test 4 Flashcards

1
Q

Shunt Blood Flow is quantitated in terms of:

A
  • PULMONARY BLOOD FLOW (Qp)
  • SYSTEMIC BLOOD FLOW (Qs)
  • This gives us a ratio of Qp/Qs
  • This will equal 1:1 (or 1) in a normal individual
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2
Q

implications of a Qp/Qs ratio > 1???

A
  • Pulmonary flow is greater than systemic flow
  • Left to right shunt
  • Not cyonotic
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3
Q

implications of a Qp/Qs ratio < 1???

A
  • Pulmonary flow is less than systemic flow
  • Right to left shunt
  • Can be cyanotic
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4
Q

(Qp/Qs) < 1.5

A

• Shunts that DO NOT cause an increase in right heart size do NOT require treatment
• pulmonary blood flow is 1.5 times greater than systemic blood flow
• pulmonary “over circulation”
• Shunts > 1.8 will usually produce an increase in pulmonary pressure that will damage the pulmonary blood vessels
- causes dilation and hypertension

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5
Q

Calculating Shunt Ratio From Saturations and what saturations need to be known

A

Qp/Qs= (SaO2 − SvO2) / (SatPV − SatPA)
- sats that need to be known to calculate:
• SaO2
• SvO2 (mixed venous) (more closely approximates SVC)
• Pulmonary vein saturation (Left atrium saturation)
• Pulmonary artery saturation

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6
Q

What to know for congenital lesions (need to know)

A
  • Anatomy
  • Pathophysiology
  • Surgical Correction
  • CPB Circuitry Considerations
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7
Q

Cardiac Septation

A
  • Occurs at Day 27
  • Lasts 10 days
  • The formation of the cardiac septa occur simultaneously
  • During this time, no major changes in external appearance
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8
Q

Atrial Septum

A
  • Right side: embryonic septum secundum
    * Contains the foramen ovale
  • Left side: embryonic septum primum
    * Contains ostium secundum
  • Form one-way flap so blood flow from RA to LA
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9
Q

Atrial Septal Defects

A
  • Most commonly occur as defects in the septum primum within the fossa ovalis (secundum ASD)
  • Will cause pressure mediated shunting
    * What conditions needed for Left to Right shunt -> LA pressure higher than RA pressure pushing blood back to RA
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10
Q

Common Types of Atrial Septal Defects

A
  • Ostium Secundum (the most common)
  • Patent Foramen Ovale
  • Ostium Primum
  • Sinus Venosus
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11
Q

ASD locations

A

LOOK AT THE PICTURE

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12
Q

Ostium Secundum ASD

A

• Most common ASD
• Formed by failed growth of the septum secundum OR
rapid reabsorption of the septum primum
• Left to right shunt
• Dilated RA and RV
• Increased Qp:Qs
• Big increase in pulmonary flow
• Decrease in systemic blood flow (i.e. CO)
• Sometimes suitable for percutaneous closure

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13
Q

Patent Foramen Ovale (PFO)

A
  • A patent foramen ovale (PFO) is a small channel that has little hemodynamic consequence
  • It is a remnant of the fetal foramen ovale.
  • Normally closes due to pressure change at birth
  • In some cases the PFO can be larger and require treatment
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14
Q

PFO Closure

A

• The initial inflation of the lungs causes changes:
• Decreases PVR results in increased blood flow from PA.
• The increased amount of blood flow from the RA to the RV and into the PA means less blood flows through the foramen ovale to the left atrium.
• In addition, more blood returns from the lungs which increases the
pressure in the LA.
• The increased LA pressure and decreased right atrial pressure (due to decreased pulmonary resistance) forces blood against the septum primum causing the foramen ovale to close.
- This action functionally completes the separation of the heart into two pumps.

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15
Q

Ostium Primum ASD

A
  • Located low in the septum
  • Can be considered a type of AV septal defect
  • Formed by failed fusion of the superior and inferior endocardial cushions
  • Commonly seen with a cleft in the anterior leaflet of the mitral valve
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16
Q

Sinus Venosus ASD

A

• Usually located high in the septum where the superior vena cava intersects with the right atrium
• Frequently associated with partial anomalous venous return (PAPVR)
• One or more of the pulmonary veins enter the RA
- May be inferior and/or superior

17
Q

ASD Pathophysiology

A

• In the case of a large ASD (> 9 mm) (ratios of 1.8 and above), a clinically significant left-to-right shunt will be present
• Blood will shunt from the LA to the RA.
• Extra blood from the left atrium may cause a volume overload of both the RA and the RV
• RA dilatation can lead to RA fibrosis
- If untreated, this condition can result in enlargement of the right side of the heart and ultimately heart failure

18
Q

ASD present leads to:

A

• Increased right sided volume -> Right atrial and right ventricular dilatation -> Tricuspid annular dilatation (TR) -> Pulmonary congestion -> Pulmonary hypertension

19
Q

ASD Pathophysiology: Any process that increases the pressure in the LV

A
  • can cause worsening of the left-to-right shunt.
    • Which affects the right heart
    • Included are systemic hypertension, which increases the pressure that the left ventricle has to generate in order to open the aortic valve
20
Q

ASD Pathophysiology: RV

A

• The RV will have to push out more blood than the left ventricle due to the L to R shunt.
• This constant overload of the right side of the heart will cause an overload of the entire pulmonary vasculature. (Pulmonary over-circulation)
- Qp/Qs > 1.5-1.8 / 1.0 is a problem
• Eventually pulmonary hypertension will develop.

