Complications of Acute Myocardial Infarction Willis E. Godin, DO.

Complications of Acute Complications of Acute Myocardial InfarctionMyocardial Infarction

Willis E. Godin, DOWillis E. Godin, DO

OverviewOverview

Recurrent Ischemia/InfarctionRecurrent Ischemia/Infarction Congestive Heart Failure/LV FailureCongestive Heart Failure/LV Failure Cardiogenic ShockCardiogenic Shock Interventricular Septal RuptureInterventricular Septal Rupture Free Wall RuptureFree Wall Rupture Acute Mitral RegurgitationAcute Mitral Regurgitation Right Ventricular InfarctionRight Ventricular Infarction ArrhythmiasArrhythmias Pericardial Effusion and PericarditisPericardial Effusion and Pericarditis

Recurrent Ischemia and Recurrent Ischemia and InfarctionInfarction

Incidence of postinfarction angina without Incidence of postinfarction angina without reinfarction is 20-30%reinfarction is 20-30%

Reduced incidence with primary PTCAReduced incidence with primary PTCA May be due to occlusion of an initially May be due to occlusion of an initially

patent vessel, reocclusion of an initially patent vessel, reocclusion of an initially recanalized vessel, or coronary spasm.recanalized vessel, or coronary spasm.

Left Ventricular FailureLeft Ventricular Failure

THE single most important predictor of mortality THE single most important predictor of mortality after AMIafter AMI

Characterized by either systolic dysfunction alone Characterized by either systolic dysfunction alone or both systolic and diastolic dysfunctionor both systolic and diastolic dysfunction

Increased clinical manifestations as the extent of Increased clinical manifestations as the extent of the injury to the LV increasesthe injury to the LV increases

Other predictors of development of symptomatic Other predictors of development of symptomatic LV dysfunction include advanced age and diabetesLV dysfunction include advanced age and diabetes

Mortality increases with the severity of the Mortality increases with the severity of the hemodynamic deficithemodynamic deficit


LV failure – Congestive Heart FailureLV failure – Congestive Heart Failure Characteristically develop hypoxemia due Characteristically develop hypoxemia due

to pulmonary vascular engorgementto pulmonary vascular engorgement Managed most effectively first by reduction Managed most effectively first by reduction

of ventricular preload and then, if possible, of ventricular preload and then, if possible, by lowering afterloadby lowering afterload


Treatment:Treatment:– DiureticsDiuretics– NitroglycerinNitroglycerin– VasodilatorsVasodilators– DigitalisDigitalis– Beta-adrenoceptor agonistsBeta-adrenoceptor agonists– Other positive inotropic agentsOther positive inotropic agents

Cardiogenic ShockCardiogenic Shock

Most severe clinical expression of left Most severe clinical expression of left ventricular failureventricular failure

Occurs in up to 7% of patients with AMIOccurs in up to 7% of patients with AMI Low output state characterized by elevated Low output state characterized by elevated

ventricular filling pressures, low cardiac ventricular filling pressures, low cardiac output, systemic hypotension, and evidence output, systemic hypotension, and evidence of vital organ hypoperfusionof vital organ hypoperfusion


At autopsy, more than 2/3 of patients with At autopsy, more than 2/3 of patients with cardiogenic shock demonstrate stenosis of cardiogenic shock demonstrate stenosis of 75 percent or more of the luminal diameter 75 percent or more of the luminal diameter of all 3 major coronary vessels and loss of of all 3 major coronary vessels and loss of about 40 percent of LV massabout 40 percent of LV mass


Medical ManagementMedical Management– Same as tx for LV failureSame as tx for LV failure– Intraaortic balloon counterpulsationIntraaortic balloon counterpulsation– RevascularizationRevascularization

Interventricular Septal RuptureInterventricular Septal Rupture

Occurs in 0.2 percent of patients with AMIOccurs in 0.2 percent of patients with AMI Clinical features associated with increased risk of Clinical features associated with increased risk of

rupture:rupture:– Lack of development of collateral networkLack of development of collateral network– Advanced ageAdvanced age– HypertensionHypertension– Anterior location of infarctionAnterior location of infarction– thombolysisthombolysis

