Downloaded 61 times
More Related Content
![[20170216][Journal Club][Enhanced recovery pathways versus standard care afte...](https://cdn.slidesharecdn.com/ss_thumbnails/20170216journalclub-171114232901-thumbnail.jpg?width=640&height=640&fit=bounds)
Similar to 2013 sept 20_final__acute_decompensated_heart_failure
2013 sept 20_final__acute_decompensated_heart_failure
- 1. Acute Decompensated Heart Failure: Optimizing Outcome Dr Jaganmohan Tharakan Professor of Cardiology SCTIMST, Trivandrum
- 2. Acute Decompensated Heart Failure •Syndrome complex characterized by rapidly developing symptoms of new onset de novo heart failure or worsening of chronic heart failure culminating in acute decompensation and requiring monitored therapy including hospitalization • Sentinel prognostic event with 50% risk of rehospitalization at 6 months and 30% mortality at 1 year
- 3.
- 4. Acute Heart Failure •>80% have decompensation of existing HF • Often several days of gradual weight gain and worsening dyspnoea precede ADHF • Fluid overloading is the acute presentation • Close to 50% have HF and preserved EF • Cardiogenic shock is a rare presentation • ACS and renal dysfunction to be assessed early
- 5. Acute Decompensated HeartFailure Optimize Outcome: Opportunities • Recognition of AHF and instituting prompt life saving intervention: time saved is life saved • Aggressive intervention to support circulation when a treatable/ reversible cause is identified: especially in De novo AHF • Optimize disease modifying medications/ interventions once stabilized • Prognostic markers/ risk score for intense out of hospital monitoring • At hospital discharge: Guideline directed medical therapy as re-hospitalization for AHF is 50% at 6 months
- 6. ADHF: Reversible/ Treatablecauses • Non adherence to medications, salt/ fluid restriction • Acute myocardial ischemia/ACS • Hypertension • AF/ tachy/ brady arrhythmias • Negative inotropic drugs/ NSAIDS/ Steroids/ thiazolidinediones • Alcohol/ cocaine • Endocrine disorders( DM, thyroid) • Infections/ anaemia/renal dysfunction/ • Other CV disorders(IE/ valve disease)
- 7.
- 8. Acute heart Failure (TVM HF Registry 624 pts) • Mean Age 60 years • Acute de novo HF 40% • Males 69% • IHD 69.5% • DCM 14.5% • RHD 8% • Diastolic HF 3% • HT55%, DM 52%, Smoking 44%, AF 14%, CKD 15% • In hospital mortality 9%
- 9. ADHF pts characteristics (OPTIMISEregistry) • Preserved LV function • EF 55% • Age 75yrs • Males 38% • IHD 38% • BNP 601pg/ml • Reduced LV function • EF 24% • Age 70 yrs • Male 62% • IHD 55% • BNP 1170 pg/ml
- 10. General Concepts inmanagement of ADHF • 1. Severity of ADHF presentation does not always predict long term outcome • 2. LVEF at presentation and improvement/ worsening influence outcome • 3. Hemodynamic improvement should come from amelioration of myocardial dysfunction rather than by increasing contractility with inotropes
- 11. General Concepts inmanagement of ADHF • 4. Ischemic Viable myocardium requires revascularization • 5. Attempt to limit myocardial and renal damage: intervention to improve clinical signs and symptoms like diuretics, vasodilators, inotropes may worsen myocardial and renal damage
- 12. Clinical Scenario atpresentation • High SBP > 160 mmHg 25% • Normal to High normal BP 50% • Hypotension (SBP<90) 10% • Cardiogenic shock 1% • Flash pulmonary edema 3%
- 14.
