AcidBase.Fluids.Lytes Flashcards
What is the composition of LRS: Include osmolarity, organi anions and pH
Na: 130 Cl 109 K 4 Ca 3
Os: 272 mOsm/L
Lactate 28
pH 6.5
What is the composition of Norm-R: Include osmolarity, organi anions and pH
Na: 140 Cl 98 K 5 Mg 3
Os: 296 mOsm/L
acetate 23 / Gluconate 27
pH 6.4
What is the composition of Plyte-A: Include osmolarity, organi anions and pH
Na: 140 Cl 98 K 5 Mg 3
Os: 294 mOsm/L
acetate 23 / Gluconate 27
pH 7.4
What is the composition of Plyte 148: Include osmolarity, organi anions and pH
Na: 140 Cl 98 K 5 Mg 3
Os: 296 mOsm/L
acetate 23 / Gluconate 27
pH 5.5
What is the composition of 0.9% NaCl: Include osmolarity, organi anions and pH
Na: 154 Cl 154
Os: 308 mOsm/L
pH 5.0
What is the composition of 0.45%: Include osmolarity, organi anions and pH
Na: 77 Cl 77
Os: 154 mOsm/L
pH 5.0
What is the composition of D5W: Include osmolarity, organi anions and pH
Na: 0 Cl 0
Os: 252 mOsm/L
pH 4.0
What is the composition of 7.5% NaCl: Include osmolarity, organi anions and pH
Na: 1282 Cl 1282
Os: 2564 mOsm/L
pH 5.0
Summarize some of the recent controversies associated with the use of 0.9% sodium chloride in hospitalized human patients. What is the proposed mechanism for acute kidney injury (AKI) after administration of 0.9% NaCl?
Large volumes can lead to hyperchloremic metabolic acidosis results in greater extravascular expansion, increasing risk for interstitial edema. May also see hyperchloremic metabolic acidosis due to chloride load, AKI with reduced urine output, damaged vascular permeability and stiffness, increased in proinflammatory mediators, detrimental gastrointestinal perfusion and function.
Renal vasoconstriction and reduced GFR resulting in NaCl retention and water retention.
When compared to a balanced electrolyte solution has been shown to result in significantly increased in hospital mortality in critically ill people.
0.9% sodium chloride is commonly called “physiologic” saline. What are three reasons why “physiologic” saline is considered a misnomer?
- Cl level is much higher than physiologic values
- pH is lower (5.0) than physiologic pH 7.4
- NaCl are not the only electrolytes that matter in a physiological basis such as K, Ca, MG
- VetStarch 6% 130/0.4/9:1 is a currently available synthetic colloid solution. What do the numbers associated with VetStarch indicate?
6% =6 g of HES/ 100 ml
130 = Molecular weight
0.4 = tetrastarch- average number of hydroxethyl residues per glucose
9:1= C2:C6 Ration. Higher ratio will be slower to breakdown.
What three factors would increase the plasma half-life of a synthetic starch colloid
High C2:C6 Ratio
High molecular weight
High Molar substitution
Why might dogs have different HES metabolism than people
Dogs have more amylase therefore may breakdown more quickly.
