CVS Physiology mecical physiology le .pdf

◼ The blood circulates in a closed system
called the cardiovascular system (CVS),
which consists of the heart and blood
vessels.
◼ The heart is a muscular organ divided
into right and left sides. Each side is
formed of two chambers (atrium and
ventricle).

◼ The wall of the heart is formed of
cardiac muscle (myocardium).
◼ The atrial myocardium is thinner
that of the ventricles.
◼ The atria act mainly as blood
reservoirs, while the ventricles act
mainly as pumping chambers.

◼There are 4 valves in the heart:
◼a) Two valves called
atrioventricular valves (A-V
valves), one between right atrium
(RA) and right ventricle (RV) called
tricuspid valve, the other between
left atrium (LA) and left ventricle (LV)
called mitral valve.

◼b)Two semilunar valves, the
aortic valve between LV and
aorta, the pulmonary valve
between RV and pulmonary
artery.

◼Division of circulation:
◼ 1- The systemic (greater) circulation:
◼ This starts from the left ventricle→
aorta → large arteries→ small
arteries→ arterioles→ capillaries→
venules→ veins→ superior and inferior
venae cavae→ right atrium.

◼2-The pulmonary (lesser)
circulation:
◼It starts from the right
ventricle→ pulmonary artery→
lungs→ pulmonary capillaries→
4 pulmonary veins → left atrium.

◼3-The special circulations:
◼These include the circulations
at specific sites e.g. the
capillary, venous, lymph,
coronary and cerebral
circulations.

◼Characteristic of the different
blood vessels:
◼ 1- The aorta, pulmonary artery and
large arteries are elastic vessels.
◼ 2- The medium- size and small
arteries are muscular low- resistance
vessels.

◼3- The arterioles are muscular
high- resistance vessels.
◼4- The capillaries are exchange
vessels.
◼5- The veins and pulmonary
vessels are volume reservoir.

◼Functions of the heart:
◼a)Function of the ventricles:
The only function of ventricles is
pumping of the blood into large
artery (LV→ aorta and RV →
pulmonary).

◼Function of the atria:
◼ 1- They are the entry- ways to the
ventricles.
◼ 2- Booster pump action.
◼ 2- The atrial walls contain stretch
receptors.
◼ 3- The atrial cells secrete the atrial
natriuretic peptide (ANP).

◼The cardiac muscle fibers
◼ There 3 types of cardiac muscle fibers:
◼ 1- The contractile cardiac muscle
fibers (99 %).
◼ These form the atrial and ventricular walls.
◼ They contain actin and myosin filaments.
◼ They perform the mechanical work of
pumping.

◼2-The nodal conducting
fibers.
◼They are modified cardiac
muscle fibers present in both
the sinoatrial and
atrioventricular nodes.

◼They contain more sarcoplasm
and very little myofibrils.
◼The nodal muscle fibers are
smaller than the contractile
fibers and are poor in gap
junctions.

◼ 3- The purkinje conducting fibers.
◼ They are modified cardiac muscle
fibers present in the His purkinje
system.
◼ They contain more sarcoplasm and
very little myofibrils.
◼ The fibers are larger than the
contractile fibers and are rich in gap
junctions

◼The nodal and the purkinje
conducting fibers form the
conduction system of the heart.
◼They do not contract, but are
specialized for initiation and
conduction of the impulses.

◼Nerve supply to the heart:
◼The heart receives
autonomic nerve supply
(sympathetic and
parasympathetic).

◼The fuel of the heart
◼ The heart is characterized by its ability to
oxidize several types of fuel substances.
◼ The major substances for the heart during
rest are the free fatty acids, glucose
and lactate.
◼ During muscular exercise the main
substrate becomes the lactate.

◼The cardiac conduction system:
This consists of the following:
◼1- The nodal system: this includes 2
nodes present in the right atrium
◼ a- The sinoatrial node (SAN).
◼ b- The atrioventricular node (AVN).

◼2-The internodal system: This
consists of 3 bundles called
the anterior, middle and
posterior internodal bundles
found in the right atrial wall.

