CARDIAC DISEASE PART II Nicole Weiss, MD Tulane University, December 13, 2012 Time Crunch… Valvular Heart Disease Hypertrophic Cardiomyopathy The Transplanted Heart Congenital Heart Disease Simple Shunts Complex Shunts Antibiotic Prophylaxis Pacemaker Classification New York Classification of Functional Heart Disease Class I: Asymptomatic except during Severe Exertion Class II: Symptomatic with Moderate Activity Class III: Symptomatic with Minimal Activity Class IV: Symptomatic at Rest Valvular Disease Mitral Stenosis Most common etiology is rheumatic disease Symptoms develop 20-30 years later when mitral valve area decreases from 4-6 cm2 to less than 2cm2 Prone to Pulmonary Hypertension & Pulmonary Edema as Left Atrial Pressures Increase Anesthetic Goals for Mitral Stenosis Pulmonary Artery Catheter? Yes, pulmonary artery pressures help guide fluid management Patients are prone to volume overload and pulmonary edema SVR? High, flow through the stenotic valve is limited and the heart cannot compensate for decreases in preload Heart Rate? Normal Sinus Rhythm, Filling is dependent on atrial kick, but too low and the cardiac output may not be sufficient Supraventricular Tachycardia may cause sudden hemodynamic collapse Clinical Correlations Ephedrine or Phenylephrine? Phenylephrine Ketamine? Bad Pancuronium? Bad Neuraxial Anesthesia? Spinal probably not the best choice Epidurals give us time to stabilize the hemodynamics Aortic Stenosis Critical Valve Area: 0.5-0.7 cm2 Similar management to MS Management Goals: Normal Intravascular Volume High SVR Normal Sinus Heart Rate (60-90) Cardiac Output does not increase with exertion Myocardial Oxygen Demand High (Hypertrophied Ventricle) Aortic & Mitral Regurgitation Management Goals: Fast Heart Rate (80-100) Decreased Afterload to Promote Forward Flow Mitral Regurgitation Pulmonary Artery Waveform: Large V Wave, Rapid Y Descent A 70 y/o male with severe aortic stenosis has a preinduction HR of 63 and BP of 125/70. Following induction, his HR is 90 and BP is 85/45. The EKG has a new ST Elevation. Drug of Choice? 1. Epinephrine 2. Isoproterenol 3. Calcium Chloride 4. Phenylephrine 5. Ephedrine Pulse Variations Bisferiens Pulse Characteristic of Aortic Regurgitation First Systolic Peak=LV Ejection Second Systolic Peak= Reflected Pressure Wave in the Periphery Pulses Tardus et Parvus Characteristic of Aortic Stenosis Delayed Pulse Wave with a Diminished Upstroke Hypertrophic Cardiomyopathy Hypertrophic Cardiomyopathy Diastolic Dysfunction Dynamic Obstruction of the LV Outflow Tract (25% of patients) Caused by Narrowing in the Subaortic Area by Systolic Anterior Motion (SAM) of the Anterior Mitral Valve Leaflet Against the Hypertrophied Septum Supraventricular & Ventricular Arrhythmias Anesthetic Management Factors that Worsen Obstruction: Enhanced Contractility Decreased Ventricular Volume Decreased LV Afterload B-Blockers & Ca-Channel Blockers Amiodarone for Arrhythmias Ideal Anesthetic: Halothane Decreases Myocardial Contractility Maintains SVR Avoid: Nitrates, Digoxin, Diuretics The Transplanted Heart The Transplanted Heart Denervated No sympathetic or parasympathetic input Resting Heart Rate 100-120 (no vagal) Responsive to catecholamines Low cardiac output, slow to pick up EKG shows two P waves Pharmacology Direct agents are the best: Epinephrine & Isoproterenol Indirect vasopressors also work, but are dependent on catecholamine stores Heart rate is NOT affected by: Anticholinergics Pancuronium Meperidine Opiods Cholinesterase Inhibitors A patient has a heart rate of 110 after heart transplant. The most likely etiology is: 1. Altered Barorecepter Sensitivity 2. Cardiac Denervation 3. Compensation for a fixed Stroke Volume 4. Cyclosporine 5. Prednisone Left to Right (Simple) Shunts Qp : Qs= (CaO2-CvO2)/(CpvO2-CpaO2) Ratios < 1 Right->Left Ratios >1 Left->Right Ratios = 1 No Shunting or Bidirectional Shunts of Equal Magnitude Factors Altering Shunts SVR Increase: Phenylephrine, Norepinephrine, Ketamine