Cardiology: Cardiology Emergencies (Complete)

• Overview: At a Glance | Acute Chest Pain: The First 10 Minutes | The Unstable Patient: Adverse Features
• Cardiac arrest: Cardiac Arrest: Adult ALS | Reversible Causes (4 Hs and 4 Ts) | Special Circumstances | Post-resuscitation Care
• Arrhythmias: Bradycardia | Tachycardia: Approach | Narrow Complex Tachycardia (SVT) | Fast Atrial Fibrillation | Broad Complex Tachycardia and VT | Torsades de Pointes | ICD Shocks and Electrical Storm
• Coronary: STEMI | NSTEMI and Unstable Angina | Complications of MI
• Pump failure: Acute Heart Failure and Pulmonary Oedema | Cardiogenic Shock
• Aorta, lungs and pericardium: Acute Aortic Dissection | Ruptured Abdominal Aortic Aneurysm | High-risk Pulmonary Embolism | Cardiac Tamponade
• Other emergencies: Hypertensive Emergency | Acute Infective Endocarditis | Syncope: Red Flags | Hyperkalaemia | Cardiotoxic Poisoning
• Revision: Drug Reference Table | Spot the Emergency | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🚑 Cardiac emergencies kill quickly, but most respond to fast, simple actions: early defibrillation, opening a blocked artery, slowing or speeding the heart, draining a tamponade. This chapter is a ward-ready guide to recognising them and acting in the first hour. Background on each condition is in the cardiology chapters.
Your four questions for every patient: Is there a pulse, and is the patient stable (shock, syncope, ischaemia, heart failure)? What does the 12-lead ECG show? What is the likely cause, and is it reversible? Who needs to come now - resus team, cath lab, cardiothoracics, ICU?

At a Glance

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Acute Chest Pain: The First 10 Minutes

The six chest pains that kill: Treat every acute chest pain as dangerous until these are considered:

• Acute coronary syndrome.
• Aortic dissection.
• Pulmonary embolism.
• Tension pneumothorax.
• Cardiac tamponade.
• Oesophageal rupture (Boerhaave's syndrome - after vomiting).

Within 10 minutes:

• ABCDE assessment; oxygen only if SpO2 is below 94% (88–92% in COPD with CO2 retention).
• 12-lead ECG within 10 minutes of arrival - and repeat it if pain continues or changes. A normal first ECG does not exclude ACS.
• BP in both arms (dissection) and pulses.
• IV access and bloods: High-sensitivity troponin, FBC, U&E, glucose, lipids, clotting; group and save if dissection or bleeding is possible.
• Chest X-ray (pneumothorax, widened mediastinum, pulmonary oedema).
• Bedside echo if available - pericardial effusion, RV dilatation, regional wall motion.
• Analgesia: GTN for ischaemic pain if BP allows; IV opioid with antiemetic if needed.

High-sensitivity troponin: Use the local rapid rule-in and rule-out pathway (e.g. 0 and 1 hour, or 0 and 3 hours; NICE DG40). A single very low result more than 3 hours after symptom onset may rule out MI. Troponin also rises in PE, myocarditis, sepsis, AKI, tachyarrhythmias and heart failure - always interpret it with the clinical picture and the change between samples.

⚠️ Safety Pearl: Never give thrombolysis or full anticoagulation for "STEMI" without considering aortic dissection - a dissection can involve the right coronary artery and cause inferior ST elevation. Check both arm pressures, pulses and the mediastinum.

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The Unstable Patient: Adverse Features

For any arrhythmia, the first decision is whether the patient is stable. Resuscitation Council UK lists four adverse features:

• Shock - hypotension (systolic below 90 mmHg), pallor, sweating, cold clammy peripheries, confusion or reduced consciousness.
• Syncope - transient loss of consciousness due to reduced brain blood flow.
• Myocardial ischaemia - ischaemic chest pain or ECG evidence of ischaemia.
• Severe heart failure - pulmonary oedema or raised JVP.

Rule: Adverse features with a tachycardia mean synchronised DC cardioversion. Adverse features with a bradycardia mean atropine and preparation for pacing. If the patient has no pulse, it is a cardiac arrest - start CPR.

