MYOCARDIAL

INFARCTION
(MI)
►Ischemic myocardial cell necrosis
Etiology:

► causes of MI include coronary

artery obstruction due to the
progressive development of
atherosclerosis; coronary artery
spasm; embolism.
 Pathophysiology processes and
manifestations
1. The severity of the disease depends on the
size of the damaged area and the effect of
the damage on cardiac output.
2. While cell death is occurring, the heart is
using oxygen and glycogen stores; as a
result, lactic acid accumulates.
3. As areas of the heart become necrotic,
changes will occur in the ECG reading in the
respective leads.
4. Symptoms can include:
► Chest pain (described as substernal, crushing with
radiation to the arm, neck, jaw, or back; pain is
unrelieved by nitroglycerine)
► Dsypnea
► Changes in heart area
► Nausea
► Vomiting
► Fever (up to 101ºF over the first 24 to 48 hours)
► Increased WBC count and sedimentation rate
5. 12-lead ECG may show ST elevation as the
MI is evolving or Q waves when the MI is
complete.
6. After the onset of MI, enzyme elevation
occurs as follows:
► CPK-MB elevates in 2 to 4 hours.
► CPK enzymes, with the cardiac specific
CPK-MB fraction, peak in 12 to 18 hours.
► Serum glutamic –oxaloacetic transaminase
(SGOT) peaks in 23 to 36 hours.
► LDH peaks in 48 to 72 hours.
 Overview of nursing interventions
1. Establish perfusion as soon as possible, because
the heart cells can sustain ischemia for only about
20 minutes before cell death occurs.
2. Administer morphine sulfate or nitrates, as
prescribed, to relieve chest pain.
3. Administer thrombolytic agents as streptokinase or
tissue plasminogen activator (TPA), as prescribed,
to limit infarct size.
4. Provide supplemental oxygen via nasal cannula.
5. Monitor vital signs every 1 to 2 hours.
 6. Monitor cardiac rhythm for dsyrhythmias, such as
premature ventricular contractions (PVCs),
ventricular tachycardia, second-degree type II
atrioventicular (AV) block, and complete heart
block.
7. Monitor for signs of congestive heart failure.
8. Maintain intravenous line for emergency access.
9. Maintain bedrest, with the patient in Semi-Fowler’s
position, for the first 24 hours.
10. Administer medications (eg, digitalis,
antiarrhythmics, vasodilators, vasopressors,
anticoagulants, diuretics, potassium, Colace, and
sedatives) to limit the potential of complications,
as ordered.
11. Institute measures to decrease the oxygen
demand (eg, provide a calm and restful
environment, encourage the patient to rest,
control pain).
12. Provide patient teaching to identify and
reduce risk factors.
13. Prepare the patient for surgical interventions
such as percutaneous transluminal coronary
angioplasty (PCTA) or coronary artery
bypass graft (CABG), if indicated.
 CARDIOGENIC
SHOCK
►Insufficient tissue perfusion due to
the heart’s inability to pump
enough blood.
Etiology
1. Causes of cardiogenic shock include:
a. Myocardial infarction
b. Congestive heart failure
c. Cardiomyopathy
d. Pulmonary edema
e. Cardiac tamponade
2. It may also result from ineffective pumping
due to cardiac dysrhythmias and from acute
disruption of valvular function.
Pathophysiologic processes and
manifestations
1. The effects of inadequate tissue perfusion
on the body’s organs result in systemic
symptoms.
2. Decreased cerebral perfusion causes
restlessness, lethargy, confusion, and
altered level of consciousness.
3. Respiratory manifestations include increased
respiratory rate as the need for oxygen
increases; as circulation through the lungs
decreases, cough, crackles, lo2 PAO2, and
increasing PACO2 result.
4. Cardiovascular manifestations include:
▪ Rapid weak pulse
▪ Elevated CVP readings (Normal CVP is
approximately 4 to 10 cmH2O)
▪ Elevated PCWP readings (normal PCWP is
4 to 13 mmHg).
▪ As perfusion to the periphery decreases,
the skin becomes cool and pale.
▪ Reduced renal perfusion results in
oliguria.
Overview of nursing interventions
1. Administer medications to improve cardiac output
(eg, inotropic drugs, preload and afterload
reducers, diuretics, and sedatives, as prescribed.
2. Monitor PCWP to determine left ventricular
function.
3. Prepare the patient for insertion of an intraaortic
balloon pump, if indicated.
4. Monitor oxygenation status including respirator
rate, lung sounds, pulse oximetry, and ABGs.
5. Institute ventilator support, if indicated.
6. Monitor vital signs closely.
7. Maintain strict intake and output measurements;
measure output hourly.
