Funtabulously Frivolous Friday Five 167

Just when you thought your brain could unwind on a Friday, you realise that it would rather be challenged with some good old fashioned medical trivia FFFF…introducing Funtabulously Frivolous Friday Five 167

Question 1

What is Asturian leprosy?

  • Pellagra or vitamin B3 (niacin) deficiency as a result of a corn based diet (Noted in the Asturias community in Spain).
  • In 1915, back when such practices were legal and under the Surgeon General’s sanction in the USA, Dr. Goldberger offered prisoners of a southern prison freedom in return for cooperation in his experiment. Eleven healthy men volunteered, and were put on an all-corn diet. Goldberger kept the patients’ housing meticulously clean and regulated, from changing the sheets and clothing everyday to screening in the doors and windows. Three weeks into the diet, seven of the eleven men developed pellagra. The men actually begged to be put back in prison. Dr. Goldberger then supplemented their diets with other vegetables and fruit and the disease cleared up. [Reference]
  • Pellagra typically causes the 3 “D’s” – Diarrhoea, dementia and dermatitis.


Question 2

What condition did Andre The Giant have?

  • Acromegaly
  • There is a book called “As You Wish” about the making of The Princess Bride with stories about Andre The Giant (Fezzig). He called everyone “Boss” because he wanted to put them at ease. When filming, he got drunk and fell and broke a table and afterwards had a dedicated police unit follow him around for damage control. He took care of Robin Wright by using his hand as an umbrella for her when it was raining and he carried Wallace Shawn on his back while climbing.
  • His acromegaly gave him chronic pain and he wore a back brace throughout the entire movie
  • He sadly died of CHF a few years after its filming [Reference]

Question 3

What is the “Jake Leg“?

  • Refers to an organophosphate-induced delayed neuropathy (OPIDN) from consumption of Jamaican Ginger, aka Jake.
  • Jake leg affected thousands in the American South and Midwest during prohibition due to the adulteration of bootlegged Jamaican Ginger (~80% ethanol) with tri-ortho cresyl phosphate. [Reference]

Question 4

A competitive athlete asks for your advice about an embarrassing medical problem she has developed… a unilaterally swollen labia majora. What sport does she most likely compete in?

  • Cycling
  • She most likely suffers from a condition known as ‘bicyclist’s vulva’.
  • That’s right as if cyclist’s nipples, cycling-related peripheral neuropathies and saddle sores weren’t bad enough there is a condition known as ‘bicyclist’s vulva’.
  • Bayaens and colleagues described 6 cases in a 2002 paper in the BMJ (the patients cycled an average of 462.5 km per week). They all had unilateral lymphoedema thought to be due to compression of the inguinal lymphatics. [Reference]

Question 5

What did Brown-Sequard repeatedly inject himself at the age of 72, in order to rejuvenate himself?Édouard_Brown-SéquardÉdouard_Brown-Séquard

  • Extracts of guinea-pig testes.
  • He wrote “The day after the first subcutaneous injection, and still more after the two succeeding ones, a radical change took place in me . . . I had regained at least all the strength I possessed a good many years ago . . . My limbs, tested with a dynamometer, for a week before my trial and during the month following the first injection, showed a decided gain of strength . . . I have had a greater improvement with regard to the expulsion of fecal matters than in any other function . . . With regard to the facility of intellectual labour, which had diminished within the last few years, a return to my previous ordinary condition became quite manifest”
  • Brown-Séquard also reported that similarly dramatic benefits of extracts from rabbit and guinea pig testes had been observed in three men, aged 54, 56 and 68 years, whereas injections of water in two other men had had no effect. This has been proven to still be due to the placebo effect. [Reference]

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Tachycardic Arrhythmias in Pregnancy: Management

Author: Jennifer Robertson, MD, MSEd (Assistant Professor, Emory University, Atlanta GA) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Case 1: A 37 yo G1P0 female at approximately 17 weeks gestational age presents to the emergency department (ED) with a chief complaint of a racing heart.  She denies any past medical history. Her heart rate is 180 beats per minute (bpm) but otherwise her vital signs are within normal limits. She denies chest pain. Her electrocardiogram (EKG) is shown below:


Case 2:  A 21 year old G1P0 female at approximately 16 weeks gestational age presents with a chief complaint of syncope. She arrives to the ED with a complaint of lightheadedness but is alert and oriented and able to converse. She does complain of some mild chest pain. Her heart rate is 160 bpm and her blood pressure is 85/60 mmHg. Her other vital signs are within normal limits.


Case 3: A 40-year-old G4P3 female at approximately 12 weeks gestational age presents after feeling palpitations for the last several days. She denies chest pain, syncope or shortness of breath. She denies any past medical history and denies taking any medications. Her initial heart rate is 165 bpm (irregular) and her blood pressure is 130/80 mmHg. Her EKG is shown as follows:



Compared to the non-pregnant population, cardiac arrhythmias are rare in pregnancy, with an incidence of about 1.2 per 1000 pregnant women (1). However, they can negatively affect the health of both the mother and child, especially if they lead to hypoperfusion. Thus, emergently addressing them is important. Additionally, it is important to understand that the management of arrhythmias in pregnancy may vary considerably from the non-pregnant patient due to the potential effects of anti-arrhythmic medications and electrical therapy with sedation (2). Thus, this is a brief review of the evaluation and management of the pregnant patient who may present to the emergency department with a tachy-arrhythmia. Pathologic bradycardia is very rare in pregnancy and will not be covered in this current article (3).

