ABG Diagnostics Flashcards

1
Q

What is the numerical value that serves as the clinical cut-off for determining acidosis versus alkalosis based on pH?

A

7.4. This is the clinical cut-off point used to distinguish between acidosis (pH below 7.4) and alkalosis (pH above 7.4).

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2
Q

Name the most commonly used artery for obtaining an ABG sample, and explain why it’s preferred.

A

Radial artery. It’s preferred due to its superficial location, easy palpation, and collateral circulation provided by the ulnar artery.

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3
Q

What is the calculated concentration in arterial blood that reflects the kidneys’ effort to neutralize acid, and what is its normal range?

A

HCO3 (Bicarbonate), normal range is 22-26 mEq/L. This reflects the metabolic component of acid-base balance.

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4
Q

Besides pH, identify the two other ABG components that must be analyzed to determine the primary acid-base disorder.

A

PaCO2 (reflecting the respiratory component) and HCO3 (reflecting the metabolic component). These help determine whether the primary disturbance is respiratory or metabolic.

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5
Q

Describe the expected compensatory mechanism for metabolic acidosis, including the specific physiological changes involved.

A

The body compensates by increasing minute ventilation (hyperventilation), leading to a decrease in PaCO2, which helps increase pH toward the normal range.

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6
Q

What is the term for an acid-base disturbance where the expected compensation occurs but the pH remains outside the normal range?

A

Partially compensated. Compensation is occurring, but it’s insufficient to fully correct the pH imbalance.

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7
Q

State Winter’s formula and explain how it’s used to identify a concomitant acid-base disorder in metabolic acidosis.

A

Winter’s formula: PaCO2 = (1.5 x HCO3) + 8. In metabolic acidosis, if the actual PaCO2 is lower than the calculated value using this formula, it suggests a concomitant respiratory alkalosis.

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8
Q

List the three components used to calculate the anion gap, and provide the formula.

A

The three components are sodium (Na), chloride (Cl), and bicarbonate (HCO3). The formula is: AG = (Na - (Cl + HCO3)).

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9
Q

What are the two most common causes of high anion gap metabolic acidosis (HAGMA)?

A

Lactic acidosis (due to tissue ischemia or altered cellular metabolism) and diabetic ketoacidosis. These are frequently encountered in clinical practice.

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10
Q

Provide three specific examples of gastrointestinal conditions that can lead to non-anion gap metabolic acidosis (NAGMA).

A

Diarrhea, ileostomy, and proximal colostomy. These conditions lead to loss of bicarbonate-rich fluids from the GI tract.

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11
Q

Explain how the ratio of change in anion gap to change in bicarbonate is used to determine the presence of concurrent acid-base disorders in HAGMA.

A

A ratio between 1.0 and 2.0 indicates uncomplicated anion gap metabolic acidosis. A ratio less than 1 suggests a concurrent NAGMA, while a ratio greater than 2 suggests a concurrent metabolic alkalosis.

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12
Q

State the formula for calculating the desired PaO2 based on age.

A

Expected PaO2 for age = 104 - (age x 0.43). This helps determine if a patient’s oxygenation is adequate for their age.

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13
Q

A patient presents with a pH of 7.32, PaCO2 of 55 mmHg, and HCO3 of 28 mEq/L. Identify the primary acid-base disorder and determine if compensation is present.

A

The patient has respiratory acidosis. The elevated PaCO2 indicates a respiratory origin, and the HCO3 is within the normal range, suggesting no compensation has occurred yet.

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14
Q

A patient with a history of COPD has an ABG showing pH of 7.36, PaCO2 of 50 mmHg, and HCO3 of 32 mEq/L. What does this ABG reveal about the patient’s acid-base status?

A

The patient has compensated respiratory acidosis. The elevated PaCO2 indicates respiratory acidosis, but the elevated HCO3 shows the kidneys are compensating to normalize the pH.

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15
Q

A patient experiencing an anxiety attack has an ABG with a pH of 7.50, PaCO2 of 30 mmHg, and HCO3 of 23 mEq/L. Interpret these findings.

