Nirosshan Thiruchelvam, MD

A 43-year-old man with no medical history presented with pain and swelling in his left arm for 2 weeks. He was a regular weight lifter, and his exercise routine included repetitive hyperextension and hyperabduction of his arms while lifting heavy weights.

He had no history of recent trauma or venous cannulation of the left arm. His family history was negative for thrombophilic disorders. Physical examination revealed a swollen and erythematous left arm and visible venous collaterals at the neck, shoulder, and chest. There was no evidence of arterial insufficiency.

Duplex ultrasonography confirmed thrombosis of the left brachial, axillary, and subclavian veins. Further evaluation with computed tomography showed no intrathoracic mass but revealed several subsegmental pulmonary thrombi in the right lung. A screen for thrombophilia was negative. Venography confirmed complete thrombotic occlusion of the subclavian, axillary, and brachial veins (Figure 1).

Catheter-directed thrombolysis with tissue plasminogen activator resulted in complete resolution of the thrombosis, but venography after 3 days of thrombolysis showed 50% residual stenosis of the left subclavian vein where it passes under the first rib (Figure 2). The redness and swelling had markedly improved 2 days after thrombolytic therapy. He was discharged home on rivaroxaban 20 mg daily.

Follow-up venography 2 months later (Figure 3), with the patient performing hyperabduction of the arms, showed a patent subclavian vein with no thrombosis, but dynamic compression and occlusion of the subclavian vein where it passes the first rib. Magnetic resonance imaging (MRI) of the neck showed no cervical (ie, extra) rib and no soft-tissue abnormalities of the scalene triangle.

Following this, the patient underwent resection of the left first rib for decompression of the venous thoracic outlet, which resulted in resolution of his symptoms. He remained asymptomatic at 6-month follow-up.

PAGET-SCHROETTER SYNDROME

Paget-Schroetter syndrome, also referred to as effort-induced or effort thrombosis, is thrombosis of the axillary or subclavian vein associated with strenuous and repetitive activity of the arms. Anatomic abnormalities at the thoracic outlet—cervical rib, congenital bands, hypertrophy of scalene tendons, abnormal insertion of the costoclavicular ligament—and repetitive trauma to the endothelium of the subclavian vein are key factors in its initiation and progression.

The condition is seen primarily in young people who participate in strenuous activities such as rowing, weight lifting, and baseball pitching. It is estimated to be the cause of 40% of cases of primary upper-extremity deep vein thrombosis in the absence of an obvious risk factor or trigger such as a central venous catheter, pacemaker, port, or occult malignancy.¹

A provocative test such as the Adson test or hyperabduction test during MRI or venography helps confirm thoracic outlet obstruction by demonstrating dynamic obstruction.²

TREATMENT CONSIDERATIONS

There are no universal guidelines for the treatment of Paget-Schroetter syndrome. However, the available data^3–5 suggest a multimodal approach that involves early catheter-directed thrombolysis and subsequent surgical decompression of the thoracic outlet. This can restore venous patency and reduce the risk of long-term complications such as rethrombosis and postthrombotic syndrome.^3–5

Surgical treatment includes resection of the first rib and division of the scalene muscles and the costoclavicular ligament. MRI with provocative testing helps guide the surgical approach. Anticoagulation therapy alone—ie, without thrombolysis and surgical decompression—is inadequate as it leads to recurrence of thrombosis and residual symptoms.⁶

Paget-Schroetter syndrome should not be managed the same as lower-extremity deep vein thrombosis because the cause and the exacerbating factors are different.

Unanswered questions

Because we have no data from randomized controlled trials, questions about management remain. What should be the duration of anticoagulation, especially in the absence of coexisting thrombophilia? Is thrombophilia screening useful? What is the optimal timing for starting thrombolytic therapy?

A careful history and heightened suspicion are required to make this diagnosis. If undiagnosed, it carries a risk of significant long-term morbidity and death. Dynamic obstruction during venography, in addition to MRI, can help identify an anatomic obstruction.

A 43-year-old man with no medical history presented with pain and swelling in his left arm for 2 weeks. He was a regular weight lifter, and his exercise routine included repetitive hyperextension and hyperabduction of his arms while lifting heavy weights.

He had no history of recent trauma or venous cannulation of the left arm. His family history was negative for thrombophilic disorders. Physical examination revealed a swollen and erythematous left arm and visible venous collaterals at the neck, shoulder, and chest. There was no evidence of arterial insufficiency.

