AAN 204 GROUP COURSEWORK

In Partial Fulfillment of the Requirements for the course

CARDIOVASCULAR NURSING

for the degree Master of Science in Nursing – Adult Health

Submitted by:
GROUP#
Peralta, Mark A
Name
Name
Name
Name
SPUP MSN 2019 Student/s

Submitted to:
Melanie Adolfo, DNS, RN
SPUP Graduate School Faculty
Coursework #1
Hypertension
• Chronic elevation in BP > 140/90
• Etiology unknown in 90-95% of pts (“essential hypertension”)
• Always consider a secondary correctable form of hypertension, especially in pts under
age 30 or those who become hypertensive after 55.
• Isolated systolic hypertension (systolic > 160, diastolic < 90) most common in elderly pts,
due to reduced vascular compliance.
• Hypertension is the most important modifiable risk factor for coronary heart disease,
stroke, congestive heart failure, ESRD, and peripheral vascular disease.

Classifications
Labile Hypertension
• Intermittently elevated BP Persistent/Resistant hypertension
• Hypertension that does not respond to usual treatment
• One of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm,
and is a leading cause of chronic renal failure.
• Even moderate elevation of blood pressure leads to shortened life expectancy.
 Malignant hypertension
• Is severe, rapidly progressive elevation in BP that causes rapid onset of end organ
complications
 White coat hypertension
• Is elevation of BP only during clinic visits.

Hypertension can be classified either essential(primary) or secondary:

Essential hypertension indicates that no specific medical cause can be found to explain a
patient’s condition.

Secondary hypertension indicates that the high blood pressure is a result of another condition,
such as kidney disease or tumors (pheochromocytoma and paraganglioma)
Etiologies of Secondary hypertension

Renal artery stenosis

• Due to either to atherosclerosis (older men) or fibromuscular dysplasia (young women)
• Sudden onset of hypertension
• Refractory to usual antihypertensive therapy
• Abdominal bruit often audible
• Mild hypokalemia may be present due to activation of the renin-angiotensin-
aldosterone system

Renal Parenchymal Disease

• Elevated serum creatinine and abnormal urinalysis, containing protein, cells.
• Coarctation of Aorta
• Presents in children or young adults
• Constriction is usually present in aorta at origin of left subclavian artery
• Exam shows diminished, delayed femoral pulsations
• Late systolic murmur loudest over the midback

Pheochromocytoma
• A catecholamine-secreting tumor, typically of the adrenal medulla, that presents as
paroxysmal or sustained hypertension in young to middle-aged pts.
• Sudden episodes of headache, palpitations and profuse diaphoresis are common.
• Hyperaldosteronism
• Due to aldosterone-secreting adenoma or bilateral adrenal hyperplasia
• Should be suspected when hypokalemia is present in a hypertensive pt off diuretic

Hypertensive Crisis

Hypertensive emergencies
• Represent severe hypertension with acute impairment of an organ system (eg. Central
Nervous System, Cardiovascular system, Renal system)
• In these conditions, the BP should be lowered aggressively over minutes to hours
Hypertensive urgency
• Defined as a severe elevation of BP, without evidence of progressive target organ
dysfunction.
• These patients require BP control over several days to weeks

Risk Factors
• Family History
• Age
• High salt-intake
• Low potassium intake
• Obesity
• Excess alcohol consumption
• Smoking
• Stress
• Signs and Symptoms
• Headache (especially upon waking). This is the most characteristic sign.
• Epistaxis
• Dizziness
• Tinnitus
• Unsteadiness
• Blurred vision
• Depression
• Nocturia
• Retinopathy, papilledema (on fundoscopy)

Hypertension Pathophysiology (narrative form)

Arterial pressure is continuously monitored by various sensors located within the body.
Whenever arterial pressure varies from normal, multiple reflex responses are initiated, which
cause adjustments in cardiac output and total peripheral resistance, needed to return arterial
pressure to its normal value. In the short term (seconds), these adjustments are brought about
by changes in the activity of the autonomic nerves leading to the heart and peripheral vessels.
In the long term (minutes to days), other mechanisms such as changes in cardiac output
brought about by changes in blood volume play an increasingly important role in the control of
arterial pressure. Arterial hypertension is the condition of persistent, abnormal elevation of
systemic arterial or blood pressure. Hypertension affects a substantial proportion of the adult
population worldwide. Numerous genetic, environmental and behavioral factors influence the
development of hypertension. In turn, hypertension has been identified as a major causative
risk factor for cardiovascular diseases including heart and kidney disease, peripheral vascular
disease, and stroke. Authors are welcomed to send manuscripts dealing with the
pathophysiology, diagnosis and treatment of arterial hypertension, at all levels,
epidemiological, experimental, or clinical investigations.
Laboratory and Diagnostic Procedure

Recommended Laboratory tests:

• CBC
• Urinalysis
• Potassium
• FBS
• Creatinine
• Calcium
• Total Cholesterol
• HDL, LDL, and Triglycerides

Arterial line
• It is used for patients receiving more than small amounts of vasoactive drip to properly
manage blood pressure.
• It is also preferred in sick patients who are labile and whose BP is unstable.
• Certain situations absolutely require an a-line for BP monitoring: any use of any dose of
nipride, for example. This is a truly powerful drug – it works very quickly, and your
patient can rapidly get into all sorts of trouble unless you’re monitoring BP continuously.
• Also serves as a port for obtaining ABG for lab testing.

Medical treatment: Choice of antihypertensive drugs based on Patient

characteristics
• Diabetic patients and those with chronic kidney disease:
Use ACE-inhibitors or Angiotensin II antagonists to delay diabetic nephropathy
• Young patients:
Use beta-blockers unless contraindicated
• Coronary Artery Disease (CAD) patients:
Use beta-blockers, calcium channel-blockers. Avoid hydralazine(Apresoline) which is a
direct vasodilator.
• Heart Failure Patients:
 Use ACE-inhibitors and/or diuretics. Generally avoid beta-blockers and calcium-
antagonists.
• Athletes:
Avoid beta-blockers and diuretics
• Broncho-pulmonary disease patients:
Use verapamil and other calcium-antagonist. Avoid beta-blockers.
• Peripheral Vascular Disease patients:
Use calcium-antagonist(nifedipine), vasodilators, or ACE-inhibitors. Avoid beta-blockers.
• Dyslipidemic patients:
Avoid beta-blockers and diuretics.
• End-stage Renal Disease (ESRD) patients:
Use calcium-antagonists, diuretics and centrally-acting agents(clonidine, methyldopa).
Caution on ACE-inhibitors.
• For stroke patients:
Use ACE-inhibitors and/or diuretics.
• Elderly patients:
Use diuretics. Generally use lower dosages. Be wary of pseudo hypertension wherein
the elevated BP is due to brachial artery atherosclerosis and not hypertension per se.

Nursing Interventions
• Patient Teaching/Counselling
• Teaching about hypertension
• Teaching about the risk factors
• Stress therapy o Low sodium, low saturated fat diet
• Avoid stimulants (eg. Caffeine, alcohol, cigarette)
• Regular pattern of exercise
• Weight reduction if obese
• Teaching about medication
• The most common side effects of diuretics are potassium depletion and orthostatic
hypotension
• The most common side effect of the different antihypertensive drugs is orthostatic
hypotension
• Take antihypertensive medications at regular basis
• Assume sitting or lying position for few minutes
• Change position gradually
• Avoid very warm bath
• Avoid prolonged sitting or standing
• Avoid alcoholic beverages
• Lie down immediately if faintness, weakness, nausea and vomiting occur; put feet
higher than head; flex thigh muscles and wiggle toes.
• Use caution when driving or operating heavy or dangerous machinery
• Avoid cheese, beer, or wine when taking a Monoamine oxidase inhibitor (e.g. pargyline).
A severe reaction might occur, with a possibility or cerebral hemorrhage.
• Should hypotensive crisis occur, wrap legs firmly with ace bandages when ambulating.
Ace bandage helps promote venous return
• Preventing Non-compliance
• Inform the client that absence of symptoms does not indicate control of BP.
• Advise the client against abrupt withdrawal of medication; rebound hypertension may
occur.
• Device ways to facilitate remembering of taking medications(e.g. labelled containers)
Rheumatic fever

Alternative names
Acute rheumatic fever

Definition
Rheumatic fever is an inflammatory disease that may develop after an infection with
streptococcus bacteria (such as strep throat or scarlet fever ) and can involve the heart, joints,
skin, and brain.

Causes, incidence, and risk factors

Rheumatic fever is common worldwide and is responsible for many cases of damaged heart
valves. While it is far less common in the U.S. since the beginning of the 20th century, there
have been a few outbreaks since the 1980s.
Rheumatic fever primarily affects children between ages 6 and 15 and occurs approximately 20
days after strep throat or scarlet fever. In up to a third of cases, the underlying strep infection
may not have caused any symptoms.
The rate of development of rheumatic fever in individuals with untreated strep infection is
estimated to be 3%. Persons who have suffered a case of rheumatic fever have a tendency to
develop flare-ups with repeated strep infections.

Epidemiology.
A sequelae of group A streptococcal pharyngitis. Rheumatic fever is observed in the age group
susceptible to group A streptococcal infections, from 5–15 yr of age. Overcrowding is frequent
in certain group of population. streptococcal skin infection does not result in acute rheumatic
fever, but infection of the upper respiratory tract or the skin may lead to another non-
suppurative complication of streptococcal infection, acute post streptococcal
glomerulonephritis. Difference in Rheumatogenic potential of “skin strains” and “throat
strains,” can explain the phenomenon. Untreated or inadequately treated infection, leads to
rheumatic fever. Carriers are at reduced risk for development of acute rheumatic fever and
they cause spread of the organism to close family or school contacts. M types 1, 3, 5, 6, and 18
are associated with rheumatic fever.
Pathogenesis.

Two theories are:

1. a toxic effect produced by an extracellular toxin of group A streptococci on target organs
such as myocardium, valves, synovium, and brain;

2. an abnormal immune response by the human host.

Antibodies cause the immunologic damage. The latent period, 1–3 wk between the onset of the
actual group A streptococcal infection and the onset of symptoms of acute rheumatic fever,
supports immunologic mechanism.
The M protein is responsible for the organism's ability to resist phagocytosis. M protein shares
amino acid sequences with some human tissues. In Sydenham’s chorea, common antibodies to
antigens are found in the group A streptococcal cell membrane and the caudate nucleus of the
brain.

Clinical manifestations: Modified Jone’s Criteria

Carditis: mild or severe carditis, leading to heart failure. Pancarditis involves the pericardium,
epicardium, myocardium, and endocardium Carditis results in chronic changes. Valvular
insufficiency, most frequently affecting mitral and the aortic valve. Isolated involvement of the
aortic valve is rare. In chronic stage, scarring of the valve or calcified valve tissue may lead to
stenosis. A combination of insufficiency and stenosis is found. pericarditis, pericardial effusion,
and arrhythmias (usually first-degree heart block, third degree or complete heart block may
occur).

Polyarthritis. The arthritis of is tender. Refuse even bed sheets or clothing to cover an affected
joint. The joints are red, warm, and swollen. Migratory and affects several joints: the elbows,
knees, ankles, and wrists. Rare in the fingers, toes, or spine. Effusions may be present. Aspirate
= polymorphonuclear leukocytosis is found - no specific laboratory findings in the synovial fluid.
The arthritis does not result in chronic joint disease. After anti-inflammatory therapy is begun,
the arthritis may disappear in 12–24 hr. Untreated, it may persist for a week or more. Because
of treatment with anti-inflammatory drugs, the migratory nature does not develop.
Chorea: Sydenham chorea occurs much later than other manifestations. Choreoathetoid
movements may begin insidiously. The period following pharyngitis may be several months, and
the movements are often very difficult to detect at the onset. Deterioration in their
handwriting. Emotional lability is a frequent finding. Sydenham chorea may affect all four
extremities or may be unilateral. frequently it is the only symptom of rheumatic fever. It usually
disappears within weeks to months. It may recur. Pronator sign, Bishop’s sign, milk maid sign,
hung up reflex, poor handwriting, no abnormal movement in sleep.

Erythema Marginatum: Major manifestation, very difficult to diagnose. Nonspecific pink

macules that are seen over the trunk, later in its fully developed form, blanching occurs in the
middle of the lesions, sometimes with fusing of the borders, resulting in a serpiginous-looking
lesion. This rash can be made worse with application of heat, but characteristically it is transient
– that is disappears in a few hours. The rash does not itch. It often occurs in patients with
chronic carditis. The rash of erythema marginatum can be mistaken for the rash seen with Lyme
disease.

Subcutaneous Nodules: observed in patients with severe carditis. pea-sized nodules are firm
and nontender, and there is no inflammation. They are seen on the extensor surfaces of the
joints, such as the knees and elbows, and over the spine.

Symptoms
• Fever
• Joint pain, migratory arthritis -- involving primarily knees, elbows, ankles, and wrists
• Joint swelling; redness or warmth
• Abdominal pain
• Skin rash (erythema marginatum)
 Skin eruption on the trunk and upper part of arms or legs
 Eruptions that are ring-shaped or snake-like in appearance
• Skin nodules
• Sydenham's chorea -- emotional instability, muscular weakness and rapid,
uncoordinated jerky movements affecting primarily the face, feet and hands
• Epistaxis (nosebleeds)
• Cardiac (heart) involvement which may be asymptomatic or may result in shortness of
breath, chest pain

Signs and tests

Given the different manifestations of this disease, there is no specific test which can definitively
establish a diagnosis. In addition to a careful physical examination of heart sounds, skin, and
joints, blood samples may be taken as part of the evaluation. These include tests for recurrent
strep infection (ASO or antiDNAse B), complete blood counts, and sedimentation rate (ESR). As
part of the cardiac evaluation, an electrocardiogram may also be done.
In order to standardize the diagnosis of rheumatic fever, several minor and major criteria have
been developed. These criteria, in conjunction with evidence of recent streptococcal infection,
establish a diagnosis of rheumatic fever.

The major diagnostic criteria include:

• Carditis (heart inflammation)
• Polyarthritis
• Subcutaneous skin nodules
• Chorea (Sydenham's chorea)
• Erythema marginatum.

The minor criteria include fever, arthralgia (joint pain), elevated erythrocyte sedimentation
rate, and other laboratory findings.
Two major criteria, or one major and two minor criteria, when there is also evidence of a
previous strep infection (positive culture or rising antibody level -- ASO or antiDNAse B) support
the diagnosis of rheumatic fever.

Treatment
The management of acute rheumatic fever is geared towards the reduction of inflammation
with anti-inflammatory medications such as aspirin or corticosteroids. Individuals with positive
cultures for strep throat should also be treated with antibiotics. Another important cornerstone
in treating rheumatic fever includes the continuous use of low dose antibiotics (such as
penicillin, sulfadiazine, or erythromycin) to prevent recurrence.

Expectations (prognosis)
The recurrence of rheumatic fever is relatively common in the absence of maintenance of low
dose antibiotics, especially during the first 3 - 5 years after the first episode of rheumatic fever.
Heart complications may be long-term and severe, particularly if the heart valves are involved.

Complications
 • Damage to heart valves (in particular, mitral stenosis and aortic stenosis)
• Endocarditis
• Heart failure
• Arrhythmias
• Pericarditis
• Sydenham's chorea

Nursing management:
• Assess pain level and joints for inflammation—effects on mobility/ADLs
• Assess pain level and joints for inflammation—effects on mobility/ADLs
• Administer pain medication if needed
• Assess fatigue/energy level and whether patient is getting sufficient rest
• Instruct patient on balancing energy and rest during illness
• Reduce physical/environmental discomforts, limit environmental stimuli
Clinical Practice Guidelines in the management of Cardiovascular Disorders

Coronary Artery Disease – Unstable Angina, NSTEMI, STEMI

An acute coronary syndrome (ACS) occurs when atherosclerotic coronary plaque

becomes unstable, leading to a series of events that eventually results in partial or complete
thrombotic occlusion of a coronary artery. Acute Coronary Syndromes are classified or
categorized into unstable angina, Non-ST Segment Elevation Myocardial Infarction (NSTEMI)
and ST Segment Elevation Myocardial Infarction (STEMI).

Unstable Angina Pectoris – the cardiac enzymes remain normal or are only very minimally
elevated.
Three different presentations of unstable angina exist:
1. Exertional angina of new onset (even it relieved with rest and requiring a consistent
amount of exertion to produce symptoms, angina is considered unstable when it
first occurs)
2. Exertional angina that was previously stable and now occurs with less physical
exertion.
3. Angina symptoms at rest without physical exertion

Non-ST Segment Elevation Myocardial Infarction (NSTEMI)

Anginal symptoms occurs at rest that result in myocardial necrosis with no ST segment
elevation on the 12-lead ECG; identified by elevated cardiac biomarkers.

ST Segment Elevation Myocardial Infarction (STEMI)

Anginal symptoms occurs at rest that result in myocardial necrosis with ST segment
elevation on the 12-lead ECG; identified by elevated cardiac biomarkers.

Pathophysiology

The vulnerable plaque that formed from the atherosclerotic process is responsible for
the acute coronary syndromes and coronary artery thrombosis. Within the necrotic core of the
plaque is a tissue factor which when exposed to the bloodstream, activates the clotting cascade
resulting to thrombosis.
 Plaque rupture or erosion and thrombosis frequently occur at the site of modest
coronary stenosis (˂50% luminal narrowing) which suggests that even if the stress test results
were normal, the risk for an ACS is still present. Take note that stress testing is the most
sensitive method to detect stenosis of 70% or greater.

Unstable angina deals with blood flow obstacles causing a lack of perfusion to the
myocardium. Initial perfusion starts directly from the heart into the aorta and subsequently
into the coronary arteries which supply their respective portions of the heart. The left coronary
artery will divide into the circumflex and the left anterior descending artery. Subsequently, this
will divide into much smaller branches, the same with the right coronary artery. Unstable
angina results when the blood flow is impeded to the myocardium. Usually, this block can be
from intraluminal plaque formation, intraluminal thrombosis, vasospasm, and elevated blood
pressure. Most often, combination of these is the provoking factor.

Factors that increase myocardial oxygen demand:

• Arrhythmias
• Fever
• Hypertension
• Cocaine use
• Aortic stenosis
• AV shunts
• Anemia
• Thyrotoxicosis
• Pheochromocytoma
• Congestive Heart Failure

Epidemiology

Coronary artery disease affects a large portion of the population. It is estimated that
coronary artery disease causes more than a third of deaths in people over the age of 35. It is
the leading cause of death in this particular age group. Roughly 18 million within the United
States alone are estimated to be affected by this disease. The incidence is higher in men, but as
individuals surpass the age of 75, the incidence of males and females becomes much closer.
Other risk factors include obesity, diabetes, hypertension, high cholesterol, smoking history,
cocaine or amphetamine abuse, family history, chronic kidney disease, HIV, autoimmune
disorders, and anemia.
 The mean age of presentation is 62 and women tend to be older than men. African
Americans tend to present at a younger age.

History and Physical Examination

Patients will often present with chest pain and shortness of breath. The chest pain will
often be described as pressure-like. Tightness, burning, sharp type of pain can be described.
Usually, patients will report discomfort as opposed to actual pain. The pain will often radiate to
the jaw or arms, both left and right sides can be affected. Constitutional symptoms such as
nausea, vomiting, diaphoresis, dizziness, and palpitations may also be present. Exertion may
worsen and rest can ease the pain. Nitroglycerin and aspirin administration may also improve
the pain. One distinguishing factor of unstable angina is that the pain may not completely
resolve with these reported relieving factors. A patient’s report of an increase in episodes of
chest pain that takes longer to resolve and an increase in the severity of symptoms is suggestive
of unstable angina as the more likely diagnosis. This is important to note as it indicates
impending myocardial infarction, and ST Segment Elevation Myocardial Infarction (STEMI)
should be evaluated expeditiously as the risk of morbidity and mortality are higher in these
cases.

The exam will likely be normal, but the patient may be clutching at their chest, sweating,
have labored breathing, their heart sounds may be tachycardic, and rales may be heard due to
pulmonary edema.