◼3- The purkinje system:
This consists of 3 components:
◼ a- The atrioventricular bundle
(bundle of His).
◼ b- The right and left bundle
branches.
◼ c- The purkinje fibers.

◼ This is the lateral pressure exerted
by the blood on the arterial walls.
◼It is generated by:
◼ 1- Pumping of the blood by the
ventricle into the aorta.
◼ 2- Presence of the peripheral
resistance to blood flow.

◼The systolic B.P:
◼Normally averages 120 mmHg
(range 90 -140 mmHg) and is
produced by ejection of blood
into the aorta during left
ventricular systole.

◼The diastolic B.P:
◼ Normally averages 80 mmHg (range 60 -
90 mmHg) and is produced as result of
the elastic recoil of the aorta during
ventricular diastole.
◼ The arterial B.P is often reported as
the systolic over the diastolic
pressure (e.g. 120/80).

◼The function of the arterial
blood pressure:
◼ 1- It maintains tissue perfusion
(blood flow) throughout different
tissues.
◼ 2- It produces the capillary
hydrostatic pressure.

◼3-The diastolic B.P performs
the following functions:
◼ a) It maintains blood flow to the tissues
during ventricular diastole.
◼ b) It is essential for normal coronary
blood flow.
◼ c) It prevents blood stasis in the arteries
during ventricular diastole.

◼Physiological factors that
affect the arterial B.P:
◼ 1- Body region.
◼ 2- Age.
◼ 3- Sex.
◼ 4- Body built.
◼ 5- Diurnal variation.

◼6- Meals.
◼7- Exercise.
◼8- Emotion.
◼9- Sexual intercourse.
◼10-Sleep.
◼11-Temperature.

◼Factors that determine and
maintain A.B.P:
◼1-Cardiac output (CO):
◼ It is the amount of blood pumped by
each ventricle per minute.
◼2-Peripheral resistance (PR):
it is determined by 3 factors:

◼ a) The diameter of the vessels.
◼ b) Blood viscosity.
◼ c) The length of the vessels.
◼3- Elasticity of the aorta and
large arteries.
◼4- Blood volume and circulatory
capacity.

A) Short- term mechanisms:
◼ These are potent mechanisms that
maintain survival. They act within a
few seconds and their action lasts for
several hours. They are mostly
nervous reflexes and include the
following:

◼(1)Arterial baroreflexes
(pressure buffer system):
◼ The receptors of these reflexes are located in
the carotid sinus and aortic arch.
◼ Arterial B.P. increases →stimulation of the
CIC and VDC and inhibition of the
VCC this results in reduction of the arterial
B.P by decreasing:

◼ (a) The cardiac pumping power
and CO (through causing
bradycardia)
◼ (b) The peripheral resistance
(through producing V.D. in both
the arterioles and venules)
◼ (c) Catecholamine secretion from
the adrenal medullae.

◼(2) Arterial chemoreflexes:
◼ The receptors of these reflexes are
located in the carotid and aortic
bodies and they are stimulated
when the arterial B.P. is reduced
below 60 mmHg (mainly as a result
of local ischaemia and hypoxia).

◼Arterial B.P. decreases
→stimulation of the VCC and
inhibition of the CIC and
VDC this results in elevation
of the arterial B.P by
increasing:

◼ (a) The cardiac pumping power and CO
(through causing tachycardia)
◼ (b) The peripheral resistance (through
producing V.C. in both the arterioles
and venules)
◼ (c) Catecholamine secretion from the
adrenal medullae.

◼3- The CNS ischaemic response:
◼Reduction of ABP below 60 mmHg
→ brain ischaemia → local
hypoxia → stimulation of the VCC
→ generalizes VC → ↑ ABP and
maintains the cerebral blood flow.

◼4-The abdominal compression
reflex:
◼ When the VCC is stimulated →
contraction of abdominal muscles → ↑
intra-abdominal pressure →
compresses the abdominal veins → ↑
venous return → ↑ cardiac output → ↑
ABP.

