Acute MyocArdiAl infrAction

Presented by Omar AL-Rawajfah, RN, PhD

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Lecture Outlines

• Etiology and pathophysiology • Classification of infarctions • Homodynamic consequences • Assessment • Nursing diagnosis • Collaborative management • Patient education

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Atheroma

0 % 30 % 65 % 90 %

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Pathophysiology

• AMI: irreversible myocardial cell damage caused by prolonged ischemia

• Atherosclerosis is the primary cause of AMI • Plaque rupture is believed to be the

triggering mechanism • Cellular death occurs when there is no O2

supply to some portion of the myocardium • Irreversible damage occurs as early as 20-40

minutes after the thrombus formation • Reperfusion within the first 6hrs save larger

portion of the heart muscle (time is muscle)

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Pathophysiology

• Zone of infarction: the area myocardial tissue death

• Zone of infarction is identified by pathologic Q wave on the ECG

• The extent of cell damage is influenced by – The degree of collateral circulation – Duration of ischemia the size of the vessels – The status of the intrinsic fibrinolytic system – Metabolic demands of the myocardium

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Pathophysiology

• Pathologic Q wave usually persists lifelong • Necrotic cells are replaced by scare tissue

within 6 weeks • Injury zone: not fully capable of contraction,

evidenced by ST-segment elevation • Ischemic zone: impaired repolarization,

evidenced by T-wave inversion • Conduction defects and dysrhythmias are

caused by increase lactic acid release & K from the dead cell into the extracellular fluid

Collateral circulation

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Size of the infarction

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Transmural or full thickness

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Classification of Infraction • Transmural or full thickness (pathologic Q)

• Nontransmural or partial-thickness (no pathologic Q)

• Classification according to the location (table 21-1) – Inferior MI – Anterior MI – Anteroseptal – Anterolateral

• Q wave MI: – Greater loss of heart tissue – Dyskinetic or Akinetic areas of myocardium – Greater incidence of CHF – 70% experience pericardial friction rub

• Non-Q-wave MI: – Smaller areas of necrosis – Lower level of cardiac enzymes – Less incidence of CHF – Higher rates of postinfraction angina

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Classification of Infraction • Type 1: Spontaneous myocardial infarction

– related to atherosclerotic plaque rupture, ulceration – resulting intraluminal thrombus in one or more of the coronary arteries – leading to decreased myocardial blood flow or distal platelet emboli with

ensuing myocyte necrosis

• Type 2: Myocardial infarction secondary to an ischemic imbalance

– myocardial injury with necrosis where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand,

– e.g. coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy-/brady-arrhythmias, anemia, respiratory failure, hypotension, and hypertension with or without LVH

• Type 3: Myocardial infarction resulting in death when

biomarker values are unavailable – Cardiac death with symptoms suggestive of myocardial ischemia and

presumed new ischemic ECG changes or new LBBB, but death occurring before blood

– samples could be obtained, before cardiac biomarker could rise, or in rare cases cardiac biomarkers were not collected.

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Classification of Infraction • Type 4a: Myocardial infarction related to

percutaneous coronary intervention (PCI) – Rise of cTn values – angiographic loss of patency of a major coronary artery or a side branch or – Persistent slow- or no-flow or embolization

• Type 4b: Myocardial infarction related to stent thrombosis

– Same criteria of type 4a

• Type 5: Myocardial infarction related to coronary artery bypass grafting (CABG)

– Rise of cTn values – angiographic documented new graft or new – native coronary artery occlusion, or – Imaging evidence of new loss of viable myocardium or new regional wall

motion abnormality

Views of the Heart Some leads get a

good view of the:

Anterior portion of the heart

Lateral portion of the heart

Inferior portion of the heart

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Evolution of Acute MI

• Evolution of the ECG during a myocardial infarct see figure change minutes not in figure b

