Spring 2016 Adult Acute Care Bulletin

Spring 2016 Adult Acute Care Bulletin

Chair
Keith Lamb, RRT-ACCS
Adult Critical Care Supervisor
UnityPoint Health System
Des Moines, IA
keith.lamb@unitypoint.org
Editor
Joe Hylton, RRT-NPS, CPFT
Co-Editor
J. Brady Scott, MSc, RRT-ACCS, FAARC
Director of Clinical Education
Assistant Professor
Department of Cardiopulmonary Sciences
Division of Respiratory Care
Rush University
Chicago, IL 60612
Jonathan_B_Scott@rush.edu

Specialty Practitioner of the Year: Maria Madden, BS, RRT-ACCS

The Section was pleased to present its 2015 Specialty Practitioner of the Year award to Maria Madden, BS, RRT-ACCS, at AARC Congress 2015 in Tampa, FL, last November.

Maria is the clinical resource for respiratory therapists in the multi-trauma ICU, neuro trauma ICU, specialty trauma ICU, trauma resuscitation unit, and post anesthesia care unit at the R Adams Cowley Shock Trauma Center (STC) at the University of Maryland Medical Center in Baltimore, MD. In addition to assisting with daily departmental operations, her administrative and leadership duties include the development, updating, and maintenance of respiratory therapy policies, procedures, and protocols, and she also chairs the Respiratory Spinal Cord Committee, Respiratory Education Committee, and Respiratory Scholarly Committee.

Maria serves as the clinical coordinator of the Diaphragm Pacing Program as well, and is also an ECMO specialist. She is involved in multiple ongoing research projects and has had multiple abstracts/posters accepted for presentation at various conferences, including the AARC Congress and Neuro Critical Care Society meeting. Maria lectures nationally on a wide variety of topics, sharing her expertise with groups around the country.

Maria has received numerous honors for her dedication to high quality patient care. She was named Support Services Champion of the Year by The Living Legacy Foundation of Maryland, nominated for the 2012 Shock Trauma Collaborative (STC) Care Award, and presented the Shock Trauma Hero Award at the 2014 STC Gala.


The Many Forms of Hypoxia

Tom Pietrantonio, BSRT, RRT
Venice Regional Bayfront Health, Venice, FL

Oxygen is able to move throughout the tissues by the process of diffusion. Diffusion occurs because there is a partial pressure gradient between two points. When a partial pressure gradient exists, oxygen will readily diffuse from an area of higher concentration to an area of lower concentration. According to Fick’s Law, the rate of diffusion is directly proportional to the difference in pressures and inversely proportional to the thickness of the membrane through which oxygen must diffuse; thus, the larger the pressure gradient, the greater the rate of diffusion. The thicker the membrane, the lower the rate of diffusion.

Oxygen transport relies on a normal functioning respiratory and cardiovascular system. That is, there must be a sufficient amount of oxygen in the lungs and the blood, adequate blood flow and hemoglobin availability to transport oxygen, and the ability of the body tissue cells to use and metabolize oxygen. Anything that disrupts the normal physiologic process of oxygen transport will create a condition of hypoxia.

 What is hypoxia

 Hypoxia is the result of a deficient supply of oxygen to the body tissues. If hypoxia is not corrected and is allowed to manifest to a severe state, the ultimate outcome is cell death.1 The addition of supplemental oxygen is typically the necessary corrective action; however, depending on the type of hypoxia, supplemental oxygen can have little to no value.1 It is important to understand the different types of hypoxia in order to determine the value of providing supplemental oxygen therapy.

Hypoxic hypoxia

Arguably the most common type of hypoxia encountered, hypoxic hypoxia is caused by inadequate oxygen at the tissues in response to a low partial pressure of oxygen in arterial blood (PaO2).2 This type of hypoxia occurs as a result of a variety of respiratory complications, such as a low partial pressure of oxygen in the lungs (PAO2), diffusion defects, V/Q mismatching, and pulmonary shunting. Oxygen transport is impaired because there is a decreased amount of oxygen in the blood (hypoxemia). Hypoxic hypoxia results from a problem with the respiratory system. Compensation occurs naturally as vessels dilate to increase perfusion and oxygen delivery; however, the administration of supplemental oxygen is of high value and should be provided to correct the situation.

