Severe acidosis affects most systems in the body, in particular it may predispose patients to cardiac arrhythmias, decrease cardiac output, cause arterial dilation and hypotension, changes in oxygen delivery, changes in energy metabolism, and impaired immune responses. At the moment, the effects on the cardiovascular system are probably the biggest concern. The metabolic acidosis may be due to sepsis, hypoperfusion, or other causes, most of which may not be amenable to a ‘quick fix.’
The respiratory acidosis, on the other hand, should be easy – the patient is already intubated, we need to manually or mechanically deliver breaths. Start with a tidal volume about 10cc/kg, 10 times a minute. You can use an anesthesia ventilator, critical care ventilator, or have someone manually ventilate the patient. If manually ventilating the patient with a bag-valve-mask (BVM, also sometimes referred to by the brand name Ambu-bag) or using an anesthesia circuit, make sure that they aren’t delivering excessively large tidal volumes or excessively fast rates – even experienced people can excessively ventilate patients in stressful situations, and excessive ventilation needs to be carefully avoided in this patient. Large tidal volumes and fast rates are going to further decrease venous return and cardiac output, which might be enough to make this patient arrest. Consistent, controlled ventilations will bring the CO2 down. Adding 3-5cm H2O of PEEP, either by programming it on the ventilator or by using a peep valve with the BVM should help to resolve any atelectasis, but avoid going higher, at least initially – high PEEP also decreases venous return and cardiac output.
With regards to the critical hypotension, the team handing the dog over to the ICU has already told us that his hypotension has not been volume responsive – it’s time to do something else. Fixing many of the other things on the list should help, but in the mean time getting a vasopressor drip going would be high on the list of priorities. A norepinephrine, vasopressin (if you can get it), epinephrine, or dopamine CRI would be good starting places. Go with the one that is most accessible and familiar to you in this situation.
The hyperkalemia, hypoglycemia, and hypocalcemia will all be addressed simultaneously: calcium gluconate 100mg/kg diluted and given IV over 10-15 minutes while monitoring the ECG and heart rate will address the hypocalcemia and is the fastest acting of the rescue/temporizing measures for cardiac arrhythmias secondary to hyperkalemia. The simple math on this one is 1cc/kg of 10% calcium gluconate diluted with 3cc/kg sterile saline. If the IV fluids that are running have supplemental potassium in them, or if there is any concern there could have been a mix-up with the additives, temporarily stop those bags/syringes of fluids. Be sure to get something in their place quickly.
Administration of a dextrose bolus should stimulate the pancreas to secrete insulin ultimately resulting in translocation of potassium into the intracellular space, neatly treating both the hypoglycemia and (temporarily) the hyperkalemia. This reduces the chance of additional hypoglycemic events, but you do still have to recheck to ensure the CRI is meeting the patient’s needs. There are many different formulas for dextrose supplementation. In resuscitation emergencies I prefer 2cc/kg of 25% dextrose because it is very easy and requires basically no calculations: draw up 1cc/kg of 50% stock dextrose solution, mix with an equal volume of sterile water or sterile saline. Administer over 3-5 minutes.
The dextrose bolus should be followed by a recheck blood glucose 10-15 minutes after administration plus starting a dextrose CRI until the patient has stabilized and no longer requires dextrose support. During a busy resuscitation when the patient is hypoglycemic I like to start the CRI and back off if the patient is hyperglycemic later rather than wait for the recheck to see if they become hypoglycemic again – that way if the recheck gets delayed for some reason (like it’s 2am and just me and one technician trying to resuscitate a patient) the patient is less likely to become hypoglycemic again – it’s still possible, which is why the recheck is important, but hopefully will maintain the patient for the first few busy minutes of the resuscitation. There are a plethora of formulas for dextrose CRIs. I like to start with 50mg/kg/h (the rough equivalent of 2.5% dextrose solution at “maintenance” fluid rate), and again I like minimal math for folks during the resuscitation, especially if I’m asking a less experienced person to mix up drips so that the more experienced individuals can be actively involved in patient care. My go-to for this first hour dextrose drip is to draw up 0.1cc/kg of stock 50% dextrose (take the patient’s weight and move the decimal 1 place to the left, see – no math to get the volume of stock dextrose solution) and dilute it with 0.9% saline to a volume equal to the patient’s weight. Put it on a syringe driver, plug it into the patient, the rate is equal to the patient’s weight as ml/kg/h (a 22kg dog would get 22cc/g), push start and keep moving with resuscitation. This is a 1 hour supply of dextrose at 50mg/kg/h, it is 5% in concentration so it can still go through a peripheral vessel safely, is not likely to cause severe tissue damage if the catheter blows without being noticed for a few minutes, and means I only add a volume of 1cc/kg/h to the patient’s total ins. Go with something that is easy for you to explain how to mix up, and that you are familiar with using, then titrate to effect.
Reassess the patient. Now that we have made several rapid and meaningful interventions take a look and see what they have done for the patient. Look at the monitors, feel pulses and extremities (warming up?), get the patient off wet bedding/blankets and cover him to reduce further heat loss, re-assess the blood glucose, electrolytes, and blood gas. Re-triage your problems and continue resuscitating.
