SCCM Resource Library-Pharmacologic Therapy for Acute RV Failure

Video Transcription

Hi everyone, my name is Kayla Nichols. I'm a CVSEU pharmacist at Emory University Hospital in Atlanta, Georgia, and today I'm going to talk about pharmacological therapy for acute  RV failure. I have no disclosures to reveal. This slide highlights the difference in how both preload and afterload affect the ejection  fraction output of the right and the left ventricle. The left graph has the atrial pressure on the x-axis as a marker of preload for the ventricle, and the y-axis is measuring  the ejection fraction of the ventricle with the left and the right ventricle graphed. You can see that while preload improvement can drastically improve right ventricular  function, this also becomes easily saturated and maxed out in comparison to the left ventricle. This highlights why volume optimization is so important in right-sided heart failure  management, and it also highlights why giving volume to treat right-sided heart failure is often recommended but is really a simplification of the problem.  The second graph with the afterload of the ventricle on the x-axis and the ventricle's output on the y-axis again highlights that the right ventricle is much more sensitive  to changes in afterload than its left ventricle counterpart. Acute right-sided heart failure is characterized by acute RV dilation, which results in bowing  of the septum into the left ventricle. The bowing of the septum into the left ventricle  then impacts LV filling via ventricular interdependent effects, and then therefore reduces the cardiac  output of the left ventricle. Reduced left ventricle flow and the ventricle interdependent effect results in reduced RV forward flow. This reduces the perfusion of the RV, which  perfuses in both systole and diastole. And then lastly, this reduced forward flow in the LV and the RV results in elevated systemic venous pressures.  So this is the RV diagram. RV dilation limits RV filling and reduces RV forward flow, leading  to elevated systemic venous pressures. Afterload is the primary determinant of normal RV function,  and right ventricular adjunction fraction is inversely proportional to pulmonary artery pressure. Acute right-sided heart failure usually occurs because of either abruptly  increased RV afterload or decreased RV contractility, and our pharmacological targets optimization of these areas. Just like with left-sided heart failure, in  right-sided heart failure, we are optimizing our preload, our contractility, and our afterload.  How we think about these terms is slightly different because our location is different, right? Our perspective from the right ventricle is going to be slightly altered than from  the left ventricle, but conceptually, they're going to be similar. So first, we're going to optimize preload by managing our volume status, which is important for the reasons  that we showed demonstrated earlier on the graphs. Two, we're going to augment contractility,  and three, we're going to reduce our afterload, which will help us not only eject blood, but  restore perfusion to the right side, again, because it perfuses in both systole and diastole.  Before we can decide whether to give volume or remove volume, we have to be able to assess the volume status for the right ventricle. There are a couple of things we will be looking  at simultaneously, depending on our access and the values available to us. Frequently, our central venous pressure is used as a surrogate for volume status for the right ventricle,  but a point-of-care ultrasound or a bedside echo to assess the RV is probably the best place to start. Usually, if the problem is volume overload, you expect to see a septal  shift during diastole. If the problem is in pressure overload, you can see a septal shift during both systole and diastole. This can kind of help us identify where we are on  the preload graph that I demonstrated earlier. If we look at our bedside echo and CVP and decide that we are under-resuscitated, I'm going to recommend gentle volume replacement,  usually looking at volumes of like 500 cc over an hour, preferably with a crystal lid. People are going to email me after this and tell me that albumin is their resuscitation  fluid of choice and that normal saline hurts the kidneys, but I would like to highlight that albumin is normal saline with protein in it that costs 25 times more with only a  theoretical benefit via oncotic pressure without a demonstrated advantage in clinical trials.  If we decide we are volume overloaded, we can proceed with diuresis or with renal replacement therapy if the patient doesn't respond or cannot produce urine.  Loop diuretics are the mainstay of treatment, working in the loop of Henle to prevent the  reabsorption of sodium via the sodium potassium chloride pump. Water is going to follow sodium  and so stay in the urine and this increases our diuresis. Our loop diuretics will always be administered IV in this setting and they include furosemide or bumetanide, bumetanide  being 20 times more potent than IV furosemide as shown with our starting doses here. You see a peak effect at about a half hour and a duration of approximately two hours. Ethacrynic  acid can be utilized in the setting of a sulfamoyety allergy, understanding that the use of ethacrynic acid is going to be associated with a higher risk of adverse effects.  We can further augment diuresis with the administration of a thiazide diuretic, such as IV chlorothiazide,  which can overcome the compensation of sodium reabsorption seen in loop diuretic resistance and can also reduce hypernatremia caused by loop diuretics by the prevention of distal  reabsorption of sodium at the sodium chloride channel. You could also utilize an oral thiazide  diuretic, but in the setting of acute right-sided decompensation, I would recommend utilizing  IV so that you're not worried about absorption. Potassium-expiring diuretics can further augment  diuresis similarly by reducing any further sodium reabsorption and also reducing potassium loss.  