- Hyperkalemia is one of the reversible causes of refractory cardiac arrest covered in the H's and T's. It is common in patients with kidney disease, and would probably be an initial consideration in a dialysis patient's refractory cardiac arrest or PEA. Those with a truly excessive amount of dietary potassium are also at risk. The severity of hyperkalemia not only depends on the total serum potassium level, but on how rapidly the level has risen (in other words, has the body had time to adjust?)
Remember- hyperkalemia is considered a REVERSIBLE cause of arrest, and there are a few things that can be done to drive the potassium into tissue cells (and, therefore out of the bloodstream) and assist this patient if high serum potassium levels are considered a primary factor.
- Calcium IV can be given to strengthen muscular contraction, and override some of the symptoms of hyperkalemia. This is probably the best initial response when hyperkalemia is considered to be a contributing factor to refractory arrest.
Sodium Bicarbonate can also be considered, as acidosis is a primary contributor of hyperkalemia.
A glucose and insulin infusion can be helpful in this case, as it can drive potassium into the cells.
Albuterol by nebulization can also drive potassium into cells.
So, your cardiac arrest patient now has a pulse. Great work! Now what?
The new AHA guidelines really stress post-resuscitative care, and have a true post-arrest algorithm. Induction of "therapeutic hypothermia" immediately after return of spontaneous circulation has been clinically proven to preserve brain function. This is due to the decreased metabolic demands on the brain in the hypothermic patient.
The criteria for this is essentially any patient post arrest who is comatose, and not septic. Most studies were done on post-arrest patients that had been in ventricular fibrillation, but patients with a history of PEA or asystole are also candidates for therapy.
The goal is to induce low body temperature for the first 24 hours post-arrest. There is a widening of the range with the 2015 guidelines for target temperature. The goal temperature is 32-36 Celsius (about 90-96 Fahrenheit.) This can be accomplished with ice packs to the armpits and groin, but that takes a while. A faster way is to begin chilled saline boluses. Fridge temperature saline is fine. If given at around 100ml per minute IV, (via a pressure bag,) each 1000ml is expected to drop body temperature around 1 degree Celsius every 10 minutes. A 500ml bolus may even be sufficient, as the average adult body temperature is 37 Celsius. So, rechecking a temperature in 30 minutes should reveal a temp of about 34 Celsius.
The one caveat here is that the patient should be maintained at a CONSTANT temperature after cooling measures for the 24 hour time period. One thing that can not be done is cooling the patient to say 32, then letting them warm to 36, then cooling again. Constant temperature is desired! If cooling ceases at 36, that is where the patient stays for 24 hours, with tight control.
To maintain this temp for 24 hours, automatic cooling blankets are best. They often are placed under and over the patient. These utilize a temperature probe (esophageal probe, or bladder probe, perhaps a rectal temp probe) connected to the device to maintain the temperature of the patient within the desired range.
There are medications that are also commonly used to assist in maintaining the temperature. A Fentanyl drip can be useful here, as it decreases the body's shivering response (shivering will raise temperature) as well as keeping the patient sedated. A non-sedated patient may have increased brain activity, which is counter- productive. Tylenol via suppository is also useful to blunt the body's hypothalamic (temperature control) response.
The patient does not necessarily need to be paralyzed. Some would say don't paralyze the patient, as the non-sedated, (or poorly sedated) paralyzed patient will surely have increased brain activity which will not be recognized. Remember, the goal is to literally and figuratively make the patient "chill out!"
Potential complications include coagulopathy- hypothermia can cause bleeding. Another problem is that hypothermia causes a decreased immune response, so it is not really indicated for septic patients. Frequent blood sugar checks are also important. Again, the non-comatose patient who achieves return of spontaneous circulation is not a candidate for this therapy.
Cessation of therapeutic hypothermia generally consists of ceasing cooling measures, and allowing the body temperature to come up naturally. As patients can rebound to hyperthermia, there is increased attention being paid to this now, and worry that rebound hyperthermia may increase morbidity. Stay tuned!
Author: Scott Carpenter
Image Credit: Anonimski / Wikimedia Commons / CC-BY-SA-3.0 / GFDL
An Ischemic stroke occurs when a clot forms or lodges in one of the arteries of the brain, causing a loss of blood supply to the affected area. Ischemic strokes account for more than 85% of all strokes. The goal is to act fast- within 3 hours of onset of symptoms (or 4.5 hours for a select group of patients) to break up the clot and restore perfusion. In order to accomplish this, several things must fall into place.
