Acid-Base Balance PDF

Acid-Base Balance Primary Goal: maintain acid base homeostasis Lungs (Respiratory) Kidneys (Metabolic) RECAP Tissues produce waste (CO2) which gets transported into the blood, delivered to the lungs, and exhaled out. If the blood has too much CO2 the brain will kick...

Acid-Base Balance Primary Goal: maintain acid base homeostasis Lungs (Respiratory) Kidneys (Metabolic) RECAP Tissues produce waste (CO2) which gets transported into the blood, delivered to the lungs, and exhaled out. If the blood has too much CO2 the brain will kick in and regulate how much CO2 will be removed by controlling the depth and rate of breathing. The respiratory system adjusts quickly to these changes An INCREASE in pH reflects decrease in H+ A decrease in pH reflects an INCREASE in H+ 2 Clinical Interpretation of Arterial Blood Gases Terminology: Acute ventilatory failure: A sudden rise in PaCO2 with a corresponding decrease in pH and there is no compensation by the kidneys Chronic ventilatory failure: A chronically elevated PaCO2 with a normal (compensated) or near normal pH and elevated HCO3 Acute ventilatory failure superimposed on chronic ventilatory failure: A sudden rise in PaCO2 in a patient with chronic ventilatory failure. Clinical Interpretation of Arterial Blood Gases Acute alveolar hyperventilation: A sudden fall in PaCO2 with a corresponding increase in pH, no metabolic compensation is occuring Chronic alveolar hyperventilation: A chronically decreased PaCO2 with a normal (compensated) or near normal pH. Acute alveolar hyperventilation superimposed on chronic ventilatory failure: A sudden decrease in PaCO2 in a patient with chronic ventilatory failure. Lungs and kidneys work together to ensure acid base balance Lungs remove the bulk of the acid through ventilation and CO2 excretion Kidneys remove smaller amounts of acid but it does help to restore the buffer capacity by replenishing HCO3 levels When there is a failure in either one of these systems it can create and acid-base imbalance The Role of The Lungs Ideally the lungs excrete carbonic acid (H2CO3) (significant volatile acid) at the same exact rate the tissues are producing CO2 In normal conditions the brain regulates the amount of carbon dioxide that is exhaled by controlling the speed and depth of breathing The Role of the Kidneys Bicarbonate (HCO3-) is produced by the renal system (kidneys) and is the primary buffer system for fixed acids In order to keep the blood pH within a normal range, the kidneys will either excrete or retain bicarbonate (HCO3-) As the blood pH decreases (acidic), the kidneys will compensate by retaining the HCO3- (alkalotic) Relationship between pH and H+ pH is a negative log of free H+ and there the relationship of pH and H+ is inverse. An INCREASE in pH reflects decrease in H+ A decrease in pH reflects an INCREASE in H+ pH Homeostasis Regulating blood pH is an interaction between Kidneys Lungs Blood buffers Lungs and kidneys do the most work, blood buffers serve a protecting role to prevent large changes in pH It is important the body excrete acid at a rate equivalent to its production in order to maintain homeostasis Acids and Bases Acids Substance that releases (or donates) H+ The more acids, the more H+ and the lower the pH Bases Can combine with or accept H+ Kidneys regulate blood bases HCO3 is controlled in the nephron, which is the functional unit of the kidney Acids and bases can dissociate H+ ion Regulation H+ formed in the body are either volatile or fixed (non-volatile) Fixed (non-volatile acids) sulfuric & phosphoric acids, lactic acid cannot be excreted by the lungs ONLY kidneys Volatile acids (H2CO3) can dissolve in gas & is excreted by ventilation (lungs) Diabetic Ketoacidosis Untreated diabetes increases acid production and the increased H+ stimulate the respiratory centers in the brain to increase ventilation and CO2 removal Diabetic ketoacidosis develops when your body is unable to produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as an alternate fuel. This process produces a buildup of toxic acids in the bloodstream called ketones Bicarbonate (OPEN) buffer