MYOCARDIAL INFARCTION (MI)

The formation of localized necrotic areas within the myocardium. MI

usually follows sudden coronary occlusion and the abrupt cessation of blood
and oxygen flow to the heart muscle. Myocardial Infarction is caused by an
in a coronary artery resulting in necrosis (death) to the tissues supplied by
the artery. The obstruction usually due to atherosclerotic plaque, a
thrombus or an embolism. The area most commonly affected is the left
ventricle.
ETIOLOGY
Coronary Atherosclerotic: Heart Disease, Coronary,
Thrombosis/Embolism, Decreased blood flow with shock and/or
Hemorrhage and Direct Trauma
PATHOPHYSIOLOGY

Coronary Atherosclerotic: Heart Disease

Coronary Thrombosis/Embolism
Decreased blood flow with shock and/or Hemorrhage
Direct Trauma

Myocardial Ischemia Decreased Myocardial Cellular Hypoxia

Oxygen Supply
Altered Cell
Decreased Cardiac Decreased Myocardial Membrane
Output Oxygen Supply Integrity

Stimulation of
Decreased Arterial Stimulation of
Sympathetic
Pressure Baroreceptors
Receptors

Increased Peripheral Increased

Vasoconstriction Afterload

Increased Myocardial Increased Decreased Decreased

Contractility Heart in Diastolic Tissue
Rate Filling Perfusion

Increased
Myocardial Oxygen
Demand
SIGNS AND SYMPTOMS
 Pain
– Crushing, severe, prolonged, unrelieved by rest or nitroglycerine; often radiating to
one or both arms, the neck and the back.
– Characterized by “Levine’s sign” (chest hand
clutching). This is the universal sign of distress in
angina pectoris or MI.
Pathophysiology basis: Cessation of blood supply to
myocardium due to thrombotic occlusion causes
accumulation of metabolites (e.g., lactic acid) within
ischemic part of myocardium. Lactic Acid irritates
nerves endings, resulting to pain.
 Anxiety and Apprehension
– Feeling of “doom”, restlessness.
Pathophysiology basis: Severe pain of a heart attack is terrifying; most clients are
aware of the significance of a heart attack; restlessness results from shock and pain.
 Shock
– This is manifested by systolic pressure below 80mmHg, gray, facial color, lethargy,
cold diaphoresis, peripheral cyanosis, tachycardia/bradycardia, weak pulse.
Pathophysiology basis: This may be due to severe pain, severe reduction in cardiac
output and inadequate tissue perfusion, thereby causing tissue hypoxia.
– Oliguria. Urine flow of less than 30ml/hour.
Pathophysiology basis: This indicates renal hypoxia due to inadequate tissue
perfusion.
 Fever
– Slight elevation of temperature occurs within 24 hours and extends 3 to 7 days
accompanied by leukocytosis and elevated ESR.
Pathophysiology basis: Fever and leukocytosis result from destruction of myocardial
tissue and ensuing inflammatory process.
– Indigestion. Gas pains around the heart. Nausea and vomiting.
Pathophysiology basis: Client may prefer to believe that pain is caused by “gas” or
“Indigestion” rather than by heart disease; nausea and vomiting may result from
severe pain or from vasovagal reflexes conducted from an area of damaged
myocardium to gastrointestinal tract.
 Acute Pulmonary Edema
 – Sense of suffocation, dyspnea, orthopnea, gurgling or bubbling respiration.
Pathophysiology basis: Left ventricle becomes severly weaknened in pumping action
owing to infarction; severe pulmonary congestion. ECG Changes
– MI causes elevation of ST segment, inversion of T wave and enlargement of Q wave.
Pathophysiology basis: Pathologic Q wave develop from the area of infarction;
elevated ST segment results from the area of injury; and inverted T wave originates
from the zone of ischemia. Elevation of ST segment heralds a pattern of injury and
usually occurs as an initial ECG change in acute MI.
 Elevated CK-MB, elevated LDH, elevated AST
Pathophysiology basis: These cardiac enzymes are produced in abnormally large
amounts because of cellular damage and death. CK-MB is the most cardiac-specific
enzyme. Elevated CK-MB in the presence of increased levels of LDH strongly support
presence of MI
 Elevated Troponin levels. These are the most definitive laboratory findings in MI.
DIAGNOSTIC TESTS AND RESULTS
il
NURSING DIAGNOSIS
 Risk for decreased cardiac tissue perfusion related to reduced coronary blood flow.
 Risk for ineffective peripheral tissue perfusion related to decreased cardiac output.
 Risk for Activity Intolerance related to decreased circulation to body tissues.
 Acute Pain related to decreased oxygenation of myocardial tissue.
 Decreased Cardiac Output related to damaged heart tissue.
 Deficient knowledge about post-MI self care.
 Anxiety related to cardiac event.
MANAGEMENT
A. NURSING MANAGEMENT
