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Lecture 37 Hypertension Klassen BLOOD PRESSURE:
Pressure inside blood vessels/heart o Relative to atmospheric pressure (mmHg) o Exerted on walls of blood vessels
Blood pressure (BP) o Directly proportional to:
Cardiac output (CO) – amount of blood/time (L/min)
Heart rate (beats/min) x stroke volume (volume pumped / beat) CO = HR x SV Peripheral vascular resistance (PVR) – resistance through vessels BP = CO x PVR
DEFINITIONS:
Diastolic blood pressure (DBP) o Blood pressure after cardiac contraction (chamber filling) o Overall low aortic pressure o NADIR VALUE
Preload – tension in heart and end of diastole o Ventricular end diastolic volume o Volume of blood in heart diastole
Systolic blood pressure (SBP) o Blood pressure during cardiac contraction o PEAK VALUE o Overall high aortic pressure
Afterload – arterial pressure heart empties into o If increased afterload the result is increased systolic pressure
Mean arterial pressure (MAP) o Average pressure through the cardiac cycle
Pule pressure – pulsatile change in pressure related to cardiac cycle o Pulse pressure = SBP – DBP o Can be used as a measure of cardiac wall stiffness/ tension o Aorta absorbs high pressure stress on cardiac emptying to buffer pulse pressure into the body
Aging stiffens aorta resulting in higher BP
CARDIAC CYCLE: 5 stages 1. EARLY DIASTOLE: 80% passive heart filling
Heart relaxed
AV valves open (SL values closed) 2. ATRIAL SYSTOLE: atrial contraction
AV valves open (SL stay closed)
20% more filling of ventricles ATRIAL KICK 3. ISOVOLUMIC VENTRICULAR CONTRACTION
Ventricle myocyte contraction
All values closed
NO FILLING 4. VENTRICULAR EJECTION – full ventricular contraction
SL valves open
Blood pumps to body/lungs 5. ISOVOLUMIC VENTRICULAR RELAXATION – ventricles relax
All valves closed
Atria begin filling
FRANK STERLING LAW OF THE HEART:
More stretch of muscle fibers = more force in contraction (UP TO A MAXIMUM)
o Stronger force of contraction = greater stroke volume (increases BP)
More stretch in heart results in INCREASED end diastolic volume causes greater stroke volume
o Heart ejects more blood
Lecture 37 Hypertension Klassen
OVERVIEW OF BLOOD PRESSURE REGULATION:
PHYSICAL FACTORS:
Heart rate: increased heart rate = increased cardiac output
Contractility: depends on anatomical structure o Heart: ↑ contraction = ↑stroke volume o Blood vessels: vasoconstriction = ↑ resistance
Baroreceptors: stretch receptors sense and transduce signal for response o Effect on blood pressure depends on which
baroreceptors are activated
CHEMICAL FACTORS:
Humoral o Vasoconstrictors: angiotensin II, catecholamines,
thromboxane, endothelin, vasopressin o Vasodilators: nitric oxide, kinins, prostaglandins
Local: autoregulation, ionic concentration (H+, Na+,
K+, pH buffer) Neural: fight/flight
o α – adrenergic receptors Smooth muscle constriction
o β – adrenergic receptors Increase heart rate and stroke volume Smooth muscle relaxation
OVERVIEW OF REGULATION:
REGULATION OF BP: BAROREFLEX
BARORECEPTORS:
High pressure sensing baroreceptors o Carotid sinuses and aortic arch o Stretch more action potential
firing autonomic nervous response
o PERIPHERAL VASODILATION
Low pressure sensing baroreceptors o Heart and vena cavae o Regulating secretions o ADH/vasopressin, renin and
aldosterone o PERIPHERAL VASOCONSTRICTION
NEGATIVE FEEDBACK LOOP:
Stretch receptors detect elevated BP
Reflex neuron firing (CAROTID): heart rate decrease decreased BP
