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88 Cards in this Set
- Front
- Back
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WHAT ARE THE MANAGEMENT GOALS WITH HEART FAILURE?
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IMPROVE PATIENT QUALITY OF LIFE; INCREASE THE ABILITY TO ENGAGE IN SYMPTOM FREE ACTIVITY
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WHAT IS THE DEFINITION OF HEART FAILURE?
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THE HEART FAILS TO PUMP SUFFICIENT BLOOD TO MEET METABOLIC OUTPUT
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WHAT IS HIGH OUTPUT?
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HEART PUMPS NORMAL VOLUME BUT METABOLIC DEMAND IS ABOVE NORMAL
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CONDITIONS THAT CAUSE HIGH OUTPUT
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THYROTOXICOSIS, SEVERE ANEMIA, AND PHEOCHROMOCYTOMA
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WHAT IS LOW OUTPUT?
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HEART PUMPING VOLUME IS DIMINISHED AND CAN'T MEET NORMAL METABOLIC NEEDS (MAJORITY OF HF CASES)
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SYSTOLIC DYSFUNCTION
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INADEQUATE FORCE TO EJECT BLOOD, DECREASED CONTRACTILITY,
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SYMPTOMS OF LEFT VENTRICULAR FAILURE
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DYSPNEA ON EXERTION, ORTHOPNEA, PAROXYSMAL NOCTURNAL DYSPNEA, COUGH
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SIGNS OF LEFT VENTRICULAR HEART FAILURE
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S3 GALLOP, ELEVATED PULMONARY VENOUS PRESSURE, PULMONARY EDEMA, CARDIAC ENLARGEMENT
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MOST COMMON FORM OF LOW OUTPUT HEART FAILURE
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LEFT VENTRICULAR FAILURE
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SYMPTOMS OF RIGHT VENTRICULAR FAILURE
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ANOREXIA, ABDOMINAL PAIN, CONSTIPATION, AND BLOATING
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SIGNS OF RIGHT VENTRICULAR HEART FAILURE
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ELEVATED VENOUS PRESSURE, PERIPHERAL EDEMA, JUGULAR VEIN DISTENTION, HEPATOMEGALY, ASCITES
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SYMPTOMS OF BIVENTRICULAR FAILURE
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NONSPECIFIC- REDUCED EXERCISE TOLERANCE, FATIGUE, WEAKNESS
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SIGNS OF BIVENTRICULAR FAILURE
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TACHYCARDIA, PALLOR, CYANOSIS OF DIGITS
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`IN CHRONIC HEART THERAPY, WHAT IS THE ONLY CURE?
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HEART TRANSPLANT
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TREATMENT FOR HEART FAILURE INCLUDES (3)
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TREAT THE UNDERLYING CAUSE (SURGICAL CORRECTION OF ABNORMALITY OR MEDICAL TREATMENT OF HYPERTENSION); MINIMIZE PRECIPITATING FACTORS THAT WORSEN HF (ARRHYTHMIAS, DRUGS, AND ANEMIAS); DRUG THERAPY TO CONTROL HF AND IMPROVE SURVIVAL
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HF CLASS I
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ASYMPTOMATIC
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HF CLASS II
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SYMPTOMATIC WITH MODERATE ACTIVITY
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HF CLASS III
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SYMPTOMATIC WITH MILD ACTIVITY
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HF CLASS IV
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SYMPTOMATIC AT REST
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MEASURES THAT CAN REDUCE HF SYMPTOMS IN PATIENTS IN CLASS I THROUGH III
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REGULAR EXERCISE, LIMIT SALT TO 6 G PER DAY, REDUCE ALCOHOL INTAKE, AVOID EXCESSIVE FLUID INTAKE, STOP SMOKING
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DRUG MANAGEMENT OF TYPE I THROUGH III INVOLVES WHAT REGIMENT?