Duplex ultrasonography confirmed thrombosis of the left brachial, axillary, and subclavian veins. Further evaluation with computed tomography showed no intrathoracic mass but revealed several subsegmental pulmonary thrombi in the right lung. A screen for thrombophilia was negative. Venography confirmed complete thrombotic occlusion of the subclavian, axillary, and brachial veins (Figure 1).

Catheter-directed thrombolysis with tissue plasminogen activator resulted in complete resolution of the thrombosis, but venography after 3 days of thrombolysis showed 50% residual stenosis of the left subclavian vein where it passes under the first rib (Figure 2). The redness and swelling had markedly improved 2 days after thrombolytic therapy. He was discharged home on rivaroxaban 20 mg daily.

Follow-up venography 2 months later (Figure 3), with the patient performing hyperabduction of the arms, showed a patent subclavian vein with no thrombosis, but dynamic compression and occlusion of the subclavian vein where it passes the first rib. Magnetic resonance imaging (MRI) of the neck showed no cervical (ie, extra) rib and no soft-tissue abnormalities of the scalene triangle.

Following this, the patient underwent resection of the left first rib for decompression of the venous thoracic outlet, which resulted in resolution of his symptoms. He remained asymptomatic at 6-month follow-up.

PAGET-SCHROETTER SYNDROME

Paget-Schroetter syndrome, also referred to as effort-induced or effort thrombosis, is thrombosis of the axillary or subclavian vein associated with strenuous and repetitive activity of the arms. Anatomic abnormalities at the thoracic outlet—cervical rib, congenital bands, hypertrophy of scalene tendons, abnormal insertion of the costoclavicular ligament—and repetitive trauma to the endothelium of the subclavian vein are key factors in its initiation and progression.

The condition is seen primarily in young people who participate in strenuous activities such as rowing, weight lifting, and baseball pitching. It is estimated to be the cause of 40% of cases of primary upper-extremity deep vein thrombosis in the absence of an obvious risk factor or trigger such as a central venous catheter, pacemaker, port, or occult malignancy.¹

A provocative test such as the Adson test or hyperabduction test during MRI or venography helps confirm thoracic outlet obstruction by demonstrating dynamic obstruction.²

TREATMENT CONSIDERATIONS

There are no universal guidelines for the treatment of Paget-Schroetter syndrome. However, the available data^3–5 suggest a multimodal approach that involves early catheter-directed thrombolysis and subsequent surgical decompression of the thoracic outlet. This can restore venous patency and reduce the risk of long-term complications such as rethrombosis and postthrombotic syndrome.^3–5

Surgical treatment includes resection of the first rib and division of the scalene muscles and the costoclavicular ligament. MRI with provocative testing helps guide the surgical approach. Anticoagulation therapy alone—ie, without thrombolysis and surgical decompression—is inadequate as it leads to recurrence of thrombosis and residual symptoms.⁶

Paget-Schroetter syndrome should not be managed the same as lower-extremity deep vein thrombosis because the cause and the exacerbating factors are different.

Unanswered questions

Because we have no data from randomized controlled trials, questions about management remain. What should be the duration of anticoagulation, especially in the absence of coexisting thrombophilia? Is thrombophilia screening useful? What is the optimal timing for starting thrombolytic therapy?

A careful history and heightened suspicion are required to make this diagnosis. If undiagnosed, it carries a risk of significant long-term morbidity and death. Dynamic obstruction during venography, in addition to MRI, can help identify an anatomic obstruction.

A 43-year-old man with no medical history presented with pain and swelling in his left arm for 2 weeks. He was a regular weight lifter, and his exercise routine included repetitive hyperextension and hyperabduction of his arms while lifting heavy weights.

He had no history of recent trauma or venous cannulation of the left arm. His family history was negative for thrombophilic disorders. Physical examination revealed a swollen and erythematous left arm and visible venous collaterals at the neck, shoulder, and chest. There was no evidence of arterial insufficiency.

Duplex ultrasonography confirmed thrombosis of the left brachial, axillary, and subclavian veins. Further evaluation with computed tomography showed no intrathoracic mass but revealed several subsegmental pulmonary thrombi in the right lung. A screen for thrombophilia was negative. Venography confirmed complete thrombotic occlusion of the subclavian, axillary, and brachial veins (Figure 1).

