ANATOMY AND PHYSIOLOGY OF
CARDIOVASCULAR SYSTEM
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ANATOMY OF HEART
ANATOMY
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The heart, a vital organ in the circulatory system, is a
hollow, muscular organ situated in the mediastinum,
the central area of the thoracic cavity, between the
lungs, and resting on the diaphragm.
Its average weight is 300 grams (10.6 oz), and its size
and weight are influenced by factors such as age,
gender, body weight, physical activity, and any
underlying heart disease.
STRUCTURE OF THE HEART
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Heart Layers:
○ Endocardium: The inner layer, made up of
endothelial tissue, lines the heart's interior,
including the valves.
○ Myocardium: The middle layer consists of
muscle fibers that are responsible for the
heart's pumping action.
○ Epicardium: The outermost layer, covering
the heart's surface.
Pericardium (Heart’s Protective Sac):
○ The heart is encased in a pericardium, a
fibrous sac that has two layers:
■ Visceral Pericardium: Closely
adheres to the epicardium.
■ Parietal Pericardium: A tough,
fibrous layer that attaches to the
great vessels, diaphragm, sternum,
and vertebral column, providing
structural support to the heart within
the mediastinum.
○ Pericardial Space: This space between the
visceral and parietal pericardium contains
about 20 mL of fluid, which lubricates the
heart's surface and reduces friction during its
contraction and relaxation cycles (systole
and diastole).
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Ventricular systole follows atrial systole.
This synchronization allows the ventricles to
fully fill before ejecting blood.
The right side of the heart (right atrium and right
ventricle):
○ Distributes venous (deoxygenated) blood to
the lungs via the pulmonary artery
(pulmonary circulation) for oxygenation.
○ Pulmonary artery is the only artery in the
body carrying deoxygenated blood.
○ The right atrium receives venous blood
returning from the superior vena cava (head,
neck, and upper extremities), inferior vena
cava (trunk and lower extremities), and
coronary sinus (coronary circulation).
The left side of the heart (left atrium and left ventricle):
○ Distributes oxygenated blood to the rest of
the body via the aorta (systemic circulation).
○ The left atrium receives oxygenated blood
from the pulmonary circulation through four
pulmonary veins.
The heart lies in a rotated position within the chest
cavity.
Right ventricle is positioned anteriorly (just beneath
the sternum).
Left ventricle is located posteriorly.
Due to its proximity to the chest wall, the apical
impulse (or point of maximal impulse [PMI]) is
easily detected during normal ventricular contraction.
In a normal heart, the PMI is found at the intersection
of the midclavicular line on the left chest wall and
the fifth intercostal space.
HEART CHAMBERS
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The heart's pumping action is achieved through the
rhythmic relaxation and contraction of its muscular
walls in two top chambers (atria) and two bottom
chambers (ventricles).
Diastole (relaxation phase):
○ All four chambers relax simultaneously.
○ Allows ventricles to fill in preparation for
contraction.
○ Often referred to as the period of
ventricular filling.
Systole (contraction phase):
○ Refers to events during the contraction of
atria and ventricles.
○ Atrial and ventricular systoles do not occur
simultaneously.
○ Atrial systole happens first, at the end of
diastole.
BSN 3-4
JOSHUA ALLAN G. ARELLANO, SN
HEART VALVES
ATRIOVENTRICULAR VALVES
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AV valves separate the atria from the ventricles.
Tricuspid valve (three cusps/leaflets) separates the
right atrium from the right ventricle.
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Mitral (bicuspid) valve (two cusps) separates the
left atrium from the left ventricle.
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DURING DIASTOLE
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The tricuspid and mitral valves are open.
Blood flows freely from the atria into the relaxed
ventricles.
DURING VENTRICULAR SYSTOLE
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Ventricles contract, causing blood to flow upward into
the cusps of the tricuspid and mitral valves, leading to
valve closure.
Papillary muscles and chordae tendineae help
maintain valve closure by preventing backflow.
