Summer 2015 Adult Acute Care Bulletin

Summer 2015 Adult Acute Care Bulletin

Keith Lamb, RRT-ACCS
Adult Critical Care Supervisor
UnityPoint Health System
Des Moines, IA
Joe Hylton, RRT-NPS, CPFT
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

In this issue:

Notes from the Chair

Keith D. Lamb, BS, RRT-ACCS

What is a respiratory therapist? What does it mean to you to BE a respiratory therapist? What do others think we do? All good questions, and I am glad you asked.

I think this all depends on whom you ask. A general care floor nurse may tell you we give nebulizer treatments. An ICU nurse may say we set up mechanical ventilators and change the settings. A nurse in the emergency department may say something in between. The average citizen may be uncertain of our daily duties. But they’ve certainly heard the ever common, “respiratory stat,” called overhead during their favorite primetime television dramas, or perhaps they have had a family member cared for by a respiratory therapist.

So who are we? What message should we be sending?

First and foremost we are professionals. There are varying ideas of exactly what a “professional” is, but I think most would agree that RT professionals are people who are engaged in what they do. They participate in lifelong learning activities, educational endeavors, and experiences that expand their knowledge of their chosen craft. They volunteer their time to their community and contribute to society as a whole. They mentor new RTs, nurses, and providers. They are hungry to learn and to teach, and they are committed to improving the lives of others.

About four years ago, I wrote a short article titled the “Art and Science of Respiratory Care” and published it here in our Adult Acute Care Bulletin. I’d like to share a couple of excerpts from that article because they are still relevant today –

In college we are taught that mastering our profession requires knowledge of chemical equations and gas laws, and owning a calculator with fresh batteries. What we may not have been fully aware of when we put on that cap and gown was that our future would be just as much about learning the art of respiratory care as the science.

Practicing without solid science is art. It requires one to be reasonable, intuitive, and creative. It means that we cannot be tethered to formulae and laws, but free to individualize our bedside care to a particular and specific problem as it is presented to us. Such is the problem of dyspnea. Much of what we do is simply observing the interaction and interface between human and machine, and “crafting” a more synchronous connection.

The art of maneuvering our strategies and customizing our care has evolved into the perfect match for today’s professional respiratory therapist. The respect, autonomy, and rapport that are garnered by employing this finesse cannot be earned by all, and should not be taken for granted. This privilege has allowed us to become the scientists and artisans that we, as RTs, must be today.

I believe today’s respiratory therapists understand these concepts. Perhaps it is not clear in the beginning, but certainly something that becomes well known over time. THESE are the things that define who we are. We are the consummate professionals who are unwavering in the pursuit of those things that perfect our understanding of the art and science of respiratory care, and what it means to be a professional.

Get the word out! Get the word out with your dialogue but more importantly get the word out with your actions! Introduce yourself to the health care team and family as someone who is here to help. Let them know you are the cardiopulmonary expert who can help navigate the illness at hand. Then make it so . . . go beyond words. Be the best that you can be at providing excellent patient care! Volunteer in your community. Get involved with your professional organization, the AARC. Get involved in research and contribute to the literature and science. Mentor a student or new graduate who is eager to learn. Help an “experienced” clinician understand new technology. Recruit high school students and tell them how great your profession is and how you positively impact lives . . . every single day.

That’s who we are and that is what we do!

Back to the Basics: Metabolic Alkalosis

J. Brady Scott, MS, RRT-ACCS, FAARC

As a common, simple acid-base disorder, metabolic alkalosis can be defined as an increase in bicarbonate (HCO3-) concentration in the plasma.1 This imbalance of the pH may be caused by the loss of hydrogen ions (H+) or the accumulation of base.2 Loss of hydrogen ions may occur via renal and/or gastrointestinal routes. Also, loss may be due to a shift in hydrogen ions into body cells. Contraction of blood volume or the administration of base may also cause a metabolic alkalosis.

