Acute Heart Failure Management in the ICU.pptx

Acute Heart Failure in ICU

1. ACUTE HEART FAILURE in ICU SOE MIN MYAT

2. Content Introduction Pathophysiology Causes of AHF Investigations Management of AHF in ICU

3. Introduction Heart failure (HF) is a chronic and progressive clinical syndrome induced by structural or functional cardiac abnormalities displaying either reduced (in HF with reduced ejection fraction ( HFrEF ) or preserved (in HF with preserved ejection fraction ( HFpEF ) Structural & Functional Cardiac dysfunction elevated cardiac filling pressures at rest and during stress HF symptoms dyspnoea (shortness of breath) and fatigue swollen ankles exercise intole rance HF cardinal signs pulmonary rales (abnormal crackling sounds) peripheral oedema distended jugular veins palpable liver tachycardia third heart sound

4. Introduction Acute Heart Faiilure (AHF) is defined as new or worsening of symptoms and signs of HF de novo HF ( symptoms occur in patients without a previous history of HF ) Acute HF (AHF) acutely decompensated HF (ADHF) ( symptoms increase in patients with previously diagnosed chronic HF ) *De novo requires more extensive diadnostic process to investigate the underlying pathology

5. Pathophysiology The pathophysiology of AHF is heterogeneous cardiac abnormalities greatly affected by the nature of the underlying cardiac diseases ( Hypertension, AMI, valvular diseases, etc ) Underlying pathophysiological mechanisms of AHF LV systolic and diastolic dysfunction Fluid retention Fluid redistribution

6. Pathophysiology LV systolic and diastolic dysfunction Acute change in cardiac function worsening of left ventricular (LV) diastolic function increase in LV filling pressures and pulmonary congestion AHF ( example of such sudden changes is acute myocardial ischaemia )

7. LV Filling LV contraction is highly dependent on oxidative energy generation Ischaemia triggers systolic impairment Reduction in oxidative ATP generation in cardiomyocytes impairs myocardial relaxation early LV filling and further increasing filling pressures an early rapid phase that is highly dependent upon fast myocardial relaxation LV filling normally occurs in two phases, later phase that is dependent on left atrial contraction and the atrial-to-ventricular pressure gradient

8. Pathophysiology Increased filling time  increased preloads  congrestion (+)  LV stiffness (+) Factors causing LV stiffness Chronic LV systolic dysfunction with raised LV end-diastolic volume Structural fibrosis and/or hypertrophy C hronic hypertension Chronic kidney disease Chronic aortic stenosis A geing Factors increasing LV filling volume sudden development of atrial fibrillation with the accompanying loss of atrial contraction substantially increase filling pressures when there is already pre-existing diastolic dysfunction ( For example, severe mitral stenosis )

9. Pathophysiology Fluid retention an increase in the volume of extracellular fluid & a change in the compliance of venous beds can lead to an increase in filling pressure

10. Pathophysiology Interstitial glycosaminoglycan The majority of the retained sodium is stored in the extracellular compartment In healthy individuals, increased total body sodium is usually not accompanied by oedema formation, interstitial glycosaminoglycan network acts likea buffer and prevents fluid accumulation in the interstitium In patients with HF , when sodium accumulation persists, the glycosaminoglycan network may become dysfunctional, resulting in reduced buffering capacity, increased interstitial compliance and oedema formation

11. Pathophysiology Neurohumoral activation Activation of the renin– angiotensin–aldosterone system and the vasopressin system renal salt and water retention The neurohumoral pathway is already activated during disease progression in patients with chronic HF or kidney disease Resulting organ dysfunction contributes to self-perpetuation of congestion T hese patients are particularly prone to fluid accumulation

12. Pathophysiology Fluid redistribution Sympathetic stimulation transient vasoconstriction leading to a sudden displacement of volume from the splanchnic and peripheral venous system to the pulmonary circulation, without exogenous fluid retention causes fluid redistribution Fluid accumulation and fluid redistribution both produce systemic congestion in AHF