Findings suggestive of a high-risk situation include:

• Dyskinetic apex
• Elevated jugular vein pressure
• Presence of S3 or S4
• New apical systolic murmur
• Presence of rales and crackles
• Hypotension

Diagnosis

The diagnosis of unstable angina, STEMI, and/or NSTEMI is predominantly based on the
ECG and cardiac enzymes or biomarkers.
 The patient should have an ECG to evaluate for ischemic signs or possible STEMI. The
ECG in unstable angina may show hyperacute T-wave, flattening of the T-waves, inverted T-
waves, and ST depression. ST elevations indicate STEMI and these patients should be treated
with percutaneous coronary intervention or thrombolytics while they wait on the availability of
a catheterization lab. Any number of arrhythmias may be present in acute coronary syndrome
including junctional rhythms, sinus tachycardia, ventricular tachycardia, ventricular fibrillation,
left bundle branch block, and others. However, most commonly, the patient will be in sinus
rhythm, especially in the scenario of unstable angina as opposed to infarcted tissue.

The patient should also have lab work that includes a complete blood count evaluating
for anemia, platelet count, and basic metabolic profile evaluating for electrolyte abnormalities.
A troponin test should be performed to determine if any of the myocardium has infarcted. A
pro-brain natriuretic peptide (Pro-BNP) can also be checked, as an elevated level is associated
with higher mortality. Coagulation studies may be appropriate if the patient will be
anticoagulated or anticoagulation is anticipated. Often, a chest x - ray will show the heart size
and the size of the mediastinum so the physician may screen for dissection and other
explanations of chest pain.

It should be made clear that the history should be screened for other emergent causes
of chest pain, shortness of breath, pulmonary embolism, aortic dissection esophageal rupture,
pneumonia, and pneumothorax. The patient should be kept on a cardiac monitor to evaluate
for any rhythm changes. Further testing may include any number of cardiac stress tests –
walking treadmill stress test, stress echocardiogram, myocardial perfusion imaging, cardiac
CT/MRI, or the gold standard, cardiac catheterization.

Acute coronary syndrome risk assessment:

• Prior MI, or known history of CAD

• Transient ECG or hemodynamic changes during chest pain
• Chest, neck or left arm with documented angina
• ST depression or elevation of more than 1 mm
• Marked symmetrical T wave inversion

Treatment/Management

Early Invasive vs. Initial Conservative

 An early invasive strategy refers to proceeding to coronary angiography with possible
percutaneous coronary intervention – also known as PCI or coronary stenting – within 4 to 24
hours of hospital admission. An initial conservative management consists of medical therapy
only, without plans to proceed to coronary angiography and PCI.

Factors that would warrant an early invasive strategy:

• Increased cardiac biomarkers (troponin, CK-MB)

• New ST segment depression
• Signs or symptoms of CHF
• Hemodynamic instability
• Sustained ventricular tachycardia or ventricular fibrillation
• Recent coronary intervention within 6 months
• Prior coronary artery bypass grafting
• Reduced left ventricular systolic function
• Recurrent angina at rest or with low level activity
• High-risk findings from non-invasive testing

The mainstay of treatment focuses on improving perfusion of the coronary arteries

which is done in several ways.

Patients are often treated with aspirin for its antiplatelet therapies, 162 to 325mg per
orem or 300mg rectally if the patient is unable to swallow. The aspirin should be administered
within 30 minutes. Nitroglycerin improves perfusion by vasodilation of the coronaries allowing
improved flow and improved blood pressure. This decreases the recently workload the heart
has to perform and decreases the energy demand of the heart.

Clopidogrel is an option for patients not able to tolerate aspirin. Prasugrel is more
effective than clopidogrel but is associated with a higher risk of bleeding. Recently ticagrelor
has been approved in addition to aspirin to reduce the rate of thrombotic cardiac events.

Supplemental oxygen should be given as well via nasal cannula to maintain appropriate
oxygen saturation. These 3 actions are the quickest and most important functions to be
performed in evaluating and treating for unstable angina. In patients with continued pain or
longer recovery time, the patient’s response should be evaluated because they are at much
higher risk for myocardial infarction.
Other potential therapies include anticoagulation with either low or high molecular weight
heparin. Beta – blockers also can decrease the energy demand by decreasing blood pressure
and heart rate.

Cardiac angiography is indicated in unstable angina if the patient has:

• Cardiogenic shock
• Depressed ejection fraction
• Angina refractory to pharmacological therapy
• Unstable arrhythmias

Early PCI in NSTEMI (within 6 hours) has been shown to have lower mortality than those who
undergo delayed PCI.

Differential Diagnosis
• Aortic dissection
• Pericarditis
• Pneumothorax
• Pulmonary embolism
• Peptic ulcer disease

The medical management of unstable angina and non-STEMI consists of beta blocker therapy,
angiotensin converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs),
aldosterone antagonists, HMG-CoA reductase inhibitors, calcium channel blockers, nitrates,
antiplatelet therapy and anticoagulation therapy. Treatment with fibrinolytics, or tPA, is not
recommended for unstable angina and non-STEMI management – and only for STEMI in certain
instances.

Prognosis

The key complications of unstable angina include:

• Myocardial Infarction
• Stroke
• Death
Negative prognostic factors include:
• Low ejection fraction
• Ongoing congestive heart failure
• Hemodynamic instability
• Recurrent episodes of angina despite maximal therapy

Prevention, Deterrence, Patient Education and Nursing Responsibilities

The goals of prevention are to enable the patient to resume all daily living activities,
preserve myocardial function and prevent future cardiac events.

Primary prevention refers to controlling cardiovascular disease risk factors to stop the
first CV event from occurring. It consist predominantly of controlling CVD risk factors such as
LDL cholesterol, tobacco use, hypertension and obesity. Treatment of lipid disorders for primary
prevention include dietary and lifestyle modifications and medical therapy with HMG-CoA
reductase inhibitors. The American college of Cardiology/American Heart Association guidelines
released in 2013 recommend high-intensity statin therapy (defined as a ˃50% reduction in LDL)
without any specific target LDL levels in patients with clinical vascular disease, such as ACS, less
than age 75 years. Those older than 75 years should receive moderate-intensity statin therapy
(defined as 30-50% reduction in LDL) without specific targets to achieve.

Secondary prevention refers to therapy aimed at reducing the risk for ACS in patient
with diagnosed CAD or a coronary risk equivalents. Coronary risk equivalents (10-year risk for
cardiac event ˃20%) include the following:
• Non-coronary atherosclerotic disease: peripheral arterial disease, or PAD, carotid artery
disease, renal artery disease, abdominal aortic aneurysm
• Type 2 diabetes
• Multiple risk factors: using the Framingham risk score, a 10-year risk for a cardiac event
is greater than 20%
• Chronic Kidney disease

Secondary prevention includes antiplatelet therapy and a HMG-CoA reductase inhibitor

regardless of the serum LDL cholesterol level.
Lifestyle
Smoking cessation is mandatory to prevent recurrent cardiac events. This applies to
everyone in the household. Lipid-lowering should try and obtain a target LDL cholesterol level
of 70mg/dl or lower, an HDL level of at least 35mg/dl, and a triglyceride level of less than
200mg/dl.

Control of Hypertension
The target blood pressure should be below 140/90mmHg, at the same time the patient
should decrease the intake of sodium and alcohol.

Diabetes Mellitus Management

Blood sugar levels may be decreased with diet, exercise or pharmacotherapy.

Weight Management and Nutritional Counseling

The patient should be encouraged to lose weight and achieve a body mass index (BMI)
of 25kg/m

Activity Management
Patients at risk for unstable angina should avoid intense physical activity especially in cold
weather.

Congestive Heart Failure (CHF)

Description
Congestive heart failure (CHF) is a chronic progressive condition that affects the
pumping power of your heart muscles. While often referred to simply as “heart failure,” CHF
specifically refers to the stage in which fluid builds up around the heart and causes it to pump
inefficiently.

Pathophysiology
The syndrome of CHF arises as a consequence of an abnormality in cardiac structure,
function, rhythm, or conduction. In developed countries, ventricular dysfunction accounts for
the majority of cases and results mainly from myocardial infarction (systolic dysfunction),
hypertension (diastolic and systolic dysfunction), or in many cases both. Degenerative valve
disease, idiopathic cardiomyopathy, and alcoholic cardiomyopathy are also major causes of
heart failure. Heart failure often occurs in elderly patients who have multiple comorbid
conditions (eg, angina, hypertension, diabetes, and chronic lung disease). Some common
comorbidities such as renal dysfunction are multifactorial (decreased perfusion or volume
depletion from overdiuresis), whereas others (eg, anemia, depression, disorders of breathing,
and cachexia) are poorly understood.
CHF indicates not only an inability of the heart to maintain adequate oxygen delivery; it
is also a systemic response attempting to compensate for the inadequacy. The determinants of
cardiac output include heart rate and stroke volume. The stroke volume is further determined
by the preload (the volume that enters the left ventricle), contractility, and afterload (the
impedance of the flow from the left ventricle). These variables are important in under standing
the pathophysiologic consequences of heart failure and the potential treatments. Furthermore,
an appreciation of cardiopulmonary interactions is important in our understanding of heart
failure. In the simplest terms, the heart can be viewed as a dynamic pump. It is not only
dependent on its inherent properties, but also on what is pumped in and what it must pump
against. The preload characterizes the volume that the pump is given to send forward, the
contractility characterizes the pump, and the afterload determines what the heart must work
against.
The preload is often expressed as the end-diastolic pressure/volume of the left ventricle
and is clinically assessed by measuring the right atrial pressure. However, the preload is not
only dependent on intravascular volume; it is also influenced by any restriction to ventricular
filling. Since the heart resides in the thoracic cavity, an increased positive pleural pressure (as
seen with dynamic hyperinflation in chronic obstructive pulmonary disease or asthma) can
reduce right-atrial pressure (which equals central venous pressure minus pleural pressure) and
thus reduce ventricular filling. The cardiac pump is a muscle and will respond to the volume it is
given with a determined output. If volume increases, so will the amount pumped out in a
normal physiologic state, to a determined plateau; this relationship is described by the Frank-
Starling law.
A concept that is often poorly understood is the diastolic function of the heart. Diastolic
function is determined by 2 factors: the elasticity or distensibility of the left ventricle, which is a
passive phenomenon, and the process of myocardial relaxation, which is an active process that
requires metabolic energy.6 Relaxation of the myocardium occurs in early diastole, and the
“untwisting” of the left ventricle is an active process that produces a suction effect that
augments left-ventricular filling. Loss of normal leftventricular distensibility or relaxation by
either structural changes (eg, left-ventricular hypertrophy) or functional changes (eg, ischemia)
impairs ventricular filling (preload). The exercise intolerance seen with diastolic dysfunction
largely results from the impairment of ventricular filling, which elevates left-atrial pressure and
pulmonary venous pressure and causes pulmonary congestion. Additionally, inadequate cardiac
output during exercise results in poor perfusion of skeletal muscles, especially the leg muscles
and the accessory muscles of respiration.
 The second variable of stroke volume is cardiac contractility, which represents the
muscular pumping of the heart and is commonly expressed as the ejection fraction. Based on
autonomic input, the heart will respond to the same preload with different stroke volumes,
depending on inherent characteristics of the heart. A heart with normal systolic function will
maintain an ejection fraction of over 50–55%. A previous myocardial infarction may result in
nonfunctioning myocardium that will impair contractility. A recent concept is that ischemic
myocardial tissue can be nonfunctioning (hibernating) but revitalized by surgical or medical
therapy directed at ischemic heart disease. Other depressants of myocardial systolic function
include pharmacologic agents (calcium-channel blockers), hypoxemia, and severe acidosis.
The final determinant of stroke volume is afterload. In basic terms, afterload is the load
that the pump has to work against, which is usually clinically estimated by the mean arterial
pressure. The normal cardiac output is relatively insensitive to afterload up to 140 mm Hg.
However, the afterload represents not only the vascular resistance but also the wall tension
and intrathoracic pressure that the myocardium must work against. Together, these 3 variables
are impaired in the patient with CHF.
The failing heart in CHF can be best evaluated with the above variables considered
together. If cardiac output falls, either the heart rate or stroke volume must change in order to
maintain perfusion. If stroke volume cannot be maintained, then heart rate must increase to
maintain cardiac output. However, the pathophysiology behind CHF includes not only a
structural abnormality; it also includes the cardiovascular response to poor perfusion with the
activation of the neurohumoral system. Activation of the renin-angiotensin system attempts to
increase preload by stimulating retention of salt and water, increasing vasoconstriction (and,
thus, afterload), and augmenting cardiac contractility. Initially, this response will suffice, but
prolonged activation results in loss of myocytes and maladaptive changes in the surviving
myocytes and the extracellular matrix. The stressed myocardium undergoes remodeling and
dilation in response to the insult. This process also has detrimental effects on the functioning of
the lungs, kidneys, muscles, blood vessels, and probably other organs. Remodeling also results
in additional cardiac decompensation from complications, including mitral regurgitation from
valvular annulus stretching, and cardiac arrhythmias from atrial remodeling.
The respiratory care provider often becomes involved with the CHF patient as the
elevated end-diastolic pressure leads to pulmonary edema and dyspnea. Patients’ presentation
can greatly differ, depending on the chronicity of the disease. For instance, most patients
experience dyspnea when pulmonary-artery occlusion pressure exceeds 25 mm Hg. However,
the patient with longstanding CHF can tolerate filling pressure up to 40 mm Hg. The lung
provides multiple mechanisms to avoid the consequences of pulmonary edema. Initially, as
pressure increases, pulmonary capillaries are recruited and increase capacitance to deal with
the added volume. As pressure continues to increase, volume can be diverted from the alveoli
to the interstitium. At this point, by action of pressure gradients, fluid will form in the
interlobular septae and the perihilar region. As noted above, chronic heart failure is associated
with increased venous capacitance and lymphatic drainage of the lung. As a result, crackles are
often absent, even in the setting of elevated pulmonary capillary pressure. Continued sodium
retention preferentially results in peripheral edema and, ultimately, in the development of
pleural effusions. With acute decompensation, the pulmonarycapillary membrane may
succumb to increased pressure, with shearing of the capillary and release of fluid, protein, and
occasionally red blood cells into the alveoli. The lungs’ response will include cough, to expel the
fluid in the alveoli. The long-term response to elevated pulmonary venous pressure includes
interstitial fibrosis with thickening of the alveolar membrane. Thus, severe, chronic heartfailure
can result in interstitial fibrosis and a restrictivelung disease.

Types of Heart Failure

Left-sided heart failure

The heart's pumping action moves oxygen-rich blood as it travels from the lungs to the
left atrium, then on to the left ventricle, which pumps it to the rest of the body. The left
ventricle supplies most of the heart's pumping power, so it's larger than the other chambers
and essential for normal function. In left-sided or left ventricular (LV) heart failure, the left side
of the heart must work harder to pump the same amount of blood.
There are two types of left-sided heart failure. Drug treatments are different for the two types.

• Heart failure with reduced ejection fraction (HFrEF), also called systolic failure: The left
ventricle loses its ability to contract normally. The heart can't pump with enough force
to push enough blood into circulation.
• Heart failure with preserved ejection fraction (HFpEF), also called diastolic failure (or
diastolic dysfunction): The left ventricle loses its ability to relax normally (because the
muscle has become stiff). The heart can't properly fill with blood during the resting
period between each beat.
Right-sided heart failure
The heart's pumping action moves "used" blood that returns to the heart through the
veins through the right atrium into the right ventricle. The right ventricle then pumps the blood
back out of the heart into the lungs to be replenished with oxygen.
Right-sided or right ventricular (RV) heart failure usually occurs as a result of left-sided
failure. When the left ventricle fails, increased fluid pressure is, in effect, transferred back
through the lungs, ultimately damaging the heart's right side. When the right side loses
pumping power, blood backs up in the body's veins. This usually causes swelling or congestion
in the legs, ankles and swelling within the abdomen such as the GI tract and liver (causing
ascites).
Causes
Heart failure often develops after other conditions have damaged or weakened your
heart. However, the heart doesn't need to be weakened to cause heart failure. It can also occur
if the heart becomes too stiff.
In heart failure, the main pumping chambers of your heart (the ventricles) may become
stiff and not fill properly between beats. In some cases of heart failure, your heart muscle may
become damaged and weakened, and the ventricles stretch (dilate) to the point that the heart
can't pump blood efficiently throughout your body.
Over time, the heart can no longer keep up with the normal demands placed on it to
pump blood to the rest of your body.
An ejection fraction is an important measurement of how well your heart is pumping
and is used to help classify heart failure and guide treatment. In a healthy heart, the ejection
fraction is 50 percent or higher — meaning that more than half of the blood that fills the
ventricle is pumped out with each beat.
But heart failure can occur even with a normal ejection fraction. This happens if the
heart muscle becomes stiff from conditions such as high blood pressure.
Heart failure can involve the left side (left ventricle), right side (right ventricle) or both
sides of your heart. Generally, heart failure begins with the left side, specifically the left
ventricle — your heart's main pumping chamber.

Clinical Manifestations/Diagnosis
Patients with heart failure can have decreased exercise tolerance with dyspnea, fatigue,
generalized weakness, and fluid retention, with peripheral or abdominal swelling and possibly
orthopnea. Patient history and physical examination are useful to evaluate for alternative or
reversible causes. Nearly all patients with heart failure have dyspnea on exertion. However,
heart failure accounts for only 30 percent of the causes of dyspnea in the primary care setting.
The absence of dyspnea on exertion only slightly decreases the probability of systolic heart
failure, and the presence of orthopnea or paroxysmal nocturnal dyspnea has a small effect in
increasing the probability of heart failure.
The presence of a third heart sound (ventricular filling gallop) is an indication of
increased left ventricular end-diastolic pressure and a decreased LVEF. Despite being relatively
uncommon findings, a third heart sound and displaced cardiac apex are good predictors of left
ventricular dysfunction and effectively rule in the diagnosis of systolic heart failure.
The presence of jugular venous distention, hepatojugular reflux, pulmonary rales, and
pitting peripheral edema is indicative of volume overload and enhances the probability of a
heart failure diagnosis. Jugular venous distention and hepatojugular reflex have a moderate
effect, whereas the others, along with cardiac murmurs, have only a small effect on the
diagnostic probability. The absence of any of these findings is of little help in ruling out heart
failure.

Laboratory Evaluation for Heart Failure and Selected Alternative Causes

Initial tests
• B-type natriuretic peptide level
• Calcium and magnesium levels (diuretics, cause of arrhythmia)
• Complete blood count (anemia)
• Liver function (hepatic congestion, volume overload)
• Renal function (renal causes)
• Serum electrolyte level (electrolyte imbalance)
• Thyroid-stimulating hormone level (thyroid disorders)
• Urinalysis (renal causes)

Other tests for alternative causes

• Arterial blood gases (hypoxia, pulmonary disease)
• Blood cultures (endocarditis, systemic infection)
• Human immunodeficiency virus (cardiomyopathy)
• Lyme serology (bradycardia/heart block)
• Serum ferritin level, transferrin saturation (macrocytic anemia, hemochromatosis)
• Thiamine level (deficiency, beriberi, alcoholism)
• Troponin and creatine kinase-MB levels (myocardial infarction, myocardial injury)

Tests for comorbid conditions, risk management

A1C level (diabetes mellitus)

Lipid profile (hyperlipidemia)

Complications

If you have heart failure, your outlook depends on the cause and the severity, your overall
health, and other factors such as your age. Complications can include:
Kidney damage or failure. Heart failure can reduce the blood flow to your kidneys, which can
eventually cause kidney failure if left untreated. Kidney damage from heart failure can require
dialysis for treatment.

Heart valve problems. The valves of your heart, which keep blood flowing in the proper
direction through your heart, may not function properly if your heart is enlarged or if the
pressure in your heart is very high due to heart failure.

Heart rhythm problems. Heart rhythm problems (arrhythmias) can be a potential complication
of heart failure.

