ABG Electrolytes

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Electrolytes and Arterial Blood Gases

James H. Harrison, Jr., M.D., Ph.D.

Center for Oncology and Pathology Informatics

Department of Pathology

Cancer Pavilion 310

University of Pittsburgh Medical CenterPittsburgh, PA

[email protected]

12/2/2003



Agenda

• Quick review of renal tubular function

• Quick review of pulmonary function

• Pulmonary-renal cooperation in maintaining pH

• Respiratory acid-base imbalances

• Metabolic acid-base imbalances

• Sodium, potassium, chloride and bicarbonate balance

• Measurement of blood gases and electrolytes

• Case studies



Nephron Function

• Maintenance of internal fluid volumes

• Maintenance of appropriate plasma concentrations of dissolved ions

> Excitable membrane function and osmotic balance

• Internal pH balance

• Metabolic conversion of a variety of substrates

• Hormone production

• Waste product excretion

Nephron Animation

• The systems managing water balance, ion concentration, and pH are inter-related.

• Problems may appear as overlapping pH, electrolyte and water balance disorders.



Pulmonary Function: Oxygenation

• The lungs absorb oxygen from inspired air

> Expected PaO2 = 95 ± 5 mm Hg

> Expected O2 saturation = 97 ± 2 %

> Age-related: PaO2 = 104.2 - (0.27 * age)

• Or about 100 - 1/3 of the patients age

> PaO2 < 55 is hypoxemic (O2 sat < 90%)

• Alveolar:arterial oxygen gradient (A - a gradient)

> PAO2 = 150 - 1.25(PaCO2)

> Normal A-a gradient is 10-20 mm Hg

> If on O2: PAO2 = FIO2(760-47) - 1.25(PaCO2)



Pulmonary Function: CO2 Removal

• Expected value: PaCO2 = 40 ± 2 mm Hg

• CO2 diffuses easily through tissue

> CO2 retention based on gas exchange problems only in

severe (end-stage) pulmonary fibrosis or COPD

• CO2 elimination can be increased by increased

respiration and decreased by decreased respiration

• Internal pH strongly influenced by PaCO2



• Normal metabolism continually produces acid

• Carbonic acid/bicarbonate is the body’s main buffer (pKa = 6.1)

• The lungs eliminate acid as carbon dioxide, maintaining a normal

PCO2 of about 40 mm Hg• The kidneys remove H+ (DT) and conserve bicarbonate (PT),

maintaining a normal bicarbonate of about 24 meq/l

• This cooperative relationship maintains an internal pH very close

to 7.4 (< 6.8 or > 7.8 is incompatible with life)

Internal pH Depends on Renal-Pulmonary

Cooperation



Normal Lung and Kidney pH Balance



Respiratory Acidosis: Impaired Lung Function

• Retention of carbon dioxide (PaCO2 > 40)

• CNS depression (trauma, anesthesia, drugs):hypoventilation

• Neuromuscular disorders/paralysis: hypoventilation

• Severe COPD: chronic bronchitis/emphysema (V/Q

mismatch)

• Severe restrictive lung disease (pulmonary fibrosis)



Respiratory Acidosis

with Metabolic Compensation

Respiratory acidosis Metabolic compensation

when chronic



Respiratory Alkalosis: Hyperventilation

• Excess respiratory loss of carbon dioxide (pCO2 < 40)

• Chronic hypoxia in COPD

• Excitement, anxiety

• Moderate or early salicylate toxicity



Respiratory Alkalosis

with Renal Compensation

Respiratory alkalosis Metabolic compensation

when chronic



Metabolic Acidosis (bicarbonate depletion)

• Retention of protons or loss of bicarbonate (bicarb < 24)

> Urine more alkaline than expected

• Pulmonary compensation (rapid and robust)



Metabolic Acidosis

with Respiratory Compensation

Metabolic acidosis

(rarely seen uncompensated)

Respiratory compensation

(rapid)



The Anion Gap in Metabolic Acidosis

• Increased "anion gap" in metabolic acidosis (expected,6 - 18 meq/l)

• Anion Gap

> Renal failure

> Ketosis

> Lactic acidosis

> Poisoning

• Non-Anion Gap

> Renal tubular dysfunction (Fanconi's syndrome, carb. anh.)