13. Pathophysiology Congestion and organ dysfunction CVS  Elevated ventricular filling pressures lead to increased ventricular wall tension & myocardial stretch progressive worsening in cardiac contractility valvular regurgitation systemic congestion Increases in left atrial pressure and mitral valve regurgitation will increase the hydrostatic pressure in thepulmonary capillaries, thereby increasing fluid filtration rate from the capillaries to the pulmonary interstitium , causing lung stiffness and dyspnoea

14. Pathophysiology ( Renal )  Elevated central venous pressure renal venous hypertension increases renal interstitial pressure the hydrostatic pressure in the renal interstitium exceeds the intratubular hydrostatic pressure resulting in the collapse of tubules reduced glomerular filtration rate In addition, renal venous hypertension induces a reduction in renal blood flow, renal hypoxia and ultimately interstitial fibrosis

15. Causes of AHF (1) Decompensstion of chronic heart failure (2) Accute coronary syndrome (3) Hypertensive crisis (4) acute arrhythmia ( VT, VF, AF, SVT) (5) Cardiomyopathy and myocarditis (6) Valvular regurgitation (7) Aortic stenosis (8) Cardiac tamponade (9) Aortic dissection

16. Causes of AHF (10) Non cardiovascular precipitating factors - poor compliance for medical treatment - volume overload - infections ( pneumonia, septicaemia ) - severe brain injury - major surgery - reduced renal function - asthma

17. Causes of AHF (11) High output syndromes - septicaemia - thyrotoxicosis - anaemia - shunt syndromes

18. Investigations History taking - a thorough history assessing symptoms - prior cardiovascular history - potential cardiac and non-cardiac precipitants

19. Investigations Physical examination -Look for increased signs of congestion - Look for decreased peripheral pefusion signs Vital signs ( Hyper/hypotension, Fever, Respiratory rate, SpO2) Body weight ( Fluid overload or response to therapy, Urine output) Jugular venous pressure ( volume status and response to therapy  need more or less diuretics) Heart sound ( elevated S3  elevated LV pressure and poor LV function), (MR, TR signs of reduction of ventricular filling pressure and volume)

20. Investigations Breath sound - signs of lung congestion or pleural effusion, pneumonia Extremities - oedema  fluid overload - extremities temperature  distal perfusion

21. Investigations

22. Investigations Biochemistry studies BNP & NT- proBNP  increased in elevated LV pressure and volume  BNP <100pg/dl suggests nonheart failure aetiology of dyspnoea  BNP > 400 pg /dl reflects AHF  BNP 100-400 pg /dl is indeterminate Renal function markers BUN Creatinine

23. Investigations Troponin - increased troponin  myocardial damage * AHF itself can lead to mild-to-moderate troponin elevation Troponinemia distinguishing from AHF or AMI can be challenging problem D dimer  elevated in PE Procalcitonin  for infection suspected patients  to guide antibiotic therapy Thyroid function test  to exclude thyrotoxicosis

24. Investigations Imaging studies ECG  information of myocardial ischaemia , chamber dilatation or hypertrophy, arrhythmias CXR  pulmonary congestion or pleural effusion  changes in cardiac silhouette reflects cardiomegaly or pericardial effusion Lung Ultrasound  multiple B lines show pulmonary congestion

25. Investigations Echocardiography - structure and function of all cardiac chambers and valves - wall motion abnormalities and estimate of haemodynaemics

26. Management AHF is a life threatening medical emergency Confirmation of diagnosis, identification of coexisting life threatening conditions and/or life threatening precipitants of AHF are parallel process Coexistent life threatening condition refers to cardiogenic shock and respiratory failure

27. Management Manage Respiratory Failure in Suspected AHF Pulmonary congestion an intrapulmonary shunt physiology resulting in hypoxemia, Oxygen therapy should be initiated with aim to keep saturation 92–94% In suspected AHF without hypoxemia oxygen is not recommended as it causes vasoconstriction and a reduction in cardiac output Oxygen therapy is initiated if PaO2 < 60 mmHg or SpO2 < 90%. An arterial blood gas to measure pH and PCO2 and lactates should be done in all patients with congestive symptoms or a background of COPD without hypoxemia without hypoxemia without hypoxemia without hypoxemia

