Heart Failure Flashcards
Goals of therapy
Improve QOL -Prevention of symptom onset -Reduction of sx and/or severity of sx Prolong survival Slow dz progression Prevent exacerbations -Reduce hospitalization Treat modifiable risk factors
Guidelines for HFpEF
Control BP
Use diuretics to control sx due to volume overload
Reasonable to have coronary revascularization in pts with angina/MI that is making HF worse
Manage a fib according to published guidelines
Stage A
Pts at high risk for HF
Not symptomatic and NO current evidence of structural heart dz
Stage A tx
Aggressive risk factor control
- Control HTN per current guideline recommendations
- Smoking cessation
- Control dyslipidemia per current guideline recommendations
- Increased physical activity
- Encourage weight loss if obese
- Control diabetes per current guideline recommendations
- Discourage EtOH and illicit drug use
Stage B
Pts with structural heart dz but are asymptomatic
-Previous MI, LV remodeling, low EF, valvular dz
Stage B tx
All txs for Stage A ACE inhibitor or ARB -Pts s/p ACS/MI or reduced EF BB (select medications) -Pts s/p ACS/MI or reduced EF
MOA of BBs
Inhibitor/block beta receptors
Net effect:
-Decreased sensivity to circulating catecholamines (SNS)
-Decreased HR/BP
Caution for BBs
Only initiate beta blocker when HF is stable and pt is euvolemic
HF indication for BBs
1st line for all pts with HFrEF
-Reduction in all-cause mortality, hospitalizations, improve EF
Not a class effect!! Only 3 meds indicated:
-Carvedilol
-Bisoprolol
-Metoprolol succinate
Goal dose carvedilol
25 mg PO BID (wt <85 kg)
50 mg PO BID (wt >85 kg)
Goal dose bisoprolol
10 mg PO daily
Goal dose metoprolol succinate
200 mg PO daily
Side effects of BBs
Depression Worsening HF sx Sexual dysfunction Alterations in glucose metabolism Bradycardia/hypotension Bronchospasm
HF indications for ACE inhibitors
1st line for all pts with HFrEF
-Reduction in all-cause mortality and hospitalizations, improved QOL, improved LV side and function, reduces likelihood of developing HF in at risk pts
MOA of ACE-Is
Block conversion of angiotensin I to angiotensin II
-Decreased vasoconstriction and cardiac remodeling
-Reduction in bradykinin breakdown (increased vasodilation)
Net effect:
-Arterial and venous vasodilation
-Reduction of preload and afterload (reduced workload on heart)
Absolute CIs for ACE-Is
Hx of angioedema secondary to ACE-I
Pregnancy (category X)
Bilateral renal artery stenosis
Relative CIs/SEs of ACE-Is
Cough Unilateral renal artery stenosis Renal insufficiency Hypotension Hyperkalemia
Additional facts of ACE-Is
0.5 increase in SrCr is fine, anything above, d/c and try again
K over 5.0, stop drug for a few weeks, and try again
ACE and ARBs are indicated in preventing nephropathy in DM
HF indication for ARBs
2nd line for all pts with HFrEF who cannot tolerate an ACE inhibitor
Reduction in all-cause mortality and hospitalizations, improved QOL
MOA of ARBs
Block the AT1 receptor to stop the actions of angiotensin II
Decreased vasoconstriction, aldosterone release, cellular growth promotion
Net effect:
-Arterial and venous vasodilation
-Reduction of preload and afterload (reduced workload on heart)
Situations when ACE and ARBs can be combined
Pt already on BB and ACE inhibitor AND Symptomatic AND Cannot take an aldosterone antagonist Carefully monitor K, SCr, BUN Should not combine ACE inhibitor, ARB and aldosterone antagonist
SEs of ARBs
Similar to ACE-Is
Not associated with cough
Can be considered if ACE-I associated angioedema
-Cross reactivity has been reported
Monitoring for ARBs
BUN, SCr, K, BP
Stage C
Pts with structural heart dz AND prior/current sx of HF
-Sx can be classified via NYHA system
Tx for Stage C
All tx for Stage A ACEI or ARB BB (select meds) Diuretics Devices -Biventricular pacing -Implantable defibrilators Can add spironolactone or bidil
HF indication for loop diuretics
Decreases sx associated with fluid retention
-Shown to decrease hospitalizations
Use in pts with hx of or current sx of fluid retention to maintain euvolemia
MOA of loop diuretics
Block Na reabsorption at the thick ascending loop of Henle
SEs of loop diuretics
Azotemia (increased BUN) Hypokalemia -Arrhythmias Hypomagnesemia AKI Ototoxicity Hypotension Hyperuricemia Hyponatremia Caution in true sulfonamide allergy
HF indication for aldosterone antagonist
Pts with stage II-IV HFrEF to reduce morbidity and mortality
MOA for aldosterone antagonists
Inhibits aldosterone
-Increased levels of aldosterone in HF to increase NA/H2O retention and “improve” CO
Weak diuretic effect
SEs of aldosterone antagonists
Hypotension
Hyperkalemia
Gynecomastia (spironolone only)
Breast tenderness/menstrual irregularities (spironolactone only)
Spironolactone initial dose
12.5-25 mg once daily
Target/max dose of spironolactone
25 mg once or twice daily
Monitoring for spironolactone and eplerenone
BP
Electrolytes (K)
Baseline
1 wk after starting or changing dose
