ACT RAPID

Arrhythmias Congestive Heart Failure Tamponade / Thromboembolic disorder Rupture (Ventricle, septum, papillary muscle) Aneurysm (Ventricle) Pericarditis Infection Death / Dresslers Syndrome

Common post mi Blocks, atrial/ ventricular arrhythmias If the arrhythmia precipitates hemodynamic compromise tx aggressively Address exacerbating conditions Electrolytes, Hypoxia, acidosis, drug effects

1. 2. 3. 4. 5. 6. 7. 8. 9.

VFib Sustained VTach PVCs / nonsustained VTach Accelerated idioventricular rhythm AFib/Flutter SVT PACs Need for pacing Sinus bradycardia

VFib defibrillate, reduce ischemia and adrenergic stimulation (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

PVCs or nonsustained, and stable no rx

Historically a warning sign for arrhythmia, but

since B-blocker, ACEI and reperfusion, this is not true.

Accelerated idioventricular rhythm slow VT. If stable, no rx.

Atrial Fibrillation/Flutter often occurs 2/2 ischemia

Unstable cardioversion, and if not effective use

IV amio or IV dig (in severe LV dysfxn) Stable but ischemic B-block, CCB (dilt, verapamil), cardioversion Stable, no ischemia rate control + anticoagulation

Reentrant supraventricular tachycardia carotid massage, adenosine, IV B-blocker, IV CCB, IV digoxin PACs no rx

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

Sinus bradycardia treat with atropine (0.61mg) if

Pause > 3sec

HR < 40 with symptoms

If still brady, need temporary pacing

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.

 rupture of the left ventricular free

wall; rupture of the interventricular septum; and the development of mitral regurgitation. Aneurysm of LV
J Am Coll Cardiol. 1998;32(1):135.

Acute or subacute myocardial rupture is a serious and often lethal complication of STEMI Increased risk:
No history of previous angina or MI ST-segment elevation or Q wave development on

the 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

Myocardial rupture occurs within the first five days 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 commonly affects the anterior and lateral walls of the left ventricle near the junction of the infarcted and normal myocardium.

Complete rupture of the left ventricular free wall usually leads to hemopericardium and cardiac tamponade sudden profound right heart failure and shock, often progressing rapidly to pulseless electrical activity (electromechanical dissociation) and death. Emergent pericardiocentesis Transthoracic echocardiography can further confirm the diagnosis

beta blockers, which are routinely administered to patients with an acute MI, reduce the rate of death from free wall rupture compared to placebo fibrinolytic therapy early after MI improves survival and decreases the risk of cardiac rupture

Mechanisms for the early mortality reduction produced by beta-blockade started early in acute myocardial infarction: ISIS-1. ISIS-1 (First International Study of Infarct Survival) Collaborative Group. Lancet. 1988;1(8591):921.

The frequency of septal rupture has been reported to be about half that of free wall rupture. It typically occurs three to five days after an acute MI. It may, however, develop within the first 24 hours or as late as two weeks. Risk factors An increased risk of septal rupture may observed in patients with single-vessel disease (especially the left anterior descending artery), extensive myocardial damage, and poor septal collateral circulation.

precipitous onset of hemodynamic compromise

hypotension, biventricular failure (often predominantly right-sided

failure) new murmur. The murmur is harsh, loud, and holosystolic, and is heard best at the lower left and usually right sternal borders, with occasionally widespread radiation. In some cases, the murmur is heard best at the apex and may be mistaken for acute mitral regurgitation.

Confirmation of the diagnosis usually requires insertion of a pulmonary artery balloon catheter to document the left-toright shunt The defect can also be diagnosed by twodimensional transthoracic echocardiography with color flow Doppler imaging

The 2004 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on ST elevation MI and on CABG recommended emergent surgery, with coronary artery bypass grafting (CABG) if indicated, for these mechanical complications of an acute MI [2,3]. No changes to this approach were made in the 2007 ACC/AHA focused update [4].

Medical therapy aimed at hemodynamic stabilization should also be instituted.

fluids,

inotropic support,
vasopressors, pericardiocentesis, intraaortic-balloon pump counterpulsation, and percutaneous cardiopulmonary bypass (if

available and necessary)

ischemic papillary muscle displacement or rupture Some patients with moderate to severe MR (but without papillary muscle rupture) are hemodynamically stable. Many such patients improve with medical therapy and revascularization (by fibrinolysis or primary angioplasty); a minority will eventually require mitral valve repair or replacement with coronary artery bypass grafting

Papillary muscle rupture is a lifethreatening complication of acute MI usually occurs two to seven days after the infarct Papillary muscle rupture occurs in both ST elevation and non-ST elevation infarcts. Risk factors: prolonged admission delay beyond 24 hours and recurrent anginal pain before or during hospitalization

The clinical manifestations of papillary muscle rupture include the acute onset of hypotension and pulmonary edema with a hyperactive precordium and a mid-, late-, or holosystolic murmur that may have widespread radiation. Although the murmur may be loud, a thrill is generally not present.