Papillary muscles are located on the ventricular
walls and are connected to the valve leaflets via
chordae tendineae (thin fibrous bands).
Contraction of papillary muscles makes the chordae
tendineae taut, keeping the valves closed and
preventing regurgitation (backflow of blood) into the
atria.
Blood is then ejected into the pulmonary artery and
aorta.
SEMILUNAR VALVES
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The semilunar valves consist of three leaflets
shaped like half-moons.
Pulmonic valve is located between the right
ventricle and the pulmonary artery.
Aortic valve is located between the left ventricle
and the aorta.
DURING DIASTOLE
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The semilunar valves are closed.
Pressure in the pulmonary artery and aorta
decreases, causing blood to flow back toward the
valves.
This backflow fills the cusps with blood and closes
the semilunar valves.
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LEFT CORONARY ARTERY
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The semilunar valves are forced open as blood is
ejected from the right and left ventricles into the
pulmonary artery and aorta, respectively.
CORONARY ARTERIES
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The left and right coronary arteries supply arterial
blood to the heart.
These arteries originate from the aorta, just above the
aortic valve leaflets.
Coronary arteries are perfused during diastole
(unlike other arteries).
With a normal heart rate (60 to 80 bpm), there is
enough time for myocardial perfusion during
diastole.
Increased heart rate shortens diastolic time,
reducing perfusion time, and may lead to myocardial
ischemia (inadequate oxygen supply).
RIGHT CORONARY ARTERY
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Supplies the right side of the heart and travels to the
inferior wall.
BSN 3-4
JOSHUA ALLAN G. ARELLANO, SN
Has three branches:
1. Left main coronary artery (from the point of
origin to the first major branch).
2. Left anterior descending artery (supplies
the anterior wall of the heart).
3. Circumflex artery (circles around to the
lateral left wall of the heart).
Patients with CAD are at risk for myocardial
ischemia during tachycardia (heart rate >100 bpm).
MYOCARDIUM
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The myocardium is the middle muscular layer of
the atrial and ventricular walls.
Composed of specialized cells called myocytes,
which form an interconnected network of muscle
fibers.
The muscle fibers encircle the heart in a
figure-of-eight pattern, spiraling from the base (top)
to the apex (bottom).
During contraction, this muscular configuration allows
for a twisting and compressive movement of the
heart.
This movement starts in the atria and progresses to
the ventricles.
The sequential and rhythmic pattern of contraction
and relaxation of the muscle fibers maximizes the
volume of blood ejected with each contraction.
The cyclical pattern of myocardial contraction is
controlled by the heart's conduction system.
FUNCTION OF THE HEART
CARDIAC ELECTROPHYSIOLOGY
DURING VENTRICULAR ASYSTOLE
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Branches into the posterior descending artery,
which supplies the posterior wall of the heart.
Coronary veins are superficial to the coronary
arteries.
Venous blood returns to the heart through the
coronary sinus, located in the right atrium.
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The cardiac conduction system generates and
transmits
electrical
impulses
that
stimulate
myocardial contraction.
Normally, the conduction system first stimulates
contraction of the atria, followed by the ventricles.
This synchronization allows the ventricles to fill
completely before ventricular ejection, maximizing
cardiac output.
PHYSIOLOGIC CHARACTERISTICS OF
SPECIALIZED ELECTRIC CELLS
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Nodal
cells
and
Purkinje
cells
provide
synchronization through three key characteristics:
● Automaticity: Ability to initiate an electrical
impulse.
● Excitability: Ability to respond to an
electrical impulse.
● Conductivity: Ability to transmit an electrical
impulse from one cell to another.
KEY COMPONENTS OF CARDIAC CONDUCTION
SYSTEM
SINOATRIAL (SA) NODE
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Primary pacemaker of the heart.
Located at the junction of the superior vena cava
and the right atrium.
Inherent firing rate: 60 to 100 impulses per minute;
rate adjusts based on metabolic demands.
