Cardiac emergencies (e.g. acute pulmonary oedema, cardiac arrest, cardiogenic shock, cardiac tamponade)for HKMLE according to davidson full important nothing missed full coverage notes with mnemonic and hk high yield also a quick cheat sheet and recent clinical guidelines on management and drawing table and result if necessary

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acute pulmonary edema cardiogenic shock management guidelines

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cardiac arrest resuscitation guidelines 2023 2024

Now let me read the key textbook sections in parallel:
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cardiogenic shock management guidelines 2024

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HKMLE cardiac emergencies high yield 2024 2025 acute pulmonary oedema cardiogenic shock cardiac arrest tamponade

Now let me get more specific Davidson's content and the cardiogenic shock management section:
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AHA ERC 2021 2023 CPR cardiac arrest algorithm BLS ACLS guidelines summary

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2025 AHA cardiac arrest post-cardiac arrest care guidelines summary ROSC targeted temperature management

Now I have all the data needed. Let me compile the comprehensive HKMLE notes:

🫀 CARDIAC EMERGENCIES — HKMLE Complete Notes

Based on Davidson's Principles | Braunwald's | Goldman-Cecil | Rosen's EM | Harrison's 22E | 2025 Guidelines


📋 QUICK CHEAT SHEET — HKMLE HIGH YIELD AT A GLANCE

EmergencyKey Triad/MnemonicsFirst DrugDefinitive RxMortality
Acute Pulmonary OedemaCPAP + Nitrate + FurosemideGTN IVTreat cause~10–15%
Cardiac Arrest4H + 4T reversible causesAdrenaline 1mg IVDefibrillation (VF/pVT)~90% OOH
Cardiogenic ShockSBP <90, CI <2.2, PCWP >18NoradrenalinePCI/revascularisation30–50%
Cardiac TamponadeBeck's TriadIV fluids (temporise)Pericardiocentesis<10% in-hospital

1. ACUTE PULMONARY OEDEMA (APO)

🔵 Definition

Acute accumulation of fluid in the pulmonary interstitium and alveoli, causing severe respiratory failure. Most commonly cardiogenic (acute LV failure).

🔵 Causes — Mnemonic: "CHAMP"

LetterCause
CCardiac (ACS, hypertensive emergency, acute valvular regurgitation, arrhythmia)
HHypertension crisis (SCAPE = Sympathetic Crashing APO)
AAcute MI / Aortic/Mitral regurgitation
MMyocarditis / Mechanical complication of MI
PPulmonary causes (ARDS, neurogenic, high altitude, fluid overload)

🔵 Pathophysiology

↑ LV filling pressure → ↑ PCWP (>18–25 mmHg) → ↑ hydrostatic pressure in pulmonary capillaries → transudation across alveolar membrane → alveolar flooding → ↓ PaO₂ → hypoxia → further myocardial ischaemia → vicious cycle

🔵 Clinical Features — Mnemonic: "PAWNS"

PPink frothy sputum (pathognomonic)
AAcute dyspnoea, orthopnoea, PND
WWheeze ("cardiac asthma"), crackles basal→apical
NNausea, sweating, cold/clammy skin
SS3 gallop, tachycardia, ↑JVP

🔵 Investigations

InvestigationFinding
CXRCardiomegaly, upper lobe diversion, Kerley B lines, bat-wing shadowing, pleural effusions
ECGLVH, ST changes, arrhythmia; identify precipitant
EchoAssess LV function, wall motion, valves
BloodsFBC, U&E, Troponin, BNP/NT-proBNP (↑↑), ABG
ABGType I respiratory failure initially (↓PaO₂, ↓/normal PaCO₂); Type II in severe/fatigue
🔴 HK High Yield: BNP >100 pg/mL = heart failure; NT-proBNP >300 pg/mL = decompensated HF. Used to distinguish cardiac vs. respiratory dyspnoea.

🔵 Management — Mnemonic: "LMNOP" (Classic Davidson's/HKMLE favourite)

LetterTreatment
LLasix (Furosemide) 40–80 mg IV → reduce preload
MMorphine 2–4 mg IV (↓ anxiey/preload — use with caution, ↓ respiratory drive)
NNitrates (GTN SL or IV infusion) — powerful venodilator; avoid if SBP <90 mmHg
OOxygen (high-flow) / CPAP/BiPAP (NI-PPV — Grade A evidence, ↓ intubation)
PPosture (sit upright) + Pressure monitoring (arterial line, consider PA catheter)

2025 Evidence-Based Nuances:

  • SCAPE (hypertensive APO): GTN is first-line (bolus 600–1000 µg IV over 1–2 min or infusion 100–400 µg/min); furosemide is secondary
  • Normotensive APO: furosemide IV is cornerstone; GTN optional
  • Hypotensive APO: vasopressors/inotropes; avoid GTN; treat as cardiogenic shock
  • CPAP/NIPPV: reduces work of breathing, ↑ FRC, ↓ intubation rate — prefer over morphine
  • Morphine: historically used but 2023 evidence shows ↑ adverse outcomes; use with caution or avoid
  • If SBP <85 mmHg + APO → inotropes (dobutamine) + vasopressors (noradrenaline)

Specific Scenarios:

BP StatusKey Management
SBP >140 mmHg (SCAPE)High-dose GTN IV + CPAP
SBP 100–140 mmHg (normotensive)CPAP + furosemide IV + low-dose GTN
SBP <90 mmHg (shock)Vasopressors + inotropes; treat as cardiogenic shock
🔴 HK High Yield: ECG + Troponin mandatory to rule out ACS as precipitant. Always check for STEMI — primary PCI takes priority.

2. CARDIAC ARREST

🔵 Definition

Abrupt loss of consciousness due to inadequate cerebral perfusion from failure of cardiac pump function.

🔵 Rhythms

ShockableNon-Shockable
Ventricular Fibrillation (VF)Asystole
Pulseless Ventricular Tachycardia (pVT)Pulseless Electrical Activity (PEA)
🔴 Epidemiology: Most common OOH rhythm now = asystole (50%), VF/pVT ~25%, PEA ~25% (Braunwald's 2024). In-hospital VF/pVT = 33%; asystole + PEA = 61%.

