Flashcards in Fluids Deck (34):
Human serum albumin (HSA) can be used for volume expansion but is utilized more often for treatment of severe hypoalbuminemia. Hypoalbuminemia is often a consequence of critical illness and is associated with increased morbidity and mortality in both humans and dogs (Box 4-4). HSA has been shown to effectively increase__________, ___________, and ___________ in critically ill dogs (Trow et al, 2008). However, administration of HSA is controversial, as it is associated with potentially serious adverse reactions. Data in the veterinary literature regarding the incidence of complications with HSA use are variable, with a low number of mild adverse reactions reported in some studies (Viganó et al, 2010; Mathews and Barry, 2005), and several serious complications potentially attributable to HSA administration in others (Trow et al, 2008). In addition, HSA has been shown to be highly antigenic in both ill and normal dogs and presents a significant risk if administered more than once (Martin et al, 2008). Goals for HSA administration in dogs are to increase serum albumin to 2.0 to 2.5 g/dl and COP to 14 to 20 mmHg (see Box 4-5). (Fossum 36)
Fossum, Theresa Welch. Small Animal Surgery Textbook, 4th Edition. Mosby, 2013. .
Human serum albumin (HSA) can be used for volume expansion but is utilized more often for treatment of severe hypoalbuminemia. Hypoalbuminemia is often a consequence of critical illness and is associated with increased morbidity and mortality in both humans and dogs (Box 4-4). HSA has been shown to effectively increase serum albumin, total solids, and COP in critically ill dogs (Trow et al, 2008).
Data in the veterinary literature regarding the incidence of complications with HSA use are variable, with a low number of mild adverse reactions reported in some studies (Viganó et al, 2010; ???, and several serious complications???? potentially attributable to HSA administration in others (Trow et al, 2008).
Vigano: no severe hypersensitivity reactions reported
Trow: 23% had at least 1 immediate complication and 4% had severe delayed complications
Goals for HSA administration in dogs are to increase serum albumin to___- ___ g/dl and COP to ___ -___ mmHg (ranges)
increase albumin to 2.0 to 2.5 g/dL
COP 14-20 mm Hg
Normal COP in an animal with TP of 7.3 is __mmHg. Albumin’s colloidal oncotic pressure is __ mmHg
The plasma half-life of albumin is ___ hours and >90% of infused alb remains in the intravascular space.
• HES is a complex carb similar to glycogen. HES COP is __ mmHg; average ___% increase in plasma volum. Plasma half-life of HES is ___ hours and duration of volume expansion is 12-48 hrs. HES is hydrolyzed in the plasma by a-amylase, resulting in hyperamylasemia.
Normal colloid oncotic pressure in an animal with 7.3 g/dl protein is 28mmHg. Albumin’s colloidal oncotic pressure is 25mmHg
The plasma half-life of albumin is 16 hours and >90% of infused alb remains in the intravascular space.
• Hetastarch: Hydroxyethyl
Hydroxyethyl is a complex carbohydrate similar to glycogen
Hydroxyethyl’s colloidal oncotic pressure is 30mmHg ® average 141% increase in plasma volume
The plasma half-life of hydroxyethyl is 25.5 hours and duration of volume expansion is 12-48 hrs
Hydroxyethyl is hydrolyzed in the plasma by a-amylase, resulting in hyperamylasemia.
• Dobutamine: MOA and Dosage
• Dobutamine: Synthetic sympathomimetic increases cardiac output without dramatic BP changes
o Dosage is 2-5 mg/kg/min
o Exerts effects on the b1 myocardium adrenoceptors to force of contraction
o Exerts weak effects on the b2 blood vessels adrenoceptors to produce mild vasodilation.
• Dopamine: MOA
o Low dosage
o Intermediate dosage
o High dosage
• Dopamine: norepinephrine precursor with dose dependant effects (table 6-8 pg 88 Tobias)
Low dosage is 0.5-2mcg/kg/min is dopaminergic causes vasodilation renal, coronary, cerebral arterial dilation
Intermediate dose is 2-10mcg/kg/min is sympathomimetic on the b1 myocardium adrenoceptors stimulates contractility (greater effect on BP than dobutamine)
High dose 10-20mcg/kg/min effects a1 adrenergic receptors in the arterial walls causing vasoconstriction
reduced hemoglobin is 3.5 times as effective as oxyhemoglobin in buffering H+
Haldane effect: the fact that deoxygenated blood increases its ability to carry CO2
Hemoglobin: responsible for __% of the non-bicarbonate buffering capacity of blood and __% of the body’s buffering capacity.
