Treatment of congestive cardiac failure – Flashcards
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Chronotropy
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Heart RATE
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Inotropy
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Myocardial CONTRACTILITY
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Dromotropy
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Conduction SPEED
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Lusitropy
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Rate of RELAXATION after contraction
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Preload vs Afterload
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Preload: Ventricular end DIASTOLIC volume (stretch after blood fills ventricles) Afterload: The amount of resistance the heart must overcome to open the aortic valve and push the blood volume out into the systemic circulation
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Hear failure
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Cardiac pump DYSFUNCTION-> congestion + DECREASED perfusion Will have: -Dyspnea -Orthopnea -Fatigue -Rales -JVD -Pitting edema Exercise-> Mycoardial oxygen demand increases-> inadequate compensation-> Heart Failure -Graph shows Ventricular Performance in Heart Failure
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HF classification
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Class I (A): NO limitation of physical activity (risk factors are present) Class II (B): Slight limitation of physical activity (severe exercise) Class III (C): MARKED limitation of physical activity Class IV (D): Unable to carry on any physical activity WITHOUT discomfort-> symptoms present even at rest (Severe symptoms at rest!)
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Chronic Cardiac Failure (CCF)
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Heart failure develops and progresses SLOWLY -Edema and congestion are hallmark symptoms Goal of Therapy: IMPROVE symptoms and PREVENT progression of CHF
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Acute Heart Failure (ACF)
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-May develop suddenly during CCF->SHOCK!!! -Usually due to myocardial damage-> infarction -Goal of Therapy in ACF: Re-establish adequate tissue perfusion and O2 delivery to end organs -ENSURE airway, breathing, and circulation (ABC)!
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Drugs to treat CCF
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*Diuretics*: DECREASE congestion -Thiazide diuretics -Loop diuretics -Natriuretic peptides: *Nesiritide* -Vasodilators (dilate arteries and veins): ACEI -Angiotensin receptor blockers (ARBs) -Nitrodilators -Direct-acting arterial dilators -Natriuretic peptides
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Drugs used to treat heart failure
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Drug selection depends on patient's initial clinical state and responsiveness to initial therapy (CHF) ABCDE -ACE inhibitors -?-blockers: mild-to-moderate HF only -Cardiac Glycosides -Diuretic agents -Eplerenone/ Spironolactone: Aldosterone inhibitors Additional Agents for severe or acutely decompensated HF: -Vasodilators -Parenteral inotropic agents DO NOT use CCBs!
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Choice of Agent based on Degree of HF
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ACE Inhibitor Beta blocker Cardiac glycoside: DIGOXIN Diuretic --- Decrease mortality with Ace inhibitors, beta blockers, and spironolactone
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Vasodilators for Heart Failure
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-*ACEIs and ARBs are FIRST line agents* -*Direct Vasodilators*: Isosorbide dinitrate, nitroprusside, hydralazine, amlodipine, and prazosin ;Used specially in patients who cannot tolerate ACE inhibitors -Use limited by high incidence of *side effects in HF* *All can help REDUCE symptoms of heart failure by DECREASING myocardial oxygen demand*
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Diuretics Used in Heart Failure
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INCREASED elimination of edematous fluid improve tissue perfusion and pulmonary function -DECREASE fluid volume and relieve symptoms of heart failure -Produce few side effects-; often used in combination with other HF drugs to REDUCE patient's symptoms -Potent diuretics such as *furosemide* (loop diuretic) are particularly valuable in treating acute HF ---- Aldosterone inhibitor: *Spironolactone and Eplerenone* -*K+-sparing diuretics* -> DECREASE hypokalemia caused by thiazides and loop diuretics
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Spironolactone (Indications)
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Treatment of CHF -Spironolactone administration in patients with severe heart failure improved symptoms, decreasing mortality by 27%, and also DECREASING rate of hospitalization --- Other uses: -Primary hyperaldosteronism -Edematous conditions -Hypokalemia -Essential HTN
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Spironolactone (Contraindications)
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-HYPERkalemia -Patients with significant *renal impairment*
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ACEIs (& ARBs) for Heart Failure
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ACEI: (-prils) Captopril, Enalapril, Lisinopril, and Others -1st-line drugs in the treatment of HF ARBs: (-sartan) Losartan, Candesartan, and Others) may be used when ACEIs NOT tolerated! Improve heart failure by DECREASING peripheral edema and INCREASING cardiac output -Effective and have relatively LOW potential for serious adverse effects! -Decrease peripheral edema and increase CO
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Beta Blockers
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*Metoprolol, Propranolol, Carvedilol* Use with caution in Heart Failure -Nearly always used in combination with other drugs in HF -Recommended for use in patients with *LV ejection fraction <35%* and NYHA class II or III symptoms in conjunction with an *ACEI or ARB and diuretics*
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Beta Blockers (effects on HF)
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DECREASE myocardial contractility, heart rate, and blood pressure ->DECREASES symptoms of HF -Start at very LOW doses (~1/10 of final target and titrate cautiously upwards)
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Digoxin and cardiac Glycosides
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*Cardiac glycosides: DIGITOXIN and DIGOXIN* Selective inhibition of the *plasma membrane Na+ pump* -Cardiac myocytes extrude LESS Na+ causing RISE in INTRAcellular Na+ concentration -ELEVATED intracellular Na+ alters the equilibrium of the Na+/Ca2+ exchanger ->Decreased Ca2+ efflux due to gradient for Na+ entry, while Ca2+ INFLUX is INCREASED due to INCREASED gradient for Na+ efflux! -Positive INOTOROPIC -Vagal stimulation-> Decreases sympathetic activation and HR --- Slide shows that blockage of 3Na+/2K+ exchange causes accumulation of intracellular sodium-> REpolarization is INHIBITED!
