Chapter 8. Interpretation of Blood Gases Part 2 PDF

ASSESSMENT OF ACID-BASE BALANCE RT 3025 HYDROGEN ION CONCENTRATION (pH)  Normal pH: 7.35 - 7.45  pH is measurement of H+ ions in the plasma.  Changes in pH of 1 unit represent a tenfold change in [H+]. pH [H+] in nanomols/L 7.6 26 7.5...

ASSESSMENT OF ACID-BASE BALANCE RT 3025 HYDROGEN ION CONCENTRATION (pH)  Normal pH: 7.35 - 7.45  pH is measurement of H+ ions in the plasma.  Changes in pH of 1 unit represent a tenfold change in [H+]. pH [H+] in nanomols/L 7.6 26 7.5 32 7.4 40 7.3 50 7.2 63 7.1 80 7.0 100 6.9 125  ACIDEMIA VS ALKALEMIA  pH > 7.45 = alkalemia.  pH < 7.35 = acidemia.  Allbody functions occur optimally around a pH of 7.40.  Acidosis results in depression of the CNS.  Lethargic and disoriented to comatose.  Acidosis reduces cardiac contractility.  Alkalosis results in hyperexcitability of CNS and peripheral nerves.  muscle spasm. PaCO2  Normal value: 35-45 mmHg.  It is the most reliable measurement for evaluating effectiveness of ventilation.  It is a reflection of the respiratory component of the acid-base status.  CO2 is a waste product of metabolism; therefore, PaCO2 identifies degree of ventilation in relation to metabolic rate.  Fever or exercise increase metabolic rate (CO2 production) leading to hyperventilation (CO2 elimination).  PaCO2  Hypercapnia or hypercarbia >45 mmHg  Hypocapnia or hypocarbia < 35 mmHg  PaCO2 alters pH according to the equation: CO2 + H2O < >H2CO3< > HCO3 + H+  Increase in PaCO2 = increase H+ = respiratory acidosis  CNS chemoreceptors respond by increasing RR  Decrease in PaCO2 = decrease H+ = respiratory alkalosis  Decrease in RR  PaCO2 and Minute Ventilation  Normal PaCO2 should be accompanied by normal minute ventilation = V E  Normal MV = 5-10 L/min in adult  Increased VE results in hypocapnia unless:  Metabolic rate is increased.  Dead space ventilation reduced lung perfusion.  Reduction in V E below normal results in hypercapnia unless:  Metabolic rate is decreased.  VE reduced, PaCO2 increased  Neuromuscular disease or respiratory depressants (morphine). EXPECTED CO2 BASED ON MINUTE VENTILATION Minute Ventilation PACO2 (mm Hg) PaCO2 (mm Hg) Normal 40 35-45 2 times normal 30 25-35 4 times normal 20 15-25  HCO3 -  Normal value: 22-26 mEq/L.(Standard at PaCO2 of 40)  This is a calculated value based on the H-H equation.  Plasma HCO3- is a reflection of the metabolic component of acid-base balance.  Metabolic acidosis:  Decrease plasma HCO¯3.  Decrease pH  Acute changes in PaCO2 slightly affect plasma HCO3- according to the equation: CO2 + H2O < > H2CO3 < > HCO¯3 + H+  Total CO2  Plasma bicarb can be reported as Total CO2  Plasma bicarb can be approximated from the total CO2  May see this on ABG report or lab sample for electrolytes from venous blood. Total CO2 = (dissolved CO2) + HCO3 = (PaCO2 x 0.03* mEq/L/mm Hg) + 24 1.2 + 24 = 25.2 mEq/L * Conversion factor to change mm Hg to mEq/L PaCO2, pH, HCO3- RELATIONSHIP  The HCO3- level may change to compensate changes in PaCO2 but it requires 12-24h to occur.  For every 10 mmHg increase in PaCO 2 > 40 mmHg:  pH decreases by 0.05  Serum HCO3- increases 1mEq/L.  PaCO2 40, pH-7.40, HCO3¯-24  PaCO2-50, pH-7.35, HCO3¯-25  PaCO2-60, pH-7.30, HCO3¯-26  PaCO2-70, pH 7.25, HCO3¯-27 PaCO2, pH, HCO3- RELATIONSHIP  For every 10 mmHg decrease in PaCO2 below normal:  pH increases by 0.10  Serum HCO3- decreases by 1 mEq/L.  