Dr: Ayub Abdulcadir Sheikh:
• Postgraduate MBBS, at University of Somalia.
• Resident physician at Sureya Medical Center.
• A lecturer physiology at Frontier University.
To all my family especially may parents (Allah may bless you), also my student
in frontier university.
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2. Heart (cardiac).
3. Blood vessels.
1. Interatrial septum.
2. Interventricular Septum
Layers of heart:
a. Outer parietal pericardium :-
b. Inner visceral (Epicardium)
Chambers of heart:
1. Right Atrium.
2. Left Atrium.
3. Right Ventricle.
4. Left Ventricle.
1. Atriovantriclular Valve:
(Tricuspid and Mitral).
2. Semilunar Valve:
(Pulmonary and Aortic)
1. Superior & Inferior Vena Cava.
2. Right atrium.
3. Right ventricle.
4. Pulmonary artery.
6. Pulmonary veins.
7. Left atrium.
8. Left ventricle.
10. Whole the body
Actions of heart:
1. Chronotropic: heart rate.
2. Inotropic: contraction.
3. Dromotropic: velocity.
4. Bathmptropic: excitability.
Types of cardiac muscles:
Histological cardiac muscle:
• Intercalated disc.
• Gap junction.
• Myofibril (Actin & Myosin filaments)
Cardiac has 2 pumps:
a) Right or left blood pump.
b) Upper or lower blood
➢ Size of your fist.
➢ 250 g (female)
➢ 300 g (male).
➢ Superior surface of
➢ Left of the midline
➢ Anterior to the vertebral
column, posterior to the
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Cardiac Action Potential:
1. Fast Sodium Channel.
2. Slow Calcium Channel (Na Ca Channel)
Phases of Action Potential in Cardiac muscle:
1. Phase 0 = Depolarization (Na influx).
2. Phase 1 = Initial repolarization (K outflux).
3. Phase 2 = Plateau (Ca influx).
4. Phase 3 = Rapid repolarization (K outflux).
5. Phase 4 = Resting membrane potential (Na-K
Excitation – Contraction of cardiac muscle:
1. Arrival of action potential on T-Tube.
2. Activation of Ca channel.
3. Ca from extracellular enters the cell.
4. Binding Ca to Ryanodine receptors of
5. Release of sarcolasmic calcium.
6. Accumulation of Calcium in the cell.
7. Formation of Ca signals.
8. Ca binds to TnC.
9. Opening of actin myosin binding site.
10. ATP activates Myosin head.
11. Formation of Cross-bridge b/w
actin and Myosin.
12. Cardiac muscle contraction occurs
(pumping of blood).
13. Again ATP binds to myosin head.
14. Detachment of Actin and Myocin.
15. Ca released from TnC.
16. Relaxation will occur.
17. Closure of Actin binding sites.
18. Some Ca is pumped in the ECF
whereas the others pumped in the
Velocity of signal conduction in cardiac muscle:
1. Atria = 0.3 m/s.
2. Ventricle = 0.5 m/s.
3. Purkinje fiber = 4 m/s
Refractory period of cardiac muscle:
Relative refractory period.
The strength of contraction of cardiac muscle depends
to a great extent on the concentration of calcium ions in
the extracellular fluids.
Calcium Induced Calcium Release (CICR):
Look at Step 4 and 5
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Normal range of cardiac cycle = 0.8 s
During exercise: systole, more diastole.
1. Atrial systole.
2. Ventricular systole:
a) Isometric contraction.
b) Ejection period.
1. Atrial diastole.
2. Ventricular diastole:
b) Isometric relaxation.
c) Rapid filling.
d) Slow filling.
e) Last rapid filling.
1. First sound: Closure of Atrioventricular valve.
2. Second sound: Closure of seminular valve.
3. Third sound: Rushing of blood into ventricles.
4. Fourth sound: Contraction of atrial musculature.
End Systolic Volume:
60 – 80 ml.
End Diastolic Volume:
130 – 150 ml.
(EDV - ESV)
(130 - 60)
Normal = 70 ml
(SV / EDV) X 100.
Normal = > 50%
Events of the cardiac cycle for left ventricular function, showing changes in left atrial pressure, left ventricular
pressure, aortic pressure, ventricular volume, the electrocardiogram, and the phonocardiogram.
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The volume-pressure diagram:
Phase I: Period of filling.
Phase II: Period of isovolumic contraction.
