Medical Treatment for acute Decompensated Heart Failure. Vlasis Ninios Cardiologist St. Luke s s Hospital Thessaloniki 2011

Transcription

1 Medical Treatment for acute Decompensated Heart Failure Vlasis Ninios Cardiologist St. Luke s s Hospital Thessaloniki 2011

2 2010 HFSA guidelines for ADHF 2009 focused update of the 2005 American College of Cardiology/American Heart Association (ACC/AHA) HF guidelines 2008 European Society of Cardiology (ESC) guidelines for acute heart failure

3 General Approach Clinical signs and symptoms Cough, dyspnea,, fatigue Tachypnea,, wheezing, hypertension, hypotension, tachycardia Perfusion status Volume status

4 Precipitating Factors MI, Ischemia Arrhythmias (AF,VT, etc.) Hypertension Renal Failure Anemia, infection, thyroid disease Drugs

5 Tests ECG CXR Lab data BNP, pro-bnp Echo Cardiac catheterisation Coronary angiography

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9 Differential Diagnosis Pulmonary embolism Pneumonia Asthma ARDS

10 PATHOPHYSIOLOGY Fluid transudation into the pulmonary interstitium or alveolar spaces Rapid and acute increase in left ventricular filling pressures and left atrial pressure Role of lymphatics

11 Predisposing conditions Systolic dysfunction Diastolic dysfunction LVOT obstruction Mitral stenosis

12 Treatment-general considerations Hospital admission Hypotension, renal dysfunction, hypoperfusion Rest dyspnea Arrhythmia ACS

13 MONITORING Vital signs Fluid balance, daily weight Electrolytes, BNP, blood gas Telemetry Hemodynamic monitoring Echo monitoring

14 Treatment goals Hemodynamic stability, improve symptoms Oxygenation, ventilation 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 Identify risk of thromboembolism and need for anticoagulant therapy Educate patients and relatives

15 Systolic vs diastolic Similar: Diuresis,, Oxygen, vasodilation Hypertension and tachycardia management in diastolic Inotropes usually in systolic

16 Arrhythmia management AF Rate control Cardiogenic shock (DC cardioversion) VT DC shock

17 Initial stabilization Airway assessment to assure adequate oxygenation and ventilation, including continuous pulse oximetry Vital signs assessment with attention to hypotension or hypertension Continuous cardiac monitoring Intravenous access Seated posture Diuretic therapy Vasodilator therapy Urine output monitoring

18 Oxygen and assisted vantilation Face mask high flow of O2 noninvasive positive pressure ventilation (NPPV) Intubation- ventilation

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20 Diuretics No randomised trials but extensive experience Hypotension, cardiogenic shock Aortic stenosis IV use is preferred Loop diuretics Dose similar to oral dose or frusemide to a naïve patient Monitoring of urine, electrolytes, renal function Beware of hypotension ie diastolic dysfunction

21 Diuretics and renal dysfunction Other causes If fliud overloaded, fluid removal If Creatinine rises, consider inotropes Ultrafiltration,, dialysis

22 Diuretic resistance Increase Add thiazide (metolazone) Continuous iv infusion Ultrafiltration Fluid restriction

23 Vasodilator therapy Nitroglycerine, nitroprusside, nesiritide Absence of hypotension and congestive symptoms Pulmonary edema and hypertension

24 Nitroglycerine Venodilation,, reduces LV filling pressure Reduces afterload at higher doses Tachyphylaxis Never with sildenafil Iv administration

25 Nitroprusside Potent venous and arterial dilator Reduces afterload Hypertensive emergencies, acute AR, acute MR Beware of cyanide toxicity Reflex tachycardia Usually for hrs

26 Nesiritide Recombinant human BNP Initial trials have shown favourable hemodynamic effects and symptom relief No effect on mortality (some concerns towards increase in mortality) Conflicting results on the effect on renal function Alternative in patient without hypotension and persistent symptoms despite conventional therapy. Close monitoring is recommended

27 Additional therapy ACE inhibitors and ARBs B-blockers Inotropes DVT prophylaxis Morphine

28 ACE-I I and ARBs Continued therapy Decrease or stop in Hypotension, Acute Heart Failure, Hyperkalemia Initiation of therapy Best NOT to initiate early ( hours) Borderline blood pressure, hyponatremia Exception is in AMI

29 B-blockers Reduce mortality long-term Cautious use in acute phase of patients with systolic dysfunction If on chronic therapy, continue if tolerated (OPTIMISE HF, Italian survey on AHF) Decrease or withdraw if patient is compromised Do not initiate in the acute phase Initiate prior to discharge in stable patients (no evidence of fluid retention) Low dose and careful titration

30 Inotropes Severe systolic LV dysfunction and low output state Hypotension Elevated filling pressure Evidence of end-organ hypoperfusion Continuous monitoring is essential Increase heart rate and myocardial O2 demand May provoke arrhythmias OPTIME-CHF (Milrinone( vs palcebo). Hypotension and arrhythmias

31 Milrinone Phosphodiesterase inhibitor Potent positive inotrope Reduces systemic and pulmonary vascular resistance Improves LV diastolic compliance Concomitant use of b-blockers b blockers does not diminish drug effect OPTIME-CHF (Milrinone( vs palcebo). Hypotension and arrhythmias. Worse outcome in IHD

32 Dobutamine B1 receptor agonist Increase SV and CO Modest decrease in SVR and PWP Dobutamine holiday No survival benefit Effect is offset by b-blocker b blocker use (carvedilol( more than metoprolol)

33 Levosimendan Enhance myocardial response to a given calcium concentration Reduction in cardiac filling pressures and increase in cardiac index Active metabolite that persists for up to 5 days LIDO trial acute hemodynamic effects were superior to Dobutamine,, survival benefit at 6 months RUSSLAN trial post MI, trend to survival benefit at 6 months SURVIVE and REVIVE trials no benefit or harm in mortality

34 DVT prophylaxis LMWH, fondaparinux

35 Morphine sulphate Limited data Reduces anxiety and work of breathing Arteriolar and venous dilatation due to reduction of sympathetic outflow Some safety concerns Avoid unless in AMI

36 ULTRAFILTRATION ADVANTAGES Effective, adjustable rates No effect on electrolytes Decreased neurohumoral activity Renal failure, diuretic resistance, excessive fluid overload RAPID-CHF, UNLOAD, more effective fluid removal, less hospitalizations No safety data

37 Vasopressin receptor antagonists Tolvaptan EVEREST trial, SALT-1 1 and 2, SALTWATER Increase Na by water excretion Limitations Thirst Neurological events by rapid Na correction Cost

38 Conclusion Accurate assessment, rapid diagnosis, life- saving measures are essential O2, diuretics, vasodilators mainstay of treatment Close monitoring is essential Ultrafiltration,, and/or inotropes may be required Mechanical assistance in severely compromised patients ACE-I I and b-blockers b blockers are best initiated after initial stabilization has been achieved