ACUTE MYOCARDIAL INFARCTION

CAROLINE POBLETE- GREGORIO,RN,MSN

ACUTE MYOCARDIAL INFARCTION

Also

known as heart attack, coronary occlusion Life threatening condition characterized by the formation of localized necrotic areas within the myocardium Usually follows sudden occlusion of a Coronary Artery and the abrupt cessation of blood and oxygen flow to the heart muscle( myocardium)

Etiology/Risk Factors: 1.Atherosclerosis- vessel lumen slowly occludes and is often blocked by a thrombus - Blood flow ceases abruptly- myocardial tissue supplied by that artery dies 2. Coronary spasm and hemorrhage into a plaque

PATHOPHYSIOLOGY

MI- end point of CAD Prolonged unrelieved ischemia causes irreversible damage to the myocardium Cardiac cells can withstand ischemia for 20 minutes before cellular death occurs Myocardium metabolically active- signs of ischemia can be seen within 8 to 10 seconds of decreased blood flow

Not sustained by blood and O2

Converts into Aneorobic metabolism

Creates less ATP( Adenosine triphostate) and more Lactic acid Acidosis- makes myocardium more vulnerable to the effects of lysosomal enzyme within the cells leads to conduction system disorder

Dysrrythmia develop

reduced contractility
decreased ability to pump blood

myocardial cell necrosis

intracellular enzyme in the bloodstream

Most common site: Anterior wall of the left ventricle near the apex left anterior descending artery)

Posterior wall of the left ventricle near the base Inferior surface of the heart (right coronary artery)

OTHER MI LOCATIONS
First, take a look again at this picture of the heart. Lateral portion of the heart(circumflex artery)

Anterior portion of the heart(left anterior descending artery)

Inferior portion of the heart(right coronary artery)

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CLINICAL MANIFESTATIONS:
Chest pains (cardinal symptom)- major clinical manifestation, similar to angina pectoris but more severe and unrelieved by REST and NTG May radiate to the neck, jaw, shoulder, back or left arm, present near the epigastrium, simulating indigestion 2. Hypotension 3. Gray facial color 4. Cold diaphoresis 5. Weak pulse 6. Peripheral cyanosis
1.

7. tachy/ bradycardia 8. Lethargy 9. anxiety- great fear of death, apprehension 10. N/V 11. dyspnea, orthopnea 12. Palpitations LABORATORY FINDINGS: 1. ECG- ELECTROCARDIOGRAM > Visual representation of the activity of the heart from various angles of the skin surface

Useful in evaluation of conditions that interfere with normal functions Shows the area where there is myocardial damage

ST ELEVATION (INJURY)
One way to diagnose an acute MI is to look for elevation of the ST segment. R

P waves represents atrial muscle depolarization( CONTRACTION) 2.5 mm high or less Impulse generated from the SA node

Q wave- first negative deflection after the P wave Normally less than 0.03 second in duration

R wave- first positive deflection after P wave S wave- first negative deflection after the R wave

T wave- represents ventricular muscle repolarization( RELAXATION) Return to resting state It follows the QRS complex ST segment represents early ventricular repolarization Analyzed for ISCHEMIA Completion of ventricular contraction

PR interval- measured from P wave to the beginning of the Q or R waves represents the time required for ATRIAL DEPOLARIZATION and the delay of the impulse in the AV node before ventricular depolarization normally ranges from 0.12 to 0.20 sec in duration time it takes for impulse to spread from atria to ventricle delay impulses at the AV node and Bundle of His to promote ventricular filling. QRS Complex- represents VENTRICULAR DEPOLARIZATION

0.04 TO 0.10 second in duration

U wave- follow the T wave > Thought to represent repolarization of the Purkinjie fibers Seen in patient with hypokalemia QT interval- represents the total time for ventricular depolarization and repolarization

Abnormal Findings: MYOCARDIAL ISCHEMIA- causes the T wave to be larger and inverted because of altered repolarization( relaxation) Ischemic region remains DEPOLARIZED Causes ST segment changes- injured cells depolarize normally but repolarize more rapidly than do normal cells- ST elevation MI > Q wave or non Q wave infarction- abnormal q waves develop within 1 to 3 days

Because of both the absence of depolarization current from necrotic tissue and opposing currents from other parts of the heart ST segment- represents completion of ventricular contraction and early repolarization

DIAGNOSING A MI
To diagnose a myocardial infarction you need to go beyond looking at a rhythm strip and obtain a 12-Lead ECG.