◼B) intermediate- term
mechanisms:
◼ They act within a few minutes and
their action lasts for several days.
◼ During this time, the nervous (rapid)
mechanisms usually fatigue and
become less effective. They include
the following:

◼1-Capillary fluid shift
mechanism:
◼Increases in the blood volume →
↑ capillary hydrostatic pressure →
↑ fluid filtration into tissue spaces
→ ↓ blood volume → ↓ ABP.

◼2- Stress relaxation mechanism:
◼↑ ABP → stretches the arteries
and increases the tension in their
walls → after sometime, the
arteries relax and tension in
their decreases → ↓ ABP.

◼ 3- Renin - angiotensin mechanism:
◼ ↓ ABP → renal ischaemia →
stimulates secretion of renin →
convert the angiotensinogen to
angiotensin I which converted to
angiotensin II by angiotensin-
converting enzyme → VC effect → ↑
ABP.

◼4-Right atrial mechanism:
◼ Increases in the blood volume →
stimulates the volume receptors in the
right atrium → following effects:
◼ a) Generalized VD.
◼ b) Reflex inhibition of secretion of
antidiuretic hormone.
◼ c) Secretion of atrial natriuretic
peptide (ANP).

◼C) long- term mechanisms:
◼ These mechanisms control the ABP by
adjusting the body fluids and blood
volume through modifying the
excretion of water and salt by the
kidneys. This occurs by:
◼ 1- Glomerular filtration.
◼ 2- Secretion of the aldosterone
hormone.

◼ ↓ ABP → ↓ glomerular filtration →
↓ renal excretion of water and salt
→ ↑ body fluid and blood volume
→ ↑ ABP.
◼ At the same time, renin is secreted
and angiotensin II is formed → VC
and stimulates aldosterone
secretion.

◼The electrocardiogram is a record of
the electrical activity of the heart from
the surface of the body.
◼ It is produced by the sum of all action
potentials occurring in the cardiac
muscle fibers with each cardiac cycle.

◼The ECG is useful for the
diagnosis of:
◼ 1- Atrial and ventricular hypertrophy.
◼ 2- Myocardial infarction and ischaemia.
◼ 3- Arrhythmias.
◼ 4- Disturbances of electrolyte metabolism.
◼ 5- Drugs effect (digitalis).
◼ 6- Pericarditis.

◼Recording points on the body
surface:
◼There are nine standard points on
the body surface from which the
ECG should be recorded.
◼Six points are on the chest wall and the
other three points are at the limbs.

◼Chest points:
◼V1: at the right 4 intercostal
space near the sternum.
◼V2: at the left 4 intercostal
space near the sternum.
◼V3: midway between V2 and V4.

◼V4: at the 5 left intercostal space at
the midclavicular line.
◼V5: at the 5 left intercostal space
at the anterior axillary line.
◼V6: at the 5 left intercostal space
at the midaxillary line.

◼Limb points:
◼VL: at the junction of the left
arm with the trunk.
◼VR: at the junction of the right
arm with the trunk.
◼VF: at the junction of the left
lower limb with the trunk.

◼The ECG leads:
◼There are 3 types of leads:
◼Unipolar leads: (chest leads and
limb leads)
◼Bipolar leads: (LI, LII and LIII)
◼Augmented leads: (aVL, aVR and
aVF)

◼ The ECG consists of 5 main waves
called P, Q, R, S, T and sometimes
U wave.
◼ The Q, R and S waves form a
complex called the QRS complex.
◼ The termination of the QRS
complex at the isoelectric line is
called the J point.

◼P wave
◼ This is a small blunt wave that is
produced as a result of atrial
depolarization.
◼ Its amplitude averages 0.1(up to
0.25) mV while its duration averages
0.08 (up to o.11) seconds.

◼It is +ve in the leads that face
the LV.
◼The first part of the wave is
due to RA activation while
its terminal part is due to LA
activation.

◼ Abnormalities of the P wave
◼ In the LA hypertrophy → P mitrale
(broad and notched) and their duration
increases.
◼ In the RA hypertrophy → P pulmonale (tall
and peaked) with less normal duration.
◼ In AV nodal rhythm → inverted P wave.
◼ In atrial fibrillation → disappear of P wave.

