Data interpretation Flashcards
7 LFTs
ALT AST ALP GGT bilirubin albumin prothrombin time
2 things ALT, AST, ALP and GGT are used to distinguish between
hepatocellular damage and cholestasis
what are bilirubin, albumin and PT used to assess
liver’s synthetic function
what is ALT a marker of
raised in acute hepatocellular injury
what is ALP a marker of
raised in cholestasis
what is a raised ALP, GGT and bilirubin suggestive of
cholestasis
4 causes of an isolated rise in ALP (i.e. GGT not raised too)
bony metastases/primary bone tumours
vit D deficiency
recent bone fractures
renal osteodystrophy
this is because ALP is also present in bone
what is an isolated rise in bilirubin suggestive of
pre-hepatic cause of jaundice
most common cause of isolated jaundice (just bilirubin raised)
Gilbert’s syndrome (also haemolysis common)
where is albumin made
liver
3 reasons why albumin levels can fall
liver disease e.g. cirrhosis = decreased production
inflammation
protein-losing enteropathies or nephrotic syndrome = excessive loss
when is ALT>AST seen
chronic liver disease
when is AST>ALT seen
cirrhosis
acute alcoholic hepatitis
what does a low paO2 and high paCO2 suggest
type TWO respiratory failure
what would a high HCO3 indicate in respiratory acidosis
metabolic compensation for respiratory acidosis = chronic
how does a high HCO3 affect base excess
increases base excess
cause of type 2 respiratory failure
ventilatory failure e.g. COPD, asthma, opiates, chronic bronchitis, MND, ankylosing spondylitis
what does a high pH and low CO2 show
respiratory alkalosis
ABG result if there was metabolic alkalosis
high HCO3/BE
cause of respiratory alkalosis
increased ventilation (increased RR) e.g. anxiety, pain, PE, pneumothorax
what does a high pH, normal CO2 and high HCO3/BE indicate
metabolic alkalosis
common cause of metabolic alkalosis
vomiting = lose stomach acid (less H+ to bind to HCO3 so more HCO3)
what should paO2 level be if a patient is on oxygen
10kPa less than the inspired concentration (FiO2) of oxygen e.g. 22% when there is 32% oxygen given
what does a normal paO2, low pH, normal paCO2 and low HCO3/BE indicate
metabolic acidosis
2 potential causes of metabolic acidosis
sepsis - lactic acidosis from tissue hypoxia
DKA
what would indicate respiratory compensation in metabolic acidosis
low CO2 (hyperventilation)
what does a low paO2 and a normal paCO2 suggest
type ONE respiratory failure
7 uses of PURPLE blood bottle (whole blood)
FBC ESR blood film reticulocytes monospot test (EBV) HbA1c PTH
2 uses of PINK blood bottle (transfusion lab)
group and save
crossmatch
4 uses of BLUE blood bottle (clotting)
coagulation screen (PT, APTT, TT)
D-dimer
INR
anti-Xa assay
9 uses of GOLD blood bottle (wide range of tests)
U&Es CRP LFTs amylase TFTs vitamins troponins and CK lipid profile tumour markers
2 uses of GREY blood bottle
glucose
lactate
3 uses of DARK GREEN blood bottle
ammonia
insulin
renin and aldosterone
lid colour of blood culture bottle for aerobic culture media
blue
lid colour of blood culture bottle for anaerobic culture media
purple
lid colour of blood culture bottle for mycobacterial cultures
black
order of draw of blood bottles
blood cultures light blue gold purple pink grey
cause of type ONE respiratory failure (low paO2 and normal paCO2)
V/Q mismatch - e.g. from pulmonary oedema, bronchoconstriction, PE
how is INR calculated
from a prothrombin time result
normal INR in healthy people
<1.1
INR range to aim for in those taking warfarin
2-3
what does a high INR mean
blood clots more slowly than desired
what does a low INR mean
blood clots more quickly than desired
4 causes of high INR (and therefore slow clotting)
Blood-thinning medications
Liver problems
Inadequate levels of blood clotting proteins
Vitamin K deficiency
2 causes of low INR (and therefore fast clotting)
high vit K levels e.g. supplements
high oestrogen e.g. HRT or OCP
normal speed of paper on an ECG
25mm/s
what does PR interval represent
time taken for electrical activity to move between atria and ventricles
what does ST segment represent
time between depolarisation and repolarisation of ventricles (CONTRACTION) - end of S-wave to start of T-wave
how is ventricular repolarisation represented
T-wave
how is the time taken between ventricular depolarisation and repolarisation represented
QT interval
where to put V1
4th intercostal space - right sternal edge
where to put V2
4th intercostal space - left sternal edge
where to put V3
midway between V2 and V4
where to put V4
5th intercostal space - midclavicular line
where to put V5
left anterior axillary line - same horizontal level as V4
where to put V6
left mid-axillary line - same horizontal level as V4 and 5
mnemonic for 4 limb electrodes
ride (red - right arm)
your (yellow - left arm)
green (green - left leg)
bike (black - right leg)
3 leads representing inferior heart
II
III
aVF
4 leads representing lateral heart
I
aVL
V5
V6
2 leads representing anterior heart
V3
V4
2 leads representing septal heart
V1
V2
how much does one small square on ECG represent
0.04 seconds
how many large squares is 1 second
5 - each is 0.2 seconds
how many large squares in 1 minute
300
normal cardiac axis?
