Hypercarbia Flashcards

(21 cards)

1
Q

Normal PaCO2 levels

A

36-44mmHg

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2
Q

Hypoxemia

A

abnormally low PaO2 (low oxygen content in the blood)

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3
Q

Hypoxia

A

tissue oxygenation inadequate to meet metabolic needs

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4
Q

Factors contributing to hypoxia:

A
  • low FiO2
  • hypoventilation
  • diffusion abnormalities
  • dead space ventilation
  • shunting
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5
Q

Dead space vs shunting

A
  • Dead space ventilation = ventilation without perfusion
  • Shunting = perfusion without ventilation
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6
Q

hypercarbia

A

Hypercarbia reflects inadequate ventilation and / or increased CO2 production

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7
Q

How hypercapnia causes marked physiological effects:

A
  • CO2 crosses lipid barriers
  • Acidosis
  • Enzyme functions imparied
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8
Q

Sensors, controllers, effectors of hypercarbia

A

Sensors
- chemical chemo-R
- peripheral chemo-R
- other

Controllers
- higher CNS
- Pain
- Voluntary control
- Temp

Effectors
- muscles of insp and exp
- accessory mm
- abdominal mm

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9
Q

Centrol sensors of hypercarbia

A

Medulla = respond to changes in [H+] in the adjacent brain ECF
CO2 can cross the BBB  leading to immediate changes in the [H+]\
The pH changes will stimulate the respiratory centre to inc minute vol

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10
Q

Peripheral sensors of hypercarbia

A
  • Aortic- and carotid bodies
  • Respond to changes in PaO2
  • Also responds to PaCO2 and pH
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11
Q

Other sensors

A
  • Stretch receptors  in lungs!
  • Irritant receptors
  • J receptors
  • Muscle- and joint receptors
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12
Q

PaCO2 vs PACO2

A
  • PACO2 = partial pressure of CO2 in the alveoli
  • PaCO2 = partial pressure of CO2 in arterial blood
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13
Q

PEtCO2

A
  • PEtCO2 = partial pressure of CO2 at the end of expiration
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14
Q

Causes of increased carbon dioxide production (VCO2):

A
  • Sepsis
  • Fever
  • Malignant hyperthermia
  • Thyrotoxicosis
  • Shivering
  • Convulsions
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15
Q

Neurogenic causes ofo hypoventilation

A

o CVA
o Encephalopathy
o Hypothermia
o Prematurity

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16
Q

CNS effects of hypercarbia

A
  • Cerebral vasodilatation
  • Increased CBF … NB to control this in head injury patients as they can’t afford a further increase in CO2 (every 1 mmHg increase in CO2 = 4% increase in CBF)
  • Increased ICP
  • Trigger chemoreceptor stimulation of ventilation
  • Sympathetic stimulation
  • Hypoxia also affect CNS
  • Central depression at very high levels
  • During recovery they must  CO2 to get the patient to have a respiratory drive but >60mmHg = CO2 narcosis thus there is a fine balance
17
Q

Sx of hypercarbia

A
  • Disorientation / confusion
  • Headache
  • Mentally obtund  blunted
  • Focal neurological signs
  • Coma
18
Q

CVS effects of hypercarbia

A

o Increased CBF
o General peripheral vasodilatation
o Depressed myocardial contractility
o Increased risk of arrhythmias
o Sympathetic stimulation

  • Warm & flushed
  • Sweaty
  • Tachycardia with bounding pulses
19
Q

Hypercarbia under anaesthesia sx

A
  • Hypertension
  • Hypotension
  • Tachypnoea (in absence of muscle relaxant)
  • Tachycardia
  • Dysrhythmias
20
Q

Sx of HYPOcarbia

A
  • Hyperventilation
  • Intracellular alkalosis (decr H+ ions)
  • decr cardiac output
  • decr cerebral blood flow
  • Respiratory depression
  • left shift of oxyhaemoglobin curve