92 terms

Cardiac Pharm


Terms in this set (...)

Heart Failure
Heart failure occurs when cardiac output is inadequate to provide the oxygen needed by the body

Heart failure may be low output (more common) or high output (rare)

insufficient cardiac output to adequately perfuse the tissues, despite normal filling of the heart
Most Common Cause of Heart Failure
The most common cause of heart failure is coronary artery disease
-Other risk factors contribute
Congestive heart failure:
combined right and left heart failure to produce pulmonary congestion and peripheral edema
Causes of Heart Failure

Valvular disease
-aortic valve disease
-mitral valve disease

Coronary artery disease
Most common
Most Common type of HF
Left sided
Systolic HF
(most common)
contractile failure of the ventricles with reduced EF and cardiac output
Diastolic HF
Often seen in normal aging, LVH, hypertrophic CM, restrictive CM and ischemic heart disease.
Know Classes and Stages of HF -slide 8
Clinical Presentation Due to excess fluid accumulation:
Dyspnea (most sensitive symptom)
Hepatic congestion
Orthopnea, Paroxysmal Nocturnal Dyspnea (PND)
Clinical Presentation Due to reduction in cardiac ouput:
Fatigue (especially with exertion)
Treatment of mild HF starts with an
angiotensin converting enzyme inhibitor (ACEI)
In addition to lifestyle changes
Increase cardiac output
By decreasing both arterial and venous resistance

Prevent the increase in angiotensin II (which is a vasoconstrictor) that is often present in HF
This decreases renovascular resistance

*Angiotensin II antagonists(ARBs) may not have the same benefits as ACE inhibitors
ACEI Decreases
load on the heart
patient symptoms
slow disease progression (esp in pts with LVF <40%)
ACEI Increases
inhibits ACE, interfering with conversion of angiotensin I to angiotensin II (which usually constrict vessels)
-This results in blood vessel relaxation & dilation
-Increases water and sodium excretion into urine
-These both lower BP
-Lower BP makes it easier for the heart to pump blood

Don't use with ARBs
ACEI Side Effects
AA patients 5x risk
Decreased renal fcn
Need to monitor BUN/Cr
ACEI Contraindications
& Lactation
Advanced renal disease
Hx of Angioedema
ACEI Dosing HF
Start low dose:
Captopril 6.25mg TID (target dose: 50mg TID)
*Enalapril- best drug for HF- 2.5 BID (target dose: 20mg BID)
Lisinopril 5mg QD (target dose: 40mg QD)

Titrate doses up as tolerated:
Higher doses shown to be very effective in treating HF
Angiotensin Receptor Blockers (ARBs)
ARBs block the binding of angiotensin-II to the angiotensin-II receptor
-Inhibits vasoconstriction effects of angiotensin-II
-Prevent the angiotensin-II-mediated release of aldosterone

ARBs indirectly inhibit fluid volume increases that would result from the actions of aldosterone

Reminder: Aldosterone promotes sodium and water retention (ARBs prevent release of Aldosterone which reduces Na+ and H2O retention)

Indications: Use ARBs only if ACEI is unable to be tolerated
ARB Drugs
Candesartan (Atacand)
*Irbesartan (Avapro)
*Losartan (Cozaar)
Telmisartan (Micardis)
*Valsartan (Diovan)
ARB Adverse Reactions
Same as ACEI
-No Cough
-Less risk of angioedema
ARB Contraindications
Pregnancy & Lactation
Advanced renal dz
Beta Blockers
Beta Blockers should only be added on when appropriate
-These drugs can initially cause acute decompensation of cardiac function