8. Promote rest and provide comfort measures.
 ACUTE PULMONARY
EDEMA
►A medical emergency in which fluid
accumulates in the interstitial spaces and
alveoli of the lung, interfering with gas
exchange and resulting in severe hypoxia.
Etiology
1. Inadequate contractility of the left ventricle, as in
CHF (the most common). Pumping is impaired to
the extent that the pulmonary capillary pressure
for exceeds the capillary osmotic pressure, causing
fluid to move rapidly from the capillaries to the
interstitial tissue and the alveoli.
2. Can result from other causes of increased
pulmonary capillary permeability, - exposure to
toxic gases, infectious processes, drug reactions,
and rapid infusion of intravenous fluid or blood.
Pathophysiologic processes and
manifestations
1. When cardiac output drops, the heart is not able
to circulate blood. Blood then pools in the
pulmonary circulation.
2. Acute pulmonary edema may occur at night, after
a person has been reclining for some time.
Dependent lower extremity edema fluid returns to
the vascular compartment and is redistributed to
the pulmonary circulation, because the heart is
unable to pump the fluid effectively.
3. Manifestations include respsiratory
alterations, such as:
a. Dyspnea
b. Orthopnea
c. Air hunger
d. Tachypnea
e. Wheezes
f. Crackles
g. Productive cough with frothy or blood-tinged
sputum (due to rapid fluid shifts that rupture
capillaries
1. Signs and symptoms resulting from
decreased cardiac output, which can occur
at any time, include:
a. Restlessness c. Weak, rapid pulse
b. Anxiety d. Pallor
c. Confusion e. Cyanosis
2. PCWP will be elevated as fluid accumulation
causes increased pressure in the vessels of
the lungs.
Overview of nursing interventions
1. Administer supplemental oxygen to maintain gas
exchange, as ordered.
2. Institute ventilatory support, if indicated.
3. Reduce fluid volume in the pulmonary circulation by
positioning the patient in high Fowler’s, using
rotating tourniquets, administering morphine,
diuretics, aminophylline, and vasodilators, as
prescribed.
4. Administer digitalis, as prescribed, to improve left
ventricular contractility.
5. Monitor vital signs and electrolyte status.
6. Provide a calm, restful, and supportive
environment.
7. Educate the patient to prevent recurrent episodes
 COR PULMONALE
►Right-sided disorder of the heart
resulting from pulmonary disease
Etiology
► Occurs secondary to chronic
obstructive lung disease or any
disorder that causes long-term
pressure increases in the lungs
Pathophysiologic processes and
manifestations
1. Lung disease increases the pressure on the
pulmonary vessels, this pressure is known as
pulmonary vascular resistance (PVR).
2. Increased vascular pressure backs up to the right
ventricle, the chamber that supplies the lung,
causing increased pressure.
3. This pressure rise causes hypertrophy of the heart
muscle in the right ventricle, because the right
ventricle must work harder to move blood through
the lungs.
4. As the disease progresses, symptoms of right-sided
heart failure (eg, edema in the liver and legs) may
develop.
5. If a second disease develops (eg, MI,
pneumonia, or infection), heart failure may
occur.
6. Right ventricular hypertrophy is noted on
the chest x-ray and ECG.
7. Other manifestations may include:
a. Chest pain
b. Louder-than-normal pulmonary component of
S2 (the second heart sound)
c. Pulmonic valve murmur
d. Tricuspid valve murmur (may accompany
Overview of nursing interventions
1. Reduce cardiac workload by allowing the
patient to rest and providing a calm
environment.
2. Institute measures to reverse underlying
lung disease.
3. Undertake the same interventions if heart
failure is present
 PULMONARY
EMBOLISM
►Partial occlusion of the pulmonary
circulation by a blood clot (embolus)
Etiology
1. Any conditions that produce or accelerate blood
clotting can cause embolism development
2. Venous stasis
3. Hypercoaguability (resulting from certain
medications [birth control pills] or metabolic
conditions [infection])
4. Emboli may also occur from substances other than
blood.
5. Fat emboli (administration of lipids or release of fat
from the bone marrow due to long bone
trauma/surgery).
6. Amniotic fluid (travel from the uterus to the
bloodstream during childbirth.)
7. Air emboli may enter the bloodstream during
hemodialysis or insertion of a central line.
Pathophysiologic processes and
manifestations
Clot formation (embolus when released to the blood)

