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Blood Pressure
Dr. Arpan Kumar Ghosh
M.B.B.S., M.D
Determinants of Arterial Pressure
Interactions between the components that regulate cardiac
output and arterial pressure. Solid arrows indicate increases,
and the dashed arrow indicates a decrease.
Normal Arterial Blood Pressure
• The blood pressure in the brachial artery in young adults in the sitting position at
rest is approximately 120/70 mm Hg.
• Because the arterial pressure is the product of the cardiac output and peripheral
resistance, it is affected by conditions that affect either or both of these factors.
• Emotion increases the cardiac output and peripheral resistance, and about 20%
of hypertensive patients have blood pressures that are higher in the doctor's
office than at home, with regular daily activities ("white coat hypertension").
• Blood pressure normally falls up to 20 mm Hg during sleep (night dip). This fall is
reduced or absent in hypertension.
• There is general agreement that blood pressure rises with advancing age. But DBP
starts to fall in middle age as the stiffness of arteries increases. Consequently,
pulse pressure rises with advancing age.
• It is interesting that systolic and diastolic BPs are lower in young women than in
young men until age 55 to 65, after which they become comparable.
Classification of Blood Pressure for adults (JNC 7)
The “Seventh Report of the Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure”
Hypertension is a sustained elevation of the systemic arterial pressure.
Cardiovascular risk factors
* Components of the metabolic syndrome.
Estimated Frequency of Various Forms of Hypertension in
the General Hypertensive Population
Isolated office hypertension
(white-coat hypertension)
• Office BP persistently elevated (> 140/90 mmHg)
• Ambulatory or home BP values normal.
• In these subjects, cardiovascular risk is less than in individuals with
raised office and ambulatory or home BP.
• However, it may not be an entirely innocent condition, and these
subjects should be followed up rather closely.
REGULATION OF BLOOD PRESSURE
(A) Intravascular Volume
• Vascular volume is a primary determinant of arterial pressure over
the long term.
• Sodium is predominantly an extracellular ion and is a primary
determinant of the extracellular fluid volume.
• When NaCl intake exceeds the capacity of the kidney to excrete
sodium, vascular volume initially expands and cardiac output
increases.
• Antihypertensive: Diuretics (excretes Na and water)
(B) Autonomic Nervous System
• Adrenergic reflexes modulate BP over the short term. Adrenergic function, in concert with
hormonal and volume-related factors, contributes to the long-term regulation of BP.
• The three endogenous catecholamines are norepinephrine, epinephrine, and dopamine.
• Adrenergic neurons synthesize NE and dopamine, Epinephrine in the adrenal medulla
• Adrenergic receptors - two principal types: α and β. Subtypes:α1, α2, β1, and β2 receptors.
• α Receptors are activated by norepinephrine; βreceptors by Epinephrine.
• α1 Receptors cause vasoconstriction; α2 Receptors inhibit further NE release.
• Different classes of antihypertensive agents inhibit α1 receptors or activate α2 receptors
and reduce sympathetic outflow.
• Activation of myocardial β1 receptors stimulates the rate and strength of cardiac
contraction and increases cardiac output. β1 Receptor activation also stimulates renin
release from the kidney.
• A class of antihypertensive agents acts by inhibiting β1 receptors – Propranolol, metoprolol
• Activation of β2 receptors relaxes vascular smooth muscle resulting vasodilation.
(C) Renin-Angiotensin-Aldosterone System
The RAAS contributes to the regulation of arterial pressure primarily via the
vasoconstrictor properties of angiotensin II
sodium-retaining properties of aldosterone.
(D) Vascular Mechanisms
• Vascular radius and compliance of resistance arteries - determinants of arterial pressure.
• Resistance to flow varies inversely with the fourth power of the radius, R ∞ 1/R4 ,and
consequently, small decreases in lumen size significantly increase resistance.
• Remodeling refers to geometric alterations in the vessel wall without a change in vessel
volume → decreased lumen size → increased peripheral resistance.
• Vascular endothelial function also modulates vascular tone.
• The vascular endothelium synthesizes and releases nitric oxide, a potent vasodilator.
• Endothelin is a vasoconstrictor peptide produced by the endothelium.
• Different classes of antihypertensive agents affect vascular structure and function.
Calcium channel blockers - Amlodipine
Direct vasodilators – hydralazine, minoxidil
NO suppliers – nitroglycerine
Effect of Posture on BP
• BP measurements are typically recorded in the sitting position.
• Normally, standing is accompanied by a small increase in DBP and a
small decrease in SBP when compared to supine values.
• SBP: Supine > Sitting > Standing
• DBP: Standing > Sitting > Supine (by > 5 mm Hg)
• Orthostatic Hypotension (OH) is present when there is a supine-to-
standing BP decrease >20 mmHg systolic or >10 mmHg diastolic.
