The document outlines the various mechanisms that regulate arterial blood pressure (ABP), including rapidly-acting nervous system reflexes, intermediate-acting hormone systems, and long-term renal control. It discusses the baroreceptor reflex, which senses changes in blood pressure and activates the sympathetic nervous system to rapidly constrict blood vessels and increase cardiac output. The renin-angiotensin system is an intermediate mechanism where low blood pressure triggers renin release to produce angiotensin II, a vasoconstrictor that also causes sodium retention. In the long-term, the kidneys regulate blood volume and pressure through pressure natriuresis, where higher pressure causes sodium excretion, and the renal control of fluid levels via
HEART RATE
REGULATION OF HEART RATE
VASOMOTOR CENTER – CARDIAC CENTER
MOTOR (EFFERENT) NERVE FIBERS TO HEART
FACTORS AFFECTING VASOMOTOR CENTER
for all medical & health care students
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
Heart rate by Pandian M, Tutor, Dept of Physiology, DYPMCKOP,MHPandian M
Heart rate
Regulation of heart rate
Vasomotor center – cardiac center
Motor (efferent) nerve fibers to heart
Factors affecting vasomotor center
Applied
A comprehensive presentation on glomerular filtration rate (GFR) & renal blood flow and how these entities are impacted by intrinsic and extrinsic regulation.
This was presented by the author in the finals of the physiology seminar presentation in medical school.
Regulation of arterial blood pressure (The Guyton and Hall Physiology)Maryam Fida
BLOOD PRESSURE
The pressure exerted by the blood on vessel wall is known as blood pressure.
SYSTOLIC BLOOD PRESSURE
The maximum pressure exerted in the arteries during systole of heart.
Normal systolic pressure: 120 mm Hg.
DIASTOLIC BLOOD PRESSURE
The minimum pressure exerted in the arteries during diastole of heart.
Normal diastolic pressure: 80 mm Hg.
PULSE PRESSURE
The difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
MEAN ARTERIAL BLOOD PRESSURE
The average pressure existing in the arteries.
Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure
Pulse Pressure = (Systolic – Diastolic)
Mean Arterial Blood Pressure =Diastolic Pressure+1/3(Systolic – Diastolic)
HEART RATE
REGULATION OF HEART RATE
VASOMOTOR CENTER – CARDIAC CENTER
MOTOR (EFFERENT) NERVE FIBERS TO HEART
FACTORS AFFECTING VASOMOTOR CENTER
for all medical & health care students
Cardiac output (The Guyton and Hall Physiology)Maryam Fida
The volume of blood pumped by each ventricle per minute is called cardiac output
Cardiac output = Stroke Volume X Heart Rate
Normal value = 5 Liters /Minute
Cardiac output = Stroke Volume X Heart Rate
The factors which regulate stroke volume and Heart rate are basically regulating Cardiac output
Volume of blood ejected by each ventricle in single systole; Normal Value = 70 ml/beat
Stroke Volume = End diastolic Volume – End Systolic Volume
So stroke volume is mainly controlled by
EDV
ESV
VENOUS RETURN: What ever blood volume returns to the heart, same is pumped forward through the Frank’s Starlings Law. According to this law 13- 15 liters of blood volume can be pumped out without cardiac stimulation.
DURATION OF DIASTOLE OR FILLING TIME: ventricular filling occurs during diastole, so there must be adequate ventricular filling time.
DISTENSIBILITY OF THE VENTRICLES: Normally ventricles are distensible to accommodate adequate blood volume. Infarction decreases the distensibility which decreases the EDV.
ATRIAL CONTRACTION: There must be adequate atrial contraction to have adequate EDV. If atrial function is not adequate then EDV will decrease.
E.S.V is basically CONTROLLED BY MYOCARDIAL CONTRACTION
FORCE OF MYOCARDIAL CONTRACTION: It depends upon the initial length of muscle fibers according to frank’s starlings law.
