Clinical approach to acid-base disorders US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Clinical approach to acid-base disorders. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Clinical approach to acid-base disorders US Medical PG Question 1: A 65-year-old man is brought to the emergency department from his home. He is unresponsive. His son requested a wellness check because he had not heard from his father in 2 weeks. He reports that his father was sounding depressed during a telephone call. The paramedics found a suicide note and a half-empty bottle of antifreeze near the patient. The medical history includes hypertension and hyperlipidemia. The vital signs include: blood pressure 120/80 mm Hg, respiratory rate 25/min, heart rate 95/min, and temperature 37.0°C (98.5°F). He is admitted to the hospital. What do you expect the blood gas analysis to show?
- A. Non-anion gap metabolic acidosis
- B. Metabolic alkalosis
- C. Respiratory acidosis
- D. Anion gap metabolic acidosis (Correct Answer)
- E. Mixed acid-base disorder
Clinical approach to acid-base disorders Explanation: ***Anion gap metabolic acidosis***
- The patient's history of **antifreeze ingestion** indicates likely exposure to **ethylene glycol**, which is metabolized into toxic acids (glycolic and oxalic acid).
- These accumulating acids lead to an **increased anion gap metabolic acidosis**.
*Non-anion gap metabolic acidosis*
- This type of acidosis typically results from **bicarbonate loss** (e.g., severe diarrhea) or **excessive chloride intake**, which is not indicated by the antifreeze ingestion.
- It involves a normal anion gap because other unmeasured anions do not accumulate.
*Metabolic alkalosis*
- This imbalance is characterized by an **increase in bicarbonate** or a significant loss of acid, often due to vomiting or diuretic use.
- Antifreeze poisoning directly leads to acid accumulation, precisely the opposite of metabolic alkalosis.
*Respiratory acidosis*
- This occurs due to **hypoventilation** and subsequent buildup of CO2, leading to increased carbonic acid.
- While respiratory rate is elevated, the primary problem here is metabolic due to toxin ingestion, not respiratory CO2 retention.
*Mixed acid-base disorder*
- While a mixed disorder is possible in complex cases, the presentation with antifreeze poisoning is classically dominated by a **severe anion gap metabolic acidosis**.
- There is no clear indication of a separate primary respiratory or alkalotic disorder at onset to warrant a "mixed" label as the primary anticipated finding.
Clinical approach to acid-base disorders US Medical PG Question 2: A 32-year-old man is brought to the emergency department after he was found unresponsive on the street. Upon admission, he is lethargic and cyanotic with small, symmetrical pinpoint pupils. The following vital signs were registered: blood pressure of 100/60 mm Hg, heart rate of 70/min, respiratory rate of 8/min, and a body temperature of 36.0°C (96.8°F). While being assessed and resuscitated, a sample for arterial blood gas (ABG) analysis was taken, in addition to the following biochemistry tests:
Laboratory test
Serum Na+ 138 mEq/L
Serum Cl- 101 mEq/L
Serum K+ 4.0 mEq/L
Serum creatinine (SCr) 0.58 mg/dL
Which of the following values would you most likely expect to see in this patient’s ABG results?
- A. pH: decreased, HCO3- : increased, Pco2: increased (Correct Answer)
- B. pH: increased, HCO3- : decreased, Pco2: decreased
- C. pH: decreased, HCO3- : decreased, Pco2: decreased
- D. pH: increased, HCO3- : increased, Pco2: increased
- E. pH: normal, HCO3- : increased, Pco2: increased
Clinical approach to acid-base disorders Explanation: ***pH: decreased, HCO3- : increased, Pco2: increased***
- The patient's **depressed respiratory rate** (8/min) indicates severe hypoventilation, leading to **CO2 retention** and subsequent **respiratory acidosis** (decreased pH, increased PaCO2).
