Epiglottitis and Awake Intubation

Mikhail Podlog, DO                Anna Van Tuyl, MD

Let's start with a case..

HPI:  41 year old male with no PMH presents to ED for sore throat and fever measured at home for 3 days. Patent was seen at urgent care yesterday and was prescribed azithromycin and prednisone for pharyngitis. Today patient started complaining of swelling in his throat and difficulty breathing so came to the emergency department for evaluation. No cough, chest pain, abdominal pain, nausea, or vomiting. No allergies, new food, or new medication.

Vital signs:       T 100.6 Oral     HR 103    RR 26    BP 170/87    SaO2 95% on RA

Physical Exam:  “Erythematous pharynx with elongation of the uvula. Muffled voice. Tender anterior cervical adenopathy”. Otherwise unremarkable exam.

Progress Notes:  ENT called to bedside for laryngoscopy. Patient found to have swollen and beefy red epiglottis with tight airway. Recommendation made for prophylactic intubation

Diagnosis:  Epiglottitis

Management: Treatment consists of three parts: airway, antibiotics, steroids.


The first priority is protecting the airway. The swelling can cause airway obstruction; therefore prophylactic intubation is frequently performed. Because intubation can be difficult, the safest approach is to perform it in the operating room with surgery on standby if an emergency surgical airway is needed. If this is not an option, the safest approach is to perform an awake intubation. During an awake intubation, the patient is consciously sedation but because they are not paralyzed they maintain their respiratory drive. Therefore, if the intubation is unsuccessful, they can continue to maintain their respiratory drive.

Awake intubation steps

  1. Dry the oropharynx - This not only helps with better visualization during intubation but allows the numbing medication to work better
    1. Glycopyrrolate 0.2 mg IV push - anticholinergic agent without CNS effect, takes about 10-20 minutes to take effect
    2. Use gauze in patients mouth to dry it as much as possible
  2. Blunt gag reflex
    1. Zofran 4-8 mg IV push
  3. Numb the oropharynx - once mucosa is dry
    1. Nebulized lidocaine
      1. 5 cc of 2-4% lidocaine
      2. Can use 2% lidocaine with epinephrine to vasoconstrict mucosa and decrease swelling
    2. Viscous lidocaine
      1. Draw up 3-5 cc of 2% viscous lidocaine in syringe and use plastic angiocath to drip down back of tongue
      2. Can alternatively place 3-5 cc of 2% viscous lidocaine on tongue depressor and place upside down on tongue and let drip down
    3. Mucosal atomization device
      1. Advance blade into pharynx slowly and spray about 5 cc of 2-4% lidocaine as you progress towards the vallecula, epiglottis, and cords
  4. Sedate
    1. Similar to procedural sedation
    2. Can use ketamine alone
      1. Start with 10-20 mg IV and push an additional 5-10 mg every minute or so as needed
    3. Ketafol (ketamine with propofol in a 1:1 to a 3:1 ratio)
      1. If using a 10 mg/mL concentration of both sedatives, mix in desired ration and place mixture in 10 cc syringe
      2. Start with 1-2 mL IV and push an additional 5-10 mg every minute or so as needed
    4. Other options include midazolam with fentanyl, or dexmedetomidine
  5. Oxygenation
    1. Preoxygenate with NRB or CPAP (with NC)
    2. Optimally position for oxygenation
    3. Maintain NC at 15L/min for entire procedure
  6. Intubation
    1. Option 1 - Video laryngoscopy
      1. Use buogie and then place endotracheal tube over bougie
    2. Option 2 - Nasal fiberoptic intubation - if you have a fiberoptic scope you can use this route
      1. Spray nasal phenylephrine prior to sedation
      2. Use nasal trumpte coated with viscous lidocaine during preoxygenation to numb nasal cavity, then remove when ready to intubate
      3. Preload endotracheal tube onto fiberoptic cable and nasally intubate
      4. Preloading the endotracheal tube allows you to confirm that it is inserted past the vocal cord by visualizing them as you withdraw the fiberoptic cable
    3. Confirm tube placement!
  7. Sedate

Patient should then be started on empiric combination therapy with a third generation cephalosporin (ceftrimraxone, cefotaxime) and staphylococcal coverage with strong consideration for MRSA coverage (clindamycin, vancomycin).  Corticosteroids such as dexamethasone are frequently administered and have been show to decrease length of stay in the ICU and overall.