Obstructs blood flow to the lung

Cell necrosis (pulmonary infaraction)

Massive occlusion occurs when a major artery is

obstructed.
 Symptoms vary depending on the size and position
of the embolism

Dyspnea
Pleural pain
Hemoptysis
Fever
Leukocytosis
Crackles
Productive cough with frothy or blood-tinged sputum
(due to rapid fluid shifts that rupture capillaries)
► Embolism with infarction - condition in which a
portion of the lung has died from hypoxia.

► Embolism without infarction - condition in which

there is a clot in the lung, but cell death has not
occurred.

► Multiple emboli - condition in which there is more

than one clot in the lung.

► Shock, hypotension, tachypnea, tachycardia, and

chest pain are signs of more massive embolic
occlusion and usually result in death; the larger
the vessel occluded, the larger the area affected.
 Overview of nursing interventions
1. Administer anticoagulants to prevent further
clot formation; the body’s fibronolytic
system will destroy the original clot.
2. Prevent the development of additional
emboli by analyzing the patient’s risk
factors.
 CARDIAC ARREST
►Cessation of breathing and circulation due
to the loss of cardiac pump functions; a
medical emergency.
Etiology
1. The most common causes are ventricular
tachycardia and ventricular fibrillation due to:
a. Congenital heart disease
b. MI
c. Heart failure
d. Drug effects
e. Electrical shock
f. Hypoxia
g. Hemorrhage
2. Severe bradyarrhythmias due to electrolyte
imbalances, near drowning, or hypothermia may
also lead to cardiac arrest.
Pathophysiologic processes and
manifestations
1. Manifestations are absence of pulse and
absence of breathing in an unconscious
victim.
2. The victim’s skin will appear ashen gray.
Overview of nursing interventions
1. Identify this medical emergency promptly in order
to restore heart function.

2. Initiate CPR after the cardiac arrest to avoid

irreversible brain damage.

3. Undertake ACLS, including defibrillation or

cardioversion, oxygenation and ventilation,
intravenous catheter insertion, drug therapy,
dysrhythmia identification, acid-base balance. And
blood pressure support.
VALVULAR DISEASE
1. Refers to dysfunction of the heart valves.
2. Types:
a. Narrowing of the valve opening (stenosis)
b. Failure of a valve to close properly
(regurgitation)
3. Typically involves the mitral and aortic
valves, although any of the heart valves
may be affected.
Etiology
1. The most common cause: RHD;
inflammation changes resulting from it can
cause scar tissue to form on the valves,
causing shortening the deformation of the
valve structure.
2. Other causes of valvular disease include:
a. Infective endocarditis
b. Atherosclerosis
c. Congenital valve defects
Pathophysiologic processes and
manifestations
1. The significance of valvular disease is
determined by the degree of cardiac
dysfunction.
2. Mitral valve stenosis leads to left atrial
hypertrophy, increased left atrial pressure,
and eventually, increased pulmonary
pressures. It can cause atrial fibrillation
with thrombus formation and CHF
3. Common symptoms of mitral valve stenosis
include:
a. Palpitation
b. Chest pain
c. Weakness
d. Fatigue
4. Mitral valve regurgitation 🡪 left atrial and left
ventricular hypertophy. 🡪 atrial fibrillation,
systemic embolization, elevated lift-sided heart
pressures, and CHF. Patients with this disorder can
remain asymptomatic for 10 to 20 years, despite
severe regurgitation.

5. Aortic valve stenosis 🡪 left ventricular hypertrophy

🡪 CHF, pulmonary edema, atrial fibrillation, vertigo
and syncope. Exertional dyspnea is a common
symptom.

6. Aortic valve regurgitation leads to left ventricular

hypertrophy and a widening pulse pressure. It can
cause left heart failure, dysrhythmias and throbbing
peripheral pulses.

