Pharm Test 2 HF

Heart fails to pump sufficient blood to meet metabolic needs
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What are some signs of RV failure?elevated venous pressure peripheral edema jvd hepatomegaly ascitesS/S of biventricular failureReduced exercise tolerance, fatigue, weakness Tachycardia, pallor, cyanosis of digits.What is the treatment of increased preload?nitroglycerin ACE-IsWhat is treatment of increased afterload?ACE-IsWhat is the treatment for decreased CO induced SNS stimulation?B-blockersWhat is the treatment for decreased CO induced RAAS stimulation?B-blockers aldosterone antagonists2 Most frequent etiologies that lead to systolic dysfunction?Ischemic heart disease (AMI) 50-60% Hypertension (30-40%)What is the only cure for chronic HF?transplantNYHA: Class IasymptomaticNYHA: Class IIsymptomatic with moderate activityNYHA: Class IIIsymptomatic with mild activityNYHA: Class IVsymptomatic at restACC/AHA: Stage APts at high riskACC/AHA: Stage Bstructural disorder but no symptoms of HFACC/AHA: Stage Cpast or current symptoms of HF associated with underlying heart disease (structural)ACC/AHA: Stage Dend-stage diseaseFirst line agents in HF tx. Sole therapy in patients with fatigue or mild dyspnea on exertion and who do not have signs or symptoms of volume overload.ACE-IShould be added in HF patients who have signs or symptoms of volume overload after the target dose of the ACE inhibitor is reacheddiureticsACTION HF suggests that stable patients with class II or III HF due to left ventricular systolic dysfunction should receive this tx.B-blockerAdded to regimen of patients who remain symptomatic after optimal management and ACE inhibitors and diuretics. May be beneficial for HF if there is a second indication for the drug such as supraventricular arrhythmiaDigoxinAll drugs should be initiated how?started at low doses and titrated to effectConcept that HF involves endogenous neurohormones and cytokines in response to acute injuryneurohormonal modelNeurohormones: - Tachycardia and vasoconstriction - Excessive amounts cause down-regulation of β-receptors leading to reduced receptor stimulation - Contributes to ventricular hypertrophy and remodelingnorepinephrineNeurohormones: - Vasoconstriction - facilitates release of other neurohormone - Promotes Na+ restriction by direct effects on renal tubules - Stimulates ventricular hypertrophy and remodelingangiotensin IINeurohormones: Released from the posterior pituitaryvasopressin (ADH)Neurohormones: Potent vasoconstrictorendothelinNeurohormones: Inflammatory cytokineTNF-aNeurohormones: - Causes sodium and water retention - Produces interstitial cardiac fibrosis which decreases systolic and diastolic functionAldosteroneNeurohormones: - Increases in response to stress and stretch of the ventricles - Hemodynamically causes vasodilation of arteries, veins, and coronary arteries - Neurohormonally decreases aldosterone, endothelin, and norepinephrine - Renally increases diuresis, naturesisHuman b-type natiuretic peptide (BNP)Renin release from kidney is stimulated by renal arterial pressure, sympathetic neural stimulation (β1), sodium concentration in the distal renal tubule. Which drugs work at this step?B-blockers A2 agonistsAldosterone binds to receptors in collecting tubule of kidney and causes sodium and water retention. Which drugs work at this step?sipronolactone / eplerenoneWhat effect does bradykinin have on prostaglandins?Bradykinin increases prostaglandin synthesisAngiotensin II: vasoconstrictor or vasodilator?vasoconstrictorACE-I increase or decrease bradykinin levels?increaseBradykinin: vasoconstrictor or vasodilator?vasodilatorAll diabetics should be on _____ due to their renal protective effect (at least all Type 1 diabetics)ACE-Imediate afferent arterioleprostaglandinsmediates efferent arterioleangiotensin IIAs renal blood flow declines, vasoconstriction is needed to maintain renal perfusion. What natural substance causes this vasoconstriction?angiotensin IIAllergic reaction causing difficulty breathing, speaking and swallowing along with swelling of the lips, face and neckangioedemaBCF ACE-I approved for HFcaptopril lisinoprilHow soon after starting ACE-I for HF should you begin to monitor renal function and K+ levels?in 1-2 weeks after starting and then periodicallyBCF ARB used for HFTelmisartanWhat effect do B-blockers have on B1 down regulation?SNS stimulation constantly tries to increase CO. Long-term exposure to norepinephrine causes down regulation of B1 receptors. B-blockers bind to the receptors to reduce exposure and prevent down regulation.What condition must Pts be in before B-Blockers are administered?Pts