Heart physiology Flashcards
What ions determine the SAN pacemaker potential?
Na+ in via voltage gated channels (NOT fast ones), Ca2+ (different ones to SAN action potential ones) in and decrease in K+ conductance
What ions determine the SAN action potential?
Ca2+ moves in (different channels to SAN pacemaker potential ones) and further decrease in K+ conductance during the depolarisation phase, and outward movement of K+ later on in repolarisation phase.
How long does the SAN action potential last in ms?
200ms
How does autonomic control of heart rate occur?
By altering pacemaker potential
How is heart rate decreased by the autonomic nervous system?
Heart has M2 parasympathetic system receptors and Ach –> decrease in HR via vagal. Reduces slope of pacemaker potential (becomes less vertical) + hyperpolarises. So action potentials space out in the graph.
How is heart rate increased by the autonomic nervous system?
β1 receptors in the heart and NA via nerves lead to a steeper slope and more frequent action potentials so faster heart rate.
What is the conduction rate through the atria?
0.5m/s, complete within 0.09s of the SAN firing
Does atrial muscle electrical signals have resting or pacemaker potentials?
Resting membrane potential
What is the conduction rate in AVN?
Falls to 0.05m/s (can be increased by SA)
What potential does the AVN have; resting or pacemaker?
Pacemaker BUT less steep than SAN pacemaker potential
Why is there an AV delay?
Ensures atrial depolarisation, contraction and ejection before ventricles depolarise
How fast is conduction through Bundle of His?
2m/s
How fast is conduction through Left and Right branches
2m/s
How fast is conduction through Purkinje fibres and ventricular muscle?
4m/s, depolarisation takes place endocardium moving outwards to epicardium
What does the ventricular myocyte action potential look like and what are the phases?
(Stable) resting potential (phase 4), straight line up (phase 0), small fall (phase 1), plateau a bit (phase 2), then falls not 100% vertically down but nearly to stable resting potential again (phase 4)
How fast is the ventricular myocyte depolarisation?
250-300ms
What ion movements are there in ventricular action potential?
Phase 0 - depolarisation - Na+ goes in via fast voltage gated channels, phase 1 Na+ fast voltage gated channels inactivate, there is partial repolarisation, phase 2 - plateau - inward movement of Ca2+ and outward of K+, phase 3 - repolarisation - outward movement of K+
What are the classes of anti-dysrhythmic drugs?
Class I - Na+ channel blockers
Class II - β blockers
Class III - drugs that prolong cardiac action potential
Class IV - calcium antagonists
How long is the absolute refractory period in ventricular myocytes?
200ms - Na+ channels are inactivated and unresponsive
How long is the relative refractory period in ventricular myocytes?
50ms - Na+ channels are inactivated and recovering but cant’t yet really support an action potential
What Class of anti-dysrhythmics can affect the ventricular action potential?
Class I can inhibit fast Na+ voltage gated channels only found in ventricular myocyte action potential to depolarise. In SAN depolarisation its Ca2+ that leads to depolarisation so don’t have an effect on those channels.
What can Class IV anti-dysrhythmics block and in what action potential (s) of the heart?
Can affect SAN and ventricular action potentials; they are Ca2+ channel blockers.
What are the 3 subdivisions of Class I antidysrhythmics?
Ia - disopyramide
Ib - lidocaine
Ic - flecainide
Give an example of a Class III antidysrhythmic
Amiodarone
Effect: suppresses dysrhythmias
Mechanism of action: affects repolarisation prolonging cardiac action potential (more than one mechanism but) thought to be via blocking K+ channels involved in cardiac repolarisation (including outward delayed rectifier). Action potential prolongation increases the refractory period–>e.g. interrupts re-entrant tachycardias and suppressing ectopic activities.
Site of action: ventricular a.p.
Side effects: pro-arrhythmic; the increase in action potential duration can produce torsades de pointes (a type of ventricular tachycardia), especially in patients with long-QT syndrome. pulmonary fibrosis (late onset)
Need to monitor K+ levels
This drug increase the QT interval in an ECG
Contraindications: Amiodarone, because of its Class IV effects, can cause bradycardia and atrioventricular block, and therefore is contraindicated in patients with heart block, or sinoatrial node dysfunction