-Long-term studies have shown to improve the survival of stable patients with HF blocking the damaging effects of overactive sympathetic activity
Beta Blocker MOA
Blockade of Beta-1 receptors primarily located in cardiac tissue results in:
-decreased heart rate
-decreased contractility
-slowed AV conduction
-suppression of automaticity
Beta Blockers Drugs of Choice
Carvedilol (Coreg)- only indicated for HF
Bisprolol (Ziac)
Metoprolol succinate (Toprol XL)
Beta Blocker Side Effects
Decreased libido
Beta Blocker Caution
Patients must be tapered off B-blockers
abrupt cessation may cause MI, ventricular arrhythmia
Beta Blocker Contraindications
Severe bradycardia
2nd or 3rd degree heart block
Cardiogenic shock
Bronchial asthma
Beta Blocker Adverse Events
asthma exacerbation
Beta Blocker Dosing
Start with a low dose and gradually titrate up over wks-to-mos

Carvedilol (Coreg) 3.125mg BID (target: 25-50mg BID)

Bisoprolol (Ziac) 1.25mg QD (target: 5-10mg QD)

Metoprolol succinate (Toprol) 12.5mg -25mg QD (target: 200mg QD)

All 3 of these Beta Blockers have been shown to reduce mortality
Treatment of HF w/ fluid overload
Addition of Loop Diuretics (stage C or D)

Relieve signs and symptoms of volume overload
-dyspnea and peripheral edema

Improvement can occur within hours to days
-Reasonable weight loss goal of 1kg/day
-Monitor for adverse effects
Diuretic Therapy of CHF
Diuretic drugs are used to eliminate excess sodium and fluid retention*

Elimination of excess fluid allows the heart to function more efficiently

Diuretics can be administered with cardiac glycosides (digoxin) and other drugs used to treat CHF
Loop Diuretics Drugs
Furosemide (Lasix) - Drug of choice
Torsemide (Demadex)
Butenamide (Bumex)

However: some pts respond better to bumetanide or torsemide superior or more predictable absorption
Loop Diuretics MOA
inhibit the sodium-potassium-chloride cotransporter in the thick ascending limb
-Blocks tubular reabsorption of Na+ which leads to diuresis of water into urine
-Also leads to excretion of K+ and Chloride
Loop Diuretics Indications
Heart failure with volume overload
-Monitor electrolytes and renal fxn closely, replace potassium as needed
Loop Diuretics Side Effects
Urinary frequency*
Worsening kidney fcn
Loop Diuretics Contraindications
Hypersensitvity to sulfonylureas
Baseline electrolyte abnormality
Loop Diuretics Adverse Effects
Ototoxicity (if given with fast IV push)
Renal failure
Dosing for Loop Diuretics
-Furosemide (Lasix) 40-80mg QD
(MAX dose: 400mg QD)
-Torsemide (Demadex) 10mg QD (Max: 20-50mg)
-Bumetanide (Bumex) 1mg (Max: 2-3mg)

Diurese as you monitor for side effects
-IV is much more powerful

Long term use of furosemide is to prevent edema
-Diuretic use reduces mortality
-May add on Thiazide diuretics for synergy as needed
Aldosterone Antagonist
AKA: Potassium sparing diuretics

Indicated for use in pts with:
-NYHA functional class II HF and LVEF ≤30%
-NYHA functional class III to IV HF and LVEF <35%

*These pts must be carefully monitored for serum potassium and renal function
Potassium-sparing diuretic MOA
antagonizes distal convoluted tubule aldosterone receptors (potassium-sparing diuretic)
-increase urinary excretion of Na+ and H2O

Aldosterone Antagonist
Potassium-sparing diuretic Indications
Potassium-sparing diuretic Adverse Effects
Severe hyperkalemia
renal failure
Potassium-sparing diuretic Side Effects
Potassium-sparing diuretic Contraindications
renal impairment
Potassium-sparing diuretic dosing
Spironolactone & Eplerenone

Spironolactone (Aldactone) 12.5- 25 mg QD
(target: 50 mg QD)

Eplerenone (Inspra) 25 mg QD (target: 50 mg QD)

*MUST monitor electrolytes & kidney function *
Eplerenone :
fewer endocrine side vs spironolactone

