Fundamentals of Anesthesia Nursing 2 Module 1 Cardiovascular and Trauma Anesthesia Congestive Heart Failure 1 2013 ACCF/AHA Guideline for the Management of Heart Failure Developed in Collaboration With the American Academy of Family Physicians, American College of Chest Physicians, Heart Rhythm Society, and International Society for Heart and Lung Transplantation Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation © American College of Cardiology Foundation and American Heart Association, Inc. • • • • • • • • • • Outline Definition of Heart Failure Incidence/Significance Pathophysiology Classification of Heart Failure Stages, Phenotypes and Treatment of HF Adaptive Mechanisms Symptoms of CHF, Right and Left Sided Failure Treatment of CHF Anesthetic Management of CHF Ventricular Assist Devices 3 Definition of Heart Failure • Inability of the heart to maintain sufficient CO to meet metabolic demands of the body • Pathophysiologic hallmarks include: – Decreased CO – Increased Left or Right VEDP – Increased SVR – Metabolic Acidosis • CHF usually EF < 40%, normal EF 55-75% 4 Definition of Heart Failure 2013 ACCF/AHA Guidelines for Management of Heart Failure Classification I. Heart Failure with Reduced Ejection Fraction (HFrEF) II. Heart Failure with Preserved Ejection Fraction (HFpEF) Ejection Fraction ≤40% ≥50% a. HFpEF, Borderline 41% to 49% b. HFpEF, Improved >40% Description Also referred to as systolic HF. Randomized clinical trials have mainly enrolled patients with HFrEF and it is only in these patients that efficacious therapies have been demonstrated to date. Also referred to as diastolic HF. Several different criteria have been used to further define HFpEF. The diagnosis of HFpEF is challenging because it is largely one of excluding other potential noncardiac causes of symptoms suggestive of HF. To date, efficacious therapies have not been identified. These patients fall into a borderline or intermediate group. Their characteristics, treatment patterns, and outcomes appear similar to those of patient with HFpEF. It has been recognized that a subset of patients with HFpEF previously had HFrEF. These patients with improvement or recovery in EF may be clinically distinct from those with persistently preserved or reduced EF. Further research is needed to better characterize these patients. 5 Incidence/Significance • Affects 5 million individuals (2% of the population) with 550,000 new cases diagnosed annually • Affects 1% of individuals between 50-59 years and >10% of individuals >80 years **Mortality from coronary heart disease heart failure has remained the same** 6 Incidence/Significance • 1 in 5 lifetime risk • Prognosis after diagnosis grim – median survival of 1.7 years in men and 3.2 years in women 7 Pathophysiology • Impairment of the heart’s ability to fill or empty the left ventricle • Ischemic heart disease and hypertension common causes http://www.integrativebiology.ac.uk/images/heart.jpg 8 • • • • • • • • • • • Pathophysiology (cont) Valvular diseases Hypertrophic cardiomyopathies (HCM) Arrhythmogenic right ventricular (RV) cardiomyopathy Restrictive/infiltrative conditions (sarcoidosis, hemochromatosis, amyloidosis) Myocarditis HIV Metabolic conditions Toxicity (drug or chemical) Peripartum disorders Muscular dystrophies Idiopathic HF http://www.integrativebiology.ac.uk/images/heart.jpg 9 Pathophysiology (cont) • Heart failure may be one of the following or both: – Systolic (decreased LV ejection fraction) – Diastolic (elevated filling pressures and abnormal relaxation but normal LVEF) – Combination of both 10 Pathophysiology (cont) • Systolic dysfunction - decreased contractility • Decreased LV ejection fraction, decreased LV volume, increased LVEDV, and abnormal contraction • IHD and resultant myocardial damage • Idiopathic dilated cardiomyopathy 11 Pathophysiology (cont) • Systolic dysfunction - excessive workload • Increased resistance to ventricular ejection (right or