“Asthma” by Gerhard Wolf, MD for OPENPediatrics
24
August

By Adem Lewis / in , , , , , , , , , , , /


The purpose of this video is to provide general
information and education about the care of a critically ill child. It is in no way a
substitute for the independent decision-making and judgment by a qualified health care professional.
The information contained in this video should not be used to make a diagnosis or to overrule
the advice of a qualified health care provider, nor should it be used to provide advice for
emergency medical treatment. Asthma, by Dr Gerhard Wolf. Hello, my name is Dr. Gerhard Wolf. I work
at the division of Critical Care Medicine at Children’s Hospital Boston. I will be talking
about asthma today. We’re going to review the epidemiology and pathophysiology of acute
and severe asthma. I will describe the current management strategies in the pediatric ICU,
and we will talk about considerations for the pediatric intensivists taking care of
a child child with severe asthma. Terminology. Asthma is a very common disease, in fact,
the most common disease of childhood, and that’s why it’s very likely that as pediatric
intensivists we will encounter a child with asthma in the pediatric ICU. The terminology
of asthma has been quite confusing, and let me just present to you a child with wheezing,
an inter-viral illness, and who presents with respiratory distress. How are we going to
call this diagnosis? Do we call it reactive airway disease? Do we call it ‘wheezy bronchitis?’
Asthmatic bronchitis? Wheezing-associated respiratory illness? Parainfectious bronchial
hyperactivity? Or asthma? Probably all of those terms can be used, and are sort of suitable
as a diagnosis. Reactive airway disease is a recurrent, viral-induced wheezing that occurs
in toddlers, and asthma describes a more chronic condition, has several triggers, respiratory
infections being one of them, and usually has a poor prognosis for spontaneous resolution. Pathophysiology. I want to show you a chest radiograph; this
is out of the New England Journal review article, and, on panel A, you see a chest X-ray; very
hyper-inflated lungs, typical in asthma. The big arrows show some subcutaneous air associated
with possible pneumomediastinum, and on B, in the big arrow you can see a big anterior
pneumothorax. All those can be complications that we see in patients with severe asthma
in the intensive care unit. Note also the areas of atelectasis pointed out by the small
arrows here. Let me take you through the normal airway and the asthmatic airway. On the left
side you see an image of the normal airway; you see the smooth muscle cells, the fibroblasts,
and the capillaries. The role of the smooth muscles in healthy patients is to provide
support of the airway and to facilitate gas exchange, as well as to help with mucus clearance.
On the right side, you see the airway of a patient with asthma, and as you can see, the
number of smooth muscle cells is increased, as is the size of the smooth muscle cells.
And in asthma, the smooth muscle cells mediate much of the pathology we see, the bronchoconstriction,
the hyper-responsiveness, the inflammation. Medications. Let me talk to you about managing asthma exacerbations,
and all those recommendations come from the recommendations from the National Heart, Lung,
and Blood Institute, and the guidelines for the diagnosis and management of asthma, released
in 2007. Beta-agonists, as we know, are one of the mainstay of therapies in patients with
asthma, but only selective beta-2 agonists are recommended. Albuterolis one of the main
beta-2 agonists we use in asthma, at the dose of 0.15 mg/kg every twenty minutes, or as
a continuous nebulization at 0.5 mg/kg per hour. We should use inhaled beta-agonists
if possible; the efficacy of IV, or intravenous beta-agonists, is unproven. We do use terbutaline
or other intravenous beta- 2 agonists, if we have a patient with asthma exacerbations
already on continuous nebulizers, but normally, inhaled beta-agonists have much less side
effects and a greater efficacy than IV beta-agonists, and the recommendation is to stay away from
drugs like isoproterenol, which have both beta-1 and beta-2 effects, since there are
more side effect of cardio- toxicity involved with those drugs. Epinephrine can be used
in an asthma attack and has been used, because apart from being a vasoconstricter, it’s also
a bronchodilator; it has both alpha-1 andalpha-2, beta-1 and beta-2 activities, and if it’s
