Fluid, Electrolytes and Acid-base Flashcards
The anion gap is defined as which of the following?
a. The difference between sodium and potassium
b. The combination of all electrolytes
c. The difference between cations and anions
d. The difference between osmolarity and osmolality
C
What is the replacement volume for a 17^kg dog that is 7% dehydrated?
a. 540^mL
b. 1190^mL
c. 2420^mL
d. 119^mL
B
Which mineral helps with cellular regulation of Na, K, and Ca and should be examined in cases of refractory hypokalemia and hypocalcemia?
a. Calcium
b. Manganese
c. Magnesium
d. Phosphorus
C
What percentage of total body water is contained within the intracellular space?
a. 1/3
b. 2/3
c. 1/4
d. 3/4
B
Which of the following is not an example of an electrolyte?
a. Calcium
b. Magnesium
c. Oxygen
d. Phosphate
C
Which is the most abundant intracellular cation?
a. Sodium
b. Potassium
c. Magnesium
d. Calcium
B
The ability of a substance to make water move across cellular membranes is referred to as what?
a. Osmosis
b. Osmolality
c. Tonicity
d. Diffusion
C
According to Stewart’s strong ion approach to acid–base analysis, hyponatremia and hyperchloremia result in which metabolic condition?
a. Metabolic acidosis
b. Respiratory acidosis
c. Metabolic alkalosis
d. Respiratory alkalosis
A
Which of the following is a weak acid buffer?
a. Cl-
b. Na+
c. Albumin
d. Lactate
C
What is the total number of solutes per liter called?
a. Osmolarity
b. Osmolality
c. Tonicity
d. Diffusion
A
Interstitial oedema
Increased fluid within the interstitial spaces and broadly a result of one of the following
- Hypertension
- Hyproteinaemia
- Increased microvascular permeability
- Impaired lymph flow
- Inflammatory oedema
Oedema results in
Impaired oxygen delivery to the tissues and disrupts cellular functions
Major ECF cation
Sodium
Major Intracellular anion
Phophate
Even small fluctuations within reference range of sodium can be detrimental, true or false.
True
Effective osmoles
Those that are unable to pass freely across cellular membrane and contribute to osmotic pressure i.e. Na, K
Ineffective osmoles
Those that can pass freely across cellular membranes i.e. H2O
Low circulating volume triggers what response
RAAS
Preservation of H2O and Na to increase IV vol
increased ADH release and thirst to increase free water intake which may lead to hyponatraemia (and therefore a decrease in osmolality).
Free water deficit calculation
((Na, current / Na, normal) - 1) x (0.6 X BW)
Causes of hypernatraemia
Vomiting & Diarrhoea
PU
Water withheld
Activated charcoal
Osmotic diuresis (i.e. mannitol)
Diabetes insipidus
HTS
Salt water ingestion
Diet
Severe hypernatraemia
> 180mmol/L and may result in clinical signs
Neuro: ataxia, seizures, obtundation, heap pressing, coma, death
Cells: shrink as water moves out of the cell (hyperosmolar ECF)
Treatment of hypernaatraemia
Increase FW via hypo-osmolar fluids
Correct no quicker than 0.5-1mEq/kg/hr
Hyponatraemia
Severe retention of FW.
The body may sense low circulating volume causing ADH to be released and increased water and salt reabsorption.
Considered severe <120mEq/L and causes cellular swelling as water enters cells > cerebral oedema and increased tissue hydrostatic pressure.
How much potassium is located within the cell compared to ECF?