Liver damage. Heart failure can lead to a buildup of fluid that puts too much pressure on the
liver. This fluid backup can lead to scarring, which makes it more difficult for your liver to
function properly.

Some people's symptoms and heart function will improve with proper treatment. However,
heart failure can be life-threatening. People with heart failure may have severe symptoms, and
some may require heart transplantation or support with a ventricular assist device.

Prevention

The key to preventing heart failure is to reduce your risk factors. You can control or eliminate
many of the risk factors for heart disease — high blood pressure and coronary artery disease,
for example — by making lifestyle changes along with the help of any needed medications.

Lifestyle changes you can make to help prevent heart failure include:

Not smoking
Controlling certain conditions, such as high blood pressure and diabetes
Staying physically active
Eating healthy foods
Maintaining a healthy weight
Reducing and managing stress

Treatment
Heart failure is a chronic disease needing lifelong management. However, with treatment, signs
and symptoms of heart failure can improve, and the heart sometimes becomes stronger.
Treatment may help you live longer and reduce your chance of dying suddenly.

Doctors sometimes can correct heart failure by treating the underlying cause. For example,
repairing a heart valve or controlling a fast heart rhythm may reverse heart failure. But for most
people, the treatment of heart failure involves a balance of the right medications and, in some
cases, use of devices that help the heart beat and contract properly.

Medications
Doctors usually treat heart failure with a combination of medications. Depending on your
symptoms, you might take one or more medications, including:

Angiotensin-converting enzyme (ACE) inhibitors. These drugs help people with systolic heart
failure live longer and feel better. ACE inhibitors are a type of vasodilator, a drug that widens
blood vessels to lower blood pressure, improve blood flow and decrease the workload on the
heart. Examples include enalapril (Vasotec), lisinopril (Zestril) and captopril (Capoten).

Angiotensin II receptor blockers. These drugs, which include losartan (Cozaar) and valsartan
(Diovan), have many of the same benefits as ACE inhibitors. They may be an alternative for
people who can't tolerate ACE inhibitors.

Beta blockers. This class of drugs not only slows your heart rate and reduces blood pressure but
also limits or reverses some of the damage to your heart if you have systolic heart failure.
Examples include carvedilol (Coreg), metoprolol (Lopressor) and bisoprolol (Zebeta).

These medicines reduce the risk of some abnormal heart rhythms and lessen your chance of
dying unexpectedly. Beta blockers may reduce signs and symptoms of heart failure, improve
heart function, and help you live longer.
Diuretics. Often called water pills, diuretics make you urinate more frequently and keep fluid
from collecting in your body. Diuretics, such as furosemide (Lasix), also decrease fluid in your
lungs so you can breathe more easily.

Because diuretics make your body lose potassium and magnesium, your doctor may also
prescribe supplements of these minerals. If you're taking a diuretic, your doctor will likely
monitor levels of potassium and magnesium in your blood through regular blood tests.

Aldosterone antagonists. These drugs include spironolactone (Aldactone) and eplerenone

(Inspra). These are potassium-sparing diuretics, which also have additional properties that may
help people with severe systolic heart failure live longer.

Unlike some other diuretics, spironolactone and eplerenone can raise the level of potassium in
your blood to dangerous levels, so talk to your doctor if increased potassium is a concern, and
learn if you need to modify your intake of food that's high in potassium.

Inotropes. These are intravenous medications used in people with severe heart failure in the
hospital to improve heart pumping function and maintain blood pressure.

Digoxin (Lanoxin). This drug, also referred to as digitalis, increases the strength of your heart
muscle contractions. It also tends to slow the heartbeat. Digoxin reduces heart failure
symptoms in systolic heart failure. It may be more likely to be given to someone with a heart
rhythm problem, such as atrial fibrillation.

You may need to take two or more medications to treat heart failure. Your doctor may
prescribe other heart medications as well — such as nitrates for chest pain, a statin to lower
cholesterol or blood-thinning medications to help prevent blood clots — along with heart
failure medications. Your doctor may need to adjust your doses frequently, especially when
you've just started a new medication or when your condition is worsening.

You may be hospitalized if you have a flare-up of heart failure symptoms. While in the hospital,
you may receive additional medications to help your heart pump better and relieve your
symptoms. You may also receive supplemental oxygen through a mask or small tubes placed in
your nose. If you have severe heart failure, you may need to use supplemental oxygen long
term.
Surgery and medical devices
In some cases, doctors recommend surgery to treat the underlying problem that led to heart
failure. Some treatments being studied and used in certain people include:

Coronary bypass surgery. If severely blocked arteries are contributing to your heart failure, your
doctor may recommend coronary artery bypass surgery. In this procedure, blood vessels from
your leg, arm or chest bypass a blocked artery in your heart to allow blood to flow through your
heart more freely.

Heart valve repair or replacement. If a faulty heart valve causes your heart failure, your doctor
may recommend repairing or replacing the valve. The surgeon can modify the original valve to
eliminate backward blood flow. Surgeons can also repair the valve by reconnecting valve
leaflets or by removing excess valve tissue so that the leaflets can close tightly. Sometimes
repairing the valve includes tightening or replacing the ring around the valve (annuloplasty).

Valve replacement is done when valve repair isn't possible. In valve replacement surgery, the
damaged valve is replaced by an artificial (prosthetic) valve.

Certain types of heart valve repair or replacement can now be done without open heart
surgery, using either minimally invasive surgery or cardiac catheterization techniques.

Implantable cardioverter-defibrillators (ICDs). An ICD is a device similar to a pacemaker. It's

implanted under the skin in your chest with wires leading through your veins and into your
heart.

The ICD monitors the heart rhythm. If the heart starts beating at a dangerous rhythm, or if your
heart stops, the ICD tries to pace your heart or shock it back into normal rhythm. An ICD can
also function as a pacemaker and speed your heart up if it is going too slow.

Cardiac resynchronization therapy (CRT), or biventricular pacing. A biventricular pacemaker

sends timed electrical impulses to both of the heart's lower chambers (the left and right
ventricles) so that they pump in a more efficient, coordinated manner.
Many people with heart failure have problems with their heart's electrical system that cause
their already-weak heart muscle to beat in an uncoordinated fashion. This inefficient muscle
contraction may cause heart failure to worsen. Often a biventricular pacemaker is combined
with an ICD for people with heart failure.

Ventricular assist devices (VADs). A VAD, also known as a mechanical circulatory support device,
is an implantable mechanical pump that helps pump blood from the lower chambers of your
heart (the ventricles) to the rest of your body. A VAD is implanted into the abdomen or chest
and attached to a weakened heart to help it pump blood to the rest of your body.

Doctors first used heart pumps to help keep heart transplant candidates alive while they waited
for a donor heart. VADs may also be used as an alternative to transplantation. Implanted heart
pumps can enhance the quality of life of some people with severe heart failure who aren't
eligible for or able to undergo heart transplantation or are waiting for a new heart.

Heart transplant. Some people have such severe heart failure that surgery or medications don't
help. They may need to have their diseased heart replaced with a healthy donor heart.

Heart transplants can improve the survival and quality of life of some people with severe heart
failure. However, candidates for transplantation often have to wait a long time before a
suitable donor heart is found. Some transplant candidates improve during this waiting period
through drug treatment or device therapy and can be removed from the transplant waiting list.

A heart transplant isn't the right treatment for everyone. A team of doctors at a transplant
center will evaluate you to determine whether the procedure may be safe and beneficial for
you.

Care Plan & Management

Decreased Cardiac Output

Assessment
The patient may manifest the following:
• Pale conjunctiva, nail beds, and buccal mucosa
• irregular rhythm of pulse
 • bradycardia
• generalized weakness

Diagnosis
• Decreased cardiac output r/t [altered heart rate and rhythm] AEB [bradycardia]
• Planning
• Short Term: After 3-4 hours of nursing interventions, the patient will participate in
activities that reduce the workload of the heart.
• Long Term: After 2-3 days of nursing interventions, the patient will be able to display
hemodynamic stability.
• Nursing Interventions
• Assess for abnormal heart and lung sounds.
• Rationale: Allows detection of left-sided heart failure that may occur with chronic renal
failure patients due to fluid volume excess as the diseased kidneys are unable to excrete
water.
• Monitor blood pressure and pulse.
• Rationale: Patients with renal failure are most often hypertensive, which is attributable
to excess fluid and the initiation of the rennin-angiotensin mechanism.
• Assess mental status and level of consciousness.
• Rationale: The accumulation of waste products in the bloodstream impairs oxygen
transport and intake by cerebral tissues, which may manifest itself as confusion,
lethargy, and altered consciousness.
• Assess patient’s skin temperature and peripheral pulses.
• Rationale: Decreased perfusion and oxygenation of tissues secondary to anemia and
pump ineffectiveness may lead to decreased in temperature and peripheral pulses that
are diminished and difficult to palpate.
• Monitor results of laboratory and diagnostic tests.
• Rationale: Results of the test provide clues to the status of the disease and response to
treatments.
• Monitor oxygen saturation and ABGs.
• Rationale: Provides information regarding the heart’s ability to perfuse distal tissues
with oxygenated blood
• Give oxygen as indicated by patient symptoms, oxygen saturation and ABGs.
• Rationale: Makes more oxygen available for gas exchange, assisting to alleviate signs of
hypoxia and subsequent activity intolerance.
• Implement strategies to treat fluid and electrolyte imbalances.
• Rationale: Decreases the risk for development of cardiac output due to imbalances.
• Administer cardiac glycoside agents, as ordered, for signs of left sided failure, and
monitor for toxicity.
• Rationale: Digitalis has a positive isotropic effect on the myocardium that strengthens
contractility, thus improving cardiac output.
• Encourage periods of rest and assist with all activities.
 • Rationale: Reduces cardiac workload and minimizes myocardial oxygen consumption.
• Assist the patient in assuming a high Fowler’s position.
• Rationale: Allows for better chest expansion, thereby improving pulmonary capacity.
• Teach patient the pathophysiology of disease, medications
• Rationale: Provides the patient with needed information for management of disease
and for compliance.
• Reposition patient every 2 hours
• Rationale: To prevent occurrence of bed sores
• Instruct patient to get adequate bed rest and sleep
• Rationale: To promote relaxation to the body
• Instruct the SO not to leave the client unattended
• Rationale: To ensure safety and reduce risk for falls that may lead to injury

Evaluation
• After nursing interventions, the patient shall have participated in activities that reduce
the workload of the heart.
• After 2-3 days of nursing interventions, the patient shall have been able to display
hemodynamic stability.

Excess Fluid Volume

Assessment
The patient may manifest the following:
• Edema of extremities
• Difficulty of breathing
• Crackles
• Change in mental status
• Restlessness and anxiety
•
Diagnosis
• Excessive Fluid volume related to decreased cardiac output and sodium and water
retention
Planning & Desired Outcomes
• Patient will verbalize understanding of causative factors and demonstrate behaviors to
resolve excess fluid volume.
• Patient will demonstrate adequate fluid balanced AEB output equal to exceeding intake,
clearing breath sounds, and decreasing edema.
Nursing Interventions
• Establish rapport
• Rationale: To gain patient’s trust and cooperation
• Monitor and record VS
• Rationale: To obtain baseline data
• Assess patient’s general condition
• Rationale: To determine what approach to use in treatment
• Monitor I&O every 4 hours
• Rationale: I&O balance reflects fluid status
• Weigh patient daily and compare to previous weights.
• Rationale: Body weight is a sensitive indicator of fluid balance and an increase indicates
fluid volume excess.
• Auscultate breath sounds q 2hr and pm for the presence of crackles and monitor for
frothy sputum production
• Rationale: When increased pulmonary capillary hydrostatic pressure exceeds oncotic
pressure, fluid moves within the alveolar septum and is evidenced by the auscultation of
crackles. Frothy, pink-tinged sputum is an indicator that the client is developing
pulmonary edema
• Assess for presence of peripheral edema. Do not elevate legs if the client is dyspneic.
• Rationale: Decreased systemic blood pressure to stimulation of aldosterone, which
causes increased renal tubular absorption of sodium Low-sodium diet helps prevent
increased sodium retention, which decreases water retention. Fluid restriction may be
used to decrease fluid intake, hence decreasing fluid volume excess.
• Follow low-sodium diet and/or fluid restriction
• Rationale: The client senses thirst because the body senses dehydration. Oral care can
alleviate the sensation without an increase in fluid intake.
• Encourage or provide oral care q2
• Rationale: Heart failure causes venous congestion, resulting in increased capillary
pressure. When hydrostatis pressure exceeds interstitial pressure, fluids leak out of ht
ecpaillaries and present as edema in the legs, and sacrum. Elevation of legs increases
venous return to the heart.
• Obtain patient history to ascertain the probable cause of the fluid disturbance.
• Rationale: May include increased fluids or sodium intake, or compromised regulatory
mechanisms.
• Monitor for distended neck veins and ascites
• Rationale: Indicates fluid overload
• Evaluate urine output in response to diuretic therapy.
• Rationale: Focus is on monitoring the response to the diuretics, rather than the actual
amount voided
• Assess the need for an indwelling urinary catheter.
• Rationale: Treatment focuses on diuresis of excess fluid.
• Institute/instruct patient regarding fluid restrictions as appropriate.
• Rationale: This helps reduce extracellular volume.
Ineffective Tissue Perfusion
Assessment
• Pale conjunctiva, nail beds, and buccal mucosa
• Generalized weakness
• Chest pain
• Difficulty of breathing
• Abnormal pulse rate and rhythm
• Bradycardia
• Altered BP readings
• With pitting edema on both forearms and hands
• Bipedal pitting edema

Diagnosis
• Ineffective tissue perfusion related to decreased cardiac output.

Planning & Desired Outcomes

• Patient will demonstrate behaviors to improve circulation.
• Display vital signs within acceptable limits, dysrhythmias absent/controlled,and no
symptoms of failure
Nursing Interventions
• Assess patient pain for intensity using a pain rating scale, for location and for
precipitating factors.
• Rationale: To identify intensity, precipitating factors and location to assist in accurate
diagnosis.
• Administer or assist with self administration of vasodilators, as ordered.
• Rationale: The vasodilator nitroglycerin enhances blood flow to the myocardium. It
reduces the amount of blood returning to the heart, decreasing preload which in turn
decreases the workload of the heart.
• Assess the response to medications every 5 minutes.
• Rationale: Assessing response determines effectiveness of medication and whether
further interventions are required.
• Give beta blockers as ordered.
• Rationale: Beta blockers decrease oxygen consumption by the myocardium and are
given to prevent subsequent angina episodes.
• Establish a quiet environment.
 • Rationale: A quiet environment reduces the energy demands on the patient.
• Elevate head of bed.
• Rationale: Elevation improves chest expansion and oxygenation.
• Monitor vital signs, especially pulse and blood pressure, every 5 minutes until pain
subsides.
• Rationale: Tachycardia and elevated blood pressure usually occur with angina and
reflect compensatory mechanisms secondary to sympathetic nervous system
stimulation.
• Provide oxygen and monitor oxygen saturation via pulse oximetry, as ordered.
• Rationale: Oxygenation increases the amount of oxygen circulating in the blood and,
therefore, increases the amount of available oxygen to the myocardium, decreasing
myocardial ischemia and pain.
• Assess results of cardiac markers—creatinine phosphokinase, CK- MB, total LDH, LDH-1,
LDH-2, troponin, and myoglobin ordered by physician.
• Rationale: These enzymes elevate in the presence of myocardial infarction at differing
times and assist in ruling out a myocardial infarction as the cause of chest pain.
• Assess cardiac and circulatory status.
• Rationale: Assessment establishes a baseline and detects changes that may indicate a
change in cardiac output or perfusion.
• Monitor cardiac rhythms on patient monitor and results of 12 lead ECG.
• Rationale: Notes abnormal tracings that would indicate ischemia.
• Teach patient relaxation techniques and how to use them to reduce stress.
• Rationale: Anginal pain is often precipitated by emotional stress that can be relieved
non-pharmacological measures such as relaxation.
• Teach the patient how to distinguish between angina pain and signs and symptoms of
myocardial infarction.
• Rationale: In some case, the chest pain may be more serious than stable angina. The
patient needs to understand the differences in order to seek emergency care in a timely
fashion.
• Reposition the patient every 2 hours
• Rationale: To prevent bedsores
• Instruct patient on eating a small frequent feedings
• Rationale: To prevent heartburn and acid indigestion

Activity Intolerance
Assessment
• Weakness
• Limited range of motion
• Abnormal pulse rate and rhythm
Diagnosis
• Activity intolerance r/t imbalance O2 supply and demand

Planning & Desired Outcomes

• Patient will use identified techniques to improve activity intolerance
• Patient will report measurable increase in activity intolerance

Nursing Interventions
• Establish Rapport
• Rationale: To gain clients participation and cooperation in the nurse patient interaction
• Monitor and record Vital Signs
• Rationale: To obtain baseline data
• Assess patient’s general condition
• Rationale: To note for any abnormalities and deformities present within the body
• Adjust client’s daily activities and reduce intensity of level. Discontinue activities that
cause undesired psychological changes
• Rationale: To prevent strain and overexertion
• Instruct client in unfamiliar activities and in alternate ways of conserve energy
• Rationale: To conserve energy and promote safety
• Encourage patient to have adequate bed rest and sleep
• Rationale: to relax the body
• Provide the patient with a calm and quiet environment
• Rationale: to provide relaxation
• Assist the client in ambulation
• Rationale: to prevent risk for falls that could lead to injury
• Note presence of factors that could contribute to fatigue
• Rationale: fatigue affects both the client’s actual and perceived ability to participate in
activities
• Ascertain client’s ability to stand and move about and degree of assistance needed or
use of equipment
• Rationale: to determine current status and needs associated with participation in
needed or desired activities
• Give client information that provides evidence of daily or weekly progress
• Rationale: to sustain motivation of client
• Encourage the client to maintain a positive attitude
 • Rationale: to enhance sense of well being
• Assist the client in a semi-fowlers position
• Rationale: to promote easy breathing
• Elevate the head of the bed
• Rationale: to maintain an open airway
• Assist the client in learning and demonstrating appropriate safety measures
• Rationale: to prevent injuries
• Instruct the SO not to leave the client unattended
• Rationale: to avoid risk for falls
• Provide client with a positive atmosphere
• Rationale: to help minimize frustration and rechannel energy
• Instruct the SO to monitor response of patient to an activity and recognize the signs and
symptoms
• Rationale: to indicate need to alter activity level

Arrhythmia

Description
An arrhythmia is a problem with the rate or rhythm of your heartbeat. It means that your heart
beats too quickly, too slowly, or with an irregular pattern. When the heart beats faster than
normal, it is called tachycardia. When the heart beats too slowly, it is called bradycardia. The
most common type of arrhythmia is atrial fibrillation, which causes an irregular and fast
heartbeat.

Pathophysiology
Most cardiac arrhythmias result from disorders of impulse formation, impulse conduction or a
combination of both. Disturbances in impulse formation or automaticity can involve no
pathological change in the pacemaker site generating sinus bradycardia (< 60 bpm) due to
slowed spontaneous sinoatrial (SA) firing or sinus tachycardia (> 100 bpm) due to rapid firing of
the SA node. The development of an ectopic focus can also lead to impulse formation
abnormalities. An ectopic focus is an impulse originating outside the SA node and can develop
as a result of electrolyte disturbances, ischemia, excessive myocardial fiber stretch, drugs, or
toxins.

Disorders in impulse conduction involve heart blocks, which result in slowed or blocked
conduction through the myocardium. The pathological process of reentry is also an impulse
conduction abnormality. This figure is animated allowing student to visually comprehend how
impulse conduction circles through the reentry pathway; the animation also draws a
corresponding action potential for correlation to heart rate (see web link). In order for a reentry
pathway to develop, there must be a unidirectional block within the conduction pathway. This
unidirectional block can be the result of ischemia (e.g. following a myocardial infarction). A
unidirectional block alone is not sufficient to generate the arrhythmia. At least one of the
following characteristics must be present for the arrhythmia to develop; long reentry pathway,
short refractory period, or slowed conduction velocity. All three of these conditions will allow
the surrounding myocardial tissue to be out of its refractory period so when the circulating
impulse reaches the myocardium a premature contraction is generated. Each of these events is
explained in detail. Hand drawings of the reentry pathway illustrating all three pathological
events are given to the class. Genetic abnormalities in voltage-gated ion channel function have
also been linked to arrhythmia generation. For example, the inherited potassium channel
disorder that results in the long-QT syndrome.