ATRIOVENTRICULAR (AV) NODE
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Secondary pacemaker of the heart.
Located in the right atrial wall near the tricuspid
valve.
Coordinates incoming electrical impulses from the
atria and relays them to the ventricles after a slight
delay, allowing for ventricular filling.
RESTING STATE
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CELLULAR SIMULATION
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CONDUCTION PATHWAY
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Impulse conduction begins with the bundle of His,
which divides into:
Right bundle branch: Conducts impulses to the
right ventricle.
Left bundle branch: Conducts impulses to the left
ventricle; further divides into:
○ Left anterior bundle branch.
○ Left posterior bundle branch.
Impulses travel through the Purkinje fibers,
composed of Purkinje cells, which rapidly conduct
impulses
throughout
the
ventricular walls,
stimulating contraction.
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Heart rate is determined by the myocardial cells with
the fastest inherent firing rate:
SA node: 60 to 100 impulses per minute (highest).
AV node: 40 to 60 impulses per minute (second
highest).
Ventricular pacemaker sites: 30 to 40 impulses per
minute (lowest).
If the SA node malfunctions, the AV node typically
takes over as pacemaker at its inherently lower rate.
If both the SA and AV nodes fail, a pacemaker site in
the ventricle will fire at a bradycardic rate of 30 to 40
impulses per minute.
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Nodal and Purkinje cells (electrical cells) generate
and transmit impulses, stimulating cardiac myocytes
(working cells) to contract.
MECHANISM OF ACTION
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Stimulation of myocytes occurs due to the exchange
of electrically charged particles, called ions, across
channels in the cell membrane.
The channels regulate the movement and speed of
specific ions:
○ Sodium (Na⁺): Rapidly enters the cell
through sodium-fast channels.
○ Calcium (Ca²⁺): Enters the cell through
calcium-slow channels.
○ Potassium (K⁺): Primarily found inside the
cell in the resting state.
BSN 3-4
JOSHUA ALLAN G. ARELLANO, SN
Once depolarization is complete, the exchange of
ions reverts to its resting state:
○ This period is known as repolarization.
CARDIAC ACTION POTENTIAL CYCLE
CARDIAC ACTION POTENTIAL CYCLE
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CARDIAC ACTION POTENTIAL
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During cellular stimulation:
○ Sodium or calcium crosses the cell
membrane into the cell.
○ Potassium ions exit into the extracellular
space.
○ This exchange creates a positively charged
intracellular space and a negatively
charged extracellular space, characterizing
depolarization.
RECOVERY PHASE
HEART RATE REGULATION
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In the resting (polarized) state:
○ Sodium is the primary extracellular ion.
○ Potassium is the primary intracellular ion.
○ The inside of the cell has a negative charge
compared to the positive charge on the
outside.
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The repeated cycle of depolarization and
repolarization is called the cardiac action potential.
Phase 0:
○ Cellular depolarization is initiated as positive
ions influx into the cell.
○ During this phase, the atrial and ventricular
myocytes rapidly depolarize as sodium
moves into the cells through sodiumfast
channels.
○ The myocytes have a fast-response action
potential. In contrast, the cells of the SA and
AV node depolarize when calcium enters
these cells through calcium-slow channels.
○ These cells have a slow-response action
potential.
Phase 1: Early cellular repolarization begins during
this phase as potassium exits the intracellular space.
Phase 2: This phase is called the plateau phase
because the rate of repolarization slows. Calcium ions
enter the intracellular space.
Phase 3: This phase marks the completion of
repolarization and return of the cell to its resting state.
Phase 4: This phase is considered the resting phase
before the next depolarization.
MAJOR EVENT IN CARDIAC CYCLE
1.
2.
REFRACTORY PERIOD
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Myocardial cells must completely repolarize before
they can depolarize again.
During the repolarization process, the cells are in a
refractory period, which has two phases:
PHASES OF REFRACTORY PERIOD
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2.
3.
