Chapter 8_2 flashcards

Question 1

Respiratory Compensation for Acidic pH (Metabolic Acidosis)

Answer 1

Lungs INCREASE ventilation (rate and depth) to blow off CO2. This shifts the buffer equation (CO2 + H2O <=> H2CO3 <=> H+ + HCO3-) to the LEFT, reducing H+ concentration and raising pH. [cite: 11, 12]

Question 2

Respiratory Compensation for Basic pH (Metabolic Alkalosis)

Answer 2

Lungs DECREASE ventilation (slow down breathing) to retain CO2. This shifts the buffer equation (CO2 + H2O <=> H2CO3 <=> H+ + HCO3-) to the RIGHT, increasing H+ concentration and lowering pH. [cite: 11, 12]

Question 3

Normal PCO2 Range & Role of Chemoreceptors

Answer 3

Normal PCO2: 35-45 mm Hg. [cite: 12, 15] Chemoreceptors in the brain monitor H+ ion levels and send signals to the medullary respiratory center to adjust ventilation and CO2 levels as needed. [cite: 12]

Question 4

Renal Compensation for Acidic pH (Respiratory Acidosis)

Answer 4

Kidneys RETAIN HCO3- (bicarbonate, a base) and EXCRETE H+ (acid) to lessen acidity and raise blood pH. [cite: 13]

Question 5

Renal Compensation for Basic pH (Respiratory Alkalosis)

Answer 5

Kidneys RETAIN H+ (acid) and EXCRETE HCO3- (bicarbonate, a base) to increase acidity and lower blood pH. [cite: 13]

Question 6

Respiratory Acidosis: Defining ABG Criteria

Answer 6

Blood pH < 7.35 AND PCO2 > 45 mm Hg. [cite: 28]

Question 7

Respiratory Acidosis: Pathophysiology

Answer 7

Lungs unable to remove sufficient CO2 (hypoventilation) -> CO2 accumulates -> equation (CO2 + H2O <=> H2CO3 <=> H+ + HCO3-) shifts to the RIGHT -> increased H+ -> decreased pH. [cite: 28]

Question 8

Respiratory Acidosis: Common Causes (Box 8-3)

Answer 8

Pulmonary: COPD (asthma, emphysema), pulmonary edema, pneumonia, airway obstruction, underventilation by mechanical ventilation, respiratory muscle weakness. Nonpulmonary: Overdosage of anesthetics/sedatives/narcotics, neuromuscular disorders (Guillain-Barré, myasthenia gravis), CNS depression. [cite: 29]

Question 9

Respiratory Acidosis: Clinical Presentation

Answer 9

Anxiety, restlessness, headache, lethargy, fatigue, shortness of breath, rapid shallow breathing, cough. Advanced: Confusion, somnolence, coma (“carbon dioxide narcosis”). [cite: 29, 30]

Question 10

Respiratory Acidosis: Physical Assessment Findings

Answer 10

Obstructive lung disease signs (wheezing, hyperinflation, barrel chest, decreased breath sounds). Cyanosis, clubbing (if chronic hypoxia). Confusion, disorientation, stupor. [cite: 29]

Question 11

Respiratory Acidosis: Compensation

Answer 11

Kidneys attempt to compensate by reabsorbing HCO3- and excreting H+. Uncompensated: pH < 7.35, PCO2 > 45 mmHg. Compensated: pH normal or nearing normal, PCO2 > 45 mmHg, HCO3- > 26 mEq/L. [cite: 28]

Question 12

Respiratory Acidosis: Treatment

Answer 12

Improve gas exchange: Oxygen administration, bronchodilation, treat underlying pulmonary infection/condition. Severe: Endotracheal intubation and mechanical ventilation. [cite: 29]

Question 13

Respiratory Alkalosis: Defining ABG Criteria

Answer 13

Blood pH > 7.45 AND PCO2 < 35 mm Hg. [cite: 31]

Question 14

Respiratory Alkalosis: Pathophysiology

Answer 14

Hyperventilation -> excessive CO2 exhalation -> low PCO2 -> equation (CO2 + H2O <=> H2CO3 <=> H+ + HCO3-) shifts to the LEFT -> decreased H+ -> increased pH. Often due to anxiety. Hypocalcemia and hypokalemia may develop. [cite: 31]