Catheter-directed thrombolysis with tissue plasminogen activator resulted in complete resolution of the thrombosis, but venography after 3 days of thrombolysis showed 50% residual stenosis of the left subclavian vein where it passes under the first rib (Figure 2). The redness and swelling had markedly improved 2 days after thrombolytic therapy. He was discharged home on rivaroxaban 20 mg daily.

Follow-up venography 2 months later (Figure 3), with the patient performing hyperabduction of the arms, showed a patent subclavian vein with no thrombosis, but dynamic compression and occlusion of the subclavian vein where it passes the first rib. Magnetic resonance imaging (MRI) of the neck showed no cervical (ie, extra) rib and no soft-tissue abnormalities of the scalene triangle.

Following this, the patient underwent resection of the left first rib for decompression of the venous thoracic outlet, which resulted in resolution of his symptoms. He remained asymptomatic at 6-month follow-up.

PAGET-SCHROETTER SYNDROME

Paget-Schroetter syndrome, also referred to as effort-induced or effort thrombosis, is thrombosis of the axillary or subclavian vein associated with strenuous and repetitive activity of the arms. Anatomic abnormalities at the thoracic outlet—cervical rib, congenital bands, hypertrophy of scalene tendons, abnormal insertion of the costoclavicular ligament—and repetitive trauma to the endothelium of the subclavian vein are key factors in its initiation and progression.

The condition is seen primarily in young people who participate in strenuous activities such as rowing, weight lifting, and baseball pitching. It is estimated to be the cause of 40% of cases of primary upper-extremity deep vein thrombosis in the absence of an obvious risk factor or trigger such as a central venous catheter, pacemaker, port, or occult malignancy.¹

A provocative test such as the Adson test or hyperabduction test during MRI or venography helps confirm thoracic outlet obstruction by demonstrating dynamic obstruction.²

TREATMENT CONSIDERATIONS

There are no universal guidelines for the treatment of Paget-Schroetter syndrome. However, the available data^3–5 suggest a multimodal approach that involves early catheter-directed thrombolysis and subsequent surgical decompression of the thoracic outlet. This can restore venous patency and reduce the risk of long-term complications such as rethrombosis and postthrombotic syndrome.^3–5

Surgical treatment includes resection of the first rib and division of the scalene muscles and the costoclavicular ligament. MRI with provocative testing helps guide the surgical approach. Anticoagulation therapy alone—ie, without thrombolysis and surgical decompression—is inadequate as it leads to recurrence of thrombosis and residual symptoms.⁶

Paget-Schroetter syndrome should not be managed the same as lower-extremity deep vein thrombosis because the cause and the exacerbating factors are different.

Unanswered questions

Because we have no data from randomized controlled trials, questions about management remain. What should be the duration of anticoagulation, especially in the absence of coexisting thrombophilia? Is thrombophilia screening useful? What is the optimal timing for starting thrombolytic therapy?

A careful history and heightened suspicion are required to make this diagnosis. If undiagnosed, it carries a risk of significant long-term morbidity and death. Dynamic obstruction during venography, in addition to MRI, can help identify an anatomic obstruction.

A 49-year-old woman with a history of depression, bipolar disorder, and chronic back pain was brought to the emergency department unresponsive after having taken an unknown quantity of amitriptyline tablets.

On arrival, she was comatose, with a score of 3 (the lowest possible score) on the 15-point Glasgow Coma Scale. Her blood pressure was 65/22 mm Hg, heart rate 121 beats per minute, respiratory rate 14 per minute, and oxygen saturation 88% on room air. The rest of the initial physical examination was normal.

She was immediately intubated, put on mechanical ventilation, and given an infusion of a 1-L bolus of normal saline and 50 mmol (1 mmol/kg) of sodium bicarbonate. Norepinephrine infusion was started. Gastric lavage was not done.

Results of initial laboratory testing showed a serum potassium of 2.9 mmol/L (reference range 3.5–5.0) and a serum magnesium of 1.6 mmol/L (1.7–2.6), which were corrected with infusion of 60 mmol of potassium chloride and 2 g of magnesium sulfate. The serum amitriptyline measurement was ordered at the time of her presentation to the emergency department.

