CARDIOVASCULAR

DISORDERS
LEARNING OBJECTIVES:
At the end of the lecture, the students will
be able to:
1.Identify the major organs and structures of
cardiovascular system
2.Discuss the risk factors associated in the
development of cardiovascular disorder
3.Discuss the physical assessment that
provide information about the functioning
of the cardiovascular disorder
LEARNING OBJECTIVES:
At the end of the lecture, the students will be
able to:
4.Describe common diagnostic tests and
their nursing responsibilities
5.Discuss the pathophysiology of clients with
cardiovascular disorder
6.Enumerate the different clinical
manifestations associated with each illness
of clients with cardiovascular disorder
LEARNING OBJECTIVES:
At the end of the lecture, the students will be
able to:
7.Identify actual and at-risk nursing diagnosis
8.Discuss medical and surgical interventions
9.Discuss the appropriate nursing
interventions with client/s and family for
identified nursing interventions
10.Implement plan of care with clients and
family
CARDIOVASCULAR
SYSTEM
is a closed system consisting
of the heart and blood vessels
FUNCTION
- to supply body cells
and tissues with
oxygen-rich blood
and eliminate carbon
dioxide and cellular
wastes
HEART
- a cone-shaped
muscle with four
chambers; a double
pump about the size
of a clenched fist
-pumps blood throughout circulatory
system
RIGHT SIDE
RIGHT ATRIUM
- upper chamber of
right heart
- receives
unoxygenated blood
from superior and
inferior vena cava
RIGHT SIDE
TRICUSPID VALVE
-Right AV valve with
three cusps
(tricuspid)
-Valve between right
atrium and right
ventricle
RIGHT SIDE
RIGHT VENTRICLE
-lower chamber of
right heart
-receives blood from
right atrium and
pumps it into
pulmonary circuit
RIGHT SIDE
PULMONARY SEMILUNAR VALVE
-composed of three
cusps
-valve between right
ventricle and main
pulmonary artery
RIGHT SIDE
MAIN PULMONARY ARTERY
-artery leading from
right ventricle to lungs
-divides into right and
left branches supplying
respective lungs
-carries unoxygenated
blood from right
ventricle to lungs
RIGHT SIDE
PULMONARY VEINS
-veins leading from
lungs to left atrium
-carry oxygenated
blood to left atrium
LEFT SIDE
LEFT ATRIUM
- upper chamber of
left heart.
- receives
oxygenated blood
from lungs through
pulmonary veins
LEFT SIDE
MITRAL VALVE
-AV valve with two
cusps (bicuspid)
-valve between left
atrium and left
ventricle
LEFT SIDE
LEFT VENTRICLE
-lower chamber of left
half of heart
- receives blood from
left atrium and pumps
oxygenated blood
through systemic
circulation
LEFT SIDE
AORTIC VALVE
- composed of three
cusps
- valve between left
ventricle and aorta.
LEFT SIDE
INTERVENTRICULAR SEPTUM
- wall between left
and right ventricles.
- vertically separates
left and right sides of
heart
LAYERS OF THE HEART
ENDOCARDIUM
- inner layer of
heart; a smooth,
thin layer of
endothelium and
connective tissue.
-smooth inner
lining of the heart
LAYERS OF THE HEART
MYOCARDIUM
- middle and thickest layer of heart;

heart muscle.
-responsible for cardiac contraction
EPICARDIUM
- the layer of serous pericardium on
heart’s surface.
- contains main coronary blood vessels
LAYERS OF THE HEART
PERICARDIUM
- Sac that surrounds the heart and roots
of the great vessels.
-Composed of two layers:
Fibrous pericardium (outer layer of
fibrous connective tissue) and
serous pericardium
SYSTEMIC AND
PULMONARY
CIRCULATION
LAYERS OF ARTERIES AND VEINS
ARTERIES
- blood vessels with three coats:

tunica intima, tunica media, and tunica

adventitia.
- carry oxygenated blood away from
left heart and unoxygenated blood to
lungs via pulmonary arteries
LAYERS OF ARTERIES AND VEINS

ARTERIOLES
- Smallest arteries; contain large

amount of smooth muscle cells that

can dilate and constrict.
- Carry blood to capillaries and control
blood flow to capillaries through
dilation/constriction
LAYERS OF ARTERIES AND VEINS

CAPILLARIES
- Single layer of microscopic

endothelial cells.
- Connect arterial and venous system
for exchange of gases, fluids,
nutrients, and wastes.
LAYERS OF ARTERIES AND VEINS

VEINS
- Contain same three layers as
arteries, but are thinner with less
elastic and collagenous tissue and
smooth muscle.
- BP in venous system is low; veins
have valves to prevent backflow.
- VEINS carry
unoxygenated
blood back to
right heart, except
for pulmonary
veins, which carry
oxygenated blood
from lungs to left
heart.
REGULATION OF HEART RATE
- HEART RATE
fluctuates according to
stimulation from
autonomic nervous
system, baroreceptors,
and chemoreceptors
- AUTONOMIC
NERVOUS SYSTEM
affects heart rate
through sympathetic
and parasympathetic
nervous system
innervation
- SYMPATHETIC NERVE FIBERS,
adrenergic neurotransmitters
(norepinephrine, epinephrine) excite SA
and AV nodes in the conduction system,
thus INCREASING HEART RATE
- The same neurotransmitters also
stimulate
BETA ADRENERGIC RECEPTORS
in the atria ventricles, increasing force of
myocardial contraction
- Heart rate slows when parasympathetic
nerve fibers from the cardiac branches of
the vagus nerve release the
CHOLINERGIC neurotransmitter
ACETYLCHOLINE
CARDIAC OUTPUT
– is the amount of
blood pumped out of
the left ventricle
each minute
PROPERTIES OF CARDIAC CYCLE
AUTOMATICITY: Generates electrical

impulse independently,
without involving the nervous system
EXCITABILITY: Responds to electrical
stimulation
PROPERTIES OF CARDIAC CYCLE
CONDUCTIVITY: Passes or propagates
electrical impulses from cell to cell

CONTRACTILITY: Shortens in
response to electrical stimulation
ELECTRICAL
CONDUCTION SYSTEM OF
THE HEART
Conduction System
Structures and
Functions
ELECTRICAL CONDUCTION SYSTEM
OF THE HEART
SINOATRIAL (SA)
NODE: Dominant
pacemaker of the
heart, located in
upper portion of right
atrium. Intrinsic rate
60–100 bpm.
SA NODE
ELECTRICAL CONDUCTION SYSTEM
OF THE HEART
INTERNODAL
PATHWAYS: Direct

electrical impulses
between SA and AV
nodes.
INTERNODAL
PATHWAYS
ELECTRICAL CONDUCTION SYSTEM
OF THE HEART
ATRIO VENTRICULAR
(AV) NODE: Part of AV
junctional tissue. Slows
conduction, creating a
slight delay before
impulses reach
ventricles. Intrinsic rate
40–60 bpm
AV NODE
ELECTRICAL CONDUCTION SYSTEM
OF THE HEART
BUNDLE OF HIS:

