Question Of The Day #30

question of the day
qod30

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

This patient arrives to the Emergency department with the return of spontaneous circulation (ROSC) from a ventricular fibrillation cardiac arrest. His regaining of pulses was likely due to his limited downtime, prompt initiation of CPR, and prompt diagnosis and treatment of ventricular fibrillation with electrical defibrillation. Important elements of emergency post-ROSC care include avoiding hypotension, hypoxia, hyperthermia, and hypo or hyperglycemia. Maintaining proper perfusion to the brain and peripheral organs is crucial in all ROSC patients. A 12-lead EKG should always be obtained early after ROSC is achieved in order to look for signs of cardiac ischemia. Cardiac catheterization should be considered in all post-ROSC patients, but especially in patients with cardiac arrest from ventricular fibrillation or ventricular tachycardia.

Patients who achieve ROSC can vary markedly in terms of their clinical exam. Some patients may be awake and conversive, while others are comatose and non-responsive. The neurological exam immediately post-ROSC does not predict long-term outcomes, so decisions on prognosis should not be based on these factors in the emergency department. For this reason, resuscitation efforts should not be considered medically futile in this scenario (Choice A). Vasopressors (Choice B) are medications useful in post-ROSC patients who have signs of hemodynamic collapse, such as hypotension. This patient is not hypotensive and does not meet the criteria for initiation of vasopressors. A CT scan of the head (Choice D) is a study to consider in any patient who presents to the emergency department with collapse to evaluate intracranial bleeding (i.e., subarachnoid bleeding). Although not impossible, the history of chest pain before collapse makes brain bleeding a less likely cause of death in this patient. Targeted Temperature Management (Choice C), also known as Therapeutic Hypothermia, is the best next step in this patient’s management.

Targeted Temperature Management involves a controlled lowering of the patient’s body temperature to 32-34ᵒC in the first 24 hours after cardiac arrest. This treatment has been shown to improve neurologic and survival outcomes. The theory behind this treatment is that hypothermia post-ROSC reduces free radical damage and decreases cerebral metabolism. Data behind targeted temperature management shows the greatest benefit in cardiac arrest patients due to ventricular fibrillation, but arrest from ventricular tachycardia, pulseless electrical activity, and asystole may also show benefit. Adverse effects of this treatment include coagulopathy, bradycardia, electrolyte abnormalities (i.e., hypokalemia), and shivering. Important contraindications to this treatment are an awake or alert patient (post-ROSC GCS >6), DNR or DNI status, another reason to explain comatose state (i.e., intracranial bleeding, spinal cord injury), age under 17 years old, a poor functional status prior to the cardiac arrest (i.e., nonverbal, bedbound), or an arrest caused by trauma. Correct Answer: C

References

 

Cite this article as: Joseph Ciano, USA, "Question Of The Day #30," in International Emergency Medicine Education Project, March 12, 2021, https://iem-student.org/2021/03/12/question-of-the-day-30/, date accessed: August 5, 2021

Question Of The Day #29

question of the day
qod29
842 - Wide QRS complex tachycardia

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

This patient presents to the emergency department with seven days of severe vomiting, diarrhea, tachycardia, and borderline hypotension. The clinician should be concerned about dehydration and potential electrolyte derangements induced by the vomiting and diarrhea. Certain electrolyte derangements can put a patient at risk for cardiac dysrhythmias, so ordering a 12-lead EKG is an important step in evaluating any patient with a potential electrolyte disturbance. Dangerous electrolyte disturbances that can predispose a patient to cardiac dysrhythmias include hyperkalemia, hypokalemia, hypomagnesemia, and hypocalcemia. Signs of hyperkalemia on the EKG include peaked T waves, absent or flattened P waves, widened QRS complexes, or a sine wave morphology. Low potassium, magnesium, and calcium can all prolong the QT interval and predispose the patient to polymorphic ventricular tachycardia (Torsades de Pointes). Hypokalemia on EKG may also be associated with a U wave, which is an upward wave that follows the T wave.

