Arrhythmias Flashcard 1

B. Rationale: Emergency cardiovascular care guidelines suggest that transcutaneous pacing is probably indicated if patients with bradycardia are unresponsive to drugs.

C. Rationale: This patient likely has significant internal bleeding from his multiple traumatic injuries. Cardiac arrest is most likely secondary to hypovolemia from the blood loss. As this is an extracardiac problem leading to hypovolemia, he will likely have PEA. PEA is a common finding in hypoxia and hypovolemia, which are highly treatable causes of cardiac arrest. The patient will need volume resuscitation and management of any ongoing sources of bleeding. It is unlikely that a young, healthy individual will have any another cardiac arrest arrhythmia with hypovolemia as a cause for the arrest.

B. Rationale: This patient has hemodynamic instability from bradycardia that has failed standard therapy. TCP can be used as a temporizing mechanism. The ECG shows bradycardia with a wide QRS. The pacer spikes are noted as negative square deflections, however, there is no subsequent QRS wave with the T waves. Consequently, capture is not occurring. The initial step to manage this is to increase the pacer current to above the threshold needed to capture. Following this, adjusting the pacer pads may be necessary. It is also important to ensure there are no comorbidities interfering with capture such as intrathoracic air (pneumothorax), fluid (pericardial effusion) or severe hyperkalemia. There has been no capture, so it is unlikely the pulse will be changed. It is premature to start chest compressions when capture has not occurred, although this may be the next step if capture occurs and the patient is still pulseless. The patient does not have a shockable rhythm at this point. A large electrical artifact from the pacer can obscure a shockable rhythm. While this may be a finding if monitor blanking is not completed, ensuring capture will be the first step before looking for underlying VF. Additionally, the pulse should be checked again before defibrillation.

A. Rationale: This man likely has an AV node reentry tachycardia (or AVNRT). This can be due to an alternate conduction pathway, or it can occur in healthy individuals with stimulants or environmental factors such as caffeine, hypoxia, tachycardia, or anxiety. It can also be seen in patients with underlying cardiac or pulmonary conditions such as CAD. ECG findings of a sudden run of narrow QRS tachycardia that resolves spontaneously suggests the diagnosis. The initial symptomatic treatment is vagal stimulation or adenosine. In a patient with increasing frequency and no known stimulus, the team should assess for an underlying etiology. Amiodarone or digoxin are not the initial treatment in a mildly symptomatic patient.

B. Rationale: This patient likely has hyperkalemia. He has several risk factors (renal failure and medication history), signs of potassium toxicity, and ECG findings consistent with increased potassium (e.g., peaked T waves and wide QRS). While hypokalemia can also lead to weakness, the associated ECG changes are different (e.g., flattened T waves and wide QRS), and it is typically associated with GI or renal losses rather than chronic renal failure. Sodium changes (hypo- or hypernatremia) are less likely to cause such significant ECG findings. Typically, there will be more neurologic abnormalities, including confusion, irritability, and seizures. Sodium abnormalities are typically associated with total body water changes.

A. Rationale: Even though the rhythm looks like sinus bradycardia, the fact that there is no pulse means that the patient is in cardiac arrest secondary to pulseless electrical activity. Rescuers must recognize this as soon as possible so that high-quality CPR can be provided immediately. (ACLS Case: Adult Cardiac Arrest: Dynamic PEA rhythm)

B. Rationale: The patient has atrial fibrillation. He is at increased risk for stroke or transient ischemic attack (TIA) in the long term due to the risk of thrombus from the atrium to the cerebral circulation causing a stroke. Atrial fibrillation is associated with many underlying cardiac and pulmonary conditions, such as ACS, valvular disease, and pulmonary emboli.

C. Rationale: Bradyarrhythmia’s that are unlikely to respond to atropine are second-degree AV block (Mobitz type 2) and third-degree AV block or a block of non-nodal origin.

B. Rationale: One of the important factors for successful advanced cardiac life support is the shortest time to defibrillation. When a shockable rhythm is diagnosed, then defibrillation should not be delayed.

D. Rationale: Wide QRS tachycardia is typically assumed to originate in the ventricles, however, this is not always the case. With a left bundle branch block, a supraventricular tachycardia can appear wide due to the slowed conduction via the right bundle branch. Polymorphic wide QRS should be managed similarly to VF, with defibrillation. Adenosine is used for symptomatic tachycardias but is not used in the management of unstable wide QRS tachycardias. It can help differentiate a supraventricular from ventricular etiology. However, there is a risk of VF in this case. Verapamil should not be given to patients with ventricular tachycardias as this can precipitate hemodynamically significant hypotension.