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Ventilators Part 2

Alexandra Wilson MD

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Topics

APRV/Bilevel
VDR
Complications of mechanical ventilation
Weaning the ventilator
Summary
NIPPV
HFNC

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Bi-level

Can be thought of as giving a patient two different levels of CPAP
Set “high” and “low” pressures with release time
Length of time at “high” pressure greater than length of time at “low” pressure
By “releasing” to lower pressure, allow lung volume to decrease to FRC

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APRV/BILEVEL

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APRV settings

Flow

P_aw

T_high

T_low

P_high

P_low

insp

exp

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Bi-level

P-high = oxygenation

-set ~ 125% current MAP

Time high 2-5 sec
P low = 0
T low 0.2- 0.8 sec

end when peak expiratory flow reaches between 25% and 50%.

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Initial Settings

	Neonates	Peds	Adults
P high	2-3> MAP	2-3>MAP	2-3 >MAP
P low	0	0	0
T high	2-3	2-5	4-6
T low	0.2-0.3 *	0.2-0.8*	0.5-0.8*

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APRV/Bilevel: adjusting

To improve oxygenation?

A. increase P high and T high

B decrease p high and T high

C increase T low

To improve ventilation?

A. decrease P high and T high

B. decrease T high

C. increase T low

To improve oxygenation and ventilation?

increase P high
decrease P high
Increase T high

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wean= “drop and stretch”

Decrease PHigh by 1.0 – 2.0cm H20 as tolerated
Increase THigh by 0.5 – 1.0 second as tolerated.

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Case 4

You are caring for a 9 mo with RSV+ bronchiolitis on Bilevel (APRV). Their last ABG is 7.24/60/55/24 . What would you like to do?

Increase P high
Increase T high
Decrease P high

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VDR:Volumetric Diffusive Ventilation

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THERE ARE 3 TYPES OF HIGH FREQUENCY VENTILATION.

The VDR4 is a pneumatically powered, high frequency percussive, bi-level ventilator. Exhalation happens with every micro breath.

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What is so different about this ventilator?

Ventilation:

Works well ventilating multiple lung types:

bronchospastic
atelectactic
inflamed (ARDS)
hyper-expanded.

Oxygenation:

Adding kinetic energy (Percussion) will aid with molecular diffusion (gas exchange).

Secretion removal:, sputum, soot

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Starting the VDR

VDR

Pulsatile flow rate (PIP) = CV titrate to chest expansion
PEEP (as OCPAP) = CV setting, adjust to 9 rib expansion
Respiratory Rate = CV settings
Pulse Frequency = 500-600 pulses per minute

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Titration of the VDR

For Treatment of Hypoxemia – increase the MAP

Increase OCPAP
Increase Pulsatile Flow
Increase Pulse Frequency (if CO_{2 o} ok)

For Treatment of Hypercarbia – increase ventilation

Increase Pulsatile Flow
Decrease Pulse Frequency but (if SpO₂ ok)

For Treatment of Hypocarbia – decrease ventilation

Increase Pulse Frequency
Decrease Pulsatile Flow

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Knowledge check

Patients in APRV (Bilevel) should receive NMB

True
False

Patients with severe pneumonia and purulent secretions are good candidates for HFOV

True
False

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Ventilator complications

Ventilator Induced Lung Injury

Oxygen toxicity
Barotrauma / Volutrauma

Peak Pressure
Plateau Pressure
Shear Injury (tidal volume)

Positive pressure ventilation can be injurious to the lungs, which were designed as a negative pressure circuit. What exactly qualifies as a dangerous pressure or even what is the best pressure to follow is not exactly known. Recently, a plateau pressure of >35 mmH₂O has been proposed as a limit. Plateau pressures are measured during an inspiratory “pause” - the lungs are kept inflated but there is no gas flow occurring. Also, recent studies have demonstrated that cyclic overdistention/collapse of an alveolus can contribute to lung injury by causing the release of inflammatory mediators. You want to keep the alveolus on the steep part of the compliance curve - not ride between the bottom plateau and the upper plateau .What constitutes a safe FiO₂ is also not exactly known. 0.60 is an acceptable limit to some, albeit arbitrary. Oxygen toxicity results in the production of free radicals with resulting cell damage and death.

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Barotrauma

High airway pressures during PPV can cause lung over distension with gross tissue injury.
This injury can allow the transfer of air into the interstitial tissues at the proximal airways.
Clinically, barotrauma presents as pneumothorax, pneumomediastinum, pneumopericardium, and subcutaneous emphysema.

Slutsky, Chest, 1999

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Volutrauma

Lung overdistension can cause diffuse alveolar damage at the pulmonary capillary membrane.
This may result in increased epithelial and microvascular permeability, thus, allowing fluid filtration into the alveoli (pulmonary edema).
Excessive end-inspiratory alveolar volumes are the major determinant of volutrauma.

