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Cardiac System

Cardiac assessment and management for paramedicine: the electrophysiology behind the ECG, acute coronary syndromes and the conditions that mimic them, the shock states, and cardiac arrest.

Cardiac Electrophysiology

Cardiac muscle structure, action potentials, conduction pathway, and ECG correlates.

Cardiac Muscle Structure

Key Structures

  • Sarcolemma — Cell membrane of cardiac myocyte. Maintains resting membrane potential, houses ion channels for action potentials
  • Sarcoplasm — Cytoplasm of the cardiac myocyte. Contains enzymes, substrates and ions for contraction
  • Sarcoplasmic reticulum — Calcium storage network
  • Sarcomere — Basic contractile unit of cardiac muscle
  • Troponin & Tropomyosin — Regulatory proteins. Troponin binds calcium and shifts tropomyosin to allow myosin attachment. Released into blood on myocardial cell death
  • Gap junctions — Direct cell-to-cell pathways for ion flow, enabling rapid electrical spread
  • Desmosomes — Anchoring junctions that ensure heart muscle acts as a functional syncytium

Conduction Pathway

  • 1
    SA Node — Natural pacemaker (60–100 bpm). P wave = atrial depolarisation
  • 2
    AV Node — Conduction slows (0.05 m/s), allowing atria to finish before ventricles. PR interval reflects this delay. Escape rate 40–60 bpm
  • 3
    Bundle of His → Bundle Branches → Purkinje Fibres — Fastest conduction (~4 m/s). Narrow QRS = simultaneous ventricular contraction. Escape rate 20–40 bpm

Ventricular Action Potential — 5 Phases

PhaseNameIon MovementECG Correlate
0Rapid depolarisationNa⁺ rapid influxOnset of QRS complex
1Initial repolarisationTransient K⁺ outflowQRS downstroke
2PlateauCa²⁺ influx balances K⁺ effluxST segment (mechanical contraction peaking)
3RepolarisationIncreased K⁺ effluxT wave
4Return to RMP (−90mV)Baseline ion balance restoredBaseline between T wave and next P wave

Pacemaker Cells

Pacemaker cells lack true phases 1 and 2. They have an unstable Phase 4 — gradual spontaneous depolarisation via slow Na⁺ currents. This is why the SA node can depolarise spontaneously and produce regular P waves.

Refractory Periods

  • Absolute refractory period — No new action potential possible. Correlates with QRS through first half of T wave
  • Relative refractory period — Stronger than normal stimulus can trigger AP. Corresponds to downslope of T wave (R-on-T phenomenon risk)
Ventricular Action Potential — Interactive Diagram
Ventricular cardiac action potential — membrane potential in millivolts over time, showing phases 0 to 4 with threshold and resting levels and the corresponding ECG waveform. +40+200−20−40−60−80−100 mV threshold Na⁺ in ↑↑fast Na⁺ channels K⁺ outtransient outward Ca²⁺ inK⁺ outbalanced inward/outward K⁺ out ↑↑Ca²⁺ channels close Na⁺/K⁺ ATPase pumprestores ion gradients 4 0 1 2 3 4 ECG QRS ST Segment T Wave P wave (atrial, schematic) Absolute refractory period Relative refractory
Click any phase of the action potential to see ion channel details and clinical relevance.

Ventricular myocyte action potential. Phases 0–4. ECG correlation shown in lower band. Waveform is schematic — not to exact timescale.

ECG Basics

ECG waveforms, intervals, and what each component represents.

