Conference Notes 7-20-2016

Barounis     Management of the Hypotensive Patient

Recent study on HelmetNon-Invasive Ventilation

Results  Eighty-three patients (45% women; median age, 59 years; median Acute Physiology and Chronic Health Evaluation [APACHE] II score, 26) were included in the analysis after the trial was stopped early based on predefined criteria for efficacy. The intubation rate was 61.5% (n = 24) for the face mask group and 18.2% (n = 8) for the helmet group (absolute difference, −43.3%; 95% CI, −62.4% to −24.3%; P < .001). The number of ventilator-free days was significantly higher in the helmet group (28 vs 12.5, P  < .001). At 90 days, 15 patients (34.1%) in the helmet group died compared with 22 patients (56.4%) in the face mask group (absolute difference, −22.3%; 95% CI, −43.3 to −1.4; P = .02). Adverse events included 3 interface-related skin ulcers for each group (ie, 7.6% in the face mask group had nose ulcers and 6.8% in the helmet group had neck ulcers).

Conclusions and Relevance  Among patients with ARDS, treatment with helmet NIV resulted in a significant reduction of intubation rates. There was also a statistically significant reduction in 90-day mortality with helmet NIV. Multicenter studies are needed to replicate these findings.

*Helmet NIV


*AVAPScan be used in patients who are not getting optimaltidal volumes with NIV.  It gradually increases IPAP.  Usually used in COPDer’s.

Management strategy with BIPAP: For COPDer’s move up on the IPAP.   For CHF, go up on the EPAP.   For ARDS go up on EPAP.

Dave’s first two steps when evaluating hypotensive patients are: 1. Touch the patient to evaluate their peripheral perfusion.  2. Put an ultrasound probe on the patient to evaluate their cardiac pump function.   Mitral valve movement directly correlates with LV function.  The other method he likes is calculating fractional shortening.

*Fractional shortening.  You drop an M mode line through the left ventrical and the machine will calculate the percentage change in width of the left ventrical.   Less than 50% is c/w heart failure.

Dave brought up the situation of unilateral R side CHF.  This can be caused by severe mitral valve disease causing an eccentric regurgitant jet into the left atrium forcing backflow preferentially into the right pulmonary vein.   If you see a patient with a right unilateral big infiltrate that looks like unilateral CHF, throw an ultrasound probe on the heart.  If the mitral valve looks abnormal, get a formal echo to evaluate for an eccentric reurgitant jet. 


*Unilateral Pulmonary Edema   Editorial comment: Unilateral right side pulmonary edema is a Zebra diagnosis but you could look amazingly good if you pick this one up. 


 *Eccentric mitral regurgitant jets.


*Sonographic B lines go all the way to the bottom of the screen.  These indicate most commonly CHF but could also be due to other fluid in the alveoli.

In hypotensive patients with Afib and RVR don’t use diltiazem.   Give magnesium 2-4 grams.   Don’t worry to much about the magnesium level.  Patients can tolerate mag levels up to 4.9.  2nd line drug is Amiodarone 150mg bolus followed by 1mg /min.

E. Kulstad       CV Study Guide

*Indications for Transcutaneous Pacing

Compared to placebo, Heparin and LMWH do not provide morality benefit in non-STEMI acute coronary syndromes.

Compared to placebo, Heparin and LMWH demonstrate a trend toward mortality benefit in STEMI’s.


*Sgarbossa Criteria


*Heart Score Components

*HEART Score Outcomes MACE (Major Adverse Coronary Events)


Carlson       Toxicology Cases

*Acetaminophen Overdose Decision-making

*Rumack Matthews Nomogram

*Acetaminophen Toxicity Mechanism.  The amount of acetaminophen overwhelms the conjugation pathways and the excess acetaminophen instead gets metabolized to NAPQI which is toxic.

*NAC Dosing

Dextromethorphan can give you a positive toxicology screen for PCP.  It is a dissociative drug similar to ketamine.  It is commonly mixed with marijuana.  Patients can have bad trips.  Treat patients with benzo’sto manage the agitation.

Drugs that cause a positive toxicology screen for PCP: PCP, dextromethorphan, and ketamine.

Caffeine is a methyl xanthine that binds the adenosine receptor. If you are treating SVT for caffeine overdose you will need to use higher dosing of adenosine.  You should start at 12 mg of adenosine.

Caffeine will cause vomiting and hypokalemia.  Caffeine acts at the kidney to increase potassium diuresis.   Hypokalemia is variable in caffeine overdose and the level of hypokalemia should not be used to risk stratify or rule in/out the diagnosis.

Toxidrome: Anxiety/agitation, tachycardia, vomiting and hypokalemia think caffeine toxicity.

Iron toxicity causes an anion gap acidosis, hyperglycemia, and leukocytosis.  Serum iron levels >500 are dangerous.