Eplerenone is much more expensive
Endocrine side effects due to nonselective binding to androgen & progesterone receptors

Less expensive
Digoxin is a cardiac glycoside
-extracted from foxglove leaves (Digitalis sp)
-Most important inotropic drug
-Can increase cardiac output by 15%
-Positive inotropic agent enhances contractility
Digoxin Indications
-Atrial fibrillation
-NYHA functional class II, III, and IV symptoms
-Who are also taking ACEI, diuretics and Beta Blockers
Digoxin MOA
Inhibition of the Na+/K+ATPase mainly in myocardium
-Reverses Sodium-Calcium exchanger making more calcium ions available for contractile proteins in myocardium
-Increases contractions
Digoxin important note
Must be monitored on regular basis to avoid toxicity
-Narrow therapeutic range
-Therapeutic drug level is 0.5 to 2 ng/mL*
Digoxin Indirect Effects
Digoxin increases vagal activity and facilitates muscarinic transmission to the heart which:
-slows HR
-slows AV node conduction
-prolongs the refractory period of the AV node
Digoxin Adverse effects
visual disturbances (yellow-blue-green halos)*
blurred vision
toxicity (which can include seizures)*
Digoxin Dosing
Digoxin 0.125mg or less QD
-Based on renal function
-NEED to monitor dose
-Therapeutic serum digoxin levels range from 0.5-2 ng/mL
Hydralazine/Isosorbide dinitrate
Hydralazine plus oral nitrate therapy is recommended for patients with:
-Persistent NYHA class III to IV HF and LVEF <40 percent despite optimal therapy
-beta blocker, ACE inhibitor (or ARB), aldosterone antagonist (if indicated), and diuretics
-Especially if patient is Black*

Decreased mortality, lower rates of hospitalization, and improvement in quality of life*
Hydralazine MOA
hydralazine molecules combine with receptors in the endothelium of arterioles
-this causes relaxation of vascular smooth muscle (directly dilates peripheral vessels)
Hydralazine Side Effects
Hydralazine Adverse Effects
MI, neutropenia, SLE
Monitor ANA, CBC and Cr at baseline and periodically with ongoing treatment
Isosorbide dinitrate MOA
Vasodilator (nitrate family)
-relaxes smooth muscle via dilation of arterial and venous beds
-reduces both preload and afterload
-Reduces myocardial oxygen demand

Improves coronary collateral circulation
-lowering blood pressure
-increasing heart rate
Isosorbide dinitrate Adverse Effects
hypotension/orthostatic hypotension/syncope*
Hydralazine/Isosorbide dinitrate dosing
Start at low dose and titrate up every 2-4 weeks based on patient symptoms:
-Hydralazine 25 mg TID (target:75mg TID)
-Isosorbide dinitrate 20mg TID (target: 40mg TID)
-Hydralazine/Isorbide dinitrate (BiDil) 20/37.5mg QD (target TID) $$

Caution: dose should not be increased if symptomatic hypotension develops
Angina pectoris
- ischemia of the heart muscle as a result of coronary artery occlusion or blockage
Angina pectoris med goals
Medications are given to decrease work load of the heart and cardiac O2 demand
-This decreases chest pain
3 classes of Angina Pectoris meds
Beta Blockers
Calcium Channel Blockers
Nitrates MOA
considered 1st-line drugs:
MOA: Drugs stimulate the formation of nitric oxide which cause peripheral vasodilation
Nitrate Adverse Effects
reflex tachycardia
possible tolerance if 24hrs of continuous use
Multiple formulations: Sublingual, oral, transdermal, buccal, IV

IV: Sodium nitroprusside
used in severe cases & hypertensive emergencies
potential risk of cyanide toxicity

Onset and duration: dependent on route of administration
SL may last 35-45 minutes

Dose: Nitroglycerin SL tabs: 0.4mg Take 1 tablet SL at onset of sxs, may repeat up to 3 tabs max

