medic429

:roll: are you kidding me?

just want to say "thank you" flight......could not have said it any better!

Background: Aortic stenosis (AS) is the obstruction of blood flow across the aortic valve. AS has several etiologies: congenital unicuspid or bicuspid valve, rheumatic fever, and degenerative calcific changes of the valve. Pathophysiology: When the aortic valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta. Stenotic aortic valves have a decreased aperture that leads to a progressive increase in left ventricular systolic pressure. This leads to pressure overload in the left ventricle, which, over time, causes an increase in ventricular wall thickness (ie, concentric hypertrophy). At this stage, the chamber is not dilated and ventricular function is preserved, although diastolic compliance may be affected. Eventually, however, the left ventricle dilates. This, coupled with a decrease in compliance, is associated with an increase in left ventricular end-diastolic pressure, which is increased further by a rise in atrial systolic pressure. A sustained pressure overload eventually leads to myocardial decompensation. The contractility of the myocardium diminishes, which leads to a decrease in cardiac output. The elevated left ventricular end-diastolic pressure causes a corresponding increase in pulmonary capillary arterial pressures and a decrease in ejection fraction and cardiac output. Ultimately, congestive heart failure (CHF) develops. Frequency: In the US: This is a relatively common congenital cardiac defect. Incidence is 4 in 1000 live births. Mortality/Morbidity: Sudden cardiac death occurs in 3-5% of patients with AS. Adults with AS have a 9% mortality rate per year. Once symptoms develop, the incidence of sudden death increases to 15-20%, with average survival duration of less than 5 years. Patients with exertional angina or syncope survive an average of 3 years. After the development of left ventricular failure, life expectancy is slightly greater than 1 year. Sex: Among children, 75% of cases of AS are in males. Age: AS usually is not detected until individuals are school aged. AS exists in up to 2% of those who are younger than 70 years. The etiology of AS in those aged 30-70 years can be rheumatic disease or calcification of a congenital bicuspid valve. In those older than 70 years, degenerative calcification is the primary cause of AS. Among people older than 75 years, 3% have critical AS. History: AS usually has an asymptomatic latent period of 10-20 years. Symptoms develop gradually. Ultimately, patients experience the classic triad of chest pain, heart failure, and syncope. Typical symptoms include the following: Palpitations Fatigue (may be an early symptom among children) Visual disturbances Gradual decrease in physical activity with insidious progression of fatigue and dyspnea on exertion Angina pectoris (30-40%) Patients may have a higher incidence of nitroglycerin-induced syncope than the general population. Always consider AS as a possible etiology for a patient in the ED with particular hemodynamic sensitivity to nitrates. Syncope during exertion: Proposed mechanisms include arrhythmias and left ventricular failure with an abrupt decline in cardiac output. Symptoms of left ventricular failure (eg, dyspnea on exertion, nocturnal cough, orthopnea, paroxysmal nocturnal dyspnea, hemoptysis) may occur. This is due to an elevation of the pulmonary capillary pressure from left ventricular dilation and reduced compliance. Physical: Palpation reveals a laterally displaced apex reflecting the presence of left ventricular hypertrophy. A systolic thrill may be palpable at the base of the heart, in the jugular notch, and along the carotid arteries. Crescendo-decrescendo systolic ejection murmur begins shortly after the first heart sound. The intensity increases toward midsystole, then decreases, and the murmur ends just before the second heart sound. It is generally a rough, low-pitched sound that is loudest at the base of the heart and most commonly is appreciated in the second right intercostal space. An ejection click may be auscultated. This is associated with bicuspid valves. An audible fourth heart sound indicates the presence of left ventricular hypertrophy in severe AS. Once the left ventricle dilates and fails, a third heart sound may be audible. Pulsus parvus et tardus: This is an arterial pulse with a delayed and plateaued peak, decreased amplitude, and gradual downslope. A high-pitched, diastolic blowing murmur may be present if the patient has associated aortic regurgitation. Causes: The ventricular pressure required to deliver a certain cardiac output at the required perfusion pressure is the pressure gradient across the valve in systole. This pressure gradient defines the degree of aortic valve obstruction. Newborns with significant AS develop CHF within the first week of life. The left ventricle is often too small to be compatible with life. The newborn heart develops left-to-right shunting through the patent foramen ovale, which leads to worsening CHF. Congenital AS caused by a congenital unicuspid or bicuspid aortic valve is usually asymptomatic in the otherwise healthy developing child. It often is diagnosed on routine physical examination, although a child may present with angina pectoris with exercise. As rheumatic fever decreases in frequency, so does rheumatic fever–induced AS. These patients have a fibrous contracture with shortening of the cusps due to recurrent inflammation from rheumatic carditis. Adjacent cusps tend to fuse at the commissures. This causes a form of acquired unicuspid or bicuspid aortic valve. Calcifications may develop, but the primary cause of stenosis is the adhesions that fuse the cusps. In patients older than 70 years, the most common cause of AS is degenerative calcification of the valve. Mönckeberg senile calcific AS occurs in elderly patients in whom all 3 cusps are highly calcified. Calcific AS also occurs in older patients with congenital or acquired bicuspid valves. Congenital bicuspid valves cause calcific AS 4 times more frequently than acquired forms do. Emergency Department Care: Prehospital and ED management is focused on acute exacerbations of the symptoms of AS. As always, assess and address airway, breathing, and circulation. If the patient is in cardiopulmonary arrest, perform resuscitation according to the recommendations of the American Heart Association in their Advanced Cardiac Life Support guidelines. A patient presenting with uncontrolled CHF should be treated supportively with oxygen, cardiac and oximetry monitoring, intravenous access, loop diuretics, nitrates (remembering the potential nitrate sensitivity of patients with AS), morphine (as needed and tolerated), and noninvasive or invasive ventilatory support (as indicated). Diagnostic studies in the ED should include ECG, chest radiograph, serum electrolytes, cardiac enzymes, CBC, and arterial blood gases (if hypoxemia or a mixed respiratory disease state is suspected). Emergency formal ultrasound may be useful in centers that have this capability. Vasodilators should be used judiciously in patients with AS, as they may cause a significant drop in blood pressure. Patients with heart failure due to AS that is resistant to medical management should be considered for emergent surgery. A patient presenting with angina pectoris requires monitoring and studies as listed above. Measures should be taken to relieve the chest discomfort. This may include administration of nitrates, oxygen, and morphine. Nitroglycerin-induced syncope occurs more often in patients with AS than in those without AS. This information should be obtained through the history at presentation. Syncope in the face of AS should be assessed and treated as in any patient presenting with a syncopal episode. A patient with AS may present initially with one or more of the above complaints. A thorough history and physical should be obtained in addition to baseline laboratory studies, a chest radiograph, and an ECG. Hospital admission, telemetry/intensive care unit admission, and cardiology consultation all should be considered. If available, an echocardiogram may be indicated in the ED. Atrial fibrillation in the setting of AS is considered a medical emergency and should be converted urgently in patients who are hemodynamically unstable. Associated symptoms also should be treated urgently. FROM eMedicine-http://www.emedicine.com/EMERG/topic40.htm How about Marfan Syndrome?

