Lecture 20 Acid-Base Disturbances

Acid- Base Balance  Acid-Base Balance Refers to the steady state of the pH of the body Normal metabolic processes continually generate acids Normal pH range is 7.35 to 7.45 If the pH falls out of this range, proteins are diminished or destroyed. Below 7.3 = acidosis (excess H...

Acid- Base Balance  Acid-Base Balance Refers to the steady state of the pH of the body Normal metabolic processes continually generate acids Normal pH range is 7.35 to 7.45 If the pH falls out of this range, proteins are diminished or destroyed. Below 7.3 = acidosis (excess H+) = causes acidemia Above 7.4 = alkalosis (low H+) = causes alkalemia Importance of pH Normal blood pH is between 7.35 and 7.45. Blood pH below 7.35 is known as acidemia. Blood pH above 7.45 is known as alkalemia. Values less than 6.8 or greater than 7.8 often result in death. The body’s pH influences the function of enzymes and thus the speed of cellular reactions, cell permeability, and the integrity of cell structure. Effects of pH Changes on the Body Effect of Acidosis ↓ blood pH (acidemia) Depression of the CNS- disoriented/comatose Effect of Alkalosis ↑ blood pH (alkaemia) Hyperexcitability of the nervous system- able to generate impulses without normal stimuli Spasms/tetanic contractions Death with severe alkalemia is due to spasms of muscles of respiration Regulatory Systems for Acid-Base Balance Chemical buffers Renal system (kidneys) 1st line of defense 3rd line of defense react in seconds react in hours to days 3 main systems is the most powerful and Bicarbonate Buffer lasts the longest Protein Buffer Phosphate Buffer Respiratory system (lungs) 2nd line of defense react in minutes Chemical Buffers: review Acid Base a substance that gives a substance that up/donates a proton accepts/binds a proton (hydrogen ion, H + Acid) (hydrogen ion, H + ) Buffer a compound that can accept OR donate a proton (H+ ) buffers are usually weak acids with their corresponding salts. Chemical Buffer Systems work to counteract H+ imbalance created by metabolic processes Buffers Substances that alter the H+ concentration If H+ are added , the buffer will combine with the extra H+ ions to help maintain the pH. If H+ are lost, the buffer will release H+ ions to combine with the base to help maintain the pH Work both intracellularly and extracellularly 3 main systems Bicarbonate Buffer* Protein Buffer Phosphate Buffer Bicarbonate (HCO3 ) Buffer - Remember: CO2 is produced as a waste product during aerobic cellular respiration CO2 combines with H2O to form carbonic acid (H2CO3) most of which rapidly dissociates to form H+ and bicarbonate (HCO3 − ) CO2 acts like an acid because it can combine with water to form carbonic acid H+ acts as an acid, and HCO3 − acts as a base Any disturbance of the system will be compensated by a shift in the chemical equilibrium by the law of mass action. Bicarbonate (HCO3 ) Buffer - Lungs and kidneys play a large role in bicarbonate buffer system Lungs can blow off or conserve CO2 through regulating ventilation Kidneys actively secrete or resorb bicarbonate. Reaction is reversible. Bicarbonate (HCO3-) Buffer In Response to a Decrease in Blood pH (Acidosis) Bicarbonate (HCO ) Buffer In 3 - Response to an Increase in Blood pH (Alkalosis) Acid-Base  Acidosis and Alkalosis Categorized by the cause of the disturbance Respiratory acidosis or alkalosis Abnormalities in the respiratory system Metabolic acidosis or alkalosis All causes other than respiratory system Respiratory system and Renal system are primary systems that regulate pH of body fluids malfunctions/disease of either system can result in acidosis or alkalosis Respiratory Acidosis/Alkalosis Respiratory acidosis Respiratory alkalosis causes a pH below 7.35 and a causes a pH above 7.45 PCO2 above 45 mm Hg. and a PCO2 below 35 mm HCO3 − is normal. Hg. HCO3 − is normal. If respiratory rate decreases less CO2 is eliminated→ If respiratory rate increase in partial pressure increases CO2 (PCO2) within the blood = decrease in PCO2 within hypercapnia the blood = hypocapnia Causes hypoventilation or Caused by impaired gas exchange hyperventilation  Respiratory Acidosis (high PCO2) Caused by diseases that will impair gas exchange within the lungs Pneumonia, cystic fibrosis, emphysema, etc Hypoventilation increases CO2 shifting equilibrium to right and thus results in an increase in H2CO3 and ultimately increase in H+ Kidneys compensate by secreting more H+ in urine and reabsorbing more HCO3- However this compensation may take up to 24 hrs to be effective Treatment: improve ventilation capability  Respiratory Alkalosis (low PCO2) Hyperventilation results in a decrease in PCO2 due to the elimination of too much CO2 Causing a reduction in H+ ions HCO3- levels are normal PRIOR to renal compensation Kidneys compensate by reabsorbing H+ ions and excreting