Some food for thought…

Controversial evidence & some reasoning.

Nitroglycerine is Contraindicated With Tachycardia?

-       BP = Cardiac Output (CO) x Systemic Vascular Resistance

-       CO = Stroke Volume x Heart Rate

An acute coronary event does not cause tachycardia.  Tachycardia (without exertion) is almost always a result of decreased stroke volume.  Stroke volume is dependant on venus return.  So if stroke volume is down, and your body is trying to maintain normal cardiac output, so it may maintain a normal BP, the heart rate may be increased.

If the patient does not have pulmonary congestion (edema), nitro should be withheld if the patient is tachycardic.  This is because the patient may be preload dependant as a result of dehydration, or some other hypovolemic condition.  The tachycardia will most likely be compensatory, and the nitro will worsen the patients condition.

But anxiety can cause tachycardia…

Then console your patient and see if the tachycardia persists after they are calmed.  If the tachycardia seems to accompany anxiety then nitrates may be acceptable.  Be very weary of persistent tachycardia, whether they are anxious or not.

Patients Experiencing a Heart Attack Don’t Need O2?

Oxygen has recently shown to be much less benign a treatment than it was once thought to be.   Hyperoxia leads to increased morbidity and mortality in stroke patients, post-arrest patients, head trauma patients, and it has most recently been discovered that hyperoxygenation may lead to poor outcomes in patients experiencing an AMI.

Why?

The answer isn’t so easy to understand.  First of all, the research is still new.  Just understand that these patients are not generally suffering from hypoxia.  They are suffering from ischemic heart tissue, more specifically—myocardium.  If their oxygen saturation is sufficient, than no additional O2 should be supplemented.  Reasoning includes an elaborate explanation regarding free radicals.  O2 is a free radical and may be toxic, leading to residual oxidative stress.  This causes increased damage.  Use of oxygen in MI patients questioned by new Cochrane review.

What is the Deal With Morphine?

Morphine is associated with an increase in morbidity when given to a patient experiencing an acute coronary event (an AMI).

Once again, there is no conclusive answer, but researchers from a CRUSADE study have three possible explanations.

-       The first explanation is that patients treated with Morphine exhibit signs and symptoms of heart failure, and are treated as such.  This isn’t really accepted as a plausible cause.

-       The second, more widely accepted explanation is that Morphine masks symptoms of angina without correcting the underlined pathology.  This means that caregivers may be less apt to provide follow-up treatments, procedures, and consults.

-       The third explanation is that Morphine decreases the respiratory drive as well as causing CNS depression.  Increased ischemia has been associated with these side effects, and extended infarction has been linked to Morphine itself.

End point	No morphine (n=40 036)	Morphine (n=17 003)	Adjusted OR (95% CI)
Death (%)	4.7	5.5	1.48 (1.33-1.64)
Death or MI (%)	7.1	8.5	1.44 (1.34-1.56)
Postadmission MI (%)	3.0	3.8	1.34 (1.22-1.48)

Morphine has bad effects when administered to patients with CHF.

Yes, it is in most prehospital guidelines as a recommended treatment for congestive heart failure.  This will soon change…

The Acute Decompenstated Heart Failure National Registry (ADHERE) conducted a study on patients admitted with CHF who received morphine and yielded important results. There was a five-fold increase in mortality (13% versus 2.4%), a five-fold increase in need for intubation and ventilation (39.7% versus 14.4%), the intensive care unit admission rate was (15% versus 3.0%), and those patients who were admitted had a prolonged hospital stay (5.6 days versus 4.2 days). Although this was an observational study, it has had a major impact on the use of morphine for CHF patients.  We know that morphine causes histamine release and subsequent hypotheses have been made concluding that this may increase catecholamine release. This may be the link to the poor outcomes. Additionally, there is a lack of evidence that morphine is related to any clinically significant preload reduction.

No More Intubations?

There has been a new paradigm shift in the way we think of resuscitation.  This has brought with it, some new terminology—cardiocerebral resuscitation (CCR).  CCR is meant to replace CPR, or cardiopulmonary resuscitation.  The focus is shifting from the lungs, or pulmonary system, to the brain, or cerebrum.

There have been suggestions from the result of much research, advocating CCR for witnessed cardiac arrest, and CPR for primary respiratory arrest.  This makes perfect sense, considering the pathologies.  Overall though, there has been much more success when emphasis has been on chest compressions, as opposed to airway management.

Blind insertion, supraglotic airways are now rapidly finding their way into prehospital cardiac arrest guidelines throughout the country.  The Combitube, Laryngeal Mask, and King LT/LTD are a few of the most common devices being utilized.  The big sell, is the ability to insert these devices without any pauses in chest compressions.

This emphasis on chest compressions comes from research showing the need to prime the pump during the circulatory phase of cardiac arrest.  This basically means that the heart and brain need to be perfused as good as possible up until defibrillation.  Immediate defibrillation is only indicated within the electrical phase; which only lasts for approximately the first five minutes of pulselessness.

Despite the turmoil and mixed opinions about ETI in cardiac arrest, the evidence is clear—survival is better when the main focus is on adequate chest compressions.  By taking the ETI aspect, and all of the complications that accompany it, out of the equation, resuscitation efforts consequently improve.

We haven’t even gone to the extreme yet.  One study has shown that by simply placing a non-rebreather mask on a cardiac arrest victim and providing high-quality chest compressions, they increased neurologically intact survival rates from 15 to 39%.

Remember:  Nearly all-medical research is flawed.  This is one reason why medicine will remain ever changing.  Fortunately the good evidence usually trumps the biased or bad evidence.  No single study should change anything.