AZCEP

I will go so far as to say that those of us that are responsible for our own actions just might be responsible for those that don't want to take responsibility for theirs. As crazy as it may sound, if you go to work each day knowing that your agency will take care of all the CEU's, QA/QI, equipment supply, etc., then why would you take it upon yourself to do these things? The management of resources from the top down creates this type of mindset. When the individual provider comes to the realization that the department is not going to ensure that each piece of equipment is where it should be, only then do they decide they have to make sure of it for themself. The classes that I've taught over the last few years, make this pretty obvious. The students don't want to take responsibility for what they have to learn, and more and more seem to believe that it is the instructor's job to give them the information to pass a test. I continue to refuse to give the answers to their questions directly. When a question is asked, I force them to think about the mechanisms at work. Hopefully, when they are placed in this position later, they will be able to work the problem on their own. Some appreciate this approach, some wish on a daily basis for me to come to great bodily harm. Sorry, I'm not here to make your life easy. Take it upon yourself to learn the material, ask questions about said material, understand the process inside out, and then you will be able to pass any test that is given to you.

The individual is responsible for everything good and bad that happens to themselves. The generation of entitlement that we are currently struggling through doesn't seem to be able to grasp this concept. Part of the problem may very well be too many wanting to make things easier for them. When this begins to happen it very quickly snowballs out of control. Let me make this very clear to all that are reading. I am responsible for what I do on a scene, I am responsible for what you do on a scene. If you decide to do something stupid, don't be surprised when I ask you to leave. I will not willingly give up my safety so that the uninitiated can feel good about themselves.

Shame on you Rid! Back in the box, no cookie for you! Bad, thinking medic!

Consideration needs to be made that while RSI may well stop the motor activity of the seizure, it will not stop the actual seizure activity in the brain. I've witnessed a number of providers wrongly assuming that because the patient is no longer moving, they are not seizing. The sedative agent that is used will greatly determine whether the seizure recurs or remains controlled. Versed is a very good, rapidly acting agent to break a benzodiazepine responsive event, but it does not last long enough to prevent recurrence. Ativan has a much longer duration, but it's onset is also significantly slower. Valium is a good middle ground, and still the most commonly used agent. If prolonged sedation is the goal, break the seizure with Versed, then add some Ativan in shortly thereafter. A close watch on vital signs must be maintained for these patients that have been given a paralytic. Heart rate, in particular, can help you to determine whether the sedation has worn off, or the seizure has recurred. A short acting paralytic, such as Succinylcholine, will also cause a situation where you may have to re-dose due to it's short duration. An unacceptable amount of damage can be done by a provider trying to limit motion of the patient, while trying to maintain a secured ETT.

Check NREMT.org for the testing requirements in the U.S. for EMT's, NAEMT might have a better description of the actual work though. Most Canadian provinces use the Primary Care Paramedic as the designation for the BLS provider, so that might be where the confusion lies.

Not to devolve into the whole "Volunteer vs. Paid" debate, but you are allowed to be a person when you are a volunteer, but not when you are paid? This is a pretty good argument against the use of volunteer services, but that has been discussed elsewhere.

Wow. Sorry for slamming on the brakes so hard. I really expected someone to be able to answer this one. Here you go. Ashman's aberrancy is a type of rate related bundle branch block. Here is the description from Advanced ECG: Boards and Beyond 2nd edition 1. The refractory period of the cardiac tissues depends on the rate. The slower the rate, the longer the refractory period. The faster the rate, the shorter the refractory period. If this didn't happen the heart rate couldn't increase by very much. 2. The refractory period is set one beat at a time. The refractory period of a given beat depends on the distance between two beats. Therefore, if the R-R interval is constantly changing, as in atrial fibrillation, the refractory period will be constantly changing also. 3. The phenomena is reliant on having a long R-R interval followed by a short R-R. The short interval will cause the stimuli to land in a portion of the refractory period as set by the previous interval. Here is a link to a strip:http://www.tveatch.org/ekgs/ekg9.html You will notice that the upper strip has a long R-R with normally conducted complexes, followed by a widened premature beat. How about something a little more common now? AORTIC STENOSIS

Depending on local statute, it can fall under the mandatory reporting of child neglect. Chances are the local law enforcement isn't going to do anything about it directly, but the driver might get a citation in the mail.

