HEY GUYS! In this video, I will be going over Right Ventricular Myocardial Infarction in great detail. I will explain pathophysiology, clinical manifestations, EKG findings and management with the use animation. I really hope you guys will enjoy it :-)
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Anatomy of Right ventricle and its blood supply -
Coronary blood - RCA and LCA.
LCA is divided into LAD and circumflex.
RCA divides into right marginal arteries and posterior descending artery.
Marginal supply the RV and posterior supplies the posterior left ventricle
Right ventricular myocardial infarction is a rare event. It is associated with about 30-50% of inferior wall MI and inferior wall MI accounts for about 40% of all myocardial infarctions. You guys might be wandering as to why we are going over this if it occurs rarely. Well the reason for that is that RVMI is associated with high in hospital morbidity and mortality due to its profound hemodynamic and electrical complications, but long term prognosis is generally good as long as the patient survives the acute event. So our main goal is to recognize this pathology and get the patient thru the acute phase.
Now let me explain why acutely RV can be devastating but there is a long term prognosis.
There are 3 factors that decrease the chances of developing infarction in RV
1. Oxygen demand is significantly lower as compare to LV
2. If there is NO right ventricular hypertrophy then the coronary perfusion occurs in both during the systolic and diastolic phase, whereas in the LV it only happens during diastole. This is because the intramural vessels get compressed when the cardiac muscles contracts during systole. Rv gets blood flow thru out the cardiac cycle.
3. Extensive collateral. RV gets perfusion from RCA and the LAD.
Why is RVMI devastating acutely?
Ischemia of the RV causes it to lose its contractility and it becomes very stiff. Because of that it doesnt effectively dilate or contract -- decreases both the preload and afterload -- decrease LV output and decrease peripheral perfusion even if LV is intact.
RV is heavily reliant on the inter-ventricular septum to pump the blood so if the affected patient has hx of a pathology that decreases LV systolic function then that would affect RV function esp during an acute MI
Secondly if the lesion is very proximal to the origin of the RCA then both the RA and RV. If RA is involved that it will also become stiff and lose contractility further decreasing amount of blood being pumped into the circulation.
Thirdly, if the ischemia specifically affects the papillary muscles attached to the tricuspid valve then it rupture and result in severe TR. This will further decrease output from the the RV because some of it will go to the lungs and other back into he right atrium
Lastly, if there is a ventricular septal rupture then the patient will develop left to right shift severely reducing CO. On exam, if you notice that lungs are clear to auscultation but there is elevated JVD in the setting of hypotension then that should make suspicious of RVMI. Now the reason why lungs are clear is because there is no pulmonary congestion and thats why the elevated JVD.
Risk at developing bradyarrhythmias or tachyarrhythmias.
High risk of developing heart blocks.
Sinus bradycardia can also be seen and it may be secondary to Bezold-Jarisch Reflex
Bezold Jarisch reflex is an inhibitory reflex that when stimulated activates the parasymthatic NS and inhibits the sympathetic causing hypotension thru systemic vasodilation. It charactered by a triad of bradycardia, hypotension and apnea.
Hypotension and bradyarrhythmias are common in inferior and posterior wall MI
Lungs clear to auscultation + elevated JVD + hypotension = high suspicious for RVMI.
EKG
ST or T wave changes in leads II, III and aVF - warrants right sided leads to be performed
ST depression in lateral leads along with inferior wall MI
ST elevation is greater in lead III than II and the ST elevation in aVF is greater than ST depression in lead V2.
*Both V1 and V2 provide partial view of the right ventricular free wall.*
The most accurate finding is ST elevation of greater 1mm the V4R lead. It has 100% sensitivity, 87% specificity and 92% predictive accuracy.
Once you have a suspicion that patient might have RVMI then avoid giving diuretics, beta blocks, morphine and nitrates. These interventions will just further decrease the preload and result in hypotension. Mainstay of treatment should be increase preload and cardiac output thru resuscitation with IVF and pressers if needed, followed by PCI. These patients have good long term prognosis so we just need to get thru the acute phase effectively without any delays to give the patient best outcome possible.
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13 июл 2024
