Surgical Critical Care

Eating Batteries, Drinking Alien’s Blood – Part 2

Anger is an acid that can do more harm to the vessel in which it’s stored than to anything on which it is poured.

Mark Twain

Welcome back, guys… Last time we left with an overview of how to read a blood gas. In this post, we will go through the main causes of acid-base derangements, and how to identify them on the blood gas…

Let’s don’t waste time and start…

Introduction

As we have seen the last time, four main groups of disorders alter the acid-base balance within our body, and these groups belong to two main regulatory systems:

  • Metabolic system
    • Metabolic acidosis
    • Metabolic alkalosis
  • Respiratory system
    • Respiratory acidosis
    • Respiratory alkalosis

Let’s see each one of them separately…

1. Metabolic Acidosis

The causes of this derangement can be divided into two main groups:

  • Increase in H+
    • Diabetic ketoacidosis
    • Chronic renal failure
    • Sepsis (increase in lactates)
    • Intoxication (e.g. salicylic acid, ethylene glycol)
  • Decrease in HCO3
    • Gastrointestinal loss (e.g. diarrhea)
    • Reduced renal reabsorption (e.g. tubular acidosis)

In this setting, the anion gap (AG) takes its importance. In fact:

  • ↑AG (aka high AG acidosis) – represents an elevation in strong (readily dissociated) acids (i.e. H+) in the extracellular fluid. Possible causes are lactic acidosis, ketoacidosis, end-stage renal failure (secondary to the loss of function in the distal renal tubules to secrete/eliminate H+), ingestion of methanol, ethylene glycol, or salicylic acid.
  • Normal AG (aka normal AG acidosis or hyperchloremic metabolic acidosis) – represents the loss of bicarbonates. Possible causes are diarrhea, high volume of normal saline infusion, early renal failure (secondary to the loss of function in the proximal tubules to reabsorb HCO3), acetazolamide intake, ureteroenterostomy.
  • ↓AG – may be found in the case of nephrotic syndrome (loss of albumin), lithium intoxication, or hyperviscosity due to hyperlipidemia.

Remember that albumin is the principal unmeasured anion, contributing to about 3 mEq/L to the AG for each 1 g/dL of albumin in the plasma at a normal pH. Therefore, hypoalbuminemia lowers the AG, requiring an adjustment in its value:

AG adjusted = AG + [2.5 x (4.5 – Plasma Albumin in g/dL)]

From the clinical point of view, patients with metabolic acidosis may have:

  • Headache, confusion, loss of consciousness, coma
  • Hyperventilation (this is the compensatory response, trying to eliminate CO2)
  • Vasodilation, decreased blood pressure, warm and flushed skin
  • Fatigue, muscle twitching
  • Nausea, vomiting (to eliminate H+)
  • Arrhythmias (if hyperkalemia)

The treatment is based on treating the underlying cause. The correction of the acidosis with sodium bicarbonate should be used only in severe cases (i.e. pH <7.2).

Now, let’s briefly talk about the main causes of metabolic acidosis…

  1. Lactic Acidosis
    Serum lactates are normally below 2.2 mmol/L. When their level increases above that value something’s wrong. There are two main causes for lactic acidosis, dividing this condition into two groups:
    1. Type A Lactic Acidosis – secondary to tissue hypoperfusion or hypoxia (e.g. cardiogenic shock, septic shock, hemorrhagic shock, acute hypoxia, carbon monoxide poisoning, anemia, etc…);
    2. Type B Lactic Acidosis – not associated with hypotension and hypoxia (e.g. hereditary enzyme deficiency (glucose 6-phosphatase), drugs and toxins (e.g. metformin, cyanide, salicylic acid, ethylene glycol, methanol, linezolid, propofol, isoniazid, etc…), systemic disease (e.g. liver failure, malignancy)).
  2. Alcoholic Ketoacidosis
    This is a sporadic condition that occurs in alcoholics who binge drink. It manifests after 1-3 days of heavy drinking with abdominal pain, vomiting, dehydration, electrolytes, and metabolic imbalances (e.g. hypokalemia, hypomagnesemia, hypoglycemia, hypophosphatemia). The diagnosis is obtained by measuring the β-hydroxybutyrate levels in the blood. It resolves in 24 hours administering dextrose-based solutions and thiamine.
  3. Renal Tubular Acidosis
    It is a sort of chronic metabolic acidosis that can be divided into 4 types according to the level of the renal tubules involved and the mechanism behind it:
    1. Type 1 – Distal: the kidney is not able to eliminate H+ at the level of collecting tubules. This leads to a reduction of K+ that is not resorbed anymore, and it is expelled with the urine. In this type of renal tubular acidosis, acidosis may be very severe;
    2. Type 2 – Proximal: the reabsorption of HCO3 is insufficient in the proximal tubules, causing an osmotic effect leading to an increased diuresis and, consequently, hypovolemia. To mitigate this effect, the kidney starts increasing the reabsorption of Na+ distally, eliminating K+ in the process;
    3. Type 3 – Combined Proximal and Distal;
    4. Type 4 – Absolute Hypoaldosteronism or Aldosterone Insensitivity.