12-Lead ECG

Rhythm Strip
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ST ELEVATION (CONT)
Elevation of the ST segment (greater than 1 small box) in 2 leads is consistent with a myocardial infarction.

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ANTERIOR VIEW OF THE HEART

The anterior portion of the heart is best viewed using leads V1- V4.
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INTERPRETATION
Yes, this person is having an acute anterior wall myocardial infarction.

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2. Laboratory findings: a. SERUM CREATININE KINASE(CK MB) Myocardial isoenzyme, found in cardiac muscle CK-MM( skeletal muscle, CK-BB( brain) Increased 3 to 6 hours after the onset of chest pains, reach peak in 12 to 18 hours(24 hours) and returns to normal in 2 to 4 days b. MYOGLOBIN- heme protein helps transportO2 found in cardiac muscle Increase within 1 to 3 hours Peaks in 12 hours( 6 to 8 hours)

>Returns to normal in 20 36 hours >have false positives with skeletal muscle injury and renal failure c. LACTATE DEHYDROGENASE(LDH0 Is increased Sub unit is plentiful in heart muscle and is released into the serum when myocardial damage occurs Elevates 14 to 24 hours after onset of myocardial damage Peaks in 48 to 72 hours

Return to normal over next 7 to 14 days

d. SERUM AST( aspartate aminotransferase)- SGOT( serum glutamic oxalo acetic transaminase)increased Peak in 12 to 18 hours Return to normal 3 to 4 days

e. WBC- increased of 10,000 to 20,000 mm3appears on second day and disappears in 1 week

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 Troponin assays are not only more sensitive but are also more specific than CK-MB assays. Expression of CK-MB is not unique to the heart. CK-MB is found in skeletal muscle and the gastrointestinal tract as well as in the uterus of pregnant women.

COMPLICATIONS: > Possibility of death from complications always accompanies an acute MI 1. DYSRYTHMIAS- major cause of death after an MI, 40 t0 50% of deaths Notify the physician if more than 6 PVCs Premature ventricular contractions (PVCs) are premature heartbeats originating from the ventricles of the heart. Premature ventricular contractions are premature because they occur before the regular heartbeat.

> the ventricle electrically discharges (and contracts) prematurely before the normal electrical discharges arrive from the SA node. > premature discharges are due to electrical "irritability" of the heart muscle of the ventricles and can be caused by heart attacks, electrolyte imbalances, lack of oxygen, or medications. >Immediately after a premature ventricular contraction, the electrical system of the heart resets. >This resetting causes a brief pause in heartbeat, and some patients report feeling the heart briefly stopping after a premature ventricular contraction.

Report to the physician if the client is symptomatichypotension, chest pains Management: A. Ventricular tachycardia- Lidocaine, Procainamide or cardioversion Electrical impulses cause muscle, including heart muscle, to contract. During a normal heart rhythm, each impulse moves in a standardized and orderly manner over nerves from the atria to the ventricles, with each impulse resulting in one heart beat

Under normal conditions, the electrical impulses are generated from an area of specialized nerve cells called the sinus node, located in the right atrium (the upper right chamber of the heart) After leaving the sinus node, the impulse travels through and activates both atria. The impulse then travels through specialized heart fibers that transmit the impulse rapidly to various parts of the right and left ventricles; this causes the heart to contract. Each individual muscle cell of the ventricles is activated. If this pattern of conduction and activation is altered in any way, an abnormal heart rhythm (arrhythmia) may occur.

CARDIOVERSION Cardioversion involves the delivery of a high-energy shock to the heart muscle. This high-energy impulse activates all of the cardiac muscle and conduction tissue simultaneously Reentrant circuits are interrupted, breaking the repeating cycle and stopping the arrhythmia. reentrant circuit is broken and the arrhythmia stops, the sinus node begins to fire again and a normal heart rhythm is restored

electrical "shock" is delivered to the heart to restore its rhythm to a normal pattern. The electrical energy can be delivered externally, with electrodes placed on the chest or directly to the heart using paddles on the heart during an open chest surgery 2. Cardiac monitoring 3. O2 therapy B. CARDIOGENIC SHOCK- accounts for only 9% of deaths of MI but 80% of clients who develop shock die from it

