Blood Pressure: Variations & Homeostasis- Physiology

Blood Pressure (BP)

The force exerted by blood on the walls of blood vessels

Vascular compliance

ΔV/ΔP, ability of vessel to expand with pressure

Veins compliance vs arteries

Veins are 8× more compliant than arteries

Veins as capacitance vessels

Veins accommodate large blood volume with minimal pressure change

Systolic Pressure (SP)

Pressure during ventricular systole

Diastolic Pressure (DP)

Pressure during ventricular diastole

Pulse Pressure (PP)

SP − DP

Mean Arterial Pressure (MAP)

DP + 1/3 PP

MAP significance

Average pressure throughout cardiac cycle, reflects tissue perfusion

Blood flow equation

Q = ΔP / R

Driving force of blood flow

Pressure gradient between two ends of vessel

Importance of BP regulation

Maintains adequate tissue perfusion, prevents rupture or ischemia

High BP danger

Vessel rupture, organ damage

Low BP danger

Inadequate perfusion, especially brain, heart, kidneys

Threshold for hypertension <65 yrs

140/90 mmHg

Threshold for hypertension ≥65 yrs

150/80 mmHg

Two determinants of arterial BP

Cardiac Output (CO) and Total Peripheral Resistance (TPR)

Arterial BP equation

ABP

Factors affecting TPR

Arteriolar diameter, blood viscosity, vessel length

Arteriolar radius effect

Resistance ∝ 1/r⁴

Vasoconstriction effect

↑ TPR → ↑ BP

Vasodilation effect

↓ TPR → ↓ BP

Blood viscosity determinants

Hematocrit, RBC shape, plasma proteins, velocity of flow

Anaemia effect on BP

↓ viscosity → ↓ BP

Polycythemia effect on BP

↑ viscosity → ↑ BP

Spherocytosis effect on BP

Altered RBC shape → ↑ viscosity → ↑ BP

Plasma protein concentration effect

↑ viscosity → ↑ BP

Major factors affecting SP

Stroke volume, arterial compliance

Minor factors affecting SP

Heart rate

Major factors affecting DP

Total peripheral resistance

Minor factors affecting DP

Stroke volume, heart rate

Increase in SP

↑ SV, ↑ HR, ↓ arterial compliance

Decrease in DP

↓ TPR, ↓ SV, ↓ HR

Physiological BP variation during sleep

BP falls ~20 mmHg

Physiological BP variation with emotion

↑ BP (white coat hypertension)

BP in obesity

Higher due to ↑ resistance and sympathetic tone

Factors causing BP variation

Sleep, emotion, body build, gender, diurnal rhythm, age, posture

Diurnal BP variation

↓ at night, ↑ before waking, peaks mid‑afternoon, ↓ evening

Circadian BP significance

Reflects autonomic tone and cardiovascular risk patterns

Gender difference in BP (young adults)

Women lower BP than men

Gender difference in BP (post‑menopause)

Women higher BP than men

Estrogen vascular effects

Vasodilator, antioxidant, ↑ eNOS, ↓ ACE → ↓ Ang II

Post‑menopause sympathetic activity

↑ sympathetic tone → ↑ BP

Age effect on BP

↑ SBP, MAP, PP due to arterial stiffness and ↓ renal efficiency

Age effect on vascular compliance

↓ compliance → ↑ pressure at any volume

Gravity effect on vascular pressure

BP ↑ below heart, ↓ above heart

Venous pressure at feet

+80 mmHg

Venous pressure at neck veins

~0 mmHg

Venous pressure in sagittal sinus

−10 mmHg (risk of air embolism in surgery)

Case study: vomiting/diarrhea low BP

Hypovolemia → ↓ preload → ↓ CO → ↓ BP

Case study: rapid pulse

Compensation for low CO

Case study: cold hands

Peripheral vasoconstriction due to sympathetic activation

Short‑term BP regulation

Neural (baroreceptors, chemoreceptors, hormones)

Long‑term BP regulation

Hormonal and renal (RAAS)

Baroreceptors location

Aortic arch, carotid sinuses

Baroreceptors function

Stretch receptors, moment‑to‑moment BP control

Baroreceptor reflex pathway

IX/X → NTS → CVC → autonomic output → heart/vessels

Chemoreceptors location

Carotid and aortic bodies (peripheral), medulla (central)

Peripheral chemoreceptor stimuli

↓ PO₂, ↓ pH, ↑ PCO₂

Peripheral chemoreceptor response

↑ sympathetic tone, ↑ HR, ↑ TPR → ↑ BP

Central chemoreceptor stimuli

Changes in CSF PCO₂, pH, PO₂

Central chemoreceptor response

↑ sympathetic stimulation → ↑ HR, vasoconstriction

Cushing reflex

CNS ischemic response to ↑ ICP

Cushing triad

↑ MAP, ↓ HR, irregular respiration

Cushing reflex mechanism

Brain ischemia → chemoreceptor activation → ↑ CO, TPR, MAP → baroreceptor reflex → ↓ HR

RAAS activation trigger

↓ MAP → ↓ renal blood flow → ↓ GFR → renin release

Angiotensin II effects

Vasoconstriction, ↑ TPR, ↑ BP

Aldosterone effects

↑ Na⁺ and water retention → ↑ blood volume → ↑ BP

Vasopressin (ADH) effects

↑ water reabsorption → ↑ blood volume → ↑ BP

ANP effects

↑ Na⁺ excretion, ↑ urine output → ↓ blood volume → ↓ BP

Volume receptors location

Atria, veins, pulmonary arteries

Volume receptor response to ↑ blood volume

↓ ADH, ↑ ANP, ↓ RAAS → ↑ urine output → ↓ BP

Hormones raising BP

Adrenaline, noradrenaline, thyroxine, aldosterone, vasopressin, angiotensin, serotonin, cortisol

Hormones lowering BP

VIP, bradykinin, prostaglandin, histamine, acetylcholine, ANP

Lowest velocity of blood flow

Capillaries

Highest pressure vessels

Arteries

Lowest pressure vessels

Veins

Lowest velocity vessels

Capillaries

Highest cross‑sectional area vessels

Capillaries

Lowest cross‑sectional area vessels

Aorta

Significance of vessel differences

Optimize exchange (capillaries), maintain flow (arteries), reservoir (veins)

Factors affecting systolic BP

Stroke volume, arterial compliance, HR

Factors affecting diastolic BP

TPR, stroke volume, HR

Factors affecting pulse pressure

Difference between SP and DP, influenced by SV and compliance

Integrated regulation of BP (↑ blood volume)

Volume receptors → ↓ ADH, ↑ ANP, ↓ RAAS → ↑ urine output → ↓ blood volume → ↓ BP

Integrated regulation of BP (↓ blood volume)

RAAS activation → ↑ Ang II, ↑ aldosterone, ↑ vasopressin → ↑ blood volume → ↑ BP

BP homeostasis significance

Maintains tissue perfusion, prevents damage from extremes