given in an asthma attack it’s normally given subcutaneously, at the dose of 0.01 mg/kg
up to a total dose of 0.3 to 0.5 mg. Again, epinephrine is a non- selective beta-agonist,
as it also has alpha activities, so we do expect more cardiac side effects if we use
epinephrine. Anticholinergics reduce the vagal tone of the airways, and ipratropium bromide
has been used a dose of .25 mg every twenty minutes. Corticosteroids are important to
reduce inflammation in the airways of a patient with an asthma attack because apart from vasoconstriction
,the inflammation is a main component of the disease. We usually use prednisone at a dose
of 1mg/kg every six hours, for 48 hours, or methylprednisolone IV at the same dose, and
after two days, we normally use 2 mg/kg per day. Magnesium has been used in asthma attacks,
and it works as an antagonistic to calcium on the smooth muscles, and therefore mediates
bronchial dilation. Much of the data supporting magnesium comes from studies done in the emergency
room, where patients who receive magnesium, in some studies, had a lower rate of admissions
to the hospital. We typically use magnesium at the same dose that we would use it for
resuscitation, which is 2g IV in an adult patient, or in a larger child, or otherwise,
25-50 mg/kg. The following treatments are not recommended in a patient with an asthma
attack, by the guidelines, or by the National Heart, Lung, and Blood institute, and their
guidelines from 2007. Theophylline is usually not recommended; antibiotics are not routinely
recommended; if a patient has a pneumonia or sinusitis, it should be treated. Aggressive
hydration therapy is not recommended. Chest physiotherapy can be stressful for the child
was asthma, and can lead to increased coughing, and worsened hypoxia, and is therefore not
recommended and is not beneficial. The same applies for mucolytics; they are not routinely
recommended, and sedation is not recommended; although patients and children with an asthma
attack often present with a large amount of anxiety, sedation can lead to worsening respiratory
failure, as it can lead to a respiratory depression. Endotracheal Intubation. Now, about 5-10% of all children who get admitted
to the ICU with an asthma attack will get intubated. And what should we base our decision
to intubate a child with asthma on? It is mainly based on clinical judgment, and on
arterial blood gas analysis, such as, worsening acidosis or rising carbon dioxide levels.
If a patient has more and more exhaustion, or has impending respiratory failure, which
means the patient does not have the full degree of respiratory failure yet, but we think he
will fail in the next half an hour, this is impending respiratory failure; then, we should
intubate those patients before they have a respiratory or cardiac arrest. Depressed mental
status can be an indication to intubate, as well as refractory hypoxemia, and hemodynamic
instability. When we think about intubating a patient with asthma, we have to think about
cardiopulmonary interactions. The first cardio- pulmonary interaction that comes to mind is
decreased preload. The pre-load of a patient with asthma may be decreased because he has
been ill for a couple of days. He may have had decreased fluid intake, he may have had
an intercurrent illness, with fever, and he’s probably been tachypneic in the setting of
his asthma attack, leading to increased insensible water losses. Also, his lungs are hyper-inflated,
and that may provide some limitation to venous return. We also have to think about his pulmonary
vascular resistance. In a patient with an asthma attack who has a fair amount of bronchial
constriction, his pulmonary vascular resistance may be increased, and his right ventricle
may be stressed. The third interaction that comes to mind is the myocardium itself. Patients
with hypoxia and acidosis may have decreased myocardial contractility. So all are things
we have to keep in mind when we think about intubation of anasthmatic. Here is an image
of pulsus paradoxus. Panel A shows a tracing of pulsus paradoxus, whereas panel B shows
a normal arterial tracing. Pulsus paradoxus was described by Kussmaul, 1878, in Vienna,
in a patient with constrictive pericarditis .Patients with asthma may have pulsus paradoxus
as well. What Kussmaul actually found, paradox in a patient with pulsus paradoxus, is that
he had a regular precordial activity, but when he felt the pulse of that patient, during
inspiration, there was a decrease in pulse pressure and a decrease in pulse amplitude.