PRELOAD: The effect of EDV on initial length is called preload. So EDV also effects the ESV.
AFTER LOAD: Force of contraction is also dependant upon the resistance against which the ventricles have to pump
CONDITION OF THE MYOCARDIUM : It also effects the force of contraction.
AUTONOMIC NERVES : Sympathetic stimulation increases and parasympathetic stimulation decreases force of contraction
HORMONES: Catecholamines, thyroxine, glucagon, digitalis, calcium, increased temp, caffeine, theophyline increase the force.
Force decreases by hypoxia, acidosis, barniturates, procainamide and quinidine decrease the force of contraction.
Heart rate by Pandian M, Tutor, Dept of Physiology, DYPMCKOP,MHPandian M
Heart rate
Regulation of heart rate
Vasomotor center – cardiac center
Motor (efferent) nerve fibers to heart
Factors affecting vasomotor center
Applied
A comprehensive presentation on glomerular filtration rate (GFR) & renal blood flow and how these entities are impacted by intrinsic and extrinsic regulation.
This was presented by the author in the finals of the physiology seminar presentation in medical school.
Regulation of arterial blood pressure (The Guyton and Hall Physiology)Maryam Fida
BLOOD PRESSURE
The pressure exerted by the blood on vessel wall is known as blood pressure.
SYSTOLIC BLOOD PRESSURE
The maximum pressure exerted in the arteries during systole of heart.
Normal systolic pressure: 120 mm Hg.
DIASTOLIC BLOOD PRESSURE
The minimum pressure exerted in the arteries during diastole of heart.
Normal diastolic pressure: 80 mm Hg.
PULSE PRESSURE
The difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
MEAN ARTERIAL BLOOD PRESSURE
The average pressure existing in the arteries.
Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure
Pulse Pressure = (Systolic – Diastolic)
Mean Arterial Blood Pressure =Diastolic Pressure+1/3(Systolic – Diastolic)
BLOOD PRESSURE
BY: SAIYED FALAKAARA
ASSISTANT PROFESSOR
DEPARTMENT OF PHARMACY
SUMANDEEP VIDYAPEETH
Definition
Arterial blood pressure can be defined as the lateral pressure exerted by moving the column of blood on the walls of the arteries.
Significance
To ensure the blood flow to various organs
Plays an important role in exchange of nutrients and gases across the capillaries
Required to form urine
Required for the formation of lymph
Normal values
Normal adult range can fluctuate within a wide range and still be normal
Systolic/diastolic
100/60 – 140/80
Unit - mmHg
This presentation gives you a brief, understandable, captivating and presentable idea on the physiology of blood pressure regulation both on hypertension and hypotension cases.
Operation “Blue Star” is the only event in the history of Independent India where the state went into war with its own people. Even after about 40 years it is not clear if it was culmination of states anger over people of the region, a political game of power or start of dictatorial chapter in the democratic setup.
The people of Punjab felt alienated from main stream due to denial of their just demands during a long democratic struggle since independence. As it happen all over the word, it led to militant struggle with great loss of lives of military, police and civilian personnel. Killing of Indira Gandhi and massacre of innocent Sikhs in Delhi and other India cities was also associated with this movement.
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Embracing GenAI - A Strategic ImperativePeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
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2. Objectives
By the end of this session, the student should be able
to:
a) Outline the different mechanisms involved in
regulation of ABP.
b) Discuss the role of reflexes especially
baroreceptor reflex in regulation of ABP.
c) Discuss the role of renin-angiotensin system in
regulation of ABP.
d) Discuss the role of renal-body fluid in long-
term regulation of ABP.