140mEq/L compared to 4mEq/L
Hypokalaemia and hyperkalaemia limits
<3.5mmol/L
>5.5mmol/L
Conseuqences of low K
Metabolic: glucose intolerance, insulin form B-cell impaired
Neuromuscular: weakness, ventroflexion, hyperpolarised myocytes
Renal: CKD
Cardiovascular: prolonged action potential, AV dissociation, VT, decreased ST segment, prolonged QT
Treatment of low K
CRI/Supplementation based on severity
Not to exceed 0.5mEq/kg/hr but in very severe cases may have short period of 1-1.5mEq/kg/hr
- Avoid bicarb and insulin until K normalising (at least 3.5)
Treatment of high K
Transcellular shifting: insulin, glucose & terbutaline
IVFT
Relieving urinary obstruction
Dietary adjustment
ACE inhibitors
Mannitol/diuretics
+- bicarb
10% CaGlu
Dialysis
Cardiac findings with high K
Atrial standstill
Bradycardia ++
Due to long depolarisation and repolarisation of myocardial conduction system
Cardiac findings with high K
Atrial standstill
Bradycardia ++
Due to long depolarisation and repolarisation of myocardial conduction system
iCa
Mediates acetylcholine release during neuromuscular transmission and also stabilises nerve cell membranes
What hormones/metabolites are involved in Ca regulation?
Parathyroid hormone
Vit D metabolites
Calcitonin
What samples should be avoided when testing Ca
EDTA
Oxalate
Citrate
- heparinized serum sample ideal
Signs of hypercalcaemia
PU/PD
Anorexia
Constipation
Letahrgy & weakness
Ataxia
Obtundation/coma
Twitching/seizures
Arrhythmias
Treatment of hypercalcaemia
Remove underlying cause
IVFT
Diuretics
Glucocorticoids
Bicarb
Pamidronate/biphosphamates
Clinical signs of low iCa
Bradycarida (decreased inotropy & chronotropy)
‘itchy’ face
Neuro changes
Cramping lethargy
Myocardial failure
Respiratory arrest
Treatment of low iCa
Ca IV (NEVER SQ)
Calcitriol
Magnesium homesostasis
Absorbed from the jejunum and ileum of the small intestine and reabsorbed by the LOH. The kidneys are the main regulator of Mg
Clinical signs of low Mg
Arrhythmias (tachy)
Neuromuscular weakness
Increased acetylcholine release
Decreased K, Na, Ca
Enhanced digoxin uptake Increased
Treatment of low Mg
Milder cases will resolve with therapy of underlying disorder
Can supplement orally or IV.
- IV = 30mg/kg or 0.15-0.3mEq/kg over 5-15min (life-threatening VT)
Presence of high Mg
Renal failure
Endocrinopathies
Iatrogenic OD (cathartics, laxatives)
Signs of high Mg
Lethargy/depression/weakness
Hyporeflexia
Respiratory depression
Blockade of ANS
Vascular collapse
Prolonged PR
Therapy of high Mg
Removing exogenous sources
Ca will antagonise Mg so given to reverse cardiovascular signs
Saline diuresis and frusemide
Phosphate
Main intracelluar anion
- production of ATP
- maintains cellular membrane integrity
- maintenance of normal bone and teeth matrix
- regulates tissue oxygenation
Low P
Poor absorption from GIT, transcellular shifts or increased urinary excretion (malabsorptive diseases and malnutrition, insulin admin, alkalaemia catecholamines, glucose, diuresis).
Consequences of low P
Haemolysis (loss of mebrane integrity)
Spherocytosis
Tissue hypoxia
Increased risk of infection
Generalised weakness
Tremors
Muscle pain
Treatment of low P
KPhos common
0.01-0.12mmol/kg/hr
** avoid mixing with LRS as can bind to Ca and cause precipitation
Causes of high P
Decreased renal excretion
Tumor lysis syndrome
Iatrogenic
Can result in renal tubular mineralisation
Clinical signs of high P
Seizures and tetany
Dysrhythmias
Low Mg
Low Ca
Metabolic acidosis
Henderson-Hasselbalch equation
pH = 6.1 + log ([HCO3] / [0.03 X PCO2])
Normal pH range
7.35 - 7.45
Low pH
Acidaemia
High pH
Alkalaemia
pCO2
Is an acid controlled by pulmonary ventilation
Base excess (BE)
Amount of acid or base that must be added to a sample of oxygenated whole blood to restore a pH of 7.4 @ 37C @ CO2 40mmHg.
