You are called to an ST-segment elevated myocardial infarction (STEMI) in the middle of the night. On the way to the hospital, you are thinking about several things. Am I driving safely (yet quickly enough for the door-to-balloon time)? Where is my ID card? Who is going to pick up the patient? Where are my lucent leads? Who will watch the kids if I am not back in time for school? Most of the time, you are not worrying or thinking about what kind of STEMI it is, and what problems you may encounter once you get to the lab. As experienced personnel in critical care areas, most of the time, you are preparing for the worst, and hoping for the best. While talking to my fellows about the different kinds of STEMIs and how each STEMI behaves, I thought it might be helpful to the cath lab team to review the clinical associations and problems seen with the most common kinds of acute myocardial infarctions (AMIs). For each type of MI, there are characteristic electrocardiogram (ECG) changes localizing the region of infarction, and corresponding clinical symptom and physical findings, reflecting the function of the infarcted myocardium and the patient’s response to the infarction.
Anterior MI
In anterior MI, ST-segment elevation (STE) occurs in leads V2-4 (Figure 1). When the STE extends to V5 and 6, the size of the MI tends to be large. When STE occurs in V1-2, ventricular septal muscle is infarcting. Since this location often involves the conduction system, it suggests to us that later bundle branch blocks or high degree heart block may develop.
The infarct-related artery is almost always the left anterior descending coronary artery (LAD) (Figure 2). Anterior infarctions can also be due to variants that include a large ramus branch running in the course along with a diminutive LAD or rarely, might involve the distal left main segment. Ultra-rare anatomy of AMI might be an anomalous left main (LM) originating from the right coronary artery (RCA), but I have yet to personally encounter this variant (thankfully). (See also the article by Mike Lee, MD, in CLD September 2010, “Unprotected LM PCI in Acute Myocardial Infarction”.)
The clinical presentation is mostly related to low cardiac output. When the anterior wall of the heart is infarcting, contractility is decreased and blood pressure is reduced, but heart rate is usually increased (>100 bpm), as a compensatory response to maintain stroke volume (ml/beat=cardiac output). Patients on beta blockers may not have this compensatory increase in heart rate, but may instead have rates of 80-90/bpm. Slower heart rates in AMI suggest either potent beta blocker effects, injury to the conduction system, or possible compromise of blood flow to the RCA from prior left to right collateral supply in a patient with multi-vessel disease. Usually, the key observation that this is a straightforward AMI is tachycardia and relatively low blood pressure. With slow heart rates and preserved blood pressure, unless there is heart block, new left bundle branch block (LBBB), or new first degree block with left axis and RBBB, a pacemaker is not needed.
In the AMI patient, if hypotension persists, despite initial fluid resuscitation in the emergency department and cath lab, an intra-aortic balloon pump (IABP) is needed. Alternatively, an Impella support device may be placed during high-risk intervention. For the hypotensive AMI, it is worthwhile, before beginning PCI, to obtain a second arterial access in the contralateral femoral artery. In critically ill patients with AMI, radial access may be suitable initially, but for support equipment in the more complicated patient, femoral access is needed.
Special precautions for AMI should include standby IABP, vasopressors, and second arterial access. In patients in shock who survive the emergent procedure, critical care physicians often request a pulmonary artery line to gauge left ventricular (LV) filling pressures over the recovery period. Consider inserting a large venous sheath in the internal jugular or femoral vein (short term only).
Inferior MI
ST-segment elevation of leads II, III, F is the rule (Figure 3). Some teachings suggest that more STE in lead II than III indicate the circumflex (CFX) and not the RCA is the culprit vessel. If the lateral leads I and aVL, V5-6 show STE, the infarction is extensive and one should anticipate more problems. In some hospitals, posterior leads behind the heart, such as V7-8 leads, are obtained and if STE is seen, the diagnosis of right ventricular (RV) infarction can be made. Recall that RV infarction is a clinical diagnosis and presents with 3 findings: elevated neck veins, clear lung fields [i.e. normal pulmonary capillary wedge (PCW)] and hypotension in the setting of inferior STE.
The infarct-related artery is the RCA (Figure 4) and less commonly, a dominant CFX. The more proximal the occlusion, the higher the likelihood of RV dysfunction, as well as inferior LV dysfunction. Since the sinoatrial (SA) and atrioventricular (AV) nodes often arise from the RCA, conduction disturbances are more common than with other infarctions. Regardless of which vessel is causing the infarct, whether the RCA or CFX, as a general rule, the inferior MI is often less dramatic and better tolerated than an AMI.
Clinically, in contrast to AMI, the heart rate in inferior MI is usually bradycardia, because of stimulation of the vagal system and the Bezold-Jarish reflexes. A higher likelihood of vomiting occurs in patients with inferior MI. A low heart rate with preserved blood pressure is common and does not require a pacemaker, unless 2nd or 3rd heart block is present. An irregular rhythm may be due to Mobitz type I (Wenkebach) block and likewise, does not need a pacemaker. Initially, low blood pressure often responds to normal saline infusions and may also benefit from dopamine, if the blood pressure does not respond quickly to fluids. Like AMI, the inferior MI in shock will need LV support or rarely, RV support (but this is not yet available routinely).
Special precautions in inferior MI include standby pacemaker, atropine, volume loading with saline, dopamine, and early consideration for right heart cath. Remember, the hemodynamic waveforms of RV infarction resemble the RV diastolic pressure dip and plateau of constrictive pericardial disease.
Lateral MI
STE in the leads I, L and V5-6 localize the infarct to the lateral wall. This location is variable in its presentation between inferior and anterior MI, and has features that may be seen in either or both. The lab team will have to respond to the problems of rhythm and pressure as they arise. No special precautions are needed.
Now that you have arrived in the cath lab to begin treating the STEMI patient, I hope you will have something more to think about. In addition, it is a well-known phenomenon in the cath lab that if you prepare the IABP well in advance, the odds are unlikely that you will need to use it, and of course, the converse is also true — if you don’t prepare the IABP, sure enough, you will need it and won’t be able to find all the parts. Be your own Boy Scout. Be prepared!
Disclosure: Dr. Kern reports that he is a speaker for Volcano Therapeutics and St. Jude Medical, and is a consultant for Merit Medical and InfraReDx, Inc.
Dr. Kern can be reached at mortonkern005@hotmail.com
Check out Dr. Kern’s latest book, “Notes from the Editor’s Corner of Cath Lab Digest” at www.mortonkernmd.com
