Acute decompensated heart failure

adhf

1. Acute Decompensated Heart Failure- Pathogenesis And Diagnosis

2. overlapping terms have been used to describe AHF. “acute heart failure syndrome” (AHFS), “acute decompensated heart failure” (ADHF), “acute decompensation of chronic heart failure” (ADCHF), “hospitalization for heart failure” (HHF)

3. AHF can be defined as the new onset or recurrence of symptoms and signs of HF requiring urgent or emergent therapy and resulting in unscheduled care or hospitalization.

4. Epidemiology AHF represents a major disease burden in the developed world. In the United States, HF is the primary diagnosis for more than 1 million hospitalized patients annually, and a secondary diagnosis for an additional 3 million hospitalizations.

5. Epidemiology - Preserved Versus Reduced Ejection Fraction HF On the basis of available registry data, 40% to 50% of patients hospitalized have HFpEF . The in-hospital mortality of patients with HFpEF appears to be lower compared with that of patients with HFrEF , but postdischarge rehospitalization rates are similarly high for both groups. Patients with AHF and HFpEF are more likely to be rehospitalized for and to die from noncardiovascular causes than patients with AHF and reduced EF, reflecting their more advanced age and greater burden of comorbidity .

6. AHF disproportionally affects elderly people, with a mean age of 75 years in large registries. AHF affects men and women almost equally, but there are important differences by gender. In the ADHERE Registry- women admitted for AHF were older than men (74 versus 70 years) and more frequently had preserved systolic function (51% versus 28%)

7. Comorbidities Hypertension, present in approximately two thirds of AHF patients coronary artery disease (CAD) is present in about half dyslipidemia in more than one third. Other conditions Cerebrovascular accident (stroke) peripheral vascular disease chronic renal insufficiency

8. Diabetes mellitus is present in more than 40% of U.S. patients with AHF, most likely related to increasing incidence of obesity, and ranges from 27% to 38% in Europe. Chronic obstructive pulmonary disease (COPD) is also present in approximately 25% to 30%, which confounds the presenting symptoms of dyspnea . Atrial fibrillation (AF) can both precipitate AHF and complicate its management.

9. Classification Depending on Whether patients have a past history of heart failure or not Systolic blood pressure (SBP) at presentation Presence or absence of signs of congestion and signs of low cardiac output and peripheral hypoperfusion at rest . Symptomatic severity of heart failure-NYHA functional classification. Heart failure with preserved, mid-range and reduced ejection fraction.

10. Depending on whether patients have a past history of heart failure or not Acutely decompensated chronic heart failure (ADCHF) more frequent representing about 65–75% of patients hospitalized for AHF De novo AHF remaining one third or less of AHF patients history of risk factors such as arterial hypertension, diabetes mellitus or advanced age

11. Systolic blood pressure (SBP) at presentation SBP > 140 and < 90 acc. to ESC guidelines Hypertensive AHF 50% or more of AHF cases . more likely to be elderly and female. preserved LVEF. mortality rates in this subgroup are significantly lower, with in-hospital mortality ranging from 1.7–2.5% and post-discharge 2–3- month mortality from 5.4 to 6%

12. Normotensive AHF (SBP) at presentation falls between 90 and 140 mmHg. represent 40% or more of AHF cases and usually have ADCHF and reduced LVEF. in-hospital mortality ranges between 8 and 10%

13. Hypotensive AHF, SBP at presentation is <90 mm Hg advanced or end-stage heart failure signs of low cardiac output, tissue hypoperfusion in-hospital mortality is higher than 15, reaching 30% or more

14. New York Heart Association (NYHA) functional classification

15. Precipitants of Acute heart failure Acute coronary ischaemia Valvular dysfunction Cardiac arrhythmia Pulmonary embolism Myocarditis Hypertensive emergency Pericardial tamponade Severe anemia Worsening renal failure Sepsis Drug noncompliance Dietary indiscretion Medication side effect / change Thyroid dysfunction

16. Pathophysiology Initiating mechanisms or triggers Amplifying mechanisms

17. Congestion Hallmark of AHF Peripheral- weight gain, peripheral oedema , jugular vein distension, hepatic enlargement, and/or pain, hepato -jugular reflux and ascites or Pulmonary- dyspnoea of varying severity and lung rales . The two main mechanisms leading to congestion is fluid retention and fluid redistribution

18. Fluid retention- Cardiac dysfunction leads to a low cardiac output Activates neurohormonal compensatory mechanisms Increased release of aldosterone and arginine vasopressin that cause Na and water retention in the kidneys Peripheral and pulmonary congestion.