Again, I would like to highlight that these are all in the oral and so you could be limited by absorption, especially if you have super edematous bowels. Lastly, we have carbonic  anhydrase inhibitors, such as IV acetazolamide, which can reduce the alkalosis that aggressive diuresis can cause. As we know, alkalosis can worsen pulmonary arterial hypertension,  and so this is something that we could really consider to augment our diuresis and reduce  our pulmonary vascular resistance, which would be representative of our afterload in the right-sided  heart failure. Next, we want to augment contractility. Again, conceptually, this is similar in treatment to left ventricular contractility augmentation.  We have our options as dobutamine, milrinone, and epinephrine as our kinotubes of choice.  Dobutamine is our beta-selective agent versus epinephrine, which tends to be beta-selective  at lower doses but does have alpha activity, and milrinone, of course, is our phosphodiesterase  3 inhibitor. All of these agents run the risk of arrhythmia, since they are stimulating the heart  to beat. I tend to think of milrinone as having a lesser risk of this than the other two, and a greater propensity for hypotension, especially in renal dysfunction, since this  is renally cleared. Another important point to think of is that epinephrine, especially at higher  doses, does have this alpha effect, and so, again, might increase your pulmonary vascular resistance.  So, again, just like with the left ventricle, we want to optimize the right ventricle's afterload,  which is represented by the pressure in the pulmonary vasculature. This is why I keep highlighting about effects on the pulmonary vascular resistance. We can do this with pulmonary  vasodilators, including inhaled epiprostanol and inhaled nitric oxide, with our goal to reduce the  pulmonary vascular resistance. Epiprostanol is an inhaled prostacyclin, and it is a strong  vasodilator of vascular beds. Nitric oxide is an inhaled and endogenous vasodilator, and so  inhaling it delivers it directly to our location of action in the pulmonary vasculature. Neither  has shown to be superior in the setting of acute right-sided heart failure, and so the choice of  this is usually of the intensivist, although it is important to note that nitric oxide is  traditionally more expensive. Another pharmacological method to improve afterload is to utilize  vasopressors that have as little effect on the pulmonary vascular resistance as possible. You'll  notice that I highlighted this with a selection of inotropes with epinephrine, and the same is  true with utilization of vasopressors. This is why vasopressin is frequently the vasopressor of choice  in these patients, because of its neutrality on pulmonary vascular resistance while it improves  systemic vascular resistance. This dosing that I've provided here for you is based off of the  VENX trial where they titrated it as a vasopressor in comparison to other sepsis dosing of vasopressin  where they have a fixed dose of 0.02 to 0.04 units per minute. In this dose, again, in the VENX trial,  we're looking at cardiac surgery patients. Part of our assessment of this acute decompensation  is evaluating for causes of the decompensation, and if the cause of acute right-sided heart failure  is from pulmonary embolism, then antifibrinolytic therapy may be indicated. Most physicians would  agree to administer TPA in the setting of a PE, especially if it was causing a right-sided  heart failure, but there is some controversy on the dosing and administration of this medication  if you have not yet reached the point of hemodynamic collapse, you know, as a massive PE.  The MOPIT trial looks at submassive PEs that received 50 milligrams of alteplase, given as 10 milligrams over 10 minutes, and then 40 milligrams over four hours, and they assessed  this with anticoagulation, the presence of heparin, in addition to the TPA versus heparin by itself.  They found that this reduced the risk of pulmonary hypertension at 28 months  for follow-up after submassive PE in comparison to the anticoagulation regimen alone.  The PATHOS trial was, again, assessing submassive PEs that were treated with weight-based  tenecteplase, which is a different fibrinolytic, and it was pushed over five to 10 seconds in conjunction with anticoagulation versus anticoagulation itself, and they reached  statistical significance in their composite outcome of death versus hemodynamic instability,  but it was mostly driven by hemodynamic instability, so they really didn't see a benefit from mortality, but it did have less patients that had hemodynamic collapse.  I provide these to you as a couple different options for dosing strategies, assuming that your patient has not yet entered hemodynamic collapse yet as a result of their obstruction,  and I would also like to acknowledge that if you start compressions and you decide to give  fibrinolytic, you need to give compressions for an additional 20 to 30 minutes  because you need to give time to give your alteplase or your fibrinolytic time to circulate  since the patient's entire circulatory system is collapsed and your compressions are their  circulatory system, so it's important to note that if you give this, you need to give it time  to circulate and to work, and then again, this is highlighting the dosing strategies for you.  This is a summary slide just to kind of highlight that this is the strategy that most places would  take in the setting of right-sided heart failure. This is from the anesthesia ACLS guidance for  right ventricular heart failure, and this again highlights all the same points that we just  reviewed. Note that the first is optimization of volume, the second step is in the inotropy, and our third step is reducing afterload. Before again, they decided to intervene with  mechanical circulatory support. All of this is to say, conceptually, optimization of the  right ventricle is similar to the left ventricle, and it just requires us to think about our preload  or contractility and our afterload from the perspective of the right side of the heart as  opposed to the left side of the heart, and then acknowledging the unique characteristics of the  right ventricle and how it tolerates shifts in preload and afterload in comparison to the left.  By optimizing our volume with diuretics, augmenting our contractility with inotropes, and reducing our afterload with pulmonary vasodilators and vasopressors selection that  is cognizant of the PVR to SVR ratio, we can work to prevent the RV death spiral. Thank you so much for your time and this opportunity.  I look forward to taking any questions that you may have.