Increased (+ve) = alakalotic process
Decreased (-ve) = acidotic process
-2 to +2 acceptable but ideally 0
Carbonic acid equation
CO2 + H2O <> H2CO3 <> H + HCO3
Respiratory acidosis
inc CO2, low pH, compensatory inc HCO3
- compensation, increased CO2 production, depressed respiratory system, brain injury, mass lesion, neuropathies, myopathies, seizures, hyperthermia
Respiratory alkalosis
low CO2, inc pH, compensatory low HCO3
- decreased CO2 production, hypoxaemia, parenchymal disease, airway inflammation, brain injury
Metabolic acidosis
low HCO3, low pH, compensatory low CO2
- increase in HCO3 or increase in H, low chloride, diarrhoea, renal HCO3 loss, toxins, drugs, RTA, hypovolaemia, DKA, uraemia, lactate
Metabolic alkalosis
inc HCO3, inc pH, compensatory inc CO2
- decreased H or increased HCO3, gastric acid loss, renal acid loss, low chloride, alkalising therapy
Bicarbonate therapy
0.3 X BW X BE
Give 1/3 dose and then titrate to effect. Only give if persistent acidaemia despite other therapies
Glycolysis
Produces 2mole ATP, pyruvate and NADH which then in aerobic conditions enters TCA, ETC, OP to produce 36mole ATP
Lactate consuming organs
Liver (50-70%)
Renal cortex (25-30%)
Different ‘types’ of lactate
Type A: clinical evidence of relative or absolute inadequate tissue oxygen delivery.
Type B: absence of inadequate tissue oxygen delivery
- Type B1: SIRS, Sepsis etc
- Type B2: Alcohols, ethylene glycol, toxins, drugs
- Type B3: metabolic disorders (rare)
Main lactate iso-form in mammalian cells
L-lactate
Body fluid distribution
66% ICF
33% ECF (75% ISS< 25% IVS)
Isotonic fluid loss
Loss of fluid equal to ECF i.e. vomiting, diarrhoea, blood etc
- change in volume but not osmolality
- no change in ICF
- OL shows signs of interstitial overhydration
Tonicity
Effective osmoles that don’t freely permeate cell membranes and drives fluid movement into or out of cells
Na/K-ATPase pumps
Regulate cell volume by maintaining intracellular K and extracellular Na
Albumin
Contriutes 80% plasma COP to minimise fluid loss from the intravascular space into interstitial space.
It is involved in wound healing, coagulation and free radical scavenging as well as hormone substrate and weak buffer.
Adverse fluid therapy effects
Dilutional coagulopathy
Increased permeability
Inappropriate electrolyte shifts
Exacerbation of haemorrhage
Acid/base derrangements
Isotonic fluids
Similar Na and osmolarity to plasma and ECF (290-310mOsm/L)
- rapid IV restoration
- interstitial dehydration
I.e. LRS, normosol-R, P148, 0.9% NaCl
Hypotonic fluids
Lower Na & osmolarity (150-250mOsm/L) than plasma and ECF
- FW deficits
- Maintenance fluids
I.e. 0.45% NaCl + 2.5% Glu, D5W
- Will not expand IVS, Do not bolus
Hypertonic fluids
Higher Na & osmolarity than plasma or ECF
- ICH
- IVS expansion
- FW shift 3-5X their volume administered
- Severe hyponatraemia
- Transient increase in preload, SV and reduction of afterload
- reduce endothelial swelling
- slight +ve inotropy
- Anti-inflammatory effects
Fluid choice for hypochloremic acidosis
0.9% NaCl
Which buffer associated with vasodilation and hypotension if given rapidly?
