Lecture 4 Acid-Base Balance & Oxygenation PDF

Summary

This lecture provides an overview of acid-base balance and oxygenation, including blood gases, clinical significance of oxygen and carbon dioxide, as well as the role of the lungs and kidneys in acid-base regulation.

Full Transcript

Acid-Base Balance and Oxygenation 1. Blood Gases Blood gas analysis (ABGs- arterial blood gases) Utilized to determine pH, O2 and CO2 in arterial blood Pixabay.com Essential terms when discussing blood gases Partial pressure Saturation (e...

Acid-Base Balance and Oxygenation 1. Blood Gases Blood gas analysis (ABGs- arterial blood gases) Utilized to determine pH, O2 and CO2 in arterial blood Pixabay.com Essential terms when discussing blood gases Partial pressure Saturation (expressed as percentage) Arterial blood Venous blood Capillary (exchange of gases) 2. Clinical Significance of Gases Oxygen and carbon dioxide External respiration (lungs) Internal respiration (cells) Certain diseases change the partial pressures of oxygen and carbon dioxide Importance of blood gas measurements Pixabay.com Useful for respiratory and metabolic conditions Measured in mmHg 3. Clinical Significance of Gases: Oxygen Essential (ATP) Factors that can affect oxygen transport: Diffusion of oxygen through the alveolar membrane Affinity of hemoglobin for oxygen Normally, 95% of the hemoglobin in arterial blood is bound to oxygen Less than 95% oxygen saturation (s02 %) Hypoxia (medical emergency) Lack of oxygen in tissues (decreased pO2 and decreased sO2) Causes: e.g., high altitudes, pneumonia, obstructed airways, anemia Hypoxemia Decreased arterial oxygen Pixabay.com Causes: any condition that affects the exchange of oxygen in the lungs 3. Clinical Significance of Gases: Oxygen pO2 (partial pressure of oxygen) levels and degree of hypoxemia 1. Normal pO2 levels (75 to 100 mm Hg) 2. Mild hypoxemia (60 to 75 mm Hg) 3. Moderate hypoxemia (40 to 60 mm Hg) 4. Severe hypoxemia (< 40 mm Hg) E.g., Cyanosis, potential organ dysfunction 5. Hypoxemic coma Loss of consciousness 6. Anoxia Life-threatening condition, irreversible brain death 4. Clinical Significance of Gases: Carbon dioxide Transported in blood as: 70 % Bicarbonate (HCO3 -) Most generated by the transport of CO2 20-25 % Carbaminohemoglobin 5-10 % Dissolved carbon dioxide Carbonic acid 4. Clinical Significance of Gases: Carbon dioxide Hypercapnia An increase of pCO2 in arterial blood Also known as respiratory acidosis e.g., hypoventilation, lung diseases, CO2- enriched air Hypocapnia A decrease of pCO2 in arterial blood Also known as respiratory alkalosis e.g., hyperventilation 5. Acid-Base Balance in the Body Importance E.g., Enzymes, hormone and ion distribution Acid-base balance: main concern 2 ions Hydrogen (H+) and bicarbonate (HCO3-) Acid-base balance Acid-base balance involves balancing carbon dioxide and noncarbonic acids and bases in the blood. 6. Acid-Base Balance in the Body Organic acids and carbonic acid are constantly being Lungs produced as byproducts of our metabolism Metabolism Output Input Kidneys E.g., carbonic acid, lactic acid, uric acid Maintenance of Normal [H+] Buffers 7. Chemical Buffers Acids X Bases pH = negative log of hydrogen ion concentration Blood pH 7.35 – 7.45 ( [H+] 35 – 45 nmol/L) H+ is constantly produced in the body Around 60 mmol is produced daily (H+] = 4 mmol/L) Excess [H+] – excreted by kidneys Excess CO2 – excreted by lungs Buffers Substances/systems that can bind H+ or release H+ Do not remove H+ from the body Importance of kidneys Reversible reaction 7. Chemical Buffers Important buffers in the body Protein Hemoglobin https://quizlet.com/371718437/bicarbonate-buffer-system-flash-cards/ High capacity to bind H+ (it reaches equilibrium) Bicarbonate HCO3- (most important) Present in large amounts in the ECF It combines with H+ to form H2CO3 Carbonic acid Efficiently removes H+ from the ECF Controlled by lungs and kidneys 8. Principles of acid-base interpretation ECF acceptable pH range maintained by: 1. Chemical buffers React very rapidly (< 1 sec) 2. Respiratory regulation Reacts rapidly (sec to min) 3. Renal regulation Reacts slowly (min to hr) 9. Role of the Lungs in Acid-Base Regulation Regulate carbon dioxide levels and the control of pH Part of body’s compensatory mechanisms (homeostasis) 1. Eliminate CO2 from the body High CO2 in the blood can lead to low blood pH Pixabay.com 2. Bicarbonate buffering system (controlled by lungs and kidneys) CO2 is removed by the lungs Less carbonic acid in the blood (Shift) more bicarbonate binding to protons 3. Respiratory Rate and depth Controlled by the brain Varies with CO2 levels 10. Role of Kidneys in