Cardiac Physiology Part I

The video starts by introducing the two types of cardiac cells: contractile and autorhythmic. Both types generate action potentials but differ in their initiation and function. Autorhythmic cells, making up 1% of cardiac cells, are unique for not having a resting membrane potential and for their 'pacemaker potential,' a slow drift to threshold. The action potential here peaks around 0mV, unlike neuronal action potentials.

The pacemaker potential in autorhythmic cells involves three types of ion channels: voltage-gated potassium channels (closing around -60mV), funny channels (opening around -60mV, allowing sodium influx), and T-type calcium channels (opening around -50mV, leading to depolarization to threshold). The depolarization phase is dominated by L-type calcium channels, which open at threshold and close around the peak, followed by repolarization due to voltage-gated potassium efflux.

Autorhythmic cells form the cardiac conduction system. The SA node, the heart's pacemaker, fires at 70-80 action potentials/minute, driving other cells. The AV node, bundle of His, and Purkinje fibers have slower intrinsic rates (40-60 and 20-40 APs/min, respectively) but follow the SA node's pace. Damage to the SA node leads to the AV node taking over, resulting in a slower heart rate (e.g., 50 bpm). Blockage of the AV node causes 'heart block,' where atria and ventricles beat at different rates (e.g., atria at 70 bpm, ventricles at 30 bpm), requiring immediate medical intervention.

Depolarization begins in the SA node and spreads across the atria, reaching the AV node. An AV nodal delay allows complete atrial depolarization and contraction. The signal then moves down the AV bundle, bundle branches, and Purkinje fibers to the ventricular contractile cells, propagating from the apex upwards to efficiently eject blood into the major arteries.

Three criteria are vital for normal cardiac function: atrial contraction must complete before ventricular contraction to maximize ventricular filling; ventricular fibers must contract simultaneously to generate sufficient pressure for blood ejection (asynchronous contraction leads to 'fibrillation,' notably dangerous in ventricles); and paired atria and ventricles (right and left) must coordinate their contractions to prevent blood damming.

Contractile cells have a resting membrane potential of -90mV and a threshold of -70mV. Depolarization to threshold, triggered by autorhythmic cells, opens voltage-gated sodium channels, causing rapid sodium influx. After an initial slight repolarization due to transient potassium efflux, the unique 'plateau phase' occurs because of long-lasting (L-type) calcium channel opening. Repolarization follows as L-type calcium channels close and regular voltage-gated potassium channels open, leading to potassium efflux.

Excitation-contraction coupling in cardiac contractile cells involves the action potential traveling down T-tubules, opening L-type calcium channels. The small influx of extracellular calcium triggers a larger release of calcium from the sarcoplasmic reticulum (calcium-induced calcium release), creating a 'calcium spark.' This calcium binds to troponin, initiating the sliding filament mechanism and muscle contraction. Relaxation requires reducing sarcoplasmic calcium levels, achieved by active transport pumps returning calcium to the sarcoplasmic reticulum and a sodium-calcium exchanger (secondary active transport) pumping calcium out of the cell, utilizing the sodium gradient established by the Na/K pump.

The long duration (250ms) of the contractile cell action potential, including its plateau phase, results in an extended absolute refractory period. This prevents summation of contractions and tetanus in the heart, ensuring that the heart can relax and refill with blood between beats, which is crucial for its pumping function. Unlike skeletal muscle, cardiac muscle's electrical activity and mechanical contraction have similar durations.

Electrocardiography (ECG/EKG) non-invasively records the heart's collective electrical activity via electrodes on the skin. It visualizes the sum of all electrical events over time, not individual action potentials. An ECG shows voltage comparisons between different body points. The normal trace includes the P wave (atrial depolarization), QRS complex (ventricular depolarization), and T wave (ventricular repolarization). Atrial repolarization is usually masked by the QRS complex.

Key ECG segments include the PR segment, which indicates the AV nodal delay, allowing atrial emptying before ventricular contraction. The ST segment reflects the plateau phase of ventricular action potentials, when ventricles contract and eject blood. The TP interval signifies ventricular relaxation and filling. The QT interval encompasses ventricular depolarization and repolarization, representing the overall electrical activity of the ventricles.

ECGs can detect abnormalities like heart block (damaged AV node, resulting in more P waves than QRS complexes as atria beat faster than ventricles) and ventricular fibrillation (uncoordinated ventricular depolarization, appearing as chaotic 'scribble' on the ECG). Junctional rhythm, caused by a damaged SA node, leads to the AV node becoming the pacemaker, resulting in a slower heart rate and a characteristic ECG pattern without a P wave or an inverted P wave.