normal <120, <80

prehypertension  120-139, 80-89

stage 1:     140-159, 90-99

stage 2:     ≥ 160, ≥100

starting at 115/75mmHg CVD risk doubles with each increment of 20/10mmHg

thiazide

ex:  hydrochlorothiazide (HCTZ)

12.5-25 mg qday

works at distal tubule:  increases Na+ excretion, decreases plasma volume, decreases ECF, some decrease in peripheral resistance

• hypokalemia, hypomagnesemia, hyperuricemia, hyperglycemia
• works in renal insufficiency (unless SCr>2.5- than use metolazone/loop)
• mild cholesterol, increased triglycerides (both usu not significant), (indapamide: less or no cholesterol effect)

thiazides ex:  hydrochlorothiazide

potassium-sparing ex:  Spironolactone (Aldactone)

loop ex:  Furosemide (Lasix)

role is to preserve K+

is an aldosterone antagonist (therefore encourages elimination)

-used in combo with thiazide diuretics to offset K+ loss

-may cause hyperkalemia when taken with K+ supplement or ACEi, or in pts w/ renal insufficiency

-aldos-antagonist may cause gynecomastia

10-160mg/day in 1-2 divided doses

more potent diuretic effect at loop of henle

• increase Na+ excretion
• decrease plasma volume
• decrease ECF
• more effective than thiazides in heart failure

ex:  Furosemide (Lasix)

• more potent effects than thiazides on hypoK+/Mg+
• overdiuresis,  metabolic alkalosis

used over thiazides in pt with significant heart failure or renal insufficiency

bumetanide, torsemide

ACE-inhibitors (ACEI)

Lisinopril (Prinivil, Zestril)

5-40mg qday

inhibit ACE, blocking formation of angiotensin ii (pwrful vasoconstrictor)

• decreases aldosterone (decreased Na+ retention)
• increases bradykinin (causing vasodilation)
• may reduce hypertrophy of CV tissue (vessels, heart)

-hyperkalemia -->  monitor esp if on K+ supplement or K+-sparing diuretic

-cough, hypotension, rash, angioedema

-acute renal failure in pts with bilateral renal artery stenosis, significant dehyd

• these pts depend on angiotensin II to maintain pressure gradient- if block-loose angiotensin II- don't retain water-pressure gradient down or more dehydration

angiotensin II receptor blockers  (ARB)

ex:  Losartan (Cozaar)

25-100mg qday

AE:  much like ACEis except no cough or rash assoc

block angiotensin II receptor

• causing vasodilation
• decreased aldosterone (decreased Na+ retention)

Direct renin inhibitors (DRI)

ex:  Aliskiren (Tekturna)

150-300mg of once daily w/ or w/out meals

directly inhibits renin causing:

• vasodilation
• decreased aldosterone (decreased Na+ retention)

diarrhea (esp with higher dose)

cough and angioedema (less often than ACE-I)

contraindicated during pregnancy!

-consider for pts who cannot tolerate ACE-Is!

-hyperK+    monitor!  esp pt on K+ supplement or K+ sparing diuretic

-hypotension, angioedema

-acute renal failure in pt with bilateral renal artery stenosis or significant dehyd

-contraindicated in 2nd and 3rd trimesters of pregnancy

-consider decreasing or d/c diuretic before starting ARB to avoid excessive hypotension

two classes of CA2+ antagonists (CCB)

AE that both classes may cause

dihydropyridine

ex:  Amlodipine (norvasc) all end in "dipine"

non-dihydropyridine

ex:  Diltiazem (Cardizem, Cardizem CD, Dilacor XR, Tiazac)

ex:  Verapamil (Isoptin SR, Calan SR, Verelan, Covera)

AE:  headache, dizziness, peripheral (ankle) edema, eczema in elderly (3-6mo after started)

C:  pt with systolic heart failure (heart relies on Ca2+ influx)

