Will we ever see a day without CPR? Perhaps not. More importantly, will anyone ever be able to prove that it makes a difference in outcomes? I seriously doubt it. One thing seems to make a difference in non-traumatic cardiac arrest: electricity! Generally speaking, those with the best chance of survival are those with a shockable rhythm who had access to prompt defibrillation. CPR sounds like the right thing to do while your waiting for the defibrillator to arrive. After all, you can’t just stand there! In an article by Sayre it was reported that CPR without ventilation, often a deterrent to bystander CPR, was just as effective as CPR with ventilations (Circulation 2008 Apr; 117:2167). Are they saying that circulating deoxygenated blood is an effective way to perfuse a pulseless patient? Nope. What they are saying, whether they realized it or not, is that ventilations didn’t matter because CPR just doesn’t work.
I recently read a chart on a 32-year-old female with type I diabetes with pyelonephritis and sepsis. Her glucose was elevated at 668 and her serum CO2 (bicarbonate) was 15. Arterial pH was 7.19. Besides her IV fluids and insulin drip, “1 amp of NaHCO3–” was ordered as well. Intuitively, this makes sense. She has DKA and is in metabolic acidosis. So, if your “bicarb” is low, give some back, right? While “bicarb” has its place, there isn’t a shred of evidence suggesting that it improves outcomes in metabolic acidosis from any source (Chest. 2000; 117:260–267). If you’re treating metabolic acidosis, treat the underlying cause and hold the “bicarb.”
The patient above had an ABG to measure her actual pH. Although she is clearly acidotic, based on her serum CO2 level, there are some additional advantages to obtaining a blood gas. Knowing the actual pH is a more direct measure of acidosis than the serum CO2, and it gives us a good sense of how effective the patient is compensating with their respiratory system. It also gives us clues regarding the work of breathing and who is likely to experience respiratory failure from just getting way too tired from trying to compensate for the acidosis. A blood gas does all of these things. However, who ever said we have to check an “Arterial” blood gas? Plenty of physicians, for many generations have and still do. ABGs are not benign, require special skills to obtain and often special personnel to obtain them. In recent years, many have questioned this practice in lieu of a venous blood gas or VBG. It’s less expensive, safer, easier to obtain and takes less time. What do we give up with a venous sample? Not a thing! It has been conclusively determined that the differences in pH and pCO2 comparatively between an ABG and a VBG are negligible (Emerg Med J. 2006 Aug;23(8):622-4, Emerg Med J. 2007 Aug;24(8):569-71). The only expected difference is in the pO2. However, we can easily overcome that issue with pulse oximetry.
The EGDT ship sailed from port with 90% of the specialty buying its preliminary findings published by Manny Rivers in 2001 (N Engl J Med. 2001 Nov 8;345(19):1368-77). It takes no stroke of genius to throw a potpourri of interventions at a single patient and find some benefit (Chest. 2007 Aug; 132(2):425). The real question is, of the myriad of treatments employed, which of them really have beneficial effects? Bill Cosby could have added a Jell-O pudding pop to the EGDT sepsis approach and claimed its beneficial effects too. For me, if its vanilla, I’ll take the pudding pop over centrally-measured ScvO2s any day. In a nutshell, although some say EGDT may have a benefit for the sickest sepsis patients who can be identified using the MEDS score, I say the shine is fading. We know that early antibiotics and fluid resuscitation are very important. Nothing new there. We also now know that lactate may be an early marker for poor cellular perfusion associated with sepsis. This is a piece of information that has been fruitful from the sepsis literature. Interestingly, many physicians don’t know that the serum lactate will rise much more quickly than the serum CO2 will decline. Thus, if you are assessing for sepsis with a CO2 and not a lactate, you’re likely to miss some early cases. Perhaps the most important reason why sepsis patients showed improved outcomes with EGDT sepsis is because we were paying closer attention. We are detecting them earlier and managing them more aggressively (Chest 2006 Feb;129 (2): 225-232 ).
What about steroids in sepsis? “Stress dose? No benefit. Then, low dose was believed to be the way to go (Ann Intern Med. 2004 July;141(1):47). Now, that appears to have been refuted (N Engl J Med. 2008 Jan; 358(2):111). We are bound to repeat history if we are ignorant of our past. We have been studying anti-inflammatory agents for sepsis for decades. Perhaps, they just don’t work.