AHA guidelines reflect the need for a patient to undergo a whole set of procedures upon entering the ER doors in order to minimize delays.
1) Within 10 minutes of arrival, the patient should undergo a doctor's evaluation, including a stroke screen assessment, history (noting time of onset of symptoms) and lab work including a bedside blood sugar.
2) The stroke team, including neurological experts, should be notified within 15 minutes.
3) The patient should have a CT scan within 25 minutes of arrival. this is the only way to be sure that the stroke is ischemic versus hemorrhagic.
4) Within 45 minutes, the CT results and basic lab work should be reviewed, and the patient's eligibility for clot busting Tissue Plasminogen Activator (TPA) intravenously should be established.
5) TPA should be initiated within 60 minutes of the patient's arrival.
These guidelines for the "golden hour of stroke care" were established after several studies showed that patients receiving TPA could have dramatic symptom reversal, and maximize their neurological potential after suffering a stroke.
Patients should be triaged to the nearest stroke center if being transported by EMS. For example- if CT is not available at one hospital, the patient should be diverted to another facility with the capability to perform all of the steps outlined above.
TPA is not without significant risks, most notably life threatening bleeding internally or externally.
Author: Scott Carpenter
Image Credit: Blausen Medical Communications, Inc. / Wikimedia Commons / CC-BY-SA-3.0 / GFDL
Epinephrine is the initial drug administered per ACLS protocol to patients in asystole, PEA, and ventricular fibrillation/ pulseless V-tach. For asystole and PEA, it is the ONLY drug indicated, unless specifically treating a reversible cause of arrest (see H's and T's.)
Epinephrine will increase central pressure via alpha agonist effects. The dose, timing and indications for epinephrine use are based on animal studies.
Recent studies question whether epinephrine provides any overall benefit for human patients.
Studies do show that epinephrine for out-of-hospital cardiac arrest will increase the rate of pulse return. The problem is that it doesn't considerably alter longer-term survival. A large Japanese study showed that, despite an increase in pulse return, epinephrine reduces long-term survival (to hospital discharge) and patients who do survive have significantly worse neurological outcomes than patients who did not receive the drug. Perhaps harmful epinephrine-induced reductions in micro-vascular blood flow offset the useful effects of the increase in central circulation.
In a V-Fib or pulseless ventricular tachycardia code situation, epinephrine should NOT be administered until after the second shock (per guidelines) for precisely these reasons. The patient's best chance of a neurologically intact survival is immediate CPR, a shock as soon as available, and two more minutes of uninterrupted CPR. A second shock (followed by epinephrine administration) is only indicated if there is no return of ROSC by that time.
Guidelines do say that it is reasonable to administer epinephrine as soon as practical in an asystole or PEA code, as no shock is advised.
Hagihara A., Hasegawa M., Abe T., Nagata T., Wakata Y., Miyazaki S.; Prehospital epinephrine use and survival among patients with out-of-hospital cardiac arrest. JAMA. 2012;307:1161-1168.
Dumas F, Bougouin W, Geri G, et al. Is Epinephrine During Cardiac Arrest Associated With Worse Outcomes in Resuscitated Patients?. J Am Coll Cardiol. 2014;64(22):2360-2367. doi:10.1016/j.jacc.2014.09.036.
Author: Scott Carpenter
Adenosine is frequently used in the setting of supra-ventricular tachycardia (SVT), in which a patient has an abnormal pathway allowing electrical activity to re-enter the atria after it has depolarized the ventricles. This family or re-entrant tachycardias (also called AVRT) short circuit the heart's normal pacemaker (the SA node) and cause massive stimulation of the AV node, producing heart rates commonly seen in the 180 (or higher) range.
Adenosine is often thought of as "chemical cardio-version", as when it is given FAST IV push, it's effect is to terminate all cardiac activity for three seconds or so, causing asystole on the monitor. The patient will feel VERY poorly for a short period of time. Generally, upon restoration of cardiac electrical activity, the heart's normal pacemaker, the SA node, will have taken over again, and the patient will be in a normal sinus rhythm.
Adenosine works by hyper-polarizing cardiac cell membranes, particularly in the AV node, making them incapable of firing for a time, and breaking the re-entrant limb of an SVT cycle.
