Asthma, respiratory arrest: The bougie is in but I can’t pass the tube!

Asthmatic respiratory arrest, able to pass bougie but not the tube!

A scary case

We received and ambulance call informing us of a moderately unwell asthmatic in her 50s.

Next thing a paramedic pops his head in the ambulance door, points at resus and says “Chris, we’ll need you in there soon”

Intriguing (well, strange, but it was James).

I headed out to the ambulance.

It turns out the patient had been not to unwell when the paramedics got to the patient’s house: wheezy but talking easily.  They had given her a couple of nebulisers en route.  A few minutes before arrival at hospital the patient had suddenly become agitated.  The paramedics had given some IM adrenaline but she had continue to deteriorate.

So as I got to the ambulance I saw a large woman on the trolley in the back of the ambulance staring blankly into space and … not breathing.

We elected to dash to resus.

In resus I bag valve mask (BVM) ventilated her,  slowly and gently, with difficulty.

I briefly considered intubating but decide not to – the primary problem was with B not A.

I put in an oropharyngeal airway, little improvement.

I placed bilateral nasopharyngeal airways with good effect -> I could ventilate reasonably.  She had bilateral breath sounds with moderate wheeze.

Circulation check: No palpable pulse, sinus tachy on the monitor.  We started chest compressions for presumed PEA arrest.

After a minute of chest compressions we stopped and reassessed.  Good radial pulse.  I elected to give 100mcg adrenaline for immediate brondilatory effect (in retrospect 250mcg of salbutamol would have been a better idea but we had adrenaline in hand in a prefilled syringe for the PEA arrest)

Over a few minutes her oxygen sats climbed from 65 to 100%.

The senior nurse asks if I wanted any help.  “Yep, an anaesthetist might be good for this one”

An amazing nurse got in a good IV line in and baseline bloods were sent and 200mg of hydrocortisone was given.

We ventilated slowly and carefully for a few minutes.  Bedside ultrasound (at the depth limit of the linear probe) shows bilateral pleural sliding – no pneumothorax.

The anaesthetist (a good one, yay) arrives promptly. The patient is making weak respiratory effort but is unresponsive to pain.

We generally avoid intubation in asthma – patients with asthma don’t tend to do well on ventilators – so we usually try to mange them on BiPAP instead.   However it didn’t look like this patient was going to wake up anytime soon, so the anaesthetist and I decided we would intubate.

I decided to do an RSI even though the patient was unresponsive.  Intubation without drugs may have caused laryngospasm or worsened her bronchospasm.

We set up for an RSI with high flow O2 by nasal prongs and ramping (for obese patients we put lots of sheets and pillows behind their upper back and head to try to get their air way alignment optimised – this is called ramping).

Ketamine 150mg and rocuronium 100mg push.

Good view with a video laryngoscope, but she had an anterior larynx and I was unable to pass tube through cords even with a good hockey stick bend on the stylet and laryngeal manipulation.

I passed a bougie easily into the trachea but I was unable to advance a size 7.5 tube into the trachea.   The tip of the tube went through the cords but the balloon seemed to hang up at the cords.  I tried rotating the tube both ways but it wouldn’t go.

Sats had dropped to 85% by now.   I pulled out and we BVMd her until her sats were  back at 100% for a minute then started again.

Bougie, size 7.0 tube.  Same result.  I’m thinking : “Has she got a subglottic stenosis?  Are we going to have to cric (cricothyroidotomy) her?” I admit defeat for the first time in over 6 years since I’ve been a consultant, and handed over to the anaesthetist.  He has the same problem.  He then put another pillow behind the patient’s head and passed the tube easily.

He thought my initial ramping wasn’t adequate, the airway angles were wrong and the ETT tube was hitting against the anterior wall of the trachea.  Makes sense.

We generally believe that the key to ramping is  to have the tragus of the ear anterior to the sternal notch.  This is hard to see from the head of the bed and I should have got someone to have a look from the side of the bed.


The blue line indicates the line from tragus to sternal notch

(image from

Somewhere in the middle of all of this the internal medicine physician arrived and asked if we had done an ECG.  The senior nurse dryly replied “No doctor, we haven’t passed A yet.”

