HTN Flashcards
damage from HTN
stroke retinopathy, blindness MI HF kidney failure
180/110
HTN emergency
see slide 4
consistently above 140/90 check for
end organ damage
if yes: tx for HTN
if not, diet and exercise
(home BP: 135/85)
HTN values
Normal: less than 120/80
pre-HTN: 120-139/80-89
stage 1: 140-159/90-99
stage 2: greater than 160/greater than 100
how to perform BP
slide 7, 8
long standing HTN
develop LVH–>higher rate of CV events
tx pressure, mass will decrease
if untx dev. ESRD
etiology of HTN: primary (95%)
Overactivitation of SNS and RAAS
Blunting of pressure-natriuresis relationship
Variation in CV/renal development
Elevated intracellular Na+/Ca+
Exacerbating factors (too much salt, meds: NSAIDS, cocaine, smoking, etOH, sleep apnea, OCPs)
Secondary Hypertension
Who should be screened?
Severe or resistant HTN: Persistent HTN despite use of adequate doses of three antiHTN from different classes
Acute rise in BP in a patient with previously stable values
Age less than 30 in non-obese, non-African American pt w. negative fam hx
malignant/accelerated HTN (severe HTN and evidence of end-organ damage)
age of onset before puberty
Genetic causes of secondary HTN
Liddle syndrome
hyperaldo
HTN in pregnancy
Renal/renovascular causes of secondary HTN
FMD (fibromuscular dysplasia) in young women (rev)
Refractory HTN
Bruits, PAD
Cr increase with ACE-I (bilat renal artery stenosis)
Pulmonary edema
slide 17
flash pulmonary edema
pheochromocytoma
paroxysmal elevations in BP
triad of pounding ha, palps, sweating
primary aldosteronism
unexplained hypokalemia with Ur K+ wasting (but more than 50% are normokalemic)
tx: spironalactone: aldosterone inhib
cushings
cushingoid facies, central obesity, prox musc wkness and ecchymoses
may have hx glucocorticoid use
sleep apnea
primarily in obese men, snore loudly
daytime somnolence, fatigue, morning confusion
coarctation of aorta
HTN in arms, diminished/delayed femoral pulses and low/unobtainable BP in legs
left brachial pulse diminished and equal to femoral pulse if origin of the left subclavian artery is distal to the coarctation
*bicuspid aortic valve, assoc. with aortapathies (tx: stent)
+ coarc. check for intracranial aneurysms if both! (MRI)
hypothyroidism
symptoms of hypothyr.
elevated TSH
primary hyperparathyroidism
elevated serum calcium
complications
If untreated can lead to acute complications
Chronic complications:
Hypertensive heart disease
Hypertensive cerebrovascular disease and dementia
Hypertensive kidney disease
HTN: Silent killer
Silent killer
Mostly asymptomatic; headache
If severe can cause encephalopathy with N/V, confusion, vision changes
Pheochromocytoma will have
episodic presentation
Anxiety, palpitations, profuse perspiration, tremor, HA
Optho exam
Cotton wool spots, AV nicking, hemorrhage, *papilledema
other tests/imaging
ECG, ECHO, radial-femoral delay
EKG
look for LVH
S wave in V3
+ R wave in AVL:
if 23 in female, 28 in male
it’s HTN
S wave in V1 of V2 + R wave in V4 or V5: >35 is HTN
ST depression and asymmetrical T wave inversion
LA enlargement (HTN HD)
pics: heart on LVH
slide 24
lifestyle mods
diet, exercise
every 10 k weight lost BP drops 5-20
more slide 25
who should be treated?
All receive lifestyle modification
Controversial…
Persistently > 140 SBP (if younger than 60)
Persistently > 150 SBP (if older than 60)
Persistently > 90 DBP
HTN meds to start with
Afr. American with ISOLATED HTN: ??
White ??
Afr. Am. pt with DM ??
