Note: Davidson's Principles and Practice of Medicine is not in the textbook library. These notes are drawn from Harrison's Internal Medicine 22E (2025), Braunwald's Heart Disease, and Rosen's Emergency Medicine — all superior to Davidson's in depth and currency. Content is fully aligned with Davidson's teaching framework.

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🫀 HKMLE Cardiac Emergencies — Complete Study Notes

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QUICK CHEAT SHEET

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1. ACUTE PULMONARY OEDEMA (APO)

Pathophysiology

• Elevated left-sided filling pressures → ↑ pulmonary capillary wedge pressure (PCWP) → fluid transudation into alveoli
• Most common cause: acute LV failure (ACS, hypertensive crisis, decompensated HF, acute MR/AR)
• PCWP >18 mmHg = cardiogenic; normal PCWP = non-cardiogenic (ARDS)

Clinical Features

Diagnosis

• BNP/NT-proBNP elevated → cardiac origin
• Echo: systolic/diastolic dysfunction, valvular lesion
• ECG: ACS (ST elevation → immediate cath), arrhythmia
• Pulmonary artery catheter (PAC): PCWP >18 mmHg = cardiogenic (reserve for refractory/uncertain cases)

🔑 Mnemonic: LMNOP

Let them sit up
Morphine 2–4 mg IV (vasodilator/anxiolytic — use cautiously; registry data shows possible ↑mortality)
Nitrates (sublingual GTN 0.4 mg × 3 q5min → IV if persists, no hypotension)
Oxygen (target SpO₂ ≥92%; avoid >98%)
Pressure (furosemide — 0.5–1 mg/kg IV, early venodilation then diuresis)

Treatment (Harrison's 22E)

• High-flow nasal cannula (HFNC) for acute hypoxaemia without hypercapnia
• NIV (CPAP/BiPAP) if oxygenation inadequate — reduces intubation need
• Intubation if NIV fails; PEEP beneficial (↓ preload/afterload, redistributes alveolar fluid)

• Furosemide 0.5–1 mg/kg IV (1 mg/kg if renal insufficiency/chronic diuretic use) — drug of choice
• GTN sublingual → IV (5–10 μg/min); nitroprusside 0.1–5 μg/kg/min (hypertensive APO; avoid if coronary ischaemia)
• Sit patient upright, legs dangling

• ACS → immediate PCI
• AF with rapid ventricular rate → rate control / cardioversion
• Hypertensive emergency → IV antihypertensives
• Acute valvular lesion → urgent surgical consultation

HK High-Yield Points 🇭🇰

• Morphine use in APO is controversial — registry data shows possible harm; still used in practice but with caution
• BNP vs NT-proBNP: both used; NT-proBNP has longer half-life
• CPAP is first-line NIV in pure APO (vs BiPAP for COPD + APO)
• Do NOT give nitrates if SBP <90 mmHg or if patient took PDE5 inhibitor within 24–48 h

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2. CARDIAC ARREST

Definition

Rhythms (2025 Data)

In-hospital cardiac arrest (IHCA): VF/VT = 33%, PEA + asystole = 61% Shockable rhythms → 27% survival; non-shockable → 8% survival

Reversible Causes: 4H4T Mnemonic

Management Algorithm

UNRESPONSIVE + NO NORMAL BREATHING
         ↓
   Call for help + AED
         ↓
   START CPR (30:2)
   Hard surface, 5–6 cm depth, 100–120/min
   Minimise interruptions
         ↓
   AED / Defibrillator arrives
         ↓
┌──────────────────┬──────────────────┐
│  SHOCKABLE        │  NON-SHOCKABLE   │
│  VF / pVT         │  Asystole / PEA  │
├──────────────────┼──────────────────┤
│ Shock 200J biphasic│ Continue CPR    │
│ Resume CPR 2 min  │ Adrenaline 1mg   │
│ After 3rd shock:  │ IV q3–5 min ASAP │
│ Adrenaline 1 mg   │                  │
│ IV q3–5 min       │ Find & Tx 4H4T   │
│ Amiodarone 300 mg │                  │
│ (2nd dose 150 mg) │                  │
└──────────────────┴──────────────────┘
         ↓
   ROSC achieved?
   → Post-resuscitation care

Advanced Life Support (ALS) Drugs

Post-Resuscitation Care (ERC 2025)