• B: Hyperacute T waves (peaked T waves) ST-elevation

• C: ST-elevation, with terminal negative T wave negative T wave (these can last for months)

• D: ST normalized with negative T wave • E: pathological Q wave

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Anterior MI • Infarction of the anterior wall of the LtV • Mostly caused by LAD occlusion • Disruption of the LtV conducting system • The different infarct patterns are named

according to the leads with maximal ST elevation: – Septal = V1-2 – Anterior = V2-5 – Anteroseptal = V1-4 – Anterolateral = V3-6, I + aVL – Extensive anterior / anterolateral = V1-6, I + aVL

Examples

• ST elevation is maximal in the anteroseptal leads (V1-4). • Q waves are present in the septal leads (V1-2). • There is also some subtle STE in I, aVL and V5, with reciprocal ST depression in

lead III. • There are hyperacute (peaked ) T waves in V2-4. • These features indicate a hyperacute anteroseptal STEMI

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Examples

• There is progressive ST elevation and Q wave formation in V2-5 • ST elevation is now also present in I and aVL. • There is some reciprocal ST depression in lead III. • This is an acute anterior STEMI – this patient needs urgent reperfusion!

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Examples

• ST elevation in V2-6, I and aVL. • Reciprocal ST depression in III and AVF.

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Examples

• Massive ST elevation with “tombstone” morphology is present throughout the precordial (V1-6) and high lateral leads (I, aVL).

• This pattern is seen in proximal LAD occlusion and indicates a large territory infarction with a poor LV ejection fraction and high likelihood of cardiogenic shock and death

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Antero-septal

• Associated with LAD • Associated with high risk for HF, pulmonary edema,

cardiogenic shock and death • Conduction disruptions, e.g., LBBB

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Inferior MI

• Occlusion of RCA • Supply 50% -60% of SA node and 90% of AV node • Result in disruption of cardiac rhythm • Less common than Antero-septal

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Right Ventricular Infarction • Right ventricular infarction complicates 30-50% of inferior wall

MIs, and 10% of anterior wall infarcts. • ST elevation in V1 - the only standard ECG lead that looks

directly at the right ventricle • The most reliable ECG finding is ST segment elevation in the

right precordial leads, with associated ST segment elevation in II, III & aVF

• If the ST segment in V1 is isoelectric and the ST segment in V2 is markedly depressed.

• If the magnitude of ST elevation in V1 exceeds the magnitude of ST elevation in V2.

• The most useful lead is V4R, which is obtained by placing the V4 electrode in the 5th right intercostal space in the midclavicular line

• Occurs when there is an occlusion of the RCA proximal to the acute marginal branches, but it may also occur with an occlusion of the LCX in patients who have left-dominant coronary circulation

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Right Ventricular Infarction

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Example: Right Ventricle MI

• There is an inferior STEMI with ST elevation in lead III > lead II.

• There is subtle ST elevation in V1 with ST depression in V2.

• There is ST elevation in V4R.

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Example: Right Ventricle MI

• There is an inferior STEMI with ST elevation in lead III > lead II.

• V1 is isoelectric while V2 is significantly depressed. • There is ST elevation throughout the right-sided leads V3R-

V6R.

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Posterior MI • Infarction of the posterobasal wall of the

left ventricle • Posterior infarction accompanies 15-20%

of STEMIs, usually occurring in the context of an inferior or lateral infarction.

• Isolated posterior MI is less common (3-11% of infarcts).

• Isolated posterior infarction is an indication for emergent coronary reperfusion

• They usually result from occlusion of the LCX coronary artery or RCA artery

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Posterior MI

• ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI

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Posterior MI

V7 – Left posterior axillary line, in the same horizontal plane as V6. V8 – Tip of the left scapula, in the same horizontal plane as V6. V9 – Left paraspinal region, in the same horizontal plane as V6.

