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Blood pressure regulation 2013

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Nyunt Wai
Nyunt Wai

Blood pressure variation and homeostasis - physiological basis for medical and health sciences students and professionals

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Blood Pressure Regulation Nyunt Wai
What is B.P.? Pressure = force/unit area Blood pressure = pressure exerted by blood on the walls of the heart or blood vessels 2
Container vs. Content example same container; same capacity; less content same content; greater capacity as the container expands PRESSURE falls PRESSURE falls e.g. haemorrhage e.g. generalized vasodilation 3
More blood GREATER PRESSURE Since the arterial system is not very distensible Arterial BLOOD VOLUME ∞ Arterial BLOOD PRESSURE 4
GREATER PRESSURE LESSER PRESSURE PRESSURE creates FLOW PRESSURE ∞ FLOW 5
6
Functions of BP • Intraventricular BP  ejection of blood (stroke volume) • Systemic arterial BP  blood flow to tissues (tissue perfusion) • Capillary hydrostatic pressure  filtration (tissue fluid formation) • Systemic venous BP  blood flow back to the heart (venous return) The unconditional term BLOOD PRESSURE refers to SYSTEMIC ARTERIAL BLOOD PRESSURE 7
The determinants of BP blood pressure ∞ cardiac output 8
Blood pressure ∞ Total Peripheral Resistance(TPR) 9
Systemic arterial blood pressure = Cardiac output x Total peripheral resistance (TPR) or Systemic vascular reistance (SVR) The 2 Major Determinants of Arterial B.P. The other Determinants of Arterial B.P.? 10
Ventricular contraction Ventricular relaxation Aorta is the most elastic artery When aortic elasticity decreases (ageing or disease): Less expansion during systole  Incr. SBP Less elastic recoil during diastole  decr. DBP Pulse pressure ? 11
The Determinants of Arterial B.P. SBP DBP • SBP • Aortic distensibility (elasticity) • TPR • Stroke volume • Aortic distensibility (elasticity) SBP = CO x TPR DBP = CO x TPR 12
Physiological Variations in BP • Age: – SBP and DBP gradually rise with age (after about 30 years), the SBP more so and more sustained than the DBP • Sex: – the rise in BP with age is greater in males • Circadian variation (diurnal variation): – lowest during sleep (nocturnal dip) and highest in the mornings after waking up • Increased transiently during physical stress (e.g. muscular exercise), mental stress(anger, apprehension, resentment, mental concentration), emotional excitement • The effect of Gravity: When erect, BP in any vessel varies in relation to the vertical distance from the heart level
Physiological Variations in BP • Gravity – In an upright position, BP in the arteries below the heart level is increased, and that in the arteries above the heart level is decreased by 0.77 mm Hg for each cm of vertical distance below or above the heart. – Thus, routine measurement of BP should be performed with the artery at the heart level.
Effect of Gravity • Pressure in large artery in the foot 105 cm below the heart = [0.77 mmHg/cm x 105 cm = 80 mm Hg)] + • 100 mm Hg (Mean ABP at heart level) • = 180 mm Hg • Pressure in vein in the foot 105 cm below the heart = [0.77 mmHg/cm x 105 cm = 80 mm Hg)] + • 4 mm Hg (right atrial pressure) • = 84 mm Hg
REGULATION OF SYSTEMIC ARTERIAL B.P. – MAINTENANCE OF RESTING B.P. B.P. HOMEOSTASIS • SITUATIONAL ADJUSTMENT OF B.P. e.g. changes in B.P. during muscular exercise 16
Regulation of 17
Systemic arterial blood pressure Total peripheral = Cardiac output x resistance (arteriolar tone) More immediate More efficient: RESISTANCE = 1 Radius 4 More economical 18
