Acid-Base Balance — MCQs

Acid-Base Balance Indian Medical PG Practice Questions and MCQs

Question 121: A female patient presents to the casualty department following an injury. Her arterial blood gas (ABG) analysis shows a low pH, high pCO2, and normal bicarbonate. What is the diagnosis?

A. Respiratory alkalosis
B. Respiratory acidosis (Correct Answer)
C. Metabolic acidosis
D. Metabolic alkalosis

Explanation: ### Explanation **1. Understanding the Correct Answer (Respiratory Acidosis)** The diagnosis of acid-base disorders follows a systematic approach. In this case: * **Low pH (< 7.35):** Indicates **Acidosis**. * **High $pCO_2$ (> 45 mmHg):** Carbon dioxide is a volatile acid. An elevation in $pCO_2$ (hypercapnia) indicates that the primary cause of the acidosis is respiratory (hypoventilation). * **Normal Bicarbonate ($HCO_3^-$):** This suggests an **acute** process. In acute respiratory acidosis, the kidneys have not yet had time (usually takes 24–48 hours) to compensate by retaining bicarbonate. **2. Why Other Options are Incorrect** * **Respiratory Alkalosis:** This would present with a **high pH** and a **low $pCO_2$** (usually due to hyperventilation). * **Metabolic Acidosis:** While the pH would be low, the primary driver would be a **low $HCO_3^-$**. The $pCO_2$ would typically be low or normal (due to respiratory compensation/Kussmaul breathing). * **Metabolic Alkalosis:** This would present with a **high pH** and a **high $HCO_3^-$**. **3. NEET-PG High-Yield Pearls** * **The "Golden Rule":** If pH and $pCO_2$ move in **opposite** directions, the primary problem is **Respiratory**. If they move in the **same** direction, it is **Metabolic** (ROME: Respiratory Opposite, Metabolic Equal). * **Clinical Correlation:** In a trauma/injury setting, acute respiratory acidosis is often caused by chest wall injuries (flail chest), pain-induced splinting, or head injuries depressing the respiratory center. * **Compensation:** For every 10 mmHg rise in $pCO_2$, $HCO_3^-$ rises by 1 mEq/L in acute cases and 3.5–4 mEq/L in chronic cases (e.g., COPD).

Question 122: Which of the following occurs as a result of persistent vomiting?

A. Hyperkalemia
B. Hypochloremia (Correct Answer)
C. Hyperventilation
D. Acidic urine excretion

Explanation: ### Explanation Persistent vomiting leads to a classic acid-base disturbance known as **Metabolic Alkalosis with Hypokalemia and Hypochloremia**. **1. Why Hypochloremia is Correct:** Gastric juice is rich in Hydrochloric acid (HCl). Persistent vomiting results in the massive loss of both Hydrogen ions ($H^+$) and Chloride ions ($Cl^-$). The loss of $Cl^-$ leads to **hypochloremia**. As $H^+$ is lost, the body generates excess bicarbonate ($HCO_3^-$), leading to metabolic alkalosis. To maintain electrical neutrality, the kidneys reabsorb bicarbonate instead of chloride, further perpetuating the hypochloremic state. **2. Why the other options are incorrect:** * **Hyperkalemia:** Vomiting causes **Hypokalemia**. This occurs due to direct loss in vomitus, but primarily due to secondary hyperaldosteronism (triggered by volume depletion) which increases urinary $K^+$ excretion. * **Hyperventilation:** In metabolic alkalosis, the body attempts respiratory compensation by **hypoventilation** (retaining $CO_2$) to lower the pH. * **Acidic urine excretion:** Initially, the urine is alkaline due to bicarbonate excretion. However, in severe cases, "Paradoxical Aciduria" occurs. While the urine is acidic in that specific late-stage complication, **Hypochloremia** is the more direct and primary result of the vomiting itself. **Clinical Pearls for NEET-PG:** * **Paradoxical Aciduria:** In late-stage vomiting, volume depletion triggers aldosterone to save $Na^+$. Since $K^+$ is already depleted, the distal tubule is forced to secrete $H^+$ to reabsorb $Na^+$, making the urine acidic despite systemic alkalosis. * **Saline Responsiveness:** This condition is "Chloride-responsive"; it can be corrected with 0.9% Normal Saline. * **Most common electrolyte triad in pyloric stenosis:** Hypokalemic, hypochloremic, metabolic alkalosis.