Release hormones (VENA CAVA): increased blood volume increased cardiac output
REGULATION OF BP: HEART
Make natriuretic peptides
o Act on kidney
Have a role in physical BP
Changes total stroke volume
BP = CO X PVR * CO = HR X SV
Lecture 37 Hypertension Klassen
REGULATION OF BP: VESSELS
RESISTANCE VESSELS:
Regulate vessel diameter to change the volume of peripheral venous blood
Modify (resist) cardiac output/pressure
Endothelium secretes local factors o Vasodilators – NITRIC OXIDE o Vasoconstrictors – endothelin,
angiotensin II
CAPACITANCE VESSELS: 70% blood volume in veins
VENOUS COMPIANCE: ability to distend and increase diameter with increasing pressure o Higher venous compliance results in more distension
Dilation of vessel accommodates increased pressure o Results in reduction in venous resistance/ pressure o Ultimately reduces blood flow back to heart
Causes reduced PRELOAD (end diastolic volume is less) Decreases total cardiac output (less stroke volume per
beat)
REGULATION OF BP: KIDNEYS
REABSORPTION of salts and water
Regulates blood pressure via BLOOD VOLUME o RENIN ANGIOTENSIN SYSTEM
Long term adjustment to low blood pressure Activates angiotensin II for vasoconstriction
o Alters GLOMERULAR FILTRATION RATE – alters blood volume Monitors volume of fluid through kidney/time Water follows salt
o Respond to NATRIURETIC FACTORS from heart Natriuretic peptides increase glomerular filtration Prevents salt uptake and inhibits renin release Reduce blood volume
RENIN ANGIOTENSIN SYSTEM:
Hormonal regulation: blood pressure / fluid balance
Low sodium/low renal BP o Kidney juxtaglomerular cells secrete RENIN
CONVERTS liver angiotensinogen to ANGIOTENSIN I Angiotensin I ANGIOTENSIN II in lungs by ANGIOTENSIN CONVERTING ENZYME (ACE)
ANGIOTENSIN II increases BP o Kidney: release aldosterone, increase Na reabsorption, blood volume = increased preload o Vessels: vasoconstriction, increased resistance = increased afterload
GLOMERULAR FILTRATION RATE (GFR):
Volume filtered / unit time (mL/min) o Move from glomerular capillaries to Bowman’s capsule o Differential basal tone in afferent/efferent arterioles – net outward pressure
Tubuloglomerular feedback (TGF) o Change in GFR detected in renal tubules – reduced blood volume results in lower GFR o Feedback to glomerulus – get increased Na uptake; water follows salt concentration o NET INCREASED BLOOD VOLUME
NATRIURETIC PEPTIDES: peptides that induce NATIURESIS (= sodium excretion in urine) SECRETED IN HEART MYOCARDIUM:
Atrial natriuretic peptide (ANP)
Respond to volume expansion in heart
Decreases Na content in blood
Decreases concentration of endothelin and angiotensin II
FUNCTIONAL IMPACT:
Act as a vasodilator in kidney to increase GFR
Inhibit Na reabsorption inducing natiuresis
Inhibit renin release
Lecture 37 Hypertension Klassen
HYPERTENSION (HTN):
Elevated and persistent arterial blood pressure o > 140 / 90 mmHg o 2x reproducible elevated
measures 6+ hrs apart using blood pressure cuff
Increased risk of cardiovascular morbidity o Heart is working harder o Shortened life expectancy
Increased risk of o Stroke o Aneurysms o Chronic kidney disease o Ischemic heart disease o Death
RISK OF HTN: > 30% of population has high BP
Ethnicity: African American > Caucasian > White Hispanic
Gender: o < 45 years: MEN o > 45 years: WOMEN
(increasing prevalence with age)
Age: common in elderly o DIAGNOSIS: 30-50 years
old; following asymptomatic PREHYPERTENSION PHASE
