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Acute Heart Failure Management in the ICU.pptx
- 1. ACUTE HEART FAILUREin 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 intolerance • HF cardinal signs pulmonary rales (abnormal crackling sounds) peripheral oedema distended jugular veins palpable liver tachycardia third heart sound
- 4. Introduction • Acute HeartFaiilure (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 pathophysiologyof 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
- 6. Pathophysiology LV systolic anddiastolic 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
- 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 Chronic hypertension Chronic kidney disease Chronic aortic stenosis Ageing 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 increasein 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 • Themajority 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 • Activationof 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 • These patients are particularly prone to fluid accumulation
- 12. Pathophysiology • Fluid redistribution Sympatheticstimulation 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 organdysfunction 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 -Lookfor 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.
- 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 - increasedtroponin 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 - structureand function of all cardiac chambers and valves - wall motion abnormalities and estimate of haemodynaemics
- 26. Management • AHF isa 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 Failurein 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 wit hou t hyp oxe mia wit hou t hyp oxe mia wit hou t hyp oxe mia wit hou t hyp oxe mia
- 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)
- 29. Management Manage Cardiogenic Shockin 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 - Pharmologicaltherapy • 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
- 31. Management - Pharmologicaltherapy • 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 - Pharmologicaltherapy 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 - Pharmologicaltherapy (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
- 34. Management - Pharmologicaltherapy • 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 - Pharmologicaltherapy Diuretics – doses and clinical indications
- 36. Management - Pharmologicaltherapy Vasodilators • Intravenous vasodilators like nitroglycerine are commonly used in AHF • The 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 • In 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 - Pharmologicaltherapy 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
- 38. Management - Pharmologicaltherapy Vasodilators - Doses
- 39. Management - Pharmologicaltherapy Inotropes and vasodilator Doses
- 40. Management - Pharmologicaltherapy Miscellaneous Drugs • Digoxin • Used 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 - Pharmologicaltherapy • Opiates • Opiates were once considered as first line agents to relieve dyspnea and anxiety • Not routinely recommended for management of patients with AHF due to the side effects • Should 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 illnesshyperkalemia, 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
- 44.