suggested literature: Hulín et al. · 3.13 Pathological changes of the blood pressure (H....
Transcript of suggested literature: Hulín et al. · 3.13 Pathological changes of the blood pressure (H....
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
BLOOD PRESSURE MEASUREMENT
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
BLOOD PRESSURE MEASUREMENT
BLOOD PRESSURE 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
1. SHORT-TERM REGULATION
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
1. SHORT-TERM REGULATION
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
2. MEDIUM-TERM REGULATION
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
2. MEDIUM-TERM REGULATION
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
3. LONG-TERM 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
3. LONG-TERM REGULATION
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
SYSTEMIC ARTERIAL HYPERTENSION
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
SYSTEMIC ARTERIAL HYPERTENSION
SYSTEMIC ARTERIAL HYPERTENSION
SYSTEMIC ARTERIAL HYPERTENSION
↑ 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
SYSTEMIC ARTERIAL HYPERTENSION
↑ 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
SYSTEMIC ARTERIAL 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
SYSTEMIC ARTERIAL HYPERTENSION
↑ 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)
SYSTEMIC ARTERIAL HYPERTENSION
SYSTEMIC ARTERIAL HYPERTENSION
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
RISK FACTORS OF PRIMARY (ESENTIAL) HYPERTENSION
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
RISK FACTORS OF PRIMARY (ESENTIAL) HYPERTENSION
MODIFIABLE – EXOGENIOUS FACTORS:
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
RISK FACTORS OF PRIMARY (ESENTIAL) HYPERTENSION
MODIFIABLE – EXOGENIOUS FACTORS:
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
RISK FACTORS OF PRIMARY (ESENTIAL) HYPERTENSION
MODIFIABLE – EXOGENIOUS FACTORS:
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
SYSTEMIC ARTERIAL HYPERTENSION
SECONDARY HYPERTENSION
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
SECONDARY HYPERTENSION
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
SECONDARY HYPERTENSION
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
SECONDARY HYPERTENSION
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
SECONDARY HYPERTENSION
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
SECONDARY HYPERTENSION
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
SYSTEMIC ARTERIAL HYPERTENSION
CONSEQUENCES OF SYSTEMIC ARTERIAL HYPERTENSION
Asymptomatic stage long period of ↑ BP without subjective / objective symptoms if the vessel wall is not damaged
CONSEQUENCES OF SYSTEMIC ARTERIAL HYPERTENSION
SYSTEMIC ARTERIAL HYPERTENSION
symptoms often attributed to hypertension observed in case of people with elevated BP appear as often as in normatonic patients
SYSTEMIC ARTERIAL HYPERTENSION
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
CONSEQUENCES OF SYSTEMIC ARTERIAL HYPERTENSION
SYSTEMIC ARTERIAL HYPERTENSION
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
CONSEQUENCES OF SYSTEMIC ARTERIAL HYPERTENSION
SYSTEMIC ARTERIAL HYPERTENSION
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
CONSEQUENCES OF SYSTEMIC ARTERIAL HYPERTENSION
SYSTEMIC ARTERIAL HYPERTENSION
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
CONSEQUENCES OF SYSTEMIC ARTERIAL HYPERTENSION
SYSTEMIC ARTERIAL HYPERTENSION
Acute complications: HYPERTENSIVE CRISIS an acute, life-threatening condition characterized by a sudden increase in blood pressure, damage and failure of vital organs.
CONSEQUENCES OF SYSTEMIC ARTERIAL HYPERTENSION