What is the Henderson Hasselbach equation
pH = 6.1 + log [HCO3/ (0.03 x PCO2)]
How does hemoglobin affect buffering
More hemoglobin more buffering effect
Where is the most carbonic anydrase located
in RBCs
What are the compensation calculations in the standard approach for respiratory disturbances
Acute acidosis 0.15 increase in bicarb
Acute alkalosis 0.25 decrease in bicarb
Chronic acidosis 0.35 increase in bicarb
Chronic alkalosis 0.55 decrease in bicarb
What are the compensation calculations in the standard approach for metabolic disturbances
0.7 (increase/decrease) in PCO2 for acidosis/alkalosis
What is the primary underlying causes of Respiratory acidosis
alveolar hypoventilation (decreased alveolar minute ventilation)
What is the primary underlying causes of Respiratory alkalosis
hyperventilation, high altitude
What is the primary underlying causes of metabolic acidosis
acids added to blood (DUEL) for High anion gap
Bicarbonate loss - normal AG hyperchloremic metabolic acidosis (diarrhea, renal tubular acidosis, dilutional acidosis- 0.9% NaCl, addisons)
What is the primary underlying causes of metabolic alkalosis
Loss of gastric acids, renal retention of bicarb
Calculate the free water deficit
ml= [(Na measured/Na normal)-1] x BW x 0.6
Calculate the Anion Gap
Na+K - (Cl- + HCO3-)
Normal 12-20 mmol/L
Define base excess
Amount of acid or base that must be added to a sample of oxygenated whole blood to restore the pH to 7.4 at 37C and at a PCO2 of 40 mmHg
Normal 0 +/- 2
Neg = acidosis
Positive= alkalosis
What does base excess tell us
Provides a measure of metabolic componenet of acid/base that is independent of PCO2
How much sodium bicarbonate do you give
0.3 x BW x base deficit
0.3= approx value for the distribution of bicarbonate
Give about 50% of calculated dose
Dilute as hyperosmolar
How does PvCO2 compare to PaCO2
Generally close, but will see an increase in PvCO2 vs PaCO2 due to poor cardiac output not hypoventilation
How does hypoalbuminemia affect AG
It will increase less and may even be normal
Does serum potassium reflect whole body K
No. Primarily stored intracellularly
How does the body maintain normal serum K
Distribution of K between extracellular and intracellular compartments
renal excretion of excess K
What are causes of hypoK
decreased intake
Intracellular shift
Increased renal excretion
How do you treat a metabolic acidosis with a signficant hypo K
Treat the hypo K,
If pateint is not responding to treatment for ventricular arrhythmia and has Hypo K what should you do
Hypo K leaves myocardium refractory to the effects of Class 1 antiarrhythmic agents and serum K concentrations should be corrected
What is the max rate of K supplementation
0.5 mEq/Kg/hr
What other electrolyte is needed to be supplemented if K is not improving
Magnesium
What are causes of hyperkalemia
Increased supplementation/intake
Increased extracellular movement (repurfusion injury, insulin deficiency, metabolic acidosis)
Decreased renal excretion
Tumor lysis syndrome
What is pseudohyperkalemia
K+ shift from cells after blood draw (RBCs, Platelets, WBCs)
Most commonly seen with thromobcytosis, but also Leukocytosis
Japaneses origin breeds have functional Na/K atpase pump that with hemolysis
What electrolyte abnormalities occur with repeated draining of effusions
Hyper K and hypo Na
Due to a decrease in circulating volume
Differentials for a Na/K ratio < 27:1
Primary is addison’s disease
r/o GI disease - trichurasis, salmonellosis, perforated duodenal ulcers
What are ECG abnormalities in HyperK
Generally seen > 8 mEq/L but does not correlate with increase.
