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 Center Pittsburgh, PA jhrsn@pitt.edu

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

Internal pH Depends on Renal-Pulmonary Cooperation

Normal metabolism continually produces acid Carbonic acid/bicarbonate is the bodys 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)

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
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? >> 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
A patient presents with the following results from a blood gas study: pH = 7.43 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 osmotic pressure: POsm = 2(NaP) + Gluc/18 + BUN/2.8
> Expected = 280 - 296 mOsm/kg

Renal sodium management is dependent on distal tubule function 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, gradient maintained 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 tubule function

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) Dehydration Renal tubular acidosis, acute renal failure Bicarbonate loss (diarrhea) Mineralocorticoid excess (Cushing's syndrome and hyperaldosteronism) Diabetes insipidus

Hyperchloremia
> > > > >

Process specimens promptly; changes in bicarbonate with air equilibration cause 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 6 meq/l per hr Chemical assay rather than ISE, susceptible to volume 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 OR lab 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 (1015 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 included in the returned report) Erroneous results from room temp specimens and specimens with air bubbles or 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