◼QRS complex
◼ This is produced as a result of
ventricular depolarization and its
duration is 0.06 - 0.1 second.
◼ The Q wave is due to depolarization
of interventricular septum and it is
normally –ve in the leads facing the
LV.

◼ The R wave is due to depolarization
of the apex and ventricular wall and
it is +ve in the leads facing the LV.
◼ The S wave is due to depolarization
of the posterobasal part of the LV
and the pulmonary conus and it is -ve
in the leads facing the LV.

◼Abnormalities of the QRS
complex:
◼ These occur in cases of:
◼ 1- Ventricular hypertrophy.
◼ 2- Myocardial infarction.
◼ 3- Bundle branch block.
◼ 4- Electrolyte disturbances.

◼T wave
◼ This is a large blunt wave that is
produced as a result of ventricular
repolarization.
◼ Its amplitude averages 0.2 (up to 0.4)
mV, while its duration averages 0.2 (up
to 0.25) second.
◼ It is normally +ve in the leads facing the
LV.

◼Abnormalities of the T wave
◼The T wave becomes inverted in
cases of:
◼ 1- Myocardial ischaemia.
◼ 2- Ventricular hypertrophy.
◼ 3- Bundle branch block.
◼ 4- Digitalis over dosage.

◼The T wave amplitude
increases in cases of:
◼1-Sympathetic over activity.
◼2-Muscular exercise.
◼3-Hyperkalemia.

◼U wave
◼This is a small +ve wave that
sometimes follows the T wave.
◼It is due to slow repolarization of
either the papillary muscles or
the purkinje network.

◼ECG segments:
◼An ECG segment is part of
the ECG record on the
isoelectric line between 2
waves.

◼P-R segment:
◼ It is the segment of the ECG from the
end of P wave to the start of the QRS
complex.
◼ Normal duration is 0.04- 0.13 second.
◼ During this segment, the atria are
completely depolarized but the
ventricles are completely polarized.

◼S-T segment:
◼ It is the segment of the ECG from
the end of S wave to the start of the
T wave.
◼ Normal duration is 0.12 second.
◼ During this segment, all ventricular
muscle fibers are completely
depolarized.

◼T-P segment:
◼ It is the segment of the ECG from
the end of T wave to the start of the
P wave of the next cycle.
◼ Normal duration is 0.25 second.
◼ During this segment, all atrial and
ventricular muscle fibers are
polarized.

◼ECG intervals
◼An ECG interval is part of
the ECG record that
includes a segment and
one or more waves.

◼P-R interval:
◼ It is the interval on the ECG from the
start of P wave to the start of R wave.
◼ Normal duration is 0.12 – 0.21
second.
◼ It is taken as index for the duration of
the AV nodal delay.

◼It is prolonged in:
◼ 1- First degree of heart block.
◼ 2- Increased vagal tone.
◼It is shortened in:
◼ 1- A-V nodal rhythm.
◼ 2- Sympathetic over activity.
◼ 3- Wolff-Parkinson-White syndrome
(WPW).

◼Q-T interval
◼ It is the interval on the ECG from the
start of Q wave to the end of T wave.
◼ Normal duration is 0.36 – 0.42 second
and it is called the electrical systole of
the heart.
◼ It is taken as index for the duration of
both the ventricular action potential and
refractory period.

◼T-Q interval
◼It is the interval on the ECG from
the end of T wave to the onset of
the next Q wave.
◼Normal duration is 0.4 second
and it is called the electrical
diastole of the heart.

◼It is shortened before atrial
and ventricular extrasystoles
but is prolonged mainly after
ventricular extrasystoles due
to compensatory pause.

◼Axis deviation
◼This occurs if the electric axis of
the heart is beyond the normal
range (between -30 and +110)
and it may be to right or to the
left.

◼Right axis deviation: this occurs in:
◼ 1- Tall thin subjects (normally).
◼ 2- Right ventricular hypertrophy.
◼ 3- Right bundle branch block.
◼ On in ECG, there are deep –ve waves
(S waves) in lead I and high +ve waves
(R waves) in lead III.

