CARDIOVASCULAR SYSTEM

1. Physiological anatomy of heart

HEART is a small, pyramidal, muscular organ situated in the mediastinum obliquely,
2/3rd part to the left and 1/3rd part to right of midline. It has a base, apex and three
surfaces – anterior, posterior and inferior. The human heart weighs approx.300gm and
contains 4 chambers.
CHAMBERS OF THE HEART
Mammalian heart is made up of 4 chambers 2 atria + 2 ventricles.
Atria
• Two thin-walled atria separated from each other by an interatrial septum.
• Right atrium receives deoxygenated blood from tissues of the entire body through the
superior and inferior vena cava. This blood passes into the Right ventricle through the
right atrioventricular orifice which is guarded by tricuspid valve.
• Left atrium receives oxygenated blood from lung through the four pulmonary veins
(two right and two left). This blood passes into Left ventricle through the left ventricular
orifice which is guarded by mitral valve (bicuspid).
Ventricles
• Interventricular septum separates the right ventricle from left ventricle.
• Right ventricle receives blood from right atria and pumps through the pulmonary trunk
(which divides into right and left pulmonary arteries) into the lungs. Pulmonary valve
is present at the junction of right ventricle and pulmonary trunk.
• Left ventricle receives blood from the left atrium and pumps out into systemic
circulation through aorta. Aortic valve is present at the junction of left ventricle and the
ascending aorta
VALVES OF THE HEART
Atrio-ventricular Valve (AV Valves): Atria and ventricles are connected by a fibrous A-V ring,
on the right side by Tricuspid valve, and on the left side by Mitral (Bicuspid) valve. These
AV valves;
• Prevent the backward flow of blood from the ventricles to the atria during ventricular
systole; and,
• Close and open passively with the pressure gradient forces
Semilunar valves: They consist of 3 flaps (or cusps) of half-moon (semilunar) shaped
appearance, and are of two types;
➢ Pulmonary valve: situated at pulmonary orifice which leads from the RV to the
pulmonary artery.
➢ Aortic Valve: Situated at aortic orifice which leads from LV to the aorta.
These valves also open and close with passive gradient forces. It prevents backward flow of
blood from aorta and pulmonary artery towards the ventricles during ventricular relaxation.
Structure of the walls of heart
Wall of the heart are composed of thick layer of cardiac muscle, the myocardium, covered
externally by the epicardium, and lined internally by the endocardium. Wall of the atrial
portion of the heart are thin and ventricular wall are thick.
Pericardium
The entire heart is enclosed by double layered structures called pericardium. Pericardium
consists of two layers: outer fibrous and inner serous.
➢ Fibrous pericardium surrounds the heart like a bag and is attached with the
surrounding structures.
➢ Serous pericardium has parietal and visceral layers. The parietal layer of serous
pericardium lines the fibrous pericardium. The visceral layer of serous pericardium
closely covers the heart and is often called the epicardium. The slit like space between
parietal and visceral layers of serous pericardium is called pericardial cavity which
contains small amount of pericardial fluid that act as a lubricant to facilitate movement
of the heart.
Myocardium
The myocardium (muscular tissue of the heart) is the main tissue constituting the walls of the
heart. It consists of three types of muscle fibres.
• Cardiac muscles forming the walls of the atria and ventricles.
• Muscle fibres forming the pacemaker which is the site of origin of cardiac muscle.
• Muscle fibres forming the conducting system which transmits the impulse to the various
parts of the heart.
Endocardium
Endocardium is thin smooth and glistening membrane lining the myocardium internally. It
consists of a single layer of endothelial cells.
2. Conducting system of heart
Certain tissues in the heart, concerned with the initiation (generation of impulse) and
propagation (conduction) of the heartbeat, are called pacemaker tissues. They include:
1. Sino Atrial Node (SAN): on the posterior aspect of the heart at the junction of superior
venacava with right atrium. It is highly vascular; consist of thin, elongated muscle fibres, rich
in glycogen and mitochondria, fusiform in shape with longitudinal striations. These are called
P cells or Pacemaker cells. These fibres normally can generate and discharge impulses more
rapidly than any other pacemaker tissues and then the rate of discharge determines the rate at
which heart beats. That is why SAN is called cardiac pacemaker.
2. Internodal pathways: From SAN impulses passes to AVN through internodal fibers. They
are anterior (Bachmann), middle (Wnckebach) and posterior (Thorel) internodal fibers.
3. AV node (AVN): posteriorly on right side of the interatrial septum near the opening of
coronary sinus.
4. Bundle of his: it takes origin from AVN and then upwards to the posterior margin of the
membranous interventricular septum and then forwards below it. Bundle of his branches into
right and left bundle branches (RBB & LBB). LBB again branched into anterior and posterior
fascicles.
5. Purkinje fibres: takes origin from terminal division of the Rt & Lt branches of bundle of his
to penetrate the ventricular wall. These fibres are larger and thicker than cardiac muscle fibbers.
Because of larger diameter they transmit the impulse at a fast velocity of 4meter/sec as
compared to other conducting system. This allows almost immediate transmission of the
cardiac impulse throughout the entire ventricular system
3. Systemic and pulmonary circulation
Systemic circulation starts from the left ventricle through aorta. Aorta branches out into
different generation of arterial system and reaches at the capillaries. There is different regional
circulation in systemic circulation. The deoxygenated blood drain back into the heart through
two vena cava; superior and inferior vena cava. The venous blood reaches at the Right atria
and flow into right. Ventricle through tricuspid valve.
Pulmonary circulation starts from Right ventricle through pulmonary artery and branches into
pulmonary capillaries in the lungs. It gets oxygenated and oxygenated blood reaches in to Left.
Atria through two pairs of pulmonary veins. The oxygenated blood flows into the Left.
Ventricle through mitral (bicuspid) valve.
4. Nerve supply of heart
Sympathetic Nerve Supply