General Physiology: Brief Review

Arrhythmias in pregnancy can be due to a number of causes including congenital heart disease, channelopathies, and other structural heart diseases (3). Examples include Wolff Parkinson White Disease, pulmonary hypertension, Marfan syndrome with a dilated aortic root, arrhythmogenic right ventricular dysplasia, and even coronary artery disease (4,5).  They can also be due to reasons that are commonly seen in non-pregnant patients such as idiopathic, infection/sepsis, electrolyte abnormalities, medications, toxins, pulmonary emboli and hyperthyroidism (2,6,7). Similar the general population, these causes should also be considered when evaluating for the underlying cause of the arrhythmia (6, 7).

For some pregnant patients, an arrhythmia may be recurrent from a previously diagnosed cardiac disease or a first-time presentation. Due to the many physiologic changes and stresses on the cardiovascular system, pregnancy can provoke arrhythmias in some women with undiagnosed structural heart disease (s) (4). In addition, in women with known tachy-arrhythmias, pregnancy may cause an increased risk of recurrence or worsening of the dysrhythmia (3, 7). A thorough family and personal history of structural heart disease should be obtained in addition to a family history of sudden or unexplained death (3).

Palpitations are usually benign and life threatening arrhythmias are rare in pregnant patients (1, 3, 7, 8), but evaluation for more serious arrhythmia is always necessary from an emergency medicine standpoint. As previously mentioned, assessing for underlying reversible causes such as infection, hyperthyroidism and toxins is important. However, if no underlying cause can be found and/or if the patient is unstable, then medical and/or electrical management is warranted.

Unstable Rhythms

In any unstable patient, the American Heart Association (AHA) makes the following recommendations (all Level C recommendations-consensus opinion of experts, case studies or standard of care) (9):

(a) Place the patient in the full left lateral decubitus position to relieve aortocaval compression.

(b) Administer 100% oxygen by facemask to treat and prevent hypoxemia.

(c) Ideally, intravenous (IV) access should be established above the diaphragm to ensure that medications can be adequately distributed into the circulation (not obstructed by the gravid uterus)

(d) Evaluate for any underlying causes of the patient’s symptoms.

Please review the following article for any specifics about cardiac arrest in pregnancy:

Jeejeebhoy FM, Zelop CM, Lipman S, Carvalho B, Joglar J, Mhyre JM, Katz VL, Lapinsky SE, Einav S, Warnes CA, Page RL. Cardiac Arrest in Pregnancy A Scientific Statement From the American Heart Association. Circulation 2015; 132(18):1747-73.

However, just as in non-pregnant patients with an unstable tachycardia causing hemodynamic compromise, immediate direct current (DC) cardioversion is indicated (1, 2, 10, 11). Overall, DC cardioversion has been found to be safe in all trimesters of pregnancy, but it does carry a small risk of inducing a fetal arrhythmia (3). Therefore, it is strongly recommended that when possible, cardioversion should be conducted with concurrent fetal monitoring and emergency caesarean section (C-section) availability (1, 3, 6, 12).  Women in later stages of pregnancy should have their pelvis tilted to the left to relieve compression of the vena cava, however the process, including the dosing of electricity, is otherwise the same as in non-pregnant patients (3, 7, 13). Higher doses of energy (up to 360J) in refractory cases still remains safe for both the mother and fetus (13).

Medication options for sedation (for cardioversion):

This article is also not intended to be a review of safe sedation in pregnancy. However, some excellent articles on sedation in pregnancy include:

Neuman G, Koren G. MOTHERISK ROUNDS: Safety of Procedural Sedation in Pregnancy. J Obstet Gynaecol Can 2013; 35(2):168-73.

Shergill AK, Ben-Menachem T, Chandrasekhara V, et al. Guidelines for endoscopy in pregnant and lactating women. Gastrointest Endosc. 2012; 76(1):18-24.

Stable Tachyarrhythmias

The majority of arrhythmias during pregnancy are stable and can be managed with conservative therapies (7). Medication therapy should be considered in patients who are symptomatic and/or have tachyarrhythmias that may lead to negative hemodynamic or physiologic complications (7). Of course, any significant acute hemodynamic compromise should lead the provider to consider cardioversion, as mentioned in the above section (14)

In addition, as previously discussed, a thorough history and physical should be conducted to rule out any reversible causes of the arrhythmia such as a pulmonary embolism, hyperthyroidism, hemorrhage, or infections (). A history of prior episodes and/or a history of structural heart disease are also important to obtain. Once reversible causes are ruled out and a thorough history is obtained, a primary stable arrhythmia requiring drug therapy can be considered (3).

The risk of any medication on the mother and fetus should be reviewed prior to its administration. Most antiarrhythmic medications have not been systematically studied in pregnancy and thus, all should be viewed as potentially harmful in pregnancy (6, 15). Most of these drugs are labeled as a Food and Drug Administration (FDA) category C except for amiodarone and atenolol, which are labeled as category D (16). As a review, category C means that risk cannot be ruled out and any category C medication should be used only if the potential benefits outweigh any potential risks to the fetus. Category D means that there is evidence of risk. There may be a benefit of this drug but that patients should be informed of all risks of the drug prior to giving it (16).

It should be noted that as of June 2015, the FDA initiated a change to pregnancy category labeling and that the use of letters will be phased out. In place of letters, a narrative summary based on the risk of each medication will be provided (17). Any medications submitted to the FDA after June 30, 2015 will use the new format immediately and that any prior prescription medications approved after June 2001 will have new labeling within 3-5 years (17). So as of now, most of these antiarrhythmic medications are still under the old letter category labeling but may change in the future.