Everyone: Oxygen if hypoxic, IV access, 12-lead ECG, continuous monitoring, and look for and correct reversible causes - potassium, magnesium, calcium, ischaemia, drugs.

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Cardiac Arrest: Adult ALS

Recognition: Unresponsive and not breathing normally. Gasping (agonal) breaths are common in the first minutes and are not normal breathing. Call for help (2222 in hospital), get a defibrillator, and start CPR.

High-quality CPR (Resuscitation Council UK 2025):

• Compressions at 100–120 per minute, depth 5–6 cm, full recoil, minimal interruptions.
• 30:2 until the airway is secured, then continuous compressions with 10 breaths a minute.
• Change compressor every 2 minutes.
• Use waveform capnography - it confirms tube placement, monitors CPR quality, and a sudden rise in end-tidal CO2 suggests ROSC.

Shockable rhythms - VF and pulseless VT:

• Shock as soon as possible (biphasic first shock at least 150 J; escalate if the device allows), then immediately resume CPR for 2 minutes without a pulse check.
• Pad position: Right pad below the right clavicle; left pad below the left armpit in the mid-axillary line.
• After the 3rd shock: Adrenaline 1 mg IV (then every 3–5 minutes) and amiodarone 300 mg IV.
• After the 5th shock: A further amiodarone 150 mg. Lidocaine 100 mg is an alternative.
• Witnessed, monitored arrest with a defibrillator immediately available (e.g. cath lab, CCU): consider up to 3 rapid stacked shocks first.
• Refractory VF: Check pad placement and consider changing to an antero-posterior position.

Non-shockable rhythms - PEA and asystole:

• CPR 30:2. Adrenaline 1 mg IV as soon as possible, then every 3–5 minutes.
• Rhythm check every 2 minutes. Look hard for a reversible cause - PEA in particular is often due to hypovolaemia, hypoxia, tamponade, tension pneumothorax or PE.

Access: IV first; intraosseous if IV access is not quickly achieved.

Airway: Start with bag-mask ventilation or a supraglottic airway; tracheal intubation only by skilled operators with minimal interruption to compressions.

Do not routinely give: Calcium, sodium bicarbonate or IV fluids - unless a specific cause needs them (hyperkalaemia, certain overdoses, hypovolaemia).

💡 Clinical Pearl: The two things that most improve survival from VF arrest are early high-quality CPR and early defibrillation. Drugs come a distant third. Never delay a shock to give a drug or secure the airway.

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Reversible Causes (4 Hs and 4 Ts)

💡 Clinical Pearl: Point-of-care ultrasound during the rhythm check - by a skilled operator, without lengthening pauses - can rapidly show tamponade, a dilated RV (PE) or an empty heart (hypovolaemia).

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Special Circumstances

• Pregnancy:
  • From about 20 weeks, the uterus compresses the IVC - use manual left uterine displacement during CPR.
  • Call obstetric and neonatal teams immediately.
  • If there is no ROSC, prepare for resuscitative hysterotomy (perimortem caesarean section), aiming to deliver within about 5 minutes of arrest. This helps the mother as well as the baby.
  • Think of haemorrhage, PE, amniotic fluid embolism, eclampsia, magnesium toxicity, dissection and peripartum cardiomyopathy.
• Hypothermia:
  • Check for signs of life for up to 1 minute - the pulse may be very slow.
  • Below 30°C: Up to 3 shocks only, and withhold adrenaline, until warmer.
  • 30–35°C: Double the interval between adrenaline doses (every 6–10 minutes).
  • Rewarm actively; consider ECMO. "Not dead until warm and dead".
• Anaphylaxis:
  • Peri-arrest: adrenaline 500 micrograms IM (0.5 mL of 1 mg/mL), repeated after 5 minutes if needed; IV fluid bolus.
  • In arrest: standard ALS with IV adrenaline 1 mg.
• After cardiac surgery: For VF, give up to 3 stacked shocks before compressions. Plan for emergency resternotomy within about 5 minutes if there is no ROSC (tamponade, bleeding).
• Hyperkalaemia in arrest: Calcium chloride 10 mL of 10% IV, insulin 10 units with 25 g glucose, and consider dialysis during CPR in specialist settings.
• Drowning: Hypoxia is the cause - give 5 rescue breaths first.
• Trauma: Treat reversible causes immediately (hypovolaemia, tension pneumothorax, tamponade) before or alongside chest compressions.