*Amlodipine!

ex:  Amlodipine (Norvasc)

2.5-10mg qday

AE:  tachycardia

comment:  avoid immediate release nifedipine- assoc w/ increased mortality

ex:  Diltiazem-immediate release, extended release

(Cardizem, Cardizem CD, Dilacor XR, Tiazac)

30-90mg tid, 120-360mg qday

AE:  slows HR- monitor/caution

C:  pt with bradycardia, heart block, sinus node dz

ex:  Verapamil- immediate release, sustained release

(Isoptin SR, Calan SR, Verelan, Covera)

40-240mg bid, 120-480mg qday

AE:  slows HR- monitor/caution!, increase digoxin levels- monitor!, constipation

mechanism of Ca2+ channel blockers/Ca2+ antagonists

CCBs

dihydropyridines and non dihydropyridines

block intracellular influx of calcium-->preventing vascular smooth muscle contraction

end result is vascular smooth muscle relaxation or vasodilation

should watch for reflex tachycardia (inc HR  to inc BP in lower extremities)

four classes of beta-blockers (BBs)

examples and dosages

non-selective (beta 1 and beta 2)

ex:  Propranolol (Inderal) 20-120mg bid

others:  Nadolol, Timolol

cardioselective

ex:  Metoprolol (Lopressor) 25-100mg 1-2/day

ex:  Atenolol (Tenormin) 25-100mg qday

others:  Betaxolol, Bisoprolol, Nebivolol

mixed alpha-beta blocker

ex:  Lebetalol and Carvedilol

intrinsic sympathomimetic activity (ISA)

ex:  Acebutolol, Penbutolol, Pindolol

AE:  B2 blockade may aggravate asthma/other lung dz

-fatigue, insomnia, depression, nightmares, bradycardia, ED, aggravate PVD, mask signs of hypoglycemia, mild decrease in HDLs and mild increase in TG

contraindicated:  pt w/ bradycardia, heart block, sinus node dz d/t dec HR, heart failure

do not stop abruptly in pt w/ ischemic heart dz or risk reflex tachy

*Labetalol may cause postural hypotension (vasoconstriction and inc contractility blocked)

*ISA does not confer cardioprotective effects

ex:  Propranolol (Inderal) 20-120mg bid

Blocks B-1 receptors in heart to:

• decrease HR and cardiac output
• results in decreased BP
• decreased plasma renin activity

ex:  Metoprolol (Lopressor) 25-100mg 1-2/day

ex:  Atenolol (Tenormin) 25-100mg qday

cardioselective effects are dose related--> some B2 blocking effects

therefore not for asthmatics!

Nebivolol causes peripheral vasodilation by increasing NO production and release from endothelial cells

Betaxolol, Bisoprolol, Nebivolol

ex:  Labetalol, Carvedilol

mixed alpha-beta blocker blocks B1 receptors and A receptors

• vasodilation effects

ex:  Acebutolol, Penbutolol, Pindolol

slight agonist effect at beta receptors while blocking (only indicated for HTN)

...basically doesn't decrease HR as much

does not confer cardioprotective effects

centrally acting A2 agonists:  Clonidine (Catapres), Clonidine patch, Methyldopa (Aldomet)

peripherally-acting adrenergic antagonist:  Reserpine

direct vasodilators:  Hydralazine, Minoxidil

alpha-1 receptor blockers:  Doxazosin (Cardura), Prazosin, Terazosin

*end in "zosin"

mechanism and AE of centrally acting A-2 agonists

ex:  Clonidine

mechanism:  stim CNS alpha 2 receptors that work to decrease peripheral sympathetic activity --> decreases BP

