Management for Patients with Cardiovascular Disorders

 Anatomy and physiology

The cardiovascular system delivers oxygenated blood to tissues and removes waste products.
Heart
 The heart is a hollow, muscular organ about the size of a closed fist, Located between
the lungs in the mediastinum, it’s about (12.5 cm) long and (9 cm) in diameter at its
widest point. It weighs between (250 to 285 g)
 The heart, controlled by the autonomic nervous system.
 The heart has four chambers, two atria and two ventricles separated by a cardiac
septum, also the heart has four valves.
The heart has two sets of valves:
 Atrioventricular (between atria and ventricles) — tricuspid valve on the heart’s right
side and mitral (bicuspid) valve on its left
 Semilunar — pulmonary valve (between the right ventricle and pulmonary artery)
and aortic valve (between the left ventricle and aorta).
• Coronary arteries originate from the aorta just above the aortic valve leaflets
• The coronary artery perfused during diastole.

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Myocardial perfusion
With a normal heart rate of 60 to 80 bpm there is ample time during diastole for
myocardial perfusion. However, as heart rate increases, diastolic time is shortened, which
may not allow adequate time for myocardial perfusion. As a result, patients are at risk for
myocardial ischemia (inadequate oxygen supply)

Blood pathways
Blood moves to and from the heart through specific pathways.
Deoxygenated venous blood returns to the right atrium through three vessels:
Superior vena cava — returning blood from the upper body
Inferior vena cava — returning blood from the lower body
Coronary sinus — returning blood from the heart muscle
Blood in the right atrium empties into the right ventricle (diastole) and is then ejected through
the pulmonic valve into the pulmonary artery when the ventricle contracts (systole).
The blood then travels to the lungs to be oxygenated.
From the lungs, blood travels to the left atrium through the pulmonary veins. The left atrium
empties the blood into the left ventricle, which then pumps the blood through the aortic valve
into the aorta and throughout the body with each contraction.
Because the left ventricle pumps blood against a much higher pressure than the right
ventricle, its wall is three times thicker.
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Normal Heart Sound
S1: the first heart sound produced by closure of the atrioventricular (mitral and tricuspid)
valves
S2: the second heart sound produced by closure of the semilunar (aortic and pulmonic) valves
Abnormal Heart Sound
S3: an abnormal heart sound detected early in diastole as resistance is met to blood entering
either ventricle; most often due to volume overload associated with heart failure
S4: an abnormal heart sound detected late in diastole as resistance is met to blood entering
either ventricle during atrial contraction; most often caused by hypertrophy of the ventricle
Key terms
Contractility: ability of the cardiac muscle to shorten in response to an electrical impulse.
Depolarization: electrical activation of a cell caused by the influx of sodium into the cell
while potassium exits the cell.
Repolarization: return of the cell to resting state, caused by reentry of potassium into the cell
while sodium exits the cell.
Diastole: period of ventricular relaxation resulting in ventricular filling.
Systole: period of ventricular contraction resulting in ejection of blood from the ventricles
into the pulmonary artery and aorta.
Sinoatrial (SA) node: primary pacemaker of the heart, located in the right atrium.
Atrioventricular (AV) node: secondary pacemaker of the heart, located in the right atrial
wall near the tricuspid valve
Cardiac conduction system.
 The SA node has the highest inherent rate (60 to 100 impulses per minute), the AV
node has the second- highest inherent rate (40 to 60 impulses per minute), and the
ventricular pacemaker sites have the lowest inherent rate (30 to 40 impulses per
minute).
 If the SA node malfunctions, the AV node generally takes over the pacemaker
function of the heart at its inherently lower rate.
 Impulses from the autonomic nervous system affect the SA node and alter its firing
rate to meet the body’s needs.

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Sign & symptoms related to cardiovascular disorders
 Chest pain or discomfort
 Shortness of breath or dyspnea
 Peripheral edema, weight gain, abdominal distention due to enlarged spleen and liver
or ascites (HF)
 Palpitations (tachycardia)
 Vital fatigue, sometimes referred to as vital exhaustion (characterized by feeling
unusually tired or fatigued, irritable, and dejected)
 Dizziness, syncope, or changes in level of consciousness
 Change in vital signs (Blood Pressure, Pulse rate, Body temperature, Respiratory rate)
 Diagnostic Evaluation
 Cardiac Biomarker Analysis
Myocardial cells that become necrotic from prolonged ischemia or trauma release specific
enzymes (creatine kinase [CK]), CK isoenzymes (CK-MB), and proteins (myoglobin, and
troponin) *
*myocardial protein; measurement is used to assess heart muscle injury.

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Brain (B-Type) Natriuretic Peptide Brain (B-type) natriuretic peptide (BNP) is a
neurohormone that helps regulate BP and fluid volume. It is primarily secreted from the
ventricles in response to increased preload with resulting elevated ventricular pressure.
**Diagnostic, monitoring, and prognostic tool in the setting of HF
Lipid Profile
Cholesterol, triglycerides, and lipoproteins are measured to evaluate a person’s risk of
developing atherosclerotic disease, especially if there is a family history of premature heart
disease, or to diagnose a specific lipoprotein abnormality.
Cholesterol Levels
Cholesterol (normal level is less than 200 mg/dL) is a lipid required for hormone synthesis
and cell membrane formation.
Triglycerides
Triglycerides (normal range is 100 to 200 mg/dL), composed of free fatty acids and glycerol,
are stored in the adipose tissue and are a source of energy
** HDLs (normal range in men is 35 to 70 mg/dL; in women, 35 to 85 mg/dL) have a
protective action.
** They transport cholesterol away from the tissue and cells of the arterial wall to the liver
for excretion.
** The risk of CAD increases as the LDL more than HDL:
** LDLs (normal level is less than 160 mg/dL) are the primary transporters of cholesterol and
triglycerides into the cell.
** One harmful effect of LDL is the deposition of these substances in the walls of arterial
vessels.
The lipoproteins are referred to as low-density lipoproteins (LDLs) and high-density
lipoproteins (HDLs).
Chest X-Ray and Fluoroscopy
A chest x-ray is obtained to determine the size, contour, and position of the heart.
Echocardiography
• Is used routinely to diagnose valvular disease. Thickened valve leaflets, vegetations or
growths on valve leaflets, myocardial function, and chamber size can be determined, and
pulmonary artery pressures can be estimated.
Electrocardiography records the electrical impulses generated from the heart muscle and
provides a graphic illustration of the summation of these impulses and their sequence and
magnitude.
 Exercise ECG (stress test)

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Exercise ECG is a noninvasive test that helps the practitioner assess cardiovascular response
to an increased workload.
Cardiac catheterization:
Invasive diagnostic procedure in which radiopaque arterial and venous catheters are
introduced into selected blood vessels of the right and left sides of the heart?
 Right Heart Catheterization
It involves the passage of a catheter from an antecubital or femoral vein into the right atrium,
right ventricle, pulmonary artery, and pulmonary arterioles.
 Left Heart Catheterization
Left heart catheterization is performed to evaluate the patency of the coronary arteries and the
function of the left ventricle and the mitral and aortic valves.

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Ishemic heart diseases

It is classified into myocardial infraction and angina pectoris

Myocardial Infarction

Myocardial infarction is used synonymously with coronary occlusion and

heart attack, yet MI is the most preferred term as myocardial ischemia causes
acute coronary syndrome (ACS) that can result in myocardial death.

 In an MI, an area of the myocardium is permanently destroyed

because plaque rupture and subsequent thrombus formation result
in complete occlusion of the artery.
 The spectrum of ACS includes unstable angina, non-ST-segment
elevation MI, and ST-segment elevation MI.
Pathophysiology

In each case of MI, a profound imbalance exists between myocardial oxygen

supply and demand.

 Unstable angina. There is reduced blood flow in a coronary

artery, often due to rupture of an atherosclerotic plaque, but the
artery is not completely occluded.
 Development of infarction. As the cells are deprived of oxygen,
ischemia develops, cellular injury occurs, and lack of oxygen leads
to infarction or death of the cells.
Causes

The causes of MI primarily stems from the vascular system.

 Vasospasm. This is the sudden constriction or narrowing of the

coronary artery.
 Decreased oxygen supply. The decrease in oxygen supply occurs
from acute blood loss, anemia, or low blood pressure.
 Increased demand for oxygen. A rapid heart rate, thyrotoxicosis,
or ingestion of cocaine causes an increase in the demand for
oxygen.

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Clinical Manifestations

Some of the patients have prodromal symptoms or a previous diagnosis of

CAD, but about half report no previous symptoms.

 Chest pain. This is the cardinal symptom of MI. Persistent and

crushing substernal pain that may radiate to the left arm, jaw,
neck, or shoulder blades. Pain is usually described as heavy,
squeezing, or crushing and may persist for 12 hours or more.
 Shortness of breath. Because of increased oxygen demand and a
decrease in the supply of oxygen, shortness of breath occurs.
 Indigestion. Indigestion is present as a result of the stimulation
of the sympathetic nervous system.
 Tachycardia and tachypnea. To compensate for the decreased
oxygen supply, the heart rate and respiratory rate speed up.
 Catecholamine responses. The patient may experience such as
coolness in extremities, perspiration, anxiety, and restlessness.
 Fever. Unusually occurs at the onset of MI, but a low-grade
temperature elevation may develop during the next few days.

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Prevention

A healthy lifestyle could help prevent the development of MI.

Exercise. Exercising at least thrice a week could help

lower cholesterol levels that cause vasoconstriction of the blood
vessels.
 Balanced diet. Fruits, vegetables, meat and fish should be
incorporated in the patient’s daily diet to ensure that he or she
gets the right amount of nutrients he or she needs.
 Smoking cessation. Nicotine causes vasoconstriction which can
increase the pressure of the blood and result in MI.
Assessment and Diagnostic Findings

The diagnosis of MI is generally based on the presenting symptoms.

