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NRS 271B > HTN & HF > Flashcards

HTN & HF Flashcards

1
Q

When to reassess BP

A
  • If normal:
    • 1 year
  • if elevated (120-129/<80):
    • 3-6months
  • if stage 1: (130/80- 139/89)
    • ASCVD ≥ 10% = 1 month
    • ASCVD <10% =3-6 months
  • if stage 2: (≥ 140/90)
    • 1 month
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2
Q

Isolated Systolic HTN (ISH)

A

SBP > 160, but DBP <90

mostly in elderly (>60yo)

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3
Q

Masked HTN

A

BP consistently high at home, but normal in office

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4
Q

Malignant HTN

A

mod-severe HTN leads to:

  • retinopathy
  • encephalopathy
  • nephrosclerosis
  • DBP > 120 usually, but can happen at 100 mmHg
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5
Q

Hypertensive Emergency vs Urgency

A
  • Emergency:
    • DBP > 120, with evidence of acute organ damage; can be life-threatening
  • Urgency:
    • DBP > 120 mmHg, asymptomatic, no evidence of acute organ damage
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6
Q

Major Causes of Secondary HTN

A
  • Medications:
    • oral contraceptives (high in estrogen)
    • NSAIDS, TCA, & SSRIs
    • Glucocorticoids
    • decongestants
    • EPO
    • Cyclosporin
    • Stimulants
  • illicit drugs: cocaine, meth
  • primary aldosteronism: HTN + HypoK + metabolic alkalosis
  • Obstructive Sleep Apnea
  • Endocrine disorders
  • Pheochromocytoma: catecholamine secreting tumor
  • Renal Vascular Stenosis
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7
Q

Complications of HTN

A
  • LVH
  • HF
  • Ischemic Stroke
  • Intra-cerebral Hemorrhage
  • MI
  • Ischemic Heart disease
  • CKD & ESRD
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8
Q

Thiazides

A
  • The med names:
    • Hydrochlorothiazide,Chlorothiazide, Chlorthalidone (x2 as potent as HCTZ), Metolazone (10x as potent as HCTZ), Indapamide (10x as potent as HCTZ), Methyclothiazide
  • MOA: act on the distal convoluted tubule and inhibit Na+ reabsorption via the NaCl pump
  • SEs:
    • dose related
    • hypoK+ and hypoMg, hyper Ca2+
    • hyperuricemia → gout flare
    • hyperglycemia
    • increase TGs → decrease efficacy of fibrates
    • limited efficacy when CrCl <30mL/min
      *
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9
Q

Loop Diuretics

A
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10
Q

Loop Diuretics

A

40mg furosemide = 20 mg torsemide = 1 mg bumetanide

ethacrynic acid = indicated in pts with sulfa allergy

  • SEs:
    • HypoNa, HypoK, Hypo Mg, HypoCa
    • potential sulfa allergy contra-indication → use ethacrynic acid
  • torsemide and bumetanide have a greater bioavailability and duration than furosemide
  • 40mg furosemide IV → response in 30min - 1 hour (output ≥ 1mL/kg/hr)
  • can double dose if AKI pt with fluid overload is not initially responsive → if still not responsive then add thiazide
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11
Q

K+ Sparing Diuretic

A

Amiloride & Triamterene

  • MOA:
    • inhibits the sodium potassium exchange in the distal tubule by selectively blocking sodium transport
  • often used together with K+ wasting diuretics
  • have modest diuresis
  • contribute to hyperK+
  • DDI:
    • ACE, ARB, K-supplementation, NSAIDs
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12
Q

Aldosterone Antagonist

A

Spironolactone & Eplerenone

  • Indications:
    • Used together with thiazide or loop diuretic
    • low dose + ACE-I or ARB for resistant HTN
  • SEs:
    • gynecomastia
    • hyperK+
    • eplerenone minimally affects androgens and progesterone compared to spironolactone
  • Contraindications:
    • CrCl <50ml/min for HTN
    • Scr >1.8 in females
    • Scr >2 in males
    • DM with microalbuminuria
    • K >5.5 mg/dL
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13
Q

Selective Beta-blocker with positive intrinsic sympathomimetic activity

A

Acebutolol

can increase HTN due to the sympathetic activation

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14
Q

Indications for Dihydropyridines

A

HTN

Angina Pectoris

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15
Q

Indications for Verapamil & Diltiazem

A

Non-dihydropyridines

  • HTN
  • Angina
  • Supraventricular arrhythmias
    • A. Fib/Flutter
    • Paroxysmal Supraventricular Tachycardia (PSVT)
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16
Q

How do Nifedipine, Diltiazem, & Verapamil affect Vasodilation, depression of cardiac contractility, depression of SA node/ AV node