left heart) – Valvular pathology – Systemic HTN – Pulmonary HTN (secondary to left heart failure) 12 Pathophysiology (cont) • Diastolic dysfunction - decreased compliance of ventricle with increased chamber stiffness • Abn LV filling and increased filling pressures – IHD – Systemic HTN – Valvular pathology – HCM 13 Pathophysiology (cont) • Acute decompensated HF – Myocardial ischemia or infarction – Worsening valvular dysfunction – AF/other arrhythmias – Cardiotoxins – Non-cardiac factors • Severe HTN • Renal failure • PE 14 Pathogenesis of CHF 15 Classification of Heart Failure 2013 ACCF/AHA Guidelines for Management of Heart Failure A B C ACCF/AHA Stages of HF At high risk for HF but without structural heart disease or symptoms of HF. Structural heart disease but without signs or symptoms of HF. None Structural heart disease with prior or current symptoms of HF. I I II III D Refractory HF requiring specialized interventions. IV NYHA Functional Classification No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. No limitation of physical activity. Ordinary physical activity does not cause symptoms of HF. Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in symptoms of HF. Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes symptoms of HF. Unable to carry on any physical activity without symptoms of HF, or symptoms of HF at rest. ACC/AHA 2005 Pre-op BNP not routinely recommended currently due to lack of evidence of meaningful cut-off levels as well as no evidence using BNP or NT-proBNP to guide therapy improving medical management. 17 ACC/AHA 2005 N-terminal pro-brain natriuretic peptide (NT-proBNP) can be used to differentiate patients with normal and reduced left ventricular ejection fraction (LVEF) Pre-op BNP not routinely recommended currently due to lack of evidence of meaningful cut-off levels as well as no evidence using BNP or NT-proBNP to guide therapy improving medical management. 18 19 20 Stages, Phenotypes and Treatment of HF Adaptive Mechanisms • The Frank-Starling Relation • Acute catecholamine production • Renal compensation (RAAS) • Myocardial enlargement (remodeling) 22 The Frank-Starling Curve • Preload is represented on the horizontal axis • Stoke volume is represented on the vertical axis • LVEDV is synonymous with preload • Stoke volume is synonymous with ventricular work Miller’s Anesthesia, 6th ed., pg 727 23 Catecholamines • Acute damage causes CO curve to shift down and to the right (depressed) • Decreased atrial pressures activates SNS – Catecholamine cause CO curve to move up and to the left slightly – Peripheral vasoconstriction will result (increased SVR) – Heart rate will also increase 24 Catecholamines Normal CO: Point A: normal operation point (CO= 5L; RA pres:0 mmHg) After Heart damage: CO lowest, but shortly after goes to B with CO= 2L and RA pres= 4 mmHg (↑due to damming of blood); may be associated with short period of fainting. Increased Sym reflex at various at various levels compensates heart activity rapidly, while the Para↓. At this point, new CO and RA pres established at point C. Thus, a person with sudden moderate heart attack experiences only cardiac pain and a few second of fainting, which is then compensated by Sym reflex. https://quizlet.com/20430153/dphy-exam-c-flash-cards/ 25 Renal Compensation • Decreased BP will result in decreased GFR • Activation of Renin-Angiotensin-Aldosterone system • Angiotensin II = vasoconstriction + sodium and water retention • Angiotensin II stimulates aldosterone secretion • ANF/BNF in response to increased atrial stretch increases urine excretion 26 Global Compensation • Initial neurohumoral response is adaptive – Sympathetic stimulation – Salt and water retention – Vasoconstriction • Over time maladaptive – Cardiac remodeling – Pulmonary congestion – Excessive workload 27 Chronic Compensation • Increased fluid retention ( CVP EDV) • Transcapillary fluid filtration, edema formation, and congestion • Left heart failure often accompanied by pulmonary edema • Right heart failure – Distended neck veins – Peripheral edema – Ascites 28 Compensation Failure • Severe heart failure – Normal cardiac output cannot be achieved by any amount of fluid retention. 