The echocardiography probe must perform two jobs. It converts electrical energy into ultrasound during transmission, then converts returning acoustic pressure into electrical signals during reception. Piezoelectric materials make this two-way conversion possible.
The two piezoelectric effects
During transmission, an applied electrical voltage deforms a piezoelectric element. Rapid changes in voltage make the element expand and contract, creating an ultrasound pulse. This is often called the converse or reverse piezoelectric effect.
During reception, a returning pressure wave deforms the same material and generates an electrical signal. This is the direct piezoelectric effect. The system processes that signal and uses it to construct the image.
What modern transducers contain
Early teaching often refers to quartz crystals. Modern diagnostic transducers more commonly use lead zirconate titanate ceramics, piezoelectric composites or related engineered materials. These materials provide useful electromechanical conversion and can be manufactured as multiple small elements.
Component
Function
Piezoelectric elements
Generate the transmitted pulse and detect returning pressure waves.
Backing or damping material
Shortens continued vibration after excitation, producing a shorter pulse and broader bandwidth.
Matching layers
Reduce the acoustic-impedance mismatch between the element and tissue so more energy crosses the interface.
Acoustic lens and probe face
Shape the beam in the elevational plane and provide a suitable contact surface.
Electrical connections and beam former
Control the timing of each element and process received signals.
How a phased array creates a cardiac sector
A cardiac phased-array probe contains many small elements in a compact footprint. The system introduces tiny timing differences between elements. During transmission, these delays steer and focus the beam. During reception, the system applies corresponding delays before combining the signals. Repeating this process along multiple lines produces the familiar sector image.
Why damping and bandwidth matter
A transducer that continues to vibrate for many cycles produces a long spatial pulse. A long pulse makes it harder to separate two reflectors that lie close together along the beam. Backing material damps the element and shortens the pulse. This improves axial resolution, although strong damping can reduce sensitivity.
Broad bandwidth allows the probe to operate over a range of frequencies. The scanner can then select a suitable transmit frequency and receive harmonic information when that mode is used.
Practical implications
The same array transmits and receives, but it does not usually do both at the same instant.
The electrical timing across elements controls beam steering and focusing.
A short pulse improves axial resolution.
The probe frequency shown on the machine is an operating or centre frequency, not proof that every transmitted component has one exact frequency.
Damage to individual elements can create dropout or streaking and should prompt a probe check.
Common misconceptions
Modern probes are not simply one quartz crystal.
The probe does not create a continuous stream of sound during routine two-dimensional pulse-echo imaging. It alternates transmission and listening periods.
Piezoelectric conversion describes energy transfer. It does not by itself explain steering, focusing or image processing.
Matching layers and backing material have different roles. Matching improves energy transfer, while backing controls ringing and pulse length.
Key learning points
Electrical excitation produces mechanical deformation and an ultrasound pulse.
Returning pressure produces an electrical signal.
Modern probes use arrays of engineered piezoelectric elements.
Backing, matching layers and beam-forming electronics determine important aspects of image quality.
Phased-array timing allows a small cardiac probe to steer a sector through a narrow acoustic window.
Professional standards context
A working knowledge of transducer construction and beam formation helps the operator recognise probe faults, select the correct transducer and understand the trade-offs involved in frequency, bandwidth, focusing and resolution.
Echocardiography turns reflected sound into a moving image of the heart. A small number of physical relationships explain most of what you see on the screen, why some structures are poorly visualised and which controls improve the image.
What ultrasound means
Ultrasound is sound above the upper limit of human hearing. Diagnostic echocardiography uses frequencies in the megahertz range. One megahertz equals one million cycles per second. Frequency describes how many cycles occur each second. Hertz is the unit used to express frequency, not a separate property of the wave.
The main wave properties
Property
Meaning
Why it matters in echocardiography
Frequency
Number of cycles per second, measured in hertz.
Higher frequency usually improves spatial resolution but increases attenuation and reduces penetration.
Wavelength
Distance occupied by one cycle.
Shorter wavelengths help distinguish structures that lie close together.
Propagation speed
Speed at which sound travels through a medium.
The scanner assumes an average speed of about 1540 m/s in soft tissue when calculating depth.
Amplitude
Maximum change in acoustic pressure within the wave.
Larger returning echoes generate stronger electrical signals, but displayed brightness also depends on gain, compression and post-processing.
Power and intensity
Power is energy delivered per unit time. Intensity is power per unit area.
These relate to acoustic output and safety. They are not interchangeable with receiver gain.
Frequency wavelength and propagation speed
Propagation speed equals frequency multiplied by wavelength. Within a given tissue, propagation speed is relatively fixed. Increasing frequency therefore shortens wavelength. This improves the ability to resolve small structures, but high-frequency sound loses energy more quickly as it passes through tissue.
Adult transthoracic echocardiography usually requires a lower centre frequency than superficial imaging because the beam must pass through the chest wall and reach deeper structures. A smaller patient or a superficial target may permit a higher frequency. The practical aim is to use the highest frequency that still provides adequate penetration.
How pulse echo imaging calculates depth
The transducer sends a short pulse and then listens for returning echoes. The scanner measures the round-trip travel time. Because it assumes an average soft-tissue propagation speed, it can estimate how deep the reflecting interface lies. Echoes that return later are displayed deeper in the image.
This calculation is an approximation. Sound travels at different speeds in fat, muscle, blood and other tissues. A wrong speed assumption can contribute to artefacts or small positional errors.
Why echoes return
An echo forms when the beam meets a boundary between tissues with different acoustic impedances. A large, smooth interface may produce specular reflection. Small structures and irregular surfaces scatter sound in several directions. Only some of that sound returns to the transducer. The strength of the received signal depends on the tissue boundary, beam angle, attenuation and system processing.
Practical implications at the machine
If deeper structures are poorly seen, try a lower frequency before increasing output power.
If the image is uniformly too dark or bright, adjust overall gain. Gain changes the displayed received signal, not the transmitted wave.
If only the far field is too dark, adjust time-gain compensation rather than increasing all gain.
Keep the beam as perpendicular as possible to a smooth reflecting surface when the aim is to visualise that interface.
Use depth, sector width and focus deliberately because image quality and frame rate depend on how the system builds each frame.
Common misconceptions
Hertz is the unit of frequency. It is not an additional wave characteristic.
Amplitude does not translate directly into pixel brightness. Receiver gain, dynamic range, compression and processing also affect the display.
The scanner assumes a soft-tissue propagation speed. It does not measure the true speed in every tissue.
A higher frequency does not always produce a better study. The useful frequency depends on the required depth and acoustic window.
Key learning points
Frequency and wavelength are inversely related when propagation speed is fixed.
Higher frequency improves detail but reduces penetration.
Depth is estimated from the round-trip travel time of each pulse.
Displayed brightness reflects both the returning echo and machine processing.
Understanding these relationships helps you choose controls logically rather than by trial and error.
Professional standards context
Ultrasound physics, instrumentation, image formation and artefact recognition form part of the knowledge expected in echocardiography training and accreditation. The EACVI core syllabus places these principles within the foundation required for safe image acquisition and interpretation.
Shock assessment starts with a question: why are this patient’s tissues failing to receive or use enough oxygen?
A low blood pressure should prompt assessment, but the reading alone cannot tell you the mechanism or the correct treatment. Some patients need fluid. Others need urgent reperfusion, vasopressor support or relief of a mechanical obstruction. Giving the same treatment to all of them can cause harm.
This article explains the physiology and applies it to fictional adult teaching cases. It is for healthcare professionals and should be used alongside local emergency pathways and senior clinical support. Guideline sources checked on 23 September 2026.
A framework for the causes of shock
The terms pump, tank, pipes, blockage and cells provide a useful memory aid.
Term
What has failed?
