How to Treat Chest Pain and Bradycardia

Rich Greene, PA-C EM

Be Still my Beating Heart: Nitro vs Atropine in Bradycardia

Case Presentation:

A 55 y/o male presents to the Emergency Department with 1 hour of chest pain.  His initial EKG shows a sinus rhythm with a rate of 45 and no ST elevations or depressions.

What is your diagnostic approach and considerations in this patient?

You have a patient with sinus bradycardia complaining of chest pain. How can you refine your clinical gestault regarding your patient? 

Chest Pain and Bradycardia

Chest Pain Risk Factors

Before we delve into treatment for this specific case, let’s consider our approach in general to any chest pain complaint.  First of all, consider your patient’s cardiac risk factors.  The HEART score is a clinical calculation that helps predict the risk of a major adverse cardiac event within 6 weeks.  This is a great tool that will help to guide you in determining a disposition for your chest pain patients.  The major risk factors considered in the HEART score are: hypertension, hyperlipidemia, smoking, diabetes, family history, previous CAD (such as previous stroke, MI, or known peripheral artery disease), BMI > 30.  You can gather this information from reviewing the patient’s record/medication list or directly questioning the patient.  Take time for a quick 30-60 second conversation.

Patient History

The next part of the conversation (either with the patient, EMS, or both) will focus on the history. I use OPQRST.  Most educational institutions, whether teaching in-hospital or pre-hospital history taking, utilize this mnemonic as a framework for obtaining history.  (O) onset: when did this start? What were you doing when this started?  Were you sitting watching TV, sleeping, or doing cocaine?  (P) Provocative/Palliative features:  Is there anything that makes the pain better or worse?  Does it hurt when I push here? Is it better with rest or worsened with exertion? (Q) Quality: Is the pain sharp, dull, stabbing, aching, squeezing, tightness, etc? (R) Radiation: Where is the pain? Does it go anywhere else like your arm, neck, back, or abdomen?  (S) Severity: What number out of 10?  Is this like your previous heart attack or when you got stents?  (T) Timing: When did the pain start?

By combining the risk factors with the history, you should have a pretty good idea of whether your patient has ischemic chest pain or not. After considering your initial EKG and lab values (primarily troponin), it lets you risk stratify your patient into Low, Intermediate, or High Risk.  This stratification is basically the same algorithm as the HEART Score.  The HEART Score is an evidence based, clinically validated “calculator.” In the end, it helps justify or guide your patient disposition.

Now back to our patient…55yo male, 1 hour of chest pain, and sinus bradycardia EKG.  When we walk in, he is sweating and clutching his chest. EMS gave 325mg ASA before bringing him to you.  He is not on any medications that could induce a bradyarrhythmia.  Without belaboring too many details, let’s just assume this patient is giving you a vibe of ischemic chest pains.  

Treat Chest Pain or Bradycardia?

This is where I want you to consider this clinical dilemma: Which medication should you give next…nitroglycerin (NTG) or atropine?  Are you going to treat the chest pain or the bradycardia?

According to your ACLS protocols, the answer is atropine because the patient is in symptomatic bradycardia.   The thought goes that if persistent bradyarrhythmia is causing hypotension, altered mental status, ischemic chest discomfort, or acute heart failure then atropine should be your first choice.   If NTG doesn’t work consider transcutaneous pacing or dopamine or epinephrine infusions.

But Wait… Not So Fast!

I thought chest pain standard of care was that MONA met every chest pain at the ER door?  MONA stands for morphine, oxygen, NTG, and aspirin.  

So the clinical question is two-fold: 1) Is the bradycardia because of the chest pain or is the chest pain because of the bradycardia?  2) What are the clinical repercussions for each of the medication choices? A classic chicken versus egg dilemma!

One of the clinical presentations for an inferior wall MI is bradycardia.  In particular, an inferior wall MI is due to a lack of perfusion in the Right Circumflex Artery (RCA).  The right coronary artery supplies blood to the AV node In 85% of people.  It also supplies blood to the SA node 70% of the time. With an inferior wall MI, one or both of the cardiac pacemakers could sustain damage.  In turn, this would cause an escape beat elsewhere in the heart due to the cardiac cell’s unique capability of automaticity.  That is, cardiac cells will self-depolarize at a slower rate unless an earlier quicker source such as the SA or AV node depolarizes them first. The escape beat rate for the atria are between 30-60 beats per minute and will produce a P-wave on EKG, giving you an EKG that looks like sinus bradycardia.

Atropine

Atropine is the first line treatment for symptomatic bradycardia.  However, you should use caution in the presence of myocardial ischemia because it increases myocardial oxygen demand.  Atropine blocks the parasympathetic action of the heart, which increases the rate of electrical firings of the sinus node.  This increases the rate of firing at the AV node, which increases the heart rate and cardiac output.  As with any muscle, the increased work requires increased oxygen demand.  In the setting of an acute myocardial infarction, the increased oxygen demand would worsen the clinical situation (i.e. pain).

Nitroglycerin

Nitroglycerin (NTG) treats ischemic angina by vasodilation.  There are multiple routes of administration to include spray, sub-lingual, topical, and IV.  The rationale for giving NTG is that it causes venous and arterial vasodilation.  This will reduce both cardiac preload (from the venous return) and cardiac afterload (by reducing systemic resistance).  In turn this will reduce workload and oxygen demand of the heart.  

Isn’t NTG contraindicated for inferior wall/right ventricle infarctions? Yes and No.  The use of NTG in this situation is a relative contraindication and not an absolute contraindication.  The problem is that the right ventricle is not designed for systemic circulation.  It is designed for pulmonary circulation so by design the walls are thinner and the pressures are much lower.  It’s functional ability is dependent on preload.  So a reduction in venous return will result in diminished pumping pressure by the right ventricle, diminished pulmonary circulation, diminished left ventricular filling, diminished cardiac output, diminished systemic blood pressure and, if not corrected, possible dysrhythmias, shock and death.

Treat the Chest Pain!

So what is the “right” answer?  After consultation with cardiology, I chose to treat the chest pain and not the bradycardia.  The initial troponin was around 200, so it met NSTEMI criteria.  This decision is not to be taken lightly as the use of NTG could have potentially devastating consequences.  In this scenario a small dose of nitro was used as well as a small 500cc bolus of NS to help bolster the preload.  The NTG should never be given unless you have established IV access. 

It is also imperative to monitor the blood pressures for any large drop in pressure.  It is generally recommended not to give NTG with a systolic below 110mm Hg.  Because the patient presented to the ED so quickly, we did not see the typical inferior wall MI pattern of ST-T elevation in I, II, and aVF that would develop over the course of the next 3-6 hours.  In our situation, the initial EKG was a sinus rhythm with bradycardia; however the initial troponin was between 200-300 meeting NSTEMI criteria. 

The history of 1-hour of chest pain, bradycardia with no previous history of bradycardia, and no medications or underlying medical conditions that could cause bradycardia pointed us to early inferior wall MI.  This is what led to the decision to use NTG rather than atropine.  We assumed the chest pain was causing the bradycardia (because of an inferior wall MI) rather than bradycardia causing the chest pain.  Eventually, the patient was taken for cardiac cath and the RCA occlusion was identified/confirmed. The take home here is if you have a patient with chest pain and bradycardia, treat the chest pain first.

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