Transmits impulses to
bundle branches.
Located below AV
node

BUNDLE OF HIS
ELECTRICAL CONDUCTION SYSTEM
OF THE HEART
LEFT BUNDLE
BRANCH: Conducts

impulses that lead to

left ventricle

LEFT BUNDLE BRANCH

ELECTRICAL CONDUCTION SYSTEM
OF THE HEART
RIGHT BUNDLE
BRANCH: Conducts

impulses that lead to

right ventricle

RIGHT BUNDLE BRANCH

ELECTRICAL CONDUCTION SYSTEM
OF THE HEART
PURKENJE SYSTEM:
Network of fibers that
spreads impulses
rapidly throughout
ventricular walls.
Located at terminals of
bundle branches.
Intrinsic rate 20–40 bpm
PURKENJE FIBERS
ELECTROPHYSIOLOGY
DEPOLARIZATION: The electrical charge
of a cell is altered by a shift of electrolytes
on either side of the cell membrane. This
change stimulates muscle fiber to contract
ELECTROPHYSIOLOGY
REPOLARIZATION: Chemical pumps re-

establish an internal negative charge

as the cells return to their resting state
 Mechanical and electrical functions
of the heart are influenced by proper
electrolyte balance.
Important components of this balance
are sodium, calcium, potassium, and
magnesium
CARDIO
VASCULAR

ASSESSMENT
PAST MEDICAL HISTORY
REVIEW OF ALLERGIES

MEDICATION HISTORY
FAMILY HISTORY

PERSONAL AND SOCIAL HISTORY

COMMON
MANIFESTATIONS OF
HEART DISEASE

CHEST
PAIN
OTHER MANIFESTATIONS:

•shortness of
breath
•palpitations
•weakness
•fatigue
•dizziness
•syncope
•GI complaints
PHYSICAL EXAMINATION
GENERAL APPEARANCE
-non-verbal behavior and body position
(anxious, depressed, pain, uncomfortable)

PAIN
-classic sign of
ischemia
PHYSICAL EXAMINATION
VITAL SIGNS

TEMPERATURE
-note presence of fever
PULSE RATE
-note rate,
rhythm and
quality
PHYSICAL EXAMINATION
VITAL SIGNS

RESPIRATORY RATE
-note if patient has labored breathing
BLOOD PRESSURE
-take BP lying, sitting,
& standing positions
(orthostatic VS)
CARDIAC RHYTHM
-electrical activity can be
observed continuously
with bedside CARDIAC
MONITOR
-electrodes are attached to the chest &
connected to a machine that displays the
cardiac rhythm
HEART SOUNDS
“LUB” – first heart
sound – referred to S1,
is the closing of the
mitral and tricuspid
valves

“DUB” – referred to S2, is the closing of

the aortic and pulmonic valves
ABNORMAL HEART SOUNDS
S3 HEART SOUND –
or a ventricular gallop
“LUB-DUB-DEE” or
“KEN-TUCK-Y”
Normal in children, but indication of
heart failure in an adult
ABNORMAL HEART SOUNDS
S4 HEART SOUND –
or a atrial gallop, an
extra heart sound
before S1
“LUB-LUB-DUB” or
“TEN-NES-SEE” –
- often associated with hypertensive
heart disease
PERIPHERAL PULSES
-palpate the radial arteries and the
major arteries of the leg bilaterally
-record the
presence or
absence of pulses
and strength
SKIN
-note changes in skin color (cyanosis,
pallor)
-note if the skin is
warm or cold, dry
or clammy
PERIPHERAL EDEMA
EDEMA occurs when blood is not
pumped efficiently or plasma protein
levels are inadequate to maintain
osmotic pressure
AREA: feet and ankles
OTHER AREAS: fingers, hands, over the
sacrum
Evaluated on a scale of 1-4
PERIPHERAL EDEMA
PITTING EDEMA – marks of the
fingers remain
1+ PITTING EDEMA – slight indentation
(2mm), normal contours
2+ PITTING EDEMA – deeper pit after
pressing (4mm), lasts longer than 1+
PERIPHERAL EDEMA

3+ PITTING EDEMA – deep pit (6mm),

remains several seconds after pressing
4+ PITTING EDEMA – dip pit (8mm),
remains prolonged time after pressing,
possibly minutes
WEIGHT GAIN
-can indicate edema

JUGULAR VEINS
-distention of this vein usually indicates
increased fluid volume and pressure in the
right side of the heart
MENTAL STATUS
-note if patient is alert and oriented,
confused and disoriented
CONFUSION and
DISORIENTATION can
result from a decrease in the
oxygen supply to the brain
(cerebral ischemia) as a
result of poor circulation
DIAGNOSTIC
TESTS
LABORATORY
STUDIES
Enzyme,
Isoenzyme,

and Biochemical
Markers
ENZYMES

CREATINE KINASE (CK) - 98%

sensitivity for AMI 72 hours after
infarction
-present in heart muscles, skeletal
muscles, and brain tissue
ENZYMES

CK ISOENZYMES - more specific

than CK
CK-MM – skeletal muscles
CK-BB – appears primarily in the brain
and nerve tissue
CK-MB – heart muscles
-generally, CK-MB levels rise 4-8hrs after
the onset of AMI, peak after 20hrs, & may
remain elevated for up to 72hrs
ENZYMES

TROPONIN I and TROPONIN T - is

a protein found in the skeletal and
cardiac muscles
TROPONIN T – may also be found in
the skeletal muscle
TROPONIN I – found only in the
myocardium, (more specific to
myocardial damage)
TROPONIN LEVELS rises within 36hrs after myocardial damage.
Troponin I peaks in 12-24hrs, with a
return to baseline in 5-7days
Troponin T peaks in 24hrs , with a
return to baseline in 10-15days
ENZYMES

MYOGLOBIN - is a small, oxygenbinding protein found in cardiac and

skeletal muscles and is rapidly
released into the bloodstream
ENZYMES

C-REACTIVE PROTEIN (CRP) - is

an inflammatory marker that may be
an important risk factor for
atherosclerosis and ischemic heart
disease
Elevated CRP is associated with AMI,
stroke, and the progression of
peripheral vascular disease
ENZYMES

LIPOPROTEIN - a molecule that is

similar to low-density lipoprotein
cholesterol (LDL-C)
It increases cholesterol deposits in the
arterial wall, enhances oxidation of
LDL-C, and inhibits fibrinolysis,
resulting in the formation of
atherosclerotic plaque and thrombosis
ENZYMES

FACTOR I or FIBRINOGEN - is
directly linked to increased
cardiovascular risk
It is involved in the coagulation
cascade (converting fibrinogen to
fibrin by thrombin)
HEMATOLOGIC STUDIES