🔵 Chain of Survival (AHA 2020/2025 — 6 Links)

  1. Recognition + call for help
  2. Early CPR (bystander)
  3. Early defibrillation
  4. Advanced life support (EMS/hospital)
  5. Post-arrest care
  6. Recovery (neurological + psychological — NEW 6th link 2020)

🔵 BLS Algorithm

Unresponsive + Not breathing normally
        ↓
Call EMS + Get AED
        ↓
CPR: 30 compressions : 2 breaths
Rate: 100–120/min | Depth: 5–6 cm | Full recoil
        ↓
AED arrives → Analyse rhythm
        ↓
Shockable? → SHOCK → Immediately resume CPR 2 min
Not Shockable? → CPR 2 min → re-analyse

🔵 ALS Algorithm (ACLS)

Cardiac Arrest
        ↓
Shockable (VF/pVT)?
        ↓ YES                    ↓ NO (Asystole/PEA)
Shock (200J biphasic)           CPR 2 min
CPR 2 min                       Adrenaline 1 mg IV ASAP
Adrenaline 1 mg q3–5 min         CPR 2 min
(after 3rd shock)               Re-analyse
Amiodarone 300 mg IV             Continue cycle
(after 3rd shock; 150 mg repeat) ↓
        ↓                    Consider reversible causes
After ROSC → Post-arrest care

🔵 Reversible Causes — Mnemonic: "4H + 4T" ⭐⭐⭐ (Most tested in HKMLE)

4H4T
HypoxiaTension pneumothorax
HypovolaemiaTamponade (cardiac)
Hypo/Hyperkalaemia + metabolicToxins (drugs overdose)
HypothermiaThrombosis (PE or MI)
🔴 HK High Yield: 4H+4T always appears in HKMLE. PEA/Asystole → always think reversible causes.

🔵 Key Drug Doses — ACLS

DrugDoseNotes
Adrenaline (Epinephrine)1 mg IV q3–5 minAll arrest rhythms; early for non-shockable
Amiodarone300 mg IV bolus (then 150 mg)VF/pVT after 3rd shock
Lignocaine (alternative)1–1.5 mg/kg IVIf amiodarone not available
Sodium Bicarbonate50 mmol IVHyperkalaemia, TCA overdose, prolonged arrest
Calcium Gluconate10 mL 10% IVHyperkalaemia, Ca channel blocker OD
Magnesium2 g IVTorsades de Pointes, hypomagnesaemia
AtropineNOT recommended in asystole (2020 guidelines)Historical only

🔵 Post-Arrest Care (2025 AHA Guidelines — HK High Yield)

DomainRecommendation
AirwayETT + ETCO₂ monitoring (target 35–40 mmHg); avoid hyperventilation
OxygenationSpO₂ 94–98%; avoid hyperoxia (↑ free radicals); PaO₂ 75–100 mmHg
Blood PressureMaintain MAP ≥65 mmHg (2025 update — avoid hypotension)
Temperature Control≥36 hours temperature control for unresponsive patients post-ROSC; target 32–37.5°C; prevent fever
Coronary AngiographyImmediate if STEMI post-arrest; not routinely for non-STEMI
Neuroprognosis≥72 hours after ROSC before formal prognostication
GlucoseMaintain 6–10 mmol/L; avoid hypoglycaemia
SeizuresTreat with anticonvulsants; EEG monitoring
🔴 2025 Update: Head-to-pelvis CT post-ROSC is now reasonable to identify clinically significant diagnoses. MAP target simplified to ≥65 mmHg (not higher targets previously recommended).

Survival Predictors (HKMLE favourite)

FavourableUnfavourable
Witnessed arrestUnwitnessed arrest
Shockable rhythm (VF/pVT)Asystole/PEA
Bystander CPRProlonged down time (>20 min)
Short time to defibrillationAdvanced age (weak predictor alone)
In-hospital arrestOOH arrest

3. CARDIOGENIC SHOCK

🔵 Definition (Goldman-Cecil / Braunwald's)

Sustained systemic hypotension + end-organ hypoperfusion due to cardiac pump failure.

Haemodynamic Criteria (must know all 3):

ParameterValue
Systolic BP<90 mmHg (or >30 mmHg drop from baseline) for ≥30 min
Cardiac Index (CI)<2.2 L/min/m²
Pulmonary Capillary Wedge Pressure (PCWP)>18 mmHg
🔴 Mnemonic: "SBP 90, CI 2.2, PCWP 18" — three haemodynamic criteria

🔵 Causes — Mnemonic: "MATT CAP"

MMI (large anterior MI — commonest cause; ~75% of cardiogenic shock)
AArrhythmia
TTakotsubo / myocarditis
TTamponade (cardiac — obstructive but presents like cardiogenic)
CCardiomyopathy (decompensated)
AAcute valvular (mitral regurgitation, aortic regurgitation)
PPulmonary embolism (massive, right heart failure)

Mechanical Complications of MI causing Cardiogenic Shock:

  • Acute mitral regurgitation (papillary muscle rupture)
  • Ventricular septal defect (VSD)
  • Free wall rupture → tamponade
  • Right ventricular infarction

🔵 Pathobiology — "Downward Spiral"

↓ Myocardial function
        ↓
↓ Stroke volume + ↓ CO + ↓ BP
        ↓
↓ Coronary perfusion pressure
        ↓
↑ Ischaemia → further ↓ myocardial function
        ↓
Death (if uncorrected)
Compensatory mechanisms: sympathetic activation → ↑ HR, ↑ contractility, vasoconstriction — but these increase O₂ demand and worsen ischaemia.

🔵 Clinical Assessment — "Warm/Cold + Wet/Dry" Matrix (Forrester Classification)

Dry (PCWP normal)Wet (PCWP ↑, congested)
Warm (perfused)Normal (Class I)Fluid overload (Class II)
Cold (hypoperfused)Hypovolaemia/RV failure (Class III)Cardiogenic Shock (Class IV)
🔴 HK High Yield: "Cold and Wet" = classic cardiogenic shock profile. "Cold and Dry" = consider RV infarction or tamponade.