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ACE INHIBITORS (MAINSTAY), +/- DIURETICS, BETA BLOCKERS, +/- DIGOXIN, ALDOSTERONE ANTAGONIST
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DESCRIBE HOW NOREPINEPHRINE CONTRIBUTES TO VENTRICULAR HYPERTROPHY AND REMODELING
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NOREPINEPHRINE CAUSES TACHYCARDIA AND VASOCONSTRICTION; EXCESSIVE AMOUNTS CAUSE DOWN REGULATION OF B RECEPTORS LEADING TO REDUCED RECEPTOR STIMULATION CONTRIBUTING TO VENTRICULAR HYPERTROPHY AND REMODELING
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DESCRIBE HOW ANGIOTENSIN II CONTRIBUTES TO VENTRICULAR HYPERTROPHY AND REMODELING?
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IT CAUSES VASOCONSTRICTION AND FACILITATES THE RELEASE OF NOREPINEPHRINE; IT PROMOTES NA RESTRICTION BY DIRECT EFFECTS ON RENAL TUBULES AND BY ALDOSTERONE RELEASE
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THE HORMONES RESPONSIBLE FOR THE VICIOUS CYCLE THAT ALLOWS FOR REMODELING OF THE HEART AND VENTRICULAR HYPERTROPHY
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NOREPINEPHRINE, ANGIOTENSIN II, VASOPRESSIN, ENDOTHELIN, TNF-A, ALDOSTERONE, BNP
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WHAT IS ANOTHER NAME FOR VASOPRESSIN?
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ADH
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WHAT IS ENDOTHELIN (GENERAL FUNCTION)?
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A POTENT VASOCONSTRICTOR
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WHAT IS TNF-ALPHA (GENERAL FUNCTION)?
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INFLAMMATORY CYTOKINE
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WHAT IS ALDOSTERONE'S GENERAL FUNCTION AND WHAT DOES IT CAUSE IN HEART FAILURE?
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CAUSES SODIUM AND WATER RETENTION; PRODUCES INTERSTITIAL CARDIAC FIBROSIS WHICH DECREASES SYSTOLIC AND DIASTOLIC FUNCTION
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WHAT IS THE FUNCTION OF HUMAN B-TYPE NATRIURETIC PEPTIDE?
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INCREASES RESPONSE TO STRESS AND STRETCH OF THE VENTRICLES (IT SENSES INCREASED PRELOAD); CAUSES VASODILATION OF THE ARTERIES, VEINS, AND CORONARY ARTERIES; DECREASES ALDOSTERONE, ENDOTHELIN, AND NOREPINEPHRINE; RENALLY INCREASES DIURESIS AND NATURESIS
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WHAT STIMULATES RENIN RELEASE FROM THE KIDNEY?
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STIMULATED BY RENAL ARTERIAL PRESSURE, SYMPATHETIC NEURAL STIMULATION, AND SODIUM CONCENTRATION IN THE DISTAL TUBULE
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WHAT IS BRADYKININ?
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VASODILATOR THAT IS INACTIVATED BY ACE
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GOOD EFFECTS OF BRADYKININ INCREASE (A RESULT OF USE OF ACE-I)
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ACE INHIBITORS CAUSE AN INCREASE IN BRADYKININ CAUSING DECREASED PERIPHERAL VASCULAR RESISTANCE AND DECREASED BLOOD PRESSURE; ALSO INCREASES PROSTAGLANDIN SYNTHESIS
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BAD EFFECTS OF BRADYKININ INCREASE (A RESULT OF USE OF ACE-I)
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INDUCE COUGH SO WHEN WE USE ACE INHIBITORS WHICH INCREASES BRADYKININ
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THE INHIBITION OF ANGIOTENSIN II RESULTS IN WHAT
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ANGIOTENSIN II IS A VASOCONSTRICTOR SO INHIBITION RESULTS IN VASODILATION
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INHIBITION OF ALDOSTERONE CAUSES WHAT?
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FLUID REDUCTION
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WHAT IS THE RESULT OF INHIBITING ACE?
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ACE NORMALLY BREAKS DOWN BRADYKININ WHICH IS A NATURAL VASODILATOR; INHIBITION OF ACE RESULTS IN MORE BRADYKININ BEING AVAILABLE FOR VASODILATION
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CLINICAL BENEFITS OF ACE INHIBITORS IN HF
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IMPROVE EXERCISE DURATION; DECREASE DYSPNEA AND FATIGUE; INCREASED SURVIVAL
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WHAT IS ANGIOEDEMA?