ECG Waveform Components

ComponentRepresentsNormal ValueClinical Notes
P Wave Atrial depolarisation (SA node origin) Smooth, upright in lead II Notched P = left atrial delay. Tall peaked P = right atrial overload (P Pulmonale). Inverted P = non-sinus origin
PR Interval Time from atrial depolarisation to ventricular depolarisation 120–200 ms (3–5 small boxes) <120ms = junctional origin. Prolonged = AV block
QRS Complex Ventricular depolarisation <120 ms (3 small boxes) Wide QRS (>120ms) = aberrant conduction. High amplitude = ventricular hypertrophy
ST Segment Period between ventricular depolarisation and repolarisation Isoelectric (flat at baseline) Elevation = STEMI/pericarditis. Depression = ischaemia/NSTEMI. J point marks ST start
T Wave Ventricular repolarisation Upright, same direction as QRS Inverted T = ischaemia. Peaked T = hyperkalaemia
QT Interval Total ventricular depolarisation + repolarisation <440 ms (corrected) Prolonged QT = risk of torsades de pointes
U Wave Delayed Purkinje fibre repolarisation Uncommon, follows T wave Prominent U waves associated with hypokalaemia

ECG Axes

Vertical axis = amplitude (height). Standard calibration: 10mm = 1mV. Horizontal axis = time. Standard speed: 25mm/s. Each small box = 0.04s. Each large box = 0.2s. Positive deflection = electrical activity moving toward electrode. Negative deflection = moving away.
The ECG Waveform — Anatomy of a Single Beat
Loading ECG…
Click any coloured segment or legend item to see details

Grid: small box = 1 mm / 0.04 s · large box = 5 mm / 0.2 s · Standard 25 mm/s, 1 mV/cm

12-Lead ECG Interpretation

Systematic approach, STEMI identification, coronary territories, and right-sided leads.

ECG interpretation

5-Step Systematic Approach

  • 1
    Check settings — Confirm gain (×1), filter (0.05–150 Hz), speed (25 mm/s), and all 12 leads are present and readable
  • 2
    Underlying rhythm in Lead II — Rate, regularity, P waves present?, PR interval, QRS width
  • 3
    Systematically investigate abnormalities — ST elevation/depression, T wave changes, reciprocal changes
  • 4
    Check for mimics and STEMI equivalents — LBBB, paced rhythm, BER, pericarditis, LVH (see mimics section below)
  • 5
    Diagnosis — Synthesise findings into working diagnosis and clinical action

STEMI Lead Groupings & Coronary Territories

Inferior STEMI
II, III, aVF
RCA territory. Always do V4R — RV infarct complicates 40% of inferior STEMIs
Anterior STEMI
V1–V4
LAD territory. New LBBB in this context = high mortality
Lateral STEMI
I, aVL, V5–V6
LCx territory. Often occurs with anterior or inferior changes

Right Ventricular Infarction (V4R)

All inferior STEMIs require V4R. Place electrode at 5th right intercostal space, mid-clavicular line. RV infarct patients are preload sensitive — fluid loading is the treatment. GTN is contraindicated — can cause severe hypotension.

Worked 12-Leads — Normal & STEMI

Model-generated 12-lead (25 mm/s, 10 mm/mV) — one continuous 10 s recording: aVR inverted, R-wave progression V1→V6. STEMI views show ST elevation in the territory’s leads with reciprocal change. Scroll horizontally on narrow screens.

STEMI Mimics

Conditions that can produce ST elevation but are not STEMI — critical for accurate triage.

Left Bundle Branch Block (LBBB)

  • Electrical conduction blocked through left bundle branch — causes wide QRS and ST changes
  • May be chronic or acute (new LBBB in anterior infarct = high mortality)
  • Can complicate reperfusion decision-making (PCI or thrombolysis) — interpret alongside clinical context and local criteria

Pericarditis

  • Widespread concave ST elevation across most leads (whole pericardium affected)
  • PR depression is a key distinguishing feature
  • T wave inversions do not occur simultaneously with ST elevation (unlike STEMI)
  • Chest pain: sharp, pleuritic, improved by sitting forward

Benign Early Repolarisation (BER)

  • Common in young, healthy patients
  • Widespread concave ST elevation, most prominent in V2–V5
  • J-point notching present — no reciprocal ST depression