BP REGULATORY MECHANISMS NEURAL: CARDIOVASCULAR REFLEXES  Baroreceptor reflexes  Chemoreceptor reflexes  Brain(CNS) ischaemic response Short term: Rapid Short term: HORMONAL Intermediate  Catecholamines  Renin-angiotensin-aldosterone(RAA) system  Vasopressin Long term RENAL-BODY FLUID CONTROL SYSTEM 19
Integrating centres Afferents Efferents Hypothalamus Vasopressin Brain stem: Medulla X IX, X (Parasym) (Parasym) Spinal cord: SYMPATHETIC NERVOUS SYSTEM Receptors • Baroreceptors • Chemoreceptors Sym .outflow Effectors • Heart, Blood vessels • Adrenal medulla: Catecholamines 20 • Kidney: activation of RAA system
Sympathetic Nervous System • • • • Major effector system for BP control Increased sympathetic tone  incr. BP decreased sympathetic tone  decr. BP Sym.N.S. is under the control of vasomotor centre (VMC) in the medulla • Descending tracts from the VMC excites the sympathetic nervous system • Inputs from the broreceptors and other receptors go to the VMC (the integrating centre) 21
How does sympathetic N.S. activity increase BP? • Direct cardiovascular effects • Neuroendocrine effects: activation of – adrenal medulla – renin-angiotensin-aldosterone (RAA) system 22
Sympathetic tone SYMPATHETIC OUTFLOW DIRECT CARDIOVASCULAR EFFECTS HR SV Venoconstrictn Arteriolar constrictn Capillary pressure Venous return ISF formation CARDIAC OUTPUT TPR Plasma loss BLOOD PRESSURE 23
Sympathetic tone SYMPATHETIC OUTFLOW NEUROENDOCRINE EFFECTS ADRENAL MEDULLA Secretion of CATECHOLAMINES JG CELLS IN KIDNEY Activation of RENIN- ANGIOTENSINALDOSTERONE SYSTEM CARDIOVASCULAR EFFECTS VOLUME EFFECTS BLOOD PRESSURE 24
CATECHOLAMINES Adrenaline Noradrenaline Dopamine b- receptors a- receptors Vasoconstriction Cardiostimulatory effects: Automaticity (SANodal discharge) Heart Rate Conductivity Excitability Myocardial contractility TPR Stroke volume Cardiac output BLOOD PRESSURE 25
RENIN- ANGIOTENSIN-ALDOSTERONE SYSTEM BLOOD VOLUME/PRESSURE Baroreceptor reflex Sympathetic tone Renal perfusion pressure LIVER Juxtaglomerular(JG) cells in afferent arteriolar muscle coat in KIDNEY Angiotensin- Angiotensinogen RENIN Angiotensin I Converting Enzyme ANGIOTENSIN II VASCULAR and VOLUME EFFECTS Endothelial cells of pulmonary circulation 26
ANGIOTENSIN II VASOCONTRICTION Vascular smooth muscle Sympathetic nerve endings Brain: Hypothalamus TPR Facilitates release of NORADRENALINE Release of VASOPRESSIN Stimulation of THIRST Adrenal cortex Water intake Secretion of ALDOSTERONE Renal reabsorption of Sodium BLOOD VOLUME 27 Renal reabsorption of Water
THE BARORECEPTOR REFLEX  operates within seconds  for moment to moment, day to day control of BP  for BP homeostasis in the face of challenges such as blood loss  Afferents: Parasympathetic  Efferents: Sympathetic noradrenergic 28
Baroreceptors = stretch receptors in the walls of • Heart Atria Volume receptors Low pressure baroreceptors • Arteries (arterial baroreceptors) Aortic arch High pressure baroreceptors Carotid sinus Stimulation of Stretch receptors in the wall Stretch on the wall BP Wall 29
Arterial baroreceptors 30
How the baroreceptor reflex works Basic network 31
Incr. baroreceptor discharge • Stimulates the Parasympathetic centres (Dorsal motor nucleus of vagus) in the medulla • Inhibits the vasomotor centre (VMC) in the medulla (through inhibitory interneurones) – Decr. excitatory discharge from the VMC to the Sympathetic Nervous System in the spinal cord –  decr. sympathetic noradrenergic discharge 32
Carotid sinus, aortic arch Parasym. fibres in IX and X cranial nerves Inhibits VMC stimulates motor vagal nuclei 33
•Hypothalamus •Posterior pituitary •Vasopressin (ADH) •Adrenal medulla •RAA system 34
HYPOTHALAMUS VASOPRESSIN POSTERIOR PITUITARY Generalized vasoconstriction (V1 receptors) TPR Renal reabsorption of water BP (V2 receptors) plasma volume CARDIAC OUTPUT 35