Teratogenic risk is also the highest in the first eight weeks after fertilization and thus, especially careful consideration should be given to women in early pregnancy who receive drug therapy (18). This is not to say there is no risk in the other stages of pregnancy, but the risk to the fetus is significantly reduced after the first eight weeks (18).

Finally, it should be remembered that many of the physiologic changes of pregnancy will affect drug metabolism (19). Some of these changes include increased plasma volume, reduction in plasma proteins, changes in renal clearance of drugs and altered gastrointestinal absorption (7, 19). Progesterone levels also increase, which can affect hepatic metabolism (7). Thus, administering the lowest effective dose of a medication is prudent in this patient population (7).

  1. Palpitations/Premature Ventricular Contractions

Palpitations are very common during pregnancy. Along with paroxysmal supraventricular tachycardia, premature atrial and ventricular beats are the most frequently seen arrhythmias in pregnancy (3, 14). Treatment is typically not necessary but in patients with unbearable symptoms, cardioselective beta blockers can be started, but preferably after the first trimester (6).

  1. Atrioventricular (AV) Nodal Re-entrant Tachycardia (AVNRT) and AV Re-entrant Tachycardia (AVRT):

The most common supraventricular tachycardia in pregnancy is AVNRT. AVNRT occurs when there are dual AV nodal pathways (slow and fast) that form a part of a re-entry circuit. The tachycardia is initiated when a premature beat is blocked in the fast pathway but conducts over the slow pathway (20). If there is enough time for the fast pathway to recover from its refractory period, then the slow pathway impulse (initiated by the premature beat) may conduct retrogradely over the fast pathway and cause the re-entry circuit (20).

AVNRT should not be confused with AVRT, which is the second most common supraventricular tachycardia in pregnancy (21). AVRT occurs in patients with WPW. In AVNRT, the accessory pathways are located within or near the AV node, while in AVRT, the accessory pathways are located in the AV valvular rings (22). The majority of patients will have the orthodromic form with anterograde conduction through the AV conduction system and retrograde conduction via the accessory pathway, which leads to a regular, narrow complex tachycardia. On occasion, antidromic conduction can occur and cause a wide complex tachycardia (Obel et al). If there is concomitant atrial fibrillation and it is conducted via the antidromic pathway, a wide complex, irregular tachycardia can occur (22).

If AVNRT or AVRT is rapid enough, hemodynamic instability can occur and thus, cardioversion may be necessary (1, 14, 21). However, the majority of patients will not have hemodynamic instability and thus, conservative or medication therapies can be initiated.

First line therapies for stable AVNRT in pregnancy (1, 3, 4, 6, 7, 14, 23):

  1. Vagal maneuvers such as carotid massage or the Valsalva maneuver.
  2. Adenosine: safe and should be the initial drug of choice. The initial standard doses are the same as in non-pregnant patients – 6mg and 12 mg. Adenosine has a short half live and does not cross the placenta. Minor effects in the mother may include transient bradycardia and dyspnea. Note adenosine can induce bronchospasm and should be a consideration if the patient has a history of asthma.
  3. Intravenous metoprolol or propranolol can be used if adenosine is ineffective. Beta blockers are considered safe in pregnancy but they have been associated with intrauterine growth retardation. Atenolol should never be given, however as it has been associated with fetal hypotonia, neonatal respiratory depression, low birth weight and hypoglycemia.
  4. Verapamil should be considered as a third line agent if the above medications are not effective. Doses up to 10mg can be given without affecting the fetal heart rate. Watch for hypotension in the mother, however.

First line therapies for stable AVRT in pregnancy (3, 6, 7, 14, 15, 18):

  1. Vagal maneuvers
  2. Adenosine: may be used but only in regular tachycardias. Patients who have orthodromic AVRT with concomitant atrial fibrillation should not receive adenosine or any other AV nodal blocking agent as this can potentially lead to accelerated conduction through the accessory pathway and lead to dangerous ventricular tachycardias.

AV nodal blocking agents including calcium channel blockers and digoxin should also be used with caution in patients with wide complex tachycardias of unknown pathogenesis.  Just as in non-pregnant patients, procainamide is the drug of choice in these circumstances.

  1. Procainamide: IV procainamide is safe in the short-term treatment of AVRT. It should be avoided in patients with underlying structural heart disease as it can be pro-arrhythmogenic. It should not be used long term as it can cause a lupus-like syndrome.
  1. Focal Atrial Tachycardia:

Focal atrial tachycardia (FAT) is usually associated with structural heart disease and is rarely seen in pregnancy (14). FAT can be difficult to treat as many are resistant to medications and even cardioversion (7, 15). The main objective is to control the maternal heart rate so that tachycardia-induced cardiomyopathy can be prevented. Adenosine should be attempted first as it is diagnostic and may, on occasion, terminate the arrhythmia (6). If adenosine does not work, the next recommended initial therapies are beta blockers, non-dihydropyridine calcium channel blockers or digoxin. Sotalol, flecainide or propafenone can be given if the beforementioned drugs do not work. Finally, amiodarone can be given but only in severe, refractory cases (7, 15).

