Electricity and the heart Flashcards
3 types of muscle
Smooth, skeletal and cardiac
Na+ extra and intra cellular
E: 120
I: 10
Ca2+ extra and intra cellular
2 and 0
K+ extra and intra cellular
4 and 140
What is resting potential of nerve cell?
-70 mV
What causes depolarisation?
Sodium entering
What causes depolarisation?
Potassium leaving
Potential of cardiac myocyte
-85 to -90 mV
How is potential in cardiac myocyte regulated?
- ATP driven pump exchanges sodium and potassium - high Na+ outside cell and high K+ inside
- Antiport system: establishes Ca2+ gradient - exchange of sodium and calcium needed
Phase 0
Depolarisation
- Fast sodium channels open
- When cardiac cell is stimulated and depolarises, the membrane potential is more positive
- Voltage gated sodium channels open and allow Na+ into cell = depolarisation
- Membrane potential reaches +20 mV before Na+ channels close
Phase 1
Repolarisation
Na+ channels close and cell repolarises, K+ leaves cell through K+ channels
Phase 2
Plateau
- Ca2+ channels open and fast K+ channels close
- After initial repolarisation occurs, AP plateaus as a result of increased Ca2+ permeability and decreased K+ permeability
Phase 3
Rapid repolarisation
- Ca2+ channels close
- Slow K+ channels open, K+ exits cell
- Plateau ends and resting level is re-established
Phase 4
Resting potential
Averages -80 to -90 mVW
Why is there a prolonged resting potential in cardiac myocytes?
Ion channel inactivation and prevents tetany
Features of pacemaker cells
- Specialised cells in atria, especially SAN and AVN
- Autonomic firing without stimulus
- Results from continuous slow ionic leak
- Natural highest rate in SAN - others become active if SAN fails
What does pacemaker AP start at?
-60 mv
What causes depolarisation of pacemaker cells?
Ca2+ influx
Sympathetic influence on HR
Slow Na+ channel permeability increases
Slope of phase 4 steeper
Threshold reached sooner, increasing HR
Parasympathetic influence on HR
Increases resting K+ permeability
Trough potential is lowered and slope of phase 4 flatter
Threshold reached later, decreasing HR
Intra-cardiac conduction
- Non-specific conduction in atria
- AVN: gate in firewall between atria and ventricles - slows conduction and allows time for atrial emptying, protects ventricles from atrial tachyarrhythmias, also affected by autonomic NS
- His-Purkinje system - ventricles - depolarise of myometrium from in to out (opposite of perfusion)
- Branching nature of cardiac muscle also enables synchronous ventricular contraction
What are ECGs?
Surface recording of electrical activity
Polarity of impulses is +ve if moving towards electrode, -ve if away
Axis of ECGs
Lead iii at 90 degrees to axis = isoelectric trace
Characteristics of ischaemia/infarction on ECH
- Typically produces ST segment (with/without T wave) changes acutely
- Damaged cells repolarise early so ST segment is out of step with normal areas
- Division between ischaemia and infarction is now less clear (acute coronary syndrome can be reversible) but classically:
- Full thickness damage (ST elevation)
- Subendocardial damage (ST depression)
Full thickness STEMI on ECH
ST elevation
Q wave
Subendocardial damage on ECG
ST wave depression
With or without T wave inversion
Coronary artery to inferior heart
Right
Coronary artery to antero-septal heart
Left anterior descending
Coronary artery to antero-apical heart
Left anterior descending - distal
Coronary artery to antero-lateral heart
Circumflex
Coronary artery to posterior heart
Right
Inferior MI on ECG
ST elevation in leads II, III and aVF (inferior leads)
Anterior/septal MI on ECH
ST elevation in V2/3/4 - tombstoning
What is the Q wave?
First downwards deflection in PQRS pathology
Seen in lateral leads as septal depolarisation
What does deep Q wave indicate?
STEMI
Hyperkalaemia on ECG
High, peaked T waves and QRS widening
Hypertrophy on ECG
- LVH = large amplitude QRS complexes
- Negative deflection in V1, positive deflection in V5
- Add the negative deflection to the positive deflection, want it to be less than 35
Fibrillation on ECG
- Rapid, uncoordinated contraction
- Atrial fibrillation: AVN prevents VF, cardiac output less than 30%, thrombo-embolism risk
- Ventricular fibrillation: No cardiac output, fatal if not treated quickly
AF on ECG
- No P waves
- QRS normal but irregularly irregular
- To confirm irregularity, mark consecutive r peaks on paper and compare down the line
Management of AF
- Anti-thrombotics: warfarin, dabigatran, rivaroxaben, aspirin
- Rhythm: cardioversion (synchronised shock to prevent VF), rate control ( beta blocker, Ca2+ antagonist, amiodarone, digoxin)
- Plus any underlying causes
Mechanism of digoxin
- Slows conduction through AVN - reduces ventricular rate in AF
- Increases myocardial contractility
- Na+/K+ pump inhibited, increasing [Na+]
- Na+/Ca2+ exchange mechanism now less efficient, raising [Ca2+] - stored in sarcoplasmic reticulum
- Force of subsequent contraction enhanced
Ventricular fibrillation
- Continuous, bizarre, irregular trace
- No P wave
Management of VF
- Defibrillation: unsynchronised (150-200J, biphasic)
- Treat underlying causes
- Automated function - AED (paramedics, airports) and AID (implanted, high risk patients)
- Sudden death is often VF
Conduction defects
- SAN: pacemaker failure, lower site normally takes over
- AVN: heart block
- Intra-ventricular - bundle branch block
- Heart block:
- Problem with conduction through AVN
1st degree block
PR interval, prolonged but all eventually conducted
2nd degree block
Some P waves not conducted, here in 2:1 ratio (type ii)
3rd degree block
P waves unrelated to QRS complexes, usually bizarre in nature
Bundle branch blockages
- Problem with circulation through R or L branch
- 1 ventricle depolarises after the other
- Wide QRS complex after normal P wave
- RBBB: M pattern in V1, W pattern in V6
- LBBB: M pattern in V6
ventricular ectopic
- One-off can be normal
- Ventricle contracts after stimulus transported throughout heart
- Wide QRS complex
- Abnormalities in repolarisation
- No P wave
Pacing impulse
- Very brief impulse external impulse stimulates ventricle (with or without atrium)
- Wide QRS
- Short, sharp pacing spike