➢ Origin: Sympathetic fibers arise from the thoracic spinal cord (T1 to T4).
➢ Pathway: Preganglionic fibers exit the spinal cord and synapse in the sympathetic
ganglia (e.g., cervical and upper thoracic ganglia). Postganglionic fibers then travel to
the heart.
➢ Effects:
• Increases heart rate (positive chronotropic effect).
• Increases the force of contraction (positive inotropic effect).
• Enhances conduction velocity through the atrioventricular (AV) node (positive
dromotropic effect).
➢ Neurotransmitters: Primarily norepinephrine, which binds to adrenergic receptors.

Parasympathetic Nerve Supply

➢ Origin: The vagus nerve (cranial nerve X) is the main parasympathetic nerve supplying
the heart.
➢ Pathway: Vagal fibers travel to the heart and synapse in ganglia located near or within
the heart tissue.
➢ Effects:
• Decreases heart rate (negative chronotropic effect).
• Reduces the force of contraction (negative inotropic effect, though this effect is
less pronounced in the ventricles).
• Slows conduction through the AV node (negative dromotropic effect).
➢ Neurotransmitters: Primarily acetylcholine, which binds to muscarinic receptors.
Intrinsic Nerve Supply

➢ Cardiac Conduction System: The heart has its own intrinsic conduction system, which
includes:
• Sinoatrial (SA) Node: The natural pacemaker of the heart, initiating the
heartbeat.
• Atrioventricular (AV) Node: Delays the signal before it travels to the
ventricles.
• Bundle of His and Purkinje Fibers: Conduct impulses through the ventricles,
facilitating coordinated contraction

5. Cardiac muscle and its properties

➢ Cardiac muscle is an involuntary, striated muscle.
➢ The individual muscle cell is 100micro.m long and 15micro.m broad.
➢ Cardiac muscle fibre has a single centrally placed nucleus and the fibres are
interconnected through gap junctions.
➢ The fibres are branched and interdigitate freely with each other, but each is a complete
unit surrounded by a cell membrane, sarcolemma.
➢ Sarcomere is the functional unit of muscle fibre.
Properties of Cardiac muscle
1. Excitability: Cardiac muscle is excitable tissue. i.e. it forms a wave of depolarization
(excitation impulse) in response to a threshold stimulus. Excitability is due to high
resting membrane potential of cardiac muscle (RMP -90mV)
2. Functional syncytium: cardiac muscle contract as a single unit because of the presence
of gap junction between individual fibres. There are two syncytium atrial and
ventricular syncytium.
3. Autorhymicity : The heart continues to beat for quite some time even after all nerves to
it are cut. This is because of the presence of the specialized pacemaker tissue in the
heart.
4. Conductivity: Impulse conduction initiated in SAN spreads through the atrial wall to
the AV node. From AVN impulse passes through Bundle of His and its penetrates into
ventricular wall by Purkinje fibres.
5. Contractility: is the ability to respond to an impulse by contraction. Contractility is
mainly exhibited by atrial and ventricular muscles.
6. Define cardiac cycle. What are the different phases of cardiac cycle
Cardiac cycle is defined as the sequence of electrical and mechanical events which occur in the
heart during a single heartbeat. Duration of cardiac cycle =0.8 seconds.
Artal systole: 0.1 second Ventricular systole: 0.3 second
Atrial diastole: 0.7 second Ventricular diastole: 0.5 second
• Cardiac cycle is described from a point at the end of diastole and the beginning of
systole.
 • Each ventricles have 130 ml of blood is end diastolic volume (EDV). It is considered
as a preload of the ventricle. (i.e. load with which the ventricles are contracting).
• After complete ejection, some amount of blood remains in the ventricle. This end
systolic volume (ESV), which is about 60 ml.
• The difference between EDV and ESV is called stroke volume (SV), i.e. the volume
of blood ejected by each ventricle in each cardiac cycle. This is about 70 ml.
Phases of cardiac cycle
1. Atrial systole: atrial systole occurs following the impulse production in the SAN.
During this phase, blood from atria enters the ventricle due atrial contraction. 30%of
ventricular filling by atrial systole. During atrial systole turbulent pattern of blood flow
may cause law pitched sound called IV th heart sound, but it is not audible.
Atrial systole is followed by ventricular systole. Ventricular systole is divided into
isovolumetric contraction phase, rapid ejection and slow ejection phase.
2. Isovolumetric contraction phase (IVC): At the beginning of ventricular systole
myocardium contract without changing its initial length of muscle fibre and ventricular
volumes remains same. But the intraventricular pressure and myocardial tension
markedly increases. During IVC both AV valves are closed and the ventricles contract
as a closed chamber. The closure of AV valves produces a sound, called I st herat sound.
3. Rapid ejection phase (REP): As the intraventricular pressure is much above the aortic
and pulmonary arterial pressure, the semilunar valves open up there will be rapid
ejection of blood from ventricles to the corresponding vessels.
4. Slow ejection phase (SEP): As the blood reaches on aorta and pulmonary artery, the
pressure goes on rising it comes near to the ventricular pressure. Then the rapid flow of
blood turns to a slow ejection.
Ventricular diastole is divided into Protodiastole, Isovolumetric relaxation, Rapid filling and
Slow filling phases
5. Protodiatole: It is the first phase of ventricular diastole. Intraventricular pressure
decreases than aortic and pulmonary pressure. There is a tendency of backward flow of
blood from aorta and pulmonary artery. These are prevented by the closure of semilunar
valves (aortic & pulmonary) results in second heart sound.
6. Isovolumetric Relaxation (IVR): Even after ventricular systole, about 60 ml of blood
remains in the ventricle and both semilunar valves and AV valves are in the closed state.
The ventricle relaxes as a closed chamber. No change in the volume occurs since it is a
closed chamber and hence the phase is referred to as isovolumetric relaxation phase.
Here the myocardial tension and intraventricular pressure drops.
7. Rapid filling phase (RFP): As the intraventricular pressure drops down as it decreases
below atrial pressure, the AV valves suddenly open up results in rapid filling of
ventricles, referred as rapid inflow phase. Rapid flow of blood causes,
➢ Vibration of interventricular septum
➢ Oscillation of the valves and vibration of ventricular wall results in the III rd
heart sound.
 When Ist, II nd & IIIrd HS are heard it is called gallop rhythm.

