CARDIAC MUSCLE CELLS
Contractile (99%) cells contract and relax.
Autorhythmic (1%) initiate and transmit action potential.

CONDUCTION PATHWAY OF A SINGLE CARDIAC CONTRACTION

1. SINOATRIAL NODE

• The sinoatrial (SA) node is located in the upper wall of the right atrium, near the opening of the superior vena cava.
• Pacemaker: fastest rate of autorhythmicity, therefore, sets heart rate.
  — Action potential originates here.

2. ATRIOVENTRICULAR NODE

• The AV node is located at the base of right atrium, adjacent to septum.
• It is the only electrical communication between the atria and the ventricles, and that it delays impulses to facilitate peak cardiac output.
  — AV nodal delay: delays impulses, maximizes stroke volume, increases cardiac output.

3. BUNDLE OF HIS

• Originates at AV node, splits at interventricular septum into left and right bundle branches.

4. PURKINJE FIBERS

• Spread upward through ventricular walls.
  — Ventricles contract.

CARDIAC MUSCLE CELL ACTION POTENTIAL

PHASE 0: DEPOLARIZATION

The initial rise of the curve.

Sodium moves rapidly into cell; calcium moves slowly into the cell.

PHASE 1

Peak of curve.

Voltage-gated sodium channels close.

PHASE 2: PLATEAU PHASE

Curve plateaus.

Potassium moves rapidly out of cell, while calcium moves slowly into the cell.
— Calcium enters from both the extracellular space and sarcoplasmic reticulum, and is the cause of the plateau.

PHASE 3: RAPID REPOLARIZATION

Curve declines.

Calcium channels close and potassium moves rapidly out of cell.
Potassium and sodium ion positions in regards to the sarcolemma are reversed.

PHASE 4: RESTING POTENTIAL

Low curve.

The resting potential is maintained by leaky potassium channels.
The sarcolemma is impermeable to sodium during this period.

• Long absolute refractory period in cardiac muscle cells: phase 0 to phase 3
  Second action potential cannot be initiated; thus, it is a protective mechanism against tetanus (state of maximal contraction).