  1. Atrial fibrillation/Atrial Flutter:

Unless there is underlying structural heart disease or hyperthyroidism, atrial flutter and atrial fibrillation are rarely seen during pregnancy (15, 21). However, if atrial flutter (AFL) or atrial fibrillation (AF) with a rapid ventricular response is present in pregnancy, serious hemodynamic effects can occur to both mother and fetus (15). Thus, urgent treatment is important in these patients.

Therapeutic options for stable patients with AFL or AF with rapid ventricular response:

  1. DC or pharmacologic cardioversion: similar to the non-pregnant population, stable pregnant patients who have had AFL or AF for > 48 hours duration will require 3 weeks of anticoagulation and/or a transesophageal echocardiogram to evaluate for a left atrial thrombus prior to the procedure (15). However, if the duration of the arrhythmia is less than 48 hours and the patient’s CHADS2-VASC score is < 2, post-cardioversion anticoagulation may not be necessary (7, 15). In this case, the patient should receive a dose of heparin or weight adjusted low molecular weight heparin (LMWH) prior to and during cardioversion (15). For patients who require anticoagulation after cardioversion, LMWH is the drug of choice (15). Warfarin can be used in the second and third trimesters but not in the first trimester or last month of pregnancy (6, 15). As of now, given the limited research, the new oral anticoagulants should not be used in pregnant patients (6, 15).

If pharmacologic cardioversion is considered, ibutilide or flecainide can be given but only in patients with structurally normal hearts (15, 21, 24). Ibutilide is particularly useful in treating AF in patients with pre-excitation syndromes. It can prolong the QT and thus, pre-treatment with magnesium is recommended (7). Again, amiodarone can be given but only as a last resort. There is less experience with propafenone so it should be avoided unless it must be used as a last resort as well (15).

  1. Rate control: For stable patients who are not candidates for cardioversion and/or have refractory AF or AFL, rate control is recommended (6, 7, 14, 15, 25). The AHA/ACC do not define what adequate rate control in pregnancy is, nor could any other literature be found regarding a goal maternal heart rate (26).

With the exception of atenolol, beta blockers are recommended as first line rate control medications in patients with rapid AF or AFL who do not have acute heart failure (6, 7, 14, 15, 25).Metoprolol 5mg IV over 5 minutes and repeated, if necessary, is an option for initial rate control (14). Verapamil, diltiazem and digoxin are second line agents (6, 14, 15, 25). Remember that these drugs should not be given if a pre-excitation syndrome is present.

  1. Ventricular Tachycardia:

Ventricular tachycardia (VT) is rare during pregnancy and inherited disorders should be considered when asking patients about their past medical and family histories (15). Some of the more common causes of VT in pregnancy may include idiopathic right ventricular (RV) outflow tract tachycardia, long QT syndrome, valvular heart disease and hypertrophic cardiomyopathy (3, 6, 15, 27). Rarely does ischemia cause a cardiomyopathy or arrhythmias in pregnant patients but coronary artery dissection or vasospasm has been known to occur in pregnant patients (6).  Post-partum cardiomyopathy should also be ruled out in women presenting with new onset VT during the last 6 weeks of pregnancy or in the early post-partum period (15).

The most important goal for pregnant patients with VT is timely conversion back to normal sinus rhythm because eventually, poor perfusion to both mother and fetus can occur (15).Just as in unstable supraventricular rhythms, acute treatment of any unstable VT should always be treated with DC cardioversion (15). Conversely, pharmacotherapy may be considered in pregnant patients with stable VT (6, 13, 15, 27). Importantly, any pregnant patient with a wide complex tachycardia should be evaluated by obstetric and cardiology specialists (18).

Idiopathic RV outflow tract tachycardia is one of the more common types of VT seen in pregnancy. It is almost always a stable tachycardia and most of the time, it is not sustained. The recommended treatment is beta blockade or verapamil. Idiopathic LV tachycardia is not as common but it responds well to verapamil (3, 15).

In pregnant patients with stable monomorphic VT, lidocaine, procainamide, or sotalol are recommend as first line agents (3, 15, 27).

Polymorphic VT is definitely most concerning as it has a higher likelihood of converting to ventricular fibrillation (3). Long QT syndrome should be a concern in patients with polymorphic VT and thus, all medications that may prolong the QT should be eliminated. In addition, treatment should include magnesium and correction of any electrolyte disturbances (3). Magnesium should be given at a dose of 1-2 grams IV over 1-2 minutes (13). It is controversial whether pregnant patients with long QT are at risk for VT during pregnancy, but it has been demonstrated that patients with long QT are definitely at an increased risk for arrhythmias post-partum (28, 29). Thus, any post-partum patient who presents in VT should have long QT syndrome as a possible etiology of her condition.


While there are a few differences, the management of tachycardic arrhythmias in pregnancy is quite similar to the non-pregnant patient. DC cardioversion should always be conducted in patients with hemodynamic instability. Pharmacologic cardioversion of supraventricular and ventricular arrhythmias is possible in the stable patient. No drugs are completely safe in pregnancy, but most are rated category C in pregnancy and if the benefit exceeds the risk, then the medication may be given.  Amiodarone and atenolol are two medications that should be avoided in the pregnant patient, especially in the first trimester. Rate control with beta blockers or calcium channel blockers is an option in patients with supraventricular tachycardias who are not immediate candidates for cardioversion. Stroke risk should still be accounted for and at risk patients should be anticoagulated with LMWH or vitamin K antagonists (only in the 2nd and 3rd trimesters and not in the last month of pregnancy). Finally, close cardiac monitoring of both the mother and fetus and availability of emergency C section should be available whenever medication or cardioversion is indicated. Finally, but importantly, obstetrics and cardiology consultation is prudent whenever a pregnant patient with an abnormal tachycardic arrhythmia presents to the ED.