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 Patient history. The patient history includes the description of
the presenting symptoms, the history of previous cardiac and
other illnesses, and the family history of heart diseases.
 ECG. ST elevation signifying ischemia; peaked upright or inverted
T wave indicating injury; development of Q waves signifying
prolonged ischemia or necrosis.
 Cardiac enzymes and isoenzymes. CPK-MB (isoenzyme in
cardiac muscle): Elevates within 4–8 hr, peaks in 12–20 hr, returns
to normal in 48–72 hr.
 LDH. Elevates within 8–24 hr, peaks within 72–144 hr, and may
take as long as 14 days to return to normal. An LDH 1 greater than
LDH2 (flipped ratio) helps confirm/diagnose MI if not detected in
acute phase.
 Troponins. Troponin I (cTnI) and troponin T (cTnT): Levels are
elevated at 4–6 hr, peak at 14–18 hr, and return to baseline over
6–7 days. These enzymes have increased specificity for necrosis
and are therefore useful in diagnosing postoperative MI when
MB-CPK may be elevated related to skeletal trauma.
 Myoglobin. A heme protein of small molecular weight that is
more rapidly released from damaged muscle tissue with elevation
within 2 hr after an acute MI, and peak levels occurring in 3–15 hr.
 Electrolytes. Imbalances of sodium and potassium can alter
conduction and compromise contractility.
 WBC. Leukocytosis (10,000–20,000) usually appears on the
second day after MI because of the inflammatory process.
 ESR. Rises on second or third day after MI, indicating
inflammatory response.
 Chemistry profiles. May be abnormal, depending on
acute/chronic abnormal organ function/perfusion.
 ABGs/pulse oximetry. May indicate hypoxia or acute/chronic
lung disease processes.
 Lipids (total lipids, HDL, LDL, VLDL, total cholesterol,
triglycerides, phospholipids). Elevations may reflect
arteriosclerosis as a cause for coronary narrowing or spasm.
 Chest x-ray. May be normal or show an enlarged cardiac shadow
suggestive of HF or ventricular aneurysm.
 Two-dimensional echocardiogram. May be done to determine
dimensions of chambers, septal/ventricular wall motion, ejection
fraction (blood flow), and valve configuration/function.

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 Nuclear imaging studies: Persantine or Thallium. Evaluates
myocardial blood flow and status of myocardial cells, e.g.,
location/extent of acute/previous MI.
 Cardiac blood imaging/MUGA. Evaluates specific and general
ventricular performance, regional wall motion, and ejection
fraction.
 Technetium. Accumulates in ischemic cells, outlining necrotic
area(s).
 Coronary angiography. Visualizes narrowing/occlusion of
coronary arteries and is usually done in conjunction with
measurements of chamber pressures and assessment of left
ventricular function (ejection fraction). Procedure is not usually
done in acute phase of MI unless angioplasty or emergency
heart surgery is imminent.
 Digital subtraction angiography (DSA). Technique used to
visualize status of arterial bypass grafts and to detect peripheral
artery disease.
 Magnetic resonance imaging (MRI). Allows visualization of
blood flow, cardiac chambers or intraventricular septum, valves,
vascular lesions, plaque formations, areas of necrosis/infarction,
and blood clots.
 Exercise stress test. Determines cardiovascular response to
activity (often done in conjunction with thallium imaging in the
recovery phase).
Medical Management

The goals of medical management are to minimize myocardial damage,

preserve myocardial function, and prevent complications.

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Mnemonics for Myocardial Infarction
Pharmacologic Therapy

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  Morphine administered in IV boluses is used for MI to reduce
pain and anxiety.
 ACE Inhibitors. ACE inhibitors prevent the conversion of
angiotensin I to angiotensin II to decrease blood pressure and for
the kidneys to secrete sodium and fluid, decreasing the oxygen
demand of the heart.
 Thrombolytics. Thrombolytics dissolve the thrombus in the
coronary artery,allowing blood to flow through the coronary
artery again, minimizing the size of the infarction and preserving
ventricular function.
Emergent Percutaneous Coronary Intervention

 The procedure is used to open the occluded coronary artery and

promote reperfusion to the area that has been deprived of
oxygen.
 PCI may also be indicated in patients with unstable angina and
NSTEMI for patients who are at high risk due to persistent
ischemia.
Nursing Management

The nursing management involved in MI is critical and systematic, and

efficiency is needed to implement the care for a patient with MI.

Nursing Assessment

One of the most important aspects of care of the patient with MI is the
assessment.

 Assess for chest pain not relieved by rest or medications.

 Monitor vital signs, especially the blood pressure and pulse rate.
 Assess for presence of shortness of breath, dyspnea, tachypnea,
and crackles.
 Assess for nausea and vomiting.
 Assess for decreased urinary output.
 Assess for the history of illnesses.
 Perform a precise and complete physical assessment to detect
complications and changes in the patient’s status.
 Assess IV sites frequently.
Diagnosis

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Based on the clinical manifestations, history, and diagnostic assessment data,
major nursing diagnoses may include.

 Ineffective cardiac tissue perfusion related to reduced coronary

blood flow.
 Risk for ineffective peripheral tissue perfusion related
to decreased cardiac output from left ventricular dysfunction.
 Deficient knowledge related to post-MI self-care.
Planning & Goals

To establish a plan of care, the focus should be on the following:

 Relief of pain or ischemic signs and symptoms.

 Prevention of myocardial damage.
 Absence of respiratory dysfunction.
 Maintenance or attainment of adequate tissue perfusion.
 Reduced anxiety.
 Absence or early detection of complications.
 Chest pain absent/controlled.
 Heart rate/rhythm sufficient to sustain adequate cardiac
output/tissue perfusion.
 Achievement of activity level sufficient for basic self-care.
 Anxiety reduced/managed.
 Disease process, treatment plan, and prognosis understood.
 Plan in place to meet needs after discharge.
Nursing Priorities

1. Relieve pain, anxiety.

2. Reduce myocardial workload.
3. Prevent/detect and assist in treatment of life-threatening
dysrhythmias or complications.
4. Promote cardiac health, self-care.
Nursing Interventions

Nursing interventions should be anchored on the goals in the nursing care

plan.

 Administer oxygen along with medication therapy to assist with

relief of symptoms.

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  Encourage bed rest with the back rest elevated to help decrease
chest discomfort and dyspnea.
 Encourage changing of positions frequently to help keep fluid
from pooling in the bases of the lungs.
 Check skin temperature and peripheral pulses frequently to
monitor tissue perfusion.
 Provide information in an honest and supportive manner.
 Monitor the patient closely for changes in cardiac rate and
rhythm, heart sounds, blood pressure, chest pain, respiratory
status, urinary output, changes in skin color, and laboratory
values.
Evaluation

After the implementation of the interventions within the time specified,

the nurse should check if:

 There is an absence of pain or ischemic signs and symptoms.

 Myocardial damage is prevented.
 Absence of respiratory dysfunction.
 Adequate tissue perfusion maintained.
 Anxiety is reduced.
Discharge and Home Care Guidelines

The most effective way to increase the probability that the patient will
implement a self-care regimen after discharge is to identify the patient’s
priorities.

 Education. This is one of the priorities that the nurse must teach
the patient about heart-healthy living.
 Home care. The home care nurse assists the patient with
scheduling and keeping up with the follow-up appointments and
with adhering to the prescribed cardiac rehabilitation
management.
 Follow-up monitoring. The patient may need reminders about
follow-up monitoring including periodic laboratory testing and
ECGs, as well as general health screening.
 Adherence. The nurse should also monitor the patient’s
adherence to dietary restrictions and prescribed medications.

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Angina Pectoris

Cardiovascular disease is the leading cause of death in the United States for
men and women of all racial and ethnic groups.

 Angina pectoris is a clinical syndrome usually characterized by

episodes of paroxysms of pain or pressure in the anterior chest.
 The cause is insufficient coronary blood flow, resulting in a
decreased oxygen supply when there is increased myocardial
demand for oxygen in response to physical exertion or emotional
stress.
Classification

There are five (5) classifications or types of angina.

Stable angina. There is predictable and consistent pain that


occurs on exertion and is relieved by rest and/or nitroglycerin.
 Unstable angina. The symptoms increase in frequency and
severity and may not be relieved with rest or nitroglycerin.
 Intractable or refractory angina. There is severe incapacitating
chest pain.
 Variant angina. There is pain at rest, with reversible ST-segment
elevation and thought to be caused by coronary artery
vasospasm.
 Silent ischemia. There is objective evidence of ischemia but the
patient reports no pain.
Pathophysiology

Angina is usually caused by atherosclerotic disease.

 Almost invariably, angina is associated with significant obstruction

of at least one major coronary artery.

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  Oxygen demands not met. Normally, the myocardium extracts a
large amount of oxygen from the coronary circulation to meet its
continuous demands.
 Increased demand. When there is an increase in demand, flow
through the coronary arteries needs to be increased.
 Ischemia. When there is blockage in a coronary artery, flow
cannot be increased, and ischemia results which may lead to
necrosis or myocardial infarction.
 Schematic Diagram for Angina Pectoris via Scribd.
Causes

Several factors are associated with angina.

 Physical exertion. This can precipitate an attack by increasing

myocardial oxygen demand.
 Exposure to cold. This can cause vasoconstriction and
elevated blood pressure, with increased oxygen demand.
 Eating a heavy meal. A heavy meal increases the blood flow to
the mesenteric area for digestion, thereby reducing the blood
supply available to the heart muscle; in a severely compromised
heart, shunting of the blood for digestion can be sufficient to
induce anginal pain.
 Stress. Stress causes the release of catecholamines, which
increased blood pressure, heart rate, and myocardial workload.
Clinical Manifestations

The severity of symptoms of angina is based on the magnitude of the

precipitating activity and its effect on activities of daily living.

Chest pain. The pain is often felt deep in the chest behind
the sternum and may radiate to the neck, jaw, and shoulders.
 Numbness. A feeling of weakness or numbness in the arms,
wrists and hands.
 Shortness of breath. An increase in oxygen demand could cause
shortness of breath.
 Pallor. Inadequate blood supply to peripheral tissues cause
pallor.
Gerontologic Considerations

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Here’s what you need to know when caring for geriatric patients with angina
pectoris:

The elderly person with angina may not exhibit the typical pain
profile because of the diminished responses of neurotransmitters
that occur with aging.
 Often, the presenting symptom in the elderly is dyspnea.
 Sometimes, there are no symptoms (“silent” CAD), making
recognition and diagnosis a clinical challenge.
 Elderly patients should be encouraged to recognize their chest
pain–like symptom (eg, weakness) as an indication that they
should rest or take prescribed medications.
Complications

Here are the common complications for patients with angina pectoris.