2. Metabolic Alkalosis

The possible causes are multiple, and even in this case it is possible to divide them into two main groups:

  • Decrease in H+
    • Gastrointestinal loss (vomiting, NG suction, high output fistula)
    • Renal loss (i.e. mineralocorticoid loss, diuretics (i.e. thiazide or loop), hypercalcemia, milk-alkali syndrome)
    • Intracellular shift (i.e. hypokalemia)
  • Increase in HCO3
    • Alkali intake (e.g. citrate, cocaine, NaHCO3)
    • “Contraction” alkalosis (e.g. over-diuresis, villous adenoma)
  • Other
    • Genetic causes (e.g. Bartter’s syndrome, Gitelman’s syndrome)
    • Antibiotics

This condition can be further classified into:

  • Chloride-Responsive [Urine Cl <15 mEq/L] – related to vomiting, NG suction, diuretics, volume depletion, laxative abuse
  • Chloride-Resistant [Urine Cl >25 mEq/L] – primary aldosteronism, licorice ingestion, severe hypokalemia (K+ <2 mEq/L)

Patients with metabolic alkalosis may present:

  • Vertigo
  • Restlessness, seizures, tetanus, tremors, muscle cramps, paresthesia
  • Irritability, dizziness, reduced level of consciousness
  • Arrhythmias (if hypokalemia)
  • Slow and shallow breath (this is the compensatory response, trying to increase CO2)

The possible treatments for metabolic alkalosis are the following (always identify and correct the primary cause):

  • Saline infusion (0.9% NS) is used to correct chloride-responsive metabolic alkalosis
    1. Cl deficit (mEq) = 0.2 x kg x (100 – plasma Cl)
    2. Volume (L) = Cl deficit / 154
    3. Infusion rate 125-150 mL/h above the hourly fluid losses
  • Edematous state
    1. If hypokalemia, correct
    2. Acetazolamide 5-10 mg/kg (PO or IV; peak effect in 15 hours)
  • Hydrochloric acid (0.1N HCl – 100 mEq/L H+): if pH>7.6, metabolic alkalosis uncorrected by other means, and harmful
    1. H+ deficit = 0.5 x kg x (plasma HCO3 – 30)
    2. Volume (L) = H+ deficit / 100
    3. Infusion rate (only via central vein) not above 0.2 mEq/kg/h (stop when pH<7.6)

3. Respiratory Acidosis

It is caused by hypoventilation, which increases the CO2 and, consequently, the dissociated H+. This condition may be secondary to:

  • Central problems
    • Brain lesion
    • Depression to the respiratory center (e.g. alcohol, opioids or benzodiazepines intoxication, anesthesia)
  • Respiratory problems
    • Lungs (e.g. pneumonia, atelectasis, emphysema, COPD, pneumothorax)
    • Airways obstruction

From the clinical point of view, patients present:

  • Slow and shallow breath, dyspnea (this is the main problem)
  • Reduced blood pressure with vasodilation
  • Headache, drowsiness, dizziness, disorientation
  • Muscle weakness, hyperreflexia, seizures
  • Arrhythmias (if hyperkalemia)

4. Respiratory Alkalosis

It is secondary to hyperventilation, which increases CO2 elimination, thus reducing the dissociated H+. It may be caused by:

  • Increased respiratory rate/depth of breath because of pain, excessive exercise, panic attack, pulmonary embolism, mechanical ventilation…
  • Central nervous system injury (e.g. encephalitis, meningitis)
  • Respiratory center hyperstimulation (e.g. fever, drug overdose)

Patients affected by this disorder may present with:

  • Tachypnea and deep breathing (this is the main problem)
  • Lightheadedness, lethargy
  • Nausea, vomiting
  • Tetanus, seizures
  • Numbness, tingling of extremities, paresthesia (if hypocalcemia)
  • Arrhythmias (if hypokalemia)

Before concluding, let’s read one last blood gas:

A 58-year-old woman who, 7 days earlier, underwent Hartmann’s procedure for Hinchey 4 acute diverticulitis. During the ward round she is pale and dyspneic, so an arterial blood gas was done: pH 7.31; pCO2 17.1 mmHg; pO2 91 mmHg; HCO3 8.5 mmol/L; BE -14.9; SatO2 97%; AG 26; Lac 1.3 mmol/L

So, what can we say?

  • pH is low, meaning acidosis;
  • Both pCO2 and HCO3 are low, meaning a metabolic origin (confirmed by the low BE);
  • This is metabolic acidosis with high AG;
  • The ΔPaCO2 in this case is: 1.2 x ΔHCO3 = 1.2 x (24 – 8.5) = 1.2 x 15.5 = 18.6;
  • The Expected PaCO2 is: 40 – 18.6 = 21.4;
  • The Expected PaCO2 is slightly higher than the real one, meaning a respiratory response and a possible respiratory alkalosis (however, the two data are not so different, so that it is more important to focus on the primary disorder);
  • This result is confirmed by the fact that HCO3 is reduced by about 15 points and the PaCO2 by 23 points when they should be reduced by about the same units;

In conclusion, the patient has a high AG metabolic acidosis with a respiratory response and a possible synchronous respiratory alkalosis.

Ok guys… That’s it…

We think we gave you enough information to think about…

Remember that the blood gas gives you more information than the ones we have analyzed in the last two posts. We did not report anything about the respiratory status.

We will talk about that later on…

You just need to remember that the blood gas, along with ultrasound and good clinical examination, can give you enough information to treat almost all the main acute conditions coming in from the ER front door.

See you next time…

References

  1. Berend K, et al. Physiological approach to assessment of acid-base disturbances. NEJM 2014:371:1434-45.
  2. Seifter JL, et al. Integration of acid-base and electrolyte disorders. NEJM 2014:371:1821-31.
  3. Berend K, et al. Diagnostic use of base excess in acid-base disorders. NEJM 2018:378:1419-28.
  4. Marino PL. The little ICU book. 2nd Ed. Philadelphia, PA: Wolters Kluwer; 2017.

How to Cite This Post

Bellio G, Marrano E. Eating Batteries, Drinking Alien’s Blood – Part 2. Surgical Pizza. Published on March 26, 2022. Accessed on June 25, 2022. Available at [https://surgicalpizza.org/critical-care/eating-batteries-drinking-alien-blood-part-2/].

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