Left Ventricular Hypertrophy (LVH)

  • Usually caused by chronic hypertension
  • Voltage criteria: S wave in V1 + tallest R wave in V5–V6 > 35mm
  • Signs of LV strain pattern on ECG

Paced Rhythms

  • Ventricular pacemakers cause ST segment elevation due to pacing lead position and altered depolarisation vector
  • Broad QRS complexes — appears similar to LBBB. Always check patient's history for pacemaker

Acute Coronary Syndrome (ACS)

Angina, NSTEMI, and STEMI — pathophysiology, clinical features, and prehospital management.

Cardiac Chest Pain — Assessment

Quality of Cardiac Pain

  • Crushing, gripping, squeezing, pressure
  • Radiates to arm/s, jaw, neck, shoulders, hands
  • Not reproducible — unchanged by breathing, coughing, swallowing, or posture
  • Often described as discomfort or aching rather than sharp pain

Risk Factors

  • Previous ischaemic heart disease (strongest predictor)
  • Dyslipidaemia / Hypercholesterolaemia
  • Hypertension
  • Smoking (pack history important)
  • Diabetes mellitus
  • Obesity, physical inactivity, poor diet
  • Family history, age, gender, ethnicity

Angina vs NSTEMI vs STEMI

Stable Angina
  • Gradual luminal narrowing, inadequate supply on demand
  • Lasts 3–5 minutes, resolves with rest
  • Relieved by GTN and rest
  • NOT an ACS — no plaque rupture
  • Associated pallor, diaphoresis, nausea, dyspnoea
Unstable Angina
  • Plaque has become complicated
  • Superficial plaque erosion → transient thrombotic occlusion
  • Lasts <20 minutes
  • May have some ST changes
  • Troponin negative
  • 20% will result in infarction
  • Requires anti-thrombotic therapy
STEMI / NSTEMI
  • Prolonged ischaemia → myocardial necrosis
  • Diagnosis: pain + ECG changes + positive troponin
  • STEMI: ST elevation, complete occlusion
  • NSTEMI: subtle ST/T changes, partial occlusion
  • Pain usually at rest, >30 minutes
  • Onset usually at rest

Myocardial Infarction — Pathophysiology Timeline

0–10 seconds

  • Myocardial O₂ reserves depleted
  • Glycogen stores decrease — anaerobic metabolism begins
  • H⁺ accumulation begins

10–60 seconds

  • Electrolyte disturbance accompanies O₂ deprivation
  • Failure of ion pumps
  • Release of catecholamines and angiotensin II

20+ minutes

  • Cell death (necrosis)
  • Release of intracellular contents
  • Troponin and cardiac enzymes detectable in blood

STEMI Management — Reperfusion Principle

  • 1
    Recognise STEMI early — the 12-lead ECG is the priority investigation
  • 2
    Assess reperfusion eligibility and screen for contraindications
  • 3
    Obtain informed consent from the patient
  • 4
    Escalate to advanced/critical care support and follow your service's reperfusion pathway
  • 5
    Antiplatelet and anticoagulant therapy are indicated per local clinical guidelines
  • 6
    Achieve timely reperfusion — emergent PCI or thrombolysis (“time is myocardium”)
  • 7
    Rapid transport to an appropriate destination

Reperfusion Strategy — PCI vs Thrombolysis

  • 1
    Primary PCI — mechanical restoration of coronary flow; generally preferred where it can be delivered within guideline timeframes
  • 2
    Thrombolysis — pharmacological reperfusion; used where timely PCI is not accessible (e.g. long transport times)
  • 3
    Thrombolysis requires careful contraindication screening due to bleeding risk
  • 4
    Transmission of the 12-lead for remote clinical decision support may guide the decision
  • 5
    Choice of strategy, agents and timing follow local clinical guidelines

ACS Pharmacology

Mechanism of action and clinical use for key ACS drugs.

