This 66-year-old man presented with a complaint of chest pain. His ECG shows a "classic" inferior wall ST-elevation M.I. (STEMI). The ST elevation is apparent in Leads II, III, and aVF, which are the leads that reflect the inferior wall of the left ventricle. In addition, this ECG shows ST elevation in Leads V5 and V6, the low lateral wall. The ST depression in V1 and V2 are reciprocal changes caused by acute injury in the posterior wall. In the majority, the RCA supplies the inferior-posterior wall, the right ventricle, the right atrium (including the SA node and the AV node), and in some, the low lateral wall. The proximal location of this man's occlusive lesion has caused damage in all these areas. The relatively slow rate is common in IWMI and can be caused by SA node injury, vagal stimulation, or medications. Clinical data is not available for this patient.
This ECG is from old files, and no patient information is available. Acute ST elevation is apparent in lateral leads I and aVL, and in Lead II. In addition, the anterior leads V1, V2, and V3 show reciprocal ST depression and, in V1 and V2, taller-than-normal R waves. This points to acute posterior - lateral M.I., probably due to occlusion of the circumflex artery. Unfortunately, we do not have angiogram confirmation for this.
The P waves are interesting. They are hard to see because of their small size and the fine baseline artifact present. The best view appears to be in the Lead II rhythm strip at the bottom. In this view, the P waves' morphology appears to be changing. What do you think?
This ECG was taken from a 66-year-old woman who presented to the emergency department complaining of chest pain and shortness of breath. She attributed her symptoms to her COPD, but stated that her aerosol treatment had not helped. She waited for some time before deciding to go to the hospital, then drove herself. In the emergency department, she had blood drawn, an I.V. started, and an aerosol treatment of albuterol. She was then taken to the radiology dept. for a chest xray. When she returned, a 12-lead ECG was done. 45 minutes had passed since she first arrived at the hospital. This ECG is shown here. It shows ST elevation in the inferior leads: II, III, and aVF. The patient was taken immediately to the cath lab, where her right coronary artery was found to have a 100% occlusion. (See image accompanying this ECG). Angioplasty was successful, and stents were placed in the artery. The patient was found to have anemia, with a hemoglobin of 5.5, and she was given a blood transfusion. During the cath procedure, a ventriculogram was performed, which showed a stunned and akinetic inferior wall. Unfortunately, subsequent ventriculogram performed several weeks later showed the lack of motion of the inferior wall to be permanent. The ventriculogram is also posted here, and at this YouTube link, so you will be able to show your students the mechanical effects on the heart of a delay to treatment in acute STEMI. See our YouTube site for more ventriculograms and cath videos.
This ECG was provided by Jamie Bisson, of E Advanced Healthcare.
The patient, in cardiogenic shock, was resuscitated in the Emergency Department, then sent to the cath lab, where his left main coronary artery was opened and stented.
Many people with complete occlusion of the left main do not survive. When there is some diminished blood flow through the blocked area in the proximal LAD or left main, this pattern may appear. Look for ST elevation in aVR greater than or equal to 1 mm, ST elevation in aVR greater than the ST elevation in V1, and widespread ST depression.
In this ECG, aVR and V1 show ST segment elevation, with widespread ST depression. For years, aVR was virtually ignored in the literature, and considered to be only a reciprocal view of the lateral inferior wall. Now, there is convincing evidence of its usefulness in discovering proximal left coronary artery occlusion and severe triple vessel disease. ST elevation in aVR can be a reliable sign of ischemia of the basal part of the heart and the proximal IV septum.
Many people with complete occlusion of the left main do not survive. When there is diminished blood flow through the blocked area in the proximal LAD or left main, this pattern may appear. Look for ST elevation in aVR greater than or equal to 1 mm, ST elevation in aVR greater than the ST elevation in V1, and widespread ST depression.
For complete discussions on this topic, go to Life in the Fast Lane,
Unbelievably, this inferolateral ST elevation M.I. was missed by the treating paramedics in the field. An elderly woman stepped off a curb and was hit by a very slow-moving car. She fell and sustained a Colle's fracture of the right wrist. While the paramedics assessed her, she complained of chest pain, prompting them to perform a 12-Lead ECG. The machine's interpretation called attention to the inferior and lateral walls' injury pattern, but the paramedics did not believe it, because "she was a trauma patient". They ran three ECGs, and still did not agree with the machine.
The patient was transported to a hospital without an interventional cath lab, and she was forced to endure a one-hour wait to be transferred to an appropriate hospital.
This is a great ECG for a discussion with your students about "distractors". The call came in as a trauma, so that, in itself, was a distractor. The rescuers saw what they expected to see. The angulated fracture distracted them - putting them into full trauma assessment mode. Then, the frequent and coupled PVCs also distracted them, possibly making it more difficult for them to evaluate the ST segments in the normal beats. Interestingly, the second and third ECGs did not have PVCs, and the ST elevation was even more clear.
PVCs which are repeating themselves in groups of two, three, or more are sinister in a chest pain patient, and may indicate LV dysfunction. They could possibly result in ventricular tachycardia, which would be disasterous for this patient.
A good teaching ECG, showing clearly elevated ST segments in V1 through V4. This patient had an LAD occlusion. In addition, he has new-onset atrial fib at a rate of about 120/min. Atrial fib has decreased cardiac output because of the loss of P waves prior to the QRS complexes, and a resultant decreased ventricular filling pressure. In addition, this fast rate contributes to increased myocardial oxygen demand and damage. An early priority, along with getting this patient to PCI, is slowing the rate.
In this ECG, there is ST elevation in II, III, and aVF and reciprocal ST depression in I and aVL, indicating acute inferior wall M.I. Also, this patient has developed pathological Q waves in III and aVF, and probably II as well, indicating permanent damage to the myocardium. A ventriculogram or echocardiogram will confirm akinesis of the inferior wall in most cases. In this ECG, there is no ST depression in V1 through V3, so we can hope the posterior wall has been spared. Notice the flattening of the ST segments in the elevated leads. This is a sign of CAD. Last week's ECG had coved upward (frowning) ST segments, which are even more sinister looking. Lead V1 has the flattening, and a pathological Q wave. When V1 looks "sick" and V2 looks "well", there is a good probability of right ventricular injury as well. Lead III has a taller ST segment than Lead II. This has also been shown to be a marker of RVMI. Regardless, a right-sided ECG, or at least a V4 right, should be obtained in any IWMI, since the RCA often supplies both the right ventricle and the inferior wall of the left ventricle.
The rhythm in this ECG is interesting, as well. It appears to be sinus, but it is difficult to evaluate P waves. In the Lead II rhythm strip, they appear to change in morphology. Because the R to R interval remains constant, we feel this change in appearance is due to baseline artifact caused most likely by patient movement such as breathing. What do you think?
Our thanks to Andrew Porter for contributing this ECG.
This ECG shows a classic inferior - posterior STEMI. This M.I. was due to complete occlusion of the right coronary artery. ST elevation apparent in Leads II, III, and aVF show the acute injury in the inferior wall, while ST depressions in V1 and V2 are reciprocal of the ST elevations in the posterior wall. The tall R waves in Leads V1 - V3 most likely are reciprocal to pathological Q waves in the posterior wall. Tall R waves in the right precordial leads can be caused by other cardiac conditions, such as right ventricular enlargement. RV hypertrophy can probably be ruled out in this case because there is no right axis deviation or P pulmonale. Because inferior wall M.I.s often extend into the posterior wall, it is the most likely cause of the tall R waves.