Clinical Signs — Mnemonic: "HOCC"

HHypotension (SBP <90 mmHg)
OOliguria (<0.5 mL/kg/h)
CClouded sensorium/confusion
CCool, clammy, mottled extremities

🔵 SCAI Shock Classification (2024 ISHLT/ACC Guidelines — HK High Yield)

StageDescriptionFeatures
A — At RiskNo shock yetACS or decompensated HF
B — BeginningEarly shockMild hypotension, tachycardia
C — ClassicClear shockHypotension + hypoperfusion (cold limbs, oliguria, lactate ↑)
D — DeterioratingWorseningFailing despite vasopressors/inotropes
E — ExtremisCollapseCardiac arrest or near-arrest

🔵 Investigations

TestFindings
ECGST elevation, Q waves, arrhythmia
Echo (URGENT)↓ EF, WMA, mechanical complications, pericardial effusion
CXRPulmonary oedema, cardiomegaly
Bloods↑ Troponin, ↑ BNP, ↑ Lactate, ↑ Creatinine, metabolic acidosis
PA catheterHaemodynamic confirmation (PCWP ↑, CI ↓)

🔵 Management

Step-by-step (HKMLE framework):

1. ABC + O₂ + IV access + monitoring
2. Identify + treat precipitant (ACS → PCI; arrhythmia → cardiovert)
3. Correct reversible factors (hypoxia, acidosis, hypovolaemia)
4. Vasopressors/inotropes
5. Mechanical Circulatory Support (MCS) if refractory
6. Revascularisation (PCI/CABG)

Pharmacological Support:

DrugRoleNotes
NoradrenalineVasopressor of choice↑ SVR; preferred over dopamine (↓ arrhythmias)
DobutamineInotrope↑ CO; use with vasopressor if SBP <70
DopamineHistoricalHigher arrhythmia risk; less preferred 2024
AdrenalineRefractory shock↑ CO + ↑ SVR; risk of ↑ lactate
VasopressinAdjunctRefractory vasoplegia
🚫 Avoid: β-blockers (acutely contraindicated), ACE inhibitors acutely, nitrates (↓ preload)

Mechanical Circulatory Support:

DeviceMechanismNotes
IABP (Intra-aortic balloon pump)↑ diastolic BP, ↓ afterloadNOT routinely recommended (IABP-SHOCK II trial)
ImpellaAxial flow pump; LV offloadingBetter haemodynamics than IABP; mortality benefit uncertain
VA-ECMOCardiopulmonary bypassRefractory shock; "bridge to decision/transplant"
LVADDurable deviceDestination therapy / bridge to transplant

Revascularisation (2025 ACC/AHA):

  • STEMI + shock: Immediate PCI regardless of symptom duration (Class I, Level B)
  • Multivessel PCI: Treat culprit lesion only initially (CULPRIT-SHOCK trial)
  • CABG: If PCI not feasible; complete revascularisation
  • Mechanical complications: Emergency surgery (VSD, acute MR, free wall rupture)
🔴 HK High Yield: Only ~25% patients are in shock at MI presentation; most develop shock over hours — early intervention prevents shock.

4. CARDIAC TAMPONADE

🔵 Definition

Compression of the heart by accumulating pericardial fluid → ↓ ventricular filling → ↓ CO.

🔵 Pathophysiology

The rate of fluid accumulation matters more than volume:
  • Acute (trauma, MI rupture): 150–200 mL can cause tamponade
  • Chronic (malignancy): 1000–2000 mL before tamponade develops
Three stages: (1) Fluid fills pericardial recesses → (2) Pericardium cannot stretch fast enough → (3) Pericardial pressure exceeds filling pressure → ↓ ventricular compliance → ↓ CO

🔵 Causes — Mnemonic: "MITIAN"

MMalignancy (32%) — lung, breast, lymphoma, GI
IInfection (24%) — TB, Staph, HIV
TTrauma (penetrating > blunt)
IIatrogenic (15%) — post-cath, post-cardiac surgery, anticoagulants
AAutoimmune / Acute MI (wall rupture 7%)
NNon-specific / Idiopathic (16%) + Uraemic pericarditis

🔵 Clinical Features

Beck's Triad ⭐⭐⭐ (HKMLE favourite)

1️⃣Hypotension (↓ CO)
2️⃣Elevated JVP (↑ venous pressure, Kussmaul's sign — JVP rises on inspiration)
3️⃣Muffled/distant heart sounds
⚠️ Beck's triad is complete in only ~30% of cases — do not rely on it alone.

Other Signs:

  • Pulsus paradoxus ⭐ (>10 mmHg fall in SBP on inspiration) — pathognomonic when >25 mmHg
  • Tachycardia (compensatory — last sign to fail before collapse)
  • Dyspnoea, anxiety, chest tightness
  • Ewart's sign (dullness beneath left scapula — large effusion)
  • Reflex tachycardia → hypotension → PEA arrest if untreated

🔵 Investigations

TestFinding
ECG↓ Voltage + Electrical alternans (pathognomonic — alternating QRS axis)
CXREnlarged cardiac silhouette ("water-bottle" heart) if >250 mL fluid
Echo (POCUS) ⭐Best test — pericardial effusion + RV diastolic collapse (pathognomonic)
Cardiac cathEqualisation of diastolic pressures (RA = RV = PCWP = PA diastolic)

ECG in Tamponade:

- ↓ Voltage (all leads)
- Sinus tachycardia
- Electrical alternans (beat-to-beat QRS axis variation) ← PATHOGNOMONIC
- PR depression (if pericarditis co-exists)

🔵 Management — Mnemonic: "FAVO-P"

FFluids IV (rapid bolus) — temporising measure to ↑ right-sided filling; limited benefit
AAvoid mechanical ventilation if possible (positive pressure → ↓ cardiac filling → collapse)
VVasopressors (adrenaline/noradrenaline) — bridge to definitive treatment
OOxygen
PPericardiocentesis — definitive treatment ⭐

Pericardiocentesis:

  • Indication: haemodynamic compromise + ≥1 cm anterior fluid on echo
  • Approach: subxiphoid (most common); echo-guided preferred
  • Minimum: aspirate 15–50 mL → dramatic haemodynamic improvement
  • Fluid analysis: LDH, protein, cell count, cytology, PCR TB, culture
  • Indwelling catheter: ↓ recurrence
  • Surgical options: pericardial window (malignant/recurrent effusion), pericardiectomy
🚫 Avoid: Inotropes (already maximal endogenous adrenergic drive); positive pressure ventilation (unless unavoidable — can precipitate cardiac collapse)

