ACUTE HEART FAILURE presentation (1) copy copy.pptx

Acute Heart Failure presentation slides

1. ACUTE HEART FAILURE BY: NKRUMAH JEPHTAH BEJNAMIN NAANA BOATEMAA KUFUOR 1

2. OUTLINE Introduction/Overview Epidemiology Etiology Pathophysiology Signs & Symptoms Investigations and Diagnosis Complications Management -Pharmacological & Non-Pharmacological Counselling Points 2

3. INTRODUCTION Heart failure(HF) is “a complex clinical syndrome that results from any structural or functional cardiac impairment of ventricle filling or ejection of blood (AHA/ACC) It results from inability of the heart to adequately pump blood sufficient to meet the metabolic needs and adequately perfuse body cells Heart failure is a progressive condition with complex possible causes, and mortality varies according to etiology and severity of symptoms.(Roger Walker,5 th edition) 3

4. TERMILOGIES PRELOAD This is the loading condition of the heart at the end of its relaxation and filling phase(diastole) just before contraction(systole) Preload represents the extent of dilation of the ventricles in diastole(end-diastolic fiber stretch) and the volume of blood the dilated ventricles can hold(end-diastolic volume) 4

5. TERMINOLOGIES CONT’D After load the tension developed in the ventricular wall as contraction (systole) occurs. It is determined by the chamber pressure in the LV and the thickness of the myocardium 5

6. TERMINOLOGIES CONT’D CARDIAC OUTPUT This is the volume of blood being pumped by the heart(ventricles),per unit time Normal CO in a healthy heart is about 5-6L/min. Co=Heart rate(HR) × Stroke volume(SV) where HR is the number of heart beats per minute and SV is the volume of blood pumped out the LV during systolic cardiac contraction. (i.e. EDV-ESV) 6

7. TERMINOLOGIES CONT’D EJECTION FRACTION Is the ratio of stroke volume to the end diastolic volume EF= It represent the percentage of blood that that was pumped out during systole The normal ejection fraction of a healthy heart ranges from 50-70% Anything lower than 40% indicates a failing heart   7

8. AETIOLOGY SYSTOLIC DYSFUNCTION Reduction in muscle mass Dilated cardiomyopathies Ventricular hypertrophy Restrictive cardiomyopathy 8

9. AETIOLOGY DIASTOLIC DYSFUNCTIONS Increased ventricular stiffness Ventricular hypertrophy Myocardial ischemia and infarction Mitral or tricuspid valve stenosis Pericardial disease (e.g., pericarditis, pericardial tamponade) 9

10. OTHER FACTORS Hypertension Viral illness Thyroid disease Excessive alcohol use Pregnancy-related heart disease Familial congenital disease 10

11. CLASSIFICATION BASED ON EF Heart Failure with reduced Ejection Fraction HFrEF – Ejection fraction ≤ 40% . In HFrEF, the LV poorly contracts and empties inadequately leading to increased diastolic volume and pressure with reduced ejection fraction. Heart Failure with Preserved Ejection Fraction HFpEF – Ejection Fraction ≥50% In HFpEF,LV filling is impaired resulting in an increase in LV end diastolic pressure at rest or during exertion usually with normal EF Heart failure with mid-range ejection fraction(HFmrEF)- Ejection fraction,41-49% 11

12. CLASSIFICATION BASED ON CARDIAC OUTPUT HIGH OUTPUT FAILURE The heart functions normally (or increase d) but unable to meet up with the increased metabolic demand of the body Eg.in anemia,hyperthyroidism,pregnancy LOW OUTPUT FAILURE- – Heart fails to generate adequate output to meet normal metabolic demands of the body. E.g. .in dilated cardiomyopathy, valvular heart disease, tamponade and bradycardia. 12

13. RIGHT AND LEFT SIDED HEART FAILURE Right sided heart failure is characterised by the presence of peripheral oedema, raised JVP and hypotension and congestive hepatomegaly. Left sided heart failure – pulmonary oedema is the striking feature. Other signs are tachypnoea, tachycardia, third heart sound, cardiomegaly. Congestive Cardiac Failure – Characterised by combination of both left and right sided heart failure. 13