- In **acute respiratory acidosis**, the body initiates immediate buffering, causing a **mild increase in HCO3-** (approximately 1 mEq/L per 10 mmHg rise in PaCO2). Over 3-5 days, renal compensation leads to more significant HCO3- retention, but in this acute presentation, some HCO3- elevation is expected from acute buffering mechanisms.
- The **decreased pH** indicates that compensation is incomplete, which is typical in the acute setting.
*pH: increased, HCO3- : decreased, Pco2: decreased*
- This pattern is characteristic of **respiratory alkalosis** (increased pH, decreased PaCO2) with metabolic compensation (decreased HCO3-), which would occur in hyperventilation, opposite to the patient's presentation.
- The patient's **slow respiratory rate** of 8/min directly contradicts the finding of decreased PaCO2.
*pH: decreased, HCO3- : decreased, Pco2: decreased*
- This suggests a **metabolic acidosis** (decreased pH, decreased HCO3-) with respiratory compensation (decreased PaCO2), typically seen in conditions like DKA or lactic acidosis.
- Although the pH is decreased, the patient's severe bradypnea (RR 8/min) indicates increased CO2 retention, not decreased CO2.
*pH: increased, HCO3- : increased, Pco2: increased*
- This combination of findings is indicative of **metabolic alkalosis** (increased pH, increased HCO3-) with respiratory compensation (increased PaCO2).
- This is inconsistent with the patient's pinpoint pupils, cyanosis, and **severe bradypnea**, which are classic signs of opioid overdose causing respiratory depression and acidosis, not alkalosis.
*pH: normal, HCO3- : increased, Pco2: increased*
- A normal pH despite increased HCO3- and PaCO2 indicates **fully compensated respiratory acidosis**, which requires days of renal compensation to develop.
- In this **acute, severe drug overdose** with profound respiratory depression, the body would not have sufficient time to achieve full compensation, thus the pH would remain low.
Clinical approach to acid-base disorders US Medical PG Question 3: A 58-year-old man presents to the emergency department with a chief complaint of ringing in his ears that started several hours previously that has progressed to confusion. The patient denies any history of medical problems except for bilateral knee arthritis. He was recently seen by an orthopedic surgeon to evaluate his bilateral knee arthritis but has opted to not undergo knee replacement and prefers medical management. His wife noted that prior to them going on a hike today, he seemed confused and not himself. They decided to stay home, and roughly 14 hours later, he was no longer making any sense. Physical exam is notable for a confused man. The patient's vitals are being performed and his labs are being drawn. Which of the following is most likely to be seen on blood gas analysis?
- A. pH: 7.30, PaCO2: 15 mmHg, HCO3-: 16 mEq/L (Correct Answer)
- B. pH: 7.37, PaCO2: 41 mmHg, HCO3-: 12 mEq/L
- C. pH: 7.41, PaCO2: 65 mmHg, HCO3-: 34 mEq/L
- D. pH: 7.47, PaCO2: 11 mmHg, HCO3-: 24 mEq/L
- E. pH: 7.31, PaCO2: 31 mmHg, HCO3-: 15 mEq/L
Clinical approach to acid-base disorders Explanation: ***pH: 7.30, PaCO2: 15 mmHg, HCO3-: 16 mEq/L***
- This blood gas analysis shows a **low pH** (acidemia), **low PaCO2** (hypocapnia), and **low HCO3-** (bicarbonate). This pattern is consistent with a **primary metabolic acidosis** with a **compensatory respiratory alkalosis**.
- In this clinical scenario, the patient likely has **salicylate toxicity** (aspirin poisoning). Salicylate toxicity initially causes respiratory alkalosis due to direct stimulation of the respiratory center, followed by a high anion gap metabolic acidosis as salicylates interfere with cellular metabolism. This specific ABG reflects a mixed disorder where metabolic acidosis is predominant and respiratory compensation is attempting to raise the pH. The **tinnitus** and **confusion** are classic symptoms of salicylate toxicity.