-patch may help compliance

-preferred agent in pregnancy

AE:  sedation, dizziness, dry mouth, fatigue, orthostatic hypotension

*avoid abrupt d/c -->may cause rebound hypertension

*Methyldopa:  liver damage, fever, hemolytic anemia

peripherally-acting adrenergic antaagonists

ex:  Reserpine

second-line agent

mechanism:  depletes catecholamine stores

AE:  orthostatic hypotension, nasal congestion, lethargy, depression

contraindicated:  depression, active peptic ulcer dz

direct vasodilators

second-line agent

ex:  Hydralazine

mechanism:  direct vascular smooth muscle relaxation (arteriolar vasodilation)

*Minoxidil is potent vasodilator

AE:  fluid retention (consider concomitant diuretic), rebound tachycardia (consider concomitant B-blocker), headache

Hydralazine assoc with lupus-like syndrome

Minoxidil may cause hirsutism

alpha-1 receptor blockers

second-line agent

ex:  Doxazosin

mechanism:  blocks alpha-1 adrenergic stimulation of vessels-->  smooth muscle relaxation (vasodilation)

AE:  postural effects- orthostatic hypotension- titrate dose based on standing BP

-1st dose phenomenon- syncope- start with low dose at bedtime (when effects are greatest... hopefully sleeping

systole:  phase of cardiac cycle in which ventricles contract

-maximal (aortic) pressure during ventricular contraction

diastole:  phase of cardiac cycle in which ventricles relax

-point of lowest arterial pressure= pressure which left ventricle must overcome to open aortic valve (systemic/peripheral resistance)

Identify the diagnostic criteria by which a definition of systolic and/or diastolic  hypertension is made

normal:  <120/80  (must meet both SBP and DBP)

prehypertension:  120-139/80-89

hypertension

stage 1:  140-159/90-99

stage 2:  ≥160/100

isolated systolic: ≥140/<90  (must meet both SBP and DBP)

must have 2 or more measurements at 2 or more visits after initial screening

Define and describe the etiology of essential hypertension

essential HTN:  (primary or idiopathic)

80-90% of all HTN cases

familial basis but combo of genetics and environment

prevalence inc with age

two subcat:

high plasma renin activity:  10-15%, vasoconstrictive form

low plasma renin activity:  25%, volume-dependent form

endocrine:  pheochromocytoma, cushings, primary aldosteronism, congenital adrenal hyperplasia, hyperparathyroidism, hyperthyroidism (systolic), hypothyroidism (diastolic)

renal:  renovascular dz (stenosis), preeclampsia, renal parenchymal dz, renin-secreting tumor

mechanical:  coarctation of aorta, a/v fistula, patent ductus arteriosus, obstructive sleep apnea

medication-induced:  stimulants, corticosteroids, SSRIs, abrupt med withdrawl, oral contraceptives, licorice

SBP ≥ 180, DBP ≥ 120

occurs in pts with long-standing, untx HTN, secondary causes

can lead to HTN encephalopathy, risk for seizures/coma if not treated

urgency/emergency and tx based on sys and PE

Recognize non-reversible and reversible risks for elevated blood pressure.

non-reversible:  age

genetic heritability

-family hx of premature CVD (men <55, women <65)

race (African Americans more susceptible)

reversible:  smoking, excess EtOH, sedentary, renal dz (microalbuminuria), obesity (BMI ≥ 30), dyslipidemia, DM factors of metabolic syndrome/syndrome X

Identify the most common clinical presentation of a patient with uncomplicated HTN.

most often an incidental finding, pt has no specific sxs

neurologic sxs:  headache- occipital in am, dizziness, palpitations, fatigue, impotence

vascular sxs:  epistaxis, hematuria, metrorrhagia, blurred vision, weakness, angina, DOE, pain (in chest/abdomen- may indicate dissection of aorta or leaking aneurysm)

Describe the initial work up on a patient with HTN with regard to findings sought on history, physical exam, laboratory, x-ray and EKG.