19. Fluid redistribution Peripheral vasoconstriction Venous constriction causes an increase in the venous return and thus preload Arterial constriction increases the afterload Increased LV pressures, increased pressures in pulmonary capillaries, and thus pulmonary congestion

20. Initiating mechanisms For patients with normal substrate (normal myocardium), a substantial insult to cardiac performance (e.g., acute myocarditis ) is required to lead to the clinical presentation of AHF. For patients with abnormal substrate at baseline (asymptomatic LV dysfunction), smaller perturbations (e.g., poorly controlled hypertension, AF, or ischemia) may precipitate an AHF episode. For patients with a substrate of compensated or stable chronic HF, medical or dietary nonadherence agents such as nonsteroidal antiinflammatory drugs (NSAIDs) or thiazolidinediones , and infectious processes are all common triggers for decompensation .

21. Amplifying Mechanisms Regardless of the substrate or initiating factors, a variety of “amplifying mechanisms” perpetuate and contribute to the episode of decompensation . These include Impaired myocaridal function Renal dysfunction Vascular mechanisms Neurohormonal and inflammatory activation

22. Impaired Myocardial function Impairments of cardiac function (systolic, diastolic, or both) remain central to the pathogenesis of AHF. Changes in systolic function and decreased arterial filling can initiate a cascade of effects that are adaptive in the short term but maladaptive when elevated chronically, including stimulation of the SNS and RAAS.

23. Activation of these neurohormonal mechanisms leads to vasoconstriction sodium and water retention volume redistribution from other vascular beds increase in diastolic filling pressures Increased LV filling pressures and changes in LV geometry can worsen functional mitral regurgitation, further decreasing cardiac output.

24. ACS are a frequent cause of AHF. AHF itself can lead to myocardial ischemia that leads to myocardial injury. Data on nearly 85000 AHF patients from the ADHERE registry published in 2008 showed that, 6% of patients had a positive troponin tests and those patients had a 2.6 times higher risk of in-hospital mortality. RELAX-AHF ( Relaxin in Acute Heart Failure) trial,-in which the new-generation high-sensitivity troponin assays were used, showed that troponin levels were higher than the upper reference limit (URL) in 93% of patients and were independently associated with 180-day mortality, while a further increase of ≥20% during the first 2 days nearly doubled the risk of death

25. In AHF, ischaemia is caused both by a decrease in the myocardial O2 supply and an increase in the myocardial O2 demand O2 supply may be impaired due to: (1) low diastolic arterial blood pressure and high LV diastolic pressure, the combination of which leads to a decrease in the coronary driving pressure, and thus impaired coronary perfusion (2) tachycardia that restricts the diastolic period, and thus the coronary perfusion time (3) potentially co-existing coronary artery disease (CAD).

26. O2 demandis increased because of High LV wall stress Tachycardia Inotropic therapy

27. Renal Mechanisms A frequent and important component of AHF pathophysiology is renal dysfunction. In the ADHERE registry, among 118 465 patients admitted with AHF, only 9% had normal renal function on admission ( glomerular filtration rate (GFR) ≥90 mL /min/1.73 m2); 71% had mild to moderate renal dysfunction (GFR 30–89 mL /min/1.73 m2) 20% had severe dysfunction (GFR <30 ml/1.73 m2)

28. The close interdependence of the heart and kidneys may lead to a vicious circle, in which heart failure causes renal dysfunction that, in turn, promotes an additional deterioration of the cardiac function that aggravates further the renal impairment, and so on.

29. Cardiorenal Syndrome defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction of one organ may induce acute or chronic dysfunction of the other.

30. Three main mechanisms (1) A low cardiac output (forward failure) that leads to a low perfusion pressure in the afferent arteriole of the glomerulus (2) A high central venous pressure (CVP) (backward failure) that increases the intra-abdominal pressure, and thus the pressure on the Bowman’s capsule (3) Drug therapy and mainly diuretics that reduce the intravascular volume and thus cause a further decrease in the glomerulus perfusion pressure, and RAAS inhibitors that cause dilatation of the efferent arteriole

31. Leads to low filtration pressure in the glomerulus , and thus a low urine output. Other causes Inflammation activation Oxidative stress Anaemia Necrosis, apoptosis, and fibrosis Resistance to ANP /BNP

32. Risk factors for CRS- Patient characteristics (age) Comorbidities (baseline renal function as assessed by GFR, diabetes mellitus, hypertension)

33. Novel biomarkers are needed –rise within few hours of onset of AKI  NGAL – neutrophil gelatinase assosiated lipocalin – earliest and sensitive marker of ischemic/ nephrotoxic injury detected in blood /urine.  Kidney injury molecule 1 is a highly specific marker for ischemic AKI.

34. Biomarkers of renal dysfunction NGAL – neutrophil gelatinase assosiated lipocalin – earliest and sensitive marker of ischemic/ nephrotoxic injury detected in blood /urine. Kidney injury molecule 1 is a highly specific marker for ischemic AKI.

35. Vascular Mechanisms Abnormalities of endothelial function related to nitric oxide (NO)–dependent regulation of vascular tone Peripheral venoconstriction redistributes blood centrally, increasing pulmonary venous congestion and edema. Peripheral arterial vasoconstriction increases afterload , LV filling pressures, and postcapillary pulmonary venous pressures, resulting in worsening of pulmonary edema and dyspnea .