Video Summary

In this video transcript, Kayla Nichols, a pharmacist, discusses pharmacological therapy for acute right ventricular (RV) failure. She explains the differences in preload and afterload between the right and left ventricles and highlights the importance of volume optimization in managing right-sided heart failure. She also discusses the use of medications to optimize preload, contractility, and afterload in the right ventricle. Nichols mentions the use of diuretics to manage volume status, inotropes to augment contractility, and vasodilators to reduce afterload. She also briefly discusses the use of antifibrinolytic therapy in the case of acute right-sided heart failure caused by pulmonary embolism. Overall, the goal is to optimize the right ventricle and prevent RV death spiral.

Asset Subtitle

Cardiovascular, Pharmacology, 2022

Asset Caption

Acute right ventricular (RV) failure is becoming more common in the ICU, especially in patients with acute respiratory distress syndrome (ARDS) on mechanical ventilation. Differences between left ventricular (LV) and RV physiology are important and are not always fully appreciated. Current treatment entails pharmacologic support while volume status is optimized. These measures are frequently insufficient to augment RV systolic function. Recent advances have resulted in several device options for mechanical RV support, both percutaneous and surgically implanted. Critical care physicians have a growing involvement in decisions about when temporary support is appropriate and how this is best accomplished. Mechanically circulatory support may be required. This session will review RV physiology, clinical scenarios warranting RV support, pharmacotherapy, and mechanical support options.

Meta Tag

Content Type Presentation

Knowledge Area Cardiovascular

Knowledge Area Pharmacology

Knowledge Level Intermediate

Knowledge Level Advanced

Learning Pathway Cardiothoracic Critical Care

Membership Level Select

Tag Ventricular Function

Tag Heart Failure

Tag Pharmacology

Tag Cardiothoracic Critical Care

Year 2022

Keywords

acute right ventricular failure

volume optimization

medications

diuretics

inotropes

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