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Monday, August 31, 2015

The Agony of the Beta Agonists PART 2 AUGUST 2015

We left off with a rather critically ill patient. EMS responded to a patient in respiratory failure:

The Agony of the Beta Agonists PART 1 of 2 JULY 2015

This was shared from a friend, provider, and colleague. Interesting case. Details changed to protect the innocent, respect privacy laws, comply with all appropriate regulations, and, well.. you get the picture.

SUBJECTIVE
HPI:
94 yo male requests 911 for shortness of breath. HPI  not obtainable due to patient presenting in extremis. The patient is alert, responsive to verbal stimuli, and is in obvious respiratory distress upon arrival. Providers appreciate audible wheezing. Family members relate that the patient is a "DNR" and was last seen acting "a little tired" 12 hours prior.
Meds: Unknown
PMH: COPD, CHF, HTN, HLD, DM

OBJECTIVE
Pt is slightly diaphoretic. BP: 134/92, R: 32, P: 90. ETC02 via NC is 20.
Supraclavicular and intercostal retractions are present as is mild JVD.

The patient's ECG was similarly concerning:

Let's review this case: 

PREHOSPITAL TREATMENT 
Prehospital treatment should be directed at symptom relief and mitigation of the underlying cause. Audible wheezing does not always indicate COPD, and this patient may be suffering from CHF, cardiac asthma, pneumonia, or a combination of entities! Fortunately, CPAP therapies have utility with respect to reducing the work of breathing and reducing preload. Of course, the concurrent rise in intrathoracic pressure may precipitate hypotension. However, this patient is alert enough to probably warrant a trial of non invasive positive pressure ventilation. Beta agonists may have utility if there is evidence of bronchospasm. However, B1 receptor stimulation may cause an increase of cardiac contractility and irritability. Nitroglycerin
wouldn't be unreasonable, but its probably safe to consider initiating IV access. The take home point in this case is that elderly patients are often highly comorbid. Physical assessment and end tidal C02 readings are often confounded by the critical presentation! Is the patient's end tidal reading low due to tachypnea alone? Is there an underlying metabolic disturbance? Is the wheezing due to bronchospasm or does it represent sequelae of pulmonary edema? Often times, more information is needed in the form of xray and bloodwork to determine the underlying diagnosis- or diagnoses. CPAP and other respiratory treatments represent reasonable therapies, and there is no all inclusive, correct answer. There is really no role for the emergent, prehospital administration of furosemide for suspected acute cardiogenic pulmonary edema. If the patient can follow the occasional verbal commands and swallow without difficulty, 325 mg of chewable aspirin is indicated. 

ECG FINDINGS AND STEMI ALERT? 
The underlying rhythm appears sinus in origin and there is evidence of a left bundle branch block (LBBB). LBBB is a common finding in elderly patients and may simply represent advanced disease. LBBB accompanies a relatively rare number of acute myocardial infarctions and is a maker of illness severity when present. A complete LBBB results from interruption of the anterior and posterior fascicles. Therefore, new onset LBBB in the setting of a critically ill patient should motivate EMS personnel to transport to a facility capable of percutaneous coronary intervention. LBBB often confounds the diagnosis of STEMI but recent literature and AHA guidelines recommend against activating the cath lab for an LBBB of unknown duration. In this setting, however, where providers are confronted with a patient in acute pulmonary edema, it may be wise to choose a cath capable hospital. 
SUBTLE SGARBOSSA
Criteria exist for the prediction of ischemia in the presence of LBBB. The Sgarbossa crtieria function to distinguish ischemia (terrible) from pre-existing conduction delay and established coronary artery disease (less terrible). In this ECG,  specifically in Lead V3, there is evidence of an "excessively discordant ST segment." In previous studies, the presence of discordant ST elevation (in leads with a negatively deflected QRS) was associated with myocardial infarction. This criteria alone is not sufficient to establish the diagnosis of STEMI but may bolster the provider's decision to transport to the cath lab. An excellent discussion of the original Sgarbossa criteria can be found on the Life in the Fast Lane Blog.



Sunday, July 19, 2015

Those Nursing Home Nurses Were Right about the Magic Nasal Cannua- Or Were They? HFNC, HFFM, Intensive Care JULY 2015

Some Nasal Background

For years, proponents of rapid sequence intubation have tried to identify the most reliable way to prevent desaturation. Pre-oxygenation is an important part of the RSI strategy, and avoidance of hypoxia in the head injured patient predicts an adverse outcome. RSI fundamentalists believe that NO positive pressure ventilation should take place during an RSI attempt. Positive pressure ventilation theoretically increases the risk for emesis and may cause gastric insufflation. Recently, the strategy\ of high flow oxygen via nasal cannula (HFNC) at flow rares in excess of 15 lpm has emerged as a feasible strategy for passive oxygenation. In patients undergoing RSI, the application of HFNC has been shown to increase "safe apnea time."