29 Myocardial Enlargement • Initially, dilation from volume overload • Hypertrophy due to chronic pressure overload – Concentric hypertrophy = nl LV chamber size w/ thickened walls • Hypertrophy due to chronic volume overload – Dilated (Eccentric) hypertrophy = Increased LV chamber size w/ nl or thickened walls • Increases muscle mass and contractile force • End result is poorly compliant ventricle that needs increased oxygen delivery • Supply vs demand mismatch 30 Myocardial Enlargement http://ccn.aacnjournals.org/content/24/6/14/F1.medium.gif 31 Myocardial Enlargement http://physiologyonline.physiology.org/content/22/1/56 32 Symptoms of CHF • Left-sided failure – Orthopnea – Dyspnea – Increased fatigability • Right-sided failure – Systemic venous hypertension – Peripheral edema 33 Left Heart Failure Clinical Presentation • Left sided failure = pulmonary – Orthopnea – Results from fluid mobilization from dependent areas – Failing LV can not manage the increases intravascular volume – Pulmonary edema develops 34 Left Heart Failure Clinical Presentation • Left sided failure = pulmonary – Dyspnea (earliest/most frequent sign) – Pulmonary edema secondary to increased pulmonary capillary pressure – Pulmonary edema increases work of breathing – Limits oxygenation of the blood 35 Clinical Presentation http://www.heartcarecenters.com/images/CHF2.jpg 36 Clinical Presentation • Left sided failure = cardiovascular – S3 ventricular gallop = significant LV dysfunction – S3 may be first sign of CHF – Increasing LV failure may display pulsus alternans – Dysrhythmias: PAT, PVC’s, Tachycardia – Elevated troponin and Natriuretic peptide levels 37 Clinical Presentation • Left sided failure = cardiovascular – Tachycardia: unexplained resting tachycardia suggests presence of CHF – Significant if patient is elderly or has heart disease – Result of increase in SNS activity 38 Clinical Presentation • Left sided failure = cardiovascular – Vasoconstriction can be present • Maintains BP so flow to brain/heart maintained • Renal blood flow: may be 25 % of normal • Results in increased blood urea nitrogen (BUN) and oliguria 39 Clinical Presentation • Left sided failure = other – Insomnia/unexplained fatigue – Decreased cardiac reserve – Low cardiac output – Above two cause fatigue at rest or with only minimal exertion 40 Clinical Presentation • Left sided failure = other – Fluid retention – Weight gain – Oliguria – Changes on CXR • Enlarged silhouette • Interstitial edema (seen as hilar and peripheral haze) • Clouding of lung fields 41 42 43 http://www.lumen.luc.edu/lumen/MedEd/MEDICINE/PULMONAR/CXR/atlas/images/328b3.jpg 44 http://www.lumen.luc.edu/lumen/MedEd/MEDICINE/PULMONAR/CXR/atlas/images/328b3.jp g Full Hazy Hilum & Pleural Effusion Clinical Presentation 45 http://www.lumen.luc.edu/lumen/MedEd/MEDICINE/PULMONAR/CXR/atlas/images/328b3.jpg Clinical Presentation Pulmonary Edema 46 Right Heart Failure Clinical Presentation • Right sided failure = pulmonary – Cor Pulmonale • Primary cause is pulmonary hypertension secondary to COPD • Loss of pulmonary capillaries • Arterial hypoxemia • Hypoxic pulmonary vasoconstriction 47 Clinical Presentation • Right sided failure = cardiovascular – Hallmark is venous congestion • JVD • Kussmaul’s sign AKA • Pulsus Paradoxus http://www.cuhk.edu.hk/cslc/materials/pclm1011/image02.gif 48 Clinical Presentation • Right sided failure = other – Edema (pitting, dependent) – Weight gain – Ascites (late manifestation) http://www.facmed.unam.mx/deptos/anatomia/ense/higado/imagenes/FIGURA30.JPG 49 Clinical Presentation • Right sided failure = other – Hepatomegaly • Distended liver causes RUQ pain • Moderate congestion results in abnormal LFT’s • Elevated serum