NBME 10 and 11. Afib, SVT Flashcards
NBME 11 62Q. A 52-year-old man is brought to the emergency department because of a 6-hour history of thirst and fatigue and a 2-hour history of light-headedness. He has been working outside during the past 2 days in temperatures reaching 90.0°F. He has no history of serious illness and takes no medications. ECG - AFIB. BP 95/64; HR 74. NExt step?
Observation only
NBME 11 62Q. afib.
Atrial fibrillation can result from a variety of factors, including dehydration, electrolyte abnormalities, alcohol or illicit drug use, and structural heart disease. For example, mitral stenosis, if severe enough, can result in left atrial enlargement, cardiogenic pulmonary edema, and arrhythmias such as atrial fibrillation and flutter. Hyperthyroidism and thyrotoxicosis are also associated with the development of atrial fibrillation
NBME 11 62Q. afib. what is rapid ventricular response?
pulse >100/min, which can result in reduced stroke volume and decreased cardiac output leading to symptomatic heart failure, and potentially hypotension and hemodynamic instability in severe cases. In these cases, rate- or rhythm-controlling agents and/or synchronized cardioversion may be necessary.
In this case - normal (HR 74)
NBME 11 62Q. afib. in this patient who is hemodynamically stable with a normal ventricular rate, no further interventions are necessary other than intravenous fluid resuscitation for the patient’s dehydration, which will likely improve his symptoms.
He will eventually require evaluation to determine if anticoagulant therapy or rate control will be needed.
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NBME 11 183Q. 67y/o, afib, HR 110; BP 126/70. Not known when started afib.
Tx?
Metoprolol therapy - for rate control
NBME 11 183 Q. afib.
In atrial fibrillation with rapid ventricular response (and in other tachyarrhythmias), diastolic filling time is reduced, so the amount of blood in the ventricles prior to ventricular systole is less than would exist had filling time been sufficient. This results in a reduced stroke volume, decreased cardiac output, symptomatic heart failure, and potentially hypotension and hemodynamic instability in severe cases.
NBME 11 183 Q. afib. 67y/o, afib, HR 110; BP 126/70. Not known when started afib.
Chemical cardioversion - why not?
It is unknown when the atrial fibrillation started and there is a risk for embolization from atrial thrombi and ischemic stroke. Typically, cardioversion is done after several weeks of anticoagulation OR after an echocardiography shows an absence of intracardiac thrombosis.
Emergent electrical cardioversion would only be indicated in a hemodynamically unstable patient.
NBME 10 109 Q. A 23-year-old man comes to the emergency department 45 minutes after the sudden onset of palpitations and mild shortness of breath that began while he was drinking beer with friends. He has not had chest pain or loss of consciousness. He has no history of serious illness and takes no medications. On arrival, he appears anxious. He is alert and fully oriented. His pulse is 138/min and regular, and blood pressure is 100/65 mm Hg; other vital signs are within normal limits. Pulse oximetry on room air shows an oxygen saturation of 99%. The patient’s tachycardia ends abruptly during the examination. The remainder of the examination shows no abnormalities. Which of the following is the most likely diagnosis?
Atrioventricular nodal reentrant tachycardia
NBME 10 109 Q. kiti ats. SVT vs sinus tachy?
Sinus tachycardia typically has a more gradual, ramping onset and decrease. An abrupt change in heart rate is more consistent with a tachyarrhythmia.
NBME 10 109 Q. Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form ….?
form of SVT that occurs in structurally normal hearts and is characterized by a regular rhythm with abrupt onset and termination.
NBME 10 109 Q. Atrioventricular nodal reentrant tachycardia (AVNRT). what provokes?
It can occur spontaneously or be provoked by alcohol, caffeine, exertion, stress, or sympathomimetic medications.
NBME 10 109 Q. In normal sinus rhythm, electrical impulses traverse the AV node via two simultaneous pathways: a fast-conducting, long refractory period pathway and a slow-conducting, short refractory period pathway. The distal end of the fast-conducting pathway interacts with the slow-conducting pathway, triggering the refractory period and preventing a second impulse from being transmitted to the ventricles. However, if the slow pathway is then activated by a premature atrial beat (as may occur spontaneously or provoked as above), the slow pathway may conduct an impulse that then reaches the distal end of the fast pathway as the refractory period ends, allowing the impulse to be transmitted in a retrograde fashion through the AV node and setting up a reentry circuit.
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NBME 10 109 Q. Atrioventricular nodal reentrant tachycardia (AVNRT). initial Tx?
vagal maneuvers, adenosine, calcium channel blockers, or β-adrenergic blockers.
NBME 10 109 Q. Atrioventricular nodal reentrant tachycardia (AVNRT). If HD unstable?
electrical cardioversion.