Case Resolution

Case 1: The patient in this case has new onset AVNRT. Her electrolytes are normal, her thyroid function is normal, and her infection workup is negative.  Since her vital signs are otherwise stable and she denies chest pain, adenosine 6mg IV push is administered. Her rhythm returns back to normal sinus rhythm and she is discharged home with close cardiology and obstetrics follow up.

Case 2: This patient has unstable ventricular tachycardia. She is immediately cardioverted with direct current. She was ultimately found to have right ventricular (RV) outflow tract tachycardia. Obstetrics and cardiology were consulted and the patient was admitted for maternal and fetal cardiac monitoring. She was eventually discharged with a beta blocker for prophylaxis and cardiology follow up.

 Case 3: The last patient has atrial fibrillation with rapid ventricular response. Her workup for infection is also negative and her thyroid function tests and electrolytes are normal. Since her symptoms had been present for several days, rate control was chosen. Metoprolol was given and she achieved adequate rate control. She was admitted for a transesophageal echo prior to cardioversion and eventually she was cardioverted back to normal sinus rhythm.

References/Further Reading

  1. Tromp CH, Nanne AC, Pernet PJ, Tukkie R, Bolte AC. Electrical cardioversion during pregnancy: safe or not? Neth Heart J 2011;19(3):134-6.
  2. Ferrero S, Colombo BM, Ragni N. Maternal arrhythmias during pregnancy. Arch Gynecol Obstet 2004; 269(4):244-53.
  3. Adamson DL, Nelson-Piercy C. Managing palpitations and arrhythmias during pregnancy. Heart. 2007; 93(12):1630-6.
  4. Newstead-Angel J, Gibson PS. Cardiac drug use in pregnancy: safety, effectiveness and obstetric implications. ExpertRev Cardiovasc Ther 2009; 7(12):1569-80.
  5. Gaiser R. Physiologic changes of pregnancy. Chestnut’s obstetric anesthesia: Principles and practice. 2009;4:15-36.
  6. Enriquez AD, Economy KE, Tedrow UB. Contemporary management of arrhythmias during pregnancy. Circ Arrhythm Electrophysiol 2014;7(5):961-7.
  7. Burkart TA, Miles WM, Conti JB. Principles of Arrhythmia Management During Pregnancy. Cardiovascular Innovations and Applications. 2016;1(2):143-55.
  8. Joglar JA, Page RL. Management of arrhythmia syndromes during pregnancy. Curr. Opin. Cardiol. 2014; 29(1):36-44.
  9. Jeejeebhoy FM, Zelop CM, Lipman S, Carvalho B, Joglar J, Mhyre JM, Katz VL, Lapinsky SE, Einav S, Warnes CA, Page RL. Cardiac Arrest in Pregnancy A Scientific Statement From the American Heart Association. Circulation. 2015;132(18):1747-73.
  10. Petrescu V, Petrescu M, Bogdan S. Arrhythmias in Pregnancy-one case report and current recommendations from a cardiological perspective. GINECO RO 2010; 6(2):124-7.
  11. Crijns HJ. Electrical cardioversion in healthy pregnant women: safe yes, but needed? NethHeartJ 2011; 19(3):105-6.
  12. Barnes EJ, Eben F, Patterson D. Direct current cardioversion during pregnancy should be performed with facilities available for fetal monitoring and emergency caesarean section. BJOG 2002; 109(12):1406-7.
  13. Trappe HJ. Emergency therapy of maternal and fetal arrhythmias during pregnancy. J EmergTraumaShock 2010; 3(2):153.
  14. Knotts RJ, Garan H. Cardiac arrhythmias in pregnancy. In Seminars in perinatology 2014 (Vol. 38, No. 5, pp. 285-288). WB Saunders.
  15. Regitz-Zagrosek V, Lundqvist CB, Borghi C, Cifkova R, Ferreira R, Foidart JM, Gibbs JS, Gohlke-Baerwolf C, Gorenek B, Iung B, Kirby M. ESC Guidelines on the management of cardiovascular diseases during pregnancy. EurHeartJ 2011:ehr218.
  16. Food and Drug Administration; Accessed Nov 15, 2016:
  17. Food and Drug Administration. Content and format of labeling for human prescription drug and biological products; requirements for pregnancy and lactation labeling. Federal registrar 2014; Vol. 79 (233): 72064-72103.
  18. Page RL. Treatment of arrhythmias during pregnancy. AmHeartJ 1995;130(4):871-6.
  19. Cox JL, Gardner MJ. Treatment of cardiac arrhythmias during pregnancy. Prog Cardiovasc Dis. 1993; 6(2):137-78.
  20. Kwaku KF, Josephson ME. Typical AVNRT—an update on mechanisms and therapy. Card Electrophysiol Rev. 2002; 6(4):414-21.
  21. Merino JL, Perez-Silva A. Tachyarrhythmias and Pregnancy.
  22. Obel OA, Camm AJ. Accessory pathway reciprocating tachycardia. EurHeartJ 1998; 19:E13-24.
  23. Elkayam U, Goodwin TM. Adenosine therapy for supraventricular tachycardia during pregnancy. Am J Cardiol 1995; 75(7):521-3.
  24. Kockova R, Kocka V, Kiernan T, Fahy GJ. Ibutilide‐Induced Cardioversion of Atrial Fibrillation During Pregnancy. J Cardiovasc Electrophysiol. 2007;18(5):545-7.
  25. Cacciotti L, Passaseo I. Management of Atrial Fibrillation in Pregnancy. J AtrFibrillation 2010;2(2).
  26. Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH, DeMets D, Guyton RA, Hochman JS, Kovacs RJ, Ohman EM. Management of patients with atrial fibrillation (compilation of 2006 ACCF/AHA/ESC and 2011 ACCF/AHA/HRS recommendations): a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61(18):1935-44.
  27. Gowda RM, Khan IA, Mehta NJ, Vasavada BC, Sacchi TJ. Cardiac arrhythmias in pregnancy: clinical and therapeutic considerations. Int J Cardiol 2003;88(2):129-33.
  28. Meregalli PG, Westendorp IC, Tan HL, Elsman P, Kok WE, Wilde AA. Pregnancy and the risk of torsades de pointes in congenital long-QT syndrome.
    Neth Heart J. 2008; 16(12):422-5.
  29. Seth R, Moss AJ, McNitt S, Zareba W, Andrews ML, Qi M, Robinson JL, Goldenberg I, Ackerman MJ, Benhorin J, Kaufman ES. Long QT syndrome and pregnancy. J Am Coll Cardiol. 2007; 49(10):1092-8.

