Resus https://www.resus.com.au Emergency Medicine Thu, 18 Jul 2019 03:19:12 +0000 en-US hourly 1 https://wordpress.org/?v=5.2.2 https://www.resus.com.au/wp-content/uploads/2019/03/cropped-favicon-32x32.png Resus https://www.resus.com.au 32 32 Emergency Medicine Resus Emergency Medicine Resus https://www.resus.com.au/wp-content/plugins/powerpress/rss_default.jpg https://www.resus.com.au Resuscitation:The Outer limits https://www.resus.com.au/resuscitationthe-outer-limits/ Thu, 07 Mar 2019 22:08:47 +0000 https://www.resus.com.au/?p=14014 https://www.resus.com.au/resuscitationthe-outer-limits/#respond https://www.resus.com.au/resuscitationthe-outer-limits/feed/ 0 <p>Resuscitation is reaching new limits, with new techniques and technologies giving results that we never thought possible. In Lazarus-like fashion, patients that a few years ago, would have been pronounced deceased, are now leaving hospital to resume their lives, with their families and their work and with very little, if any, deficit. About 8 years…</p> <p>The post <a rel="nofollow" href="https://www.resus.com.au/resuscitationthe-outer-limits/">Resuscitation:The Outer limits</a> appeared first on <a rel="nofollow" href="https://www.resus.com.au">Resus</a>.</p> Resuscitation is reaching new limits, with new techniques and technologies giving results that we never thought possible. In Lazarus-like fashion, patients that a few years ago, would have been pronounced deceased, are now leaving hospital to resume their lives, with their families and their work and with very little, if any, deficit.

About 8 years ago I spoke about a new paradigm being needed in Resuscitation. We had to think differently. The resuscitation guidelines emerged in the time of black and white television and apart from some fine tuning, have remained effectively the same.

“The evidence isn’t great, but it’s the best evidence we have”,  is the usual quote. I say:

 “It’s time to push the envelope, to reach the limits of our resuscitation capacities!”

We can’t all have ECMO, but we can push the parameters and dare to do those things that may a difference to our patients’ lives.

This year at EMCORE (Hong Kong, Melbourne and Fiji), I’m talking about: “The Outer Limits of Resuscitation”

Here’s what I mean:

  1. Why aren’t we using apnoeic oxygenation during cardiac arrest?  The theory of a negative pressure gradient oxygenating the apnoeic patient, can surely be applied here. I’m not saying don’t bag valve mask the patient. I’m saying augment that!
  2. The long standing don’t shock systole stance of the guidelines should be revisited.When initially introduced, it was based on poor studies, some of which were paediatric, where DC shocks don’t work, as the cause of arrest is respiratory, rather than cardiac. Of course these studies showed no benefit. This was a different population group! There has always been the fear of cardiac damage caused by shocking the asystole patient. Something that borders on absurdity.”You can’t kill dead!” This becomes very important when we know that a portion of asystole patients actually have coordinated cardiac activity on echo. I’ll go through some cases.
  3. What about PEA?We know that a significant number of these patients have coordinated cardiac motion. What about the use of H’s and T’s? Surely there’s a better way. There is!
  4. Let’s monitor the blood pressure…invasively.What’s measured can be altered. Let’s treat the blood pressure with increments of adrenaline, not buckets of it. I talk about the after-load effects as well as the effects in the stages of arrest. There is both the best dosing and the best timing for adrenaline.

Peter Kas

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Resuscitation is reaching new limits, with new techniques and technologies giving results that we never thought possible. In Lazarus-like fashion, patients that a few years ago, would have been pronounced deceased, Resuscitation is reaching new limits, with new techniques and technologies giving results that we never thought possible. In Lazarus-like fashion, patients that a few years ago, would have been pronounced deceased, are now leaving hospital to resume their lives, with their families and their work and with very little, if any, deficit. About 8 years… Resus
Should We Shock Patients in Asystole? https://www.resus.com.au/shock-patients-asystole/ Tue, 21 Aug 2018 07:11:54 +0000 https://www.resus.com.au/?p=13790 https://www.resus.com.au/shock-patients-asystole/#comments https://www.resus.com.au/shock-patients-asystole/feed/ 4 <p>Should cardiac arrest patients in asystole be shocked? Is there any advantage to this? What do we know about asystole in cardiac arrest? Patients in asystole are known to have a very poor prognosis, with 0% to 2% surviving to hospital discharge. There is a slightly better prognosis if the rhythm converts spontaneously to a shockable rhythm…</p> <p>The post <a rel="nofollow" href="https://www.resus.com.au/shock-patients-asystole/">Should We Shock Patients in Asystole?</a> appeared first on <a rel="nofollow" href="https://www.resus.com.au">Resus</a>.</p> Should cardiac arrest patients in asystole be shocked? Is there any advantage to this?