4. Changes in mean arterial
pressure after rapid
hemorrhage
A-return of MAP to normal
by compensatory
mechanism
B-failure of compensatory
mechanism leading to
hypovolemic shock and
death
5. Mechanisms Involved for Regulation of Arterial Blood
Pressure
Rapidly acting mechanism for regulation of blood pressure
Mostly the nervous control mechanism
• Baro receptor feed back mechanism
• Central nervous system ischemic mechanism
• Chemoreceptor mechanism
Intermediate acting mechanism for control of blood pressure
• Renin angiotensin vasoconstrictor mechanism
• Stress relaxation of vasculature
• Fluid shift across the capillary for adjustment of blood volume
Long term mechanism for control of blood pressure
• Renal blood volume pressure control mechanism
8. Role of the Nervous System in Rapid Control of
Arterial Pressure
Nervous control of arterial pressure is by far the most rapid of all our
mechanisms for pressure control.
When there is drop in arterial blood pressure there are three major
changes that occur simultaneously, each of which helps to increase
arterial pressure. They are as follows
1. Most arterioles of the systemic circulation are constricted.
2. The veins especially (but the other large vessels of the circulation
as well) are strongly constricted. This displaces blood out of the
large peripheral blood vessels toward the heart, thus increasing
the volume of blood in the heart chambers.
3. Finally, the heart itself is directly stimulated by the autonomic
nervous system, further enhancing cardiac pumping.
10. Reflex Mechanisms for Maintaining Normal Arterial Pressure
Baroreceptor reflex
•It is the baroreceptor arterial pressure control system and it is the
best known nervous mechanism for control of arterial pressure.
•Basically, this reflex is initiated by stretch receptors, called either
baroreceptors or pressoreceptors, located at specific points in the
walls of several large systemic arteries.
•Baroreceptors are spray-type nerve endings that lie in the walls of
the arteries; they are stimulated when stretched. They are extremely
abundant in (1) the wall of each internal carotid artery slightly above
the carotid bifurcation, an area known as the carotid sinus, and (2)
the wall of the aortic arch, the aortic sinus.
11. •The baroreceptors respond much more to a rapidly changing pressure
than to a stationary pressure.
•Carotid sinus <Hering’s nerve<Glossopharyngeal nerve<NTS in the
medulla; Aortic sinus < vagus nerve< NTS in medulla
•Excitation of the baroreceptors by high pressure in the arteries reflexly
causes the arterial pressure to decrease because of both a decrease in
peripheral resistance and a decrease in cardiac output. Conversely, low
pressure has opposite effects, reflexly causing the pressure to rise back
toward normal.
•Function of the Baroreceptors -During Changes in Body Posture
•Because the baroreceptor system opposes either increases or decreases
in arterial pressure, it is called a pressure buffer system and the nerves
from the baroreceptors are called buffer nerves.
•The long-term regulation of mean arterial pressure by the
baroreceptors requires interaction with additional systems, principally
the renal-body fluid-pressure control system (along with its associated
nervous and hormonal mechanisms).
12. Changes in mean aortic pressure in response to 8% blood loss in
three groups of individual (2)
13. Control of Arterial Pressure by the Carotid and Aortic Chemoreceptors-
chemoreceptor reflex
•Whenever the arterial pressure falls below a critical level, the
chemoreceptors become stimulated because diminished blood flow
causes decreased oxygen, as well as excess buildup of carbon dioxide
and hydrogen ions that are not removed by the slowly flowing blood.
The signals transmitted from the chemoreceptors excite the
vasomotor center, and this elevates the arterial pressure back toward
normal.
•However, this chemoreceptor reflex is not a powerful arterial
pressure controller until the arterial pressure falls below 80 mm Hg.
