Senior Report 5.27

Case Presentation by Dr. Meena Munshi

CHIEF COMPLAINT: “I feel short of breath.”


21-yo F with sickle cell anemia is brought into resuscitation from walk-in triage for tachycardia (HR 150s) with multiple complaints including: shortness of breath, dizzy/lightheadedness, cough with bright red blood-tinged sputum, and “bloody pee”

Shortness of breath occurs at rest and with exertion, without positional component. Has a slight cough with a few drops of blood tinged sputum. Was admitted to the hospital 10 days ago with community acquired pneumonia and acute chest syndrome, given IV antibiotics, an exchange transfusion, and discharged home 4 days ago with doxycycline of which she completed a 7 day course today. Shortness of breath began when she was diagnosed with CAP but improved during hospital stay and with home antibiotics until today when it suddenly got worse. Denies chest pain, wheezing, sick contacts, history of PE, leg swelling, or asthma.

Feels fatigued and lightheaded at rest, with exertional exacerbation. No fever, syncope, weight loss, headache, neck pain, palpitations, diaphoresis, room-spinning sensation, abdominal pain/distention, nausea or vomiting. Loose brown stools today, without melena or hematochezia.

Notes worsening yellowing of her skin related to sickle cell anemia. No petechiae, bruising, pruritis.

What really brought her in was that for the last few hours, she has been “peeing out blood.” States this is not blood-tinged urine but frank blood. Denies previous such occurrence or any suprapubic or flank pain, dysuria, polyuria, urgency, frequency, vaginal bleeding, or menstruation.


GENERAL: Generalized weakness, chills and fatigue; no fever or night sweats

HEAD:  Lightheadedness, without syncope or headache.

EAR, NOSE AND THROAT:  No bleeding gums.

CARDIAC: No chest pain, palpitations, orthopnea, PND or leg swelling.

RESPIRATORY:  Shortness of breath and hemoptysis

GI:  No abdo pain, N/V, melena, hematochezia, hemetemesis. Loose stools.

GU:  Gross hematuria, but no dysuria, urgency, frequency, vaginal bleeding

MUSCULOSKELETAL:  No myalgias, arthralgias, joint swelling

ENDOCRINE:  No heat/cold intolerance, polyuria or polydipsia.

SKIN:  Yellowing of eyes and skin, but no bruising, rashes, or pruritis

PMH:  Sickle cell anemia (HbSS), recent CAP with acute chest syndrome requiring plasma exchange transfusion and pRBCs. Multiple (4-5) prior blood transfusions for SCA.

PSH:  Cholecystectomy, left eye muscle repair.

Meds:  Tylenol with Codeine, Motrin.


FH:  DM, HTN, and Sickle cell trait. No DVT/PE, cancer or CAD

SH:  Denies use of alcohol, tobacco, or drugs.

LMP: Cannot recall; periods are irregular. Not sexually active.


VITALS:  BP 104/76, HR 152, RR 24, oral T 37.7, pulse ox 97% RA

GENERAL:  Obese female appears tired and jaundiced, but in no acute distress.

PSYCH:  Alert and oriented x4, cooperative.

HEENT:  NCAT, PERRLA (4 mm b/l), profound conjunctival pallor and scleral icterus.  No epistaxis/rhinorrhea.  Pale,  moist oral mucosa. No oropharyngeal erythema, exudates or lesions.  No cyanosis.

NECK:  Supple, no JVD, lymphadenopathy or meningismus.  Trachea is midline.

PULMONARY:  Tachypnea(30s). CTA b/l without wheeze/rales/ronchi/stidor or use of accessory muscles. Speaks in complete sentences.

CARDIOVASCULAR:  Tachycardia (140s to 150s). No murmurs/gallops/rubs/S3/S4.

ABDOMEN:  Soft, nontender, nondistended, normal BS. No hepatosplenomegaly. No guarding, rigidity or rebound tenderness.  FOBT negative.

MUSCULOSKELETAL:  Back and extremities, atraumatic, nontender with FROM. No peripheral edema, calf tenderness or asymmetry. Extremities well perfused.

NEURO:  EOMI.  Normal speech and hearing.  Face is symmetric.  Moving all extremities with good and symmetric motor strength. Sensation grossly intact. Gait not assessed.  GCS 15. Normal mental status.

SKIN:  Pallor with yellow-orange skin discoloration.  Scleral icterus.  No petechiae, contusions, hematomas or ther acute rashes or lesions.