Back to the case..

Patient's course: Awake intubation was attempted in the emergency department by the ED attending. Below is a short clip of what was seen on video laryngoscopy.

Even after multiple attempts, awake intubation was unsuccessful so patient was taken to the operating room for fiberoptic intubation with surgery on standby. The patient was successfully intubated and started on Clindamycin, vancomycin, and Decadron. The patient was successfully extubated 2 days later, down graded to a regular floor, and discharged home 2 days later on oral antibiotics. Patient was doing well at one month follow up.

Pulmonary Hypertension and Right Ventricular Failure

Mikhail Podlog, DO

Editor: Anna Van Tuyl, MD



The left ventricle (LV) is widely studied and much is known about its normal function, how it performs under stress, and the causes, sequelae, and treatments of LV failure. On the other hand, much less is understood about the right ventricle (RV), including right ventricular failure (1,3). There are many causes of right ventricular failure, the most common being failure of the left ventricle, but one important condition to always consider is pulmonary hypertension (PH), defined as a mean pulmonary artery pressure of 25 mm Hg or higher (1). As pulmonary pressures rise, the increase in afterload on the RV decreases right ventricular stroke volume and output, increasing RV volume.  Since the RV cannot adapt as rapidly as the LV to increases in afterload, this has several detrimental effects on the cardiovascular system.

First, the increased volumes and pressures in the RV causes bulging of the interventricular septum into to LV, decreasing left ventricular preload. This results in a decrease in cardiac output, leading to hypotension and cardiac ischemia (1,3). Second, increased pressures in the RV cause a rise wall tension, decreasing right coronary artery perfusion, which leads to further ischemia. (1,3) Finally, increased pressures in the RV cause tricuspid regurgitation leading to decreased cardiac output (2). All of these processes ultimately cause what is referred to as the right ventricular spiral of death. 



World Health Organization (WHO) Classifications of Pulmonary Hypertension


As always, the first step is considering the diagnosis. The most common presenting complaint is exertional dyspnea and pulmonary hypertension should always be thought about if an alternative diagnosis does not explain the patient’s presentation (1). Although a definitive diagnosis of PH requires right heart catheterization, there are several ways ED providers can assess for its presence.

Cardiac Ultrasound
1.    Apical 4 (A4) chamber – RV greater than 2/3rd-1x the size of LV (1,4)
2.    Parasternal short – flattening of interventricular septum, D-shaped LV (1,2)
3.    TAPSE (Tricuspid Annular Plane Systolic Excursion)- M mode through tricuspid annulus in A4 view, >1.6 nml, <1.0 severe dysfunction (7)

CTA Chest  - If RV is greater than 9/10ths of LV, that correlates with increased risk of adverse events and death. (1,4)


Definitive treatment of pulmonary hypertension usually involves treating the underlying causes. This includes diuretics for left heart failure, bronchodilators and steroids for lung diseases, thrombolysis for pulmonary emboli, etc. Appropriate consultations with cardiologists, pulmonologists and other specialists is also emergently indicated for further management. (1,2,3) In the meantime, there are certain things that emergency department providers must do to resuscitate and stabilize the patient in front of them.

Optimize Volume Status

Volume status in these patients is difficult to assess, as the physical exam as well as ultrasound visualization of the IVC is often unreliable. Overloading these patients can lead to further increase in RV volume causing decreased cardiac output and an accelerated path down the spiral of death. Overly diuresing these patients may also lead to a decreased cardiac output if the patient is preload dependent. Here are some tips one can use to assess these patients. (2)

1.     Assume the patient is fluid overloaded and avoid large boluses of fluids -> negative balance is usually key for these patients. (1,2,6)

2.     If there is clear volume loss (diarrhea, blood loss) -> low volume boluses of 250cc of isotonic solution and monitor for effects on blood pressure, heart rate, and urine output.  (1)

a.     If patient is anemic transfuse blood as decreased Hgb and iron has been associated with increased mortality (3,4)

3.     Use passive leg raise maneuver and assess for changes in blood pressure and heart rate (this stimulates giving a bolus and can be rapidly reversed by lowering the legs).

