Right-sided heart failure

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The RV is sensitive to sudden afterload. Acute PE, hypoxia, acidosis or high airway pressure can sharply reduce output; chronic pulmonary hypertension produces progressive pressure overload and secondary tricuspid regurgitation.

Management is a three-part problem: optimise rather than maximise preload, reduce RV afterload by treating the cause, and support contractility/perfusion when shock persists. Bedside echo is central but must be integrated with the clinical cause.

Chronic isolated right-sided signs should not be labelled 'cor pulmonale' without evaluating left-heart disease, valves, pulmonary hypertension, lung disease, thromboembolism and pericardium.

Key points

Right-sided HF causes raised systemic venous pressure: raised JVP, peripheral oedema, ascites, hepatomegaly, early satiety and congestive renal/liver dysfunction.
Common drivers are left-sided HF, pulmonary hypertension or lung disease, acute PE, RV infarction, tricuspid/pulmonary valve disease, cardiomyopathy and constrictive pericardial disease.
Acute RV failure can present with shock and clear lungs; do not exclude cardiac shock because crackles are absent.
Treat the cause while balancing RV preload: severe underfilling may justify a small monitored fluid challenge, but routine repeated boluses worsen dilation and septal shift when congestion is present.
Use loop diuretic for systemic congestion, watching renal function and perfusion; venous congestion itself can drive cardiorenal dysfunction.
Avoid nitrates and other preload-reducing drugs in hypotensive RV infarction; restore coronary flow urgently through the ACS pathway.
Pulmonary vasodilators are disease-specific specialist therapy, not empirical treatment for undifferentiated RV failure and can be harmful in some left-heart or lung-disease phenotypes.
Refractory shock needs expert vasoactive therapy and early mechanical-support/advanced-centre discussion.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Left-sided heart disease

Left-ventricular failure or left-sided valve disease can raise pulmonary venous and arterial pressure, increasing right-ventricular afterload and eventually causing secondary right-sided failure.

Pulmonary vascular or lung disease

Pulmonary hypertension, chronic hypoxic lung disease and sleep-related breathing disorders raise pulmonary resistance, producing pressure overload and eventual right-ventricular maladaptation.

Acute pulmonary embolism or right-ventricular infarction

A large embolus abruptly increases afterload, whereas right-ventricular infarction reduces contractility. Either can cause acute low output, shock and raised venous pressure with relatively clear lungs.

Valve, myocardial or pericardial disease

Severe tricuspid or pulmonary valve disease, right-ventricular cardiomyopathy and constrictive pericardial disease can impair forward flow or filling and cause systemic venous congestion.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Right-ventricular load or injury
Increased pulmonary afterload, impaired myocardial contractility, abnormal valve flow or restricted filling can reduce the right ventricle's ability to eject an adequate stroke volume.
2
Dilatation and rising wall stress
Compensatory hypertrophy or dilatation may initially support output, but progressive dilatation increases wall tension and oxygen demand, can worsen ischaemia and may stretch the tricuspid annulus.
3
Ventricular interaction reduces output
Right-sided dilatation shifts the interventricular septum and limits left-ventricular filling. Systemic cardiac output falls despite preserved left-ventricular contractility in some acute presentations.
4
Neurohormonal fluid retention
Reduced perfusion activates sympathetic and renin-angiotensin-aldosterone pathways, retaining sodium and water even though venous pressure and tissue congestion are already high.
5
Systemic venous congestion
Raised right-atrial pressure is transmitted to the systemic veins, producing oedema, ascites, hepatic congestion and impaired renal filtration, which further reinforces fluid retention.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Systemic venous congestion

Raised JVP with prominent V waves when severe TR, dependent oedema, ascites, tender hepatomegaly, hepatojugular reflux and weight gain.

Acute RV shockRed flag

Hypotension, cool peripheries, oliguria, confusion and raised JVP, sometimes with clear lungs; rising lactate signals worsening output.

RV infarctionRed flag

Inferior MI with hypotension, raised JVP and relatively clear lungs; right-sided ECG changes and echo support the diagnosis.

Pulmonary embolismRed flag

Sudden dyspnoea, pleuritic pain, syncope, hypoxaemia or shock with RV strain requires the NICE PE diagnostic and reperfusion pathway.

Pulmonary-hypertension decompensation

Progressive exertional dyspnoea, syncope, loud P2, RV heave and oedema; decompensation may follow infection, arrhythmia or treatment interruption.

