Foundations EKG II Unit 9 Instructor—Miscellaneous

Timeline:

• Divide learners into 4 groups at different tables (this approach is suggested for groups of 8 or more learners and should be modified to 1 or 2 groups so sites with lower numbers of learners)

• 5 min large group review of the Unit 9 Summary “Approach to Miscellaneous Ischemia”

• Give each group 2 copies of the Unit 9 EKG Challenges Packet (merged challenge EKG content for EKGs 33 -36), this allows learner groups to all review content and record their group's answers to the interpreta- tion and questions for each EKG

• Allow 20 minutes for groups to complete the 4 challenges (give updates at 5min increments)

• 20 minutes large group discussion of answers to challenges. May consider asking each group to present their responses to a different EKG

Meeting Resources:

• Notify learners in advance of the session that they need to review the unit summary and challenge EKGs

• Before the session, have a few copies of the unit summary (pages 2-5 of this document) printed to give to learners who forgot their copies/devices and copies of the Unit 9 EKG Challenges Packet to give to groups

• Before the session, make sure to print this document for your own reference during the group discussion

• After the meeting, send out the answer document to learners for independent review Foundations EKG II - Unit 9 Summary Miscellaneous Ischemia

Impressive inversion on EKG has a differential diagnosis that includes acute myocar- dial ischemia among others.

Diffuse T wave inversion can indicateincreased intracranial pressure. Typically T waves are asymmetric with a bulge. Most commonly caused by intra-parenchymal and non-traumatic subarachnoid hemorrhage but can also be seen with massive ischemic stroke or tumor.

Courtesy of Susan Torrey of torreyEKG.com

Created by Ashley Deutsch, MD Edited by Nick Hartman, MD & Kristen Grabow Moore, MD, MEd

Deeply inverted T waves or biphasic T waves in V2-V4 during a pain-free interval may represent Wellens Waves. Wellens waves may occur with normal enzymes when patient is not having pain, and indicate a left anterior descending (LAD) occlusion. They should prompt a discussion with cardiology about performing cardiac catheterization, although may not need immediate activation if patient is not having active pain. Serial EKGs should be obtained to evaluate for evolving ischemic disease.

Courtesy of Susan Torrey, MD of torreyEKG.com EKG findings suggestive ofright heart strain:

•

• T wave inversions in inferior and anterior leads

• Incomplete RBBB

• STE with lead III, aVR, V1

Causes of right heart strain includes pulmonary hypertension, pulmonary embolism, mitral stenosis, and chronic lung disease among others.

Courtesy of Edward Burns of Life in the Fast Lane Creative Commons License A new RBBB with a left anterior fascicular block can be seen in left main and left anterior descending artery occlusion. As a reminder, left anterior fascicular blocks are diagnosed as left axis deviation with small Q waves and tall R waves in leads I and aVL, small R waves with deep S waves in leads II, III, and aVF, and increased QRS voltage in the limb leads. This rhythm (new RBBB+LAFB) is at risk for developing into VT and presenting with cardiogenic shock.

Courtesy of Steve Smith of Dr. Smith’s ECG Blog Triage EKG—Unit 9, Case 33

37yF with ACL repair 3 weeks ago c/o SOB & CP. Hypoxic on HR: 102 BP: 100/60 room air. Repeat O2 sat of 96% on NRB. RR: 28 O2 Sat: 88%

Courtesy of Edward Burns of Life in the Fast Lane Creative Commons License Unit 9, Case 33—Right Heart Strain What is your interpretation of the EKG? History/Clinical Picture—Young woman with recent surgery presents with hypoxemic respiratory failure, and borderline hypotension. Rate— 96 Rhythm—Sinus rhythm

Axis—Normal, though approaching right axis devation P Waves—Normal Q/R/S Waves—Large S-wave in I. Subtle, non-pathologic Q waves V5-6. S1Q3T3 noted. T Waves—Deep, inverted T waves V1-4

U Waves—None apparent PR Interval—Normal, approximately 170ms QRS Width—Normal, approximately 110ms ST Segment—No ST elevation or depression QT Interval—Grossly normal

Diagnosis: EKG findings consistent with acute right heart strain.