So pulsus paradoxus, in inspiration, there is a fall in blood pressure as you see on
the top graph. And why would a patient with asthma have pulsus paradoxus? A patient with
asthma has hyperinflation of the lungs, and that in and of itself may limit venous return,
and when, during inspiration, there is more venous return normally, the right atrium may
not be able to accommodate all that increased blood volume, and therefore the septum may
bow over to the left side, in this case, limiting left atrial preload, and left ventricular
preload, leading to a decrease in blood pressure. Often patients who are intubated with asthma
have a fair amount of pulsus paradoxus, which can lead to hypotension during inspiration.
So let’s talk about strategies for a tracheal intubation. We’ve talked about decreased preload,
so obviously we should consider giving a large volume bolus, like 20 cc/kg of normal saline
or20 cc/kg of Ringer’s lactate prior to intubation. When we think about induction agents, we should
avoid agents that are direct myocardial depressants. What we would typically use is an induction
agent like etomidate, or ketamine, followed by a little bit of fentanyl or versed. We
should avoid agents such as propofol, as they may lead to significant hypotension. As we
choose our endotracheal tube, we should use acuffed endotracheal tube, as we may have
to apply higher mean air pressures later during the course of ventilation, so that we don’t
have a leak around the endotracheal tube. So, at Children’s Hospital, we often use endotracheal
tubes that are cuffed even when they are as small as 3.5. Mechanical Ventilation. Let’s talk about ventilation of a patient
with asthma. Most patients have dynamic pulmonary hyperinflation, or in other words, gas trapping,
and you can see that on this panel here; the lower panel is a normal patient who’s breathing,
and in asthmatic lungs, you can see that there’s a fair amount of end-expiratory air that remains
in the lungs and that leads to air stacking, which means that every subsequent breath,
since the lungs are not emptied, stacks on the previous one, and over time, that leads
to a fair amount of air trapping, or auto-PEEP. Now, how can we measure auto-PEEP? Let me
take you through this for a second. During a normal patient, or in normal lungs, at the
end of inspiration, say the alveolar pressure is 20 cm H20, so at the airway opening we
also measure a pressure of 20 cm H20. Let’s look at the normal lungs in end expiration.
The alveolar pressure slowly declines until it reaches 0, and so at the airway opening,
we also measure a pressure of zero. Now let’s look at obstructive physiology, and you can
see the obstruction being marked here by this black obstruction of the airway. Again, at
inspiration, the alveolar pressure is, for example, 35, and, at the airway opening, such
as with pneumotach, we measure a pressure of 35. But now during expiration, since the
airway is obstructed, they may be still some air remaining in the alveolus, leading to
a pressure of about 15, as in this example, but as there is obstruction, the pressure
of the airway opening now reads zero. And only if you do anexpiratory hold, slowly the
pressure in the alveouls equilibrates through the obstruction with the pressure at the airway
opening, and then at the airway opening you will measure the real pressure, which is now
15. So to measure auto- PEEP in a patient who is intubated and ventilated, this patient
has to be either deeply sedated, or paralyzed, since you have to go through the expiratory
hold maneuver, and if a patient is not sedated, he is very tachypneic normally, then you won’t
be able to measure the auto-PEEP reliably. What are the general goals of mechanical ventilation?
As in every patient who’s mechanically ventilated, we have to ensure adequate oxygen delivery.