This patient’s 12-lead EKG shows a wide-complex tachycardia with QRS complex “twisting” around the isoelectric line and varying QRS amplitudes. These EKG signs, along with the inferred history of severe electrolyte abnormalities, support a diagnosis of Torsades de Pointes (TdP). Another risk factor for TdP is a history of congenital prolonged QT syndromes. Similar to monomorphic ventricular tachycardia, TdP should always be treated with electrical cardioversion if there are any signs of instability (i.e., altered mental status, SBP <90mmHg). A pulseless patient with TdP always necessitates unsynchronized cardioversion, also known as defibrillation. This patient may have briefly syncopized or potentially underwent cardiac arrest. Intravenous Amiodarone (Choice A) and Procainamide (Choice B) are contraindicated in TdP as both of these agents can further prolong the QT interval. These agents can be used in a stable patient with monomorphic ventricular tachycardia. Intravenous Ciprofloxacin (Choice C) is a quinolone antibiotic that is useful for treating infections from gram-negative bacteria. This may be beneficial for this patient, especially if there is a concern for bacterial gastroenteritis. However, quinolone antibiotics also can prolong the QT interval, and this medication will not acutely stabilize this patient. Intravenous Magnesium Sulfate (Choice D) shortens the QT interval and is the preferred therapy for a TdP patient with a pulse. Correct Answer: D

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #29," in International Emergency Medicine Education Project, March 5, 2021, https://iem-student.org/2021/03/05/question-of-the-day-29/, date accessed: August 5, 2021

Question Of The Day #28

question of the day
qod28

EKG#1

710 - hyperkalemia

EKG#2

855 - bradycardia

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

This patient presents to the emergency department with vague and nonspecific symptoms of nausea, fatigue, and palpitations. The initial EKG (EKG #1) demonstrates a wide-complex tachycardia (QRS >120msec) with a regular rhythm. The differential diagnosis for wide-complex tachyarrhythmias include ventricular tachycardia (monomorphic ventricular tachycardia), torsades de pointes (polymorphic ventricular tachycardia), coarse ventricular fibrillation, supraventricular tachycardias with aberrancy (i.e. underlying Wolf Parkinson White Syndrome or Ventricular Bundle Branch Block), electrolyte abnormalities (i.e., Hyperkalemia), and from medications (i.e., Na channel blocking agents). If the history is unclear or the patient shows signs of instability, Ventricular tachycardia should always be the assumed tachyarrhythmia. This is managed with electrical cardioversion or with medications (i.e., amiodarone, procainamide, lidocaine), depending on the patient’s symptoms and hemodynamic stability.

The prior EKG for the patient (EKG #2) is helpful in showing that the patient does not have a wide QRS complex at baseline. There also are no EKG signs of Wolf Parkinson White Syndrome (Choice B) on EKG #2, making this choice incorrect. Signs of this cardiac pre-excitation syndrome on EKG include a shortened PR interval and a delta wave (slurred upstroke at the beginning of the QRS complex). Anxiety (Choice D) can cause sinus tachycardia and be a symptom associated with any arrhythmia, but it is not the underlying cause for this patient’s bizarre wide-complex tachydysrhythmia. On a closer look, the patient’s EKG (EKG #1) demonstrates tall, peaked T waves in the precordial leads. This supports a diagnosis of hyperkalemia. Other signs of hyperkalemia on EKG include flattened or absent P waves, widened QRS complexes, or a sine wave morphology. A common underlying cause of hyperkalemia is renal disease (Choice C). Ischemic heart disease (Choice A) is a common underlying cause for ventricular tachycardia. Ventricular tachycardia is less likely in this case given the presence of peaked T waves and the lack of fusion beats, capture beats, or signs of AV dissociation on the 12-lead EKG. Correct Answer: C 

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). Ventricular Tachycardia – Monomorphic VT. Life in The Fast Lane. Retrieved from https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library/

Cite this article as: Joseph Ciano, USA, "Question Of The Day #28," in International Emergency Medicine Education Project, February 26, 2021, https://iem-student.org/2021/02/26/question-of-the-day-28/, date accessed: August 5, 2021

Question Of The Day #27

question of the day
qod27
756.1 - palpitation - SOB

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

This patient has a narrow-complex, regular tachycardia that is causing the sensation of palpitations. The clinical history, rapid heart rate, and 12-lead EKG provide enough information to diagnose this patient with supraventricular tachycardia, also known as “SVT.” Supraventricular tachycardias refer to a broad range of arrhythmias, including sinus tachycardia, atrial fibrillation, atrial flutter, multifocal atrial tachycardia, and AV nodal re-entry tachycardia. This scenario specifically depicts an AV nodal re-entry tachycardia (AVNRT). AVNRT is a common type of SVT that can occur spontaneously or is triggered by sympathomimetic agents (i.e., cocaine, amphetamines), caffeine, alcohol, exercise, or beta-2 agonists using in asthma treatment (i.e., albuterol, salbutamol). AVNRTs are narrow-complex tachycardias with rates that range from 120-280bpm. P waves are typically absent in AVNRTs, but rarely they may be present as retrograde inverted P waves located immediately before or after the QRS complex. Symptoms experienced by the AVNRT patient may include pre-syncope, syncope, dizziness, palpitations, anxiety, or mild shortness of breath. Patients with AVNRTs are more likely to be young and female over male.

