CARDIOVASCULAR SYSTEM SHEET

Cardiac Anatomy

Mechanical

Heart wall structure – the four distinct layers of the heart are: 1) the pericardium, 2) the epicardium,

3) the myocardium, and 4) the endocardium.

 Pericardium – the outermost fibrous pericardium provides a physical barrier to protection. It is a thick

envelope that is tough and inelastic. Ligaments anchor the pericardium to the diaphragm and the

great vessels such that the heart is maintained in a fixed position within the thoracic cavity. Inside the

fibrous layer is a double-walled membrane called the serous pericardium. These two layers are the

parietal and visceral layers.

 Epicardium – the epicardium is tightly adhered to the heart and the base of the great vessels. The

coronary arteries lie on top of the visceral epicardium. In adults, a layer of adipose tissue is typically

present beneath the visceral pericardium and may surround the heart. This is known as epicardial fat.

 Myocardium – The next layer of the heart is the myocardium, a thick, muscular layer. This layer

includes all of the atrial and ventricular muscle fibers necessary for contraction. The fibers of the

myocardium do not have the same thickness throughout the ventricular walls. The LV is much thicker

than the RV or the atria. This is to ensure that the force of contraction is most efficient in ejecting

blood toward the outflow tracts of the heart. The myocardium is the muscle that is damaged by a

“heart attack” or transmural myocardial infarction.

 Endocardium – The innermost layer of the heart is the endocarcium, which is a thin layer of

endothelium and connective tissue lining the inside of the heart. This layer is continuous with the

endothelium of the great vessels to provide a continuous closed system. Disruption in the

endothelium as a result of surgery, trauma, or congenital abnormality can predispose the endocardium

to infection. This infective endocarditis is a devastating disease which, if left untreated, can lead to

massive valve damage or sepsis and death.

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Chambers – 4 chambers - The human heart has four chambers: the left and right atria and the left and right

ventricles. The atria are thin-walled and normally low-pressure chambers. They function to receive blood from

the vena cavae and pulmonary veins and to pump blood into their respective ventricles. Atrial contraction,

also known as atrial kick, contributes approximately 20% of blood flow to ventricular filling; the other 80%

occurs passively during diastole. The ventricles are the primary pumping chambers of the heart. The healthy

left ventricle is about 10 to 13 mm thick. The healthy right ventricle is approximately 3 mm thick. The right

ventricle pumps blood into the low-pressured pulmonary circulation, which has a normal mean pressure of

approximately 15 mm Hg. The left ventricle must generate tremendous force to eject blood into the aorta

(normal mean pressure of approximately 100 mm Hg). Because of left ventricular wall thickness and the large

force it must generate, the left ventricle is considered the major pump of the heart. When the left ventricular

muscle is damaged from cardiomyopathy or infarction, the effective pumping pressure is diminished, leading

to increased left atrial pressure, pulmonary vasculature congestion, and ultimately, systemic venous

congestion.
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Valves - Cardiac valves are composed of flexible, fibrous tissue. The valve structure allows blood to

flow in only one direction. The opening and closing of the valves depends on the relative pressure gradients on

either side of the valve. The two atrioventricular (AV) valves are named for their location between the atria

and the ventricules. These are the tricuspid valve (three leaflets) on the right and the mitral valve (two

leaflets) on the left. The AV valves are open during ventricular diastole (filling) and prevent backflow of blood

into the atria during ventricular systole (contraction). The semilunar valves are pulmonic and aortic valves and

each have three cuplike leaflets. These valves separate the ventricles from their respective outflow arteries.

During ventricular systole (contraction), semilunar valves open, allowing blood to flow out of the ventricles.

As systole ends and the pressure in the outflow arteries exceeds that of the ventricles, the semilunar valves

close, preventing blood regurgitation back into the ventricles.

