Feeling Pulses in Cardiac Arrest

This picture is the most accurate summation of this topic I have ever seen (in the form of interpretive Zoidberg) – Reproduced from a great article on this subject by Pediatric EM Morsels @ http://pedemmorsels.com/palpation-of-pulse-for/


Feeling for a pulse in a patient suffering cardiac arrest is one of the more misunderstood actions associated with advanced life support. This review aims to break down the process of pulse checking to give a better understanding of this important task.

Why: We feel for a pulse in unconscious or critically unwell patients to assess perfusion and quickly quantify cardiac output. When a patient loses their pulse we can assume that their cardiac output has dropped below the level required to perfuse the brain and other vital organs. The absence of a palpable pulse is a primary sign of cardiac arrest and should be treated aggressively.

Where: Pulses can be palpated at numerous sites around the body. Peripheral pulses like the radial may be anatomically easier to locate in a well patient, however they will often not be detectable at lower blood pressures. For this reason central pulses are more useful in the setting of cardiac arrest where time is of the essence. The two most common sites to aim for are the carotid and femoral pulses (While the carotid is typically easier to find, the femoral is often more accessible in an arrested patient).


Picture reproduced from: https://commons.wikimedia.org/wiki/File:Pulse_sites-en.svg


Historically different figures have been suggested to link the presence of different pulses to specific systolic blood pressures (i.e. Radial pulse = systolic >80, Femoral pulse = systolic 70-80 etc.); However, there is little evidence to support any reliable correlation between different pulses and specific blood pressures (Rebel EM have a good review on this topic @ http://rebelem.com/atls-wrong-palpable-blood-pressure-estimates/).


How: The process of feeling for a pulse is relatively simple:

  1. 2-3 fingers are placed over an artery.
  2. Pressure is applied until a pulsation can be felt under the tips of the clinician’s fingers.

This pulsation indicates that blood is flowing through the underlying artery, which in turn indicates that the heart is pumping. The thumb should not be used when feeling for a pulse as the ‘feeler’ of the pulse is likely to detect the pulsation of their own radial artery being transmitted through the thumb.

In an unconscious or shocked patient, even central pulses may be difficult to feel. If you are relying on the presence of a pulse to rule out cardiac arrest and you are unable to CONFIDENTLY determine that the pulse is there, treat the patient as arrested (they will respond accordingly if they are alive and you start pressing on their chest – if they don’t respond, then carry on pressing)!

One interesting study found that doctors and nurses were only able to correctly identify the presence or absence of a pulse 78% of the time. The same group was noted to incorrectly identify the presence of a pulse 14% of the time (Feeling a pulse that was not really there); potentially delaying vital treatment in an arrested patient (Tidballs & Russell, 2009). This study helps to confirm that even as health professionals, it isn’t always easy feeling the pulse of a sick patient.

When feeling pulses in the context of cardiac arrest or critical illness, it’s also helpful to confirm that the pulse you are feeling matches the electrical rhythm on the cardiac monitor. If the monitor reads 15 beats per minute and you feel a pulse of 120 bpm, you are probably feeling your own pulse. The take-home message is that you can have a rhythm without a pulse, but not a pulse without a rhythm!

How long: In the patient where cardiac arrest is suspected (unconscious, not breathing etc.) a healthcare professional should not spend longer than 10 seconds attempting to feel for a pulse. If after 10 seconds a pulse cannot be felt, it isn’t there – start CPR.

When: Assessment of central pulses can provide vital information very quickly for any acutely unwell patient. In the context of cardiac arrest – the absence of a palpable pulse is how we traditionally differentiate cardiac arrest from other causes of unconsciousness. Whenever you are worried about a patient, a finger on the pulse goes a long way.

There is a common practice of holding onto the femoral pulse of an arrested patient to determine the quality of the chest compressions being provided (the theory being that the pulse represents the blood flowing through the femoral artery resulting from the external compression of the heart). There is mixed evidence on this practice with some studies suggesting that the pulsation felt during compressions comes from the femoral vein rather than the femoral artery. My feeling is that there isn’t much merit in this practice as there are better ways to monitor the ongoing quality of chest compressions i.e. ETCO2, Arterial lines (if available) & good old fashioned visual monitoring of compression rate and depth.

Following each rhythm check there MAY be an indication for a pulse check. It is important to understand that the pauses in the ALS algorithm are NOT for pulse checks; they are for RHYTHM checks! If VF or VT is identified during a rhythm check – the patient gets a shock and you’re back onto the chest. If any organised electrical rhythm is identified during the rhythm check, the defib can be disarmed and you perform a pulse check to determine if you have ROSC or PEA.

This point becomes important when utilising a guided defibrillation tool like the COACHED pneumonic. The purpose of such a tool is to maximise the compression fraction by ensuring the amount of time spent off the chest for each rhythm check is kept to the bare minimum. When following COACHED effectively, there is a good chance a patient with a shockable rhythm will receive their shock within 5 seconds of compressions stopping. If the process is modified by having someone continually holding onto the pulse during the rhythm check there is an increased risk of delays to defibrillation or worse – pulse checkers getting a wee zap.

With coordination, the practice of holding a pulse into a rhythm check can work; however this requires the pulse checker to keep an eye on the rhythm and release the pulse if they see VF or VT on the defib. With good clear communication between the pulse checker and the defib operator this process can introduce a benefit by having an extra set of eyes (the pulse checker) to corroborate rhythms and more importantly, having the ability to differentiate PEA from ROSC more efficiently so that PEA may be treated with further high quality CPR. In an already high functioning team this concept may be useful, but for most novice to intermediate teams I feel that a structured approach to safe defibrillation provided by COACHED (or alike) may improve important measures like compression fraction and time to defibrillation while ensuring everyone stays safe.

If you think you might have trouble finding the pulse again after the rhythm check, it can be helpful to mark the pulse site quickly with a marker/pen i.e. a circle or a cross over the femoral pulse can make it much easier to find when you come back to check for a pulse in your organised rhythms.

Extra: There are a number of different adjuncts that may support the process of pulse assessment in cardiac arrest.

