Acute Management of Supraventricular Tachycardias

Acute management of SVT

The term “supraventricular tachycardia (SVT)” expresses all kinds of rhythms that meet two criteria: Firstly, the atrial rate must be faster than 100 beats per minute at rest. Secondly, the mechanism must involve tissue from the His bundle or above. Mechanism-wise, atrial fibrillation resembles SVTs. However, supraventricular tachycardia traditionally represents tachycardias apart from ventricular tachycardias (VTs) and atrial fibrillation (1,2).

Supraventricular tachycardias are frequent in the ED!

The SVT prevalence is 2.25 per 1000 persons. Women and adults older than 65 years have a higher risk of developing SVT! SVT-related symptoms include palpitations, fatigue, lightheadedness, chest discomfort, dyspnea, and altered consciousness.

How to manage supraventricular tachycardia?

In clinical practice, SVTs are likely to present as narrow regular complex tachycardias. Concomitant abduction abnormalities may cause SVTs to manifest as wide complex tachycardias or irregular rhythms. However, 80% of wide complex tachycardias are VTs. Most importantly, SVT drugs may be harmful to patients with VTs. Therefore, wide complex tachycardias should be treated as VT until proven otherwise (1,2).

The chart below summarizes acute management of regular narrow complex tachycardias:

Acute Management of Regular Narrow Tachycardias

References and Further Reading

  1. Brugada, J., Katritsis, D. G., Arbelo, E., Arribas, F., Bax, J. J., Blomström-Lundqvist, C., … & Gomez-Doblas, J. J. (2019). 2019 ESC Guidelines for the management of patients with supraventricular tachycardia: the Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). European Heart Journal, 00, 1-66.
  2. Page, R. L., Joglar, J. A., Caldwell, M. A., Calkins, H., Conti, J. B., Deal, B. J., … & Indik, J. H. (2016). 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology67(13), e27-e115.

Deadly ECG Patterns – 5 Can’t Miss ECG Findings

5 Can’t Miss ECG findings

An average ER physician performs around 100 tasks in an hour and gets interrupted at least every 6 minutes. One of the common interruptions in the ED is a request to “sign off” on an ECG of a patient who has been triaged but not seen by a doctor yet. Therefore, knowing deadly ECG patterns is an essential skill for emergency physicians, residents, as well as medical students who rotate in the emergency department.

Below are five ECG patterns that should raise concerns for red flag conditions.

ECG #1

A 37-years-old female patient presented to the ED with complains of dizziness and generalized fatigue. She was started on ACE inhibitors few months ago and missed her clinic appointments. Her bedside VBG revealed a K+ of 8.1

ECG source - Dr. Smith's ECG blog

The ECG shows severe bradycardia, wide QRS complexes and symmetrically peaked T waves in V2-V5.

Key Take Home Points

Hyperkalemia can present with multiple abnormalities on an ECG, including

  • Tall, peaked T waves with a narrow base (best seen in precordial leads)
  • Progressive flattening and eventually disappearance of P waves
  • Wide QRS complexes
  • Bradyarrhythmias (sinus bradycardia, slow AF, second and third-degree AV blocks)
  • Sine wave appearance (pre-terminal rhythm)
  • Endgame: Ventricular fibrillation

Always consider the diagnosis of hyperkalemia in a patient with a history of dialysis, renal failure, or treatment with drugs like ACE inhibitors, ARBs, spironolactone especially if the ECG shows bradycardia or complete heart block.

ECG #2

A 56-years-old patient presented to the ED with lightheadedness and dizziness. Initial vitals showed hypotension and tachycardia.

ECG source - Dr. Smith's ECG blog
ECG source - Dr. Smith's ECG blog

The above ECG shows low voltage, lectrical alternans: the beat-by-beat R-wave amplitude changes best appreciated in the precordial leads. A bedside ECHO completed after the initial ECG showed a large pericardial effusion.

Key Take Home Points

Massive pericardial effusion can produce a triad of:

  • Low QRS voltage
  • Tachycardia
  • Electrical alternans (consecutive, normally-conducted QRS complexes alternate in height)

Consider the possibility of pericardial effusion and a potential impending cardiac tamponade in patients with electrical alternans on ECG.

ECG #3

A 65-years-old patient was brought to the ED by family members in a disoriented state. Further history revealed that the patient was taking digoxin as one of his regular medications. His serum digoxin level was 2.7 ng/ml.

