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CCM Respiratory Disorders > SACCM 17: Hypoventilation > Flashcards

SACCM 17: Hypoventilation Flashcards

1
Q

What are 3 categories of causes for hypercapnia?

A
  • hypoventilation
  • increased CO2 production e.g., fever
  • increased dead space
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2
Q

Minute ventilation equation

A

VE = VT x RR

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3
Q

Alveolar ventilation equation

A

VA = VE - VD

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4
Q

Tidal volume equation

A

VT = VD + VA

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5
Q

What is the location of the anatomic dead space?

A

respiratory system down to the level of the terminal bronchioles

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6
Q

What is alveolar dead space?

A

part of the alveoli that is ventilated but does not participate in gas exchange/not perfused

< 5% normally

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7
Q

What is the physiologic dead space?

A

sum of anatomic and alveolar dead space

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8
Q

How do you determine anatomic dead space?

A

Fowler’s method
measures exhaled nitrogen after giving breath with 100% O2 -> nitrogen cc graphically displayed over time against volume exhaled
-> can derive dead space from this graph

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9
Q

How can you calculate physiologic dead space in a clinical setting

A

Enghoff modification of the Bohr equation

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10
Q

Explain the Bohr equation for physiologic dead space and its limitations

A

concept: CO2 comes from airway participating in gas exchange (i.e., not dead space) -> alveolar versus expired CO2 difference should demonstrate dead space
VT x FECO2 = (VT - VD) x FACO2 -> rearrange to:
VD/VT = (FACO2 - FECO2) / FACO2

limitations: FACO2 difficult to measure and alveolar CO2 different in part of lungs

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11
Q

Explain how the Enghoff modification is applied and what are its limitations

A

Alveolar CO2 difficult to measure -> PaCO2 as surrogate -> mixed product of all lung fields -> more representative of average CO2 of all alveoli

VD/VT = (PaCO2 - ETCO2) / PaCO2

limitations: influenced by reasons for PaCO2 - PACO2 gap, e.g., diffusion impairment, intrapulmonary shunt, V/Q mismatch

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12
Q

how do you determine the alveolar dead space

A

substract the Fowler (anatomic) dead space from the Bohr/Enghoff (physiologic) dead space

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13
Q

PACO2 is directly proportional to ________ and inversely proportional to __________

A

PACO2 is directly proportional to PACO2 produced and delivered to lungs and inversely proportional to alveolar ventilation

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14
Q

What PaCO2 levels are consistent with hyper- or hypoventilation

A

hyperventilation < 30-35 mm Hg
hypoventilation > 40-45 mm Hg

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15
Q

How does PvCO2 compare to PaCO2?

A

PvCO2 generally 3-6 mm Hg higher than PaCO2

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16
Q

Name 5 examples of causes for increased inspired CO2

A
  • faulty breathing circuits
  • excess apparatus dead space
  • inadeqaute fresh gas flow
  • exhausted absorbent
  • faulty unidirectional valves
17
Q

Name 6 examples for increased CO2 production

A
  • fever
  • sepsis
  • thyrotoxicosis
  • malignant hyperthermia
  • overfeeding
  • exercise
18
Q

why does increased CO2 production rarely lead to hypercapnia?

A

because minute ventilation changes can usually compensate for this increaed production -> will exhale more CO2

19
Q

If an animal’s tidal volume decreases and it normalizes its VE by increasing the RR, how can this still lead to hypercapnia?

A

decreaes tidal volume -> anatomic dead space volume won’t change -> proportion of alveolar ventilation will be smaller and this will not change even with increased RR

-> higher proportion of VD/VT possible even with normal VE

20
Q

What should you suspect when your patient has hypercapnia with increased arterial to end-tidal CO2 gradient but increased VE?

A

suspect increased alveolar dead space/ventilation of poorly or not perfused alveoli
e.g.,
* PTE
* Pulmonary capillary compression from pulmonary overinflation
* cardiovascular shock

21
Q

What are the cardiovascular effects of hypercapnia?

A
  • CO2 decreases myocardial contractility and SVR
22
Q

Why are the systemic cardiovascular effects of hypercapnia rarely clinically apparent?

A

concurrent increase in sympathetic tone and catecholamine release -> increased HR and vasoconstriction

23
Q

What are the effects of hypercapnia on the pulmonary/respiratory system?

A
  • vasoconstriction of the pulmonary circulation
  • bronchodilation
  • decreaed diaphragmatic contractility
24
Q

Explain the neurologic effects of hypercapnia

A
  • cerebral vasodilation -> increased cerebral blood flow -> increased intracranial pressure -> altered consciousness, seizures, altered brainstem reflexes and portural/motor responses
  • CO2 narcosis from intracellular pH changes and cellular metabolism alterations
25
Q

At what PaCO2 can CO2 narcosis develop?

A

PaCO2 > 90 mm Hg

26
Q

How can hypercapnia lead to AKI?

A

causes constriction of the renal afferent arteriole

27
Q

What leads to a leftward shift of the oxyhemoglobin dissociation curve?

A
  • decreased temperature
  • decreased PaCO2
  • increased pH
  • decreased 2,3-DPG
28
Q

What leads to a rightwards shift of the oxyhemoglobin dissociation curve?

A
  • increased temperature
  • decreased pH
  • increase PaCO2
  • increase 2,3-DPG
29
Q

How is CO2 carried in venous blood (name fraction of CO2 in % for each mechanism)

A
  • dissolved in plasma (10%)
  • buffered within RBCs as bicarbonate (90%)
30
Q

What are the 2 reasons PvCO2 increaes in states of decreased tissue perfusion?

A
  • accumulation of CO2 in underperfused tissue beds
  • anaerobic metabolism -> lactate production and hydrolysis of ATP -> increaed H+ production -> will be buffered by HCO3- -> CO2 production
31
Q

what is the normal PaCO2 to ETCO2 gradient?

A

ETCO2 2-6 mm Hg lower than PaCO2

32
Q

Name the 3 mechanisms by which O2 treatment in chronically hypoventilating patients causes worsening of hypercapnia

A
  • depression of hypoxia driven chemoreceptors (rely more on peripheral O2 sensitive chemreceptors)
  • relief of hypoxic pulmonary vasoconstriction -> increased perfusion without concomitant increased ventilation (low V/Q)
  • increased Hb O2 saturation -> less CO2 carrying capacities (Haldane effect)
33
Q

What is the currently recommended target PaO2 and SpO2 in chronically hypoventilating patients

A

PaO2 60-70 mm Hg
SpO2 90-93%

34
Q

Name 5 examples for respiratory stimulants

A
  • doxapram
  • aminophylline
  • theophylline
  • caffeine
  • progesterone

CCM Respiratory Disorders (10 decks)

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