7. Tricuspid stenosis leads to right atrial enlargement.

It can cause right-sided heart failure and a decrease
in right ventricular cardiac output.
 8. Tricuspid regurgitation leads to venous overload
and a decreased cardiac output.
9. Pulmonic stenosis leads to right ventricular
hypertrophy and systemic congestion and can
cause right-sided heart failure.
10. Pulmonic regurgitation leads to backflow of blood
into the right ventricle and can cause right-sided
heart failure.
11. Mitral valve prolapse leads to a bulging of the
valve leaflet into the left atrium during ventricular
systole. It has recently been associated with
autonomic dysfunction.
12. Manifestations of mitral valve prolapse can
include:
a. Chest pain
b. Weakness
c. Dyspnea on exertion
d. Palpitations
e. Exercise intolerance
f. Dysrhythmias
13. Signs and symptoms of CHF also may occur.
Overview of nursing interventions
1. Institute interventions associated with CHF.
2. Prepare patient for surgery to replace or
repair the defective valve. afterward,
provide appropriate postoperative care.
3. Provide patient regarding the disease
process and treatment plan.
4. Administer B –blockers, as ordered, to
manage mitral valve prolapse.
PERICARDITIS
1. Refers to inflammation of the pericardium.
2. It may be acute, chronic, or constrictive:
a. Acute pericarditis is associated with a fibrous
exudate and is usually self-limiting.
b. Chronic pericarditis is characterized by an
increase in inflammatory exudate that continues
beyond an anticipated period of time.
c. Constrictive Pericarditis is characterized by scar
tissue that forms between the visceral and
parietal layers of pericardium.
Etiology
1. Commonly associated with increased capillary
permeability, which allows plasma proteins to invade
the pericardial space.

2. Causes of acute pericarditis include idiopathic and

viral syndromes, uremia, bacterial infections, MI,
rheumatic fever, and physical and chemical agents.

3. Chronic pericarditis is associated with rheumatic

fever, congenital heart conditions, hypertension,
lupus, rheumatic arthritis, scleroderma, myxedema,
and acute and chronic renal failure. Pericarditis with
effusion commonly occurs in persons being
maintained on hemodialysis.

4. Constrictive pericarditis is associated long standing

pyrogenic infections or postviral infections.
Pathophysiologic processes and
manifestations
1. The inflammatory process of acute pericarditis
occurs in response to stimulation of immune
system, which, after insult to the pericardim from
infection or radiation therapy, causes inflammation
on the pericardial sac.

2. Chest pain worsens with deep breathing, coughing,

swallowing, and changing position.

3. This type of pericarditis preceded by fever, malaise,

and flu like symptoms.

4. Chronic pericarditis produces minimal signs and

symptoms; this type of Pericarditis is typically
identified by routine chest film.
5. In constrictive pericarditis, fibrous scarring and
calcification cause obliteration of the pericardial
cavity as the layers adhere, encasing the heart in a
rigid way.

6. Pericardial effusion

7. Cardiac tamponade is cardiac compression that

results from an excessive accumulation of fluid or
blood in the pericardial space.

8. Rapid accumulation of fluid in the pericardial space

results in increased CVP, decreased cardiac output,
tachycardia, narrowed pulse pressure, and muffled
heart sounds.
 9. Symptoms of pericarditis worsen with
effusion and tamponade. A pericardial
friction rub is the hallmark sign of
Pericarditis, but disappears in pericardial
effusion.

10. An early sign of tamponade is ascites

without peripheral edema. Kussmaul’s sign
and neck vein distention also occur.
Overview of nursing interventions
1. Prepare the patient for echocardiography,
radiation-scanning procedures, or CT Scan to
identify the location and extent of inflammation
or effusion.

2. Obtain aspiration and laboratory analysis of the

pericardial fluid and extent the causative agent,
as ordered.

3. Administer the proper antibiotic, if warranted.

4. Administer anti-inflammatory medications to

reduce inflammation, as ordered.
5. Prepare the patient in severe cardiac
tamponade for pericardiocentesis to remove
fluid from the pericardial sac.
6. Monitor vital signs frequently.
7. Provide support and reassurance.
8. Provide patient teaching covering:
a. Disease process
b. Causative factors
c. Preventive measures
 INFECTIVE
ENDOCARDITIS
1. Infective endocarditis refers to
inflammation or infection of the
pericardium or the heart valves.
2. Classifications:
a. Acute infective endocarditis commonly
affects persons with normal hearts.
b. Subacute infective endocarditis mainly
affects persons with damaged hearts.
Etiology
1. Acute infective endocarditis is caused by
Staphylococcus aureus and B-hemolytic
Streptococcus. It affects via hematogenous
spread.