A

Diltiazem & Verapamil = decrease velocity

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17
Q

ACE-Inhibitors

A
  • meds that end in “pril” → most common: captopril, enalapril, lisinopril
  • Dosing: initiate at a low dose with gradual titration to target doses (or max tolerated dose)
  • SEs: (Caused by increased Bradykinin)
    • CHAD has a cough
    • Cough, Hyperkalemia, Hyperuremia (monitor serum creatinine→ only allow increase of 30% or creatinine > 3mg/dL; and BUN)
    • Angioedema, Dose 1 syncope/hypotension
  • Contraindications:
    • Pregnancy
    • Bilateral Renal Artery Stenosis
    • K > 5.5 mEq/L
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18
Q

ARBs

A

Angiotensin-2 Receptor Blockers

end in “sartan” → Losartan, Valsartan, Candesartan

  • Only Losartan & Valsartan = approved for Heart Failure
  • Dosing: initiate at a low dose with gradual titration to target doses (or max tolerated dose)
  • SEs: Same as ACE-I WITHOUT the cough
    • Hyperkalemia, Hyperuremia (monitor serum creatinine & BUN)
    • angioedema, dose 1 hypotension/syncope
  • Contraindications:
    • Pregnancy
    • Hypersensitivity
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19
Q

Renin Inhibitors

A
  • Aliskiren (Tekturna)
    • first in class
    • MOA: directly blocks renin → reduce plasma renin activity
    • monitor serum K+, kidney fxn – similar to ACEI/ARBs
    • caution with renal dysfxn & stenosis
    • Pregnancy Cat. D – may cause harm to fetus
  • Aliskiren/amlodipine/ HCTZ
  • Aliskiren/Amlodipine
  • Aliskiren/ HCTZ
20
Q

Alpha-1 Blockers

A
  • Doxazosin, Prazosin, Terazosin
  • Indications:
    • Benign Prostatic Hyperplasia
  • SEs:
    • syncope, dizziness, palpitations
  • Contraindications:
    • Hypersensitivity
21
Q

Direct Vasodilators

A
  • Isosorbide dinitrate, hydralazine, minoxidil
  • Indications:
    • heart failure with elevated BP
      • (isosorbide dinitrate + hydralazine in African Americans)
  • SEs:
    • Edema (minoxidil)
    • Tachycardia
    • Lupus-like syndrome (hydralazine)
  • Contraindications:
    • hypersensitivity, pheochromocytoma, acute closure glaucoma, head trauma or cerebral hemorrhage
22
Q

Central Alpha-2 Agonists

A
  • Methyldopa, clonidine, guanabenz, guanfacine (also used for ADHD)
  • SEs:
    • hepatotoxicity, hemolytic anemia, peripheral edema (methyldopa)
    • Orthostatic Hypotension (methyldopa, clonidine)
    • Dry mouth, muscle weakness (clonidine)
    • Abrupt D/c of clonidine → severe rebound HTN
      • beta-blocker + clonidine → taper BB off first then clonidine
23
Q

Drug Class Recommendations for Heart Failure

A
  • Diuretic, aldosterone antagonist, Beta-Blocker, ACE-I, ARB, Direct Vasodilator
24
Q

Drug Class Recommendations for Post-MI

A
  • Aldosterone antagonist, BB, ACE-I
25
Q

Drug Class Recommendations for High Coronary Disease Risk

A

Diuretic, Beta-Blocker, CCB, ACE-I

26
Q

Drug Class Recommendation for Diabetes

A

Diuretic, Beta-blocker, CCB, ACE-I/ARB

27
Q

Drug Class Recommendation for Chronic Kidney Disease

A

ACE-I, ARB

28
Q

Tx of HTN + Diabetes

A
  1. ACE-I/ARB +/- CCB or thiazide
  2. Thiazide, CCB, ACE-I, or ARB
29
Q

Tx of HTN + nonblack, no comorbidities

A
  • Thiazide, CCB, ACE-I, or ARB
30
Q

Tx of HTN + African American & no co-morbidities

A
  • Thiazide or CCB
31
Q

Tx of HTN + CKD

A

ACEI or ARB +/- CCB or thiazide

32
Q

Tx of HTN + Stroke Hx

A
  • ACE-I or ARB +/- CCB or thiazide
33
Q

Tx of HTN + Heart failure

A

ACE-I or ARB + BB

34
Q

Tx of HTN + CAD

A

ACEI or ARB + BB

35
Q

When to have BP of pt re-checked after initiation of HTN therapy and what to do if not at goal

A
  • Reassess in 2-3 weeks
    • if not at goal: assess adherence to drugs, lifestyle changes
    • Increase dose, or add thiazide, CCB, ACE-I, or ARB
  • monitor q 2-3 weeks and increase dose/add agent until controlled
36
Q