What do we know about asystole in cardiac arrest?

Patients in asystole are known to have a very poor prognosis, with 0% to 2% surviving to hospital discharge. There is a slightly better prognosis if the rhythm converts spontaneously to a shockable rhythm early(1).

The Advanced Life Support guidelines do not recommend defibrillation in asystole. They consider shocks to confer no benefit, and go further claiming that they can cause cardiac damage; something not really founder in the evidence.

So why am I writing about this?

…..because not all asystole is true asystole. We know that false asystole can appear on our monitors and occur secondary to technical error() and that the measured amplitude, is altered by several factors including; recording conditions, movement artefact, body habits and recording devices.(3)

The above video comes from one of many case studies where the patient is in asystole, however the echo demonstrates fibrillation(4).

The FEEL Study(5) demonstrated that 38% of patients with an ECG diagnosis of asystole had coordinated cardiac motion and 58% of patients in PEA had coordinated cardiac motion.

Multiple case studies show that patients in asystole receiving shocks return to an organised rhythm, implying that they were probably in ventricular fibrillation.(6,7,8,9)

One study showed(10), that an initial defibrillatory countershock resulted in 8.4% of patients with asystole developing QRS complexes, indicating that they were in ventricular fibrillation.

Where is the evidence for the guidelines’ push for NO SHOCK in Asystole? 

In 1992 the American Heart Association stated that delivering shocks in asystole was considered dangerous (11). There was a strong concern that delivering shocks could result in parasympathetic storm(12,13). Evidence is lacking in respect to an approach to asystole, as it is in most of the resuscitation-related guidelines. Two studies are cited in the guidelines as evidence of the poor survival from shocking asystole(14,15). One is a paediatric study, which is really not applicable in the adult population as the rate of ventricular fibrillation is very different in the two groups. The second found that patients with asystole did better with no shocks delivered.

The 2015 European Resuscitation Guidelines advise that in cases of asystole, that the rhythm be checked for P waves, as these may respond to cardiac pacing. They advise against defibrillation if there is doubt as to the rhythm being asystole, or extremely fine VF. The recommendation is to continue chest compressions and ventilation, with the aim of improving the amplitude and frequency of the VF and thus the chance of a successful defibrillation(16,17,18). However the guidelines have stayed firm on no shock in asystole(19)

What do we know?

  1. We know that most adults in cardiac arrest(76%), have ventricular fibrillation as their initial rhythm and this can deteriorate to asystole(15).
  2. We also know that defibrillation is very effective in those patients with ventricular fibrillation. The average out of hospital cardiac arrest survival rate of 8%,  increases to 20% in those patients with ventricular fibrillation and early defibrillation(20).
  3. We also know that about 8% of patients in the pre-hospital environment, that present in asystole, are actually in ventricular fibrillation and this is the group of patients that may benefit.
  4. For every minute that defibrillation is delayed, the survival drops by 7-10%. This is because as the duration of the cardiac arrest increases the amplitude of the ventricular fibrillation decreases. Thus, the greater the amplitude of VF, the better the outcome, with the best outcome in those patients that have a VF amplitude of > 0.5mV. Those patients with an amplitude of <0.2mV, when shocked developed asystole.

Why might we be missing VF and calling it asystole?

Our monitors simply don’t pick it up. The defibrillators we use are usually set to read one lead only, with no capacity to scan the leads and we are not seeing all possible leads. We may not increasing the amplitude in the asystole patient, which might assist us in seeing low amplitude VF.

We may also not be using cardiac echo enough in arrests. It can show  fibrillation even when the monitor reads asystole.

Will it make a difference?

All studies done show that defibrillation of VF in the first 4 minutes make a significant difference. After this time, it may be that we are fighting an uphill battle. The evidence is not great. In a study by Steil(21) in out of hospital cardiac arrest, defibrillation made little difference to survival if too delayed.

I am not saying that all asystole should be shocked, with a hope of a return to an organised rhythm.

What I am saying is that not all asystole is the same. Some patients are not in this rhythm and may benefit from defibrillation, if we can identify them.

What could we be doing?

