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I'm not asking a question here. Just posting something I think brings many key concepts to Step 1.
http://circ.ahajournals.org/content/50/4/678.full.pdf
An article discussing left ventricular function following acute myocardial infarction. Increased end-phase, intra-chamber pressures reflect the cardiogenic dysfunction (with or without ensuing shock) accompanied by increase in PCWP (LA pressure). I'd say the increased PCWP in the setting of post-MI cardiogenic dysfunction is a salient point, as this is the basis for augmented pulmonary venular and capillary pressures, with resultant transudation and pulmonary oedema. Heart rate may increase considerably following acute MI (unless we want to get technical and consider brady in the context of RCA and nodal infarcts), which would lead one to consider that end-diastolic pressures should ebb secondary to decreased filling times. But the reduced myocardial contractility will cause stasis and increased PCWP despite the lesser time spent in diastole.
http://circ.ahajournals.org/content/50/4/678.full.pdf
An article discussing left ventricular function following acute myocardial infarction. Increased end-phase, intra-chamber pressures reflect the cardiogenic dysfunction (with or without ensuing shock) accompanied by increase in PCWP (LA pressure). I'd say the increased PCWP in the setting of post-MI cardiogenic dysfunction is a salient point, as this is the basis for augmented pulmonary venular and capillary pressures, with resultant transudation and pulmonary oedema. Heart rate may increase considerably following acute MI (unless we want to get technical and consider brady in the context of RCA and nodal infarcts), which would lead one to consider that end-diastolic pressures should ebb secondary to decreased filling times. But the reduced myocardial contractility will cause stasis and increased PCWP despite the lesser time spent in diastole.