14. FRANK STARLING MECHANISM It describes the relationship between preload and cardiac performance. It states blood contractile performance(represented by SV or CO) is proportional to preload with the normal physiologic range. 14

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16. PATHOPHYSILOGY In heart failure, the heart is unable to pump enough blood for tissue metabolic needs and as a result cardiac-related elevation of pulmonary or systemic venous pressures may cause organ congestion This condition can result from abnormalities in the systolic or diastolic function, or both. Factors such as change in cardiomyocyte function, cardiac structural defects such as valvular disorders, rhythm abnormalities and higher metabolic demands due to thyrotoxicosis can contribute to heart failure 16

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19. PATHOPHYSIOLOGY CONT’D Endothelins : cause vasoconstriction, potentiation of cardiac remodeling, and decreased renal blood flow Natriuretic Peptides : antagonism of the RAAS, inhibition of sympathetic outflow, inhibit vasopressin secretion, and ET-1 antagonism decreasing preload and afterload Vasopressin (ADH): V1a receptor stimulation: vasoconstriction V2 receptor stimulation: free water in the kidneys 19

20. Cardiac Remodeling Occurs as a compensatory adaptation to a change in wall stress It is largely regulated by neurohormonal activation Angiotensin II and aldosterone being key stimuli Leads to Ventricular hypertrophy 20

21. ACCF/AHA FUNCTIONAL CLASSIFICATION 21

22. NYHA FUNCTIONAL CLASSIFICATION 22

23. SYMPTOMS Left Heart Failure Breathlessness On exertion On lying flat ( orthopnoea ) At night (paroxysmal nocturnal dyspnoea ) Easy fatiguability Cough with frothy blood-stained sputum Wheezing Right Heart Failure Pedal/peripheral edema Abdominal swelling Right hypochondriac pain from an enlarging liver 23

24. SIGNS 24

25. INVESTIGATIONS FBC ECG Chest X-ray Blood urea, electrolytes and creatinine and eGFR (estimated glomerular filtration rate) Liver function test Fasting blood sugar Echocardiography Thyroid function tests Cardiac enzymes, if myocardial infarction is suspected Coronary angiography Echocardiogram 25

26. Management (ACC/AHA guidelines) Stage A: ACE inhibitors/ARBs Statins Stage B: ACE inhibitor or ARB, β-blockers statin 26

27. Management (ACC/AHA guidelines) Stage C ACE inhibitor, ARB, or angiotensin receptor- neprilysin inhibitor (valsartan/sacubitril, ARNI) β- blocker Aldosterone antagonists Loop diuretics, hydralazine-isosorbide dinitrate (ISDN) Digoxin Ivabradine 27

28. Management (ACC/AHA guidelines) Stage D : often referred to as advanced, refractory, or end stage HF. Diuretics Vasopressin antagonists Vasodilators Inotropes 28

29. Management 29

30. Management 30

31. MANAGEMENT 31

32. INTRODUCTION TO ACUTE HEART FAILURE Acute heart failure is the rapid onset of symptoms and signs of heart failure, severe enough to warrant emergency medical attention It is a condition with adverse prognosis, characterized by high mortality and rehospitalization rates especially in individuals aged 65 or older. Patients with AHF require urgent evaluation with subsequent initiation or intensification of treatment, including iv. therapies or procedures Despite the considerable public health and financial burden related to AHF there has very little progress in the pharmacological management of these patients, as most drugs that have been investigated failed to improve prognosis.(Tubaro et al,2018) 32

33. EPIDEMIOLOGY . AHF is a leading cause of hospitalizations in subjects aged >65 years and is associated with high mortality and rehospitalization rates. AHF predominant in males ( Dimitrios et al,2015) Majority of subjects (65–75%) have a known history of heart failure. Other comorbid conditions include arterial hypertension in about 70% of patients, documented CAD in 50–60%, and AF in 30–40%. Non-cardiovascular comorbidities include diabetes mellitus in about 40% of patients, renal dysfunction in 20–30%, COPD in 20–30%, and anemia in 15–30% 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 rates.(EHJ,2021) 33

