Animals are sometimes presented with such severe abnormalities in important blood constituents that a generic fluid plan does
not adequately address the problem. In these situations specific modifications to the fluids plan are indicated. Designing
a fluid plan for a patient with numerous such problems can be difficult, especially if one attempts to address all of the
animal's problems with one thought process. Obviously this is not possible, but, more to the point, the fluid plan can be
considerably simplified by addressing only one problem at a time. Usually each successive decision will simply fold into
the rest of the fluid plan and when you reach the bottom of the page, you have a well-considered, defensible fluid plan.
Occasionally one might have to go back and remake a previous decision based on the current problem under consideration, but
more often not.
Volume is always the first and foremost consideration; how much dehydration or hypovolemia and how much fluid would you estimate
to normalize it. Remember it is not necessarily the objective to totally normalize volume and solute concentrations right
away. The immediate objective is to move the animal away from the "death line" and then the remaining therapy can take place
over a longer period of time at a more casual, watchful manner. Second priority would be those solute concentration deviations
that represent an immediate threat to the life of the patient, such as severe hyperkalemia, severe anemia, hypoglycemia, and
severe hypocalcemia. Third priority are the rest of the solute concentration variations that can, or should, be treated over
a period of time, such as severe hypokalemia, hypo/hypernatremia, hypercalcemia, hypo/hyperphosphatemia, metabolic acidosis,
hypomagnesemia, polycythemia, and hypo/hyperproteinemia.
Severe hypovolemia is identified by a history of blood loss, the physical exam/imaging findings suggestive of low cardiac
preload (dehydration, collapsed jugular veins, low end-diastolic diameter via ultrasound, small postcava via chest radiography),
hypotension, vasoconstriction (pale mucous membrane color, prolonged capillary refill time, cool appendages, oliguria/anuria),
and metabolic markers of poor tissue oxygenation (low central veous oxygen, lactic acidosis, high oxygen extraction). Since
none of these finding are specific to severe hypovolemia, it is important to evaluate as many parameters as are available.
Severe hypovolemia requires the rapid administration of large volumes of fluid. The type of fluid is not so important as
long as it is not a low-sodium crystalloid. Iso-osmotic, isotonic, polyionic crystalloids (with a sodium concentration similar
to normal ECF and some bicarbonate-like anion [lactate, acetate, gluconate]) (20-40-60-80-100 ml/kg over 5 to 60 minutes,
depending upon the magnitude of the hypovolemia), 7.5% hypertonic saline (4-6 ml/kg over 5 minutes), an artificial colloid
(6% Dextran 70; 6% Hetastarch) (5-10-15-20-25-30 ml/kg over 5 to 60 minutes), plasma or whole blood (10-30 ml/kg) may be administered.
Isotonic crystalloids are most commonly used but might be especially indicated if the animal is also dehydrated or especially
not indicated if the animal is edematous (subcutaneous, pulmonary or cerebral). Hypertonic saline may be of use in the field
or when time is very short, but realistically, has limited use in most blood volume restoration endeavors. Artificial colloids
are more effective blood volume expanders than are isotonic crystalloids and may be especially indicated if the patient is
hypoproteinemic, edematous, or if crystalloids have failed to provide a sustained augmentation of blood volume. Plasma is
too expensive for routine blood volume support but might be especially indicated if the animal has a coexistent coagulopathy.
Whole blood is too expensive for routine blood volume support but might be especially indicated if the animal has a coexistent
anemia. Animals that are simultaneously severely hypovolemic and severely anemic are generally better served by the administration
of a clear fluid (to augment the effective circulating volume even at the expense of worsening the anemia) until such time
as red blood cells can be procured.
Cats have a smaller blood volume than dogs (50-60 ml/kg vs 80-90 ml/kg) and fluid boluses should be proportionately reduced.
