Episode 59: Pulmonary HTN with Jochen Steppan

Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Episode 59: Pulmonary HTN with Jochen Steppan

In this episode, episode 59, I welcome international pulmonary hypertension expert Dr. Jochen Steppan to the show to discuss pulmonary hypertension and how to manage the preoperative care of patients with this disease.

Outline by Brian Park: Outline

7 Replies to “Episode 59: Pulmonary HTN with Jochen Steppan”

  1. Really enjoyed this one; my perspective is that of an ICU RN taking care of these patients… every surgical case usually a SWAN is placed; and just as it was stressed low fluid status is critical, if a higher SVR is noticed with low blood pressure we will often give 250 mL 12,5 g albumin; one thing I do notice is the CVP is not a good guide for fluid volume status and can even be elevated or normal in the setting of needing fluid. Also as mentioned vasopressin seems to be the best vasoactive drug of choice, neo seems to have a very bad effect on the cardiac index.

  2. Great talk on a fascinating topic.

    First comment is regarding managing pulmonary hypertension. The most common cause of PH and RV failure is left heart disease. Can you comment on the practice of using selective pulmonary vasodilator such as iNO in this setting? Would you recommend iNO empirically for PH +/- right heart failure without a right heart cath to determine the cause of PH. The increased RV output can cause elevated left heart filling pressure and pulmonary edema.

    Second comment is regarding systemic BP and RV failure. It has been shown that the LV contraction contributes to a significant RV output in the setting of RV failure through systolic interventricular dependence via the ventricular septum. Therefore it is very important to maintain normal systemic BP and LV contraction.

    Third comment is regarding fluid responsiveness and cvp. I think cvp still is an extremely important measurement to help us with managing volume status, especially in cardiac patients. In patients with PH and concerns for right heart failure, high cvp is a defining feature of RV failure. In a hypotensive patient with low cvp, in conjunction with other dynamic measures such as a elevated PPV, I think most of us would first restore the right heart filling pressure to at least upper end of normal and observe fluid responsiveness. A low cvp rules out RV failure and it’s safe to volume resuscitate, which in turn could unmask RV failure ( old study on patients with inferior MI ). On the other hand, in a hypotensive patient with high cvp ( high teens), I would be very cautious with fluid administration since RV failure is a possibility and an echo would be needed immediately to rule out other causes of high filling pressure that could be responsive to volume and other treatments such as tamponade, constriction, restriction etc. A high cvp with high PPV or SVV would again make me very cautious about giving volume since the underlying cause of high SVV, a marker for fluid responsiveness, could actually be RV failure/enlargement causing diastolic interventricular dependence and volume loading would obviously be detrimental and futile. Lastly I want to point out that JVD is a major criteria for diagnosing congestive heart failure in Framingham Criteria. I hope to emphasize the importance of cvp and the complex physiology behind this simple measurement and how it can guide us in specific settings.

    1. Great comments. Here are Dr. Steppan’s responses:

      Thank you very much for your kind words.

      Regarding your questions / comments:

      1) I would not use iNO or another inhaled pulmonary vasodilator EMPIRICALLY for all patients with class II PH – with or without a right heart catheter. The evidence for using iNO in patients with class II PH is slim. While there is an improvement in PA pressures in some patients it is not clear if that consistently translates in improved outcomes. Secondly the majority of patients with class II PH, while often suffering from significantly elevated PA pressures, tend to have fairly well compensated right ventricular function. I agree with you that an increased RV output could increase left heart preload but I am not convinced that this is clinically significant to push a patient into LV failure – though I have not hard data to back me up. At our institution, if a patient has significant left heart disease and maybe even significant lung disease and presents with elevated PAP without any other red flags that this might be due to class I PH, we do not pursue a right heart catheterization.

      2) I do agree with you 100%. The RV does “share” a wall with the LV – well, basically the RV is attached to the LV wall, and there is an intimate interventricular interdependence between the two chambers. Also an adequate systemic BP and LV function is essential for coronary perfusion of the RV – which can be tenuous in the case of RV hypertrophy and concomitant CAD.

