The Causes of Cardiac Arrest

November 23rd, 2015
by reuben in .cardiac arrest

It has been repeatedly demonstrated that the use of drugs empirically does not work in cardiac arrest. Despite this, ACLS often feels like an algorithmic march down a menu of pharmaceuticals, one drug after the next, hold compressions, ok still asystole, have we tried bicarb? Until everyone has had enough and the patient is pronounced.

There are three things you can do to benefit your patient in cardiac arrest. The first is good chest compressions, which serves mostly to buy time. The second is shocking shockable rhythms, and the third is identifying and treating the cause of cardiac arrest. The use of a vasopressor in the right dose probably offers some benefit; unfortunately we can’t figure out what the right dose is and epinephrine 1 mg every few minutes is almost certainly way too much.

Which drug is next keeps you busy and is the focus of how ACLS is taught, which is why it’s so dangerous: it feels right but not only does not benefit the patient, which drug is next distracts you from the most important task in cardiac arrest, which is figuring out why the patient in front of you just died, so you can offer a treatment to address it.

Causes of CA

Dysrhythmia is a central cause of cardiac arrest; as soon as a cardiac monitor is available, check a rhythm and if shockable, shock immediately. If you’re not sure if the rhythm is shockable, shock. The harm caused by an unindicated shock is trivial compared to the harm of untreated pulseless vtach or vfib.

Acute coronary syndrome is a hugely important cause of cardiac arrest, but causes cardiac arrest predominantly by dysrhythmia, which you will fix by checking the rhythm early and often. ACS can also cause cardiac arrest by pump failure, these patients may benefit from emergent reperfusion and would ideally be in a cath lab, if we knew that acute coronary artery occlusion was the problem. If you think ACS is the cause of arrest, cath lab is not an option, and the patient seems salvageable, give a thrombolytic. The data is equivocal in this context but I think the majority of resuscitationists would offer it for hearts too good to die.

Any sufficiently severe insult to airway or breathing can cause cardiac arrest, fortunately they are all treated at once with 100% FiO2 through an endotracheal tube. If the cause of cardiac arrest is unlikely to be primarily A or B, intubation can be deferred in favor of a supraglottic device; however, if A or B is the problem, all efforts should be directed at establishing oxygenation, usually via endotracheal intubation. Diverting your finite cognitive powers to ACLS drugs in respiratory arrest is particularly poor care.

There are three common, crucially important obstructive causes of cardiac arrest. Pericardial tamponade and tension pneumothorax are easily excluded and should be explicitly excluded in every case of undifferentiated arrest. Massive pulmonary embolism is amenable to reperfusion therapy, usually with intravenous thrombolysis–consider risk factors, exam signs, and ultrasound the legs and RV when the context fits.

Hyperkalemia is common, immediately lethal, and readily treatable. Calcium should be given to most arrested patients with kidney disease, and hyperK is a great reason to push for point of care electrolytes testing in your shop. Hypokalemia is much less common but also easily treated and a particular consideration in malnourished patients. Likewise hypoglycemia–fingerstick testing is routine if POC blood gas not available, and empiric use of D50 is reasonable in diabetics or liver patients.

Hemorrhage is of course most relevant in trauma, which may be occult, but the peritoneum is easily sonographed and uncrossmatched blood remains one of our best therapies. Ahemorrhagic hypovolemia is even more treatable though an uncommon cause of arrest in developed countries.

There are several key antidotes to important toxins, intralipid is a rising arrest therapy to consider if a cardiotropic medication is suspected; bicarb, digibind, and hydroxocobalamin may also restore circulation in the poisoned patient.

Hyperthermia is hopefully easily identified; treatment can be tricky but should involve some form of icewater in most cases. Hypothermia is an important cause and effect of cardiac arrest and determining which can sometimes be a challenge.

Anaphylaxis as a cause of cardiac arrest will be treated by airway management and the epinephrine you’re giving anyway. Once the patient has arrested from sepsis or an aortic or intracranial catastrophe, it is unlikely that you will be able to meaningfully reverse the process.

Though excellent, step-by-step algorithms exist, it can be difficult to remember this differential while managing an arrested patient as well as your team of providers which, when large enough, invariably obstructs rather than augments care. However, once you’re used to taking care of pulseless patients, the differential can be streamlined.

Causes Highlighted

You’re not going to forget to look for and shock shockable rhythms or intubate. Hyperthermia and hypothermia announce themselves, anaphylaxis will be treated with your supportive therapies and the last three causes are more or less irreversible once the patient is dead. This just leaves eight causes which are treated with six therapies. Six is the perfect number of items for a mnemonic.


