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- 1. Acid-base disorders andits implications: Therapy in a Nursing Perspective (July 23, 2014) EMILIANO IAN B. SUSON II, ED.D, USRN, MAN, RN “SIR EYE”
- 2. Objectives Describe physiologyinvolved in acid base balance of the body Review causes and treatments of acid base disorders Identify normal arterial blood gas values Interpret results of ABG samples Interpret oxygenation state of a patient using reported ABG values 2
- 3. Interpretation of ABG »Very important for health care providers » Usefulness of this tool depends on being able to interpret correctly the results » Critically ill patients 3
- 4. Acid base disorders 12000 to 15000 mEq of volatile acids are produced daily by body and excreted as CO2 by lungs 1 mEq / kg / day of non-volatile acids (sulfuric and phosphoric acids) are produced daily by body and excreted by the kidneys The most important buffers in the body are, hemoglobin, plasma proteins and bicarbonate 4
- 5. Acid base disorders SIMPLEACID BASE DISORDER: when there is only one primary disorder MIXED ACID BASE DISORDER: when there are two or more primary disorders present at the same time 5
- 6. Normal values pH 7.35-7.457.40 PaCO2 35-45 mmHg 40 PaO2 70-100 mmHg HCO3- 24±2 24 Met-Hb <2% CO-Hb <3% BE -2 to 2 mEq/L CaO2 16-22 ml/dL A gap 10±2 12 6
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- 11. Buffers 1. Protein BufferSystems Amino Acid buffers Hemoglobin buffers Plasma Protein buffers 2. Phosphate Buffer Systems 3. Carbonic Acid – Bicarbonate Buffer System 11
- 12. 12Bicarbonate buffer SodiumBicarbonate (NaHCO3) and carbonic acid (H2CO3) Maintain a 20:1 ratio : HCO3 - : H2CO3 HCl + NaHCO3 ↔ H2CO3 + NaCl NaOH + H2CO3 ↔ NaHCO3 + H2O
- 13. 13Phosphate buffer Majorintracellular buffer H+ + HPO4 2- ↔ H2PO4- OH- + H2PO4 - ↔ H2O + H2PO4 2-
- 14. 14Protein Buffers Includeshemoglobin, work in blood and ISF Carboxyl group gives up H+ Amino Group accepts H+ Side chains that can buffer H+ are present on 27 amino acids. The 10 essential amino acids are:(PVTMATHILL) Phenylalanine, Valine, Tryptophan, Methionine, Arginine, Threonine, Histidine, Isoleucine, Leucine, Lysine 10 Amino acids the body produces: alanine, asparagine, aspartic acid, cysteine, glutamic acid, glutamine, glycine, proline, serine and tyrosine
- 15. 152. Respiratory mechanisms Exhalation of carbon dioxide Powerful, but only works with volatile acids Doesn’t affect fixed acids like lactic acid CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3 - Body pH can be adjusted by changing rate and depth of breathing
- 16. 163. Kidney excretion Can eliminate large amounts of acid Can also excrete base Can conserve and produce bicarb ions Most effective regulator of pH If kidneys fail, pH balance fails
- 17. 17Rates of correction Buffersfunction almost instantaneously Respiratory mechanisms take several minutes to hours Renal mechanisms may take several hours to days
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- 21. 21Acidosis Principal effectof acidosis is depression of the CNS through ↓ in synaptic transmission. Generalized weakness Deranged CNS function the greatest threat Severe acidosis causes Disorientation, Coma, Death
- 22. 22 Alkalosis Alkalosis causesover excitability of the central and peripheral nervous systems. Numbness Lightheadedness It can cause : Nervousness muscle spasms or tetany Convulsions Loss of consciousness Death
- 23. 23Respiratory Acidosis Acute conditons: AdultRespiratory Distress Syndrome Pulmonary edema Pneumothorax
- 24. 24Compensation for Respiratory Acidosis Kidneyseliminate hydrogen ion and retain bicarbonate ion