CBC: today                vs     baseline   

H/H 4.7/14.5              vs        8/24

WBC 30                         vs      10-17

Plt 825,000                  vs      750,000

Reticulocyte 12%         vs      25%

Retic count 186,700   vs      500,000


turbid brown

urine bilirubin 3+

blood 3+

urine protein 3+

urobilinogen 4+

RBCs 2-5

WBCa 2-5


Na                   136

K                    3.6

Cl                  101

CO2                19

BUN              29

Cr                  1.2 (baseline 0.6)

Gluc            115

T. Bilirubin      4.5 (0-1.5)

D. Bilirubin      1.7 (0-0.4)

AST                  23

ALT                  30

Alk Phos            109

Troponin: negative

Serum preg test: negative

Type and Cross: 2U pRBCs; Blood type B+

Direct Antigen Test: positive

LDH: 1476 (nml 100-240)

EKG: Sinus tachycardia (HR 152)


1)  The patient’s symptoms are most likely due to:

a) Aplastic crisis

b)  Delayed hemolytic transfusion reaction

c)  Splenic sequestration

d)  Vaso-occulsive sickle cell pain crisis

e)  Anxiety

2)  The patient was normotensive and afebrile throughout her ED stay. Her tachycardia improved (150s–> 110s) with bolus NS hydration. Tachypnea and shortness of breath improved with 2L oxygen via nasal cannula. She remains alert otherwise well. After reevaluating the scenario, you decide to:

a)  Continue supportive treatment, observe, hold off on transfusion

b)  Transfuse 2U pRBCs

c)  Transfuse 1U pRBCs

d)  Transfuse whole blood

e)  Discharge home with close Hematology follow up

3)  In this patient which condition(s) would warrant a blood transfusion?

a)  A typical pain crisis

b)  Drop in hemoglobin 2 units below baseline with symptomatic anemia

c)  Pregnancy

d)  Stroke

e)  Chest pain with cough, fever, purulent sputum



1.B            2.A            3.D and E


The patient’s final diagnosis: Delayed hemolytic transfusion reaction (DHTR). 

DHTR  is a rare, life-threatening complication of sickle cell disease that should be in the differential diagnosis of acute pain crisis especially after  a recent RBC  transfusion.  Because SCD patients have a chronic hemolytic anemia, vaso-occulusive complications often necessitate RBC transfusion to increase oxygen carrying capacity or improve blood flow.

DHTR  in an SCD patient can be tricky to diagnose especially when the presentation mimics a typical pain crisis. Ask about history of transfusion, especially within the last 5-14 days and particularly if the patient was recently hospitalized. A major risk factor for developing DHTR is a history of multiple RBC transfusions, because increased exposure to multi-donor blood antigens increases the patient’s chance for alloimmunization. Alloimmunization – the development of recipient antibodies to donor RBC antigens —  is  thought to be the major mechanism for DHTR and tends to be higher in SCD than in other chronically transfused populations.

DHTR patients will usually have a significant drop in their absolute reticulocyte count from baseline, develop a more profound anemia after transfusion than they had before the transfusion, demonstrate hemolysis with an increase in LDH and indirect bilirubin assays.

In aplastic crisis patients have a significant drop in their hemoglobin concentration, but it is associated with profound reticulocytopenia (<10,000) and a normal or mildly depressed WBC count. There is no elevation in bilirubin because the problem isn’t related to hemolysis, but to bone marrow infarction caused in a majority of SCD patients by Parvo B19 viral infection.

In hepatic/splenic sequestration, patients will have a significant drop in hemoglobin concentration associated with an elevated reticulocyte count (>100,000), indirect bilirubin and LDH levels, and a rapidly enlarging liver/spleen.

The pathophysiology of worsening anemia after an RBC transfusion is thought to be multimodal. Hemolysis occurs when recipient antibodies destroy transfused cells carrying the targeted antigen.  Hyperhemolysis refers to the immunologic response where donor RBCs that are negative for the antigen the antibody is targeting get destroyed, likely due to complement activation. Erythropoesis suppression that is seen with transfusion may also contribute, in addition to an already shortened RBC lifespan to depressed hemoglobin concentrations in SCD.

Diagnosing DHTR : History includes recent transfusion with a history of multiple prior transfusion. Physical exam shows signs of transfusion reaction: fever, chills, myalgias, weakness, dyspnea, red urine, pallor, tachycardia, jaundice and often mimics a pain crisis. Lab tests: CBC (hemoglobin concentration lower than it was prior to transfusion), reticulocyte count (usually markedly depressed), direct and indirect antiglobulin tests (looking for the development of new antibodies but can often be negative), serum bilirubin (total and indirect usually both elevated) and lactate dehydrogenase to assess for increased hemolysis, and a urinalysis to evaluate for hemoglobinuria.

(A negative antibody test does not exclude the diagnosis of a DHTR as the antibody screen often remains negative in these patients. Hemoglobin electrophoresis demonstrates marked destruction of donor RBC seen as a lack of hemoglobin A).3

Management of DHTR in SCD is still done on a case by case basis, however there are a few caveats.  If you suspect DHTR, withhold further transfusion unless absolutely necessary as you could herald a worsening hemolysis because of alloimmunization. If RBC transfusion is required, use phenotypically matched blood that is leukocyte-poor, and E, C, and Kell-negative.  Restrict the number and volume of blood draws. Do not transfuse these patients to hemoglobin levels exceeding 10-11 g/dL as blood viscosity increases with transfusion, and particularly more so in SCD patients, thereby reducing the oxygen carrying capacity. In all cases, contact Hematology as soon as you suspect DHTR because they may want to start high dose steroids  or IVIG.  Treat pain crises as you would otherwise. The patients usually improve with supportive therapy as evidenced by improving RBC counts and reticulocytosis.