Arterial blood gas analysis showed:

• pH 7.15 (normal range 7.35–7.45)
• Paco₂ 66 mm Hg (34–46)
• Pao₂ 229 mm Hg (85–95)
• Bicarbonate 22 mmol/L (22–26).

The initial electrocardiogram (ECG) (Figure 1) showed regular wide-complex tachycardia with no definite right or left bundle branch block morphology, no discernible P waves, a QRS duration of 198 msec, right axis deviation, and no Brugada criteria to suggest ventricular tachycardia.

She remained hypotensive, with regular wide-complex tachycardia on the ECG. She was given an additional 1-L bolus of normal saline and 100 mmol (2 mmol/kg) of sodium bicarbonate, and within 1 minute the wide-complex tachycardia resolved to narrow-complex sinus tachycardia (Figure 2). At this point, an infusion of 150 mmol/L of sodium bicarbonate in dextrose 5% in water was started, with serial ECGs to monitor the QRS duration and serial arterial blood gas monitoring to maintain the pH between 7.45 and 7.55.

TRANSFER TO THE ICU

She was then transferred to the intensive care unit (ICU), where she remained for 2 weeks. While in the ICU, she had a single recurrence of wide-complex tachycardia that resolved immediately with an infusion of 100 mmol of sodium bicarbonate. A urine toxicology screen was negative, and the serum amitriptyline measurement, returned from the laboratory 48 hours after her initial presentation, was 594 ng/mL (reference range 100–250 ng/mL). She was eventually weaned off the norepinephrine infusion after 20 hours, the sodium bicarbonate infusion was discontinued after 4 days, and she was taken off mechanical ventilation after 10 days. Also during her ICU stay, she had seizures on day 3 and developed aspiration pneumonia.

From the ICU, she was transferred to a regular floor, where she stayed for another week and then was transferred to a rehabilitation center. This patient was known to have clinical depression and to have attempted suicide once before. She had recently been under additional psychosocial stresses, which likely prompted this second attempt.

She reportedly had no neurologic or cardiovascular sequelae after her discharge from the hospital.

AMITRIPTYLINE OVERDOSE

Amitriptyline causes a relatively high number of fatal overdoses, at 34 per 1 million prescriptions.¹ Death is usually from hypotension and ventricular arrhythmia caused by blockage of cardiac fast sodium channels leading to disturbances of cardiac conduction such as wide-complex tachycardia.

Other manifestations of amitriptyline overdose include seizures, sedation, and anticholinergic toxicity from variable blockade of gamma-aminobutyric acid receptors, histamine 1 receptors, and alpha receptors.²

In amitriptyline overdose, sinus tachycardia is the most common finding on ECG

Of the various changes on ECG described with amitriptyline overdose, sinus tachycardia is the most common. A QRS duration greater than 100 msec, right to extreme-right axis deviation with negative QRS complexes in leads I and aVL, and an R-wave amplitude greater than 3 mm in lead aVR are indications for sodium bicarbonate infusion, especially in hemodynamically unstable patients.³ Sodium bicarbonate increases the serum concentration of sodium and thereby overcomes the sodium channel blockade. It also alkalinizes the serum, favoring an electrically neutral form of amitriptyline that binds less to receptors and binds more to alpha-1-acid glycoprotein, decreasing the fraction of free drug available for toxicity.⁴

In patients with amitriptyline overdose, wide-complex tachycardia and hypotension refractory to sodium bicarbonate infusion can be treated with lidocaine, magnesium sulfate, direct-current cardioversion, and lipid resuscitation.^5,6 Treatment with class IA, IC, and III antiarrhythmics is contraindicated, as they block sodium channels and thus can worsen conduction disturbances.

A 49-year-old woman with a history of depression, bipolar disorder, and chronic back pain was brought to the emergency department unresponsive after having taken an unknown quantity of amitriptyline tablets.

On arrival, she was comatose, with a score of 3 (the lowest possible score) on the 15-point Glasgow Coma Scale. Her blood pressure was 65/22 mm Hg, heart rate 121 beats per minute, respiratory rate 14 per minute, and oxygen saturation 88% on room air. The rest of the initial physical examination was normal.

She was immediately intubated, put on mechanical ventilation, and given an infusion of a 1-L bolus of normal saline and 50 mmol (1 mmol/kg) of sodium bicarbonate. Norepinephrine infusion was started. Gastric lavage was not done.

