Canonical Question
Cardiac Cycle
Master answer
Surface ECG to events of Cardiac Cycle
ECG:
- 12 metal electrodes on chest wall
- Detect small (0.5-2mV) changes in voltage produced by the heart
- Transfer these to an oscilloscope output
- P wave: → atrial depolarisation → atrial systole → AV valve opening
- PR interval: conduction from SA node → atrial conducting pathways → AV node (slowest) → bundle of His → LBB and RBB → Purkinje fibres
- QRS: ventricular depolarisation (endocardium → endocardium, L > R) → ventricular systole → closure of AV valves, opening of aortic and pulmonary valves
- Atrial repolarisation is low voltage, and lost within the QRS complex
- QT interval: sustained ventricular depolarisation and muscular contraction
- T wave: ventricular repolarisation (epicardium -> endocardium, L > R) -> ventricular
relaxation -> closure of aortic and pulmonary valves
ELECTRICAL EVENTS
| P0 | Fast Na opening |
| P1 | Transient K efflux |
| P2 | Influx Na & Ca |
| P3 | Efflux K > Influx Na & Ca |
| P4 | Re-establishment of RMP |
MECHANICAL EFFECTS
| A | Aortic Valve Closure |
| 1 | Isovolumetric relaxation |
| B | Mitral Valve Opening |
| 2a | Early Diastolic filling |
| 2b | Late Diastolic filling |
| C | Mitral Valve Closure |
| 3 | Isovolumetric Contraction |
| D | Aortic Valve Opening |
| 4 | Ventricular Ejection |
Action of Drugs
| Drug | Interval effects | Mechanism |
|---|---|---|
| VW (Vaughan-Williams) Class 1a | ↑QRS, ↑QT | Fast Na-channel blockade |
| VW Class 1b | ↓QT | |
| VW Class 1c | ↑↑QRS, ↑QT | |
| VW Class 2 | ↑PR | β blockade → negative chronotropy |
| VW Class 3 | ↑QT | K channel blockade → prolongation of RRP |
| VW Class 4 | Can ↑PR | Prolongation of ERP and RRP in pacemaker cells |
| Adenosine | ↑PR | Hyperpolarisation of myocardium via opening of K channels |
| Digoxin | ↑PR, ↓QT | Multiple effects, vagotonic at AVN |
| Amiodarone | ↑PR, ↑QRS, ↑QT, ↑RR (sinus rate) | Multiple |
| Mg | ↓QTc | Membrane stabilising. |
| TCAs | ↑QRS | Quinidine like Na-channel effect (class 1a) |
| SSRIs | ↑QT | Direct potassium blockade and downregulation of potassium → ↑ERP and ↑RRP. |
Digoxin
- ↑ RR interval (sinus rate), ↑PR interval, ↓RR interval
- Slowed AV conduction by increased vagal tone
- ACh → M2 receptors
- ↑KACh (ACh controlled K+ channels) → increased efflux of K+ → hyperpolarised
membrane - ↓If (funny current) → decreased influx of Na+ → decreased slope of phase 4
- ↓ICa(L) (long lasting) and iCa(T) (transient) → decreased efflux of calcium on partial
depolarisation → decreased slope of phase 4
Amiodarone
- ↑PR, ↑QRS, ↑QT, ↑RR (sinus rate)
- Main effect is K+ channel blockade
- Repolarisation is slowed → prolonged QT
- Some INa
- Slower phase 0 upstroke
- Slowed ventricular muscle conduction → prolonged QRS
- Some ICa
- Slower spontaneous depolarisation in SA node → decreased sinus rate
- Slowed conduction in AV node → prolonged PR
- Weakly downregulates adrenoreceptors
- Increased PR, decreased sinus rate
Mooney / Gladwin 2016
Exam appearances
| Exam | Exact wording | Relationship | Success |
|---|---|---|---|
| 2011A Q13 | Relate the surface electrocardiogram (ECG) to the events of the cardiac cycle (60% of marks). Briefly describe the mechanism of the effects of digoxin, and the mechanism of the effects of amiodarone, on the ECG (40% of marks) | historical_member | — |
| 2009A Q01 | Relate the surface ECG to the events of the cardiac cycle (60% of mark). Describe how the PR, 20QRS and QT intervals may be prolonged by the action of drugs. | historical_member | — |