ECG Source -
ECG Source -

The above rhythm strip shows atrial tachycardia with 2:1 AV block.

Key Take Home Points

Always have a high suspicion of digoxin toxicity in a patient taking digoxin presenting with the disoriented state.

Digoxin toxicity can cause a wide variety of arrhythmias. It is classically associated with supraventricular tachycardias but a slow ventricular response (e.g.: atrial tachycardia with high-grade AV block).

The other common rhythms include:

  • Regularized atrial fibrillation (AF with complete heart block + accelerated junctional escape rhythm which produces a paradoxically regular rhythm)
  • Bidirectional VT (polymorphic VT with QRS complexes alternating between LBBB and RBBB morphology)

Digoxin toxicity should be separated from the normal digoxin effect that can occur in patients taking the expected dose of digoxin. The digoxin effect (image below) includes sagging ST-segment depression, abnormal T waves (flat, inverted or biphasic) and a short QT.

ECG source - Dr. Smith's ECG blog

ECG #4

A 45-years-old patient presented to the ED with a history of severe central chest pain lasting about 10 – 15 minutes. Cardiac enzymes were negative. However, with the above ECG findings, the patient was sent to the Cath lab and subsequent coronary angiography revealed proximal LAD artery occlusion.

By Jer5150 - Own work, CC BY-SA 3.0,

The above ECG shows deep T wave inversions in precordial leads. This is known as the Wellen’s sign.

Key Take Home Points

Wellens syndrome is a pattern of deeply inverted or biphasic T waves in V2-V3 which is highly specific for critical stenosis of left anterior descending (LAD) artery.

There are two patterns of T wave abnormality in Wellens syndrome

  • Type A: Biphasic T waves (initially positive and terminally negative)
  • Type B: Deep and symmetrically inverted (Most common type)

Note that patients can be completely pain-free with normal cardiac enzyme levels. Patients are, however, at extremely high risk of anterior wall MI due to the critical LAD stenosis and need appropriate Cardiology consultation and management urgently.

ECG #5

A 17-years-old previously healthy male patient who had one attack of syncope earlier in the day presented to the ED.

ECG Source - Peter Allely -
ECG Source - Peter Allely -

The ECG pattern is diagnostic of Brugada syndrome – coved shaped ST-elevation > 2mm followed by an inverted T wave seen in V1 and V2.

Key Take Home Points

Such finding is very serious in a patient with a recent episode of unconsciousness.

The suspicion of Brugada syndrome must be confirmed or excluded by an urgent consultation with a cardiologist.


ECGs in isolation are usually not enough to make a diagnosis – always correlate with clinical history and/or confirmatory investigations.

Try looking at as many ECGs as possible to improve your skills of pattern recognition and picking up subtle changes in ECGs.

Cite this article as: Neha Hudlikar, UAE, "Deadly ECG Patterns – 5 Can’t Miss ECG Findings," in International Emergency Medicine Education Project, November 22, 2019,, date accessed: March 29, 2020

Pacemaker-Related Emergencies – Part 1

pacemaker related emergencies

After the initial implementation of a pacemaker in the 1950s, implanted cardiac devices have become the mainstay therapy for life-threatening arrhythmias and severe congestive heart failure (1). Thanks to technological advancements, the devices become cheaper and smaller, now improving the lives of millions of patients (2). As physicians who serve in an acute setting, we started to take care of patients with implanted cardiac devices on a daily basis. Therefore, we must know how to manage implanted cardiac devices-related emergencies.

The three most common implanted cardiac devices are pacemakers (PMs), implantable cardioverter-defibrillators (ICDs), and left ventricular assist devices (LVADs). PMs generate rhythmic electrical stimuli and consequent heart contractions when the intrinsic electrical activity is below a threshold. ICDs recognize and treat ventricular tachyarrhythmias electrically. Newer generation ICDs also function as pacemakers (3). While the PMs and ICDs mainly support the cardiac electrical function, LVADs support the mechanical function of the heart.

Pacemaker related emergencies are divided into two broad groups as complications of implantation and device malfunction. In this post (part 1), we will summarize complications of implantation.

Complications of Implantation

Although modern technology and technique have significantly decreased the complication rates., we as acute care providers still must be aware of the perioperative complications related to pacemaker implantation. Relatively common complications include pocket, lead-related, thromboembolic, mechanical complications, and pacemaker syndrome (1,4).


Hematomas are formed by perioperative arterial and venous bleeding and can spread tracking the pacemaker leads (5). Palpable hematomas require surgical evacuation as needle aspiration is ineffective, poses pacemaker damaging risk, and does not reveal the underlying source (6). Hematomas increase infection risk.

Pocket Infections

The infections of pocket or leads can occur, mostly due to cutaneous flora, namely, Staphylococcus aureus and Staphylococcus epidermidis (4). The presence of foreign bodies and hematomas contribute to the infectious process (4). Local infections may progress to lung infections, sepsis, skin erosion, and wound dehiscence. The clinical picture may vary from local inflammation and fluctuation to vague systemic complaints and even to sepsis/septic shock without origin (1, 5). Therefore, a clinician should always suspect pacemaker and lead-related infections as a source in patients with a pacemaker. In the ED, after taking blood cultures, intravenous wide-spectrum antibiotics should be started. Pocket cultures should be obtained under fluoroscopy (4). Pocket infections generally necessitate long admissions with IV antibiotics therapy and removal of the pacemaker (7).

Lead-related complications

Lead-related complications include lead malposition, dislodgment, fracture, and damage to the insulation, all of which cause various malfunctions (8, 9). Among them, lead malposition and dislodgement have some additional clinical implications.

Lead malposition

Lead malposition refers to when a lead is inadvertently placed into the left ventricle (9). Lead may land in the left ventricle through a natural orifice of intracardiac variants and defects (atrial-septum defect, patent foramen ovale, sinus venosus defect, malpositioned coronary sinus or its tributaries) or perforation of the intraventricular septum (9). Also, the operator may erroneously place the lead through the subclavian artery and aortic valve.

Lead malposition significantly increases thromboembolic event risk, including transient ischemic attack and stroke (9). Even though there are rare nonpathological right bundle branch block causes, in the acute care setting, if pacing rhythm is right bundle branch block, especially in a patient, whose previous rhythm is known to be left bundle branch block, lead malposition should be suspected (9, 10). A chest X-ray shows the lead position.

 Lead dislodgement

Leads can be dislodged from the endocardial interface, mostly, days or months after implantation (11). In dual-chamber pacemakers, atrial leads get more frequently dislodged than the ventricular leads (11). Such dislodgement produces various rhythm problems due to malfunctions. Additionally, two lead dislodgement-related syndrome is defined below:

  • Lead displacement dysrhythmia refers to when free-floating ventricular leads cause episodes of malignant arrhythmias (12). When a lead is dislodged from the endocardial interface, the patient’s pacemaker dependency determines the symptoms (11). While pacemaker-dependent patients experience episodes of bradycardia- and ventricular tachyarrhythmia-related symptoms, if the native rhythm is favorable, lead dislodgement may stay unknown until malignant arrhythmia episode. Additionally, hiccups may occur due to vagal pacing (11).
  • Macrodislocation lead-dysfunctioning syndromes include Twiddler’s syndrome (coiling of the pacemaker leads due to rotation of the pacemaker generator on its long axis), Reel syndrome (coiling of the pacemaker leads around the pacemaker generator due to rotation of the pacemaker generator on its transverse axis) and Rachet syndrome (13). For further information, please check links 13 – 14.

Thromboembolic complications

The presence of leads in the venous system may cause thrombosis in axillary, subclavian, innominate, and upper arm veins or the superior vena cava up to varying degrees (4). Extensive collateralization masks symptoms. The most common symptoms include swelling and pain of the arm on the lead insertion side (5). However, pacemaker induced thrombosis may even lead to superior vena cava syndrome (5). Standard diagnostic and therapeutic measures apply.

Mechanical complications

Pacemaker and leads implantation may cause many mechanical complications, including tricuspid regurgitation, pneumothorax, hemothorax, air embolism, pericarditis, cardiac tamponade, and perforation (1, 7). All entities have distinct clinical courses and treatments. However, acute care providers should keep in mind all these differential diagnoses when a patient with a pacemaker presents with chest pain and shortness of breath.

Pacemaker Syndrome

It refers to when a patient’s symptoms progressively worsen after pacemaker implantation due to loss of AV synchrony and subsequent reduced cardiac output (15). These symptoms include fatigue, exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea, orthostatic hypotension, presyncope, and syncope (16). The syndrome is more frequent in patients with single-chamber ventricular pacing systems; however, it also occurs in patients with dual-chamber systems. If the patient has a single-chamber device, the treatment is upgrading the pacemaker to a dual-chamber system. If the patient has a dual-chamber device, the pacemaker programming should be adjusted (17).