 Promote Oxygenation and Tissue Perfusion
- Instruct the patient to avoid overfatigue; stop activity immediately in the presence
of chest pain, dyspnea, lightheadedness or faintness.
- O2 therapy by cannula for the first 24 to 48 hours or longer if pain, hypotension,
dyspnea or dysrhythmias persist. Monitor VS changes, indicative of complications.
- Position client in semi fowler’s to allow greater diaphragm expansion, thereby
lung expansion and better carbon dioxide - oxygen exchange. Promoting
Adequate Cardiac Output
 - Monitor the following parameters: Dysrhythmias on ECG tracings, VS, Effects of
daily activities on cardiac status, rate and rhythm of pulse.
- Promote rest and minimize unnecessary disturbances.
 Promote Comfort
- Relieve pain. Administer morphine sulfate as ordered. This is to decrease
sympathetic stimulation, which increases myocardial oxygen demand. In addition,
this will prevent shock which may result from severe pain. Providing rest.
- The client is usually placed on bed rest with commole privileges for 24 to 48 hours
- Administer Diazepam (Valium) as ordered.
- Explain that the purpose of Coronary Care Unit is for continuous monitoring and
safety during the early recovery period.
- Provide psychosocial support to the client and his family. Calmness and
competency are extremely reassuring.
 Promote Activity
- Gradual increase in activity is encouraged. After the first 24 to 48 hours, the client
may be allowed to sit for increasing periods of time and begins ambulation on the
4th and 5th day.
- Monitor for signs of dysrhythmias, chest pain and changes in VS during activity.
 Promoting Nutrition and Elimination
- Provide small, frequent feedings
- Provide low-calorie, low-cholesterol, low-sodium diet
- Avoid stimulants
- Avoid taking very hot or very cold foods. Vasovagal stimulation may occur, this
may lead to bradycardia and cardiac arrest.
- Use of bedpan and straining at stool should be avoided. Valsava maneuver
causes changes in blood pressure and heart rate, which may trigger ischemia,
dysrhythmias, pulmonary embolism or cardiac arrest.
- Use bedside commode
- Administer stool softener as ordered (e.g. odium docussate (Colace)
 Promoting Relief of Anxiety and Feeling of Well-Being
- Provide an opportunity for the client and family to explore their concerns and to
identify alternative methods of coping as necessary.
 Facilitating Learning
- Teaching is started once the client is free of pain and excessive anxiety.
- Promote a positive attitude and active participation of the client and the family
B. DIET MODIFICATION
o A liquid diet is progressed to a regular low cholesterol, low salt diet is prescribed.
o The client may tolerate small frequent feedings better than three large meals.
o Caffeine and extreme hot and cold foods are avoided.
C. DRUG THERAPY
o ANALGESICS
- For relief of pain (priority)
- Morphine Sulfate, Lidocaine or Nitroglycerine are administered intravenously.
Drug of Choice is Morphine.
o THROMBOLYTIC THERAPY
- To disintegrate blood clot by activating the fibrinolytic processes.
- Streptokinase, Urokinase and tissue plasminogen activator (TPA) are currently
used.
- Administration of thrombolytics is the most crucial between 3 to 6 hours after
the initial infarction has occurred.
- Detect for occult, bleeding during and after thrombolytic therapy.
- Assess neurologic status changes which may indicate GI bleeding or Cardiac
Tamponade.
- The effectiveness of the medication is evidenced by absence of chest paint.
Absence of blood clots improves blood flow and oxygen supply to the
myocardium.
o ANTI-COAGULANTS AND ANTI-PLATELET MEDICATIONS
- Administered after thrombolytic therapy to maintain arterial patency.
o OTHER MEDICATIONS: BETA-ADRENERGIC BLOCKING AGENTS, DIAZEPAM
(VALIUM)
D. SURGICAL MANAGEMENT
Primary treatment may be PTCA instead of thrombolytic therapy. Along with
balloon compression, astent(s) may be insterted. Clients with muktiple vessels occluded,
or for whom thrombolytic therapy and PTCA have not been effective, may have the CABG
procedure performed.
CONGESTIVE HEART FAILURE
It is often the final stage of
many other heart conditions. It is a
state of circulatory congestion
produced by myocardial dysfunction.
MI compromises myocardial function
by reducing contractility and producing
abnormal wall motion. The ability of the
ventricle to empty lessens, the stroke
volume falls, residual volume increases.
Heart failure is the inability of the heart
to pump the amount of oxygenated
blood necessary to effect venous
return and to meet the metabolic
requirements of the body.

