Pediatric Airway Risks: Inefficient Mechanics of Breathing

Inefficient mechanics of breathing is one major risk factor for infants and young children because it increases work of breathing. In many ways pediatric anatomy and physiology predisposes a child to respiratory distress and respiratory failure.

(Illustrations copyright Whitten, Pediatric Airway Management: A Step By Step Guide)

Mechanics of Normal Breathing

Normal quiet breathing is effortless. The rate is neither too fast nor too slow, however, rate varies greatly depending on age and metabolic rate. The chest rises and falls easily and symmetrically. Air flows into and out of the lungs through the open airway based on changes in air pressure.

Adult Chest Cavity Anatomy Makes Breathing Efficient

Let’s start by reviewing the adult mechanics of breathing. The angulation and rigidity of the ribs during the breathing cycle maximizes efficiency in the adult. The lungs are housed in a skeletal cage formed by the ribs. In order to initiate airflow into the lungs, pressure in the lungs must drop below atmospheric pressure. The body accomplishes this by expanding the airtight chest cavity, thereby decreasing the pressure inside. Two motions are involved:

  • expansion of the rib cage by contraction of intercostal muscles
  • contraction and descent of the diaphragm

The ribs form three functional groupings. The first rib attaches rigidly to the sternum to anchor the rib cage. It hardly moves during respiration.

The 8th through 12th ribs expand mostly laterally during inhalation. This effectively increases intra-abdominal space for organs pushed downward by the diaphragm. The motion is like a bucket handle, swinging up and down toward the side away from the centerline and expanding the width of the chest cavity.

The 2nd to 7th ribs flexibly expand mostly anterior-posterior with a little lateral motion. This motion is like a pump handle — mostly up and down in the front of the chest, expanding the depth of the chest cavity.

Illustration comparing the motions of ribs 8-12 to the motion of ribs 2-7. Each set has unique movements for expanding the rib cage.

a. Ribs 8-12 expand mostly laterally, like a bucket handle. b. Ribs 2-7 expand mostly anteriorly, like a pump handle.

Diaphragmatic Contaction Is The Bellows

The diaphragms are two large dome-shaped sheets of muscle separating the thoracic cavities from the abdominal cavity. As the diaphragms contract with each inhalation, they act like a bellows. During inhalation the bellows descends and flattens, increasing intrathoracic volume and decreasing intrathoracic pressure. This pulls air into the lungs as they inflate.

During exhalation, the diaphragm and intercostals relax. As a result, the diaphragms rise and become dome shaped again, decreasing intrathoracic volume and raising intrathoracic pressure. Lungs deflate. The patient exhales. Unless there is obstruction, exhalation is passive, requiring little energy.

Full contraction of the intercostals and the diaphragm allows for much greater expansion of the chest cavity and produces a larger breath, assuming that air is free to flow into the lungs..

Illustration showing how relaxation and contraction of the diaphragm produces air flow into and out o the lungs by changing air pressure inside the thoracic cavity.

The diaphragm contracts and relaxes during breathing, expanding and contracting the volume of the thoracic cage. The associated air pressure changes inside the thoracic cavity cause the lungs to expand (a) and to deflate (b).

What Factors Affect Ease of Air Flow?

A variety of factors affect how easily that air flows:

  • breathing rate
    • too rapid or too slow a rate impairs air movement
  • inspired tidal volume
    • ventilating close to dead space volume causes CO2 levels to rise
  • airway resistance
    • smaller airways have higher resistance than larger airways
    • increased resistance impairs airflow
  • tissue resistance
    • increased frictional resistance of lung tissues and chest wall increases work of breathing and limits tidal volume
  • elastic recoil
    • with weaker elastic recoil, airways tend to remain partially collapsed on exhalation rather than passively reinflate to baseline
  • compliance
    • poor compliance makes it harder to distend the lungs, limiting air movement and increasing the work of breathing

Changes in any of these parameters can significantly affect adequacy of respiration and how hard it is to take a breath.

Anatomical Features That Increase Pediatric Work of Breathing

When the patient works hard to take a breath, for example against an obstruction, he generates a more negative pressure inside the chest cavity.  The intercostal muscles more fully contract. Retractions, noisy breathing, and a rocking chest wall motion are common. As respiratory failure progresses, the pattern of respiration becomes more and more inefficient and ineffective. Work of breathing increases.

In the patient exhausted to the point of respiratory collapse, or in the patient with respiratory depression due to altered mental status, there may be little effort to breathe. Hypoventilation worsens hypoxia, hypercarbia, and respiratory acidosis. Level of sedation increases, further depressing respiratory drive.

Normal infants and small children have significant anatomic predispositions to serious disruption of their mechanics of breathing if they become sick or injured.

Factors Increasing Infant Work of Breathing

The differences in the mechanics of breathing of small children compared to adults places them at much higher risk of respiratory failure.

Evaluating the degree of respiratory compromise is a judgment call. Mild or potential obstruction may have no signs or symptoms at all. In certain patients such as facial burn victims or patients having a severe allergic reaction, mild airway obstruction can convert to total obstruction quickly as edema forms. Constant reassessment is important so that you may intervene early if necessary — before the airway is lost.

