module 10 blood pressure Flashcards
short term regulation
occurs quickly to accomodate behavior change - position change - exercise - fear - anxiety pathologic change - fever - volume depletion
Short term SNS regulation
increase HR and systemic vascular resistance (SVR)
- baroreceptors
- increase Epi and NE
- Chemoreceptors
Epi and NE alpha 1 and A2 receptors
vasoconstriction in arterial system
A2 receptor in brain: negative feedback
Epi and NE B1 receptors
in heart -> increased rate of SA node firing
short term regulation SNS negative feedback
how often baroreceptors fire
- inc. MAP = inc. fire rate
chemoreceptors
central: within medullary center
- respond to changes in CO2 and pH
Peripheral: aortic arch and carotid bodies
- respond to dec. in arterial O2 concentration
-> SNS activation
Long term blood pressure regulation
neural
hormonal
renal
- all work together
Renal regulation of blood pressure
Balance of Na and H2O
Renin-angiotensin-aldosterone system (RAAS)
Renin-angiotensin-aldosterone system (RAAS)
juxtaglomerular cells: stimulated by dec. arterial pressure
- > renin release -> acts on circulating angiotensinogen
- > release of angiotensin I
- > angiotensin converting enzyme (ACE) in lungs
- > angiotensin II (vasoconstriction)
- > adrenal cortex -> aldosterone release
- > Na and H2O retention
- > increased blood volume and BP
Neural regulation of blood pressure
ADH
- increased osmolality -> Inc. ADH
- > inc. H2O resorption -> dec. osmolality
other influences of longterm blood pressure regulation
SNS activation
natriuretic peptides
regulation of intrarenal mechanisms
- renin releases inc when SNS binds to B1 in kidney
- dec. GFR r/t arteriolar constriction and inc. resorption
- ANP
hypertension
normal 120/80
Prehypertension: systolic between 120-140
diastolic between 80-90
Stage 1 hypertension
systolic: 140
diastolic: 90
primary hypertension (essential)
idiopathic
subtypes:
- isolated systolic HTN: S > 140, D < 90
- isolated diastolic HTN: S < 140, D > 90
- combo systolic and diastolic HTN
Risk factors for primary HTN
western population black increasing age family Hx Modifiable - obesity - sedentary lifestyle - metabolic syndrome - dietary factors (inc. fat and Na, dec. K and Ca) - tobacco - lab data (inc. BG, cholesterol, triglycerides, and LDL. Dec. HDL)
primary HTN Tx
lifestyle alterations
- modifiable risk factors
pharmacologic interventions
secondary HTN
has specific identifiable cause
- ingestion of drugs, food, chemicals
- conditions
risk of: end-organ damage
common causes of secondary HTN
Renal - artery stenosis - renal failure - polycystic kidney disease - glomerulonephritis Cardiovascular - coarctation of the aorta Tumors - pheochromocytoma - neuroblastoma - wilms tumor - adrenal adenocarcinoma endocrine - hyperthyroid - cushing disease - congenital adrenal hyperplasia - primary hyperaldosteronism Neurologic - Guillain- Barre syndrom - inc ICP other - systemic arteries - sleep apnea
hypertensive crisis
rapid onset HTN - secondary HTN - uncontrolled primary - autonomic dysfunction -- guillian- barre -- autonomic dysreflexia Diastolic > 120 Emergency - spike in BP with end-organ damage Urgency - spike in BP without end-organ damage
End organ damage HTN
CNS
- ischemic stroke
- encephalopathy
- subarachnoid and intracerebral hemorrhage
- acute HF
- pulmonary edema
- MI
Low BP
SNS activation
orthostatic hypotension: dec. BP upon standing
Orthostatic hypotension s/s
dizzy blurred vision fainting falls -> injury cardiovascular disease -> stroke, cognitive impairment, death dec. systolic > 20 dec. diastolic >10 inc. HR by 20-30
risk factors for orthostatic hypotension
vasovagal reaction dec. circulating volume dysrhythmias adverse drug therapy eldery
orthostatic hypotension Tx
education on moving slowly
avoid hot baths, saunas (vasodilation)
compression stockings
increase Na and fluids
reactive hyperemia
when blood flow is reestablished after occlusion
- build up of vasodilatory metabolies: CO2, H+, K+, lactic acid -> relaxation of arterioles.
- > period of increased blood flow upon reperfusion
active hyperemia
increased blood flow to a tissue when metabolism in the tissue is elevate (exercise)
- r/t inc. production of vasodilatory metabolites
myogenic regulation
autoregulation of blood flow that occurs when perfusion pressure is inc. (no change in metabolic activity)
- initially flow to tissue rises but returns toward baseline
low pressure baroreceptors
in heart and pulmonary circulation
- respond to changes in blood volume and modulate SNS activity and ADH release
circle of willis
collateral circulation
- ensures blood flow to all tissue sin brain
coronary circulation
supplied by coronary arteries
pressure gradient affected by
- tissue pressure in wall of heart during systole
Contraction of heart -> compression of heart vessels
local effects during bloodflow
though systemic vasoconstriction
local
- metabolic vasodialtion
– use of O2 -> inc. CO2 -> vasodialation
vessels 3 layers
tunicae
- intima
- media
- adventitia
tunicae intima
a layer of endothelial cells in direct contact of blood flow
- in veins protrudes into lumen to create valves
- arterial intima
- inner elastic membrane next to endothelial cells
tunicae media
greatest difference between arteries and veins
Arteries: thickest layer
- smooth muscle fibers all around and interspersed with elastic fibers (circular)
- elastic fiber disappears in smaller arterioles
- smooth muscle -> firmness and limits distensibility
Veins
- smooth muscle in circular pattern
- quantity of smooth muscle decreased with vein size increase
- has collagenous CT
tunica Adventitia
arteries: predominately collagenous CT
- external elastic membrane in large arteries
Veins: thickest layer
- collagenous CT and longitudinal smooth muscle
