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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/2,37/27/2019 Complications of Myocardial Infarction and their mx.pptx
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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_link7/27/2019 Complications of Myocardial Infarction and their mx.pptx
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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_link7/27/2019 Complications of Myocardial Infarction and their mx.pptx
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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.
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