Question 123: When the sympathetic nervous system is activated, what occurs?

A. Norepinephrine is released by the vascular smooth muscle cells
B. Acetylcholine is released onto vascular smooth muscle cells
C. Norepinephrine is released from axons onto the arteriolar wall (Correct Answer)
D. The arterioles constrict because nitric oxide production is suppressed

Explanation: ### Explanation **1. Why Option C is Correct:** The sympathetic nervous system (SNS) regulates vascular tone through the release of **Norepinephrine (NE)** from postganglionic sympathetic nerve terminals (axons) directly onto the **tunica media** of the arteriolar wall. NE binds to **$\alpha_1$-adrenergic receptors** on vascular smooth muscle cells, triggering a G-protein-coupled signaling cascade ($IP_3/DAG$ pathway) that increases intracellular calcium, leading to **vasoconstriction**. This is a fundamental mechanism for maintaining peripheral resistance and systemic blood pressure. **2. Why Other Options are Incorrect:** * **Option A:** Norepinephrine is synthesized and released by **sympathetic neurons**, not by the smooth muscle cells themselves. The muscle cells are the *targets* (effectors), not the source. * **Option B:** Acetylcholine (ACh) is the neurotransmitter for the parasympathetic system and preganglionic sympathetic fibers. While some specialized sympathetic fibers (to sweat glands) release ACh, they do not cause the generalized arteriolar constriction characteristic of SNS activation. * **Option D:** While Nitric Oxide (NO) is a potent vasodilator, sympathetic vasoconstriction is primarily driven by the **active release of NE** and subsequent $\alpha_1$ stimulation, rather than the mere suppression of NO. **3. High-Yield NEET-PG Pearls:** * **Exceptions to the Rule:** Most blood vessels receive only sympathetic innervation. However, skeletal muscle vessels also possess **$\beta_2$ receptors**, which cause vasodilation when stimulated by low doses of epinephrine. * **Dominant Tone:** Arterioles are the "resistance vessels" of the body; sympathetic tone is the primary determinant of Total Peripheral Resistance (TPR). * **Neurotransmitter Synthesis:** Tyrosine $\rightarrow$ L-Dopa $\rightarrow$ Dopamine $\rightarrow$ Norepinephrine $\rightarrow$ Epinephrine (in the adrenal medulla). * **Clinical Correlation:** $\alpha_1$-blockers (e.g., Prazosin) are used in hypertension to inhibit this NE-induced vasoconstriction.

Question 124: Aerial blood gas analysis in a bottle containing heparin causes a decrease in which of the following values?

A. pCO2
B. FICO3
C. pH
D. All of the above (Correct Answer)

Explanation: This question addresses the pre-analytical errors associated with **Arterial Blood Gas (ABG)** sampling, specifically the effect of **excess liquid heparin** (dilutional effect). ### Why "All of the Above" is Correct: Liquid heparin is acidic and has a low partial pressure of carbon dioxide ($pCO_2$). When a syringe contains an excessive volume of liquid heparin relative to the blood sample (dilution), the following changes occur: 1. **Decrease in $pCO_2$:** Heparin has a $pCO_2$ near 0 mmHg. Diluting blood with heparin lowers the overall $pCO_2$ of the sample. 2. **Decrease in $HCO_3^-$:** The dilution effect directly reduces the concentration of bicarbonate ions in the sample. 3. **Decrease in pH:** While heparin is a weak acid, the primary reason for the pH drop in this context is the dilution of the blood's natural buffer systems (like bicarbonate and hemoglobin), making the sample more acidic. ### Analysis of Options: * **A ($pCO_2$):** Decreases due to the dilution with a solution containing negligible dissolved $CO_2$. * **B ($HCO_3^-$):** Decreases due to direct dilution and the chemical reaction with the acidic heparin. * **C (pH):** Decreases because liquid heparin is acidic (pH ~6.4 to 7.0) and it dilutes the blood's buffering capacity. ### High-Yield Clinical Pearls for NEET-PG: * **Ideal Heparinization:** To avoid these errors, use **dry (lyophilized) lithium heparin** or ensure the syringe is only "flushed" with liquid heparin (dead space only). * **Air Bubbles:** If air bubbles are left in the syringe, $pCO_2$ decreases while $pO_2$ increases (as $O_2$ moves from the bubble into the blood and $CO_2$ moves out). * **Delayed Analysis:** If the sample is not analyzed immediately or kept on ice, ongoing cellular metabolism (glycolysis) will **decrease pH**, **decrease $pO_2$**, and **increase $pCO_2$**.