CBC - indication of the type and

number of formed elements in the
blood
HEMATOLOGIC STUDIES

HEMATOCRIT – expresses the

relationship of the formed elements in
the blood to the total volume

 LOWERED when blood volume increases

as in CHF

 RISES when blood volume is lost as in

bleeding, shock and burns
HEMATOLOGIC STUDIES

PROTHROMBIN TIME - measures

how long it takes for prothrombin to
become active in clotting process
PARTIAL THROMBOPLASTIN TIME determine deficiencies in all
coagulation factors except factor VII
HEMATOLOGIC STUDIES

ERYTHROCYTE SEDIMENTATION
RATE (ESR) - indicates the extent to
which RBC settle to the bottom of the
test tube containing a sample of blood
 ESR rises during the inflammatory
processes such as rheumatic fever and MI
BLOOD CHEMISTRIES

SERUM CHOLESTEROL
SERUM TRIGLYCERIDES
GRAPHIC
RECORDING
STUDIES
ECG
HOLTER
MONITORING
GRAPHIC RECORDING STUDIES

ECG - graphically record electrical

current generated by the heart
Helps identify primary
conduction
abnormalities,
arrhythmias, cardiac
hypertrophy, pericarditis,
electrolyte imbalance,
and MI
GRAPHIC RECORDING STUDIES

EXERCISE ECG (Stress Test) - non

invasive test that helps the doctor
assess cardiovascular response to
an increased workload
Provides diagnostic information that can’t
be obtained from a resting ECG
GRAPHIC RECORDING STUDIES

HOLTER MONITORING - records the

heart’s electrical activity for 24 hours
or longer as the patient performs his
usual activities and experiences
normal physical and emotional stress
RADIOLOGY AND
IMAGING
Chest X-ray
Myocardial Imaging
RADIOLOGY AND IMAGING

CHEST X-RAY - a noninvasive tool

used to visualize internal structures,
such as the heart, lungs, soft tissues,
and bones
RADIOLOGY AND IMAGING

MYOCARDIAL IMAGING - with the

use of radionuclides and scintillation
cameras, radionuclide angiograms
can be used to assess left ventricular
performance
RADIOLOGY AND IMAGING

ECHOCARDIOGRAPHY – a
noninvasive imaging technique,
records the reflection of ultra-high
frequency sound waves directed at
the patient’s heart
RADIOLOGY AND IMAGING

MRI (MAGNETIC RESONANCE

IMAGING)– yields high-resolution,
tomographic, three dimensional
images of body structures
Permits visualization of valve leaflets and
structures, pericardial abnormalities and
processes, ventricular hypertrophy,
cardiac neoplasm, infarcted tissue
RADIOLOGY AND IMAGING

ULTRAFAST CT SCAN – uses a

scanner that takes images as fast
speeds, resulting in high resolution
pictures
-can identify microcalcifications in the
coronary arteries
RADIOLOGY AND IMAGING

ELECTRON BEAM COMPUTED

TOMOGRAPHY – a radiologic test
that produces x-rays of the coronary
arteries using electron beam
-can detect and quantify calcified plaque
in the coronary arteries
RADIONUCLIDE
IMAGING TESTS
CARDIAC
CATHETERIZATION
AND CORONARY
ANGIOGRAPHY
RADIONUCLIDE IMAGING TESTS

CARDIAC CATHETERIZATION AND

CORONARY ANGIOGRAPHY –
invasive tests, use a catheter threaded
through an artery or vein into the heart
-to determine the size and location of a
coronary lesion, evaluate ventricular
function, measure heart pressures and
oxygen saturation
RADIONUCLIDE IMAGING TESTS

CORONARY FLOW AND PERFUSION

EVALUATION – used to assess blood
flow through the coronary arteries,
investigate myocardial anatomy and
perfusion, and determine the extent of
lesions
RADIONUCLIDE IMAGING TESTS

DSA – combines angiography with

computer processing to produce highresolution images of cardiovascular
structures
-provides a clear view of arterial
structures
RADIONUCLIDE IMAGING TESTS

VENOGRAM– Insertion of a dye into

the vein for the purpose of outlining an
obstruction or lesion
TREATMENTS
DRUG THERAPY
ADRENERGICS
ANTIANGINALS
ANTIARRHYTHMICS
ANTIHYPERTENSIVES
ANTILIPEMICS
ANTIPLATELET AGENTS
DIURETICS
INOTROPHIC AGENTS
THROMBOLYTICS
ANALGESIC

Antipyretic, Non-Steroidal Antiinflammatory drugs, acetaminophen,

acetylsalicylic acid, ibuprofen

 Relieves pain, fever, and

inflammation
ANGIOTENSIN-CONVERTING
ENZYME (ACE) INHIBITORS
Captopril, Enalapril

Prevent angiotensin I from converting

to angiotensin II, a potent
vasoconstrictor, thereby decreasinbg
peripheral vascular resistance, blocks
the secretion of aldosterone from
adrenal gland
ANGIOTENSIN II RECEPTOR
ANTAGONISTS
LOSARTAN, VALSARTAN

Block angiotensin II at the receptor

sites, thereby decreasing peripheral
vascular resistance
ANTIARRHYTHMICS
Lidocaine, propanolol, amiodarone

Reduce automaticity, slow conduction

of electrical impulses through the heart,
and prolong the refractory period of
myocardial cells
ANTIBIOTICS
Aminoglycocides (gentamycin,
tobramycin), Amoxicillin, Erythromycin,
penicillin, tetracycline

Prevent or treat infections caused by

pathogenic microorganism
ANTICHOLINERGICS

Atropine
Block effects of vagus nerve
stimulation
ANTICOAGULANTS

IV Heparin, oral warfarin sodium

Prevent recurrence of emboli but
have no effect on emboli that are
already present
ANTICOAGULANTS

Subcutaneous – low dose heparin

(5,000 units)
Prophylactically prevent deep vein
thrombosis, heparin activates
antithrombin III
ANTILIPEMIC AGENTS

Cholestyramine, clofibrate, colestipol,

lovastatin
Lower the serum cholesterol level by
binding bile salts in the bowel and
forming an insoluble complex that is
excreted in the stool
ANTIPLATELET AGENTS

Aspirin, ticlopidine
Inhibit the aggregation of platelets to
form a plug, platelets do not initiate
thrombus formation as readily when
taking antiplatelets
BETA-ADRENERGIC BLOCKERS

Atenolol, metoprolol, propanolol

Decrease the heart rate and the force
of contraction and reduce
vasoconstriction by antagonizing betareceptors in the myocardium and
vasculature
BETA-ADRENERGICS

Beta only (dobutamine), beta or alpha

plus beta – dopamine, epinephrine,
metaraminol
Increase myocardial contractility and
heart rate, which in turn raises blood
pressure, alpha plus beta-adrenergic
activity
CALCIUM CHANNEL BLOCKERS

Nifedipine, Verapamil
Inhibit calcium ions from crossing
myocardial and vascular smooth
muscle, thereby producing vasodilation
and decreased myocardial contractility
CARDIAC GLYCOSIDES

Digoxin
Increase the force of myocardial
contractions and slow heart rate and
conduction through the atrioventricular
node and bundle of His
CORTICOSTEROIDS