*pH: 7.37, PaCO2: 41 mmHg, HCO3-: 12 mEq/L*
- This blood gas shows a **normal pH**, **normal PaCO2**, and **low HCO3-**. This suggests a **compensated metabolic acidosis**, where the body has fully compensated to bring the pH back to normal.
- While the patient likely has metabolic acidosis from salicylate toxicity, full compensation to a normal pH is less characteristic of an acute, severe presentation with significant neurological symptoms.
*pH: 7.41, PaCO2: 65 mmHg, HCO3-: 34 mEq/L*
- This blood gas shows a **normal pH**, **high PaCO2**, and **high HCO3-**. This indicates a **compensated respiratory acidosis**, where the kidneys have compensated for chronic CO2 retention.
- This pattern is not consistent with salicylate toxicity, which typically causes **respiratory alkalosis** early on, and later **metabolic acidosis**.
*pH: 7.47, PaCO2: 11 mmHg, HCO3-: 24 mEq/L*
- This blood gas analysis shows a **high pH** (alkalemia), **very low PaCO2** (severe hypocapnia), and a **normal HCO3-**. This indicates a **primary respiratory alkalosis** with no significant metabolic compensation.
- While salicylate toxicity can cause respiratory alkalosis, severe confusion and the progression of symptoms suggest a more advanced stage, usually involving a metabolic acidosis component, making a pure, uncompensated respiratory alkalosis less likely.
*pH: 7.31, PaCO2: 31 mmHg, HCO3-: 15 mEq/L*
- This blood gas shows a **low pH**, **low PaCO2**, and **low HCO3-**. This also indicates a **metabolic acidosis** with **respiratory compensation**.
- However, compared to pH 7.30, PaCO2 15 mmHg, and HCO3- 16 mEq/L, this option shows slightly **less severe respiratory compensation** (PaCO2 is higher), which is less typical for the profound respiratory stimulation seen in severe salicylate poisoning. The chosen correct option demonstrates a more characteristic and maximal respiratory compensation for the degree of metabolic acidosis.
Clinical approach to acid-base disorders US Medical PG Question 4: A 75-year-old woman with late-onset autoimmune diabetes mellitus, rheumatoid arthritis, coronary artery disease, and idiopathic pulmonary fibrosis presents to the ship medic with altered mental status. While on her current cruise to the Caribbean islands, she experienced nausea, vomiting, and diarrhea. She takes aspirin, simvastatin, low-dose prednisone, glargine, and aspart. She is allergic to amoxicillin and shellfish. She works as a greeter at a warehouse and smokes 5 packs/day. Her temperature is 100.5°F (38.1°C), blood pressure is 90/55 mmHg, pulse is 130/min, and respirations are 30/min. Her pupils are equal and reactive to light bilaterally. Her lungs are clear to auscultation bilaterally, but her breath has a fruity odor. She has an early systolic murmur best appreciated at the left upper sternal border. She has reproducible peri-umbilical tenderness. Which of the following will most likely be present in this patient?
- A. Respiratory alkalosis and anion-gap metabolic acidosis (Correct Answer)
- B. Respiratory acidosis and anion-gap metabolic acidosis
- C. Respiratory alkalosis and non anion-gap metabolic acidosis
- D. Respiratory acidosis and contraction metabolic alkalosis
- E. Respiratory alkalosis and non-contraction metabolic alkalosis
Clinical approach to acid-base disorders Explanation: ***Respiratory alkalosis and anion-gap metabolic acidosis***
- The patient's **fruity-smelling breath**, history of diabetes, and symptoms of nausea, vomiting, and diarrhea strongly suggest **diabetic ketoacidosis (DKA)**, which causes a **high anion-gap metabolic acidosis** from accumulation of ketoacids (beta-hydroxybutyrate and acetoacetate).