Category
Pump
The heart cannot generate adequate forward flow
Cardiogenic
Tank
Insufficient circulating volume
Hypovolaemic
Pipes
Loss of vascular tone and abnormal distribution of flow
Distributive
Blockage
Restriction of cardiac filling or blood flow
Obstructive
Cells
Impaired oxygen carriage, release or cellular use
Sometimes called dissociative
The first four are the standard categories of circulatory shock. “Dissociative shock” is a supplementary educational term with inconsistent usage. Carbon monoxide poisoning and cyanide toxicity illustrate the problems it describes.
More than one mechanism can operate in the same patient. Classification should help identify treatment priorities rather than force the patient into a single category (Vincent and De Backer, 2013).
1. Shock, hypotension and congestion
Shock involves inadequate tissue oxygen delivery or utilisation, leading to cellular dysfunction and potentially organ injury. Hypotension is an important sign, but compensatory vasoconstriction can preserve blood pressure while cardiac output falls.
Patient
Findings
Interpretation
A
BP 88/55 mmHg, similar to baseline. Alert, warm, normal urine output
Hypotension without clear evidence of shock
B
BP 110/70 mmHg. Cold, mottled, confused, oliguric, rising lactate
Possible shock despite preserved pressure
Ask three separate questions:
Is blood pressure low?
Is organ perfusion inadequate?
Is the patient congested?
The answers may differ. A congested patient can have inadequate forward flow. A patient with a low baseline pressure may have adequate perfusion. Assessment must connect the circulation to organ function.
2. The physiology behind the bedside findings
The relationship between pressure, flow and resistance is:
MAP − RAP ≈ CO × SVR
MAP is mean arterial pressure, RAP is right atrial pressure, CO is cardiac output and SVR is systemic vascular resistance. With consistent units, this expresses the pressure gradient driving systemic flow. Numerical calculations using conventional haemodynamic units need the appropriate conversion factor.
Blood pressure can fall because output falls, resistance falls, or both.
Oxygen delivery follows a second relationship:
DO₂ = CO × CaO₂
CaO₂ is arterial oxygen content. Most blood oxygen binds to haemoglobin, so delivery depends mainly on cardiac output, haemoglobin concentration and oxygen saturation.
For calculations using CO in L/min and CaO₂ in mL oxygen/dL:
DO₂ (mL/min) = CO × CaO₂ × 10
CaO₂ ≈ 1.34 × Hb (g/dL) × SaO₂ + 0.003 × PaO₂ (mmHg), with SaO₂ expressed as a fraction.
Ignoring the small dissolved oxygen contribution gives the following examples:
Situation
Cardiac output
Hb
Saturation
Approximate oxygen delivery
Reference example
5 L/min
150 g/L
98%
985 mL/min
Low cardiac output
2 L/min
150 g/L
98%
394 mL/min
Severe anaemia
5 L/min
60 g/L
98%
394 mL/min
These are illustrative calculations, not clinical targets. All three have the same saturation. A normal SpO₂ therefore cannot establish adequate oxygen delivery.
3. Hypovolaemic shock
Reduced circulating volume lowers venous return, ventricular filling and stroke volume. Tachycardia and peripheral vasoconstriction usually compensate.
Common causes include haemorrhage, vomiting, diarrhoea, a high-output stoma, excessive diuresis and fluid loss into tissues or body cavities.
Look for:
A history of blood or fluid loss.
Cool peripheries and delayed capillary refill.
Low jugular venous pressure (JVP).
A narrow pulse pressure.
Reduced urine output and often clear lungs.
No single finding confirms the diagnosis. Beta-blockers can blunt tachycardia.
Case: a high-output stoma
A 72-year-old has three days of increased stoma output. BP is 82/48 mmHg and heart rate is 118 beats/min. Their hands are cool, JVP is low and chest is clear. Creatinine has doubled and lactate is 3.6 mmol/L.
Reduced circulating volume is the leading mechanism. Escalate, establish monitoring and give isotonic crystalloid in a measured bolus with reassessment. Measure ongoing stoma losses, check electrolytes including magnesium, review contributing medicines and investigate the increased output.
Improving capillary refill, alertness and stroke volume support a beneficial response. Urine output may recover more slowly.
After each bolus, ask whether perfusion has improved and whether further fluid is likely to help.
Variation: gastrointestinal bleeding
Replace the stoma losses with haematemesis. The priorities now include haemorrhage control and blood products through the major haemorrhage pathway when indicated.
Repeated crystalloid alone cannot restore oxygen-carrying capacity. An initially normal haemoglobin does not exclude major acute bleeding because whole blood is lost before equilibration changes the measured concentration.
Acute severe mitral regurgitation or ventricular septal rupture.
Sustained tachyarrhythmia or severe bradyarrhythmia.
Severe valve disease.
Poor perfusion commonly accompanies congestion: cold peripheries, oliguria, confusion and rising lactate may coexist with raised JVP and pulmonary oedema.
However, cardiogenic shock does not require pulmonary oedema or a severely reduced ejection fraction. RV infarction can present with clear lungs. Acute severe mitral regurgitation can reduce effective forward flow despite an apparently preserved LV ejection fraction (Sinha et al., 2025).
Case: anterior STEMI with pulmonary oedema
A 64-year-old has chest pain, BP 78/50 mmHg and heart rate 115 beats/min. They are cold, clammy and confused. JVP is raised, widespread crackles are present, the ECG shows anterior ST elevation and echo shows severe LV dysfunction.
This is a congested, low-output presentation. Priorities include immediate interventional cardiology and critical care involvement, emergency angiography and revascularisation, and respiratory support according to oxygenation and clinical state (Byrne et al., 2023).
Avoid routine fluid loading. More fluid can raise filling pressure without meaningfully improving forward flow.
Noradrenaline is generally preferred when severe hypotension requires a vasopressor. Persistent low output may require an inotrope, but these drugs can worsen tachyarrhythmia or hypotension. Refractory shock requires early specialist shock-service discussion (Sinha et al., 2025).
Variation: inferior MI with RV involvement
Hypotension, raised JVP, clear lungs and inferior ST elevation with right-sided ECG changes should raise concern for RV infarction.
A cautious fluid challenge may help when filling is inadequate. Repeated boluses can distend the RV, worsen ventricular interaction and impair LV filling. Preload dependence does not justify unlimited fluid.
5. Distributive shock
Loss of vascular tone lowers SVR. Venous dilatation also reduces effective venous return. Cardiac output may initially remain normal or high despite inadequate pressure and tissue perfusion.
Causes include sepsis, anaphylaxis, neurogenic shock, some drug effects and endocrine emergencies.
Warm skin, low diastolic pressure and a relatively wide pulse pressure suggest vasodilatation. These are patterns rather than requirements. Septic shock can present with cold peripheries.
Case: pneumonia with hypotension
A 76-year-old presents with fever, productive cough and confusion. BP is 84/36 mmHg, heart rate 122 beats/min and lactate 4.2 mmol/L. Their hands are warm.
The low diastolic pressure supports reduced vascular tone. Initial priorities include antibiotics, source assessment, appropriate fluids and early escalation.
NICE and international fluid guidance
For adults needing fluid resuscitation in suspected sepsis, NICE NG253 recommends an initial 250 mL crystalloid bolus, ideally over 10–15 minutes. Reassess after each bolus. Further 250 mL boluses may be needed, up to 1,000 mL including fluid already given, with senior advice if improvement remains inadequate. Deterioration or fluid intolerance requires earlier escalation (NICE, 2025).
The 2026 Surviving Sepsis Campaign suggests at least 30 mL/kg in the first three hours for sepsis-induced hypoperfusion or septic shock. This conditional recommendation differs from NICE’s initial bolus approach. Follow the local pathway, individualise treatment and repeatedly assess response and tolerance. Noradrenaline remains first-line vasopressor therapy in septic shock (Surviving Sepsis Campaign, 2026).
Variation: anaphylaxis
Minutes after an antibiotic, a patient develops wheeze, facial swelling and BP 70/35 mmHg.
Stop the trigger and call for emergency help.
Give adult IM adrenaline 500 micrograms into the anterolateral thigh.
