ABG's and sepsis

Alright, I had a patient recently who was septic, on dopamine and vasopressin. The nurse giving me report stated "he needs more fluid" and she was looking at his ABG. Is there some connection between fluid status and HCO3 or BE? I couldn't figure it out, I gave her report in the AM and she stated "oh, he still needs fluid" again looking at the ABG! Help...I'm lost!

Without knowing the entire patient 'picture' it's difficult to give you a straight answer. By looking at ABG's in a vaccum, you can't determine if a patient needs fluids or not.

However....

In Septic-shock type patients, profound metabolic acidosis can develope because of poor perfusion/hypotension...AND...one of the first things you do for septic shock to improve perfusion/bp is to give LOTS of fluids.

So...my guess is the ABG's showed a metabolic acidosis (most likely from hypotension/lactic acidosis)and your co-worker was thinking about 'filling the patient's tanks' so to speak...

OR...she was blowing smoke and trying to impress you (???) because you cant glance at an ABG blindly and detremine if fluids need to be given...BECAUSE there're several causes of metabolic acidosis other than sepsis-induced hypotension (ie DKA, renal failure, drugs, etc.)

So you see...difficult to answer with your limited info...but she may have been kinda sorta maybe right....in a convoluted sense...

A negative base excess general indicates the need for some fluid to correct the metabolic imbalance that exists.

If pH and Hc03 is elevated it is metabolic alkalosis. Just try to remember there are 4 types of interpretation...and 4 'relative' treatments:

Resp. Acidosis.....(not ventilating)most common--------trmt:Ventilate

Resp. alkalosis.....(hyperventilating)--------------------trmt:slow down or decrease ventilation.

Met. Acidosis........(not enough Hc03 in blood)------------------trmt:Hc03

Met

Met. Alkalosis......(to much Hc03 in blood)--------trmt:give fluids

This is kinda basic but dont put to much more into it.

www.theabgsite.com.

www.treatingmetabolicalkalosiscaremark.com.

good luck

A negative base excess general indicates the need for some fluid to correct the metabolic imbalance that exists.

Yes, you're mostly right, but there're instances where a patient can be in metabolic acidosis and fluid bolus would be detrimental. The most obvious/common would be an acute renal failure (acidotic on ABG with low Base Excess) who is also anuric and volume overloaded ...which is why you can't determine what treatment a patient needs by simply looking at an ABG in a vaccuum.

Rather than the need for fluids, a low base excess would more likely indicate a need for bicarb administration. (and fluids in many instances).

I think the nurse the OP was reporting off to was correct in that the patient may have needed fluids...but the ABG was just part of the equation though the OP asumed it was soley dependant on ABG analysis. ...i think

Why didn't you ask her what value she was looking at and how it was indicator of the need for more fluid? It can be tough admitting that you don't know something, but it's a good way to learn. Do you remember what the ABG was? Was the bicarb really high or really low?

metabolic acidosis and alkalosis

page index

metabolic acidosis.

the following is a brief summary. for additional information visit: e-medicine (christie thomas) or wikepedia

etiology: there are many causes of primary metabolic acidosis and they are commonly classified by the anion gap:

metabolic acidosis with a normal anion gap:


• longstanding diarrhea (bicarbonate loss)
  
• uretero-sigmoidostomy
  
• pancreatic fistula
  
• renal tubular acidosis
  
• intoxication, e.g., ammonium chloride, acetazolamide, bile acid sequestrants
  
• renal failure

metabolic acidosis with an elevated anion gap:


• lactic acidosis
  
• ketoacidosis
  
• chronic renal failure (accumulation of sulfates, phosphates, uric acid)
  
• intoxication, e.g., salicylates, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde, inh, toluene, sulfates, metformin.
  
• rhabdomyolysis

for further details visit: e-medicine (christie thomas).

treating severe metabolic acidosis.

the ideal treatment for metabolic acidosis is correction of the underlying cause. when urgency dictates more rapid correction, treatment is based on clinical considerations, supported by laboratory evidence. the best measure of the level of metabolic acidosis is the standard base excess (sbe) because it is independent of pco2. if it is decided to administer bicarbonate, the sbe and the size of the treatable space are used to calculate the dose required:

metabolic alkalosis

etiology: primary metabolic alkalosis may occur from various causes including:

• loss of acid via the urine stools, or vomiting
  
• transfer of hydrogen ions into the cells
  
• excessive bicarbonate administration, e.g. alkali given to patients with renal failure.
  
• contraction of the extracellular space due to excessive diuretic treatment

prolonged metabolic alkalosis may be caused by a number of different mechanisms:

• decrease in renal perfusion: occurs in dehydration, cardiac failure, or cirrhosis, stimulates the renin-angiotensis system which increases sodium reabsorption in the nephron.
  