Anemic hypoxia

When oxygen diffuses across the alveolar-capillary membrane, it binds to the hemoglobin molecules in the blood. If there is a reduction of hemoglobin availability, oxygen transport can be inefficient. Blood loss, anemia, hemoglobin abnormalities, and carbon monoxide (CO) poisoning are potential causes of anemic hypoxia; thus, the problem is blood related. Similar to hypoxic hypoxia, compensation occurs when vessels dilate to increase perfusion and oxygen delivery.

Providing supplemental oxygen is of high value when there is suspicion of CO poisoning. CO has a greater affinity for hemoglobin than oxygen, thus oxygen will have to compete to bind to hemoglobin in the presence of CO. The administration of 100% oxygen is the recommended method of treatment in the presence of CO poisoning.

In all other situations, the use of supplemental oxygen is of little value. As oxygen diffuses across the alveolar-capillary membrane, a small amount of oxygen dissolves in the blood. It is thought that by providing supplemental oxygen, the amount of oxygen dissolved in the blood can be increased. This small amount of extra oxygen may be the difference between life and death.1 Never-the-less, the primary corrective response is to administer blood. By administering blood, the oxygen carrying capacity of hemoglobin increases, and oxygen delivery is restored.

Stagnant (hypoperfusion) hypoxia

Theoretically, the amount of blood pumped from the heart should be the same amount that returns to heart. Cardiac arrest, pulmonary embolism, and even positive pressure ventilation can cause a condition of stagnant hypoxia in which cardiac output decreases. The primary culprit in this situation is the cardiovascular system, and all attempts to restore cardiac function should be of primary concern. The use of supplemental oxygen is of no value when stagnant hypoxia is present, and since the PaO2 is normal, increasing the fraction of inspired oxygen (FiO2) is not helpful to correct the problem.3

Histotoxic hypoxia

Sometimes a problem exists with the tissue cells and their inability to metabolize oxygen. Essentially, the cell is unable to use oxygen due to the inhibition of the cytochrome oxidase enzyme. The most common cause is cyanide poisoning.

Cyanide poisoning can result from alcohol or drug ingestion, smoke inhalation, metabolic disorders, and the administration of certain pharmaceutical medications. If clinical suspicion of cyanide poisoning exists, a cyanide level should be obtained by sending a sample of blood to the lab for analysis.

The use of supplemental oxygen in the presence of cyanide poisoning is of no value because the primary problem resides with the cells’ ability to use and metabolize oxygen; however, oxygen supplementation could be debatable depending on the assessment and condition of the patient. Still, the main concern is to treat the underlying cause. Antidotal treatment is indicated to correct histotoxic hypoxia and restore oxygen delivery.

Oxygen therapy in summary

In summary, the use of supplemental oxygen is of no value when treating stagnant and histotoxic hypoxia because the problem is due to impaired cardiac function and cell enzyme inhibition, respectively. Supplemental oxygen is of little value when treating anemic hypoxia because the issue is a lack of hemoglobin availability. The preferred method of treatment is to transfuse packed red blood cells.

However, when CO poisoning is present, the use of supplemental oxygen is imperative and should be provided immediately. When hypoxic hypoxia is present, the use of supplemental oxygen is of high value to restore oxygen in the lungs and blood.

Understanding how hypoxia inhibits normal oxygen transport is useful when selecting the best corrective actions to reverse hypoxia and restore normal oxygen transport.

