Cardiac Muscle Physiology

• Intercalated Discs are cell membranes between individual cardiac muscle cells that form gap junctions, allowing for rapid ion diffusion and action potentials.
• The epicardial and endocardial muscle layers' composition and opposing direction create a twisting motion, like a spring that recoils during diastole.
• Fibrous tissue separates the atrial syncytium from the ventricles, preventing action potentials from traveling outside of the AV bundle and allowing the atria to contract before ventricular contraction.
• Fast sodium channels open briefly to allow sodium to enter and create the action potential during Phase 0 for depolarization; close at +20 mV when repolarization in Phase 1 begins; potassium ions experience decreased permeability after sodium channel closure during Phase 1.
• Slow, L-type Calcium channels open slowly when -40 mV is reached during Phases 0 and 1, allowing calcium to enter the cell, and create the plateau in the action potential.
• The "all or nothing" threshold of cardiac muscle cells is reached at -40 mV.
• The strength of cardiac muscle contraction depends on the concentration of calcium ions in the extracellular fluid and the sarcoplasmic reticulum.

Ventricular Blood Volumes

• End diastolic volume: 110-120 mL
• Stroke Volume: 70 mL
• End systolic Volume: 40-50 mL
• EF=End Diastolic Volume-Stroke volume normal ~60%
• An EF <30% is associated with increased mortality and morbidity with anesthesia; vasopressors are often required to maintain adequate preload and cardiac output.

Cardiac Cycle

• Phase 1 (Filling): AV valves open, semilunar valves are closed
• Phase 2 (Isovolumetric contraction): all valves are closed
• Phase 3 (Ejection): AV valves are closed, semilunar valves are open
• Phase 4 (Isovolumetric relaxation): all valves are closed
• Preload: end-diastolic pressure when the ventricle has been filled
• Afterload: the pressure in the aorta that opposes ventricular ejection of blood
• Frank-Starling Mechanism: the strength of cardiac muscle contraction relates to the stretch caused by the amount of blood filling the ventricles.
• Increased stretch from increased blood volume returning to the heart causes more forceful contraction but can lead to dysfunction and failure if stretched too far.
• Stroke volume= venous return which is increased with increased end-diastolic volume.

Rhythmicity

• The sinoatrial (SA) node, in the right atrium, generates electrical impulses for normal cardiac contractions and has a resting membrane potential of -55 to -60 mV.
• Cardiac muscle fibers have a resting membrane potential ranging from -85 to -90 mV.
• The normal rate established by the SA node is 60 to 80 beats per minute.
• A total delay of 0.16 seconds occurs when the action potential reaches the AV node.
• This delay allows atrial contraction to push blood through the open AV valves into the ventricles.
• The action potential continues through the Bundle of His, Left, and Right bundle branches, and then to the Purkinje fibers surrounding both ventricles, causing contraction and ejection of blood into the pulmonary artery and aorta.
• The AV node will discharge an impulse at a rate of 40 to 60 bpm if the SA node cannot generate the action potential for cardiac contraction.
• The Purkinje fibers will discharge at a rate of 15 to 40 bpm if the SA and AV nodes fail to fire.
• Stimulation of the parasympathetic nervous system releases acetylcholine from the vagus nerve, increasing fiber membrane permeability to potassium ions, resulting in hyperpolarization and a decrease in impulse generation.
• Strong stimulation can completely inhibit the SA node.
• Stimulation of the sympathetic nervous system releases norepinephrine, activating beta-1 adrenergic receptors that may increase fiber membrane permeability to sodium and calcium ions.
• This causes a rise in resting membrane potential, making it easier to trigger depolarization, and influences the AV node and AV bundle.