General strategies that also apply to a patient with asthma are to apply low tidal volumes,
about 5-6 per kg, to have some degree of permissive hypercarbia, to avoid excess plateau pressures,
those are pressures that are higher than 35 cm of water, in order to prevent barotrauma,
and we try to wean the oxygen so that we apply non-toxic oxygen concentrations. It’s really
not quite clear what that is in a child. We know that there’s well documented oxygen toxicity
in neonates, but we usually try to wean, even in children, the FiO2, or the fraction of
inspired oxygen, to less than 60%. The big question that always comes up in a patient
with asthma is: how much PEEP should we apply? There are a couple of teaching opinions that
are usually mentioned in textbooks. One classic teaching opinion is that we apply no PEEP,
and the rationale for that is, we say, okay, a patient with asthma already has a fair amount
of auto-PEEP, has a fair amount of air trapping, and so every additional PEEP will increase
air trapping, and this is for sure partially true. The other teaching opinion is that we
try to adjust the positive end expiratory pressure to match the auto-PEEP, for example,
if we measure an auto-PEEP of ten, we apply a PEEP of ten, and that comes mainly I think
from the thought that if a patient triggers on the ventilator, and in older times, those
ventilators had pressure triggers, he would have to generate a negative pressure at the
airway opening. In order to generate a negative pressure at the airway opening, with a fair
amount of auto-PEEP, the patient has to overcome the auto-PEEP and then would not be able to
trigger on the ventilator. So while it is true that extrinsic PEEP in a patient with
asthma may worsen air trapping, we also have to consider that positive end expiratory pressure
reduces the work of breathing, by splinting the airway open, and also PEEP prevents end
expiratory collapse in the alveolus. So typically our respiratory therapists carefully titrate
PEEP by observing tidal volumes, by observing end tidal CO2 and flow patterns. And this,
again, is a chest X-ray of a one-year-old patient with asthma, who is intubated, you
can see the endotracheal tube, and the lungs look quite hyper-inflated, you can see that
the diaphragms is relatively flat. But this is not the only pathology we observe here.
Perihilar, there is also a fair amount of atelectasis, there is peribronchial cuffing.
And where does the atelectasis come from? Well, most of these patients with asthma have
a lot of mucus, they have swelling of the mucus membranes, they have bronchial construction,
and over time they may have a viral or bacterial pneumonia. So, they don’t only have hyperinflation
but they also have atelectasis, and here is actually where PEEP can be helpful in restoring
lung volume. When we think about impaired gas exchange in a patient with asthma, we
have to think about hypercarbia and hypoxia. Hypoxia is coming from a patient who has atelectasis
that leads to a fair amount of V/Q mismatch, which is a mismatch of ventilation and perfusion,
and leads to intrapulmonary shunting, and intrapulmonary shunting is perfusion without
ventilation. The patient with asthma also has hypercarbia, and the hypercarbia is mediated
by air trapping, that leads to decreased alveolar ventilation, but the patient with asthma also
has increased pulmonary dead space, and again, intrapulmonary dead space is ventilation of
an alveolus without perfusion, and that probably comes through that the alveolus is hyper-inflated
and therefore, perfusion of that alveolus is impaired. How do we limit gas trapping
in a patient with asthma? There’s actually three fundamental ways we can do this. We
can: A. Administer a bronchial dilator, we can B. increase the expiratory time, and we
can C. decrease the tidal volume and decrease the minute ventilation, because if we have
lower tidal volume less air is going to get into the lungs and less air has to be exhaled,
so air trapping is reduced. Let me show you this effect of an increased expiratory time
here on this graph. On the top panel you can see gas trapping with an inappropriate expiratory
time, and you can see that the expiratory flow, delineated by this red circle, does
not decelerate to zero, so expiration in this patient is not complete. And if you shorten
the inspiratory time, at the expense of lengthening expiratory time, in the lower panel you have
a shorter inspiratory time and the expiratory time is longer, and the expiration is complete,
and you can see that because the expiratory flow reaches zero. Let’s look at the end tidal
CO2 waveform of a patient with asthma. On this side, on the left side, you can see a
normal end tidal CO2 waveform, so you can see a rapid upstroke of CO2, then it reaches
a plateau phase, and at the end of expiration you can see a red circle, and that is actually
when the end tidal CO2 is measured. And right next to it, you see an end tidal CO2 waveform
of a patient with asthma. You can see that there is a much less steep upstroke of end-tidal
CO2, and why is that? It is because the patient has airway obstruction. So, often in a patient
with asthma, the end tidal CO2 value you can get from the monitor can be inaccurate, because
again, it’s measured at the end of expiration, and in a patient with obstructive airway disease,
expiration at any time may not be complete. Inhaled Gases. Heliox is a very light and inert gas and it
has the potential to turn turbulent flow into laminar flow, and if you nebulize albuterol
with heliox, it has the potential that more albuterol is reaching the terminal airways
in a patient with asthma. Here you can see a set-up that is connected in an eighty-twenty
heliox cylinder, which means that this gas mixture contains 80% helium and 20% oxygen,
and then that drives the nebulizer, through which continuous albuterol is nebulized. Heliox
has also been used in patients with severe asthma exacerbations, just to use on the ventilator,
and this is an example of how heliox can be set-up with a ventilator. Instead of oxygen
and fresh gas, heliox is connected to the ventilator, and again, heliox often comes
in eighty-twenty mixes, which means 80% helium and 20% oxygen, or 70% helium and 30% oxygen.
