A review by Holden Spivak, MD based on the course of a TICU patient who had significant hypoxia due to right heart failure and increased pulmonary pressure.
Background and Pathophysiology
When discussing right heart failure, the normal pulmonary circulation and its differences from the systemic circulation needs to be examined. The pulmonary (right sided) circulation is a low pressure, high flow circuit unlike the high pressure systemic circuit. This low pressure prevents the fluid from extravasating into the interstitial spaces and also prevents the RV from pumping against high pressures. This includes both during rest and exercise. During exercise the pulmonary vascular resistance stays the same (or decreases in young healthy patients) whilst in the left sided circulatory system, the resistance increases during exercise. Due to this, the right side remains a low pressure system at all physiologic times. Its ability to stay this way is in part due to its ability to recruit unused vessels and its lack of muscular arterioles. In the left sided circulation, there exist muscular arterioles that act as resistors and can greatly alter the general SVR. Due to this potential for SVR variation with these muscular arterioles, the left sided resistance is more easily altered and affected with vasoconstrictors and therefore more easily augmented in the acute setting. The left heart and right heart also have major differences that must be discussed. The left heart, a large four wall muscular chamber, is much better at handling these pressure differences (afterload) due to its muscular ability. However because of this musculature it is worse at handling major changes in preload due to an inability to comply to large volume changes.
The right heart is a thin free wall wrapped around this muscular left ventricle. Due to this it is ‘looser’ and more compliant and therefore more able to handle changes in preload but worse when handling changes in afterload. The cause right heart failure is due to some functional or structural process that effectively decreases the right ventricle’s ability to pump blood forward into the pulmonary (right sided) circulation.
The three major categories of etiologies are alterations in preload, excessive afterload, or impaired contractility. The most common overall cause is left heart failure. Alterations in preload may be due to sepsis, hypovolemia or volume overload. Excessive afterload may be due to pulmonary hypertension, massive PE, LV failure, or acute lung injury. Impaired contractility may be due to right ventricle ischemia, valvular disease. In sick patients in the ICU, Right heart failure is usually due to some underlying pulmonary or right heart disease exacerbated by an acute insult. In patients with hypovolemia or inflammation induced RHF such as sepsis, there is a role of TNF alpha depressing cardiac contractility.
In patients with pulmonary hypertension or some lung pathology pneumonia, ALI, PE) the right heart is pumping against increased afterload causing it to eventually fail. This is in part due to the lung’s normal physiologic reflex to constrict its vasculature in response to hypoxia (termed hypoxic pulmonary vasoconstriction) in order to shunt blood to more oxygenated parts of the lung. Left heart failure causes backup of blood which causes increased afterload in the right heart.
When a patient is in the ICU with right heart failure, it is important to address the effect of mechanical ventilation on the right heart. Mechanical ventilation increases the intrathoracic pressure which decreases the right heart’s preload and can increase the right ventricle’s afterload.
Diagnosis
Diagnosing Right heart failure presents a challenge. The physician should use the classic physical exam findings such as an elevated JVD and peripheral edema. The most reliable methods of diagnosis are pulmonary artery catheters, transthoracic, or transesophageal echocardiography. However, unlike the left heart, there are not as easily measurable values to assess the right heart’s function. It is more so assessed on general function seen during the echo. However, the Tricuspid Annular Plane Systolic Excursion value may be used to get a general estimate. It should be noted it is understudied in critically ill patients and that mechanical ventilation can cause inaccuracy. The TAPSE measures the longitudinal displacement of the RV base towards the apex. Unlike the circumferential contraction of the left ventricle, the right heart contracts in a similar fashion to how the TAPSE measures it. A normal TAPSE is 24-27 mm. Less than 18 mm has an 87% accuracy to show decreased stroke volume. Chest xray and CT of the heart do not typically show changes in Right heart failure until very late into the course.
Management
The management of RHF centers around the three main etiologies of RHF with focus directed on preload correction, afterload reduction, and contractility management. Managing preload in RHF patient poses a challenge because there exists a fine line before a patient is fluid overloaded and therefor puts more afterload strain on the heart. Also PPV can impede RV preload and sedatives and analgesics can lower SVR (and therefore decreased preload) In sepsis and hypovolemic patients, volume must be restored but not so much so it pushes the needle towards too much afterload. Afterload management due to the functional construction of the right heart is of utmost importance. As a reminder, afterload can increase due to hypoxia (hypoxic pulmonary vasoconstriction), sepsis (endothelin, IL-6, decreased NO etc. all push equilibrium towards vasocontriction, PE (mechanical obstruction) and Left heart failure. The main interventions are geared towards reduction of afterload via correction of hypoxia and hypercapnia, acidemia (acidosis causes constriction) and sepsis. Unfortunately, aiming for a high O2 sat in a patient who is ventilated can causes problems in patients with ARDS where permissive hypercapnia is allowed.
Pulmonary vasodialators can be used however these should be reserved for further down the line in management in patients where further care is not futile. Treatment options range from inhaled nitric oxide, PGE 1, and PGI2. While these have been showed to improve RV EF and right ventricle end diastolic volume, they are no statistical help in ARDS. To help contractility, vasopressors and inotropes can be added. At this institution, norepinephrine is usually first line, however epinephrine can also be used as well. Sole inotropes are usually avoided as they can cause increased strain on heart and ultimately lead to poor prognosis. Milrinone can be used due to its focus on inotropic support without much chronotropic effect.
Overall for right heart failure, the physician should focus on the cause and reverse it. If the cause cannot be immediately reversed, preload should be optimized and afterload should be decreased and PVR should be decreased. When all of these measures fail, ECMO can be used, but only as a bridge to surgical intervention when care is not futile.
References
- Lahm, Tim, et al. “Medical and Surgical Treatment of Acute Right Ventricular Failure.” Journal of the American College of Cardiology, vol. 56, no. 18, 2010, pp. 1435–1446., doi:10.1016/j.jacc.2010.05.046.
- Ventetuolo, Corey E., and James R. Klinger. “Management of Acute Right Ventricular Failure in the Intensive Care Unit.” Annals of the American Thoracic Society, vol. 11, no. 5, 2014, pp. 811–822., doi:10.1513/annalsats.201312-446fr.