Category: Cardiovascular Emergencies

Question Of The Day #85

question of the day
~ Joseph Ciano, USA ~ Leave a comment
SS Video 3 Pericardial Tamponade
Which of the following is the most likely cause for this patient’s condition?
  • A) Pulmonary embolism
  • B) Tension pneumothorax
  • C) Pneumonia with septic shock
  • D) Cardiac tamponade

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient presented to the Emergency department with 2 days of shortness of breath without chest pain, cough, or fevers.  The exam shows tachycardia, hypotension, mild tachypnea, clear lungs, and distant heart sounds.  Tension pneumothorax (Choice B) can cause hypotension and tachycardia and COPD is a risk factor for pulmonary bleb formation and rupture.  However, the lungs are equal and clear bilaterally, so this diagnosis is not likely.  Septic shock due to pneumonia (Choice C) is also less likely as there is no fever, the lungs are clear, and the patient lacks a cough.  The ultrasound image given also provides a clear explanation for the patient’s symptoms.  This patient is at risk for pulmonary embolism (Choice A) given his cancer history which can cause a hypercoagulable state and predispose him to clot formation.  Again, an understanding of the ultrasound image will provide the diagnosis.

The ultrasound image is a subxiphoid view of the heart demonstrating a pericardial effusion (red stars) with compression of the right ventricle (yellow arrow). 

This presentation is consistent with cardiac tamponade (Choice D).  Cardiac tamponade is a condition defined by the accumulation of fluid in the pericardial sac to the point of right ventricular collapse and obstructive shock.  Common presenting symptoms of cardiac tamponade include shortness of breath, chest pain, or nonspecific symptoms.  Risk factors for this diagnosis are penetrating chest trauma (hemopericardium), cancer (malignant effusion), lupus, end stage renal disease, uremia, HIV, Tuberculosis, or history of chest radiation.  The presence of hemodynamic instability (hypotension and tachycardia) is a hallmark of this condition, although early stages of tamponade can be seen on cardiac ultrasound before vital signs decompensate.  The patient may have Beck’s triad of muffled distant heart sounds, jugular venous distension, and hypotension, although the majority of patients with cardiac tamponade do not have all three of these signs together.  Treatment involves IV fluids, bedside pericardiocentesis (ultrasound guided preferred), and surgical pericardiotomy (“pericardial window”).

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Question Of The Day #84

question of the day
~ Joseph Ciano, USA ~ Leave a comment
475.3 xray abdomen series normal chest
Which of the following is the most appropriate next step in management for this patient’s condition?
  • A) IV insulin infusion
  • B) IV lactated ringers solution
  • C) Nebulized Beta-2 agonist
  • D) Endotracheal intubation

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

 

This patient arrives to the Emergency Department with shortness of breath and generalized weakness or 3 days.  On physical exam, there is tachycardia, tachypnea, normal oxygen saturation, and a markedly elevated glucose.  The Chest X-ray provided is normal; there are no lung infiltrates or pleural effusions. 

This patient has diabetic ketoacidosis (DKA).  DKA is a serious condition of insulin deficiency characterized by hyperglycemia, metabolic acidosis, and ketosis.  Presenting symptoms include weakness, increased thirst (polydipsia), increased hunger (polyphagia), increased urination (polyuria), abdominal pain, or vomiting.  Shortness of breath can also be seen in DKA as the metabolic ketoacidosis triggers an increased respiratory rate to drive more exhaled carbon dioxide out of the body.  This deep rapid breathing seen in severe DKA is known as Kussmaul breathing.  The treatment of DKA involves IV fluids for hydration, insulin infusion, and close monitoring for electrolyte derangements (potassium abnormalities are common).  DKA patients are severely dehydrated due to osmotic diuresis from their hyperglycemic state.  For this reason, IV fluid resuscitation is the first step to DKA management.  Either normal saline or lactated ringers (Choice B) can be used, although large volumes of normal saline can worsen the acidotic state by causing a hyperchloremic metabolic acidosis.  Intravenous fluids should be started with a 20-30cc/kg bolus.  IV insulin infusion (Choice A) should never be started without a potassium level, and no potassium level is provided in the question stem.  Insulin lowers potassium, and administration of insulin without a potassium level can result in hypokalemia, arrythmia, and death.  Endotracheal intubation (Choice D) should be avoided in DKA whenever possible as the patient’s respiratory status serves as a compensation for the metabolic acidosis.  This patient is tachypneic and mildly confused, but he is not somnolent and does not require immediate intubation.  Intubated DKA patients need carefully monitored ventilator settings in combination with blood gas measurements to avoid worsening acidosis and cardiac arrest.  Nebulized beta-2 agonist (i.e., albuterol, salbutamol) is helpful in asthma, however this patient has DKA and not an asthma exacerbation.  IV lactated ringers solution (Choice B) is the best next step.