Higher 30-day mortality (74%) compared to those Higher 30-day mortality (74%) compared to those patients who do not develop this complication patients who do not develop this complication (7%)(7%)


The size of the defect determines:The size of the defect determines:– The magnitude of the left-to-right shuntThe magnitude of the left-to-right shunt– Extent of hemodynamic deteriorationExtent of hemodynamic deterioration– Likelihood of survivalLikelihood of survival

Associated with complete heart block, right Associated with complete heart block, right bundle branch block, and atrial fibrillation bundle branch block, and atrial fibrillation in 20-30 percent of casesin 20-30 percent of cases


Characterized by the appearance of a new Characterized by the appearance of a new harsh, loud holosystolic murmurharsh, loud holosystolic murmur

Best heard at the lower left sternal borderBest heard at the lower left sternal border Usually accompanied by a thrillUsually accompanied by a thrill Can be recognized by 2-D Can be recognized by 2-D

echocardiographyechocardiography Catheter placement of an umbrella-shaped Catheter placement of an umbrella-shaped

device within the ruptured septumdevice within the ruptured septum

Free Wall RuptureFree Wall Rupture

Features that characterize free wall rupture:Features that characterize free wall rupture:– ElderlyElderly– HTNHTN– More frequently occurs in left ventricleMore frequently occurs in left ventricle– Seldom occurs in atriaSeldom occurs in atria– Usually involves the anterior or lateral wallsUsually involves the anterior or lateral walls– Usually associated with a relatively large transmural Usually associated with a relatively large transmural

infarction involving atleast 20% of the left ventricleinfarction involving atleast 20% of the left ventricle– It occurs between 1 day and 3 weeks, but most It occurs between 1 day and 3 weeks, but most

commonly 1 to 4 days after infarctioncommonly 1 to 4 days after infarction– Most often occurs in patients without previous infarctionMost often occurs in patients without previous infarction


Usually leads to hemopericardium and Usually leads to hemopericardium and death from cardiac tamponadedeath from cardiac tamponade

Occasionally, rupture of the free wall of the Occasionally, rupture of the free wall of the ventricle occurs as the first clinical ventricle occurs as the first clinical manifestation in patients with undetected or manifestation in patients with undetected or silent MI, and then it may be considered a silent MI, and then it may be considered a form of “sudden cardiac death”form of “sudden cardiac death”


The coarse of rupture can vary from The coarse of rupture can vary from catastrophic, with an acute tear leading to catastrophic, with an acute tear leading to immediate death, to subacute, with nausea, immediate death, to subacute, with nausea, hypotension, and pericardial type of hypotension, and pericardial type of discomfortdiscomfort

Survival depends on the recognition of this Survival depends on the recognition of this complication, on hemodynamic complication, on hemodynamic stabilization of the patient, and most stabilization of the patient, and most importantly, on prompt surgical repairimportantly, on prompt surgical repair

PseudoaneurysmPseudoaneurysm

Incomplete rupture of the heart, with Incomplete rupture of the heart, with organizing thrombus and hematoma, organizing thrombus and hematoma, together with pericardium, seal a rupture of together with pericardium, seal a rupture of the left ventriclethe left ventricle

With time this area of organized thrombus With time this area of organized thrombus and pericardium can become a and pericardium can become a pseudoaneurysm that maintains pseudoaneurysm that maintains communication with the cavity of the left communication with the cavity of the left ventricle.ventricle.

PseudoaneurysmPseudoaneurysm

Can become quite large, even equaling the Can become quite large, even equaling the true ventricular cavity in size, and they true ventricular cavity in size, and they communicate with the LV cavity through a communicate with the LV cavity through a narrow necknarrow neck

Diagnosis: 2-D echocardiography and Diagnosis: 2-D echocardiography and contrast angiographycontrast angiography

Acute Mitral RegurgitationAcute Mitral Regurgitation

Due to partial or total rupture of a papillary Due to partial or total rupture of a papillary musclemuscle

Rare but often fatal complication of transmural MIRare but often fatal complication of transmural MI Complete transection of a left ventricular papillary Complete transection of a left ventricular papillary

muscle is incompatible with life because the muscle is incompatible with life because the sudden massive mitral regurgitation that develops sudden massive mitral regurgitation that develops cannot be toleratedcannot be tolerated