Question 125: If blood gas analysis reveals pH = 7.52, pCO2 = 30, and pO2 = 105, this will be compensated by?

A. Compensatory respiratory acidosis
B. Compensatory respiratory alkalosis
C. Compensatory metabolic acidosis (Correct Answer)
D. Compensatory metabolic alkalosis

Explanation: ### Explanation To solve acid-base problems, follow a systematic three-step approach: **1. Identify the Primary Disturbance** * **pH = 7.52:** Normal pH is 7.35–7.45. Since it is >7.45, the primary condition is **Alkalosis**. * **pCO₂ = 30 mmHg:** Normal pCO₂ is 35–45 mmHg. A low pCO₂ (hypocapnia) causes alkalosis. * **Conclusion:** The primary disturbance is **Respiratory Alkalosis**. **2. Determine the Compensation** The body always attempts to return the pH toward normal by moving the opposite system in the same direction as the primary change. * In **Respiratory Alkalosis** (low pCO₂), the kidneys compensate by **excreting HCO₃⁻** (bicarbonate) and retaining H⁺. * Decreasing the base (HCO₃⁻) creates a **Metabolic Acidosis** to counter the respiratory alkalosis. --- ### Why the other options are incorrect: * **Option A & B:** Compensation is never performed by the same system that caused the primary derangement. Since the primary issue is respiratory, the compensation must be metabolic (renal). * **Option D:** Adding a metabolic alkalosis to a respiratory alkalosis would worsen the pH deviation, potentially leading to fatal alkalinity. --- ### NEET-PG High-Yield Pearls: * **The "Same Direction" Rule:** In simple acid-base disorders, the pCO₂ and HCO₃⁻ always move in the same direction (both up or both down) if compensation is occurring. * **Speed of Compensation:** Respiratory compensation (for metabolic issues) starts within minutes. Renal compensation (for respiratory issues) is slow, taking **2–5 days** to reach maximal effect. * **Expected Compensation in Acute Respiratory Alkalosis:** For every 10 mmHg drop in pCO₂, HCO₃⁻ drops by **2 mEq/L**. In chronic cases, it drops by **4–5 mEq/L**.

Question 126: Hydrogen ion is eliminated by which organ?

