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Acute decompensated heart failure

Acute decompensated heart failure

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Acute decompensated heart failure

  1. 1. Acute Decompensated Heart Failure
  2. 2. Definition • rapid onset of new or worsening signs and symptoms of HF, as a result of volume overload and/or low cardiac output .It is often a potentially life-threatening condition. • Generally requires hospitalization, intensive therapy, IV meds, intensive monitoring.
  3. 3. Etiology and Pathophysiology 1. refractory to oral therapies 2. decompensate after mild insult (eg, dietary indiscretion, nonsteroidal anti-inflammatory drug use) 3. medication nonadherence 4. concurrent noncardiac illness (eg, infection). 5. New or worsening cardiac processes, such as MI, atrial or ventricular arrhythmias, hypertensive crises, myocarditis, or acute valvular insufficiency,
  4. 4. Prognostic factors: • BUN ≥43mg/dl • SBP ≤ 115mmHg • SrCr ≥2.75 mg/dl • Hyponatremia • troponin I • Ischemic etiology • Poor functional capacity
  5. 5. Signs & symptoms: • Wt gain of at least 5kg, AMS, dyspnea, HoTN, worsening of renal fcn, polmunary or systemic congestion, arrhythmias • Labs: BNP, BUN, SCr, electrolytes (K), troponins., thyroid, LFT • Cardiac enzymes to exclude myocardial ischemia.
  6. 6. The Heart Failure Society of American guidelines recommend the following treatment goals for patients admitted for ADHF • Improve symptoms, especially congestion and low-output symptoms • Restore normal oxygenation • Optimize volume status • Identify etiology • Identify and address precipitating factors • Optimize chronic oral therapy • Minimize side effects • Identify patients who might benefit from revascularization. • Identify patients who might benefit from device therapy (LVAD) • Identify risk of thromboembolism and need for anticoagulant therapy • Educate patients concerning medications and self- management of HF
  7. 7. Subsets of Acute HF (systolic)
  8. 8. Subset I (Warm and dry) • No signs and symptoms of volume overload or hypoperfusion • values within ranges(CI >2.2 and PCWP < 18 ) • normal compensatory mechanisms in Patient significant left ventricular dysfunction or drug. • lowest risk of mortality • do not require immediate intervention just optimization PO drugs for HF
  9. 9. Subset II (Warm & Wet) • Well perfused, with congestion • CI >2.2 but a PCWP greater than 18 mm Hg. • Management - relieve symptoms of congestion by lowering PCWP - without reducing CO, increasing heart rate, provoking neurohormonal activation(SVR) .
  10. 10. Subset III Cold & Dry • Hypoperfusion w/o congestion. • CI of less than 2.2 L/min/m2 but normal range of PCWP <18. • The mortality is higher • Treatment focuses on increasing CO w/ positive inotropes, very cautious fluid replacement and vasodilators.
  11. 11. Subset IV Cold & wet • Volume overload & peripheral hypoperfusion • Worst prognosis (end stage HF) • CI <2.2 L/min/m2, PCWP >18 mm Hg • If patient compromise MAP :combined inotrope and vasopressor therapy (eg, dobutamine plus norepinephrine) or an inotrope with vasopressor activity (eg, dopamine) to rise MAP
  12. 12. Monitoring Pulmonary Artery Catheter: • Invasive hemodynamic monitoring helps evaluate volume and perfusion status • Pulmonary artery catheter (PAC) placement: • PCWP > 18mmHg -> overload • CI <2.2 l/min/m2 -> cold • BUT IT IS NOT ALWAYS REQUIRED
  13. 13. • Uses pulmonary artery (PA) - refractory to initial therapy - whose volume status is unclear, - with clinically significant hypotension (ie, systolic blood pressure <80 mm Hg) - or worsening renal function despite standard therapy. - patients being evaluated for mechanical circulatory support (MCS) or cardiac transplantation.
  14. 14. Systolic Versus Diastolic Dysfunction • In the acute setting, however, some of the initial therapies are similar in systolic and diastolic HF, including the following: • Diuresis • Supplemental oxygen and assisted ventilation, if necessary • Vasodilator therapy in selected patients • in systolic dysfunction, some medications should not be initiated or should be used with caution in the acute setting (eg, angiotensin converting enzyme inhibitors and beta blockers). • In diastolic dysfunction, treatment of hypertension and tachycardia is particularly important. • Inotropic agents are not indicated in patients with diastolic dysfunction with preserved systolic function.
  15. 15. Diuretics: • Loop diuretics are 1st line in ADHF • Furosemide, Torsemide, Bumetanide. • Reduce preload, PCWP but no effect on CO • Reduce pulmonary congestion and dyspnea • IV bolus or continuous infusion • 2 mechanisms: Reduces preload within 5 to 15 min by venodilation within 20 min by sodium and water excretion • Reduce pulmonary congestion • Titrate to U/O, PCWP, congestion, BP
  16. 16. • To overcome diuretic resistance: • increase dose, frequency, switch to continuous infusion • Add thiazide like diuretic e.g metolazone • IV vasodilator, inotropes, ultrafiltration or vasopressin antagonist. • Non-pharm strategy: limit Na and water intake.
  17. 17. Vasodilators: • NTG, nitroprusside, nesiritide • Arteriodilators reduce SVR, afterload, increase CO • Venodilators (NTG, nesitiride) relieve s/s of congestion via reducing preload and PCWP • Nitroprusside is mixed vasodilator
  18. 18. Nitroglycerin • Venodilation is predominant effect, also has mild arteriodilation at higher doses (200mcg/min) • Causes coronary dilation, ideal in HF pt w/ CAD and myocardial ischemia • Continuous infusion (short half-life 1-3mins) • Reduce preload and PCWP • Tachyphylaxis develops w/in 72h (resistance) • Initial dose 5-10 mcg/min increased every 5-10 mins • Maintenance dose: 35-200mcg/min • S.E: HoTN, excessive decrease in PCWP
  19. 19. Nesiritide • Recombinant Human BNP • Causes vensous & arterial dilation and natriuresis • Reduces PCWP, preload, afterload, SVR, BP, increases CO, no effect on HR • No tolerance build up • Longer half life than NTG and Nitroprusside • Use in cardiac ischemic • S.E: worsening of renal fcn • Natriuresis ( loss of Na & water) • Difficult to titrate due to longer half life
  20. 20. Sodium nitroprusside • Source of nitric oxide in vascular smooth muscle • Given as continuous IV infusion • Venodilation & arteriodilation at any dose • Decrease preload, congestion, PCWP, SVR, BP, • Increase CO • More potent in lowering BP than NTG • Can worsen myocardial ischemia • Cyanide and/or thiocyanate toxicity w/ liver or renal insufficiency
  21. 21. • Rapid onset of action but effects last less than 10 mins • initiated at low doses (0.1-0.2 mcg/kg/min) increments (0.1-0.2 mcg/kg/min) every 5 to 10 minutes to avoid hypotension. • Effective doses :from 0.5 to 3 mcg/kg/min • Avoid in increase ICP pts may worsen cerebral edema
  22. 22. Vasopressin antagonists • Tolvaptan & conivaptan: inhibit AVP receptors.
  23. 23. Ultrafiltration: • Renal impairment • rapid fluid removal • salt and water may be eliminated at rates of up to 500 mL/h • reduces PCWP and increases diuresis. • Potential candidates for : diuretic resistance, renal impairment following diuretic administration, or continued renal impairment despite inotropic therapy
  24. 24. • Complications of ultrafiltration: • central venous access (infection) • rapid volume removal • intravascular depletion • electrolyte depletion
  25. 25. Inotropes: • Dobutamine, Milrinone • Increase intracellular cAMP -> increase contractility • Help perfuse vital organs • May increase workload/ischemia • All are associated w/ risk for arrhythmias • Improve diuresis • Give to patient with cardiogenic shock, depressed CO and low SBP
  26. 26. Dobutamine • synthetic catecholamine, β1- and β2-receptor agonist with some α1-agonist effects. • Improve contractility and CO w/ minimal change in HR and MAP. • Increase CO-> decrease SVR • Reduce PCWP (useful in congestion) • Causes increase in myocardial oxygen consumption • Avoid use if pts is on B-blocker • Effect is observed w/in 10 mins elimination half life 2 mins • Initial dose 2.5-5 mcg/kg/min may be increase to 20mcg/kg/min • S.E tachycardia & arrhythmia
  27. 27. Milrinone • Phosphodiesterase inhibitors • Positive inotrope, vasodilator • Causes increase in SV, CO, reduce PCWP with minimal change on HR & MAP • Useful for congestion and low CO • Ideal for use in pts on B blockers • IV administration • Long half-life • S.E arrhythmia, HoTN, thrombocytopenia
  28. 28. Dopamine (inotropic & vasopressor activity) • At lower doses (3-10mcg/kg/min) activates B1, B2, D1 receptors increasing inotropy, SV, HR, CO. • At higher doses (>10mcg/kg/min) activate a1 & increase chronotropy & arrhythmia • increase BP ,CO,PCWP, coronary ischemia Highly proarrhythmic, should be reserved for pts w/ HoTN and near cardiogenic shock.
  29. 29. Arrhythmia Management • Both supraventricular and ventricular arrhythmias can occur in association with pulmonary edema , all may associate to ADHF
  30. 30. Atrial Fibrillation • there are several possible relationships: • Acute HF can precipitate AF due to increases in left atrial pressure and wall stress. • AF can cause acute HF, particularly if the ventricular response is rapid. • AF may be chronic and not directly related to the acute HF decompensation.
