He complained that the pacing was painful, and so I gave him 2mg of valium to take the edge off. His BP was now 100/62, and I thought we had done OK.
Then he went into respiratory arrest.
Diazepam (Valium) is a benzodiazepine and has the potential for causing respiratory depression. You gave 2 mg. That is such a small dose that it is not likely to have a significant effect on respiratory drive, unless he was tiny. If the patient was ready to stop breathing from working too hard to breathe, then it was probably only a matter of time until he stopped breathing. The diazepam could have contributed, but the intubation may have been inevitable. The BP and CO2 numbers (below) suggest that he was still perfusing well, which indicates that his circulation received a benefit from your treatment with the pacemaker. I do not see any reason to place any blame on your actions.
I prefer fentanyl (Sublimaze) for pacemaker pain. It has less of an effect on blood pressure than morphine or benzodiazepines, but it can have even more of a respiratory depressant effect. If sticking to benzodiazepines, and many people prefer to to use them for pacemaker pain, I prefer to use midazolam (Versed), since it wears off much more quickly than lorazepam (Ativan) or diazepam. Similarly, a big advantage is that fentanyl wears off quickly. For EMS, we do not want drugs that last a long time. We want to be titrating to effect. We can always give more (depending on protocol and amount carried).
I tubed him, and his EtCO2 looked good, and over the next few minutes, his O2 sats went from the 70’s into the upper 90s. His lungs sounded wet, but the clinical signs were there. CHF, maybe? We delivered him to the ED with vitals of: HR 80(paced), Resp 12(BVM via ETT), BP 110/70, SaO2 96, EtCO2 42.
With a misplaced tube, it is extremely unlikely to have improved oxygen saturation. There are a couple of possible reasons for the number to increase with a misplaced tube.
1. The pulse oximeter was not getting a good reading before the intubation, but was afterward. Even though the sat may be slowly dropping, when there is at least one inaccurate reading, there may appear to be a positive trend, but that is just due to an error in one, or more, readings.
2. An esophageal intubation should not lead to improved oxygenation. However, the act of inserting a laryngoscope blade and a tube may provide enough painful stimulus to inspire the patient to breathe spontaneously and adequately around a tube that is placed in the esophagus and not obstructing the airway. The tube would not be providing any benefit other than painful stimulus. Painful stimulus may be all that the patient needs, but that does not justify an endotracheal tube misplaced and unrecognized in the esophagus. The pacing may have the same effect of painful stimulus, but the patient seems to have had the respiratory arrest after capture was obtained with the pacer.
On the topic of pacemakers, it is likely that the improved cardiac output from many paced patients is not due to successful capture, but to painful stimulus. That is a topic all to itself.
Wet sounding lungs can mean many different things, but if he does have CHF, positive pressure ventilation works wonders, as long as we do not drop the blood pressure by raising his intrathoracic pressure high enough to impair venous return.
The ER doc listened to the lungs, and consulted with the RT. They decided to extubate. I pointed them to the EtCO2, and the Doc said “That stuff isn’t accurate. You are in the stomach.”
“That stuff isn’t accurate. You are in the stomach.”
Strike One!
This clown doctor needs a big tattoo on his forehead to warn people to stay away.
Accuracy-wise, waveform capnography is the most reliable method of confirmation available. The false negative rate is very low. For example false negatives might from an obstructed sample port, equipment not connected properly, equipment malfunction, a very dead patient produces little, if any CO2, . . . .
The false positive rate is almost zero. For example from a lot of air in the stomach from a lot of mouth-to-mouth ventilation. The exhaled CO2 is going into the stomach, to be returned later, when oxygen is pumped into the stomach. The possibility that consuming a lot of carbonated beverages prior to intubation would similarly result in a reservoir of CO2. Not that anybody would ever substitute carbonated beverages for the almost mandatory pre-arrest Mylanta. The patient is hooked up to the nasal cannula form of CO2 sampling device and is still spontaneously breathing around an esophageal tube well enough to produce good CO2 numbers and waveform. The monitor is showing a waveform from a simulator, rather than the patient. Although I spend a lot more space on the false positives, they are much less likely than the false negatives.
He then ordered the nurse to discontinue the pacing, and give 0.5mg epinephrine and 0.5mg atropine. I showed him the original strip and pointed out the original rhythm.
Strike Two!
Discontinuing pacing that has both electrical and mechanical capture is a very bad idea, unless you are just doing so temporarily to assess the underlying rhythm before resuming pacing. Discontinuing pacing to give a toxic dose – perhaps a lethally toxic dose – is irresponsibly dangerous.
I would suspect that the doctor, by giving both atropine and epinephrine, exacerbated an MI. A 500 mcg bolus (0.5 mg = 500 mcg), to a patient with a pulse, is way outside of the ACLS guidelines of 2 mcg/minute to 10 mcg/minute by infusion. I don’t know what happened, but I have never seen a slow push of epinephrine. Even assuming that the epinephrine was given over a full minute, that doctor still gave 50 times the maximum dose for a living patient.