Then I had an all to frequent disagreement with the anaesthetist regarding ventilator settings.  This woman was’t tall.  I thought her ideal body weight (IBW) might be 60kg.  I wanted a tidal volume (TV) of 6ml/kg IBW = 360ml (lung portective strategy).  The anaesthetist wanted a TV of 500ml.  “You don’t need to worry about the airway pressures, the alveoli won’t see that.”

I reminded him that one of his colleagues had given my last patient life threatening asthma  bilateral pneumothoraces and set the TV at 350ml.  Later it was calculated that her IBW was 53kg.  We are often fulled thinking that obese people have big lungs.  Think of those CTs with tiny lungs surrounded by lots of padding.

In retrospect I am very glad I didn’t try a crash intubation on arrival in resus.  I think that would have been a disaster.  I think it was better to manage her airway with basic airways and adjuncts first, attempt to optimise her positioning, then to a controlled RSI.  Even if she had been a normal body weight patient I think I would still avoid intubation as patients with respiratory arrest from asthma will often respond to some BVM ventilation and wake up quite quickly and not need intubation.

Bottom line

Positioning, positioning, positioning for airways in obese patients.


Bullous Impetigo

Bullous impetigo is not that common but it is worth knowing about.

This 3-year-old had had one spot on her R lateral chest about a week earlier.  She had developed more spots that were becoming more sore, and in the last day had been itchy.  A few days previously there had been one fluid filled blister.

She had no medical history and was systemically well.

She was using paracetamol and ibuprofen for pain.




At about day 3 she had seen a GP who thought she might have shingles.  Now the lesions crossed the mid line and she had some on her legs so it didn’t look dermatomal now.

With the peeling skin around the edges I wondered if this was a mild case of stapylococcal scalded skin syndrome.  Looking at these photos the on-call paediatrician quickly put me right that this is actually bullous impetigo, a less serious condition.

The strain of staphylococcus aureus releases a toxin that lyses skin.

Staphylococcal scaled skin syndrome tends to be in neonates, the child is febrile and irritable, the rash is more widespread, has more widespread erythema, and surrounding intact appearing skin shears off easily with light touch (Nikolsky’s sign)

A swab was sent and she was admitted for a couple of days if IV antibiotics: flucloxacillin 50mg/kg 4 times daily.

Everyone was encouraged to be particularly careful with their handwashing.



Thanks to the child’s mother for permission to publish these photographs.


Song on podcast Souffrance  by Orange Blossom

Diltiazem for SVT rather than adenosine

Patients hate adenosine, it makes them feel like they are going to die.  With diltiazem patients just feel the SVT stop.

In the podcast that goes with this post I have a recording of one of our midwives who has recurrent SVT.  She was very happy afer dilitazem and I don’t think you could get adenosine into her again.

Treatment of SVT

Start with vagal manoeuvres eg get the patient to lie  flat and blow into a syringe with the plunger in it,  lift the patient’s legs in the air as the patient finishes their expiration.  It is the rush of blood to the heart as the intrathoracic pressure drops and you lift the legs that in creases the cardiac output, stimulating the carotid stretch receptors and causes the vagal response.

Carotid sinus massage if the patient isn’t an arteriopath or say over 60.

Ice cold flannel of water in the face.

If these don’t work (all of them do work sometimes and are worth trying even though we love playing with drugs) then we go to medication.

Typically in an adult I’ll give a 20mg push of diltiazem.  This can be repeated after 5 minutes if needed.  The blood pressure may drop but this is almost never symptomatic.

Some backwards countries like Australia still don’t have IV diltiazem.  Slow IV verapamil is a good alternative there.  I use diltiazem rather than verapamil because it is the drug we are more familiar with as we use it frequently for rate control in AF.


Any antiarrhythmic, including adenosine, can cause cardiac arrest.  Be ready to start CPR if this happens – treat as per PEA arrest algorithm.

Caution in a patient with heart failure or hypotension – get a senior help.  Adenosine or electricity may be better options, or the patient may need preloading with IV calcium and or IV fluid.

Talk to a paediatrician before treating an SVT in a baby.

Don’t use adenosine or a calcium channel blocker (verapamil or diltiazem) to treat an irregular wide complex tachycardia as this may be Wolff-Parkinson-White  Syndrome (WPW) with atrial fibriallation.  Just about any drug you through at this may stop the slow pathway and just leave the fast pathway active and may lead to VF and death.  Electricity is the best option for these patients.



The various terms for SVTs can be confusing.