My own view is:

  • Commence CPR, this perfuses the myocardium and can increase the amplitude of VF if it is present, improving the chances of a successful cardioversion. One cycle is adequate.
  • Increase the amplitude reading on the cardiac monitor(defibrillator), to pick up fine VF
  • During the rhythm check phase, scan the leads for any signs of ventricular fibrillation- you have about 5-7 seconds (in some difibrillators, this can be achieved by disabling the VF/VT alarms)
  • Simultaneously perform a cardiac echo looking for fibrillation or coordinated cardiac motion.You have about 5-7 seconds. It is better to record this, so it can be viewed away from the arrest.
  • Start CPR Immediately after this.
  • If there is ventricular fibrillation and you believe you have maximised perfusion, deliver a shock. One shock, to see if there is any return of an organised rhythm. if nothing, I would not continue shocking.

What if you are in a situation where you can’t echo or change leads. Can you just deliver a shock? My answer is definitely yes. Deliver a shock, one shock and deliver it early. If it is unseuccessful, no further shocks need be given.

We can’t really cause harm by doing this. These patients have no chance of survival if we do nothing. They are effectively deceased by all measures. The survival is poor even if we do. However it is an approach we must consider, especially in the early stages ie., out of hospital cardiac arrest by first responders, or in hospital cardiac arrest.

WATCH THE 60 SECOND SYNOPSIS                 

A/Prof Peter Kas – I will be speaking on this topic in detail at EMCORE Byron Bay 2019

References

  1. Luo S, Zhang Y, Zhang W, et al. Prognostic significance of spontaneous shockable rhythm conversion in adult out-of-hospital cardiac arrest patients with initial non-shockable heart rhythms: A systematic review and meta-analysis. Resuscitation 2017; 121:1.
  2. Cummins RO, Austin Jr D. The frequency of ‘occult’ VF masquerading as a flat line in prehospital cardiac arrest. Ann Emerg Med 1988;17:813-7
  3. Callaway CW, Menegazzi JJ. Waveform analysis of ventricular fibrillation to predict defibrillation. Currently Open Crit Care 2005 Jun;11(3):192-9.
  4. Limb C, Siddiqui M.A. Apparent Asystole: are we missing a lifesaving opportunity? BMJ Case Rep. 2015 Mar 16. PMID: 25777487
  5. Brown DC, Lewis AJ, Criley JM. Asystole and its treatment: the possible role of the parasympathetic nervous system in cardiac arrest. JACEP 1979;8:448-52.
  6. J.P. Ornato, E.R. Gonzales, A.R. Morkunas, M.R. Coyne, C.L. Beck Treatment of presumed asystole during pre-hospital cardiac arrest: superiority of electrical countershock. Am J Emerg Med, 3 (5) (1985), pp. 395-399
  7. Amaya SC, Langsam A: Ultrasound detection of ventricular fibrillation disguised as asystole. Ann Emerg Med March 1999;33:344-346.
  8. Ewy GA, Dahl CF, Zimmerman M, et al: Ventricular fibrillation masquerading as ventricular standstill. Crit Care Med 1981;9:841-844.
  9. McDonald JL: Coarse ventricular fibrillation presenting as asystole or very low amplitude ventricular fibrillation. Crit Care Med 1982;10:790-792.
  10. Thompson BM, Brooks RC, Pionkowski RS et al. ‘Immediate countershock treatment of asystole’. Ann Emerg Med 1984;9:827–9
  11. Emergency Cardiac Care Committee and Subcommittees, American Heart Association: Guidelines for cardiopulmonary resuscitation and emergency cardiac care, part III: Adult advanced cardiac life support. JAMA 1992;268:2199-2241.
  12. Brown DC, Lewis AJ, Criley JM. Asystole and its treatment: the possible role of the parasympathetic nervous system in cardiac arrest. JACEP 1979;8:448-52.
  13. Vassalle M. On the mechanisms underlying cardiac standstill: factors determining success or failure of escape pacemakers in the heart. J Am Coll Cardiol 1985;5:35B-42B.
  14. J.D. Losek, H. Hennes, P.W. Glaeser, D.S. Smith, G. Hendley Prehospital countershock treatment of pediatric asystole. Am J Emerg Med, 7 (6) (1989), pp. 571-575
  15. Martin DR, Gavin T, Bianco J, Brown CG, Stueven H, Pepe PE, et al.Initial countershock in the treatment of asystole. Resuscitation 1993;26:63-8.
  16. Berg RA, Hilwig RW, Kern KB, Ewy GA. Precountershock cardiopul- monary resuscitation improves ventricular fibrillation median frequency and myocardial readiness for successful defibrillation from prolonged ventri- cular fibrillation: a randomized, controlled swine study. Ann Emerg Med 2002;40:563–70.
  17. Eftestol T, Sunde K, Aase SO, Husoy JH, Steen PA. “Probability of successful defi- brillation” as a monitor during CPR in out-of-hospital cardiac arrested patients. Resuscitation 2001;48:245–54.
  18. Kolarova J, Ayoub IM, Yi Z, Gazmuri RJ. Optimal timing for electrical defi- brillation after prolonged untreated ventricular fibrillation. Crit Care Med 2003;31:2022–8.
  19. Stewart JA. The prohibition on shocking apparent asystole: A history and critique of the argument. AJEM 2008, 26.618-622.
  20. McNally R, Vellano Al V, Pw Y, C S, A C, et al. Out-of-hospital cardiac arrest surveillance—Cardiac Arrest Registry to Enhance Survival (CARES), United States, October 1, 2005—December 31, 2010. Morb Mortal Wkly Rep Surveill Summ Wash DC 2002. 2011;60: 1–19.
  21. Steil et al Advanced Cardiac life support in out of hospital cardiac arrest August 12, 2004N Engl J Med 2004; 351:647-656

