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Rosens > 70. HTN > Flashcards

70. HTN Flashcards

1
Q

Uncontrolled BP strong association with which conditions?

A

HF
mi
stroke
vascular dementia
ckd

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2
Q

What % decr does antiHTN therapy decr risk of
stroke
MI
HF

A

40
25
50

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3
Q

What is a hypertensive emergency?

A

disease state defined by acute Target organ damage,
manifest by newly developed clinical sequelae or diagnostic test abnormalities. A hypertensive emergency can exist in patients with or without underlying chronic HTN. Although it has been esti- mated that 1% to 2% of patients with chronic HTN will experience a hypertensive emergency in their lifetime, hospitalization for this condition is relatively rare, occurring in only 2 of every 1000 ED presentations and 6 per 1000 HTN-related ED visits in the United States.

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4
Q

Poorly controlled chronic HTN defn

A

a presentation in which patients with established HTN are found to have elevated BP with- out specific attributable symptoms or evidence of acute target organ damage. Such presentations often result from inadequate medical management or nonadherence to treatment regimens, but may also reflect refractory disease. Concurrent use of seemingly innocuous medications, includ- ing nonsteroidal antiinflammatory drugs (NSAIDs), steroids, decon- gestants, appetite suppressants, over-the-counter stimulants, oral contraceptives, and tricyclic antidepressants or rebound from short- acting antihypertensives, such as clonidine, may be contributory.

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5
Q

Why does HTN occur in older adults? (basic physiology categories)

A

neurohormonal dysregulation
vascular modulation
Na intake
psychosocial stress
obesity

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6
Q

List 5 categories (think VINDICATE) of secondary causes of HTN

A

endocrine
pulmonary
renal
toxic/metabolic
vascular

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7
Q

name 5 causes of endocrine related secondary cause of HTN

A

cushing’s/steroid
hyperaldosteronism
OCP
pheo
thyroid
parathyroud

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8
Q

What is a pulmonary secondary cause of HTN?

A

OSA - get a sleep study with O2 sat

think of this if obese, narcolepsy

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9
Q

Name 5 secondary causes of HTN - renal

A

chr pyelo
diabetic nephropathy/other kidney dis
neprhitic and nephrotic syndrome
polycystic kidney disease
renovascular conditiosn

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10
Q

Name 3 toxic/metabolic secondary causes of HTN

A

chr etoh
sympathomimetic drug use
tyramine-containing food

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11
Q

name 2 secondary vascular causes of HTN

A

as
coarctation

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12
Q

How to assess for cushing’s?

A

hx
dexamethasone suppression test
gluc intol
purple striae

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13
Q

How to assess for hyperaldosteronism and other mineralocorticoid excess states

A

24h aldosterone level or other mineralocorticoids

*unexplained hypok

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14
Q

pheo dx test

A

24h urinary metanephrine and normometanephrine

*think of labileparoxysmal HTN with palpitations, pallor, perspiration

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15
Q

When to consider renovascular conditions like renal a stenosis as HTN cause?

A

HTN pre 30 or after 55
abdo bruit
refr htn control
recurrent pulmonary edema
unexplained renal failure

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16
Q

how to work up renal vascular conditions for secondary HTN?

A

doppler flow study

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17
Q

How does NE cause HTN?

A

potent vasoconstr to drive SVR to amplify afterload to HTN

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18
Q

How is RAAS involved in HTN?

A

renin from juxtaglomerular cells –> cleave angiotensinogen to angiotensin I then to angio II by ACE
Angiotensin II exerts systemic and renal effects: arterail vasoconstriction, na reabsorption, modulation GFR

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19
Q

How does vascular remodelling occur in HTN?

A

sns, raas, incr wall tension by HTN itself

large vessels = incr intimal thickness, minimal luminal narrowing (unless plaque build up) whereas smaller vessels = reduce lumen diameter

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20
Q

Recommended daily Na intake

A

1500mg/day

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21
Q

for every incr 5kg/m^2 in BP, how does relative risk of HTN incr?

A

1.5

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22
Q

What organs are effected by HTN?