NBME 10 109 Q. kiti ats. AVNRT vs Multifocal atrial tachycardia vs wandering atrial pacemaker?
Multifocal atrial tachycardia (Choice C) is characterized by an irregularly irregular rhythm and polymorphic P waves. It is associated with chronic pulmonary disease.
Patients with polymorphic P waves but a normal heart rate are described as having a wandering atrial pacemaker (Choice F).
NBME 10 109 Q. kiti ats. AVNRT.
Ventricular tachycardia (Choice E) is more often associated with underlying structural heart disease.
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NBME 10 166 Q.
An 18-year-old man has the sudden onset of rapid, pounding heartbeats. A previous episode occurred while he was drinking coffee and resolved abruptly after 30 minutes. His pulse is 180/min, respirations are 15/min, and blood pressure is 105/85 mm Hg. Examination shows no other abnormalities. Which of the following is the most likely diagnosis?
Paroxysmal supraventricular tachycardia
NBME 10 166 Q. SVT. where originates?
CP?
Provokes what?
Abnormally rapid heart rate and rhythm originating from above the ventricles, typically with a narrow QRS complex on ECG.
Patients with SVT can manifest with acute symptoms of light-headedness, palpitations, diaphoresis, and syncope.
SVT is typically a result of structural defects in the His-Purkinje system causing a reentrant pathway, such as in Wolff-Parkinson-White syndrome, but may also occur in structurally normal hearts spontaneously OR provoked by alcohol, caffeine, exertion, stress, or sympathomimetic medications.
NBME 10 166 Q. SVT. Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of paroxysmal SVT.
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NBME 10 166 Q. SVT. kiti ats. Paroxysmal ventricular tachycardia (Choice D) is more commonly associated with??
With underlying structural heart disease. Potentially life-threatening because of loss of adequate cardiac output and risk for devolving into ventricular fibrillation. SVT is more likely in a young, otherwise healthy patient.
NBME 10 166 Q. SVT. kiti ats.
Premature atrial beats (Choice E) are fairly common and typically present in isolation, often asymptomatic or with the patient experiencing a “skipped beat” sensation. Premature atrial beats occur more often in the presence of structural heart disease.
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NBME 10 166 Q. SVT. kiti ats.
Premature ventricular beats (Choice F) are common and increase in prevalence with age and medical comorbidities. They are typically benign and asymptomatic.
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NBME 11 4 Q. PEDS. 7-month-old girl + 2-day history of rapid breathing, sweating, pallor, decreased feeding, and increased fussiness. Pulse is 220/min, respirations are 48/min, and blood pressure is 62/42 mm Hg. Capillary refill time is 3 seconds. An ECG shows narrow complex tachycardia. NEXT STEP IN MX?
Intravenous adenosine therapy
NBME 11 4 Q. PEDS. SVT - commonly occurs in children and infants, and is characterized by paroxysmal episodes of rapid, narrow-complex tachycardia. Causes?
SVT is often idiopathic and paroxysmal but may occur secondary to accessory pathways in some children with Wolff-Parkinson-White syndrome.
NBME 11 4 Q. PEDS. SVT - how Dx is made?
Diagnosis is made by ECG, although some children may require cardiac monitoring to capture a paroxysmal event.
NBME 11 4 Q. PEDS. SVT - Tx?
AV nodal blockade with intravenous adenosine therapy is the first-line treatment for narrow complex SVT.
NBME 11 4 Q. PEDS. SVT - if adenosine fails –> what to do?
If adenosine fails, synchronized cardioversion may be attempted.
NBME 11 4 Q. PEDS. SVT - in older kids what can be done?
Children who are old enough may be trained to use vagal maneuvers to naturally induce AV nodal blockade. A similar vagal maneuver may be attempted by placing an ice bag over the eyes and face for approximately 30 seconds.
NBME 11 4 Q. PEDS. SVT - adenosine and vagal manouvers not effecitve –> second line drug?
Intravenous propranolol therapy (Choice E) can be utilized as a second-line agent if vagal maneuvers and intravenous adenosine fail to abort the tachyarrhythmia.
NBME 11 131Q. PEDS.
A previously healthy 3-month-old boy is brought to the physician because of a 24-hour history of increasingly rapid breathing, difficulty feeding, and progressive fussiness.His pulse is 250/min, respirations are 68/min, and blood pressure is 80/50 mm Hg. Shown ECG - tachy. Dx?
Supraventricular tachycardia
INBME 11 131Q. PEDS. infants who present with SVT typically have a pulse..???
pulse between 220 and 280/min
INBME 11 131Q. PEDS. SVT. For patients who are hemodynamically stable, attempts can be made to terminate the tachyarrhythmia by vagal maneuvers (eg, ice or cold water over the face) or with adenosine.
Unstable - cardioversion is indicated