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Should cardiac arrest patients in asystole be shocked? Is there any advantage to this? What do we know about asystole in cardiac arrest? Patients in asystole are known to have a very poor prognosis, with 0% to 2% surviving to hospital discharge. Should cardiac arrest patients in asystole be shocked? Is there any advantage to this? What do we know about asystole in cardiac arrest? Patients in asystole are known to have a very poor prognosis, with 0% to 2% surviving to hospital discharge. There is a slightly better prognosis if the rhythm converts spontaneously to a shockable rhythm… Resus
Pericardiocentesis https://www.resus.com.au/pericardiocentesis/ Wed, 20 Jun 2018 01:07:10 +0000 https://www.resus.com.au/?p=13653 https://www.resus.com.au/pericardiocentesis/#comments https://www.resus.com.au/pericardiocentesis/feed/ 2 <p>How to Perform Pericardiocentesis Pericardiocentesis is used to treat symptomatic pericardial effusions and cardiac tamponade. It was first described in the 1650’s and since the introduction of the subxiphoid approach in 1911, has been used very successfully, with significant reduction in morbidity and mortality. The use of echocardiography and other guidance techniques have reduced the…</p> <p>The post <a rel="nofollow" href="https://www.resus.com.au/pericardiocentesis/">Pericardiocentesis</a> appeared first on <a rel="nofollow" href="https://www.resus.com.au">Resus</a>.</p> How to Perform Pericardiocentesis

Pericardiocentesis is used to treat symptomatic pericardial effusions and cardiac tamponade. It was first described in the 1650’s and since the introduction of the subxiphoid approach in 1911, has been used very successfully, with significant reduction in morbidity and mortality. The use of echocardiography and other guidance techniques have reduced the risks even further.

A CASE WE HAD RECENTLY

An 80 yo male presents with 9/10 central chest pressure. It awoke him in the middle of the night. After several hours he called the ambulance who treated the patient with GTN spray and the pain improved markedly.

PMHx
Pacemaker inserted 2 days ago
Thyroidectomy
Type II Diabetes
Left Inguinal Hernia Repair
TURP 2009

In the emergency department the vitals were:
T 36.9, HR 60, BP 145/75, SaO2 99% on room air, Resp Rate 16.

Pericardial Effusion

Patient ECHO

The patient continued to have chest pain.  He was treated with further sublingual GTN, after which he dropped his blood pressure and required a total of 500mL of Normal Saline to return it to 115mmHg systolic. The blood pressure continued to fall reaching 70mmHg systolic and a Metaraminol Infusion was commenced.

A bedside ECHO revealed a pericardial effusion, which was felt to be responsible for the ongoing hypotension.

This tied in well with the drop in blood pressure, with the use of GTN, given that pericardial effusions usually cause a right ventricular collapse.

The decision was made to perform a pericardiocentesis.

 

Indications for Pericardiocentesis

  • A pericardial effusion causing haemodynamic compromise
  • Symptomatic large effusions not responding to medical treatment.
  • Smaller effusions that are bacterial, tuberculous or neoplastic in origin

Contraindications to Pericardiocentesis

  • There are no real absolute contraindications when the patient is decompensating and in shock
  • Relative contraindications include coagulopathy, thrombocytopaenia and anticoagulant therapy

Techniques Used

There are several techniques available including CT guided and Fluoroscopy guided, however for use in the emergency department the safest and simplest approach is echocardiography-guided.

