CARDIAC DISEASE PART IINicole 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 DiseaseClass I: Asymptomatic except during Severe

ExertionClass II: Symptomatic with Moderate ActivityClass III: Symptomatic with Minimal ActivityClass 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. Epinephrine2. Isoproterenol3. Calcium Chloride4. Phenylephrine5. 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 Sensitivity2. Cardiac Denervation3. Compensation for a fixed Stroke

Volume4. Cyclosporine5. Prednisone

Left to Right (Simple) Shunts

Qp : Qs=

Ratios < 1 Right->Left

Ratios >1 Left->Right

Ratios = 1 No Shunting or Bidirectional Shunts of

Equal Magnitude

(CaO2-CvO2)/(CpvO2-CpaO2)

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 slowed2. Induction rate for halothane is

affected more than the induction rate for nitrous oxide

3. IV induction is more rapid4. 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 Fallot1.RV Obstruction

(Infundibular Spasm)

2.RVH3.VSD4.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 ProcedureAnastamosis 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 Atresia2. Hypoplastic Left Heart Syndrome3. Pulmonary Valve Stenosis4. Truncus Arteriosus5. 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