Manual or mechanical? Either way, if you are managing the patient that requires artificial ventilation and oxygenation, you are the primary ventilator. And, it doesn’t matter if you are using a simple facemask or a machine; your objective is the same: effectively move air into and out of the lungs to optimize the circulating oxygen content and carbon dioxide concentration.
Easy, right? But it does require a few basic skills, a couple of devices and some knowledge, all of which you have or should obtain.
Creating airway patency
First thing needed is a clear pathway to the lungs. If an obstruction is present it is most often due to the tongue and that can be moved out of the way with a head tilt/chin lift or jaw thrust. It may require insertion of an oral or nasal airway or a combination of techniques.
In a worse-case-scenario, think two nasal airways, one oral and your partner is pulling the jaw forward so you can get in a few breaths while planning your next move.
On the rare occasion when the obstruction is not the tongue, more invasive procedures may be required, such as cricothyroidotomy. Always keep suction handy to clear any blood, vomit or mucous you encounter.
Once the airway is open, you can begin to move air, but how much air? We know that providing too little or too much oxygen or leaving behind too much or too little carbon dioxide can be bad for the patient.
Managing oxygen levels
Pulse oximetry indirectly measures oxygen content in the blood and capnometry measures expired carbon dioxide; this combination will give you the information you need to keep your patient in the right air zone.
Pulse oximeters are cheap; there are no excuses for not having one.
With pulse oximetry you can determine if you need to dial down the oxygen level for your COPD patient whose usual O2 saturation is 90% 1 or help maintain the post cardiac arrest patient’s O2 saturation normal but less than 100% as too much oxygen decreases survival of injured cardiac cells2.
The pulse oximeter will also inform you if your patient’s oxygen level is too low and you need to increase the percentage of delivered oxygen. If you haven’t reached your target O2 saturation on 100% inspired oxygen, it’s time to add or increase the PEEP.
Positive end expiratory pressure, PEEP3, exists normally in your alveoli due to the column of air in the bronchioles, bronchi and trachea stacked above these air sacs. Without PEEP the alveoli would collapse with each breath and that would decrease the exchange of oxygen and carbon dioxide in the alveoli.
Patients with COPD learn to increase their personal PEEP by exhaling through pursed lips. This is the same mechanism used by a PEEP valve, a device that keeps extra back pressure on the expired air to increase the pressure in the air sacs. These devices come preset with a single pressure setting or with a range of pressures. Models are available to fit any ventilating mask or tube.
If your patient has persistent hypoxia despite administration of 100% oxygen, you can increase their PEEP to help push oxygen into the circulation. Just use the lowest pressure that accomplishes your oxygenation goals. Too much PEEP can cause the blood pressure to decline.
Be cautious with asthmatics or anyone with bronchospasm requiring manual or mechanical ventilation. Bronchospasm is like a partial one-way valve, it lets more air into the air sac then it lets out. The result is hyperinflation, a steady increase in air pressure in the air sacs that can adversely affect air exchange and potentially decrease the patient’s blood pressure. Decrease the rate and volume of ventilation to allow extra time for expiration. If you use PEEP, monitor your patient closely and decrease or discontinue if the patient is not improving or gets worse.
Controlling carbon dioxide
Capnometry devices are more pricey but well worth the expense to improve your patient care. You can move a step up by using capnography which provides carbon dioxide numbers plus a waveform graph or picture of expired CO2. This waveform supplies information about lung conditions and about blood flow in general.
For example it will show you when bronchospasm is present. The normal CO2 waveform is a slightly upward sloping square. Bronchospasm changes the normal waveform to a shark fin shape. This will show up even if you don’t hear wheezing with your stethoscope. That would be useful to know especially if you have a little albuterol handy.
With capnometry you can manage changes in CO2 by changing the minute volume (respiratory rate x tidal volume) just like your brain stem does normally. Carbon dioxide is an acidic waste product from normal cell metabolism that is continuously transported by the blood stream to the lungs for disposal.
Most of the time your goal for manual or mechanical ventilation is to maintain a normal exhaled CO2 level (35-45mmHg). One important exception is the ventilated asthmatic as it is critical to decrease the rate and volume of ventilation to allow for adequate alveolar emptying while maintaining sufficient oxygenation and accepting a rise in carbon dioxide4. The patient will normalize the elevated blood CO2 over time, but may die if you over-ventilate.
Summary
Whether your fingers are on the bag or on the dials of a machine, you remain the primary ventilator. With the basic overview presented above you can begin to optimize your patient’s respiratory status and keep yourself part of the solution, and not part of the problem.
References
1. O’Driscoll BR, Howard LS, Davison AG: BTS guideline for emergency oxygen use in adult patients. Thorax. 2008;63(Suppl VI):vi1–vi68.
2. Peberdy MA, Callaway CW, Neumar RW, Geocadin RG, Zimmerman JL, Donnino M, Gabrielli A, Silvers SM, Zaritsky AL, Merchant R, VandenHoek TL, Kronick SL: Part 9: Post-Cardiac Arrest Care : 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010; 122: S768-S78
3. Neligan P: Why do we use PEEP?. Available at http://www.ccmtutorials.com/rs/PEEP/index.htm
4. Stather DR, Stewart TE: Clinical review: Mechanical ventilation in severe asthma. Critical Care. 2005; 9:581-587. Available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1414026/pdf/cc3733.pdf
