Presented BY:

Afshan AliBEMS 4th Professional

Poonch University AJ&K

MYOCARDIAL

INFARCTION

Myocardial Infarction

• Myocardial infarction or “heart attack” is an

irreversible injury to and eventual death of

myocardial tissue that results from ischemia

and hypoxia.

• Myocardial infarction is the leading killer of

both men and women in the United States.

• Critical myocardial ischemia can occur as a result of increased myocardial metabolic demand, decreased delivery of oxygen and nutrients to the myocardium via the coronary circulation, or both. An interruption in the supply of myocardial oxygen and nutrients occurs when a thrombus is superimposed on an ulcerated or unstable atherosclerotic plaque and results in coronary occlusion.

•  A high-grade (>75%) fixed coronary artery stenosis caused by atherosclerosis or a dynamic stenosis associated with coronary vasospasm can also limit the supply of oxygen and nutrients and precipitate an MI.

• Conditions associated with increased myocardial metabolic demand include extremes of physical exertion, severe hypertension (including forms of hypertrophic obstructive cardiomyopathy), and severe aortic valve stenosis.

• Other cardiac valvular pathologies and low cardiac output states associated with a decreased mean aortic pressure, which is the prime component of coronary perfusion pressure, can also precipitate MI.

Causes

• Most frequent cause is rupture of an atherosclerotic lesion within coronary wall with subsequent spasm and thrombus formation

• Coronary artery vasospasm• Ventricular hypertrophy• Hypoxia• Coronary artery emboli

Causes

• Cocaine• Arteries• Coronary anomalies• Aortic dissection• Pediatrics Kawasaki disease, Takayasu

arteritis• Increased afterload which increases

myocardial demand

Risk factors for atherosclerosis

• Age• Male gender• Smoking• Hypercholesterolemia and triglyceridemia• Diabetes Mellitus• Poorly controlled hypertension• Type A personality

Risk factors for atherosclerosis

• Family History• Sedentary lifestyle

Mechanisms of Myocardial damage

The severity of an MI is dependent of three factors

• The level of the occlusion in the coronary• The length of time of the occlusion• The presence or absence of collateral

circulation

• The death of myocardial cells first occurs in the area of myocardium most distal to the arterial blood supply: the endocardium.

• As the duration of the occlusion increases, the area of myocardial cell death enlarges, extending from the endocardium to the myocardium and ultimately to the epicardium.

• The area of myocardial cell death then spreads laterally to areas of watershed or collateral perfusion. Generally, after a 6- to 8-hour period of coronary occlusion, most of the distal myocardium has died. The extent of myocardial cell death defines the magnitude of the MI. If blood flow can be restored to at-risk myocardium, more heart muscle can be saved from irreversible damage or death

Coronary blood flow and myocardial infarction

The location of a myocardial infarction will be largely

determined by which coronary blood vessel is occluded.

The two main coronary arteries supplying the myocardium

are:

a) the left coronary artery (which subdivides into the left

anterior descending and circumflex branches) and

b) the right coronary artery

Myocardial Infarction

The two main coronary arteries supplying the myocardium are:1. the left coronary artery (which subdivides into the left anterior descending

and circumflex branches) and2. the right coronary artery

Coronary Arteries for the heart

• The left anterior descending artery supplies blood to the

bulk of the anterior left ventricular wall, while the left

circumflex artery provides blood to the left atrium and the

posterior and lateral walls of the left ventricle.

• The right coronary artery provides blood mainly to the right

atria and right ventricles.

• Nearly 50% of all myocardial infarctions involve the left

anterior descending artery that supplies blood to the

main pumping mass of the left ventricle.

• The next most common site for myocardial infarction is

the right coronary artery, followed by the left

circumflex.

Myocardial Infarction

A myocardial infarction may be:

a) transmural, meaning it involves the full thickness of the

ventricular wall, or

b) subendocardial, in which the inner one third to one half of

the ventricular wall is involved.

Transmural infarcts tend to have a greater effect on cardiac

function and pumping ability since a greater mass of

ventricular muscle is involved.

Myocardial Infarction Morphology

Signs and symptoms• Acute MI can have unique

manifestations in individual patients. The degree of symptoms ranges from none at all to sudden cardiac death. An asymptomatic MI is not necessarily less severe than a symptomatic event, but patients who experience asymptomatic MIs are more likely to be diabetic. Despite the diversity of manifesting symptoms of MI, there are some characteristic symptoms.

Signs and symptoms Contd.

• Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax

• Radiation of chest pain into the jaw or teeth, shoulder, arm, and/or back

• Associated dyspnea or shortness of breath• Associated epigastric discomfort with or without

nausea and vomiting• Associated diaphoresis or sweating• Syncope or near syncope without other cause• Impairment of cognitive function without other cause

Signs and symptoms Contd.

• An MI can occur at any time of the day, but most appear to be clustered around the early hours of the morning or are associated with demanding physical activity, or both. Approximately 50% of patients have some warning symptoms (angina pectoris or an anginal equivalent) before the infarct.

Investigation / Cardiac Biomarkers

• Cardiac biomarkers are protein molecules released into the blood stream from damaged heart muscle

• Since ECG can be inconclusive , biomarkers are frequently used to evaluate for myocardial injury

• These biomarkers have a characteristic rise and fall pattern

Troponin T and I

• These isoforms are very specific for cardiac injury

• Preferred markers for detecting myocardial cell injury

• Rise 2-6 hours after injury

Peak in 12-16 hours

Stay elevated for 5-14 days

Creatinine Kinase ( CK-MB)

• Creatinine Kinase is found in heart muscle (MB), skeletal muscle (MM), and brain (BB)

• Increased in over 90% of myocardial infraction

• However, it can be increased in muscle trauma, physical exertion, post-op, convulsions, and other conditions

Creatine Kinase (MB)

• Time sequence after myocardial infarction

Begins to rise 4-6 hours

Peaks 24 hours

returns to normal in 2 days• MB2 released from heart muscle and

converted to MB1.• A level of MB2 > or = 1 and a ratio of

MB2/MB1 > 1.5 indicates myocardial injury

Myoglobin

• Damage to skeletal or cardiac muscle release myoglobin into circulation

• Time sequence after infarction

Rises fast 2hours

Peaks at 6-8 hours

Returns to normal in 20-36 hours• Have false positives with skeletal muscle

injury and renal failure

Renal Failure and Renal Transplantation

• Diagnostic accuracy of serum markers of cardiac injury are altered in patients with renal failure

• Cardiac troponins decreased diagnostic sensitivity and specificity in patients receiving renal replacement therapy

• Current data show levels of troponin I are unaltered while levels of troponin T may be elevated

CBC

• CBC is indicated if anemia is suspected as precipitant

• Leukocytosis may be observed within several hours after myocardial injury and returns returns to levels within the reference range within one week

Chemistry Profile

• Potassium and magnesium levels should be monitored and corrected

• Creatinine levels must be considered before using contrast dye for coronary angiography and percutanous revascularization

C-reactive Protein (CRP)

• C- reactive protein is a marker of acute inflammation

• Patients without evidence of myocardial necrosis but with elevated CRP are at increased risk of an event

Chest X-Ray

• Chest radiography may provide clues to an alternative diagnosis ( aortic dissection or pneumothorax)

• Chest radiography also reveals complications of myocardial infarction such as heart failure

Echocardiography

• Use 2-dimentional and M mode echocardiography when evaluating overall ventricular function and wall motion abnormalities

• Echocardiography can also identify complications of MI ( eg. Valvular or pericardial effusion, VSD)

Electrocardiogram

• A normal ECG does not exclude ACS• High probability include ST segment

elevation in two contiguous leads or presence of q waves

• Intermediate probability ST depression• T wave inversions are less specific

As a result of the hypotension and hemodynamic changes that accompany

a myocardial infarction, the cardiovascular system initiates a number of

reflex compensatory mechanisms designed to maintain cardiac

output and adequate tissue perfusion:

1.Catecholamine release : Increases heart rate, force of contraction and

peripheral resistance.

2. Sodium and water retention.

3. Activation of renin–angiotensin system leading to peripheral

vasoconstriction.

4. Ventricular hypertrophy.

Unfortunately, these compensatory changes may increase oxygen demand

and workload on the infarcted heart and worsen overall cardiac function.

Myocardial InfarctionCompensatory mechanisms of myocardial infarction

Depending on the extent of the area involved in a myocardial infarction, a

number of complications might arise, including:

1. Rupture of weakened myocardial wall. Bleeding into pericardium may

cause cardiac tamponade and further impair cardiac pumping function.

This is most likely to occur with a transmural infarction. Rupture of the

septum between the ventricles might also occur if the septal wall is

involved in the infarction.

2. Formation of a thromboembolism from pooling of blood in the

ventricles.

3. Pericarditis : Inflammation due to pericardial friction rub. Often occurs 1

to 2 days after the infarction.

4. Arrhythmia : Common as a result of hypoxia, acidosis and altered

electrical conduction through damaged and necrotic areas of the

myocardium. May be life-threatening and lead to fibrillation.

