Fall/Winter 2017 Adult Acute Care Bulletin

Fall/Winter 2017 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

Back to Basics: Pathophysiology of Hypoxemia

Karsten Roberts, MS, RRT-ACCS
Hospital of the University of Pennsylvania, Philadelphia, PA

Clinicians often use the terms “hypoxia” and “hypoxemia” interchangeably. While hypoxemia can sometimes be described as hypoxic hypoxemia, the terms are not synonymous.

The term hypoxia refers to a decrease in tissue oxygenation, whereas hypoxemia more specifically describes a decrease in the partial pressure of oxygen in the blood.1 By measuring the PaO2 clinicians are able to calculate oxygenation deficiency using equations such as A-a (Alveolar-arterial) gradient, the oxygen index, or PaO2/FIO2 ratio.

Using these calculations gives us the ability to identify the type of hypoxemia that is present. With the exception of diffusion limitation, where PAO2 is normal, alveolar oxygenation is decreased with hypoxemia. The A-a gradient is normal in cases of hypoventilation or low inspired partial pressure of oxygen (PIO2), but will be increased in all other hypoxemic events.

It might seem obvious that the solution to hypoxemia is to increase the FIO2 being delivered to the patient, and in some cases the desired response occurs. Whenever shunting occurs, however, there will be a limited increase in PaO2 with increases in FIO2.1-3 Since it is clear that there are differences in the types of hypoxemia, the rest of this article will describe those differences in more specific detail.


Hypoventilation-induced hypoxemia results when alveolar ventilation is reduced and tissue oxygen consumption remains the same. Although all causes of hypoventilation are not fully understood, hypoventilation is often caused by extrinsic diseases, and lung function is normal.2

Some common causes of hypoventilation in a clinical setting include morbid obesity in conjunction with somnolence, abnormalities of the central nervous system, drug overdose, and obstructive sleep apnea.1

Hypoxemia is not the hallmark of hypoventilation. Rising PaCO2 is the primary concern when alveolar ventilation decreases. In the alveolar ventilation equation, CO2 output is divided by alveolar ventilation to equal PCO2; therefore, when alveolar ventilation is halved, PCO2 doubles. In cases of hypoventilation, oxygenation is improved by increasing PIO2 This concept is denoted in the alveolar air gas equation, where alveolar oxygenation is equal to the PIO2 minus alveolar PCO2 divided by the respiratory exchange ratio. If all other factors remain constant and inspired PO2 increases, hypoxemia is easily mitigated during periods of hypoventilation.

Diffusion limitation

When diffusion limitations occur, impaired oxygenation is due to limited movement of oxygen from the alveolus to the capillary bed.1 Although uncommon from a clinical perspective, some examples of diffusion limitation include idiopathic pulmonary fibrosis, sarcoidosis, and connective tissue diseases such as scleroderma.2

In these examples, diffusion limitation occurs as the blood-gas barrier is thickened; thus, equilibration between PO2 in the capillary blood and alveolar gas does not occur. Diffusion limitation also occurs in healthy individuals exercising at altitude due to lower barometric pressure, and in elite athletes due to increased cardiac output.1-3 When cardiac output increases, blood passes over the blood-gas barrier more quickly, and therefore less time is available for oxygenation to occur. Due to compensatory mechanisms, such as vasodilation, the effects of diffusion limitation are reduced.2

Low inspired PIO2

The alveolar air equation mathematically demonstrates that inspired oxygen tension is equal to FIO2 multiplied by the difference between atmospheric pressure and the partial pressure of water. Therefore, if FIO2, atmospheric pressure, or water pressure change, PAO2 will increase or decrease in the same manner. In cases of hypoxemia, if PAO2 decreases oxygen diffusion will be impaired, leading to a lower gradient across the blood-gas barrier, with the net result being hypoxemia. A common example of this is seen in higher elevations where atmospheric pressure is lower.2

 Ventilation/perfusion (V/Q) mismatch

One example of V/Q mismatch is low V/Q units or regional mismatching of ventilation and perfusion within the lung, leading to conditions in which all gas exchange becomes insufficient.3 This imbalance leads to low PAO2 in some parts of the lung, with increased PCO2 in other lung units. This type of hypoxemia is seen in COPD patients.2

