Acid-Base Disorders › Acid-Base Pathologies

Alkalosis and Acidosis

Notes

Alkalosis and Acidosis

Sections


Alkalosis and Acidosis: 4 simple acid-base disorders

Metabolic acid-base disorders present as imbalances between bicarbonate, the primary extracellular buffer, and fixed, aka, non-volatile, acids.

Respiratory acid-base disorders present as imbalances between bicarbonate and carbon dioxide, the volatile acid.

Distinguishing Features

Acid-base Disorders are distinguishable by their arterial blood profiles, compensatory respiratory and renal mechanisms, and common causes.

Acidemia

Acidemia is defined as a pH < 7.35

Metabolic acidosis

Metabolic acidosis is characterized by arterial Bicarbonate < 20 mEq/L due to either a gain in hydrogen ions and/or a loss of bicarbonate, which lowers pH.

Consequently, the arterial blood profile shows reduced bicarbonate concentration and elevated hydrogen ion concentration.

In response to a drop in pH, the respiratory system compensates with hyperventilation: excess carbon dioxide is "blown off," which lowers the partial pressure of carbon dioxide in the blood; the arterial blood profile reflects this.

Though slower to respond, renal bicarbonate conservation and acid excretion produce a more effective and longer-lasting pH elevation.

Anion Gap

Causes of metabolic acidosis into at least two categories: those associated with a normal anion gap (AG), and those associated with an elevated anion gap.

In a routine blood test, only some cations and anions are measured; the anions that are not measured constitute the "anion gap."

Because the total concentration of anions must be equal to the total concentration of cations, we know that the anion gap, the unmeasured anions, must be equal to:

The measured cations (usually sodium) minus the measured anions (usually bicarbonate and chloride).

A normal average anion gap value is 12 mEq/L (typical range = 8 – 16 mEq/L).

Thus, an increased anion gap indicates that bicarbonate, a measured anion, has been lost and replaced by the unmeasured ions

A normal anion gap indicates that chloride is the ion that replaced the lost bicarbonate, which makes sense given that it is the other measured anion in the anion gap equation.

Normal anion gap causes include:

Increased anion gap causes include: MUDPILES

  • Methanol intoxication (methanol is also called "wood alcohol," commonly found in antifreeze and industrial settings)
  • Uremia
  • Diabetic ketoacidosis
  • Paraldehyde (which is sometimes used to treat alcoholism and certain convulsive and mental disorders)
  • Iron overdose
  • Lactic acid
  • Ethylene glycol poisoning (ethylene glycol is a compound commonly found in antifreeze)
  • Salicylate ingestion (key ingredient in aspirin, poisoning is common in children)

Respiratory acidosis

Respiratory acidosis is characterized by Pco2 > 44 mmHg, due to a gain in carbon dioxide and bicarbonate.

The degree of change in pH depends on the duration of the disorder:
The pH is more reduced in acute acidosis than in chronic because, in chronic acidosis, sufficient time has elapsed for renal mechanisms to have some effect.

There is no respiratory compensation when the respiratory system is itself the source of the imbalance.

To raise pH, the nephrons conserve bicarbonate and excrete hydrogen ions; notice that this is similar to the renal response to metabolic acidosis.

Causes of respiratory acidosis: Hypoventilation

  • Inhibition of the medullary respiratory center, which can be induced by sedatives or brainstem lesions
  • Neuromuscular defects that inhibit the anatomical structures responsible for ventilation
  • Gas exchange defects, such as COPD.

Alkalemia

Alkalemia is defined as a pH > 7.45

Respiratory alkalosis

Respiratory alkalosis is characterized by Pco2 < 36 mmHg; pH is increased in proportion to the duration of the disorder.

There is no respiratory compensation for respiratory-induced acid-base disturbances.

Nephrons excrete excess bicarbonate and reduce titratable acid and ammonium ion secretion to conserve hydrogen ions; this is similar to the renal response to metabolic alkalosis.

Caused by: Hyperventilation**

Hyperventilation "blows off" too much carbon dioxide and lowers its arterial partial pressure. Can be due to stimulation of the medullary respiratory center, hypoxemia (low blood oxygen), and physical or mental distress.