In SCD, the few absolute indications for transfusion include aplastic crisis, splenic sequestration, development of new stroke-like symptoms, hemodynamic instability, or cardiovascular collapse. A low hemoglobin/hematocrit alone is not a reason for transfusion because chronically anemic SCD patients can tolerate further anemia well.


  3. Schenunemann LP, Ataga KI.  Delayed hemolytic transfusion reaction in sickle cell disease.  Am J Med Sci. 2010 Mar; 339(3):266-9.


Follow-up to the case:

The patient was admitted to Hematology floors without being transfused in the ED. The patient’s personal Hematologist had recommended against transfusion to avoid further hemolysis, however the admitting Hematologist was concerned about hemodynamic collapse and recommended transfusion of 1 Unit pRBCS (leuko-poor, etc etc). Because of difficulty with type and crossing for this patient, the blood was unavailable at the time she was admitted to the floor.

Within the first 24 hrs of admission, she dropped her hemoglobin concentration down to 2.9 and was started on high dose steroids and IVIG. She was never transfused but recovered with supportive therapy and was discharged on home a week after admission with a hemoglobin of 6g/dL and a diagnosis of DHTR. Shortly thereafter, in clinic, she was started on hydroxyurea.


Senior Report 5.26

Case Presentation by Dr. Katie Ohlendorf

Chief Complaint:

Possible stroke.

History of Present Illness:

The patient is a 78 year old female with no prior CVA.  The patient was last seen well by her son yesterday evening.  Today, the patient was supposed to go to her grandson’s birthday party.  She did not show up and her son has been trying to call the patient for the prior 3 hours without response.  EMS was called to the patients home.  Here, she was found with slurred speech, left sided gaze and left sided hemiparesis.

The patient is following commands.  She is difficult to understand secondary to severe dysarthria.  She denies dyspnea or chest pain.  She cannot tell us when her neurological symptoms started.

Review of Systems:

Per HPI – unable to obtain further secondary to patients severe dysarthria.

Past Medical History:

Hypertension, palpitations, rheumatic fever, pneumonia, and breast cancer.

Past Surgical History:

Lumpectomy, hysterectomy, cardiac ablation, and cardiac valve replacement.


Coumadin, multivitamins, metoprolol, docusate, vitamin D3, calcium carbonate, Arimidex, and alendronate.



Family History:

Not obtained. 

Social History:

Negative for alcohol and smoking.  The patient presents with her son.

Examination of Organ Systems and Body Areas:

VITAL SIGNS:  Blood pressure 184/80, pulse 101, respirations 18, temperature 37.5 temporal, and pulse ox on room air 99%.

GENERAL:  The patient is awake and alert.  Does not appear to be in acute cardiopulmonary distress.

HEENT:  Pupils equal, round andreactive, although gazing to the right.  No conjunctival injection or subconjunctival hemorrhage.  Unable to assess her hearing.  No hemotympanum.  Droop to her left face.  No pus or redness in the posterior pharynx.  Intact gag reflex.

NECK:  Supple without adenopathy.

RESPIRATORY:  Symmetrical breath sounds.  No rales, rhonchi or wheezes.

CARDIAC:  Regular rate and rhythm without murmur, rub or gallop.  Patient has a valvular click from prosthetic aortic valve.

GASTROINTESTINAL:  Soft, nontender.  Active bowel sounds.  No organomegaly, hernias or masses.  Bowel sounds present in all quadrants.

MUSCULOSKELETAL:  Hemipareses, left side.

NEUROLOGIC:  Patient awake and alert.  Dysarthric speech. Hearing unable to be assessed.  Right sided gaze preference.  Left sided facial droop.  Intact gag reflex.  Left sided hemiparesis with 0/5 muscle strength with left upper and left lower extremity.  5/5 muscle strength with right upper and right lower extremity. Receptive wise, she processes her questions fairly well.

SKIN:  No rash.


Na:  139

K:  4.3

Cl:  100

HCO3:  11

Glucose:  139

BUN:  11

Cr:  0.8

Ca:  9.3

Troponin:  <0.017

WBC:  16.7

Hb:  17.1

Hct:  47.2

Plts:  224

PTT:  40.8

PT:  43.7

INR:  4.14





1) How would you manage a warfarin induced coagulopathy if…

  1. a.     The INR is between 3.5 to 5 without significant bleeding
  2. b.    The INR is between 5-9 without significant bleeding
  3. c.     The INR is > 9 without significant bleeding
  4. d.    The patient has an elevated INR and life threatening bleeding


2) How do you manage a heparin induced coagulopathy in a patient with…

  1. e.     Minor bleeding
  2. f.      Major bleeding

3) How do you manage a patient on Pradaxa with significant bleeding?