QRS complexes in AVNRTs are often narrow (<120msec), however, wide QRS complexes may be present in AVNRTs if there is a concurrent bundle branch block or Wolff-Parkinson White Syndrome. AVNRTs are often stable and do not require electric cardioversion. Signs that indicate instability and necessitate cardioversion are hypotension (SBP <90mmHg), altered mental status, or ischemic chest pain (more common if known history of ischemic heart disease). This patient lacks all of these signs and symptoms.

Treatment of AVNRT focuses on restoring the patient to normal sinus rhythm, which leads to resolution of symptoms. First-line medications for AVNRTs are short-acting AV nodal blocking agents, like adenosine (Choice A). Beta-blockers or calcium channel blockers act as second-line agents for patients who do not respond to adenosine. Metoprolol is a beta-blocker (Choice C) and Diltiazem is a calcium channel clocker (Choice D). Prior to any medications, vagal maneuvers should always be attempted first in a stable patient with AVNRT. The Valsalva maneuver (Choice B), or “bearing down,” is a commonly used vagal maneuver in the termination of AVNRTs. Other vagal maneuvers include the carotid massage or the Diving reflex (place bag of ice and water on face). Correct Answer: B

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). Supraventricular Tachycardia (SVT). Life in the Fast Lane. Retrieved from https://litfl.com/supraventricular-tachycardia-svt-ecg-library/

Cite this article as: Joseph Ciano, USA, "Question Of The Day #27," in International Emergency Medicine Education Project, February 19, 2021, https://iem-student.org/2021/02/19/question-of-the-day-27/, date accessed: August 5, 2021

Question Of The Day #26

question of the day
qod26
38 - atrial fibrillation

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

This patient presents to the emergency department with palpitations, a narrow complex tachycardia (<120msec), and an irregularly irregular rhythm. A close look at this patient’s EKG reveals the absence of discrete P waves and QRS complexes that are spaced at varying distances from each other (most apparent in lead V6). These signs support a diagnosis of Atrial Fibrillation, or “AFib.” Atrial Fibrillation is an arrhythmia characterized by an irregularly irregular rhythm, the absence of P waves with a flat or undulating baseline, and narrow QRS complexes. Wide-QRS complexes may be present in AFib if there is a concurrent bundle branch block or Wolff-Parkinson White Syndrome. AFib is caused by the electric firing of multiple ectopic foci in the atria of the heart. This condition is triggered by a multitude of causes, including ischemic heart disease, valvular heart disease, dilated or hypertrophic cardiomyopathies (likely related to this patient’s congestive heart failure history), sepsis, hyperthyroidism, excess caffeine or alcohol intake, pulmonary embolism, and electrolyte abnormalities.

The main risk in AFib is the creation of thrombi in the atria as they fibrillate, resulting in emboli that travel to the brain and cause a stroke. The CHA2DS2VASc scoring system is used to risk stratify patients and determine if they require anticoagulation to prevent against thrombo-embolic phenomenon (i.e. stroke). This patient has a high CHA2DS2VASc score, so she would require anticoagulation. In addition to anticoagulation, A fib is treated with rate control (i.e. beta blockers or calcium channel blockers), rhythm control (i.e. anti-arrhythmic agents), or electrical cardioversion. Electrical cardioversion (choice A) is typically avoided when symptoms occur greater than 48 hours, since the risk of thrombo-emboli formation is higher in this scenario. An exception to this would be a patient with “unstable” AFib. Signs of instability in any tachyarrhythmia are hypotension, altered mental status, or ischemic chest pain. This patient lacks all of these signs and symptoms. Although this patient lacks signs of instability, this patient’s marked tachycardia should be addressed with medical treatment. General observation (Choice C) is not the best choice for this reason. Intravenous adenosine (Choice D) is the best choice for a patient with supraventricular tachycardia (SVT). This is a narrow-complex AV nodal re-entry tachycardia with rates that range from 120-280bpm. SVT also lacks discrete P waves. A key factor that differentiates A fib from SVT is that SVT has a regular rhythm, while AFib has an irregular rhythm. Intravenous metoprolol (Choice B) is the best treatment option listed in order to decrease the patient’s heart rate.

