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Video 3 - Cardiovascular Regulation, Exercise & Hemorrhage – Comprehensive Study Notes

Cardiovascular Regulation – Core Principles

  • Goal: Match tissue blood flow to metabolic need while maintaining systemic blood pressure (BP) and adequate cardiac output (CO).
  • 3 co-ordinated control levels
    • Autoregulation (local, immediate)
    • Neural mechanisms (fast, CNS-driven)
    • Endocrine mechanisms (slower; minutes → hours, sometimes chronic)

Autoregulation of Blood Flow

• Triggered by changes in the interstitial fluid surrounding a capillary bed.

• Key local factors that make precapillary sphincters DILATE

  • ↓ O$_2$
  • ↑ CO$_2$ (→ ↓ pH)
  • ↑ lactic acid (muscle anaerobic metabolism)
  • ↑ inflammatory chemicals (e.g., histamine in a mosquito bite)
  • ↑ local temperature

• Key local factor that makes them CONSTRICT

  • Physical damage to a vessel; prevents hemorrhage by diverting flow away from a “broken pipe.”

• Net effect: Shunt blood toward active or inflamed tissue and away from damaged regions.

Example connection: Red, warm, raised, itchy skin around a mosquito bite = autoregulatory hyperemia delivering immune cells to the site.


Neural Mechanisms (Medullary Cardiovascular Centers)

1. Baroreceptor Reflexes

• Sensors: carotid sinuses, aortic sinuses, right atrium.

• If BP rises

  • Parasympathetic (vagus) → ↓ HR → ↓ CO
  • Widespread vasodilation

• If BP falls

  • Sympathetic activation → ↑ HR & ↑ contractility → ↑ CO
  • Peripheral vasoconstriction

• Protective logic: Maintain cerebral and coronary perfusion.

2. Chemoreceptor Reflexes

• Sensors: carotid bodies, aortic bodies (same physical region as baroreceptors but chemically sensitive).

• Detect

  • ↑ CO$2$ (→ ↓ pH via CO2 + H2O \rightarrow H2CO_3)
  • ↓ O$2$ (less potent stimulus than CO$2$)

• Response to acidosis / hypercapnia

  • ↑ CO, ↑ respiratory rate, peripheral vasoconstriction → flush acidic blood to lungs, blow off CO$_2$.

• Response to alkalosis / hypocapnia (rarer)

  • Essentially the opposite pattern.

Neurotransmitter – Vessel Tone Pairing

• Norepinephrine ((\alpha)-adrenergic) → vasoconstriction.
• Nitric oxide → vasodilation.


Endocrine Mechanisms

Low Blood Volume / Low BP

  1. Renin–Angiotensin–Aldosterone System (RAAS)

    • Kidney releases renin → angiotensin II
    • Effects: systemic vasoconstriction, aldosterone release (Na$^+$ & water reabsorption)
  2. Antidiuretic Hormone (ADH)

    • Pituitary secretion → water retention at kidneys.
  3. Erythropoietin (EPO)

    • Kidney hormone → ↑ red-cell production; slow but ↑ O$_2$ carrying capacity.

High Blood Volume / High BP

• Atrial Natriuretic Peptide (ANP)

  • Released by stretched atrial myocardium.
  • Promotes Na$^+$ & water loss (diuresis) + peripheral vasodilation.

Ethical-clinical link: Chronic RAAS overactivation = basis for ACE-inhibitor & ARB antihypertensive drug classes.


Cardiovascular Responses to Exercise

Light (Moderate) Exercise

  • General vasodilation in active skeletal muscle & skin.
  • ↑ venous return via muscle pump.
  • Modest rise in CO.

Heavy (Strenuous) Exercise

  • Sympathetic dominance → near-maximal CO.
  • Dramatic flow increase to working muscles & coronary circulation.
  • Active shunting AWAY from “non-essential” viscera (GI tract, kidneys).
  • Marathon‐runner example: Renal hypoxia can cause transient hematuria (blood in urine).

