The 9-1-1 dispatcher reports a call from a female who says her 66-year-old mother "may be having a heart attack, but is responsive." On arrival, the crew finds the older female can answer questions, but responds in a fashion the daughter says is abnormally slow and confused. The patient, Mrs. Jones, says she had a heart attack four months ago and is now taking medication for heart failure. She has felt progressively tired over the past two weeks, and feels dizzy when standing. Today, her chest started "feeling funny" about an hour ago, with some pain at about 2 on a 10 scale. She has a history of hypertension. She is not reporting shortness of breath, sweating or nausea.
Initial physical exam reveals an elderly female with pale skin in no respiratory distress. Her vitals are: BP 90/55, pulse 48 and irregular, RR 24 with slight bilateral lower lobe crackles, pulse oximetry 92%. Her pupils are equal, round and reactive; blood glucose is 90; there is 1+ ankle edema, and the jugular veins are distended.
Oxygen is given by NRB at15 LPM; IV access and the initial lead II strip are obtained. Every third P-wave lacks a subsequent QRS complex. All P-R intervals are 0.16 seconds and regular. The QRS complexes are 0.18 seconds wide and upright in lead II. A 12-lead EKG is obtained showing a left axis. The rhythm disturbance noted in the 3-lead rhythm strip is confirmed. Lead V1 shows deep QS waves and ST segment elevation (see Figure 1). These ECG findings point to the possibility of left bundle branch block. There are Q-waves in leads II and III, which raises concerns for inferior or right-sided infarction.
The nearest hospital with invasive cardiac capability is 45 minutes away, and the patient had received treatment at the facility for a heart problem that occurred four months ago. A closer community hospital is 10 minutes transport time. Oxygen has not improved the patient's pulse oximetry reading or mental status. She shows evidence of poor perfusion and is still confused. Her daughter can't provide any history of the patient's usual blood pressure, but in a patient with a history of hypertension, a blood pressure of 90/55 is almost certainly too low. Her heart rate is low, and she is not conducting the electrical impulses effectively and regularly. The patient shows signs that her vascular volume is not compromised, with jugular venous distention, lung crackles and leg edema. To increase perfusion, the patient needs a heart rate higher than 48 beats a minute. Questions the EMS crew will need to consider are: How should the bradycardia be treated in light of a suspected left-sided bundle branch block and possible MI? If this patient deteriorates, should she be given atropine or have transcutaneous pacemaking performed? In view of these questions and how they will impact the transport decision, medical control is contacted.
BRADYCARDIA TREATMENT OPTIONS
The emergency physician on service initially asks for details regarding the patient's current health status and determines that although she continues to show symptomatic signs of hypoperfusion, her condition is not deteriorating. Therefore, transport should continue toward the hospital with invasive cardiac capability. With regard to patient care en route, the physician frames the decision into three groups: (1) supportive care only, (2) give medication, (3) use electrical intervention.
Supportive care is appropriate if the patient has been deteriorating and transport has been directed to the nearby community hospital. In this case, the biggest assist to patient care would be maintaining the airway and oxygenation, as well as expediting the patient's hospital care by obtaining serial vital signs and ECG printouts. With this short transport, the critical decisions involving invasive procedures are better made in the more controlled environment of the emergency department. The other case in which supportive care would be warranted is when the patient is maintaining perfusion. If bradycardia is present but the patient has normal mental orientation and function, then no invasive intervention in the ambulance would be indicated.
The second decision group involves the use of medication. Atropine is commonly used for patients with symptomatic bradycardias. If the patient continues to have symptomatic bradycardia, dopamine is the second-line agent after transcutaneous pacing. These agents can be used to maintain the patient's perfusion status in a symptomatic bradycardia en route to specialized care; however, keep a heightened suspicion of MI. If an infarction is present, chromotropic and inotropic medication would be minimized to prevent excessively increased oxygen demand from the myocardium before arrival at the ED and cath lab.