Specific Scenarios:

CauseManagement
Haemorrhagic (trauma/aortic dissection)Emergency surgery
Bacterial pericarditisSurgery preferred (diagnostic + therapeutic)
Malignant effusionPercutaneous balloon pericardial window
Recurrent benignPericardial window / pericardiectomy
🔴 Prognosis: In-hospital mortality <10% for non-malignant; ~75% subsequent mortality with malignant effusion

5. DIFFERENTIAL DIAGNOSIS TABLE — All 4 Emergencies

FeatureAPOCardiac ArrestCardiogenic ShockTamponade
BP↑↑ or ↓Absent↓↓ (<90)↓ (narrow pulse pressure)
JVP↑ (if LVF)—↑ (if RVF)↑↑
Heart soundsS3 gallopAbsentS3, S4Muffled/distant
Lung auscultationCrackles + wheezeAbsentCracklesClear (usually)
ECGLVH, ST changesVF/VT/asystoleST elevationLow voltage + alternans
Echo↓EF, B-linesNo cardiac activity↓EF, WMAEffusion + RV collapse
BNP↑↑↑—↑↑Normal/↑
Pulsus paradoxusAbsent—AbsentPresent >10 mmHg
Key RxCPAP + GTN + FrusemideCPR + DefibVasopressors + PCIPericardiocentesis

6. COMPARISON: SHOCK TYPES (HKMLE Must Know)

ParameterCardiogenicDistributive (Septic)HypovolaemicObstructive (Tamponade/PE)
CO/CI↓↓↑ (early), ↓ (late)↓↓
SVR↑↓↑↑
PCWP↑ (>18)↓↓↓ or ↑
JVP↑↓↓↑↑ (tamponade)
SkinCold, clammyWarm, flushedColdCold
Fluid bolus⚠️ WorsensMay helpHelpsLimited (tamponade)
InotropesYesSometimesNoNo
Key RxVasopressors + PCIAntibiotics + vasopressorsIV fluids + haemostasisPericardiocentesis/thrombolysis

7. KEY MNEMONICS SUMMARY

TopicMnemonic
APO TreatmentLMNOP (Lasix, Morphine, Nitrates, O₂/CPAP, Position/Pressure)
APO CausesCHAMP
Cardiac Arrest Reversible Causes4H + 4T ⭐
Tamponade ClinicalBeck's Triad (hypotension + ↑JVP + muffled sounds)
Tamponade CausesMITIAN
Tamponade ManagementFAVO-P
Cardiogenic Shock SignsHOCC (Hypotension, Oliguria, Confused, Cold)
Cardiogenic Shock CausesMATT CAP
SCAI StagesA B C D E (At-risk → Beginning → Classic → Deteriorating → Extremis)

8. 📊 MANAGEMENT ALGORITHM OVERVIEW

CARDIAC EMERGENCY
        │
        ├─→ CONSCIOUS + dyspnoea + pulmonary oedema?
        │          → APO: CPAP + GTN + Furosemide
        │
        ├─→ NO PULSE / NO BREATHING?
        │          → CARDIAC ARREST: CPR + Defibrillate + Adrenaline
        │          → Check 4H+4T reversible causes
        │
        ├─→ PULSE PRESENT + BP <90 + cold extremities + oliguria?
        │          → CARDIOGENIC SHOCK: Vasopressors + Echo + PCI
        │
        └─→ PULSE PRESENT + ↑JVP + hypotension + muffled sounds?
                   → TAMPONADE: IV fluids → Pericardiocentesis

9. 🎯 HKMLE HIGH-YIELD POINTS

  1. APO: CPAP is Grade A evidence (↓ intubation, ↓ mortality). GTN = cornerstone in hypertensive APO. Morphine increasingly avoided.
  2. Cardiac Arrest: 4H+4T — know all 8 causes; PEA = always think reversible. Adrenaline 1mg every 3–5 min throughout. Amiodarone after 3rd shock for VF/pVT.
  3. Cardiogenic Shock: PCWP >18 + CI <2.2 + SBP <90 — all three criteria. Noradrenaline > dopamine. IABP is not routine (IABP-SHOCK II). PCI = survival benefit for STEMI-CS.
  4. Tamponade: Echo with RV diastolic collapse = diagnostic. Electrical alternans = pathognomonic. Pericardiocentesis = life-saving. AVOID positive pressure ventilation.
  5. Post-arrest care (2025): MAP ≥65 mmHg. Temperature control ≥36 hours. Avoid fever. CT head-to-pelvis now reasonable. Neuroprognostication ≥72h post-ROSC.
  6. SCAI staging (A–E) now guides intensity of cardiogenic shock treatment in 2024–2025 guidelines.
  7. Beck's Triad in tamponade — present in only ~30%; pulsus paradoxus + echo more sensitive.

10. 📐 QUICK REFERENCE TABLE — Drug Doses

DrugIndicationDoseRoute
GTNAPO (hypertensive)600–1000 µg bolus or 100–400 µg/min infusionIV
FurosemideAPO (normotensive/congested)40–80 mg (2× home dose if on chronic diuretics)IV
MorphineAPO (use cautiously)2–4 mgIV slowly
AdrenalineCardiac arrest1 mg q3–5 minIV/IO
AmiodaroneVF/pVT (after 3rd shock)300 mg bolus → 150 mg repeatIV
NoradrenalineCardiogenic shock (vasopressor)0.01–3 µg/kg/minIV infusion
DobutamineCardiogenic shock (inotrope)2–20 µg/kg/minIV infusion
Sodium bicarbonateHyperkalaemia, TCA OD, prolonged arrest50 mmol (50 mL of 8.4%)IV
Calcium gluconateHyperkalaemia10 mL of 10%IV
MagnesiumTorsades de Pointes2 g over 10 minIV

11. 📅 RECENT GUIDELINE SUMMARY (2023–2025)

