Complications of Myocardial Infarction and their mx.pptx

7/27/2019 Complications of Myocardial Infarction and their mx.pptx

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ACT RAPID Arrhythmias

Congestive Heart Failure Tamponade / Thromboembolic disorder

Rupture (Ventricle, septum, papillary muscle)

Aneurysm (Ventricle) Pericarditis Infection Death / Dresslers Syndrome


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Common post mi Blocks, atrial/ ventricular arrhythmias

If the arrhythmia precipitates hemodynamiccompromise tx aggressively

Address exacerbating conditions Electrolytes, Hypoxia, acidosis, drug effects


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1. VFib2. Sustained VTach3. PVCs / nonsustained VTach

4. Accelerated idioventricular rhythm5. AFib/Flutter6. SVT7. PACs

8. Need for pacing9. Sinus bradycardia


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VFib defibrillate, reduce ischemia and adrenergicstimulation (B-block, IABP, revascularize)

VTach -

Sustained (>30s) polymorphic, unstable defibrillate,reduce ischemia and adrenergic stimulation

Sustained, monomorphic, unstable cardioversion

Sustained, monomorphic, stable amio or procainamide,+/- cardioversion


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PVCs or nonsustained, and stable no rx

Historically a warning sign for arrhythmia, but

since B-blocker, ACEI and reperfusion, this is nottrue.

Accelerated idioventricular rhythm slowVT. If stable, no rx.


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Atrial Fibrillation/Flutter often occurs 2/2ischemia

Unstable cardioversion, and if not effective useIV amio or IV dig (in severe LV dysfxn)

Stable but ischemic B-block, CCB (dilt,

verapamil), cardioversion

Stable, no ischemia rate control +anticoagulation


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Reentrant supraventricular tachycardia carotid massage, adenosine, IV B-blocker, IV

CCB, IV digoxin PACs no rx


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Pacemaker needed if:

2 AV block + bifascicular block

3 AV block Transient 2 or 3 AV block + BBB

Symptomatic 2 or 3 AV block

? Asymptomatic, persistent 2 or 3 AV block


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Sinus bradycardia treat with atropine (0.6-1mg) if

Pause > 3sec HR < 40 with symptoms

If still brady, need temporary pacing


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Serious. Hypotension + inadequate ventricular fxn

inability to meet tissue demands Progressive Renal failure/ SOB/ Alt. mental status

Relatively preserved SBP- Dobutamine,declining SBP Dopamine.+NE, IABP

Echo evaluate for mechanical compln.


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rupture of the left ventricular freewall;

rupture of the interventricularseptum;

and the development of mitralregurgitation.

Aneurysm of LV

J Am Coll Cardiol. 1998;32(1):135.


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Acute or subacute myocardial rupture is aserious and often lethal complication ofSTEMI

Increased risk: No history of previous angina or MI

ST-segment elevation or Q wave development onthe initial ECG

Peak MB-creatine kinase above 150 IU/L anterior location of the infarction,

age >70, and female sex

Multicenter Investigation of Limitation of Infarct Size. Pohjola-Sintonen S, Muller JE, Stone PH,Willich SN, Antman EM, Davis VG, Parker CB, Braunwald E


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Myocardial rupture occurs within the first fivedays after MI in about one-half of cases and

within two weeks in over 90 percent of cases left ventricle > right ventricle, and rarely

involves the atria. The infarct commonlyaffects the anterior and lateral walls of theleft ventricle near the junction of theinfarcted and normal myocardium.


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Complete rupture of the left ventricular free wallusually leads to hemopericardium and cardiactamponade

sudden profound right heart failure and shock,often progressing rapidly to pulseless electricalactivity (electromechanical dissociation) anddeath.

Emergent pericardiocentesis Transthoracic echocardiography can further

confirm the diagnosis


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beta blockers, which are routinelyadministered to patients with an acute MI,

reduce the rate of death from free wallrupture compared to placebo fibrinolytic therapy early after MI improves

survival and decreases the risk of cardiacrupture

Mechanisms for the early mortality reduction produced by beta-blockade started earlyin acute myocardial infarction: ISIS-1. ISIS-1 (First International Study of Infarct Survival)

Collaborative Group. Lancet. 1988;1(8591):921.


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The frequency of septal rupture has beenreported to be about half that of free wallrupture.

It typically occurs three to five days after anacute MI. It may, however, develop within thefirst 24 hours or as late as two weeks.

