congenital heart defects hemodynamics, pharmacology, and updates amanda l. affleck crna, mae...
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Congenital Heart Defects
Hemodynamics, Pharmacology, and Updates
Amanda L. Affleck CRNA, MAEProvidence 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
OBSTRUCTIONOn the left side decreases systemic
flow=hypoperfusion
SHUNTLeft-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
OBSTRUCTIONOn the right side, decreases
pulmonary flow=hypoxemia
SHUNTRight-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
How do I know where the blood will go?
PVR:SVR will determine the direction of shunt.
Blood takes the path of least resistance, therefore these pressures are manipulated in order to maintain the patient’s oxygenation & cardiac output.
PVR & SVR
SVR nml values and definition
SVR
Inhalational agents
H2 release
Ganglionic blockade
SVR
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 non- cyanotic 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.
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
smooth muscle cells
Nitric oxideProstacyclin
vasodilate
Thromboxane A2Endothelin-1
vasoconstri
ct
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, acidosisEmbolism (thrombus, CO2, air)Bone cementProtamineCardiopulmonary bypassIschemia-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 is bound by the RV free wall and the inter-ventricular 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
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 PVRAvoid metabolic acidosis
Adequate analgesia & anesthesia to avoid catecholamine surge
Avoid shivering
Maintenance
Maintain RV functionAvoid 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
NorepinephrinePhenylephrine (’s PVR)
Inotropic support of RV functionMilrinone, Dobutamine: support
RV function and PVR**vasopressor support may
be needed as it will SVR)
Pharmacologic Support
Inhaled Nitric OxidePotent and specific pulmonary
vasodilatorImmediately inactivated in the
circulation by hemoglobin binding.Sildenafil
’s PVROnly available orally