Category Archives: clinical cases

A Case of Non-bacterial Thromboembolic Endocarditis

Authors: Captain William Dirkes (EM Resident Physician, Madigan Army Medical Center), Captain Joshua Kessler (EM Resident Physician, Madigan Army Medical Center), Lieutenant Colonel Jay Baker (EM Attending Physician, Madigan Army Medical Center), and Colonel Ian Wedmore (EM Attending Physician, Madigan Army Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021)


A 59 year-old male presented to the emergency department with a chief complaint of difficulty concentrating and loss of vision. He had presented to the same facility the day prior for chest pain, chills, and a cough. During his prior visit, the patient underwent a chest x-ray which demonstrated a consolidation suggestive of a lobar pneumonia and was subsequently discharged home with a prescription for Azithromycin as well as instructions to follow-up with his primary care doctor. However, he was unable to fill his prescription. Upon attempting to drive home, the patient was pulled over by law enforcement because he was acting “delirious.” Despite the traffic incident, he was allowed to return home. The patient reported that once he arrived at home he began bumping into furniture, experiencing difficulty with concentration, and suffered vision loss. In addition, he continued to experience chills, chest pain, and shortness of breath. He denied experiencing any abdominal pain, dysuria, focal numbness or weakness, headache, hematuria, hematochezia or melena, speech disturbances, or a rash. His medical history included diabetes, hypertension, hyperlipidemia, and an unprovoked DVT (deep venous thrombosis) approximately 5 months prior. He denied any surgical history. His medications included Atorvastatin, Lantus, Metformin, Rivaroxaban, Sitagliptin, and Telmisartan. He reported smoking a ½ pack of cigarettes per day for the last 15 years, consuming alcohol occasionally, and denied any current or prior illicit drug use.

His initial vital signs in the emergency department were a blood pressure of 150/95, a heart rate of 106, a respiratory rate of 24, an oxygen saturation of 95% on room air, and a temperature of 97.8F, taken temporally. His physical exam demonstrated a male appearing his stated age, in no apparent distress but with mild tachypnea, diminished breaths sounds in the left posterior lung fields, and no cardiac murmurs on auscultation. His neurologic examination demonstrated that he was alert and oriented, but had intermittent periods of confusion and difficulty with recall during the interview. His speech was normal and his cranial nerves were grossly intact. He had a right hemianopsia on visual confrontation. He had full strength in all of his extremities and normal sensation to light touch. No dysmetria on finger-nose testing and heel-shin was normal.

He underwent a non-contrasted computed tomography (CT) scan of his head which demonstrated multifocal cortical abnormalities concerning for embolic infarcts with a dense left middle cerebral artery sign indicative of an evolving territorial infarct. A portable chest x-ray demonstrated a moderate left lung pleural effusion and prompted further imaging to characterize the lesion. A CT pulmonary arteriogram demonstrated a segmental pulmonary embolism of the right lower lung lobe with an enhancing mediastinal mass concerning for malignancy in addition to the already visualized left-sided pleural effusion. Abnormal laboratory findings included a white blood cell count of 10.4 and a platelet count of 58. The remainder of the CBC was unremarkable and his lactate, liver function tests, coagulation panel, troponin, and urinalysis were within normal limits. His electrocardiogram demonstrated a normal sinus rhythm with a rate of 85 beats/minute.

CT chest
segmental pulmonary embolism of the right lower lung lobe with an enhancing mediastinal mass concerning for malignancy in addition to the already visualized left-sided pleural effusion
ct head
multifocal cortical abnormalities concerning for embolic infarcts with a dense left middle cerebral artery sign indicative of an evolving territorial infarct.

He was admitted to the inpatient medicine service which included a neurology consultation. An inpatient MRI of his brain was obtained which demonstrated an acute ischemic infarct in the left parieto-occipital lobes. These findings were consistent with multiple chronic infarcts versus vasogenic edema possibly representing metastatic disease. A trans-esophageal echocardiogram demonstrated tricuspid vegetations. He was subsequently diagnosed with Non-Bacterial Thromboembolic Endocarditis (NBTE) and discharged home on the following day.

Non-Bacterial Thromboembolic Endocarditis (NBTE)

NBTE is also known as Libman-Sacks Endocarditis or formerly, as Marantic Endocarditis. It is a rare condition, often diagnosed on autopsy, most often found between the fourth and eighth decades of life. [1, 2, 4] NBTE is the result of platelet and/or fibrin aggregation on a heart valve secondary to an underlying hypercoagulable state. Usually, the hypercoagulable state is induced by a metastatic process or rheumatologic condition such as Systemic Lupus Erythematosus (SLE), Anti-Phospholipid Syndrome, or Rheumatoid Arthritis. [1-3] These disorders are known to have a higher prevalence in female patient populations (approximately 5-9 times their male counterparts), more specifically in African American and Hispanic ethnicities. As such, the clinician should maintain a higher degree of suspicion when treating these patient populations. Unlike bacterial vegetations, the vegetations of NBTE are symmetric with a smooth or verrucoid texture and contain little evidence of polymorphonuclear leukocytes, microorganisms, or inflammation. The disease affects the heart valves with the following predilection: aortic valve > mitral valve > tricuspid valve > pulmonary valve. Clinically, the disease presents with embolic events including stroke, delirium, pulmonary embolism, renal/splenic infarction, acute myocardial infarction, digital ischemia, and/or rash. Because of the non-invasive nature of NBTE, clinical examination may or may not reveal a new cardiac murmur. An embolic stroke may be the initial presentation to suggest a diagnosis of NBTE and if the clinician is suspicious, an Echocardiogram should be obtained to assess for valvular lesions. Emergency Department management should include evaluation for Disseminated Intravascular Coagulation (obtaining coagulation panel, d-dimer, fibrinogen), as this complication has been found in 18% of cases of NBTE.


Treatment of NBTE consists of anti-coagulation and therapy directed at the underlying metastatic process or rhematoogical condition. Unfractionated heparin should be the anti-coagulant employed as warfarin is less effective and has been associated with increased rates of thromboembolic events. Novel anticoagulants, such as Dabigatran, Apixaban and Rivaroxaban, should also be avoided as they have not been evaluated for use in this disease process. Surgical intervention may be considered in select cases where the risk-benefit ratio is favorable. Anticoagulation should be continued indefinitely, since recurrent thromboembolism has occurred in patients following its discontinuation. [5] The indications for surgical intervention in NBTE are similar to those in infective endocarditis, namely heart failure, valve rupture, and most commonly recurrent embolization despite anticoagulation. Follow-up should be considered on an individual basis. However, patients should be monitored for known complications of NBTE, specifically infective endocarditis and emobilzation despite anticoagulation. Additionally, Echocardiogram 6 weeks to 3 months after initiation should be considered to follow the progression or resolution of valvular vegetations. Prognosis is generally grim despite anticoagulation due to the underlying predisposing medical condition rather than NBTE itself; a strong association between advanced malignancy and NBTE has been demonstrated in retrospective studies. Similarly, in patients with SLE, a longitudinal, cross-sectional study reports poor outcomes due to recurrent embolic events (25%), cognitive disability (24%) and death (9%). [6]

References/Further Reading

  1. el-Shami, K, Griffiths, E, and Streiff, M. Nonbacterial Thrombotic Endocarditis in Cancer Patients: Pathogenesis, Diagnosis, and Treatment. The Oncologist. 2007;12:518-23.
  2. Deppisch LM, Fayemi AO. Non-bacterial thrombotic endocarditis: Clinicopathologic correlations. Am Heart J 1976;92:723–729.
  3. Eiken PW, Edwards WD, Tazelaar HD, McBane RD, Zehr KJ (2001).“Surgical pathology of nonbacterial thrombotic endocarditis in 30 patients, 1985–2000”. Mayo Clin. Proc.76 (12): 1204–12. doi:4065/76.12.1204. PMID 11761501.
  4. Lopez JA, Ross RS, Fishbein MC, SIegel JC. Nonobacterial thrombotic endocarditis: a review. AM Heart J 1987; 113:773.
  5. Rogers LR, Cho ES, Kempin S et al. Cerebral infarction from non-bacterial thrombotic endocarditis: Clinical and pathological study including the effects of anticoagulation. Am J Med 1987;83:746 –756.
  6. Roldan CA, Qualis CR, Sopko KS, SIbbit WL Kr. Transthoracic versus tranesophageal echocardiography for detection of Libman-Sacks endocarditis: a randomized controlled study. J Rheumatol 2008; 35:224.

The Crashing Trauma Patient

Author: Bryant Allen, MD (@bryantkallen, Assistant Profess of Emergency Medicine, Carolinas Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021, Senior Staff Physician, Henry Ford Hospital)

ABCDE: General principles for the resuscitation and treatment of the unstable trauma patient

Case 1: A 35-year-old male presents after a high-speed motor vehicle collision. He was the restrained driver of a vehicle traveling approximately 70 mph when it struck a tractor-trailer stopped in the roadway. First responders found him slumped in his seat, airbags deployed, with the seat fractured from the vehicle. The car had severe front-end damage. He was placed in a cervical collar by EMS and after a prolonged extraction was placed on a spine board. Obvious injuries included an open deformity to his right femur, a tender and distended abdomen, and multiple facial and scalp injuries. Vital signs per EMS included a maximum heart rate of 139 bpm, lowest blood pressure of 84/40 mmHg, respiratory rate of 30 bpm, and GCS of 6.


Accidental and traumatic injuries remain one of the leading causes of death worldwide, accounting for 5.8 million deaths annually and a large percentage of ED evaluations.1 Increasing disease severity creates an environment that makes patient care difficult. The American College of Surgeons has created a protocol driven framework, Advanced Trauma Life Support, in order to overcome this challenge and achieve success in the “Golden Hour”.

Management of the crashing trauma patient can be hectic and challenging. The primary role of the traumatologist is to create a calm environment in the trauma bay in order to effectively designate roles and provide cohesive, structured care. Preparing the trauma team prior to arrival can be helpful in order to obtain appropriate equipment, including an airway cart, RSI drugs, tube thoracostomy, ED thoracotomy tray, or a Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) catheter. Managing the room and all members of the trauma team can be difficult, but can often make a sloppy and potentially unsuccessful resuscitation more organized. As the Boy Scouts of America motto states, “Be prepared.”

After preparation for the resuscitation is complete, initial evaluation and management of the unstable trauma patient can be framed using the ATLS Primary Survey mnemonic ABCDE.

A – Airway maintenance and cervical spine precaution

Cervical spine precautions

Patients presenting with debilitating traumatic injury have been found to have a high prevalence of cervical spine injuries, with between 4-34% of polytrauma patients suffering from cervical spine injury.2 Given this high likelihood of injury, care should be taken with initial evaluation, transport and bed transfer of these patients, with use of appropriately sized and fitted cervical collars. Manual in-line stabilization methods during intubation are important as well, given stabilization with a cervical collar during intubation can limit jaw movement, increasing the difficulty of intubation.2 However, when such interventions limit laryngoscopic views, as has been seen in the setting of direct laryngoscope usage, relaxation of aggressive immobilization may be necessary to facilitate successful intubation.3 Efforts to limit flexion and extension, including usage of a supraglottic airway, gum-elastic bougie or video laryngoscopy, should be considered for every polytrauma patient requiring airway management.


In many cases, the unstable and crashing trauma patient will require securement of the airway through intubation. An extensive deep dive into this topic was covered recently (here). The trauma airway is an inherently difficult airway and should never be taken for granted. Patients present un-fasted and with pathology that often makes standard intubation approaches impossible. Additionally, they present with pathology that suffers greatly from even small periods of hypotension or hypoxia. As such, practitioners should have a well thought out airway management plan, with multiple backups and airway adjuvants available for immediate use at the bedside, including materials for a surgical airway.4

B – Breathing and ventilation


Traumatic pneumothorax may quickly develop tension physiology, resulting in devastating preload elimination, hypotension and hypoxia. As such, rapid identification and reversal are key to preventing decompensation or cardiac arrest. Several methods for decompression of pneumothorax are described. Needle decompression has been described and is still taught as part of ATLS; however, this method is often unsuccessful and has frequent complications, requiring the provider to be prepped for rapid conversion to finger thoracostomy.5 Recent literature has identified lack of appropriate placement of needle for decompression and inadequate angiocatheter length as potential causes of needle decompression failure.6 Given the timely need for reversal of tension physiology in the unstable trauma patient, efforts should be directed instead at performance of finger thoracostomy, a procedure used in the initial stages of tube thoracostomy placement.7  As resuscitation proceeds, immediate placement of a chest tube is reasonable over finger thoracostomy.

Several methods may be used to rapidly identify a pneumothorax, including X-ray, point-of-care ultrasound and auscultation of breath sounds. In the unstable trauma patient, auscultation of lung sounds can be extremely difficult with standard stethoscopes.8 Other components of the physical exam may point toward pneumothorax with tension physiology, such as tracheal deviation, subcutaneous emphysema with crepitus, and penetrating trauma. Supine radiographs of the chest certainly demonstrate large pneumothoraces, but there is growing literature to support improved identification of this pathology and other lung pathology with ultrasound.9-11 Examination of the intercostal spaces on the anterior chest wall with linear array probe may illustrate lack of lung sliding as evidence of pneumothorax, and in the setting of traumatic instability, should be acted upon.

In setting of rapid decompensation and pending cardiac arrest, many algorithms recommend immediate bilateral decompression in blunt, and ipsilateral decompression in penetrating trauma.5,12 Vigilance should be maintained in the post-intubation patient, given the propensity for worsening pneumothorax in the setting of positive-pressure ventilation.

C – Circulation with hemorrhage control

Hemorrhage identification and control

The most common etiology of hemodynamic collapse in the trauma patient is hemorrhagic shock. Given this, the trauma practitioner should quickly identify the shock state and determine the source of hemorrhage. ATLS teaches practitioners to look to “blood on the floor and then four more (chest, abdomen, pelvis/retroperitoneum, long bones)” as sources for major blood loss.

Superficial injuries

Blood from superficial and deep lacerations is often the most obvious source for blood loss. Despite the frequent overestimation of blood lost at the scene of a trauma, large volume exsanguination can occur without correction. Direct pressure to venous and arterial bleeding is often sufficient to prevent additional blood loss, but care should be made not to overpad dressings. Big, bulky dressings can be less effective that those that provide direct, pointed pressure to the site of hemorrhage. In the setting of continued blood loss despite pressure, the practitioner should be prepared to ligate bleeding vessels, either though whip-stitching of the vessel or closure of the wound with sutures/staples to provide tamponade. The key to a successful trauma resuscitation is exposure; a missed scalp laceration can result in severe hemorrhage that would have been easily addressed if the patient was rolled and scalp explored.