A. Kidney (Correct Answer)
B. Lungs
C. Liver
D. Stomach

Explanation: **Explanation:** The maintenance of acid-base homeostasis involves three primary systems: chemical buffers, the respiratory system, and the renal system. **1. Why the Kidney is Correct:** The **Kidney** is the only organ capable of the actual **elimination (excretion)** of fixed (non-volatile) hydrogen ions from the body. While buffers neutralize acids and lungs manage volatile acid, the kidneys perform three critical functions to maintain pH: * **Secretion of H+ ions:** Primarily in the proximal convoluted tubule (PCT) and via intercalated cells in the collecting ducts. * **Reabsorption of filtered HCO3-:** To maintain the alkaline reserve. * **Generation of new HCO3-:** Through the excretion of titratable acids (buffered by phosphate) and ammonium (NH4+) excretion. **2. Why other options are incorrect:** * **Lungs:** The lungs eliminate **volatile acid** in the form of Carbon Dioxide (CO2). They do not excrete H+ ions directly; instead, they shift the equilibrium of the bicarbonate buffer system ($H^+ + HCO_3^- \leftrightarrow H_2CO_3 \leftrightarrow H_2O + CO_2$). * **Liver:** The liver is involved in acid-base balance through the metabolism of lactate and the production of plasma proteins (buffers), but it does not serve as an excretory route for H+ ions. * **Stomach:** While the stomach secretes HCl into its lumen for digestion, this is a localized secretion, not a systemic regulatory mechanism for H+ elimination. **Clinical Pearls for NEET-PG:** * **Rate of Action:** Lungs act within minutes (fast but incomplete), while Kidneys take hours to days (slow but most powerful/complete). * **Type of Acid:** Lungs = Volatile acid (CO2); Kidneys = Non-volatile/Fixed acids (e.g., sulfuric, phosphoric, and lactic acid). * **Ammoniagenesis:** In chronic acidosis, the kidney's most important adaptive response is increasing the production and excretion of **NH4+**.

Question 127: A hyperventilating patient has the following ABG values: pH=7.53, pCO2=20 mmHg, HCO3= 26 mEq/L. What is the most likely diagnosis?

A. Metabolic alkalosis
B. Metabolic acidosis
C. Respiratory alkalosis (Correct Answer)
D. Respiratory acidosis

Explanation: ***Respiratory alkalosis*** - The pH of 7.53 indicates **alkalemia**, and the low pCO2 (20 mmHg) is the primary driver, signifying **respiratory alkalosis** - A hyperventilating patient exhales more CO2, leading to a decrease in its partial pressure in the blood and a subsequent rise in pH - The HCO3 is within normal range (26 mEq/L), indicating **uncompensated respiratory alkalosis** *Metabolic alkalosis* - This would be characterized by a high pH and an elevated **HCO3**, but the HCO3 is within the normal range (26 mEq/L) - While it causes alkalemia, the primary disturbance here is respiratory, not metabolic *Metabolic acidosis* - This would present with a **low pH** and a low **HCO3**, which is contrary to the given ABG values - The patient's pH is elevated, indicating an alkalotic state, not acidotic *Respiratory acidosis* - This would be defined by a **low pH** and an elevated **pCO2**, which is the exact opposite of the provided ABG results - The patient's high pH and low pCO2 rule out respiratory acidosis

Question 128: Acid-base imbalance is suspected in a patient. Which of the following parameters would you use for initial determination of acid-base status?

A. pH, PaCO2, and Base excess
B. pH, PaCO2, and Bicarbonate (Correct Answer)
C. pH and PaCO2
D. pH, PaCO2, Bicarbonate, and Base excess

Explanation: ***pH, PaCO2, and Bicarbonate*** - The **pH** provides immediate assessment of overall acid-base status (acidemia if <7.35 or alkalemia if >7.45) - The **PaCO2** reflects the respiratory component - elevated in respiratory acidosis or compensated metabolic alkalosis; decreased in respiratory alkalosis or compensated metabolic acidosis - The **HCO3- (bicarbonate)** reflects the metabolic component - essential for determining whether the primary disorder is metabolic or respiratory - This triad forms the **standard approach** to arterial blood gas (ABG) interpretation taught in all major medical textbooks - Together, these three parameters allow complete initial classification of acid-base disorders using the Henderson-Hasselbalch relationship *pH and PaCO2* - While pH and PaCO2 are critical measurements, **without bicarbonate**, you cannot differentiate between metabolic and respiratory disorders or assess metabolic compensation - For example, a low pH with normal PaCO2 could indicate metabolic acidosis, but you need HCO3- to confirm this diagnosis - Incomplete for initial acid-base determination *pH, PaCO2, and Base excess* - Base excess is a **calculated parameter** used to quantify the metabolic component of acid-base disturbances - While useful, it is considered a **secondary parameter** for more detailed metabolic analysis rather than essential for initial determination - Standard ABG interpretation uses bicarbonate, not base excess, as the primary metabolic parameter *pH, PaCO2, Bicarbonate, and Base excess* - While this includes all relevant parameters, **base excess is redundant** for initial determination - Base excess adds quantitative information about metabolic component but is not required for the initial classification of acid-base status - The essential triad for initial assessment is pH, PaCO2, and HCO3-

Question 129: During heavy exercise, what is the primary mechanism for maintaining arterial pH despite increased lactic acid production?