References and Further Reading

  1. Cabrera, D., & Decker, W.W. (2013). Management of Emergencies Related to Implanted Cardiac Devices. In: J.G. Adams, E.D. Barton, J.L. Collings, P.M.C. DeBlieux, M.A. Gisondi, E.S. Nadel (Eds.), Emergency Medicine: Clinical Essentials (2nd ed., pp. 547-557). Philadelphia: Elsevier. 
  2. Birnie, D., Williams, K., Guo, A., Mielniczuk, L., Davis, D., Lemery, R., … & Tang, A. (2006). Reasons for escalating pacemaker implants. The American journal of cardiology98(1), 93-97.
  3. Beyerbach, D. M. (2019). Pacemakers and Implantable Cardioverter-Defibrillators. Retrieved October 20, 2019 from
  4. Niemann, J. T. & Squire, B. Implantable cardiac devices. (2014). In: J. A. Marx, R. S. Hockberger, R. M. Walls (Eds.), Rosen’s emergency medicine: Concepts and clinical practice (8th ed., pp. 1064-1074). Philadelphia: Elsevier. 
  5. McMullan, J., Valento, M., Attari, M., & Venkat, A. (2007). Care of the pacemaker/implantable cardioverter defibrillator patient in the ED. The American Journal of Emergency Medicine25(7), 812-822.
  6. Trohman, R. G., Kim, M. H., & Pinski, S. L. (2004). Cardiac pacing: the state of the art. The Lancet364(9446), 1701-1719.
  7. Mulpuru, S. K., Madhavan, M., McLeod, C. J., Cha, Y. M., & Friedman, P. A. (2017). Cardiac pacemakers: function, troubleshooting, and management: part 1 of a 2-part series. Journal of the American College of Cardiology69(2), 189-210.
  8. Aguilera, A. L., Volokhina, Y. V., & Fisher, K. L. (2011). Radiography of cardiac conduction devices: a comprehensive review. Radiographics31(6), 1669-1682.
  9. Ohlow, M. A., Roos, M., Lauer, B., Von Korn, H., & Geller, J. C. (2015). Incidence, predictors, and outcome of inadvertent malposition of transvenous pacing or defibrillation lead in the left heart. Ep Europace18(7), 1049-1054.
  10. Erdogan, O., & Aksu, F. (2007). Right bundle branch block pattern during right ventricular permanent pacing: Is it safe or not?. Indian pacing and electrophysiology journal7(3), 187.
  11. Fuertes, B., Toquero, J., Arroyo-Espliguero, R., & Lozano, I. F. (2003). Pacemaker lead displacement: mechanisms and management. Indian pacing and electrophysiology journal3(4), 231.
  12. Burns, E. (2019). Pacemaker Malfunction. Retrieved October 20, 2019 from
  13. Alvarez-Acosta, L., Garrido, R. R., Farrais-Villalba, M., & Afonso, J. H. (2014). Reel syndrome: a rare cause of pacemaker malfunction. British Medical Journal Case Reports2014, bcr2014204545.
  14. Munawar, M., Munawar, D. L., Basalamah, F., & Pambudi, J. (2011). Reel syndrome: A variant form of Twiddler’s syndrome. journal of arrhythmia27(4), 338-342.
  15. Prinzen, F. W., Vernooy, K., Lumens, J., Auricchio, A.(2017). Physiology of Cardiac Pacing and Resynchronization. In: K. A. Ellenbogen, B. L. Wilkoff, G. N. Kay, C. Lau, A. Auricchio. (Eds.), Clinical Cardiac Pacing, Defibrillation and Resynchronization Therapy (5th Ed., pp. 213-248). Philadelphia: Elsevier. 
  16. Gillis, A. M. (2017). Pacing for Sinus Node Disease. In: K. A. Ellenbogen, B. L. Wilkoff, G. N. Kay, C. Lau, A. Auricchio. (Eds.), Clinical Cardiac Pacing, Defibrillation and Resynchronization Therapy (5th Ed., pp. 375-398). Philadelphia: Elsevier. 
  17. Stephenson, E. A. & Davis, A. M. (2009). Electrophysiology, Pacing, and Devices. In: R. H. Anderson, E. J. Baker, D. Penny, A. N. Redington, M. L. Rigby, G. Wernovsky (Eds.), Paediatric Cardiology (3rd Ed., pp. 379-413). Philadelphia: Churchill Livingstone.
Cite this article as: Elif Dilek Cakal, Turkey, "Pacemaker-Related Emergencies – Part 1," in International Emergency Medicine Education Project, November 20, 2019,, date accessed: March 29, 2020