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Question Of The Day #83

question of the day
~ Joseph Ciano, USA ~ Leave a comment
infero-lateral MI - 41 yo male - 1 h pain
Which of the following is the most appropriate next step in management for this patient’s condition?
  • A) Provide supplemental oxygen
  • B) Administer 324mg aspirin
  • C) Administer sublingual nitroglycerin
  • D) CT head to evaluate weakness

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

 

This patient arrives to the Emergency Department with several hours of shortness of breath, nausea, and generalized weakness.  On physical exam, the vital signs are normal, there is no tachypnea, no hypoxemia, no respiratory distress, and the lungs are clear.  Clear lungs in a patient with respiratory distress should raise concern for acute coronary syndrome, pulmonary embolism, cardiac tamponade, anemia, and metabolic acidosis.    

The 12-lead EKG provided shows an inferior ST-elevation Myocardial Infarction (STEMI).  This is demonstrated through the ST segment elevations in the inferior EKG leads (II, III, AvF) and the reciprocal changes in the lateral leads (most notably in AvL).  The presence or absence of chest pain is not provided in this question, but patients with acute coronary syndromes do not always have chest pain.  Elderly patients and women are more likely to present with non-chest pain anginal equivalents, like shortness of breath, lethargy, or nausea.  Diagnosis of acute coronary syndrome is done through a combination of a 12-lead EKG, blood troponin levels, and history and physical exam.  A STEMI is the most severe of all acute coronary syndromes and requires prompt recognition and treatment with antiplatelets (i.e., aspirin plus clopidogrel or ticagrelor), heparin, pain management (morphine or nitroglycerin), and percutaneous coronary intervention (PCI).  Providing supplemental oxygen (Choice A) is not necessary as the patient has no hypoxemia and a normal lung exam.  Administration of sublingual nitroglycerin (Choice C) can help alleviate ischemic chest pain and other symptoms associated with a STEMI but is contraindicated in inferior STEMIs.  Using nitroglycerin in inferior STEMIs can result in dangerous hypotension due to cardiac preload reduction.  This patient has a STEMI, and a CT head to evaluate weakness (Choice D) will not be helpful.  In general, a detailed neurological exam assessing for motor deficits will be more valuable than a CT head to determine the etiology of a patient’s weakness.  The best next step in this case is to administer 324mg aspirin (Choice B) in this patient with a STEMI.

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Question Of The Day #82

question of the day
~ Joseph Ciano, USA ~ Leave a comment
35.3 - pulmonary congestion

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

  • A) Diabetic ketoacidosis
  • B) Congestive heart failure
  • C) Myocardial infarction
  • D) Pneumonia

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

 

This patient presents to the Emergency department with 1 day of shortness of breath without chest pain, fevers, or a cough.  He has been noncompliant with his home medications for his multiple comorbid conditions.  The exam shows tachypnea, tachycardia, hypertension, a low oxygen level, pulmonary crackles, and peripheral edema.  The chest X-ray shows bilateral pulmonary congestion and infiltrates consistent with pulmonary edema.

Diabetic ketoacidosis (Choice A) can cause shortness of breath, but the severe hypertension, fluid overload on exam, and lack of hyperglycemia make DKA less likely.  Pneumonia (Choice D) can cause shortness of breath, but often has other symptoms like cough, fever, and sometimes chest pain.  It is difficult to rule out an underlying pneumonia in the presence of pulmonary edema by solely looking at the chest X-ray.  The patient’s peripheral edema, severe hypertension, and lack of cough and fever make pneumonia a less likely diagnosis responsible for that patient’s symptoms.  Myocardial infarction (Choice C) often presents with chest pain but can present with only shortness of breath.  A severe myocardial infarction with cardiogenic shock can result in acute fluid overload as seen in this patient, but hypotension would be expected.  A 12-lead EKG is required to more fully evaluate for a myocardial infarction, but the constellation of symptoms this patient has makes congestive heart failure (Choice B) the most likely diagnosis. 

Immediate initial actions for this patient should include placing the patient on a cardiac monitor, obtaining a 12-lead EKG, sitting the patient upright to assist with breathing, and providing supplemental oxygen.  Acute decompensated heart failure should be aggressively treated with Nitroglycerin to lower the blood pressure and stress on the heart (preload).  Noninvasive positive pressure ventilation (NIPPV), such as BIPAP or CPAP, is another crucial initial step to help provide oxygenation, lower the preload, and push the fluid out from the lungs.  IV diuresis to remove fluid from the body and evaluating for the underlying cause are other important steps in acute CHF management. 

