BP (including regulation) Flashcards
(32 cards)
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)
PEs, investigations for HTN
ECG Eye exam kidneys abdominal tenderness bruits thyroid
HTN management (conservative)
Weight reduction (BMI 18.5-25, waist 50 yo)
Alcohol (<2 drinks/day)
Potassium, calcium, magnesium intake
relaxation therapy
Invasive treatment of HTN
Endovascular procedures
- renovascular hypertension (pc catheter interventions or surgical reconstruction)
- aortic coarctation (excision of narrowed aortic segment, transcatheter interventions)
Resections of tumours
Pheochromocytoma - surgical resection of tumour (usually in adrenal medulla)
Primary aldosteronism - surgical removal of the adrenal adenoma
4 different types of hypotension
Hypovolemic shock
Cardiogenic shock
Distributive shock
Obstructive shock
Differentiating types of hypotension
SVR
CO
Fever
Previous Cardiac Hx
Causes of hypovolemic shock
Hemorrhagic
Non-hemorrhagic (burns, vomiting, dehydration)
S&S of hypovolemic shock
Cool and pale
SVR increased
CO decreased
Tx of hypovolemic shock
IV fluids
Blood transfusion
stop bleeding
Causes of cardiogenic shock
Inadequate coronary perfusion
- acute MI
- acute valvular dysfunction
- myocardial contusion (disruption of heart rhythm)