Scope & Guidelines

This pharmacology is general educational information. Indications, dosing and routes vary between services — always follow your own scope of practice and current clinical guidelines.
GTN (Glyceryl Trinitrate)
Nitrate Vasodilator
Commonly Used For
Used for ischaemic chest pain in ACS and for cardiogenic pulmonary oedema
Mechanism
Vasodilator — redistributes coronary blood flow, decreases preload and afterload
Contraindications
RV infarction (inferior STEMI + V4R positive) — can cause severe hypotension. Hypotension. PDE-5 inhibitor use.
Aspirin
Antiplatelet
Commonly Used For
Given in ACS across all presentations, and in cardiogenic shock and pulmonary oedema
Mechanism
Irreversible inhibitor of platelet TXA synthesis — prevents platelet aggregation
Fentanyl
Opioid Analgesic
Commonly Used For
An analgesic option in ACS, often preferred over morphine in haemodynamically unstable patients
Mechanism
Opioid receptor agonist — central analgesia, sedation
Ticagrelor
Antiplatelet (PCI)
Mechanism of Action
Direct P2Y12 receptor antagonist. Prevents ADP-induced platelet aggregation. Prevents expression of GP IIb/IIIa.
Heparin
Anticoagulant (PCI)
Mechanism of Action
Activates antithrombin III — inhibits thrombin and factor Xa.
Tenecteplase
Thrombolytic
Mechanism of Action
Binds to fibrin component of thrombus. Converts plasminogen to plasmin → clot lysis.
Clopidogrel / Enoxaparin
Antiplatelet / LMWH
Clopidogrel
Prodrug — requires metabolism by CYP2C19. P2Y12 receptor antagonist. Prevents ADP-induced platelet aggregation.
Enoxaparin (Clexane)
Antithrombin III enhancer — acts primarily on factor Xa only.

Chest Pain — Differential Diagnosis

Life-threatening causes and differentials in prehospital chest pain assessment.

Life-Threatening Causes — Exclude First

ACS · Acute aortic dissection · Pulmonary embolism · Tension pneumothorax · Cardiac tamponade · Mediastinitis (oesophageal rupture) · Myocarditis

Assume life-threatening if any of the following are present:

  • Abnormal vital signs
  • Obvious distress or signs of hypoperfusion
  • Abrupt onset of thoracic or abdominal pain
  • Variation of pulse between limbs

Duration Clues

  • Pain >30 minutes → more likely ACS than angina
  • Pain lasting multiple days → unlikely ACS or angina
  • Sudden onset + dyspnoea + cyanosis → consider massive PE
  • Pleuritic pain (worse on inspiration) → pleurisy, PE, pericarditis

General Approach — Unstable Chest Pain

  • Assess and manage airway, ventilation
  • Supplemental O₂ as needed
  • IV access
  • 12-lead ECG and continuous cardiac monitoring
  • Address dysrhythmias
  • Aspirin (if no contraindications)
  • Circulatory support as required

Acute Cardiogenic Pulmonary Oedema

LV failure leading to alveolar fluid accumulation and hypoxia.

Clinical Features

  • Sudden onset extreme breathlessness — "drowning" sensation
  • Profuse diaphoresis
  • Basal crackles on auscultation
  • Pink, frothy sputum
  • Tachypnoea and tachycardia
  • Patient prefers sitting upright

Prehospital Management

  • O₂ — reverse hypoxia
  • Aspirin (if ischaemic cause)
  • GTN — aggressive preload/afterload reduction (if BP allows)
  • 12-lead ECG
  • Early IV access
  • IPPV / CPAP / PAEP
  • Escalate to advanced/critical care support + rapid transport

Vicious Cycle — Break it Early

Hydrostatic/oncotic pressure imbalance → alveolar fluid exudate → alveolar collapse (atelectasis) → hypoxia → tachypnoea → worsens condition further. Aggressive early GTN and CPAP break this cycle.