SVT means a supraventricular tachycardia which technically includes sinus tachycardia, AF, atrial flutter and atrial reentry tachycardias + others.

In day-to-day use however SVT means a paroxysmal SVT with sudden, usually unprovoked, onset.  It may be due to atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT) or atrial tachycardia, which is all very confusing.  So we just use the term SVT.

See the table of relevant terms and definitions from the 2015 ACC/AHA/HRS guidelines at the bottom of the page.


What we call SVTs  tend to be regular, narrow complex, have no P waves, sudden and spontaneous onset, rapid heart rate.  Usually the patient is aware of it and they can be just be annoying or can leave the patient feeling quite faint and occassionally cause chest pain.  Patients tend to be in their late teens to 30s.


Always consider could this patient have a sinus tachycardia with p waves hidden in the preceding T waves.  Is this patient actually sick from something else like sepsis or rheumatic fever.

A very useful technique to sort out SVT from sinus tachycardia is to watch the monitor.  An SVT will stay and the same rate +/- a few beats/minute.  A sinus tachycardia will vary 10-20 beats per minute as the patient moves, holds their breath etc.

ST depression in SVT

As far as we know this has no significance – ignore it.  It does not mean the patient has failed an SVT stress test.

Regular wide complex SVT

Rarely we will see patients with a prexisting bundle branch block who go into an SVT.  This can be confusing.  The complexes tend to have the same morphology as typical bundle branch block so a LBBB will have a wide S wave in V1 and wide tall R waves in V6 rather than fairly similar looking complexes across the ECG in VT.

If in doubt and the patient is shocked electrically cardiovert for presumed VT.

Bottom line

Be nice to your patients – give diltiazem for SVTs


Dr Chris Cresswell MBChB, FACEM

Podcast episode

Song  on Podcast

Zhaba by DakhaBrakha

Relevant Terms and Definitions

(from the 2015 ACC/AHA/HRS SVT guideline)