Results of initial laboratory testing showed a serum potassium of 2.9 mmol/L (reference range 3.5–5.0) and a serum magnesium of 1.6 mmol/L (1.7–2.6), which were corrected with infusion of 60 mmol of potassium chloride and 2 g of magnesium sulfate. The serum amitriptyline measurement was ordered at the time of her presentation to the emergency department.

Arterial blood gas analysis showed:

• pH 7.15 (normal range 7.35–7.45)
• Paco₂ 66 mm Hg (34–46)
• Pao₂ 229 mm Hg (85–95)
• Bicarbonate 22 mmol/L (22–26).

The initial electrocardiogram (ECG) (Figure 1) showed regular wide-complex tachycardia with no definite right or left bundle branch block morphology, no discernible P waves, a QRS duration of 198 msec, right axis deviation, and no Brugada criteria to suggest ventricular tachycardia.

She remained hypotensive, with regular wide-complex tachycardia on the ECG. She was given an additional 1-L bolus of normal saline and 100 mmol (2 mmol/kg) of sodium bicarbonate, and within 1 minute the wide-complex tachycardia resolved to narrow-complex sinus tachycardia (Figure 2). At this point, an infusion of 150 mmol/L of sodium bicarbonate in dextrose 5% in water was started, with serial ECGs to monitor the QRS duration and serial arterial blood gas monitoring to maintain the pH between 7.45 and 7.55.

TRANSFER TO THE ICU

She was then transferred to the intensive care unit (ICU), where she remained for 2 weeks. While in the ICU, she had a single recurrence of wide-complex tachycardia that resolved immediately with an infusion of 100 mmol of sodium bicarbonate. A urine toxicology screen was negative, and the serum amitriptyline measurement, returned from the laboratory 48 hours after her initial presentation, was 594 ng/mL (reference range 100–250 ng/mL). She was eventually weaned off the norepinephrine infusion after 20 hours, the sodium bicarbonate infusion was discontinued after 4 days, and she was taken off mechanical ventilation after 10 days. Also during her ICU stay, she had seizures on day 3 and developed aspiration pneumonia.

From the ICU, she was transferred to a regular floor, where she stayed for another week and then was transferred to a rehabilitation center. This patient was known to have clinical depression and to have attempted suicide once before. She had recently been under additional psychosocial stresses, which likely prompted this second attempt.

She reportedly had no neurologic or cardiovascular sequelae after her discharge from the hospital.

AMITRIPTYLINE OVERDOSE

Amitriptyline causes a relatively high number of fatal overdoses, at 34 per 1 million prescriptions.¹ Death is usually from hypotension and ventricular arrhythmia caused by blockage of cardiac fast sodium channels leading to disturbances of cardiac conduction such as wide-complex tachycardia.

Other manifestations of amitriptyline overdose include seizures, sedation, and anticholinergic toxicity from variable blockade of gamma-aminobutyric acid receptors, histamine 1 receptors, and alpha receptors.²

In amitriptyline overdose, sinus tachycardia is the most common finding on ECG

Of the various changes on ECG described with amitriptyline overdose, sinus tachycardia is the most common. A QRS duration greater than 100 msec, right to extreme-right axis deviation with negative QRS complexes in leads I and aVL, and an R-wave amplitude greater than 3 mm in lead aVR are indications for sodium bicarbonate infusion, especially in hemodynamically unstable patients.³ Sodium bicarbonate increases the serum concentration of sodium and thereby overcomes the sodium channel blockade. It also alkalinizes the serum, favoring an electrically neutral form of amitriptyline that binds less to receptors and binds more to alpha-1-acid glycoprotein, decreasing the fraction of free drug available for toxicity.⁴

In patients with amitriptyline overdose, wide-complex tachycardia and hypotension refractory to sodium bicarbonate infusion can be treated with lidocaine, magnesium sulfate, direct-current cardioversion, and lipid resuscitation.^5,6 Treatment with class IA, IC, and III antiarrhythmics is contraindicated, as they block sodium channels and thus can worsen conduction disturbances.

A 49-year-old woman with a history of depression, bipolar disorder, and chronic back pain was brought to the emergency department unresponsive after having taken an unknown quantity of amitriptyline tablets.

On arrival, she was comatose, with a score of 3 (the lowest possible score) on the 15-point Glasgow Coma Scale. Her blood pressure was 65/22 mm Hg, heart rate 121 beats per minute, respiratory rate 14 per minute, and oxygen saturation 88% on room air. The rest of the initial physical examination was normal.

