A 64 yr old white female presented to EMS with n/v/d times three days and a recent episode of orthostatic syncope. She had no complaints of chest discomfort or shortness of breath. She was pale in apearance and found to be hypotensive on exam.
Although AV dissociation can be appreciated in the first three tracings, the fourth appears consistent with undifferentiated 2nd degree conduction block and prolonged (>200 ms) PR interval with bigeminal junctional escape. Close examination of II and V4-6 reveal a subtle morphological variation in the complexes, supporting the argument for multiple depolarization foci. A narrow-complex junctional escape rhythm is typical of a culprit RCA lesion resulting in often transient ischemia to the superior portion of the nodal tissue. Wide-complex 3rd degree block more frequently reflects a significant LCA infarction which has resulted in distal, more inferior conduction system damage that is less likely to recover. Note that the ST elevation in III is greater than that in II— a finding that has been correlated with RV involvement, although I know of no EBM trials to support this. It is regrettable that right-sided and posterior leads were not recorded.
AV conduction abnormalities can be appreciated in as much as 30% of inferior wall MIs owing to the ~70% prevalence of the RCA as the dominant vessel supplying the AV nodal branch. Left dominant coronary systems present a variation to the predictability of progressive conduction pathway ischemia but constitute only 10% of the populace. This leaves 20% with co-dominant systems. In the absence of confounding factors, it would be interesting if there has been a study demonstrating a decreased incidence of AV conduction blocks in pts with redundant AV nodal circulation who present with acute coronary syndrome.
Despite what appear to be convalescent ECG changes over the course of these three 12-leads, the pt. deteriorated rapidly in the ED and required pressor support and intubation before she could be transported to the cath lab. The outcome is unknown.
A 68 year old white male presenting to EMS with chest pain and a history of HTN. No further on this case in known at this time.
This ECG demonstrates a 3:2 Wenkibach phenomenon with an initial inconsistency, possibly due to an A:V ratio shift or artifactual event. Note the subtle elevation in V6; again, a 15lead tracing would have been optimal here.
It should not be forgotten that although inferior wall STEMI typically results from RCA occlusion, it may also arise from a lesion in the Circumflex; in the latter case, the right heart is spared and RCA dependent conduction system elements remain unaffected. Dr. Smith has recently presented an example of this phenomenon as well as a review of a risk stratification ECG algorhythm recently proposed to deliniate RCA vs CLX lesions on ECG. While the case above meets several of these criteria (aVR depression and V6 eleveation), the manifest conduction system involvment all but eliminates the possibility of a CLX eitiology. I hope to post a better example of the DeVerna RCA/CLX decision tool in the near future; see Dr. Smith’s ECG site for a superior and more appropriately exemplified discussion of this new research.
A 52yr old hispanic male with history of hyperlipidemia, IDDM, hypertension, and 30 pack/yr smoking presents to the ED with c/o nausea and diaphoresis. His mother had an MI at 50, and he has two sisters– one suffered an MI at 52 with subsequent CABG, and the other had an MI at 49. His BP on arrival was 92/48.
Another 3:2 Wenkibach; the second ECG shows the pathology resolving slightly to a 1st degree conduction delay, perhaps reflecting beneficial pharmacotherapy.
This pt. received medical management at an outside facility until he could be transported to the cath lab. His Pro-BNP on admission to CCU was 4668, and his Troponin peaked at 8.36ng/ml. No further is known.
A 59 yr old white male presented to his primary care physician with complaints of weakness and exertional dyspnea. The following ECG was recorded by EMS called to the scene.
Again we see the preference in RCA occlusion for a junctional rather than ventricular escape pacemaker. The low voltage baseline activity in leads I, II, and III appears artifactual, however a close examination of the precordial leads demonstrates a small blip consistantly 200ms after the beginning of the QRS, suggesting the possibility of retrograde atrial depolarization buried within the ST-segment. These findings have been marked with the red arrows below.
The disturbances marked with the blue arrows should also be noted, perhaps representing atrial depolarizations with “P-mitrale” morphology. Under this interpretation, the EKG in fact demonstrates a sinus rhythm with marked 1st degree block. Unfortunately, no additional tracings are available for study.
This pt survived to reach the cath lab, but no further is known.
A 52 yr old man, transfered from an outside hospital, pain free at this time and resting comfortably.
Included for completeness, this ECG demonstrates no AV block but is a distractor from the previous series. Individual P-waves cannot be identified; the rhythm is irregularly irregular. In the context of inferior wall MI, this pt is experiencing slow ventricular response a-fib with an associated digitalis-type ST-segment morphology.
Again, unfortunately, no follow up was possible regarding this pt’s outcome.
An 84yr old white female, s/p VT/PEA arrest.