Large volume blood loss into the chest can result from both blunt and penetrating trauma, and can potentially result in tension physiology. After identification of hemopneumothorax in the unstable trauma patient, a chest tube should be placed on the affected side. ATLS recommends placement of large bore chest tubes in the setting of any traumatic hemothorax large enough to be identified on chest radiograph.1 Often hemothorax is secondary to a lung laceration or intercostal vessel injury, and decompression with placement of chest tube may be the definitive management, with patients often not requiring further intervention. However, should the patient have massive output (see below), further surgical intervention is necessary.

Indication for surgical intervention for hemothorax
>1,500cc immediate output
>200cc/hr output for 2-4 hours
Patient requires large volume transfusion

With large volume hemorrhage, early initiation of auto-transfusion of the patient’s own whole blood should be attempted. Patient’s with suspected diaphragmatic injury, concomitant gastric injury with violation into the thorax or associated chest malignancy are potential contraindications for autotransfusion.13 Commercially available devices can be used to ensure adequate filtration when used in-line with chest tube suction devices.

Intra-abdominal hemorrhage

Damage to intra-abdominal organs, both solid and hollow, can result in large volume blood loss without significant changes to the external appearance of the patient.1 Gross examination of the abdomen and review of the mechanism of injury can lend some information as to the presence of an abdominal injury. In the absence of obvious signs of injury, the addition of the Focused Assessment Sonography in Trauma (FAST) exam can help to identify presence of intra-abdominal free fluid suggestive of traumatic hemorrhage. Given the high sensitivity and specificity, FAST examination carries an EAST Level II recommendation as the initial study for identifying intra-abdominal free fluid. Diagnostic peritoneal lavage may also be employed to identify hemorrhage in this setting. Many algorithms exist for the use of these procedures in the unstable patient instead of CT imaging. Positive studies should result in immediate surgical intervention, unless a contraindication is present.

EAST Algorithm for evaluating for intra-abdominal injury in the hemodynamically unstable trauma patient.

Pelvic fractures

The pelvis also serves as a large cavity for blood loss, with a substantial increase in volume in the setting of acute pelvic ring fractures. In one cadaveric study, fracture of the pelvis resulting in a pelvic diastasis of 5cm resulted in a 20% increase in pelvic volume, with a high association of venous injury.14 As a result, large volumes of blood can rapidly accumulate in the pelvis. Binding the pelvis, either with commercially-available devices or with an appropriately fitted sheet, has been found to decrease the volume of the pelvis, but has not been shown to have a statistically significant decrease in blood loss.15 Given the potential for decreasing pelvic volume and blood loss, placement of a temporary pelvic binder is recommended in the setting of a potential pelvic source of hemorrhage. In the patient who has no other identifiable source for hemorrhage, pelvic angiography is the EAST recommended intervention over surgical intervention.


The compartments containing long bones can serve as a large vacuum for blood loss in the setting of acute fracture, in addition to blood lost externally in the setting of open fractures. One study illustrated an average blood loss of greater than 1,200cc in the setting of isolated femur fractures in adults.16 Rapid identification of and splinting of fractures can result in improved pain control and decreased blood loss.17 For most fracture related external hemorrhage, external direct pressure is sufficient to prevent additional hemorrhage. Some devices exist for rapid wound packing which may be of benefit in this patient population. However, in the setting of massive hemorrhage with suspected arterial source, placement of a tourniquet may be indicated. Tourniquet use has illustrated decreased hemorrhage rates and improved morbidity and mortality, even when placed by first responders in the out-of-hospital environment.18,19 If placing such devices, carefully document placement location and specific time of placement to prevent prolonged tourniquet times.

General hemorrhage

One intervention proven to decrease death from bleeding and all-cause mortality at 30-days is the early administration of an antifibrinolytic agent tranexamic acid.20 This medication has shown great success when administered in the first hour after injury, though it did illustrate a slight association with increased risk of bleeding death if administered after 3 hours post-injury.20 As such, this medication is recommended in the setting of transfusion-requiring severe traumatic injury and should be given early in the evaluation, potentially in the pre-hospital setting.21 Recommended dosing is 1g administered IV over 10 minutes, with additional infusion of 1g over 8 hours. For further details, go here:

Anticoagulant reversal

Use of anticoagulants and antiplatelet agents complicate the management of traumatic hemorrhage.22 Often the hemodynamically stable patient will be unable to provide medication history, and additional data may be necessary to know of concomitant anticoagulant use. Elderly patients, patients with history or evidence of atrial fibrillation and those with history of CVA should be considered at risk for usage of either anticoagulant or antiplatelet agents. Point-of-care PT/INR may help if the patient is using warfarin, but will otherwise be of little help to the practitioner.

In the setting of anticoagulant use, efforts should be made to reverse the anticoagulated state in the setting of life-threatening hemorrhage. Use of these agents has an associated increased injury severity and mortality in elderly patients, so rapid reversal of their effects is paramount.23 Several protocols exist for reversal in the trauma patient, but consensus statements do not exist. With the addition of new reversal agents, more work should be done to create reversal protocols.


Sample reversal protocols for anticoagulant agents in traumatic, life-threatening hemorrhage.

The use of anti-platelet agents also creates an unfavorable environment for hemostasis. Some protocols call for the transfusion of platelets to reverse effects. In the hemodynamically unstable patient, platelets should be added as part of standardized massive transfusion protocols, making this intervention less important for the specific reversal of the anti-platelet agent.

Resuscitative Thoracotomy

A third subset of shock that may present in the unstable and crashing trauma patient is that of cardiogenic shock. In the setting of blunt traumatic injury, this may be related to direct cardiac contusion or free wall rupture, resulting in pericardial tamponade. In the penetrating trauma patient, this may also be due to cardiac injury resulting in pericardial tamponade. As discussed in a prior post on traumatic cardiac arrest, emergency department thoracotomy can be considered in certain situations for correction of potentially reversible causes. Pericardiocentesis, though temporizing, may only have short-lived effects, given the nature of injuries that lead to pericardial tamponade in the setting of trauma. As such, rapid transition to thoracotomy is recommended.

New therapies

REBOA: A relatively new therapy for the management of traumatic hemorrhage of the trunk and torso is the use of resuscitative endovascular balloon occlusion of the aorta (REBOA). A technique initially described in 1950s, REBOA has been used in multiple arenas related to hemorrhage, from abdominal aortic aneurysm rupture to post-partum hemorrhage.24 Through the strategic placement of a balloon catheter in various zones of the aorta, a provider can selectively prevent distal blood flow to sites of hemorrhage, hopefully temporizing the patient until more definitive management can be performed. Several protocols have been proposed for initiation of REBOA in the ED, with more facilities introducing REBOA programs.25 Despite expanding its use, one review of REBOA use illustrated no improvement in hemorrhage-related mortality.26 REBOA remains a viable option in the age of damage control resuscitation of the patient with massive traumatic torso hemorrhage, though more research is needed to identify the best populations for usage.


After identifying the potential source of exsanguination, efforts should be directed at resuscitation. “Damage control resuscitation” protocols have been developed to reduce the dangers of the “lethal triad” of trauma: acidosis, hypothermia, and coagulopathy.27 Infusion of crystalloid in large volumes has been linked to worsening acidosis and hemodilution. After initial field resuscitation with crystalloid, the unstable patient should be transitioned to blood product. The Eastern Association for the Surgery of Trauma guidelines give Level I recommendation for the transfusion of packed red blood cells in the setting of trauma and hemodynamic compromise, with less emphasis placed on hemoglobin directed transfusion.28 Combat literature has shown that the ideal transfusion product would be whole blood, though this resource is not often held in supply. The PROMMTT study found that practitioners attempted to replicate whole blood in their transfusion patterns, approaching a 1:1:1 or 1:1:2 ratio of plasma to platelets to packed red blood cells. Further investigation into ideal transfusion ratios by the PROPPR trial showed similar outcomes with these ratios, but noted a slight improvement in achievement of hemostasis and 24-hour mortality related to exsanguination in the 1:1:1 group.29

Given that hemorrhage is the most common etiology of shock in the trauma patient, little emphasis should be placed on vasopressor agents. Blood product replacement remains the gold standard in management of traumatic hemorrhagic shock. An exception to this rule involves patients with traumatic spinal cord injuries presenting with hypotension secondary to neurogenic shock.30 While guidelines recommend aggressive reversal of hypotension with fluid resuscitation, there is no one specific vasopressor agent for additional support recommended.31 Norepinephrine, phenylephrine or dopamine are all mentioned as potential agents, though phenylephrine should be avoided in those patients presenting with simultaneous bradycardia secondary to neurogenic shock.32

D – Disability; neurologic status

GCS/neurologic examination

After initial assessment, efforts should be made to perform a neurologic examination and determine the Glasgow Coma Scale of the patient. In the unstable patient, efforts may often proceed quickly to rapid sequence intubation, which can prevent adequate neurologic examination. Though protection of the patient’s airway is paramount, a neurologic exam should be performed and short-acting paralytics should be considered for RSI if possible.

Spinal cord injuries

Spinal column and cord injuries may complicate the poly-traumatized patient, leading to further injury load and potential source for hemodynamic instability. Patients will often present in a cervical collar and on spinal immobilization boards, though recent review of the literature suggests that spinal motion restriction methods may be more beneficial than immobilization boards. Efforts to minimize spinal manipulation should be attempted, with knowledge that life-saving measures may limit the ability to do so. During initial resuscitation, some elements of the physical exam may suggest spinal cord injury: focal neurologic deficit, priapism, or shock refractory to standard transfusion methods. Careful attention should be made to prevent hypoxia and hypotension, which increase morbidity and mortality.

Intracranial hemorrhage (ICH) management

Traumatic intracranial injury can complicate the course of the poly-traumatized patient. Though CT examination may be performed after the patient reaches a more hemodynamically stable state, suspicion of severe ICH should remain high so that early intervention can occur. The practitioner should look for signs of expanding ICH: palpable skull crepitus/obvious skull fracture, signs of basilar skull fracture, scalp hematoma, and facial bone fractures. Additionally, patients with diminished GCS without obvious signs of head injury should be considered high risk for ICH.

Progressively worsening ICH and associated edema can quickly progress, resulting in herniation of intracranial contents. This is often heralded by a combination of vital sign changes and lateralizing physical exam findings. Cushing’s response is the combination of bradycardia and hypertension in the herniating patient. Additionally, a unilateral dilated and unreactive pupil may be observed. Hemodynamic instability due to severe ICH and herniation requires rapid intervention. Hypertonic saline or mannitol may be used in an effort to decrease intracranial pressure, though guidelines do not exist for preferential use. The practice of hyperventilation should be avoided, unless rapid surgical decompression is possible, given the associated cerebral vasoconstriction and decreased oxygen delivery. Neurosurgical consultants should be involved as early as possible. Please go here for further details:

E – Endpoints/Markers (ATLS uses “Exposure/environmental control” here)

The ultimate goal in the resuscitation of the unstable and crashing trauma patient is to preserve life and return the patient to a normal physiologic state. However, the severity of injury may require prolonged resuscitation and multiple interventions before an external sign of response is noted by the practitioner. Surrogate markers for injury severity are the serum lactate level and base deficit. Severely elevated base deficit has been linked to increased mortality and blood product requirements, while the rate at which the base deficit is corrected in the resuscitation is associated with improved survival.33-35 Base deficit may be slightly better than lactate at this prediction, but lactate has also shown utility.36 Both are recommended as markers of resuscitation response by the most recent EAST Guidelines. Hemoglobin measurement is known to be inherently flawed in the acutely hemorrhaging patient and should not be used as an initial risk stratifying tool or resuscitation goal. Aggressive efforts to improve oxygen delivery, through prevention of further hemorrhage, application of supplemental oxygen and transfusion of blood product may be linked to more rapid correction of these physiologic markers and improved outcomes.37

Ultimately, the crashing trauma patient may require definitive surgical intervention. The initial resuscitation should be aimed at rapid identification of potentially reversible causes of hemorrhage, protection of the airway, and aggressive resuscitation. If the facility does not have the potential for surgical intervention, then the patient should quickly be prepped for transfer. Intubation, placement of chest tubes, and fracture splinting can be performed quickly in most emergency departments; however, a “stay-and-play” approach to the trauma patient is often detrimental to the patient and transport should not be delayed if available.

Case Recap

35-year-old male presents after a high speed MVC. Patient unresponsive on scene, placed in cervical collar and on spinal board by EMS after prolonged extrication. 5 minutes prior to patient arrival, EMS alerts EM providers to current vital signs and mechanism of injury. Trauma surgery paged to ED, lead EM physician briefs nursing and support staff in trauma bay prior to arrival, assures adequate procedural supplies are present and alerts blood bank to likely massive transfusion protocol event. Airway setup prepped.

Primary Survey:

A: Airway intact and without obvious obstruction

B: Spontaneous but sonorous respirations, left chest wall crepitus with diminished lung sounds

C: Thready pulses in bilateral radial locations and left dorsalis pedis; absent pulse in right DP; large volume hemorrhage from posterior scalp wound; open right femur fracture with continued hemorrhage; distended abdomen

D: GCS 6 (Eye – 1, Verbal – 2, Motor – 3)

E: Cool to touch, worse in distal right lower extremity

Vitals: HR 139 bpm, BP 84/40 mmHg manual, RR 30 bpm, SpO2 78%

Patient identified as having multiple potential sources for shock on arrival. After initial assessment, he underwent endotracheal intubation using ketamine and rocuronium. Video laryngoscope was used primarily, and intubation was successful on first attempt with no worsening hypoxia. Lack of breath sounds with associated crepitus to the left chest wall raised concern for left hemopneumothorax, and a left chest tube was placed with return of air and 500cc blood immediately. An autotransfuser device was employed, and the massive transfusion protocol was initiated at 1:1:1 ratio with 1g TXA IV. Given an open deformity to the right femur, a tourniquet was requested, but after the patient was placed in a traction splint, hemorrhage ceased. The scalp laceration was stapled for rapid hemostasis. Chest radiograph confirmed appropriate ETT placement, chest tube placement with small residual hemothorax, and left sided rib fractures. Pelvic radiograph demonstrated a sacral fracture with associated anterior diastasis, resulting in the placement of a pelvic binder. FAST examination was performed, illustrating presence of anechoic fluid collection in Morison’s pouch and peri-splenic views. After interventions and blood product administration, vital signs were notable for persistent hypotension and minimal improvement in tachycardia, resulting in immediate transit to operating room for exploratory laparotomy.