8. Reduced filling phase / Diastasis: The incoming venacaval blood and pulmonary
venous blood flows into the corresponding ventricles through the already opened AV
valves. Finally slow filling of the ventricles is called diastasis. It is longest phase of
cardiac cycle.
9. Atrial diastole: during atrial diastole, atrial muscles relax, and blood flows into the
atria from great veins (superior vena cava, inferior vena cava and pulmonary veins)

7. Heart sounds
Heart sounds are the sounds produced by the mechanical activities of the heart during each
cardiac cycle. Phonocardiography is the technique of recording the sounds produced by the
heart.
Heart sound Phase of cardiac Cause Characteristics
cycle
First Isovolumetric Closure of AV Valve Soft, low pitched
contraction phase (LUBB)
Second Protodiatole phase Closure of Semilunar valve Sharp, high
pitched (DUBB)
Third Rapid filling phase Rush of blood flow to ventricle Low pitched
➢ Vibration of
interventricular septum
➢ Oscillation of the valves
and vibration of
ventricular wall
Fourth Slow filling phase Turbulent pattern of blood flow Inaudible
during atrial systole

8. ECG: basic principles of recording, types of leads- normal ECG

Recording of electrical activities of heart is known as electrocardiography (ECG). This
technique was first devised by Sir William Einthoven in 1903.
Recording of ECG is done with the subject in the supine position. Tie the electrodes on the
right arm, left arm and left leg. 12 leads are used clinically. They are;
Unipolar: Unipolar Chest leads & augmented chest leads.
➢ Chest leads are V1 to V6. (V1, V2, V3, V4, V5, V6)
➢ Augmented leads are aVR ,aVL&aVF
Bipolar Standard Limb Leads are LI, LII & LIII. These limb leads are connected according
to Einthoven’s triangle & Einthovens law

ECG WAVES
 ➢ P wave: First wave of ECG of duration 0.1 sec, amplitude 0.5mV directed upwards,
rounded or pointed. It is due to atrial depolarization and represents the spread of impulse
from SA node to atrial muscles.
➢ PR- Segment: Following the P wave there is brief isoelectric period of 0.04 sec, called
PR-segment.
➢ QRS- Complex: The ORS complex extends from the beginning of Q wave to the end
of S wave with 0.08 – 0.12 sec duration and height is 1.5 – 2mV. QRS complex is due
to the ventricular depolarization and it is completed just before the opening of semilunar
valves.
➢ ST- Segment: Following QRS complex there is long isoelectric period which extends
from the end of S wave to the beginning of T-wave, called ST segment. Its duration is
0.04 – 0.08 sec.
➢ T- Waves: Rounded positive deflection of duration 0.1 sec and 0.5mV height. It
represents ventricular repolarization.
➢ U –wave: Rarely seen, as positive rounded wave of 0.08 sec duration and 0.2mV height.
It is due to slow repolarization of papillary muscles.
➢ PR-interval: Interval from the beginning of P wave to the beginning Q wave or R wave
(if the Q-wave is absent. It represents atrial depolarization plus conduction time of
bundle of his.
➢ QT- interval: Interval from the beginning of Q wave to the end of T wave. Duration
0.40 – 0.43 sec. It represents ventricular depolarization plus repolarization.
➢ ST- interval: Interval from the end of S-wave to the end of T-wave. Normal duration
0.32 sec.
➢ TP- Segment: Period from the end of T-wave to the beginning of P wave of next cardiac
cycle. It represents polarized state of whole heart.
➢ J Point: Point between S wave and ST-segment. It is a point of no electrical activity.
➢ RR- INTERVAL: Interval between two R-waves in the ECG pattern obtained is called
RR interval. This helps to find out the HR from ECG. If the recording is regular, then
HR is equal to 60/RR-interval. For example, if the RR interval is 0.8 sec, then
HR = 60 / 0.8 = 75 / min.