28. Management Non invasive Ventilation (NIV) NIV is indicated if there is no urgent need of intubation and no contraindication of NIV Non invasive Ventilation (NIV) reduces work of breathing and respiratory distress NIV also decreases preload and left ventricular afterload leading to increased cardiac output and decreased pulmonary congestion The provision of adequate positive end expiratory pressure (PEEP) with NIV also increases oxygenation by increasing the mean airway pressure Inspiratory positive pressure improves minute ventilation and is useful in cases of hypercapnia and concomitant chronic obstructive pulmonary disease (COPD) NIV includes both Continuous positive airway pressure (CPAP) and bilevel positive pressure ventilation (BPAP) Invasive ventilation and intubation is recommended in AHF when respiratory failure cannot be managed noninvasively

29. Management Manage Cardiogenic Shock in AHF Cardiogenic shock is defined as hypotension and signs of tissue hypoperfusion despite an adequate filling pressures In case of cardiogenic shock an immediate ECG and echocardiography are needed to diagnose the common pathogenetic conditions like STEMI, arrythmias and advanced chronic heart failure with decompensation In case of ACS as cause of AHF with cardiogenic shock immediate coronary angiography be done with an intent to revascularization All patients with AHF and cardiogenic shock should ideally have an arterial line in situ for continuous monitoring of arterial blood pressure

30. Management - Pharmological therapy Aim of pharmacologic therapy in AHF with cardiogenic shock is to increase cardiac output and improve organ perfusion Fluid challenge with 250-300 mL crystalloid over 15–20 min in patients with hypoperfusion but no congestion After the fluid challenge pharmacologic management with vasopressors and inotropes is initiated Intravenous inotropic agents like dopamine or dobutamine should be used to increase cardiac output Dose titration should be done with continuous monitoring of perfusion of organs Norepinephrine is the preferred vasopressor medication when arterial blood pressure needs support

31. Management - Pharmological therapy there is some benefit with the combination of Levosimendan with vasopressors Adding levosimendan to a combination of dobutamine and vasopressors has also been looked into with some benefit in hemodynamics For patients with preserved ejection fraction presenting with cardiogenic shock treat left ventricular outflow tract obstruction with IV fluids + norepinephrine or phenylephrine as vasopressors Mechanical circulatory support for a short term for cardiogenic shock not responding to inotropes and vasopressors

32. Management - Pharmological therapy Precipitants of AHF Which Require Immediate Management (1) Acute Coronary Syndrome (ACS) (2) Hypertensive Emergency (1) Acute Coronary Syndrome (ACS) - ST elevation MI should be treated by urgent revascularization either by primary angioplasty or by thrombolysis by fibrin specific fibrinolytic agents - NON ST elevation MI in patients with recurrent ischemia, ST changes, arrhythmia should also be managed by early angiography and intervention Invasive strategy with intention to revacularize within 2 h of presentation

33. Management - Pharmological therapy (2)Hypertensive emergency Hypertensive emergency can precipitate AHF manifests predominantly as pulmonary oedema Use vasodilators and diuretics to reduce blood pressure aggressively by 25% during the first few hours is necessary to avoid further deterioration Arrhythmias: Tachyarrhythmias or brady- arryhtmias should be tackled with medications, cardioversion, defibrillation or temporary pacing Acute pulmonary embolism: When acute pulmonary embolism is identified as the cause of shock, immediate reperfusion therapy with thrombolysis, catheter based techniques or surgical embolectomy should be considered Acute mechanical cause: ACS with mechanical complications like ventricular septal defect, acute mitral regurgitation, free wall rupture needs to be managed surgically to prevent deterioration

