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Dast 3 Final - CHF
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| Question | Answer |
|---|---|
| Digitalis extract obtained from | leaf |
| Glycoside constituents | sugar and aglycone |
| part that doesn’t have sugar | a-glycol |
| class of inamrinone and milrinone | 3,4’ bipyridines |
| glycoside part responsible for the pharmacological activity | aglycone |
| function of sugar part of glycoside | affects pharmacokinetics and stability |
| natural glycoside structure | steroid nucleus + 5 or 6 membered lactone ring |
| class with 6 membered lactone rings, with 5 | bufadienolide, cardenolide |
| -genin refers to | structures without the sugar of glycoside |
| Hexoses are mostly __ sugars, __ bond, some are __ | deoxy, B-glycosidic bond, acylated |
| Difference between Lanatoside C and A | Lanatoside C has a hydroxyl at position 12 |
| Digitoxigenin / Lanatoside __ | A |
| Digoxigenin / Lanatoside __ | C |
| difference between digitoxin and digoxin | digoxin has extra O on steroid nucleus at C12 (more polar) |
| required SAR characteristics for cardiac glycosides | alpha, beta unsaturation next to carbonyl group of lactone; C,D ring has cis-fusion, |
| essential for MAXIMUM activity but not essential for cardiac glycosides | A, B ring cis-fusion |
| more polar cardiac glycoside | Lanatoside C glycoside due to glucose (low lipophilicity) |
| relationship between partition coefficient and lipophilicity | higher the partition coefficient, the more lipophilic |
| more lipophilic, has longer half life, higher protein binding, enterohepatic cycling, and liver metabolism (5-7 days) | digitoxin |
| renally excreted, largely unchanged | digoxin |
| 4,3’ bipyridines MOA | inhibit degradation of protein kinase -> elevated Ca levels |
| More selective to phosphodiesterase-3 | milrinone |
| Exhibit increased conjugation, not as stable, decomposes with air and light (photosensitivity) | bipyridines |
| Bipyridines | inamrinone and milrinone |
| Dopamine analogs MOA | B1 adrenergic agonists with a1 activity |
| Administration of dopamine | Parenteral rapid metabolism by COMT (1st pass) |
| More selective to PDE3 | milrinone |
| difference between the EDV and ESV = volume of blood ejected with each heart beat | stroke volume |
| EF = | SV/EDV = (EDV – ESV) / EDV |
| Normal EF = | 55-65% |
| Characterized by systolic dysfunction, Moderate to severe reduction in LVEF | dilated cardiomyopathy |
| Characterized by filling abnormalities or diastolic dysfunction, Systolic function is preserved initially, normal or increased LVEF | hypertrophic cardiomyopathy |
| LVEF < 40%; Preserved LVEF | systolic dysfunction (dilated cardiomyopathy), diastolic dysfunction (hypertrophic cardiomyopathy) |
| Dilation and reduced EF results in | ↑ EDV, ↑ ESV |
| Hypertrophy and preserved EF results in | ↓ EDV, ↓/↔ ESV |
| Down-regulation of beta receptors is a type of | cardiac remodeling |
| Hypertension, Obstructive Sleep Apnea, Obesity, Sarcoidosis, Amyloidosis cause | Hypertrophic cardiomyopathy |
| Neurohormone: increased preload | aldosterone |
| Neurohormone: increased afterload | angiotensin II |
| Neurohormone: Increased afterload, decreased filling time | norepi |
| Neurohormone: decreased preload, diuresis | natriuretic peptides, cause vasodilation |
| Renin-angiotensin-aldosterone system activation: Sensitive to low CO (→ __), Stimulates vasoconstriction (↑__), Conserves sodium/water (↑__) | renin release, afterload, preload |
| SNS: Sensitive to changes in BP (→ __), Promotes vasoconstriction (↑__), Directly toxic to myocardial cells (↑__), Activates __ | NE release, afterload, arrhythmias, RAAS |
| RR monitoring | 10-14 breaths/min |
| Hypoperfusion signs regarding SCr or BUN | elevated |
| __natremia is a sign of HF | hypo |
| At high risk for HF but without structural heart disease or symptoms of HF (e.g., patients with HTN, DM, CAD or metabolic syndrome) | Stage A |