Repeat after five minutes if airway, breathing or circulation problems persist.
Provide oxygen and IV crystalloid as required.
Do not allow the patient to stand or walk.
Antihistamines do not treat shock. IV adrenaline requires appropriately experienced clinicians and monitoring (Resuscitation Council UK, 2021).
6. Obstructive shock
Obstructive shock develops when a mechanical problem restricts filling or blood flow.
Cause
Mechanism
High-risk pulmonary embolism
Abrupt RV afterload increase reduces pulmonary flow and LV filling
Cardiac tamponade
Pericardial pressure restricts cardiac filling
Tension pneumothorax
Intrathoracic pressure compromises venous return and circulation
Hypotension, raised JVP and relatively clear lungs suggest PE or tamponade, but RV infarction can look similar. History, ECG and focused imaging help distinguish them.
Case: collapse after surgery
A 58-year-old develops sudden breathlessness and syncope. BP is 76/44 mmHg, heart rate 132 beats/min and SpO₂ 86%. JVP is raised, the chest is clear and echo shows a dilated, poorly functioning RV.
High-risk PE is a major concern. Call critical care and the relevant PE team immediately. Obtain CTPA if safe. If transfer is unsafe, bedside assessment informs emergency decisions. Assess urgently for reperfusion and avoid large empirical fluid loads.
Recent surgery increases concern about thrombolysis-related bleeding and may favour an alternative reperfusion strategy where available. RV dilatation alone does not prove acute PE (Konstantinides et al., 2020).
Case: hypotension after a cardiac procedure
A patient becomes hypotensive after an invasive cardiac procedure. Echo shows pericardial fluid with chamber compression.
Possible tamponade requires urgent assessment for drainage or surgery. Fluids and vasopressors may temporarily support the circulation but cannot remove the obstruction. Do not wait for the complete classical triad (ESC, 2017).
Similarly, severe instability with suspected tension pneumothorax requires immediate decompression rather than waiting for radiography (Resuscitation Council UK, 2025).
7. Impaired oxygen carriage or cellular use
The supplementary term “dissociative shock” groups distinct problems together.
Problem
Mechanism
Carbon monoxide poisoning
Impaired oxygen carriage and release, with cellular toxicity
Methaemoglobinaemia
Abnormal haemoglobin cannot carry oxygen normally
Cyanide toxicity
Cells cannot use oxygen effectively
Profound anaemia
Reduced oxygen-carrying capacity, sometimes included in this teaching category
These conditions may cause tissue hypoxia without an initial classical circulatory shock pattern.
Case: reassuring saturation after smoke exposure
A patient rescued from a house fire is confused and tachycardic. SpO₂ is 99% and lactate is elevated, without convincing pulmonary oedema or major ventricular dysfunction.
Normal pulse oximetry does not exclude carbon monoxide poisoning. Give high-concentration oxygen, obtain blood co-oximetry, assess ECG and myocardial injury, examine neurological status and seek toxicology advice. Hyperbaric oxygen may be appropriate in selected circumstances.
PaO₂ can remain normal because it measures dissolved oxygen. Conventional pulse oximetry cannot reliably distinguish oxyhaemoglobin from carboxyhaemoglobin (CDC, 2024).
Severe smoke exposure with cardiovascular collapse or marked lactic acidosis also raises concern for cyanide toxicity. Seek urgent toxicology guidance on antidotal treatment.
8. Bedside differentiation
These are typical untreated patterns, with substantial overlap.
Finding
Hypovolaemic
Cardiogenic
Distributive
Obstructive
Cardiac output
Low
Low
Often high early, sometimes low
Low
SVR
Usually high
Usually high
Low
Usually high
JVP
Often low
Often raised
Variable
Often raised
Skin
Usually cool
Usually cool
Often warm early
Usually cool
Lungs
Often clear
May show oedema
Depends on cause
Often clear in PE or tamponade
History
Bleeding or fluid loss
MI, HF, valve disease, arrhythmia
Infection, allergen, spinal injury
Sudden dyspnoea, procedure, trauma
Treatment target
Restore volume and stop losses
Restore forward flow and treat cardiac cause
Restore vascular tone and treat cause
Relieve obstruction
Do not diagnose the mechanism from skin temperature or JVP alone. Combine:
ABCDE, repeat BP and continuous monitoring.
Mental state, capillary refill, skin temperature and mottling.
JVP, chest examination and peripheral oedema.
ECG and blood gas with lactate.
FBC, renal function, electrolytes and cause-directed investigations.
Urine output.
Focused cardiac and lung ultrasound when trained staff are available.
Serial assessment matters. ESICM 2025 supports echocardiography as first-line imaging to identify the haemodynamic mechanism and dynamic assessment before continuing fluid resuscitation in persistent shock (Monnet et al., 2025).
9. Fluid need, responsiveness and tolerance
Question
Meaning
Does the patient need resuscitation?
Is there clinically significant hypoperfusion?
Is the patient fluid responsive?
Will more preload increase stroke volume?
Can the patient tolerate fluid?
Will benefit outweigh worsening congestion?
A fluid-responsive patient does not automatically need fluid. Oedema also does not exclude inadequate effective circulating volume.
Passive leg raising
Passive leg raising produces a reversible increase in venous return. Start semi-recumbent, lower the trunk and elevate the legs. Measure the immediate change in cardiac output or stroke volume, then return to baseline and confirm reversal. BP change alone is less reliable than a flow measurement (Monnet and Teboul, 2015).
An increase of roughly 10% in measured output supports responsiveness with suitable technique. LVOT velocity time integral (VTI) can track the response, but acquisition must remain consistent and rhythm-related variability needs attention (Monnet, Marik and Teboul, 2016).
For example, VTI rising from 12 cm to 14 cm represents a 16.7% increase. That supports responsiveness, but fluid need and tolerance remain separate decisions.
IVC diameter alone cannot answer these questions. A dilated IVC may reflect RV failure, severe tricuspid regurgitation or raised intrathoracic pressure. A small LV can accompany hypovolaemia, vasodilatation or reduced filling from PE.
10. Why volume status alone is insufficient
Perfusion and congestion
Example
Implication
Poor perfusion, no congestion
Diarrhoea with volume loss
Fluid may restore flow
Poor perfusion with congestion
Severe LV failure
More fluid may worsen the problem
Congestion with preserved perfusion
Stable decompensated HF
Usually needs decongestion
Oedema with vasodilatory shock
HF plus sepsis
May need vasopressor support despite excess body fluid
“Hypervolaemic shock” is not a standard category. Raised filling pressure also does not necessarily mean increased total body volume. Tamponade illustrates this distinction.
11. Mixed shock on AMU
A 79-year-old with EF 25% develops pneumonia. BP is 80/42 mmHg and lactate 4.5 mmol/L. They have cool peripheries, raised JVP, bilateral B-lines and severe LV impairment. Passive leg raising produces no meaningful VTI increase.
Possible contributors include infection-related vasodilatation, limited cardiac reserve, septic myocardial dysfunction and pulmonary or systemic congestion.
Repeated fluid solely because the patient has sepsis risks worsening respiratory failure. The treatment direction includes:
Prompt antibiotics and source assessment.
Early critical care and cardiology input.
Vasopressor support for hypotension when required.
Further evaluation of cardiac output.
Selective inotropic support for persistent low output.
Individualised decongestion as haemodynamics allow.
Reassess the dominant mechanism as treatment changes the circulation.
12. A bedside teaching exercise
Present four patients with BP 80/50 mmHg:
Vomiting, low JVP and clear lungs.
Chest pain, raised JVP and pulmonary oedema.
Fever, warm peripheries and low diastolic pressure.
Sudden dyspnoea, raised JVP and clear lungs.
For each, ask:
What demonstrates organ hypoperfusion?
Which mechanism best explains the findings?
What would focused echo show?
Would fluid increase forward flow?
What would make you stop fluid?
Which definitive treatment must not be delayed?
The useful answer connects the likely mechanism to the clinical evidence, treatment choice and a clear plan for reassessment.