34. Management - Pharmological therapy Diuretics are the mainstay of treatment of congestive symptoms Diuretics increase renal water and salt excretion leading to vasodilatation Diuretics need to be used with caution in AHF patients with hypoperfusion For patients with AHF and pulmonary congestion, the initial treatment is the combination of intravenous diuretics and vasodilators In AHF, intravenous furosemide is the first line diuretic and dose should be uptitrted based on response - starting from a lowest possible dose - The Initial dose should at least be 2.5 times the previous oral dose in patients already on diuretics In denovo AHF, intravenous dose of 20–40 mg initially should be started  In case of diuretic resistance or to improve efficacy of diuretics, a dual nephron blocakade with a combination of a loop diuretic ( furesomide or torsemide) and a thiazide diuretic (Metolazone) This combination needs to be carefully monitored for renal dysfunction and electrolyte imbalance

35. Management - Pharmological therapy Diuretics – doses and clinical indications

36. Management - Pharmological therapy Vasodilators  Intravenous vasodilators like nitroglycerine are commonly used in AHF T he second most common agents used in AHF  Vasodilators cause veno -dilatation leading to decreased preload and also arterial dilatation leading to decreased afterload of the heart(helps the failing heart to increase stroke volume) Urgent afterload reduction is required in AHF due to acute hypertension, acute aortic regurgitation and acute mitral regurgitation Nitroprusside, an effective vasodilator in such situations I n case of SBP < 90 mmHg, they should be used with caution Vasodilators are contraindicated in patients with significant aortic stenosis and mitral stenosis

37. Management - Pharmological therapy Inotropes & vasopressors Indicated when the cardiac output is significantly reduced as in AHF with hypoperfusion Dobutamine is the inotrope of choice Adrenergic receptor stimulating inotropes can cause tachycardia and induce myocardial ischemia and arrhythmias Should always be titrated from a low dose upwards with continuous ECG monitoring Dopamine has been compared with norepinephrine in treatment of shock and there seems to be excessive mortality in the subset of cardiogenic shock with use of dopamine due to increased arrhythmogenic events Norepinephrine is the drug of choice for AHF with severe hypotension (SBP < 85 mmHg) Adrenaline (epinephrine) is used only as a vasopressor agent in refractory shock and in resuscitation protocol as per ACLS guidelines Inotropic agents are not indicated in patients of heart failure with preserved ejection fraction

38. Management - Pharmological therapy Vasodilators - Doses

39. Management - Pharmological therapy Inotropes and vasodilator Doses

40. Management - Pharmological therapy Miscellaneous Drugs Digoxin U sed in AHF with Atrial fibrillation with a rapid ventricular response (> 110/min) used as boluses of 0.25 mg to 0.5 mg Maintenance dose depends on a multitude of factors, such as age, sex and renal function Vasopressin antagonists  Drugs like tolvaptan are V2 receptor anatgonists at the renal tubules promote water excretion (aquaresis) Tolvaptan is indicated in AHF with volume overload and hyponatremia

41. Management - Pharmological therapy Opiates Opiates were once considered as first line agents to relieve dyspnea and anxiety N ot routinely recommended for management of patients with AHF due to the side effects S hould be used with caution in patients with severe dyspnea due to pulmonary oedema Anxiolytics and sedatives Use for agitation and delirium Benzodiazepines (Lorazepam or diazepam) can be used

42. Management Renal Replacement Therapy The most common modality of renal replacement therapy in AHF with congestion is generally ultrafiltration Movement of water across a semipermeable membrane due to a transmembrane pressure is called as ultrafiltration. Ultrafiltration is indicated for diuretic refractory pulmonary congestion It is not the first line therapy for patients with AHF and congestion. Indications for dialysis in AHF are the standard indications of dialysis in critical illness  hyperkalemia , acidosis and volume overload

43. Management Mechanical Assist Devices (1) Intra-aortic balloon pump (IABP): IABP can be used to support the circulation, as a bridge to surgery, in case of mechanical complications like ventricular septal rupture and acute mitral refurgitation (2) Extracorporeal membrane oxygenation (ECMO): Patients with AHF and cardiogenic shock may be supported with ECMO as temporary measure until the heart and other organs have recovered their function

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