Biventricular heart failure

Article written and reviewed by Dr Luca Moretti

Biventricular heart failure is a syndrome in which both ventricles have insufficient pump reserve and/or pathological filling pressures, with a combination of pulmonary congestion, systemic congestion, and reduced cardiac output. It is not simply the sum of left- and right-sided heart failure: the septum, pericardium, pulmonary circulation, and valves couple the two chambers, so that deterioration of one changes the loading conditions and geometry of the other. The phenotype may develop simultaneously, as in diffuse cardiomyopathies, or sequentially, most often through progression of left heart disease to pulmonary hypertension and right heart dysfunction. Reverse trajectories also exist, in which chronic right-sided overload reduces left heart filling and eventually impairs global function; left ventricular ejection fraction may be reduced, mildly reduced, or preserved. Diagnosis therefore requires a bilateral and integrated assessment of volumes, cardiac output, pressures, valves, and organ perfusion, not the use of LVEF alone.

Extensive ischemic heart disease, dilated cardiomyopathy, myocarditis, toxicity, genetic diseases, multivalvular disease, and congenital heart disease are frequent causes. In advanced forms, secondary mitral and tricuspid regurgitation amplify volume and pressure, while the kidneys and liver promote sodium retention and reduce treatment tolerance. Presentation ranges from pulmonary edema with systemic venous signs to edema and ascites with few crackles, through to biventricular shock; the distribution of congestion depends on compliance, pulmonary pressure, atrial function, the pericardium, and the speed of onset. Treatment must correct the cause, achieve decongestion without removing necessary preload, apply prognosis-modifying therapy for the left-sided phenotype, control right ventricular afterload, and assess devices, valves, and advanced therapies early.

Etiology, pathogenesis, and pathophysiology

Dilated cardiomyopathy often involves both ventricles because of genetic abnormalities, inflammation, toxicity, or tachycardia. Variants in LMNA, DSP, FLNC, RBM20, and desmosomal genes may combine biventricular dysfunction, conduction abnormalities, and arrhythmias; etiological characterization is therefore relevant even when the final appearance seems nonspecific. Ischemic heart disease produces left ventricular myocardial loss and, with right ventricular infarction or right coronary ischemia, direct injury to the right ventricle. Even without right ventricular necrosis, increased pulmonary pressure and reduced coronary perfusion may cause secondary dysfunction. Fulminant myocarditis, sarcoidosis, Chagas disease, amyloidosis, and hemochromatosis may diffusely involve the myocardium. Magnetic resonance imaging, scintigraphy, genetic testing, or biopsy are selected because specific treatments are available for some causes.

In HFrEF, elevated left atrial pressure is transmitted to the pulmonary veins and increases right ventricular afterload. Initially, the hypertension is passive and postcapillary; chronic exposure may induce vasoconstriction and remodeling, creating a precapillary component and increased pulmonary vascular resistance; the right ventricle hypertrophies and then dilates. When contractility no longer increases in proportion to the load, coupling with the pulmonary artery declines, right atrial pressure and tricuspid regurgitation increase, and prognosis worsens. In HFpEF, the stiff left ventricle and diseased atrium may generate the same progression. Thus, a normal LVEF does not prevent severe biventricular disease.

The interventricular septum transmits force and defines cavity shape. Right ventricular pressure overload flattens it in systole, and volume overload in diastole; displacement reduces left ventricular compliance and may decrease cardiac output even without additional left ventricular myocardial damage. The pericardium limits total volume. When both ventricles are dilated, a small increase in volume in one chamber takes space away from the other: this diastolic competition makes the response to fluids unpredictable and explains why volume expansion may worsen cardiac output. Intrathoracic pressure and ventilation modify venous return and the transmural gradient. High PEEP may relieve left-sided edema but increase right ventricular afterload, requiring an individual balance.

Secondary mitral regurgitation increases left atrial volume and pulmonary pressure; tricuspid regurgitation increases right-sided volume and venous pressure. The two lesions form a valvular cycle in which annular dilation and tethering progress even if the initial cause was ventricular. Atrial fibrillation eliminates the atrial contribution to filling, makes cardiac output irregular, and promotes atrial functional regurgitation. In ventricles with poor compliance, the hemodynamic cost of losing sinus rhythm is high. Dyssynchrony from bundle branch block or right ventricular pacing reduces left ventricular efficiency, alters the septum, and may worsen right heart function; CRT may improve both ventricles in responders, but scar and pulmonary disease limit the effect.