Renal and gastrointestinal loss

Excretion of hydrogen ions via the kidneys can result in a metabolic alkalosis. There are five major causes of this loss:3,4

  • Loop or thiazide diuretics
    • May cause loss of potassium in the urine resulting in hypokalemic alkalosis.
    • Loss of blood volume may cause contraction alkalosis. This is a relative elevation of plasma HCO3– due to fluid loss.
  • Renal tubular disorders
    • Genetic disorders such as Bartter and Gitelman syndromes can cause loss of both chloride and potassium.
  • Post-hypercapneic increase in HCO3
    • May occur when patients with acute ventilatory failure superimposed on chronic ventilatory failure receive mechanical ventilation.
  • Milk-alkali syndrome and hypercalcemia
    • Hypercalcemia impairs renal function. Hypovolemia (from vomiting, if present) and reduced renal function result in alkalosis.
  • Excess mineralocorticoid
    • Aldosterone (a mineralcorticoid) is synthesized in the adrenal cortex and is required for proper kidney function. Excess production of aldosterone can lead to metabolic alkalosis (and hypertension).

Removal of gastric secretions due to vomiting (or oral/nasal gastric tube) can cause a metabolic alkalosis. Gastric secretions contain high levels of hydrochloric acid, which are generally neutralized by the pancreas in response to the acid in the duodenum. The loss of the hydrochloric acid results in bicarbonate being ultimately added to extracellular fluid.5-7

Intracellular shift of hydrogen

Extracellular potassium loss will cause a shift of hydrogen ions into the cells. This lowers the plasma hydrogen ion concentration and raises the pH. Most often, this occurs with profound potassium insufficiency.

Administration of base

The intake of base can cause a metabolic alkalosis, especially when kidney function is abnormal. In general, the chronic ingestion of antacids and other substances containing bicarbonate does not increase plasma HCO3– in the setting of normal kidney function. Usually, metabolic alkalosis resulting from the administration of base is due to:8

  • Administration of sodium bicarbonate to treat severe metabolic acidosis.
  • Citrate salts from banked blood.
  • Use of crack cocaine prepared with sodium bicarbonate.

Respiratory compensation for metabolic alkalosis

In metabolic alkalosis, respiratory compensation occurs as an increase of PaCO2 of about 0.7 mm Hg for each 1 mEq/L increase in HCO3-. The compensation is rapid, but it is important to note that PaCO2 generally does not exceed 55 mm Hg. Expected compensation can be calculated by: Expected PaCO2 = 0.7 (HCO3-) + 20 (±2).


Treatment of metabolic alkalosis is directed towards the underlying cause. Specific treatment for metabolic alkalosis is beyond the focus of this article; however, it is thought that two questions must be asked in order to properly treat a metabolic alkalosis:9

  1. What is causing the increase in plasma bicarbonate (vomiting, diuretic therapy, contraction of extracellular fluid)?
  2. Why is excess bicarbonate not being removed by the kidneys?


Metabolic alkalosis is relatively common in the clinical setting and is most often caused by an excessive loss of hydrogen ions from the kidneys and gastrointestinal tract. Treatment should be aimed at reversing the underlying cause.

Editor’s Note: If you would like to write an article for the Bulletin or suggest a topic for our “Back to the Basics” section, please email either Joe Hylton or Brady Scott. Member input is always welcomed!


  1. Khanna A, Kurtzman NA. Metabolic alkalosis. Respir Care 2001;46:354-365.
  2. Emmet M. Simple and mixed acid-base disorders. In: UptoDate, Basow DS, (ed.), UptoDate, Waltham, MA, 2013.
  3. Emmet M. Causes of metabolic alkalosis. In: UptoDate, Basow DS, (ed.), UptoDate, Waltham, MA, 2013.
  4. Scott JB, Walsh BK, Shelledy DC. Blood gas analysis, hemoximetry, and acid-base balance. In: Shelledy DC, Peters JI. Respiratory care: patient assessment and care plan development, 1st Burlington, MA: Jones and Bartlett; 2016:281-346.
  5. Kassirer JP, Schwartz WB. The response of normal man to selective depletion of hydrochloric acid. Factors in the genesis of persistent gastric alkalosis. Am J Med 1966;40:10.
  6. Perez GO, Oster JR, Rogers A. Acid-base disturbances in gastrointestinal disease. Dig Dis Sci 1987;32:1033.
  7. Giovannini I, Greco F, Chiarla C, et al. Exceptional nonfatal metabolic alkalosis (blood base excess +48 mEq/l). Intensive Care Med 2005;31:166.
  8. Emmet M. Causes of metabolic alkalosis. In: UptoDate, Sterns RH, (ed.), UptoDate, Waltham, MA, 2015.
  9. Mehta A, Emmet M. Treatment of metabolic alkalosis. In: UptoDate, Sterns RH, (ed), UptoDate, 2015.