Epidemiology

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia worldwide, and it
carries an increased risk of stroke, hospitalization, and mortality, thus representing a major
public health burden. The Global Burden of Disease (GBD) project first embarked on a global
assessment of AF in 2010. It estimated, that globally at least 33.5 million individuals had AF in
the year 2010, representing 0.5% of the world population.1 In Europe and the United States,
the reported prevalence of AF in adults is 1–3%, but the actual prevalence may be even higher
due to the large number of individuals with undiagnosed AF. In the United States and Europe,
the lifetime risk for developing AF has been estimated to be approximately 25%. About half of
patients have permanent AF, whereas paroxysmal and persistent AF are present in a quarter of
patient’s each.

AF prevalence, incidence, and associated adverse outcomes have been steadily increasing.
During 1990–2010, the global burden associated with AF, measured as disability-adjusted life
years, increased nearly 20%. During the same time period, the age-adjusted prevalence of AF
increased by 4–5%, to 0.60% in men and to 0.37% in women. Similarly, AF incidence per
100,000 increased by approximately 30–35% to 77.5 in men and 59.5 in women. This clear male
dominance in the prevalence and incidence of AF is present both in high-income and low- and
middle-income countries (LMIC), but overall, AF prevalence and incidence is greater in high-
income countries compared to LMIC1. While all the contributing factors are not known, this
could in part be due to the higher prevalence of several risk factors, but there is also emerging
evidence that adults of white European descent have a higher risk of AF compared with
individuals of other races. Due to an ageing population and increase in AF risk factors both in
high-income countries and LMIC, the number of people with AF is estimated to at least double
by the year 2050.

Sick sinus syndrome is a disorder of cardiac rhythm characterized by symptomatic dysfunction

of the sinus node. It can manifest as symptomatic sinus bradycardia, sinoatrial block or sinus
arrest, and is often accompanied by atrial arrhythmias (also referred to as tachycardia-
bradycardia syndrome). The estimated incidence of sick sinus syndrome in adults is around 1
per 1000 person-years, and increases with advancing age and prevalence of cardiovascular risk
factors. The annual number of patients with sick sinus syndrome is projected to double in the
United States in the next few decades. Pacemaker implantation is the established therapy for
symptomatic sick sinus syndrome, and at present it represents the indication for approximately
30–50% of newly implanted pacemakers, although significant global differences also exist in
prevalence of pacemaker therapy for this indication. Although the presence of sick sinus
syndrome is predictive of both pacemaker therapy and AF, it is not independently associated
with increased mortality.

Sudden cardiac death (SCD) refers to death that occurs from unexpected circulatory arrest
usually caused by a cardiac arrhythmia, occurring unexpectedly in a person with or without
previously known cardiac disease. The term sudden cardiac arrest describes SCD cases in which
the process of resuscitation and advanced cardiac care reverses the event.

The annual incidence of SCD in the Western world is estimated to range from 50 to 100 per
100,000 in the general population, and globally in the range of 4–5 million cases per year. In
Asia and among Asians living in the West, the reported incidence of SCD has been somewhat
lower, but due to a lack of uniform methods and definitions, it is challenging to both compare
and combine different studies. Moreover, as opposed to AF for which there is at least some
data available from most parts of the world, estimating the incidence of SCD in countries
lacking functional first responder systems is virtually impossible. Despite significant
improvements in primary and secondary prevention that have substantially reduced overall
coronary artery disease mortality over recent decades, SCD rates in particular have declined to
a lesser extent. Estimates indicate that SCD accounts for approximately 50% of all coronary
heart disease deaths and 5–15% of overall mortality, the wide range indicating partly the lack of
standardized case adjudication in epidemiological studies. The risk of SCD increases markedly
with age,54 with a 100-fold lower incidence in adolescents and adults under 30 than in adults
older than 35.46 Approximately two-thirds of women presenting with SCD have no previously
detected cardiac disease, compared with 50% in men. In addition, women suffering from SCD
seem to have a higher prevalence of structurally normal hearts than do men. From a public
health perspective in the United States, the burden of premature death for men (2.04 million
years of potential life lost; 95% uncertainty interval 1.86–2.23 million) and women (1.29 million
years of potential life lost; 95% uncertainty interval 1.13–1.45 million) was greater for SCD than
for all individual cancers.

Ventricular fibrillation, often preceded by ventricular tachycardia, has been the predominant
arrhythmia that manifests during SCD, but pulseless electrical activity and bradycardias can also
cease mechanical activity of the heart resulting in loss of viable circulation. The proportion of
pulseless electrical activity among cardiac arrest cases has steadily increased during the last
three decades, and the proportion of ventricular fibrillation or ventricular tachycardia as the
initial documented rhythm during cardiac arrest has correspondingly decreased. Despite efforts
to increase bystander cardiopulmonary resuscitation, wider use of automated external
defibrillators, and major advances in cardiopulmonary resuscitation and post-resuscitation care,
survival from out-of-hospital cardiac arrest is still poor, with only approximately 8% of patients
surviving to hospital discharge. If the initial presenting rhythm is ventricular fibrillation or
tachycardia, survival rates of over 25% have been reported, compared to less than 5% if cardiac
arrest presents with pulseless electrical activity or asystole.

Types

Arrhythmias differ from normal heartbeats in speed or rhythm. Arrhythmias are also grouped
by where they occur—in the upper chambers of the heart, in its lower chambers, or between
the chambers. The main types of arrhythmia are bradyarrhythmias; premature, or extra, beats;
supraventricular arrhythmias; and ventricular arrhythmias.

Bradyarrhythmia is a slow heart rate—also called bradycardia. For adults, bradycardia is often
defined as a heart rate that is slower than 60 beats per minute, although some studies use a
heart rate of less than 50 beats per minute. Some people, especially people who are young or
physically fit, may normally have slow heart rates. A doctor can determine whether a slow heart
rate is appropriate for you.

A premature heartbeat happens when the signal to beat comes early. It can feel like your heart
skipped a beat. The premature, or extra, heartbeat creates a short pause, which is followed by a
stronger beat when your heart returns to its regular rhythm. These extra heartbeats are the
most common type of arrhythmia. They are called ectopic heartbeats and can trigger other
arrhythmias.

Arrhythmias that start in the heart’s upper chambers, called the atrium, or at the gateway to
the lower chambers are called supraventricular arrhythmias. Supraventricular arrhythmias are
known by their fast heart rates, or tachycardia. Tachycardia occurs when the heart, at rest, goes
above 100 beats per minute. The fast pace is sometimes paired with an uneven heart rhythm.
Sometimes the upper and lower chambers beat at different rates.

Types of supraventricular arrhythmias include:

Atrial fibrillation.
This is one of the most common types of arrhythmia. The heart can race at more than 400 beats
per minute.

Atrial flutter.
Atrial flutter can cause the upper chambers to beat 250 to 350 times per minute. The signal that
tells the upper chambers to beat may be disrupted when it encounters damaged tissue, such as
a scar. The signal may find an alternate path, creating a loop that causes the upper chamber to
beat repeatedly. As with atrial fibrillation, some but not all of these signals travel to the lower
chambers. As a result, the upper chambers and lower chambers beat at different rates.

Paroxysmal supraventricular tachycardia (PSVT).

In PSVT, electrical signals that begin in the upper chambers and travel to the lower chambers
cause extra heartbeats. This arrhythmia begins and ends suddenly. It can happen during
vigorous physical activity. It is usually not dangerous and tends to occur in young people.

These arrhythmias start in the heart’s lower chambers. They can be very dangerous and usually
require medical care right away.

Ventricular tachycardia is a fast, regular beating of the ventricles that may last for only a few
seconds or for much longer. A few beats of ventricular tachycardia often do not cause
problems. However, episodes that last for more than a few seconds can be dangerous.
Ventricular tachycardia can turn into other more serious arrhythmias, such as ventricular
fibrillation, or v-fib. Torsades de pointes is a type of arrhythmia that causes a unique pattern on
an EKG and often leads to v-fib.

Ventricular fibrillation occurs if disorganized electrical signals make the ventricles quiver instead
of pumping normally. Without the ventricles pumping blood to the body, sudden cardiac arrest
and death can occur within a few minutes.

Causes

Arrhythmia is caused by changes to heart tissue. It can also occur suddenly as a result of
exertion or stress, imbalances in the blood, medicines, or problems with electrical signals in the
heart. Typically, an arrhythmia is set off by a trigger, and the irregular heartbeat can continue if
there is a problem in the heart. Sometimes the cause of an arrhythmia is unknown.

Changes to the heart

The following conditions may cause arrhythmia:

• Changes to the heart’s anatomy

• Reduced blood flow to the heart or damage to the heart’s electrical system
• Restoring blood flow as part of treating a heart attack
• Stiffening of the heart tissue, known as fibrosis, or scarring

Exertion or strain

Strong emotional stress, anxiety, anger, pain, or a sudden surprise can make the heart work
harder, raise blood pressure, and release stress hormones. Sometimes these reactions can lead
to arrhythmias. If you have heart disease, physical activity can trigger arrhythmia due to an
excess of hormones such as adrenaline. Sometimes vomiting or coughing can trigger
arrhythmia.
Imbalances in the blood

• An excess or deficiency of electrolytes, hormones, or fluids can alter your heartbeat.

• An excess of thyroid hormone can cause the heart to beat faster, and thyroid deficiency
can slow your heart rate.
• Dehydration can cause the heart to race.
• Low blood sugar, from an eating disorder or insulin doses that are too high in someone
who has diabetes, can lead to slow or extra heartbeats.
• Low levels of potassium, magnesium, or calcium can trigger arrhythmia. These
electrolyte disturbances can occur after a heart attack or surgery

Medicines

Certain medicines can cause arrhythmia. These include medicines to treat high blood pressure
and other conditions, including arrhythmia, depression, and psychosis. Some people also need
to be careful about taking certain antibiotics and over-the-counter medicines, such as allergy
and cold medicines.

Problems with the electrical signals in the heart

An arrhythmia can occur if the electrical signals that control the heartbeat are delayed or
blocked. This can happen when the nerve cells that produce electrical signals do not work
properly or when the electrical signals do not travel normally through the heart. Another part
of the heart could start to produce electrical signals, disrupting a normal heartbeat.

Disorders of electrical signaling in the heart are called conduction disorders.

Clinical Manifestations/Diagnosis

You may be able to feel a slow or irregular heartbeat or notice pauses between heartbeats. If
you have palpitations, you may feel like your heart skipped a beat or may notice it pounding or
racing. These are all symptoms of arrhythmia.

More serious signs and symptoms include:

 • Anxiety
• Blurred vision
• Chest pain
• Difficulty breathing
• Fainting or nearly fainting
• Foggy thinking
• Fatigue
• Sweating
• Weakness, dizziness, and light-headedness

Complications
Arrhythmias that are unrecognized or left untreated can cause sometimes life-threatening
complications affecting the heart and brain.
Cognitive impairment and dementia. Alzheimer’s disease and vascular dementia are more
common in people who have arrhythmia. This may be due to reduced blood flow to the brain
over time.
Heart failure. Repeat arrhythmias can lead to a rapid decline in the ability of the lower
chambers to pump blood. Heart failure is especially likely to develop or to grow worse as a
result of arrhythmia when you already have heart disease.
Stroke. This can occur in some patients who have atrial fibrillation. With arrhythmia, blood can
pool in the atria, causing blood clots to form. If a clot breaks off and travels to the brain, it can
cause a stroke.
Sudden cardiac arrest. The heart may suddenly and unexpectedly stop beating as a result of
ventricular fibrillation.
Sudden infant death syndrome (SIDS). SIDS can be attributed to an inherited conduction
disorder that causes arrhythmia.
Worsening arrhythmia. Some arrhythmias trigger another type of arrhythmia or get worse over
time.

Prevention
If you or your child is at increased risk of arrhythmia, the doctor may want to do a screening to
assess the risk of a life-threatening event. Sometimes screening is required to participate in
competitive sports. If your child carries a genetic risk of arrhythmia, your child’s doctor may
recommend regular screening to monitor your child’s heart or other family members’ health.
The doctor may also ask about risk factors and may suggest genetic testing if your child, parent,
or other family member has a known or suspected arrhythmia or other heart condition. Heart-
healthy lifestyle changes and other precautions can help decrease the risk of triggering
arrhythmia.

Screening tests
Your doctor may recommend screening tests based on your risk factors, such as age or family
history.
An electrocardiogram (EKG or ECG) is the main test for detecting arrhythmia. An EKG records
the heart’s electrical activity. Your doctor may do the test while you are at rest or may do a
stress test, which records the heart’s activity when it is working hard. Your doctor may also give
you a portable monitor to wear for a day or several days if no arrhythmia was detected during
testing in the clinic. If you have a child who is at risk of arrhythmia because of a genetic
condition, the doctor may recommend regular testing for your child and his or her siblings.
Genetic testing can help you understand your risk when a family member has been diagnosed
with a genetic condition. Testing is especially important if your newborn or another close
relative died suddenly and had a genetic risk. Your doctor may also suggest genetic testing if
you have a history of fainting or have survived cardiac arrest or near drowning.
Imaging tests, such as cardiac magnetic resonance imaging (MRI), can help detect scarring or
other problems that can increase your risk of arrhythmia.

Learn about prevention strategies that your doctor may recommend, including:
• Avoiding triggers, such as caffeine or stimulant medicines, that can cause arrhythmias or
make them worse. Your doctor can also help if you are trying to avoid illegal drugs.
• Getting an implantable or wearable cardioverter defibrillator to prevent sudden cardiac
arrest from arrhythmia if you have heart disease. Defibrillators can correct arrhythmias
by sending an electric shock to the heart.
• Making heart-healthy lifestyle changes, such as heart-healthy eating, being physically
active, aiming for a healthy weight, quitting smoking, and managing stress
• Monitoring you after surgery, if you are having heart surgery. The surgical team may
also use medicine and maintain or supplement electrolyte levels during or after the
procedure to prevent arrhythmia.
• If you are the parents of a child with an inherited condition that increases the risk of
arrhythmia, discuss prevention strategies with your pediatrician as part of your child’s
care.
• If your child is a newborn, follow safe sleep recommendations to help reduce the risk of
sudden infant death syndrome (SIDS).
• Your doctor may recommend routine assessments of your child’s heart activity to detect
patterns or symptoms of arrhythmia that emerge over time.
Medical Management
Medicines
Your doctor may give you medicine for your arrhythmia. Some medicines are used in
combination with each other or together with a procedure or a pacemaker. If the dose is too
high, medicines to treat arrhythmia can cause an irregular rhythm. This happens more often in
women.
• Adenosine to slow a racing heart. Adenosine acts quickly to slow electrical signals. It can
cause some chest pain, flushing, and shortness of breath, but any discomfort typically
passes soon.
• Atropine to treat a slow heart rate. This medicine may cause difficulty swallowing.
• Beta blockers to treat high blood pressure or a fast heart rate or to prevent repeat
episodes of arrhythmia. Beta blockers can cause digestive trouble, sleep problems, and
sexual dysfunction and can make some conduction disorders worse.
• Blood thinners to reduce the risk of blood clots forming. This helps prevent stroke. With
blood-thinning medicines, there is a risk of bleeding.
• Calcium channel blockers to slow a rapid heart rate or the speed at which signals travel.
Typically, they are used to control arrhythmias of the upper chambers. In some cases,
calcium channel blockers can trigger ventricular fibrillation. They can also cause
digestive trouble, swollen feet, or low blood pressure.
• Digitalis, or digoxin, to treat a fast heart rate. This medicine can cause nausea and may
trigger arrhythmias.
• Potassium channel blockers to slow the heart rate. They work by lengthening the time it
takes for heart cells to recover after firing, so that they do not fire and squeeze as often.
Potassium channel blockers can cause low blood pressure or another arrhythmia.
• Sodium channel blockers to block transmission of electrical signals, lengthen cell
recovery periods, and make cells less excitable. However, these drugs can increase risks
of sudden cardiac arrest in people who have heart disease.
• If medicines do not treat your arrhythmia, your doctor may recommend one of these
procedures or devices.
• Cardioversion
• Catheter ablation
• Implantable cardioverter defibrillators (ICDs)
• Pacemakers
Treatment may also include managing any underlying condition, such as an electrolyte
imbalance, high blood pressure, heart disease, sleep apnea, or thyroid disease.

Your doctor may use supplements to treat magnesium or electrolyte deficiencies. Electrolytes
can also be an alternative to medicines that treat arrhythmia if your doctor is concerned that
those medicines might trigger an arrhythmia.
Your doctor may also perform certain techniques to slow your heart rate. The exercises
stimulate your body’s natural relaxation processes. They do this by affecting the vagus nerve,
which helps control the heart rate. Techniques can include:

• Having you cough or gag

• Having you hold your breath and bear down, which is called the Valsalva maneuver
• Having you lie down
• Putting a towel dipped in ice-cold water over your face

Nursing Management and Goal

Nursing Priorities
• Prevent/treat life-threatening dysrhythmias.
• Support patient/SO in dealing with anxiety/fear of potentially life-threatening situation.
• Assist in identification of cause/precipitating factors.
• Review information regarding condition/prognosis/treatment regimen.

Risk for Decreased Cardiac Output

Risk for Decreased Cardiac Output: At risk for inadequate blood pumped by the heart to meet
metabolic demands of the body.

Nursing Diagnosis
• Cardiac Output, risk for decreased

Risk factors may include

• Altered electrical conduction
• Reduced myocardial contractility

Desired Outcomes
• Maintain/achieve adequate cardiac output as evidenced by BP/pulse within normal
range, adequate urinary output, palpable pulses of equal quality, usual level of
mentation.
• Display reduced frequency/absence of dysrhythmia(s).
 • Participate in activities that reduce myocardial workload.

Nursing Interventions
• Palpate pulses (radial, carotid, femoral, dorsalis pedis), noting rate, regularity, amplitude
(full or thready), and symmetry. Document presence of pulsus alternans, bigeminal
pulse, or pulse deficit.
• Auscultate heart sounds, noting rate, rhythm, presence of extra heartbeats, dropped
beats.
• Monitor vital signs. Assess adequacy of cardiac output and tissue perfusion, noting
significant variations in BP/pulse rate equality, respirations, changes in skin color,
temperature, level of consciousness, sensorium, and urine output during episodes of
dysrhythmias.
• Provide quiet and calm environment. Review reasons for limitation of activities during
acute phase.
• Demonstrate and encourage use of stress management behaviors,: relaxation
techniques, guided imagery, slow/deep breathing.
• Investigate reports of chest pain, documenting location, duration, intensity (0–10 scale),
and relieving or aggravating factors. Note nonverbal pain cues: facial grimacing, crying,
and changes in BP/heart rate.
• Be prepared to initiate cardio-pulmonary resuscitation (CPR) as indicated.
• Prepare and assist with elective cardioversion.
• Assist with insertion and maintenance of pacemaker function.
• Insert and maintain IV access.
• Prepare for invasive diagnostic procedures and surgery as indicated.
• Prepare for implantation of cardioverter or defibrillator (ICD) when indicated.
References
Huether, S. E., & McCance, K. L. (2012). Understanding pathophysiology (5th ed.). St. Louis,
MO:Mosby/Elsevier.
Coven, et al., 2019 Acute Coronary Syndrome emedicine.medscape.com

Goyal, et al., 2019 Unstable Angina. NCBI Bookshelf: A service of National Library of Medicine,
National Institutes of Health

Wong, et al., 2019 Canadian cardiovascular Society/Canadian Association of Interventional

cardiology Guidelines on the Acute Management of ST-Elevation Myocardial Infarction: Focused
Update on Regionalization and Reperfusion

Yaser Al Ahmad and Mohammed T. Ali, 2018 Non-ST Elevation Myocardial Infarction: Diagnosis
and Management

Sweis, et al., Angina Pectoris. MSD Manual

Thomas F. Luscher 2018 Acute Coronary Syndromes: The Impressive Impact of guideline-based
management in NSTEMI. European Society of Cardiology
Coursework #2
HEART CATHETERIZATION

Overview/description
Cardiac catheterization is a procedure used to check for many cardiovascular conditions,
especially blockages in the arteries to your heart that could cause a heart attack. During cardiac
catheterization, a long thin tube called a catheter is inserted in an artery or vein in your groin,
neck or arm and threaded through your blood vessels to your heart. Using this catheter,
doctors can then do diagnostic tests as part of a cardiac catheterization. Some heart disease
treatments, such as coronary angioplasty, also are done using cardiac catheterization.

