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Download Update on the Treatment of Acute Decompensated Heart Failure
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ACUTE DECOMPENSATED HEART FAILURE University of Ottawa Medical School Curriculum Sharon Chih MBBS, FRACP, PhD Assistant Professor, University of Ottawa January 13h, 2016 Learning Objectives Define acute heart failure and describe its pathophysiology with reference to: impaired -contractility or ventricular filling and increased afterload. List examples of conditions that cause left and right-sided heart failure. Review the clinical manifestation of heart failure. Review the treatment of heart failure with reference to: diuretics, vasodilators, inotropic drugs Distinguish between pulmonary edema of cardiogenic vs noncardiogenic origin. Management of Acute HF - Outline Review of the clinical presentation of acute HF Causes Clinical signs and symptoms Diagnosis What are the important management strategies? What are the important prognostic markers? How do we use diuretics? How and when do we use inotropes or vasodilators Definition: Heart Failure Condition where the heart cannot pump an adequate supply of blood at normal filling pressures to meet the metabolic needs of the body Clinically Reduced cardiac output Congestion Impaired quality of life Reduced life expectancy Distinguish from cardiomyopathy: Pathologic abnormality of myocardium resulting in abnormal myocardial structure - cardiac dilatation and hypertrophy All patients with cardiomyopathy do not have HF Acute vs. Chronic HF? Acute HF or Acute heart failure syndrome or ADHF First presentation of new onset HF symptoms Acute worsening of symptoms Previously stable HF that has deteriorated Acute vs. Chronic HF Chronic HF Management Beta blockers ACE inhibitors / ARB Spironolactone ICD /CRT Acute HF Management Symptom based Relieve congestion Diuretics Improve perfusion Inotropes Remove agent precipitating General Causes of HF Coronary artery disease Myocardial infarction Valve disease Idiopathic cardiomyopathy Hypertension Myocarditis / pericarditis Arrhythmias Thyroid disease Pregnancy Toxins (alchohol, chemotherapy) Inherited cardiomyopathies Mechanisms and Causes of HF Impaired Contractility Myocardial infarction Transient ischemia Chronic volume overload MR/AR Dilated cardiomyopathy Increased Afterload AS Uncontrolled HTN Systolic Dysfunction Left Sided HF Diastolic Dysfunction Obstruction of LV filling MS Pericardial constriction or tamponade Impaired ventricular relaxation LVH Hypertrophic cardiomyopathy Restrictive cardiomyopathy Transient ischemia Mechanisms and Causes of HF Cardiac Causes Left sided HF Pulmonary stenosis Right ventricular infarction Right Sided HF Pulmonary Vascular Disease Pulmonary embolism Pulmonary HTN Right ventricular infarction Parenchymal pulmonary disease COPD Interstitial lung disease Chronic infections Adult respiratory distress syndrome Increased contractility Normal A Heart Failure Hypotension Stroke volume (cardiac output) Heart Failure: Pathophysiology B C Pulmonary congestion Left ventricular end diastolic pressure (volume) Heart Failure Neurohumoral Activation Myocardial insult LV dysfunction Neurohormonal Activation LV Remodeling •Sympathetic •Renin-angiotensin •ADH • Initially restores CO and organ perfusion • Ultimately highly negative impact on ventricular function Diagnosis of HF There is no single diagnostic test that can confirm the diagnosis of heart failure Constellation of symptoms and signs CXR findings Confirmation of cardiac abnormality Invasive hemodynamic studies Echocardiogram Serum BNP testing Symptoms and Signs of HF Increased filling pressures Congestion Poor Cardiac Output Poor Perfusion Congestion – left sided Left-Sided Symptoms Dyspnea Orthopnea Shortness of breath when supine Paroxysmal nocturnal dyspnea Acute awakening from sudden dyspnea Fatigue Signs S3 gallop Displaced apex MR Pulmonary rales Loud P2 Congestion – Right Sided Right-Sided Symptoms Peripheral edema Abdominal bloating Nausea Anorexia Signs Elevated JVP Hepatomegaly Ascites Edema Evaluating the JVP Consensus: <2 cm above the sternal angle considred normal and >4cm ASA is abnormal http://cal.fmc.flinders.edu.au /gemp/ClinicalSkills/clinskil/ year1/cardio/cardio04.htm Assessing Perfusion Symptoms Fatigue