acetate
Colloids
> 10,000 Da so remain in IVS longer and will increase blood viscosity and COP. Ideal for patients with hypoalbuminaemia and increased vascular permeability
Normal COP dogs & cats
15.3-26.3mmHg (Dogs)
17.6-33.1mmHg (Cats)
System that degrades larger colloidal molecules
reticuloendtothelial system
Colloidal side effects
- can interfere with PLT function, vWF & FVIII
- Anaphylaxis
- AKI
Max colloidal dose per day
20/ml/kg/day
3 main colloidal parts
- Albumin
- Globulins
- Fibrinogen
Calculating daily IVFT
- Deficit (ml) = BW X % DEHY X 1000
- Maintenance = 2-4ml/kg/hr
- Ongoing losses, insensible + sensible losses
1+2+3 = mls/day
What fluid osmolarity requires central catheter
> 600-700mOsm/L
Starting rate for FW
3.7ml/kg/hr (should reduce Na by 1mEq/hr)
Discontinuation of fluids
Shouldn’t be done abruptly particularly if patient has been on high fluid rates due to potential medullary wash out that can lead to hypovolaemia and dehydration.
Aim to wean fluids over 24h period and monitor pt closely
Providing shock crystalloids
Short, large bore catheter (potentially multiple)
IO obtained if venous access not possible
10-20ml/kg increments to resuscitation end points
+- permissive hypotension (80-90sys) to avoid rebleeding (haemorrhaging patients)
Shock rates for colloids
2-5ml/kg over 10-30min, re-evaluate need for more
- don’t exceed 20ml/kg/day or 10ml/kg/day in cats
Aggressive overzealous crystalloid resuscitation consequences
Volume overload & organ oedema
Decreased GI functionality & bacterial translocation
Abdominal compartment syndrome
Arrhythmias
Poor contractility & CO
Coagulation disturbances
Albumin deficit (gms)
10 X (target Alb - pt Alb) X BW X 0.3
- usually give 2g/kg
Corrected sodium calculation
Sodium Correction = measured Na + [(glucose level - 100) x 0.016]
Correct sodium for a patient with a glucose of 400mg/dL and Na+130mEq/L
Na(meas) + 1.6 ( Gluc(meas) - Gluc norm)/100)
132
Correct sodium for a patient with a glucose of 510mg/dL and sodium of 128mEq/L
136
Anion gap (cat)
Na; 140, K; 4.2
Cl; 110 HCO3; 15
(Na + K) - (Cl + HCO3)
(140 + 4.2) - (110 + 15)
19.2 (norm 13-27)
Anion gap (dog)
Na; 120 K; 6.7
Cl; 109 HCO3; 8
(Na + K) - (Cl + HCO3)
(120 + 6.7) - (109 + 8)
9.7 (Norm 10-24)
Fluid plan for a 5.5kg dog that is 5% dehydrated and has 5ml/hr ongoing losses. Lactate 3mmol/L
- 5ml/kg fluid bolus lactate normalises
- Fluid deficit = BW X 0.05 X 1000 = 275mls
- Maintenance = (5.5 X 30) + 70 = 235mls
- Ongoing losses 5ml/hr
- Total/day = 605ml/day
- Per hour = 25.2ml/hr
Fluid plan 1.8kg cat, euvolaemic
(BW^0.75) X 70 = 108.8
4.5ml/hr
Fluid plan 2kg cat, 10% dehydrated, insensible losses 22ml/kg/day
- (2 X 30) + 70 = 130ml
- 2 X 0.1 X 1000 = 200ml
- 22 X 2 = 44ml/day
- 374ml/day
- 15.5ml/hr
Albumin deficit for 10.2kg patient with albumin 12; goal albumin = 20, HSA 20%
Alb def (gm) = 10 (20-12) X 10.2 X 0.3
24.4g
therefore ml to give = 24.4g/20g/ml = 1.22ml
Albumin deficit 5kg dog with albumin 10; target albumin 20
Alb def (g) = 10 (goal alb - pt albumin) X BW X 0.3
10 (20-10) X 5 X 0.3
150g