Question 15

Respiratory Alkalosis: Common Causes (Box 8-4)

Answer 15

Pulmonary: Pneumonia, pulmonary edema/embolus, asthma, hypoxia with hyperventilation, overventilation by mechanical ventilation. Nonpulmonary: Anxiety, pain, liver disease, fever/infection/sepsis, CNS disorders, salicylate/alcohol intoxication. [cite: 31]

Question 16

Respiratory Alkalosis: Clinical Presentation

Answer 16

Tingling of extremities (paresthesia), muscle cramps, tetany (due to hypocalcemia), dizziness, syncope, confusion, anxiety, seizures, coma. Cardiac: palpitations, dysrhythmias, hypotension. [cite: 32]

Question 17

Respiratory Alkalosis: Compensation

Answer 17

Kidneys attempt to compensate by reabsorbing H+ and excreting HCO3-. Uncompensated: pH > 7.45, PCO2 < 35 mmHg. Compensated: pH normal or nearing normal, PCO2 < 35 mmHg, HCO3- < 22 mEq/L. [cite: 32]

Question 18

Respiratory Alkalosis: Treatment

Answer 18

Identify and treat underlying trigger of hyperventilation. Slow respiration (e.g., breathing into a paper bag to rebreathe CO2, CO2 rebreather mask). Pain management or sedation if needed. [cite: 32]

Question 19

Metabolic Acidosis: Defining ABG Criteria

Answer 19

Blood pH < 7.35 with normal OR low PCO2 (PCO2 < 35 mmHg if compensating). HCO3- < 22 mEq/L. [cite: 33]

Question 20

Metabolic Acidosis: Pathophysiology Mechanisms

Answer 20

1. Increased level of non-carbonic acids in bloodstream (e.g., DKA - ketones, lactic acidosis). 2. Decreased excretion of acids by kidneys. 3. Loss of base (bicarbonate) from bloodstream (e.g., prolonged diarrhea). Hyperkalemia and hypercalcemia may develop. [cite: 33]

Question 21

Metabolic Acidosis: Common Causes (Box 8-5)

Answer 21

Increased Noncarbonic Acids: DKA, lactic acidosis, alcoholic ketoacidosis, uremic acidosis, ingestion of toxins (antifreeze, aspirin), intestinal/biliary/pancreatic fistulas. Bicarbonate Loss: Prolonged diarrhea, renal tubular acidosis, interstitial renal disease, acetazolamide ingestion. [cite: 33]

Question 22

Metabolic Acidosis: Clinical Presentation

Answer 22

Respiratory distress (Kussmaul’s breathing), headache, drowsiness, confusion, seizures, neuromuscular fatigue, twitching, coma. GI: nausea, vomiting, anorexia. Cardiovascular: hypotension, dysrhythmias, decreased contractility. [cite: 34]

Question 23

Metabolic Acidosis: Compensation

Answer 23

Lungs: Increase ventilation (depth and rate - Kussmaul’s breathing) to blow off CO2 (PCO2 becomes <35 mmHg). Kidneys (if healthy): Reabsorb HCO3- and excrete H+. [cite: 34]

Question 24

Metabolic Acidosis: Treatment

Answer 24

Treat underlying cause (e.g., insulin for DKA, hemodialysis for renal failure). Correct electrolyte/fluid balance. IV sodium bicarbonate in severe cases (pH < 7.20), with caution to avoid rebound alkalosis. [cite: 34]

Question 25

Anion Gap (AG) in Metabolic Acidosis: Increased AG

Answer 25

Occurs when large amounts of unmeasured acids (e.g., ketones in DKA, lactate) enter bloodstream. Bicarbonate (measured anion) buffers these acids and decreases, while unmeasured anions increase, thus increasing the AG. [cite: 21, 22] Causes: Lactic acidosis, Ketoacidosis, Renal failure, Aspirin overdose, Methanol/glycol ingestion. [cite: 23]