  • End tidal carbon dioxide (ETCO2): May be more useful than pulse palpation for assessing the quality of chest compressions and predicting ROSC (ETCO2 decreases as compression quality falls & may suddenly increase when ROSC is achieved).
  • Arterial lines: May also be used to continually monitor the quality of chest compressions during CPR and to identify ROSC. (These are useful if they are already in situ when the arrest occurs, they can be challenging to site and their intra-arrest placement should never interrupt chest compressions).
  • Point of care ultrasound (POCUS): The use of ultrasound in cardiac arrest is becoming routine as the utility of the assessment grows. Cardiac ultrasound can help assess underlying cardiac function while providing important information relating to the presence or absence of reversible causes. In the case of PEA, cardiac ultrasound can help us differentiate true PEA from pseudo-PEA (where a pulse cannot be felt but the heart is contracting on ultrasound)

Key Points:

  1. Feel central pulses (femoral – carotid).
  2. Don’t take longer than 10 seconds.
  3. If in doubt – start compressions.
  4. Pauses in compressions are primarily for RHYTHM CHECKS not pulse checks.
  5. You can have a rhythm without a pulse – you cannot have a pulse without a rhythm.
  6. Consider adjuncts like ETCO2 and art lines to monitor CPR quality and the likelihood of ROSC.
  7. Focus on high quality compressions with a high compression fraction. Plan your interventions and interruptions for rhythm checks (use this time wisely).
  8. Use adjuncts to predict ROSC at the next rhythm check – Don’t stop compressions early unless the patient stops you.

There is a great talk by Haney Mallemat exploring these ideas in more detail with a particular focus on how we assess and manage PEA – I would highly recommend having a look @ https://www.smacc.net.au/2017/01/the-pea-paradox/


2005 American Heart Association Guidelines for Cardiopulmonary Resuscitations and Emergency Cardiovascular Care. Part 4: Adult Basic Life Support. Circulation; 112. Retrieved from: http://circ.ahajournals.org/content/112/24_suppl/IV-19

Tibballs J1, Russell P. (2009). Reliability of pulse palpation by healthcare personnel to diagnose paediatric cardiac arrest. Resuscitation;80(1):61-4

The Crunch

While many factors impact our ability to deliver effective care to our patients, positioning is one of the simplest, but most meaningful interventions we can provide. Different positions help to facilitate different interventions or physiological processes.

  • Supine: Facilitates abdominal assessment & spinal protection.
  • Prone: Helps optimize ventilation for patients with ARDS.
  • Fowlers: Supports normal physiological respiration.
  • Lateral recumbent (Sim’s position): Allows passive airway clearance in the unconscious patient, facilitates inspection of posterior surfaces.
  • Lithotomy: Facilitates lower abdominal surgery, pelvic surgery & childbirth.
  • Trendelenburg: Supports blood pressure and central perfusion.
  • Reverse Trendelenburg etc…You get the picture.

Among the many positions patients find themselves in within the confines of a hospital bed, there is one common position that continues to confound clinicians and hinder the provision of optimal care to patients. I call this position – the crunch.

This position occurs most commonly when a patient is positioned sitting up in bed (the fowler’s position) and gradually slides towards the foot of the bed. While the fowler’s position is great when the patient’s backside is in good contact with the mattress, it can cause problems when the patient begins to slip. As the patient drifts towards the bed-end their lower back rounds and their neck invariably begins to flex causing a reclined kyphotic posture that feels as awful as it looks.


For conscious, independently breathing patients – sitting up in bed (in the fowlers position) is an optimal position to facilitate ventilation and maintain airway patency.



When the patient slides downwards and ‘crunches’ themselves in the angle of the bed, the alignment of the airway and respiratory anatomy becomes less favorable.


‘Crunching’ patients is bad for a number of reasons. Primarily the combination of neck flexion and thoracic rounding provides one of the least optimal physiological environments for breathing imaginable. Secondarily, to get into this position in the first place the patient has to slide down the bed, which implies the application of a shearing force to their backside that over time sets the scene for a pressure injury. This position is also fairly rubbish for other activities like eating & drinking, taking meds or vomiting as the alignment of the GI tract and airway make choking and aspiration real considerations.

Patients can end up in this position for a number of reasons, but the causative factors in most cases will include at least one of the following:

  • Decreased level of consciousness.
  • Slide sheets left under patients for long time.
  • Poor use of bed mechanics (bed tilted downwards etc.)
  • Restricted mobility.


In order to avoid this situation we need to be mindful of our patient positioning. While the fowler’s position is one of the most common and useful positions for the bed-bound patient, the use of simple bed manipulations like raising the foot of the bed or bending the knees slightly can provide some much needed resistance against the eternal pull towards the floor. While slide sheets make our life significantly easier when actively moving patients, they can hasten a patients slide away from their ideal position if they are left in place constantly – not to mention the discomfort factor of lying on multiple layers of nylon and linen.

If you recognise this position in your unit, be sure to intervene and assist the patient up the bed. ‘Un-crunching’ patients not only helps to ensure comfort and dignity; its also a simple, effective and often overlooked way of optimising your patients anatomy to facilitate better ventilation while reducing clinical risks like aspiration and choking. Remember that a simple transfer up the bed can be the most meaningful thing you can do when troubleshooting a patient with dyspnoea – sometimes the simplest thing to do is best.

An article from American Nurse Today dives much deeper into the causes and management of ‘patient migration’, Check it out at the link below if you are that way inclined (https://www.americannursetoday.com/sliding-patient-respond-prevent-migration-bed/).

11 ECG Patterns Worth Knowing

While there are plenty of overtly abnormal ECG patterns that are universally recognized as indicators of impending trouble – there are a number of patterns that, despite looking unfamiliar can be equally significant for the patient.

While it remains important to understand the in’s and out’s of ST changes, bundle branch blocks and AV dissociation; I recommend keeping these 11 patterns in the back of your mind when assessing patients with chest pain or syncope.

Six of these patterns suggest problems with the conduction system of the heart while the remaining five are considered “STEMI equivalents” and should be treated as serious indicators of coronary vascular disease.



Prolonged QT interval

The QT interval represents the time it takes for the ventricles to depolarize and then repolarize, ready for the next heart beat. This interval is measured from the start of the QRS complex to the end of the T wave.

In some circumstances, this interval can become abnormally prolonged. This may be due to either a congenital condition or a combination of external factors i.e. toxins, electrolyte imbalance etc. Having an abnormally long QT interval increases the risk of a patient developing life threatening ventricular arrhythmias.

It is important to note that the QT interval changes proportionally to the heart rate (the QT narrows as the HR increases and widens as the HR slows). For this reason the QTc or corrected QT interval is commonly used to determine whether a patients QT is abnormally prolonged. There are many formulae for calculating QTc available, however most ECG machines will provide a QTc value for you.

In general terms, a QTc greater than 450ms is considered prolonged, while a QTc greater than 500ms will increase the risk of developing ventricular arrhythmias.

Patients with abnormally long QT intervals should be assessed for pathological causes of QT prolongation (toxicity, electrolytes etc.). If no cause is found and marked QT prolongation persists post treatment, patients should receive cardiology assessment for congenital causes of the condition.