| Structural heart disease but without signs or symptoms of HF (e.g. previous MI, LV remodeling including LVH and low EF, asymptomatic valvular heart disease) | Stage B |
| Structural heart disease with prior or current symptoms of HF (e.g. known structural heart disease and SOB and fatigue, reduced exercise tolerance) | Stage C |
| Refractory HF requiring specialized interventions (e.g. marked symptoms at rest despite maximal medical therapy) | Stage D |
| Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitations, or dyspnea | Class II |
| Marked limitation of physical activity. Comfortable at rest but less than ordinary to minimal exertion causes fatigue, palpitations, or dyspnea | Class III |
| Loop diuretics MOA | Block Na/K/2 Cl transport channel in Ascending loop of henle; Prevents Na, K, Mg, and Ca reabsorption |
| Is not affected by GFR or CrCl | efficacy of loop diuretics |
| Useful in conditions refractory to less potent diuretics (HF, renal insufficiency, nephrotic syndrome) | Loop diuretics |
| Thiazide diuretics MOA | Na/Cl co-transport channels in early distal tubule |
| Mild diuretic (less Na+ reabsorbed distally) | Thiazides |
| Relatively ineffective in CRI | Thiazides |
| Enhances reabsorption of Ca++ and uric acid in proximal tubule (gout flairs) | Thiazides |
| More effective in patients with reduced CrCl (<30-40) | Metolazone or indapamide (most potent) |
| Potassium sparing diuretics MOA | Na/K/H transport channel in Late distal tubule, Competitive aldosterone receptor antagonist (ARA), Blocks aldosterone-stimulated Na+ reabsorption and K+ excretion (Hyperkalemia) |
| Onset and half-life of furosemide | 30-60 min, 2 hrs |
| Onset and half-life of HCTZ | 2 hrs, 10-12 hrs |
| Increasing the dose until adequate response, Combination with thiazide diuretic, Intravenous dosing may be necessary, Ultrafiltration | Managing refractory patients with diuretic resistance |
| Loop diuretic po equivalent doses | furosemide 40mg = bumetanide 1mg = torsemide 20mg |
| postural hypotension, ototoxicity (high dose – transient), electrolyte abnormalities (K/Mg/Ca), hyperglycemia, hyperuricemia, dehydration, and renal dysfunction | ADRs of loops |
| ACEI MOA | prevents conversion of angiotensin I to angiotensin II, resulting in a decrease in afterload and sodium/water retention |
| agents of choice for blockade of the RAAS in HF patients with systolic dysfunction | ACEI |
| ACEI: To avoid first-dose hypotension and risk of increased sCr, | reduce (or hold) diuretic dose prior to initiation |
| Elevated sCr is not a contraindication to therapy; For an ACEI, an increase in sCr up to __ may be expected | 30% |
| Use with caution in low SBP (< 80mmHg), bilateral renal artery stensosis, contraindicated in pregnancy, SCr > 3mg/dL, and serum K >5.5 mEq/L | ACEIs |
| ARBs are not recommended in addition to ACEI and b-blocker in patients with | recent MI and LV dysfunction |
| ARBS MOA | inhibits the A1 receptors responsible for vasoconstriction and proliferation |
| reasons not to consider an ARB | Hypotension, hyperkalemia, renal dysfunction |
| Addition of a b-blocker produces greater improvement in symptoms and reduction in risk of death than | an increase in ACE inhibitor dose. |
| Anti-arrhythmic effect, Up-regulation of b-receptors, prevent NE-induced apoptosis | BBs |
| BB trial that claimed target dose titration improves LVEF and reduces mortality | MOCHA trial |
| BB Recommended in these disease states | DM, COPD, CAD |
| Only initiate or up-titrate the BB dose when | euvolemic |
| Appropriate response to BB | Fluid overload - increase diuretic dose (temporarily) + or - decrease BB dose (temporarily); Dizziness/orthostasis - decrease diuretic dose if dry + decrease ACEI dose |
| Recommended in all patients with IHD, chronic HF (symptomatic and asymptomatic patients, reduced and normal EF) | BBs |