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There’s a lady in Resus, she’s 46, she’s got a history of mental health problems.  Her husband tells you she’s been gradually more lethargic over the last few days.  He called the ambulance today because he found her on the sofa in the morning mumbling incoherently.  Her observations are okay.  Her ABC’s are okay, she’s got a normal glucose, but when you go to move her arm to cannulate you notice she’s rigid.  Hypertonic all over.  You do what you can of a neuro exam and find she’s got globally increased reflexes.  Her pupils are fine.  VBG is okay acid base wise but her Na is 154.

Now as we said last week.  Sodium is important, and it’s ubiquitous.  We need it for everything, and every single one of our cells uses a lot of energy to maintain a sodium concentration of between 135-145mmol/l.  When things go wrong with sodium homeostasis, things are very wrong indeed.  Mortality rates are higher for hypernatraemia than hyponatraemia ranging from 45-60% for all patient groups, and can be as high as 80% in the elderly.  Thankfully it is less common than hyponatraemia, and we most often see it in patients as they enter their last phase of life, this adds an ethical dimension to treatment that I’m not going to talk about here (maybe another day).

Features of severe hypernatraemia are hyperthermia, delirium, seizures, and coma.  Patients with milder symptoms can sometimes present with delirium or changes in mental status.  Patients might have features of underlying disease processes (such as Conns or Cushings).

Hypernatreamia is usually caused by combined electrolyte and water loss, it’s just that the water loss is in excess of the electrolyte loss, and is coupled with an inability to replace water via the thirst response (people with low GCS, dementia, mental health problems).  The trick is working out where the water is being lost from.

Net water loss from kidneys

Diabetes insipidus can be neurogenic, or nephrogenic.  Neurogenic is usually due to traumatic brain injury, space occupying lesions or infections.  Nephrogenic can be caused by general renal dysfunction, or electrolyte abnormalities such as hypercalcaemia or hypokalaemia, or HHS.

Net water loss from other sources:

The commonest drug cause of hypernatraemia is Lithium, though other drugs such as amphotericin, diuretics and vasopressin analgoues (demeclocycline) can also contribute to or cause it.  Lithium actually inhibits a protein called GSK3 which is part of how renal cells’ respond to vasopressin.  Colchicine, gentamicin, and rifampicin can also cause diabetes insipidus.  Unreplaced loss from the respiratory system, sweating, burns, GI tract (D+V) or any type of fistulae can also be implicated.

Hypernatraemia from sodium gain

Feeding, or increased oral salt intake (this usually needs to be massive, or Iatrogenic).  Sea water ingestion, hyptertonic enemas, or dialysis.  Primary hyperaldosteronism (Conns), or Cushings syndrome can also cause excess sodium re-absorption.



As with hyponatraemia the symptoms are vague and wide ranging.  Treatment depends on the speed of onset with those with a rapid onset (<48 hours) likely to have more severe symptoms.

Assessment of volume status again here is key, because disorders of sodium metabolism are also disorders of WATER.

Hypovolaemic hypernatraemia – patients have signs of hypovolaemia, plus a high sodium!  If you check a urinary sodium and it is low it suggests that the the loss of Na is coming from somewhere other than the kidneys (normally GI tract).  The Na in these cases is usually elevated at 150-170mmol/L.  I think this is the most common class of hypernatraemia.

Euvolaemic hypernatraemia – can be caused by either renal or extra-renal loss of water without loss of Na.  These patients usually have an inability to respond to thirst, or one of the diabetes insipiduses? Inspidies?  Urine osmolality will be lower than plasma osmolality in patients with renal losses of water.  Serum Na in these cases is usually higher >170mmol/L.

Hypernatreamia with hypervolaemia – least common, these patients have normally been given more Na+ than they need (hypertonic solutions either NG, IV) OR they may have conditions which compound this such as renal or liver dysfunction.  People in this category have sky high sodiums >190mmol/L.

Acute Ix strategy – send urine and plasma for electrolytes and osmolality.