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Question Of The Day #81

question of the day
~ Joseph Ciano, USA ~ Leave a comment
475.3 xray abdomen series normal chest
Which of the following is the most likely diagnosis for this patient’s condition?
  • A) Pneumothorax
  • B) Diabetic Ketoacidosis
  • C) Pulmonary Embolism
  • D) Pneumonia

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient presents to the Emergency Department with 1 day of acute onset shortness of breath with pleuritic chest pain. Her exam shows tachycardia, tachypnea, a normal glucose level, and clear lungs bilaterally.  The chest X-ray provided shows no acute abnormalities.  Pneumothorax (Choice A) can present as acute onset shortness of breath with pleuritic chest pain, but the chest X-ray shows no signs of pneumothorax.  Diabetic Ketoacidosis (Choice B) can cause shortness of breath, and this patient has a history of diabetes.  However, the patient lacks other symptoms of this condition such as hyperglycemia (often glucose >250mg/dL (13.8mmol/L)), polydipsia, polyphagia, polyuria, or vomiting.  This makes DKA an unlikely diagnosis. Pneumonia (Choice D) is also unlikely as there is no fever, no cough, and no infiltrate seen on the chest X-ray provided.  Pulmonary Embolism (Choice C) is the most likely diagnosis and the correct answer.

The most common presenting symptom in pulmonary embolism (PE) is shortness of breath.  Other symptoms seen in PE include chest pain worsened by deep inspiration, unilateral leg swelling, hemoptysis, and fever.  Risk factors for PE include immobility, recent surgery or hospitalization, trauma, or hypercoagulable states (malignancy, estrogen use, Factor V Leiden mutation, antiphospholipid syndrome).  Common signs of PE on physical examination include tachycardia (common), fever (less common), and sometimes hypotension in a massive PE causing obstructive shock.  The gold standard for PE diagnosis is CT pulmonary angiography, but D-dimer blood testing, bedside ultrasound, and other tests can be useful in PE diagnosis.  The mainstay of treatment in PE is anticoagulation.  Unfractionated heparin and low molecular weight heparin are equally effective in PE.  Surgical treatment (embolectomy) and thrombolysis (alteplase) are other treatment options fo larger PEs.

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Seizure: Lethal Dissection

Lethal Dissection Seizure
~ Naveen Paila, India ~ 1 Comment

Case Presentation

A 49-year old female without any co-morbidities presented to the emergency department (ED) with seizures. On arrival, she was in a postictal state.

She had recently visited a local hospital with complaints of severe dysmenorrhea and low back pain. The attenders informed us that she was very sleepy and weak at that time, was treated for pain and given tranexamic acid, and sent home. The next day, she had one episode of Generalized Tonic-Clonic Seizure, and she arrived in our ED in a postictal phase. She vomited twice in the ED.

Her vitals were as follows: 

  • Blood pressure (BP): 160/100 mmHg.
  • Heart rate (HR): 22/min
  • Peripheral capillary oxygen saturation (SPO2): 98% on room air
  • General Random Blood Sugar (GRBS): 233 mg/dl
  • Glasgow Coma Scale (GCS): E2V5M6

Her examination was as follows:

  • The patient was drowsy but arousable. 
  • Pupils bilateral reacting to light. No anisocoria.
  • CNS examination could not be completed as the patient was drowsy.
  • A normal pattern of breathing. The respiratory examination was normal.
  • The abdomen was soft, symmetric, and non-tender without distention.

Point-of-care ultrasound (POCUS) showed a flap in the abdominal aorta. (See Figure 1 and 2 for transverse and longitudinal views of the aorta, respectively) Upon this finding, cardiac surgery and neurology consultations were sought.

Transverse section of the abdominal aorta showing a flap.
https://ibb.co/N6VyMD8

Image shows transverse section of the abdominal aorta showing a flap.

Abdominal aorta showing a flap
https://ibb.co/wwkYHJY

Image shows abdominal aorta showing a flap.

The laboratory results were as follows:

  • D-dimer: 1192 ng/ml
  • Haemoglobin (Hb): 10 g/dl
  • The international normalized ratio (INR): 1.25
  • Platelets: 260000 per mcL
  • Total leucocyte count (TLC): 22000 cells/mm3
  • Creatinine :1.6 mg/dl.

Meanwhile, the patient was suffering multiple seizure-like episodes, characterized by staring, deviation of the mouth, and irregular limb movements, but these episodes lasted for few minutes and ended without the postictal phase. The patient was drowsy but obeyed commands and did not have any recollection of those few minutes.

Head computed tomography (CT) showed no infarct or bleeding. It was normal.

CT angiogram and aortogram revealed that the patient had Stanford Type A aortic dissection with the flap extending to the entire left subclavian artery, with severely occluding filling defects and thrombosis of the false lumen into bilateral common carotid arteries (See Figure 3, 4 and 5). On the other end, the dissection extended to the common iliac arteries (See Figure 6).

CT Aortogram showing bilateral common carotid artery filling defects
https://ibb.co/M6TMqpq

Image shows CT Aortogram showing bilateral common carotid artery filling defects

And on the other loose of the string the dissection was extending till the common iliac arteries.
Ascending and descending aortic dissection
https://ibb.co/n8Rbdvm

Image shows ascending and descending aortic dissection

Dissection of the common iliac artery before bifurcation
https://ibb.co/jVjL0qJ

Image shows dissection of the common iliac artery before bifurcation.

