Clase 6 Fisiología - Regulación del equilibrio Ácido-Base (IG:@doctor.paiva)

Regulation of Acid-Base Balance in Physiology

In this section, the instructor delves into the regulation of acid-base balance in physiology and pathophysiology, covering topics such as acids and bases, pH measurement, Henderson-Hasselbalch equation, acidosis, and alkalosis.

Generalities of Acids and Bases

• The pH scale measures acidity or alkalinity in a solution based on hydrogen ion concentration.

• The pH is the negative logarithm of hydrogen ions concentration expressed in equivalents per liter.

• Normal hydrogen ion concentration is low compared to other ions like potassium in extracellular fluid.

pH Measurement and Interpretation

• Normal body pH is around 7.4.

• Calculating the log of hydrogen ions concentration yields a value close to 7.4.

• The pH scale ranges from 0 (acidic) to 14 (alkaline), with lower values indicating acidity and higher values indicating alkalinity.

Importance of Maintaining pH Levels

• Human body tolerates a narrow range of pH for survival.

• Deviations outside the range can disrupt cellular functions.

• Early detection and correction of abnormal pH levels are crucial for cellular function.

Electrolytes and Acid-Base Balance

This part focuses on electrolytes' role in maintaining acid-base balance within the body, emphasizing the impact of imbalances on cellular functions.

Electrolyte Imbalance Effects

• Abnormal electrolyte levels disrupt protein structures, enzyme activity, muscle contraction, and neural transmission.

• The internal environment tends towards acidity due to metabolic processes producing volatile (CO2) and non-volatile acids (e.g., phosphoric acid).

Gasometry Values for Assessment

• Essential gasometry values aid in detecting acid-base imbalances promptly.

• Key values include normal pH (7.35–7.45), partial pressure of CO2 (35–45 mmHg), and bicarbonate levels (22–26 mEq/L).

Acids and Bases: Defenses Against pH Changes

Exploring how the body defends against shifts in pH through buffering systems involving bicarbonate, proteins, and phosphates.

Buffering Systems

• Rapid defense mechanisms involve buffer systems that stabilize pH changes within seconds to minutes using bicarbonate, phosphate, and protein buffers.

Understanding Acid-Base Balance in the Body

In this section, the speaker delves into the different defense mechanisms of the body related to acid-base balance, focusing on the respiratory and renal systems.

The Role of the Respiratory System

• The lungs play a crucial role in regulating carbon dioxide elimination through changes in alveolar ventilation.

• The kidneys act as a potent defense mechanism, albeit slower than the respiratory system, by absorbing or excreting hydrogen ions to maintain balance.

Maintaining pH Balance Through Buffer Systems

This part emphasizes how various buffer systems within the body contribute to maintaining pH balance effectively.

Intracellular Proteins and Buffers

• Urine can vary widely in pH from 4.5 (acidic) to 8 (alkaline), showcasing the body's ability to regulate acidity levels.

• Henderson-Hasselbalch equation allows for calculating pH based on bicarbonate and carbon dioxide partial pressure values.

Compensating for Metabolic Acidosis

Exploring metabolic acidosis and how the body compensates for excess hydrogen ions.

Mechanisms of Metabolic Acidosis

• Excess hydrogen ions in metabolic acidosis combine with bicarbonate, forming carbonic acid through carbonic anhydrase enzyme action.

• Carbonic acid dissociates into water and carbon dioxide, which are eliminated via urine and lungs respectively for compensation.

Effects of Compensation on Blood Parameters

Understanding how compensation impacts blood parameters during metabolic acidosis.

Impact on Blood Parameters

• Increased hydrogen ion levels lead to decreased pH and bicarbonate levels due to their interaction with each other.

• Lung compensation involves hyperventilation to eliminate excess carbon dioxide, lowering its partial pressure.

Types of Metabolic Acidosis

Differentiating between types of metabolic acidosis based on specific characteristics.

Classification of Metabolic Acidosis

Acid-Base Disorders in Clinical Practice

In this section, the speaker delves into acid-base disorders commonly encountered in clinical practice, focusing on metabolic acidosis and its various etiologies.

Metabolic Acidosis Causes and Mechanisms

• : Metabolic acidosis can result from an excess of hydrogen ions rather than bicarbonate loss. Causes include diabetic ketoacidosis due to the body utilizing fatty acids for energy production.

• : Lactic acidosis can occur from conditions like cancer, liver failure, seizures, or alcohol intoxication. It involves an accumulation of lactic acid in the body.

• : The formula for calculating the anion gap is emphasized: (Sodium + Potassium) - (Chloride + Bicarbonate). An elevated anion gap indicates excess hydrogen ions.

Compensation and Assessment of Metabolic Acidosis

• : Compensation mechanisms for metabolic acidosis involve decreased pH, bicarbonate levels, and partial pressure of CO2. The respiratory center compensates by adjusting ventilation rates.

• : Understanding how to assess compensation in metabolic acidosis is crucial. The Henderson-Hasselbalch equation helps determine if compensation is adequate based on bicarbonate levels.

Clinical Case Example and Diagnosis

• : A clinical case presents a patient with a low pH, low carbon dioxide pressure, low bicarbonate levels but normal sodium and chloride levels. This pattern indicates uncompensated metabolic acidosis.

• : Calculations using the anion gap formula reveal that the patient's condition stems from bicarbonate deficiency. Assessing compensation through specific ranges aids in diagnosing compensated or uncompensated states.

Understanding Respiratory Acidosis

In this section, the speaker explains the process of respiratory acidosis and its impact on the body's pH balance.

The Process of Respiratory Acidosis

• Carbon dioxide buildup in the lungs leads to excess carbon dioxide in the body.

