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Acid/Base and Electrolytes > Respiratory Acid-Base Disorders > Flashcards

Respiratory Acid-Base Disorders Flashcards

1
Q

How is CO2 regulated?

A

Alveolar ventilation

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2
Q

Where is the respiratory centre?

A

Medulla

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3
Q

What receptors are responsible for sensory inputs concerning changes in CO2 and O2

A

Chemoreceptors

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4
Q

What are the two main stimuli for changes in alveolar ventilation?

A

Hypoxaemia (pao2< 60mmHg) and pCO2
a lot more sensitive to CO2 changes

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5
Q

Where are most oxygen-sensitive chemoreceptors located?

A

carotid body and to a lesser extent aortic bodies
play a minimal role in normal ventilation in the absence of hypoxemia

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6
Q

Where are the primary CO2/pH-sensitive receptors noted

A

in the CNS - retrapezoid nucleus, serotonergic, noradrenergic neurons and Gabaergic neurons

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7
Q

What is the portion of gas not making it to the gas exchange units called?

A

dead space

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8
Q

From where do respiratory mechanoreceptor inputs come from

A

chest wall, pulmonary and airway
receptors

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9
Q

Gas diffusion and transport during respiration

A
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10
Q

How much more soluble is is CO2 when compared to O2

A

20 to 24x

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11
Q

How do RBCs remain electroneutral when buffering CO2

A

As HCO3 moves out of the cell easily and H+ is trapped within the cell Cl- moves into the cell to maintain electroneutrality.

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12
Q

How is most CO2 transported to the lungs?

A

As HCO3 after being buffered by RBCs (approximately 81%), small amount (8%) transported dissolved in plasma, some combined with amino acids (11%)

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13
Q

How much oxygen is dissolved in blood?

A

0.003 mL dissolved O2 per 100 mL of blood/mm Hg
PO2

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14
Q

What factors aid in the unloading of oxygen to tissues

A

increased H
þ
ion and carbon dioxide
concentrations (as seen in respiratory acidosis),
increased temperature, and increased 2,3-diphosphogycerate
(2,3-DPG)

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15
Q

How is the aa gradient useful

A

To determine the degree of pulmonary impairment and excluding hypoventilation as a component

R= diffusability of of CO2 but also the metabolism of CO2 (varies between animals and diet)

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16
Q

What value of aa gradient is considered normal?

A

bellow 15mmHg

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17
Q

Above what value is pulmonary disease very likely?

A

25

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18
Q

WHat are the 5 main reasons for hypoxemia?

A

low fraction of inspired oxygen,

hypoventilation - on room air,
diffusion impairment,
ventilation-perfusion
mismatching,
and shunt

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19
Q

What conditions may result in alveolar hypoventilation?

A

CNS disease,
respiratory depressant pharmacologic agents, neuromuscular
diseases affecting the respiratory muscles, chest wall
injury, upper airway obstruction, and severe diffuse
pulmonary disease.

20
Q

What is diffusion impairment ?

A

whenever there is incomplete
equilibration of alveolar gas and pulmonary end capillary blood. may be seen with
the thickening of the alveolar-capillary membrane. seen in diffuse pulmonary (interstitial disease), or loss of alveolar or capillary surface
area (e.g., emphysema or vasculitis)

21
Q

What is a normal mammalian V-Q ratio?

A

approximately 0.8. if V-Q drops to 0.1 blood essentially remains unoxygenated as it moves through the lungs

22
Q

What conditions may cause derangements in V-Q matching

A

Low vq - less vent, fine perfusion. –> asthma, bronchitis, pneumonia
High Vq - fine vent, less perfusion –> emphysema, low output states, PE

23
Q

what is right to left shunting

A

a severe form of V-Q mismatch
and results when mixed venous blood completely
bypasses ventilated pulmonary alveoli and returns to the arterial circulation.

24
Q

how much shunting is present in normal animals?

A

2-3% - due to bronchial perfusion

25
Q

What causes shunting?