The Infant’s Chest Wall Increases The Work Of Breathing

In the infant or small child, the chest wall is more box-like in shape compared to the adult’s. The ribs are more at right angles to the vertebral column and won’t be angulated like an adult until age 10 years. This makes the pediatric chest wall mechanically less efficient and limits potential lung expansion.

comparison infant vs adult rib angulation

The shape and flexibility of the infant chest, and the shape and immaturity of the diaphragmatic muscle both increase the risk of respiratory failure when the child is ill.

Babies “belly breathe”. To take a deep breath, the infant’s chest therefore expands a little and the abdomen rises a lot as the diaphragm descends, pushing abdominal contents down and out of the way.  Anything that interferes with descent of the diaphragm, such as a stomach or intestines distended with air or liquid, can seriously impair an infant’s breathing.

The infant’s chest wall is also more compliant than an adult’s, with an elastic recoil close to zero because of the lack of rib cage ossification. When the infant takes a breath against resistance, such as with airway obstruction or poor pulmonary compliance from pneumonia, the chest wall actually moves inward as the belly moves outward. The inward movement of the chest wall decreases the amount of air that enters. A rocking chest wall motion is very common in children with even partial airway obstruction.

Illustration showing the components of infant anatomy that make the mechanics of breathing inefficient, increasing risk of respiratory failure.

The inefficient mechanics of infant/toddler breathing increases the risk of respiratory failure.

Because chest wall structure and “belly breathing” limit the ability to increase tidal volume, the baby must rely on respiratory rate increases to compensate for stress. The harder a child tries to breathe, the less efficient and more labored breathing becomes.

You can see video of a toddler with croup and the signs of airway obstruction described above here.

Monitor Your Pediatric Patient Carefully

Watch for signs of airway obstruction.

chart listing the signs of airway obstruction

Infants and toddlers tire easily when they have airway or respiratory compromise. Respiratory distress can easily progress to respiratory failure. Assess your patients carefully and monitor for change. Always ask yourself: “How well is my patient breathing?” Follow the link below for discussions and video of recognizing and treating airway obstruction.

Recognizing Airway Obstruction May Save Your Patient’s Life

Click here see a video clip comparing the signs of airway obstruction in a pediatric patient with a more normal breathing pattern once the obstruction is relieved.

May The Force Be With You

Christine E Whitten MD, author:
Anyone Can Intubate: A Step By Step Guide
and
Pediatric Airway Management: A Step By Step Guide

Button to see inside or buy the book Pediatric Airway Management: A Step-by-Step Guide by Christine Whitten    Button link to see inside or buy the book Anyone Can Intubate, A Step By Step Guide to Intubation and Airway Management, 5th edition on amazon

Click on the covers to preview books at amazon.com

ETCO2: Valuable Vital Sign To Assess Perfusion

Like pulse oximetry before it alerting us to changes in oxygenation, end-tidal CO2 monitoring, or ETCO2, is rapidly becoming an additional vital sign. We routinely use ETCO2 to provide information on ventilation. But ETCO2 can also provide valuable information on the adequacy of cardiac perfusion. It can be an essential tool in ensuring optimal, high quality chest compressions during cardiac resuscitation.

Some Physiology

Ventilation and oxygenation are different. Ventilation exchanges air between the lungs and the atmosphere so that oxygen can be absorbed and carbon dioxide can be eliminated. Oxygenation is simply the addition of oxygen to the body. Under normal circumstances, hyperventilation with room air will lower your arterial carbon dioxide content (PaCO2) significantly, but not change your oxygen levels much at all. On the other hand, if you breathe a high concentration of oxygen without changing your respiratory rate, your arterial oxygen content (PaO2) will greatly increase. However, your PaCO2 won’t change.

Oxygenation changes PaO2. Ventilation changes PaCO2.

Some History Of Old Fashioned Monitors

When I started my anesthesia training in 1980, we monitored the patient with a manual blood pressure cuff, EKG, pulse, and temperature. Pulse oximetry and capnography were not yet in clinical use. If we wanted to determine PaO2, or PaCO2, we needed to draw a blood gas. Frequent blood gas determinations, or the need to monitor continuous perfusion pressures, often necessitated placement of an arterial line.

To provide an indirect indicator of perfusion, we used a precordial stethoscope attached to an earpiece to continuously listen to heart sounds. An attentive anesthesiologist could use changes in the loudness or crispness of the heart tones to alert him or her to changes in cardiac output. As the patient got lighter or if the blood pressure rose, heart tones got louder and sharper. Low blood pressure brought muffled, faint heart tones independent of heart rate. We were essentially using our ears in place of the plethysmograph waveform that pulse oximetry would eventually provide.