4.     Consider expedited admission to the ICU where a pulmonary artery catheter can be used to obtain accurate central pressures and guide further fluid management, although the efficacy of this is highly debated. (2)

Consider early pressor support

Systemic vasopressors can help prevent the downward spiral of RV failure several ways. Increasing left ventricular afterload can decrease interventricular septum bowing into the LV, increasing cardiac output. Vasopressors also assist in maintaining coronary perfusion to the right ventricle, decreasing effects of ischemia. Although literature is very scant comparing the variety of pressors available, certain pressors have advantages over others in treating pulmonary hypertension.

1.     Norepinephrine – proven benefits in several types of shock; helps maintain coronary perfusion of right ventricle; may increase pulmonary vascular resistance (1,4)

2.     Vasopressin – peripheral vasopressor just like norepinephrine, may actually decrease pulmonary vascular resistance through a NO-induced mechanism (1,2)

3.     Phenylephrine – avoid due to increase in pulmonary vascular resistance when compared to other pressors available (1,5)

4.     Dobutamine – augments myocardial contractility and reduces RV and LV afterload -> increased CO; but disadvantages include decreased SVR and tachycardia so may need to combine with a vasopressor (1,2,3,4)

5.     Milrinone – Unlike dobutamine, PDE3 inhibitors are inotropic and augment cardiac output without chronotropic effects, but disadvantages include decreased SVR as well so may need to combine with a vasopressor; may consider inhaled milrinone if available (2,3,4)

Treat atrial arrhythmias

Patient with pulmonary hypertension are predisposed to atrial tachyarrhythmias. These patients do not tolerate atrial arrhythmias as cardiac output is preload dependent and any minor change can have drastic effects.  Calcium channel blockers and beta blockers should be avoided as they may further impair cardiac function. Cardioversion should always be strongly considered as first line especially for unstable patients (1). Amiodarone can be tried if the patient is stable, and can also be used to pretreat the patient prior to cardioversion. (2,3)

Pulmonary Vasodilations

Pulmonary vasodilators are the only medications that directly reverse the symptom-causing pathology. These are very useful in patients with idiopathic pulmonary hypertension (Category 1) and must be quickly given if a patient is on an IV pump of these medications that has malfunctioned. Inhaled preparations of these medications are also very effective at delivery the medication to highly ventilated portions of the lung, causing local vasodilation and improving V/Q mismatch. Below is a table that lists the categories of pulmonary vasodilators and their potential uses in emergencies.



Airway and ventilation management

Maintaining tight control of ventilation and oxygenation is crucial in these patients. Hypoxemia as well as hypercarbic respiratory acidosis can lead to increased pulmonary vasoconstriction, further exacerbating the underlying pathology. Therefore oxygen saturations and carbon dioxide levels in the blood must be maintained in the normal range. (1,4)

If a patient is in respiratory failure, intubation should be avoided at all costs. Intubating these patients can lead to a fatal hemodynamic collapse for two main reasons:

1.     Sedation -> Loss of native catecholamines -> decreased SVR/vasodilation -> decreased venous return -> cardiovascular collapse (1)

2.     Positive pressure ventilation -> increase RV and LV afterload and decreased RV preload -> decreased CO -> cardiovascular collapse (1)

Therefore try to avoid intubating these patients. If respiratory support is needed, first try NIPPV. This avoids the adverse effect of eliminating the patient’s innate catecholamine surge. In addition, the NIPPV can be removed rapidly if the patient begins to deteriorate. (1) If a patient needs to be intubated, following these guidelines can increase your chance of success.

1.     Place an arterial line prior to intubation in order to quickly assess any hemodynamic changes and respond appropriately.

2.     Avoid hypoxia -> preoxygenate the patient and utilize apneic oxygenation during the intubation

3.     Avoid hypercarbia -> induce respiratory alkalosis prior to intubation (4). Hypercarbia worsens pulmonary vasoconstriction.