Phase III: Period of ejection.
Phase IV: Period of isovolumic relaxation.
Fig: Changes in intraventricular volume and pressure during a single
cardiac cycle (red line). The shaded area represents the net external
work (EW) output by the left ventricle during the cardiac cycle.
Shift to right: (if increased time of filling).
Ex: increased volume of blood
Shift to left: (if decreased time of filling).
Ex: increased sympathetic activity.
P wave: Atrial depolarization (Atrial contraction).
QRS complex: Ventricular Depolarization (Ventricular
T wave: Ventricular Repolarization (Ventricular
Atrial relaxation is mixed in QRS complex but does not
appear in ECG.
Is the pressure during filling of the ventricle.
End Diastolic pressure
Is the arterial pressure against which the
ventricle must contract.
End Systolic pressure
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Regulation of Heart Pumping:
1. Frank Starling Mechanism (Venous
2. Autonomic Nervous System
(Sympathetic & Parasympathetic)
3. Other factors.
1. Frank Starling Mechanism (intrinsic control) states that:
A. If increased venous return leads.
B. greater the heart muscle is stretched during filling &
C. the greater is the force of contraction &
D. the greater the quantity of blood pumped into the aorta.
2. Distribution and function of Autonomic Nervous
A) Sympathetic A N S:
In SA node, AV node, Septum, Whole the heart.
• Increases heart rate = 70 -220 bpm.
• Increases force of contraction.
• Increases volume of blood pumping.
• Increases ejection pressure.
• Increases cardiac output = 5 – 30L/minute.
B) Parasympathetic A N S:
In SA node, AV node.
• Strongly decreases heart rate = <50 bpm.
• Slightly decreases force of contraction.
• Slightly decreases volume of blood pumping.
• Slightly decreases ejection pressure.
• Normal or slight decrease cardiac output =
Increasing the arterial pressure load (up to a
limit) does not decrease the cardiac output
3. Other factors:
• Hyperkalemia: (cardiac weakness,
abnormal rhythmus, or block
• Hypocalcemia: (decreased excitability
• Hypercalcemia: (spastic contraction).
Due to less development of sarcoplasmic
reticulum of cardiac muscle, the contraction of
heart muscle is depending among the
concentration of Extracellular calcium.
• Slightly increase in temperature:
(increases the permeability of ions also
increases the contractility of heart).
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1. Sino Atrial Node (Pacemaker):
Three Internodal fibers:
A. Anterior (Bachman) Internoadal F.
B. Middle (Wenckebach) Internoadal F.
C. Posterior (Thorel) Internoadal F.
2. Atrioventricular Node.
3. Atrioventricular Bundle (Bundle of Hiss):
A. Right Bundle Branch.
B. Left Bundle Branch.
4. Purkinje Fiber.
Importance of Conductive System:
1) Generation of self rhythmical excitation of heart.
2) Conduction or propagation of these rhythmical
Average human age of 100 year the heart will
beat approximately 3 billion times.
Velocity of Conduction:
1. SA node = 70 – 80 bpm.
2. AV node = 40 – 60 bpm.
3. Purkinje fiber = 20 – 40 bpm
Total velocity conduction before ventricular contraction
is 0.16 s.
➢ Slow conduction in the transitional, nodal, penetrating
AV bundle is due to diminished number of Gap junction.
➢ Rapid conduction in Purkinje fiber is due to presence of
large number of Gap junction.
Properties of conductive system:
1. Self excitation continually due to:
➢ Opening and Influx of Na & Ca ions in the node.
2. Hyperpolarization continually due to:
➢ Opening and Outflux of K ions in the node.
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➢ Parasympathetic nerve fiber:
1. Release of Acetylcholine (Ach).
2. Ach binds with Muscarinic
3. Activation of G protein.
4. Activation &opening of K channel,
then K outflux.
5. G protein also Inactivates Adenyl
6. Decreased production of cAMP.
7. Closure of Na and Ca channels leads.
“Cardiac cycle” = more than 0.8 s
➢ Sympathetic nerve fiber:
1. Release of Epi/Nor-epinephrine
2. These binds with Adrenergic
3. Activation of G protein.
4. Activates Adenyl Cyclase.
5. Increased production of cAMP.
6. Opening & influx of Na and Ca
7. Inactivation & closing of K channel
“Cardiac cycle” =less than 0.8 s
Ventricular Escape: when severe stimulation
of parasympathetic fiber causes the heart to
stop, then after 5 – 20 s the heart will beat
ECTOPIC PACEMAKER: is a pacemaker that
is not in the original position (sinus node).