Tx of Chronic HTN in pregnancy

A

Methyldopa = first line therapy

  • labetalol
  • Beta-blockers
37
Q

Compensatory Mechanisms of Heart Failure

A
  • Frank-Starling Law: ability to change force of contraction and thus stroke volume in response to changes in venous return
  • Neurohormonal Activation
  • Ventricular Remodeling
38
Q

ACCF/AHA Stages of HF: Structural Changes and Symptoms

A
  • Stage A:
    • At high risk for HF but without structural heart disease or symptoms of HF
  • Stage B:
    • Structural heart disease but without signs or symptoms of HF
  • Stage C:
    • Structural heart disease with prior or current symptoms of HF
  • Stage D:
    • Refractory HF requiring specialized interventions
39
Q

Stage A Heart Failure Tx

A

High risk but no structural changes or s/sxs

  • HTN & lipid disorders should be controlled
  • Other conditions should be managed such as:
    • obesity, DM, tobacco use, & known cardiotoxic agents
40
Q

Stage B Heart Failure Tx

A

Structural heart disease but without signs or symptoms of HF

  • in all pts with a recent or remote hx of MI or ACS and reduced EF
  • ACE-I
    • to prevent symptomatic HF and reduce mortality
  • Beta-Blockers
  • Statins
    • to prevent symptomatic HF and cardiovascular events
  • Non-dihydropyridine CCBs with negative inotropic effects:
    • May be harmful in asymptomatic patients with low LVEF and no sxs of HF after MI
41
Q

What med classes do we give to ALL pts with reduced EF even if they do not have a hx of MI?

A

ACE-I & Beta-blockers

42
Q

Effects of RAAS inhibitors

A
  • Decrease ventricular remodeling
  • Decrease myocardial fibrosis
  • Decrease myocyte apoptosis
  • Decrease cardiac hypertrophy
  • Decrease NE release
  • Decrease vasoconstriction
  • Decrease Na/H20 absorption
  • Increase vasodilation
43
Q

Stage C Heart Failure Tx (HFrEF Stage C)

A
  • ACE-I or ARB and Beta-blocker
    • For all volume overload NYHA class II-IV pts: Loop diuretics
    • For persistently symptomatic African Americans, NYHA class III-IV add: hydralazine + long-acting nitrates
    • For NYHA class II-IV patients add: Aldosterone Antagonists (eplerenone, spironolactone) Provided estimated creatinine > 30mL/min and K+ < 5.0 mEg/dL
44
Q

Hydralazine/Isosorbide Dinitrate

A
  • MOA:
    • hydralazine: direct arterial vasodilator (decreases afterload)
    • Isosorbide Dinitrate: venodilator (decreases preload)
  • Clinical Considerations:
    • Benefits in AAs
      • decreased rate of the first hospitalization for HF
      • improved quality of life score
      • useful in pts unable to tolerate RAAS inhibitors
  • SEs:
    • headache, dizziness & GI complaints → all due to vasodilation in periphery
45
Q

Digoxin

A
  • MOA: inhibits the Na-K ATPase
    • leads to positive inotropic (contractility) effects
    • parasympathomimetic actions (increased vagal tone), decreased RAAS output
  • Dosing: 125-250 mcg/day
    • loading dose not required for managing HF
  • Adverse Effects:
    • CNS (dizziness, HA, confusion), GI intolerance (N/V)
    • toxicity can occur at any level (frequently >2ng/mL)
  • Monitoring:
    • electrolytes (Ca, Mg, K), vital signs (BP&HR), digoxin serum levels
  • Indications:
    • symptom improvement
46
Q

Stage D Advanced (or End-Stage) Heart Failure Tx

A
  • tx s/sxs of fluid retention
  • evaluate need for cardiac transplant or medical intervention (LV assist device)
  • consider use of positive inotropes IV in outpatient setting

Positive Inotropic Therapy:

  • Dobutamine (Dobutrex):
    • MOA: stimulates Beta receptors on heart
      • mild chronotropic, vasodilative & arrhythmogenic effect
  • Milrinone (Primacor):
    • MOA: inhibits the cAMP phosphodiesterase III isoenzyme
      • increased intracellular ionized Ca2+ and heart contractile forces
      • arrhythmogenic effects
47
Q

Sacubitril-Valsartan (Entresto)

A
  • MOA: Neprilysin (enzyme that breaks down BNP) inhibitor and angiotensin receptor blocker
    • Increased levels of vasoactive peptides, including natriuretic peptides, bradykinin, and adrenomedullin
  • Clinical Considerations:
    • mortality benefiting therapy
    • reduced cardiovascular-related hospitalization
    • fetal-toxicity – d/c as soon as pregnancy is detected
  • Contraindicated:
    • Hx of angioedema; concomitant use of ACEI or aliskiren

NRS 271B (10 decks)

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