Pulse Oximetry

Pulse oximetry revolutionized anesthetic safety. Pulse oximetry was a non-invasive way of measuring oxygen saturation. Oxygen saturation  is the percent of Hemoglobin (Hgb) binding sites in the blood that are carrying oxygen. Hemoglobin is a chemical molecule in the red blood cell (RBC) that carries oxygen on specific binding sites. Each Hgb molecule, if fully saturated, can bind four oxygen molecules. Depending on conditions, Hgb releases some percentage of the oxygen molecules to the tissues when the RBC passes through the capillaries.  We can measure how many of these binding sites are combined, or saturated, with oxygen. This number, given as a percentage, is called the oxygen saturation or simply O2 Sat, commonly pronounced “Oh Two SAT”. it is also referred to as SPO2. When all the Hgb binding sites are filled, Hgb is 100% saturated.

Oxygen saturation and PaO2 are NOT equivalent, and they have significant clinical differences that you can read about here.

What’s The Difference Between Oxygen Saturation And PaO2?

However, with pulse oximetry we could now measure oxygen saturation. We could immediately see in real time if our patient was hypoxemic or hypoxic and, if so, diagnose the cause and treat it before harm was done.

Watching the quality of the waveform, along with the oxygen saturation, told us valuable information about perfusion. The higher the amplitude of the wave, the stronger the pulse was. The more damped out the waveform appeared, the weaker the pulse.

With this new tool, and with the OR environment becoming increasingly noisy, use of the precordial stethoscope has largely faded away. Pulse oximetry quickly spread to ICUs, on wards, and clinics to monitor patients at risk. Pulse oximetry has become a fifth vital sign.

I believe we are seeing the same transition with end-tidal CO2 monitoring.

END TIDAL CO2 Has Many Uses

What Is ETCO2?

Capnography refers to the process of measuring the partial pressure of end-tidal CO2 in each expired breath. Providers measure the value of ETCO2 in each exhaled breath with a very thin tube inserted into the breathing circuit or the patients oxygen mask or nasal prongs.

The waveform (capnogram) that you then see on the capnography monitor provides a real time recording of the patient’s respiratory rate, pattern and depth of breathing, and of course the value of CO2 exhaled. These measurements help the provider evaluate adequacy of ventilation.

The author looks at the capnography waveforms during an anesthetic to evaluate ETCO2 values and the adequacy of ventilation.

The author looks at the capnography waveforms during an anesthetic to evaluate end-tidal CO2 (ETCO2) values and the adequacy of ventilation.

ETCO2 Helps Assess Adequacy of Ventilation

We routinely measure ETCO2 for every patient in the operating room. We use it increasingly for conscious sedation provided in treatment rooms and on the wards. ETCO2 and PaCO2 are not the same value. PaCO2 is the concentration of CO2 in arterial blood. ETCO2 is the concentration of CO2 in the exhaled breath, and is close to alveolar CO2. ETCO2 is usually about 5 mmHg below PaCO2. This makes sense. If the concentration of CO2 in the alveoli were higher than in the blood stream, CO2 could not enter the lungs and would not be exhaled.

ETCO2 offers a valuable trending tool to monitor and control ventilation. It alerts us immediately if the patient hyperventilates, hypoventilates, or becomes apneic.

  • A normal trace appears as a series of rectangular waves in sequence, with a numeric reading (capnometry) that shows the value of exhaled CO2. “Normal” ETCO2 is in the range of 35 to 45 mmHg.
  • In hyperventilation, the CO2 waveform becomes smaller and more frequent, and the numeric reading falls below the normal range.
  • In hypoventilation), the waveform becomes taller and less frequent, and the numeric reading rises above the normal range.
  • Fattening of the waveform indicates an airway obstruction.
  • If the series of rectangular waves become a flat line, the patient is not breathing.

Use ETCO2 In The Perioperative Areas

I believe we should increase our use of ETCO2 in our perioperative areas and procedure rooms. Patients receiving conscious sedation on the ward or recovering from anesthesia are arguably at more risk of airway compromise than patients in the operation room. They are often under more intermittent observation. I encourage my recovery room nurses to use end-tidal CO2 monitoring when they are caring for patients at risk of hypovention or obstruction such as those:

  • exhibiting prolonged sedation,
  • with opioid induced respiratory depression,
  • history of sleep apnea,
  • any cardiovascular instability
  • any time they are worried about a particular patient.

For clinical examples of how ETCO2 can change during clinical care and how we can use ETCO2 to guide our treatment, read more here.

How Does Hypoventilation Cause Hypoxemia?

Anatomic Dead Space Affects Hypoventilation

Don’t Withhold Oxygen From That CO2 Retainer

ETCO2 Helps Verify Intubation

Esophageal intubation or accidental extubation are always risks.  Monitoring ETCO2 increases safety. The continued presence of CO2 in the exhaled breath can only mean placement of the tube in the trachea. Loss of the ETCO2 trace indicates extubation or disconnection from the circuit the ETCO2.

The shape of the capnography waveform can also indicate the severity of problems such as bronchospasm or other cause of increased resistance to breathing or exhalation.

