Respiratory Acid-Base Disorders Flashcards
How is CO2 regulated?
Alveolar ventilation
Where is the respiratory centre?
Medulla
What receptors are responsible for sensory inputs concerning changes in CO2 and O2
Chemoreceptors
What are the two main stimuli for changes in alveolar ventilation?
Hypoxaemia (pao2< 60mmHg) and pCO2
a lot more sensitive to CO2 changes
Where are most oxygen-sensitive chemoreceptors located?
carotid body and to a lesser extent aortic bodies
play a minimal role in normal ventilation in the absence of hypoxemia
Where are the primary CO2/pH-sensitive receptors noted
in the CNS - retrapezoid nucleus, serotonergic, noradrenergic neurons and Gabaergic neurons
What is the portion of gas not making it to the gas exchange units called?
dead space
From where do respiratory mechanoreceptor inputs come from
chest wall, pulmonary and airway
receptors
Gas diffusion and transport during respiration
How much more soluble is is CO2 when compared to O2
20 to 24x
How do RBCs remain electroneutral when buffering CO2
As HCO3 moves out of the cell easily and H+ is trapped within the cell Cl- moves into the cell to maintain electroneutrality.
How is most CO2 transported to the lungs?
As HCO3 after being buffered by RBCs (approximately 81%), small amount (8%) transported dissolved in plasma, some combined with amino acids (11%)
How much oxygen is dissolved in blood?
0.003 mL dissolved O2 per 100 mL of blood/mm Hg
PO2
What factors aid in the unloading of oxygen to tissues
increased H
þ
ion and carbon dioxide
concentrations (as seen in respiratory acidosis),
increased temperature, and increased 2,3-diphosphogycerate
(2,3-DPG)
How is the aa gradient useful
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)
What value of aa gradient is considered normal?
bellow 15mmHg
Above what value is pulmonary disease very likely?
25
WHat are the 5 main reasons for hypoxemia?
low fraction of inspired oxygen,
hypoventilation - on room air,
diffusion impairment,
ventilation-perfusion
mismatching,
and shunt
What conditions may result in alveolar hypoventilation?
CNS disease,
respiratory depressant pharmacologic agents, neuromuscular
diseases affecting the respiratory muscles, chest wall
injury, upper airway obstruction, and severe diffuse
pulmonary disease.
What is diffusion impairment ?
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)
What is a normal mammalian V-Q ratio?
approximately 0.8. if V-Q drops to 0.1 blood essentially remains unoxygenated as it moves through the lungs
What conditions may cause derangements in V-Q matching
Low vq - less vent, fine perfusion. –> asthma, bronchitis, pneumonia
High Vq - fine vent, less perfusion –> emphysema, low output states, PE
what is right to left shunting
a severe form of V-Q mismatch
and results when mixed venous blood completely
bypasses ventilated pulmonary alveoli and returns to the arterial circulation.
how much shunting is present in normal animals?
2-3% - due to bronchial perfusion
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
Is shunting O2 responsive
no
Respiratory Acidosis
What is almost always the cause of respiratory acidosis
respiratory failure - increase in
PaCO2, decreased pH, and a compensatory increase in blood HCO3 concentration
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
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
What conditions may result in central hypoventilation?
CNS trauma, neoplasia,
infection, inhalant anesthetics, narcotics, and cerebral
edema
How long does abrupt apnea have to be to cause death
4 mins
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
how does hypercapnea shift The oxyhaemoglobin dissociation curve
To the right - allowing easier O2 unloading
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
When may neuro signs be seen with acute hypercapnia
As the CO2 approaches 70-100mmHg –> anxiety, restlessness, somnolence, coma
How is resp acidosis treated?
Quickly treat the cause - or mech vent
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
Resp Alkalosis
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
What compensation is expected for chronic resp alk
0.55mEq/L decrease in HCO3 for every 1 mmHG decrease in CO2
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
At what CO2 may neurological signs be noted
<25mmHg - confusion and seizures
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
What electrolyte change may be noted in resp alkalosis?
hypokalaemia
What is the definition of dyspnoea?
as difficult or labored breathing - likely associated with a negative sensory experience
WHat are the three types of dyspnoea
air hunger - pulmonary disease
increased work of breathing - LMN, boas
thoracic tightness - asthma
