brock8024

I have loved reading all of the post on this topic. I am gay and have been pretty much all of my life, well as much as I remember. I have been with my partner for 3 years. We are looking at buying a house very soon. We are complete opposites when it comes to certain views, but it makes life interesting. We was going to church every sunday but have not been able to go since college and work. We are going to start back up soon. I am out to anyone who ask me. I am one you could not pick out of a crowd. It is funny, I have came out to all of my class that I am graduating with and most was shocked. They never thought I was. I am lucky that everyone is cool with it and have had not problems. Me and Rusty are complete opposites when it comes to looks. I am overweight and have a beard , while he is skinny as hell and well lets just say you could tell he was in a crowd. We do not sleep around or go to clubs. We lead a normal life if that is what you want to call it. I mean what is normal anyways. My family is awesome and I am so lucky to have them. My mom has told me she wish I was strait but loves me anyway. My 79 year old grandparents tell rusty they love him and give him hugs all the time. My grandma even cooks certain foods for him since he is picky. My aunts and uncles are aweomse with it too. They have invited him down to stay with them and everything. I will say I did not choose this lifestyle. I mean can you chose to be gay then strait then back. I knew something was up when I was younger just never knew what it was. I have almost commited suicide but thought WHY? so people may not like it but who cares. Most who do not like it have something they are hiding whether it is drug use or something. I think mostly it is your personal relationship with GOD. I mean there are how many different branches of Christianity? sorry for spelling. There are baptist to penicostal to mormans. I mean all are christians but have different thoughts. I mean there are how many different types of baptist alone. I can say this being raised a baptist. LOL Oh well. I think it is weird that I am the only one so far that has came out and said they were gay. Brock

Case 1- I would say AMI vs CHF until proven otherwise then I would think about a pulmonary problem. tx would be IV,O2,Monitor, EKG, as a basic o2 via NRB. Case 2- I would say either CHF, AMI, or Acute Liver Failure of some sort. Tx would be IV, Monitor, V/S EKG, as a medic. Basic tc would be o2 via NRB and watch him Case 3- I would say Croupe vs Epiglottitis hard to tell the difference in a 3 year old. Just try to keep them from crying and high flow o2 via blow by.

http://www.bored.com/malerestrooms/index.htm i thought it was funny.

See it is amazing that I was flogged for the treatment that I would have done for this patient, and was told that someone hoped I was just starting out as a medic student and never to come to PA to practice. Well I am graduating soon, may to be more to the point. I will never come to Pa. is this is how people are treated. See I was taught that is a heart is hypoxic you need to fix the hypoxemia before moving on. This is why we now do 2 mins of CPR before we defib a patient, and why we can do 2 mins of CPR after we get a pulse back to help the Hypoxemia and acidosis. I still think that it was a respiratory problem that caused the tachycardia. I mean how many people can have SHOB for 2 DAYS and have that much edema and it be from a tachycardia? I doubt this guys heart had been going that fast both days. I am sure he got into a CHF or COPD problem did not call and though he could do ok on his own or would not let his wife call EMS. Then as time went on from his breathing difficulty, his heart speeds up to compensate for the impending respiratory arrest. I think that if we was to caridovert first one of two things would happen 1) We would send him into cardiac arrest 2) we would convert him but he would speed right back up due to the hypoxemia Brock

This is my whole thing right here, IT COULD BE A PUMP PROBLEM OR A LUNG PROBLEM!!! If it was a heart problem I will agree that is can cause the Fluid in the lungs and such. If it is a Lung problem it can cause the fluid and Rapid Heart Rate. How do you or can you tell which can first. It is like the chicken or the egg question. For this reason I will go back to A- Airway B- Breathing C- Circulation Airway before Breathing and Breathing before Circulation. So you cardiovert this guy and throw him inot respiratiory aresst, which you can fix but why not go in order. I do not understand, from this no one can tell which caused the problems. The heart causing the breathing problems or the breathign problems causing the heart problems. So I say fix the breathing then the circulation.

I support a 2 year degree program and will graduate in may with my degree from the only nationally accredited college for EMS in oklahoma.

Ok I have read this again and I personally think that the respiratiory problem is causing the tachy heart rate. I can not prove it but if you think about it if you are full of fluid and having to use a lot of energy to breath your heart rate is going to increase. This patient's heart is already irritable and I am sure it would not take much for it to get the job done. the problem with this is that the filling time is going to be low which will cause low Cardiac out put. I would ask the patient and his wife about meds and when he last took them. He has had a increasing SHOB over the last 2 days and now has 4+ edema in his legs. Lungs are full of fluid and his is using all muscles to breath. I would give him the lasix and MONA if possible. It takes lasix a few mins to work and with all the edema and fluid it should help. The Morphine will help with moving fluid also as well as Nitro. I am looking at getting the fluid out and fixing the breathing problem before cardiac since I personally believe this is the true problem. This guy also should be cpap or intubated. I always go back to basic and follow ABC way of doing things. This guy has a Airway, His breathing is well not the best to say the least. So we need to fix that before going on to Circulation. It has been drilled into my head but my instructors to TREAT THE PATIENT NOT THE MONITOR!!!!!! I am also taught to think about what is going on. I believe and RID tell me if I am wrong, but my school also teaches us to think out side the box and not cook book medicine. I think if cardioversion is the top thing to do for this person then they have either forgot the ABC's of assessment or are treating the MONITOR not the PATIENT. In the end of all this if it is hard to read 1) treat the SHOB that has been going on for 2 days. 2) Meds to help with one 3) advanced airways if needed 4) Treat the Cardiac issues Lets face it we can fix the rate but if we do not fix what is causing the problem the Heart rate will go right back up and take more oxygen. Brock

I have learned the age plus percent burned (2nd and 3rd degree) equals mortality. After working in a burn center and loving it, I have been taught that burns generally do not kill the patient but rather the inhalation injury does along with other core morbities. I have seen patients be totally healed, all the grafts healed everything and still die from kidney failure, ARDS, or some other problem.

