Continuing on with right heart failure with the final part of the 4-part series. If you have not read Management of acute right ventricular failure in the intensive care unit by Ventetuolo, et al. I recommend reading it, especially for this section.
Breaking down cardiac output in terms of the right heart.
Let’s relook at the breakdown of cardiac output into its four core components (Figure 1). I have added all the components from parts 1 - 3.
Figure 1: Cardiac output breakdown
Creating an RV Failure Treatment Algorithm
Disease physiology:
In order to understand the treatment, it is important to understand the physiology. There is a spiral or feedback loop where the patient will continue to worsen unless the loop can be interrupted. The most common cause of RV failure in the ICU is due to increased afterload and it is the most complicated to treat. Increased preload as the primary cause is due to too much volume. Treatment is diuresis or ultrafiltration while treating the underlying condition. Decreased contractility as the primary cause is usually due to right-sided MI with decreased contractility leading to poor forward flow, increased preload, and organ congestion. In this case, depending on the extent of the dysfunction, inotropic support or right-sided mechanical support is needed.
As stated in part 3, when there is increased afterload it is more difficult for the RV to eject blood over to the left heart. The right ventricle is more sensitive than the left ventricle to afterload due to it being thin-walled. The increased afterload leads to decreased stroke volume causing increased volume in the RV at the end of systole and diastole. The increased preload enlarges the RV and stretches the RV inflow causing tricuspid regurgitation and reversal of flow. The increased afterload and preload both cause decreased contractility as it moves the ventricle to the descending limb of the Starling curve. Additionally, the increased pressure and volume will increase wall tension and compress small arterioles and capillaries in the thin wall of the ventricle and lead to ischemia. The ischemia leads to worsening contractility which further worsens stroke volume. The decreased stroke volume results in low cardiac output. Low cardiac output decreases right coronary perfusion which also worsens RV function. The worsening RV function leads to further RV function and the patient goes into a death spiral (Figure 2).
Figure 2: RV Failure Spiral (3)
Treating RV failure, therefore, involves trying to break the spiral by reversing or stopping these processes.
How to approach RV Failure
Afterload
The first hemodynamic component to focus on is the afterload. With it being the most common cause and realizing it can cause increased preload and decreased contractility, it makes sense to try and fix the afterload and the other two may improve.
Evaluating afterload can be difficult. Figure 3 is from part 3 and looks at ways of measuring RV afterload. Additionally, a D-sign during systole on echo is another indicator of increased RV pressure compared to LV pressure. Any signs of afterload abnormalities, I would have a low threshold to treat.
Figure 3: Measuring Afterload
Figure 4: D-Sign during Systole - RV Pressure Overload (Parasternal Short)
The initial evaluation should look at the estimated PASP and the D-sign since they are both non-invasive.
1. Non-pharmacological treatments of afterload:
Hypoxia and Acidosis:
Pulmonary vascular resistance is very sensitive to changes in oxygen and pH. Hypoxia and acidosis significantly increase pulmonary vascular resistance and correcting these will make a huge difference in afterload. As shown in Figure 5, acidosis and hypoxia can quickly increase PVR by more than 200%.
Figure 5: Oxygen/Acidosis and PVR (1)
These are not the patients to do permissive hypercapnia and let them be mildly acidotic. The goal should be normal saturation and normal pH.
Positive pressure:
Positive pressure is an interesting topic for RV afterload. Often it is taught to decrease PEEP as low as possible to help decrease PVR. It is true that overdistention of the alveoli with positive pressure can increase PVR, but under “PEEPing” them will lead to atelectasis. This will cause vasoconstriction to the atelectatic areas which also increases PVR. The PEEP needs to be at the minimum pressure to be above the lower inflection point (LIP) on the pressure-volume loop and create a positive transpulmonary pressure (TPP). Figure 6 shows this relationship between over and under PEEPing and Figure 7 shows the pressure-volume loop and the LIP.
Figure 6: PEEP and PVR Relationship (4)
Figure 7: Pulmonary Pressure-Volume Loop
https://derangedphysiology.com/main/cicm-primary-exam/required-reading/respiratory-system/Chapter%20554/interpreting-shape-pressure-volume-loop
When patients are not intubated and intubation is considered, the abrupt change from negative pressure to positive pressure will cause a large afterload increase, a sharp decline in stroke volume, and typically cardiac arrest. Intubating a patient with acute severe pulmonary hypertension, for example, an acute massive/sub-massive PE, should be avoided or done with extreme caution. Increasing the MAP with vasopressors or start an epinephrine infusion or giving small push doses may help prevent cardiac arrest.
2. Pharmacological treatment:
The most efficient way to reduce RV afterload is to start pulmonary vasodilators. There are primary pulmonary vasodilators whose main mechanism of action is to reduce pulmonary vascular resistance and there are medications used for other reasons that also reduce PVR secondarily.
Primary pulmonary vasodilators:
These medications are becoming more readily available and at least one should be available in most hospitals. Guanylate cyclase stimulators, prostacyclins and phosphodiesterase inhibitors are the three most commonly seen in the ICU (1).
Table 1: Primary Pulmonary Vasodilators
Inhaled pulmonary vasodilators should be used first. They do not cause hypotension like the systemic pulmonary vasodilators. Also, since they are only dilating the vasculature that is matched with the alveoli, it should improve oxygenation and reduce shunting. Systemic vasodilators will dilate all of the pulmonary vasculature and can worsen shunting.