CBC (anemia, polycythemia?)

serum K+ (rule out hypokalemia, mineralocorticoid excess)

BUN/Cr (assess renal function)

Ca2+/PO4- (parathyroid dz, hyperCa2+/PO4-?)

fasting glucose (screen for DM, establish baseline)

hx:  onset/duration of sxs, PMH, PSH, FH, SH

-age of onset may clue to secondary HTN (<35, >55?)

-potential target organs affected

ROS:  general (weight changes, fatigue), neuro (deficits, sxs), visual phenomena, cardiac (palpittations, angina), dysuria, polyuria, polydipsia, vascular (impotence, exercise intolerance)

general appearance:  Cushingoid (abd obesity/chix legs), musc develp in upper vs lower extremities, abdominal/general obesity

fundoscopy:  look for retinopathy

cv exam:  displaced PMI, S3 or S4, carotid bruits

abdominal exam:  renal artery bruits, abdominal aortic width, palpate for enlarged kidneys

peripheral vascular exam:  equality of peripheral pulses, femoral artery bruits, missing hair on legs (low circulation)

renal:  IVP or MRA to image renal arteries, suppressed or stimulated plasma renin activity (PRA), uric acid

primary aldosteronism:  serum/urine K+, PRA test

pheochromocytoma:  urine/serum catecholamines, metanephrine, VMA

cushing's syndrome:  serum cortisol, urinary free cortisol, dexamethasone suppression test

Describe the significance of non-pharmacologic management for reducing hypertension by using diet, exercise, weight loss, and smoking cessation.

diet:  dietary approaches to stop HTN (DASH)- rish in K+, Ca2+, fruit/veg

-Low sodium diet- (1600mg/day)...  DASH + low sodium shown to be as effective as drug monotherapy

exercise:  30min aerobic daily

weight reduction:  goal BMI 18.5-24.9

smoking cessation and EtOH consumption to 1-2 servings/day

any of two listed above has been proven to help lower bp, enhance efficacy of HTN meds, reduce cardiovascular risk

Discuss end organ damage secondary to HTN found at the eyes, renal, cardiac and vascular systems.

eyes:  retinopathy-  papilledemea (optic nerve swelling), A/V nicking (compressed retinal veins), hemorrhage, exudates (lipid deposits after pinpoint hemorrhage), cotton wool spots (ischemic regions of retina- nerve fiber layer)

renal:  proteinuria, renal insufficiency

cardiac system:  congestive heart failure, left ventricular hypertrophy- S4 heart sound "stiff ventricle", cardiomegaly on CXR, EKG changes (Framingham criteria)

peripheral arterial dz:  hair loss on legs, diminished peripheral pulses, cool extremities, sluggish capillary refill (> 3 seconds)

brain:  stroke (hemorrhagic or ischemic), TIAs, encephalopathy (loss of brain volume)

Describe the etiology, pathology for orthostatic/postural hypotension.

significant drop in arterial blood pressure with position change

pathology:  defect in vasomotor reflexes impeded by something pathological (like ANS disorders) or age (causes syncope in elderly)

ANS etiology:  multiple sclerosis, Parkinson's dz, Peripheral neuropathy (DM or other), Guillain-Barre Syndrome, Raynaud's Syndrome, Reflex Sympathetic distrophy

other etiologies:  drugs (vasodilators, antihypertensives, antidepressants), physically deconditioned (blood pools), sympathectomy, dec blood volume (gi bleed, dehydration, adrenal insufficiency), idiopathic (familial), advanced age (sluggish baroreceptors)

dx:  bp/hr from supine to stand (wait 2 min btwn position change, SUSTAINED drop of SBP > 20mmHg or DBP > 10mmHg, absence of HR increase (15 beats) suggests neuro etiology, presence suggest nonneuro, tilt table

management:  reduce/eliminate offending drugs, possible high Na+ diet, maybe drug therapy

pt edu:  caution on position changes, elevate head of bed, compressive stockings

both loop diuretics and thiazide diuretics do the following:

and which one is more potent and effective in the tx of HTN in heart failure patients

increase Na+ excretion

decreases plasma volume and ECF volume

loop diuretics more potent

distal tubule diuretic

microzide

12.5-25mg qday

lasix

loop diuretic

10-160mg qday 1-2 div doses

tenormin

cardioselective B-blocker

25-100mg qday

zestril, prinivil

ACE-I

5-40mg qday

norvasc

Ca2+ channel blocker (dihydropyridine)