 

Management

Initially, the patient was treated symptomatically by anti-epileptics and analgesics. After the cardio-thoracic and vascular surgeon consultations, we decided to airlift the patient to a higher centre as our hospital was tertiary care and there were no grafts for the urgent repair of the extensive aortic dissection. We intubated the patient for secure transportation. However, we learned that the patient expired in the higher centre before reaching the operating room.

Discussion

Before I shed light on the important part of this discussion, I know that the outcome of this case was unfortunately grave. However, I chose this case because of it.

In this case, the patient had low back pain in her previous hospital visit. However, she was sent home with symptomatic management, implying that it could have been addressed more carefully. She visited our ED one day later, and POCUS let us diagnose the dissection in 15 minutes, which was confirmed by a CT aortogram within 40 minutes. After consultations and finding the available facility, we airlifted the patient to a higher centre for urgent repair, but the patient could not make it to the operating room.     

We all know acute aortic dissection is the most common life-threatening disorder affecting the aorta. Over the first several hours, the mortality rate increase up to 1% per hour; therefore, early intervention is critical (1). In our case, the involvement of bilateral carotid arteries caused seizure-like episodes and altered mental status. Also, studies show that patients with similarly located dissections may experience neck pain, transient ischemic attacks (TIA), cerebral ischemia, transient monocular blindness and subarachnoid haemorrhage (SAH) but not seizure(2). In our case, the global hypo-perfusion caused recurrent TIAs, which resembled seizure-like clinical episodes. That’s why emergency physicians should be vigilant about the underlying causes of seizure-like activities, even if altered mental status similar to postictal state is present, especially if the patient does not have a history of seizures and the complaints are unclear. Keep the aortic dissection in mind as a differential. Also, I cannot stress the use of POCUS in the ED enough. It is a game-changer, and in our case, it detected a lethal disease successfully.

Learning Points

  1. Never ignore back pain that does not subside after adequate pain management.
  2. POCUS is always a game-changer. It saves a lot of time and lives, as in my case.
  3. Seizures or not, you must keep a high suspicion for lethal vascular diseases. Remember the basics: If unclear, go back to history.
  4. Once you confirm an aortic dissection, never delay treatment because time = life.
  5. Never ever send a patient back home unless you are completely sure about the cause of the presenting symptom. Over investigating is ok when compared to under investigating, when it might cost a life.

References and Further Reading

  1. Braverman AC. Acute aortic dissection: clinician update. Circulation. 2010;122(2):184-188. doi:10.1161/CIRCULATIONAHA.110.958975
  2. Debette S, Grond-Ginsbach C, Bodenant M, et al. Differential features of carotid and vertebral artery dissections: the CADISP study. Neurology. 2011;77(12):1174-1181. doi:10.1212/WNL.0b013e31822f03fc
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Out of Proportion: Acute Leg Pain

~ J. Austin Lee, USA ~ Leave a comment

Case Presentation

A 48-year-old male, with history of hypertension and diabetes and prior intravenous drug use (now on methadone) presents with acute onset right leg pain from his calf to the ankle, that woke him from sleep overnight. The pain has been constant, with no modifying or relieving factors. He hasn’t taken anything other than his daily dose of methadone. He hasn’t had any fevers or chills and denies any recent trauma or injuries.

Any thoughts on what else you might want to ask or know?

  • Any recent travel or prolonged immobilization?
  • Have you ever had a blood clot?
  • Are you on any blood thinners?
  • Have you used IV drugs recently?
  • Any numbness or weakness in your leg?
  • Any associated rash or color change?
  • Any back pain or abdominal pain? Any bowel or bladder incontinence?
  • Any recent antibiotics (or other medication changes)?
  • Have you ever had anything like this before?
[all of these are negative/normal]

Pause here -- what is your initial differential diagnosis looking like?

  • Deep vein thrombosis
  • Superficial vein thrombosis
  • Pyomyositis
  • Necrotizing fasciitis
  • Muscle sprain or tear
  • Arterial thromboembolism
  • Bakers cyst
  • Achilles tendonitis, Achilles tendon rupture

What are some key parts of your targeted physical exam?

  • VITAL SIGNS! [BP was slightly hypertensive, and he is slightly tachycardic, normothermic]
  • Neurologic exam of the affected extremity (motor and sensory)
  • Vascular exam of the affected extremity (femoral/popliteal/posterior tibialis/dorsalis pedis)
  • Musculoskeletal exam including ranging the hip, knee, ankle and palpating throughout the entire leg
  • Skin exam for signs of injury or rashes etc.
  • Consider a cardiopulmonary and abdominal exam, particularly the lower abdomen

On this patient’s exam, he was overall uncomfortable appearing and had slight tachycardia (110s, EKG shows normal sinus rhythm), normal cardiopulmonary exam, normal abdominal exam. He had a 2+ right femoral pulse and faintly palpable DP pulse that had a good biphasic waveform on doppler. His hip/knee/ankle all have painless range of motion. The compartments are soft in the upper and lower leg. He does have some diffuse calf tenderness and the medial aspect feels slightly cool compared to the contralateral side, but his foot is warm and well perfused. There isn’t any spot that is most tender. There is no rash, no crepitus, no bullae or bruising or other evidence of injury.