Therefore, it is at the lower pressures that this reflex becomes
important to help prevent further decreases in arterial pressure
14. Atrial and Pulmonary Artery Reflexes Regulate Arterial Pressure
Both the atria and the pulmonary arteries have in their walls stretch
receptors called low-pressure receptors
These low-pressure receptors play an important role, especially in
minimizing arterial pressure changes in response to changes in blood
volume
They do detect simultaneous increases in pressure in the low-pressure
areas of the circulation caused by increase in volume, and they elicit
reflexes parallel to the baroreceptor reflexes to make the total reflex
system more potent for control of arterial pressure
15. Atrial Reflexes That Activate the Kidneys-The "Volume Reflex."
•Stretch of the atria also causes significant reflex dilation of the
afferent arterioles in the kidneys. Signals are also transmitted
simultaneously from the atria to the hypothalamus to decrease
secretion of antidiuretic hormone (ADH). Combination of these two
effects-increase in glomerular filtration and decrease in
reabsorption of the fluid-increases fluid loss by the kidneys and
reduces an increased blood volume back toward normal
•Atrial stretch caused by increased blood volume also elicits a
hormonal effect on the kidneys-release of atrial natriuretic
peptide-that adds still further to the excretion of fluid in the urine
and return of blood volume toward normal
16. Atrial Reflex Control of Heart Rate (the Bainbridge Reflex)
•An increase in atrial pressure also causes an increase in heart rate,
sometimes increasing the heart rate as much as 75 percent
•The stretch receptors of the atria that elicit the Bainbridge reflex
transmit their afferent signals through the vagus nerves to the
medulla of the brain. Then efferent signals are transmitted back
through vagal and sympathetic nerves to increase heart rate and
strength of heart contraction. Thus, this reflex helps prevent
damming of blood in the veins, atria, and pulmonary circulation
Central Nervous System Ischemic Response
This arterial pressure elevation in response to cerebral ischemia is
known as the central nervous system (CNS) ischemic response. It is
one of the most powerful of all the activators of the sympathetic
vasoconstrictor system
18. Components of the Renin-Angiotensin System
Renin is synthesized and stored in an inactive form called
prorenin in the juxtaglomerular cells (JG cells) of the kidneys.
The JG cells are modified smooth muscle cells located in the walls
of the afferent arterioles immediately proximal to the glomeruli.
When the arterial pressure falls, intrinsic reactions in the kidneys
themselves cause many of the prorenin molecules in the JG cells
to split and release renin.
Most of the renin enters the renal blood and then passes out of
the kidneys to circulate throughout the entire body
21. Angiotensin II is an extremely powerful vasoconstrictor, and it also
affects circulatory function in other ways as well.
During its persistence in the blood, angiotensin II has two principal
effects that can elevate arterial pressure.
i. The first of these, vasoconstriction in many areas of the body,
occurs rapidly. Vasoconstriction occurs intensely in the
arterioles and much less so in the veins. Constriction of the
arterioles increases the total peripheral resistance, thereby
raising the arterial pressure.
ii. The second principal means by which angiotensin II increases
the arterial pressure is to decrease excretion of both salt and
water by the kidneys. This long-term effect, acting through the
extracellular fluid volume mechanism, is even more powerful
than the acute vasoconstrictor mechanism in eventually raising
the arterial pressure.
22. Angiotensin II causes the kidneys to retain both salt and water in
two major ways:
1. Angiotensin II acts directly on the kidneys to cause salt and water
retention.
2. Angiotensin II causes the adrenal glands to secrete aldosterone,
and the aldosterone in turn increases salt and water reabsorption
by the kidney tubules.
Thus both the direct effect of angiotensin on the kidney and its
effect acting through aldosterone are important in long-term
arterial pressure control. However, research has suggested that
the direct effect of angiotensin on the kidneys is perhaps three or
more times as potent as the indirect effect acting through
aldosterone-even though the indirect effect is the one most
widely known.
25. Delayed compliance (Stress relaxation) of vessels
The principle of delayed compliance is the mechanism by which a
blood vessels attempts to return back to its original pressure when
it is loaded with blood or blood is withdrawn from it , this is a
property of smooth muscles and is exhibited by blood vessels as
well as hollow viscera like urinary bladder
When a segment of a vein is exposed to increased volume , then
immediately its pressure increases but after some time the pressure
returns back to normal due to stretching of the vessel wall,
similarly after drop in original volume due to any fluid loss the
blood pressure decreases for some time and then it returns back to
normal due to changes in the arrangement of smooth muscle.