Just Some Broken Ribs

Just Some Broken Ribs

The phone was ringing incessantly. I barely woke up. In my pitch dark bedroom, the ringing phone was the only light source. I slowly grabbed my phone while involuntarily rubbing my eyes. I looked at the caller I.D. It was my father. And what time was it? 1:30 am! In a typical day, this might be an early hour for me, but I was attending a local Emergency Medicine conference that day; so I went to bed early.

I cradled the phone between my ear and shoulder. My father’s voice was fussy. “Someone lies unconscious on the street,” he said hastily. “Can you come and help us?” I asked him to call for an ambulance by that time. He said that he already called. 

While I was preparing in a hurry, my heart started to beat faster and my mind swelled with CPR guidelines, syncope algorithms and my past experiences.

My home is down the block from my parents. I ran there and saw a crowd gathered around a man who was lying on the street. When I passed through I realized someone was doing CPR. I have spotted my parents standing in the crowd and my eyes met with my father. He pointed my younger brother, a trainee surgeon also lives in the same area and was taking his turn on the CPR and checking his pulse. I rushed near them and he filled me in with all they know about the citizen at that point.

The first responder to the cries of the patient’s wife was an ambulance driver with ten years of experience. He said he pulled the patient out of his vehicle. He laid down the man in his 50s suffered from heartburn for the last couple of hours and was about to go to the hospital but lost his consciousness as soon as he started the engine. Since the man wasn’t responding, the former driver started the CPR. About 3 minutes later, my brother showed up along with my father and he took the turn while they kept checking for any response. He said that the rhythm never lasted longer than 10 seconds. So I asked them to keep it up and I took my turn till the ambulance shows up.

It was clear that the patient endured a heart-related condition, probably a myocardial infarction. And I knew by experience that with a proper CPR and early defibrillation, these patients have a high chance of returning of spontaneous circulation, and survival.

The ambulance arrived in a couple of minutes. Paramedics jumped out of the vehicle and rushed to the scene and recognized that I am an Emergency Medicine resident at the State Research and Education Hospital. They let me control the situation. The first rhythm was read on the screen as ventricular fibrillation (VF) and we delivered a shock and started chest compressions again. With the equipment they’ve brought, I intubated the patient while they monitored him with the defibrillator from the ambulance. The nearest hospital was 10 minutes away, and we have shocked-compressed for at least 4 or 5 times in an ambulance moving fast. IT-WAS-HARD!

We have arrived at the hospital. After 10 minutes of additional CPR and proper mediations, spontaneous circulation of the patient returned spontaneous circulation. And a control ECG was consistent with Inferior MI. In a couple of minutes, we were in a different ambulance, headed to the nearest hospital with a coronary angiography unit and ICU.

I took a deep breath after we have delivered the patient to the ICU safe and sound. It was over, for now. One week later, he returned to his home with full recovery, without any neurological sequelae. They were very thankful.

Later on, I’ve heard many funny words people were chattering about this incident. One has particularly given me the giggle. It was coming from an ENT specialist. He said, “So that was no big deal, they probably overreacted and caused him a couple of broken ribs.”

Yeah, there were just some broken ribs… and a life saved.

Further Reading

Cite this article as: Ibrahim Sarbay, Turkey, "Just Some Broken Ribs," in International Emergency Medicine Education Project, August 16, 2019,, date accessed: March 29, 2020

A 19-year-old female presents with sharp right flank pain and shortness of breath

by Stacey Chamberlain

A 19-year-old female presents with sharp right flank pain and shortness of breath that started suddenly the day prior to arrival. The pain is worse with deep inspiration but not related to exertion and not relieved with ibuprofen. She denies anterior chest pain, cough, and fever. She denies leg pain or swelling and recent travel, immobilization, trauma, or surgery. She has no anterior abdominal pain, no dysuria or hematuria and no personal or family history of gallstones, kidney stones, or blood clots. She’s never had this pain before, has no significant past medical history and her only medication is birth control pills. On exam, her vital signs are within normal range, she has normal cardiac and pulmonary exams, no costovertebral angle tenderness, no chest wall or abdominal tenderness and no leg swelling.