Arrhythmia/Term Definition
Supraventricular tachycardia (SVT) An umbrella term used to describe tachycardias (atrial and/or ventricular rates in excess of 100 bpm at rest), the mechanism of which involves tissue from the His bundle or above. These SVTs include inappropriate sinus tachycardia, AT (including focal and multifocal AT), macroreentrant AT (including typical atrial flutter), junctional tachycardia, AVNRT, and various forms of accessory pathway-mediated reentrant tachycardias. In this guideline, the term does not include AF.
Paroxysmal supraventricular tachycardia (PSVT) A clinical syndrome characterized by the presence of a regular and rapid tachycardia of abrupt onset and termination. These features are characteristic of AVNRT or AVRT, and, less frequently, AT. PSVT represents a subset of SVT.
Atrial fibrillation (AF) A supraventricular arrhythmia with uncoordinated atrial activation and, consequently, ineffective atrial contraction. ECG characteristics include: 1) irregular atrial activity, 2) absence of distinct P waves, and 3) irregular R-R intervals (when atrioventricular conduction is present). AF is not addressed in this document.
Sinus tachycardia Rhythm arising from the sinus node in which the rate of impulses exceeds 100 bpm.
 • Physiologic sinus tachycardia Appropriate increased sinus rate in response to exercise and other situations that increase sympathetic tone.
 • Inappropriate sinus tachycardia Sinus heart rate >100 bpm at rest, with a mean 24-h heart rate >90 bpm not due to appropriate physiological responses or primary causes such as hyperthyroidism or anemia.
Atrial tachycardia (AT)
 • Focal AT An SVT arising from a localized atrial site, characterized by regular, organized atrial activity with discrete P waves and typically an isoelectric segment between P waves. At times, irregularity is seen, especially at onset (“warm-up”) and termination (“warm-down”). Atrial mapping reveals a focal point of origin.
 • Sinus node reentry tachycardia A specific type of focal AT that is due to microreentry arising from the sinus node complex, characterized by abrupt onset and termination, resulting in a P-wave morphology that is indistinguishable from sinus rhythm.
 • Multifocal atrial tachycardia (MAT) An irregular SVT characterized by ≥3 distinct P-wave morphologies and/or patterns of atrial activation at different rates. The rhythm is always irregular.
Atrial flutter
 • Cavotricuspid isthmus–dependent atrial flutter: typical Macroreentrant AT propagating around the tricuspid annulus, proceeding superiorly along the atrial septum, inferiorly along the right atrial wall, and through the cavotricuspid isthmus between the tricuspid valve annulus and the Eustachian valve and ridge. This activation sequence produces predominantly negative “sawtooth” flutter waves on the ECG in leads 2, 3, and aVF and a late positive deflection in V1. The atrial rate can be slower than the typical 300 bpm (cycle length 200 ms) in the presence of antiarrhythmic drugs or scarring. It is also known as “typical atrial flutter” or “cavotricuspid isthmus–dependent atrial flutter” or “counterclockwise atrial flutter.”
 • Cavotricuspid isthmus–dependent atrial flutter: reverse typical Macroreentrant AT that propagates around in the direction reverse that of typical atrial flutter. Flutter waves typically appear positive in the inferior leads and negative in V1. This type of atrial flutter is also referred to as “reverse typical” atrial flutter or “clockwise typical atrial flutter.”
 • Atypical or non–cavotricuspid isthmus–dependent atrial flutter Macroreentrant ATs that do not involve the cavotricuspid isthmus. A variety of reentrant circuits may include reentry around the mitral valve annulus or scar tissue within the left or right atrium. A variety of terms have been applied to these arrhythmias according to the re-entry circuit location, including particular forms, such as “LA flutter” and “LA macroreentrant tachycardia” or incisional atrial re-entrant tachycardia due to re-entry around surgical scars.
Junctional tachycardia A nonreentrant SVT that arises from the AV junction (including the His bundle).
Atrioventricular nodal reentrant tachycardia (AVNRT) A reentrant tachycardia involving 2 functionally distinct pathways, generally referred to as “fast” and “slow” pathways. Most commonly, the fast pathway is located near the apex of Koch’s triangle, and the slow pathway inferoposterior to the compact AV node tissue. Variant pathways have been described, allowing for “slow-slow” AVNRT.
 • Typical AVNRT AVNRT in which a slow pathway serves as the anterograde limb of the circuit and the fast pathway serves as the retrograde limb (also called “slow-fast AVNRT”).
 • Atypical AVNRT AVNRT in which the fast pathway serves as the anterograde limb of the circuit and a slow pathway serves as the retrograde limb (also called “fast-slow AV node reentry”) or a slow pathway serves as the anterograde limb and a second slow pathway serves as the retrograde limb (also called “slow-slow AVNRT”).
Accessory pathway For the purpose of this guideline, an accessory pathway is defined as an extranodal AV pathway that connects the myocardium of the atrium to the ventricle across the AV groove. Accessory pathways can be classified by their location, type of conduction (decremental or nondecremental), and whether they are capable of conducting anterogradely, retrogradely, or in both directions. Of note, accessory pathways of other types (such as atriofascicular, nodo-fascicular, nodo-ventricular, and fasciculoventricular pathways) are uncommon and are discussed only briefly in this document (Section 7).
 • Manifest accessory pathways A pathway that conducts anterogradely to cause ventricular pre-excitation pattern on the ECG.
 • Concealed accessory pathway A pathway that conducts only retrogradely and does not affect the ECG pattern during sinus rhythm.
 • Pre-excitation pattern An ECG pattern reflecting the presence of a manifest accessory pathway connecting the atrium to the ventricle. Pre-excited ventricular activation over the accessory pathway competes with the anterograde conduction over the AV node and spreads from the accessory pathway insertion point in the ventricular myocardium. Depending on the relative contribution from ventricular activation by the normal AV nodal/His Purkinje system versus the manifest accessory pathway, a variable degree of pre-excitation, with its characteristic pattern of a short P-R interval with slurring of the initial upstroke of the QRS complex (delta wave), is observed. Pre-excitation can be intermittent or not easily appreciated for some pathways capable of anterograde conduction; this is usually associated with a low-risk pathway, but exceptions occur.
 • Asymptomatic pre-excitation (isolated pre-excitation) The abnormal pre-excitation ECG pattern in the absence of documented SVT or symptoms consistent with SVT.
 • Wolff-Parkinson-White syndrome Syndrome characterized by documented SVT or symptoms consistent with SVT in a patient with ventricular pre-excitation during sinus rhythm.
Atrioventricular reentrant tachycardia (AVRT) A reentrant tachycardia, the electrical pathway of which requires an accessory pathway, the atrium, atrioventricular node (or second accessory pathway), and ventricle.
 • Orthodromic AVRT An AVRT in which the reentrant impulse uses the accessory pathway in the retrograde direction from the ventricle to the atrium, and the AV node in the anterograde direction. The QRS complex is generally narrow or may be wide because of pre-existing bundle-branch block or aberrant conduction.
 • Antidromic AVRT An AVRT in which the reentrant impulse uses the accessory pathway in the anterograde direction from the atrium to the ventricle, and the AV node for the retrograde direction. Occasionally, instead of the AV node, another accessory pathway can be used in the retrograde direction, which is referred to as pre-excited AVRT. The QRS complex is wide (maximally pre-excited).
Permanent form of junctional reciprocating tachycardia (PJRT) A rare form of nearly incessant orthodromic AVRT involving a slowly conducting, concealed, usually posteroseptal accessory pathway.
Pre-excited AF AF with ventricular pre-excitation caused by conduction over ≥1 accessory pathway(s).
  • AF indicates atrial fibrillation; AT, atrial tachycardia; AV, atrioventricular; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentrant tachycardia; bpm, beats per minute; ECG, electrocardiogram/electrocardiographic; LA, left atrial; MAT, multifocal atrial tachycardia; PJRT, permanent form of junctional reciprocating tachycardia; PSVT, paroxysmal supraventricular tachycardia; SVT, supraventricular tachycardia; and WPW, Wolff-Parkinson-White.