Answer Choices:

I.  Administer 10 mg of vitamin K with a slow IV push and 10 – 15 ml/kg of FFP

II.  Hold next 1 – 2 doses and consider oral vitamin K 1 – 2.5 mg

III. Consider hemodialysis, PCC and rFVIIa

IV.  Stop heparin administration

V. Hold next 1 – 2 doses and administer oral vitamin K 2.5 – 5 mg

VI.  Lower or admit next dose of warfarin

VII.  Protamine 1 mg per 100 units of total amount of IV heparin administered within the past 3 hours



1) a.  VI.

     b.  II.

     c.  V.

     d.  I.

2) a.  IV.

     b.  VII.

3) III.



There are several anticoagulants on the market today.  Anticoagulants are used in the management of many conditions – they may stop further thrombosis reduce the risk of a thromboembolic event, or help prevent thrombi from forming.  One of the biggest risks of using these agents is hemorrhage and life threatening bleeding.  We will discuss the pharmacology and the complications and management of the various anticoagulants available today.

Warfarin (Coumadin)

Warfarin is the most common oral anticoagulant encountered in the emergency department.  It works by blocking the activation of vitamin K and therefore interferes with the vitamin K dependent clotting factors II, VII, IX and X.  This provides the antithrombotic effect via the extrinsic coagulation pathway (“The EX patriot went to WARfarin”).  Warfarin also has a pro-thrombotic effect via inhibition of proteins C and S.  During maintenance therapy, the antithrombotic effect outweighs the pro-thrombotic effect.

The pro-thrombotic effect is greatest when starting and discontinuing warfarin therapy.  Therefore, when starting warfarin therapy it is necessary to bridge with a parental anticoagulant (such as heparin) until the international normalized ratio (INR) reaches the therapeutic range.  It is also necessary to gradually taper warfarin when discontinuing this medication.  This is due to the differences in the half-lives of the clotting factors and proteins C and S.  The clotting factor half-lives vary from 7 hours (factor VII) to 60 hours (factor II), whereas the antithrombotic proteins have shorter half-lives of 8 hours.

Dosing of warfarin is guided by measuring the INR.  Normal therapeutic range is 2-3.  The INR of 2.5 to 3.5 is goal for those with mechanical heart valves and those who have antiphospholipid antibody syndrome.  The risk of bleeding increases with the increasing INR.

To manage a warfarin coagulopathy you must consider the INR, the patient status, and whether or not they have significant bleeding.  To reverse a warfarin coagulopathy the first step is to hold warfarin, the next to administer vitamin K, and the final is to administer fresh frozen plasma (FFP), prothrombin complex concentrate (PCC) or recombinant Factor VIIa (rFVIIa).

For asymptomatic patients the first step is to hold the next dose to two doses of warfarin.  If the patient is at a high risk of bleeding with an INR of 5-9, consider PO vitamin K administration.  If the INR is > 9 and no significant bleeding then administer 2.5 to 5 mg of PO vitamin K.

Oral vitamin K will decrease the INR in approximately 16 hours (longer if INR > 10).  Oral vitamin K will decrease the INR faster than subcutaneous vitamin K if the INR is < 10.  IV vitamin K may also be used.  This is associated with risk of anaphylaxis and is not used in the routine reversal of anticoagulation.  IV vitamin K also carries a risk of over correction and is reserved for those with life threatening bleeds or those who ingested a rodenticide.  The peak effect from vitamin K is seen in 1-2 days.

FFP is used if there is life threatening bleeding present.  It is the fastest way to reverse the anticoagulant effects of warfarin, and is considered safe.  Administer FFP at a dose of 10-15 mL/kg (typically 3-4 units).

Rapid (and complete) reversal of warfarin may be achieved by PCC or rFVIIa.  PCC contains factors II, VII, IX and X and works in under 30 minutes.  The dose is 25-50 units/kg.  rFVIIa dose is 5 mcg/kg (typical dose is one 1200 mcg vial).  May repeat the dose if INR remains elevated.


Heparin and Low Molecular Weight Heparin

Unfractionated heparin (UFH) activates antithrombin III (AT III), leading to the inhibition of Factor Xa and thrombin.   Heparin has a very short half life (30-150 minutes) and must be given arenterally.  It has a relatively unpredictable anticoagulation effect and requires frequent monitoring of the activated partial thromboplastin time (aPTT).  Goals with therapy are usually an aPTT 1.5 to 2.5 times the normal range.  Heparin may affect the PT and INR, but this is not used to guide therapy.

If bleeding develops while a patient is on UFH, you must first stop the heparin administration.  The aPTT may lag behind the actual anticoagulation dosing; therefore you cannot rely on the aPTT to predict whether your patient has a serious bleed.

Protamine is used to reverse UFH in severe bleeding.  One milligram IV protamine neutralizes 100 units of UFH administered in the prior 3 hours.  Protamine has a risk of anaphylaxis.  It should be given slowly over 1 to 3 minutes and not exceed 50 mg in a 10 minute period.  Protamine has a very short half life (7 minutes) therefore may require more than one dose.

Low molecular weight heparin (LMWH) also work by binding  AT III and deactivation of Factor Xa.  LMWH’s include enoxaparin (Lovenox), dilteparin and tinzaparin.  The half life is longer than UFH and therefore allows for once or twice a day dosing.

