Cardiac disease - Tulane University Department of Anesthesiology
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Transcript Cardiac disease - Tulane University Department of Anesthesiology
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