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Digoxin Uses
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HF -Increases inotropy -INCREASES Ejection Fraction -DECREASES preload -Decreases pulmonary congestion/edema Arrhythmias -DECREASES AV nodal conduction-> PNS effect: Prolongs the effective refractory period -DECREASES ventricular rate in *atrial flutter and fibrillation* (SA node depression) --- -Sinus node: decreases rate -Atrial muscle: Decreases refractory period -AV node: INCREASES refractory period + decreases conduction velocity -Purkinje system/Ventricular muscle: SLIGHT DECREASE refractory period -Electrocardiogram: INCREASED PR Interval, DECREASED QT interval
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Digoxin (Adverse effects)
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-*Narrow Therapeutic Index: Requires monitoring!* Extracardiac (symptoms similar to the flu): -Anorexia -NVD -Abdominal pain -Blurred vision >Abnormal color perception: Yellow or green spots -Anxiety -Nightmares -Hallucinations -Delirium -Fatigue -Muscle weakness -Gynecomastia -Toxicity Management Digibind-> Digoxin immune FAB ==== Toxic doses: -Can lead to atrial muscle having arrhythmias -Tachycardia, fibrillation, extrasystoles
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Digoxin (Contraindications)
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-*Ventricular tachycardia* -*Heart block* -*Hypokalemia* -Hypercalcemia -Renal impairment (*Digoxin removed by KIDNEYS*) -Do NOT give with verapamil, amiodarone, quinidine, diuretics: Displace from binding site and decrease CLEARANCE -Treat overdose with DiGiBind: Anti-Digoxin Fab fragments
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Management of CHF: Summary
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REMEMBER: ABCDE -ACE inhibitors -?-blockers: mild-to-moderate HF only -Cardiac Glycosides -Diuretic agents -Eplerenone/ Spironolactone: Aldosterone inhibitors
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Acute Heart failure (AHF): management
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Beta adrenergic agonists: *isoproterenol* -Beta 1 agonist: *Dobutamine* -*Dopamine* (low and medium doses) -*Phosphodiesterase-III Inhibitors (PDEI)*: Milrinone, Inamrinone, Theophylline, Calcium chloride -*Pressor Agents*: Agents to restore tissue perfusion >Epinephrine/ Norepinephrine >HIGH dose Dopamine
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Beta-Adrenergic Receptor Agonists (Indications)
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ACUTE conditions where there is LOW cardiac output (CO)-> *cardiogenic shock*
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Beta-Adrenergic Receptor Agonists (In Congestive Heart Failure)
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-Have had LIMITED use in chronic management of CHF -BETA adrenergic receptor agonist efficacy limited by REDUCTION in receptor numbers and Desensitization: a significant LOSS of Beta-1 receptors (~ 50%) occurs
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Dobutamine
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Racemic mixture that binds to and activates ?-1 and ?-2 adrenoceptors -Positive inotropic action mediated by ?-receptor activation predominates -Does NOT activate *dopamine receptors* and therefore does NOT increase renal blood flow Mechanism of action: LOW doses *Beta-1 selective adrenergic agonist * -*INCREASES CONTRACTILITY (inotropic) WITHOUT substantially increasing either HR or peripheral resistance* -LESS arrhythmogenic and LESS tachycardia than endogenous catecholamines or *isoproterenol*
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Dobutamine (Indications)
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SHORT-term *inotropic* (elevate heart contractility) support in patients with cardiac decompensation due to depressed contractility
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Dobutamine (Adverse Effects)
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-INCREASES systolic blood pressure by 10-20 mm and heart rate by ~5-15 beats/minute in most patients *Increased SBP and HR*
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Dopamine
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DOSE DEPENDENT Low Doses: Selectively activate D1 receptors in several vascular beds (kidneys)-> VASODILATION-> INCREASES renal blood flow (ex: in the TREATMENT OF SHOCK) Intermediate Doses: ACTIVATE cardiac BETA-1 receptors -Improve myocardial contractility (* +ve inotropic effect*) -Produces LESS of an INCREASE in heart rate compared to isoproterenol! --- Low and medium is therapeutic; high will cause vasoconstriction (alpha agonist)-> NOT wanted
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Dopamine (mechanism)
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-Dilates renal arteries achieves *better renal perfusion than dobutamine or isoproterenol* -*Corrects hemodynamic disturbances* in shock due to *myocardial infarction, trauma, septicemia, open-heart surgery, and renal failure * *Tolerance may develop with continued infusion!*
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Dopamine (Indications)
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In Chronic cardiac decompensation (Congestive HF) -> Corrects hemodynamic IMBALANCES in SHOCK-> MI, trauma, septicemia, open-heart surgery, *renal failure*, etc
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Dopamine (Side effects)
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-Cardiac arrhythmias -Dyspnea -Nausea -Vomiting -Headache