21
Q

Pulmonary hypertension

A
  • RV pumps against an increased afterload (PVR) AND the RV has to handle the increased preload caused by the blood shunted blood from the LA to RA caused.
    • The RV will be forced to generate higher tension/pressures to overcome the pulmonary hypertension.
    • This may lead to right ventricular failure
    • Dilatation and decreased systolic function of the right ventricle
22
Q

If ASD left uncorrected

A
  • Pressure in the right heart > left heart.
  • RA pressure > LA pressure
  • The pressure gradient reverses across the ASD causing the shunt to reverse so a right-to-left shunt (R to L) will now exist
    * This shunt reversal phenomena is known as EISENMENGER’S SYNDROME
  • Once a right-to-left shunting occurs, oxygen-poor blood gets shunted to the left side of the heart
    * This will cause signs of cyanosis
23
Q

Percutaneous Closure of the ASD (Amplatzer)

A
  • feed catheter in vein up to RA through the ASD
    1. inflate one side of the Amplatzer device
    2. pull back against the wall of the atrium
    3. inflate other side of the balloon
    4. unscrew and remove form vein
  • CORRECTIVE SURGERY
24
Q

Surgical Correction of ASD’s

A
  • Incision
    • Median sternotomy
    • Right thoracotomy (going between the ribs on the right side)
  • Surgical closure
    • Primary Closure: Direct vision, close defect with suture
    • Patch Closure: Uses pericardial tissue or Gore-Tex patch for closure
    • Usually use running suture vs. interrupted
    • not absorbable stitches so they stay in there
    • If PAPVR is present with sinus venosus ASD, must reroute the PV to the left atrium
25
Q

CPB case notes for ASD

A
  • Case is very, very quick with 10-15 min pump run
  • Stay warm or drift
  • Can be challenging because of the speed: (on CPB, XC, give CP, warm, correct Ca++,lytes, ABG’s, off CPB-MUF, charting)
26
Q

Ventricular Septation

A
  • The ventricular septum is formed by the outgrowth of the muscular ridge at the interventricular foramen.
  • The ventricular septum grows upward from the apex of the heart to the base of the heart.
27
Q

The ventricular septum consists of

A
  • Inferior muscular portion
  • Superior membranous portion
    * Last part of the septum to close
28
Q

Common Sites of Ventricular Septal Defects

A
  1. Supracristal (outlet)
  2. Perimembranous
  3. Anterior muscular
  4. Apical
  5. Mid-muscular
  6. Inlet
29
Q

Types of Ventricular Septal Defects

A

• Membranous 75 %
• Muscular 20 %
• Supracristal (Outflow) 5 %
LOOK AT PICTURE

30
Q

Muscular VSD - Anatomy

A
  • Muscular ventricular septal defect is found in four locations
    * Anterior
    * Mid-ventricular (most common)
    * Posterior
    * Apical
  • Many small muscular VSDs will close spontaneously by 2 years of age
  • Multiple called “swiss cheese” VSD’s
31
Q

Membranous VSD - Anatomy

A

• Located in the membranous portion of septum close to the atrioventricular node
• Membranous VSDs are located near the heart valves
• Most common in adults and older children
- These VSDs can close at any time

32
Q

Supracristal VSD - Anatomy

A
  • Supracristal VSD is an outflow tract VSD sub-valvular in nature
  • The crista supraventricularis can be considered synonymous with the infundibular (or conus) ventricular septum
  • Outlet VSDs are found in the part of the ventricle where blood leaves the heart
  • These are the rarest type of VSD
  • The infundibular (or conus) septum separates the tricuspid and pulmonary valves and accounts for the more superior placement of the pulmonary valve relative to the aortic valve
  • This portion of the septum also provides muscular rigid support for the aortic valve, especially the right coronary cusp
33
Q

VSD Pathophysiology

A

• During systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium.
• This may cause the following effects:
• First, the circuitous refluxing of blood causes volume overload on the LV.
• Second, because the left ventricle normally has a much higher systolic pressure (~120 mm Hg) than the right ventricle (~20 mm Hg), a L to R shunt persists
- Leakage of blood into the right ventricle elevates right ventricular pressure and volume, causing pulmonary hypertension

34
Q

CPB Circuitry Considerations: Cannulation

A
  • Arterial: Aortic
  • Venous: Bicaval [Total CPB]
    * Single Atrial if the infant is small and DHCA is anticipated
  • Venting
    * May use direct venting with a flexible catheter since the heart is open
35
Q

CPB Circuitry Considerations: Cardioplegia

A

• Antegrade, usually a single dose will suffice

36
Q

CPB case notes VSD

A
  • Case is usually quick depending on location of defect
  • Usually cool to 32°C, or DHCA if a small infant
  • Can be challenging, but usually you have more time with VSD
  • Ventricular function may be related to of the length of time the VSD has been present
37
Q

Surgical Correction of VSD’s

A
  • Percutaneous closure (Amplatzer)
  • Can be tough to close VSDs percutaneously
  • Surgical Closure
    * Probably will not see primary closures