Electrical intervention for symptomatic bradycardias in the prehospital setting involves transcutaneous pacing. For cases of third-degree heart block in which there is complete atrioventricular dissociation, or in a rapidly deteriorating patient, this is the primary treatment. There are a couple of considerations with regard to pacing, one of which is that transcutaneous pacing is painful. The increased sympathetic response to pain can in itself act as a stimulant, but there are more humane ways to accomplish this, such as using atropine. Sedatives are therefore given to facilitate pacing, which presents its own set of dilemmas. The sedative may dampen any remaining sympathetic stimulus to maintain heart rate and respirations. Also, it becomes more difficult to assess the effectiveness of treatment when the patient's mental status has been altered. Finally, pacing itself lessens the diagnostic effectiveness of ECGs, so on arrival at the ED, not only is the patient's mental status unreliable from sedation, but the paced rhythm may have masked ECG changes. These are factors to be considered when ordering pacing. Nevertheless, it is the indicated treatment for third-degree block or a deteriorating patient with bradycardia (Figure 2).
In this case, the report was given to the ED physician, who asked that in addition to aspirin and two large IVs, the patient be given 0.5 mg atropine and be monitored for any changes in vital signs, ECG findings and mental status.
Atropine is one of the oldest drugs in the medical pharmacopeia. It was used in ancient times, not as a chronotropic agent, but as a cosmetic drug. The belladonna plant, which is a source of atropine, means "beautiful lady" in Italian. It was known for its ability to redden cheeks and dilate the pupils, thereby enhancing beauty. Atropine has also been a first-line treatment for bradycardia for hundreds of years. In modern times it is used to antagonize the effects of acetylcholine, which plays a large role in regulating the sinoatrial node and transmission of impulses to the atrioventricular node in the heart. It is accepted practice to treat bradycardias with SA nodal input by giving atropine.
There have been conflicting views regarding treatment with atropine for bradycardias resulting from heart blocks. The American Heart Association, as well as most EMS protocols, recommends pacing without delay in treatment of high-degree heart blocks, which include both Mobitz II and third-degree blocks. Keeping the creed "First do no harm" in mind, it is difficult to go straight to the painful administration of transcutaneous pacing. It is an equally difficult decision to sedate a patient who is minimally responsive. Therefore, questions arise concerning the use of atropine as an initial treatment and what factors might be considered beforehand. The focus is on atropine, because there is much confusion and debate among paramedics on its role and implementation, especially in regard to heart block. Opinions about the use of atropine in heart block generally follow one of three statements: (a) It is relatively contraindicated in high-degree blocks; (b) atropine is ineffective for high-degree blocks and should therefore not be considered; (c) the ACLS guideline says atropine should be considered, but should not delay prompt pacing.
So what are the considerations at play? There is not much guidance on the issue in ACLS or in most protocols, so the statement "consider atropine but do not delay pacing" has not been entirely clear to many medics. A major source of confusion on the issue stems from the fact that a common cause of high-degree heart block is myocardial infarction. Since the actions of atropine are to block the binding of acetylcholine to muscarinic receptors, thereby (a) reducing vagal input at the SA node, and (b) increasing conduction velocity through the AV node, the thought is that atropine would be a poor choice for reducing oxygen demand in heart-block therapy when an MI is present. This case study was intended to take some of the mystery out of the decision of whether to use atropine in treating high-degree heart block along with pacing. The discussion hopefully provides some clarity in the standard that is already in place. Working up these cases in a logical manner will provide guidance on treatment, minimize adverse effects and improve patient outcomes.
GIVING ATROPINE WHERE HEART BLOCK IS PRESENT ON EKG
In the scenario, there are indeed factors pointing in the direction of right ventricular or septal MI, especially the V1 ST segment elevations and pathological Q-waves. Confounding the interpretation, however, the possibility exists that the Q-waves were residual indicators of previous MI. The ST segment elevations in lead V1 may be entirely due to a prior existing left bundle branch block, which often has ECG features of an elevated ST segment. The point here is that what looks like MI on the ECG can be misleading, possibly leading a medic to not use atropine in heart block. Furthermore, making a diagnosis based on ECG interpretation can be difficult in any practice, especially in a prehospital setting. Therefore, the initial decision of whether to treat the bradycardia with atropine or pacing should be primarily based on the patient's hemodynamic presentation.
