Conference Notes 7-24-2012

Conference Notes 7-24-2012


Junctional rhythm does not occur in healthy hearts so you have to investigate for ischemia or other pathology.

Brugada Syndrome is a genetic condtion that affects phase 0 sodium channels.  Causes sudden death in structurally normal hearts.   Affects asian men more commonly.   EKG demonstrates RBBB with j point elevation and widening in leads V1-3.   

Elise comment:  not everything that looks like Brugada is Brugada so you need cardiology to consult on these EKG’s if there is a question.

Treat WPW with afib with procainamide if stable.  If unstable, cardiovert. 

Norepi is a good pressor to use if you don’t want to increase tachycardia too much.  Alpha effects (vasoconstriction) are more prominent.

When resuscitating a patient with septic shock, vasopressors work best with a full vascular bed.   Pressors can falsely elevate cvp so be sure you are giving adequate fluids.   There is no evidence that trandelenburg position improves pt outcome or cardiopulmonary function.  There is some evidence it may worsen cv status.  So don’t use it.

For massive transfusions, pt’s should receive prbc’s/platelets/ffp in 1:1:1 ratio.

For pelvic or abdominal injuries  you want iv access above the diaphragm.  IO in the proximal humerus is a great second line access means is you can’t get peripheral iv access.

Anaphylaxis is an IGE-mediated immune reaction.   IM Epinephrine in the thigh (0.3-0.5mg) is the treatment for adults.  If you have two of the following: skin/respiratory/gi/cardiovascular symptoms you have anaphylaxis.  

Transvenous pacing for an unstable patient with bradycardia or heart block is indicated if transcutaneous pacing at max output is not getting good capture.  In the meantime try atropine. 

Barounis comment: Check for  hyperkalemia if transcutaneous pacing is unsuccessful.

Initial management of rapid afib is rate control with cardizem.

Barounis comment: I would prefer elective cardioversion for acute rapid afib.  Elise comment: totally would want to be shocked for rapid afib of less than 48 hours.




SIRS: hr>90, tachypnea, elevated wbc, abnormal temp either hi or low

Sepsis is SIRS plus an infection

Severe sepsis is sepsis with hypotension prior to IV fluids

Septic Shock: severe sepsis not responding to fluid bolus of 20cc/kg

 Sepsis patients need at least 20ml/kg of NS with a minimum of 1 liter over 30 minutes.

Broad spectrum in the first hour improves mortality.  Delay of antibiotics increases mortality of about 7% per hour.

Early Goal Directed Therapy: has been shown to reduce sepsis mortality compared to standard care.  Indication of EGDT is persistent hypotension or lactate >4 despite initial fluids.  Place a CVP line above the diaphragm.  CVP is a proxy for preload.  CVP helps you to optimize volume status.  Goal is CVP of 8-12 or 12-15 if the patient is on a ventilator.  If CVP less than 8 give more fluids.   Next step is to start vasopressors.  Vasopressors do not improve mortality.  No data to say which pressor is superior.   Norepi however is the drug of choice due to less adverse effects.    Central venous oxygen satuation is a marker of success/mortality.  So get a VBG off your central line.   If Scv02 is <70% you got problems.   Intubate/Check hgb/start dobutamine as an inotrope.  Transfuse if hgb less than  7. 7-10 is a grey zone.  Lactate  clearance is a reasonable proxy for Scvo2.  

No steroid use/not indicated for sepsis. Steroids only if pt’s on chronic steroids and are steroid dependent.   Procalcitonin if nl may be a sign you can stop antibiotics but evidence is weak.

Wise comment: if Scvo2 is low, early intubation with neuromuscular blockade is indicated.

C Kulstad: Sepsis patients ned high fluid maintenance rates like 200ml/hr

Lovell comment:  If you give fluid bolus to patients give a liter not 200ml bolus.  Also use EGDT protocol in our EMR.

Hermann comment:  IV infusion pumps do not get the fluids in fast enough.  You have to hang fluids with a pressure bag and no pump.   Corroborated by Dr. E Kulstad/Lovell

Harwood comment: Questioned that pressors in septic shock don’t improve mortality.


Definition: increase in symptoms of cough/sputum/dyspnea.  All copdr’s  have a decreased FEV1/FVC ratio.

Treatment priority is to ensure oxygenation.   Hypercapnea is well tolerated.    Get O2 sat to 92% and 95% in dark skinned patients.   Can use venti masks but usually 4L pnc is enough to correct oxygenation problems in copdr’s.  If you need more oxygen support you gotta think about other things.

Bipap has been shown to decrease need for intubation, decrease risk of nosocomial infection, and decrease mortality.    Intial settings are 8-12 inspiratory and 3-5 expiratory.  If you need to adjust settings a reasonable move would be 15/7.

Vent management for intubated patients: high inspiratory flow rates and low tidal volumes (5-7ml/kg) and low rates.  This will help to minimize airway pressures.

Treatment: Nebs are more effective than in mdi’s in COPD exacerbation.   Magnesium can be used.  Theophylline has not been shown to improve outcomes in COPD.  Chest PT also not indicated in acute COPD exacerbation because it can worsen an acute exacerbation.   Steroids have been shown to improve symptoms, lung function and decrease hospital stay.  About a third of COPD exacerbations are triggered by bacterial infection so antibiotics are indicated for acute exacerbations.  Sputum cultures are not useful.   Pseudomonas risk factors:4 episodes/year, recent hospitalization, previous pseudomonas, or severe copd.   If risk factors for pseudomonas are present give zosyn, if not then ceftriaxone.    

Most common causes of death in an admitted COPD patient: heart failure, pneumonia, PE, then COPD.

Work UP: CXR, EKG, Troponin, CBC, BMP,  ABG,  +/- Blood cultures.

Girzadas comment: What triggers PE work up (one study showed 20% incidence of pe in COPD exacerbation but my experience does not match that)?    Robbie: persistent hypoxia or remarkable risk factors,  exam findings, lab or cxr findings suggestive of PE.

Harwood comment:   CO2 narcosis is very common due to excess O2 administration.  Beware of giving too much oxygen to COPDR’s.   If the patient needs to be intubated for CO2 narcosis, they likely will be hard to get off the ventilator.   Try bipap first to reduce CO2 retention but for very high PCO2’s it may not work.


  Common ED clinical conundrum is separating out pneumonia/chf/copd.

Bipap has been shows to decrease intubations/admissions/mortality.   PEEP helps.  12/5 again is a reasonable starting point for the bipap machine.

Nitroglycerine (both IV and Sublingual) is the key medication treatment.   Give 4 sprays of ntg to give a 1600microgram bolus rapidly.   Start 50mcg/min drip and titrate up rapidly to around 200 mcg/min.  If patient still not improving and BP still up, you can add nitroprusside drip.

Beckemeyer and Harwood comments: Look for improvement from ntg by improved dyspnea and improved blood pressure.   You will only be at the very high levels of ntg administration for a short while because BP will start going down.  You will need to be alert as to when to start going down on ntg dose.

Diuretics alone can increase mortality. Diuretics can worsen renal function.  You need to not give lasix until you have ntg going.

ACE-I ‘s have been shown to improve patient outcomes.

Contraindications to  NTG vasodilatation:  RV infarct, aortic stenosis, hypertrophic cardiomyopathy, hypotension.

Barounis comment: how do you manage patient pulling off bipap mask?   Elise and Christine say give ativan cautiously.   If they either keep pulling of mask or become too somnolent you proceed to intubation.

Girzadas comment: Be alittle bit patient for the NTG to work for the first 15 minutes.  Most patients don’t need to be intubated.  The nitro will work magic if given alittle time.