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Physiology 3% exam weight

Cardiovascular System

Part of the INI CET (AIIMS PG) study roadmap. Physiology topic physio-005 of Physiology.

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Hemodynamics and Blood Pressure Regulation covers hemodynamics and blood pressure regulation for INI CET (AIIMS PG).

Blood Circulation:

  • Systemic circulation: LV → aorta → arteries → arterioles → capillaries → venules → veins → RA (high pressure ~100 mmHg)
  • Pulmonary circulation: RV → pulmonary artery → pulmonary capillaries → pulmonary vein → LA (low pressure ~15 mmHg)
  • Mean Arterial Pressure (MAP): MAP = CO × TPR (Ohm’s law for circulation)
    • Normal: 70–100 mmHg; MAP ≈ DBP + 1/3 pulse pressure (for DBP 80, PP 40 → MAP ≈ 93)

Cardiac Output (CO):

  • CO = HR × SV (normal: ~5 L/min at rest)
  • Stroke Volume determined by: Preload, Afterload, Contractility
  • Frank-Starling mechanism: Increased venous return → increased end-diastolic volume → increased SV
  • Factors increasing CO: ↑HR (sympathetic), ↑SV (↑contractility, ↑preload), ↓afterload

Blood Pressure Regulation:

Short-term (seconds to minutes):

  • Baroreceptor reflex: Most important rapid regulator
    • Arterial baroreceptors (carotid sinus, aortic arch): Detect ↑BP → stretch → ↑nerve firing → medulla → ↑parasympathetic (↓HR) + ↓sympathetic (vasodilation) → ↓BP
    • Cardiopulmonary baroreceptors: Low-pressure receptors; respond to volume changes
  • Chemoreceptors: Detect hypoxia, hypercapnia, acidosis → ↑BP (via sympathetic activation)
  • CNS ischemic response: Severe hypoxia of vasomotor center → powerful sympathetic activation → ↑BP

Medium-term (minutes to hours):

  • Renin-Angiotensin-Aldosterone System (RAAS):
    1. Renin (from juxtaglomerular cells — low perfusion pressure, ↓Na⁺ delivery, β₁ stimulation) converts Angiotensinogen → Angiotensin I
    2. ACE (lung endothelium) converts Ang I → Angiotensin II (active)
    3. Ang II: Potent vasoconstrictor; stimulates aldosterone (Na⁺/water retention); ADH release; thirst; sympathetic activation; cardiac remodeling
    4. Aldosterone: Distal tubule Na⁺ reabsorption + K⁺ secretion → ↑blood volume → ↑BP
  • ADH (Vasopressin): ↑aquaporin channels → water reabsorption; V1 receptors → vasoconstriction (at high concentrations)

Long-term (hours to days):

  • Kidney pressure-natriuresis mechanism: ↑BP → ↑Na⁺ excretion (pressure natriuresis) → ↓blood volume → restores BP
  • ACE inhibitors and ARBs interrupt RAAS → used in hypertension, heart failure, diabetic nephropathy

Microcirculation:

  • Arterioles: Main resistance vessels (~65% of TPR); smooth muscle with sympathetic innervation (α₁ → vasoconstriction); locally regulated by metabolic factors (↓O₂, ↑CO₂, ↑K⁺, adenosine → vasodilation)
  • Capillaries: Site of exchange (nutrients, wastes, fluids); no innervation; regulated by pre-capillary sphincters
  • Venules: Low resistance; capacitance vessels (~65% of blood volume at rest)

Starling Forces and Fluid Exchange:

  • Capillary filtration: Driven by net hydrostatic pressure (P_c) — forces fluid out
  • Capillary reabsorption: Driven by oncotic pressure (π_c) — pulls fluid in
  • Net Filtration Pressure = (P_c – P_i) – (π_c – π_i)
  • At arterial end: P_c > π_c → net filtration (tissue fluid formation)
  • At venous end: P_c drops (resistance) + π_c maintained → net reabsorption
  • Edema: When net filtration pressure is increased (↑P_c from venous congestion, ↑P_i from tumors, ↓π_c from hypoalbuminemia, ↑ capillary permeability) or impaired lymph drainage

⚡ Exam Tip for INI CET (AIIMS PG): ACE inhibitors (–pril: enalapril, lisinopril) block ACE → ↓Ang II → ↓aldosterone → ↓Na⁺/water retention. Side effects: Dry cough (bradykinin accumulation), angioedema, hyperkalemia. CONTRAINDICATED in pregnancy (teratogenic — fetal renal damage). ARBs (–sartan) have fewer cough side effects.