Causes: decreased myocardial contraction, diminished CO, undetected dysrhythmias or sepsis Clinical manifestations: Decreased systolic BP, diaphoresis, rapid pulse, restlessness, cold clammy skin, gray skin color Prevention: relief of pain, sufficient IVF- prevent circulating collapse, identify dysrhythmia Management: 1. Vasopressors- + inotropic agents- increase cardiac contractility and cardiac output, improve tissue perfusion

Prescribe to raise BP by increasing peripheral resistance Ex. Norepinephrine, dopamine, dobutamine, metaraminal( aramine)

C. HEART FAILURE AND PULMONARY EDEMA Secondary decreased myocardial contraction Will disable 20% of clients, responsible for 1/3 of deaths after MI Clinical Manifestations: dyspnea, orthopnea, weight gain, edema, enlarged tender liver, distended neck veins and crackles

1.
2. 3.

NI Decreased sodium diet Fluid restrictions Digitalis therapy as ordered

D. PULMONARY EMBOLISM- develops secondary to phlebitis of the leg or pelvic veins or from atrial fibrillation Occurs in 10% to 20% of patients NI: > Anticoagulant therapy

>ROM during bed rest Elastic stockings E. RECURRENT MYOCARDIAL INFARCTION Within 6 years after initial MI 23% - men, 31%- women Causes: overexertion, embolization or further thrombotic occlusion of a coronary A. by an atheroma NI: > strict, progressive activity program

Anticoagulant therapy

MANAGEMENT:
I.

Goal: to decrease pain and increase myocardial O2. Semifowlers position O2 inhalation- increase O2 supply Administration of E med- MORPHINE SO4- pain reliever, decrease O2 demand to myocardium

NI:
1. 2. 3.

s/s of morphine toxicity Respiratory depression Bilateral constriction of pupils Antidote: NARCAN (naloxone) is indicated for the complete or partial reversal of opioiddepression, including respiratory depression, - is specifically used to counteract life-threatening depression of the central nervous system and respiratory system an opioid antagonist drug developed by Sankyo in the 1960s[

4. Maintain a calm and reassuring environment 5. Stay with the client- for anxious patient( apprehensions) II. Maintain homeostatsis and decrease effects of MI 1. Cardiac monitoring 2. Administration of meds a. anti- arrhythmic Lidocaine, Xylocaine, procaine b. Stool softener- Colace- decreases straining during

Bowel movement- causes bradycardia c. Anticoagulant therapy 1. HEPARIN- given SQ, with tissue destruction if IM site: iliac region, lower abdominal region Destroyed by gastric contents so its not given orally Short acting Ist sign of toxicity- bleeding( hematuria) NI: > Give at the same time of the day

Avoid activities that increases chance of bleeding Antidote: PROTAMINE SO4 Lab exam to determine level- PTT 2. ORAL ANTICOAGULANT(Coumadin/warfarin) antidote: Vit. K Lab Exam- PT Long lasting- takes 3-4 days to take effect 3. THROMBOLYTIC- or "clot-busting" therapy is used to stop a heart attack in its tracks, it prevents or limit heart muscle damage by dissolving clots that block an artery. This opens up the artery and restores the blood flow.

Given 4-6 hours after onset of chest pains Eg Currently, the standard thrombolytic drug is tissuetype plasminogen activator (tPA), also calledalteplase (Activase). According to one study, it was the most effective in restoring blood flow to the heart, followed by reteplase (Retavase), urokinase (Abbokinase), and finally streptokinase(Kabikinase, Streptase)

low molecular weight heparins, can be injected under the skin - usually in the abdomen - and there is less risk of unwanted bleeding Enoxaparin (Lovenox) Dalteparin (Fragmin)

3. DIET: initially NPO then clear liquids- decrease O2 demand >low Na Low fat/ cholesterol 4. Frequent assessment of V/s , chest pains

5. Decrease anxiety Keep client informed Decrease sensory overload Encourage verbalization III. To assist the client to return to optimum level of wellness within limitations of condition 1. Monitored exercise 2. Dietary modifications 3. Stress reductions 4. Sexual counselling

4. Relaxed atmosphere 5. Lifestyle modifications Surgical Management: CORONARY ARTERY BYPASS GRAFT(CABG) >blood flow is rerouted through a new artery or vein that is grafted around diseased sections of your coronary arteries to increase blood flow to the heart muscle tissue > requires open-chest surgery and the use of a heartlung bypass machine to circulate the blood and add oxygen

