|Year : 2019 | Volume
| Issue : 2 | Page : 111-115
Isolated acute right heart failure syndrome in a young male with severe sepsis: An unusual pathophysiology in a normal heart
Raghuram Palaparti, Sudarshan Palaparthi, Gopala Krishna Koduru, PS S Chowdary, Hari Krishna Marri, Purnachandra Rao Kondru, Somasekhar Ghanta, Prasad Maganti, Sasidhar Yendapalli
Department of Cardiology, Aayush Hospitals, Vijayawada, Andhra Pradesh, India
|Date of Web Publication||23-Sep-2019|
Dr. Raghuram Palaparti
Aayush Hospitals, Ramachandra Nagar, Vijayawada - 520 008, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
Acute right heart failure is being increasingly recognized in intensive care unit (ICU) and when severe, can contribute to hemodynamic instability. Sepsis-induced myocardial dysfunction is also a known entity in critical care ICU. However, isolated right ventricle (RV) dysfunction in patients with sepsis after excluding chronic heart and lung disease is underdiagnosed and reported uncommonly. Whether RV is a bystander or a major contributor to hemodynamic instability in that scenario has not been studied clearly. Here, we report a 42-year-old male patient with no major cardiovascular risk factors who presented to us in shock with a history of low-grade fever, generalized weakness, and decreased urine output for 3 days. On physical examination, he had pedal edema and neck vein distension. He was found to have neutrophilic leukocytosis, deranged renal function test, and liver function test. His chest X-ray posteroanterior view showed cardiomegaly with pulmonary congestion. His electrocardiography (ECG) showed right bundle branch block (RBBB). He was anuric and started on dialysis for severe acidosis. In view of shock, renal failure and RBBB on ECG, a transthoracic echocardiography was done which showed gross dilatation of right atrium, and RV with severe RV dysfunction with normal left ventricle function. Contrast-enhanced computerized tomography chest was negative for pulmonary thromboembolism. His blood culture has grown Escherichia coli. With intravascular (IV) fluids, ionotropic support, renal replacement therapy, IV antibiotics, and other supportive therapy, he gradually improved. His serial ECGs showed resolution of RBBB. Two-dimensional echo showed improved RV function. He was discharged on day 9 and his 2-week follow-up echo showed normalization of RV function. During follow-up, his coronary angiogram showed normal coronaries. This case illustrates the importance of identifying acute RV failure in patients with severe sepsis with shock. It also underscores the necessity for more studies and research on understanding the pathophysiology of RV dysfunction in critical care patients and its contribution to hemodynamic instability.
Keywords: Acute right heart failure, isolated, normal heart, severe sepsis
|How to cite this article:|
Palaparti R, Palaparthi S, Koduru GK, S Chowdary P S, Marri HK, Kondru PR, Ghanta S, Maganti P, Yendapalli S. Isolated acute right heart failure syndrome in a young male with severe sepsis: An unusual pathophysiology in a normal heart. J Indian coll cardiol 2019;9:111-5
|How to cite this URL:|
Palaparti R, Palaparthi S, Koduru GK, S Chowdary P S, Marri HK, Kondru PR, Ghanta S, Maganti P, Yendapalli S. Isolated acute right heart failure syndrome in a young male with severe sepsis: An unusual pathophysiology in a normal heart. J Indian coll cardiol [serial online] 2019 [cited 2019 Oct 22];9:111-5. Available from: http://www.joicc.org/text.asp?2019/9/2/111/267494
| Introduction|| |
Acute right heart syndrome (ARHS) may be defined as sudden compromise of RV function and failure of heart to deliver adequate blood flow to the pulmonary circulation, resulting in systemic hypoperfusion. It is seen in critically ill patients and contributes to poor outcomes.