Management: This EKG suggests acute right heart strain. In the ED, acute right strain is most commonly due to pulmonary embolus, however, worsening pulmonary hypertension from any cause could be the culprit. EKG findings suggestive of right heart strain include: tachycardia and non-specific -T wave changes (most common abnormalities however very non- specific), T-wave inversions inferiorly and anteriorly, right axis deviation, incomplete RBBB, and STE in the rightward leads (III, aVR, V1). This patient’s presentation is highly suggestive of acute PE. A CT angiogram should be obtained to confirm the diagnosis (Wells 6—tachy, surg, most likely). A bedside echo, troponin, and BNP would be useful for determining the extent of RV dysfunction. If the patient remains hemodynamically stable, systemic anticoagulation should be initiated, and expert consultation obtained to discuss the risks and benefits of catheter directed thrombolytics. If the patient develops frank shock or , consideration must be given to the administration of systemic lytics, mechanical circulatory support, and (if available at your institution) consultation for surgical thrombectomy. Resource Links: Life in the Fast Lane — great overview Dr. Steve Smith’s Blog – good case

Created by William Burns, MD & Duncan Wilson, MD Edited by Nick Hartman, MD & Kristen Grabow Moore, MD, MEd Triage EKG—Unit 9, Case 34

37 year-old female with history of migraines complaining of a HR: 55 BP: 210/120 sudden onset, severe headache. RR: 18 O2 Sat: 97% Unit 9, Case 34—Cerebral T Waves What is your interpretation of the EKG? History/Clinical Picture—Young woman with a primary complaint of sudden, severe headache without chest pain or other anginal equivalent Rate—55 Rhythm—Sinus

Axis—Borderline Left Axis Deviation at ~-30 P Waves—Normal morphology Q, R, S Waves—No pathologic Q waves, normal R/S waves T Waves—Deep T wave inversions that are most prominent in the precordial leads but also in high lateral and inferior leads

U Waves—None apparent PR Interval—Normal at ~140ms QRS Width—Slightly prolonged at ~120ms ST Segment—No ST elevation or depression QT Interval—Prolonged at ~540ms Diagnosis: Cerebral T-waves in the setting of CNS insult

Discussion: Diffuse, deep T wave inversions and prolonged QTc in setting of severe headache is concerning for severe CNS in- sult with elevated intracranial pressure. Cerebral T-waves are most commonly seen with intra-parenchymal hemorrhage and non-traumatic SAH. Massive ischemic stroke with cytotoxic edema, severe TBI, and intracranial tumor have also been associ- ated. Cerebral T-waves may be the result of microvascular spasm, or stress induced (Takotsubo) in the setting of high levels of circulating catecholamines. ED therapy should focus on diagnosing the intracranial insult and lower- ing intracranial pressure. This patient is critically ill and has vital sign derangements concerning for imminent herniation. Air- way management, elevating the head of the bead, aggressive blood pressure lowering, hyperosmolar therapy, and emergent neurosurgical consultation should take priority. The patient may go on to manifest signs of left , and this should be managed with diuresis, afterload reduction, and inotropic support as appropriate.

Resource Links: Life in the Fast Lane — great overview Dr. Steve Smith’s Blog – good case

Created by William Burns, MD & Duncan Wilson, MD Edited by Nick Hartman, MD & Kristen Grabow Moore, MD, MEd Triage EKG—Unit 9, Case 35

45 y/o M with PMH of obesity, HTN, DM, HL presents by EMS for HR: 65 BP: 164/102 45 minutes of crushing substernal chest pressure and diaphoresis. RR: 12 O2 Sat: 97% By ED arrival the pain has completely resolved.

