Acid Base Discorders MIU BCPS 2015

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

Acid Base Disorders Taher Hegab 2


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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?

Acid Base Disorders Taher Hegab26


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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)


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)


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



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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= 8 + (17-12)= 13

Corrected HCO3< 20acidosis



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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



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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



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Step 6:Are other metabolic disturbance present? Calculate corrected HCO3:


Corrected HCO3= 15 + (22-12)= 25

Corrected HCO3is between 20-28, no additional

metabolic disorder



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Assessment: Respiratory alkalosis + metabolic acidosis

Initial management:

Treat salicylate toxicity



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Pharmacotherapy: Principles and Practice,2013.

Acid Base Discorders MIU BCPS 2015

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