Note • BP may not fall with minor haemorrhage • Fall in venous return is detected by low pressure baroreceptors  increase in TPR  compensates for fall in CO  BP unchnaged • When blood loss is >20% of circulating blood volume, the fall in CO is great enough to cause a fall in BP • BP = CO x TPR 36
SENSITIVITY BARORECEPTORS CHEMORECEPTORS 50 110 mm Hg MEAN ARTERIAL B.P. 37
Neural regulation of B.P. 120 Baroreceptor reflex 100 B.P. mmHg 80 60 40 Chemoreceptor reflex CNS ischaemic response 38
The chemoreceptor reflex 39
ARTERIAL CHEMORECEPTORS CAROTID BODIES AORTIC BODIES 40
BP BLOOD FLOW  STAGNATION O2 delivery to tissues (stagnant hypoxia) CO2 uptake from tissues O2 CO2 (in tissues) Stimulation of chemoreceptors IX, X nerves •Stimulation of medullary respiratory centre •Stimulation of medullary VMC sympathetic discharge BP
The CNS ischaemic response Medulla oblongata CEREBRAL BLOOD FLOW CNS ISCHAEMIA PO2 BLOOD PRESSURE VASOMOTOR PCO2 Stagnant hypoxia CENTRE Spinal Cord (+) (+) SYMPATHETIC OUTFLOW Sympathetic tone 42
CUSHING’S REFLEX HEAD INJURY Increased intracranial pressure Pressure on cerebral arteries CNS ISCHAEMIA CEREBRAL BLOOD FLOW BLOOD PRESSURE Normal BARORECEPTOR REFLEX PO2 VMC PCO2 Stagnant hypoxia VAGAL TONE HEART RATE (+) (+) SYMPATHETIC OUTFLOW Sympathetic tone 43
Head injury CNS ischaemia The rise in BP • Baroreceptor reflex –  stimulation of vagus  fall in HR (since parasympathetic control of HR is dominant over sympathetic control) –  but baroreflex-mediated inhibition of VMC is counterbalanced by direct stimulation of VMC by CNS ischaemia –  sympathetic-mediated generalized vasoconstriction maintained  Incr. in BP Slow, full and bounding pulse CUSHING’S REFLEX 44
Cushing's reflex • Because the skull is rigid after infancy, intracranial masses or swelling may increase intracranial pressure. When intracranial pressure is increased sufficiently, regardless of the cause, Cushing's reflex and other autonomic abnormalities can occur. • Cushing's reflex includes systolic hypertension, increased pulse pressure, and bradycardia. 45
Renal regulation of B.P. I. Physical : by variation of Glomerular filtration pressure  variation in urine formation II. Hormonal : by secretion of renin •  Renin-Angiotensin (AGII)Aldosterone system (RAAS) 46
Renal regulation of B.P. When blood volume and BP is increased, KIDNEYS excrete excess fluid by • Pressure diuresis increased urine formation as a result of increased glomerular filtration due to raised renal perfusion pressure • Pressure natriuresis increased urinary excretion of sodium as a result of increased glomerular filtration of sodium due to raised renal perfusion pressure 47
Renal regulation of B.P. When blood volume and BP is decreased:  decr. glomerular capillary H.P.  decr.GFR  • Oliguria (deceased urine formation) • Anuria (renal shutdown – no urine formation) Thus KIDNEYS conserve ECF Volume 48
Anuria 49
Summary :Systemic Arterial Blood Pressure • Varies with the amount of blood in the systemic arterial system (begins at the aorta, ends at arterioles in various tissues) • This is because the systemic arteries are not very distensible • The greater the cardiac output, the greater the inflow of blood into the systemic arterial system, the higher is the BP • The greater the TPR, the lesser the outflow of blood out of the systemic arterial system, the 50 higher is the BP
Systemic Arterial Blood Pressure • Sympathetic nervous system and the RAA system are powerful systems that can increase BP • Moment to moment control is by baroreceptor reflex. • What is the use of increasing the BP when blood supply to almost all tissues are shut down by arteriolar constriction? • Ans. Local vasodilatory mechanisms in the vital organs- the brain and the heart, will overcome the systemic vasoconstrictor effect– diverting blood flow to them at the expense of other organs and tissues End 51

