Fall 2015 Adult Acute Care Bulletin

Point of Care Testing: What Can Be Determined at the Bedside?

Karsten Roberts, MS, RRT-ACCS, RCP
Clinical Education Coordinator, Respiratory Care Services, Stanford Health Care, San Francisco, CA

In critical care, interpretation of arterial blood gases, venous blood gases, and other laboratory values are vital to ventilator management and real time decision making. Valuable time and resources are potentially wasted by sending samples to the clinical lab and waiting for results.¹ Point of care testing tools such as handheld blood gas analyzers and glucometers exist to aid clinicians in quickly determining the course of patient care during emergency care, intensive care, and rapid response. In recent years, point of care testing has moved beyond blood analysis to procedures such as handheld and portable ultrasonography.

Benefits of point of care testing include:

• Positive patient identification
• Reduction or elimination of specimen transport
• Reduced blood specimen volume
• Data management and connectivity, including transcription error reduction
• Patient-centric care

Perhaps the biggest benefit to these tests, however, is not only immediate data analysis and diagnostics, but also immediate treatment.

By definition, point of care testing takes place by utilizing portable and/or handheld instruments and test kits.² Three areas of testing will be described here: blood analysis, ultrasound, and indirect calorimetry. Although the evidence is not robust, some studies have shown that point of care testing can even help reduce patients’ hospital length of stay.³

Blood analysis

Perhaps most commonly used at the point of care is arterial blood gas and glucose testing. Technologic advances have allowed clinicians to move beyond basic testing, and the number of tests available at the bedside has grown from simple blood glucose and blood gases to electrolytes balance and co-oximetry. In fact, there are approximately 110 different tests that clinicians can run at the bedside with handheld or desktop sized devices.²

However, the level of accuracy with point of care blood testing is variable. Examples of how blood analysis can and cannot be used at the point of care include electrolyte analysis, hemoglobin and hematocrit testing, and cardiac markers. For example, lactic acidosis and glucose monitoring have been used to predict mortality in emergency medicine,⁴ whereas hemoglobin and hematocrit test results tend to be inaccurate.⁵

In post-surgical cardiac care, the preferred method is to use co-oximetry and other methodologies to accurately determine test results.⁶ In order to rule out myocardial infarction, troponin can be analyzed at the bedside, but low sensitivity has led to decreased optimization of results. So, while a wealth of information is available at the bedside, clinicians should be aware of variability and inaccuracy.

Point of care ultrasound

This procedure can be used by clinicians as a diagnostic tool or to guide invasive procedures. Common procedures include vascular access, thoracentesis, paracentesis, lumbar puncture, arthrocentesis, and pericardiocentesis.⁷ Diagnostics can be performed on multiple organ systems, including, but not limited to, the heart, lungs, deep veins of the lower extremities, and bladder. During resuscitation efforts ultrasound devices can be used to visualize tension pneumothorax, cardiac tamponade, pulmonary embolism, and acute right ventricular failure.⁷

 Indirect calorimetry

The study of the metabolic needs required by critically ill patients is yet another area in which respiratory care practitioners can gather data using point of care tests. Patients for which these studies may be of benefit include the morbidly obese, malnourished, and those with a prolonged duration of mechanical ventilation.⁸

So-called metabolic cart studies are accomplished by collecting exhaled gas via a “mass flow sensor.” Collected gas is analyzed for oxygen consumption and carbon dioxide production. Using these measurements, resting energy expenditure is calculated as a means of comparing measured to predicted caloric intake.⁸ Respiratory care practitioners then share these results with clinical nutritionists, who in turn order the appropriate diet for the patient’s needs. Any combination of carbohydrates, protein, and lipids maybe used, depending on desired patient outcome.⁸ All of this is accomplished in real time at the point of care.

Good potential

Point of care testing plays an important role in the diagnosis and management of critically ill patients. Much data can be collected via testing at or near the bedside. These tests have the potential to decrease costs and hospital stays while helping clinicians make timely and consequential decisions.

