Amy Bardin, MS, RRT, VA-BC, Senior Clinical Marketing Specialist, Vascular, Teleflex, Reading, PA
When creating a health care culture that is patient-centered and outcome-focused, clinicians need to remain agile; seek and adapt technology and practices that enhance outcomes; and promote collaborative, safe, and effective practices. One such advancement is the growing use of bedside ultrasound. Real time bedside ultrasound has been adopted over the last decade, with success attributed to ease of use, portability, and reductions in complications.1 This adjunct to bedside invasive procedures has added value and resources to the bedside clinician. Ultrasound has changed the care delivery model while reducing associated risk, improving patient outcomes, and enhancing bedside procedures for both the clinician and patient.2
Ultrasound involves a wide array of clinicians, including nurses, respiratory therapists, and physician assistants. The goal of these clinicians is to provide the best possible outcome, device, and experience to their patients the first time, every time.
Current care models include highly trained groups of respiratory therapists who serve as vascular access specialists in inserting, monitoring, and maintaining all types of vascular access devices.3 Ultrasound aids this team in vessel selection by providing direct vessel visualization throughout otherwise blind procedures. Creating this type of highly skilled collaborative team and vascular access culture takes time, a unified passion, and a sincere desire to provide the most efficient care model. Integration of a “no blind stick” approach empowers safe advancement in scope of practice, changes patient outcome, enhances the patient’s experience, and utilizes a best practice that is relevant and should be applied to each invasive procedure.
For the advancing respiratory therapists, incorporating the use of ultrasound is an opportunity to enhance their professional scope of practice.4 As we move forward with utilization of a multifaceted, multidisciplinary approach to patient-centered care, it is easy to see how adjuncts like ultrasound provide a bridge of opportunity for all bedside clinicians. Utilization of this tool with adaptive real-time training for procedures that include ultrasound guided arterial catheterization, peripheral IV insertion, and peripherally inserted central catheters, as well as simple blood collection procedures, will allow qualified clinicians, regardless of discipline, to maximize their individual scopes of practice while enhancing the patient experience and improving patient outcomes.
<>Back to the Basics: Metabolic Acidosis
Carlos Jones, MSc, RRT, Rush-Copley Medical Center, Aurora, IL
Metabolic acidosis is described as a disease process that results in a loss of serum bicarbonate and a decrease in the body’s pH level. To accurately identify and treat the specific source of the acidemia, a clinician must be able to understand the process of metabolic acidosis and correctly interpret the anion gap calculation.
Three main avenues participate in the generation of metabolic acidosis: an increase in acid generation, a loss of sodium bicarbonate, or a decrease in renal acid excretion.1,2 Under normal circumstances, metabolism occurs in the presence of oxygen and glucose. With a lack of oxygen, cellular respiration is conducted in anaerobic conditions. As a result, lactic acid production is increased as a waste product.3 Patients with severe hypoxemia or those who have exceeded their aerobic threshold through strenuous exercise may present with increased lactic acid production.1-3
A cellular metabolism without sufficient amounts of glucose also contributes to an increase in acid production. As seen in diabetes, a lack of insulin hampers the ability of cells to utilize glucose. Therefore, the body must break down proteins for energy.1,3 The breakdown of proteins through this avenue produces keto acids, or ketones, as a byproduct.1,3 Ketoacidosis can not only be seen with diabetes, but it can also accompany starvation and alcohol abuse.1-3
The kidneys play an important role in the regulation of blood bases. Kidneys regulate the reabsorption of bicarbonate (HCO3), and the excretion of excessive H+ ions. Diminished renal function can contribute to metabolic acidosis in two ways. The first is due to a decrease in the glomerular filtration rate in combination with a reduction in H+ excretion.2 Secondly, tubular dysfunction with an intact glomerular filtration rate can contribute to renal tubular acidosis.2 In an attempt to regulate pH levels, the kidneys also excrete and retain HCO3 to maintain proper pH levels.3 Any form of renal failure may disrupt this process, and metabolic acidosis may develop as a result.1 Processes such as severe diarrhea and proximal renal tubular acidosis may contribute to a loss of bicarbonate.2,3