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Post-resuscitation Care

Return of spontaneous circulation (ROSC) is only the start. Brain injury, myocardial stunning and the underlying cause decide the outcome. The targets below follow the RCUK/ERC 2025 post-resuscitation guidance:

• Airway and breathing: Secure airway; SpO2 94–98% (avoid hypoxia and hyperoxia); normal PaCO2.
• Circulation:
  • 12-lead ECG and echo.
  • Mean arterial pressure above 65 mmHg, with fluids, noradrenaline and dobutamine as needed.
  • Emergency coronary angiography if there is ST elevation (or new LBBB) with a likely cardiac cause. Consider it in others with no obvious non-cardiac cause.
• Disability (brain):
  • Prevent fever - keep the temperature at or below about 37.5–37.7°C for at least 72 hours in comatose patients.
  • Treat seizures.
  • Glucose about 7.8–10 mmol/L; avoid hypoglycaemia.
  • CT head (and chest) if the cause is unclear.
• Prognosis: Do not make decisions too early. Prognostication is multimodal (examination, EEG, CT or MRI, biomarkers such as neuron-specific enolase), and usually at least 72 hours after ROSC.
• Afterwards: Investigate the cause. Consider an ICD for survivors of VF or VT arrest without a reversible cause. Offer rehabilitation and family support.

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Bradycardia

Definition: Heart rate below 60 beats per minute. It matters when there are adverse features (shock, syncope, ischaemia, heart failure) or a risk of asystole.

Common causes:

• Drugs: Beta-blockers, rate-limiting calcium channel blockers (verapamil, diltiazem), digoxin, amiodarone, ivabradine.
• Inferior MI - often transient AV block.
• Conduction disease: Sick sinus syndrome, degenerative AV block.
• Hyperkalaemia, hypothyroidism, hypothermia.
• Raised intracranial pressure (Cushing's reflex: bradycardia with hypertension).
• Vagal (vasovagal, vomiting); athletes (normal).

Risk of asystole - seek pacing even if the patient responds to atropine:

• Recent asystole.
• Mobitz type II AV block.
• Complete heart block with broad QRS.
• Ventricular pauses longer than 3 seconds.

Management (RCUK):

• Atropine 500 micrograms IV, repeated every 3–5 minutes to a maximum of 3 mg.
• If not effective:
  • Isoprenaline infusion (starting at 5 micrograms/minute), or
  • Adrenaline infusion (2–10 micrograms/minute).
• Pacing: Arrange transvenous pacing early in unstable patients. Transcutaneous pacing (with analgesia and sedation) is a bridge - check that each pacing spike captures with a pulse.
• Special situations:
  • Do not give atropine after heart transplant (it can cause paradoxical block) - use aminophylline or isoprenaline.
  • Atropine is often ineffective in broad-complex complete heart block - go to isoprenaline or pacing.
  • Beta-blocker or calcium channel blocker toxicity: Consider glucagon and high-dose insulin (see Cardiotoxic Poisoning).
  • Hyperkalaemia: Treat the potassium.

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Tachycardia: Approach

Step 1 - Is there a pulse? If not, follow the cardiac arrest algorithm.

Step 2 - Adverse features? If present (shock, syncope, ischaemia, heart failure) and the rhythm is the cause:

• Synchronised DC cardioversion, up to 3 attempts, under sedation or anaesthesia.
  • AF: start at maximum output.
  • Atrial flutter or SVT: start at 70–120 J and increase.
  • VT with a pulse: start at 120–150 J and increase.
• If unsuccessful: Amiodarone 300 mg IV over 10–20 minutes (or procainamide), then repeat cardioversion. Follow with amiodarone 900 mg over 24 hours.

Step 3 - If stable, look at the 12-lead ECG:

• Narrow (QRS below 0.12 s) and regular: Usually SVT (AVNRT, AVRT) or atrial flutter with 2:1 block (rate about 150).
• Narrow and irregular: Usually AF.
• Broad (QRS 0.12 s or more) and regular: Treat as VT - especially with known heart disease.
• Broad and irregular: AF with bundle branch block, pre-excited AF (WPW), or polymorphic VT / torsades.