Dr. Rich Levitan, a nationally recognized (and emergency medicine trained) airway expert has published on the "NO-DESAT" protocol. This protocol advocates for HFNC in addition to the usual measures can prevent and perhaps maintain oxygen saturation during rapid sequence intubation.

Nice summary of "NO-DESAT" here:
http://www.epmonthly.com/archives/features/no-desat-/

THE PREOXYFLOW TRIAL
A recent study published in Intensive Care Medicine looks more specifically at the use of HFNC in hypoxic patients. The study randomized patients to either high flow oxygen via face mask or high flow (>60 lpm!) nasal cannula. The primary outcome of interest was the lowest saturation of oxygen measured by pulse oximetry.

The study randomized over 120 ***sick*** adult patients. These patients exhibited respiratory failure as evidenced by a high Fi02 requirement, tachypnea, or hypoxia. The study results did not establish the superiority of the HFNC technique, and both patient groups (HFFM and HFNC) experienced significant medical complications.

Does this study urge practitioners to back off the cannula?
Should HFNC be abandoned for patients exhibiting significant respiratory distress?

Before attempting to summarize this trial, we've got to remember that when talking about HFNC, we're still comparing oral airways to king LTs. That is to say, there's quite a lot of difference between the use of HFNC as an adjunct and the use of HFNC as a primary strategy for avoidance of hypoxia. Also, this study uses nasal cannulae specifically designed to accommodate high flow rates. Can the ordinary oxygen regulators supply flow rates in excess of 60 lpm? Probably not. Given peri-intubation hypoxia's association with adverse outcomes, it makes sense that airway practitioners should try to maximize a patients oxygen reserve. Sustaining normoxic values in distressed patients is always a challenging endeavor, and emergency medicine regularly encounters patients at risk for desaturation. Whether its poor respiratory mechanics, morbid obesity, acute blood loss, or baseline pulmonary disease, there are many threats to address in the pre-intubation phase of RSI. Furthermore, its pretty clear that a higher preintubation oximetry reading is linked to that precious "safe apnea" time... that wonderful interval prior to the obnoxious cascade of alarms that herald impending doom.

BOTTOM LINE:
-The PREOXYFLOW trial (HFNC vs HFFM) is NOT an indictment o the NO-DESAT protocol and does not mean that HFNC is bad for patients
-Hypoxia is, in general, something to avoid during RSI
-Use HFNC to complement preoxygenation efforts
-Severely hypoxemic patients may require more active measures to increase and maintain a satisfactory pre-oxygenation level
-In patients with respiratory failure, HFNC as a "stand alone" hypoxia prevention strategy may not represent best practice

Keep the high flow flowing!

The Agony of the Beta Agonists PART 1 of 2 JULY 2015

This was shared from a friend, provider, and colleague. Interesting case. Details changed to protect the innocent, respect privacy laws, comply with all appropriate regulations, and, well.. you get the picture.

SUBJECTIVE
HPI:
94 yo male requests 911 for shortness of breath. HPI  not obtainable due to patient presenting in extremis. The patient is alert, responsive to verbal stimuli, and is in obvious respiratory distress upon arrival. Providers appreciate audible wheezing. Family members relate that the patient is a "DNR" and was last seen acting "a little tired" 12 hours prior.
Meds: Unknown
PMH: COPD, CHF, HTN, HLD, DM

OBJECTIVE
Pt is slightly diaphoretic. BP: 134/92, R: 32, P: 90. ETC02 via NC is 20.
Supraclavicular and intercostal retractions are present as is mild JVD.

12 LEAD ECG:












Case related questions: 
1. What is your prehospital treatment?
2. What are some concerning ECG findings?
3. Is this patient treated as a STEMI alert?

Thursday, April 23, 2015

April 2015: Sighting the Subtlety Down Below



CASE: 

A 63 y/o gentleman calls 911 for "chest pressure" and indigestion. The patient is nauseated but denies LOC, SOB, or dizzinesss. The pressure started approximately 1 hour prior to 911 arrival. The patient has a history of hypertension and takes an aspirin daily. He is hemodynamically stable. BP is 110/70, P: 82, R: 16. Sp02: 95% on RA.

12 LEAD ECG:
























12 LEAD ECG DISCUSSION:

There is a sinus rhythm. PR depression is present in lead II. There is slight ST segment elevation present in II, III, and aVF. Elevation measures about 1 mm. There is no evidence of recriprocal change. A biphasic T wave is present in lead III and terminal T wave inversion is present in the lateral precordial leads. The QRS axis appears physiologic.

