PHYSIOLOGY
DOCTOR SMART
CARDIOVASCULAR
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PHYSIOLOGY
CARDIOVASCULAR
PHYSIOLOGICAL ANATOMY OF THE HEART
The heart is a four-chamber pump composed of 2 atria and 2 ventricles.
Contraction of the atria (atrial systole) is followed by contraction of the ventricles (ventricular
systole) and all four chambers are relaxed during diastole.
PROPERTIES OF THE CARDIAC MUSCLE
1) Rhythmicity
It is the ability of the cardiac muscle to beat regularly. It is myogenic in nature.
It does not depend upon nerve supply of the heart.
Rhythmicity of different parts of the heart:
•
Sino-atrial node (SA node):
It has the biggest rhythm 120 impulses/min (Pacemaker).
•
Atrioventricular node (AV node):100 impulses/min.
•
Purkinje fibers: 35–40 impulses/min.
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PHYSIOLOGY
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FACTORS AFFECTING RHYTHMICITY
1. Changes in temperature:
o
Moderate warming increases rhythmicity.
o
Moderate cooling decreases rhythmicity.
o
Excessive heating or cooling stops the heart.
2. Effect of ions:
o
Na⁺ ion initiates rhythmicity.
o
K⁺ ion favors diastole.
o
Ca²⁺ ion favors systole.
3. Effect of pH changes:
o
Acids favor relaxation.
o
Alkalies favor systole.
4. Effect of drugs:
o
Adrenaline stimulates rhythmicity.
o
Acetylcholine decreases rhythmicity.
5. Nervous regulation:
o
Sympathetic stimulation increases rhythmicity.
o
Parasympathetic stimulation decreases rhythmicity.
6. Oxygen:
o
Complete absence of oxygen stops the heart.
CARDIAC OUTPUT
It is the amount of blood pumped by each ventricle per minute. Normal value: 5.5 L/min.
Cardiac output = heart rate × stroke volume.
Normal variations of CO:
•
CO increases in anxiety, exercise, after meals and pregnancy.
•
CO decreases in sitting or standing from lying down, also in heart diseases.
STROKE VOLUME amount of blood pumped by each ventricle per beat. Normal value: 70 ml/beat.
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2) Excitability
It is the ability of cardiac muscle to respond to an adequate stimulus.
Absolute Refractory Period:
This period extends throughout the whole period of contraction.
Any stimulus, however strong, will fail to elicit a response if it falls within this period.
II) Relative Refractory Period:
This starts immediately after the absolute refractory period and involves the first part of
relaxation. Only a very strong stimulus will be effective.
III) Supernormal Period:
There is another type of refractory period observed after the relative refractory period which is
known as supernormal period. A weak stimulus will be effective.
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PHYSIOLOGY
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3) Conductivity
It is the ability of cardiac muscle to transmit excitation wave.
Conductive system of the heart:
1. SA node.
2. Internodal fibers.
3. AV node: the slowest part 0.02 m/sec.
4. Bundle of His.
5. Purkinje fibers: the fastest fibers.
6. Ventricular fibers.
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PHYSIOLOGY
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4) Contractility
It is the ability of cardiac muscle to contract and push blood into circulation.
Factors affecting Contractility:
FACTOR
EFFECT ON CONTRACTILITY
• Moderate warming increases contractility
CHANGES IN TEMPERATURE
• Moderate cooling decreases contractility
• Excessive heating or cooling stops the heart
EFFECT OF IONS
EFFECT OF PH CHANGES
EFFECT OF DRUGS
• K⁺ ion favors diastole
• Ca²⁺ ion favors systole
• Acids favor relaxation
• Alkalies favor systole
• Adrenaline stimulates contractility
• Acetylcholine decreases contractility
FRANK-STARLING LAW
Within physiological limits, the strength of contraction is increased by increasing the initial
length of cardiac muscle fibers.
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PHYSIOLOGY
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HEART RATE AND ITS REGULATION Average: 70 beats/min. (Range: 60–100 beats/min).
Physiological variations:
1. Age: Newly born: 120 beats/min. It decreases gradually until it reaches its normal value at
age of 20 years.
