The Cardiac Compass | Clinical Cardiology

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

Mechanism	Examples	Findings that direct assessment	Immediate therapeutic objective
Hypovolaemic	Haemorrhage, gastrointestinal losses, excessive diuresis	Relevant losses, reduced filling, peripheral vasoconstriction	Replace the deficit and control ongoing loss
Distributive	Sepsis, anaphylaxis	Infective or exposure history, vasodilatation, sometimes warm extremities	Treat the trigger and restore vascular tone and effective circulating volume
Cardiogenic	Acute myocardial infarction, ventricular failure, severe valve disease, arrhythmia	Ischaemia, congestion, abnormal rhythm or impaired ventricular function	Restore effective cardiac output and treat the cardiac cause
Obstructive	Pulmonary embolism, tamponade, tension pneumothorax	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.

Trial	Population and comparison	Principal result	Interpretation
CLOVERS, 2023 10	1,563 patients with sepsis-induced hypotension after 1–3 L initial fluid. Restrictive fluid with earlier vasopressors versus liberal fluid.	Death before discharge home by day 90: 14.0% versus 14.9%. Estimated difference −0.9 percentage points, 95% CI −4.4 to 2.6.	Neither strategy demonstrated superiority for the primary endpoint. This endpoint is not simply all-cause 90-day mortality.
CLASSIC, 2022 11	1,554 ICU patients with septic shock after at least 1 L. Restricted versus standard fluid.	Ninety-day mortality: 42.3% versus 42.1%. Adjusted difference 0.1 percentage points, 95% CI −4.7 to 4.9.	Lower fluid exposure did not improve overall survival. Findings apply to the studied post-initial-resuscitation setting.
ANDROMEDA-SHOCK-2, 2025 12	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.

13. Resuscitation Council UK. Emergency treatment of anaphylaxis: guidelines for healthcare providers. 2021. Official guidance and guideline download.

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.