Decrease: Propofol, Inhaled Agents (Iso, Sevo, Des), Dexmetomidine Nitroprusside, Nitroglycerin, Nicardipine, Milrinone, Fenoldopam, Adenosine PVR Increase: Hypercapnea, Acidosis, Hypoxemia, Positive Pressure Ventilation, Hypothermia, Reactions to the ETT Shunts & Induction of Anesthesia R->L Shunt Longer Inhalation Induction Shorter IV Induction L->R Shunt Shorter Inhalation Induction Longer IV Induction Compared with a normal patient, which of the following is true in a patient with a right->left intracardiac shunt? (More than one answer) 1. Inhalation Induction is slowed 2. Induction rate for halothane is affected more than the induction rate for nitrous oxide 3. IV induction is more rapid 4. Increased doses of IV agents are required Atrial Septal Defects Ostium Secundum Most Common Area of Fossa Ovalis Usually Isolated Defects Usually Asymptomatic Ostium Primus & Sinus Venosus Associated with Other Cardiac Defects Large Ostium Primum can cause a Large Shunt and Mitral Regurgitation Atrioventricular Septal Defects Endocardial Cushion Defects Contiguous Atrial & Ventricular Defects Associated with Downs Large Shunts Ventricular Septal Defects Most common congenital defect Small VSDs often close during childhood Restrictive are associated with small L->R Large defects produce large L->R shunts that vary with SVR and PVR Large VSDs are surgically repaired before pulmonary disease and Eisenmenger develop Patent Ductus Arteriosus •Closes within 15 hrs •Factors that Keep Open: •High Prostaglandins •Hypoxemia •Nitric Oxide •Factors that Close •Low Prostaglandins •High Oxygen •Endothelin-1 •Norepinephrine •Ach •Left Untreated-> Eisenmenger Right to Left (Complex) Shunts Tetralogy of Fallot 1. RV Obstruction (Infundibular Spasm) 2. RVH 3. VSD 4. Overriding Aorta 5. 20% have Pulmonic Stenosis Management of Tetralogy Two components of Shunt (R->L) Fixed (Obstruction of the Outflow Tract) Dynamic (PVR: SVR or Qp:Qs) Decrease the Shunt Propranolol Propranolol decreases infundibular spasm SVR Keep SVR high! Tetralogy of Fallot… Four Parts? RV Outflow Obstruction, RVH, Overriding Aorta, VSD Ketamine? Maintains SVR Propranolol? Decreases Infundibular Spasm Prostaglandin E1? Keeps PDA open Augments Pulmonary Blood Flow in the case of Right Ventricular Obstruction Tricuspid Atresia Small RV Large LV Limited Pulmonary Blood Flow Arterial Hypoxemia ASD: Mixes oxygenated with deoxygenated, Ejects through LV Pulmonary Blood Flow is via a VSD, PDA, or Bronchial Vessels Fontan Procedure Anastamosis of the Right Atrial Appendage to the Pulmonary Artery Used to correct decreased pulmonary Artery blood flow or for patients with a single ventricle After CPB: Maintain increased right atrial pressures to Facilitates pulmonary blood flow Patients with a Fontan: Monitor CVP (which equals the PAP ) Follow intravascular fluid volume, pulmonary pressures and detect LV impairment Transposition of the Great Arteries Parallel Systems Treatment: Prostaglandin E Balloon Atrial Septoplasty Decrease PVR, Increase SVR Hypoplastic Left Heart LV Hypoplasia MV Hypoplasia AV Atresia Aortic Hypoplasia Prone to Ventricular Arrhythmias Increased Pulmonary Blood Flow-> Systemic & Myocardial Ischemia Delicate Balance Between PVR & SVR Truncus Arteriosus Increased Pulmonary Blood Flow-> Myocardial Ischemia Management: Phenylephrine & Fluids PEEP Anastamosis of the right atrium to the pulmonary arter (Fontan procedure is useful surgical treatment for each of the following except: 1. Tricuspid Atresia 2. Hypoplastic Left Heart Syndrome 3. Pulmonary Valve Stenosis 4. Truncus Arteriosus 5. Pulmonary Artery Atresia Appropriate therapy for “tet spells” include (may be more than one): 1. Propranolol 2. Dobutamine 3. Phenylephrine 4. Ephedrine Antibiotic Prophylaxis High Risk: Previous Infective Endocarditis Prosthetic Valves CHD (some) Transplants Procedure Type None for GI/GU Bronchoscopy- depends Dental Procedures- depends Pacemaker Codes Chamber Paced OAVD Chamber Sensed OAVD Response to Sensing OTID