Acid-base Balance and Blood Gas Analysis

Question 1

What is Base excess?

Answer 1

Base excess (BE) is usually defined as the amount of strong acid (hydrochloric acid for BE greater than zero) or strong base (sodium hydroxide for BE less than zero) required to return 1 L of whole blood exposed in vitro to a Pco2 of 40 mm Hg to a pH of 7.4

Question 2

What is a buffer system?

Answer 2

A buffer is defined as a substance within a solution that can prevent extreme changes in pH. A buffer system is composed of a base molecule and its weak conjugate acid. The base molecules of the buffer system bind excess hydrogen ions, and the weak acid protonates excess base molecules

Question 3

The most important buffer systems in blood, in order of importance, are

Answer 3

(1) bicarbonate buffer system (H2CO3/HCO3 )

(2) hemoglobin buffer system (HbH/Hb )

(3) other protein buffer systems (PrH/Pr )

(4) phosphate buffer system (H2PO4 / HPO42−)

(5) ammonia buffer system (NH3/NH4+).

Question 4

There is a very wide variation in individual Paco2/ventilation response curves, but minute ventilation generally increases … for every 1 mm Hg increase in Paco2

Answer 4

1 to 4 L/min

Question 5

What is the maximum pH in which is possible a respiratory compensation (patient breathing room air) in a case of metabolic alkalosis?

Answer 5

The stimulus from central and peripheral chemoreceptors to either increase or decrease alveolar ventilation diminishes as the pH approaches 7.4 such that complete correction or overcorrection is not possible. The pulmonary response to metabolic alkalosis is usually less than the response to metabolic acidosis. The reason is because progressive hypoventilation results in hypoxemia when breathing room air. Hypoxemia activates oxygen-sensitive chemoreceptors and limits the compen- satory decrease in minute ventilation. Because of this, Paco2 usually does not rise above 55 mm Hg in response to metabolic alkalosis for patients not receiving oxygen supplementation

Question 6

Which are the mechanisms of the renal response in a case of acid-base disorder?

Answer 6

(1) reabsorption of the filtered HCO3
(2)excretion of titratable acids
(3) ammonia

Question 7

What is the leukocyte larceny

Answer 7

A delay in analysis of ABG can lead to oxygen consumption and carbon dioxide generation by the metabolically active white blood cells. Usually this error is small and can be reduced by placing the sample on ice. In some leukemia patients with a markedly increased white blood cell count this error can be large and lead to a falsely low Po2 even though the patient’s oxygenation is acceptable. This phenomenon is often referred to as leukocyte larceny

Question 8

How hypothermia affects the ABG measure?

Answer 8

Decreases in temperature decrease the partial pressure of a gas in solution, even though the total gas content does not change. Both Pco2 and Po2 decrease during hypothermia, but serum bicarbonate is unchanged. This leads to an increase in pH if the blood could be measured at the patient’s temperature.
Unfortunately, all blood gas samples are measured at 37°C, which raises the issue of how to best manage the ABG measurement in hypothermic patients

Question 9

Causes of respiratory acidosis

Answer 9

1) Increased CO2 production
Malignant hyperthermia Hyperthyroidism
Sepsis
Overfeeding

2) Decreased CO2 elimination
Intrinsic pulmonary disease (pneumonia, ARDS, fibrosis, edema)
Upper airway obstruction (laryngospasm, foreign body, OSA)
Lower airway obstruction (asthma, COPD)
Chest wall restriction (obesity, scoliosis, burns)
CNS depression (anesthetics, opioids, CNS lesions)
Decreased skeletal muscle strength (residual effects of neuromuscular blocking drugs, myopathy, neuropathy)

3) Increased CO2 rebreathing or absorption
Exhausted soda lime
Incompetent one-way valve in breathing circuit
Laparoscopic surgery

Question 10

Explain the hemoglobin buffer system

Answer 10

The hemoglobin protein serves as an effective buffering system because it contains multiple histidine residues. Histidine is an effective buffer from pH 5.7 to 7.7 (pKa 6.8) because of multiple protonatable sites on the imidazole side chains. Buffering by hemoglobin depends on the bicarbonate system to facilitate the movement of carbon dioxide intracellularly.

At the lungs, the reverse process occurs. Chloride ions move out of the red blood cells as bicarbonate enters for conversion back to carbon dioxide. The carbon dioxide is released back into plasma and is eliminated by the lungs.

Question 11

Causes of respiratory alkalosis

Answer 11

1) Increased minute ventilation
Hypoxia (high altitude, low Fio2, severe anemia)
Iatrogenic (mechanical ventilation)
Anxiety and pain
CNS disease (tumor, infection, trauma)
Fever, sepsis
Drugs (salicylates, progesterone, doxapram)
Liver disease
Pregnancy
Restrictive lung disease
Pulmonary embolism

Question 12

Causes of metabolic acidosis

Answer 12

1) Anion Gap Acidosis
Methanol, ethylene glycol
Uremia
Lactic acidosis (e.g., from CHF, sepsis, cyanide toxicity)
Ethanol
Paraldehyde
Aspirin, INH (isoniazid)
Ketones (e.g., starvation, diabetic ketoacidosis)

2) Non gap Acidosis
Excessive chloride administration (e.g., 0.9% saline infusion)
GI losses (diarrhea, ileostomy, neobladder, pancreatic fistula Renal losses)
RTA
Drugs (acetazolamide)

Question 13

How albumin blood levels change the anion gap?

Answer 13

each 1.0 g/dL decrease or increase in serum albumin less or more than 4.4 g/dL decreases or increases the actual concentration of unmeasured anions by approximately 2.5 mEq/L

Question 14

Where is lactate metabolized?

Answer 14

The liver metabolizes approximately 60% of lactate produced, with the kidneys metabolizing 30%. A small amount of lactate is converted back to glucose via gluconeogenesis

Question 15

Causes of elevated lactate

Answer 15

Type A—Perfusion Related
Distributive: sepsis, anaphylaxis
Cardiogenic/cardiac arrest
Hypovolemia: hemorrhagic
Obstructive: pulmonary embolism, cardiac tamponade
Tissue ischemia: mesenteric ischemia, burns, trauma, compartment syndrome, necrotizing soft tissue infections
Muscle activity: tonic-clonic seizures, increased work of breathing, disorders with acute muscle rigidity (e.g.,
serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia)

Type B—Nonperfusion Related
Toxins: cyanide, carbon monoxide, cocaine, alcohol
Medications: metformin, linezolid, HIV reverse transcriptase inhibitors, epinephrine, inhaled β2-agonists, propofol
infusion syndrome Malignancy
Liver failure

Question 16

How is saline infusions associated with metabolic acidosis?

Answer 16

Aggressive fluid resuscitation with normal saline (>30 mL/kg/h) will induce a nonanion gap metabolic acidosis secondary to excessive chloride administration, which impairs bicarbonate reabsorption in the kidneys

Question 17

Describe the Stewart approach for acid-base disorders

Answer 17

His major tenet is that although serum bicarbonate and BE can be used to determine the extent of a clinical acid–base disorder, they do not help determine the mechanism of the abnormality.

Instead, he proposed that the independent variables responsible for changes in acid–base balance are the SID* (the difference between the completely dissociated cations and anions in plasma), the plasma concentration of non- volatile weak acids (ATOT), and the arterial carbon dioxide tension (Paco2). The strong ion approach distinguishes six primary acid–base disturbances (acidosis caused by decreased SID, alkalosis caused by increased SID, acidosis caused by increased ATOT, alkalosis caused by decreased ATOT, respiratory acidosis, or respiratory alkalosis)

• SID = [strong cations] – [strong anions]

[Na+] + [K+] + [Ca2+] + [Mg2+] – ([Cl ] + [SO42–] + [organic acids ])

Or ~ [ Na+] + [K+] – [Cl ]

Question 18

Is the Stewart approach better than the tradicional approach?

Answer 18

The major practical difference between the two theories (Stewart vs. Henderson-Hasselbalch) is the inclusion of the serum albumin concentration in the Stewart approach, which provides some increase in accuracy in certain clinical settings. If changes in serum albumin concentration are accounted for in measurement of the anion gap, the more complex Stewart approach does not appear to offer a clinically significant advantage over the traditional approach to acid–base disturbances

Question 19

Causes of metabolic alkalosis

Answer 19

1) Chloride Responsive
Renal loss (diuretic therapy)
GI loss (vomiting, NG suction)
Alkali administration (citrate in blood products, acetate in TPN, bicarbonate)

Chloride Resistant
Hyperaldosteronism
Refeeding syndrome
Profound hypokalemia

Question 20

Describe the gas equation

Answer 20

Alveolar gas equation: PAo2 = (PB – PH2O)Fio2 – PaCO2/RQ

PAo2 = alveolar partial pressure oxygen (mm Hg)
PB = barometric pressure (760 mm Hg at sea level)
PH2O = partial pressure of water vapor (47 mm Hg at 37 C) Fio2 = fraction inspired oxygen concentration
RQ = respiratory quotient (0.8 for normal diet)

Question 21

How to calculate the pulmonary shunt?

Answer 21

To estimate the amount of shunt present, when Pao2 is higher than 150 mm Hg, the shunt fraction is approximately 1% of cardiac output for every 20 mm Hg difference in the A-a gradient. When Pao2 is less than 150 mm Hg or when cardiac output is increased relative to metabolism, this guideline will underestimate the actual amount of venous admixture

% shunt = 1% for every 20 mm Hg of A-a gradient

Exemple:
For patient with Pao2 of 363 mmHg and PaCO2 of 40 mmHg breathing Fio2 1.0
PAo2 = (760 − 47)(1.0) – 40/0.8 = (713) − 50 = 663 mm Hg

A-a gradient = 663 − 363 = 300 mm Hg

% shunt = 1% for every 20 mm Hg of A-a gradient = 300/20 = 15%

Question 22

How to interpret the A-a gradient

Answer 22

The A-a gradient for- mula calculates the difference in oxygen partial pres- sure between alveolar (Pao2) and arterial (Pao2) blood. Normally, the A-a gradient is less than 15 mm Hg while breathing room air as a result of shunting via the Thebesian and bronchial veins.

Larger A-a gradients suggest the presence of pathollogic shunting, such as right-to-left intrapulmonary shunts (atelectasis, pneumonia, endobronchial intubation) or intracardiac shunts (congenital heart disease)