💡 Clinical Pearl: A sinus tachycardia is a symptom, not a diagnosis. Find the cause - pain, fever, sepsis, bleeding, PE, hypoxia, thyrotoxicosis - and never try to cardiovert it or "slow it down" with drugs.

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Narrow Complex Tachycardia (SVT)

Mechanism: Most regular narrow complex tachycardias in young, otherwise well people are re-entry circuits involving the AV node - AV nodal re-entrant tachycardia (AVNRT) or AV re-entrant tachycardia via an accessory pathway (AVRT). Because the AV node is part of the circuit, briefly blocking it stops the tachycardia.

Management of stable regular narrow complex tachycardia:

• Vagal manoeuvres: The modified Valsalva manoeuvre - strain against a closed glottis (e.g. blowing into a 10 mL syringe) for 15 seconds sitting up, then lie flat and raise the legs. Works in about 1 in 4 (REVERT trial). Avoid carotid sinus massage in older patients (stroke risk).
• Adenosine - rapid IV bolus into a large vein, followed by a fast saline flush, with ECG recording:
  • 6 mg; if unsuccessful, 12 mg; then 18 mg.
  • Warn the patient: brief sense of doom, chest tightness and flushing are normal.
  • Use a lower dose (e.g. 3 mg) via a central line, after heart transplant, or with dipyridamole. Effect reduced by theophylline and caffeine.
  • Avoid in severe asthma - use verapamil 2.5–5 mg IV instead (never with a beta-blocker, and avoid in heart failure or broad-complex tachycardia).
• If adenosine reveals atrial flutter (sawtooth waves): Rate control (beta-blocker), and anticoagulation and cardioversion planning as for AF.
• If it fails or recurs: Beta-blocker or verapamil; DC cardioversion if adverse features develop.
• Afterwards: Look for pre-excitation (short PR, delta wave) on the resting ECG. Refer to cardiology - catheter ablation cures most SVTs.

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Fast Atrial Fibrillation

Unstable (shock, syncope, ischaemia, heart failure, with AF as the cause): synchronised DC cardioversion at maximum output; heparin if possible without delay.

Stable - rate or rhythm?

• Look for and treat triggers: Sepsis, dehydration, thyrotoxicosis, PE, alcohol, electrolyte disturbance, post-operative state. Rate control drugs can be harmful when AF is compensating for sepsis or hypovolaemia.
• Rate control (most patients):
  • Beta-blocker (e.g. bisoprolol orally, or IV metoprolol in increments) or rate-limiting calcium channel blocker (diltiazem, verapamil) - avoid calcium channel blockers in heart failure with reduced EF.
  • Digoxin in heart failure or sedentary patients, or added to a beta-blocker.
  • Amiodarone in critically ill patients or acute heart failure where other drugs are unsuitable.
• Rhythm control (NICE NG196):
  • Onset clearly under 48 hours: Can be cardioverted - electrically, or with flecainide (no structural or ischaemic heart disease) or amiodarone (structural disease). Give heparin first.
  • Onset 48 hours or more, or unknown: Rate control first; cardioversion only after at least 3 weeks of therapeutic anticoagulation, or after a TOE excludes left atrial thrombus.
• Anticoagulation: Assess stroke risk with CHA2DS2-VASc (NICE now uses CHA2DS2-VASc with ORBIT for bleeding risk). A DOAC is usually first-line.

⚠️ Safety Pearl: Very fast, irregular, broad-complex AF in a young person suggests pre-excited AF (WPW). Do not give AV nodal blockers (adenosine, verapamil, diltiazem, digoxin, beta-blockers) - they can push conduction down the accessory pathway and cause VF. Use DC cardioversion (or specialist drugs such as procainamide).

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Broad Complex Tachycardia and VT

Rule: A regular broad complex tachycardia is VT until proven otherwise, especially in someone with previous MI or heart failure. Haemodynamic stability does not make it SVT.

Clues to VT:

• Known structural or ischaemic heart disease.
• AV dissociation (P waves marching through), fusion or capture beats.
• Very broad QRS (above 0.16 s), extreme axis ("northwest").
• Concordance across the chest leads (all positive or all negative).