Discharge problem list following 15-day hospitalization:

Right-sided subdural hematoma, status post surgical decompression
Right maxillary, frontal sinus fractures
Rib fractures (R 3-5, L 3-8)
Left hemopneumothorax
Liver laceration
Splenic laceration, status post splenectomy
Sacral fracture
Pelvic ring fracture
Right open femoral shaft fracture, status post ORIF

References / Further Reading

  1. ATLS Student Course Manual, 10th edition
  2. Aoi Y, Inagawa G, Hashimoto K, Tashima H, Tsuboi S, Takahata T, Nakamura K, Goto T. Airway scope laryngoscopy under manual inline stabilization and cervical collar immobilization: a crossover in vivo cinefluoroscopic study. J Trauma. 2011; 71(1): 32-6.
  3. Manoach S, Paladino L. Manual in-line stabilization for acute airway management of suspected cervical spine injury: historical review and current questions. Ann Emerg Med 2007; 50(3): 236-45.
  4. Stephens CT, Kahntroff S, Dutton RP. The success of emergency endotracheal intubation in trauma patients: a 10-year experience at a major adult trauma referral center. Anesth Analg. 2009 Sep;109(3):866-72.
  5. Leigh-Smith S. Tension pneumothorax – time for a re-think? Emerg Med J 2005; 22:8-16.
  6. Chang SJ, Ros SW, Kiefer DJ, Anderson WE, Rogers AT, Sing RF, Callaway DW. Evaluation of 8.0cm needle at the fourth anterior axillary line for needle chest decompression of tension pneumothorax. J Trauma Acute Care Surg 2014; 76(4):1029-34.
  7. Aylwin CJ, Brohl K, Davies GD, et al. Pre-hospital and in-hospital thoracostomy indications and complications. Ann R Coll Surg Engl 2008; 90:54-7.
  8. Gaydos S. Clinical auscultation in noisy environments. J Emerg Med. 2012; 43(3): 492-3.
  9. Zanobetti M, Poggioni C, Pini R. Can chest ultrasonography replace standard chest radiography for evaluation of acute dyspnea in the ED? Chest. 2011; 139(5):1140-7.
  10. Zhang M, Liu ZH, Yang JX, Gan JX, Xu SW, You XD, Jiang GY. Rapid detection of pneumothorax by ultrasonography in patients with multiple trauma. Crit Care. 2006; 10(4): R112.
  11. Tasci O, Hatipoglu ON, Cagli B, Ermis V. Sonography of the chest using linear-array versus sector transducers: Correlation with auscultation, chest radiography, and computed tomography. J Clin Ultrasound. 2016 Feb 11 [Epub ahead of print]
  12. Sherren PB, Reid C, Habig K, Burns BJ. Algorithm for the resuscitation of traumatic cardiac arrest patients in a physician-staffed helicopter emergency medical service. Crit Care 2013; 17(2): 308.
  13. Salhanick M, Corneille M, Higgins R, Olson J, Michalek J, Harrison C, Stewart R, Dent D. Autotransfusion of hemothorax blood in trauma patients: is it the same as fresh whole blood? Am J Surg 202(6):817-822, 2011
  14. Baque P, Trojani C, Delotte J, et al. Anatomical consequences of “open-book” pelvic ring disruption: a cadaver experimental study. Surg Radiol Anat. 2005;27:487–490.
  15. Sadri H, Nguyen-Tang T, Stern R, Hoffmeyer P, Peter R. Control of severe hemorrhage using C-clamp and arterial embolization in hemodynamically unstable patients with pelvic ring disruption. Arch Orthop Trauma Surg. 2005;125:443–447.
  16. Lieurance R; Benjamin JB; Rappaport WD. Blood loss and transfusion in patients with isolated femur fractures. J Orthop Trauma. 1992; 6(2):175-9.
  17. Wood SP, Vrahas M, Wedel SK. Femur fracture immobilization with traction splints in multisystem trauma patients. Prehosp Emerg Care, 2003 Apr–Jun; 7(2): 241–3.
  18. Kragh JF, Littrel ML, Jones JA, et al. Battle casualty survival with emergency tourniquet use to stop limb bleeding. J Emerg Med 2011;41:590-597.
  19. Callaway DW, Robertson J, Sztajnkrycer MD. Law enforcement-applied tourniquets: a case series of life-saving interventions. Prehosp Emerg Care. 2015 Apr-Jun;19(2):320-7.
  20. Roberts I, Shakur H, Coats T, et al. The CRASH-2 trial: a randomized controlled trial and economic evaluation of the effects of tranexamic acid on death, vascular occlusive events and transfusion requirement in bleeding trauma patients. Health Technol Assess. 2013; 17(10).
  21. Napolitano J. et al. Tranexamic acid in trauma: how should we use it? J Trauma Acute Care Surg. 2013 Jun;74(6):1575-86.
  22. Pieracci FM, Eachempati SR, Shou J, Hydo LJ, Barie PS. Use of long-term anticoagulation is associated with traumatic intracranial hemorrhage and subsequent mortality in elderly patients hospitalized after falls: analysis of the New York State Administrative Database. J Trauma. 2007 Sep;63(3):519-24.
  23. Boltz MM, Podany AB, Hollenbeak CS, Armen SB. Injuries and outcomes associated with traumatic falls in the elderly population on oral anticoagulant therapy. Injury. 2015 Sep;46(9):1765-71.
  24. Stannard A, Eliason JL, Rasmussen TE. Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) as an adjunct for hemorrhagic shock. J Trauma. 2011; 71(6): 1869-72.
  25. Biffl WL, Fox CJ, Moore EE. The role of REBOA in the control of exsanguinating torso hemorrhage. J Trauma Acute Care Surg. 2015; 78(5): 1054-8.
  26. Morrison JJ, Galgon RE, Jansen JO, Cannon JW, Rasmussen TE, Eliason JL. A systematic review of the use of resuscitative endovascular balloon occlusion of the aorta in the management of hemorrhage shock. J Trauma Acute Care Surg. 2016; 80(2): 324-34.
  28. EAST Guidelines Napolitano LM, Kurek S, Luchette FA, et al. Red Blood Cell Transfusion in Adult Trauma and Critical Care. J Trauma. 2009; 67(6): 1439-42.
  29. Holcomb JB, Tilley BC, Baraniuk S, Fox EE, et al; PROPPR Study Group. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA. 2015 Feb 3;313(5):471-82.
  30. Atkinson PP, Atkinson JL. Spinal shock. Mayo Clin Proc. 1996 Apr;71(4):384-9.
  31. Stein DM, Roddy V, Marx J, Smith WS, Weingart SD. Emergency neurological life support: traumatic spine injury. Neurocrit Care. 2012 Sep;17 Suppl 1:S102-11.
  32. Wing PC, et al. Early Acute Management in Adults with Spinal Cord Injury. J Spinal Cord Med. 2008; 31(4): 403–479.
  33. Davis JW, Kaups KL, Parks SN: Base deficit is superior to pH in evaluating clearance of acidosis after traumatic shock. J Trauma 1998;44:114-118.
  34. Davis JW, Shackford SR, MacKersie RC, Hoyt DB: Base deficit as a guide to volume resuscitation. J Trauma 1988;28:1464-1467.
  35. Rixen D, Raum M, Bouillon B, et al: Base deficit development and its prognostic significance in posttrauma critical illness: an analysis by the trauma registry of the Deutsche Gesellschaft für unfallchirurgie. Shock 2001;15:83-89.
  36. Shoemaker WC, Appel P, Bland R: Use of physiologic monitoring to predict outcome and to assist in clinical decisions in critically ill postoperative patients. Am J Surg 1983;146:43-38.
  37. Abramson D, Scalea TM, Hitchcock R, Trooskin SZ, Henry SM, Greenspan J: Lactate clearance and survival following injury. J Trauma 1993;35:584-589.

Additional FOAMed resources:

Taking Ownership of the Ventilator – How to Manage and Troubleshoot

Evan Miller, DO (EM Resident Physician, Allegheny General Hospital) and Maxim Dzeba, MD (EM Attending Physician, Allegheny General Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) & Justin Bright, MD (@JBright2021)

Case Scenarios

You are the overnight senior resident in the ED managing a 27 year-old asthmatic male who has been in respiratory distress for the past few hours. You make the decision to intubate given the patient’s declining mental status and increasing fatigue. The respiratory therapist asks if you want to set the patient’s respiratory rate at his current 24 breaths per minute.

You received sign-out from the day resident about an intubated patient in room 5. The patient is an 81 year-old female who presented seven hours prior and was intubated after being diagnosed with severe sepsis due to pneumonia. The patient’s blood pressure has been steadily decreasing and repeat chest xray showed diffuse bilateral opacities which was worse than prior imaging. The patient is 80 kg and 5’3” tall. She was started on VCV rate 14, tidal volume 600, PEEP 10, FiO2 80%. Are these the correct settings?

Your overnight junior calls for your help with his decompensating intubated patient. The patient is a 54 year-old male with a history of COPD who was intubated ten minutes ago. The ventilator is alarming due to high pressures. The patient’s current vitals are HR 140, BP 80/50, SpO2 82%. The ventilator settings are VCV rate 12, tidal volume 450, PEEP 15, FiO2 100%. You quickly disconnect the circuit but the patient is not improving. What do you do next?

As you are managing these critical patients, a nurse tells you that the 16 year-old female in room 1 who was intubated for airway protection for a suspected drug-induced encephalopathy has a low pressure alarm. You enter the room and see an obese young female who is bucking the vent and thrashing around. You perform an inspiratory pause and find the plateau pressure to be low with a continuously low peak pressure.


The care of critically ill, mechanically ventilated (MV) patients is essential to the practice of emergency medicine. While emergency physicians are experts at securing even the most difficult airways, much less time is spent on learning the intricacies of mechanical ventilation. Increasing emergency department (ED) boarding time has been associated with negative outcomes.1 Fuller et al (2015) found emergency physicians had suboptimal adherence to best practice guidelines for mechanically ventilated patients in the ED. This was correlated with increased intensive care unit (ICU) length of stay (LOS) and higher rates of morbidity and mortality. In that study the median ED LOS was 3.4 hours with a range of 1.1 to 18.3 hours. Due to this increased ED LOS, it is imperative ED physicians are comfortable with initial ventilator settings, best practices, and perhaps the most difficult yet most important task of ventilator troubleshooting.2

Basics of Mechanical Ventilation

Indications and Pathophysiology

The emergency physician will intubate for one of four main reasons: a) inability to ventilate; b) inability to oxygenate; c) anticipated clinical course; and d) airway protection.3

There are two main goals of respiration: supplying oxygen demand and eliminating carbon dioxide (CO2). Ventilation is defined as the elimination of CO2 from the body. Adequate ventilation is matching minute ventilation with metabolic demand, while hypoventilation is the inability to keep up with metabolic demand resulting in hypercapnia and eventually acidosis.

Minute ventilation (VE) is the measurement of air inhaled or exhaled per minute and is found by multiplying the respiratory rate (RR) by the tidal volume (VT) [VE = RR x VT]. When dealing with a patient who was intubated for inability to ventilate, these two parameters (RR, VT) can be modified to correct the hypoventilation. Common causes of low RR include any CNS depressant/injury, while causes of low VT include poor respiratory muscle contraction due to neuromuscular disorders or poor chest wall mechanics.4

Oxygenation is any process that leads to the delivery of O2 to the tissues. There are many causes of hypoxemia including low inspired FiO2 (altitude, medical error), V/Q mismatch, hypoventilation, diffusion defect, and low mixed venous oxygen.5  Shunt and dead space ventilation are the two major mechanisms that cause significant abnormalities in gas exchange.

Shunt is perfusion without ventilation. This occurs when the blood passes from the right heart to the left heart without passing any areas of ventilation. An intra-cardiac right to left shunt is an easy representation of this. Intrapulmonary causes include consolidation, pulmonary edema, and atelectasis. In these situations, increasing the FiO2 to 100% will not improve the oxygenation as the blood is not being exposed to areas of ventilation. The treatment for shunt induced hypoxemic respiratory failure is positive end expiratory pressure (PEEP).6,7 PEEP recruits collapsed alveoli and works to decrease the shunted areas. One method to determine the proper amount of PEEP is to use the Acute Respiratory Distress Syndrome Network (ARDSNet) PEEP/FiO2 table ( Ideally, the goal is to use the lowest amount of PEEP to maintain an oxygen saturation of 88 – 95%.8

Dead space is any area of ventilation without perfusion. The traditional example of dead space is seen with a massive pulmonary embolism, but this can also be seen in cases of low cardiac output. Iatrogenic causes of dead space include alveoli over distension secondary to breath-stacking in an intubated COPD patient. Increased dead space can lead to both hypoxemia and hypercapnia.4

Modes and variables

There are several different modes and variables to understand when setting up MV.

Breath types: There are three main types of breaths that a ventilator can supply. The most basic is a mandatory breath which is initiated, controlled, and ended by the machine itself. The second type is an assisted breath which is initiated by the patient but controlled and ended by the machine (based on variables set by the provider).  The third type is a spontaneous breath which is initiated, controlled, and ended by the patient.

Trigger: An assisted breath is triggered by a set negative airway pressure or flow. When an intubated patient attempts to take a breath, the negative pressure or change in flow is sensed by the vent and a breath is delivered. This setting is generally standard and not often manipulated by ED physicians.

Cycle: The cycle is the main distinction between ventilator modes. The “cycling” is when the ventilator switches from inspiration to expiration. Volume-cycled: the machine delivers a set volume at which point it stops the flow and allows for expiration. Pressure-cycled: the machine delivers a breath until it reaches a set pressure at which point it stops the flow and allows for expiration. The volume will vary with each breath depending on lung compliance.

Respiratory rate: This variable sets a minimum number of breaths that must be given per minute. For example, in an assist mode, if you set the rate at 12 the ventilator will break the minute up into 12 five second blocks. If the patient initiates a breath during these five seconds, the ventilator will count that breath. If the patient does not initiate a breath by that time, the ventilator will deliver a mandatory breath ensuring a minimum number of breaths per minute.9

Inspiratory to expiratory (I:E) ratio: This variable is a factor of the inspiratory time which is the VT divided by the flow rate (VT / FR). The standard flow rate is 60 L/min. The I:E can be increased by: 1) decreasing the tidal volume; 2) increasing the inspiratory flow; or 3) decreasing the respiratory rate. A normal I:E would be 1:2 or 1:3 vs. a patient with COPD where an appropriate I:E would be 1:4 or above.

