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
Renin–Angiotensin–Aldosterone System (RAAS)
- Kidney releases renin → angiotensin II
- Effects: systemic vasoconstriction, aldosterone release (Na$^+$ & water reabsorption)
Antidiuretic Hormone (ADH)
- Pituitary secretion → water retention at kidneys.
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
Situation | Superior Mesenteric (gut) | Common Iliac (legs) |
---|
After big meal | Dilated (↑ digestion) | Constricted (legs elevated) |
Playing soccer | Constricted | Dilated (↑ 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
- ↑ 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}.