Cardiac System
Educational use only. This content is derived from paramedicine study notes and is intended as a study and revision aid. Always follow your service's current clinical practice guidelines and defer to senior clinicians in practice.
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
- 1SA Node — Natural pacemaker (60–100 bpm). P wave = atrial depolarisation
- 2AV Node — Conduction slows (0.05 m/s), allowing atria to finish before ventricles. PR interval reflects this delay. Escape rate 40–60 bpm
- 3Bundle 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
| Phase | Name | Ion Movement | ECG Correlate |
|---|---|---|---|
| 0 | Rapid depolarisation | Na⁺ rapid influx | Onset of QRS complex |
| 1 | Initial repolarisation | Transient K⁺ outflow | QRS downstroke |
| 2 | Plateau | Ca²⁺ influx balances K⁺ efflux | ST segment (mechanical contraction peaking) |
| 3 | Repolarisation | Increased K⁺ efflux | T wave |
| 4 | Return to RMP (−90mV) | Baseline ion balance restored | Baseline 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)
ECG Waveform Components
| Component | Represents | Normal Value | Clinical 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.
5-Step Systematic Approach
- 1Check settings — Confirm gain (×1), filter (0.05–150 Hz), speed (25 mm/s), and all 12 leads are present and readable
- 2Underlying rhythm in Lead II — Rate, regularity, P waves present?, PR interval, QRS width
- 3Systematically investigate abnormalities — ST elevation/depression, T wave changes, reciprocal changes
- 4Check for mimics and STEMI equivalents — LBBB, paced rhythm, BER, pericarditis, LVH (see mimics section below)
- 5Diagnosis — 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.
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)
- !Currently a contraindication for PCI referral or thrombolysis
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
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 — PCI Referral (ppCI)
- 1Request CCP backup
- 2Confirm patient is indicated for PCI referral
- 3Complete STEMI checklist
- 4Obtain informed consent from patient
- 5Contact referral line
- 6Administer Heparin and Ticagrelor
- 7Transport Code 1 to hospital
STEMI Management — Thrombolysis (Rural/Remote)
- 1Request CCP backup
- 2Confirm indicated for decision-supported thrombolysis
- 3Complete thrombolysis checklist
- 4Send photo of 12-lead to thrombolysis consult line
- 5Contact consult line
- 6Obtain informed consent
- 7Administer Clexane, Tenecteplase, Clopidogrel, Enoxaparin
- 8Transport Code 2 to hospital
GTN (Glyceryl Trinitrate)
Nitrate Vasodilator
400 mcg
Sublingual
Contraindications
RV infarction (inferior STEMI + V4R positive) — can cause severe hypotension. Hypotension. PDE-5 inhibitor use.
Aspirin
Antiplatelet
300 mg
PO (loading)
Fentanyl
Opioid Analgesic
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.
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
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
- →CCP backup + 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.
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
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
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.
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)
Defibrillation within 3 minutes = 50–70% survival. Chance of reversion decreases 7–10% per minute without defibrillation.
Non-Shockable — CPR + Treat Cause
Pulseless Electrical Activity (PEA)
Asystole
Focus on high-quality CPR and identifying reversible causes (4H 4T).
Asystole
Focus on high-quality CPR and identifying reversible causes (4H 4T).
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
1 mg IV
Every 3–5 min
Amiodarone
Anti-arrhythmic — VF/VT
300 mg IV
1st dose
150 mg IV
2nd dose
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
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. Dose: 0.5–1 mg IV every 3–5 min, max 3 mg
- →Transcutaneous pacing — Used when pharmacology fails or risk of asystole. Temporary cardiac pacing via external pads
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
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 300 mg IV
Unstable — Synchronised Cardioversion
- →Energy delivered across myocardium, synchronised to R wave
- →Performed with sedation
- !AF with aberrancy + Torsades De Pointes → IV Magnesium Sulphate
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