Image reproduced from the Cleveland Clinic @ https://my.clevelandclinic.org/health/articles/long-qt-syndrome


Wolff Parkinson White Syndrome

Wolff Parkinson White (WPW) syndrome is a condition characterized by the pre-excitation of the ventricles via an additional electrical pathway known as the bundle of Kent (linking the atria to the ventricles).

Typically electrical currents from the SA node are ‘slowed down’ as they pass through the AV node before moving into the ventricles. In WPW, the electricity can enter the ventricles via the bundle of Kent without being slowed by the resistance of the AV node. This means that part of the ventricles will be stimulated fractionally earlier than the AV node can convey the message to the bundle of HIS.

As with other accessory pathways, electrical impulses may travel back up the bundle of Kent from the ventricles into the atria. This type of circuit allows electrical impulses to rapidly travel in a cycle from the AV node, through the ventricles and back to the AV node via retrograde (backward) conduction through the bundle of Kent. This is known Atrioventricular reciprocating tachycardia (a type of SVT).

Patients with WPW are at an increased risk of AVRT and are also at a slightly higher risk of sudden cardiac death.

Symptomatic patients with WPW should be referred to a cardiologist for further assessment and management (patients may require treatment with medication of ablation).

WPW patients with palpitations or extreme tachycardia should be treated according to their clinical condition and ECG findings. WPW patients with SVT may be responsive to vagal maneuvers or medications but as with all tachyarrhythmia’s, DC cardioversion may be required if the patient is unstable.

ECG characteristics of WPW are:

  • A short PR interval (less than 120 milliseconds)
  • The presence of a delta wave (an early upward slurring of the initial section of the QRS complex signifying early excitation of the ventricles).
  • Patients may also present with AVRT (a type of SVT).



Globally shortened PR interval with delta waves evident in all leads – ECG reproduced from life in the fast lane @ https://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes/


Brugada Syndrome

Brugada syndrome is characterized by a mutation of the gene responsible for controlling sodium channels within the myocardium. Dysfunction of these channels can lead to abnormal depolarization and potentially the development of lethal tachyarrhythmias.

Brugada was only recently discovered 1992 but has since been linked to a high risk of sudden cardiac death with an estimated 10% annual risk of sudden death.

The one ECG finding characteristic of Brugada syndrome is the presence of the ‘Brugada sign’ – coved (down-sloping) ST elevation of greater than 2mm followed immediately by an inverted T wave in more than one of the following leads (V1, V2 or V3).

Brugada sign may not always be present on a patients ECG and may only be uncovered by particular stimulus i.e. drugs, cardioversion, fever, ischemia or electrolyte imbalances.

Brugada can only be diagnosed when the Brugada sign is present on an ECG and the patient presents with relevant clinical signs i.e. episodes of VT or VF, family history of sudden death under 45, Brugada sign on the ECG of family members, syncope, agonal respirations during sleep etc.

Patients with Brugada sign and relevant clinical history should be referred for urgent cardiology assessment to determine whether their risk of sudden cardiac death necessitates the insertion of an implantable automated cardioverter defibrillator.



Typical ‘Brugada sign’ in V1-3 – ECG reproduced from The Student Physiologist @ https://thephysiologist.org/study-materials/brugada-syndrome/


Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is characterized by the abnormal thickening of the myocardial muscles comprising the ventricle walls. Typically HCM involves hypertrophy (thickening) of the left ventricle, however different patterns exist including hypertrophy of the inter-ventricular septum and concentric hypertrophy.

HCM is relatively common and has been attributed to a genetic mutation that affects the regulation of the proteins responsible for building and repairing the myocardium.

HCM is associated with a 1-2% annual risk of sudden cardiac death and is the leading cause of sudden death in young athletes. As the walls of the myocardium thicken, the naturally occurring conduction pathways are interrupted and various accessory pathways may develop which put the patient at a greatly increased risk of conduction abnormalities and lethal arrhythmias.

Patients with HCM may present with chest pain, dyspnea or exertional syncope. If any of these symptoms are present, patients should be urgently referred for cardiology assessment to determine whether an AICD is required. Further testing (including echocardiography) will be required to establish a formal diagnosis, but ECG clues can be the first step in uncovering this condition in young adults.

Wolff-Parkinson White syndrome may be present in up to 30% of patients with HCM due to the development of accessory pathways such as the bundle of Kent.

ECG characteristics of HCM vary depending on the area of the heart affected but can include:

  • Increased QRS voltages (QRS complexes which are much taller than normal) and non-specific ST segment changes in the chest leads (signifying ventricular hypertrophy).
  • Deep narrow Q waves in lateral and inferior leads (signifying asymmetrical septal hypertrophy).
  • P mitrale (M shaped doubled P waves) may signify left atrial hypertrophy, which may follow ventricular enlargement.
  • Giant T wave inversion may be present in the case of apical hypertrophy.
  • Atrial arrhythmias and VT may also be seen in conjunction with HCM.



Increased QRS voltages in the inferior and precordial leads, Dagger like Q waves in the inferolateral leads, Deep T wave inversion in the lateral leads – ECG reproduced from life in the fast lane @ https://lifeinthefastlane.com/ecg-library/hcm/


Second Degree AV Block – Mobitz 2

Mobitz type 2 refers to the intermittent failure of an impulse generated in the atria to conduct through to the ventricles. Where mobitz type 1 indicates a gradual fatigue of the working AV node which leads to regular failure, type 2 indicates a mechanical failure at or below the level of the bundle of HIS. Typically this failure is due to damage or injury to the electrical conduction systems from cellular necrosis, fibrosis or inflammation.

Mobitz type 2 is more clinically significant than mobitz 2 as patients are more likely to present with symptomatic bradycardia and insufficient cardiac output. Mobitz type 2 is also significantly more likely to deteriorate to complete (third degree) heart block. This rhythm is associated with a 35% risk of Asystole and sudden cardiac death each year.

The reason Mobitz 2 is so important to remember is that can be quite subtle on an ECG while still flagging potentially significant complications for the patient. Third-degree block is obviously more significant, however it is much more obvious. First degree and Mobitz 1 can also be subtle, however they pose little risk to the patient if left unmanaged. Mobitz 2 is sneaky and can cause patients problems.

A cardiologist should assess the need for pacemaker insertion in patients with a mobitz 2 ECG and concerning symptoms such as syncope.

Mobitz type 2 ECG’s are characterized by:

  • The intermittent presence of P waves that are not followed by QRS complexes and are not preceded by the gradual lengthening of PR intervals.
  • P waves will maintain a regular rate with an even P-P interval. PR intervals remain constant.
  • Multiple P waves may occur together with absent QRS complexes.



