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RajaHTN
lecture 22 raja
| Question | |
|---|---|
| 4 main organ systems that are damaged as a result of HTN | heart, kidneys, brain and blood vessels |
| BP that warrants further investigation to r/o HTN | 130/80 typically |
| BP at which pt is stage I hypertensive | 140/90 |
| 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. |
| 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 |
| 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 |
| 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 |
| 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 |
| "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 |
| "white coat aggravation" | superimposition of adrenergic response while in physician's office onto an already elevated mean daytime BP = cause for alert |
| "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 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| CV risk factors | men 55+ and women 65+, FMHx of premature CV dz, dyslipidemia, DM, chronic kidney dz, smoking, obesity, physical inactivity |
| high-risk hypertensives typically have (other dz): | DM, chronic kidney dz, established coronary dz, atherosclerosis of other aa., high risk for CAD, heart failure |
| overall CV risk = high BP + other major risk factors + target organ damage | |
| DM as risk factor | very high risk factor, pts with DM that develop HTN usually need 3-4 meds to be maintained in normotension |
| 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 |
| essential (primary) HTN | describes up to 90% of cases of HTN - specific disease-causing mechanism is not identfiable |
| 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 |
| sympathetic derangements that can serve secondary causes of HTN | pheochromocytoma, sympathomimetics like cocaine, . obstructive sleep apnea? |
Created by:
sirprakes
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