Chapter-6a)

Definition and Significance of BP

blood pressure lateral pressure exerted by the flowing blood on aortic vessel wall
Pressure

Definition

Physio. significance

Systolic

highest pressure during cardiac cycle

work done by heart

Diastolic

lowest pressure during cardiac cycle

peripheral resistance

Pulse

systolic diastolic

stroke Volume

diastolic+ 1/3 pulse pressure (PP)

perfusion pressure

pressure
Mean blood
pressure
b)

Factors affecting BP

Physical

BP= CO X PR or BP = SV X HR X PR

(determinants) CO in turn depends on blood volume, venous return

And PR depends on diameter of vessel, viscosity, velocity

Physiological

Factors increasing BP- obesity, salt intake, exercise, anxiety, meals, cold, old
age
Factors decreasing BP- child, female, sleep, standing,

Pathological

Factors increasing BP (cause of Hypertension )- essential HT,

(Clinical)

secondary(Renal)
Factors decreasing BP (cause of hypotension )- shock
Vasomotor centre (VMC)

Structure of VMC
1) Vasoconstrictor area or area C-l. - located bilaterally in the anterolateral portions of
upper medulla.
2) Vasodilator area or area A-l- located bilaterally in anterolateral portions of lower half of
medulla.
3) Sensory area or A-2- located bilaterally in the tractus solitarius, in the poster lateral
portions of the medulla and lower pons.
Inputs of VMC
1) inhibitory inputs- from baroreceptors (carotid and aortic sinus thro 9 and 10 cranial
nerves to NTS), lungs, parts of cerebral cortex and limbic system including hypothalamus.
1) excitatory inputs- from chemoreceptors (carotid and aortic body thro 9 and 10 cranial
nerves to NTS), pain receptors from skin and joints, parts of cerebral cortex and limbic
system including hypothalamus. Hypoxia and hypercapnia in brain (due to cerebral
ischemia) is strong direct stimulus for VMC
outputs of VMC
Stimulation of VMC causes stimulation of sympathetic and inhibition of parasympathetic
nervous system (vagus) and vice versa.

c)

Regulation of BP

Short term regulation (mainly by nervous

reflexes, starts in secs to mts)

1) baroreceptors reflex
2) atrial low pressure / cardio-pulmonary

Long term regulation (takes hours to days to

starts )

8) renal blood volume pressure control

mechanism

10) renin angiotensin (AII) aldosterone

mechanism

reflex
3) chemo receptor reflex

11) role of other hormones (ANP, ADH,

adrenaline,

4) CNS-Ischemic reflex
5) abdominal compression reflex
6) stress relaxation and reverse stress
relaxation
7) capillary fluid shift mechanism

d)

14) role of local vasoconstrictors- endothelins

(ET1,2), serotonin
15) role of local vasodilators- NO, PGE2,
histamine, bradykinin

Short term regulation (mainly by nervous reflexes, starts in secs to mts)

1) Baroreceptors reflex
Physiological Anatomy
Baroreceptors or pressoreceptors are the stretch receptors and are located in the walls of
large systemic arteries. They are extremely abundant in two areas:
-Wall of internal carotid artery slightly above the carotid bifurcation is known as carotid
sinus.
-Wall of aortic arch is known as aortic sinus. Baroreceptors are spray type nerve endings
lying in the walls. They are stimulated when stretched.
InnervationsImpulses from carotid sinus are carried by Herings nerves to the glossopharyngeal nerve
and then to tractus solitarius of medulla. Impulses from aortic sinus are carried through
vagus nerve to the tractus solitarius
How it works
When the blood pressure increases above the normal level, it causes baroreceptor reflex as
follows:
Increased blood pressure Signals from baroreceptors to tractus solitarius of medulla
Secondary signals from tractus solitarius to inhibit vasomotor area
Inhibition of VMC Inhibition of sympathetic and stimulation of para sympathetic
nervous system vasodilatation, decreased heart rate & decreased force of contraction of

the heart Decreased cardiac output Decreased blood pressure

Thus blood pressure returns back to normal.
Exactly opposite sequence of events occurs when blood pressure is lowered.
Characteristicsi) Operates between 60 to 160mmHg (best at 100 mm Hg)
ii) Respond more to change in BP than stationary BP
iii) Act as buffer system and 9 and 10 nerves are called buffer nerves as this system correct
postural & day to day variation in BP.
iv) Reset in two three days to changed value of BP so very fast and powerful short term
regulator but not valuable in long term regulation of BP.
v) Respond to pulse pressure but most sensitive to MBP

