Show notes
CardioNerd (Daniel Ambinder) and series co-chairs Mark Belkin (AHFT Fellow, University of Chicago) and Karan Desai (Cardiologist, Johns Hopkins), join fellow lead, Dr. Pablo Sanchez (FIT, Stanford) for a discussion with Dr. Ryan Tedford (Professor of Medicine at the Medical University of South Carolina) about Right Ventricular (RV) predominant cardiogenic shock. In this episode we explore risk factors, pathophysiology, hemodynamics, and treatment strategies in this common and complex problem. We dissect three cases that epitomize the range of diagnostic dilemmas and management decisions in RV predominant shock, as Dr. Tedford expertly weaves us through the pathophysiology and decision-making involved in managing the “people’s ventricle.” Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds internship program, CardioNerds academy fellow, and IM resident at Brigham and Women’s Hospital).
The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif.
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Pearls and Quotes - RV Predominant Cardiogenic Shock
The degree of RV dysfunction and failure are modulated by stretching its capacity to tolerate insults from deranged afterload, preload, and contractility.Afterload insults are MUCH LESS tolerated than other insults and broadly comprise the most common pathophysiologic cause of both acute and chronic RV failure.RV and left ventricular (LV) function are anatomically and physiologically connected. Progressive derangements in RV function can lead to the deadly “RV spiral,” in which poor RV function causes lower LV preload, leading to hypotension, and thus worsening RV perfusion and function.In RV failure/shock, some basic tenets including treating reversible causes, optimizing preload and afterload, and using inotropes and/or temporary MCS for as limited time as possible.Many acute RV failure patients can recover, but multiorgan injury plays an important role. Therefore, thoughtful and expeditious use of mechanical circulatory support is important.
Show notes - RV Predominant Cardiogenic Shock
Notes drafted by Dr. Pablo Sanchez.
What is the basic difference between RV dysfunction and failure?Dysfunction: Abnormalities in systolic/diastolic function of the RV, but not necessarily to the point of leading to end-organ perfusion defects. RV dysfunction leads to poor outcomes regardless of mechanism.1Failure: Clinical syndrome of inability of RV to maintain adequate output despite adequate preload. 1
How is the RV different from the LV and what impact does it have on pathophysiology and hemodynamics?The LV and RV originate from different embryologic “heart fields.”1,2The RV wall is thinner and more compliant and has only two layers (instead of 3 like the LV).3 Furthermore, unlike the LV which has a significant proportion of endocardial and epicardial transverse myocardial fibers, the RV myocardial fibers are aligned in a longitudinal plane for the most part. Thus, a more significant proportion of RV systolic contraction is longitudinal – base of the ventricle moving towards the apex.The RV is crescent-shaped and has a large surface-to-volume ratio meaning smaller inward motion ejects the same stroke volume. 1Hemodynamically, the RV takes blood from a low-pressure venous system and gives it to a distensible system with low impedance (the normal pulmonary circuit at baseline typically has a resistance one-tenth of the systemic resistance). Therefore, volume loads (preload) are much better handled than pressure (afterload).1
What is RV-PA coupling?As Dr. Tedford noted, RV-PA coupling describes “the interaction of RV contractility and afterload (resistive and pulsatile components). It is the most comprehensive description of RV function and therefore the Gold Standard.” Whether we are referring to the LV or RV, the basic concept of coupling describes the energy transfer between ventricular contractility and arterial afterload.RV-PA coupling has typically been assessed by pressure-volume loops, with ventricular contractility assessed by end-systolic elastance (a load-independent measure of systolic function) and arterial afterload by effective arterial elastance.MODUS OPERANDI: RV dysfunction and eventual failure is modulated by stretching its capacity to tolerate insults from afterload, preload, and contractility.
What leads to ACUTE right heart failure?Most commonly results from:1Abrupt increases in afterload (e.g., think PE, hypoxia, and acidemia).Decreased contractility (e.g., think ischemia such as RV infarction, myocarditis, and post-cardiotomy).Volume overload can sometimes lead to acute right heart failure, particularly in the setting of another categorical insult such as septic cardiomyopathy or LVAD support.