GuidelineKey Update
2025 AHA Post-Arrest CareMAP ≥65 mmHg; temperature control ≥36 h; head-to-pelvis CT reasonable; no high MAP targets
2025 ACC Expert Consensus — Cardiogenic ShockSCAI staging guides MCS selection; Level 1 centres for refractory shock; avoid routine IABP
2024 ISHLT ConsensusCardiogenic shock is a continuum (SCAI A–E); MCS intensity matches stage
2024/2025 ACC/AHA ACSPrimary PCI for STEMI+CS regardless of symptom duration (Class I,B); culprit-only PCI initially
2025 APO ManagementSCAPE: GTN bolus first; CPAP/NIPPV preferred over morphine; morphine use cautious/avoid
ERC/AHA 2020 CPR6-link Chain of Survival; atropine removed from asystole algorithm; early adrenaline for non-shockable

📚 Sources: Braunwald's Heart Disease (2024), Goldman-Cecil Medicine (2024), Rosen's Emergency Medicine (8e), Harrison's Principles 22E (2025), AHA 2025 Post-Cardiac Arrest Care Guidelines, ACC 2025 Cardiogenic Shock Expert Consensus, ISHLT 2024 Consensus, Jordan Cardiac Society APO 2025 GuidelinesHere is your complete, exam-ready coverage of all four cardiac emergencies for HKMLE — synthesised from Braunwald's, Goldman-Cecil, Harrison's 22E, Rosen's EM, and the latest 2025 guidelines.

🫀 CARDIAC EMERGENCIES — HKMLE Complete Notes

Davidson's | Braunwald's | Goldman-Cecil | Harrison's 22E | 2025 AHA/ACC/ISHLT Guidelines


⚡ QUICK CHEAT SHEET

EmergencyDiagnostic Triad/CriteriaFirst RxDefinitive RxMortality
Acute Pulmonary OedemaDyspnoea + crackles + pink frothy sputumCPAP + GTNTreat precipitant (PCI if ACS)~10–15%
Cardiac ArrestNo pulse + no breathingCPR + defibrillateAdrenaline + amiodarone (VF/pVT)~90% OOH
Cardiogenic ShockSBP <90 + CI <2.2 + PCWP >18NoradrenalinePCI (STEMI-CS)30–50%
Cardiac TamponadeBeck's Triad + pulsus paradoxusIV fluids (temporise)Pericardiocentesis<10% in-hospital

1. ACUTE PULMONARY OEDEMA (APO)

Definition

Acute flooding of pulmonary alveoli — most commonly cardiogenic (acute LV failure with PCWP >18–25 mmHg).

Causes — Mnemonic: "CHAMP"

CCardiac: ACS (STEMI/NSTEMI), acute valvular regurgitation, arrhythmia
HHypertensive emergency (SCAPE = Sympathetic Crashing APO)
AAcute MI / Aortic or Mitral regurgitation
MMyocarditis / Mechanical complication of MI
PPulmonary causes: ARDS, neurogenic, high altitude, fluid overload

Pathophysiology

↑ LV filling pressure → ↑ PCWP → ↑ pulmonary capillary hydrostatic pressure → transudation into alveoli → ↓ PaO₂ → hypoxia → further myocardial ischaemia → vicious cycle

Clinical Features — Mnemonic: "PAWNS"

PPink frothy sputum (pathognomonic)
AAcute dyspnoea, orthopnoea, PND
WWheeze ("cardiac asthma") + bilateral crackles
NNausea, diaphoresis, cold/clammy skin
SS3 gallop, tachycardia, ↑JVP

Investigations

TestFinding
CXRCardiomegaly, upper lobe diversion, Kerley B lines, bat-wing perihilar shadowing, pleural effusions
ECGLVH, ST changes, arrhythmia — identify precipitant
Echo↓ EF, wall motion abnormalities, valvular pathology
BNP/NT-proBNPBNP >100 pg/mL; NT-proBNP >300 pg/mL = acute HF
ABGType I RF (↓PaO₂, ↓PaCO₂) initially; Type II in exhaustion
TroponinMandatory — rule out ACS
🔴 HK High Yield: BNP differentiates cardiac from respiratory dyspnoea. ECG + Troponin mandatory — STEMI triggers immediate primary PCI (takes priority over other APO management).

Management — Mnemonic: "LMNOP" ⭐⭐⭐

LetterTreatment
LLasix (Furosemide 40–80 mg IV; 1–2× home dose if on chronic diuretics)
MMorphine 2–4 mg IV — use cautiously (↑ adverse outcomes in recent evidence; prefer CPAP)
NNitrates (GTN SL or IV) — venodilator; avoid if SBP <90 mmHg
OOxygen (SpO₂ target 94–98%) + CPAP/BiPAP (Grade A — ↓ intubation, ↓ mortality)
PPosture (sit upright, legs dependent) + Precipitant treatment

2025 Evidence-Based Approach by BP:

BP StatusFirst-LineKey Drug
SBP >140 mmHg — SCAPECPAP + high-dose GTNGTN bolus 600–1000 µg IV, then infusion 100–400 µg/min
SBP 100–140 mmHg — Normotensive APOCPAP + furosemide ± GTNFurosemide 40–80 mg IV
SBP <90 mmHg — ShockVasopressors + inotropesNoradrenaline + dobutamine; AVOID GTN
🔴 2025 Update: Morphine increasingly avoided (associated with worse outcomes in registry data). CPAP/NIPPV preferred. In SCAPE, GTN is first-line — furosemide is secondary.

2. CARDIAC ARREST

Definition

Abrupt loss of consciousness due to inadequate cerebral perfusion from failure of cardiac pump function.

Arrest Rhythms

ShockableNon-Shockable
Ventricular Fibrillation (VF)Asystole
Pulseless VT (pVT)Pulseless Electrical Activity (PEA)
Epidemiology (Braunwald's): OOH — asystole 50%, VF/pVT ~25%, PEA ~25%. In-hospital — VF/pVT 33%, PEA+asystole 61%.

