Blood pressure in detail

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Blood Pressure - A Detailed Overview

1. Definition and Basic Formula

Blood pressure (BP) is the force exerted by circulating blood on the walls of blood vessels. It is governed by the hydraulic equation:

BP = Cardiac Output (CO) × Peripheral Vascular Resistance (PVR)

Both components are regulated through multiple overlapping neural, humoral, and local mechanisms to maintain pressure within the narrow range needed for adequate organ perfusion.

Robbins & Kumar Basic Pathology, p. 309
Katzung's Basic and Clinical Pharmacology, 16th Ed., p. 268

2. Normal Values

Blood Pressure Category	Systolic (mmHg)	Diastolic (mmHg)
Low	70-90	40-60
Normal	90-120	60-80
Elevated	120-129	<80
Hypertension Stage I	130-139	80-90
Hypertension Stage II	>140	>90
Malignant HTN	>180	>120

Starting at 115/75 mmHg, cardiovascular disease risk doubles with each increment of 20/10 mmHg throughout the blood pressure range. - Katzung's, p. 268

3. Components of Blood Pressure

A. Cardiac Output

Cardiac output = stroke volume × heart rate.

Stroke volume is primarily determined by filling pressure, which depends on sodium homeostasis and blood volume.
Heart rate and contractility are controlled by α- and β-adrenergic systems.
Blood volume is influenced by sodium, mineralocorticoids, and atrial natriuretic peptide (ANP).

B. Peripheral Vascular Resistance

Regulated mainly at the arteriole level by a balance of:

Vasoconstrictors:

Angiotensin II
Catecholamines (via α-adrenergic receptors)
Endothelin-1
Thromboxane, leukotrienes

Vasodilators:

Nitric oxide (NO)
Prostaglandins
Kinins
β-adrenergic stimulation

4. Regulatory Mechanisms

Here is the master diagram summarizing all factors governing blood pressure:

Blood pressure regulation diagram showing BP = Cardiac Output × Peripheral Resistance, with humoral factors (vasoconstrictors: Angiotensin II, Catecholamines, Thromboxane, Leukotrienes, Endothelin; dilators: Prostaglandins, Kinins, NO), cardiac factors (heart rate, contractility), blood volume factors (sodium, mineralocorticoids, ANP), neural factors (alpha and beta adrenergic), and local factors (autoregulation, pH, hypoxia)

Fig. 8.2 - Blood Pressure Regulation. (Robbins & Kumar Basic Pathology)

The four anatomic control sites coordinated by the CNS are shown below:

Anatomic sites of blood pressure control: (1) Resistance arterioles, (2) Capacitance venules, (3) Heart (pump output), (4) Kidneys (volume via Renin-Angiotensin-Aldosterone), all regulated by CNS-Sympathetic nerves

Fig. 11-1 - Anatomic sites of blood pressure control (Katzung's Pharmacology)

A. The Renin-Angiotensin-Aldosterone System (RAAS)

This is the primary long-term BP regulator:

Renin - released by renal juxtaglomerular cells when renal perfusion pressure falls or sodium is low
Renin cleaves angiotensinogen → Angiotensin I
ACE (on vascular endothelium) converts it → Angiotensin II
Angiotensin II acts by:
- Directly constricting arteriolar smooth muscle (↑ PVR)
- Stimulating aldosterone secretion from the adrenal cortex
- Increasing tubular sodium resorption directly
Aldosterone increases Na+ (and water) resorption in the distal tubule → ↑ blood volume → ↑ CO

B. Baroreflex (Short-term, rapid regulation)

Carotid baroreceptors sense arterial wall stretch. When BP falls:

Reduced baroreceptor firing → reduced inhibition of the medullary vasomotor center
Increased sympathetic outflow → vasoconstriction (↑ PVR) + increased heart rate/contractility (↑ CO)
This restores BP within seconds

When BP rises, the opposite occurs. In hypertensive patients, this baroreflex is reset to a higher set point. - Katzung's, p. 270

