BP/HTN Pathophysiology

need to add factors incfluencing blood pressure and hypertension epidemiology

arteries

arteries

• made up of connective tissue, muscle, and endothelial cells

• take blood from heart to organs/tissues

• offer resistance to blood flow = resistance vessels

capillaries

terminal portions of arteries that deliver oxygen/nutrients to organs

venules/veins

• made up of small amount of muscle and connective tissue

• drain blood back from capillaries to heart

intima

inner artery layer; endothelium maintains structural, metabolic, and signaling functions to maintain homeostasis

media

middle artery layer; muscle innervated by noradrenergic nerve fibers, constrictor in function

adventitia

outer artery layer; connective tissue

systolic

peak pressure during cardiac contraction

diastolic

nadir pressure when cardiac chambers are filling

factors that increase cardiac output

increased cardiac preload; sodium and water retention from excess sodium intake or kidney sodium retention

factors that increase total vascular resistance

vascular constriction; excess stimulation of RAAS; sympathetic system overactivity; endothelial derived factors

normal blood pressure

SBP <120mmHg and DBP <80mmHg

elevated blood pressure

SBP 120-129mmHg and DBP <80mmHg

stage 1 HTN

SBP 130-139mmHg or 80-89mmHg

stage 2 HTN

SBP ≥ 140mmHg or ≥ 90mmHg

HTN urgency/emergency

SBP ≥180mmHg and/or DBP ≥120mmHg

primary hypertension

• 90% of patients

• cannot be attributed to any other single cause

• cannot be cured, but can be medically managed

secondary hypertension

• 10% of patients

• attributed to another disease or medications

clinical presentation

• asymptomatic

• silent killer

• headache, dizziness, epistaxis are possible with very elevated BP

endothelial derived factors that cause vasodilation and decreased total vascular resistance

• nitric oxide

• prostacyclin

• bradykinin

endothelial derived factors that cause vasoconstriction and increased total vascular resistance

• endothelin I

non-endothelial derived regulators that cause vasoconstriction

• increased intracellular calcium

• angiotensin II

• serotonin

• norepinephrine/ epinephrine

environmental factors that led to hypertension

• high sodium diet

• low potassium diet

• low calcium diet

• obesity/physical inactivity

high sodium diet

exact mechanism unknown; appears to affect TVR

low potassium diet

increased total peripheral resistance

low calcium diet

increased vascular smooth muscle contraction due to increased gradient of intracellular vs. extracellular calcium

obesity/physical inactivity

overactivation of SNS; renal compression

secondary hypertension diseases

• chronic kidney disease

• Cushing’s disease (hypercortisolemia)

• obstructive sleep apnea

• pheochromocytoma

• primary aldosteronism

• hyperthyroidism

secondary hypertension medications

• amphetamines

• corticosteroids

• estrogen-containing oral contraceptives

• testosterone

• decongestants

• erythropoiesis stimulating agents

• NSAIDs

• certain anti-depressants: desvenlafaxine, venlafaxine, bupropion

• cocaine

• abrupt withdrawal of central alpha-agonist (clonidine) or beta-blocker

secondary hypertension diet

• high sodium diet

• excessive ethanol consumption

• licorice

natriuretic hormones

• atrial-derived natriuretic protein (ANP)

• B-type natriuretic protein (BNP)

natriuretic hormone effect

increased ANP and/or BNP —> increased Na/H2O excretion via kidney —> decreased BP

peripheral autoregulation

kidneys regulate BP through regulation of plasma volume (sodium and water excretion vs. retention)

intrinsic defect in kidney adaptive mechanisms → plasma volume expansion → increased blood flow to peripheral tissues → vasoconstriction at tissues (arterioles)

acute: increased BP due to reversible increased total vascular resistance

chronically: arteriolar hypertrophy and thickening causing irreversible increase in total vascular resistance

baroreceptor reflex system

senses volume in large arteries (carotids and aortic arch)

• decreased volume → vasoconstriction, increased HR, increases contractility → increased BP

• increased volume → vasodilation, decreased HR, decreased contractility → decreased BP

mediated via sympathetic vasomotor outflow (catecholamines) and vagus nerve

a1 receptors (arterioles and venules)

stimulation causes vasoconstriction → increased total vascular resistance (TVR)

a2 receptors (central nervous system)

stimulation causes decreased release of peripheral catecholamines → decreased BP

b1 receptors (heart)

stimulation causes increased HR (chronotropy) and increased force of contraction (inotropy) → increased BP

b2 receptors (arterioles and venules)

stimulation causes vasodilation → decreased total vascular resistance (TVR)

mechanisms of essential hypertension; RAAS

• environmental factors

• disruption in natriuretic hormones

• abnormal neuronal mechanisms

• defects in peripheral autoregulation

what contributes to hypertension

• autoregulation

• adrenergic tone (sympathetic nervous system)

• humoral response

• diet and lifestyle

factors playing a role in elevated blood pressure

genetics, diet, physical activity, alcohol consumption, obesity