Peripheral vascular resistance
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"peripheral vascular resistance" physiology regulation
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Peripheral Vascular Resistance (PVR)
Definition and the Fundamental Equation
Peripheral vascular resistance (PVR), also called total peripheral resistance (TPR), is the resistance offered by the systemic vasculature to blood flow. It is the principal determinant of afterload.
The foundational hemodynamic equation (hydraulic/Ohm's law analogy) is:
BP = CO × PVR
where BP = arterial blood pressure, CO = cardiac output.
Rearranged: PVR = BP / CO
Units are expressed as peripheral resistance units (PRU) = mmHg per mL/sec. - Medical Physiology (Boron & Boulpaep), p. 606
Determinants of PVR - Poiseuille's Law
From the Hagen-Poiseuille equation, the resistance of any vascular segment is:
R = (8ηl) / (πr⁴)
Where:
- η = blood viscosity
- l = vessel length
- r = vessel radius (most important - resistance varies with the 4th power of radius)
This means a 2-fold decrease in radius increases resistance 16-fold. - Medical Physiology, p. 606
Key factors governing PVR:
| Factor | Effect on PVR | Notes |
|---|---|---|
| Vessel radius (r) | ↑r → PVR ↓↓↓↓ | Most powerful determinant (r⁴ relationship) |
| Blood viscosity (η) | ↑η → PVR ↑ | Normal blood ~3-4× water viscosity |
| Hematocrit | ↑Hct → ↑η → ↑PVR | Polycythemia raises PVR; anemia lowers it |
| Vessel length (l) | ↑l → PVR ↑ | Fixed in adults; obesity increases it |
| Number of parallel vessels | ↑N → PVR ↓ | Parallel arrangement reduces aggregate resistance |
- Guyton & Hall Textbook of Medical Physiology, Chapter 14
Site of Greatest Vascular Resistance: Arterioles
Although capillaries have the smallest individual radii, arterioles account for the greatest aggregate resistance in the systemic circulation - and therefore the steepest pressure drop occurs across them.
Why? Because capillaries vastly outnumber arterioles (10¹⁰ vs 10⁷). The larger number in parallel dramatically reduces their aggregate resistance:
| Vessel | Internal Radius | Individual R | Number | Total R |
|---|---|---|---|---|
| Arterioles | 15 µm | ~15×10⁷ dyne·s/cm⁵ | 10⁷ | 15 dyne·s/cm⁵ |
| Capillaries | 4 µm | ~3000×10⁷ dyne·s/cm⁵ | 10¹⁰ | 3 dyne·s/cm⁵ |
- Medical Physiology (Boron & Boulpaep), Table 19-4
This is why arterioles are called "resistance vessels" - they are the primary site of blood pressure regulation.
Regulation of PVR
PVR is regulated at four anatomic sites; blood pressure is maintained by moment-to-moment adjustments at all four: - Katzung's Basic & Clinical Pharmacology, 16e, p. 269
1. Arterioles (primary)
- Vasodilation/vasoconstriction via smooth muscle tone
- Regulated by both neural and humoral mechanisms
2. Postcapillary Venules (capacitance vessels)
- Control venous return and preload
- Indirectly affect CO, which modifies overall hemodynamics
3. Heart
- CO adjustments via heart rate and contractility
4. Kidney
- Long-term BP regulation via volume control (RAAS axis)
Neural and Humoral Control of PVR
A. Sympathetic Nervous System (Baroreceptor Reflex)
- Central sympathetic neurons from the vasomotor area of the medulla are tonically active
- Carotid baroreceptors sense arterial wall stretch → inhibit sympathetic outflow
- Drop in BP (e.g., standing up, hemorrhage) → ↓ baroreceptor stretch → ↑ sympathetic discharge → arteriolar constriction → ↑ PVR → restores BP
- α₁-receptor stimulation (e.g., norepinephrine) → vasoconstriction → ↑ PVR
- Chronic excess catecholamines (pheochromocytoma): sustained ↑ PVR → hypertension, LV hypertrophy, myocardial ischemia - Morgan & Mikhail's Clinical Anesthesiology, 7e
B. Renin-Angiotensin-Aldosterone System (RAAS)
- Decreased renal perfusion → ↑ renin → ↑ angiotensin II → direct constriction of resistance vessels → ↑ PVR
- Aldosterone → ↑ Na⁺ reabsorption → ↑ intravascular volume → ↑ CO
C. Local / Endothelial Factors
Vascular tone reflects a balance between: - Robbins & Kumar Basic Pathology
| Vasoconstrictors | Vasodilators |
|---|---|
| Angiotensin II | Nitric oxide (NO) |
| Catecholamines | Prostacyclin (PGI₂) |
| Endothelin-1 | Kinins (bradykinin) |
| Thromboxane A₂ | Atrial natriuretic peptide |
Autoregulation: Increased blood flow induces vasoconstriction to protect downstream capillaries (myogenic response + metabolic signaling).
PVR and Cardiac Output - The Inverse Relationship
In the long term, increases in TPR do not raise arterial pressure if the kidney's fluid-pressure control is intact - Guyton's "whole-body autoregulation" principle. Instead:
- ↑ TPR → ↓ CO (inverse relationship at constant BP)
- Conditions reducing TPR (AV fistulas, anemia, pregnancy, beriberi, Paget's disease) → ↑ CO → high-output states - Guyton & Hall, Chapter 20
Clinical Relevance
| Condition | PVR Change | Mechanism |
|---|---|---|
| Hypertension | ↑ | Increased arteriolar tone (sympathetic/RAAS) |
| Septic shock | ↓↓ | Massive vasodilation (NO, cytokines) |
| Cardiogenic shock | ↑ | Compensatory vasoconstriction |
| Polycythemia | ↑ | ↑ blood viscosity |
| Anemia | ↓ | ↓ viscosity + ↑ CO compensation |
| CCBs | ↓ | Block Ca²⁺-dependent arteriolar tone (↓ PVR regardless of age, sex, ancestry) - Brenner & Rector's The Kidney |
| Alpha-blockers | ↓ | Block α₁ receptors → vasodilation |
| Vasopressors (norepinephrine) | ↑ | α₁ stimulation |
Summary Formula
$$\text{MAP} = \text{CO} \times \text{TPR}$$
$$\text{TPR} = \frac{8\eta l}{\pi r^4} \propto \frac{\text{viscosity} \times \text{length}}{r^4}$$
The arteriole is the master rheostat of peripheral vascular resistance, and its radius - controlled by neural, humoral, and local endothelial signals - is the most physiologically important variable.
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