Category: ECG

Question Of The Day #25

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod25
835 - 3rd degree heart block

Which of the following is the most likely diagnosis of this patient’s condition?

  • A) Sinus bradycardia
  • B) First-Degree AV Block
  • C) Second-Degree AV Block (Mobitz type II)
  • D) Third-Degree AV Block

This patient has marked bradycardia on exam with a borderline low blood pressure. These vital sign abnormalities are likely the cause of the patient’s dizziness. Bradycardia is defined as any heart rate under 60 beats/min. The most common cause of bradycardia is sinus bradycardia (Choice A). Other types of bradycardia include conduction blocks (i.e. type 2 or type 3 AV blocks), junctional rhythms (lack of P waves with slow SA nodal conduction), idioventricular rhythms (wide QRS complex rhythms that originate from the ventricles, not atria), or low atrial fibrillation or atrial flutter. About 80% of all bradycardias are caused by factors external to the cardiac conduction system, such as hypoxia, drug effects (i.e., beta block or calcium channel blocker use or overdose), or acute coronary syndromes.

ecg qod25Sinus bradycardia (Choice A) occurs when the electrical impulse originates from the SA node in the atria. Signs of sinus bradycardia on EKG are the presence of a P wave prior to every QRS complex. This EKG shows P waves prior to each QRS complex, but there are extra P waves that are not followed by QRS complexes. Some P waves are “buried” within QRS complexes or within T waves. The EKG below marks each P wave with a red line and each QRS complex with a blue line.

 

First-degree AV Block (Choice B) is a benign arrhythmia characterized by a prolonged PR interval. This patient’s EKG has variable PR intervals (some prolonged, some normal). This is a result of a more severe AV conduction block. Second-Degree AV Blocks are divided into Mobitz type I and Mobitz Type II. Mobitz type I, also known as Wenckebach, is characterized by a progressive lengthening PR interval followed by a dropped QRS complex. This can be remembered by the phrase, “longer, longer, longer, drop.” Wenckebach is a benign arrhythmia that does not typically require any treatment. Mobitz type II (Choice C) is characterized by a normal PR interval with random intermittent dropping of QRS complexes. This patient’s EKG has consistent spacing between each QRS complex (blue lines) and consistent spacing between each P wave (red lines). However, the P waves and QRS complexes are not associated with each other. This phenomenon is known as AV dissociation. These EKG changes are signs of a complete heart block, also known as Third-Degree AV Block (Choice D). Both Second-Degree AV block- Mobitz type II (Choice C) and Third-Degree AV Block (Choice D) are more serious conduction blocks that require cardiac pacemakers. Correct Answer: D

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References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Nickson, C. (2020). Heart Block and Conduction Abnormalities. Life in the Fast Lane. Retrieved from https://litfl.com/heart-block-and-conduction-abnormalities/

 

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Question Of The Day #24

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod24
738.1 - Prior ECG before 738.2 - STEMI

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) Begin transcutaneous pacing
  • B) Begin transvenous pacing
  • C) Administer IV Amiodarone
  • D) Administer IV Metoprolol

This patient is suffering from severe bradycardia with signs of poor cardiac output, shock, and diminished perfusion to the brain. Bradycardia is defined as any heart rate under 60 beats/min. Many individuals may be bradycardic at rest with no danger to the patient (i.e. young patients or athletes). Bradycardia in these scenarios is physiologic and is not associated with difficulty in perfusing the brain and other organs. This patient’s 12-lead EKG shows sinus bradycardia since there is a P wave prior to every QRS complex. Sinus bradycardia is the most common type of bradycardia. Other types of bradycardia include conduction blocks (i.e. type 2 or type 3 AV blocks), junctional rhythms (lack of P waves with slow SA nodal conduction), idioventricular rhythms (wide QRS complex rhythms that originate from the ventricles, not atria), or slow atrial fibrillation or atrial flutter. About 80% of all bradycardias are caused by factors external to the cardiac conduction system, such as hypoxia, drug effects (i.e. beta block or calcium channel blocker use or overdose), or acute coronary syndromes.  

For any patient with a bradyarrhythmia or tachyarrhythmia, it is crucial to determine if the arrythmia is “stable” or “unstable”. Signs that an arrhythmia is unstable include altered mental status, hypotension with systolic blood pressure under 90mmHg, chest pain, or shortness of breath. Patients with a stable arrhythmia can be managed supportively with observation and less invasive medical management. Patients with unstable arrhythmia are managed more aggressively with the use of electricity, often in combination with other medical treatments. This patient has an unstable bradyarrhythmia, given her altered mental status and hypotension. Intravenous metoprolol (Choice D) would make the patient more bradycardic since this medication blocks beta-adrenergic receptors of the heart that control heart rate and contractility. Intravenous Amiodarone (Choice C) is an antiarrhythmic agent used often in wide complex tachyarrhythmias (i.e. Ventricular Tachycardia). Intravenous atropine or epinephrine are agents that can be used in this patient prior to preparing for electric pacing. Transcutaneous pacing (Choice A) should always be attempted prior to Transvenous pacing (Choice B), as Transcutaneous pacing is less invasive and quicker to set up. If Transcutaneous pacing does not result in electrical “capture” or change the heart rate, the next step is Transvenous pacing. Correct Answer: A 

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References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Burns, E. (2020). Sinus Bradycardia. Life in the Fast Lane. Retrieved from https://litfl.com/sinus-bradycardia-ecg-library/
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Hypertrophic Cardiomyopathies

Hypertrophic Cardiomyopathies
~ Maryam Bagherzadeh, Canada ~ Leave a comment

Hypertrophic cardiomyopathy is an inherited cardiovascular disease [1]. The condition can lead to sudden death in young adults and other problems such as heart failure, arrhythmias and stroke. It is prevalent in the world, with cases reported in over 50 countries and in people of all sexes, ethnicities and races. In diverse regions including the USA, Europe and East Africa, the prevalence of hypertrophic cardiomyopathy is 1 in 500 in the general population [2]. While considered a common and possibly fatal disease, most affected individuals remain undiagnosed in their lifetime and do not experience symptoms or reduced life expectancy [1].