- The markedly increased respiratory rate (30/min) represents **Kussmaul breathing** - a compensatory hyperventilation mechanism attempting to blow off CO2 and normalize pH. While this is technically **respiratory compensation for metabolic acidosis** rather than a primary respiratory alkalosis, the arterial blood gas will show a **low PaCO2** (respiratory alkalosis pattern) alongside the **low pH and low HCO3** (metabolic acidosis).
- This represents a **partially compensated metabolic acidosis** with high anion gap, which is the classic acid-base disturbance in DKA.
*Respiratory acidosis and anion-gap metabolic acidosis*
- **Respiratory acidosis** would imply hypoventilation (decreased respiratory rate or impaired ventilation) with CO2 retention, which is contrary to the patient's markedly elevated respiratory rate (30/min). The patient is hyperventilating, not hypoventilating.
- While **anion-gap metabolic acidosis** is correct due to DKA, the respiratory component is incorrect.
*Respiratory alkalosis and non anion-gap metabolic acidosis*
- While the low PaCO2 from compensatory hyperventilation would be present, **non-anion-gap metabolic acidosis** is incorrect.
- **Non-anion-gap metabolic acidosis** is typically caused by conditions like diarrhea (GI HCO3 loss) or renal tubular acidosis, whereas DKA characteristically causes a **high anion-gap metabolic acidosis** due to accumulation of unmeasured anions (ketoacids).
*Respiratory acidosis and contraction metabolic alkalosis*
- This option incorrectly identifies both acid-base components. The patient is **hyperventilating** (not hypoventilating), ruling out respiratory acidosis.
- **Contraction alkalosis** occurs with severe volume depletion and diuretic use when chloride depletion leads to metabolic alkalosis, which does not fit the DKA presentation where ketoacid accumulation causes metabolic acidosis.
*Respiratory alkalosis and non-contraction metabolic alkalosis*
- While the compensatory hyperventilation results in low PaCO2, **metabolic alkalosis** (whether contraction or non-contraction) is inconsistent with DKA, which causes metabolic **acidosis**, not alkalosis.
- **Non-contraction metabolic alkalosis** is associated with conditions like hyperaldosteronism or vomiting with gastric acid loss, not with ketoacid accumulation.
Clinical approach to acid-base disorders US Medical PG Question 5: A 24-year-old male is brought in by ambulance to the emergency department after he was found unresponsive at home for an unknown length of time. Upon arrival, he is found to be severely altered and unable to answer questions about his medical history. Based on clinical suspicion, a panel of basic blood tests are obtained including an arterial blood gas, which shows a pH of 7.32, a pCO2 of 70, and a bicarbonate level of 30 mEq/L. Which of the following is most likely the primary disturbance leading to the values found in the ABG?
- A. Respiratory acidosis (Correct Answer)
- B. Metabolic alkalosis
- C. Respiratory alkalosis
- D. Metabolic acidosis
- E. Mixed alkalosis
Clinical approach to acid-base disorders Explanation: ***Respiratory acidosis***
- The **pH (7.32)** is acidic (normal 7.35-7.45), and the **pCO2 (70 mmHg)** is significantly elevated (normal 35-45 mmHg), indicating **primary respiratory acidosis** due to hypoventilation.
- The **bicarbonate (30 mEq/L)** is elevated above normal (22-26 mEq/L), indicating **partial metabolic compensation** by the kidneys retaining bicarbonate to buffer the acidosis.
- This pattern suggests **chronic respiratory acidosis** (e.g., from COPD, CNS depression, neuromuscular disease) with renal compensation.
*Metabolic alkalosis*
- This would present with **elevated pH** (>7.45) and **elevated bicarbonate** as the primary disturbance, often with compensatory elevation in pCO2.
- The patient's **pH is acidic (7.32)**, not alkalotic, ruling out metabolic alkalosis as the primary process.
*Respiratory alkalosis*
- This would present with **elevated pH** (>7.45) and **decreased pCO2** (<35 mmHg) due to hyperventilation.
