70. HTN Flashcards
Uncontrolled BP strong association with which conditions?
HF
mi
stroke
vascular dementia
ckd
What % decr does antiHTN therapy decr risk of
stroke
MI
HF
40
25
50
What is a hypertensive emergency?
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.
Poorly controlled chronic HTN defn
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.
Why does HTN occur in older adults? (basic physiology categories)
neurohormonal dysregulation
vascular modulation
Na intake
psychosocial stress
obesity
List 5 categories (think VINDICATE) of secondary causes of HTN
endocrine
pulmonary
renal
toxic/metabolic
vascular
name 5 causes of endocrine related secondary cause of HTN
cushing’s/steroid
hyperaldosteronism
OCP
pheo
thyroid
parathyroud
What is a pulmonary secondary cause of HTN?
OSA - get a sleep study with O2 sat
think of this if obese, narcolepsy
Name 5 secondary causes of HTN - renal
chr pyelo
diabetic nephropathy/other kidney dis
neprhitic and nephrotic syndrome
polycystic kidney disease
renovascular conditiosn
Name 3 toxic/metabolic secondary causes of HTN
chr etoh
sympathomimetic drug use
tyramine-containing food
name 2 secondary vascular causes of HTN
as
coarctation
How to assess for cushing’s?
hx
dexamethasone suppression test
gluc intol
purple striae
How to assess for hyperaldosteronism and other mineralocorticoid excess states
24h aldosterone level or other mineralocorticoids
*unexplained hypok
pheo dx test
24h urinary metanephrine and normometanephrine
*think of labileparoxysmal HTN with palpitations, pallor, perspiration
When to consider renovascular conditions like renal a stenosis as HTN cause?
HTN pre 30 or after 55
abdo bruit
refr htn control
recurrent pulmonary edema
unexplained renal failure
how to work up renal vascular conditions for secondary HTN?
doppler flow study
How does NE cause HTN?
potent vasoconstr to drive SVR to amplify afterload to HTN
How is RAAS involved in HTN?
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
How does vascular remodelling occur in HTN?
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
Recommended daily Na intake
1500mg/day
for every incr 5kg/m^2 in BP, how does relative risk of HTN incr?
1.5
What organs are effected by HTN?
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
How does a hypertensive emergency effect flow/autoregulation of BP mechanisms?
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
MC top HTN emergencies by organ system
Heart overall - HF, ACS
Brain - stroke/ICH/hpertensive encephalopathy
Acute renal risk kidney
Why does hypertensive encephalopathy occur?
diffuse vasogenic cerebral edema –> failure autoregulation of brain with vasospasm, ischemia, incr vascular permeability, punctate hemorrhage and interstitial edema
Hypertensive encephalopathy symptom features
headache
vomit
MAS
seizure coma
blurry vision
papilledema
Hypertensive encephalopathy imaging
may or may not show punctate hemorrhage on CT
What is Posterior reversible leukoencephalopathy?
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
DDX for elevated BP in the ED? 3 categories
- 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
Findings of acute hypertensive retinopathy?
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
Box 70.2: Name the 5 grades of fundoscopic grading of suspected hypertensive retinopathy and their description
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
What is the MAP
summary measure representing average arterial pressure in one cardiac cycle, described by co times svr plus central venous pressure
What does CVP indicate?
intravascular vol/preload and effective hydrostatic force in circulatory system
MC 2 antiHTN in ED?
labetalol
NTG
nicardipine in states?
Optimal reduction of MAP in acute hypertensive emergency?
MAP 20-25% in first hour and goal BP 160/100 by 2-6 hours
Why is a decrease in MAP 20-25% optimal in a HTN emergency?
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.
Effect on CO, SVR, CVP:
alpha blockers
phentolamine
incr/decr/incr
Effect on CO, SVR, CVP:
beta 1 blocker
esmolol, metop
decr/can incr or decr/can incr or decr
Effect on CO, SVR, CVP:
ACEi
incror decr/decr/ incr or decr
Effect on CO, SVR, CVP:
dihydro like nicardipine vs nondihidro (dilt/verapamil)
incr/decr/either
vs
decr/decr/either
Effect on CO, SVR, CVP:
hydralazine/direct acting vasodilator
incr/decr/either
Effect on CO, SVR, CVP:
loop diuretics
either/decr/decr
Effect on CO, SVR, CVP:
NO donor like nitroprusside, ntg
incr/decr/decr
AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments
Phentolamine
5-15mg q5min
0.2-0.5mg/min
1-2 min
10-30min
cannot use in CAD
AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments
metoprolol
5mg q5min
none
10-30min
5-8h
AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments
labetalol
20-80mg q10min
1-2mg/min
2-5min
3-6h
AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments
Nicardipine
none
5-15mg/h
5-15min
4-6h
AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments
hydralazine
5-20min q30min
none
10-20min
2-4h
AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments
furosemide
40-240mg q12h
10-40mg/h
30-60min
2-4h (really 6)
AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments
Na nitroprusside
none
0.25-10 microgram/kg/min
immed
1-2min
AntiHTN therapy bolus or load/infusion/time to onset/duration of action/comments
ntg
1-2mg q5min
5-200 microgram/min
2-5min
5-10min
Nitroprusside risk
cn toxicity
ACS and HTN - goal of BP reduction and primary agent
decr cardiac work and improve perfusion, combat rise in SVR
NTG best!
goal of BP reduction and primary agent - HF
reduce impedence to foward flow and diminish cardiac workload
NTG, furos
goal of BP reduction and primary agent - ao dissection
reduce shear force and change in pressure over change in time
esmolol +/- nitropruside; secondary labetalol
goal of BP reduction and primary agent - acute ischemic stroke
reduce hemorrhagic conversion and edema, don’t go hypotensive
nicardipine, secondary labetalol
goal of BP reduction and primary agent - acute ICH
reduce hematoma expansion and perihematomal edema; nicardipine, labetalol
goal of BP reduction and primary agent - HTN encephalopathy
decr brain edema, reduce IC pressure, improve autoreg control
nicardipine, labetalol
goal of BP reduction and primary agent - AKI
decr pressure in renal parenchyma and glomerular apparatus
clevidipine, nicardipine
goal of BP reduction and primary agent - preeclampsia, eclampsia
decrease ICP while maintaining placental perfusion
hydralazine, labetalol
goal of BP reduction and primary agent - sympathetic crisis
reduce alpha 1 adr metadiated vasoconstriction
phentolamine, ntg
BUN/Cr ratio >20 and FENa <1% indiates ? cause
prerenal
First line preeclampsia mag sulf dose
then BP meds of choice?
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
Pheochromocytoma SPECIFIC BP meds
1.phentolamine FIRST
2. then beta bocker to decr HR (typically paired with vasodilator to ensure no unopposed alpha)
Untreated chronic Hypertension or new diagnosis? start ? two options
- Start thiazide diuretic.
- Hydrochlorothizide 25 mg
qd - Chlorthalidone 25 mg qd
Uncontrolled chronic hypertension on monotherapy: can start ?
- 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)
Uncontrolled chronic hypertension on dual therapy - how to tx?
double med dose up to max
add on third class of med
