lecture 22 raja
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| 4 main organ systems that are damaged as a result of HTN | heart, kidneys, brain and blood vessels
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| BP that warrants further investigation to r/o HTN | 130/80 typically
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| BP at which pt is stage I hypertensive | 140/90
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| typical BP at which starts showing dangerous PEx signs of hypertensive damage | 160/100 or more --> pt may have papilledema, ischemia anywhere, renal damage, ST changes on EKG, etc.
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| hypertensive emergency | acute severe elevation of BP to at least 160/100 that causes target organ damage such as coronary ischemia, cerebral dysfunction, stroke, renal failure or pulmonary edema. pt must be admitted
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| hypertensive urgency | severe elevations in BP to at least 160/100 without any evidence of progressive target organ dysfunction . pt can be managed medically and sent home
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| 3 goals of the initial evaluation for HTN | accurately stage the BP, assess overall CV risk and seek clues for rarer secondary causes for HTN
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| describe requirements for correct technique of measuring BP | pt must rest seated for @ least 5 min before, when taking BP: pt's back supported with feet on the floor, arm @ heart level, appropriate size cuff on bare arm. take 2 readings - one in each arm seated and standing
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| "white coat" HTN | HTN likely due to adrenergic response to being in physician office and having BP measured. pt typically has mean daytime BP that is normal when measured outside of the office
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| "white coat aggravation" | superimposition of adrenergic response while in physician's office onto an already elevated mean daytime BP = cause for alert
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| "masked" HTN | BP is nl in the physician's office but if set up with ambulatory monitoring one will note nocturnal and ambulatory HTN. could be fatal as risk of stroke continues without dx and subsequent tx
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| BP changes with aging | younger ppl can elevate their SBP easily/without consequence. high DBP in them is more concerning, but in ppl 50+ y/o, SBP tends to be more elevated. pulse pressure widens with age
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| persistent nocturnal HTN increases the aggregate BP burden on the CV system and greatly increases risk of target organ dz and CV death | the morning surge (on top of nocturnal HTN) is strongly associated with peak incidence of stroke, MI and sudden cardiac death
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| residual lifetime risk in anyone greater than 65 even if in perfect health and normotensive is ______ | 90% especially by age 85, usually due to increasing noncompliance of arteries and arterioles due to collagen replacing elastin in aorta. accelerated by atherosclerosis and HTN
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| isolated systemic HTN | usually in pts who developed HTN after the age of 50 - their SBP is > 140 mmHg but DBP is usually nl or < 80-90 mmHg; this is due to decreased distensibility of large conduit arteries
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| the pt with isolated systolic HTN and wide pulse pressure is most at risk for fatal heart attack | the pt with pulse pressure of 100 mmHg carries twice the risk of fatal CAD as compared with pt whose pulse pressure is 40 mmHg
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| CV risk factors | men 55+ and women 65+, FMHx of premature CV dz, dyslipidemia, DM, chronic kidney dz, smoking, obesity, physical inactivity
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| high-risk hypertensives typically have (other dz): | DM, chronic kidney dz, established coronary dz, atherosclerosis of other aa., high risk for CAD, heart failure
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| overall CV risk = high BP + other major risk factors + target organ damage |
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| DM as risk factor | very high risk factor, pts with DM that develop HTN usually need 3-4 meds to be maintained in normotension
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| PEx findings that might indicate HTN | neuro dysfunction, papilledema, retinal hemorrhage, AV nicking, carotid bruits, thyroid enlargement, rhonchi and crackles, audible S4, bruits over renal artery or AA, dec peripheral pulses or edema
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| essential (primary) HTN | describes up to 90% of cases of HTN - specific disease-causing mechanism is not identfiable
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| RAAS derangements that can serve as secondary causes of HTN | chronic kidney dz (hypertensive nephrosclerosis), renal art.stenosis or fibromuscular dysplasia, aortic coarctation, primary aldosteronism (Conn syndrome with 20-30:1 aldo: renin levels), mineralocorticoid excess aka Cushing's syndrome, NSAIDs
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| sympathetic derangements that can serve secondary causes of HTN | pheochromocytoma, sympathomimetics like cocaine, . obstructive sleep apnea?
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