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8/9/2019 Acid Base Discorders MIU BCPS 2015
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Taher Hegab, PharmD, PhD, BCPS
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Identify acid/base disorders Discuss etiologies for primary acid/base
disorders
Interpret acid/based disorders by interpretingarterial blood gas & serum chemistry values
Develop optimal pharmacotherapy plans foracid/base disorders
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What is acid?
Acids are H+ donors.
What is base
Bases are H+ acceptors
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What is pH?
pH = - log [H+]
Range is from 0 14 A change of 1 pH unit corresponds to a 10-fold
change in hydrogen ion concentration
If [H+] is high, the solution is acidic; pH < 7
If [H+] is low, the solution is basic or alkaline ;pH > 7
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What is the normal pH of the blood and ECF?
Blood and Extracellular fluid has a pH of7.35 7.45
(average 7.4)
Blood is:
A. AcidicB. Basic
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Physiological sources of acids in blood and ECF: CO2(volatile acid, from carbohydrate and fat
metabolism)
Metabolism of proteins (sulfur and phosphorus
containing amino acids). Incomplete oxidation of carbohydrates and fats (lactic
and keto-acid generation)
Acid excretion: Lung (CO2)
Kidney (non volatile acids, as ammonium and phosphate)
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Physiological sources of bases in blood andECF: HCO3
-from kidneys (production and reclamation)
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Buffers are solutions which can resist changes in pH whenacid or base is added.
Physiological buffers:
Bicarbonate: most important Extracellular buffer
H
+
+ HCO3-
H2CO3CO2+ H2O
Proteins: important intracellular and plasma buffers H++ Hb-HHb
Phosphate: important intracellular and renal tubular buffer
H++ HPO42-H2PO4
-
Ammonia: important renal tubular buffer
H++ NH3NH4
+
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Acidemia is pH < 7.35 Alkalemia is pH > 7.45
Acidosis: process of causing acidemia Alkalosis: process of causing alkalemia
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Compensation: pH is returned toward normal by altering the
component NOT primarily affected
Correction: pH is returned toward normal by altering the
component PRIMARILY affected
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Maintaining near constant hydrogen ionconcentration is essential for life
The lung and kidney work to maintain pHaround 7.4
The compensation for pH alteration isdescribed as respiratory if it wasaccomplished through the lung.
Metabolic compensation is done through thekidney
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PCO2is pressure of
CO2gas in the blood
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blood test that is performed using blood froman artery and is used to measure blood pH
The most common puncture site is the radialartery at the wrist
Alternate sites include femoral artery
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Measure pH, CO2, and O2in arterial blood Arterial blood is used as is best reflect the
ability of the lung to perform the gasexchange as O2and CO2level are measuredbefore blood enter tissues
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Respiratory disease that carries a risk ofinadequate lung ventilation and inadequatetissue oxygenation (Pulse oximetry indicates anO2saturation < 95%) COPD Severe asthma
Metabolic disease that carries a risk of acid-baseabnormalities Acute renal failure Sepsis
DKA
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Arterial blood gas sampling is used for:
A. only in patients with pulmonary disease
B. only in patients with renal disease
C. to assess lung ventilation, tissue oxygenation, andacid base status
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Arterial Mixed VenouspH 7.4 (7.35-7.45) 7.38 (7.33-7.43)
PO2 80-100 mmHg 35-40 mmHg
SaO2 95% 70 75%
PCO2 35-45 mmHg 45-51 mmHg
HCO3 22-26 mEq/L 24-28 mEq/L
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PrimaryDisorder
Primaryproblem
Effecton pH
Compensatorymechanism
Respiratoryacidosis
PCO2 HCO3
Respiratoryalkalosis
PCO2 HCO3
Metabolicacidosis
HCO3 PCO2
Metabolic
alkalosis
HCO3 PCO2
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Disorder Rate of Compensation
Metabolic acidosis For 1mEq/L HCO3PCO2 1 1.5 mmHg
Metabolic alkalosis For 1mEq/L HCO3
PCO2 0.5 2 mmHgRespiratory Acidosis(acute)
For 10 mmHg PCO2 ,HCO3 1 mEq/L
Respiratory Acidosis(chronic)
For 10 mmHg PCO2 ,HCO3 4 mEq/L
RespiratoryAlkalosis (acute)
For 10 mmHg PCO2 ,HCO3 1-3 mEq/L
RespiratoryAlkalosis (chronic)
For 10 mmHg PCO2 ,HCO3 2-5 mEq/L
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Normal value: Check you lab!!!