4.     Consider performing awake intubation.

5.     Medications

a.     Induce with etomidate -> cardiovascular neutral (2)

b.     Paralyze the patient -> increases chances of first pass success

c.     Push dose pressors -> Have ready at the bedside along with your induction/paralytics (1)

d.     Have norepinephrine drip ready -> Have the pump primed and connected; just having the medication in the room is not good enough (1)

6.     Vent settings -> keep intrathoracic pressures low (similar to ARDS protocol) -> low TV, PEEP, low plateau pressures (2,3)

Further management

LVAD, ECMO, atrial septostomy, lung transplant, PH referral center (1,2,3)


1.     Pulmonary Hypertension and Right Ventricular Failure in Emergency Medicine, Wilcox

2.     Hoeper MM, Granton J. Intensive care unit management of patients with severe pulmonary hypertension and right heart failure. Am J Respir Crit Care Med. 2011;184:1114-1124

3.     Acute Right Ventricular Failure in the Setting of Acute Pulmonary Embolism or Chronic Pulmonary Hypertension: A Detailed Review of the Pathophysiology, Diagnosis, and Management

4.     Lahm T, McCaslin CA, Wozniak TC, et al. Medical and surgical treatment of acute right ventricular failure. J Am Coll Cardiol. 2010;56:1435-1446.

5.     Kwak YL, Lee CS, Park YH, et al. The effect of phenylephrine and norepinephrine in patients with chronic pulmonary hypertension. Anaesthesia. 2002;57:9-14

6.     Ternacle J, Gallet R, Mekontso-Dessap A et al. Diuretics in normotensive patients with acute pulmonary embolism and right ventricular dilatation. Circ J 2013;77:2612–2618.

7.     Schmid E, Hilberath JN, Blumenstock G, Shekar PS, Kling S, Shernan SK, Rosenberge P, Nowak-Machen M. Tricuspid annular plane systolic excursion (TAPSE) predicts poor outcome in patients undergoing acute pulmonary embolectomy. Heart, Lung and Vessels. 2015; 7(2): 151-158

8.     https://emcrit.org/podcasts/pulmonary-hypertension-right-ventricular-failure/

9.     https://www.nhlbi.nih.gov/health/health-topics/topics/pah/types

Double Sequential Defibrillation

Double Sequential External Defibrillation for Refractory Ventricular Fibrillation

Ilya Litvak, DO             Mikhail Podlog, DO            Anna Van Tuyl, MD


Ventricular fibrillation (VF) is the most common initial dysrhythmia after out-of-hospital cardiac arrest(OHCA) occurring in approximately 70 % of the cases.  VF  is also considered the rhythm with the highest likelihood of neurologically intact survival (1). Unfortunately, there is a subset of patients who do not respond to standard ACLS algorithm for VF and are termed to have refractory ventricular fibrillation (RVF).


What is refractory ventricular fibrillation?

The exact definition of RVF is subject of debate. However, the literature in the past has used persistent VF without response to at least five single defibrillations (including AED) as the definition of RVF.  One intervention that has been reported to terminate RVF is double sequential defibrillation (DSD).


What factors affect successful defibrillation?

Successful defibrillation depends on several variables, including pad placement, total energy used, length of stay in VF, and patient’s body habitus (2). Zhang et al. demonstrated in swine models that body mass had inverse relationship with the success of defibrillation (3).  Other studies have shown lower success rates in cardioversion of atrial fibrillation in patients with BMI >25 (4).

The amount of energy is also an important factor in successful defibrillation. Although there are concerns that higher energy may result in myocardial injury or chest wall trauma, several studies have shown safety of high energy defibrillation in humans. For example, Stiell et al. found no deleteriouseffects of biphasic defibrillation up to 360 J (5).  Multiple other studies have found no deleterious effects in subjects cardioverted for atrial fibrillation with energy levels of up to 720 J monophasic. 


What is Double Sequential Defibrillation?

