Acute pulmonary edema: Come’on let us blame it on Right ventricle
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Basic science lessons are promptly forgotten by the time we reach the final year of medical school. How about recalling them decades into clinical practice ? The mechanism of systemic edema revolves around the interplay between hydrostatic pressure, colloid pressure, interstitial pressure. However, In the pulmonary circuit, it gets a little more complex. Acute pulmonary edema begins to occur at around 18mmhg PCWP. What is special about this number 18? Nothing great. The lung begins to ooze when the LVEDP/LA mean pressure exceeds the colloid osmotic pressure, (that keeps fluid in situ) within the pulmonary capillaries, which is about 18mmhg. Interstitial fluid begins to collect as the basal rales go onto develop frank alveolar edema at 25mmhg. Of course, chronic situations like mitral stenosis both lymphatic reserve and thickened interstitial fibrotic process keep threshold still higher)
To simplify, whatever be the mechanism on the left heart, during acute pulmonary edema for the lungs to get flooded, we need a well-functioning right ventricle. If only the RV has enough wisdom*, it should take the cue and slow down and help the LV out by reducing its preload. (RV’s afterload is LV’s preload right )
We know, the lungs are protected from congestion in a number of chronic right ventricular diseases, pericardial disorders, severe PH. This happens in RV infarction. This lung-protective effect might explain the heterogeneous nature of outcome in RVMI (bad to excellent)
Final message
We know, the commonest cause of pulmonary edema is due to acute LVF. Now add one more mechanism in the genesis/and or maintenance of pulmonary edema. Vigorously contracting, RV is equally culpable.
Here is an Important paper that discusses the key role of RV in the precipitation of acute pulmonary edema.
Some more questions relevant to this topic
1.What is the effect of RV dysfunction on paroxysmal nocturnal dyspnea & orthopnea?
2.Explain class 3 Forrester’s hemodynamic grading of acute MI. (Why PCWP goes down in grade 3 compared to grade 2?)
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