◼Left axis deviation: this occurs in:
◼ 1- Short subjects and pregnant women
(normally).
◼ 2- Left ventricular hypertrophy.
◼ 3- Left bundle branch block.
◼ On in ECG, there are high +ve waves
(R waves) in lead I and deep –ve waves
(S waves) in lead III.

◼ECG manifestation of
ventricular hypertrophy
◼1- Right ventricular hypertrophy.
◼2- Left ventricular hypertrophy.

◼ ECG characteristics of coronary
insufficiency:
◼ According to severity, coronary
insufficiency is associated with either:
◼ 1-Ischaemia: (inverted symmetric T wave)
◼ 2- Injury: (S-T segment elevation or
depression).
◼ 3- Necrosis (infarction): deep
(pathological) Q wave.

◼When a coronary artery is
occluded:
◼ 1- Necrosis usually occurs in the centre of
the affected area (deep Q wave).
◼ 2- This is surrounded by area of injury (S-
T segment shift).
◼ 3- This is surrounded by an ischaemic
area (inversion of T wave).

◼The cardiovascular centres:
◼These are collections of neurons
located in the medulla oblongata
which regulate the functions of
the CVS:

◼ 1- The cardioinhibitory centre
(CIC).
◼ 2- The vasomotor centre (VMC):
this includes 2 component:
◼ a- Vasoconstrictor centre (VCC or
pressor area).
◼ b- Vasodilator centre (VDC or
depressor area).

◼ Physiological variation of heart rate:
◼ 1- Age.
◼ 2- Sex.
◼ 3- Time of the day (circadian rhythm).
◼ 4- Rest and sleep.
◼ 5- Physical training.
◼ 6- Posture.

◼Regulation of the heart rate
◼The heart rate refers to the
ventricular rate of beating /
minute.
◼Normally, it averages 75 beats
/minute (60 – 100 b/minute).

◼A heart rate higher than 100
beats/min is called
tachycardia.
◼A heart rate lower than 60
beats/min is called
bradycardia.

◼The frequency of discharge of
the S-A node is regulated by:
◼ 1- Nervous factor.
◼ 2- Chemical factors.
◼ 3- Certain factors that directly affected
the SA node activity.

◼Nervous regulation of the H.R
◼ The activity of these centres is affected by:
◼a-Supraspinal centres:
◼ 1- The cerebral cortex: the HR is
affected by emotions and conditioned
reflexes.
◼ 2- The hypothalamus and limbic
system: these structures are concerned
with emotional reactions.

◼3-The respiratory centre:
◼Respiratory sinus arrhythmia:
this term refers to increase of HR
during inspiration and its
decrease during expiration.
◼The tachycardia that occurs
during inspiration is due to:

◼ a- Irradiation of impulses from the
inspiratory centre which excite the
VCC.
◼ b- Lung inflation through a
pulmonary stretch reflex.
◼ c- Bainbridge reflex or effect.

◼b-Reflexes initiated from the
CVS:
◼1-Marey,s reflex or law
◼ ↑of ABP → ↓ HR.
◼ ↓of ABP → ↑ HR.
◼Effects of stimulation of arterial
baroreceptors:

◼ a- Stimulation of both the CIC and
VDC and inhibition of the VCC.
◼ b- Inhibition of respiratory centre
→ apnea.
◼ c- Inhibition of secretion of the
ADH.
◼ d- Inhibition of the brain activity
and muscle tone.

◼2- Bainbridge reflex
(atrial stretch reflex):
◼An increase in the right
atrial pressure leads to heart
acceleration.

◼ Increase in RA pressure →
Stimulation of the type A atrial
receptors → stimulate VCC → heart
acceleration.
◼ Atrial distension → Stimulation of
the type B atrial receptors → heart
slowing.

◼Effects of rise of the right atrial
pressure:
◼ a- Tachycardia (Bainbridge reflex).
◼ b- Tachypnea (Harrison,s reflex).
◼ c- Generalized VD and decrease of the
ABP.
◼ d- Coronary VD (anrep,s reflex).
◼ e- Inhibition of secretion of ADH.
◼ f- Stimulation of secretion of ANP.