Oral hydrocortisone, oral

methylprednisolone, oral prednisone
Strengthen the biologic membrane,
which inhibits capillary permeability and
prevents leakage of fluid into the
injured area and development of
edema
DIURETICS
Loop diuretics – furosemide, potassium
sparing diuretic – spironolactone,
thiazide diuretic

Decrease blood volume, which

decreases the workload of the heart
OPIOD ANALGESICS
Codeine, morpine, hydromorphone

Release moderate to severe pain by

reducing pain sensation, producing
sedation, and decreasing the emotional
upset often associated with pain
NITRATES

Isosorbide dinitrate, nitroglycerine –

sublingual, topical, patch, tablet, IV
Reduce myocardial oxygen demand
by promoting vasodilation and by
increasing oxygen supply to myocardial
tissue
STOOL SOFTENERS

Docusate calcium, docusate sodium

Decrease the surface tension of the
fecal mass to allow water to penetrate
into the stool; prevents the client from
straining from defecation
THROMBOLYTIC AGENTS

Streptokinase, urokinase
Dissolve thrombus or emboli in the
coronary arteries
VASODILATORS

Hydralazine, nitroprusside sodium

Decrease preload (venous dilators)
and afterload (arterial dilators); act
directly on blood vessels to cause
dilation and decrease peripheral
vascular resistance
AUTONOMIC NERVOUS SYSTEM
- critical to the stability of our internal
environment (homeostasis)

DIVISIONS:
SYMPATHETIC NERVOUS SYSTEM
PARASYMPATHETIC NERVOUS SYSTEM

-generally function antagonistically

toward each other
SYMPATHETIC NERVOUS SYSTEM
- regulates the expenditure of energy
- Neurotransmitter are known as
CATECHOLAMINES – epinephrine,
norepinephrine, and dopamine

- controls “fight-or-flight responses”

SYMPATHETIC NERVOUS SYSTEM
ENZYMES:
Monoamine oxidase (MAO) &
Catechol-O-methyltransferase
(COMT)
4 TYPES OF RECEPTORS:
alpha1, alpha2, beta1, beta2
PARASYMPATHETIC NERVOUS
SYSTEM
-Works to conserve body energy and
is partly responsible for slowing
heart rate, digesting food, and
eliminating body wastes

- “rest and digest”

-Neurotransmitter: ACETYLCHOLINE
PARASYMPATHETIC NERVOUS
SYSTEM
ENZYME:
Acetylcholinesterase
2 TYPES OF RECEPTORS:
Nicotinic, Muscarinic (both are
alkaloids)
ADRENERGIC FIBERS – are
NERVE ENDINGS that secrete
NOREPINEPHRINE

CHOLINERGIC FIBERS – are

NERVE ENDINGS that liberate
ACETYLCHOLINE

- They produce opposite responses

EXAMPLE:

HEART
ADRENERGIC AGENTS
increase the heart rate

CHOLINERGIC AGENTS
slow the heart rate
RESPONSES TO
SYMPATHETIC
ACTIVATION
RESPONSES TO
PARASYMPATHETIC

ACTIVATION
CARDIAC
PACING
CARDIAC PACEMAKER

- is an electronic device
that delivers direct
electrical stimulation to
stimulate the
myocardium to
depolarize, initiating a
mechanical contraction
The PACEMAKER initiates and
maintains the heart rate when the
heart's natural pacemaker is unable
to do so
PACEMAKERS can be used to
correct bradycardias, tachycardias,
sick sinus syndrome, and secondand third-degree heart blocks, and for
prophylaxis
Pacing may be
accomplished through a
permanent implantable
system, a temporary
system with an external
pulse generator and
percutaneously threaded
leads, or a transcutaneous
external system with
electrode pads placed
over the chest
CARDIAC PACEMAKER

INDICATIONS
1. Symptomatic bradydysrhythmias
2. Symptomatic heart block
a. Mobitz II second-degree heart block
b. Complete heart block
c. Bifascicular and trifascicular bundle
branch blocks
CARDIAC PACEMAKER

INDICATIONS
3. Prophylaxis
a. After acute MI: dysrhythmia and
conduction defects
b. Before or after cardiac surgery
c. During diagnostic testing
CARDIAC PACEMAKER

INDICATIONS
4. Tachydysrhythmias; to break rapid
rhythm disturbances
a. Supraventricular tachycardia
b. Ventricular tachycardia
CARDIAC PACEMAKER

TYPES
PERMANENT PACEMAKERS
•Used to treat chronic heart conditions;
surgically placed, utilizing a local
anesthetic, the leads are placed
transvenously in the appropriate
chamber of the heart and then
anchored to the endocardium
CARDIAC PACEMAKER

TYPES
PERMANENT PACEMAKERS
• The pulse generator is placed in a
surgically made pocket in
subcutaneous tissue under the
clavicle.
• Once placed and programmed it can
be adjusted externally as needed.
CARDIAC PACEMAKER

TYPES
TEMPORARY PACEMAKERS
• are usually placed during an
emergency, such as when a patient
demonstrates signs of decreased
CO until the temporary condition is
resolved
CARDIAC PACEMAKER

TYPES
TEMPORARY PACEMAKERS

• Indicated for patients with highgrade AV blocks, bradycardia, or

low CO
Temporary
transvenous
pacer wire with
external pulse
generator
SURGERY
CORONARY ARTERY BYPASS
GRAFTING
• CABG circumvents an occluded
coronary artery with an autogenous
graft (usually a segment of
saphenous vein or internal mammary
artery, thereby restoring blood flow to
the myocardium
Coronary artery
bypass graft
surgery is done
primarily to
alleviate anginal
symptoms as well
as improve
survival
CORONARY ARTERY BYPASS
GRAFTING
CANDIDATES FOR CABG
- Severe angina from atherosclerosis
- CAD with high risk of MI
TRANSMYOCARDIAL
REVASCULARIZATION
• TMR is a relatively new procedure.
• Can provide relief for sever angina
when medical therapy fails or the
patient isn’t a candidate for
angioplasty or by-pass surgery
• Is performed through an incision on
the left side of the chest
TRANSMYOCARDIAL
REVASCULARIZATION
POTENTIAL COMPLICATIONS:

- Arrhythmias, bleeding, damage to the

great vessels, valves, and coronary
arteries
MINIMALLY INVASIVE CORONARY
ARTERY BYPASS
• is CABG surgery done through a left
anterior small thoracotomy (LAST)
• a short parasternal incision, or small
incisions using port access and videoassisted technology
Minimally
invasive direct
grafting of left
internal
mammary
bypass graft to
left anterior
descending
coronary artery
(LAD).
Surgery is performed on the beating heart.
To allow suturing of the graft anastomosis
to the beating heart, pharmacologic
measures such as adenosine and betablockers are used to slow or temporarily
stop the heart
PORT ACCESS CARDIAC SURGERY
• is another minimally invasive surgical
technique that uses femorofemoral
bypass through a small incision with
aid of videoscopes.
• is performed using a small anterior
thoracotomy and several small “port”
chest incisions
VASCULAR REPAIR
• may treat:
- Vessels damaged by arteriosclerotic or
thromboembolic disorders (such as
aortic aneurysm or arterial occlusive
disease), trauma, infections, or
congenital defects
- Vascular obstructions that severely
compromise circulation
VASCULAR REPAIR
• may treat:
- Vascular disease that doesn’t repsond
to drug therapy
- Life-threatening dissecting or ruptured
aortic aneurysm
VASCULAR REPAIR
• includes aneurysm resection, grafting,
embolectomy, vena caval filtering, and
vein stripping
VASCULAR REPAIR
TYPES:
AORTIC ANEURYSM REPAIR
- Removes an aneurysmal segment of the
aorta
VEIN STRIPPING
- Removes the
saphenous vein and
it's branches to treat
varicosities
VASCULAR REPAIR
TYPES:
VENA CAVAL FILTER INSERTION
- Traps emboli in the vena cava,
preventing them from reaching the
pulmonary vessels
EMBOLECTOMY
- Removes an embolism from an artery
VASCULAR REPAIR
TYPES:
BYPASS GRAFTING
- bypasses an arterial obstruction
resulting from arteriosclerosis
BALLOON CATHETER TREATMENTS

PERCUTANEOUS BALLOON
VALVULOPLASTY
PERCUTANEOUS
TRANSLUMINAL CORONARY
ANGIOPLASTY (PTCA)
PERCUTANEOUS BALLOON
VALVULOPLASTY
-can be performed in the cardiac
catheterization laboratory
- seeks to improve valvular function by
enlarging the orifice of a stenotic heart
valve caused by congenital defect,
calcification, rheumatic fever, or aging
PTCA
-offers a nonsurgical alternative to
coronary artery bypass surgery
- uses a balloon-tipped catheter to dilate
a coronary artery that has become
narrowed because of atherosclerotic
plaque
-can open an occluded coronary artery
without opening the chest
DISEASES OF
THE HEART
Thrombus
• A thrombus
– a blood clot that can develop
anywhere in the vascular system
– causing the narrowing of a
vessel.
– blood flow can be occluded
(reduced or totally blocked)
Thrombus

– develop from any injury to the vessel wall

• endothelial cell injury draws platelets and
other mediators of inflammation to the
area.
• substances stimulate clotting and activation
of the coagulation cascade.
• formation can occur when blood flow
through a vessel is sluggish,
• when blood flow is irregular or erratic
–during periods of irregular heartbeat or
cardiac arrest
Thrombus
Embolus
• Embolus
– a substance that travels in the
bloodstream from a primary site to a
secondary site
– becomes trapped in the vessels at the
secondary site
– causes blood flow obstruction.
– Most emboli are blood clots
(thromboemboli)
• usually deep leg veins
Embolus
–Other sources of emboli
• fat
–released during the break of a long bone
–produced in response to any physical
trauma, and amniotic fluid
»which may enter maternal circulation
during the intense pressure gradients
generated by labor contractions.

• Air and displaced tumor cells also may

act as emboli to obstruct flow.
CORONARY ARTERY DISEASE
-focal narrowing of the large and
medium-sized coronary arteries
- due to deposition of atheromatous
plaque in the vessel wall
- LIPID or FATTY Substance
- FIBROUS TISSUE
ARTERIOSCLEROSIS – hardening of
the arteries, which results in loss of
elasticity of intimal layer of the artery
ATHEROSCLEROSIS – accumulated
fatty plaques made of lipids in the
arteries
CORONARY ARTERY DISEASE
RISK FACTORS
- Hereditary,
including race
- Age, Gender

- Cigarette Smoking
- HTN
- Elevated Serum
Cholesterol Level
- Diabetes Mellitus
- Physical Inactivity
- Obesity
- fatty, fibrous
plaques
- occlude the
coronary
arteries
- reduce volume of blood flow
leading to myocardial ischemia
Progression of atheromatous plaque from initial
lesion to complex and ruptured plaque
CORONARY ARTERY DISEASE
SIGNS AND SYMPTOMS
ANGINA – classic symptom
occurs as burning,
squeezing or crushing
tightness in the
substernal or precordial
chest
- may radiate to the left arm, neck, jaw or
shoulder blade
4 MAJOR FORMS OF ANGINA

STABLE – pain that’s predictable in

frequency and duration and can be
relieved with nitrates and rest
UNSTABLE – increased pain that’s
easily induced
4 MAJOR FORMS OF ANGINA

PRINZMETAL’S or VARIANT – from

unpredictable coronary artery spasm
MICROVASCULAR – impairment of
vasodilator reserve, which causes
angina-like chest pain in a patient with
normal coronary arteries
CORONARY ARTERY DISEASE
OTHER SIGNS AND SYMPTOMS
Nausea
Vomiting
Weakness
Diaphoresis
Cool extremities
CORONARY ARTERY DISEASE
DIAGNOSTICS
ECG – shows ischemia
Exercise ECG – provoke chest pain
Coronary Angiography – reveals
coronary artery stenosis or obstruction,
shows arteries beyond narrowing
CORONARY ARTERY DISEASE
DIAGNOSTICS
Laboratory evaluation– to eliminate
a diagnosis of MI
Serum lipid studies – to detect
hyperlipidemia
CORONARY ARTERY DISEASE
NURSING DIAGNOSIS
Acute Pain
Decreased Cardiac Output
Anxiety
CORONARY ARTERY DISEASE
TREATMENT
MEDICATIONS:
Nitrates
Antiplatelets
Antilipemics
Beta-adrenergic blockers
Calcium channel blockers
CORONARY ARTERY DISEASE
NURSING MANAGEMENT
Provide care during an acute anginal
attack
- Nitrates (SL)
-stat 12-Lead ECG
CORONARY ARTERY DISEASE
NURSING MANAGEMENT
PROMOTE PAIN RELIEF
-reduce activity to a point at which pain
does not occur
-Position patient for comfort; Fowler's
position promotes ventilation
-Administer oxygen if prescribed
CORONARY ARTERY DISEASE
NURSING MANAGEMENT
MAINTAIN CARDIAC OUTPUT
-monitor vital signs, note changes in BP
-note patient complaints of headache
(especially with use of nitrates)
-evaluate for development of heart
failure
CORONARY ARTERY DISEASE
NURSING MANAGEMENT
DECREASING ANXIETY
-Rule out physiologic etiologies for
increasing or new onset of anxiety
-Explain to patient and family reasons
for hospitalization
Encourage patient to verbalize fears
and concerns
CORONARY ARTERY DISEASE
SURGERY
Obstructive lesions may necessitate
CORONARY ARTERY BYPASS surgery
or PTCA
CORONARY ARTERY DISEASE
PREVENTION
Cessation of smoking
Control of high BP
Diet low in saturated fat, cholesterol
Limit alcohol intake
Physical exercise
Weight control
Control of diabetes mellitus
MYOCARDIAL INFARCTION
refers to a dynamic process by which
one or more regions of the heart
experience a severe and prolonged
decrease in oxygen supply because of
insufficient coronary blood flow;
subsequently, necrosis or death to the
myocardial tissue occurs
MYOCARDIAL INFARCTION
Obstruction in a coronary artery
resulting in necrosis
Due to:
Atherosclerotic plaque
Thrombus
Embolism
MYOCARDIAL INFARCTION
CLINICAL MANIFESTATIONS
CHEST PAIN
Typically, persistent
and crushing, located
substernally with
radiation to the arm,
neck, jaw and unrelieved
by rest or nitrates
MYOCARDIAL INFARCTION
CLINICAL MANIFESTATIONS
CHEST PAIN