References 

1. Pecoraro V, Germagnoli L, Banfi G. Point-of-care testing: where is the evidence? A systematic survey. Clin Chem Lab Med 2014;52(3):313-324.
2. DuBois JA. The role of POCT and rapid testing: September 2013. http://mlo-online.com/articles/201309/the-role-of-poct-and-rapid-testing.php Accessed August 29, 2015.
3. Singer AJ, Ardise J, Gulla J, et al. Point-of-care testing reduces length of stay in emergency department chest pain patients. Ann Emerg Med 2005;45:587-591.
4. Martin J, Blobner M, Busch R, Moser N, Kochs E, Luppa P. Point-of-care testing on admission to the intensive care unit: lactate and glucose independently predict mortality. Clin Chem Lab Med 2013;51(2):405-412.
5. Hopfer SM, Nadeau FL, Sundra M, Makowski GS. Effect of protein on hemoglobin and hematocrit assays with a conductivity-based point-of-care testing device: comparison with optical methods. Ann Clin Lab Sci 2004;34(1):75-82.
6. Myers GJ, Browne J. Point of care hematocrit and hemoglobin in cardiac surgery: a review. Perfusion 2007;22(3):179-183.
7. Soni NJ, Arntfield R, Kory P. Point of care ultrasound, chapter 1. Philadelphia, PA: Elsevier-Saunders; 2015: 3-8.e1.
8. Siobal MS, Baltz JE. A guide to the nutritional assessment and treatment of the critically ill patient. AARC 2013;1-45.

Permissive Hypercapnia

Nicholas Dearth
Respiratory Care Student, Rush University, Chicago, IL

Mechanical ventilation is a complex support system for the lungs involving delivery of gases while targeting safe volumes and pressures. Certain disease processes, such as acute respiratory distress syndrome (ARDS) or asthma, make ventilation difficult.

ARDS, for example, involves inflammation of the lung, which causes the alveoli to fill with fluid, leading to lower lung compliance. This reduction in compliance makes ventilation with normal tidal volumes more difficult in terms of keeping the lungs safe. When delivery of normal tidal volumes becomes impossible without damaging the alveoli, the concept of permissive hypercapnia may be utilized.

Permissive hypercapnia occurs when mechanical ventilator settings are reduced (for lung protection) with a resultant increase in carbon dioxide. Under normal circumstances, the lungs are able to maintain an arterial partial pressure of carbon dioxide at 35-45 mm Hg, but during permissive hypercapnia, the normal CO₂ threshold is allowed to rise, thus allowing a subsequent drop in pH.¹ The lowered pH and elevated CO2 may cause effects within the body that may have a substantial impact (supportive and detrimental) on the patient.

Immunologic response

Normally, the immune response to lung damage involves the release of pro-inflammatory mediators and neutrophils to destroy infection and repair tissue. Permissive hypercapnia has been shown to suppress certain pro-inflammatory modulators such as nuclear factor-kB, which is involved in the production of other pro-inflammatory mediators.²

Permissive hypercapnia further reduces not only cytokine production, but proliferation of the neutrophil to the site of the damage as well.³ This acts as a double sided effect. The reduced cytokine production results in a reduction of the inflammation, but the reduction in neutrophil proliferation may lead to further damage from possible bacteria at the site of the damage. In the case of sepsis, this has been shown to be helpful in early stages of the disease. When applied early, hypercapnia may suppress the body’s inflammatory response and reduce any further cellular damage.