In healthy individuals, regional differences exist when comparing the PAO2 in the apices versus the PAO2 in the bases of the lung. Clinically, hypoxemia due to V/Q mismatch is also seen in cases of interstitial lung disease and pulmonary embolism.2 In addition to calculations such as the A-a gradient, V/Q mismatch can be diagnosed by ruling out the other causes of hypoxemia.1

Another example of V/Q mismatch is shunt. When regions of the lung are unventilated but perfused, a pulmonary shunt exists. In other words, blood is passed from the right side of the heart through the pulmonary vasculature to the left side of the heart without being normally oxygenated.

Shunting can be due to intra-cardiac malformations causing anatomic shunts, where some blood bypasses the alveoli,1 or physiologic shunts, where blood may reach the blood-gas barrier but oxygenation does not occur. Physiologic shunts, such as atelectasis, pneumonia, pneumothorax, and ARDS can occur clinically in many different settings.2 In all of these cases simply using supplemental oxygen may be insufficient in the attempt to correct hypoxemia. Advanced interventions such as mechanical ventilation, either invasive or noninvasive, are required to alleviate shunt in critically ill patients.


Hypoxemia is a complex condition facing respiratory therapists on a daily basis. By understanding the underlying cause of hypoxemia, clinicians can be efficient and effective in reversing it before cell death occurs. A keen understanding of the aforementioned reasons why hypoxemia occurs may be the difference between life or death for our patients.


  1. Theodore AC. Oxygenation and the mechanisms of hypoxemia. Up-to-Date. https://uptodate.com/contents/oxygenation-and-mechanisms-of-hypoxemia. Updated May 31, 2017. Accessed on July 15, 2017.
  2. West JB. Pulmonary pathophysiology: The essentials. 8th Baltimore: Lippincott Williams & Wilkins, 2013.
  3. Petersson J, Glenny RW. Gas exchange and ventilation-perfusion relationships in the lung. Eur Respir J 2014;44(4):1023-1041.

The Basics of Capnography and Monitoring the Partial Pressure of End-Tidal Carbon Dioxide: What You Need to Know

Tom Pietrantonio, BSRT, RRT-ACCS
MedCenter Air, Carolinas HealthCare System, Charlotte, NC

The partial pressure of end-tidal carbon dioxide (PETCO2) is arguably one of the most important vital signs to monitor; however, it is also one of the least used methods today. Capnography is much more than just a numerical value with a corresponding waveform. With a basic understanding of the body’s physiologic processes of CO2 production, transport, and removal, and the clinical uses of capnography, clinicians can make decisions that will affect patient care and potential outcomes based on real time data obtained from capnography.

Physiologic parameters of ETCO2

There are three physiologic parameters of ETCO2:

  • Cellular metabolism
  • Perfusion
  • Ventilation

 Cellular metabolism

The oxidation of carbohydrates, fats, and proteins within the mitochondria produces high energy adenosine triphosphate (ATP) molecules and produces CO2 as a metabolic waste product. If CO2 is not being produced, then ATP is not being produced and the energy utilizing and energy producing functions of the body cease to exist.1


CO2 is transported from the cells to the lungs through systemic circulation by a process known as perfusion. As CO2 diffuses out of the cell and into the bloodstream, it is transported in both the plasma and the red blood cells; the most abundant transport mechanism being the red blood cells.2 CO2 is primarily transported in red blood cells in the form of bicarb until it reaches the lungs. Once the red blood cells reach the lungs, bicarb is then converted back into CO2. In general, perfusion status directly influences PETCO2 values.


There must be a working ventilation-to-perfusion relationship if effective ventilation is to occur. In general, O2 and CO2 are exchanged across the alveolar-capillary membrane. O2 diffuses into the bloodstream and is transported to the tissues and cells, whereas CO2 diffuses out of the bloodstream and into the alveoli, where it is spontaneously or mechanically exhaled.

The relationship between ventilation and perfusion (V/Q) is often expressed as a ratio, and under normal conditions, is 0.8. In critically ill patients, this ratio becomes altered, resulting in a V/Q mismatch and it is the primary culprit for the development of hypoxemia and hypercapnia. Using capnography to monitor critically ill patients with V/Q abnormalities hasn’t gained widespread acceptance yet, but it certainly does have its advantages.