I will agree that we do have to do stuff to our patients in times of need. What I am saying is that no matter if we think they can hear us or not, we should still explain what we are doing to them. Yes on my patients that have a low blood sugar that I am giving glucose I still explain that I am starting the IV and what I am giving them. If I had to cardiovert someone I would still explain what was happening. I believe that we are all smart enough to multi-task and explain what we are doing when we are doing it. I have never been told not to explain what I was doing. Heck I intubated a cardiac arrest patient and Was explaining everything. Did he hear me nope but did it hurt Nope. I believe that you can never go wrong with explaining things. We might know what a patient needs but that does not mean that we do not explain. If you believe that a patient does not hear you wait til you get sued for saying something Now the one thing I want to know is why I was attacked. What did I say or do for Fire to tell em I should never practice in his state, and that he hopes that I am just starting out. We are all learning no matter if we have been doing this for 1 month or 30 years. I will graduate in may with a A.A.S 2 year degree. My school is the only nationally accredited school in oklahoma. I take great pride in what I learn and my job. I always act as a Professional. I do not see anything in my post that should have been attacked. So please humor me and tell me why you acted so unprofessional. Thanks I was not bragging but I take great pride in my education.

You are so right. I do not understand why we can not give the proper meds or at least explain what we are doing. I mean it does not take that long, or why we do not explain stuff to ouor older patients just because they have not responded to stimulus in years. Who cares they are still human.

thanks for ur opinion we are all allowed to think what we will. Hope you have a great day.

