If this is your first visit, be sure to check out the FAQ by clicking the link above. You may have to register before you can post: click the register link above to proceed. To start viewing messages, select the forum that you want to visit from the selection below. |
|
|
Thread Tools | Display Modes |
#151
|
|||
|
|||
Dentist uses Nitrous Oxide?
V35B writes:
Nitrous Oxide is not potent enough to induce a state of general anesthesia ... That's one of the reasons why it is dangerous for that purpose. Still, it is a general anesthetic in its mechanism of action (i.e., it's not a local anesthetic by any means). General anesthetics require greater caution than local anesthetics. -- Transpose hotmail and mxsmanic in my e-mail address to reach me directly. |
#152
|
|||
|
|||
Dentist uses Nitrous Oxide?
Your logic is incorrect. I am a professor of pharmacology at a Pharmacy
School. That's one of the reasons why it is dangerous for that purpose. It is not dangerous, you cannot be rendered unoncious with it. How can it be dangerous? General anesthetics require greater caution than local anesthetics. You cannot compare the two in this way. They are different classes of drugs that are used for different purposes.... |
#153
|
|||
|
|||
Dentist uses Nitrous Oxide?
There have been accidental deaths from N2O.
One hospital case happened where the plumbers couldn't figure out the mismatched pipe sizes and cut them off and incorrectly rematched them. **The mismatch PREVENTS people from mixing up the hoses ~ normally it is impossible to crank up the N2O/O2 ratio past 80/20. The 20% O2 is required for life. After the plumbers did their work the tragedy happened. The docs thought there were on 100% O2 but it was really 100% N2O. Tragic. Joel On Fri, 19 Sep 2003 13:43:27 +0200, Mxsmanic wrote: V35B writes: Nitrous Oxide is not potent enough to induce a state of general anesthesia ... That's one of the reasons why it is dangerous for that purpose. Still, it is a general anesthetic in its mechanism of action (i.e., it's not a local anesthetic by any means). General anesthetics require greater caution than local anesthetics. -- Joel M. Eichen, . Philadelphia PA STANDARD DISCLAIMER applies: You fill it in |
#154
|
|||
|
|||
Dentist uses Nitrous Oxide?
Please see my post above about mismatching hoses .....
Joel' On Fri, 19 Sep 2003 12:09:57 GMT, "V35B" wrote: Your logic is incorrect. I am a professor of pharmacology at a Pharmacy School. That's one of the reasons why it is dangerous for that purpose. It is not dangerous, you cannot be rendered unoncious with it. How can it be dangerous? General anesthetics require greater caution than local anesthetics. You cannot compare the two in this way. They are different classes of drugs that are used for different purposes.... -- Joel M. Eichen, . Philadelphia PA STANDARD DISCLAIMER applies: You fill it in |
#155
|
|||
|
|||
Dentist uses Nitrous Oxide?
We agree .......
........say ....... WAIT! Mothers' milk in IV lines ........ isn't that a new treatment for removing amalgam from your bloodstream? I gotta check with that erstwhile nursery school teacher, Miss Jan Drew! I'll be back later ........ right now she is Line Dancing in the park ....... Joel On Fri, 19 Sep 2003 13:02:00 GMT, "V35B" wrote: Of course if you place mothers milk in an IV line it can kill you too. The point is N20 is arguably safer than local anesthetics, when used within its therapeutic realm. No chance of anaphylactic hypersensitivity reaction... etc. The point also is that the two are not interchangable... "Joel M. Eichen D.D.S." wrote in message .. . There have been accidental deaths from N2O. One hospital case happened where the plumbers couldn't figure out the mismatched pipe sizes and cut them off and incorrectly rematched them. **The mismatch PREVENTS people from mixing up the hoses ~ normally it is impossible to crank up the N2O/O2 ratio past 80/20. The 20% O2 is required for life. After the plumbers did their work the tragedy happened. The docs thought there were on 100% O2 but it was really 100% N2O. Tragic. Joel On Fri, 19 Sep 2003 13:43:27 +0200, Mxsmanic wrote: V35B writes: Nitrous Oxide is not potent enough to induce a state of general anesthesia ... That's one of the reasons why it is dangerous for that purpose. Still, it is a general anesthetic in its mechanism of action (i.e., it's not a local anesthetic by any means). General anesthetics require greater caution than local anesthetics. -- Joel M. Eichen, . Philadelphia PA STANDARD DISCLAIMER applies: You fill it in -- Joel M. Eichen, . Philadelphia PA STANDARD DISCLAIMER applies: You fill it in |
#156
|
|||
|
|||
Dentist uses Nitrous Oxide?