References
Byrne, R.A. et al. (2023) ‘2023 ESC Guidelines for the management of acute coronary syndromes’, European Heart Journal, 44, pp. 3720–3826. doi:10.1093/eurheartj/ehad191.
Konstantinides, S.V. et al. (2020) ‘2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism’, European Heart Journal, 41, pp. 543–603. doi:10.1093/eurheartj/ehz405.
Monnet, X. and Teboul, J.-L. (2015) ‘Passive leg raising: five rules, not a drop of fluid!’, Critical Care, 19, 18. doi:10.1186/s13054-014-0708-5.
Monnet, X., Marik, P. and Teboul, J.-L. (2016) ‘Passive leg raising for predicting fluid responsiveness: a systematic review and meta-analysis’, Intensive Care Medicine, 42, pp. 193–205. doi:10.1007/s00134-015-4134-1.
Monnet, X. et al. (2025) ‘ESICM guidelines on circulatory shock and hemodynamic monitoring 2025’, Intensive Care Medicine, 51, pp. 1971–2012. doi:10.1007/s00134-025-08137-z.
Sinha, S.S. et al. (2025) ‘2025 concise clinical guidance: an ACC expert consensus statement on the evaluation and management of cardiogenic shock’, Journal of the American College of Cardiology, 85, pp. 1618–1641. doi:10.1016/j.jacc.2025.02.018.
Publication date: 21 September 2026. Last reviewed: 21 September 2026.
Abstract
Hypotension requires interpretation in the context of tissue perfusion, baseline blood pressure and the clinical trajectory. The immediate task is to identify circulatory failure, establish its likely mechanism and select treatment that addresses the cause. This focused narrative review examines bedside assessment, fluid decisions and time-critical interventions in adult acute care. Contemporary guidance and randomised trials support repeated haemodynamic assessment rather than uncritical fluid administration. Particular attention is given to differences between current sepsis fluid recommendations, the distinction between fluid responsiveness and fluid requirement, and the limitations of extrapolating intensive care evidence to ward practice.
Hypotension and shock are different clinical concepts
A low blood pressure is a finding. Shock is a syndrome of circulatory failure with inadequate tissue perfusion. Compensatory vasoconstriction can preserve blood pressure despite falling cardiac output. Conversely, a low reading does not establish shock without clinical assessment. Mental state, peripheral perfusion and urine output provide essential context. 1
Consider two fictional patients. One has a blood pressure of 92/60 mmHg, feels well and has consistently similar previous readings. The other has a pressure of 108/76 mmHg with new confusion, cold extremities and declining urine output. The second presentation may require more urgent intervention despite the higher pressure. These examples illustrate clinical interpretation, not validated diagnostic rules.
The useful opening question is: “Is organ perfusion impaired, what mechanism explains it, and which intervention is likely to help?”
Identify the dominant mechanism
Blood pressure depends on cardiac output and vascular resistance. More precisely, mean arterial pressure minus right atrial pressure approximates cardiac output multiplied by systemic vascular resistance. Cardiac output equals heart rate multiplied by stroke volume. These relationships explain why volume loss, pump failure, mechanical obstruction, vasodilatation and major rhythm disturbances can produce hypotension.
The following framework is an educational synthesis. Mixed mechanisms are common, and findings should be interpreted together. 1,2,3
Sudden deterioration, right-sided pressure elevation or procedure-related clues
Relieve the obstruction
The first bedside assessment
Use an ABCDE assessment, call for help early and treat immediate threats as they are identified. Monitoring, intravenous access, ECG acquisition and blood sampling can proceed simultaneously. Confirm an unexpected pressure with a repeat measurement and appropriate cuff technique, without delaying treatment of a clinically deteriorating patient. Review the trend and previous baseline. 4
The focused history should establish the timing of deterioration, fluid losses, bleeding, infection, chest symptoms, recent procedures and medication changes. Examine for altered consciousness, impaired peripheral perfusion, congestion and a specific reversible cause. Raised jugular venous pressure with clear lungs should prompt consideration of right ventricular or obstructive pathology. It should not automatically trigger treatment for dehydration. 2,3,4
Investigations should address an immediate question. Obtain an ECG and relevant blood tests, including blood count, renal function, electrolytes, glucose and blood gas analysis. Arrange coagulation testing and crossmatching when bleeding is suspected. In suspected sepsis, obtain cultures promptly, ideally before antibiotics. 4,5,6
Lactate supports assessment and follow-up but should not become an isolated fluid target. SSC 2026 specifically advises individualisation rather than continuing fluid until lactate normalises. 6
Use ultrasound to refine, rather than replace, clinical reasoning
ESICM 2025 suggests echocardiography as the first imaging modality for identifying the type of shock. Relevant questions include ventricular function, right ventricular enlargement, pericardial fluid and major structural abnormalities. Persistent shock warrants reassessment of the haemodynamic mechanism and response to treatment. 7
An abnormal image must fit the clinical context. Right ventricular dilatation does not independently establish acute pulmonary embolism. Focused imaging should guide further investigation and expert review, especially when the diagnosis will determine an invasive or reperfusion treatment. 3
Fluid therapy: indication, responsiveness and tolerance
Three questions should precede further fluid: does the patient need improved perfusion, is additional preload likely to increase cardiac output, and is the risk of congestion acceptable?
Passive leg raising provides a reversible preload challenge. Its interpretation is more reliable when paired with real-time cardiac output or stroke volume measurement than with blood pressure alone. A positive response demonstrates preload responsiveness, not an automatic indication for fluid. Technique, measurement quality and the risk of overload remain important. 8
ESICM recommends dynamic assessment over static preload markers when applicable, and assessment of responsiveness before continuing fluids in persistent shock after initial resuscitation. 7
Why the recommended bolus volume depends on context
Clinical context
Verified recommendation
Interpretation
General adult hospital fluid resuscitation
NICE CG174: 500 mL crystalloid over less than 15 minutes when resuscitation is indicated. 9
This is not a prescription for every low blood pressure.
Suspected sepsis in the NG253 population
NICE: initial 250 mL, ideally over 10–15 minutes. Reassess after each bolus. Further 250 mL boluses may be given if required, up to 1,000 mL including previous fluid. Seek senior advice if improvement remains inadequate. 5
NG253 concerns people aged at least 16 who are not pregnant or recently pregnant.
Sepsis-induced hypoperfusion or septic shock
SSC 2026: conditionally suggests at least 30 mL/kg crystalloid within three hours, with individualisation and frequent reassessment. Certainty is low. 6
This is a different recommendation and scope, not an interchangeable version of the NICE regimen.
For UK practice, apply the relevant local pathway and escalate according to severity. The NICE 1,000 mL threshold must not be interpreted as an instruction to postpone senior involvement until that volume has been delivered. 5
After an intervention, document both benefit and tolerance. Reassess perfusion alongside respiratory rate, oxygen requirement and signs of congestion. New dyspnoea or pulmonary congestion should prompt review of further fluid. Resuscitation, maintenance and replacement of ongoing losses are separate prescribing tasks. 4,9
What the fluid trials establish
The major trials studied defined sepsis populations, generally after some initial fluid. They do not justify withholding resuscitation from untreated hypovolaemia or haemorrhage.
1,501 randomised, 1,467 in the primary analysis. Personalised resuscitation targeting capillary refill versus usual care.
Hierarchical composite of mortality, vital-support duration and hospital stay favoured intervention: win ratio 1.16, 95% CI 1.02–1.33.
The advantage mainly reflected shorter vital support. Twenty-eight-day mortality was 26.5% versus 26.6%.
CLOVERS and CLASSIC were open-label strategy trials. Their neutral primary results do not prove equivalence or exclude clinically relevant differences in particular patients. ANDROMEDA-SHOCK-2 tested a structured treatment protocol, not capillary refill measurement in isolation. Its composite result should not be described as a demonstrated mortality reduction. 10,11,12
The clinical interpretation is that the next intervention should follow the evolving haemodynamic problem. A fluid strategy cannot replace diagnosis, source control or reassessment.