Laboratory Analysis of Blood Components


The complete blood count (CBC) can offer clues to many diseases and conditions, and a thorough understanding of this standard test is essential for proper diagnosis and treatment. As respiratory therapists charged with the care of adult acute care patients, we should all have a good understanding of the basic components of the CBC. The following tutorial provides a brief overview —

Hematocrit (Hct): Hematocrit possesses a high sensitivity for disease, but a low specificity. Hematocrit is the percentage of formed elements (predominately red blood cells) in a venous blood sample. A low percentage of hematocrit can indicate a decreased capacity of the blood to deliver oxygen to the tissues. Low readings are associated with anemia, hemorrhage, leukemia, lupus, endocarditis, rheumatic fever, poor nutrition, over-hydration, and chronic infections. High readings can be seen with polycythemia and dehydration. The normal range for hematocrit is 41-50%.

Hemoglobin (Hgb): This primary iron-rich protein is responsible for oxygen transport to the cells, and to a much lesser extent, transporting carbon dioxide to the lungs. Elevated levels may be seen with disease states that decrease fluid levels in the blood, such as dehydration, severe burns, or vomiting. Low hemoglobin levels, or anemia, can be caused by iron deficiency, poor dietary intake, hyperthyroidism, aplastic anemia, hemolytic anemia, sickle cell anemia, chemotherapy liver disease, and kidney disease. High levels can be associated with COPD, CHF, polycythemia, and altitude sickness. The normal range for hemoglobin is 14.0-17.5 g/dL for males, and 12.0-16.0 g/dL for females.

Red Blood Cell (RBC) Count: This is the total number of red blood cells measured in a microliter of blood. Low RBC levels may be seen with anemia, hemorrhage, leukemia, over-hydration, and chronic infections. High levels can be seen with polycythemia, dehydration, cardiovascular disease, and hemoconcentration. The normal range is 3.9-5.5 x 106/µL.

White Blood Cell (WBC) Count: This is a total measure of the leukocytes in the blood. The WBC is a global or non-differentiated view, so the information gained from this test is limited. Low levels are associated with leukemia, bone marrow diseases, viral infections, radiation, and late-stage AIDS. High levels can be seen in viral/bacterial infections, leukemia, hemorrhage, vascular disease, and traumatic tissue injuries. A differential analysis will provide information on segmented and unsegmented neutrophils, basophils (or mast cells), lymphocytes, eosinophils, monocytes, and thrombocytes. The normal range is 4500-11,000/µL.

Platelets: Platelets play an essential role in clot formation. They adhere to exposed collagen in the sub-endothelium, promoting fibrin strand production and thrombus formation. Low platelet levels are associated with cancers, leukemia, sickle cell disease, and lupus. High levels are associated with pulmonary embolism, hemorrhage, metastatic cancer, and surgical stress. The normal range is 150-350 x 103/µL.


  • Fundamental Critical Care Support, Fourth Edition, 2007. Society of Critical Care Medicine. Mount Prospect, IL.
  • Critical Care Transport, First Edition, 2010. Jones and Bartlett Publishers, Sudbury, MA.
  • Critical Care Medicine, Third Edition, 2006. Lippincott, Williams and Wilkins Publishers, Philadelphia, PA.
  • The ICU Book, Third Edition, 2007. Lippincott, Williams and Wilkins Publishers, Philadelphia, PA.
  • Critical Care Paramedic, First Edition, 2006. Pearson Education, Inc., Upper Saddle River, NJ.

Section Connection

Specialty Practitioner of the Year: Use our online nomination form to nominate a fellow section member for our 2015 Specialty Practitioner of the Year award.

Recruit a New Member: Know an AARC member who could benefit from section membership? Direct them to online sign-up. It’s the easiest way to add section membership to their overall membership package.

AARConnect: Visit our section page to take advantage of our discussion list and other online resources and networking activities.

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