• There is more OH in diabetic individuals. The causes of OH include
severe volume depletion, baroreflex dysfunction, autonomic
insufficiency, and certain antihypertensive drugs.
Effect of Exercise on BP
Effect on Systolic BP
Effect on Diastolic BP
• Isometric Exercise: Increased DBP
Cause: Tonic contraction of muscles compress on
blood vessels causing increased peripheral
resistance
 Isometric Exercise: ↑ SBP, ↑ DBP, ↑ MBP
• Isotonic Exercise: ↓ or unchanged DBP
• Cause: Vasodilation causing decrease in
peripheral resistance due to:
i. ↓PO2, ↑PCO2, ↑H+, ↑K+, ↑ temp, ↑
adenosine → vasodilator metabolites
ii. ↑ Adrenaline acts on β2 receptors on
Vascular smooth muscles → vasodilation
iii. Sympathetic cholinergic vasodilator system
in skeletal muscle
Isotonic Exercise: ↑ SBP, ↓ or unchanged
DBP
Hypertensive Crises: Emergencies and Urgencies
Clinical Characteristics of Hypertensive Crisis
• The basic difference between the two conditions with high BP, usually
>180/120 mmHg, is the presence or absence of target organ damage.
• Hypertensive emergencies: Target organ damage that includes any of the
features of neurologic or myocardial or retinal or renal involvement; require
hospitalization and parenteral drug therapy.
Hypertension Management
• Goals of Therapy:
• Treating SBP and DBP to targets that are <140/90 mmHg is associated
with a decrease in CVD complications.
• In patients with hypertension and diabetes or renal disease, the BP
goal is <130/80 mmHg.
• Lifestyle Modifications:
• Weight Reduction
• Adopt DASH Diet
• Antihypertensive drugs
Lifestyle modifications to manage hypertension
Thank You
https://www.youtube.com/watch?v=O-lbLyopcuo
PAHO, WHL, the Lancet Commission on Hypertension Group, Hypertension Canada and Resolve to Save
Lives have developed a free brief training and certification course in blood pressure measurement.
http://www.whleague.org/index.php/j-stuff/awareness-and-screening/new-online-bp-certification-course
Virtual Course on accurate automated blood pressure measurement (2020)
https://www.campusvirtualsp.org/en/node/29166

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BP.pdf

  • 1. Blood Pressure Dr. Arpan Kumar Ghosh M.B.B.S., M.D
  • 2. Determinants of Arterial Pressure Interactions between the components that regulate cardiac output and arterial pressure. Solid arrows indicate increases, and the dashed arrow indicates a decrease.
  • 3. Normal Arterial Blood Pressure • The blood pressure in the brachial artery in young adults in the sitting position at rest is approximately 120/70 mm Hg. • Because the arterial pressure is the product of the cardiac output and peripheral resistance, it is affected by conditions that affect either or both of these factors. • Emotion increases the cardiac output and peripheral resistance, and about 20% of hypertensive patients have blood pressures that are higher in the doctor's office than at home, with regular daily activities ("white coat hypertension"). • Blood pressure normally falls up to 20 mm Hg during sleep (night dip). This fall is reduced or absent in hypertension. • There is general agreement that blood pressure rises with advancing age. But DBP starts to fall in middle age as the stiffness of arteries increases. Consequently, pulse pressure rises with advancing age. • It is interesting that systolic and diastolic BPs are lower in young women than in young men until age 55 to 65, after which they become comparable.
  • 4. Classification of Blood Pressure for adults (JNC 7) The “Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure” Hypertension is a sustained elevation of the systemic arterial pressure.
  • 5. Cardiovascular risk factors * Components of the metabolic syndrome.
  • 6. Estimated Frequency of Various Forms of Hypertension in the General Hypertensive Population
  • 7.
  • 8. Isolated office hypertension (white-coat hypertension) • Office BP persistently elevated (> 140/90 mmHg) • Ambulatory or home BP values normal. • In these subjects, cardiovascular risk is less than in individuals with raised office and ambulatory or home BP. • However, it may not be an entirely innocent condition, and these subjects should be followed up rather closely.