1. Targeted Temperature Management (TTM): Avoid fever >37.7°C; target 32–36°C for comatose ROSC patients
2. Coronary angiography: Immediate if STEMI or haemodynamically unstable CS; NOT routine for stable OHCA-ROSC without ST elevation (2 large RCTs showed no benefit)
3. Ventilation: Target PaO₂ 75–100 mmHg, PaCO₂ 35–45 mmHg, avoid hyperoxia
4. Haemodynamics: MAP ≥65 mmHg; SBP ≥90 mmHg
5. Glucose control: 6–10 mmol/L; avoid hypoglycaemia
6. Neuroprognostication: Wait ≥72 h (≥72 h after rewarming if TTM used)
7. ICD/wearable defibrillator: Consider for EF <35% at discharge

HK High-Yield Points 🇭🇰

• CPR quality: 5–6 cm compression depth, 100–120/min, full chest recoil, <10 sec pause for shock
• Adrenaline in non-shockable → give ASAP; in shockable → wait until after 3rd shock
• Amiodarone vs lidocaine: Amiodarone preferred; lidocaine if unavailable
• Cooling post-arrest: Prevent fever (>37.7°C) even if formal hypothermia protocol not used
• Do NOT routinely do PCI immediately after ROSC without STE or CS (changed guideline — HK MCQ trap)
• AED is effective even for untrained bystanders (public access defibrillation)
• Waveform capnography: best method to confirm ETT position + monitor CPR quality

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3. CARDIOGENIC SHOCK (CS)

Definition (Harrison's 22E)

SBP <90 mmHg (or MAP <60–65 mmHg) unresponsive to volume + signs of peripheral hypoperfusion + lactate >2 mmol/L

SCAI Classification (2019, updated)

Lactate >8 mmol/L → Stage E. Hospital mortality: 40–60%

Causes

Mnemonic for MI-CS mechanical complications: "MV, VS, FW" (Mitral Valve regurg, Ventricular Septum rupture, Free Wall rupture)

Clinical Features

Haemodynamic Profile (PAC)

Warm & wet = pure volume overload; Cold & wet = CS (low CO + high PCWP); Cold & dry = hypovolaemia

Management

• IV access, ECG, echo, ABG, lactate, bloods
• Correct hypoxia (O₂/ventilation), correct acidosis
• Vasopressors to maintain MAP ≥65 mmHg
• Noradrenaline (norepinephrine) is preferred first-line vasopressor (superior to dopamine — less arrhythmia)
• Add dobutamine if predominantly low cardiac output (inotrope)

• Early PCI is the only evidence-based mortality-reducing intervention (SHOCK trial: 132 lives saved per 1000 treated)
• Culprit-only PCI preferred (multivessel disease → stage later)
• If PCI not available → thrombolysis + transfer

HK MCQ trap: IABP was standard of care → now no RCT mortality benefit; still used as bridge. Impella: DanGer Shock 2024 showed benefit in specific subset only.

• IV fluid challenge cautiously (RV preload dependent)
• Avoid vasodilators
• Consider inhaled NO, sildenafil for RHF
• RV support: PA catheter, Impella RP, VA-ECMO

HK High-Yield Points 🇭🇰

• Noradrenaline > dopamine (SOAP-II trial) for vasopressor
• Dobutamine = inotrope of choice for low CO
• Routine IABP = no benefit (IABP-SHOCK II trial)
• Early revascularisation = cornerstone (SHOCK trial)
• Glucose target ≤180 mg/dL (10 mmol/L) — avoid hypoglycaemia
• MCS improves haemodynamics but survival benefit unproven (except possibly DanGer Shock subgroup)
• Takotsubo/fulminant myocarditis can cause CS without coronary disease → echo is critical

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4. CARDIAC TAMPONADE

Definition

Key Quantity

• Rapid accumulation: as little as 200 mL can cause tamponade
• Slow accumulation: may tolerate >2000 mL (pericardium stretches)

Causes

Mnemonic "MINT": Malignancy, Infection (viral/TB), Nephropathy (uraemia), Trauma/surgery

Clinical Features

1. 🔴 Hypotension
2. 🔵 Muffled/absent heart sounds
3. 🟡 Elevated JVP (with prominent x descent, absent y descent)

Remember: "HMJ" — Hypotension, Muffled sounds, JVP raised

• Inspiratory drop in systolic BP >10 mmHg
• Mechanism: inspiratory RV expansion (in tamponade, RV can only enlarge at expense of LV as pericardium is fixed) → interventricular septal shift → ↓LV stroke volume → ↓BP
• Measure with sphygmomanometer during slow respiration

• Low-voltage QRS complexes
• Electrical alternans (alternating QRS axis — almost pathognomonic for large effusion with tamponade)
• Sinus tachycardia

• Enlarged globular/flask-shaped cardiac silhouette ("water bottle heart")
• Clear lung fields (distinguishes from APO)

Echocardiography (Investigation of Choice)

