A 10 month, intact female retriever mix is presented for lethargy and inappetence. She a less playful than usual yesterday, but seemed normal the day prior. This morning she declined food, seems a little uncoordinated, and over the last few hours the owners report difficulty breathing. Triage vitals:
T 100.1P 135R 42mm pinkCRT 1s BCS 5/9Weight 37kg BP 186/99 (128mmHg)
On physical exam the dog is not interactive, seems photophobic, has low head carriage, tachycardia with bounding pulses, and respiratory changes characterized by a mild but noticeable increase in rate and depth of breathing (nasal breathing/closed mouth) without obvious increase in effort or respiratory sounds. She has sluggish pupillary light reflexes, does not react to stimulation of the left nostril, and has delayed postural reactions in all 4 limbs. She is reluctant to walk making gait assessment difficult, but you do not see any obvious gate abnormalities. She does not have any spinal pain, and segmental spinal reflexes are normal. You estimate she is 8% dehydrated based on exam findings.
Chest and abdominal radiographs, CBC (including differential), serum chemistry, and urinalysis are all completely normal. An arterial blood gas is obtained. Interpret the blood gas:
Note: since this is an arterial blood gas (instead of our usual venous blood gasses), in the hospital we would evaluate the oxygenation and ventilation status of the patient as step 1 (this is largely why the blood gas was obtained in this patient) and then move on to the acid-base analysis. However, for the purposes of discussing acid-base cases, we are skipping this step. Assessment of the respiratory system using an arterial blood gas will be covered in Wednesday’s follow-up discussion of this case. In the mean time, if you are interested in respiratory system evaluation using blood gasses, look at Silverstein & Hopper’s Small Animal Critical Care Medicine (start with the oxygen therapy chapter) or a similar reference.
Alkalemia can be caused by a high bicarbonate or a low carbon dioxide. In this case both the bicarbonate and carbon dioxide are low. Since the low CO2 is an alkalinizing process (and the low bicarbonate is an acidifying process), the process represented by the CO2 is the cause of the high pH – this is a primary respiratory alkalosis.
The expected compensation process with a respiratory alkalosis is a metabolic acidosis – a low bicarbonate. This patient’s bicarbonate is 15.5 – a little low, so it fits the pattern for a compensated respiratory alkalosis. Next we should check mathematically to see if this is all a compensatory process, or if there is more than one process happening.
With a primary respiratory process the first thing we have to do is decide if this is an acute or chronic process. The history for this patient suggests an acute problem. With an acute respiratory alkalosis, for every 1 point decrease in the pCO2 there should be a corresponding 0.25 point decrease in the bicarbonate
This patient’s pCO2 is 23 points lower than normal:
40 – 17 = 23
This means there should be an approximately 6 point decrease in the bicarbonate to compensate:
23 x 0.25 = 5.75 (we will round to 6)
The normal bicarbonate is about 20, so this means we expect the bicarbonate to be about 14 if our patient is compensating for her respiratory alkalosis
20 – 6 = 14
BUT there is a range for normal (both bicarbonate and CO2) that we need to account for, so generally we say that the range is the calculated bicarbonate value +/- 2. So for this patient the range for the bicarbonate would be about 12-16:
14 – 2 = 12 (low end of range)
14 + 2 = 16 (high end of range)
Our patient’s bicarbonate is 15.5 – neatly inside the range for a compensated process. So, this patient has a compensated acute respiratory alkalosis.
What is the source of this patient’s respiratory distress (is it really distressed?)?
The patient is tachypneic but doesn’t clinically appear to be distressed – at least not from the description in the physical exam findings. Owners will sometimes describe fast breathing as ‘having trouble breathing’ and differentiating the two can be helpful in generating a differential diagnosis list.
This patient is hyperventilating (clinically he is breathing harder and faster than usual; from a laboratory perspective on the blood gas the pCO2 is low) but has normal oxygen levels assessed 3 different ways: pulse oximetry, red blood cell saturation measured on the blood gas, and normal partial pressure of oxygen (PaO2) also measured on the arterial blood gas. The first thing that comes to mind is primary respiratory disease. As respiratory disease develops and oxygenating ability decreases, minute ventilation (total volume of air the patient breathes per minute, which is manipulated by increasing or decreasing how many breaths per minute, and how deep (how much air is pulled in) the breath is) will increase to maintain oxygenation. Early in the respiratory disease process we can see mildly tachypneic patients who have a low pCO2 and still have a normal oxygen saturation. The majority of these patients would have notable changes on their chest X-ray or other thoracic imaging – things like pulmonary infiltrate from pneumonia or congestive heart failure, or obvious pleural space disease from pleural effusion, pneumothorax, etc. The decrease in pCO2 from these causes is generally mild early in the disease process. As disease and therefore gas exchange in the alveoli worsens, the oxygen levels begin to fall and pCO2 begins to rise. A pCO2 of 17 from primary respiratory disease is rare. All of these reasons plus the normal chest X-rays for this patient mean we should go looking for non-respiratory causes of hypocapnea.
The major non-respiratory causes of hyperventilation are pain, fear, and agitation (uncommon to cause pCO2 to get this low); cardiovascular causes such as pericardial effusion causing tamponade or pulmonary embolus; anemia; severe metabolic acidosis (these patients get a respiratory pattern called Kussmaul breathing where they breathe fast and deep to blow off excess acid in the form of CO2); and disease affecting the respiratory center in the brain. Note that panting does NOT cause respiratory alkalosis – panting is dead-space ventilation only and does not result in gas exchange at the alveoli – and therefore cannot result in respiratory alkalosis.
This patient’s pCO2 is 17 – too low to be from behavioral causes of hyperventilation like fear or agitation. Chest X-rays ruled out primary respiratory diseases like pneumonia and pleural space disease. A normal cardiac silhouette makes pericardial effusion and tamponade less likely and can easily be ruled out with ultrasound. Anemia is ruled out with blood work (this patient has a normal CBC), and we have diagnosed a primary respiratory alkalosis in our patient so we know a severe metabolic acidosis isn’t the cause.
That leaves us with pulmonary embolus (a contrast CT scan +/- echocardiogram will help to rule this in/out), and neurologic disease affecting the respiratory center of the brain (an MRI and cerebrospinal fluid analysis will help with this differential).
The age and comorbidities of a patient can further help us – in this case we are talking about a young, previously healthy dog. As with almost every case we will ever see, the answer is in the history and physical examination for this patient. This is a young, previously healthy dog with about 48 hour history of progressive decline (not consistent with pulmonary embolus), and who has a neurologic examination with multifocal intracranial localization. This is probably central neurogenic hyperventilation.
The top differentials for this patient’s signalment, history, and examination/localization are infectious, inflammatory, and neoplasia. In order of probability they would be inflammatory, infectious, neoplastic (lymphoma would be the primary differential in the neoplasia category). This dog went on to have MRI and CSF analysis with a final diagnosis of CNS lymphoma.
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