Management:

• Pulseless: Cardiac arrest algorithm.
• Adverse features: Synchronised DC cardioversion under sedation.
• Stable:
  • Amiodarone 300 mg IV over 10–60 minutes (preferably via a central line), then 900 mg over 24 hours. Procainamide is an alternative (ERC/RCUK 2025).
  • Elective cardioversion if drugs fail.
• Correct potassium (aim 4.0–5.0), magnesium and ischaemia.
• Afterwards: Echo, coronary assessment, cardiac MRI; consider an ICD for secondary prevention.
• Known SVT with aberrancy: Can be treated as SVT - but only if certain from a previous ECG.

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Torsades de Pointes

Mechanism: A polymorphic VT in which the QRS complexes appear to "twist" around the baseline. It happens on a background of a long QT interval, often triggered by a pause. It can degenerate into VF.

Causes of long QT:

• Drugs:
  • Antiarrhythmics (sotalol, amiodarone).
  • Macrolides (clarithromycin, erythromycin), quinolones.
  • Antipsychotics (haloperidol), citalopram, escitalopram, methadone, ondansetron, domperidone.
• Electrolytes: Low potassium, low magnesium, low calcium.
• Bradycardia, ischaemia, hypothermia, hypothyroidism.
• Congenital long QT syndromes.

Management:

• Pulseless: Defibrillate (unsynchronised) and follow ALS.
• Magnesium sulfate 2 g IV over 10 minutes - even if magnesium is normal.
• Stop all QT-prolonging drugs; correct potassium (aim 4.5–5.0) and calcium.
• Increase the heart rate to shorten the QT if it recurs: isoprenaline infusion or overdrive pacing (specialist).
• Do not give amiodarone - it prolongs the QT further.

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ICD Shocks and Electrical Storm

• A single shock with full recovery: Usually needs a device check (often the next working day) and a review of the trigger.
• Seek urgent assessment if:
  • Two or more shocks in 24 hours.
  • Shock with chest pain, breathlessness or ongoing symptoms.
  • Shocks while conscious and well (possible inappropriate shocks - AF, lead fracture, oversensing).
• Electrical storm: Three or more episodes of VT or VF (or appropriate shocks) within 24 hours. A medical emergency:
  • Correct potassium and magnesium; look for ischaemia, heart failure, thyroid disease and drugs.
  • Beta-blocker (e.g. propranolol), amiodarone.
  • Sedation - reduces sympathetic drive.
  • Urgent cardiology and electrophysiology input; catheter ablation.
• Magnet: A clinical magnet placed over an ICD suspends shock therapy (but usually does not change pacing). Use it for repeated inappropriate shocks - and make sure the patient is on a monitor with an external defibrillator ready, because true VT or VF will no longer be treated by the device.
• Cardiac arrest with an ICD: Standard ALS. Place pads at least 8 cm from the device.

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STEMI

Mechanism: A coronary artery is completely blocked by thrombus on a ruptured plaque. Heart muscle starts dying within minutes - "time is muscle". Every minute's delay to reopening the artery means more permanent damage.

ECG criteria: New ST elevation at the J point in 2 or more contiguous leads:

• 1 mm or more in limb leads and V4–V6.
• In V2–V3: 2 mm or more in men aged 40 or over; 2.5 mm or more in men under 40; 1.5 mm or more in women.

STEMI equivalents - treat as STEMI and call the cath lab:

• New LBBB (or paced rhythm) with ischaemic symptoms, especially with concordant ST changes (Sgarbossa criteria).
• Posterior MI: ST depression in V1–V3 with tall R waves - record V7–V9.
• De Winter T waves: Upsloping ST depression with tall symmetrical T waves in V1–V6 (proximal LAD occlusion).
• ST elevation in aVR with widespread ST depression (left main or multivessel disease) - discuss urgently.
• Ongoing ischaemic pain with haemodynamic instability despite a non-diagnostic ECG.

