Dead of Night shift

http://en.wikipedia.org/wiki/File:DeadOfNight1.jpg

After six years of being a day walker I have returned to my origin as a night shift healthcare provider. I enjoy the pace and the autonomy of night shift however, it is sometimes torturous. 

I feel like “Walter Craig” in the 1945 British film “Dead of Night”, in which the character experiences a recurring nightmare with the same cast of house guests. Instead of “Pilgrims Farm” I’m stuck in a hospital interacting with it's own recurring cast of personalities; the non-compliant patient, the substance abuse patient, the medical resident who thinks he’s M.D. “House”, the nurses who are fueled on cigarettes & Red Bull.  Yes, I’m dead of night shift; indifferent, cold, and apathetic. Additionally, night shift is slowly killing me.

Night shift work has been associated with a number of maladies including:

Metabolic syndrome [1& 2]

Increased vascular stress [3 & 4]

Induced Apnea [5]

In regards to me it is vitamin D deficiency. Yearly, I have a few blood tests performed to check for abnormal values. Before returning to night shift my previous vitamin D levels were normal, I lived in the Midwest, and had no additional vitamin D supplementation. After starting night shift I began supplementing my vitamin D intake with 1000 micro units/day & I also moved to the east coast (more sun), conversely my results were below normal. I always have these test performed in February, so the amount of sunlight/day/month is not a factor.

[1] Biggi, N. et. Al. (2008). Metabolic Syndrome in Permanent Night Shift Workers. Chronobiol Int.

[2] Pietroiusti, A. et. Al. (2010). Incidence of Metabolic Syndrome Among Night-Shift Healthcare Workers. Occup Environ Med.

[3] Lo, SH. et.al. (2010). Working Night Shift Causes Increased Vascular Stress and Delayed Recovery in Young Women. Chronobiol Int.

[4] McCubbin, JA. et. Al. (2010). Blood Pressure Increases During a Simulated Night Shift in Persons at Risk for Hypertension. Int J Behav Med.

[5] Laudencka, A. et. Al. (2007). Does Night-Shift Work Induce Apnea Events in Obstructive Sleep Apnea Patients? J Physiol Pharmacol.

Setting Ventilator Alarms Diagnostically

Many practitioners set alarm thresholds thoughtlessly due to the fact that many ventilators do a poor job of filtering alarm nuisances versus 'high-risk' alarms. Many times I see the high respiratory rate alarm set at threshold in which the patient would have severe air trapping and dynamic hyperinflation before the alarm threshold is met.

When using controlled modes of ventilation (VC-CMV & PC-CMV) it is extremely important to set the high respiratory rate alarm threshold appropriately.

During both machine and patient initiated breaths the inspiratory time is fixed, so any additional breaths takes away from the expiratory time which can quickly lead to a inverse inspiratory-to-expiratory (I: E) ratios.

How to set the High Respiratory Rate Alarm Diagnostically

In patients with obstructive airway disease I prefer to set my high
respiratory rate based on a 1:1, I: E ratio. 
That is when the patient sets off the high respiratory rate alarm I know that they are breathing at a 1:1 ratio and that any additional breaths will be an inverse I: E ratio, putting the patient at a increased risk for dynamic hyperinflation.

This is easy to calculate based on the patient's set inspiratory time.

Formula: x = 60/(I-time * 2)
X (high respiratory rate alarm)
60 (total cycle time)
I-time (machine set I-time)

A common I-time is 1.0 second this would equal a high respiratory rate alarm of 30 breaths/minute. This stays the same if the set rate is 8 or 25; the 1:1 threshold is at 30 breaths/min.

The 0.25 Second difference

If air trapping is a concern just decrease the I-time.
A 0.25 second change is significant. 


Decreasing the I-time from 1.0 second to 0.75 second increases the
alarm threshold to 40 bpm.

Low Peak Inspiratory Pressures During Adaptive Pressure Control Ventilation: an Indication for Weaning

Low Peak Inspiratory Pressures (PIP) during Adaptive Pressure Control (APC) may be a sign of distress in patients with increased inspiratory efforts (e.g. high metabolic rate, sepsis, and hypercapnea) [1], or may be a sign that the patient is ready for spontaneous breathing trials.




In the patient that is not in distress and the PIP is low (≤ 15 cmH20) consider evaluation for liberation. If the PIP is low one can presume that the patients’ pulmonary mechanics have improved or within the normal range and that the workload imposed by low compliances or high resistances have decreased.


