Chapter 5: Fluids Flashcards
Canine blood donors ideally should be erythrocyte antigen ____ and ___, negative if possible? and why is this?
1.1 and 7, as a dog is most likely to have a clinically significant transfusion reaction to these.
How many naturally occurring dog erythrocyte antigens have been identified?
8
How do you work out how much blood is needed in a transfusion?
Vol(ml) = 1.5 x desired PCV x kg BW
What is the blood volume of a dog and of a cat?
dog - 90ml/kg
cat - 50ml/kg
Animals with colloid osmotic pressure of <___mmHg may benefit from synthetic colloid administration?
<16mmHg
What antigen is associated with incompatible cross match results in cats?
Mik antigen
Type A cats rarely have naturally occurring anti-B antibodies, but type B cats often have strong naturally occurring anti-A antibodies - What results if type A blood is given to type B cat?
Severe and potentially fatal transfusion reactions and RBC lifespan of aprrox. 1 hour
What are the most common side effects in dogs associated with synthetic colloid administration?
coagulopathies - decrease in factor 8 and vWF, impairement of platelet function, interference with stability of fibrin clots making clot more susceptible to fibrinolysis
Patients with severe head trauma should be administered what fluid?
0.9% NaCl - as has higher sodium and is less likely to cause a decrease in osmolarity and subsequent water movement into brain interstitium
What fluid should you use for hyperchloremic metabolic acidosis?
0.9% NaCl
Fluid type for patient with severe metabolic acidosis?
LRS
what are the two most common transfusion reactions in dogs?
- TACO (transfusion associated circulatory overload)
- non-hemolytic febrile reactions
Chronic hyponatremia should be corrected slowly (no more than 0.5mEq/L/h)- if not it could result in what?
Osmotic demyelination syndrome (central pontine myelinolysis)
Clinical signs of hypernatremia are usually only seen over what number in dogs?
170mEq/L dogs
Cats 175mEq/L
Chronic hypernatremia can result in the formation of what?
Idiogenic osmoles
- maintain the intracellular osmolarity similar to that of the extracellular and prevent fluid from moving out of the cell
- if the cell was to shrink it can result in vascular damage and hemorrhage within the brain
How is free water deficit usually replaced?
FW is most commonly replaced using 5% dextrose in water IV - as dextrose is rapidly metabolized - effectively leaving free water
Loop diuretics can facilitate natriuresis particularly in animals with hypervolemic hypernatremia
potassium moves intracellularly with?
Potassium moves extracellularly with?
- Intracellular: glucose, insulin, catecholamines and metabollic alkalosis
- Extracellular: metabolic acidosis or hyperosmolarity
What is meant by the term paradoxical aciduria?
From vomiting, when chloride is low, sodium is reabsorbed from the kidneys in exchange for K+ and H+ (acids in urine)
- worsens the hypokalemia and metabolic alkalosis
If K+ serum concentration is<3 what can result?
<2?
< 3: muscle weakness, cardiac arrythmias and PU
< 2: rhabdomyolysis with increased CK concentrations and respiratory muscle paralysis
Animals with refractory hypokalemia should have what checked?
Their serum Mg levels checked and supplementation instituted
What are expected ECG changes with K+ of:
5.7-6 ?
7-8.5?
>8.5?
10-12?
5.7-6: Spiked T waves and shortened QT interval
7-8.5: Prolonged PR interval and widening of QRS
>8.5: P waves disappear, R-wave amplitude decreases and S-wave prominence increases resulting in a sinoatrial wave
10-12: asystole and atrial fibrillation
Treatment options for hyperkalemia? (5)
Calcium gluconate - raises threshold membrane potential
Insulin and glucose - moves potassium into the cell
Sodium bicarbonate - moves potassium into the cell
Beta-2 agonists (albuterol or terbutaline) -moves potassium into the cell
Dialysis
Kidney failure can cause hypocalcemia how?
Reduced ability of kidney to convert 25-hydroxycholecalciferol to vitamin D - resulting in decreased intestinal absorption of calcium
Does hypoalbuminaemia affect ionised calcium levels?
no
What is the most common cause of hypercalcemia in dogs / cats?
Malignancy in dogs
Idiopathic in cats
HypoMg+ causes?
malabsorption: Decrease absorption: pancreatic insufficiency, cholestatic liver disease, short bowel syndrome, generalised malabsorption syndrome or starvation
excessive urinary losses: Renal tubular abnormalities - decreased resorption - renal tubular acidosis, postop diuresis, polyuric renal failure and diuresis,
drugs: aminoglycosides, digoxin, cisplatin and cyclosporin
redistribution: insulin, catecholamines,
Causes of hypermagnesemia?
Renal failure: acute or chronic
Endocrine disorders: hypoadrenocorticism, hyperparathyroidism, hypothyroidism
Iatrogenic over administration - cathartic, laxatives, antacids
Causes of hypophosphatemia?
Increased renal loss: primary hyperPTH, Diabetes, eclampsia, diuretic, Cushing’s, hyperaldosteronism
Decreased Gut absorption: vitamin D deficiency, malabsorption, vomiting, diarrhea, phosphate binders and antacids, diet deficiency
Translocation: DKA, insulin admin, glucose, bicarbonate, total parenteral nutrition, refeeding syndrome, hypothermia, resp alkalosis or hyperventilation
Causes of hyperphosphatemia?
