Last week I posted on some of the problems with this precordial thump study.^[1] This week I will look at some of the positives. While the data do not suggest that we should start using precordial thump. The data suggest that we should be doing more research. Is this harmless when it is not effective? This is an important question that the study seems not to address. I already wrote about that enough.

Here are some of the positives. The ECGs from the actual thumps are impressive:


ECG 1.

Figure 1. Restoration of cardiac activity following pre-cordial thump delivery after 52 s of asystole. Cardiac arrest was witnessed by the emergency medical service personnel during ambulance transport.

Patient 1

A 64-year-old man with a history of hypertension and syncope developed CAAS during hospital transportation. Asystole was treated solely by PT, causing prompt ROSC. The patient was discharged alive, neurologically intact, after electrical pacemaker implantation (#1 in Table 3; see Figure 1).^[2]

ECG 2.

Figure 2. Patient recording of pre-cordial thump induced cardioversion during witnessed out-of-hospital cardiac arrest (OOH-CA). Subsequent to the development of asystole, a pre-cordial thump is delivered after 22 s (see arrow), restoring a palpable pulse.

Patient 2

A 51-year-old female with a history of migraine called EMS, suffering from headache, nausea and vomiting. During transportation the patient became progressively bradycardic (in the absence of further vomiting), developed 1st degree atrio-ventricular block, and suddenly lost consciousness. After 22 s of documented CAAS, PT was delivered and sinus rhythm achieved (Figure 2). The patient received an implanted pacemaker and was discharged neurologically intact (#2 in Table 3).²

ECG 3.

Figure 3. First episode of asystole successfully treated by pre-cordial thump on the scene. Two more episodes were observed during ambulance transport to the hospital, all responsive to a single pre-cordial thump.

Patient 3

A 78-year-old man experienced 160 s of EMS-witnessed CAAS. PT was followed by restoration of spontaneous circulation. P waves were recognized during post hoc analysis of the defibrillator memory card for the first 120 s of CAAS. During transportation, two additional episodes of CAAS occurred, both converted successfully into an organized viable rhythm by prompt administration of a single PT (Figure 3). The patient was conscious when admitted to the coronary care unit, and transferred to the department of internal medicine without pace-maker implantation, where he subsequently died of pneumonia complicating chronic obstructive respiratory disease (#3 in Table 3).²

Some of you may be thinking that this is all the convincing you need to start thumping patients. Especially the ones in cardiac arrest. Not so fast.

Look at these rhythms without looking at the thumps. Are they clearly asystole?

I don't think so. True, the strips are not as clear as we would like, but they are dealing with a witnessed cardiac arrest in each of these cases. Some are during transport, so there are plenty of reasons for artifact. If three beats make a rhythm, what would three beats of asystole be? Three very bradycardic beats? Three of whatever was the previous rhythm, if we already have the patient on the monitor and know what the previous rhythm was? This is really more of an answer to a documentation question. Patients are not documentation questions.

ECG 1. I have labeled the individual strips with letters, so that it is easier to specify what I am describing. What do you see?

Each is a 14 second strip. We do not know if the ECG is continuous in the same lead. Strips A and D do look alike, so they probably are the same lead. Strip B begins with a beat that looks different. Is it a different lead? Then there is asystole for 52 seconds before something is done? We are missing a lot of information.

I am more patient than most people. I am not going to wait 52 seconds after cardiac arrest to do something, except if I have given adenosine or if there is some kind of an advance directive (such as a DNR - Do Not Resuscitate order). His heart rate was already in the mid-30s. Was he symptomatic? We do not know. What was the original call for?

He has a history of syncope. He may vagal down to something that looks asystolic, but with something that could be atrial activity, somebody may shake him to see if he is OK, and his heart remembers what it was doing.

Or he could be in an ambulance, repeat that behavior, and be awoken by a medic punching him in the chest.

Or he might not need any stimulus. When he does this, it may be something that resolves spontaneously.

Does he have Cheyne-Stokes respirations? His heart rate may vary with his rspiratory pattern. 52 seconds of asystole does seem unlikely, but we do seem to be in zebra territory.

His QT segment seems to be longer after the thump (strip A vs strip D). Is this related to the thump? Is this related to the ventricular standstill? Is this at all relevant? A lot of unknowns with this patient. We don't know anything about vital signs, except ECG heart rate. Let's move on to the next one.

Should he have received atropine or transcutaneous pacing prior to arresting? Difficult to tell. Does the transcutaneous pacer work more by obtaining capture, or by painful stimulus? Maybe it is a little of both, because some of the pacer applications I have seen have not been good for anything but painful stimulus. Why should we give more credit to the precordial thump?

Is the original rhythm sinus? Is the final rhythm sinus?

Figure 1. Restoration of cardiac activity following pre-cordial thump delivery after 52 s of asystole. Cardiac arrest was witnessed by the emergency medical service personnel during ambulance transport.

Patient 1

A 64-year-old man with a history of hypertension and syncope developed CAAS (Cardiac Arrest - ASystole) during hospital transportation. Asystole was treated solely by PT, causing prompt ROSC. The patient was discharged alive, neurologically intact, after electrical pacemaker implantation (#1 in Table 3; see Figure 1).²

ECG 2. Each is a 6 second strip. As with ECG 1., there appears to be some atrial activity. Sinus rhythm with a first degree block. This seems to progress to a more serious form of first degree block - one without ventricular activity. The rate is about 80 before the arrest, so it does not appear that this would have been prevented by treating the presenting rhythm. The resuscitated rate is only about 60 (strip Cand it seems to take its time getting there if strip B is any indication.