Example Case


80 female patient with the following ventilator settings:


Mode- APC, Rate- 12, Vt- 500, Fio2- 35%, PEEP- +5 cmH2O


Discovered from the ventilator patient assessment that the patient’s PIP was only 13 cmH2O and the patient was resting comfortably. At this institution spontaneous breathing trials are performed with CSV-PS, Pressure Support of 7 cmH2O & a PEEP +5 (PIP total 12 cmH2O).


The measured PIP over the previous 48 hours was a ~ mean of 13 cmH2O.


This was significant, the patient was basically on the same control pressure as what this facility does SBT’s on, indicating that the patient should have been weaned or liberated 48 hours earlier.


After this finding the patient was immediately placed on a Trach collar trial. The trial was successful with no complications and the patient was transferred to a general medical floor within 48 hours.


Conclusion


Low PIP during APC ventilation should always be evaluated further for the potential for liberation from mechanical ventilation or the need for adjusting ventilator settings to decrease the work of breathing.

[1] The Problem With Adaptive Pressure Control Modes of Ventilation: a Case Study.

Delayed Cycling

One form of delayed cycling  is when the operator inappropriately sets the inspiratory time too
long.

However, delayed cycling is also very common during CSV-PS.

A pressure spike at the end of inspiration may indicate delayed cycling however this is not always associated with expiratory muscle activity . The spike may also be due to the relaxation of the inspiratory muscles, the spike is caused by the returning of pressure creating a temporary increase in pressure (usually associated with higher levels of pressure support > 10 cmH2O). 

Always evaluate the patient for distress to determine if it is delayed cycling vs. muscle relaxation. If the patient looks relaxed and the P0.1 is within limits then the spike is most likely due to muscle relaxation.

A 25% expiratory cycling threshold is a common default setting in most mechanical ventilators. This setting is appropriate in a large percent of the patient population. As previously mentioned a default setting of 25% may be too short in patients recovering from ALI, conversely , in patients with histories of airway obstruction this setting may be too long.


Prolonged expiratory cycling in the COPD patient may increase work of breathing, intrinsic PEEP, and trigger asynchronies (ineffective efforts).Waveform book  at 

Is the T-Piece Trial Futile? 3 Cases that Justify a T-Piece Trial.

In a current Blog posting “No More T-Piece” author Rick Frea states that at his facility T-piece trials are pretty much non-existent.

I don’t remember the last time I have preformed a T-piece trial on a patient with an E.T. Tube? It is very popular these days to perform the Spontaneous Breathing Trial (SBT) inline with the mechanical ventilator, due to the advance physiological monitoring and the extra alarm capabilities.

Most institutions I’m familiar with use a small amount of pressure support (~5 cmH2O) or Automatic Tube Compensation (a.k.a. Tube Comp, ATC, or Tube Resistance Compensation) if it is available on the machine to overcome the resistance of the artificial airway.

Even though the t-piece method is rarely used I believe it can be beneficial and more diagnostic in some cases to prevent false positives created by spontaneous breathing augmented with pressure support & PEEP.

3 examples:

Premature Cycling

Image 1: Patient coughing, notice the peak pressure spikes (yellow pressure waveform) this may lead to premature cycling. 

Premature Cycling
Premature cycling  also known as premature termination or short cycling occurs when the ventilator breath cycle ceases abruptly, while the patient requires a longer inspiratory phase. It is defined by the delivered inspiratory time is less than 50% of the mean inspiratory time [1,2].

Premature cycling may be attributed to pressure over-shots, causing the breath to cycle-off when the generated pressure meets the safety threshold setting. A good example of this is when a patient coughs during volume controlled ventilation (VC-CMV, VC-SIMV), in which the exhalation valve is closed throughout the set inspiratory time. 

Adaptive Support Ventilation: the “Pareto Principle” of Mechanical Ventilation.

One reader asked me “what do you think about ASV” (Adaptive Support Ventilation) in which I replied back “I think it is the Pareto Principle or Pareto Efficiency of mechanical ventilation”.

So what is the Pareto Principle?

Oral Exam: 99.9 % Failure Rate Among ICU Nurses

Question 1. What is pictured in image 1?

Image 1

Question 2. What is it used for?

If you answered “Bite Block” you must be an ICU nurse.

 I cannot count how many times nurses have tried to use the “oropharyngeal airway” as a bite block and complain about how the patient is fighting the tube & airway, gagging, and fighting the ventilator.

The next step, they usually heavily sedate or paralyze the patient.

An oropharyngeal airway is to help keep the airway patent (open) & should not be used in the conscious patient with a gag reflex.

Now this is a bite block (image 2), which can be used for that patient biting on an  E.T. tube. 

Image 2 "Bite Block"