The tie is between “B” and “D ”
We know in hypertensive hearts LV primarily fails in diastole . Lungs get congested due to raised LVEDP .Here is a catch . . . if diastole is terribly dysfunctional how can be systole be near normal ? (After all . . . systole is not a distant cousin of diastole !)
How is that high blood pressure maintained in spite of LV failure* ?
Is it due to well-preserved EF and cardiac Index ? or Is it due to extreme levels of peripheral sympathetic activity mediated by catecholamine surge triggered by LVF.
We have attempted to measure LVEF in patients with flash pulmonary edema and acute severe hypertension .It was a real messy echocardiography . We could not conclude much but one thing is clear in acute hypertensive LVF the LV was vigorously contracting in , probably making the option D more correct .
* The other way of reasoning is . . . it is because of high blood pressure the LVF has occurred . LV contractility has no contribution in maintaining the high BP ( Not in line with the age old concept of LV contractility a major determinant of systolic blood pressure !)
(Having said that . . . we also see patients with severe LV dysfunction with severely stunned , ventricles in association with hypertension and LVF . In fact many of the reversible DCMs are due to sudden surge in blood pressure )
Other mechansims of LVF and lung congestion is
- Extreme tachycardia and shortening of diastole
- Mitral regurgitation
- Assocaited CAD unmasked by sudden raaise in heart rate .
If this article has confused you a little , It has achieved one of it’s objective . ! I expect more from young cardiology fellows to address the issue !
This NEJM article authored by Sanjay Gandhi has almost answered the hemodynamics of acute LVF and HT .