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Right ventricular failure

Right ventricular failure (RVF), also known as right-sided heart failure, occurs when the right ventricle of the heart cannot pump blood efficiently to the lungs to be oxygenated. 

Right heart failure, also known as right-sided heart failure, occurs when the right side of the heart is unable to pump blood effectively. 

The heart consists of two sides: the left side and the right side. 

The left side receives oxygenated blood from the lungs and pumps it to the rest of the body, while the right side receives deoxygenated blood from the body and pumps it to the lungs for oxygenation.

In right heart failure, the weakened right side of the heart is unable to adequately pump blood, leading to a buildup of fluid and congestion in the body, particularly in the veins, liver, and lower extremities. 

Common causes of right heart failure include left heart failure, chronic lung diseases, such as chronic obstructive pulmonary disease or pulmonary hypertension, heart valve disorders, and certain congenital heart defects.

Symptoms of right heart failure may include:

1. Peripheral edema

2. Hepatomegaly

3. Ascites

4. Jugular venous distention

5. Rapid weight gain:

6. Shortness of breath

7. Fatigue and weakness

8. Decreased urine output

9. Cyanosis

Acute increases in afterload are poorly tolerated by the right ventricle as demonstrated by acute pulmonary embolus.

Treatment options for right heart failure depend on the underlying cause but may involve medications to manage fluid buildup, such as diuretics, medications to improve heart function, such as ACE inhibitors or beta-blockers, oxygen therapy, lifestyle modifications and in severe cases, surgical interventions like heart transplantation or the placement of a ventricular assist device.

The right ventricle plays a critical pathophysiological and prognostic role in left heart failure, pulmonary arterial hypertension, and severe acute respiratory distress syndrome..

Treatment for RVF typically focuses on addressing the underlying cause, such as treating heart or lung disease, reducing fluid buildup, and improving heart function.

Some treatments include medications such as diuretics to reduce fluid buildup, oxygen therapy to improve breathing, and medications to improve heart function. 

In severe cases, surgical interventions such as heart valve replacement or transplantation may be necessary. 

The major determinants of right ventricular function include: preload, afterload, contractility, and lusitropy.

Mechanisms of RVF can be acute or chronic abnormalities of the right ventricular load-preload or afterload, or myocardial function, contractility, and active relaxation (lusitropy).

In RVF these mechanisms frequently coexist.

RVF can be initiated or promoted by myocyte hypertrophy, fibrosis, ischemia, neurohormonal activation, Inflammation, and shifts in metabolic substrates.

As fibrosis progresses right ventricular, diastolic function and contraction coupling worsen and contraction is impaired.

Chronic increased afterload from any cause resulting RVH, which initially adapts and is accompanied by increasing contractility and preserved stroke volume, achieved in part  by neural hormonal activation with increased adrenergic tone. 

Eventually, neurohormonal activation is maladaptive with reduced rate ventricular beta adrenergic receptor density, depletion of tissue adrenergic effects and failure of myocyte adenylate cyclase stimulation in response to beta agonists.

Overtime, right ventricular contractility declines, or afterload further increases, and the right ventricle dilates to maintain stroke volume.

Eventually, right ventricular ischemia, reduced right coronary artery flow, excessive oxygen demand exceeds supply, contractility declines, resulting  in the state of ventriculoarterial uncoupling and right ventricular failure.

Mechanical stress, ischemia, and neurohormonal activation, stimulate the production of cardiac fibroblast collagen.

Insulin resistance and obesity may be modifiable risk factors for right ventricular dysfunction as diabetes is associated with worse right and systolic diastolic function in patients with dilated cardiomyopathy or pulmonary hypertension.

Right ventricular remodeling is present in patients with diabetes or prediabetes, and add potential mechanisms of damage by promoting myocardial fibrosis, inflammation, microvascular, ischemia, and lipotoxicity.

Obesity contributes to right ventricular dysfunction by affects on ventricular preload, afterload, and contractility,  myocyte function, increased circulating pro inflammatory adipokines, and lipotoxicity from excess myocardial lipid delivery, hypoxia from obesity associated hypo ventilation, and sleep apnea, increased pulmonary and systemic blood pressure.

Diagnosis:

Evaluation is suggested by history and physical findings that include dyspnea, lower extremity edema, early satiety abdominal fullness, fatigue, exertional intolerance, and right upper quadrant tenderness, along with historical features of the presence of coronary disease, left heart failure, valvular disease, chronic lung disease, venous thrombosis, or embolism, connective tissue, disease, and HIV.

Clinical findings suggestive of right ventricular failure include elevated jugular venous pressure, right ventricular heaves, prominent pulmonic heart sound, murmur of tricuspid regurgitation, palpable and pulsatile liver, hepatojugular reflux, ascites, and lower extremity edema.

Elevated BNP levels are diagnostically sensitive, but not specific.

EKG may show signs of right atrial dilation, right axis deviation, or right ventricular hypertrophy.

Transthoracic echocardiography provides rapid assessment of the right ventricular size and function, and can estimate primary systolic pressure in most patients.

Transthoracic echocardiography provides reproducible information with prognostic value, including function, ventricular wall longitudinal strain,  dilation of the inferior vena cava,  and assesses the left ventricular size, left atrial size, systolic, and diastolic function, valve function, and pericardial constraints, which help narrow the differential diagnosis.

Echocardiogram is the initial screening tool to detect an increase in afterload.

Cardiac MRI can assess right ventricular ejection fraction and mass, right ventricular and systolic volume index, providing information for prognosis and risk stratification.

Right heart catheterization can directly measure intracardiac and pulmonary pressures, as well as cardiac output and estimates right ventricular preload (right atrial pressure or right ventricular end diastolic pressure) and afterload (pulmonary vascular resistance, pulmonary arterial compliance, and pulmonary arterial elastance).

Right heart catheterization can estimate right ventricular function, stroke volume, stroke volume index, the ratio of right arterial pressure to pulmonary artery wedge pressure, right ventricular stroke work index, and pulmonary artery pulse index.

Tricuspid regurgitation is commonly identified with right ventricular heart failure, due to the presence of excessive preload.

An acute reduction in right ventricular contractibility can occur with myocardial infarction or myocarditis or as a result of cardiac surgery.

Post surgical right ventricular contractor dysfunction is common and manifests as difficulty in weaning a patient from cardio pulmonary bypass along with low cardiac output.

Right ventricular failure is common in patients with left heart failure receiving left ventricular assist device management.

Chronic right ventricular failure due to impaired contractility activity can occur as part of a cardiomyopathy and left heart failure is the most common cause of right ventricular failure.

The majority of the right ventricle’s blood supply comes from the right coronary artery through right ventricular marginal branches.

 

 

 

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