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ALLERGIC REACTION TO ACE INHIBITORS CAUSING DIFFICULTY BREATHING, SPEAKING, AND SWALLOWING ALONG WITH SWELLING OF THE LIPS, FACE AND NECK
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WHAT ARE THE TWO ACE INHIBITORS FOR HF?
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CAPTOPRIL (CAPOTEN) AND LISINOPRIL (ZASTRIL, PRINIVIL)
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WHAT ARE THE KEY THINGS TO MONITOR IN A PATIENT WITH HF THAT IS ON ACE INHIBITORS?
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POTASSIUM LEVEL/KIDNEY FUNCTION; BLOOD PRESSURE AND HYPOTENSION
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WHAT IS THE CURRENT BCF ARB?
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TELMISARTAN (MICARDIS)
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WHAT ARB'S HAVE HAD DOCUMENTED TRIALS IN HF?
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CANDESARTAN AND VALSARTAN
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WHAT IS THE PURPOSE OF ADDING A BETA BLOCKER TO ACE INHIBITOR IN HEART FAILURE PATIENTS?
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BETA BLOCKER IS USED TO PREVENT CARDIAC REMODELING
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WHAT ARE THE THREE BETA BLOCKERS WITH AN INDICATION FOR HEART FAILURE?
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CARVEDILOL (COREG), METOPROLOL (LOPRESSOR0, AND BISOPROLOL (ZEBETA)
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THIS IS A MIXED A AND B BLOCKER WITH NON SELECTIVE BETA BLOCKER ACTION THAT IMPROVES LEFT VENTRICULAR FUNCTION, EXERCISE TOLERANCE AND NYHA CLASSIFICATION
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CARVEDILOL (COREG)
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THIS IS A BETA 1 SELECTIVE BETA BLOCKER THAT IS USED AS IMMEDIATE RELEASE FOR HTN OR TOPROL XL FOR HTN AND HF TOGETHER
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METOPROLOL
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BISOPROPOL IS _______ SELECTIVE
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B1
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DO NOT USED BETA BLOCKERS IN HF IF THESE THREE CONDITIONS ARE PRESENT
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RECENTLY HAD CLASS IV SYMPTOMS, BRONCHOSPASTIC DISEASE, OR BRADYCARDIA
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WHAT IS THE MAJOR BENEFIT OF SPIRONOLACTONE/EPLERENONE IN CHF?
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IT HAS THE ABILITY TO BLOCK ALDOSTERONE. ALDOSTERONE NATURALLY STIFFENS THE HEART AND BLOOD VESSELS AND CAUSES WATER AND SODIUM RETENTION
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USE THIS DRUG IN ALL CLASS III/IV HF PATIENTS
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SPIRONOLACTONE
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THIS IS A POSITIVE INOTROPIC AGENT THAT INCREASES THE FORCE OF CARDIAC CONTRACTILITY AND MODULATES NEUROHORMONAL ACTION
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DIGOXIN (LANOXIN)
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WHAT IS THE MOA FOR LOW DOSE DIGOXIN?
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REDUCES SYMPATHETIC NERVOUS SYSTEM ACTIVATION AND INCREASES PARASYMPATHETIC ACTIVITY LEADING TO DECREASED HR AND ENHANCED DIASTOLIC FILLING
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WHAT IS THE MOA FOR REGULAR DOSE DIGOXIN?
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POSITIVE INOTROPIC EFFECT BY BINDING TO AND INHIBITING NA/K ATPASE OF CARDIAC MEMBRANE RESULTING IN DECREASED INTRACELLULAR K AND INCREASED NA AND CA. THE INCREASED INTRACELLULAR CA CAUSES INCREASED ACTIVATION OF CONTRACTILE ELEMENTS
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WHEN DO YOU USE DIGOXIN FOR HF?
