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
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.
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.