Hypertrophic cardiomyopathy is passed on by an autosomal dominant fashion through mutations in more than 12 genes that encode for thick and thin myofilament proteins. However, sporadic cases caused by de-novo mutations in the predisposing genes can also occur [3]. Genetic testing for the identification of causative mutations can be conducted via DNA sequencing; however, pathogenic mutations are identified in roughly fewer than 50% of clinically affected patients [1].

Clinical Presentation, Signs and Symptoms

Clinical diagnosis of hypertrophic cardiomyopathy entails a hypertrophied but non-dilated left ventricle without evidence of any other disorders, such as cardiac or systemic diseases that may cause cardiomyocyte hypertrophy [4]. Often, patients with hypertrophic cardiomyopathy do not have any symptoms, and diagnosis is made either incidentally or through familial genetic screening. However, symptomatic patients may experience chest pain with exertion and varying rates of dyspnoea on a daily basis. Chest pain may also present at rest and can be caused by large meals. Some patients can also experience syncope [5]. Dyspnoea, chest pain and syncope are common symptoms that we faced in the emergency department. Although there are more common and deadly presentations with those symptoms, hypertrophic cardiomyopathy should always be in our differential diagnoses, particularly in cases with additional findings explained below.

Clinical Exam and Investigations

Clinical examination of patients with hypertrophic cardiomyopathy often reveals little information. In patients with dynamic left ventricular outflow tract obstruction, a systolic murmur may be heard with auscultation at the left sternal edge, radiating to the aortic and mitral areas [5]. However, if hypertrophic cardiomyopathy is suspected, either due to familial screening, the presence of a murmur or an abnormal 12-lead electrocardiogram (ECG), its diagnosis needs to be confirmed with either echocardiography and/or cardiovascular MRI [1].

Natural History and Clinical Course of Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathies can present at any age from infancy to adulthood. Many patients with this cardiovascular disease are expected to have a normal life expectancy without any major complications or even therapeutic interventions [6]. However, complications may occur in some patients and can include a range of events. Sudden death may occur in patients who are mildly symptomatic or even asymptomatic. Progressive heart failure with possible obstructive outflow obstruction and normal systolic function can occur, which may slowly lead to systolic dysfunction [4]. Cardiac arrhythmias may also develop – most commonly atrial fibrillation. This can lead to symptoms of heart failure and embolic stroke in 20% of the patients [7].

Sudden Death

Sudden death is the most unpredictable and devastating consequence of hypertrophic cardiomyopathy and is the most common cause of sudden death in young patients (under the age of 30) and young athletes [1,4,8]. However, the risk of sudden death falls gradually with older age. Although sudden death from mild physical activity or even inactivity can occur, death due to vigorous exertion amongst this patient population is more common [1]. Sudden death from hypertrophic cardiomyopathy usually occurs due to ventricular fibrillation and tachycardia. Risk stratification of high-risk patients for sudden death is important and can lead to the prevention of sudden death using various approaches, such as an implantable defibrillator [1,9]. Additionally, young professional athletes should be screened to detect silent signs of cardiovascular disorders that may lead to sudden death. Unfortunately, if young athletes are found to have hypertrophic cardiomyopathy, implementation of a cardiovert-defibrillator is not sufficient to grant athletes to return to competing. Athletes are often advised to stop participating in competitive sports, unless it is of low intensity such as golf [8].

Heart Failure

Symptoms of heart failure associated with preserved left-ventricular systolic function most often occur in middle-aged patients but can occur at any age [13]. Functional limitations can occur at differing rates but are often gradual and involve day to day variability. Women with hypertrophic cardiomyopathy have been shown to experience more severe symptoms of heart failure later in life compared to male patients. Frequently, these symptoms experienced in women have been associated with left-ventricular outflow-tract obstruction [14]. Some causes of heart failure in hypertrophic cardiomyopathy patients include left-ventricular outflow-tract obstruction, atrial fibrillation and diastolic dysfunction [1,4]. Treatment strategies include drugs and surgical myectomy or alcohol septal ablation for relief of symptoms of heart failure and outflow obstruction, and pharmacological strategies to treat atrial fibrillation and prevent stroke (such as blood thinners).

Hypertrophic Cardiomyopathy Management in the ED

Patients with hypertrophic cardiomyopathy exacerbation may present to the ED with a range of symptoms including syncope, chest pain, dyspnea, cardiac arrhythmia and worst of all, sudden cardiac death [10]. Diagnosis of hypertrophic cardiomyopathy patients presenting with these symptoms to the ED may be difficult as most of these patients are not aware of their underlying cardiovascular disease. Therefore, ED staff should keep this differential in mind and should be aware of certain diagnostic tools and approaches for acute management of hypertrophic cardiomyopathy.