34. EPIDEMIOLOGY CONT’D 34

35. INVESTIGATIONS ECG [ Arrhythmias, Myocardial Ischemia ] Chest X-ray [ Congestion, Lung infection ] Lung Ultrasound [ Congestion ] Echocardiography [Congestion, Cardiac dysfunction ] Natriuretic Peptides [ Congestion ] Serum Troponin [ Myocardial injury(ACS) ] Serum Creatinine [ Renal dysfunction ] 35

36. INVESTIGATIONS Serum Electrolytes [ Electrolyte disorders ] Iron status [ Iron depletion ] Thyroid Stimulating Hormone [ Hypo and hyperthyroidism ] Procalcitonin [ Pneumonia ] Lactate [ Lactic Acidosis ] Pulse Oximetry and Arterial Blood gas [ Respiratory failure ] D-dimer [ Pulmonary Embolism ] 36

37. DIAGNOSIS 37

38. COMPLICATIONS According to the 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure, Acute heart failure may present as 4 major complications; Acute Decompensated Heart Failure Acute Pulmonary Oedema Isolated Right Ventricular Failure Cardiogenic Shock 38

39. ACUTE DECOMPENSATED HEART FAILURE Most common presentation of Acute Heart Failure ( 50%-70% of hospital presentations) Gradual onset (days) Main Cause Sodium and water retention Left ventricular dysfunction with or without hypoperfusion Main Clinical Presentation Wet and warm Dry and cold 39

40. ACUTE DECOMPENSATED HEART FAILURE Treatment Objectives Identification of precipitating factors Decongestion with Diuretic therapy Hypoperfusion correction with Inotropes and Vasopressors 40

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42. ACUTE PULMONARY OEDEMA Rapid onset( Hours) Clinical criteria; RR> 25 breaths/min Dyspnea with Orthopnea Respiratory failure Tachypnoea Main Clinical Presentation; Lung congestion ( Wet and warm) 42

43. ACUTE PULMONARY OEDEMA Treatment Objectives; Oxygen given as continuous positive airway pressure or high flow nasal cannula IV Diuretics IV Vasodilators( If SBP is high to redu ce afterload ) 43

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45. ISOLATED RIGHT VENTRICULAR FAILURE Onset may be gradual or rapid Main clinical presentation; Associated with increased right ventricular and atrial and systemic congestion Impairs left ventricular failing ultimately reducing Cardiac output May present as wet and warm or dry and cold Treatment Objectives; IV Diuretics( for Venus systemic congestion) Vasopressor and/or Inotropes (For low cardiac output and hemodynamic instability) 45

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47. CARDIOGENIC SHOCK Cardiogenic shock is a syndrome due to primary cardiac dysfunction resulting in an inadequate cardiac output, comprising a life-threatening state of tissue hypoperfusion, which can result in multi-organ failure and death Onset may be gradual or rapid Main Clinical Presentation is associated with Hypoperfusion; Cold sweatered extremities Oliguria Mental confusion Dizziness Narrow pulse pressure 47

48. CARDIOGENIC SHOCK Relevant Biochemical Markers; Elevated serum Creatinine Metabolic acidosis ( Elevated blood pH) Elevated serum lactate 48

49. CARDIOGENIC SHOCK Treatment Objectives; Identification and treatment of underlying cause Hemodynamic stabilization Management of organ dysfunction 49

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51. PHARMACOLOGICAL MANAGEMENT OF AHF Oxygen Therapy and/or Ventilatory Support ; Oxygen should not be used routinely in non-hypoxemic patients, as it causes vasoconstriction and a reduction in cardiac output. Oxygen Therapy is recommended in patients with AHF with SpO 2 <92% to correct hypoxemia, increase oxygenation and pH and decreased work of breathing. 51

52. PHARMACOLIGICAL MANAGEMENT OF AHF During oxygen therapy, acid base balance,SpO 2 and BP should be monitored regularly. Intubation is recommended for progressive respiratory failure in spite of oxygen administration 52

53. PHARMACOLOGICAL MANAGEMENT OF AHF 2. Diuretics Intravenous diuretics are the cornerstone of AHF treatment. They increase renal excretion of salt and water and are indicated for the treatment of fluid overload and congestion in the vast majority of AHF patients. Loop diuretics are commonly used due to their rapid onset of action and efficacy. It is appropriate that when starting diuretic treatment, to use low doses, to assess the diuretic response and increase the dose when that is insufficient. 53

54. PHARMACOLOGICAL MANAGEMENT OF AHF Diuretic treatment should be started with an initial iv. dose of furosemide, or equivalent dose of bumetanide or torsemide at a starting dose of; 0.5-1 mg/kg or 20-40mg IV Furosemide over 1-2min every 8-12 hrs. which may be increased to 80 mg if there is no adequate response within 1 hour without exceeding maximum dose of 160-200mg/dose. 10-20 mg IV Bolus Torsemide daily 54

55. PHARMACOLOGICAL MANAGEMENT OF AHF If the diuretic response remains inadequate, e.g. <100 mL hourly diuresis despite doubling loop diuretic dose, concomitant administration of other diuretics acting at different sites, namely thiazides or metolazone or acetazolamide, may be considered. However, this combination requires careful monitoring of serum electrolytes and renal function. Transition to oral treatment should be commenced when the patient’s clinical condition is stable. It is recommended that, after achievement of congestion relief, oral loop diuretics are continued at the lowest dose possible to avoid congestion 55

56. PHARMACOLOGICAL MANAGEMENT OF AHF 3. Vasodilators; Intravenous vasodilators, namely nitrates or nitroprusside dilate venous and arterial vessels leading to a reduction in venous return to the heart, less congestion, lower afterload, increased stroke volume and consequent relief of symptoms. Nitrates act mainly on peripheral veins whereas nitroprusside is more a balanced arterial and venous dilator hence may be more effective than diuretics in those patients whose acute pulmonary oedema is caused by increased afterload and fluid redistribution to the lungs in the absence or with minimal fluid accumulation and also in patients with SBP>/= 110 mmHg. 56

57. PHARMACOLOGICAL MANAGEMENT OF AHF Sodium Nitroprusside should be given at an infusion rate of 0.3mcg/kg/min monitoring for BP at least 5 min before titrating to higher or lower dose to achieve desired BP. 57

58. PHARMACOLOGICAL MANAGEMENT OF AHF 4. Inotropes; Inotropes are still needed for treatment of patients with low cardiac output and hypotension and should be reserved for patients with LV systolic dysfunction, low cardiac output and low SBP (e.g. <90 mmHg) resulting in poor vital organ perfusion. Phosphodiesterase III inhibitors ( Amrinone, Milrinone ) may be preferred over dobutamine for patients on beta-blockers as they act through independent mechanisms. Excessive peripheral vasodilation and hypotension can be major limitations of type-3-phosphodiesterase inhibitors especially when administered at high doses. 58

59. PHARMACOLOGICAL MANAGEMENT OF AHF IV Amrinone ; 0.5mg/kg IV bolus over 2-3 mins, then 5-10 mcg/kg/min IV not exceeding a total daily dose of 10 mg/kg/day. IV Milrinone ; 50mcg/kg loading dose IV over 10 mins then 0.375-0.75 mcg/kg/min IV with a maintenance dose of 1.13mg/kg/day. 59

60. PHARMACOLOGICAL MANAGEMENT OF AHF 5. Vasopressors; Among drugs (Norepinephrine, Epinephrine, Dopamine, Dobutamine ) with a prominent peripheral arterial vasoconstrictor action, norepinephrine may be preferred in patients with severe hypotension. The aim is to increase perfusion to the vital organs. However, this is at the expense of an increase in LV afterload. Therefore, a combination of norepinephrine and inotropic agents may be considered, especially in patients with advanced HF and cardiogenic shock and patients with SBP<90 mmHg with hypotension and/or hypoperfusion. 60

61. PHARMACOLOGICAL MANAGEMENT OF AHF IV Norepinephrine ; 0.2-1.0 mcg/kg/min IV Epinephrine ; 0.05-0.5 mcg/kg/min IV Dobutamine ; 2-20 mcg/kg/min IV Dopamine ; 3-5 mcg/kg/min 61

