acute heart failure final power point presentation

acute heart failure final power point presentation

1. Acute Heart Failure Management Presenter: Dr. Rebeka.A (IMR3) Moderator: Dr. Adane (Consultant internist and cardiologist) July 2025

2. Outline Introduction Epidemiology Pathophysiology Evaluation Management 4/15/2025 2

3. Acute heart failure AHF refers to rapid or gradual onset of symptoms and/or signs of HF, severe enough for the patient to seek urgent medical attention, leading to an unplanned hospital admission or an emergency department visit. AHF may be the first manifestation of HF (new onset) or, more frequently, be due to an acute decompensation of chronic HF

4. Leading cause of hospitalizations in subjects aged >65 years and is associated with high mortality and hospitalization rates . In-hospital mortality ranges from 4% to 10 %.Post-discharge 1-year mortality can be 25>30 % with up to more than 45% deaths or readmission Clinical severity the determined by precipitants, the underlying cardiac substrate, and the patient’s comorbidities.

5. An institution based retrospective cohort study was conducted at Asella Referral Teaching hospital,Ethiopia,from sep2022< Augest 2023 The mean age was 56 years, and 52.4% were female IHD ( 36.4%) was the most frequent cause of HF In-hospital mortality was 13 .4%. The leadng precipitating factor was pneumonia,24% 4/15/2025 8

6. AHF is to consider as the result of the interaction Underlying substrate, Initiating mechanisms or triggers, and Amplifying mechanisms Contribute to a common set of clinical signs and symptoms (primarily related to congestion, end-organ dysfunction, or both ) that define AHF 4/15/2025 9 Pathophysiology of AHF

7. Pathophysiology of AHF … 4/15/2025 10

8. Pathophysiology of AHF … Congestion Systemic/pulmonary congestion, caused by a high VDP , dominates the clinical presentation of most patients hospitalized for AHF. Final common pathway producing clinical symptoms leading to hospitalization Gradual increases in intravascular volume lead to symptoms of congestion and clinical presentation Hemodynamic Congestion (increased VDP) precedes clinical congestion Hemodynamic congestion may contribute to the progression of HF 4/15/2025 11

9. Pathophysiology of AHF … Myocardial Changes in systolic function and decreased arterial filling initiate a cascade(SNS and RAAS) of result in adaptive in the short term but maladaptive when elevated chronically Activation of these neurohormonal axes leads vasoconstriction, sodium and water retention, volume redistribution from other vascular beds, increases in diastolic filling pressures , and clinical symptoms Underlying IHD, initial defects in systolic function may initiate a vicious cycle of decreasing coronary perfusion , increased myocardial wall stress, and progressively worsening cardiac performance 4/15/2025 12

10. Pathophysiology of AHF … Myocardial Impairment of diastolic function are present in HF patients regardless of EF and related to passive stiffness, abnormal active relaxation of the left ventricle, or both Hypertension, tachycardia, and myocardial ischemia (even in the absence of CAD) can further impair diastolic filling. Contribute to increase LV end-diastolic pressures , which are reflected back to the pulmonary capillary circulation 4/15/2025 13

11. Pathophysiology of AHF… Vascular mechanism Involves endothelial dysfunction , Arterial stiffness , Peripheral vasoconstriction Redistributes blood centrally, increasing pulmonary venous congestion and edema. Increases afterload, LV filling pressures, and postcapillary pulmonary venous pressures, resulting in worsening of Pulmonary Edema and dyspnea Causes ventricular wall stress and increased myocardial ischemia and arrhythmias Elevated central venous pressure reduces renal function, resulting in greater fluid retention that further elevates venous pressures 4/15/2025 14

12. Neurohormonal mechanism Increased plasma concentrations of norepinephrine, plasma renin activity, aldosterone, and endothelin (ET)-1 reported in patients with AHF Associated with vasoconstriction and volume retention , Contribute to myocardial ischemia and congestion, thus exacerbating cardiac decompensation. Proinflammatory cytokines ( TNF- α and IL-6 ) are elevated in patients with AHF Direct negative inotropic effects on the myocardium Increasing capillary permeability and inducing endothelial dysfunction 4/15/2025 15