- The patient has the opposite: **acidic pH and elevated pCO2**, ruling out respiratory alkalosis.
*Metabolic acidosis*
- This would present with **decreased pH** and **decreased bicarbonate** (<22 mEq/L) as the primary disturbance.
- While the pH is low, the **bicarbonate is elevated (30 mEq/L)**, not decreased, ruling out metabolic acidosis as the primary disorder.
*Mixed alkalosis*
- A mixed alkalosis would involve simultaneous respiratory and metabolic processes causing **elevated pH**.
- The patient's **pH is acidic (7.32)**, making any form of alkalosis impossible as the primary disturbance.
Clinical approach to acid-base disorders US Medical PG Question 6: A 52-year-old man with a history of Type 1 diabetes mellitus presents to the emergency room with increasing fatigue. Two days ago, he ran out of insulin and has not had time to obtain a new prescription. He denies fevers or chills. His temperature is 37.2 degrees Celsius, blood pressure 84/56 mmHg, heart rate 100/min, respiratory rate 20/min, and SpO2 97% on room air. His physical exam is otherwise within normal limits. An arterial blood gas analysis shows the following:
pH 7.25, PCO2 29, PO2 95, HCO3- 15.
Which of the following acid-base disorders is present?
- A. Respiratory alkalosis with appropriate metabolic compensation
- B. Respiratory acidosis with appropriate metabolic compensation
- C. Mixed metabolic and respiratory acidosis
- D. Metabolic acidosis with appropriate respiratory compensation (Correct Answer)
- E. Metabolic alkalosis with appropriate respiratory compensation
Clinical approach to acid-base disorders Explanation: ***Metabolic acidosis with appropriate respiratory compensation***
- The patient's pH of 7.25 and HCO3- of 15 indicate **metabolic acidosis**, while the PCO2 of 29 indicates **respiratory compensation**.
- The compensation is **appropriate** as suggested by Winter's formula [Expected PCO2 = (1.5 x HCO3-) + 8 +/- 2; (1.5 x 15) + 8 = 30.5, which is close to 29].
*Respiratory alkalosis with appropriate metabolic compensation*
- This would involve a **pH > 7.45** and **low PCO2** with a secondary drop in HCO3-, which is not seen here.
- The patient's primary problem is a metabolic disturbance due to insulin deficiency.
*Respiratory acidosis with appropriate metabolic compensation*
- This disorder is characterized by a **low pH** and a **high PCO2**, with a secondary rise in HCO3-.
- The patient's PCO2 is low, indicating a compensatory response rather than a primary respiratory acidosis.
*Mixed metabolic and respiratory acidosis*
- A mixed disorder would show a **low pH** due to both **low HCO3-** and **high PCO2**.
- The patient's PCO2 is low, indicating a compensatory response to metabolic acidosis, not an additional respiratory acidosis.
*Metabolic alkalosis with appropriate respiratory compensation*
- This would present with a **high pH (>7.45)** and **high HCO3-**, with compensatory **elevated PCO2**.
- The patient's pH and HCO3- are low, indicating acidosis, not alkalosis.
Clinical approach to acid-base disorders US Medical PG Question 7: A 37-year-old G1P0 woman presents to her primary care physician for a routine checkup. She has a history of diabetes and hypertension but has otherwise been healthy with no change in her health status since the last visit. She is expecting her first child 8 weeks from now. She also enrolled in a study about pregnancy where serial metabolic panels and arterial blood gases are obtained. Partial results from these studies are shown below:
Serum:
Na+: 141 mEq/L
Cl-: 108 mEq/L
pH: 7.47
pCO2: 30 mmHg
HCO3-: 21 mEq/L
Which of the following disease processes would most likely present with a similar panel of metabolic results?