• Kidneys compensate for respiratory acidosis by excreting hydrogen ions and reabsorbing bicarbonate.

• Respiratory issues like bronchitis or emphysema can cause elevated carbon dioxide levels, leading to acidosis.

Compensation Mechanisms for Respiratory Acidosis

This section delves into how the body compensates for respiratory acidosis through various mechanisms.

Compensation Mechanisms

• Acute and chronic respiratory issues can lead to different forms of compensation by the body.

• Chronic conditions like COPD can result in weight gain due to CO2 retention.

Treatment Considerations for Respiratory Acidosis

Here, treatment considerations for patients with respiratory acidosis are discussed.

Treatment Guidelines

• Avoid administering bicarbonate in respiratory acidosis as it can worsen the condition.

Expected Compensation in Respiratory Acidosis

This part focuses on expected compensation mechanisms in cases of respiratory acidosis.

Expected Compensation

• Bicarbonate levels increase based on CO2 levels, aiming to maintain pH balance within a specific range.

Chronic Respiratory Acidosis Compensation

The discussion shifts towards compensation mechanisms in chronic respiratory acidosis scenarios.

Chronic Compensation

Clinical Case Analysis: Acid-Base Disorders

In this section, a clinical case of a patient with acute bronchitis is analyzed to understand acid-base disorders and compensatory mechanisms.

Understanding the Clinical Case

• The patient presents with low pH, high partial pressure of carbon dioxide (90), and elevated bicarbonate levels.

• Compensation in acute cases involves an increase of 1 in bicarbonate for every 10 mmHg increase in partial pressure of carbon dioxide.

• Calculations show that the expected compensation leads to an increase in bicarbonate levels within the normal range.

Diagnosis and Compensatory Mechanisms

• The final diagnosis is compensated respiratory acidosis due to acute conditions, with specific changes in pH, base excess, and bicarbonate levels.

• Chronic cases involve different compensatory mechanisms where bicarbonate levels are adjusted based on specific rules.

Final Diagnosis and Interpretation

• A bicarbonate level of 29 falls within the expected compensation range for respiratory acidosis, leading to a confirmed diagnosis.

• Another case analysis reveals metabolic acidosis, highlighting the importance of understanding compensatory mechanisms for accurate diagnosis.

Metabolic Acidosis: Compensation Analysis

This section delves into a case study focusing on metabolic acidosis and explores compensatory responses within the body.

Analyzing Metabolic Acidosis

• Calculation involving sodium, chloride, and bicarbonate levels helps determine metabolic acidosis severity.

• Expected compensation involves adjustments in partial pressure of carbon dioxide based on changes in bicarbonate concentrations.

Compensatory Responses and Diagnosis

• Excess carbon dioxide indicates inadequate elimination by the lungs, leading to a mixed acid-base disorder diagnosis.

Understanding Acid-Base Disorders

In this section, the speaker delves into the intricacies of acid-base disorders, focusing on scenarios involving bicarbonate levels, carbon dioxide partial pressure, and compensatory mechanisms in acute and chronic respiratory alkalosis.

Bicarbonate Levels and Compensation in Acute Respiratory Alkalosis

• : Bicarbonate decreases by 2 mEq/L for every 10 mmHg decrease in carbon dioxide partial pressure.

• : Example calculation: With a CO2 partial pressure of 10 (lower than normal 40), bicarbonate decreases by 6 mEq/L.

• : Expected compensation range for CO2 partial pressure of 10 is a bicarbonate level between 16 and 20; above 20 indicates mixed alkalosis, below 16 indicates decompensation.

Respiratory Alkalosis Scenarios

• : Individuals experiencing acute respiratory alkalosis due to hyperventilation from panic may exhibit compensatory mechanisms.

• : Hyperventilation in panic states can lead to respiratory alkalosis, causing excessive loss of carbon dioxide.

Effects of Acidosis on Potassium Levels

This segment explores the impact of acid-base disturbances on potassium levels within cells and extracellular fluid, emphasizing the critical relationship between acidosis correction and potassium balance.

Acidosis Influence on Potassium Dynamics

• : Excess hydrogen ions during acidosis cause potassium to shift into cells via ion exchange mechanisms.

• : Acidotic conditions elevate plasma potassium levels, potentially leading to dangerous extracellular imbalances.

• : Correcting acidosis before addressing hypokalemia is crucial to prevent cardiac complications like arrhythmias or arrest.

Neuronal Activity in Acid-Base Disorders

The discussion shifts towards neuronal responses in acid-base disorders, elucidating how acidemia and alkalemia influence neuronal excitability with implications for seizures and coma development.

Neuronal Response to Acidemia vs. Alkalemia

• : Acidemia reduces neuronal activity, possibly inducing coma; conversely, alkalemia heightens excitability, increasing seizure risk.

Clinical Case Discussion: Acid-Base Disorders

In this section, the speaker discusses a clinical case involving a patient with chronic obstructive pulmonary disease and presents symptoms of respiratory distress. The focus is on analyzing the acid-base status of the patient.

Patient Presentation and Initial Assessment

• The patient is a smoker with chronic obstructive pulmonary disease (COPD) in an advanced state, presenting with hypertension, dyspnea, fever, and purulent sputum.

Diagnosis of Respiratory Acidosis

• Analysis reveals respiratory acidosis due to COPD.

Compensation Mechanisms and Final Diagnosis

• Compensation for respiratory acidosis occurs through increased bicarbonate levels in chronic conditions like COPD.

• Calculation of expected compensation shows an increase in bicarbonate levels from 22 to 38, indicating metabolic acidosis alongside respiratory acidosis.

• The final diagnosis is confirmed as mixed acidosis comprising both respiratory and metabolic components.