Classical value: 12 2 mEq/L
Newer instrumentation 9-11 mEq/L
Again check your lab
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Anion gap is expected to increase withaccumulation of acids that consumebicarbonate in serum
Example of acid are: Lactic acid
Ketoacids
Phosphoric acid
Sulfuric acid
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Steps to perform Acid Base Analysis
1 Determine if the ABG is acidemic, alkalemic, or normal (assess pH)
2Determine if the disturbance is respiratory or metabolic (Assess PCO2and HCO3)
3If the disturbance is respiratory, determine if it is acute or chronic
(Compare measured HCO3with expected HCO3)
4If the disturbance is metabolic acidosis, determine if it is an anion gapor non-anion gap
5
If metabolic, determine if the respiratory system is adequately
compensating
6 If an anion gap exists, are other metabolic disturbances present?
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A 22 year old student is admitted to the EDafter taking an overdose of morphine. He isunconscious and breathing at a rate of 6-7breaths per minute.
His ABG values on room air are pH 7.25, PCO260, PO274, HCO3 26.
What is wrong with him?
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Primary change is an increase in PCO2(hypercapnea) due to decreased CO2excretion
CO2
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Causes Central nervous system depression
Drugs, CNS events
Acute airway obstruction Upper airway, laryngospasm, bronchospasm
Severe pneumonia or pulmonary edema Impaired lung motion
Hemothorax, pneumothorax
Thoracic cage injury Flail chest
Neuromuscular disorders Myopathies, neuropathies
Ventilator dysfunction
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Signs and symptoms Acute
Marked restlessness, dyspnea and tachypnea
May progress to stupor and coma
Chronic SOB and fatigue with or without right-sided heart
failure (cor pulmonale)
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Acute Increased PCO2, moderately elevated HCO3(25-30
mEq/L) and a dramatic decrease in pH
Also see decreased PO2on room air
Normal plasma Na, K and Cl with an increased totalCO2 content
Compensatory increase in HCO3 For each 10 mmHg increase in PCO2, HCO3increases1
mEq/L
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Chronic Moderately decreased arterial pH (7.25-7.4),
elevated HCO3and PCO2 In a patient with chronic bronchitis:
PCO250-60, PO245-60 Normal plasma Na and K
Compensatory increase in HCO3 For each 10 mmHg increase in PCO2, HCO3increases 4
mEq/L
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Acute Goal of therapy: normalize arterial blood pH within
8-24 hours
Administer oxygen; intubate and mechanically
ventilate if needed
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Chronic Goal of therapy: make patient comfortable and able
to continue with daily activities
Supportive care
Lung transplantation
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A 22 yo student is admitted to the ED aftertaking an overdose of morphine. He isunconscious and breathing at a rate of 6-7breaths per minute.
His ABG values on room air are pH 7.25, PCO260, PO274, HCO3 26.
What is wrong with him?
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ABG interpretation: Step 1: assess pH
pH 7.25 (acidemia)
Step 2:Assess PCO2
and HCO3
PCO2 60 (), HCO3 26 () = respiratory acidosis
Primary disorder = respiratory acidosis
Step 3: Compare measured HCO3with expected
HCO3 PCO2 by 20, HCO3 by 2 10/1 Appropriate
metabolic compensations for acute respiratory acidosis
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Assessment: Acute respiratory acidosis secondary to narcotic
overdose resulting in hypoventilation
Initial management Oxygen therapy
Naloxone
Intubate and mechanically ventilate, if necessary
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A 67 yo man presents with complaints ofincreased cough and shortness of breath forthe past 12 hrs. PMH includes severe COPD.Current labs are: ABG: pH 7.2, PCO280, PO247 Electrolytes: Na 135, K 4.0, Cl 90, HCO3 34
3 months ago her serum HCO3 was 34
What is your acid/base assessment?
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Step 1: assess pH pH 7.2 (acidemia)
Step 2:Assess PCO2and HCO3
PCO2 80 (), HCO3 34 () = respiratory acidosis Primary disorder = respiratory acidosis
Step 3: Compare measured HCO3with expectedHCO3
PCO2 by 40, HCO3 by 10 10/2.5 Closer toexpected compensation for chronic respiratoryacidosis
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Assessment: Chronic respiratory acidosis secondary to severe
COPD
Initial management Oxygen therapy
Optimize COPD medications
Lung transplant
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A 55 yo woman is admitted to the hospital fora breast biopsy. While the resident isexplaining the procedure to her she becomesnoticeably anxious and says she feels dizzy.
