Biochemistry Flashcards
VBG flow chart
How do you work out the anion gap?
Interpret
Anion Gap = Na – (Cl + HCO3)
4-12 normal
What are the cause of a HAGMA
Causes (CATMUDPILES)
- CO, CN
- Alcoholic ketoacidosis and starvation ketoacidosis
- Toluene
- Metformin, Methanol
- Uremia
- DKA
- Paracetamol,
- Iron, Isoniazid
- Lactic acidosis
- Ethylene glycol
- Salicylates
What are the causes of a NAGMA
Causes (CAGE)
- Chloride excess
- Acetazolamide/Addisons
- GI causes – diarrhea/vomiting, fistulae (pancreatic, ureters, billary, small bowel, ileostomy)
- Extra – RTA
What are the main causes of acute respiratory acidosis
things that cause hypoventilation:
* CNS depression - injury, stroke, drugs
* respiratory depression - myopathy, drugs, spinal injury
* mechanical hypoventilation - pain, chest wall injury, raised intra abdominal pressure
* Resp failure - pneumonia, pneumothorax, oedema, bronchial obstruction
what are the causes of chronic resp acidosis
COPD
restrictive lung disease
How do you work out if the resp acidosis is acute or chronic?
What does it mean if the expected value is not met?
Acute - bicarb to increase by 1mmol/l for every 10mmhg of co2 above 40
Chronic- increases by 4
if expected is below measured then concurrent metabolic acidosis
What are the causes of respiratory alkalosis
CHAMPS
- CNS disease - stroke, haemorrhage
- Hypoxia - PE, asthma
- Anxiety and pain
- Mechanical or excessive ventilation
- Progesterone and pregnancy
- Salicylates and sepsis
What are the causes of metbolic alkalosis?
CLEVER PD
- Contraction - volume contraction
- Liquorice abuse
- Endocrine - cons, Cushings
- Vomiting
- Excess alkali - Antacids
- Renal - Bartlers
- Post hypercapnia
- Diuretics
How do you work out if the resp alkalosis is acute or chronic?
Acute -Bicarb should reduce by 2mmol/l for every 10mmhg under 40
Chronic - reduce by 5
When do you use Winters formula?
Has the metabolic acidosis been compensated for or is there also a respiratory acidosis?
Expected Pc02 = (1.5 x bicarb) + 8 (+/-2)
if expected is correct then its compensation
How do you calculate the delta gap?
When do you use the delta ratio?
(AG -12) / (24-bicarb)
to work out the metabolic acidosis component
<0.4 pure NAGMA
0.4-0.8 mixed
0.8 - 2 Pure Hagma
Over - Hagma plus metabolic alkalosis or resp acidosis
What is the respiratory acid base status
Marked respiratory alkalosis
sepsis
What is the metabolic acid base status. Show working and differentials
HAGMA - 137 – (98 + 18) = 21
Delta ratio (AG -12) / (24-bicarb) =9/6 = 1.5 therefore pure HAGMA
Causes (CATMUDPILES)
Alcoholic with epigastric pain and vomiting.
Comment on:
Sodium
Potassium
Chloride
Calcium
Why abnormal?
- Hyponatremia moderately low
‐ Likely GI losses or other cause
K 3.5 – corrected for pH => 2.5
‐ GI losses likely
Hypochloremia ‐
‐ Vomiting, electrical neutrality
Ionised Ca – severe hypocalcaemia
‐ Pancreatitis, renal failure, rhabdo a possibility
list major abnormalities and differentials
High anion gap metabolic acidosis
‐ Ketones – DKA, alcoholic
‐ Lactate (type A or B with liver failure)
Inadequate respiratory compensation (expect CO2 to be lower)
‐ Decreased consciousness eg alcohol, head injury, other drugs
Delta ratio (42‐12)/(22‐11) = v. high almost (1 mark)
No differential acceptable
Lactate high
‐ Type A hypoperfusion
‐ Type B – liver failure
Hyperglycaemia
‐ DKA
what are the major abnormalities and clinical implications?
