Cardiovascular Physiology - Cardiac Action Potential Flashcards
Divide answer into phases, this is not the pacemaker action potential
Draw and explain the cardiac action potential
IMAGE
The graph has Time (ms) on the X axis (0-500), and Membrane Potential (mV) on the Y axis (-90 - +30).
Five phases, numbered 0-4.
Phase 0
Rapid depolarisation, fast sodium channels open
(A vertical upstroke on the graph)
Phase 1
Repolarisation (short), Na channels close, K channels open to allow K out.
Does not repolarise beyond zero mV
(Exponential decay towards 0)
Phase 2
Plateau phase, L type Ca channels allow Ca in to slow repolarisation
(Sigmoid decay to 0)
Phase 1 and 2 are part of the absolute refractory period, precluding cardiac tetany
Phase 3
Repolarisation, L type Ca channels close, K channels remain open
(Steep downslope to near the resting membrane potential)
Phase 4
Na/K/ATPase restores balance
(Exponential decay to the resting membrane potential)
Phase 3 and 4 are part of the relative refractory period
Divide answer into phases, this is not the cardiac action potential
Draw and explain the cardiac pacemaker action potential
IMAGE - Pacemaker potential
The graph has Time (ms) on the X axis (0-500), and Membrane Potential (mV) on the Y axis (-90 - +30).
Of the 5 phases of the cardiac action potential, the pacemaker only has phases 0, 3 and 4
Phase 0
Depolarisation is triggered at -40,V
Slow L type Ca channels allow Ca ingress into the cell
Phase 3
Repolarisation, Ca channels close and K channels open
Phase 4
Transient ‘overshoot’ hyperpolarisation (maximum diastolic potential of -65mV)
K channels close
Gradual depolarisation until threshold potential is met, due to:
Sodium ion leak
T type Ca channels allowing Ca in
Sodium-Calcium pump
The speed of depolarisation in phase 4 is affected by (para)sympathetic stimulation.
Explain the Vaughan-Williams classification of antiarrhythmic agents
Based on their target ion channel
Class 1 - Sodium Channel Blockers
1A) Intermediate onset, prolong refractory period (Quinidine/Procainamide)
1B) Fast onset, shorten refractory period (Lidocaine/Phenytoin)
1C) Slow onset, no effect on refractory period (Flecainide/Propafenone)
Class 2 - Beta Blockers (Propranolol/Metoprolol) (Indirect Ca channel blockade)
Class 3 - Potassium Channel Blockers (Amiodarone/Sotalol) (Delay repolarisation)
Class 4 - Calcium Channel Blockers
(Verapamil/Diltiazem) (Directly block Ca)
Sotalol fits into group 2 and 3, and Amiodarone into all groups)
Class 5 - Direct Nodal Inhibition (Digoxin/Adenosine)
https://www.youtube.com/shorts/AgHRzs8WDwE
Classify anti-arrhythmic agents by their clinical indication
SVT Adenosine, Beta blockers, Verapamil, Digoxin
VT Lidocaine
SVT & VT Amiodarone, Procainamide, Flecainide
Phenytoin is used for digoxin toxicity
Explain where each class of antiarrhythmic drug acts throughout the cardiac action potential
IMAGE
Class 1 Membrane stabilisers, inhibiting the rapid influx of sodium ions responsible for phase 0.
They also slow phase 4 depolarisation in pacemaker cells
1A prolong the refractory period, acting in the atria, ventricles, and accessory pathways
1B shorten the refractory period, but only in the ventricles
1C have no effect on the refractory period, acting in the atria, ventricles and accessory pathways
Class 2 inhibit sympathetic tone.
They reduce the slope of phase 4 deoplarisation in pacemaker cells
Reduce the maximum rate of depolarisation (phase 0)
Prolong the duration of the action potential
Class 3 prolong the duration of the AP and refractory period by inhibiting K channels
Class 4 modify the plateau phase in non-pacemaker cells.
In pacemaker cells, inhibit depolarisation in phase 0 by inhibiting Ca channels.
Where does the autonomic system innervate the heart
IMAGE
Parasympathetic:
Right Vagus: ACh lowers SA node rate to 60-100bpm (flattens phase 4 gradient)
Left Vagus: ACh increases AV node conduction delay (increased K+ permeability)
Sympathetic
NA increases SA node rate
NA decreases AV node conduction delay (via Ca)
Why do children frequently develop bradycardia in response to an insult?
Their parasympathetic system is more developed than their sympathetic system, so any significant autonomic stimulation will produce dominant parasympathetic responses, such as bradycardia
What considerations regarding heart rate are necessary after heart transpant?
Loss of innervation to the heart - any drug that alters HR via (para)sympathetic stimulation will be ineffective.
Atropine/Glycopyrrolate will not increase HR
Ephedrine will only work via its direct action (indirect agents have no effecT)
Adrenaline and isoprenaline will continue to work and increase HR
Why do tachyarrhythmias occur?
Increased automaticity of atrial or ventricular myocytres resulting in premature depolarisation before the SA node.
Can be triggered by anything that enables the membrane potential to reach the depolarisation threshold more quickly - for instance ionic imbalance (HypoK) and ischaemia
Re-entry tachyarrhythmias can occur if there is an ectopic focus and a conducting pathway that allows a circuit of repolarisation and depolarisation to occur.
Why might a patient become bradycardic?
Physiological responses
Vagal stimulation
1. Surgical (Pneumoperitoneum, cervical dilatation, pressure on the eye)
2. Anaesthetic (Laryngoscopy, particularly miller blade in children)
3. Medication (Opioids, neostigmine)
Conduction pathology
Failure of AV node to conduct atrial impulses
Type II or complete HB (MI/ischaemia)
Explain an atrioventricular nodal re-entrant tachycardia
NEEDS MORE INFORMATION IN ANSWER
There are two distinct conduction pathways in the AV node.
A fast pathway with a long refractory period
A slow pathway with a short refractory period
The AP travels down both pathways, but reaching the conducting system through the fast pathway first. When the AP reaches the end of the slow pathway, it cannot propagate, as the conducting system is during its refractory period.
If at the time of the next impulse, the fast pathway has not reset, the slow pathway takes up the impulse, which can then travel back up the node via the fast pathway in a retrograde fashion.
This generates a circular route, forming the basis of the re-entry nodal tachycardia.
An example is Wolf-Parkinson-White syndrome, but via the bundle of Kent