She was immediately intubated, put on mechanical ventilation, and given an infusion of a 1-L bolus of normal saline and 50 mmol (1 mmol/kg) of sodium bicarbonate. Norepinephrine infusion was started. Gastric lavage was not done.

Results of initial laboratory testing showed a serum potassium of 2.9 mmol/L (reference range 3.5–5.0) and a serum magnesium of 1.6 mmol/L (1.7–2.6), which were corrected with infusion of 60 mmol of potassium chloride and 2 g of magnesium sulfate. The serum amitriptyline measurement was ordered at the time of her presentation to the emergency department.

Arterial blood gas analysis showed:

• pH 7.15 (normal range 7.35–7.45)
• Paco₂ 66 mm Hg (34–46)
• Pao₂ 229 mm Hg (85–95)
• Bicarbonate 22 mmol/L (22–26).

The initial electrocardiogram (ECG) (Figure 1) showed regular wide-complex tachycardia with no definite right or left bundle branch block morphology, no discernible P waves, a QRS duration of 198 msec, right axis deviation, and no Brugada criteria to suggest ventricular tachycardia.

She remained hypotensive, with regular wide-complex tachycardia on the ECG. She was given an additional 1-L bolus of normal saline and 100 mmol (2 mmol/kg) of sodium bicarbonate, and within 1 minute the wide-complex tachycardia resolved to narrow-complex sinus tachycardia (Figure 2). At this point, an infusion of 150 mmol/L of sodium bicarbonate in dextrose 5% in water was started, with serial ECGs to monitor the QRS duration and serial arterial blood gas monitoring to maintain the pH between 7.45 and 7.55.

TRANSFER TO THE ICU

She was then transferred to the intensive care unit (ICU), where she remained for 2 weeks. While in the ICU, she had a single recurrence of wide-complex tachycardia that resolved immediately with an infusion of 100 mmol of sodium bicarbonate. A urine toxicology screen was negative, and the serum amitriptyline measurement, returned from the laboratory 48 hours after her initial presentation, was 594 ng/mL (reference range 100–250 ng/mL). She was eventually weaned off the norepinephrine infusion after 20 hours, the sodium bicarbonate infusion was discontinued after 4 days, and she was taken off mechanical ventilation after 10 days. Also during her ICU stay, she had seizures on day 3 and developed aspiration pneumonia.

From the ICU, she was transferred to a regular floor, where she stayed for another week and then was transferred to a rehabilitation center. This patient was known to have clinical depression and to have attempted suicide once before. She had recently been under additional psychosocial stresses, which likely prompted this second attempt.

She reportedly had no neurologic or cardiovascular sequelae after her discharge from the hospital.

AMITRIPTYLINE OVERDOSE

Amitriptyline causes a relatively high number of fatal overdoses, at 34 per 1 million prescriptions.¹ Death is usually from hypotension and ventricular arrhythmia caused by blockage of cardiac fast sodium channels leading to disturbances of cardiac conduction such as wide-complex tachycardia.

Other manifestations of amitriptyline overdose include seizures, sedation, and anticholinergic toxicity from variable blockade of gamma-aminobutyric acid receptors, histamine 1 receptors, and alpha receptors.²

In amitriptyline overdose, sinus tachycardia is the most common finding on ECG

Of the various changes on ECG described with amitriptyline overdose, sinus tachycardia is the most common. A QRS duration greater than 100 msec, right to extreme-right axis deviation with negative QRS complexes in leads I and aVL, and an R-wave amplitude greater than 3 mm in lead aVR are indications for sodium bicarbonate infusion, especially in hemodynamically unstable patients.³ Sodium bicarbonate increases the serum concentration of sodium and thereby overcomes the sodium channel blockade. It also alkalinizes the serum, favoring an electrically neutral form of amitriptyline that binds less to receptors and binds more to alpha-1-acid glycoprotein, decreasing the fraction of free drug available for toxicity.⁴

In patients with amitriptyline overdose, wide-complex tachycardia and hypotension refractory to sodium bicarbonate infusion can be treated with lidocaine, magnesium sulfate, direct-current cardioversion, and lipid resuscitation.^5,6 Treatment with class IA, IC, and III antiarrhythmics is contraindicated, as they block sodium channels and thus can worsen conduction disturbances.