A

no ventilation because of atelectasis or consolidation - or anatomic shunt vessels
main cause for hypoxemia in pulmonary edema, atelectasis, pneumonia, and in congenital abnormal cardiac communications between
the systemic and pulmonary circulations

26
Q

Is shunting O2 responsive

A

no

27
Q

Respiratory Acidosis

A
28
Q

What is almost always the cause of respiratory acidosis

A

respiratory failure - increase in
PaCO2, decreased pH, and a compensatory increase in blood HCO3 concentration

29
Q

In acute respiratory acidosis - what mechanisms handle the majority of the acid load?

A

intracellular buffers - hemoglobin. 97%
extracellular buffers - plasma proteins. 3%

for each 1-mm Hg increase in PCO2, these buffers increase HCO3 0.15 mEq/L in dogs and cats - Acute
0.35mEq/L increase in HCO3 - chronic

30
Q

When and how does renal compensation occur due to respiratory acidosis?

A

renal compensation occurs after 5 days
causes intracellular H to increase in the renal tubular cells. Upregulation
of the Na-H antiporter of the renal brush border
occurs, and hydrogen ions are exchanged for sodium and then excreted as NH4Cl

Intracellular HCO3 is reabsorbed and exchanged for Cl , resulting in an increase in plasma SID, chloruresis, an negative chloride balance

31
Q

What conditions may result in central hypoventilation?

A

CNS trauma, neoplasia,
infection, inhalant anesthetics, narcotics, and cerebral
edema

32
Q

How long does abrupt apnea have to be to cause death

A

4 mins

33
Q

What CV clinical signs may be seen with hypercapnia

A

Tachyarrhythmias
Results in increased sympathetic tone - increased HR and CO however also results in vasodilation and poor contractility –> often present as hyperdynamic

34
Q

how does hypercapnea shift The oxyhaemoglobin dissociation curve

A

To the right - allowing easier O2 unloading

35
Q

What are he metabolic consequences of hypercapnea?

A

retention of both sodium and water, due to
increased antidiuretic hormone release, increased cortisol secretion, and activation of the renin-angiotensin system
also may cause gastroparesis

36
Q

When may neuro signs be seen with acute hypercapnia

A

As the CO2 approaches 70-100mmHg –> anxiety, restlessness, somnolence, coma

37
Q

How is resp acidosis treated?

A

Quickly treat the cause - or mech vent

38
Q

Why may giving a chronically hypercapnic and hypoxic patient O2 supplementation be dangerous?

A

Due to chronicity chemoreceptors have become insensitive to CO2 - therefore rely on hypoxemia as the driver of respiration - O2 supp may result in worsening hypovent

39
Q

Resp Alkalosis

A
40
Q

What occurs during acute compensation to a respiratory alkalosis?

A

Chloride ions leave red blood cells in exchange for HCO3, causing a decrease in plasma HCO3 concentration.
H+ moves extracellularly in exchange for na/k

In dogs and cats, a compensatory decrease of
0.25 mEq/L in HCO3 concentration for each 1-mm Hg decrease in PCO2 is expected

41
Q

What compensation is expected for chronic resp alk

A

0.55mEq/L decrease in HCO3 for every 1 mmHG decrease in CO2

42
Q

What are the main causes of resp alk?

A

Fear, pain, stress
overzealous mech vent
Centrally mediated –> sepsis, CNS disease, exercise, cushings
Pulmonary disease (stretch and nociception) - independent of hypoxemia
Hypoxaemia

43
Q

At what CO2 may neurological signs be noted

A

<25mmHg - confusion and seizures

44
Q

How does alkalaemia affect the oxyhaemoglbin dissociation curve?

A

to the left, reducing the release of oxygen to
the tissues by increasing affinity of hemoglobin for oxygen
Chronic alkalemia
negates this effect by increasing the concentration of
2,3-DPG in red cells

45
Q

What electrolyte change may be noted in resp alkalosis?

A

hypokalaemia

46
Q

What is the definition of dyspnoea?

A

as difficult or labored breathing - likely associated with a negative sensory experience

47
Q

WHat are the three types of dyspnoea

A

air hunger - pulmonary disease
increased work of breathing - LMN, boas
thoracic tightness - asthma

Acid/Base and Electrolytes (12 decks)

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