What diagnostic studies would you like to send?

  • CBC, BMP
  • CPK, lactate
  • DVT ultrasound?
  • Anything else?

What treatments would you like to provide?

  • Analgesia (mutli-modal)?
  • Maybe a bolus of IV fluids to help with the tachycardia?

The patient is having a lot of pain despite already getting NSAIDs, acetaminophen, and a dose of morphine. You decide to re-medicate the patient with more morphine and send him for DVT ultrasound. As soon as he gets back, he’s frustrated that you still haven’t treated his pain “at all” and he really does look uncomfortable and in a lot of pain.  You start to wonder if he’s faking it giving his history of IV drug use.

His DVT ultrasound comes back as normal. The lab work is also coming back and unrevealing. A normal CBC, metabolic panel, normal CPK, normal lactate. His pain is not really improving. You reexamine the leg, and the exam is unchanged. It really seems like his pain is out of proportion to the exam.

Pain is out of proportion to the exam should catch your attention every time. While we always need to keep malingering and less emergent causes for pain that seems to be more than expected in the back of our minds. But! Several emergent diagnoses have patients presenting in pain in a way that doesn’t fit what you can objectively identify as a cause. Diagnoses like compartment syndrome and mesenteric ischemia can be erroneously dismissed by emergency providers, and it is crucial you don’t just stop looking for the cause of pain out of proportion. In fact, it’s important you dig in deeper and rule out all potentially life and limb threatening causes.

In this case, the pain was recalcitrant to multiple doses of IV opiates and several other modes of treatment. The patient was getting so frustrated that he pulled out his IV and threatened to leave the ED. After talking with him further, he agreed to stay and a new IV was placed, more pain medication given, and a CTA with lower extremity run-off was performed, which showed the acute thrombus of the proximal popliteal artery, just below the level of the knee.

He was started on a heparin infusion and vascular surgery was consulted; the patient was admitted from the ED and taken for thrombectomy. No source of embolism was identified, and his occlusion was presumed to be thrombotic (most commonly from a ruptured atheromatous plaque leading to activation of the coagulation cascade), with particular attention to his history of diabetes and hypertension raising his risk for this. He had a fair amount of collateralization from other arteries around the occlusion, such that his foot wasn’t cold, and he had a doppler-able DP pulse. 

Remember

Go with your gut and don’t minimize pain that is out of proportion to the exam. Keep hunting for a reasonable explanation or you may miss a life or limb threatening cause of an atypical emergency presentation.

Further Reading

Deep Vein Thrombosis (DVT)

July 14, 2018 No Comments

by Elif Dilek Cakal Case Presentation An 85-year-old woman, with a history of congestive heart failure, presented with right leg pain and swelling of 2

Read More »

Acute Mesenteric Ischemia

July 1, 2018 No Comments

by Rabind Antony Charles Case Presentation A 75-year-old woman presents to your Emergency Department (ED) with diffuse abdominal pain for the past day, associated with

Read More »

Abdominal Pain

April 29, 2018 2 Comments

by Shaza Karrar Case Presentation A 39-year-old female presented to the emergency department (ED) complaining of right-lower-quadrant (RLQ) pain; pain duration was for 1-day, associated

Read More »
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Question Of The Day #59

question of the day
~ Joseph Ciano, USA ~ Leave a comment
38 - atrial fibrillation

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

  • A) Pulmonary embolism
  • B) Cardiac arrythmia
  • C) Dehydration
  • D) Systemic infection

This patient presents to the Emergency Department with palpitations, generalized weakness, and shortness of breath after discontinuing all her home medications.  She has hypotension, marked tachycardia, and pulmonary edema (crackles on lung auscultation).  The 12-lead EKG demonstrates atrial fibrillation with a rapid ventricular rate.  This patient is in a state of cardiogenic shock and requires prompt oxygen support, blood pressure support, and heart rate control. 

Pulmonary embolism (Choice A) can sometimes manifest as new atrial fibrillation with shortness of breath and tachycardia, but pulmonary embolism initially causes obstructive shock.  If a pulmonary embolism goes untreated, it can progress to right ventricular failure, pulmonary edema, and cardiogenic shock.  This patient has known atrial fibrillation and stopped all her home medications.  The abrupt medication change is a more likely cause of the patient’s cardiogenic shock.  Dehydration (Choice D) and systemic infection (Choice D) are less likely given the above history of abruptly stopping home maintenance medications.  Untreated cardiac arrythmia (Choice B) is the most likely cause for this patient’s pulmonary edema and cardiogenic shock. 

