Air leak or Air trapping?
Respiratory Failure & Mechanical Ventilation
Changing from square flow waveform to decelerating flow waveform with decreasing peak pressure
62 years old female who was intubated for acute on chronic hypercapnic respiratory failure secondary to COPD exacerbation. Her ideal body weight is 67 Kg. CXR shows severely hyperinflated lungs.
Patient was placed on AC mode of ventilation with VT of 450 mL, RR of 22 per minute, and an inspiratory flow of 60 L/min. Her minute ventilation was 10 liters per minute.
Blood gases revealed acute on chronic respiratory acidosis with pH of 7.22 and pCO2 of 75
An inspiratory hold maneuver was done and shown in the following screenshot:
I guess all the answers are right, the goal is to prolong the expiratory time to allow for complete exhalation of the air. I would start by increasing the flow rate trying to decrease the inspiratory time and I:E ratio without changing the minute ventilation. Then I would decrease the tidal volume and/or the rate and accepting permissive hypercapnea. Adding external PERP can help triggering on the ventilator as this would allow the patient to exert less efforts.
This screenshot shows an increased flow rate to 70 L/min, decreased rate to 14, and decreased tidal volume to 450:
inspiratory hold now shows improved plateau pressure to 22:
And expiratory hold shows improved autoPEEP to around 5-7:
Blood gases improved despite decreased minutes ventilation:
Ventilator graphic of an intubated asthmatic patient on mechanical ventilation showing mild persistent flow at end of expiration indicating auto-PEEP:
The ventilator settings were changed as the following:
VT decreased from 470 to 420 mL.
Rate decreased from 20 to 16 breaths per minute but the patient is still breathing over.
The inspiratory time was decreased from 0.9 second to 0.6 second.
Improving in auto PEEP , it can be achieved by :
1) decrease in RR ,
2) decrease in Tidal Volume,
3) by decreasing inspiration time, expiration time will be automatically increased.
PRVC mode of ventilation with a targeted VT of 400, RR 26 and I:E ratio of 1:1.5. Notice the dynamic hyperinflation (autoPEEP) with persistent flow at end of expiration and the ineffective triggers.
Ventilator settings were adjusted to allow longer expiration by decreasing the rate to 20 per minute, and decreasing inspiratory time with I:E at 1:2.9. The volume was also increased to 450 ml.
Dynamic hyperinflation improved remarkably and now the ventilator is triggered with every inspiratory effort of the patient.
In the first setting of ventilator, there were two issues discovered
1) Auto Peep due to low expiration time, leading to air trapping- Auto Peep, by decreasing RR expiration time increased lead to resolved the auto peep issue as shown in second picture.
2) The second issue discovered what I observed was “ Air Hunger or Starvation ” in flow time waves, which was resolved by increasing Tidal Volume or Peak flow.
Thanks Dr. Mazen for sharing such interesting articles.
As you know, patients with severe asthma and status asthmaticus develop dynamic hyperinflation syndrome and autoPEEP meaning that the inhaled air does not get exhaled completely and the pressure is built up inside the alveoli. This is caused by not enough expiratory time due to the high time constant of the airways. My question, what will happen next if the process continues?
How does dynamic hyperinflation progress if no change in the expiratory time made on the ventilator?
0%Continues to build till the lung ruptures
0%Stops on its own due to increased driving pressure
0%I do not know!
You may want to see this video to help you understand the concept.
It should stop when the higher elastic recoil caused by the hyperinflation permits the expiration to be be faster enough to be completed (provided this equilibrium takes Place within the limits of lung parenchima integrity otherwise barotrauma May result). Time constant (compliance x resistance) Is the core variabile.Shall we Say that the equilibrium Is found without barotrauma when the decrease in compliance can compensate for the increased resistance?and on the other end that we may have a PNX when the residence Is so High that the compliance required to balance It must be so low that in would require the lung to be that overstached that It goes beyond its limits?
47 years old female with status asthmatics who got intubated and placed on mechanical ventilation. An inspiratory hold was applied as shown in this snapshot of the ventilator screen:
Notice the limitation of the expiratory flow in the first breath before the inspiratory hold. Also notice that the peak pressure is elevated at 46 cm H2O, the plateau is elevated at 30 cm H2O and the difference is at 16 cm H2O representing the increased airway resistance due to bronchospasm.
What is the most likely explanation of the increased plateau pressure in this asthmatic patient?
0%Pneumonia
0%Pneumothorax
0%AutoPEEP
0%Lung collapse
You can vote for more than one answer.