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Papillary muscles – The chordae tendineae and papillary muscles, which attach to the tricuspid and

mitral valves, give the valves stability and prevent valve leaflet eversion during systole. Papillary muscles arise

from the ventricular myocardium and derive their blood supply from the coronary arteries. Each papillary

muscle gives rise to approximately 4 to 10 main chordae tendineae, which divide into increasingly finer cords

as they approach and attach to the valve leaflets. Papillary muscle rupture may be auscultated as a

holosystolic, blowing murmur at the cardiac apex and is a surgical emergency.

Chordae tendineae – The chordae tendineae are fibrous, avascular structures covered by a thin layer

of endocardium. Dysfunction of the chordae tendineae or of a papillary muscle may cause incomplete closure

of an AV valve, wich results in backflow of blood into the atrium.

Blood flow RA -> Tricuspid Valve -> RV -> Pulmonic Valve -> Pulmonary Artery -> Lungs -> Pulmonary

vein -> LA -> Bicuspid Valve -> LV -> AV -> Aorta -> Body

Electrical Conduction System - To analyze electrical activity within the heart, it is helpful to understand the

three main areas of impulse propagation and conduction: 1) the sinoatrial (SA) node, 2) the AV node, and 3)

the conduction fibers within the ventricle, specifically the bundle of His, the bundle branches, and the Purkinje

fibers.

SA Node – The SA node is the natural pacemaker of the heart because it has the highest degree of

automaticity, producing the fastest intrinsic heart rate at a rate of 60-100 beats/min.

AV Node – the AV node depolarizes at a rate of 40-60 beats/minute and is the backup pacemaker of the heart.

The AV node performs 4 major functions:

1. Delays the conduction impulse from the atria (0.8 to 1.2 seconds) to provide time for the ventricles to

fill during diastole

2. Controls the number of impulses transmitted from the atria to the ventricles, preventing rapid irregular

atrial heart rhythms from destabilizing the ventricular rhythm.

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3. Acts as a backup pacemaker if the SA node fails

4. Can conduct retrograde (backwards) impulses through the node, so if the SA and AV pacemaker cells

fail to fire, an electrical impulse can ben initiated in the ventricles and conducted backward via the AV

node.

Bundle of His, Bundle Branches, and Purkinjie fibers - Electrical impulses are conducted in the

ventricles through the bundle of His, the bundle branches, and the Purkinje fibers. The bundle of His divides

into the right and left bundle branches. The right bundle branch continues down the right side of the

interventricular septum toward the right apex. The left bundle branch is thicker than the right. Functionally,

when one of the left branches is blocked, it is referred to as a hemiblock. All of the bundle branches are

subject to conduction defects (bundle branch blocks) that give rise to characteristic changes in the 12-lead

electrocardiogram (ECG). The right bundle branch and the two divisions of the left bundle branch eventually

divide into the Purkinje fibers, which have the fastest conduction velocity of all heart tissue. Purkinje fibers

have an intrinsic rate of 10 – 39 beats/min. This is followed by ventricular muscle depolarization.

SA node-->AV node-->Bundle of His--> Bundle Branches -> Purkinje fibers

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Action potential – In a myocardial cell, when a sudden increase in permeability of the membrane to Na +

occurs, it is followed by a rapid sequence of events that lasts a fraction of a second. This sequence of events is

termed depolarization.

TABLE 12-5 PHASES 0 THROUGH 4 OF A CARDIAC CELL ACTION POTENTIAL

PHASE DESCRIPTION IONIC MOVEMENT MECHANISMS

0 Upstroke Na+ into cell Fast Na+ channels open
1 Overshoot — Fast Na+ channels close
2 Plateau Na+ and Ca2+ into cell, Multiple channels (Ca2+, Na+, K+) open to maintain membrane

K+out voltage
3 Repolarization K+ out of cell Ca2+ and Na+ channels close; K+ channel remains open
4 Resting membrane Na+ out, K+ in Na+–K+ pump

potential
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Properties of the heart –
 Excitability- the ability of the cardiac muscle cells to reach threshold (and therefore contract) in
response to a stimulus. The smaller the stimulus requirement, the greater the excitability.
 Automaticity-the ability of the cardiac cells to generate electrical impulses without external stimulus.
Determines it’s own rhythmicity-impulses are formed at regular intervals. Permeability of cardiac cells
to potassium and sodium ions; when concentration of ions is reached, an impulse is generated.
 Conductivity-the ability to transmit those impulses from one cell to another.
 Contractility-the ability of myocardial cells to shorten or contract when electrically stimulated;
referring to the inotropic state of the muscle.