Indications
Main reasons a cardiac catheterization is recommended for a patient with chronic stable angina
(according to American College of Cardiology Foundation and American Heart Association):
• Patients with disabling chronic stable angina despite medical therapy
• High-risk criteria on clinical assessment or noninvasive testing regardless of anginal
severity
• Patient who have survived sudden cardiac death or serious ventricular arrhythmia
• Patients with angina and symptoms and signs of congestive heart failure

Pre, Intra and Post-Op Instructions/Care

PRE-OPERATIVE:
1. Assess for allergies to radiopaque dye, iodine, or shellfish. Patient may be pretreated for
the allergies.
2. Written, informed consent by physician
3. NPO for 6-8 hours prior to procedure
4. Adequate hydration
a. IV insertion with fluids as ordered
b. Clear liquids up to 4 hours before procedure may be allowed
5. Use of N-acetylcysteine (Mycomyst) prior to and post cardiac catheterization in patients
who are at risk for contrast nephropathy (for example, may treat if creatinine > 1.5, but
depends on the hospital policy)
6. Assessment of baseline vital signs, oxygen saturation, and peripheral pulses. Abnormal
labs that may affect the catheterization should be communicated to the cath lab
(information on front of chart, called to cath lab).
 7. Explain the procedure to the patient. Explain that they will be awake and may
experience a flushing sensation as the dye is injected or feel fluttering as the catheter
passes through the heart.
8. Medications: Hold metformin (Glucophage). Generally, hold low molecular weight
heparin (for example, Lovenox) on the day of the catheterization. Check adjusted insulin
order for day of catheterization.

INTRAOPERATIVE

1. You’ll put on a hospital gown. A nurse will put an intravenous (IV) needle in your arm
in order to give you medications and fluids.
2. The cardiac cath room looks like an operating room. You’ll lie on a special table. A
large camera and several TV monitors will be above you. You can watch the pictures
from your cardiac cath on the monitors.
3. The nurse will clean and possibly shave the site where they’ll insert the catheter (in
your arm or groin). Sterile cloths will cover the site and help prevent infection. Keep
your arms and hands at your sides so you don’t move the drapes.
4. The nurse will put electrodes (small, flat, sticky patches) on your chest. The
electrodes are attached to an EKG machine that charts your heart's electrical
activity.
5. Your doctor will give you a mild drug to help you relax, but you’ll be awake during
the procedure. Your doctor will use a medication called a local anesthetic to numb
the area where the catheter goes in. This could be at your groin (they’ll call this the
femoral approach) or on your wrist (the radial approach).
6. Your doctor will make a small cut over the blood vessel. They’ll insert a device called
an introducer sheath and thread the catheter through it into the arteries of your
heart. You might feel some pressure but shouldn’t feel pain. If you feel any pain, tell
your health care providers.
7. When the catheter is in place, they’ll dim the lights and insert a small amount of dye
(also called contrast material) through the catheters into your arteries and heart
chambers. The contrast material outlines your vessels, valves, and chambers.
8. When the doctor injects the dye into your heart, you may feel hot or flushed. This is
normal and will go away in a few seconds. Tell the doctor or nurses if you feel itching
or tightness in your throat, nausea, chest discomfort, or any other symptoms.
9. The X-ray camera will take photographs of your arteries and heart chambers. Your
doctor may ask you to take a deep breath, hold your breath, or cough during the
procedure. You’ll need to hold your breath while they’re taking the X-rays. When all
the photos are done, the team will remove the catheter and turn on the lights.
POST-OPERATIVE:
1. View post procedure orders and agency policy
2. Maintain strict bedrest per physician’s orders (up to 4-6 hours) with head of bed
elevated < 15-30 degrees
3. Continuous EKG monitoring
4. Monitor VS, oxygen saturation per agency protocol.
5. Assess peripheral pulses, color, sensation, temperature of extremity, signs of
bleeding or hematoma at insertion site with vital signs
6. Maintain dressing at insertion site
7. Maintain IV, encourage oral fluids, and monitor intake and output
8. Report significant problems to physician: chest pain, dysrhythmias, bleeding,
hematoma, significant changes in vital signs or peripheral pulses

Complications and Interventions

The risk of major complications during diagnostic cardiac catheterization procedure is usually
less than 1%, and the risk and the risk of mortality of 0.05% for diagnostic procedures.[5] For
any patient, the complication rate is dependent on multiple factors and is dependent on the
demographics of the patient, vascular anatomy, co-morbid conditions, clinical presentation, the
procedure being performed, and the experience of the operator. The complications can be
minor as discomfort at the site of catheterization to major ones like death.

Local Vascular Complications

Hematoma/Retroperitoneal Bleeding
These are among the most common complications seen after cardiac catheterization
procedures. Hematomas are usually formed following poorly controlled hemostasis post sheath
removal. Most hematomas are self-limiting and benign, but large rapidly expanding hematomas
can cause hemodynamic instability requiring resuscitation with fluids and blood. The incidence
of this complication is significantly reduced in transradial access. In patients with transfemoral
access, retroperitoneal bleeding should be suspected if there is a sudden change in the
hemodynamic stability of the patient with or without back pain as there may not be any visible
swelling in the groin for some of these patients. The incidence of this complication is less than
0.2%.[6] Strong clinical suspicion along with immediate imaging, usually with CT scan, helps
make a diagnosis of this problem. Identification of the bleeding source is essential for patients
with continued hemodynamic deterioration. These life-threatening bleeds are more frequent
when the artery is punctured above the inguinal ligament. Most patients are managed with a
reversal of anticoagulation, application of manual compression and volume resuscitation and
observation. Patients with continued deterioration with need coiling of the bleeding source
vessel, or balloon angioplasty or covered stents for bleeding from larger vessels.

Pseudoaneurysm

When the hematoma maintains continuity with the lumen of the artery, it results in the
formation of a pulsatile mass locally, defined as a pseudoaneurysm. This will be associated with
bruit on examination. They happen following low access in the superficial femoral artery as
opposed to the common femoral artery. These are usually diagnosed by ultrasound Doppler
imaging or CT angiography. Small pseudoaneurysms of the less than 2 to 3 cm in size may heal
of spontaneously and can be followed by serial Doppler examinations. Large symptomatic
pseudoaneurysms can be treated by either ultrasound-guided compression of the neck of
pseudoaneurysm or percutaneous injection of the thrombin using ultrasound guidance or may
need surgical intervention.

Arteriovenous Fistula

Direct communication between the arterial and venous puncture sites with ongoing bleeding
from the arterial access site leads to the fistula formation and are associated with a thrill or
continuous bruit on examination. These usually will require surgical exploration as they are
unlikely to heal spontaneously and may expand with time.

Dissection

This is an infrequent complication and occurs in patients with an increased atherosclerotic

burden, tortuous arteries, or traumatic sheath placement. Non-flow limiting dissections usually
heal spontaneously following sheath removal. A flow limiting large dissections could lead to
acute limb ischemia and should be treated immediately with angioplasty and stenting. Vascular
surgery is usually reserved for patients with failed percutaneous techniques.

Thrombosis and Embolism

This complication is extremely rare with the use of the low profile catheters and predisposing
factors include small vessel lumen, and associated peripheral arterial disease, diabetes mellitus,
female sex, large diameter sheath, and prolonged catheter dwell time. Treatment involves
removal of the occlusive sheath, percutaneous thrombectomy in conjunction with vascular
surgery consultation.

Vascular Complications after Transradial Access

The most frequent complication after transradial access is about a 5% risk of radial artery
occlusion. This is a clinically insignificant complication if the Allen test is normal. Patients with
incomplete palmar arch and abnormal Allen test may have symptoms of hand ischemia after
radial artery occlusion.

Radial artery spasm is another frequent complication, and this can be avoided by the use of
local vasodilatory medications and systemic anxiolytics. Perforation of the radial artery is an
extremely rare complication and is usually managed with prolonged external compression and
rarely requires vascular surgery intervention.

Other Major Complications

Death

The incidence of death with cardiac catheterization has decreased progressively and is less than
0.05% for diagnostic procedures. Patients with depressed left ventricular systolic function and
those presenting with shock in the setting of acute myocardial infarction are at increased risk.
In some subsets of patients, the risk of mortality can be more than 1%. Other factors that would
increase the risk include old age, the presence of multivessel disease, left main coronary artery
disease, or valvular heart disease like severe aortic stenosis.

Myocardial Infarction

The reported incidence of periprocedural myocardial infarction for a diagnostic angiography is

less than 0.1%. This is mostly influenced by patient-related factors like the extent and severity
of underlying coronary artery disease, recent acute coronary syndrome, diabetes requiring
insulin, and technique-related factors.
Stroke

The overall risk of stroke in recently reported series is low at 0.05% to 0.1% in diagnostic
procedures and can increase to 0.18% to 0.4% in patients undergoing intervention.[7] This can
be a very debilitating complication associated with a high rate of morbidity and mortality. The
risk is higher in patients with extensive atherosclerotic plaque in the aorta and aortic arch,
complex anatomy, procedures requiring multiple catheter exchanges or excessive catheter
manipulation, or the need for large-bore catheters and stiff wires.

Dissection and Perforation of the Great Vessels

Dissection of the aorta, perforation of the cardiac chambers, perforation of the coronary
arteries is an extremely rare complication. The risk is higher in procedures with intervention as
opposed to diagnostic procedures only. Patients with type A aortic dissection involving the
ascending aorta will require surgical correction. Patients with a cardiac chamber or coronary
perforation resulting in the accumulation of the blood in the pericardial space will need urgent
pericardiocentesis to restore hemodynamic stability and immediate surgical consultation.

Atheroembolism

Cholesterol emboli from friable vascular plaques can give rise to distal embolization in multiple
vascular beds. These are usually recognized by digital discoloration (blue toes), livedo
reticularis. This can also manifest as a neurological squeal or renal impairment. The risk of this
complication is minimized by exchanging catheters over a long wire and minimizing the
catheter exchanges. Retinal artery occlusion causes Hollenhorst plaque.

Allergic Reactions

Allergic reactions can be related to the use of local anesthetic, contrast agents, heparin or other
medications used during the procedure. Reactions to the contrast agents can occur in up to 1%
of the patients, and people with prior reactions are pretreated with corticosteroids and
antihistamines. Use of iso-osmolar agents decreases the risk compared to high osmolar agents.
When severe reactions do occur, they are treated similarly to anaphylaxis with intravenous (IV)
epinephrine (initial dose 1 ml of 1:10000 epinephrine).
Acute Renal Failure

The incidence of the reported contrast nephropathy is quite variable (range 3.3% to 16.5%) in
the patients undergoing cardiac catheterization resulting in a transient increase in the serum
creatinine levels after exposure to contrast material. In the National Cardiovascular Data
Registry, the incidence of contrast-induced acute kidney injury was 7.1%, among the patients
undergoing elective and urgent coronary intervention.[8] The risk is higher in patients with
underlying moderate to severe renal disease, people with diabetes, elderly, females, patients
on diuretics, ACEI, and metformin. Adequate pre-hydration, use of iso-osmolar agents, and
techniques to minimize the amount of dye used will help prevent this complication. Renal
atheroemboli can also cause renal failure and are associated with other signs of embolization.

Infection

Cardiac catheterization is performed using sterile technique, and local or systemic infection is
extremely rare. Routine prophylaxis for endocarditis is not recommended during cardiac
catheterization procedures.

Radiation Injury

Radiation skin injury can occur if a patient is exposed to excessive doses of radiation to one
particular area of the body and manifestation could range from mild erythema to deep
ulceration. Skin biopsies should be avoided for these lesions as they would make the underlying
condition worse. This complication should be managed by a combined team of cardiologists,
dermatologists, and plastic surgeons.

Arrythmias

The occurrence of the ventricular fibrillation or ventricular tachycardia during the procedure
could be related to irritation or ischemia of the myocardium by the catheter, contrast material
or occlusive balloons. These arrhythmias occur more frequently in people presenting with acute
ST-elevation myocardial infarction and treatment includes cardioversion along with anti
arrhythmic drugs and restoration of the flow to the occluded artery. Atrial tachyarrhythmias
can occur following the irritation of the right atrium during right heart catheterization and is
usually self-limiting.
Transient brady arrhythmias are also a common occurrence in the cardiac cath lab. Prolonged
episodes resulting in hypotension will need treatment with intravenous atropine, or temporary
transvenous pacing. In people with preexisting right bundle branch block, development of the
left bundle branch block during right heart catheterization may result in complete heart block,
and this can be avoided by minimal catheter manipulation in right ventricular outflow tract.
Nursing Responsibilities/Patient Teaching

1. Patients who have undergone cardiac catheterization will require cardiac monitoring.
2. Assess cardiovascular function using the following schedule: q 15 minutes x 4, q 30
minutes x 4, q 1 hour x 2, then routine or per practitioner order. Assess for changes in
vital signs, bleeding or hematoma at catheter insertion site and for changes in
circulation, sensation, motion, and pulses in extremity where catheter was placed.
3. If femoral approach was used: Position patient in supine position, head gatched no more
than 30¬, and leg with insertion site extended, not flexed. Bed rest as per practitioner
order.
4. If radial approach was used: The patient should remain on bedrest for 4 hours;
bathroom privileges with assistance after 1 hour.
a. HOB 45 degrees for 1 hour, then level of patient comfort
b. After 4 hours, increase activity per orders
5. Administer intravenous hydration as per practitioner order.

Notify practitioner for:

1. Bleeding at catheter site.

2. Swelling/hematoma at catheter site.
3. Circulation, motor and sensation changes in extremity.
4. Vital sign changes (parameters specified in post procedure orders).
5. Chest pain.
6. Heart rhythm changes.
7. Urinary retention.
PACEMAKER/IMPLANTED DEFIBRILLATOR
Overview/description
A pacemaker is an electrically charged medical device. Your surgeon implants it under your skin
to help manage irregular heartbeats called arrhythmias.
Modern pacemakers have two parts. One part, called the pulse generator, contains the battery
and the electronics that control your heartbeat. The other part is one or more leads to send
electrical signals to your heart. Leads are small wires that run from the pulse generator to your
heart.
Pacemakers generally treat two types of arrhythmias:
• tachycardia, a heartbeat that’s too fast
• bradycardia, a heartbeat that’s too slow
Some people need a special type of pacemaker called a biventricular pacemaker, or bivent. You
may need a bivent if you have severe heart failure. A bivent makes the two sides of the heart
beat in sync. This is known as cardiac resynchronization therapy (CRT).
An implantable cardioverter-defibrillator (ICD) is a small battery-powered device placed in your
chest to monitor your heart rhythm and detect irregular heartbeats. An ICD can deliver electric
shocks via one or more wires connected to your heart to fix an abnormal heart rhythm.
You might need an ICD if you have a dangerously fast heartbeat (ventricular tachycardia) or a
chaotic heartbeat that keeps your heart from supplying enough blood to the rest of your body
(ventricular fibrillation). Ventricles are the lower chambers of your heart.
ICDs detect and stop abnormal heartbeats (arrhythmias). The device continuously monitors
your heartbeat and delivers electrical pulses to restore a normal heart rhythm when necessary.
An ICD differs from a pacemaker — another implantable device used to help control abnormal
heart rhythms.

Indications
You're a candidate for an ICD if you've had sustained ventricular tachycardia, survived a cardiac
arrest or fainted from a ventricular arrhythmia. You might also benefit from an ICD if you have:
• A history of coronary artery disease and heart attack that has weakened your heart.
• A heart condition that involves abnormal heart muscle, such as enlarged or
thickened heart muscle.
• An inherited heart defect that makes your heart beat abnormally. These include long
QT syndrome, which can cause ventricular fibrillation and death even in young
people with no signs or symptoms of heart problems.
• Other rare conditions that may affect your heart rhythm.
Pre, Intra and Post-Op Instructions/Care
PRE-OPERATIVE

• Please arrive at the hospital “fasting” (nothing to eat) from the previous midnight
• You may take your morning medications with a small sip of water
• If you have been instructed to have blood drawn, please do not forget (you may be
instructed to have this done several days before your procedure)
• Please make sure you have consulted with your physician if you are on coumadin or
insulinfor diabetes. For most procedures, your coumadin will be discontinued or
adjusted several days prior.
• If you have not received a phone call from the hospital or our office by the day
before the procedure to let you know what time to arrive, please call us.
• Please arrange to have someone drive you to the hospital and home after the
procedure as driving is typically limited for at least 1 week after device implantation
• If you develop a cold or are sick, please consult your physician immediately as we
may need to postpone your procedure.

INTRAOPERATIVE
Usually, the procedure to implant an ICD can be performed with numbing medication and a
sedative that relaxes you but allows you to remain aware of your surroundings. In some cases,
general anesthesia may be used so that you're unconscious for the procedure.
During surgery, one or more flexible, insulated wires (leads) are inserted into veins near your
collarbone and guided, with the help of X-ray images, to your heart. The ends of the leads are
secured to your heart, while the other ends are attached to the generator, which is usually
implanted under the skin beneath your collarbone. The procedure usually takes a few hours.
Once the ICD is in place, your doctor will test it and program it for your heart rhythm problem.
Testing the ICD might require speeding up your heart and then shocking it back into normal
rhythm.

POST-OPERATIVE
As you recover from ICD or S-ICD implant procedure, it’s important to follow your doctor’s
instructions, including:

• Walk, exercise, and bathe according to your doctor’s instructions.

• Don’t wear tight clothing that could irritate the skin over your device.
 • Avoid rubbing your device or the surrounding chest area.
• Tell your other doctors, dentists, and emergency personnel that you have an
implanted device and show them your Medical Device ID Card.
• Ask your doctor any questions you may have about your device, heart rhythm, or
medication.

Please call the physician or seek care if:

• Your bandage at the catheter site has become soaked with blood
• Any evidence of frank pus from the incision site
• Any increased swelling or pain since hospital discharge
• Any red or hot area around your incision site
• If you have a temperature >38.0 C
• If you have any chest pain, shortness of breath, or significant change in your vision.
These may be signs of an emergency – call 911.

Complications and Interventions

Once you are past the surgical implantation of an ICD and are completely healed, you should
expect to be able to return to your normal life. However, there is still a small risk of developing
post-surgical complications.

Post-surgical complications of ICD therapy include:

• Lead complications, such as lead "dislodgement"(movement of the leads out of their
proper position) or lead fracture. A malfunctioning lead can cause the loss of
effectiveness of the ICD system, or inappropriate shocks (see below).
• Movement of the ICD generator out of its proper position, which can cause pain,
skin erosion or bleeding.
• Inappropriate shocks, which cause pain, and can produce psychological trauma.
• ICD malfunction.

The most common of these complications are inappropriate shocks, that is, shocks delivered by
the ICD because the device “thinks” a life-treating arrhythmia is occurring when actually it is
not.

ICD shocks are not particularly dangerous, but they hurt. While the shocks are designed to be
delivered only when a life-threatening arrhythmia occurs, about 20% of people with ICDs at one
time or another will receive shocks for other reasons. These inappropriate shocks can be caused
by any very rapid heart rhythm such as atrial fibrillation, or by the rapid heart rate that you get
from strenuous exercise.