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Dopamine (contraindications)
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Contraindicated in: -Pheochromocytoma -Uncorrected tachyarrhythmias -Ventricular fibrillation
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Nesiritide
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Recombinant *B-type natriuretic peptide* -Arterial and venous VASODILATOR with modest diuretic and natriuretic properties -Used to treat acutely *decompensated congestive heart failure with dyspnea at rest* -Normally produced by the ventricular myocardium
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Nesiritide (Mechanism of action)
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INCREASE cardiac output by VASODILATION without increasing heart rate or oxygen consumption -Counterregulation of the renin-angiotensin-aldoesterone system via stimulation of cGMP-> smooth muscle relaxation-> Promotes vasodilation, natriuresis, and diuresis
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Ivabradine
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In patients on maximally tolerated -blocker therapy >HR or in whom Beta-blockers are contraindicated, or resting HR ?70 & (LVEF ? 35%) >For anti-anginal (chronic stable angina), anti-ischemic, and symptomatic CHF. Mechanism: Selective blocker of If (funny channels are blocked)-> DECREASED pacemaker activity-> HR only decreases Side effects: -Inappropriate sinus tachycardia is an uncommon disorder characterized by multiple symptoms, including palpitations, dizziness, orthostatic intolerance, and elevated heart rates. -Visual disturbances
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Milrinone and Inamrinone
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-NONE drugs *Phosphodiesterase III inhibitors* used for the SHORT-term management of HF -INCREASE force of contraction (inotropic) and cause VASODILATION -Only given IV and can produce potentially SERIOUS adverse effects -Used for a SHORT time when HF refractory to other drugs
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Milrinone and Inamrinone (side effects)
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IV ONLY and short time use Clinically significant *thrombocytopenia* occurs in ~10% of patients receiving inamrinone (rare with milrinone)
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ACUTE HEART FAILURE: EKG manifestations of Damage to the myocardium
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*ST Segment elevation*: Myocardial damage may cause elevation of S portion and T wave elevates( can be close or even higher than R wave) >Typically with MI (ST elevated MI= STMI) >Starts in ventricles and moves outwards (affects electrical activation) *INVERSION of T wave*: Appears later on-> ISCHEMIA *Q waves can go further down*= EXAGGERATION>DEAD tissue NOT conducting anymore in the ventricles (NECROSIS)-> rest may look normal
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Possible Consequences of MI: Types of shock
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-Hypovolemic Shock -Cardiogenic Shock -Distributive Shock -Neurogenic Shock -Septic shock >Thirst and dry mouth >Low blood sugar >Fever
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Possible Consequences of MI: Anaphylaxis
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Hives and swelling of the face and throat
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Possible Consequences of MI: Signs and symptoms
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-Rapid, weak, or ABSENT pulse and irregular heart rate -Cool, clammy skin -Rapid and shallow breathing -Decreased BP and urine output -Chest pain and nausea -Confusion, anxiety, and light headedness -DILATED pupils or lackluster eyes
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Cardiogenic Shock
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Cardiac dysfunction persistent hypotension (SBP <80 to 90 mm Hg or MAP 30 mmHg lower than baseline) with severely cardiac index (<1.8 L/ min per m2 without support or Patients most commonly succumb to MULTI-organ dysfunction due to ongoing ischemia -- Cardiogenic shock may follow MI, acute decompensated heart failure, and low CO states after cardiac surgery
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Cardiogenic shock: Causes and pathogenesis
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-Acute myocardial infarction: usually ST elevation myocardial infarction + Left ventricular failure -Mechanical complications: Acute mitral regurgitation or rupture of either the ventricular septal or free walls -Acute, severe left or right ventricular dysfunction may lead to cardiogenic shock
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Cardiogenic shock: General measures
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-Ventilation support (O2) to correct hypoxemia and acidosis -Optimize intravascular volume -Sodium bicarbonate only for severe metabolic acidosis (arterial pH less than 7.10 to 7.15) -ASPIRIN -*IV Heparin (UFH)* -Possible glycoprotein IIb/IIIa inhibitor with NSTEMI -Insertion of pulmonary artery catheter
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Cardiogenic shock: Treatment
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Shock is a medical emergency -Goal find and treat the cause of shock -Supportive therapy to maintain tissue perfusion and oxygenation -Drugs to INCREASE blood pressure and improve heart function: *-Dobutamine -Dopamine -Epinephrine -Norepinephrine -Milrinone and amrinone*