Primarily, ED staff should conduct a complete history of the patients, including family history of relatives with early cardiovascular disorders or sudden death at a young age. Physical examination of the patient may be inconclusive, as patients usually don’t present with any specific cardiovascular symptoms, unless their disease has progressed to having left-ventricular outflow obstruction tract. An electrocardiogram (EKG) should be conducted, as most patients with hypertrophic cardiomyopathy will have abnormal EKGs. Specifically, their EKGs will show signs of left ventricular hypertrophy through large amplitude QRS, and deep, narrow Q waves particularly in the lateral leads if the patient has septal hypertrophy [11]. Physical examination should be coupled with EKG to rule out other cardiac problems.

HCM-pattern-with-asymmetrical-septal-hypertrophy
Adopted from - Ed Burns. Hypertrophic Cardiomyopathy (HCM). https://litfl.com/hypertrophic-cardiomyopathy-hcm-ecg-library/

Deep narrow Q waves in chest leads are typical ECG finding of the hypertrophic cardiomyopathy patients. For more ECG information please visit – https://litfl.com/hypertrophic-cardiomyopathy-hcm-ecg-library/

In managing hypertrophic cardiomyopathy patients, following the ACLS algorithm if the patient is hemodynamically unstable is first priority. Otherwise, the goal of acute treatment of hypertrophic cardiomyopathy is to restore normal sinus rhythm or control the ventricular rate. Appropriate vasopressors should be given if patients are experiencing volume fluctuations due to diarrhea or other consequences of their disease. If patients present with a new onset of atrial fibrillation, approach of rate versus rhythm control and thromboembolism risk management should be considered [10]. If acute pharmacological treatment of hypertrophic cardiomyopathy patients is required, caution should be taken considering the state of their disease. For example, caution must be exercised when giving diuretics to patients with severe heart failure, as reduction in left ventricular preload can exacerbate obstruction and lead to hypotension [12]. The same considerations must be applied to any other treatment and guidelines should be followed closely. In conclusion, quick identification of the patient’s underlying cardiovascular problem and acute pharmacological management in the ED is critical to help the patient until a specialist can see them.

References and Further Reading

  1. Maron, B. J., & Maron, M. S. (2013). Hypertrophic cardiomyopathy. The Lancet, 381(9862), 242-255.
  2. Maron, B. J., Gardin, J. M., Flack, J. M., Gidding, S. S., Kurosaki, T. T., & Bild, D. E. (1995). Prevalence of hypertrophic cardiomyopathy in a general population of young adults: echocardiographic analysis of 4111 subjects in the CARDIA study. Circulation, 92(4), 785-789.
  3. Alcalai, R., Seidman, J. G., & Seidman, C. E. (2008). Genetic basis of hypertrophic cardiomyopathy: from bench to the clinics. Journal of cardiovascular electrophysiology, 19(1), 104-110.
  4. Maron, B. J. (2002). Hypertrophic cardiomyopathy: a systematic review. Jama, 287(10), 1308-1320.
  5. Elliott, P., & McKenna, W. J. (2004). Hypertrophic cardiomyopathy. The Lancet, 363(9424), 1881-1891.
  6. Maron, B. J., Casey, S. A., Hauser, R. G., & Aeppli, D. M. (2003). Clinical course of hypertrophiccardiomyopathy with survival to advanced age. Journal of the American College of Cardiology, 42(5), 882-888.
  7. Olivotto, I., Cecchi, F., Casey, S. A., Dolara, A., Traverse, J. H., & Maron, B. J. (2001). Impact of atrial fibrillation on the clinical course of hypertrophic cardiomyopathy. Circulation, 104(21), 2517-2524.
  8. Maron, B. J. (2003). Sudden death in young athletes.New England Journal of Medicine, 349(11), 1064-1075.
  9. Maron, B. J., Shen, W. K., Link, M. S., Epstein, A. E., Almquist, A. K., Daubert, J. P., … & Estes, N. M. (2000). Efficacy of implantable cardioverter–defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy.New England Journal of Medicine, 342(6), 365-373.
  10. Gardner, M., Nair, V., Hu, D., & Derry, S. (2018). The evaluation and management of decompensated hypertrophic cardiomyopathy in the emergency department.The American journal of emergency medicine, 36(12), 2286-2288.
  11. Kelly, B. S., Mattu, A., & Brady, W. J. (2007). Hypertrophic cardiomyopathy: electrocardiographic manifestations and other important considerations for the emergency physician.The American journal of emergency medicine, 25(1), 72-79.
  12. Efthimiadis, G. K., Pagourelias, E., Zegkos, T., Parcharidou, D., Panagiotidis, T., Arvanitaki, A., … & Karvounis, H. (2016). An overview of pharmacotherapy in hypertrophic cardiomyopathy: current speculations and clinical perspectives.Reviews in Cardiovascular Medicine, 17(3-4), 115-123.
  13. Melacini, P., Basso, C., Angelini, A., Calore, C., Bobbo, F., Tokajuk, B., … & Thiene, G. (2010). Clinicopathological profiles of progressive heart failure in hypertrophic cardiomyopathy.European heart journal, 31(17), 2111-2123.
  14. Olivotto, I., Maron, M. S., Adabag, A. S., Casey, S. A., Vargiu, D., Link, M. S., … & Maron, B. J. (2005). Gender-related differences in the clinical presentation and outcome of hypertrophic cardiomyopathy.Journal of the American College of Cardiology, 46(3), 480-487.

 

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Question Of The Day #23

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod23
3. PEA

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) Administer intravenous sodium bicarbonate
  • B) Administer intravenous calcium gluconate
  • C) Administer thrombolytics
  • D) Administer blood products

This patient presented to the emergency department with acute pleuritic chest pain, dyspnea, and experienced a cardiac arrest prior to a detailed physical examination. The cardiac monitor shows a narrow complex sinus rhythm morphology. In the setting of a cardiac arrest and pulselessness, this cardiac rhythm is known as pulseless electric activity (PEA). PEA includes any cardiac rhythm that is not asystole, ventricular fibrillation, or pulseless ventricular tachycardia. The ACLS algorithm divides the management of patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole. Assuming adequate staff and medical resources are present, patients with all of these rhythms receive high-quality CPR, IV epinephrine, and airway management. Patients with pVT or VF receive electrical cardioversion, while patients with PEA or asystole do not receive electrical cardioversion. Patients with PEA or asystole generally have a poorer prognosis than those with pVT or VF. Out of hospital cardiac arrests that present to the emergency department with PEA or asystole on initial rhythm have a survival rate of under 3%. The etiology of PEA in cardiac arrest includes a wide variety of causes. A traditional approach to remembering the reversible causes of PEA are the “Hs & Ts”. The list of the “Hs & Ts” along with their individual treatments are listed in the table below.

PEA treatments

Sodium bicarbonate (Choice A) would be the correct choice for a patient whose PEA arrest was caused by severe acidosis. This can occur in severe lactic acidosis (i.e. sepsis), diabetic ketoacidosis, certain toxic ingestions (i.e. iron, salicylates, tricyclic antidepressants), as well as other causes. Calcium gluconate (Choice B) would be the correct choice for a patient whose PEA arrest was caused by hyperkalemia. This can occur in renal failure, in the setting of certain medications, rhabdomyolysis (muscle tissue breakdown), and other causes. Blood products (Choice D) would be the correct choice for a patient whose PEA arrest was due to severe hemorrhage, such as gastrointestinal bleeding or in the setting of traumatic injuries. This patient has symptoms and risk factors for pulmonary embolism, including pleuritic chest pain, dyspnea, and a cancer history. These details make pulmonary embolism the most likely cause of PEA arrest in this scenario. The best treatment for this diagnosis would be thrombolysis (Choice C).

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References

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Question Of The Day #22

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod22
1. VFib

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) Continue chest compressions
  • B) Perform unsynchronized cardioversion at 200 Joules
  • C) Administer Amiodarone
  • D) Administer Sodium Bicarbonate

This patient presents to the Emergency Department after a cardiac arrest with an unknown medical history. Important components of Basic Life Support (BLS) include early initiation of high-quality CPR at a rate of 100-120 compressions/minute, compressing the chest to a depth of 5 cm (5 inches), providing 2 rescue breaths after every 30 compressions (30:2 ratio), avoiding interruptions to CPR, and allowing for adequate chest recoil after each compression. In the Advanced Cardiovascular Life Support (ACLS) algorithm, intravenous epinephrine is administered every 3-5 minutes and a “pulse check” is performed after every 2 minutes of CPR. The patient’s cardiac rhythm, along with the clinical history, helps decide if the patient should receive additional medications or receive unsynchronized cardioversion (defibrillation, or “electrical shock. The ACLS algorithm divides management in patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole.

The cardiac rhythm seen during the pulse check for this patient is ventricular fibrillation. The ACLS algorithm advises unsynchronized cardioversion at 150-200 Joules for patients with pVT or VF. Continuing chest compressions (Choice A) with minimal interruptions is a crucial component of BLS, however, this patient’s cardiac rhythm is shockable. Defibrillation (Choice B) takes precedence over CPR in this scenario. Amiodarone (Choice C) is an antiarrhythmic agent that is recommended in patients with pVT, in addition to unsynchronized cardioversion. This patient has VF, not pVT. Sodium bicarbonate (Choice D) is an alkaline medication that is helpful in cardiac arrests caused by severe acidosis or certain toxins (i.e. salicylates or tricyclic antidepressants). The next best step in this patient scenario would be defibrillation for the patient’s VF (Choice B).

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References

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Question Of The Day #21

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod21

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) Watch the cardiac monitor for a rhythm change
  • B) Continue chest compressions
  • C) Administer intravenous adrenaline
  • D) Check for a pulse

This patient experienced a witnessed cardiac arrest at home, after which pre-hospital providers initiated cardiopulmonary resuscitation (CPR, or “chest compressions”) and Advanced Cardiovascular Life Support (ACLS). ACLS includes the tenets of Basic Life Support (BLS), such as early initiation of high-quality CPR at a rate of 100-120 compressions/minute, compressing the chest to a depth of 5 cm (2 inches), providing 2 rescue breaths after every 30 compressions (30:2 ratio), avoiding interruptions to CPR, and allowing for adequate chest recoil after each compression. In the ACLS algorithm, intravenous epinephrine is administered every 3-5 minutes and a “pulse check” is performed after every 2 minutes of CPR. The patient’s cardiac rhythm, along with the clinical history, helps decide if the patient should receive defibrillation (“electrical shock”) or additional medications. The ACLS algorithm divides management into patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole.

The cardiac rhythm seen during the pulse check for this patient is a wide complex tachycardia with a regular rhythm. In the setting of cardiac arrest, chest pain prior to collapse, and a history of acute coronary syndrome, ventricular tachycardia is the most likely cause. The ACLS algorithm advises unsynchronized cardioversion at 150-200 Joules for patients with pVT or VF. Watching the cardiac monitor for a rhythm change (Choice A) or checking for a pulse (Choice D) are not recommended after defibrillation. A major priority of both BLS and ACLS is to avoid interruptions to CPR, so the best next step in management is to continue CPR (Choice B) after defibrillation. Administration of intravenous adrenaline (Choice C) is helpful for cardiac arrests to initiate shockable rhythm and should be repeated every 3-5 minute or every 2 cycle of CPR, particularly valuable in asystole patients. Calcium gluconate is another drug that can be used in patients with hyperkalemia and indicated in a patient with known kidney disease, missed hemodialysis sessions, or a history of usage of medications that can cause hyperkalemia. Magnesium can be used for patients who show polymorphic VT, particularly Torsades de Pointes. The next best step in this scenario is to continue CPR, regardless of the etiology of the cardiac arrest. Correct Answer: B.

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References

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Question Of The Day #20

question of the day
~ Joseph Ciano, USA ~ Leave a comment
cod20
608 - Figure3 - pericardial effusion - ECG

Which of the following is the most appropriate next investigation for this patient’s condition?

  • A) Arterial blood gas
  • B) Bedside cardiac sonogram
  • C) Chest radiography
  • D) CT pulmonary angiography

This patient’s EKG demonstrates alternating amplitudes of QRS complexes, a phenomenon known as electrical alternans. This is caused by the heart swinging back and forth within a large pericardial effusion. The patient is tachycardic and borderline hypotensive, which should raise concern over impending cardiac tamponade. The next best investigation to definitively diagnose a large pericardial effusion with possible tamponade would be a cardiac sonogram (Choice B). This investigation could also guide treatment with pericardiocentesis in the event of hemodynamic decompensation and the development of obstructive shock. Other EKG signs of a large pericardial effusion are diffusely low QRS voltages and sinus tachycardia. Chest radiography (Choice C) may show an enlarged cardiac silhouette in this case and evaluate for alternative diagnoses (i.e. pneumothorax, pleural effusions, pneumonia, atelectasis), however, cardiac echocardiography is the best next investigation. CT pulmonary angiography (Choice D) would demonstrate the presence of a pericardial effusion along with differences in cardiac chamber size indicative of tamponade. Still, bedside cardiac sonogram is a faster test that prevents a delay in diagnosis. Sending a potentially unstable patient for a CT scan may also be dangerous. Arterial blood gas testing (Choice A) has no role in diagnosing pericardial effusion or cardiac tamponade. Correct Answer: B

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References

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From Missed Hemodialysis to Multiple Arrhythmias

From Missed Hemodialysis to Multiple Arrhythmias
~ Gayatri Lekshmi Madhavan, India ~ 2 Comments

Case Presentation

A 78-year-old male, known case of Chronic Kidney Disease on maintenance hemodialysis, presented to the Emergency Department with dizziness and lethargy complaints about 2 days. He had missed his last hemodialysis session due to personal reasons. We could not elicit any further history details as was significantly dyspneic (no bystanders with him at the time of presentation). Hence, the patient was received in Bay 1 for immediate resuscitative measures. The patient was afebrile, conscious, and well oriented, but unable to communicate because of severe dyspnea.

Vitals

HR – 142 beats/min
BP – not recordable
RR – 36 breaths/min
SpO2 – poor tracing, intermittently showed 98% on room air (15 LO2 via Non Rebreathing Mask was initiated nevertheless)

ECG

ECG on presentation
Monomorphic ventricular tachycardia

He was immediately connected to a defibrillator in anticipation of possible synchronized cardioversion. Simultaneously, the cause of the possible rhythm was being evaluated for and a thorough examination was carried out. On examination, his lung fields were clear. His left arm AV Fistula had a feeble thrill on palpation.

In suspicion of hyperkalemia as the cause of VT, patient was immediately started on potassium reduction measures while the point of care ABG report was awaited. He was treated with salbutamol nebulization 10mg, sodium bicarbonate 50 ml IV and 10% calcium gluconate 10ml IV. In view of hemodynamic instability, he was also started on intravenous noradrenaline infusion.

ABG Findings

pH – 7.010, pCO2 – 20.8 mmHg, pO2 – 125 mmHg, HCO3 – 7 mmol/L, Na – 126 mmol/L, K – 9.6 mmol/L

As hyperkalemia was confirmed, the patient was also given 200 ml of 25% dextrose with 12 units of Rapid-acting insulin IV. With the above measures, the patient’s cardiac rhythm came to a sine wave pattern. 

He was later taken up for emergency hemodialysis (HD) – Sustained Low Efficacy Dialysis (SLED) in the ICU, using a low potassium dialysate. Since his AV fistula was non-functioning, HD was done after placement of a femoral dialysis catheter. 2 hours into HD, the patient’s cardiac monitor showed a normal sinus rhythm. His hemodynamic status significantly improved. Noradrenaline infusion was gradually tapered and stopped by the end of the HD session, and repeat blood gas analysis and serum electrolytes showed improvement of all parameters. 

after hemodialysis

The patient was discharged 2 days later, after another session of hemodialysis (through AV fistula) and a detailed cardiology evaluation (ECHO – LVH, normal EF).

For the Inquisitive Minds

  1. The patient underwent a detailed POCUS evaluation, both in the ER and ICU. What findings do you expect to find on the RUSH examination for this patient?
  2. His previous ECHO report (done 1 month ago) mentioned left ventricular hypertrophy and normal ejection fraction. So what would be the reason behind the POCUS findings? Is it reversible?
  3. Why was the AV fistula non-functioning at the time of presentation? When would it have started to function again?
  4. Despite not having hypoxia, this patient was given supplemental oxygen. Did he really require it, and if so, what was the rationale?
  5. What was the necessity for carrying out SLED for this patient?
  6. Why was this patient not immediately cardioverted in the ER?
  7. If this patient had gone into cardiac arrest, what drugs would you have given for management of hyperkalemia?
  8. How differently would you have managed this patient?

Please give your answers and comments into "leave a reply" area below.

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Question Of The Day #19

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod19
52 - Perforated Viscus

Which of the following is the most likely cause of the patient’s condition?

  • A) Pulmonary embolism
  • B) Pancreatitis
  • C) Peptic ulcer disease
  • D) Gastroesophageal Reflux Disorder

All patients who present to the emergency department with chest pain should be evaluated for the top life-threatening conditions causing chest pain. Some of these include myocardial infarction, pulmonary embolism, esophageal rupture, tension pneumothorax, cardiac tamponade, and aortic dissection. Many of these diagnoses can be ruled-out or deemed less likely with a detailed history, physical exam, EKG, and sometimes imaging and blood testing. This patient presents with vague, burning chest pain, nausea, and tachycardia on exam. Pulmonary embolism (Choice A) is hinted by the patient’s tachycardia, but the patient has no tachypnea or risk factors mentioned for PE. Additionally, the chest X-ray findings demonstrate an abnormality that can explain the patient’s symptoms. Pancreatitis (Choice B) and Gastroesophageal reflux disorder (Choice D) are also possible diagnoses, especially with the location and description of the patient’s pain. However, Chest X-ray imaging offers an explanation for the patient’s symptoms. The patient’s Chest X-ray demonstrates the presence of pneumoperitoneum. In the presence of NSAID use, this radiological finding raises concern over a perforated viscus from advanced peptic ulcer disease (Choice C). Peptic ulcer disease (PUD) is most commonly caused by Helicobacter pylori infection, but NSAIDs, iron supplements, alcohol, cocaine, corrosive substance ingestions, and local infections can cause PUD. PUD is a clinical diagnosis which can be confirmed visually via endoscopy. The treatment for PUD includes initiation of a proton pump inhibitor (H2-receptor blockers are 2nd line), avoiding the inciting agent, and H.pylori antibiotic regimens in confirmed H.pylori cases. The treatment for a perforated peptic ulcer with pneumoperitoneum is IV fluids, IV antibiotics, Nasogastric tube placement, and surgical consultation for repair.

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References

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You may want to read these

Acute Coronary Syndrome – https://iem-student.org/acute-coronary-syndome-acs/ 

Acute Management Of Supraventricular Tachycardias – https://iem-student.org/2020/01/10/acute-management-of-supraventricular-tachycardias/

Deadly ECG Patterns – 5 Can’t Miss ECG Findings – https://iem-student.org/2019/11/22/deadly-ecg-patterns-5-cant-miss-ecg-findings/

Cardiac Monitoring – https://iem-student.org/cardiac-monitoring/

The EKG Case of No Symptoms

the ecg case of no symptoms
~ Anthony Rodigin, USA ~ Leave a comment

Case Presentation

A 52-year-old woman presents to the ED from an outpatient dialysis center with a rather vague history. She has no symptoms and feels normal, but she was told something “was either too low or too high” on her vital signs at dialysis, so dialysis staff did not perform her scheduled dialysis session. No one had called ahead to alert the emergency department, and the patient had driven herself to the ED, as she was instructed. Vitals show a normal temperature, respiratory rate, oxygen saturation, blood pressure of 102/47 mm Hg, and a heart rate of 138 beats per minute. The physical exam is normal besides a mild regular tachycardia and a working AV dialysis fistula on the right arm. EKG is done, and a representative portion is shown below:

EKG from the prior year is shown for comparison.

How would you interpret the first EKG, and what are your next steps?

Discussion

While you are thinking, I will discuss a few of my practical observations from working in the pit. I want to focus not so much on the diagnosis but on working with these types of scenarios.

Treat the patient and not the chief complaint, vitals, labs, EKGs, studies, or referral information.

Anthony Rodigin Tweet

When they are feeling great and have no symptoms, they are feeling great and have no symptoms! Your nurses will not necessarily think this way, but one does not feel great while having a real STEMI apparent on the triage EKG. So what is it then, if the patient is here for a contact lens stuck in their eye, but has an EKG STEMI? Worst case – a prior STEMI that never corrected or evolved on the EKG. A ventricular aneurysm? Leads misplaced? Did your EKG tech do an EKG on themselves? A silent MI can occur, but an incidental STEMI is unlikely. 

Of course, the patient has to be alert, competent, and not intoxicated. They should not be lying about or hiding their symptoms and should not have a secondary interest like the need to make it to a daughter’s wedding - live or die. The easiest thing is to ask directly.

What is the rhythm's rate doing when it is left alone?

Afibs and MATs will tend to vary greatly in the second to second heart rate, sinus tachycardias will fluctuate some, while A-flutters and SVTs will tend to stick to a single number no matter what you do and no matter if the patient is walking, talking, or snoozing. Stable Vtachs will depend on a number of factors like being monomorphic or polymorphic – but we are talking about narrow QRS dysrhythmias or ones with an obvious bundle. 

