IV fluids
Function
N saline
Hypertonic
saline (7.5%)
0.45% saline
Hartmann’s
Ringer’s
lactate
5% dex
10% dex
NaHCO3
Gelofusin
4% Albumin
20% Albumin
Mannitol
Crystalloids vs
colloids
PRBC
300ml bags
(500ml in
whole blood)
Restore IV vol sufficient for critical organ perfusion; maintain O2-carrying capacity of blood for adequate delivery;
correct derangement in coag
Na 150
Cl 150
Osm 300
pH 5.3
Indications: replacement of ECF losses, hypoNa, shocked paeds
SE: hyperCl metabolic acidosis if large amounts
CI: hyperNa, hyperCl, maintenance in paeds
Na Cl Osm pH
Draws water from ISF to IVF  rapid expansion of intravascular space in minimal time; decr SVR (due to vasoD);
interstitial dehydration  decr ICP and cerebral oedema
Indication: HI
Dose: 250ml dose (equivalent of 2L saline)
SE: phelbitis, fluid overload, hyperNa, osmotic demyelination syndrome
Na 75
Cl 75
Osm pH
nd
Indication: in 2 hr of trt of DKA (avoid hyperCl), trt of hyperNa due to ECF loss
Na 131
Cl 111
K5
Ca 2
Osm 278
pH 6
Lactate 29
Physiological electrolyte replacement
CI: lactic acidosis, hyperCa/K, hypothermia, clots with blood transfusion
Pros: buffers acidaemia
Cons: hyperK if renal insufficiency
Na Cl Osm 278 pH
Glu 50g/L
Indications: DM, hyperNa, most effective for establishing urine flow in euvolaemic patient
Na Cl Osm pH Glu 100g/L
Indications: DKA where normoG but still incr ketones; persistent hypoG unable to eat; sick neonate
See below
Na 154
Cl 120
Osm 274
pH; vascular expansion lasts 3-4hs; anaphylactoid reactions
Na 140
Cl 128
K 0.12
Osm 250
pH 7
Alb 40g/L
Indications: hypoV with incr cap perm or hypoAlb; burns after 12hrs; shock and alb <20; therapeutic plasma exchange
SE’s: fluid overload, infection, expensive
Na 5.5
Cl
Osm 80
Alb 20g/100ml
Indications: diuresis in hypoproteinaemia; shock and alb <20; haemolytic disease of newborn
0,.5-1g/kg over 30mins
SAFE study: No significant difference between albumin (colloid) and saline (crystalloid) in fluid resus of ICU patients in
terms of ICU/hospital LOS, duration of mechanical ventilation; subset showed decr mortality in sepsis (statistically
insignificant), incr mortality in HI
Interstitial dehydration may be good in some circumstances (eg. ARDS, HI)
Indications: Hb <7, Hb <10 and symptoms or active bleeding
O neg low titre: immediate
Group specific: 10mins; O 46% > A 39% > B 11% > AB 3.5%; Rh +ive 80%, Rh-ive 20%
XM: 30mins; clinically significant ab’s present in 2% ED patients (5% haem/onc patients), incr with age
Effects of storage: incr pH, K, rigidity of cell membrane, citrate
decr T, Ca (due to citrate), 2,3,DPG  L shift
no factor V/VIII activity, no plts
Technique: infuse no faster than 5ml/min for 1st 15mins; compatible only with N saline and 4% alb; slowest rate is
1iu/4hrs; can be stored for up to 30/7; Hct 60-70% (35-40% in whole blood)
Pros: longer life, less storage problems, less Ags
Cons: slower flow, smaller vol, higher viscosity; can’t give meds through same line
Complications:
Microaggregates (activate coagulation cascade and complement, impairs microcirculation and O2 delivery)
ABO incompatibility (usually misidentification error)
Citrate toxicity (if >100ml/min; decr ionised Ca, metabolic acidosis, metallic taste / perioral paraesthesia)
HyperK (usually if blood >2/52 old); hyperNa
Hypothermia (shifts curve to L, decr CO)
Febrile non-haemolytic reaction (incidence 0.1-1%; often in multip/multiple transfusions; recipient ab to donor RBC;
dose related, towards end of transfusion 30-120mins in or after transfusion; stop transfusion, check pt and blood
details  if mild (T change <1.5, no rash), restart / if mod (T incr >1.5, urticaria), give anti-histamines and
paracetamol, restart after 20mins / if severe stop, send rpt sample; more common with plts)
Allergy (recipient reaction to pp’s in donor blood; most common with FFP; 1-3% incidence mild reaction, 1:2050,000 anaphylaxis; trt as fever)
FFP
180ml bags
Cryo
Plt
50ml bags
PTX
Factor VIIa
Haemolysis (1:12-77,000; shock, fever, headache, pain, Hburia, ARF, DIC)
Tranfusion related acute lung inj (1:5-10,000; can be fatal; donor ab’s to patient’s WBC’s  pul damage 
SOB, cough, fever, APO within 1-6hrs)
Bacterial contamination (1:500,000; more common with plt)
Immune suppression
Jaundice (30% transfused RBC don’t survive)
Transfusion related disease (eg. HIV 1:5400000, Hep C 1:2700000, Hep B 1:739000, malaria etc..)