Confusion Dyspnea Sweating Signs Hypotension Tachycardia Cool extremities Altered mental status Decreased urine output/Rising creatinine Liver enzyme abnormalities Pulmonary Edema General Considerations Increase in the fluid in the lung Generally, divided into cardiogenic and non-cardiogenic categories. Pathophysiology Fluid first accumulates in and around the capillaries in the interlobular septa (typically at a wedge pressure of about 15 mm Hg) Further accumulation occurs in the interstitial tissues of the lungs Finally, with increasing fluid, the alveoli fill with edema fluid (typically wedge pressure is 25 mm Hg or more) Cardiogenic vs. Noncardiogenic pulmonary edema Cardiogenic pulmonary edema Heart failure Coronary artery disease with left ventricular failure. Cardiac arrhythmias Fluid overload -- for example, kidney failure. Cardiomyopathy Obstructing valvular lesions Myocarditis and infectious endocarditis Non-cardiogenic pulmonary edema - due to changes in capillary permeability Smoke inhalation. Head trauma Overwhelming sepsis. Hypovolemia shock Acute lung re-expansion High altitude pulmonary edema Disseminated intravascular coagulopathy (DIC) Near-drowning Overwhelming aspiration Acute Respiratory Distress Syndrome (ARDS) CXR Findings of Pulmonary Edema Cardiogenic pulmonary edema Kerley B lines (septal lines) Seen at the lung bases, usually no more than 1 mm thick and 1 cm long, perpendicular to the pleural surface Pleural effusions Usually bilateral, frequently the right side being larger than the left If unilateral, more often on the right Fluid in the fissures Thickening of the major or minor fissure Peribronchial cuffing Visualization of small doughnutshaped rings representing fluid in thickened bronchial walls Non-cardiogenic pulmonary edema Bilateral, peripheral air space disease with air bronchograms or central bat-wing pattern Kerley B lines and pleural effusions are uncommon Typically occurs 48 hours or more after the initial insult Stabilizes at around five days and may take weeks to completely clear On CT Gravity-dependent consolidation or ground glass opacification cuffing Alveolar edema Kerley B Clinical Presentation of Acute HF Hypertension and acute pulmonary edema 10-20% Hypotension and markedly low CI <10% Gradual worsening of symptoms 60-80% -less pulmonary congestion and more edema or weight gain ->70% ADHF is worsening chronic HF -50% of these patients may have SBP>140 Presentation – Symptoms and Signs Patient profile Older - median 75y.o Female ~50% HFpEF ~50% Comorbidities common: AF, DM, CKD Dyspnoea 70-90% Other: oedema, fatigue, subtle Young: abdo pain, nausea, anorexia Old: confusion and lethargy JVP most sensitive Estimate of left sided filling pressures (PCWP) R = 0.64 for JVP and PCWP Dissociation b/w JVP and PCWP in lung disease, obesity, PE, RV infarct Poor sensitivity: rales, oedema, S3 Majority hypertensive 50% SBP >140 mmHg; 45% SBP 90 – 140 mmHg; 5% SBP <90 mmHg Predictors of Adverse Outcome During Acute HF Clinical Hypotension (SBP <100) Older age Ischemic etiology Recurrent hospitalisations NYHA IV (>90 days) Laboratory Renal dysfunction (Cr >220) Anemia (acute or chronic) Hyponatremia (Na <132) EF<40% Elevated troponin or BNP (>500) ADHF Treatment Goals 1. 2. 3. 4. 5. 6. 7. Relieve symptoms: congestion and low out-put Optimise volume status Identify aetiology Identify precipitating factors Initiate and optimise chronic oral therapy Minimise side effects Educate patient/family: medications and self assessment HFSA guidelines: Journal of Cardiac Failure Vol. 16 No. 6 2010 Precipitants of HF Increased metabolic demands Fever, anemia, infection, tachycardia, hyperthyroidism, pregnancy Increased circulating volume Excessive salt or fluid in diet Progression of Renal failure underlying disease Increased afterload Hypertension PE Impaired contractility Negative inotropes Ischemia Failure to take medications ADHF Evaluation and Treatment According to clinical haemodynamic profiles ↓BP ↑Cr P E R F U S I O N Dry & Warm Wet & Warm ACEI/BB/Aldost inhib Diuretics ± IV Vasodilators Dry & Cold Wet & Cold ↓Vasodilators ↓Diuretics Diuretics Inotropes/Vasodilators CONGESTION Stevenson et al. Eur J Heart Failure 1999: 1: 251-257 ↑JVP Crackles Oedema Therapy Diuretics 1. Reduce fluid overload Vasodilators 2. Decrease preload and/or