Increased intestinal absorption: vitamin D toxicosis, phosphate containing enemas,
IV over admin
Decreased renal excretion: renal failure, urinary obstruction, uroabdomen, hypoPTH,
Translocation: tumor cell lysis, tissue trauma or rhabdomyolysis, hemolysis, metabolic acidosis
young growing animals
lab error
Calculation for corrected Chloride?
Cl measured x 146/Na measured - dog
Cl measured x 156/Na measured - cat
Causes of hypochloridemia?
Excessive loss - GI loss - vomiting, other GI disease - trichuriasis, salmonellosis, duodenal perforation
Renal loss - thiazide or loop diuretics, chronic resp acidosis, HAC
Excessive gain of sodium relative to chloride - sodium bicarbonate administration
Causes of hyperchloridemia?
Excessive loss: diarrhea
Excessive gain: NaCl, total parenteral nutrition, salt poisoning
Renal chloride retention: renal failure, renal tubular acidosis, Addisons, diabetes, Chronic resp alkalosis and spironolactone
Pseudohyperchloremia - potassium bromide therapy
What is Whipple’s triad?
Hypoglycemia
Clinical signs of hypoglycemia
Resolution of signs once supplemented
Causes of hypoglycemia?
Excess insulin: overdose, insulinoma, PNS, toxins and meds - xylitol
Excess glucose use: infection, exercise induced, pregnancy, pns, polycythemia, leukocytosis
Decreased glucose production: liver, neonatal, toy breed, PSS, neoplasia, cirrhosis, glycogen storage disease, Addison’s, betablockers
Causes of hyperglycemia?
Postprandial hyperglycemia
Endocrine - Diabetes, pancreatitis
Increased gluco-counterregulatory hormones: glucocorticoids, stress, critical illness, catecholamines - pain, exertion, excitement, growth hormones, progesterone, hyperthyroidism
Drugs: adrenocorticotropic, progesterone, xylazine, ketamine, morphine, glucose/dextrose containing fluids
What is the only significant volatile acid in the body?
Carbonic acid
Dissociation of a weak acid is described by what equation?
Henderson - Hasselbach Equation
In terms of Acid/Base - what is a buffer?
Main buffers in body?
What is the main extracellular buffer?
Main intracellular buffers?
Other part of the body with buffering capacity?
A buffer is a weak acid and its conjugate salt that can accept or donate a proton to minimize changes in fluid pH after the addition of a strong acid or base
Main: Bicarbonate, proteins, phosphate
Main extracellular: Bicarbonate - open buffering system
Main intracellular: Hemoglobin, plasma proteins and organic/inorganic phosphate - closed buffering system
Bone also has important buffering capacity in the body.
What is the pKa of bicarbonate?
6.1
How do you calculate anion gap?
What are the causes of increased anion gap?
AG = (Na + K) - (Cl + HCO3)
DKA, lactic acidosis, ethylene glycol, salicylate toxicosis, uremic states
(DUELS)
*Albumin can be associated with an increase in AG
What are the causes of respiratory acidosis?
What are the acute and chronic compensations?
Hypoventilation
- Less commonly increased CO2 production by tissues - (CPR, malignant hyperthermia, heatstroke)
For every 1mmHg increase in PaCO2:
- acute 0.15mEq/L increase in HCO3
- chronic 0.35mEq/L increase in HCO3
You suspect a patient has a chronic respiratory acidosis - you give oxygen but hypercapnia worsens, why?
In some chronic cases the respiratory center is no longer sensitive to elevated CO2 levels
- instead ventilation is driven by hypoxia and so supplemental oxygen may decrease ventilatory drive and worsen hypercapnia
What is the compensatory response in acute and chronic respiratory alkalosis?
For every 1mmHg decrease in PaCO2:
- Acute decrease of 0.25mEq/L of HCO3
- Chronic decrease of 0.55mEq/L of HCO3
Causes of metabolic acidosis?
- Normochloremic (increased anion gap): DUELS
- Hyperchloremic - diarrhea, renal tubular acidosis, giving carbonic anhydrase inhibitors
- Hypochloremic: Addison’s
Compensation for metabolic acidosis?
For every decrease 1mEq/L of HCO3 - 0.7mmHg decrease in PaCO2
Dose of bicarbonate required to return base deficit to 0 is calculate by what formula?
Bicarb Dose = 0.3 x bodyweight (kg) x base deficit (mEq/L)
Causes of metabolic alkalosis?
Vomiting, suctioning gastric contents, admin of diuretics that induce chloride excretion (Furosemide)
Hyperaldosteronism
Cushing’s
What are the four questions to ask in interpreting a blood gas?
- Is an acid-base disturbance present? (check pH, HCO3, PaCO2)
- What is the primary disturbance?
- alkalosis vs acidosis
- metabolic vs respiratory
- Is is compensated? Mixed? - Is the compensatory response appropriate?
- if not consider a mixed
4.What underlying diseases are present?