So if you cannot tell from the EKG – observe what the thing does while left alone. As long as the patient is otherwise stable or has had symptoms for a while, you have some time.

Adenosine – not just for SVT conversion

“SVT = adenosine” should not be an automatic equation. First of all, there are contraindications to adenosine based on past history or current medications taken. But adenosine can also be used to “stretch out” weird or equivocal fast rhythms to make flutter waves or hidden P waves come out, so you can see and diagnose the arrhythmia vs. sinus. 

You have to have continuous EKG recording going or printing the monitor strip to spot the temporary effect.

Hypotension + tachy-dysrhythmia: does not necessarily add up to Joules.

The textbook mantra of shocking any dysrhythmia associated with hypotension does not hold up in reality. In reality, you will find that most of your Afibs with a rapid response, your new-onset atrial flutters and your SVTs will have a lousy blood pressure: systolic of 80s and 90s are almost to be expected, and may even dip down to 70s on occasion. It also depends on a prior BP baseline, if the person is petite or dehydrated. But if the patient is mentating well and is not suffocating or experiencing crushing chest pain with diaphoresis, please don’t feel like you have to shock them. The body is not used to the new arrhythmia, and the rapid rate compromises the cardiac output. 

Yes, you can still use your rate and rhythm controllers. Give the patient a gentle fluid bolus if you must. Of course, pacer pads do have to be on ahead of time.

Be afraid of shocking dialysis patients. Check electrolytes.

Hypotension with normal mentation is much better than a PEA arrest. Shocking extremes of electrolyte and acid/base abnormalities, whether due to TCA and other overdoses or in dialysis patients, will give you exactly that. This is especially true for the so-called “slow-X” arrhythmias: slow Afib, slow SVT, or even V-slow (Vtach with a rate of 130) that dialysis patients like to present in. 

Just like airplane travel in transportation, electricity is in general the safest rhythm conversion strategy. But there are exceptions, and you only need to crash once.

A-flutter and the stuck rate of 150

You already know this, but just as a reminder. If the rate is a steady 150, plus or minus, and it is stuck there, you should think of atrial flutter. 

Even if you do not see obvious classic flutter waves, there is a high chance of 2:1 conduction. In this case, I thought of it. Fortunately, it did not think of me.

Adenosine (again)….the 6, the 12…the 24??

Sometimes adenosine is not pushed correctly, but sometimes it just does not work or only works for a few seconds. Sometimes the patient’s Mom knows best what works, so you should listen. Sometimes the last time it was used, the patient really did feel like they were going to die – so they do not ever want it again. Ever. That you should try 6mg, then 12mg, then stop is generally true, but it is also a dead-end. What is your back up plan? Electricity? In the past I have given the doses in reverse, combined 6mg with the Valsalva maneuver and had given a preemptive beta-blocker or calcium channel blocker dose 10-15 minutes before adenosine to massage a stubborn heart into adenosine submission. It is ok to experiment a little. Another practical point – how much does your ED freak an SVT patient out while he or she is being triaged and roomed? I still do not completely understand why an SVT tends to be rushed up in the same fashion as a STEMI with cardiogenic shock and bradycardia, judging from staff adrenaline levels. 

Calm the patient down, turn the lights off and let them change. It's like a kid with croup. Remember, it is lack of the sympathetic influx that we want, not an excess. Otherwise, why try the Valsalva at all? Has anyone attempted a stellate ganglion block Vfib-style for a refractory SVT? An overkill, I know….but could be fun, and practice for the real deal.

Aren’t all AVNRTs verapamil sensitive?

Years ago, in my first year of solo practice, I had a case of a refractory SVT in a young teenager, which a pediatric cardiologist consulting by phone called a “verapamil-sensitive AVNRT” based on the EKG alone. I was impressed. Hours later, I decided to flash my newly acquired cool knowledge and relayed the same to my in-house cardiologist, who looked at me with a grin and a raised eyebrow and said, “Anthony, all AVNRTs are verapamil sensitive”. At that time, I was also sensitive, and so my feelings were hurt. Lately I have gotten into the habit of treating my SVTs with diltiazem – as a purer verapamil relative. With generally good results and no need to stand in front of the patient during administration by the nurse. 

The bottom line is – you have choices. Especially, if the patient is already on a beta-blocker or a calcium channel blocker, give them a beta or a calcium blocker IV, see what happens.

Case Concluded

Despite a single nadir of blood pressure of 75 systolic, the rest holding steadily in the high 90s, the patient received a single dose of IV diltiazem and a small IV fluid bolus. Labs reviewed prior showed normal potassium, calcium, sodium, magnesium and the rest of them. Her average heart rate reduced to about 106 and a repeat EKG is shown, accidentally capturing an event: 

She, of course, had a “verapamil sensitive” SVT. The patient’s new right bundle block had also improved to an incomplete, proving to be either SVT- or rate-related. The patient had never experienced any symptoms while in the ED. She was observed for a short time, scheduled for an out-of-sequence dialysis the next day and discharged home with a normal heart rate. I guess, in this case, we did treat the EKG and not the patient.

[cite]

Want to read more, take a look this post from September

Question Of The Day #18

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod18
839 - diffuse ST elevation - pericarditis?

Which of the following is the most appropriate next step in management for the patient’s condition?

