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Cards HTN Tx

Cardiology

QuestionAnswer
Firstline tx in HTN: MOA (eg, diuretics, BB) decrease vascular volume, decrease afterload and systolic BP
Most potent type of diuretics & MOA = loop (furosemide): inhibit Cl reabsorption in TAL -> Na follows Cl and H2) follows Na&Cl. Results in high K+ losses.
Thiazide diuretics MOA = HCTZ & chlorthalidone: inhibit K+ & Na+ reabsorption in TAL. Decrease plasma volume, increase Na excretion
Thiazide diuretics AEs = Volume depletion, low K+ & Na, hyperglycemia / insulin resistance; hyperuricemia/gout, photosensitivity, decreased placental flow. May increase serum cholesterol & digoxin
Hypertensive Emergency: tx Controlled, gradual lowering of BP; 10% decrease in first hour, then 15% over next 3–12 hrs to BP of no less than 160/110; rapid correction of BP to normal levels puts pt at high risk for worsening cerebral, renal or cardiac ischemia
Cushing Syndrome: tx for HTN HTN is reversible if cause is eliminated (ie, pituitary adenoma, corticosteroid Rx)
Beta blocker: MOA Blockade of parts of the sympathetic NS (reduce PVR); Lowers HR; Initially lowers cardiac output; Reduces circulating renin
ACEI AEs Cough; Angioedema; Hyperkalemia & hyponatremia (2/2 low aldosterone); Rash. CI in pregnancy, and use cautiously in renal artery stenosis (RAS)
ARBs: MOA Act to block Angiotensin II from binding points; same effect as ACEI, without some of the AEs
ARBs AEs Hyperkalemia; Angioedema (rare, 10% cross-over); CI in PG; Cautious use in RAS
CCBs: MOA Inhibit Ca+ influx -> block vascular smooth mx contractility -> vasodilatation & afterload reduction (aoso preload). Also coronary vasodilatation: CCBs are used in coronary artery spasm (Prinzmetal, Raynaud)
CCBs: Dihydropyridines (DHPs) vs nonDHPs DHPs more vascular selective (fewer cardiac conduction fx): tx HTN/angina. NonDHPs more cardio-selective with more inhibitory fx on SA/AV node (CAUTION in CHF)
DHP CCBs (amlodipine, nifedipine): AEs Ankle edema; Flushing; HA; Increased HR
Non-DHP CCBs (diltiazem, verapamil): AEs Bradycardia, constipation, hotn, edema, CHF, AV node block
HTN lifestyle mods Wt reduction (BMI 18.5 - 25) (biggest fx on bp); ETOH; aerobic activity 30 min; Na+ to 2.4 mg/day; K+; DASH diet
Most single HTN meds lower BP: at most 20/10 mm Hg (so most pts on more than 1 drug)
Beta-1 stimulation causes (a), and beta-2 stimulation causes (b) (a) tachycardia; (b) bronchodilation
BBs (2) used for migraine, SVT, V-tach, tremors, EtOH W/D = Inderal (propranolol) and atenolol
BB used to reduce IOP in glaucoma = nadolol
BBs are contraindicated in: any resp dz (asthma, COPD, DF); type 1 DM. Also pt may have W/D and increase in CP (2/2 CAD) bc of increased HR & thus increasing O2 demand
CCBs are contraindicated in: CHF, LV dysfunction, AV block, sick sinus syndrome
First Line Tx for HTN *Thiazide*; beta; ACEI; ARB; other diuretics; CCB
ACEI MOA: Inhibit ACE in lung -> block formation of angiotensin II -> increased vasodilatation and Na+ loss
ACEI work less well in AA popultion bc of: lower blood renin levels
Rx of choice for DM nephropathy ACEI (increase blood flow to kidneys -> promote renal repair); act synergistically with a diuretic
Presynaptic adrenergic release inhibitors: 2 types central and peripheral
Central presynaptic adrenergic release inhibitors (anti-adrenergic meds) MOA prevent adrenergic outflow from the brain, by stimulating inhibitory alpha-2 receptors (eg, clonidine)
Peripheral presynaptic adrenergic release inhibitors (anti-adrenergic meds) MOA prevent norepinephrine release from peripheral nerve terminals (eg, in heart) -> block alpha-1 receptors (eg, prazosin)
Sudden DC of anti-adrenergic meds can cause: rebound HTN
Firstline & 2ndline HTN tx in pregnant patient = 1st: methyldopa (Aldomet). 2nd: hydralazine
Secondary indications of anti-adrenergic meds Central: nicotine/heroin W/D; Ppx for migraine, glaucoma, DM-assoc diarrhea. Peripheral: BPH; asthma (relax smooth mx); meds lower LDL & inc HDL
Nitrates MOA 1) dilate large myocardial arteries -> increase blood flow to heart; 2) reduce venous tone -> blood pooling in periphery -> reduces preload -> reduces cardiac work (so: increase O2 supply & decrease O2 demand)
Nitrates AEs hotn, rebound tachycardia, facial flushing, HA
JNC8: tx of uncomplicated HTN for most (non-AA) patients Firstline: ACEI, ARB, CCB, thiazide diuretics
JNC 8: essential HTN tx for AA patients CCBs and thiazide diuretics
For pts with DM regardless of race), HTN tx should include: ACEI or ARB
Hypertensive emergency tx nitroprusside (CI in PG) or labetolol; to 110 over several hours
HTN Compelling Indications: CHF 1st: ACE plus diuretic (HCTZ / Lasix); 2) Beta blocker (atenolol); 3) clonidine. Also ARB
HTN Compelling Indications: High Coronary Dz Risk Beta; ACEI; CCB; Diuretic
HTN Compelling Indications: Post-MI 1 Beta; 2 ACEI; CCB
HTN Compelling Indications: DM 1 ACEI; 2 Beta (for DM2); 3 Verapamil or clonidine
HTN Compelling Indications: Recurrent Stroke Prevention ACEI; Diuretic
JNC 8: in patients >60, start tx at: SBP >150 or DBP >90
JNC 8: in patients <60, start tx at: 140/90 (same used in pts >18 yo with either CKD or DM)
1stline (&2nd & 3rd) tx for uncomplicated isolated systolic HTN (elderly) 1) HCTZ; 2) Atenolol; 3) captopril or verapamil
HTN Compelling Indications: CKD 1 ACE; 2 BB (atenolol) or verapamil or HCTZ; 3 clonidine
Tx for BPH Prazosin +/- tamsulosin
Tx for migraine (w/HTN meds): 1 atenolol; 2 verapamil
Tx osteoporosis (w/HTN med): HCTZ
Tx for pre-op HTN Atenolol
1stline HTN tx in pregnancy 1 Methyldopa; 2 hydralazine
Pt just started on ACEI develops weakness. What test (lab, UA, CT, US) is most specific to dx pt? Renal US
HTN Tx in CVD BB
HTN Tx in DM ARB
Alternate to ACEI if CHF or other intolerance ARB
HTN tx if BP >20/10 over goal: 2 meds
Created by: Abarnard
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