Nurs614 Exam 3 Pulmonary Ventilation

Front 1

How does unilateral phrenic nerve block or palsy affect pulmonary function?

Back 1

Unilateral phrenic nerve block or palsy only modestly reduces most indices of pulmonary function (25%)

Front 2

How are interostal muscles innervated?

Back 2

By their respective nerve roots

Front 3

Why do cervical cord injuries above C5 lead to lack of spontaneous breathing?

Back 3

Because both phrenic and intercostal nerves are affected

Front 4

What provides sensory innervation to the trahecobronchial tree?

Back 4

The vagus nerve

Front 5

What mediates bronchial dilation?

Back 5

SNS (T1-T4) mediates bronchial dilation via beta 2.

Front 6

Where does basic breathing rhythm originate?

Back 6

In the medulla

Front 7

Regarding the central respiratory center:
what are the two medullary groups of neurons generally recognized in respiration?

Back 7

Dorsal respiratory group which is primarily active during inspiration and a ventral respiratory group, which is active during expiration

Front 8

Regarding the central respiratory center:
two pontine areas influence the dorsal medullary center, what are they?

Back 8

A lower pontine (apneustic) center which is excitatory and upper pontine (pneumotaxic) center which is inhibitory. These centers fine tune rate & rhythm.

Front 9

Regarding the central sensors:
What are the most important of the central sensors?

Back 9

The chemoreceptors that respond to changes in hydrogen ion concentration

Front 10

Describe how the chemoreceptors of the medulla work

Back 10

The central chemoreceptors lie on the surface of the medulla and respond primarily to changes in the hydrogen ions of CSF. This is effective in regulating PaCO2 b/c the blood-brain barrier is permeable to dissolved CO2 but not to arterial HCO3.
Acute changes in PaCO2 but not in bicarb are reflected in CSF, thus a change in CO2 must result in change in hydrogen. CO2 in the body bonds with water to make HCO3 & hydrogen ions. CO2 crosses into the CSF reacts with water to form HCO3 & hydrogen. The chemoreceptors respond to the hydrogen ions.

Front 11

What are the peripheral chemoreceptors?

Back 11

Peripheral chemoreceptors include the carotid bodies (at the bifurcation of the common carotid arteries) and the aortic bodies (surrounding the aortic arch).

Front 12

What are the principal peripheral chemoreceptors?

Back 12

Carotid bodies.
They are sensitive to changes in PaO2, PaCO2 & pH and arterial perfusion pressure.
They interact with the central resp centers via glossopharyngeal nerves, producing reflex increases in alveolar ventilation in response to reduction in PaO2.

Front 13

How do zones change as we go from nondependent to dependent?

Back 13

Alveoli/arterial/venous partial pressure changes.

Front 14

Compare the alveolar, arterial and venous partial pressure in west zone 1(most nondependent)

Back 14

Alveoli > arterial > venous

Front 15

Compare the alveolar, arterial and venous partial pressure in west zone 2

Back 15

arterial > Alveoli > venous

Front 16

Compare the partial pressure in west zone 2 of the alveolar, arterial and venous oxygenation

Back 16

arterial > alveoli > venous

Front 17

What are the 3 primary forces that affect pulmonary vasculature

Back 17

Hyrdrostatic - comes from the force created by the pumping of blood. It wants to push fluid from the vessels.
Oncotic - comes from the pressure exreted by proteins particales. It wants to pull fluid back into the vessels.
Lymphatics - draws extra fluid in. Lymphatics follow arteries & veins. If we alter lymph system, it does not change hydrostatic pressure
Hydrostatic pressure next to heart is high.
In lungs there is a high net hydrostatic pressure

Front 18

What is the pathway of the lymphatics?

Back 18

Lymphatics follow arteries & veins.

Front 19

If we alter the lymph system how does it affect hydrostatic pressure?

Back 19

It does not change hydrostatic pressure.

Front 20

What is PEEP?

Back 20

A pressure threshold that allows expiratory flow to occur only when airway pressure equals or exceeds the selected PEEP level.

Front 21

What is CPAP?

Back 21

It is an application of a positive-pressure threshold during both inspiration and expiration with spontaneous breathing.

Front 22

How does the body try to match ventilation with perfusion with the pt in the supine position?

Back 22

With inspiration, zone 2 is biggest --> more negative pressure to zone 3 --> increase ventilation in zone 3

Front 23

What causes ventilation changes?

Back 23

Abdominal Content Shift;
Mediastinal Shift.

Front 24

How does GA affect ventilation

Back 24

GA --> decreased lung volumes which causes increased hypoxic vasoconstriction --> shunt.

Front 25

What is metabolic requirement?

