Identifying right ventricular failure
November 14th, 2023 
You respond to a call for a 48-year-old woman with a chief complaint of shortness of breath and chest pain. The husband states the patient just underwent hip surgery, and has a history of hypertension and DM. He states she has recently taken herself off her anticoagulant medication and she is supposed to follow up with her doctor tomorrow.
Upon arrival, you note the patient is in visible distress with two-word dyspnea. Her vital signs are as follows: BP: 90/62; RR: 34; Pulse: 122; SPO2: 86% on room air; ETCO2: 23. The 12-lead ECG reveals sinus tachycardia with T-wave inversions in V1-V3 as well as the inferior leads.
You place the patient on a non-rebreather at 15 Lpm and obtain IV access. You administer a 500 mL fluid bolus of normal saline and reassess. The patient does not seem to be improving and she is becoming more obtunded. Blood pressure is now 74/52. You elect to intubate the patient. Shortly after intubation, the patient goes into cardiac arrest and cannot be resuscitated. What happened?
Physiology considerations
When discussing the right ventricle (RV), I like to conceptualize it as the diva of the heart. Structurally, it’s a weak system compared to the left heart because it doesn’t have to pump as hard against the high pressures of the systemic circulation. The RV is part of a low-pressure system that is built for compliance and does not handle increased afterload – or pulmonary hypertension – very well. While the RV can adapt through hypertrophy in the same way the left ventricle (LV) adapts to systemic hypertension, contractility will decrease due to dilation during acutely increased afterload (as in massive pulmonary embolism), or chronically increased afterload (like the patient with pulmonary hypertension).
When there is an obstruction in the pulmonary artery, blood flow will begin to back up into the right ventricle, further increasing the strain on the RV, and cause ventricular dilation [1]. A severely dilated RV will then push the interventricular septum into the space otherwise occupied by the LV. This is the concept of ventricular interdependence. In decompensated RV failure with volume overload, the interventricular septum shifts into the LV during end-diastole, resulting in decreased LV preload.
As the left ventricular end diastolic volume is further decreased, systemic blood pressure falls and becomes closer to the right ventricular pressure. The pressure gradient the RV is perfused over is smaller, and the RV is susceptible to ischemia. Once ischemic, the RV contractility falls further, and the sequence self-perpetuates [2]. To further compound this problem, blood flow is not reaching the alveolar capillary membrane for the exchange of CO2 and oxygen. The lack of oxygenated blood causes hypoxic pulmonary vasoconstriction, which causes further increases in pulmonary vascular resistance and strain on the RV. Oxygenated blood is no longer perfusing the tissues of the body, and the cells switch from aerobic to anerobic metabolism to preserve metabolic function. This lack of cellular oxygenation creates acidosis, which further increases pulmonary vascular resistance and exacerbates the situation. This is often referred to as the RV spiral of death.
Listen for more: Heart matters: What providers need to know about congestive heart failure
POCUS presentation of RV dysfunction
If point-of-care ultrasound is available, this modality provides a quick way to identify RV dysfunction in the undifferentiated critically ill patient [3]. The apical four-chamber view, if attainable, is best for comparing chamber size. An RV:LV chamber size ratio >1 or an RV end-diastolic diameter >30 mm (at mid-level) indicate the RV is dilated and that right sided pressures may be elevated. In the parasternal short axis view, flattening of the interventricular septum causes the LV to take on a characteristic “D” shape, illustrating the presence of ventricular interdependence (Figure 1) [1].
ECG in RV failure
While the ECG is not sensitive nor specific for pulmonary embolism (PE)/acute RV failure, when coupled with the history and other signs and symptoms, it can help the clinician differentiate RV failure. Many people are taught the SQQ3T3 pattern on the ECG as being diagnostic for PE. This ECG pattern is only present in 20% of patients with a large PE. Sinus tachycardia is more prevalent in about 44% of patients with PE and acute right heart strain. Another finding that has been found to be highly specific for large pulmonary embolism and high pulmonary pressures are T-wave inversions in the right precordial leads and inferior leads (Figure 2). This finding has a been shown to be present in up to 33% of patients, with one study showing a specificity of up to 99% [4].
References
1. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: A report from the American society of echocardiography: Endorsed by the European association of echocardiography, a registered branch of the European society of cardiology, and the Canadian society of echocardiography. Journal of the American Society of Echocardiography. 2010;23(7):685-713.
2. Wolferen SA, Marcus JT, Westerhof N, et al. Right coronary artery flow impairment in patients with pulmonary hypertension. Eur Heart J. 2008;29(1):120-127. doi: ehm567 [pii].
3. Goldstein JA. Pathophysiology and management of right heart ischemia. J Am Coll Cardiol. 2002;40(5):841-853.
4. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: A report from the American society of echocardiography: Endorsed by the European association of echocardiography, a registered branch of the European society of cardiology, and the Canadian society of echocardiography. Journal of the American Society of Echocardiography. 2010;23(7):685-713.
5. Said, S. A., Bloo, R., de Nooijer, R., & Slootweg, A. (2015). Cardiac and non-cardiac causes of T-wave inversion in the precordial leads in adult subjects: A Dutch case series and review of the literature. World journal of cardiology, 7(2), 86–100. https://doi.org/10.4330/wjc.v7.i2.86