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ADD TO REGIME WHEN THE PATIENT IS STILL SYMPTOMATIC EVEN AFTER TAKING ACE INHIBITORS, B BLOCKERS, SPIRONOLACTONE, AND DIURETIC THERAPY
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IF PATIENTS WILL PROB NEED DIGOXIN AND BETA BLOCKERS, WHAT DO YOU DO?
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START THE B BLOCKER FIRST SO THAT THE BRADYCARDIC EFFECT OF DIGOXIN DOES NOT PRECLUDE B BLOCKER USE
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CLASSIC SYMPTOM OF DIGOXIN TOXICITY
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BLURRING OR COLOR CHANGES IN VISION (YELLOW OR GREEN HALOES)
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IF A PATIENT IS HAVING DIG TOXICITY BUT THERE IS NO ARRYTHMIA OR ELECTROLYTE IMBALANCE, WHAT CAN YOU DO?
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STOP THE DIG FOR 2-3 DAYS AND THEN RESTART
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DIGITALIS TOXICITY IS ASSOCIATED TO THESE ELECTROLYTE IMBALANCES
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HYPOKALEMIA, HYPERCALCEMIA, AND HYPOMAGNESEMIA
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WHEN USING AMIODARONE AND DIGOXIN TOGETHER WHAT IS THE CONCERN?
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AMIODARONE REDUCES RENAL EXCRETION AND INCREASED DIGOXIN LEVEL
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WHAT IS THE EFFECT OF POTASSIUM DEPLETING DRUGS ON A PATIENT TAKING DIGOXIN?
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INCREASE THE LIKELIHOOD OF DIGOXIN TOXICITY
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WHAT DIURETIC IS PREFERRED IN PATIENTS WITH SEVERE HEART FAILURE?
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LOOP DIURETICS BECAUSE THEY ARE MORE EFFECTIVE THAN THIAZIDES AT GETTING RID OF EXCESS FLUID
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WHAT IS THE USE FOR DIURETICS IN HEART FAILURE?
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TO PULL OF EXCESS FLUID; THEY RELIEVE SYMPTOMS BUT THERE IS NO LONG TERM EFFECT ON MORTALITY
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WHAT IS THE PRIMARY GOAL OF DIURETICS IN HF?
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TO DECREASE EDEMA AND PULMONARY CONGESTION BY REDUCING PRELOAD
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YOU SHOULD AVOID EXCESSIVE USE OD DIURETICS BEFORE STARTING AN (BLANK- TYPE OF DRUG).
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ACE INHIBITOR
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WHEN DO YOU CONSIDER LOOP DIURETICS?
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WHEN RENAL CLEARANCE IN BELOW 30 ML PER MIN
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SUBSET 1 OF DECOMPENSATED HF
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CI AND FLUID STATUS ARE WITHIN NORMAL LIMITS
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BISOPROPOL IS _______ SELECTIVE
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B1
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DO NOT USED BETA BLOCKERS IN HF IF THESE THREE CONDITIONS ARE PRESENT
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RECENTLY HAD CLASS IV SYMPTOMS, BRONCHOSPASTIC DISEASE, OR BRADYCARDIA
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WHAT IS THE MAJOR BENEFIT OF SPIRONOLACTONE/EPLERENONE IN CHF?
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IT HAS THE ABILITY TO BLOCK ALDOSTERONE. ALDOSTERONE NATURALLY STIFFENS THE HEART AND BLOOD VESSELS AND CAUSES WATER AND SODIUM RETENTION
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USE THIS DRUG IN ALL CLASS III/IV HF PATIENTS
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SPIRONOLACTONE
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THIS IS A POSITIVE INOTROPIC AGENT THAT INCREASES THE FORCE OF CARDIAC CONTRACTILITY AND MODULATES NEUROHORMONAL ACTION
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DIGOXIN (LANOXIN)
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WHAT IS THE MOA FOR LOW DOSE DIGOXIN?
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REDUCES SYMPATHETIC NERVOUS SYSTEM ACTIVATION AND INCREASES PARASYMPATHETIC ACTIVITY LEADING TO DECREASED HR AND ENHANCED DIASTOLIC FILLING
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WHAT IS THE MOA FOR REGULAR DOSE DIGOXIN?