| Case Report|| |
A 42-year-old male patient with no major cardiovascular risk factors who presented to us with history of low-grade fever, generalized weakness, and decreased urine output for 3 days. At presentation, he was in shock. His blood picture showed neutrophilic leukocytosis, deranged renal function test, and liver function test (LFT). His LFT was suggestive of shock liver (severe transaminitis with enzymes in thousands). There was no history suggestive of any toxin exposure. He was started on intravascular (IV) fluids and inotropic support (noradrenaline and dobutamine). His blood gas analysis showed severe acidosis. He was started on hemodialysis. His chest X-ray (CXR) posteroanterior view showed cardiomegaly with pulmonary congestion [Figure 1]. His electrocardiography (ECG) showed right bundle branch block (RBBB) [Figure 2]. On physical examination, he had pedal edema, neck vein distension, and a tricuspid regurgitation murmur. In view of shock, renal failure, shock liver, and RBBB on ECG, a transthoracic echocardiography was done which showed gross dilatation of the right atrium (RA) and right ventricle (RV) with severe RV dysfunction. Tricuspid annulus planar systolic excursion (TAPSE) was 1.1. RV systolic pressure was around 50 mmHg when his systemic systolic blood pressure was 80 mmHg [Figure 3], [Figure 4] and Videos 1-5. His left ventricle (LV) function was normal. After stabilization and correction of electrolytes and acidosis, we have done contrast-enhanced computerized tomography (CECT) chest to rule out pulmonary thromboembolism (PTE). CECT chest was negative for PTE and also confirmed gross dilatation of RA and RV [Figure 5]. His brain natriuretic peptide (BNP) was 1800 ng/dl and his troponins were only mildly elevated. He never had chest pain. His blood culture has grown Escherichia More Details coli and he was started on injection piperacillin + tazobactam according to sensitivity. With IV fluids, inotropic support, renal replacement therapy, IV antibiotics, and other supportive therapy, he gradually improved. With gradual negative fluid balance of around 6 l during the recovery phase from sepsis and renal failure, his RV function improved. His serial ECGs showed resolution of RBBB [Figure 6] and [Figure 7]. We presumed this to be related to RV stretch, which later disappeared. We ruled out other possible causes of acute RV failure in young adults such as sickle cell crisis and epidemic dropsy. He was discharged on day 9. His predischarge echo showed only mild RV dysfunction. He is in follow-up since then doing well. His 2-week follow-up echo showed normalization of RV function [Figure 8], [Figure 9] and Videos 6-10. At 2-month follow-up, coronary angiogram has been done to rule out coronary artery disease which showed normal coronaries.
|Figure 1: Electrocardiography at presentation showing right bundle branch block|
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|Figure 2: Chest X-ray at presentation showing cardiomegaly and pulmonary congestion|
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|Figure 3: Echo still image showing D-shaped left ventricle and dilated right ventricle|
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|Figure 4: Echo still image showing grossly dilated right atrium, right ventricle|
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|Figure 5: Contrast-enhanced computerized tomography chest excluding pulmonary thromboembolism|
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|Figure 8: Echo still image predischarge showing normal-sized right ventricle|
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|Figure 9: Echo predischarge still image showing normal-sized right atrium and right ventricle|
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| Discussion|| |
Acute right heart failure is being increasingly recognized in intensive care unit (ICU) setting and when severe, can contribute to hemodynamic instability. Right ventricular failure occurs when the RV fails to maintain enough blood flow through the pulmonary circulation to achieve adequate left ventricular filling. This can occur suddenly in a previously healthy heart due to massive pulmonary embolism or right-sided myocardial infarction (MI), but many cases encountered in the ICU involve worsening of compensated RV failure in the setting of chronic heart and lung disease. The recent focus on RV function in critically ill patients is majorly attributed to the rapid growth in our understanding of pulmonary vascular biology and the subsequent development of several new classes of pulmonary vasodilator medications. Technical advances in extracorporeal life support have provided us the ability to support patients with acute RV failure through their illness and enhance our understanding of how the failing RV should be managed. Sepsis-induced myocardial dysfunction is also a known entity in critical care ICU. Whether RV is a bystander or a major contributor to hemodynamic instability in that scenario has not been studied clearly.
Causes of acute RV failure in critical illness according to the pathophysiology can be divided into three main categories: (1) excessive preload, (2) excessive afterload, and (3) insufficient myocardial contractility. Etiological causes for acute right heart syndrome have been tabulated in [Table 1]. In our case, we propose the following causes for acute RV failure (1) decreased cardiac contractility because of severe acidosis and sepsis; (2) endotoxin- and cytokine-induced decreases in systolic and diastolic LV and RV function, as well as afterload increases from endothelial dysfunction, hypoxic pulmonary vasoconstriction, and pulmonary microthrombi; and (3) disproportionate increase in preload (volume overload) because of renal failure.
Assessment of RV function in the critically ill patient should begin with physical examination and consideration of the patient's presentation and medical history. Evidence of elevated right-sided filling pressures, as suggested by jugular venous distension and peripheral edema, may be the most recognizable signs. Splitting of the second heart sound, tricuspid regurgitation murmur heard best over the right sternal border may be present. Signs of RV failure may be evident on CXR, although the anterior position of the RV makes it difficult to evaluate RV size unless a lateral film can be obtained. Contrast-enhanced computed tomography studies of the chest can provide a better assessment of RV size and position of the interventricular septum. Widely used biomarkers, such as plasma BNP or cardiac troponin levels, are not specific for RV failure but can signal RV dysfunction in the absence of left-sided heart disease. Transthoracic echocardiography provides estimates of RV size and function and may help elucidate possible precipitating factors for RV failure, including LV dysfunction and valvular heart disease. RV systolic function can be assessed by measuring the longitudinal systolic displacement of the RV base toward the RV apex. This is commonly referred to as the TAPSE and is relatively simple to perform, highly reproducible, and has been shown to correlate well with RV ejection fraction derived from radionuclide angiography., RVs prime, RV free wall strain, and fractional area change are other important parameters to be measured in RV dysfunction.