  31. 31. • In some patients with AF and ADHF, effective treatment of pulmonary edema results in slowing of the ventricular rate or spontaneous reversion of the arrhythmia. • If AF persists, it is treated in the same fashion as AF in other situations , rate control are preferred
  32. 32. • Restoration of sinus rhythm should be considered in the following settings (DC Shock): • If AF is associated with hypotension or evidence of cardiogenic shock • If AF is clearly the cause for pulmonary edema • If AF is associated with new or increased ischemia • If the response to effective therapy of pulmonary edema is slow or suboptimal • Heparin should be started prior to cardioversion if possible
  33. 33. Ventricular Arrhythmia • Ventricular tachycardia during pulmonary edema is usually life-threatening. • As a result, prompt electrical cardioversion or defibrillation is required. • If the arrhythmia recurs after reversion, antiarrhythmic therapy, particularly with amiodarone, may be effective.
  34. 34. Renovascular Hypertension • Recurrent unexplained heart failure (HF) decompensation and/or flash (sudden-onset) pulmonary edema occurs in some patients with renovascular hypertension. • often with preserved (normal or near normal) left ventricular systolic function. • Flash pulmonary edema appears to be more common in patients with bilateral renal artery stenosis as compared to those with unilateral disease.
  35. 35. • The combination of bilateral renal artery stenosis and flash pulmonary edema has been named the Pickering syndrome. • Acute treatment of acute decompensate HF in patients with this syndrome includes blood pressure control , diuresis. • In patients who are euvolemic or dehydrated, diuresis should be avoided, as it may lead to renal insufficiency, and preload reduction with nitrates is preferable.
  36. 36. Monitoring • daily monitoring of vital signs (including orthostatic blood pressure) and at least daily monitoring of weight, fluid intake and output, symptoms and signs of congestion, serum electrolytes, blood urea nitrogen, serum creatinine, and oxygen saturation until stable Serum potassium and magnesium levels should be monitored at least daily, and more frequent monitoring may be required when diuresis is rapid. • Routine tests include blood glucose, troponin, complete blood count, and the International Normalized Ratio if warfarin is used.
  37. 37. • Evaluation of liver function tests, and urinalysis is frequently indicated and arterial blood gas testing is occasionally indicated (eg, to detect carbon dioxide retention). • Measurement of brain natriuretic peptide (BNP) or N-terminal pro BNP can be of value in clarifying the cardiac basis of respiratory distress and/or guiding therapy.
  38. 38. Summary And Recommendations • Hospital admission is recommended for patients with acute decompensated heart failure (ADHF) with evidence of severe decompensation (including hypotension, worsening renal function, or altered mentation), dyspnea at rest, hemodynamically significant arrhythmia including new onset atrial fibrillation, or acute coronary syndrome. • Hospitalization should be considered for other patients with ADHF, including those with signs or symptoms of pulmonary or systemic congestion (with or without weight gain), major electrolyte disturbance, or associated comorbid conditions. • High hospital readmission rates are partly due to ineffective fluid removal. Daily assessment of patient weight may be the most effective method for documenting effective diuresis. For accurate comparisons, daily measurements should use the same scale and should be performed at the same time each day, usually in the morning, prior to eating and after voiding.
  39. 39. • Treatment goals for patients admitted with ADHF include improving symptoms, optimizing volume status, identifying etiology and precipitating factors (particularly ischemia), initiating and optimizing oral therapy, minimizing side effects, educating patients, and considering a disease management program. • The following initial therapies are similar in systolic and diastolic HF: diuresis, supplemental oxygen and assisted ventilation, and vasodilator therapy in selected patients. • Some medications should be avoided or used with caution in the acute setting (eg, angiotensin converting enzyme [ACE] inhibitors and beta-blockers) in patients with systolic dysfunction. In patients on ACE inhibitors and beta blockers, the medications can be continued if the patient is relatively stable (eg, just needs diuresis). Inotropic agents are not indicated in patients with diastolic dysfunction with preserved systolic function.
  40. 40. • Atrial fibrillation can precipitate ADHF and ADHF can promote atrial fibrillation (AF). • An initial strategy of rate control is reasonable if AF does not appear to be the precipitant of ADHF. • Restoration of sinus rhythm should be considered if AF is associated with hypotension or cardiogenic shock, if AF is the cause for pulmonary edema, or if the response to therapy of pulmonary edema is suboptimal.
  41. 41. • Ventricular tachycardia during pulmonary edema generally requires prompt electrical cardioversion or defibrillation. • Careful discharge planning and transition to outpatient care is indicated to reduce the risk of post-discharge mortality and readmission

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