Page 95 - Basic Monitoring in Canine and Feline Emergency Patients

Table 5.1. Differentials for hyperventilation and hypoventilation.

VetBooks.ir Anatomical location Common causes 2 Physiological stimulation Common causes
Hyperventilation (PCO )
Hypoventilation (PCO )
2
Central respiratory Any significant CNS disease Hypoxemia (See Table 6)
centers (trauma, inflammation/
(brainstem) infection, neoplasia)
Sedative or anesthetic drugs
Cervical spinal Cervical IVDD, trauma Stimulation of pulmonary Pneumonia, pulmonary
cord receptors edema, inhalation of irritants,
pulmonary thromboembolism
Phrenic nerves/ NM diseases (myasthenia Centrally detected stimuli: SIRS/sepsis,
NMJ gravis) circulating drugs, hyperadrenocorticism/
NM blocking drugs metabolites, or cytokines steroids, liver disease,
CNS diseases, exercise,
heatstroke/hyperthermia
Diaphragm Diaphragmatic hernia Central: conscious Pain, stress, fear
Respiratory muscle fatigue perception of environment
Excessive abdominal pressure
(ascites, GDV, severe obesity)
Pleural space Chest wall injury, severe Iatrogenic Excessive mechanical
accumulations of fluid or air ventilation
Pulmonary Restrictive pleuritis, severe
compliance diffuse pulmonary disease
Upper and lower Airway obstruction,
airways bronchoconstriction
CNS, central nervous system; GDV, gastric dilatation volvulus; IVDD, intervertebral disc disease; NMJ, neuromuscular junction; NM,
neuromuscular; SIRS, systemic inflammatory response syndrome.
Adapted from Dibartola, S.P. (ed.), Fluid, Electrolyte and Acid–Base Disorders in Small Animal Practice, 4th edn. Elsevier, St. Louis, Missouri, USA.
Table 5.2. Common differentials for metabolic acidosis.

High anion gap a Normal gap (hyperchloremic)
Lactate (including d-lactate) GI loss of bicarb (vomiting, diarrhea)
Uremia (retention of phosphates and sulfates) Renal loss of bicarb/acid retention (renal tubular acidosis,
Ketones carbonic anhydrase inhibitors)
Ethylene glycol/ethanol/methanol Iatrogenic administration of chloride (NaCl, KCl, etc.)
Salicylate intoxication Excess free water
(Other less common toxins such as paraldehyde, iron, Rebound post chronic respiratory alkalosis
cyanide, etc.) IV nutrition
Inborn errors of metabolism Hypoadrenocorticism
a Using the traditional approach to define metabolic acidosis as a low pH caused by a low bicarbonate, causes of metabolic acidosis
can be further subdivided into ‘high-gap’ versus ‘normal gap’ (hyperchloremic) metabolic acidosis by calculation of the anion gap (see
the text). This helps the clinician sort which differentials are more likely the underlying cause of the metabolic acidosis. While there are
many mnemonic aids used to recall causes for metabolic acidosis, the author prefers the mnemonic ‘LUKES’ as shown in bold for the
commonly encountered clinical abnormalities causing an elevated anion gap.
Cl, chloride; GI, gastrointestinal; K, potassium; Na, sodium; IV, intravenous.
Adapted from Dibartola, S.P. (ed.), Fluid, Electrolyte and Acid–Base Disorders in Small Animal Practice, 4th edn. Elsevier, St. Louis, Missouri, USA.
+
to the right, producing both HCO − and H . of base that must be theoretically added or removed
3
To overcome this influence, the mathematical con- from 1 L of oxygenated whole blood that has been
cept of BE was developed. Base excess is a value normalized to 37°C and a PCO of 40 mmHg in
2
calculated by the analyzer to represent the amount order to restore the pH of the sample to 7.4.
Venous and Arterial Blood Gas Analysis 87