Isolated RV dysfunction in patients with sepsis after excluding chronic heart and lung disease has been reported and studied but underdiagnosed. However, what makes our case challenging is associated with shock and anuria. This makes the fluid resuscitation in this patient cumbersome. We initially started him on liberal fluid resuscitation based on central venous pressure monitoring, while the patient was on inotropic support and dialysis. Later, in the phase of recovery from sepsis and renal failure, he required gradual diuresis with furosemide infusion. Ideally, invasive hemodynamic monitoring with Swan–Ganz catheter would have given a better insight into his hemodynamics, however, could not be implemented due to financial constraints.
Initial management in patients with acute RV failure should focus on determining the cause of RV decompensation and reversing it. In our case, we ruled out PTE with a CECT chest. It is very unlikely to be RV MI because of the absence of typical ECG changes, no chest pain, mild elevation of troponins, and spontaneous recovery of RV function. We ruled out other rare causes of acute right heart failure in a young adult without lung diseases such as sickle cell crisis and epidemic dropsy. When a reversal is not possible, efforts should be directed toward optimizing RV preload and mitigating any factors that can increase pulmonary vascular resistance. If RV failure persists, short-acting pulmonary vasodilators should be used, preferably through inhalation in an attempt to lower RV afterload. When these efforts fail, the judicious use of vasopressors and inotropes should be considered in an attempt to improve RV perfusion and contractility. Extracorporeal life support is effective at restoring circulatory support when other measures fail and may be indicated in patients who are expected to recover from the cause of their RV failure, or as a bridge to surgical interventions, such as pulmonary endarterectomy or lung transplantation.
Although not an uncommon entity, this case illustrates the importance of identifying RV failure in patients with severe sepsis and septic shock, which may significantly contribute to circulatory collapse. Screening is recommended in all patients with severe sepsis and septic shock for RV dysfunction. There is a certain necessity for more research on understanding the pathophysiology of RV dysfunction in critical care patients and its contribution to hemodynamic disturbances.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc 2014;11:811-22.
Lepper PM, Hörsch SI, Seiler F, Kamp A, Becker SL, Lensch C, et al.
Percutaneous mechanical circulation support combined with extracorporeal membrane oxygenation (oxyRVAD) in secondary right heart failure. ASAIO J 2018;64:e64-7.
Lahm T, McCaslin CA, Wozniak TC, Ghumman W, Fadl YY, Obeidat OS, et al.
Medical and surgical treatment of acute right ventricular failure. J Am Coll Cardiol 2010;56:1435-46.
Boxt LM. Radiology of the right ventricle. Radiol Clin North Am 1999;37:379-400.
Kaul S, Tei C, Hopkins JM, Shah PM. Assessment of right ventricular function using two-dimensional echocardiography. Am Heart J 1984;107:526-31.
Lee CY, Chang SM, Hsiao SH, Tseng JC, Lin SK, Liu CP, et al.
Right heart function and scleroderma: Insights from tricuspid annular plane systolic excursion. Echocardiography 2007;24:118-25.
Lakshmanadoss U, Levitan BM, Hsi DH. Right ventricle failure in sepsis: A case report. Cardiol Res 2011;2:48-9.
Vallabhajosyula S, Kumar M, Pandompatam G, Sakhuja A, Kashyap R, Kashani K, et al.
Prognostic impact of isolated right ventricular dysfunction in sepsis and septic shock: An 8-year historical cohort study. Ann Intensive Care 2017;7:94.
Novelli EM, Gladwin MT. Crises in sickle cell disease. Chest 2016;149:1082-93.
Sharma BD, Bhatia V, Rahtee M, Kumar R, Mukharjee A. Epidemic dropsy: Observations on pathophysiology and clinical features during the Delhi epidemic of 1998. Trop Doct 2002;32:70-5.
Kapur NK, Esposito ML, Bader Y, Morine KJ, Kiernan MS, Pham DT, et al.
Mechanical circulatory support devices for acute right ventricular failure. Circulation 2017;136:314-26.
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