- 25. 25Signs and Symptomsof Respiratory Acidosis Breathlessness Restlessness Lethargy and disorientation Tremors, convulsions, coma Respiratory rate rapid, then gradually depressed Skin warm and flushed due to vasodilation caused by excess CO2
- 26. 26Treatment of Respiratory Acidosis Restoreventilation IV lactate solution Treat underlying dysfunction or disease
- 27. 27Respiratory Alkalosis Conditionsthat stimulate respiratory center: Oxygen deficiency at high altitudes Pulmonary disease and Congestive heart failure – caused by hypoxia Acute anxiety Fever, anemia Early salicylate intoxication Cirrhosis Gram-negative sepsis
- 28. 28Compensation of Respiratory Alkalosis Kidneys conserve hydrogen ion Excrete bicarbonate ion
- 29. 29Treatment of Respiratory Alkalosis Treat underlying cause Breathe into a paper bag IV Chloride containing solution – Cl- ions replace lost bicarbonate ions
- 30. 30Metabolic Acidosis Bicarbonatedeficit - blood concentrations of bicarb drop below 22mEq/L Causes: Loss of bicarbonate through diarrhea or renal dysfunction Accumulation of acids (lactic acid or ketones) Failure of kidneys to excrete H+
- 31. 31Symptoms of Metabolic Acidosis Headache,lethargy Nausea, vomiting, diarrhea Coma Death
- 32. 32Compensation for Metabolic Acidosis Increased ventilation Renal excretion of hydrogen ions if possible K+ exchanges with excess H+ in ECF ( H+ into cells, K+ out of cells)
- 33. 33Treatment of Metabolic Acidosis IVlactate solution
- 34. 34Metabolic Alkalosis Bicarbonateexcess - concentration in blood is greater than 26 mEq/L Causes: Excess vomiting = loss of stomach acid Excessive use of alkaline drugs Certain diuretics Endocrine disorders Heavy ingestion of antacids Severe dehydration
- 35. 35Symptoms of Metabolic Alkalosis Respiration slow and shallow Hyperactive reflexes ; tetany Often related to depletion of electrolytes Atrial tachycardia Dysrhythmias
- 36. 36Treatment of Metabolic Alkalosis Electrolytesto replace those lost IV chloride containing solution Treat underlying disorder
- 37. 37Example A patientis in intensive care because he suffered a severe myocardial infarction 3 days ago. The lab reports the following values from an arterial blood sample: pH 7.3 HCO3- = 20 mEq / L ( 22 - 26) pCO2 = 32 mm Hg (35 - 45)
- 38. 38Diagnosis Metabolic acidosis With compensation
- 39. Acid base disorders METABOLIC ACIDOSIS: HCO3 <24 OR Anion Gap >12 METABOLIC ALKALOSIS: HCO3 >24 RESPIRATORY ALKALOSIS: PCO2 <40 or PCO2 less than expected for primary metabolic abnormality RESPIRATORY ACIDOSIS: PCO2 >40 or PCO2 higher than expected for primary metabolic abnormality HIGH ANION GAP (>12-20) always indicates primary metabolic acidosis 39
- 40. Acid base disordersand compensatory response pH HCO3- PaCO2 Metabolic acidosis Metabolic alkalosis Respiratory acidosis Respiratory alkalosis Compensatory response never brings the pH back to normal if the pH is in acidic direction, it tells you that the process or processes in acidic direction are the primary disorders 40
- 41. Anion Gap Na-(Cl+HCO3)= 12±2 Estimates unmeasured anions Normal is 12 Hypoalbuminemia: Correct anion gap: 2.5 per gram of albumin below 4 Calculate osmolal gap if anion gap is elevated OSM gap = measured OSM-2(Na)-glu/18-BUN/2.8 = <10 41
- 42. Urinary anion gap Useful in differential diagnosis of non gap acidosis U anion gap= Na + K – Cl A negative U. Anion Gap ie Cl >> Na + K suggests appropriate urinary NH4 excretion and G.I. loss of HCO3 A positive U. Anion Gap ie. Cl << Na + K suggests RTA with distal acidification defect and inadequate NH4 excretion in urine 42
- 43. Acidosis (Low pH) Lowering extracellular pH by rising concentration of hydrogen ions Fall in bicarbonate concentration Elevation in PCO2 Decreases force of cardiac contractions Decreases vascular response to catecholamines Decreases response of certain medications 43
