lntroduction

What happens to the right ventricle may be deter -mined by resistance in the pulmonary circulation.For example,if there is disease in the microcirculation of the lung then there is increased pulmonary vascular resistance to R V emptying and increased pressure overload of the right ventricle.

Increased pulmonary vascular resistance may be related to pulmonary disease but the pulmonary venous circulation can also increase and raise P A resistance as a result of increased left atrial pressure due to mitral regurgitation,mitral stenosis or a stiff and abnormal left ventricle from any cause which increases LV filling pressures.A cardiac ultrasound of the short axis of the ventricle in this type of patient reveals a D shaped left ventricle and systolic septal f attening.When the R V is dysfunctional,peripheral signs are usually apparent,e.g.distended neck veins,tender enlar ged liver and peripheral edema,particularly if the tricuspid valve is insuff cient.

Some Problems that may Result in RV Dysfunction

When RV dysfunction is present it is usually associated with LV failure or pulmonary hypertension due to pulmonary disease.Cardiomyopathy patients due to myocarditis or myocardial ischemia generally show poor function of both ventricles.Symptoms are usually due to left heart disease.Increased pulmonary venous pressure is usually related to increased L VEDP,which increases pulmonary artery pressure,which increases resistance to R V outflow.

Arrhythmogenic RV cardiomyopathies are unique and demonstrate dilation and aneurysms of the free wall,flbro fatty replacement,and severely reduced myocardial strain by echo.I am not aware of patients with ARVD dying of heart failure but patients do die suddenly of arrhythmias and may require an ICD to prevent SCD.In a few cases some patients have disease of the L V and the RV.These changes are clearly shown in the central f gure illustration of “ Anatomy Function and Dysfunction of the Right Ventricle” JACC State of the art review [1].

Right Ventricular Infarction may accompany many inferior infarctions,usually the result of an occluded RCA,but may not occur without some insult to the L V.My concern is related to the fact that RV infarction is often treated with infusion of f uid,particularly if the patient remains symptomatic.This is OK if the L VEDP is normal or low but if the LVEDP is high the infusion of f uid could precipitate pulmonary edema.To me RV failure,in the setting of an acute inferior myocardial infarction means that the inferior infarction is extensive rather than small and the prognosis may not be as good as if RV failure was not present.

Pulmonary embolus may increase pulmonary artery resistance which may result in decreased emptying of the RV and symptoms of RV dysfunction.

Amyloid usually involves both ventricles and thus is not isolated R V dysfunction.Biopsy of the RV septum is usually positive or amyloid.

Sarcoid:in contrast cardiac sarcoid is not as diffuse as cardiac amyloid but often involves the R V septum.Despite the involvement of the septum,biopsy of the heart may miss the pathology of car -diac sarcoid because of the dif fuse nature of the disease.

The RV as a Conduit

I guess where I am coming from is related to an article published in 1943 in which Starr et al.reported the absence of conspicuous increments of venous pressure after severe burn damage to the right ventricle of the dog [2].This concept was further validated by completely excluding the right ventricle in patients (Fontan circulation).Flow from the venous chamber (e.g.R Atrium) bypasses the RV and fills the pulmonary arteries and can only occur if the P A pressure is low.Fontan and Baudet reported minimal increases in peripheral venous pressure and that led to the conclusion that the right ventricle wall is not necessary for the maintenance of a “ normal” circulation since the procedure completely excludes the right ventricle [3],particularly if the PA is tied off.In the animal laboratory,one can create increased resistance to emptying of the RV into the PA by banding the PA,a procedure that is no longer done.Adults who have received a Fontan procedure in childhood may develop symptoms of right heart failure as a young adult when the left ventricle fails and increases the pulmonary artery pressure and decreased RV emptying.

Causes of RV Failure

The commonest cause of R V failure is pulmonary hypertension and the commonest cause of pulmonary hypertension is left heart failure due to systolic or diastolic failure or severe mitral valve disease.However,RV failure can result from disease affecting both ventricles e.g.myocarditis,cardiomyopathy,ischemia or arrhythmias.

Evaluation of Ventricular Function (Left and Right)

The LV has the shape of a “ proloid elipse ”,has thick walls and cardiac output can be calculated using a standard formula in the catheterization laboratory.In contrast,the RV is a triangular structure,and has thin walls that seem to wrap around the LV.With the exception of magnetic resonance,cardiac output of the RV cannot be accurately calculated.It is important to point out that the ventricular septum belongs to both the right and left ventricles.

In experimental animals,the L V may contribute to RV ejection probably mainly due to septal contraction and not due to contraction of the right ventricular free wall.

The overall function of the R V is not to gener -ate pressure.The pressure that the RV does generate probably comes from the septum (which is both LV and RV).

Volume Overloaded RV

It is well known that the RV can withstand a volume overload for many years e.g.in adult ASD patients,the volume overloaded R V shows dilation as well as diastolic septal f attening and the patient may not have any symptoms.

In the past few years,I have observed a patient with isolated tricuspid valve regurgitation probably due to isolated endocarditis who had no symptoms of RV failure such as peripheral edema or ascites.How long this volume overload will persist in this patient is not known,but at least early in the course of this disease the patient described above did not have any symptoms.

I have never seen isolated R V dysfunction in patients without some elevation of the L VEDP or increased resistance in the pulmonary circulation.I believe that RV failure is the end result of L V or pulmonary failure because it is a thin walled structure that cannot tolerate increased resistance to emptying.