USES OF ECG
• To find out the heart rate HR = 60/RR interval
• Diagnosis of cardiac arrhythmia- diagnosis of abnormal rhythm.
• Diagnosis of ischemia of heart disease- by noting elevation and depression of ST
segment.
• Diagnosis of electrolyte disturbances (hypokalemia, Hyperkalemia)
• Diagnosis of drug toxicity (digitalis)
• To assess the ventricular dimensions and thickness of ventricular wall.

9. Cardiac output: factors affecting and regulation of cardiac output

The amount of blood pumped by each ventricle per minute is cardiac output (CO). Normal
cardiac output is 5-6 L/min. it is the product of stroke volume (SV) and heart rate (HR).
CO = SV x HR= 70ml x 72/min = 5 L/min. Cardiac index is CO/min/square meter body surface
area and is approximately 3.4 L/min/m2. (2.8-4.2 L).
Factors affecting cardiac output
1. Heart rate: when HR rate increases CO also increases. Any factors which change HR
will also change CO.
a. Sympathetic tone: increase sympathetic tone will increase HR and inturn increase
CO.
b. Parasympathetic tone: increase in parasympathetic tone will decrease HR and inturn
decrease CO.
2. Force of contraction of heart and Stroke volume: when force of contraction of the heart
increases, stroke volume increase. Therefore, CO will increase. Force of contraction
and stroke volume is influenced by,
a. End diastolic volume (EDV): as EDV increases, SV increases and CO increases
b. Sympathetic stimulation and adrenalin: both will increase the force of contraction,
it will increase SV and CO.
3. Blood volume (BV): when BV increase CO will increase
4. Venous Return (VR): it is defined as the amount of blood returned to the heart by
venacava per minute. Any factors influencing VR will change the CO. E.g,
a. Muscular exercise- Muscle pump: during muscular exercise VR increases due to
squeezing of the veins so mor blood come to the heart. This increases co.
b. Thoracic pump or Respiratory pump: during inspiration intrapleural pressure and
intrathoracic pressure becomes more negative. The intraabdominal pressure rises
due to the descent of diaphragm. These factors favour VR.
c. Total blood volume: increase in blood volume will increase VR.
d. Body position and gravity: in standing position peripheral pooling of blood occurs
and this decrease venous return.
Regulation of cardiac output
Regulation of cardiac output includes all factors that regulate stroke volume and heart rate,
since cardiac output is the product of heart rate and stroke volume.

Heart Rate (HR): The number of beats per minute.

➢ Autonomic Nervous System: Sympathetic stimulation increases HR, while
parasympathetic stimulation decreases it.
➢ Hormones: Epinephrine increases HR during stress.
Stroke Volume (SV): The amount of blood pumped by the heart with each beat.

➢ Preload: The degree of stretch of the heart muscle before contraction. Increased preload
(e.g., due to increased venous return) can enhance stroke volume.
➢ Afterload: The resistance the heart must overcome to eject blood. Higher afterload can
decrease stroke volume.
➢ Contractility: The strength of the heart’s contraction. Increased contractility (e.g.,
through sympathetic stimulation) increases stroke volume.

Venous Return: The flow of blood back to the heart.

➢ Blood Volume: More blood volume increases venous return.

➢ Body Position: Standing can reduce venous return compared to lying down.
➢ Muscle Pump: Skeletal muscle contraction aids venous return.
Intrinsic Regulation

➢ Frank-Starling Law: The heart can increase its force of contraction in response to
increased end-diastolic volume, leading to a higher stroke volume.

Hormonal Regulation

➢ Catecholamines (e.g., epinephrine): Increase heart rate and contractility.

➢ Aldosterone and Antidiuretic Hormone (ADH): Affect blood volume and venous
return.

Exercise

➢ Increases demand for oxygen and nutrients, leading to higher cardiac output through
increased heart rate and stroke volume.

10. Heart rate and its regulation

The rate at which heart beats per minute. Normal rate is 72 beats/min. Normal range 70-90/min
The pacemaker, i.e., the SAN generates impulses and the conducting tissue conduct impulses
to the different parts of the heart. If the pacemaker is out of order, the rest of the heart can
generate impulses at a lower rate. Normally in humans, HR is kept constant. HR varies
depending on the body surface area and depending on the species. Increase in HR from normal
is called tachycardia. Decrease in HR is called bradycardia.
Regulation of heart rate
Regulation of heart rate includes following factors
➢ Neural factors
➢ Chemical factors
➢ Physical factors