bilirubin and transaminase • Severe enlargement may have prolonged PT 50 Clinical Presentation • Right sided failure = other – Radiographic changes • Enlarged cardiac silhouette • Pleural effusions – Laboratory values • Elevated troponin • Elevated BNP 51 52 http://www.heartcarecenters.com/images/CHF2.jp g Overview 53 Treatment of CHF • Based on four principles – Improve contractility – Reduce cardiac workload – Control excess salt and water retention – Prolong survival 54 Treatment of CHF • Early stages of chronic CHF – Bed rest to decrease MVO2 – Sodium restricted diet 55 Treatment of CHF • Early stages of chronic CHF - Pharmacology – Usually combination therapy – Goal is to optimize cardiac function by manipulating peripheral circulation, decreasing preload, and improving myocardial performance 56 Treatment of CHF • Beta blockers – Previously contraindicated – Current research suggest that betablockers improve survivability, decreases hospitalizations and improve LV function – In failing heart beta adrenergic system is desensitized – Catecholamines are directly cardiotoxic – Beta-blockade attenuates these effects – May attenuate remodeling 57 Treatment of CHF • Angiotensin-Converting Enzyme Inhibitors – Degree of activation of renin-angiotensinaldosterone system (RAAS) correlates directly with poor outcome in heart failure – Increased preload and afterload – Myocardial remodeling – ACEIs decrease mortality – ACEIs decrease hospitalizations **Evidence based practice suggests this is the most appropriate medical treatment for CHF** 58 Treatment of CHF • Angiotensin II receptor blockers (ARB) – Advantage over ACEIs in that blocks Angiotensin II generated through non-ACE pathway – Research not clear regarding benefits of angiotensin II blockers over ACEIs alone or in combination with ACEIs – Some research suggests possible higher mortality, but better EF and quality of life – As with ACEIs, may produce hypotension, hyperkalemia, and renal dysfunction Hypotensive during induction - possibly bradycardic Prophylactic glycopyrolate (0.2 mg) in elderly taking chronic ARB 59 Treatment of CHF • Aldosterone antagonists – Aldosterone levels significantly high in CHF – May lead to remodeling (or reverse remodeling although not a direct effect on cardiomyocytes) – ACEIs may only transiently reduce aldosterone – Aldosterone secretion may be independent of angiotensin II levels – Research limited ***May cause hyperkalemia- measure K+ intraop*** 60 Treatment of CHF • Digoxin (Lanoxin, Lanoxicaps, Cardoxin, Digitek) – LVEDP decreases which decreases wall tension – Digoxin is now recommended only in patients who continue to experience symptoms while receiving optimal medical treatment, including ACE inhibitors and [beta]-blockers. – Not indicated for patients with acute MI in sinus rhythm, mild failure, isolated RV failure 61 Treatment of CHF • Digoxin (Lanoxin, Lanoxicaps, Cardoxin, Digitek) – Recent evidence suggests that digoxin • Sensitizes cardiac baroreceptors • Decreases sympathetic outflow by its vagolytic effect • Suppresses renin secretion from the kidneys – In heart failure, digoxin probably acts primarily as a neurohormonal modulator rather than a weak positive inotropic agent. Only positive inotrope that does not increase mortality in HF 62 Treatment of CHF • Other pharmacological agents – Diuretics promote excretion of excess body water • May deplete K+ – Vasodilators decrease afterload • VA study-hydralazine and isosorbide (organic nitrate) improved survival • Beneficial in patients with renal dysfunction who cannot tolerate ACEI or ARB. 63 Treatment of CHF • Other pharmacological agents – Calcium channel blockers generally contraindicated – Antiarrhythmic agents not routinely prescribed for CHF • However, if indicated for treatment of symptomatic atrial arrhythmias, amiodarone should be used (known CHF-safe) • Antithrombolyitics agents not routinely prescribed for CHF 64 Treatment of CHF • Other