CSMLS Blood Gas Chemistry Quiz

Blood gas abnormalities reflect impaired oxygenation, ventilation, or metabolic regulation. Conditions such as airway obstruction or COPD reduce oxygen intake, CO₂ retention increases acidity, and renal dysfunction disrupts acid-base balance. Minor conditions like headaches or broken bones do not directly affect gas exchange or systemic pH regulation.

After collection, cells continue metabolizing glucose and oxygen. This increases CO₂ production, decreases oxygen levels, and lowers pH. Potassium leaks from RBCs, and glucose decreases due to glycolysis. These predictable changes explain why delayed processing alters blood gas results significantly.

The bicarbonate buffer system has a pKa of 6.1. A 20:1 ratio of bicarbonate to carbonic acid results in a physiologic pH of 7.4. This ratio allows effective buffering of acids generated during metabolism while maintaining normal blood pH.

Normal arterial values reflect effective gas exchange and acid-base balance. pH remains tightly regulated between 7.35 and 7.45. pO₂ reflects adequate oxygenation at 80–100 mmHg, and pCO₂ indicates ventilation efficiency at 35–45 mmHg.

Deoxyhemoglobin is hemoglobin not bound to oxygen. Each hemoglobin molecule can carry up to four oxygen molecules due to its four heme groups. Oxygen binding is reversible, allowing efficient loading in lungs and unloading in tissues.

Carboxyhemoglobin forms when carbon monoxide binds hemoglobin. Although reversible, CO binds with 200 times greater affinity than oxygen, preventing oxygen delivery. This strong binding explains CO poisoning’s severity and prolonged hypoxia.

Methemoglobin contains iron in the ferric (Fe³⁺) state, which cannot bind oxygen. RBC enzymes like methemoglobin reductase can convert Fe³⁺ back to Fe²⁺, restoring oxygen-carrying capacity under normal conditions.

Delayed centrifugation allows intracellular analytes to leak from RBCs. Potassium, LD, phosphorus, and magnesium increase due to membrane breakdown and ongoing metabolism, falsely elevating measured concentrations.

Glucose decreases due to glycolysis. Ionized calcium binds intracellularly, and bicarbonate decreases as CO₂ accumulates. These predictable decreases result from continued cellular metabolism in unseparated blood samples.

Hemolysis releases intracellular components into plasma. Potassium, LD, AST, ALT, iron, ammonia, magnesium, phosphorus, and protein increase, potentially causing false elevations and misleading clinical interpretations.

Smoking introduces ammonia-producing compounds in saliva. Ammonia diffuses into blood, falsely elevating measured levels. This pre-analytical variable highlights the importance of patient preparation before specimen collection.

Dehydration concentrates plasma proteins. Multiple myeloma and amyloidosis increase immunoglobulins. Chronic infections stimulate protein synthesis. These mechanisms elevate total protein levels.

Nephrotic syndrome causes urinary protein loss. Liver disease reduces protein synthesis. Pregnancy and burns increase protein demand or loss. These mechanisms lower total protein concentration.

AST is present in liver, heart, and skeletal muscle. Damage to these tissues releases AST into circulation, causing elevated levels. It is not specific to liver injury alone.

ALP increases with bile duct obstruction and bone turnover. Paget’s disease, biliary blockage, and parathyroid disorders elevate ALP due to increased enzyme production in affected tissues.

Ionized calcium regulates myocardial contraction, blood clotting, and nerve-muscle signaling. These functions are critical for survival and tightly regulated by parathyroid hormone and vitamin D.

Potassium maintains membrane potential in cardiac and skeletal muscle cells. Abnormal levels disrupt electrical conduction, leading to arrhythmias and muscle weakness.

Renal failure limits potassium excretion. Acidosis shifts potassium from cells into plasma. Both mechanisms elevate serum potassium levels, causing hyperkalemia.

Hypernatremia results from water loss exceeding sodium loss. Dehydration, burns, diarrhea, and steroid use reduce free water, concentrating sodium levels.

Excess water intake dilutes sodium. Renal failure and diuretics impair sodium regulation. These conditions lower serum sodium, causing hyponatremia.

Guaiac paper reacts with hemoglobin’s peroxidase activity. Hydrogen peroxide oxidizes guaiac, producing a blue color, indicating occult blood presence.

Atmospheric air contains approximately 21% oxygen, translating to a partial pressure of about 150 mmHg. Carbon dioxide is minimal at roughly 0.03%, yielding about 1 mmHg. These baseline values drive diffusion gradients essential for pulmonary gas exchange.

In acidosis, the body compensates by increasing ventilation to remove excess CO₂. Lowering pCO₂ shifts the bicarbonate buffer system, increasing pH toward normal. This respiratory response is rapid and effective in correcting metabolic disturbances.

Sulfhemoglobin forms when sulfur irreversibly binds hemoglobin. This altered hemoglobin cannot carry oxygen and persists for the lifespan of the RBC. No enzymatic pathway exists to reverse this binding.

Relative Centrifugal Force depends on rotor radius and speed. The formula 1.118×10⁻⁵ × radius (cm) × RPM² accurately calculates RCF, ensuring proper specimen separation without cellular damage.

Ammonia is unstable and increases rapidly at room temperature. Cold spinning minimizes cellular metabolism. Refrigeration is acceptable briefly, but freezing plasma preserves accuracy during prolonged analyzer downtime.

Renal failure impairs calcium reabsorption and vitamin D activation, lowering calcium levels. Alkalosis increases protein binding of calcium, reducing ionized calcium availability.

Hypokalemia results from losses through vomiting, diarrhea, diuretics, or intracellular shifts caused by insulin and alkalosis. These mechanisms reduce circulating potassium.

Drug screening cutoffs define positivity. Results at or above the cutoff are reported as positive. Values below are negative. This ensures standardized interpretation.

Urine drug screens remain stable when refrigerated up to 48 hours. Proper storage preserves analyte integrity. Longer storage requires freezing to prevent degradation.