Acute left ventricular failure

Dr Md Seebat Masrur
Indoor Medical Officer
Cardiology Dept
Bangladesh

1. Dr Md Seebat Masrur IMO at Cardiology at TMC & RCH ACUTE LEFT VENTRICULAR FAILURE

2. Defining Heart Failure Generally defined as a complex clinical syndrome in which an abnormality of cardiac function and connected system is responsible for failure of the heart to move blood forward at a rate commensurate with the requirement of the metabolizing tissues. Ref.1.Braunwald`s Heart Disease 2.Hurts`s the heart

3. Acute Left Ventricular Failure A clinical syndrome in which the dominant feature is fluid congestion in the lung(pulmonary oedema) rather in the systemic circulation If left atrial pressure rises acutely it may cause pulmonary oedema and if rises gradually there will be reflex pulmonary vesoncstriction .

4. Incidence & Prevalance Approximatly 5.1 million persons in the USA have clinically manifest HF, and the prevalance continues to rise The lifetime risk of developing HF is 20% for Americans more or equal 40 years of age. Acute Heart Failure syndromes constitue the most common indication for hospitalization in adults over the age of 65 years. There are no available data for HF in Bnagladesh .

5. Bangladesh Heart Journal Overall , the prevalence of heart failure in Asia is 1.26% to 6.7 %.In Bangladesh, rheumatic heart disease still plays an important role in the incidence of heart failure, complicating the scenario. In a study conducted in National Institute of Cardiovascular Diseases and different medical colleges of Bangladesh revealed that IHD was responsible for 65% of chronic heart failure, rheumatic heart disease for 18% cases, hypertension for 12% cases and idiopathic cardiomyopathy for 5% cases.

6. Etiology Loss of Muscles Volume overload Pressure overload Restricted Filling Post MI Chronic Ischemia Connective Tissue Disease Infection Poisons( Alcohol,cobalt,doxorubicin ) Regurgitative Valve High Output Status Systemic Hypertension Outflow obstruction Pericardial Diseases Restrictive Cardiomyopathy Tachyarrhythmias

7. Pathophysiology several key factors play varying roles in the initiation and propagation of AHF, including but not limited to ( 1) Acute or subacute worsening of cardiac dysfunction, either systolic or diastolic ( 2) Neurohormonal activation ( 3) The cardiorenal syndrome resulting from the complex interplay between the kidney and the heart (4 ) Impaired vascular/endothelial function ( 5) Inflammation and oxidative stress and ( 6) Hemodynamic Factors

8. Pathophysiology

9. The cardiorenal syndrome

10. The N it roso -redox imbalance and acute heart failure (AHF)

11. Classification

12. NYHA Functional Classification

13. The ACC/AHA Stages of Heart Failure ACC/AHA Stage Symptoms A At high risk for heart failure but without structural heart disease or symptoms of heart failure. B Structural heart disease but without signs or symptoms of heart failure. C Structural heart disease with prior or current symptoms of heart failure. D Refractory heart failure requiring specialized interventions.

14. Killip classification Killip class I Includes individuals with no clinical signs of heart failure Killip class II Includes individuals with rales or crackles in the lungs, an S  3  gallop, and elevated jugular venous pressure Killip class III D escribes individuals with frank acute pulmonary edema Killip class IV  Describes individuals in cardiogenic shock or hypotension (measured as systolic blood pressure <90 mmHg), and evidence of low cardiac output (oliguria, cyanosis, or impaired mental status).

15. Forrester classification (Clinical classification of the mode of heart failure)

16. Forrester classification (Clinical classification of the mode of heart failure) Subset PCWP Cardiac Index Mortality Rate I < 18 > 2.2 3 II > 18 > 2.2 9 III < 18 < 2.2 23 IV > 18 < 2.2 51

17. Categorization of Left Ventricular Failure… Systolic Diastolic Both Impaired contractility of the left ventricle(EF%) Associated with chamber dilation Poor Ventricular Filling and high LV end diastolic pressure Left ventricular hypertrophy-stiff noncompliant ventricle Often coexist particularly in patients with CAD.

18. Categorization of Left Ventricular Failure… Acute Chronic Acute on Chronic 1.Acute MI 2.Acute native valve failure e.g Chordal rupture, Endocarditis 3.Acute myocarditis 1.ICM 2.DCM 3.Hypertensive & diastolic cardiomyopathy 4.Valvular disorders 5.Thiamine deficiency Infection( Viral,Bacterial )

19. RISK STRATIFICATION IN ACUTE HEART FAILURE The Acute Decompensated Heart Failure National Registry (ADHERE) “risk tree ”. The Enhanced Feedback for Effective Cardiac Treatment (EFFECT) risk index. Get With the Guidelines–Heart Failure (GWTGHF) risk score. The ESCAPE discharge risk score PROTECT risk score

20. General Approach for ALVF patient History taking and general examination Functional and haemodynamic assessment Diagnostic investigations Management plan Lifestyle modification Phamrmacological management Device therapy Revascularization Vaccination

