CARDIOVASCULAR SYSTEM

HEART

Rubina Shoukat
 INTRODUCTION

• 4 chambers
• Atrium and Ventricles
• Right side deliver blood to lungs, left to systemic circulation
• Two layered protective sac called pericardium
• Special mechanisms in the heart cause a continuing succession of
contractions called cardiac rhythmicity, transmitting action
potentials throughout the cardiac muscle to cause the heart’s
rhythmical beat.
 LAYERS OF HEART WALL

• The wall of the heart consists of three layers: the epicardium (external
layer), the myocardium (middle layer), and the endocardium (inner
layer).
• The epicardium is composed of two tissue layers. The epicardium
contains blood vessels, lymphatics, and vessels that supply the
myocardium.
• The middle myocardium is responsible for the pumping action of the
heart and is composed of cardiac muscle tissue.
• The innermost endocardium is a thin layer of endothelium overlying a
thin layer of connective tissue. The smooth endothelial lining
minimizes the surface friction as blood passes through the heart.
 CHAMBERS OF THE HEART

• The heart has four chambers.

• The two superior receiving chambers are the atria and the two
inferior pumping chambers are the ventricles.
• The paired atria receive blood from blood vessels returning blood
to the heart, called veins, while the ventricles eject the blood from
the heart into blood vessels called arteries.
• On the anterior surface of each atrium is a wrinkled pouch like
structure called an auricle.
• Also on the surface of the heart are a series of grooves, called
sulci , that contain coronary blood vessels and a variable amount
of fat.
• The anterior interventricular sulcus that marks the external boundary between
the right and left ventricles on the anterior aspect of the heart.
• This sulcus continues the posterior interventricular sulcus, which marks the
external boundary between the ventricles on the posterior aspect of the heart.
SYSTEMIC AND PULMONARY CIRCULATIONS
 CORONARY CIRCULATION

• Nutrients are not able to diffuse quickly enough from blood in the chambers of
the heart to supply all layers of cells that make up the heart wall.
• For this reason, the myocardium has its own network of blood vessels, the
coronary circulation or cardiac circulation.
• The coronary arteries branch from the ascending aorta and encircle the heart
like a crown encircles the head.
• While the heart is contracting, little blood flows in the coronary arteries
because they are squeezed shut.
• When the heart relaxes, however, the high pressure of blood in the aorta
propels blood through the coronary arteries, into capillaries, and then into
coronary veins.
 CORONARY ARTERIES

• Left Coronary Artery Pathway:

• The left coronary artery passes inferior to the left auricle and divides into two main
branches:
• Anterior Interventricular Branch (LAD Artery):
• Supplies oxygenated blood to the walls of both ventricles.
• Circumflex Branch:
• Distributes oxygenated blood to the walls of the left ventricle and left atrium.
• Right Coronary Artery Pathway:
• The right coronary artery supplies small branches (atrial branches) to the right atrium.
• It continues inferior to the right auricle and divides into two main branches:
• Posterior Interventricular Branch:
• Supplies the walls of both ventricles.
• Marginal branch: (the walls of right ventricles)
 CORONARY VEINS

• Most of the deoxygenated blood from the myocardium drains into a

large vascular sinus in the coronary sulcus on the posterior surface
of the heart, called the coronary sinus.
• The deoxygenated blood in the coronary sinus empties into the right
atrium.
• Principal Tributaries to Coronary Sinus:
• Great Cardiac Vein
• Middle Cardiac Vein:
• Small Cardiac Vein:
• Anterior Cardiac Veins:
 HISTOLOGY OF CARDIAC MUSCLE TISSUE

• A typical cardiac muscle fiber is 50–100 𝜇m long and has a diameter

of about 14 𝜇m.
• The ends of cardiac muscle fibers connect to neighboring fibers by
irregular transverse thickenings of the sarcolemma called
intercalated discs.
• The discs contain desmosomes, which hold the fibers together, and
gap junctions, which allow muscle action potentials to conduct
from one muscle fiber to its neighbors.
• Mitochondria are larger and more numerous in cardiac muscle fibers
than in skeletal muscle fibers. they take up 25% of the cytosolic
space.
 AUTORHYTHMIC FIBERS: THE CONDUCTION
SYSTEM