Of course if you place mothers milk in an IV line it can kill you too. The
point is N20 is arguably safer than local anesthetics, when used within its therapeutic realm. No chance of anaphylactic hypersensitivity reaction... etc. The point also is that the two are not interchangable... "Joel M. Eichen D.D.S." wrote in message ... There have been accidental deaths from N2O. One hospital case happened where the plumbers couldn't figure out the mismatched pipe sizes and cut them off and incorrectly rematched them. **The mismatch PREVENTS people from mixing up the hoses ~ normally it is impossible to crank up the N2O/O2 ratio past 80/20. The 20% O2 is required for life. After the plumbers did their work the tragedy happened. The docs thought there were on 100% O2 but it was really 100% N2O. Tragic. Joel On Fri, 19 Sep 2003 13:43:27 +0200, Mxsmanic wrote: V35B writes: Nitrous Oxide is not potent enough to induce a state of general anesthesia ... That's one of the reasons why it is dangerous for that purpose. Still, it is a general anesthetic in its mechanism of action (i.e., it's not a local anesthetic by any means). General anesthetics require greater caution than local anesthetics. -- Joel M. Eichen, . Philadelphia PA STANDARD DISCLAIMER applies: You fill it in |
#157
|
|||
|
|||
Allergy to epinephine - (?)
While we got you here .........
Some people claim they are "allergic" to epinephrine. Of course we know that the problem when epinephrine/local anesthetic (1:100,000 or 1:50,000) is accidentally injected into a vein it is vasovagal sympathomimetic reaction, not anaphylactic or allergic reaction. I say that it is impossible for someone to be "allergic" to epinephrine. What do you say? Joel PS- Here is a checklist for laymen who want to learn more ...... EM guidemap - Syncope Click on any of the headings or sub-headings to rapidly navigate to the relevant section of the guidemap Introduction and general principles History of present illness clinical clue table Risk factors for syncope Examination Diagnostic testing Cardiac monitoring EKG Pulse oximetry Blood testing Carotid massage Orthostatic vital signs Echocardiography Exercise stress testing Signal-averaged electrocardiography Intracardiac electrophysiologic studies Neurological testing Medical decision-making Indications for admission Continuous ambulatory electrocardiographic monitoring Long-term event and memory loop recorders Implantable loop recorders Tilt table testing Psychiatric evaluation Appendix Causes of syncope table differentiating syncope from seizure suggested algorithm for workup of syncope Introduction and general principles - syncope is defined as a transient loss of consciousness associated with a loss of postural tone, and most diseases causing syncope produce a transient LOC by temporarily decreasing cerebral blood flow An emergency physician, when faced with a syncope-patient in an ED setting, should first seek to exclude life-threatening causes of syncope, which require immediate diagnostic evaluation/treatment + hospital admission AMI PE aortic dissection cardiac tamponade tension pneumothorax leaking AAA active internal bleeding malignant cardiac arrhythmias ectopic pregnancy SAH carotid artery/vertebral artery dissection air embolism If there are no overt life-threatening causes of syncope, then an emergency physician should attempt to identify patients with situational syncope, vasovagal syncope and benign orthostatic (postural) syncope - who are candidates for home discharge after any necessary stabilization treatment in the ED - young patients ( 45 years), who have a history of a short-lived syncopal episode with no other associated ongoing symptoms, rarely have serious causes of syncope if the syncope did not occur during exertion, and hospital admission and/or an extensive workup is rarely necessary - emergency physicians are often faced with the dilemma that the cause of the syncope is not immediately apparent after a brief clinical examination, and a decision has to be made whether it is necessary to admit the patient to hospital If the cause of the syncope is not readily apparent after initial clinical evaluation in the ED, then an emergency physician should attempt to decide whether certain categories of syncope-patients require admission to hospital - examples of syncope patients warranting hospitalization include:- elderly patients 60 years with no apparent cause of the syncope sudden syncope occurring in a non-erect patient with no premonitory symptoms or prodrome sudden syncope occurring during exertion sudden syncope in a patient with a family history of syncope or sudden death patient has overt evidence of structural heart disease by history or examination patient has an abnormal ECG (* see the medical decision-making section for further details) - there is no universally accepted approach to the further inpatient/outpatient workup of patients, whose cause of syncope is not readily apparent = a suggested algorithm is included in the appendix section as a general guide History of the present illness - critical historical elements include the mode of onset and progression of event, body position at onset of event, the depth of altered consciousness, the duration of