In most ventilators, the oxygen calibration really gets out of range when heliox is used,
that’s why an external O2analyzer has been used to get the correct concentration of oxygen.
In some newer ventilators, the helium-oxygen mixture can just be plugged in. What about
inhalation anesthetics? Isoflurane is the preferred agent, and we know that it’s a strong
anesthetic agent, but also a strong bronchodilator, and hence it has been used in patients with
asthma. The primary effect is that you really get improved ventilation, due to its bronchodilatory
effects. But, there are pretty significant side effects that have to be considered when
isoflurane is used in the ICU, and those side effects are hypotension. Most patients with
asthma, once they have a severe asthma exacerbation, are at risk for hypotensive episodes, and
hence, we often place a central line before we start the patient on isoflurane, and we
also have a vasopressor or an inotrope, such as dopamine, ready to infuse in case the patient
has a drop in blood pressure. Here is how isoflurane can be administered. This is a
Servo 900C ventilator; at this point, you can see that the isoflurane vaporizer is attached
to it, and on top you see a monitor, through which the minimal alveolar concentration of
isoflurane can be measured. Sedating the Intubated Asthmatic. Let’s talk
about sedation once a patient is ventilated. The standard sedation regimen that we use
would be midazolam and morphine, because we use it in other patients who are ventilated
as well. In a patient with asthma, alternatives come to mind, for example, ketamine, because
ketamine has some bronchodilatory effects, as well as isoflurane for sedation because
it also has a bronchodilatory effect as we’ve seen before. With all sedation effects, you
have to consider that the patient has hemodynamic side effects, such as hypotension, and once
the patient is weaned off the ventilator, typically after he’s been on morphine and
midazolam for more than five days, you have to consider that the patient will withdraw
from those medications, so you have to taper, and wean the sedation accordingly. What about
neuromuscular blockade in a patient with asthma? We try, as with all patients, not to paralyze
patients with asthma on a ventilator, however sometimes, it becomes necessary when there
is a very pronounced patient- ventilator asynchrony. The complications that we are fearful of are
critical illness myopathies, especially when patients receive both steroids, as asthmatics
do, and neuromuscular blocking agents. The strategies we try to implement whenever we
paralyze a patient with asthma is that we give them a paralytic holiday, at least once
a day, and let him wake up, and show that he can move around a little bit, and we can
also use peripheral nerve stimulation to assess the deepness of paralysis. So let’s summarize
again what we talked about for ventilation during asthma. We try to use a strategy where
we have low tidal volumes and a low respiratory rate, again, a low respiratory rate to give
the patient a proper expiratory time. We can try to shorten the inspiratory time at the
expense of the expiratory time; that can help to make the expiratory time even longer, and
we have to constantly monitor for the development of dynamic hyperinflation and air trapping.
Thank you very much. That concludes our video on asthma. Thank you. Please help us improve
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4 thoughts on ““Asthma” by Gerhard Wolf, MD for OPENPediatrics

  1. Excellent video but it would be great to explain more about management of status asthmatics specially timing of nebulization and IV brinchodilators.
    Thanks

  2. Excellent presentation sir ,, could u please add more videos about cardiopulmonary interactions in different disease states “ heart disease , sepsis , croup , bronchiolitis, effusion empyema ?? Basics to specifics disease !!
    Thank u

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