Electrical Activity of the Heart

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Cardiac Conduction Channels:

• Ungated-K: always open, unless membrane reaches -94mV.

• Voltage-gated Na: fast; depolarization opens them; won't respond to second stimulus until cell repolarizes.

• Voltage-gated Ca: slow; depolarization opens them.

• Voltage-gated K: open under resting conditions; close at depolarization.

Ventricular Muscle Action Potential:

Ventricular Muscle Action Potential

Cardiac Conduction Ion Flow:

Sodium Potassium Chloride Calcium
Phase 0 inflow
Phase 1 inactive outflow inflow
Phase 2 inactive closed/outflow inflow inflow
Phase 3 inactive reopening/outflow closed closed
Phase 4 Na/K active open/outflow

Cardiac muscle:

• Length of refactory period = length of mechanical event; no tetany. The specialized cells of the heart possess an unstable phase 4.

Sinoatrial Nodal (Pacemaker) Action Potential:

Sinoatrial Nodal Action Potential

Sinoatrial Nodal Cells:

• Pacemaker potential or prepotential.

• Unstable phase 4; Na influx.

• Phase 0: Ca spike.

• Phase 3: rapid K efflux.

• Sympathetics: intrinsic firing rate increases.

• Parasympathetics: intrinsic firing rate decreases.

Sinoatrial: pacemaker greater than atrial muscle greater than AV (slow) greater than Purkinje (fast) greater than ventricles.

Automaticity:

• Sinoatrial: 100-120/min.

• AV: 40-60/min.

• Purkinje: 30-40/min.

ECG Waves:

• P: atrial depolarization.

• QRS: ventricular depolarization and atrial repolariztion.

• T: ventricular repolarization.

• PR: AV conduction delay.

Random Notes on Cardiac Conduction:

• Conduction velocity in atrial/ventricular fibers is 0.3-0.5 m/sec.

• Velocity in purkinje fibers is 4 m/sec.

• Absolute refractory: heart cannot conduct even if stimulus is very strong.

• Relative refractory period: heart can conduct if stimulus is strong; this results in premature contractions.

• Cardiac muscle has larger T-tubules; only in cardiac muscle are T-tubules coupled with sarcoplasmic reticulum through sarcoplasmic tubules; and this causes extra Ca to be released into the cardiac muscle sarcoplasm producing prolonged depolarization.

• Ruptured chordae tendineae cause weak connection between cardiac valves and papillary muscles, producing mitral regurgitation.

• Note that chordae tendineae are not present with aortic and pulmonary valves.

• Excess K ions lead to slowed heart rate, or even CHF.

• Excess Ca ions lead to a faster heart rate, or spastic contractions.

Additional Reading:

Basic Cardiology

1. Electrical Activity of the Heart
2. Heart Muscle Mechanics
3. Heart Sounds and Murmurs
4. Additional FAQ on Heart Sounds and Murmurs
5. Cardiac Conduction Diagram
6. Blood Pressures in Cardiac Chambers
7. What is Pulsus Paradoxus?
8. FAQ on Heart Murmurs and Mechanisms of Turbulent Flow
9. Notes on Fetal Circulation
10. FAQ on Ischemic Myocardial Infarction
11. FAQ on Electrocardiograms / ECG / EKG
12. FAQ on Cardiac Conduction
13. The Heart as a Pump, the Cardiac cycle and Cardiac Output
14. What are the most common causes of aortic stenosis?
15. What is Pulseless Electrical Activity?
16. Causes and Complications of Arteriovenous Fistulas
17. CHADS2 Score for Atrial Fibrillation Stroke Risk
18. How to Reduce Blood Pressure without Medications?
19. Types of Shock
20. Locations of Heart Murmurs on Chest Wall
21. Types of Heart Blocks

Electrocardiogram (EKG/ECG) Topics

1. EKG Chest Leads
2. EKG Limb Leads
3. Quick 12-Lead ECG/EKG Format

Cardiology Videos

1. Video of Cardiology Examination in a Clinical Setting

Medical Images

Useful Medical Images & Diagrams (link opens in a new window)

Related Topics

1. Thorax Anatomy
2. Vascular Disorders
3. Heart Disorders
4. Histology of the Cardiovascular System
5. Jugular Venous Distention Workup
6. ER Chest Pain Workup
7. Cardiac Examination for Internal Medicine
8. FAQ on Blood Pressure
9. FAQ on principles of fluid and flow dynamics of Blood

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