• chloride depletion: may occur via vomiting or through the use of loop diiuretics and this enhances bicarbonate reabsorption with associated hydrogen ion loss.
  
• hypokalemia: metabolic alkalosis may be associated with hypokalemia which can then maintain metabolic alkalosis by various mechanisms:
  • shift of hydrogen ions intracellularly which enhances bicarbonate reabsorption in the collecting duct.
    
  • stimulation of the h+/k+ atpase in the collecting duct: this leads to potassium ion reabsorption and hydrogen ion secretion. the net gain of bicarbonate maintains the metabolic alkalosis.
    
  • renal ammonia genesis: ammonium ions (nh4+) are produced in the proximal tubule from glutamine metabolism. alpha-ketoglutarate is produced the metabolism generates bicarbonate.
    
  • impaired chloride ion reabsorption in the distal nephron increases luminal electronegativity with enhanced hydrogen ion secretion.
    
  • lowered glomerular filtration rate (gfr). hypokalemia may decrease gfr, which in turn decreases the filtered load of bicarbonate. in volume depletion this impairs excretion of the excess bicarbonate.

treating severe metabolic alkalosis

physiological response: adequate hydration normally allows the kidneys to correct the problem. however, in severe cases accompanied by hypokalemia, correction of the hypokalemia may be necessary first.

as with metabolic acidosis, ideal treatment is the correction of the underlying abnormality. more active intervention is occasionally required and various techniques are available. a common transient cause is iatrogenic; correction of acute metabolic acidosis with sodium bicarbonate leaves a residual metabolic alkalosis. time, hydration, and renal function should gradually correct this.

contraction alkalosis is one of the easier causes to understand and treat. dehydration concentrates the body's electrolytes. as the extracellular fluid (ph = 7.4) is on the alkaline side of neutral (ph = 6.8), the relative alkaline mixture of electrolytes is concentrated and shifts the ph to more alkaline value. rehydration, e.g., with oral fluids or intravenous ringer's lactate, restores the normal electrolyte concentration and, therefore, the ph.

other therapies: intravenous dilute hydrochloric acid is occasionally used but carries the risk of hemolysis. potassium chloride may also be used unless there is kidney failure. in severe cases which are unresponsive to other measures ammonium chloride may be given (1 to 2 g orally every 4 to 6 hours up to 4 g every 2 hours. it may also given by intravenous infusion (100 to 200 meq dissolved in 500 to 1000 ml of isotonic saline) in addition to potassium replacement. in severe unresponsive metabolic alkalosis it may be necessary to administer hydrochloric acid or institute peritoneal dialysis.

specific therapy depends on the underlying pathology. for details visit: e-medicine (christie thomas).

emergency therapy.

the body's metabolism produces respiratory (carbonic) acid and, in ischemia or cardiorespiratory failure, metabolic (lactic) acid. in emergencies, therefore, urgent correction is most commonly required for metabolic or respiratory acidosis.

calculating the bicarbonate dose.

(move mouse over the diagram)

the diagram shows an example of a patient with a (pure) metabolic acidosis, sbe = -18 meq/l. to achieve complete correction for someone weighing 70 kg:

dose (meq) = 0.3 x wt (kg) x sbe (meq/l)

378 = 0.3 x 70 x 18

this assumes that the treatable compartment is about 30% of the body, i.e., about 21 liters. our intention , of

Maybe someone can make heads or tails of this:w00t:

good luck!

I'm guessing like most other posters that the ABG was part of the puzzle. It is very difficult to claim that a patient needs more fluid on the basis of a single factor. Most experienced crit care nurses can read the monitor and gain insight into the patient's fluid state and needs by putting together all the information that is generally available on site from the monitor eg Hr BP BP waveform (resp swing) CVP etc. ?Perhaps the ABG was just the icing on the cake?

I'm guessing like most other posters that the ABG was part of the puzzle. It is very difficult to claim that a patient needs more fluid on the basis of a single factor. Most experienced crit care nurses can read the monitor and gain insight into the patient's fluid state and needs by putting together all the information that is generally available on site from the monitor eg Hr BP BP waveform (resp swing) CVP etc. ?Perhaps the ABG was just the icing on the cake?

What's "resp swing"?

Thanks!

What's "resp swing"?

Thanks!

I'm assuming the poster was referring to resp variation in the CVP waveform - not in the A-line tracing?

No I am refering to the change in a line tracing on inspiration for the ventilated patient. Increased thoracic pressure increases afterload and decreases preload resulting in reduced stroke volume in patients who are vascularly dry. This is similar to the stroke volume variance via PICCO etc though unlike the SVV there is no objective measure. CVP may swing however the changes in pressure will be so small that it would be difficult to see from the end of the bed. Again however it is difficult to make the call whether someone is vascularly dry and requires more fluids based on a single piece of data.

:cheers: