Assessment and care of an acute myocardial infarction
EKG findings and prehospital 12-lead EKG interpretation point to the cause of the patient's problem and a course of treatment
Article updated July 19, 2017
You are transporting a 50-year-old diaphoretic Caucasian male patient (read the EKG case) complaining of 8/10 restrosternal chest pain for the last 45 minutes that started while sitting on a couch watching the evening news. The patient’s pain is unresolved after two doses of nitroglycerin. He has a regular and strong radial pulse at 44 bpm, blood pressure 138/46 mm Hg, 14 rpm, and a SpO2 of 97 percent on 4 lpm by nasal cannula. You are en route to the tertiary center and will arrive in approximately 10 minutes.
Expert panel discussion of patient with chest pain
- Rate & Rhythm: 3rd deg AV block at 42 bpm
- P wave: P waves dissociated from QRS at a rate of 100 per minute
- PR interval: Irregularly irregular
- QRS interval: 0.12 sec
- QRS complex and mean axis: Wide complexes. Normal axis
- ST segment: Isoelectric
- T wave: Are discordant with the QRS, meaning they are deflected in the opposite direction of the "bulk" of the QRS complex, a normal finding in LBBB
- U wave: Present on V1, V2, and V3
- QT interval: 0.48/0.39 corrected
The first QRS complex of this EKG has a P wave immediately preceding it. By measuring the distance between P waves and the R-R interval we can see that this timing is coincidental. The third QRS complex has a P wave "hidden" behind the ST segment. The last QRS complex again has a P wave preceding the QRS. This is a good example of a potential confounder and why even a non-diagnostic rhythm strip duration of ten or more seconds can be helpful. The QRS interval measures approximately 0.12ms, which is consistent with a QRS that originates in the ventricles.
While an acute myocardial infarction could be the culprit for this patient, you can’t be certain without ST segment elevation. When the clinical picture is combined with the EKG, however, an astute clinician should be concerned and should treat the patient with AMI high on the list of differential diagnosis.
A symptomatic bradycardia is not an uncommon scenario. Your treatment plan should be directed at treating the symptoms presented and should be directed towards minimizing the load on the heart while transporting to a facility with interventional cardiology. With this patient, determining the sequence of events may be difficult in the field.
- Is the bradycardia the result of an electrolyte imbalance such as hyperkalemia or is the patient's heart ischemic?
- Or is it normal for this particular patient?
These questions should rise quickly to the top of choices to consider. The patient is diabetic, but has not expressed a history of recent illness or chronic renal failure, making ischemia or AMI the most likely cause.
The next consideration is of the chest pain that remains unrelieved by nitroglycerin and oxygen. This could be due to an ongoing AMI, but take a moment to think about other potential causes. What effect would TCP have on ischemic heart muscle? The best treatment is to continue providing oxygen, maintaining a low flow patent IV, and reassuring comments intended to calm the patient.
One final tidbit is in regard to the recognition of the patient holding a clenched fist over his chest. This is known as Levine’s Sign, named after the physician who found this particular gesture to be somewhat specific to chest pain resulting from cardiac causes.
- Basic Level: Evaluation of a patient complaining of chest pain suggestive of Acute Coronary Syndrome (ACS). Identifying an atrioventricular (AV) block.
The initial approach to this patient should include 3-lead EKG monitoring. Lead II is a very good lead for the purpose of determining heart rate and cardiac rhythm. The EKG strip for this case clearly shows P waves that are not conducting to the ventricles. The P waves appear at a regular rate and the QRS complexes also appear to be regular. This tells us the patient has complete AV disassociation, which is also known as a "complete" AV block or third degree AV block.
With any patient complaining of chest pain, it is important to obtain a 12-lead EKG. You should set a benchmark for a rapid 12-lead EKG on any patient suspected of suffering from ACS. Some EMS agencies have set a benchmark time for 12-lead acquisition at five minutes. With a little practice, good teamwork, and solid clinical evaluation, you can evaluate a chest pain or ACS patient and obtain the 12-lead in five minutes. Many studies and current medical literature point to the benefits of reducing the time it takes to identify an acute myocardial infarction (AMI), particularly one with ST segment elevation (STEMI), and rapidly directing that patient towards interventional cardiology providers.
- Intermediate Level: Evaluating a list of differential diagnoses for any patient with chest pain and an atrioventricular block even without evidence of ST elevation myocardial infarction (STEMI).
The list of differential diagnosis possibilities need not be long. Based on past medical history of non-insulin dependent diabetes without chronic renal failure and without recent illness and with no other findings suggestive of hyperkalemia, this is not a likely cause of the bradycardia. Bradycardia could also be cause by an AMI, whether it is a STEMI or non-STEMI. Many bradycardia causing AMIs are localized to the right ventricle. A right-sided EKG may show ST elevation in lead V4R.
In some systems it would be appropriate to obtain a right-sided EKG, particularly for lead V4R. This is located at the V4 position on the right side of the chest. This lead view is particularly well-suited for detecting ST elevation in the right ventricle, a common culprit in bradycardia causing AMIs. The patient tolerated the nitroglycerin; however, if he was preload dependent, the reduction in preload caused by nitroglycerin administration could have caused a precipitous drop in blood pressure. This would have provided further clues of a right ventricular AMI.
- Advanced Level: Determining appropriateness of external pacing for a symptomatic but stable patient with an atrioventricular block.
There are few patient presentations which highlight the old medical adage "treat the patient and not the monitor" more than cases of third degree AV block resulting in a ventricular escape bradycardia. Although this patient seems to be compensating well, as evidenced by his good mentation, skin color, and adequate blood pressure, this could change quickly.
Atropine, normally a first line treatment for bradycardia, may be used with caution in this patient. Why? For two primary reasons the use of atropine in the setting of AMI is cautioned against by the American Heart Association/American College of Cardiology. The second reason can be evaluated in this patient whose 12-lead hints at an inconsistent ventricular pacemaker site. Notice the fourth and fifth complexes have differing morphologies. The fourth originates in the right ventricle and the fifth originates in the left ventricle. Neither appear to originate in the AV node itself based on the QRS width and the shape of the QRS complexes found in lead V1. One must consider the desired effect of atropine and whether it would benefit this patient. Atropine works by blocking and reversing the vagal tone. Remember, the vagal tone serves to slow conduction through the AV node. The ventricular pacemaker sites(?) this patient is exhibiting are too low to be effected by the AV node, thus making atropine not-indicated. When faced with complete heart block, you should prepare for Transcutaneous Pacing (TCP), but do not begin pacing until signs and symptoms of inadequate perfusion are evident.
Additional Teaching Points
Cardiac chest pain: does body language help the diagnosis? W M Edmondstone. BMJ 1995;311:1660-1661 (23 December).