Courtesy of Edward Burns of Life in the Fast Lane Creative Commons License Unit 9, Case 35—Wellens’ Syndrome What is your interpretation of the EKG? History/Clinical Picture— Middle aged man with cardiac risk factors presents with anginal type chest pain now resolved Rate— 60-70 Rhythm— sinus rhythm

Axis— left axis deviation P Waves— normal Q, R, S Waves— pathologic q-wave in V2 vs poor R-wave progression. S-waves inferiorly T Waves— deep biphasic T-waves in V1-5 and lateral TWI

U Waves— none PR Interval— normal QRS Width— normal ST Segment— no notable STE/STD QT Interval— normal

Diagnosis: Wellens’ syndrome

Discussion: Biphasic T-waves across the precordium (Wellens’ pattern type A) and deep symmetric T-wave inversions across the precordium (Wellens’ pattern type B) are concerning for critical LAD stenosis. The fact that our patient had chest pain that is now resolved suggests that he had an occluded proximal LAD that spontaneously reperfused. He nevertheless has a very unstable plaque in the proximal portion of a large artery, and immediate cath is a reasonable option. If the cath team opts to defer immediate transfer from the ED to the cath lab, which is reasonable given that the artery is currently open, the patient should be treated aggressively for ACS (heparin, dual antiplatelet therapy, high dose statin) and should be monitored in an ICU (ideally with continuous 12-lead) as he is very high risk for re-occlusion and subsequent STEMI.

Resource Links: Life in the Fast Lane — great overview Dr. Steve Smith’s Blog – good case

Created by Duncan Wilson, MD Edited by Nick Hartman, MD & Kristen Grabow Moore, MD, MEd Triage EKG—Unit 9, Case 36

68 y/o M with PMH of obesity, DM2, and a heavy smoking history presents HR: 105 BP: 66/52 for acute onset crushing chest pain and shortness of breath. Previous EKG RR: 20 O2 Sat: 88% shows a narrow QRS and a normal axis.

Courtesy of Steve Smith of Dr. Smith’s ECG Blog Unit 9, Case 33—New RBBB & Anterolateral STEMI What is your interpretation of the EKG? History/Clinical Picture— High risk middle aged man presents with anginal chest pain, cardiogenic shock and hypoxia. Rate— 100-110 Rhythm— sinus rhythm

Axis— left axis deviation P Waves— present Q, R, S Waves— no pathologic q-waves, large s-waves inferiorly, large R waves with abnormal progression across precordium. T Waves— inverted V1-3

U Waves— not present PR Interval— normal QRS Width— wide ST Segment— STE in V1-V4, aVR, aVL, and sub-millimeter STE in I. There are reciprocal STD inferiorly QT Interval— normal

Diagnosis: new RBBB w LAFB w large anterolateral STEMI

Discussion: This case is particularly challenging because while there is a large STEMI, the ST-segments are difficult to appreci- ate due to the right and left anterior fascicular block. It is important to note that new RBBB+LAFB can be seen in acute left main occlusion and acute LAD occlusion. STEMIs that cause this degree of conduction system disturb- ance are usually very large and can present with cardiogenic shock. This patient needs to go emergently to the cath lab. He is at high risk for degenerating into VT. If he arrests, consideration should be given to transporting him to the cath lab with ongoing CPR and accompanying MD/RN to provide ACLS. The emergency team must consider the risks/benefits of intuba- tion, obtaining central access, and initiating vasopressor and inotropic support prior to transport. While it may be tempting to think this is VT, notice that there are clear -p waves and the rate is too slow for VT (<120 bpm). Attempting cardioversion would be counter-productive.

Resource Links: Dr. Steve Smith’s Blog— good case Dr. Steve Smith’s Blog – another good case

Created by Duncan Wilson, MD Edited by Nick Hartman, MD & Kristen Grabow Moore, MD, MEd