Cardiac Cell Action Potentials

• Action potentials in cardiac cells result from ion movement across the cell membrane through voltage-gated ion channels.

Action Potential Phases in Contractile Cells (Myocytes)

• Phase 0 (Depolarization): Rapid Na⁺ influx due to open Na⁺ channels causes depolarization.
• Phase 1 (Initial Repolarization): Na⁺ channels close; brief repolarization occurs as transient outward K⁺ channels open.
• Phase 2 (Plateau): Ca²⁺ influx through open Ca²⁺ channels balances K⁺ efflux, sustaining the plateau phase.
• Phase 3 (Repolarization): Ca²⁺ channels close; K⁺ efflux through open potassium channels causes repolarization.
• Phase 4 (Resting Potential): Achieved and maintained by the Na⁺/K⁺ pump.

Action Potential in Autorhythmic Cells

• Autorhythmic cells spontaneously generate action potentials due to gradual depolarization (pacemaker potential) during Phase 4.
• Pacemaker potential results from Na⁺ and Ca²⁺ influx and reduced K⁺ efflux.

Refractory Periods

• The refractory period is when cardiac cells cannot be re-excited during and after an action potential.
• Absolute refractory period: No stimulation can trigger a new action potential, preventing tetany (sustained contraction).
• Relative refractory period: Only a stronger-than-normal stimulus can induce an action potential.

Absence of Summation

• Cardiac muscle contraction lacks summation due to the long refractory period.
• The heart contracts fully then relaxes before it can be stimulated again, ensuring proper rhythm.

Heart Sounds

• Heart sounds originate from the closing of heart valves.
• "Lub" (S1): Closure of atrioventricular (AV) valves (tricuspid and mitral) at the start of ventricular contraction (systole).
• "Dup" (S2): Closure of semilunar valves (aortic and pulmonary) at the end of ventricular systole, marking the start of diastole.

Cardiac Cycle - Electrical Events (ECG)

• P wave: Atrial depolarization.
• QRS complex: Ventricular depolarization.
• T wave: Ventricular repolarization.

Cardiac Cycle - Mechanical Events

• Atrial contraction follows the P wave.
• Ventricular contraction (systole) follows the QRS complex.
• Ventricular relaxation (diastole) follows the T wave.

Heart Rhythms

• Normal Sinus Rhythm (NSR): Regular rhythm originating from the sinoatrial (SA) node, with a heart rate of 60-100 bpm.
• Bradycardia: Slow heart rate (
• Arrhythmias: Abnormal rhythms like atrial fibrillation, ventricular tachycardia, or heart block.

Graphs During Cardiac Cycle

• Ventricular Volume graph: Shows changes in end-diastolic volume (EDV) and end-systolic volume (ESV).
  • EDV is highest at the end of diastole.
  • ESV is lowest at the end of systole.
• Heart Sounds graph:
  • The S1 sound occurs with AV valve closure (start of systole).
  • The S2 sound occurs with semilunar valve closure (end of systole).
• ECG graph: Depicts electrical activity.
  • P wave, QRS complex, and T wave correlate with atrial depolarization, ventricular depolarization, and ventricular repolarization.

EDV and ESV During Exercise

• End-Diastolic Volume (EDV): Increases during exercise due to enhanced venous return and increased ventricular filling.
• End-Systolic Volume (ESV): Decreases during exercise as stronger contractions (due to sympathetic stimulation) eject more blood, increasing stroke volume.

Cardiac Output

• Cardiac Output (CO): The amount of blood the heart pumps per minute.
  • Formula: CO = Heart Rate (HR) × Stroke Volume (SV)
• Heart rate (HR) increases during exercise to pump more blood per minute.
• Stroke volume (SV) increases with exercise due to enhanced contractility and increased venous return.

Autonomic Nervous System

• Sympathetic Nervous System: Increases heart rate (positive chronotropic effect) and contractility (positive inotropic effect) via norepinephrine release.
• Parasympathetic Nervous System: Decreases heart rate (negative chronotropic effect) via acetylcholine release, acting primarily on the SA node.

Cardiac Output Equation

• Cardiac Output (CO) = HR × SV

Stroke Volume

• Preload: Stretch of heart muscle fibers before contraction (related to venous return). Increased preload increases stroke volume (Frank-Starling mechanism).
• Contractility: Intrinsic ability of heart muscle to contract, enhanced by sympathetic stimulation.
• Afterload: Resistance ventricles overcome to eject blood. Increased afterload decreases stroke volume.

Venous Return

• Venous pressure: Higher pressure facilitates blood flow back to the heart.
• Muscle pump: Skeletal muscle contractions aid blood return.
• Respiratory pump: Negative thoracic pressure during inspiration aids venous return.
• Blood volume: Increased blood volume increases venous return.