the syncopal episode and the rate of recovery of consciousness (* by paying close attention to the details, an emergency physician should be able to differentiate syncope from seizures, non-specific near-syncopal events, non-specific ligheadedness and dysequilibrium syndromes) - sudden unheralded syncope at rest, particularly in a non-erect posture, is ominous - especially if significant injury results = suggests a cardiac arrhythmia - associated palpitations or an irregular heart beat suggests cardiac syncope secondary to a cardiac arrhythmia - certain antecedent symptoms lasting 10 seconds (darkening vision or tunnel vision or graying vision, lightheadedness, swaying sensation, nausea, sweating, feeling "hot", face and distal limb numbness), especially if preceded by a provocative emotional event and occurring in an upright position suggest vaso-vagal syncope (also called vasodepressor or reflex or neurocardiogenic syncope) (* vasovagal syncope is also more likely to happen in overcrowded social settings where prolonged mandatory standing is a requirement eg. church, military parades in hot weather) - antecedent/accompanying chest pain (AMI or PE) or abdominal pain (ectopic pregnancy) or back pain (ruptured abdominal aortic aneurysm or dissecting aortic aneurysm) or headache (SAH) suggests serious pathology - prominent antecedent/accompanying dyspnea suggests hyperventilation syndrome, pulmonary embolism or pulmonary hypertension - accompanying brainstem symptoms (diplopia or blurred vision, dysarthria, dysphagia, deafness, vertigo, ataxia, limb weakness or hypoesthesia, face pain or hypoesthesia) suggest vertebro-basilar artery insufficiency or basilar artery migraine - the patient’s posture at the time of syncope is very important – sudden syncope in a non-erect position signifies serious pathology , while lightheadedness for 30 - 60 seconds after suddenly standing/walking and immediately preceding the syncopal episode suggests underlying orthostatic hypotensive syndromes (autonomic neuropathy and/or volume depletion and/or drug-induced vasodilatation) - sudden syncope related to turning or hyperextending the head (eg. when shaving or while wearing tight constricting neckwear) suggests carotid sinus syncope - sudden syncope during strenuous physical activity (exertional syncope ) suggests potentially serious pathology (HOCM or aortic stenosis, or atrial myxoma or anomalous coronary artery; or a malignant arrhythmia eg. torsade des pointes and VT) - pscyhological triggering events (painful stimuli, sudden bad news) suggest vasovagal syncope (* however sudden stress/excitement in patients with long QT syndrome can trigger torsades des pointes) - evidence of volume loss may precede syncope (vomiting, diarrhea) or accompany syncope (hematemesis or melena) - syncope related to strenuous unilateral upper arm activity suggests subclavian steal syndrome - situational syncope is self-diagnostic - cough syncope, micturition syncope, defecation syncope, hair-grooming syncope, adolescent stretch syncope, deglutition (swallow) syncope, glossopharyngeal syncope and "weight-lifter blackouts" - antecedent "glue-sniffing" or "huffing" suggests a ventricular arrhythmia and/or hypoxia as the cause of the syncope; sympathomimetic drug abuse (cocaine or amphetamines) suggest a tachyarhythmia - recurrent bouts of progressive gradual loss of consciousness over several minutes while walking or standing + NO sweating + NO pallor + fixed heart rate suggest chronic dysautonomic syncope (* patients often also have a history of hypohidrosis, impotence, blurred vision, urinary difficulties, constipation, nocturnal polyuria and " coat-hanger" pain [neck and shoulders ache - present only when standing]) - recent meal ingestion in an elderly patient may suggest post-prandial hypotensive syncope - short-lived myoclonic seizures or twitching are compatible with convulsive syncope, and do not imply a true seizure (* a true seizure is more likely if an aura and/or convulsions precede the fall, tongue biting and/or urinary incontinence occurs, convulsions are generalized and last longer than 30 seconds, prolonged post-ictal confusion-lethargy occurs = see the table in the appendix section for further details) Clinical clue table Clinical clue Suggests Sudden syncope at rest when non-erect Cardiac arrhythmia, atrial myxoma Sudden syncope on exertion Aortic stenosis, HOCM, atrial myxoma, malignant cardiac arrhythmia Preceding "lightheadness" prodrome when erect Vasovagal syncope, orthostatic hypotension Preceding palpitations Cardiac arrhythmia Preceding or accompanying dyspnea Pulmonary embolism, tension pneumothorax, cardiac tamponade, air embolism Preceding or accompanying chest pain AMI, PE, cardiac tamponade, dissecting aneurysm, tension pneumothorax, mitral valve prolapse Preceding or accompanying back pain Dissecting aortic aneurysm, leaking AAA Preceding or accompanying abdominal pain Leaking AAA, ectopic pregnancy Occurring when turning head to side, or looking up Carotid sinus syncope Occurring when exercising upper arm Subclavian steal syndrome Occurring during (or immediately after) coughing, laughing, vomiting, swallowing, urination, defecation, combing hair, stretching Situational