Respiratory Failure & Mechanical Ventilation
Dear Sir,
Excellent graphics presentation in simple way and easily understandable.
Airway obstruction is most likely due to endotracheal from the blood stained secretions, which is indicated to be changed as soon as possible.
Ventilator initiated breath with positive pressure of about 17-18 cm H2O (controlled breath but notice the flow #4 and the volume #6)
Pressure dropped from 18 cm H2O to -10 cm H2O as a result of patient's effort
Ventilator breath triggered by patient's efforts in #2 (assisted breath with slightly higher pressure than #1; pressure regulation)
Very minimal inspiratory flow associated with breath #1(positive pressure but no flow)
Very high flow (about 100 L/min) generated as the result of patient's effort in the second breath in association with the assisted breath.
Hello, just yesterday, I had a patient with very high PIP, which did not exceed 40 cmH2O because the maximum pressure (Pmax) was set at this level. The flow vs. time scalar displayed no inspiratory and expiratory flow, and the etCO2 was about 120 mmHg. We found copious fluid secretion in the ETT. After ETT suctioning, everything normalized (PIP, inspiratory and expiratory flow started displaying on the ventilator monitor, and etCO2 normalized). Unfortunately, I had to attend to the situation, and I did not take a screenshot of the ventilator.
VT 1200
Rate 40’s
Minute ventilation of 45 liters.
The highest I have ever seen!
Patient's expiratory effort during ventilator inspiratory phase
Patient's inspiratory effort during expiration
Red arrow: expiratory effort during inspiration. Green arrow: inspiratory effort during inspiration in a PC mode of ventilation. @Ibrahim Ameen
Air leak or Air trapping?
69 years old with anoxic encephalopathy and acute right parietal infarct after cardiac arrest. On Volume control mode of ventilation with VT of 510 breathing
What do you think?
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:
Age/gender : 54y/o male
📝 Diagnosed as ARDS, H1N1 positive, later found to have ICH
🗂️ Medical history : Nil
🏋🏻♂️ Adm wt.60kg, ht.168cm.
Current wt: 54.0
Interesting answers, it looks like this is a case of delayed cycling indicated by increase inspiratory flow at end of inspiration in every single breath. Notice the increase in volume at the same time. This may lead to double triggering if the inspiratory negative pressure continued and was at the level to trigger another breath. However, we need to rule out reverse triggering by applying expiratory hold and notice if these efforts disappear. If they disappear then the answer to the question would be resuming paralysis, if they did not then we need to shorten inspiratory time on the ventilator first and re-evaluate.
67 year old who eas intubated and placed on the ventilator for COPD exacerbation. Respiratory rate increased from 13 to 142 per minute
What should you do?
Your next step is
0%Decrease trigger sensitivity
0%Increase inspiratory time
0%Sedate the patient
Thank you all for your answers, this is auto cycling due to low sensitivity responding to heart pulsation.
64 years old male who is a heavy smoker with COPD and laryngeal carcinoma, s/p tracheostomy. He is addmitted now to the ICU complaining of air hunger. When connected to the ventilator; it showed the waves you see and the patient felt suffocation. Unfortunately, this is the only screenshot that was provided by Dr. Abdulhaseeb Tarabulsi.
Knowing that this is not a ventilator malfunction or circuit disconnection, what do you thing is happening?
With this huge leak, I think tracheo-bronchial fistula is very likely and should be investigated
Suction me please!
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.
How do you explain the the drop in the pressure indicated by the white arrows on the pressure/time scalar?
@Everyone
Please answer the question and provide your input in the comment section!
The drop in the pressure on the pressure waveform is caused by:
0%Ventilator malfunction
0%Double triggering
0%Patient’s inspiratory efforts
0%Early cycling
having this phenomena in each breath at the same time will trigger me to find if it is a type of reverse trigger or just additional inspiratory efforts that do not cause another trigger.
the scalar does not show if the initiation of the cycle is triggered by time or by the patient.
Reverse trigger may manifest by a nigative deviation in the pressure wave after the beginning of the inspiration by the ventilator. However, the initial trigger should be time.
I tried to compare the total frequency to the set frequency. They are not the same, 41 vs 24, which may indicate that its not time triggered but patient triggered. If this is true then it is not a reverse trigger.
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.
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
65 years old with submasdive pulmonary embolism, DVT, atrial flutter, and non-ischemic cardiomyopathy. Intubated and placed on mechanical ventilation at night (A/C mode VT 500, Flow of 50, RR 22 and PEEP 5). The following was observed during the morning round:
Based on the pressure over time waveform, how would you approach this case?
What would you do next?
0%Increase flow
0%Decrease flow
0%Increase tidal volume
0%Increase fentanyl
You can vote for more than one answer.
Please see comments for the answer!
And this is at 80 liters per minute then we increased fentanyl and much improved.
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.
Please examine the pressure and flow waveforms in the above graph and determine the abnormality:
What is the abnormality in the above waveforms?
0%Oscillations due to vibration device
0%Airway secretions
0%Ventilator malfunction
Observe the flow/time and the volume/time waveforms, compare with the flow/volume loop and make your diagnosis:
What is your diagnosis?
0%Auto PEEP
0%Air Leak
0%Ventilator malfunction
Please notice that the exhaled volume is lower than the inhaled volume but there is no persistent flow at end of expiration indicating that this is air leak.
Double-triggering seen in flow and volume waveforms from volume-controlled ventilation. Continued subject effort during the second breath causes the airway pressure to drop below the trigger threshold, which initiates an additional “stacked” breath. Note the large increase in peak airway pressure caused by the stacked breath and the high peak expiratory flow following the stacked breath.
How can you explain the pressure/time and flow/time tracings in the above scalars?
..so no "technical problem" rathar my technical ignorance about HFV... Very interesting post! It would be nice to have a webinar about HFV. I 've no experience with such a modality, apparently It's not very popular now as It was in the past. In the hospital where I work we don t even have the equipment required to deliver It. According to prof Gattinoni in a recent webinar it's Just a metter of time and it'll reagain the deserved attention. What Is your point of view?
Decreasing plateau pressure with inspiratory hold in a patient with a pneumothorax and chest tube in place indicating continued air leak!
Dr Kherallah this was very helpful. can you also do an example of using volumetric capnography to measure peep and explain the concept of P0.1 in measuring respiratory drive and vent weaning.