suggested literature: Hulín et al. · 3.13 Pathological changes of the blood pressure (H. Sapáková, pp. 152-155) 3.14 Systemic arterial hypertension (H. Sapáková, pp. 155-162)

suggested literature: Hulín et al.: PATHOPHYSIOLOGY Bratislava, SAP 1997 available at https://zona.fmed.uniba.sk/patfyz-zona/ Chapters: 3 Pathophysiology of the cardiovascular system ( I. Hulín, F. Šimko et al. ): 3.13 Pathological changes of the blood pressure (H. Sapáková, pp. 152-155) 3.14 Systemic arterial hypertension (H. Sapáková, pp. 155-162) 3.15 Secondary arterial hypertension (H. Sapáková, pp. 162-169)

BLOOD PRESSURE REGULATION & HYPERTENSION Simona Trubačová [email protected]

𝑓𝑜𝑟𝑐𝑒 (𝐹)

𝑠𝑢𝑟𝑓𝑎𝑐𝑒(𝑆) = pressure (P)

o Blood pressure (BP) = hydrostatic pressure of circulating blood (F), acting on surface of vessel wall (S)

o BP value is dependent on: • blood volume in blood vessels - cardiac output • vascular wall compliance - peripheral vascular resistance

What is BLOOD PRESSURE?

120/80

systolic blood pressure– SBP the highest pressure in the arteries when the ventricles

contract diastolic blood pressure- DBP minimal arterial pressure when the ventricles are filling with blood

pulse blood pressure - SBP - DBP

BLOOD PRESSURE MEASUREMENT

120

8O

O time

(mmHg)

systole diastole

120/80 BLOOD PRESSURE MEASUREMENT

mean arterial pressure – MAP average arterial blood pressure in an individual during a single heart cycle

MAP = 70-110 mmHg

120/80

systole diastole

𝐌𝐀𝐏 ≃ DBP + 1 3 (SBP – DBP) 𝐌𝐀𝐏 ≃ 23 DBP + 1 3 SBP

(mmHg)

time (t)

or

duration of

diastole 2/3 t

duration of

systole 1/3 t

a sudden drop in MAP below 70 mmHg or a decrease of 40 mmHg can indicate a circulatory failure


non-invasive blood pressure measurement: (heart rate registration after inflated cuff is released) • sphygmomanometrically - inflated cuff

with mercury tonometer and stethoscope - determination of Korotkoff phenomena

• oscillometric - detection of oscillation after cuff release detected above the artery

• Doppler technique - detection of blood

movement by probe over the artery

invasive blood pressure measurement: • intra-arterial measurement



BP in SYSTEMIC CIRCULATION vs PULMONARY CIRCULATION

) pressure (120/80 mmHg, MAP = 100 mmHg) resistance compliance

pressure (25/8 mmHg, MAP = 12-16 mmHg) resistance (1/6 – 1/10 of systemic circulation) compliance

cardiac output (CO) peripheral resistance (PR)

stroke volume (SV) heart rate (HR)

preload

afterload contractility

blood volume(BV) compliance of veins

arterial diameter

arterial length

blood viscosity

compliance of large arteries

vasoconstriction/vasodilation

arterial wall remodeling

BLOOD PRESSURE DETERMINANTS

blood pressure

BP = CO x PR

BLOOD PRESSURE REGULATION

BP - ratio between

change in BP → change in ratio

change in capacity of blood circulation- fast, short-term, urgent regulation change in blood volume - slow, long-term regulation BP CONTROL MECHANISMS according to the rate of onset and duration of action 1. short-term regulation seconds - minutes 2. medium-term regulation minutes - hours 3. long-term regulation hours - days

1. SHORT-TERM REGULATION

BAROREFLEXES

high-pressure baroreceptors in aortic arch and sinus caroticus

↑ BP impulses to CNS

↓ sympathetic tone

↓ stroke volume

↑ stimulation of n. vagus

↓ BP

peripheral vasodilation

if the hypotensive effect is not sufficient and ↑ BP persists, the baroreceptors adapt to the new ↑ BP value