ETIOLOGY
 Direct damage to the heart, e.g. mitral myocarditis, ventricular aneurysm.
 Ventricular Overload
 Increased preload, e.g. mitral or aortic regurgitation, atrial or ventricular septal
defects, or rapid infusion of large volumes of IV Fluids.
 Increased afterload, e.g. aortic or pulmonary valve stenosis, systemic hypotension,
pulmonary hypertension.
 Constriction of the ventricles, e.g. Cardiac Tamponade, Pericarditis, Restrictive
Cardiomyopathies.

CLASSIFICATION OF HEART FAILURE

1. Backward Heart Failure – results from damming up of the blood in the vessels proximal
to the heart.
2. Forward Heart Failure – results from inability of the heart to maintain cardiac output.
 PATHOPHYSIOLOGY (LEFT – SIDED CONGESTIVE HEART FAILURE)

Causes:
MI
Hypertension
Arterial Stenosis/Insufficiency
Mitral Stenosis/Insufficiency

Reduced Myocardial Contractility

Increased Cardiac Workload
Decreased Diastolic Filling
Obstruction of Left Atrial Emptying

Increase in Left Atrial Pressure

Left – sided CHF

Blood Dams Back Into Decrease in Stroke Volume

The Pulmonary
Capillary Bed
Tissue Perfusion

Pressure of Blood Into the

Pulmonary Capillary Bed
Increases
Increased Cellular Hypoxia Decreased Blood Flow into the Kidneys
Fluid shifts into the
intraalveolar and
interalveolar spaces RAAS Stimulation

Pulmonary edema Vasoconstriction and Reabsorption of Na

and water

Signs and Symptoms: Increased in ECF volume

Dyspnea, Paroxysmal Nocturnal Dyspnea,
Orthopnea, Rales/Crackles ,Blood tinged frothy
sputum, Wheezing (cardiac asthma), Dizziness, Increased Total Blood Volume
Syncope, Fatigue, Weakness, Anorexia, Increased Systemic BP
Hypokalemia, Increased level of aldosterone,
Clubbing of fingers, Polycythemia, S3, S4 heart
sounds; Pulsus Alterans and Elevated PAP, PCWP,
LVEDP.
PATHOPHYSIOLOGY (RIGHT – SIDED CONGESTIVE HEART FAILURE)

Causes:
LSCHF
Pulmonary Embolism
Right Ventricular Infarction
Congenital Septal Defects

Reduced Myocardial Contractility

Increased Cardiac Workload
Decreased Diastolic Filling
Obstruction of Right Atrial Emptying

Increased Right Atrial Pressure

Right – Sided CHF

Pressure of Blood into the

pulmonary capillary bed
increases

Increased pressure in the

venous circuit (venous backup)

Signs and Symptoms:

Neck Vein Engorgement (Jugular Vein
Distention), Hepatomegaly, Portal Hypotension which
leads to Cardiac Cirrhosis, Ascites, Peripheral Edema
(Pitting/Dependent), Splenomegaly, Jaundice,
Hemolytic Anemia, Internal hemorrhoids, Leg
varicosities, Weight gain, S3 S4 heart sounds,
Elevated CVP Reading
SIGNS AND SYMPTOMS
 Congested Lungs
- Fluid backup in the lungs can cause shortness of breath with exercise or difficulty
breathing at rest or when lying flat in bed. Lung congestion can also cause a dry, hacking
cough or wheezing.
 Fluid and Water Retention
- Less blood to your kidneys causes fluid and water retention, resulting in swollen
ankles, legs, abdomen (called edema) and weight gain. Symptoms may cause an
increased need to urinate during the night. Bloating in your stomach may cause a loss of
appetite or nausea.
 Dizziness, Fatigue, and Weakness
- Less blood to your major organs and muscles makes you feel tired and weak.
Less blood to the brain can cause dizziness or confusion.
 Rapid or Irregular Heartbeats
- The heart beats faster to pump enough blood to the body. This can cause a rapid
or irregular heart beat.
DIAGNOSTIC TESTS AND RESULTS
ii
NURSING DIAGNOSIS
 Decreased Cardiac Output related to mechanical failure of heart muscle.
 Impaired Gas Exchange related to decreased cardiac output and pulmonary edema.
 Excess Fluid Volume related to decreased cardiac output and decreased renal output.
 Risk Activity Intolerance related to edema, dyspnea and fatigue.
 Anxiety related to change in health status, lifestyle, changes, or fear of death.
 Deficient Knowledge related to disease process, medications, diet and plan for recovery.
MANAGEMENT
A. NURSING MANAGEMENT
 Providing Oxygenation
- Administer oxygen therapy per nasal cannula at 2 to 6L/min as ordered.
- Evaluate arterial blood gas analysis results.
- Maintain high or semi-fowler’s position to maximize oxygenation by promoting
greater lung expansion.
 Promoting rest and activity
- Bed rest or limited activity may be necessary during the acute phase
 - Provide an overbed table close to the patients to allow resting the head and
arms.
- The arms may be supported on pillows to reduce the pull on the shoulder
muscles when in high fowler’s position, which is most comfortable for the
patient.
- Administer Diazepam (Valium) 2 to 10mg 3 to 4 times a day as ordered to
allay apprehension.
- Gradual ambulation is encouraged to prevent risk of venous thrombosis and
embolism due to prolonged immobility.
- Activities should progress through dangling, sitting up in a chair and then
walking in increased distances under close suspension.
- Assess for signs of activity intolerance such as dyspnea, fatigue and
increased pulse rate that do not stabilize readily.
 Decreasing anxiety
- Identifying feelings and concerns related to these feelings
- Identify strengths that can be used for coping
- Learn what can be done to decrease anxiety
 Facilitating Fluid Balance
- Control of sodium intake
- Administer diuretics and digitalis as prescribed
- Monitor I/O, weight and VS
 Providing skin care
- Edematous skin is poorly nourished and susceptible to pressure sores.
- Change position at frequent intervals
- Assess the sacral area regularly
- Use protective devices to prevent pressure sores.
 Promoting nutrition
- Provide bland, low calorie, low residue, with vitamin supplement during the acute
phase.
- Frequent small feedings minimize exertion and reduce gastrointestinal blood
requirements.
- There may be no need to severely restrict sodium intake of the client who receives
diuretic. However, “no added salt” diet is prescribed. Salty foods must be omitted.
 Promoting elimination
 - Advise client to avoid straining at defecation which involves Valsalva’s
maneuver. Valsalva’s maneuver increases cardiac workload.
- Encourage use of bedside commole.
 Facilitating learning
- Teach the client and his family about the disorder and self-care
o Monitor sign and symptoms of recurring CHF (e.g. weight gain, loss of
appetite, dyspnea, orthopnea, edema of the legs, persistent cough,
Report these to the physician.
o Avoid fatigue, balance rest with activity.
o Observe prescribed sodium restrictions.
o Eat small, frequent meals rather than 3 large meals a day.
o Take prescribed medications at regular basis (e.g. digitalis, diuretics,
vasodilators)
o Observe regular follow up care as directed.
 If acute pulmonary edema occurs in the client with CHF, the following are the