The other ECG sign mentioned that might lead medics to discard the use of atropine was the wide QRS complexes. This is the basis for the perception that atropine is ineffective in wide-complex Mobitz II block. A wide QRS complex is an indication that the electrical origin of ventricular depolarization is not from the SA or AV nodes, but from the ventricles themselves. The point that must be made here is that bundle branch blocks (a) don't always show the RSR morphology (that is, they don't always have two distinct points at the apex) and (b) bundle branch blocks prolong the QRS width, appearing falsely to be a ventricular rhythm, especially when it's hard to discern the P-wave. The point here is that a Mobitz II block is commonly a block in the bundle branches and therefore shows widened QRS patterns similar to a ventricular rhythm.
So, just as described above in regard to ECG signs in BBB overlapping with an MI, ECG signs in BBBs can also overlap with what appear to be ventricular rhythms. Again, careful consideration of the patient's hematological status and presenting appearance must be made before deciding to withdraw atropine therapy. This was true in Mrs. Jones' case, in which two out of three atrial depolarizations caused ventricular contraction, but not rapidly enough to keep the tissues adequately perfused. Stated another way, if there is ventricular response to nodal impulses in a BBB and the patient is symptomatic, it cannot be argued that atropine will have no effect.
USING ATROPINE IN THE ACUTE MI PATIENT
Given that an acute MI would ordinarily exclude the use of atropine's accelerating effects, the question now is, would the risk of harm by giving atropine in MI outweigh its usefulness? The decision is especially crucial in a poorly perfused patient like Mrs. Jones, for whom the adverse effects of pain from pacing and the risks of sedation may be large. To continue the theme described above, it must be recognized that along with false positive readings for MI, there are also commonly true MIs in which there are absolutely no ECG signs. An example of how timing can make an ECG falsely normal is to obtain an ECG during a phase when the T-wave is moving upward from an inverted position (ischemia) to an upright position and pulling the depressed ST segment upwards with it. For a small period of time, the ECG will appear to be completely normal, when in fact death is imminent. The point is that an ECG is a flash in time. Although decisions in the emergency setting must be made with speed, having the benefit of establishing a trend will lead to better-quality decisions. This luxury is generally not available to paramedics in the field; therefore, emphasis must be on the patient's lack of perfusion from bradycardia in order to make a decision regarding atropine.
As stated, it is difficult to make a treatment decision based solely on ECG signs; therefore, we base the decision of whether to use atropine primarily on patient presentation. However, one case in which the use of atropine can more confidently be excluded is left coronary artery infarct. The LCA supplies the left ventricle, left lateral side, septum and, in 15% of cases, the inferior wall. The signs of LCA infarct are usually the more classic signs of "heart attack" because the LCA branches supply such a large area of myocardium. The highly sensitive presentation is a history of severe, crushing, substernal, radiating chest pain, diaphoresis and characteristic ECG indications of hypoxic left myocardium. The problem from a diagnostic standpoint is that the interventricular septum containing the bundle branches is supplied by the septal branch of the LAD. So a LAD infarct may give high-degree heart block signs, yet it would be incorrect in this case to irritate the myocardium further by giving atropine as the primary treatment. Left-sided infarction has a classic presentation. In addition, the intact SA node will usually respond to hypoperfusion with tachycardia. Thus, in the case of high-degree block in the face of left-sided MI, patient presentation can again, along with tachycardia, guide the treatment, in this case away from atropine.
Mrs. Jones did not show most of the classic signs of LAD infarct, but what if she was in the midst of a right coronary artery infarction? Should this possibility exclude the use of atropine in a symptomatic patient? RCA infarct is more difficult to identify because the signs are more subtle, but in addition to inferior lead II, III, aVF and V4R ST segment changes, there are common right-sided features of (a) hypotension, (b) jugular venous distension, with (c) clear breath sounds. Mrs. Jones did have slight crackles, but these may have been a chronic condition resulting from her recent MI. Otherwise, she fits the picture. Our next question then is, does atropine help or hinder our treatment in the case of RCA infarct?