You note that her respirations have increasedto 45 bpm. The resident orders ABGs and theresults are as follows:
pH 7.5, PCO229, PO280, HCO322.
Interpret this ABG and discuss initialmanagement for this patient
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Primary change is a decrease in PCO2due toincrease in elimination of CO2
CO2
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Causes: Anxiety
Hypoxia
Central nervous system disease
Drug-induced: Salicylates, catecholamines,progesterone
Pregnancy
Sepsis
Mechanical ventilation
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Signs and symptoms Neuromuscular irritability
Periorbital and extremity parathesias, muscle cramps,tinnitus, hyperreflexia, seizures
Cerebral thrombosis or ischemic events in patientswith sickle cell disease
Ischemic changes in ECG or arrhythmias
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Acute: pH > 7.45, PCO2< 35 and a small compensatory
decrease in HCO3 For each 10 mm Hg decrease in PCO2, HCO3
decreases1-3 mEq/L
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Chronic: Normal-high pH with hypocapnea, mild
hypokalemia, hyperchloremia and metabolicacidosis
Compensatory decrease in HCO3 For each 10 mm Hg decrease in PCO2, HCO3decreases
2-5 mEq/L
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No specific treatment Treat cause or underlying condition
Stop hyperventilation, manage pain/anxiety
Use of acidifying agents is generally NOTrecommended
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A 55 yo woman is admitted to the hospital fora breast biopsy. While the resident isexplaining the procedure to her she becomesnoticeably anxious and says she feels dizzy.
You note that her respirations have increasedto 45 bpm. The resident orders ABGs and theresults are as follows:
pH 7.5, PCO229, PO280, HCO322.
Interpret this ABG and discuss initialmanagement for this patient
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Step 1: assess pH pH 7.5 (alkalemia)
Step 2:Assess PCO2and HCO3
PCO2 29 (), HCO3 22 () = respiratory alkalosisPrimary disorder = respiratory alkalosis
Step 3: Compare measured HCO3with expectedHCO3
PCO2by 11, HCO3by 2 10/2 Closer toexpected compensation for acute respiratory alkalosis
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Assessment: Acute respiratory alkalosis secondary to
hyperventilation related to pre-procedure anxiety
Initial management Calm and reassure the patient
Encourage slow, deep breathing
Have patient breathe into a paper bag or place an
oxygen mask with a CO2reservoir on the patient
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EW is a 19 yo diabetic female who recentlybecame engaged. Over the past week she hasbeen staying up late each night planning herwedding after working full time during the day.She has not been watching her diet closely and
developed flu-like symptoms 3 days ago. Todayshe called her MD who referred her to the ED. Onassessment in the ED you note rapid breathingand a fruity odor to EWs breath.
Her ABGs and glucose values are: pH 7.2, PCO
221, PO
294, HCO
38, glucose 460.
Interpret this ABG and describe initialmanagement for this patient
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Primary change is a decrease in plasma HCO3with a decrease in arterial pH below 7.35
Causes of metabolic acidosis: Buffering of added strong acids by HCO3 Loss of HCO3through the GI tract or kidneys
Rapid dilution of extracellular fluid by HCO3-freesolutions
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Increased anion gap acidosis (more acidsadded to plasma, increase in unmeasurableanions) Renal failure
Ketoacidosis Diabetic, alcoholic
Lactic acidosis
Rhabdomyolysis
Toxins Methanol, ethylene glycol, paraldehyde, salicylates
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Causes of normal anion gap acidosis (loss of HCO3, noincrease in unmeasurable anions)
Renal bicarbonate loss Renal tubular acidosis Early renal failure
Carbonic anhydrase inhibitors Aldosterone inhibitors
GI bicarbonate loss Diarrhea Ureteral diversion
Small bowel, biliary, pancreatic or fistula drainage
Hyperalimentation (TPN)
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Signs and symptoms: Severe
Kussmaul hyperventilation:
Rapid, deep, irregular respirations
Atrial tachycardia Ventricular fibrillation
Arterial vasodilation and hypotension
Hyperkalemia
CNS depression
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Arterial pH, plasma HCO3, PCO2
Compensatory decrease in PCO2: For each 1 mEq/L in HCO3, PCO2decreases 1-1.5 mmHg
Increased AG is diagnostic An indication of the etiology can be made by evaluating the AG
and the plasma K+
Hyperchloremic, hypokalemic metabolic acidosis >> GIlosses of HCO3and GI or ureteral diversions
Hyperchloremic, hyperkalemic metabolic acidosis >>decreased ability of kidney to excrete H+ and K+ >>Hypoaldosteronism or mineralocorticoid deficiencies
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Goal: restore hemodynamic stability by pH
Correct electrolyte abnormalities
Treat underlying causes
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NaHCO3 Mainstay of therapy
Initial doses range from 100-150 mEq
Monitor ABG 30 minutes after each dose
Bolus then continuous NaHCO3infusion 150 mEq NaHCO3 in 1 L D5W
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NaHCO3 HCO3deficit:
NaHCO3dose = (25 [HCO3] observed) X 50% TBW (kg) If thearterial blood pH < 7.1, use 80% TBW
Administer 30-50% of the calculate dose initially Increase pH over 3-6 hours, but not > 7.25
Monitor serum K+ closely
ADRs Left shift in the oxyhemoglobin curve, increased serum
osmolality, hypernatremia, volume overload, worsening
of intracellular acidosis
THAM
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EW is a 19 yo diabetic female who recentlybecame engaged. Over the past week she hasbeen staying up late each night planning herwedding after working full time during the day.She has not been watching her diet closely anddeveloped flu-like symptoms 3 days ago. Todayshe called her MD who referred her to the ED. Onassessment in the ED you note rapid breathingand a fruity odor to EWs breath.