Initial dose of eplerenone
25 mg once daily
Max/target dose of eplerenone
50 mg once daily
Caution in aldosterone antagonists
SCr >2.5 (men)
SCr >2.0 (women)
K >5.0
HF indication of hydralazine-isosorbide dinitrate
Pts with stage II-IV HFrEF to reduce morbidity and mortality
-First med to show mortality benefit
MOA of hydralazine-isosorbide dinitrate
Hydralazine
-Directly causes smooth muscle relaxation
-Net effect: reduced afterload
Isosorbide dinitrate
-Activation of guanylate cyclase that causes an increase in cGMP in vascular smooth muscle
-Net effect: reduced preload via venous vasodilation
Place of hydralazine-isosorbide dinitrate in therapy
Substitute in pts who cannot tolerate either an ACE inhibitor or ARB
-ACEI and ARBs are vasodilators that have higher mortality benefit than hydralazine/isosorbide dinitrate
Add-on therapy in pts self-described as AA who are on optimal therapy with ACE-I/ARB and BB but still symptomatic
-Prospective-randomized trial found more mortality benefit in this pt group
HF indication of digoxin
Add-on therapy in pts already on ACE-I/ARB, BB and other mortality benefiting meds who are still symptomatic
- Reduction in hospitalizations only
- No effect on mortality or dz progression
- -If levels >1.2 ng/mL may have increased relative risk of mortality
MOA of digoxin
Inhibition of Na/K ATPase pump in myocardial cells leads to increase in intracellular Na leads to increased Ca influx
- Neurohormonal modulation
- Net effect: Increased contractility (pos inotrope)
When to start with a lower dose in digoxin
Age >65-70 yo
CrCl <60 mL/min
Low lean body mass
Dosing of digoxin
0.125-0.25 mg PO once daily
Titrate to goal level of 0.5-0.9 ng/mL
Can dose every other day in decreased renal function
Monitoring of digoxin
If signs of toxicity, change in renal function, new drug interaction, dose change, after IV load (atrial fibrillation)
When is cardiac manifestation more likely in digoxin?
Decreased Mg, K, and Ca levels
Digoxin toxicity
Associated with levels >2.0 ng/mL Fatigue/weakness Confusion Delirium Psychosis N/V/anorexia Visual disturbances -Halos, photophobia, red-green/yellow-green vision Arrhythmias -Vtach, vfib, AV block, sinus brady
Reversal agent for digoxin
Digibind
Antibody that binds digoxin to be excreted via kidneys
Stage D
Pts with significant sx at rest even though on optimal and maximum medical therapy
Stage D tx
All txs for Stage A-C Heart transplant Chronic inotropic meds Mechanical support Palliative care/hospice
Causes of HF exacerbation
ACS Med nonadherence Na/fluid restriction nonadherence Uncontrolled BP A fib Addition of drugs that worsen HF Pulmonary embolus Infection Excessive EtOH use
Warm and dry characteristics
Nl pt
Warm and wet characteristics
Congestion
Cold and dry characteristics
Hypoperfusion
Cold and wet characteristics
Congestion and hypoperfusion
Cardiac index is low
S/sx of ADHF (acute decompensated HF)
Hypoperfusion -Cool extremities -Sleepy -Declining Na levels Congestion -Orthopnea -DOE -High JVP -Pulmonary edema -Peripheral edema -Elevated BNP -Weight gain
Goals of tx of ADHF
Correct underlying precipitating factor Relieve the pt's sx Improve hemodynamics -Optimize chronic oral med regimen -Educate pt on adherence to lifestyle modifications and drug regimen
Tx of warm and wet
Loop diuretics
+/- vasodilators
Tx of cold and dry
Pos inotropes
+/- fluid replacement
Tx of cold and wet
Mixture of diuretics, vasodilators, inotropes
Diuretics with warm and wet
IV furosemide, bumetanide, torsemide
Cautions for diuresing in ADHF
Excessive preload reduction can cause decreased CO
-Reflex increase in sympathetic tone
Over-diuresis can cause AKI
-Monitor SCr/BUN daily to assess intravascular volume depletion
Electrolyte depletion
-Monitor and replete K and Mg
Diuretic resistance
Failure to decrease weight by 0.5 kg (neg fluid balance of 500 mL) after several IV diuretic doses
Strategies to overcome diuretic resistance
Increase dose of the diuretic
Increase frequency of diuretic administration
Change to continuous infusion of loop diuretic
Change loop diuretic (furosemide to bumetanide)
Combine to loop diuretic with thiazide diuretic
Effects of vasodilators for warm and wet
Decreased arterial tone causing decreased SVR and increased CO
Decreased wedge pressure and ventricular workload
Nitroprusside dose
0.25-3 mcg/kg/min
Nitroprusside pearls
Potent venous and arterial vasodilator
Cyanide and thiocyanate toxicity
-Esp in hepatic/renal insufficient and/or >3 days administration and/or receiving high doses
Monitor: BP, HR, liver and kidney
Nitro dose
5-200+ mcg/min
Nitro pearls
Primary venous vasodilator
Tolerance after 12 hrs requiring escalating doses
Adverse effects: HA, hypotension, tachycardia
Monitor: BP, HR, ECG, change in ischemic sx
Nesiritide dose
Bolus: 2 mcg/kg
Infusion: 0.01 mcg/kg/min
Nesiritide pearls
Recombinant BNP
Improves dyspnea and fatigue
Adverse effect: hypotension