syncope Occurring after prolonged standing Vasovagal syncope Occurring after emotional upset Vasovagal syncope, prolonged QT interval and torsade Recent illicit drug use Cardiac arrhythmia, air or foreign body embolism Recent sudden headache SAH Recent neurological symptoms Brain stem stroke, vertebro-basilar artery insufficiency, basilar migraine, carotid or vertebral artery dissection, dissecting aortic aneurysm Recent vaginal insufflation Air embolism Recent black stools GI bleed Recent fluid loss (diarrhea, vomiting, sweating) Orthostatic hypotension, Addisonian crisis Recent meal Postprandial hypotensive syncope Polypharmacy, recent sialdenafil use Orthostatic syncope History of fever or myalgia or arthalgia or rash Atrial myxoma, cardiac tamponade History of known cardiac ischemia or structural heart disease Cardiac arrhythmia, pro-arrhythmia drug effect, valve dysfunction History of mechanical heart valve Thrombosis of valve Recent history of cancer, prolonged immobilization, leg injury or surgery Pulmonary embolism History of autonomic dysfunction (impotence, anhydrosis, sphincter dysfunction) Orthostatic hypotension secondary to autonomic neuropathy History of recurrent syncope Cardiac arrhythmia, carotid sinus syncope, atrial myxoma, aortic stenosis, subclavian steal syndrome, prolonged QT interval - torsade Family history of syncope or sudden death HOCM, prolonged QT syndrome Pacemaker Pacemaker failure Risk factors for syncope Underlying causes of orthostatic hypotension - volume depletion (vomiting, diarrhea, excessive perspiration, diuretic use) - blood loss - adrenal insufficiency - primary or secondary dysautonomias (multiple sclerosis, Guillane-Barre syndrome, spinal cord injury, tabes dorsalis, Parkinsonism, Shy-Drager syndrome, diabetic autonomic neuropathy) - peripheral neuropathy (chronic alcoholism, diabetes) - polypharmacy in elderly patients with impaired baroreceptor reflexes - prolonged recumbency and secondary "cardiac-deconditioning" Drugs predisposing to syncope - vasodilators (alpha blockers, beta blockers, ACEI’s, calcium channel blockers, nitrates, phenothiazines) - cardio-inhibitor drugs (beta blockers, digoxin) - psycho-active drugs (anti-convulsants, CNS sedative-depressants, anti-histamines, anti-depressants, anti-psychotics) Conditions predisposing to a prolonged QT interval and torsade des pointes Acquired causes Enviromental and endocrinological causes Medicinal and toxicological causes Congenital causes Neurological causes Ischemic coronary artery disease Hypothermia Class 1A antidysrhythmics - quinidine, procainamide, disopyramide Jervell-Lange-Nielsen syndrome Subarachnoid hemorrhage Congestive heart failure Bulemia, stringent dieting Class 1C antidysrhythmics - flecainide, encainide Romano-Ward sydrome Cerebrovascular occlusive disease Rheumatic heart disease Hypothyroidism Phenothiazine overdose Refsum syndrome Traumatic brain injury Myocarditis Hypokalemia Butyrophenone overdose Mitral valve prolapse Encephalitis Hypocalcemia Tetracyclic/tricyclic antidepressant overdose Hypomagnesemia Organophosphate overdose Macrolide antibiotics + terfenadine or astemizole or cisapride Azole antigungals + terfenadine or astemizole or cisapride Examination - a selective examination can offer clinical clues as to the etiology of the syncope Blood pressure - difference in blood pressure between left and right upper limbs 20mmHg is abnormal (suggests dissecting aortic aneurysm or subclavian steal syndrome) - difference in blood pressure between upper and lower limbs 20mmHg when recumbent is abnormal (suggests a dissecting aortic aneurysm) Pulse volume - decreased and delayed upstoke (aortic stenosis/hypertrophic obstructive cardiomyopathy) - positive pulsus paradoxus (cardiac tamponade, massive pulmonary embolism) - absent pulses (dissection of the aorta, cardiac emboli) Neck bruits - suggests great artery stenosis eg. subclavian steal syndrome or carotid artery dissection Jugular venous pressure - increased in heart failure or pulmonary embolism or cardiac tamponade (positive Kussmaul’s sign) - 'cannon' a waves suggests AV conduction block Apex beat - displaced and forceful (LVH), forceful (RVH) Heart sounds - decreased (pericardial tamponade) - 3rd/4th heart sounds (ventricular failure or LV overload) - loud second heart sound (pulmonary embolism or pulmonary hypertension) - ejection systolic murmurs (aortic stenosis or hypertrophic cardiomyopathy - increased murmur when standing, decreased when squatting) - machinary murmur (air embolism) - "tumor plop" or diastolic murmur (atrial myxoma) - varying heart sounds/murmurs (thrombotic occlusion of a prosthetic valve) Abdomen - pulsatile masses (abdominal aneurysm) - rectal exam for melena or heme-occult positive stools (gastro-intestinal bleeding) - absent/decreased femoral pulses (dissection of the aorta) Neuro exam - signs of vertebro-basilar artery TIA/CVA or neuropathy or myelopathy Diagnostic testing Cardiac monitoring - immediate and continuous monitoring during the ED evaluation period is highly recommended - arrhythmias may be etiologically significant (* no study has determined the ideal duration of ED cardiac monitoring ECG - an abnormal ECG may be etiologically