The Cardiac Compass
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.
4. Cardiogenic shock
Cardiogenic shock develops when cardiac dysfunction prevents adequate forward flow. Causes include:
- Acute myocardial infarction.
- Severe ventricular dysfunction or myocarditis.
- 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.
- Centers for Disease Control and Prevention (2024) Clinical guidance for carbon monoxide poisoning.
- European Society of Cardiology (2017) Pericardiocentesis in patients on thrombolytic drugs.
- 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.
- NICE (2025) NG253: Suspected sepsis in people aged 16 or over: recognition, assessment and early management.
- Resuscitation Council UK (2021) Emergency treatment of anaphylaxis.
- Resuscitation Council UK (2025) Special circumstances guidelines.
- 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.
- Surviving Sepsis Campaign (2026) International guidelines for management of sepsis and septic shock 2026.
- Vincent, J.-L. and De Backer, D. (2013) ‘Circulatory shock’, New England Journal of Medicine, 369, pp. 1726–1734. doi:10.1056/NEJMra1208943.