Author: Scott Carpenter
Image Credit: Original art by Monica Murray. Photo by Leisa Marshall. Used with permission.
New classroom course books are in stock with your preferred AHA vendor. Online courses followed by skills sessions do not require a manual, as one is supplied online with that portion of the course
Please be aware, Carpenter CPR does not supply books for classroom courses. Obtaining necessary course materials is a student responsibility. Please note that the new 2016 tests are OPEN BOOK!
If you would like, you may purchase your manuals from Laerdal, an authorized AHA materials provider. Current manuals are the 2016 version.
AHA is also offering E-books at: http://ebooks.heart.org/catalog/show/all
At a recent live code, I again noted how common it is for less experienced teams to attempt to "do everything at once" and priorities can easily become confused in the hurried rush to save a life. I have put together a few reflections from this event.
The most important part of any resuscitation attempt is to do the basic things well!
One of the first things I noted was the hesitancy to initiate CPR. This is a decision point that all CPR students struggle with. If I suggest to you that you may feel a pulse, in which case there is no need to start an aggressive act, you may decide that you feel one. This is the reason that the AHA guidelines are so clear. If you do not DEFINITELY feel a pulse within 10 seconds, it is time to get on the chest.
Another thing that I saw was the incessant "need" of the provider to hyperventilate the patient. Multiple individuals took turns using a bag mask on the patient prior to intubation, and providers were bagging the patient approximately once per second, even during CPR (when it should be 30 compression to 2 breaths). After intubation, providers were attempting to bag the patient approximately every three seconds (should be one every 6 seconds at this point). (for more on the dangers of hyperventilation, see: http://www.carpentercprsolutions.com/-blog/key-components-of-high-quality-cpr-continued-part-2)
My advice is that you take care not to make your need to "do something" into a process that hurts the victim. AHA guidelines are evidence based, and the evidence clearly states that hyperventilated patients have poor outcomes.
Provider "need" to do something, and act, can easily turn into detrimental outcomes for the patient. This patient had no need for hyperventilation, yet all healthcare providers seem to do it.
In this code, there was a rush to intubate, and a rush to get the monitor set up, and to get an IV line in place, but a decided delay in placing the pads, hooking the bag mask to oxygen, and defibrillation.
REMEMBER, in order to save a life, the emphasis must be on doing the basic things correctly-- early, HIGH quality CPR and early defibrillation are the keys here. Everything else is just theory. In codes done correctly, there will be little other activity going on. Providers feel the need to ACT, and ACT NOW, but please don't forget that much of a code is spent doing nothing more than the basics, and those measures are the real life savers, not the advanced stuff done in a hurried fashion.
This particular patient was ultimately resuscitated with HIGH quality CPR, and defibrillation, with CPR being done during defibrillator charging, and resumption immediately after the shock.
Author: Scott Carpenter
Image credit: By Aditya Suseno (Own work) [CC BY-SA 3.0 (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons
The 2015 AHA guidelines have included the addition of intravenous lipid infusion as a treatment for local anesthetic toxicity. Local anesthetics (think: Lidocaine, bupivicaine) are generally very safe, and are usually given in fairly small amounts. These drugs are lipid soluble, and their effects wear off as they diffuse into the body's fat.
Occasionally, relatively large amounts of these products are given for procedures in the extremities (for example, Bier's block procedures.) These drugs can also be used for spinal anesthesia. A locally injected anesthetic may inadvertently find it's way directly into the circulatory system.
Signs of local anesthetic toxicity can be tongue numbness, dizziness, drowsiness, disorientation. Large doses can lead to convulsions, respiratory depression, chest pain, and hypotension.
If local anesthetic toxicity is suspected (usually in an operating room type environment) a lipid emulsion infusion can be started in order to rapidly bind the drug. This, of course, should not take the place of initial stabilization and life saving measures such as airway support.
Lipid infusion may also be reasonable to consider in other forms of drug toxicity that have failed standard measures as well, although the data on this is conflicting.
There is no standard for preferred method of infusion, but one possibility (according to http://www.lipidrescue.org/) is: 20% lipid emulsion:
1.5 mL/kg as an initial bolus, followed by
0.25 mL/kg/min for 30-60 minutes
Bolus could be repeated 1-2 times for persistent asystole
Infusion rate could be increased if the BP declines.
Author: Scott Carpenter
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