Do you need to do any studies to evaluate this patient for a pulmonary embolism?

Pulmonary Embolism Rule-Out Criteria (PERC)

  • Age ≥ 50
  • Heart rate ≥ 100
  • O2 sat on room air < 95%
  • Prior history of venous thromboembolism
  • Trauma or surgery within 4 weeks
  • Hemoptysis
  • Exogenous estrogen
  • Unilateral leg swelling

The PERC CDR was originally derived and validated in 2004 and with a subsequent multi-study center validation in 2008. In the larger validation study, the rule was only to be applied in those patients with a pre-test probability of < 15%, therefore incorporating clinical gestalt prior to using the rule. PERC is a one-way rule, as mentioned above, which tried to identify patients who are so low-risk for pulmonary embolism (PE) as to not require any testing. It does not imply that testing should be done for patients who do not meet criteria, and it is not meant for risk stratification, as opposed to the Wells’ and Geneva scores.

Case Discussion

In order to apply the PERC CDR to the case study patient, the ED physician pre-supposes a pre-test probability of < 15%. If the ED physician has a higher pre-test probability than that, he/she should not use the PERC CDR. If the ED physician, in this case, did indeed have a pre-test probability of < 15%, the case study patient would fail the rule-out due to her use of oral contraceptives. In that case, the ED physician would need to determine if he/she would do further testing which could include a D-dimer, CT chest with contrast, ventilation/perfusion scan, or lower extremity Doppler studies to evaluate for deep vein thromboses (DVTs). The PERC CDR gives no guidance in this case.

Cite this article as: iEM Education Project Team, "A 19-year-old female presents with sharp right flank pain and shortness of breath," in International Emergency Medicine Education Project, June 17, 2019,, date accessed: March 29, 2020

Sinus Tachycardia: Think Simple!

You walk into a patient’s room and notice on the monitor: heart rate of 135. Your patient appears alert and oriented, speaking in full sentences, and telling you, “I have no pain, doctor.”

755.3 - tachycardia

You leave the room, scratching your head, wondering,

“why is the heart rate so high?”

Sinus tachycardia is one of the most common presentations you will find in the Emergency Department, defined as a heart rate greater than 100 beats per minute. Remember, sinus tachycardia will always include p-waves on EKG and telemetry monitoring. This rhythm can be a ‘great masquerader’ in emergency medicine, given that many different etiologies can cause it.

Often, sinus tachycardia – equivalent to an elevated heart rate (HR) – is a compensatory response to an underlying etiology. To explain this concept, let’s recall the delivery of oxygen equation:

CaO2 = (1.34 x Hb x SaO2) + 0.003 x PaO2

The equation for oxygen delivery (CaO2 = arterial oxygen content, Hb = hemoglobin, SaO2 = arterial saturation of oxygen, PaO2 = partial pressure of oxygen in the arterial blood).

All cells require oxygen to survive, and In the lungs, oxygen attaches to hemoglobin molecules so that it can be transported – courtesy of the cardiac output – to the rest of the body. When the delivery of oxygen diminishes, the cardiac output (equal to HR multiplied by the stroke volume) may increase to help compensate for the total delivery of oxygen (as seen by the above equation) (1).

How does this concept apply to sinus tachycardia and the patient in front of you?

Firstly, you want to consider whether your patient has adequate oxygenation and circulation. Check their airway, pulse oximetry, and work of breathing to ensure they are not hypoxemic. Could your patient have a pulmonary embolism? Consider checking for right ventricular dilation with an ultrasound machine or determining whether they may have missed their regularly prescribed anticoagulation.

Enlarged Right Ventricle is seen apical 4 chamber view of the heart and in Para-Sternal short axis (on the right) D shape Left Ventricle. These findings should warn physicians to think about massive pulmonary embolism in a patient with appropriate history, physical examination or risk factors.

For perfusion, check their capillary refill (normal is less than 3 seconds) and palpate their distal extremities to ensure they are warm and not likely in cardiogenic shock. Ensure they are not dehydrated and do not simply need more fluid. Without adequate volume, the body fails to deliver a sustainable amount of oxygen to its tissues. 

Make sure they are not experiencing acute coronary syndrome, either, since sinus tachycardia can occur in one-third or more of patients suffering from ACS due to either pain, hypoxia, anxiety or impending cardiogenic shock(2).