13. Evaluation of AHF Initial evaluation of the patient with AHF focuses on : Establishing a definitive diagnosis as rapidly as possible Emergent treatment for life-threatening conditions (e.g., Shock, RF) Identifying and addressing any relevant clinical triggers/conditions requiring specific treatment (e.g., ACS, acute pulmonary embolism) Risk stratification in order to triage patient to appropriate level of care Defining the clinical profile of the patient ( based on BP, volume status ) in order to rapidly implement the most appropriate therapy 4/15/2025 16

14. Evaluation… Classification Based on the presence or absence of a prior history of HF 1.New-onset/de novo HF makes up about 20% of hospitalizations for AHF Mostly they have a background of risk factors for HF (stage A heart failure) 2.Acute Decompensated chronic heart failure Less dramatic clinical presentation, since the chronic nature of the disorder has allowed for recruitment of compensatory mechanisms and remodeling (e.g., increased pulmonary lymphatic capacity ) Neurohormonal activation may be less profound Diuretic resistance more common 4/15/2025 17

15. Evaluation of AHF…. Symptoms Related to Volume Overload(backward failure) Dyspnea (exertional, PND, orthopnea, or at rest), cough, wheezing Foot and leg discomfort Abdominal discomfort/bloating; early satiety or anorexia Related to Hypoperfusion(forward failure) Fatigue Altered mental status, daytime drowsiness, confusion, or difficulty concentrating Dizziness, presyncope, or syncope 4/15/2025 19

16. Evaluation of AHF…. Signs Related to Volume Overload(backward failure) Rales, pleural effusion ,Peripheral edema (legs, sacral) Ascites, right upper quadrant pain, hepatomegaly/ splenomegaly Increased weight Elevated JVP, abdominojugular reflux Increasing S3, accentuated P2 Related to Hypoperfusion(forward failure) Cool extremities with/without palpable peripheral pulse Pallor, dusky skin discoloration Hypotension and narrow Pulse pressure 4/15/2025 20

17. Evaluation of AHF…. Clinical Triggers Onset and increase in systemic congestion of AHF can be triggered by several factors either directly or indirectly ACS, arrhythmias (AF), lung process (Pneumonia and PE), uncontrolled HTN and non-compliance with dietary recommendations and drug prescriptions are the most common identified precipitants About (~40–50%), no precipitants could be identified, whereas a combination of multiple factors were present in ~5–20% of patients 4/15/2025 21 OPTIMIZE-HF Registry

18. Evaluation of AHF…. Investigation CBC, RFT , electrolytes, Cardiac troponin , TSH, Lactate Chest X-ray/LUS – Congestion, lung infection ECG – rhythm , LVH signs, ischemic signs /ACS Echo – LV size and function, RWM (MI), Valvular diseases, pulmonary pressure, Estimate right/left side filling pressure, pericardial Disease Natriuretic peptides (BNP, NT- proBNP , MR- proANP ) High negative predictive value to rule out AHF if BNP <100 pg / Ml .NT- proBNP <300 pg /mL MR- proANP <120 pg /mL 4/15/2025 22

19. Management of AHF Management of AHF patients may be considered in the context of four phases of treatment with distinct goals Phase I- urgent/emergent treatment Phase II-hospital care Phase III- predischarge planning Phase IV-post discharge management 4/15/2025 23

20. Management… Congestion With Normotensive Congestion With Hypertensive Congestion With Hypotensive Congestion With Shock 4/15/2025 24

21. Management… Phase I- urgent/emergent treatment Evalute for CHAMPIT Symptom relief- Dyspnea(oxygen, Diuresis and/vasodilators) Identify etiology and precipitating triggers Hemodynamic stabilization Optimizing proven long-term therapies . 4/15/2025 25

22. 3CPO trial- 1069 pts- pulm . Edema Standard O2,with CPAP/NIPPV NIPPV-improvement of dyspnea, HR, acidosis after 1 hr. No decrease 7 day mortality, intubation