LMWH usually cause less bleeding than UFH.  Protamine will not completely reverse the anticoagulant effect of LMWH, only reversing 60% of function.  rFVIIa has been reported to stop severe bleeding with use of LMWH.

Fondaparinux  (Arixtra)is a synthetic drug that is a selective Factor Xa inhibitor.  The use of protamine does NOT reverse fondaparinux.  Hemodialysis (HD) will reduce the level by 20%.  rFVIIa may be used to reverse serious bleeds.


Dibigatran (Pradaxa)

Dibigatran is a competitive, direct thrombin inhibitor.  This prevents development of a thrombus via direct clotting factor inhibition (not depletion).  It is approved for use in atrial fibrillation to help prevent thromboembolism.

Laboratory testing may help determine if dibigatran is contributing to the bleeding event.  aPTT is insensitive to the effects of dibigatran.  If the aPTT is normal this suggests little anticoagulant activity present, but even mild elevations in aPTT can be associated with significant bleeding.  Thrombin time (TT) is less helpful in overdose, but a normal TT excludes the presence of significant dibigatran levels.  Ecarin clotting time (ECT) has a linear relationship with dibigatran levels, although this test is not available at all facilities.

There is no reversal agent for dibigatran.  In an acute overdose, activated charcoal may help in absorbing dibigatran.  Because dibigatran is a direct thrombin inhibitor, administration of clotting factors (FFP, PCC) is unlikely to be helpful in reversal of coagulation.  They may be administered only as a last resort when supportive measures fail to control the bleed.  If a patient develops life threatening bleeding while on dibigratan, consider hemodialysis (primarily excreted in urine, HD will remove approximately 60% of the drug) and the use of rFVIIa and PCC.


Rivaroxaban (Xarelto)

Rivaroxaban is a direct Factor Xa inhibitor.  It is approved for the prevention of stroke and thromboembolism in patients with atrial fibrillation and prevention of thrombus in those who are undergoing knee or hip replacement surgery.

Laboratory testing will show a dose dependent effect on PT and aPTT, however this is not a reliable test.  Similarly the INR is not sensitive to the effects of rivaroxaban.  There are new laboratory testing under development to help determine the level of anticoagulation achieved with rivaroxaban.

There are no reversal agents available.  If a patient has minor bleeding either discontinue therapy or delay the next dose.  If there is moderate to severe bleeding, initiate supportive treatment (blood, IVF, cardiac monitoring)and try to control the site of the bleeding.  Oral charcoal may be administered if rivaroxaban was administered within the prior 2 hours.  Unlike dibigatran, rivaroxaban is NOT dialyzable.  If severe/life threatening bleeding PCC may be tried.

Great resource on anticoagulant reversal:

Senior Report 5.25

Case Presentation by Dr. Dan Seitz

A middle aged African-American John Doe, presents as a medical code. On arrival the patient is actively seizing. According to EMS the patient has been seizing for approximately 40 minutes prehospital. After eight rounds of lorazepam pushes the patient continues to have seizure activity. The decision is made to load the patient with one gram of phenytoin, start a lorazepam drip and intubate the patient. Rapid sequence intubation is performed using etomidate and succinylcholine. For post-intubation sedation and to facilitate imaging studies the patient receives morphine, the lorazepam drip and gets two doses of vecuronium while in the ED. The patient is transferred to the Neuro ICU for further management.


1)  The patient receives a considerable amount of both lorazepam and phenytoin. What solvent must you be aware of which can cause hyperosmolarity and metabolic acidosis?
a) Ethylene glycol
b) Fluoxetine hydrochloride
c) Levamisole
d) Propylene glycol

2)  The patient is found to be severely hyperkalemic. Which medication likely worsened this?
a) Etomindate
b) Lorazepam
c) Phenytoin
d) Succinylcholine

3)  What is the most common complication of multiple doses of paralytics?
a) Hyperkalemia
b) Paresthesias and peripheral neuropathies
c) Prolonged paralysis and myopathy
d) Rhabdomyolysis

4)  In the ICU the patient is found to be septic. He develops hypotension that is refractory to IV fluids and pressors. Administration of which medication should be considered?
a) Hydrocortisone
b) Neostigmine
c) None – permissive hypotension is appropriate in this setting
d) Xigris (activated protein C)

5)  After administering a paralytic agent – the patients eyes will be:
a) Reactive to light
b) Non-reactive to light


1) D   2) D   3) C   4) A   5) reactive

An awareness of the potential adverse effects of medications that we order is essential in becoming a competent physician.  We often administer medications in the Emergency Department and these adverse effects do not materialize until the patient reaches the floor or the ICU.  This case highlights just a few of these potential adverse effects.

1)  D.   In some instances adverse effects are the result of a medication additive.  Propylene glycol is the primary solvent in lorazepam, phenytoin, etomidate and some “environmentally safe” antifreeze preparations.   Propylene glycol is a clear, odorless, colorless viscous liquid – which is hepatically metabolized to lactic acid.  Adverse effects of large volumes of propylene glycol include cardiovascular toxicity (hypotension, bradycardia and QRS widening), neurotoxicity (seizures – in particularly in small infants), and electrolyte/metabolic disturbances (hyperosmolality and lactic acidosis).  Alternatives to these agents include midazolam, phosphenytoin and ketamine – which do not contain propylene glycol.