The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.  

 

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References

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Question Of The Day #56

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

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

  • A) Hypovolemic shock
  • B) Distributive shock
  • C) Obstructive shock
  • D) Cardiogenic shock

This trauma patient arrives with hypotension, tachycardia, absent unilateral lung sounds, and distended neck veins. This should raise high concern for tension pneumothorax, which is a type of obstructive shock (Choice C). This diagnosis should be made clinically without X-ray imaging. Bedside ultrasound can assist in making the diagnosis by looking for bilateral lung sliding, if available. Treatment of tension pneumothorax should be prompt and includes needle decompression followed by tube thoracostomy. Other types of shock outlined in Choices A, B, and D do not fit the clinical scenario with information that is given.

Recall that shock is an emergency medical state characterized by cardiovascular or circulatory failure. Shock prevents peripheral tissues from receiving adequate perfusion, resulting in organ dysfunction and failure. Shock can be categorized as hypovolemic, distributive, obstructive, or cardiogenic. The different categories of shock are defined by their underlying cause (i.e., sepsis, hemorrhage, pulmonary embolism, etc.) and their hemodynamics which sometimes overlap. The diagnosis of shock is largely clinical and supported by the history, vital signs, and physical exam. Additional studies, such as laboratory investigations, bedside ultrasound, and imaging tests help narrow down the type of shock, potential triggers, and guide management. The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.

 

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References

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Question Of The Day #55

question of the day
~ Joseph Ciano, USA ~ Leave a comment
738.2 - STEMI
Which of the following is the most likely cause for this patient’s condition?  
  • A) Hypovolemia
  • B) Systemic infection
  • C) Pulmonary embolism
  • D) Poor cardiac output

This patient presents with chest pressure at rest and an anterior ST segment elevation myocardial infraction (STEMI) seen on 12-lead EKG.  This patient should be given aspirin, IV fluids to increase the preload status, and receive immediate coronary reperfusion therapy.  This patient’s hypotension is likely due to infarction of the left ventricle causing poor cardiac output (Choice D).  This is known as cardiogenic shock.  The patient has been vomiting, but the acute onset of symptoms and STEMI on EKG make poor cardiac output (Choice D) more likely than hypovolemia (Choice A) as the cause for the patient’s condition.  Systemic infection (Choice B) and pulmonary embolism (Choice C) are also less likely given the clinical information in the case and the STEMI on EKG.  The best answer is Choice D.  Please see the chart below for further detailing of the different types of shock.   

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References

[cite]

Acute Atrial Fibrillation in the ED: Almost all goes home

~ Israa M Salih, UAE ~ Leave a comment

Atrial fibrillation (AF) is the most common dysrhythmia presenting to ED. The management options depend on patient stability, presence of underlying causes and factors in the patient history. In stable patients presenting in AF with a rapid ventricular response, both rate and rhythm control are acceptable approaches. Physicians often tend toward rate control because evidence has shown no mortality benefit between the two approaches. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial contributed to this trend when it concluded no survival advantage and higher risk of adverse drug effects with rhythm control. However, rhythm control is the preferred approach for the management of acute stable AF in Canadian guidelines. The advantages are a higher rate of symptom resolution, restoration of sinus rhythm and avoiding the need for rate control prescriptions, decreased ED length of stay, and hospital admissions.

In the electrical versus pharmacological cardioversion for emergency department patients with acute atrial fibrillation (RAFF2) trial, it was found that both drug–shock and shock-only strategies were effective, rapid, and safe with 96% of patients discharged home in sinus rhythm. The drug infusion worked for 50% of patients avoiding procedural sedation.

The evidence that supports the management of acute AF in the ED without hospital admission is increasing. Implementing practices to achieve that will markedly decrease the burden on the health care system.

ED Management

Approach of Atrial fibrillation

AF might be secondary to variable causes, including ACS, Heart failure, PE, sepsis and bleeding. In patients with secondary AF, cardioversion might be harmful, and the mainstay of treatment is tackling the underlying cause. Those patients will require hospital admission. For primary AF, if the patient is unstable, electrical cardioversion should be done without delay. Stable primary AF may be managed with rate or rhythm control.

Rate control can be achieved with the following:

CCB: Diltiazim 0.25 mg/kg over ten mins, repeat q15-20 mins, up to three doses (avoid in heart failure)

BB: Metoprolol 2.5-5 mg q15-20 mins

Digoxin: 0.25-0.5 mg loading dose then 0.25 mg q4-6 hs (if hypotension or acute HF occur)

Target is HR <100 at rest or <110 walking

Rhythm control is safe with the following according to The CAEP AF best practice guidelines:

  1. Anticoagulated for three or more weeks.
  2. No valvular heart disease, prior stroke or TIA plus: 
  • Onset in 12 hours or less
  • Onset more than 12 hours but less than 48 hours plus less than two of :
    • Age less than 65, DM, HTN, HF.
  • Cleared by TOE

Methods:

  • Procainamide 15mg/kg in 500 ml of NS over an hour.