Neural factors: heart is supplied by sympathetic and parasympathetic divisions of nervous

system.
➢ Sympathetic fibers supply the whole of the heart, i.e. the nodal tissues, atrial and
ventricular musculature. Norepinephrine is the neurotransmitter. Sympathetic
stimulation produces positive chronotropic effect (increase in HR)
➢ Parasympathetic preganglionic fibers reach the heart through the right and left vagus
nerves. The ganglion is close to the heart. Postganglionic parasympathetic fibers supply
the SA node, AV node and atrial musculature. Ventricle is devoid of parasympathetic
supply. Parasympathetic stimulation has an inhibitory effect on heart, i.e. they depress
the SA node and decrease HR. neurotransmitter at the postganglionic ending is
acetylcholine.
Control of heart rate by medullary centers: in the reticular formation of medulla, many vital
centers are present that control cardiac function called cardiac centers. The medullary centers
are;
➢ Cardioinhibitory centers is a group of neurons constituted by dorsal motor nucleus of
vagus, nucleus tractus solitarius and nucleus ambiguous. When these centers are
stimulated, reduction in heart rate.
 ➢ Vasomotor centers: when the vasomotor centers are stimulated due to sympathetic
stimulation, there is increase in heart rate.
The cardiac centers receive afferents from baroreceptors, from chemoreceptors and respiratory
system and from receptors within the heart and blood vessels.
• Impulses from baroreceptos: baroreceptors are the receptors give response to change
in blood pressure, located in the carotid sinus and aortic arch. When the baroreceptors
are stimulated reduces sympathetic tone and decrease in heart rate. Marey’ s law states
that heart rate is inversely proportional to blood pressure. Whenever BP is increased,
there will be reflex bradycardia, and whenever BP falls, there will be reflex tachycardia.
• Respiratory afferents: in forced respiration, changes in heart rate are observed which
is called sinus arrhythmia. Forced inspiration produces increase in heart rate, and forced
expiration decrease in heart rate.
• Afferents from chemoreceptors: chemoreceptors are the receptors give response to
changes in blood chemistry, present in carotid and aortic body. The chemoreceptor
afferents stimulate the inspiratory centers and increase in heart rate.
Chemical factors: chemical factors that affect heart rate are;
➢ Catecholamines: increase rhythmicity and contractility of the heart.
➢ Increased level of thyroid hormones increases heart rate. In hypothyroidism,
there is decrease in heart rate.
➢ Hypercapnia (increase in PCo2) decreases heart rate and hypocapnia increases
heart rate
➢ Hypoxia (decrease in PO2) in the initial stages increases heart rate. When the
degree of hypoxia become severe, heart rate becomes irregular and arrhythmias
occur.
➢ Acidosis decreases heart rate
➢ Parasympatholytic drugs increase heart rate. Parasympathomimetic drugs
decrease heart rate. Nicotine increases heart rate.
Physical factors: when there is an increase in body temperature as in increased metabolic
activity, heart rate is increased. Muscular exercise increases heart rate.

11. Arterial pulse and venous pulse

Arterial pulse is the expansion of the arterial walls passively produced by pressure changes
during systole and diastole. Pulse waves are obtained only up to the smallest arteries.
Venous pulse is the positive and negative pressure changes occurring in the right atrium during
each cardiac cycle transmitted in the form of a wave to the veins near the heart. Venous pulse
is observed only in larger veins near the heart like Jugular vein.

12. Define blood pressure. What are the components and give its normal values
The Arterial BP is the lateral pressure exerted by a column of blood on the vessel wall while
flowing through it. It can be measured by Sphygmomanometer.
Clinically B.P is expressed as SBP/DBP. Normal: 120/80mmHg.

Components of Blood Pressure

➢ Systolic BP: Is the max. pressure exerted during systole; normal 100-130mmHg
 (average 120mmHg)
➢ Diastolic BP: Is the min. pressure exerted during diastole; normal:70-85mmHg
(average 80mmHg)
➢ Pulse Pressure: It is the difference of systolic and diastolic BP; normal 40mmHg.
➢ Mean BP: It is the average pressure throughout the cardiac cycle and computed as
DBP+1/3PP; normal: 95-100mmHg.

13. Determination Blood pressure

BP can be measured by two methods; direct and indirect.
• Direct method: In this method a cannula is introduced in to an artery and secured in
position with help of ligature; the other end of the cannula is connected to a mercury
manometer, consequently the mercury column will rise. Direct method is unsafe,
inconvenient and involves high risk of infection. It is appropriate only for research
purposes such as measurement of B.P in animals.
• Indirect method: It involves balancing of pressure in a bag i.e. Air pressure against the
pressure of the blood in an artery. The air pressure is estimated by means of mercury
manometer.
Sphygmomanometer
• It consists of an inflatable rubber bag covered by a non-distensible cloth envelop called
Riva-Rocci Cuff. The cavity of the bag is connected by a longer tube to manometer and
by a short tube to a rubber pump; by this means the bag can be inflated to any desired
pressure.
• A small valve is provided between the pump and the bag which permits the escape of
air and reduction of the pressure as required compensating tissue resistance.
• The manometer is a U-shaped tube, one limb being broader than other. The broader
limb is the reservoir for mercury and the narrow limb is graduated from 0 to 300mmHg.
Palpatory method:

➢ Allow the subject to sit comfortably in a chair or to lie supine position.

➢ The uninflated cuff of sphygmomanometer is wrapped firmly around the bare upper
arm 2-3cm above the elbow joint (antecubital fossa) at the heart level.
➢ Feel for the radial pulse and inflate the rubber bag to increase the pressure above the
point at which the radial pulse will disappear at the wrist.
➢ Now deflate the cuff slowly, releasing the pressure, while lowering the pressure, keep
palpating the radial artery and reading is take just when pulse starts reappearing. This
gives the systolic B.P

Disadvantages of Palpatory Method

➢ DBP cannot be estimated.
➢ SBP estimated is lower than the actual by 6-10mmHg.

Auscultatory Method

➢ This method was introduced by Russian physician, Korotkoff, in 1905.

➢ Method: Allow the subject to sit comfortably in a chair or to lie in supine position.
➢ The uninflated cuff of sphygmomanometer is wrapped firmly around the upper arm
2-5cm above the elbow joint at the heart level.
➢ Place the chest piece of stethoscope over the arm medial to the tendon of biceps
where pulsations of brachial artery are felt. Under ordinary circumstances, if a
stethoscope is placed over an artery, no sound can be heard, as the streamline flow
 of blood through the unconstricted blood vessels produce no sound.
➢ Inflate the cuff until the pressure in it is well above the SBP as measured by
palpatory method. The brachial artery gets occluded by the cuff and no sound can
be heard with stethoscope.
➢ Now gradually lower the cuff pressure by opening the valve till a clear sharp tapping
sound is heard. The cuff pressure at which the sound is heard first, is SBP
➢ The pressure in the cuff is further lowered, while listening for the appearance of the
sound of Korotkoff’s. The sound under-goes a series of changes in quality and
becomes dull and muffled, to finally disappear. The cuff pressure at which the sound
becomes muffled or disappears is the DBP

14. Determinants of Blood pressure or factors regulating blood pressure

Determinants of blood pressure: BP = CO X PR

➢ Cardiac Output/ Pumping action of heart: CO mainly determines SBP. As CO

increases SBP increases.
➢ Peripheral Resistance: PR mainly determines DBP. In conditions of increase in PR
(atherosclerosis) results in increase in DBP.
➢ Blood volume: increase in BV increases SBP. Increased BV cause increasing VR, EDV,
Force of contraction, SV, CO, increases SBP.
➢ Elasticity of vessel wall: having inverse relationship with PR. Elasticity of the vessel
wall and PR act together to maintain DBP. Elasticity of vessel wall also affects the SBP.
The distensibility of vessel wall determines SBP.
➢ Velocity of blood: velocity having an inverse relationship with lateral pressure.
➢ Viscosity of blood: PR depends on viscosity of blood. Greater the viscosity greater will
be the pressure required to force blood through the blood vessel in a given time. As the
viscosity increases PR increases, so DBP increases. For e.g. in polycythaemia,
leukaemia etc the viscosity is increased and there is an increase in the DBP.

15. Mechanism of regulation of blood pressure

The various mechanisms exist within the body to regulate systemic arterial BP. These
mechanisms are well interconnected and their main aim is to maintain normal mean blood
pressure (MBP) within narrow range, between 95-100mmHg. The different mechanisms are,
➢ Short-term regulation &
➢ Long term regulation

Short-term Regulation
➢ It is achieved through the neural mechanism. It very quick in action, but may not be
accurate enough.
➢ This begins to act within seconds to minute after arterial BP becomes abnormal.
➢ These are primarily circulatory reflexes, which begin to act within seconds and help to
control BP from rising extremely high or falling extremely low.
The circulatory reflexes are;
➢ Baroreceptor reflex
➢ Chemoreceptor reflex
➢ CNS Ischemic response.

Baroreceptor Reflex
➢ Baroreceptors are extremely abundant in the wall of carotid sinus & aortic arch
 ➢ Baroreceptors get stimulated when pressure increases and sends stimulus to sensory
area of vasomotor center (tractus solitarius)
➢ Signals from carotid baroreceptors are transmitted through glossopharyngeal nerve.
And aortic receptors transmit through vagus nerve.

When baroreceptor signals reach tractus solitarius, it inhibits the VMC & excites vagal para-
sympathetic center. This results in vasodilation (veins & arterioles), ↓heart rate & ↓strength of
heart contraction. Causing ↓ peripheral resistance & ↓CO, which result in ↓BP
Chemoreceptor Reflex: Chemoreceptors are present in Carotid & aortic bodies
➢ Stimuli - ↓O2, ↑CO2 & ↑H+ion.
➢ Signals from chemoreceptor excite vasomotor center, which elevates BP

➢ The chemoreceptors are chemo-sensitive cell sensitive to O2 lack, Co2 excess or H2 ion
excess. They are located in carotid bodies and aortic bodies. The chemoreceptor excites
nerve fibres pass through Hering's nerve and vagus nerve in to the VMC of the brain
stem.
➢ Each carotid and aortic body is supplied with an abundant blood flow through a small
nutrient artery, so that chemoreceptors are always in contact with arterial blood.
Whenever BP fall below critical level, the chemoreceptors become stimulated, because
diminished blood flow causes decreased O2 as well as building up of CO2 and H2 ions,
that are nor removed by slow flow of blood.
➢ The signals transmitted from chemoreceptors in to the VMC excite VMC and this
elevates arterial pressure back to the normal. This reflex helps to return the lateral
pressure back towards the normal level whenever it falls too below.
CNS Ischaemic Response

➢ This mechanism considered as Last ditch stand mechanism to prevent the final death of
a person.
➢ When the MBP drops below 40mmHg (20-30mmHg), to cause CNS ischaemia, which
causes CO2 accumulation in the VMC, which directly stimulates VMC. Excitation of
VMC causes tremendous powerful sympathetic discharge throughout the body. Thus
HR & BP increase to maintain normal supply of blood to the brain.