- A. Diarrheal disease
- B. Loop diuretic abuse
- C. Living at high altitude (Correct Answer)
- D. Ingestion of metformin
- E. Anxiety attack
Clinical approach to acid-base disorders Explanation: ***Living at high altitude***
- Chronic exposure to **high altitude** leads to sustained **hypoxia**, which stimulates **hyperventilation** as a compensatory mechanism.
- This persistent hyperventilation causes a **respiratory alkalosis** (high pH, low pCO2) and a compensatory **metabolic acidosis** (low HCO3-) to normalize pH, mimicking the presented metabolic panel.
*Diarrheal disease*
- Severe **diarrhea** leads to the loss of bicarbonate from the gastrointestinal tract, causing a **non-anion gap metabolic acidosis**.
- This would present with a **low pH**, **low HCO3-**, and a **compensatory drop in pCO2**, not a respiratory alkalosis with a high pH.
*Loop diuretic abuse*
- Chronic abuse of **loop diuretics** can cause **metabolic alkalosis** due to increased renal excretion of hydrogen ions and potassium, leading to volume contraction.
- This would typically present with a **high pH**, high HCO3-, and a compensatory rise in pCO2, which is different from the given values.
*Ingestion of metformin*
- **Metformin** can cause **lactic acidosis** (a type of high anion gap metabolic acidosis), especially in patients with renal impairment.
- This would manifest as a **low pH**, **low HCO3-**, and a **compensatory decrease in pCO2**, along with an elevated anion gap, not the respiratory alkalosis seen here.
*Anxiety attack*
- An **anxiety attack** causes acute **hyperventilation**, leading to **acute respiratory alkalosis** (high pH, low pCO2).
- However, in an acute setting, there is insufficient time for significant renal compensation, so the HCO3- would remain near normal, unlike the compensated state shown in the panel.
Clinical approach to acid-base disorders US Medical PG Question 8: A 72-year-old man being treated for benign prostatic hyperplasia (BPH) is admitted to the emergency department for 1 week of dysuria, nocturia, urge incontinence, and difficulty initiating micturition. His medical history is relevant for hypertension, active tobacco use, chronic obstructive pulmonary disease, and BPH with multiple urinary tract infections. Upon admission, he is found with a heart rate of 130/min, respiratory rate of 19/min, body temperature of 39.0°C (102.2°F), and blood pressure of 80/50 mm Hg. Additional findings during the physical examination include decreased breath sounds, wheezes, crackles at the lung bases, and intense right flank pain. A complete blood count shows leukocytosis and neutrophilia with a left shift. A sample for arterial blood gas analysis (ABG) was taken, which is shown below.
Laboratory test
Serum Na+ 140 mEq/L
Serum Cl- 102 mEq/L
Serum K+ 4.8 mEq/L
Serum creatinine (SCr) 2.3 mg/dL
Arterial blood gas
pH 7.12
Po2 82 mm Hg
Pco2 60 mm Hg
SO2% 92%
HCO3- 12.0 mEq/L
Which of the following best explains the patient’s condition?
- A. Metabolic acidosis complicated by respiratory alkalosis
- B. Non-anion gap metabolic acidosis
- C. Respiratory alkalosis complicated by metabolic acidosis
- D. Respiratory acidosis complicated by metabolic alkalosis
- E. Metabolic acidosis complicated by respiratory acidosis (Correct Answer)
Clinical approach to acid-base disorders Explanation: ***Metabolic acidosis complicated by respiratory acidosis***
- The patient's pH is significantly low (7.12), indicating **acidemia**. The **HCO3- is markedly low (12 mEq/L)**, and PCO2 is elevated (60 mm Hg), suggesting both a metabolic and a respiratory component to the acidosis.
- The severe infection (fever, elevated heart rate, hypotension, flank pain, leukocytosis, elevated creatinine) and the signs of hypoperfusion contribute to **lactic acidosis (metabolic acidosis)**, while his history of COPD and lung findings (decreased breath sounds, wheezes, crackles) explain the impaired ventilation leading to **respiratory acidosis**.
