Acid-Base Balance in Physiology

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Questions and Answers

What is the effect of adding hydrogen ions to the blood, assuming all other factors remain consistent?

Increase in blood bicarbonate concentration

No change in blood hydrogen ion concentration

Increase in blood hydrogen ion concentration (correct)

Decrease in blood hydrogen ion concentration

What enzyme facilitates the conversion of carbon dioxide to carbonic acid within red blood cells?

Glutaminase

Deaminase

Bicarbonate synthase

Carbonic anhydrase (correct)

Which of the following physiological changes would lead to a decrease in blood hydrogen ion concentration?

Addition of hydrogen ions

Removal of bicarbonate

Increased PCO2

Addition of bicarbonate (correct)

In the context of renal tubular cells, what molecule is produced as a result of glutamine deamination?

Ammonia Signup and view all the answers

What is the primary cause of a 'metabolic' acid-base disorder?

Change in bicarbonate concentration Signup and view all the answers

What is the primary form in which carbon dioxide is transported in the blood?

Bicarbonate Signup and view all the answers

A patient is hyperventilating which ultimately causes a decrease in PCO2. This would be most accurately described as which type of acid-base imbalance disorder?

Respiratory alkalosis Signup and view all the answers

Which of the following indicates a primary respiratory disorder causing an acid-base imbalance?

High PCO2 levels Signup and view all the answers

What process occurs in the lungs that leads to the excretion of carbon dioxide?

Bicarbonate is converted to carbonic acid, then to carbon dioxide Signup and view all the answers

According to the bicarbonate buffer system formula $H^+ \propto \frac{PCO_2}{HCO_3^-}$, what is the relationship between hydrogen ion concentration and bicarbonate concentration?

Inversely proportional Signup and view all the answers

What is the role of renal compensation in acid-base disorders?

To increase the excretion of hydrogen ions Signup and view all the answers

Which of the following best defines the term 'acidemia'?

A condition where the blood hydrogen ion concentration is higher than normal. Signup and view all the answers

If excess hydrogen ions are present in the blood, what is the immediate action of the bicarbonate buffer system?

Bicarbonate ions bind to hydrogen ions forming carbonic acid. Signup and view all the answers

If a patient has a fully compensated acid-base disorder, what would be true about their blood hydrogen ion levels?

They would be within the normal range. Signup and view all the answers

What is the role of chloride ions in red blood cells during carbon dioxide transport?

To move into red blood cells while bicarbonate moves out Signup and view all the answers

What happens to carbon dioxide after being buffered by bicarbonate?

It is converted to carbon dioxide and lost in the expired air Signup and view all the answers

What is the primary cause of non-respiratory acidosis?

Increased production or decreased excretion of hydrogen ions Signup and view all the answers

Which of the following conditions can lead to non-respiratory acidosis due to increased hydrogen ion formation?

Ketoacidosis Signup and view all the answers

What effect does hyperventilation provide in a person experiencing non-respiratory acidosis?

It lowers the PCO2 by removing carbon dioxide Signup and view all the answers

A patient presents with a deep, rapid, and gasping respiratory pattern. What is this pattern known as?

Kussmaul breathing Signup and view all the answers

Which of the following is a typical characteristic of blood in a person with non-respiratory acidosis?

High [H+], low pH, low PCO2, low [HCO3-] Signup and view all the answers

What could result from loss of alkaline secretions from the small intestine?

Non-respiratory acidosis Signup and view all the answers

Besides the kidneys, what body system can compensate for the change in pH due to metabolic acidosis?

Respiratory Signup and view all the answers

What is commonly observed in patients with acidosis and related to potassium levels?

Hyperkalemia Signup and view all the answers

Which condition is most likely to increase the risk of cardiac arrest in the context of acidosis?

Hyperkalemia Signup and view all the answers

In metabolic alkalosis, what is the primary change observed in the extracellular fluid (ECF)?

Increase in bicarbonate concentration Signup and view all the answers

What is a typical renal response to increased plasma bicarbonate concentration under normal conditions?

Increased excretion of bicarbonate in the urine Signup and view all the answers

Which of the following is NOT a typical cause of increased renal bicarbonate reabsorption in non-respiratory alkalosis?

Increased ECF volume Signup and view all the answers

What characterizes respiratory acidosis?

Increase in PCO2 and increase in HCO3- Signup and view all the answers

What occurs when there is a loss of hydrogen ions in gastric fluid during vomiting without equivalent bicarbonate loss?

Metabolic alkalosis Signup and view all the answers

In acute respiratory acidosis, the primary physiological problem is:

Alveolar hypoventilation leading to CO2 retention. Signup and view all the answers

What physiological changes are likely to occur as a consequence of decreased unbound plasma calcium concentration due to alkalosis?

Muscle cramps, tetany, and paraesthesia Signup and view all the answers

What is the primary physiological effect of a low arterial [H+] concentration?

Inhibition of the respiratory center, leading to hypoventilation Signup and view all the answers

In the context of acute non-respiratory alkalosis, why might respiratory compensation be self-limiting?

An increase in PCO2 is a powerful stimulus to respiration Signup and view all the answers

What is a typical management strategy for non-respiratory alkalosis when hypovolemia is present?

Infusion of isotonic sodium chloride to correct hypovolemia and alkalosis Signup and view all the answers

Which scenario would require exceptionally large quantities of ingested alkali to produce sustained alkalosis?

The patient has normal renal function Signup and view all the answers

During respiratory acidosis, for every hydrogen ion produced, what else is generated?

A bicarbonate ion. Signup and view all the answers

Why might a patient with metabolic alkalosis paradoxically pass acidic urine?

Hydrogen ions being retained inside cells to replace missing potassium ions Signup and view all the answers

Which of the following scenarios would result in a mixed acid-base disorder of metabolic alkalosis and respiratory acidosis?

Prolonged nasogastric suction and chronic obstructive airway disease Signup and view all the answers

What distinguishes acute respiratory acidosis from chronic respiratory acidosis?

Acute has no time for renal compensation to develop, while chronic does. Signup and view all the answers

In a patient with chronic bronchitis, the development of renal impairment would likely result in which condition?

Respiratory acidosis and decreased bicarbonate concentration Signup and view all the answers

Which of the following best describes the acid-base disturbances seen in salicylate poisoning?

Metabolic acidosis and respiratory alkalosis Signup and view all the answers

A patient with chronic obstructive airway disease develops thiazide-induced potassium depletion. What acid-base derangements are most likely?

Respiratory acidosis and metabolic alkalosis Signup and view all the answers

A normal blood pH value can still indicate an acid-base disorder when which condition is present?

Either a fully compensated disturbance or two primary disturbances that offset each other Signup and view all the answers

If a patient has an increased PCO2 in the context of an acidosis, what can be immediately concluded?

There is a respiratory component to the acidosis. Signup and view all the answers

Which of the following factors is NOT described in the content as part of the compensatory mechanism for non-respiratory alkalosis?

Renal adjustment of bicarbonate reabsorption. Signup and view all the answers

What is the starting point in evaluating acid-base disturbances, regardless of other conditions?

Hydrogen ion concentration or pH Signup and view all the answers

What does an abnormal PCO2 value indicate about an acid-base disorder?

It indicates a respiratory component to the disturbance. Signup and view all the answers

Study Notes

Water and Electrolytes

Water, sodium, potassium, chloride are electrolytes crucial for bodily functions.
Acid-base balance is vital for maintaining homeostasis.

Acid-Base Homeostasis

Blood hydrogen ion concentration is tightly regulated.
Normal levels are 35-45 nmol/L (pH 7.35-7.46) in extracellular fluid.
Intracellular fluid has a slightly higher pH which is still tightly controlled.
Normal pH for arterial blood is 7.4.
Venous blood and interstitial fluid pH is 7.35.
Intracellular fluid pH is 7.0.
Alkalosis/alkalemia: arterial blood pH above 7.45.
Acidosis/acidemia: arterial blood pH below 7.35 (physiological acidosis).

