HTN & HF Flashcards
When to reassess BP
- 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
Isolated Systolic HTN (ISH)
SBP > 160, but DBP <90
mostly in elderly (>60yo)
Masked HTN
BP consistently high at home, but normal in office
Malignant HTN
mod-severe HTN leads to:
- retinopathy
- encephalopathy
- nephrosclerosis
- DBP > 120 usually, but can happen at 100 mmHg
Hypertensive Emergency vs Urgency
-
Emergency:
- DBP > 120, with evidence of acute organ damage; can be life-threatening
-
Urgency:
- DBP > 120 mmHg, asymptomatic, no evidence of acute organ damage
Major Causes of Secondary HTN
-
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
Complications of HTN
- LVH
- HF
- Ischemic Stroke
- Intra-cerebral Hemorrhage
- MI
- Ischemic Heart disease
- CKD & ESRD
Thiazides
-
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
*
Loop Diuretics
Loop Diuretics
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
K+ Sparing Diuretic
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
Aldosterone Antagonist
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
Selective Beta-blocker with positive intrinsic sympathomimetic activity
Acebutolol
can increase HTN due to the sympathetic activation
Indications for Dihydropyridines
HTN
Angina Pectoris
Indications for Verapamil & Diltiazem
Non-dihydropyridines
- HTN
- Angina
- Supraventricular arrhythmias
- A. Fib/Flutter
- Paroxysmal Supraventricular Tachycardia (PSVT)
How do Nifedipine, Diltiazem, & Verapamil affect Vasodilation, depression of cardiac contractility, depression of SA node/ AV node
Diltiazem & Verapamil = decrease velocity
ACE-Inhibitors
- 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
ARBs
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
Renin Inhibitors
-
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
Alpha-1 Blockers
- Doxazosin, Prazosin, Terazosin
-
Indications:
- Benign Prostatic Hyperplasia
-
SEs:
- syncope, dizziness, palpitations
-
Contraindications:
- Hypersensitivity
Direct Vasodilators
- Isosorbide dinitrate, hydralazine, minoxidil
-
Indications:
- heart failure with elevated BP
- (isosorbide dinitrate + hydralazine in African Americans)
- heart failure with elevated BP
-
SEs:
- Edema (minoxidil)
- Tachycardia
- Lupus-like syndrome (hydralazine)
-
Contraindications:
- hypersensitivity, pheochromocytoma, acute closure glaucoma, head trauma or cerebral hemorrhage
Central Alpha-2 Agonists
- 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
Drug Class Recommendations for Heart Failure
- Diuretic, aldosterone antagonist, Beta-Blocker, ACE-I, ARB, Direct Vasodilator
Drug Class Recommendations for Post-MI
- Aldosterone antagonist, BB, ACE-I
Drug Class Recommendations for High Coronary Disease Risk
Diuretic, Beta-Blocker, CCB, ACE-I
Drug Class Recommendation for Diabetes
Diuretic, Beta-blocker, CCB, ACE-I/ARB
Drug Class Recommendation for Chronic Kidney Disease
ACE-I, ARB
Tx of HTN + Diabetes
- ACE-I/ARB +/- CCB or thiazide
- Thiazide, CCB, ACE-I, or ARB
Tx of HTN + nonblack, no comorbidities
- Thiazide, CCB, ACE-I, or ARB
Tx of HTN + African American & no co-morbidities
- Thiazide or CCB
Tx of HTN + CKD
ACEI or ARB +/- CCB or thiazide
Tx of HTN + Stroke Hx
- ACE-I or ARB +/- CCB or thiazide
Tx of HTN + Heart failure
ACE-I or ARB + BB
Tx of HTN + CAD
ACEI or ARB + BB
When to have BP of pt re-checked after initiation of HTN therapy and what to do if not at goal
- 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
Tx of Chronic HTN in pregnancy
Methyldopa = first line therapy
- labetalol
- Beta-blockers
Compensatory Mechanisms of Heart Failure
- Frank-Starling Law: ability to change force of contraction and thus stroke volume in response to changes in venous return
- Neurohormonal Activation
- Ventricular Remodeling
ACCF/AHA Stages of HF: Structural Changes and Symptoms
-
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
Stage A Heart Failure Tx
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
Stage B Heart Failure Tx
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
What med classes do we give to ALL pts with reduced EF even if they do not have a hx of MI?
ACE-I & Beta-blockers
Effects of RAAS inhibitors
- Decrease ventricular remodeling
- Decrease myocardial fibrosis
- Decrease myocyte apoptosis
- Decrease cardiac hypertrophy
- Decrease NE release
- Decrease vasoconstriction
- Decrease Na/H20 absorption
- Increase vasodilation
Stage C Heart Failure Tx (HFrEF Stage C)
- 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
Hydralazine/Isosorbide Dinitrate
-
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
- Benefits in AAs
-
SEs:
- headache, dizziness & GI complaints → all due to vasodilation in periphery
Digoxin
-
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
Stage D Advanced (or End-Stage) Heart Failure Tx
- 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
-
MOA: stimulates Beta receptors on heart
-
Milrinone (Primacor):
-
MOA: inhibits the cAMP phosphodiesterase III isoenzyme
- increased intracellular ionized Ca2+ and heart contractile forces
- arrhythmogenic effects
-
MOA: inhibits the cAMP phosphodiesterase III isoenzyme
Sacubitril-Valsartan (Entresto)
-
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