Arrows indicate P waves with no associated QRS complexes – Rhythm strip reproduced from EKG Strip Search @ http://www.ekgstripsearch.com/2nd_2.htm


Arrhythmogenic Right Ventricular Dysplasia

Arrhythmogenic right ventricular dysplasia is a congenital heart disease that is characterized by the pathological replacement of myocardial cells in the right ventricle with fatty or fibrous tissue. This tissue is not conductive like myocardial tissue and as such the presence of this tissue obstructs and interferes with the conduction of normal electrical signals within the heart.

ARVD is the second leading cause of sudden cardiac death in young people (following behind HCM). For some patients the first sign that they have this disease will be the development of a ventricular arrhythmia and possible cardiac arrest.

While echocardiography and radiological investigation are the most sensitive investigations for this condition, there are some important ECG findings that we should be mindful of in patients with symptoms of palpitations, syncope or exertional collapse.

Patients diagnosed with ARVD who are deemed high risk may be treated with medication to prevent arrhythmias or have an AICD inserted. As such, any patient suspected to have findings suggestive of ARVD should receive cardiology assessment.

ECG characteristics that suggest ARVD include:

  • The presence of an epsilon wave (a small positive inflection buried in the end of the QRS complex)
  • T wave inversion and QRS widening in the anterior leads (v1-3)
  • Episodes of ventricular tachycardia with a left bundle branch block appearance.



Epsilon waves present in all QRS complexes, T wave inversion V1-5 (also in inferior leads) – ECG reproduced from life in the fast lane @ https://lifeinthefastlane.com/ecg-library/basics/arrhythmogenic-right-ventricular-cardiomyopathy/



Through the use of universal ‘STEMI’ criteria, we are hoping to identify patients in the acute phase of a myocardial infarction who will benefit from the timely delivery of therapy (like PCI or TPA) to restore coronary blood flow and potentially circumvent permanent heart damage.

In New South Wales the diagnostic criteria from a STEMI is “persistent ST segment elevation greater than or equal to 1mm in two or more contiguous limb leads or ST segment elevation greater than or equal to 2mm in two contiguous chest leads or presumed new LBBB pattern” (NSW Chest pain pathway, 2011). While this definition fits (for the most part) with different guidelines around the world, there are some important exceptions to the rule.

The following patterns are commonly referred to as ‘STEMI equivalents’. While these ECG’s don’t fit the traditional mold of an acute infarct, the patient outcomes and treatment requirements are in line with more recognizable patterns of ST elevation. If any of these patterns are identified in a patient with ongoing chest pain or hemodynamic compromise urgent cardiology review should be arranged.

Wellens Syndrome

This pattern is very specific for a critical stenosis of the proximal segment of the LAD coronary artery. While this pattern is not necessarily a ‘STEMI equivalent’, it should be taken very seriously as these patients are at significant risk of imminent anterior infarct without appropriate and timely treatment.

These patients should be monitored closely and reviewed by a cardiologist. Care should be taken to differentiate Wellens from an anterior STEMI pattern (STEMI = more than 2mm ST elevation, poor R wave progression, unrelieved pain, higher troponin levels).

Wellens ECG’s are characterized by:

  • Slight ST elevation (0 – 1mm) in the anterior leads (may extend through all chest leads) – combined with – inverted or biphasic T waves in the anterior leads (may extend through all chest leads).



ST elevation with associated T wave inversion V1-4 – ECG reproduced from RebelEM @ http://rebelem.com/r-e-b-e-l-ecg-week-wellens-syndrome-stemi/


De Winters T waves

De Winters T waves are predictive of an acute occlusion of the proximal left anterior descending (LAD) coronary artery. This pattern has been seen in 2% of patients with acute LAD occlusion in the literature. Because the pattern is unfamiliar to many clinicians, De Winters T waves may be associated with an increased risk of under treatment. This pattern should be treated as being equivalent to an anterior STEMI.

ECG characteristics of De Winters T waves include:

  • Tall (often very prominent) T waves in the precordial leads
  • More than 1mm of ST depression in the precordial leads
  • Very slight (0.5-1mm) ST elevation in lead aVR.


T waves associated with De Winters are often referred to as being ‘hyper acute’. Symmetrical hyper acute T waves in the absence of hyperkalemia should be considered as an indicator of myocardial ischemia.


ST depression with very tall T waves V2-6 – ECG reproduced from Dr Smiths ECG Blog @ https://hqmeded-ecg.blogspot.com.au/2014/04/chest-pain.html


Sgarbossa Criteria

While the new onset of a left bundle branch block is always considered pathological, this pattern is no longer routinely associated with a STEMI. Instead, different formulas have been developed to help us determine when acute myocardial ischemia is present in the patient with a concurrent LBBB (this includes patients with permanent pacemakers who typically exhibit LBBB morphology on their ECGs). One such formula is the Sgarbossa criteria.

In patients with LBBB, there is typically some element of ST segment discordance, meaning the ST segment will be shifted in the opposite direction to the QRS complex. If the majority of the QRS complex is below the isoelectric line (negative) then you can expect the ST segment to be elevated above the isoelectric line (positive). This also means that ST segments will be negative when QRS complexes are positive.

Sgarbossa criteria focuses on patients with alterations to this rule of ‘normal discordance’. There are three main variations to this pattern and each of these variations is associated with a numerical score. If the patient has a cumulative score of greater than (or equal to) three, their ECG is 90% specific for diagnosing myocardial ischemia.

The three variations considered in Sgarbossa criteria are included below with their respective numerical score:

  • Concordant ST elevation > 1mm (Positive ST segment in a lead with a positive QRS complex) = 5 points
  • Concordant ST depression > 1mm (Negative ST segment in a lead with a negative QRS complex i.e. V1-3) = 3 points
  • Excessively discordant ST elevation > 5mm (very positive ST segment in a lead with a negative QRS complex) = 2 points



Original Sgarbossa criteria reproduced from https://www.aliem.com/2013/12/modified-sgarbossa-criteria-ready-primetime/ referenced as “Cai, Mehta, Sgarbossa et al, 2013”.


In order to improve the sensitivity of the original Sgarbossa criteria the Smith-Modified Sgarbossa criteria was developed. These modified criteria essentially replace the third variant (excessively discordant ST elevation > 5mm) to the following:

  • 1 lead anywhere with > 1mm ST elevation and proportionally excessive discordant ST elevation as defined by > 25% of the depth of the preceding S wave.

This modification is useful as the un-quantified inclusion of discordant ST elevation as a diagnostic feature did not account well for patients with high voltage ECG’s.


Image reproduced from Wikem @ https://wikem.org/wiki/Sgarbossa%27s_criteria


Left Main Coronary Artery Occlusion

Occlusion or critical stenosis of the left main coronary artery is commonly associated with an ECG pattern that does not fit the routinely accepted definitions of a STEMI. Nevertheless, this condition necessitates immediate treatment and potential revascularization just the same as a more commonly recognized STEMI.

This pattern is caused by a widespread myocardial perfusion deficit (as would be the case if flow through the left main was restricted). This pattern can also be seen in other conditions causing diffuse ischemia of the myocardium such as severe triple vessel disease, proximal LAD occlusion or any other condition causing global tissue hypoxia i.e. post cardiac arrest.

ECG characteristics of this pattern include:

  • ST elevation > 1mm in aVR
  • ST elevation in aVR > V1
  • Widespread ST depression in the inferolateral leads (II, III, aVF, V4-6).



ST Elevation in aVR with diffuse ST depression in the inferolateral leads – ECG reproduced from Johnson Francis (Cardiophile MD) @ https://cardiophile.org/ecg-in-left-main-coronary-artery-stenosis/


Posterior STEMI

A standard 12 lead ECG doesn’t look at the posterior wall of the heart. For this reason any injury to the posterior wall can only be identified on a standard ECG through the presence of reciprocal changes. When considering an infarct causing ST elevation in the posterior territory of the heart, the opposite territory that will reciprocate these changes is the anterior surface of the heart.

Posterior STEMI is most commonly associated with either inferior or lateral STEMI as the same vessels (right coronary & circumflex) supply the posterior wall. Posterior STEMI without inferior or lateral ST elevation is possible but less common. If posterior STEMI changes are present in the context of an inferior or lateral infarct, the area of ischemic myocardium is considerably larger and may be associated with worse patient outcomes.

If ECG changes are seen on a standard 12 lead ECG that suggest a posterior infarct, it may be helpful to perform a posterior ECG by moving V4-6 further around the patients chest to look more directly at the posterior wall of the heart.

ECG characteristics of a posterior STEMI include:

  • Horizontal ST depression with upright T waves and tall broad R waves V1-3 (supported by >1mm ST elevation in the posterior leads V7-9).



Horizontal ST depression can be seen with upright T waves in the anterior leads (V1-3) – Associated with inferolateral ST elevation – ECG reproduced from life in the fast lane @ https://lifeinthefastlane.com/ecg-library/pmi/



Cai Q, Mehta N, Sgarbossa E, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: from falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? Am Heart J. 2013;166(3):409-413.


Assessing the ECG

As with the interpretation of any test, having a systematic approach to ECG interpretation can make a daunting task more manageable while minimizing the likelihood of missing important details. Most nurses will perform thousands of these tests through the course of their career, giving us a great opportunity to refine our ECG literacy and potentially identify trouble early in patients with cardiac trouble.

If you talk to any ECG boffin you’ll typically find they have a specific approach to breaking down ECGs into their vital elements to ensure their assessment is thorough and reproducible. I try to look at ECG’s the same way I look at physical assessments; you follow certain steps to gather information that will come together to show the bigger picture and reveal the diagnosis. While there are lots of different ways of breaking down ECGs, I use the following steps to assess the important elements of every ECG I perform:


  1. The first step is to identify the rate.
  • Determine whether the rate is normal (60-100bpm), fast (>100bpm) or slow (<60bpm).
  • Most ECG machines will automatically interpret the rate for you (this is perfectly acceptable – the machines are clever).
  • Alternatively, just count the number of QRS complexes on the rhythm strip and multiply this by 6 (a 12 lead ECG records for 10 seconds – 6 lots of 10 seconds in a minute).


  1. The second step is to determine if the rhythm is regular or irregular.
  • The easiest way to do this is to run a sheet of paper across the top of the QRS complexes on your ECG, using a pen mark the location of the first and second QRS complexes.
  • Now move the paper to the right so that the mark from the first complex is over the second complex. If the rhythm is regular the mark from the second complex will now be over the third. This should apply for any complex you move your marker to.


  1. The third step is to identify whether all features of the waveform are present
  • Is there a P wave?
  • Is there a QRS complex? If there is not, immediately recheck your patient – They are probably in trouble!
  • Is there a T wave?
  • Are there any additional elements i.e. U waves, J waves etc.?



  1. The fourth step involves identifying whether different intervals and features have a normal appearance. This step is often the most difficult but helps us to identify and differentiate between various rhythms and disease states in a more definitive manner. I find if you work through the different features in the order they appear you are less likely to miss steps or get fixated on particular points.
  • P waves – Are they upright and symmetrical or do they exhibit abnormal morphology (i.e. fibrillation waves, flutter waves, inversion, asymmetry)
  • PR interval – Is it fixed or does it change from beat to beat?
  • QRS complex – Does it follow every P wave? Is it wide or narrow?
  • ST segment – Is there ST elevation or depression?
  • T waves – Are they upright or inverted? Is the amplitude (size) normal?
  • QT interval – Is it abnormally long?
  • Other – Are there any other features that are not usual i.e. abnormal Q waves, U waves, J waves etc.?

If you identify any abnormal features, it is also important to identify if they are generalized (present in all/most leads) or localized (present in only certain leads).


While breakdown process gives you a lot of information, it doesn’t tell you whether there is a problem or directly establish a ‘diagnosis’. To ‘diagnose’ an ECG, you need a bit more information on how this data fits together.

By far the most important aspect of understanding ECGs is having the ability to identify a ‘normal’ ECG. This means, confidently identifying an ECG in sinus rhythm with no evidence of acute ischemia or pathology. If you’re comfortable using a systematic approach to interpret an ECG of normal sinus rhythm, you will be able to determine when something is NOT normal sinus rhythm and escalate appropriately.

Normal sinus rhythm represents the rhythmic contraction of the heart muscle when stimulated by an electrical impulse generated in the SA node that moves through the atrium, AV node and ventricular conduction system without interruption.