ETCO2 Is An Early Sign Of Poor Perfusion or Cardiac Arrest

Oxygen delivery and carbon dioxide removal depend on three systems: lungs, blood and circulation. It’s important to remember that adequate oxygen absorption and delivery depends on the interaction between lung function and circulation. As soon as cardiac output starts to fall, blood perfusion through the lungs falls. CO2 now has more difficulty being carried to the lungs for exhalation. This leads to a rise in PaCO2 in the blood stream and a fall in ETCO2.

Oxygen delivery and CO2 removal from the lungs depend on lung function, blood hemoglobin concentration, and circulation. Disturbance in any of these risks respiratory distress or failure. If lung function and Hgb are stable, then changes in ETCO2 imply changes in perfusion.

Oxygen delivery and CO2 removal from the lungs depend on lung function, blood hemoglobin concentration, and circulation. Disturbance in any of these risks respiratory distress or failure. If lung function and Hgb are stable, then changes in ETCO2 imply changes in perfusion.

In the operating room, I often see a drop in ETCO2 even before blood pressure itself starts to fall. As long as there is some circulation, there will be some ETCO2 present, even if you can’t feel a weakened peripheral pulse. ETCO2 can therefore be an early warning of developing shock, or pulmonary embolus.

If ETCO2 drops to zero, then the heart has stopped. This is true even for patients who are continuing to receive manual ventilation, because although air is moving into and out of the lungs, there is no CO2 being delivered to exhale. Loss of ETCO2 can also be the first sign of cardiac arrest. A patient may still have an EKG trace in pulseless electrical activity, but not have circulation and therefore will not have a measurable ETCO2.

Here is a simplified flow chart for using ETCO2 to alert you to perfusion or ventilation problems.

ETCO2 is a valuable tool for early recognition of poor perfusion and cardiac arrest.

ETCO2 is a valuable tool for early recognition of poor perfusion and cardiac arrest.

Adequacy Of Chest Compressions

Good quality CPR depends on high quality chest compressions. When I practice with my staff during Critical Event Training, failure to perform adequate chest compressions is common, a fact that reinforces the need to routinely practice.

During one particular exercise, one diminutive RN was having trouble making her compressions meet the 2-2.5 inch depth, 100 compressions per minute on the manikin (as measured by our test device). The rest of the team encouraged her until she got it correct. The following weekend her Dad suffered a cardiac arrest in her living room. She went into action delivering chest compressions while the family dialed 911. Her father made a full recovery, and she gave credit to the training she had just received.

Good quality compressions can save lives. ETCO2 is one valuable tool we have to tell us that good quality compressions are being delivered. The higher the ETCO2 measured during compressions, the better the perfusion being supplied by CPR. The goal should be to maintain ETCO2 no lower than 10-20 mmHg. An ETCO2 below 10 mmHg is associated with poor outcome.

Good quality chest compressions will also generate a waveform on the ETCO2 capnograph that allows you to estimate the rate of compressions.

Return of Spontaneous Circulation

Return Of Spontaneous Circulation (ROSC) is accompanied by a sharp rise in ETCO2, usually within a range higher of 35-45 mmHg or higher as CO2 is now delivered to the lungs and then exhaled. This is often accompanied by a palpable pulse and a rising blood pressure.

Good news. However, the next 10 minutes are a very dangerous time for your patient. The heart is still stunned and cardiac output may still be poor. Current consensus guidelines for cardiopulmonary resuscitation (CPR) recommend that chest compressions resume immediately after defibrillation attempts and that rhythm and pulse checks be deferred until completion of 5 compression:ventilation cycles or minimally for 2min.

One study showed that perfusion remained poor for greater than 2 minutes in 25% of patients successfully defibrillated [1]. Continue to monitor that ETCO2! This is now your powerful tool to see if perfusion is adequate and being maintained. Assuming ventilation is consistent, a drop in ETCO2 during this period can indicate failing circulation. A loss in ETCO2 can mean re-arrest.

Check to make sure your endotracheal tube is still properly positioned, check a pulse, and decide your appropriate actions.

Prognosis During CPR Efforts

ETCO2 below 10 mmHg can be caused by poor compression technique.  It can also be caused by low perfusion and metabolism from prolonged shock despite good compressions — in other words the cardiac pump is damaged and failing. If high quality compressions are being delivered, and an advanced airway is in place allowing accurate ETCO2 measurements, then an ETCO2 persistently below 10mmHg after 20 minute of resuscitation is a poor prognostic sign. It can be used as an indication to consider terminating resuscitation efforts.

On the other hand if ETCO2 is above 15mmHg, or it continues to rise, that is one indication that resuscitation efforts should continue, as the brain and heart are being perfused. There are case reports of patients surviving prolonged CPR with higher ETCO2 readings.

We’ve come a long way since I had to depend on a precordial stethoscope, skin color and finger on the pulse to supplement blood pressure and EKG to assess perfusion in my patients. Capnography and pulse oximetry are powerful tools. However, don’t forget that in the absence of either, you can still look at your patient and be vigilant. Without vigilance, all the tools in the world will not protect your patient.