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(ECG): is the interpretation of
the electrical activity of the heart
over a period of time.
Advantages of ECG:
1. Heart rate.
2. Heart rhythm.
3. Abnormal electrical conduction.
4. Poor blood ﬂow to heart muscle
5. Heart Attack.
6. Coronary artery disease.
7. Hypertrophy of heart chambers.
A. Light line of Small square = 1 X 1 mm.
B. Dark line of Large square = 5 X 5 mm.
C. X axis of one small square = 0.04 s.
D. Y axis of one small square = 0.1 mV
12 ECG lead:
1. Bipolar Limb leads:
• Limb lead I: Between the right arm (negative electrode) and
the left arm (positive electrode).
• Limb lead II: Between the right arm (negative electrode) and
the left leg (positive electrode).
• Limb lead III: Between the left arm (negative electrode) and
the left leg (positive electrode).
2. Unipolar limb lead (augmented leads):
• aVR: Between the right arm (positive electrode) and left arm +
left leg (negative electrode).
• aVL: Between the left arm (positive electrode) and right arm +
left leg (negative electrode)
• aVF: Between the left foot (positive electrode) and right arm +
left arm (negative electrode).
3. Unipolar Chest lead (precardial leads):
• V 1 : Over 4th intercostal space near right sternal margin
• V 2 : Over 4th intercostal space near left sternal margin
• V 3 : In between V2 and V4
• V 4 : Over left 5th intercostal space on the mid clavicular line
• V 5 : Over left 5th intercostal space on the anterior axillary
• V 6 : Over left 5th intercostal space on the mid axillary line.
Einthoven triangle: The Heart is said to be in the center of an
imaginary equilateral triangle drawn by connecting the roots of
three limbs (Rt Arm, Lt Arm, Lt Leg).
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• Normal ECG consists of waves,
complexes, intervals and segments.
• Waves of ECG recorded by limb lead
II are considered as the typical
• Isoelectric line: above (Positive
wave) and below (Negative wave)
1. Abnormal pattern of cardiac excitation resulting in
different types of arrhythmias.
2. Abnormalities of myocardium.
3. Cardiac abnormalities due to alteration in plasma
4. Cardiac involvement secondary to other diseases.
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Arrhythmia: irregular heartbeat or
disturbance in the rhythm of heart
Causes of Arrhythmia:
1. Scarring of heart tissue from a prior
2. High blood pressure
5. Alcohol, drug abuse
6. Stress, diabetes.
Sign & Symptoms of Arrhythmia:
1. Palpitation, Chest pain, Shortness of
2. Lightheadedness or dizziness,
4. Fainting (syncope) or near fainting.
2. Heart Failure.
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Cardiac output: “The quantity of blood
pumped into the aorta each minute.
by the heart”.
Normal CO: in males (5.6L/min), in
• Cardiac index: “is the minute volume
expressed in relation to square meter of
body surface area”.
• Cardiac index = CO/ body surface area.
• Normal Range: 2.6–4.2 L/min/m2
• Below 2.2 L/min/m2
Body Surface Area = Height (cm) X Weight (Kg)
• Cardiac Reserve: “difference b/w the rate at
which the heart pumps blood and its maximum
capacity for pumping blood at any given time”.
• Cardiac Reserve = Maximum CO – Normal CO X
100 / Normal CO.
• It’s expresses as percentage %.
• Example Normal person = 400% (if Max CO =
25L/min & Norm CO = 5l /min)
Distribution of CO in the body
When total peripheral resistance is more than 100, both
the cardiac output and the Arterial pressure are
decreased, vice verse.
Factors that cause Hypereffective heart (age, sex,
exercise, pregnancy, nervous stimulation, physiological
ventricular hypertrophy, environment, emotional).
Factors that cause Hypoeffective heart (severe
increased arterial pressure, inhibition of nervous
stimulation, congenital and heart disease, fever).
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Blood flow through tissues is
determined by interaction of these:
1. Tissue needs.
2. Cardiac output.
3. Arterial blood pressure.
Function of circulation:
1. Transport: nutrients, O2, waste
products, hormones, drugs.
