Cardiac Physiology

Pulmonary Circulation

The pathway that carries deoxygenated blood from the right side of the heart to the lungs and returns oxygenated blood to the left atrium.

Systemic Circulation

The pathway that carries oxygenated blood from the left ventricle to body tissues and returns deoxygenated blood to the right atrium.

Four Chambers of the Heart

Right atrium, right ventricle, left atrium, left ventricle; arranged so that blood flows RA → RV → lungs → LA → LV → body.

tricuspid blood flow

RA→RV

pulmonary blood flow

RV→pulmonary artery

mitral/bicuspid blood flow

LA→LV

aortic blood flow

LV→aorta

Cardiac Muscle Fibers

Intercalated discs with gap junctions allow rapid spread of electrical impulses and synchronized contraction.

Pericardial Sac

A double-layered membrane surrounding the heart; reduces friction and anchors the heart in place.

Blood Flow Pathway

Vena cavae → right atrium → tricuspid valve → right ventricle → pulmonary valve → pulmonary arteries → lungs → pulmonary veins → left atrium → mitral valve → left ventricle → aortic valve → aorta → body.

Chordae Tendineae

Fibrous cords that anchor AV valve leaflets to papillary muscles, preventing valve prolapse during ventricular contraction.

Fibrous Skeleton of Heart

Rings of dense connective tissue that support valves and prevent dilation during high pressure.

Systole

The contraction phase of the heart that pumps blood out of a chamber.

Diastole

The relaxation phase of the heart that allows chambers to fill with blood.

Atrial Systole

Atria contract, pushing blood into ventricles through open AV valves.

Ventricular Systole (First Phase)

Ventricles contract isovolumetrically; all valves closed, pressure rises.

Ventricular Systole (Second Phase)

Semilunar valves open, blood ejected into arteries.

Ventricular Diastole (First Phase)

Semilunar valves close, ventricles relax isovolumetrically.

Ventricular Diastole (Second Phase)

AV valves open, ventricles fill passively with blood.

Heart Pump Coordination

The right and left sides of the heart contract simultaneously, not sequentially.

Cardiac Cell Types

Autorhythmic cells (pacemakers) and contractile cells (muscle fibers that contract).

Pacemaker Potential Channels

Caused by “funny” Na⁺ channels (influx of Na⁺) and T-type Ca²⁺ channels (transient influx of Ca²⁺).

Autorhythmic Tissue Pathway

SA node → AV node → Bundle of His → Purkinje fibers.

SA Node

Primary pacemaker; sets heart rate around 70–80 bpm.

AV Node

Secondary pacemaker; sets heart rate around 40–60 bpm if SA node fails.

Bundle of His & Purkinje Fibers

Tertiary pacemakers; can set rate around 20–40 bpm if higher pacemakers fail.

Controlled Spread of Excitation

Ensures coordinated contraction — atria contract before ventricles.

Parasympathetic Effects on SA/AV Nodes

Decreases heart rate and conduction velocity (via ACh).

Sympathetic Effects on SA/AV Nodes

Increases heart rate and conduction velocity (via norepinephrine).

Electrocardiogram (ECG)

A recording of the heart’s electrical activity through electrodes on the skin.

P Wave

Atrial depolarization (atrial contraction).

QRS Complex

Ventricular depolarization (ventricular contraction).

T Wave

Ventricular repolarization (ventricular relaxation).

Cardiac Output (CO)

CO = Heart Rate (HR) × Stroke Volume (SV).

Stroke Volume (SV)

The volume of blood ejected by one ventricle per beat.

Intrinsic Control of SV

Determined by venous return and Frank-Starling mechanism (greater stretch → stronger contraction).

Extrinsic Control of SV

Controlled by sympathetic stimulation, which increases contractility.

Frank-Starling Law

The greater the stretch of cardiac fibers (from increased venous return), the greater the stroke volume.

Preload

The degree of stretch of the ventricle before contraction; related to venous return.

Afterload

The resistance the ventricle must overcome to eject blood (arterial pressure).

Heart Failure

A condition where the heart cannot pump enough blood to meet the body’s metabolic needs.