May The Force BeWith You

Christine E Whitten MD, author
Anyone Can Intubate: A Step By Step Guide
and
Pediatric Intubation: A Step By Step Guide

Button link to see inside or buy the book Anyone Can Intubate, A Step By Step Guide to Intubation and Airway Management, 5th edition on amazon      Button to see inside or buy the book Pediatric Airway Management: A Step-by-Step Guide by Christine Whitten

References

1. Pierce AE, Roppolo LP, Owens PC, Pepe PE, Idris AH. The need to resume chest compressions immediately after defibrillation attempts: an analysis of post-shock rhythms and duration of pulselessness following out-of-hospital cardiac arrest. Resuscitation. 2015 Apr;89:162-8. doi: 10.1016/j.resuscitation.2014.12.023. Epub 2015 Jan 15.

Conscious Sedation: Is Your Patient Breathing?

Change in mental status can occur from conscious sedation or opioid administration, hypotension, sepsis, head trauma, acid-base imbalance, alcohol, drugs, or toxins. Change in level of consciousness often affects breathing, sometimes to the point of causing severe hypoxia, arrythmias and cardiac arrest. Let me repeat that. Anything that alters consciousness can alter respiration, which can lead to the vicious cycle of hypoventilation, hypercarbia, and hypoxia. If you don’t recognize inadequate respiration —and treat it— the patient can suffer injury or die. Let’s look at a common clinical example of altered consciousness — conscious sedation.

Everyday, in all of our practices, we purposefully try to alter our patient’s level of consciousness in order to tolerate a procedure. We often take the safety of procedural conscious sedation for granted. After all, we’re only giving a little sedation to make the patient relaxed, calm and more comfortable. Although problems are rare, patients can become hypoxic, hypercarbic, and apneic with conscious sedation, and some have died. The deaths of the celebrities Michael Jackson in 2009, and Joan Rivers in 2014 were related to hypoxia from loss of the airway under deep sedation. Respiratory depression represents the principal potential risk introduced with conscious sedation. If left unrecognized and untreated, it can be the cause of serious complications.

Sleep and Sedation Affect Respiration

To understand why mental status change increases respiratory risk, let’s start with the respiratory effects of sleep.

Janet Smith is a 44 year-old healthy patient who is scheduled for correction of a trigger finger with ambulatory surgery under conscious sedation tomorrow at the surgicenter. She’s worried, so it takes her a long while to fall asleep. When she finally does sleep, her respiratory drive begins to change.

Does oxygen saturation change with normal sleep? For healthy young people between 19-25 years of age, there appears to be no change in oxygen saturation with sleep (1). Other studies looking at a more varied population up to age 64 did find up to an 11% drop in oxygen saturation(2,3,4). Adding a comorbidity such as chronic bronchitis is also associated with saturation drops of about 10%. So the answer seems to depend on age, presence of comorbidities and how ventilation changes with sleep for that particular person due to such things as snoring.

With normal non-REM sleep, PaCO2 rises about 3-7 mmHg as the body’s response to increased CO2, or hypercarbia, is blunted. Tidal volume and respiratory rate decrease. Pharyngeal muscles as well as muscles of the tracheobronchial tree relax, increasing airway resistance and predisposing to potential obstruction, such as snoring.

Although some of us sleep more deeply than others, we usually awaken easily if someone talks to us, or the alarm goes off. If we obstruct our airway and begin to snore, we typically rouse ourselves enough to take a deep breath and turn over. When we don’t easily rouse from sleep induced airway obstruction then we may have sleep apnea. Now, let’s look at how giving sedation to a patient like Janet Smith interferes with her ability to rouse.

Conscious Sedation

When Janet gets to the preop area, she’s nervous and tells her nurse that she didn’t sleep much the night before. Her anesthesia provider gives her 1 mg of midazolam IV to relax her. Her care team then takes her to the OR.

With light conscious sedation she will continue to respond to verbal commands. Cognitive function and coordination may be impaired. She can still carry on a conversation, although she may not remember details of it.  Cardiac and ventilatory function are usually not altered a lot. Like natural sleep, it’s common for the patient’s respiratory rate and tidal volume to decrease slightly. She’ll lie comfortably on the OR bed while we’re attaching her monitors and going through the final safety checks.

Moderate Sedation

Of course, many patients like to nap during their surgical procedure and in this case the anesthesiologist starts a background infusion of propofol at a low rate of 25 mcg/kg/hr to induce a moderate level of conscious sedation while things are being set up. Using this technique, the level of propofol in Janet’s bloodstream builds slowly and she will get progressively sleepier until she’s moderately sedated.

With moderate sedation, a patient still responds to commands, but she might require a tap on the shoulder to rouse and answer a question. She still shouldn’t require any help holding her airway open, but there may be more of a tendency to snore, especially if the patient has a history of snoring. Snoring is a sign of airway obstruction and is a warning sign that the patient needs to be monitored more closely.

Injecting local anesthetic can be a bit painful. As the surgeon gets ready to inject the local anesthetic the anesthesiologist will often give just a little more sedation so that the patient does not remember the injection. This could be more midazolam, or a short acting opioid like fentanyl. However, in this case Janet is given a small bolus of 50 mg of propofol IV. The strategy behind this technique is to temporarily induce a deeper level of sedation during the local anesthetic injection itself. Sedation from a Propofol bolus wears off in a few minutes, allowing Janet’s level of consciousness to return back to the prior moderate level of sedation for the rest of the procedure.

