BP (including regulation) Flashcards
Arterial baroceptor location
aortic arch
carotid sinuses
aortic arch baroreceptor innervation
Vagus (X)
Carotid sinus baroreceptor innervation
Glossopharyngeal (IX)
Baroreceptor response (direct)
Respond to pressure 50-200 mmHg
Increase firing rate
Increase PNS output to the heart –> decrease HR and contractility
Decrease in SNS activity to the heart (same as above)
Decrease SNS activity to peripheral vessels –> relaxes smooth muscles, thereby decreasing SVR
Adaptation of baroreceptor
Prolonged exposure (>10 min) to high BP –> resetting of normal range
Baroreceptor response (renal)
Decreased firing rate of baroreceptors
increased renal SNS –> renin release –> activation of RAAS
AII: increase Na resorption at PT
- v/c of renal and systemic blood vessels
- triggers release of aldosterone (increases Na reabsorption at the DT and CT in exchange for K+)
- stimulates thirst and triggers further release of vasopressin
Increased release of vasopressin from post. pituitary gland –> increased resorption of water at CT, moderate vasoconstriction effect
Endothelin
family of peptides that are synthesized and released from endothelial cells
ETa receptors in vascular smooth muscle cells –> vasoconstrictors
ETb receptors in endothelial cell membrane –> cause release of NO
Lung - hypoxia is a potent inducer of ET release, vasoconstricts to direct blood away from poorly ventilated areas
NO
synthesized and secreted from endothelial cells
produced from L-Arg by nitric oxide synthase
vasodilator
Nitroglycerin breaks down to nitric oxide
- venodilator
- vasodilator for coronary arteries
- activates cGMP-dependent protein kinases (PKG) to phosphorylate myosin light chain kinase (MLCK) and prevent myosin/actin interaction
Primary HTN
cause unknown
genetics likely plays a role
obesity, DM, hyperlipidemia?
enhanced response to catecholamines
Secondary HTN
5-10% Suspect when: - extremes of age with unexpected target organ damage - occurs abruptly - response to therapy is atypical - renal failure present - hypokalemia or hypercalcemia
Causes of secondary HTN
ABCDE
A: accuracy, sleep apnea, primary aldosteronism
B: bruits, bad kidneys
C: Catecholamines, aortic Coarctation, Cushing’s
D: diets, prescription drugs (corticosteroids, NSAIDs, oral contraceptives or high doses of estradiol), non-Rx drugs
E: erythropoietin, endocrine disorders
Etiologies of HTN
Age: increased v/c
Race: darker skin
Smoking: accumulation of chemicals on vessel walls
Others: reduction in vitamin D, low K, excessive consumption of alcohol, and stress
Diagnosis of HTN
> 160 S or 100 D avged across 3 visits at least one week apart
up to 5 visits necessary when BP is 140-160/90-100
Ambulatory BP: (mean awake S >135 or D>85)
Target values lowered for patients with DM or chronic failure: >130/80
HTN can be diagnosed if it is >180/110 on the second visit
Target organ damage in HTN
Stroke - #1 risk factor, every 2-3 mmHg reduction = 10% lowered risk
CAD
LV hypertrophy
AAA (exceeding normal diameter by more than 50%)
Chronic renal failure (increased vascular resistance, parenchymal scarring)
General tests that may be ordered for HTN
Urianalysis - kidney function Hematocrit BUN and/or creatinine - monitor kidney function Potassium fasting glucose calcium TSH and T4 lipid profile Basic metabolic profile (aldosterone and renin, cortisol - Cushing's, catecholamines, metanephrines)