Inhaled nitric oxide is very expensive, so inhaled epoprostenol is usually more readily available. It can be done while intubated or can be used with a high-flow device or BiPAP. If a high-flow oxygen cannula is used, it is typically done at a lower flow to ensure the medication is delivered, 30L of flow or less.
Secondary pulmonary vasodilators:
Often, I will use the secondary pulmonary vasodilators first since they have two functions and reevaluate before adding a primary pulmonary vasodilator.
Table 2: Medications with Secondary Pulmonary Vasodilation
If an inotrope is needed, milrinone is ideal, if the patient can tolerate the vasodilation. If a vasopressor is needed I will use vasopressin first-line.
Preload:
The preload and volume status of RV failure is the second component to be evaluated. The increased afterload quickly leads to an increased RVEDV, venous congestion, and edema. The increased RVEDV will cause a decrease in contractility as it over-distends the actin-myosin bridge and moves to the descending limb of the Starling Curve. The volume overload will lead to renal and hepatic congestion and worsen outcomes. Measuring preload can be difficult and CVP is unreliable.
Table 3: Right Ventricular Preload Assessment
Figure 8: D-Sign during Diastole - RV Volume Overload (Parasternal Short)
1. Diuretics
Aggressive diuresis should be started since these patients are often resistant due to renal venous congestion. Loop diuretics or dual nephron blockade with loop and thiazide seem to work best.
2. Ultrafiltration:
There should be a low threshold to place a hemodialysis catheter and begin ultrafiltration.
Decreasing RVEDV with volume removal will place the patient on the better part of the Starling curve and will actually increase blood pressure. These patients love having volume removed and like removal at a fast rate. CRRT can have the ultrafiltration turned up to >500mL.hr net removal and the blood pressure will usually improve as the removal increases. Do not be apprehensive to remove fluid! Look at the IVC, the venous pulsatility, TR improvement, or the resolution of diastolic D-sign to guide fluid removal.
Contractility:
I look at contractility third, the contractility will often improve with afterload and preload reduction. I will still start an inotrope when I see reduced contractility to help with forward flow and help reduce preload and venous congestion. This will help optimize diuresis. RV contractility is assessed in a number of ways, with most of them being invasive with a pulmonary artery catheter (Figure 9).
Figure 9: RV Contractility Measurement
Due to TAPSE being the least invasive and easy to re-evaluate, I use TAPSE to decide on starting inotropic agents.
Table 4: Inotropic Medications for RV Failure
Milrinone is the ideal medication if the patient can tolerate systemic vasodilation.
Other Factors to Consider:
Vasopressors:
When there is acute RV failure with high afterload the RV free wall is thin and prone to ischemia due to increased wall tension. Increasing the MAP goal to ≥70 mmHg helps ensure coronary perfusion and reduces the risk of ischemia. In acute on chronic RV failure, the free wall is often hypertrophic and may have poor blood supply due to the hypertrophy and so a MAP goal ≥70 mmHg is also used.
Table 5: Vasopressor Medications for RV Failure
Refractory Shock:
If everything non-pharmacological and pharmacological has been done to optimize the patient, and the patient continues to be in shock, then mechanical support should be initiated. VA ECMO is the preferred treatment if the primary cause is increased afterload. The primary problem is the obstruction to go from right to left. VA will take blood from the venous side and return it to the arterial side in parallel to the heart and therefore bypasses the obstruction.
Figure 10: VA ECMO
http://icuecmo.ca/icuECMO_content/icuECMO_ECMO_configuration_VA.html
My RV Failure Algorithm:
I will try to look with point-of-care ultrasound (POCUS) or look at the official TTE for the TR velocity and any signs of septal flattening. The septum may also have a shutter to it that changes based on breathing which is a sign of increasing RV pressure with respiration. I will make sure I look at the septum and TR through a couple of breathing cycles to assess for any changes.
When I get a patient with RV failure with increased afterload I will order this 4 medication cocktail:
1. Inhaled Epoprostenol
2. Furosemide/Bumetanide
3. Milrinone
4. Vasopressin
Table 6: Algorithm Steps with Evaluation Methods
Summary:
Increased afterload is the most common cause of RV dysfunction in the ICU and can lead to contractility and preload issues. It should be the first component of RV failure that should be evaluated and optimized. This will save a lot of time, effort, and resources. If increased afterload is leading to decreased contractility and increased preload, then treating it should improve the other two. Working down this algorithm has made a difference for me.
References:
1. Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc. 2014;11(5):811-822. doi:10.1513/AnnalsATS.201312-446FR
2. Tedford RJ. Determinants of right ventricular afterload (2013 Grover Conference series). Pulm Circ. 2014;4(2):211-219. doi:10.1086/676020
3. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur Respir J. 2019;54(3):1901647. Published 2019 Oct 9. doi:10.1183/13993003.01647-2019
4. Alviar CL, Miller PE, McAreavey D, et al. Positive Pressure Ventilation in the Cardiac Intensive Care Unit. J Am Coll Cardiol. 2018;72(13):1532-1553. doi:10.1016/j.jacc.2018.06.074
5. Nguyen A, Deschamps A, Varin F, Perrault L, Denault A. A Pathophysiological Approach to Understanding Pulmonary Hypertension n Cardiac Surgery. Perioperative Considerations in Cardiac Surgery. 2012. 277-306.
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