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
What causes shunting?
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
Is shunting O2 responsive
no
27
Respiratory Acidosis
28
What is almost always the cause of respiratory acidosis
respiratory failure - increase in PaCO2, decreased pH, and a compensatory increase in blood HCO3 concentration
29
In acute respiratory acidosis - what mechanisms handle the majority of the acid load?
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
When and how does renal compensation occur due to respiratory acidosis?
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
What conditions may result in central hypoventilation?
CNS trauma, neoplasia, infection, inhalant anesthetics, narcotics, and cerebral edema
32
How long does abrupt apnea have to be to cause death
4 mins
33
What CV clinical signs may be seen with hypercapnia
Tachyarrhythmias Results in increased sympathetic tone - increased HR and CO however also results in vasodilation and poor contractility --> often present as hyperdynamic
34
how does hypercapnea shift The oxyhaemoglobin dissociation curve
To the right - allowing easier O2 unloading
35
What are he metabolic consequences of hypercapnea?
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
When may neuro signs be seen with acute hypercapnia
As the CO2 approaches 70-100mmHg --> anxiety, restlessness, somnolence, coma
37
How is resp acidosis treated?
Quickly treat the cause - or mech vent
38
Why may giving a chronically hypercapnic and hypoxic patient O2 supplementation be dangerous?
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
Resp Alkalosis
40
What occurs during acute compensation to a respiratory alkalosis?
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
What compensation is expected for chronic resp alk
0.55mEq/L decrease in HCO3 for every 1 mmHG decrease in CO2
42
What are the main causes of resp alk?
Fear, pain, stress overzealous mech vent Centrally mediated --> sepsis, CNS disease, exercise, cushings Pulmonary disease (stretch and nociception) - independent of hypoxemia Hypoxaemia
43
At what CO2 may neurological signs be noted
<25mmHg - confusion and seizures
44
How does alkalaemia affect the oxyhaemoglbin dissociation curve?
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
What electrolyte change may be noted in resp alkalosis?
hypokalaemia
46
What is the definition of dyspnoea?
as difficult or labored breathing - likely associated with a negative sensory experience
47
WHat are the three types of dyspnoea
air hunger - pulmonary disease increased work of breathing - LMN, boas thoracic tightness - asthma