The Cardiovascular System: The Heart

The Pulmonary and Systemic Circuits

The right side of the heart is the pulmonary circuit pump.

Pumps blood through the lungs, where CO2 is unloaded and O2 is picked up.

The left side of the heart is the systemic circuit pump.

Pumps blood to the tissues, delivering O2 and nutrients and picking up CO2 and wastes.

Heart Anatomy

Size, Location, and Orientation

The heart is the size of a fist and weighs 250–300 grams.

The heart is found in mediastinum and two-thirds lies left of the midsternal line.

The base is directed toward the right shoulder and the apex points toward the left hip.

Coverings of the Heart

The heart is enclosed in a doubled-walled sac called the pericardium.

Deep to pericardium is the serous pericardium.

The parietal pericardium lines the inside of the pericardium.

The visceral pericardium, or epicardium, covers the surface of the heart.

Layers of the Heart Wall

The myocardium is composed mainly of cardiac muscle and forms the bulk of the heart.

The endocardium lines the chambers of the heart.

Chambers and Associated Great Vessels

The right and left atria are the receiving chambers of the heart.

The right ventricle pumps blood into the pulmonary trunk; the left ventricle pumps blood into the aorta.

Heart Valves

The tricuspid and bicuspid valves prevent backflow into the atria when the ventricles contract.

When the heart is relaxed the AV valves are open, and when the heart contracts the AV valves close.

The aortic and pulmonary valves are found in the major arteries leaving the heart. They prevent backflow of blood into the ventricles.

When the heart is relaxed the aortic and pulmonary valves are closed, and when the heart contracts they are open.

Pathway of Blood Through the Heart

The right side of the heart pumps blood into the pulmonary circuit; the left side of the heart pumps blood into the systemic circuit.


Coronary Circulation

The heart receives no nourishment from the blood as it passes through the chamber.

The coronary circulation provides the blood supply for the heart cells.

In a myocardial infarction, there is prolonged coronary blockage that leads to cell death.

Properties of Cardiac Muscle Fibers

Microscopic Anatomy

Cardiac muscle is striated and contraction occurs via the sliding filament mechanism.

The cells are short, fat, branched, and interconnected by intercalated discs.

Mechanism and Events of Contraction

Some cardiac muscle cells are self-excitable or autorhythmic. These cells generate an action potential that spreads throughout the myocardium, causing the heart to contract as a single unit.

Unlike skeletal muscle there are no individual motor units and no motor unit recruitment. In addition, the heart’s absolute refractory period is longer than a skeletal muscle’s, preventing tetanic contractions.

Energy Requirements

The heart relies exclusively on aerobic respiration for its energy demands.

Cardiac muscle is capable of switching nutrient pathways to use whatever nutrient supply is available. It doesn't matter if the acetyl-CoA comes from glucose, fatty acids, lactate converted to pyruvate, or amino acids, ATP is primarily generated by oxidative phosphorylation.

Heart Physiology

Electrical Events

The intrinsic conduction system is made up of specialized cardiac cells that initiate and distribute impulses, ensuring that the heart depolarizes in an orderly fashion.

The autorhythmic cells have an unstable or drifting resting potential, called a pacemaker potential, which results in a slow depolarization. When the resting potenital "drifts up" to threshold the cells rapidly generate an action potential. Depolarization is followed by repolarization, although the inward flux of Ca++ extends the absolute refractory period and inhibits rapid sequential depolarizations.

Impulses pass from the autorhythmic cardiac cells in the sinoatrial node through atrial myocytes to the atrioventricular node, down the atrioventricular bundle (bundle of His) to the right and left bundle branches and on to the Purkinje fibers.

Cells at SA node depolarize approximately 100 times per minute. Cells at the AV node depolarized approximately 60 times per minute and can support cardiac function if the cells of the SA node fail to function properly but are overridden by action potentials that originate in the SA node under normal circumstances. This is why the SA node is known as "the pacemaker of the heart".

Fibers of the bundle branches and the Purkinje cells spontaneously depolarize about 32 times per minute but that is insufficient to supply the body.

The autonomic nervous system modifies the heartbeat: the sympathetic center increases rate and strength of the heartbeat, and the parasympathetic center slows the heartbeat.


The dominant extrinsic influence on heart rate at rest is inhibitory due to parasympathetic stimulation through the vagus nerve.

Parasympathetic stimulation "puts the brakes on" the rate set by the SA node, resulting in a resting heart rate considerably less than 100 bpm (72 -75 bpm, depending on aerobic conditioning)

Sympathetic fibers innervate both the SA and AV nodes and the myocardium. Sympathetic stimulation will cause an increase in heart rate and contractility of the ventricles, especially the left ventricle.

An electrocardiograph monitors and amplifies the electrical signals of the heart and records it as an electrocardiogram (ECG).