Urine osmolality

Lower than plasma or <300

[very dilute]

Normal 400-800 High >800

[super concentrated]

Central or nephrogenic diabetes insipidus


Incomplete Central or nephrogenic diabetes insipidus



Lots of water loss (and your patient has just run out of free H20)


Total Na+ gain


Extra-renal losses, D+V, burns etc

The mainstay of emergency treatment is infusion of the right amount of normal saline to bring the sodium back down.  You want to do this slowly in chronic hypernatreamia (drop the Na by no more than 10mmol/day).  I think this is why Normal Saline is suggested in the emergency phase rather than 5% Dextrose.

Most sources suggest we calculate the water deficit, and replace the lost fluid (after initial resuscitation fluids) over 24-48 hours with oral or 5% dextrose.  The formulae are similar but I encountered 3 different ones in the 3 sources I used (BMJ best evidence, Life in the Fast Lane, Mushin article).  Most of them changed either B or the way you calculate the Na excess.  The one below is from BMJ best evidence I found it the easiest to actually use (for me).

Deficit = A x B x ([Serum Na/140]-1)

A = is their weight

B = % water (0.6 for men, 0.4 for women)


Patients with hypervolaemic hypernatraemia might require that dirtiest of treatments;  fluid AND diuretics, as by expanding their intravascular volume with IV fluid you will downregulate vasopressin excretion further, compounding the problem.  This group of patients might benefit from dialysis to remove the volume and improve the sodium (carefully).

Once we’ve corrected this (and unless your bed-state is really really bad) most patients will be out of your department but further diagnostic tests may be done to confirm the cause.

Tests that may be required:

Plasma Aldosterone:Renin ratio: a high PCA:PRA ratio supports the diagnosis of Conns.  The ratio should be >1000 and a random aldosterone level should be >250pmol/L. (requires patient to be K+ replete, and have all diuretics and antihypertensives stopped for a few weeks beforehand  ).  If you get an equivocal result you might need to get a saline infusion test for hyperaldosteronism (this is an outpatient thing).

Dexamethasone suppression test (Cushings).  Patient takes 1mg dexamethasone at 23:00 and at 09:00 has blood taken for plasma cortisol.  A positive result is <50nmol/L.

Water deprivation test (for euvolaemic hypernatraemias)

When everything is back to normal.  Water restriction starts in the early morning, with baseline vasopressin level, with hourly Na checks.  Once the sodium is >148mmol/L another vaspopressin level should be taken.  At this point DDAVP (vasopressin agonist) should be given.  Patients with nephrogenic DI fail to respond to DDAVP, and their urine osmolality increases by <50% or <150mOsm/kg from baseline pointing to another cause.

CT or MRI head for cranial DI

CT or MRI adrenals for primary aldosteronism.


So just like our hyponatraemia patients, hypernatraemia patients need a serum and urine electrolytes and osmolality.  We need to decide on their volume status.  We need to resuscitate if required with normal saline, or replace slowly with 5% dextrose.  It is possible to calculate their fluid requirements and we should do this too.  In some circumstances we might even need to infuse 5% dextrose while giving diuretics.

The key question to answer is “Where has all the water gone?”


Hypovolaemic Euvolemic Hypervolaemic


Renal Losses

Renal failure


Post-obstructive diuresis


Non Renal Losses (urinary sodium low)




Failure to drink (psychological, behavioral, inability)


Nephrogenic DI

Drugs, AKI, Electrolytes


Neurogenic DI



Failure to drink (psychological, behavioral, inability)


Iatrogenic infusion/feeding of high Na fluid


Co-existing renal or liver dysfunction



Primary Aldosteronism

Resuscitate with Normal Saline


Calculate deficit and replace losses with 5% dextrose over 48 hours.


Aim for <10mmol/day increase in Na

Calculate deficit and replace losses with 5% dextrose over 48 hours.


Aim for <10mmol/day increase in Na

Calculate deficit, replace any losses carefully to avoid worsening overload using 5% dextrose.


Use IV Furosemide


Aim for <10mmol/day increase in Na

PS if you are wondering about that lady, she ended up having neuroleptic malignant syndrome plus a partial neurogenic diabetes insipidus from mass effect from maxillary bone osteomyelitis.  You know, one of those simple diagnoses…



BMJ best practice Hypernatraemia ( Accessed 24/11/2016

Mushin, A, Mount D Diagnosis and Treatment of Hypernatraemia.  Best Practive and Research Clinical Endocrinology and Metabolism 30;2 March 2016 189-203.  [paywall]

Running Hurdles With Ruth Bader Ginsburg

In 1993, when Ruth Bader Ginsburg was appointed the second woman to serve on the Supreme Court, I was nine years old and growing up in a house and a community that made this seem the norm. I now recognize the magnitude of this appointment. It took another three men and 16 years before the third woman would be appointed.  However, it is her journey to the appointment over a 40-year career starting with simultaneous law school and motherhood in the 1950s that is truly remarkable. Last month, The New York Times published the essay, “Ruth Bader Ginsburg’s Advice for Living,” an excerpt from her recent book, My Own Words, in which  she focuses on how she overcame gender challenges while reaching the top of her profession in a man’s world. Though much has changed in gender roles in the professional world, unfortunately not enough has. Twenty-three years after her appointment, as a young physician, I still identify with the hurdles she has overcome that lay ahead on my career path.  