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) Atrial Fibrillation. Life in The Fast Lane. Retrieved from https://litfl.com/atrial-fibrillation-ecg-library/

 

Cite this article as: Joseph Ciano, USA, "Question Of The Day #26," in International Emergency Medicine Education Project, February 12, 2021, https://iem-student.org/2021/02/12/question-of-the-day-26/, date accessed: August 5, 2021

Question Of The Day #25

question of the day
qod25
835 - 3rd degree heart block

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

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

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/

 

Cite this article as: Joseph Ciano, USA, "Question Of The Day #25," in International Emergency Medicine Education Project, February 5, 2021, https://iem-student.org/2021/02/05/question-of-the-day-25/, date accessed: August 5, 2021

Question Of The Day #24

question of the day
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?

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 

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/
Cite this article as: Joseph Ciano, USA, "Question Of The Day #24," in International Emergency Medicine Education Project, December 11, 2020, https://iem-student.org/2020/12/11/question-of-the-day-24/, date accessed: August 5, 2021

Question Of The Day #23

question of the day
qod23
3. PEA

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

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).

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #23," in International Emergency Medicine Education Project, December 4, 2020, https://iem-student.org/2020/12/04/question-of-the-day-23/, date accessed: August 5, 2021

Question Of The Day #22

question of the day
qod22
1. VFib

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

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).

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #22," in International Emergency Medicine Education Project, November 27, 2020, https://iem-student.org/2020/11/27/question-of-the-day-22/, date accessed: August 5, 2021

Physiologically Difficult Airway – Metabolic Acidosis

Physiologically Difficult Airway - Metabolic Acidosis

Case Presentation

A 32-year-old male with insulin-dependent diabetes mellitus came to your emergency department for shortness of breath. He was referred to the suspected COVID-19 area. His vitals were as follows: Blood pressure, 100/55 mmHg; pulse rate, 135 bpm; respiratory rate, 40/min; saturation on 10 liters of oxygen per minute, 91%; body temperature, 36.7 C. His finger-prick glucose was 350 mg/dl.

The patient reported that he had started to feel ill and had an episode of diarrhea 1 week ago. He developed a dry cough and fever in time. He started to feel shortness of breath for 2 days. He sought out the ER today because of the difficulty breathing and abdominal pain.

The patient seemed alert but mildly agitated. He was breathing effortfully and sweating excessively. On physical examination of the lungs, you noticed fine crackles on the right. Despite the patient reported abdominal pain, there were no signs of peritonitis on palpation.

An arterial blood gas analysis showed: pH 7.0, PCO2: 24, pO2: 56 HCO3: 8 Lactate: 3.

The point-of-care ultrasound of the lungs showed B lines and small foci of subpleural consolidations on the right.
At this point, what are your diagnostic hypotheses?

Two main diagnostic hypotheses here are:

  • Diabetic ketoacidosis (Hyperglycemia + metabolic acidosis)
  • SARS-CoV2 pneumonia

We avoid intubating patients with pure metabolic decompensation of DKA if possible, as they respond to hydration + insulin therapy + electrolyte replacement well and quickly. 

But in this scenario, the patient is extremely sick and has complicating medical issues, such as an acute lung disease decompensating the diabetic condition, probably COVID19. Considering these extra issues may complicate the recovery time and increase the risk of respiratory failure, you decide to intubate the patient in addition to the treatment of DKA.

You order lab tests and cultures. You start hydration and empirical antibiotics while starting preoxygenation and preparing for intubation.

Will this be a Difficult Airway?

Evaluating the patient for the predictors of a difficult airway is a part of the preparation for intubation. Based on your evaluation, you should create an intubation plan. 

This assessment is usually focused on anatomical changes that would make it difficult to manage the airway (visualization of the vocal cords, tube passage, ventilation, surgical airway), thereby placing the patient at risk.

“Does this patient have any changes that will hinder opening the mouth, mobilizing the cervical region, or cause any obstruction for laryngoscopy? Does this patient have any changes that hinder the use of Balloon-Valve-Mask properly, such as a large beard? What about the use of the supraglottic device? Does this patient have an anatomical alteration that would hinder emergency cricothyroidotomy or make it impossible, like a radiation scar? ”

So the anatomically difficult airway is when the patient is at risk if you are unable to intubate him due to anatomical problems.

The physiologically difficult airway, however, is when the patient has physiological changes that put him at risk of a bad outcome during or shortly after intubation. Despite intubation. Or because of intubation, because of its physiological changes due to positive pressure ventilation.

These changes need to be identified early and must be mitigated. You need to recognize the risks and stabilize the patient before proceeding to intubation or be prepared to deal with the potential complications immediately if they happen.

5 main physiological changes need attention before intubation are: hypoxemia, hypotension, severe metabolic acidosis, right ventricular failure, severe bronchospasm.