Her ABGs and glucose values are: pH 7.2, PCO
2
21, PO2
94, HCO3
8, glucose 460.
Interpret this ABG and describe initialmanagement for this patient
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Step 1: assess pH pH 7.2 (acidemia)
Step 2:Assess PCO2and HCO3
PCO221 (), HCO38 () = metabolic acidosis Primary disorder = metabolic acidosis likely due to
DKA
Initial management
Treat DKA Insulin, volume resuscitation, correct electrolyte
abnormalities (e.g., hypokalemia)
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A 59 yo male is admitted to the hospital with ccof increased SOB and acute pulmonary edema.PHM includes 2 MIs and chronic CHF. Currentmedications include metoprolol, ASA, enalapril,
digoxin and furosemide. On day 3, his ABG are asfollows:
pH 7.5, PCO248, PO285, HCO336. His K is 2.5.
Interpret this ABG and discuss interventions forthis patient
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Primary change is an increase in HCO3with anincrease in pH
Caused by a loss of H+from the body or a netgain in HCO3
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Signs and symptoms: Mild to moderate:
Usually asymptomatic
Severe: Compromised cerebral and myocardial perfusion Neurologic abnormalities
Headache, tetany, seizures, lethargy, delirium, stupor
Hypoventilation
SVT and ventricular arrhythmias Hypokalemia (muscle weakness)
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Diagnosis Characterized by elevated arterial blood HCO3
and pH and hypokalemia
Compensatory increase in PCO2 For each 1 mEq/L increase in HCO3, PCO2increases
0.5-2 mm Hg
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Goal: normalize blood pressure, heart rate,urine output and laboratory parameterswithin 24-48 hours
Therapy based on diagnosis of the underlying
disorder Address precipitating causes
Administration of alkali, mineralocorticoid, potentdiuretics, excessive NG suction, etc.
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Chloride-responsive metabolic alkalosis: NS volume replacement
Acetazolamide
HCl infusion
Dose (mEq)=[(0.5L/kg)(Wt kg)][desired currentHCO3]
Ammonium chloride limited value
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Chloride unresponsive metabolic alkalosis: Treat underlying cause of mineralocorticoid excess
Diuretics (spironolactone, amiloride, triamterene)
Potassium repletion
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A 59 y/o male is admitted to the hospital withc/o increased SOB and acute pulmonary edema.PHM includes 2 MIs and chronic CHF. Currentmedications include metoprolol, ASA, enalapril,
digoxin and furosemide. On day 3, his ABG are asfollows:
pH 7.5, PCO248, PO285, HCO336. His K is 2.5.
Interpret this ABG and discuss interventions forthis patient
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Step 1: assess pH pH 7.5 (alkalemia)
Step 2:Assess PCO2and HCO3 PCO248 (), HCO336 () = metabolic alkalosis
Primary disorder = metabolic alkalosis
Step 3:respiratory compensation Appropriate respiratory compensation
HCO3 by 12; PCO2 by 8 (between 0.5 - 1)
Acute metabolic alkalosis secondary to diuresis Hypokalemia secondary to diuresis and metabolic alkalosis
Initial management NaCl and K replacement
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Two or three acid-base disturbances occursimultaneously
Determine the expected compensatory response to aprimary acid-base disorder, any value that fallsoutside that range represents an additional primary
disorder
Diagnosis Based on history, concurrent medical conditions,
medication history and laboratory abnormalities
Treatment Similar to the management for simple acid-base disorders
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When to suspect a mixed acid base disorder:1. The expected compensatory response does notoccur
2. Compensatory response occurs, but level of
compensation is inadequate or too extreme
3. Whenever the PCO2and HCO3becomesabnormal in the opposite direction. (i.e. one iselevated while the other is reduced). In simple
acid base disorders, the direction of thecompensatory response is always the same asthe direction of the initial abnormal change.
