ABG Interpretation 1

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Arterial Blood Gas and Electrolytes

Caesar Antonio O. Ligo, M.D. Holy Child Hospital Dumaguete City

Indications of ABG
Determine

acid-base or oxygenation problem May indicate onset or culmination of cardiopulmonary crises May serve as a gauge to the appropriateness or effectiveness of therapy

The Allen Test

Have the patient clench his/her fist Press on both radial and ulnar arteries Have the patient unclench fist Test for good collateral flow.

Collection of Blood Gas

Extend patients wrist 300 downward, palm up Locate pulse of radial artery proximal to skin crease at the wrist Palpate for size, direction, depth of the artery.

Arterial Blood Gas Collection

Cleanse the site Puncture skin 5-10 mm distal to palpating finger, at an angle of 450 Withdraw from patient and apply direct pressure.

Potential Complications

Pain
Hematoma, hemorrhage Trauma to vessel

Arteriospasm
Air or clotted-blood emboli

Vasovagal response
Arterial occlusion Infection

Arterial Blood Gas Interpretation

Normal ABG Values


pH 7.35 7.45

paCO2
paO2 HCO3 BE SaO2

35 45 mmHg
80 100 mm Hg 22 26 meq/L -2 - +2 97 98%

Steps in Acid-Base Classification


pH

classification PaCO2 classification Metabolic classification Compensation evaluation Complete acid-base classification

Severity of Generalized Acid-Base Disturbances


pH
< 7.20 7.20 7.29 7.30 7.34 7.35 7.45
Degree of Impairment

Severe acidemia Moderate acidemia Mild acidemia Normal pH

7.46 7.50
7.51 7.55 > 7.55

Mild alkalemia
Moderate alkalemia Severe alkalemia

Classification of PaO2 in the Adult


Classification
Hyperoxemia

PaO2 (mmHg)
>100

Normoxemia
Mild hypoxemia Moderate hypoxemia Severe hypoxemia

80 100
60 79 45 59 < 45

pH
7.80

Symptoms
Death Convulsions Arrythmias Irritability Normal Drowsiness Lethargy Coma Death

7.40

6.80

Acid-Base Classification
Acid-base disturbance
Respiratory acidosis Respiratory alkalosis

pH

PaCO2

N0 or
N0 or

HCO3
N0 or N0 or

Metabolic acidosis
Metabolic alkalosis

Cases

Case
V.M., 59 year old male
Moderate COPD; NIDDM 2-week cough with yellow sputum Intermittent low-grade fever Cefuroxime, Paracetamol, Fenoterol+Ipratropium Br x 3 days Sought consult at ER due to dyspnea and pleuritic chest pain

Case
At ER, he was agitated with the ff v/s: BP 130/90mmHg HR 110/min RR 28/min T 380C Chest/Lungs: decreased breath sounds and tactile fremitus at the right lower lung field, crackles on both lower lung fields

Case

Chest x-ray: lobar pneumonia at


the right lower lobe, hazy densities

at the left base and blunting of the


right costophrenic angle

Case

ABG taken at room air


7.50 31 mmHg 60 mmHg 22 meq/L 1.6 meq/L 90%

pH paCO2 paO2 HCO3 BE SaO2

What is the acid-base problem?


A. Respiratory alkalosis B. Respiratory acidosis C.A. Respiratory alkalosis Metabolic alkalosis D. Metabolic acidosis

Respiratory Alkalosis
Hallmark

pH, PaCO2 Compensation


Cellular Renal

buffering

response: retention of endogenous acids, excretion of HCO3

Respiratory Alkalosis
Formula

for compensation

HCO3 by 2 - 4 meq/L

Respiratory Alkalosis
Primary central disorders Hyperventilation syndrome, anxiety Cerebrovascular disease Meningitis, encephalitis Pulmonary disease Interstitial fibrosis Pneumonia Pulmonary embolism Pulmonary edema (some patients) Hypoxia Septicemia, hypotension Hepatic failure Drugs Salicylates Nicotine Xanthines Progestational hormones High altitude Mechanical ventilators

Respiratory Alkalosis

Treatment

Paralyze CMV

Treat the primary cause Control the patients ventilation


the patient

Carbonic anhydrase inhibitor (acetazolamide)


To

decrease HCO3 of limited value

* Most frequently, requires no specific therapy

Case

Given O2 at 4L/min via nasal cannula

SaO2 98%
Given Ceftazidime, Amikacin
WBC Segmenters Potassium Sodium Creatinine 30 x 106/uL 98%; (+) toxic granules 4 mmol/L 135 mmol/L 0.12 mmol/L

Case

Eight hours later drowsy with labored breathing and cyanosis ABG at 10L/min O2
7.23 86 mmHg 69 mmHg 25 meq/L - 4.8 meq/L 91%

pH PaCO2 PaO2 HCO3 BE SaO2

Case

Repeat Chest X-Ray: progression of hazy densities on the left lower lung field, with no significant interval change in the previously noted right lower lobe pneumonia. Patient admitted to ICU

What is the acid-base problem?


A. Respiratory alkalosis B. Respiratory acidosis C. B. Respiratory acidosis Metabolic alkalosis D. Metabolic acidosis

Respiratory Acidosis
Hallmark

pH, PaCO2 Compensation


Cellular

buffering: HCO3 Renal adaptation: H+ secretion, Cl- reabsorption, net acid excretion

Respiratory Acidosis
Formula

for compensation

HCO3 by 3 - 4 meq/L

Respiratory Acidosis

COPD O2 excess in COPD Drugs Barbiturates Anesthetics Narcotics Sedatives Extreme ventilation-perfusion mismatch Exhaustion Inadequate MV Neurologic disorders

Neuromuscular disease Poliomyelitis ALL G-B syndrome Electrolyte deficiencies (K+, PO4-) Myasthenia gravis Excessive CO2 production TPN Sepsis Severe burns NaHCO3 administration

Respiratory Acidosis
Treatment:
Correct

precipitating cause Restore alveolar ventilation Correct CO2 retention Intubation and assisted ventilation O2 administration

Case

Third ICU day

blood C/S: Klebsiella pneumoniae


Sensitive:

piperacillin/tazobactam, meropenem, cefepime ceftazidime, amikacin

Resistant:

Decreasing urine output at 10ml/hr Impression: acute renal failure Referred to nephrologist

Case

Laboratories
145 mmol/L 5 mmol/L 106 mmol/L 0.48 mmol/L 300 mg/dL

sodium potassium chloride creatinine CBG

Case

ABG at 40% FiO2, BUR 20/min


400ml VT, PEEP 5cmH2O
7.20 25 mmHg 114 mmHg 11 meq/L - 15.9 meq/L 98.4%

pH PaCO2 PaO2 HCO3 BE SaO2

What is the acid-base problem?


A. Respiratory alkalosis B. Respiratory acidosis C. Metabolic alkalosis D. Metabolic acidosis D. Metabolic acidosis

Metabolic Acidosis

Metabolic Acidosis
Hallmark: pH HCO3 base deficit accumulation of fixed acids

Metabolic Acidosis
Abnormalities: Overproduction of acids Loss of buffer stores Underexcretion of acids

Metabolic Acidosis
Compensation pCO2 (hyperventilation) Pathway:
HCO3 pCO2 ratio HCO3 H+ conc pH Acidification of ECF Stimulation of brainstem Normalization of pH ECF

RR

pCO2

Metabolic Acidosis
Compensation Ionic shift
K+

moves extracellularly for H+ HCO3 generation, H+ excretion

Metabolic Acidosis
Effects Stimulate epinephrine release Leukocytosis Hyperkalemia Hypercalcemia / hypercalciuria Myocardial failure

Anion Gap
Numerical difference Na+ and HCO3, Cl Helpful

between

tool in suggesting the presence and clarifying the differential diagnosis of metabolic acidosis
Anion Gap = [Na+] [HCO3 + Cl-] N0 value = 12 2 meq/L