must be clinically stableA mixed α and β blocker with non-selective beta blocker action that is used in HFcarvedilolβ1 selective beta blockers used in HF. Must be started at a very low dose and titrated very slowly every two weeksmetoprololB1 selective B-blockersused in HFmetoprolol bisoprololDO NOT USE B-Blocks in these HF Pts:recent NYHA Class IV symptoms bronchospasmic disease bradycardiaWhat can happen in Pts with HF if dose of B-blockers is too high?worsening of HFIf B-blockers are administered and there is lab evidence of liver abnormalities, what should you do?discontinue B-blocker useMajor benefit is it's ability to block aldosterone (not diuresis)spironolactone / eplerenoneShould be used in all class III / IV HF patientsspironolactone / eplerenonePositive Inotropic Agent - Increases the force of cardiac contractility and modulates neurohormonal actiondigoxinReduces sympathetic nervous system activation and increases parasympathetic activity leading to decreased HR and enhanced diastolic fillinglow dose digoxinPositive inotropic effect by binding to and inhibiting Na+/K+ ATPase of cardiac membrane resulting in decreased intracellular K+ and increased intracellular Na+ and Ca++. The increased intracellular Ca++ causes increased activation of contractile elements.regular dose digoxinAdd to patient's regimen when they remain symptomatic on ACE inhibitors, β-blockers, spironolactone (if appropriate) and diuretic therapydigoxindigoxin is recommended in Pts with HF who have what complication?rapid atrial fibrillationDescribe digoxin dosing in HFmust be individualized. Adjust with lab monitoringWhat is the time to steady state with digoxin in HF?usually a week but 2-3 weeks in renal impairmentAnorexia, nausea, headache, blurring or color changes to vision (yellow or green haloes), disorientation and arrhythmiasdigoxin toxicityDigoxin toxicity is linked to what electrolyte presentations?hypokalemia, hypercalcemia, hypomagnesiaAntiarrythmics used to treat dig tox.lidocaine phenytoinWorks by binding free digoxin and then the complex is excreted in the urinedigoxin immune FABdescribe therapeutic index for digoxinnarrowReduces renal excretion and increases digoxin level. Use caution with digoxin administration.amiodaroneThese diuretics should be used in mild HF or in Pts with both HF and HTNthiazide diureticsThese diuretics are preferred in most HF Pts with more severe HFloop diureticsWhat are intermediate benefits to diuretic use in HF?increase exercise tolerance and improve symptomsHow should you initiate ACE-I in HF Pts with severe edema?take fluid off first with diuretics then start an ACE Inhibitor about 3 days after diureticWhat level of weight loss is your dosing marker for diuretic therapy?increase dose unitl weight decreases by 0.5 to 1.0 kg per daySelection of diuretic is based on what?renal function - creatinine clearanceThiazides not effective if creatinine clearance is below ~30ml/min. What diuretics should then be cosidered?loop diureticsif a chronic heart failure patient has fluid overload that needs to be reversed, when should diuretics be used?before other agentsmost effective means of providing symptomatic relief in HFdiureticsbetter for hypertension - longer duration of action and only require daily dosingthiazidesbest when fluid overload is excessive, needs to be done quickly, or when the kidney is impaired. GFR below 25 to 30mL/minloop diureticsAdvanced or Decompensated HF: Subset 1Cardiac index and fluid status are within acceptable limitsTreatment of Subset 1monitor and maximize oral therapyAdvanced or Decompensated HF: Subset 2Cardiac index is adequate but patient has fluid overloadTreatment of Subset 2IV loop or nitroglycerin will reduce preloadAdvanced or Decompensated HF: Subset 3Cardiac index is less than adequate and fluid status is adequateTreatment of Subset 3Vasodilator - Nitrates Positive inotropic - IV DobutamineAdvanced or Decompensated HF: Subset 4Cardiac index and fluid status are both less than adequateTreatment of Subset 4Combination of agents for subset 2 and 3inotropic agent: β1 and β2 receptor agonist with a small amount of α1dobutamineWhat is the effect of dobutamine?Increase cardiac output with only a small increase to ratemay cause tachyphylaxisdobutaminehBNP: Neurohormone secreted from the ventricles in response to symptomatic CHF; Results in arterial and venous dilation, enhanced Na+ excretion, suppression of the RAAS, and the SNSnesiritideAdverse effects of nesiritideHOTN V. TachPatients in heart failure who have atrial fibrillation or who have had recent myocardial infarctions should be on what type of therapy?anticoagulant therapy Warfarin (Coumadin)