This ECG demonstrates AV dual sequenced pacing with loss of atrial capture. Note the high left axis in the x-y plane, consistent with typical pacer findings, but an atypical rightward shift of electrical forces across the precordial z-axis (inverse R-wave progression). Traditionally ventricular pacing electrodes are deployed in the right heart and result in a LBBB ECG morphology as the myocardial tissue depolarizes from right to left. Yet in this case we see a dramatic RBBB pattern, raising concerns about displacement or septal perforation, particularly given that the pt. has received CPR. The etiology of RBBB pacer morphology is not exclusively pathological, however, and receives a good discussion on Dr. S. Venkatesan’s Cardiology Blog. Note that the QRS in this case is elongated above 160ms, and necessarily reflects slow and poorly coordinated ventricular contraction, perhaps betraying a newly aberrant interventricular conduction pathway, even for this 100% paced patient.
Another interesting example of a similar RBBB effect can be seen at Dr. M. Rosengarten’s electrocardiography site, and there is a thorough case report and research analysis of the phenomenon in The Journal of Electrocardiography Vol.6 No. 1, 2003.
Shortly after this 12-lead was captured, the pt. again deteriorated into PEA and was lost to resuscitative efforts.
A 19yr old white male, s/p cardiac arrest, now with transtentorial herniation.
As with this case, ECG patterns in the context of acute CNS disease have been primarily associated with ventricular repolarization, i.e. the morphology of the QT segment and T-wave, and the presence of prominent U-waves (not present here). Although little sensitivity or specificity has been accorded to this connection, the phenomenon raises interesting questions of nerocardiac interrelation. Most explicitly, bradycardia as a result of hypervagotonia is often noted in the setting increased intracranial pressure. Yet more difficult to explain are the deep, symmetrical T-wave inversions and prolonged Q-T frequently described as more specific indicators of intracranial pathology. It has been hypothesized that these effects are due to an autonomicaly mediated catocholamine surge causing transient coronary vasospasm and subsequent myocardial ischemia.
The ST segments in this case are of a somewhat novel morphology, perhaps even reminiscent of the scooped out troughs seen as a common Digitalis effect.
This pt. was taken to the OR for withdrawal of ventilatory support and organ donation later in the night.
This patient is a 64 year-old cachectic white male, admitted to ICU with a five day history of nausea, vomiting, and upper abdominal discomfort. The following EKGs were collected in the ED before and after treatment. His history includes HTN, alcoholism, and IDDM.
Classic electrocardiographic indications of hyperkalemia include sharply peaked, symmetrical T-waves, suppression of atrial activity, bradycardia, a markedly widened QRS and a short QT interval. Note how the rhythm in this case approaches the appearance of a sign wave as the QT narrows and the ventricular complexes widen; this is representative of the course in worsening hyperkalemia and is sometimes responsible for the idoventricular or agonal appearance of some hyperkalemic EKGs. This should not be considered a mere “agonal appearance,” however, as typically broad and flattened P-waves with an elongated PR interval will progress toward complete atrial paralysis, frank idoventricular activity below 40bpm, and subsequent hemodynamic collapse.
Distinguishing between the T-wave morphologies of hyperkaemia, early-repolarization, and hyperacuity in early MI can become problematic for pt. outcomes in the acute setting, particularly in the latter case, and a good discussion of this issue can be found at Dr. Smith’s EKG blog. It has been said that hyperkalemic T-waves are “tented” and should be pointed enough to prick your finger. Also note Lipman and Massie’s observation that, “The uniformly wide complex in hyperkalemia differs from the wide QRS in bundle branch block (terminal QRS sluring) or pre-excitation (initial sluring) in that the uniform widening of the QRS in hyperpotassemia affects both the initial and terminal QRS portions.” Lab values are as follows:
Despite resuscitation in the ED this patient arrived in the ICU with a BP of 70/40, HR 60bpm, RR of 30, and a room air SpO2 of 88%. The patient was ultimately stabilized over a matter of days but required extensive pressor support for evolving bacteremia and HHNKC. An ultrasound of the upper abdomen revealed fatty infiltration of the liver but no cholecystitis or cholangitis. It should be noted that although a history of recent complaints could be obtained from the patient’s family members, he initially presented in a comatose state.
Of additional relevance in this case may be Lipman-Massie’s further contention that, “Low sodium levels tend to exaggerate and high sodium levels tend to neutralize the ECG effects of hyperpotassemia.”
Dramatic recordings of progressing or resolving hyperkalemia are not difficult to find about the internet. Dr. M. Rosengarten has a fine series here.
Quotations from Lipman-Massie Clinical Electrocardiography, 8th Ed. Marvin I. Dunn MD, Bernard S. Lipman MD. Yearbook Medical Publisher Inc. ©1989. See pp. 240-243.