Arrhythmia Flashcards
What controls the cardiac muscle contractions?
Pacemaker cells ≈ self-excitable (autorythmic) ≈ SAN in RA (by sulcus terminalis, between SVC and coronary sinus) ≈ myogenic ≈ determines HR ≈ chronotropy
What adjusts the control of contractions?
Hormonal, neuronal and local factors ≈ ∆ SAN ≈ ∆ adjacent cell depolarisation + contraction ≈ depolarisation propagation wave ≈ ∆ contractility ≈ ∆ chronotropy + inotropy + lusitropy
What are the three types of cardiac action potentials and what are the distinguished by?
Distinguished by spontaneous pacemaker activity + speed of depolarisation
1) Pacemaker potentials
- Spontaneous depolarisation
- Slow depolarisation
- Driven by calcium slowly
2) Non-pacemaker potentials
- Rapid depolarisation
- Driven by sodium rapidly and prolonged by calcium
3) His-Purkinje potentials
- Rapid depolarisation
- Spontaneous depolarisation
- Driven by sodium rapidly and prolonged by calcium
What is the membrane potential changes in nodal tissue?
Sinoatrial node depolarisation occurs through 3 phases with a unique waveform
- No true resting potential
- Regular, spontaneous APs
- Depolarising currents carried by L-type CaVG
- Slower AP ≈ ’slow response AP’
Phase 1: If ≈ Na+ open at -60mV ≈ Na+ in;
-50mv ≈ T-type CaVg open ≈ Ca++ in;
Phase 2
-40mV ≈ L-type CaVf open ≈ Ca++ in
Phase 3
+ 20mV ≈KVg open ≈ K+ efflux ≈ repolarisation
What is the membrane potential changes in atrial and ventricular cardiac tissue?
Phase 0: - Rapid depolarisation due to NaVg opening at -75mV ≈ gNa+ ≈ Na+ in
Phase 1: - NaVg close ≈ reduced gNa+
Phase 2: - L-type CaVg open @ 10mV ≈ gCa++ ≈ Ca++ in ≈ plateau
Phase 3: - Rapid repolarisation: gCa++ ≈ increased IC Ca++ ≈ K+ channels open ≈ gK+ efflux - L-type CaVg close ≈ reduced gCa++
Phase 4: - Stable resting membrane potential where gK+ > gNa+ (50:1)
What is the effect of hypoxia on heart rate and why?
Cellular hypoxia ≈ depolarises the cell ≈ ∆ phase 3 hyper-polarisation ≈ reduced pacemaker rate ≈ bradycardia
What effects do the respective functional divisions of the ANS have on pacemaker activity?
1) PSNS: Vagus nerve (CN X) —> SAN + AVN
- ACh @ M2R ≈ Gai ≈ reduce cAMP ≈ reduce rate of phase 0 depolarisation + hyperpolarise membrane potential (= increase extent + duration of opening of K+ channels ≈ increase gK+)
2) SNS: Sympathetic chain ≈ sympathetic nerves —> atria + ventricles
- NA @ ß1R ≈ Gas ≈ increase cAMP ≈ increase rate of phase 0 depolarisation ≈ increase gCa++ + increase gNa+ via funny channels
What is the electrical conduction pathway in the heart?
Coordinated electrical activity: pacemaker activity of SAN (RA) ≈ initiate process ≈ depolarisation spreads due to functional syncytium (electrically connected via GAP junctions) ≈ SAN in RA —> internodal pathway + interatrial pathway —> AVN (critical delay ≈atrioventricular flow) —> L + R Bundle of His (interatrial septa) —> Purkinje fibres
What is a dysrhythmia (arrhythmia)?
Conditions where co-ordinated sequence of electrical activity in the heart is disrupted ≈
- ∆ in heart cells
- ∆ in conduction of impulse through heart
- ∆ in heart cells + ∆ impulse conduction through heart
What are the classifications of dysrhythmias (arrhythmias)?
Dysrhythmias (arrhythmia) classified by origin site of abnormality + speed (tachycardia or bradycardia)
- Atrial (supra-ventricular)
- Junctional (associated with the AV node)
- Ventricular - Tachycardia or bradycardia
What are the four broad categories of event which can be used to physiologically classify a dysrhythmia (arrhythmia)?
- Ectopic pacemaker activity (Intrinsic ability to set AP)
- Delayed after-depolarisations (pumping out Ca++ and Na++ in via NCX and Na+, K+-ATPase where Na+ out and K+ in ≈ cell trying to pump calcium out and sodium in h/e ∆ pumps ≈ increased Na+ ≈ increased depolarisation AP during plateau period)
- Circus re-entry (impulses pass down conduction pathway h/e block in impulse circulating tissue)
- Heart block (Nodal tissue block ≈ atria and ventricles beat at different rhythms)
How are antidysrhythmic drugs classified?
Vaughan Williams system
How can the Vaughan Williams System for Antidysrhythmic drugs be transposed onto the action potential of a cardiomyocyte?
Vaughan Williams system can go on anti-clockwise to the cardiomyocyte action potential
Class 1 @ Na+ (stage 0)
- Lidocaine
- Procainamide
- Flecainide
Class 2 @ K+ rectifier (stage 4)
- Bisoprolol
- Atenolol
- Propanolol
Class 3 @ K+ out (Stage 3)
- Amiodarone
- Sotalol
Class 4 @ Ca2+ in (Stage 2)
- Diltiazem
- Verapamil
When do sodium channel blockers work?
Binds domains of voltage-gated sodium channels ≈ block if ion channels in open state (use-dependent sodium channel blockers), refractory or resting
What are the clinical uses of class 1 antidysrhythmics?
Sodium channel blockers
