Good morning, thank you for that introduction, Paul. And thanks for the society for asking me to give this presentation today. So the topic is the management of right heart failure and pulmonary hypertension in the ICU. And I would like to focus on some basic concepts of anatomy and physiology of the right ventricle because it's important to understand right ventricular function and physiology, which allows us to then make good decisions regarding management of a failing right ventricle. I have no disclosures. So I'll review the anatomy and physiology of a normal right ventricle and a right ventricle of a failing right ventricle, discuss mechanics and ventricular interdependence, review some of the potential etiologies of right heart failure that are commonly seen, and then we will get into management. So there's a lot to cover, and hopefully we'll get this wrapped up in 15 minutes. It is important to recognize that the RV and the LV are fundamentally different. And the right ventricle is a complex, has got a complex anatomy, chrysanthic shape, and it doesn't conform to a simple geometric model like the left ventricle does. And anatomically, it has two layers of circumferential and longitudinal fibers in contrast to the left ventricle, which has three layers. And this is important. So when the anatomy is different, the function during normal state is different, and when the ventricle becomes dysfunctional, it behaves differently. The contractile properties of the right ventricle are different than the left ventricle. RV contraction happens at a higher end diastolic volume. Right ventricle has a lower ejection fraction than the left ventricle. And the contraction is longitudinal and bellows-like on the right side, and this is different than the left side. So everybody knows that the basic physiologic principles that are involved in ventricular dysfunction, whether it's the right or the left side, are preload, afterload, and contractility. So that's very similar here. But the interaction of these physiologic determinants is different between the two ventricles. For example, right ventricular stroke volume decreases with acute increases in right ventricular afterload, and that's pulmonary hypertension. And compared to the left ventricle, right ventricle demonstrates a heightened sensitivity to changes in afterloads. So you can see on the slide that the stroke volume vascular resistance curve is much more steep for the right ventricle compared to the left ventricle. And importantly, a normal right ventricle cannot generate a systolic pressure of greater than 45 millimeters mercury as a result of this heightened sensitivity to afterload. So what are the hemodynamic and clinical definitions of pulmonary hypertension? So the World Health Organization has classified pulmonary hypertension into group one through group five. Group one is pulmonary arterial hypertension, and then group two is the pulmonary hypertension due to left heart disease. Group three, pulmonary hypertension due to lung diseases. Group four, pulmonary hypertension due to pulmonary arterial vascular obstructions, chronic thromboembolic pulmonary hypertension. And then group five, where the mechanism is unclear or multifactorial. From a hemodynamic perspective, pre-capillary pulmonary hypertension and post-capillary pulmonary hypertension are still commonly used terms to describe pulmonary hypertension. And the hemodynamic definitions are shown on this slide. Mean pulmonary artery pressure is greater than 20 whenever there is pulmonary hypertension. And then the vascular resistance is elevated and the wedge pressure is less than 15 in pre-capillary and more than 15 in post-capillary. And post-capillary can be an isolated post-capillary or a combined pre- and post-capillary. Two other hemodynamic variables that one must know about when you are managing pulmonary hypertension right heart failure is pulmonary artery pulsatility index or PAPI, which is systolic pulmonary pressure minus diastolic pulmonary pressure over mean right atrial pressure and cardiac power output, which is mean arterial pressure times cardiac output times a constant. The pathogenic mechanisms of pulmonary hypertension are shown here. It's a rather complex and busy slide. I apologize for that. But I just wanted to highlight that there are numerous triggers. There are multiple cellular signaling pathways. Some of these have been very well delineated and have allowed us to develop molecular targets to help manage pulmonary hypertension. And collectively, you have remodeling of the pulmonary vascular bed and this progressive remodeling, intimal thickening, intimal hyperplasia, fibrosis then results in the development of pulmonary vascular disease and consequently right heart failure due to increased afterload. So mechanics of the right ventricle. So you have a neurohormonal and other activation, other mediator activation, pressure overload, adaptive hypertrophy, maladaptive hypertrophy, increased wall stress. Coronary perfusion is affected. There is right ventricular ischemia. And you navigate from a compensated phase of right heart failure to a decompensated phase of right heart failure. And this progressive change in the right ventricular mechanics affect adversely the function of the left ventricle as well through a phenomenon called ventricular interdependence. So this is a photograph of an echocardiogram. On the left side, you see a normal right ventricle and the septum is midline and you can see the right ventricle is adequately filled. But on the right side, you see a failing right ventricle which is dilated and the septum is shifted and pushed into the left ventricle. The left ventricular cavity is small. So changes in right ventricular function invariably affects performance of the left ventricle. And three other additional physiologic principles to quickly review are ventricular arterial coupling which is probably the most important determinant of RV performance, interdependence I already mentioned and dyssynchrony. And RVPA coupling is really the impact of the right ventricle, impact of afterload on the right ventricle and it's proportional to the contractile state of the right ventricle. So you can have a coupled right ventricle which is tolerating the high pulmonary vascular resistance and then you have an uncoupled right ventricle which is failing rapidly and is unable to tolerate because its contractile state is compromised. I mentioned ventricular interdependence already and moving on to dyssynchrony. Dyssynchrony is where the activity of the right and left ventricle is not