PaCO2-40, pH-7.40, HCO3¯-24  PaCO2-30, pH-7.50, HCO3¯-23  PaCO2-20, pH-7.60, HCO3¯-22 BASE EXCESS AND BASE DEFICIT  Normal value: + 2 mEq/L.  It is a reflection of the pure metabolic components of acid-base balance.  Takes into account the RBC buffering ability  Calculation is made from measurement of pH, PaCO2, and hematocrit Hb.  Hb Hct: significant amount of blood buffers.  45-50 mEq/L, approx. twice that of HCO3¯.  Reported as base excess or deficit.  (+) base either has  Acid depletion or base added  (-) base either has  Acid added or base depleted BASE EXCESS/DEFICIT  pH7.37, PaCO2 58 mm Hg, HCO3¯ 34 mEq/L  Base excess (+) 10 mEq/L  34-10 = 24 mEq/L  A base deficit of 10 means that 10 mEq/L of buffer has been used up to neutralize metabolic acids (like lactic acid) BASE EXCESS AND BASE DEFICIT  BE provides a more complete analysis of the metabolic buffering capabilities.  The larger the value, the more severe the deviation in the metabolic component.  Base Excess- base has been added or acid has been removed  Base deficit-acid added or base removed  Metabolic changes in HCO3¯ alter base excess  Acute changes in HCO3¯ due to PaCO2 do not cause base excess changes. RESPIRATORY AND METABOLIC ACID-BASE DISORDERS  RESPIRATORY AND METABOLIC DISORDERS  The effects of PaCO2 and plasma HCO3¯ on acid-base balance are defined in the Henderson-Hasselbach equation: pH=pK(6.1) + log (HCO3¯/PaCO2 x 0.03)  HCO3¯/PaCO2 ratio 20:1.  pH is determined by this ratio.  Normal pH does not rule out acid-base disorder.  May indicate compensation.  CO2 CO2 RESPIRATORY ACIDOSIS  Reduction in alveolar ventilation relative to CO2 production. Inadequate ventilation  Respiratory causes:  Acute upper airway obstruction  Diffuse airway obstruction  Massive pulmonary edema  Non-respiratory causes:  Drug overdose  Spinal cord injury  Neuromuscular disease  Head/chest trauma  RESPIRATORY ACIDOSIS  Uncompensated or acute respiratory acidosis:  High PaCO2, low pH, normal HCO3¯, normal BE  pH-7.30, PaCO2-60 mmHg, HCO3¯ – 24 mEq/L, BE 0 mEq/L.  Partially compensated  High PaCO2, Low pH, Elevated HCO3¯, BE increased  pH- 7.32, PaCO2- 60mmHg, HCO3 ¯ 27 mEq/L, BE + 3 mEq/L  Fully compensated  High PaCO2, Normal pH, Elevated HCO3¯, BE ++increased  pH 7.37, PaCO2 60 mmHg, HCO3¯ -34 mEq/L, BE + 8 mEq/L  COMPENSATION Determine degree of compensation:  CHRONIC –greater increase in HCO3¯  Acute increase PaCO2 by 10 mm Hg- increase1 mEq/L HCO3¯  COPD-PaCO2 increases from 55 to 65 mmHg  HCO3¯ increases from 34 to 35 mEq/L  Chronic Increase PaCO2 by 10 mmHg CO2 : increase 4 mEq/L HCO3¯.  COPD increases PaCO 2 from 40 to 60 mm Hg  HCO3¯ increases from 24 to 32 mEq/L (this takes longer than acute change)  This brings the pH back to acceptable value HYPERCAPNIA  Cardiovascular  Peripheral vasodilation  Increased CO  Flushed, warm skin  Bounding pulse  Cerebral vasodilation  Arrhythmia’s  CNS  Headache  Lethargy  Coma (acute hypercapnia >70 mmHg)  Cerebral vasodilation  Increased ICP  RESPIRATORY ALKALOSIS  Increase in alveolar ventilation relative to CO2 production.  Causes:  Pain  Hypoxemia-PaO2 < 60 mmHg  Acidosis  Anxiety  Compensation:  Renal compensation-excrete HCO3¯  ACUTE decrease PaCO2 by 5 mmHg : decrease 1 mEq/L in HCO3¯.  