EKG - The P wave represents atrial depolarization, followed immediately by atrial systole. The QRS

represents ventricular depolarization, followed immediately by ventricular systole. The ST segment

corresponds to phase 2 of the action potential, during which time the heart muscle is completely depolarized

and contraction normally occurs. The T wave represents ventricular repolarization. The PR interval, measured

from the beginning of the P wave to the beginning of the QRS, corresponds to atrial depolarization and

impulse delay in the atrioventricular (AV) node. The QT interval, measured from the beginning of the QRS

complex to the end of the T wave, represents the time from initial depolarization of the ventricles to the end

of ventricular repolarization.

EKG
P wave: Atrial depolarization
PRI: 0.12-0.2
QRS: 0.8-0.12, depolarization of
ventricles
T wave: ventricle repolarization
QT/QTc: </= 0.44sec (prolonged-risk
for dysrhythmias)
U wave: hypokalemia, inverted in heart
disease, may be purkinji fibers
repolarizing
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Vasculature – Major cardiac vessels include the aorta, the vena cava, pulmonary artery, and pulmonary veins.

The heart itself receives its own supply of blood from the coronary arteries. The Right Coronary Artery (RCA)

serves the right atrium and right ventricle. The LCA divides into the LAD and Circumflex artery, and these

serve the left atrium and most of the left ventricle. Blockage of coronary artery blood flow, especially LAD

usually results in death. The coronary veins, which carry deoxygenated blood, are adjacent to the paths of the

coronary arteries and ultimately join together to become the coronary sinus, the largest cardiac vein and

empties into the right atrium.

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Hemodynamics

Blood Pressure – Systolic blood pressure (SBP) represents the ventricular volume ejection and the response of

the arterial system to that ejection. The diastolic blood pressure (DBP) value indicates the ventricular resting

state of the arterial system. The pulse pressure is the difference between the SBP and the DBP. The mean

arterial pressure (MAP) is the mean value of the area under the blood pressure curve.

Systolic – Less than 120 Diastolic – Less than 80 MAP – 70 – 100 mmHg

Venous Oxygen Saturation (SVO2) – Normal SvO2 is 75% in the healthy adult with a range of 60% - 80% and is

evidence of adequate balance between oxygen supply and demand.

Central Venous Oxygen Saturation (ScVO2) – The normal values for the SCVO2 catheter are slightly higher

because the reading is taken before the blood enters the right heart chambers. The heavily desaturated

myocardial blood decreases the oxygen saturation slightly. For this reason, SVO2 values are always slightly

lower than SVCO2 readings in the same patient.

Myocardial Oxygen Consumption (MVO2) – Is the balance between oxygen supply and demand of the heart.

Factors that enhance myocardial tension on the cardiac muscle cells, such as tachydysrhythmias, increase

MV02.

Preload – the volume of blood in the left ventricle at the end of diastole. Factors affecting preload include

venous return to the heart, total blood volume, and atrial kick. One way to measure preload is through the

pulmonary artery wedge pressure. (Starling’s Law: force of contraction r/t myocardial fiber length prior to

contraction)

Afterload – Is the ventricular wall tension or stress during systolic ejection. It is also called systemic vascular

resistance (SVR). An increase in afterload usually means an increase in the work of the heart. Afterload is

increased by factors that oppose ejection such as vasoconstriction or hypertension.

