Ashley, another nice job explaining the nearly inexplicable. Afterload always reminds me of Potter Stewart and his discussion of pornograhy. “I shall not attempt to further define it, but I know it when I see it”.
One thing that has puzzled me for a while: where do you think dynamic arterial elastance fits into the afterload description you have provided?
Thanks Jan. It’s clever, but it is trying to infer a clinically useful response from a ratio of two respiratory percentage variations, neither of which is MAP, and then use that to predict whether a later, sustained increase in stroke volume will raise MAP. That is quite a long inferential chain!
Mechanistically, it does not give you a clean physical variable like resistance, compliance or wall stress. It gives you a dynamic pressure–flow coupling descriptor whose value depends on several interacting arterial and ventricular factors, and whose clinical meaning comes more from observed prediction than from a single clear mechanism.
So I would not build much bedside reasoning around it. It may be useful as a predictor in selected patients, but for me it is more complicated than physiologically illuminating.
Ashley, another nice job explaining the nearly inexplicable. Afterload always reminds me of Potter Stewart and his discussion of pornograhy. “I shall not attempt to further define it, but I know it when I see it”.
One thing that has puzzled me for a while: where do you think dynamic arterial elastance fits into the afterload description you have provided?
Thanks again
Thanks Jan. It’s clever, but it is trying to infer a clinically useful response from a ratio of two respiratory percentage variations, neither of which is MAP, and then use that to predict whether a later, sustained increase in stroke volume will raise MAP. That is quite a long inferential chain!
Mechanistically, it does not give you a clean physical variable like resistance, compliance or wall stress. It gives you a dynamic pressure–flow coupling descriptor whose value depends on several interacting arterial and ventricular factors, and whose clinical meaning comes more from observed prediction than from a single clear mechanism.
So I would not build much bedside reasoning around it. It may be useful as a predictor in selected patients, but for me it is more complicated than physiologically illuminating.