Guidelines Schmidelines – how do i apply them?

https://resus.com.au/guidelines-schmidelines-how-do-i-apply-them/

Hi everyone.  Just finished a great week at the ASM 2011 conference in Sydney. Thanks to all the people that came up and said “hi”. One of the talks I gave was on “Guidelines Schmidelines”. A lot of people came up after the talk and asked if I could write it up. So here it is.

AIRWAY I was specifically looking at the guidelines in terms of adult VF/pulseless VT. The current guidelines really are a result of the first closed heart massage that has been practiced since the 1960’s. In fact the sad thing has been that the outcomes from out of hospital cardiac arrest have not really changed in the last 30 years. Advanced Cardiac life support is really about AIRWAY and DRUGS and we know they really add very little. Steil et published the OPALS study in the NEJM 2004;351:647-656. This really looked at the effect of adding ACLS to defibrillation in out of hospital cardiac arrest. It made NO DIFFERENCE to the rate of intact discharges from hospital. In fact there was an observable delay in CPR as a direct result of the need to intubate.

SO WHAT DO WE KNOW ABOUT CARDIAC ARREST? We know that in adults, it is not a problem of oxygen saturation in the blood. It is a problem with the pump. When collapse occurs that person’s oxygen saturation may have been 97% and their PaO2 may have been > 90mmHg. So they have a reserve. The continued requirement for oxygen, is also reduced during arrest, as the cardiac output achieved by CPR is about 30% of normal. So here we go. TO INTUBATE OR NOT TO INTUBATE that is the question. One of the biggest problems with intubating patients is the potential delay in CPR that it causes. CPR has to be stopped in some cases to get that tube in. I’m not sure how that applies to video assisted devices. In a study by Garza et al Circulation 2009, 119;2597-2605, intubation actually resulted in an increase in mortality. So we don’t really know if it makes a difference and there are no studies looking at the best time to intubate. Other issues are whether the tube is in the trachea. There is the possibility of false positives with ETCO2, however, over about 6 waveforms, the amplitude of the waveforms decreases and should indicate if it is in or out. There can also be false negatives in cases such as pulmonary embolism and acute pulmonary oedema.

WHAT ABOUT RATE, VOLUME AND CONCENTRATION? We don’t know the optimal rate of oxygen concentration. We tend to always give 100%, but due to free radicals, this may be detrimental. Some work coming out now is indicating a lower saturation is appropriate, but early days yet. The volume to give per breath is about 600mL. This is probably adequate given the reduced oxygen requirements due to decreased output. Also it is a volume that doesn’t promote hyperinflation of the stomach and potential regurgitation. It is also a volume that minimises hyperinflation of the thorax. Finally the rate. This is of extreme importance. We know that >10 breaths / minute results in zero return of spontaneous circulation(ROSC). This is due to the hyperinflation that occurs. Beware as the rates of ventilation can be high during resuscitation attempts. Also ensure that the breath is delivered in the relaxation phase of CPR, other wise there is a decrease in coronary perfusion pressure. So remember to BAG SLOWLY and SOFTLY.

WHAT ABOUT SUPRAGLOTTIC DEVICES? These are very helpful as they do not interrupt CPR and they can be inserted blindly. They also reduce the rate of regurgitation as compared to the bag-valve-mask. However they are not a secure and protected airway, in the same way as the endotracheal tube(Ett) is. Take care with supraglottic devices in interpreting the ETCO2 readings. We know that persistent ETCO2 of <10mmHg with an Ett, predicts a significant risk of no ROSC. This can’t be interpreted in the same way with a supraglottic device. Let’s talk about CPR Chest compressions are now recognised as being extremely important. More specifically a lack or delay in CPR is important. The reason for this is, that when we start CPR, a pressure head builds, to the point that it provides a perfusing pressure for the coronary arteries. When we stop CPR, we don’t just drop that blood pressure a little. It drops to nothing, then takes a period of time and a number of chest compressions to get to a perfusing blood pressure again.

WHAT ABOUT CHECKING THE PULSE? Studies have shown that laypersons make significant errors when checking the pulse. It is appropriate for a health professional to check the pulse in a hospital cardiac arrest. The only time a pulse makes sense is when there is no CPR going on. During CPR a femoral pulse felt, may be no more than the retrograde pulsations through the valveless inferior vena cava. A palpable carotid pulse during CPR does not guarantee cerebral or coronary perfusion.

HOW DEEP TO PRESS? The guidelines recommend 1/3 the distance form from to back of the chest or 5cm. We really don’t know the correct depth, but we do know that the deeper we press, the better the perfusing pressure becomes. Beware not to misjudge the depth of your compressions. The mattress on a bed can be compressed and add to the illusion of a deeper compression. It can also fool the accelerometer on the new defibrillators. If a patient is brought in by ambulance it may be beneficial to leave the backboard in place.

HOW FAST? We know that <80 and >120 compressions diminish the blood pressure. So an attempt to get 100 is recommended. To ensure this occurs, a metronome in the department is a great idea. Others prefer the music to ‘Staying alive’ by the Bee Gees, to practice with. I don’t advocate this be on during a resus, but that people have practiced to it beforehand and know the beat.

DUTY CYCLE This is the time that the hand is spent compressing the chest, as a percentage of the total time from first to second compression. A duty cycle of 50% is recommended, but no greater. The chest must be allowed to recoil.

HOW TO MEASURE EFFECTIVE CPR? What we really want to know is, when there is ROSC. The reason for this is, that giving 1mg of adrenaline, when the heart has just started to work again can be detrimental. The reason for this is that it creates a large afterload, against which this newly started heart must work. The ETCO2 can be used as an indicator of ROSC. To actually measure the blood pressure would be ideal. We know that a coronary perfusion pressure of >15mmHg is associated with ROSC. This correlates with a diastolic blood pressure of 35-40mmHg. One way to do this is to attempt an arterial line at some point early in the resuscitation.

So there it is, a summary of what was said. In essence Bag SLOWLY and GENTLY. Push HARD and FAST. Good luck with your resuscitations.