What leads to CHRONIC right heart failure?This is different than acute right heart failure. Most commonly chronic right heart failure results from:1Gradual increases in afterload (e.g., think pulmonary arterial hypertension).Chronic volume overload (e.g., longstanding tricuspid regurgitation, atrial septal defect, and other congenital lesions like double outlet RV).Contractility (e.g., including the isolated RV cardiomyopathies like arrhythmogenic right ventricular cardiomyopathy or ischemic cardiomyopathy).Other pathologies certainly affect multiple categories (e.g., Ebstein’s anomaly which is a function of contractility and volume overload or single ventricle physiology like post-Fontan patients – for more on these and other ACHD lesions, enjoy the CardioNerds ACHD Series!)MODUS OPERANDI: The cardiovascular system is wholly connected, and acute decompensation leads to progressive derangements in the above levers (including LV function). This phenomenon is called the RV spiral.
How do we manage RV failure?The most important and first step is the treatment of reversible causes. For instance, acute coronary syndrome involving the RV requires percutaneous intervention (PCI) or pulmonary embolism requires anticoagulation and/or thrombolytic/device/surgical therapy.PRELOAD OPTIMIZATIONEnsuring that there is adequate preload is a key tenet of diagnosing and treating RV failure. This may require diuresis or judicious volume resuscitation to maintain cardiac output.While guiding fluid management in the setting of RV failure, one should STRONGLY consider invasive hemodynamic monitoring (e.g., over-resuscitation can lead to decreased LV output through septal shift and ventricular interdependence from pericardial constraint).1General target: We could consider a CVP 10-15 mmHg; however, this will be individualized. Another general rule would also be if that a bolus of 500 cc of crystalloid does not result in hemodynamic improvement, further loading should not be continued, especially without invasive hemodynamic guidance.AFTERLOAD OPTIMIZATION The goal should be to correct reversible causes of elevated pulmonary vascular resistance (e.g., acidosis, hypercapnia, hypoxia, and generally in ventilated patients avoid elevated inspiratory pressures 30mmHg).1With specialized expert guidance, we can consider selective pulmonary vasodilators (acutely and short-term):One example includes inhaled NO, and in observational studies, short-term use lowered PVR and increased RV ejection.4We also have to remember the consequences of reducing RV afterload. Acutely increasing LV preload in a baseline abnormal LV may lead to distention, lowered cardiac output, and pulmonary edema.1Pulmonary vasodilators can act on specific pathways (e.g., nitric oxide, prostacyclin, endothelin-1, and soluble guanylate cyclase stimulators) and come in various forms (oral, inhaled, and intravenous).CONTRACTILITY AUGMENTATION (INOTROPES)We typically utilize inotropes in concert with the prior two but optimize loading so the time we need inotropes is minimal.1Short-term use can improve hemodynamics. Longer-term use will typically increase myocardial O2 consumption and is associated with increased mortality. The RV has coronary perfusion in systole and diastole, so peripheral vasopressors are helpful to maintain perfusion, especially if systolic blood pressure is less than RV systolic pressure.1GOAL: Increase contractility without increasing RV afterload.For those failing to respond to these above measures to optimize preload, afterload, and contractility, there may be a role for temporary mechanical circulatory support (see #10 below).
How do we decide between dobutamine and milrinone?BOTH inotropes can lead to hypotension, have similar clinical outcomes, hemodynamic efficacy and arrhythmogenic potential1 (despite the adage that attributes more arrhythmias to dobutamine, studies show the risk is typically the same in both5).Milrinone is a more potent vasodilator (systemic and pulmonary) typically leading to greater decreases in end-diastolic pressures in the ventricles.1 It is renally cleared, has a longer half-life, and acts through a separate mechanism pathway compared to beta-blockade, thus patients can be on milrinone and beta blockers at the same time on a case-by-case basis.1Dobutamine has a shorter half-life, with rapid onset/offset and so may be more ideal in unstable/hypotensive patients.1
What if the patient is hypotensive?In this circumstance, we would need an ino-constrictor or peripheral vasoconstrictor.Vasopressin has almost no impact on PVR, so unlike catecholamines, it does not directly worsen RV afterload.1
What are some important invasive hemodynamic parameters to be aware of?