◼3- The ventricular stretch reflex:
◼ Distension of the LV leads to
bradycardia and hypotension.
◼ Stimulation of certain baroreceptors
located near the coronary vessels →
stimulation of CIC and VDC and
inhibition of the VCC.

◼4- The Bezold- Jarisch reflex
(coronary chemoreflex):
◼ Injection of certain substances
(serotonin) into the coronary
arteries that supply the LV leads to
apnea followed by rapid breathing,
hypotension and bradycardia.

◼c- Reflexes initiated from
extravascular structures:
◼1- From the lungs
◼ a- The pulmonary stretch reflex:
◼ Lung inflation leads to tachycardia.
◼ Stimulation of baroreceptors located in
bronchial walls → stimulation of VCC →
tachycardia.
◼ b- The pulmonary chemoreflex.

◼2- From skeletal muscles (Alam-
Smirk reflex):
◼ Voluntary contraction of the skeletal
muscles leads to tachycardia and
tachypnea.
◼3- From the skin and viscera:
◼ Cold and mild pain → tachycardia.
◼ Severe pain → bradycardia.

◼4-From the eye (oculo- cardiac
reflex):
◼Applying pressure to the eyeball
results in reflex decrease of the
heart rate.

◼5-From the trigger zones
(trigger zone reflexes):
◼Signals from certain sensitive
areas in the body as the trigger
area (larynx, testes and
epigastric region) → slowing of
the heart.

◼2- Chemical regulation of the heart
rate
◼ A-Effects of changes in blood gases
◼1- Hypoxia:
◼ A moderate O2 lack increases the heart
rate by 3 mechanisms:
◼ a- Direct mechanism.
◼ b- Central mechanism.
◼ c- Reflex mechanism

◼Severe hypoxia → ↓ HR
due to:
◼- Inhibition of S-A node
activity.
◼- Paralysis of CVS center in
medulla oblongata.

◼2-Hypercapnia and acidosis
◼ Moderate hypercapnia and acidosis
→ ↑ HR by 3 mechanisms:
◼ a- Inhibition of the CIC.
◼ b- Stimulation of the VCC
(peripheral chemoreceptors).
◼ c- Stimulation of the VCC (central
chemoreceptors).

◼Severe hypercapnia → ↓ HR
due to:
◼- Inhibition of S-A node activity.
◼- Paralysis of CVS center in
medulla oblongata.

◼B- Effects of hormones ,
drugs and chemical:
◼ 1- Adrenaline. 2-Noradrenaline.
◼ 3- Thyroxin. 4-Atropine.
◼ 5- Histamine.
◼ 6- Bile salts.
◼ 7- Autonomic drugs.

◼3- Factors that directly
affect the S-A node activity:
◼1-Physical factors.
◼2-Mechanical factors.
◼3-Chemical factors.

◼Cardiac output is the volume of
blood pumped by each ventricle per
minute.
◼ It equals the stroke volume x heart rate.
◼ In normal adult male during rest, it is
about 5.5 L/ min.
◼ Stroke volume is the volume of blood
pumped by each ventricle per beat.

◼Factors that affect the end
diastolic volume:
◼ 1- Right atrial pressure (RAP).
◼ 2- Blood volume:
Hypovolaemia → ↓ MCP → ↓ VR
and EDV.

◼3- Venous tone:
Venoconstriction → ↑MCP → ↑
VR and EDV.
◼4- Intrapericardial pressure:
↑ intrapericradial pressure → ↓
EDV.

◼5- Atrial fibrillation:
AF → weakness of atrial contraction
→ ↓ EDV.
◼6- Intrathoracic pressure:
↑ of its negativity → help ventricular
relaxation and ↑VR → ↑ EDV.

◼7- Skeletal muscle contraction.
◼8- Posture.
◼9- Ventricular stiffness and
compliance.
◼10- Atrial systole.

◼Factors that affect the cardiac
output:
◼The cardiac output is affected
by changes in either HR or
the stroke volume.

◼ Effects of changes in the HR on the
CO:
◼ If the HR decreases below 70 beats /
minute.
◼ If the HR decreases below 50 beats /
minute.
◼ If the HR increases from 70 to 180 beats /
minute.
◼ If the HR increases above 180 beats /
minute.