I started the last paragraph with the assumption that he had both electrical and mechanical capture with the pacemaker. If there is any question about whether this is the case, the waveform capnography gives a pretty good indication of the quality of circulation. There is more that I would want to know to make a more definite statement, but I do not doubt that he had full pacemaker capture. That the patient coded after discontinuation of the pacing, and the addition of an extremely toxic dose of epinephrine only adds to the confirmation that the EMS treatment was appropriate.
Maybe the doctor placed the tube in the esophagus, since he clearly does not know how to confirm tube placement. Expecting correct placement (if he did attempt to re-intubate) from Dr. Deadly would be an example of unreasonable optimism. We might as well allow him to be the only unreasonable person in the room.
Picture Credit[1] You know how to make it bigger.
To create a continuous infusion of epinephrine hydrochloride for treatment of bradycardia or hypotension, add 1 mg (1 mL of a 1:1000 solution) to 500 mL of normal saline or D5W. The initial dose for adults is 1 µg/min titrated to the desired hemodynamic response, which is typically achieved in doses of 2 to 10 µg/min. Note that this is the nonarrest infusion preparation and dose (ie, for bradycardia or hypotension).[2]
What if Dr. Deadly was assessing the patient as pulseless and was giving the dose for cardiac arrest, so the dose could be appropriate.
Let’s see if the AHA has a mostly dead dose for doctors, who just can’t commit to a full milligram in cardiac arrest –
It is appropriate to administer a 1-mg dose of epinephrine IV/IO every 3 to 5 minutes during adult cardiac arrest (Class IIb). Higher doses may be indicated to treat specific problems, such as ß-blocker or calcium channel blocker overdose. If IV/IO access is delayed or cannot be established, epinephrine may be given by the endotracheal route at a dose of 2 to 2.5 mg.[3]
It looks as if Dr. Deadly was using a dose of epinephrine that is half of an adult cardiac arrest dose combined with a dose of atropine that is half of an adult cardiac arrest dose. Dr. Deadly appears to be a complete half wit.
Maybe he was giving the appropriate dose of atropine for a living patient combined with a ridiculously inappropriate dose of epinephrine for a living patient
Maybe he was, but I would rather not speculate about the motives of this malpractitioner. He could be 50 times more witless. At least if we use the ratio of his dosing to the actual recommended doses.
What about dopamine? The chart includes dopamine.
Dopamine is just epinephrine light. It is a little more complicated than that, but the dopamine is going to be much weaker than the epinephrine. Dopamine is also not to be given as a bolus to live patients.
As I was leaving, the doctor came out and informed her that her husband had passed away. He then told her, right in my presence, that if the paramedic had not placed the tube incorrectly, her husband may have lived. I felt about three inches tall.
Strike Three!
He blames others for his incompetence.
At least the doctors reviewing the case were able to recognize the signs of a properly placed tube.
Did you tell the family that the outcome of the complaint against you was that you did nothing wrong. If anyone killed this patient, I would suspect that the doctor, by giving both atropine and epinephrine, exacerbated an MI. A 500 mcg bolus, to a patient with a pulse, is way outside of the ACLS guidelines of 2 mcg/minute to 10 mcg/minute by infusion. I don’t know what happened, but I have never seen a slow push of epinephrine. Assuming that the epinephrine was given over a full minute, that doctor gave 50 times the maximum dose for a living patient.
It is difficult to tell a lot of what is going on without the strips and other information. Not that anyone needs to be blamed, but when those taking care of patients are clueless people, such as Dr. Deadly, patients seem to die more often.
While I intended to start by saying nice things about the review board for recognizing that you did the right thing, I am disappointed if they failed to report this doctor to the state medical board.
People, who automatically blame others for their mistakes, such as Dr. Deadly, seem to do this because they have a lot of practice making very bad mistakes. They also seem to be incapable of learning.
Footnotes:
^ 1 Management of Symptomatic Bradycardia and Tachycardia
Circulation. 2005;112:IV-67 – IV-77.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.3: Management of Symptomatic Bradycardia and Tachycardia
Bradycardia
Free Full Text . . . . Free PDF
^ 2 Monitoring and Medications
Circulation. 2005;112:IV-78 – IV-83.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.4: Monitoring and Medications
Medications for Cardiovascular Support
Epinephrine
Free Full Text . . . . Free PDF
^ 3 Management of Cardiac Arrest
Circulation. 2005;112:IV-58 – IV-66.
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.2: Management of Cardiac Arrest
Medications for Arrest Rhythms
Epinephrine and Vasopressin
VF and Pulseless VT
Epinephrine
Free Full Text . . . . Free PDF
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