system. Called “open” because H2CO3 can be removed through ventilation (exhaled out of the body). Can only buffer fixed acid. Open Buffer System (Bicarbonate) 53% Total Buffering Plasma 35% Erythrocyte 18% Because the bicarbonate buffer system can only buffer fixed acids, what happens where there in as increase in lactic acid? Increases H+, reacts with HCO3 to increase H2CO3 which breaks down into CO2 and H2O and exhaled out. As long as the lungs are able to ventilate well this is not a problem. If there is a problem with ventilation, the bicarbonate buffer system cannot buffer H2CO3 at the rate it is being produced, which will accumulate in the blood when ventilation fails to remove the CO2. The non-bicarbonate system can buffer H2CO3 NON-bicarbonate (CLOSED) buffer system. Called “closed” because all components of the acid-base reactions remain in the system Closed System (Nonbicarbonate) 47% Total Buffering Hb 35% - most important, it is the most abundant in this system Organic phosphates 3% Non organic phosphates 2% Plasma proteins 7% Non-bicarbonate system can buffer H+ produced by any fixed or volatile acid but is slower to respond Kidneys and Acid Base Control Kidneys excrete fixed acids (nonvolatile) Kidneys also reabsorb filtered bicarbonate Proximal tubes in the kidneys: main site for bicarbonate reabsorption which is regulated by four factors: Luminal HCO3- concentration Luminal flow rate Arterial PaCO2 Angiotensin II ✓An increase in any of these factors causes and increase in bicarbonate reabsorption Acid-Base Disturbances Normal acid-base balance Kidneys maintain HCO3– of ~22-26 mEq/L. Lungs maintain CO2 of ~35-45 mm Hg. These produce a pH of ~7.40 (H-H equation). 16 Terminology PaCO2 greater than 45 mmHg = hypercapnia Alveolar ventilation is not sufficient to remove CO2 at an acceptable rate (hypoventilation) PaCO2 less than 35 mmHg = hypocapnia Alveolar ventilation is excessive relative to metabolic needs (hyperventilation)  Acid Base Balance & ABG Components pH = H+ concentration (calculated) Normal pH is 7.35 to 7.45 PaCO2 = carbon dioxide or “waste” Normal CO2 is 35 to 45 mmHg (lungs) Normal PO2 is 80 to 100 mmHg PaO2 = amount of oxygen in the blood Normal HCO3- is 22 to 26 meq/L HCO3- = bicarbonate (kidneys) - metabolic Step One – Label the pH Normal pH values range from 7.35 to 7.45 pH >7.45 = alkalosis pH < 7.35 = acidosis Step 2 – Label PCO2 PCO2 < 35 = alkalosis PCO2 > 45 = acidosis Step 3 – Label HCO3- (Metabolic) HCO3- < 22 = acidosis HCO3- > 26 = alkalosis  Label the ABG values pH = 7.30 Acidosis PCO2 = 55 Acidosis (Respiratory) HCO3- = 26 Normal (metabolic) Match the abnormal value with the pH Because PCO2 is related to the lungs this is called Respiratory Acidosis To correct the imbalance, the kidneys will try to reabsorb the HCO3- Respiratory Acidosis aka Acute Ventilatory Failure aka hypercapnia aka hypoventilation Compensation occurs by renal reabsorption of HCO3- If the respiratory acidosis is compensated, a chronic respiratory acidosis may be present, which may be called chronic ventilatory failure Causes include: Respiratory – upper airway obstruction, severe diffuse airway obstruction (acute or chronic), massive pulmonary edema Nonrespiratory – drug OD, spinal cord trauma, neuromuscular disease (ALS, GB, MG), head trauma, thoracic trauma, gross obesity 23 Respiratory Acidosis aka Acute Ventilatory Failure aka hypercapnia Can cause systemic vasodilation. Peripheral vasodilation and increased CO promote warm flushed skin and bounding pulse Cerebral vasodilation can also occur which could elevate ICP’s, retinal venous distention, papilledma and headache. RT’s must understand this mechanism. When a patient has an elevated ICP we must closely monitor the PaCO2 so that we are not contributing to the increase 24 Chronic Ventilatory Failure In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (ie, >26 mEq/L). Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including the following: Decreased responsiveness to hypoxia and hypercapnia Increased ventilation-perfusion mismatch leading to increased dead space ventilation Decreased diaphragmatic function due to fatigue and hyperinflation Ventilatory Failure (Respiratory Acidosis) Ventilatory failure is abnormally elevated PaCO2 (respiratory acidosis or hypercapnia). Caused by a reduction in alveolar ventilation (hypoventilation) Acute ventilatory failure is a sudden rise in PaCO2 with a corresponding decrease in pH (uncompensated respiratory acidosis). Common causes include reduced lung compliance, increased airway resistance, reduced drive to breathe, or a reduced ability to breathe due to neuromuscular disease. Chronicventilatory failure is a chronic elevation in PaCO2 with a normal or near normal pH. Common causes are COPD and other forms of chronic lung disease.  Label the ABG values pH = 7.50 Alkalosis PCO2 = 42 Normal (Respiratory) HCO3- = 33 Alkalosis (Metabolic) Again, match the abnormal value to the pH. The pH is alkalosis and the HCO3- is alkalosis this is a Metabolic Alkalosis The respiratory system tries to compensate by holding on to carbonic acid (which contains PaCO2) Metabolic Alkalosis Gain in buffer base or loss in fixed acids Elevated pH with elevated HCO3- Compensation is by the respiratory system to hypoventilate as an attempt to increase PaCO2 28 Metabolic Alkalosis Common causes include Hypokalemia (moves H+ ions into the intracellular fluid in exchange for K+, this increases renal excretion of H+)or hypochloremia NG suction (loss of stomach acid) Persistent vomiting (loss of stomach acid) Diuretic therapy Steroid therapy Excessive sodium bicarb given  Label the ABG values pH = 7.31 Acidosis PCO2 = 39 Normal (Respiratory) HCO3- = 17 Acidosis (Metabolic) Again, match the abnormal value with the pH This is called a Metabolic Acidosis The body tries to compensate by breathing faster to get rid of acid (H2CO3-) Metabolic Acidosis Net gain in fixed blood acids or reductions in buffer bases To differentiate between acidosis due to acid gain and loss of base use the anion gap. Anion gap is the difference between major serum cations and major anions Anion gap = [Na+] – ([Cl-] + [HCO3-]) Normal is 7 to 16 mEq/L Metabolic acidosis caused by increase in fixed acids depletes stores and increases the anion gap When caused by loss of HCO3-, the anion gap usually remains within the normal range. Acute metabolic acidosis is rarely seen because the respiratory system responds through hyperventilation 31 Metabolic Acidosis (continued) To predict the PaCO2 level needed to fully compensate for metabolic acidosis use the Winter’s Formula PaCO2 = [(1.5 x HCO3-) + 8] ±2 Vasoconstriction can occur which may shift blood flow to the lungs and cause pulmonary edema. https://youtu.be/TG0vpKae3Js DKA breathing pattern 32 Metabolic Acidosis (continued) Increased Fixed Acids Loss of Base Ketoacidosis (diabetes, starvation) Diarrhea Renal failure Pancreatic fistula Lactic acidosis (shock, anaerobic Renal failure metabolism) Hyperalimentation (TPN feeding) Acid ingestion (methanol)  Metabolic Acidosis Definedas a decrease in the concentration of bicarbonate in the plasma (decrease HCO3–) to < 22 mEq/L. Caused by: Increasedfixed acid production Ingestion of acids (methanol, ethylene glycol, aspirin, or toluene) Decreased renal excretion of acids: When the kidneys fail to excrete fixed organic and inorganic acids there is usually an increase in the anion gap value Loss of bicarbonate Renal tubular acidosis (RTA): Typically causes a normal anion gap acidosis Metabolic acidosis due to loss of HCO3–: Typically causes a normal anion gap acidosis Total Parenteral Nutrition and Acid-Base Balance Total parenteral nutrition (TPN) refers to IV hyperalimentation. Consider in patients who are malnourished and who have contraindications to enteral nutrition. Parenteral nutrition provides carbohydrate, fat, protein, electrolytes, vitamins, minerals, trace elements, and fluids. TPN solutions are acidic (in order to ensure stability) and contain both preformed acids and nutrients which are metabolized to acids.34–36  Label the ABG values pH = 7.50 Alkalosis PCO2 = 30 Alkalosis (Respiratory) HCO3- = 24 Normal (Metabolic) Match the abnormal value to the pH This is a Respiratory Alkalosis. The kidneys try to compensate