2. Maintain appropriate internal
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Blood flow through a blood vessel
is determined by two factors:
(1) Pressure difference.
(2) Vascular resistance.
Ohm’s law: “the blood flow is
directly proportional to the
pressure difference but inversely
proportional to the resistance”.
Two type of Blood flow
through a blood vessel:
1. Streamline (linear) flow.
2. Turbulent flow.
Vascular resistance of two types:
1. Total peripheral vascular resistance:
1 PRU (peripheral resistance unit)
2. Total pulmonary vascular resistance:
A valuable characteristic of the vascular system is that “all
blood vessels are distensible”.
The most distensible by far of all the vessels are the veins.
Steps in measuring Blood
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❖ Structure of Capillary:
a) Unicellular layer of endothelial cells.
b) Surrounded by a thin basement membrane.
c) Two pores or pathways:
• Intercellular cleft: water & water soluble ions
• Caveolae: Transport of plasma protiens
Function of the microcirculation: is transport of nutrients to the
tissues and removal of cell excreta.
The metarterioles and the precapillary sphincters are in close
contact with the tissues that serve as open and close for
controlling tissue blood flow
❖ Types of Capillary:
When the molecular weight
of the substance is less, the
permeability of that
substance is more.
• Is the space between cells of the total volume of the body
• The structure of the interstitium:
1. Collagen fiber bundles.
2. Proteoglycan filaments.
3. Small rivulets of “free” ﬂuid and small free ﬂuid vesicles.
❖ Starling forces:
• The four primary forces that determine whether
ﬂuid will move through capillary & interstitium:
1. Capillary pressure (Pc).
2. Interstitial ﬂuid pressure (Pif)
3. Capillary plasma colloid osmotic pressure (Πp)
4. Interstitial ﬂuid colloid osmotic pressure (Πif)
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Types of Control tissue blood flow by:
4. Local control.
5. Endothelial Derived Factors.
6. Nutrient and Ions control.
7. Humoral control.
8. Nervous control.
Factors determine the Control tissue blood flow:
1. Increase or decrease in Heart Rate.
2. Vasoconstriction or Vasodilatation.
1. Local Control of blood Flow:
B) Acute local control: rapid changes
in local vasodilatation or
A) Long Term control: slow, controlled
changes in ﬂow over a period of days,
weeks, or even months.
1. Increases in Tissue Metabolism Increase
Tissue Blood Flow.
2. Reduced Oxygen Availability Increases
Tissue Blood Flow.
3. Two theories that increase tissue blood
a) Vasodilator Theory (increased rate
metabolism and decreased O2 &
nutrient availability = formation of
b) Oxygen Demand Theory (decrease O2
concentration leads vasodilatation).
Example of Acute local control:
1. “Reactive Hyperemia” Occurs
after the Tissue Blood Supply Is
Blocked for a Short Time.
2. “Active Hyperemia” Occurs When
Tissue Metabolic Rate Increases.
1. Increase or decrease in the physical
2. Increase or decrease in numbers of
blood vessels supplying the tissues.
Example of Long Term control:
1. “Tissue Vascularity” occurs if the
metabolism in a tissue is increased
for a prolonged period, vascularity
2. “Role of Oxygen in Long-Term
Regulation” occurs at high altitudes,
3. Development of Collateral
2. Endothelial Derived Factors:
A) Nitric Oxide:
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(+/-) (+/-) (+/-)
5. Nervous Control of blood Flow:
A) Cardioaccelator Center:
• Pressor area
• Give sympathetic activity:
1. Increase heart rate.
2. Increase heart contractility.
3. Release of epi-norepinephrine
from adrenal medulla.
B) Vasomotor center:
• Pressor area
• Give sympathetic activity:
1. Maintainance of normal
vascular tone (Arteries & Veins).
2. Vasoconstrictor both “Artery
C) Cardioinhibitory center:
• Depressor area from “sensory
• Give Parasympathetic activity:
1. Decrease heart rate.
2. Decrease heart contractility.
Sensory Areas from:
• Nucleus Tractus Solitarus, Nucleus Ambigious and Dorsal
Motor Nucleus Activity depends on the blood pressure:
1. Activates or inhibit the Cardioaceletor & Vasomotor
2. Activates or inhibit the Cardioinhibitory center.
• Carotid sinus:
• Aortic Arch: (Vagus)
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Autoregulation: the mechanism in which
returning normal blood flow to optimal level.
