Anesthesia And Respiration

Front 1

With light anesthesia, expiration becomes?

Back 1

active and moderately forceful, with a larger than normal tidal volume

Front 2

What also happens with the respiratory pattern with light anesthesia?

Back 2

can be irregular and vary from breath-holding to hyperventilation

Front 3

What is the pattern with deeper anesthesia?

Back 3

more regular and depends on the anesthetic agent

Front 4

What breathing pattern do halogenated agents tend to produce?

Back 4

rapid, shallow breathing

Front 5

What breathing pattern do nitrous oxide-opioid regimens produce?

Back 5

slower, deeper breathing

Front 6

In the supine and prone position what occurs?

Back 6

the abdominal contents push against the diaphragm, elevating the level of the diaphragm in the chest, reducing chest compliance, and reducing FRC by 0.5-1L

Front 7

In the trendelenburg position what happens to FRC

Back 7

reduces even more than the supine position due to an increase in intrathoracic blood volume

Front 8

In the lateral decubitus position, awake, and breathing spontaneously...what happens to VA?

Back 8

is greater in the lower (dependent) lung than in the upper (nondependent) lung

Front 9

Why is ventilation greater in the lower lung than the upper lung?

Back 9

the alveoli in lower lung lie on the steeper portion of compliance curve

Front 10

Where is perfusion greater, the lower (dependent) lung or upper (nondependent) lung?

Back 10

Greater in the lower lung than the upper lung (always zone 3 flow)

Front 11

In a patient who is in the supine position, induction of anesthesia causes a ____-____% reduction in FRC.

Back 11

15-20% (in addition to the reduction in FRC caused by the supine position)

Front 12

What occurs with induction of anesthesia that causes this further reduction in FRC?

Back 12

loss of end-expiratory tone in the diaphragm and appearance of end-expiratory tone in abdominal muscles so abd. contents push diaphragm farther forward and produce a further decrease in chest compliance

Front 13

Is the decrease in FRC related to anesthetic depth?

Back 13

no

Front 14

Can the reduction of FRC persist into the post-op period?

Back 14

yes

Front 15

What can exaggerate the decrease in FRC?

Back 15

1. paralysis
2.placement of surgical retractors and packs
3. Obese patients

Front 16

Are the reductions in FRC proportional to BMI?

Back 16

yes

Front 17

Does anesthesia alter CC?

Back 17

no

Front 18

What occurs in the patient that is in the lateral decubitus position, anesthetized and breathing spontaneously?

Back 18

Anesthesia shifts the dependent lung to a lower volume position on the compliance curve, while the nondependent lung shifts to a steeper position on the curve

Front 19

So in the anesthetized, lateral decubitus breathing spontaneously patient, which lung is better ventilated? and why?

Back 19

the nondependent lung, greater cephalad displacement of the dependent hemidiaphragm by abd contents and mediastinal structures compress the dependent lung

Front 20

Lateral decubitus, anesthetized, spont. breathing, which lung better perfused?

Back 20

the dependent lung is better perfused, 40% of CO goes to the nondependent lung while 60% goes to the dependent lung

Front 21

In the lateral decubitus, anesthetized, spont. breathing patient is there VA/Q mismatch?

Back 21

Yes

Front 22

Lateral decubitus position, anesthetized, paralyzed, positional changes?

Back 22

cephalad displacement of the dependent hemidiaphragm by abd. contents is exaggerated by paralysis

Front 23

Lateral decubitus position, anesthetized, paralyzed, excursion?

Back 23

excursion of the nondependent hemidiaphragm by positive pressure ventilation is more effective than excursion of the dependent hemidiaphragm

Front 24

Is VA/Q mismatch exaggerated with the lateral decubitus position, anesthetized, paralyzed patient?

Back 24

Yes

Front 25

What would happen if you opened the chest of the lateral, anesthetized, paralyzed patient?

Back 25

increases compliance of the nondependent lung, enhancing its ventilation, and creates furter VA/Q mismatching

Front 26

In a one-lung ventilated, anesthetized, paralyzed and chest-open patient what would you expect of the VA/Q of the nonventilated lung?