Myocardial infarction. Myocardial infarction is the end result of

angina pectoris if left untreated.
 Cardiac arrest. The heart pumps more and more blood to
compensate the decreased oxygen supply, and.the cardiac muscle
would ultimately fail leading to cardiac arrest.
 Cardiogenic shock. MI also predisposes the patient
to cardiogenic shock.
Assessment and Diagnostic Findings

The diagnosis of angina pectoris is determined through:

 ECG: Often normal when a patient at rest or when pain-

free; depression of the ST segment or T wave inversion signifies
ischemia. Dysrhythmias and heart block may also be present.
Significant Q waves are consistent with a prior MI.
 24-hour ECG monitoring (Holter): Done to see whether pain
episodes correlate with or change during exercise or activity. ST
depression without pain is highly indicative of ischemia.
 Exercise or
pharmacological stress electrocardiography: Provides more
diagnostic information, such as duration and level of activity
attained before the onset of angina. A markedly positive test is
indicative of severe CAD. Note: Studies have shown stress echo

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 studies to be more accurate in some groups than exercise stress
testing alone.
 Cardiac enzymes (AST, CPK, CK, and CK-MB; LDH and
isoenzymes LD1, LD2): Usually within normal limits (WNL);
elevation indicates myocardial damage.
 Chest x-ray: Usually normal; however, infiltrates may be present,
reflecting cardiac decompensation or pulmonary complications.
 Pco2, potassium, and myocardial lactate: May be elevated
during the anginal attack (all play a role in myocardial ischemia
and may perpetuate it).
 Serum lipids (total lipids, lipoprotein electrophoresis, and
isoenzymes cholesterols [HDL, LDL, VLDL]; triglycerides;
phospholipids): May be elevated (CAD risk factor).
 Echocardiogram: May reveal abnormal valvular action as the
cause of chest pain.
 Nuclear imaging studies (rest or stress scan): Thallium-
201: Ischemic regions appear as areas of decreased thallium
uptake.
 MUGA: Evaluates specific and general ventricle performance,
regional wall motion, and ejection fraction.
 Cardiac catheterization with angiography: Definitive test for
CAD in patients with known ischemic disease with angina or
incapacitating chest pain, in patients with cholesterolemia and
familial heart disease who are experiencing chest pain, and in
patients with abnormal resting ECGs. Abnormal results are
present in valvular disease, altered contractility, ventricular failure,
and circulatory abnormalities. Note: Ten percent of patients with
unstable angina have normal-appearing coronary arteries.
 Ergonovine (Ergotrate) injection: On occasion, may be used for
patients who have angina at rest to demonstrate hyper spastic
coronary vessels. (Patients with resting angina usually experience
chest pain, ST elevation, or depression and/or pronounced rise in
left ventricular end-diastolic pressure [LVEDP], fall in systemic
systolic pressure, and/or high-grade coronary artery narrowing.
Some patients may also have severe ventricular dysrhythmias.)
Medical Management

The objectives of the medical management of angina are to increase the

oxygen demand of the myocardium and to increase the oxygen supply.

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  Oxygen therapy. Oxygen therapy is usually initiated at the onset
of chest pain in an attempt to increase the amount of oxygen
delivered to the myocardium and reduce pain.

Pharmacologic Therapy

 Nitroglycerin gives long-term and short-term reduction of

myocardial oxygen consumption through selective vasodilation
within three (3) minutes.
 Beta-blockers reduces myocardial oxygen consumption by
blocking beta-adrenergic stimulation of the heart.
 Calcium channel blockers have negative inotropic effects.
 Antiplatelet medications prevent platelet aggregation,
and anticoagulants prevent thrombus formation.

Nursing Care Plan and Management

Nursing care management for chest pain involves prompt assessment,

effective pain management, and close monitoring of vital signs to ensure
timely intervention and promote patient well-being. In this section, we’ll dive
into the nursing care management for patients with angina pectoris (chest
pain).

Nursing Problem Priorities

The following are the nursing priorities for patients with chest pain:

1. Chest pain management. Addressing the patient’s chest pain

and managing it effectively to provide relief and prevent
complications.

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 2. Preventing complications. Providing interventions to prevent
potential myocardial complications and risks (i.e., myocardial
infarction, cardiac arrest, and cardiogenic shock).
3. Decreasing oxygen demand. Balancing activity and rest to
manage risk for decrease in cardiac output.
4. Reducing anxiety. Providing emotional support for relief of
anxiety and fear by addressing the patient’s emotional distress.
5. Patient education and teaching. Assessing the patient’s
understanding of chest pain and its management, self-
care strategies, lifestyle changes, and providing education to fill
any deficits in knowledge.

Nursing Assessment

Thorough nursing assessment of patients experiencing chest pain is essential

to accurately identify the underlying cause, assess the severity of symptoms,
and determine appropriate interventions, thereby facilitating timely and
effective care for optimal patient outcomes

Assess for the following subjective and objective data:

 Reports of pain varying in frequency, duration, and intensity

(especially as the condition worsens)
 Narrowed focus
 Distraction behaviors (moaning, crying, pacing, restlessness)
 Autonomic responses (e.g., diaphoresis, blood pressure, and pulse
rate changes, pupillary dilation, increased/decreased respiratory
rate)
 Situational crisis and reports of anxiety
Assess for factors related to the cause of chest pain:

 Decreased myocardial blood flow

 Increased cardiac workload and oxygen consumption
 Myocardial tissue ischemia
Nursing Diagnosis

Following a thorough assessment, a nursing diagnosis is formulated to

specifically address the challenges associated with chest pain (angina) based

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on the nurse’s clinical judgement and understanding of the patient’s unique
health condition. While nursing diagnoses serve as a framework for organizing
care, their usefulness may vary in different clinical situations. In real-life clinical
settings, it is important to note that the use of specific nursing diagnostic
labels may not be as prominent or commonly utilized as other components of
the care plan. It is ultimately the nurse’s clinical expertise and judgment that
shape the care plan to meet the unique needs of each patient, prioritizing their
health concerns and priorities.

Nursing Goals

Goals and expected outcomes should include:

The client will report anginal episodes decreased in frequency,

duration, and severity.
 The client will demonstrate relief of pain as evidenced by stable
vital signs, absence of muscle tension, and restlessness.
 The client will verbalize understanding of their disease
process, therapeutic regimen and management, and potential
complications.
 The client will initiate necessary lifestyle changes to prevent
potential myocardial complications of chest pain.
Nursing Interventions and Actions

Actions and interventions for a patient with chest pain (angina pectoris)
include:

 1. Managing Acute Chest Pain and Discomfort

 2. Administering Medications and Providing Pharmacologic
Interventions
 3. Decreasing Oxygen Demand and Managing Decreased Cardiac
Output
 4. Monitoring and Preventing Potential Myocardial Complications
 5. Providing Emotional Support and Reducing Anxiety

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  6. Providing Patient Education and Teachings for for Lifestyle
Changes

Evaluation

The expected patient outcomes and evaluation for patients with chest pain
may include the following:

 Reported pain is relieved.

 Reported decrease in anxiety.
 Understood ways to avoid complications and is free of
complications.
 Adhered to self-care program.

Discharge and Home Care Guidelines

The goals of education are to reduce the frequency and severity of anginal
attacks, to delay the progress of the underlying disease if possible, and to
prevent complications.

Reduce anginal attacks. Activities should be planned to


minimize the occurrence of angina episodes.
 Follow-up monitoring. The patient may need reminders about
follow-up monitoring, including periodic blood laboratory testing
and ECGs.
 Compliance to therapeutic regimen. The home care nurse may
monitor the patient’s compliance to dietary restrictions and to
prescribed antianginal medications.
Documentation Guidelines

The focus of documentation in a patient with angina pectoris includes:

 Nature, extent, and duration of problem.

 Effect on independence and lifestyle.
 Characteristics of pain, precipitators, and what relieves pain.
 Pulses and BP.
 Client’s fear and signs and symptoms exhibited.
 Responses and actions of family/SOs.

23
  Deviation from prescribed treatment plan and client’s reasons in
own words.
 Consequences of actions to date.
 Plan of care.
 Teaching plan.

Heart Failure

Heart failure, also known as congestive heart failure, is recognized as a clinical

syndrome characterized by signs and symptoms of fluid overload or of
inadequate tissue perfusion.

 Heart failure is the inability of the heart to pump

sufficient blood to meet the needs of the tissues for oxygen and
nutrients.
 The term heart failure indicates myocardial disease in which
there is a problem with contraction of the heart (systolic
dysfunction) or filling of the heart (diastolic dysfunction) that
may or may not cause pulmonary or systemic congestion.
 Heart failure is most often a progressive, life-long condition that
is managed with lifestyle changes and medications to prevent
episodes of acute decompensated heart failure.
Classification

Heart failure is classified into two types: left-sided heart failure and right-sided
heart failure.

Left-Sided Heart Failure

24
  Left-sided heart failure or left ventricular failure have different
manifestations with right-sided heart failure.
 Pulmonary congestion occurs when the left ventricle cannot
effectively pump blood out of the ventricle into the aorta and the
systemic circulation.
 Pulmonary venous blood volume and pressure increase, forcing
fluid from the pulmonary capillaries into the pulmonary tissues
and alveoli, causing pulmonary interstitial edema and impaired
gas exchange.
Right-Sided Heart Failure

 When the right ventricle fails, congestion in the peripheral tissues

and the viscera predominates.
 The right side of the heart cannot eject blood and cannot
accommodate all the blood that normally returns to it from the
venous circulation.
 Increased venous pressure leads to JVD and increased capillary
hydrostatic pressure throughout the venous system.
The American College of Cardiology and American Heart Association have
classifications of heart failure.

Stage A. Patients at high risk for developing left ventricular

dysfunction but without structural heart disease or symptoms of
heart failure.
 Stage B. Patients with left ventricular dysfunction or structural
heart disease that has not developed symptoms of heart failure.
 Stage C. Patients with left ventricular dysfunction or structural
heart disease with current or prior symptoms of heart failure.
 Stage D. Patients with refractory end-stage heart failure requiring
specialized interventions.
Pathophysiology

Heart failure results from a variety of cardiovascular conditions, including

chronic hypertension, coronary artery disease, and valvular disease.

 As HF develops, the body activates neurohormonal compensatory

mechanisms.
 Systolic HF results in decreased blood volume being ejected from
the ventricle.

25
  The sympathetic nervous system is then stimulated to
release epinephrine and norepinephrine.
 Decrease in renal perfusion causes renin release, and then
promotes the formation of angiotensin I.
 Angiotensin I is converted to angiotensin II by ACE which
constricts the blood vessels and stimulates aldosterone release
that causes sodium and fluid retention.
 There is a reduction in the contractility of the muscle fibers of the
heart as the workload increases.
 Compensation. The heart compensates for the increased
workload by increasing the thickness of the heart muscle.
Incidences

Heart failure can affect both women and men, although the mortality is higher
among women.

 There are also racial differences; at all ages death rates are higher
in African American than in non-Hispanic whites.
 Heart failure is primarily a disease of older adults, affecting 6% to
10% of those older than 65.
 It is also the leading cause of hospitalization in older people.
Causes

Systemic diseases are usually one of the most common causes of heart failure.

 Coronary artery disease. Atherosclerosis of the coronary

arteries is the primary cause of HF, and coronary artery disease is
found in more than 60% of the patients with HF.
 Ischemia. Ischemia deprives heart cells of oxygen and leads
to acidosis from the accumulation of lactic acid.
 Cardiomyopathy. HF due to cardiomyopathy is usually chronic
and progressive.
 Systemic or pulmonary hypertension. Increase in afterload
results from hypertension, which increases the workload of the
heart and leads to hypertrophy of myocardial muscle fibers.
 Valvular heart disease. Blood has increasing difficulty moving
forward, increasing pressure within the heart and increasing
cardiac workload.

Clinical Manifestations

26
The clinical manifestations produced y the different types of HF are similar and
therefore do not assist in differentiating the types of HF. The signs and
symptoms can be related to the ventricle affected.

Left-sided HF

 Dyspnea or shortness of breath may be precipitated by minimal

to moderate activity.
 Cough. The cough associated with left ventricular failure is
initially dry and nonproductive.
 Pulmonary crackles. Bibasilar crackles are detected earlier and
as it worsens, crackles can be auscultated across all lung fields.
 Low oxygen saturation levels. Oxygen saturation may decrease
because of increased pulmonary pressures.

27
from Cardiovascular Mnemonics

28
from Cardiovascular Mnemonics

29
Right-sided HF

 Enlargement of the liver result from venous engorgement of the

liver.
 Accumulation of fluid in the peritoneal cavity may increase
pressure on the stomach and intestines and cause gastrointestinal
distress.
 Loss of appetite results from venous engorgement and venous
stasis within the abdominal organs.
Prevention

Prevention of heart failure mainly lies in lifestyle management.

Healthy diet. Avoiding intake of fatty and salty foods greatly

improves the cardiovascular health of an individual.
 Engaging in cardiovascular exercises thrice a week could keep
the cardiovascular system up and running smoothly.
 Smoking cessation. Nicotine causes vasoconstriction that
increases the pressure along the vessels.
Complications

Many potential problems associated with HF therapy relate to the use

of diuretics.

Hypokalemia. Excessive and repeated dieresis can lead

to hypokalemia.
 Hyperkalemia. Hyperkalemia may occur with the use of ACE
inhibitors, ARBs, or spironolactone.
 Prolonged diuretic therapy might lead to hyponatremia and result
in disorientation, fatigue, apprehension, weakness, and muscle
cramps.
 Dehydration and hypotension. Volume depletion from
excessive fluid loss may lead to dehydration and hypotension.
Assessment and Diagnostic Findings

HF may go undetected until the patient presents with signs and symptoms of
pulmonary and peripheral edema.

30
  ECG: May show hypertrophy, axis deviation, ischemia, and
damage patterns. Dysrhythmias and ST-T segment abnormalities
may be present.
 Chest x-ray: May show enlarged cardiac shadow or abnormal
contour indicating ventricular aneurysm.
 Sonograms (echocardiography, Doppler, and transesophageal
echocardiography): May reveal chamber dimensions, valvular
function/structure, and ventricular dilation and dysfunction.
 Heart scan (MUGA): Measures cardiac volume, ejection fraction,
and wall motion.
 Exercise or pharmacological stress myocardial perfusion:
Determines presence of myocardial ischemia and wall motion
abnormalities.
 PET scan: Sensitive test for evaluating myocardial ischemia and
viability.
 Cardiac catheterization: Assesses pressures, differentiates right-
versus left-sided heart failure, and evaluates coronary artery
patency.
 Liver enzymes: Elevated in liver congestion/failure.
 Digoxin and other cardiac drug levels: Determines therapeutic
range.
 Bleeding and clotting times: Identifies clotting risks and
therapeutic range.
 Electrolytes: May be altered due to fluid shifts, renal function, or
diuretic therapy.
 Pulse oximetry: Measures oxygen saturation, especially in
conjunction with COPD or chronic HF.
 Arterial blood gases (ABGs): Reflects respiratory and acid-base
status.
 BUN/creatinine: Evaluates renal perfusion and function.
 Serum albumin/transferrin: Indicates protein intake and liver
function.
 Complete blood count (CBC): Assesses for anemia, polycythemia,
and dilutional changes.
 ESR: Evaluates acute inflammatory reaction.
 Thyroid studies: Determines thyroid activity as a potential
precipitator of HF.

Medical Management

31
The overall goals of management of HF are to relieve patient symptoms, to
improve functional status and quality of life, and to extend survival.

from Cardiovascular Care Nursing Mnemonics.

32
Pharmacologic Therapy

 ACE Inhibitors. ACE inhibitors slow the progression of HF,

improve exercise tolerance, decrease the number of
hospitalizations for HF, and promote vasodilation and diuresis by
decreasing afterload and preload.
 Angiotensin II Receptor Blockers. ARBs block the conversion of
angiotensin I at the angiotensin II receptor and cause decreased
blood pressure, decreased systemic vascular resistance, and
improved cardiac output.
 Beta Blockers. Beta blockers reduce the adverse effects from
the constant stimulation of the sympathetic nervous system.
 Diuretics. Diuretics are prescribed to remove excess
extracellular fluid by increasing the rate of urine produced in
patients with signs and symptoms of fluid overload.
 Calcium Channel Blockers. CCBs cause vasodilation, reducing
systemic vascular resistance but contraindicated in patients with
systolic HF.
Nutritional Therapy

 Sodium restriction. A low sodium diet of 2 to 3g/day reduces

fluid retention and the symptoms of peripheral and pulmonary
congestion, and decrease the amount of circulating blood
volume, which decreases myocardial work.
 Patient compliance. Patient compliance is important because
dietary indiscretions may result in severe exacerbations of HF
requiring hospitalizations.
Additional Therapy

 Supplemental Oxygen. The need for supplemental oxygen is

based on the degree of pulmonary congestion and resulting
hypoxia.
 Cardiac Resynchronization Therapy. CRT involves the use of a
biventricular pacemaker to treat electrical conduction defects.
 Ultrafiltration. Ultrafiltration is an alternative intervention for
patients with severe fluid overload.

33
  Cardiac Transplant. For some patients with end-stage heart
failure, cardiac transplant is the only option for long term survival.

Nursing Care Plans & Management

Nurses greatly influence the outcomes of patients with heart failure through
education and monitoring despite high morbidity and mortality rates.
Education empowers patients, improving adherence and preventing
complications. Vigilant monitoring enables early intervention, reducing risks.
Nurses play a crucial role in reducing HF morbidity and mortality.

Nursing Problem Priorities

The following are the nursing priorities for patients with congestive heart
failure:

Improve myocardial contractility and perfusion. Enhance

heart’s pumping function to ensure adequate blood flow to
organs through medications, monitoring vital signs, and
optimizing fluid balance.
 Manage fluid volume. Monitor fluid balance, assess for signs of
retention, administer diuretics, monitor weight, and promote
adherence to a low-sodium diet.
 Prevent complications. Monitor for and manage complications
such as pulmonary edema, arrhythmias, and thromboembolism
through close monitoring, medication administration, and patient
education.
 Promote activity tolerance. Encourage 30 minutes of daily
physical activity (as tolerated), collaborate on a schedule, and
prioritize activities.
 Reduce anxiety. Provide comfort, psychological support, and
teach anxiety management techniques.
 Minimize powerlessness. Encourage patient expression of
concerns and involve them in decision-making.
 Provide disease information and prevention
education. Educate patients about heart failure, its impact,
prognosis, lifestyle modifications, medication adherence, and
seeking timely care to prevent worsening of symptoms.
Nursing Assessment

34
Nursing assessment for patients with heart failure emphasizes evaluating the
efficacy of treatment and the patient’s adherence to self-management
strategies. Monitoring and reporting worsening signs and symptoms of heart
failure are essential for adjusting therapy. Additionally, the nurse addresses the
patient’s emotional well-being, as heart failure is a chronic condition linked
to depression and psychosocial concerns

Health History

 Assess the signs and symptoms such as dyspnea, shortness of

breath, fatigue, and edema.
 Assess for sleep disturbances, especially sleep suddenly
interrupted by shortness of breath.
 Explore the patient’s understanding of HF, self management
strategies, and the ability and willingness to adhere to those
strategies.
Physical Examination

 Auscultate the lungs for presence of crackles and wheezes.

 Auscultate the heart for the presence of an S3 heart sound.
 Assess JVD for presence of distention.
 Evaluate the sensorium and level of consciousness.
 Assess the dependent parts of the patient’s body for perfusion
and edema.
 Assess the liver for hepatojugular reflux.
 Measure the urinary output carefully to establish a baseline
against which to assess the effectiveness of diuretic therapy.
 Weigh the patient daily in the hospital or at home.
Assess for the following subjective and objective data:

 Increased heart rate (tachycardia)

 ECG changes
 Changes in BP (hypotension/hypertension)
 Extra heart sounds (S3, S4)
 Decreased urine output (oliguria)
 Diminished peripheral pulses
 Orthopnea
 Crackles
 Jugular vein distention
 Edema

35
  Chest pain
 Weakness
 Fatigue
 Changes in vital signs
 Presence of dysrhythmias
 Dyspnea
 Pallor
 Diaphoresis
 Weight gain
 Respiratory distress
 Abnormal breath sounds
Assess for factors related to the cause of congestive heart failure:

 Altered circulation
 Altered myocardial contractility/inotropic changes
 Alterations in rate, rhythm, electrical conduction
 Decreased cardiac output
 Structural changes (e.g., valvular defects, ventricular aneurysm)
 Poor cardiac reserve
 Side effects of medication
 Imbalance between oxygen supply/demand
 Prolonged bed rest
 Immobility
 Reduced glomerular filtration rate (decreased cardiac
output)/increased antidiuretic hormone (ADH) production, and
sodium/water retention.
 Changes in glomerular filtration rate
 Use of diuretics
 Lack of understanding
 Misconceptions about interrelatedness of cardiac
function/disease/failure
 Invasive procedures
 Prolonged hospitalization
 Alveolar edema secondary to increased ventricular pressure
 Retained secretions
 Increased metabolic rate secondary to pneumonia
Nursing Diagnosis

Following a thorough assessment, a nursing diagnosis is formulated to

specifically address the challenges associated with heart failure based on the

36
nurse’s clinical judgement and understanding of the patient’s unique health
condition. While nursing diagnoses serve as a framework for organizing care,
their usefulness may vary in different clinical situations. In real-life clinical
settings, it is important to note that the use of specific nursing diagnostic
labels may not be as prominent or commonly utilized as other components of
the care plan. It is ultimately the nurse’s clinical expertise and judgment that
shape the care plan to meet the unique needs of each patient, prioritizing their
health concerns and priorities.

Nursing Goals

Major goals for patients with heart failure include promoting physical activity,
reducing fatigue, alleviating symptoms of fluid overload, managing anxiety,
fostering patient empowerment in decision-making, and providing
comprehensive health education to the patient and their family. Goals and
expected outcomes may also include:

 The patient will exhibit optimal cardiac output, indicated by vital

signs within acceptable ranges, absence/control of dysrhythmias,
and absence of heart failure symptoms.
 The patient will engage in activities that reduce cardiac workload.
 The patient will actively participate in desired activities and meet
their own self-care needs.
 The patient will maintain stable fluid volume, with balanced intake
and output, clear/clearing breath sounds, vital signs within
acceptable range, stable weight, and absence of edema.
 The patient will verbalize understanding of individual dietary and
fluid restrictions.
 The patient will prioritize maintaining skin integrity.
 The patient will effectively manage pain.
 The patient will identify strategies to reduce anxiety.
 The patient will exhibit improved concentration.
 The patient will actively participate in their treatment regimen
based on their abilities and situation.
Nursing Interventions and Actions

Therapeutic interventions and nursing actions for patients with congestive

heart failure may include:

 1. Initiating Interventions for Decrease in Cardiac Output

37
 2. Monitoring Diagnostic Procedures and Laboratory Studies
 3. Administering Medication and Providing Pharmacological
Interventions
 4. Maintaining or Improving Respiratory Function
 5. Managing Fluid Volume and Electrolyte Imbalance
 6. Providing Perioperative Nursing Care
 7. Managing Acute Pain and Discomfort
 8. Promoting Adequate Tissue Perfusion and Managing Decreased
Cardiac Tissue Perfusion
 9. Promoting Optimal Nutritional Balance and Adherence to Low-
Sodium Diet
 10. Maintaining Skin Integrity & Preventing Pressure Ulcers
 11. Managing Decreased Tolerance to Activity and Fatigue
 12. Reducing Anxiety, Fear and Improving Coping
 13. Initiating Health Teaching and Patient Education

38
Cardiogenic Shock

Cardiogenic shock is also sometimes called “pump failure”.

Cardiogenic shock is a condition of diminished cardiac output

that severely impairs cardiac perfusion.
 It reflects severe left-sided heart failure.
Pathophysiology

This is what happens in cardiogenic shock:

1. Inability to contract. When the myocardium can’t contract

sufficiently to maintain adequate cardiac output, stroke volume
decreases and the heart can’t eject an adequate volume
of blood with each contraction.
2. Pulmonary congestion.The blood backs up behind the
weakened left ventricle, increasing preload and causing
pulmonary congestion.
3. Compensation. In addition, to compensate for the drop
in stroke volume, the heart rate increases in an attempt to
maintain cardiac output.
4. Diminished stroke volume.As a result of the diminished stroke
volume, coronary artery perfusion and collateral blood flow is
decreased.
5. Increased workload. All of these mechanisms increase the heart’s
workload and enhance left-sided heart failure.
6. End result. The result is myocardial hypoxia, further decreased
cardiac output, and a triggering of compensatory mechanisms to
prevent decompensation and death.
Classification

The causes of cardiogenic shock are known as either coronary or non-

coronary.

39
  Coronary. Coronary cardiogenic shock is more common than non
coronary cardiogenic shock and is seen most often in patients
with acute myocardial infarction.
 Noncoronary. Noncoronary cardiogenic shock is related to
conditions that stress the myocardium as well as conditions that
result in an ineffective myocardial function.

Statistics and Incidences

Cardiogenic shock could be fatal if left untreated.

 Cardiogenic shock occurs as a serious complication in 5% to

10% of patients hospitalized with acute myocardial infarction.
 Historically, mortality for cardiogenic shock had been 80% to
90%, but recent studies indicate that the rate has dropped
to 56% to 67% due to the advent of thrombolytics, improved
interventional procedures, and better therapies.
 Incidence of cardiogenic shock is more common in men than in
women because of their higher incidence of coronary artery
disease.
Causes

Cardiogenic shock can result from any condition that causes significant left
ventricular dysfunction with reduced cardiac output.

 Myocardial infarction (MI).Regardless of the underlying cause,

left ventricular dysfunction sets in motion a series of
compensatory mechanisms that attempt to increase cardiac
output, but later on leads to deterioration.
 Myocardial ischemia. Compensatory mechanisms may initially
stabilize the patient but later on would cause deterioration with
the rising demands of oxygen of the already compromised
myocardium.
 End-stage cardiomyopathy.The inability of the heart to pump
enough blood for the systems causes cardiogenic shock.
Clinical Manifestations

Cardiogenic shock produces symptoms of poor tissue perfusion.

40
 Clammy skin. The patient experiences cool, clammy skin as the
blood could not circulate properly to the peripheries.
 Decreased systolic blood pressure.The systolic blood pressure
decreases to 30 mmHg below baseline.
 Tachycardia. Tachycardia occurs because the heart pumps faster
than normal to compensate for the decreased output all over the
body.
 Rapid respirations. The patient experiences rapid, shallow
respirations because there is not enough oxygen circulating in the
body.
 Oliguria. An output of less than 20ml/hour is indicative of
oliguria.
 Mental confusion. Insufficient oxygenated blood in
the brain could gradually cause mental confusion and
obtundation.
 Cyanosis. Cyanosis occurs because there is insufficient
oxygenated blood that is being distributed to all body systems.
Assessment and Diagnostic Findings

Diagnosis of cardiogenic shock may include the following diagnostic tests:

 Auscultation. Auscultation may detect gallop rhythm, faint heart

sounds and, possibly, if the shock results from rupture of the
ventricular septum or papillary muscles, a holosystolic murmur.
 Pulmonary artery pressure (PAP).PAP monitoring may show
increase in PAP, reflecting a rise in left ventricular end-diastolic
pressure and increased resistance to the afterload.
 Arterial pressure monitoring. Invasive arterial pressure
monitoring may indicate hypotension due to impaired ventricular
ejection.
 ABG analysis. Arterial blood gas analysis may show metabolic
acidosis and hypoxia.
 Electrocardiography. Electrocardiography may show possible
evidence of acute MI, ischemia, or ventricular aneurysm.
 Echocardiography. Echocardiography can determine left
ventricular function and reveal valvular abnormalities.
 Enzyme levels. Enzyme levels such as lactic dehydrogenase,
creatine kinase. Aspartate aminotransferase and alanine
aminotransferase may confirm MI.

41
Medical Management

The aim of treatment is to enhance cardiovascular status by:

 Oxygen. Oxygen is prescribed to minimize damage to muscles

and organs.
 Angioplasty and stenting. A catheter is inserted into the blocked
artery to open it up.
 Balloon pump. A balloon pump is inserted into the aorta to help
blood flow and reduce workload of the heart.
 Pain control. In a patient that experiences chest pain,
IV morphine is administered for pain relief.
 Hemodynamic monitoring.An arterial line is inserted to enable
accurate and continuous monitoring of BP and provides a port
from which to obtain frequent arterial blood samples.
 Fluid therapy.Administration of fluids must be monitored closely
to detect signs of fluid overload.
Pharmacologic Therapy

Drug therapy may include:

 IV dopamine. Dopamine, a vasopressor, increases cardiac output,

blood pressure, and renal blood flow.
 IV dobutamine. Dobutamine is an inotropic agent that increase
myocardial contractility.
 Norepinephrine. Norepinephrine is a more potent
vasoconstrictor that is taken when necessary.
 IV nitroprusside. Nitroprusside is a vasodilator that may be used
with a vasopressor to further improve cardiac output by
decreasing peripheral vascular resistance and reducing preload.
Surgical Management

When the drug therapy and medical procedures don’t work, then the last
option is for surgical procedure.

 Intra-aortic balloon pump (IABP).The IABP is a mechanical-

assist device that attempts to improve the coronary artery
perfusion and decrease cardiac workload through an inflatable
balloon pump which is percutaneously or surgically inserted
through the femoral artery into the descending thoracic aorta.

42
Nursing Care Plans and Management

The nursing care plan for clients with cardiogenic shock involves carefully
assessing the client, observing cardiac rhythm, monitoring hemodynamic
parameters, monitoring fluid status, and adjusting medications and therapies
based on the assessment data.