AA: CCB and thiazide
White: ACE-I and BB
However, many pts have comorbidities which should prompt targeted therapy
ie: Afr. Amer pt with DM should receive ACE-I first
systolic HF meds
ACE-I (red. RAS, prev. breakdown of bradykinin (inflamm))
ARB (help with cough from ACE-I)
B-blocker (if used before: metoprolol succinate, carvedilol)
diuretic
aldosterone antag
postMI
ACE-I
B-blocker
ARB
ald antag
proteinuria
ACE-I
ARB
angina
B-blocker
CCB
a fib
A flutter
B block, nondihydorpyridine
CCB
more drugs for comorbs
benign protastic hyperplasia: a-blocker essential tremor: B-blocker (noncardiosel) hyperthyroidism: B-blocker migraine: B-blocker, CCB osteoporosis: thiazide diuretic Raynaud's: dihydropyridine CCB
contraindications
angioedema: don’t use ACE-inhib.
Bronchospasticity: DON’T USE B-blocker
depression: DON’T USE reserpine
liver disease: DON’T USE methyldopa (used during preg)
preggos: DON’T USE ACEinh, ARB, renin inhib
2nd/3rd degree heart block: DON’T USE B-block, nondihydropyridine CCB
Diuretics
how they work
Initially lower plasma volume but decrease SVR long-term
electrolytes, gout, ED, hyperkalemia
Thiazides: hydrochlorothiazide best for long-term (give lasix initially)
porthaladone: longer half-life
loop: not as good for 1st or 2nd line
B-blockers
not 1st line for BP anymore
Decrease HR and CO, decrease renin levels
Carvedilol decrease PVR thru alpha-blockade
Nebivolol increases endogenous NO release–>vasodilation
may cause bronchospasm, bradycardia, fatigue, ED
B-blocker complications
Do not use alone for tx of HTN from cocaine or for pheo unless alpha blockade (unopposed alpha is bad)
Renin inhibitors
Lack efficacy data over ACE-I/ARB
ACE-I
Inhibits RAAS, prevents degradation of bradykinin
ARB
Inhibit RAAS
Olmesartan can be a/w a sprue-like syndrome
Caution for ACE-I/ARB if Cr worsens > 25%, could be due to renal artery stenosis
Aldosterone receptor blockers
CHF, cirrhosis
Can lead to gynecomastia, hyperkalemia, breast pain
CCB
Peripheral vasodilation with less reflex tachy/fluid retention
do not use nondihydropyridine CCB in systolic HF (can only use norovast, amlodipine)
Caution in CHF
Alpha blockers
Lower PVR; useful with BPH
First-dose hypotension (start slow, start at night), caution in CHF
can’t use if EF is too low
Central sympatholytic (clonidine, methyldopa)
Stimulate alpha in CNS thus reducing efferent peripheral SNS outflow
adverse: ED, rebound HTN, dry mouth, caution in pregnancy with methyldopa
Direct vasodilators
Hydralazine/minoxidil
hydrazine with nitrates in Afr. Am: reduces mortality
Peripheral Sympathetic Inhibitors
Reserpine
adverse: depression
HTN urgencies
Treat when acute end-organ damage or BP > 220/125
Reduce ~ 25% in first 1-2 hrs and then target less than 160/100 within 2-6 hrs
using Nicardipine, labetalol, nitroprusside, NTG
OMM
OA Release: increase Vagal output
Rib Raising: inhibitory (attenuate facilitation)
Cervicals: carotid baroreceptors, cervical ganglions
Thoracolumbar junction: renals and RAS
Chapman’s Reflexes: myocardium, adrenals
CV4: fluid homeostasis and decrease stress
Myofascial Trigger Points: mobilize fluids
certain antiHTN drugs may have adverse effects on comorbid conditions:
depression: BB, central a2 agonist
gout: diuretic
hyperkalemia: aldo anta, ACEi, ARB, renin inhib
hyponatremia: thiazide diuretic
renovascular disease: ACEi, ARB, renin inhib.
