Hemodynamics, Pharmacology, and Updates
Amanda L. Affleck CRNA, MAE
Providence Anesthesia Services

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
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.

On the left side decreases systemic flow=hypoperfusion
Left-to-right
Pulmonary over-circulation may lead to pulm htn, and eventually pulmonary vascular obstructive disease
(Eisenmenger’s Syndrome)

Ventricular Septal Defect
Atrial Septal Defect
Persistent Ductus Arteriosus
Aortic Stenosis
Coarctation of the Aorta
Complete Common Atrioventricular
Canal

What increases left-to-right shunt?
Dramatic increase in SVR relative to PVR.
Dramatic decrease in PVR relative to SVR.

On the right side, decreases pulmonary flow=hypoxemia
Right-to-left
Less blood reaches the lungs for oxygenation
Venous blood mixes with systemic flow

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

What increases right-to-left shunt?
Decrease in SVR.
Increase in PVR.

How do I know where the blood will go?

SVR nml values and definition
 SVR
Inhalational agents
H
2 release
Ganglionic blockade
 SVR
RX

PVR
Normal 90-250 dynes/s/cm -5
 PVR
Hypoxemia
Acidosis
N
2
O
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 SpO
2
.
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 O
2 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 I
2
, prostaglandin E
2
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 SpO
2
.
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 SpO
2 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:
EtCO
2
significantly underestimates PaCO
2
.
Increases in physiologic dead space (ventilation without perfusion)
Increases in venous admixture (right-to-left shunt)
As right-to-left shunt increases, etCO
2 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.

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 A
2
, serotonin) which act on the smooth muscle cells.

endothelial cells
Endothelin-1
Thromboxane A2
Prostacyclin Nitric oxide smooth muscle cells

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)

Hypoxia, hypercarbia, acidosis
Embolism (thrombus, CO
2
Bone cement
, air)
Protamine
Cardiopulmonary bypass
Ischemia-reperfusion syndrome (clamping, declamping of aorta)
Loss of lung vessels (pneumonectomy)

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.

Maintain any current pulmonary vasodilator therapy to avoid rebound pulmonary hypertension.
Careful sedation to avoid respiratory acidosis and subsequent  in PVR.

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.

Arterial line
Central venous pressure monitoring of fluid trends
Trans esophageal echo

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.

Reduce PVR
Avoid metabolic acidosis
Adequate analgesia & anesthesia to avoid catecholamine surge
Avoid shivering

Maintain RV function
Avoid hypovolemia or fluid overload (RV is less pre-load responsive compared to
LV)
Appropriate fluid challenge is 250-500ml

Avoid HPV with high FiO
2
Moderate hyperventilation (PaCO
2
30-35)
PEEP <15cmH
2
O (compression of alveolar vessels  RV afterload)
Avoid high airway pressures which compress pulmonary vasculature.
No Nitrous!!!

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)

Inhaled Nitric Oxide
Potent and specific pulmonary vasodilator
Immediately inactivated in the circulation by hemoglobin binding.
Sildenafil
 ’s PVR
Only available orally

Factors that increase PVR
Hypoxemia
Acidosis
Hypercapnia
Hypothermia
Increased sympathetic stimulation