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Infants often require a shoulder roll to optimally align their airway for intubation.
Children can align well with their heads flat on a surface, adults might require a roll under their head to align their airway.
Placing child into sniffing position
Aligning the pharyngeal, oral and laryngeal axes
Create full seal of mouth and nose with an appropriately sized mask by placing mask on face and then pulling the mandible up towards you and the mask.
Can use one handed C-E hold, or two handed hold of mask with another operator squeezing the bag
Can place a nasal trumpet or an oral airway to move the tongue from obstructing the retropharynx
Consider nasogastric sump placement to decompress stomach and empty gastric contents (prevent emesis).
Flow inflating bag - MUST BE CONNECTED TO OXYGEN (10-15 L/min)
Self-Inflating bag - if simply placed on face, no air flow and can't do "blow by" with this device
Oral airway - size from center of mouth to the angel of the jaw/corner of the mouth to the earlobe
Nasopharyngeal airway - size from tip of the nose to the tragus of the ear
(A-a) = PAO2 - PaO2
Assessing the gradient can help determine the cause of hypoxia
Estimate of normal A–a gradient is less than [age in years/4] + 4
The 5 causes of hypoxemia:
Elevated A-a gradient:
V-Q mismatch (improves with 100% FiO2)
R to L shunt (does NOT improve with 100% FiO2)
Diffusion restriction
Normal A-a gradient:
Hypoventilation
Decreased Partial Pressure of O2 (scuba diving, high altitude, CO poisoning)
Used to assess severity of ARDS (see ARDS section for more information)
MV = Respiratory Rate x Tidal Volume
Total Dead Space ventilation (VD): ventilation that does not participate in gas exchange – physiological dead space is ~ 2ml/kg
Anatomic Dead Space: volume of conducting airways from nose to terminal bronchioles (and ventilator tubing if intubated) -- this is usually constant
Alveolar Dead Space: alveoli that are ventilated but not perfused -- this can change significantly in disease states and will cause an elevated ratio
CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.003)
Note that hemoglobin has more significant contribution to the equation and contributes more to the overall oxygen delivery.
See Shock section in CV for more on oxygen delivery vs demand
Decreased Inhaled O2
At high elevations above sea level, atmospheric pressure drops. (260mmHg on top of Mt. Everest) - decreased PaO2
Hypoventilation
CNS depression (sedatives, GBS, ALS)
Obesity
Neuromuscular disease
Rib fractures, Scoliosis
Diffusion limitation
Alveolar fibrosis
Will increase A-a gradient as alveoli can see high O2 but cannot get into blood stream
V/Q mismatch
Right to left shunt
Physiologic R-L shunt includes bronchial veins that drain into the pulmonary veins and Thebesian veins which drain coronary venous return into the LV
Extreme V/Q mismatch where there is no ventilation and only perfusion.
Shunts do not respond to O2
Usually does not affect CO2 clearance until > 50% shunt
Pathologic shunt can come from pneumonia, ARDS etc
Shunt vs Dead Space Ventilation
Two types:
1. Type 1 respiratory failure- failure to oxygenate
2. Type 2 respiratory failure – failure to ventilate/remove CO2 failure hypercapnia
- It is generally a clinical (and billing) diagnosis, defined by a patient requiring a higher level of respiratory support from baseline (any form of O2)
Signs & Symptoms:
Increased work of breathing, tachypnea, grunting, nasal flaring, and retractions
Signs of increased work of breathing are blunted in those with neuromuscular disorders and these patients instead present with tachypnea and shallow breathing without retractions.
What’s on a blood gas?
