AcidBase Flashcards
1
Q
- What is the importance of maintaining a physiologic acid-base status?
A
- A physiologic acid-base status optimizes enzyme function, myocardial contractility, and the saturation of hemoglobin with oxygen. (363)
2
Q
- What are acids and bases?
A
- According to Brønsted and Lowry, an acid is a molecule that can act as a proton (H+) donor and a base is a molecule that can act as a proton acceptor; in biological systems, weak acids or bases can reversibly donate or bind H+. (363)
3
Q
- How are acidemia and alkalemia defined?
A
- Acidemia is defined as an arterial pH less than 7.35, and alkalemia is defined as an arterial pH greater than 7.45. (363)
4
Q
- How are acidosis and alkalosis defined?
A
- An acidosis is the underlying process that lowers pH, while an alkalosis is the process that raises pH; a patient may have a mixed disorder but will ultimately be either acidemic or alkalemic. (363)
5
Q
- What is the definition of base excess?
A
- Base excess is defined as the amount of strong acid or strong base required to return 1 L of whole blood (at a PCO2 of 40 mm Hg) to a pH of 7.4. (364)
6
Q
- What is the clinical utility of measuring the base excess?
A
- The base excess indicates the nonrespiratory (metabolic) component of an acid-base disorder: a negative value suggests metabolic acidosis and a positive value suggests metabolic alkalosis; it is also used as a surrogate for lactic acidosis to assess volume resuscitation. (364)
7
Q
- What is the normal plasma H+ concentration, the normal plasma HCO3− concentration, and the normal arterial pH of blood?
A
- At 37° C, the normal plasma H+ concentration is 35 to 45 nmol/L, the normal plasma HCO3− concentration is 24 ± 2 mEq/L, and the normal arterial pH is between 7.36 and 7.44. (364)
8
Q
- How does the body regulate acid-base disturbances to maintain normal arterial pH?
A
- Normal arterial pH is maintained through three systems: buffering (immediate), respiratory adjustments (minutes), and renal responses (12 to 48 hours, up to 5 days for maximal effect). (364)
9
Q
- What is a buffer?
A
- A buffer is a substance that minimizes pH changes in a solution by reversibly binding or releasing hydrogen ions; it consists of a weak acid and its conjugate base. (364)
10
Q
- What is the pKa?
A
- The pKa is the pH at which an acid is 50% protonated and 50% deprotonated. (364)
11
Q
- What are the buffering systems in blood? Which buffering system has the greatest contribution to the total buffering capacity of blood?
A
- The buffering systems include bicarbonate, hemoglobin, phosphate, plasma proteins, and ammonia; the bicarbonate system contributes about 50% of the total buffering capacity, while hemoglobin accounts for about 35%. (364)
12
Q
- How does the bicarbonate buffering system work? What enzyme facilitates this reaction?
A
- Carbonic anhydrase catalyzes the hydration of carbon dioxide to form carbonic acid (H2CO3), which then dissociates into hydrogen ions and bicarbonate (HCO3−), thus buffering changes in pH. (364)
13
Q
- How does hemoglobin act as a buffer?
A
- Hemoglobin acts as a weak acid by binding hydrogen ions generated in the bicarbonate buffering process; additionally, deoxyhemoglobin binds more CO2, enhancing its buffering capacity in venous blood. (364-365)
14
Q
- How does the respiratory system respond to acid-base disorders?
A
- The respiratory system adjusts alveolar ventilation via central and peripheral chemoreceptors to alter CO2 elimination, thereby influencing blood pH. (365)
15
Q
- How does the renal system respond to acid-base disorders?
A
- The kidneys regulate pH by reabsorbing bicarbonate, secreting hydrogen ions, and generating ammonia to buffer excess acid. (365)
16
Q
- How quickly can the buffering system, respiratory system, and renal system respond to physiologic changes in arterial pH?
A
- The buffering system responds almost instantaneously; the respiratory response occurs within minutes; and the renal response takes 12 to 48 hours, with maximal compensation in up to 5 days. (365)
17
Q
- What is the relationship between a venous and arterial blood gas drawn from the same patient concurrently?
A
- Venous blood gases have a pH slightly (0.03 to 0.04) lower than arterial values, but venous blood is not reliable for oxygenation assessment because PvO2 is much lower than PaO2. (366)
18
Q
- What errors can occur if heparin or air is present in an arterial blood gas sample?
A
- Excess heparin can dilute blood gas measurements, and air bubbles can alter gas tensions by diffusion, typically causing a decrease in measured CO2; the effect on O2 depends on the patient’s actual oxygen tension. (367)
19
Q
- What happens if there is a delay in analysis of the blood gas sample?
A
- Delays allow metabolic activity (especially by white blood cells) to consume oxygen and produce CO2, potentially altering the blood gas values; this is minimized by placing the sample on ice. (367)
20
Q
- How does temperature affect the arterial blood gas (ABG)?
A
- Lower temperatures reduce the partial pressures of gases in solution: for instance, a blood gas at 37° C with pH 7.4 and PCO2 40 mm Hg will have a pH of 7.58 and PCO2 of 23 mm Hg at 25° C, and PO2 decreases roughly 6% for each °C below 37° C. (367)
21
Q
- How does an anesthesia provider manage the patient when using alpha stat during cardiopulmonary bypass?
A
- Using alpha stat, management is based on an ABG measured at 37° C with a target pH of 7.4, without adjusting for the patient’s actual hypothermia. (367)
22
Q
- How does an anesthesia provider manage the patient when using pH stat during cardiopulmonary bypass?
A
- With pH stat, the ABG is corrected for the patient’s temperature, often requiring the addition of CO2 so that the temperature-corrected blood gas maintains a pH of 7.4. (367)
23
Q
- What is the difference between a primary disturbance and a compensatory disturbance in acid-base status?
A
- A primary disturbance is the initial alteration in pH due to a respiratory or metabolic cause, while a compensatory disturbance is the body’s secondary response aimed at partially correcting the pH deviation. (368)
24
Q
- What defines a primary metabolic acidosis or alkalosis?
A
- Primary metabolic acidosis is characterized by a pH < 7.35 with HCO3− < 22 mEq/L; metabolic alkalosis by a pH > 7.45 with HCO3− > 26 mEq/L. (368)
25
Q
- What defines a primary respiratory acidosis or alkalosis?
A
- A primary respiratory acidosis is indicated by a PCO2 > 43 mm Hg, while a primary respiratory alkalosis is indicated by a PCO2 < 37 mm Hg. (368)
26
Q
- What adverse responses are associated with severe acidemia?
A
- Severe acidemia leads to decreased myocardial contractility, hypotension, and in the brain, confusion, loss of consciousness, or seizures; respiratory acidosis may produce more rapid and pronounced myocardial depression. (369)
27
Q
- What adverse responses are associated with severe alkalemia?
A
- Severe alkalemia can result in decreased cerebral and coronary blood flow due to arteriolar vasoconstriction, leading to confusion, myoclonus, depressed consciousness, and seizures. (369)
28
Q
- What are the causes of a respiratory acidosis?
A
- Respiratory acidosis may result from increased CO2 production (eg, malignant hyperthermia, sepsis), decreased CO2 elimination (eg, CNS depressants, pulmonary disease, airway obstruction), or rebreathing due to exhausted soda lime, incompetent valves, or laparoscopic surgery. (369)
29
Q
- What is the compensatory response for a respiratory acidosis?
A
- The kidneys compensate for respiratory acidosis by increasing hydrogen ion secretion and bicarbonate reabsorption over hours to days, leading to elevated HCO3− levels in chronic cases. (369)
30
Q
- What is the treatment for a respiratory acidosis?
A
- Treatment is directed at correcting the underlying cause; if pH falls below 7.2, mechanical ventilation may be required to reduce PCO2. (369)
31
Q
- What are the causes of a respiratory alkalosis?
A
- Respiratory alkalosis may result from increased minute ventilation relative to CO2 production (eg, anxiety, pain, CNS disorders) or decreased CO2 production (eg, hypothermia, muscle paralysis). (369)
32
Q
- What is the compensatory response for a respiratory alkalosis?
A
- The kidneys compensate by decreasing bicarbonate reabsorption and increasing urinary excretion of bicarbonate. (369)
33
Q
- What is the treatment for a respiratory alkalosis?
A
- Treatment involves addressing the underlying cause; mild cases often require no specific therapy, though during general anesthesia, minute ventilation may be reduced. (369)
34
Q
- What are the causes of a metabolic acidosis?
A
- Metabolic acidosis may be due to an increased anion gap (eg, lactic acidosis, ketoacidosis, toxins) or a normal anion gap (eg, bicarbonate loss via diarrhea or renal tubular acidosis). (369)
35
Q
- How is the anion gap calculated?
A
- Anion gap = Na+ − (Cl− + HCO3−), with normal values of 8 to 12 mEq/L; lower albumin levels reduce the gap. (370)
36
Q
- How does the Stewart strong ion approach to understanding acid-base status differ from the classic Henderson-Hasselbalch approach?
A
- The Stewart approach distinguishes six primary disturbances (strong ion, nonvolatile buffer, and respiratory acidosis/alkalosis) and incorporates variables like albumin, whereas the Henderson-Hasselbalch method classifies disorders into metabolic and respiratory categories. (370)
37
Q
- What is the compensatory response for a metabolic acidosis?
A
- Compensation for metabolic acidosis includes increased alveolar ventilation (to lower CO2) and renal excretion of hydrogen ions with bicarbonate reabsorption; chronic metabolic acidosis can also lead to bone buffering. (370)
38
Q
- What is the treatment for a metabolic acidosis?