Cardiogenic Shock

Inadequate oxygen delivery at cellular level due to cardiac pump failure.

Key Formula

CO = HR × SV. If stroke volume falls, HR compensates — to a point. When compensation fails, cardiac output drops and shock ensues. Most common cause is AMI.

Clinical Features

  • Chest pain, diaphoresis
  • Pallor / cyanosis
  • Altered LOC (ALOC)
  • Tachycardia
  • Hypotension
  • Respiratory distress
  • Cold, clammy skin / oliguria

Management

  • If dysrhythmia — treat underlying rhythm
  • If STEMI — manage per ACS protocol
  • Oxygen
  • 12-lead ECG
  • IPPV / CPAP
  • IV access / fluids
  • Aspirin
  • Adrenaline (if required)
  • Rapid transport

Pericarditis

Inflammation of the pericardial sac — key differentiator from STEMI.

Clinical Features

  • Chest pain — sharp, pleuritic, sudden onset. Improved by sitting up and leaning forward. Worsened by inspiration/coughing
  • Pericardial friction rub — superficial scratchy/squeaky sound on auscultation
  • ECG changes — widespread ST elevation + PR depression
  • Fever if infectious aetiology

Diagnosis — ≥2 of:

  • ✓Chest pain typical of pericarditis
  • ✓Pericardial friction rub
  • ✓Characteristic ECG changes
  • ✓New/worsening pericardial effusion

Pericarditis vs STEMI on ECG

  • ST elevation is concave (saddle-shaped) in pericarditis; convex in STEMI
  • ST changes are generalised across leads in pericarditis (whole pericardium); anatomically grouped in STEMI
  • T wave inversions do not occur simultaneously with ST elevation in pericarditis
  • PR elevation in aVR with PR depression elsewhere = common in pericarditis, rare in STEMI

Cardiac Tamponade

Pericardial effusion compressing the heart — impaired filling and reduced stroke volume.

Clinical Features

  • Tachycardia + hypotension
  • Elevated JVP — venous distension neck, forehead, scalp
  • Pulsus paradoxus — abnormally large decrease in systolic BP on inspiration
  • Muffled heart sounds (Beck's Triad)
  • Fever if infectious aetiology

Types

  • Acute — occurs within minutes, causes cardiogenic shock. Urgent pericardiocentesis required
  • Subacute — develops over days to weeks, may be initially asymptomatic
  • Low pressure — occurs in severely hypovolaemic patients
  • Regional — localised effusion affecting one or more but not all chambers

Beck's Triad

Hypotension + elevated JVP + muffled heart sounds. Classic triad for cardiac tamponade. ECG typically shows sinus tachycardia. Electrical alternans (alternating QRS amplitude) is a sign of large pericardial effusion.

Cardiac Arrest

Recognition, CPR, shockable rhythms, defibrillation, reversible causes, drugs, and ROSC.

CPR Standards

Compression Rate
100–120
per minute
Depth
5–6 cm
or ⅓ chest depth. Full recoil required
Interruptions
Minimal
Regular swap to minimise fatigue

Shockable vs Non-Shockable Rhythms

Shockable — Defibrillate

Pulseless Ventricular Tachycardia (pVT)
Ventricular Fibrillation (VF)
Defibrillation within 3 minutes = 50–70% survival. Chance of reversion decreases 7–10% per minute without defibrillation.
Ventricular Fibrillation (VF)
Pulseless VT (pVT)

Non-Shockable — CPR + Treat Cause

Pulseless Electrical Activity (PEA)
Asystole
Focus on high-quality CPR and identifying reversible causes (4H 4T).
Asystole
Pulseless Electrical Activity (PEA)

Reversible Causes — 4H 4T

4 H's

  • HHypoxia
  • HHypovolaemia
  • HHypo/Hyperkalaemia / metabolic disorders
  • HHypo/Hyperthermia