Other agents: Amiodarone, Ibutilide, flecainide, etc.

  • Electrical: 150-200 J synchronized. Requires sedation.

Anticoagulation:

If CHADS positive then discharge on DOAC or Warfarin.

Disposition:

Almost all patients can be discharged home after cardioversion or effective rate control with appropriate follow up: within a week if warfarin or rate control agent prescribed, otherwise in 4 weeks.

Patients will require admission if one of the following:

  • Highly symptomatic after treatment.
  • ACS
  • Acute heart failure not improved in the ED

References and Further Reading

  1. Stiell, I. G., Macle, L., & CCS Atrial Fibrillation Guidelines Committee (2011). Canadian Cardiovascular Society atrial fibrillation guidelines 2010: management of recent-onset atrial fibrillation and flutter in the emergency department. The Canadian journal of cardiology, 27(1), 38–46. https://doi.org/10.1016/j.cjca.2010.11.014
  2. Wyse, D. G., Waldo, A. L., DiMarco, J. P., Domanski, M. J., Rosenberg, Y., Schron, E. B., Kellen, J. C., Greene, H. L., Mickel, M. C., Dalquist, J. E., Corley, S. D., & Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators (2002). A comparison of rate control and rhythm control in patients with atrial fibrillation. The New England journal of medicine, 347(23), 1825–1833. https://doi.org/10.1056/NEJMoa021328
  3. Baymon, D. E., & Baugh, C. E. (2020). Patients with Atrial Fibrillation in the Emergency Department: Strategies to Achieve Best Outcomes. https://www.hmpgloballearningnetwork.com/site/eplab/patients-atrial-fibrillation-emergency-department-strategies-achieve-best-outcomes
  4. Martín, A., Coll-Vinent, B., Suero, C., Fernández-Simón, A., Sánchez, J., Varona, M., Cancio, M., Sánchez, S., Carbajosa, J., Malagón, F., Montull, E., Del Arco, C., & HERMES-AF investigators (2019). Benefits of Rhythm Control and Rate Control in Recent-onset Atrial Fibrillation: The HERMES-AF Study. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 26(9), 1034–1043. https://doi.org/10.1111/acem.13703
  5. Stiell, I. G., Sivilotti, M., Taljaard, M., Birnie, D., Vadeboncoeur, A., Hohl, C. M., McRae, A. D., Rowe, B. H., Brison, R. J., Thiruganasambandamoorthy, V., Macle, L., Borgundvaag, B., Morris, J., Mercier, E., Clement, C. M., Brinkhurst, J., Sheehan, C., Brown, E., Nemnom, M. J., Wells, G. A., … Perry, J. J. (2020). Electrical versus pharmacological cardioversion for emergency department patients with acute atrial fibrillation (RAFF2): a partial factorial randomised trial. Lancet (London, England), 395(10221), 339–349. https://doi.org/10.1016/S0140-6736(19)32994-0
  6. Ian G. Stiell, et al. (2021). 2021 CAEP Acute Atrial Fibrillation/Flutter Best Practices Checklist.https://caep.ca/wp-content/uploads/2021/06/2021-CAEP-AAF-Checklist-FINAL-6-June-2021.pdf
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Defibrillator: Clear!

Defibrillator clear
~ Jule Santos, Brasil ~ Leave a comment

So, this is your first day at your internship rotation in the Emergency Department. You see some movement in the resuscitation room, and someone shouts: CODE!

Then, you approach the team, excited to learn and help with cardiopulmonary resuscitation (CPR). The attending physician looks at you and asks: Do you know how to use the defibrillator?

What would your answer be?

Knowing the main functions of the defibrillator is essential but not enough; you need to get used to the model in your hospital to be able to help safely with an emergency.

Defibrillators are devices used to apply electrical energy manually or automatically. Their use is indicated for electrical cardioversion, defibrillation or as a transcutaneous pacemaker.

Later that day, another patient presents with unstable atrial fibrillation (AFib).

The attending suggests cardioverting the patient. Do you know how to prepare the defibrillator?

Defibrillation versus cardioversion

Both defibrillation and cardioversion are techniques in which an electrical current is applied to the patient, through a defibrillator, to reverse a cardiac arrhythmia.

Defibrillation

Defibrillation is a non-synchronized electrical discharge applied to the chest, which aims to depolarize all myocardial muscle fibres, thus literally restarting the heart, allowing the sinoatrial node to resume the generation and control of the heart rhythm, and reversing the severe arrhythmias. It is indicated for pulseless ventricular tachycardia and ventricular fibrillation during CPR.