Post-prandial vs. Exercise Vascular Patterns

SituationSuperior Mesenteric (gut)Common Iliac (legs)
After big mealDilated (↑ digestion)Constricted (legs elevated)
Playing soccerConstrictedDilated (↑ leg perfusion)

Take-home: Walking after Thanksgiving dinner redistributes some blood away from the gut → modestly lowers caloric absorption & aids glucose handling.


Quantitative Redistribution of Flow (Rest vs. Max Exercise)

• Resting flow (ml min$^{-1}$)

  • Brain ≈ 750
  • Heart ≈ 200
  • Kidneys ≈ 1{,}100
  • GI ≈ 1{,}400
  • Skeletal muscle ≈ 1{,}200

• Max exercise flow

  • Brain ≈ 750 (nearly unchanged; protected)
  • Heart ≈ 750 (( \uparrow 275\% ))
  • Kidneys ≈ 250 (( \downarrow 75\% ))
  • GI ≈ 250 (( \downarrow 80\% ))
  • Skeletal muscle ≈ 12{,}500 (( \uparrow \approx 10\times ))
  • Skin ↑ markedly for heat loss

Mechanistic importance: Cutaneous vasodilation balances muscular vasoconstriction in core to prevent hyperthermia.


Acute Hemorrhage & Circulatory Shock

Immediate (Short-Term) Response

  • ↑ HR & contractility (↑ CO)
  • Peripheral vasoconstriction (↑ total peripheral resistance)
  • Goal: restore BP and perfusion

If bleeding continues → Decompensation

  • “Runaway train” – heart works harder against falling volume → failure risk.

Long-Term Response

  • ADH + RAAS water retention
  • Thirst
  • Erythropoiesis to replace lost RBCs

Circulatory Shock – Causes & Hallmarks

• Causes: severe hemorrhage, dehydration, extensive burns, MI.
• Symptoms: confusion, tachycardia with weak pulse, cool clammy skin.
• Treatment: stop loss, fluid/blood replacement, vasoactive drugs if necessary.


Special Circulation Considerations

• Brain: Autoregulation keeps cerebral flow constant despite systemic BP swings.

• Coronary Vessels: Epinephrine & local hypoxia → vasodilation; ensures heart O$_2$ supply during stress.

• Pulmonary Capillaries: Constrict in low-O$_2$ regions (opposite of systemic pattern) to divert blood toward well-ventilated alveoli; optimizes gas exchange.


Transition to Next Topic – Lymphatic & Immune Systems

  • Upcoming lecture covers lymphatic vessels, innate & adaptive immunity, and clinical examples (e.g., parasitic worms).
  • Instructor note: Some images may be unsettling; avoid snacking on gummy worms while viewing.
  • Action items before next class:
    • Complete the Circulation Quiz.
    • After immunity lectures, take the Immune/Lymphatic Quiz.
    • Begin preparing for Test 2.

Integrative Connections & Implications

• Homeostasis: Cardiovascular, renal, and respiratory systems function as an interlocking triad (BP ↔ gas exchange ↔ volume).

• Pathophysiology: Chronic hypertension often reflects maladaptive neural (sympathetic over-activity) and endocrine (RAAS) responses; therapeutic interventions target these pathways.

• Exercise Physiology: Training improves maximal CO and augments coronary reserve, explaining lower resting HR in athletes.

• Everyday Practice: Simple lifestyle choices (post-meal walks, hydration, gradual exercise warm-ups) exploit natural regulatory mechanisms for health gains.


Key Numbers & Values (quick reference)

  • Right atrial pressure at rest: \approx 2\;\text{mm Hg}
  • Cerebral flow protected at \approx 750\;\text{ml min}^{-1}.
  • Coronary flow rest → exercise: 200 \rightarrow 750\;\text{ml min}^{-1}.
  • Skeletal muscle flow rest → max: 1{,}200 \rightarrow 12{,}500\;\text{ml min}^{-1}.