significant, although the 'definitive' diagnostic yield is low ( 5%) - ECG abnormalities include:- previous or acute cardiac ischemic changes signs of pericarditis or electrical alternans (cardiac tamponade) LVH (hypertension, aortic stenosis, HOCM) RVH (PE or pulmonary hypertension) classical/non-specific ECG signs of PE WPW syndrome LBBB or bifasicular block (conducting system disease) bradyarrythmias or tachyarrhythmias long QT interval Brugada syndrome (partial RBBB with elevated ST segments in leads V1-3 and peculiar downsloping of the elevated ST segments + inverted T waves in those leads) arrhythmogenic right ventricular dysplasia (RBBB, QRS complex 110 msec in leads V 1-3, inverted T wave or epislon wave Pulse oximetry - a low reading may suggest a possible etiology (cyanotic congenital heart disease, pulmonary embolism, pulmonary hypertension Blood testing - not generally useful - Hb/Hct helpful in establishing baseline in bleeding patients - glucose and electrolytes have no/little utility (* hyponatremia + hyperkalemia may rarely suggest Addison's disease; hypoglycemnia rarely produces syncope without ongoing symptoms of hypoglycemia) - serum HCG rarely helpful in reproductive age female patients (* very rare patient with an ectopic pregnancy presenting as syncope without any abdominal pain/vaginal bleeding) Carotid sinus massage - may be useful in diagnosing carotid sinus syncope in elderly patients - first performed on the right side for a minimum of 5 seconds (preferably 15 seconds) = measure pulse rate and blood pressure = wait 120 seconds = repeat test on the left side - positive response = longer than 3 seconds of asystole, and/or systolic blood pressure drop of 50 mmHg when supine - borderline positive response = slowing of heart rate 30 - 40% and/or systolic blood pressure drop of 30mmHg when supine - 90% of positive-test patients have the cardio-inhibitory or combined response, while only 10% have the vaso-depressor response - up to 10% of elderly patients have carotid sinus hypersensitivity to some degree, however only 5 - 20% of these patients have carotid sinus syndrome (carotid sinus syncope etiologically related to carotid artery hypersensitivity) - carotid sinus syncope can only be definitively diagnosed when syncope or near-syncope occurs during carotid massage (* carotid sinus massage is contra-indicated in patients with a history of a CVA, a recent AMI or when a neck bruit is present Orthostatic vital signs - the patient should be recumbent for at least 5 minutes prior to performing the test and the patient should stand for at least 2 minutes - a positive test is defined as a systolic blood pressure decrease of 20 - 30mmHg, a diastolic decrease of 10 - 15mmHg and/or heart rate increase of greater than 30 bpm when standing - the test is non-dependable, often inconsistent and has a low specificity - a significant drop in blood pressure + fixed heart rate suggests dysautonomia - a significant drop in blood pressure + increased heart rate suggests volume depletion and/or excessive vasodilatation - an insignificant drop in blood pressure + marked increase in heart rate suggests postural tachycardia syndrome, which is a heterogenous entity (history of frequent fainting, symptoms of autonomic overactivity - palpitations, diaphoresis, tremulousness, visual blurring, non-anginal chest pain, "spaced-out" feelings, inability to concentrate, inability to breathe, sensations of impending doom) Echocardiography - diagnostic yield low in the absence of historical or physical signs of organic heart disease - only definitely indicated in patients with exertion-related syncope, in all patients who have a prosthetic heart valve, or when the clinical suspicion of organic heart disease is high (eg. strong clinical suspicion of obstructive cardiac lesions - HOCM, AS or atrial myxoma) -some conservative physicians believe that organic heart disease cannot be fully excluded prior to performing echocardiography (unsuspected findings are found in 5 - 10% of unselected patients) and that echocardiograph should routinely be performed in all patients, or definitely in patients 50 years Exercise-stress testing - indicated for patients with exertion-related syncope or suspected CAD - should always be preceded by echocardiography to first rule-out cardiac obstructive pathology eg. HOCM, aortic stenosis, atrial myxoma Signal-averaged electrocardiography - not usually helpful with many false-positives - may be useful in selecting patients for electrophysiological studies when CAD is present and secondary VT suspected Intracardiac electrophysiologic studies - expensive, invasive and with low yield - not indicated in patients with clinically normal hearts and a normal ECG - most useful in patients with known organic heart disease (patients with a history of a MI or CHF - especially if the ejection fraction 40%) and/or an abnormal ECG - usefulness is mainly based on the ability of EPS testing to induce malignant arrhythmias eg. sustained monomorphic ventricular tachycardia - induction of non-sustained VT, polymorphic VT and VF during testing is of no/uncertain clinical usefulness - less useful for detecting bradyarrhythmias - sinus node recovery time 3 seconds may reflect