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33 Cards in this Set

  • Front
  • Back
Causes of Systolic Dysfunction
Reduction of functional mass
Dilated Cardiomyopathies
Ventricular hypertrophy
Cause of Dystolic Dysfuncation
Increased ventricular stiffness
Mitral or tricupsid valve stenosis
Pericardial disease
Compensatory Mechanisms of the cardiac system
Cardiac dilation
Activation of SNS
(sympathetic nervous system)
Activation of RAAS
(renin-angiotensin-aldosterone system)
Retention of water
Symptoms of Left-Sided HF
Dyspnea - Difficult breathing
Orthopnea - Difficult breathing except when sitting or standing up
Paroxysmal nocturnal dyspnea (PND) - an urgent form of respiratory distress that occurs during sleep
Symptoms of Right-Sided HF
Peripheral edema - excess accumulation of fluid in the peripheral tissue spaces
Hepatomegaly - enlarged liver
Jugular venous distention (JVD) - enlargement of the jugular veins of the neck due to internal pressure
Hepatojugular reflux (HJR) - distention of the jugular veins of the neck resulting from abdominal compressions
Exercise intolerance
Weight gain
New York Heart Association Functional Classification
I: No symptoms and no limitations.
II: Mild symptoms and slight limitation. Comfortable at rest.
III: Marked limitation in activity due to symptoms, even during mild activity. Comfortable only at rest.
IV: Severe limitations. Experience symptoms while at rest.
ACC/AHA Stages
Stage A:
At high risk. No structural disease or symptoms.
Stage B:
Structural disease without symptoms.
Stage C:
Structural disease with symptoms.
Stage D:
Advanced disease with marked symptoms at rest.
Requires specialized interventions.
GOALS OF DRUG THERAPY IN THE TREATMENT OF HF
Increase CO (ventricular emptying)
Decrease preload
Decrease afterload
Increase sodium and water excretion
ACE INHIBITORS IN THE TREATMENT OF HF
Venous and arterial dilating properties
Potent inhibitor of angiotensin-converting enzyme which is a vasoconstrictor
Clinical Benefit of ACE inhibitors
Multiple, large, prospective, randomized trials have consistently demonstrated a significant reduction in mortality
Play a role in cardiac remodeling and hemodynamic changes that result from decreased cardiac output
Ace Inhibitors ends with
"pril"
Dosing of ACE Inhibitors
Begin with low dose and titrate up
Reduces complications (e.g. hypotension, azotemia)
If tolerated, the dose is titrated up
Enalipril 10mg bid
Captopril 50mg tid
Lisinopril 40mg daily
Higher doses were used in the studies
Side-Effects of ACE Inhibitors
Hypotension
Decline in renal function
Hyperkalemia
Cough
Angioedema
ANGIOTENSIN RECEPTOR BLOCKERS (ARBs)
Reserved for patients who do not tolerate ACE inhibitors
Losartan (Cozaar®)
Candesartan (Atacand®)
Valasartan (Diovan®)
HYDRALAZINE / NITRATE COMBINATION
Clinical Benefits of Vasodilators
Hydralazine in combination with a nitrate may prolong survival in HF
Only use in patients who do not tolerate an ACE inhibitor or ARB
Vasodilators:
Hydralazine (started at 25 mg TID and titrated upward to 100 mg TID) and
Isosorbide Dinitrate (40 mg TID or QID)
Large number of tablets required and greater incidence of ADRs can result in non-compliance
Isosorbide dinitrate (Isordil®)
Hydralazine (Apresoline®)
Combination product (BiDil®)
Approved in 2005 only for African Americans
Side-effects of Vasodilators
Dizziness
Lightheadedness
Orthostatic hypotension
Tachycardia
Flushing of face and neck
Headache
DIURETICS IN THE TREATMENT OF HF
Sodium and water retention lead to the common congestive symptoms of pulmonary and peripheral edema.
Clinical Benefit of Diuretics
Reduction of fluid overload.
Improvement in symptoms can occur within hours to days
Loop Diuretics
Inhibit reabsorption of sodium and chloride in the ascending Loop of Henle
Causes increased excretion of:
Water
Sodium
Chloride
Magnesium
Potassium
Examples:
Furosemide (Lasix®)
Bumetanide (Bumex®
Thiazide Diuretics
Inhibits sodium reabsorption in the distal tubules
Causes increased secretion of:
Water
Sodium
Potassium
Examples:Hydrochlorothiazide (HydroDIURIL®), Metolazone (Zaroxolyn®)
Dosing of Diuretics
For volume overload
Reasonable goal is weight reduction of 0.5 to 1.0 kg/day.
A loop diuretic:
Control pulmonary and/or peripheral edema.
Thiazide diuretics (hydrochlorothiazide, metolazone)
Can be given 30 minutes prior to loop diuretic
Added synergistic effect
Side effects of Diuretics
Electrolyte disturbances
Hypokalemia
Hypomagnesemia
Thirst
Restlessness
Constipation
Hypotension
Decline in renal function
ALDOSTERONE ANTAGONISTS
Compete with aldosterone for receptors in distal renal tubules
Increase sodium and water excretion

Examples:
Spironolactone (Aldactone®)
Eplerenone (Inspra®)

AKA: Potassium-sparing diuretics
ALDOSTERONE ANTAGONISTS
In RALES study (NEJM 9/2/99) spironolactone demonstrated a decrease in mortality in patients with severe HF

Eplerenone can improve survival of:
stable patients with left ventricular systolic dysfunction (EF<40%)
clinical evidence of HF after an acute MI
Side Effects of Aldosterone Antagonists
Hyperkalemia
Gynecomastia (spironolactone only)
BETA ADRENERGIC BLOCKING AGENTS
Antagonize the increase in sympathetic nervous system activity responsible for the progression of heart failure
May decrease the energy requirements of the heart by decreasing HR and blood pressure
Examples:
Carvedilol (Coreg®)
Metoprolol sustained release (Toprol XL®)
Bisoprolol (Zebeta®)
BETA ADRENERGIC BLOCKING AGENTS
Carvedilol, metoprolol, and bisoprolol have shown to decrease:
Symptoms
Risk of death
Hospitalizations
Beta blockers with intrinsic sympathomimetic activity (such as pindolol and acebutolol) should be avoided.
Need to start with very low doses.
side effects of BETA ADRENERGIC BLOCKING AGENTS
Hypotension
Bradycardia
Bronchoconstriction
Fluid Retention
Worsening HF
Heart Block
Digoxin
Digoxin therapy may cause:
Decrease hospitalizations for HF
Reduction in symptoms of HF
Increase exercise tolerance
No benefit in terms of overall mortality
Digoxin improves symptoms of HF by:
Increasing CO
More complete systolic emptying
Reducing preload
Reducing sympathetic tone
digitalization
The administration of digoxin (either rapidly or slowly) until sufficient amounts of the drug have accumulated in the body to produce a therapeutic response without signs and symptoms of toxicity
Digoxin Pharmalogical properties
Positive inotropic action
Increases myocardial systolic contraction
Slows conduction through the AV node
Sensitizes the heart
to vagal stimulation
Digoxin absoroption and metabolism
Absorption
Tablets and elixir are 60-85% absorbed following oral administration
Digoxin encapsulated solution (Lanoxicaps) 90-100% absorbed
Many drugs can inhibit absorption
Metabolism and excretion
Primarily excreted in the urine as unchanged drug
Requires dosage decrease in patients with renal failure
Dogoxin Toxicity
Therapeutic plasma levels: 0.5-0.8 ng/ml
Toxicity does not correlate with digoxin levels
Infants require and tolerate higher levels of digoxin
Hypokalemia, hypomagnesemia, and hypercalcemia may predispose patients to digoxin toxicity
Adverse effects/Signs of Digoxin Toxicity
GI
anorexia, nausea, vomiting
CNS
headache, fatigue, malaise, drowsiness
disorientation, confusion, depression
color vision changes
Cardiotoxicity
May occur with or without other toxic signs
Manifested as all types of cardiac arrhythmias
DRUG SELECTION IN THE TREATMENT OF HF
All patients with HF (LV systolic dysfunction) need an ACE inhibitor
Unless contraindication or intolerance is present
Effective for prevention of HF in high risk patients (recovery phase post-MI)
All patients with stable NYHA class II or III HF should receive a beta-blocker
Use a loop diuretic in combination with an ACE inhibitor and a Beta-blocker.
Spironolactone should be used in patients with severe HF
Digoxin is reserved for symptomatic patients on ACEI/BB/diuretic