http://www.blackwell-synergy.com/doi/abs/1....2000.tb00662.x An 86-year-old female developed supraventricular tachycardia 36 hours after a myocardial infarction (MI). She developed atrial fibrillation and polymorphic ventricular tachycardia (PVT) following administration of 12 mg ofadenosine. The PVT caused hemodynamic instability with no response to cardioversion, but termination with procainamide. The heart is vulnerable to hemodynamically unstable, possibly lethal, PVT early after MI under some circumstances. This vulnerability may be exposed following administration of adenosine. Extra caution is warranted when using adenosine in the post-Mi period. The link and article which I think is intersting. http://www.aafp.org/afp/20020615/2479.html Management of Common Arrhythmias: Part I. Supraventricular Arrhythmias A. KESH HEBBAR, M.D., and WILLIAM J. HUESTON, M.D. Medical University of South Carolina, Charleston, South Carolina Family physicians frequently encounter patients with symptoms that could be related to cardiac arrhythmias, most commonly atrial fibrillation or supraventricular tachycardias. The initial management of atrial fibrillation includes ventricular rate control to provide adequate cardiac output. In patients with severely depressed cardiac output and recent-onset atrial fibrillation, immediate electrical cardioversion is the treatment of choice. Hemodynamically stable patients with atrial fibrillation for more than two days or for an unknown period should be assessed for the presence of atrial thrombi. If thrombi are detected on transesophageal echocardiography, anticoagulation with warfarin for a minimum of 21 days is recommended before electrical cardioversion is attempted. Patients with other supraventricular arrhythmias may be treated with adenosine, a calcium channel blocker, or a short-acting beta blocker to disrupt reentrant pathways. When initial medications are ineffective, radiofrequency ablation of ectopic sites is an increasingly popular treatment option. (Am Fam Physician 2002;65:2479-86. Copyright© 2002 American Academy of Family Physicians.) A PDF version of this document is available. Download PDF now (8 pages / 129 KB). More information on using PDF files. Heart palpitations and cardiac arrhythmias are common problems encountered by family physicians. Patients may present with acute cardiac rhythm abnormalities. Although these arrhythmias are usually benign, they can indicate significant underlying heart disease. More often, patients have chronic arrhythmias, such as atrial fibrillation, that may require treatment to reduce the risk of future complications. The challenges for the family physician are to determine which arrhythmias are benign and which indicate probable cardiac malfunction, and to manage recurrent or chronic rhythm abnormalities. Atrial fibrillation is the most common cardiac arrhythmia family physicians are likely to encounter. This two-part article reviews common atrial and ventricular arrhythmias, with a focus on initial management decisions. Part I discusses supraventricular arrhythmias. Part II discusses ventricular arrhythmias and the management of rhythm abnormalities in special populations, including pregnant women, athletes, and children. Atrial Fibrillation Atrial fibrillation is the most common cardiac arrhythmia family physicians are likely to encounter. This rhythm abnormality affects 3 to 5 percent of patients more than 60 years of age1 and becomes increasingly common with advancing age. The median age of patients with atrial fibrillation is 75 years, and the prevalence of the arrhythmia doubles every 10 years after the age of 55.2,3 In the United States, atrial fibrillation is estimated to affect almost 9 percent of patients more than 75 years of age.2 Most risk factors for atrial fibrillation are associated with structural or ischemic heart disease. Risk factors include hypertension, left ventricular hypertrophy, dilated and restrictive cardiomyopathies, coronary artery disease, chronic obstructive pulmonary disease, and diabetes in women.1 The annual risk of stroke in patients with atrial fibrillation and normal valve function has been reported to be 4.5 percent per year.4 Anticoagulation with warfarin (Coumadin) reduces the risk by about two thirds.4 The mortality rate for stroke in patients with atrial fibrillation is approximately twice as high as the rate in patients without this rhythm abnormality.5 Although anticoagulation is contraindicated in some elderly patients, a study in Great Britain6 found that about 60 percent of patients identified in community screenings as having atrial fibrillation were eligible for, and would benefit from, this treatment. The annual risk of stroke in patients with atrial fibrillation and normal valve function has been reported to be 4.5 percent per year. MANAGEMENT The first step in managing a patient with atrial fibrillation is to decide whether there is a high likelihood of safe conversion to sinus rhythm or whether the patient should be allowed to remain in atrial fibrillation. A patient with recent onset of atrial fibrillation (within the previous 12 months) and no evidence of enlargement of the left atrium has a greater chance of achieving and maintaining sinus rhythm. If the arrhythmia is long-standing and the patient is not a suitable candidate for rate cardioversion, initial treatment should focus on ventricular rate control, with consideration given to long-term stroke prophylaxis. Restoration of Sinus Rhythm. Patients who present within 48 hours of the onset of new atrial fibrillation are candidates for cardioversion with a low risk of embolism. Conversion to sinus rhythm can be attempted by electrical shock or with antiarrhythmic drugs. Patients who have been in atrial fibrillation for more than 48 hours or for an undetermined period are more likely to have atrial thrombi and may develop emboli with immediate electrical or medical (pharmacologic) cardioversion. Atrial thrombi are not evident on transthoracic echocardiograms, but they can been seen on transesophageal echocardiograms.7 If the transesophageal echocardiogram reveals thrombi, anticoagulation is recommended before cardioversion is attempted. Anticoagulation can be accomplished using warfarin, with the dosage adjusted to achieve an International Normalized Ratio (INR) between 2.0 and 3.0 for a minimum of 21 days.8 If the transesophageal echocardiogram does not show thrombi on multiplane views, cardioversion can be attempted. Short-term anticoagulation with heparin should be started before the procedure, and warfarin therapy should be initiated after cardioversion.8 When rhythm conversion is indicated, it can be accomplished using direct-current cardioversion or pharmacologic therapy. Synchronized cardioversion is currently considered the treatment of choice for the restoration of sinus rhythm and, in appropriately selected patients, has a success rate of at least 80 percent.4 Cardioversion is also indicated in patients with hypotension, angina, heart failure, or other evidence of severe compromise caused by atrial fibrillation.5 Medical cardioversion of atrial fibrillation may be achieved with class IA drugs (quinidine, disopyramide [Norpace], procainamide [Procanbid]) or with amiodarone (Cordarone). In the past, quinidine was frequently used for both cardioversion and maintenance of sinus rhythm in patients who had undergone electrical cardioversion. However, because of the proarrhythmic action of class IA agents and their detrimental effects on left ventricular function, these drugs are now used less often than amiodarone for primary therapy of atrial fibrillation.4 Amiodarone therapy is successful in 86 percent of patients who have had atrial fibrillation for less than two years.4,9 Treatment is also effective in 40 to 60 percent of patients with long-standing atrial fibrillation that has been resistant to other agents and to electrical cardioversion.4 Amiodarone can be given in a dosage of 200 mg a day, which is lower than the dosages that have been associated with thyroid abnormalities and pulmonary fibrosis. Although there is little risk of toxicity when amiodarone is given in a low dosage, it is prudent to monitor patients for the development of thyroid, pulmonary, hepatic, and cardiac side effects. Findings on the usefulness of various agents for the conversion of atrial fibrillation, based on the evidence-based practice program of the Agency for Healthcare Research and Quality, are summarized in Table 1.10 Although drugs such as digitalis preparations and sotalol (Betapace) are sometimes used for rate control, they are not effective for converting atrial fibrillation to sinus rhythm.10,11 TABLE 1 Medications for Converting Atrial Fibrillation to Sinus Rhythm -------------------------------------------------------------------------------- Drug and class Usual oral dosing Odds ratio for conversion compared with placebo (95% CI)* Flecainide (Tambocor): class IC 50 mg every 12 hours; increase by 50 mg per day every 4 days to maximum of 300 mg per day. 24.7 (CI: 9.0 to 68.3) Ibutilide (Corvert) given IV, followed by dofetilide (Tikosyn) given orally: both class III Ibutilide: 0.01 mg per kg IV over 10 minutes; if first dose is not effective, give second infusion 10 minutes later (maximum dose: 1 mg). Dofetilide: 0.1 to 0.5 mg every 12 hours 29.1 (CI: 9.8 to 86.1) Disopyramide (Norpace): class IA 100 to 200 mg every 6 to 8 hours 7.0 (CI: 0.3 to 153) Amiodarone (Cordarone): class III 800 to 1,600 mg per day for 7 to 14 days; then 200 to 400 mg per day as maintenance 5.7 (CI: 1.0 to 33.4) Propafenone (Rythmol): class IC 150 mg every 12 hours; if needed, increase dose every 3 to 4 days to maximum of 300 mg every 12 hours. 