Vasopressors and pressure targets
SSC 2026 recommends an initial MAP target of 65 mmHg in septic shock and conditionally suggests 60–65 mmHg for adults aged at least 65. Noradrenaline remains the principal first-line vasopressor. Peripheral initiation may avoid delay, with appropriate monitoring and local protocols. These are recommendations for actively managed shock, not permission to disregard ward deterioration. 6
Conditions in which specific treatment is decisive
Cardiogenic shock
Chest pain, cold extremities and pulmonary congestion should prompt urgent ECG, echocardiography and cardiology assessment. Acute coronary occlusion requires rapid access to the reperfusion pathway. The ACC 2025 consensus emphasises early recognition, characterisation of haemodynamics and timely specialist escalation. Routine additional fluid is difficult to justify in a clearly congested patient without evidence that it will improve output. 2
Right ventricular involvement may produce hypotension with relatively clear lungs. The practical implication is to assess ventricular function and filling rather than infer volume depletion from lung auscultation alone. 2
Obstructive shock
Sudden dyspnoea, collapse and right ventricular dysfunction raise concern for high-risk pulmonary embolism. Urgent multidisciplinary assessment should address confirmation and the appropriate reperfusion option. Recent surgery or bleeding risk materially affects that decision. Tamponade and tension pneumothorax require urgent relief of the mechanical cause. Repeated fluid does not remove an obstruction. 3
Anaphylaxis
In an adult with suspected anaphylaxis and airway, breathing or circulation compromise, give adrenaline 500 micrograms intramuscularly into the anterolateral thigh. This is 0.5 mL of 1 mg/mL solution. Repeat after five minutes if compromise persists. Stop the trigger where feasible, summon emergency help and give crystalloid for shock. Antihistamines do not treat cardiovascular collapse, and corticosteroids are not routine first-line emergency treatment. Persistent compromise after two appropriate IM doses requires the refractory-anaphylaxis pathway and expert support. 13
Adrenal crisis
Consider adrenal crisis in an unwell patient with hypotension and known adrenal insufficiency or relevant glucocorticoid exposure. Give hydrocortisone 100 mg intravenously or intramuscularly immediately, followed by 200 mg over 24 hours, or 50 mg every six hours. Restore circulating volume with isotonic fluid, assess glucose and treat the precipitant. Diagnostic testing must not delay emergency treatment. 14
Bradyarrhythmia or tachyarrhythmia
For bradycardia with adverse signs, RCUK 2025 recommends atropine 500 micrograms IV where appropriate, repeated every 3–5 minutes to a maximum of 3 mg. However, it specifically advises against atropine in high-degree AV block with a wide QRS, and in cardiac transplant recipients. Arrange early pacing support for unstable high-grade block. A tachyarrhythmia causing life-threatening instability may require synchronised cardioversion. Establish whether tachycardia is causal or compensatory before selecting treatment. 15
Orthostatic hypotension requires a different assessment
Once acute instability has been excluded, posture-related symptoms warrant lying and standing blood pressure assessment, medication review and evaluation of reversible contributors. The distinction between neurogenic and non-neurogenic causes informs further management. Treatment should be individualised and usually begins with non-pharmacological measures and review of contributing drugs, rather than immediate pressor therapy. 16
Applying the evidence: three fictional clinical scenarios
Gastrointestinal losses and hypotension
A patient presents after several days of diarrhoea with tachycardia, reduced intake and no clinical congestion. The working diagnosis is volume depletion. Initial resuscitation should be followed by reassessment, electrolyte review and a separate plan for ongoing losses. Failure to improve should reopen the differential diagnosis rather than automatically generate repeated boluses. 9
Deterioration after femoral arterial access
A patient develops back pain, pallor and hypotension after a procedure, despite little visible groin swelling. Concealed haemorrhage must be considered. Escalation to the procedural team, transfusion preparation and a plan for haemorrhage control take priority over treating the pressure reading alone. 2,4
Pneumonia in a patient with severe ventricular dysfunction
A patient with established heart failure develops pneumonia, confusion, hypotension and increasing oxygen requirements. Infection-related vasodilatation and cardiac dysfunction may coexist. The clinical task is to treat the infection while reassessing output, congestion and the likely benefit of further fluid, with early critical care involvement. This is a teaching synthesis of the sepsis and cardiogenic shock guidance, not a trial-tested protocol. 2,5,6
Key learning points
Assess perfusion and the trajectory alongside blood pressure.
Identify the likely mechanism before committing to repeated treatment.
Distinguish fluid responsiveness from clinical need and fluid tolerance.
Use disease-specific treatment promptly when the cause is recognised.
Interpret trial results within their populations and endpoint definitions.
Escalate with a clear account of the suspected mechanism, treatment response and unresolved problem.
Evidence scope and limitations
This is a focused educational narrative review, checked on 21 September 2026. Targeted web searches located official guidelines, PubMed records and accessible original publications. It is not a systematic review. No comprehensive database search, independent screening or formal risk-of-bias assessment was undertaken. No Consensus-assisted search was performed for this article.
Numerical results for CLOVERS and CLASSIC were checked against their PubMed abstracts. The ANDROMEDA-SHOCK-2 results were checked against accessible full text. Guideline checking used official recommendation pages or the issuing organisation’s text hosted in a recognised repository. CG174 was checked through indexed official recommendation text because direct retrieval failed. ESICM recommendations were checked against the publisher’s abstract. The orthostatic hypotension reference supports only the broad principles presented, using its accessible abstract. The accompanying editorial audit records these access limits.
The article concerns adult professional education. Paediatric and obstetric resuscitation require their own guidance. The fictional scenarios are teaching examples, not patient reports or individual medical advice.
References
1. Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Medicine. 2014;40:1795–1815. doi:10.1007/s00134-014-3525-z. Full text. Cited for foundational definitions, not current treatment targets.
2. Sinha SS, Morrow DA, Kapur NK, Kataria R, Roswell RO. 2025 concise clinical guidance: an ACC expert consensus statement on the evaluation and management of cardiogenic shock: a report of the American College of Cardiology Solution Set Oversight Committee. Journal of the American College of Cardiology. 2025;85:1618–1641. doi:10.1016/j.jacc.2025.02.018. PubMed. Author-institution full-text copy.
3. Resuscitation Council UK. Special circumstances guidelines. 2025. Official guidance.
4. Resuscitation Council UK. The ABCDE approach. Official guidance. Accessed 21 September 2026.
5. National Institute for Health and Care Excellence. Suspected sepsis in people aged 16 or over: recognition, assessment and early management. NG253. 2025. Official recommendations. NICE text in NCBI Bookshelf.
6. Society of Critical Care Medicine. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2026. Published 23 March 2026. Official recommendations.
7. Monnet X, Messina A, Greco M, et al. ESICM guidelines on circulatory shock and hemodynamic monitoring 2025. Intensive Care Medicine. 2025;51:1971–2012. Publisher record and abstract.
8. Monnet X, Teboul JL. Passive leg raising: five rules, not a drop of fluid! Critical Care. 2015;19:18. Full text.
9. National Institute for Health and Care Excellence. Intravenous fluid therapy in adults in hospital. CG174. 2013, updated 2017. Official recommendations.
10. Shapiro NI, Douglas IS, Brower RG, et al. Early restrictive or liberal fluid management for sepsis-induced hypotension. New England Journal of Medicine. 2023;388:499–510. doi:10.1056/NEJMoa2212663. PubMed.
11. Meyhoff TS, Hjortrup PB, Wetterslev J, et al. Restriction of intravenous fluid in ICU patients with septic shock. New England Journal of Medicine. 2022;386:2459–2470. doi:10.1056/NEJMoa2202707. PubMed.
12. ANDROMEDA-SHOCK-2 Investigators, et al. Personalized hemodynamic resuscitation targeting capillary refill time in early septic shock: the ANDROMEDA-SHOCK-2 randomized clinical trial. JAMA. 2025;334:1988–1999. PubMed. Full text.