Risk factors An increased risk of septal rupturemay observed in patients with single-vesseldisease (especially the left anterior descendingartery), extensive myocardial damage, and poorseptal collateral circulation.


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precipitous onset of hemodynamic compromise

hypotension,

biventricular failure (often predominantly right-sidedfailure)

new murmur. The murmur is harsh, loud, andholosystolic, and is heard best at the lower left and

usually right sternal borders, with occasionallywidespread radiation. In some cases, the murmur isheard best at the apex and may be mistaken for acutemitral regurgitation.


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Confirmation of the diagnosis usuallyrequires insertion of a pulmonary artery

balloon catheter to document the left-to-right shunt The defect can also be diagnosed by two-

dimensional transthoracic echocardiographywith color flow Doppler imaging


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The 2004 American College ofCardiology/American Heart Association

(ACC/AHA) guidelines on ST elevation MI andon CABG recommended emergent surgery,with coronary artery bypass grafting (CABG)if indicated, for these mechanicalcomplications of an acute MI [2,3]. Nochanges to this approach were made in the2007 ACC/AHA focused update [4].
http://www.uptodate.com/contents/mechanical-complications-of-acute-myocardial-infarction/abstract/2,3http://www.uptodate.com/contents/mechanical-complications-of-acute-myocardial-infarction/abstract/4http://www.uptodate.com/contents/mechanical-complications-of-acute-myocardial-infarction/abstract/4http://www.uptodate.com/contents/mechanical-complications-of-acute-myocardial-infarction/abstract/2,3


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Medical therapy aimed at hemodynamicstabilization should also be instituted.

fluids, inotropic support,

vasopressors,

pericardiocentesis, intraaortic-balloon pump counterpulsation,

and percutaneous cardiopulmonary bypass (if

available and necessary)


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ischemic papillary muscle displacement orrupture

Some patients with moderate to severe MR(but without papillary muscle rupture) arehemodynamically stable. Many such patientsimprove with medical therapy and

revascularization (by fibrinolysis or primaryangioplasty); a minority will eventuallyrequire mitral valve repair or replacementwith coronary artery bypass grafting


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Papillary muscle rupture is a life-threatening complication of acute MI

usually occurs two to seven days after theinfarct Papillary muscle rupture occurs in both ST

elevation and non-ST elevation infarcts. Risk factors: prolonged admission delay

beyond 24 hours and recurrent anginal painbefore or during hospitalization


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The clinical manifestations of papillarymuscle rupture include the acute onset of

hypotension and pulmonary edema with ahyperactive precordium and a mid-, late-, orholosystolic murmur that may havewidespread radiation. Although the murmurmay be loud, a thrill is generally not present.


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Usually anterior wall MI ant wall/ apex

Affected myocardium

infarct expansion/thinning and fibrosis

involved wall segment is either akinetic(without movement) or dyskinetic (withparadoxical ballooning) during systole


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Cardiac enlargement with a diffuse apicalimpulse that is displaced to the left of the

midclavicular line. A third and/or fourth heart sound is often

heard, indicating blood flow into a dilatedand stiffened left ventricular chamber.

A systolic murmur of mitral regurgitationmay be appreciated


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Heart failure and angina

Ventricular arrhythmias, which can lead tosudden cardiac death

Systemic embolization

Ventricular rupture LVAs may enlarge overtime but rarely rupture


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Treatment of an LVA consists of medicaltherapy of the complications that can occur

and consideration of aneurysmectomy.

Small to moderate size asymptomaticaneurysms can be safely treated medically

ACE I, antiischemic medications for angina, andanticoagulation if there is significant LV

dysfunction or evidence of thrombus


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The 2004 American College ofCardiology/American Heart Association(ACC/AHA) guidelines on ST elevation MIconcluded that it is reasonable (class IIarecommendation) to consideraneurysmectomy, accompanied by CABG, in

patients with an LVA who have intractableventricular arrhythmias and/or heart failureunresponsive to medical and catheter-basedtherapy


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A left ventricular pseudoaneurysm or falseaneurysm forms when cardiac rupture is

contained by adherent pericardium or scartissue. Unlike a true aneurysm, apseudoaneurysm contains no endocardium ormyocardium.

