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Pediatrics > Ped perfusion blood gases and hypothermia > Flashcards

Ped perfusion blood gases and hypothermia Flashcards

1
Q

Why Pediatrics are NOT Small Adults

A

Major differences exist between adult and pediatric cardiopulmonary bypass, stemming from:
Anatomic differences Metabolic differences Physiologic differences

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2
Q

myocytes and myofibrils are ______ in peds

A

larger

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3
Q

the # of mitochondria in peds

A

increases as the oxygen requirements of the heart rises.

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4
Q

The amount of sarcoplasmic reticulum and its ability

A

to sequester calcium similarly increase in early development.

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5
Q

Activity of Na+/K+ adenosine triphosphatase (ATPase)

A

increases with maturation, and affects the sodium-calcium exchange.

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6
Q

what factors affect the way in which the immature heart handles calcium (monitor calcium closely)

A

The amount of SR and ability to sequester calcium increase. Na+, K+ and Ca++ movement have increased activity

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7
Q

Ca++ handling in immature myocardium

A

↑’s intracellular Ca ++ concentrations post ischemia/reperfusion.

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8
Q

↑’s intracellular Ca ++ concentrations causes

A

Activates energy-consuming processesdecreased levels of adenosine triphosphatase (ATPase)lack of energy sources for cardiac function
Contributes to dysfunction observed after CPB
Abnormal and uncontrolled activation of these enzymes leads to cellular damage after CPB

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9
Q

Increased myocardial oxygen demands  associated with

A

a switch from anaerobic metabolism after birth to

a more aerobic metabolism

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10
Q

The immature myocardium uses

A

several substrates

carbohydrates, glucose, medium, and long-chain fatty acids, ketones, and amino acids.

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11
Q

In the mature (3-12 mo) heart,

A

ong-chain fatty acids are the primary substrates

enzymes and an increased number of mitochondria are needed.

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12
Q

Bottom Line:

Because of the increased ability of the immature myocardium to rely on anaerobic glycolysis,

A

it can withstand ischemic injury better than an adult myocardium can.

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13
Q

Premature infants prone to

A

hypocalcemia hypoxia, infection, stress, diabetes (mom)

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14
Q

Effects of hemodilution is

A

enhanced in neonates decreased plasma proteins, coagulation factors, and
Hgb
reduction increases organ edema, coagulopathy, and transfusion requirements

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15
Q

Infants/neonates have high

A

oxygen-consumption rates

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16
Q

require flow rates

A

as high as 200 mL/kg/min at normal temperature (kg based flow rates)

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17
Q

unique anatomic and physiologic findings in patients with congenital cardiac disease

A

Intra-cardiac and extra-cardiac shunts and the reactive pulmonary vasculature

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18
Q

glucose in adults

A

ontrol high blood sugar CPB => stress response => hyperglycemia Studies link hyperglycemia with adverse outcomes

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19
Q

glucose in peds

A

control low blood sugar Hyperglycemia has not been linked to adverse
outcomes in pediatric CPB more common on pediatric CPB is hypoglycemia
( ↓ glycogen stores)

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20
Q

Hematologic

 Adult:

A

Inflammatory response upon surgery/CPB

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21
Q

Hematologic Peds

A

Exaggerated response to surgery/CPB

Inflammatory response inversely proportional to age

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22
Q

The events that trigger stress:

A

Ischemia

Hypothermia Anesthesia Surgery

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23
Q

CPB causes hormone release and also releases:

A

Catecholamines
Cortisol ACTH TSH Endorphins
Immature organs affect the release

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24
Q

Cardiac

Adult

A

Less ischemia tolerance May/may not be preconditioned to ischemia More tolerant of overfilling

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25
Q

cardiac Peds

A

Tolerate ischemia Higher lactates seen (cost of tolerating

ischemia) Prone to stretch injury (overfilling)

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26
Q

CNS

Adult

A

More neurological injuries Multifaceted etiology Stem from disease processes

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27
Q

CNS Peds

A

Neuro problems rare with routine CPB Increased with DHCA (?25%)

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28
Q

Pulmonary

Adult

A

Lungs fully developed Less reactive vasculature May have preexisting disease

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29
Q

Pulmonary Peds

A

Lungs not fully developed More reactive vasculature Usually without existing disease

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30
Q

Renal

Adults

A

The normal urine output for adults can be 0.5 to 1 ml/min, regardless of weight. That translates to 60 ml/hr.
Average 70kg adult would be expected to produce 35-70 mL/hour of urine.

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31
Q

Renal Peds

A

For children, the expected urine output is closer to 1ml/kg/hour of urine.
Average 5 kg child would be expected to produce
5 mL/hour

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32
Q

Pediatric CPB Techniques

A

Hypothermia

Deep Hypothermic Circulatory Arrest (DHCA)

33
Q

Hypothermia in Children: What can you expect?