2. Sex: It is faster in female than in male.
3. Physical training: It is faster in non-trained individuals than in athletes.
Regulation of Heart Rate
SOURCE OF IMPULSES
MECHANISM / EFFECT ON HEART RATE
• Baroreceptors (Mary’s Law): Heart rate is inversely proportional to
arterial blood pressure provided other factors remain constant.
A) FROM CIRCULATORY
SYSTEM
Increase in arterial blood pressure → reflex decrease in heart rate
and vice versa.
• Bainbridge reflex:
Increase in venous return and venous pressure → distension of right
atrium → reflex cardiac acceleration.
1. Respiratory center: Heart rate accelerates during inspiration and
slows down during expiration.
2. Cerebral cortex:
B) FROM HIGHER CENTERS • Conditioned reflex in response to visual, smell, or auditory
stimuli.
• Emotions: heart rate increases in fear and anger, decreases in
sudden emotions and shock.
• Hypothalamus.
C) FROM OTHER PARTS OF • Light and moderate pain: cardiac acceleration.
• Severe pain: may stop the heart.
THE BODY
Hormones (Adrenaline, Noradrenaline, Thyroxine) and increased body temperature raise heart
rate, while decreased body temperature lowers it.
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FACTORS CONTROLLING CARDIAC OUTPUT (CO)
A) Stroke Volume (SV)
1. Venous return.
2. Arterial blood pressure.
3. Contractility.
Venous Return (VR)
Increase in venous return and filling capacity of the heart results in increase strength of
contraction with increasing stroke volume and cardiac output.
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PHYSIOLOGY
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FACTORS AFFECTING VR
FACTOR AFFECTING
VENOUS RETURN (VR)
1. THE PRESSURE
GRADIENT
MECHANISM / EFFECT
The blood pressure in the venular end of the capillaries is about 15
mmHg and in the big veins just outside the thorax is zero.
This pressure difference is responsible for moving the blood
towards the heart. The venous return is directly proportional to the
pressure gradient.
2. THE RESPIRATORY
MUSCLE
During resting inspiration, venous return increases. So blood is
sucked from extrathoracic to intrathoracic veins.
3. SKELETAL MUSCLE
PUMP
During contraction of skeletal muscles, the increased muscle
tension around the soft-walled veins squeezes their blood content
and helps propel the blood towards the heart.
4. DIAMETER OF
ARTERIOLES
Dilatation of the arterioles accelerates the blood flow from the
arteries to the veins. The venous return and the cardiac output are
increased.
5. CAPILLARY TONE
6. VENOUS TONE
7. ARTERIAL PULSATION
8. CONTRACTION OF
SPLEEN AND BLOOD
RESERVOIRS
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If capillaries are widely dilated, they would accommodate a great
volume of blood. So venous return and cardiac output are reduced.
Excess vasodilatation of veins may lead to pooling of blood in the
venous system and decreases venous return.
Helps venous return in places where a vein runs parallel to and
near an artery.
When pulsations are mechanically transmitted to the venous wall,
they propel blood towards the heart.
Increase venous return.
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II) Contractility
An increase in force of ventricular contraction (e.g., produced by sympathetic activation of the
heart) increases cardiac output.
While decrease in force of ventricular contraction as in coronary thrombosis leads to decrease
cardiac output.
III) Arterial Blood Pressure
An increase or decrease in arterial blood pressure has no effect on cardiac output in case of
healthy normal heart.
B) Heart Rate
In general, physiological (moderate) changes in heart rate leads to non-significant effect on
cardiac output because stroke volume can compensate for this change.
However, excessive change in heart rate reduces cardiac output because stroke volume cannot
compensate for these changes.
ARTERIAL BLOOD PRESSURE (ABP)
Definitions and Physiological Standards
Arterial blood pressure is the pressure exerted by blood on the lateral walls of the arteries,
leading to their distension.
THE SYSTOLIC BLOOD PRESSURE:
It is defined as the maximum pressure in the arteries, which occurs at systole.
THE DIASTOLIC BLOOD PRESSURE:
It is the lowest pressure at diastole.