62. PHARMACOLOGICAL MANAGEMENT OF AHF 5. Digoxin ; It is indicated in AHF with fast atrial fibrillation or in sinus rhythm with systolic dysfunction. According to the ACCF/AHA Guidelines a loading dose to initiate therapy in AHF is not necessary. Digoxin ; 0.125-0.25mg PO/IV daily 62

63. PHARMACOLOGICAL MANAGEMENT OF AHF 6. Opiates ; Opiates relieve dyspnea and anxiety. They may be used as sedative agents during non-invasive positive pressure ventilation to improve patient adaptation. Dose-dependent side effects include nausea, hypotension, bradycardia, and respiratory depression. Morphine; SC/IM 5-10 mg q4hr PRN (dose range 5-20mg) or IV 2.5-5mg q3-4hrs PRN infused over 4-5mins (dose range 4-10mg) 63

64. PHARMACOLOGICAL MANAGEMENT OF AHF 7. Thromboembolism Prophylaxis ; SC Enoxaparin 1.5 mg/kg daily should be used as prophylactic anticoagulation against venous thrombosis. 8. Short term Mechanical Circulatory Support ; MCS may be necessary to augment cardiac output and support end organ perfusion in patients presenting with cardiogenic shock. 64

65. NON PHARMACOLOGICAL MANAGEMENT OF AHF Patientswithheartfailureshouldbeadvisedtomake lifestyle changes to reduce the risk of progression of their heart failure and associated co-morbidities. These include ; Smoking cessation R educing alcohol consumption I ncreasing physical exercise if appropriate W eight control D ietary changes such as increasing fruit and vegetable consumption and reducing saturated fat intake. 65

66. NON PHARMACOLOGICAL MANAGEMENT OF AHF Salt and fluid intake should only be restricted if these are high, and a salt intake of less than 6 g per day is advised. Bed rest only( in Acute failure and exacerbation of chronic failure) Prop up in bed 66

67. COUNSELING POINTS Patient should be counseled on lifestyle modifications to help reduce rate of acute exacerbations. Patients should be counseled and encouraged to adhere strictly to the pharmacotherapy of their comorbid conditions that predispose the to AHF. Patients experiencing side effects and sub optimal therapy from the management of their co morbid conditions should let their physicians know so as to optimize therapy and reduce the risk of acquiring AHF. Contraception and pregnancy should be discussed with women of childbearing potential and heart failure. Advice from a heart failure specialist and an obstetrician should be sought if pregnancy occurs or is being considered. 67

68. COUNSELING POINTS Patients should be encouraged to join a personalised rehabilitation programme including education, psychological support, and exercise when appropriate. Reduce salt intake Reduce weight in overweight and obese individuals Avoid alcohol Avoid or quit smoking Encourage moderate exercise Bed rest (in acute heart failure or exacerbations of chronic heart failure) 68

69. REFERENCES 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: Developed by the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) With the special contribution of the Heart Failure Association (HFA) of the ESC , European Heart Journal , Volume 42, Issue 36, 21 September 2021, Pages 3599–3726, British National Formulary 80 (September 2020, March 2021). Royal Pharmaceutical Society of Great Britain. Pages 204-260 K ode-Kimble & Young (2013). Applied Therapeutics: The Clinical Use of Drugs. 10th edition, Lippincott Williams & Wilkins, USA. Pages 235-238 69

70. REFERENCES Dipiro J., et al. (2020). Pharmacotherapy: A PathophysiologicApproach. 11TH Edition. McGraw- Hill, New York. Page 586-673 Ministry of Health (2017). Standard Treatment Guidelines. Seventh Edition. Yamens Press Limited, Accra. Pages 133-140 Zeind , C. & Carvalho, M. (2018). Applied Therapeutics: The Clinical Use Of Drugs. 11 th Edition. Wolters Kluwer, China. Pages 261-278 Whittlesea C. & Hodson K. (2019). Clinical Pharmacy and Therapeutics. 6th Edition. Elsevier, China. Pages 357-365 70