Rupture of a portion of a papillary muscle Rupture of a portion of a papillary muscle resulting in severe mitral regurgitation is much resulting in severe mitral regurgitation is much more frequent and is not immediately fatalmore frequent and is not immediately fatal

Acute Mitral RegurgitationAcute Mitral Regurgitation

Patients manifest a new holosystolic Patients manifest a new holosystolic murmur and develop increasingly severe murmur and develop increasingly severe heart failureheart failure

The murmur may become softer or The murmur may become softer or disappear as arterial pressure fallsdisappear as arterial pressure falls

Recognized by 2-D echocardiography with Recognized by 2-D echocardiography with color flow Dopplercolor flow Doppler

Right Ventricular InfarctionRight Ventricular Infarction

Frequently accompanies inferior LV Frequently accompanies inferior LV infarction or rarely occurs in isolated forminfarction or rarely occurs in isolated form

Right-sided filling pressures are elevated, Right-sided filling pressures are elevated, whereas left ventricular filling pressure is whereas left ventricular filling pressure is normal or only slighty raisednormal or only slighty raised

Cardiac output is often markedly depressedCardiac output is often markedly depressed


Common among patients with inferior LV Common among patients with inferior LV infarctioninfarction

Unexplained systemic arterial hypotension Unexplained systemic arterial hypotension or diminished cardiac output or marked or diminished cardiac output or marked hypotension in response to small doses of hypotension in response to small doses of nitroglycerine in patients with inferior nitroglycerine in patients with inferior infarction should lead to the prompt infarction should lead to the prompt consideration of this diagnosisconsideration of this diagnosis


Most patients with RV infarction have ST Most patients with RV infarction have ST segment elevation in lead V4R (right segment elevation in lead V4R (right precordial lead in V4 position)precordial lead in V4 position)

2-D echocardiography : abnormal wall 2-D echocardiography : abnormal wall motion of the right ventricle as well as right motion of the right ventricle as well as right ventricular dilitation and depressed RV ventricular dilitation and depressed RV ejection fractionejection fraction


Medications routinely prescribed for LV Medications routinely prescribed for LV infarction may produce profound infarction may produce profound hypotension in patients with RV infarction hypotension in patients with RV infarction (especially nitroglycerine)(especially nitroglycerine)

Initial treatment of hypotension in patients Initial treatment of hypotension in patients with RV infarction include volume with RV infarction include volume expansionexpansion

ArrhythmiasArrhythmias

Ventricular arrhythmiasVentricular arrhythmias– Ventricular Premature BeatsVentricular Premature Beats– Accelerated Idioventricular RhythmAccelerated Idioventricular Rhythm– Ventricular TachycardiaVentricular Tachycardia– Ventricular FibrillationVentricular Fibrillation

BradyarrhythmiasBradyarrhythmias– Sinus BradycardiaSinus Bradycardia

ArrhythmiasArrhythmias

Atrioventricular and Intraventricular BlockAtrioventricular and Intraventricular Block– First-Degree AV blockFirst-Degree AV block– Second-Degree AV Block (Mobitz I / II)Second-Degree AV Block (Mobitz I / II)– Third degree (Complete) AV blockThird degree (Complete) AV block– Intraventricular BlockIntraventricular Block– AsystoleAsystole

Supraventricular TachyarrhythmiasSupraventricular Tachyarrhythmias– Sinus TachycardiaSinus Tachycardia– Atrial Premature ContractionsAtrial Premature Contractions– Atrial FlutterAtrial Flutter– Atrial FibrillationAtrial Fibrillation– Paroxysmal Supraventricular TachycardiaParoxysmal Supraventricular Tachycardia

Ventricular ArrhythmiasVentricular Arrhythmias

Ventricular Premature Beats (PVCs)Ventricular Premature Beats (PVCs) Commonly seen in patients with acute MICommonly seen in patients with acute MI Usually pursue a conservative approach and Usually pursue a conservative approach and

do not routinely prescribe antiarrhythmic do not routinely prescribe antiarrhythmic drugs but instead determine whether drugs but instead determine whether recurrent ischemia or electrolyte/metabolic recurrent ischemia or electrolyte/metabolic disturbances are presentdisturbances are present