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Blood pressure regulation 2013

  • 2. What is B.P.? Pressure = force/unit area Blood pressure = pressure exerted by blood on the walls of the heart or blood vessels 2
  • 3. Container vs. Content example same container; same capacity; less content same content; greater capacity as the container expands PRESSURE falls PRESSURE falls e.g. haemorrhage e.g. generalized vasodilation 3
  • 4. More blood GREATER PRESSURE Since the arterial system is not very distensible Arterial BLOOD VOLUME ∞ Arterial BLOOD PRESSURE 4
  • 5. GREATER PRESSURE LESSER PRESSURE PRESSURE creates FLOW PRESSURE ∞ FLOW 5
  • 6. 6
  • 7. Functions of BP • Intraventricular BP  ejection of blood (stroke volume) • Systemic arterial BP  blood flow to tissues (tissue perfusion) • Capillary hydrostatic pressure  filtration (tissue fluid formation) • Systemic venous BP  blood flow back to the heart (venous return) The unconditional term BLOOD PRESSURE refers to SYSTEMIC ARTERIAL BLOOD PRESSURE 7
  • 8. The determinants of BP blood pressure ∞ cardiac output 8
  • 9. Blood pressure ∞ Total Peripheral Resistance(TPR) 9
  • 10. Systemic arterial blood pressure = Cardiac output x Total peripheral resistance (TPR) or Systemic vascular reistance (SVR) The 2 Major Determinants of Arterial B.P. The other Determinants of Arterial B.P.? 10
  • 11. Ventricular contraction Ventricular relaxation Aorta is the most elastic artery When aortic elasticity decreases (ageing or disease): Less expansion during systole  Incr. SBP Less elastic recoil during diastole  decr. DBP Pulse pressure ? 11
  • 12. The Determinants of Arterial B.P. SBP DBP • SBP • Aortic distensibility (elasticity) • TPR • Stroke volume • Aortic distensibility (elasticity) SBP = CO x TPR DBP = CO x TPR 12
  • 13. Physiological Variations in BP • Age: – SBP and DBP gradually rise with age (after about 30 years), the SBP more so and more sustained than the DBP • Sex: – the rise in BP with age is greater in males • Circadian variation (diurnal variation): – lowest during sleep (nocturnal dip) and highest in the mornings after waking up • Increased transiently during physical stress (e.g. muscular exercise), mental stress(anger, apprehension, resentment, mental concentration), emotional excitement • The effect of Gravity: When erect, BP in any vessel varies in relation to the vertical distance from the heart level
  • 14. Physiological Variations in BP • Gravity – In an upright position, BP in the arteries below the heart level is increased, and that in the arteries above the heart level is decreased by 0.77 mm Hg for each cm of vertical distance below or above the heart. – Thus, routine measurement of BP should be performed with the artery at the heart level.
  • 15. Effect of Gravity • Pressure in large artery in the foot 105 cm below the heart = [0.77 mmHg/cm x 105 cm = 80 mm Hg)] + • 100 mm Hg (Mean ABP at heart level) • = 180 mm Hg • Pressure in vein in the foot 105 cm below the heart = [0.77 mmHg/cm x 105 cm = 80 mm Hg)] + • 4 mm Hg (right atrial pressure) • = 84 mm Hg
  • 16. REGULATION OF SYSTEMIC ARTERIAL B.P. – MAINTENANCE OF RESTING B.P. B.P. HOMEOSTASIS • SITUATIONAL ADJUSTMENT OF B.P. e.g. changes in B.P. during muscular exercise 16
  • 18. Systemic arterial blood pressure Total peripheral = Cardiac output x resistance (arteriolar tone) More immediate More efficient: RESISTANCE = 1 Radius 4 More economical 18
  • 19. BP REGULATORY MECHANISMS NEURAL: CARDIOVASCULAR REFLEXES  Baroreceptor reflexes  Chemoreceptor reflexes  Brain(CNS) ischaemic response Short term: Rapid Short term: HORMONAL Intermediate  Catecholamines  Renin-angiotensin-aldosterone(RAA) system  Vasopressin Long term RENAL-BODY FLUID CONTROL SYSTEM 19