To distinguish between the causes of metabolic acidosis, a calculation of the anion gap can be used. This can assist in determining if the cause is a buildup of fixed acids or a loss of HCO3.1,2,4,5
The law of electroneutrality governs measurement of the anion gap. This states that the number of cations must equal the number of anions in bodily fluids.4 The measured anions for calculation are chloride (Cl–) and bicarbonate (HCO3–). The cations used for measurement are sodium (Na+) ions. With these electrolytes, the calculation for the anion gap is:
Anion Gap = [Na+] – ([Cl–] + [HCO3–])
With all electrolytes being within normal limits, this would put the normal anion gap measurement at 9-14 mEq/L.4 However, new methods of measuring electrolytes indicate that a normal anion gap is less than 11 mEq/L.3,4
An anion gap measurement greater than 11 mEq/L in the presence of metabolic acidosis can be associated with an accumulation of fixed acids.2-4 Lactic acidosis, ketoacidosis, and salicylate intoxication (e.g. aspirin overdose) can contribute to an increase in fixed acids.3-5 Ingestion of acids such as methanol and ethylene glycol can also increase the amount of fixed acids in the body.3,4 H+ ions created by these fixed acids are buffered by HCO3–. Buffering hydrogen ions by bicarbonate is responsible for a decrease in bicarbonate concentration and causes an increase in the anion gap.3,5 Unmeasured anions are commonly the source of the increased anion gap measurement.5 However, an elevated anion gap can be associated with nonacids.5 Although uncommon, conditions such as hyperalbuminemia and hyperphosphatemia have also raised anion gap levels.5
When metabolic acidosis is present with a normal anion gap measurement, this could be associated with loss of bicarbonate.3,4 As stated earlier, renal failure and severe diarrhea can contribute to this loss of HCO3–.1-5 The loss of bicarbonate, however, does not increase the anion gap because as HCO3 is lost, Cl replaces it in an attempt to maintain electroneutrality.4 This type of metabolic acidosis is referred to as hyperchloremic metabolic acidosis.4
Some processes can be seen in both hyperchloremic and anion gap acidosis. These include severe diarrhea, ketoacidosis, and renal failure.2-5 In some cases of severe diarrhea, hypoperfusion-induced lactic acidosis and hypovolemia-induced hyperalbuminemia can increase the anion gap.2,5
In an effort to counter the acidemia caused by metabolic acidosis, the respiratory system tries to compensate for the decrease in pH.1,3,6 The respiratory system’s main response to the decrease in bicarbonate is to decrease PaCO2 levels through hyperventilation.1,3,5,6 This mechanical decrease in PaCO2 is used to offset the H+ concentration. Under normal conditions, this process initializes quickly, usually within 30 minutes, and is complete in 24 hours.3 PaCO2 is expected to fall approximately 1.2 mm Hg for each mEq/L of bicarbonate lost.1,3 The presence of metabolic acidosis without respiratory compensation is a rare occurrence.1,3,6 If PaCO2 is not at the expected levels, a respiratory defect may be present.1,3 In patients with respiratory defects, mechanical ventilation can be used to achieve the appropriate compensatory levels of hypocapnia.6
Resolving the underlying pathophysiology of metabolic acidosis should be the goal of treatment. Identification and initiation of treatment will assist with the overall goals to resolve the acidemia.6 The treatment plan should include normalizing cardiac output and vascular volume, as well as ensuring adequate oxygenation .3,6
To summarize, metabolic acidosis is associated with a decrease in bicarbonate concentration accompanied by a drop in pH. This process is facilitated by a loss of HCO3, a decline in renal acid excretion, or an increase in acid generation. Localizing the cause of the metabolic acidosis can be achieved through calculation of the anion gap. This calculation will determine if the source of the acidosis is due to an increase in fixed acids or a loss of bicarbonate. Once the cause of the acidosis has been identified, treatment can focus on resolving that pathophysiology.
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