An ECG of normal sinus rhythm contains the following features:

  • A regular rhythm with a rate of 60-100 beats per minute.
  • A single P wave which is upright in leads I, II and is inverted in aVR,
  • A single narrow QRS complex
  • A T wave that is upright (inverted in aVR)
  • Fixed PR interval (less than 200ms)
  • Isoelectric PR and ST segments.
This ECG is a good example of sinus rhythm: The rate is normal, it’s regular, all the bits are there and predominantly they appear normal (ignoring some benign looking ST elevation V1-3)


When you come across something that is NOT normal sinus rhythm, it can initially help to use a tool to assist in determining the nature of the rhythm. There are loads of great charts and info-graphics around designed to take you through the steps of pulling apart different rhythms. Joanne Reading has a great flowchart for rhythm interpretation on her blog that you can find at:


The way I break ECGs down is a little different so I took some time to try and map my thought process. Using the steps from above, you should have all the data you need to follow this chart through to a potential diagnosis. You should always be mindful that while these types of charts will get you close to a definitive answer, there are occasionally confounding factors like funky conduction and anatomical disturbance that can send you off track. Also worth noting that if you reach a diagnosis of VF by taking a 12 lead ECG and following a flow chart – something has gone very wrong! If you are concerned about either the appearance of the patient or the appearance of their ECG – you have all the information you need, go get help.

But for what it’s worth, here’s my chart…

ecg chart




Once you have determined the rhythm, it is important to check for the telltale signs of cardiac disease or dysfunction. Primarily this will involve looking for signs of ischemia associated with myocardial infarction, however, it can involve looking for signs of electrolyte imbalance or even secondary organ dysfunction (i.e. raised ICP). While there are too many individual syndromes and diseases to fit into one blog post, essentially you can cover most bases by looking for any of the following abnormalities:

1 – ST elevation or depression: suggestive of abnormal ventricular depolarization / repolarization that may be caused by myocardial ischemia.

Here ST elevation can be seen highlighted in yellow, while ST depression is highlighted in blue.

2 – T wave abnormalities: suggestive of abnormal ventricular repolarization that may be caused by myocardial ischemia. Most importantly look for T waves that are inverted or disproportionately large in more than one lead.

3 – A really wide QRS: suggestive of poor ventricular conduction that may indicate serious conduction problems or electrolyte abnormalities.


Using this information, try to ‘diagnose’ the ECGs you perform in your workplace. Think critically about whether each ECG is normal; if it isn’t, think about why it isn’t. When getting abnormal ECG’s checked, talk to your colleagues about what you think is wrong and ask them what they see. Having these discussions with your workmates is one of the best ways of developing not only skills in ECG reading but also more broadly developing skills in critical thinking and analysis.

If you want more comprehensive resources exploring different arrhythmias and abnormalities, I would encourage you to take a look at both ‘Life in the fast lane’ http://lifeinthefastlane.com/ecg-library/ and Dr. Smith’s ECG blog at https://hqmeded-ecg.blogspot.ae. Both of these sites are awesome free resources with a huge supply of knowledge about all things ECG.



Is There a Medical Professional on Board This Aircraft: Responding to a Medical Emergency on a Commercial Flight

In the coming days, my wife and I will be embarking on a trip to Europe. Predominantly this trip will be for a bit of adventure, however, the underlying motivation is the SMACC conference in Berlin towards the end of June.

I have flown internationally a handful of times in the past. On one of these occasions I was given some pause to think more critically about how I would respond in future if the call came over the loud speaker:


Is there a medical professional on board this aircraft?


Several years ago, I responded to one such call. My wife and I were traveling abroad for our honeymoon – we were peacefully reclining in the economy section of the plane when the first call came over the speaker:


If there is a doctor on board this flight could you please make yourself known to cabin staff?”


I wondered to myself what could be happening and allowed my mind to wander, all the while assuming that there would be some able and willing physician on the plane who would sweep in and address any emergency that could be unfolding (n.b. I was relatively green at this point). After about ten minutes, a second call came over:


If there is a doctor, nurse or other health professional on board would you please make yourself known to cabin staff?


My wife looked at me, knowing quite well that I was already unbuckling my seatbelt. I presented to the nearest member of the cabin crew, introduced myself as an emergency nurse and asked if they still needed assistance. I was taken to the back of the plane where I found a patient who was experiencing a condition that I saw quite commonly in the ED (However, this condition suddenly felt very foreign when transposed several thousand meters above the ground).

For the sake of this post, I won’t talk about any specific details of the patient’s problem, firstly for privacy reasons and secondly because I think the nature of a patient’s problem often takes a backseat to the non-technical and logistic aspects of managing an unwell patient on a plane.

After helping the patient find a comfortable position and performing a brief primary assessment. I was briefed by another member of the cabin staff who informed me of the resources I had at my disposal. I was informed there was oxygen available and I was handed a large, reasonably well-equipped medical kit.

The medical kit was well stocked with various drugs, IV access equipment, fluids, dressings and limited assessment equipment. In a doctor and nurse team, there would be ample medication and equipment to provide throughout initial management to patients with a wide variety of presenting problems. The thing that stuck out to me was the variety of cardiac drugs available: aspirin, GTN, adrenaline all immediately accessible. There were also a wide variety of analgesic agents ranging from simple stuff like paracetamol to parenteral narcotics. However, being a lone nurse responder I felt myself highly unlikely to have the inclination to administer any drugs (thank god the patient in my case didn’t require any).

I was shown the automated defibrillator that was situated in the locker with the other medical gear. I was pleased to see this included, even in the early days of my practice. With my expanded comprehension of the concepts related to effective resuscitation, I feel even more reassured that these devices are widely available on commercial flights. As most will know, there are few well-validated interventions that improve outcomes for patients suffering cardiac arrest, and with these devices on board we have access to both of the big-ticket items – High-quality CPR and timely defibrillation. As someone who values the high-flying (no pun intended), cutting edge aspects of resuscitation, I would feel comfortable attempting resuscitation using oxygen, an AED and the assistance of the first aid trained cabin staff.

Fortunately again, my patient was not suffering cardiac arrest. They were, however, looking a little pale. I proceeded to take the sphygmomanometer and stethoscope and performed a simple assessment gathering the patient’s history and vitals. My patient was ever so slightly hypotensive. In the hospital setting, I would almost reflexively establish IV access and continue my assessment using more intensive tests to establish the cause of the hypotension. In the back of a plane with a basic medical kit, an ECG and full blood panel was unfortunately out of the question. So what do you do?

Sure there was enough gear for a line and some fluids, but again, as a reasonably junior nurse I would not feel comfortable poking a patient in the back of a plane, let alone starting a drip (which is something I wouldn’t have done without clarification even in the hospital setting). So I decided to utilize the planes ergonomics to help me out. The plane was flying (as planes often do) with the nose elevated above the tail. This allowed us to lay the patient down with her head on a pillow pointing towards the tail of the plane, giving us a kind of modified trendenleburg position.