23. Management… Diuretics Loop Diuretics -25% of filtered Na Iv administration – rapid onset of action and avoids variable bioavailability Initial doses Low vs High Doubling of dose based on response( threshold type dose-response curve)  No increase in natriuresis until the threshold concentration of luminal diuretic is reached and, O nce the threshold is exceeded, the degree of natriuresis increases until a maximal ceiling is reached 4/15/2025 30

24. DOSE trial randomized 308 patients compared diuretic strategies in AHF I ntermittent vs. continuous and L ow-dose ( home dose ) vs. high-dose ( 2.5x home dose) with IV loop diuretics The primary end points patients' global assessment of symptoms, and the change in the serum creatinine level from baseline to 72 hours . No significant difference in either of the co–primary endpoints with administration by bolus compared to infusion or with the low- versus high-dose strategy High-dose strategy associated with greater diuresis and more favorable outcomes in some secondary measures( relief of dyspnea and net fluid loss at 72 hours) but also with transient worsening of renal function . 4/15/2025 31 Management… Diuretics

25. Management… Diuretics Evidences of benefit Observational studies-global improvement of dyspnea Early treatment (60 mins) reduces in hospital mortality Hemodynamic effects Morphine like effect - fall in cardiac filling pressures and decreased pulmonary congestion prior to the onset of the diuresis Adverse effect Volume depletion, electrolyte abnormality, alkalosis Worsening RFT 4/15/2025 32

26. Management… Diuretics Diuretic response should be evaluated. Urinary sodium content together with urine volume helpful for assessment of diuretic response on 1st day Refractory to loop diuretics add other diuretics (HCTZ, Metozalone , chlorothizide or spirolactone ) NSAIDs greatly reduce the efficacy of diuretics should be avoided 4/15/2025 33

27. Management… Diuretics 4/15/2025 34

28. Management… Diuretics resistance F ailure to achieve effective congestion relief despite appropriate or escalating doses of diuretics Reduced delivery of the diuretic to its site of action Tubular compensatory readaptation Neurohormonal activation strategies to overcome Diuretics resistance salt restriction, Higher effective single dose/higher dose frequency of loop diuretics, continuous infusion of diuretics Sequential nephron blockade through combination of two or more diuretics from different classes 4/15/2025 35

29. Conclusion The addition of acetazolamide to loop diuretic therapy in patients with acute decompensated heart failure resulted in a greater incidence of successful decongestion.

30. Management… Diuretics 4/15/2025 37

31. Management… Vasodilators For patients with acute pulmonary edema caused by increased afterload and fluid redistribution to the lungs in the absence/minimal fluid accumulation. In Clinical trials (TRUE-AHF, RELAX AHF2, GALACTIC) have not show a long-term survival benefit . Show an improvement in dyspnea and some short-term outcomes 4/15/2025 38

32. Management… Vasodilators Selection depends on the needed hemodynamic effect Afterload reduction- arterial dilators – nitroprusside Avoid in Acute MI , due to coronary steal phenomenon. Filling pressure reduction- nitroglycerin Use in hypertension, Acute MR, Acute AR Suggested as an adjunct to diuretic therapy for patients without adequate response to diuretics , Avoid ; RV infarction, AS, PDE-5Is use In patients with AHF and SBP >110 mmHg, i.v. vasodilators may be considered as initial therapy to improve symptoms and reduce congestion 4/15/2025 39

33. Management… Vasodilators 4/15/2025 40

34. Management… Inotropes Depending on mechanism of action classify into four: Catecholamine(NE, Dopamine, and dobutamine) Phosphodiesterase 3 inhibiter(Milrinone) Calcium sensitizer ( Levosimendan ) Digoxin Considered in patients with SBP <90 mmHg a,low cardiac out put, LV systolic dysfunction to improve peripheral perfusion and maintain end-organ function Associated with significant side effects, such as hypotension, atrial or ventricular arrhythmias , and an increase in in-hospital and possibly long-term mortality 4/15/2025 41

35. Management… Digoxin Rapidly improves hemodynamics without increasing heart rate or decreasing BP and may be considered in patients with a low BP caused by low cardiac output In patients who continue to have signs and symptoms of HF, digoxin therapy should be continued in addition to other therapies, with a dose resulting in a trough serum concentration less than 1 ng/ mL. 4/15/2025 42