● pH, pCO2, pO2, a calculated bicarbonate value, and base deficit/excess
● Electrolytes (Na, K, Cl: not as accurate as an RFP but still helpful to trend; iCa and glucose: much more accurate and safer to intervene on)
● Lactate, mixed venous saturation (SvO2), and hemoglobin and hematocrit (much more accurate on a CBC, but still sometimes helpful to trend)
Can get an arterial sample (ABG) or a venous sample (VBG)
Mixed venous saturation (SvO2)
● A measure of the body’s oxygen consumption and is most accurately measured if sampled from the right atrium (RA)
● Normal SvO2 should be 75%, assuming the patient has normal lungs from which blood in the pulmonary veins that is sent out to the body via the aorta is 100% saturated, and knowing the body uses about 25% of the O2 it is supplied under normal conditions.
● A lower SvO2 may indicate increased oxygen consumption or demand (i.e. sepsis, anemia, fever)
A higher SvO2 may indicate increased oxygen delivery, decreased oxygen demand (i.e. if the patient is receiving 100% FiO2 or is currently sedated), or decreased oxygen extraction ability
Includes Low Flow and High Flow Oxygen Delivery Devices as well as Non-Invasive Positive Pressure Devices (CPAP, BiPAP)
Ensure optimal positioning and controlled environment for successful intubation
Effective bag mask ventilation is essential for ensuring patient safety
Equipment needed for intubation procedure:
Bag / appropriately sized mask
Suction
Appropriately sized ETT and backup 1/2 size smaller
CMAC /Laryngoscope
End Tidal monitor
Ventilator
Airway bag (with oral airways, LMA)
Push-pull IV fluid setup
Personnel (important to have team leader, proceduralist (fellow intubating), RT, Bedside RN, Charge RN, Attending
Pneumonic to remember the items to have during intubation
RSI - NO bag-mask ventilation meds are all rapidly given, followed by saline flush, patient receives passive oxygenation, and intubation is attempted
Modified RSI - pre-oxygenating the patient with 100% FiO2, often via bag-mask ventilation prior to intubation.
BMV with slow med administration
Optimal placement of endotracheal tube is between T1 and the carina (visualized on frontal CXR, ~ T4)
Neck flexion shortens the trachea and displaces the ETT downward
Neck extension elongates the trachea and displaces the ETT upwards
This is one reason we get daily CXR on intubated patients, to ensure safe ETT placement
Yan and Zhang. BMC Anesth. 2020
Indications
Respiratory failure not improved with non-invasive methods
Airway protection
Decrease overall metabolic demand in states of shock
Trigger - initiation of the breath. This can be time (set by ventilator) or detection of air flow change within the ventilator circuit (patient effort sets this)
Limit - what tells the ventilator to stop the inhalation part of the breath. This is flow, pressure or volume limited
Cycling - what tells the ventilator to switch to exhalation. This is time, flow, pressure or volume cyled.
PEEP- the amount of pressure in the aveoli at the end of exhalation - at "baseline" prior to next breath.
Nice description here by Deranged Physiology
Below is a visual representation of lung volumes during a respiratory cycle.
With invasive mechanial ventilation, you are converting the patient from NEGATIVE pressure ventilation to POSITVE pressure ventilation.
The effects of this on your cardiac and respiratory physiology is known as cardiopulmonary interactions. This will be explained in the section below on this page.
Below is a pressure volume curve. As volume increases in the lung, more aveoli are recruited and ultimately causes pressure to rise. The slope of how fast the pressure rises is the lung compliance. The steeper the sloop, the more compliant the lung.
Barotrauma can occur when you pass the upper inflection point, i.e, have increase in presure with no additional increase in volume. This is often referred to as "beaking."
Two main forms of ventilation:
Pressure Control (PC) - you guessed it, you tell the ventilator what PRESSURES you want. Volume is variable since you are only controlling the pressure. Pressure is maintained for the duration of the inspiratory phase.