Positive end-expiratory pressure: PEEP is used to increase functional residual capacity (FRC) by preventing alveolar collapse at the end of expiration and recruiting fluid filled or atelectatic alveoli. The starting PEEP is usually set at 5 cm H2O as this is believed to be equivalent to physiologic levels. In patients with ARDS, the PEEP is adjusted based on the PEEP / FiO2 tables.8

Fraction of inspired oxygen: FiO2 is usually started at 100% and is titrated down to a SpO2 of > 88% (or PaO2 > 55 mm Hg) with a goal FiO2 of < 60% as soon as possible.10 In patients who are intubated for airway protection and have no issues with ventilation or oxygenation, it is reasonable to start the FiO2 at lower levels. Increased FiO2 allows for a higher PAO2 at a low alveolar ventilation L/min.

Tidal Volume: VT is set in volume-cycled modes and is the minimum volume delivered per breath. It is important to note that the tidal volume should be calculate using the ideal body weight (aka predicted body weight) rather than the actual weight.

Predicted body weight (in kg)
Males: 50 + 2.3 (height [inches] – 60)
Females: 45.5 + 2.3 (height [inches] – 60)


Assist-control ventilation (ACV) provides the highest level of ventilatory support3. In this mode, every breath is supported by the ventilator, including any breaths above the set rate. ACV can be either volume-cycled (volume-targeted) or pressure-cycled (pressure-targeted).

In volume-cycled ACV the physician will establish a set VT to be delivered with each breath ensuring a minimum volume per breath. The trigger can either be an elapsed time (minimum set rate) or a spontaneous breath. Major disadvantages of this include auto-PEEP with associated lung injury (discussed later) and decreased cardiac output.

In pressure-cycled ACV the physician will establish a set rate, flow, and pressure. Each breath will cycle after the set pressure is reached thereby decreasing peak inspiratory pressure (discussed later). However the tidal volume is variable which each breath and is dependent upon the lung compliance.

Pressure-support ventilation (PSV) is used primary for weaning purposes or during stable ventilatory support periods. Each breath is patient-triggered and pressure-cycled. This mode provides extra pressure support to help the patient overcome the inherent resistance of the ventilator circuit.

Other available modes include synchronized intermittent mandatory ventilation, bilevel, and control mode ventilation.

Ventilatory settings

General settings for initiation of MV using the “lung-protective” strategy are as follows:8,10

  • Assist control mode – volume-cycled
  • Tidal volume 6 mL/kg IBW
    • Alternatively starting at 8 mL/kg IBW and reducing by 1 mL/kg every 2 hours until tidal volume is 6 mL/kg4
  • RR 14-16 breaths/min (can titrate to a max of 35 to keep pH above 7.15)
  • FiO2 100% with rapid titration based on SpO2
  • PEEP 5 to 7 cm H2O
  • Keep plateau pressures below 30 cm H2O

For patients with contraindications for permissive hypercapnia (discussed below):

  • Tidal volume 8 mL/kg IBW
  • RR 12-20 breaths per minute

Special Scenarios

Acute Respiratory Distress Syndrome (ARDS)

Acute respiratory distress syndrome is a severe cause of hypoxemic respiratory failure. ARDS is caused by both direct and indirect lung injury which causes an exudative alveolar filling. This leads to a severe VQ mismatch. While ARDS is not commonly encountered in the ED due to its delayed time of onset, most patients that are intubated in the ED have significant risk factors for its development. These risk factors include severe sepsis, chest trauma, and pneumonia.

Historically, tidal volumes were set as 10-12 mL/kg even though the normal tidal volumes of spontaneous breathing is 5-7 mL/kg IBW. It was later discovered that these elevated volumes lead to alveolar over distension causing alveolar rupture and release of inflammatory cytokines. These effects in turn can lead to: 1) Barotrauma, which includes pneumothorax, pneumomediastinum, and pneumopericardium, occurs when the structural integrity of the alveolus is disrupted due to elevated transalveolar pressures; 2) Volutrauma is due to the overdistention of the alveolus resulting in lung parenchyma damage; and 3) Biotrauma which is a multi-organ injury due to the inflammatory cytokines.11

The high mortality of ARDS led to a randomized control trial performed by ARDSNet in 2000 which found a significant reduction in morbidity and mortality when volumes were set at 6 mL/kg IBW and plateau pressures were kept below 30 cm H2O.8 The low tidal volume strategy is designed to prevent worsening lung injury that could be caused by alveolar over-distension. These lower tidal volume are combined with higher respiratory rates to provide adequate minute ventilation.8

Table (1): Berlin Definition of Acute respiratory Distress Syndrome.12

Permissive hypercapnia

The lung-protective settings usually result in a retention of CO2 and therefore a degree of acidosis, this is referred to as permissive hypercapnia. Previously, MV was used to normalize arterial blood gas numbers, specifically the pH and arterial carbon dioxide tension (PaCO2). The current thought process is to minimize the risks of MV while still maintaining an adequate gas exchange. Permissive hypercapnia is acceptable as long as the pH remains above 7.15-7.20. If the pH falls below 7.15, you can increased the RR to a maximum of 30-35 breaths/min.10 Due to this acidosis, permissive hypercapnia is contraindicated in patients with acute brain injury, fulminant hepatic failure, severe pulmonary hypertension, or severe metabolic acidosis.9,13

Asthma and COPD

The major concern for mechanically ventilated patients with obstructive airway disease is dynamic hyperinflation (also known as auto-PEEP, intrinsic PEEP, breath stacking, or air trapping). This condition occurs when gas becomes trapped in the lungs during mechanical ventilation. The air trapping is caused by inadequate time for exhalation allowing for delivery of the next breath before the patient has time to completely exhale. This leads to increased alveolar pressures, decreased venous return, and decreased cardiac output ultimately leading to hemodynamic instability. Auto-PEEP can be detected on the ventilator waveform because the flow will not return to zero before the next breath (figure 1).

Figure (1). Dynamic hyperinflation: Top image shows how the trapped gas will result in increased lung volume resulting in decreased ventilation/oxygenation and increased intrathoracic pressure. Bottom image shows how the waveform does not reach zero/baseline before delivery of the next breath.11

Strategies to avoid auto-PEEP would be any factor that increases the I:E ratio which include decreasing the respiratory rate and/or tidal volume, or increasing the inspiratory flow rate (the standard flow rate is 60 L/min, this can be increased up to 80-100 L/min).6 These factors allow more time for the patient to complete exhalation minimizing the risk of hyperinflation. In severe cases, deep sedation and paralysis may be necessary to improve ventilator synchrony and avoid auto-PEEP.11

Other special topics

Elevated intracranial pressure: Ii any case of elevated ICP, hypoxia and hypercapnia need to be avoided. Permissive hypercapnia is contraindicated due to association with cerebral vasodilatation which could lead to increased cerebral blood flow and therefore increased intracranial pressure.11

Severe metabolic acidosis: Patients with severe metabolic acidosis (e.g. diabetic ketoacidosis or salicylate toxicity) usually increase their minute ventilation to help compensate for the acidosis. This is usually accomplished by increasing their respiratory rate. When these patients are placed on MV, it is important to consider setting the RR close to the pre-intubation rate as well as closely monitoring the pH.6

Shock: High amounts of PEEP can result in increased intrathoracic pressures which decrease cardiac preload and exacerbate hypotension. Addressing volume status, preferably prior to intubation, and keeping PEEP at 5 cm H2O is advised.7

Troubleshooting the ventilator

General effects of intubation include:

  • Post-intubation hypotension
  • Decreased venous return due to increased intrathoracic pressure
  • Acidemia
  • Acute lung injury / acute respiratory distress syndrome
  • Increased intracranial pressure
  • Ventilator-induced pneumonia
    • Strategies to reduce this include:
      • Elevate the head of the bed 30-45 degrees
      • Maintaining endotracheal tube cuff pressure at 20 cm H2O
      • Placing a naso- or oro-gastric tube to avoid overdistention
    • Oxygen toxicity – the exact cause and mechanism is still controversial however supraphysiologic levels of oxygen has been associated with increased mortality and worse neurologic outcomes in post arrest patients

Step-wise approach

There is a broad differential in any mechanically ventilated distressed patient including anxiety and pain as well as tension pneumothorax and auto-PEEP. The first step is identifying the level of distress as well as the overall hemodynamic stability.

In a hemodynamically stable patient, a focused systematic approach can be safely utilized.7,15

1) Obtaining a history from the bedside staff – this includes reason for and difficulty of intubation, ETT depth, current ventilator settings, and any recent changes including ventilator settings, new medications, or invasive procedure attempts (e.g. chest tube, central line).

2) Performing a physical exam – this includes examining the ETT for migration, air leak, or kinking. This also includes assessing need for continued intubation. For example, if a previously healthy patient was intubated for airway protection for a suspected drug overdose and is now awake and following commands, weaning to extubate could be an option. Evaluation for equal breath sounds and chest rise should be performed as well. Assess for hypoxia via pulse oximetry and/or arterial blood gas.

3) Checking the ventilator – evaluate the patient’s synchrony with the machine as well as the waveform searching of possible auto-PEEP.

4) Monitoring lung mechanics – please see measuring pressures section below.

5) Examining a chest x-ray or bedside ultrasound – examine the chest x-ray for worsening clinical condition, pneumothorax, and ETT tube position. Bedside ultrasound can be utilized for evaluation of pneumothorax.

6) Evaluating adequacy of analgosedation – after all other causes have been evaluated, the patient’s need for analgesia, sedation, and possibly paralysis should be assessed (e). The modified Society for Critical Care Medicine’s algorithm for sedation and analgesia on UpToDate can be utilized.

Measuring pressures – monitoring lung mechanics

Peak airway pressure (PAP): The peak pressure (Ppeak) is the amount of pressure that is required to deliver the set tidal volume from the ventilator circuit to the alveoli. The PAP is measured at the end of inspiration and is a function of both the airway resistance and the compliance of the lung. Therefore, if the tidal volume remains constant, a change in the PAP would be due to either a change in the airway resistance or in the compliance.  In VCV, the increase in PAP would not affect the delivery of the set volume. However, in PCV, the increase in the peak pressure would result in less volume be delivered (since the set pressure is constant).

Ppeak ≈ (Resistance + Compliance)

Plateau pressure (Pplat): The plateau pressure is measured by using the “inspiratory hold” technique. After the ventilator completes delivery of the breath, the machine will pause resulting in no airflow between the ventilator and patient; this allows for the equalization of pressures. Since the plateau pressure is measure when there is no airflow, it is therefore only a measurement of compliance.

Pplateau ≈ Compliance

Based on the above information, the difference between the Ppeak and Pplat would be proportional to the airway resistance.

Ppeak — PPlateau≈ Airway resistance

The normal measured airway resistance should be less than 10 cm H2O (with an adequate sized ETT).11

Using Pressures to troubleshoot

We can now apply the above information in a case of a crashing ventilator-dependent patient.

  1. If the peak pressure is elevated while the plateau pressure remains unchanged, that means there is an issue with the airway resistance. [ΔPPeak – PPlat would be increased]
  2. If both pressures are increased, then this would mean there is an issue with the compliance of the lungs and chest wall. [ΔPPeak – PPlat would be unchanged or decreased]
  3. If the peak pressure would be decreased, then there is either an air leak or the patient is hyperventilating enough to pull the air instead of having it pushed under pressure.
  4. No change in peak or plateau and patient still having respiratory distress, pulmonary embolism should be considered.11
Using pressures to troubleshoot
Increased Resistance

High peak pressure

Increased Compliance

High peak and plateau

Low Peak
·    ETT obstruction by kinking or patient biting tube

·    Airway obstruction (secretions, mucus, blood)

·    Bronchospasm


·    Abdominal compartment syndrome

·    Ascites

·    Large body habitus

·    Positioning


·    Pneumothorax

·    Pneumonia

·    ARDS

·    Atelectasis

·    Auto-peep

·    Pulmonary edema

·    R mainstem intubation


·  Cuff Leak

·  ETT dislodgement

·  Ventilator malfunction

·  Vent circuit is disconnected


Abdominal compartment syndrome is due to elevated abdominal compartment pressures. These elevated pressure result in compression of the diaphragm and lead to elevated peak and plateau pressures. Symptoms include hypotension, difficulty ventilating, decreased urine output, and cardiac arrest. Treatment includes decompression, sedation and/or paralysis, and urgent surgical consultation.6

In a hemodynamically unstable patient, the EM physician must know how to quickly react in order to prevent worsening patient condition and death. A common mnemonic used to respond to a deteriorating patient is DOPE. This stands 1) Dislodgement, 2) Obstruction, 3) Pneumothorax, and 4) Equipment failure.7,11

The first step should be disconnecting the patient from the ventilator and proceeding to manually bag with a bag valve mask and 100% FiO2. This step alone will help identify if the distress is due to the equipment failure or auto-PEEP. If there was a large exhalation immediately after disconnecting the circuit with immediate improvement in stability, auto-PEEP was likely to be the cause. If the patient improves with BVM then the ventilator needs to be investigated for equipment failure or patient-ventilator asynchrony due to inadequate sedation. Asynchrony can be improved by addressing adequacy of sedation as well as tailoring vent settings to match the patient’s efforts with required support.11 Double-cycling is an example of asynchrony in which there are back to back ventilator delivered breaths. This occurs when the patient wants a higher flow rate than what is set. This can be alleviated by increasing the flow rate.13

If the patient does not improve, next assess the difficulty of ventilation. If it is “too easy” to ventilate, a dislodgement or air leak could have occurred. If it is “too difficult” to ventilate, a suction catheter should be passed through the tube to asses for ETT obstruction or kinking.

If the above measures fail and the patient continues to decline, pneumothorax must be considered. This can be evaluated with auscultation, chest x-ray, or bedside ultrasound. If necessary, a needle chest decompression followed by a decompressive chest tube should be performed.

Case answers

Case #1: No. This patient is at risk for auto-PEEP. If this patient’s vent was set for a rate of 24 this would allow for 2.5 seconds per breath. Even if the inspiratory flow would be increased to 100 L/min, that would only allow for a maximum of 2.4 seconds for exhalation. This would result in an I:E of 1:2.4 which is significantly less than the recommended 1:4 to 1:5.

Case #2: The tidal volume in the scenario was set to 600 mL. Given this patient’s current condition she would be at risk for ARDS and the lung protective strategy should be utilized. The patient’s height is 5’3” and an appropriate tidal volume would be 400 mL (

Case #3: This is an example of a hemodynamically unstable patient. In the case, the patient was removed from the ventilator and BVM was utilized. In going through the stepwise approach you find that the ETT is in good place and is not obstructed. You place the ultrasound on the left chest and quickly identify an acute tension pneumothorax. You perform a needle decompression with immediate patient improvement. Afterwards you place a tube thoracostomy and decrease the PEEP to 5.