Different Pericardiocentesis Approaches and Risks

Source: European Society of Cardiology Journals. E-Journal of Cardiology Practice. Volume 15

There are 3 anatomical approaches to needle insertion:

  1. Parasternal: Catheter insertion is at the left 5th intercostal space adjacent(<<1cm) to the sternal margin. This approach carries a risk of pneumothorax, and damage to the internal thoracic vessels.
  2. Apical:Catheter insertion in the 5-7th intercostal space, 1-2 cm lateral to the apex beat. There is an increased risk of pneumothorax and of ventricular puncture.
  3. Subxiphoid(also called paraxiphoid):The catheter is inserted between the xiphisternum and the left costal margin, directed towards the left shoulder. There is a lower risk of pneumothorax, however there is a risk of entering the peritoneal cavity, of puncturing the right atrium and puncturing the left lobe of the liver.

How to Perform a Pericardiocentesis

The video below goes through the procedure performed in this case. The following steps are involved:

  1. Explain to the patient what you are going to so.
  2. Place patient in semi-reclining position with head up about 20 degrees.
  3. Aseptic Technique, use a pericardiocentesis tray.
  4. Paraxiphoid approach is used and the needle is directed towards the opposite shoulder at about 40 degrees to the skin.
  5. The catheter insertion is guided by echocardiography.
  6. When the pericardial space is entered and there is flashback of fluid into the syringe, ‘agitated’ normal saline is injected. This allows confirmation that you are in the right space.
  7. Feed the guidewire as per Seldinger technique and then dilate with the introducer and feed the pigtail catheter over this.
  8. Aspirate blood from the cavity and then allow drainage etc.

A few things to remember:

Pericardial fluid does not clot, but blood does.

The volume of fluid is calculated by the size of the effusion on echo.

  • Normally the pericardial sac can contain up to 50mL of fluid.
  • 5-10 mm: 100-250 mL
  • 10-20 mm: 250-500 mL
  • >20 mm: >500 mL

Watch the 4 minute video below

BACK TO THE CASE

A total of 260mL of fluid was removed and a pigtail catheter was inserted. The Metaraminol infusion was stopped whilst the aspiration was under way. On completion, the blood pressure rose naturally to a normal level.

This is not a procedure we take lightly. However in a situation like this, it was necessary and showing you the way it was done, I think you will agree, it is straightforward, thanks to echocardiography.

Peter Kas

 

 

 

Peter Kas

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How to Perform Pericardiocentesis Pericardiocentesis is used to treat symptomatic pericardial effusions and cardiac tamponade. It was first described in the 1650’s and since the introduction of the subxiphoid approach in 1911, How to Perform Pericardiocentesis Pericardiocentesis is used to treat symptomatic pericardial effusions and cardiac tamponade. It was first described in the 1650’s and since the introduction of the subxiphoid approach in 1911, has been used very successfully, with significant reduction in morbidity and mortality. The use of echocardiography and other guidance techniques have reduced the… Resus
How to Diagnose the Patient with Vertigo in 5 steps https://www.resus.com.au/diagnose-patient-vertigo-5-steps/ Wed, 13 Jun 2018 10:55:51 +0000 https://www.resus.com.au/?p=13622 https://www.resus.com.au/diagnose-patient-vertigo-5-steps/#comments https://www.resus.com.au/diagnose-patient-vertigo-5-steps/feed/ 1 <p>How to Diagnose the Patient with Vertigo in 5 steps This week it’s all about the ‘dizzy’ patient, or that patient with vertigo. I recently spoke at EMCORE Melbourne and went through my step by step approach of sorting, in my mind at least, the potential causes of the ‘dizzy’ patient. Below is a summary…</p> <p>The post <a rel="nofollow" href="https://www.resus.com.au/diagnose-patient-vertigo-5-steps/">How to Diagnose the Patient with Vertigo in 5 steps</a> appeared first on <a rel="nofollow" href="https://www.resus.com.au">Resus</a>.</p> How to Diagnose the Patient with Vertigo in 5 steps

This week it’s all about the ‘dizzy’ patient, or that patient with vertigo.

I recently spoke at EMCORE Melbourne and went through my step by step approach of sorting, in my mind at least, the potential causes of the ‘dizzy’ patient. Below is a summary of those points and a short podcast that goes over all the issues.

An algorithm for diagnosing the patient with vertigo

The Miss Rate of Strokes in the Emergency Department

The miss rate, of patients returning to the Emergency Department, with a diagnosis of stroke, in the first month after discharge, is about 1:500 (Annals Of Emergency Medicine. Vol 57, Issue 1, pp34-41 2011).

When the only complaint is Solitary Vertigo, the misdiagnosis rate is only 0.67% (Stroke 2006, 37:2484-2487) That is a vast improvement and shows that when we get down to solitary vertigo, the diagnosis is easier to make.