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POSITIVE INOTROPIC EFFECT BY BINDING TO AND INHIBITING NA/K ATPASE OF CARDIAC MEMBRANE RESULTING IN DECREASED INTRACELLULAR K AND INCREASED NA AND CA. THE INCREASED INTRACELLULAR CA CAUSES INCREASED ACTIVATION OF CONTRACTILE ELEMENTS
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WHEN DO YOU USE DIGOXIN FOR HF?
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ADD TO REGIME WHEN THE PATIENT IS STILL SYMPTOMATIC EVEN AFTER TAKING ACE INHIBITORS, B BLOCKERS, SPIRONOLACTONE, AND DIURETIC THERAPY
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IF PATIENTS WILL PROB NEED DIGOXIN AND BETA BLOCKERS, WHAT DO YOU DO?
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START THE B BLOCKER FIRST SO THAT THE BRADYCARDIC EFFECT OF DIGOXIN DOES NOT PRECLUDE B BLOCKER USE
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CLASSIC SYMPTOM OF DIGOXIN TOXICITY
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BLURRING OR COLOR CHANGES IN VISION (YELLOW OR GREEN HALOES)
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FUNCTION OF BNP
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NATURAL VASODILATOR- ARTERIOLE AND VENOUS SIDE, ENHANCED NA EXCRETION, SUPPRESSION OF THE RAAS SYSTEM, AND THE SYMPATHETIC NERVOUS SYSTEM
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WHAT IS NESIRITIDE OR NATRECOR?
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HUMAN B TYPE NATRIURETIC PEPTIDE
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WHAT HF PATIENTS SHOULD ALSO BE ON ANTICOAGULATION THERAPY?
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PATIENTS WHO ALSO HAVE A FIB OR WHO HAVE HAD RECENT MYOCARDIAL INFARCTIONS
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WHAT IS WARFARIN (COUMADIN)?
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ANTICOAGULANT THERAPY USED IN PATIENTS WHO HAVE HF AND ALSO A RECENT MI OR A FIB
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DRUGS THAT CAUSE AN NEGATIVE INOTROPIC EFFECT THUS PRECIPITATING OR EXACERBATING CHF
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CALCIUM CHANNEL BLOCKERS (AMIODIPINE ONLY ONE APPROVED FOR HF- USED WHEN THERE IS ALSO HTN OR ANGINA), BETA BLOCKERS WHEN NOT APPROPRIATELY USED
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DRUGS THAT CAUSE SODIUM AND WATER RETENTION THUS EXACERBATING OR PRECIPITATING CHF
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NSAID'S, GLUCOCORTICOIDS, ANDROGENS AND ESTROGENS, DIRECT VASODILATORS
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DRUGS THAT PRECIPITATE OR EXACERBATE CHF BY CAUSING TACHYCARDIA AND ARRHYTHMIAS
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CCB (EXCEPT AMIODIPINE/FELODIPINE); AMPHETAMINES; CILOSTAZOL (PLETAL); AND CLASS I AND III ANTIARRYTHMICS EXCEPT AMIODARONE AND DEFETILIDE
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IF A PERSON HAS ASYMPTOMATIC LV SYSTOLIC DYSFUNCTION, WHAT IS THE MINIMUM DRUG REGIME?
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ACEI AND A BB ADDED ONCE STABLE
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IF A PERSON HAS SYMPTOMATIC LV SYSTOLIC DYSFUNCTION, WHAT IS THE DRUG REGIME?
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DIURETICS FOR CONGESTION, ACE-I UNLESS CONTRAINDICATED, BB FOR STABLE PATIENTS, DIGITALIS IF THEY ALSO HAVE A FIB, SPIRINOLACTONE FOR CLASS III OR IV
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3 BETA BLOCKERS APPROVED FOR HF
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BISOPROPOL, METOPROPOL, AND CARVEDILOL
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USE THIS DRUG IN ALL CLASS III/IV HF PATIENTS
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SPIRONOLACTONE/EPLERENONE
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SIDE EFFECTS OF SPIRONOLACTONE
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GYNECOMASTIA AND MENSTRUAL IRREGULARITIES
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