From Mayoclinic.com A grand mal seizure — also known as a tonic-clonic seizure — is a type of seizure characterized by loss of consciousness, falling down, loss of bowel or bladder control, and rhythmic convulsions. Seizures result from an abnormal electrical discharge in the brain. Other types of seizures include petit mal seizure and temporal lobe seizure. Repeated brain seizures characterize a seizure disorder known as epilepsy. Only a small percentage of people who experience at least a single seizure episode go on to develop epilepsy. The causes of seizures can vary. Often, the cause is unknown. Sometimes seizures run in families. Finding the underlying cause can help stop seizures. Petit mal seizure — also known as absence seizure — is a type of seizure that most often occurs in children. An abnormal electrical discharge in the brain causes seizures. Other types of seizures include grand mal seizure and temporal lobe seizure. Signs and Symptoms A typical grand mal seizure starts with a loss of consciousness and falling down. This is followed by a 15- to 20-second period with muscle rigidity (tonic phase) and then a one- to two-minute period of violent, rhythmic convulsions (clonic phase). During a grand mal seizure, you may take on a dusky appearance, resulting from decreased blood oxygen levels due to impaired breathing during the seizure. Most grand mal seizures last from 30 seconds to five minutes. After the seizure, you may experience a headache and drowsiness or confusion. Seizures often occur randomly, though in rare cases, stimulation by light, sound or touch can trigger a seizure in susceptible people. Sleep deprivation and excessive alcohol use also may trigger seizures. Sometimes the seizures involve only a few muscles, such as one side of the face or one arm or leg. This is called a focal seizure. Usually, a petit mal seizure involves only a brief, sudden lapse of conscious activity. Each seizure lasts only seconds or minutes, but hundreds may occur each day. During a petit mal seizure, small jerks sometimes occur involving the facial muscles or hands. A person who experiences a petit mal seizure can usually resume normal activities immediately after the seizure ends. Repeated seizures characterize a seizure disorder known as epilepsy. Only a small percentage of people who have seizures will develop epilepsy. Medications can be effective in eliminating or reducing the number of seizures. Signs and Symptoms In a typical petit mal seizure, a brief, sudden absence of consciousness may occur. There may not be any movement at all, only what appears to be staring. In other cases, a seizure may cause: Lip smacking Fluttering eyelids Chewing Hand movements Petit mal seizures last only a few seconds. Full recovery is almost instant. Afterward, there is no confusion, but also no memory of the incident. Petit mal seizures may occur for weeks or months before an adult notices them, because they're so brief. Also, they often occur when a child is sitting quietly and seldom during physical activity. Because these seizures come and go so quickly, a noticeable decline in a child's learning ability may be the first sign of this disorder. Teachers also may comment about a child's inability to pay attention. ****Respiratory Acidosis?*****

One that sticks in my mind happened while I was a Basic during a routine transfer. Picked up a patient from the hospital for discharge back to his nursing home. Found patient sitting on edge of bed. He had a stoma. Said the usual "hello sir, how are...blah, blah, blah". He had had a larygectomy years ago. Well, I kept bending down and putting my ear near his mouth so I could hear him better. After a few minutes, he gently tapped my shoulder and said to me "It's better if you look at my face when I'm talking, and anyone who's in my position. You may be able to read my lips if you miss something I'm trying to say." Lesson learned--thank you sir. This guy was great...even suctioned himself and everything. Just one of those patient's you remember. Finding out that this is also true in the opposite for people who are HOH. Instead of bending down and talking to the hearing aid like so many people do, a lot, though not all, of these people can read your lips if you look directly at them and talk slowly.

I'll take a stab at Fifth Disease, since both kids had it...my oldest while I was pregnant with my youngest :shock: Fifth disease is a virus and usually starts with a fever and general ill feeling. After a few days a bright red rash appears on the body and usually on the face. Fifth disease is usually seen and spread among young children. Once a child gets it, they usually build immunity and do not contract it again. Pregnant women need to be very careful with exposure to Fifth Disease. The virus can cause severe anemia in the fetus. Handwashing is of utmost importance. Called fifth because it's one of the five rash causing diseases...and the only one I can think of at one a.m. is measels! That's what I can remember. We'll stick with Rid's question: Cor Pulmonale

also... don't forget....it's usually the BEST answer, not the RIGHT answer they are looking for and don't read into the question that is posed! good luck

:shock: what was the question?

Strippel! like marty said...thank god it was only paint balls!! be safe,

PRPG!! I hear you....HUGE pet peeve!!!