A
- Treatment depends on the presence of an anion gap: for nongap acidosis, sodium bicarbonate may be given; for anion gap acidosis, the underlying cause must be addressed (eg, oxygen, fluids, insulin for diabetic ketoacidosis). (371)
39
Q
- What are some of the concerns regarding the administration of bicarbonate for the treatment of metabolic acidosis?
A
- Administration of bicarbonate is controversial because it produces CO2, which can worsen acidosis if ventilation is inadequate. (371)
40
Q
- What are the causes of a metabolic alkalosis?
A
- Metabolic alkalosis may result from bicarbonate gain or hydrogen ion loss; causes are classified as chloride-responsive (eg, diuretics, vomiting) or chloride-resistant (eg, hyperaldosteronism, refeeding syndrome, hypovolemia, severe hypokalemia). (371)
41
Q
- What is the compensatory response for a metabolic alkalosis?
A
- The body compensates by increasing hydrogen ion reabsorption, decreasing its secretion, and inducing alveolar hypoventilation; the effectiveness depends on sodium, potassium, and chloride availability. (371)
42
Q
- What is the treatment for a metabolic alkalosis?
A
- Treatment involves correcting the underlying cause, such as stopping acid loss, administering saline with potassium chloride, and sometimes acetazolamide to induce bicarbonaturia. (371)
43
Q
- What are the steps for diagnosing an acid-base disorder?
A
- Steps: 1) Assess oxygenation via the A-a gradient; 2) Determine acidemia (pH <7.35) or alkalemia (pH >7.45); 3) Identify whether the primary disturbance is respiratory (PCO2 deviation) or metabolic (HCO3− deviation); 4) For respiratory disorders, assess if the process is acute or chronic; 5) For metabolic acidosis, calculate the anion gap; 6) Determine the Δgap; 7) Evaluate if respiratory compensation is appropriate. (371)
44
Q
- How can an acute respiratory process be distinguished from a chronic process?
A
- An acute respiratory acidosis shows a pH change of about 0.08 per 10 mm Hg increase in PCO2 from 40 mm Hg, whereas a chronic process shows a change of only about 0.03 per 10 mm Hg, reflecting renal compensation. (371)
45
Q
- How is the ∆gap determined?
A
- The ∆gap is determined by subtracting 12 from the measured anion gap and adding this value to the serum bicarbonate level; values <22 mEq/L suggest a concurrent nongap acidosis, and >26 mEq/L suggest a concurrent metabolic alkalosis. (371)
46
Q
- What formula is used to determine if there is appropriate respiratory compensation for a metabolic process?
A
- In metabolic acidosis, the Winter formula (PCO2 = [1.5 × HCO3−] + 8) is used; in metabolic alkalosis, PCO2 = (0.7 × HCO3−) + 21; deviations from these values indicate an additional respiratory disorder. (371)
47
Q
- How does measurement of the PaCO2 help to determine the adequacy of ventilation?
A
- PaCO2 reflects the effectiveness of CO2 removal: values >45 mm Hg suggest hypoventilation, while values <35 mm Hg suggest hyperventilation. (372)
48
Q
- What is the dead space to tidal volume (VD/VT) ratio?
A
- The VD/VT ratio represents the fraction of each tidal volume that is dead space ventilation; a normal value is less than 0.3, predominantly due to anatomic dead space. (372)
49
Q
- What are some causes of arterial hypoxemia?
A
- Arterial hypoxemia may be due to low inspired PO2, hypoventilation, or increased venous admixture from shunts (intrapulmonary or intracardiac). (372)
50
Q
- What does the alveolar gas equation calculate?
A
- The alveolar gas equation calculates the partial pressure of alveolar oxygen (PAO2) based on barometric pressure, water vapor pressure, FIO2, and PCO2. (373)
51
Q
- How is the alveolar-arterial (A-a) gradient calculated? What is the significance of the gradient?
A
- The A-a gradient is calculated as PAO2 minus PaO2; an increased gradient indicates the presence of shunt or ventilation-perfusion mismatch and helps estimate the shunt fraction. (373)
52
Q
- What is the PaO2/FIO2 (P/F) ratio?
A
- The P/F ratio is the ratio of arterial oxygen tension (PaO2) to the fraction of inspired oxygen (FIO2) and is used to assess the severity of hypoxemia; a ratio below 200 is consistent with moderate ARDS and a shunt fraction >20%. (374)
53
Q
- What is the normal mixed venous PO2?
A
- The normal mixed venous PO2 is approximately 40 mm Hg. (374)
54
Q
- What is the clinical utility of the Fick equation?
A
- The Fick equation calculates cardiac output by relating oxygen consumption to the difference between arterial and venous oxygen content, thereby assessing the adequacy of oxygen delivery. (374)
55
Q
- What is the clinical utility of the arteriovenous difference?
A
- The arteriovenous oxygen difference indicates the extent of oxygen extraction by tissues; a normal difference is 4 to 6 mL O2/dL, with higher values suggesting increased extraction (eg, in low cardiac output states) and lower values indicating high output states. (375)