Volume Control (VC) - you guessed it, you tell the ventilator what VOLUME you want. Pressures needed to generate this volume vary. Set the volume, and once that is reached in the breath, then the ventilator cycles to exhalation
Typically two ways the ventilator supports each breath: SIMV (synchronized intermittent mandatory ventilation) and Assist Control (AC)
SIMV - the ventilator synchronizes mandatory breaths with patient’s spontaneous breaths
Ventilator will not give a breath while patient is trying to exhale or immediately after the patient has just taken a breath. The patient's spontaneous breaths are only supported with additional pressure support, but no guaranteed tidal volume or rate
AC - every breath, whether mechanical or spontaneous (by the patient) is fully supported
Ventilator modes combine SIMV/AC with PC or VC. Visualizations of these are below.
Common modes of ventilation
SIMV - Pressure Regulated Volume Guaranteed/Volume Control (PRVG/PRVC)
The most commonly used ventilator mode used in the PICU
Ventilator will adjust pressure needed to provide desired tidal volume
Benefit of having the "decelerating flow" pattern of PC, but able to manipulate a patient's minute ventilation.
Also lower overall PIP when compared to traditional VC modes. Will need to monitor PIP though as not setting pressure to achieve volumes.
Patient will get set PS when taking spontaneous breaths above the set rate
Each breath stops (cycles off) when the airflow reaches 30% of maximal flow
Set: Rate, PEEP, Tidal Volume, Pressure Support, FiO2, iT, max PIP
SIMV - Pressure Control Ventilation (PCV)
Ventilator gives each breath with a pressure above the PEEP (the pressure control, PC)
PIP will be PEEP + PC for mandatory breaths
Tidal volume will be variable as you are no longer dictating a tidal volume. Report tidal volumes patient pulls
Each breath stops (cycled off) by the set inspiratory time
Set: Rate, PEEP, PC, FiO2, iT
SIMV - Volume Control Ventilation (VCV)
Ventilator will deliver a set volume using whatever pressure is required - must monitor PIP as will change with each breath
Set: Rate, PEEP, Tidal Volume, FiO2, iT, PIP max
Pressure Support Ventilation (PSV)
All breaths are patient generated and supported with extra pressure support. Weaning ventilator support.
Monitor patient’s RR, tidal volumes, work of breathing, SpO2 while on the pressure support trial to assess patient distress.
Set: PEEP, PS, back-up rate, FiO2
Airway Pressure Release Ventilation (APRV)
Continuous postive airwya pressure (CPAP) with intermittent release phase
Have a CPAP (P high) for a set amount of time (T high) to maintaine FRC and alveolar recruitment
Then have time-cylced release phase at a low pressure (P low) for a short period of time (T low) where ventilation/CO2 removal occurs
Set: Phigh, Plow, Thigh, Tlow, FiO2
APRV Pressure vs Time
Cardiac:
Remember oxygen is a vasodilator and giving O2 to a cardiac patient with lesions that unbalanced pulmonary to systemic circulation (e.g HLHS) can result in increased pulmonary blood flow and decreased systemic flow.
SMA:
Due to neuromuscular weakness, will not clinically display increase in work of breathing even when ill
Administering oxygen without optimizing ventilation may mask hypercarbia/worsening hypercarbic respiratory failure
Optimize airway clearance and ventilation strategies prior to increasing FiO2 in hypoxemic SMA patients
Ventilator alarming? Patient’s SpO2 suddenly worse? What to do?
Go to the bedside!
Call RT & Call your Fellow/Attending
Disconnect patient from the ventilator and bag with anesthesia bag and 100% FiO2
Determine the issue with the help of the DOPE pneumonic!
Patients are assessed daily via an Extubation Readniess Protocol to see patient is on low amounts of mechanical ventilation and thus qualify for a trial of PSV.