2. Subacute infective endocarditis is caused by

organisms normally present in the body (eg,
Streptococcus viridans, non hemolytic and
microaerophilic streptococci).
3. Other causative organisms include
Escherichia coli, Klebsiella, Proteus,
Pseudomonas, Salmonella, Candida, and
Histoplasma.

4. Predisposing conditions include congenital

heart disease, rheumatic heart disease,
mitral valve prolapse, and cardiac defects;
however, 50% to 60% of acute infective
endocarditis cases occur without previous
cardiac deformities.
 Pathophysiologic processes and
manifestations
Valve with damage (due to colonization)

Microbes that are in the blood adhere to the area

then proliferate.

Initial damage to the valves (also known as endothelium)

exposes the basement membrane
 Attracts platelets; causes clot formation

Sloughing of disease, with erosion of valve leaflets

or myocardial damage

Congestive heart failure

1. Irregular vegetation on the heart valves can
cause brain, kidney, spleen, or mesenteric
embolization.
2. Manifestation of acute infective endocarditis
may include:
a. Sudden fever
b. Septicemia
c. Valvular insufficiency
d. Heart failure
e. Stroke
3. Manifestations of subacute infective endocarditis
may include:
a. Chronic low-grade fever
b. Anemia
c. Weight loss
d. Splenomegaly
e. Heart murmur
4. Peripheral manifestations may include petechiae,
splinter hemorrhages, Roth’s spots, and Osler’s
nodes. Allergic vasculitis is thought to be
responsible for producing peripheral
manifestations.
5. Blood cultures are positive: leukocytosis and an
elevated sedimentation rate are usually present.
Overview of nursing interventions
1. Institute appropriate testing to identify the
pathogen, as ordered.

2. Minimize the organism’s effect on the heart by

using appropriate antibiotic therapy, as prescribed,
for 4 to 6 weeks.

3. Institute broad-spectrum antibiotic therapy, as

ordered, while awaiting bacteriologic confirmation
(eg, intravenous high-dose penicillin with
gentamycin, streptomycin, or vancomycin).
4. Provide supportive therapy to prevent and
manage heart failure.
5. Prepare the patient for valve replacement
surgery if medical intervention fails.
6. Prevent the disease by administering
antibiotics prophylactically before the patient
undergoes any procedure that may cause
bacteremia.
 MYOCARDITIS
►Focal
or diffuse inflammation of the
myocardium; may be viral (most
common) or bacterial (rare).
Etiology
1. Viral myocarditis may be caused by coxsackie
virus.

2. Bacterial myocarditis is associated with rheumatic

fever and the diphtheria toxin.

3. Other causes include hypersensitivity reactions,

autoimmune responses, chemical and physical
agents, and radiation therapy.
Pathophysiologic processes and
manifestations:
1. Myocarditis can be asymptomatic or can
produce symptoms of heart failure.
2. Manifestations of viral myocarditis may
include:
a. Tachycardia
b. Dyspnea
c. Low grade fever
d. Malaise
e. History of upper respiratory infection
3. In young adults, sudden death has
occurred; in adults, viral myocarditis is likely
to be benign and self-limiting.

4. Laboratory analysis reveals leukocytosis and

elevated ALT, AST and LDH.

5. Manifestation of right and left heart failure

can occur with advanced disease.
Overview of nursing interventions
1. Obtain viral antigen detection or serologic
testing, as ordered, to aid in diagnosis.
2. Prepare the patient for myocardial biopsy,
which may also aid diagnosis.
3. Administer appropriate antibiotics for
bacterial myocarditis, as ordered.
4. Institute measures to decrease cardiac
workload, such as bed rest.
5. For the patient with heart failure:
a. Administer digitalis, diuretics, and oxygen
therapy, as ordered.
b. Restrict sodium.
c. Encourage activities that improve oxygen supply
and decrease oxygen demand.
6. Administer antiarrthymics, with caution, for
dysrhythmias; administer anticoagulants for
thromboembolic events, as prescribed.
7. Use immunosuppressive therapy, as
prescribed, to resolve inflammation.