| slows electrical conduction between the atria and ventricles to help with ventricular rate control | digoxin |
| Digoxin MOA | decreases SNS outflow from CNS, decreasing Na reabsorption in the distal tubules causing ↓renin release, Positive inotrope (inhibits Na+/K+ ATPase exchange so high IC Na+ and EC K+ activates the Na+/Ca+2 ATPase exchanger to pump Na+ out & Ca+2 in |
| Digoxin: NOT necessary to use loading dose for | HF |
| LD of digoxin, MD | 5 mcg/kg x LBW (kg); MD = LD x % daily loss or (CrCl ÷ 5) + 14 (Round to the nearest 125mcg) |
| Digoxin: expect steady state in __ days after dose adjustments | 5-7 |
| Consider using digoxin in patients being treated with an ACEI (or ARB), BB, and diuretics (to maintain euvolemia) for ___ with or without an aldosterone antagonist | symptomatic improvement and to reduce recurrent hospitalization |
| Recommended in patients with NYHA class III or IV HF from LV dysfunction (LVEF < 35%) in addition to standard therapy; should be considered in patients post-MI with clinical HF signs/symptoms and an LVEF < 40% in addition to standard therapy | ARAs therapy |
| Initiate ARA therapy at low doses, Spironolactone __ mg/d or eplerenone __mg/d; Uptitrate to sprionolactone __mg/d or eplerenone __mg/d as tolerated | 12.5, 25, 50, 50 |
| Drug class that should be avoided during ARA therapy | NSAIDs and COX2-inhibitors |
| ARAs: Assess K+ and sCr in | 3 days, at 1 wk, then monthly for 3 months and every 3 months thereafter |
| MOA of ARAs | reduces potassium excretion and myocardial fibrosis |
| Benefit of ___: decrease mortality from SCD and progression of HF (NYHA class III/IV and post-MI with LV dysfunction), decrease hospitalizations | ARAs |
| Recommendation: add to regimen of patients with mild-severe HF who are symptomatic despite optimal therapy and have recently been hospitalized | ARAs |
| Monitoring for ARAs | serum potassium, renal |
| MOA of Hydralazine | direct relaxation of arterial smooth muscle resulting in vasodilation |
| African American patients do not receive the same benefit from ACE inhibitors due to ___; retrospective analysis of ___ | ↑ renin expression; SOLVD and V-HeFT II trials |
| African American patients may derive greatest benefit from ___; retrospective analysis of ___ | the HYD / ISDN combination; V-HeFT I and II trials, Prospective A-HeFT trial |
| Recommended in African Americans with LV dysfunction in addition to standard therapy of ACE inhibitor and b-blocker. (NYHA class III/ IV - Evidence A, NYHA class II – Evidence B) | Hydralazine/ISDN |
| ¯ preload, ¯ afterload, improve endothelial function | Hydralazine/ISDN |
| Interacts with Hydralazine/ISDN | phosphodiesterase inhibitors (e.g. Viagra) |
| hydralazine decreases | nitrate tolerance |
| Hydralazine/ISDN Monitoring | hypotension, headache, dizziness, lupus-like reaction (hydralazine). Nitrate-free interval not required |
| Meds to Avoid in HF: Non-Dihydropyridine CCBs - __ inotrope | negative |
| Meds to Avoid in HF: safe, but provide no clinical benefit | Dihydropyridine CCBs |
| Meds to Avoid in HF: NSAIDS, COX-1 (___), COX-2 (___) | Ibuprofen, naproxen, ketoralac; celecoxib, meloxicam |
| Meds to Avoid in HF: use sparingly as needed and monitor | corticosteroids |
| Meds to Avoid in HF: increase mortality | Flecaininde and propafenone |
| Antiarrhythmics appropriate for use in HF | Amiodarone and dofetilde |
| Avoid if NYHA Class III or IV within 6 months | Dronedarone |
| Therapy Goals and drugs in Stage A | lifestyle modifications, ACEI/ARB for vascular disease or diabetes |
| Therapy Goals and drugs in Stage B | lifestyle modifications, ACEI/ARB for appropriate pts, BBs in appropriate pts, implantable defibrillators in select pts |
| Therapy Goals and drugs in Stage C | dietary salt restriction, diuretic, ACEI, BB; ARA, ARB, Digitalis, Hydralazine/nitrates in selected pts; Biventricular pacing, implantable defibrillators in selected patients |