Effective (Absolute) Refractory Period:
○ The cell is completely unresponsive to any
electrical stimulus.
○ Incapable of initiating an early
depolarization.
○ Corresponds with the time from phase 0 to
the middle of phase 3 of the action potential.
Relative Refractory Period:
○ Corresponds with the short time at the end
of phase 3.
○ During this period, if an electrical stimulus is
stronger than normal, the cell may
depolarize prematurely.
IMPLICATION OF EARLY DEPOLARIZATION
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Early depolarizations of the atrium or ventricle can
cause premature contractions, increasing the risk
for arrhythmias.
Premature Ventricular Contractions (PVCs):
○ PVCs are concerning, especially in the
presence of myocardial ischemia.
○ Early ventricular depolarizations can trigger
life-threatening arrhythmias such as:
■ Ventricular tachycardia
■ Ventricular fibrillation
CARDIAC HEMODYNAMICS
HEMODYNAMIC MONITORING
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Cardiac Cycle: Refers to the events that occur in the
heart from the beginning of one heartbeat to the next.
The number of cardiac cycles completed in a minute
depends on the heart rate.
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BSN 3-4
JOSHUA ALLAN G. ARELLANO, SN
Chamber pressures can be measured using special
monitoring catheters and equipment, a technique
known as hemodynamic monitoring.
Methods of hemodynamic monitoring are covered in
more detail later in the chapter.
CARDIAC OUTPUT
CARDIAC CYCLE
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Diastole:
○ All four heart chambers are relaxed.
○ AV valves are open; semilunar valves are
closed.
○ Pressures in all chambers are at their
lowest, facilitating ventricular filling.
○ Venous blood returns to:
■ Right atrium from the superior
and inferior vena cava.
■ Right ventricle.
■ Left atrium from the lungs via the
four pulmonary veins into the left
ventricle.
Atrial Systole:
○ Occurs toward the end of diastole as the
atrial muscles contract in response to an
electrical impulse from the SA node.
○ Increases pressure inside the atria, ejecting
the remaining blood into the ventricles.
○ Augments ventricular blood volume by
15% to 25%, sometimes referred to as the
atrial kick.
Ventricular Systole:
○ Begins in response to the electrical impulse
propagated from the SA node.
○ Pressure inside the ventricles rapidly
increases, forcing the AV valves to close.
○ Prevents regurgitation (backflow) of blood
into the atria.
○ Increased pressure forces the pulmonic and
aortic valves to open, ejecting blood into:
■ Pulmonary artery (right ventricle).
■ Aorta (left ventricle).
○ Blood exit is initially rapid; flow gradually
decreases as pressures equalize.
○ At the end of systole, pressures in the
ventricles rapidly decrease, leading to
closure of the semilunar valves.
○ Marks the onset of diastole, and the cycle
repeats.
Cardiac Output:
○ Refers to the total amount of blood ejected
by one of the ventricles in liters per minute.
○ In a resting adult, cardiac output is typically 4
to 6 L/min.
○ Varies greatly depending on the metabolic
needs of the body.
Calculation of Cardiac Output
○ Formula:
○ Cardiac Output = Stroke Volume × Heart
Rate.
Stroke Volume
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Defined as the amount of blood ejected from
one of the ventricles per heartbeat.
The average resting stroke volume is
approximately 60 to 130 mL.
EFFECT OF HEART RATE IN CARDIAC OUTPUT
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Cardiac Output Response:
○ Cardiac output adjusts to changes in the
metabolic demands of tissues due to:
■ Stress
■ Physical exercise
■ Illness
○ Enhanced by increases in both stroke
volume and heart rate.
■
EFFECT OF STROKE VOLUME ON CARDIAC
OUTPUT
Stroke volume is primarily determined by three factors:
1. Preload
2. Afterload
3. Contractility
PRELOAD
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REGULATION OF HEART RATE
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Changes in heart rate result from inhibition or
stimulation of the SA node, mediated by:
○ Parasympathetic Nervous System:
■ Branches travel to the SA node via
the vagus nerve.