Normal sinus rhythm is driven by the SA node.






Junctional rhythm is driven by the AV node.


Heart block:

1st degree = prolongation of the p-q interval due to refractoriness of conductive cells in the AV node.

2nd degree = a fraction of atrial depolarizations are conducted through the AV node, resulting in more p waves than QRS complexes. The ratio is usually that of 2 small integers (2:1, 3:1, 3:2). The block may be above or below the bundle. If the block is below the bundle the ramifications are more severe.

3rd degree = complete heart block, no atrial depolarizations are conducted through the AV node. Atrial and ventricular contractions are completely independent. The intrinsic depolarization of the ventricles (about 32 bpm) often results in syncope. This condition is one of the most common requiring artificial pacemakers.

Ectopic foci may cause premature atrial or ventricular contractions, which prevent proper ventricular filling.


Heart Sounds


The first heart sound, lub, corresponds to closure of the AV valves, and occurs during ventricular systole.

The second heart sound, dup, corresponds to the closure of the aortic and pulmonary valves, and occurs during ventricular diastole.


Heart murmurs are extraneous heart sounds due to turbulent flow of blood backwards through a valve that does not close tightly (regurgitation) or forward through a valve that doesn't open completely (stenosis).

Mechanical Events: The Cardiac Cycle

Systole is the contractile phase of the cardiac cycle and diastole is the relaxation phase of the cardiac cycle.

Cardiac Cycle

Ventricular filling: Mid-to-late ventricular diastole (includes atrial systole, P-Q interval)

Ventricular systole: isovolumetric contraction and ejection phase (Q-T interval)

Quiescent phase: isovolumetric relaxation in early ventricular diastole until atrial contraction (end of T wave to beginning of next P wave)

Cardiac Output

Cardiac output is defined as the amount of blood pumped out of a ventricle per minute, and is calculated as the product of stroke volume and heart rate.

Regulation of Stroke Volume

Stroke volume is regulated by three things: preload, contractility, and afterload.


Preload: the Frank-Starling law of the heart states that the critical factor controlling stroke volume is the degree of stretch of cardiac muscle cells immediately before they contract.








Stretch allows the sarcomer to contract farther, generating more force.



Afterload: ventricular pressure that must be overcome before blood can be ejected from the heart. (Afterload is indicated by the diastolic blood pressure)


Contractility: contractile strength increases if there is an increase in cytoplasmic calcium ion concentration.

Regulation of Heart Rate

Regulation of Heart Rate

Factor Type

Increase Rate

Decrease Rate


Autonomic NS



Sympathetic (stimulation of pacemaker cells increases heart rate and contractility)



Parasympathetic (inhibition of cardiac pacemaker cells decreases heart rate)




Thyroxine (increases BMR and potentiates epi and NE)











Hypernatremia (inhibits calcium transport)

Hyperkalemia (lowers resting membrane potential)

Hypokalemia (causes both abnormal contractions and decreases contractility


Other factors










Exercise* (long term aerobic conditioning)




Homeostatic Imbalance of Cardiac Output

Congestive heart failure occurs when the pumping efficiency of the heart is so low that blood circulation cannot meet tissue needs.

Pulmonary congestion occurs when one side of the heart fails, resulting in pulmonary edema.

Developmental Aspects of the Heart

Embryological Development


The heart begins as a pair of endothelial tubes that fuse to make a single heart tube with four bulges representing the four chambers.

Referring to (b) in the figure above:

The sinus venosus receives all embryonic venous blood. It becomes the smooth-walled part of the right atrium and the coronary sinus and gives rise to the sinoatrial node.

The atrium gives rise to the pectinate muscle-ridged parts of the atria.

The ventricle becomes the left ventricle.

The bulbus cordis and the truncus arteriosus give rise to the pulmonary trunk, the first part of the aorta, and most of the right ventricle.

The foramen ovale is an opening in the interatrial septum that allows blood returning to the pulmonary circuit to be directed into the atrium of the systemic circuit.

The ductus arteriosus is a vessel extending between the pulmonary trunk to the aortic arch that allows blood in the pulmonary trunk to be shunted to the aorta.

Congenital Heart Defects

1. mixing of oxygen-poor blood wiht oxygenated blood

Septal defects

Patent ductus arteriosus

2. Narrowed valves or vessels that increase the workload of the heart

Coarctation of the aorta

Tetralogy of Fallot


Aging Aspects of the Heart

Sclerosis and thickening of the valve flaps occurs over time, in response to constant pressure of the blood against the valve flaps.

Decline in cardiac reserve occurs due to a decline in efficiency of sympathetic stimulation.

Fibrosis of cardiac muscle may occur in the nodes of the intrinsic conduction system, resulting in arrhythmias.

Atherosclerosis is the gradual deposit of fatty plaques in the walls of the systemic vessels.