sinus node disease requiring a pacemaker - an HV interval exceeding 100 msec or infranodal block induced by pacing suggest AV nodal disease and a bradycarrhythmic cause of the syncope Neurological testing - EEG, CT scan, transcranial/carotid Dopplers - not indicated unless there is substantial reason to suspect a seizure or other significant neuropathology Medical decision-making An overriding concern and uncertainty about what may happen to the patient in the near future may cause an emergency physician to unnecessarily admit too many patients Patients who can clearly be discharged include those with a classical presentation of vasovagal syncope (irrespective of age), those with situational syncope, those with mild, reversible orthostatic syncope (including polypharmacy syndrome in the elderly patient) and patients with hysterical conversion syncope Indications for admission of patients presenting with syncope include: new clinical evidence of structural heart disease significant antecedent/associated chest pain or ECG evidence of cardiac ischemia history of previous CHF or myocardial ischemia history of a previous malignant arrhythmia sudden syncope preceded by and/or associated with palpitations or an irregular heart beat significant malignant arrhythmia detected in the ED high-grade conduction block or high-grade carotid sinus syncope sudden onset syncope without premonitory symptoms, especially if occurring when non-erect and associated with injury exercise-induced syncope (irrespective of age) syncope associated with moderate/severe orthostatic hypotension resistant to ED treatment or due to life-threatening pathology eg. ectopic pregnancy syncope associated with any significant neurological symptoms/signs syncope suggestive of pulmonary embolism or pulmonary hypertension strong family history of sudden syncope/sudden death syncope in a patient with an abnormal ECG - long QT interval or Brugada syndrome or WPW syndrome age 60 years with no evidence of vasovagal syncope or readily reversible chronic-or-benign orthostatic causes syncope due to cardiac tamponade or active internal bleeding patient taking pro-arrhythmia medications that may potentially cause malignant arrhythmias eg. quinidine, sotalol, amiodarone ACEP task force recommendations for admission include: Admit patients with syncope and any of the following: 1. A history of congestive heart failure or ventricular arrhythmias 2. Associated chest pain or other symptoms compatible with acute coronary syndrome 3. Evidence of significant congestive heart failure or valvular heart disease on physical examination 4. ECG findings of ischemia, arrhythmia, prolonged QT interval, or bundle branch block Consider admission for patients with syncope and any of the following: 1. Age older than 60 years 2. History of coronary artery disease or congenital heart disease 3. Family history of unexpected sudden death 4. Exertional syncope in younger patients without an obvious benign etiology for the syncope 24-hour Holter (continuous ambulatory electrocardiographic) monitoring - traditional approach to syncope of unknown etiology with low yield - 4% true positives (symptoms correlate with arrhythmia) and 15% false positives (symptoms without any arrhythmia); 14% of patients have an asymptomatic arrhythmia which may suggest a cause for the syncope (sinus pauses, non-sustained VT, Mobitz type II block) - extending the continuous ambulatory electrocardiograhic monitoring to 72 hours results in a slightly higher yield - if no symptoms/arrhythmias are detected, arrhythmogenic syncope cannot be excluded = further testing is required for patients with recurrent syncope, or if there is a strong clinical suspicion of malignant cardiac arrythmias eg. known severe structural heart disease +/- history of recurrent palpitations Long-term event and memory loop recorders - provide continuous ambulatory electrocardiographic recordings for prolonged periods (weeks) - useful for patients who have recurrent syncope ( 1x/4 weeks) Implantable loop recoders - latest development based on a loop-based memory system capable of providing continuous ambulatory electrocardiographic recording for up to 18 months - indicated for patients with recurrent syncope with no definite organic heart disease Tilt table testing - used to confirm neurocardiogenic syncope in a patient, who does not have a classical history of vaso-vagal (vasodepressor) syncope; has also been useful in diagnosing neurally-mediated syncope, which manifests as post-exertional syncope - used to investigate recurrent syncope in elderly patients with probable autonomic neuropathy - some cardiologists reserve tilt testing for patients with unexplained, recurrent syncope in whom cardiac causes of syncope, including arrhythmias, have been excluded by echocardiography and Holter monitoring and EPS testing - can also be used to differentiate convulsive syncope from true seizures Psychiatric evaluation - may be indicated in young patients who faint frequently for no apparent reason, especially when symptoms are suggestive of postural tachycardia syndrome Appendix Causes of syncope Vasomotor/vascular Hypovolemia dehydration fluid loss "third" spacing osmotic/iatrogenic diuresis Hemorrhage