Action potential in myocardial cell and pacemaker cell
Reading File
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Finding Sources
Searching the Web
cardiac action potential myocardial cell vs pacemaker cell phases ions
Reading Web Page
https://cvphysiology.com/arrhythmias/a010
I now have comprehensive information. Here is the detailed explanation:
Action Potentials: Myocardial Cell vs. Pacemaker Cell
The heart has two fundamentally different types of action potentials. Understanding both is essential for cardiac physiology and pharmacology.
1. Non-Pacemaker (Myocardial / Ventricular) Action Potential - "Fast Response"
These are found in atrial myocytes, ventricular myocytes, and His-Purkinje fibers. They are called "fast response" because of their rapid phase 0 upstroke.
Resting membrane potential: -85 to -90 mV (stable - no spontaneous depolarization)
Phases
| Phase | Name | Mechanism | Ions |
|---|---|---|---|
| Phase 4 | Resting potential | Stable. Inward rectifier K+ channels (IK1) keep the cell polarized | K+ leaks out, maintaining ~-90 mV |
| Phase 0 | Rapid depolarization | Fast voltage-gated Na+ channels (INa) open rapidly | Na+ rushes IN; membrane potential rises to ~+20 to +30 mV |
| Phase 1 | Early repolarization | Fast Na+ channels inactivate; transient outward K+ channels (Ito) open | K+ flows OUT briefly; slight dip in potential |
| Phase 2 | Plateau | L-type (slow) Ca2+ channels open (ICa-L), balancing K+ efflux | Ca2+ flows IN; sustains ~0 mV plateau for ~200 ms |
| Phase 3 | Final repolarization | Delayed rectifier K+ channels (IKr, IKs) open; Ca2+ channels close | K+ flows OUT, repolarizes cell back to -90 mV |
Key features:
- Duration: 200-400 ms (much longer than nerve/skeletal muscle)
- The plateau (Phase 2) is unique to cardiac cells - it prevents tetanic contraction by enforcing a long refractory period
- Ca2+ entry during Phase 2 triggers calcium-induced calcium release (CICR) from the sarcoplasmic reticulum, coupling excitation to contraction
- No automaticity - requires an external trigger to fire
2. Pacemaker Cell Action Potential - "Slow Response"
Found in the SA node and AV node. Called "slow response" because phase 0 rises slowly.
Resting membrane potential: -50 to -65 mV (unstable - undergoes spontaneous depolarization)
Phases
| Phase | Name | Mechanism | Ions |
|---|---|---|---|
| Phase 4 | Pacemaker potential ("funny current") | HCN channels (If - hyperpolarization-activated, cyclic nucleotide-gated) open spontaneously; gradual depolarization toward threshold (~-40 mV) | Na+ flows IN slowly; late contribution from T-type Ca2+ channels (ICa-T) |
| Phase 0 | Slow depolarization / upstroke | L-type Ca2+ channels (ICa-L) open at threshold | Ca2+ flows IN; slow rise (no fast Na+ channels active here) |
| Phase 3 | Repolarization | Voltage-gated K+ channels open; Ca2+ channels inactivate | K+ flows OUT, restoring negative membrane potential |
Key features:
- Only 3 recognizable phases (0, 3, 4) - phases 1 and 2 are absent
- No fast Na+ channels (or they are inactivated at the less negative resting potential)
- Upstroke velocity (dV/dt) is ~1-10 V/s vs. ~200-1000 V/s in myocardial cells
- Conduction velocity is slow (0.05-0.1 m/s in SA node) - allows rate regulation without rapid propagation
- Automaticity is the defining property - they fire spontaneously
Side-by-Side Comparison
| Feature | Myocardial Cell (Fast) | Pacemaker Cell (Slow) |
|---|---|---|
| Location | Atria, ventricles, Purkinje | SA node, AV node |
| Resting potential | -85 to -90 mV (stable) | -50 to -65 mV (unstable) |
| Phase 0 carrier | Fast Na+ (INa) | L-type Ca2+ (ICa-L) |
| Phase 0 velocity | Very fast (200-1000 V/s) | Slow (1-10 V/s) |
| Plateau (Phase 2) | Present | Absent |
| Phase 4 | Flat (no spontaneous depolarization) | Slow, spontaneous depolarization (If) |
| Automaticity | No | Yes |
| Conduction velocity | Fast (0.5-2 m/s) | Very slow (0.05-0.2 m/s) |
| Action potential duration | 200-400 ms | Shorter, no distinct plateau |
The "Funny" Current (If) - The Engine of Automaticity
The funny current (If) is the cornerstone of pacemaker automaticity:
- Carried through HCN channels (HCN1, HCN2, HCN4 isoforms predominate in SA node)
- Activated by hyperpolarization (hence "hyperpolarization-activated") - paradoxically, the current switches on when the cell is most negative after Phase 3
- Carries mixed Na+/K+ inward current (net inward, so it depolarizes the cell)
- cAMP binding to HCN channels increases channel opening speed - this is how sympathetic stimulation (adrenaline) increases heart rate: cAMP shifts the If activation curve, speeds up Phase 4, fires faster
- Parasympathetic stimulation (ACh) does the opposite - reduces cAMP, slows If, slows heart rate
Drug Targets - Practical Relevance
- Beta-blockers (propranolol, metoprolol): Block beta-1 receptors on SA node - reduce cAMP, slow If, decrease heart rate
- Ivabradine: Directly blocks HCN channels (If), selectively slows heart rate without affecting contractility - used in heart failure and stable angina
- Calcium channel blockers (verapamil, diltiazem): Block L-type Ca2+ channels - suppress pacemaker Phase 0 and slow AV conduction; effective for SVT and rate control in AF
- Sodium channel blockers (lidocaine, flecainide): Target Phase 0 fast Na+ channels in working myocardium and Purkinje fibers - have minimal effect on SA/AV nodes (which don't rely on INa)
- Digoxin: Slows AV node conduction mainly via vagal (parasympathetic) enhancement
Why This Matters Clinically
The long refractory period imposed by the Phase 2 plateau is why the heart cannot be tetanized - this is a life-saving feature. The slow conduction at the AV node (pacemaker-type action potential) provides the PR interval delay, giving the atria time to fill the ventricles before they contract.
This is a shared conversation. Sign in to Orris to start your own chat.