To round out the year, here are three tutorials on the blood gas machine, blood gas analysis and the blood gas printout.
The first tutorial looks at how oxygen is measured using the Clark Electrode on the blood gas analyser and demonstrates the importance of co-oximetry in modern blood analysis. From that the fractional saturation of hemoglobin with oxygen is derived.
The second tutorial explains the Glass Electrode that measures pH and PCO2. Subsequently I cover problems you might encounter with blood gas sampling. If you don’t want to watch the technical stuff, I strongly recommend you scroll to the middle of the tutorial (12 minutes in) as it covers information that all healthcare practitioners must know.
The final tutorial looks at all of that other data that appears on blood gas printouts that you may never have understood – and it can be really confusing – DERIVED or calculated variables (bicarbonate, temperature correction, TCO2, O2 content, Base Excess, Standard Bicarbonate, Anion Gap etc.). I cover both the Radiometer ABL machines and the GEM 5000. I guarantee you’ll learn something.
As part of my fundamentals of Anesthesiology and Critical Care Series I have posted 3 tutorials on the Role of CO2 /HCO3 in Acid Base Balance. These are entirely new tutorials (not part of the previous acid base series – that I have not finished yet! There is some overlap and updated facts and figures) and I have put a lot of work into getting the message of why the respiratory system is so important in acid base. Tutorial 1 is the basics of acid base. Tutorial 2 discusses respiratory acidosis, acute and chronic, and respiratory alkalosis. Tutorial 3 discusses respiratory compensation for acute metabolic acidosis. Although I cover the respiratory component in great depth, I also explain what metabolic acidosis is, what causes it and briefly discuss the anion gap, expected bicarbonate, base deficit and base deficit gap. I guarantee that you will learn something.
Hyperchloremic Acidosis is a common problem. It is usually an iatrogenic problem. Unfortunately, the majority of doctors who cause a patient to have Hyperchloremic Acidosis (HCA) are either unaware of the problem or ambivalent to it. For the most part, HCA is caused by the intravenous administration of isotonic saline solution (NS – “normal saline – NaCl 0.9%). This problem has been known about for more than 100 years and led Alexis Hartmann, a pediatrician from St Louis, to construct a balanced intravenous fluids, that he called “Lactated Ringers” solution. Ironically, in clinical practice, HCA is induced as part of the local hospital “protocol” for management of Diabetic Ketoacidosis. Inevitably, as the ketones fall, the Chloride rises, and the acidosis persists.
HCA is the only cause of “normal” anion gap metabolic acidosis and is almost always caused, . In the tutorial I explain that HCA is caused by a reduction in the Na-Cl strong ion difference (SID). The acidosis associated with NaCl 0.9% is more complex that merely a rise in plasma Chloride. Other serum electrolytes, Albumin and Hemoglobin are diluted – and this has an alkalinizing effect. Other resuscitation fluids have different impacts on acid base. Hyperchloremia is also a feature of Renal Tubular Acidosis (RTA), various other nephropathies, the administration of acetazolamide and other drugs, and following surgical transplantation of the ureters into the small bowel, If renal function is normal, and the Chloride level is lower than 125mmol/L, then the patient’s kidneys will resolve the problem over 36 to 48 hours. If the Chloride is very high, acidosis will persist, particularly in patients with poor renal function, and Sodium Bicarbonate infusions may be warranted.
This is an opinion piece – a rant if you like about the perceptions and understanding of most healthcare professionals regarding the status of Lactate and Lactic Acidosis. It seems to me that everyone has an opinion on Lactic Acidosis, in my own opinion – they are often misinformed. The bottom line is that the body manufactures and processes vast quantities of Lactate each day and that accumulation of Lactate in the blood – Lactic Acidosis – is a sign of acute illness and multifactorial in origin. The Lactate is not the problem. The Lactate will eventually be processed by the liver and kidneys. You need to identify the underlying problem and control the source. Moreover, as Lactate is a signalling molecule and part of a multi-system process for energy transmission (the “Lactate Shuttle”), particularly when there is a lot of white blood cell activity, a raised lactate late in critical illness is frequently a sign of tissue healing, rather than acute inflammation. The biggest problem that I encounter, on a daily basis is the binary belief that hyperlactatemia means global oxygen debt. Certainly it is associated with hypovolemia (which can be identified by capillary refill time and mixed venous oxygen saturation) but more often it is associated with increased catecholamines associated with the stress response. If you are playing lactate-fluid “whack a mole” – each blood sample leads to a fluid bolus, your patient will become fluid overloaded very quickly. The latter is strongly associated with worse outcomes in critical illness.