CHRONIC decrease PaCO 2 by 10 mmHg : decrease 5 mEq/L in HCO3¯.  RESPIRATORY ALKALOSIS  Acute Respiratory Alkalosis  pH 7.50 PaCO2 30, HCO3¯23  Partially compensated  pH 7.47, PaCO2 30, HCO3¯21  Completely Compensated  pH 7.42, PaCO2 33, HCO3¯17  HYPOCAPNIA  Clinical manifestations  Tachypnea  Dizziness  Sweating  Tingling in the fingers and toes  Muscle weakness  Muscle spasm INTERPRETATION pH PaCO2 HCO3¯ 7.30 60 26 7.35 50 25 7.40 40 24 7.50 30 22 7.32 55 30 7.37 58 35 7.60 20 22 CALCULATION OF EXPECTED PH  In Hypocarbia  Expected pH = 7.4 + (40 mm Hg – PaCO2) 0.01  Example: With a measured PaCO2 = 30 mm Hg what is the expected pH/  7.40 + (40 – 30) 0.01  7.40 + ( 10 x 0.01)  7.40 + ( 0.1) = 7.5 CALCULATION OF EXPECTED PH  In Hypercarbia  Expected pH = 7.4 + (PaCO2 - 40 mm Hg) 0.006  Example: With a measured PaCO2 = 50 mm Hg what is the expected pH/  7.40 + (50 – 40) 0.006  7.40 + ( 10 x 0.006)  7.40 + ( 0.06) = 7.34 METABOLIC ACIDOSIS  Reduced plasma HCO3¯ or base deficit.  Base depleting drugs Aspirin  Loss of HCO3¯  Diarrhea  Renal disease or failure  Increase metabolic acid production.  Ketoacidosis (lack of cellular glucose).  Lactic acidosis (lack of cellular oxygen).  Starvation.  Intoxication  Ethanol, ethylene glycol  METABOLIC ACIDOSIS  When metabolic acidosis due to buildup of organic and inorganic acids in the body, anion gap is elevated > 16 mEq/L.  Hypoxemia and hypoglycemia: increased amount of nonvolatile acids.  Renal Failure  Disruption of excretion of H+ or reabsorption of HCO3.  Also show signs of Increase BUN and creatinine Reduced urine output  COMPENSATION  Reduction of PaCO2 by hyperventilation.  Uncompensated metabolic acidosis is rare. Hyperventilation blows off CO2 quickly-Kussmauls’ respirations-diabetic ketoacidosis  pH 7.15, PaCO2 26 mmHg, HCO3 - 11  Predictedalteration in PaCO 2 for simple metabolic acidosis: Winter’s Formula PaCO2 = (1.5 x HCO3-) + 8 + 2 (1.5 x 11) =17 + 8 = 23-25-27 A normal or elevated PaCO2 in metabolic acidosis indicates a ventilatory defect is present  pH 7.25, PaCO2 48, HCO3-16  Metabolic Acidosis A elevated PaCO2 in metabolic acidosis indicates a ventilatory defect is present.  pH 7.25, PaCO2 48, HCO3-16 PaCO2 = (1.5 x HCO3-) + 8 + 2 (1.5 x 16) =24 + 8 = 32 (30-34) But the PaCO2 is 48 mm Hg. So patient has a ventilatory problem on top of their metabolic acidosis. EXAMPLE OF METABOLIC ACIDOSIS  Acute  pH=7.21, PaCO2=37 mm Hg, HCO3¯=19 mEq/L  Partly compensated  pH=7.31, PaCO2= 27 mm Hg, HCO3¯=14 mEq/L  Completely compensated  pH=7.37, PaCO2=19 mm Hg, HCO3¯=11 mEq/L CLINICAL MANIFESTATIONS  Rapid and deep breathing: Kussmaul’s.  Dyspnea, headache, nausea, vomiting.  Confusion and stupor.  Arrhythmias. LACTIC ACID (PLASMA LACTATE)  Lactate-product of carbohydrate metabolism  Lactic acid produced during anaerobic metabolism from:  Cells not receiving adequate oxygen  Single most important cause of lactic acidosis is deficient cell oxygenation in shock  Hypovolemic-trauma  Cardiogenic-heart failure  Septic-bacterial infection in blood  Therefore increase lactic acid is a marker for hypoxia  Lactic acid increases quickly within minutes of hypoxia LACTIC ACID (PLASMA LACTATE)  Accumulation of lactic acid from:  Excessive production  Reduced removal from blood by liver  