BAROREFLEXES

low-pressure baroreceptors in right atrium and pulmonary artery

• reaction to ↓ venous return

↑ BP

impulses to CNS

↑ sympathetic tone

↓ venous return / ↓ blood volume

vasoconstriction

↑ Na+ & water reabsorption in kidneys

↑ CO


HUMORAL MECHANISMS

CATECHOLAMINES

↑ contractility

↑ vasoconstriction ↑ heart rate vasodilation

↑ CO ↑ BP

2. MEDIUM-TERM REGULATION

RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM

bleeding dehydration heart failure

↓ blood volume

↓ BP

↓ renal blood flow

stenosis of a. renalis

RENIN release

main effector peptide

ANGIOTENSIN II

vasoconstriction

thirst

aldosterone

Na+ & water retention

pituitary gland

ADH

↑ blood volume

↑ afterload

↑ preload ↑ BP


ANTIDIURETIC HORMONE – ADH, VASOPRESSIN

↑ osmolality of ECT ↓ volume of ECT ↓ BP

ADH release from pituitary

↑ water reabsorption

↑ blood volume

↑ BP

↑ number of aquaporins in collecting tubules


ATRIAL NATRIURETIC PEPTIDE (ANP)

ANP release from cardiomyocytes of

heart atria

↑ glomerular filtration

↑ volume of ECT

heart failure hyperhydration ↑ Na+ intake

↓ secretion of : aldosterone

renin ADH ↑ Na+ excretion

↓ peripheral resistance

↑ natriuresis & diuresis

↓ blood volume

↓ preload

↓ BP

3. LONG-TERM REGULATION

PRESSURE NATRIURESIS

• major system that prevents long-term BP increase

• control mechanism, which is not subject to adaptation and its action lasts until BP, as a result of ↓ intravascular volume, reaches a value ensuring a long-term balance between intake and excretion of water and Na +

↑ BP

↑ renal blood flow

mechanical ↑in tubular Na+ permeability

↑ Na+ & water excretion

inner renal baroreflex activation

↓ renin release

↓ blood volume ↓ BP

CIRCADIAN REGULATION


The circadian rhythms are regulated by MELATONIN

Changes in BP, HR undergo circadian rhythms:

• change of body position

• intensity of physical activity

• intensity of mental activity

• food, drug intake, …

CIRCADIAN REGULATION

impaired in 10 -30 % of patients with essential hypertension • patients who do not exhibit BP

circadian rhythm with a drop in the night

normal BP fluctuation within 24 hours, reaching a maximum shortly after waking

physiological decrease – dipper - 10 – 20 % of daytime BP non-dipper – less than 10 % ↓ of daytime BP extreme dipper - 20 % or more ↓ of daytime BP reverse dipper - BP ↑ during night


SYSTEMIC ARTERIAL HYPERTENSION

for most adults (age of 18 and above), systemic arterial hypertension is present if the resting blood pressure is persistently (repeated readings) at or above

according to diastolic BP: 90 – 104 mmHg mild AH 105 – 115 mmHg moderate AH > 115 mmHg severe AH


permanent increase of arterial blood pressure above arbitrarily determined values, which increases the risk of damage to the organism and their normalization can be expected to improve health arterial BP = variable adapts to the immediate need of the organism optimal BP = BP as low as possible ktorý ešte zabezpečí to ensure sufficient tissue and organ perfusion

curve in shape of the letter J

BLOOD PRESSURE CLASSIFICATION

Class Systolic BP

mmHg

Diastolic BP

mmHg

Optimal < 120 and < 80

Normal 120-129 and/or 80-84

High Normal 130-139 and/or 85-89

Grade 1 Hypertension 140-159 and/or 90-99

Grade 2 Hypertension 160-179 and/or 100-109

Grade 3 Hypertension ≥ 180 and/or ≥ 110

Isolated Systolic Hypertension ≥ 140 and < 90




↑ stiffness of arteries - remodeling

↑ circulating blood volume

↑ cardiac output ↑ total peripheral resistance

compliance hypertension

volume hypertension

resistance hypertension

BP value is dependent on compliance of vascular wall & blood volume in blood vessels


↑ arterial stiffness - COMPLIANCE HYPERTENSION

as a result of

• increased sympathetic tone - vasoconstriction

• aging

e.g. loss of elastic fibers, accumulation of myocytes, lipids, connective tissue, calcium (atherosclerosis, diabetes mellitus, hypercholesterolemia) wall thickening ↓ arterial volume ↑ volume of circulating blood

↑ systolic BP , ↑ pulse BP , ↓ diastolic BP

main cause of isolated systolic hypertension


↑ blood volume - ↑ cardiac output – VOLUME HYPERTENSION

↑ 1 ml blood increase in circulation = ↑ ∿ 1 mmHg increase of BP

as a result of:

↑ venous return e.g. in case of aortic regurgitation or patent ductus arteriosus ↑ volume of extracellular fluids associated with an increase in intravascular fluid = ↑ venous return • if water intake > excretion • renal demerge - ↓ renal excretion function is

compensated by ↑ arterial BP

↑ systolic BP and ↕ or ↓ diastolic BP

shifted curve


↑ blood volme - ↑ total peripheral resistance - RESISTANCE HYPERTENSION

as a result of:

constriction of arterioles – slowing the flow of blood from the arteries into the capillary circulation arterioles = 50 % of total peripheral resistance blood flow depends on myocytes contractions degree of contraction - ratio between vasodilatory / vasoconstrictive signals

even small changes in diameter of arterioles cause significant changes in vascular resistance

dominance of vasoconstrictive mediators (e.g. noradrenalin, angiotensin II, endothelin) • vasoconstriction + hypertrophy and hyperplasia of muscle and non-muscle cells

vessel wall remodeling

PRIMARY (ESENCIAL) HYPERTENION:

• a persisting increase in arterial blood pressure above arbitrarily determined

values without a detectable cause

• effecting 15 – 20 % of the world population

• accounts for 90–95 % all cases of hypertension

• onset usually between 50 – 60 age of life

• in 70-80% cases positive family history

• higher predisposition in some ethnic groups

(e.g. African Americans)



RISK FACTORS OF PRIMARY (ESENTIAL) HYPERTENSION:

RISK FACTORS OF PRIMARY (ESENTIAL) HYPERTENSION

Non-MODIFIABLE FACTORS:

• age > 60 years of age • sex ♂ • ethnicity African Americans • family history (mutations of genes associated with BP regulation

Age-specific and age-adjusted prevalence of hypertension among adults aged 18 and over: United States, 2009–2010


MODIFIABLE – EXOGENIOUS FACTORS:

factors associated with poor nutrition

OBESITY • hypertension detected in 15 – 35 % cases of

obese patients • associated with metabolic consequences

• insulin resistance • hyperinsulinemia • glucose intolerance • hypercholesterolemia • hypertriglyceridemia • hyperaminoacidemia

the most pronounced correlation between

obesity and hypertension in the android type of obesity



DIABETES MELLITUS

• coexistence of DM and hypertension –

↑ development of micro / macroangiopathies

• DM type I – hypertension develops later and can induce renal damage DM type II – hypertension develops with insulin resistance and obesity

• hyperglycemia ↑ reabsorption of Na+ endothelial dysfunction ↑ synthesis of collagen a expression of fibronectin



LACK OF PHYSICAL ACTIVITY

stopping progression / regression of hypertension-induced structural changes with 5-6 hours of aerobic exercise / weekly

• physical activity has an antihypertensive effect despite an increased pressor response

• ↑ blood flow and shear stress of endothelial cells

- ↑ NO & prostacyclines release vasodilatory & antiproliferative effect



ALCOHOL AND TOBACCO CONSUMPTION

• low doses of ethanol - hypotensive effect • higher doses of ethanol (60-80 g / day) -

hypertensive effect • smoking

• vascular endothelial damage - disturbance of the balance between vasoconstriction / vasodilation

• induction of noradrenaline secretion

progressive ↑ in BP of 1 mmHg per 100 ml of ethanol consumed weekly

SECONDARY HYPERTENSION

• 5 – 10 % of all hypertension cases

• typical clinical signs of primary disease (e.g. Cushing syndrome)

• patients younger than 30 years of age, often with severe diastolic hypertension

• patients do not react to common combined therapy

• often sudden aggravation of hypertension

• often atypical course of disease

• abnormalities in laboratory tests, ECG



RENAL HYPERTENSION: caused by kidney disease (impaired excretion of renal vasoactive mediators and/or impaired Na+ and water excretion

1. Renovascular hypertension (vasorenal hypertension)

• ↑ renin secretion as a result of ↓renal perfusion (e.g. stenosis or obstruction of renal artery, atherosclerosis)

• ↑ circulating angiotensin II – vasoconstriction – ↑ vascular resistance - ↑ BP

• Na+ and water retention – ↑ aldosterone secretion ↑ venous return

subsequent damage to the contralateral kidney


RENAL HYPERTENSION: caused by kidney disease (impaired excretion of renal vasoactive mediators and/or impaired Na+ and water excretion 2. Renal parenchymal hypertension • may be due to various kidney diseases

(e.g. hypertensive nephrosclerosis, diabetic nephropathy, chronic glomerulonephritis)

• ↓ ability to excrete Na + and water

• ↑ BP due to ↑ intravascular volume

• ↓ glomerular filtration

• complete destruction of some nephons is compensated by other nephrons - in healthy nephrons ↑ glomerular filtration


RENAL HYPERTENSION: caused by kidney disease (impaired excretion of renal vasoactive mediators and/or impaired Na+ and water excretion