| Determines how much volume the ventricle receives during diastole and degree of ventricular stretch | preload |
| Determined by systemic vascular resistance (SVR) or pulmonary vascular resistance (PVR) | afterload |
| Dependent on central venous pressure (CVP) or Pulmonary Capillary Wedge Pressure (PCWP) | preload |
| Normal range of PCWP (preload - estimates LVED) | 8-12 mm Hg |
| Normal CO | 4-7 L/min |
| Normal Cardiac Index (CO corrected for BSA) | >2.6-3.6 L/min/m2 |
| Normal range for SVR (approximates afterload) | 800-1200 |
| Fatigue, Altered mental status, Narrow pulse pressure, Increased lactic acid, Hypotension, Tachycardia, Cool extremities, Worsening renal function | hypoperfusion (AHFS signs and symptoms) |
| BNP < 100 pg/mL | HF highly unlikely |
| BNP 100 – 500 pg/mL | Consider HF history and other potential causes |
| BNP > 500 pg/mL | HF highly likely |
| CI >2.2 and PCWP <15 mmHg | Subset 1 (normal) warm and dry |
| CI >2.2 and PCWP >18 mmHg | Subset 2 (congestion) warm and wet |
| CI <2.2 and PCWP <15 mmHg | Subset 3 (hypoperfusion) cold and dry |
| CI <2.2 and PCWP >18 mmHg | Subset 4 (congestion and hypoperfusion) cold and wet |
| Goal of diuretics in AHFS, used in subsets __ | to relieve congestion; II (warm and wet) and IV (cold and wet) |
| Reduce preload by venodilation and Na/water excretion | IV diuretics (furosemide, bumetanide, and torsemide) |
| Can cause sympathetic and RAAS activation and reduction in CO | IV diuretics (furosemide, bumetanide, and torsemide) |
| IV furosemide dose | 40 mg bolus, 5-40 mg/hr infusion |
| IV bumetanide dose | 1 mg bolus, 0.5-2 mg/hr infusion |
| IV torsemide dose | 20 mg bolus, followed by infusion |
| Monitor for symptom relief, intake/output, daily weight, vital signs, BUN, SCr, electrolytes | IV diuretics |
| When congestion fails to improve in response to diuretic therapy, the following options should be considered | Sodium and fluid restriction, Increased doses of loop diuretic, Continuous infusion of a loop diuretic, or addition of a second type of diuretic orally (metolazone or spironolactone) or intravenously (chlorothiazide), , ultrafiltration may be considered |
| Rapidly removes salt and water (up to 500 mL/hr), Allows for a predictable amount of fluid to be removed, Isotonic removal of fluid, May prevent neurohormonal activation | ultrafiltration |
| Potential indications: Patients with diuretic resistance, with renal impairment | ultrafiltration |
| Recommended for patients with a recent decompensation of HF after optimization of volume status, including inotropic support | BB therapy |
| Recommended in most patients experiencing a symptomatic exacerbation of HF during chronic maintenance therapy. (Evidence C) If necessary, consider temporary dose reduction. Avoid abrupt discontinuation | BB therapy |
| Greater weight loss and dyspnea score in UF vs. aggressive IV diuretic therapy | UNLOAD trial |
| Dyspnea on exertion, Orthopnea, PND, Early satiety, Nausea/vomiting, Rales, Peripheral edema, __ JVP, __ HJR, Hepato-/splenomegaly, Ascites | Volume Overload; increased, positive |
| Indication for vasodilator therapy with NTP, Nesiritide, and NTG | warm and wet |
| NTP dosing | 0.2 mcg/kg/min (titrate upward) |
| Nesiritide dosing | 2mcg/kg IV bolus, 0.01 mcg/kg/min |
| NTG dosing | 5-10 mcg/min (titrate every 5 min) |
| Efficacy in HF, Tachycardia, Tachyphylaxis, Flushing and redness, Neurohormonal activation due to reflexive sympathetic activity | limitations of NTG |
| Requires arterial line monitoring, Tachycardia, Coronary steal, Pulmonary shunting, Thiocyanate toxicity, Neurohormonal activation due to reflexive sympathetic activity | limitations of nitroprusside |
| Endogenous peptide secreted from cardiac myocytes in response to volume and pressure overload, an independent predictor of elevated left ventricular end-diastolic pressure in patients with HF | brain natriuretic peptide (BNP) |
