Total Peripheral Resistance
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Direct answer
Total peripheral resistance equals mean arterial pressure minus right atrial pressure, divided by cardiac output — roughly (93 − 3)/5, about 18 mmHg per litre per minute, or around 1000-1400 dyn.s.cm-5 in physiological units. The arterioles generate most of this resistance: pressure falls from about 85 mmHg in the aorta to roughly 30 mmHg at the capillary, and because resistance varies with the fourth power of radius (Poiseuille), tiny calibre changes dominate. Control is layered — basal sympathetic alpha-1 tone, hormones (angiotensin II, vasopressin), and local metabolic and endothelial factors (nitric oxide) that fine-tune each bed.
What you must remember
- Formula and values: TPR = (MAP − RAP)/CO; with MAP 93, RAP 3 and CO 5 L/min, about 18 units — multiply mmHg.min/L by 80 for dyn.s.cm-5 (about 1440).
- Resistance vessels: arterioles, with their single-to-double smooth muscle layer, hold the steepest pressure drop; capillaries are exchange vessels, not resistance vessels.
- Poiseuille's law: resistance = 8 × viscosity × length divided by pi times radius to the fourth; a 19 per cent fall in radius doubles resistance — calibre is everything.
- Viscosity: anaemia lowers viscosity and TPR (producing flow murmurs and a hyperdynamic circulation); polycythaemia raises both — viscosity tracks haematocrit.
- Neural control: tonic sympathetic vasoconstrictor discharge (alpha-1) sets the baseline; baroreflex adjusts it beat to beat.
- Hormonal control: angiotensin II is the most potent vasoconstrictor, vasopressin next; adrenaline at low concentrations vasodilates muscle and splanchnic beds through beta-2 receptors.
- Local control: metabolic vasodilators (adenosine, CO2, lactate, potassium, hydrogen ion) and endothelial nitric oxide keep a basal dilator tone — the reason endothelial injury (atherosclerosis, diabetes) produces paradoxic constriction.
- Parallel arrangement: organs in parallel lower net resistance and allow independent regulation of each bed's flow — the architectural reason MAP stays similar across tissues with very different flows.
- Exercise physiology: TPR falls in exercise (massive muscle bed vasodilation) even as cardiac output triples, so mean pressure rises only modestly — mostly systolic.
Working through a septic shock patient
A 50-year-old man with urinary sepsis is warm, flushed and tachycardic, with a cardiac index of 4.5 L/min/m2 yet a mean arterial pressure of 55 mmHg. Calculate: his systemic vascular resistance is about 600 dyn.s.cm-5 — half of normal. Nitric oxide and prostaglandins poured out by cytokine-activated endothelium have relaxed the arterioles body-wide; the heart, initially buoyed by reduced afterload and increased preload, cannot keep the pressure product (MAP = CO × TPR) above perfusion thresholds once resistance collapses. Noradrenaline, an alpha-1 agonist, is first-line precisely because it restores the missing variable, tone, rather than the ample cardiac output. Contrast cold cardiogenic shock: cardiac index 1.8, resistance 2000-plus as compensatory vasoconstriction squeezes the periphery — the same low blood pressure, an opposite physiology, and dopamine or inotropes rather than vasopressors as the primary lever. One formula, MAP = CO × TPR, sorts every shock at the bedside.
Where students slip
The MAP formula trap: mean arterial pressure is not the arithmetic mean — it is diastolic plus one-third of pulse pressure (93 at 120/80), because diastole occupies two-thirds of the cycle at resting heart rates. The second slip is forgetting the fourth-power law cuts both ways: the same exponent that makes vasodilators powerful makes vasoconstriction expensive — an arteriole halving its radius needs sixteen times the pressure for the same flow. Third, students call capillaries the resistance vessels because they are narrow; they are numerous and in parallel, so their collective resistance is modest — the arteriole, with pre-capillary sphincter control, is where regulation lives.
Frequently asked questions
State the formula for total peripheral resistance with normal values.
TPR = (mean arterial pressure − right atrial pressure) / cardiac output; approximately 18 mmHg.min/L, or about 1000-1400 dyn.s.cm-5.
Why are arterioles called resistance vessels?
Their small radius and muscular walls create the steepest pressure drop in the circuit, and their calibre — controlled by sympathetic tone and local factors — regulates both upstream pressure and downstream organ flow.
How does anaemia affect total peripheral resistance?
Reduced haematocrit lowers blood viscosity, lowering resistance and producing a hyperdynamic circulation with flow murmurs — resistance varies directly with viscosity per Poiseuille's law.
Why does total peripheral resistance fall during exercise?
Massive metabolic vasodilation in working muscle opens enormous parallel capacity, so net resistance falls despite reflex constriction elsewhere, letting cardiac output rise with only a modest pressure increase.
What is the role of nitric oxide in basal vascular tone?
Endothelium continuously releases nitric oxide that relaxes smooth muscle; losing this dilator tone (atherosclerosis, diabetes) causes paradoxic vasoconstriction and hypertension.