Long-Term Regulation of BP

The long-term regulation is mainly achieved through the kidney by altering ECFV or BV as
such. These mechanisms are slow to begin acting. Generally, it takes 3-10 days. These
mechanisms have the ability to bring the arterial BP all way back to normal.
Long term mechanisms broadly operate in two ways.
➢ Direct mechanism (Renal fluid or ECFV mechanism)
➢ Indirect mechanism (Hormonal mechanism)

Direct Mechanism
➢ These mechanisms involve control of BV by kidneys directly, therefore also called renal
fluid mechanism or ECFV mechanism.
➢ When ECFV increases, the BV increases. This will tend to increase BP.
➢ However, when the pressure is increased, kidney excrete more amount of water and
salt, particularly sodium. This reduces ECFV and in-turn BP is reduced.
➢ Even slight increases in BP can double the water excretion which is known as pressure
diuresis. Elevated BP also leads to sodium excretion which is called pressure
natriuresis.
➢ When the BP falls due to decreased ECFV, reabsorption of water from renal tubule is
increased and the volume of ECF is restored

ECFV
BP

BP
Renal Ischaemia

GFR
GFR

Filter Na
Water & electrolyte retention

BV
ECFV

BP
BV

CO BP
Indirect Mechanism: These mechanisms involve control of kidney functions via hormonal
system.
Aldosterone system: Aldosterone causes retention of sodium & water and thereby increases
ECFV and BV, increases BP.

In arterial BP

Tissue perfusion

Stimulate Adrenal Cortex

Aldosterone Secretion
Via kidney

Water & electrolyte retention

ECFV

BV

CO

BP

Renin-angiotensinogen system: When BP decreased renin secreted from JGA, which act on
angiotensinogen (alpha 2 globulin in plasma) and convert it in to angiotensin I. Angiotensin
converting enzyme convert angiotensin I in to Angiotensin II. Angiotensin II causes
constriction of arterioles in the body, so that PR is increased and the BP rises. Simultaneous
constriction of afferent arterioles in kidneys causes retention of water and salts, so that the
ECFV is increased. This in turn restores the normal BP. Angiotensin II also stimulates adrenal
cortex to secrete aldosterone. This increases reabsorption of sodium from renal tubules. Sodium
reabsorption is followed by water reabsorption and thereby ECFV increase and BP becomes
normal.
Other Hormones Regulating BP
➢ Adrenalin increases SBP by increasing force f contraction and increasing CO. But it
decreases DBP. Adrenalin causes constriction of blood vessels through alpha receptors.
It also causes dilation of blood vessels through the beta receptors in some areas of the
body like skeletal muscle, liver and heart.
➢ Nor adrenalin: increases DBP due to general vasoconstriction. It has a stronger effect
on blood vessels. It causes constriction of all blood vessels throughout the body via
alpha receptors. The action of nor- adrenalin increases total PR and thereby elevate BP
➢ Thyroxine: increases SBP by increasing CO & Decreases DBP due to increased
metabolic activity by thyroxin. These metabolites cause vasodilation and so the PR is
reduced. This decreases the DBP.
➢ Aldosterone: increases BP
➢ ADH: increase BP
➢ Angiotensin: increases BP
➢ Serotonin (5HT): Serotonin secreted in hypothalamus, limbic system, cerebellum,
spinal cord, retina and GIT. It produces vasoconstriction and increases BP.
➢ VIP (Vasoactive intestinal peptide): is a polypeptide is secreted in the stomach and
SI. A small amount of this hormone is also secreted in LI. VIP is a vasodilator and cause
dilation of blood vessels and decreases BP.
➢ Bradykinin: is produced in the blood during conditions like inflammation. It is a
vasodilator substance and cause reduction in BP.
➢ Histamine: vasodilator
➢ Acetylcholine: vasodilator
➢ Atrial natriuretic peptide (ANP): Is a hormone secreted by the musculature of the
atria of the heart. It causes the dilation of blood vessels and decreases BP.

16. Hypertension and hypotension

Feature Hypertension (High Blood Hypotension (Low Blood Pressure
Pressure)
Definition Blood pressure consistently above Blood pressure consistently below
normal levels normal levels
Normal Generally above 130/80 mmHg Typically, below 90/60 mmHg
Range
Causes - Genetics - Dehydration
- Poor diet (high salt, low - Blood loss
potassium - Heart problem
- Lack of exercise - Endocrine issues
- Obesity - Severe infection (septicemia)
- Chronic stress

Symptoms - Often asymptomatic - Dizziness

- Headaches - Fainting
- Shortness of breath - Fatigue
- Nosebleeds - Blurred vision
17. Coronary circulation
The myocardium is supplied by coronary arteries and the blood flow through the heart is
referred to as coronary circulation.