Normal values  Venous blood-0.5-2.2 mEq/L  Arterial blood-0.5-1.6 mEq/L  Values > 2.0 mEq/L in arterial blood is considered abnormal  Most lactate produced from skeletal muscle, brain, and circulating erythrocytes  Normal metabolism of lactate within liver which converts it to glucose. LACTIC ACID (PLASMA LACTATE)  Increase in lactic acid from:  Liver disease  Cardiac failure  Respiratory failure  Hemorrhage  Hypoxia LACTIC ACID (PLASMA LACTATE)  In severe shock (CV, hypovolemic, septic)  System is not delivering enough oxygen to the tissue because of reduced cardiac output.  Metabolism produces pyruvate which metabolizes to lactic acid  Since this is non-volatile acid it must be removed by liver  Treatment  Treat shock situation  Give high FiO2  This will quickly convert lactic acid to glucose and can be utilized by tissues LACTIC ACID (PLASMA LACTATE)  An unexplained decrease in pH of the blood with hypoxia-producing condition is reason to suspect lactic acidosis. pH – 7.40 PaO2 – 80 mm Hg PaCO2-40 mm Hg pH – 7.25 PaO2 – 50 mm Hg PaCO2-40 mm Hg METABOLIC ALKALOSIS  HCO3-accumulation or excessive H + loss.  Compensation is hypoventilation  Can only raise PaCO2 to 55 mm Hg  Common causes:  Hypokalemia or hypochloremia.  Nasogastric suction.  Persistent vomiting.  Diuretic therapy.  Steroid therapy.  Excessive administration of HCO3-. METABOLIC ALKALOSIS EXAMPLES pH PaCO2 HCO3¯ Acute 7.59 42 29 P.C. 7.52 52 34 Comp 7.43 58 39 LIMITATIONS TO COMPENSATION FOR ACID- BASE DISORDERS  When one component has severe acid base imbalance complete compensation is not always possible.  Metabolic imbalance can be adjusted by the respiratory system but not completely  Kidney compensation for the resp imbalance does not adjust completely.  The greater the disturbance the less likely the compensation occurs completely. MIXED ACID-BASE DISORDERS MIXED ACID-BASE DISORDERS  A mixed acid-base disorder comprise 2 or more primary disorders.  RESPIRATORY AND METABOLIC ACIDOSIS  RESPIRATORY AND METABOLIC ALKALOSIS RESPIRATORY AND METABOLIC ACIDOSIS  Elevated PaCO2 and reduced plasma HCO3- are a result of different situations.  CPR  Lack of perfusion-hypoxia  Hypoventilation-hypercarbia  pH 6.98, PaCO2 98 mmHg, HCO3¯ 10 mEq/L, PaO2 35 mmHg RESPIRATORY AND METABOLIC ACIDOSIS  COPD and hypoxia  Chronic elevation of CO2  Reduced PaO2  Adequate tissue oxygenation because of hematocrit and increased cardiac output  Severe hypotension and anemia  Reduced perfusion and anemia causes tissue hypoxia and lactic acidosis.  Before  pH 7.37, PaCO2 57, PaO2 55, HCO3¯ 34  After  pH 7.30, PaCO2 57, PaO2 43, HCO3¯ 34 RESPIRATORY AND METABOLIC ACIDOSIS  Poisoning or Drug Overdose  Results in depression of respiratory center and hypoventilation=respiratory acidosis.  CNS depressants  Anticulvusants  Drugs break down and form acids producing metabolic acidosis-propylene glycol, formaldehyde  Lactic acid may contribute to the acidosis  Hypoxia  pH 7.07, PaCO2, 76, HCO3¯15, PaO2 40 PaCO2 AND HCO3¯  Pure metabolic acidosis?  