References / further reading

Atrioventricular nodal reentrant tachycardia from EM Core Content

Verapamil for SVT from the Rage Podcast 2014

A debate on the safety of verapamil in children from the Rage Podcast 2014

Cochrane review of calcium channel blockers vs adenosine for SVT from 2007

Adenosine level I evidence, calcium channel blockers level IIa only.  “Intravenous beta blockers, diltiazem, or verapamil are reasonable for acute
treatment in hemodynamically stable patients with AVNRT”

Engage your brain when reading ECGs

Click on ECG to enlarge

Fast AF

An 80 year old presented with mild nausea and shortness of breath.  His vital signs were normal other than the tachycardia.

He had a history of chronic atrial fibrillation, moderate chronic kidney disease and type 2 diabetes.

This ECG was given to a doctor to interpret

The doctor correctly identified that there were no signs of an MI, signed off the ECG and left the patient in the queue to be seen.

An hour later the patient was seen by another doctor.  By this time the patient’s heart rate was still 170, his blood pressure was sagging and the was febrile.

10 minutes later the patient’s blood pressure was 80/60.

His lactate was 6.0

No septic source was found but the patient had a history of multiple abdominal surgeries and a colostomy and similar episodes which grew enteric bacteria.  It is presumed that he has episodic bacteraemia from his gut.  The surgeons understandably were not keen to go hunting for a surgical remedy.

He was started on broad spectrum antibiotics to cover gut flora (cefuroxime and metronidazole), given IV fluids and started immediately on a vasopressor.

We chose to use phenylephrine in the hope that it’s alpha receptor agonism would cause vasoconstriction and cause a reflex drop in heart rate (rather than using a mixed alpha and beta agonist such as noradrenaline).  You could equally argue that noradrenaline would give some Beta 1 mediated inotropy which may have increased cardiac output and thus led to a decreased heart rate.  Often it is trail and error to see what works for a particular patient.

A vasporessor was used straight away as it was thought an 80 year old heart would not tolerate sepsis and a HR of 170 for long.

This patient’s heart rate and BP improved fairly quickly but if they hadn’t we get into the tricky situation of needing a negative chronotrope (to reduce the rate) but most negative chronotropes also drop the blood pressure.  In this setting most clinicians will use diltiazem, though a beta blocker has as much evidence for it.  Some will use IV digoxin, though most argue this takes too long to work.

Moral of the story

Engage your brain when reading ECGs.

You are not only looking for myocardial ischaemia – ECGs can tell us a lot about other badness.

This ECG was screaming “This patient is sick, or is going to become sick very soon”

Old hearts can not tolerate going at 170/min for long.  This is an old cardiovascular system attempting to compensate for badness, maxed out and about to decompensate.

For someone in fast AF always looks for a driver eg sepsis, congestive heart failure, thyrotoxicosis (rare and it is debated whether we should look for it).

This ECG should have led to a fairly immediate bedside review of the patient.


Music (on the podcast:

Fire by Sol3 Mio