2.5-10mg qday

lipitor

HMG-CoA reductase inhibitor/statin

10mg qday

tricor

fibric acid lipid lowering agent- increases lipoprotein lipase activity

201mg qday

niacor, niaspan

nicotinic acid

1-2g tid

lanoxin

anti-arrhythmic agent

0.125-0.5mg PO qday

or

0.5mg IV followed by 0.25mg q4-6h X 2

nitrolingual

vasodilator for angina, CHF (IV), pulm HTN, peri/intraoperative HTN

1 tab q5minutes X 3doses in 15min

IV:  10mcg/min X 48hours

coumadin

anti-coagulant, vitamin k antagonist

PO 4-5mg qday

H1N1

enterovirus

coxsackie B

adenovirus

CMV

HIV

streptococcus

Borrelia Burgdorferi

cocaine

Coxsackie B5, B6

echovirus

adenovirus

EBV

influenza

VZV

HIV

usually microorganism related

streptococci accts for 65% (s. epidermis MC in pt with prosthetic valve)

• usually affects left side of heart

all normal- may see diffuse ST elevations and PR depressions

look for signs of pericardial effusion on TTE

pericarditis only one that really has pain (btwn peri, myo, and endocarditis)

all abnormal

cxr- pulm edema

ekg- show injury pattern or tachycardia

tte- hypokinesis

cardiac enzymes will be normal

everything else abnormal

cxr- pulm edema/infiltrate

ekg- sinus tach

tte- look for vegetations and valve malfunctions

uncomplicated HTN  <140/90

DM or renal dz  <130/80

Left ventricular dysfunction (HF)  <130/80; consider <120/80

HTN

coronary artery disease

viral cardiomyopathy

EtOH induced cardiomyopathy

mostly seen in 2/3 of pts w/ LVD

tachy, brady

-increase preload

-vasoconstriction

-tachy and inc contractility

-ventricular hypertrophy

dyspnea

fatigue

edema

negative inotropic effect- decreases force of contraction:  antiarrhythmics, BB, CCBs, intraconazole, terbinafine

cardiotoxic:  most are chemotherapy, ethanole, amphetamines

NA2+ AND h20 RETENTION:  NSAIDS, glucocorticoids/corticosteroids, androgens, estrogens, salicylates (high dose asprin), drugs with high Na2+ content (IV), DM meds, COX-2 inhibitors

cardiac workload determinants:

OPTIMIZE PRELOAD:  need enough blood volume to perfuse, but not too much to overload

REDUCE AFTERLOAD:  make as easy as possible for heart to perfuse

INCREASE CONTRACTILITY

ACE-I

BB

diuretics

digoxin

lisinopril dosing in HF

if someone has angioedema or another contraindication to lisinopril what is a good alternative

start at 5mg qday and titrate to 20-40mg qday

ARB, or hydralazine +isosorbide

BB used in treatment of HF

effect on ventricular workload (remember, we want to optimize preload, reduce afterload, and increase contractility

benefit

Carvedilol, Metoprolol CR/IL, Bisoprolol

decrease HR

antiarrhythmic (HF pt at greater risk for v-tach)

cause reverse of ventricular remodeling!  (which is a large part of what increases the workload in the first place)