pH 7.01, PaCO2 15 mm Hg, HCO3¯ 3.5 mEq/L  Winter’s formula  HCO3¯ x 1.5 + 8 = PCO2 ((± 2 mm Hg) 3.5 x 1.5 + 8 =13 mm Hg(± 2 mEq/L) so 11-15 mm Hg  Combined metabolic and respiratory acidosis  pH 6.92, PaCO2 34 mm Hg, HCO3¯ 3.5 mEq/L  Winter’s formula  HCO3¯ x 1.5 + 8 = PCO2 ((± 2 mm Hg) 3.5 x 1.5 + 8 =13 mm Hg(± 2 mEq/L) so 11-15 mm Hg  Pts PaCO2 higher than normal so respiratory acidosis from hypoventilation. METABOLIC AND RESPIRATORY ALKALOSIS  Recognized by elevated HCO3¯ and low PaCO2  Causes  Respiratory alkalosis-pain, anxiety, hypotension, hypoxemia, excessive mechanical ventilation or combination of all.  Metabolic alkalosis-NG suctioning, vomiting, antacid therapy  pH: 7.59, PaCO2: 42, HCO3¯: 29  Combined Metabolic and Respiratory Alkalosis  pH: 7.56, PaCO2: 32, HCO3¯:37, PaO2: 67 METABOLIC AND RESPIRATORY ALKALOSIS  Ventilator induced alkalosis occurs  COPD patients are intubated placed on mechanical ventilation.  Typical ABG’s  pH 7.38, PaCO2 56, HCO3¯34, PaO2 50  COPD in acute exacerbation  pH 7.31, PaCO2 67, HCO3¯38, PaO2 43  Excessive ventilation ABG’s  pH 7.45, PaCO2 50, HCO3¯ 31, PaO2 68  - METABOLIC ACIDOSIS AND RESPIRATORY ALKALOSIS  Met acidosis  pH 7.31, PaCO2 28, HCO3¯ 14  Met Acidosis and Resp Alkalosis  pH 7.26, PaCO2 21, HCO3¯ 14  Why PaCO2 = 14 + 7 = 21 + 8 = 29 ± 2 (27- 31) METABOLIC ALKALOSIS AND RESPIRATORY ACIDOSIS  Administration of diuretics  Met alkalosis and Resp Acidosis  pH-7.37, PaCO2-59, HCO3¯ 34  pH-7.30, PaCO2-65, HCO3¯ 36 FACTORS THAT COMPLICATE CLINICAL ACID-BASE BALANCE Respiratory and Metabolic Imbalances TYPICAL END-STAGE COPD pH – 7.38 PaCO2 – 55 mm Hg BE – 8 mEq/L HCO3¯ – 33 mEq/L PaO2 – 55 mm Hg Chronic respiratory acidosis with metabolic compensation (high HCO3¯ -metabolic alkalosis) RELATIVE HYPERVENTILATION IN COPD pH – 7.52 PaCO2 – 40 mm Hg BE – 8 mEq/L HCO3¯ – 33 mEq/L PaO2 – 50 mm Hg Hyperventilation due to hypoxemia. What is a way to tell: Look at the pH and PaCO2 Winters Formula-Given the level of HCO3¯ the PaCO2 should be closer to 58 mm Hg. RELATIVE HYPERVENTILATION WITH LACTIC ACIDOSIS pH – 7.38 PaCO2 – 40 mm Hg BE – 1 mEq/L HCO3¯ – 24 mEq/L PaO2 – 44 mm Hg Increase in lactic acid drops pH, HCO3¯ and BE decreases. Pt. increase respiratory rate in response to hypoxemia. ACUTE HYPERCAPNIA IN COPD pH – 7.30 PaCO2 – 75 mm Hg BE – 8 mEq/L HCO3¯ – 35 mEq/L PaO2 – 48 mm Hg Acute exacerbation in the ED. Notice the relatively normal pH in spite of high PaCO2. ACUTE HYPERCAPNIA WITH LACTIC ACIDOSIS IN COPD pH – 7.20 PaCO2 – 75 mm Hg BE – 0 mEq/L HCO3¯ – 28 mEq/L PaO2 – 43 mm Hg Again the patient comes in the ED with severe exacerbation of COPD…may need some positive pressure ventilation if no response from oxygen and other medications. 2 problems exist-respiratory acidosis and metabolic acidosis. CASE STUDIES STEPS TO A-B ASSESSMENT  1. Identify pH  Is it acidosis or alkalosis?  Is it respiratory or metabolic or mixed?  Resp: pH and PaCO 2  Metabolic: pH and HCO3¯  See-saw effect (resp) vs elevator effect (metabolic)  Mixed-both PCO2 and HCO3¯ are out of range.  2. Compensation  Acute, uncompensated, chronic CASE 1 GI DISTURBANCE 1. Classify the ABG 2. What is the status of her ventilation? 3. What is the status of her oxygenation? 4. Assess her vital signs for any abnormalities. 5. Any problems with her plasma electrolytes? CASE STUDY 2 WHEEZING CHILD 1. Interpret the ABG. 2. What is the ventilatory status? 3. What is the oxygenation status? 4. Assess the child’s vital signs. CASE STUDY 2 CONTINUED 1. Has the oxygenation improved with the increase in FiO2? 