Normal blood pressure in case of complete physical, mental and digestive rest in a healthy adult
human is approximately: 120 mmHg systolic, 80 mmHg diastolic, Written as 120/80 mmHg.
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PHYSIOLOGY
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PHYSIOLOGICAL VARIATIONS INFLUENCING ABP
1. Age:
The arterial blood pressure is very low at birth (50/30 mmHg).
It rapidly rises during the first few weeks to 90/60 mmHg, then gradually increases with age
up to adult age to be about 120/80 mmHg.
Then a progressive but slight increase continues with advancing age.
2. Sex:
a) In children: arterial blood pressure is more or less identical in both sexes before puberty.
b) In adult age: arterial blood pressure is slightly lower in females than males.
c) At menopause: arterial blood pressure is higher in females than males.
3. Body build:
In obese people, arterial blood pressure is usually higher than that of normal individuals.
They are liable to have pathological hypertension more than normal weight persons.
4. Effect of gravity:
The pressure in any vessel below heart level is increased, and that in any vessel above heart
level is decreased by the effect of gravity.
5. Meals:
During digestion, arterial blood pressure increases 5–10 mmHg due to contraction of spleen
and blood reservoirs.
6. Circadian rhythm:
Arterial blood pressure shows lowest level at early morning (about 4 a.m.) and highest level
in the afternoon (about 4 p.m.).
7. Emotions and muscular exercise:
Emotions increase arterial blood pressure by more than 30 mmHg due to increase in
adrenaline secretion.
In muscular exercise, arterial blood pressure increases temporarily to high level (up to 180
mmHg), and after exercise the arterial blood pressure drops to the normal level.
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PHYSIOLOGY
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8. Sleep:
Deep quiet sleep lowers arterial blood pressure by 15–30 mmHg.
But when accompanied by dreams of emotional activity, arterial blood pressure may rise to
high level.
9. Pregnancy:
Arterial blood pressure drops during normal pregnancy due to both hormonal factors and
fetal circulation.
10. Physical factors:
Exposure to cold causes cutaneous vasoconstriction with increasing mean arterial blood
pressure by about 10 mmHg.
Exposure to heat causes vasodilatation and decreased arterial blood pressure.
In severe hot weather, diastolic pressure may decrease markedly leading to hypotension and
syncope.
11. Respiratory phases:
Arterial blood pressure rises 4–6 mmHg during inspiration and falls towards normal level
with expiration.
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PHYSIOLOGY
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FACTORS MAINTAINING NORMAL ARTERIAL BLOOD PRESSURE
1) Peripheral Resistance (PR)
Definition:
It is the resistance which the blood meets during
its passage in the peripheral arteries and capillaries.
Increase in peripheral resistance leads to increase
diastolic blood pressure while systolic pressure remain constant.
Peripheral resistance depends on:
A) Diameter of arteries:
Decrease in diameter (vasoconstriction) leads to increase diastolic blood pressure.
B) Viscosity of blood:
Increase in viscosity (increase plasma proteins or RBCs) leads to increase diastolic blood
pressure.
2) Cardiac Output
Arterial blood pressure is directly proportional to cardiac output.
Increase stroke volume leads to increase systolic blood pressure.
Increase heart rate leads to increase diastolic blood pressure.
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PHYSIOLOGY
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3) Elasticity of Arteries
Normal physiological elasticity buffers excessive change in arterial blood pressure.
During systole, the arteries are distended to prevent excessive increase in systolic blood
pressure. during diastole, recoil of the wall prevents excessive decrease in diastolic blood
pressure.
CLINICAL CORRELATION: ARTERIOSCLEROSIS
A pathological condition caused by precipitation of cholesterol in the arterial wall leading to
loss of normal arterial elasticity and converting the arteries into rigid tubes.
Therefore, arterial blood pressure becomes higher than normal.
4) Blood Volume and Capacity of the Circulation
Moderate changes:
Adjustment occurs by corresponding changes in capacity and heart rate without change in BP.
Severe changes:
As in severe hemorrhage, arterial blood pressure decreases in spite of change of heart rate and
capacity.