We need to remember that 50% of causes of dizziness are medical ie., new medications, arrhythmias GIT bleeds etc., so we need to look for these.

Beware Depending on the CT brain.

A CT brain has a yield of < 2%, in patients presenting with vertigo. We should not be using it to clear patients. The reassurance it gives is false, evidenced by the fact that twice the number of patients that returned to hospital with a diagnosis of stroke, had been investigated with a CT brain and cleared before discharge.

The 5 Step Approach to Diagnosis

STEP 1

Perform a neurological examination, looking for specifics.
A patient with any neurology (except a positive Rhomberg), means a Neurology referral.

  • Is there Nystagmus?
    • Dizziness or vertigo must be present to be able to test for nystagmus.
    • Vertigo and NO nystagmus is of central cause until proven otherwise.
    • Any nystagmus other than simple unilateral horizontal nystagmus, is assumed to be of central origin ie., it is bi-directional, vertical, pendular, see-saw, etc.
  • Perform a test of skew
    • Cover and uncover each eye in turn, whilst asking the patient to look straight ahead. If there is any vertical correction of the eye, when uncovered, it is a positive test and of central cause.
  • Test Cranial nerves III, IV, VI: Is there diplopia?
  • Test the other cranial nerves including V, VII, VIII, IX, X
    • Look for facial numbness and facial paresis
    • This is the time to test cranial nerve VIII and assess the hearing
      • If there is hearing loss and tinnitus, the diagnosis is probably Meniere’s Disease, however beware not to miss acoustic schwannoma. (See step 2 below.)
  • Test dysphonia, dysarthria and dysphasia
  • Look for long tract signs
  • Perform a Cerebellar Examination
  • Test GAIT: Stand the patient. Those patients with a central lesion, have difficulty walking. Those with a peripheral lesion may be able to mobilise by holding onto furniture etc. Whilst the patient begins to sit up in bed look for TRUNCAL ATAXIA. Patients that have this, have great difficulty sitting up. It is of a central cause.

STEP 2

Is there hearing loss? Beware the patient with hearing loss and tinnitus. The most likely diagnosis is Meniere’s Disease, however in a small number of cases it may be an acoustic Schwannoma. In an acoustic Schwannoma beware of the following:

  • If the cochlear nerve is affected, there is the customary hearing loss and tinnitus
  • If the vestibular nerve is affected, the patient may have an unsteady gait. This is usually a broad-based gait.
  • If the trigeminal is affected, the patient may complain of facial numbness, hyperaesthesia or pain
  • If the facial nerve is affected there may be facial paresis.

STEP 3

Is there a headache?
If so, this is a central cause and a neurological referral is needed,  unless there is an associated migraine and we then need to consider Vestibular Migraine as a diagnosis. However there are strict criteria for doing this. These include:

  • Episodic vertigo
  • Familial history
  • Migraine has accompanied more than two episodes
  • The precipitants of vertigo are similar to those of migraines.

If everything in the above two steps is normal, we have now arrived at SOLITARY VERTIGO. Go to step 4

STEP 4

The Dix-Hallpike Manoeuvre
The history is very important here. If the history is brief, sudden and positional, then think of Benign Paroxysmal Positional Vertigo(BPPV). The symptoms are of short duration and tend to occur when the patient moves their head. Keep in mind that cerebellar or brainstem causes that are vascular in origin, may also have a sudden onset.

The Dix Hallpike manoeuvre assists us in diagnosing a peripheral cause of vertigo. It should probably be done following the examination of gait, so that the person is not too distressed to perform gait. There should be direct visualisation of eye movements. Frenzel lenses can be used to assist. If the test is positive, ie., it is reproducible on one side and there is delay of onset of nystagmus and the nystagmus itself decays after a short period, the diagnosis of BPPV can be made. The manoeuvre tests the posterior semicircular canals, which are affected in about 85% of cases. If this is negative consider performing the ‘Supine Roll Test’ described below.

Performing the Dix-Hallpike

  • Explain the procedure.
  • Sit the patient up, such that when they lie down, the patient’s shoulders will be level with the end of the bed and their head can lie below the bed.
  • Turn their head 45 degrees towards the suspected affected side. This is usually the side opposite to the nystagmus.
  • Ask the patient to look directly in front.
  • Support the patients head and neck and rapidly bring the head down, so that it hangs 15-20 degrees below the horizontal.
  • There should be a delay until the onset of nystagmus.
  • If nystagmus occurs, the patient should be kept in this position for up to 2 minutes.
    • Look for nystagmus decay. If there is no decay, the cause of the nystagmus may be central.
    • If nystagmus does occur, repeat the procedure to reproduce the nystagmus after the patient has settled.
  • If there is no nystagmus, carefully and slowly sit the patient back up and prepare to test the opposite side.

