RV Infarction



RV Infarction

Epidemiology

-Occurs in nearly half of all IMI

-3% of all MIs result in isolated RV infarctions, but may result in considerable morbidity

RV Physiology

-The RV has same cardiac output as LV, but 1/6 muscle mass; PVR lateral wall

-PDA -> posterior wall/septum

-conus artery -> anterior wall

Pathogenesis

-RV infarct occurs when occ RCA prox to acute marginals or LCx if left dominant

-Only half of all occ prox acute marg result in RV involvement (better collaterals, O2 delivery)

-Often associated with LV infarction (14-84%)

Pathophys of RV Infarcts

-Reduction of RVSP, LVEDV, CO, Ao pressure, equalization RV/LV diastolic Pressures

-Severity depends on extent of infarct and restraining effect of pericardium/interaction c LV

-LV septal contraction that bulges into RV generates systolic force sufficient pulm perfusion

-Augmented atrial contractility overcomes RV stiffnes

-Diminution of preload (diuretics/nitrates) or AV synchrony -> profound hemodynamic effects

Diagnosis

-Accurate dx important because management differs from LV infarction

-Suspicion warranted in inferior MIs

-On PE, clinical triad: hypotension, clear lungs, elevated JVP ( nearly pathognomonic)

-Hemodynamics – RA pressure > 10mm Hg and within 1-5mm Hg PCWP

-EKG – 1mm STE in V4R: 70% sensitive, 100% specific

-Echo – RV dilatation, RV wall asynergy, abnormal interventricular septal motion

Complications

-Shock is most serious complication

-High degree heart block – poor prognosis, found in 48% pts

-Atrial fib in 1/3, possibly 2/2 atrial infarction or RA dilatation

-Increased incidence of VT/VF

-VSD, RV thrombus formation, TR, pericarditis

Treatment

-Early maintenance of RV preload, reduction of RV afterload

-Inotropic support of dysfunctional RV

-Early reperfusion

-Diuretics/Nitrates may produce severe hypotension

-Volume loading several liters initial first step, dobutamine if CO fails to improve

-AV synchrony is essential; consider cardioversion of afib early if hemodynamic compromise

-“Unloading” LV with afterload reduction may be beneficial if LV dysfn also present (IABP)

Prognosis

- In-hosptial mortality up to 31% vs. 6% for IMI without RV infarction

-In vast majority survivors, RV dysfunction returns to normal, hemodynamics return to normal

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