Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Right Ventricular Failure Clinical Problem This case was chosen as it highlights the high index of suspicion required in order to diagnose and treat RVF. (Domain 3) A 66 year old retired electrician presented acutely to A+E with a 2 day history of productive cough, fatigue and pyrexia. He was referred by the A+E team due to his type 1 respiratory failure and “white out” of the right hemithorax on CXR. Further history from the patient revealed a preceding gradual decline in exercise tolerance over the past 18 months together with a history of significant exposure to asbestos during his working life. This was accompanied by the discovery of marked clubbing, peripheral oedema, hepatomegaly and raised JVP on examination. ECG showed atrial fibrillation with a ventricular rate of 120 whilst chest USS confirmed a massive right sided plural effusion. Immediate management of the patient involved insertion of an intercostal chest drain and CPAP whilst a HDU bed was organized. Management The patient’s dysponea was markedly improved by the drainage of 2L plural fluid (transudate) from his pleural cavity. Despite this he remained in type 1 respiratory failure, desaturating rapidly when his CPAP was discontinued. Repeat CXR confirmed drainage of the effusion but also showed appearances suggestive of pulmonary fibrosis with pleural plaques. Transthoracic echocardiography revealed pulmonary hypertension and an enlarged right ventricle with impaired contractility (as assessed by the degree of systolic excursion of the tricuspid annular plane) consistent with the clinical diagnosis of RVF. Invasive monitoring was established and the patient was given a cautious fluid challenge whilst also being started upon a dobutamine infusion. Diuresis was induced with combined intravenous frusemide and spironolactone. His atrial fibrillation was treated with magnesium sulphate and digoxin (amiodarone was avoided in view of the suspected pulmonary fibrosis). The patient was also anticoagulated with subcutaneous low molecular weight heparin. His clinical condition gradually improved over 48 hours and he was weaned off CPAP and dobutamine. A subsequent CTPA ruled out pulmonary embolism but confirmed the presence of subpleural fibrotic changes particularly in the lower lobes. He was discharged under the joint care of the cardiologists and respiratory physicians where his subsequent management involved commencement of Bosartan and warfarinisation. He was eventually discharged home. Discussion Classically the right ventricle of the heart has been viewed as subordinate to the more important left ventricle even described in one study as merely a ”passive conduit”(1). This view has been challenged and corrected over the subsequent years with RVF now recognised as having an equal prevalence but much worse prognosis than LVF (2,3) . Unlike the left ventricle which generates a high pressure pulsatile flow through a arterial tree with low compliance, the right ventricle is anatomically adapted for the low resistance, high compliance pulmonary circuit (4). The right ventricle wall is 3-4 times thinner than the left ventricle, contracting from the apex to the outflow tract with a peristalsis-like motion which generates one sixth of the work of the left ventricle whilst moving the same volume of blood. When one compares the pressure-volume relationships of the right and left ventricles, the right ventricular loop is much more triangular in shape with shorter periods of isovolumetric contraction and relaxation (5). This leads to a prolonged low pressure emptying that renders the right ventricle extremely sensitive to changes in afterload, such as those which occur in chronic pulmonary disease and pulmonary hypertension. RVF may occur due to either Volume overload (as occurs in tricuspid or pulmonary valve incompetence). Pressure overload (as occurs in pulmonary embolism, pulmonary hypertension, ARDS or pericardial disease). Impaired contractility (myocardial infarction, sepsis). However frequently a combination of these mechanisms is involved. Diagnosis is by high index of clinical suspicion as no one sign, symptom or test is infallible. The absence of pulmonary congestion with a raised JVP is considered most specific for RVF however this is unlikely to be helpful in the average ventilated ICU patient. Various imaging modalities including MRI, radionuclide scanning and contrast ventriculography may all help assess right ventricular function but again are impractical in the vast majority of ICU patients. As a result echocardiography is the mainstay of right ventricular functional assessment. This allows measurement of right ventricular size, pulmonary artery pressures (via Doppler techniques) and estimation of contractility via measuring the systolic excursion of the tricuspid annular plane. There are a numerous treatment strategies for RVF, these can be divided into supportive measures and vasodilatory agents. Supportive measures include Initial trial of volume replacement as right ventricular failure is often preload dependent, however if signs of ventricular overload are present (raised CVP or septal shift on echocardiography) then this is to be avoided. Ventilatory support to prevent hypoxia and thus increasing pulmonary vascular resistance. Dobutamine is the inotrope of choice due to its beneficial effect on right ventricular contractility and minimal effect on pulmonary vascular resistance (6). Diuretics. The aim of vasodilator therapy is to improve right ventricular function via a reduction in afterload and as such predominantly target the pulmonary circulation. Available agents include Prostaglandins such as epoprostenol (prostocyclin) which has been shown to improve survival in patients with pulmonary hypertension (7). Endothelin receptor anatagonists. Bosartan, a dual ET A/ETB endothelin receptor antagonist, has been shown to improve right heart function in clinical trials (8). Phosphodiesterase inhibitors (Sildenafil). However despite the variety of treatment agents the prognosis remains poor particularly if, as in this case, the RVF is a marker of the severity of the underlying disease process. Lessons learnt This was a challenging case and required a multidisciplinary approach in order to allow the patient to be discharged home. It highlighted to me that in order to diagnose RVF a high index of clinical suspicion is required but also that the condition is much more common than I had previously suspected. References 1) Starr I et al. The absence of conspcious increments of venous pressure after severe damage to the RV of the dog, with discussion of the relation between clinical congestive heart failure and heart disease. Am Heart J. 1943; 26: 291-301. 2) Cohen JN et al. Right ventricular infarction, clinical and haemodynamic features. Am J Cardiol. 1974; 33: 209-14. 3) Mehta SR et al. Impact of right ventricular involvement on mortality and morbidity in patients with inferior myocardial infarction. J Am Coll Cardiol. 2001; 37: 37-43. 4) Mebazaa A et al. Acute right ventricular failure- from pathophysiology to new treatments. Intensive Care Med. 2004; 30: 185-196. 5) Redington AN et al. Characteristics of the normal right ventricular pressure-volume relation by biplane angiography and simultaneous micromanometer pressure measurements. Br Heart J. 1988; 59: 23-30. 6) Pagnamenta A et al. Pulmonary vascular effects of dobutamine in experimental pulmonary hypertension. Crit Care Med. 2003; 31: 1140-6. 7) Barst RJ et al. A comparison of continuous intravenous epoprostenol with conventional therapy for primary pulmonary hypertension. NEJM. 1996; 334: 296-302. 8) Channick RN et al. Effects of the dual endothelin receptor antagonist bosartan in patients with pulmonary hypertension: a randomized placebo controlled study. Lancet. 2001; 47: 2049-56. List of Abbreviations RVF (Right Ventricular Failure). A+E (Accident and Emergency). CXR ( Chest X-ray). USS (Ultrasound). CPAP (Continuous Positive Airway Pressure). HDU (High Dependency Unit). CTPA (Computer Tomography Pulmonary Angiogram). LVF (Left Ventricular Failure). ARDS (Acute Respiratory Distress Syndrome). ICU ( Intensive Care Unit).