Cellular repair

Despite permissive hypercapnia’s effects on reducing initial cell damage from inflammation, recent studies have found it to hinder the repair of cells already damaged.^4,5 A study of 72 rats ventilated for 20 minutes at a tidal volume of 40 mL/kg evaluated the effects of CO₂ and tissue repair after damage had occurred. Results showed that lung tissue ventilated under hypercapnic conditions had a greater number of permanently damaged plasma membranes than did the cells under normal CO₂ conditions. Lung weights within the hypercapnic group were also lower than that of the normocapnic.⁴

Not only does hypercapnia weaken cellular repair, but it is also thought to damage the type II alveolar cells. The mitochondria within these cells become dysfunctional under hypercapnic conditions. Mitochondria begin to become dysfunctional around a partial pressure of carbon dioxide of 120 mm Hg.⁶ The damage to the mitochondria within these cells restricts them from differentiating and repairing the alveoli.⁵ Hypercapnia further damages cellular tissue by reducing fluid clearance from the alveoli. Under these circumstances, the sodium channels responsible for fluid clearance become dysfunctional and cannot clear edematous fluid at a normal rate.⁵

Cardiovascular effects

The effects of hypercapnia are not limited to the pulmonary system but also adversely affect the cardiovascular system. Basic physiologic principles still apply and may be hazardous. The disease process of ARDS raises pulmonary vascular resistance (PVR) by constricting the pulmonary blood vessels. Carbon dioxide is a pulmonary vasoconstrictor, and when combined with the already elevated constriction from ARDS, can cause high pulmonary artery pressures that may create an excessive amount of work on the right heart. The increased PVR would cause blood flow to the lungs to back up into the right heart, eventually causing cor pulmonale.

Hypoxemia, another pulmonary vasoconstrictor, is a possible result of permissive hypercapnia. Hypercapnia shifts the oxygen dissociation curve to the right, making oxygen loading more difficult, but unloading easier.⁶ If there is difficulty loading oxygen within the lungs, hypoxemia may result and further add to the already increased PVR.

Clinical application

Permissive hypercapnia is a relatively new treatment modality, and its use is generalized and working CO₂ limits have yet to be established. The effects of hypercapnia and the resultant drop in pH may be more harmful in one disease population than another. ARDS has many different causes, all of which work differently. Head trauma, pneumonia, and sepsis may all lead to the development of ARDS, but they vary in pathophysiology and may be affected adversely.

Before instituting permissive hypercapnia, measures should be taken to control any other underlying health conditions that may worsen with an increase in pulmonary vascular pressure, such as pulmonary hypertension or right heart failure. People with right heart failure already have reduced heart function, and further strain on the heart could be detrimental.

More study needed

Permissive hypercapnia is often viewed clinically as a protective strategy to reduce dangerously high mechanical ventilation pressures. The effects of elevated CO₂ levels have adverse effects on the immune and cardiovascular systems, as well as tissue repair, that may either promote or impede healing. The potential impact of permissive hypercapnia on patient outcomes is still unknown, but some data suggest it may be helpful.

References

1. Cairo JM, Pilbeam SP. Mechanical ventilation. Pilbeam’s mechanical ventilation: physiological and clinical applications, 5th edition. St. Louis, MO: Elsevier Mosby; 2012:591.
2. Chiu S, Kanter J, Sun H, Bharat A, Sporn PS, Bharat A. Effects of hypercapnia in lung tissue repair and transplant. Curr Transplant Rep 2015;2(1):98-103.
3. Curley G, Contreras MM, Nichol AD, Higgins BD, Laffey JG. Hypercapnia and acidosis in sepsis: a double-edged sword? Anesthesiology 2010;112(2):462-472.
4. Curley G, Hayes M, Laffey JG. Can ‘permissive’ hypercapnia modulate the severity of sepsis-induced ALI/ARDS? Crit Care 2011;15(2):212.
5. Curley GF, Laffey JG. Acidosis in the critically ill – balancing risks and benefits to optimize outcome. Crit Care 2014;18(2):129.
6. Doerr CH, Gajic O, Berrios JC, Caples S, Abdel M, Lymp JF, et al. Hypercapnic acidosis impairs plasma membrane wound resealing in ventilator-injured lungs. Am J Respir Crit Care Med 2005;171(12):1371-1377.

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