  • 9. REGULATION OF BLOOD PRESSURE (A) Intravascular Volume • Vascular volume is a primary determinant of arterial pressure over the long term. • Sodium is predominantly an extracellular ion and is a primary determinant of the extracellular fluid volume. • When NaCl intake exceeds the capacity of the kidney to excrete sodium, vascular volume initially expands and cardiac output increases. • Antihypertensive: Diuretics (excretes Na and water)
  • 10. (B) Autonomic Nervous System • Adrenergic reflexes modulate BP over the short term. Adrenergic function, in concert with hormonal and volume-related factors, contributes to the long-term regulation of BP. • The three endogenous catecholamines are norepinephrine, epinephrine, and dopamine. • Adrenergic neurons synthesize NE and dopamine, Epinephrine in the adrenal medulla • Adrenergic receptors - two principal types: α and β. Subtypes:α1, α2, β1, and β2 receptors. • α Receptors are activated by norepinephrine; βreceptors by Epinephrine. • α1 Receptors cause vasoconstriction; α2 Receptors inhibit further NE release. • Different classes of antihypertensive agents inhibit α1 receptors or activate α2 receptors and reduce sympathetic outflow. • Activation of myocardial β1 receptors stimulates the rate and strength of cardiac contraction and increases cardiac output. β1 Receptor activation also stimulates renin release from the kidney. • A class of antihypertensive agents acts by inhibiting β1 receptors – Propranolol, metoprolol • Activation of β2 receptors relaxes vascular smooth muscle resulting vasodilation.
  • 11. (C) Renin-Angiotensin-Aldosterone System The RAAS contributes to the regulation of arterial pressure primarily via the vasoconstrictor properties of angiotensin II sodium-retaining properties of aldosterone.
  • 12. (D) Vascular Mechanisms • Vascular radius and compliance of resistance arteries - determinants of arterial pressure. • Resistance to flow varies inversely with the fourth power of the radius, R ∞ 1/R4 ,and consequently, small decreases in lumen size significantly increase resistance. • Remodeling refers to geometric alterations in the vessel wall without a change in vessel volume → decreased lumen size → increased peripheral resistance. • Vascular endothelial function also modulates vascular tone. • The vascular endothelium synthesizes and releases nitric oxide, a potent vasodilator. • Endothelin is a vasoconstrictor peptide produced by the endothelium. • Different classes of antihypertensive agents affect vascular structure and function. Calcium channel blockers - Amlodipine Direct vasodilators – hydralazine, minoxidil NO suppliers – nitroglycerine
  • 13. Effect of Posture on BP • BP measurements are typically recorded in the sitting position. • Normally, standing is accompanied by a small increase in DBP and a small decrease in SBP when compared to supine values. • SBP: Supine > Sitting > Standing • DBP: Standing > Sitting > Supine (by > 5 mm Hg) • Orthostatic Hypotension (OH) is present when there is a supine-to- standing BP decrease >20 mmHg systolic or >10 mmHg diastolic. • There is more OH in diabetic individuals. The causes of OH include severe volume depletion, baroreflex dysfunction, autonomic insufficiency, and certain antihypertensive drugs.
  • 14. Effect of Exercise on BP Effect on Systolic BP Effect on Diastolic BP • Isometric Exercise: Increased DBP Cause: Tonic contraction of muscles compress on blood vessels causing increased peripheral resistance  Isometric Exercise: ↑ SBP, ↑ DBP, ↑ MBP • Isotonic Exercise: ↓ or unchanged DBP • Cause: Vasodilation causing decrease in peripheral resistance due to: i. ↓PO2, ↑PCO2, ↑H+, ↑K+, ↑ temp, ↑ adenosine → vasodilator metabolites ii. ↑ Adrenaline acts on β2 receptors on Vascular smooth muscles → vasodilation iii. Sympathetic cholinergic vasodilator system in skeletal muscle Isotonic Exercise: ↑ SBP, ↓ or unchanged DBP
  • 15. Hypertensive Crises: Emergencies and Urgencies Clinical Characteristics of Hypertensive Crisis • The basic difference between the two conditions with high BP, usually >180/120 mmHg, is the presence or absence of target organ damage. • Hypertensive emergencies: Target organ damage that includes any of the features of neurologic or myocardial or retinal or renal involvement; require hospitalization and parenteral drug therapy.
  • 16. Hypertension Management • Goals of Therapy: • Treating SBP and DBP to targets that are <140/90 mmHg is associated with a decrease in CVD complications. • In patients with hypertension and diabetes or renal disease, the BP goal is <130/80 mmHg. • Lifestyle Modifications: • Weight Reduction • Adopt DASH Diet • Antihypertensive drugs
  • 17. Lifestyle modifications to manage hypertension
  • 18. Thank You https://www.youtube.com/watch?v=O-lbLyopcuo PAHO, WHL, the Lancet Commission on Hypertension Group, Hypertension Canada and Resolve to Save Lives have developed a free brief training and certification course in blood pressure measurement. http://www.whleague.org/index.php/j-stuff/awareness-and-screening/new-online-bp-certification-course Virtual Course on accurate automated blood pressure measurement (2020) https://www.campusvirtualsp.org/en/node/29166