14. Society for Endocrinology. Adrenal crisis. Emergency guidance. Accessed 21 September 2026.
15. Resuscitation Council UK. Adult advanced life support guidelines. 2025. Official guidance.
16. Wieling W, Kaufmann H, Claydon VE, et al. Diagnosis and treatment of orthostatic hypotension. Lancet Neurology. 2022;21:735–746. doi:10.1016/S1474-4422(22)00169-7. PubMed.
The 2026 European Society of Cardiology (ESC) guideline is a substantial update to heart-failure practice. It replaces the 2021 guideline and its 2023 focused update as the current ESC reference. Its main clinical message is to treat heart failure across a continuum: reduce risk early, recognise structural disease before symptoms where possible, and apply evidence-based treatment promptly once heart failure is established.12
The most visible changes are a simplified ejection-fraction classification, a stage-based framework, revised terminology for therapy, and new recommendations on mineralocorticoid-receptor antagonists (MRAs) and obesity treatment. These changes should improve clarity, but they do not replace careful phenotyping, aetiological investigation, or local prescribing and device pathways.
What has changed?
1. The LVEF classification has been simplified
The ESC now uses two heart-failure phenotypes based on left-ventricular ejection fraction (LVEF): heart failure with reduced ejection fraction (HFrEF) for LVEF <50%, and heart failure with preserved ejection fraction (HFpEF) for LVEF ≥50%. The previous separate category of heart failure with mildly reduced ejection fraction (HFmrEF; LVEF 41–49%) has been removed.13
This reflects the view that patients with LVEF in the 41–49% range often have a similar biology and treatment response to those with lower LVEF. It should not lead to treatment decisions being made from a single LVEF value. Image quality, loading conditions, rhythm, method of measurement and biological variation all matter. A patient with an LVEF close to 50% still needs an integrated assessment of symptoms, congestion, natriuretic peptides, structural heart disease, co-morbidity and cause.
The guideline also replaces the broad label acute heart failure with decompensated heart failure. This better captures patients whose deterioration is progressive rather than abrupt.3
2. Heart failure is framed as a staged condition
The new framework places greater emphasis on prevention and earlier intervention. It follows the progression from people at risk of heart failure (stage A), through pre-heart failure with structural or functional abnormalities but no symptoms (stage B), to symptomatic heart failure (stage C) and advanced heart failure (stage D).13
For day-to-day practice, this reinforces three points. First, hypertension, diabetes, obesity, chronic kidney disease, coronary disease and cardiotoxic exposure should be addressed before symptomatic heart failure develops. Second, asymptomatic left-ventricular dysfunction or structural heart disease warrants active follow-up rather than passive labelling. Third, advanced-heart-failure referral should not be delayed until every conventional option has been exhausted.
Medical therapies with the strongest evidence for an unselected heart-failure population.
Establish and optimise these first, unless contraindicated or not tolerated.
Additional medical therapy (AMT)
Therapies with benefit in defined clinical settings or for selected outcomes.
Add according to phenotype, rhythm, symptoms, co-morbidity and residual risk.
Guideline-directed interventional therapy (GDIT)
Recommended device or structural interventions.
Consider after appropriate medical optimisation and multidisciplinary assessment.
For symptomatic HFrEF, the familiar disease-modifying foundation remains a beta-blocker, renin–angiotensin system inhibition with an angiotensin-converting-enzyme inhibitor or an angiotensin-receptor neprilysin inhibitor, an MRA, and an SGLT2 inhibitor, tailored to clinical status and tolerance. The guideline recommends reviewing and uptitrating foundational treatment at least every one to two weeks, guided by symptoms, observations and laboratory results.1
Treatment updates most likely to affect practice
MRA treatment now spans the LVEF spectrum
A major change is the Class I recommendation for an MRA in chronic heart failure irrespective of LVEF.3 This is an important move beyond the previous evidence boundary between reduced and preserved ejection fraction.
The recommendation is supported by the established mortality and hospitalisation benefit of steroidal MRAs in HFrEF, together with newer evidence in patients with LVEF ≥40%. In FINEARTS-HF, finerenone reduced the rate of the composite of total worsening heart-failure events and cardiovascular death. The observed benefit was driven mainly by fewer worsening heart-failure events; cardiovascular death alone was not clearly reduced. Hyperkalaemia was more frequent.4
This does not mean that MRAs are interchangeable or suitable for every patient. Choice of agent, renal function and potassium thresholds, monitoring, interaction checks, local formulary rules and the product licence remain essential. In particular, this recommendation should not be used to bypass the need for repeat renal-function and potassium testing after initiation or dose change.
Obesity is treated as a therapeutic target in selected HFpEF-spectrum patients
The guideline gives a Class IIa, Level B recommendation that semaglutide or tirzepatide should be considered for patients with symptomatic heart failure, LVEF ≥45% and body-mass index ≥30 kg/m², regardless of diabetes status, to reduce weight and improve exercise capacity and quality of life.1
This recommendation is deliberately selective. In STEP-HFpEF, semaglutide improved symptoms, physical limitations, 6-minute walk distance and weight loss over 52 weeks in patients with HFpEF and obesity.5 In SUMMIT, tirzepatide reduced the composite of cardiovascular death or worsening heart failure and improved health status in patients with HFpEF and obesity; the trial was not powered to establish a reduction in cardiovascular death alone.6
For practice, these agents should be considered in addition to, not instead of, foundational heart-failure care, congestion management, rehabilitation and structured lifestyle support. Patient selection still requires attention to frailty, nutritional risk, gastrointestinal adverse effects, renal function, diabetes treatment and local eligibility or commissioning arrangements.
Selected therapies have a clearer place after foundational treatment
The guideline retains a selective role for cardiac glycosides. Digoxin or digitoxin should be considered in patients with symptomatic HFrEF, LVEF ≤40%, despite optimal foundational treatment, to reduce heart-failure hospitalisation.1 This is not a return to routine digoxin prescribing: there remains no established mortality benefit, and renal function, potassium, dose, interactions and toxicity risk must guide use. See our related review: Digoxin in Contemporary Heart-Failure Practice.
For selected patients with stable symptomatic HFrEF and severe secondary mitral regurgitation despite optimised foundational therapy and cardiac resynchronisation therapy where indicated, mitral transcatheter edge-to-edge repair is recommended when defined clinical and echocardiographic criteria are met.1 This remains a Heart Team decision, not an alternative to medical optimisation.
What should change in a practical heart-failure review?
A useful review now starts by recording the current phenotype as HFrEF (<50%) or HFpEF (≥50%), while documenting the actual LVEF and its context. Avoid carrying the historical HFmrEF label forward as if it were a current ESC category.
For a patient with symptomatic chronic heart failure, establish whether foundational treatment is complete and tolerated before moving to additional therapies. In HFrEF, this includes early sequencing and regular review rather than prolonged, single-drug titration. For all phenotypes, assess congestion, blood pressure, renal function, potassium, rhythm, iron status, diabetes, kidney disease, obesity, frailty and adherence.
For a patient with LVEF ≥45% and obesity, assess whether semaglutide or tirzepatide fits the individual’s phenotype and goals. The strongest guideline-supported outcomes are weight loss, exercise capacity and quality of life; treatment should not be presented as a universal heart-failure mortality therapy.
For every patient, reinforce self-management, medication review, exercise-based cardiac rehabilitation where appropriate, multidisciplinary follow-up and an early plan for deterioration. The guideline gives these elements a central—not optional—place in care.1
Pitfalls and limitations
The new LVEF threshold does not eliminate measurement uncertainty. A value near 50% should prompt clinical interpretation, not automatic reclassification without context.
An ESC Class I recommendation for MRAs does not remove safety constraints. Hyperkalaemia, worsening renal function, hypotension and interacting medication remain common barriers and require proactive monitoring.