Reduced cardiac output activates the sympathetic nervous system, the renin-angiotensin-aldosterone system, and vasopressin; venous pressure reduces renal filtration. The kidney interprets low effective arterial blood volume as depletion, retaining sodium despite edema: this dual renal insult makes congestion more resistant. The liver experiences sinusoidal stasis from right-sided pressure and centrilobular hypoxia from reduced cardiac output. Bilirubin, INR, and albumin reflect different components and influence procedural risk and eligibility for advanced therapies. Intestinal edema, inflammation, and satiety cause malnutrition; sarcopenia reduces the venous muscle pump and functional capacity, promoting inactivity and further retention.

In biventricular shock, hypoperfusion and reduced cardiac output coexist, with possible hypotension and elevated right and left filling pressures according to the hemodynamic phenotype. The ratio of right atrial pressure to wedge pressure, the pulmonary artery pulsatility index, and cardiac power output help identify the dominant ventricle, but do not replace the overall clinical assessment. A right-dominant phenotype may require reduction of pulmonary afterload and right-sided support; a left-dominant phenotype requires greater left ventricular unloading; an isolated LV device may fail if the right ventricle cannot sustain flow through the lungs. Acidosis, hypoxia, and ventilation further increase right ventricular load; resuscitation must therefore address systemic blood pressure, oxygenation, and congestion simultaneously.

Clinical manifestations

Exertional dyspnea, orthopnea, and nocturnal dyspnea arise from the left-sided component; edema, abdominal distention, satiety, and nausea from the right-sided component; the combination is typical, but the distribution of symptoms changes with therapy and chronicity. Fatigability, confusion, oliguria, and coldness indicate low cardiac output. Blood pressure may remain normal because of vasoconstriction until reserve is exhausted; a reduction from usual blood pressure is significant even above 90 mmHg. Palpitations, syncope, and ICD shocks suggest arrhythmia. Syncope may also result from pulmonary hypertension or valvular stenosis and requires rapid assessment.

Elevated jugular venous pressure, hepatojugular reflux, and the v wave document right-sided pressure; crackles, a third heart sound, and effusions support pulmonary congestion; absence of crackles is common in chronic congestion and does not exclude elevated wedge pressure. Examination may show a biventricular impulse, a laterally displaced apex beat, a parasternal heave, and mitral and tricuspid murmurs. An accentuated P2 suggests pulmonary hypertension. Hepatomegaly, ascites, sacral edema, and anasarca indicate advanced stasis. Cold skin and a narrow pulse pressure distinguish the hypoperfused component from isolated congestion.

Weight alone does not quantify volume. Ascites, effusions, and muscle loss may mask changes; subclinical congestion may persist at discharge despite weight reduction. Bedside lung and venous ultrasound complements the examination, but B-lines, the vena cava, and venous patterns depend on the lungs, ventilation, and regurgitation; the finding should modify a clinical probability, not become an isolated target. A reduced diuretic response manifests as low urine output and failure of symptoms to regress. It may result from an insufficient dose, absorption, kidney function, abdominal pressure, or tubular adaptation.

Acute decompensation may be precipitated by ischemia, arrhythmia, infection, embolism, hypertensive crisis, progression of valvular disease, NSAIDs, or treatment omission. Multiple factors often interact, and the dominant precipitant must be treated without neglecting the others; rapid pulmonary edema often indicates redistribution and afterload; progressive anasarca reflects sodium accumulation. In biventricular disease, these may coexist and require vasodilation and decongestion in different proportions; deterioration with hypotension, elevated lactate, oliguria, or altered mental status constitutes an emergency and requires assessment for shock and the need for support.

NYHA class measures limitation but does not distinguish mechanisms. KCCQ, the six-minute walk test, and cardiopulmonary exercise testing quantify burden and response; the VE/VCO2 slope may be particularly elevated with right heart dysfunction and pulmonary hypertension. Frailty and cognition influence adherence and prognosis. Repeated hospitalizations cause deconditioning, loss of independence, and delirium, which may persist after decongestion. Depression, sleep disorders, and isolation are frequent; multidimensional assessment is necessary before complex procedures and advanced therapies.

Investigations and diagnosis

ECG assesses ischemia, fibrillation, conduction blocks, a wide QRS, hypertrophy, and arrhythmias; radiography evaluates edema, effusions, cardiomegaly, and pulmonary arteries, but may have low sensitivity in chronic congestion. BNP or NT-proBNP confirms wall stress but does not identify the responsible chamber. Troponin, complete blood count, kidney function, electrolytes, liver function, TSH, iron status, blood gases, and lactate define the cause and systemic severity. Urine testing and albumin distinguish renal or hepatic components of edema; elevated bilirubin with jugular venous distention and regurgitation supports congestion, while massive aminotransferase elevations suggest hypoxia.