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Example: Posterior MI

• Standard interior leads

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Example: Posterior MI

• Same patients with posterior leads

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Hemodynamic consequences • Scare tissue lacks the contractile (dyskintic or a

kinetic), elastic, and conductive properties • When the infraction area is large, SV & CO are

reduced • Ventricular remodeling:

– Occurs within weeks to months after the attack – Hypercontractile for healthy myocardium & thins the infarct

area – Expansion and dilation of healthy myocardium – It may precedes aneurysm formation

• Patient with loss of 40% or more of the LV function, usually develop cardiogenic shock with a death rate of 85%

• Heart block disorders are very common with large MI

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Assessment • “Time is Muscle”: initiation of treatment early

saves the myocardium • Ideally, treatment should be started within

60 – 90 min of the onset of symptoms • Prehospital delay range from 2 – 6.5 hr • Factors affect time of delay:

– Pt decision making – Responding and transporting Pt to the ER – Initiation of treatment

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Sings and Symptoms • History

– Persistent chest pain last more than 30 min, unrelieved by rest or nitrates

– The pain usually described as “burning, crushing, tightness, squeezing in the chest”

– Pain may radiate to shoulders, neck, back, jaws, ears, or arms

– Pain may be associated with nausea, vomiting, & diaphoresis

– Elderly people usually don’t have the classical presentation of AMI

– Women are more often experience “Silent AMI” – Nurse should used focused approach in

obtaining the history of chest pain (PQRST)

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Physical Examination

• General appearance: – Distress and pain – Labored and rapid breathing

• Cardiovascular – High BP early – Low BP → HF – Low HR → high mortality rate – Loss of point of maximal impulses

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Laboratory and Diagnostic Tests

• 12-lead ECG – For the first hours of the symptoms ST segment and T

inversion are presented – Q wave is usually associated with post MI – Pathological Q waves: 25% or more of the height of the R

wave and/or they are greater than 0.04 seconds and greater than 2mm: many time need at least 24-48hrs

– Some time it is not very diagnostic, about 50% of Pt with chest pain and they have AMI they have normal or nondiagnostic ECG

• Cardiac enzymes are more accurate (table 17-3) – CK, CK-MB1 & CK-MB2, LDH1, LDH2, Mgb, Troponin I&T – CK-MB2: raises within 2 hrs of the onset of AMI – Mgb: increase to twice their normal values within 2 hr and

peaks within 4 hr – cTnT: appear in circulation within 3-4 hrs and remains 6-20

days – cTnTi: rise in about 3 hr and peaks within 14 hrs

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Evolution of Acute MI

• Evolution of the ECG during a myocardial infarct see figure change minutes not in figure b

• B: Hyperacute T waves (peaked T waves) ST-elevation

• C: ST-elevation, with terminal negative T wave negative T wave (these can last for months)

• D: ST normalized with negative T wave • E: pathological Q wave

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Nursing Diagnoses

• Emergency department – Pain – Decreased CO – Anxiety

• ICU or CCU – Sleep pattern disturbance – Ineffective coping – Impaired adjustment

• Intermediate care unit – Alter role performance – Self-esteem disturbance – Knowledge deficit

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Collaborative Management • Emergency Department

– “Door-to-drug” : 30 min – MOVE: Monitor, O2, venous access, ECG – Rapid assessment of the chest pain (see app-13)

• Reperfusion Strategies 1. Thrombolytic Therapy (see table 10-5)

• Optimal results are obtained if given within 1 hr • 60 – 80% experienced patency of occluded artery • They convert plasminogen to plasmin which catalyzes

the fibrin clot • They limit the size of infraction, yielding a non-Q-wave

AMI with borderline rise of CK enzyme

Coagulation cascade.