Back to our patient: Does he have physiologically difficult airway predictors?

  • SI (Shock Index): 1.35 (Normal <0.8) – signs of shock
  • P / F: 93 (Normal> 300) – Severe hypoxemia
  • pH: 7.0: Severe metabolic acidosis – expected pCO2: 20 (not compensating)
  • qSOFA: 2 + Lactate: 3 (severity predictor)

Physiologically Difficult Airway

"Severely critical patients with severe physiological changes who are at increased risk for cardiopulmonary collapse during or immediately after intubation."

Sakles JC, Pacheco GS, Kovacs G, Mosier JM. The difficult airway refocused.

Severe Metabolic Acidosis

In this post, we will focus only on the compensation of the metabolic part, but do not forget that this is a patient who needs attention on oxygenation and hemodynamics as well. That is, this is intubation with very difficult predictions.

What happens during the rapid sequence of intubation in severe metabolic acidosis?

To perform the procedure, the patient needs to be in apnea. During an apnea, pulmonary ventilation is decreased and the CO2 is not “washed” from the airway. These generate an accumulation of CO2, an acid, decreasing blood pH. In a patient with normal or slightly altered pH, this can be very well-tolerated, but in a patient with a pH of 7.0, an abrupt drop in this value can be ominous.

We know that the respiratory system is one of the most important compensation mechanisms for metabolic acidosis and it starts its action in seconds, increasing the pH by 50 to 75% in 2 to 3 minutes, guaranteeing the organism time to recover. So, even seconds without your proper actions can be risky for critical patients.

In addition, it must be remembered that increased RF is the very defense for the compensation of metabolic acidosis, and most of the time the organism does this very well. So if after the intubation the NORMAL FR and NORMAL minute volume are placed in the mechanical ventilator parameters, again there is an increase in CO2 and a further decrease in pH.

And what’s wrong? After all, a little bit of acidosis even facilitates the release of oxygen in the tissues because it deflects the oxyhemoglobin curve to the right, right?

Severe metabolic acidosis (pH <7.1) can have serious deleterious effects:

  • Arterial vasodilation (worsening shock)
  • Decreased myocardial contractility
  • Risks of arrhythmias
  • Resistance to the action of DVAs
  • Cellular dysfunction

What to do?

Always the primary initial treatment is: treating the underlying cause! In patients with severe metabolic acidosis, it is best to avoid intubation! Especially in metabolic ketoacidosis, which as hydration and insulin intake improves, there is a progressive improvement in blood pH.

Sodium bicarbonate

The use of sodium bicarbonate to treat metabolic acidosis is controversial, especially in non-critical acidosis values ​​(pH> 7.2). If you have acute renal failure associated, its use may be beneficial by postponing the need for renal replacement therapy (pH <7.2).

As for DKA, where sodium bicarbonate is used to the ketoacidosis formed by erratic metabolism due to the lack of insulin and no real deficiency is present, its use becomes limited to situations with pH <6.9.

The dose is empirical, and dilution requires a lot of attention (avoid performing HCO3 without diluting!)

NaHCO3 100mEq + AD 400ml

Run EV in 2h

If K <5.3: Associate KCl 10% 2amp

I would make this solution and leave it running while proceeding with the intubation preparations.

Attention: Remember, according to the formula below, that HCO3 is converted to CO2, and if done in excess, is associated with progressive improvement of the ketoacidosis and recovery of HCO3 from the buffering molecules. In a patient already with limited ventilation, its increase can cause deviation of the curve for the CO2 increase, which is also easily diffused to the cells and paradoxically decrease the intracellular pH, in addition to carrying K into the cell.

H + + HCO3 – = H2CO3 = CO2 + H2O

Mechanical ventilation

I think the most important part of the management of these patients is the respiratory part.

If you choose the Rapid Sequence Intubation: Prepare for the intubation to be performed as quickly as possible: Use your best material, choose the most experienced intubator, put the patient in ideal positioning, decide and apply medications skillfully, to ensure the shortest time possible apnea.

You will need personnel experienced in Mechanical Ventilation and you must remember to leave the ventilatory parameters adjusted to what the patient needs and not to what would be normal!

I found this practice very interesting: First, you calculate what the expected pCO2 should be for the patient, according to HCO3:

Winter’s Equation (Goal C02) = 1.5 X HCO3 + 8 (+/- 2)

And then, according to this table, you try to reach the VM Volume Minute value.
Goal CO2 Minute Ventilation
40 mmHg
6-8 L
30 mmHg
12-14 L
20 mmHg
18-20 L

These are just initial parameters. With each new blood gas analysis repeated in 30 minutes to an hour, you re-make fine adjustments using the formula below:

Minute volume = [PaCO2 x Minute volume (from VM)] / CO2 Desired

With the treatment of ketoacidosis, new parameters should be adjusted, hopefully for the better.