Severe tricuspid regurgitation

Large JVP V waves, pulsatile liver and pansystolic murmur that increases with inspiration; quantify mechanism and RV function on expert echo.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
12-lead ECG including right-sided leads when RV infarction suspectedFirst step
Why
Identify inferior/RV MI, RV strain, AF or other arrhythmia.
Interpretation and limitations
ST elevation in right-sided leads supports RV infarction; an ECG cannot exclude PE or RV failure.
02
Urgent transthoracic echocardiography
Why
Assess RV size/function, septal shape, TR, pulmonary pressure, LV and pericardium.
Interpretation and limitations
RV dilation/poor function confirms haemodynamic involvement but is not specific for cause; acute severe instability may require immediate treatment before complete imaging.
03
FBC, U&E/eGFR, LFT, coagulation, troponin, natriuretic peptide and blood gas/lactate
Why
Assess trigger, congestion, injury and perfusion.
Interpretation and limitations
Congestive cholestasis and renal dysfunction track venous pressure; troponin/BNP show strain but do not establish PE or ACS alone.
04
Chest imaging and oxygen assessment
Why
Find lung disease, oedema, effusion or alternative pathology.
Interpretation and limitations
Hypoxia and acidosis raise pulmonary vascular resistance and should be corrected; clear lungs can coexist with severe RV shock.
05
CT pulmonary angiography or V/Q imaging
Why
Confirm suspected PE through the NICE Wells/D-dimer pathway.
Interpretation and limitations
In haemodynamic instability, bedside echo and immediate specialist reperfusion decisions may precede definitive CT when transport is unsafe.
06
Right-heart catheterisation in selected patients
Why
Confirm pulmonary hypertension and define haemodynamics when non-invasive tests are insufficient.
Interpretation and limitations
Perform in a specialist pulmonary-hypertension/advanced-HF pathway; it distinguishes pre- from post-capillary physiology.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Chronic venous insufficiency or lymphoedema

Leg swelling without raised jugular venous pressure, hepatomegaly or right-heart abnormalities favours local venous or lymphatic disease rather than systemic cardiac congestion.

Cirrhosis or portal hypertension

Ascites, liver stigmata and portal-flow abnormalities may indicate primary hepatic disease; raised venous pressure and a cardiac abnormality support congestive hepatopathy, and both processes can coexist.

Renal or nephrotic disease

Heavy proteinuria, low serum albumin or intrinsic renal findings support renal oedema, although venous congestion can itself reduce filtration and create overlap.

Pericardial tamponade or constriction

Marked venous pressure with impaired filling, ventricular interaction or pericardial abnormalities suggests tamponade or constriction, which requires a cause-specific rather than generic heart-failure pathway.

Acute pulmonary embolism or RV infarction

Sudden dyspnoea or chest pain, hypoxaemia, an inferior infarct pattern or abrupt shock raises concern for an urgent cause of acute right-sided failure requiring reperfusion assessment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-lineAcute RV failureFirst stepFirst lineRaised JVP with hypoperfusion, hypoxaemia or shock

1Start ABCDE, cardiac monitoring, blood gas/lactate and urgent echo; call cardiology and critical care.
2Treat hypoxia, acidosis and the driver: activate ACS reperfusion for RV infarct or NICE PE diagnosis/reperfusion for suspected high-risk PE.
3Assess preload with examination and echo; use only a small monitored fluid challenge if clearly underfilled and stop if congestion/output worsens.
4Avoid empirical nitrate or aggressive ventilation pressures that can collapse preload in a hypotensive, preload-dependent patient.

02Second-lineCongested chronic right HFSecond lineOedema, ascites or congestive organ dysfunction without shock

1Use loop diuretic and monitor weight, urine output, renal function and electrolytes; address adherence and sodium/fluid excess rather than routine blanket restriction.
2Treat left-HF, valve, lung, sleep, rhythm or thromboembolic cause through the appropriate NICE pathway.
3Refer suspected pulmonary hypertension to a specialist service before disease-specific vasodilator treatment.
4Offer rehabilitation, vaccination and a written deterioration plan.

03Third-linePersistent low outputThird lineShock despite cause treatment and appropriate preload

1Use invasive BP and specialist haemodynamic monitoring; reassess tamponade, PE, RV infarction and mechanical ventilation effects.
2Titrate noradrenaline to maintain coronary/systemic perfusion; add dobutamine for persistent low output when appropriate.
3Avoid prolonged high-dose vasoactive therapy without a recovery or bridge plan.
4Discuss temporary RV/biventricular support or VA-ECMO early at an experienced centre when the cause is potentially reversible.