References

  1. Guyton AC, Hall JE. Textbook of medical physiology, 11th Philadelphia: Elsevier Health; 2008.
  2. Des Jardins TR. Cardiopulmonary anatomy & physiology: essentials for respiratory care, 5th Clifton Park, NY: Thomson Delmar Learning; 2008.
  3. Pittman RN. Regulation of tissue oxygenation. San Rafael, CA: Morgan & Claypool Life Sciences; 2011. http://be-md.ncbi.nlm.nih.gov/books/NBK54104/

Back to the Basics: Understanding Hypoxic Drive and the Release of Hypoxic Vasoconstriction

Jon C. Inkrott, RRT-ACCS
Flight Respiratory Therapist, Florida Flight 1, Florida Hospital Orlando, Orlando, FL

I have been a respiratory therapist since 1993 and I frequently find that the concept of hypoxic drive and the release of hypoxic vasoconstriction is misunderstood and even somewhat confusing. Like many, I was taught that too much oxygen is not good for COPD patients. Because of the hypoxic drive theory, too much oxygen will further slow the respiratory drive and cause further complications. My professors taught it, the doctors preached it, so it shall be so!

Not so fast, my friends!

In getting back to the basics, what is the hypoxic drive and how does increased supplemental oxygen play into its function? Further, what is the rationale for withholding “too much oxygen” in a patient who is hypoxemic? In this article we’ll review the two processes involved in drive to breathe and the delivery of oxygen in “at risk” patients.

Under normal conditions, breathing maintains homeostasis within the body by maintaining a normal level of oxygen, carbon dioxide, and acid-base balance. Essentially, we’re breathing in oxygen and blowing out carbon dioxide. The normal breathing pattern is modified by differentiations in these stimuli. The major factor responsible for changes in ventilation is the neural input from medullary centers through the chemoreceptors. These are nerve cells that sense and respond to changes in the chemical composition of their environment.

There are two sets of chemoreceptors: central and peripheral. The central receptors lie on the surface of the medulla and the peripheral receptors are located in both the carotid arteries and the aortic arch. Because of their location, the central receptors are not in contact with blood, but rather, in direct contact with cerebrospinal fluid (CSF), which is separated from the blood by a semi-permeable membrane known as the blood-brain barrier.

Without too much of a physiology recap, elevations in blood CO2 cause rapid diffusion of molecular carbon dioxide to diffuse across this membrane and dissociate into H+ and HCO3-, lowering the pH of the CSF, which in turn stimulates the central chemoreceptors that tell the medullary centers to increase ventilation. According to Egan’s Fundamentals of Respiratory Care, Fifth Edition, this central mechanism for chemical control is so extraordinary that the PaCO2 does not vary more than 3 mm Hg over the course of 24 hours!1

Now . . . take a deep breath.

The peripheral receptors, as compared to the central receptors, are not as sensitive to changes in CO2. With respect to the phenomenal control the central receptors have on chemical regulation, the peripheral receptors would need to recognize a 20-30 mm Hg increase in CO2 before a significant increase in ventilation would occur. So, although they are responsive to hypercapnia and changes in H+ concentrations (such as in metabolic acidosis), their primary role appears to be in response to hypoxia.

The response to hypoxia, however, requires a much greater deviation from normal to stimulate increases in ventilation. According to Mosby’s Respiratory Physiology, Fifth Edition, ventilation is not stimulated significantly until the inspired concentrations fall below about 12%, which is equivalent to a PaO2 of about 50-60 mm Hg. In normal individuals living at sea level, the hypoxic stimulus to breathing is not considered part of the regular respiratory mechanism.2

In other words, the peripheral chemoreceptors only play a minor role during normal respirations, and only send a signal to breathe when the PO2 is 50-60 mm Hg. This response is far slower than the signal sent by the central chemoreceptors. Thus, the peripheral chemoreceptors only play a minor role in breathing . . .

Unless . . .

Let’s discuss the COPD patient and what happens over time in these patients. The pathophysiology of these patients eventually creates ventilation/perfusion (V/Q) inequalities. These V/Q mismatches result in hypoxemia.