Myocardial InfarctionComplications of myocardial infarction

5. Reduced cardiac function : Typically presents with reduced

myocardial contractility, reduced wall compliance, decreased stroke

volume and increased left ventricular end diastolic volume.

6. Congestive heart failure may result if a large enough area of the

myocardium has been damaged such that the heart no longer

pumps effectively.

7. Cardiogenic shock : Marked hypotension that can result from

extensive damage to the left ventricle. The resulting hypotension will

trigger cardiovascular compensatory mechanisms that will further tax

the damaged myocardium and exacerbate impaired function.

Cardiogenic shock is associated with a mortality rate of 80% or

greater.

Myocardial InfarctionComplications of myocardial infarction

A main goal of intervention for myocardial infarction is to limit the

size of the infarcted area and thus preserve cardiac function.

Early recognition and intervention in a myocardial infarction have

been shown to significantly improve the outcome and reduce

mortality in patients.

If employed in the early stages of myocardial infarction, antiplatelet-

aggregating drugs such as aspirin and clot-dissolving agents such

as streptokinase and tissue plasminogen activator may be very

effective at improving myocardial blood flow and limiting damage to

the heart muscle.

Myocardial InfarctionRationale for

therapy

Other drugs such as vasodilators, β -adrenergic blockers and ACE

inhibitors can also improve blood flow and reduce workload on the

injured myocardium and thus reduce the extent of myocardial

damage.

The development of potentially life-threatening arrhythmias is also

common during myocardial infarction as a consequence of hypoxia,

acidosis and enhanced autonomic activity and must be treated with

appropriate antiarrhythmic drugs.

Supportive therapies such as oxygen, sedatives and analgesics are

also utilized.

Myocardial InfarctionRationale for

therapy

1. Oxygen : Used to maintain blood oxygenation as well as tissue and

cardiac O2 levels.

2. Aspirin : If administered when myocardial infarction is detected, the

antiplatelet properties of aspirin may reduce the overall size of the

infarction.

3. Thrombolytic therapy :If employed in the first 1 to 4 hours following the

onset of a myocardial infarction, these drugs may dissolve clots in

coronary blood vessels and re-establish blood flow.

4. Vasodilator drugs : Intravenous nitroglycerin can increase blood flow to

the myocardium and reduce myocardial work.

Treatment for myocardial infarction

Myocardial Infarction

5.β -Blockers : Blunt the effect of catecholamine release on the

myocardium, reduce heart rate and myocardial work.

6. Pain management : Sublingual nitroglycerin, morphine if necessary

7. Antiarrhythmic drugs : To treat and prevent a number of potentially

life-threatening arrhythmias that might arise following a myocardial

infarction.

8. ACE inhibitors : the negative effects of vasoconstriction and salt and

water retention on the myocardium.

Treatment for myocardial infarction

Myocardial Infarction

a. Streptokinase : Derived from β -hemolytic streptococcus bacteria;

involved in the activation of plasmin

b. Anistreplase (APSAC) : Complex of human lys-plasminogen and

streptokinase; Administered as a prodrug

c. Alteplase (TPA): Recombinant tissue plasminogen activator

d. Urokinase : Endogenous human enzyme that converts

plasminogen to active plasmin

e. Routes of administration : Intravenous. for all of the above

f. Major unwanted effects : Internal bleeding, gastrointestinal

bleeding, stroke, allergic reactions

Myocardial InfarctionThrombolytic Agents Used Clinically

a. Sublingual nitroglycerin : Potent vasodilator of coronary

arteries, also dilates

b. peripheral arteries and veins to reduce preload and

afterload on the heart

c. Morphine sulfate : Powerful opioid analgesic that also

provides a degree of

d. sedation and vasodilatation; although the opioid

analgesics have little effect on

e. the myocardium, they are powerful respiratory

depressants

Myocardial InfarctionPain Management in Myocardial Infarction

• Inhibits the cyclo-oxygenase pathway for the synthesis of

prostaglandins, prostacyclins and thromboxanes.

• Inhibits aggregation of platelets and is effective in

reducing myocardial infarction, stroke and mortality in

high-risk patients.

Myocardial InfarctionAspirin

Key terms

• Cardiac tamponade : Excessive pressure that develops from the accumulation of fluid in the pericardium.

• Pericarditis : Inflammation of the pericardium.

• Stroke volume : Volume of blood ejected from each ventricle per beat.

• End-diastolic volume : Volume of blood remaining in the ventricle at the end of systole (contraction).

Myocardial Infarction