ruptured abdominal aortic aneurysm ectopic pregnancy GIT bleeding trauma-induced Vasomotor insufficiency Postural orthostasis Vasodepressor (vaso-vagal) syncope Glossopharyngeal neuralgia Trigeminal neuralgia Autonomic/peripheral neuropathy Subclavian steal syndrome Anaphylactic shock Cardiac Dysrhythmias tachyarrhythmias bradyarrhythmias Carotid sinus hypersensitivity Pacemaker malfunction Myocardial ischemia Dissection of the aorta Mechanical outflow obstruction or venous return impedance aortic stenosis hypertrophic obstructive cardiomyopathy pulmonary stenosis pulmonary embolus primary pulmonary hypertension atrial myxoma prosthetic valve malfunction/thrombosis pericardial tamponade tricuspid stenosis mitral stenosis retrictive cardiomyopathy tension pneumothorax Congenital heart disease anomalous origin of the left coronary artery Eisenmenger's syndrome Tetralogy of Fallot Situational cough (post-tussive) micturition defecation swallowing postprandial weight-lifters adolescent stretch hair grooming trumpet player's Metabolic "hypoglycemia" addisonian crises pheochromocytoma hypothyroidism Central nervous system subarachnoid hemorrhage "seizures" basilar migraine posterior circulation TIA's vertebral artery dissection carotid artery dissection Miscellaneous air embolism amniotic fluid embolism foreign body embolism asphyxia/hypoxia carbon monoxide poisoning breath-holding attacks hyperventilation syndrome conversion disorder pro-arrhythmic drugs polypharmacy "glue sniffing or huffing" postural tachycardia syndrome Differentiating syncope from seizure Feature Syncope Seizure Aura Absent Rarely present Antecedent "dizziness-prodrome" prior to event Sometimes present Absent Color at onset of event Sometimes pale Sometimes florid/purple Jerking movements Infrequent and short-lived (seconds) Common and longer-lasting (minutes) Pattern of convulsions Uncoordinated myoclonic jerks and twitches - after LOC Generalized tonic and/or clonic movements - coincident with LOC Upturning of eyes Common Uncommon Forced conjugate deviation of eyes Absent Common Tongue biting - lateral Absent Common Urinary incontinence Rare Common Duration of event Seconds Minutes Prolonged disorientation or sleepiness after event Absent-rare Present-common Increase in CK enzyme or lactate Absent Present Suggested algorithm for workup of syncope Disclaimer : My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use. On Fri, 19 Sep 2003 13:02:00 GMT, "V35B" wrote: Of course if you place mothers milk in an IV line it can kill you too. The point is N20 is arguably safer than local anesthetics, when used within its therapeutic realm. No chance of anaphylactic hypersensitivity reaction... etc. The point also is that the two are not interchangable... "Joel M. Eichen D.D.S." wrote in message .. . There have been accidental deaths from N2O. One hospital case happened where the plumbers couldn't figure out the mismatched pipe sizes and cut them off and incorrectly rematched them. **The mismatch PREVENTS people from mixing up the hoses ~ normally it is impossible to crank up the N2O/O2 ratio past 80/20. The 20% O2 is required for life. After the plumbers did their work the tragedy happened. The docs thought there were on 100% O2 but it was really 100% N2O. Tragic. Joel On Fri, 19 Sep 2003 13:43:27 +0200, Mxsmanic wrote: V35B writes: Nitrous Oxide is not potent enough to induce a state of general anesthesia ... That's one of the reasons why it is dangerous for that purpose. Still, it is a general anesthetic in its mechanism of action (i.e., it's not a local anesthetic by any means). General anesthetics require greater caution than local anesthetics. -- Joel M. Eichen, . Philadelphia PA STANDARD DISCLAIMER applies: You fill it in -- Joel M. Eichen, . Philadelphia PA STANDARD DISCLAIMER applies: You fill it in |
#158
|
|||
|
|||
Acute case of balonitis ~ can anyone help?
Agreed!
To be more specific, there are actual medical cases where PN (peripheral neuropathy) exists. Of course that describes a symptom, not a diagnosis. The one that readily comes to mind is a sign or sequelae of diabetes. As for Jan Drew syle PN, meaning she gets her amalgams out and the next day is cured, that suggests Baloney! In medical terms its called, "Jansterbalonitis." I suggest getting out more! Joel On Fri, 19 Sep 2003 13:12:10 GMT, "Tony Bad" wrote: "ChuckMSRD" wrote in message ... Here come Vaughn sucking up to the dentists, even though he knows Joel is EXACTLY what you stated. What is up with that Vaughn? For a seemingly intelligent guy to defend or ignore the things that Joel says is pretty comical. ie: "laziness causes PN" no comment but I say "Hg is the second most toxic metal" WAAAAAAAA it is 3.7th most according to OSHA.... Whats the agenda here? Chuck That last question is one you should answer as well. You want to debate the odd posting behavior of some here or something more important. You seem to be leaning toward the former. As someone else suggested, do a google search on this group and you may have a better understanding of the personality dynamics here. What is your agenda? T -- Joel M. Eichen, . Philadelphia PA STANDARD DISCLAIMER applies: You fill it in |
#159
|
|||
|
|||
Dentist uses Nitrous Oxide?