Occurs without cause, primarily

early morning
NOT relieved by rest or
nitroglycerin
Lasts 30 minutes or longer
MYOCARDIAL INFARCTION
CLINICAL MANIFESTATIONS
Diaphoresis, cool clammy skin, facial
pallor
Hypertension or hypotension
Bradycardia or tachycardia
Premature ventricular and/or atrial
beats
Palpitations, severe anxiety, dyspnea
MYOCARDIAL INFARCTION
CLINICAL MANIFESTATIONS
Disorientation, confusion,
restlessness
Fainting, marked weakness
Nausea, vomiting, hiccups
Atypical symptoms: epigastric or
abdominal distress, dull aching or
tingling sensations, shortness of breath,
extreme fatigue
MYOCARDIAL INFARCTION
DIAGNOSTICS
•ST segment is
ELEVATED.
T wave inversion,
presence of Q
wave
- Elevated CK-MB, LDH and Troponin levels
CBC - Elevated WBC count
MYOCARDIAL INFARCTION
NURSING DIAGNOSIS
•Acute Pain
•Anxiety related to chest pain, fear of
death, threatening environment
•Decreased Cardiac Output related to
impaired contractility
•Activity Intolerance
•Risk for Injury (bleeding) related to
dissolution of protective clots
MYOCARDIAL INFARCTION
MANAGEMENT
M – Morphine sulfate
O – O2 therapy
N – Nitrates
A – Aspirin/Adequate rest
MYOCARDIAL INFARCTION
MANAGEMENT
O2 – to increase oxygenation of the
blood
NITRATES – to relieve chestpain
MORPHINE – for analgesia
ASPIRIN – to inhibit platelet
aggregation
MYOCARDIAL INFARCTION
MANAGEMENT
-Relieve pain
-Stabilize heart rhythm
-Revascularize the coronary artery
-Reduce cardiac workload
-PTCA
MYOCARDIAL INFARCTION
NURSING MANAGEMENT
 Administer prescribed medications
– morphine, nitrates, antilipemics,
thrombolytics, anticoagulants
 Provide ongoing assessment
-monitor cardiac enzymes
MYOCARDIAL INFARCTION
NURSING MANAGEMENT
 Minimize anxiety

 Minimize metabolic demands

-institute a liquid diet, advance to a low
sodium, low cholesterol, low fat diet
MYOCARDIAL INFARCTION
NURSING MANAGEMENT
 prepare the client for treatment, such
as percutaneous transluminal coronary
angioplasty and coronary artery bypass
grafting
HEART FAILURE
 is a syndrome of pulmonary or
systemic circulatory congestion caused
by decreased myocardial contractility,
resulting in inadequate CO to meet
oxygen requirements of tissues.
HEART FAILURE
CLASSIFICATION:
LEFT-SIDED (or
left ventricular)

RIGHT-SIDED (or
right ventricular)
HEART FAILURE
LEFT-SIDED - congestion occurs primarily in
the lungs from backup of blood into
pulmonary veins and capillaries because of
left ventricular pump failure.
As blood backs up into the pulmonary bed,
increased hydrostatic pressure causes fluid
accumulation in the lungs.
Blood flow is consequently decreased to the
brain, kidneys, and other tissues
HEART FAILURE
RIGHT-SIDED - congestion in systemic
circulation results from right ventricular pump
failure.

As blood backs up into the pulmonary bed,

increased hydrostatic pressure produces
peripheral and dependent pitting edema.
Venous congestion in the kidneys, liver, and
GI tract also develops.
HEART FAILURE
CAUSES:
-atherosclerotic heart disease
-MI
-hypertension
-Rheumatic heart disease
-congenital heart disease
-ischemic heart disease
-Arrhythmias
HEART FAILURE
DIAGNOSTICS:
ECHOCARDIOGRAPHY - depressed

cardiac output, evidence of

cardiomegaly
CHEST X-RAY-reveals cardiomegaly
ABG-decreased partial pressure of arterial
O2
HEART FAILURE
CLINICAL MANIFESTATIONS
LEFT SIDED HEART FAILURE
-dyspnea on exertion, paroxysmal
nocturnal dyspnea, or orthopnea
-crackles on lung auscultation
-frothy blood-tinged sputum
-tachycardia with S3 heart sound
-pale, cool extremities
-peripheral and central cyanosis
HEART FAILURE
CLINICAL MANIFESTATIONS
LEFT SIDED HEART FAILURE
-decreased peripheral pulses and capillary
refill
Decreased urinary output
easy fatigability
Insomnia and restlessness
HEART FAILURE
CLINICAL MANIFESTATIONS
RIGHT SIDED HEART FAILURE
•dependent pitting edema
(peripheral and sacral)
•Weight gain
•Nausea and anorexia
•Jugular vein distention
•Liver congestion, ascites,
weakness
HEART FAILURE
NURSING DIAGNOSIS:
Decreased CO related to an ineffective
ventricular pump
HEART FAILURE
PHARMACOLOGIC TREATMENT:
Vasodilators
Diuretics
Digoxin

Dobutamine
Beta-adrenergic blocking agents
(metoprolol, carvedilol)
HEART FAILURE
NURSING MANAGEMENT:
☺ Administer medications as ordered
☺ Provide ongoing assessment
-Monitor hemodynamic parameters, HR,
rhythm,
-weigh OD

☺ Prevent complications of immobility

HEART FAILURE
NURSING MANAGEMENT:
☺ Provide a low-sodium diet, as
prescribed
☺ provide client and family teaching
HYPERTENSION
 refers to an intermittent or sustained
elevation in diastolic or systolic blood
pressure
HYPERTENSION
TYPES:
ESSENTIAL (IDIOPATHIC) – most
common form
SECONDARY – results from a number
of disorders that impair blood pressure
regulation
MALIGNANT HYPERTENSION –
severe, fulminant form of hypertension
common to both types
HYPERTENSION
CAUSES:
ESSENTIAL (IDIOPATHIC) –associated
with risk factors such as genetic
predisposition, stress, obesity, and a
high-sodium diet
HYPERTENSION
CAUSES:
SECONDARY – results from underlying
disorders that impair blood pressure
regulation, particularly renal, endocrine,
vascular, and neurological disorders;
hypertensive disease of pregnancy
(formerly known as toxemia); and use of
estrogen-containing oral contraceptives
HYPERTENSION
CAUSES:
MALIGNANT HYPERTENSION – not
known, but it may be associated with
dilation of cerebral arteries and
generalized arteriolar fibrinoid necrosis,
which increases intracerebral
blood flow, resulting in encephalopathy
Guidelines for Determining
Hypertension
Category