Effective for treating/prevention of variant and unstable angina*
Beta Blockers angina
AHA recommends beta blockers as 1st line therapy to reduce anginal episodes & improve exercise tolerance in pts with ischemic heart disease
Beta Blockers relieve anginal sxs by
reducing heart rate and contractility
Beta blockers are the only antianginal drugs proven to
prevent reinfarction
improve survival in pts who have sustained MI
Since beta blockers reduce "heart rate-blood pressure product" during exercise:
onset of angina during exercise is delayed or avoided
Beta Blocker meds for angina
All types of beta blockers appear to be equally effective in exertional angina
-Atenolol or Metoprolol (cardioselective)
Do not use Beta Blockers in this type of angina
Prinzmetal or vasospastic angina
Calcium channel blockers are used in combo with Beta blockers when:
initial treatment with Beta blockers is not successful


as a substitute for a beta blocker when beta blockers cannot be used
Calcium channel blockers improve angina by
Causing coronary & peripheral dilation
Reducing contractility of the heart

The degree by which these changes occur depends on the type of CCB used
-Non-Dihydropiridines (Non-DHPs)
-Verapamil (Calan) or Diltiazem
CCB: Non-Dihydropiridine MOA
inhibits calcium ion influx into vascular smooth muscle and myocardium
-Dilating coronary arteries (more)
-Prolonging AV node refractory period (more)
-Relaxing smooth muscle (less)
-Decreasing peripheral vascular resistance (less)

Cause less vasodilation and more cardiac depression than DHP CCBs
CCB: Non-Dihydropiridine Indications
HTN, Angina, SVT, non-obstructive cardiomyopathy, rate control in a-fib
-Have negative effects at the SA and AV node*
-Cause reductions in heart rate and contractility*
-Verapamil has the most pronounced negative inotropic effect (reduces myocardial O2 demand)*
CCB: Non-Dihydropiridine Dosing
Diltiazem (Cardizem) CD 120-480mg/qd
Verapamil (Calan) 80-120 mg TID
CCB: Non-Dihydropiridine Side Effects
Edema (less)
CCB: Non-Dihydropiridine Contraindications
Severe LV dysfunction
2nd or 3rd degree heart block
CCB: Non-Dihydropiridine Adverse Events
Severe bradycardia
Heart block
Severe HYPOtension
Antiplatelet therapy

In the absence of contraindications, all pts should be treated with Aspirin
75mg-325mg QD
-Associated with best risk/benefit ration
Ranolazine (Ranexa)
Approved for the use in Chronic Stable Angina
-Often used in pts who cannot tolerate Nitrates*
Ranolazine (Ranexa) MOA
Exact MOA is unknown but seems to increase the efficiency of energy production in the heart
-This maintains cardiac function without reducing heart rate or blood pressure
Ranolazine (Ranexa) Adverse Effects
headaches, dizziness
Ranolazine (Ranexa) Dosing
Ranexa 500-1000mg PO BID
The pharmacologic management of the pt post MI aims to achieve several goals:
Chief among these is to prevent subsequent events - death, reinfarction, & rehospitalization

Secondary goals include:
-preventing arrhythmias
-minimizing left ventricular (LV) remodeling
-preventing progression to heart failure
All patients post MI require:
ACEI (or ARB if ACEI cannot be tolerated)
Antiplatelet therapy
-Aspirin (162-325mgQD)

Beta Blockers
-reduce short-term complications and improve long-term survival (STEMI and NSTEMI)
-Esp: Carvedilol (Coreg)
Aldosterone blockade
recommended long-term for patients post MI with
LVEF ≤40% and either symptomatic heart failure or diabetes
Pts with ACS and/or lipid abnormalities
Atorvastatin (Lipitor) 80mg qpm
Platelet inhibitors (P2Y12)
Clodipogrel (Plavix) 75mg QD
-In patients who cannot tolerate ASA
-OR need additional anticoagulation due to increased risk, procedures, etc...