Immediate management (NICE NG185 / ESC):

• Aspirin 300 mg chewed or dispersed - as soon as possible.
• Pain relief: GTN sublingual (if systolic above 90 and not RV infarction); IV morphine or diamorphine with an antiemetic if needed.
• Oxygen only if SpO2 is below 94%.
• Primary PCI if presentation is within 12 hours of symptom onset and PCI can be delivered within 120 minutes of when fibrinolysis could have been given. Call the PPCI centre directly and transfer straight to the cath lab.
• Second antiplatelet (per local PPCI protocol): prasugrel (60 mg loading, then 10 mg daily; 5 mg if aged 75 or over or under 60 kg) if not on an oral anticoagulant, or ticagrelor (180 mg loading, then 90 mg twice daily). Clopidogrel if high bleeding risk or on an anticoagulant.
• Anticoagulation during PCI: Unfractionated heparin (radial access preferred).
• Fibrinolysis (e.g. tenecteplase, weight-adjusted) if PPCI cannot be delivered in time: give with an antithrombin, then transfer for angiography - immediately if ST elevation has not resolved by 60–90 minutes (rescue PCI).
• Late presenters (12–48 hours) with ongoing ischaemia, heart failure or arrhythmia still benefit from PCI.

Contraindications to fibrinolysis (main ones):

• Previous haemorrhagic stroke; ischaemic stroke within 6 months.
• Active bleeding; recent major trauma or surgery.
• Aortic dissection.
• CNS tumour; severe uncontrolled hypertension.

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NSTEMI and Unstable Angina

Mechanism: A partly blocked coronary artery. In NSTEMI troponin rises (heart muscle damage); in unstable angina it does not. The ECG may show ST depression, T wave inversion, or be normal.

Immediate management (NICE NG185):

• Aspirin 300 mg loading, then 75 mg daily.
• Fondaparinux 2.5 mg SC daily unless high bleeding risk or angiography is planned within 24 hours. Avoid if eGFR is below 20 - use unfractionated heparin.
• Pain relief; GTN; oxygen only if hypoxic.
• Risk stratify with the GRACE score (predicted 6-month mortality).

Angiography:

• Immediate (as for STEMI) if clinically unstable:
  • Ongoing or recurrent pain despite treatment.
  • Haemodynamic instability or cardiogenic shock.
  • Life-threatening arrhythmias or cardiac arrest.
  • Acute heart failure, or dynamic ST changes.
• Within 72 hours of admission if the predicted 6-month mortality is above 3% (intermediate or higher risk).
• Low risk: conservative management, with ischaemia testing if needed.

Second antiplatelet (NICE NG185):

• PCI planned: Prasugrel or ticagrelor.
• Conservative management: Ticagrelor (or clopidogrel if high bleeding risk).
• Usually continue dual antiplatelet therapy for 12 months.

Then secondary prevention for everyone:

• High-intensity statin (atorvastatin 80 mg).
• ACE inhibitor.
• Beta-blocker (especially with reduced EF).
• Cardiac rehabilitation; smoking cessation.

💡 Clinical Pearl: A raised troponin is not always a type 1 MI. In a septic, anaemic or tachycardic patient, a "type 2" MI (supply–demand mismatch) or myocardial injury is more likely - treat the cause, not with dual antiplatelets and an urgent angiogram.

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Complications of MI

• Arrhythmias (first hours to days):
  • VF - commonest cause of early death.
  • AV block with inferior MI (right coronary artery supplies the AV node) - often transient and responds to atropine.
  • AV block with anterior MI means extensive damage - poor prognosis, often needs pacing.
• Right ventricular infarction (with inferior MI):
  • Hypotension, raised JVP, clear lungs; ST elevation in V4R.
  • Give IV fluids; avoid nitrates and diuretics, which drop the preload the RV depends on.
• Mechanical complications (typically 2–7 days, but can be earlier; urgent echo and cardiothoracic surgery):
  • Papillary muscle rupture → sudden acute mitral regurgitation, flash pulmonary oedema, new pansystolic murmur (may be quiet).
  • Ventricular septal rupture → new loud pansystolic murmur with a thrill, shock, step-up in oxygen saturation in the right heart.
  • Free wall rupture → sudden tamponade and PEA arrest.
• Cardiogenic shock - see Cardiogenic Shock.
• Acute pericarditis (days 1–3) - pleuritic pain, rub.
• Dressler's syndrome (weeks later) - autoimmune pericarditis, fever, effusion. NSAIDs or colchicine.
• LV thrombus (large anterior MI) → embolic stroke; anticoagulate.
• LV aneurysm - persistent ST elevation weeks after MI, heart failure, VT, thrombus.