-30 to +90 degrees
how to see if there is a normal cardiac axis
look at lead I and lead III/aVF - both pointing up = no axis deviation
how to see if there is left axis deviation
I and III/aVF leaving each other - LEFT = left deviation
how to see if there is right axis deviation
I and III/aVF are pointing towards each other - Reaching = Right deviation
right ventricular hypertrophy, pulmonary conditions and very tall people can all show what on ECG?
right axis deviation (+90 to +180)
conduction defects can show what on ECG?
left axis deviation (-30 to -90)
how to calculate heart rate from ECG if regular
count number of large squares in 1 RR interval and divide 300 by this number
how to calculate heart from ECG if irregular
count number of complexes on rhythm strip (each strip = 10 seconds) then X by 6
what should PR interval be
120-200ms (3-5 small squares)
sign of 1st degree heart block (AV delay)
PR interval >200ms or 5 squares (long)
cause of 2nd degree heart block
intermittent failure of conduction from SAN - often from drugs or structural heart defects e.g. post MI when arteries aren’t supplying some of the nerve fibres
sign of Mobitz type 1 2nd degree heart block
progressive lengthening of PR interval until non-conducted P wave
sign of Mobitz type 2 2nd degree heart block
PR interval constant and 1 P wave not conducted
sign of 3rd degree heart block (complete heart block)
completely unrelated P waves and QRS complexes
only treatment for complete heart block
pacemaker
location of 1st, 2nd and 3rd degree heart block on the heart
1st = between SAN and AVN
Mobitz 1 = in AVN
Mobitz 2 = after AVN in bundle of His or Purkinje fibres
complete = anywhere from AVN down
normal QRS complex length
<0.12 seconds
2 signs of Wolff-Parkinson white syndrome on ECG
- short PR interval (uses a faster shortcut pathway)
- delta wave (slurred upstroke of QRS)
sign of ventricular hypertrophy on ECG
tall QRS complex
when is ST elevation significant
> 1mm (1 small square) in 2+ contiguous limb leads
> 2mm in 2+ chest leads
sign of myocardial ischaemia on ECG
ST depression >0.5mm in >2 contiguous leads
2 causes of tall T waves
hyperkalaemia
hyper acute STEMI (first 30 mins)
2 leads where T waves are normally inverted
V1 III (normal variant)
5 causes of inverted T waves in other leads
ischaemia bundle branch block PE LVH hypertrophic cardiomyopathy
T waves are inverted in which 3 leads in LBBB
V4
V5
V6
T waves are inverted in which 3 leads in RBBB
V1
V2
V3
are there Q waves in NSTEMI
no - but there is ST depression and T wave inversion
2 causes of biphasic T waves
ischaemia
hypokalaemia
2 causes of U waves
hypokalaemia or hypothermia
anti-arrythmic therapy e.g. digoxin or amiodarone
SBARR stands for
- situation (who where when what why)
- background
- assessment
- recommendation (both state diagnosis and ask for advice)
- response/review/read back
8 things to include in background
PC date of admission current diagnosis relevant past medical and surgical history medications allergies investigation results any interventions tried and patient's clinical response to them
3 things to include in assessment
vital signs
clinical exam findings
overall clinical impression
length of time to administer bolus of IV drugs
3-5 minutes
length of time to administer intermittent infusion of IV drugs
15 min-2 hours
size syringe for flushing
10ml
technique used to flush
positive pressure technique (push-pause injecting 1ml at a time)
2 types of IV fluids
crystalloid (small particles e.g. 0.9% saline, 5% dextrose
colloid (large particles e.g. gelofusin)
3 parts to the GCS
eye opening (out of 4) verbal response (out of 5) motor response (out of 6)
4 aspects of eye opening for GCS (4, 3, 2, 1)
spontaneously = 4
to speech = 3
to pain = 2
no eye opening = 1
5 aspects of verbal response for GCS (5, 4, 3, 2, 1)
oriented, time, place, person = 5 confused, conversation = 4 inappropriate words = 3 incomprehensible words = 2 no verbal response = 1
6 aspects of motor response for GCS (6, 5, 4, 3, 2, 1)
obeys commands = 6 moves to localised pain = 5 flexion withdrawal from pain = 4 abnormal flexion = 3 abnormal extension = 2 no response = 1
monitoring if NEWS 0
12 hourly
monitoring if NEWS 1-4
minimum 4-6 hourly, inform nurse who needs to assess
monitoring if NEWS 3 in one parameter, or 5-7
minimum 1 hourly, med team urgent assessment
monitoring if NEWS 7+
continuous monitoring, med team immediately informed, emergency assessment, HDU/ITU