■ Stimulation of the vagus nerve
slows the heart rate.
○ Sympathetic Nervous System:
■ Increases heart rate by innervating
beta-1 receptor sites in the SA
node.
■ Increases heart rate through:
■ Elevated levels of
circulating
catecholamines (secreted
by the adrenal gland).
■ Excess thyroid hormone,
which has a
catecholamine-like effect.
Baroreceptors:
○ Specialized nerve cells located in the aortic
arch and both right and left internal
carotid arteries (at the bifurcation from the
common carotid arteries).
○ Sensitive to changes in blood pressure
(BP).
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RESPONSE TO BLOOD PRESSURE CHANGES
1.
2.
Hypertension (High BP):
○ Increased baroreceptor discharge.
○ Transmits impulses to the cerebral medulla.
○ Initiates parasympathetic activity and
inhibits sympathetic response.
○ Results in:
■ Lowered heart rate.
■ Decreased blood pressure.
Hypotension (Low BP):
○ Decreased baroreceptor stimulation.
○ Prompts a decrease in parasympathetic
activity and enhances sympathetic
responses.
○ Results in:
■ Elevated blood pressure through
vasoconstriction.
BSN 3-4
JOSHUA ALLAN G. ARELLANO, SN
Definition: The degree of stretch of the ventricular
cardiac muscle fibers at the end of diastole.
Characteristics:
○ Highest filling volume in the ventricles leads
to the greatest stretch.
○ Preload is commonly referred to as left
ventricular end-diastolic pressure.
○ Frank–Starling Law:
■ Greater initial stretch of sarcomeres
(cardiac muscle cells) leads to a
greater degree of shortening.
■ Increased blood volume returning to
the heart increases preload,
resulting in stronger contractions
and greater stroke volume.
○ Factors Reducing Preload:
■ Diuresis, venodilating agents (e.g.,
nitrates), excessive blood loss,
dehydration (due to vomiting,
diarrhea, or diaphoresis).
○ Factors Increasing Preload:
■ Blood volume replacement (e.g.,
blood transfusions, intravenous
fluids).
AFTERLOAD
BARORECEPTOR ACTIVITY
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Increased heart rate.
Definition: Resistance to the ejection of blood from
the ventricle.
Characteristics:
○ Systemic Vascular Resistance: Resistance
of systemic blood pressure to left ventricular
ejection.
○ Pulmonary Vascular Resistance:
Resistance of pulmonary blood pressure to
right ventricular ejection.
○ Relationship with Stroke Volume:
■ Inverse relationship; increased
afterload decreases stroke volume.
■ Increased by arterial
vasoconstriction; decreased by
arterial vasodilation.
CONTRACTILITY
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Definition: The force generated by the contracting
myocardium.
Characteristics:
○ Enhanced By: Circulating catecholamines,
sympathetic neuronal activity, certain
medications (e.g., digoxin, dopamine,
dobutamine).
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Depressed By: Hypoxemia, acidosis, certain
medications (e.g., beta-adrenergic blockers
like metoprolol).
Increased contractility leads to increased
stroke volume.
STROKE VOLUME MECHANICS
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The heart can increase stroke volume during exercise
by:
○ Increasing preload through increased
venous return.
○ Increasing contractility via sympathetic
nervous system activation.
○ Decreasing afterload through peripheral
vasodilation and decreased aortic pressure.
EJECTION FRACTION
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Definition: The percentage of end-diastolic blood
volume ejected with each heartbeat.
Normal Range:
○ Left Ventricular Ejection Fraction: 55% to
65%.
○ Right Ventricular Ejection Fraction: Rarely
measured.
Clinical Significance:
○ Used as a measure of myocardial
contractility.
○ An ejection fraction of less than 40%
indicates decreased left ventricular function
and may require treatment for heart failure
(HF).
BSN 3-4
JOSHUA ALLAN G. ARELLANO, SN