Similar phenomenon can be seen in urinary bladder.
27. •The arterial hypotension, arteriolar constriction, and reduced
venous pressure during hemorrhagic hypotension lower hydrostatic
pressure in the capillaries. The balance of these forces promotes the
net reabsorption of interstitial fluid into the vascular compartment
•Considerable quantities of fluid may thus be drawn into the
circulation during hemorrhage. About 0.25 mL of fluid per minute
per kilogram of body weight may be reabsorbed by the capillaries.
Thus, approximately 1 L of fluid per hour might be autoinfused from
the interstitial spaces into the circulatory system of an average
individual after acute blood loss
•Substantial quantities of fluid may shift slowly from the intracellular
to the extracellular space. This fluid exchange is probably mediated
by secretion of cortisol from the adrenal cortex in response to
hemorrhage. Cortisol appears to be essential for the full restoration of
plasma volume after hemorrhage
28. Role of renal-body fluid control mechanism in long-term
regulation of ABP
29. An increase in arterial pressure in the human of only a few mm Hg
can double renal output of water, which is called pressure diuresis,
as well as double the output of salt, which is called pressure
natriuresis.
30. Control of renal NaCl and water excretion
Renal Sympathetic Nerves (↑ Activity: ↓ NaCl Excretion)
↓GFR
↑ Renin secretion
↑ Na+ reabsorption along the nephron
Renin-Angiotensin-Aldosterone (↑ Secretion: ↓ NaCl Excretion)
↑ Angiotensin II stimulates reabsorption of Na+ along the nephron
↑ Aldosterone stimulates Na+ reabsorption in the thick ascending limb of Henle's loop,
distal tubule, and collecting duct
↑ Angiotensin II stimulates secretion of ADH
Natriuretic Peptides: ANP, BNP, and Urodilatin (↑ Secretion: ↑ NaCl Excretion)
↑ GFR
↓ Renin secretion
↓ Aldosterone secretion (indirect via ↓ in angiotensin II and direct on the adrenal
gland)
↓ NaCl and water reabsorption by the collecting duct
↓ ADH secretion and inhibition of ADH action on the distal tubule and collecting duct
ADH (↑ Secretion: ↓ H2O Excretion)
↑ H2O reabsorption by the distal tubule and collecting duct
31. Renal Urinary Output Curve
The approximate average effect of
different arterial pressure levels
on urinary volume output by an
isolated kidney, demonstrating
markedly increased urine volume
output as the pressure rises. This
increased urinary output is the
phenomenon of pressure diuresis.
Not only does increasing the
arterial pressure increase urine
volume output, but it causes
approximately equal increase in
sodium output, which is the
phenomenon of pressure
natriuresis.
32. Increases in cardiac output,
urinary output, and arterial
pressure caused by
increased blood volume in
dogs whose nervous
pressure control
mechanisms had been
blocked. This figure shows
return of arterial pressure
to normal after about an
hour of fluid loss into the
urine
33. Near infinite feedback gain
This return of the arterial
pressure always back to the
equilibrium point is the near
infinite feedback gain principle
for control of arterial pressure by
the renal-body fluid mechanism.
34. Two ways in which the
arterial pressure can be
increased:
A, by shifting the renal
output curve in the right-
hand direction toward a
higher pressure level or
B, by increasing the intake
level of salt and water
35. Summary
a) Outline the different mechanisms involved in
regulation of ABP.
b) Discuss the role of reflexes especially
baroreceptor reflex in regulation of ABP.
c) Discuss the role of renin-angiotensin system
in regulation of ABP.
d) Discuss the role of renal-body fluid in long-
term regulation of ABP.