If the Dix-Hallpike is negative, perform a Supine Roll Test. This tests the horizontal canals, which are responsible for about 10% of cases of Benign Paroxysmal Positional Vertigo. The head is simply turned from side to side whilst the patient is lying in bed and we note the presence or absence of vertigo and nystagmus.

The presence of vertigo, with no nystagmus, is of central origin, unless proven otherwise.

STEP 5

Perform the Head Impulse test.
This test has been covered before on this blog. It tests the Vestibulo-Ocular Reflex(VOR). Usually the nystagmus occurs, on the opposite side to which the VOR is affected. When the test is positive, it indicates a peripheral lesion.

  • Hold the patients head with both hands
  • Ask the patient to look straight at your nose.
  • Explain to them, that you will move their head from side to side, however they should continue to look straight ahead at your nose.
  • When the head is turned towards the side of the affected VOR, the eyes start to move with the head, for a brief instant. Then there is a rapid saccadic correction back towards the centre. This is a positive test, as shown in the video below and indicates a peripheral lesion.

Head Impulse Test

Putting it all together

Below is my approach to the patient with vertigo:

  1. If there are any positive neurological signs(except a Rhomberg, which may be positive in patients with peripheral balance problems), which include cranial nerves, long tract signs, positive test of skew, the cause is assumed to be central and the patient is referred to neurology
  2. Is there any hearing loss? If so assess the possibility of Meniere’s Disease, however be suspicious of an acoustic schwannoma.
  3. If there is any headache, except what might be a migraine-related headache, this is a neurological referral.
  4. When down to solitary vertigo, consider 3 things:
    1. Benign Paroxysmal Positional Vertigo is of short duration and positional and the Dix-Hallpike manoeuvre is positive
    2. If there is vertigo and no nystagmus, consider this to be central
    3. If there is vertigo and nystagmus and a positive head impulse test, this is of peripheral cause.

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How to Diagnose the Patient with Vertigo in 5 steps This week it’s all about the ‘dizzy’ patient, or that patient with vertigo. I recently spoke at EMCORE Melbourne and went through my step by step approach of sorting, in my mind at least, How to Diagnose the Patient with Vertigo in 5 steps This week it’s all about the ‘dizzy’ patient, or that patient with vertigo. I recently spoke at EMCORE Melbourne and went through my step by step approach of sorting, in my mind at least, the potential causes of the ‘dizzy’ patient. Below is a summary… Resus
How to Read the ECG https://www.resus.com.au/how-to-read-the-ecg/ Mon, 15 Aug 2016 10:20:36 +0000 https://sites.ckpcreative.com.au/resus/?p=17979 https://www.resus.com.au/how-to-read-the-ecg/#respond https://www.resus.com.au/how-to-read-the-ecg/feed/ 0 <p>Reading the ECG, is one of the most important skills in Medicine. We are expected to read them expertly and read them quickly. In most cases we have about 20 seconds to recognise that an ECG isn’t normal. That’s why I came up with my own system: “The ECG in 20 Seconds”, because that’s really…</p> <p>The post <a rel="nofollow" href="https://www.resus.com.au/how-to-read-the-ecg/">How to Read the ECG</a> appeared first on <a rel="nofollow" href="https://www.resus.com.au">Resus</a>.</p>

Reading the ECG, is one of the most important skills in Medicine. We are expected to read them expertly and read them quickly. In most cases we have about 20 seconds to recognise that an ECG isn’t normal. That’s why I came up with my own system: “The ECG in 20 Seconds”, because that’s really all the time we have to recognise abnormality. Now if it is abnormal, then certainly, we can spend more time reviewing it. However, if we don’t pick up the potential issues, it can be disastrous. I share the elements the system on several blogs that I’ll link below.  Reading ECG’s will be straightforward if you follow a formula.

This PODCAST shares the formula I use to read ECG’s with you.