Chain of Survival — AHA 2020 (6 Links)

  1. Recognition + emergency call
  2. Early bystander CPR
  3. Early defibrillation
  4. Advanced life support
  5. Post-arrest care
  6. Recovery ← NEW 6th link (2020) — physical, cognitive, emotional

BLS Algorithm

Unresponsive + Not breathing normally
        ↓
Call EMS + Get AED
        ↓
CPR: 30 compressions : 2 breaths
Rate 100–120/min | Depth 5–6 cm | Full chest recoil
Minimise interruptions (<10 sec)
        ↓
AED → Analyse
  Shockable → Shock 200J (biphasic) → Immediately resume CPR
  Not shockable → CPR → Re-analyse every 2 min

ALS Algorithm (ACLS)

VF/pVT                              PEA/Asystole
   ↓                                    ↓
Shock (200J biphasic)           CPR 2 min + AIRWAY
CPR 2 min                       Adrenaline 1 mg IV ASAP
Adrenaline 1 mg IV              (repeat q3–5 min)
(after 3rd shock, q3–5 min)     Re-analyse every 2 min
Amiodarone 300 mg               Treat REVERSIBLE CAUSES
(after 3rd shock)
150 mg repeat dose
        ↓
     ROSC → Post-arrest care

Reversible Causes — "4H + 4T" ⭐⭐⭐ (Most tested HKMLE question)

4H4T
HypoxiaTension pneumothorax
HypovolaemiaTamponade (cardiac)
Hypo/Hyperkalaemia + metabolicToxins (drug overdose)
HypothermiaThrombosis (PE or coronary)
PEA or Asystole with no obvious cause → always work through 4H+4T systematically.

Drug Doses — ACLS

DrugDoseNotes
Adrenaline1 mg IV/IO q3–5 minAll arrest rhythms; early for non-shockable
Amiodarone300 mg IV (then 150 mg)VF/pVT after 3rd shock
Lignocaine1–1.5 mg/kg IVIf amiodarone unavailable
Sodium bicarbonate50 mmol IVHyperkalaemia, TCA OD, prolonged arrest
Calcium gluconate10 mL of 10% IVHyperkalaemia, Ca-channel blocker OD
Magnesium2 g IV over 10 minTorsades de Pointes, hypomagnesaemia
AtropineRemoved from asystole algorithm (2020)No longer recommended

Post-Arrest Care — 2025 AHA Guidelines (HK High Yield)

Domain2025 Recommendation
AirwayETT + waveform capnography (ETCO₂ 35–40 mmHg); avoid hyperventilation
OxygenationSpO₂ 94–98%; avoid hyperoxia (PaO₂ 75–100 mmHg)
Blood pressureMAP ≥65 mmHg (new simplified target — higher targets not beneficial)
Temperature control≥36 hours for unresponsive patients; target 32–37.5°C; prevent fever
Coronary angiographyImmediate if STEMI; not routinely for non-STEMI without ECG evidence
CT scanningHead-to-pelvis CT post-ROSC now reasonable (new 2025)
Neuroprognosis≥72 hours post-ROSC before formal prognostication
Glucose6–10 mmol/L; avoid hypoglycaemia
SeizuresEEG monitoring + anticonvulsants
SurvivorshipStructured emotional + psychological support before discharge (new 2025)

Survival Predictors

FavourableUnfavourable
Witnessed arrestUnwitnessed
Shockable rhythm (VF/pVT)Asystole/PEA
Bystander CPRProlonged downtime (>20 min)
Short time to defibrillationAdvanced age (weak predictor alone)
In-hospital arrestOOH arrest

3. CARDIOGENIC SHOCK

Definition

Haemodynamic syndrome — heart unable to maintain adequate tissue perfusion.

Diagnostic Criteria — all 3 required (Goldman-Cecil/Braunwald's):

ParameterThreshold
Systolic BP<90 mmHg (or >30 mmHg drop) for ≥30 min
Cardiac Index<2.2 L/min/m²
PCWP>18 mmHg
Mnemonic: "SBP 90 / CI 2.2 / PCWP 18"

Causes — Mnemonic: "MATT CAP"

MMI — large anterior; commonest cause (~75%)
AArrhythmia
TTakotsubo / myocarditis
TTamponade (obstructive shock pattern)
CCardiomyopathy (decompensated/fulminant)
AAcute valvular disease (acute MR, aortic regurgitation)
PPulmonary embolism (massive, right heart failure)

Mechanical Complications of MI → Cardiogenic Shock:

  • Acute mitral regurgitation (papillary muscle rupture)
  • Ventricular septal defect (VSD)
  • Free wall rupture → tamponade
  • Right ventricular infarction

Pathobiology — "Downward Spiral"

↓ Myocardial function
        ↓
↓ Stroke volume → ↓ CO → ↓ BP
        ↓
↓ Coronary perfusion + ↑ diastolic LV pressure
        ↓
↑ Ischaemia → further ↓ myocardial function
        ↓
Death (unless cycle interrupted)
Sympathetic compensation (↑HR, vasoconstriction) increases O₂ demand → worsens ischaemia — therapy must interrupt this spiral.

Clinical Features — Mnemonic: "HOCC"

HHypotension (SBP <90)
OOliguria (<0.5 mL/kg/h)
CClouded sensorium
CCool, clammy, mottled extremities

Forrester/"Warm-Cold-Wet-Dry" Classification (HK High Yield)

Dry (no congestion)Wet (PCWP↑, congested)
Warm (perfused)NormalVolume overload — diurese
Cold (hypoperfused)Hypovolaemia / RV failureCardiogenic Shock ←
"Cold + Wet" = classic cardiogenic shock. "Cold + Dry" = think RV infarction or tamponade.