A

Due to the complex nature of congenital heart repairs you will see that children are often brought to colder temperatures more frequently than adults
Different temperature monitoring sites in pediatrics Smaller children cool more rapidly than adults DHCA is more often utilize

34
Q

hypothermia definitions

A

“The importance of the preservation of tissue viability can not be overstated”

 Warm 36-37°C Mild Hypothermia 32-35°C Moderate Hypothermia 28-31°C Deep Hypothermia 18-27°C Profound Hypothermia < 18°C

35
Q

Q10 Principle (temperature coefficient)

A

The temperature coefficient (Q10) represents the factor by which the rate (R) of a reaction increases for every 10-degree rise in the temperature (T)
Remember: Oxygen consumption is a reaction

36
Q

Q10 factor (a unitless quantity) How is it obtained?

A 
R1 = reaction rate at temperature T1 (where T1 < T2) R2 = reaction rate at temperature T2 (where T2 > T1)
T1 = temperature at which the reaction rate R1 is measured (where T1 < T2)
T2 = temperature at which the reaction rate R2 is measured (where T2 > T1)
Temps = C0 or K, R1 and R2 units must be the same
37
Q

7° C Principle

A

• This reduction in metabolic rates can be summarized as follows:
• Every 7°C drop in temperature will result in a 50% decrease in oxygen consumption
37°C Normothermic 34°C 25% decrease 30°C 50% decrease 23°C 75% decrease 16°C 87.5% decrease
9°C 94% decrease

38
Q

Temperature monitoring locations:

I. Core (central)

A

 Bladder (not on small children)  Nasopharyngeal  Tympanic  Esophageal
 Venous

39
Q

Pediatric Monitoring of Temperature during Hypothermia:

II. Shell (peripheral)

A

 Rectal  Skin

40
Q

Protective effects of hypothermia

A
  • Excitatory neurotransmitter release is reduced with hypothermia
  • Hypothermia helps to protect organs against injury caused by the compromised substrate supply to tissues resulting from reduced flow.
41
Q

why Protective effects of hypothermia occur

A

This protection occurs because of a reduced metabolic rate and decreased oxygen consumption.
The metabolic rate is determined by enzymatic activity, which, in turn, depends on temperature.
The safe period of hypothermic cardiopulmonary bypass (CPB) is longer than the period predicted on the basis of reduced metabolic activity alone

42
Q

PHCA/DHCA “Safe period durations”

A

> 320C= < 18 0 C =45-60 minutes

43
Q

Negative effects of hypothermia

A

brain blood flow loses autoregulation at extreme temperatures which makes blood flow highly dependent on extracorporeal perfusion.
As we will later see, this uncoupling of autoregulation is a serious issue and is the basis for the Alpha stat/pH stat debate

44
Q

DHCA provides

A

excellent surgical exposure by eliminating the need for several cannulas in the surgical field and by providing a motionless and bloodless field.

45
Q

Cooling is started before

A

CPB by simply cooling room

46
Q

CPB is started and cooling is begins for at least

A

20-30 minutes. The patient’s body temperature is monitored. After adequate cooling is achieved, the circulation is arrested. The desired duration of DHCA is limited to the shortest time possible.

47
Q

After circulation is resumed,

A

the final repairs are done on warming

48
Q

Cannulation for PHCA/DHCA is usually

A

a SAC  The heart is not opened until circulatory arrest

49
Q

Cannulation for PHCA/DHCA can and will be done with

A

BICAVAL also

 The heart is can be opened before circulatory arrest

50
Q

DHCA the good

A

Allows exposure Reduces metabolic rate and
Allows cessation of
circulation

51
Q

DHCA the Bad

A

Neurologic injury & morbidity
Brain is at the most risk >60 min arrest is detrimental
>40 min increases risk MUST monitor temp gradients closely

52
Q

he finding that DHCA was associated with neurologi morbidity led researchers to investigate the

A

HLFB

53
Q

Trials to compare the 2 methods (DHCA vs. HLFB) ha demonstrated lowered rates of neural dysfunction in patients undergoing

A

HLFB

54
Q

Finally, some groups have combined the 2 approaches mentioned above by using

A

approaches mentioned above by using DHCA with INTERMITTENT LOW FLOW BYPASS (ILFB) for 1-2 minutes every 15-20 minutes

55
Q

Cerebral Perfusion

Antegrade

A

Perfusing the head vessels in an antegrade fashion to perfuse the brain during DHCA
Via head vessels/shunt

56
Q

Cerebral Perfusion Retrograde

A

Perfusing the head vessels in an retrograde fashion to perfuse the brain during DHCA
Via SVC

57
Q

The concept of RCP originated in

A

the treatment of massive air embolism during CPB.