- 15. ADHF: Noninvasive Investigations •Chest X ray, ECG • 2D Echo Doppler: EF, LV dimension, wall thickness, wall motion, valve function, PAH, RV function • Myo. Viability/ reversible ischemia study if CAD suspected and suitable for revascularization • CMRI for myocardial infiltration/ fibrosis/ scar
- 16. ADHF: Invasive Investigations •PA catheterization: hypoperfusion with uncertain volume status/respiratory disease • CAD suspected and eligible for revascularization • Endo myocardial Biopsy when specific diagnosis suspected & can alter therapy Transplant rejection, giant cell myocarditis, infiltrative process, active myocarditis with progressive ventricular dysfunction
- 17. Acute De-compensated HF:Management Hypoxemia and respiratory failure due to pulmonary Edema • Usual treatment for acute pulmonary edema • O2 by mask : O2 sat>= 90%/ – Noninvasive ventilation CPAP, NIPPV (avoid if hypotension/altered sensorium) – Intubated ventilation • Vasodilators if SBP >110mmHg – NTG – Nitroprusside – Nesiritide
- 18. Acute De-compensated HF DiureticTherapy • Bolus parenteral Loop diuretics: equal to pt’s oral maintenance dose: Infusion / intermittent bolus/ high dose diuretics • Add another diuretic like thiazide group/ metolazone • Add small dose dobutamine at 2-5 mic/kg/m • Resistant fluid overload: Ultra filtration • Aquaretics if euvolumic hyponatremia
- 19. Ultra filtration inADHF CARESS trial(188 pts) • In patients with volume overload ADHF as it reduces volume and electrolytes equally • UNLOAD(200 pts): superior to diuretics • CARESS study:High risk ADHF pts.: Similar outcome for weight reduction, but higher rise in ser creatinine, need for dialysis, and other adverse events. • AVOID HF: Ongoing trial
- 20. Inotropes in Heartfailure Inotropes/ Vasopressors/ both • Inotrope: Dobutamine: minimal vasodilatory effect (beta 2 stimulation) • Inotrope with vaso dilatation: Milrinone, Levosimendan • Vasopressor with Inotropic action: Dopamine, Nor epinephrine
- 21. Pts with hypotension/Hypo- perfusion SBP <85 mmHg/ reduced urine output/ lactate • Exclude hypovolumia • Modify dose of ACEI/ beta blockers • Dobutamine infusion • Short term circulatory support • I/V levosimendan if exposed to beta blockers • Vasopressor like dopamine/ norepinephrine if in cardiogenic shock despite an inotrope, to maintain SBP and end organ perfusion
- 22. ADHF: Inotropic Support Indications •Until definitive therapy( MCS/transplant) or resolution of precipitating cause in Pts with cardiogenic shock , to maintain systemic perfusion and preserve end organ function • Short term inotropic support in pts with severe systolic LV dysfunction, low BP, low CO : to preserve end organ function • Long term palliation with inotropic support
- 23. Mechanical Circulatory Support •MCS for resistant HF: definitive management ( transplant) or recovery anticipated. • Percutaneous/ extra corporeal assist devices: bridge to recovery/ bridge to decision when in acute profound hypotension
- 24. Pts with AFand fast VR • Anticoagulation with heparin • Rhythm control: – Emergent DC cardioversion if hemodynamically unstable -- Elective DC cardioversion if recent AF(<48hrs) or TEE echo excludes LA thrombus • Rate control: Digoxin, ? amiodarone
- 26. Potential New Therapies •Cinaciguat: Soluble Guanilate cyclase activators • Chimeric natriuretic peptides: Avoids arterodilating hypotensive effects of BNP, with venodilating and natriuretic action intact • Istaroxime: membrane Na+ K+ ATPase inhibitor with SERCA2a activation. • Stresscopin: Human peptide Urocortin2: Activates myocardial reperfusion injury protection pathways: increase EF and CO, decrease SVR,
- 27. Vaso active drugsin ADHF Relaxin • Endogenous peptide associated with pregnancy and acts through relaxin receptor: reduce inflammation, decrease fibrosis, increase vasodilation, promote renal blood flow, increase vascular endothelial growth factor, and angiogenesis.