Metabolic alkalosis

Metabolic alkalosis is characterized by arterial Bicarbonate > 28 mEq/L, due to a loss of hydrogen ions and/or a gain in bicarbonate, which raises pH.

Consequently, the arterial blood profile shows elevated bicarbonate concentration, and decreased hydrogen concentration.

In response to elevated pH, hypoventilation retains carbon dioxide, which increases its arterial partial pressure; this is reflected in the arterial blood profile.

The nephrons increase bicarbonate excretion, and, by reducing secretion of titratable acids and ammonium, conserve hydrogen ions; these actions lower pH.

Metabolic alkalosis is most commonly caused by vomiting (HCL is lost from the body).

Other causes include loop and thiazide diuretics, which increase bicarbonate excretion in the urine, and hyperaldosteronism (excessive aldosterone secretion), which causes over-excretion of hydrogen ions.

Vomiting and diuretics cause extracellular fluid volume contraction, which, as we've learned elsewhere, triggers hormonal responses that increase bicarbonate reabsorption and maintain the metabolic alkalosis.

Clinical Cases

Case 1: Hyperventilating patient

A 26-year-old female presents to the emergency department with complaints of dizziness and tingling (paresthesia) around her mouth and distal upper extremities. She denies any recent drug or alcohol use. Staff reports her symptoms have worsened since she arrived, and also inform you that the patient has demanded to "see a doctor immediately" because she is "dying".

On physical examination, the patient is visibly agitated, and demonstrates pressured speech and difficulty concentrating. Her blood pressure is 140/70 mm Hg, heart rate is 110/min, respiratory rate is 30/min, and her temperature is 37 degrees Celsius (96.8 degrees Fahrenheit).

The patient is breathing shallow and rapidly (tachypnea), so you order a STAT arterial blood gas (ABG). Her ABG values on room air are as follows: pH 7.52, PaO2 90 mm Hg, SaO2 97 percent, PaCO2 25 mm Hg, and HCO3 18 mEq/L.

Which of the following processes is most likely causing this patient's acid-base imbalance?

Answer

  • Respiratory alkalosis with metabolic compensation

Explanation

This patient has a respiratory alkalosis with metabolic compensation. The arterial blood gas (ABG) demonstrates pH above 7.45, PaCO2 less than 33 mm Hg, and HCO3 (bicarbonate) less than 22 mEq/L. Respiratory alkalosis is the result of hyperventilation. Specific causes of hyperventilation include catastrophic central nervous system (CNS) events such as hemorrhage, drugs such as salicylates, interstitial lung diseases, pregnancy (especially in the third trimester), and as in this scenario, anxiety. In respiratory alkalosis, a decrease in HCO3 compensates for the decrease in PaCO2.

In acute cases, HCO3 decreases 2 mEq/L for every 10 mm Hg decrease in PaCO2. In chronic cases, HCO3 decreases 4 mEq/L for every 10 mm Hg decrease in PaCO2. Acute respiratory alkalosis causes the pH to increase by 0.08 for every 10 mm Hg decrease in PaCO2.

Respiratory acidosis is the result of either decreased alveolar ventilation or increased carbon dioxide (CO2) production. Decreased alveolar ventilation is seen in chronic obstructive pulmonary disease (COPD), acute respiratory failure, neuromuscular disorders that result in peripheral muscle weakness such as myasthenia gravis, and central nervous system (CNS) depression as seen with narcotic overdoses and general anesthetics. Increased carbon dioxide (CO2) production occurs in hypermetabolic states such as sepsis or fever.

Metabolic alkalosis with respiratory compensation is a common metabolic disturbance seen in patients related to loss of hydrogen ions as seen with vomiting, nasogastric (NG) suction, and hypokalemia as a result of diuretics. In metabolic alkalosis the PaCO2 increases 6 mm Hg for every 10 mEq/L increase in HCO3.

Metabolic acidosis can be divided into anion gap acidosis and non-anion gap acidosis. The anion gap value is the difference between negatively and positively charged electrolytes, and is calculated as follows: Na (sodium) minus (Cl (chloride) plus HCO3). Although there are differences between laboratories and assays, the normal anion gap has traditionally been set between 8 mEq/L to 12 mEq/L. If the anion gap is greater than 12, this suggests an increased accumulation of acidic metabolites. Specific causes of anion gap acidosis (anion gap greater than 12 mEq/L) include ketoacidosis, lactic acidosis, renal failure, and toxic doses of salicylates.

For a metabolic acidosis, determine whether an anion gap is present as follows: Na minus (Cl plus HCO3). Non-anion gap acidosis (anion gap less than 8 mEq/L) results from loss of bicarbonate or external acid infusion. Specific causes of non-anion gap acidosis include diarrhea, renal tubular acidosis, and hyperalimentation. In metabolic acidosis, PaCO2 decreases 1.2 mm Hg for every 1 mEq/L decrease in HCO3.

Case 2: Hypoventilating Patient

An obese 50-year-woman presents to her PCP for fatigue and shortness of breath upon exertion. She states the SOB has worsened during the past nine months. About one year ago she was diagnosed with obstructive sleep apnea due to being overweight, but due to lack of insurance coverage was unable to purchase a CPAP machine. She has never smoked, denies any marijuana use, and does not let anyone smoke in her home. She is five feet, eight inches tall and weighs 295 pounds.

There are no abnormalities on cardiorespiratory examination. Chest x-ray is unremarkable.

Morning arterial blood gas shows:
PaO2: 65 mm Hg
PaCO2: 57 mm Hg
pH: 7.35
Serum HCO3–: 30 mEq/L

How can you explain the patient's arterial blood gas values and the resultant clinical complications?

Answer

  • Obesity hypoventilation syndrome with resultant pulmonary hypertension

Explanation

The patient is suffering from obesity hypoventilation syndrome (categorized by a BMI over 30, in this case 44.8). The patient's obesity makes it difficult for the lungs to expand, resulting in low ventilation and the retention of CO2. At night, the pressure on the patient's chest also decreases her ability to inhale, thus resulting in decreased O2 intake and further retention of CO2. This causes the right side of the heart to work harder in an attempt to get more blood to the lungs for diffusion, thus resulting in pulmonary hypertension.

Case 3: Altitude Sickness

A 20-year-old college athlete, male, presents at his PCP's office in preparation for a mountain climbing trip with his friends. In particular, the group is travelling to Alaska to climb Mount Saint Elias which peaks at 18,000 feet. The patient asks his physician if there is a medication that can help him adjust to the altitude and avoid acute mountain sickness. The patient is healthy, not on any prescription medications, has no known allergies, and as a college athlete he is regularly tested for steroids or other illegal substances. The physician prescribes Diamox (acetazolamide).

Which of the medication's side effects can help alleviate acute mountain sickness?

Answer

  • Metabolic Acidosis

Explanation

Metabolic acidosis helps to combat the oxidative stress that occurs at high elevations, improving the ability of red blood cells to carry oxygen through the body and serving as a treatment for pulmonary edema. Diamox is a carbonic anhydrase inhibitor. It limits the effects of the enzyme carbonic anhydrase, which is needed to convert water and carbon dioxide into bicarbonate and hydrogen ions in your body. It reduces the amount of acid excreted when you urinate. This causes the kidneys to excrete more bicarbonate, sodium, potassium, and water, with the urine becoming more alkaline. Diamox thus produces a metabolic acidosis by increasing the urinary excretion of bicarbonate.

Metabolic alkalosis would amplify the oxidative stress already occurring.

Respiratory acidosis occurs when the lungs are unable to remove CO2 from the blood; this results in the creation of bicarbonate in the blood and also the release of free acidic hydrogen ions. This will not aid a systemic increase in bicarbonate and therefore not help in hemoglobin oxygen binding.

Respiratory alkalosis will not only increase acidity levels in already acidic blood, but will enhance removal of CO2 through the lungs thus reducing the ability to create bicarbonate. This would rapidly increase the effects of high altitude sickness and could lead to serious health issues.