Sources of Hydrogen Ions

Carbon dioxide transport as bicarbonate releases hydrogen ions.
Breakdown of sulfur-containing proteins releases hydrogen ions into extracellular fluid (ECF).
Incomplete oxidation of energy substrates (e.g., lactic acid from anaerobic respiration of glucose, organic acids and ketone bodies from fat metabolism).
Temporary imbalances between the rates of production and consumption can occur (e.g., lactic acid accumulation during anaerobic exercise).
Increased hydrogen ion production in disease contributes to acidosis.
The total amount of hydrogen ions produced daily is 100,000 times greater than normal.

Hydrogen Ion Regulation

Hydrogen ion concentration is regulated sequentially by chemical buffer systems, the respiratory center, and renal mechanisms.
Chemical buffer systems act within seconds.
The respiratory center (in the brain stem) acts within 1-3 minutes.
Renal mechanisms require hours to days to effect pH changes.

Chemical Buffer Systems

Three major chemical buffer systems: bicarbonate, phosphate, and protein buffer systems.
These buffer systems resist any pH changes.

Buffering of Hydrogen Ions

Buffers limit the rise in hydrogen ion concentration by combining with hydrogen ions.
A buffer is a solution containing a weak acid or salt that can bind hydrogen ions.
When hydrogen ions are added to a buffer, they combine with the conjugate base, forming the undissociated acid.

Buffer Solution Mechanism

Buffers resist changes in pH when either a strong acid or base is added.
When a strong acid is added, hydrogen ions combine with bicarbonate to form carbonic acid.
When a strong base is added, it reacts with carbonic acid to from sodium bicarbonate.

Buffering of Hydrogen Ions (Continued)

Buffers do not remove hydrogen ions, but temporarily neutralize excess hydrogen ions.
Buffering is a short-term solution.
Buffer efficiency is limited by concentration and equilibrium position.

Bicarbonate Reabsorption

Virtually all filtered bicarbonate in kidneys is reabsorbed.
Bicarbonate reabsorption is an indirect process that utilizes carbonic anhydrase.
Carbon dioxide (CO2) and water (H2O) form carbonic acid (H2CO3); H2CO3 dissociates into bicarbonate and hydrogen ions (H+).
Bicarbonate ions move from tubular cells into interstitial fluid.

Bicarbonate Reabsorption and Hydrogen Ion Excretion

Excretion of hydrogen ions must be buffered.
Bicarbonate reabsorption is indirect, occurring within the renal tubular cells.
Carbonic acid forms from carbon dioxide and water, catalyzed by carbonic anhydrase.
Bicarbonate moves into interstitial fluid with sodium ions.

Bicarbonate Buffer System (Continued)

The capacity of the bicarbonate buffer system is limited and the bicarbonate must be regenerated.
Excretion of hydrogen ions depends on the same reactions as bicarbonate reabsorption but is influenced by an appropriate urine buffer.

How is CO2 Exported?

Most carbon dioxide is carried as bicarbonate.
Dissolved carbon dioxide, carbonic acid, and carbamino compounds contribute a smaller amount to the total carbon dioxide.

Transport of Carbon Dioxide

Aerobic metabolism produces carbon dioxide that diffuses out of cells and into Extracellular Fluid (ECF).
A small amount combines with water to form carbonic acid.
In red blood cells, carbon dioxide diffuses into red blood cells.
Carbon dioxide is converted to bicarbonate inside red blood cells and is facilitated by carbonic anhydrase which enhances the conversion of carbon dioxide.
Bicarbonate diffuses out of red blood cells in exchange for chloride ions.

Assessing Acid-Base Status

Acid-base status is assessed by measuring bicarbonate buffer system components (water, CO2, H2CO3, H+, HCO3- (bicarbonate)).
Excess hydrogen ions are buffered. Carbon dioxide is lost in expired air.
Hydrogen ion concentration is proportional to PCO2.

Assessing Acid-Base Status (Continued)

Hydrogen ion concentration in blood varies with bicarbonate concentration and PCO2 changes.
Adding hydrogen ions, or removing bicarbonate, or increasing PCO2 increases [H+].
Removing hydrogen ions, or adding bicarbonate, or lowering PCO2 decreases [H+].
Normal blood [H+] is 40 nmol/L controlled by respiration and kidney function.