2)  D.  The most important adverse effect of Succinylcholine is its potential to induce hyperkalemia.  Which has been lethal and life threatening in many case reports.  Succinylcholine will typically cause a 0.5 mEq/L elevation in a patient’s potassium.  This only become clinically significant in patients who present with diseases that cause ACh regulator upregulation:

  • Denervating injuries or diseases (eg, stroke, spinal cord injury, MS, ALS
  • Inherited myopathies (eg, muscular dystrophy)
  • Burns – subacute
  • Crush injuries
  • Rhabdomyolysis or risk of rhabdomyolysis

3)  C.  The most important thing to remember when redosing paralytics is that they have no analgesic or amnestic properties.  Never give paralytics as monotherapy.  The most common side effect of multi-dose paralytics is myopathy and prolonged paralysis.  This “critical illness polyneuromyopathy” is associated with prolonged ventilation and worse outcomes.  As with all medication weight the pros and cons (risk of self extubation – is never a good thing), and act in the best interest of your patients.

4)  A.  There is a long standing debate regarding the usage of etomidate as an induction agent.  Proponents of drug argue that in these septic patients you should not risk immediate hemodynamic stability (etomidate does not worsen hypotension), that cortisol levels do not fall below physiological levels, and that in prospective randomized controlled trials there has been no differences shown in mortality.  Opponents of the drug argue that etomidate inhibits cortisol synthesis, depressing cortisol levels for 12-24 hours; this is logically not beneficial for sick patients who are attempting to mount a stress response.  Opponents also argue that while mortality may be the same, morbidity is not.  Single dose Etomidate has been shown to increase ICU stays, duration of intubation and hospital length of stays.  Whatever side of the fence that you may fall on; in our clinical scenario consideration should be made for the possibility of adrenal suppression and 100 mg of hydrocortisone should be administered.

As an aside Xigris is officially dead.

Pupillary light reflex is NOT altered by neuromuscular blocking drugs.  As shown in Archives of Neurology in 1997, and re-proven in Annals of EM – March, 2011.  The second article has lots of discussion on the Annals Journal Club website.  Read the articles and see for yourself the next time that you intubate a patient.



Manual of Toxicologic Emergencies.  Goldfrank.

Samantha Wood, Michael E. Winters, Care of the Intubated Emergency Department Patient, The Journal of Emergency Medicine, Volume 40, Issue 4, April 2011, Pages 419-427, ISSN 0736-4679, 10.1016/j.jemermed.2010.02.021.

The effect of etomidate on adrenal function in critical illness: a systematic review.  Albert SG, Ariyan S, Rather A.  Intensive Care Med. 2011 Jun;37(6):901-10. Epub 2011 Mar 4

Gray AT, Krejci ST, Larson MD. Neuromuscular blocking drugs do not alter the pupillary light reflex of anesthetized humans. Arch Neurol. 1997;54(5):579-584.

David A. Caro, Steven Andescavage, Mohsen Akhlaghi, Colleen Kalynych, Robert L. Wears, Pupillary Response to Light Is Preserved in the Majority of Patients Undergoing Rapid Sequence Intubation, Annals of Emergency Medicine, Volume 57, Issue 3, March 2011, Pages 234-237, ISSN 0196-0644, 10.1016/j.annemergmed.2010.10.017.

Senior Report 5.24

Case Presentation by Dr. Matt Steimle

You are starting your shift at a small rural hospital with limited resources.

At the start of your shift during transition of care, you receive sign out about a 63-year-old male who has chest pain, is undergoing a cardiac workup, and is admitted to his own internal medicine doctor with a cardiology consult. You are told his first EKG has first-degree atrioventricular block unchanged from prior EKGs and that his first troponin I is negative. He has received aspirin and a dose of nitroglycerin.

His vital signs at the time of transition of care: BP 145/94, P 65, R 20, T 37.1, and 100% saturation on 2L O2 by nasal cannula

His repeat EKG and troponin I are ordered to be drawn in 3 hours.

2 hours into your shift you notice that the patient is lightheaded and confused, and the family and the nursing staff indicate that this is a sudden change. You examine him and order another 12-lead EKG.