4.6 (CI: 2.6 to 8.2) Quinidines: class IA Quinidine sulfate (Quinidex): 400 mg every 6 hours Quinidine gluconate (Quinaglute): 648 mg every 8 to 12 hours 2.9 (CI: 1.2 to 7.0) -------------------------------------------------------------------------------- CI = confidence interval; IV = intravenous. *--Odds ratio is expressed as the number of times conversion is more likely with drug compared with placebo. Information from Management of new onset atrial fibrillation. Summary, evidence report/technology assessment: no. 12. Rockville, Md.: Agency for Healthcare Research and Quality, May 2000; AHRQ publication no. 00-E006. Retrieved April 23, 2002, from www.ahcpr. gov/clinic/epcsums/atrialsum.htm. If external electrical cardioversion is unsuccessful and antiarrhythmic drug therapy fails, other measures can be used. However, these approaches are usually reserved for use in patients who cannot tolerate atrial fibrillation and patients who have associated systolic dysfunction. Techniques include internal electrical cardioversion through the application of electrical current to pulmonary veins via a transcatheter cathode4 and radiofrequency ablation of the atrioventricular node with insertion of a ventricular pacemaker.12 In addition, an implantable atrial defibrillator can be used to provide rapid cardioversion in patients with atrial fibrillation that cannot be controlled with medications.13 Rate Control in Chronic Atrial Fibrillation. In patients in whom rhythm conversion is not indicated or those who have new-onset atrial fibrillation with a rapid ventricular response, treatment may be needed to control the ventricular rhythm. Excessive ventricular rates may result in diminished cardiac output because of poor filling time, and in ischemia because of increased myocardial oxygen demand. Medications used for ventricular rate control in patients with atrial fibrillation are listed in Table 2.14 TABLE 2 Medications for Ventricular Rate Control in Atrial Fibrillation -------------------------------------------------------------------------------- Drug Dosing Side effects and complications Calcium channel blockers Diltiazem (Cardizem) Acute IV: 0.25 mg per kg over 2 minutes; then 0.35 mg per kg after 15 minutes if needed; then 10 mg per hour in drip if needed Acute: heart block, CHF, hypotension (~3%) Long-term: constipation Oral maintenance: 180 to 240 mg per day Verapamil (Calan) Acute IV: bolus of 5 to 10 mg over 2 minutes; may repeat 10 mg in 15 to 30 minutes Acute: heart block, CHF, hypotension (~5% to 10%) Oral maintenance: 240 to 320 mg per day Long-term: constipation Beta blockers Acute IV: 1 to 3 mg at 1 mg per minute; repeat in 2 minutes if needed. Acute: heart block, bronchospasm, CHF Propranolol (Inderal) Oral maintenance: 10 to 30 mg every 6 to 8 hours Long-term: fatigue, depression Esmolol (Brevibloc) Acute IV: 0.5 mg per kg over 1 minute; then 0.05 mg per kg per minute by IV drip for 4 minutes Acute: hypotension (20% to 50%), heart block, CHF Digoxin (Lanoxin) Acute IV: 0.25 to 0.50 mg; then 0.25 mg every 4 to 6 hours to total of 1.0 mg Heart click, visual disturbances, delirium, hallucinations Oral maintenance: 0.125 to 0.25 mg per day -------------------------------------------------------------------------------- CHF = congestive heart failure. Information on side effects and complications from Physicians' desk reference. 56th ed. Montvale, N.J.: Medical Economics, 2002. Acute management of ventricular rates can usually be achieved with intravenously administered diltiazem (Cardizem), given in an initial bolus of 15 to 20 mg (0.25 mg per kg) over two minutes, or with an intravenously administered beta blocker such as propranolol (Inderal), given in a dose of 0.5 to 1 mg (up to 3 to 5 mg if needed). A number of medications, including calcium channel blockers, beta blockers, and digoxin (Lanoxin), are effective for maintaining ventricular rates within acceptable ranges. Because calcium channel blockers are associated with better exercise tolerance, they may be preferable to beta blockers.15 Digoxin is associated with a high degree of exercise intolerance; therefore, it should be reserved for use in patients who are relatively immobile, who cannot tolerate other treatment options, or who have significant ventricular dysfunction. Paroxysmal Supraventricular Tachycardias Based on duration, supraventricular tachycardias are usually categorized as paroxysmal, persistent, or chronic. Paroxysmal supraventricular tachycardia (PSVT) is the most common of these arrhythmias and the one that is most often encountered in the primary care setting. Longer-duration supraventricular tachycardias can be treated similarly to PSVT, but cardiology consultation is often required to identify the electrophysiologic mechanism responsible for sustaining the arrhythmia. In contrast to ventricular tachycardias (discussed in part II of this article) and atrial fibrillation, PSVT is usually a narrow-complex tachycardia with a regular rate. MECHANISMS Atrioventricular Nodal Reentry Causing PSVT. Atrioventricular nodal reentry, the most common mechanism of PSVT, occurs when two pathways exist with different conduction rates. A premature atrial complex that is blocked in the fast pathway and redirected through the slow pathway usually triggers the tachycardia (Figure 1). The electrical signal proceeds down the slow pathway and then reenters the fast pathway in a retrograde direction. By the time the signal has propagated down the slow pathway and back around on the fast pathway, the slow pathway is no longer refractory and is ready to conduct the signal again, completing a continuous circuit. Reentry Paroxysmal Supraventricular Tachycardia FIGURE 1. Mechanism for reentrant paroxysmal supraventricular tachycardia. (A) A premature atrial complex (PAC) occurs and is blocked in a fast pathway, but it can propagate down the slower pathway. ( By the time the electrical signal reaches the end of the slow pathway, the fast pathway has repolarized, and retrograde conduction of the wave occurs. © The wave then returns down the slow pathway, setting up a closed circuit that is self-sustaining. FIGURE 2. Atrial tachycardia from reentry (lead II), with negatively conducted P waves (arrows) buried in the ST segment. Reentrant tachycardias usually produce a narrow-complex tachycardia with no discernible P wave. The rate is usually between 160 and 190 beats per minute. In a less common form of atrioventricular nodal reentrant tachycardia, the circulating wavefront proceeds in an antegrade fashion down the fast pathway and in a retrograde fashion up the slow pathway. In this form, inverted P waves (Figure 2) are clearly visible in lead II of the electrocardiogram (ECG). It is important to note that atrioventricular nodal reentrant tachycardia can result in a wide-complex tachycardia if the patient has preexisting bundle branch block. Accessory Pathways Causing PSVT. Accessory pathways (Wolff-Parkinson-White syndrome) and other bypass tracts can cause PSVT. In patients with Wolff-Parkinson-White syndrome, a shortened PR interval and a slurred upstrike to the QRS complex "delta wave" on the resting ECG indicate the presence of an accessory pathway (Figure 3). It should be noted that the resting ECG may be normal in some patients with Wolff-Parkinson-White syndrome, because of the inability of the accessory pathway to conduct in the antegrade direction. The usual mechanism of PSVT in this setting is antegrade conduction down the normal pathways through the atrioventricular node and retrograde conduction through the accessory pathway. The ECG in an atrial arrhythmia with an accessory pathway usually shows a narrow-complex tachycardia at rates of 160 to 240 beats per minute. Delta waves are absent because the normal pathways are