  • 20. Integrating centres Afferents Efferents Hypothalamus Vasopressin Brain stem: Medulla X IX, X (Parasym) (Parasym) Spinal cord: SYMPATHETIC NERVOUS SYSTEM Receptors • Baroreceptors • Chemoreceptors Sym .outflow Effectors • Heart, Blood vessels • Adrenal medulla: Catecholamines 20 • Kidney: activation of RAA system
  • 21. Sympathetic Nervous System • • • • Major effector system for BP control Increased sympathetic tone  incr. BP decreased sympathetic tone  decr. BP Sym.N.S. is under the control of vasomotor centre (VMC) in the medulla • Descending tracts from the VMC excites the sympathetic nervous system • Inputs from the broreceptors and other receptors go to the VMC (the integrating centre) 21
  • 22. How does sympathetic N.S. activity increase BP? • Direct cardiovascular effects • Neuroendocrine effects: activation of – adrenal medulla – renin-angiotensin-aldosterone (RAA) system 22
  • 23. Sympathetic tone SYMPATHETIC OUTFLOW DIRECT CARDIOVASCULAR EFFECTS HR SV Venoconstrictn Arteriolar constrictn Capillary pressure Venous return ISF formation CARDIAC OUTPUT TPR Plasma loss BLOOD PRESSURE 23
  • 24. Sympathetic tone SYMPATHETIC OUTFLOW NEUROENDOCRINE EFFECTS ADRENAL MEDULLA Secretion of CATECHOLAMINES JG CELLS IN KIDNEY Activation of RENIN- ANGIOTENSINALDOSTERONE SYSTEM CARDIOVASCULAR EFFECTS VOLUME EFFECTS BLOOD PRESSURE 24
  • 25. CATECHOLAMINES Adrenaline Noradrenaline Dopamine b- receptors a- receptors Vasoconstriction Cardiostimulatory effects: Automaticity (SANodal discharge) Heart Rate Conductivity Excitability Myocardial contractility TPR Stroke volume Cardiac output BLOOD PRESSURE 25
  • 26. RENIN- ANGIOTENSIN-ALDOSTERONE SYSTEM BLOOD VOLUME/PRESSURE Baroreceptor reflex Sympathetic tone Renal perfusion pressure LIVER Juxtaglomerular(JG) cells in afferent arteriolar muscle coat in KIDNEY Angiotensin- Angiotensinogen RENIN Angiotensin I Converting Enzyme ANGIOTENSIN II VASCULAR and VOLUME EFFECTS Endothelial cells of pulmonary circulation 26
  • 27. ANGIOTENSIN II VASOCONTRICTION Vascular smooth muscle Sympathetic nerve endings Brain: Hypothalamus TPR Facilitates release of NORADRENALINE Release of VASOPRESSIN Stimulation of THIRST Adrenal cortex Water intake Secretion of ALDOSTERONE Renal reabsorption of Sodium BLOOD VOLUME 27 Renal reabsorption of Water
  • 28. THE BARORECEPTOR REFLEX  operates within seconds  for moment to moment, day to day control of BP  for BP homeostasis in the face of challenges such as blood loss  Afferents: Parasympathetic  Efferents: Sympathetic noradrenergic 28
  • 29. Baroreceptors = stretch receptors in the walls of • Heart Atria Volume receptors Low pressure baroreceptors • Arteries (arterial baroreceptors) Aortic arch High pressure baroreceptors Carotid sinus Stimulation of Stretch receptors in the wall Stretch on the wall BP Wall 29
  • 31. How the baroreceptor reflex works Basic network 31
  • 32. Incr. baroreceptor discharge • Stimulates the Parasympathetic centres (Dorsal motor nucleus of vagus) in the medulla • Inhibits the vasomotor centre (VMC) in the medulla (through inhibitory interneurones) – Decr. excitatory discharge from the VMC to the Sympathetic Nervous System in the spinal cord –  decr. sympathetic noradrenergic discharge 32
  • 33. Carotid sinus, aortic arch Parasym. fibres in IX and X cranial nerves Inhibits VMC stimulates motor vagal nuclei 33
  • 35. HYPOTHALAMUS VASOPRESSIN POSTERIOR PITUITARY Generalized vasoconstriction (V1 receptors) TPR Renal reabsorption of water BP (V2 receptors) plasma volume CARDIAC OUTPUT 35