Consider at some point in a cardiac arrest, the majority of patients--adult or pediatric--will exhibit a period of VF. The short downtime, or witnessed collapse, is more likely than the longer, unwitnessed collapse. In the pediatric population the period of VF is so short there is really no way for EMS to arrive on scene early enough to witness and treat it.

Background: Hyperviscosity syndrome (HVS) refers to the clinical sequelae of increased blood viscosity. Increased serum viscosity usually results from increased circulating serum immunoglobulins and can be seen in Waldenström macroglobulinemia and multiple myeloma. It can also result from increased cellular blood components (typically white or red blood cells) in hyperproliferative states such as the leukemias, polycythemia, and the myeloproliferative disorders. The complications most commonly associated with this syndrome include mucous membrane bleeding, neurologic and pulmonary symptoms, and the associated retinopathy. Pathophysiology: Viscosity is a property of liquid and is described as the resistance that a liquid exhibits to the flow of one layer over another. As serum proteins or cellular components increase, the blood becomes more viscous, leading to the clinical symptoms of hyperviscosity syndrome secondary to the vascular stasis and resultant hypoperfusion. The normal relative serum viscosity ranges from 1.4-1.8 units (reported as Centipoises). Symptoms usually are not seen at viscosities of less than 4 units, and the hyperviscosity syndrome typically requires a viscosity greater than 5 units. Hyperviscosity syndrome is associated most commonly with plasma cell dyscrasias (the paraproteinemias) and is due to the large size of the excess immunoglobulin M (IgM) paraproteins in these disorders. Waldenström macroglobulinemia is the most common cause and accounts for about 85% of cases of HVS. Less frequently, the disease can occur in multiple myeloma (especially with myeloma proteins of the IgA and IgG3 types) and connective tissue diseases. Hyperviscosity syndrome can also be caused by the bone marrow hyperproliferative states: the leukemias, polycythemia, essential thrombocytosis, and the myelodysplastic disorders, which also increase serum viscosity. Confusion and mental status changes result from the increased viscosity of the blood and decreased cerebral blood flow. This sludging leads to segmental dilatation of retinal veins and retinal hemorrhages. Mucosal bleeding may occur from prolonged bleeding time caused by myeloma proteins interfering with platelet function. Cardiopulmonary symptoms such as shortness of breath, hypoxemia, acute respiratory failure, and hypotension also result from this sludging of blood and decreased microvascular circulation. History: Clinical symptoms generally are related to the triad of mucosal bleeding, visual changes, and neurologic symptoms. Constitutional symptoms and cardiorespiratory symptoms also contribute to the clinical presentation. Tendency to bleed is the most common symptom of hyperviscosity syndrome. Spontaneous gum bleeding Epistaxis Rectal bleeding Menorrhagia Persistent bleeding after minor procedures Visual changes range from blurred vision to vision loss. Neurologic manifestations are frequent and varied. The neurologic symptoms of hyperviscosity have been referred to as the Bing-Neal syndrome. Vertigo Hearing loss Paresthesias Ataxia Headaches Seizures Somnolence progressing to stupor and coma Other manifestations may include heart failure, shortness of breath, hypoxia, fatigue, and anorexia. In fact, one should have a high index of suspicion for HVS in patients with unexplained coma/altered mental status or unexplained shortness of breath especially in those with an underlying hematologic disorder. Physical: Physical findings are related to the major organ systems involved. Bruises, epistaxis, or gum bleeding may be noted. Ophthalmic examination may reveal decreased visual acuity, dilated retinal veins, “sausage-linked” or “boxcar segmentation” of the retinal veins, or retinal hemorrhages. Neurologic examination may reveal various findings, including diminished mental status, confusion, ataxia, or nystagmus. Cardiopulmonary examination may reveal signs of congestive heart failure with volume overload (rales, lower extremity edema, elevated JVP, and hypoxia). Causes: Increased serum viscosity usually results from increased circulating serum immunoglobulins and can be seen in Waldenström macroglobulinemia and multiple myeloma. Less commonly, the hyperproliferative blood cell disorders such as the leukemias, myeloproliferative diseases, polycythemia, and thrombocytosis may be implicated for the increased viscosity caused by proliferation of their respective cellular components. Prehospital Care: Be attentive to the ABCs and symptomatic support. Emergency Department Care: Plasmapheresis is the treatment of choice for initial treatment and stabilization of the hyperviscosity syndrome caused by the paraproteinemias (the majority of cases), while leukapheresis, plateletpheresis, and phlebotomy are indicated for leukostasis, and symptomatic thrombocytosis, and polycythemia, respectively. As plasmapheresis removes the circulating paraproteins, the serum viscosity decreases and symptoms improve. In similar fashion leukapheresis, plateletpheresis, and phlebotomy also decrease the serum viscosity by decreasing the existing cellular component in excess. Although symptoms of CHF from hyperviscosity may not respond to standard therapies, and, in fact, can be exacerbated due to the resultant dehydration from diuresis causing increased viscosity; plasmapheresis and/or cellular pheresis reverses these symptoms. While arranging for plasmapheresis, treat hemorrhage, CHF, and metabolic imbalances with standard therapies. Caveat: Use caution with the decision to proceed with packed red blood cell transfusion (pRBCs) for minor bleeding because a single unit of pRBCs may increase the viscosity enough to cause worsening symptoms and clinical decompensation. If plasma/cellular pheresis is not readily available and the patient is decompensating, one may try vigorous intravenous hydration coupled with a 2-3 unit phlebotomy in the interim as a temporizing measure. Upon commencing pheresis (especially leukapheresis) one should prepare for the possibility of tumor lysis syndrome and treat accordingly. Thank God for eMedicine, eh? Let's see, what next? How about Ashman's aberrancy?

One question, did you work as a basic prior to your medic class? The quality of assessment might not have been there, but the interaction with patients would have made things progress more easily. One of the great misguided notions about EMS is the BLS assessment is different from the ALS assessment. Truth be told, they are and should be the same. Same A-B-C's, same head to toe exam, same system by system evaluation. The difference lies in the amount of information that can be used when you find something. If you can't do an assessment, how do you expect to know when to use a medication? How do you determine that a patient needs a procedure? I will endanger my own sanity, and once again agree with Dustdevil. If you don't know assessment, you really have no business performing patient care. The fact that you are looking for help bodes well for you, but how did your program graduate anyone without the ability to figure out what is wrong with patients? Get yourself to an ER, or do some extra ride-outs so that you can get this down. Perhaps discuss the issue with the preceptor that you are working with. There is a good possibility that you are doing some form of assessment without realizing it.

On to the "blue baby" syndromes, eh? Fallot was the doctor that got the honor of having it named after him, but it was recognized long before his time. The tetrology is: A ventricular septal defect Pulmonary stenosis An overriding aorta Right ventricular hypertrophy These defects create a situation that allows for de-oxygenated blood from the right side of the heart to mix with oxygenated blood in the left, and also reduce the amount of oxygenated blood that is available. Usually corrected with open-heart surgery in the first few months, depending on severity of presentation. These children have "blue periods", when exposed to increased oxygen demand they will become cyanotic. Removal of the stimulation, and placement of the child in a knee-chest position will help mitigate the effects.

Very good Ace, but you didn't describe the why's and how's. And it is Paraquat/diaquat exposure. Kumquats will only give you diarrhea.