by excreting HCO3- Respiratory Alkalosis aka Acute Alveolar Hyperventilation Increase in alveolar ventilation, removing too much PaCO2 Kidneys compensate by increasing HCO3- excretion Expected compensation depends on severity and duration of hyperventilation Signs & Symptoms Tachypnea, dizziness, sweating, tingling in fingers or toes, muscle weakness or spasm Mosby items and derived items © 2014, 2010, 2005, 2000, 1995, 1990, 37 1985 by Mosby, Inc., an imprint of Elsevier Inc. Alveolar Hyperventilation (Respiratory Alkalosis) Acute alveolar hyperventilation is a sudden decrease in PaCO2 with a corresponding increase in pH. Caused by hypoxemia, pain, anxiety, respiratory distress, or neurologic disorders Chronicalveolar hyperventilation is a chronic decrease in PaCO2 with a normal or near normal pH. Treatmentshould address the underlying cause of alveolar hyperventilation. Label the ABG using 7.40 as a normal pH to identify abnormality pH = 7.38 Acidosis PCO2 = 56 Acidosis (lungs) HCO3- = 35 Alkalosis (kidneys) Match the abnormal values; in this case it is Respiratory Acidosis The kidneys try to compensate by reabsorbing the HCO3- Mixed Disturbance 7.12 / 60 mmHg/ 40 mmHg / 19 mEq/L Mixed respiratory & metabolic acidosis Cardiac arrest – blood flow and ventilation stops, lack of blood flow causes tissue hypoxia, which causes anaerobic metabolism, which increases lactic acidosis COPD – They chronically have an elevated PaCO2 and with severe electrolyte disturbances, sudden hypotension, renal failure or anemia can cause metabolic acidosis to develop on top of a respiratory acidosis Poison and drug OD depresses the respiratory center Mixed Disturbance 7.58 / 32 mmHg / 48 mmHg / 30 mEq/L Metabolic and Respiratory Alkalosis Critically ill patients – anxiety, pain, hypoxemia, hypotension, neurologic damage. Metabolic alkalosis can occur with NG suction, vomiting, blood transfusions, antacid therapy Ventilator-Induced Alkalosis, the RT can over ventilate a patient. Extra care must be given when intubating and ventilating a chronic COPD patient  Determine Compensation If pH is normal = fully compensation Partially compensated = the opposite system is attempting to balance Uncompensated = the opposite has not moved outside normal range to help balance out Oxygenation (PO2) Oxygenation refers to the amount of oxygen that is in our blood. Hypoxemia is defined as an abnormally low concentration of oxygen in the blood. Normal PO2 values are 80 to 100 mmHg 60 – 79 mmHG = mild hypoxemia 40 – 59 mmHG = moderate hypoxemia Less than 40 mmHG = severe hypoxemia Oxygenation Status PO2 = 88 mmHg Normal PO2 = 48 mmHg Moderate Hypoxemia PO2 = 65 mmHg Mild Hypoxemia Label the ABG pH = 7.39 Normal PCO2 = 44 mmHg Normal HCO3- = 25 mEq/L Normal PO2 = 89 mmHg Normal This ABG is NORMAL Base Excess or Deficit Base excess (BE) or deficit (BD) is the amount of acid or base needed to return the pH to normal with a normal PaCO2 (e.g., PaCO2 = 40 mm Hg). Normal range -2 to +2 mEq/L (norms) A positive BE indicates either there is more base or loss of acid A negative BE indicates there is excess acid or loss of base. (AKA base deficit) Anion Gap The anion gap (AG) represents the concentration of all the unmeasured anions in the plasma. ❑7 – 16 mEq/L – normal range ❑AG = Na+ - (Cl- + HCO3) Indicates metabolic acidosis is due to an increase in acid (rather than a decrease in base) oIncrease in anion gap may be due to DKA, lactic acidosis, salicylate or ethylene glycol poison, dehydration oDecrease may be due to renal failure Anion Gap Evaluation Assessment of the anion gap is helpful in determining if an acidosis is caused by a gain in fixed acids or a loss of HCO3–: Anion gap (mEq/L) = [Na+] – ([Cl–] + [HCO3–]) Normal range of 8 to 16 mEq/L or as low as 3 to 11 mEq/L.29 Increased anion gap acidosis indicates an elevation of fixed acids in the body. Causes are from lactic acidosis, ketoacidosis, or ingestion of acids. Normal anion gap acidosis has HCO3– loss, failure to reabsorb HCO3–, or ingestion of certain substances. Causes are diarrhea, pancreatic fistula, ureteral diversion, and ingestion of certain substances.