Echocardiography must be comprehensive: left ventricular ejection fraction and volumes, strain, diastolic function, atria, valves, TAPSE, S’, right ventricular area, free-wall strain, pulmonary pressure, vena cava, and pericardium. A description of “reduced right heart function” without measurements is insufficient to track the trajectory; the severity of functional regurgitation varies with volume and pressure; multiparametric methods and three-dimensional imaging improve assessment. Device leads and acoustic windows may require transesophageal echocardiography. TAPSE/sPAP estimates right ventricular-pulmonary arterial coupling. In massive regurgitation and at very low pressures it may appear falsely favorable, so it must be integrated with cardiac output and signs of stasis.

Magnetic resonance imaging accurately measures both ventricles and identifies fibrosis, infarction, infiltration, myocarditis, noncompaction, and arrhythmogenic heart disease; late enhancement has etiological and prognostic value, particularly when the ICD decision is not explained by ejection fraction. Coronary CT or angiography defines ischemia; chest CT and ventilation-perfusion scintigraphy investigate pulmonary and thromboembolic disease; the clinical question determines the choice, avoiding an indiscriminate sequence of tests. Genetic testing is indicated in selected cardiomyopathies and must be accompanied by counseling and family screening. A high-risk genotype may modify arrhythmic protection.

Right heart catheterization is useful when the hemodynamic profile is uncertain, treatment produces no response, shock is present, or transplantation, mechanical support, or pulmonary hypertension is being evaluated. It measures atrial pressure, wedge pressure, cardiac output, vascular resistance, and oxygen saturations with rigorous technique. Elevated pressures in both compartments confirm biventricular congestion; disproportionate right-sided pressure may indicate right ventricular failure or substantial regurgitation; wedge pressure may be distorted by v waves, ventilation, or position. In shock, the catheter allows the response to be tracked, but static values do not define the perfect fluid dose. Trends and a cautious therapeutic trial are more useful.

Cardiopulmonary exercise testing quantifies peak VO2, ventilatory efficiency, and prognosis. In advanced assessment, a low peak is insufficient: effort, therapy, obesity, anemia, and the pulmonary component must be considered; exercise hemodynamics may reveal pathological pressures when resting findings do not explain symptoms. Measurement of the pressure-flow relationship characterizes the reserve of both circulations. Endomyocardial biopsy is reserved for suspected myocarditis, infiltration, or diseases in which histology changes treatment. It is not necessary in unselected chronic biventricular heart failure.

The differential diagnosis includes constriction, tamponade, cirrhosis, nephrosis, pulmonary diseases, and high-output conditions. Constriction may mimic bilateral congestion and requires respiratory Doppler assessment, pericardial imaging, and sometimes simultaneous pressures. Once the syndrome is defined, the report must specify the dominant ventricle, congested or hypoperfused profile, left ventricular ejection fraction, right heart function, pulmonary pressure, valves, and cause. This description guides treatment better than the generic label; monitoring compares weight, signs, peptides, kidney function, liver function, and imaging. Clinical changes often precede a significant change in ejection fraction.

Treatment and prognosis

Decongestion with loop diuretics is the main symptomatic treatment. Intravenous dose, early response, and sequential blockade are adapted to kidney function, blood pressure, and urinary sodium; the goal is to reduce both pressures without causing left ventricular underfilling or hypoperfusion. A moderate rise in creatinine during effective decongestion does not always equate to structural injury, whereas residual congestion is unfavorable; organ signs and the overall response guide management more than a single value. Tense ascites and effusions may require selected drainage for symptoms or pressure, accompanied by control of the cardiac condition and assessment of coagulation and infection.

If HFrEF is present, ARNI or ACEi/ARB, an evidence-based beta-blocker, MRA, and SGLT2 inhibitors are introduced early according to stability. In HFpEF or HFrEF, specific therapies are applied, maintaining the principle that right heart function does not negate the benefit on the left ventricle. Hypotension and kidney dysfunction require removal of unnecessary drugs, correction of volume status, and rational sequencing. Reducing all classes simultaneously may accelerate deterioration. Atrial fibrillation is anticoagulated according to risk and managed with individualized rate or rhythm control. In the phenotype dependent on atrial systole, rhythm control may offer a substantial hemodynamic advantage.

Ischemia is treated with revascularization when indicated; myocarditis, amyloidosis, sarcoidosis, and metabolic cardiomyopathies follow dedicated therapies. Embolism and pulmonary hypertension require correct classification before vascular drugs; reducing pulmonary afterload by correcting hypoxia, acidosis, embolism, or left-sided pressure is often more important than an inotrope. Specific pulmonary vasodilators are not a general treatment for the biventricular form due to left heart disease. In the acute setting, norepinephrine supports blood pressure; dobutamine or milrinone is reserved for hypoperfusion. Tachycardia and hypotension necessitate the minimum effective dose.