I make the following points in this tutorial.
Most clinicians overestimate their knowledge of lactate and consider it a waste product of aerobic metabolism. Lactate is likely the end product of glycolysis and a major fuel source for the body. Lactate is always an Arrhenius acid in the body. Lactate is not a good endpoint of resuscitation (“clearance”). Using Lactate “clearance” as an endpoint usually results in excessive fluid resuscitation. High Lactate and Low Glucose is an Ominous Sign. Nobody can be really sure what is in a bag of Hartmann’s Solution (Ringers Lactate). D-Lactate is likely more harmful than you think. There is no specific treatment for Lactic Acidosis.
This is Tutorial 4 in the Acid Base Series – on the topic of Metabolic Acidosis. The tutorial is based on a single blood gas – a random sample that was handed to me in the ICU recently. Blood Gas Used in This Tutorial: pH 7.19 PaCO2 32mmHg (4.1kPa) HCO3- 13.1 BE – 16.5 AG 20 Na+ 126 K+ 3.1 Cl- 96 Lactate- 7.2 Ketones- 0.6mmol/L Albumin 21g/L Creatinine 3.3mg/dl (293mmol/l)
Metabolic Acidosis is characterized by an increase in the relative ratio of strong anions to strong cations in the plasma. The PaCO2 and the Bicarbonate fall in a predictable manner. It is possible to compute the effectiveness of respiratory compensation for metabolic acidosis by using the Winters equation.
To understand the mechanism of metabolic acidosis – caused by accumulation of mineral (Chloride) and organic (Lactate, Ketones, Metabolic Junk Products) anions – one needs to apply the law of Electrical Neutrality. All of the positive charges must equal all of the negative charges. As Bicarbonate is consumed in the process of buffering metabolic acidosis, the change in the Bicarbonate level (downwards) can be used to quantify the degree of acidosis. This is important because the pH may be within the normal range due to respiratory compensation. Be aware that the HCO3- quantum that is displayed on a blood gas is derived from the pH and PCO2 by the Henderson Hasselbalch equation.
Unfortunately, because respiratory abnormalities may complicate the diagnosis of metabolic acidosis, and pH and PCO2 are altered by changes in temperature, the precision of a single reading of PCO2 and HCO3- may be poor. Consequently, the Standard Base Excess was developed to excise the respiratory component from the change in bicarbonate. Again it is a derived variable and may be imprecise. Nevertheless, BE (or 1-BE the Base Deficit BD) is a terrific scanning tool to identify the presence of a metabolic acidosis (BD) or alkalosis (BE). It is defined as the amount of strong cation (BD) or strong anion (BE) required to bring the pH back to 7.4 when the temperature is 37 degrees Celcius and the the PaCO2 is 40mmHg or 5.3kPa.
The Base Deficit does not indicate the source of the acidosis, but it can be recalculated to remove the impact of the [Na+], the [Cl-], the body water and the serum Albumin (and the Lactate) to determine the Base Deficit Gap – indicative of the quantity of Unmeasured Anions (UMA, Ketones, if not measured, and Renal Acids (metabolic junk products – MJP).
Traditionally clinicians use the Anion Gap to determine whether a patient has a Hyperchloremic Acidosis (no gap) from a UMA acidosis. I find this quite a dated concept. If the [Cl-] exceeds 105 and the plasma Sodium is normal, the patient has a Hypercloremic acidosis. We can easily measure Ketones and Lactate. The AG is imprecise and should be adjusted for the Albumin level, which tends to hover around 25g per liter in critically ill patients (narrowing the Gap and alkalinizing the patient). I do think if you are calculating the AG that you must include the K+ on the Cation side, the Lactate on the Anion side and adjust the Albumin.
The Strong Ion Gap is a more advanced, more precise and more cumbersome version of the AG. Regardless of the approach, one eventually ends up with a quantify of unidentifiable anions (SIG) that may be of medley origin (metabolism, poisoning etc). It is my opinion that it is useful to tease out all of the different acidifying and alkalinizing processes (the Fencl approach) to determine what is going on with the patient. All of these calculations can be done in seconds with smartphone apps and spreadsheets.
ORtoICU 