Heart Failure: What Happens to the Circulation?
Heart failure is not one single problem with the heart. It is a clinical syndrome that develops when the heart cannot maintain the circulation normally without changes in blood flow, filling pressure or both.
Sometimes the ventricle cannot contract effectively. Sometimes it contracts reasonably well but has become stiff and difficult to fill. Valve disease, myocardial damage, longstanding hypertension and abnormal rhythms can all alter the way blood moves through the heart.
The effects are seen well beyond the myocardium. Pressure building behind the left side of the heart can congest the lungs. Raised systemic venous pressure can contribute to peripheral oedema and abdominal congestion. Reduced cardiac reserve can leave a patient exhausted or breathless with activity that was previously manageable.
Following those changes through the circulation makes the symptoms of heart failure much easier to connect with the underlying physiology.
Heart failure is a problem of flow and pressure
Each minute, the heart must receive venous blood, fill, contract and eject enough blood to maintain tissue perfusion. Cardiac output is the volume pumped by one ventricle each minute and is broadly determined by heart rate multiplied by stroke volume. Stroke volume is influenced by ventricular filling, the strength of contraction and the resistance against which the ventricle ejects.
Heart failure can disturb several parts of that process. A ventricle may be weakened and unable to contract effectively. It may be abnormally stiff and unable to relax and fill without a substantial rise in pressure. Valve disease may obstruct forward flow or allow blood to move backwards. A persistent tachyarrhythmia can shorten filling time and increase myocardial demand, while longstanding hypertension can leave the left ventricle working against increased resistance for years.
The body initially tries to protect perfusion. Sympathetic activation increases heart rate and contractility. The renin-angiotensin-aldosterone system encourages vasoconstriction and retention of sodium and water. These responses may support blood pressure in the short term, but persistent activation increases cardiac workload, promotes fluid retention and contributes to adverse ventricular remodelling. A compensatory response can therefore become part of the problem.
Ejection fraction helps describe the type of heart failure
The left ventricular ejection fraction is the proportion of blood in the left ventricle that is ejected during systole. It is usually estimated during echocardiography. It is not the same as cardiac output, and a normal-looking percentage does not prove that the heart is functioning normally.
In heart failure with reduced ejection fraction, usually abbreviated to HFrEF, left ventricular systolic contraction is impaired and the ejection fraction is reduced. The ventricle may become dilated and eject a smaller proportion of its filled volume.
In heart failure with preserved ejection fraction, or HFpEF, the ejection fraction is generally at least 50%, but the ventricle is commonly stiff and relaxes poorly. It may fill with a smaller volume or require abnormally high filling pressure. The percentage ejected can remain preserved even though the actual filling, pressure and output are not normal. Between these categories sits heart failure with mildly reduced ejection fraction.
These labels help guide treatment and describe ventricular function, but they do not replace the wider clinical picture. Symptoms, examination, natriuretic peptides, echocardiography and the likely underlying cause all matter.
Why left-sided failure causes breathlessness
If the left ventricle cannot accept or eject blood without raised pressure, pressure is transmitted backwards into the left atrium and pulmonary veins. Increased pulmonary capillary hydrostatic pressure encourages fluid to move into the lung interstitium and, when more severe, into the alveoli. The lungs become less compliant and gas exchange may be impaired.
This helps explain exertional breathlessness. Activity increases the circulation's demand, but the failing heart has limited reserve and pulmonary pressures rise. Orthopnoea, breathlessness when lying flat, can occur because recumbency redistributes blood from the lower body towards the chest. Some patients wake suddenly at night severely breathless, described as paroxysmal nocturnal dyspnoea. Fine inspiratory crackles may be heard when pulmonary congestion is present, although their absence does not exclude heart failure.
Acute pulmonary oedema is a medical emergency. The patient may become profoundly breathless, hypoxic, clammy and distressed, sometimes with widespread crackles or pink frothy sputum. This is not simply a more uncomfortable version of chronic breathlessness. It signals severe decompensation requiring urgent assessment and treatment.