used for ventricular activation. Inverted P waves may be seen in the inferior leads. In a much less common form of PSVT, antegrade conduction is down the bypass tract and results in a wide-complex tachycardia. Increased Automaticity Causing PSVT. Increased automaticity usually occurs when the atrium is enlarged, as in patients with chronic lung disease, congestive heart failure, or electrolyte and acid-base disturbances. Usually, the stretched atria fire irregularly, producing multiple premature beats that emanate from different areas of the atria. Because the foci for the ectopic beats are in multiple sites, the P waves vary in morphology, giving rise to the term "multifocal atrial tachycardia." FIGURE 3. Patient with Wolff-Parkinson-White syndrome. Note the short PR interval and slurred upstrike (arrows), termed a "delta wave." FIGURE 4. Blocked premature atrial complex. In the complex preceding the pause, note the altered morphology of the T wave (arrow), caused by superimposition of a P wave on the T wave. The diagnosis of multifocal atrial tachycardia depends on the identification of an irregular rhythm with three or more different P-wave morphologies. The rate is usually between 130 and 180 beats per minute. Treatment is directed at correcting the underlying cause. Antiarrhythmic drugs are usually not helpful. MANAGEMENT In most patients, PSVT is benign and self-limited. However, some patients can have angina, hypotension, and intense anxiety. The first step in the management of PSVT is to determine whether the patient is hemodynamically stable. If PSVT is sustained and there is any indication of instability (i.e., angina, shortness of breath, decreased level of consciousness, hypotension, or congestive heart failure), electrical cardioversion should be performed urgently. If the symptoms are restricted to discomfort (e.g., palpitations and anxiety), conservative measures should be applied. Conservative management of PSVT can include both nonpharmacologic and pharmacologic measures (Table 3).16 Vagal maneuvers to increase parasympathetic tone and slow conduction through the atrioventricular node should be the first approach. Patients should be taught some of these maneuvers for use in future episodes. They should also be instructed to avoid inciting factors, such as caffeine, tobacco, alcohol, pseudoephedrine, and stress. Carotid sinus massage can be attempted, but its role has become more limited because of the effectiveness of drug therapy and the risk of embolism from carotid pressure in some patients. The goal of pharmacologic management is to slow or block atrioventricular nodal conduction. Agents used for this purpose include adenosine (Adenocard), calcium channel blockers (verapamil [Calan] or diltiazem), and beta blockers (e.g., esmolol [brevibloc]). Adenosine is an ultra­short-acting agent that is cleared quickly (half-life of 1 to 6 seconds). This agent is given intravenously in an initial dose of 6 mg, which is followed by one or two 12-mg boluses. Adenosine works by reducing conductance along the slow antegrade pathway. Side effects include flushing, dyspnea, and chest pain. Because of the short half-life of adenosine, these effects are usually very brief and do not ordinarily result in complications. One advantage of adenosine is that it lacks the negative inotropic effects of calcium channel blockers. Adenosine can also decrease the sinus rate transiently and produce a "rebound" sinus tachycardia. Adenosine should not be used in patients with heart transplants, because such patients may be too sensitive to its effects.17 Calcium channel blockers can also be used to disrupt a reentrant pathway. Verapamil can be given in a 5- to 10-mg bolus over 2 minutes, followed by 10 mg in 15 to 30 minutes if the initial dose does not convert the arrhythmia.18 Verapamil and other calcium channel blockers should not be used in patients with an undiagnosed wide-complex tachycardia, because of the risk of fatal hypotension or ventricular fibrillation if the arrhythmia is actually ventricular tachycardia and not PSVT.19 Intravenously administered diltiazem is also effective.20 Initial treatment consists of a bolus of 0.25 mg per kg administered over two minutes. A repeat bolus of 0.35 mg per kg given over two minutes can be administered 15 minutes later. Esmolol, a short-acting beta blocker, can be given in an intravenous bolus of 0.5 mg per kg over 1 minute or in an infusion at a rate of 0.5 mg per kg per minute after an initial loading dose of 0.5 mg per kg. An advantage of esmolol over other beta blockers is its short half-life (four to five minutes), compared with the much longer half-lives (three hours or more) of most other beta blockers. Because of a similar depressive effect on left ventricular contractility, esmolol should be used with caution if initial treatment with a calcium channel blocker is not successful. Other antiarrhythmic drugs, including quinidine, procainamide, flecainide (Tambocor), and amiodarone, may be used in patients who do not respond to initial medications. However, selective radiofrequency ablation is rapidly becoming the treatment of choice in this situation. Long-term control of recurrent PSVT caused by atrioventricular nodal reentry may be achieved with pharmacologic therapy or radiofrequency ablation. Patients who have infrequent, well-tolerated recurrences may manage these episodes with self-administered physiologic maneuvers. Radiofrequency ablation is now used early in the management of patients with PSVT caused by an accessory pathway (Wolff-Parkinson-White syndrome), atrioventricular nodal reentrant tachycardia, or atrial tachycardia.21 The success rate for radiofrequency ablation is 95 percent in patients with an accessory pathway or atrioventricular nodal reentrant tachycardia, and approximately 80 percent in patients with atrial tachycardia.21 TABLE 3 Treatment Options for Supraventricular Tachycardias -------------------------------------------------------------------------------- Physiologic interventions Rest Valsalva maneuvers: gag reflex, ice packs, etc. Carotid massage* Avoidance of inciting factors: caffeine, tobacco, alcohol, pseudoephedrine, stress, etc. Medications Drugs with direct effect on atrioventricular node or accessory pathway: amiodarone (Cordarone), sotalol (Betapace), class IC drugs (flecainide [Tambocor], propafenone [Rythmol], etc.) Drugs that work primarily on atrioventricular node: adenosine (Adenocard), calcium channel blockers, beta blockers, digoxin (Lanoxin) Drugs that work primarily on accessory pathway: class IA drugs (quinidine, disopyramide [Norpace], etc.) Radiofrequency ablation Electronic pacing -------------------------------------------------------------------------------- *--Controversial because of risk of embolism. Adapted with permission from Myerburg RJ, Kessler KM, Castellanos A. Recognition, clinical assessment, and management of arrhythmias and conduction disturbances. In: Alexander RW, Schlant RC, Fuster V, eds. Hurst's The heart, arteries and veins. 9th ed. New York: McGraw-Hill, Health Professions Division, 1998:873-942. Other Atrial Arrhythmias SINUS ARRYTHMIA Sinus arrhythmia is usually a normal event in young persons and athletes. In fact, it occurs with such high frequency that it may considered a normal variant rather than a true arrhythmia. There are two forms of sinus arrhythmia. In the "respiratory" form, the RR interval shortens during inspiration and slows during expiration. Breath-holding eliminates the variation. In the "nonrespiratory" form, the same phasic variation is seen in the RR interval but is not related to respirations. This form of sinus arrhythmia occurs in elderly patients, patients with digoxin overdose, and patients with increased intracranial pressure. Sinus arrhythmia is usually asymptomatic. Sometimes, however, the long pauses can cause dizziness or syncope. Treatment is usually unnecessary. WANDERING ATRIAL PACEMAKER Patients with wandering atrial pacemaker are usually not symptomatic. The condition is most often an isolated finding on the ECG and requires no treatment. Sometimes it is noted on physical examination as an irregularly irregular rhythm. With wandering atrial pacemaker, the ECG shows variable P-wave morphology and PR intervals. The atrial impulses conduct in a 1:1 fashion and usually control the rhythm for several beats before shifting to another focus. The normal heart rate in wandering atrial pacemaker differentiates this condition from multifocal atrial tachycardia. PREMATURE ATRIAL COMPLEXES A premature atrial complex is generated from an ectopic focus in the atria. Therefore, the P wave is usually different in morphology from the usual sinus P wave. The impulse conducts along the normal pathways, generating