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Transcript
Congenital Heart Defects
Hemodynamics, Pharmacology, and Updates
Amanda L. Affleck CRNA, MAE
Providence Anesthesia Services
Five Basic Questions
Is the patient acyanotic or cyanotic?
Is pulmonary arterial blood flow increased or not?
Does the malformation originate in the left or right side of the heart?
Which is the dominant ventricle?
Is pulmonary hypertension present or not?
Acyanotic vs Cyanotic
ACYANOTIC
Left-to-right shunt
Oxygenated blood mixes with venous return
Impediment to systemic perfusion
CYANOTIC
Right-to-left shunt
Venous blood mixes with systemic flow, as well as
less blood going to the lungs for oxygenation.
Impediment to pulmonary perfusion.
Acyanotic Defects
OBSTRUCTION
On the left side decreases systemic flow=hypoperfusion
SHUNT
Left-to-right
Pulmonary over-circulation may lead to pulm htn, and
eventually pulmonary vascular obstructive disease
(Eisenmenger’s Syndrome)
Acyanotic Defects
Ventricular Septal Defect
Atrial Septal Defect
Persistent Ductus Arteriosus
Aortic Stenosis
Coarctation of the Aorta
Complete Common Atrioventricular
Canal
Acyanotic Defects
What increases left-to-right shunt?
Dramatic increase in SVR relative to PVR.
Dramatic decrease in PVR relative to SVR.
Cyanotic Defects
OBSTRUCTION
On the right side, decreases pulmonary
flow=hypoxemia
SHUNT
Right-to-left
Less blood reaches the lungs for
oxygenation
Venous blood mixes with systemic flow
Cyanotic Defects
Pulmonary Stenosis
Tetralogy of Fallot
Transposition of the Great Arteries
Tricuspid Atresia
Pulmonary Atresia
Atresia:
absence or closure of a
natural passage of the body
Cyanotic Defects
What increases right-to-left shunt?
Decrease in SVR.
Increase in PVR.
How do I know where the blood
will go?
PVR & SVR
SVR nml values and definition
 SVR
Inhalational agents
H2 release
Ganglionic blockade
 SVR
RX
PVR & SVR
PVR
Normal 90-250 dynes/s/cm-5
 PVR
Hypoxemia
Acidosis
N2O
Pain
RX
Anesthetic Considerations for
Acyanotic Defects
GOAL: Decrease shunt & maintain adequate oxygenation and
perfusion
PreOp: How big is the shunt? (echo)
What palliative or corrective work has been done? Do you
understand the plumbing?
Baseline cardiorespiratory status. Functional status, exercise
tolerance. Baseline VS, including RA SpO2.
De-bubble and filter IV lines.
Anesthetic Considerations for
Acyanotic Defects
SBE prophylaxis?
Recommended in shunts with cyanotic disease or patients with
surgical or percutaneous procedure in the last 6 months.
Otherwise endocarditis prophylaxis is not recommended for simple noncyanotic lesions.
Anesthetic Considerations for
Acyanotic Defects
Induction:
An inhalation induction is generally tolerable, if necessary (i.e.,
peds).
Patients with severe pulmonary htn or RV failure should have an IV
induction.
Theoretically, left-to-right shunt may speed inhalation induction by
decreasing the aterial-venous gradient of agent in the lungs.
Anesthetic Considerations for
Acyanotic Defects
Induction:
Potent intravenous and inhalational agents will decrease SVR.
Anesthetic Considerations for
Acyanotic Defects
IntraOp:
Avoid acute & long-term increases in SVR or decreases in PVR
(worsens the left-to-right shunt).
High O2 concentrations decrease PVR and increase SVR.
Hypoxemia increases PVR & decreases SVR.
Acidosis increases PVR.
IV bolus meperidine may increase PA pressures.
Anesthetic Considerations for
Acyanotic Defects
IntraOp:
Positive pressure ventilation and Valsalva maneuvers may cause
transient reversal of flow in left-to-right shunts.
Anesthetic Considerations for
Acyanotic Defects
PostOp:
Drugs to decrease pulmonary htn:
Inhaled nitric oxide, prostacyclin, prostaglandin I2,
prostaglandin E2
Phosphodiesterase inhibitors
NTG, Nitroprusside
Pain control: Pain causes increased sympathetic stimulation=inc
PVR, but oversedation causes hypercapnia=inc PVR.
Anesthetic Considerations for
Cyanotic Defects
GOAL:
Decrease shunt & maintain adequate perfusion &
oxygenation.
PreOp:
How big is the shunt? (echo)
What palliative or corrective work has been done? Do you
understand the plumbing?
Baseline cardiorespiratory status. Functional status, exercise
tolerance. Baseline VS, including RA SpO2.
De-bubble and filter IV lines!!! A bubble can easily pass through a
right-to-left shunt to the systemic circulation to the brain or
another end organ.
Anesthetic Considerations for
Cyanotic Defects
PreOp:
Avoid preoperative dehydration (esp. with ToF, polycythemia, &
Fontan physiology).
Dehydration combined with polycythemia may cause stroke.
Preop admission for overnight hydration may be necessary.
Anesthetic Considerations for
Cyanotic Defects
Induction:
Maintain SVR>PVR to reduce right-to-left shunt.
An inhalation induction is generally tolerable.
Ketamine may maintain SVR.