*5 Stages of Iron poisoning.   Treat with deferoxamine.

Vitamin A is really the only dangerous vitamin overdose.  It can cause cerebral edema.

If you identify a patient with an anion gap metabolic acidosis and a respiratory alkalosis they have ASA toxicity.  Death from salicylate is a CNS death, not a pulmonary or cardiovascular death. Alkalinize serum to keep salicylate out of CNS.  Alkalinize urine to enhance elimination. Replace potassium.  Finally, hemodialysis can be life-saving.

Tinnitus is common with a salicylate level above 20. 

*Indications for dialysis in ASA toxicity

Hart    Code STEMI

Goal: Get the patient to the Cath Lab in less than 60 minutes for a STEMI.  Identify alternative critical diagnoses such as PE, Aortic dissection, perforated ulcer, GI bleed,  hyperkalemia, pericardial effusion, valve rupture.

No need for O2 if a Code STEMI patient is sating at or above 94% on room air. 

Air Versus Oxygen in ST-Elevation Myocardial Infarction (AVOID) trial compared supplemental oxygen vs no oxygen unless O2 fell below 94%.

"The AVOID study found that in patients with ST-elevation myocardial infarction who were not hypoxic, there was this suggestion that, potentially, oxygen is increasing myocardial injury, recurrent myocardial infarction, and major cardiac arrhythmia and may be associated with greater infarct size at 6 months," lead author Dr Dion Stub (St Paul's Hospital, Vancouver, BC, and the Baker IDI Heart and Diabetes Institute, Melbourne, Australia) concluded.

Methods and Results—We conducted a multicenter, prospective, randomized, controlled trial comparing oxygen (8 L/min) with no supplemental oxygen in patients with STEMI diagnosed on paramedic 12-lead electrocardiogram. Of 638 patients randomized, 441 were confirmed STEMI patients who underwent primary endpoint analysis. The primary endpoint was myocardial infarct size as assessed by cardiac enzymes, troponin (cTnI) and creatine kinase (CK). Secondary endpoints included recurrent myocardial infarction, cardiac arrhythmia and myocardial infarct size assessed by cardiac magnetic resonance (CMR) imaging at 6 months. Mean peak troponin was similar in the oxygen and no oxygen groups (57.4 mcg/L vs. 48.0 mcg/L; ratio, 1.20; 95% confidence interval [CI], 0.92 to 1.56; P=0.18). There was a significant increase in mean peak CK in the oxygen group compared to the no oxygen group (1948 U/L vs. 1543 U/L; means ratio, 1.27; 95% CI, 1.04 to 1.52; P= 0.01). There was an increase in the rate of recurrent myocardial infarction in the oxygen group compared to the no oxygen group (5.5%vs.0.9%, P=0.006) and an increase in frequency of cardiac arrhythmia (40.4% vs. 31.4%; P=0.05). At 6-months the oxygen group had an increase in myocardial infarct size on CMR (n=139; 20.3 grams vs. 13.1 grams; P=0.04).

Conclusions—Supplemental oxygen therapy in patients with STEMI but without hypoxia may increase early myocardial injury and was associated with larger myocardial infarct size assessed at six months.


 For STEMI’s make sure all patients get 4 chewable baby ASA.  If the patient received ASA from EMS or took it at home, document that.  Start IV Heparin (max dose 4000u).  Discuss anti-platelet agents with your cardiology consultant.  Some cardiologists may choose not to use an anti-platelet agent to avoid bleeding complications if the patient requires CABG.

If you have a patient with an inferior STEMI with ST elevation in lead 3>lead 2 get a right-sided EKG to identify a possible Right ventricular infarction.

*DeWinter’s Syndrome

*Dewinter Teaching Points


Unfortunately I missed this excellent lecture. 

Nand    Observation Service and Care Management

Basically if you are admitting for a symptom, the patient should be brought in as observation.  For the most part, if you have a diagnosis for the patient then  bring them in as a full admit.  Exceptions would be TIA, syncope, and cellulitis which can be observation status.  If you have a doubt, start as an observation. Social issues should be brought in as an observation.

When patients are brought in as an observation patient, theyhave more personal financial exposure than they would as a regular admission.  If the patient is expressing concerns about the financials of an OBS admission, consult the ED Care Manager to help with this discussion.

If you have to change the admit or observation order, cancel and reorder the bed request. This action will re-generate a new level of care order.

If the patient will be staying for 2 midnights that is a patient who should be a full admit.

Don’t use the word “observation” as a verb.  Use “monitor” or “watch” instead.   For example don’t write “we will observe the patient in the ICU”.  Instead write, “we will monitor in the ICU”  Using the word “observation” as a verb in your note causes confusion for reviewers regarding whether the patient is admitted or Observation status.