Another safer option for these patients would be to use the Awake Patient Intubation technique so that you would avoid the apnea period. However, Awake Patient Intubation Technique is contraindicated in suspected or confirmed COVID-19 cases due to the risk of contamination.

That’s it, folks, send your feedback, your experiences, and if you have other sources!

Further Reading

  1. Frank Lodeserto MD, “Simplifying Mechanical Ventilation – Part 3: Severe Metabolic Acidosis”, REBEL EM blog, June 18, 2018. Available at: https://rebelem.com/simplifying-mechanical-ventilation-part-3-severe-metabolic-acidosis/.
  2. Justin Morgenstern, “Emergency Airway Management Part 2: Is the patient ready for intubation?”, First10EM blog, November 6, 2017. Available at: https://first10em.com/airway-is-the-patient-ready/.
  3. Salim Rezaie, “How to Intubate the Critically Ill Like a Boss”, REBEL EM blog, May 3, 2019. Available at: https://rebelem.com/how-to-intubate-the-critically-ill-like-a-boss/.
  4. Salim Rezaie, “RSI, Predictors of Cardiac Arrest Post-Intubation, and Critically Ill Adults”, REBEL EM blog, May 10, 2018. Available at: https://rebelem.com/rsi-predictors-of-cardiac-arrest-post-intubation-and-critically-ill-adults/.
  5. Salim Rezaie, “Critical Care Updates: Resuscitation Sequence Intubation – pH Kills (Part 3 of 3)”, REBEL EM blog, October 3, 2016. Available at: https://rebelem.com/critical-care-updates-resuscitation-sequence-intubation-ph-kills-part-3-of-3/.
  6. Lauren Lacroix, “APPROACH TO THE PHYSIOLOGICALLY DIFFICULT AIRWAY”, https://emottawablog.com/2017/09/approach-to-the-physiologically-difficult-airway/
  7. Scott Weingart. The HOP Mnemonic and AirwayWorld.com Next Week. EMCrit Blog. Published on June 21, 2012. Accessed on July 15th 2020. Available at [https://emcrit.org/emcrit/hop-mnemonic/ ].
  8. IG: @pocusjedi: “Pocus e Coronavirus: o que sabemos até agora?”https://www.instagram.com/p/B-NxhrqFPI1/?igshid=14gs224a4pbff

References

  1. Sakles JC, Pacheco GS, Kovacs G, Mosier JM. The difficult airway refocused. Br J Anaesth. 2020;125(1):e18-e21. doi:10.1016/j.bja.2020.04.008
  2. Mosier JM, Joshi R, Hypes C, Pacheco G, Valenzuela T, Sakles JC. The Physiologically Difficult Airway. West J Emerg Med. 2015;16(7):1109-1117. doi:10.5811/westjem.2015.8.27467
  3. Irl B Hirsch, MDMichael Emmett, MD. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed on July 15, 2020.)
  4. Cabrera JL, Auerbach JS, Merelman AH, Levitan RM. The High-Risk Airway. Emerg Med Clin North Am. 2020;38(2):401-417. doi:10.1016/j.emc.2020.01.008
  5. Guyton AC, HALL JE. Tratado de fisiologia medica. 13a ed. Rio de Janeiro(RJ): Elsevier, 2017. 1176 p.
  6. Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol. 2010;6(5):274-285. doi:10.1038/nrneph.2010.33
  7. Calvin A. Brown III, John C. Sakles, Nathan W. Mick. Manual de Walls para o Manejo da Via Aérea na Emergência. 5. ed. – Porto Alegre: Artmed, 2019.
  8. Smith MJ, Hayward SA, Innes SM, Miller ASC. Point-of-care lung ultrasound in patients with COVID-19 – a narrative review [published online ahead of print, 2020 Apr 10]. Anaesthesia. 2020;10.1111/anae.15082. doi:10.1111/anae.15082
Cite this article as: Jule Santos, Brasil, "Physiologically Difficult Airway – Metabolic Acidosis," in International Emergency Medicine Education Project, November 25, 2020, https://iem-student.org/2020/11/25/physiologically-difficult-airway-metabolic-acidosis/, date accessed: August 5, 2021

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Question Of The Day #21

question of the day
qod21

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

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.

