Conference Notes 11-6-2012

Conference Notes 11-6-2012

Girzadas    Recruiting Season Prep

Lambert  Study Guide  Resuscitation

Discussion of management of witnessed VF arrest between Harwood and Lambert.  If you are by yourself managing the patient defibrillate first.  If you have someone else helping you, first  start CPR while another person gets the defibrillator.

 Procainamide infusion is stopped if you reach 17mg/kg, QRS widens by 50%, pt becomes hypotensive, or arrhythmia is terminated.

Most common common underlying cause of CHF is coronary artery disease.

Cuffed ET tubes in pediatric patients are recommended to eliminate oropharyngeal contamination into the airway.

Co2 detectors on ET tubes can have false negative results if pt has no circulation.  Meaning the ET tube can be in the trachea but patient with no circulation is not expiring any CO2

There was a discussion of the appropriate tidal volume for ventilated patients between Lambert and Barounis.   Smaller tidal volumes are becoming more recommended 6-8ml/kg for all ventilated patients is now considered lung protective.

There was a discussion of whether or not to sedate patients prior to giving adenosine.  No general agreement about the necessity of this.  Most did agree that if there is time and adequate help, giving sedation is the kind thing to do to limit pt discomfort with adenosine.

Most common adverse effect of IV amiodarone is hypotension.

IV diltiazem is contraindicated in wide complex tachycardia.

In a choking patient, if they can speak or cough do not intervene.  Let them try to clear their throat spontaneously.

Eastvold        Acute Decompensated Heart Failure

There are few guidelines regarding acute decompensated CHF.  This is because most decompensated CHF patients in the ER are suffering from diastolic dysfunction and most CHF research is on patients with systolic dysfunction.

Pearl #1 Chf is not gout.  It is not a one treatment/one approach illness.

Up to 50% of patients arriving to the ED with pulmonary edema are not fluid overloaded.  However, afterload mismatch/vascular failure  can cause body fluid to be shifted to the lungs even if the patient is not total body fluid overloaded.

In a patient with acute chf who is hypertensive, they are less likely to have systolic dysfunction.

Pearl #2 Pts with CHF and HTN suggest vascular failure and fluid predominantly shunted to lungs with diastolic dysfunction.

5 reasons the patient in front of you doesn’t have  chf: no hx of chf, no DOE, no rales, no cardiomegaly, nl ekg, BNP<100.  The more of these that are present the less likely it is to be CHF.

BNP may be falsely low due to flash pulmonary edema (it takes time to increase the bnp) or acute mitral insufficiency.

Vascular pedical width (width just below the aortic knob >71mm) and cardiomegaly on CXR increase chance of chf.   Using the cardiac or abdominal probe, Ultrasound findings of at least  4 lung rockets/b-lines/headlights/searchlights in the fog are indicative for alveolar/interstitial fluid. Put the probe on the anterior chest bilat.    This ultrasound finding can be due to pulmonary edema, pulmonary fibrosis, or Aids lung and a few  others.

 PT with CHF and a Bun>43, SBP<115, Cr>2.75=22% mortality in hospital.   Elevated troponin and hyponatremia are another two markers for high risk CHF.

To categorize CHF patients in the ED look at the BP

CHF with HTN (>140 systolic): Rapid onset.  Fluid is in the wrong place (vascular failure).  Bipap and nitrates are the work horses for this category.  +/- Lasix 20-30 min after treatment started.    For the severely dyspneic patient with very high BP, you can load the pt with NTG by giving multiple suplingual sprays.     

Normotensive: Gradual onset.  Chronic CHF patients.  Give NTP or IV NTG and lasix. These patients can have a high mortality though.

Hypotensive: Cardiogenic shock. 

CHF with ACS: This does not mean isolated troponin leak.  Pt’s should have chest pain, ekg changes or pattern of troponin changes.

Isolated RV failure: nt discussed in this lecture

Morphine: Increases mortality and rate of intubation and ICU admission.

Acute CHF patients only have 20% of normal renal flow.  This risks renal injury from lasix if you over diurese.  It also may not be much help in patients with vascular mismatch CHF.  If you use lasix, start with low dose.  If the patient is on lasix at home, match their usual po dose with iv Lasix.  Josh feels EMS should not be giving lasix because it is often misused.

NTG is the drug of choice for decompensated heart failure.

IV ACE-I is usually not needed if you are using NTG aggressively.

BiPap has been shown decrease mortality.  Use it for patients who arehypoxic and/or dyspneic.

Harwood comment: Give 4 sprays of NTG pretty much out of the gate to the severely hypertensive patient.   Intubating a acutely decompensated CHF patient  should be considered a failure of EM management.

Tomasello     ST Depression on EKG

ST depression in AVL suggests inferior wall AMI.  Get serial ekg’s and watch for inferior ST elevation.

High lateral AMI’s are usually due to circumflex occlusions and mostly don’t have much ST elevation because the high lateral region has low voltage generally.  Look for minimal st elevation in high lateral leads and inferior st depression.

Think posterior MI with tall anterior R wave, horizontal st depression anteriorly, upright t waves anteriorly. Posterior MI’s  affect  the posterior or far lateral aspect of the left ventricle.

 Discussion about DeWinter wave vs. Wellen’s.  Both are related to LAD occlusion and are found anteriorly, but Wellen’s is usually seen when pt is pain free.

With an EKG with diffuse ST segment depressions think either three vessel disease or left main (left coronary prior to bifurcation of LAD and circumflex)occlusion.   You need st depression in 6 leads or more with st elevation in AVR  to call left main.  Most need CABG so don’t give plavix.  


Ryan   Med Student Review