  • 36. Note • BP may not fall with minor haemorrhage • Fall in venous return is detected by low pressure baroreceptors  increase in TPR  compensates for fall in CO  BP unchnaged • When blood loss is >20% of circulating blood volume, the fall in CO is great enough to cause a fall in BP • BP = CO x TPR 36
  • 38. Neural regulation of B.P. 120 Baroreceptor reflex 100 B.P. mmHg 80 60 40 Chemoreceptor reflex CNS ischaemic response 38
  • 41. BP BLOOD FLOW  STAGNATION O2 delivery to tissues (stagnant hypoxia) CO2 uptake from tissues O2 CO2 (in tissues) Stimulation of chemoreceptors IX, X nerves •Stimulation of medullary respiratory centre •Stimulation of medullary VMC sympathetic discharge BP
  • 42. The CNS ischaemic response Medulla oblongata CEREBRAL BLOOD FLOW CNS ISCHAEMIA PO2 BLOOD PRESSURE VASOMOTOR PCO2 Stagnant hypoxia CENTRE Spinal Cord (+) (+) SYMPATHETIC OUTFLOW Sympathetic tone 42
  • 43. CUSHING’S REFLEX HEAD INJURY Increased intracranial pressure Pressure on cerebral arteries CNS ISCHAEMIA CEREBRAL BLOOD FLOW BLOOD PRESSURE Normal BARORECEPTOR REFLEX PO2 VMC PCO2 Stagnant hypoxia VAGAL TONE HEART RATE (+) (+) SYMPATHETIC OUTFLOW Sympathetic tone 43
  • 44. Head injury CNS ischaemia The rise in BP • Baroreceptor reflex –  stimulation of vagus  fall in HR (since parasympathetic control of HR is dominant over sympathetic control) –  but baroreflex-mediated inhibition of VMC is counterbalanced by direct stimulation of VMC by CNS ischaemia –  sympathetic-mediated generalized vasoconstriction maintained  Incr. in BP Slow, full and bounding pulse CUSHING’S REFLEX 44
  • 45. Cushing's reflex • Because the skull is rigid after infancy, intracranial masses or swelling may increase intracranial pressure. When intracranial pressure is increased sufficiently, regardless of the cause, Cushing's reflex and other autonomic abnormalities can occur. • Cushing's reflex includes systolic hypertension, increased pulse pressure, and bradycardia. 45
  • 46. Renal regulation of B.P. I. Physical : by variation of Glomerular filtration pressure  variation in urine formation II. Hormonal : by secretion of renin •  Renin-Angiotensin (AGII)Aldosterone system (RAAS) 46
  • 47. Renal regulation of B.P. When blood volume and BP is increased, KIDNEYS excrete excess fluid by • Pressure diuresis increased urine formation as a result of increased glomerular filtration due to raised renal perfusion pressure • Pressure natriuresis increased urinary excretion of sodium as a result of increased glomerular filtration of sodium due to raised renal perfusion pressure 47
  • 48. Renal regulation of B.P. When blood volume and BP is decreased:  decr. glomerular capillary H.P.  decr.GFR  • Oliguria (deceased urine formation) • Anuria (renal shutdown – no urine formation) Thus KIDNEYS conserve ECF Volume 48
  • 50. Summary :Systemic Arterial Blood Pressure • Varies with the amount of blood in the systemic arterial system (begins at the aorta, ends at arterioles in various tissues) • This is because the systemic arteries are not very distensible • The greater the cardiac output, the greater the inflow of blood into the systemic arterial system, the higher is the BP • The greater the TPR, the lesser the outflow of blood out of the systemic arterial system, the 50 higher is the BP
  • 51. Systemic Arterial Blood Pressure • Sympathetic nervous system and the RAA system are powerful systems that can increase BP • Moment to moment control is by baroreceptor reflex. • What is the use of increasing the BP when blood supply to almost all tissues are shut down by arteriolar constriction? • Ans. Local vasodilatory mechanisms in the vital organs- the brain and the heart, will overcome the systemic vasoconstrictor effect– diverting blood flow to them at the expense of other organs and tissues End 51