*Metabolic acidosis complicated by respiratory alkalosis*
- While a **metabolic acidosis** is clearly present due to the low pH and HCO3-, the PCO2 is elevated, indicating **respiratory acidosis**, not alkalosis.
- Respiratory alkalosis would be characterized by a **low PCO2** due to hyperventilation.
*Non-anion gap metabolic acidosis*
- To determine the anion gap, we use the formula: **Na+ - (Cl- + HCO3-)**. In this case, 140 - (102 + 12) = 140 - 114 = **26 mEq/L**.
- An anion gap of 26 mEq/L, which is significantly elevated (normal range is typically 8-12 mEq/L), indicates an **anion gap metabolic acidosis**, not a non-anion gap one.
*Respiratory alkalosis complicated by metabolic acidosis*
- The low pH and HCO3- confirm **metabolic acidosis**, but the elevated PCO2 (60 mm Hg) indicates **respiratory acidosis**, not alkalosis, as the respiratory component is also acidotic.
- Respiratory alkalosis would result from **hyperventilation and a low PCO2**.
*Respiratory acidosis complicated by metabolic alkalosis*
- While the elevated PCO2 indicates **respiratory acidosis**, the HCO3- is significantly low (12 mEq/L), which points to a **metabolic acidosis**, not metabolic alkalosis.
- **Metabolic alkalosis** would be characterized by an **elevated HCO3-**.
Clinical approach to acid-base disorders US Medical PG Question 9: A 30-year-old woman presents to the emergency department with breathlessness for the last hour. She is unable to provide any history due to her dyspnea. Her vitals include: respiratory rate 20/min, pulse 100/min, and blood pressure 144/84 mm Hg. On physical examination, she is visibly obese, and her breathing is labored. There are decreased breath sounds and hyperresonance to percussion across all lung fields bilaterally. An arterial blood gas is drawn, and the patient is placed on inhaled oxygen. Laboratory findings reveal:
pH 7.34
pO2 63 mm Hg
pCO2 50 mm Hg
HCO3 22 mEq/L
Her alveolar partial pressure of oxygen is 70 mm Hg. Which of the following is the most likely etiology of this patient’s symptoms?
- A. Right to left shunt
- B. Alveolar hypoventilation (Correct Answer)
- C. Ventricular septal defect
- D. Impaired gas diffusion
- E. Ventilation/perfusion mismatch
Clinical approach to acid-base disorders Explanation: ***Alveolar hypoventilation***
- The patient exhibits features of **obesity** and **labored breathing** with decreased breath sounds and hyperresonance, along with arterial blood gas results showing **respiratory acidosis** (pH 7.34, pCO2 50 mmHg) and **hypoxia** (pO2 63 mmHg).
- The calculated A-a gradient (Alveolar O2 - arterial O2) is low (70 mmHg - 63 mmHg = 7 mmHg), indicating that the problem is primarily with **overall ventilation** rather than a defect in gas exchange across the alveolar-capillary membrane.
*Right to left shunt*
- A right-to-left shunt would cause a **large A-a gradient**, as deoxygenated blood bypasses the lungs and mixes with oxygenated blood.
- While it causes **hypoxemia**, it would not typically be associated with hypercapnia unless very severe, and the A-a gradient calculation here does not support a significant shunt.
*Ventricular septal defect*
- A ventricular septal defect is a **structural heart abnormality** that can cause a left-to-right shunt initially, leading to pulmonary hypertension and eventually a right-to-left shunt (Eisenmenger syndrome).
- While it can cause hypoxemia due to shunting, it would not primarily manifest with increased pCO2 or the specific lung physical exam findings of decreased breath sounds and hyperresonance in the absence of other cardiac signs.