| Causes vasodilation of veins, arteries, and coronary arteries, decreases aldosterone, endothelin, and noradrenaline, brochodilation, increases sodium and water excretion | BNP |
| In the absence of symptomatic hypotension, ______ may be considered as an addition to diuretic therapy for rapid improvement of congestive symptoms in patients admitted with ADHF | intravenous vasodilators (nitroglycerin, nitroprusside, or nesiritide) |
| Recommended for rapid symptom relief in patients with acute pulmonary edema or severe hypertension. (Strength of Evidence = C) | Intravenous vasodilators (nitroglycerin or nitroprusside) and diuretics |
| May be considered in patients with ADHF and advanced HF who have persistent severe HF despite aggressive treatment with diuretics and standard oral therapies (Strength of Evidence = C) | Intravenous vasodilators (nitroglycerin or nitroprusside) |
| Indication for inotropes dobutamine or milrinone | ADHF short-term management, cold and wet |
| b-1agonist to increase contractility, slight peripheral vasodilation | dobutamine |
| PDE-3 inhibitor which increases cAMP to augment myocyte Ca utilization, moderate vasodilation | milrinone |
| Dobutamine dose | 5-20 mcg/kg/min |
| Milrinone dose | 50 mcg/kg, 0.375-0.75 mcg/kg/min |
| Recommended if hypotensive; recommended if receiving a BB | dobutamine, milrinone |
| Dobutamine: __SV, __SVR, and thus __ CO, __PCWP | increased, decreased, increased, decreased |
| direct vasodilatory properties (greater decrease in SVR), may lead to a decrease in BP with/without a reflex increase in HR, consistent decrease in PCWP, long half-life (2-4 hr in healthy patient and 12 hr in heart failure) with renal dysfunction | Milrinone |
| Increased mortality, Arrhythmias, Neurohormonal activation, Tachyphylaxis, Physiologic effects antagonized by b-blockade | Limitations of Positive Inotropes |
| May be considered in pts with advanced HF and low output (LV dilation,↓end-organ dysfunction), marginal systolic blood pressure (<90 mm Hg), symptomatic hypotension despite adequate filling pressure, Unresponsive/intolerant to IV vasodilators, reduced EF | Intravenous inotropes (milrinone or dobutamine) |
| These agents may be considered in similar patients with evidence of fluid overload if they respond poorly to intravenous diuretics or manifest diminished or worsening renal function. (Strength of Evidence = C) | Intravenous inotropes (milrinone or dobutamine) |
| When adjunctive therapy is needed in other patients with ADHF, administration of __ should be considered instead of intravenous inotropes. (Strength of Evidence = B) | vasodilators |
| Intravenous inotropes are not recommended unless left heart filling pressures are known to be __ based on direct measurement or clear clinical signs. (Strength of Evidence = B) | elevated |
| Long term use of an infusion of ___ may be harmful and is not recommended for patients with current or prior symptoms of HF and reduced EF, except as palliation for patients with end-stage disease who cannot be stabilized with standard medical treatment | positive inotropes |
| Risk of hyperkalemia increases progressively with sCr > | 1.6 mg/dL |
| Natriuretic effects on RAAS: Vaso__, Sodium __, __ aldosterone release, __ cellular growth, __ sympathetic nervous system activity | constriction, retention, Increased, Increased, Increased |
| Natriuretic effects on Natriuretic Peptide System: Vaso__, Sodium __, __ aldosterone release, __ cellular growth, __ sympathetic nervous system activity | dilation, excretion, Decreased, Decreased, Decreased |
| Avoid ARAs: If elderly or low muscle mass with CrCl __, Serum creatinine __ mg/dL, if baseline serum K+ __ mEq/L | >30, >2.5, >5 |
| ACE inhibitors are recommended in all patients with a __ including symptomatic and asymptomatic patients | LVEF< 40% |
Created by:
sreeja
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