What would you do next to confirm your diagnosis?
Here is a screenshot of the ventilator waveforms of the pressure, flow, and volume over time in this patient prior the the inspiratory and expiratory hold.
@Everyone
65 year-old male with acute respiratory failure secondary to pulmonary edema who was intubated and placed on mechanical ventilation. His course was complicated with left parietal occipital and temporal infarction. The following graphs have been observed;
Please identify the abnormality and answer the following question:
This patient-ventilator asynchrony is caused by:
0%Early cycling
0%Delayed cycling
0%Flow asynchrony
0%Malfunction
Please notice the volume over time scalar as indicated by the light orange arrow and provide your feedback:
@Everyone
Please select your answer and you may provide your explanation in the comment section.
The noticed abnormality is caused by:
0%Leak
0%Auto-PEEP
0%Malfunction
Please see comments for explanation!
So the main problem in the first breath is that the exhaled volume is less than the inhaled, then you would ask where did the air go, has it leaked or trapped, then if you look at the second breath, you see that the exhaled volume is more the than the inhaled indicating that the patient exhaled the trapped air from the first breath. The expiratory phase of the second breath is prolonged and patient had an inspiratory effort during it but was ineffective as he did not reach the trigger threshold.
Now, if this is trapped air in the first breath, why the flow did not persist at end of expiration? The answer is that he has a high central respiratory drive from massive stroke and his inspiratory efforts every 2 seconds cut off his expiratory flow and decreased to zero and in fact reached 3.66 L/min as you see at the dot and was able to trigger the ventilator for the second breath.
So this is trapped air or auto-peep.
here is what happened when I decreased the tidal volume to 450 from 540!
The respiratory drive is the intensity of the neural stimulus that determines how much the respiratory muscles contract. Excessive or low respiratory drive can be encountered in different clinical scenarios in patients on mechanical ventilation. High respiratory drive potentially leads to an injurious effect on the diaphragm (myotrauma), and on the lung (patient-self-inflicted lung injury). The low respiratory drive may cause disuse atrophy which leads to difficulty in weaning off the ventilator. Occlusion pressure at 100 ms (P 0.1) is the negative pressure measured 100 ms after the initiation of an inspiratory effort performed against a closed respiratory circuit and has been used as an indirect measure of the respiratory drive.
Please observe the P0.1 procedure and value in the. Above graph and provide your answer to this question:
What does a value of P0.1 of -3.5 indicate?
0%High respiratory drive
0%Normal respiratory drive
0%Low respiratory drive
0%Weak respiratory muscles
Sources of errors and potential pitfalls
There is a significant breath-to-breath variability of P0.1, and an average of 3–4 values of P0.1 in one patient in one clinical condition should be obtained to represent a reli- able index of respiratory drive . Range of values
In healthy subjects, P0.1 varies between 0.5 and 1.5 cmH2O . In stable, non-intubated patients with COPD, P0.1 varies between 2.5 and 5.0 cmH2O [3]. Ranges of P0.1 from 3.0 to 6.0 cmH2O have been reported in patients with ARDS under mechanical ventilation, and from 1.0 to as high as 13 cmH2O during weaning.
Ventilation strategy combining very low tidal volume (VT) with extracorporeal carbon dioxide removal (ECCO2R) is evaluated in patients with acute hypoxemic respiratory failure.
The effect of ECCO2R on mortality varies based on the ventilatory ratio (VR) and the severity of hypoxemia.
High VR (3 or higher) is associated with a higher probability of benefit and reduced mortality with the intervention.
Low VR (less than 3) is associated with a higher probability of increased mortality with the intervention.
The effect of the intervention also varies based on the severity of hypoxemia (PaO2:FiO2 ratio).
As the inspiratory pressure is fixed in Pressure Control Ventilation (PCV), when the patient starts breathing, transpulmonary pressure would be higher in pressure controlled ventilation compared to volume controlled ventilation, thus volume would be also higher.
There are two fundamental methods to control the delivery of a breath. The clinician can choose to keep either volume or pressure constant from breath to breath. The control variables most commonly used to describe modes of ventilation are volume-controlled (VC) ventilation and pressure-controlled (PC) ventilation. Within these two categories are multiple ways to tailor specific modes. In volume-controlled ventilator, clinician sets flow magnitude and pattern; the pressures used to deliver the set tidal volume will vary as a function of the patient’s pulmonary resistance and compliance and the his or her efforts in order to deliver that flow.
Air leak as tidal volume drops after 3rd breath to zero.