Assessment of V/Q mismatch using time and volume capnography

The phase III segment on a time capnogram is where the severity of V/Q abnormalities will be seen. The slope of the phase III segment is dependent on time constants and the gas emptying ability of alveolar units, and the severity of V/Q mismatching greatly affects the slope. In general, the more severe the V/Q mismatch, the steeper the slope, and this is what makes capnography a useful tool to monitor and detect V/Q abnormalities.3

The PaCO2-PETCO2 gradient

“V/Q mismatch” is a rather ambiguous term and it offers the clinician very little additional information other than the fact that some form of ventilation or perfusion problem exists. More appropriately, V/Q mismatching can further be characterized by a high or low V/Q abnormality, which alerts the clinician to a dead space ventilation and shunt perfusion complication, respectively. Incorporating and comparing the PaCO2 to the PETCO2 can offer valuable information regarding a patient’s clinical status, as the gradient is widened and altered by dead space ventilation or shunt perfusion complications.3

PaCO2-PETCO2 and dead space ventilation (high V/Q)

The PaCO2-PETCO2 difference is a direct reflection of alveolar dead space and is useful to assess the severity of V/Q mismatching. In healthy adults, a normal PaCO2-PETCO2 is 3-5mmHg. In the presence of V/Q mismatching, an increase in PaCO2-PETCO2 is suggestive of increased dead space ventilation because the PETCO2 is decreased due to a reduction in cardiac output and pulmonary blood flow. As cardiac output and pulmonary blood flow improve, the PaCO2-PETCO2 difference begins to narrow more towards normal.

It is important to understand that PETCO2 can differ substantially from PaCO2, where changes in PETCO2 may or may not have accompanying changes in PaCO2.3 Because PaCO2 is always at least as high as PETCO2, providing care solely on PETCO2 without an arterial blood gas can be risky in patients with lung disease.

In summary, PaCO2-PETCO2 reflects alveolar dead space and will increase and decrease based on a worsening or improving V/Q relationship, respectively.

PaCO2-PETCO2, shunt (low V/Q) and PEEP titration

Shunt is characterized by a low V/Q mismatch, and it occurs when alveoli are inadequately ventilated despite adequate perfusion. Atelectasis, pneumonia, and ARDS are common pulmonary disease states that are responsible for increasing the PaCO2-PETCO2 gradient.

Unlike dead space ventilation, where restoring perfusion is the primary goal, shunt requires the recruitment of alveoli by applying the appropriate amount of PEEP to restore adequate ventilation. With successful alveolar recruitment, the PaCO2-PETCO2 gradient decreases and remains closer to normal so long as the lungs remain open.

Once PEEP falls below the pressure needed to stabilize the lung open, derecruitment occurs and the PaCO2-PETCO2 gradient begins to increase.3 This was further validated in a 2006 study by Tusman, et al. where they performed PEEP titration trials on an experimental animal model with acute lung injury to determine optimal PEEP levels that would sustain lung recruitment following a recruitment maneuver. The results showed a 95% sensitivity and 93% specificity for detecting lung collapse that correlated well with the use of the PaCO2-PETCO2 gradient.4

Uses of capnography

Currently, there are many clinical conditions that warrant the use of capnography and PETCO2 monitoring, such as:

  • Endotracheal tube placement and confirmation
  • Cardiopulmonary resuscitation
  • Transport
  • Trauma
  • — Head trauma and intracranial pressure
  • — Hypovolemic shock
  • — Cardiogenic shock
  • — Septic shock
  • Medical
  • — Respiratory distress
  • — Pulmonary embolism
  • — Diabetic ketoacidosis
  • — Obtunded or unconscious patients
  • — Seizures

 Endotracheal tube placement and confirmation

 Condensation in the endotracheal tube, auscultation of breath sounds with absent epigastric sounds, and chest rise and fall can be reliable methods of confirming endotracheal tube placement; however, the gold standard is waveform capnography.