3. Diabetic nephropathy • hypertrophy of glomerular and tubular elements, extracellular tissue

accumulation mass, basal membrane thickening, tubulointerstitial fibrosis, renal arterial sclerosis

• interaction of metabolic consequences of diabetes (hyperglycemia) + hemodynamic alteration of renal circulation

• ↑ basal membrane permeability – microproteinuria

• hyperglycemia - ↑ collagen synthesis - epithelial cell hypertrophy – ↓ filtration area and glomerular filtration

4. RENIN secreting tumors

5. Kidney transplantation • stenosis of a. renalis, kidney rejection, persistent ↑ of renin secretion from

contralateral kidney or „transplantation of hypertension with donor kidney


ENDOCRINAL HYPERTENSION clinically proven ↑ action of hormones that - ↑ of Na + and water reabsorption - ↑ cardiac output - ↑ vasoconstriction - have mitogenic effects

1. Estrogen contraception

• 2x higher risk of hypertension (+ smoking, ↑ age, obesity) • alteration of estrogen balance

2. Aldosteronism • ↑ aldosterone secretion – Na+ and water reabsorption - ↑ extracellular

volume • primary aldosteronism - ↑ aldosterone production from adrenal cortex

adenoma – Conn syndrome • congenital hyperaldosteronism • aldosterone-producing extra-adrenal tumors • secondary hyperaldosteronism


ENDOCRINAL HYPERTENSION

3. Cushing‘s syndrome • adrenal cortex hyperfunction - ↑ glucocorticoid (cortisol) production • stimulation of angiotensinogen production + ↑ vascular reactivity to

vasoconstriction

4. Pheochromocytoma • adrenal medullary tumors - continuous/intermitent secretion of catecholamines • variable adrenaline: noradrenaline ratio • bad prognosis - massive secretion of catecholamines – intracranial bleeding,

myocardial infarction, rhythm disorders

5. Hyperparathyroidism • ↑ extracellular Ca input into cells - ↑ secretion of norepinephrine from

sympathicus endings - increased contraction of vascular myocytes, positiv chrono- and inotropic effects

6. Metabolic syndrome ↑ insulinemia + ↑ glycemia + ↑ triglyceridemia + ↓ HDL in plasma - atherogenic processes, ↓ vasodilating effect, ↑ reabsorption of Na+ and water


HYPERTENSION IN GRAVIDITY

arterial hypertension during pregnancy - continued primary / secondary hypertension prior to pregnancy or - part of pre-eclamptic syndrome

- onset usually in III. trimester, disappears after delivery

• gestational changes in hemodynamics ↑ cardiac output (40 %) in II. trimester - ↓ total vascular resistance ↓ BP

• endothelial dysfunction

due to placental hypoperfusion ↓ prostacyclin production, platelet activation, fibrin deposits, vasoconstriction, Na + and water retention - edema


CONSEQUENCES OF SYSTEMIC ARTERIAL HYPERTENSION

Asymptomatic stage long period of ↑ BP without subjective / objective symptoms if the vessel wall is not damaged



symptoms often attributed to hypertension observed in case of people with elevated BP appear as often as in normatonic patients


Complications

1. hypertensive vascular damage

adaptation to ↑ BP – hypertrophy of myocytes

• atherosclerotic vascular remodeling

• sick vessel syndrome - ↓ activity of K+ channels + endothelial dysfunction – ↓ hypoxia-driven vasodilatation , platelet and leukocyte adhesion

2. hypertensive heart disease

• left ventricle hypertrophy • left ventricle failure • coronary artery disease



Complications

3. hypertensive kidney disease

• sclerotic changes of afferent and efferent arterioles, damage to glomerular capillaries, glomerular destruction

• damage of glomerular filtration: proteinuria microscopic hematuria



Complications

4. brain damage

• cerebral hemorrhage & ischemia atherosclerotic brain damage + damage of cerebral arteries - microaneurism

• progression of hypertension – local spasms and narrowing of the retinal arterioles

retinal bleeding



Complications

4. brain damage

• hypertensive encephalopathy approx. 1 % of hypertensive pacients

• ↑ BP – constriction of cerebral vessels – ensuring normal blood flow

• sudden exceeding of upper BP limit - vasodilation

↑ vascular wall permeability

CEREBRAL EDEMA



Acute complications: HYPERTENSIVE CRISIS an acute, life-threatening condition characterized by a sudden increase in blood pressure, damage and failure of vital organs.


suggested literature: Hulín et al. · 3.13 Pathological changes of the blood pressure (H. Sapáková, pp. 152-155) 3.14 Systemic arterial hypertension (H. Sapáková, pp. 155-162)

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