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Plasminogen Activator

Thrombolytic Drugs • Alteplase (fibrin selective)

– Known as tissue plasminogen activator – Originally derived from cultured human melanoma

cell – It has low affinity for free plasminogen in the

plasma – Activates plasminogen that bound to fibrin – It has short half-life (5-30min) – Given infusion over one hours – Optimal results if given with 3 hours of stroke

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Thrombolytic Therapy • Indications

• AMI Chest pain that is less than 6hrs in duration • ST-segment elevation > 1mm in two contiguous leads • Absence of absolute contraindications

• Absolute contraindications (see chart 21-10)

• Active or recent internal bleeding • Intracranial neoplasm • Prolonged, traumatic CPR • Suspected aortic dissection • BP > 180/110 • Trauma or surgery within 4 weeks

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Thrombolytic Therapy • S&S of Success Treatment: (within 2-3hr of starting the therapy)

• Resolution of chest pain • Early peaking of CK-MB • Reperfusion dysrhythmias (e.g., PVC, VT, AV blocks) • Normalization of ST segment

• No ST-segment resolution indicate failure of the treatment

• Approximately 50% of patients with patent infarction artery have none of these S&S

• Reocclusion occurs 5-25% of patients

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Collaborative Management • Invasive Techniques

– Rescue angioplasty – Primary angioplasty

• Elder and ineligible for thrombolytic therapy • S&S of cardiogenic shock • Presenting within 12hr of acute anterior infraction

• Surgical Techniques – Coronary artery bypass graft (CABG)

• Evidence of major multivessel disease • Failed thrombolytic and angioplasty options

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Collaborative Management • Pharmacotherapy • Aspirin

– Inhibit thromobxane A2, thus inhibiting platelet aggregation – 80 – 160 mg per day – Also reduce the inflammation in blood vessels in the progression of

atherosclerosis – For patient who can’t take it, other antiplatelet therapy are available

(e.g., Ticopidine, dipyridamole) • Heparin

– Given to prevent the reocclusion after thrombolytic therapy – Does is regulated according to the aPTT (see table 10-8) – Maintain the PTT at 1.5-2.5 the control

• Nitrates – Initially given sublingual in a 5 minutes interval, 3 times – 5-10 µg per min increase every 5-10 min – It has effect on the peripheral (↓preload) & coronary vessels

(↑collateral flow) – Close monitoring of the BP is required

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Pharmacotherapeutics • Analgesics (Morphine sulfate IV)

• 2-5mg IV repeated 5-15min • It has analgesic, anxiolytic, and homodynamic effects • It cause vasodilatation and ↓HR • Close monitoring of BP, & respiratory depression is

needed

• B- blockers (e.g. Propranolol, Metoprolol) • Inhibit catecholamines at B1 receptor in the myocardium

resulting in ↓HR, contractility, and BP • ↓O2 consumption of the myocardium • Should be given with caution for patient with asthma,

DM, & cardiomyopathy • Contraindications: AV block, hypotension, bradycardia

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Pharmacotherapeutics • Magnesium

• Demonstrate good outcome • Used to moderate negative effect of increase increased

intracellular CA, and depletion of high-energy phosphates at early reperfusion

• ACE inhibitors (e.g. captopril, analpril) • Block the conversion of angiotensin I to II. • They are effective vasodilators • Improve ventricular function • Close monitoring of BP is required special at the

beginning of the therapy

• O2 • By nasal cannula 2 – 4 L/min • Maximize myocardial oxygenation • Minimize dysrhythmias

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Cardiac Monitoring • Continuous cardiac monitoring • Chest pain assessment • 12-lead ECG in case of chest pain • Monitoring of HR, rhythm, and dysrhythmias

including ECG evidence of infraction, reperfusion, & reocclusion

• Vital sings monitoring • Intake and output monitoring

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Complications • See box 21-10 • Vascular complications

– Recurrent ischemia (10-15%) – Recurrent infraction

• Myocardial complications – Cardiogenic shock (5-15%) of MI patients

• Most likely with 40% or more loss • Mortality very high even about 80% • S &S: narrow pulse pressure, dyspnea, inspiratory

crackles, chest pain, moist skin, oliguria, PAWP > 18mm Hg, systolic BP< 85mm Hg, & other symptoms