1. Metabolic theory:
When the arterial pressure
becomes too great, the excess
flow provides too much oxygen
and too many other nutrients to
the tissues and “washes out” the
vasodilators released by the
2. Myogenic theory:
When high arterial pressure stretches
the vessel, this in turn causes reactive
vascular constriction that reduces
blood flow nearly back to normal.
N.B: “A rapid increase in arterial pressure
causes an immediate rise in blood flow.
Then blood flow in most tissues returns
almost to the normal level, even though
the arterial pressure is kept elevated”.
Autoregulation Organs Are:
Heart, Kidney, Brain.
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Calculatiob of Mean arterial pressure (MAP):
1. Diastolic pressure + 1/3 of pulse pressure.
2. MAP = Systolic Pressure + 2(Diastolic Pressure)
Arterial blood pressure: is pressure exerted
by the column of blood on wall of
• It is expressed in four different terms:
1. Systolic blood pressure - 120 mm Hg (110
mm Hg to 140 mm Hg.
2. Diastolic blood pressure - 80 mm Hg (60
mm Hg to 80 mm Hg.
3. Pulse pressure - 40 mm Hg (SP 120 – DP
80 = 40).
4. Mean arterial blood pressure: the
average pressure existing in the arteries -
• Two factors influence the variation of
arterial blood pressure:
1. Physiological variation: age, sex, body
build, after meal, during sleep, etc.
2. Pathological variation: hypertension,
Systolic pressure is quickly and easily
variable in contrast to diastolic pressure.
4 regulatory mechanisms to maintain the blood pressure within
1) Nervous mechanism or short - term regulatory mechanism.
2) Renal mechanism or long - term regulatory mechanism.
3) Hormonal mechanism.
4) Local mechanism.
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Venous pressure is the pressure exerted by
the contained blood in the veins.
• Two factors influence the variation of
1. Physiological variation: Changing
from standing to supine position,
Forced expiration, Contraction of
abdominal and limb muscles, etc.
2. Pathological variation:
a) Increases in: Low cardiac output, venous
obstruction, Paralysis of muscles, renal
b) Decreases in: Severe hemorrhage,
• Types of venous pressure:
1. Central venous pressure: is the
pressure in the vena cava and right
2. Peripheral venous pressure: is the
pressure in peripheral veins.
• FACTORS REGULATING VENOUS PRESSURE:
1. Contraction of the left ventricles and its pressure leads forward
of blood to the veins then to the right atrium.
2. Set points of right atrial pressure of 0mmHg maintain the
3. Resistance offered by venous wall.
4. Volume of blood flowing through veins.
5. Peripheral resistance is inversely to venous pressure.
• Relation of respiration and venous pressure:
1. Valsalva maneuver: is the forced expiratory effort with
a) intrathoracic pressure becomes positive (+50mmHg).
b) Decrease in central venous pressure.
c) 30 seconds endurance test.
d) It is used to correct the abnormal heart rhythms
2. Müeller maneuver: is the forced inspiratory effort with
a) intrathoracic pressure decreases (-70mmHg).
b) Increase in central venous pressure.
c) Is used to evaluate Upper respiratory tract problems & Sleep
The Veins Function as Blood
Reservoirs in these locations:
c) Large abdominal veins,
d) Venous plexus of skin.
• Venous pulse is observed only in larger veins near the heart such as
• Venous pulse recording is used to determine the rate of atrial
• Recording of jugular venous pulse is called phlebogram.
• Kussmaul sign: increase in venous distention + increase in venous
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• Also called capillary hydrostatic pressure.
• Is responsible for the exchange of various substances between blood and interstitial fluid through capillary wall.
• Normal value of different type capillary pressure:
a) Arterial end of the capillary = 30 - 32mmHg.
b) Venous end of capillary = 15mmHg.
c) Glomerular capillary pressure = 60mmHg.
d) Pulmonary capillary pressure = 7mmHg.
• Arterioles play an important role in regulating
the capillary pressure.
➢ Capillary membrane is permeable to all substances
except plasma proteins (albumin).
➢ Normal oncotic pressure is about 25 mm Hg.
➢ Oncotic pressure plays an important role in filtration
across capillary membrane, particularly in renal
1. Coronary Circulation.
2. Cerebral Circulation.
3. Splanchnic Circulation.
4. Skeletal Muscle Circulation.
5. Cutaneous Circulation.