Why right-sided congestion looks different
The right ventricle receives systemic venous blood and ejects it into the pulmonary circulation. Right ventricular failure can occur because of primary right-sided disease, pulmonary hypertension, lung disease or the effects of left-sided heart failure transmitted through the pulmonary circulation.
When right-sided filling pressure rises, congestion develops in the systemic venous circulation. The patient may have raised jugular venous pressure, dependent peripheral oedema, hepatic congestion, abdominal discomfort or ascites. Oedema is often most visible around the ankles in an ambulant patient, but gravity changes where fluid collects. In someone who remains in bed, sacral oedema may be more apparent.
Left- and right-sided patterns are useful for understanding the physiology, but real patients often have features of both. A patient with chronic left ventricular failure can develop pulmonary hypertension and secondary right ventricular dysfunction, producing breathlessness alongside peripheral oedema and abdominal congestion.
Forward failure affects the rest of the body
Congestion is only part of the picture. Reduced forward flow can leave skeletal muscles and organs with less perfusion, particularly during activity. Patients may describe fatigue, reduced exercise tolerance, dizziness, poor concentration or weakness. Renal perfusion can fall, while venous congestion can also impair kidney function. This makes fluid management more complex because the heart and kidneys influence one another.
Cool peripheries, prolonged capillary refill, hypotension, reduced urine output and altered cognition are concerning findings in an acutely unwell patient. They may indicate compromised perfusion, but each must be interpreted in context rather than used as a single diagnostic sign.
What causes heart failure?
Heart failure is a syndrome with an underlying cause, not a single disease. Coronary artery disease and previous myocardial infarction can leave damaged myocardium that contracts poorly. Longstanding hypertension produces pressure overload and ventricular hypertrophy. Cardiomyopathies directly affect the heart muscle, while valve disease can create pressure or volume overload.
Other contributors include atrial fibrillation and other arrhythmias, congenital heart disease, myocarditis, thyroid disease, severe anaemia, alcohol-related myocardial damage and some cancer treatments. Acute deterioration in a person with established heart failure may be triggered by infection, myocardial ischaemia, an arrhythmia, uncontrolled blood pressure, worsening renal function, missed medicines or medicines that promote fluid retention. Sometimes several factors are present together.
Looking for the cause matters because treatment is not limited to removing excess fluid. A reversible trigger, valve lesion, ischaemic problem or rhythm disturbance may need specific management.
From suspicion to diagnosis
Breathlessness and ankle swelling are common and have many possible causes. Assessment therefore begins with the story, clinical examination and an awareness of alternative explanations such as respiratory disease, venous disease, renal disease, liver disease, anaemia or deconditioning.
In suspected chronic heart failure, National Institute for Health and Care Excellence (NICE) guidance uses measurement of N-terminal pro-B-type natriuretic peptide (NT-proBNP) to help determine the urgency of specialist assessment and echocardiography. Natriuretic peptide levels rise when myocardial wall stress increases. They support the diagnostic pathway, but they do not tell you the cause or, by themselves, confirm the diagnosis. Levels may be affected by factors including age, atrial fibrillation, renal dysfunction, obesity and treatment already being taken.
An echocardiogram gives information about chamber size, ventricular systolic function, valve structure and function, wall motion and other haemodynamic features. An electrocardiogram may identify previous infarction, conduction abnormalities or arrhythmia. Blood tests commonly help assess renal function, electrolytes, full blood count, liver and thyroid function, while chest imaging may show pulmonary congestion or another cause for breathlessness.
Treatment is more than giving a diuretic
Diuretics such as loop diuretics help relieve congestion by increasing sodium and water excretion. They can improve breathlessness and oedema, but response must be monitored alongside weight, symptoms, urine output, blood pressure, renal function and electrolytes. A rapidly falling weight may reflect successful fluid removal, but excessive diuresis can contribute to hypotension, kidney injury and electrolyte disturbance.