Electrical Cardioversion

Electrical cardioversion is the application of shock in a synchronized way to ensure the electric discharge is released in the R wave, that is, in the refractory period because accidental delivery of the shock during the vulnerable period, that is, the T wave, can trigger VF. It is reserved for severe arrhythmias in unstable patients with a pulse. It can usually be an elective procedure.

Special Situations

Digital Intoxication

Digital intoxication can present with any type of tachyarrhythmia or bradyarrhythmia. Cardioversion in this situation is a relative contraindication, as digital makes the heart sensitive to electrical stimulation. Before considering cardioversion, correct all electrolyte imbalances, otherwise, the cardioversion can degenerate the rhythm to a VF.

Pacemaker / Implantable cardioverter-defibrillator (ICD)

Cardioversion can be performed, but with care. The inadequate technique can damage the generator, the conductive system, or the heart muscle, leading to dysfunction of the device. The blades must be positioned at least 12 cm away from the generator, preferably in the anteroposterior position. The lowest possible electrical charge must be used.

Pregnancy

Cardioversion can be used safely during pregnancy. The fetal beat should be monitored throughout the procedure.

Things To Consider

Keep your devices tested!

Working in the ED is not easy. This is the place where organization and preparation should be routine. Constant checking of materials and operation of the equipment must be the rule because the smallest detail can cause a difference in saving a life.

During adversity, it is necessary to remain calm, trying to not affect the reasoning and disposition of the team. It is an arduous job, it takes practice and a lot of effort. Errors can only be corrected after they are recognized and must have the right time to be exposed. It happens.

There is no time for despair, yelling and stress when it comes to CPR.

No conductive gel, what can we do?

The main guidelines regarding the use of the conductive gel used in the defibrillator paddles are:

  • Using the proper gel for this purpose is essential. The gel is an electrically conductive material that decreases the resistance to the flow of electric current between the paddle and the chest wall. The absence of conductive material can lead to the production of an arc that causes burns in the patient and the risk of explosion if there is an oxygen source very close, among others.
  • Avoid the use of gauze soaked in saline solution, as the excess serum can cause burns on the patient’s skin, but it is a reasonable option, in an emergency
  • Do not use the ultrasound gel
  • The preference is to use adhesive paddles that already come with their own conductive gel (but this is rare in Brazil).

Location recommended by Advanced Cardiac Life Support (ACLS)

Antero-lateral

One paddle is placed on the right side of the sternum, right below the clavicle and the other laterally where the cardiac appendix would be in the anterior or medial axillary line (V5-V6).

Adhesive paddles can also be placed in an anteroposterior position: The anterior one is placed in the cardiac appendage or precordial region, and the posterior one is placed on the back in the right or left infrascapular region.

During the shock, the provider must ensure that no one is in contact with the patient. A force of approximately 8k must be used to increase the contact of the paddles with the chest. Do not allow a continuous flow of oxygen over the patient’s chest to avoid accidents with sparks.

Complications

  • Electric arc (when electricity travels through the air between the electrodes and can cause explosive noises, burns and impair current delivery)
  • Electrical injuries in spectators
  • Risk of explosion if there is a continuous flow of oxygen during the shock
  • Burning of the skin by repeated shocks
  • Myocardial injury and post-defibrillation arrhythmias and myocardial stunning
  • Skeletal muscle injury
  • Fracture of thoracic vertebrae

References and Further Reading

  1. Sunde, K., Jacobs, I., Deakin, C. D., Hazinski, M. F., Kerber, R. E., Koster, R. W., Morrison, L. J., Nolan, J. P., Sayre, M. R., & Defibrillation Chapter Collaborators (2010). Part 6: Defibrillation: 2010 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation, 81 Suppl 1, e71–e85. https://doi.org/10.1016/j.resuscitation.2010.08.025
  2. Panchal, A. R., Bartos, J. A., Cabañas, J. G., Donnino, M. W., Drennan, I. R., Hirsch, K. G., Kudenchuk, P. J., Kurz, M. C., Lavonas, E. J., Morley, P. T., O’Neil, B. J., Peberdy, M. A., Rittenberger, J. C., Rodriguez, A. J., Sawyer, K. N., Berg, K. M., & Adult Basic and Advanced Life Support Writing Group (2020). Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation, 142(16_suppl_2), S366–S468. https://doi.org/10.1161/CIR.0000000000000916
  3. Ionmhain, U. N. (2020). Defibrillation Basics. Life in The Fastlane. Retrieved April 26, 2020, from https://litfl.com/defibrillation-basics/
  4. Paradis, N. A., Halperin, H. R., Kern, K. B., Wenzel, V., & Chamberlain, D. A. (Eds.). (2007). Cardiac arrest: the science and practice of resuscitation medicine. Cambridge University Press.
  5. Nickson, C. (2020). Defibrillation Pads and Paddles. Life in The Fastlane. Retrieved April 26, 2020, from https://litfl.com/defibrillation-pads-and-paddles/
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