Systolic Pressure

Diastolic Pressure

Normal

<120 mm Hg

<80 mm Hg

Prehypertension

120-139 mm Hg

80-89 mm Hg

Stage 1
hypertension

140-159 mm H g

90-99 mm Hg

Stage 2
hypertension

>160 mm Hg

>100 mm Hg
HYPERTENSION
RISK FACTORS
Family history of hypertension
Race (more common in blacks)
Gender
Diabetes mellitus
Stress
Obesity
HYPERTENSION
RISK FACTORS

High dietary intake of saturated fats

or sodium
Tobacco use
Hormonal contraceptive use
Sedentary lifestyle
aging
HYPERTENSION
SYMPTOMS:
blood pressure measurements of more
than 140/90mmHg
Throbbing occipital headaches upon
waking
Drowsiness
Confusion

vision problems
nausea
HYPERTENSION
DIAGNOSTICS:
BUN - May be elevated
SERUM CREATININE - determines if
renal dysfunction is present as a
complication of hypertension
Total cholesterol, Triglycerides
Electrocardiogram
HYPERTENSION
TREATMENT:
SECONDARY HPN - correcting the
underlying cause and controlling
hypertensive effects

LIFESTYLE MODIFICATIONS:
change in diet, relaxation techniques,
exercise, smoking cessation,
limited intake of alcohol
HYPERTENSION
TREATMENT:
DRUG THERAPY

THIAZIDE – for uncomplicated HPN

ACE INHIBITOR
BETA-ADRENERGIC BLOCKER
HYPERTENSION
TREATMENT:
DRUG THERAPY

Angiotensin II receptor blockers

Alpha-receptor blockers
Calcium channel blockers
HYPERTENSION
NURSING DIAGNOSIS:
Knowledge deficit related to chronic

disease management
INTERVENTIONS: Health education;
Teaching: Diet, Disease process, Health
behaviors, Medication, Prescribed
activity, Treatment regimen
INFLAMMATORY
DISORDERS OF THE
PERIPHERAL BLOOD
VESSELS
VARICOSE VEINS
• Permanently distended
veins that develop from
loss of valvular
competency
• Faulty valves elevate
venous pressure
• Causes distension and
tortuosity
Predisposing Factors

• Pregnancy
• Obesity
• Heart disease
Assessment Findings

• Aching, a feeling of
heaviness in the legs
• Itching, moderate swelling
• Superficial inflammation
• Dilated tortuous skin veins
Diagnostic test

• Trendelenberg test:
• Doppler ultrasound
– Decrease or no blood flow
heard after calf or thigh
compression
Medical Management
Reduce
venous
pooling

Prevent
complication

Improve
comfort
levels

Compression stocking
THROMBOPHLEBITIS
-is an inflammation of a vein
accompanied by clot or thrombus
formation
DEEP VEIN
THROMBOSIS –
veins that are
deep in the lower
extremeties
THROMBOPHLEBITIS
-when inner lining of a vein is irritated or
injured, platelets clump together, forming
a clot

Clot interferes with blood flow, causing
congestion of venous blood
THROMBOPHLEBITIS
SIGNS AND SYMPTOMS
-complaints of discomfort in the affected
extremity
-Calf pain (+Homan’s sign)
-heat, redness, swelling on the affected
vein
THROMBOPHLEBITIS
DIAGNOSTICS

VENOGRAPHY –
indicates a filling
defect in the area
of the clot
THROMBOPHLEBITIS
MANAGEMENT
Complete rest of the affected part
anticoagulant therapy (heparin)
Continues warm, wet packs – to
improve circulation, ease pain, decrease
inflammation
THROMBECTOMY- surgical removal
of the clot
THROMBOANGITIS OBLITERANS
(BUERGER’S DISEASE)
 Inflammatory, nonatheromatous
occlusive condition that causes
segmental lesions and subsequent
thrombus formation
- affects small arteries and veins of the
legs
THROMBOANGITIS OBLITERANS
(BUERGER’S DISEASE)
CAUSE:
-unknown but definite link to smoking
CLINICAL MANIFESTATIONS:
-Intermittent Claudication
THROMBOANGITIS OBLITERANS
(BUERGER’S DISEASE)
- No specific treatment exist, except
smoking cessation
- Amputation
maybe necessary
for patients with
gangrene
formation
INFECTIOUS AND
INFLAMMATORY
DISORDERS OF THE
HEART
RHEUMATIC FEVER
is a systemic inflammatory disease
that sometimes follows a group A
streptococcal infection of the throat

RHEUMATIC CARDITIS
refers to the inflammatory cardiac
manifestations of Rheumatic Fever in
either the acute or later stage
RHEUMATIC FEVER
STRUCTURES AFFECTED:

heart valves, praticularly mitral valve

endocardium
myocardium
pericardium
RHEUMATIC FEVER
STREPTOCOCCAL INFECTION


Antistreptococcal antibodies attack normal
heart cells

Myocarditis and valvulitis develop


Rheumatic carditis develops
RHEUMATIC FEVER
SIGNS AND SYMPTOMS:
most common in children 2-3 weeks
after a streptococcal infection
CARDITIS – inflammation of the layers
of the heart
RHEUMATIC FEVER
POLYARTHRITIS – inflammation of
more than 1 joint
rash, subcutaneous nodules,
chorea (characterized by involuntary
grimacing & an inability to use skeletal
muscles in coordinated manner
RHEUMATIC FEVER
SIGNS AND SYMPTOMS:
mild fever
Heart rate (rapid, rhythm abnormal)
Red, spotty rash (trunk, disappears
rapidly)
Swollen, warm, red & painful joints
RHEUMATIC FEVER
DIAGNOSTICS:

no specific laboratory tests

ASO titer
ESR, C-reactive protein – elevated,
ECG, ECHOCARDIOGRAPHY –
structural changes in the heart
RHEUMATIC FEVER
MEDICAL MANAGEMENT:

IV ANTIBIOTICS:
PENICILLIN – drug of choice
Others: AZYTHROMYCIN
(ZYTHROMAX), CLINDAMYCIN,
VANCOMYCIN
CEPHALOSPORINS:
Cephalexin, Cefadroxil
RHEUMATIC FEVER
MEDICAL MANAGEMENT:
ASPIRIN – to control the formation of
blood clots around heart valves
STEROIDS – to suppress the
inflammatory response