appropriate collaborative management:
 Place in high fowler’s position, with legs slightly lowered to facilitate breathing
and reduce preload.
 Morphine Sulfate 10 to 15 mg/IV as ordered. To primarily reduce preload and
afterload and to allay anxiety.
 Oxygen Therapy at 40% to 70 % by nasal cannula or face mask.
 Aminophylline/IV as ordered. To relieve bronchospasm, increase urinary
output and increase cardiac output.
 Rapid digitalization
 Diuretic therapy
 Vasodilators
 Dopamine or dobutamine
 Monitor serum potassium. Diuresis may result to hypokalemia.
B. DIET MODIFICATION
o A daily weight and strict intake and output are necessary to assess fluid
retention.
o Sometimes fluid intake is limited. Eat small, frequent meals rather than 3 large
meals a day.
o Provide bland, low calorie, low residue, with vitamin supplement during the acute
phase.
 o Frequent small feedings minimize exertion and reduce gastrointestinal blood
requirements.
o There may be no need to severely restrict sodium intake of the client who receives
diuretic. However, “no added salt” diet is prescribed. Salty foods must be omitted.
C. DRUG THERAPY
o DIGITALIS THERAPY
- It the major therapy of CHF. It has positive inotropic effect (strengthens force of
cardiac contractility), negative chronotropic effect (decreases conduction of the
heart cells)
- Assess heart rate before administration of digitalis. If the heart rate is 60 bpm
and below or 120 bpm and above, withhold the drug. Bradycardia or rebound
tachycardia may occur.
- Monitor serum potassium level. Hypokalemia enhances digitalis toxicity because
it potentiates the effect of the drug. Commonly used digitalis (cardiac glycosides)
 Lanoxin (Digoxin)
 Crystodigin (Digitoxin)
 Lanatoside C (Cedilanid C)
 Destanoside (Cedilanid D)
- Evaluate effectiveness of digitalis. There should be increased cardiac output,
increased urine output, stronger pulse, lowering BP, absence of ales and
crackles.
- Assess for the signs and symptoms of digitalis toxicity:
 Bradycardia
 GI Manifestations (Anorexia, Nausea and Vomiting, Diarrhea)
 Dsyrhythmias (most dangerous)
 Altered visual perceptions (yellow or green vision; blurred vision; halos or
rainbows around lights among elderly)
 In males: Antiadrogenic effects (Gynecomastia, Decreased libido and
Impotence)
o DIURETIC THERAPY
- Purpose is the decrease cardiac workload by reducing circulating volume and
thereby reducing reload,
- Assess for signs and symptoms for hypokalemia when administering Thiazides
and loop diuretics.
- Give potassium supplement and potassium-rich foods.
 - Diuretics are best administered early morning and/or early afternoon to prevent
sleep pattern disturbance related to nocturia.\
- If Thiazides are ineffective, an oral aldosterone antagonist (potassium-sparing
diuretic) may be given with Thiazide.
- The diuretics used in the treatment of CHF are as follows:
 Thiazides (potassium-wasting): Chlorothiazide (Diruril),
Hydrochlorothiazide (Esidrix, Hydrodiuril)
 Loop Diuretics (potassium-wasting): Furosemide (Lasix), Bumetamide
(Bumex)
 Potassium-sparing: Spironolactone (Aldactone), Triamterene (Dyrenium)
o VASODILATORS
- To decrease afterload by decreasing resistance to ventricular emptying.
- The most commonly used drugs are as follows: Nitroglycerine (Nipride),
Hydralazine (Apresoline), Nifedipine (a calcium-channel blocker with vasodilator
effect), Captopril (Capoten) – also has a vasodilator effect.
o OTHER DRUGS
- Sympathomimetics (Dopamine and Dobutamine)
D. SURGICAL MANAGEMENT
Cardiac transplantation is the definitive surgical treatment for patients with severe
left ventricular dysfunction and congestive heart failure. Unfortunately, however, the
supply of donor hearts remains severely limited, so transplantation is an option for only a
minority of these patients. Even after being approved for a heart transplant, patients often
have a long wait until a suitable donor heart can be found. This waiting period entails a
significant mortality rate. Because the supply of donor hearts is not expected to increase,
surgeons have introduced several alternatives to heart transplantation, including partial
left ventriculectomy, mitral valve repair, myocardial revascularization, and endoventricular
circular patch plasty. For maximal benefit, surgeons must refine the selection criteria for
determining which patients are the best candidates for each of these procedures.
PULMONARY EDEMA