• Dysrhythmias – Reperfusion dysrhythmias – Dysrhythmias as results of myocardial ischemia

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Complications • Implantable cardioverter defibrillator (ICD)

– indications: • Pt who survived an episode of sudden cardiac arrest • Pt who has documented life-threatening ventricular

dysrhythmias • Pt with medication-refractory dysrhythmias

– Like pacemaker powered by lithium battery with life expectancy of > 5 years

– Placed subcataneous – The ICD consists of tripolar lead tip – 2 of electrodes detect dysrhythmias and giving the

shock and the 3rd for sense the HR

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Complications • Implantable cardioverter defibrillator (ICD)

– Functions • Anti tachycardia Pacing (ATP) • Cardioversion • Defibrillation • Anti bradycardia pacing (ABP)

– Perioperative Management • Patient and family education • Need general anesthesia • The thresholds is determined by inducing malignant

dysrhythmias • Device usually left inactive 2-3 days post op

– Discharge education • Patient and family education about the device • Importance of carrying device identification • CPR training for the family • External magnetic exposure • Activity guidelines

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Complications • Premature Ventricular Contractions (PVCs)

– May cause by hypoxia, ischemia, acid-based-imbalance, hypokalemia, hypomagnesemia, & Digoxin

– Treat the cause – Lidocaine hydrochloride IV, or oral Procainmide

and Amiodarone hydrochlorides • AV blocks

– Seen in 15-33% of patients with inferior MI • Intraventricular conduction defects

– Common with anterior MIs – Mostly associated with LAD stenosis

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Structural Defects • Papillary Muscle Rupture

– May be partial or complete – Both presented with mitral regurgitation and

cardiogenic shock – With complete rupture death rate is 95% – Partial rupture can be stabilized with intra-aortic

balloon pump and inotropic agents (Dobutamine) • Ventricular septal rupture

– 2% - 4% of all MI – Presented with sudden hypotension, chest pain – Diagnosed by echocardiography – Emergency correction for both condition with high

death rates

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Structural Defects • Ventricular aneurysms

– Thin-walled, noncontractile outpouchings of the ventricle (usually LV in the apex region)

– Suspected in Pt with persistent ST elevation – Diagnosed by echocardiography – CHF, LV thromoembolism, VT are common

complications – Treatment include prevention of HF,

antiarrhythmias, and Warfarin for 3 moths after the infraction

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Ventricular Aneurysms

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Hemodynamic Alterations • Cardiogenic shock

– Rt-sided HF associated with ascites & peripheral edema – Lt-sided HF associated with pulmonary edema

• Inflammatory Reponses – Pericarditis

• Occur 2 – 4 days after an AMI • Chest pain increased with deep respiration, cough, lying flat • Pricardial friction rub in auscultation • Treatment: Indomethacin for 3-5 days

• Dressler’s Syndrome – Precarditis occur after 1 week to several moths of AMI – Associated with fever, pericardial effusion – Treatment: oral corticosteroids

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Psychosocial support • Anxiety, Denial, and Depression

– All are associated with the diagnosis, life style changes, self-esteem changes, role changes, sense of loss of control, & powerlessness

• Needs of families – Reducing anxiety – Enhance coping – Communicating information to family members

• Hospital environment – Level of noise – Interruption in sleep – Family and relative visits

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Cardiac Rehabilitation • Phase I

– Start in the hospital – ROM exercises – Progressive daily activities

• Phase II – Outside the hospital – Risk factor modifications – Exercise training – Counseling – Behavioral interventions

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Patient Education • Explanation of procedures throughout the

hospitalization • Health information:

– Desire to know: disease process, risk factors, medication,

– Need to know: chest pain management, activity restriction, follow up instructions

– See table 21-2

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Questions and answers