pharmacological agents – Positive inotropes such as phosphodiesterase inhibitors were used in the past – No long term survival benefit from these drugs – Used in acute refractory CHF only 65 Treatment of CHF 66 67 ACC/AHA Stages with Treatment 68 Anesthetic Management 69 Anesthetic Management of CHF • Elective procedures are contraindicated – CHF is the single MOST important predictor of perioperative cardiac morbidity and mortality – Must maximize CO if surgery is emergent • Patients with CHF at increased risk for postoperative complications – Presence of S3/JVD: 16% – History CHF: 6 % – Patient history is important 70 Anesthetic Management of CHF • Central concepts for management – Use drugs that decrease SVR and have minimal depressant effect on the heart – Invasive hemodynamic monitoring frequently required – Hypotension due to poor cardiac output may require use of positive inotropic agents – Perioperative CHF : diuretics, NTG, inotropes – Afterload reduction to decrease ventricular wall tension and myocardial oxygen consumption – Inotropic support often needed for hypotension resulting from poor cardiac output 71 Anesthetic Management of CHF • Induction – Opioids – Etomidate – Propofol…carefully – CHF pt’s myocytes are more sensitive to neg effects on velocity of shortening* – Propofol/Ketamine mixture – Benzodiazapines *Armstrong, CS, et al. (2006). Anesth and CHF. MEJ Anesth, 18(5) 72 Anesthetic Management of CHF • Treatment of hypotension and decreased CO – Oxygen! – Do not bolus fluids unless absolute emergency. These patients are run “dry”. – Adm inotropic agents: • Dobutamine 2-20 mcg/kg/min • Dopamine 2-20 mcg/kg/min • Norepinephrine 4-8 mcg IVP • Epinephrine 5-10 mcg IVP 73 Anesthetic Management of CHF • Maintenance – Isoflurane: good choice since it decreases SVR with little effect on CO (+/-) – Cardiac depression from volatile agent superimposed on CHF is much greater than in the absence of CHF – Addition of nitrous oxide to opioids or opioids + bz’s may cause significant myocardial depression 74 Anesthetic Management of CHF • Maintenance – Nitrous oxide may cause pulmonary vasoconstriction leading to pulmonary HTN and may worsen RV failure – High dose fentanyl or sufentanil as single drug may be warranted if myocardial depression is severe 75 Anesthetic Management of CHF • Maintenance – PPV may decrease pulmonary congestion and improve arterial oxygenation – Invasive monitors depend on the complexity of the procedure and severity of disease 76 Anesthetic Management of CHF • Monitoring considerations – Pre-induction intra-arterial catheter – CV catheter to monitor central volume status plus vasoactive drug administration – PA catheter not routinely recommended due to increased possibility of complications and damage from malplacement and use – TEE if equipment and expertise available 77 Anesthetic Management of CHF • Monitoring considerations (cont) – The Vigileo monitor – Continuous monitoring of essential hemodynamic information, such as CCO, SVV / SV, SVR 78 Anesthetic Management of CHF • Regional anesthesia - Neuraxial – Sympathetic blockade resulting in decreased SVR may improve CO – Decreased SVR is unpredictable – Decreased SVR is not easily controlled 79 Anesthetic Management of CHF • Combined technique – Epidural narcotics, LA, or both may help decrease stress response to surgery – More likely to select epidural narcotics without LA 80 Ventricular Assist Devices Ventricular Assist Devices 81 Ventricular Assist Devices Ventricular Assist Devices 82 Ventricular Assist Devices Intra-Aortic Balloon Pump 83 Ventricular Assist Devices Impella Device (2.5 and 5 L) 84 • • • • • • • • • • Outline Definition of Heart Failure Incidence/Significance Pathophysiology Classification of Heart Failure Stages, Phenotypes and Treatment of HF Adaptive Mechanisms Symptoms of CHF, Right and Left Sided Failure Treatment of CHF Anesthetic Management of CHF Ventricular Assist Devices 85 Questions 86