o > 60 years: 65%
CLASSIFICATION IN ADULTS ≥ 18 YEARS:
Uncontrolled blood pressure decreases lifespan by 10-20 years
HTN CLASSIFICATION:
Primary (essential) – unknown (idiopathic) cause – 90% o NO CURE o Control only o Mainly asymptomatic o Detected on routine
clinical visits
Secondary: < 10% o Renal disease o Cushing’s or Conn’s
syndrome (endocrine) o Hyper/hypo thyroidism o Obesity o Pregnancy o Sleep apnea o Medication Amphetamines Decongestants NSAIDs Steroids Cocaine
PRIMARY HYPERTENSION: MANY PROPOSED PATHOGENIC MECHANISMS…
GENETICS – monogenic/polygenic dysregulation o Family history o Common variants small effect AND rare
variants large effect
Ionic balance/excitability
Urinary excretion
Nitric oxide release
Adrenal hormone release
LIFESTYLE o High salt intake o Fatty foods o Sedentary lifestyle o Alcohol o Stress o Caffeine o Inactivity
PATHOPHYSIOLOGY:
CARDIAC OUTPUT remains normal in primary HTN
Inappropriate peripheral vascular resistance o Arteriole remodeling – artery narrowing
(smaller lumen) o Capillary beds – ↓number and/or density o Aorta stiffening o Endothelium decrease production NO
Decreased peripheral venous compliance o Results in increased venous return o Results in increased cardiac preload o Leads to diastolic dysfunction via decline in
ventricular ability
Lecture 37 Hypertension Klassen
SECONDARY HTN:
General complaints – lightheaded, dizzy, fainting, headaches, altered vision
Secondary hypertension (HTN) can be asymptomatic
SYMPTOMS CAN BE INDICATIVE OF UNDERLYING CAUSE:
PHEOCHROMOCYTOMA: adrenal tumor o Increased sodium/water reabsorption o Headaches, sweating, tachycardia, palpitations
PRIMARY ALDOSTERONISM: excess aldosterone o Muscle cramps, weakness
CUSHING’S SYNDROME: excess adrenocorticotropic hormone (ACTH) o System hypersensitive to epinephrine/norepinephrine o Weight gain, polyuria, edema, muscle weakness
KIDNEY DISEASE: loss in kidney function o Activation of renin angiotensin system o General malaise, loss of appetite, diabetes, anemia
PREGNACNY HYPERTENSION
Increased risk in pregnancy o 10% of pregnancies o May have pre-existing
pre-hypertension o Gestational htn –
elevated BP only o Diagnosed after 20
weeks pregnancy o 2 readings 140/90 6+ hrs
apart
Initial sign of pre-eclampsia o Elevated BP and protein
in urine (kidney dysfunction)
o Damage to maternal endothelium, kidneys, liver Release of
vasoconstrictors
HYPERTENSINVE EMERGENCY/CRISIS: 1% of patients with HTN per year
Up to 90% mortality
Acute and immediate elevation in BP: 180/110 mmHg
Due to: o Failure of normal autoregulatory function o Leads to a sharp increase in systemic vascular resistance o Endovascular injury with arteriole necrosis o Ischemia, platelet deposition and release of vasoactive substances o Further loss of autoregulatory mechanism o Exposes organs to increased pressure
END ORGAN DAMAGE:
Brain: headache, altered consciousness
Eyes: optic disk swelling or bleeding in eye
Heart: myocardial distress
Lungs: pulmonary edema
Kidney: acute injury/ damage ARTERIO VS. ATHERO VS. ARTERIOLOSCLEROSIS
Any artery hardening/thickening
Loss of ELASTICITY (generally with age) o ARTERIOSCLEROSIS OBLITERANS): fibrosis of tunica intima &
calcification of tunica media o ATHEROSCLEROSIS: artery wall thickening/lumen shrinking
FATTY DEPOSITS: cholesterol, triglyceride o ARTERIOSCLEROSIS: damage to small arteries/arterioles
Hyaline or fibrotic necrosis of intima/media Common in HYPERTENSIVE EMERGENCY: primarily impacts
kidney