In a study by Kelly et al., it was reported that condensation observed in the endotracheal tube occurred in 83% of esophageal intubations.5 Birmingham, et al., stated that movement of the chest wall alone can be seen with an endotracheal tube positioned in the esophagus due to various diaphragmatic “mimic” movements and that air passing through the esophagus can produce similar adventitial lung sounds, explaining why an endotracheal tube placed in the esophagus may be mistakenly identified as lung breath sounds.6

Per Goldberg, et al., the accuracy of using capnography to confirm proper ET tube placement in the trachea has been shown to demonstrate 100% sensitivity and 100% specificity in those patients with spontaneous circulation.7 Even in states of hypoperfusion, MacLeod, et al., demonstrated that the accuracy of capnography to confirm endotracheal tube placement in the trachea during cardiac arrest had a 72% sensitivity.8

Cardiopulmonary resuscitation (CPR)

Back in 1988, Falk, et al., determined that PETCO2 may be a practical, noninvasive method for monitoring blood flow generated by chest compressions during CPR and an almost immediate indicator of successful resuscitation.9 Advanced Cardiac Life Support (ACLS) guidelines highly recommend the use of capnography during resuscitation efforts. The use of capnography during CPR provides the following benefits:

  • PETCO2 concentration varies directly with the cardiac output produced by chest compressions.
  • PETCO2 monitoring eliminates the need to interrupt chest compressions to assess for the presence of a pulse.
  • Per ACLS guidelines, the quality of CPR must be improved if the PETCO2 is less than 10mmHg.
  • Higher PETCO2 values during CPR correlate with increased ROSC and survival.
  • ROSC is associated with an immediate and sustained increase in PETCO2 — typically around 40mmHg.
  • Chest compressions can be safely interrupted to assess for the presence of a pulse and blood pressure after an increase in PETCO2 to verify ROSC.


Using capnography to monitor PETCO2 during transport improves clinical decision making and reduces complications and mishaps due to the increased number of patient movements and/or vehicle noise levels within the transport environment. Monitoring PETCO2 during transport allows the clinician to continually assess the following:

  • Endotracheal tube placement
  • Ventilator circuit integrity
  • Effectiveness of mechanical ventilation
  • Administration and management of sedatives and analgesics
  • Cardiac output
  • Resuscitation efforts


Decreased cardiac output and blood flow secondary to the mechanism of injury results in increased alveolar dead space and subsequent V/Q mismatching. Implementing capnography with patients who have sustained significant trauma is beneficial to help guide resuscitation efforts.

Head trauma and intracranial pressure (ICP)

Using PETCO2 alone to target ventilation can have detrimental effects and outcomes in patients with suspected or known head injuries. Inadvertently hyperventilating a patient with a head injury decreases CO2 concentrations and results in a reduction of cerebral blood flow.3 Today, hyperventilating a patient is only considered a last chance effort during resuscitation, and this tactic is only used when the patient is actively herniating. CO2 affects cerebral blood flow in the following ways:

  • ↑ CO2 = Results in cerebral vasodilation
  • ↓ CO2 = Results in cerebral vasoconstriction

Shock: hypovolemic, cardiogenic, septic

In states of hypoperfusion such as hypovolemic, septic, and cardiogenic shock, PETCO2 is reduced and the goal of treatment is to increase intravascular volume and cardiac output. Monitoring PETCO2 during the administration of intravenous fluid and/or blood is useful to guide and determine the effectiveness of therapy. Thus:

  • ↑ Intravascular Volume = ↑ Cardiac Output = ↑ PETCO2


Respiratory distress

The use of capnography with a patient presenting in respiratory distress will alert the clinician if the patient is responding or not responding to therapy by an increasing, decreasing, or stabilized trend in PETCO2.

  • Decreasing PETCO2: Patient is responding to treatment with improvements in ventilation.
  • Stabilized PETCO2: Patient is not getting better or worse despite treatment.
  • Increasing PETCO2: Patient is not responding to treatment with worsening ventilation.