a narrow QRS complex followed by a pause. Sometimes the premature atrial complex is not conducted and can mimic heart block (Figure 4). Premature atrial complexes are found in a variety of settings, including the excessive consumption of caffeine or alcohol and the use of sympathomimetic drugs. These complexes can also be present in patients with structural heart disease. Patients with premature atrial complexes are usually asymptomatic and require no treatment. A beta blocker given in a low dosage can be tried in patients with uncomfortable symptoms, but no studies of efficacy have been reported. Patients should be counseled to decrease their intake of caffeine, tobacco, and alcohol, and their use of over-the-counter sympathomimetic substances, which are often present in cold medicines and weight-loss preparations. It is important to note that premature atrial complexes sometimes precipitate supraventricular tachycardia, atrial flutter, or atrial fibrillation. Patients with sustained paroxysmal supraventricular tachycardia who are unstable should undergo emergency cardioversion. Sinus Nodal Arrhythmias SINUS PAUSE AND SINOATRIAL EXIT BLOCK Sinus pause or arrest occurs when the sinoatrial node fails to discharge. The ECG shows a pause in the sinus rhythm, with no preceding P wave. Patients usually have no symptoms, but if the pause is prolonged, they may have lightheadedness, palpitations, syncope, and falls. In sinus arrest, the length of the pause has no relationship to the PP interval. Sinoatrial exit block is recognized by the pauses being multiples of PP intervals. Sinus node dysfunction is usually caused by drugs such as digoxin, quinidine, or procainamide. It can also be caused by ischemia, myocarditis, or fibrosis. From a therapeutic standpoint, it is probably not important to distinguish between sinus arrest and sinoatrial exit block. Both can occur in well-trained athletes22 and can be a factor in sick sinus syndrome.23 SICK SINUS SYNDROME The term "sick sinus syndrome" encompasses a number of abnormalities, including sinus bradycardia, sinus arrest or exit block, combinations of sinoatrial and atrioventricular nodal conduction disturbances, and atrial tachyarrhythmias. More than one of these arrhythmias may be recorded in the same patient (bradycardia-tachycardia syndrome). The abnormalities in sick sinus syndrome are usually due to ischemia, fibrosis, or drug-induced or autonomic dysfunction. Signs and symptoms are related to cerebral hypoperfusion and reduced cardiac output. Treatment of recurrent symptomatic bradycardia or prolonged pauses requires implantation of a permanent pacemaker.24 The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported. Members of various family practice departments develop articles for "Practical Therapeutics." This article is one in a series coordinated by the Department of Family Medicine at the Medical University of South Carolina, Charleston. Guest editor of the series is William J. Hueston, M.D. This is part I of a two-part article on common arrhythmias. Part II, "Ventricular Arrhythmias and Arrhythmias in Special Populations," appears on page 2491 of this issue. -------------------------------------------------------------------------------- The Authors A. KESH HEBBAR, M.D., is assistant professor in the Department of Family Medicine at the Medical University of South Carolina, Charleston. He graduated from the University of Madras Medical School, India, and received postgraduate training in internal medicine and general practice in Great Britain. Dr. Hebbar completed a family practice residency at the Medical University of South Carolina, where he currently coordinates cardiology training for family practice residents. WILLIAM J. HUESTON, M.D., is professor and chair of the Department of Family Medicine at the Medical University of South Carolina. Dr. Hueston received his medical degree from Case Western Reserve University School of Medicine, Cleveland, and completed a family practice residency at Riverside Methodist Hospital, Columbus, Ohio. Address correspondence to William J. Hueston, M.D., Department of Family Medicine, Medical University of South Carolina, P.O. Box 250192, Charleston, SC 29425 (e-mail: huestowj@musc.edu). Reprints are not available from the authors. REFERENCES Levy S. Epidemiology and classification of atrial fibrillation. J Cardiovasc Electrophysiol 1998;9(8 suppl):S78-82. Ryder KM, Benjamin EJ. Epidemiology and significance of atrial fibrillation. Am J Cardiol 1999;84(9A):R131-8. Benjamin EJ, Levy D, Vaziri SM, D'Agostino RB, Belanger AJ, Wolf PA. Independent risk factors for atrial fibrillation in a population-based cohort. The Framingham Heart Study. JAMA 1994;271:840-4. Golzari H, Cebul RD, Bahler RC. Atrial fibrillation: restoration and maintenance of sinus rhythm and indications for anticoagulation therapy. Ann Intern Med 1996;125:311-23. Pritchett EL. Management of atrial fibrillation. N Engl J Med 1992; 326:1264-71. Sudlow M, Thomson R, Thwaites B, Rodgers H, Kenny RA. Prevalence of atrial fibrillation and eligibility for anticoagulants in the community. Lancet 1998;352:1167-71. Falk RH. Atrial fibrillation. N Engl J Med 2001;344:1067-78. Manning WJ, Silverman DI, Keighley CS, Oettgen P, Douglas PS. Transesophageal echocardiographically facilitated early cardioversion from atrial fibrillation using short-term anticoagulation: final results of a prospective 4.5-year study. J Am Coll Cardiol 1995; 25:1354-61. Santos AL, Aleixo AM, Landieri J, Luis AS. Conversion of atrial fibrillation to sinus rhythm with amiodarone. Acta Med Port 1979;1:15-23. Management of new onset atrial fibrillation. Summary, evidence report/technology assessment: no. 12. Rockville, Md.: Agency for Healthcare Research and Quality, May 2000; AHRQ publication no. 00-E006. Retrieved April 23, 2002, from www.ahcpr.gov/ clinic/epcsums/atrialsum.htm. Falk RH, Knowlton AA, Bernard SA, Gotlieb NE, Battinelli NJ. Digoxin for converting recent-onset atrial fibrillation to sinus rhythm. A randomized, double-blinded trial. Ann Intern Med 1987;106:503-6. Pappone C, Rosanio S, Oreto G, Tocchi M, Gugliotta F, Vicedomini G, et al. Circumferential radiofrequency ablation of pulmonary vein ostia: a new anatomic approach for curing atrial fibrillation. Circulation 2000;102:2619-28. Swerdlow CD, Schsls W, Dijkman B, Jung W, Sheth NV, Olson WH, et al. Detection of atrial fibrillation and flutter by a dual-chamber implantable cardioverter-defibrillator. For the Worldwide Jewel AF Investigators. Circulation 2000;101:878-85. Physicians' desk reference. 56th ed. Montvale, N.J.: Medical Economics, 2002. Segal JB, McNamara RL, Miller MR, Kim N, Goodman SN, Powe NR, et al. The evidence regarding the drugs used for ventricular rate control. J Fam Pract 2000;49:47-59. Myerburg RJ, Kessler KM, Castellanos A. Recognition, clinical assessment, and management of arrhythmias and conduction disturbances. In: Alexander RW, Schlant RC, Fuster V, eds. Hurst's The heart, arteries and veins. 9th ed. New York: McGraw-Hill, Health Professions Division, 1998:873-942. O'Nunain S, Jennison S, Bashir Y, Garratt C, McKenna W, Camm AJ. Effects of adenosine on atrial repolarization in the transplanted human heart. Am J Cardiol 1993;71:248-51. Rinkenberger RL, Prystowsky EN, Heger JJ, Troup PJ, Jackman WM, Zipes DP. Effects of intravenous and chronic oral verapamil administration in patients with supraventricular tachyarrhythmias. Circulation 1980;62:996-1010. Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia: misdiagnosis and outcome after emergent therapy. Ann Intern Med 1986;104:766-71. Betriu A, Chaitman BR, Bourassa MG, Brevers G, Scholl JM, Bruneau P, et al. Beneficial effect of intravenous diltiazem in the acute management of paroxysmal supraventricular tachyarrhythmias. Circulation 1983;67:88-94. Morady F. Radio-frequency ablation as treatment for cardiac arrhythmias. N Engl J Med 1999;340:534-44. Bjornstad H, Storstein L, Meen HD, Hals O. Ambulatory electrocardiographic findings in top athletes, athletic students and control subjects. Cardiology 1994;84:42-50. Wu DL, Yeh SJ, Lin FC, Wang CC, Cherng WJ. Sinus automaticity and sinoatrial conduction in severe symptomatic sick sinus syndrome. J Am Coll Cardiol 1992;19:355-64. Haywood GA, Katritsis D, Ward J, Leigh-Jones M, Ward DE, Camm AJ. Atrial adaptive rate pacing in sick sinus syndrome: effects on exercise capacity and arrhythmias. Br Heart J 1993; 69:174-8. -------------------------------------------------------------------------------- Copyright © 2002 by the American Academy of Family Physicians. This content is owned by the AAFP. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP. Contact afpserv@aafp.org for copyright questions and/or permission requests.