GVHD (transfusion of immunocompetent WBC to immunosupp patient; onset 10-14/7  fever, skin rash,
pancytopenia, diarrhoea, abnormal LFT’s; prevent by irradiating blood products)
Available in 30mins; do require ABO compatibility; contains all CF’s + fibrinogen; give at 10ml/min (ie over <1hr); give
4-6iu per 5L blood
Indications: haemorrhage and coagulopathy; reversal of warfarin OD; factor def; AT III def; TTP
Available in 30mins; better if ABO compatibility; contains VIII/XIII, fibrinogen, vWF; give at 10ml/min (ie over <1hr);
give 1iu / 10kg body weight
Indications: bleeding and fib <1
Available in 15-30mins; do not require ABO compatibility; can only be stored 3/7; 1iu  incr plt 5; give 12 units per 5L blood
Indications: plt <10
<20 and fever / antibiotics / evidence of systemic haemostatic failure
<50 and bleeding (or skin bleeding time >2x normal) or OT (<100 if eye / neuro); neurosurg OT on antiplt
DIC / ITP with life-threatening haemorrhage
Contains II/V/VII/IX/X, anti-thrombin and heparin; DOA 12-24hrs; give 3ml/min; give 25-50iu/kg (50iu if INR >6, 35iu if
INR 4-6, 25iu if INR 2-4)
Indications: congenital CF def, warfarin OD and significant bleeding
Pros: small vol, rapid admin, no time delay in thawing (unlike FFP), no ABO typing (unlike FFP), INR reversal within
15mins, no disease transmission
Not demonstrated to improve any clinically significant outcomes in trials; incr mortality in blunt trauma in CONTROL
trial, expensive, requires normal pH and T to be effective; 5% absolute incr risk of VTE; give 90-120mcg/kg
Indications: last resort in generalised bleeding only after control of bleeding obtained; inhibitors to CF VIII/X;
congenital CF VII def; Glanzmann’s thrombasthenia
Notes from: Dunn
MOA
Indications
Use of NaHCO3
8.4% = 1mmol/ml
Bicarbonate load  buffer H, alkaline urine
Na load  additive effect to above to help with Na channel blockade
Hydrofluoric acid toxicity
Correction of severe metabolic acidosis: 0.5mmol/kg for each desired incr in HCO3; endpoint HCO3 >8, clinical
improvement of shock / dysrhythmias; incr pH to no greater than 7.2
HCO3 <3, pH <7.2, severe hyperchloraemic acidaemia
Cyanide poisoning
Isoniazid OD
Ethylene glycol, methanol, other toxic alcohols
Prolonged cardiac arrest (evidence unclear):
Cons: doesn’t improve ability to defib / survival rates in animals; can compromise coronary perfusion
pressure; shifts Ox-Hb curve to L (Hb holds on to O2  tissue hypoxia); produces CO2 
intracellular acidosis; causes hyperosm and hyperNa; exacerbates central venous acidosis; may
inactive adrenaline given; precipitates with Ca; does not correct causes of acidosis
Cardiotoxicity 2Y to fast Na channel blockade (cardiac arrest, VF/VT, hypoT): repeated doses of 2mmol/kg IV until
stability achieved  100mmol diluted in 1000ml N saline at 100-250ml/hr; aim pH 7.5-7.55; stop when no longer
cardiotoxic; will likely need K supplementation
TCA, Type 1a and 1c antiarrhythmics: flecainide, quinidine
Chloroquine / hydroxychloroquine
Antihistamines
Antimalarials (quinine)
Phenothiazines (eg. Stemetil, chlorprom)
Cocaine, carbamazepine
Propanolol, LA, type IV, amantadine
Urinary alkalinisation in OD  enhanced elimination: 1-2mmol/kg IV bolus  100mmol in 1L 5% dex at 250ml/hr;
add 20mmol KCl to infusion to maintain normal K; aim urinary pH >7.5
Salicylate – moderate severity not requiring haemodialysis (pH <7.1)
Phenobarbitone – if continued toxicity despite MDAC
Methotrexate
Methanol
Rhabdo and myoglobinuria renal failure
Urinary sepsis, RTA type 1
Prevention of drug redistribution to CNS – incr unionized amount of drug
Salicylate
SE’s
CI’s
Severe hyperK: 50-100mmol slow IV (1mmol/kg in children)
Extravasation, gastric distension, hyperNa, hyperosmolality, vol overload, pul oedema, alkalosis (pH >7.6 bad for CV
function), L shift of O2-Hb diss curve (impaired O2 unloading), hypoK, hypoCa (usually not clinically significant); incr
lactate production (decr citrate and lactate metabolism); resp acidosis (ventilation must account for incr CO2
production)
HypoK, hypoCa, alkalosis, acute pul oedema, renal failure, severe hyperNa
tone