58
Q

When RCP is started, the superior vena cava

A

is snared, antegrade arterial flow is terminated, and the arterial cannula is connected to the arterial return line to the SVC cannula pressure in the superior vena cava is maintained at 15-20 mm Hg

59
Q

Mechanisms with which retrograde cerebral perfusion may accomplish neuroprotection include

A

the flushing of air and atheromatous embolic material from the cerebral circulation
the maintenance of cerebral hypothermia, and the provision of nutritive cerebral flow
RCP can be given continuously or intermittently
However, incidents of cerebral edema after retrograde cerebral perfusion, particularly when the perfusion pressure exceeds 25 mm Hg, are reported.`

60
Q

Despite signs of oxygen uptake observed in several studies, the amount of perfusate that provides cerebral nutrition IS

A

ow, corresponding to only about 5% of total retrograde flow.
Most of this flow is drained from the SVC into the inferior vena cava given the rich network of collaterals between the veins.
This technique is used less commonly than ACP used in the pediatric population.

61
Q

Antegrade cerebral perfusion can be achieved by using an

A

open end of a modified Blalock-Taussig (BTT) shunt after the proximal anastomosis is constructed in neonates who require arch reconstruction (i.e Norwood operation).

62
Q

The perfusate temperature, flow, and pressure is usually set at for ACP

A

18°C, and the flow is set at 10-20 mL/kg/min or adjusted to maintain a pressure of 40-50 mm Hg in the right radial artery.
Higher flows of 30-40 mL/kg/min are recommended for neonates.

63
Q

Several drawbacks are associated with those various cannulation techniques and are mainly related to complications of direct cannulation of arch vessels such as

A

dissection of the arterial wall air atheromatous plaque embolization malposition of the cannula overcrowding of the operative field with cannulas ACP can be given continuously or intermittently

64
Q

However, incidents of cerebral edema antegrade cerebral perfusion, particularly when the perfusion pressure exceeds

A

25 mm Hg, are reported

65
Q

During hypothermia, the solubility of carbon dioxide in blood increases and

A

for a given concentration of carbon dioxide in blood, PCO2 decreases and the blood becomes alkalotic.

66
Q

During pH-stat acid-base management, the patient’s pH is managed

A

at the patient’s temperature.

67
Q

Compared to alpha-stat, pH stat (which aims for a pCO2 of 40 and pH of 7.40 at the patient’s actual temperature) leads to

A 
higher pCO2 (respiratory acidosis), and increased cerebral blood flow.
CO2 is deliberately added to maintain a pCO2 of 40 mm Hg during hypothermia.
68
Q

In pH-stat , to compensate for increased carbon dioxide solubility,

A

carbon dioxide is added to the gas mixture in the oxygenator to maintain the hypothermic pH at 7.40 and the PCO2 at 40 mm Hg.

69
Q

When blood samples are warmed to room temperature, blood gases are

A

hypercapnic and acidotic.

CDI: READ ABG’s AT PERFUSATE TEMPERATURE

70
Q

Ph stat - GOOD

A

Improved neurologic outcome, hastened EEG recovery times, and reduced number of postop seizures.

71
Q

reasons for better neuro outcomes

A

Increased cortical oxygen saturation before arrest,
Decreased cortical oxygen metabolic rates during arrest
Increased brain-cooling rates.
CBF during reperfusion increases by using a pH- stat management strategy.

72
Q

Ph stat -BAD

A

 increased CBF that can increase embolic events, high CBFs during reperfusion, and reperfusion injury
Acid load induced by pH-stat strategy may impair enzymatic function and metabolic recovery. To retain the benefits of the pH- stat method on cooling and to eliminate its negative effect on enzymatic function
Lose autoregulation.

73
Q

During alpha-stat acid-base management, the ionization state of histidine is perfusion pressure then rules

A

maintained by managing a standardized pH (measured at 37C)
Alpha-stat pH management is not temperature-corrected as the patient’s temperature falls, the partial pressure of CO2 decreases (and solubility increases)

74
Q

The alpha-stat method allows blood pH

A

increase during cooling, which leads to hypocapnic and alkalotic blood in vivo.

75
Q

alpha stat Blood samples warmed to room temperature have a pH

A

7.4 and a PCO2 of 40 mm Hg. These conditions allow the alpha- imidazole group of the histidine moiety on blood/cellular proteins to maintain a constant buffering capacity, which enhances enzyme function and metabolic activity.

76
Q

Furthermore, the increase in pH parallels

A

the increase in the hydrogen ion dissociation constant of water during cooling, which can maintain a constant ratio of OH- ions to H+ ions. READ ABG’s AT 37°C

77
Q

Alpha- stat: good

A

With the alpha-stat approach:
• Cerebral Blood Flow (CBF) autoregulation is maintained, which allows for metabolism and blood flow coupling. CBF can be adjusted depending on the patient’s cerebral metabolic activity and oxygen needs.
• Autoregulation is intact • Normal enzyme function
 Most studies of this approach have been performed in adults.

78
Q

Alpha–stat: bad

A

With the alpha-stat approach: • Vasoconstriction

• Poor Cooling, which potentiates problems at the cellular level

79
Q

initial cooling is accomplished with

A

the pH- stat method, which is then switched to alpha-stat method to normalize the pH in the brain before ischemic arrest is induced (some do it on the last gas before arrest)

Pediatrics (14 decks)

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