Let’s start with the basic questions:

  1. Is it ischaemia or arrhythmia
    1. This is about the history. If the patient presents with palpitations or syncope, then an arrhythmia may be more likely
    2. If the patient has chest pain, you may look more closely at the arterial territories of the leads and the ST segments.
  2. What is the rate? If its tachycardia, is it wide or narrow complex? If its bradycardia is it a junctional or a block? Are there more P’s than QRS’s: if so look for the Mobitz.
    1. Being able to know if the rhythm is sinus, is the first step.
    2. Knowing how to pick up Blocks is important, whether these are Mobitz, or triphasicular .
  3. What are the QRS complexes doing? Are they tall/small/wide/narrow and do they have abnormal morphology, or are they clumped?
    1. Is this a wide complex rhythm? Do you have differentials for a wide complex?
    2. Is there hypertrophy?
    3. Is there WPW?
  4. What are the ST-T segments doing? What is there morphology?
    1. Is it ischaemia?
    2. Is it pericarditis?
    3. Hyper/Hypokalaemia?
    4. Is it Wellen’s, Brugada’s
    5. Are there de-Winter’s T waves?
  5. What are the intervals doing? PR and QT?
    1. Prolonged PR on its own may not mean much, but with a left axis and right bundle branch block, may explain why the patient suffered syncope.
    2. PR depression may also be meaningful in the presence of other changes, signifying pericarditis.
    3. A QT interval that is too long or even short, can predispose to arrhythmias
  6. Are there pacing spikes?
    1. It’s important to look closely in all leads
    2. It may be a malfunctioning pacemaker causing the problem.

That’s it. Now listen to the podcast and then read some of these links. Share them.

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Reading the ECG, is one of the most important skills in Medicine. We are expected to read them expertly and read them quickly. In most cases we have about 20 seconds to recognise that an ECG isn’t normal. That’s why I came up with my own system: “The E... Reading the ECG, is one of the most important skills in Medicine. We are expected to read them expertly and read them quickly. In most cases we have about 20 seconds to recognise that an ECG isn’t normal. That’s why I came up with my own system: “The ECG in 20 Seconds”, because that’s really… Resus
Non-Invasive Ventilation https://www.resus.com.au/non-invasive-ventilation/ Thu, 11 Feb 2016 03:16:04 +0000 http://www.resus.com.au/?p=7536 https://www.resus.com.au/non-invasive-ventilation/#respond https://www.resus.com.au/non-invasive-ventilation/feed/ 0 <p>Introduction If find myself reaching more and more for the non-invasive ventilation, in the COPD patient. I’ve always loved it for acute pulmonary oedema. However, there is something about assisting the patient’s work of breathing, that allows me to ‘titrate’ what I give. A Case The ambulance bring a patient in on a rebreather. She…</p> <p>The post <a rel="nofollow" href="https://www.resus.com.au/non-invasive-ventilation/">Non-Invasive Ventilation</a> appeared first on <a rel="nofollow" href="https://www.resus.com.au">Resus</a>.</p> Introduction

If find myself reaching more and more for the non-invasive ventilation, in the COPD patient. I’ve always loved it for acute pulmonary oedema. However, there is something about assisting the patient’s work of breathing, that allows me to ‘titrate’ what I give.

A Case

The ambulance bring a patient in on a rebreather. She is elderly and has been unwell for the last few days.

Her respiratory rate is 32, heart rate is 125 and sats are 90%. She is afebrile and examination is normal apart for a few creeps in both bases.

A set of gases reveals the following:

pH 7.3
PaO2 63
PaCO2 37
HCO3 20
SaO2 90%

Does she meet Criteria for Non-Invasive Ventilation? Yes she does?

What type of Non-Invasive Ventilation would you use; CPAP or BiPAP?

What type of NonInvasive Ventilation would you use for:
(A) Acute Pulmonary Oedema?
(b) COPD?
(c) Asthma?
…. and why   … all answers in the 9 minute video below:

You place the patient on BiPAP (settings EPAP 6 / IPAP 11) and wean down to 50% and the patients gases improve markedly:

paO2 137
paCO2 39

The patients respiratory rate is still high at 28 breaths  per minute.
What setting would you change on the machine to assist the patient? This is all about work of breathing, so increase the IPAP, whist keeping EPAP constant.

Answers in the 9 minute video below as well as an explanation of how Non-Invasive Ventilation works. (If the video doesn’t play, just click this link)

 

<iframe src=”https://player.vimeo.com/video/154941178″ width=”640″ height=”400″ frameborder=”0″ webkitallowfullscreen mozallowfullscreen allowfullscreen></iframe>

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Introduction If find myself reaching more and more for the non-invasive ventilation, in the COPD patient. I’ve always loved it for acute pulmonary oedema. However, there is something about assisting the patient’s work of breathing, Introduction If find myself reaching more and more for the non-invasive ventilation, in the COPD patient. I’ve always loved it for acute pulmonary oedema. However, there is something about assisting the patient’s work of breathing, that allows me to ‘titrate’ what I give. A Case The ambulance bring a patient in on a rebreather. She… Resus