2) Atrial low pressure or cardio-pulmonary reflex

Atria contain stretch receptors. These are also called low pressure receptors. They play role
in minimizing the effect of decreased blood volume on arterial blood pressure. The reflex
occurs as follows:
Increased blood volume Increased cardiac output Increased blood pressure Stretch
of atria Reflex dilatation of afferent arterioles of kidneys (This effect occurs at other
arterioles also) which Increases GFR that in turn increases output of water and diminishes
release to antidiuretic hormone (ADH) that in turn decreases water absorption from distal
nephron Decreased blood volume Lowering of blood pressure back to normal

3) Chemo receptor reflex

Carotid and aortic bodies contain chemoreceptors which are mainly stimulated by chemical
stimuli such as oxygen lack, carbon dioxide excess and hydrogen ion excess. They are
profusely supplied with blood and therefore when blood pressure falls below a critical level
80 mm Hg chemoreceptors are stimulated because of diminished blood flow resulting into
diminished O2 supply and building up of CO2 and H+ ions. They send impulse through
Herings nerves (from carotid bodies) and vagi nerves (from aortic bodies) to the vasomotor
centre. This elevates arterial pressure. Thus reflex is responsible for bringing arterial

pressure back to normal. But this reflex is not very powerful controller of arterial blood
pressure. Still it is important as it is stimulated at low pressure and helps in preventing
further fall in blood pressure.
4) CNS-Ischemic reflex
When blood flow to the vasomotor centre in the brain stem is decreased enough to cause
nutritional deficiency (i.e. cerebral ischemia) the neurons in the vasomotor centre are
strongly excited. This is due to accumulation of CO2, lactic acid locally near the vasomotor
centre. Excitation of vasomotor centre causes strong sympathetic stimulation leading to
vasoconstriction leading to increase in blood pressure. Peripheral vessels become totally
occluded at certain areas, e.g. kidneys. This most powerful response that activates
sympathetic vasoconstrictor system strongly is called as CNS ischemic response. It is
initiated when blood pressure falls below 60 mm Hg. This acts as an emergency arterial
pressure control system. If rise of pressure does not relieve CNS ischemia, neuronal cells
begin to suffer and within 3 to 10 minutes become totally inactive.
Example of CNS-Ischemic reflex is Cushing reaction- When CSF pressure rises and becomes
equal to arterial pressure; it compresses the arteries in the brain and cuts off the blood
supply to the brain. This initiates the CNS ischemic response. This causes rise in blood
pressure. When blood pressure becomes greater than CSF pressure, blood flows through
the vessels of brain and ischemia is relieved. Blood pressure comes to equilibrium at a new
level. This effect is called Cushing reaction. It protects the vital centers in the brain.

5) Abdominal compression reflex

Whenever vasomotor centre is stimulated (e.g. baroreceptor reflex, chemoreceptor reflex)
other reticular areas of brain stem are also stimulated. They send simultaneous impulses
through skeletal nerves to skeletal muscles of the body especially abdominal muscles.
Contraction of abdominal muscles compresses the abdominal venous reservoirs. This
causes increased venous return to the heart and therefore increased cardiac output. This
overall response is called abdominal compression reflex. During exercise the skeletal
muscles contract and compress the blood vessels. This causes translocation of large
quantities of blood from the peripheral vessels into the heart and lungs. This increases the
cardiac output.

6) Stress relaxation and reverse stress relaxation

When blood pressure is high, after some time smooth muscle of blood vessel relaxes
leading to vasodilatation and fall in blood pressure this is termed stress relaxation.