A. Increased bicarbonate reabsorption
B. Phosphate buffering
C. Increased hydrogen secretion
D. Hyperventilation (Correct Answer)

Explanation: ***Hyperventilation*** - **Hyperventilation** during heavy exercise increases the expulsion of **carbon dioxide (CO2)**, shifting the **bicarbonate buffer system** equilibrium to the left. - This reduction in **CO2** effectively removes **hydrogen ions (H+)**, thereby helping to maintain **arterial pH** despite rising **lactic acid** levels. *Increased bicarbonate reabsorption* - While the kidneys adapt by increasing **bicarbonate reabsorption** to compensate for acidosis, this is a **slower renal mechanism** for pH regulation, taking hours to days, rather than an immediate response during acute exercise. - The rapid pH regulation during exercise primarily relies on respiratory and chemical buffer systems, not renal function. *Phosphate buffering* - The **phosphate buffer system** is indeed important for intracellular and renal tubular fluid buffering. - However, its buffering capacity in the extracellular fluid and plasma is relatively limited compared to the **bicarbonate system** due to its lower concentration. *Increased hydrogen secretion* - **Increased hydrogen secretion** by the renal tubules is a long-term mechanism for compensating for acidosis, which helps excrete excess **acid** and regenerate **bicarbonate**. - This is a slow, renal regulatory process and not the primary rapid mechanism for maintaining pH during the immediate demands of heavy exercise.

Question 130: What is the primary mechanism for maintaining acid-base balance during prolonged vomiting?

A. Increased chloride reabsorption
B. Increased potassium excretion
C. Increased bicarbonate excretion (Correct Answer)
D. Decreased hydrogen secretion

Explanation: ***Increased bicarbonate excretion*** - Prolonged vomiting leads to the loss of **gastric acid (HCl)**, causing **metabolic alkalosis**. The kidneys compensate by increasing the excretion of **bicarbonate (HCO3-)** to restore acid-base balance. - This renal compensation is the primary mechanism to eliminate the excess alkali from the body. *Increased chloride reabsorption* - In **metabolic alkalosis** due to vomiting, the body tends to reabsorb less chloride, not more, in an attempt to excrete bicarbonate. - **Chloride depletion** can actually hinder bicarbonate excretion by promoting sodium reabsorption with bicarbonate. *Increased potassium excretion* - **Hypokalemia** can occur with prolonged vomiting due to increased aldosterone activity and direct renal loss associated with metabolic alkalosis. - However, increased potassium excretion itself is not the primary mechanism for correcting the acid-base disorder; rather, it is a consequence or a contributing factor to the imbalance. *Decreased hydrogen secretion* - In response to alkalosis, the kidneys would typically decrease, not increase, **hydrogen ion (H+) secretion** in an effort to retain H+ and normalize pH. - Decreased H+ secretion is a compensatory mechanism, but the direct excretion of bicarbonate is more crucial for correcting the metabolic alkalosis.

Practice by Chapter

Acid-Base Chemistry

Practice Questions

Respiratory Regulation of Acid-Base Balance

Practice Questions

Renal Regulation of Acid-Base Balance

Practice Questions

Bicarbonate Buffer System

Practice Questions

Non-Bicarbonate Buffer Systems

Practice Questions

Respiratory Acidosis and Alkalosis

Practice Questions

Metabolic Acidosis and Alkalosis

Practice Questions

Mixed Acid-Base Disorders

Practice Questions

Compensatory Mechanisms

Practice Questions

Clinical Assessment of Acid-Base Status

Practice Questions

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