- 44. Alkalosis (High pH) Elevation of the pH of the extra cellular fluid Lowering hydrogen ion concentration Elevation in plasma bicarbonate Reduction in PCO2 Impairs oxygenation Impairs muscular function Impairs neurological function 44
- 45. Metabolic acidosis Anion Gap Methanol Uremia DKA Paraldehyde INH Lactic acidosis Ethylene glycol Salicylate Non Gap Hyperalimentation Acetazolamide Renal tubular acidosis Diarrhea Ureterosigmoidostomy Pancreatic fistula 45
- 46. Metabolic alkalosis Gainof bicarbonate by abnormal renal absorption Volume contraction (low urine chloride) Vomiting: loss of H+ Diuretics: depletion ECF Severe hypokalemia Renal failure Mineralocorticoid excess (high urine chloride) 46
- 47. At a GlanceAcid- Base Disorders Acid-base disorder Causes Signs and Symptoms Respiratory acidosis Hypoventilation, Neuromuscular disorders, Airway obstruction, CNS depression ↑PR, ↑RR, ↑BP, Mental cloudiness, Feeling of fullness in the Head, ↑ICP Ventricular Fibrillation, Papilledema, Dilated Conjunctival Blood vessel, Hyperkalemia, Tachypnea, Cyanosis
- 48. Acid-base disorder Causes Signs and Symptoms Respiratory alkalosis Hyperventilation, Sepsis, Pregnancy, Mechanical Ventilation,fever Lightheadedness Inability to Concentrate, Numbness and Tingling, Tinnitus Loss of consciousness At a Glance Acid- Base Disorders
- 49. Acid-base disorder Causes Signs and Symptoms Metabolic acidosis Diabetic Ketoacidosis, Renalfailure Methanol/aspirin Overdose, Renal tubular Acidosis, Diarrhea, Chronic alcoholism Headache, ↓ BP Confusion Drowsiness ↑ RR and depth Nausea, Vomiting ↓Cardiac output Cold and clammy Skin, Shock, Dysrhythmias At a Glance Acid- Base Disorders
- 50. Acid-base disorder Causes Signs and Symptoms Metabolic alkalosis vomiting diuretics alkaliingestion Tingling of fingers and toes, Dizziness, Hypertonic muscles, Symptoms of Hypocalcemia, ↓ RR, Atrial tachycardia Hypokalemia, Paralytic Ileus, Dysrhythmia At a Glance Acid- Base Disorders
- 51. Acid-Base Imbalances Management TYPEOF IMBALANCE MANAGEMENT Respiratory Acidosis - Improving ventilation - Bronchodilators - Antibiotics for infection - Thrombolytics & anticoagulants (pulmonary emboli) - Pulmonary hygiene - Mechanical ventilation - Semi-Fowler’s position
- 52. Acid-Base Imbalances Management TYPEOF IMBALANCE MANAGEMENT Respiratory Alkalosis - Treatment of the underlying cause - Breathe into a paper bag - Sedative
- 53. Acid-Base Imbalances Management TYPEOF IMBALANCE MANAGEMENT Metabolic Acidosis - Treatment is correcting the underlying defect. - Eliminating source of chloride - Bicarbonate - Alkalizing agents - Hemodialysis - Peritoneal dialysis
- 54. Acid-Base Imbalances Management TYPEOF IMBALANCE MANAGEMENT Metabolic Alkalosis - Treatment of underlying disorder - Chloride supply - Sodium chloride fluids - KCl - H2-receptor antagonists (Cimitidine) - Carbonic anhydrase inhibitors
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- 58. 58 Hemoglobin – thisis the part of your red blood cell which carries oxygen all over the body. If your hemoglobin levels are decreased it could pertain to anemia, bleeding, patients with chronic kidney disease, or a possible blood dyscrasia. If your hemoglobin levels are elevated we could consider polycythemia vera and dehydration. Red Blood Cell (RBC) – this part of the CBC tells you the number of cells that could carry oxygen in the body. Same with hemoglobin, decrease levels of RBC could also be secondary to anemia or bleeding and increase levels could also be secondary to polycythemia or dehydration. Hematocrit – this measures the amount of space in the blood being occupied by your red blood cells. Causes for the increased and decreased of hematocrit are the same with your hemoglobin and red blood cells.