When blood volume and pressure is low the vessel constricts over a small volume and
pressure inside rises, this is termed reverse stress relaxation.

7) Capillary fluid shift mechanism

When arterial blood pressure rises, the pressure at arterial end of capillaries becomes
higher than normal. This causes greater fluid to be shifted from capillaries to interstitial
fluid. This in turn reduces the total circulating blood volume and venous return and thus
reduces the blood pressure.
When arterial blood pressure falls, pressure at arterial end of capillaries and therefore at
venous end of capillaries is reduced.
This causes greater absorption of fluid from interstitial space into the capillary. This
increases blood volume and therefore the blood pressure.

Long term regulation (takes hours to days to starts)

8) Renal blood volume pressure control mechanism
When there is increase in extracellular fluid volume, it causes rise in blood volume and
therefore rise in blood pressure. Rising pressure has a direct effect on kidneys to excrete
excess of water (pressure diuresis) and also increase output of sodium (pressure
natriuresis). Pressure diuresis and pressure natriuresis bring blood volume back to normal
and therefore returning blood pressure back to normal.
Example- decrease BP decrease GFR decrease urine output increase blood volume
increase BP
Increase BP increase GFR increase urine output decrease blood volume
decrease BP
Thus pressure diuresis and natriuresis is the fundamental mechanism of long-term
regulation of blood pressure. With evolution however multiple refinements have been
added to make the fundamental system more exact in its control. Especially important
refinement is renin-angiotensin mechanism.
Characteristicsi) Phylogenitically oldest, ii) although take hours to days to start but most effective &

powerful mechanism, iii) work on infinite gain principle means makes 100% correction in BP.

10) Role of renin angiotensin (AII) aldosterone mechanism

Despite variable salt intake, long term level of arterial pressure is maintained normal
because of renin-angiotensin system as given below.
Accumulation of salt indirectly increases the extracellular fluid volume because of two
reasons:
1. When there is excess salt in the body, there is increased osmolality of body fluids. This
increased osmolality stimulates the thirst centre, making person drink large quantities of
water to dilute the extracellular fluid. Thus there is increase in extracellular fluid volume.
2. Increased osmolality of body fluids also stimulates hypothalamic posterior pituitary gland
system to secrete increased quantities of ADH (antidiuretic hormone). This causes increased
reabsorption of fluid from the distal renal tubules. This causes increase in extracellular fluid
volume.
Example- Increased salt intake Increase osmolarity Increased ECF volume due to
stimulation of thirst and ADH release Increased blood volume Increased blood pressure
Increased Renal blood flow Decreased renin and angiotensin Decreased retention
of salt and water Increased decreased ECF volume Increased blood volume
Returning blood pressure back to normal
Decrease in salt intake will have exactly opposite effects.

Other mechanisms
11) Some role is played by other hormones like ANP, ADH, adrenaline etc especially in
emergency conditions.
14) Some role by local vasoconstrictors like - endothelins (ET1,2), serotonin
15) And some role by local vasodilators- NO, PGE2, histamine, bradykinin

e)

Experimental studies

one kidney Goldblatts hypertensionWhen one kidney is removed and a constrictor is placed on the renal artery of the remaining
kidney, then within few minutes arterial pressure begins to rise and continues to rise for
several days. The hypertension produced in this way is called one kidney Goldblatts
hypertension. The early rise in blood pressure is due to renin-angiotensin vasoconstrictor
mechanism. The second rise is caused by fluid retention.

two kidney Goldblatts hypertensionHypertension that develops when the artery to one kidney is constricted while artery to the
other kidney is still normal is called two kidney Goldblatts hypertension.

f)

Measurement of BP

direct & indirect

g)

-Clinical- hypertension (HT)

What is HT3 consecutive reading more than 140/90 in adult male.

Causesessential (90%), secondary (renal, endocrine, cns disease, oral contra)
type, c/f, diagnosis, complications
Hypertension if left untreated can cause following lethal effects:
-Coronary heart disease, heart attack, heart failure
-Brain hemorrhages, infarcts
-Hemorrhages in kidneys leading to renal failure, uremia and death.