Deep Sedation

With deep sedation the patient is not easily arousable, but will still respond with repeated or painful stimulation. The deeply sedated patient might occasionally require help holding her airway open and spontaneous ventilation might become inadequate. Cardiovascular stability is usually maintained.

Janet tolerates the injection well and appears to be sleeping. However, after the injection is finished, the anesthesiologist notices that Janet is no longer breathing well. Her airway is obstructed. He tips her chin back and lifts her jaw to open her airway and she takes a deep breath. He has to periodically shake her shoulder for the next few minutes to remind her to take deep breaths. After about 2 minutes she starts breathing well again on her own.

Unconsciousness: General Anesthesia

What just happened? It can be easy to take a patient from deep sedation to general anesthesia. With general anesthesia the patient is completely unresponsive and airway support of some type is often required, even when the patient is breathing spontaneously. Cardiovascular changes are common. After the extra Propofol bolus was given, Janet continued to breathe well — as long as she was being stimulated by the pain of the injection. After that stimulus stopped, she slipped into an even deeper plane of sedation. The same scenario can happen postoperatively upon arrival in the recovery room when stimulation ceases (see prior discussion).

Perhaps Janet was just more sensitive to sedatives than some patients. Perhaps it was because she was sleep deprived from her insomnia the night before. Maybe it was the speed with which she got repeated doses of medications in such a short time that added up to too much sedation.

In our case, the anesthesiologist was watching carefully and noticed immediately that he needed to assist Janet’s breathing. Janet’s level of sedation could have eventually become light enough, or her CO2 levels high enough, to allow her to start breathing again on her own. The question is whether she would start breathing again quickly enough — before she became hypoxic or extremely hypercarbic. Prolonged hypoxia and hypercarbia can cause complications, including potential cardiac arrest. And hypoxia and hypercarbia both depress mental status, which, if severe enough can further depress respiration, making complications more likely.

Sedation Is A Continuum

All four stages of sedation are a continuum. At any point with just a little more sedation or a little less stimulation, your patient can stop breathing well. In my job as an anesthesiologist, I see on a daily basis how easy it is to overshoot and cause a patient to become apneic using moderate to deep sedation. And if the patient is frail or sick, or extremely old or young, sometimes even a small dose of sedative or opioid, — one that would normally induce just light sedation — can cause apnea and hypoxia. Sedation, and its effect on respiration, are not just dose related, they depend on the status of the patient receiving that dose and what else is happening to that patient at that time. Be vigilant.

Related Articles

May The Force Be With You

Christine Whitten MD, author

Anyone Can Intubate: A Step By Step Guide
and
Pediatric Airway Management: A Step By Step Guide

Button to see inside or buy the book Pediatric Airway Management: A Step-by-Step Guide by Christine WhittenButton link to see inside or buy the book Anyone Can Intubate, A Step By Step Guide to Intubation and Airway Management, 5th edition on amazon

Click the cover to preview or purchase book at Amazon.com

References

  1. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC459897/pdf/thorax00225-0033.pdf
  2. Gimeno F, Peset R. Changes in oxygen saturation and heart frequency during sleep in young normal subjects. Thorax 1984;39(9):673-675.
  3. Block AJ, Boysen PG, Wynne JW, Hunt LA. Sleep apnea, hypopnea and oxygen desaturation in normal subjects. A strong male predominance. N Engl J Med. 1979 Mar 8;300(10):513–517. [PubMed]
  4. Douglas NJ, Calverley PM, Leggett RJ, Brash HM, Flenley DC, Brezinova V. Transient hypoxaemia during sleep in chronic bronchitis and emphysema. Lancet. 1979 Jan 6;1(8106):1–4. [PubMed]

Anatomic Dead Space Affects Hypoventilation

Understanding anatomic dead space is important to recognizing subtle hypoventilation. Hypoventilation from sedation, pain medications, anesthesia in the immediate postoperative period is common. The most obvious sign is slowing of the rate of breathing. A more subtle sign is that tidal volume becomes shallower. Having a tidal volume close to, or smaller than the patient’s dead space can lead to significant hypercarbia, hypoxia, and respiratory failure. This article discusses the concept of dead space and it’s clinical use in recognizing hypoventilation and preventing hypoxia and hypercarbia. Continue reading

Remember That Respiratory Failure Is Not Always Due to Lung Failure

There are many causes of respiratory failure. Some causes of respiratory failure result from disease or damage to the respiratory system. However disease or injury to other organ systems such as the central nervous system, the musculoskeletal system, or the presence of cardiac or septic shock can also cause respiratory dysfunction.

While final diagnosis will certainly affect treatment, assessing and managing the patient’s ability to breathe will not change with diagnosis.  However, once the airway is secure, you then have to diagnose and treat the real problem in order to resolve the respiratory failure.