- 28. Vaso active drugsin ADHF Relaxin: Serelaxin • RELAX HF:1161 pt. of ADHF with preserved SBP >115 mmHg. • Serelaxin 30 ug/kg/day x48 hrs vs Placebo • Significant improvement in dyspnoea scale • No impact on short term mortality/ HF readmission at 60 days, though 180 day mortality was significantly lower. • Hypotensive episodes higher but renal dysfunction less than placebe group
- 29. Investigational drugs inADHF Omecamptive Mecabril • First selective cardiac Myosin activator: acts through greater binding of myosin to actin: – Increases myo. contractility without increase in O2 consumption: increased EF, stroke volume, decreased LVES and LVED volume – Chest pain, tachycardia and myo. Ischemia more common ATOMIC- AHF study is Phase 3 trial: ongoing
- 30. Vaso active drugsin ADHF Ularitide • Synthetic form of Urodilantin: human natriuretic peptide produced in kidney: induces natriuresis and diuresis. Also potent vasodilator( increases intracellular cyclic GMP) and increased renal blood flow) : Two double blind studies have shown favorable outcome in ADHF by symptom improvement and hemodynamics • Phase 3 trial(TRUE-AHF >2110 pts) ongoing
- 31. Investigational drugs inADHF Adenosine A1 receptor antagonist: Rolophylline • Preserve GFR, improve diuresis, increase sodium excretion by kidney • Phase 2 trial: better relief of dyspnoea and lesser renal dysfunction • Phase 3 trial: PROTEC:2033 pts.: negative trial with none of the primary end points significant and safety was questioned due to neurological side effects: seizure and stroke
- 32. Newer Molecules intreatment of AHF • Overall impact in treatment is small • Mechanical Circulatory support will continue to be used more frequently to bridge to recovery/ transplant/ destination therapy • Newer strategies will be required, for any major impact in management of AHF
- 33. ADHERE Registry: Mortalityin ADHF : SBP and Ser Creatinine
- 34. Biomarkers in AHF •To diagnose HF in ER • To predict outcome of HF therapy • To plan follow up strategy at discharge and prognostication
- 35. Acute Heart Failure Biomarkers:BNP • BNP/ NT pro BNP : to support clinical judgement for diagnosis of ADHF • BNP/ NT pro BNP and/or cardiac troponins in establishig diagnosis severity and prognosis of ADHF • BNP/ NT pro BNP to guide therapy in ADHF • Other biomarkers of myocardial injury/ fibrosis: ST2
- 36. Biomarkers in HF BNP/NT pro BNP • PROTECT (150 pts): Compensated CHF • HOME HF outpatient monitoring evaluation(350 pt.)ADHF pts: BNP based home management vs BNP blinded (use wt/ symptoms/signs) vs Controls (usual care) • GUID-IT: ADHF pts monitored with NT pro BNP guided therapy
- 37. Novel Cardiac Biomarkersin ADHF • Soluble ST2 receptor: interleukin family: upregulated by myocardial strech: predicts 1 year mortality • NGAL: neutrophil gelatinase ass. Lipocalin: marker of kidney injury: higher levels predict 30 day mortality • Copeptin: C terminal protein of pre pro vasopressin: highest quartile predicted very high 90 day mortality
- 38. Novel Cardiac Biomarkersin ADHF: contd. • Midregion pro adrenomedullin • Galactin 3: indicator of myocardial collagen deposition and fibrosis: marker of early HF Will a multi marker approach help in prognostication of ADHF
- 39. Post ADHF discharge:Mortality 25% at 1 year EVEREST trial
- 40. HF: Monitoring topredict/ prevent ADHF admissions • Devices: Externally applied Impedance Cardiography (PREDICT study 211 pts) • Internally placed devices measuring intra thoracic impedance(PARTNER 2HF: CRT device with Impedance monitoring): predicted subsequent admission for ADHF • PA / LA/ LVEDP monitoring devices Usefulness uncertain for mortality benefit
