Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Advanced Principles of Anesthesia > Week 5 - Pediatric Congenital Heart Disorders > Flashcards

Week 5 - Pediatric Congenital Heart Disorders Flashcards

1
Q

What are the functional shunts in fetal circulation?

A

Ductus Venosus: allows blood to bypass the unnecessary liver – closes with clamping of umbilical cord

Foramen Ovale: shunts oxygenated blood from RA to LA (blood entering through IVC) – closes around 3 days of life

Ductus Arteriosus: shunts blood from pulmonary artery to aorta (returned from SVC) – can remain open for several weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What changes occur after birth causing fetal functional shunts to close?

A
  • First breath –> lung expansion and increased PaO2/decreased CO2 (reduction in PVR)
  • Clamping of umbilical cord –> increased SVR
  • Reduced PVR and increased SVR = LAP>RAP (foramen ovale closes)
  • Reduced PVR –> blood flow reversal through DA leading to increased PaO2 and ductal closure (decreased prostaglandins from removal of placenta causes DA closure – why we avoid NSAIDs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What increases pulmonary vascular resistance? (9)

A
  • PEEP
  • High airway pressures
  • Atelectasis
  • Low FiO2
  • Respiratory and metabolic acidosis
  • Increased hematocrit
  • Sympathetic stimulation
  • Direct surgical manipulation
  • Vasoconstrictors: phenylephrine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What decreases pulmonary vascular resistance?

A
  • No PEEP
  • Low airway pressures
  • Lung expansion to FRC
  • High FiO2
  • Respiratory and metabolic alkalosis
  • Low hematocrit
  • Blunted stress response (deep anesthesia)
  • Nitric oxide
  • Vasodilators: milrinone, prostacyclin, others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are examples of cyanotic lesions in congenital heart disease? (5)

A
  • Tetralogy of Fallot
  • Transposition of the Great Vessels
  • Tricuspid abnormality (Ebstein)
  • Truncus Arteriosus
  • Total Anomalous Pulmonary Venous Connection

*O2 saturation of 75-85% goal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are examples of acyanotic lesions in congenital heart disease? (4)

A
  • ASD/PFO
  • VSD
  • PDA
  • Coarctation of the Aorta

*left to right shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the characteristics of ASD/VSD

A

Causes left to right shunt, but are generally asymptomatic

  • may be found in conjunction with other forms of CHD
  • provide mixing of oxygenated and deoxygenated blood
  • may require patch or may be created

*VSD are not initially significant in neonatal period, but become symptomatic over first few months of life (as kids age PVR decreases and SVR increases causing shunting across the VSD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the four abnormalities in Tetralogy of Fallot?

A
  • RVH (right ventricular hypertrophy)
  • RVOT narrowing/PS
  • VSD
  • Overriding Aorta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do you manage a TET spell in a kid with Tetralogy of Fallot?

A

Intraop: SVR, volume, negative inotrope, reduction in PVR
*dont give epi

Awake kids may squat/knees to chest (occluds femoral vessels essentially increasing SVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does a right to left shunt affect an inhalation induction and an IV induction? What about left to right shunt?

A

Right to Left Shunt:

  • inhalation = slower
  • IV = faster

Left to Right Shunt:

  • inhalation = minimal effect
  • IV = slower (not really clinically)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is circulation in parallel?

A

Pulmonary (Qp) and systemic (Qs) blood flow arises from a single ventricle, and there is mixing of oxygenated and deoxygenated blood

  • balance Qp:Qs with goal close to 1:1 (equal splitting)
  • as one changes, the opposite does so in inverse fashion
  • PVR high following birth, then decreases (increased Qp:Qs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is circulation in series?

A

blood flow to the pulmonary system is separate from blood flow to the systemic system

*what we all have

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the characteristics of hypoplastic left heart (or right heart)?

A

Diminutive left or right ventricle

  • at birth major systemic blood supply is through the ductus arteriosus
  • RV not meant to be pumping chamber of the body
  • require ASD for mixing
  • staged approach for repair
  • hypoplastic aorta

*given prostaglandins to keep ductus open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is stage 1 palliation procedure for Hypoplastic Left Heart Syndrome?

A

Norwood

  • perform atrial septostomy (to allow mixing)
  • reconstruct diminutive aorta with pulmonary artery (systemic flow) – pulm valve becomes neo-aortic valve
  • create shunt for pulmonary blood flow (can either be systemic-PA or RV-PA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is stage 2 palliation procedure for Hypoplastic Left Heart Syndrome?

A

Glenn

  • bidirectional Glenn – SVC drains passively into RPA
  • PaCO2 levels are important for CBF and ultimately SVC drainage/Pulmonary blood flow (high CO2 levels pulmonary vessels constrict increasing resistance of flow into pulmonary system)
  • may see venous engorgement in head and neck with increasing pulmonary pressures
  • PBF is now passive, and circulation is in series not parallel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is stage 3 palliation procedure for Hypoplastic Left Heart Syndrome?