> Diarrhea (bicarbonate loss)



Metabolic Alkalosis (bicarbonate retention)

• Loss of acid or retention of bicarbonate

• Pulmonary compensation (rapid but limited)

• Vomiting (loss of gastric acid)

• Diuretics (renal loss of potassium and acid in the distal tubule)

• Elevated corticosteroids (Cushing's syndrome and

hyperaldosteronism; distal tubule)

• Severe potassium depletion

• Acute alkali ingestion



Metabolic Alkalosis

with Respiratory Compensation

Metabolic alkalosis Respiratory compensation

(rapid but limited)



Practice Case

A patient presents with the following results from a blood gas study:pH = 7.43

pCO2 = 21 mm Hg

Bicarb = 14 meq/l

Questions:

1. What is the patient's acid-base status?

2. Is the lung retaining or removing acid?

3. Is the kidney retaining or removing bicarbonate?

4. Which organ is the primary culprit in this problem?



Method 1: Eyeball


pCO2 = 21 mm Hg

Bicarb = 14 meq/l

Questions:

1. What is the patient's acid-base status? >> Look at pH

2. Is the lung retaining or removing acid? >> Compare pCO2 to 40

3. Is the kidney retaining or removing bicarbonate? >> Compare bicarb to 28

4. Which organ is the primary culprit in this problem?

>> The organ producing the effect seen in the pH is the primary problem



Method 2: Math


pCO2 = 21 mm Hg

Bicarb = 14 meq/l



Serum Electrolytes: Sodium

• The major extracellular cation

• In general, sodium balance defines water balance

• Sodium is the most important contributor to plasma osmoticpressure: POsm = 2(NaP) + Gluc/18 + BUN/2.8> Expected = 280 - 296 mOsm/kg

• Renal sodium management is dependent on distal tubulefunction

• Reference range about 136-145 meq/l (mmol/l)¸ < 120 produces muscular weakness

¸ < 100 causes neurological symptoms

• Sodium deficit/excess must be corrected carefully



Hyponatremia

• Assess plasma osmolality first, then clinical volume status and urine osmolality

• Low plasma osmolality with elevated urine osmolality

> Hypovolemia: GI, dermal, renal fluid loss; salt wasting states; potassium depletion;

ketoacidosis

> “Effective volume depletion” (dilution): heart failure, cirrhosis, nephrotic syndrome

> Diuretics, chronic renal disease, SIADH, hypocortisolism, hypoaldosteronism

• Low plasma osmolality with low urine osmolality

> Replacement of lost fluid (vomiting, burns, etc.) with hypotonic solutions

> Primary polydipsia

• Increased plasma osmolality

> Elevated glucose, mannitol (not clinically significant from a sodium standpoint)

• Clinical hyponatremia is associated with decreased plasma osmolality

• Pseudohyponatremia with flame photometry in hyperproteinemia and

hyperlipidemia; plasma osm is normal (not a problem with ISE)



Hypernatremia

• Poor fluid intake or excess loss from skin (diaphoresis, burns)

• Water loss from the kidney (diabetes insipidus, osmotic diuresis)

• GI loss (vomiting, diarrhea)• Increased mineralocorticoids (hyperaldosteronism)

• Cushing's syndrome

• Evaluate volume status, serum/urine osmolality and sodium

> Low urine osmolality: osmotic diuresis or diabetes insipidus

> Elevated urine osmolality

• Hypervolemic: renal water/sodium retention (mineralocorticoid excess)

• Hypovolemic: extrarenal water loss (diaphoresis, diarrhea)



Potassium Balance

• The major intracellular cation (ca. 150 meq/l, gradientmaintained by Na-K ATPase)