Disorders of Hydrogen Ion Homeostasis

"Metabolic" acid-base disorders directly affect bicarbonate concentration.
Insulin deficiency, buildup of ketone bodies, or bicarbonate loss from ECF can cause metabolic disorders.
"Respiratory" acid-base disorders affect PCO2, such as impaired respiration or hyperventilation which causes a decreased PCO2.

Non-Respiratory (Metabolic) Acidosis

Increased production or decreased excretion of hydrogen ions can cause non-respiratory acidosis.
Causes of non-respiratory acidosis include ketoacidosis, lactic acidosis, poisoning, acid ingestion, decreased H+ excretion, and loss of bicarbonate.

Causes of Non-Respiratory Acidosis (Continued)

Ketoacidosis (often diabetic or alcoholic).
Lactic acid.
Poisoning (ethanol, methanol, ethylene glycol, salicylate).
Acid ingestion (acid poisoning).
Renal tubular acidosis.
Generalized renal failure.
Carbonate anhydrase inhibitors.
Diarrhea, pancreatic, intestinal or biliary fistulae or drainage.

Metabolic Acidosis

Acidosis develops when hydrogen ions accumulate or bicarbonate is lost.
Respiratory compensation occurs quickly in response to an increase in hydrogen ions concentration or a reduction in bicarbonate.

Non-Respiratory Acidosis (Further Details)

Characterized as high [H+], low pH, low PCO2, and low [HCO3-].
Compensation via hyperventilation, increasing CO2 removal and lowering PCO2.
Hyperventilation is stimulated by increased [H+].

Non-Respiratory Acidosis (Continued)

In a healthy person, hyperventilation causes respiratory alkalosis.
Excess hydrogen ions can be excreted by the kidneys when renal function is healthy.
Complete correction requires reversing the primary cause (e.g., rehydration or insulin for diabetic ketoacidosis).
Hyperkalemia is common in acidotic patients.

Clinical Effects of Acidosis

Compensatory response to metabolic acidosis is hyperventilation.
Increased [H+] leads to increased neuromuscular irritability.
Arrhythmias may result, particularly with hyperkalemia.

Metabolic Alkalosis (Non-Respiratory Alkalosis)

Characterized by a primary increase in ECF bicarbonate concentration and a consequent reduction in [H+].
Normally, increased plasma bicarbonate causes incomplete bicarbonate reabsorption and excretion in urine.
In non-respiratory alkalosis, high renal bicarbonate reabsorption occurs, contributing factors may include decreased ECF volume, mineralocorticoid excess, increased sodium and carbonate reabsorption, and potassium depletion.
Ingestion of massive quantities of bicarbonate can produce sustained alkalosis.

Causes of Non-Respiratory Alkalosis

Gastrointestinal causes (gastric aspiration, vomiting with pyloric stenosis, congenital chloride-losing diarrhoea).
Renal causes (mineralocorticoid excess; Cushing's syndrome, Conn's syndrome; drugs with mineralocorticoid activity; diuretic therapy (but not K+ sparing drugs); rapid correction of chronically high PCO2, potassium depletion).
Administration of alkali (inappropriate treatment of acidotic states, chronic alkali ingestion).

Metabolic Alkalosis (Continued)

Loss of hydrogen ions in the gastric fluid during vomiting, especially when there is no parallel loss of bicarbonate.
Ingestion of absorbable alkali (sodium bicarbonate) can create alkalosis.
Severe potassium depletion can cause hydrogen ions to be retained in cells (to replace the missing potassium), resulting in more hydrogen being exchanged for sodium reabsorption (causing acidic urine).

Clinical Effects of Metabolic Alkalosis

Hypoventilation, confusion, eventually coma.
Muscle cramps, tetany, and paraesthesia associated with decreased unbound plasma calcium concentration.

Metabolic Alkalosis (Correction)

Correction of non-respiratory alkalosis requires reversal of the primary cause and maintenance mechanisms.
The expected compensatory response is an increase in PCO2. A low arterial [H+] will inhibit the respiratory center, triggering hypoventilation and increasing PCO2.

Metabolic Alkalosis (Further Details)

While increased PCO2 is a powerful respiratory stimulus, compensation in acute non-respiratory alkalosis may self-limit.
In chronic disorders, significant compensation may occur because the respiratory center becomes less sensitive to carbon dioxide.
Hypoventilation causing further hypoxemia can provide a powerful stimulus to respiratory compensation.