If you’re not familiar with the release of hypoxic pulmonary vasoconstriction and what can happen if 100% oxygen is administered, let’s take a moment to review. In looking at the alveolar ventilation in COPD patients, under-ventilated alveoli usually have a low oxygen content and increased CO2 levels. Let’s assume the local PO2 to be less than 50-60 mm Hg. The low oxygen level leads to localized vasoconstriction, limiting blood flow to that lung tissue and redistributing it to alveoli that are better ventilated.

When 100% supplemental oxygen is administered, the PO2 hypothetically would be greater than 50-60 mm Hg and this would negate the localized vasoconstriction, leading to enhanced V/Q mismatching. This redistribution of blood to areas of the lung with poor ventilation reduces the amount of carbon dioxide eliminated from the system and actually increases the level of CO2. And herein lies the focus of oxygen-induced hypercapnia. V/Q matching is not optimal.

As COPD progresses, hypoxemia worsens, and hence stimulation of the peripheral chemoreceptors results. This stimulation may result in hyperventilation to correct for the hypoxemia. Over time, if this pattern persists, the oxygen consumption by the patient’s respiratory muscles exceeds the benefits received by hyperventilating. The percent of total oxygen consumption being used for ventilation becomes greatly increased due to the efficiency of the respiratory system being greatly decreased by disease progression and accessory muscle use.

As the body can no longer maintain the level of alveolar ventilation necessary to maintain adequate PaO2 without sacrificing delivery to other organs, the depressed respiratory drive, in an attempt to conserve energy, results in increased CO2 levels. Hence the patient is deemed a “CO2 retainer” and the primary stimulus to breathe is oxygen. When hypoxemia exists with chronic hypercapnia, the central response to carbon dioxide is blunted and the primary stimulus to breathe is mediated through hypoxic stimulation of the peripheral chemoreceptors. This is known as the hypoxic drive. And it’s real.

But what about the hypoxic drive theory? That is, supplemental oxygen in higher percentages is thought to be harmful to COPD patients, causing them to stop breathing because it knocks out their drive to breathe.

After learning all of the above, some confusion remains, as in my experience many RNs and even some RTs continue to believe that all COPD patients are CO2 retainers when in fact the retainers are the minority. In a well-known editorial in the September 1997 issue of Critical Care Medicine titled “Debunking Myths of Chronic Obstructive Lung Disease,” Dr. John Hoyt emphasized the importance of recognizing these myths.3

In summation Dr. Hoyt stated that the premise of shutting down a COPD patient’s drive to breathe by administering oxygen has entered into the medical decision making process like a virus infects a computer. It has taken hold and festered and multiplied and seems to stick with physicians and practitioners throughout their careers, despite the lack of evidence-based science behind it. The body’s vital organs are “unforgiving” when exposed to low oxygen levels and this treatment strategy, to withhold oxygen from a COPD patient in fear of increasing CO2 levels, is essentially fatal for the patient and career tragedy for the misinformed practitioner.

As Dr. Hoyt stated in his article, “. . . one should not fear apnea and cardio-respiratory arrest when giving oxygen to a patient with an exacerbated chronic obstructive lung disease and respiratory failure. Instead, one should be prepared to help the patient eliminate CO2 when deadspace increases. Providing assistance with the elimination of CO2 has been around since the beginning of critical care medicine. It is called mechanical ventilation.”3

References

  1. Scanlan CL, Spearman CB, Sheldon RL. Egan’s fundamentals of respiratory care, 5th St. Louis: CV Mosby; 1990:226-250.
  2. Slonim NB, Hamilton LH. Respiratory physiology, 5th St. Louis: CV Mosby; 1985.
  3. Hoyt JW. Debunking myths of chronic obstructive lung disease. Crit Care Med 1997;25(9):1450-1451.

Section Connection

Specialty Practitioner of the Year: Use our online nomination form to nominate a fellow section member for our 2016 Specialty Practitioner of the Year award.

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Next Bulletin Deadline: Fall Issue: August 1.