Double sequential external defibrillation refers to the use of two simultaneous defibrillator pads to deliver the shock. In addition, to increased energy, another theory behind this set-up is that the addition of a second pair of defibrillator pads allows for two alternative vectors of energy delivered to fibrillating myocytes. This allows the energy to overcome limiting factors, such as poorly placed electrodes and the air in the lungs, which otherwise divert the vectors from fibrillating myocardium.(6). Yet another theory postulates that the first defibrillation serves to lower the threshold for successful shock with the second defibrillation (7).


How should the pads be positioned?

There is no clear evidence on which pad placement is ideal. Two sets of pads can be placed in anterior-posterior (AP) orientation, antero-lateral (AL) or AP/AL orientation. 



The first report of DSD in VF patient was described in 1994 by Hoch et al. in the electrophysiology literature (8). This case series paper described 5 patients with WPW or other cardiomyopathies undergoing routine studies in the electrophysiology lab. All five subjects had VF intentionally induced as part of their evaluation. In this study, patients failed to convert to normal sinus rhythm with monophasic energies ranging from 200-360 J, but all of them responded to double shock with a total of 720 J. However, until recently there has been paucity of data (limited mostly to case reports) supporting the use of DSD in the Emergency Department or OHCA. 

One recent paper in Resuscitation by Cortez et. Al from August 2016 shows promising evidence for the use of DSD for RVF in OHCA  (9).  In this retrospective chart review, 2428 OHCA events were reviewed with 12 patients treated with DSD. Nine patients out of twelve were successfully converted out of ventricular fibrillation. Of the patients treated with DSD, three patients survived to hospital discharge with good neurologic function.

Also important to note is that the median time to DSD was 27 minutes in the above study. This is significantly shorter than reported values in other papers. This may mean that DSD maybe more effective when incorporated earlier in resuscitation efforts of VF arrest.

Although the above paper provides promising evidence for DSD it has several important limitations including small sample size and retrospective case series nature of the study. Unfortunately, to date there are no double blind randomized control studies on DSD to determine its efficacy.



Management of RFV remains challenging and when standard ACLS measures have failed DSD may be another tool that can be utilized to achieve ROSC in RVF patients.



1 Holmberg M. Holmberg S. Herlitz J. Incidence, duration and survival of ventricular fibrillation in out-of-hospital cardiac arrest patients in Sweden. Resuscitation 2000.44:7-17

2 Morrison LJ, Dorian P, Long J. et al Out- of- hospital cardiac arrest rectilinear biphasic to mopnophasic damped sine defibrillation waveforms with advanced life support intervention trial (ORBIT). Resuscitation 2005; 66 :149-57

3 Zhang Y, Clark CB, Davies LR, Karlsson G, Zimmerman MB, Kerber R. Body weight is a predictor of biphasic shock success for low energy thranthorasic defibrillation. Resuscitation 2002; 54:281-7.

4 Glover BM, Walsh SJ, McCann CJ, et al. Biphasic energy selection for transthoracic cardioversion of atrial fibrillation. The BEST AF Trial. Heart 2008;94:884-7

5 Stiell IG, Walker RG, Nesbitt LP, et al, BIPHASIC Trial: a randomized comparison of fixed lower versus escalating higher energy levels for defibrillation in out-of-hospital cardiac arrest. Circulation 2007;115:1511-7

6 Ristagno G, Yu T, Quan W, Freeman G, Li Y. Comparison of defibrillation efficacy between two pads placements in a pediatric porcine model of cardiac arrest. Resuscitation 2012;83:755-9

7 Kerber RE. Indications and techniques of electrical defibrillation and cardioversion. In: Fuster V, Walsh R, Harrington RA, editor. Hurst's the heart. 13th ed. New York, New York: McGraw-Hill; 2011

8 Hoch DH, Batsford WP, Greenberg SM, et al Double sequential external shocks for refractory ventricular fibrillation. J Am Coll Cardiol 1994;23:1141-5

9 Cortez E et al. Use of Double Sequential External Defibrillation for Refractory Ventricular Fibrillation During Out-of-Hospital Cardiac Arrest. Resuscitation 2016. S0300-9572(16): 30398 – 7.


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