Case #4: On your physical exam you notice the patient has “tongued” the tube out of place and therefore has self-extubated. You reassess the patient’s mental status and confirm that the patient is currently alert and oriented, following commands, and is able to protect her airway. The patient is eventually discharged from the department in the custody of her concerned parents.

Must Know Information

Vent Basics

  • Understand the importance of the initial ventilator settings
  • Utilize the lung protective settings when applicable
    • Use 6-8 mL/kg using predicted/ideal body weight
  • Understand how permissive hypercapnia can be utilized to prevent ARDS

Crashing Patients

  • Have a standardized approach to a crashing patient
  • Understand the DOPE mnemonic
    • Dislodgement, obstruction, pneumothorax, equipment failure
  • Consider adequate sedation/analgesia
  • Understand how peak and plateau pressures can be utilized to help diagnose an acutely crashing patient

References / Further Reading

  1. Chalfin DB, et al. Impact of delayed transfer of critically ill patients from the emergency department to the intensive care unit. Crit Care Med 2007;35:1477-1483
  2. Fuller BM, Mohr NM, Miller CN. et al. Mechanical ventilation and acute respiratory distress syndrome in the emergency department: a multi-center observational, prospective, cross-sectional study. Chest. 2015;148:365-374
  3. Adams J. Emergency Medicine: Clinical Essentials. Philadelphia, PA: Elsevier/Saunders; 2013.
  4. Marino, P. L., & Sutin, K. M. (2007). The ICU book. Philadelphia: Lippincott Williams & Wilkins.
  5. Mosier JM, Hypes C, Joshi R, Whitmore S, Parthasarathy S, Cairns CB. Ventilator Strategies and Rescue Therapies for Management of Acute Respiratory Failure in the Emergency Department. Annals of Emergency Medicine2015;66(5):529–541.
  6. Wood SL, Kloot TVder. Ventilator Management in The Intubated Emergency Department Patient. EM Critical Care2013;3(4). Available at: Accessed January 15, 2016.
  7. Owens W. Ventilator Management And Troubleshooting In The Emergency Department. EM Critical Care2014;4(5). Available at: Accessed January 15, 2016.
  8. Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and the Acute Respiratory Distress Syndrome. New England Journal of Medicine N Engl J Med2000;342(18):1301–1308.
  9. Rosen, P., Marx, J. A., Hockberger, R. S., Walls, R. M., & Adams, J. (2006). Rosen’s emergency medicine: Concepts and clinical practice. Philadelphia, PA: Mosby Elsevier.
  10. Wood S, Winters ME. Care of the Intubated Emergency Department Patient. The Journal of Emergency Medicine2011;40(4):419–427.
  11. Archambault PM, St-Onge M. Invasive and Noninvasive Ventilation in the Emergency Department. Emergency Medicine Clinics of North America30:421–449.
  12. Acute Respiratory Distress Syndrome. Jama 2012;307(23).
  13. Santanilla JI, Daniel B, Yoew M-E. Mechanical Ventilation. Emergency Medicine Clinics of North America2008;26:849–862.
  14. Kilgannon JH, Jones AE, Shapiro NL, et al. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA. 2010;303(21):2165-2171.
  15. Winters ME, DeBlieux PMC, Santanilla JI. Emergency Department Resuscitation of the Critically Ill. Dallas, TX: American College of Emergency Physicians; 2011.
  16. Please see the NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary

Case – Blunt Trauma to the Neck

Author: Brett A Hayzen, MD (EM Chief Resident, UTSW / Parkland Memorial Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF)


A 23 year-old male who was riding a motorcycle in front of a High School crowd lost control and ran into the bleachers, with trauma to the anterior neck. EMS arrived and placed King Tube and C-collar. Upon arrival in ED, the patient was noted to have blood spurting out of King Tube, was tachycardic and hypotensive, GCS 5, but with no other outward signs of trauma (no abrasions, lacerations, ecchymosis) – impressively unimpressive visual appearance.

Initial vital signs – HR: 130s, BP: 80/60, O2: 61%

Upon exam, the patient had gurgling breath sounds bilaterally and significant crepitus from neck down to below the nipple line bilaterally. The ED team managing the airway immediately recognized that this would be a very difficult airway – the oropharynx was full of blood, tongue was swollen, and neck was enlarged secondary to subcutaneous emphysema. The decision was made to perform cricothyrotomy. A large vertical incision was made, and it was immediately apparent that the trachea was completely transected, with the distal portion at the level of the sternal notch. An endotracheal tube was placed in the distal portion. Bilateral chest tubes were also placed simultaneously with minimal return of air. The patient was taken emergently to the OR where a sternotomy was performed and ENT repaired the trachea and placed a tracheostomy. The cricoid cartilage and membrane were fractured and were therefore resected. He underwent a primary repair with an anastomosis from thyroid cartilage to 2nd tracheal ring. The patient also had esophageal repair and G-tube placed.

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List of injuries: Tracheal transection, esophageal injury, acute right MCA infarct, subdural hematoma, C1 posterior arch fracture, type III Odontoid fracture, T2 burst fx with minimal retropulsion, right 1st rib fracture, bilateral hemopneumothoraces, and bilateral pulmonary contusions.

Tracheal Injuries are rare diagnoses with < 2% occurring after chest trauma. Injuries sufficient to result in severe laryngotracheal damage can also easily damage the cervical spine (as many as 50% of cases), esophagus, and vascular structures.

Iatrogenic damage is more common with up to 18% of emergent intubations end up with tracheal injuries, often as a result of overinflated cuffs, or perforation from the stylet/ETT. Those most likely to suffer tracheal injuries are the elderly, very young, or patients with history of heavy steroid use or chemotherapy and/or radiation.

There is significant mortality associated with tracheal injuries (approximately 30%), half of which occurring in the first hour due to inadequate airway and tension pneumothorax. Associated morbidity includes tracheal stenosis, atelectasis, pneumonia, mediastinitis, sepsis, and decreased pulmonary function.


The two main classifications of trauma are blunt and penetrating:

Blunt trauma – The most common cause of blunt laryngotracheal trauma is motor vehicle accidents. Patients typically present with dyspnea, dysphonia, neck pain, dysphagia, odynophagia, and hemoptysis. Physical findings may include subcutaneous emphysema, tenderness, edema, hematoma, ecchymosis, and distortion or loss of laryngeal landmarks. Laryngotracheal injuries are often unrecognized because the severity of the symptoms does not always correspond with the extent of injury. 

Penetrating trauma – Usually more obvious, but it is vital to fully assess both entry and exit wounds carefully as there may be bone/cartilage fragments causing obstruction. Additionally, penetrating objects are more likely to causes damage to surrounding structures. Injuries may be obscured by subcutaneous emphysema. Patients often have pneumothoraces / pneumomediastinum – which may delay detection of laryngotracheal injuries. 


Initial management – As always, securing an adequate airway and immobilizing the cervical spine should be the first steps. Airway management may entail cricothyroidotomy / tracheotomy. Endotracheal intubation may be difficult in the presence of spinal, facial, or cervical trauma. Even in cases of only limited intraluminal injury, intubation may exacerbate the situation, so tracheotomy is preferred for patients with a severe laryngeal injury. Also concomitant injuries – such as those to the tongue, jaw, or spine – may preclude safe intubation. In these cases, a controlled tracheotomy over a laryngeal mask airway or over a rigid ventilating bronchoscope can be performed.

Intubation is best performed under direct vision (preferably fiber-optic or rigid endoscopy). A smaller tube with a high-volume, low-pressure cuff is preferable. Early involvement of ENT is highly recommended, as the larynx and trachea need to be fully assessed as they may become affected by secondary inflammation, infection, and further damage secondary to the superimposed presence of the tube. Prolonged intubation poses a significant risk of complications that must not be overlooked or underestimated.


Take home points:

-Traumatic injuries to the larynx or trachea are not always very obvious – have a high suspicion when you have trauma to the anterior neck

-Always look for concomitant injuries to adjacent structures (c-spine, vascular, esophagus)

-Use fiber-optics to intubate and to fully assess the oropharynx and laryngotracheal structures

-Get ENT involved early


References / Further Reading:

-Walter et al. Acute external laryngotracheal trauma: Diagnosis and management. Ear Nose & Throat J 2006 v85 p179-84

-Brett T. Comer, MD, and Thomas J. Gal, MD; Recognition and Management of the Spectrum of Acute Laryngeal Trauma; The Journal of Emergency Medicine, Vol. 43, No. 5, pp. e289–e293, 2012

-Randall et al.: Laryngotracheal Trauma Incidence and Outcomes; Laryngoscope 124: April 2014

-Natarajan A, Sanders GM, et al. A case of anterior tracheal rupture following trivial trauma. Chest Medicine On Line. January 2006. January 23, 2008. On-Line

-Barmada H, Gibbons JR, et al. Tracheobronchial injury in blunt and penetrating chest trauma. Chest 1994. July;106 (1):74 78.

Splenic Infarction in Mononucleosis: Pearls and Pitfalls

Author: Kristen Kann, MD (EM Staff Physician, SAUSHEC, USAF) // Edited by: Brit Long, MD (@long_brit, EM Chief Resident at SAUSHEC, USAF) and Alex Koyfman, MD (@EMHighAK)

An 18 year-old male recently diagnosed with infectious mononucleosis by Monospot presents to the Emergency Department complaining of three days of left upper quadrant pain. He denies any recent trauma or participation in contact sports. His review of systems is otherwise negative, with no fever, nausea, rashes, or other complaints noted. He appears mildly uncomfortable on exam but otherwise is in no acute distress. His initial vital signs include BP 119/55, HR 97, RR 16, T 98.8F, Sat 99%, and a pain scale of 6/10. His lungs and heart are normal, but his abdominal exam is significant for moderate left upper quadrant tenderness to palpation without rebound or guarding. No organomegaly is appreciated on exam. The remainder of his physical exam is unremarkable, including skin and lymph nodes.

A review of recent workup reveals a splenic ultrasound three days prior to the patient’s presentation, which he reports coincided with the onset of the left upper quadrant pain. The ultrasound was significant for multiple hypodensities in the spleen and splenomegaly.



The spleen is a large reticuloendothelial organ in the left upper quadrant that functions to filter red blood cells, produce antibodies (specifically IgM), and remove antibody-coated bacteria from the bloodstream.

The spleen can become infarcted when flow from the splenic artery or one of its branches is interrupted, causing hypoperfusion of splenic segments and eventual tissue death. Causes of splenic infarction can be broken down into three main categories: hematologic conditions that result in splenomegaly, systemic thromboembolic conditions, and trauma.

Splenomegaly occurs with splenic enlargement. The differential for splenomegaly is very large and includes diseases that increase demand for splenic filtration (autoimmune hemolytic anemia, polycythemia vera, spherocytosis, early sickle cell anemia, thalassemias), certain infectious diseases (infectious mononucleosis, AIDS, CMV, and malaria, among others), and splenic infiltration (sarcoidosis, myelofibrosis, metastatic disease, amyloidosis, leukemias, and lymphomas). Infectious mononucleosis was previously diagnosed in this patient and was his only known risk factor. Splenic infarction has been reported as a rare complication of infectious mononucleosis/Epstein Barr Virus infection, but the incidence is unknown.

The vascular network of the spleen can also become the site of thromboembolic disease, such as in the case of malignancy, antiphospholipid antibody syndrome, infectious endocarditis, atrial fibrillation, and sickle cell disease. Interestingly, splenic infarction has been reported in patients with sickle cell trait who were otherwise asymptomatic but presented with left upper quadrant pain after heavy exertion at altitude.

Trauma that affects the blood flow to the spleen, either directly or as a result of compression (ex. splenic hematomas) can also cause splenic infarction. In addition, the Emergency Physician may encounter a patient who has symptomatic splenic infarction after splenic artery embolization.

Rarely, the splenic artery can become torsed in “wandering spleen syndrome,” a rare condition seen in children and young adults in which the spleen is more mobile than usual, leading to infarction of the entire spleen.



Patients with splenic infarction can present in a myriad of ways. Up to 30% may be completely asymptomatic, especially those with nonmalignant hematologic conditions. The most common signs and symptoms in patients with complaints include left sided abdominal pain, fever, nausea/vomiting, elevated LDH, and leukocytosis. While abdominal tenderness to palpation is relatively easy to elicit, splenomegaly is notoriously difficult to appreciate on physical exam. One study compared percussion and palpation by physicians with the gold standard of ultrasonographic measurement and found palpation to have a sensitivity of 56-71% for splenomegaly, with similar results for percussion. Thus, the Emergency Physician should not rely on physical exam alone to exclude splenomegaly, and certainly not to exclude splenic infarction, as there are many causes that can occur in normal or even shrunken spleens (such as advanced sickle cell anemia).



For a patient in whom you suspect splenic infarction, the basic work up should likely include a complete blood count and LDH, with a consideration for peripheral blood smears and manual differentials based on the suspicion for underlying causes. Initial imaging can include ultrasound or computed tomography. Ultrasound has the benefit of being radiation free, relatively fast, and being able to reliably exclude splenomegaly, though some splenic infarcts may be hard to visualize if they are very small and/or more centrally located in the abdomen. Computed tomography, though it does involve an IV dye load and radiation, has the advantage of visualizing the entire spleen while also showing the rest of the abdominal organs in the cases in which the differential is broad.



For the vast majority of splenic infarctions, the main concerns for the Emergency Physician are the determination of the underlying cause and providing proper disposition. If there is no obvious cause already known, but the patient is stable, pain is well controlled, and follow up can be reliably obtained, most patients can be discharged home with outpatient follow up, either with their primary care physician or a hematologist. If the patient is hemodynamically unstable, or if there is evidence of splenic rupture or abscess associated with the infarction, then consultation with Surgery or Interventional Radiology for further treatment and admission should be obtained. While many cases of splenic rupture can be managed non-operatively, the patient will require close observation and consideration for splenic artery embolization or splenectomy. Splenic abscess will require antibiotics as well as drainage or splenectomy. In any patient with a significant portion of their spleen affected by infarction, resultant functional hyposplenia should be anticipated, and the patient will need follow up to provide the appropriate vaccinations and monitoring.