Figure 2. Patient recording of pre-cordial thump induced cardioversion during witnessed out-of-hospital cardiac arrest (OOH-CA). Subsequent to the development of asystole, a pre-cordial thump is delivered after 22 s (see arrow), restoring a palpable pulse.

Patient 2

A 51-year-old female with a history of migraine called EMS, suffering from headache, nausea and vomiting. During transportation the patient became progressively bradycardic (in the absence of further vomiting), developed 1st degree atrio-ventricular block, and suddenly lost consciousness. After 22 s of documented CAAS, PT was delivered and sinus rhythm achieved (Figure 2). The patient received an implanted pacemaker and was discharged neurologically intact (#2 in Table 3).²

ECG 3. Again, each is a 6 second strip. This patient arrests 3 times. What are the rhythms before the asystoles? I thought 52 seconds of asystole was demonstrating extreme patience. This patient was in asystole for 160 seconds before being thumped. 2 minutes 40 seconds. Top marathoners will run over half a mile in that time - at a pace that they will maintain for over 26 miles. Try holding your breath for that amount of time. This is a small amount of time for many things, but for going without a heartbeat during a witnessed cardiac arrest, this can be a lifetime - at least for the patient. I've had to explain to some patients that they were dead for a few minutes, but at least I was treating them during that time. In this study, the patients received a precordial thump as the first treatment. If not they were not included in the precordial thump treatment group. This patient was included in the precordial thump treatment group. This is described as an EMS witnessed cardiac arrest. Were they waiting for the P waves to go away? Were they trying to see what interesting colors the patient could demonstrate? Was someone preventing them from treating the patient? Again, there are a lot questions, but not enough answers. Since no CPR was described for this patient, what were they doing for almost 3 minutes? After 3 minutes it is more likely to be time to repeat a treatment, rather than to decide to finally initiate treatment.

We have three different looking post-arrest rhythms. Do they begin to look more alike after a few beats? In describing him, there is almost as much space used as for both Patient 1 and Patient 2 combined. It is almost as if they view the death in the hospital after resuscitation with return of consciousness as a failure of the precordial thump, that needs to be explained.

What was the original call for?

Figure 3. First episode of asystole successfully treated by pre-cordial thump on the scene. Two more episodes were observed during ambulance transport to the hospital, all responsive to a single pre-cordial thump.

Patient 3

A 78-year-old man experienced 160 s of EMS-witnessed CAAS. PT was followed by restoration of spontaneous circulation. P waves were recognized during post hoc analysis of the defibrillator memory card for the first 120 s of CAAS. During transportation, two additional episodes of CAAS occurred, both converted successfully into an organized viable rhythm by prompt administration of a single PT (Figure 3). The patient was conscious when admitted to the coronary care unit, and transferred to the department of internal medicine without pace-maker implantation, where he subsequently died of pneumonia complicating chronic obstructive respiratory disease (#3 in Table 3).²

These problems with the research did not go completely unnoticed outside of this blog. In the same issue there is an article pointing out some of these problems. Here is a quote:

In this study therefore, the precordial thump may have played only a marginal role. Pellis et al, nevertheless, do recommend the continued use of the precordial thump in out-of-hospital cardiac arrest and cite an “interesting cost-to-benefit potential” for patients in EMS-witnessed asystole. Let us, for the sake of argument, accept that the cost of the precordial thump is low, maybe even zero. But is there any benefit? I am not convinced. As discussed by the authors, the ambulance-witnessed asystole cannot be the late asystole from end-stage VF as this, almost by definition, is associated with late arrival of the ambulance and no bystander CPR. In the tracings, at least in two out of the three cases, p waves are visible, suggesting complete AV block with lack of an escape activity as the cause of the asystole. But why was the ambulance called in the first place? The authors do not answer this question, but it is not unlikely that an earlier symptomatic episode of asystole was the reason to call for ambulance help, confirming the transient and repetitive nature of the conduction disturbance. In any case, no alternative diagnosis was apparent and the uncontrolled nature of this cohort makes it impossible to establish a causal relation between the precordial thump and the positive outcome in the two surviving patients. While the abnormal shaped QRS complex from the thump in Figs. 1 and 3 are good examples of the relation between thump and electrical activity, this cannot be seen in Figure 2. Here it is questionable if there is any relation between the suggested moment of the thump and the QRS complex at that position, given the shape that appears identical to all other QRS complexes. Nevertheless, it is possible that in asystole caused by a conduction disturbance (a small minority in out-of hospital cardiac arrest) the thump may have played a role in the good outcome in two of three patients.^[3]

Are these high grade heart blocks or are they cardiac arrests?

We do not know.


Footnotes:

^ ¹ Utility of pre-cordial thump for treatment of out of hospital cardiac arrest: A prospective study
Pellis T, Kette F, Lovisa D, Franceschino E, Magagnin L, Mercante WP, Kohl P.
Resuscitation. 2009 Jan;80(1):17-23. Epub 2008 Nov 17.
PMID: 19010581 [PubMed - indexed for MEDLINE]


^ ² Utility of pre-cordial thump for treatment of out of hospital cardiac arrest: A prospective study
Pellis T, Kette F, Lovisa D, Franceschino E, Magagnin L, Mercante WP, Kohl P.
Resuscitation. 2009 Jan;80(1):17-23. Epub 2008 Nov 17.
PMID: 19010581 [PubMed - indexed for MEDLINE]
The same study.


^ ³ Precordial thump: friend or enemy?
Koster RW.
Resuscitation. 2009 Jan;80(1):2-3. No abstract available.
PMID: 19103396 [PubMed - indexed for MEDLINE]

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