BED REST
RHEUMATIC FEVER
MEDICAL MANAGEMENT:
SURGERY may be required to treat
constrictive pericarditis and damage to
heart valves
RHEUMATIC FEVER
NURSING MANAGEMENT:
 Administer prescribed
drug therapy and monitor
for therapeutic and
adverse effects
 Plan diversional activities that require
minimal activity
INFECTIVE ENDOCARDITIS
formerly called BACTERIAL
ENDOCARDITIS
 is inflammation of the inner layer of
heart tissue as a result of an infectious
microorganism
MICROORGANISM – bacteria and fungi
BACTERIA: Streptococcus viridans,
Staphylococcus aureus
INFECTIVE ENDOCARDITIS
SIGNS AND SYMPTOMS:
-can have an acute onset – less than one week
-fever, chills, muscle aches in the lower
back and thighs, joint pain
ADVANCE:
OSLER NODES - purplish, painful
nodules, appear on the pads of the
fingers & toes
INFECTIVE ENDOCARDITIS
SIGNS AND SYMPTOMS:
-SPLINTER HEMORRHAGES – black
longitudinal lines can be seen in the nails
-JANEWAY LESIONS – small, painless,
red-blue macular lesions on the palms
and soles of the feet
INFECTIVE ENDOCARDITIS
SIGNS AND SYMPTOMS:
-ROTH’S SPOT – white areas in the
retina surrounded by areas of
hemorrhage
-HEART MURMUR – may be present
from malfunctioning valves
INFECTIVE ENDOCARDITIS
SIGNS AND SYMPTOMS:
-PETECHIAE – tiny red-dish
hemorrhagic spots on the skin and
mucous membranes
-weakness, anorexia, weight loss
INFECTIVE ENDOCARDITIS
DIAGNOSTICS
-BLOOD CULTURE – to determine
microorganism circulating in the blood
-ECG
INFECTIVE ENDOCARDITIS
MEDICAL MANAGEMENT
High doses of IV Antibiotics
Antibiotic Therapy extends at least 26 weeks
Bed rest
SURGERY – valve replacement if
heart valve is severely damaged
INFECTIVE ENDOCARDITIS
NURSING MANAGEMENT
Remind client to limit activity
Assess for changes in weight and pulse
rate and rhythm
Administer prescribed antibiotics
Inform client that periodic antibiotic
therapy is a lifelong necessity because
they will be vulnerable to the disease for
the rest of their lives
MYOCARDITIS
is an inflammation of the
myocardium (the muscle layer
of the heart)
CAUSES: Viral, bacterial,
fungal, or parasitic infections
VIRAL AGENTS: coxsackie virus A & B,
influenza A & B, measles, adenovirus,
mumps, rubeola, rubella
MYOCARDITIS
Inflammatory response causes
the cardiac muscle to swell

Interferes with the myocardium’s ability to
stretch and recoil

Cardiac output is reduced and blood
circulation is impaired, predisposing the
client to CHF
MYOCARDITIS
CLINICAL MANIFESTATIONS:
-sharp stabbing pain or squeezing chest
discomfort that resembles a MI (pain is
relieved by sitting up)
-Low-grade fever, tachycardia,
dysrhythmias
-Dyspnea, malaise, fatigue, anorexia
-Skin is pale and cyanotic
MYOCARDITIS
CLINICAL MANIFESTATIONS:
IF THERE’S IMPAIRED HEART’S PUMPING
ACTIVITY:

-Neck vein distention, ascites,

-Peripheral edema,
-crackles
MYOCARDITIS
DIAGNOSTICS:
-WBC – elevated
-C-Reactive protein – elevated,
inflammatory conditions
-CARDIAC ISOENZYMES-elevated
-CHEST X-RAY – heart enlargement, fluid
infiltration in the lungs
MYOCARDITIS
MANAGEMENT
Treat underlying cause and prevent
complications
ANTIBIOTICS if bacterial
Bed Rest
Sodium-restricted diet
Cardiotonic drugs – digitalis to prevent
or treat heart failure
MYOCARDITIS
MANAGEMENT
Heart transplant is necessary in severe
cases of cardiomyopathy
MYOCARDITIS
NURSING MANAGEMENT
Monitor client’s cardiopulmonary status
(daily weights, vital signs, I & O, heart &
lung sounds, edema)
Maintain bed rest
Administer antipyretics if patient has
fever
Elevate head of the bed for maximal
breathing potential
CARDIOMYOPATHY
is a chronic condition characterized by
structural changes in the heart muscle
TYPES:
DILATED CARDIOMYOPATHY
HYPERTROPHIC CARDIOMYOPATHY
RESTRICTIVE CARDIOMYOPATHY
CARDIOMYOPATHY
DILATED CARDIOMYOPATHY
-dyspnea on exertion & when lying down,
fatigue, edema, palpitations, chestpain

HYPERTROPHIC CARDIOMYOPATHY
-syncope, fatigue, shortness of breath,
chestpain
-some are asymptomatic
CARDIOMYOPATHY
RESTRICTIVE CARDIOMYOPATHY
-exertional dyspnea, dependent edema in the
legs, ascites, hepatomegaly
CARDIOMYOPATHY
DILATED CARDIOMYOPATHY
-the cavity of the heart is stretched (dilated)
CAUSES: Viral myocarditis, Autoimmune
response, chemicals (chronic alcohol ingestion)

TREATMENT: Drug Therapy to minimize

symptoms & prevent complications,
abstinence from alcohol, salt restriction,
weight loss, possible heart transplantation
CARDIOMYOPATHY
HYPERTROPHIC CARDIOMYOPATHY
-the muscle of the left ventricle & septum
thickens, causing heart enlargement)
CAUSES: hereditary, unknown

TREATMENT: Drug Therapy to reduce heart

rate & force of contraction, antidysrhythmic
drugs, artificial pacemaker
CARDIOMYOPATHY
RESTRICTIVE CARDIOMYOPATHY
-heart muscle stiffens, which interferes with
its ability to stretch & fill with blood
CAUSES: deposits of amyloid, scleroderma,

TREATMENT: no specific treatment, drugs

such as diuretics & antihypertensives used to
control symptoms
CARDIOMYOPATHY
TREATMENT:
-DIURETICS
-CARDIAC GLYCOSIDES
-ANTIHYPERTENSIVE
PERICARDITIS
inflammation of the pericardium
PRIMARY – develops
independently of any
other condition
SECONDARY – develops because of
another condition
PERICARDITIS
Usually secondary to endocarditis,
myocarditis, chest trauma or MI

OTHER CAUSES: tuberculosis,

malignant tumors, uremia
PERICARDITIS
SIGNS AND SYMPTOMS
Fever and malaise
Dyspnea, or complaints of chest
heaviness
PRECORDIAL PAIN (relieved by upright
or leaning forward)
PERICARDITIS
DIAGNOSTICS
ECG – ST segment elevation (cardiac
isoenzymes normal)
ECHOCARDIOGRAPHY
WBC & ESR - elevated
PERICARDITIS
MANAGEMENT
Rest
DRUGS: Analgesics, antipyretics,
NSAIDs, corticosteroids
PERICARDIOCENTESIS – needle
aspiration of fluid from between the
visceral and parietal pericardium