Back 26

is zero, creating a substantial right-to-left transpulmonary shunt

Front 27

In a one-lung, anesthetized, paralyzed, and chest-open patient what would HPV do?

Back 27

reduce perfusion of the nondependent lung to approx 22% of CO, lessening the degree of actual shunt

Front 28

What about the dependent lung in one-lung ventilation, anesthetized, paralyzed, chest open patient?

Back 28

is well perfused, receiving approximately 78% of CO; however, ventilation of the dependent lung is compromised by anesthesia and paralysis and possibly by factors such as secretions and absorption atelectasis

Front 29

What are possible in one-lung, anesthetized, paralyzed, chest open patient?

Back 29

VA/Q mismatching and hypoxemia

Front 30

Does anesthesia increase the work of breathing? Primarly?

Back 30

yes, an increase in compliance work

Front 31

What causes an increase in airway resistance?

Back 31

decreased FRC caused by anesthesia and the supine position but may be offset by bronchodilator activity of inhalational agents

Front 32

Increased airway resistance is most likely to result from? examples?

Back 32

pathophysiologic factors or equipment problems, such as: laryngospasm, bronchoconstriction, secretions, small ET tube, obstruction of breathing circuit

Front 33

Gas exchange, can anesthesia and equipment cause alterations?

Back 33

yes

Front 34

In relation to gas exchange what in particular can anesthesia and equipment increase?

Back 34

physiologic dead space and physiologic shunt

Front 35

During sponataneous ventilation, VD/VT is approximately? and VD/VA is?

Back 35

0.33, 1:2

Front 36

During positive pressure, VD/VT is? and VD/VA is?

Back 36

0.5, 1:1

Front 37

If the requirement of minute ventilation is greater than predicted to maintain arterial PCO02 then you can predict?

Back 37

that either physiologic dead space (VD) or VC02 is increased

Front 38

End-tidal C02 (PETCO2) is usually less than?

Back 38

arterial PC02 due to dead space ventilation

Front 39

PETCO2 and _____ are inversely related.

Back 39

VD/VT

Front 40

What is a sensitive, though nonspecific, monitor of pulmonary perfusion?

Back 40

PETC02

Front 41

How much does general anesthesia increase physiologic shunt?

Back 41

approximately 10%

Front 42

Why do you think physiologic shunt increases with GA?

Back 42

airway collapse and atelectasis in dependent areas of the lung

Front 43

What may alleviate an increased shunt?

Back 43

PEEP (provided cardiac output is maintained)

Front 44

At high doses (ED50=2 MAC), volatile anesthetics may inhibit?

Back 44

HPV, consequence is exaggerating physiologic shunt

Front 45

What else may also increase physiologic shunt?

Back 45

prolonged administration of high Fi02- probably due to absortion atelectasis in alveoli that had low VA/Q ratios prior to collapse

Front 46

Most GAs tend to cause ______ in proportion to the depth of anesthesia

Back 46

hypoventilation

Front 47

Is there a progressive decrease in spontaneous MV with deepening anesthesia?

Back 47

yes

Front 48

Why is there a decrease in MV with GA? (2)

Back 48

1. Depression of central chemoreceptors
2. Depression of external intercostal muscle activity

Front 49

With GA, which way does the arterial PCO2 curve shift?

Back 49

to the right and the slope decreases

Front 50

What abolishes the hypoxic drive to the peripheral chemoreceptors?

Back 50

inhalational agents and many IV agents

Front 51

In a mechanically ventilated patient, doubling VE will reduce arterial PCO2 from?

Back 51

40 to 30mmHg

Front 52

Quadrupling VE, will reduce arterial PC02 from?

Back 52

40 to 20mmHg

Front 53

In an anesthetized, apneic patient, how much does arterial PCO2 increase in the first minute of apnea? and then how much thereafter?

Back 53

12 mmHg, then 3.5 mmHg/min