A

The patient has respiratory alkalosis. The low PaCO2 and elevated pH point to a respiratory origin. The near-normal HCO3 suggests minimal compensation.

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16
Q

Describe the two main categories of causes of metabolic alkalosis, providing examples of conditions for each category.

A

The two main categories are hypovolemia with chloride depletion (e.g., vomiting, gastric suction) and hypervolemia and chloride expansion (e.g., heart failure, hyperaldosteronism).

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17
Q

List five distinct causes of respiratory acidosis, ensuring they represent different underlying mechanisms.

A

Airway obstruction (e.g., COPD), CNS depression (e.g., opioid overdose), neuromuscular impairment (e.g., Guillain-Barré syndrome), ventilatory restriction (e.g., chest wall deformity), and increased CO2 production (e.g., malignant hyperthermia).

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18
Q

Explain why a patient with myasthenia gravis might develop respiratory acidosis.

A

Myasthenia gravis can cause muscle weakness, including the muscles involved in breathing (diaphragm, intercostal muscles), leading to hypoventilation and CO2 retention.

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19
Q

Identify one key cause of metabolic acidosis in chronic kidney disease (CKD).

A

Loss of renal function impairs acid excretion, leading to an accumulation of metabolic acids.

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20
Q

Which electrolyte abnormality commonly accompanies metabolic alkalosis?

A

Hypokalemia. It often co-occurs due to intracellular shifting of potassium or renal losses.

21
Q

What is the classic triad of symptoms seen in diabetic ketoacidosis (DKA)?

A

Polyuria, polydipsia, and polyphagia.

22
Q

How does hyperventilation affect blood pH, and what is this condition called?

A

Hyperventilation decreases PaCO2, which increases blood pH, leading to respiratory alkalosis.

23
Q

Explain how renal tubular acidosis (RTA) can result in metabolic acidosis.

A

RTA involves impaired bicarbonate reabsorption or hydrogen ion excretion, resulting in a net acid gain and a decrease in bicarbonate levels.

24
Q

Differentiate between type I and type II renal tubular acidosis in terms of their primary defect.

A

Type I RTA involves a defect in distal H+ excretion, while type II RTA involves a defect in proximal HCO3 reabsorption.

25
Q

Explain why vomiting can lead to metabolic alkalosis.

A

Vomiting leads to a loss of gastric acid (HCl), reducing the acid load and increasing the serum bicarbonate concentration.

26
Q

Name a condition that can cause a mixed acid-base disorder, where both metabolic acidosis and respiratory acidosis are present.

A

Severe asthma exacerbation can lead to both metabolic acidosis (due to hypoxia and lactic acidosis) and respiratory acidosis (due to hypoventilation).

27
Q

Explain why hyperaldosteronism can cause metabolic alkalosis.

A

Hyperaldosteronism leads to increased sodium reabsorption and potassium and hydrogen ion excretion, resulting in an increase in bicarbonate levels and a shift toward alkalosis.

28
Q

What is the effect of acute kidney injury (AKI) on acid-base status, and what disorder is typically seen?

A

AKI can impair the kidney’s ability to excrete acid, leading to the development of metabolic acidosis, often characterized by a low bicarbonate level.

29
Q

State two common causes of respiratory alkalosis.

A

Anxiety (due to hyperventilation) and hypoxia (such as in pulmonary embolism or high altitude).

30
Q

Describe the classic ABG findings in a patient with chronic obstructive pulmonary disease (COPD) exacerbation.

A

Patients often present with respiratory acidosis (elevated PaCO2) and a compensatory increase in bicarbonate (HCO3), along with a reduced pH.

31
Q

Explain the term ‘compensated metabolic alkalosis’.

A

Compensated metabolic alkalosis occurs when the respiratory system compensates for the metabolic alkalosis by hypoventilating (increasing PaCO2) to increase the acidic load and balance the elevated bicarbonate levels.

32
Q

What acid-base disorder might you expect in a patient with severe sepsis and why?

A

Metabolic acidosis, typically due to lactic acidosis. Sepsis often leads to tissue hypoxia and increased lactate production.