While I was crouched down beside the patient, I noticed that the crew had done a marvelous job of cordoning off the back of the plane with curtains to ensure the patient was not subjected to a plane full of passengers peering around corners to get a glimpse at the spectacle. While this was fantastic, I did notice that the patient still have five or six crew standing around them for much of the assessment period. As in any location, care should be taken to maintain the privacy and dignity of all the people we look after – and consent should always be sought before attending any tests or treatments.

I stayed with the patient and after a few minutes, they began to feel better. Much to my delight (and to the benefit of my own blood pressure), they remained stable for the remainder of the flight. I continued to keep an eye on the blood pressure and watched for signs of mischief, but for the most part the management remained conservative. I took the rest of my time on standby to formulate contingencies against any change in condition i.e. what would I do if the BP remained low or if the patient needed pain relief. At the time, the truth of the matter is that I didn’t know the answer to a lot of these questions, and in mid-air it was not as simple and whipping out my phone for a sneaky Google search.

Since this scenario, I have had more time to think about the ins and outs of emergency response in an airplane. The more I thought and read, the more I came to feel that nurses (and particularly emergency / critical care nurses) can play a few major roles in the management of these situations.


  • Assessment – Nurses generally have well-established assessment skills. Being able to perform a general assessment including a visual assessment, vitals, and a history can help establish some management goals. Even if achieving those goals is beyond your means as a lone nurse in a big plane, it can help you to escalate the situation as needed.


  • First aid – Having the ability to perform advanced first aid with a high degree of proficiency can be useful in the management of a wide variety of different situations. In the aircraft environment, consider the case of the unrestrained passenger during turbulence. Occasionally you will hear a story in the news about ‘passengers injured during turbulence’. In this instance, an emergency nurses assessment and first aid skills may be very applicable. Having the ability to control bleeding, apply dressings and immobilize injuries could potentially save a great deal of misery for the passengers and the crew.


  • Basic life support – This is the most obvious but also the most terrifying case. While most airline staff will have received training in first aid and CPR, the likelihood that they have had to use their skills in anger is probably fairly low as a general rule. As critical care providers, we often have advanced skills in resuscitation – commonly including ACLS training. From this perspective, it is easy to imagine that we might feel like fish out of water when removed from our defibs and vents. However, if we remember that timely defibrillation and well delivered and coordinated CPR are the most meaningful interventions for an arrested patient (even in our current ACLS guideline), you can see that you have the potential to make a difference. While higher-level airway equipment may not be available, remember that removing foreign bodies and providing simple airway maneuvers is still very useful.


After the first hour with the afflicted passenger, another member of the crew greeted me. This time it was the first officer (or co-pilot of the plane). He thanked me for helping out before hitting me with another question I had not considered.


Do we need to divert the plane or should we carry on to the destination


Again, as you could imagine I was puzzled by how to respond to this question. In hindsight, this is where the value of a high-quality assessment comes into play. Effectively this is mid-air triage. I did another set of vitals and discussed this proposition with the patient who had requested that we continue to the final destination for reasons that were well substantiated. At this point, I felt comfortable that the additional 2 hours was manageable and confirmed with the officer that we could continue.

This area is a little tricky, and to be completely honest there isn’t a good ‘one size fits all’ answer on how to approach these questions. I mention this because I think it’s worth keeping in the back of your mind if you have to perform this type of assessment. Even in comparison to some of the decisions I make daily, the decision to divert hundreds of people to land in an unexpected country weighed on my mind (with no real consideration to the cost of diverting an airplane of that size – vaguely discussed on the web as fitting between $65,000-$100,000). However, in making these decisions it’s worth remembering why you responded in the first place – for the benefit of the patient. If at any point you are worried that this patient will have a worse outcome if they have to wait for the final destination, this should be clearly communicated to the flight crew.

Curiously, after four hours of continuously observing this patient in the back of the plane, I was introduced to a professedly well-regarded doctor who seemed quite concerned he had not been involved in this scenario from the start. While I was initially taken aback by his blunt address, I explained that I too was curious as to why I was left with this patient when there was potentially a more qualified provider only meters away from me the entire time. I think the communication associated with this scenario was limiting in that once any provider was located (i.e. Me – Emergency Nurse with mild to moderate level of experience), the appeal for assistance ceased. In future, I would make a point of asking the cabin staff to continue asking for medical assistance if I was the sole provider responding to an in-flight emergency.

One thing that I was not previously aware of but I think is essential for all responders to know about is the availability of ‘MedLink’ – a telecommunication-based advisory link to an emergency physician provided by a company called MedAire. While MedLink is available in aircraft from a wide variety of providers around the world, it is worth asking if this service or something like it is available if you find yourself in such a situation. In future, this would be among my first questions.

The quote below is from MedAire’s own website and I think it summarizes the service nicely:


Medical volunteers can assist the MedAire physician with gathering vital signs and administering any medications or treatment recommendations. Volunteers can rely on the immediate knowledge MedAire physicians have on the medical equipment available on the aircraft, medications available, and their location within the medical kit. If no medical volunteer is present, MedAire can confidently provide instruction to crewmembers



A paper published in the New England Journal of Medicine in 2015 reported that a medical emergency took place once for every 604 flights. This equates to 16 emergencies per million passengers or 44,000 cases each year around the globe. The NEJM article reported that this figure was likely underestimated as the data was collected by a telemedicine call center (like MedLink) who were probably not consulted for minor mishaps.

The moral of the story is that while these events are not THAT common, they are common enough for us to think about them. Moreover, in our current climate where people and living longer and subsequently living sicker it would be fair to assume that this number has the potential to increase in the coming years.



In NSW, part 8 of the Civil Liability Act (2002, No 22) outlines the legal standing of ‘Good Samaritans’. The general idea of the ‘Good Samaritan’ Act is that a person who comes to the assistance of someone who is injured or at risk of being injured will not incur civil liability for acts or omissions made in an emergency situation if they are acting in ‘good faith’. To loosely paraphrase, if you have relevant skills in an emergency situation and you attempt to provide assistance to ensure the well-being of another person you are protected from lawsuits to a degree if your intention is to help and not harm.

Limitations and variations of this legislation exist in most parts of the world and often the variation of the law that is invoked stems from the region in which the aircraft is registered. For this reason, I would suggest checking your local legislation. In NSW, ‘Good Samaritans’ are also expected to assist ‘in good faith and without expectation of payment or reward’ – this seems obvious but if you are rendering assistance in ‘good faith’ you shouldn’t expect to be compensated for your service.

Also, this act does not remove liability from people who act against the best interest of the patient, performing actions that cause intentional harm or are intentionally negligent. Additionally, errors made while functioning under the influence of drugs or alcohol are not granted an exemption under this act.

