Cardiac disease - Tulane University Department of Anesthesiology

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
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
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
 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
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
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
 Direct agents are the best:
 Epinephrine & Isoproterenol
 Indirect vasopressors also work, but are
dependent on catecholamine stores
 Heart rate is NOT affected by:
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)
Qp : Qs=
 Ratios < 1
 Right->Left
 Ratios >1
 Left->Right
 Ratios = 1
 No Shunting or Bidirectional Shunts of Equal
Factors Altering Shunts
 Increase:
 Phenylephrine, Norepinephrine, Ketamine
 Decrease:
 Propofol, Inhaled Agents (Iso, Sevo, Des),
 Nitroprusside, Nitroglycerin, Nicardipine, Milrinone,
Fenoldopam, Adenosine
 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
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
 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
•Nitric Oxide
•Factors that Close
•Low Prostaglandins
•High Oxygen
•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
Management of
 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
 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
 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
 Decrease PVR, Increase
Hypoplastic Left Heart
LV Hypoplasia
MV Hypoplasia
AV Atresia
Aortic Hypoplasia
 Prone to Ventricular
 Increased Pulmonary
Blood Flow-> Systemic
& Myocardial Ischemia
 Delicate Balance
Between PVR & SVR
Truncus Arteriosus
 Increased Pulmonary
Blood Flow->
 Myocardial Ischemia
 Management:
 Phenylephrine & Fluids
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
 Chamber Sensed
 Response to Sensing

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