BB decreases contractility (negative ionotropic effect)

there fore pt must be:

stable ,started at low doses and titrated upward slowly (double dose over two weeks), and monitored for hypotension, bradycardia, and fluid status

definitely not for asthmatics

diuretics

effect on ventricular workload

benefit

who should use a diuretic

devcreases preload (vascular volume)

major benefit is symptomatic relief

only for pt with congestive sxs (volume overload)- otherwise may dry them out and kick the renin-angiotensin sys in to retain Na2+ and H20

digoxin

effects on ventricular workload

benefit

caveats

positive inotrope (increases contractility)

antiarrhythmic for pt with a-fib

relieves sxs

-but no sig effect on survival of HF pt

-IF NO ATRIAL ARRHYTHMIA START AFTER BB, so decreased HR  from digoxin does not preclude BB

decrease preload, decrease afterload, increase contractility

correcting this will also help pulm edema

inability of heart to generate a sufficient CO to meet metabolic demands of body

c/cs by:  sxs of intrvascular/interstitial volume overload (SOB, rales, edema)

and

manifestations of inadequate tissue perfusion (fatigue, poor exercise tolerance)

dyspnea:  on exertion, at rest, supine (orthopnea), paroxysmal (PND)

-cough, hemoptysis

fatigue:  postural lightheadedness

-decreases mental acuity

edema:  bloating/nausea, weight gain, anorexia/weight loss, palpitation

Discuss the etiology of right ventricular, left ventricular, and biventricular failure.

L:  MI, CAD, HTN, idiopathic dilated cardiomyopathy, EtOH abuse

R:  pulm embolism, pulm HTN, RV infart, cardiomyopathy

Describe the symptoms and physical exam findings of HF and list additional asymptomatic clues on physical exam associated with left and right sided heart failure.

sxs:  dyspnea, fatigue, edema

PE:  abnormal BP, HR, RR

-distended neck veins

-Heart:  enlarged, murmurs, diminished tones, S3 gallop sounds

-Lungs:  pulm noise

-distended abdomen 

-extremity edema

-pallor/tired appearing

what are the reversible causes of CHF

what types of things worsen CHF

valvular lesions

mi

uncontrolled hypertension

arrhythmias

EtOH induced myo depression

CCBs, anti-arrhythmics, NSAIDS

List and discuss the merits and limitations of adjunctive aids (imaging, EKG, and laboratory studies) in the diagnosis of suspected HF.  

lab:  Hbg (anemia?), metabolic panel (Cr, BUN), TSH, lipid panel, BNP level

EKG:  look for prior MI, LVH, conduction abn, ischemia

imaging:  CXR (infiltrates, effusions, heart size?)

BNP alone 83% BNP< "negative" predictive value- can tell person don't have CHF

Framingham 73%

NHANES critria 67%

pt must comply with meds

no NSAIDS- counteract effect of ACEi, may worsen renal function

check for drugs that are negative inotropes

COPD, fever

ongoing MI

progressing valvular lesions

HTN

heat/humidity, cold

low CO, high pulm pressure, dyspnea

Diastolic HF:  diastolic pressure elevated even though volume is normal or small

dilated/congestive cardiomyopathy in LV

ETIOLOGY:  EtOH cardiomyopathy, viral myocarditis, idiopathic cardiomyopathy, infiltrated dz (chromatosis, sarcoidosis, amyloidosis), degenerative and congenital valve dz

EXERTIONAL DYSPNEA, COUGH, FATIGUE, ORTHOPNEA, PAROXYSMAL NOCTURNAL DYSPNEA, CARDIOMEGALY, RALES, GALLOP, PULM CONGESTION

vital signs normal or tach, hypotension, reduced pulse pressure may also present

class 1:  no sxs with ordinary activity

class 2:  slight limitation of physical activity.  comfortable at rest, ordinary physical activity results in fatigue, dyspnea, palpitation, or angina

class 3:  very limited during physical activity.  comfortable at rest, less than ordinary physical activity results in fatigue, palpitations, dyspnea, or angina

class 4:  unable to carry out physical activity w/out discomfort.  sxs of cardiac insufficiency may present at rest

stage a:  at risk for HF (HTN, valvular dz, hx of MI)

stage b:  asymptomatic LV dysfunction (NYHA Class 1)

stage c:  mild to moderate heart failure sxs (NYHA Class 2-3)

stage d:  severe heart failure sxs not responsive to medical tx (NYHA Class 4)

