In-House Diagnostics Module 1 Flashcards
What is the minimum database?
PCV/TP
BG
BUN
Lactate
Blood smear
What is the extended database?
EPOC
Coags
Saline agg
Bloody typing
Arterial blood gas
Biochem
FELV/FIV
Urinalysis
What is PaO2 and SaO2
PaO2 = partial pressure of oxygen in arterial blood
SaO2 = measures HB saturation via pulse oximetry
What is oxygenation?
Measurement of oxygen in the blood
What is ventilation?
Measurement of CO2
What are causes of hyperventilation?
Low CO2
Pain/fear/stress
Decreased arterial O2 content
Neurological disease
Hyperthermia
Compensation for metabolic acidosis
What are causes of hypoventilation?
High CO2
Airway obstruction
Neurological disease/drugs
Neuromuscular disease
Restrictive pleural disease
Respiratory muscle fatigue
What are the 4 types of acid/base disturbances?
Respiratory alkalosis - removal of CO2 by ventilation more than it is produced
Respiratory acidosis - Retention of CO2 due to alveolar ventilation not keeping up with CO2 production
Metabolic alkalosis - primary gain in base or loss of acid
Metabolic acidosis - a primary gain in acid of loss of base
What is the base excess?
It is a calculated value that reflects the non-respiratory portion of acid base, closely related to bicarb. It takes into account all the body’s buffering systems and is an estimate of how much base needs to be added or taken away from the system to achieve a normal pH
What can the anion gap be used to determine?
Can help determine whether the acidosis is caused by creation/addition of acid or loss of bicarb
- production of lactate/ketones
- lack of secretion - kidneys (resorb bicarb and secrete H+)
- ingestion of acid
Loss of bicarb rich fluid (D+)
What are the seven step to evaluating acid base
- pH
- Evaluate resp system - Evaluate PCO2 - the difference between PvCO2 should be is 5mmHg PCO2
- Evaluate metabolic system - based on the assessment of bicarb concentrations
- Base excess: represent metabolic portion of acid/base balance - measurement of how much base needs to be added or taken away to achieve a normal pH at a normal temp
- Looking at primary problem
pH = HCO3/CO2 - if pH and CO2 opposite directions = primary resp IF HCO3 changes in same direction as CO2 = metabolic primary - Evaluate compensatory changes - lung compensate quickly, kidneys take a few hours (gives an idea of chronicity)
- Assessment of oxygenation and ventilation - need arterial sample
What are causes of primary metabolic acidosis?
DUEL
D - DKA/diarrhea - ketones or loss of bicarb rich fluid
U - Uremic acidosis - kidneys
E - Ethylene glycol/aspirin
L - Lactic acidosis
What is the anion gap
(Na+K) - (Cl + HCO3) = anion gap
The anion gap is made up of unmeasured anions (cations/ions) such as lactate, ketones, toxins, uraemic toxins
Helps to categorise the metabolic disturbance and refine differential list
What are causes of metabolic alkalosis
- Vomiting - loss of acid
- Renal acid losses
- Loop diuretic administration
- NG suctioning - getting rid of acidic fluid
- compensatory
A metabolic acidosis with a normal AG means?
Suggestive of bicarb losses - most commonly through GI or renal
A metabolic acidosis with a high AG means?
Suggestive of acid gain - DUEL
What is potassium important for?
Important for determining the resting potential for excitable tissues - serum concentration doesnt account for body concentration
What is K+ metabolism
Intake via - GI tracts
Excreted via - Kidneys with aldosterone being the princiople hormone affecting excitation in distal tubule
What are some causes of hyperkalaemia?
- Decreased urinary excretion: renal failure, uroabdomen, urethral obstruction, hypoadrenocortism, effusive disease, GI disease, Drugs (ACE inhibitor, spirinolactone)
- Translocation from intra to extracellular compartment
- massive cell death - reperfusion injury, trauma, tumor lysis
-insulin deficiency - Iatrogenic/artefact
Treatment of hyperkalaemia
Calcium gluconate 3x
Dextrose - promotes insulin release causing cell uptake
IV regular insulin with dextrose - promotes cell uptake
Bicarb - changes plasma pH and pushes K+ into cells
What are causes of hypocalcaemia
Decreased intake - inappettance, diet
Increased loss - GIT (V/D), Urinary tract (renal failure, post ob diuresis, drugs (loop diuretic), excess mineralocorticoid
Translocation - insulin/glucose fluids, alkalaemia, catecholamine release
What is the treatment of hypocalcaemia?
oral or intravenous
How is Na regulated grossly?
Regulation is tied to water - Na doesnt move freely betweeen cell membranes while H20 does depending on the concentration of active osmoles
- Body measures Na concentration in the brain and corrects this by losing or retaining water
What are the three ways sodium is controlled by the body?
- Kidneys - Filtered via GFR, large portion
- Volume regulation via carotid sinus, aortic arch, glomerular arterioles and cardiac atria - water
- Hormones
Aldosterone - major control (adrenals) - increased sodium retention
Angiotensin 2 - Na/H port
Natrureitic peptide (ANP) - inhibits Na collection and inhibits aldosterone
Catecholamines - increased Na resorption and stimulates renin
ADH (vasopressor)
Causes of hypernatraemia
- Hypervolaemia: iatrogenic, toxicity: salami, saltwater, playdo
- Pure water deficit: fever, diabetes insipidus
- Loss of more H20 than Na: renal failure, v/d, burn injuries, drug induced (frusemide/mannitol)
Causes of hyponatraemia
- Pseudo - very lipid filled sample
- other molecules in blood affecting water loss: Glucose
- Hyponatraemia + hypovolaemia - Body detects low fluid so retains sodium and water - CHf, ascites, nephrotic syndrome
-HypoNa + Normovolaemia: inappropriate ADH secretion, drugs, psychogenic
Treatment of chronic hyponatraemia
- 0.5mEq/L sodium per hour
- Give time for body to dissolve idiogenic osmoles
- Correct hypovolaemia first but use fluid with less Na than serum concentration
- Calculate free water deficit