Umm I graduate in May. Is there something wrong with my post? Please tell me why I should not come to PA?

I am disappointed, I only got $640. I was thinking it would be much higher.

Well this is very interesting on many different levels. First off how can anyone just say well I am doing this and if you do not want me too say so now because I am doing it, well that is just wrong. I always try to explain to my patients what I am about to do to them. I do not care what their GCS is I still explain, just for the reason it is professional and they are a HUMAN. I think it is sad when we stop treating people like they are humans. In my classes we are taught that if someone calls you for a stubbed toe take them and treat them like they have a million dollars. We got into this not for the money but to help people. I have been told that if you are only in this for the trauma or the "good" calls where people are near dead or what ever then you are in this for the wrong reason. I mean some places run anywhere from 1 to 12 calls a shift but it is what we went to school for, so that is my rant on that. I think that every patient should have the treatments explained to them no matter what the mental state is. As far as what to do to the pt it seems that we are damned if we do damned if we do not. One thing I did not notice was what a ECG showed, this can change things greatly. I would not give this patient adenocard just for the fact that I can not tell if it is A-fib or what ever. If I remember right it is a big no no to give adenocard to a patient in A-fib. Please correct me if I am wrong. I would start off with my ABC's and start either a NRB or explain that I am going to apply a BVM and assist his breathing. Again if I remember right you can assist ventilations on a consiouse patient, you just have to corridnate the breaths with them. Then I would figure out intubate or not to intubate. Yes the rate is a problem but we can think about two things at once, and if we ever get stumped ABC. As far as treating the rate I would run a ECG and try to figure out what is going on. I know there is a setting on the Lifepak 12 where you can speed the paper up making the tracing easier to interpret. I would for sure start a IV and NS tko for meds. I would start off with lasix if he could tolerate it, then MONA as long as the BP held up. As far as the rate I would let my ER doctor help me with that. I would call medical control and see what he wanted me to do. I do not know what protocols say about cardioverting but I would call the ER and let them know because there may be a better answer. Remember sometimes two heads or three heads are better than one. Plus if something happens I know have documentation that med control gave me the order. Takes some of the liability off me, which may be a good thing if the patient dies after you cardiovert them. I know one of my instructors said it looks bad if your patient has a pulse and loses it because of the treatment espicially if they could have made it to the ER with out the treatment. Remember ACLS guidelines are not set is stone they are just that GUIDELINES Yes if they need cardioverting then why waste the time in giving pain meds or versed. Who cares they needed it. Well if you put 100J or 360J through me, I think my BP and anxiety is going to go through the roof and if it did not work with the fisrt 100J and then you tell me you have to go higher hell no. That is why you explain stuff to your patient. And it may take a few mins for the meds to work but if you shock them while it is working they may know what you are doing right then, but they might not remember after the meds take affect. I have seen doctors give a med not wait for it to work and re-set a bone or what ever and the patient wakes up later not remembering. Why because the med had time to do its job. Ok enough with my rant and what I think. I am just a paramedic student that is all. I do not know anything but it is fun to pretend. LOL Sorry for any spelling mistakes.