Have you considered whether they may be experiencing a GI bleed, or have an abnormal hemoglobin result with your basic lab studies? Remember: if their oxygen content (as determined by their respiratory and circulatory systems) falls below normal, their cardiac output will try to compensate. Hemoglobin is an important component of the oxygen delivery equation.

720 - variceal bleeding

Image: 17 years old girl, previously healthy, vomited blood suddenly at night, and in the ED.

Secondly, think of non-oxygen related causes including drug and hormone-related effects. Drug intoxication (including amphetamines, cocaine, TCAs plus others) plus opiate, benzodiazepine and/or alcohol withdrawal can lead to sinus tachycardia, too. Albuterol and epinephrine are other common precipitants.

Abnormal glucose and thyroid hormone regulation can also lead to sinus tachycardia. Is your patient hypoglycemic? Remember that low glucose can lead to tachycardia in response to stress (and be associated with altered mental status plus seizure activity). Have your patient’s thyroid levels been checked recently? Hyperthyroidism can easily lead to sinus tachycardia.

755.1 - exophthalmos

A 23 yo female presented with palpitation. Palpitation for 3 days and fever (reaching 39C at home). Weight loss of 24kg (90 to 66) and fatigue in the past three months. ROS: hair loss, heat intolerance, tremor, inability to close her eyes properly, irritability and anxiety. Check the thyroid hormone levels!

Finally, pain and fever! These two important aspects can easily be missed. With pain, your body implements a stress response, often leading to tachycardia. With fever and/or infection, cells require more oxygen.

There are many causes to sinus tachycardia but remember the basics: human cells need oxygen, and if it does not receive this critical element, the body will attempt to compensate by elevating the heart rate. Sometimes, your patient may be experiencing a life-threatening issue (like ACS or pulmonary embolism) or may simply be anxious!

Regardless, always think hard about potential causes and do not anchor on a presumed diagnosis too early. If you follow the basic rules, you can save a life!


  1. Patil, A, Ranjit, S. Hemodynamic Monitoring in PICU. In: Journal of Pediatric Critical Care. New Delhi : Intensive Care Chapter of India Academy of Pediatrics; 2014:267-292.
  2. DeSanctis RW, Block P, Hutter, Jr AM. Tachyarrhythmias in myocardial infarction. Circulation. 1972 Mar;45(3):681-702.

Further Reading

Cite this article as: Erik Blutinger, USA, "Sinus Tachycardia: Think Simple!," in International Emergency Medicine Education Project, May 27, 2019,, date accessed: March 29, 2020

Bat Sign

Dear students/interns, learn ultrasonographic anatomy and clinical ultrasound basics to improve your decision making processes.


The bat sign is critical for correct identification of the pleural line. Always begin lung ultrasound by identifying the bat sign before proceeding to look for artifacts and pathologies.

This sign is formed when scanning across 2 ribs with the intervening intercostal space.

The wings are formed by the 2 ribs, casting an acoustic shadow. The body is the first continuous horizontal hyperechoic line that starts below one rib and extends all the way to the other. (see above video) The body is the pleural line, i.e., parietal pleural. Normally, the pleural line is opposed to and hence indistinguishable from the lung line (formed by the visceral pleura).

To learn more about it, read chapter below.

Read "Blue Protocol" Chapter

Causes of ST Elevation

Stanford A or B?

In case you didn’t encounter a patient with sudden onset chest pain today!

68.2 - AD CT2

iEM Education Project Team uploads many clinical picture and videos to the Flickr and YouTube. These images are free to use in education. You can also support this global EM education initiative by providing your resources. Sharing is caring!

Audio files – Selected Cardiovascular Emergencies

What is your next action?

In case you didn’t encounter an elderly with chest discomfort today!

A 78-year-old male patient presented with chest discomfort and SOB. BP: 89/48 mmHg, HR: 128 bpm, RR: 26/min, T: 37, SpO2: 92% in room air. He has a history of lung cancer, hypertension and diabetes mellitus. Bed side ECG is done. What is your next action?

Feel free to give your answers at the comment box below.

608 - Figure3 - pericardial effusion - ECG

iEM Education Project Team uploads many clinical picture and videos to the Flickr and YouTube. These images are free to use in education. You can also support this global EM education initiative by providing your resources. Sharing is caring!

Cardiac Monitoring Pearls

Cardiac Monitoring chapter written by Stacey Chamberlain from USA is just uploaded to the Website!