als_medic_uk

Etomidate is a good sedative for RSI; it is advisable but not a necessity to give a preventative dose of hydrocortisone, as Etomidate as a long term sedative (ICU) can increase mortality rates due to the suppression of steroid production. However, there is no evidence that a single dose can cause this suppression. It is not used in the critical care environment, only in the emergency care scenario. So with its short half life and relatively low LD50 comparison it is an effective RSI sedative. Regards.

Neither of those links you included mentioned an abnormally high mortality rate when using inhaled furosemide at 2mg/Kg. I was curious as to where that data was obtained certainly not the BPJ. May I point out there is a difference between relieving the feeling of the issue at cause and alternating the physiology. I merely stated what has been shown in numerous research examples. That when inhaled, a COPD patient may show relief from the feeling of dyspnoea. It also improves bronchodilation which in turn is beneficial to the patient. Maybe it isn’t a convenient pre-hospital medication; however, the context was regarding the treatment of COPD with Furosemide. As for the use of spirometry, in a patient with dyspnoea, I find that not only futile but also bizarrely interdictory to the patient’s well-being. I understand your issues, but I think your data, and medical knowledge is rather fundamental when it comes to the mechanisms of drugs, not being derogatory. Regards.

The use of a diuretic in COPD patients is not all that uncommon. If the patient were to have taken furosemide by direct inhalation that may have proved beneficial by alleviating the feeling of dyspnoea, there is also considerable bronchodilation post inhalation. Sometimes COPD can be mistaken for CHF symptomatically. Regards

Ventilation is maintained throughout the intubation sequence by means of using a cuffed oropharyngeal airway. Reagrds

That sounds like a P wave with a PR interval prolongation, if you think of a junction being blocked [a short escape interval] then the next junction or conducted P wave would be shorter due to the block in the escaping QRS complex, and in turn a shorter PR interval. Ending up with two P waves, at the “R” junction blockage. Reagrds

Paroxysmal supraventricular tachycardia, [with Atrial flutter; if you check the pulse you will find that it is slower than the ECG reading because not all of the electrical impulses become contractions in the ventricles]. It sounds like atrioventricular nodal reentrant supraventricular tachycardia and that would cause the internal defibrillator to go off, as this tends to stop and start, it is the palpitations that are uncomfortable. You can correct the arrhythmia by using a vagus nerve stimulation maneuver [does'nt always work]. The pharmacon of choice would be adenosine or verapamil. But remember this person is already undergoing cardioversion, not of choice. Digoxin or propafenone would be amognst many long term antiarrhythmic drug treatments. Regards.

The morphology of the ECG of Wolff-Parkinson-White [WPW] syndrome may vary from a classic presentation to near normal, one can not be addiment that a specific factor must be presented when viewing a WPW ECG print out. You would normally see a widened QRS interval, but again it can vary substantially, the morphology of the ECG of WPW depends on the level of preexcitation, you can have a normal QRS interval with a shortened PR interval. What helps more is the dysrhythmia, which can be much more indicative especially if CMT. It is the dysrhythmia that can kill, and hence how it is normally discovered, you can have normal ECG [in a sense] with CMT or A-Fib, which in turns calls for further investigative tools. And the dysrhythmia is treated with Adenosine or Procainamide. There are other clinical findings that are usually present with WPW sufferers, which include tachycardia, palpitations, dizziness, hypotension and PVC made be heard when examining the lungs. One can not rely on ECG readings for complete diagnosis, and often many 'off-shot' ECG readings are misinterpreted, one must also view the most important factors; clinical history and presenting symptoms (if symptomatic). Regards.

I don't know many web sites [generally don't trust - unless electronic Journals], but there are many books from the basic care provider to the advanced. If you browse amazon, for ECG for the beginner or the Basics of 12 Lead ECG, then I am sure you will find many. I do know that McGraw-Hill have some very interesting and relatively board based electronic books, available on their web site, however, I am unaware if there are any specific ECG books. Regards

It depends if the patient has been diagnosed with recurrent atrial fibrillation, and therefore paroxysmal or persistent. Paroxysmal atrial fibrillation, is whereby the abnormal rhythm will last for short periods [max. 1 week] and maybe become benign for a certain period, in this benign phase then the patient will have with normal sinus rhythm, after this period the atrial fibrillation will reappear again for short periods. Persistent atrial fibrillation, as it says, will last for long periods [min. 1 week], and the patient may never have a normal sinus rhythm, unless medicated, as yours is. You should also consider Lone Atrial Fibrillation. you where referring to a scenario whereby the patient was taking a cardiac glucoside, you will see NO change in the arrythmia, the AV flutter will still be present, you cannot rid it [we are talking persistent AF here] what the drug will do is increase the force of contraction, not alter the arrythmia. If the patient suffers paroxysmal AF and in sinus rhythm then a cardiac glucoside would not be used, so that scenario is out of the window [sorry pun]. So no the AF does not disappear, but the contraction improves. Regards hope that helps

The caps are a little off putting, but there is nothing wrong with spelling mistakes, some people are dyslexic, nothing they can do! Spelling does not justify your competence. Regards.

Mature patients may be more sensitive to the anticholinergic properties of the medicine; however, I do expect that 25 mg would be perfectly acceptable, although if the patient has had previous reactions/effects to the drug, them a lower dosage ought to be used, along the lines of paediatric administration. Nalbuphine has been discontinued since 2003 in the UK, due to its associated sex references [regarding pain]. Regards.

If you are robust, and your control is good, then your risk from having a tattoo is the same, as for anyone else. Which are the risks of infection, at the location of the injections, the pain of the process, and the nuisance related with removal of the tattoo if you get fed up with it. I do, however, see no need, in having a tattoo when a bracelet is good enough. Regards

So I gather this person was an alcoholic, although no-one mentioned the odour of alcohol, never the less, one has to realise that many as people grow older [a large percent of the population] we have to change in order to prepare, we don't want manifestations, we want understanding. Many people, have a care-less attitude when it comes to the elderly, especially the mentally impaired elderly, these people require individual care, otherwise you end up with a patient like the one described. These patients, need a care assistant to come 2-4 times a day, with this in act, the level of need/stress on the EMS structure will be reduced. People are left to rot, literally, with more and more cases ever so more present. As for Korsakoff's syndrome, as someone mentioned, what gave you that diagnosis?, deficiency of thiamine, and encephalopathy rolled in one, lol, you must have just read your neuropathology book, and there is/was a contradiction. Regards.

The mortality rate of a ruptured Aorta is very high around 50% will die, you want to keep them sat, as the main 'stand point' in emergency care is reduce the BP and heart rate [usually using BP lowering drugs] and either a beta blocker or verapamil to slow the pulse and make the heart beat with less strength. Ideally feet over the side of the bed/ gurney or rest sitting up with the legs hanging down. Aortic dissections are uncommon, but definitely not rare. Regards.

Angioplasty should not be delayed, more so for the patients who have presented prior to the 3 hours of pain onset. When a delay for angioplasty is going to be longer than the recommended 60 minutes, then post delivery of fibrinolytic drugs/fibrinolysis is generally used. Regards.

You don't elevate legs, because you want to return venous flow, CPR isn't just about arterial blood circulation, I remember some research into the prone position and its increased effectiveness in CPR [for both v and a return] however, my Journals seem to had excluded this, although knowing me, I have misplaced it. Regards.

There is no need for rudeness, if you can't be constructive don't post, we don't all use the ridiculous google search engine [that is 99.99% pornography, and false links]. Try www.wikipedia.org or http://www.britannica.com/ or encarta.msn.com or http://www.nlm.nih.gov/medlineplus/encyclopedia.html or www.accessscience.com/ Some may cost, but worth while, as contain valid authenticated research. Regards

Burns are the time IO's are needed, IV's are really hard, unless you remove top layer of skin, plus you need to do the escharotomy [for neck burns]. Such a terrible event is a serve burn. Regards.

You could try this, http://www.stillwaterfire.com/ems.htm although I am not quite sure what you are looking for. Regards.

I was not trying to criticise your medical judgment, I was merely stating that for a paramedic to beg for resuscitation to discontinue seems to be rather occlusive, hence the funeral statement I made, maybe I lacked sympathy, but again I don't understand why anyone would beg, after administering two drugs. A paramedic ought to be able to make a discission without consulting an 'operator', maybe things operate different in America. No harm intended. Regards.

In london we have voluntary ALS and BLS, which are dispatched to 999 [911] calls, and operate at public occasions [such as football matches]. Whilst I am currently reading medicine, at weekends, when possible I volunteer with the local ALS unit. As I previously [prior to reading medicine] worked for the London Ambulance Service. Regards

The question was not the causes it was the mechanisms [the person knows the causes], and its called the 5 H's and 5T's, not 4. Regards.

What about Sodium Bicarbonate or TCP? I know you have a funeral parlor, are you in need of the money? Regards.

Yes, however, in Haemolytic anaemia, the production of RBC's are insufficient and cause a crisis, a transfusion is normally needed. Regards

Hello there, you are referring to a massive pulmonary embolism [saddle] that can cause PEA, pathophysiological actions that cause the PEA, are the inotropic states of cardiac muscle and most importantly the sudden changes in preload or after load [cardiac]. You must remember that most PEA's are caused by hypoxia and respiratory failure. A classical mechanical description for PEA due to MPE is decreased preload [inadequate optimal extent], this occurs because the pulmonary embolism causes a 'decreased' venous return from the left atrium, and hence the left ventricle is unable to acquire significant force to cause a contraction. Similar to cardiac tamponade which can have the same effect. I do apologise if I was too technical, you may want to read some books regarding decreased preload. Regards