H-O-N-K: Another in a long line of descriptions for Hyperglycemic (high blood sugar) Hyperosmolar (increased osmolar fluid loss) Non-Ketotic (no ketones produced) syndrome. This is a sister syndrome to DKA, with a few differences. 1. No ketone production. These patients have just enough insulin available that the body does not utilize fatty acids for fuel sources. 2. Typically an older patient with pre-existing type II diabetes. Because of the usual regimen of insulin sensitizing agents, the body becomes more sensitive to the insulin that is available, and lesser amounts are released from the pancreatic beta cells. See #1 3. Higher blood sugars. DKA begins with BGL's of 250-300, and usually tops out in the 600-750 mg/dL range. HHNK, or HONK, will have blood glucose levels >800 mg/dL. Blood sugars in excess of 1000 mg/dL are not uncommon. 4. Ungodly amount of extremely dilute urine. DKA will run out of fluid, or the urine will become so concentrated with glucose and ketoacids the kidneys can't produce as much. HHNK will continually diurese the patient so the urine becomes diluted and it's specific gravity drops like a rock. Management is focused on fluid replacement and normalizing the blood glucose level over an extended period. Too rapid a drop in blood sugar will cause just as many CNS dysfunctions as leaving it too high for too long. Usual rates of decrease are 100 mg/dL per hour until the blood sugar reaches 250 mg/dL. QUESTION: What is the contraindication (relative or absolute) to the prehospital administration of oxygen? NOT ASSOCIATED WITH THE PATIENT BEING ON FIRE.

From Medscape today: Intravenous Plus Intra-Arterial Thrombolysis Sometimes Helpful in Stroke NEW YORK (Reuters Health) Jul 05 - Using a combination of intravenous (IV) and intra-arterial (IA) thrombolysis can be advantageous in certain patients with acute stroke, European researchers report in the July issue of Stroke. Senior investigator Dr. Roman F. Sztajzel of University Hospital and Medical School, Geneva, Switzerland, told Reuters Health that "combined IV-IA versus IV thrombolysis guided by transcranial color-coded duplex sonography is feasible and safe." "Recanalization after 30 minutes of intravenous thrombolysis led to a favorable outcome in about 60% of patients," he noted. However, "in the absence of early recanalization during IV thrombolysis, there is a clinical benefit to proceed to intra-arterial therapy for a significant proportion of patients." Dr. Sztajzel and colleagues studied 33 patients, who, within 3 hours of symptom onset, underwent IV thrombolysis with tissue plasminogen activator. If this was not successful, they went on to IA thrombolysis. At 3 months, 10 of the 17 patients (59%) in the IV group who had had complete or partial recanalization after 30 minutes of therapy had a favorable outcome. This was also the case in 9 of 16 patients (56%) who did not achieve such a result and went on to IA. "These findings," concluded Dr. Sztajzel, "may support the systematic use of transcranial color-coded duplex sonography during thrombolysis in order to select patients without early recanalization for a more aggressive therapy such as intra-arterial thrombolysis." Stroke 2006;37:1805-1809.

The nearest available stroke center is 40-45 minutes by air. Most of the prehospital triaged patients with CVA presentations get direct flights from the scene. The local receiving hospital has a tough time justifying using IV tPA with the close proximity of a stroke center. As chbare already said, most strokes don't present early enough to be included anyway.

If only there were more "French maids" willing to perform.

1. Students without a sense of entitlement. 2. An educational system that demands, and holds to, a high standard 3. A national EMS administration that is able to make a positive influence in what happens on the street.

Instead of ALS vs. BLS, maybe we should be looking at urban vs. rural. ALS two blocks from a trauma center is not going to make a difference. ALS 20-30 minutes from a trauma center can. Is it more cost effective to have the highest trained providers further from the tax base that can support them? Probably not, but that is where they are most needed.

A "saved" patient is one that is able to resume a level of function that they had prior to arresting. If we keep them alive in ICU for several weeks, and they die on a ventilator, that does not count.

Not doubting the possibility of narcotics, but why use Narcan for a meth overdose?

Maintain perfusion, elevate the head of the LSB to facilitate venous drainage, maintain normal ventilation, monitor BGL.

Your brain has given up. Keep practicing the system that works for you until you see them in your sleep.

Yep, this won't make it out of the bargain DVD bin, much less to the theaters.

And the crowd goes wild!!!!!