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Lowered Expectations

Permissive Hypercapnia

accept higher PaCO2s in exchange for limiting peak airway pressures and tidal volume
can titrate pH as desired with THAM or sodium bicarbonate

Permissive Hypoxemia

SaO2 88-90% in exchange for limiting FiO2 (<.60) and PEEP
can maintain oxygen content by keeping hematocrit > 30%

What is an acceptable level of P_aO₂ or P_aCO₂ ? Like so many things in life, an acceptable level is often determined by what you are willing to do to get there. Ideally, a patient should have a S_aO₂ greater than 95%. If this can be accomplished with a PEEP of 7 and an FiO₂ of <0.60, that would be acceptable. If achieving a S_aO₂ greater than 95% means that the PEEP is 12 and the FiO₂is 1.0, this is not acceptable. Along these same lines, if achieving a P_aCO₂ of 40 mmHg results in a peak pressure of 30 mmH₂O, this is acceptable. Peak pressures greater than 35-40 mmH₂O are not as acceptable. In general, the upper limit for an acceptable FiO₂ is 0.60; peak pressures ideally would be less than 35-40 mmH₂O; PEEP should probably be kept at 15 mmH₂O or less. Recognize that these limits are arbitrary in nature and no study has ever demonstrated what a safe PIP or FiO₂ is. Furthermore, these “limits” must be made in the context of the patient’s clinical situation and expected clinical course.

When you reach your limits with the ventilator, you must decide to either exceed these limits or change your goals. P_aCO₂ is somewhat easier to deal with.Hypercarbia in of itself does not pose much danger (CO₂ narcosis should not be of concern for a patient on a ventilator). It does result in a respiratory acidosis. One must decide what pH they will accept. Some may accept a pH of 7.20, other 7.30, still others in between or even lower than 7.20. You can buffer the pH with bicarbonate or let the kidneys do it for you and accept the metabolic alkalosis. Again, the clinical situation must be taken into account - you will not accept the same P_aCO₂ for the child with ARDS as you would for the child with head trauma. You may also want a normal pH if the patient is receiving vasopressor support.

Oxygen can be somewhat trickier. The body has a significant ability to tolerate decreases in oxygen delivery without a change in oxygen consumption. When this changes however can be difficult to predict, especially in critically ill patients, who may have altered delivery-consumption relationships. Recall that contributes very little to oxygen content. Also, increasing the S_aO₂ from 90% to 95% increases oxygen content by 6% but may require significant increases in ventilatory support. If you increase the hemoglobin from 9 mg/dL to 12 then you have increased oxygen content by 33%. For this reason a S_aO₂, of 88-90% may be tolerated if an acceptable hematocrit is maintained. Again these numbers are arbitrary and this strategy has never been proven to decrease mortality. For the patient in shock, you may want a greater than 93%. For the patient with cyanotic heart disease, a of 70% may be acceptable. Decide what you want and what you will pay (or what the patient can pay).

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Complications

Cardiovascular Complications

Impaired venous return to RH
Bowing of the Interventricular Septum

🡺decrease preload

LV afterload is decreased (good)
RV afterload (decreased or increased)

Increasing the intrathoracic pressure, as mechanical ventilation does, has several effects on the heart. First and foremost, it decreases venous return to the right side of the heart and subsequently to the left side of the heart. Patients may need a higher CVP to maintain cardiac output. Positive pressure also causes the interventricular septum to bow to the left, which decreases the filling capacity of the left ventricle and thus its output. Positive pressure does decrease the afterload the LV faces. This can be of use in patients with left heart failure. The effects on right sided afterload depend on the lung volumes. If positive pressure increases the total lung volume to FRC then pulmonary vascular resistance will decrease (as hypoxic vasoconstriction is relieved) and right sided afterload will decrease. If positive pressure increases lung volumes beyond FRC, then overdistended alveoli will compress blood vessels, increasing PVR and right sided afterload.

More often than not, a patient will have decreased cardiac output when on positive pressure. This can often be ameliorated by fluid administration. The degree of cardiac compromise may often limit the amount of PEEP a patient can tolerate and hence what you are willing to use.

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Complications

Other Complications

Ventilator Associated Pneumonia
Sinusitis
Sedation
Risks from associated devices (CVLs, A-lines)
Unplanned Extubation

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Extubation

Weaning

Is the cause of respiratory failure/or other disease requiring ventilation gone or getting better ?
Is the patient well oxygenated and ventilated ?
Can the heart tolerate the increased work of breathing ?

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Extubation

Weaning – depends on the mode

What you want to do is decrease what the vent does and see if the patient can make up the difference….

Weaning is really the transfer of demands from the ventilator to the patient. By decreasing the rate, the FiO₂ and the PEEP, you are asking the patient to do more. The rate at these parameters are decreased will often depend on the acuity of the disease process. The patient who was intubated because of sedation secondary to a drug overdose may wean rapidly when they are awake as compared to the child recovering from ARDS who may take weeks to completely wean from mechanical ventilatory support. The rate can be decreased in increments of 2-5 breaths/minute (or more) as dictated by the clinical situation. An arterial blood gas or end tidal CO₂ monitor can be used to assess the P_aCO₂ after these changes. PEEP is generally lowered in increments of 1-2 mmH₂O per change. As changes in oxygenation or ventilation may not be immediately apparent after a decrease in PEEP, these changes are not made more often than every 6-8 hours. [fair statement?]

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Extubation

Extubation

Control of airway reflexes
Patent upper airway (air leak around tube?)
Minimal oxygen requirement
Minimal MV *
Make sure pressure support is not excessive *
“Awake ” patient
SBT

* in CV

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Summary

Don’t wait until your patient is in respiratory failure to start resp support
Match the patient’s clinical status to the appropriate mode of support
When addressing ventilator issues think about what you are trying to achieve

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Summary

Remember what changes oxygenation/ventilation when you are presented with a blood gas
Don’t be stubborn… reevaluate your patient and be prepared to move on to next level of support
Remember the RTs are your friends!