CRT is indicated in patients meeting criteria for ejection fraction, QRS duration, morphology, and therapy and may produce remodeling of both ventricles. ICD prevents arrhythmic death in appropriate profiles; genotype and scar may broaden assessment beyond ejection fraction. Secondary mitral regurgitation may be treated with a transcatheter approach in selected patients after maximal therapy and CRT; tricuspid intervention requires judgment regarding pulmonary pressure, right heart function, liver function, kidney function, and anatomy, because an excessively advanced stage limits benefit. Primary valvular diseases are managed through the Heart Team. Correcting one valve alone may change the load on the other and requires serial reassessment.

In shock, temporary support is selected according to the dominant ventricle. An intra-aortic balloon pump, left-sided pumps, right-sided support, and ECMO produce different effects; balanced unloading avoids pulmonary congestion or inadequate emptying of the device; a durable LVAD requires right heart function capable of providing preload. Elevated atrial pressure, regurgitation, kidney dysfunction, and liver dysfunction increase the risk of postimplantation right heart failure and may require preventive strategies or biventricular support. Transplantation is evaluated before pulmonary vascular resistance, cirrhosis, or frailty becomes irreversible. Palliative care is integrated throughout the pathway, not only after exclusion from advanced therapies.

Rehabilitation, nutrition, vaccinations, and control of diabetes, sleep apnea, obesity, and iron status improve reserve; exercise is adapted to stability and pulmonary pressure; strength and balance protect against frailty. Prognosis is worse than with isolated dysfunction and depends on right ventricular function, hospitalizations, cardiac output, atrial pressure, kidney function, liver function, sodium, and functional capacity. Improvement in LVEF without right heart recovery leaves high risk. Close follow-up after hospitalization allows optimization of diuretics and therapy; an increasing dose requirement, hypotension, or intolerance signals advanced heart failure.

Complications

Acute decompensations cause pulmonary edema, ascites, effusions, and anasarca; residual congestion promotes rehospitalization; discharge based solely on improvement in dyspnea may leave systemic venous pressure elevated. Diuretic resistance results from kidney function, perfusion, venous congestion, intestinal absorption, and nephron adaptation. Sequential strategies increase the risk of hyponatremia, hypokalemia, and alkalosis and require frequent laboratory monitoring; excessive depletion may reduce left ventricular filling and cardiac output, particularly with pulmonary hypertension and marked interdependence.

Biventricular shock leads to kidney failure, hypoxic liver injury, intestinal ischemia, and neurological impairment. Lactate may be influenced by adrenergic drugs and the liver, but trends and clearance complement perfusion assessment; right heart failure after LVAD implantation is a feared complication and may require inotropes, inhaled vasodilators, or support. Perioperative prevention begins with selection and decongestion; support devices may cause hemolysis, bleeding, ischemia, thrombosis, and infection. The proportionality of benefit and risk is reassessed daily.

Atrial fibrillation and ventricular arrhythmias reduce cardiac output and cause sudden death. Potassium and magnesium disturbances, ischemia, and inotropic drugs increase risk; electrical monitoring is essential during unstable phases. Intracardiac thrombi and thromboembolism may occur with dilated chambers and low cardiac output; anticoagulation follows defined indications and balances hepatic congestion, kidney function, and procedures. Device-related or valvular endocarditis may cause acute regurgitation and sepsis. Fever and sudden worsening require blood cultures and appropriate imaging.

Cardiorenal and cardiohepatic syndromes become chronic with venous pressure exposure. Advanced hepatic fibrosis, hypoalbuminemia, and coagulopathy reduce eligibility and increase bleeding; damage may be partially reversible if corrected before the structural phase. Intestinal edema, cardiac cachexia, and sarcopenia impair absorption, immunity, and rehabilitation. Weight and albumin do not readily distinguish water from tissue and must be integrated with nutritional assessment. Frailty and cognitive decline increase treatment errors. Caregivers and community care become part of readmission prevention.

Progressive valvular disease may make regurgitation massive and less treatable; late intervention, after severe right heart dysfunction or organ damage, offers inferior outcomes; surveillance must anticipate the point of no return. Fixed pulmonary hypertension may preclude isolated heart transplantation; early advanced assessment allows reversibility testing and strategies before vascular resistance and frailty increase. In the terminal phase, dyspnea, edema, pain, and anxiety require palliative treatment together with planning for devices and resuscitation. Clarity about goals avoids inconsistent procedures.