• The source of this electrical activity is a network of specialized

cardiac muscle fibers called autorhythmic fibers because they
are self-excitable.
• These relatively rare fibers have two important functions:
• They act as a pacemaker,
• They form the cardiac conduction system.
• Cardiac action potentials propagate through the conduction system in the
following sequence.
• Cardiac excitation normally begins in the sinoatrial (SA) node, located
in the right atrial wall just inferior and lateral to the opening of the
superior vena cava. SA node cells do not have a stable resting potential.
Rather, they repeatedly depolarize to threshold spontaneously. The
spontaneous depolarization is a pacemaker potential.
• By conducting along atrial muscle fibers, the action potential reaches the
atrioventricular (AV) node, located in the interatrial septum, just
anterior to the opening of the coronary sinus.
• From the AV node, the action potential enters the atrioventricular (AV)
bundle.
• After propagating through the AV bundle, the action potential enters both
the right and left bundle branches. The bundle branches extend through
the interventricular septum toward the apex of the heart.
• Finally, the large-diameter Purkinje fibers rapidly conduct the action
potential beginning at the apex of the heart upward to the remainder of
the ventricular myocardium. Then the ventricles contract, pushing the
blood upward toward the semilunar valves.
ACTION POTENTIAL AND CONTRACTION OF
CONTRACTILE FIBERS
 ELECTROCARDIOGRAM

• As action potentials propagate through the

heart, they generate electrical currents that
can be detected at the surface of the body.
• An electrocardiogram ,abbreviated either
ECG or EKG is a recording of these
electrical signals.
• The ECG is a composite record of action
potentials produced by all of the heart
muscle fibers during each heartbeat.
• The first, called the P wave, is a small upward deflection on the ECG. The P
wave represents atrial depolarization, which spreads from the SA node
through contractile fibers in both atria.
• The second wave, called the QRS complex, begins as a downward deflection,
continues as a large, upright, triangular wave, and ends as a downward wave.
• The QRS complex represents rapid ventricular depolarization, as the
action potential spreads through ventricular contractile fibers.
• The third wave is a dome-shaped upward deflection called the T wave. It
indicates ventricular repolarization and occurs just as the ventricles are
starting to relax. The T wave is smaller and wider than the QRS complex
because repolarization occurs more slowly than depolarization.
• During the plateau period of steady depolarization, the ECG tracing is flat.
• In reading an ECG, the size of the waves can provide clues to abnormalities.
• Larger P waves indicate enlargement of an atrium; an enlarged Q wave may
indicate a myocardial infarction; and an enlarged R wave generally indicates
enlarged ventricles.
• The T wave is flatter than normal when the heart muscle is receiving insuff
icient oxygen—as, for example, in coronary artery disease. The T wave may
be elevated in hyperkalemia (high blood K+ level).
 THE CARDIAC CYCLE

• Atrial Systole
• During atrial systole, which lasts about 0.1 sec, the atria are contracting. At the same
time, the ventricles are relaxed.
• Depolarization of the SA node causes atrial depolarization, marked by the P wave in the
ECG.
• Atrial depolarization causes atrial systole. As the atria contract, they exert pressure on
the blood within, which forces blood through the open AV valves into the ventricles.
• Atrial systole contributes a final 25 mL of blood to the volume already in each ventricle
(about 105 mL). The end of atrial systole is also the end of ventricular diastole
(relaxation). Thus, each ventricle contains about 130 mL at the end of its relaxation
period (diastole). This blood volume is called the end-diastolic volume (EDV).
• The QRS complex in the ECG marks the onset of ventricular depolarization.
• Ventricular Systole
• During ventricular systole, which lasts about 0.3 sec, the ventricles are contracting.
At the same time, the atria are relaxed in atrial diastole.
• Ventricular depolarization causes ventricular systole. As ventricular systole begins,
pressure rises inside the ventricles and pushes blood up against the atrioventricular
(AV) valves, forcing them shut.
• Continued contraction of the ventricles causes pressure inside the chambers to rise
sharply. At this point, ejection of blood from the heart begins. The period when the
SL valves are open is ventricular ejection and lasts for about 0.25 sec. The pressure
in the left ventricle continues to rise to about 120 mmHg, and the pressure in the
right ventricle climbs to about 25–30 mmHg.
• The left ventricle ejects about 70 mL of blood into the aorta and the right ventricle
ejects the same volume of blood into the pulmonary trunk. The volume remaining in
each ventricle at the end of systole, about 60 mL, is the end-systolic volume (ESV).
Relaxation Period
• Ventricular repolarization causes ventricular diastole. As the ventricles relax,
pressure within the chambers falls, and blood in the aorta and pulmonary
trunk begins to flow backward toward the regions of lower pressure in the
ventricles. Backflowing blood catches in the valve cusps and closes the SL
valves. After the SL valves close, there is a brief interval when ventricular
blood volume does not change because all four valves are closed. This is the
period of isovolumetric relaxation.
• As the ventricles continue to relax, the pressure falls quickly. When
ventricular pressure drops below atrial pressure, the AV valves open, and
ventricular filling begins. The major part of ventricular filling occurs just after
the AV valves open.
 HEART SOUNDS