36. Management… Vasopressors Vasopressors( NE, Dopamine and phenylephrine) reserved for patients with Marked hypotension in whom central organ hypoperfusion is evident Used to redistribute cardiac output centrally at the expense of peripheral perfusion and increased afterload NE is the preferred vasopressor for cardiogenic shock All these agents may induce end-organ hypoperfusion and tissue necrosis 4/15/2025 43

37. Management… Vasopressin- antagonists Arginine vasopressin (AVP), also known as antidiuretic hormone Main regulator of plasma osmolality inappropriately high in both acute and chronic HF Block V2-receptor of renal tubules- Promotes Aquaresis Tolvaptan –is the most studied drug No significant benefit :EVEREST Limited for use in volume overload and resistant hyponatremia 4/15/2025 44

38. Management… Ultrafiltration Peripheral ultrafiltration is an available modality to remove sodium and water in hospitalized patients with HF ultrafiltration is the removal of isotonic fluid , resulting in greater salt removal, potentially without the neurohormonal activation seen with diuretics CARRESS study 188 patients with AHF, WRF, and persistent congestion compare stepped pharmacologic care (IV diuretics dosed) to maintain UOP of 3 to 5 L/day plus IV vasodilators/inotropes if needed) with ultrafiltration (fluid removal rate, 200 mL/ hr ) Ultrafiltration resulted in similar Wt loss but increase in creatinine levels, compared to standard care, and associated with more adverse events, AKI, bleeding, and IV catheter-related complications 4/15/2025 45

39. Management… Mechanical circulatory support In patients presenting with cardiogenic shock, short-term MCS(IABP) may be necessary to augment cardiac output and support end-organ perfusion. IABP is not routinely recommended in cardiogenic shock post-MI 4/15/2025 47

40. Management… Opiates(Morphine) R educes patient anxiety and decreases the work of breathing . D iminish central sympathetic outflow, leading to arteriolar and venous dilatation with a resultant decrease in cardiac filling pressures May be used as sedative agents during NIPPV to improve patient adaptation Routine use of opiates in AHF is not recommended although they may be considered in selected patients,(severe/intractable pain or anxiety)or in the setting of palliation. 4/15/2025 48

41. Management… Phase II-hospital care Optimize hemodynamic profile, volume status, clinical symptoms Monitoring of daily weights, fluid balance, and vital signs, daily assessment of symptoms and signs are crucial . Laboratory monitoring should include daily analysis of electrolytes and RF DVT prophylaxis(all patients) and Treat comorbidities Continue/optimize/ Initiate oral medication unless contraindicated 4/15/2025 49

42. Management… Phase III- predischarge planning Goals of evaluating readiness for discharge, optimizing chronic oral therapy, minimizing the side effects of treatments, and ultimately preventing early readmission and improving symptoms and survival . Persistent clinical congestion and elevations of discharge BNP level at discharge is associated with a high risk for rehospitalization Drugs to improve long-term outcomes in chronic HF( beta blockers, RAAS, and MRA , should be initiated as soon as reasonable during the hospitalization and before discharge in hemodynamically-stable, appropriate patients. 4/15/2025 50

43. Discharge checklist-discharge planning goals Guideline-directed medical therapy has been reviewed and patient has been stable for 24 h Potential exacerbating/confounding comorbidities have been addressed Exercise tolerance has returned to New York Heart Association Class II Volume status has been optimized Education has been provided Clinic follow-up has been scheduled

44. Prognostic markers

45. Blood urea nitrogen: BUN blood concentration >37 mg/dL (urea > 43 mg/dL) is the other strong predictor of significantly increased mortality. Other factors of concern but with less impact on the mortality are: Low serum sodium concentration; Elevated serum creatinine; Advanced age; Dyspnoea at rest; Congestion despite diuresis/refractory

46. REFERENCES Braunwald's Heart Disease -A textbook of cardiovascular medicine(12 th edition) 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure UpToDate online 56

47. Thank you

48. SUMMARY 4/15/2025 58

49. 1, what is diuretic breaking phenomonia 2, how do you over come this situation 3,when do you use inotropes in HF 4, 3 causes of diuretic resistance 5 what are the spectrum of AHF