Tall tented T waves, depressed p-wave, prolonged QRS and PR interval
In severe get atrial standstill, bradycardia, and ventricular astolye
What is the MOA for Ca Gluconate treatment with HyperK
restablishses normal gradient between resting membrane potential and threshold potential
Does not decrease K
What is the MOA for dextrose and insulin dextrose with Tx of Hyper K
Insulin (both endogenous and exogenous) promotes intracellular shift of K through ativation of NaK atpase pump
What is the MOA of Na bicarbonate with tx of hyperK
Increase extracelluar pH and promotes intracellular shift of K+ in exchange for H+
What is the MOA of beta adrenergic agonists in the tx of Hyper K
Promotes intracellular shift of K through activation of NaK ATPase pump
Where is phosphorus stored in the body
80% skeletal
19-20% intracellular
1% plasma
What regulates storage and absorption of phosphorus
Vitamin D- enhances GI absorption
PTH, VitD, and calcitonin regulate storage
What regulates excretion of phosphorus by the kidney
PTH
fibroblast growth factor 23 (FGF 23
How does Fibroblast growth factor (FGF) 23 work
Secreted by osteoblasts in response to increase phos intake
Inhibits production and stimulates 1-25 dihydroxyvitamin D (calcitriol)
Promotes excretion in the kidneys indepent mechanism of PTH and Vit D
What is the main site of renal Phosphorus regulation
Renal tubular NaPO4 co transportor
Inhibited with metabolic acidosis
What are the causes of hypophosphatemia
Transcellular shfits (refeeding, respiratory alkalosis) Increased renal excretion (eclampsia, etc) Decreased intake/abosrption
What rate of supplementation is generally started for phos
0.03 mmol/kg/hr
What are causes of hyperphosphatemia
Increased endogenous release (tumor lysis syndrome, crush injury)
increased exogenous uptake ( vit d toxicosis, phsophate enemas
Decreased renal excretion (CKD)
How does furosemide alter phosphorus in the kidneys
May promote phosphorus excretion
How does calcium levels affect voltage gated ion channels
Extracellular low Ca: open too easily
Extracellular high Ca: prevent/reduce opening
What are the concentrations of calcium in the plasma
55% ionized
10% non ionized
35% protein bound (albumin)
what is believed to be the mechanism of hypo Ca with pancreatitis
Soponafication
What do you want to avoid in treating hypocalcium
at calcium x phosphorus ration of > 70
What are causes of HyperCa
1) generally increase PTH or hormonally related peptide
2) bone destruction, bone inflammation, or bone infection
Thiazied diruetics, toxicity: Vit D analogues rodenticides
In life threatening hyperCa what are treatment options
calcium chelating agents
calcium channel blockers
extracorpeal therapies
bisphosphonate agents (pamidronate)
Where is Magnesium found in the body
Most is intracellular second highest to K
How is Magnesium uptake regulated
Dogs- colonic absorption Cats unknown
Active uptake when whole body stores are low; Passive uptake with normal to high Mg
Signs attributed to HypoMg
ECF composition-- HypoK, HypoCa Neuromuscular signs Neurologic- nystagmus CV GI ileus unresponsive to traditional tx
How to treat HypoMg with normal whole body stores
If not whole body deficiency then oral supplementation won’t work and will act as laxative
Cellular uptake of Mg slow and may take 24hrs to equilibrate. Therefore need CRI
What is the recommended supplementation of Mg
Daily dose
Small 0.5 g/day
Dog 6-20 kg 1 g/day
Dogs > 20 kg 2 g/day
What are causes of HyperMg
decrease renal function/GFR
Less likely due to increase uptake due to passive nature
What are signs of hyper Mg
weakenss, hypotension, respiratory difficulty
rarely asytole—- Mg is a calcium channel blocker
What is the treatment for hyperMg
Diruresis/ increase GFR
Insulin/dextrose improves cellular uptake
Ca gluconate if signs are severe
Bicarbonate therapy potential adverse effects
increase hemoglobin affinity for Oxygen increase blood lactate concentration paradoxical intracellular acidosis (CO2 into the cell ) Hypercapnia Hypervolemia Hyperosmolarlity HypoiCa, HypoK, Pheblitis
If you didn’t get base deficit on your machine how can you estimate the bicarb to give a patient
replace base deficit with Bicarb patient- normal bicarb
In the stewart approach to Acid/Base what are the 3 independent determinants
Partial pressure of CO2 (PCO2)
Strong ion difference