Question 26

Anion Gap (AG) in Metabolic Acidosis: Normal AG

Answer 26

Occurs when metabolic acidosis is due to loss of bicarbonate (a measured anion), which is often replaced by chloride (another measured anion), keeping the AG normal. Causes: GI loss of bicarbonate (diarrhea), Increased renal bicarbonate loss, Hypoaldosteronism, Ingestion of ammonium chloride. [cite: 21, 23]

Question 27

Metabolic Alkalosis: Defining ABG Criteria

Answer 27

Blood pH > 7.45 with normal OR high PCO2 (PCO2 > 45 mmHg if compensating). HCO3- > 26 mEq/L. [cite: 35]

Question 28

Metabolic Alkalosis: Pathophysiology Mechanisms

Answer 28

1. Excessive loss of acids unrelated to CO2 (e.g., loss of H+ from GI tract via vomiting/NG suction, or kidneys via diuretics). 2. Increase in bicarbonate levels (e.g., bicarbonate ingestion, retention of sodium bicarbonate). Hypocalcemia and hypokalemia may develop. [cite: 35]

Question 29

Metabolic Alkalosis: Common Causes (Box 8-6)

Answer 29

Bicarbonate ingestion/IV admin, K+-wasting diuretics, loss of gastric fluids (vomiting, NG suction, bulimia), Cushing’s syndrome, hyperaldosteronism. [cite: 35]

Question 30

Metabolic Alkalosis: Clinical Presentation

Answer 30

Confusion, dizziness, agitation, weakness, vomiting, diarrhea, seizures. Related electrolyte imbalances cause muscle weakness, myalgia, spasms, cardiac arrhythmias (hypokalemia); tetany, Chvostek’s/Trousseau’s signs (hypocalcemia). [cite: 36]

Question 31

Metabolic Alkalosis: Compensation

Answer 31

Lungs: Decrease ventilation to retain CO2 (PCO2 becomes >45 mmHg), lowering pH. Kidneys: Excrete HCO3- and retain H+. [cite: 36]

Question 32

Metabolic Alkalosis: Treatment

Answer 32

Treat underlying cause. Electrolyte and fluid replacement. Potassium-sparing diuretics if diuretic-induced. Acetazolamide (increases HCO3- excretion) for moderate/severe cases. [cite: 36]

Question 33

Relationship between pH and Potassium (K+)

Answer 33

Acidosis: H+ shifts into cells, K+ shifts out of cells into ECF -> hyperkalemia. Kidneys excrete H+ instead of K+. [cite: 25] Alkalosis: K+ shifts into cells from ECF, H+ shifts out -> hypokalemia. Kidneys excrete more K+. [cite: 25] Hyperkalemia can cause H+ to shift out of cells -> acidosis. Hypokalemia can cause H+ to shift into cells -> alkalosis. [cite: 25]

Question 34

Relationship between pH and Calcium (Ca++)

Answer 34

Acidosis: Increased H+ competes with Ca++ for albumin binding sites -> increased free, ionized Ca++ -> hypercalcemia. [cite: 26] Alkalosis: Decreased H+ -> less competition -> more Ca++ binds to albumin -> decreased free, ionized Ca++ -> hypocalcemia. [cite: 26]

Question 35

Effect of K+ and Ca++ Disturbances (from pH changes) on Cell Excitability

Answer 35

Hyperkalemia (acidosis): Resting membrane potential more positive -> cells hyperexcitable. [cite: 26] Hypokalemia (alkalosis): Resting membrane potential less positive -> cells less excitable. [cite: 26] Hypercalcemia (acidosis): Increases depolarization threshold -> cells less excitable. [cite: 26] Hypocalcemia (alkalosis): Lowers depolarization threshold -> cells more excitable (tetany). [cite: 26]

Question 36

Interpretation of ABGs: ROME Mnemonic

Answer 36

Respiratory Opposite (pH and PCO2 move in opposite directions). Metabolic Equal (pH and PCO2 move in the same direction, or PCO2 is normal and HCO3- is the primary derangement reflecting pH). [cite: 40]

Question 37

Mixed Acid-Base Disorders

Answer 37

More than one type of acid-base disturbance present simultaneously, often due to multiple underlying conditions. Requires careful analysis of ABGs, anion gap, and patient presentation. [cite: 37]