The plasma potassium measurement defines the magnitude of the hyperkalemia; the ECG changes defines the cardiac electrical
problems from it. Hyperkalemia causes membrane hypopolarization which may result in extrasystoles/fibrillation if the resting
membrane potential is slightly more negative than threshold potential or asystole when resting membrane potential is slightly
less negative. Hyperkalemia also increases potassium permeability which augments the repolarization phases of the electrocardiograph
(tall, tented, narrow T-wave) and diminishes the depolarization phases (small P waves; prolonged P-R intervals; bradycardia,
and widened QRS complexes). Hyperkalemia may also be associated with peripheral muscle weakness, decreased contractility,
and weak pulse quality. Finally there is a blending of the QRS and T waves (a sinusoidal pattern), hypotension, and either
ventricular asystole or fibrillation.
Imminently life-threatening hyperkalemia should be treated with calcium (0.2 ml of 10% calcium chloride or 0.6 ml or 10% calcium
gluconate per kilogram of body weight , administered intravenously). Calcium effects membrane threshold potential and thereby
antagonizes the effect of hyperkalemia. Therapy immediately returns the electrical performance toward normal. The effects
of calcium are, however, short-lived, lasting only until the calcium is redistributed. Not so immediately life-threatening
hyperkalemia should be treated with insulin and glucose (0.1 to 0.25 units of regular insulin/kg, administered as an intravenous
bolus and 0.5 to 1.5 G of glucose/kg, respectively, administered as an intravenous infusion over two hours). Patients should
be monitored to make sure that they do not become hypoglycemic.
Bicarbonate will also cause the intracellular redistribution of potassium if it is going to be administered for acidosis.
It is not a common choice for the treatment of hyperkalemia because animals commonly do not need to be alkalinized. Sympathomimetic
drugs with beta2-agonist activity will also cause the intracellular redistribution of potassium. There are not commonly used for this purpose,
however, because their therapeutic margin is narrow. Specific beta2 drugs (terbutaline) are associated with tachycardia and hypotension; while general beta1&2 drugs (epinephrine, dopamine) are associated with tachycardia, arrhythmias, and hypertension.
In humans, the trigger for a hemoglobin transfusion has traditionally been a hemoglobin concentration of 10 g/dL (a packed
cell volume [PCV] of 30%), however recent studies suggest that a more relaxed trigger of 7 g/dL (PCV = 21%) might represent
a better benefit:risk ratio. In veterinary medicine, a packed cell volume of 20% (hemoglobin of about 7 gm/dl) has been a
common trigger for blood transfusion.
Oxygen delivery is the product of oxygen content (hemoglobin and PO2) and cardiac output. Early compensation for anemia is an increase in cardiac output to maintain oxygen delivery. In situations
where the heart is well able to compensate, hemoglobin levels might justifiably be allowed to drop to a lower level (immune
mediated anemia), however, in situations where cardiac output is impaired (organic heart disease, circulating cardio-depressants
including general anesthetics) blood transfusion triggers should be higher than 7 g/dl. Metabolic markers of poor tissue
oxygenation, such as a low PvO2 or a metabolic (lactic) acidosis, may help guide the need for hemoglobin transfusions.
Whole blood may need to be administered in volumes of 10 to 30 ml/kg, depending on the magnitude of anemia and hypovolemia
(cats: 5 to 15 ml/kg). These volumes should be halved if packed red blood cell products are used. The rate of administration
depends upon the magnitude of the hypovolemia. The amount of blood to administer can also be calculated: (desired PCV - current
PCV) x body weight (kg) x 2 ml whole blood (assumes a PCV of about 40%) (or 1 ml packed red blood cells [assumes a PCV of
The brain normally lives on glucose and severe hypoglycemia causes seizures, coma, and brain damage. If blood glucose concentration
is below about 60 mg/dl, glucose (0.25 g/kg IV) should be administered IV over a minute to restore blood glucose (this dose
should increase the ECF blood glucose concentration by 100 mg/dl). A glucose infusion (2.5 to 5% or 0.1 to 0.3 g/kg/hr) should
then be started to maintain an acceptable blood glucose concentration (80 to 120 mg/dl by serial measurement).