>surgeon will use either an artery or a vein from your body >vein may be removed from your leg. One end of it is attached to the aorta and the other end to the diseased coronary artery just past the blocked area NI: Initially: patients care is focused on achieving or maintaining hemodynamic stability Recovery from anesthesia Wound care

Progressive activity Diet Most common vein- greater saphenous vein or lesser s. v., basilic and cephalic vein Removed from leg or arm and grafted to ascending aorta and coronary artery distal to the lesions Candidates for CABG 1. Angina that cannot be controlled by medical therapies 2. Unstable angina

3. Lesions that cannot be treated by PTCA 4. Left main coronary artery lesions of more than 60% 5. Individuals who have complications from or unsuccessful PTCAs > Occlusion of blood vessel less than 70%- enough to prevent adequate blood flow through CABG

INVASIVE HEMODYNAMIC MONITORING

PURPOSES OF INVASIVE HEMODYNAMIC MONITORING

Early detection, identification, and treatment of lifethreatening conditions such as heart failure and cardiac tampanade Evaluate the patients immediate response to treatment such as drugs and mechanical support Evaluate the effectiveness of cardiovascular function such as cardiac output and index

COMPONENTS OF A PULMONARY

ARTERY
CATHETER

COMPONENTS OF SWAN-GANZ [CONT]

Normally

has four[4] ports Proximal port [Blue] used to measure central venous pressure/RAP and injectate port for measurement of cardiac output Distal port [Yellow] used to measure pulmonary artery pressure Balloon port [Red] used to determine pulmonary wedge pressure;1.5 special syringe is connected Infusion port [White] used for fluid infusion

PULMONARY CAPILLARY WEDGE PRESSURE

>provides an indirect estimate of left atrial pressure (LAP). > measured by inserting balloon-tipped, multi-lumen catheter (Swan-Ganz catheter) into a peripheral vein, then advancing the catheter into the right atrium, right ventricle, pulmonary artery, and then into a branch of the pulmonary artery. >behind the tip of the catheter is a small balloon that can be inflated with air >catheter has one opening (port) at the tip (distal to the balloon) and a second port several centimeters proximal to the balloon. These ports are connected to pressure transducers.

Why is it measured? diagnose the severity of left ventricular failure and to quantify the degree of mitral valve stenosis. Both of these conditions elevate LAP and therefore PCWP. These pressures are normally 8-10(4-12) mmHg. Aortic valve stenosis and regurgitation, and mitral regurgitation also elevate LAP When these pressures are above 20 mmHg,pulmonary edema is likely to be present, which is a life-threatening condition

by measuring PCWP, the physician can titrate the dose of diuretic drugs and other drugs that are used to reduce pulmonary venous and capillary pressure, and thereby reduce pulmonary edema also important to measure when evaluating pulmonary hypertension. Pulmonary hypertension is often caused by increased pulmonary vascular resistance. Pulmonary hypertension can also result from increases in pulmonary venous pressure and pulmonary blood volume secondary to left ventricular failure or mitral or aortic valve disease.

PCWP is also useful in evaluating blood volume status when fluids are administered during hypotensive shock. One practice is to administer fluids at a rate that maintains PCWP between 12-14 mmHg Measures status of left sided heart function, pressure in the left ventricle= diastolic pressure in the PA, pulmocapillaries and left atrium

CENTRAL VENOUS PRESSURE Pressure of the blood in the thoracic vena cava near the right atrium of the heart Simplified as the right atrial pressure Reflects the amount of blood returning to the heart and the ability of the heart to pump the blood in the atrial system Major determinant of right ventricular end diastolic volume and right ventricular preload Change in CVP= change in volume, change in venous compliance

CVP is increased by venous blood volume or by increase in venous tone Good indicator of right ventricular function Normal pressure- 2-12mmHg Case scenarios of increased CVP(increase circulating volume) Hypervolemia Forced exhilation Being on ventilator Tension pnemothorax Pleural effusion Heart failure

Decreased CVP( decreased in circulating blood volume) >hypovolemia Septic shock DHN For accurate CVP reading: > Zero point of manometer must be at the level of right atrium located at mid axillary line at the 4th ICS