• The first sound (S1), which can be described as a lubb sound, is louder and a
bit longer than the second sound.
• S1 is caused by blood turbulence associated with closure of the AV valves
soon after ventricular systole begins.
• The second sound (S2), which is shorter and not as loud as the first, can be
described as a dupp sound. S2 is caused by blood turbulence associated with
closure of the SL valves at the beginning of ventricular diastole.
• S3 is due to blood turbulence during rapid ventricular filling, and S4 is due to
blood turbulence during atrial systole.
 CARDIAC OUTPUT

• Cardiac output (CO) is the volume of blood ejected from the left
ventricle (or the right ventricle) into the aorta (or pulmonary trunk) each
minute.
• Cardiac output equals the stroke volume (SV), the volume of blood ejected
by the ventricle during each contraction, multiplied by the heart rate (HR),
the number of heartbeats per minute.
• Cardiac reserve is the difference between a person’s maximum cardiac
output and cardiac output at rest. The average person has a cardiac reserve
of four or five times the resting value.
 REGULATION OF STROKE VOLUME

• At rest, the stroke volume is 50–60% of the end-diastolic volume

because 40–50% of the blood remains in the ventricles after each
contraction (end-systolic volume).
• Three factors regulate stroke volume and ensure that the left and
right ventricles pump equal volumes of blood:
• Preload, the degree of stretch on the heart before it contracts;
• Contractility, the forcefulness of contraction of individual
ventricular muscle fibers; and
• Afterload, the pressure that must be exceeded before ejection of
blood from the ventricles can occur.
 PRELOAD: EFFECT OF STRETCHING

• A greater preload (stretch) on cardiac muscle fibers prior to contraction

increases their force of contraction.
• Within limits, the more the heart fills with blood during diastole, the
greater the force of contraction during systole. This relationship is known
as the Frank–Starling law of the heart.
• The preload is proportional to the end-diastolic volume (EDV). Normally,
the greater the EDV, the more forceful the next contraction.
• Two key factors determine EDV: (1) the duration of ventricular diastole
and (2) venous return, the volume of blood returning to the right ventricle.
• When heart rate increases, the duration of diastole is shorter. Less filling
time means a smaller EDV, and the ventricles may contract before they are
adequately filled.
• By contrast, when venous return increases, a greater volume of blood flows
into the ventricles, and the EDV is increased.
• When heart rate exceeds about 160 beats/min, stroke volume usually
declines due to the short filling time. At such rapid heart rates, EDV is less,
and the preload is lower.
• People who have slow resting heart rates usually have large resting stroke
volumes because filling time is prolonged and preload is large.
 CONTRACTILITY

• The second factor that influences stroke volume is myocardial

contractility, the strength of contraction at any given preload.
• Substances that increase contractility are positive inotropic agents.
• Those that decrease contractility are negative inotropic agents.
• Thus, for a constant preload, the stroke volume increases when a
positive inotropic substance is present.
 AFTER LOAD

• Ejection of blood from the heart begins when pressure in the right
ventricle exceeds the pressure in the pulmonary trunk (about 20
mmHg), and when the pressure in the left ventricle exceeds the
pressure in the aorta (about 80 mmHg).
• At that point, the higher pressure in the ventricles causes blood to
push the semilunar valves open.
• The pressure that must be overcome before a semilunar valve can
open is termed the afterload.
• An increase in afterload causes stroke volume to decrease, so that
more blood remains in the ventricles at the end of systole.
 REGULATION OF HEART RATE

Autonomic Regulation of Heart Rate

• Sympathetic neurons extend from the medulla oblongata into the
spinal cord. From the thoracic region of the spinal cord,
sympathetic cardiac accelerator nerves extend out to the SA
node, AV node, and most portions of the myocardium.
• Parasympathetic nerve impulses reach the heart via the right and
left vagus (X) nerves. Vagal axons terminate in the SA node, AV
node, and atrial myocardium. They release acetylcholine, which
decreases heart rate by slowing the rate of spontaneous
depolarization in autorhythmic fibers.
 CHEMICAL REGULATION OF HEART RATE

Hormones
• Epinephrine and norepinephrine enhance the heart’s pumping
effectiveness. Thyroid hormones also enhance cardiac
contractility and increase heart rate. One sign of hyperthyroidism
is tachycardia.
Cations
• In particular, the relative concentrations of three cations—K+,
Ca2+, and Na+— have a large eff ect on cardiac function.