Accelerated Idioventricular RhythmAccelerated Idioventricular Rhythm Defined as a ventricular rhythm with a rate of 60-Defined as a ventricular rhythm with a rate of 60-

125 beats/min125 beats/min Frequently called “slow v. tach”Frequently called “slow v. tach” Seen in up to 20% of patients with AMISeen in up to 20% of patients with AMI Occurs frequently during the first 2 daysOccurs frequently during the first 2 days Probably results from enhanced automaticity of Probably results from enhanced automaticity of

the Purkinje fibersthe Purkinje fibers Often observed shortly after successful Often observed shortly after successful

reperfusionreperfusion


Ventricular TachycardiaVentricular Tachycardia When continuous ECG recordings during When continuous ECG recordings during

the first 12 hours of AMI are analyzed, the first 12 hours of AMI are analyzed, nonsustained paroxysms of VT may be seen nonsustained paroxysms of VT may be seen in up to 67% of patientsin up to 67% of patients

Hypokalemia and hypomagnesemia may Hypokalemia and hypomagnesemia may increase the risk of developing VTincrease the risk of developing VT

Treatment may include: lidocaine, Treatment may include: lidocaine, procainamide, amiodaroneprocainamide, amiodarone


Ventricular FibrillationVentricular Fibrillation Ventricular fibrillation occuring in Ventricular fibrillation occuring in

association with marked LV failure or association with marked LV failure or cardiogenic shock entails a poor prognosis, cardiogenic shock entails a poor prognosis, with an in-hospital mortality rate of 40-60%with an in-hospital mortality rate of 40-60%

Tx : defibrillatorTx : defibrillator Management : lidocaine, amiodarone, Management : lidocaine, amiodarone,

bretyliumbretylium

BradyarrhythmiasBradyarrhythmias

Sinus BradycardiaSinus Bradycardia Common arrhythmia occuring during the early Common arrhythmia occuring during the early

phases of AMIphases of AMI Particularly frequent in patients with inferior and Particularly frequent in patients with inferior and

posterior infarctionposterior infarction Isolated sinus bradycardia, unaccompanied by Isolated sinus bradycardia, unaccompanied by

hypotension or ventricular ectopy, should be hypotension or ventricular ectopy, should be observed rather than treated initiallyobserved rather than treated initially

Atropine should be utilized if hypotension Atropine should be utilized if hypotension accompanies any degree of sinus bradycardiaaccompanies any degree of sinus bradycardia

Atrioventricular and Atrioventricular and Intraventricular BlockIntraventricular Block

First Degree AV BlockFirst Degree AV Block Occurs in less than 15% of patients with Occurs in less than 15% of patients with

AMI admitted to CCUsAMI admitted to CCUs Generally does not require specific Generally does not require specific

treatmenttreatment (Digitalis, B-blockers, Calcium antagonists)(Digitalis, B-blockers, Calcium antagonists)


Second-Degree AV blockSecond-Degree AV block– Mobitz Type I or WenckebachMobitz Type I or Wenckebach

Usually transient and does not persist more Usually transient and does not persist more than 72 hours after infarctionthan 72 hours after infarction

Rarely progresses to complete AV blockRarely progresses to complete AV block Do not appear to affect survivalDo not appear to affect survival Caused by ischemia of the AV nodeCaused by ischemia of the AV node Specific therapy not requiredSpecific therapy not required


Second Degree AV blockSecond Degree AV block– Mobitz Type IIMobitz Type II

Rare conduction defect after AMIRare conduction defect after AMI Often progresses suddenly to complete AV Often progresses suddenly to complete AV

blockblock Treated with a temporary external or Treated with a temporary external or

transvenous demand pacemakertransvenous demand pacemaker


Complete (Third Degree) AV blockComplete (Third Degree) AV block Often develops gradually, progressing from Often develops gradually, progressing from

first-degree or type II second-degree blockfirst-degree or type II second-degree block Treat with temporary external or Treat with temporary external or

transvenous demand pacemakertransvenous demand pacemaker


Intraventricular BlockIntraventricular Block– Isolated fasicular blocksIsolated fasicular blocks