HCO3- into the urine Can take up to 24 hours to be Can result from: effective Fear/anxiety Not effective if Resp. Alkalosis Pain develops quickly More effective if Resp. Alkalosis Hypoxemia- CHF, high altitudes, pulmonary develops more gradually disease Hypermetabolic states: fever, anemia, Treatment: slow breathing thyrotoxicosis Pain relief, anxiolytics, rebreathing CO2  Metabolic Acidosis/Alkalosis Increase in acid production (H+) or a decrease in bicarbonate levels that are not caused by respiratory problems Decrease in HCO3- = Metabolic Increase in HCO3- = Acidosis Metabolic Alkalosis Gain in acid to point at which HCO3- Loss of H+ (vomiting) buffer system is overwhelmed Gain of HCO3- (abnormal e.g. DKA, decreased renal retention of HCO by excretion of H+ kidneys in response to Loss of HCO3- dehydration due to vomiting/gastric retention e.g. large amount of fluid loss of fluids) through GI tract- diarrhea, renal tubular dysfunction resulting in  Respiratory Compensation Hyperventilation due to Metabolic Acidosis reduce pH influence on respiratory centers of the Rise in H+ due to either an brain. increase in production or a Eliminates more CO2 and decrease in excretion thus less carbonic acid can DKA be formed Starvation Lactic Acidosis (poor oxygen Renal Compensation perfusion to tissues- GDV) Increase H+ secrection & Depletion of HCO3- reserve HCO3- resorption either due to decreased resorption by kidneys or excess loss Renal failure Diarrhea  Metabolic Alkalosis Caused by a decrease or loss of metabolic acids or an increase in bicarbonate concentration not due to respiratory problems  Metabolic Alkalosis Increase in HCO3- = Respiratory Metabolic Alkalosis Compensation Hypoventilation in Loss of H (vomiting) + Gain of HCO3- (abnormal retention of response to effects of increased pH on the HCO3- by kidneys in response to dehydration due to vomiting/gastric respiratory centers of the retention of fluids) brain Excessive ingestion of antacids CO2 accumulates thus (increase in -HCO3-) shifting carbonic acid/bicarbonate equation to the right Renal Compensation Blood Gases Value of Blood Gases Allow for the assessment of patient’s oxygenation ventilation acid-base status BG, electrolytes, iCa2+, and lactate levels Can help in the diagnosis, monitoring, and treatment of disease processes that are directly related to metabolic or respiratory dysfunction 4 Basic Types of Acid-Base Disturbances Metabolic acidosis Primary gain in acid or loss of base Metabolic alkalosis Primary gain in base or loss of acid Respiratory acidosis Retention of CO2 due to CO2 production outpacing alveolar ventilation Respiratory alkalosis Removal of CO2 by ventilation which outpaces CO2 production Clarification of Terms PaO2 – partial pressure of oxygen dissolved in arterial blood A measure of oxygenation not ventilation PaCO2 – partial pressure of carbon dioxide dissolved in arterial blood. Provided the best measurement of patients ability to ventilate Determines whether resp. acidosis or resp. alkalosis is present PVCO2 – partial pressure of carbon dioxide dissolved in venous blood When obtained properly it is a measure of the patients ability to ventilate. Base Excess/Deficit (BE)- calculated value that estimates how much base needs to be added/subtracted to achieve a normal pH @ a normal temperature Reflects the metabolic portion of acid balance Evaluates for metabolic acidosis or alkalosis Potential Sampling Errors Peripheral vein sampling in patients with poor-perfusion Sample may reflect acid-base status of limb and not of whole body Prolonged occlusion of sampled limb vein Sample may reflect lactic acidosis specific only to that limb Sample not immediately evaluated or placed on ice Continued cellular metabolism by RBCs will continue to use O2 and produce CO2 Exposing sample to air Oxygen from atmosphere will diffuse into sample and CO2 will diffuse out altering PaO2, PaCO2, and pH Thus causing error in calculated values (HCO3- & BE) Steps in Interpreting Blood Gas Results 1. Venous or Arterial Sample? 2. Is there an acidemia or alkalemia present> Acidemia = decrease in blood pH Alkalemia = increase in blood pH 3.Determine Primary disturbance ROME Respiratory Opposite Metabolic Equal  Steps in Interpreting Blood Gas Results 4. Assess Oxygenation if arterial sample FiO2 of room air is 21% PaO2 - should equal 5x FiO2 5. Determine whether compensatory changes have occurred A change in the resp. or metabolic component of the acid- base status normally induces an opposite compensatory response in effort to normalize pH Absence or degree of compensation can provide some insight into chronicity of the disturbance Overcompensation does not occur Case Studies Example 1 Example 2 Value Reference Range pH 7.48 7.35-7.45 paO2 mmHg 63 90-100mmHg paCO2 mmHg 25.9 36-40 mmHg HCO3 mEq/L 18.8 20-24 mEq/L BE -4.8 -4 to +4