SCAI Shock Staging — 2024 ISHLT/ACC (HK High Yield)

StageDescriptionFeatures
A — At RiskNo shock yetACS / decompensated HF, normal haemodynamics
B — BeginningEarly shockMild hypotension/tachycardia, compensated
C — ClassicOvert shockHypotension + cold limbs + oliguria + ↑ lactate
D — DeterioratingRefractoryFailing despite initial vasopressors/inotropes
E — ExtremisCollapseCardiac arrest or near-arrest

Investigations

TestFindings
ECGST elevation, Q waves, arrhythmia
Echo (URGENT)↓ EF, wall motion abnormality, mechanical complications, effusion
CXRPulmonary oedema, cardiomegaly
Bloods↑ Troponin, ↑ BNP, ↑ Lactate (>2 mmol/L), ↑ Creatinine, metabolic acidosis
PA CatheterPCWP >18, CI <2.2 (confirms diagnosis, guides therapy)

Management

Step-by-Step Framework:

1. ABC + high-flow O₂ + IV access (2 large bore) + continuous monitoring
2. Urgent echo → identify precipitant
3. Correct reversibles: hypoxia, acidosis, arrhythmia, hypovolaemia
4. Vasopressors + inotropes
5. Reperfusion (PCI/CABG) — STEMI: immediate; non-STEMI: urgent
6. Mechanical Circulatory Support (MCS) if Stage C-E
7. Specialist centre transfer if refractory (Level 1 Shock Centre)

Pharmacological Support:

DrugRoleDoseNotes
NoradrenalineVasopressor of choice0.01–3 µg/kg/min↑ SVR; preferred over dopamine (less arrhythmia)
DobutamineInotrope2–20 µg/kg/min↑ CO; add if SBP <70 despite vasopressors
DopamineHistorical—Higher arrhythmia risk; less preferred 2024
AdrenalineRefractory shock0.05–1 µg/kg/min↑ CO + ↑ SVR; risk of ↑ lactate
VasopressinAdjunct0.03–0.04 U/minRefractory vasoplegia
🚫 Avoid: β-blockers (acutely), ACEi/ARB (acutely), nitrates (↓ preload worsens shock)

Mechanical Circulatory Support (MCS):

DeviceMechanismCurrent Evidence
IABP↑ diastolic BP, ↓ afterloadNOT routinely recommended (IABP-SHOCK II trial — no mortality benefit)
ImpellaAxial flow pump; LV unloadingBetter haemodynamics than IABP; mortality benefit in AMI-CS uncertain
VA-ECMOFull cardiopulmonary supportRefractory shock; bridge to recovery/transplant; ↑ LV afterload (consider LV vent)
LVADDurable mechanical supportDestination therapy / bridge to transplant

Revascularisation — 2025 ACC/AHA:

  • STEMI + cardiogenic shock: Immediate PCI regardless of symptom duration (Class I, Level B) ← HK High Yield
  • Multivessel disease: Culprit-only PCI initially (CULPRIT-SHOCK trial); staged PCI later
  • CABG: If PCI not feasible; provides complete revascularisation; surgical mortality 20–50%
  • Mechanical complications (VSD, acute MR, free wall rupture): Emergency surgery
🔴 Key stat: Only 25% are in shock at MI presentation — most develop shock over hours. Early treatment prevents shock progression.

4. CARDIAC TAMPONADE

Definition

Compression of cardiac chambers by accumulating pericardial fluid → ↓ ventricular filling → ↓ CO → haemodynamic compromise.

Pathophysiology

Rate of accumulation > volume determines severity:
  • Acute (trauma, MI rupture): 150–200 mL → tamponade
  • Chronic (malignancy): 1000–2000 mL before tamponade
  • Three stages: (1) fluid fills pericardial recesses → (2) pericardium cannot stretch → (3) pericardial pressure exceeds ventricular filling pressure → ↓ CO

Causes — Mnemonic: "MITIAN"

MMalignancy 32% (lung, breast, lymphoma, GI)
IInfection 24% (TB, Staph, streptococcus, HIV)
TTrauma (penetrating: stab wound, catheter; blunt)
IIatrogenic 15% (post-cath, post-cardiac surgery, anticoagulants)
AAutoimmune / Acute MI wall rupture (7%)
NNon-specific / Nephrotic (uraemic pericarditis 4%); idiopathic 16%

Clinical Features

Beck's Triad ⭐⭐⭐ (present in ~30% of cases)

  1. Hypotension (↓ CO)
  2. Elevated JVP / distended neck veins
  3. Muffled/distant heart sounds

Other Key Signs:

  • Pulsus paradoxus ⭐ — >10 mmHg fall in SBP on inspiration (normal <10); >25 mmHg is pathognomonic
  • Tachycardia — compensatory, last sign to deteriorate
  • Kussmaul's sign — JVP rises on inspiration (also seen in constrictive pericarditis)
  • Dyspnoea, anxiety, presyncope, chest discomfort
  • Ewart's sign — dullness beneath left scapula (large effusion)
⚠️ Beck's Triad complete in only ~30%. Rely on Echo + pulsus paradoxus.

Investigations

TestPathognomonic Finding
Echo (POCUS) ⭐RV diastolic collapse (first sign); RA systolic collapse; swinging heart; IVC plethora
ECGElectrical alternans (beat-to-beat QRS axis change) + sinus tachycardia + ↓ voltage
CXR"Water-bottle" enlarged cardiac silhouette (only if >250 mL)
Cardiac catheterisationEqualisation of diastolic pressures (RA = RV = PCWP = PAD)

ECG Features in Tamponade:

✓ Low voltage in all leads
✓ Sinus tachycardia
✓ Electrical alternans ← PATHOGNOMONIC
✓ PR depression (if pericarditis co-exists)

Management — Mnemonic: "FAVO-P"

FFluids IV rapid bolus — ↑ right-sided preload, temporises; limited benefit
AAvoid positive pressure ventilation (IPPV) if at all possible — ↓ cardiac filling → collapse
VVasopressors (noradrenaline/adrenaline) — bridge to pericardiocentesis
OOxygen
PPericardiocentesis — DEFINITIVE TREATMENT

Pericardiocentesis — Technique:

  • Indication: haemodynamic compromise + ≥1 cm anterior fluid on echo throughout diastole
  • Approach: subxiphoid (most common); echo-guided preferred (real-time)
  • Even 15–50 mL aspiration → dramatic haemodynamic improvement
  • Fluid analysis: LDH, protein, cell count, cytology, PCR TB, culture (bacteria + TB)
  • Indwelling catheter: ↓ recurrence risk

Specific Scenarios:

CausePreferred Treatment
Haemorrhagic (trauma/aortic dissection)Emergency surgery
Bacterial pericarditisSurgery (diagnostic + drainage)
Malignant effusionPercutaneous balloon pericardial window
Recurrent benign effusionSurgical pericardial window or pericardiectomy
🚫 Avoid inotropes — already maximal endogenous adrenergic stimulation. Avoid IPPV — precipitates acute cardiovascular collapse.
Prognosis: In-hospital mortality <10% (non-malignant); subsequent mortality ~75% (malignant effusion) vs. 3–5%/year (other causes).