Preventing further inappropriate shocks depends on what is causing them. If an inappropriate

shock occurs due to atrial fibrillation or exercise, in most cases the doctor can "re-program" the
ICD to reduce the chance of further inappropriate shocks.

But sometimes inappropriate shocks can happen because one of the leads has become loose or
has developed a tiny fracture. Preventing inappropriate shocks caused by an ICD lead problem
usually requires a surgical procedure.

Finally, because ICDs are complex electronic devices that contain numerous essential (and
delicate) components, sometimes one of these components can fail to operate normally. If this
happens, the ICD may not be able to deliver therapy when it is needed, or it may deliver
inappropriate shocks. An ICD that fails to function normally almost always needs to be removed
and replaced with a new device.

In the effort to reduce complications that sometimes occur with standard ICDs, subcutaneous
ICDs have been developed recently. These devices are implanted under the skin in the chest
area, and entirely avoid having to place leads within blood vessels. This avoids any
complications related to the heart and blood vessels that sometimes occur with a standard ICD.
While subcutaneous ICDs have their own set of problems, early experience suggests that the
incidence of dangerous complications may be reduced with these devices.

Fortunately, the large majority of people who have ICDs never experience any serious
complications with their devices.
The idea of receiving an ICD is simply to protect you from dangerous arrhythmias; it is not
meant to drastically change your life.

Nursing Responsibilities/Patient Teaching

Monitor for complications of insertion such as:
• Pneumothorax (collapsed lung)
• Hemothorax (collection of blood in the pleural cavity)
• Perforation from the pacemaker lead
• Cardiac tamponade (pressure on the heart caused by fluid build-up around the
heart)
These complications are seen as shortness of breath, low blood pressure, chest pain, or a rapid
heart rate.
• Monitor for lead dislodgement, seen as ECG changes or hiccups if diaphragm is being
paced.
• Monitor ECG for loss of sensing, loss of capture, or failure to pace.
• Provide pain medications & interventions as needed.
• Assess insertion site for bleeding and infection.
• Apply ice pack to minimize pain and swelling for first 6 hours.
• Maintain bedrest for 12 hours.
• Restrict movement of the affected arm for 12-24 hours. After 24 hours, assist with
gentle ROM exercises 3 times daily, to restore normal movement & prevent stiffness.
• Do not give aspirin or heparin for 48 hours.
• If defibrillation is necessary, avoid the area surrounding generator site.

Discharge instructions to teach the patient:

 Placement of the pacemaker generator & leads, how it works, & the rate at which it is
set.
 Monitor site for bleeding & infection for the first week; bruising may be present.
 Avoid immersing the site in water for 3 days.
 Minimize arm & shoulder activity of affected arm and wear loose covering over
incision for 1-2 weeks, to prevent dislodgement of new leads.
 Avoid contact sports and heavy lifting for 2 months after surgery.
 Contact physician with fatigue, palpitations, or recurrence of symptoms (may indicate
pacemaker malfunction or battery depletion).
 Take radial pulse daily before arising & notify physician for rates outside those
programmed (may indicate pacemaker malfunction or battery depletion).
 Carry pacemaker information at all times & wear a MedicAlert bracelet (pacemaker
will trigger some airport security alarms).
• Discuss any possible procedures with cardiologist (somebprocedures - MRI,
electrocautery - may affect the pacemaker). Household appliances such as microwave
ovens, radios, & gardening tools will not affect the pacemaker. Cell phones currently
don’t appear to affect pacemakers.
CARDIAC ABLATION

Overview/description
Cardiac ablation is a procedure that can correct heart rhythm problems (arrhythmias).

Cardiac ablation works by scarring or destroying tissue in your heart that triggers or sustains an
abnormal heart rhythm. In some cases, cardiac ablation prevents abnormal electrical signals
from entering your heart and, thus, stops the arrhythmia.

Cardiac ablation usually uses long, flexible tubes (catheters) inserted through a vein or artery in
your groin and threaded to your heart to deliver energy in the form of heat or extreme cold to
modify the tissues in your heart that cause an arrhythmia.

Cardiac ablation is sometimes done through open-heart surgery, but it's often done using
catheters, making the procedure less invasive and shortening recovery times.

Indications
Cardiac ablation is a procedure that's used to correct heart rhythm problems.
When your heart beats, the electrical impulses that cause it to contract must follow a precise
pathway through your heart. Any interruption in these impulses can cause an abnormal
heartbeat (arrhythmia), which can sometimes be treated with cardiac ablation.
Ablation isn't usually your first treatment option. Ablation is a treatment option for people
who:
• Have tried medications to treat an arrhythmia without success
• Have had serious side effects from medications to treat arrhythmias
• Have certain types of arrhythmias that respond well to ablation, such as Wolff-
Parkinson-White syndrome and supraventricular tachycardia
• Have a high risk of complications from their arrhythmias, such as sudden cardiac arrest
Pre, Intra and Post-Op Instructions/Care

PREOPERATIVE

Pre-procedure testing
• EKG, event monitor if available
• LABS: BUN, Cr, electrolytes, PT/INR, pregnancy test
• Stress test
• Echocardiogram
• MRI/CT

Pre-procedure teaching
• Informed consent including procedural risks-cardiac and noncardiac
• Pre-op testing, medication instructions
• Expectations during the procedure
• Immediate post-procedure course
• ‘curative’ statistics for that ablation

Informed consent
• Non-delegable duty of cardiologist
• Must include:
o why ablation is recommended
o benefits of having the ablation
o risks associated with ablation
o risks of not having ablation
o alternatives (Babb, 2011)

Pre-procedure testing, medication

• Indication for labs, echo, ECG, MRI/CT
• Need to hold antiarrhythmic meds
• When/if to hold anticoagulant medications
• When to resume medications
• Follow-up lab tests as indicated
INTRAOPERATIVE
During cardiac ablation
Catheter ablation is performed in the hospital. Before your procedure begins, a specialist will
insert an intravenous line into your forearm or hand, and you'll be given a sedative to help you
relax. In some situations, general anesthesia may be used instead to place you in a sleep-like
state. What type of anesthesia you receive depends on your particular situation.
After your sedative takes effect, your doctor or another specialist will numb a small area near a
vein on your groin, neck or forearm. Your doctor will insert a needle into the vein and place a
tube (sheath) through the needle.
Your doctor will thread catheters through the sheath and guide them to several places within
your heart. Your doctor may inject dye into the catheter, which helps your care team see your
blood vessels and heart using X-ray imaging. The catheters have electrodes at the tips that can
be used to send electrical impulses to your heart and record your heart's electrical activity.
This process of using imaging and other tests to determine what's causing your arrhythmia is
called an electrophysiology (EP) study. An EP study is usually done before cardiac ablation in
order to determine the most effective way to treat your arrhythmia.
Once the abnormal heart tissue that's causing the arrhythmia is identified, your doctor will aim
the catheter tips at the area of abnormal heart tissue. Energy will travel through the catheter
tips to create a scar or destroy the tissue that triggers your arrhythmia.
In some cases, ablation blocks the electrical signals traveling through your heart to stop the
abnormal rhythm and allow signals to travel over a normal pathway instead.
The energy used in your procedure can come from:
• Extreme cold (cryoablation)
• Heat (radiofrequency)
• Lasers
Cardiac ablation usually takes three to six hours to complete, but complicated procedures may
take longer.
During the procedure, it's possible you'll feel some minor discomfort when the catheter is
moved in your heart and when energy is being delivered. If you experience any type of severe
pain or shortness of breath, let your doctor know.
POST-OPERATIVE
The physical examination should include surveillance of the following:

Puncture site assessment

Assess puncture site for:

• Bleeding- check pressure dressing for any oozing or bleeding from puncture site and
mark the size of bleed if possible
• Note: check for bleeding immediately after vomiting or vigorous coughing.
• Haematoma- assess site for swelling, redness and pain and mark the size of haematoma
if possible
• Note: A haematoma can indicate internal bleeding into the thigh, pelvis or
retroperitoneal space.
• Infection- assess site for heat, pain and redness. Also assess for other signs of infection
including an increase in temperature, tachycardia, and rigors.
• Ecchymosis- assess skin around site for purple discoloration.
• Assessment of potential complications
• Assess for retroperitoneal bleeding
• Assess vital signs- fluctuating BP response, bradycardia and hypotension are signs of
retroperitoneal bleeding.
• Assess for abdominal pain, groin pain and back pain.
• Note: Retroperitoneal haematomas are ipsilateral to the puncture site so pain on the
same side of the access site needs further investigations.
• Assess for diaphoresis.
• Assess for signs of bleeding - tachycardia, hypotension, decreased peripheral perfusion,
widening pulse pressure, agitation, decreased haemoglobin level
• Assess for arrhythmias
• Assess patient’s ECG rhythm on the cardiac monitor. Ensure patient is in sinus rhythm
(Link- Sinus rhythm)or is in a rhythm deemed normal for the patient
• Assess for thrombus
• Neurovascular observations: assess limb for colour, warmth, CRT, pulse strength,
sensation, movement and pain.
• In the presence of venous access site clot, the affected limb will appear red, swollen, the
patient will have an increase in pain levels and delayed CRT due to pooling of blood.
• In the presence of an arterial access site clot, the affected limb will appear pale, cool,
have diminished or absent pulses distal to the insertion site, have decreased sensation
and delayed CRT due to lack of supply of arterial blood.
Note: If you notice a limb with decreased perfusion assess pressure dressing to ensure it is not
too tight.
Note: For accurate assessment of the pulse, mark the pulse position on the patient’s foot. A
doppler can be utilised if a pulse is not palpable.
• Assess and document intake and output.

Complications and Interventions

Cardiac ablation carries a risk of complications, including:
• Bleeding or infection at the site where your catheter was inserted
• Damage to your blood vessels where the catheter may have scraped as it traveled to
your heart
• Puncture of your heart
• Damage to your heart valves
• Damage to your heart's electrical system, which could worsen your arrhythmia and
require a pacemaker to correct
• Blood clots in your legs or lungs (venous thromboembolism)
• Stroke or heart attack
• Narrowing of the veins that carry blood between your lungs and heart (pulmonary vein
stenosis)
• Damage to your kidneys from dye used during the procedure
• Death in rare cases

Discuss the risks and benefits of cardiac ablation with your doctor to understand if this
procedure is right for you.

Nursing Responsibilities/Patient Teaching

What happens after I get home?
Follow the instructions your nurse or doctor gave you. Most people can return to their normal
activities on the day after they leave the hospital.
• Don’t drive for 24 hours after you leave the hospital.
• Don’t drink alcohol for 24 hours after you leave the hospital.
• Avoid heavy physical activity for three days. Ask your doctor when you can return to
strenuous exercise.
• A small bruise at the puncture site is normal. If the site starts to bleed, lie flat and press
firmly on top of it. Have someone call the doctor or hospital.
Call 911 if you notice:
• The puncture site swells up very fast.
• Bleeding from the puncture site does not slow down when you press on it firmly.

Call your doctor if:

• Your leg with the puncture becomes numb or tingles, or your foot feels cold or turns
blue.
• The area around a puncture site looks more bruised.
• The spot begins to swell, or fluids drain from it.
• You feel pain or discomfort in your chest that moves into your neck, jaw or arm.
• You feel sick to your stomach or sweat a lot.
• You have a fast or irregular heartbeat.
• You feel short of breath.
• You feel dizzy or lightheaded enough to have to lie down.

ANGIOPLASTY/CARDIAC BYPASS
Overview/description

ANGIOPLASTY is the mechanical widening of a narrowed or totally obstructed blood vessel.

These obstructions are often caused by atherosclerosis.

DIFFERENT KINDS OF ANGIOPLASTY

• Coronary Angioplasty /Percutaneous Coronary Intervention (PCI) is a therapeutic

procedure to treat the stenotic coronary arteries of the heart found in coronary heart
disease. These stenotic segments are due to the build up of cholesterol-laden plaques
that form due to atherosclerosis
• Peripheral Angioplasty/PercutaneousTransluminal Angioplasty (PTA) is most commonly
done to treat narrowings in the leg arteries, especially the common iliac, external iliac,
superficial femoral and popliteal arteries. PTA can also be done to treat narrowings in
veins
• Renal Artery Angioplasty/Percutaneous Transluminal Renal Angioplasty(PTRA)
 Atherosclerotic obstruction of the renal artery can be treated with angioplasty.
  Renal artery stenosis can lead to hypertension and loss of renal function.

Indications

• Greatly increases blood flow through the blocked artery.

• Decreases chest pain (angina).
• Increases ability for physical activity that has been limited by angina or ischemia.
• Can also be used to open neck and brain arteries to help prevent stroke.

Pre, Intra and Post-Op Instructions/Care

PREOPERATIVE

You should not eat or drink anything for four hours prior to the procedure. You will be given
special instructions if you are diabetic. Your groin area will be washed and shaved in
preparation for the PTCA. If you have had coronary angiography prior to the angioplasty, this
will have been completed already.

INTRAOPERATIVE

The length of time of each procedure depends on the complexity of the individual diagnosis and
situation. Procedures last between 1-3 hours for most patients. Of course, due to the nature of
the procedure, each individual will encounter different parameters. Variables include the extent
and nature of each blockage, as well as the number of blockages.

You will receive various medications through an intravenous line in your arm. As with
angiography, you be drowsy during the procedure. The doctor may want to give you directions
during the procedure.

• As with Cardiac Catheterisation, you will be placed on an x-ray table upon your arrival in
the lab. Surgical sheets will cover you. Your groin will be cleansed with antiseptic and
numbed. (You will feel the sting of the needle, but then your groin will feel quite numb.)
 • Heart monitoring equipment will be placed on your arms and legs, and you may be
given oxygen to breathe.

• The angioplasty catheter (balloon-tipped) is inserted at the numb area, and advanced to
your heart, using x-ray guidance. Your cardiologist will inflate the tiny balloon in the
area where the blockage occurs. It is normal when the balloon is inflated at the point of
the blockage to feel chest pressure, or discomfort. Once the balloon is deflated, this will
subside. Some patients feel a stronger thumping of the heart or skipping of beats. Some
also feel a flushed feeling. All these sensations are normal. You will be asked at times to
hold your breath for a few seconds. You may also be asked to cough.
• The cardiologist may also put stents (tiny tubular shaped mesh devices that hold the
arteries open) in to the arteries to inhibit the reforming of the narrowing. Newer drug
eluting stents offer even greater assurance of the longevity of the repair.
• This procedure may be repeated several times if there is more than one narrowing or a
narrowing that is particularly long.

POST OPERATIVE

At the end of the procedure, a closure device for the groin incision may be used.

You will be moved to a recovery area for a short time, and then taken to your room. Your vital
signs and general well-being will be monitored in the room. Your groin area and dressing will be
frequently checked and you will remain in bed and keep your leg immobilised. Pain medication
will be given as required and you will be required to take other postoperative medication. You
will be able to eat as soon as you wish after the procedure.

Discharge

You will be required to stay in hospital at least overnight. Your cardiologist will discuss your
individual requirements with you prior to discharge. Your cardiologist will see you the morning
of discharge and discuss any further needs including follow-up consultations in the rooms and
also medication. The hospital staff may also discuss these requirements with you after this
consultation. You will receive prescriptions for the medicines you will need.

Complications and Interventions

No invasive procedure occurs without a certain amount of potential risk and complications.
Your doctor and the hospital staff follow your recovery closely so that if any complications arise,
corrective action can be taken immediately. Although the incidence is low, you should be aware
that the following complications may rarely occur:

• Allergic reaction to the dye or to other medications.

• A tear in the artery during the procedure.
• Severe bruising/bleeding into the groin area of the procedure leg. This may come to the
surface over the next few days.
• Changes in heart rhythm.
• Blood clotting o A heart attack or stroke

Nursing Responsibilities/Patient Teaching

Any surgical or invasive procedure carries risks. Before proceeding, you should seek a second
opinion from an appropriately qualified health practitioner.’ Follow-up Care Periodic follow-ups
with your cardiologist are quite important. Your cardiologist will discuss when your next
appointment should be made. After this, there will be a schedule of follow-ups and at least
yearly consultations. In some patients, re-narrowing of the artery may occur in the future. It is
important to realise that angioplasty and stenting, whilst removing the immediate problem, do
not cure coronary artery disease. It is vital that you maintain both your health and have regular
visits with your cardiologist and your GP to ensure continued health. Be aware of the signs and
symptoms of reoccurring heart problems and take measures to seek medical help immediately.
It is also vital to ensure that any medications you are prescribed are taken as prescribed. In
patients who have had stents, there is a life-long commitment to medication.

Current Trends in Cardiovascular Management

Ventricular Assisted Devices (VAD)

Overview

A ventricular assisted device is also known as a mechanical circulatory support device. It

is an implantable mechanical pump that helps pump blood from the lower chambers of the
heart to the different organs of the body. It is used in patients who have heart failure.
 A ventricular assisted device can be placed in the right, left or both ventricles of the
heart but, it is often used in the left and is commonly called left ventricular assisted device
(LVAD). Depending on the doctor, it can be implanted while waiting for a heart transplant or as
a long-term treatment if heart transplant is not possible for a variety of reasons.

Indications

A ventricular assisted device is a mechanical device that supports the lower left heart
chamber (LVAD), the lower right heart chamber (RVAD), or both lower heart chambers termed
as biventricular assisted device or BIVAD.

Depending on the case, the doctor may recommend that a person may have a VAD
implanted as in the following situations:

• Waiting for a heart transplant – referred to as a “bridge to transplant”

• As a long-term, permanent treatment referred to as “destination therapy” – such as in
the case of a patient who is not currently eligible for a heart transplant due to his/her
age or other conditions.
• As a “bridge to recovery” – that is in the case of those whose heart failure is temporary
until the heart is healthy enough to pump blood on its own.

Preparation for Surgery

• The doctor and the treatment team will have to explain to the patient on what to expect
before, during, and after the surgery including the associated potential risk of surgery.
• Talk to your doctor regarding food and medications you are taking in, when to stop
taking it, when to withhold and when to resume, or if it has potential effects that will
affect the outcome of the surgery.
• Your treatment team may ask you to bring several items which you will need to include:
1. A list of your medications
2. Eyeglasses, hearing aids or dentures
3. Personal care items
4. Loose-fitting, comfortable clothing
5. A copy of your advance directive
6. Portable music players, books, etc., that may help you relax
• During the surgery, do not wear jewelries, eyeglasses, contact lenses, dentures, and nail
polish
 • It is very important that you tell your doctor about any allergies to food and
medications.
The Perioperative Surgical Experience

Before the Surgery

1. The patient will have to stay in the hospital for comprehensive assessment and will
likely to receive treatment for heart failure.
2. The doctor will review several factors to decide if a VAD is the most appropriate
treatment option and to determine which VAD is the most appropriate depending
on his/her assessment of the patient’s condition which will include, among others,
the following:
• The severity of heart failure as appropriate for VAD.
• Other serious medical conditions that may affect health or quality of life with a
VAD.
• Areas or chambers of the heart that needs support. It could be the right, left, or
both ventricles.
• Tolerance to taking blood-thinning medications for a long period of time.
• Availability of strong social support from family and friends.
• Emotional and mental stability to take care of a VAD.
3. Your doctor will order several tests to evaluate your condition including:
• Echocardiogram – to determine the pumping function of the heart, assess your
heart valves and help determine the cause of your heart failure.
• Chest X-ray – to see the size and shape of your heart and lungs
• Blood tests – to check the liver, kidney, and thyroid function of your body, and to
check for symptoms of infection
• ECG – to record the electrical activity of the heart
• Cardiac catheterization – to measure the pressure and blood flow in your heart.
4. Your treatment team will educate you and your support system regarding VAD to
include:
• How your VAD works to support your heart
• Safety measures
• What to do if your control unit signals a problem with your VAD.
• How to respond to emergencies, such as failed battery
• How to care for your VAD, how to clean and check the equipment.
• How to shower without damaging the device (VAD).
• How to monitor for infections, and other complications after the surgery.
• Travel safety and restrictions with VAD
• Managing Stress regarding VAD along with your support systems
During the Procedure – What to expect or tell the patient

• The procedure will be done in the operating room with your cardiac surgeons, surgical
nurses, and anesthesiologists.
• The procedure is an open heart surgery that usually takes four to six hours.
• It will be done under general anesthesia or the patient will be asleep and won’t feel pain
during the entire procedure.
• The patient will be connected to a ventilator which can extend for several days after the
surgery.
• If the heart is stopped using medications during the surgery, the patient will be
connected to heart-lung bypass machine.
• Your surgical team will implant the VAD during the procedure. (Note that VAD comes in
different types).
• After your VAD is implanted and is working properly, your doctors will take you off the
heart-lung bypass machine so that the VAD can begin pumping through your heart.