Normal vs. Elevated Anion Gap


Normal Anion Gap Reduced HCO3 is counterbalanced by a measurable anion

GI disorders (diarrhea, pancreatic fistulas) Uterosigmoidoscopy, ileostomy Ingestion of acids, parenteral hyperalimentation Carbonic anhydrase inhibitors Renal acidification defects

Normal vs. Elevated Anion Gap


Elevated Anion Gap Reduced HCO3 is replaced by an unmeasurable organic anion

Ketoacidosis (starvation, alcoholinduced) Lactic acidosis Chronic renal failure Methyl alcohol / ethyl alcohol ingestion Paraldehyde ingestion Salicylate overdose

Metabolic Acidosis

Compensation

Expected pCO2 = HCO3 x 1.5 + 8.4 Limit = 10 mmHg

Metabolic Acidosis
Management Sustain normality of blood acid base parameters
Maintain serum HCO3 = 10 to 15 meq/L HCO3 administration for pH < 7.2 Treat the underlying cause

NaHCO3 Deficit Computation


HCO3 = (desired actual HCO3) x 0.4 x wt (kg)

HCO3 = BE x 0.3 x wt (kg) 2

Case
Urine output improved after fluid challenge Few hours later tachypneic PEEP increased to 8 cmH2O

pH PaCO2 PaO2 HCO3 BE SaO2

7.36 34 mmHg 89 mmHg 18 meq/L - 6.1 meq/L 96.6%

Case
Furosemide drip started at 10mg/hr Laboratories:

sodium potassium chloride creatinine albumin

140 mmol/L 2 mmol/L 100 mmol/L 0.34 mmol/L 26 g/dL

Case

Repeat ABG at 40% FiO2, VT400ml,


BUR 20/min, PEEP 8cmH2O
7.53 47 mmHg 109 mmHg 36 meq/L 11.3 meq/L 98.5%

pH PaCO2 PaO2 HCO3 BE SaO2

What is the acid-base problem?


A. Respiratory alkalosis B. Respiratory acidosis C. Metabolic alkalosis C. Metabolic alkalosis D. Metabolic acidosis

Metabolic Alkalosis
Hallmark

pH, HCO3
Compensation

PaCO2 (hypoventilation)

Metabolic Alkalosis
Pathway

HCO3

PaCO2 ratio HCO3

H+ conc

Alkalinization of ECF

PaCO2 with mild hypoxemia

Normalization of pH

Metabolic Alkalosis

Compensation

Expected PaCO2= ( O.8 x HCO3 ) + 16 4

Every 1 mEq increase in HCO3 will increase PaCO2 by 0.5-1 mmHg

Causes of Metabolic Alkalosis


Hypokalemia* Ingestion of large amounts of alkali or licorice Gastric fluid loss: Vomiting, NG suctioning* Hyperaldosteronism 20 to nonadrenal factors Bartters syndrome Inadequate renal perfusion diuretics (inhibiting NaCl reabsorption)* Bicarbonate administration Sodium bicarbonate overcorrection Blood transfusion Adrenocortical hypersecretion (e.g tumor) Steroids* Eucapnic ventilation posthypercapnia * Common in the ICU

Why is Correction of Metabolic Alkalosis Important ?


Decrease CO Depress central ventilation Shift the oxyhemoglobin saturation curve to the left Worsen hypokalemia and hypophosphatemia Negatively affect ability to wean patient from the mechanical ventilator

Correction of Metabolic Alkalosis


Increase Minute Ventilation Increase Arterial O2 & mixed venous O2 Tension Decrease O2 consumption

Treatment of Metabolic Alkalosis


Replace fluids (with Normal Saline) Replace electrolyte deficit

K supplementation (K > 4.5 mEq/L) Ammonium chloride Hydrochloric acid

Acetazolamide (carbonic anhydrase inhibitor) -promotes renal excretion of HCO3-

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