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Pulmonary Artery Pressure (PAP) – pulsatile pressure in the pulmonary artery measured by an indwelling

catheter.

Systolic – 20 – 30 mmHg Diastolic – 5 – 10 mmHg PAPMean – 10 – 15 mmHg

Stroke volume (SV) – Amount of blood ejected by the ventricle with each heartbeat. Calculate SV by dividing

CO by the HR then multiplying by 1000 to change L to mL. Normal SV is 60-70mL

Cardiac output (CO) – the volume of blood ejected from the heart in 1 minute. The determinants of CO are SV

x HR = CO. Normal CO is 4-6 L/min at rest, 4-8 L/min with exercise.

Cardiac index (CI) – 2.2 – 4 L/min/square meter. CI is determined by CO divided by BSA. This is considered to

be more accurate than CO because it is individualized by height and weight.

Ejection Fraction (EF) – The percentage of preload volume ejected from the left ventricle per meat is the

ejection fraction. Not all of the preload volume of the heart is ejected with every heartbeat. This is often

measured during a cardiac catheterization or echocardiogram. Most cardiologists accept 50% as adequate

and 70% as a healthy heart.

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EXTRAS – ACTION POTENTIAL
In a myocardial cell, when a sudden increase in permeability of the membrane to Na + occurs, it is
followed by a rapid sequence of events that lasts a fraction of a second. This sequence of events is
termed depolarization. The graphic representation of depolarization and repolarization is termed the
action potential (AP) (Fig. 12-23). Ionic currents cause changes in electrical potentials, which are known
as AP phases 0, 1, 2, 3, and 4. These phases give the AP a characteristic shape.
Phase 0.
The sodium crossing the cell membrane causes the cell to become depolarized and the interior of the
cell to become more positive. At approximately −65 mV, the membrane reaches the threshold, the
point at which the inward Na+ current overcomes the efflux of K+. This is accomplished by means of
the fast Na+ channels. With the fast Na+ channels open, the inward rush of Na+ is extremely rapid and
briefly causes the inside of the cell to become slightly more positive than the outside of the cell. This
series of events is graphically described as phase 0 of the AP and is reflected in the overshoot of the
AP, during which the charge is 20 to 30 mV.
Phase 1 and Phase 2.
When the rapid influx of Na+ is terminated, a brief period of partial repolarization occurs as the AP
slope returns toward zero (phase 1 of the AP). The plateau that follows is described as phase 2.
During this phase, another set of channels, the slow Na+ and Ca2+ channels, open to allow the influx of
Ca2+ and Na+. During phase 2, K+ tends to diffuse out of the cell, balancing the slow inward flux of Na +
and Ca2+ thereby maintaining the plateau of the AP. The Ca2+ entering the cell at this phase causes
cardiac contraction, which is described later in this chapter. The inward flux of Ca2+ during this phase
can be influenced by many factors. For example, calcium channel–blocking medications such as
verapamil and diltiazem inhibit the inward Ca2+ current into pacemaker tissue, especially the AV
node. For this reason, this class of medications is used therapeutically to slow the rate of atrial
tachydysrhythmias and protect the ventricle from excessive atrial impulses.
Phase 3.
The repolarization phase is described as phase 3, and it depends on two processes. The first is the
inactivation of the slow channels, which prevents further influx of Ca 2+ and Na+. The other is the
continued efflux of K+ out of the cell. Both processes cause the intracellular environment to become
more negative, thereby re-establishing the RMP. On the AP, phase 3 is seen as a gradual descent
during which the interior of the cell becomes more negative relative to the outside.
Phase 4.
In phase 4, the AP returns to an RMP of −80 to −90 mV. The excess Na+ that entered the cell during
depolarization is removed from the cell in exchange for K+ by means of the Na+–K+ pump. This
mechanism returns the intracellular concentrations of Na + and K+ to the levels present before
depolarization and is essential for normal ionic balance and preparation for the next depolarization