Treatment
-life style-Drugs- There are many antihypertensive drugs. The common drugs are:
-Which decrease the activity of sympathetic nervous system, e.g. beta blockers.
-Which decrease tubular absorption of salt and water, e.g. diuretics
-Which block the action of renin-angiotensin, e.g. angiotensin converting enzyme inhibitors.
-Drugs paralyzing the smooth muscle of renal vasculature, e.g. calcium channel blockers

Chapter-5- Heart rate

a)

Definition and value of heart rate

No of heart beats per minute. Normal value- 60-100 /mt (72) in adult.

b)

Factors affecting heart rate

Physiological

Factors increasing heart rate- anxiety, exercise, infant, pregnancy

Factors decreasing heart rate athletes (due to high vagal tone),
, sleep

Pathological
(Clinical)

Factors increasing heart rate (cause of tachycardia- heart rate 100 /mt or
more)- fever, anemia, hypoxia, hyperthyroidism
Factors decreasing heart rate (cause of bradycardia- heart rate 60 /mt or
less)- hypothyroidism, hypothermia, increase BP, increase ICP, drugs

c)

Regulation of heart rate

Mediated via vasomotor center (VMC)

1) Marey reflex (via Baroreceptor reflex) - Increased B.P. stimulation of baroreceptors
Impulses through IX and X cranial nerves nucleus of tractus solitarius stimulation of
vasodilator area and inhibition of vasoconstrictor area increase in vagal tone and
decrease sympathetic tone reflex bradycardia
2) Bain bridge reflex (via Cardiopulmonary reflex) - Increased venous return stimulation of
stretch receptors in right atrium afferent impulses through vagus
Inhibition of vasodilator area decrease in vagal tone tachycardia
3) Chemo receptor reflex- low po2, high pco2 and acidosis stimulation of chemoreceptors
Impulses through IX and X cranial nerves nucleus of tractus solitarius stimulation of
vasomotor center tachycardia
3) Cushing reflex (via CNS ischemic reflex) - Increase ICP Increases B.P. due to CNS
ischemic reflex Increase B.P. in turn causes reflex bradycardia by Baroreceptor reflex
4) Role of higher centers- some parts of cerebral cortex and limbic system including
hypothalamus increases heart rate while some other parts decreases heart rate
5) Role of peripheral afferents- example- painful stimuli produces tachycardia
while nasal mucosa irritation (by v nerve) produces bradycardia.
6) Role of respiratory center- during inspiration impulse spill over from respiratory center to
VMC and heart rate increases (it is called sinus arrhythmia)

Mediated without vasomotor center (VMC)

7) Role of thyroid hormones- T3, T4 directly stimulates SA node and cause tachycardia
8) Role of temperature- increase temperature directly stimulates SA node and cause
tachycardia

Shock

a)

Definition of shock
Inadequate blood flow to body cells specially vital organs heart / brain

b)

Causes of shock
Shock caused by reduced cardiac output
1) Hypovolumic shock. There is decrease in blood volume due to any cause, e.g.
hemorrhagic shock (injury, fracture), dehydration shock (diarrhea, vomiting, excess
sweating, and burns), and surgical shock.
2) Cardiogenic shock, due to decreased pmping ability of the heart because of cardiac
abnormalities, e.g. myocardial infarction, toxic states of heart, severe heart valve
dysfunction, heart arrhythmias.
3) Obstructive shock, caused by obstructive blood flow, e.g. tension pneumothorax,
pulmonary embolism, cardiac tumor, etc.
4) Neurogenic shock, caused by general or spinal anesthesia, brain damage, emotional
fainting.
5) Anaphylactic shock, an allergic reaction which causes marked venous and arteriolar
dilatation and increased capillary permeability due to release of histamine or histamine like
substances.