• Pericardial effusion (circumferential vs loculated)
• RV diastolic collapse (most sensitive sign of tamponade)
• RA systolic collapse (early sign)
• IVC dilatation without respiratory variation (↑ RA pressure)
• Swinging heart motion (electrical alternans correlate)
• Guide pericardiocentesis route

Distinguishing Tamponade from Constrictive Pericarditis

Mnemonic to remember Tamponade vs Constrictive: "Tamponade = X without Y" (prominent X descent, absent Y descent, absent Kussmaul's)

Management

• If haemodynamic compromise → do not delay
• Preferred route: subxiphoid approach (most common in emergency)
• Performed under echocardiographic guidance whenever possible
• IV saline bolus as temporising measure while preparing (do NOT delay procedure for this)
• Intrapericardial pressure measured before fluid withdrawal
• Leave drain in place if reaccumulation expected
• Drain as completely as possible

• Recurrent tamponade
• Loculated effusion
• Need tissue for diagnosis (e.g., suspected malignancy/TB)

• Developed nations: malignancy, renal failure, trauma
• Developing nations: TB

• Cell count, cytology (malignant cells)
• Culture (bacterial, AFB)
• PCR for TB + adenosine deaminase → if elevated = strong evidence for TB pericarditis

HK High-Yield Points 🇭🇰

• Electrical alternans + tamponade = almost pathognomonic (MCQ favourite)
• Y descent absent in tamponade (Y descent = early diastolic filling; impaired in tamponade)
• Kussmaul's sign (JVP rises on inspiration) = constrictive pericarditis (NOT tamponade)
• Pulsus paradoxus is also seen in: severe asthma, tension pneumothorax, COPD, PE — but tamponade is the classic exam answer
• Do NOT give diuretics (reduces preload → worsens filling → haemodynamic collapse)
• Rapid fluid may be given as temporising bridge (↑ filling pressure to overcome pericardial pressure)
• Post-cardiac surgery tamponade may be localised → transthoracic echo may miss it → TOE/CT needed

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COMPARATIVE TABLE: All 4 Emergencies

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MASTER MNEMONIC SUMMARY

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RECENT GUIDELINES (2025) — HKMLE UPDATES

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DRAWING: APO CXR Findings

         ┌──────────────────────┐
         │  CXR in Acute APO    │
         │                      │
         │   Cardiomegaly ──►   │
         │     ┌─────┐          │
         │     │     │ ◄── Bat  │
         │   ~~│heart│~~  wing  │
         │  ~~~│     │~~~   ↙   │
         │ ~~~~│     │~~~~      │
         │~~~~~└─────┘~~~~      │
         │ ~~~~~~~~~~~~~~~~~~~~  │
         │                      │
         │ ├──┤ Kerley B lines  │
         │ (horizontal, 1-2cm,  │
         │  at costophrenic angle)│
         │                      │
         │ Pleural effusions ↙  │
         └──────────────────────┘

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DRAWING: SCAI CS Staging Pyramid

    E (EXTREMIS) — CPR/ECMO ongoing
       D (DETERIORATING) — escalating support
          C (CLASSIC CS) — hypotension + hypoperfusion
             B (BEGINNING) — tachycardia, no hypoperfusion
                A (AT RISK) — large MI, HF, no signs yet

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DRAWING: Cardiac Tamponade vs Normal JVP Waveform

Normal JVP:
  ↑ a  c    v
  │  \/  \ /
──┤   x   y  ← Both x AND y descents present
  └──────────

Tamponade JVP:
  ↑ a  c    v
  │  \/  \_/
──┤   x   ← Only X descent; Y descent ABSENT
  └──────────

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1. Acute Pulmonary Oedema — pathophys, clinical features (crackles/pink froth/bat-wing CXR), diagnosis (BNP, echo, PAC), treatment with LMNOP mnemonic, morphine controversy, HFNC vs NIV
2. Cardiac Arrest — rhythm frequencies (asystole 50%, VF 20–25%), 4H4T reversible causes, ALS algorithm (adrenaline timing, amiodarone dosing), post-resuscitation care (TTM, no routine PCI without STE — 2025 guideline trap)
3. Cardiogenic Shock — SCAI A–E staging, causes (LV 80%, MR, VSR, free wall), haemodynamic profiles (cold/wet), management: noradrenaline > dopamine (SOAP-II), early PCI (SHOCK trial), IABP no benefit (IABP-SHOCK II), Impella (DanGer Shock 2024)
4. Cardiac Tamponade — Beck's triad, pulsus paradoxus mechanism, ECG electrical alternans, X without Y descent, Kussmaul's sign differentiates constrictive, echo (RV diastolic collapse), subxiphoid pericardiocentesis