synchronous and dyssynchrony is often evident and can be picked up on cardiac MRI as well as tissue Doppler imaging. Okay, so etiologies of RV failure are listed here and everyone is familiar with that and the etiologies can be acute or chronic. They can be related primarily due to elevated afterload or impaired contractility or elevated preload. And potential triggers have to be identified when one deals with a patient with acute right heart failure. It could be just progression of underlying pulmonary vascular disease. It could be pulmonary embolism. It could be a new or worsening intrinsic pulmonary process or it could be a post-operative state and it could be associated with other medical conditions, high cardiac output states such as hyperthyroidism and then of course cardiac arrhythmias. So the management. Now obviously we often talk about managing, management of right ventricular failure but really it should start even before a patient develops right ventricular failure and I think it's important to recognize that especially in chronic pulmonary hypertension, it is important to make every effort to prevent acute right ventricular failure. So you determine the etiology and chronicity, you evaluate hemodynamics both by right heart catheterization, you do imaging studies, echocardiography as well as cardiac MRI to look at the anatomy of the right ventricle and look for changes in right ventricular physiology. You treat predisposing factors and you tailor your medical and surgical management to optimize preload, afterload and contractility. Atrial arrhythmias in particular are poorly tolerated in bi-pulmonary hypertension patients and it is important to treat them effectively, quickly. General recommendations are the use of digoxin or amiodarone. One should have a low threshold for electrical cardioversion. Optimal management requires a multifaceted approach that addresses preload, afterload and contractility and so all three of these physiologic determinants have to be addressed in every patient. Preload optimization is critical. Fluid administration if the CVP is low and treating excessive preload if the CVP is high. It is important, optimizing preload is critical to restore normal interventricular dependence and you can use diuretics and sometimes ultrafiltration or renal replacement therapy may be necessary as appropriate. Contractility management to optimize hemodynamics and cardiac output and end organ perfusion. Use of inotropes, dubutamine, dopamine, epinephrine. Of course one must avoid hypotension and make sure that the systemic vascular resistance is greater than the pulmonary vascular resistance and vasopressors should be used when appropriate. The preferred vasopressor in the ICU is vasopressin. It is somewhat selective to the systemic circulation. Afterload management, obviously the most important of the three determinants. You can use inhaled agents such as nitric oxide or epiprostanol. If a patient is already on a parenteral prostacyclin or other oral agents for pulmonary arterial hypertension, they must be continued without interruption. Intravenous prostacyclin can sometimes be, can often be initiated to help manage right ventricular failure. Respiratory insufficiency should be treated by supplemental oxygen, noninvasive ventilation or mechanical ventilation as necessary and when mechanical ventilation is utilized, avoid high PEEP levels and make sure that you are avoiding high and low extremes of lung volumes and using lung ventilation protective strategies as appropriate and of course in extreme cases, VV ECMO may be needed to maintain adequate oxygenation. When a patient fails to respond to these measures, there are some additional measures that could be considered. Atrial septostomy is being shown to be palliative in patients with refractory right heart failure. Of course lung transplantation is often effective but unfortunately is only available for select patients and may not be available in a timely fashion. Mechanical circulatory support is utilized but must be utilized judiciously as there is a risk of pulmonary hemorrhage via ECMO in patients who have markedly reduced cardiac output and hypotension. And in special circumstances, other measures may be necessary. Right ventricular failure due to chronic left ventricular failure. One must again utilize the same sort of strategies but again optimize them as necessary to achieve optimal hemodynamics. Pulmonary vasodilators may be effective in select patients, particularly right heart failure after LVAD implantation or early after post heart transplantation. I think these are some strategies that are available. Acute pulmonary embolism, just two points to make here. One is that the clot burden is what determines how the right ventricle behaves in acute PE. It is important to focus on clot dissolution. The clot dissolution can be done by a variety of methods. You can do it acutely in interventional radiology or the cardiac catheterization laboratory. You can give lytics to dissolve these clots or you can do surgical embolectomy. And in chronic thromboembolic pulmonary hypertension, select cases, you can consider doing pulmonary thromboendarterectomy. Cardiogenic shock, especially right ventricular shock, is often very serious and associated with very poor outcomes. This is the algorithm that has been proposed for the management of shock, both left ventricular shock, right ventricular shock, and biventricular shock. And I refer you to this algorithm which was published in Jack Heart Failure two years ago. Mechanical circulatory support, there are some devices that are available and the use of these devices is growing and we are gaining experience. There are no good clinical trials with these devices, so much to learn about their appropriate utility in the setting of right ventricular failure. Impella RP, TandemHeart, VA ECMO are all options available to patients. So in conclusion, right ventricle has a fundamentally distinct anatomy and physiology relative to the left ventricle and it responds differently to changes in afterload and the changes in the right ventricle can in turn affect the performance of the left ventricle. And in evaluating right ventricular failure, it is critical to determine the etiology and chronicity as that will tailor your appropriateness of therapy in this condition. But regardless of etiology, the treatment should include a combination of strategies that are aimed to optimize preload, contractility, and afterload. Thank you for your attention.

right heart failure

pulmonary hypertension

ICU

management

ventricular failure