- 59. 59 White Blood Cell(WBC) – this are the cells in the body that fight off invaders like infections. An increase or decrease in WBC count could represent an ongoing infection or a malignancy like your leukemia. Also included in the CBC is the 5 differential count for your WBC, namely: Neutrophils or segmenters – this type of WBC are the primary cells that respond to a bacterial infection. High levels of your neutrophils usually represent and ongoing infection, an inflammation, malignancy, cause by some drugs, etc. Low levels of your neutrophils could be seen in patients with viral infection, autoimmune diseases, some medications and malignancy. Lymphocytes – this type of WBC represent 20-40% of your circulating WBC in the blood. An increased in lymphocyte count usually represents an acute infection especially viral infections, leukemia, smoking, etc. Low lymphocyte count is usually not significant.
- 60. 60 Monocytes – thiscomprises 3-8% of all white blood cells in the body. An increase in monocyte could signify a chronic infection like your tuberculosis or a chronic inflammation condition like your inflammatory bowel disease and malignancy. Low levels of monocytes are usually none significant if other cells are normal. Basophils – this comprises only 0.01-0.3% of all white blood cells in the blood. This type could produce histamine. Increased numbers could represent a myeloproliferative disorder. Eosinophils – comprises 1 – 6% of all white blood cells in the blood stream. They are usually increase in cases of allergy, asthma and in parasitic infections. Low levels are usually not significant. Platelet Count – the normal platelet count ranges from 150,000 – 400,000 /L and this cell is involved in the clotting cascade of the body. Low levels of this cell could cause easy bruising and bleeding. Causes of low platelet count include infections (ex: dengue fever), autoimmune disease, liver disease, idiopathic thrombocytopenic purpura, etc.
- 61. 61 Red Cell Indices– this are investigated when considering diseases like your thalassemia or sickle cell anemia. MCV (mean corpuscle volume) – telling you the average size of the red blood cell (80-100) MCH (mean corpuscle hemoglobin) – shows the average amount of hemoglobin in each red blood cell (26-34) MCHC (mean corpuscle hemoglobin concentration) – average amount of hemoglobin in the red blood cell compared to their average size. (31-37) RDW – (11.5 -14.5)
- 62. ABG SHORTCUT Laboratory studies ABG:pH/PaCO2/PaO2/HCO3/O2sat ABG: 7.38-7.44/35-45/80-100/22-26/95-100 What is the acid base disturbance and what is the cause Na 135-145 62 K 3.5-5.1 AG 7-16 CO2 22-30 BUN 5-25 Crea 0.6-1.2 Glu 70-110 Ca 8.5-10.1 Cl 98-107
- 63. CHEMICAL COMPOSITIONS OFBODY FLUIDS Extracellular Fluid Intracellular Fluid Na+ 142 mEq/L 10mEq/L K+ 4mEq/L 140 mEq/L Ca2+ 2.4 mEq/L 0.0001 mEq/L Mg2+ 1.2 mEq/L 58 mEq/L Cl- 103 mEq/L 4 mEq/L HCO3- 28 mEq/L 10 mEq/L Phosphates 4 mEq/L 75 mEq/L SO42- 1 mEq/L 2 mEq/L Glucose 90 mg/dl 0-20 mg/dl Amino Acids 30 mg/dl 200 mg/dl
- 64. CHEMICAL COMPOSITIONS OFBODY FLUIDS Extracellular Fluid Intracellular Fluid Cholesterol 0.5 g/dl 2-95 g/dl Phospholipids 0.5 g/dl 2-95 g/dl Neutral fat 0.5 g/dl 2-95 g/dl PO2 35 mm Hg 20 mm Hg PCO2 46 mm Hg 50 mm Hg pH 7.4 7.0 Proteins 2 g/dl 16 g/dl 5 mEq/L 40 mEq/L
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- 66. Indications To assess. RespiratoryStatus Assess oxygenation and ventilation Acid Base Balance Phlebotomy. Used if venous route is unavailable or inaccessible due to trauma or burns. Usually a femoral puncture, uncommon variation.