The Emergency Department workup for this patient consisted of a complete blood count, a comprehensive metabolic profile, and coagulation studies in addition to a CT scan of the abdomen with IV contrast, as requested by radiology. A CT was selected to better characterize the total number and size of the lesions and to evaluate for any complications such as abscess or rupture. Laboratory work up was all within normal limits, and the CT scan revealed multiple peripheral small wedge-shaped hypodensities within the spleen measuring up to 1.9 cm. The patient remained hemodynamically stable throughout his ED stay, and his pain was well controlled. He was counseled to continue to avoid contact sports and to return to the Emergency Department for any increase in pain, fever, or other concerns. He was discharged with Hematology follow up. His clinical course remained unremarkable, and given the large portion of unaffected splenic tissue, he did not require any additional vaccines.

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Splenic infarction is a rare complication of infectious mononucleosis, and a rare disease in general, but should be considered in the ED differential of patients with left upper quadrant pain. Special consideration for this diagnosis should be given to those patients with a history of conditions predisposing to splenomegaly, a history of thromboembolic disease, and in those with a history of abdominal trauma. Management for most patients will consist of supportive case and avoidance of splenic injury (no contact sports), while some patients will require admission and consideration for splenectomy, especially if splenic abscess or splenic rupture develop.


References / Further Reading

-Harrison’s Principles of Internal Medicine 19ed

-Tintinalli’s Emergency Medicine 8ed

-Sabiston Textbook of Surgery

-The clinical spectrum of splenic infarction.

Nores M, Phillips EH, Morgenstern L, Hiatt JR

Am Surg. 1998;64(2):182.

PMID: 9486895

-Splenic infarction: an update on William Osler’s observations.

Lawrence YR, Pokroy R, Berlowitz D, Aharoni D, Hain D, Breuer GS

Isr Med Assoc J. 2010;12(6):362.

PMID: 20928991

-Splenic infarction: 10 years of experience.

Antopolsky M, Hiller N, Salameh S, Goldshtein B, Stalnikowicz et al .

Am J Emerg Med 2009;27:262–5.

Subtle ECG Findings in ACS: Part III Benign Early Repolarization vs. Anterior STEMI

Author: Jamie Santistevan, MD (@jamie_rae_EMDoc, Senior EM Resident Physician, University of Wisconsin) // Edited by: Alex Koyfman, MD (EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital, @EMHighAK) & Justin Bright, MD (EM Attending, Henry Ford Hospital, @JBright2021)


Look at these two snakes: One is a deadly coral snake, the other a friendly harmless mimic. I learned to tell them apart in the 5th grade using this rhyme: “Red next to black, you’re alright Jack. Red next to yellow, you’re a dead fellow.”


You may be wondering what reptiles have to do with ECGs. Well, welcome to the third blog post in a series on subtle ECG findings in ACS. This post about mimics: benign early repolarization (BER) and the anterior STEMI. Each of these can mimic the other. The problem is that one of these diagnoses is deadly and the other is a normal variant. Today I am going to discuss the key differences between benign ST-segment elevation, also known as J-point elevation or benign early repolarization (BER), and the subtle ST-segment elevation seen occasionally in acute LAD occlusion.

In the previous post concerning hyperacute T-waves, I said that the STEMI criteria are poorly sensitive for diagnosing vessel occlusion.  This means that some patients with acute coronary occlusion may not meet criteria for STEMI.  In fact, about one quarter of NSTEMI patients have complete vessel occlusion on angiogram [1]. Wang and colleagues studied 1,957 NSTEMI patients and compared baseline characteristics, ECG findings, and long term outcomes, between patients with and without occluded arteries. The group of researchers found that 27% had an occluded culprit artery and those patients had larger infarcts and higher six-month mortality compared to NSTEMI patients without an occluded artery [1].

Remember, the STEMI criteria are arbitrary, based solely on the size (in millimeters) of ST-segment elevation and are only guidelines for reperfusion therapy. We typically use the term “STEMI” to mean complete coronary artery occlusion. “NSTEMI” traditionally means that the patient has had an MI (elevated troponin), but without complete coronary artery occlusion. However, as Wang and colleagues data shows us, some patients have an occluded vessel but do not develop diagnostic ST-segment elevation. These patients, therefore, have a “STEMI-equivalent”, or may be described as having a “subtle-STEMI”.

The subtle STEMI, as defined by 0.1-1mm of ST-segment elevation, occurs in about 18% of patients with an occluded coronary artery [2]. These patients have smaller infarcts compared to patients with obvious STEMI, however subtle STEMI patients are more likely to experience greater delays to reperfusion [2, 3]. Interestingly, subtle STEMI patients do not have better outcomes than those with obvious STEMI [2].  Marti and colleagues studied 504 patients who were taken to the cardiac cath lab for suspected coronary artery occlusion. Patients with subtle and obvious ST-elevation MI had similar rates of pre-interventional TIMI flow of 0/1 (86% of the patients in the subtle STE group and in 87% of the patients in the marked STE group).  Among patients with coronary artery occlusion, 18.3% did not have any lead with at least 1 full millimeter of ST-segment elevation. Subtle STEMI patients were more likely to have multi-vessel disease and experienced greater delays to reperfusion.  Comparing the subtle-STEMI patients to those with obvious STEMI, the authors found that the rate of reinfarction or death were similar between the two groups (10.0% vs 12.6%, P = .467) [2].

Therefore, recognizing the subtle findings of coronary artery occlusion and taking the next steps to rapidly evaluate for ACS may allow us to recognize these subtle-STEMI patients early and provide timely revascularization. Anterior MI carries the worst prognosis compared to other anatomic areas; it has the highest mortality and rates of complications [4,5]. Early anterior MI can have less than 1mm of ST-segment elevation and can mimic benign early repolarization. So today I will discuss the findings that differentiate BER and LAD occlusion by exploring 5 different ECG features.

Benign early repolarization

The ST segment represents the period between ventricular depolarization and repolarization. In a normal ECG the ST-segment is isoelectric, meaning neither elevated nor depressed relative to the TP-segment [6]. Benign early repolarization is the most common normal ECG variant. It has been reported in both men and women of all age groups and various ethnicities [6] and occurs in about 1% of the population [7] with higher occurrence in black males 20-40 years old [8].

ECG characteristics that are more likely to be seen in BER include:

  1. ST elevation at the J-point with upward concavity
  2. Notching of the J-point
  3. Diffuse ST elevation (typically highest in V3-4)
  4. Concordant, prominent T-waves with large amplitudes
  5. Normal R-wave progression
  6. Relative stability from one ECG to the next

Here is a classic example of benign early repolarization:


The ST-segment elevation is most pronounced in V2-4. There is upsloping ST elevation. The T-waves are asymmetric: they have a concave upslope and a steep downslope. There is good R-wave progression across the precordium with a very tall R-wave in V4. Also, notice the absence of certain features: there is no ST-segment depression and there are no anterior Q-waves.

Acute LAD occlusion will also manifest as anterior ST-segment elevation, often maximal in V2-3. So how does anterior MI differ from BER? To answer this question we are going to discuss 5 ECG features:

  1. ST-segment morphology
  2. Reciprocal changes
  3. Poor R-wave progression
  4. Anterior Q-waves
  5. Terminal QRS distortion

ST segment morphology

It is often taught that up-sloping ST segments are benign. However, you should not rely on ST-segment morphology alone to rule out ACS. While convex (“tombstone”) ST-segment elevation is highly specific for AMI [9], it is less common than either straight or upsloping (concave) elevation in acute anterior MI [2, 10]. Straight ST-segment elevation is the most common ST morphology in anterior MI [11]. However, in one retrospective review of patients with LAD occlusion on angiogram, 43% (16/37) had concave morphology [9].

Reciprocal changes

Reciprocal change is ST-segment depression in the leads opposite of the ST-elevation. Occasionally reciprocal ST-segment depression is the first (and rarely, the only) ECG findings in AMI. It is important to look specifically for ST-segment depression because it may be subtle. The absence of ST depression does not rule out AMI, but its presence does make the ST-elevation more specific for coronary artery occlusion [4, 12].  And, the presence of ST depression correlates with a larger infarct area at risk and higher mortality, independent of ST elevation [13].

Reciprocal ST depression can occur in either anterior or lateral MI. An anterior MI will manifest ST-segment depression in the inferior leads when there is a more proximal LAD occlusion (the first diagonal branch is occluded) [4, 14]. If you see ST-depression leads II, III, or aVF, you should carefully scrutinize the ECG for subtle anterior (V1-4) or high lateral (I, aVL) ST-segment elevation or hyperacute T-waves. The bottom line is that in the presence of reciprocal ST-segment depression in the inferior leads, you should be very cautious about diagnosing benign early repolarization.

Poor R-wave progression

Normally, the height of the R-wave increases gradually across the precordial leads to the point where the R-wave is bigger than the S-wave at V3 or V4 and eventually there is only a very small S-wave remaining in V6. One commonly accepted definition of poor R-wave progression is R-wave height ≤ 3 mm in V3. Causes of poor R-wave progression include left ventricular hypertrophy (LVH), inaccurate lead placement, old anterior infarct and acute anterior MI. Remember that BER should always have good R-wave progression.

Here is normal R-wave progression in BER:



Here is a patient who has poor R-wave progression secondary to old anterior infarct:


Notice there are QS-waves in V1-3 and only a very small R-wave in V4.


Pathologic Q-waves result from the absence of electrical myocardial activity secondary to ischemic cell death. The infarcted area of myocardium does not conduct electricity, so the deflection on the ECG paper is negative (downward). Q-waves are classically taught to develop in MI after several hours to days [10]. However, Q-waves can form early in acute MI, as early as less than 1 hour [4, 15].

Pathologic Q-waves in the anterior leads are defined as Q-waves in leads V2–V3 ≥ 20ms [16]. A general rule of thumb is that in acute MI the most common type of Q-wave is a QR-wave. QS-waves may develop later in anterior MI, so they may be suggestive of a subacute presentation, or they can be there from a previous MI. However, when anterior QS-wave are paired with very large, wide and towering T-wave (hyperacute T-waves), this may be a sign of acute LAD occlusion [17].

Here are QR-waves accompanied by ST-segment elevation:


Contrast that to these QS-waves paired with a hyperacute T-wave:

This image originally appeared at:

In summary, in the presence of anterior Q-waves, anterior ST-segment elevation cannot be considered benign early repolarization. The ST segment elevation may be due to:

  • Acute anterior MI
  • Subacute anterior MI
  • Old anterior infarct with persistent ST-segment elevation (possibly due to LV aneurysm formation)

This is an example of a patient with LAD occlusion who’s ECG demonstrates all 4 ECG criteria discussed here:

This ECG originally appeared at:

This ECG shows upsloping anterior ST-segment elevation. Although this may be confused for normal variant ST-elevation, there are four concerning features make this ECG diagnostic for LAD occlusion. There is a QS-wave in V1-V2 paired with hyperacute anterior T-waves. There is reciprocal ST-segment depression in lead III and poor R wave progression across the precordium.

Dr. Smith’s ECG formula

I would like to make special mention of a mathematical formula developed specifically to differentiate BER and acute LAD occlusion [18]. Smith and colleagues conducted a retrospective study comparing patients with subtle anterior STEMI to those with proven early repolarization. They found that several ECG measurements were independently predictive of STEMI versus BER:

  • Greater height of ST-segment elevation (measured at 60ms after the J point)
  • Longer QTc interval
  • Lower R-wave amplitude
  • Higher T-wave/R-wave amplitude ratio in leads V2-V4

Using logistic regression, they derived and validated an ECG-based formula using the first three measurements as follows:

[1.196 x ST-segment elevation 60 ms after the J point in lead V3 in mm]+[0.059 x QTc in ms]-[0.326 x R-wave amplitude in lead V4 in mm]

A value of >23.4 was found to predict STEMI, and </= 23.4 predicted early repolarization with an overall sensitivity and specificity of 86%, 91% respectively [18]. A calculator for this formula and further explanation can be found at

Before applying the formula there are some things you must consider:

The equation only applies when trying to distinguish between subtle LAD occlusion and early repolarization. The rule does not apply if there is left ventricular hypertrophy (LVH). Most importantly, if there are other findings on the ECG that support the diagnosis of LAD occlusion such as inferior ST depression, ST-segment convexity, terminal QRS distortion, or Q-waves, then the equation does NOT apply because these kinds of cases were excluded from the study as representing an obvious STEMI.

Terminal QRS distortion

Terminal QRS distortion is defined as emergence of the J point ≥50% of the R wave in leads with QR-wave, or disappearance of the S wave in leads with an RS-wave. [19] In acute MI, terminal QRS distortion predicts greater size of infarct and higher mortality [20].

Here are two examples of terminal QRS distortion:


This is the more obvious, with emergence of the J point ≥50% of the R wave in leads with QR-wave

This ECG first appeared at: LITFL

This is more subtle terminal QRS distortion. Notice how the S-wave does not extend below the isoelectric line.


As always, it is important to correlate the ECG findings with the clinical picture. You should be incredibly cautious diagnosing BER in a patient over 55 years old, or anyone with concerning symptoms or history. If the ECG is subtle and you are concerned about ACS, get serial ECGs (every 15 minutes) and use adjunctive information such as comparison to an old ECG or obtain echocardiogram. Remember that ACS is a dynamic process and can present subtly. The ECG is a cheap, noninvasive and fast tool, which can provide valuable diagnostic and prognostic information. Missing subtle presentation of ACS can have dire consequences for our patients who may be inappropriately discharged or experience significant delays to reperfusion. As emergency physicians, it is our job to own the ECG and we should strive for mastery to recognize even the subtlest cases.


  • Anterior STEMI can be subtle and present with less than 1mm ST-segment elevation anteriorly and can mimic benign early repolarization.
  • Do not rely on ST-segment morphology alone to rule out AMI because about 40% of patients with anterior MI have upsloping (concave) ST-segment elevation.
  • Be very cautious about diagnosing BER when there is poor R-wave progression, anterior Q-waves, inferior ST depression, or terminal QRS-distortion.
  • Be cautious diagnosing BER in patients older than 55 years old or anyone with concerning symptoms.
  • When concerned for subtle STEMI, use adjunctive information such as serial ECGs, comparison to prior ECGs, and/or echocardiogram.