      3) CVP continuous to be a topic of hot debate and clash of opinions. Please let me state from the outset that I am not trying to discount CVP as useless, or as shown in multiple studies as not having any predictive value for fluid responsiveness (though mostly in the ICU) – either as a single number nor a trend measurement. It does make intuit sense to follow CVP, especially in cardiac patients for the reasons you mentioned. In fact, I do follow CVPs in cardiac patients and in selected patients with severe PH myself. However, in my opinion, this is one of many measurements that are needed to establish a clinical diagnosis / suspicion and one parameter among many to follow treatment. For example the one you are mentioning below: PPV or SSV.
      In the example you are giving (In a hypotensive patient with low cvp, in conjunction with other dynamic measures such as an elevated PPV), I politely disagree with restoring “filling pressure to at least upper end of normal”. While careful administration of volume is justified, I would be cautious with increasing volume to a point that get you close to the upper limit as it becomes very easy to go beyond that point and drive the RV in overt failure due to volume overload and, though it sounds cliché, it is easier to give fluid than to take it out quickly. I also disagree that a low CVP rules out RV failure. In medicine, like so many places in live, it is dangerous to speak in absolutes. Yes, a low CVP makes RV failure unlikely, but it does not necessarily exclude it with all certainty – for example a patient with RV failure after bypass who is also vasoplegic can have a low CVP despite being in RV failure (same can be true for the hypovolemic patient in RV failure, or the one with concomitant LV failure). I do agree with your other example: ” in a hypotensive patient with high cvp ( high teens), I would be very cautious with fluid administration since RV failure is a possibility, as well as with your last point, of JVD being a major criteria in the Framingham Criteria.

      Thank you again for your critical response and passionate argument of the importance of CVP and the complex physiology it is connected to. My intention was not to discount CVP as useless or insignificant but rather to put into perspective that it is one measure and that we need to be cautious with making assumption solely based on one number.

  3. Thank you for your thorough discussion! My comment about restoring right heart filling pressure to upper end of normal is a bit of a simplification. We should always observe incremental changes to fluid resuscitation. In all honesty, it is really hard to accurately measure CVP within a few cm of H2O pressure and normal CVP is only 2-6 mmHg.

    Can I pick your brain on a perhaps more important point, what is your definition of RV failure? You mentioned that a vasoplegic or hypovolemic patient can have low CVP with concomitant RV failure after bypass. I assume that knowledge of RV failure is based on either echo, pre-op RV status, or visual examination of the RV. But isn’t RV failure, like heart failure, a clinical diagnosis and the commonly accepted definition is low RV output with a high CVP? (Although I have heard of high-output RV failure and that further emphasizes the term “failure” is a clinical diagnosis.) Many patients have reduced RV systolic function with dilation on echo but not all are in failure. To your point, they can be pushed into RV failure if too much volume is given or if RV encounters sudden increases in afterload. The point I was trying to make is that even in patients with structurally or functionally abnormal RV, if they are hypotensive, have low filling pressure due to the underlying disorder, and they are fluid responsive, then careful fluid resuscitation is still warranted. We were taught back in medical school to give fluid in inferior MI with RV failure to improve cardiac output and BP. Animal study showed the most supportive evidence. Studies done on humans with acute inferior MI and RV failure were less definitive. But the recommendation in this setting is still volume resuscitation toward a normal to mildly elevated CVP. An even more interesting scenario is patients with biventricular dysfunction in cardiogenic shock, for those of us who don’t have ECMO, which side needs support? Impella or impella RP or both? Measurements of CVP and wedge pressure are equally important in this setting.

    1. Per Dr. Steppan:

      My definition of RV failure: A clinical syndrome characterized by perfusion that is inadequate to meet the body’s metabolic demands as a result of impaired right ventricular function. As you mentioned that is difficult to establish directly in the OR, so we use surrogate markers such as mTAPSE on TEE (on example among many others).
      To clarify the point about fluid in your example. I was not saying to give no fluids, also I do agree that the patient you are mentioning does need fluid and should receive it. The point I was making is that one needs to be cautious about over-transfusing those patients and CVP should be one parameter among many to follow. As for the matter of using CVP, as you are stating yourself, animals studies do support it and it does make sense, but the data in humans is less strong and in the end it comes down to expert opinions on what appears to be the right thing to do. Expert opinions are exactly that – opinions. That does not mean they are wrong or unfounded, but they have less evidence behind them and not everyone will share them in every detail.
      Regarding your last point of biventricular dysfunction, in the absence of ECMO. Given that it is really biventricular failure, I would favor mechanical left ventricular support first, before using it on the right side – simply because it is more established and therefore easier to implement in most hands. So using an impella or an IABP would be my first choice. In most cases that should unload the LV, shift the septum back, reduce the congestion (decrease RV afterload), improve coronary blood flow (reduce RV ischemia), and increase RV preload. Only if that plus pharmacological support fails, would I consider right sided mechanical support.

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