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Acute Heart Failure and Pulmonary Oedema

Mechanism: The heart cannot pump forward fast enough, so pressure rises behind it and fluid floods the lungs. It may be a first presentation or decompensation of chronic heart failure.

Common triggers:

• ACS.
• Arrhythmia - especially fast AF.
• Uncontrolled hypertension.
• Infection.
• Non-adherence to drugs or fluid and salt restriction.
• NSAIDs, steroids, rate-limiting calcium channel blockers.
• Acute valve problems (endocarditis, papillary muscle rupture); anaemia; thyroid disease; renal failure.

Clinical pattern: Severe breathlessness, orthopnoea, pink frothy sputum, sweating, tachycardia, crackles, raised JVP, third heart sound, peripheral oedema. Check whether the patient is "warm" or "cold" (perfused or not) and "wet" or "dry" (congested or not).

Investigations: ECG, chest X-ray, troponin, U&E, FBC, TFTs, NT-proBNP (normal levels make heart failure unlikely), arterial or venous gas, and echocardiogram (within 48 hours for new suspected heart failure; urgently if shocked or valve disease suspected).

Management (NICE CG187):

• Sit the patient upright; oxygen to target saturations.
• IV loop diuretic: e.g. furosemide 40–80 mg IV - or at least the usual oral dose given IV if already on a loop diuretic. Monitor urine output, weight and U&E.
• CPAP or NIV for severe breathlessness with acidaemia that does not settle quickly.
• Nitrates (IV GTN infusion): not routinely, but consider if there is myocardial ischaemia, severe hypertension, or regurgitant aortic or mitral valve disease. Avoid if systolic BP is below 90.
• Opioids: Not routinely.
• Treat the trigger: ACS, arrhythmia, hypertension, infection.
• Beta-blockers: Continue in people already on them, unless HR is below 50, there is second- or third-degree AV block, or shock.
• Before discharge: Start or optimise heart failure drugs for reduced EF; heart failure specialist nurse follow-up within 2 weeks.

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Cardiogenic Shock

Definition: Low cardiac output causing tissue hypoperfusion:

• Systolic BP below 90 mmHg for more than 30 minutes, or needing vasopressors.
• Signs of poor perfusion: cold peripheries, confusion, oliguria, raised lactate (above 2 mmol/L).

Causes:

• Large MI - the commonest cause, with mortality around 40–50%.
• Mechanical complications of MI.
• Myocarditis, Takotsubo, end-stage cardiomyopathy.
• Severe valve disease (critical aortic stenosis, acute regurgitation).
• Arrhythmias.
• Obstructive causes that look like it: massive PE, tamponade, tension pneumothorax.

Management:

• Early senior, cardiology and ICU involvement; ideally transfer to a cardiac shock centre.
• Urgent echo - LV and RV function, valves, mechanical complications, tamponade.
• Emergency coronary angiography and PCI of the culprit artery in MI-related shock (culprit-only PCI is preferred at first).
• Fluids: Only if not congested (or in RV infarction).
• Vasopressor: Noradrenaline first-line to maintain MAP about 65 mmHg.
• Inotrope: Dobutamine to improve output if perfusion remains poor.
• Mechanical circulatory support (specialist): Microaxial flow pumps (e.g. Impella) improved survival in selected STEMI shock patients (DanGer Shock trial); VA-ECMO in selected cases. Routine intra-aortic balloon pump is not recommended.
• Correct acidosis, electrolytes and arrhythmias; ventilate if needed.

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Acute Aortic Dissection

Mechanism: A tear in the inner lining of the aorta lets blood split the wall, creating a false channel. It can extend, block branch arteries, rupture, or tear back into the aortic valve or pericardium.

• Stanford type A: Involves the ascending aorta - a surgical emergency. Mortality rises by about 1–2% per hour without surgery.
• Stanford type B: Starts beyond the left subclavian artery - usually managed medically, with endovascular repair (TEVAR) if complicated.

Risk factors:

• Hypertension - the commonest.
• Connective tissue disease - Marfan, vascular Ehlers–Danlos, Loeys–Dietz.
• Bicuspid aortic valve, coarctation, Turner syndrome.
• Cocaine; pregnancy; previous cardiac or aortic surgery.

Clinical pattern:

• Sudden, severe, "tearing" chest or back pain, maximal at onset; may migrate.
• Pulse deficit or BP difference between arms above 20 mmHg.
• New aortic regurgitation murmur (type A).
• Stroke, paraplegia, limb ischaemia, mesenteric or renal ischaemia (branch involvement).
• Syncope, tamponade, inferior STEMI (right coronary involvement).

Diagnosis:

• CT aortogram - the key test. Bedside echo may show a flap, aortic regurgitation or effusion.
• Chest X-ray may show a widened mediastinum, but a normal film does not exclude dissection.
• The aortic dissection detection risk score (ADD-RS) with D-dimer can help decide who needs CT in lower-risk patients.

Management:

• Analgesia (IV opioid) - pain drives BP and heart rate.
• Lower heart rate and BP to reduce stress on the aortic wall:
  • IV labetalol or esmolol first, aiming for heart rate below 60 and systolic BP 100–120 mmHg.
  • Add a vasodilator (e.g. GTN) only after beta-blockade, if BP remains high.
• Type A: Immediate referral for emergency cardiothoracic surgery.
• Type B: Vascular and cardiothoracic MDT; TEVAR for rupture, malperfusion, uncontrolled pain or hypertension.
• Never give thrombolysis or anticoagulation.

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Ruptured Abdominal Aortic Aneurysm

• Who: Usually older men who smoke, with hypertension or a family history. Many do not know they have an aneurysm.
• Classic triad:
  • Abdominal, back or flank pain - often misdiagnosed as renal colic.
  • Hypotension or collapse.
  • Pulsatile abdominal mass (often not felt in obese patients).
• Management:
  • Call the vascular surgeon immediately - before imaging.
  • Two large-bore cannulas; crossmatch; activate the major haemorrhage protocol.
  • Permissive hypotension - give fluid or blood only to keep the patient conscious (systolic around 70–90 mmHg). Over-resuscitation worsens bleeding.
  • CT angiography only if haemodynamically stable enough - it helps plan endovascular repair.
  • Endovascular (EVAR) or open repair (NICE NG156).

💡 Clinical Pearl: "Renal colic" in a man over 60 with no previous stones is a ruptured AAA until proven otherwise - bedside ultrasound of the aorta takes seconds.

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High-risk Pulmonary Embolism

Mechanism: A large clot blocks the pulmonary arteries. The right ventricle cannot pump against the obstruction, dilates and fails, and the left ventricle is starved of blood - causing shock and PEA arrest.

Risk groups (ESC):

• High risk (massive): Haemodynamic instability - cardiac arrest, systolic below 90 mmHg (or needing vasopressors), or persistent hypotension.
• Intermediate risk: Normotensive, but with RV dysfunction on imaging and/or raised troponin.
• Low risk: Neither - may be suitable for outpatient care.

Clinical pattern:

• Sudden breathlessness, pleuritic pain, haemoptysis, syncope.
• Tachycardia, hypoxia, raised JVP, shock.
• ECG: sinus tachycardia (commonest), right heart strain (T inversion V1–V4, RBBB, right axis); S1Q3T3 is uncommon.

Diagnosis:

• CTPA if stable enough.
• If too unstable to scan: bedside echo showing a dilated, poorly contracting RV in the right setting is enough to justify thrombolysis.

Management:

• High-risk PE: systemic thrombolysis - e.g. alteplase 10 mg IV bolus over 1–2 minutes, then 90 mg over 2 hours (maximum 1.5 mg/kg if under 65 kg). In cardiac arrest, alteplase 50 mg bolus and continue CPR for 60–90 minutes.
• Unfractionated heparin (rather than LMWH) if thrombolysis may be needed.
• If thrombolysis is contraindicated or fails: surgical embolectomy or catheter-directed treatment (specialist).
• Careful fluids only - too much fluid worsens RV dilatation. Noradrenaline for hypotension.
• Intermediate-high risk: Anticoagulate and monitor closely; give "rescue" thrombolysis if the patient deteriorates.
• Everyone else: Anticoagulation - usually a DOAC (NICE NG158).