2. Interpret the ABG. 3. Assess the vital signs. CASE 3 HEAD TRAUMA FROM AUTOMOBILE INJURY 1. Interpret the ABG. 2. Assess her ventilator status. 3. Assess her oxygenation status. 4. Assess her vital signs. CASE 4 WOMAN WITH INTESTINAL OBSTRUCTION 1. Interpret her ABG. 2. Assess her vital signs. 3. Assess her plasma electrolytes. 4. Assess her ventilatory status. 5. Assess her oxygenation status. 6. What is the cause of this acid-base change? STEPS TO A-B ASSESSMENT  3. PaO2 (< 60 years of age)  Determine extent of hypoxemia  60-79 mild  40-60 moderate  < 40 severe  Determine if the hypoxemia has been corrected with the FiO2  Give FiO2 of 0.40 and PaO2 is still < 79-uncorrected.  PaO2 80 or above with increased FiO2-corrected  For > 60 years of age-determine the normal level for the age then apply the above. STEPS TO A-B ASSESSMENT  4. Hemoglobin and CaO2 (if available)  Normal hgb value (men and women)  Normal CaO2.  5. Tissue oxygenation-look at  Sensorium  Blood pressure  Extremity temperature  Pulses  PvO2 if available.  6. Patient’s reaction to the ABG being obtained-hyperventilation vs comatose. INTERPRETATION pH PaCO2 PaO2 HCO3¯ (mm Hg) (mm Hg) (mEq/L) 1 7.39 44 89 25 Normal 2 7.12 42 155 13 Uncomp met acidosis with hyperoxemia 3 7.25 65 55 28 P artially comp resp acidosis with moderate hypoxemia 4 7.52 32 105 26 Uncomp resp alk with hyperoxemia 5 7.42 33 103 21 Comp resp alk with hyperoxemia ABG’S pH PaCO2 PaO2 HCO3 6. 7.55 38 98 32 Uncomp met alkalosis 7. 7.37 66 68 36 Comp resp acid with mild hypoxemia 8. 7.29 73 69 34 Partially comp resp acid with mild hypoxemia 9. 7.33 65 78 33 Part comp resp acid with mild hypoxemia 10.7.52 25 99 20 Part comp resp alkalosis INTERPRETATION 1. Normal 2. Uncomp met acidosis with hyperoxemia 3. Partially comp resp acidosis with moderate hypoxemia 4. Uncomp resp alk with hyperoxemia 5. Comp resp alk with hyperoxemia 6. Uncomp met alk 7. Comp resp acid with mild hypoxemia 8. Partially comp resp acid with mild hypoxemia 9. Part comp resp acid with mild hypoxemia 10. Part comp resp alkalosis CASES 1. A 23 yo asthmatic female presents in the ED with moderate respiratory distress. Her initial ABG; pH 7.56, PaCO2 20 mm Hg, HCO3 22 mEq/L, PaO2 85 mm Hg. Acute Respiratory alkalosis, no hypoxemia 2. 59 yo male presents in ED with vomiting over the last few days. ABG’s are pH 7.55, PaCO2 47 mm Hg, HCO3 34 mEq/L, PaO2 85 mm Hg. Partly compensated metabolic alkalosis, no hypoxemia CASES 3. A 16 yo found, obtunded, shallow and slow breathing. A bottle of diazepam (valium) found at her bedside. In the ED on 100% oxygen. ABG’s are: pH 6.98, PaCO2 40 mm Hg, HCO3¯ 7 mEq/L, PaO2 456 mm Hg Mixed Metabolic Acidosis and Respiratory Acidosis What should the PaCO2 be given the HCO3¯ of 7? 7 x 1.5 = 10 + 8 = 18 ± 2 = 16-20 mEq/L A 39-year-old female presents to the Emergency Department after being found unconscious by family members up to 2 days prior to presentation. Initial vital signs include: temperature, 29.5 Celsius (rectal); heart rate, 100 beats per minute; respiratory rate, 20 breaths per minute; blood pressure, 139/86 mmHg. Physical examination was significant for depressed mental status, unresponsive to deep pain. Pupils were 4-5 mm and minimally reactive. Initial laboratory testing revealed sodium of 150 mEq/L, chloride of 115 mEq/L, bicarbonate of