» LAFBLAFB

» LPFBLPFB

– Right bundle branch blockRight bundle branch block– Bifasicular blockBifasicular block

Supraventricular Supraventricular TachyarrhythmiasTachyarrhythmias

Sinus TachycardiaSinus Tachycardia Typically associated with augmented Typically associated with augmented

sympathetic activity (anxiety, persistent sympathetic activity (anxiety, persistent pain, LV failure, hypovolemia, epinephrine, pain, LV failure, hypovolemia, epinephrine, atropine, etc.)atropine, etc.)

Beta-adrenoceptor blocking agents Beta-adrenoceptor blocking agents frequently utilizedfrequently utilized


Paroxysmal Supraventricular TachycardiaParoxysmal Supraventricular Tachycardia Requires aggressive management because Requires aggressive management because

of the rapid ventricular rateof the rapid ventricular rate Augmentation of vagal tone – manual Augmentation of vagal tone – manual

carotid massagecarotid massage Drug of choice – adenosine (in non-AMI Drug of choice – adenosine (in non-AMI

patients)patients) Alternatives: IV verapamil, diltiazem, Alternatives: IV verapamil, diltiazem,

metoprololmetoprolol


Atrial Flutter and FibrillationAtrial Flutter and Fibrillation Atrial flutter – usually transientAtrial flutter – usually transient Atrial Fibrillation occurs in 10-20% of Atrial Fibrillation occurs in 10-20% of

patients with AMIpatients with AMI The increased ventricular rate and the loss The increased ventricular rate and the loss

of atrial contribution to LV filling result in a of atrial contribution to LV filling result in a significant reduction in cardiac outputsignificant reduction in cardiac output

Atrial fibrillation in AMI is associated with Atrial fibrillation in AMI is associated with increased mortality and strokeincreased mortality and stroke

Pericardial EffusionPericardial Effusion

Generally detected by 2-D Generally detected by 2-D echocardiographyechocardiography

More common in patients with anterior MI More common in patients with anterior MI and with larger infarcts and when and with larger infarcts and when congestive heart failure is presentcongestive heart failure is present

Majority do not cause hemodynamic Majority do not cause hemodynamic compromise; when tamponade occurs, it is compromise; when tamponade occurs, it is usually due to ventricular rupture or usually due to ventricular rupture or hemorrhagic pericarditishemorrhagic pericarditis

PericarditisPericarditis

When secondary to transmural MI, When secondary to transmural MI, pericarditis may produce pain as early as pericarditis may produce pain as early as the first day and as late as 6 weeks after MIthe first day and as late as 6 weeks after MI

Treatment of pericardial discomfort consists Treatment of pericardial discomfort consists of aspirin at does as high as 650mg every 4-of aspirin at does as high as 650mg every 4-6 hours. (corticosteroids should be avoided 6 hours. (corticosteroids should be avoided because they may interfere with myocardial because they may interfere with myocardial scar formation)scar formation)

Dressler SyndromeDressler Syndrome

Dressler SyndromeDressler Syndrome

Post-myocardial infarction syndromePost-myocardial infarction syndrome Usually occurs 1 to 8 weeks after infarctionUsually occurs 1 to 8 weeks after infarction Patients present with malaise, fever, Patients present with malaise, fever,

pericardial discomfort, leukocytosis, pericardial discomfort, leukocytosis, elevated ESR,and a pericardial effusionelevated ESR,and a pericardial effusion

Cause of this syndrome not clearly Cause of this syndrome not clearly established (? Immunopathological process)established (? Immunopathological process)

Treatment : ASA 650mg Q4hrsTreatment : ASA 650mg Q4hrs

SummarySummary

Be aware of all the potential complications Be aware of all the potential complications that can arise from myocardial infarction, that can arise from myocardial infarction, diagnose these complications when they diagnose these complications when they occur, and treat the patient appropriately in occur, and treat the patient appropriately in a timely manner to reduce morbidity and a timely manner to reduce morbidity and mortality.mortality.

Complications of Acute Myocardial Infarction Willis E. Godin, DO.

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