References

Cite this article as: Joseph Ciano, USA, "Question Of The Day #21," in International Emergency Medicine Education Project, November 13, 2020, https://iem-student.org/2020/11/13/question-of-the-day-21/, date accessed: August 5, 2021

Push Th(d)ose Vasopressors

Push Th(d)ose Vasopressors

Background

Since Scott Weingart first advocated for using push-dose pressors in the Emergency Department (ED) over a decade ago(1), push-dose vasopressors, also known as bolus-dose vasopressors have seemingly found their way into many EDs. However, recent studies have sought to ask more questions regarding its use and safety in the Emergency Department.

Vasopressors such as epinephrine and norepinephrine are commonly used for regulating and maintaining adequate blood pressure or mean arterial pressure (MAP). While these are usually administered as a continuous infusion via central access, administering them as a small bolus through peripheral access came to be known as push-dose vasopressor in practice.

Traditionally, this small bolus strategy was used in the operating room (OR) by anesthetists to treat transient hypotension due to sedating agents or spinal anesthesia. Multiple studies have supported the safety and efficacy of push-dose vasopressors in this clinical setting/patient population (2).

Swensen, et al. (3) studied the safety of bolus-dose phenylephrine for hypotension in the Emergency Department, however, data on the efficacy and safety of push-dose pressors remains sparse in ED and in-patient settings. Studies published in the past few years have questioned the lack of evidence regarding the safety and efficacy of push-dose pressor use in ED settings and highlighted some negative consequences of its use (4). To understand the concerns, it’s important we first understand the vasopressors, indications for use, and preparation in the ED.

Push-dose pressors in the Emergency Department

The two common vasopressors used as push-dose pressors in the Emergency Department are Epinephrine and Phenylephrine. Patients needing emergency airway, traumatic brain injury, and post-cardiac arrest with the return of spontaneous circulation may all experience hypotension which could lead to adverse outcomes. Push-does pressors have been proposed as a temporary measure to limit the hypotension while a vasopressor infusion/definitive treatment is being set up (5).

phenilephrine vs epinephrine
push dose epinephrine
push dose phenilephrine

Clinical settings in the ED where the use of push-dose pressor is proposed:

  1. Airway management: Hypotension prior, during, and post-intubation could be treated with bolus-dose vasopressors. Panchal et al. (6) did a retrospective chart review of intubated hypotensive patients in which phenylephrine was used. Bolus-dose phenylephrine demonstrated an increase in systolic blood pressure and the authors recommended further studies to understand the best use of phenylephrine for post-intubation hypotension.
  2. Return of spontaneous circulation (ROSC): In patients with ROSC, bolus-dose pressors may aid in the maintenance of end-organ perfusion, which is often impaired after ROSC (7).
  3. Traumatic brain injury: By rapidly increasing mean arterial pressure and thus cerebral perfusion pressure, bolus-dose vasopressors may help to prevent secondary brain injury.

What are the concerns regarding the use of push-dose pressors in the ED?

Acquisto and Bodkin (8) cited a few dosing errors while using push-dose pressors and highlighted that emergency physicians are less familiar with the practice of medication preparation/manipulation and hence dosing errors are expected, inadvertently causing patients more harm than benefit. They also emphasized on the lack of evidence in the literature regarding the efficacy and safety of push-dose pressors in a stressful environment like the ED.

Rotando and Picard et al. (9) in their prospective observational study of 146 patients receiving push-dose pressors in the ICU had thirteen (11.2%) patients have a dose-related medication error and seventeen (11.6%) adverse events. They concluded while push-dose pressors where efficacious, they were associated with adverse drug events and medication errors.

Cole et al (10). performed a retrospective analysis of 249 patients receiving push-dose pressors and found a higher incidence of adverse hemodynamic effects (39%) and human errors (19%). They emphasized the need for further studies to question whether push-dose pressors improve outcomes, and if so, how to safely implement them in practice.

Another concern raised is whether physicians may bypass standard resuscitation practices of fluid boluses in favor of using push-dose pressors. Schwartz et al. (11) found that only 34% of patients received an appropriate fluid challenge before using push-dose pressors in a retrospective chart review of 73 patients receiving push-dose pressors for acute hypotension in the ED. Furthermore, it appeared that patients who did not receive an appropriate fluid bolus needed more doses of bolus-dose pressors followed by the need for continuous vasopressor infusion within 30 minutes of bolus-dose pressor use.

Emergency physicians work in stressful environments which raises concerns on the ability of the physician to perform accurate dose calculations under duress (4). The prepared syringe also contains multiple individual doses, and using more concentrated solutions potentially increases the risk of overdose and extravasation injury (12).

