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Peripheral resistance
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I now have comprehensive information to give a detailed answer. Here is the full explanation of Peripheral Resistance based on your textbook page and supplemented by Costanzo, Guyton & Hall, and Medical Physiology textbooks:
Peripheral Resistance
Definition
Peripheral resistance is the resistance offered to blood flow at peripheral blood vessels - specifically, it is the load against which the heart must pump blood. It is also called Total Peripheral Resistance (TPR) or Systemic Vascular Resistance (SVR).
- Costanzo Physiology, p. 168
Site of Maximum Resistance
- Arterioles are the primary site of resistance to blood flow. Small changes in their caliber produce large changes in total peripheral resistance. They are therefore called "resistant vessels".
- In the body, the maximum peripheral resistance is offered at the splanchnic region.
- Ganong's Review of Medical Physiology
Relationship to Cardiac Output
$$\text{Cardiac Output} \propto \frac{1}{\text{Peripheral Resistance}}$$
Cardiac output is inversely proportional to peripheral resistance. When TPR increases, the heart faces greater afterload, which reduces cardiac output. When TPR decreases, cardiac output increases.
Formula (Ohm's Law of Hydrodynamics)
$$R = \frac{\Delta P}{Q}$$
Where:
- R = resistance
- ΔP = pressure gradient (aortic pressure - vena caval pressure)
- Q = cardiac output (blood flow)
Units: mm Hg / (mL/sec) = Peripheral Resistance Units (PRUs)
- Medical Physiology, p. 828
Determinants of Resistance (Poiseuille's Law)
$$R = \frac{8 \eta l}{\pi r^4}$$
| Factor | Relationship to Resistance |
|---|---|
| Vessel radius (r) | Inversely proportional to r⁴ (most important factor) |
| Vessel length (l) | Directly proportional |
| Blood viscosity (η) | Directly proportional |
The 4th power relationship with radius means even small changes in arteriolar caliber have enormous effects on resistance. Halving the radius increases resistance 16-fold.
- Medical Physiology, p. 835
Effects of Changing TPR
| Change in TPR | Effect |
|---|---|
| Increased TPR (arteriolar constriction) | ↑ Arterial blood pressure, ↑ afterload, ↓ cardiac output, ↓ venous return |
| Decreased TPR (arteriolar dilation) | ↓ Arterial blood pressure, ↓ afterload, ↑ cardiac output, ↑ venous return |
- Costanzo Physiology, p. 168
Regulation of Peripheral Resistance
- Sympathetic nervous system - sympathetic activation causes arteriolar vasoconstriction via α₁ adrenoceptors → increases TPR (key response in hemorrhage and exercise)
- Local metabolic factors - CO₂, H⁺, hypoxia cause local vasodilation, reducing local resistance
- Hormones - Angiotensin II, catecholamines increase resistance; ANP decreases it
- Endothelium - releases NO (vasodilator) and endothelin (vasoconstrictor)
Clinical Relevance
- Hypertension - often caused by chronically elevated peripheral vascular resistance, largely driven by structural and functional changes in arterioles. Harrison's 22E
- Hemorrhagic shock - early sympathetic activation increases TPR to maintain blood pressure; prolonged shock causes failure of this vasoconstrictor response
- Heart failure - compensatory increase in TPR initially maintains BP but worsens cardiac output over time
Relationship to Other Cardiac Output Determinants (from your textbook page)
| Factor | Relationship to Cardiac Output |
|---|---|
| Preload | Directly proportional |
| Afterload | Inversely proportional |
| Heart rate | Directly proportional |
| Peripheral resistance | Inversely proportional |
The arterioles are the key control point for peripheral resistance - vasodilation or vasoconstriction here is the primary mechanism by which the cardiovascular system redistributes blood flow to meet metabolic demands.
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