04EscalationRefractory chronic RV failureEscalationRecurrent admission, escalating diuretic, worsening renal/liver function or severe TR/PH

1Obtain expert valve, pulmonary-hypertension and advanced-HF MDT review.
2Clarify candidacy for tricuspid intervention, pulmonary endarterectomy/balloon treatment, transplant or durable/temporary support according to cause.
3Optimise rhythm and left-heart therapy and reassess frailty, nutrition and end-organ reversibility.
4Integrate palliative symptom support when needs persist, alongside active specialist management.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Relieves systemic venous congestion and ascites.

Furosemide

For chronic oedema a common oral start is 20–40 mg in the morning; acute congestion commonly starts 20–40 mg IV if loop-naive, with higher response-led IV dosing when already exposed.

Over-diuresis can reduce RV preload/output; under-diuresis leaves renal/hepatic congestion. Monitor BP, urine, weight, creatinine, sodium, potassium and magnesium.

Selected hypotensive RV shock to preserve systemic and right-coronary perfusion.

Noradrenaline

The cited ready-to-use SmPC, licensed for adults weighing over 50 kg, starts noradrenaline base at 0.05–0.15 micrograms/kg/min by central IV infusion pump, titrated in critical care to adequate MAP/perfusion.

For this product use a central venous catheter and preferably arterial BP monitoring; concentrations and labels differ between preparations. Watch for excessive vasoconstriction, arrhythmia, ischaemia and extravasation, and treat the cause concurrently.

Inotropic support for persistent low-output RV failure after preload and pressure are addressed.

Dobutamine

Usually 2.5–10 micrograms/kg/min by continuous IV infusion, titrated to perfusion/output.

Tachyarrhythmia, ischaemia and hypotension; ICU/cardiology use only and avoid without a defined bridge/recovery goal.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cardiorenal dysfunction

Raised renal venous pressure and reduced arterial perfusion impair filtration. Sodium retention then worsens congestion, creating a cycle of oedema, diuretic escalation and renal vulnerability.

Congestive hepatopathy

Chronic hepatic venous hypertension can cause tender hepatomegaly and cholestatic blood-test abnormalities; prolonged severe congestion may progress to fibrosis, impaired synthetic function and altered drug clearance.

Ascites, gut oedema and malnutrition

Splanchnic congestion can produce ascites, early satiety and gut oedema, which may impair nutrition, contribute to frailty and make oral medicine absorption or fluid management less predictable.

Functional tricuspid regurgitation and arrhythmia

Chamber and annular dilatation worsen tricuspid leakage and stretch the atria, promoting atrial arrhythmias that further reduce filling and forward output.

Low-output shock

Severe right-ventricular failure reduces pulmonary and left-sided filling, causing hypotension, tissue hypoperfusion, rising lactate and potentially cardiac arrest without rapid cause control.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

JVP, oedema/ascites, daily weight, abdominal symptoms and functional capacity.
BP, pulse/rhythm, perfusion, urine output and lactate during acute failure.
Creatinine/eGFR, sodium, potassium, magnesium and LFT during active decongestion.
Oxygenation and acid-base status; review ventilation settings that may increase RV afterload or reduce venous return.
Serial echo for RV function, TR and pulmonary pressure when clinical trajectory or intervention decisions change.
Cause-specific follow-up: anticoagulation for PE, ACS prevention, pulmonary-hypertension therapy or valve/advanced-HF review.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Clear lungs do not mean low risk

Severe RV infarction or PE can produce profound shock without pulmonary crackles.

The kidney sees the veins

Raised renal venous pressure can impair filtration; appropriate decongestion may improve kidney function despite an early creatinine fluctuation.

Fluid is a diagnostic treatment

If underfilling is plausible, give a small monitored challenge and assess output/congestion; repeated blind litres are not RV therapy.

Ventilation affects the RV

Hypoxia/acidosis raise pulmonary resistance, while excessive positive pressure reduces venous return and increases RV afterload.

Pulmonary vasodilators are phenotype-specific

They belong in specialist pulmonary-hypertension pathways and can worsen pulmonary oedema in left-heart disease.

11Common pitfallsFrequent interpretation and management errors.

01
Giving repeated large fluid boluses to a dilated, congested RV because the BP is low.
02
Using nitrates in hypotensive RV infarction or another clearly preload-dependent state.
03
Empirically starting pulmonary-arterial-hypertension drugs before specialist haemodynamic classification.
04
Ignoring left-heart, valve, PE and pericardial causes of right-sided signs.
05
Escalating vasoactive support without urgent cause control or a bridge plan.