For HFrEF, disease-modifying treatment aims to reduce symptoms, hospital admission and mortality. Current therapy commonly brings together medicines acting on the renin-angiotensin system, evidence-based beta-blockade, mineralocorticoid receptor antagonism and sodium-glucose cotransporter-2 inhibition, with selection, sequencing and dose titration guided by the specialist team, comorbidities, renal function, blood pressure and tolerance. Some patients benefit from devices such as cardiac resynchronisation therapy or an implantable cardioverter defibrillator. Revascularisation or valve intervention may be appropriate when the underlying problem requires it.
Management of HFpEF includes treating congestion and the conditions that drive it, such as hypertension, atrial fibrillation, coronary disease, obesity, diabetes and chronic kidney disease. Sodium-glucose cotransporter-2 inhibitors now have an important role for many people with HFpEF, but prescribing decisions remain individual.
Cardiac rehabilitation, appropriate physical activity, smoking cessation, vaccination, medication support and honest conversations about prognosis and future care are also part of treatment. Fluid or salt restrictions should not be imposed automatically on every patient. Advice should follow the person's clinical situation and the plan from their heart failure team.
What the nurse is watching
Good heart failure nursing care is built on patterns rather than isolated numbers. Compare the patient's breathlessness with their usual baseline. Ask about sleeping position, night-time symptoms and activity tolerance. Look for changes in oedema, abdominal swelling, appetite and fatigue. Check whether the weight has moved over several days and whether the measurement conditions are consistent.
Observations need interpretation. A rising respiratory rate or increasing oxygen requirement may be an early sign of pulmonary congestion or another acute problem. Blood pressure affects the safety and tolerance of treatment. Pulse rate and rhythm may reveal a new arrhythmia. Fluid balance can be useful, but only when intake and output are recorded accurately and considered alongside weight, examination, renal function and the patient's overall condition.
Medicines deserve the same attention. Monitor for dizziness, symptomatic hypotension, bradycardia where relevant, renal deterioration and potassium disturbance. Check what the patient was actually taking before admission and whether practical problems, side effects or unclear instructions have affected adherence. Do not describe non-adherence as carelessness without understanding what has made the regimen difficult.
Escalate new or worsening breathlessness, falling oxygen saturation, chest pain, acute confusion, reduced urine output, hypotension, rapidly increasing oedema or weight, or signs of poor peripheral perfusion according to the patient's condition and local pathway. In an acutely deteriorating patient, use a structured assessment such as ABCDE while seeking timely senior support.
Putting the findings together
By this point, breathlessness, orthopnoea, peripheral oedema and rapid fluid-related weight gain should no longer feel like an unrelated list of heart failure symptoms. They can be traced back through the circulation. Raised left-sided filling pressure can contribute to pulmonary congestion, while systemic venous congestion and sodium and water retention can contribute to peripheral oedema. Fatigue and reduced exercise tolerance may reflect limited cardiac reserve alongside the effects of breathlessness and disturbed sleep.
At the bedside, the aim is not to diagnose heart failure from one finding. It is to notice patterns, establish what has changed from the person's usual baseline and communicate that clearly. “More breathless than usual, now needing three pillows, weight up 2.5 kg in four days, bilateral oedema to the shins and respiratory rate increased from 18 to 26” gives the team much more useful information than “looks fluid overloaded”.
Understanding the physiology helps you decide which observations belong together, what needs closer assessment and when a change needs escalation, while still leaving room for differential diagnosis, investigation and professional judgement.
References
British Heart Foundation (2026) Heart failure: causes, symptoms and treatment.
McDonagh, T.A., Metra, M., Adamo, M. et al. (2021) ‘2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure’, European Heart Journal, 42(36), pp. 3599–3726.
McDonagh, T.A., Metra, M., Adamo, M. et al. (2023) ‘2023 focused update of the 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure’, European Heart Journal, 44(37), pp. 3627–3639.
National Institute for Health and Care Excellence (NICE) (2014, updated 2021) Acute heart failure: diagnosis and management. CG187. London: NICE.
National Institute for Health and Care Excellence (NICE) (2018, updated 2025) Chronic heart failure in adults: diagnosis and management. NG106. London: NICE.
NHS (2026) Heart failure.