References / Further Reading

  1. Wang TY et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non-ST-elevation acute coronary syndromes undergoing diagnostic angiography. Am Heart J. Apr 2009;157(4):716-23.
  2. Martí D et al. Incidence, angiographic features and outcomes of patients presenting with subtle ST-elevation myocardial infarction. Am Heart J. Dec 2014;168(6):884-90.
  3. Sharkey SW et al. Impact of the electrocardiogram on the delivery of thrombolytic therapy for acute myocardial infarction. Am J Cardiol. Mar 1994;15;73(8):550-3.
  4. Smith SW. The ECG in Acute MI: An evidence-based manual of reperfusion therapy. Lippincott Williams & Wilkins 2002.
  5. Lee KL et al. Predictors of 30-day mortality in the era of reperfusion for acute myocardial infarction. Results from an international trial of 41,021 patients. GUSTO-I Investigators. Circulation. 1995 Mar;91(6):1659-68.
  6. Somers, MP et al. The prominent T wave: electrocardiographic differential diagnosis. Am J Emerg Med. 2002 May;20(3):243-51.
  7. Mehta MC, Jain AC: Early repolarization on scalar electrocardiogram. Am J Med Sci 1995;309:305-311
  8. Thomas J, Harris E, Lassiter G: Observations on the T wave and S-T segment changes in the precordial electrocardiogram of 320 young Negro adults. Am J Cardiol 1960;5:368-374
  9. Smith SW. Upwardly concave ST segment morphology is common in acute left anterior descending coronary occlusion. J Emerg Med. Jul 2006;31(1):69-77
  10. Nable, JV and Brady, W. The evolution of electrocardiographic changes in ST-segment elevation myocardial infarction. Am J Emerg Med. 2009 Jul;27(6):734-46.
  11. Kosuge et al. Value of ST-segment elevation pattern in predicting infarct size and left ventricular function at discharge in patients with reperfused acute anterior myocardial infarction. Am Heart J. 1999 Mar;137(3):522-7.
  12. Brady WJ et al. Reciprocal ST segment depression: impact on the electrocardiographic diagnosis of ST segment elevation acute myocardial infarction. Am J Emerg Med. 2002 Jan;20(1):35-8.
  13. Willems JL et al. Circulation. Significance of initial ST segment elevation and depression for the management of thrombolytic therapy in acute myocardial infarction. European Cooperative Study Group for Recombinant Tissue-Type Plasminogen Activator. 1990 Oct;82(4):1147-58.
  14. Engelen DJ et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol. 1999 Aug;34(2):389-95.
  15. Raitt, MH, et al. Appearance of abnormal Q waves early in the course of acute myocardial infarction: implications for efficacy of thrombolytic therapy. J Am Coll Cardiol. 1995 Apr;25(5):1084-8.
  16. Pathologic Q waves. ECGPedia. Web. 12 Dec 2015.
  17. Left ventricular Aneurysm Morphology Distorted by Right Bundle Branch Block, Mimicking Acute STEMI with RBBB.
  18. Smith S et al. Electrocardiographic differentiation of early repolarization from subtle anterior ST-segment elevation myocardial infarction. Ann Emerg Med. Jul 2012;60(1):45-56
  19. Birnbaum Y, et al. Distortion of the terminal portion of the QRS on the admission electrocardiogram in acute myocardial infarction and correlation with infarct size and long-term prognosis (Thrombolysis in Myocardial Infarction 4 Trial).Am J Cardiol. 1996 Aug 15;78(4):396-403.
  20. Mulay DV, Mukhedkar SM. Prognostic significance of the distortion of terminal portion of QRS complex on admission electrocardiogram in ST segment elevation myocardial infarction. Indian Heart J. 2013 Dec;65(6):671-7.
  21. Flickr photo. Web. 12. Dec 2015.
  22. “Anterior Myocardial Infarction”. Life in the Fast Lane Medical Blog. Web. 12 Dec 2015.
  23. ”Conclusin to snapshot case: 44 year old male-chest tightness”. EMS 12 Lead Blog, 2014. Web. 12 Dec 2015.

Subtle ECG findings in ACS: Part II Hyperacute T-Waves

Author: Jamie Santistevan MD (@jamie_rae_EMDoc, EM Resident Physician, University of Wisconsin) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) & Justin Bright, MD (EM Attending Physician, Henry Ford Hospital, @JBright2021)


What if you could identify a patient with complete coronary vessel occlusion almost immediately after it occurs, before the ST segments begin to elevate? What if you could pick up the very subtle, early MI? We know that early recognition and intervention improves outcomes in patients with coronary artery occlusion. Sometimes patients presenting with ACS are obvious. Sometimes it seems that the patient has read the textbook. However, more often than not, patients are not obvious, especially in the early stages of ACS. That is why we are concerning ourselves with subtlety.

Welcome to Part II of a three-part series on subtle ECG findings in ACS. Last time we reviewed the ECG findings associated with left main coronary artery disease, where we discussed the meaning of ST elevation in lead aVR. Now we are going to turn our attention to the T-waves.

The T-wave represents the period of ventricular repolarization on the ECG. The normal T-wave appearance varies based on lead placement, age, and sex. In general, T-waves are tallest in leads II and V4 and will decrease in size with age. A normal T-wave usually has amplitude of less than 5mm in the precordial leads and less than 10mm in the limb leads [1]. The normal shape of a T-wave is asymmetric, with a slow upstroke and a rapid down stroke. Normal T-waves are always upright except in leads aVR and V1 and have a normal QT interval (QTc of 350-440ms in men or 350-460ms in women). Additionally, the R-wave amplitude should progress normally across the precordial leads.

In this post, we are going to review 4 causes of abnormal T-waves:

  1. Hyperacute T-waves in AMI
  2. The de Winter T-wave pattern
  3. Pseudonormalization of T-waves
  4. Hyperkalemia

Hyperacute T-waves

Immediately after coronary artery occlusion, the ECG undergoes predictable temporal changes. Classically, coronary vessel occlusion leads to elevation of the ST-segments (producing STEMI). However, the earliest findings on an ECG are subtle changes in the T-wave shape and size. When a coronary artery is occluded, within the first 30 minutes, the T-wave amplitude increases [2]. The next changes are ST-segment elevation and loss of the R-wave amplitude.  If the vessel remains occluded, Q-waves develop. Without intervention, the ECG will then begin to exhibit T-wave inversions and eventually, the ST-segments will normalize [3]. Persistent ST-segment elevation suggests aneurysm formation.

This image originally appeared at


Early in the course of AMI, biochemical markers may not be elevated, although this may be changing in the era of highly sensitive troponin assays. Regardless, the development of T-wave changes is the first sign that we can see on the ECG and the ECG is fast, cheap, noninvasive, and readily available in the ED. In the early stages of MI, prior to the development of necrosis, the myocardium is suffering from ischemia. Timely revascularization may actually prevent complete infarction and death of the affected portion of the myocardium. Therefore, recognizing ACS early is beneficial because patients have improved outcome the timelier revascularization occurs [3], and delay to reperfusion causes larger infarction size and worse functional outcomes [4].

It is well known that new ST-segment elevation represents complete vessel occlusion and transmural infarct. However, the STEMI criteria have limited sensitivity in diagnosing coronary artery occlusion [5, 6, 7]. This means that some patients ultimately diagnosed with NSTEMI will also have complete coronary artery occlusion.

Below are the AHA criteria that define STEMI [7]:


Of course, it is important to recognize an obvious STEMI, but patients may present initially with only subtle ECG changes and minimal ST-segment elevation they may not meet the official criteria. These “subtle STEMI” patients have higher rates of inappropriate ED discharge and significant delays to reperfusion [8, 9, 10]. It is true that more ST elevation indicates a larger area of infarcted myocardium, however patients with subtle ST elevation MI experience similar functional outcomes and mortality rates as those with obvious STEMI [10]. Furthermore, approximately 25% of patients who do not meet the STEMI criteria, and are diagnosed with NSTEMI, have a completely occluded artery on angiography [11]. Some experts would argue that patients with subtle findings of coronary vessel occlusion should be treated as expeditiously as patients with obvious STEMI [10].

 The T-wave is often the first deflection on the ECG to change in acute vessel occlusion. Initial changes to the T-wave are straightening of the ST-segment and enlargement of the T-wave height and width.  The T-wave becomes disproportionately large when compared to the QRS. The prominent T-waves seen early in coronary vessel occlusion are called hyperacute T-waves. They were first described in 1947 as an early marker of coronary artery occlusion [2].

Hyperacute T-waves are often bulky, and wide at the base and are localized to an anatomic area of infarct. The widening of the T-wave may also lengthen the QT interval. It must be emphasized that hyperacute T-waves are not necessarily always tall, they may only be relatively large when compared to the R-wave. This means that even a small T-wave can still be hyperacute if paired with a low-voltage QRS. It is important to note that there is no acceptable universal definition of hyperacute T-waves, but there can be other clues on the ECG. During the development of hyperacute T-waves, there can be associated ST-segment depression in the reciprocal leads.

Here is an example of an ECG with hyperacute T-waves localized to the anterior region:

This ECG originally appeared at

Do not be distracted by the first-degree AV block or by the PVCs. This ECG shows very prominent, broad-based T-waves in the anterior leads (V2-6). Notice also the loss of R-wave height throughout the precordium and the how the T-waves are massive in comparison to the QRS complexes. This ECG is concerning for LAD occlusion.

 The patient underwent repeat ECG 40 minutes later, which showed obvious anterior ST elevation:

This ECG originally appeared at

Now there is obvious ST elevation in the anterior leads (V2 and V3), as well as ST elevation in the lateral leads (I, aVL, V5 and V6) with reciprocal depression in lead III. Also, the Q-waves are deepening in the leads V2 and V3.

Here is another example of hyperacute T-waves, this time in the inferior leads. This is the ECG of a 75 year-old woman presenting with chest pain:


Notice the large T waves in the inferior leads. The total height of the T-waves is not all that impressive, but when compared to the QRS complexes, especially in aVF, the T-wave is massive. The ST-segments are straighter than normal and there is subtle ST elevation in lead III, aVF, V5-V6. Notice the subtle reciprocal ST depression and T-wave inversion in aVL. The machine read this ECG as Early Repolarization. Her Troponin I came back slightly elevated (0.07 ng/mL). She was found to have complete occlusion of the RCA on angiogram and was diagnosed with “NSTEMI”.

De Winter T-waves

An interesting variant of hyperacute T-waves are those paired with J-point depression. This causes a T-wave takeoff point that is below the isoelectric line. This “depressed T-wave takeoff” pattern was first described in 2009 by Verouden and colleagues and was found to represent complete LAD occlusion (a STEMI-equivalent) [15]. This pattern of up sloping ST-segment depression paired with a tall, prominent T-wave is present in about 2% of patients with LAD occlusion [15]. It was initially postulated that these findings are not dynamic, but rather that they remain static throughout coronary vessel occlusion until the time of reperfusion [15, 16]. However, some experts have documented de Winter T-waves developing during anterior STEMI and would argue that these findings may represent subtotal occlusion of the LAD. Regardless, these patients require immediate reperfusion.

This ECG initially appeared at:

Notice the up sloping ST depression seen in leads V2-V6 followed by very tall and symmetric T-waves. Notice also the subtle reciprocal depression in the inferior leads (II, III, and aVF).

For an interesting case of the de Winter T-wave pattern occurring in a patient who initially presented with an obvious anterior STEMI, read this case on Dr. Smith’s ECG blog:


Another interesting phenomenon of the T-waves is the pseudonormalization in AMI. This occurs when a patient with baseline T-wave inversions presents with acute coronary occlusion. Hyperacute T-waves in these patients manifest as upright T-waves, which may be confused for a normal ECG. This finding highlights the fact that it is not solely the height, but rather the increase in positive amplitude, that signifies a hyperacute T-wave [2]. The other scenario for pseudonormalization is a patient who presents with re-occlusion of a recently reperfused artery, also known as Wellens’ Syndrome.

Here is the classic appearance of Wellens’ syndrome, type A (left) and type B (right):


These images originally appeared at:

It is important to note that this pattern appears when the patient is asymptomatic because this represents a reperfusion pattern on ECG. Type A, the biphasic T-waves, are seen immediately upon reperfusion. As the artery remains open, the T-waves evolve to be more deeply inverted, a Type B pattern. When the patient becomes symptomatic it is because the vessel re-occludes. When that happens the T-waves become upright (pseudonormalization) and if it remains occluded, ST-segment elevation will appear. These lesions are unstable because the vessel can re-occlude at any time and the patient requires revascularization.


Perhaps the most well known cause of prominent T-waves is the peaked T-waves seen with hyperkalemia, and they can be confused with the hyperacute T-waves of ACS. There is no exact correlation between serum potassium and onset of ECG changes but about 80% of patients begin to exhibit ECG changes at 6.8-7.0mEq/L. The typical progression of ECG changes in hyperkalemia is first the development of peaked T-waves, followed by decreased P-wave amplitude, widening of the QRS complex and finally development of a sine wave. But, as we know, hyperkalemia can cause a myriad of ECG changes including AV and bundle branch blocks, bradycardias, and even a STEMI mimic. Here are the typical changes with hyperkalemia.

This image originally appeared at

Although the T-waves of early hyperkalemia are very tall and prominent, the key differentiator from hyperacute T-waves is the shape of the T-wave.  Hyperacute T-waves are fat and wide with a more blunted peak. The T-waves of hyperkalemia are very pointy, peaked or “tented” with a narrow base, they have sharp apex and tend to be extraordinarily symmetric [1].

Here is the ECG of a patient with a history of type I diabetes who presented with nausea and vomiting. EMS reported that the patient was in sinus tachycardia with a rate of 300.

ECG Courtesy of Dr. Morgan Wilbanks, University of Wisconsin.

Notice the very tall, pointy T waves, which have a narrow base and are extremely symmetric. This patient was found to be in severe DKA, with a pH of 7.17 and a potassium of 7.1 mmol/L. The tall T-waves were likely being mistaken for QRS complexes and cardiac monitor misread the rate to be 300, when in fact it is about 150.


The earliest changes on an ECG after acute vessel occlusion are hyperacute T-waves and patients with coronary vessel occlusion can present with only subtle ECG changes. The ECG is an important tool, but should not always be used in isolation (unless clearly diagnostic). The clinical picture and adjunctive information should always be considered. If suspicious for vessel occlusion by the appearance of the ECG, it is important to look carefully for reciprocal changes and get serial ECGs every 15 minutes (not in an hour or two) and look for evolving changes because ACS is a dynamic process. Other adjuncts that may help diagnose ACS in patients with subtle ECG changes include continuous ST-segment monitoring, echocardiogram to evaluate for wall motion abnormality, and cardiac biomarkers.