The diagnosis needs to be established early,since these aneurysms are prone to rupture


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Chest pain, SOB, murmur

Echocardiography can usually distinguish apseudoaneurysm from a true aneurysm bythe appearance of the connection betweenthe aneurysm and ventricular cavity

Surgery is the preferred therapeutic option.


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Early infarct-associated pericarditis (oftentermed peri-infarction pericarditis)

Pericardial effusion (with or withouttamponade) Postcardiac injury (Dressler's) syndrome


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Acute pericarditis, detected by thepericardial friction rub with or without chest

discomfort usually occurs soon after the MI and is

transient. strongly associated with larger infarct size, as

manifested by higher creatine kinase andtroponin levels, lower ejection fraction, morefrequent anterior location of the MI


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The ECG changes seen with other forms ofpericarditis are usually overshadowed by thechanges due to the myocardial infarction.

However, ST segments that remain elevated,with persistence of upright T waves, maysuggest PIP

Echocardiography should be performed inpatients suspected of having PIP to evaluatefor the presence of a pericardial effusion


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The treatment of PIP is generallysupportive as most cases are self-limited.

treatment with routine anti-inflammatorytherapy is generally avoided

Do antiplatelets promote the development of

a hemorrhagic pericardial effusion in patientswith PIP?

Do not alter antiplatelet or anticoagulationtherapy in most patients with PIP


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The 2004 ACC/AHA guidelines recommendaspirin as the preferred agent for thetreatment of PIP, noting that doses as high as

650 mg every four to six hours may beneeded

Other agents considered reasonable (class IIa

recommendation) by the ACC/AHA guidelinesincluded colchicine (0.6 mg every 12 hours)and acetaminophen (500 mg every six hours)
http://www.uptodate.com/contents/colchicine-drug-information?source=see_linkhttp://www.uptodate.com/contents/acetaminophen-paracetamol-drug-information?source=see_linkhttp://www.uptodate.com/contents/acetaminophen-paracetamol-drug-information?source=see_linkhttp://www.uptodate.com/contents/colchicine-drug-information?source=see_link


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monitor the size of the pericardial effusion andthe patients hemodynamic status to assess forsigns of cardiac tamponade

Anticoagulation - a large effusion or earlytamponade requires consideration of lessaggressive treatment.

Guidelines recommended that anticoagulationshould be immediately discontinued if a

pericardial effusion develops or increases.


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A 2004 European Society of Cardiology (ESC)task force recommended ibuprofen as thetreatment of choice for PIP

Anti-inflammatory agents have been shownto lead to scar thinning and infarct expansion 2004 ACC/AHA guidelines gave class IIb

recommendations (usefulness or efficacy is

less well established) to corticosteroids ornon-steroidal anti-inflammatory agents inthis setting, while a class III indication (maybe harmful) was given to ibuprofen
http://www.uptodate.com/contents/ibuprofen-drug-information?source=see_linkhttp://www.uptodate.com/contents/ibuprofen-drug-information?source=see_linkhttp://www.uptodate.com/contents/ibuprofen-drug-information?source=see_linkhttp://www.uptodate.com/contents/ibuprofen-drug-information?source=see_link


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The postcardiac injury syndrome (PCIS) hasalso been called Dressler's syndrome

It is not limited to patients with MI, alsooccurring in other settings, particularly aftercardiac surgery or pulmonary embolism.


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It is usually a late complication, developingweeks to months after the acute MI, but

rarely may be evident within the first weekpost-MI. The clinical manifestations include pleuritic

chest pain, a pericardial friction rub, fever,

leukocytosis, and sometimes pleural effusionor pulmonary infiltrates.


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Immunologic factors are thought to be ofprimary importance in PCIS.

myocardial injury releases cardiac antigens

stimulates antibody formation.

immune complexes deposit onto thepericardium, pleura, and lungs

eliciting an inflammatory response.


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ESR

Symptoms of post-MI PCIS generally resolveafter the administration of a nonsteroidalanti-inflammatory drug (NSAID).Corticosteroids may be required in refractory

cases but could delay myocardial healing


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Mechanical, inflammatory, ischemiccomplications

Warning signs: Haemodynamic compromise,

New murmur, Friction rub, recurrent CP/SOB Look out in anterior wall mi Surgical and medical mx

Early- rupture, pericarditis,effusion/tamponade Late- dresslersNSAIDs, steroids PseudoaneurysmSurgery


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For references please see me, most wereRCTs with a few observational studies.

Complications of Myocardial Infarction and their mx.pptx

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