Pertinent findings on repeat physical exam:

Vitals: BP 70/40, P 39, R 20, T 37.2, 100% saturation on 2L O2 by nasal cannula

General: complains of feeling presycopal and lightheaded

Cardiac: bradycardic, no M/R/G, s1 and s2 normal

Neuro: a+ox3, but is slow to respond; otherwise the rest of your neuro exam is unremarakable


1. Which venous site is preferred for transvenous pacemaker placement?
a) brachial
b) left internal jugular
c) right internal jugular
d) right subclavian

2. What should the initial settings be on the pulse generator?
a) rate 60 beats/min or 10 beats faster than the underlying ventricular rhythm, output 5 mA, sensitivity 10 mV
b) rate 70 beats/min or 10 beats faster than the underlying ventricular rhythm, output 5 mA, sensitivity 10 mV
c) rate 80 beats/min or 10 beats faster than the underlying ventricular rhythm, output 5 mA, sensitivity 10 mV
d) rate 80 beats/min or 10 beats faster than the underlying ventricular rhythm, output 5 mA, sensitivity 3 mV

3. Which EKG lead do you connect the pacemaker to?a) II

b) III
c) AVL
d) V1

4. When do you inflate the balloon?
a) 10-12 cm for a subclavian or internal jugular insertion
b) 14-16 cm for a subclavian or internal jugular insertion
c) 16-18 cm for a subclavian or internal jugular insertion
d) 8-10 cm for a subclavian or internal jugular insertion

5. What will the EKG show when the pacemaker is in the right ventricle?
a) both the P-wave and QRS complex will be negative
b) P-wave becomes large and biphasic
c) P-wave becomes smaller and the QRS complex becomes larger
d) P-wave is larger than the QRS complex and deeply inverted

6. When the sensitivity control is in the demand (synchronous) mode, the pacemaker does not sense ventricular depolarizations.

a) False

b) True


1. c

2. d

3. d

4. a

5. c

6. a


Heart block is a known complication of acute myocardial infarction (AMI).  15% to 19% of AMI patients progress to some degree of heart block. First-degree atrioventricular (AV) block progresses to second- or third-degree AV block 33% of the time, and second-degree AV block progresses to third-degree AV block about 33% of the time.

AV block occurring during anterior wall AMI is believed to occur due to diffuse ischemia of the septum and infranodal conduction tissue. These patients can progress to higher-degree AV block without warning, and consideration should be given to “prophylactic” cardiac pacemaker placement in such patients. Hemodynamically unstable patients unresponsive to medical therapy should be paced. One should try transcutaneous cardiac pacing until a transvenous pacemaker can be placed.

Temporary cardiac pacing for bradyarrhythmias in acute myocardial infarction may be necessary, even though permanent cardiac pacing may not be required. Revascularization strategies with thrombolysis and angioplasty have reduced the need for permanent pacing since there is less myocardial damage and a greater chance that bradycardia and conduction abnormalities will resolve. Therefore, there may be a need for temporary cardiac pacing.

An important consideration in the setting of AMI is that bradycardia, even if asymptomatic or transient, can cause decreased coronary blood flow and reduced myocardial perfusion.

Guidelines from the American Heart Association and American College of Cardiology recommend temporary cardiac pacing in patients with AMI and the following cardiac rhythms and conduction abnormalities:

1.            Asystole

2.            Symptomatic bradycardia due to sinus node dysfunction, or Mobitz type I             (Wenckebach) second degree AV block that is not responsive to atropine therapy

3.            Mobitz type II second degree or complete heart block

4.            Bilateral or alternating bundle branch block, including right bundle branch block             with left anterior fascicular block or left posterior fascicular block

5.            A new bundle branch block with either old or new first degree AV block

6.            An old right bundle branch block with first degree AV block and a new fascicular             block

There are complications with the insertion of a endocardial pacemaker in a patient who has received thrombolytic therapy and is being treated with aggressive anticoagulant and antiplatelet therapy. In these settings, transcutaneous pacing is preferred. Insert endocardial pacemaker only if warranted due to recurrence of symptoms.

Avoid temporary pacing:

1. When the risks outweigh the benefits

2. When there are intermittent, mild or rare symptoms, and the bradycardia is well tolerated. This includes mildly symptomatic (mild or rare symptoms) complete heart block with an adequate and “stable” escape rhythm or symptomatic sick sinus syndrome with only rare pauses

3. In the presence of a prosthetic tricuspid valve or right ventricle infarct (remember to obtain right-sided leads RV3 and RV4), a circumstance in which it may not be possible to achieve right ventricle capture

4. In a patient with AMI who has received thrombolytic therapy and is being aggressively treated with anticoagulation or antiplatelet agents. Insertion of the pacemaker by a cutdown or the right internal jugular may be associated with significant bleeding in such patients.

5. When there is no informed consent, unless temporary pacing is considered life-saving

Procedure basics:

Continuous electrocardiographic monitoring is recommended. Fluoroscopy is desirable, safer, and insures proper placement under direct fluoroscopic guidance, but is not always feasible. If fluoroscopy is not available, a balloon-tipped catheter is recommended as long as the patient has intact circulation to help “float” the pacemaker wire to the desired location within the right ventricle.

Access site- the best access site for temporary pacing is via the left subclavian vein or right internal jugular vein. Brachial and femoral vein approaches are not recommended because of the risk of cardiac puncture and instability using a brachial approach, and the risk of deep vein thrombosis and infection using the femoral approach. The right internal jugular and the left subclavian veins have the straightest anatomic pathway to the right ventricle and are generally preferred for transvenous pacing. You will need an introducer set or sheath. Some pacing catheters are prepackaged with the appropriate equipment, others require a separate set. The introducer sheath must be larger than the pacing wire to allow it to pass!