33
Q

Describe the typical ABG changes in a patient with early stages of acute respiratory distress syndrome (ARDS).

A

In the early stages of ARDS, patients may develop respiratory alkalosis due to hyperventilation from hypoxia, leading to a reduced PaCO2 and elevated pH.

34
Q

Explain how hypovolemic shock can lead to metabolic acidosis.

A

Hypovolemic shock leads to decreased tissue perfusion, causing anaerobic metabolism and lactic acid accumulation, which results in metabolic acidosis.

35
Q

What is the primary compensatory response in metabolic alkalosis, and how does it affect PaCO2?

A

The primary compensatory response to metabolic alkalosis is hypoventilation, leading to an increase in PaCO2 as the body retains CO2 to counterbalance the alkalosis.

36
Q

List two common causes of high anion gap metabolic acidosis (HAGMA) that involve toxins or poisons.

A

Methanol ingestion and ethylene glycol poisoning are common causes of high anion gap metabolic acidosis due to the accumulation of toxic metabolites.

37
Q

How does acute respiratory acidosis affect the kidney’s compensatory response?

A

In acute respiratory acidosis, the kidneys will attempt to compensate by retaining bicarbonate over a period of hours to days, though compensation may not be sufficient in the acute phase.

38
Q

Explain the concept of ‘corrected bicarbonate’ in the context of mixed acid-base disorders.

A

Corrected bicarbonate refers to adjusting the bicarbonate level based on a patient’s current PaCO2 to account for the respiratory component in the assessment of mixed acid-base disturbances.

39
Q

Name one condition that can cause a normal anion gap metabolic acidosis but result in a significant shift in chloride levels.

A

Diarrhea is a common cause of normal anion gap metabolic acidosis, where the loss of bicarbonate is matched by an increase in chloride levels (hyperchloremic acidosis).

40
Q

What compensatory mechanism is seen in respiratory alkalosis, and how does it affect bicarbonate levels?

A

In respiratory alkalosis, the kidneys compensate by excreting bicarbonate, leading to a decrease in bicarbonate levels to help restore pH balance.

41
Q

What are the hallmark ABG findings in a patient with hyperventilation due to anxiety?

A

In hyperventilation due to anxiety, ABG findings typically include respiratory alkalosis with a decreased PaCO2 and increased pH, along with normal or slightly reduced bicarbonate levels as compensation.

42
Q

Describe the pathophysiology behind lactic acidosis as a cause of metabolic acidosis.

A

Lactic acidosis results from the accumulation of lactate due to anaerobic metabolism, often triggered by conditions such as shock, sepsis, or severe hypoxia, leading to a decreased pH and a low bicarbonate level.

43
Q

Identify a condition in which both metabolic acidosis and metabolic alkalosis could be present simultaneously.

A

Chronic kidney disease with vomiting can present with both metabolic acidosis (due to kidney failure) and metabolic alkalosis (due to loss of gastric acid).

44
Q

Explain the concept of ‘buffering capacity’ in acid-base physiology.

A

Buffering capacity refers to the ability of a system to resist changes in pH when an acid or base is added. The bicarbonate buffer system is the primary extracellular buffer.

45
Q

How does hypercapnia contribute to acidosis?

A

Hypercapnia (elevated PaCO2) leads to increased carbonic acid concentration in the blood, which dissociates to release hydrogen ions, thus lowering pH and causing respiratory acidosis.

46
Q

Explain the pathophysiological mechanism behind diabetic ketoacidosis (DKA) and its effect on acid-base status.

A

DKA leads to the production of ketoacids due to the lack of insulin and increased fatty acid metabolism. The accumulation of these acids results in metabolic acidosis.

47
Q

Which acid-base disturbance is most commonly associated with severe asthma attacks?

A

Respiratory acidosis is commonly seen during severe asthma attacks due to hypercapnia from impaired ventilation.

48
Q

Describe the role of the kidneys in compensating for respiratory alkalosis.

A

In respiratory alkalosis, the kidneys compensate by decreasing bicarbonate reabsorption and increasing its excretion to reduce the buffering capacity and lower pH.