A

heart- HF, ACS
large blood vessels - vascular (ao dissection)
kidneys - acute renal risk and kidney injury
brain - stroke/ICH/HTN encephalopathy
Eyes - retinopathy
Pregnant - ecclampsia

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23
Q

How does a hypertensive emergency effect flow/autoregulation of BP mechanisms?

A

acute endothelial injury –> rapid rise fo vascular pressure overwhelming regulatory measures
drop NO and excess release endothelin = incre SVR - incr BP ++
unchecked wall tension occurs so terminal arterioles dilate and can rupture –> proinflamm/hypercoag state, fibrin deposition and ishcmeia

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24
Q

MC top HTN emergencies by organ system

A

Heart overall - HF, ACS
Brain - stroke/ICH/hpertensive encephalopathy
Acute renal risk kidney

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25
Q

Why does hypertensive encephalopathy occur?

A

diffuse vasogenic cerebral edema –> failure autoregulation of brain with vasospasm, ischemia, incr vascular permeability, punctate hemorrhage and interstitial edema

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26
Q

Hypertensive encephalopathy symptom features

A

headache
vomit
MAS
seizure coma
blurry vision
papilledema

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27
Q

Hypertensive encephalopathy imaging

A

may or may not show punctate hemorrhage on CT

28
Q

What is Posterior reversible leukoencephalopathy?

A

neuro presentation similar to hypertensive encephalopathy: posterior cerebral impairment (vision changes, h/a, ams, seizure) –> dx on MR: change WM edema in parietal/temporal/occipital regions

29
Q

DDX for elevated BP in the ED? 3 categories

A
  • True hypertensive emergencies (i.e., acute heart failure, ischemic stroke, pre-eclampsia)
  • Elevated blood secondary to pain, anxiety, transient physiological condi- tions, and medications
  • Inaccuratemeasurement
30
Q

Findings of acute hypertensive retinopathy?

A

focal intraretinal periarterio- lar transudates (whitish ovoid lesions deep in the retina), focal retinal pigment epithelial lesions (evidence of choroidal injury), macular and optic disk edema, and cotton wool spots (fluffy white lesions that con- sist of swollen ischemic axons caused by small vessel occlusion). Hard exudates, which consist of lipid deposits located deep in the retina, are also a common but late occurrence

31
Q

Box 70.2: Name the 5 grades of fundoscopic grading of suspected hypertensive retinopathy and their description

A

Grade 0—normal
Grade 1—minimal arterial narrowing
Grade 2—obvious arterial narrowing with focal irregularities
Grade 3—arterial narrowing with retinal hemorrhages and/or exudate Grade 4—grade 3 plus disk swelling

32
Q

What is the MAP

A

summary measure representing average arterial pressure in one cardiac cycle, described by co times svr plus central venous pressure

33
Q

What does CVP indicate?

A

intravascular vol/preload and effective hydrostatic force in circulatory system

34
Q

MC 2 antiHTN in ED?

A

labetalol
NTG

nicardipine in states?

35
Q

Optimal reduction of MAP in acute hypertensive emergency?

A

MAP 20-25% in first hour and goal BP 160/100 by 2-6 hours

36
Q

Why is a decrease in MAP 20-25% optimal in a HTN emergency?

A

This arises from an under- standing of the cerebral autoregulation curve, which maintains stable blood flow within a range of pressures (MAP of 60 to 160 mm Hg) under normal circumstances but resets in chronic HTN with a shift of the lower limit toward the right. This shift tends to settle approximately 25% below baseline MAP, resulting in concern for decreased cerebral blood flow with BP reduction beyond this.

37
Q

Effect on CO, SVR, CVP:
alpha blockers

A

phentolamine
incr/decr/incr

38
Q

Effect on CO, SVR, CVP:
beta 1 blocker

A

esmolol, metop

decr/can incr or decr/can incr or decr

39
Q

Effect on CO, SVR, CVP:
ACEi

A

incror decr/decr/ incr or decr

40
Q

Effect on CO, SVR, CVP:
dihydro like nicardipine vs nondihidro (dilt/verapamil)