=D> =D> very well said....

OK...can someone enlighten me--maybe I missed something...does anyone know if these protocols that have been quoted are actually for BLS PROVIDERS?? I did not check out all the links, and maybe I did miss something...but on the one page I did see I don't remeber seeing it stated that these were BLS protocols!! and if it was there, i apologize for missing it...my head felt a little :offtheair: half way thorough this thread..... ugh.

:glasses7: heading to the pool...but for now.....my turn!!

:boxing: just 5 minutes...that's all i want!!

:tongue: my turn!!

THAT was funny

personally--i wear one. i don't feel they are heavy or hurt my neck. and yes, i agree....why a seatbelt and no helmet?? however, it is a choice here and some choose not to. i guess it's a lot of the "it would never happen to me, i'm a safe rider" thing.....

I agree with Race. I'd probably ride it in. I too would want a finger stick and monitor. And I'd try to get a little more out of her...is it true vertigo or is she lightheaded? Any recent head trauma? What was she doing when the "dizziness" occurred? Any other info??

Regardless of the "bashing", the holier than thou attitudes, etc......my question is this..... why in the he!! do people take things so seriously?? If you have a question about a call or treatment , etc...there are a lot of very very bright and talented people here that are more than happy to answer any questions, give you food for thought, etc......and remember -- you asked!! SO WHAT if they want you to not type in caps, or use spell check (which...I agree with) and all the other little things that get said..... I cannot understand why people feel they need their hands held all the time......if someone disagrees on here, they tell you--and I for one appreciate the honesty.....if you don't like what someone has to say.... move on...and don't give it another thought......I have seen plenty of posts that have been very 'nice' when people needed a "'atta boy"...... Of course, it's just my opinion....and I doubt that I'm alone. Maybe I didn't really answer the question posed...and like I said...just my opinion.

agree with the above posters...

WOW! I agree that this isn't so much about intubating as it is a WAKE UP about documentation! I too was told over and over, if "you don't write it, you didn't do it" and the opposite of that, if you write it, you better have done it. Definitley an eye opener.....

AK, I agree with what you're saying. Yes, we want to get paid, no we shouldn't be free. BUT, when you go to a hospital, doctor's office, etc. it's not the person treating you that's asking the insurance questions...it's the registrar or secretary or clerk whatever....that's where I have a problem....not even a 'problem' per se, I just don't do it.

I gave my number to a banana because that's how i roll! 8) ACK!

If you HAVE to do it, then DSmitty's response is a good one.... I have a problem with having to ask anyone if they have insurance....we usually get a financial sheet from the hospitals once the patient is registered.....if we don't, and we bill the patient, we attach a card they fill out and send back with that info. Maybe there is a better billing program out there....... I don't know....just a pet peeve of mine.... good luck!

I got the scoop from my boss who attended the debate between Dr. Wang and one of our Command docs....here's the deal, as I understood -- Dr. Wang's study was strictly on trauma patients...no medical ETI's. How about the medical pt's that get intubated?? The debate was very good, and it was packed. NO ONE disagrred that we need more practice...but is the OR really the place to do it?? How often do we get to intubate with a patient paralized, in bright white lights, lying in a perfect position on a nice hard table?? Our command doc. had pictures of where hospital personell get to intubate versus where we get to intubate (ER versus dark street-seeing as the study was on trauma patients) How about the dark narrow hallways, or the cramped bathrooms...and even the back of an ambulance?? A LOT different than a hospital. The debate went on for about an hour and a half with a Q & A session afterward. Dr. Wang himself said he does a "handful" of ETI's a year.....a handful! But he did say he supervises 300......hmmmmmmm........ I have a problem with just yanking the skill......I'd feel better about the entire Dr. Wang issue if he would have a plan in mind to correct the problem, not just say we shouldn't do it. If I can get the audio CD I'll let you know, if anyone would be interested.