The Case

In this case, I was an anesthesia resident doing my pediatric rotation at a children’s hospital. It was my turn to be on call for the weekend. At this particular hospital back in 1982, the anesthesia department managed the airway emergencies in the Emergency Department so when I got the page to go to the ED, I ran.

Inside the triage cubicle a 6 year-old girl was clearly unresponsive. She had been sick with fever, nausea, vomiting and diarrhea for several days according to her mother, who was crying in the corner. She hadn’t been able to hold down any food or fluids for over 24 hours. Her temperature was 102F. She was breathing rapidly but very shallowly. We did not as yet have pulse oximetry, but her color was dusky blue. Her blood pressure was 60/40 and her pulse was 150. She looked septic.

I placed an oral airway and assisted her breathing. She didn’t react at all to the oral airway — no gag reflex. We decided to intubate.

My colleagues quickly placed an IV and I decided to intubate without induction agent or muscle relaxant. If she didn’t need those agents then I didn’t want to potentially compromise her status by giving them. Had she reacted at all when I started to perform direct laryngoscopy I would have aborted and changed the plan.

She didn’t respond at all as I slid the endotracheal tube into the trachea.

We gave her two boluses of 20ml/kg of normal saline. Her color improved, her pulse came down to 110 and her blood pressure rose to 80/50, appropriate for her age. But she still hadn’t woken up.

Ten minutes later the first blood test results returned. Her blood glucose was 10, extremely low. We gave her 2 ml/kg of D25W. Within two minutes she woke up and started fighting the endotracheal tube. As her other vital signs looked much improved and she was now awake and protecting her airway, we elected to extubate her.

The child was admitted to the pediatric ward, was treated for gastroenterits and she did well.

Learnings: Hypovolemia and Hypoglycemia Can Cause Respiratory Failure

This was the first experience that I remember seeing in my career that demonstrated that hypovolemic shock and hypoglycemia can cause profound respiratory failure without lung pathology.  It’s important to remember that respiratory failure can result from a variety of other systemic problems, not just dysfunction of the respiratory system.

Table showing the difference multi-system causes of respiratory distress and respiratory failure

Respiratory distress or respiratory failure can come from many causes.

While assisting ventilation and protecting the airway are first priorities to stabilize a patient, treating the cause of the respiratory failure may require more than just ventilation and/or intubation. In fact, treating the cause can sometimes help you avoid the progression of respiratory distress to respiratory failure. If you don’t consider a potential problem or cause, you’re not going to be able to diagnosis it.

May The Force Be With You

Christine Whitten MD
Author of Anyone Can Intubate: a Step by Step Guide, 5th Edition
and
Pediatric Airway Management: a Step by Step Guide

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Communication In A Crisis: A Case of Respiratory Depression In A Child:

When I’m teaching communication in a crisis to my Perioperative/OR nurses, I often recount the story of what happened during one particular child’s recovery years ago. This case, involving a 2 year old child who developed respiratory depression in the recovery room, demonstrates how good communication in a crisis, including the ability to challenge an authority figure, can improve patient safety and allow collaborative teamwork in a crisis management situation. Continue reading

Difference in Manual Ventilation: Self-Inflating Ventilation Bag vs. a Free Flow Inflating Bag

Manual ventilation with a bag-valve-mask device requires a good mask seal against the face in order to generate the pressure to inflate the lungs. But it also requires knowledge of how to effectively use the ventilation device to deliver a breath. This article will discuss the differences in ventilation technique for self-inflating vs free-flow ventilation bags. Understanding those differences is important for successful manual ventilation of your patient. Continue reading

Ventilation Perfusion Mismatch

Alveolar gas exchange depends not only on ventilation of the alveoli but also on circulation of blood through the alveolar capillaries. In other words it depends both on ventilation and perfusion. This makes sense. You need both oxygen in the alveoli, and adequate blood flow past alveoli to pick up oxygen, other wise oxygen cannot be delivered. When the proper balance is lost between ventilated alveoli and good blood flow through the lungs, ventilation perfusion mismatch is said to exist.

The ventilation/perfusion ratio is often abbreviated V/Q. V/Q mismatch is common and often effects our patient’s ventilation and oxygenation. There are 2 types of mismatch: dead space and shunt.

Imbalance between perfusion and ventilation is called ventilation perfusion mismatch. This illustration compares shunt, the perfusion of poorly ventilated alveoli; and Physiologic dead space: the ventilation of poor perfused alveoli.

Shunt is perfusion of poorly ventilated alveoli. Physiologic dead space is ventilation of poor perfused alveoli.