A

incr/decr/either
vs
decr/decr/either

41
Q

Effect on CO, SVR, CVP:
hydralazine/direct acting vasodilator

A

incr/decr/either

42
Q

Effect on CO, SVR, CVP:
loop diuretics

A

either/decr/decr

43
Q

Effect on CO, SVR, CVP:
NO donor like nitroprusside, ntg

A

incr/decr/decr

44
Q

AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments

Phentolamine

A

5-15mg q5min
0.2-0.5mg/min
1-2 min
10-30min

cannot use in CAD

45
Q

AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments

metoprolol

A

5mg q5min
none
10-30min
5-8h

46
Q

AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments

labetalol

A

20-80mg q10min
1-2mg/min
2-5min
3-6h

47
Q

AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments

Nicardipine

A

none
5-15mg/h
5-15min
4-6h

48
Q

AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments

hydralazine

A

5-20min q30min
none
10-20min
2-4h

49
Q

AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments

furosemide

A

40-240mg q12h
10-40mg/h
30-60min
2-4h (really 6)

50
Q

AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments

Na nitroprusside

A

none
0.25-10 microgram/kg/min
immed
1-2min

51
Q

AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments

ntg

A

1-2mg q5min
5-200 microgram/min
2-5min
5-10min

52
Q

Nitroprusside risk

A

cn toxicity

53
Q

ACS and HTN - goal of BP reduction and primary agent

A

decr cardiac work and improve perfusion, combat rise in SVR
NTG best!

54
Q

goal of BP reduction and primary agent - HF

A

reduce impedence to foward flow and diminish cardiac workload

NTG, furos

55
Q

goal of BP reduction and primary agent - ao dissection

A

reduce shear force and change in pressure over change in time

esmolol +/- nitropruside; secondary labetalol

56
Q

goal of BP reduction and primary agent - acute ischemic stroke

A

reduce hemorrhagic conversion and edema, don’t go hypotensive

nicardipine, secondary labetalol

57
Q

goal of BP reduction and primary agent - acute ICH

A

reduce hematoma expansion and perihematomal edema; nicardipine, labetalol

58
Q

goal of BP reduction and primary agent - HTN encephalopathy

A

decr brain edema, reduce IC pressure, improve autoreg control

nicardipine, labetalol

59
Q

goal of BP reduction and primary agent - AKI

A

decr pressure in renal parenchyma and glomerular apparatus

clevidipine, nicardipine

60
Q

goal of BP reduction and primary agent - preeclampsia, eclampsia

A

decrease ICP while maintaining placental perfusion

hydralazine, labetalol

61
Q

goal of BP reduction and primary agent - sympathetic crisis

A

reduce alpha 1 adr metadiated vasoconstriction

phentolamine, ntg

62
Q

BUN/Cr ratio >20 and FENa <1% indiates ? cause

A

prerenal

63
Q

First line preeclampsia mag sulf dose

then BP meds of choice?

A

4 g IV loading dose, followed by 1 to 2 g/ hour) is considered first-line therapy for all cases of preeclampsia and eclampsia. It relaxes the smooth muscle (partly through calcium antag- onism),

Hydralazine (10 mg IV) and labetalol (20 mg IV) by IV bolus are equally useful for this purpose and have a limited impact on placental blood flow

64
Q

Pheochromocytoma SPECIFIC BP meds

A

1.phentolamine FIRST
2. then beta bocker to decr HR (typically paired with vasodilator to ensure no unopposed alpha)

65
Q

Untreated chronic Hypertension or new diagnosis? start ? two options

A
  • Start thiazide diuretic.
  • Hydrochlorothizide 25 mg
    qd
  • Chlorthalidone 25 mg qd
66
Q

Uncontrolled chronic hypertension on monotherapy: can start ?

A
  • Start dual therapy, adding a new class of medication.
    1. Calcium channel blocker
  • Amlodipine 5 mg qd
    2. Angiotensin-converting
    enzyme inhibitor
  • Lisinopril 10–20 mg qd
  • Angiotensin receptor
    blocker
  • Losartan 50 mg qd
    3. Thiazide diuretic (if not
    already on one)
67
Q

Uncontrolled chronic hypertension on dual therapy - how to tx?

A

double med dose up to max
add on third class of med

Rosens (48 decks)

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