Other things to consider when determining if you patient is ready for the ETT to be removed are:
Very important for PICU patients to treat atelectasis and mobilize/clear secretions
Typically contraindicated in severe TBI patients & after some surgeries
Not effective for asthma or bronchiolitis
Try to time BH with nebulizer treatments and in between feeds, if able
Types of Bronchial Hygiene:
PDs: Manual chest percussion to help loosen up secretions
Vibes: A vibrating tool that works similar to PDs
High Frequency Chest Wall Oscillation (Vest): A device that is wrapped around the patient’s chest and vibrates at a high frequency in 5 min intervals to help loosen up secretions
EZPAP: Positive pressure is provided while the patient breathes spontaneously to improve/prevent atelectasis.
Cough Assist: Used on patients who have a poor/weak cough -- provides alternating positive and negative pressure to mimic coughing and loosen/mobilize secretions.
IPV (intrapulmonary percussive ventilator): Used on intubated patients; provides rapid low volume breaths to help with mucus clearance. Should not be used on patients at risk for PTX/obstructive processes (eg. asthma)
Bag Lavage Suction: Small amount of saline is bagged into the patient’s lungs followed by suctioning. Can help clear out thicker, copious secretions. Used on intubated/trached patients.
New 2023 Guidelines here (with Rainbow’s own Drs. Shein & Cheifetz!)
Definition: Rapid onset of respiratory failure with hypoxemia in conjunction with severe pulmonary or systemic inflammation.
Direct causes: pneumonia, aspiration, inhalation, lung contusion, and mechanical ventilation.
Indirect causes: sepsis/multi-organ dysfunction syndrome, pancreatitis, multiple trauma, severe burns, major surgery, and ischemia-reperfusion injury.
Main goals: reversal/treatment of the underlying cause, support of organ function, and mechanical ventilation until patient improves
Overall ventilator concept is lung protective
Tolerate hypercarbia (pH >7.2), hypoxemia (>88%) to help prevent toxic ventilator settings
Consider prone positioning in severe cases
Avoid/treat fluid overload, use NMB if needed (especially early on)
Corticosteroids, iNO, surfactant, etc. are generally not recommended. Corticosteroids and iNO are sometimes considered in cases of severe pARDS
ECMO is useful for severe ARDS (OI > 40)
Summary of Management Recommendations from 2023 PARDS Guidelines
Summary of Management Recommendations from 2023 PARDS Guidelines Continued
Definition: an extreme form of asthma exacerbation characterized by hypoxemia, hypercarbia, and secondary respiratory failure. All patients with bronchial asthma are at risk of developing this
~ 190-200 deaths/per in US
6.2% of children in US have asthma
> 1 million ER visits a year
Clinical Presentation:
Tachypnea, increased work of breathing with retractions, forced exhalation, unable to speak, wheezing (or "silent chest" due to lack of air flow), tachycardia, hypoxemia, encephalopathy
on CXR, will see hyperinflation of the bilateral lung fields with flattened diaphragms
May also see pulsus paradoxus on pulse oximetry
Decrease in SBP by > 10 mmHg with inspiration (can also see in cardiac tamponade)
Due to large intrathoracic negative pressure, increased preload, bowing of the interventricular septum into the LV, reducing LV preload
Also large intrathoracic negative pressure increased LV afterload and thus decreaed SBP
Pathophysiology of Asthma
Goals of Treatment:
reverse bronchospasm
reduce inflammation
improve work of breathing
improve ventilation and oxygenation
These goals are achieved with bronchodilators, systemic steroids, non-invasive ventilation, and …TIME.
In the RBC PICU we have a protocol for patients with asthma, called the Asthma Care Path in the PICU (almost all Children’s Hospitals have similar protocols). Our Respiratory Therapists score patients and administer medications in the PICU.