Hemoglobin: responsible for 80% of the non-bicarbonate buffering capacity of blood and 60% of the body’s buffering capacity.
HbO2 + H2O + CO2 « (finish equation)
HbO2 + H2O + CO2 « H+ · Hb + O2- + HCO3-
Another Buffer: protein- Albumin is responsible for __% of non-bicarbonate buffering and how?
20% via histidine rings
___________: buffers only in the face of pathologic changes such as renal failure.
(Name that body buffer!)
Bicarbonate Buffering System: ____% of the body’s buffering system?
Equation = ????
H2O + CO2 « H2CO3 « H+ + HCO3-
Name the enzyme catalyst for this reaction H2O + CO2 « H+ + HCO3-
Carbonic anhydrase is the enzyme catalyst for this reaction H2O + CO2 « H+ + HCO3-
where is carbonic anhydrase found? (name 4 places) and not found? (1 important place you will not find me!)
Carbonic anhydrase is found in renal epithelium, pulmonary tissue, erythrocytes, vascular endothelium, but not the plasma
4 regulators of free water balance (brief MOA) and why do you care
Vasopressin (ADH) = osmo and baroreceptor controlled. Hypovolemia will result in continued ADH release even if hypoosmolar
Thirst = same control as ADH
Aldosterone (=increased Na retention in kidney) Juxtag cells detect decreased renal perfusion (hypovolemia) and release renin that increases aldosterone levels.
Atrial natriuretic peptide = from kidney in response to increased perfusion (neg feed back on aldosterone production too) causes increased renal excretion of Na
regulating it regulates Na
Serum Na under 140 D and 149 C
Clinical signs don't show until below 120 or if drops faster than 0.5mEq/L/hr
Can be w/ hyper, hypo or normal osmolarity
Hypo most common and can be with hyper, normo or hypovolemia (w normovolemia is uncommon)
What role does physical exam findings have in the diagnosis of hyponatremia
Used to differentiate volume status of patient. Hypo, hyper, or normovolemia which is critical to determining the cause of hyponatremia
When you get hyponatremia on blood work when pet has hyperlipidemia and or hyperproteinemia. Its a test error. Not common anymore - test ran differently
Clinical signs of hyponatremia
Related more to rapidity of onset than the degree of decrease
Acute = CNS depression, ataxia, coma, seizures secondary to cerebral edema
Chronic = similar but rarely seen in Vet
Treatment of hyponotremia
Asymptomatic chronic - can treat with water restriction and watch Na closely.
Symptomatic - dont correct faster than 0.5mEq/L/hr
Greater than 150 D and 160 C
Results from free water loss or increased sodium ingestion
2 types of free water loss.
Which is more common?
Hypotonic water loss (more common) and pure water loss
What type of hypernatremia does hypotonic water loss result in and some causes
Water and electrolytes are lost through vomiting, diarrhea, osmotic diuresis, 3rd space fluid loss
What are the findings in a blood gas consistent with a respiratory acidosis or alkalosis
The PaCO2 will move opposite the pH.
Alkalosis = High pH and low PaCO2
Acidosis = Low pH and high PaCO2
What are the findings in a blood gas with a metabolic acidosis or alkalosis
The HCO3 will move in the same direction as the pH
Acidosis = Low pH and low HCO3
Alkalosis = High pH and high HCO3
What is the expected compensation for a respiratory acidosis in a dog
Actue and chronic
For every 1mmHg increase in PaCO2 a 0.15mEq/l increase in HCO3 (acute) and 0.35 (chronic)
What is the expected compensation for a respiratory alkalosis in a dog
Actue and chronic
For every 1mmHg drop in PaCO2 a 0.25mEq/l drop in HCO3 (acute) and 0.55 chronic
What is the expected compensation for a metabolic acidosis in a dog
For each 1mEq/l drop in HCO3 a 0.7mmHg drop in PaCO2
What is the expected compensation for a metabolic alkalosis in a dog
For each 1mEq/l increase in HCO3 a 0.7mmHg increase in PaCO2
What findings suggest a mixed disturbance
- When HCO3 and PaCO2 move in opposite directions
- Normal pH with very abnormal PaCO2 or HCO3 (secondary compensation never brings the pH back to normal)
- If the compensatory response exceeds or falls short of expected
If have a metabolic acidosis and the respiratory compensation falls short you have a
metabolic acidosis with a respiratory alkalosis
What fluids have calcium
LRS, Plasmalyte 56(?)