afterload Inotropes 3. Augment contractility 4. Mechanical circulatory support Unresponsive to medical therapy Intravenous Diuretics Essential for the management of congestion Restore volume by increasing excretion of Na and water Loop diuretics are first line Diuretic resistance Dosing Combination therapy with thiazide Neurohormonal blockade Lasix Administration and Dosing Bioavailability of oral dosing variable (20-80%) Gut wall edema, reduced blood flow, protein binding IV rate preferred in acute HF Initial dose should be double maintenance or 40-80 mg IV – titrate to clinical response Consider continuous infusions if large bolus ineffective Dose trial: no difference between bolus vs. infusion Associated with hypotension, renal dysfunction, electrolyte disturbance (K, Mg, Ca), RAAS activation Diuretic Responsiveness Ellison et al. Cardiology 2001; 96:132-143 Beneficial effects of volume restoration Negative sodium and water balance Decreased cardiac filling pressure Decreased ventricular dilatation Decreased ventricular wall stress and endomyocardial ischemia Improved pulmonary congestion Decreased functional MR/TR Improved myocardial function Improved renal function Vasodilators Reduce filling pressures, afterload: increase CO Class IIa Recommendation, Level of evidence B In patients with evidence of severely symptomatic fluid overload in the absence of systemic hypotension, vasodilators such as intravenous nitroglycerin, nitroprusside, or nesiritide can be beneficial when added to diuretics and/or those who do not respond to diuretics alone Little data for specific choice: Nitroglycerin vs. Nitroprusside vs. Nesiritide Vasodilator Therapy in Acute HF Nitroglycerin Stimulates guanylate cyclase Dose dependent venous and arteriole dilatation Decreases filling pressures without increasing oxygen demand Headache Nitrate tolerance Nitroprusside Equipotent venous and arteriolar dilation Useful for HTN, valvular dysfunction (AR, MR) Short half life Methemoglobinaemia Cyanide toxicity Who is the Ideal Candidate for IV vasodilator therapy? “wet and warm” profile Patients with acute pulmonary edema/dyspnea and preserved BP (SBP >90) Acute HF and concurrent cardiac ischemia Vasodilator Dosing Nitroglycerin Intravenous infusions 5-10 ug/min titrated for desired clinical effect Oral: isordil 10-30 mg tid Transdermal:0.2-0.8 mg/hr by patch Inotropic Use in Acute HF Dobutamine PDE Milrinone Levosimendan Adapted from Dorn; Circulation 2004 Inotropes and Harm Increased mortality through variety mechanisms Increase HR Arrhythmias Increase myocardial oxygen demand Direct toxic effect to myocardium: accelerated apoptosis NOT effective in broad populations of patients with ADHF Routine use in “wet and warm” detrimental (OPTIME-HF) Majority of ADHF patients are not in low output state Increased rates of HF rehospitalisation, mortality with inotropes (ESCAPE, ADHERE) Role of Inotropic Therapy Reserved for those with low output HF “wet and cold” Evidence of poor tissue perfusion Symptomatic hypotension despite adequate filling pressures Poor response to diuretics with worsening renal function Unresponsive or intolerant to vasodilators Short term Lowest dose No evidence that one is agent is superior to other Inotrope Dosing Dobutamine 2-6 ug/kg/min infusions –larger doses needed if profound shock/hypotension Milrinone 0.25-0.75 ug/kg/min infusion Dopamine 2-5 ug/kg/min infusions What about oral HF medications? Beta blockers ACE Inhibitors Usually maintained in mild-moderate acute HF Dose reduced or held when patients felt to have significant reduction in perfusion or need for inotropes Dose escalation not advised in setting of acute HF Dose usually maintained unless significantly hypotensive or acute renal failure Dose escalation ok once acute symptoms improved (if no worsening renal function) Digoxin Dose maintained unless digoxin toxicity Acute HF: Summary Acute HF results when heart function can no longer meet needs of body Can be caused by pump failure, or resistance on either side of heart Key strategy in management is to identify underlying cause Diuretics are essential Vasodilators reserved for acute HF with HTN, ischemia or pulmoary edema Inotropes should only be used in patients with poor perfusion Novel inotropes have not proved more safe or effective than current care
