We recently responded to a call for chest pain for a 53 year old woman who was at home working out. We arrived on scene and evaluated a patient who was pale, nauseated, weak, and extremely diaphoretic. The patient denied any cardiac history. The resulting assessment and care is a great case study in things both obvious and hidden.
The patient’s initial blood pressure was 112/80, with a pulse of 50, respirations of 18 and a room air pulse oximetry reading of 98%. The patient’s pulse remained in the high 40’s-low 50’s range throughout treatment. There is a lot going on in the initial 12 lead. The obvious issue is the STEMI in the inferior leads: II, III, and AVF. This patient is definitely having an inferior MI. One very common characteristic of an inferior infarction is the reciprocal changes in leads I and AVL. The down-sloped ST depressions are seen in almost all inferior STEMI’s and are very obvious here. If you are unsure of an inferior diagnosis, look for the depressions in I and AVL.
This patient showed a textbook example of an inferior presentation. She was weak, pale, bradycardic, hypotensive and diaphoretic. Inferiors often have intranodal blocks associated with AV dysfunction. The same artery that supplies the inferior heart with oxygenated blood also supplies blood to the SA node, AV node and other critical parts of the heart’s electrical conduction system.
Careful analysis of the patient’s cardiac rhythm reveals extreme AV node dysfunction. Trace the occurrence of P waves across Leads I, AVR and V1 at the top of the strip. There is a very regular pattern of P waves every 20 mm representing a depolarization of the SA node at a rate of about 75. The QRS complexes are also fairly regular but are 30 mm apart, representing a ventricular depolarization rate of about 50. The atrial and ventricular complexes have different rates and are not synchronized. This patient was experiencing complete atrioventricular dissociation (third degree heart block). The dysrhythmia is not uncommon with in inferior MI because the same arterial occlusion that causes the inferior is responsible for hypoperfusion of the AV node. AV node dysfunction is demonstrated here by the completely refractory pathway from the atria to the ventricles.
Inferior STEMI’s are caused by an arterial occlusion of the right coronary artery (RCA). The standard 12 lead EKG is not really set up to see the areas of the heart served by the RCA very well. As a matter of fact, about the only finding indicative of RCA occlusion that can be seen on a standard 12 lead is an inferior MI. There are many areas of the heart served by the RCA that are endangered by this occlusion, but are practically invisible on the 12 lead. One of these areas is the posterior heart wall. About 85% of people get their posterior heart perfusion from the RCA (the other 15% use the circumflex artery). We cannot see the posterior heart directly but we can get a hint of problems with the posterior heart by looking for reciprocal changes in the septal leads: V1-V3. Notice the ST depressions in leads V1 and V2. If we were to flip those leads over 180 degrees we would be looking at the characteristic STEMI pattern of ST segment elevation.
The right ventricle is another area of the heart that depends on the RCA for blood supply. The electrical activity of the right ventricle is completely overwhelmed by the magnitude and vector of the left ventricle. The standard 12 lead EKG is not set up to examine the right ventricle. If we want to see the activity of the right ventricle, we have to go looking for it. We do this by running a right-sided 12 lead. This is usually done by moving V4, V5, and V6 from the left chest wall to mirror image positions on the right chest wall. The positions are called V4R, V5R and V6R. When the 12 lead is printed in this configuration, any ST elevation that show up in V4R, V5R, or V6R are indicative of a right ventricular myocardial infarction (RVMI)
How often do these “hidden” infactions happen and how do we make sure that we never miss when they occur? It all comes back to recognizing that the RCA is involved. Whenever you see significant ST changes in the inferior leads (II, III, AVF), it is important to examine the posterior reciprocal leads (V1-V3) and to run another 12 lead with V4, V5, and V6 moved to the right side of the chest (V4R, V5R, V6R). This patient was having an inferior, posterior, and right ventricular infarction and that’s a real game-changer as far as treatment goes. Cardiac output from the right ventricle can be significantly diminished in cases of RVMI. It’s possible that this can cause deficits in left ventricular preload. This patient becomes very dependant on preload to maintain their systemic blood pressure. We want to avoid vasodilators like nitroglycerine and we want to establish an IV line for fluids to inflate venous preload.
If you suspect an inferior MI:
· Check V1-V3 for reciprocal changes that may indicated posterior involvement
· Check V4R-V6R for ST elevation (right ventricular involvement)
If you have evidence of right ventricular involvement:
· Avoid vasodilators like nitroglycerine
· Be prepared to fluid bolus the patient to maintain systemic pressure