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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).