Right heart failure

Learning objectives

Right heart failure (RHF) is defined as dysfunction of the right heart structures, predominantly the right ventricle (RV), but also the tricuspid valve and right atrium
Impaired vena cava flow, resulting in an impaired ability of the right heart to perfuse the lungs at normal central venous pressures, can also cause RHF
Ventricular interdependence, the phenomenon whereby the function, volume, or pressure in one ventricle can directly influence that of the other, contributes to right heart failure in case of left ventricular dysfunction
Vice versa, when RV pressure or volume overload occurs, the RV can affect LV performance and result in a decreased LV preload and contractility
Elevated filling pressures on the right side of the heart lead to backward failure and systemic venous congestion

Backward failure:
- Negatively affects the hepatic function
- Causes acute kidney injury and aggravates further fluid retention and worsening RHF
Fundamental management principles involve optimizing rate, rhythm, perfusion, and preload, whilst maintaining contractility and minimizing afterload

	Decreased RV contractility	RV volume overload	RV pressure overload
Acute	Sepsis		Acidosis
	LVAD support		Hypoxia
	Myocarditis		Acute Respiratory Distress Syndrome
	Perioperative injury/ischemia (postcardiotomy)		Positive pressure ventilation
			Pneumonia
			Mechanical ventilation
Chronic	Right ventricular cardiomyopathy	Left heart disease
	Arrhythmogenic right ventricular cardiomyopathy	Single ventricle
	Ebstein anomaly		Pericardial disease
		Pulmonary regurgitation	Pulmonary hypertension (PH)
		Transposition of the great arteries	Chronic thromboembolic Pulmonary hypertension (PH)
		Tricuspid regurgitation (TR)	Pulmonary stenosis
		Congenital heart disease with a shunt (ASD or anomalous pulmonary venous return)	Left-sided valvular heart disease
			Restrictive cardiomyopathy
			Chronic obstructive pulmonary disease
			Right ventricular outflow tract obstruction

Another important mechanism that leads to RHF is intrinsic RV myocardial disease:

RHF may be caused by impaired filling which is seen in the following conditions:

Acute RHF

Chronic RHF

Diuretics and sodium restriction
- Combination therapy: loop diuretics with thiazides
Renin-angiotensin-aldosterone system inhibitors, beta-blockers, and hydralazine
Digoxin
Pulmonary vasodilators
- Prostacyclin analogs
  - Epoprostenol
  - Treprostinil
  - Iloprost
- Phosphodiesterase-5 inhibitors
- Endothelin receptor antagonists
Mechanical circulatory support
- ECMO
- RVAD
- LVAD
Transplantation

	Classification	Dose (i.v. unless stated)	Effects	Advantages	Disadvantages
Noradrenaline	Vasopressor	0.02-0.2 µg/kg/min	Vasoconstriction, ↑SVR, ↑myocardial O2 delivery, ↑PVR	Cheap, easy to titrate, familiarity	Arrhythmias, ↑PVR in higher doses
Vasopressin	Vasopressor	1-4 units/min	Vasoconstriction, ↑SVR, pulmonary vasodilatation at low doses via endothelial nitric oxide pathway, ↑myocardial O2 delivery	Catecholamine-sparing, less ↑PVR than noradrenaline, easy to titrate	Expensive, bradycardia, splanchnic ischemia
Dobutamine	Inodilator	2.5-10 µg/kg/min	Inotropy, ↑contractility, ↓SVR, PVR	Easy to titrate, cheap	↑O2 demand, tachyarrhythmias, systemic hypotension
Milrinone	Inodilator	0.75-0.75 µg/kg/min	Inotropy, ↑contractility, ↓SVR, PVR	Pulmonary vasodilatation	Systemic hypotension
Levosimendan	Inodilator	Loading dose: 6-12 µg/kg/min over 10 min followed by infusion of 0.1 µg/kg/min	↑Contractility	No effect on myocardial oxygen demand	Expensive, tachycardia, hypotension, headache
Sildenafil	Pulmonaryvasodilator	10 mg t.d.s. Oral: 20-100 mg t.d.s	↓PVR, ↑Contractility	Oral administration for patients with chronic disease	Long terminal half-life (4e18 h), ↓SVR
Epoprostenol	Pulmonaryvasodilator	1-2 ng/kg/min Nebulized: 0.2-0.3 ml/min of a 10-20 µg/mil solution	↓PVR, ↑V/Qmismatch	As efficient as nitric oxide	Systemic hypotension with i.v. administration, flushing, headaches