A

Fontan (3-4 years)

  • bring IVC into RPA as well – all venous return to RPA
  • fenestration made to relieve increases in pulmonary pressures secondary to increased PBF – increased pulmonary pressures over time (PHTN)
  • PBF is again passive
17
Q

What are major complications associated with Fontan physiology?

A

Arrhythmias
Thromboembolic events
Protein losing enteropathy
Plastic bronchitis

18
Q

What is the key point of pulmonary blood flow in fontan physiology?

A

PBF largely reliant on sub-atmospheric intrathoracic pressures, low PVR, and absence of anatomical barriers, and CO is dependent on PBF

*anything that affect PVR will affect venous return

19
Q

What are the anesthetic considerations for Fontan physiology?

A
  • Do better with spontaneous ventilation and adequate preload (passive PBF)
  • Avoid hypovolemia
  • Maintain PaCO2 (remember PVR as well)
  • Maintain normal sinus rhythm
  • Assess baseline SpO2
  • Assess most recent cardiac cath and ECHO
  • Caution with neuraxial anesthesia due to effects on SNS and preload
20
Q

What is the mPAP, PCWP, and PVR to be considered pulmonary hypertension?

A

mPAP > 25 mmHg

PCWP < 15 mmHg (indicates post capillary etiology - L heart)

PVR > 3 Woods U

21
Q

What is believed to be the cause of pulmonary HTN?

A

Believed that cellular changes lead to abnormal proliferation of endothelial cells, smooth muscle, and immune cells leading to vascular remodeling

*imbalance between PGI2 and thromboxane

22
Q

What does pulmonary HTN cause?

A

Progressive pulmonary vascular obstruction with vascular remodeling leads to increases in RV afterload, strain, failure, and eventually death

  • normally RV receives perfusion during diastole/systole – in pulmonary HTN, RV systolic pressures approach aortic pressures leading to compromise in RV coronary flow
  • ventricular septum shift left leading to reduced LV preload, CO, and coronary blood flow –> further RV compromise
23
Q

What medications are used to treat pulmonary HTN?

A
  • Endothelin Receptor Antagonist (Bosentan, Ambrisentan): inhibit vasoconstriction and smooth muscle cell proliferation
  • PDE-5 Inhibitor (Sildenafil): decrease breakdown of cGMP – vascular relax
  • PDE-3 Inhibitor (Milrinone): decrease PVR>SVR, positive inotrope
  • iNO: increases cGMP (can cause rebound and direct lung damage over time)
  • Prostacyclin (Epoprostenol): pulmonary dilator, anti-inflammatory, and anti- platelet

*Calcium Channel Blockers – however only work in 10%

24
Q

What are the overall anesthesia goals for pulmonary hypertension?

A
  • Prevent systemic hypotension (RV ischemia) – treat with norepi or vaso (less affect of PVR) and fluids
  • Decrease PVR (RV failure)
  • Avoid hypoxia, hypercapnia, acidosis, and hypothermia
  • Avoid aggressive positive pressure ventilation (may lead to increased PVR)
25
Q

What medications should you avoid in pulmonary hypertension?

A

N2O

Beta Blockers

High Volatile levels (excessive negative inotropy)

26
Q

What should be included in the preop for pulmonary hypertension?

A
  • Assess most recent ECHO, EKG, and cath reports — EKG usually shows RAD and RVH, ECHO shows ventricular septum flattening (systole), and D-shaped LV
  • Assess number/types of pulmonary dilators
  • Syncope is an ominous sign (poor LV preload/CO)
  • Most important thing is the recognize if pt can be managed in a given facility
27
Q

What is homemetric autoregulation?

A

Adaptive mechanism in the RV to allow it to tolerate acute increases in afterload while preserving mechanical coupling between RV and PA

  • can be inhibited by central neuraxial blockade leading to critically reduced CO and RV failure
  • especially bad with hypoventilation from MAC
28
Q

What is pulmonary hypertensive crisis? How do you treat it?

A

Stressors can lead to increases in PVR, leading to RV failure and CV collapse – can occur with induction, transfer from spontaneous ventilation to positive pressure ventilation with PEEP, with potential hypoxia/hypercapnia (gentle induction with pre-oxygenation)

  • Avoid increases in PVR and RV strain
  • Optimize preload and ensure reduced RV afterload
  • Maintain NSR
  • May need vasopressors (NE, vaso), inotropes (Epi, dobutamine, milrinone), availability of pulm dilators (iNO, Epo), and ECMO

Advanced Principles of Anesthesia (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions