Cardiovascular System Anatomy and Physiology

A dual pump that circulates blood around the body and through the lungs.

The pattern of electrical activity recorded at the body surface.

Includes blood vessels that carry blood to and from the lungs where oxygen is picked up and carbon dioxide is released.

Includes blood vessels that transport blood to and from all body tissues.

Carry blood away from the heart.

Carry blood toward the heart.

The medial cavity of the thorax where the heart is enclosed.

A sac that encloses the heart.

Inflammation of the pericardium.

The thick cardiac muscle layer of the heart.

Crisscrossing collagen and elastic connective tissue fibers that strengthens and anchors the heart.

The innermost layer of the heart.

Lines the heart valves and chambers.

Allow for additional filling of the atria.

Muscular ridges in the atria and ventricles, respectively.

Allows fetal blood to bypass the pulmonary circuit.

Natural pacemaker of the heart.

Atria activation (depolarization).

Phase 1 of the cardiac cycle; includes late diastole, ventricular filling, and atrial contraction.

Phase 2a of the cardiac cycle; ventricular systole, isovolumetric contraction.

Phase 2b of the cardiac cycle; ventricular ejection stage.

Phase 3 of the cardiac cycle; early diastole, isovolumetric relaxation.

Volume of blood in the left ventricle at the end of diastole (filling).

Receives blood from the superior and inferior vena cava & coronary sinus.

Receives blood from the four pulmonary veins.

Prevent AV valves from everting into the atria during ventricular contraction.

Left ventricle pumps blood to the entire body, higher pressure, higher resistance.

Chest pain caused by fleeting insufficiency of blood supply to the myocardium.

Prolonged blockage of coronary arteries leading to oxygen and nutrient deficit and tissue death.

Anchoring junctions that prevent cells from separating during contraction.

Allow ions to pass rapidly between cardiac cells for coordinated contraction.

Allows for rapid and coordinated electrical coupling of the entire heart.

Specialized non-contractile cells that spontaneously depolarize.

The inner lining of the heart, composed of endothelium.

The serous membrane lining the fibrous pericardium; part of the pericardium.

Irregular ridges of muscle on the ventricular walls.

Pericardial cavity filled with serous fluid that reduces friction.

The sequence includes atrial depolarization, septal depolarization, apical depolarization, left ventricular depolarization, ventricular depolarization, and ventricular repolarization.

A rapid change in membrane potential due to fast voltage-gated sodium channels opening.

A sustained depolarization phase in cardiac cells, caused by slow voltage-gated calcium channels opening.

Return to resting membrane potential, potassium channels open.

Ensures efficient blood ejection and prevents tetanus.

Represents ventricular depolarization and atrial repolarization.

Enlargement of the ventricles.

Wave indicates atrial depolarization.

Volume of blood pumped out by one ventricle with each beat.

Volume of blood in the ventricle at the end of diastole (relaxation/filling).

Volume of blood remaining in the ventricle after systole (contraction).

Volume of blood pumped out by one ventricle in one minute.

Difference between maximum and resting cardiac output.

Cardiac contractions don't need nerves; the vagus nerve slows the heart down while sympathetic nerves speed it up.

Action potentials spread from the SA node, through the atria, to the atrioventricular (AV) node. This leads to atrial contraction and blood flow to the ventricles.

The AV node delays the action potential to allow the atria to contract fully, then rapidly transmits it through the AV bundle and Purkinje fibers to the ventricles.

Rapid spread of action potential down the Purkinje fibers leads to ventricular depolarization.

Defects in the conduction system can cause arrhythmia, where the heart rhythm is irregular, and in severe cases, fibrillation.

Fibrillating ventricles twitch ineffectively and can't pump blood. Defibrillation shocks the heart to reset the SA node's control.

If the SA node fails and is replaced by the AV node, the heart rate slows down, and the ECG will have a slower rhythm without a P wave.

An extra beat is followed by a longer pause for filling, leading to a stronger next beat.

In second-degree heart block, some SA node impulses don't reach the ventricles, leading to more P waves than QRS complexes on an ECG.

Valves which prevent backflow from the ventricles into the atria.

Valves that prevent backflow of blood from the aorta and pulmonary arteries into the ventricles.

The 'lub' sound. Occurs during early ventricular contraction when the AV valves close.

The 'dup' sound. Occurs when the semilunar valves close as the ventricles relax.

Abnormal heart sound due to turbulent blood flow often caused by valve malfunctions.

A condition where the major visceral organs are mirrored.

A valve defect that allows blood to flow backward, reducing heart efficiency.

A condition where valve flaps are stiff and narrowed, forcing the heart to work harder.

The phase in the cardiac cycle when the ventricles cannot change volume. Pressure increases but volume is static.

Volume of blood remaining in the ventricle after systole (contraction).

Increased heart muscle contraction.

Decreases heart rate by signaling for the opening of potassium channels via acetylcholine.

Natural rate of the SA node without any nerve input (approx. 100 bpm).

Respond to blood vessel stretch, signaling the autonomic nervous system to maintain blood pressure.

Reflex activated by increased atrial filling, leading to increased sympathetic output and heart rate.

Increases heart rate, similarly to norepinephrine.

Hormone from the thyroid gland that increases heart rate.

Abnormally fast heart rate (greater than 100 bpm).

Abnormally slow heart rate (less than 60 bpm).

Heart rate less than 60 bpm due to high-level physical fitness.

Heart's weakened ability to pump blood efficiently due to structural or functional impairment.

Fatty buildup and scar tissue clogs the coronary arteries.

The force against which the heart must pump.

When the ventricles stretch out and deteriorate, causing CHF.