Intensive care Flashcards
Is it reasonable to start renal replacement therapy for a fluid overload pt unresponsive to diuretics?
Yes
What are some indications for renal replacement therapy?
- Fluid overload unresponsive to diuresis
- Dialyzable toxins (lithium, toxic alcohols, theophylline, salicylate, sodium valproate)
- Hyperkalemia (eg. >6.5 & rapidly rising, refractory to medical therapy)
- Severe temp derangement (eg. >40deg C)
- severe electrolyte derangements (eg. Na <110 or >160mmol/L)
- symptomatic uraemia (esp if >35mmol/L)
- uncompensated metabolic acidosis (pH <7.1)
What’s the preferred site for a vas Cath?
femoral, then 2nd choice is internal jugular & subclavian= last choice. Because the femoral has longest mean run time.
What are benefits of the subclavian site for central access but why are they the last resort for vas cath?
have the lowest infection rates, they are more comfortable BUT they have higher complication rate (eg. DVT, PE, chronic limb oedema) & are a contraindication to future formation of AVF for LT dialysis if brachiocephalic vein thrombosis & stenosis. Also provide relatively ineffective flows.
Which site is preferred for vas cath when it comes to the IJ.. R) or L)?
right
When should the femoral vein site be avoided for venous access?
- aiming for early mobilisation (esp in the case of dialysis)
- renal transplant pts (because thrombosis of femoral veins would seriously impair venous outflow from the transplant)
- massively obese (higher risk CRBI & risk of access failure w femoral placement)
What French catheter is used for vas Cath for RRT? why?
14.5
balance btwn thrombosis risk (higher w larger catheters) & achieving adequate flow (need 200-300mL/min for adequate RRT & maximising filter life)
what does French refer to? how to calculate the diameter?
French= the external circumference in mm
divide it by pi to get diameter
Where should the tip of a vas Cath be?
in the SVC-RA junction or even in the RA
What’s the purpose of the underwater seal drain?
The underwater seal prevents the inward movement of air. It excludes air from re-entering the chest cavity via the chest tube
Systematic approach to ABGs:
1-pH: what’s the primary process? academia or alkalemia, is the pCO2 contributing or reacting to the change in pH?
2-Is there compensation for the primary disorder? (assess respiratory compensation according to the CO2, metabolic according to SBE with normal being -3 to +3)
Is the compensation adequate? (chronic acid-base disorders may compensate the pH fully, acute respiratory disorders or metabolic acid-base disorders will not)
respiratory acidosis: acute: bicarb incr 1mmol per 10mmHg PaCO2 above 40, chronic: bicarb incr 4mmol for every 10mmHg PaCO2 above 40
resp alkalosis: acute: 2mmol decr bicarb for every pA CO2 decr of 10mmHg (acute res disturbance rarely results in bicarb <18; if so, suggests coexisting met acidosis), chronic bicarb 5mmol decr for every 10mmHg CO2
metabolic disorders:
PaCO2= (1.5x bicarb) + 8 for met acid
(0.7 x bicarb) +20 for met alk
also, for met acidosis, change in PaCO2 = 1.2 x SBE
met all: change in PaCO2 is 0.7 x SBE
-If a metabolic acidosis/alkalosis is present, how severe is it? stratify according to magnitude of SBE derangement (+/-4= mild, +/-10=mod, +/-14=severe)
3-What’s the anion gap? (normal=12, not including potassium, so use: ( [Na+] - [Cl- + HCO3-] ). it drops by 1 for every 4g/L of alb lost. delta ratio is the (change in anion gap/change in bicarb)
4-Is the increase in anion gap accompanied by a reduction in SBE or bicarb? the DELTA RATIO= (change in AG/change in bicarb); any incr in AG should be matched by a decr in SBE or bicarb, mole for mole- any deviation= mixed disorder, ie:
DR <0.4= pure NAGMA
0.4-0.8= combined HAGMA & NAGMA
0.8-2= pure HAGMA
>2= magma and co-existing met alk
5-What’s the cause of increased anion gap?
Causes of a metabolic acid-base disorder:
HAGMA=
MUDPILES
methanol, uraemia, DKA, pyroglutamic acidosis, iron overdose, lactic acidosis, ethylene glycol, salicylates
NAGMA: PANDARUSH
pancreatic secretion loss, acetazolamide, N/S intoxication, diarrhoea, aldosterone antagonists, RTA1 (distal), ureteric diversion, small bowel fistula, hyperalimentation (TPN)
Metabolic alkalosis
Cl depletion:
gastric losses (vomit/drainage), diuretics (loop or thiazides),diarrhoea, posthypercapnic state, dietary Cl deprivation, gastrocystoplasty, CF (high sweat Cl depletion)
bicarb excess (renal or apparent):
iatrogenic alkalisation, recovery from starvation, hypoallergenic
potassium depletion:
primary hyperaldosteronism, mineralocorticoid over supplementation, liquorice, B-lactams, severe HTN, laxative abuse
Ca++ excess:
malignancy, milk-alkali syndrome
- is there hypoxaemia?
- what’s the A-a gradient? (PAO2) = (FiO2 x 713(760-47)) - (PaCO2 x 1.25); normal is 10mmHg, add 1mmHg per decade of life
- P/F ratio for ARDS: 300-200 = “mild” ARDS, 27% mortality, 200-100= moderate, 32% <100= severe (45%)