➢ Heart is supplied by the right and left coronary arteries, which arise from the base of
the aorta.
➢ The left coronary artery divides into left circumflex artery and anterior descending
artery. The left circumflex artery passes along the AV groove, comes posterior and
passes down as the posterior descending artery. The anterior descending artery passes
down along the interventricular groove.
➢ The right coronary artery goes along the right AV groove for some distance and then
splits into several descending branches.
Parts supplied by right and left coronaries
Right coronary Left coronary
Right atrium Anterior and lateral portions of left ventricle
Posterior portion of interventricular septum Anterior portion of interventricular septum
Right ventricle Left atrium
Posterior part of left ventricle

18. Circulatory shock and classification of shock

Shock is a general term that means depression or suppression of body functions produced by
any disorder. Circulatory shock is shock developed by inadequate blood flow throughout the
body. It is life threatening condition and if the affected person is not treated immediately, it
may result in death.
Clinical features of shock
➢ Cardiovascular system: fall in arterial blood pressure which results decreased blood
flow to all organs
➢ Respiratory system: breathing become rapid and shallow resulting in hypoventilation.
Some person may develop respiratory distress syndrome.
➢ Renal system: initially urine output is reduced. Later tubular necrosis develops resulting
in acute renal failure.
➢ Skin: because of stagnant hypoxia, skin become pale and cold. Cyanosis develops in
many parts of the body, particularly in ear lobes and fingertips. There is excess
sweating.
➢ Vital organs such as liver and endocrine glands fails to function due to necrosis
➢ Central nervous system: lack of blood flow to brain produces ischemia resulting in
fainting and irreparable damage of brain tissue.
TYPES OF SHOCK
Circulatory shock is primarily classified in four types
➢ Hypovolemic shock: due to decrease blood flow
➢ Vasogenic shock: due to increased vascular capacity
➢ Cardiogenic shock: due to cardiac disease
➢ Obstructive shock: due to obstruction to blood flow
Hypovolemic shock/cold shock: Shock due to decreased blood volume is called hypovolemic
shock. Important manifestations of hypovolemic shock are decrease in cardiac output, low,
blood pressure, increase in respiratory rate and restlessness a or lethargy
Some common types of hypovolemic shock are,
➢ Hemorrhage shock: due to hemorrhage.
➢ Traumatic shock: due serious injury or wound caused by some external force
➢ Burn shock: caused the effect of burn
➢ Dehydration shock: develops during severe dehydration

Vasogenic shock: Shock occurs because of inadequate blood supply to the tissues. Types of
vasogenic shock are,
➢ Neurogenic shock: during severe emotional outbursts like over excitement, fear and
anger autonomic nervous system dysfunction can happen. This produces sudden
marked vasodilation, fall in venous return, decrease in cardiac output and hypotension.
Fainting or syncope is commonly seen.
➢ Anaphylactic shock: some hypersensitivity reactions can lead to release of histamine or
other substances which produce vasodilation as well as increase in capillary
permeability. Decrease in blood volume and decrease in cardiac output.
➢ Septic shock: sepsis is the condition characterized by the presence of pathogenic
organisms or their toxins in blood or tissue. Shock developed during sepsis is known as
septic shock or blood poisoning.
Cardiogenic shock: Shock due to cardiac disease is called cardiogenic shock
Types of cardiogenic shock
➢ Shock due to arrhythmia (abnormal heart beat)
➢ Shock due myocardial ischemia
➢ Shock due to congestive heart failure
Obstructive shock: Shock due to the obstruction to blood flow through circulatory system is
called obstructive shock.
Causes of obstructive shock;
➢ Tumor in myocardium
➢ Cardiac tamponade (compression of heart due accumulation of fluid in pericardial
space)
➢ Obstruction of blood vessels in lungs due to embolism.

19. Cardiovascular changes during exercise

During exercise, the cardiovascular system undergoes several important changes to meet the
increased demands of the body.

1. Increased Heart Rate: The heart rate increases significantly. Reason: To pump more blood
(and therefore more oxygen) to the working muscles.

2. Increased Stroke Volume: The amount of blood ejected by the heart with each beat
increases. Reason: The heart becomes more efficient at pumping blood due to improved
contractility and increased venous return.
3. Increased Cardiac Output: Cardiac output (the total volume of blood the heart pumps per
minute) rises dramatically. Cardiac Output = Heart Rate × Stroke Volume. Reason: To deliver
more oxygen and nutrients to muscles while removing waste products like carbon dioxide.

4. Redistribution of Blood Flow: Blood flow is redirected from non-essential organs (like the
digestive system) to the working muscles and skin. Reason: To prioritize oxygen delivery to
areas that need it most during exercise.

5. Increased Blood Pressure: Systolic blood pressure rises significantly, while diastolic
pressure may remain stable or rise slightly. Reason: Increased cardiac output and vascular
resistance in exercising muscles.

6. Enhanced Blood Vessel Dilation: Blood vessels in the muscles dilate (widen) to
accommodate increased blood flow. Reason: This process, known as vasodilation, helps lower
resistance and allows more blood to reach active tissues.

7. Improved Oxygen Utilization: Muscles become better at using oxygen during exercise.
Reason: Enhanced efficiency of cellular respiration and increased capillary density in muscle
tissues.

8. Increased Respiratory Rate: Breathing rate and depth increase. Reason: To facilitate
greater oxygen intake and carbon dioxide removal, complementing cardiovascular changes.