MC:  CAD

RHD

cardiomyopathy

trauma

congenital

notable points of an inferior infarction

and posterior infarct

ST elevations and T wave inversions in leads (II, III, aVF)

look for reciprocal changes in V1 or do a 15-18 lead EKG

both right cornary artery

anterior infarct

lateral infarct

leads V2-V4

ST elevations, T wave inversion

left anterior descending artery

leads I, aVL, V5, V6

ST elevations, T wave inversion

left circumflex artery

must be 1/3 the height of QRS complex

greater than 0.04seconds in duration (one small box)

describe the pathophysiology and presenting features for obstructive sleep apnea

central:  less drive to breath

obstructive: narrowing or collapsing of upper airway

presenting features:  shallow breathing during sleeping, excessive sleepiness in daytime, morning headaches, nocturnal arousals, intellectual deterioration, chronic fatigue

diagnostic evaluation: 

gold standard:  overnight polysomnography “sleep study”

Epworth sleepiness scale, history from significant other, PE

treatment:

-weight loss

-avoid EtOH, tobacco, sedatives

-nasal saline/decongestants

-CPAP, BiPAP, airway appliances, surgery

-Mondafinil for daytime sleepiness

weight reduction (BMI 18.5-24.9) can result in 5-20mmHg/10Kg

DASH diet

reduced Na+ intake to <2.4gm Na+ or <6gm NaCl

physical activity

moderation of EtOH consumption

uncompmlicated HTN <140/90

DM/renal dz <130/80

• includes CAD or equivalent or 10 yr Famingham risk score ≥10%

therapy is determined by what stage of HTN the pt is in:

all therapies prescribe lifestyle modifications

Drugs not really considered until Stage 1, Stage 2 HTN

stage 1:  Thiazide diuretic

• may consider ACEI, ARB, CCB, or combo

-respond best to diuretics or CCBs, decreased response to BB, ACEI, ARB monotherapies (although when used with large dose of diuretic, decrease response is not as bad)

-risk for angioedema 2-4 X more likely with use of ACEIs

at greater risk for orthostasis

• start with low dose to minimize risk (esp with diuretics and ACEIs)!

pro:  may slow demineralization in osteoporosis

con:  use cautiously in gout or history of significant hyponatremia

pro:  useful in tx of atrial tachy/fibrillation, migraine, short-term thyrotoxicosis, essential tremor, or perioperative HTN

con:  avoid in pt with asthma, reactive airways dz, or second/third degree heart block

CCBs:  useful in Raynaud's syndrome and certain arrhythmias

alpha-blocker:  useful in prostatism

which anti-HTN is CONTRAINDICATED in pregnant women and those trying?

which should be avoided in individuals with a hx of angioedema

anti-HTN drugs that are more likely to cause hyperkalemia

ACE-Is and ARBs

ACE-Is

aldosterone antagonists and K+ SPARING DIURETICS

in pt with CAD and/or heart failure

CAD:  BB and ACE-I/ARB

Heart failure:  BB, ACE-I/ARB, diuretic, and aldosterone agent

pt should return for follow-ups/med adjustments until BP goal reached

• check BP and pt tolerance 2-4 wks after start of or change of HTN dose
• assess response after 4-6wks
• pts with stage 2 or with complicating comorbid conditions need more frequent visits!

DBP >130 and TOD present

goal:  reduce DBP to 110 w/in 30min (avoid drastic reduction!)

• then to 100 w/in 12-24hrs

DBP >130 but NO TOD present

goal:  reduce DBP to 100 w/in 24 hrs

tx:  oral agents