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Acid-base balance (ABB) is one of the strictest homeostatic parameters of the body. In this chapter, we analyze how blood pH is maintained and what happens when compensatory mechanisms fail.
This section covers basic ABB parameters, the function of buffer systems, and physiological regulatory mechanisms (respiratory and renal). We examine the classification of disorders in detail: from respiratory and metabolic acidosis/alkalosis to excretory, exogenous, and complex mixed disorders.
During practical classes and pathophysiology exams, students are most often required to be able to "read" blood gas panels, distinguish between primary metabolic and respiratory shifts, and determine the stage of compensation. Pay special attention to the mechanisms underlying mixed disorders—these form the basis of the most interesting and complex clinical cases.
What is the main parameter used to assess acid-base balance?
The fundamental criterion for assessing acid-base balance is the pH value, which reflects the concentration of hydrogen ions in biological fluids.
Which blood buffer is the most powerful?
Hemoglobin buffer. It accounts for more than 50% of the total blood buffering capacity, while operating exclusively inside erythrocytes.
Why do the lungs react to ABB shifts faster than the kidneys?
The lungs utilize a mechanism of alveolar ventilation changes, which is reflexively triggered within 1–2 minutes. Renal mechanisms require time for enzymatic processes and ion transport in the tubules.
What is alkalosis in simple terms?
This is a pathological condition in which the concentration of hydrogen ions (H⁺) in the body decreases, and the blood pH rises above the neutral mark of 7.39.
What is the difference between immediate and long-term compensation?
Immediate compensation (buffers, $Cl^-/HCO_3^-$ exchange) is activated instantly to neutralize $H^+$. Long-term compensation (kidneys) takes time but provides radical elimination of acids.
Why do muscle spasms (tetany) develop in respiratory alkalosis?
Due to a pH shift, plasma proteins (albumins) begin to actively bind ionized calcium (Ca2+). The decrease in its active fraction in the blood sharply increases neuromuscular excitability.
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