Nursing Problem Priorities

The following are the nursing priorities for patients with cardiogenic shock:

Managing decreased cardiac output. Cardiogenic shock is

characterized by a significant decrease in cardiac output, resulting
in insufficient blood supply to meet the body’s oxygen and
nutrient demands. Improving cardiac output is crucial to address
the underlying problem.
 Maintaining hemodynamic stability and monitoring vital
signs. Implementing interventions to stabilize blood pressure and
heart rate, such as administering vasoactive medications, and
regularly and closely monitoring vital signs to detect any changes
or signs of deterioration.
 Improving gas exchange and oxygenation. The decreased
cardiac output in cardiogenic shock can lead to impaired balance
of gas exchange. Optimizing gas exchange is essential to ensure
adequate oxygen delivery and removal of waste products.
Nursing Assessment

Proper nursing assessment allows for early identification of changes, facilitates

monitoring of treatment response, aids in detecting complications, and
provides essential information for effective care planning, intervention, and
collaboration with the healthcare team.

Assess for the following subjective and objective data:

43
 1. Vital signs. Monitor blood pressure, heart rate, respiratory rate,
oxygen saturation, and temperature regularly to assess
hemodynamic stability and detect any changes or signs of
deterioration.
2. Cardiac status. Assess heart sounds, including the presence of
murmurs or extra heart sounds, and monitor for any signs of
impaired cardiac function, such as jugular vein distention or
peripheral edema.
3. Respiratory status. Assess respiratory effort, assess lung sounds,
and monitor for signs of respiratory distress, such as increased
work of breathing or decreased oxygen saturation.
4. Neurological assessment. Assess level of consciousness,
orientation, and neurological function, monitoring for any signs of
cerebral hypoperfusion, such as confusion, restlessness, or
decreased responsiveness.
5. Urine output. Measure and record urine output to assess renal
perfusion and function, monitoring for any signs of decreased
urine output or oliguria.
Assess for factors related to the cause of cardiogenic shock:

1. Dysrhythmias. Dysrhythmias, stemming from factors like

electrolyte imbalances, ischemia, or structural heart abnormalities,
can disrupt effective blood pumping, leading to inadequate
cardiac output and subsequent cardiogenic shock.
2. Increased or decreased preload or afterload. Increased preload
or afterload can strain the heart, impairing its effective pumping
ability and potentially leading to cardiogenic shock.
3. Impaired left ventricular (LV) contractility. Reduced
contractility of the left ventricle can result from conditions
like myocardial infarction, myocarditis, or cardiomyopathy,
impairing the heart’s ability to eject blood adequately and
decreasing cardiac output.
4. Septal defects. Structural defects in the septum, such as VSDs or
ASDs, can disrupt blood flow patterns, cause volume overload on
the heart chambers, and potentially lead to cardiac dysfunction.
5. Valve dysfunction. Valvular abnormalities like severe aortic
stenosis or mitral regurgitation can compromise the heart’s
pumping efficiency by disrupting the normal flow of blood,
leading to decreased cardiac output.

44
 6. Changes in the alveolar-capillary membrane. Impaired gas
exchange and reduced oxygen delivery resulting from conditions
affecting the alveolar-capillary membrane, like acute respiratory
distress syndrome (ARDS) or pulmonary edema, can decrease
cardiac output due to inadequate oxygenation.
7. Impaired ventilation-perfusion. Imbalances in ventilation and
perfusion, as seen in conditions like pulmonary embolism or
severe bronchospasm, can impair gas exchange, reduce oxygen
availability, and potentially impact cardiac function.
8. Decrease in renal organ perfusion. Reduced blood flow to the
kidneys can compromise renal function and impairs the kidneys’
ability to regulate fluid balance and eliminate waste products
effectively leading to compromised cardiac function.
9. Increased sodium and water retention. Impaired cardiac
function may lead to activation of compensatory mechanisms,
including the renin-angiotensin-aldosterone system. This can
result in increased sodium and water retention by the kidneys,
contributing to fluid overload, increased preload, and
exacerbation of cardiac dysfunction.
Nursing Diagnosis

Here are some common nursing diagnosis for cardiogenic shock:

Decreased cardiac output

Nursing Goals

Goals and expected outcomes may include:

 The client will maintain adequate cardiac output as evidenced by

strong peripheral pulses, HR 60 to 100 beats per minute with a
regular rhythm, systolic BP within 20 mm Hg of baseline, urinary
output 30 ml hr or greater, warm and dry skin, and normal level of
consciousness.
 The client will maintain optimal gas exchange, as evidenced
by ABGs within the normal range, oxygen saturation of 90% or
greater, alert responsive mentation or no further reduction in the
level of consciousness, relaxed breathing, and baseline HR for the
client.
 The client will demonstrate increased perfusion as individually
appropriate as evidenced by strong peripheral pulses, HR 60 to

45
 100 beats per minute with a regular rhythm, systolic BP within 20
mm Hg of baseline, balanced intake and output, warm and dry
skin, and alert/oriented.
 The client will report reduction in level of anxiety and use effective
coping mechanisms.

Nursing Interventions and Actions

Therapeutic interventions and nursing actions for patients with cardiogenic

shock may include:

1. Managing Decrease in Cardiac Output

2. Monitoring Diagnostic Procedures and Laboratory Studies
3. Promoting Optimal Oxygenation and Improving Gas Exchange
4. Improving Tissue Perfusion
5. Administering Medications and Providing Pharmacological
Interventions
6. Managing Fluid and Electrolyte Imbalance
7. Providing Perioperative Nursing Care
8. Reducing Anxiety

Evaluation

Expected outcomes include:

 Prevented recurrence of cardiogenic shock.

 Monitored hemodynamic status.
 Administered medications and intravenous fluids.
 Maintained intra-aortic balloon counterpulsation.
Discharge and Home Care Guidelines

Lifestyle changes must be made to avoid the recurrence of cardiogenic shock.

 Control hypertension. Exercise, manage stress, maintain a

healthy weight, and limit salt and alcohol intake.
 Avoid smoking. The risk of stroke is the same for smokers and
nonsmokers years after you stop smoking
 Maintain a healthy weight.Losing those extra pounds would be
helpful in lowering the cholesterol and blood pressure.

46
  Diet. Eat less saturated fat and cholesterol to reduce heart
disease.
 Exercise. Exercise daily to lower blood pressure, increase high-
density lipoproteins, and improve the overall health of the blood
vessels and the heart.

Documentation Guidelines

The focus of documentation include:

 Baseline and subsequent findings and individual hemodynamic

parameters, heart and breath sounds, ECG pattern,
presence/strength of peripheral pulses, skin/tissue status, renal
output, and mentation.
 Respiratory rate, character of breath sounds, frequency, amount,
and appearance of secretions, presence of cyanosis, laboratory
findings, and mentation level.
 Conditions that may interfere with oxygen supply.
 Conditions contributing to the degree of fluid retention.
 I&O, fluid balance.
 Pulses and BP.
 Client’s description of response to pain.
 Acceptable level of pain.
 Specifics of pain inventory.
 Prior medication use.
 Plan of care.
 Teaching plan.
 Client’s responses to interventions, teaching, and actions
performed.
 Status and disposition at discharge.
 Attainment or progress toward desired outcomes.
 Modifications to plan of care.

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Hypertension

Hypertension is one of the most common lifestyle diseases to date. It affects

people from all walks of life. Let us get to know hypertension more by its
definitions.

 Hypertension is defined as a systolic blood pressure greater than

140 mmHg and a diastolic pressure of more than 90 mmHg.
 This is based on the average of two or more accurate blood
pressure measurements during two or more consultations with
the healthcare provider.
 The definition is taken from the Seventh Report of the Joint
National Committee on Prevention, Detection, Evaluation,
and Treatment of High Blood Pressure.
Classification

In 2017, the American College of Cardiology and the American Heart

Association revised their hypertension guidelines. The previous guidelines set
the threshold at 140/90 mm Hg for younger people and 150/80 mm Hg for
those ages 65 and older.

 Normal. The normal range for blood pressure is between, less

than 120 mmHg and less than 80 mmHg.
 Elevated. Elevated stage starts from 120 mmHg to 129 mmHg for
systolic blood pressure and less than 80 mmHg for diastolic
pressure.
 Stage 1 hypertension. Stage 1 starts when the patient has a
systolic pressure of 130 to 139 mmHg and a diastolic pressure of
80 to 89 mmHg.

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  Stage 2 hypertension. Stage 2 starts when the systolic pressure
is already more than or equal than 140 mmHg and the diastolic is
more than or equal than 90 mmHg.

Pathophysiology

In a normal circulation, pressure is transferred from the heart muscle to the

blood each time the heart contracts and then pressure is exerted by the blood
as it flows through the blood vessels.

The pathophysiology of hypertension follows.

 Hypertension is a multifactorial
 When there is excess sodium intake, renal sodium retention
occurs, which increases fluid volume resulting in increased
preload and increase in contractility.
 Obesity is also a factor in hypertension because hyperinsulinemia
develops and structural hypertrophy results leading to increased
peripheral vascular resistance.

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  Genetic alteration also plays a role in the development of
hypertension because when there is cell membrane alteration,
functional constriction may follow and also results in increased
peripheral vascular resistance.

Epidemiology

Hypertension is slowly rising to the top as one of the primary causes of

morbidity in the world. Here are the current statistics of the status of
hypertension in some of the leading countries.

 About 31% of the adults in the United States have hypertension.

 African-Americans have the highest prevalence rate of 37%.
 In the total US population of persons with hypertension, 90% to
95% have primary hypertension or high blood pressure from an
unidentified cause.
 The remaining 5% to 10% of this group have secondary
hypertension or high blood pressure related to identified causes.
 Hypertension is also termed as the “silent killer” because 24% of
people who had pressures exceeding 140/90 mmHg
were unaware that their blood pressures were elevated.
Causes

Hypertension has a lot of causes just like how fever has many causes. The
factors that are implicated as causes of hypertension are:

 Increased sympathetic nervous system activity. Sympathetic

nervous system activity increases because there is dysfunction in
the autonomic nervous system.
 Increase renal reabsorption. There is an increase reabsorption of
sodium, chloride, and water which is related to a genetic
variation in the pathways by which the kidneys handle sodium.
 Increased RAAS activity. The renin-angiotensin-aldosterone
system increases its activity leading to
the expansion of extracellular fluid volume and increased
systemic vascular resistance.
 Decreased vasodilation of the arterioles. The vascular
endothelium is damaged because of the decrease in the
vasodilation of the arterioles.

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Clinical Manifestations

Many people who have hypertension are asymptomatic at first. Physical

examination may reveal no abnormalities except for an elevated blood
pressure, so one must be prepared to recognize hypertension at its earliest.

 Headache. The red blood cells carrying oxygen is having a hard

time reaching the brain because of constricted vessels, causing
headache.
 Dizziness occurs due to the low concentration of oxygen that
reaches the brain.
 Chest pain. Chest pain occurs also due to decreased oxygen
levels.
 Blurred vision. Blurred vision may occur later on because of too
much constriction in the blood vessels of the eye that red
blood cells carrying oxygen cannot pass through.
Prevention

Prevention of hypertension mainly relies on a healthy lifestyle and self-

discipline.

Weight reduction. Maintenance of normal body weight can

help prevent hypertension.
 Adopt DASH. DASH or the Dietary Approaches to Stop
Hypertension includes consummation of a diet rich in fruits,
vegetable, and low-fat dairy.
 Dietary sodium retention. Sodium contributes to an elevated
blood pressure, so reducing the dietary intake to no more than
2.4 g sodium per day can be really helpful.
 Physical activity. Engage in regular aerobic physical activity for
30 minutes thrice every week.
 Moderation of alcohol consumption. Limit alcohol consumption
to no more than 2 drinks per day in men and one drink for
women and people who are lighter in weight.
Complications

If hypertension is left untreated, it could progress to complications of the

different body organs.

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 Heart failure. With increased blood pressure, the heart pumps
blood faster than normal until the heart muscle goes weak from
too much exertion.
 Myocardial infarction. Decreased oxygen due to constriction of
blood vessels may lead to MI.
 Impaired vision. Ineffective peripheral perfusion affects the
eye, causing problems in vision because of decreased oxygen.
 Renal failure. Blood carrying oxygen and nutrients could not
reach the renal system because of the constricted blood vessels.
Assessment and Diagnostic Findings

Assessment of the patient with hypertension must be detailed and thorough.

There are also diagnostic tests that can be performed to establish the
diagnosis of hypertension.

Assessment

 Assess the patient’s health history

 Perform physical examination as appropriate.
 The retinas are examined to assess possible organ damage.
 Laboratory tests are also taken to check target organ damage.
Diagnostic Tests

 Urinalysis is performed to check the concentration of sodium in

the urine though the specific gravity.
 Blood chemistry (e.g. analysis of sodium, potassium, creatinine,
fasting glucose, and total and high density lipoprotein cholesterol
levels). These tests are done to determine the level of sodium and
fat in the body.
 12-lead ECG. ECG needs to be performed to rule presence of
cardiovascular damage.
 Echocardiography. Echocardiography assesses the presence
of left ventricular hypertrophy.
 Creatinine clearance. Creatinine clearance is performed to check
for the level of BUN and creatinine that can determine if there is
renal damage or not.
 Renin level. Renin level should be assessed to determine how
RAAS is coping.

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 Hemoglobin/hematocrit: Not diagnostic but assesses
relationship of cells to fluid volume (viscosity) and may indicate
risk factors such as hypercoagulability, anemia.
 Blood urea nitrogen (BUN)/creatinine: Provides information
about renal perfusion/function.
 Glucose: Hyperglycemia (diabetes mellitus is a precipitator of
hypertension) may result from elevated catecholamine levels
(increases hypertension).
 Serum potassium: Hypokalemia may indicate the presence of
primary aldosteronism (cause) or be a side effect of diuretic -
therapy.
 Serum calcium: Imbalance may contribute to hypertension.
 Lipid panel (total lipids, high-density lipoprotein [HDL], low-
density lipoprotein [LDL], cholesterol, triglycerides,
phospholipids): Elevated level may indicate predisposition
for/presence of atheromatous plaques.
 Thyroid studies: Hyperthyroidism may lead or contribute to
vasoconstriction and hypertension.
 Serum/urine aldosterone level: May be done to assess for
primary aldosteronism (cause).
 Urinalysis: May show blood, protein, or white blood cells;
or glucose suggests renal dysfunction and/or presence
of diabetes.
 Creatinine clearance: May be reduced, reflecting renal damage.
 Urine vanillylmandelic acid (VMA) (catecholamine
metabolite): Elevation may indicate presence of
pheochromocytoma (cause); 24-hour urine VMA may be done
for assessment of pheochromocytoma if hypertension is
intermittent.
 Uric acid: Hyperuricemia has been implicated as a risk factor for
the development of hypertension.
 Renin: Elevated in renovascular and malignant hypertension, salt-
wasting disorders.
 Urine steroids: Elevation may indicate hyperadrenalism,
pheochromocytoma, pituitary dysfunction, Cushing’s syndrome.
 Intravenous pyelogram (IVP): May identify cause of secondary
hypertension, e.g., renal parenchymal disease, renal/ureteral -
calculi.
 Kidney and renography nuclear scan: Evaluates renal status
(TOD).

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  Excretory urography: May reveal renal atrophy, indicating
chronic renal disease.
 Chest x-ray: May demonstrate obstructing calcification in valve
areas; deposits in and/or notching of aorta; cardiac enlargement.
 Computed tomography (CT) scan: Assesses for cerebral tumor,
CVA, or encephalopathy or to rule out pheochromocytoma.
 Electrocardiogram (ECG): May demonstrate enlarged heart,
strain patterns, conduction disturbances. Note: Broad, notched P
wave is one of the earliest signs of hypertensive heart disease.
Medical Management

Main Topic: Antihypertensive Drugs

The goal of hypertensive treatment I to prevent complications and death by

achieving and maintaining the arterial blood pressure at 40/90 mmHg or
lower.

Pharmacologic Therapy

 The medications used for treating hypertension decrease

peripheral resistance, blood volume, or the strength and rate
of myocardial contraction.
 For uncomplicated hypertension, the initial medications
recommended are diuretics and beta blockers.
 Only low doses are given, but if blood pressure still exceeds
140/90 mmHg, the dose is increased gradually.
 Thiazide diuretics decrease blood volume, renal blood flow,
and cardiac output.
 ARBs are competitive inhibitors of aldosterone binding.
 Beta blockers block the sympathetic nervous system to
produce a slower heart rate and a lower blood pressure.
 ACE inhibitors inhibit the conversion of angiotensin I to
angiotensin II and lowers peripheral resistance.
Stage 1 Hypertension

 Thiazide diuretic is recommended for most and angiotensin-

converting enzyme-1, aldosterone receptor blocker, beta
blocker, or calcium channel blocker is considered.
Stage 2 Hypertension

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 Two-drug combination is followed, usually including thiazide
diuretic and angiotensin-converting enzyme-1, or beta-blocker, or
calcium channel blocker.
Nursing Management

The goal of nursing management is to help achieve a normal blood pressure

through independent and dependent interventions.

Nursing Assessment

Nursing assessment must involve careful monitoring of the blood pressure at

frequent and routinely scheduled intervals.

 If patient is on antihypertensive medications, blood pressure is

assessed to determine the effectiveness and detect changes in
the blood pressure.
 Complete history should be obtained to assess for signs and
symptoms that indicate target organ damage.
 Pay attention to the rate, rhythm, and character of the apical and
peripheral pulses.
Diagnosis

Based on the assessment data, nursing diagnoses may include the following:

 Deficient knowledge regarding the relation between the

treatment regimen and control of the disease process.
 Noncompliance with the therapeutic regimen related to side
effects of the prescribed therapy.
 Risk for activity intolerance related to imbalance between
oxygen supply and demand.
 Risk-prone health behavior related to condition requiring
change in lifestyle.
Nursing Care Plan and Goals

Main article: 6 Hypertension Nursing Care Plans

The major goals for a patient with hypertension are as follows:

 Understanding of the disease process and its treatment.

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  Participation in a self-care program.
 Absence of complications.
 BP within acceptable limits for individual.
 Cardiovascular and systemic complications prevented/minimized.
 Disease process/prognosis and therapeutic regimen understood.
 Necessary lifestyle/behavioral changes initiated.
 Plan in place to meet needs after discharge.
Nursing Priorities

1. Maintain/enhance cardiovascular functioning.

2. Prevent complications.
3. Provide information about disease process/prognosis and
treatment regimen.
4. Support active patient control of condition.
Nursing Interventions

The objective of nursing care focuses on lowering and controlling the blood
pressure without adverse effects and without undue cost.

 Encourage the patient to consult a dietitian to help develop a

plan for improving nutrient intake or for weight loss.
 Encourage restriction of sodium and fat
 Emphasize increase intake of fruits and vegetables.
 Implement regular physical activity.
 Advise patient to limit alcohol consumption and avoidance of
tobacco.
 Assist the patient to develop and adhere to an appropriate
exercise regimen.
Evaluation

At the end of the treatment regimen, the following are expected to be

achieved:

 Maintain blood pressure at less than 140/90 mmHg with

lifestyle modifications, medications, or both.
 Demonstrate no symptoms of angina, palpitations, or visual
changes.
 Has stable BUN and serum creatinine levels.
 Has palpable peripheral pulses.
 Adheres to the dietary regimen as prescribed.

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  Exercises regularly.
 Takes medications as prescribed and reports side effects.
 Measures blood pressure routinely.
 Abstains from tobacco and alcohol intake.
 Exhibits no complications.
Discharge and Home Care Guidelines

Following discharge, the nurse should promote self-care and independence of

the patient.

 The nurse can help the patient achieve blood pressure control
through education about managing blood pressure.
 Assist the patient in setting goal blood pressures.
 Provide assistance with social support.
 Encourage the involvement of family members in the education
program to support the patient’s efforts to control hypertension.
 Provide written information about expected effects and side
effects.
 Encourage and teach patients to measure their blood pressures at
home.
 Emphasize strict compliance of follow-up check up.
Documentation Guidelines

These are the following data that should be documented for the patient’s
record:

 Effects of behavior on health status/condition.