36. Increased afterload causes greater ventricular wall stress increased myocardial ischemia cardiac arrhythmias.

37. Neurohormonal and Inflammatory Mechanisms Increased plasma concentrations of norepinephrine , plasma renin activity, aldosterone , and endothelin (ET)-1. vasoconstriction and volume retention, which could contribute to myocardial ischemia and congestion, thus exacerbating cardiac decompensation .

38. Inflammatory activation and oxidative stress may also play a role. Proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-6 are elevated in patients with AHF and have direct negative inotropic effects on the myocardium as well as increasing capillary permeability and inducing endothelial dysfunction.

39. Evaluation of the Patient With Acute Heart Failure The initial evaluation of the patient with acute HF focuses on the following critical aspects: (1) establishing a definitive diagnosis of AHF as rapidly and efficiently as possible (2) emergent treatment for potentially life-threatening conditions (e.g., shock, respiratory failure) (3) identifying and addressing any relevant clinical triggers or other conditions requiring specific treatment (e.g., ACS, acute pulmonary embolism)

40. Clinical features

41. Symptoms Dyspnea the most common symptom present in more than 90% of patients Orthopnea , Paroxysmal nocturnal dyspnea Can be very acute onset over minutes to slow worsening of chronic symptoms until patients present to medical attention.

42. symptoms Edema (of extremities, scrotum, or elsewhere) Increasing abdominal girth or bloating Abdominal pain (particularly if confined to right upper quadrant) Cough, wheezing Weight gain/weight loss Somnolence or diminished mental acuity

43. Physical Examination

44. Hypotension-strongest predictors of poor outcomes SBP is typically normal or elevated in patients with AHF, with almost 50% presenting with SBP greater than 140 mm Hg. hypertensive urgencies or emergencies (12% of patients can had SBP >180 mm Hg on admission in ADHERE).

45. Pulse pressure (the difference between systolic and diastolic blood pressure) an indirect marker of cardiac output. A low pulse pressure-low cardiac output and confers an increased risk in patients admitted with AHF. A high pulse pressure-possibility of unrecognized thyrotoxicosis , aortic regurgitation, or anemia

46. The jugular venous pressure (JVP) Literally barometer of systemic venous hypertension reflects the right atrial pressure, which typically (although not always) is an indirect measure of LV filling pressures.

47. Rales or inspiratory crackles most common physical examination finding 66% to 87% of patients admitted for AHF. Cool extremities with palpable peripheral pulses suggest decreased peripheral perfusion

48. Peripheral edema dependent, symmetric, and pitting minimum of 4 liters of extracellular fluid is accumulated to produce clinically detectable edema.

49. Routine Laboratory Assessment Chest Radiography “butterfly” pattern of interstitial and alveolar opacities bilaterally fanning out to the periphery of the lungs. Kerley B lines (thin horizontal linear opacities extending to the pleural surface caused by accumulation of fluid in the interstitial space) peribronchial cuffing, and evidence of prominent upper lobe vasculature (indicating pulmonary venous hypertension) are the most prominent findings. Pleural effusions and fluid in the right minor fissure may also be seen.

50. Biomarkers

51. Natriuretic Peptides useful biomarkers for HF Diagnosis estimation of HF severity Prognosis B-type natriuretic peptide (BNP) and its amino-terminal (N-terminal) cleavage propeptide equivalent, NTproBNP are most commonly measured.

52. Because of the differences in their clearance, BNP and NT- proBNP have considerably different halflives (BNP: 20 minutes; NT- proBNP : 90 minutes), and thus they circulate with very different concentrations

53. Other biomarkers Soluble ST2 Galectin 3 Growth differentiation factor-15

54. Cardiac troponins Frequently elevated in patients presenting with AHF Elevated levels are associated with worse in-hospital and postdischarge outcomes. Can help to identify concurrent ACS.

55. ECG - electrocardiogram ACS Arrhythmias are also a common trigger for AHF, and AF is present in 20% to 30%. Clue to etiology.

56. Other investigations Renal function (estimated by BUN, creatinine , and GFR) is an important predictor of prognosis in patients with AHF. D- dimer to evaluate for pulmonary embolism or procalcitonin to evaluate for evidence of infection Thyroid function (cause of failure)

57. Echocardiography evaluating the etiology of the patient with AHF. global systolic and diastolic function regional wall motion abnormalities valvular function hemodynamics including estimates of filling pressures and cardiac output pericardial disease assessing RV size and pulmonary pressures

58. Differential Diagnosis for Patients Presenting With Dyspnea (mimics AHF) Pulmonary embolism Pneumonia Acute coronary syndromes Aortic dissection Pericarditis or pericardial effusion Pneumothorax Chronic obstructive pulmonary disease Asthma