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Vocabulary flashcards covering primary acid-base disorders, buffer mechanisms, normal blood gas values, compensation responses, and serum anion gap calculations from lecture notes.
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Acid
A substance that can donate protons (hydrogen ions, H+), such as hydrochloric acid (HCl).
Base
A substance that can accept protons (hydrogen ions, H+), such as ammonia (NH3).
Acidemia
A clinical state characterized by low blood pH values (<7.35).
Alkalemia
A clinical state characterized by high blood pH values (>7.45).
Henderson-Hasselbalch Equation (Acid-Base)
The equation used to determine blood pH, expressed as pH=6.1+log0.03×pCO2[HCO3−].
Basic Metabolic Panel (BMP) Bicarbonate Reporting
Laboratory reporting where bicarbonate is reported as CO2 because it is measured as total dissolved CO2, which is approximately 95% bicarbonate.
Normal Arterial Blood Gas (ABG) Values
Standard arterial blood reference values: pH 7.35−7.45, PO2 of 80−100 mmHg, SaO2 of 95%, PCO2 of 35−45 mmHg, and HCO3− of 22−26 mEq/L.
Extracellular Buffering
The rapid first defense mechanism against a sudden increase in hydrogen ion concentration, comprising the bicarbonate/carbonic acid system, proteins, and phosphates.
Ventilatory Regulation
The second process maintaining acid-base homeostasis, in which changes in pulmonary ventilation alter blood PCO2 to regulate carbonic acid levels, maintaining PCO2 at approximately 40 mmHg.
Renal Regulation
The renal process that independently regulates blood bicarbonate concentration by filtration at the glomerulus and reabsorption in the proximal tubule through the apical Na+−H+ exchanger, maintaining serum bicarbonate at approximately 24 mEq/L.
Respiratory Acidosis
An acid-base disorder characterized by a pH<7.4 with a primary disturbance of increased PCO2 resulting from hypoventilation, compensated by an increased HCO3− concentration.
Respiratory Alkalosis
An acid-base disorder characterized by a pH>7.4 with a primary disturbance of decreased PCO2 resulting from hyperventilation, compensated by a decreased HCO3− concentration.
Metabolic Acidosis
An acid-base disorder characterized by a pH<7.4 resulting from a primary decrease in serum bicarbonate (HCO3−) concentration, compensated by a decreased PCO2.
Metabolic Alkalosis
An acid-base disorder characterized by a pH>7.4 with a primary disturbance of increased HCO3− resulting from gain of HCO3− or loss of H+, compensated by an increased PCO2.
Respiratory Compensatory Response
A rapid compensatory response occurring within minutes to hours that alters the rate and depth of respiration to correct the HCO3− to PCO2 ratio.
Metabolic Compensatory Response
A slow compensatory response occurring over days that involves the excretion or reabsorption of HCO3− by the kidneys, excretion of H+, or generation of new HCO3−.
Serum Anion Gap (SAG)
A parameter calculated to maintain electroneutrality in serum using the formula SAG=[Na+]−[Cl−]−[HCO3−], with a normal value of 10 mEq/L (range of 8−12 mEq/L).
Serum Anion Gap Albumin Correction
An adjustment rule where for every decrease in serum albumin by 1 g/dL from normal (4 g/dL), the calculated serum anion gap decreases by 2.5 mEq/L.
Anion-Gap Metabolic Acidosis (AGMA)
A category of metabolic acidosis resulting from excess formation of endogenous organic acids, such as in lactic acidosis, ketoacidosis, alcohol intoxication, starvation, or toxic ingestions of methanol or ethylene glycol.
Non-Anion Gap Metabolic Acidosis (NAGMA)
A category of metabolic acidosis caused primarily by renal or gastrointestinal loss of bicarbonate (HCO3−).