Cardiac failure in pregnancy is a common enough reason for ICU admission, and is worth knowing about for exam purposes as well as in real life terms. Very likely neither the obstetrician nor the cardiologist get as much exposure to this condition as the intensivist is going to get during their career. As the most interesting part of peripartum cardiomyopathy is its association with pregnancy, this chapter got shoved into the O&G section (whereas the cardiomyopathy aspect of it is a fairly boring one, and generic with a lot of other management of heart failure).
Though rarely, this does tend to come up in the exams. Question 28 from the first paper of 2017 asked specifically for diagnostic ciriteria of peripartum cardiomyopathy, which are discussed below. Question 16 from the second paper of 2010 asked specifically for pregnancy-associated causes of left and right heart failure in pregnancy, which was tricky because not all of the possible causes of heart failure in pregnancy are related to the pregnancy itself. For instance, a fair proportion of girls with congenital heart disease are cared for so well these days that they grow up into women, and then go on to get pregnant. The college answer to that question actually cheated by including such things as PE, which is not a strictly pregnancy-associated issue - but is common enough to warrant discussion in this context. Lastly, Question 15 from the second paper of 2021 asked about how one might go about managing these pregnancy-associated cardiac failure states. A brief discussion of the important issues is offered below. Wherever possible, juicyness of detail was sacrificed to brevity and precision.
This works best as a table. In fact, in Sliwa et al (2010) there is an even better table (Table 3. p.772)
Question 28 from the first paper of 2017 asked for a specific definition of this disease, which is weird because it does not seem to have a widely agreed-upon definition. The ESC statement from 2010 (Sliwa et al) offers the following criteria for diagnosis:
Is this meaningful? Of course not. The pragmatic intensivist would spit with derision at the very idea. There are no specific treatments to offer, for PPCM or for most other aetiologies of acute heart failure; and the non-specific management is exactly the same for all of them. So what does it matter what the diagnosis is?
Well, it certainly matters when 30% of a CICM SAQ asks you to "list the diagnostic criteria for peri-partum cardiomyopathy". The college answer to this question is available, and is therefore canonic - the definitive diagnostic criteria, no matter what the wold literature says. These diagnostic criteria are as follows:
"This level of detail not expected", the college allows generously at their end of their ultra-detailed highly specific answer. So, that is fine. But where did they get their details from? Well. If the candidate selects their entire LV echocardiographic criteria and uses it as a Google search string, several prominent textbooks of cardiology pop up. One such book is Volume 1 of Management of Heart Failure by Baliga and Haas. In fact there one may find the college answer in completely unchanged verbatim copy. Unlike the college answer, Baliga and Haas use responsible referencing, and offer us an explanation as to where these criteria came from. They were concocted by a panel of fourteen experts during a conference workshop (Pearson et al, 2000).
In actual fact there are several competing definitions, of which the abovementioned one is probably the least vague. Observe (from the same article):
Characteristic features of peripartum cardiomyopathy (also from Sliwa et al):
Pathophysiology? Who the hell knows. Certainly not these guys. Possibilities which have been considered:
Management is same as you would manage acute heart failure from any cause:
A large selection of the drugs which you would normally use are contraindicated during pregnancy, for example:
Experimental techniques specific to PPCM:
Specific issues in PPCM:
Pisani et al (1988) desribe this condition which is fairly rare these days. In the 1980s, tocolytic therapies had consisted of beta-agonists such as terbutaline, isoxsuprine, ritodrine, and salbutamol. Pregnant women develop pulmonary oedema in association with the use of these agents, whereas non-pregnant women do not. This is because of several factors (see this discussion by R.F Lamont, 2000), some of which change the variables of the Starling equation:
Predictably, management consists of stopping the offensive tocolytic agent, or - like most modern O&G services - by eschewing the use of these primitive methods. In this day's kingdom of reason, we prefer to use nifedipine.