Conclusion

While the practice of using push-dose pressors has found its way into the Emergency Department, it is crucial to acknowledge that evidence regarding its safety and benefits is limited. However, rather than disregarding the practice, high-quality research should be encouraged, which could potentially be practice-changing. Holden et al. (12) offer a framework of operational and safety considerations for the use of push-dose pressors in the ED and is a must-read for all using push-dose pressors in their current practice.

References

  1. Scott Weingart. EMCrit Podcast 6 – Push-Dose Pressors. EMCrit Blog. Published on July 10, 2009. Accessed on September 25th 2020. Available at [https://emcrit.org/emcrit/bolus-dose-pressors/ ].
  2. Lee A, Ngan Kee WD, Gin T. A quantitative, systematic review of randomized controlled trials of ephedrine versus phenylephrine for the management of hypotension during spinal anesthesia for cesarean delivery. Anesth Analg. 2002 Apr;94(4):920-6, table of contents. doi: 10.1097/00000539-200204000-00028. PMID: 11916798.
  3. Swenson K, Rankin S, Daconti L, Villarreal T, Langsjoen J, Braude D. Safety of bolus-dose phenylephrine for hypotensive emergency department patients. Am J Emerg Med. 2018 Oct;36(10):1802-1806. doi: 10.1016/j.ajem.2018.01.095. Epub 2018 Feb 19. PMID: 29472039.
  4. Cole JB. Bolus-Dose Vasopressors in the Emergency Department: First, Do No Harm; Second, More Evidence Is Needed. Ann Emerg Med. 2018 Jan;71(1):93-95. doi: 10.1016/j.annemergmed.2017.05.039. Epub 2017 Jul 26. PMID: 28754354.
  5. Weingart S. Push-dose pressors for immediate blood pressure control. Clin Exp Emerg Med. 2015;2(2):131-132. Published 2015 Jun 30. doi:10.15441/ceem.15.010
  6. Panchal AR, Satyanarayan A, Bahadir JD, Hays D, Mosier J. Efficacy of Bolus-dose Phenylephrine for Peri-intubation Hypotension. J Emerg Med. 2015 Oct;49(4):488-94. doi: 10.1016/j.jemermed.2015.04.033. Epub 2015 Jun 20. PMID: 26104846.
  7. Gottlieb M. Bolus dose of epinephrine for refractory post-arrest hypotension. CJEM. 2018 Oct;20(S2):S9-S13. doi: 10.1017/cem.2016.409. Epub 2017 Jan 10. PMID: 28069098.
  8. Acquisto NM, Bodkin RP, Johnstone C. Medication errors with push dose pressors in the emergency department and intensive care units. Am J Emerg Med. 2017 Dec;35(12):1964-1965. doi: 10.1016/j.ajem.2017.06.013. Epub 2017 Jun 7. PMID: 28625533.
  9. Rotando A, Picard L, Delibert S, Chase K, Jones CMC, Acquisto NM. Push dose pressors: Experience in critically ill patients outside of the operating room. Am J Emerg Med. 2019 Mar;37(3):494-498. doi: 10.1016/j.ajem.2018.12.001. Epub 2018 Dec 3. PMID: 30553634.
  10. Cole JB, Knack SK, Karl ER, Horton GB, Satpathy R, Driver BE. Human Errors and Adverse Hemodynamic Events Related to “Push Dose Pressors” in the Emergency Department. J Med Toxicol. 2019 Oct;15(4):276-286. doi: 10.1007/s13181-019-00716-z. Epub 2019 Jul 3. PMID: 31270748; PMCID: PMC6825064.
  11. Schwartz MB, Ferreira JA, Aaronson PM. The impact of push-dose phenylephrine use on subsequent preload expansion in the ED setting. Am J Emerg Med. 2016 Dec;34(12):2419-2422. doi: 10.1016/j.ajem.2016.09.041. Epub 2016 Sep 22. PMID: 27720568.
  12. Holden D, Ramich J, Timm E, Pauze D, Lesar T. Safety Considerations and Guideline-Based Safe Use Recommendations for “Bolus-Dose” Vasopressors in the Emergency Department. Ann Emerg Med. 2018 Jan;71(1):83-92. doi: 10.1016/j.annemergmed.2017.04.021. PMID: 28601272.
Cite this article as: Neha Hudlikar, UAE, "Push Th(d)ose Vasopressors," in International Emergency Medicine Education Project, November 11, 2020, https://iem-student.org/2020/11/11/push-thdose-vasopressors/, date accessed: August 5, 2021

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