If you’ve ever been to Antwerp you know it is gloomy as hell, and you would never, ever carry bling through gloomy Antwerp. Needle, calcium, blood/fluid, thrombolytic, glucose and antidote are the six things to remind yourself to consider in the arrested patient. It’s the Hs and Ts, evolved for our post-ACLS age.

Lastly, if you are able to put arrested patients on bypass/ECMO, you are playing a different game than the rest of us and that game has a different set of rules. Come up with your own mnemonic that includes Antwerp.

Lecture is 35 minutes, then questions for 20 minutes. On Vimeo.


Opioids are extraordinary agents that have been used for millennia for the relief of pain and suffering; however, the history of opioids is also one of abuse and addiction. In the US, we are in the midst of a devastating iatrogenic chapter in this history, a prescription opioid epidemic that kills 15,000 Americans per year by overdose and destroys hundreds of thousands of lives and families.

In this presentation we will consider the magnitude and consequences of the current epidemic; describe how clinical organizations and clinicians were appropriated by the pharmaceutical industry so that Americans–5% of the world’s population–consume more prescription opioids than the rest of the world combined; and discuss strategies for managing patients who present to emergency departments with acute or chronic pain complaints that account for our competing mandates to palliate and protect.

These strategies center on an assessment of the likelihood that using opioids will deliver benefit or cause harm. For patients at low risk to be harmed by opioids, utilize aggressive multimodal analgesia, including opioids as needed to control acute pain, and prescribe optimal outpatient non-opioid analgesia with a small number of breakthrough opioids if indicated. For patients at high risk to be harmed by opioids, including patients with chronic pain and patients with flags for opioid misuse, avoid using opioids in the ED and outpatient settings, utilize non-opioids to manage symptoms, and, when misuse is suspected, nudge the patient to addiction treatment. The goals of optimal opioid stewardship are to provide effective symptom relief while preventing de novo cases of addiction, to control the supply of opioids in the community, and to protect existing addicts from further harm while promoting recovery.

For slides, the HELPCard treatment referral business card, and phraseology to use when managing patients at risk for opioid misuse, go to

Most of us were taught to place central lines using the wire through needle Seldinger technique, but using the introduction catheter instead of the needle makes successful wire insertion more likely and facilitates venous confirmation. A 7 minute screencast.

on vimeo

operating room video of wire through catheter technique. recommend viewing at 2x speed.

Update 1 Lee 2015 compares wire through needle and wire through catheter and shows that wire through needle is (slightly) better. The operators were anesthesiologists very experienced in central line insertion, which may account for their results. In the less controlled ED environment, with providers who don’t place a lot of lines (especially learners), the tendency of the needle to move before the wire can be transmitted may be more important. Also they did not confirm venous location in this study, which should be done whenever feasible and is greatly facilitated by the wire through catheter technique. Still, I’m aware of no data comparing the two techniques other than this (which appeared a few weeks after I posted the video), so though my success rate is definitely higher since I switched to wire through catheter, your mileage may vary.

Update 2  There are two advantages of the wire through needle (conventional approach): the needle is functionally slightly longer than the catheter, and the needle doesn’t kink. Neither of these advantages make a difference at the IJ site, and where I work almost all lines are IJ, so I didn’t mention this in the video. Based on feedback, I am surprised (and pleased) at how many non-IJ lines are being placed out there. If there is a lot of flesh in between the skin and the vein, for example at the femoral site in an obese person, the catheter can kink. This can be managed by keeping the pannus out of the way and keeping the skin taut throughout the procedure (flabby groin tissue can interfere with wire advancement as well, regardless of which technique you use to transmit the wire), but this requires an extra set of hands. At the subclavian site, the problem is not flesh but distance–sometimes you enter the vein relatively far away from where you enter the skin, and in this case the couple of millimeter difference between the wire and the catheter can be relevant. You can overcome this problem, in cases where you have to hub the catheter to get into the vein, by applying gentle continuous forward pressure on the hub until the wire is in the vein.





Cardiologists use calipers. Intensivists write little marks on a page and march them across. Emergency providers fold the ECG in half and hold it up to the light. Or the sun.


Fold the tracing in half. Hold up to the light.
















Now align the QRS complexes. The rhythm is regular.

2 regular rhythm overlap
















Here is another example.

3 irregular rhythm prelim fold

















Irregular. Cannot line up QRS complexes.

4 irregular rhythm overlap