Basic Physiology + Anatomy Flashcards
What is the resting membrane potential of the pacemaker cell?
-40-65mV
What is responsible for phase 0 of the cardiac myocyte action potential?
Activation of voltage gated Na+ channels resulting in fast sodium influx into the cell
What is responsible for phase 1 of the cardiac myocyte action potential and what does it resemble on the diagram?
Decay of the sodium current following closure of the fast Na gated channels and activation of outward K+
Resembles a small notch directly after the rapid upstroke of depolarisation
What is responsible for phase 2 of the cardiac myocyte action potential? What does it resemble on the AP diagram?
Slow calcium entry + calcium mediated calcium release
Ongoing outward K+ movement
Represents the plateau in the diagram
What makes phase 3 of the cardiac myocyte action potential and what does it resemble on the AP diagram?
Decay in calcium influx and increase in outward movement of K+
Represents repolarisation on the AP diagram, sharp downslope after the plateau, cell back to resting membrane potential at end of phase 3
What channels present in a normal cardiac myocyte AP but not a pacemaker cell AP?
Voltage gated fast Na channels
What is the resting membrane potential of a ventricular cardiac myocyte? What electrolyte is this due to?
-80-90mV
Due to the equilibrium potential of K+
What is meant by the diastolic depolarisation phase (or phase 4) of the pacemaker cell action potential?
The gradual process of the cell reaching the threshold for depolarisation (ie the resting membrane potential is not static, it is gradually moving towards the threshold potential)
This occurs by the slow inward movement of Na (funny current), decrease in outward K+ and slow inward movement of calcium
What causes depolarisation of the pacemaker cell?
Rapid inward calcium movement through L-type calcium channels (these have a slower velocity then the fast gated sodium channels that are responsible for the depolarisation of the normal cardiac myocyte)
What is automaticity in relation to the cardiac pacemaker cells?
What cells exhibit automaticity?
The ability of cells to self-depolarise
It resembles the progressive slow depolarisation of the membrane potential until threshold potential is reached
Cells the exhibit this normally are SA node, AV junction
Under pathological circumstances (ie ischaemia, drugs, stretch) purkinje, atrial and ventricular cells can develop automaticity
What are the four classes of antiarrythmics? (Vaughan-Williams)
Class 1= blockage of sodium channels Split into 3 subgroups below based on the rate of drug binding and dissociation 1a - intermediate 1b - fast 1c - slow Class II = inhibit sympathetic activity Class III = inhibit K+ channels Class IV = inhibit Ca channels
Give examples of antiarrythmics in each drug class?
Ia - Quinidine, Procainamide Ib - Lignocaine, Mexiltine Ic - Flecainide, Propafenone II - B-blockers III - Amiodarone, Sotalol, Dronedarone IV - Verapamil, Diltiazem
- remember a lot of antiarrythmics have actions across a lot of classes - ie. amiodarone has I,II,III + IV actions! Sotalol has some class II effects as it is a beta-blocker
What does use dependance mean in relation to anti-arrhythmic drugs?
If a drug has use dependance it means that it works more effectively at fast heart rates
If a drug has reverse use dependance it means it works more effectively at slower heart rates
A good example is Sotalol (reverse use dependence) works better at slow rates therefore maintaining sinus rhythm but is a poor rate control agent because it sucks at fast heart rates
On the other hand flecainide (use dependence) works well at fast heart rates therefore is used to cardiovert
What are the normal durations for the PR, QRS and QTc?
PR - 120-200ms (3-5 small squares)
QRS-
What is a formula used to calculate the QTc?
Bazetts
QTc = QT divided by the square root of the RR interval
Only reliable in HR less then 100
Remember QT should be calculated from a sinus beat that follows a sinus beat