Steroids may benefit critically ill patients with adrenal suppression. However, identifying those patients is challenging. Some data suggests that cortisol levels have no predictive value for those who will benefit from corticosteroid administration compared to those who won’t (Arch Surg. 2005 July; 140:661). The key is, if you suspect adrenal insufficiency (i.e. hypotension, refractory hypoglycemia, hyponatremia, vomiting and hyperkalemia, etc.) just treat it. Steroids are cheap!
Where adrenal insufficiency has emerged as a critical consideration for EPs is in the case of etomidate for rapid sequence intubation (RSI). In continuous infusion, three days and beyond, adrenal suppression and increased mortality has been shown to be higher in trauma patients. Other patient subsets have experienced this phenomena as well (i.e. sepsis patients). What really isn’t clear is whether or not one dose for RSI will have that same result. My money is on the logical explanation. Although some patients do worse with etomidate, they tend to be the sicker patients who might already have developed adrenal insufficiency from sepsis, etc…, regardless of exposure to etomidate. Honestly, we don’t have the definitive answer yet. However, we should all be mindful of this potential phenomena and recognize that this response to etomidate is both cumulative and dose-dependant. Thus, repeat doses of etomidate in critically ill or injured patients is ill advised and consider the use of alternatives for patients with known septic shock (Chest. 2005 Mar;127(3):1031-8, Acad Emerg Med. 2009 Jan; 16(1):11).
For years, and most recently with the “Surviving Sepsis” campaign, the evidence suggested that hyperglycemia was a bad prognostic indicator for those with significant disease (i.e. sepsis, pneumonia, CAD, trauma, etc.). Well it might be, since sicker patients tend to have higher serum glucose levels, but hyperglycemia may not be acutely harmful. Emerging data has put the brakes on “Tight glucose control” (JAMA 2008 Aug; 300(8):933). Sure, if your patient is substantially hyperglycemic, treat it. That’s not what we’re talking about. The past evidence suggested that critically ill or injured patients should be kept in fairly tight glucose control during their illness. What we know now is that hyperglycemia in critical illness is most likely a self-protective mechanism in response to physiologic stress. So, if the body has this figured out, stay out of the way. If the glucose is only mildly or moderately elevated and that elevation is likely in response to other problems, resist the temptation to treat it.
Although there are many critics of therapeutic hypothermia, this concept has been endorsed for years by the International Liaison Committee on Resuscitation (ILCOR). While the data is limited, it is still fairly compelling. (New England Journal of Medicine. 2002 Vol. 346, No. 8). In patients with a primary v-fib arrest who have spontaneous return of circulation, but do not regain consciousness, their chances for a better neurological outcome may be enhanced by doing this. Hey, if they survive in the ED, we’re sending them to the ICU anyway. Why don’t we give them every possible chance at survival? The only strong argument against this modality is cost. If you keep the medical device companies out of this and stick to the basics, this can be a bit messy, but not expensive. Ice is cheap!
Everyone using amiodarone instead of lidocaine? If so, why? This move was made by the American Heart Association in the 2000 guidelines. Interestingly, this was based on the ARREST trial, (N Engl J Med. 1999; 341:871–878), comparing amiodarone to placebo. The ALIVE trial compared amiodarone to lidocaine (N Engl J Med. 2002; 326:884–890). In both studies, more treated with amiodarone survived to ICU admission. I think the AHA stopped reading the articles at that point. The numbers discharged from the ICU with a good neurological recovery were equal in both groups for both studies. All amiodarone accomplishes is taking up an ICU bed you’ll need for someone else and jacking up the costs for the family who’ll lose their loved one anyway.
If your favorite procedure is the rectal examination, you’ll be sadly disappointed. The ACS now states that rectal examinations are not mandatory in all trauma patients. Further, they support the literature, which confirms that patients don’t conceal their bladder or urethral injuries. These patients will have physical findings, such as hematuria, trauma in the perineum or signs of a pelvic fracture that should raise your index of suspicion (J Trauma. 2005 Dec;59(6):1314-9). If these signs are not present, no need to glove up! Also of importance is that the practice of checking for poor rectal tone as a sign of spinal cord injury is nearly worthless. If this sign is relied upon, 63% of spinal cord injuries could be missed (Ann Emerg Med. 2007 Jul;50(1):25-33, 33.e1).
Resuscitation is one of the most critical areas of emergency medicine. And although it’s rich with assumptions and dogma, it is short on evidence. Perhaps, one of the most critical resuscitation skills all EPs should develop is when to ask, “Why?” Being critical of the “Why” will prompt better answers for future generations of physicians and better care for our patients.