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PHYSIOLOGY
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HEMORRHAGE
Definition: It is the loss of blood from the heart and blood vessels.
Special effects of hemorrhage depend on:
a) The amount of blood loss:
If it is less than 30% of blood volume, the body can compensate for it.
But if it is more than 30% (sudden loss), the body cannot compensate for it and death occurs
unless blood transfusion and other therapies are given.
b) The speed of blood loss:
Small repeated hemorrhage is not dangerous because the body can compensate for it.
But rapid severe hemorrhage is dangerous.
The following characters occur after severe hemorrhage:
1. The primary event is reduction in blood volume, cardiac output and arterial pressure.
2. The pulse is rapid and weak.
3. Breathing is shallow and rapid.
4. Skin is pale and cold.
5. The mouth is dry and thirst is common.
6. Reduction in urine output.
7. Loss of consciousness and death.
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PHYSIOLOGY
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COMPENSATORY REACTIONS OF HEMORRHAGE
I) Rapid (Immediate) Compensatory Mechanisms
Aim: To maintain adequate arterial blood pressure.
Onset: Starts within seconds to few minutes.
1) Blood coagulation
Aims to close the wound and prevent further blood loss.
2) Cardiovascular changes
a) Increase heart rate
To increase diastolic blood pressure and maintain blood flow through cerebral and coronary
blood vessels.
Causes:
1. When arterial blood pressure decreases, arterial baroreceptors are stimulated leading to
increase heart rate (Mary’s Law).
2. Hypoxia stimulates chemoreceptors that increase heart rate.
3. Increased adrenaline secretion directly stimulates the SA node.
b) Increased vasoconstrictor discharges
Vasoconstriction mainly affects blood vessels of less important areas (skin, splanchnic area
and muscle vascular beds) leading to redistribution of blood flow and ensuring adequate
circulation through coronary and cerebral vessels.
3) Respiratory changes
Respiration is accelerated to increase venous return and ensure complete oxygenation of blood.
Causes:
1. Hypoxia stimulates chemoreceptors that activate the respiratory center.
2. Local accumulation of metabolites in cells of the respiratory center due to its ischemia.
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4) Endocrine changes (increase secretion of):
A. Epinephrine and norepinephrine
Responsible for:
a) Enhancing vasoconstriction of skin and splanchnic area.
b) Dilating coronary arteries and helping coronary blood flow.
c) Increasing heart rate and improving contractility.
d) Contraction of spleen.
B. Aldosterone
Responsible for sodium and water reabsorption by the kidney leading to increase blood volume
and return arterial blood pressure towards normal.
C. Antidiuretic hormone (ADH)
Responsible for water reabsorption by the kidney and restoration of blood volume and arterial
blood pressure.
D. Angiotensin II
Responsible for generalized vasoconstricting effect.
E. Glucocorticoids
Responsible for increasing resistance to stress condition.
F. Erythropoietin
Responsible for stimulation of red blood cell formation by the bone marrow.
5) Splenic contraction
It squeezes 200–500 cc of blood rich in RBCs into circulation leading to restoration of blood
volume, arterial blood pressure and RBC number.
6) Renal changes
Urine formation is decreased due to:
•
Decrease arterial blood pressure and renal blood flow.
•
Increase secretion of ADH.
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II) Long-Term (Delayed) Compensatory Reactions
Aim: To restore blood volume.
1) Restoration of water and electrolytes
Occurs within 12–72 hours through:
a) Decrease arterial blood pressure and filtration force with normal reabsorption force leading
to withdrawal of water from interstitial space.
b) Greater reabsorption of water by the kidney.
c) Increase in water intake.
2) Restoration of plasma proteins
Occurs through:
•
Rapid addition: within one hour from labile protein of the liver and tissues.
•
Delayed addition: by synthesis of new protein in the liver.
3) Restoration of red blood cells
Occurs through:
•
Rapid mechanism: squeeze of spleen.
•
Slow mechanism: stimulation of bone marrow by erythropoietin hormone produced by the
kidney under effect of hypoxia.
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