What is the most likely cause of the acid base abnormality?
Metformin-associated lactic acidosis + Acute renal failure impairing excretion of metformin and also contributing to acidaemia
What is the difference between Type A and B lactic acidosis?
Causes?
product of anaerobic glycolysis which reflects:
type A oxygen delivery
type B altered metabolism with no evidence of inadequate tissue delivery
Type A causes:
anaerobic muscular activity
hypoperfusion eg shock or cardiac arrest
hypoxaemia eg anaemia
Type B causes:
pancreatitis
diabetes
leukemia
drugs - panadol, salicylates, methanol
What are the management priorities?
how do you treat low bicarb
50-100ml 8.4% bicard
list four metabolic abnormalities and calculations
Sever metabolic acidosis ( Low HCo3)
Expected Resp compensation with low Pco2 but actual Pco2 very high
Concurrent Resp acidosis
HAGMA - pure HAGMA with delta ratio
Urea/Creatinine ratio 18/0.12= > 100
à Pre-renal failure
63 year old male with chronic pancreatitis and nausea and vomiting.
What are the main abnormalities
Is real chronic or acute???
High anion gap (approx. 31) metabolic acidosis
Profound hypochloraemia
Gastric losses and fluid depletion causing chloride loss and metabolic alkalosis
Metabolic acidosis secondary to renal failure (acute? Acute on chronic?) +/- sepsis
from pancreatitis and/or gastro-enteritis
CO2 retention as compensation for severe metabolic alkalosis
What are the clinical features of severe hypocalcaemia and how do you manage?
Features:
* Tetany
* carpopedal spasm
* decreased cardiac output
* seizures
* Prolonged QT
Management
* make sure to treat low mg with IV mg
* IV 10% calcium gluconate and then calcium infusion
List four point of care/bedside tests and justifications
BSL -?hypoglycaemia
VBG - low or high K
ECG - signs of electrolyte disturbance
US - tampanade
CXR - ?oedema
VBG - acid/base disturbance
lactate - hypoperfusion or sepsis
List three diagnostic abnormalities and what does it suggest
Peaked T
Wide QRS
LAD
Hyperkalaemia
What are the signs of hyperkalaemia on ECG?
- Peaked T
- Wide QRS/bundle branch blocks
- P wave widening or flattening
- Bradyarrhytmias
What are the signs of hypokalaemia ECG
ST depression
T wave flattening
prominent U waves
prolonged PR
given ECG findings of hyperkalaemia how do you treat?
- stabilise myocardium with calcium chloride or calcium carbonate
- move K to intracelluar space with salbutamol and insulin dextrose
- remove K via frusemide or dialysis
How do you manage life threatening hypokalemia/
risk of VF/VT so keep cardiac monitored
Check MG as need to replace this
replace 10mm/hr peripherally or quicker centrally
discuss with family in case of deterioration
check Cl
Disposition - HDU v ICU
What are the causes of hyponaetremia
what are important features of a history when investigating low sodium
- Hx organ failure – heart, renal, liver – causes hypervolemic hypoNa
- Drug history – drugs that cause SIADH, diuretics
- Mental health history – drugs that cause SIADH, water intake for psychogenic polydipsia
- Intercurrent illnesses – eg sepsis, pancreatitis, gastroenteritis– causes of hypovolemic hypoNa
- Malignancy – SIADH
What are the risk factors for osmotic demyelination syndrome?
- Sodium level at presentation - most occur if under 105. Unusual over 120
- Duration of hyponaetremia - rare if developed over hours to a day eg ingesting large volumes of water
- Over rapid correction - should be 6-12 mmol/day
- other risk factors associated with ODS with less severe levels - alcoholics, liver disease, malnutrition
How do you use hypertonic saline in TBI?What are the targets and end points?