- 41. Heart Failure RiskScores Circ HF 2013 End point: Death/ transplant/ Assist device • Heart Failure Survival Score(200pts): – IHD, QRS>120ms, LVEF, Resting HR, mean BP, O2 consumption, ser Na • Seattle Heart Failure model: (1100pts) – Age, LVEF, NYHA class, SBP, Diuretic dose, Na+, uric acid, ser. Chol., lymph. count - Sex, IHD, QRS >120ms, ICD, CRT, betablockers, ACEI, Statins, Allopurinol,
- 42. Heart Failure RiskScores • SHOCKED predictor: (900pts): Age>75, NYHA>II, AF, COPD, CKD, LVEF<20%, DM • PACE: (900 pts) PVD, Age >70, Creatinine >2, EF < 20%, • ADHERE registry( for acute mortality): SBP, Ser creatinine and BUN • Frankenstein: BNP , 6 WT′
- 43. In multivariable models,nearly all tested covariates performed similarly across LVEF strata for the outcome of death from any cause, as well as for HF-related and all- cause hospitalizations. Conclusions—We found that in a large, diverse contemporary HF population, risk assessment was strikingly similar across all LVEF categories. These data suggest that, although many HF therapies are uniquely applied to patients with reduced LVEF, individual prognostic factor performance does not seem to be significantly related to level of left ventricular systolic function. (Circ Heart Fail. 2013;6:635-646.)
- 44. Post Discharge Multidisciplinary Management Program • Cardiac Rehabilitation: periodic follow up, education, optimize drug treatment, general medical care, exercise program, ensure access to hospital care • Palliative Care: frequent hospitalization, not listed fro transplant or mechanical circulatory support, poor quality of life, dependence for daily needs, close to end of life • Heart failure team: practitioner, nurse, pharmacist, dietician, psychologist, physiotherapist
- 45. Conclusion • Acute HeartFailure, is a medical emergency and rapid, coordinated multi disciplinary approach can significantly reduce mortality. • Stabilized patients of AHF, to have GDMT/ devices/ revascularization as indicated • At discharge: patient education, counseling, compliance with GDMT and frequent clinic visits can prevent re-hospitalization for AHF
- 46.
- 47. I/V Vasodilators inAHF • Nitroglycerine: 10 – 100 ugm/min • Nitroprusside: 0.03 to 0.3 mic/kg/min • Nesiritide: 0.1 mic/kg/min
- 48. General Concepts inmanagement of ADHF • 1. AHF with preserved EF is being recognized more often and carry similar long term prognosis • 2. Severity of ADHF presentation does not always predict long term outcome • 3. LVEF at presentation and improvement/ worsening influence outcome • 4. Hemodynamic improvement should come from amelioration of myocardial dysfunction rather than by increasing contractility with inotropes
- 49. General Concepts inmanagement of ADHF • 5. Ischemic Viable myocardium requires revascularization • 6. Attempt to limit myocardial and renal damage: intervention to improve clinical signs and symptoms like diuretics, vasodilators, inotropes may worsen myocardial and renal damage
- 50. Risk Score toPredict Acute Decompensated HF: PRIDE Score • Elevated NT Pro BNP>450 pg/ml(<50yrs) 4 • Interstitial pulm edema 2 • Orthopnea 2 • Lack of fever(r/o infection) 2 • Current diuretic use/Age>75/ rales on lung exam/ lack of cough 1 • Early identification and institution of treatment/ correction of causative factors improve outcome
- 51. European Heart failureStudy • Worsening of chronic HF: 65% • Acute pulmonary edema: 16% • Hypertensive HF: 11% • Cardiogenic shock: 4% • Acute right heart failure: 4% ACS presenting as HF :10% of all ACS
- 52. ADHF: Prognostic markers •Mathematical model using NT pro BNP value as a continuous variable with age and pretest probability of HF had 96% sensitivity and 84% specificity for predicting a ADHF • Mid regional pro ANP >120pmol/l: also affected by age, ender, BMI, AF,renal function
- 53. Positive Inotropes inHF Indications • Advaced HF, • Reduced EF, LV dilatation, • Euvolumic hypotensive ( adequate filling pressure) • Intolerant to vaso dilators • Signs of diminished peripheral perfusion or renal other end organ dysfunction
- 54. Old drugs: Newdosage strategy Dopamine and furosemide • Low dose dopamine 5 mic/kg/min and low dose furosemide appears safer for renal fuction deterioration (DAD HF study) • Phase 3 trials ongoing : DAD HF 2, ROSE AHF
- 55. Diuretic Strategy inADHF Low vs high dose furosemide: DOSE trial(308pts) • Low( usual Furosemide dose)vs High(2.5 times) X continuous vs intermittent parenteral dosing • No significant difference in safety/ efficacy • Acutely, high dose group had higher creatinine elevation, but at 7 days, this was not significant • Secondary end points: greater dyspnoea relief, fluid loss and weight loss with higher dose
Editor's Notes
- #10 Characteristics, treatments, and outcomes of patients with preserved systolic function hospitalized for heart failure: A report from the OPTIMIZE-HF Registry. J Am Coll Cardiol 50:768, 2007.
- #15 Noninvasive positive airway pressure ventilation/ continuous positive airway pressure ventilation
- #34 Data from the ADHERE registry have been used to develop a classification and regression tree (CART) analysis to identify the best predictors of in-hospital mortality and to develop a risk stratification model. Of the 39 variables evaluated, the CART method identified elevated blood urea nitrogen (BUN), lower systolic blood pressure (SBP), and higher serum creatinine at the time of admission to be the best discriminators between hospital survivors and nonsurvivors. A similar model from the OPTIMIZE registry identified serum creatinine, SBP, age, heart rate, and serum sodium as the most powerful predictors of in-hospital mortality in AHFS.[52] A combination of two variables (creatinine concentration and SBP) that were powerful predictors in both ADHERE and OPTIMIZE-HF was able to risk stratify patients into risk groups (Fig. 27-5). FIGURE 27-5 In-hospital mortality by serum creatinine (SCr) concentration and systolic blood pressure (SBP) in the ADHERE registry.(From Abraham WT, Fonarow GC, Albert NM, et al: Predictors of in-hospital mortality in patients hospitalized for heart failure: Insights from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients With Heart Failure [OPTIMIZE-HF]. J Am Coll Cardiol 52:347, 2008.)
- #40 Mortality and rehospitalization rates postdischarge in patients admitted with HF may be as high as 15% and 30% within 60 to 90 days, respectively. Recent claims data using the U.S. Medicare sample suggest an even more striking rate of rehospitalization in elderly patients, with a 30-day rehospitalization rate of 27%.[49] Approximately 30% of patients hospitalized with HF and reduced ejection fraction die suddenly within several months after discharge, and 40% die of progressive HF in spite of receiving evidence-based therapy (Fig. 27-4).[50] Of note, approximately half of the rehospitalizations are not HF related.[50] Rates of early postdischarge events in patients with HFpEF appear to be similar to those in patients with reduced ejection fraction. However, the modes of death and reasons for rehospitalization have not been studied in the former group. It is possible that a significant number of morbid events in the HFpEF population are related to coexisting cardiac or noncardiac comorbidities, such as CAD, hypertension, atrial fibrillation, renal insufficiency, or stroke.[17] FIGURE 27-4 Postrandomization causes of death of 4,133 patients admitted with worsening HF and reduced ejection fraction in the EVEREST trial. The overall mortality at 9.9 months was 26%.(From O’Connor CM, Miller AB, Blair JE, et al: Causes of death and rehospitalization in patients hospitalized with worsening heart failure and reduced left ventricular ejection fraction: Results from Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan [EVEREST] program. Am Heart J 159:841, 2010.)