The obesity recommendation applies to a defined symptomatic population with LVEF ≥45% and BMI ≥30 kg/m². It should not be extrapolated automatically to HFrEF below this range, to patients without obesity, or to those who cannot safely tolerate weight-reducing treatment.
ESC guidance informs practice in the UK, but it is not a substitute for NICE guidance, a medicine’s UK licence, local formulary approval or a specialist heart-failure pathway. Where these differ, clinicians should follow local governance while considering the evidence and the patient’s circumstances.
Key learning points
The 2026 ESC guideline replaces the separate HFmrEF category with HFrEF <50% and HFpEF ≥50%.
Heart failure is now framed as a staged condition, strengthening prevention, earlier recognition and timely referral.
The guideline uses the terms foundational medical therapy, additional medical therapy and guideline-directed interventional therapy to clarify treatment priorities.
MRAs now have a Class I recommendation in chronic heart failure across the LVEF spectrum, but agent choice and renal/potassium surveillance remain individualised.
Semaglutide or tirzepatide should be considered only for selected patients with symptomatic HF, LVEF ≥45% and BMI ≥30 kg/m²; the recommended aims are weight loss, exercise capacity and quality of life.
Digoxin remains a selected, safety-sensitive additional therapy rather than foundational treatment.
Educational note: This article summarises guideline changes for clinicians. It is not a prescribing protocol. Treatment decisions should incorporate the current medicine licence, local pathway, renal function, potassium, haemodynamics, co-morbidity and patient preference.
Publication date: 19 September 2026 Last reviewed: 19 September 2026
Audience: echocardiographers, cardiologists and acute physicians. Evidence reviewed: September 2026.
Key message
A left-atrial mass attached near the fossa ovalis is suggestive of myxoma, but attachment, mobility, vascularity and clinical context must be defined before diagnosis. Important mimics include thrombus, other tumours, vegetation and extracardiac compression. Once a probable myxoma is identified, prompt specialist surgical assessment is usual because embolic and obstructive complications can be sudden.
Clinical presentation
Obstruction: exertional dyspnoea, orthopnoea, syncope or positional symptoms from intermittent mitral inflow obstruction.
Embolism: cerebral, coronary, retinal or systemic arterial events.
Constitutional features: fever, weight loss, raised inflammatory markers and anaemia.
Incidental discovery: an asymptomatic mass found during unrelated imaging.
Echocardiographic assessment
Transthoracic echocardiography is the usual first test. Record the mass in multiple planes and describe size, shape, surface, mobility, stalk, precise attachment and relationship to the mitral valve and pulmonary veins. Assess functional mitral obstruction with Doppler at a stated heart rate, associated regurgitation, chamber size, pulmonary-pressure probability and pericardial effusion.
Transoesophageal echocardiography improves definition of attachment, small lesions and surgical anatomy. Three-dimensional echo may clarify the stalk and spatial relationship. Avoid declaring histology from echogenicity alone.
Possibility
Features that may support it
Important caution
Myxoma
Mobile pedunculated mass, often arising from interatrial septum near fossa ovalis
Valve-related oscillating mass with infection or valve destruction
Blood cultures and clinical criteria are essential.
Other tumour/metastasis
Broad attachment, infiltration, multiple lesions or known malignancy
Requires tissue and multimodality context.
When CT or CMR helps
CMR can assess tissue signal, perfusion and enhancement; CT defines calcification, coronary anatomy and extracardiac disease. Neither modality removes the need for pathology. If malignancy or thrombus remains plausible, imaging and treatment decisions should be coordinated across cardiology, radiology, oncology/infectious diseases and surgery as relevant.
Management
Probable cardiac myxoma is generally referred promptly for surgical excision, including the attachment site where feasible. Urgency reflects mobility, prior embolism, obstruction, tumour size and clinical stability. Coronary assessment follows age, symptoms and surgical protocol; tumour neovascularisation may occasionally be demonstrated.
Histopathology confirms the diagnosis. Follow-up echocardiography checks for recurrence, which is uncommon after complete excision but more likely in familial syndromes, multiple tumours or incomplete resection. Younger patients, multiple or recurrent myxomas, or suggestive endocrine/skin features should prompt consideration of Carney complex and genetic assessment.
Educational material only. A suspected intracardiac tumour or thrombus requires timely specialist assessment; acute obstruction or embolism is an emergency.
Audience: acute-cardiology, interventional-cardiology and cardiothoracic teams. Evidence reviewed: September 2026.
Key message
In acute coronary syndrome (ACS), culprit treatment and complete revascularisation are related but distinct decisions. CABG should remain in the index-admission pathway when anatomy, diabetes, ventricular dysfunction, mechanical complications or PCI feasibility suggests a prognostic or technical advantage—provided timing balances recurrent-ischaemia and bleeding risks.
Stabilise first, then define the problem
Immediate management follows ACS severity: resuscitation, antithrombotic therapy, urgent angiography and culprit reperfusion when indicated. Cardiogenic shock, ongoing ischaemia, failed PCI or a mechanical complication demands rapid multidisciplinary escalation; the ideal revascularisation mode may differ from that in a stable NSTEMI patient.
Anatomy that should trigger surgical discussion
Significant left-main disease, especially complex distal bifurcation disease.
Complex three-vessel disease not amenable to durable complete PCI.
Diabetes with multivessel coronary disease where long-term evidence favours surgery in suitable patients.
Need for concomitant valve, aortic or mechanical-complication surgery.
Failed or complicated PCI with ongoing jeopardised myocardium.
The index-admission Heart Team
Domain
Questions
Clinical stability
Ongoing pain, shock, arrhythmia, heart failure or mechanical complication?
Coronary anatomy
Left main, complexity, targets, chronic occlusions, likelihood of complete revascularisation?
Myocardium
LV function, infarct territory, viability where genuinely uncertain?
Patient factors
Frailty, cognition, renal/pulmonary disease, prior surgery, preferences and rehabilitation potential?
Treatment constraints
Recent P2Y12 inhibitor, bleeding, anticoagulation, infection and theatre availability?
Timing is an individual risk balance
Emergency CABG may be necessary for failed reperfusion, anatomy unsuitable for PCI with ongoing ischaemia, or mechanical complications. In stable patients, surgery is often delayed sufficiently to reduce perioperative bleeding and allow antiplatelet washout, but unnecessary discharge can expose patients to recurrent ischaemia and fragmented decision-making. The plan should state the reason for timing, antithrombotic strategy and triggers for acceleration.
Routine platelet-transfusion or bridging strategies should not be improvised. Follow the current guideline, local surgical protocol and patient-specific thrombotic and bleeding risks. Aspirin is commonly continued, while interruption intervals for P2Y12 inhibitors depend on the agent and urgency.
Communication standard
Document: culprit and residual anatomy; whether PCI achieved stable reperfusion; why CABG, PCI or medical therapy is preferred; estimated surgical and bleeding risk; antiplatelet stop dates; intended timing; contingency plan; and the patient’s informed preference. “For outpatient discussion” is not an adequate plan when prognostically important disease remains untreated.
Educational material only. Revascularisation strategy and timing require case-specific Heart Team decisions and current local antithrombotic/surgical protocols.
Audience: heart-failure clinicians, general physicians and trainees. Evidence reviewed: September 2026.
Key message
Digoxin remains useful for selected patients, but it is not a foundational mortality-reducing therapy for heart failure. Its narrow therapeutic index makes indication, renal function, dose, drug interactions and clinical monitoring inseparable from prescribing.
Two distinct indications
Setting
Potential role
What it does not establish
HFrEF in sinus rhythm
May reduce heart-failure hospitalisation in persistently symptomatic patients despite guideline-directed therapy
No proven survival benefit in the pivotal DIG trial
HFrEF with atrial fibrillation
May support resting rate control, often with another agent
Less reliable rate control during exertion
Evidence in HFrEF
In the Digitalis Investigation Group trial, digoxin did not reduce all-cause mortality but reduced hospital admission for worsening heart failure. The trial pre-dated angiotensin-receptor neprilysin inhibitors, SGLT2 inhibitors and widespread modern device therapy, so absolute benefits in present practice are uncertain. Contemporary guidelines therefore position digoxin as an option for selected symptomatic HFrEF rather than routine foundational treatment.
