mi complications[1]
TRANSCRIPT
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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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Papillary Muscle Rupture
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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Papillary Muscle Rupture
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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Papillary Muscle Rupture
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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Ventricular Septal Rupture
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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Ventricular Septal Rupture
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