 Plan for adjustments and interventions for achieving the plan and
the people involved.
 Client responses to the interventions, teaching, and action plan
performed.
 Attainment or progress towards desired outcome.
 Modifications to plan care.
 Individual findings including deviation from prescribed treatment
plan.
 Consequences of actions to date.

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 DYSRHYTHMIAS

Sinus Tachycardia

Sinus tachycardia is a heart rate greater than 100 beats per minute originating
from the sinus node.

 Rate: 100 to 180 beats per minute

 P Waves precede each QRS complex
 PR interval is normal
 QRS complex is normal
 Conduction is normal
 Rhythm is regular

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Causes of sinus tachycardia may include exercise, anxiety, fever,
drugs, anemia, heart failure, hypovolemia, and shock. Sinus tachycardia is
often asymptomatic. Management, however is directed at the treatment of the
primary cause. Carotid sinus pressure (carotid massage) or a beta-blocker may
be used to reduce heart rate.

Sinus Bradycardia

Sinus bradycardia is a heart rate of less than 60 beats per minute and
originates from the sinus node (as the term “sinus” refers to the sinoatrial
node). It has the following characteristics

 Rate is less than 60 beats per minute

 P Waves precede each QRS complex
 PR interval is normal
 QRS complex is normal
 Conduction is normal
 Rhythm is regular

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Causes may include drugs, vagal stimulation, hypoendocrine
states, hypothermia, or sinus node involvement in MI. This arrhythmia may be
normal in athletes as they have quality stroke volume. It is often
asymptomatic but manifestations may include: syncope, fatigue, dizziness.
Management includes treating the underlying cause and administering
anticholinergic drugs like atropine sulfate as prescribed.

Premature Atrial Contraction

Premature Atrial Contraction are ectopic beats that originates from the atria
and they are not rhythms. Cells in the heart starts to fire or go off before the
normal heartbeat is supposed to occur. These are called heart palpitations and
has the following characteristics:

 Premature and abnormal-looking P waves that differ in

configuration from normal P waves

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  QRS complex after P waves except in very early or blocked PACs
 P waves often buried in the preceding T wave or identified in the
preceding T wave.
Causes includes coronary or valvular heart diseases, atrial ischemia, coronary
artery atherosclerosis, heart failure, COPD, electrolyte imbalance and hypoxia.
Usually there is no treatment needed but may include procainamide and
quinidine administration (antidysrhythmic drugs) and carotid sinus massage.

Atrial Flutter

Atrial flutter is an abnormal rhythm that occurs in the atria of the heart. Atrial
flutter has an atrial rhythm that is regular but has an atrial rate of 250 to 400
beats/minute. It has sawtooth appearance. QRS complexes are uniform in
shape but often irregular in rate.

 Normal atrial rhythm

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  Abnormal atrial rate: 250 to 400 beats/minute
 Sawtooth P wave configuration
 QRS complexes uniform in shape but irregular in rate
Causes includes heart failure, tricuspid valve or mitral valve
diseases, pulmonary embolism, cor pulmonale, inferior wall MI, carditis
and digoxin toxicity.

Management if the patient is unstable with ventricular rate of greater than 150
bpm, prepare for immediate cardioversion. If patient is stable, drug therapy
may include calcium channel blocker, beta-adrenergic blockers, or
antiarhythmics. Anticoagulation may be necessary as there would be pooling
of blood in the atria.

Atrial Fibrillation

Atrial fibrillation is disorganized and uncoordinated twitching of atrial

musculature caused by overly rapid production of atrial impulses. This
arrhythmia has the following characteristics:

 Atrial Rate: 350 to 600 bpm

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  Ventricular Rate: 120 to 200 bpm
 P wave is not discernible with an irregular baseline
 PR interval is not measurable
 QRS complex is normal
 Rhythm is irregular and usually rapid unless controlled.
Causes includes atherosclerosis, heart failure, congenital heart disease, chronic
obstructive pulmonary disease, hypothyroidism and thyrotoxicosis. Atrial
fibrillation may be asymptomatic but clinical manifestation may include
palpitations, dyspnea, and pulmonary edema. Nursing goal is towards
administration of prescribed treatment to decrease ventricular response,
decrease atrial irritability and eliminate the cause.

Premature Junctional Contraction

Premature Junctional Contraction (PJC) occurs when some regions of the heart
becomes excitable than normal. It has the following characteristics.

 PR interval less than 0.12 seconds if P wave precedes QRS

complex
 QRS complex configuration and duration is normal

63
  P wave is inverted
 Atrial and ventricular rhythms irregular
Causes of PJC may include myocardial infarction or ischemia, digoxin toxicity,
excessive caffeine or amphetamine use. Management includes correction of
underlying cause, discontinuation of digoxin if appropriate.

Atrioventricular Blocks

AV blocks are conduction defects within the AV junction that impairs

conduction of atrial impulses to ventricular pathways. The three types are first
degree, second degree and third degree.

First Degree AV Block

 Rate is usually 60 to 100 bpm

 PR intervals are prolonged for usually 0.20 seconds
 QRS complex is usually normal
 Rhythm is regular

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First degree AV block is asymptomatic and may be caused by inferior wall MI
or ischemia, hyperkalemia, hypokalemia, digoxin toxicity, calcium channel
blockers, amiodarone and use of antidysrhythmics. Management includes
correction of underlying cause. Administer atropine if PR interval exceeds 0.26
second or symptomatic bradycardia develops.

Second Degree AV Block Mobitz I (Wenckebach)

 Atrial rhythm is regular

 Ventricular rhythm is irregular
65
  Atrial rate exceeds ventricular rate
 PR interval progressively but only slightly, longer with each cycle
until QRS complex disappears (dropped beat)
 PR Interval shorter after dropped beat.
Clinical manifestations include vertigo, weakness, and an irregular pulse. This
may be caused by Inferior wall MI, cardiac surgery, acute rheumatic fever,
vagal stimulation. Treatment includes correction of underlying cause, atropine
or temporary pacemaker for symptomatic bradycardia and discontinuation of
digoxin if appropriate.

Second Degree AV Block Mobitz II

 Atrial rhythm is regular

 Ventricular rhythm maybe regular or irregular depending on the
degree of block
 P-P interval constant

66
  QRS complex periodically absent or disappears
Clinical manifestations same as Mobitz I. Causes includes: severe coronary
artery diseases, anterior wall MI, acute myocarditis and digoxin toxicity.
Treatment includes: atropine, epinephrine, and dopamine for symptomatic
bradycardia. Discontinuation of digoxin if appropriate. Installation of
pacemaker.

Third Degree AV Block (Complete Heart Block)

 Atrial rhythm regular

 Ventricular rhythm regular and rate slower than atrial rate
 No relation between P waves and QRS complexes

67
  NO constant PR interval
 QRS interval normal or wide and bizarre
Manifestations include hypotension, angina, and heart failure. This may be
caused by congenital abnormalities, rheumatic fever, hypoxia, MI, LEv’s
disease, Lenegre’s disease and digoxin toxicity. Management includes
atropine, epinephrine, and dopamine for bradycardia. Installation of
pacemaker may also be considered.

Premature Ventricular Contractions (PVC)

Early or premature ventricular contractions are caused by increased

automaticity of ventricular muscle cells. PVCs usually are not considered
68
harmful but are of concern if more than six occur in 1 minute, if they occur in
pairs or triplets if they are multifocal or if they occur or near a T wave.

 Atrial rhythm is regular

 Ventricular rhythm is irregular
 QRS complex premature, usually followed by a complete
compensatory pause
 QRS complex is also wide and distorted, usually >0.14 second.
 Premature QRS complexes occurring singly, in pairs, or in threes
Clinical manifestations includes palpitations, weakness, lightheadedness but it
is most of the time asymptomatic. Management includes assessment of the
cause and treat as indicated. Treatment is indicated if the client has underlying
disease because PVCs may precipitate ventricular tachycardia or fibrillation.
Assess for life threatening PVCs. Administer antiarrhythmic medication as
prescribed.

Ventricular Tachycardia

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Ventricular tachycardia (VT) is three or more consecutive PVCs. it is considered
a medical emergency because cardiac output (CO) cannot be maintained
because of decreased diastolic filling (preload).

 Rate is 100 to 250 beats per minute

 P wave is blurred in the QRS complex but the QRS complex has
no associate with P wave.
 PR Interval is not present
 QRS complex is wide and bizarre; T wave is in the opposite
direction
 Rhythm is usually regular
 May start and stop suddenly
Clinical manifestations of VT includes lightheadedness, weakness, dyspnea and
unconsciousness. Causes includes MI, aneurysm, CAD, rheumatic heart
diseases, mitral valve prolapse, hypokalemia, hyperkalemia, and pulmonary
embolism. Anxiety may also caused VT.

Pulseless Ventricular Tachycardia

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Management for Pulseless VT: Initiate cardiopulmonary resuscitation; follow
ACLS protocol for defibrillation, ET intubation and administration of
epinephrine or vasopressin.

Ventricular Tachycardia with Pulse

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Management with Pulse VT: If hemodynamically stable, follow ACLS protocol
for administration of amiodarone, if ineffective, initiate synchronized
cardioversion.

Ventricular Fibrillation

Ventricular fibrillation is rapid, ineffective quivering of ventricles that may be

rapidly fatal.

 Rate is rapid and uncoordinated, with ineffective contractions

 Rhythm is chaotic
 QRS complexes wide and irregular
 P wave is not seen
 PR interval is not seen
Causes of ventricular fibrillation is most commonly myocardia ischemia or
infarction. It ma result from untreated ventricular tachycardia, electrolyte
imbalances, digoxin or quinide toxicity, or hypothermia. Clinical manifestations
may include loss of consciousness, pulselessness, loss of blood pressure,
cessation of respirations, possible seizures and sudden death.

Start CPR is pulseless. Follow ACLS protocol for defibrillation, ET intubation

and administration of epinephrine or vasopressin.

Other Arrhythmias
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Atrial Tachycardia

2nd Degree AV Block Type 1, Mobitz I

Torsade de Pointes

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Pulseless Ventricular Tachycardia

Supraventricular Tachycardia

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ST Depression

EKG Interpretation Cheat Sheets

Download the printable cheat sheet for EKG interpretation below. To

download, simply click on the images below and save.

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