Mi Complications[1]

8/3/2019 Mi Complications[1]

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HPI

Male Pt 77yrs withoutprior history of heartdisease

Presented to ER C/O SOB for one day whichbecame progressive and on presentation to ERhe required intubation


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History

Emphysema, on OTC Primatene

Rt Knee surgery

No DM, HTN or CA MEDS: Primatene

Social Hx: Smoker


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Physical Exam

B/P 90/70 Pulse 115 Diaphoretic, intubated

HEENT: unremarkable

Neck: supple, no JVD

Ht: RRR S1S2 audible, no murmurs or gallops

Lungs: CTAs (anteriorly and laterally)

Abdomen: Soft, non tender without organomegally

Ex: No edema +PP

Neuro: No apparent focal deficits


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Labs

TCPK: 307, CKMB: 35.5, CK Index: 11.6 Troponin I:28.7

HGB: 13.6, HCT:43, WBC 4.56, Plat: 334

Gluc: 152, Cr 2.0, BUN 118, Na 129, K 5.0, Cl 100CO2 19

ABGs: 7.12/61/385/99.9 IMV,100%,750,12


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EKG


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Cardiac Cath

Mid LCX 70%---0% stent

LAD 80%---5% stent

OM2 99%---0% stent RCA 100% Chronic occlusion?

Pt in Cardiogenic Shock---IABP placed


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Complications of MI

Ischemic Complications

Hypotension

Cardiogenic ShockAneurism formation

Mural Thrombus

Papillary muscle ruptureAcute Mitral Regurgiation


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Ischemic Complications

Reocclusion of the IRA (infarct related artery)not always symptomatic due to development ofcollaterals

Therapy:ASA, heparin, IIBIIIa inhibitor, nitrates, beta

blockers for ongoing ischemic symptoms

Balloon pump for patients with severe hemodynamicinstability

Revascularization


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Hypotension

Hypovolemia

Nitrate induced vasodilitation

Reduced LV filling due to RV infarction Reduced LV contraction due to extensive

myocardial injury or mechanical complications


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Cardiogenic Shock

Characterized byhypotension, tachycardia,reduced urine output, mental confusion,diaphoresis, and cold extremities, has a mortality

of >= 65% Most often associated with massive anterior

infarction and > 50% loss of LV functioning

myocardium May be associated with IMI with RV

involvement


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Cardiogenic Shock - Treatment

Identify and treat underlying cause if possible

RV Infarction: push fluids

Hypovolemia: optimize Starling

Ongoing ischemia: PCI or CABG

Mechanical Complications: consider IABP andconsider surgical intervention


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Myocardial rupture

Occurs in three forms:

ventricular septal rupture

papillary muscle rupture free wall rupture


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Papillary Muscle Rupture

Mild to moderate MR found in 13-45% of patients afterMI

Reduced incidence in post-thrombolytic era, howevernow occurs earlier

Day 2-7 in pre-thrombolytic era

Median time to papillary rupture 13 hrs in SHOCK TrialRegistry

Contributes to 5% of total mortality


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Most often associated with aninferiorinfarct

due to right coronary artery occlusion.

Posteromedial papillary muscle generallyperfused by PDA

It produces acute, severe mitral regurgitation

and is characterized by the sudden appearanceof a loud apical systolic murmur and thrill,usually with pulmonary edema.


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Diagnosis:

Exam: sudden appearance of a loud apical systolicmurmur and thrill, usually with pulmonary edema

ECG: Recent inferior of posterior MI

CXR: Focal pulmonary edema (right upper lobe)

Echo: Frequent finding of severe MR, often with

flair posterior leaflet Hemodynamic monitoring: large v-wave


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Therapy:

Aggressive medical treatment while surgery is beingconsidered

Vasodilators (nitroprusside)

Intra-aortic balloon pump

Definitive treatment: Surgery


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Ventricular Septal Rupture

It is rare, but 8 to 10 times more common than ruptureof the papillary muscle

Incidence significantly reduced in post thrombolytic era

Increased incidence in:

Older

Female

Hypertension

Non-smokers

Anterior infarction


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Diagnosis: Bedside: New onset of loud, harsh holosystolic

murmur at left lower sternal border. Thrill presentin 50%

ECG: AV nodal and infranodal conductionabnormalities

Echo with color doppler:


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Treatment: Early surgical closure is preferred treatment

Medical treatment associated with 72 hr mortality of

24% and 3 week mortality of 75% Intensive medical treatment before surgery

should include:

Intra-aortic balloon pumpVasodilators with hemodynamic monitoring


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Free Wall Rupture

Occurs in 3% of MI patients and responsible for10% of mortality after MI

Increasing incidence associated with

Advanced age

Female gender

Hypertension

First MI

Poor collateral vessels


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Free Wall Rupture

Diagnosis:

It is characterized by sudden loss of arterial pressurewith momentary persistence of sinus rhythm and

often by signs of cardiac tamponade If contained rupture course may be more subacute

Bedside: JVD, reduced heart sounds, pericardialfriction rub, new to-and-frow murmur

Only therapy is emergent surgery

Usually fatal


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Pseudoaneurysm

Rupture of the free LV wall in which ananeurysmal wall containing clot and pericardiumprevent exsanguination. AKA contained free

wall rupture

May be clinically silent and diagnosed duringroutine investigation

Treatment: Since spontaneous rupture mayoccur without warning, surgery is recommended


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Mural Thombosis

Occurs in about 20% of acute MI patients(60% of patients with large anterior infarcts).

Systemic embolism occurs in about 10% ofpatients with LV thrombus (best diagnosedby echocardiography);

Risk is highest in the first 10 days but persists

at least 3 mo.


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Pericarditis

May cause a pericardial friction rub in about 1/3of patients with acute transmural MI.

The friction rub usually begins 24 to 96 h after

MI onset. Earlier onset is unusual and suggests other diagnoses (eg, acute

pericarditis), although hemorrhagic pericarditis occasionally complicatesthe early phase of MI.

Acute tamponade is rareAssociated with larger infarctions and worse

prognosis


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Dresslers Syndrome

Develops in a few patients days to weeks oreven months after acute MI, although the incidenceappears to have declined in recent years.

Characterized by:

fever pericarditis with friction rub

pericardial effusion

Pleurisy pleural effusions

pulmonary infiltrates

joint pains.


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RV Infarction

RV involvement occurs in 40% of inferior orinferoposterior MIs

Degree of RV involvement dependent upon: Proximal location of occlusion in RCA Presence of collaterals from left coronary artery

Diagnositic Triad:

Hypotension Elevated jugular pressure

Clear lungs


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RV Infarction

Diagnosis:

RV Leads on ECG

Echocardiography is definitive test and is useful in

ruling out cardiac tamponade

Hemodynamic monitoring:

High right atrial pressure

Low PCWP


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RV Infarction

Treatment:

Volume loading to incrase LV preload (often withhemodynamic monitoring)

Inotropic agents if volume not enough

Reperfusion therapy

Consider RV assist device

Course: most patients spontaneously improvewithin 48-72 hrs

Mi Complications[1]

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