Shock occurring without decrease in cardiac output

6) Excessive metabolism of the body due to which normal cardiac output is inadequate.
7) Septic shock. Abnormal tissue perfusion patterns so that most of the cardiac output is
passing through blood vessels besides those that are supplying the local tissues with
nutrition. It occurs due to blood borne infection, e.g. peritonitis. Usually there is high fever,
vasodilatation, high cardiac output and slugging of blood.

c)

Stages of shock
1. Non-progressive stage (compensated stages).
Following circulatory compensatory mechanisms (- feedback mechanisms) eventually cause

full recovery without help of outside therapy.

Short term mechanisms1) baroreceptors reflex, 2) atrial low pressure / cardio-pulmonary reflex, 3) chemo receptor
reflex, 4) CNS-Ischemic reflex
Intermediate term mechanisms5) abdominal compression reflex, 6) stress relaxation and reverse stress relaxation
7) capillary fluid shift mechanism
Long term mechanisms8) role of kidneys & hormones (specially renin angiotensin (AII) aldosterone mechanism)
2. Progressive stage.
When shock becomes severe enough structures of circulatory system begin to deteriorate
and various types of positive feedback mechanisms develop. These cause vicious cycle of
progressively decreasing cardiac output. This is called progressive shock.
3. Irreversible stage.
Shock progresses to such an extent that all forms of known therapy are inadequate to save
persons life.

d)

Effects of shock (Ex- Hemorrhage)

1.
2.
3.
4.
5.

Decreased blood pressure, tachycardia, reduced stroke volume,

Reduction in velocity of blood flow producing stagnant hypoxia and cyanosis,
Pale and cold skin due to vasoconstriction,
Decreased urine output due to reduced renal blood flow and GFR.
Blood flow to vital organs is affected. Reduced blood flow to brain causes fainting and
ischemic injuries on kidney, skin, GIT, lung, liver, heart.
6. Lactic acidosis
7. Respiration becomes rapid.
8. If patient is conscious, there is intense thirst, agitation, restlessness etc.

e)

Treatment of shock

1. Fluid replacement therapy

-Blood or plasma transfusion. If the shock is due to hemorrhage transfusion of blood is the
best therapy. If shock if due to plasma loss, plasma or appropriate electrolytic solution can
correct the shock. Plasma substitute such as dextran can be used.
-Saline. Less effective.
2. Sympathomimetic drugs
They mimic sympathetic stimulation. They are most useful in neurogenic and anaphylactic
shock. They are not useful in hemorrhagic shock.
3. Other therapies
-Head low position
-Oxygen
-Glucocorticoids: They are useful because they increase the strength of heart in last stages
of shock, by stabilizing lysosomal membranes they prevent release of enzymes of cells and
help in metabolism of glucose by the severely damaged cells.

f)

Hemorrhage

1) Causesaccidental, postpartum, internal, placenta previa

2) Typeshemorrhage can be acute or chronic
3) stages of shock-Immediate compensatory mechanisms (- feedback) by nervous reflexes (via VMC
sympathetic stimulation)
-Long term mechanisms- by kidney and hormones
-delayed compensation- by restoration of plasma, plasma proteins (in 4days) & blood cells
(in 4 weeks)

-Uncompensated stage (due to + feedback mechanisms) in this stage vicious cycle starts.
shock itself leads shock finally death
4) Treatmenti) Fluid replacement therapy- in hemorrhage transfusion of blood is the best therapy.
ii) Other therapies- -Head low position, oxygen, glucocorticoids

Chapter-7- Cardiac failure

Definition, effects and causes of cardiac failure

Definition and effects-Failure of the heart to pump enough blood to satisfy the needs of the
body is called cardiac failure. It may be manifested in two ways:
-forward failure or decrease in cardiac output which causes weakness or fainting.
-By damming of blood in the veins behind the left causing pulmonary edema and dyspnea or
behind the right heart causing peripheral edema.
Causes -Acute or chronically progressive coronary artery disease, Malfunction of heart
valves, Congenital abnormalities of the heart, Severe hypertension.