Total weak acids Atot
In the Stewart approach to acid/base what are the possible abnormalities
Increased SID metabolic alkalosis Decreased SID metabolic acidosis Decreased Atot metabolic alkalosis Increased Atot Metabolic acidosis Increased SIG metabolic Acidosis
What is a strong ion
Ions that fully dissociate at physiologic pH
What is used to calculate SID
Cations: Na + K + Ca + Mg subtract anions anion Cl- If Atot remains constant the change in SID will reflect changes in HCO3 Normal 40-45 mEq/L
Define total weak acids
partially dissociated at physiologic pH
albumin and phosphate
How do you calculate SIG
SID- (HCO3- + Atot)
How is Atot estimated
Dogs (Albx4.9) - AG
Cats (Alb x 7.4) - AG
If phos is elevated need to adjust AG
AG + (2.52 - .58 x phos concentration)
What are the semiquantitive formulas
Free water effect Chloride effect albumin effect Phosphorus effect lactate effect
How due you calculate the semiquantative approach
Sum = free H20 + Chloride effect + Alb effect + Phosphate effect + Lactate effect
How do you measure unmeasured anions in the semiquantative approach
Base excess - sum
How doe you calculate the free H2O effect in the semiquantitive approach
(Na measured - Na normal)/4
How doe you calculate the chloride effect in the semiquantitive approach
Corrected chloride= Measured cl x (Normal Na/Measured Na)
Chloride effect= normal Cl - corrected chloride
How doe you calculate the albumin effect in the semiquantitive approach
(normal alb- measured alb)/ 4
How doe you calculate the phosphorus effect in the semiquantitive approach
(Normal phos - Measured phos)/2
How doe you calculate the lactate effect in the semiquantitive approach
Measured lactate x (-1)
What are the systemic consequences of acidemia
Decreased cardiac contractility, decreased cardiac output, increased susceptibility to arrythmias
impairs response to catecholamines
Promotes systemic inflammatory state
pH < 7.15 decreases systemic and increases pulmonary vascular resistance— hypotension worse
What are the sources of fluid acidity
Container- PVC generates acid- small amount
CO2 absorbed from air (largest contributor)
Salts added increase hydronium ions (H3O+) favoring H+ actitivity- decrease pH
What is the SID of IV fluids
In vitro is 0 due to law of electroneutrality
In vivo is 0-50 mEq/L because of metabolizable organic anions
What is the mechanism that IV fluids change plasma pH
primarily due to change in SID, not in dilution
What is the in vivo SID of PLyte and Norm R
SID 50
Increases plasma pH
How is the water in the body divided
Total body water 60% of BW
Intracellular= 67%
Extracellular= 33%
Interstitial= 75%
Intravasculature= 25%What is the difference of osmoalitlity and osmolarity
Osmolality: number of particles (mOsm) per kg of water
Osmolarity- Number of particles per liters of H20
What are the two mechanism for ADH release
Osmotic: hyperosmolarity
Nonosmotic: decrease in circulationg volume
how to calculate sodium deficiency
BW(kg) x 0.6 x (Normal na- patient Na)
How to calculate change serum Na expected with 1 Liter
(infusate Na + K - patient Na)/ (BWx0.6 +1)
What is the equivilant volume of cyrstalloid to 1 colloid
3-4 times crystalloid to 1 collowed to get equal intravascular volume
How much plasma is needed to increase albumin 1 g/dl
40 ml/kg
What are possible adervese effects with human serum albumin
type III hypersensitivity reactions in healthy dogs
But reported in critically ill dogs
What are adverse effects of crystalloids
Specific fluid tyype complications: Saline, LRS (hypotonic) Acetate may cause vasodiluation/hypoperfusion with rapid admin
Resuscitation injury, upregulation of pro inflammatory cytokines, augmented neutrophil adhesion to vascular endothelium, stimulate neutorphil oxidative burst, increase cellular apoptosis
Fluid overload
What are adverse effects of HES
Coagulopathy, AKI, Tissue accumulation, trends toward mortality
What is the proposed MOA for HES induced AKI
hyperviscosity mediated, ischemic injruy, osmotic nephrons
renal uptake by interstial reticuloendothelial system
What is the MOA for HES induced coagulopathy
decrease vWF, F VIII activity and acquired fibrinogen deficiency
What are the coefficents in the starlings equation and what do they mean
K= filtration- ease with which fluids moves across membranes sigma= represents the pore size or permeability of the membrane