Initial treatment:
First line treatment: Albuterol, systemic steroids, +/- Magnesium sulfate, ipratropium, isotonic fluid resusciatation
IV fluid can help augment cardiac output due to elevated PVR, dehydration, improve V/Q mismatch
Second line treatment: BiPaP -great if patient has worsening work of breathing
can receive continuous albuterol through BiPaP mask
Third line treatment: terbutaline/aminophylline, Heliox, ketamine
Fourth line treatment (severe cases): invasive mechanical ventilation, inhaled anesthetics, ECMO
A note on IMV (i.e. intubation)- only performed in extreme circumstances because patients are at incredibly high risk for cardiopulmonary arrest. It is also incredibly challenging to ventilate asthma patients on a ventilator because can't mimic the rate and large tidal volumes they were taking prior to being in extremis. Absolute indications for invasive ventilation in asthma include apnea, cardiopulmonary arrest, and acute encephalopathy.
Ventilator Strategies: Beyond the scope of this website, but in general large tidal volumes, generous pressure support, low PEEP or 0 PEEP, low respiratory rate. Need to monitor plateau pressures to be cognizant of barotrauma/risk of pneumothorax (PIPs not reliable/accurate of alveolar pressure)
Pictorial representation of PIP vs Plateau Pressures
caused by resistance to airflow in the non-conducting portions of the airway --> supraglottic, glottic, subglottic and tracheal
Causes: croup, vocal cord dysfunction, subglottic stenosis, tracheal/laryngomalacia, epiglottis, angioedema, anaphylaxis, burns, foreign body, post-operative edema from T+A, sedation, poor airway/muscle tone, laryngeal web/mass
Symptoms: stridor, tripod positioning, drooling, suprasternal retractions, hypoxemia, snoring
Treatment: racemic epinephrine, steroids (Decadron), Heliox, and ultimately intubation
What is helilox?
Mixture of helium and oxygen of various blends: 80% Helium/20% Oxygen or 70% Helium/30% Oxygen
Really requires > 70% helium to be beneficial, so may have limited use in hypoxemic patients requiring more than 30% FIO2
Mechanism of Action: Helium is less dense than nitrogen and oxygen. Decreasing the density of the air flow helps promote laminar flow → less resistance → decreased work of breathing.
■ This reduces a patient’s Reynolds number --> the lower the number, the more laminiar the fluid/airflow is
Definition: typically viral infection causing inflammation of the lower respiratory tract in children < 2 years of age and can present with signs of symptoms of respiratory distress, ranging from mild to life-threatening
Pathophysiology:
Typical viruses: RSV (most common), rhinovirus, parainfluenza, human metapneumovirus, adenovirus
Infects epithelial cells can causes cell death/edema leading to air trapping, increased mucous production, atelectasis, increased work of breathing and imparied ventiation
Treatment:
Mostly supportive care (frequent nasal suctioning, IVF, fever/pain control, close monitoring)
SpO2 goals > 92% but < 97%
Can be with low flow or high flow nasal cannula, as well as non invasive positive pressure (see earlier discussion on these on this page)
Can trial bronchodilators and steroids in select patients
For apneas, cardiopulmonary instability, or severe respiratory distress/acidosis, may warrant invasive mechanical ventilation
New vaccines on the horizon!
***lots of work done by Intensivists in our own RBC Group. Check them out!***
Shein SL, Slain KN, Rotta AT, Milési C, Cambonie G. High-flow nasal cannula flow rate in young infants with severe viral bronchiolitis: the question is still open. Intensive Care Med. 2019 Jan;45(1):134-135. doi: 10.1007/s00134-018-5474-4. Epub 2018 Nov 27. PMID: 30483835.
Shein SL, Slain KN, Clayton JA, McKee B, Rotta AT, Wilson-Costello D. Neurologic and Functional Morbidity in Critically Ill Children With Bronchiolitis. Pediatr Crit Care Med. 2017 Dec;18(12):1106-1113. doi: 10.1097/PCC.0000000000001337. PMID: 28930814.
Clayton JA, Slain KN, Shein SL, Cheifetz IM. High flow nasal cannula in the pediatric intensive care unit. Expert Rev Respir Med. 2022 Apr;16(4):409-417. doi: 10.1080/17476348.2022.2049761. Epub 2022 Mar 7. PMID: 35240901.