Congenital Heart Defects PowerPoint Presentation, PPT - DocSlides

Congenital Heart Defects PowerPoint Presentation, PPT - DocSlides

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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?. ID: 401707

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Presentations text content in Congenital Heart Defects

Slide1

Congenital Heart Defects

Hemodynamics, Pharmacology, and Updates

Amanda L. Affleck CRNA, MAE

Providence Anesthesia Services

Slide2

Slide3

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?

Slide4

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.

Slide5

Slide6

Acyanotic Defects

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

Slide7

Acyanotic Defects

Ventricular Septal DefectAtrial Septal DefectPersistent Ductus ArteriosusAortic StenosisCoarctation of the AortaComplete Common Atrioventricular Canal

Slide8

Acyanotic Defects

What increases

left-to-right

shunt?

Dramatic increase in SVR relative to PVR.

Dramatic decrease in PVR relative to SVR.

Slide9

Cyanotic Defects

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

Slide10

Cyanotic Defects

Pulmonary StenosisTetralogy of FallotTransposition of the Great ArteriesTricuspid AtresiaPulmonary Atresia

Atresia: absence or closure of a natural passage of the body

Slide11

Cyanotic Defects

What increases

right-to-left

shunt?

Decrease in SVR.

Increase in PVR.

Slide12

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.

Slide13

PVR & SVR

SVR

nml

values and definition

SVR

Inhalational agents

H

2

release

Ganglionic blockade

SVR

RX

Slide14

PVR & SVR

PVR

Normal 90-250 dynes/s/cm

-5

PVR

Hypoxemia

Acidosis

N

2

O

Pain

RX

Slide15

Slide16

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.

Slide17

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.

Slide18

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.

Slide19

Anesthetic Considerations for Acyanotic Defects

Induction:

Potent intravenous and inhalational agents will decrease SVR.

Slide20

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.

Slide21

Anesthetic Considerations for Acyanotic Defects

IntraOp

:

Positive pressure ventilation and

Valsalva

maneuvers may cause transient reversal of flow in left-to-right shunts.

Slide22

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.

Slide23

Slide24

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.

Slide25

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.

Slide26

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

Slide27

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.

Slide28

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.

Slide29

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.

Slide30

Anesthetic Considerations for Cyanotic Defects

PostOp:

Adequate analgesia without sedation-induced

hypercapnia

.

Pain yields sympathetic stimulations which

PVR.

Over-sedation yields

hypercapnia

which

PVR.

Slide31

Right Ventricular Failure

&

Pulmonary Arterial Hypertension

Slide32

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 A

2

, serotonin) which act on the smooth muscle cells.

Slide33

endothelial cells

smooth muscle cells

Nitric oxide

Prostacyclin

vasodilate

Thromboxane A2

Endothelin-1

vasoconstrict

Slide34

Pulmonary Hypertension

mPAP greater than 25 mmHgPVR greater than 240 dynes/cm/-5

Slide35

WHO Classification of Pulmonary Hypertension

Pulmonary arterial hypertension (ex. familial, congenital left-to-right shunt)

II. Pulmonary venous hypertension (ex. left-sided

valvular

heart disease)

PH with disorders of the respiratory system (ex. COPD)

PH d/t chronic embolic disease (ex. PE)

V. PH d/t disorders affecting pulmonary vasculature directly (ex.

sarcoidosis

)

Slide36

Intraoperative causes of PH

Hypoxia,

hypercarbia

, acidosis

Embolism (thrombus, CO

2

, air)

Bone cement

Protamine

Cardiopulmonary bypass

Ischemia-reperfusion syndrome (clamping,

declamping

of aorta)

Loss of lung vessels (

pneumonectomy

)

Slide37

Right Ventricle

Thin-walled, highly compliant, but poorly contractile chamber.

Under normal conditions ejects blood against 25% of the afterload, compared to the LV.

Slide38

*

*RV failure

Slide39

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.

Slide40

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.

Slide41

Thin-walled RV dilates in the face of increased afterload.

Septal shift compresses the LV chamber, further compromising systemic output.

Slide42

Anesthetic Management

Slide43

Anesthetic Management

PreOp

:

Maintain any current pulmonary vasodilator therapy to avoid rebound pulmonary hypertension.

Careful sedation to avoid respiratory acidosis and subsequent

in PVR.

Slide44

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.

Slide45

Anesthetic Management

Arterial line

Central venous pressure monitoring of fluid trends

Trans esophageal echo

Slide46

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.

Slide47

Maintenance

Reduce PVR

Avoid metabolic acidosis

Adequate analgesia & anesthesia to avoid catecholamine surge

Avoid shivering

Slide48

Maintenance

Maintain RV function

Avoid

hypovolemia

or

fluid overload (RV is less pre-load responsive compared to LV)

Appropriate fluid challenge is 250-500ml

Slide49

Ventilatory Strategies

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!!!

Slide50

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)

Slide51

Pharmacologic Support

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

Slide52

Post Op

Factors that increase PVR

Hypoxemia

Acidosis

Hypercapnia

Hypothermia

Increased sympathetic stimulation

Slide53

Slide54

Slide55

Slide56

Slide57


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