Hypertension Flashcards
isolated [systolic/diastolic] hypertension increases with age
systolic - due to decreased vascular compliance (calcification)
with decreased compliance, similar volumes produce larger pressure changes
what is the major influencer of CO and TPR, respectively?
stroke volume —> cardiac output
arteriolar tone —> total peripheral resistance
1 determinant of extracellular fluid volume
sodium
sodium causes water intention —> increased circulatory volume —> HTN
NaCl intake may exceed capacity of kidney to excrete sodium
which of these is NOT an effect of high sodium?
a. increase in peripheral vascular resistance
b. decreased extracellular volume
c. reduced NO synthesis
d. decreased compliance of large arteries
e. increased SNS
a. increase in peripheral vascular resistance —> arteriolar remodeling
b. INCREASED extracellular volume (#1 determinant)
c. reduced NO synthesis - due to endothelial dysfunction
d. decreased compliance of large arteries
e. increased SNS —> increased vascular tone, HTN
when should you consider secondary HTN for a patient?
age <20 or >50 with new HTN
dramatic increase in BP
abrupt onset
difficult to control
signs/symptoms of other issues, family history
why does it make sense that PMI is shifted in systolic HF, but not diastolic HF?
systolic HF due to eccentric hypertrophy - heart chamber becomes huge —> lateral shift of PMI
diastolic HF due to concentric hypertrophy - ventricle doesn’t really get bigger, the walls are just really thick
why might a patient with HTN develop ischemia without coronary artery disease?
HTN increases afterload —> LV hypertrophy —> myocardial oxygen demand without increase in blood flow
also at risk for arrhythmias due to fibrosis
what are the 2 forms of vascular pathology related to HTN?
hyaline arteriosclerosis: plasma proteins leak across damaged endothelial and deposit in wall, making it thicker
hyperplastic arteriosclerosis: worse pathology, “onion skin” appearance due to smooth muscle cell proliferation and wall thickening
hyaline vs hyperplastic arteriosclerosis
hyaline arteriosclerosis: plasma proteins leak across damaged endothelial and deposit in wall, making it thicker
hyperplastic arteriosclerosis: worse pathology, “onion skin” appearance due to smooth muscle cell proliferation and wall thickening
atherothrombotic stroke vs hemorrhagic stroke vs lacunar infarct
atherothrombotic stroke: piece of lipid becomes embolus
hemorrhagic: due to damaged piece of blood vessel
lacunar infarct: seen in patients with chronic HTN, caused by occlusion of single penetrating branch of large cerebral artery
If a patient presented to the ER with hypertensive encephalopathy, acute hypertensive nephroslcerosis, or acute heart failure, what kind of emergency would this indicate? What is the most immediate goal in this situation?
hypertensive emergency - presents with signs/symptoms of acute end-organ damage
SBP > 180, DBP > 120
MUST decrease BP
what is usually the first pharmacological intervention for essential hypertension?
start with thiazide diuretic
add from there as necessary, use drugs with different modes of action and long duration of action (rather than extended release formulation)
*treat essential hypertension by diuresis and vasodilation (increases renal blood flow)
describe what occurs in renovascular hypertension (secondary cause of HTN) - what are the possible causes?
narrow/stenosis of one or both renal arteries by
1. atherosclerosis: 70%, older patients, M>F
2. fibromuscular dysplasia: young patients, idiopathic, F>M, “string of beads” appearance
—> RAAS activation
usually will hear abnormal bruit, but only listen for one if there is high BP (bruits are common even without narrowing)