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4. pH is normal but PCO2or HCO3is abnormal
4. In anion gap metabolic acidosis, if thechange in bicarbonate level is not
proportional to the change of the anion gap.
5. In simple acid base disorders, the
compensatory response should never returnthe pH to normal. If that happens, suspect amixed disorder.
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Calculate corrected HCO3: Corrected HCO3= HCO3+ AG
Corrected HCO3> 28Alkalosis
Corrected HCO3< 20Acidosis
Calculate delta ratio Delta ratio = AG / HCO3
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AG / HCO3=1-2 uncomplicated high anion gapmetabolic acidosis
AG / HCO3 2 Combined high AG metabolicacidosis and concurrent metabolic alkalosis
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A diabetic patient with viral gastroenteritispresents to your service with the followinglaboratory parameters:
Na 130, K 2.5, Cl 80, HCO310, pH 7.2, PCO225
Interpret this ABG and discuss interventionsfor this patient
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Step 5:Is respiratory compensation adequate PCO2by 15 for HCO3by 14 1/1 (expected PCO2
by14-21) Adequate respiratory compensation
No added respiratory disorder
Step 6:Are other metabolic disturbance present?
Calculate corrected HCO3:
Corrected HCO3= HCO3+ AG
Corrected HCO3= 10 + (40-12)= 38
Corrected HCO3> 28Alkalosis
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Assessment: Anion gap metabolic acidosis (from DKA?) + metabolic
alkalosis (vomiting?)
Initial management:
Treat DKA and volume resuscitate
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EMTs bring a patient to your ED who wasfound down on the street. The patient ispresumed homeless and no PMH is available.The following labs are obtained on
admission: Na 125, K 2.5, Cl 100, HCO38, pH 7.07, PCO2
28
Interpret this ABG and discuss interventions
for this patient
Acid Base Disorders Taher Hegab 87
8/9/2019 Acid Base Discorders MIU BCPS 2015
88/95
Acid Base Disorders Taher Hegab 88
8/9/2019 Acid Base Discorders MIU BCPS 2015
89/95
Step 5:Is respiratory compensation adequate PCO2by 12 for HCO3by 16 < 1/1 (expected
PCO2 by 16-24) Not adequate respiratorycompensation, higher PCO2
Respiratory acidosis
Step 6:Are other metabolic disturbance present?
Calculate corrected HCO3:
Corrected HCO3= HCO3+ AG
Corrected HCO3= 8 + (17-12)= 13
Corrected HCO3< 20acidosis
Acid Base Disorders Taher Hegab 89
8/9/2019 Acid Base Discorders MIU BCPS 2015
90/95
Assessment: Anion gap metabolic acidosis + respiratory acidosis +
non anion gap metabolic acidosis
Initial management:
Protect air (intubate) and determine underlying causeof metabolic acidosis and treat accordingly
Acid Base Disorders Taher Hegab 90
8/9/2019 Acid Base Discorders MIU BCPS 2015
91/95
A patient just arrived to the emergencydepartment following ingestions of a largequantity of aspirin. His initial laboratory panelis as follows:
pH 7.5, PCO220, HCO315, Na 140, Cl 103 Interpret this ABG and discuss interventions
for this patient
Acid Base Disorders Taher Hegab 91
8/9/2019 Acid Base Discorders MIU BCPS 2015
92/95
Acid Base Disorders Taher Hegab 92
8/9/2019 Acid Base Discorders MIU BCPS 2015
93/95
Step 6:Are other metabolic disturbance present? Calculate corrected HCO3:
Corrected HCO3= HCO3+ AG
Corrected HCO3= 15 + (22-12)= 25
Corrected HCO3is between 20-28, no additional
metabolic disorder
Acid Base Disorders Taher Hegab 93
8/9/2019 Acid Base Discorders MIU BCPS 2015
94/95
Assessment: Respiratory alkalosis + metabolic acidosis
Initial management:
Treat salicylate toxicity
Acid Base Disorders Taher Hegab 94
8/9/2019 Acid Base Discorders MIU BCPS 2015
95/95
Pharmacotherapy: Principles and Practice,2013.
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