• Serum concentration of about 3.5 - 5 meq/l, plasma values 0.1 -

0.7 lower• Potassium concentration dramatically affects excitable

membrane function (muscle and nerve)

• Symptoms: muscle weakness, nausea, lethargy, arrhythmias,characteristic EKG changes, cardiac arrest

• Levels < 3 produce marked neuromuscular symptoms, levels > 7.5 produce symptoms and levels > 10 are lethal

• Renal potassium management is dependent on distal tubulefunction



Hypokalemia

• Inadequate intake

• Treatment of normokalemic dehydration without

potassium supplementation• Mineralocorticoid excess (Cushing's syndrome

and hyperaldosteronism)

• Renal loss (diuretics and corticosteroids)

• Insulin treatment (K enters cells with glucose)• Alkalosis (H+ exits cells in exchange for K)

• GI loss (protracted vomiting or diarrhea)



Hyperkalemia

• Dehydration

• Shock, severe hemolysis, tumor lysis, burns (cellular

release)• Renal failure (decreased excretion)

• Endocrine diseases with mineralocorticoid deficiency

• "Potassium sparing" diuretics

• Acidosis (K exits cells in exchange for H)• Artifactual hemolysis of blood specimens; K leak in

chilled or unprocessed specimens



Chloride Balance

• The major extracellular anion (expected, 118 - 132 meq/l in serum)

• Important in water distribution, osmotic pressure, and anion-cation balance

• Hypochloremia

> Fluid volume expansion (dilution)

> Renal diseases (reabsorption failure)> Metabolic acidosis with increased "unmeasured anions" (e.g. DKA)

> SIADH

> GI loss (protracted vomiting)

• Hyperchloremia

> Dehydration

> Renal tubular acidosis, acute renal failure

> Bicarbonate loss (diarrhea)

> Mineralocorticoid excess (Cushing's syndrome and hyperaldosteronism)

> Diabetes insipidus

• Process specimens promptly; changes in bicarbonate with air equilibrationcause shifts in chloride between the extra- and intracellular compartments



Bicarbonate Balance

• The primary acid-base buffer in the body

• Serum/plasma concentration of about 23 - 29 meq/l

• Provides a rough assessment of acid-base balance,but is subject to error

• Equilibration vs. pCO2 of 0.25 in air; decline of 6meq/l per hr

• Chemical assay rather than ISE, susceptible tovolume effects

• Bicarbonate < 10 is a critical value (reflects low pH)



Blood Gas Testing

• Blood gas analysis may be carried out in a main laboratory, in an ER or ORlab or using POC devices

• Provides accurate measurement of PO2, PCO2, pH, hemoglobin saturation,

bicarbonate and hematocrit (some analyzers also offer electrolytes, lactate,glucose, Hgb, CO-Hgb, met- and sulfHgb)

• Arterial blood, drawn in appropriate equipment and transported quickly (10-15 min) on ice to the lab

• Check ulnar artery patency before radial artery draws

• "Arterialized capillary blood" (warmed heel or earlobe) may be acceptable in

some cases• Specimen is accompanied by history with FIO2 and clinical status of patient,

and patient temperature (all are important for interpretation and are includedin the returned report)

• Erroneous results from room temp specimens and specimens with air bubblesor improper capping



Blood Gas Instrumentation

Radiometer 625

Pulse Oximetry



Electrolyte Measurement

• Standard serum or heparinized venous plasma specimen (Li or NH4 heparin)

• Chem 7: sodium, potassium, chloride, CO2 content (bicarb), BUN, creatinine, glucose

Vitros 250/Slide technology

• Issues of frequency and utility for this test

panel

• Hemolysis, refrigeration, waiting, high

leukocytes or platelets increase K

• CO2 content not particularly accurate(equilibration vs. pCO2 of 0.25 in air; decline

of 6 meq/l per hr)

• Na, K, Cl measured by ion-selective electrodes

• Bicarbonate measured using a carboxylation

reaction followed by NADH oxidation

ABG Electrolytes

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