After the Surgery

• After the surgery, the patient will need to stay in the ICU for intensive monitoring.
He/she will be given fluids, nutrition and medications through IV lines. There will also be
other tubes to drain urine from the bladder and drain fluid and blood from the heart
and chest.
• The patient will need to stay connected to a ventilator for a few days until he/she is able
to breathe well on his/her own.
• Depending on the patient’s response to surgery and towards recovery, his/her doctor
upon assessment will order for his/her transfer to a regular room.
• Once the patient is transferred to a regular room, the treatment team and nurses will
aid him/her to gradual ambulation to help in his/her recovery, and to prevent post-
surgery complications.
• Your doctor will prescribe antibiotics and blood-thinning medications to prevent
infections and other complications. It is very important to follow the instructions for
taking these medications.
• The patient will have to undergo regular blood tests to monitor the effects of blood-
thinning drugs and other medications.
• Once the patient has recovered and gained strength, his/her doctors and the treatment
team can agree on his/her discharge from the hospital.
 • Just before going home, the patient and his/her support system should be informed
about schedules of follow-up care including numbers and persons to contact for all
matters relating to his/her care.

Associated Complications Related to Surgery

• Blood clots – this can slow or block normal blood flow through the heart which can
potentially lead to stroke or heart attack, or cause the implanted VAD to stop working.
• Interventions include taking blood-thinning medications such as warfarin and aspirin
which should be taken as prescribed. The patient will have to be informed that he/she
will undergo regular blood tests for monitoring.
• Bleeding – educate the patient and his/her support system about the signs and
symptoms of bleeding, what to do initially, and to report it immediately. Tell the patient
to avoid injuries and minimize green leafy vegetables in his/her meal as it is rich in Vit.K
that can worsen the potential of bleeding.
• Infection – educate the patient and his/her support system to recognize and
immediately report the signs and symptoms of infection such as fluid draining in the
site, soreness or redness near the port, and/or fever. Teach them also skills on the
proper care and disinfection of the hands and ports to prevent infection.
• Device malfunctions – Teach the patient and his/her primary caregiver to recognize and
immediately report device malfunction so urgent attention can outright be given.
• Right heart failure – educate, empower, and encourage the patient to report any
subjective and objective experience of the signs and symptoms so necessary treatment
can be initiated through medications, and/or another surgery as assessed by the doctor.
References:

Starrh L. et al., 2018 Ventricular Assist Devices: The Basics. The Journal of Nurse Practitioners

Saeed D. 2018 Right Ventricular Failure and Biventricular support strategies. Cardiology Clinics.

Yancy CW, et al. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guidelines for the
management of heart failure. Journal of the American College of Cardiology
Heart Transplant

Overview

A heart transplant is an operation in which a diseased, failing heart is replaced with a

healthier donor heart. While it is considered a major operation, the chance of survival is good
with appropriate care and treatment.

Indications

Heart transplants are performed when other treatments for heart problems have failed
resulting to heart failure.

In adults, heart failure can be due to:

1. A weakening of the heart muscle (cardiomyopathy)
2. Coronary artery disease
3. Herat valve disease
4. Congenital heart defect
5. Recurrent ventricular arrhythmias not controlled by other treatments
6. Failure of a previous heart transplant

In children, heart failure is usually due to either a congenital heart defect and/or
cardiomyopathy.

Multi-organ transplant in which another organ transplant can be done at the same time
as a heart transplant in selected medical centers.

• Heart-kidney transplant
• Heart-liver transplant
• Heart-lung transplant

The Perioperative Surgical Experience

Before the Surgery

Preparations for a heart transplant often begins weeks or months before a patient
receive a donor heart. When your doctor recommends a heart transplant, you may be referred
to a heart transplant center or you can select one on your own. Factors to consider when
selecting a heart transplant center are the number of heart transplants performed each year
and the survival rates, health insurance coverage, and the availability of other services which
the patient might be needing after surgery including support groups, travel arrangements, and
local housing during the recovery period. Once you have chosen one, you will be screened if
you are eligible for a heart transplant to see if you:
• Have a heart condition that would benefit from transplantation
• Might benefit from other, less aggressive treatment choices
• Are healthy enough to undergo surgery and post-transplant treatments
• Will agree to quit smoking, if you smoke
• Are willing and able to follow the medical program outlined by the transplant team
• Can emotionally handle the wait for a donor heart
• Have a supportive network of family and friends to help you during stressful times

If the transplant center medical team determines that you’re a good candidate for a heart
transplant, they will put you on a waiting list while underdoing the necessary treatment for
heart failure. In the event that these fails and there isn’t available donor heart yet, they might
advise that you may be implanted with a ventricular assisted device (VAD) depending on your
case.

Immediately before transplant surgery

A heart transplant usually needs to occur within four (4) hours of organ removal for the
donor organ to remain usable. So the patient must be ready at all times once notified because
the transplant team have a limited time to accept the donation.

During the Procedure

Heart transplant is an open-heart surgical procedure that takes several hours. The
patient will be under general anesthesia and will be connected to a heart-lung bypass machine.
The operating surgeon will make an incision in the chest, separates the chest bone, open the rib
cage, and operate on the heart. He/she then removes the diseased heart and sews the donor
heart into place. He or she then attaches the major blood vessels to the donor heart. The new
heart usually starts beating when blood flow is restored. At certain times, an electric shock is
needed to make the donor heart beating properly. The patient will also be connected to a
ventilator and chest tube to drain fluids and blood from around the heart and lungs, and a
urinary catheter will also be in place.

After the Surgery

1. The patient will initially stay in the ICU for few days or depending on his/her
response to the surgery and towards recovery. He/She will be given the necessary
treatment until weaned from the ventilator and can be transferred to a regular
room.
2. Once the patient is transferred to a regular room, he/she will be assisted by the
nurses to gradual ambulation. The treatment continues until the patient can be
finally discharged from the hospital.
3. Upon discharge, the patient will be frequently and intensely monitored so it is
advised that he/she stays close to the transplant center for few months to a year.
4. The patient will be closely monitored for signs and symptoms of rejection such as
shortness of breath, fever, fatigue, anuria and/or weight gain. He/she should be
taught to report these immediately once experienced or observed.
5. Frequent heart biopsies will be done to determine whether his/her body is rejecting
the new heart. This is necessary and decreases over time.
6. There will be long-term adjustments after undergoing a heart transplant that
includes the following:
• Taking immunosuppresants – to decrease the activity of the immune system to prevent
it from attacking the donated heart. Taking these medications will be for a lifetime. The
patient will also likely to be given antimicrobials as he/she will be more prone to
infection. Taking these medications could result to some iatrogenic effects leading to
high blood pressure, high cholesterol, and diabetes among others.
Over time, as the risk of rejection decreases, the doses and the number of anti-rejection drugs
can be reduced.

• Managing medications, therapies and a lifelong care plan – your doctor will give
instructions regarding lifestyle changes, activity and exercise restrictions, smoking
cessation, and the importance of medical nutrition therapy. It is very important that you
strictly follow your doctor’s advice.

• Cardiac rehabilitation – these programs incorporate exercise and education to improve

your health that can start prior to discharge from the hospital.
Complications associated with surgery

Besides the risks of having open-heart surgery, which include bleeding, infection,. Blood
clot formations, risks and complications of a heart transplant include:

• Rejection of the donor heart – Educate the patient about this possibility and encourage
him/her to report signs and symptoms on initial experience or observation immediately
to his/her doctor. Make him/her realize the importance of compliance to
immunosuppresants or anti-rejection medications and the frequency of necessary heart
biopsies to determine rejection as it can also occur even without symptoms.
• Primary graft failure – this is the most common cause of death in the first few months
after transplant.
• Problems with arteries – cardiac allograft vasculopathy that can potentially lead to a
cardiac attack, heart failure, arrhythmias, or sudden cardiac death.
• Medication side effects – immunosuppressants lowers your immune system so you are
more prone to infections and it can cause serious kidney damage.
• Cancer – increased risk due to immunosuppressants.
References:

Kittleson, et al. 2017 Cardiac Transplantation: Current outcomes and contemporary

controversies, Journal of the American College of Cardiology

McCartney, et al., 2017 Long-term outcomes and management of the heart transplant
recipient. Best Practice and Research Clinical Anesthesiology

Yardley, et al., 2018 Importance of Physical capacity and the effects of exercise in heart
transplant recipients. World Journal of Transplantation

Coyne, C., Baier, W., Perra B., & Sherer, B.K. (1994). Controlled trial of backrest elevation after
coronary angiography. American Journal of Critical Care 3:282-288.

Keeling, A.W., Knight, E., Taylor, V., & Nordt, L.A. (1994). Postcardiac catheterization time-in-
bed study: Enhancing patient comfort through nursing research. Applied Nursing Research 7:14-
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Prinkey, L.A. (1992). Diagnostic testing. In C.E. Guzzetta & B.M. Dossey (Eds). Cardiovascular
Nursing: Holistic Practice, pp. 126-159. St. Louis: C.V. Mosby.

Nursing Department Policy, "Care of Patients with Arterial Lines", January 1995.

Nursing Department Standard of Practice, "Care of the Patient with an Arterial Line (Radial and
Brachial)", August 1994.

National Institute for Cardiovascular Outcomes Research. National Audit of Cardiac Rhythm
Management Devices 2013–2014. Available from www.devicesurvey.com (accessed 25
November 2015)

Brignole M , Auricchio A, Baron-Esquivias Get al. . 2013 ESC Guidelines on cardiac pacing and
cardiac resynchronization therapy. Eur Heart J2013; 34: 2281–329
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National Institute for Health and Care Excellence. Implantable cardioverter defibrillators and
cardiac resynchronisation therapy for arrhythmias and heart failure. NICE technology appraisal
(TA314) 2014. Available from https://www.nice.org.uk/guidance/ta314 (accessed 25 November
2015)

Bernstein AD , Daubert JC, Fletcher RDet al. . The revised NASPE/BPEG generic code for
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Electrophysiology/British Pacing and Electrophysiology Group. Pacing Clin Electrophysiol2002;
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patients with implantable defibrillators, pacemakers and arrhythmia monitors: facilities and
patient management. Heart Rhythm2011; 8: 1114–54
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Coursework #3
SINUS RHYTHM
 Sinus Rhythm
 Sinus Arrhythmia
 Sinus Bradycardia
 Sinus Tachycardia
 Sinus Pause

1. Sinus Rhythm

Defining Criteria
- There is a P wave, followed by a QRS complex at a regular rhythm and rate of 60 – 100
bpm.
- P:QRS ratio 1:1
- PR interval: Normal
- QRS width: Normal

2. Sinus Arrhythmia

Defining Criteria
- Rate: 60 – 100 bpm
- P wave present
- P:QRS ratio: 1:1
- PR interval: Normal
- QRS width: Normal
Clinical Manifestation
Sinus arrhythmia is a common incidental finding seen on presenting EKGs. The finding is
normal and found at a higher prevalence in younger individuals. Lack of sinus arrhythmia
may be a sign of underlying chronic disease requiring further investigation. It is rare for
patients with sinus arrhythmia to display symptoms. If present, symptoms such as shortness
of breath, lower extremity edema, dyspnea on exertion, or peripheral neuropathy are likely
due to some underlying cause and not sinus arrhythmia.

Etiology
Sinus arrhythmia is a common rhythm variation. It is seen more often in children and young
adults. Respirations lead to vagal stimuli resulting in R-R interval variations. Typically, its
presence is an indicator of good cardiovascular health. Loss of sinus arrhythmia may
indicate underlying heart failure or structural heart disease.

Treatment and Management

Sinus arrhythmia is a common finding on telemetry. It is considered to be a normal variation
found in healthy young adults. Upon confirming the diagnosis of sinus arrhythmia on EKG,
there are no further recommendations regarding treatment. Patients found to have sinus
arrhythmia should receive education that this is a common finding seen in young healthy
persons. It rarely requires further evaluation upon establishment of the diagnosis.

3. Sinus Bradycardia
Defining Criteria
- Rate: less than 60 bpm
- Rhythm: Regular
- P wave present
- P:QRS ratio: 1:1
- PR interval: Normal
- QRS width: Normal

Clinical manifestation
Majority of patients with sinus bradycardia do not have symptoms. Healthy young adults
and athletes tend to have an increased vagal tone which keeps them in sinus bradycardia at
rest. Also, patients above the age of 65 tend to have sinus bradycardia during sleep
secondary to the aging of the sino-atrial node. Using history to relate to the symptoms of a
patient with sinus bradycardia on an electrocardiogram is essential to come to the correct
diagnosis. Those who present with symptoms may present with the following:
  Fatigue
 Exercise intolerance
 Lightheadedness
 Dizziness
 syncope or presyncope
 worsening of anginal symptoms
 worsening of heart failure or cognitive slowing
When taking a history, a health care provider must include relevant questions which help
narrow down the differential. Such as any recent medication changes, medication
overdoses, chest pain, shortness of breath, history of prior myocardial infarction, symptoms
of intermittent palpitations, history of chest trauma, rash or recent tick bite, current or past
diagnosis of streptococcus pharyngitis, family history of sinus bradycardia, family history of
muscular dystrophy. Moreover, physical exam findings should be correlated with the history
given by the patient to help narrow the differential diagnosis, such as any murmur heard
during the physical exam or any skin exam findings of a developing rash.

Etiology
Sinus bradycardia has many intrinsic and extrinsic etiologies:
Inherent Etiologies 

 Chest trauma                                                            
 Ischemic heart disease
 Acute myocardial infarction
 Acute and chronic coronary artery disease
 Repair of congenital heart disease
 Sick sinus syndrome
 Radiation therapy
 Amyloidosis
 Pericarditis
 Lyme disease
 Rheumatic fever
 Collagen vascular disease
 Myocarditis
 Neuromuscular disorder
 X-linked muscular dystrophy
 Familial disorder
 Inherited channelopathy

Extrinsic Etiologies
 Vasovagal simulation (endotracheal suctioning)
 Carotid sinus hypersensitivity
 Beta-blockers
 Calcium channel blockers
 Digoxin
 Ivabradine
 Clonidine
 Reserpine
 Adenosine
 Cimetidine
 Antiarrhythmic Class I to IV
 Lithium
 Amitriptyline
 Narcotics
 Cannabinoids
 Hypothyroidism
 Sleep apnea
 Hypoxia
 Intracranial hypertension
 Hyperkalemia
 Anorexia nervosa

Actual management Standard management Applicability of care

1. Assessment  A patient in sinus  Educating patients

 Check for drug bradycardia should be at risk for this rhythm
toxicity evaluated for and making a closed loop
2. Medication hemodynamic instability. communication between
 Atropi If found to be them and their providers
ne hemodynamically can help further improve
 If due unstable patient can be the management of
to drug toxicity: treated with intravenous these rhythms.
 Calcium
(IV) atropine
Channel 0.5 mg push
Blocker every 3 to 5 minutes up to
 Beta
3 mg
Blocker
total.
 Digoxin
3. Pacemaker  If the patient's
symptoms and heart rate
do not improve, the
patient is a candidate for
a temporary pacemaker.
 If the patient on
arrival is
hemodynamically stable
but has signs and
symptoms of acute
myocardial infarction,
they should be treated for
an acute myocardial
infarction appropriately.

 If there are no signs

or symptoms of acute
myocardial infarction in a
hemodynamically stable
patient, then workup
should be initiated for an
infectious etiology
(including chest x-ray,
blood cultures, urinary
analysis, viral panel)
together with thyroid
function tests.

 If a patient is found
to have an infectious
etiology or a thyroid
abnormality, the patient
should be appropriately
treated for these
underlying etiologies and
re-evaluated.

 Upon re-evaluation,
if this patient is no longer
symptomatic and his
heart rate returns to
within normal limits
patient could be
evaluated for a possible
sick sinus syndrome or a
long-term implantable
loop recorder.

 While management
 decisions are being made
for a patient with sinus
bradycardia patient's
medication list should also
be reviewed for possible
causes of bradycardia,
and those medications
should be withdrawn if
possible. If a patient has
comorbid conditions that
require him to be on
certain medications which
may be causing his sinus
bradycardia than in that
case-patient may be a
candidate for a
permanent pacemaker.

 In cases where
medication can be
withdrawn than
medication, withdrawal is
made and if symptoms
and heart rate still do not
improve than the patient
may be evaluated for a
permanent pacemaker.

4. Sinus Tachycardia
Defining Criteria
- Rate: Greater yhan 100
 - Rhythm: Regular
- P wave present
- P:QRS ratio 1:1
- PR Interval normal
- QRS width: normal

Clinical Manifestation:
Tachycardias are characterized on the basis of origin; those that originate above the ventricle
are referred to as supraventricular tachycardias (SVTs) and those that originate from the
ventricle or purkinje fibers are characterized as ventricular tachycardias. The distinction
between the two types of tachycardias is critical at the beginning due to difference in their
prognosis. Ventricular tachycardias overall have grave prognosis and usually result from
significant heart disease. On the other hand, SVTs are usually nonlethal and have a more
benign prognosis.

Etiology

Most of the time, sinus tachycardia is a normal response of the cardiovascular system to
triggers that increase the heart rate. Normal sinus tachycardia may occur as part of the body's
response to certain conditions, such as intense physical activity or emotional distress. During
exercise, the heart rate typically increases as it needs to pump more oxygen to the muscles.
Emotional stress or anxiety can trigger an increase in neurotransmitters, such as dopamine and
epinephrine, which make the heart beat faster.

Other potential causes of normal sinus tachycardia include:

 stimulants, such as nicotine or caffeine

 alcohol
 anxiety
 stress
 low blood pressure
 infection

Less common causes of sinus tachycardia include:

 damage to cardiac tissue
 thyroid problems
 anemia
Actual Management Standard Management Applicability of Care
The primary management  reducing caffeine Tachycardia, a common
strategy in TMC is focused on intake problem in clinical practice,
aggressive attempts to  quitting smoking and can be secondary to
control tachycardia with the avoiding other physiological and/or
aim of improving heart sources of nicotine pathological causes. One
failure symptoms and  exercising regularly major adverse consequence
reversing left ventricular  drinking enough of pathological tachycardia is
dysfunction [6]. Depending water development of
on the clinical condition of consuming less than 2,300 cardiomyopathy with
the patient and type of milligrams of sodium per day subsequent heart failure.
tachycardia, rate control Early recognition is
and/or rhythm control important, and an aggressive
strategies are usually approach towards rate and
employed. Underlying rhythm control of the culprit
disease conditions, if present, tachycardia can result in
should be optimized as much resolution of symptoms and
as possible and as soon as partial or complete recovery
possible. of left ventricular function.
Concomitant heart failure
therapy to aid favorable
remodeling is recommended.
Close surveillance for
arrhythmia recurrence during
follow-up is warranted to
avoid further decline in
ventricular function

5. Sinus Pause/Arrest

Defining Criteria

- Rate: Varies
- Rhythm: Irregular
- P wave present
- P:QRS ratio 1:1
- PR Interval: Normal
- QRS width: Normal

Clinical Manifestation
Characterized by temporary cessation of sinus node discharges.
Electrocardiographically, there are no P waves and associated QRS-T during sinus pause.
This pause is sometimes followed by junctional rhythm or idioventricular rhythm.
Absence of escape rhythm results in asystole. Sinus pause less than 3 seconds usually
needs no investigation and may be seen in normal people; however, longer pauses (≥3
seconds) require further investigation and treatment.
Most patients with sinus node dysfunction (SND) present with one or more of the
following nonspecific symptoms, primarily due to bradycardia, sinus pause, and sinus
arrest:

 Fatigue

 Lightheadedness

 Palpitations

 Presyncope/syncope

 Dyspnea on exertion

 Chest discomfort

Etiology

Sinus pause, arrest, and exit block may arise from ischemic, inflammatory, or infiltrative
or fibrotic disease of the SA node, excessive vagal tone, sleep apnea, digitalis, and some
antiarrhythmic and other drugs. The causes of SND are discussed in detail elsewhere.