Usually anterior wall MI ant wall/ apex

Affected myocardium infarct expansion/ thinning and fibrosis involved wall segment is either akinetic (without movement) or dyskinetic (with paradoxical ballooning) during systole

Cardiac enlargement with a diffuse apical impulse 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 dilated and stiffened left ventricular chamber. A systolic murmur of mitral regurgitation may be appreciated

Heart failure and angina

Ventricular arrhythmias, which can lead to sudden cardiac death Systemic embolization Ventricular rupture LVAs may enlarge over time but rarely rupture

Treatment of an LVA consists of medical therapy of the complications that can occur and consideration of aneurysmectomy.
Small to moderate size asymptomatic aneurysms can be safely treated medically
ACE I, antiischemic medications for angina, and

anticoagulation if there is significant LV dysfunction or evidence of thrombus

The 2004 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on ST elevation MI concluded that it is reasonable (class IIa recommendation) to consider aneurysmectomy, accompanied by CABG, in patients with an LVA who have intractable ventricular arrhythmias and/or heart failure unresponsive to medical and catheter-based therapy

A left ventricular pseudoaneurysm or false aneurysm forms when cardiac rupture is contained by adherent pericardium or scar tissue. Unlike a true aneurysm, a pseudoaneurysm contains no endocardium or myocardium. The diagnosis needs to be established early, since these aneurysms are prone to rupture

Chest pain, SOB, murmur

Echocardiography can usually distinguish a pseudoaneurysm from a true aneurysm by the appearance of the connection between the aneurysm and ventricular cavity Surgery is the preferred therapeutic option.

Early infarct-associated pericarditis (often termed peri-infarction pericarditis) Pericardial effusion (with or without tamponade) Postcardiac injury (Dressler's) syndrome

Acute pericarditis, detected by the pericardial 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 and troponin levels, lower ejection fraction, more frequent anterior location of the MI

The ECG changes seen with other forms of pericarditis are usually overshadowed by the changes due to the myocardial infarction.
However, ST segments that remain elevated, with persistence of upright T waves, may suggest PIP Echocardiography should be performed in patients suspected of having PIP to evaluate for the presence of a pericardial effusion

The treatment of PIP is generally supportive as most cases are self-limited. treatment with routine anti-inflammatory therapy is generally avoided Do antiplatelets promote the development of a hemorrhagic pericardial effusion in patients with PIP? Do not alter antiplatelet or anticoagulation therapy in most patients with PIP

The 2004 ACC/AHA guidelines recommend aspirin as the preferred agent for the treatment of PIP, noting that doses as high as 650 mg every four to six hours may be needed Other agents considered reasonable (class IIa recommendation) by the ACC/AHA guidelines included colchicine (0.6 mg every 12 hours) and acetaminophen (500 mg every six hours)

monitor the size of the pericardial effusion and the patients hemodynamic status to assess for signs of cardiac tamponade
Anticoagulation - a large effusion or early tamponade requires consideration of less aggressive treatment. Guidelines recommended that anticoagulation should be immediately discontinued if a pericardial effusion develops or increases.

A 2004 European Society of Cardiology (ESC) task force recommended ibuprofen as the treatment of choice for PIP Anti-inflammatory agents have been shown to lead to scar thinning and infarct expansion 2004 ACC/AHA guidelines gave class IIb recommendations (usefulness or efficacy is less well established) to corticosteroids or non-steroidal anti-inflammatory agents in this setting, while a class III indication (may be harmful) was given to ibuprofen

The postcardiac injury syndrome (PCIS) has also been called Dressler's syndrome It is not limited to patients with MI, also occurring in other settings, particularly after cardiac surgery or pulmonary embolism.

It is usually a late complication, developing weeks to months after the acute MI, but rarely may be evident within the first week post-MI. The clinical manifestations include pleuritic chest pain, a pericardial friction rub, fever, leukocytosis, and sometimes pleural effusion or pulmonary infiltrates.

Immunologic factors are thought to be of primary importance in PCIS. myocardial injury releases cardiac antigens stimulates antibody formation. immune complexes deposit onto the pericardium, pleura, and lungs eliciting an inflammatory response.

ESR
Symptoms of post-MI PCIS generally resolve after the administration of a nonsteroidal anti-inflammatory drug (NSAID). Corticosteroids may be required in refractory cases but could delay myocardial healing

Mechanical, inflammatory, ischemic complications 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 Pseudoaneurysm Surgery

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