Pulmonary embolism

Pulmonary embolism is a classic example of dead space ventilation with a concurrently increased PaCO2-PETCO2. Essentially, the CO2 in the affected alveoli decreases, and this alveolar gas mixes with the exhaled gas of well-perfused alveoli, which results in a decreased PETCO2 and increased PaCO2. Despite its potential, capnography remains a screening tool only, and cannot be considered a replacement for the gold standard diagnostic tests used for the diagnosis of a pulmonary embolism.3

Diabetic ketoacidosis (DKA)

Patients who present in DKA develop an underlying metabolic acidosis. The patient will compensate for the metabolic acidosis by increasing minute ventilation, which results in decreased PETCO2 values. Kartal, et al., determined that PETCO2 values correlate moderately with HCO3-levels and that capnography can be used as a noninvasive diagnostic tool for ruling out suspected severe metabolic disturbances in the ED.10 Soleimanpour, et al., also found that capnography could be used to rule out DKA in patients with increased blood sugar levels, with a sensitivity and specificity of 90%.11

Obtunded or unconscious patients

Capnography can be used to assess the adequacy of ventilation in a patient who presents with alcohol intoxication, drug overdose, altered mental status, and any other medical condition with the potential for respiratory impairment by allowing the clinician to observe increasing, decreasing, or stabilized trends in PETCO2.

  • Decreasing PETCO2: Patient is hyperventilating, which could result in impaired ventilatory function overtime as the patient begins to tire out.
  • Stabilized PETCO2: Patient can adequately ventilate.
  • Increasing PETCO2: Impending respiratory failure.


Capnography assesses ventilation and perfusion status and is not affected by the presence of artifact during a seizure. This advantage makes monitoring PETCO2 ideal in these situations:

  • Seizing with apnea: Flat capnography waveform with no associated PETCO2
  • Seizing with ineffective ventilation: Small capnography waveforms with decreased PETCO2
  • Seizing with effective ventilation: Normal capnography waveforms with normal PETCO2 values.  


While the routine use of capnography has yet to be accepted, its abilities make implementing capnography and monitoring PETCO2 paramount in an ever-evolving world of medicine. With a basic understanding of the body’s physiologic processes of CO2 production, transport, and removal, along with the many clinical uses of capnography, clinicians can optimize patient care and outcomes.


  1. Guyton AC, Hall JE. Textbook of medical physiology. Philadelphia: Elsevier Saunders. 2006.
  2. Des Jardins T. Cardiopulmonary anatomy & physiology: essentials of respiratory care. Clifton Park: Thomson Delmar Learning. 2008.
  3. Gravenstein JS, Jaffe MB, Gravenstein N, Paulus DA. Capnography. Cambridge: Cambridge University Press. 2011.
  4. Tusman G, Suarez-Sipmann F, Bohm S, Pech T, Reissmann H, Meschino G, Hedenstiema G. Monitoring dead space during recruitment and PEEP titration in an experimental model. Intensive Care Med 2006;32(11):1863-1871.
  5. Kelly J, Eynon C, Kaplan J, de Garavilla L, Dalsey W. Use of tube condensation as an indicator of endotracheal tube placement. Ann Emerg Med 1998;31(5):575-578.
  6. Birmingham PK, Cheney F, Ward RJ. Esophageal intubation: a review of detection techniques. Anesth Analg 1986;65(8):886-891.
  7. Goldberg J, Rawle P, Zehnder J, Sladen R. Colorimetric end-tidal carbon dioxide monitoring for tracheal intubation. Anesth Analg 1990;70(2):191-194.
  8. MacLeod BA, Heller MB, Gerard J, Yealy DM, Menegazzi JJ. Verification of endotracheal tube placement with colorimetric end-tidal CO2 detection. Ann Emerg Med 1991;20(3):267-270.
  9. Falk J, Rackow E, Weil M. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med 1988;318(10):607-611.
  10. Kartal M, Eray O, Rinnert S, Goksu E, Bektas F, Eken C. ETCO2: a predictive tool for excluding metabolic disturbances in nonintubated patients. Am J Emerg Med 2011;29(1):65-69.
  11. Soleimanpour H, Taghizadieh A, Niafar M, Rahmani F, Golzari S, Esfanjani R. Predictive value of capnography for suspected diabetic ketoacidosis in the emergency department. West J Emerg Med 2013;14(6):590-594.

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Next Bulletin Deadline: Spring/Summer Issue: February 1, 2018.