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33 Cards in this Set
- Front
- Back
Causes of Systolic Dysfunction
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Reduction of functional mass
Dilated Cardiomyopathies Ventricular hypertrophy |
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Cause of Dystolic Dysfuncation
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Increased ventricular stiffness
Mitral or tricupsid valve stenosis Pericardial disease |
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Compensatory Mechanisms of the cardiac system
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Cardiac dilation
Activation of SNS (sympathetic nervous system) Activation of RAAS (renin-angiotensin-aldosterone system) Retention of water |
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Symptoms of Left-Sided HF
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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 |
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Symptoms of Right-Sided HF
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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 |
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New York Heart Association Functional Classification
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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. |
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ACC/AHA Stages
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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. |
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GOALS OF DRUG THERAPY IN THE TREATMENT OF HF
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Increase CO (ventricular emptying)
Decrease preload Decrease afterload Increase sodium and water excretion |
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ACE INHIBITORS IN THE TREATMENT OF HF
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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 |
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Ace Inhibitors ends with
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"pril"
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Dosing of ACE Inhibitors
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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 |
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Side-Effects of ACE Inhibitors
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Hypotension
Decline in renal function Hyperkalemia Cough Angioedema |
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ANGIOTENSIN RECEPTOR BLOCKERS (ARBs)
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Reserved for patients who do not tolerate ACE inhibitors
Losartan (Cozaar®) Candesartan (Atacand®) Valasartan (Diovan®) |
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HYDRALAZINE / NITRATE COMBINATION
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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 |
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Side-effects of Vasodilators
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Dizziness
Lightheadedness Orthostatic hypotension Tachycardia Flushing of face and neck Headache |
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DIURETICS IN THE TREATMENT OF HF
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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 |
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Loop Diuretics
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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® |
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Thiazide Diuretics
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Inhibits sodium reabsorption in the distal tubules
Causes increased secretion of: Water Sodium Potassium Examples:Hydrochlorothiazide (HydroDIURIL®), Metolazone (Zaroxolyn®) |
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Dosing of Diuretics
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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 |
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Side effects of Diuretics
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Electrolyte disturbances
Hypokalemia Hypomagnesemia Thirst Restlessness Constipation Hypotension Decline in renal function |
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ALDOSTERONE ANTAGONISTS
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Compete with aldosterone for receptors in distal renal tubules
Increase sodium and water excretion Examples: Spironolactone (Aldactone®) Eplerenone (Inspra®) AKA: Potassium-sparing diuretics |
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ALDOSTERONE ANTAGONISTS
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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 |
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Side Effects of Aldosterone Antagonists
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Hyperkalemia
Gynecomastia (spironolactone only) |
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BETA ADRENERGIC BLOCKING AGENTS
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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®) |
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BETA ADRENERGIC BLOCKING AGENTS
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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. |
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side effects of BETA ADRENERGIC BLOCKING AGENTS
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Hypotension
Bradycardia Bronchoconstriction Fluid Retention Worsening HF Heart Block |
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Digoxin
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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 |
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digitalization
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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
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Digoxin Pharmalogical properties
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Positive inotropic action
Increases myocardial systolic contraction Slows conduction through the AV node Sensitizes the heart to vagal stimulation |
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Digoxin absoroption and metabolism
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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 |
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Dogoxin Toxicity
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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 |
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Adverse effects/Signs of Digoxin Toxicity
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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 |
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DRUG SELECTION IN THE TREATMENT OF HF
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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 |