21. History A patient with AHF typically presents with some combination of increased congestion and, less frequently, decreased peripheral perfusion. In addition to disturbances in oxygenation due to pulmonary edema , renal dysfunction is a frequent manifestation of AHF and reflects the multisystem nature of this disease. The mean age of patients with AHF is in the mid-70s, with about half of each sex and the majority with normal or elevated blood pressure. Most frequent symptoms at presentation: Dyspnea (including increasing dyspnea on exertion, dyspnea at rest, orthopnea , and paroxysmal nocturnal dyspnea ) Fatigue (including confusion) Cough Abdominal discomfort (including early satiety, bloating, anorexia) Leg pain (secondary to tense peripheral edema ) Sleep disturbances

22. History The typical patient presents with signs and symptoms of congestion, usually with some combination of lower extremity edema and pulmonary congestion, normal or elevated blood pressure and heart rate, and compromised oxygenation proportional to the extent of the pulmonary edema . A significant minority of patients may manifest worsening of their heart failure with predominantly abdominal congestion symptoms and signs, rather than lower extremity edema . Other patients, often elderly with hypertension, can present with rapid, if not fulminant, pulmonary edema with no or mild increase in total body fluid. Patients with recurrent heart failure exacerbations tend to recapitulate their clinical presentations in subsequent episodes, so obtaining a history of the time course, triggers, signs and symptoms, and response to therapy of prior events can increase the sensitivity to early decompensation .

23. Left Sided Heart failure

24. Physical Examination Findings. Most frequent signs at presentation Edema (legs, abdomen, sacral) Pulmonary rales , pleural effusion Elevated jugular venous pressure Positive abdominojugular reflux ( hepatojugular reflux) Increased body weight Increased abdominal girth Normal or elevated blood pressure Tachypnea Increased heart rate Third heart sound Less common signs at presentation, suggestive of low cardiac output Cool extremities Hypotension Narrow pulse pressure Pulsus alternans Impaired end organ function, such as decreased urine output

25. Physical Examination Findings. There are no physical exam findings that individually establish a definitive diagnosis of AHF, but relevant findings may be considered in two main categories. First, there are findings that suggest the presence of underlying cardiac dysfunction that provides the substrate for the AHF episode. These findings include evidence of left ventricular systolic dysfunction (laterally displaced and/or diffuse PMI, S3, decreased stroke volume on carotid pulse), diastolic dysfunction (S4), or both. Second, physical exam signs can support the diagnosis of AHF by suggesting the predominant pathophysiologic process involved in the decompensation , such as volume overload (peripheral edema , pleural effusions, rales , ascites, elevated jugular venous pressure, hepatojugular reflux), vascular redistribution (elevated jugular venous pressure, hepatojugular reflux, often elevated blood pressure), or low cardiac output (cool extremities, low blood pressure, often narrow pulse pressure, pulsus alternans ). Note that patients with chronic heart failure may have markedly elevated pulmonary venous pressure causing significant dyspnea with relatively mild rales . Patients with AHF due to vascular redistribution frequently have rapid onset of symptoms that can occur in the absence of signs of marked volume overload.

26. Investigations 12 Leads ECG CXR(P/A) Blood It may reveal MI LVH Arrhythmia IHD Enlarged hilar vessels Ground glass/reticular shadowing of alveolar oedema Prominance of upper lobe vessels Septal or kerley`s B line Pulmonary oedema NT Pro BNP Complete Blood Count Blood urea Serum Electrolytes Serum Creatinine Blood Sugar TSH

27. Biomarkers for Diagnosis & Prognosis 2017 ACC/AHA Heart failure focused uypdate Class I In patient with dyspnea , measurement of BNP or NT-pro BNP is useful to support a diagnosis or exclusion of HF Class I Measurement of BNP or NT- ProBNP is useful for establishing prognosis or disease severity in chronic HF Class I Measurement of baselione levels of Natriuretic peptide biomarkers and/or cardiac troponin on admission to the hospital is useful to establish a prognosis in acutely decompensated HF.

28. What`s to look for in an Xray ?

29. CXR…

30. CXR…

31. CXR…

32. Before Vs After treatment

33. Any other Investigations???

34. Echocardiography Most useful diagnostic test in the evaluation of patients with heart failure. Provide information about aetiology and prognosis of heart failure. Regional wall abnormalities, EF, LV dimensions, LV mass, the myocardial performance index( T ei index),measures of diastolic dysfunction all can be done by ECHO.

35. Echocardiography

36. Echocardiography

37. Echocardiography

38. Echocardiography

39. Immediate management: The first step in management of the patient with AHF is to address life-threatening issues, including, but not limited to: Respiratory failure : The most common presenting symptom of subjects with AHF is dyspnea and respiratory failure is the most frequent life-threatening condition for these patients. Immediate administration of the following is recommended: Reposition the patient : If it is safe to do so, support the patient in assuming an upright, sitting posture. Many patients will do this on their own to optimize their ventilator efficiency Oxygen : Although no randomized study has been performed, immediate administration of supplemental oxygen is the most readily available means to increase end organ oxygen delivery. Ventilatory support : If the above measures remain inadequate Management

40. Immediate management Nitrates : Sublingual or intravenous nitrates can be very effective as vasodilators, decreasing pulmonary venous pressure and relieving dyspnea . Rapid administration of intravenous nitrates in patients with severe pulmonary edema decreased the need for mechanical ventilation and myocardial infarction compared to a high-dose furosemide strategy in a randomized study. Diuretic : Most patients will also have significant volume overload contributing to the respiratory insufficiency, so if there is evidence of volume overload (as opposed to volume redistribution), rapid administration of intravenous loop diuretics is recommended. Although it has remained controversial, one early study suggested that furosemide also directly dilates pulmonary veins.