First, it must be understood that just as the septal branch of the LAD supplies the interventricular septum and bundle, the nodal branches of the RCA supply the SA and AV nodes via different branches. So both infarct locations will affect signal conduction. But there is a major difference between right and left coronary infarct. Sympathetic division autonomic innervations travel by blood vessels. Parasympathetics in the thorax travel via vagal nerve branches. When there is ischemia to the nodal branches of the RCA, there is a relative decrease in sympathetic input and a relative increase in vagal input, leading to sinus bradycardia, as well as a conduction delay, leading to heart block. So both LCA and RCA infarctions can lead to heart block by differing mechanisms.
One commonly noted case review: Atropine associated with RCA infarct is a declining perfusion status upon administration of nitrates. It is for this reason that, if RCA infarct is suspected, a V4R ECG is obtained, along with two large-bore IV sites for rapid fluid infusion capability. When there is ST segment elevation in leads II, III, aVF and V4R, administration of nitroglycerin can cause blood pressure to rapidly drop due to a decrease in preload. Using atropine to reverse the nitroglycerin-induced preload reduction would not offer benefit, since the hypotension is due to low preload. However, there is no way to know whether the SA or AV node remain functional. If they are, then atropine would offer some benefit in increasing perfusion and could be an appropriate bridge to maintain the patient's status on the way to the ED and cath lab. Again in the case of RCA infarct, the decision to administer atropine is based on the degree of symptomatic presentation of bradycardia.
Upon administration of atropine, Mrs. Jones' heart rate increased into the high 50s and her mental status improved. There were no further ECG changes noted, but she was found to have ST segment elevation in lead V4R. She arrived at the ED in stable condition and soon thereafter underwent cardiac catheterization and stenting of the right coronary artery. She later received an implanted pacemaker.
This case study examined a situation in which the use of atropine was considered in a symptomatic patient who suffered from hypoperfusion due to bradycardia. The case reflects the need to treat the patient, but recognizes the concern of "causing no harm" with the intervention. The "harms" of particular concern include increased oxygen demand from the atropine, or if atropine is discarded in lieu of pacing, then the "harm" of concern would be the pain of pacing, as well as the concern of sedating a minimally responsive patient. The question of whether to use atropine can be confounded by co-existing factors like heart block and MI. Due to the practical difficulty of making a diagnosis based exclusively on an ECG, it has been shown that the decision should be primarily based on the degree of hypoperfusion the patient is displaying.
One instance where harm is minimized by withholding atropine administration from heart block treatment is an LCA infarction, which is typically accompanied by classic signs combined with ECG changes and tachycardia. For paramedics, the first question, which must be continuously considered, is, "Does the patient need any intervention at all at this time?" If the answer is "no," the patient would be better served by being transported directly to the ED and cath lab, where medical staff possess the advantage of technology and experience to identify specific causes of hypoperfusion and treat based on that knowledge. On the converse, we also recognize that tissue hypoxia and hypoperfusion are acute issues that will become the highest priority necessitating our consideration of atropine or pacing.
Hopefully, this article has had the effect of not only highlighting an actual case and prompting a discussion, but also of providing paramedics with the luxury of forethought into a situation that they may face.
1. Aehlert P, ed. The 12-Lead ECG in Acute Coronary Syndromes, Mosby, 2006.
2. American Heart Association, Handbook of Emergency Cardiovascular Care, AHA 2006.
3. Blackwelder R. EKG Interpretation, 2008.
4. Hayashi T, et al. Usefulness of ST segment elevation in the inferior leads in predicting ventricular septal rupture in patients with anterior wall acute myocardial infarction. Am J Cardiol 96(8):1037–1041, 2005.
5. Netter F, ed. Atlas of Human Anatomy, 4th edition, Saunders Elsevier, 2006.
After working and volunteering in EMS since 2003, Stewart Stancil entered medical school under the U.S. Army Health Professions Scholarship Program. He is currently a CCEMT-P and a third-year medical student at East Tennessee State University and will begin a residency in emergency medicine in 2011.