C. Renal Volume Control (Long-term)

Reduced renal perfusion → salt and water retention → expanded blood volume → ↑ CO
The kidney controls BP by regulating intravascular volume over days to weeks
Vasopressin (ADH) from the posterior pituitary also contributes by regulating water reabsorption

D. Natriuretic Peptides (Counter-regulatory)

ANP (from atria) and BNP (from ventricles) are released in response to volume expansion / elevated filling pressures
They inhibit sodium resorption in distal renal tubules → natriuresis and diuresis
They also cause systemic vasodilation
Net effect: reduce blood volume and BP

E. Local Autoregulation

Resistance vessels respond to increased blood flow with vasoconstriction to protect against hyperperfusion
Tissue pH and hypoxia fine-tune local blood flow to match metabolic demands

5. Measurement

Blood pressure is expressed as systolic/diastolic in mmHg, measured via sphygmomanometry. Key points:

Two readings are taken; the average is used
"White coat hypertension" (elevated in office, normal at home) should be confirmed with ambulatory BP monitoring (ABPM) or home readings
Hypertension is asymptomatic until end-organ damage is imminent - Katzung's, p. 268

6. Hypertension

Classification by Cause

Type	Frequency	Examples
Primary (essential/idiopathic)	90-95%	Multifactorial; no identifiable cause
Secondary	5-10%	Renal artery stenosis, primary aldosteronism, pheochromocytoma, Cushing's, coarctation of aorta, obstructive sleep apnea

Primary hypertension arises from a combination of: genetic factors, psychological stress, high dietary sodium, low potassium/calcium, alcohol consumption, obesity, and physical inactivity. - Robbins Pathology, p. 310

Risk Stratification

Additional risk factors that worsen prognosis at any BP level:

Smoking (including secondhand)
Diabetes mellitus
Metabolic syndrome (obesity, dyslipidemia)
Physical inactivity
End-organ damage at diagnosis
Family history of cardiovascular disease
African American ethnicity (higher prevalence + severity)
Male sex (premenopausal women are relatively protected)

Malignant Hypertension

Systolic >180 mmHg or diastolic >120 mmHg
Rapidly rising; leads to death within 1-2 years if untreated
Associated with renal failure, retinal hemorrhages, papilledema
Most commonly superimposed on pre-existing primary hypertension

7. Consequences of Hypertension

Without treatment, approximately:

50% of hypertensive patients die of ischemic heart disease or congestive heart failure
33% die of stroke
Others develop aortic dissection, renal failure, multifocal dementia

Target organs damaged by sustained hypertension:

Heart - left ventricular hypertrophy, heart failure
Brain - stroke, hypertensive encephalopathy, vascular dementia
Kidneys - nephrosclerosis, renal failure
Eyes - retinopathy, retinal hemorrhages
Arteries - accelerated atherosclerosis, aortic dissection

8. Antihypertensive Drug Classes

All antihypertensive drugs work by interfering with normal BP regulatory mechanisms at one or more of the four anatomic control sites:

Diuretics - deplete sodium, reduce blood volume (e.g., hydrochlorothiazide, furosemide)
RAAS blockers - ACE inhibitors, ARBs, direct renin inhibitors; reduce angiotensin II effect → vasodilation + reduced aldosterone
Direct vasodilators - relax vascular smooth muscle (e.g., hydralazine, minoxidil)
Sympathoplegic agents - reduce sympathetic outflow; subdivided by site of action:
- Central acting (e.g., clonidine, methyldopa)
- Ganglionic blockers
- β-blockers (reduce HR and CO)
- α-blockers (reduce PVR)
- Combined α/β blockers (e.g., labetalol)
Calcium channel blockers - reduce vascular smooth muscle contraction

Katzung's, p. 271

Sources:

Robbins & Kumar Basic Pathology (Robbins Pathology), pp. 309-311
Katzung's Basic and Clinical Pharmacology, 16th Ed., pp. 268-271

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