Back 25

Metabolic requirement of a kid = 6ml of oxygen per kg
Adults = 3ml/kg

Front 26

TVs historically have been 10-15cc/kg. What is the current accept range & why did it change ?

Back 26

Recent data and observed risks of barotrauma have created a movement to decrease TV to 6-8cc/kg.

Front 27

What is the typical inspiratory flow rates?

Back 27

It is typically set at 60L/min

Front 28

Where do we typically set the RR on the vent?

Back 28

Adults 10-12
Peds 16

Front 29

What is the vent mode of Continuous Mandatory Ventilation (CMV)?

Back 29

The vent cycles from expiration to inspiration after a fixed interval, despite patient effort.

Front 30

What the vent mode of Synchronous Intermittent Mandatory Ventilation (SIMV)?

Back 30

The vent times the mandatory mechanical breath to coordinate with the patient effort. It reduced barotrauma.

Front 31

What is AC ventilation?

Back 31

Coordinated breaths with patient breathing. (Better tolerated)

Front 32

What is Intermittent Mandatory Ventilation?

Back 32

Coordinated breaths with patient breathing with no support to limit WOB.

Front 33

How does ventilator pressure mode work?

Back 33

As compliance vary, so does TV. TV is dependent on pressure (intrathoracic pressure being generated by the vent pushing in air)

Front 34

What is the goal of volume modes of ventilation?

Back 34

Getting a certain TV in inspiratory time (usually 1-2 secs). **It looks like an inverted V on the graph

Front 35

What is the goal of pressure modes of ventilation?

Back 35

Deliver a set pressure in a set time.

Front 36

What does the TV waveform of pressure modes of ventilation looks like?

Back 36

Waveform is square with the descending limb of the waveform is the same as that in pressure mode. Inspired air stays in the lungs a little longer before expiration. (it recruits better)
Pressure is good for pts with lung disease.

Front 37

What happens if pressure exceeds the upper inflection point (>50cmH2O)?

Back 37

Barotrauma occurs

Front 38

What happens if pressure is less than that at the lower inflection point?

Back 38

Atelectasis trauma occurs b/c of the effort to open the alveoli.

Front 39

If your SaO2 falls and you arbitrarily increase TV, what may happen?

Back 39

You may increase dead space b/c you risk of over distension of the non dependent alveoli and ultimately volutrauma. In addition, increasing pressure may reduce flow due to over distension of the alveoli into the pulmonary capillaries.

Front 40

FiO2 is often not changed unless PaO2 fails below ____?

Back 40

60mm Hg

Front 41

What does preferential inflation of non dependent lung causes?

Back 41

A vicious cycle and over time atelectasis increases until further regions of ventilation are lost.

Front 42

Sheer force (opening/closing) will cause?

Back 42

Low volume injuries.

Front 43

What does breath stacking lead to?

Back 43

Resp acidosis

Front 44

Acidosis vs akalosis, which is better for the pt?

Back 44

Acidosis is better b/c O2 can be unloaded to the tissue easier than with alkalosis

Front 45

How does PEEP assist ventilation?

Back 45

PEEP increased FRC and decreased need for “high” FiO2.

Front 46

As a result of the ARDSNet findings, what is the recomendation for plateau pressure?

Back 46

32cm H2O

Front 47

True/false? According to the ARDSNet findings,
Plateau Pressures below 32 have no benefit.

Back 47

True

Front 48

What does longer I:E ratio do?

Back 48

Acts like “auto peep”
Increases mean airway pressure
Reduced interstitial fluid
Increased PaO2
Decreases atelecteasis

Front 49

How does inverse ratio ventilation affects inspiartory & expiratory phases

Back 49

IRV extends the inspiratory phase and decreases the expiratory phase. This increases the overall mean airway pressure (MAP). (MAP is considered the primary determinant of arterial oxygenation.

Front 50

How does increases in mean airway pressure (MAP)affect PaO2?

Back 50

Increases in MAP results in increases in PaO2.
Increases in MAP can be thought of as an auto-PEEP where the alveoli are maintained moderately distended decreasing interstitial fluid by hydrostatic forces and driving gas across the membrane.

Front 51

How does inverse ratio ventilation affect ventilation?

Back 51

IRV decreases PaCO2, physiologic dead space and improve CO2 clearance

Front 52

How may time constants does healthy alveoli have?

Back 52

One because in theory they act in a homogenous manner

Front 53

Why does atelectatic alveoli have longer than one time constant?

Back 53

ARDS alveoli (atelectatic) are spread randomly throughout the lung fields (heterogeneously) and take longer to fill because they are collapsed.

Front 54

What is the main disadvantage of inverse ratio ventilation?

Back 54

It helps to resolve/prevent retained CO2.