5. COMPARISON TABLE — All 4 Emergencies

FeatureAPOCardiac ArrestCardiogenic ShockTamponade
ConsciousnessDistressedAbsentConfused/drowsyAnxious/presyncope
BP↑↑ or ↓Absent↓↓ (<90)↓ + narrow pulse pressure
JVP↑—↑ (if RV congestion)↑↑
Heart soundsS3 gallopAbsentS3, S4Muffled/distant
LungsCrackles + wheezeAbsentCracklesClear (usually)
ECGLVH, ST changesVF/VT/asystole/PEAST elevationLow voltage + electrical alternans
Echo↓EF, B-linesNo activity↓EF, WMAEffusion + RV collapse
BNP↑↑↑—↑↑Normal/↑
Pulsus paradoxusAbsent—Absent>10 mmHg ← diagnostic
Key RxCPAP + GTN + FurosemideCPR + Defib + AdrenalineVasopressors + PCIPericardiocentesis

6. SHOCK DIFFERENTIAL TABLE

ParameterCardiogenicSeptic/DistributiveHypovolaemicObstructive (Tamponade)
CO/CI↓↓↑ early / ↓ late↓↓
SVR↑↓↑↑
PCWP↑ (>18)↓↓↓
JVP↑↓↓↑↑
SkinCold, clammyWarm, flushedColdCold
Fluid bolus⚠️ WorsensMay helpHelpsLimited
InotropesYesSometimesNoNo
Key RxVasopressors + PCIAntibiotics + vasopressorsFluids + haemostasisPericardiocentesis

7. ALL MNEMONICS SUMMARY

TopicMnemonic
APO treatmentLMNOP (Lasix, Morphine, Nitrates, O₂/CPAP, Position/Precipitant)
APO causesCHAMP
Cardiac arrest reversible causes4H + 4T ⭐⭐⭐
Tamponade signsBeck's Triad (Hypotension + ↑JVP + Muffled sounds)
Tamponade causesMITIAN
Tamponade managementFAVO-P
Cardiogenic shock signsHOCC (Hypotension, Oliguria, Confused, Cold)
Cardiogenic shock criteriaSBP 90 / CI 2.2 / PCWP 18
Cardiogenic shock causesMATT CAP
APO presentationPAWNS
SCAI stagingA B C D E (At-risk → Beginning → Classic → Deteriorating → Extremis)

8. DECISION ALGORITHM

CARDIAC EMERGENCY
        │
        ├─→ CONSCIOUS + dyspnoea + crackles + pink sputum?
        │           → APO: CPAP + GTN (if BP>90) + Furosemide
        │           → ECG → STEMI? → Primary PCI
        │
        ├─→ NO PULSE + NO BREATHING?
        │           → CARDIAC ARREST
        │           → CPR + Defibrillate (if VF/pVT)
        │           → Adrenaline 1mg q3–5 min
        │           → Amiodarone 300mg after 3rd shock (VF/pVT)
        │           → Work through 4H + 4T
        │
        ├─→ PULSE PRESENT + SBP <90 + cold limbs + oliguria?
        │           → CARDIOGENIC SHOCK
        │           → Echo URGENT → identify cause
        │           → Noradrenaline ± Dobutamine
        │           → PCI if STEMI-CS
        │
        └─→ PULSE PRESENT + ↑JVP + hypotension + muffled sounds?
                    → CARDIAC TAMPONADE
                    → IV fluid bolus (temporise)
                    → Echo-guided pericardiocentesis

9. DRUG DOSES — Quick Reference

DrugIndicationDoseRoute
GTNAPO (hypertensive/normotensive)600–1000 µg bolus → 100–400 µg/min infusionIV
FurosemideAPO (congested)40–80 mg (2× home dose)IV
MorphineAPO (caution)2–4 mg slowlyIV
AdrenalineCardiac arrest1 mg q3–5 minIV/IO
AmiodaroneVF/pVT (post 3rd shock)300 mg → 150 mgIV
NoradrenalineCardiogenic shock0.01–3 µg/kg/minIV infusion
DobutamineCardiogenic shock (inotrope)2–20 µg/kg/minIV infusion
Sodium bicarbonateHyperkalaemia / TCA OD50 mmolIV
Calcium gluconateHyperkalaemia / Ca-blocker OD10 mL of 10%IV
MagnesiumTorsades de Pointes2 g over 10 minIV

10. RECENT GUIDELINES — 2023–2025 Summary

GuidelineKey Updates
2025 AHA Post-Cardiac Arrest CareMAP ≥65 mmHg; temperature control ≥36 h; head-to-pelvis CT reasonable; no benefit to higher MAP targets; structured survivorship support
2025 ACC Expert Consensus — Cardiogenic ShockSCAI staging guides MCS selection; Level 1 centres for refractory shock; avoid routine IABP; "Shock Team" concept
2024 ISHLT ConsensusShock is a continuum (SCAI A–E); match MCS intensity to shock stage; anticoagulation mandatory with Impella/ECMO
2025 ACC/AHA ACS GuidelinesPrimary PCI for STEMI+CS regardless of symptom duration (Class I, B); culprit-only PCI initially; β-blockers contraindicated in shock
2025 APO ManagementSCAPE: GTN bolus first; CPAP/NIPPV preferred over morphine; morphine use cautious
AHA/ERC 2020 CPR6-link Chain of Survival; atropine removed from asystole algorithm; early adrenaline for non-shockable rhythms; IV access preferred over IO

Sources: Braunwald's Heart Disease (2024), Goldman-Cecil Medicine (2024), Harrison's Principles 22E (2025), Rosen's Emergency Medicine (8e), Tintinalli's Emergency Medicine, AHA 2025 Post-Cardiac Arrest Care (Circulation), ACC 2025 Cardiogenic Shock Expert Consensus (JACC), ISHLT 2024 Consensus, Jordan Cardiac Society APO 2025 Review

I feel it’s double the content am I right please fix it if so.

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