In medicine, it is well documented that we have gender disparities in our academic leadership. In 1990, when ~50% of medical school graduates were women, there was hope that this would equate to more women in positions of leadership and that women would become equal contributors to the field of research. In a 2014 AAMC report on the state of women in medicine, it is noted that despite a continued 50% female graduation rate over the past 24 years, we haven’t come close to equal representation of female physicians in leadership roles.  In the US, only 16% of medical schools’ vice deans are women (1).  In academic medicine, women make up a smaller portion of tenured professors, on average publish fewer articles, and are likely to have a lower H-index.  Interestingly, if the data on publications is adjusted to compare women who don’t have children to men, there is no statistical difference (2).  This suggests that child bearing has a significant impact on career trajectory.  As there was no difference between men with or without children, it also is apparent that it has a different trajectory on male and female career paths.  As one female physician and vice president of research points out, when plotting her own life on a graph, her publication productivity was virtually a flat line over the 5 years that her three children were born.  After that, her productivity exponentially increased and her promotion to professor took three quarters of the time it took her to reach associate professor (1).  Though clearly she has overcome the hurdles, many don’t.  Some studies speculate that the early years of academic productivity that typically overlap with our childbearing years are paramount in career trajectory and may have long lasting effects that contribute to why things don’t equalize later on.  

The challenge of work-life-balance and career advancement has been, and continues to be, universal to the professional woman. In her essay, Justice Ginsburg notes fear of going to law school because she had an infant to care for.  Had it not been for her father-in-law who suggested that if she wanted to be a lawyer, she would figure out a way to do both, she might not have gone to law school then or ever. To balance her responsibilities she split her workday into the time before 4pm and after her daughter’s bedtime. In between was dedicated to her daughter. She credits this time away from her studies as making her a better law student. Maybe there is a silver lining to our childbearing years and the many directions we are pulled in that gives us a balance we have not yet effectively harnessed. Or maybe these are the stories we tell ourselves to get through it.

At a recent American Association of Women Emergency Physicians (AAWEP) meeting this past week at ACEP, two Academic Emergency Medicine chairs offered opposite advice on childbearing. One said she tells women to have children early so that they are more available to focus on their career after having had their kids.  The other stated he recommends waiting to have children until their academic career is already in progress, stating it may be easier to step away without losing ground.

In Justice Ginsberg’s case, she had her second child 10 years after the first. In effect she tried the early and late approach and was successful with both. Regardless of when you have children, something all AAWEP speakers that day seemed to agree upon is the need to prioritize your time; the things you can’t do—be in two places at once—or don’t enjoy doing should be outsourced.  This means enlisting child care to allow you time to get your work done or hiring someone to clean your house, do your laundry or prepare your meals. For Justice Ginsburg this included a nanny and a husband who took on the role of lead cook, something she hated to do.  

The final challenge in career advancement Justice Ginsburg touched on is the professional support we need to get to the next level. She shares that at the time she graduated from law school, the combination of being a woman and having a young child was generally prohibitive of getting a job as a clerk in a federal court. If it were not for what she calls the “heroic efforts” of one of her professors, she never would have gotten the job. Justice Ginsburg had a sponsor long before we were talking about “sponsorship.” Most are familiar with “mentorship” and think of it as important for career advancement. The new hot topic in the world of executives is “sponsorship.” Both have the goal of helping you succeed, but they do it in different ways. Mentors offer advice and guidance while sponsors advocate for you and put themselves on the line on your behalf (3). Dr. Azita Hamedani, Chair of the Department of Emergency Medicine at the University of Wisconsin, stated in her recent keynote address at the AAWEP meeting that we don’t find sponsors, they find us for the work we have done. Though data does not show that mentoring provides objective career advancement, she acknowledges that women probably benefit from cultivating both forms of relationships; mentorship for guidance while navigating your career and sponsorship for concrete career advancement. Justice Ginsburg even attributes her final appointment to the Supreme Court as a result of the sponsorship of her husband who lobbied important members of the legal community and state senators on her behalf.  

Much has changed since Justice Ginsburg walked this road, and she is one of many who has paved the way for women to follow in her footsteps as judges, CEOs, department chairs or deans. There are more women in positions of rank than 30 years ago, but it is not enough. We are still jumping through the same hoops of balancing when to have children, how to balance both shifts—at home and at work—and how to make the professional relationships that lead to our promotion. As we move forward, it is our responsibility as women physicians to not only jump the hurdles, but to cut them down until they are the same height as the ones our male counterparts seem to more easily walk through.


  1. Rochon PA., Davidoff, F., & Levinson, W., (2016). Women in Academic Medicine Leadership. Academic Medicine, 91(8), 1053-6. doi:10.1097/ACM.0000000000001281. PubMed PMID: 27306972.
  2. Raj, A., Carr, P. L., Kaplan, S. E., Terrin, N., Breeze, J. L., & Freund, K. M. (2016). Longitudinal Analysis of Gender Differences in Academic Productivity Among Medical Faculty Across 24 Medical Schools in the United States. Academic Medicine, 91(8), 1.
  3. Forum FL. Mentorship vs. Sponsorship, and how to maximize Both. Forbes. October 2, 2015. Accessed October 23, 2016.

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CRACKCast E015 – Syncope

This episode of CRACKCast covers Rosen’s Chapter 15, Syncope. This short but high yield chapter covers Syncope, a common reason for emergency visits that may be benign, but sometimes can have more sinister diagnoses lurking that cannot be missed! Shownotes – PDF Link Rosen’s in Perspective: Syncope is defined as a sudden, transient, loss of consciousness with loss of postural tone accompanied by a rapid return to baseline. prevalence: 1 in 5 in ...

The post CRACKCast E015 – Syncope appeared first on CanadiEM and was written by Adam Thomas.