12 LEAD INTERPRETATION: 

Inferior wall STEMI

TREATMENT

The patient was transported to a hospital capable of percutasneous coronary intervention. A right sided ECG was not performed, and NTG was withheld due to the patient's marginal blood pressure or relative hypotension. 325 mg of ASA was administered. The patient's RCA was 75% occluded.

Thanks always to the Baltimore City Fire Department for its endless supply of pathologic 12 lead tracings.

Wednesday, March 11, 2015

Fix the Rate First ?


CASE PRESENTATION:
Providers respond to a 68 yo female with a sudden onset of paroxysmal nocturnal dyspnea. The patient reports slight dyspnea on exertion for the past few weeks and endorses a mild, non productive cough. The patient speaks in 2-3 word sentences and appears in severe respiratory distress. The patient denies chest discomfort, nausea, vomiting or fever. The patient is in severe respiratory distress and is profoundly diaphoretic. Another paramedic provider onscene diagnoses SVT and readies adenosine for administration.

EXAM:

BP:     220/120
P:        168
R:        40
Spo2:  88%


12 LEAD ECG:




12 LEAD ECG ANALYSIS:

There is a supraventricular tachycardia. P waves are difficult to discern but the QRS complexes are narrow and occur at regular intervals. Diffuse repolarization abnormalities in the form of biphasic T waves are present in the inferior leads. There is no obvious ST segment elevation.

TREATMENT:

High flow oxygen is administered and an intravenous line is inserted. The senior paramedic recommends against adenosine administration. A total of 1.2 mg of nitroglycerin is administered sublingually. 324 mg of aspirin is administered. As the patient is prepared for transportation, CPAP is started at 10 cm H20. The patient experiences rapid improvement and the hypoxia resolves. A repeat ECG shows sinus rhythm with some lateral ST segment depression. Vital signs following CPAP and NTG are as follows: BP: 180/100, P: 110, R: 22, Sp02: 100%. A chest xray shows cardiomegaly and bilateral opacities consistent with pulmonary edema are present.

DISCUSSION:

Though fixing a fast heart rate can reduce ischemia, it is important to consider the underlying cause of a dysrhythmia. Administration of adenosine could convert this ECG but the SVT is very likely due to the catecholamine surge that accompanies acute pulmonary edema. A reduction in cardiac output and afterload results in improved oxygenation, reduced work of breathing, and resolution of the supraventricular tachycardia. Following a hospitalization for acute heart failure, the patient was discharged to home on an aggressive medical regimen targeted at maintaining an acceptable blood pressure. The prehospital application of CPAP is consistently linked to a reduced endotracheal intubation and improved mortality.



Sunday, March 8, 2015

Non Sustained VT: Making a Lasting Impression!

Putting on the Pressure

A 60 yo male presents to EMS with several hours of chest pressure and diaphoresis. A 12 lead ECG is obtained following a 10 beat run of non sustained ventricular tachycardia. Despite the EMT's excitement at "firing up the paddles," the paramedic administers 324 mg of aspirin and prepares for transport to the nearest facility capable of percutaneous coronary intervention. Your partner informs you that the monitor discerns the presence of a paced rhythm. The patient has no previous medical history.


12 LEAD ECG:




12 LEAD ECG Analysis:

A sinus rhythm is present and the rate is regular. Diffuse and concerning ST segment changes appear in this tracing. First, pathologic ST segment elevation occurs in leads V2, V3 and V4. Q waves also appear throughout the tracing. The monitor misinterprets the ischemic Q wave as a pacer spike. The QRS is narrow, so an interventricular conduction delay is less likely responsible for the "false pacer" call. Reciprocal changes appear in lead aVF. There is minimal J point depression in lead III and V6. The baseline is also irregular.


12 Lead ECG Interpretation: 

Sinus rhythm, anterior wall ST segment myocardial infarction.

Comments:
  • It is difficult to discern the location of the anatomic lesion based upon this ECG. The large ST segment elevation in the precordial leads suggests involvement of the LAD. The findings of lateral wall ischemia could implicate the circumflex as well. 
  • The run of VT was likely due to ventricular irritability. Remember that the most devastating complications of anterior wall ischemia are lethal dysrhythmia and cardiogenuc pulmonary edema 
  • Pathologic Q waves generally follow a few rules: (1) larger than a third of the corresponding R wave or (2) measure in excess of 0.03 seconds. Q waves that accompany poor R wave progression are more likely to indicate ischemia.