Acid-Base Regulation Responsible for renal regulation of H+ and bicarbonate Initiation: too much CO2 in blood or too little bicarbonate Consequence: H+ ion excretion and regeneration of bicarbonate Consequence: Bicarbonate reabsorption (recovery) Retaining the used bicarbonate Acid-Base Imbalances 11. Acid-Base Disorders Disorders that can affect: pCO2 (known as respiratory) Bicarbonate concentration (known as metabolic) E.g., diabetes mellitus, impaired respiratory functions The clinical terms for acid base disorders are associated with the primary acid-base disturbance: 1. Metabolic acidosis ❖Metabolic disorders involve bicarbonate 2. Metabolic alkalosis concentrations 3. Respiratory acidosis ❖Respiratory disorders involve dissolved 4. Respiratory alkalosis carbon dioxide concentrations 11.1 Metabolic Acid-Base Disorders Origin of the disorder should be known Pixabay.com Metabolic acid-base disorders are caused by: Increase in H+ production or a loss of H+, resulting in loss or gain of HCO3- Direct loss or gain of HCO3- Inspection of bicarbonate concentration is necessary Arterial blood gas analysis (ABGs) ❖ Anion Gap Calculated parameter to assess acid-base conditions Sum of all cations=sum of all anions (law of electroneutrality) Anion gap = [Na+ + K+ ] - [Cl- + HCO3- ] RI: (8 and 16 mmol/L) Plasma proteins, ketones, lactic acid are negatively charged but are not included in the formula There is no real gap Increases in the anion gap = increase in unmeasured anions Metabolic disorders with increased concentrations of acid Metabolic Acidosis A. Metabolic Acidosis Metabolic acidosis represents a bicarbonate deficit of the ECF (always low!) [H+] can be high or even normal (normal anion gap) Chloride can increase Main causes Evaluation of metabolic acidosis: Clinical history Anion Gap (helpful) pH < 7.35 A. Metabolic Acidosis – clinical significance ❖Metabolic acidosis with elevated anion ❖Metabolic acidosis with normal anion gap: gap: Diabetic ketoacidosis (most common Loss of bicarbonate cause) Also known as hyperchloremic Renal disease (no H+ excretion) acidosis Reduced HCO3- is balanced by Bicarbonate is consumed through increased Cl- concentration in ECF buffering Chronic diarrhea or intestinal fistula Renal tubular acidosis (no excretion Clinical effects of acidosis: H+, loss bicarbonate) Hyperventilation “air hunger” –deep, rapid- compensatory response Increased [H+] Neuromuscular irritability (arrhythmias – cardiac arrest) A. Metabolic Acidosis – clinical significance Laboratory findings pH < 7.35 Decreased pCO2 Low bicarbonate levels Metabolic Alkalosis B. Metabolic Alkalosis Decrease in [H+] Bicarbonate excess pH > 7.45 Causes Clinical effects: Hypoventilation (compensatory response) Confusion Coma B. Metabolic Alkalosis Laboratory findings pH > 7.45 Increased bicarbonate levels Elevated pCO2 levels 11.2 Respiratory Acid-Base Disorders Origin of the disorder Changes in air moving in and out of the lungs Changes in gas exchange Changes in arterial blood pCO2 and increase/decrease in carbonic acid concentration Inspection of pCO2 is necessary (ABGs) Respiratory Acidosis A. Respiratory Acidosis Hypoventilation (accumulation of pCO2) May be acute or chronic Acute respiratory acidosis: Depressed respiratory center (drugs), choking, asthma Not compensated Renal compensation takes 48 to 72 hours to become fully effective Chronic (compensated) respiratory acidosis Chronic respiratory conditions Compensation: many patients will have extensive renal compensation [H+] near normal Excretion of carbonic acid and reabsorption of bicarbonate Respiratory Acidosis Laboratory findings Acute respiratory acidosis High pCO2 (> 45 mmHg) Low pH (< 7.35) Chronic respiratory acidosis High pCO2 (> 45 mmHg) Normal or slightly low pH Due to renal compensation Respiratory Alkalosis B. Respiratory Alkalosis Hyperventilation (decreased pCO2) Increases ration of bicarbonate to pCO2 pH > 7.45 Less common than acidosis Usually acute conditions (uncompensated) Compensation Kidneys excrete bicarbonate Buffer systems release H+ Laboratory findings Decreased pCO2 pH > 7.45 Interpreting the Results Interpreting the H+, pCO2, HCO3- results help to classify the acid- base disorder Results: 1. Is it acidosis or alkalosis? Look at the pH a. pH < 7.35 b. pH > 7.45 Answer: low pH (acidosis), high pH (alkalosis) 2. Is it respiratory or metabolic? Look at the pCO2 Answer: increased= respiratory acidosis Look at the bicarbonate Answer: decreased= metabolic acidosis Interpreting the Results 3. Determine if compensation has occurred (is body reacting to try to bring pH within normal limits)

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