◼Factors that affect the stroke
volume:
◼1- The cardiac pumping power
(maximal CO that can be pumped
per minute) : it is affected by the
following factors:

◼A- The preload (EDV):
This is an intrinsic autoregulatory
mechanism that controls the power
of cardiac contractility by Starling's
law.
◼The resting cardiac pumping
power is about 10 L/min.

◼B- Sympathetic nerve supply:
The resting cardiac sympathetic
tone increases the cardiac
pumping power to 13-15 L/min.
◼Maximal sympathetic stimulation
increases it to about 25 L/min.

◼C-The afterload: an increase in
the afterload reduces the cardiac
pumping power.
◼D- Ventricular hypertrophy: in
athletes, the cardiac pumping
power increase up to 35 L/min.

◼2-The venous return (VR): The
volume of the venous return is
affected by the following factors:
◼ A-The mean circulatory pressure
(MCP): this the main pressure in
systemic circulation.
◼ Normally, it is about 7 mmHg and it
affects venous return directly.

◼B-The right atrial pressure:
It is closely related to the central
venous pressure (CVP) and VR
is inversely proportional to it.

◼C- The resistance to the VR
(RVR):
◼This occurs mostly in the
veins and normally, it is about
1.4 mmHg/ liter of blood flow
and it affects the VR inversely.

◼Regulation of the cardiac
output:
◼1- Extrinsic regulation
◼This regulates both the stroke
volume and heart rate by effect
of:

◼a-The autonomic nerves to
the heart:
◼1-Sympathetic stimulation:
◼ Sympathetic stimulation increases
the cardiac output by increasing the
stroke volume and heart rate
because sympathetic stimulation
leads to:

◼ ↑ the rhythmicity of SA node
(+ve chronotropic effect).
◼ ↑ the force of cardiac muscle
contraction (+ve inotropic
effect).
◼ ↑ the coronary blood flow.

◼2- Parasympathetic stimulation:
◼ Parasympathetic stimulation decreases the
cardiac output by:
◼ ↓ the rhythmicity of SA node (-ve
chronotropic effect).
◼ ↓ the force of cardiac muscle contraction
(-ve inotropic effect).
◼ ↓ the coronary blood flow.

◼b-Hormones and drugs:
◼1- Glucagon hormone: increase
the cardiac output by increasing the
force of cardiac muscle contration.
◼2- Catecholamines: increase the
cardiac output by increasing SV and
HR.

◼3- Acetylcholine: decrease the
cardiac output by decreasing the HR.
◼4- Thyroxin: increase the cardiac
output by increasing the HR.
◼5- Xanthines: such as caffeine:
increase the cardiac output by
increasing the force of contraction.

◼6- Digitalis: increase the cardiac
output by increasing the force of
contraction.
◼7- Hypoxia, hypercapnia,
acidosis and myocardial
ischemia: decrease the cardiac
output by decreasing the HR and
cardiac contractility.

◼2-Intrinsic regulation:
◼This regulates the stroke
volume only and it includes
heterometric and homeometric
autoregulation.

◼a-Heterometric autoregulation:
◼ This regulation of the stroke volume
through changing the initial length of the
muscle fibers.
◼ Filling of the ventricle → ventricular
expansion → ↑ in EDV and length of
muscle fibers → ↑ the force of contraction
→ ↑ stroke volume.

◼B- Homeometric autoregulation:
◼ This regulation of the stroke volume
without change in the length of the
muscle fibers.
◼ A prolonged increase in EDV is
followed by its decrease to its normal
level.

◼ESV decreases less than its
normal level by more forceful
ventricular contraction.
◼The stroke volume remains
elevated.

◼Physiological variations of
the cardiac output:
◼1-Sleep.
◼2-Posture.
◼3-Meals.

◼4-Temperature.
◼5-Pregnancy.
◼6-Emotions.
◼7-Muscular exercise.

CVS Physiology mecical physiology le .pdf

CVS Physiology mecical physiology le .pdf

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CVS Physiology mecical physiology le .pdf