Well, I give ASA for chest pain of a cardiac nature. Whilst I assess thoroughly and consider the whole spectrum of acute coronary syndrome from angina/UA/NSTEMI/STEMI, I do not have the ability to check cardiac markers to rule out infarct as opposed to angina. Therefore the risk/benefit ratio is clearly in favour of giving ASA. If we give it, and they are having an infarct, we have significantly impacted on mortality and morbidity in a positive manner. If we give it and they are not having an infarct, they have had an aspirin...
As for the BP question for acute pulmonary edema, I do not necessarily know the rationale your MD's may have had. I will hazard a guess though: In the later stages of acute cardiogenic pumonary edema there is significant myocardial dysfunction from a number of causes such as excess left ventricular end diastolic pressure (LVEDP) overwhelming the Frank-Starling mechanism, and then myocardial hypoxia. Whilst initially LV function is impaired, this impairment extends to the right ventricle. The RV is normally able to cope with hypoxia a lot better than the left ventricle as it is a low pressure system that requires less workload, and it is also able to enhance it's utilization of O2 in hypoxic states in a fashion that the LV is not capable of.
However as the hypoxia continues, there is an increase in pulmonary vascular pressure causing an increase in RVEDP which impairs right ventricular function, and there is also a limit to how well the RV will cope with prolonged hypoxia. The increased RVEDP also impinges upon the LV, which worsens LVF as well, incidently.
So, this then leads to a situation of right ventricular impairment, which of course renders the patient preload dependant to ensure adequate cardiac output. In this setting nitrates may cause a precipitous drop in blood pressure which then leaves you with a patient with pulmonary edema and cardiogenic shock: i.e. about as sick as you can get. They may then need inotropic support which is associated with poor outcomes from heart failure.
So, after all that, I suspect that possibly the higher BP for APE is to provide a safety buffer in this setting. Now, I'm not entirely sure that I agree with it, as APE at it's heart is a problem of hypertension causing maldistribution of fluid and we need to attack that hypertension vigorously.
What would perhaps be more applicable would be to look at both systolic and diastolic pressures. A very wide pulse pressure with a low diastolic pressure may indicate that the BP is being maintained by the last gasp of the sympathetic nervous system, in which case you would want to tread very carefully with nitrates for the above reasons.
I could of course be entirely wrong.
Anyone else have other thoughts?