OTHER INDUCTION DRUGS
Theoretically, right-to-left shunt may dilute the inhaled anesthetic
agent in the LV, decreasing the amount of IA reaching the brain,
slowing induction. CHECK THIS IV AND IA OR IA ONLY
Anesthetic Considerations for
Cyanotic Defects
Induction:
By decreasing SVR IA’s may increase shunt and cyanosis, so titrate
agents up slowly.
A fall in SpO2 may actually reflect a fall in SVR, as more blood
shunts right-to-left
Desaturation not readily attributable to respiratory difficulty is
likely d/t  SVR with  right-to-left shunt, & should be
treated with a direct vasoconstrictor.
Anesthetic Considerations for
Cyanotic Defects
IntraOp:
Maintain SVR
A decrease in SVR and/or an increase in PVR worsens shunt and
hypoxia.
Avoid excessive positive airway pressure and excessive PEEP in
patients with decreased pulmonary flow (ToF, pulmonary
stenosis), as they will further decrease flow.
Anesthetic Considerations for
Cyanotic Defects
IntraOp:
EtCO2 significantly underestimates PaCO2.
Increases in physiologic dead space (ventilation without
perfusion)
Increases in venous admixture (right-to-left shunt)
As right-to-left shunt increases, etCO2 is less accurate.
Anesthetic Considerations for
Cyanotic Defects
PostOp:
Adequate analgesia without sedation-induced hypercapnia.
Pain yields sympathetic stimulations which  PVR.
Over-sedation yields hypercapnia which  PVR.
Right Ventricular Failure
&
Pulmonary Arterial
Hypertension
Pulmonary Vascular Bed
A high flow, low pressure
system
Tone is maintained via balanced production by
the pulmonary endothelium of vasodilators
(prostacyclin, nitric oxide) & vasoconstrictors
(endothelin-1, thromboxane A2, serotonin)
which act on the smooth muscle cells.
endothelial cells
Endothelin-1
Thromboxane A2
Prostacyclin
smooth muscle cells
Nitric oxide
Pulmonary Hypertension
mPAP greater than 25 mmHg
PVR greater than 240 dynes/cm/-5
WHO Classification of
Pulmonary Hypertension
I. Pulmonary arterial hypertension (ex. familial,
congenital left-to-right shunt)
II. Pulmonary venous hypertension (ex. left-sided valvular
heart disease)
III. PH with disorders of the respiratory system (ex.
COPD)
IV. PH d/t chronic embolic disease (ex. PE)
V. PH d/t disorders affecting pulmonary vasculature
directly (ex. sarcoidosis)
Intraoperative causes of PH
Hypoxia, hypercarbia, acidosis
Embolism (thrombus, CO2, air)
Bone cement
Protamine
Cardiopulmonary bypass
Ischemia-reperfusion syndrome (clamping,
declamping of aorta)
Loss of lung vessels (pneumonectomy)
Right Ventricle
Thin-walled, highly
compliant, but poorly
contractile chamber.
Under normal conditions ejects blood against 25%
of the afterload, compared to the LV.
*
*RV failure
RV is bound by the RV free wall and the interventricular septum. Failure of both to
contract normally ultimately leads to reduced
LV filling and cardiac output.
The free wall of the RV is served by the right
coronary artery.
Perfusion occurs during both systole and diastole.
Perfusion pressure depends on the gradient between
the aorta and RV pressures.
Systemic hypotension or increased RV pressure
result in decreased RV coronary perfusion.
Thin-walled RV dilates in the face of increased
afterload.
Septal shift compresses the LV chamber, further
compromising systemic output.
Anesthetic Management
Anesthetic Management
PreOp:
Maintain any current pulmonary vasodilator
therapy to avoid rebound pulmonary
hypertension.
Careful sedation to avoid respiratory acidosis and
subsequent  in PVR.
Anesthetic Management
Spinal anesthesia is not safe d/t the
sympathectomy.
Epidural anesthesia may be safely used if the level
is raised slowly and close attention is paid to
volume status and
SVR.
Anesthetic Management
Arterial line
Central venous pressure monitoring of fluid
trends
Trans esophageal echo
Induction Agents
Fentanyl, Sufentanil, Propofol, Etomidate, and
Thiopental have no effect on pulmonary
tone.
Ketamine may  PVR d/t catecholamine
effect. However pt’s with RV failure may
be catecholamine depeleted.
Caution with  SVR leading to inadequate
RV function.
Maintenance
Reduce PVR
Avoid metabolic acidosis
Adequate analgesia & anesthesia to avoid
catecholamine surge
Avoid shivering
Maintenance
Maintain RV function
Avoid hypovolemia or fluid overload (RV is
less pre-load responsive compared to
LV)
Appropriate fluid challenge is 250-500ml
Ventilatory Strategies
Avoid HPV with high FiO2
Moderate hyperventilation (PaCO2
30-35)
PEEP <15cmH2O (compression of
alveolar vessels  RV afterload)
Avoid high airway pressures which compress
pulmonary vasculature.
No Nitrous!!!
Pharmacologic Support
Maintain SVR to support coronary perfusion
Norepinephrine
Phenylephrine (’s PVR)
Inotropic support of RV function
Milrinone, Dobutamine: support RV
function and  PVR
**vasopressor support may be
needed as it will  SVR)
Pharmacologic Support
Inhaled Nitric Oxide
Potent and specific pulmonary
vasodilator
Immediately inactivated in the
circulation by hemoglobin binding.
Sildenafil
’s PVR
Only available orally
Post Op
Factors that increase PVR
Hypoxemia
Acidosis
Hypercapnia
Hypothermia
Increased sympathetic stimulation