3% 3ml/kg bolus IV repeating every 2-4 hours
Target:
ICP <20mmhg
osmolality 300-320mosm/l
Sodium 145-150
What are the advantages and disadvantages of hypertonic saline vs mannitol in TBI?
hypertonic saline:
- more effective in lowering ICP
- more prolonged effect on ICP
- more haemodynamically stable as less change of diuresis and hypotension
What are the most common causes of renal failure in young indiginous women
- diabetic nephropathy
- post strep glomerulonephritis
- Drug side effect
Management priorities?
Move to monitored bed. Need for ECG
Needs potassium replacement in monitored environment, likely to need central line for
IV potassium replacement.
Need to contact HDU
Need for IVF as likely element of pre-renal failure in view of mild CK rise
How do you calculate
Corrected sodium
Corrected sodium = Na + (glucose/4)
You notice the patient is making some spontaneous respiratory efforts which are triggering the high pressure alarms.
Give your strategy for improving this patient’s ventilation, stating your desired endpoints.
1 - Achieve synchrony – sedate further +/‐ drug paralyse patient
2 - Improve Ventilation – increase RR to 16‐20
3 - Improve Oxygenation –
4 - increase PEEP to 10‐15cm H20
5 - Tidal volume to 480‐500mls (6mls/kg)
State four (4) important principles regarding your fluid and electrolyte treatment of
this patient while in ED, and give a justifying statement (which may include doses) for
why it is an important principle.
- rehydrate over 48 hours - 10% dehydrated so want to ensure no fluid shifts
- insulin infusion early to shift glucose into cells
- closely monitor glucose to watch for rapid falls
- monitor K closely as insulin can cause it to move intracellularly
What are the management priorities for HHS
- Fluids- This patient is likely to be severely dehydrated. Aim correction over next 24 hours. Example N/S 500ml/hr for first 2 hours. Then 250ml/hr next 4 hours.
- Insulin- 0.05-0.1units/kg/hr. No bolus.
- Electrolytes- Watch K, will need to add extra potassium as pH improves and blood K levels drop.
- Seek and treat precipitant of current state
- Anticipate and treat complications eg cerebral oedema.
- Disposition to ICU as requiring close observation and possibility for
deterioration.
How do you alter potassium for PH?
Inversely proportional.
0.1 PH = 0.6 k
What is the Aa gradient
PA02 - Pa02
- PA02 = Partial pressure of oxygen in alveoli Pa02 = partial pressure of oxygen in the blood
- PA02 worked out from alveolar gas equation
Pa02 from Gas
The ‘short’ form of the alveolar gas equation is: PAO2 = PiO2 (which is 713 x fi02) – PaCO2/0.8
where PiO2 = (Patm – PH2O) x FiO2
Patm - Ph20 = 713 at sea level
Pi02 = 713 x fi02
- Pa02 from Gas
What is a normal Aa Gradient?
What can cause an abnormal gradient?
normal is 5-10mmHg in a non smoker on air. Increaes by 1 with each decade of life
Causes
- Diffusion defect
- V/Qmismatch
- right to left shunt - cardiac or pulmonary
- increased 02 extraction
What are the causes of a low anion gap
Decrease in unmeasured anions (albumin, dilution)
Increase in unmeasured cations (multimyeloma (cationic IgG paraprotein), hypercalcaemia, hypermagnesaemia, lithium OD, polymixin B)
bromide OD (causes falsely elevated chloride measurements)
How do you work out expected co2 in metabolic alkalosis
Expected pco2=
(0.7 x HCO)+ 20 (+/-5)
How do you work out expected co2 in metabolic alkalosis
Expected pco2=
(0.7 x HCO)+ 20 (+/-5)
what are the causes of SIADH
MADCHOP
MAjor surgery eg abdo
ADH from tumours
Drugs - TCA/SSRI
CNS - cerebral tumours/SAH
Hormone deficiency - hypothyroid
Others - GBS/HIV
Pulmonary - pneumonia/TB
