Lecture 37 Hypertension Klassen BLOOD PRESSURE · 2018-04-07 · Lecture 37 Hypertension Klassen HYPERTENSION (HTN): Elevated and persistent arterial blood pressure o > 140 / 90 mmHg

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