  • A) Aspirin
  • B) Steroids
  • C) Ibuprofen
  • D) Colchicine

This patient presents to the emergency department with signs and symptoms consistent with acute pericarditis from a likely viral etiology. Common causes of acute pericarditis include idiopathic, infectious (viral, bacterial, or fungal), malignancy, drug-induced, rheumatic disease-associated (lupus, rheumatoid arthritis, etc.), radiation, post-MI (Dressler’s Syndrome), uremia, and severe hypothyroidism. The chest pain associated with this diagnosis is typically worse with supine positioning, improved with sitting forward, worse with inspiration, and may radiate to the back. A pericardial friction rub may be heard on auscultation of the chest, and there may be a low-grade fever on the exam. The hallmark EKG demonstrates diffuse ST-segment elevation with PR segment depression, although normal ST segments or T wave inversions can be seen on EKG later in the disease process. The treatment of acute pericarditis depends on the underlying cause of the disease. This patient has likely viral pericarditis with no clinical signs of myocarditis (i.e. fluid overload, cardiogenic shock, etc.) or cardiac tamponade (i.e. obstructive shock, distended neck veins, muffled heart sounds, low voltage QRS complexes or electrical alternans on EKG). A cardiac sonogram would be prudent to evaluate for a pericardial effusion. This patient’s disease course likely will resolve with NSAIDs in 1-2 weeks. Ibuprofen (Choice C) is the preferred treatment over aspirin (Choice A) or steroids (Choice B). Colchicine (Choice D) can be useful in recurrent episodes of pericarditis to reduce recurrence and in acute pericarditis not responding to NSAIDs. Correct Answer: C 

Want Another Question?

References

[cite]

You may want to read these

Acute Coronary Syndrome – https://iem-student.org/acute-coronary-syndome-acs/ 

Acute Management Of Supraventricular Tachycardias – https://iem-student.org/2020/01/10/acute-management-of-supraventricular-tachycardias/

Deadly ECG Patterns – 5 Can’t Miss ECG Findings – https://iem-student.org/2019/11/22/deadly-ecg-patterns-5-cant-miss-ecg-findings/

Cardiac Monitoring – https://iem-student.org/cardiac-monitoring/

Question Of The Day #15

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod 15 - pleuritic chest pain

Which of the following is the best course of action to further evaluate for a diagnosis of pulmonary embolism?

  • A) Perform a V/Q scan
  • B) Draw a D-Dimer test
  • C) Perform a CT Pulmonary Angiogram
  • D) Give lorazepam
Pulmonary embolism (PE) is a potentially lethal diagnosis evaluated by a combination of a thorough history, physical exam, and the use of risk stratification scoring tools. The Wells criteria and the PE rule-out criteria (PERC) are two well-accepted risk stratification tools for PE. These criteria are each listed below (Wieters et al., 2020).

Wells’ Criteria for Pulmonary Embolism

CriteriaPoint Value
Clinical signs and symptoms of DVT+3
PE is #1 diagnosis, or equally likely+3
Heart rate > 100+1.5
Immobilization at least 3 days, or Surgery in the Previous 4 weeks+1.5
Previous, objectively diagnosed PE or DVT+1.5
Hemoptysis+1
Malignancy w/ Treatment within 6 mo, or palliative+1
Interpretation
Score >4 = High probability
Score 2–4 = Moderate probability
Score <2 = Low probability

Pulmonary Embolism Rule Out Criteria

All Variables Must Be Present for <2% Chance of PE
Pulse oximetry >94% (room air)
HR <100
No prior PE or DVT
No recent surgery or trauma within prior 4 wk
No hemoptysis
No estrogen use
No unilateral leg swelling
The patient in this clinical vignette would have a Wells score of 1.5 (low risk) due to her persistent tachycardia of unknown etiology. The PERC rule can not be applied to this patient as she is over 50-years-old and has tachycardia. If the patient was low risk on Wells score and meet all the PERC rule criteria, she would have a less than 2% likelihood of her symptoms being due to a PE. It is important to note that only patients with a low-risk Wells score (low pretest probability for PE) can be subjected to the PERC rule. A low-risk Wells score (<2) is investigated with a D-Dimer test (Choice B), while moderate to high-risk Wells scores are investigated with a CT Pulmonary Angiogram (CTPA) (Choice C). A V/Q Scan (Choice A) is not a first-line test for the diagnosis of PE as it is less sensitive than a CTPA scan. Unlike a CTPA scan, a V/Q scan may be nondiagnostic in the setting of lung consolidation, effusions, or other airspace diseases. V/Q scans are second-line tests to CTPA when there are contraindications to a CTPA (i.e., renal failure). Lorazepam (Choice D) is a benzodiazepine that may be helpful in reducing tachycardia, which is secondary to anxiety. However, this therapy does not help further discern if the patient may have a PE. Correct Answer: B 

References

Wieters J, McDonough J, Catral J. Chest Pain. In: Stone C, Humphries RL. eds. CURRENT Diagnosis & Treatment: Emergency Medicine, 8e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2172&sectionid=165059275

Nickson, C. (2019). Pulmonary Embolism. Life in the Fastlane. Accessed on August 17, 2020. https://litfl.com/pulmonary-embolism/

[cite]

You may want to read these

Pulmonary Embolism – https://iem-student.org/pulmonary-embolism/

Clinical Decision Rules – https://iem-student.org/clinical-decision-rules/

Question of The Day #6 – https://iem-student.org/2020/07/31/question-of-the-day-6/