Types of shock
left and right sided failure
In large number of patients with acute failure, left sided failure predominates over right
sided failure leading to unilateral left sided failure. Very rarely there is unilateral right sided
failure. When there is predominant left heart failure, right heart pumps normal quantity of
blood to the lungs but blood is not pumped out of lungs into the systemic circulation
because of left sided failure. This causes increased volume of blood to be retained in the
lungs, increased pulmonary capillary pressure (pulmonary vascular congestion) and

pulmonary edema.

high and low output cardiac failure

High and low output failure- When persons cardiac output is much higher than normal, and
he has signs of heart failure (high right and left atrial pressures, edema), it is called high
output failure. This is due to over beating of heart with increased venous return and not
due to decreased pumping ability of the heart. This is caused due to circulatory abnormality
that drastically decreases the total peripheral resistance.
Causes: Arteriovenous fistula, Beriberi, Thyrotoxicosis.
Low output cardiac failure-In many cases of acute heart attacks, there is slow progressive
cardiac deterioration and heart becomes incapable of pumping adequate blood flow to keep
the body alive. All body tissues suffer and begin to deteriorate, ultimately leading to death,
within few hours or few days. This type of circulatory shock is called as cardiogenic shock or
cardiac shock or power failure syndrome. Patient dies of cardiogenic shock before
compensatory processes can return cardiac output to normal.

Patho-Physiology of heart failure

Compensated heart failure

Acute stage of compensated failure- When there is sudden damage to the heart as in
myocardial infarction, pumping ability of the heart is immediately depressed. This causes
reduction in cardiac output to as low as 2 1/min. It also causes damming of blood in the
veins resulting into increased systemic venous pressure so that right atrial pressure rises to 4
mm Hg. This low cardiac output still sustains life but is associated with fainting.
When cardiac output becomes low, different circulatory reflexes are activated within 30
seconds, e.g. baroreceptor reflex, chemoreceptor reflex, CNS ischemic response, reflexes
originating in heart. Due to these reflexes, there is strong sympathetic stimulation within
few seconds which causes
Direct effect on the heart. If musculature of the heart is diffusely damaged but still
functional, it strengthens the musculature. Or if the part of the muscle has become non-

functional, normal muscle is stimulated and compensates for non-functional muscle. Thus
heart becomes a stronger pump. Sympathetic stimulation also causes increased tone in the
blood vessels, especially the veins. This results into increased venous return. This, in turn,
increases the pumping ability of the heart increasing cardiac output to about 4.2 1/min
adequate to sustain life.

Chronic stage of compensated failure- After the few minutes of acute attack, a prolonged
secondary state begins which causes: (a) retention of fluid by the kidneys, and (b)
progressive recovery of the heart.
-Retention of fluid by the kidneys. Decreased cardiac output decreases the urine output and
therefore causes retention of fluid and increase in blood volume. When it is moderate, it
helps in compensating the diminished pumping ability of the heart. It increases mean
systemic filling pressure causing flow of blood towards the heart. Secondly it distends the
veins, reduces the venous resistance and increases the flow of blood towards the heart.
If cardiac pumping ability is greatly reduced (less than 25 to 50% of normal) then blood flow
to kidneys is greatly reduced and there is low urinary output. Also there is retention of
excess fluid but it has no beneficial effect on circulation as heart is already pumping at its
maximal ability. This leads to development of edema which is detrimental.
-Progressive recovery of the heart. Heart gradually recovers because of new collateral blood
supply and hypertrophy of undamaged musculature. This is achieved ordinarily within 5 to 7
weeks.
Thus there is compensation for the damage (compensated heart failure) and person has
normal resting cardiac output but if he performs heavy exercise, pumping ability of the heart
cannot be increased to a desired level and symptoms of acute failure may return, i.e. cardiac
reserve is reduced in compensated heart failure.

Decompensated heart failure.

If heart is severely damaged, sympathetic reflexes, fluid retention are not useful in causing
weakened heart to pump a normal output. Therefore, cardiac output can never rise enough.
Fluid continues to be retained and person develops more and more edema progressively
eventually leading to death. This is called decompensated heart failure.

Treatment of heart failure

This is treated by: (i) strengthen the heart by giving cardiotonic drugs, (ii) by administering
diuretic drugs and (iii) by diet (by reducing salt and water intake)