- 67. Contraindications Overlying infectionor burn at insertion site. Absent collateral circulation. Arteriovenous shunt. Often radial or brachial. Severe atherosclerosis Raynauds disease. Coagulopathy.
- 68. Sites Preferred radialor femoral arteries. Less common. Dorsalis pedis and posterior tibial. Avoid. Branches without collateral supply. Example is the brachial artery.
- 69. Complications Bleeding causinghematoma. Arterial occlusion causing thrombus or dissection. Infection causing arteritis or cellulitis. Embolization Last 3 uncommon.
- 70. Normal Values pH,7.36 to 7.44. For acid base status of blood. pCO2, 38 to 44 mmHg. Reflects ventillation. pO2, 85 to 95 mmHg. Reflects oxygenation. HCO3, 21 to 27 meq per litre. Key blood buffer. Base excess, plus or minus 2 meq per litre ABG quiz. http://www.vectors.cx/med/apps/abg.cgi
- 71. Pathophysiology Metabolic alkalosis Metabolic acidosis Respiratory alkalosis Respiratory acidosis
- 72. Initial Preparation Washhands Gloves Protective eye wear Iodine swab. Povidone-iodine, betadine. Followed by alcohol swab Arterial blood gas sampling kit 2 x 2 cm gauze Bag of ice. To store sample
- 73. Allens Test Indicatescollateral circulation to hand. Radial artery on non dominant hand. Palpate radial artery. Simultaneouslys palpate ulnar artery, or as close to that area as possible. Patient makes a fist. Palpate both arteries for10 seconds. Release ulnar artery and witness blood flow and pinking of the hand via collateral radial artery Radial artery is now a candidate for testing.
- 74. Set Up Patientseated on stretcher Rolled up towel under wrist. That hyperextends wrist, bringing artery closer to surface. Clean area in a cicular motion with iodine. Allow to dry. Wipe away iodine with alcohol. While drying, open sampling kit.
- 75. Sampling Kit 3pieces 1. Orange air ball or cube. Used to expel excess air from the syringe. 2. Black cap for syringe, used for transport. 3. 3 cc, cubic centimetres heparinised syringe. With needle attached.
- 76. Sampling Kit Use Pull back slightly on plunger, so once needle is in artery, natural pulsations will fill the syringe. Remove clear needle cap. Locate the bevel. Bevel is a slanted opening on one side of the needle tip. We want bevel facing upward, so you can see it.
- 77. Syringe Use 45degrees, sharper angle. Hold like a dart or pen. Feeling pulse under non syringe finger is the only landmark for orientation. Before piercing skin, roll finger back slightly from artery, so you dont stab yourself in the finger. Flash of blood into hub of needle. Artery has been accessed. Blood will pulse into syringe. 1.5 to 2.0 cc required. Cover needle with gauze. Quickly remove needle.
- 78. After Care Physicianapplies pressure to gauze for 5 minutes. 10 minutes if patient is on anticoaggulant therapy. Optional to ask patient to do this instead.
- 79. Blood Care Insertneedle into orange air cube or ball. Want bevel covered, dont want needle to go through cube. Push down on plunger to expell excess air. So it doesnt affect results. Key point because we are measuring air component levels in blood. Remove cube and needle as one. Attach black cap to syringe. Roll test tube between hands, to ensure blood heparinisation. Place in iced bag. Send to lab. Needle and cube to sharps container.
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- 81. References Bishop, M.,Fody, E., & Schoeff, l. (2010). Clinical Chemistry: Techniques, principles, Correlations. Baltimore: Wolters Kluwer Lippincott Williams & Wilkins. Carreiro-Lewandowski, E. (2008). Blood Gas Analysis and Interpretation. Denver, Colorado: Colorado Association for Continuing Medical Laboratory Education, Inc. Sunheimer, R., & Graves, L. (2010). Clinical Laboratory Chemistry. Upper Saddle River: Pearson . 81
- 82. Resources to learnmore www.acid-base.com www.acidbasedisorders.com Haber RJ. A practical approach to acid-base disorders. West J Med 1991; 155: 146 www.postgradmed.com/issues/2000/03_00/fall.ht m http://medicine.ucsf.edu/housestaff/handbook/H ospH2002_C5.htm