*Impaired gas diffusion*
- Impaired gas diffusion would lead to a **large A-a gradient** and **hypoxemia**, but typically not significant hypercapnia unless the impairment is extremely severe.
- Conditions like **pulmonary fibrosis** or **emphysema** cause impaired diffusion, but the patient's presentation and particularly the low A-a gradient do not support this.
*Ventilation/perfusion mismatch*
- A V/Q mismatch also causes a **large A-a gradient** and **hypoxemia**, as some areas of the lung are either poorly ventilated or poorly perfused.
- While it can cause hypercapnia in severe cases, the primary issue indicated by the low A-a gradient here is one of overall inadequate ventilation, not selective areas of ventilation-perfusion imbalance.
Clinical approach to acid-base disorders US Medical PG Question 10: A 54-year-old man presents with 3 days of non-bloody and non-bilious emesis every time he eats or drinks. He has become progressively weaker and the emesis has not improved. He denies diarrhea, fever, or chills and thinks his symptoms may be related to a recent event that involved sampling many different foods. His temperature is 97.5°F (36.4°C), blood pressure is 133/82 mmHg, pulse is 105/min, respirations are 15/min, and oxygen saturation is 98% on room air. Physical exam is notable for a weak appearing man with dry mucous membranes. His abdomen is nontender. Which of the following laboratory changes would most likely be seen in this patient?
- A. Metabolic alkalosis and hyperkalemia
- B. Non-anion gap metabolic acidosis and hypokalemia
- C. Respiratory acidosis and hyperkalemia
- D. Metabolic alkalosis and hypokalemia (Correct Answer)
- E. Anion gap metabolic acidosis and hypokalemia
Clinical approach to acid-base disorders Explanation: ***Metabolic alkalosis and hypokalemia***
- Persistent **vomiting** leads to the loss of **gastric acid** (HCl) and **potassium**, resulting in **metabolic alkalosis** and **hypokalemia**. The loss of HCl directly removes acid from the body, and the subsequent renal compensation to conserve volume often exacerbates potassium loss.
- The patient's presentation with **dry mucous membranes**, increased heart rate (pulse 105/min), and persistent non-bloody, non-bilious emesis suggests significant volume depletion and electrolyte imbalances consistent with prolonged vomiting.
*Metabolic alkalosis and hyperkalemia*
- While metabolic alkalosis is expected due to gastric acid loss from vomiting, **hyperkalemia** is unlikely. Vomiting typically causes **hypokalemia** due to direct potassium loss and renal compensation mechanisms.
- The body attempts to compensate for volume depletion, leading to increased activity of the **renin-angiotensin-aldosterone system**, which promotes potassium excretion in the urine.
*Non-anion gap metabolic acidosis and hypokalemia*
- **Metabolic acidosis** is characterized by a decrease in blood pH and bicarbonate; however, profuse vomiting of gastric contents primarily leads to **alkalosis** due to the loss of hydrogen ions.
- **Non-anion gap metabolic acidosis** is usually seen in conditions involving bicarbonate loss from the kidneys or gut (e.g., diarrhea, renal tubular acidosis), not vomiting.
*Respiratory acidosis and hyperkalemia*
- **Respiratory acidosis** results from hypoventilation, leading to an increase in blood CO2, which is not suggested by the patient's normal respiratory rate and oxygen saturation.
- Profuse vomiting causes a loss of gastric acid and can lead to compensatory **hypoventilation** to retain CO2 (acid), but this is a secondary response to metabolic alkalosis, and primary respiratory acidosis is not the underlying issue.
*Anion gap metabolic acidosis and hypokalemia*
- **Anion gap metabolic acidosis** typically occurs with the accumulation of unmeasured acids (e.g., lactic acidosis, ketoacidosis, renal failure, poisoning), which is not indicated by the patient's symptoms.
- While **hypokalemia** is consistent with vomiting, the primary acid-base disturbance from prolonged emesis is metabolic alkalosis, not acidosis.
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