Please remember that this is purely one nurse’s interpretation of the NSW legislation in conjunction with a review of the related literature. I don’t profess to have any formal legal training, I am just trying to be armed with as much knowledge as possible.

For a far more in-depth analysis of the ins and outs of Good Samaritan legislation I highly recommend having a look at Dr. Michael Eburn’s page. He is a Barrister (not a Barista) and his page hosts a smorgasbord of legal questions relating to emergency situations as answered by a pro (if you’re into that sort of thing). The link below will take you to a great description of how your individual ‘scope of practice’ is considered when applying the Good Samaritan principle.




The whole NSW Act can be found by following the link below. This links directly to the Good Samaritan section and is a very quick read.




My Tips

Know your rights and responsibilities – Understand your own scope of practice and the legislation surrounding emergency aid.

Introduce yourself – To the crew, state your qualification. Introduce yourself to the patient, use an interpreter as necessary and always ask for permission before performing an assessment or intervention.

Know your environment – Ask what resources you have available i.e. Medical packs, defibrillators, oxygen etc.

Know how to call for help – Ask cabin staff about MedLink or any other medical correspondence service that may be available. As a sole nurse responder ensure cabin staff continues to look for medical practitioners willing to help if they are available (due to their wider autonomous scope of practice).

Know your role – Provide high-quality first aid within your scope of practice. This will vary from practitioner to practitioner but as a rule, general first aid principles including patient positioning, injury management, and even basic life support measures are reasonable to attend if you are qualified provider and the patient requires these interventions. Do not perform treatments you are not qualified to provide or would not provide in your daily practice.

Avoid working outside of your scope of practice – While it is tempting to function with the level of autonomy that you work with in your acute care setting, it is important to remember that the standing orders and medical support we rely on for backup is not available in the majority of these cases. Performing good quality assessment and first aid can make a great deal of difference for an unwell patient.

Worst Case Scenario – In the case of a cardiac arrest on an airplane, remember that good quality CPR and timely defibrillation are by far the most meaningful interventions you can provide. Don’t get caught up in the things you don’t have and make the most of the things you do.

Document – It is always a good idea to keep a record of your encounter for your own records in case you are asked about your treatment at a later date.


Further Reading


The articles found at the links above provide further interesting perspectives into the logistics and principles surrounding medical emergencies on commercial aircraft. While covering similar principles I think they are worth a read if this subject peaks your interest. As is the NEJM article listed below.



Vable, J., Tupe, C., Gehle, B. & Brady, W. (2015). In-flight medical emergencies during commercial travel. NEJM. 373: 939-945.

Best Blogs

With the Internet being so content saturated it’s often tricky to find the things that matter to you. In the context of emergency nursing there are a ton of great sites that help curate content that is both meaningful and entertaining.

Through my endless late night nerd sessions I have developed a few favorite sites that I think are worth a look if you want to stay up to date or gain an insight into the cutting edge resus theories and techniques that are emerging from around the world.

https://thenursepath.blog – A beautifully curated blog created by an experienced emergency nurse, for all nurses. Lots of helpful insights and practical philosophies. A very pure nursing resource.

https://lifeinthefastlane.com – One of the original free open access medical education resources. This blog has miles of useful information specific to the critical care world. It also has one of the most accessible and comprehensive ECG resources I have found anywhere.

http://dontforgetthebubbles.com – A great paediatric page with digestible bites of knowledge and a very useful selection of paeds specific resources i.e. age appropriate ECG morphology charts & x-ray interpretation resources.

https://www.smacc.net.au – The social media and critical care conference page provides details related to the big daddy of contemporary crit care conferences. There is an indispensable selection of videos on their page covering all of the talks given at previous SMACC conferences. Effectively the TED talks of critical care.

http://injectableorange.com – Another very nicely put together nursing focused site with a slightly heavier focus on critical care concepts. Home to a number of excellent resources on mechanical ventilation and managing the critically ill patient.

http://ragepodcast.com – The home page for a great podcast hosted by a group of critical care doctors focusing on the provision of high-level evidence-based resuscitation.

http://intensiveblog.com – lots of useful information relating to the intensive care setting from the team at the Alfred ICU. This site also has a lot of interesting example cases and images to get you thinking.

http://stemlynsblog.org – A great emergency and crit care blog with information and updates that are current and well written. St Emlyns also has a number of novel associated projects including a virtual hospital populated with various teaching cases.

https://emcrit.org – Scott Weingart publishes an excellent blog that digs deep into the clinical concepts that matter when caring for critically ill patients. Scott is an excellent speaker and his podcasts are engaging for clinicians with varying levels of experience.

https://www.aliem.com – An awesome resource providing insight into both the clinical and non-clinical sides of emergency medicine. The ‘Academic life in emergency medicine’ page contains valuable information about teamwork, communication and self-preservation in a challenging environment – as well as the obligatory clinical pearls.

http://www.tamingthesru.com – An interesting blog containing clinical insights from a resus unit in US. Regular ‘grand rounds’ segments dissect clinical cases and apply best practice info in context making it particularly easy to digest.

http://blog.clinicalmonster.com – This resident authored from King’s County emergency department has a lot a great emergency management insights as well as a link to a number of interesting ED lectures the hospital has made available on YouTube.

https://hqmeded-ecg.blogspot.com.au – The best ECG site available. Dr Smith’s blog contains a myriad of weird and wonderful ECGs with associated cases to help you become more in touch with this widely used and commonly misunderstood investigation.

http://rebelem.com – A frequently updated site containing excellent reviews of critical care literature covering a wide range of topics.

This is only a tiny sample of the high-quality resources that can be found all over the web. If there are blogs you love that I have left out I would love to hear about them in the comments.






If you’re reading this it means the WordPress ad was correct and I now have a blog.

Primarily the purpose of this page will be for me to share the cognitive ‘bleeps’ and ‘bloops’ that come into and out of my head in my daily practice.

Currently, that practice takes place in a busy Australian Emergency Department. Through my time in ED, I have developed a keen interest in practical critical care and the pragmatic application of the various principles related to the care of sick patients.

While many high-quality resources can be found around the web relating to resuscitation from a medical point-of-view, this blog will have a decidedly ‘Nursecentric’ twist.

This Blog will in no way try to reinvent the wheel; instead, my posts will aim to communicate my thoughts on things that matter to me. All opinions expressed in this blog are mine alone unless they are explicitly attributed to someone else with a bigger brain.

In the weeks, months and years to come, I hope this can become a place where we can challenge and learn from one another in the spirit of becoming more capable and passionate as resuscitation nurses.

Welcome to my resus scrapbook.