These are good points to follow. I am a student and if I was ever caught sleeping or doing something I was not suppose to I know what will happen to me. Professionalism has been drilled into my head so much and what is expected of me that I would be ashamed of myself if I done anything that would embarrass my instructors or my school. I have seen many other students not be aggressive or lazy on a clinical and yes some from my school and it makes me mad. Like others have said we are there to learn and act like we are there on our real job. Oh and do not be LATE!!! I am sure that is something that will get you in big trouble.

I know you know who taught this. He is one of my favorite teachers.

I agree with this 100%. Why can we not put our egos to the side and take care of our patients like we went to school to do. I also live in oklahoma and it is starting to get scary for ems here. I think last year we had over 10 services close due to funding. The only problem I have with regional ems is the medical directors. I mean we have some that are awesome and that are more knowledgeable in ems and want to help ems forwards but have others that know nothing and would set us back and not let us think for ourselves.

In my PC III class we was taught to do this only if the patient was 50 and we felt and listened to the carotids. We was also not allowed to use SVT we had to tell the difference between atrial tachycardia and junctional tachycardia.

I understand that on some people we will not be able to get a IV. I have learned that there is always the neck to start a IV in. I know it is not the best place, but if you had to use it I am sure you would. I am a paramedic student and will graduate in may so take me with a grain of salt. I was taught that you need to get a med with out a IV. In my acls part of school if we gave nitro without a IV the patient crashed. It taught us to make sure we had our life net in place in case something happened. I mean what if you was to give nitro and they went hypotensive and that caused them to use more O2 due to the strain of having to fight to keep a BP. Now they are going to vasoconstrict I would think due to the fact that their brain is telling the body to do what it has to do to keep it alive. So now are you going to be able to get a IV? I think it would be harder to get a IV after the drop in pressure than before if it was going to happen. In todays worlds there is a ER very close unless you are in the sticks. Even then there are many sites to choose from. I hope that everyone is taught about EJ's, different sites on the hands and arms. Hell I have even started IVs in the foot on a patient in cardiac arrest. So trust me there has to be something that can be done to get a IV. I would hate to face a medical director or attorney because I did not have a IV before giving a med. I mean why would you give a med with out a way of treating the possible out comes good or bad.

Sorry for any spelling errors!!!! I am human I hope that a lot of people who are on here calling others names and thinking they are better than others look at the title of this thread. The senior members on this board so far have been very respectful of everyone and the ones with the hot heads are being unprofessional. Now how to fix the whole ems problems? Get young people who are willing to fight for better ems along with the older people of ems. We should stand together and make a difference in our profession. I go to the only national recognized paramedic school in oklahoma. It is not a easy road to get through by any means, but I chose the road. I could have picked a 11 month course or school with less standards but I am DAMN proud of what I am about to accoplish. I am not saying that others are not better or harder but come and see what we have to do to get our A.A.S. I have talked to other EMT students and they do not know near what I will know or my classmates. Hell some do not even know how to do a 12 lead which I find scary. Here is what I am tested on affectively Integrity,empathy, self motivation, appearance and personal hygiene, self confidence, communitcation, time management, teamwork and diplomacy, respect, patient advocacy, careful delivery of service. I have other student tell me that I have to do way to much stuff to get through medic school but I do not care. I like knowing that when I walk across that stage and get my degree that I have gotten probly the best education in the state. As far as the whole Volley thing goes, I will have to agree that they hurt the rest of us. I mean they pay everyother city offical there and probley pay them more than they are worth. Trust me if all the volleys stopped working and that mayor's wife ro kids got hurt the would find a way to have a ambulance. Why can they not make a deal with other towns and put stations between the towns? Or hell increase their water tax or something to make money for a ambulance. I think it is funny that there is no money for a ambulance but they will pay for joe blow to go to school to be a EMT B. There is no money for a ambulance but they can have picnics, parades, all the city officals they do not need, but do not want to pay for a ambulance. WTF What is wrong with our world. I got into EMS for one reason and that was to help people. I chose to be a medic so I could make the choice. I did not want to be that EMT I or EMT B that gets on these boards bashing the medic because "THEY" would have done it different. I mean get off your butts work a little harder to get through a good school and be a professional. Stop gripping about everyone else and take the steps to make your community a better place, not getting on here throwing stones at others because you community is in trouble. Brock

I have seen this one time. Me and my partner walking in a house on xmas day at noon for a person down. When we got there he was in full arrest and both daughters asked us no to do anything. We had already called them from the ambulance and asked them to call the family doctor since he did not have a DNR. The doctor they had called was being a prick and told us to transport him and let the ER doctor call him there. We looked confussed because this man wanted us to drive a dead man to ther ER so another doctor could call him. We both called our ER doctor told him what was going on and was like give me five mins and do not start treatment. He called us back and told us that he talked to the family doctor and that he was calling it over the phone. We chose to help the family out a little by taking him down the road to meet the funeral home. Seeing it was xmas day and we backed our vech to eachother it worked well. The family was greatful he did not have to stay in the floor and that we followed the wishes. The grandkids were there and I am sure it helped since they was all out of the house until we removed him.

I will have to agree, if he lost his paramedic stuff why not fire him from the firefighter position? I mean if he was to lazy or stupid to do his job right, how do they know he will on a fire scene where alot more people could be hurt or killed. Brock

Dang that is a lot too. We also have to take a comprehensive final and skills just like a mock National Registry test to graduate.

I was wondering what other people have to do to graduate. I am going to be graduating from a 2 year associate degree program in May, and we got a lot to do. As a matter of fact we have homework from our instructor for that semester. In order for us to graduate we have to do the following 1) 204 hours of clinicals 2) 10 page paper 3) 30 min speeches x 2 4) Go into the basic class and help teach class and lab 5) Community service project 6) two 12 hour gatekeeper shifts with paramedic 7) two 12 gatekeeper shifts with our medical director for program Now this is just for our last semester, each of the others had projects in them too. I have already got my topic for my paper so that is not to bad. This is also our Pals and PEPP training semester. So I was just wondering what other people have to do to graduate. Brock