4 T's

  • TTension pneumothorax
  • TTamponade — pericardial compression
  • TToxins
  • TThrombosis — pulmonary or coronary

Cardiac Arrest Drugs

Adrenaline
Catecholamine — Cardiac Arrest
Commonly Used For
Often a first-line vasopressor in cardiac arrest
Mechanism
Alpha-1 agonist. Increases systemic vasomotor tone → increased diastolic BP and coronary perfusion pressure. Evidence for outcome benefit is uncertain.
Amiodarone
Anti-arrhythmic — VF/VT
Commonly Used For
Used for shock-refractory VF or pulseless VT
Mechanism
Often the anti-arrhythmic of choice for VF/VT. Prolongs action potential duration and refractory period of atrial, nodal, and ventricular tissues.

ROSC Goals

  • Continue respiratory support
  • Maintain cerebral perfusion
  • Treat and prevent cardiac arrhythmias
  • Determine and treat the cause of arrest
  • Resuscitation does not stop at ROSC

Withholding CPR / ROLE

Obvious Signs of Death

  • Decomposition / putrefaction
  • Hypostasis (fluid accumulation)
  • Rigor mortis
  • Injuries incompatible with life (decapitation, hemicorporectomy, incineration)

ROLE Criteria

  • No palpable carotid pulse
  • No heart sounds for 30 seconds
  • No breath sounds for 30 seconds
  • Fixed, dilated pupils
  • No response to central stimuli

Arrhythmias

Bradyarrhythmias, SVT, WPW, broad complex tachycardia, and AF.

Bradycardia (<60 bpm)

Causes

  • Myocardial ischaemia / infarction
  • Hypoxia
  • Electrolyte disturbances

Symptoms

  • Syncope, dizziness
  • Chest pain, shortness of breath, diaphoresis

Management

  • Atropine — Acetylcholine antagonist at muscarinic receptor. Inhibits parasympathetic system.
  • Transcutaneous pacing — Used when pharmacology fails or risk of asystole. Temporary cardiac pacing via external pads
Sinus Bradycardia (<60/min)

Supraventricular Tachycardia (SVT)

Key Features

  • Tachyarrhythmia arising from above the Bundle of His
  • No aberrancy = narrow complex QRS
  • Primary focus: AVNRT (AV nodal re-entry) and AVRT (AV re-entry with accessory pathway)

AVNRT

  • HR typically 140–240 bpm, regular rhythm
  • Spontaneous or provoked (exertion, caffeine, stress)
  • No structural abnormalities
  • Initial management: modified Valsalva manoeuvre

WPW Syndrome (AVRT with accessory pathway)

  • Bundle of Kent = accessory pathway
  • Delta wave visible on ECG
  • Unstable criteria: BP <90mmHg, HR >150, chest pain, heart failure, ALOC
  • Peri-arrest/unstable → immediate synchronised cardioversion
SVT — narrow-complex, regular (~180/min)

Broad/Wide Complex Tachycardia

Rule of Thumb

Regular rhythm + QRS >0.12s + tachycardia = treat as ventricular tachycardia (VT) until proven otherwise.

Stable Broad Complex

  • Amiodarone

Unstable — Synchronised Cardioversion

  • Energy delivered across myocardium, synchronised to R wave
  • Performed with sedation
  • AF with aberrancy + Torsades De Pointes → IV Magnesium Sulphate
Monomorphic VT — broad, regular

Atrial Fibrillation (AF)

  • Atrial cells contracting spontaneously — no organised atrial activity
  • Rhythm is irregularly irregular with no clear isoelectric baseline
  • No distinct P waves — fibrillatory baseline
  • Ventricular rate rapid and irregular — affects cardiac output
  • AF with fixed AV conduction (2:1 atrial rate 300 = ventricular 150, 3:1 = 100, 4:1 = 75) → suspect atrial flutter
Atrial Fibrillation — irregularly irregular, no P waves

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