41. Immediate management Opiates (morphine) in the setting of AHF have been associated with increased rates of mechanical intubation, prolonged hospitalization, more frequent ICU admissions, and higher mortality. While this association may be reflective of the greater disease severity of patients receiving morphine, these findings argue against routine use of morphine in patients with dyspnea , as well as for careful monitoring in the select patients who receive opiates . Beta-blocker therapy in particular should be continued during the hospital course, unless there is cardiogenic shock, symptomatic bradycardia , or advanced heart block.  IVABRADIN can be beneficial to reduce HF hospitalization for patients with symptoms(NYHA Class II-III) stable chronic HFrEF9LVEF<35%) who are receiving a beta blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of &) bpm or greater at rest(2016 ACC/AHA/HFSA focused update for HF) Immediate management

42. Immediate management Circulatory failure: Surprisingly few (approximately 5%) patients present with low output syndromes in the general HF population, but these patients require aggressive management of their shock to mitigate or prevent the related end organ damage. Positive inotropes: To date, there are no “pure” inotropes, since all of the currently available agents also have some vascular effects, and the selection of the specific agent should account for these differences. All of these agents increase cAMP and intracellular calcium, with the related increases in heart rate, myocardial oxygen consumption, and arrhythmias, potentially resulting in myocardial ischemia, infarction, or death. Immediate management

43. Monitoring of response to these therapies B lood pressure P eripheral perfusion Respiratory status U rine output M ental status and other end organ function . Laboratory Tests to Monitor Response To, and Adjustments in, Management Serial evaluation of electrolytes and renal function

44. Mechanical support Intraaortic balloon pumps (IABP ) V entricular assist devices (VADs)  E xtracorporeal membrane oxygenation (ECMO )

45. Long-term management. The long-term management of a patient admitted for AHF is directed to three main issues (also see section on chronic heart failure): First, establishing the etiology of the heart failure is important, so that measures may be taken to address potentially reversible causes. Selected patients with ischemic cardiomyopathies may benefit from revascularization; patients with hypertensive cardiomyopathy should have an aggressive antihypertensive regimen. Alcoholic cardiomyopathies may resolve with cessation of alcohol consumption. Second, identification of precipitating factors for the AHF episode and intensive education to avoid future hospitalizations (see later section). Third, optimization of therapies with demonstrated long-term benefits (see section on Chronic heart failure). In patients with heart failure and reduced ejection fraction, these pharmacologic therapies include beta-blockers, ACE inhibitors, possibly angiotensin receptor blockers, mineralocorticoid receptor antagonists (spironolactone, eplerenone ), possibly isosorbide dinitrate /hydralazine, and possibly digoxin. It is absolutely imperative that these therapies be initiated as much as possible during the hospitalization and not be left to the outpatient setting. In addition, consideration and scheduling of device therapy, such as cardiac resynchronization therapy (CRT)/biventricular pacemaker and implantable defibrillator device (ICD), should be done while the patient is still hospitalized, if appropriate. The hospitalization for AHF is one of the most potent “teachable moments” and care providers are strongly encouraged to take advantage of the patient as a captive audience.

46. Management with Co-Morbidities Treatment of Atrial fibrillation. In patients with preserved ejection fraction, beta-blockers and calcium channel blockers are often effective. In any patient presenting with AHF, it is important to consider the diagnosis of an ACS with an ECG for the evaluation of myocardial ischemia/infarction. Treatment of Chronic obstructive pulmonary disease (COPD ). Renal insufficiency: In patients who present with renal failure as evidenced by an elevated creatinine (i.e., >3.0 mg/ dL ), consideration should be given to withholding ACE inhibitors, ARBs, and mineralocorticoid receptor antagonists (spironolactone, eplerenone ). Diuretic doses need to be adjusted upward in the setting of renal failure, with doubling of initial doses until a diuretic effect is achieved or until concerns of toxicity arise.

47. Advice before discharge This education should include, but not be limited to, instruction on: Low-salt and weight loss diets (as appropriate) Daily use of a scale and a mechanism to record body weights, including directions on the specific actions to take in the event of a change in body weight Self-titration of diuretics, in appropriate patients. For example, if weight increases by 3 to 5 lb above baseline, double the diuretic dose for 3 to 5 days. If body weight returns to baseline, resume prior dose of diuretics. If symptoms of hypotension ensue, hold diuretics, and if the symptoms of hypotension do not resolve, call care provider. If weight does not improve or if increasing symptoms of dyspnea or other symptoms of congestion, call a care provider. Chronic heart failure management programs, if available Exercise or rehabilitation program Other health-related issues such as smoking cessation

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