Obtain pacing generator:

The rate control or (top control) is where you set the rate or beats per minute.

The ouput control (middle control) allows the operator to vary the amount of electrical current (amperage, amps) delivered to the myocardium; increasing this setting increases the output and improves the likelihood of capture.

The pacing control/sensitivity (the most inferior control), is determined by adjusting the gain setting for the sensing function of the generator. By increasing the sensitivity one can convert the unit from a fixed-rate (asynchronous mode) to a demand (synchronous mode) pacemaker. The voltage setting represents the minimum strength of electrical signal that the pacer is able to detect. Decreasing the setting increases the sensitivity and improves the likelihood of sensing myocardial depolarization.

In the fixed-rate mode(asynchronous) the unit fires despite the underlying intrinsic rhythm, the unit does not sense any intrinsic electrical activity. In the full demand mode, (synchronous mode similar idea to synchronized cardioversion) the pacemaker senses the underlying ventricular depolarizations and the unit does not fire as long as the patients ventricular rate is equal to or faster than the set rate of the pacing generator.

Initial settings: Set Rate (80 beats/min or 10 beats faster than the underlying ventricular rhythm, output 5 mA, sensitivity 3 mV)

Obtain central venous access with an introducer. Attach the still-compressed sterile sheath to the introducer hub (make sure the connector of the sheath is firmly attached to the hub of the introducer), open the hub of the introducer by turning it counter clockwise to allow passage of the pacing wire.

Inflate then deflate the balloon on the pacing wire before it is introduced to test for integrity. There is a valve that keeps the balloon inflated; it must be turned to inflate /deflate the balloon. Use 1.2-1.5 mL of air for the balloon. An assistant attaches the proximal pacing wire to the nonsterile energy source. Use the demand mode and turn on the pacer output to the highest level, rate about 80/min, with the balloon deflated.

Insert the pacing wire into the still collapsed sheath and into the hub of the introducer. Slowly advance the wire through the introducer. Inflate the balloon when the tip of the pacing wire is in the superior vena cava (10-12 cm) and continue to advance. Close the valve to keep the to keep the balloon inflated. Watch the ECG and look for capture, demonstrated by a wide QRS pattern after each pacer spike. The right ventricle should be encountered by 15-20 cm as noted by markings on the pacer wire. If no capture is seen by 25 cm, deflate the balloon, withdraw the wire and try again. When consistent capture is seen, deflate the balloon and advance the wire 1-2 cm more to seat the wire in the endocardium. Tighten the valve on the sheath introducer to stop subsequent movement of the wire, and extend the sheath its full length. If required suture the wire in place. The lead should be tied down in at least two different sites, one where the lead exits from the skin and other to a loop formed with the lead.

Turn down the output control (middle control), then slowly turn it up to determine pacing threshold (first sign of capture). Set the output at two to three times the stimulation threshold and set the desired rate. Leave the pacer in the demand mode until stability is assured.  Obtain chest x-ray and 12-lead EKG.

EKG Guidance: The patient should be connected to the limb leads of an EKG machine, The pacemaker may be attached to any of the V leads (usually V1 or V5)

When the pacing wire enters the superior vena cava (10-12 cm for a subclavian or internal jugular insertion) the balloon is inflated.

The V lead ( usually V1 or V5) should be monitored. The P wave and QRS complex should be observed to ascertain the position of the catheter tip. As the pacing wire passes through the tricuspid valve, the P-wave becomes smaller and the QRS complex becomes larger. After successful passage of the pacing wire into the right ventricle, the tip should be advanced until contact is made with the endocardial wall. When this occurs, the QRS segment will show ST segment elevation.

Complications related to Central Venous Catheterization:

1.            Inadvertent arterial puncture (compress)

2.            Venous thrombosis and thrombophlebitis uncommon (Femoral vein thrombosis             more common)

3.            Pneumothorax

4.            Hemothorax

5.            Thoracic duct laceration chylothorax (left-sided insertion)

6.            Air embolism

7.            Wound infection

8.            Pneumomediastinum

9.            Hydromediastinum, hemomediastinum

10.            Phrenic nerve injury

11.            Fracture of guide wire and embolization

Complications of right-sided heart catheterization:

1.            Dysrhthymia with pvc’s bing a common occurrence

2.            Ventricular tachycardia

3.            Pacer in pulmonary artery

4.            Pacer in coronary sinus

5.            Left ventricle through ASD,VSD

6.            Septal puncture

7.            Extraluminal insertion

8.            Arterial insertion

9.            Perforation of the ventricle can result in loss of capture, hemopericardium,             tamponade

10.            Local infection

11.            Balloon rupture

12.            Pulmonary infarction

13.            Phrenic nerve pacing

14.            Rupture of the chordae tindinae

Defibrillation and cardioversion are safe in patients who have temporary pacemakers


1. Roberts: Clinical Procedures in Emergency Medicine, 5th ed; 2009

  1. UpToDate: temporary cardiac pacing; 2012