Actual Management Standard Management Applicability of Care

Management of the Dual-chamber pacing
patient is determined by versus single ventricular
the results of diagnostic pacing has been shown to
testing and more result in less atrial
importantly the correlation fibrillation, stroke, and
of results with the congestive heart failure,
presence or absence of but no difference in
symptoms. Patients with mortality. Ventricular
symptomatic SND and pacing even in the DDDR
bradyarrhythmias usually mode can promote heart
are indicated for failure, and newer
permanent pacemaker pacemakers employ
therapy. algorithms that favor
 maximizing atrial pacing,
Immediate management is with back-up dual chamber
rarely required. pacing.
Intravenous atropine or
beta-agonist for Patients who receive
symptomatic severe sinus permanent pacemakers
node dysfunction may be should be monitored for
warranted. signs and symptoms of
congestive heart failure. If
In a hospital or other heart failure develops, they
health care facility setting, should then have the
external pacing pads may pacemaker, if possible (no
be employed until more AV nodal disease present)
definitive treatment is programmed to minimize
administered (temporary ventricular pacing.
or permanent transvenous
pacing). Discontinuation of If left ventricular
any possibly offensive dysfunction develops as a
cardioactive drug is cause of necessary
warranted until pacing ventricular pacing,
therapy is instituted. consideration should be
given to upgrade the
pacemaker to a cardiac
resynchronization device.
For patients with atrial
tachyarrhythmias, one
should monitor for signs or
symptoms of congestive
heart failure or coronary
artery disease, which may
be related to the
tachyarrhythmias or
inappropriate ventricular
tracking of such
arrhythmias in patients
with AV block.

The pacemaker diagnostic

data (giving duration and
ventricular rates of
tachyarrhythmias) should
be used to guide
antiarrhythmic drug
therapy.
The patient with clinically
significant
bradyarrhythmias,
tachyarrhythmias, or both,
regardless of having
received a permanent
pacemaker requires long-
term follow-up. If a
pacemaker is not
implanted, clinical
reevaluation is warranted
to check for progression of
bradycardia and/or
symptoms, progression of
sinus node disease to
involve AV nodal or
infranodal disease (which
might signal a change of
medications or pacemaker
prescriptive therapy).

In addition, patients with

SND often have
concomitant (or develop
later) hypertension and/or
coronary artery disease,
and if present would be
diagnoses that also require
long-term follow-up.
Pacemaker evaluation
should include
interrogation of arrhythmia
logs (looking for atrial and
ventricular
tachyarrhythmias),
percentage of ventricular
pacing, rate histograms,
and automatic threshold
checks performed by the
pacemaker.

Patients indicated for long-

term antithrombotic
 therapy for atrial
tachyarrhythmias should
be evaluated for signs and
symptoms of bleeding, and
have regular INR checks if
taking warfarin.

Atrial Rhythm
1. Sinoatrial Block

Defining Criteria:

- Rate: Varies
- Rhythm: Irregular
- P present except in areas of dropped beat
- P:QRS ratio 1:1
- PR Interval: Normal
- QRS width: Normal
- Dropped beat: yes

Clinical Manifestation
Sinoatrial blocks are typically well-tolerated. They are not as serious as an AV block and most
often do not require treatment. In some people, they can cause fainting, altered mental status,
chest pain, hypoperfusion, and signs of shock. They can also lead to cessation of the SA node
and more serious dysrhythmias.

Etiology
The following conditions causes sinoatrial block:
 Sinus Node Dysfunction
  Perimyocarditis
 Acute Myocardial Infarction
 Ischemia
 Drug side effects e.g. Procainamide & Digitalis
 Well trained athletes display sinoatrial block as a physiological and normal finding
Actual Management Standard Management Applicability of Care

Sinoatrial blocks may cause 1. Administration of Nursing care for patients with
bradycardia. Evidence shows Atropine Sulfate sinoatrial blocks depend on
that the bradycardia and the 2. Transcutaneous how the block affects the
sinoatrial block itself do not Pacing patient. Lower-degree blocks
convey any significant 3. Permanent are less likely to cause
increase in mortality. Pacemaker hemo¬dynamic alterations
However, sinoatrial block and usually require only
may compromise cardiac monitoring for progression.
output and cause symptoms But as the block progresses,
or worsen symptoms. hemodynamic instability may
Symptomatic sinoatrial block lead to signs and symptoms.
is therefore frequently Nursing diagnoses that may
treated with external be appropriate include:
artificial pacemaker.
 decreased cardiac
output
 increased fluid volume
 acute pain related to
ischemia
 ineffective breathing
patterns
 ineffective tissue
perfusion
 activity intolerance,
fatigue, or both
 impaired gas exchange.

Focus care in these areas

while assisting the
management team to treat
underlying causes and
restore impulse conduction.
to as near normal as possible.
Once near-normal
conduction returns, many
signs and symptoms resolve
 and treatment is no longer
necessary.

2. Atrial Flutter

Defining Criteria:
- Rate: atrial 250 – 350, ventricular 125 – 175
- Rhythm: regular
- P wave-flutter waves
- P:QRS ratio: often 2:1
- PR interval: variable
- QRS width: normal
Clinical Manifestation
The electrical signal that causes Atrial Flutter circulates in an organized, predictable pattern.
This means that people with this usually continue to have a steady heartbeat, even though it is
faster than normal. It is possible that people with Atrial Flutter may feel no symptoms at all.
Others do experience symptoms, which may include:
 Heart palpitations (feeling like your heart is racing, pounding, or fluttering)
 Fast, steady pulse
 Shortness of breath
 Trouble with everyday exercises or activities
 Pain, pressure, tightness, or discomfort in your chest
 Dizziness, lightheadedness, or fainting
Etiology
The etiology of atrial flutter is similar to that of atrial fibrillation. Identifying the etiology of
cannot be under-emphasized, as treating the cause is frequently necessary to eliminate
recurrences of atrial flutter.
The classic mnemonic “PIRATES” encompases a vast majority of the causes:
 Pulmonary embolus, pulmonary disease, post-operative, pericarditis
 Ischemic heart disease, idiopathic (“lone AF”), intravenous central line (in right atrium)
 Rheumatic valvular disease (specifically mitral stenosis or mitral regurgitation)
 Anemia, alcohol (“holiday heart”), advanced age, autonomic tone (vagally-mediated
atrial fibrillation)
 Thyroid disease (hyperthyroidism)
 Elevated blood pressure (hypertension), electrocution
 Sleep apnea, sepsis, surgery
Historically, hypertension was thought to be the most common cause of atrial flutter; however,
obstructive sleep apnea is present in about 40% of patients, and it is well known that OSA
causes hypertension. The exact proportion of atrial flutter caused directly by OSA remains
unclear

Actual Management Standard Management Applicability of Care

The approach to the There are two main
management of patients with approaches which can be
atrial flutter requires the utilized to alleviate
consideration of two distinct symptoms of atrial fibrillation
areas ― alleviating — a “rate control” strategy
symptoms of atrial flutter or a “rhythm control”
and preventing strategy.
thromboembolism.
Rate Control:
Commonly, controlling the
ventricular rate in atrial
flutter can completely
resolve symptoms, and no
further therapy is needed.
This is done using AV
blocking medications, either
intravenously in the acute
setting or orally for long-term
therapy. Atrial flutter tends
to be more difficult to control
with AV blocking medications
than atrial fibrillation.
  Beta blockers
 Nondihydropyridine
Ca Ch. Blockers
 Digoxin

Rhythm Control:
Arhythm control strategy is
employed when rate control
is not successful in
completely eliminating
symptoms from atrial flutter
or if the ventricular rate is
refractory to the above-
mentioned AV blocking
medications.

 Cardioversion
 Antiarrhythmic drug
 Ablation

Atrial Fibrillation

Defining Criteria
The electrical signal that circles uncoordinated through the muscles of the atria causing them to
quiver (sometimes more than 400 times per minute) without contracting. The ventricles do not
receive regular impulses and contract out of rhythm, and the heartbeat becomes uncontrolled
and irregular.It is the most common arrhythmia, and 85 percent of people who experience it
are older than 65 years.
Rate: atrial: 350-400 bpm
Rhythm: Irregular
P wave present
PR interval length: not discernalble
Clinical Manifestation
▪ Heart palpitations
▪ Irregular pulse which feels too rapid or too
slow, racing, pounding or fluttering
▪ Dizziness or light-headedness
▪ Fainting
▪ Confusion
▪ Fatigue
▪ Trouble breathing
▪ Difficulty breathing when lying down
▪ Sensation of tightness in the chest

Etiology:
▪ Hypoxia
▪ Hypertension
▪ Congestive heart failure
▪ Coronary artery disease
▪ Dysfunction of the sinus node
▪ Mitral valve disorders
▪ Rheumatic heart disease
▪ Pericarditis
▪ Hyperthyroidism
▪ Excessive alcohol or caffeine consumption

Actual Management Standard Management Applicability of Care

Medical Treatment Chemical or electrical
▪ Rate control cardioversion
(slow ventricular rate to 80-
100 beats/minute)
▪ Digoxin
▪ Beta-adrenergic
blockers
▪ Calcium channel
blockers
 ▪ Example - Verapamil
(give IV if needed for quick
rate control)
▪ Antithrombotic
therapy
▪ Correction of rhythm
▪ Chemical or electrical
cardioversion

Supraventricular Tachycardia (SVT)

Encompasses all fast (tachy) dysrhythmias in which heart rate is greater than 150 beats per
minute (bpm)

Defining Criteria

Rate: Atrial 150-250bpm

Rhythm: Irregular
Not discernable P wave
Not discernable PR interval

Clinical Manifestation

Signs and Symptoms

▪ Palpitations
▪ Chest discomfort (pressure, tightness, pain)
▪ Lightheadedness or dizziness
▪ Syncope
▪ Shortness of breath
▪ A pounding pulse.
▪ Sweating
▪ Tightness or fullness in the throat
▪ Tiredness (fatigue)
▪ Excessive urine production

Etiology:

▪ Find underlying cause

• Stimulants
• Hypoxia
• Stress or over-exertion
• Hypokalemia
• Atherosclerotic heart disease

Actual Managenent Standard Management Applicability of care

▪ Stable patient’s
▪ Stable patient’s (asymptomatic)
(asymptomatic) ▪ Vagal maneuvers
▪ Vagal maneuvers ▪ Drug management
▪ Drug management ▪ Adenosine
▪ Adenosine ▪ Cardioversion if
▪ Cardioversion if unstable
unstable

Premature atrial contractions (PAC)

Defining Criteria

- Rate: usually regular but depends on the underlying cause

- Rhythm: Irregular
- P wave: usually up right but premature and abnormal in shape

Clinical Manifestation:

 Palpitations
 Skipped beat

Etiology:

▪ Occurs in healthy patients without

heart disease
▪ Stress
▪ Stimulants
▪ Hypertension
▪ Valvular condition
▪ Infectious diseases
▪ Hypoxia

Medical Treatment:

▪ No treatment necessary if
asymptomatic
▪ Treat the cause
▪ Drug therapy
▪ Beta Blockers
▪ Calcium Channel Blockers

Premature Ventricular Contractions

A PVC is not a rhythm, but an ectopic beat that arises from an irritable site in
the ventricles. PVCs appear in many different patterns and shapes, but are always wide and
bizarre compared to a “normal” beat

Defining criteria:

Rate: usually normal

Rhythm: Irregular
P wave: absent
QRS complex: varies

Clinical Manifestation:

▪ Palpitations
▪ Weakness
▪ Dizziness
▪ Hypotension

Etiology

▪ Exercise
▪ Stress
▪ Caffeine
▪ Heart disease: MI, CHF, Cardiomyopathy, Mitral valve prolapse
▪ Electrolyte imbalances
▪ Hypoxia
▪ Tricyclic antidepressants
▪ Digitalis toxicity

Actual Management Standard Management

• Assess patient ▪ Oxygen

• O2 at 2 liters; Oxygen may abate the ▪ Treat the cause
PVC’s ▪ Lidocaine is the drug of choice,
• Start IV if not already established and although procainamide is sometimes used
hang NS
• Monitor for frequent PVC’s and
 deterioration to more serious rhythms

Idioventricular Rhythm

Idioventricular arrhythmia is also termed ventricular escape rhythm. It is considered a last-

ditch effort of the ventricles to try to prevent cardiac standstill.
▪ The SA node and AV node have failed
▪ Rate usually between 20 to 40 beats per minute (bpm)

Defining Criteria:

-Rate: Ventricular 20-40 bpm

- Rhythm: Usually regular
- P wave: absent
- PR interval: not measurable
-QRS complexes: wide and bizarre

Clinical Manifestation

▪ Pale
▪ Cool with mottled skin
▪ Weakness
▪ Dizziness
▪ Hypotension
▪ Alteration in mental status

Etiology:

• Drugs- Digitalis
• MI
• Metabolic imbalances
• Hyperkalemia
• Cardiomyopathy

Actual Management Standard Management

 • Assess your patient: patient will most ▪ Atropine
likely be symptomatic with a weak, thready ▪ Pacing
pulse ▪ Dopamine when hypotensive
• Run continuous monitor strips/record ▪ CPR
• Begin CPR
• Call Code Blue
• Notify MD
• Start IV if not already established and
hang NS

Accelerated Idioventricular Rhythm

Accelerated idioventricular arrhythmia is last-ditch effort of the

ventricles to try to prevent cardiac standstill.
• The SA node and AV node have failed
• Rate usually between 40 to 100 beats per minute (bpm)
• Cardiac output is compromised

Defining Criteria

Rate: 41-100
Rhythm: Regular
P wave: absent
PR interval: not measurable
QRS comples: wide bizarre

Clinical Manifestation

▪ Pale
▪ Cool with mottled skin
▪ Weakness
▪ Dizziness
▪ Hypotension
▪ Alterations in mental status
Etiology

• Drugs- Digitalis
• MI
• Metabolic imbalances
• Hyperkalemia
• Cardiomyopathy

Actual Management Standard Management

▪ Atropine
• Assess your patient: patient will most ▪ Pacing
likely be symptomatic with a weak, thready ▪ Dopamine when hypotensive
pulse ▪ CPR
• Run continuous monitor strips/record
• Begin CPR
• Call Code Blue
• Notify MD
• Start IV if not already established and
hang NS

Ventricular Tachycardia

▪ Ventricular tachycardia almost always occurs in diseased hearts.

▪ Rhythm in which three or more PVCs arise in sequence at a rate greater than 100 beats
per minute.
▪ V-tach can occur in short bursts lasting less than 30 seconds, causing few or no
symptoms.
▪ Sustained v-tach lasts for more than 30 seconds and requires immediate treatment to
prevent death.
▪ V-tach can quickly deteriorate into ventricular fibrillation.

Defining Criteria:

Rate: 101-250bpm
Rhythm: atrial rhythm not distinguishable, ventricular rhythm usually regular
P wave: no p wave
QRS complex: wide bizarre

Clinical Manifestation

▪ Chest discomfort (angina)

▪ Syncope
▪ Light-headedness or dizziness
▪ Palpitations
▪ Shortness of breath
▪ Absent or rapid pulse
▪ Loss of consciousness
▪ Hypotension

Etiology

▪ Usually occurs with underlying heart

disease
▪ Commonly occurs with myocardial
ischemia or infarction
▪ Certain medications may prolong the QT interval predisposing the patient to ventricular
tachycardia
▪ Electrolyte imbalance
▪ Digitalis toxicity
▪ Congestive heart failure

Actual Management Standard Management

Assess your patient ▪ If there is no pulse, begin CPR
If symptomatic, treatment must be and follow ACLS protocol
aggressive and immediate ▪ If there is a pulse and the patient is
Pulse present unstable - cardiovert and begin drug therapy
• Oxygen ▪ Amiodarone
• Patent IV (preferably x2) ▪ Lidocaine
• Monitor patient very closely ▪ With chronic or recurrent VT
Pulseless ▪ Give antiarrhythmics
• Call Code Blue ▪ Long term may need ICD placed
• Begin CPR ▪ Ablation may be used for reentry
• Defibrillate ASAP
• Start IV if not already established and
hang NS
• Notify MD
Ventricular Fibrillation

V-Fib (coarse and fine)

Occurs as a result of multiple weak ectopic foci in the ventricles
No coordinated atrial or ventricular contraction
Electrical impulses initiated by multiple ventricular sites; impulses are not transmitted through
normal conduction pathway

Defining Criteria:

Rate: Not discernible

Rhythm: Rapid, unorganized, not discernable
Pwave: no
PR interval: None
QRS complex: none

Clinical Manifestation:

▪ Loss of consciousness
▪ Absent pulse

Etiology:

▪ AMI
▪ Untreated VT
▪ Electrolyte imbalance
▪ Hypothermia
▪ Myocardial ischemia
▪ Drug toxicity or overdose
▪ Trauma

Actual Management Standard Management

• Assess your patient ▪ CPR with immediate
• Many things can mimic v-fib on a defibrillation
monitor strip such as electric razor or ▪ Initiate ACLS algorithm
shivering
• You must check your patient!
• Treatment must be aggressive and
immediate
• Start CPR/ACLS
• Call a Code Blue
• Defibrillate ASAP

• Start IV if not already established and

hang NS
• Notify MD

Torsades de Pointes Rhythm

▪ Torsades de pointes is associated with a prolonged QT interval. Torsades usually

terminates spontaneously but frequently recurs and may degenerate into ventricular
fibrillation.
▪ The hallmark of this rhythm is the upward and downward deflection of the QRS
complexes around the baseline. The term Torsades de Pointes means “twisting about the
points.”

Defining Criteria:
Rate: Ventricular 150-250 bpm
Rhythm: Regular or irregular
Pwave: No
PR interval length: not measurable
QRS complexes: wide and bizarre

Clinical Manifestation:

▪ Chest pain
▪ Loss of consciousness
▪ Dizziness
▪ Nausea
▪ Shortness of breath

Etiology

▪ Is associated with prolonged QT

interval
▪ Is often caused by drugs conventionally recommended in treating VT
▪ Phenothiazine or tricyclic antidepressant overdose
▪ Electrolyte disturbances, especially hypokalemia and hypomagnesemia

Actual Management Standard Management

• Assess your patient ▪ Begin CPR and other code
• Make sure there aren’t any loose measures
leads or leads that have come off the patient ▪ Eliminate predisposing factors -
• Start CPR rhythm has tendency to recur unless
• Call a Code Blue precipitating factors are eliminated
• Start IV if not already established and ▪ Administrate magnesium sulfate
hang NS bolus
• Notify MD ▪ Synchronized cardioversion is
• Must treat the cause – usually giving indicated when the patient in unstable if
Magnesium possible or defibrillate

Asystole
Rate: No
Rhythm: No
P wave: none
PR interval length: none
QRS complex: none

Clinical Manifestation

▪ No palpable pulse
▪ No measurable BP
▪ Loss of consciousness

Etiology

▪ Extensive myocardial damage, secondary to acute myocardial infarction

▪ Failure of higher pacemakers
▪ Cardiac tamponade
▪ Prolonged v-fib
▪ Pulmonary embolism

Actual Management Standard Management

Assess your patient ▪ CPR
▪ ACLS protocol
Make sure their aren’t any loose leads or
leads that have come off the patient

Treatment must be aggressive and

immediate
• Call a Code Blue
• Start CPR/ACLS
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