Management

Management of non-respiratory alkalosis depends on the severity and cause.
Hypovolemia is corrected simultaneously by isotonic saline infusion.
Rapid pH correction (e.g., ammonium chloride) is only rarely necessary.
Mild potassium depletion may require correction.

Respiratory Acidosis

Primary disorder is an increased PCO2(CO2 retention).
For each hydrogen ion produced, a bicarbonate ion is generated.
The primary effect of adding hydrogen ion to a concentration of 40 nmol/l is much greater than adding one bicarbonate molecule to 26 mmol/l.
Majority of hydrogen ions are buffered by intracellular buffers (e.g., hemoglobin).

Respiratory Acidosis (Continued)

Renal compensation occurs slowly as the mechanisms to adjust bicarbonate reabsorption take 48-72 hours.

Respiratory Acidosis (Acute conditions)

Acute conditions occur within minutes or hours.
Alveolar hypoventilation leads to increased PCO2 in the blood, causing a quick rise in [H+].

Respiratory Acidosis (Further Details)

Low PO2 and high PCO2 can cause coma.
Examples include acute airway obstruction, choking, bronchopneumonia, acute asthma exacerbation, and depression of respiratory centers (anesthetics or sedatives).

Chronic Respiratory Acidosis

Results from chronic obstructive airway disease and is usually a long-standing condition accompanied by maximum renal compensation.
Primary problem in chronic respiratory acidosis is impaired alveolar oxygen ventilation.
The kidney increases hydrogen ion excretion and ECF bicarbonate levels rise, causing a trend towards normal [H+].

Management of Acidosis

Aim when treating respiratory acidosis is to improve alveolar ventilation and lower PCO2.
In acute alveolar hypoventilation, hypoxia is the main threat.
Treatment of chronic respiratory acidosis focuses on addressing the underlying cause and maximizing alveolar ventilation (physiotherapy, bronchodilators, antibiotics).

Respiratory Alkalosis

Respiratory alkalosis is less common than acidosis but can occur from stimulated respiration.
Acute conditions are usually present with little or no renal compensation.
Renal compensation occurs slowly.
Treatment is focused on inhibiting hyperventilation, which restores acid-base balance to normal levels.

Causes of Respiratory Alkalosis

Hysterical hyperventilation.
Mechanical overventilation of an intensive care patient.
Raised intracranial pressure.
Hypoxia (which stimulates the respiratory center).

Mixed Acid-Base Disorders

Patients can have more than one acid-base disorder.
Examples include chronic bronchitis with renal impairment (resulting in increased PCO2 and decreased bicarbonate).
Prolonged nasogastric suction causes hyperventilation, leading to respiratory alkalosis and metabolic alkalosis.

Mixed Acid-Base Disorders (Continued)

Two acid-base conditions can be antagonistic in affecting [H+], a metabolic acidosis with a co-existing respiratory alkalosis.
Examples include patients with chronic obstructive airway disease with thiazide-induced potassium depletion or patients with salicylate poisoning.

Interpretation of Acid-Base Data

A comprehensive understanding of acid-base homeostasis is essential.
The starting point is the hydrogen ion concentration (or pH).
A normal value does not exclude an acid-base disorder (e.g., a compensated disturbance or two primary disturbances cancelling each other out).

Interpretation of Acid-Base Data (Continued)

Abnormal PCO2 indicates a respiratory component to the disturbance (high PCO2 in acidosis suggests respiratory acidosis; low PCO2 in acidosis suggests a non-respiratory component).
A similar rationale applies to alkalotic states.

Case Studies (Examples)

Provided case studies include patient history, blood gas results, and questions about acid-base disorders and assessment.
Demonstrates application of knowledge to interpret acid-base disorders and appropriate clinical reasoning.

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Description

This quiz explores key concepts related to acid-base balance in the human body, focusing on mechanisms involving hydrogen ions, carbon dioxide, and bicarbonate. Test your knowledge on the physiological changes, enzyme functions, and disorders that influence acid-base equilibrium within the blood and lungs.