Choosing and monitoring treatment
Confirm the goal: symptom/hospitalisation reduction or ventricular-rate control.
Use a low maintenance dose tailored to age, lean body mass and renal function; loading is rarely needed in stable chronic care.
Check renal function and potassium before treatment and after clinically important changes.
Review interacting medicines, including amiodarone, verapamil, macrolides and other P-glycoprotein inhibitors.
If a serum concentration is required, sample at steady state and at least 6–8 hours after the last dose; interpret the result with symptoms, ECG and renal function.
For heart failure, many experts aim for a low serum concentration, commonly 0.5–0.9 ng/mL, when measurement is clinically indicated. A number within a laboratory “therapeutic range” does not exclude toxicity, particularly in older adults, renal impairment, hypokalaemia, hypomagnesaemia or hypothyroidism.
Recognising toxicity
Toxicity may cause anorexia, nausea, confusion, visual disturbance, bradyarrhythmia, atrioventricular block or almost any tachyarrhythmia. Stop digoxin, obtain an ECG, electrolytes, renal function and an appropriately timed level, and assess severity urgently. Life-threatening arrhythmia or significant hyperkalaemia may require digoxin-specific antibody fragments under emergency/toxicology guidance.
When to reconsider
Reassess digoxin when renal function changes, interacting therapy is added, bradycardia develops, the original indication disappears or adherence/monitoring is unreliable. Withdrawal may worsen symptoms or rate control in some patients, so deprescribing should be planned rather than automatic.
Educational material only. Dose and monitoring must follow the current product information, renal function, local formulary and individual clinical context.
Audience: cardiology clinicians and trainees. Evidence reviewed: September 2026.
Key message
In symptomatic obstructive hypertrophic cardiomyopathy (HCM), first confirm that dynamic left-ventricular outflow-tract (LVOT) obstruction explains the symptoms. Treatment then proceeds from physiology-aware medical therapy to specialist myosin-inhibitor or septal-reduction strategies, while sudden-death risk is assessed on a separate track.
1. Confirm the phenotype and mechanism
Document maximal wall thickness, distribution of hypertrophy and LV systolic/diastolic function.
Identify systolic anterior motion, mitral–septal contact and the mechanism/severity of mitral regurgitation.
Measure resting and provoked LVOT gradients with correctly aligned CW Doppler. Exercise stress echocardiography is valuable when symptoms and resting/Valsalva gradients disagree.
Use CMR for anatomy, apical disease, scar burden and alternative diagnoses.
Exclude important mimics and contributors such as hypertension, valve disease, coronary disease, anaemia and arrhythmia.
2. Define what limits the patient
Record NYHA class, exertional chest pain, presyncope/syncope, palpitations and exercise capacity. Review volume status, blood pressure and drugs that reduce preload or afterload. New atrial fibrillation can sharply worsen filling and symptoms and requires prompt rhythm/rate and anticoagulation assessment.
3. Start physiology-directed treatment
A non-vasodilating beta-blocker is generally first-line for symptoms attributable to obstruction. Verapamil or diltiazem may be considered when beta-blockers are ineffective or not tolerated, but caution is required with hypotension, severe obstruction or advanced congestion. Disopyramide can reduce obstruction when added under expert supervision, with attention to anticholinergic effects and QT prolongation.
Step
Decision
Safety focus
Initial drug
Non-vasodilating beta-blocker
Heart rate, blood pressure, conduction disease
Alternative
Verapamil or diltiazem in selected patients
Hypotension, pulmonary congestion, drug interactions
Add-on
Disopyramide in expert care
QT interval and anticholinergic burden
Advanced option
Cardiac myosin inhibitor where licensed and appropriate
Serial LVEF, interactions and mandated monitoring
4. Escalate persistent severe symptoms
Patients with substantial symptoms despite maximally tolerated therapy should be referred to an experienced HCM centre. Options include a cardiac myosin inhibitor and septal reduction. Surgical myectomy is preferred when concomitant cardiac surgery or complex mitral/subvalvular anatomy requires correction. Alcohol septal ablation is an alternative for selected anatomy and risk profiles. Operator and centre experience materially affect outcomes.
5. Run parallel risk pathways
Sudden-cardiac-death risk assessment is not replaced by symptom control or gradient reduction. Evaluate previous cardiac arrest or sustained ventricular tachycardia, unexplained syncope, family history, maximal wall thickness, apical aneurysm, LV systolic dysfunction, non-sustained ventricular tachycardia and CMR scar within the applicable guideline framework. Also address genetics and family screening, atrial fibrillation, stroke prevention, pregnancy, exercise and endocarditis advice.
Educational material only. Myosin-inhibitor and septal-reduction decisions require specialist HCM-centre assessment and current local prescribing guidance.
Audience: heart-failure clinicians, trainees and evidence-based-medicine readers. Evidence reviewed: September 2026.
Bottom line
FINEARTS-HF showed that finerenone reduced the rate of the composite of total worsening heart-failure events and cardiovascular death in symptomatic heart failure with left-ventricular ejection fraction (LVEF) ≥40%. The benefit was driven mainly by fewer worsening heart-failure events, with more hyperkalaemia but less hypokalaemia.
Clinical question
Does the non-steroidal mineralocorticoid-receptor antagonist finerenone improve outcomes in patients with heart failure and mildly reduced or preserved ejection fraction?
Design and population
FINEARTS-HF was an international, double-blind, randomised, placebo-controlled trial. It enrolled 6,001 patients aged 40 years or older with symptomatic heart failure, LVEF ≥40%, structural heart disease and elevated natriuretic peptides. Participants received finerenone or placebo in addition to usual therapy. The primary endpoint was a recurrent-event composite: total worsening heart-failure events plus cardiovascular death.
Feature
Why it matters
Recurrent-event analysis
Counts first and subsequent worsening-HF events rather than only time to first event.
LVEF ≥40%
Addresses HFmrEF/HFpEF, where evidence for steroidal MRAs had been uncertain.
Biomarker and structural criteria
Enriched the population for objectively supported heart failure.
Active contemporary background care
Improves relevance, although uptake of some newer therapies varied.
Results
During a median follow-up of 32 months, 1,083 primary-outcome events occurred in the finerenone group and 1,283 in the placebo group. The rate ratio was 0.84 (95% confidence interval 0.74–0.95; P=0.007). Worsening heart-failure events numbered 842 versus 1,024 (rate ratio 0.82, 95% CI 0.71–0.94). Cardiovascular death occurred in 8.1% versus 8.7% of participants; the trial did not demonstrate a clear mortality reduction.
Treatment effects were broadly consistent across prespecified subgroups, including the range of LVEF studied. Finerenone increased creatinine and hyperkalaemia risk but reduced hypokalaemia. The clinical trade-off therefore includes renal-function and potassium surveillance.
Strengths and limitations
Strengths: large randomised design, blinded outcome assessment, broad geography and clinically meaningful recurrent-event endpoint.
Endpoint interpretation: the primary benefit was morbidity rather than proven cardiovascular survival.
Generalisability: trial eligibility and monitoring may not represent frail patients, advanced kidney disease or routine-care adherence.
Background therapy: evolving SGLT2-inhibitor use complicates direct extrapolation to every present-day regimen.
Clinical application
Finerenone is a disease-modifying option for appropriately selected patients with HFmrEF/HFpEF, particularly when recurrent decompensation risk is important. Before initiation, confirm the indication, estimated glomerular filtration rate, serum potassium, interacting medicines and the ability to repeat blood tests. Do not assume interchangeability with spironolactone or eplerenone: molecular properties, evidence bases and licensed indications differ.
Educational critical appraisal only. Prescribing must follow the current licence, formulary, renal/potassium criteria and local heart-failure pathways.