This article will describe how dead space is different from shunt. It will help you understand how you can use these concepts to care for your patient. Continue reading

Apneic Oxygenation: Increase Your Patient’s Margin Of Safety During Intubation

While breathing room air, oxygen saturation drops precipitously to below 90% within about a minute of the start of apnea in the average healthy adult. As we saw in a previous blog post, preoxygenation is one of the most important safety measures we can use prior to induction of anesthesia and in preparation for intubation. Adequate preoxygenation can more than double the time to hypoxia during open airway apnea, allowing more time for intubation to occur. However, increasing the time to critical hypoxia from 1 minute to 2 or 3 minutes with preoxygeation, as important as that is, can still be too short if the intubation turns out to be truly challenging. Apneic oxygenation is an easy technique to increase the time to desaturation significantly. However you have to know how to optimally provide it in order to safeguard your patient  Continue reading

Preoxygenation Can More Than Double The Time To Hypoxia During Apnea

While breathing room air, oxygen saturation drops precipitously to below 90% within about a minute of the start of apnea in the average healthy adult. One of the most important safety measures we use in anesthesia is to preoxygenate our patients prior to induction of anesthesia and in preparation for intubation. This is especially true if we are planning a rapid sequence induction. Adequate preoxygenation can more than double the time to hypoxia during apnea, allowing more time for intubation to occur.

Preoxygenation increases the margin for safety. It treats any pre-existing hypoxemia in the critically ill patient. It also postpones the onset of hypoxia while the patient is apneic during the intubation attempt. This becomes especially important if the intubation attempt becomes difficult and prolonged.

Speed of onset of hypoxia with apnea depends on metabolic rate and on the actual amount of oxygen available in the patient’s functional residual capacity. To see how preoxygenation can effect this let’s review some physiology. Continue reading

Assisting Ventilation With Bag-Valve-Mask

As an anesthesiologist, I often run to emergencies where the patient is not breathing adequately and requires intubation. However, before any intubation, a patient in respiratory distress/failure needs ventilation. Providers who have passed ACLS are often able to ventilate an apneic patient well because they have practiced on the manikin. However, I often see that providers have more difficulty trying to assist ventilation of a patient who is still breathing spontaneously.

The typical inexperienced provider will try to provide large, slow breaths just as they were taught in ACLS. Unfortunately these breaths are often out of synch with the patient’s own breathing. Squeezing the bag while the patient is exhaling means that your inflation pressure must not only overcome the diaphragm, but also reverse the passive outflow of air, the elastic recoil of the lungs, and the rebound of the chest wall combined. The vocal cords may be closed. Ventilating out of synch with the patient won’t be as effective. The breath you deliver will take the path of least resistance to enter the stomach or escape from the mask. It often makes the patient cough.

Even worse,  providers will occasionally hesitate to try to assist a patient’s breathing while waiting for the intubation team because they feel they don’t know how. Delay in improving ventilation can place your patient at higher risk of complication. This is unfortunate because in many ways assisting ventilation is even easier than manually ventilating an apneic patient. Let’s see why. Continue reading

Don’t Withhold Oxygen From That CO2 Retainer

There is often a great deal of confusion about how to manage the care of a patient with COPD because of unwarranted, and incorrect, concern that all patients with COPD are CO2 retainers. This fear of causing CO2 retention sometimes causes providers to withhold or withdraw oxygen inappropriately. Understanding some of the respiratory physiology behind CO2 retention will allow you to make more informed decisions. Let’s start at the beginning. Some of this material comes from my book Anyone Can Intubate, 5th Edition. Continue reading

What’s The Difference Between Oxygen Saturation And PaO2?

I often teach classes for RNs who are orienting to our preoperative and recovery areas. Hypoxemia and hypoxia occur commonly among our perioperative patients so I spend a lot of time on recognizing early signs of respiratory distress such as tachycardia, tachypnea, cyanosis, agitation, and changes in mental status.

Pulse oximetry is one obvious monitoring tool to identify hypoxemia and hypoxia. I find that one frequent area of confusion relates to understanding the important distinction between arterial partial pressure of oxygen (PaO2) and oxygen saturation (O2 sat). I am not alone. Multiple studies have identified this as a knowledge gap. One study of pediatric nurses showed that while 84% of the clinicians felt they had received adequate training, only 40% correctly identified how a pulse oximeter worked, and only 15% had a correct understanding of the oxyhemoglobin dissociation curve. This is such a key concept that we all must take pains to ensure our staff understands how to use this valuable monitoring tool. Some of the material below is from my book Anyone Can Intubate. Continue reading

How Does Hypoventilation Cause Hypoxemia?

I often find that my students sometimes confuse oxygenation and ventilation as the same process. In reality they are really very different. Ventilation exchanges air between the lungs and the atmosphere so that oxygen can be absorbed and carbon dioxide can be eliminated. Oxygenation is simply the addition of oxygen to the body. You must understand the difference to understand how hypoventilation causes hypoxia.

If you hyperventilate with room air, you will lower your arterial carbon dioxide content (PaCO2) significantly, but your oxygen levels won’t change much at all. On the other hand, if  you breathe a high concentration of oxygen, but don’t increase or decrease your respiratory rate, your arterial oxygen content (PaO2) will greatly increase, but your PaCO2 won’t change.

Ventilation changes PaCO2. Oxygenation changes PaO2.

Why do we need to understand this? Let’s look at some common examples. Along the way we will painlessly use the Alveolar Gas Equation to explain two common scenarios:

  • how hypoventilation causes hypoxia,
  • why abruptly taking all supplemental oxygen away from a carbon dioxide retainer will hurt them.

Continue reading