  • Hyperacute T-waves are often the first manifestation of complete vessel occlusion; they are wide, bulky and prominent.
  • Hyperacute T-waves are not necessarily tall, and small T-waves can still be hyperacute when paired with a low-amplitude QRS complex.
  • De Winter T-waves represent LAD occlusion (a STEMI equivalent) requiring immediate revascularization.
  • Previously inverted T-waves can appear normal and upright in the setting of acute vessel occlusion. This is known as pseudonormalization.
  • The tall T-waves associated with hyperkalemia are sharp, pointy, symmetric, and have a narrow base.
  • When in doubt, get serial ECGs (every 15 minutes) and use adjunctive information.

Well, that concludes this post on hyperacute T-waves and other T-wave abnormalities. Please stay tuned for the third installment on subtle ECG findings: the subtle anterior STEMI mimicking benign early repolarization!


References / Further Reading

  1. Somers, MP et al. The prominent T wave: electrocardiographic differential diagnosis. Am J Emerg Med. 2002 May;20(3):243-51.
  2. Dressler, W and Roesler, H. High T waves in the earliest stage of myocardial infarction. Am Heart J. 1947 Nov;34(5):627-45.
  3. Nable, JV and Brady, W. The evolution of electrocardiographic changes in ST-segment elevation myocardial infarction. Am J Emerg Med. 2009 Jul;27(6):734-46.
  4. Keeley, EC et al. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003 Jan 4;361(9351):13-20.
  5. Zarling, EJ et al. Failure to diagnose acute myocardial infarction: The clinicopathologic experience at a large community hospital. JAMA. Sep 1983;250(9):1177-81.
  6. Scott, PJ et al. Optimization of the precordial leads of the 12-lead electrocardiogram may improve detection of ST-segment elevation myocardial infarction. J Electrocardiol. Jul-Aug 2011;44(4):425-31.
  7. Thygesen, K et al; Third universal definition of myocardial infarction.  Circulation. Oct 2012;126(16):2020-2035.
  8. Pope, JH et al. Missed diagnoses of acute cardiac ischemia in the emergency department. N Engl J Med. Apr 2000;20;342(16):1163-70.
  9. Sharkey, SW et al. Impact of the electrocardiogram on the delivery of thrombolytic therapy for acute myocardial infarction. Am J Cardiol. Mar 1994;15;73(8):550-3.
  10. Martí, D et al. Incidence, angiographic features and outcomes of patients presenting with subtle ST-elevation myocardial infarction. Am Heart J. Dec 2014;168(6):884-90.
  11. Wang, TY et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non-ST-elevation acute coronary syndromes undergoing diagnostic angiography. Am Heart J. Apr 2009;157(4):716-23.
  12. “ECG changes in acute MI”. Doctors Gates Blog. 22 Oct 2015. Web.
  13. “Anterior Myocardial Infarction” Life in the Fast Lane Medical Blog. 22 Nov. 2015. Web.
  14. “Is the LAD really completely occluded when there are de Winter’s waves? Dr. Smith’s ECG Blog. 22 Nov. 2015. Web.
  15. Verouden, NJ et al. Persistent precordial “hyperacute” T-waves signify proximal left anterior descending artery occlusion. Heart. 2009 Oct;95(20):1701-6.
  16. de Winter, RW et al. Precordial junctional ST-segment depression with tall symmetric T-waves signifying proximal LAD occlusion, case reports of STEMI equivalence. J Electrocardiol. 2015 Oct 13.
  17. “Hyperkalemia” Life in the Fast Lane Medical Blog. 02 Dec 2015. Web.
  18. “De Winter’s T-waves”. Life in the Fast Lane Medical Blog. 02 Dec 2015. Web.
  19. “Wellens’ Syndrome”. Life in the Fast Lane Medical Blog. 02. Dec 2015. Web.

Subtle ECG Findings in ACS: Part I Left Main Coronary Artery Disease

Authors: Jamie Santistevan, MD (EM Resident Physician, University of Wisconsin, @Jamie_Rae_EMDoc) // Edited by: Alex Koyfman, MD (EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital, @EMHighAK) & Justin Bright, MD (EM Attending, Henry Ford Hospital, @JBright2021)


A patient with a history of hypertension and hyperlipidemia presents to the emergency department with crushing, substernal chest pain. He is diaphoretic and has this ECG:


It is quite obvious that this patient is having an anterior STEMI. But acute coronary syndrome (ACS) is not always so obvious, in fact sometimes it is very subtle.

One hallmark of our profession is being able to delicately discriminate the sick from the not sick. It is only through careful refinement of our clinical skills that we can develop the ability to pick up a very subtle diagnosis. Unfortunately, it is the subtle cases that are at risk of being missed; and it is through the subtle presentations that we can be made a fool by disease processes.

When it comes to ACS, some ECGs are obvious. This article is not about those ECGs. This article will be the first in a series of blog posts related to subtle ECG findings in ACS. In this post we will look at ECG findings associated with left main coronary artery disease and explore the significance of ST-segment elevation in the “forgotten lead”. In the next post, we will review the appearance and significance of hyperacute T-waves, which may be the first, subtle sign of coronary vessel occlusion. Finally, we will discuss a mimicker: the subtle anterior STEMI, which may be mistaken for benign early repolarization.

Left main coronary artery disease

Early identification of left main coronary artery (LMCA) disease is critical because acute occlusion can cause rapid hemodynamic and electrical deterioration [1, 2]. LMCA insufficiency due to critical stenosis of the left main artery is important to recognize because these patients can progress to complete occlusion and are likely to require surgical intervention (such as CABG)[3]. Below, we will discuss the significance of ST elevation in lead aVR and review difference between LMCA occlusion and insufficiency.

Classic findings on ECG that are taught to represent LMCA “occlusion” are:

  • ST depression in leads I, II, aVL and V4-6 [4]
  • ST elevation in aVR ≥ 1mm [2]
  • ST elevation in aVR ≥ V1 [5]

Lead aVR has often been called the “forgotten lead”, but it is worth paying attention to because ST-segment elevation in aVR portents a worse prognosis in ACS [1, 2, 3, 6]. ST elevation in aVR ≥ 1mm is the strongest independent predictor of either severe LMCA or triple-vessel disease requiring CABG in patients with NSTEMI [3, 7]. Elevation in aVR of ≥ 0.5 mm is an independent predictor of mortality in patients with STEMI [6].

ST-elevation in aVR occurs by the following mechanisms:

  1. Critical narrowing of the LMCA causing subendocardial ischemia due to insufficient blood flow.
  2. Transmural infarction of the basal septum due to a very proximal LAD occlusion or complete LMCA occlusion.
  3. Severe multi-vessel coronary artery disease.
  4. Diffuse subendocardial ischemia from oxygen supply/demand mismatch.

Understanding these mechanisms first requires visualization of the anatomic location of aVR.  Lead aVR is an augmented limb lead, with its vector pointing toward the right shoulder. Therefore, it is recording activity from the right upper portion of the heart. This includes the basal (upper) portion of the interventricular septum, which is perfused by the first septal perforator, a branch of the proximal LAD.

This image originally appeared at

In mechanism 1, critical narrowing of the LMCA produces subendocardial ischemia due to insufficient blood flow through a tight left main artery. This causes widespread ST-segment depression in nearly all leads, but it is often most pronounced in the left-sided leads (I, II, aVL and V4-6). Because aVR is anatomically opposite from the left-sided leads, ST depression due to ischemia is met with reciprocal ST elevation in aVR (also often in V1, which is a right-sided lead).  This produces the classic findings on ECG described above. Remember, in this mechanism, there is still some flow through the tight LMCA, but it is not enough to match the demand. This is known as LMCA insufficiency.

Critical stenosis of the LMCA is quite dangerous. The entire artery can become occluded if the thrombus propagates. In addition, a large portion of the myocardium is ischemic due to lack of sufficient blood flow. Therefore, these patients require prompt recognition, and most experts agree that they should go to the cath lab immediately for revascularization.

This ECG demonstrates critical LMCA stenosis:

This ECG originally appeared at

Notice the diffuse ST depression in multiple leads (I, II, aVF, aVL, V2-V6) with reciprocal elevation in aVR. This pattern represents diffuse subendocardial ischemia due to flow limitation through the LMCA. This patient presented in cardiogenic shock and was found to have critical stenosis of the LMCA on angiography.

In Mechanism 2, ST elevation in AVR is produced by transmural infarct to the basal septum. Remember, the LMCA gives rise to the LAD and the left circumflex. The first septal perforator arising from the proximal LAD supplies the basal septum. Infarct of the basal septum occurs secondary to either complete occlusion of the proximal LAD (before the takeoff of the first septal perforator) or complete occlusion of the LMCA. When either occurs, the patient will have STEMI in all areas of the heart supplied by these vessels. This can include the anterior wall (supplied by the LAD), the lateral wall (supplied by the left circumflex), and occasionally the posterior wall (if the left circumflex gives rise to the posterior descending artery).

Therefore, complete left main occlusion causes at least two syndromes to occur simultaneously: a proximal anterior STEMI producing ST elevation in aVR and V1-4 in addition to a lateral STEMI producing ST elevation in I, aVL and V5-6. If the posterior wall is involved, then posterior STEMI will produce ST depression in the anterior leads, which may be superimposed or even hidden within the ST elevation from the anterior STEMI.  The bottom line is that a complete, very proximal LAD occlusion or a complete LMCA occlusion will produce STEMI in the locations supplied by those arteries.

This case demonstrates a very proximal LAD occlusion:

This ECG originally appeared at

Notice that there is RBBB, a septal STEMI (ST elevation in V1-V3) plus ST elevation in aVR. This suggests an LAD occlusion proximal to the first septal perforator. This patient presented post-VF arrest and was found to have 100% occlusion of the proximal LAD on angiography.

An ECG demonstrating acute, complete occlusion of the LMCA is difficult to find, because patients with complete LMCA occlusion often have rapid electrical-mechanical dissociation and death [1,2]. This probably explains why only a very small percentage (0.19-1.3%) of patients with STEMI are found to have complete LMCA occlusion in the cath lab [1,8]. The need for cath lab activation in patients with complete LMCA occlusion is typically apparent based on their clinical picture (they often are in cardiogenic shock), as opposed to relying on their ECG findings alone [2].

Here is an excellent case of STEMI in more than one territory due to LMCA occlusion of a patient who presented in cardiogenic shock after VF arrest:

In mechanism 3, ST elevation in aVR is caused by multi-vessel coronary artery disease. In this mechanism, diffuse subendocardial ischemia produces widespread ST depression and therefore reciprocal ST elevation in aVR. This is similar to patients with critical stenosis of the LMCA. Here is an ECG of a patient who was found to have triple-vessel coronary artery disease.

This ECG shows ST elevation in aVR and ST depression in multiple leads (V2-6, I, aVL). This patient was found to have high-grade stenosis of the LMCA, LAD and left circumflex requiring CABG.

Severe multi-vessel disease and LMCA disease appear similar on ECG and, coincidentally, both entities are likely to require CABG. Because they are often treated the same, the fact that they cannot be differentiated on ECG is not so important. Many authors agree that Clopidogrel should be avoided in patients found to have NSTEMI and STE in aVR ≥ 1mm due to likelihood of requiring CABG [2, 3, 7, 9].

In Mechanism 4, diffuse subendocardial ischemia due to oxygen supply/demand mismatch produces widespread ST depression and reciprocal ST elevation in aVR. This is similar to the other mechanisms whereby diffuse subendocardial ischemia produces ST depression most pronounced in the lateral leads with reciprocal elevation in AVR.

Differentiating the ECG of mechanism 4 from the other three requires analysis of axis of the ST segment elevation. For a detailed explanation of the ST-segment elevation axis please visit Dr. Smith’s ECG blog and read this post at


  • ST-segment elevation in lead aVR portends a worse prognosis in ACS and often predicts the need for CABG.
  • ST-segment elevation in aVR can be caused by any of the following 4 mechanisms:
    • LMCA insufficiency
    • Very proximal LAD occlusion or complete LMCA occlusion
    • Multi-vessel coronary artery disease
    • Diffuse subendocardial ischemia
  • Patients with complete occlusion of the LMCA often present in cardiogenic shock and require immediate revascularization.
  • Patients with NSTEMI and ST elevation ≥ 1mm in aVR are likely to have multi-vessel or LMCA disease and are likely to require CABG, therefore withholding Clopidogrel may be prudent.

Well, that concludes this post on LMCA disease. Please stay tuned for the next installment on subtle ECG findings: Hyperacute T-waves!

References / Further Reading

  1. Baek JY et al. Clinical outcomes and predictors of unprotected left main stem culprit lesions in patients with acute ST segment elevation myocardial infarction. Catheter Cardiovasc Interv. 2014 Jun 1;83(7):E243-50.
  2. Smith, SW. Updates on the Electrocardiogram in Acute Coronary Syndromes Curr Emerg Hosp Med Rep (2013) 1:43–52.
  3. Barrabes, JA et al. Prognostic value of lead aVR in patients with a first non-ST-segment elevation acute myocardial infarction. Circulation. 2003 Aug 19;108(7):814-9.
  4. Gorgels, AP et al. Value of the electrocardiogram in diagnosing the number of severely narrowed coronary arteries in rest angina pectoris. Am J Cardiol. 1993 Nov 1;72(14):999-1003.
  5. Yamaji, H et al. Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography. ST segment elevation in lead aVR with less ST segment elevation in lead V(1). J Am Coll Cardiol. 2001 Nov 1;38(5):1348-54.
  6. Aygul N et al. Value of lead aVR in predicting acute occlusion of proximal left anterior descending coronary artery and in-hospital outcome in ST-elevation myocardial infarction: an electrocardiographic predictor of poor prognosis. J Electrocardiol. 2008;41(4):335–41.
  7. Kosuge, M et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol. 2011 Feb 15;107(4):495-500.
  8. Zoghbi GJ et al. ST elevation myocardial infarction due to left main culprit lesions: percutaneous coronary intervention outcomes free. J Am Coll Cardiol. 2010;55(10s1): E1712.
  9. “Anterior Myocardial Infarction” Life in the Fast Lane Medical Blog. 19 Oct. 2015. Web.
  10. “MI Localisation” Life in the Fast Lane Medical Blog. 19 Oct. 2015. Web.
  11. “Five primary patterns of ischemic ST depression, without ST elevation. Some STEMI equivalents” Dr. Smith’s ECG Blog. 19. Oct. 2015. Web.
  12. “Head on motor vehicle collision. ST depression. Myocardial contusion?” Dr. Smith’s ECG Blog. 19 Oct. 2015. Web.
  13. “The difference between left main occlusion and left main insufficiency” Dr. Smith’s ECG Blog. Web. 19 Oct. 2015. Web.