In article ,
Joel M. Eichen D.D.S. wrote: There have been accidental deaths from N2O. One hospital case happened where the plumbers couldn't figure out the mismatched pipe sizes and cut them off and incorrectly rematched them. **The mismatch PREVENTS people from mixing up the hoses ~ normally it is impossible to crank up the N2O/O2 ratio past 80/20. The 20% O2 is required for life. After the plumbers did their work the tragedy happened. The docs thought there were on 100% O2 but it was really 100% N2O. Tragic. Then the N2O didn't kill the patient. The lack of O2 killed the patient. And yes, the distinction matters. It's why we have to be careful if we let kids suck the helium out of a balloon: the helium won't hurt them, but the lack of oxygen if they do it several times in a row without a "real" breath between may -- and, since both are gases, they don't feel like they aren't breathing. meh -- Children won't care how much you know until they know how much you care |
#160
|
|||
|
|||
Allergy to epinephine - (?)
One cannot be allergic to epinephrine it occurs naturally in the human body.
People tend to get allergy and adverse reaction confused. Allergy would have to come under the umbrella of on of the 4 types of hypersensitivity reactions. Soem one who gets a rapid heartbeat or headache is not showing sgins of an "allergy" "Joel M. Eichen D.D.S." wrote in message ... While we got you here ......... Some people claim they are "allergic" to epinephrine. Of course we know that the problem when epinephrine/local anesthetic (1:100,000 or 1:50,000) is accidentally injected into a vein it is vasovagal sympathomimetic reaction, not anaphylactic or allergic reaction. I say that it is impossible for someone to be "allergic" to epinephrine. What do you say? Joel PS- Here is a checklist for laymen who want to learn more ...... EM guidemap - Syncope Click on any of the headings or sub-headings to rapidly navigate to the relevant section of the guidemap Introduction and general principles History of present illness clinical clue table Risk factors for syncope Examination Diagnostic testing Cardiac monitoring EKG Pulse oximetry Blood testing Carotid massage Orthostatic vital signs Echocardiography Exercise stress testing Signal-averaged electrocardiography Intracardiac electrophysiologic studies Neurological testing Medical decision-making Indications for admission Continuous ambulatory electrocardiographic monitoring Long-term event and memory loop recorders Implantable loop recorders Tilt table testing Psychiatric evaluation Appendix Causes of syncope table differentiating syncope from seizure suggested algorithm for workup of syncope Introduction and general principles - syncope is defined as a transient loss of consciousness associated with a loss of postural tone, and most diseases causing syncope produce a transient LOC by temporarily decreasing cerebral blood flow An emergency physician, when faced with a syncope-patient in an ED setting, should first seek to exclude life-threatening causes of syncope, which require immediate diagnostic evaluation/treatment + hospital admission AMI PE aortic dissection cardiac tamponade tension pneumothorax leaking AAA active internal bleeding malignant cardiac arrhythmias ectopic pregnancy SAH carotid artery/vertebral artery dissection air embolism If there are no overt life-threatening causes of syncope, then an emergency physician should attempt to identify patients with situational syncope, vasovagal syncope and benign orthostatic (postural) syncope - who are candidates for home discharge after any necessary stabilization treatment in the ED - young patients ( 45 years), who have a history of a short-lived syncopal episode with no other associated ongoing symptoms, rarely have serious causes of syncope if the syncope did not occur during exertion, and hospital admission and/or an extensive workup is rarely necessary - emergency physicians are often faced with the dilemma that the cause of the syncope is not immediately apparent after a brief clinical examination, and a decision has to be made whether it is necessary to admit the patient to hospital If the cause of the syncope is not readily apparent after initial clinical evaluation in the ED, then an emergency physician should attempt to decide whether certain categories of syncope-patients require admission to hospital - examples of syncope patients warranting hospitalization include:- elderly patients 60 years with no apparent cause of the syncope sudden syncope occurring in a non-erect patient with no premonitory symptoms or prodrome sudden syncope occurring during exertion sudden syncope in a patient with a family history of syncope or sudden death patient has overt evidence of structural heart disease by history or examination patient has an abnormal ECG (* see the medical decision-making section for further details) - there is no universally accepted approach to the further inpatient/outpatient workup of patients, whose cause of syncope is not readily apparent = a suggested algorithm is included in the appendix section as a general guide History of the present illness - critical historical elements include the mode of onset and progression of event, body position at onset of event, the depth of altered consciousness, the duration of the syncopal episode and the rate of recovery of consciousness (* by paying close attention to the details, an emergency physician should be able to differentiate syncope from seizures, non-specific near-syncopal events, non-specific ligheadedness and dysequilibrium syndromes) - sudden unheralded syncope at rest, particularly in a non-erect posture, is ominous - especially if significant injury results = suggests a cardiac arrhythmia - associated palpitations or an irregular heart beat suggests cardiac syncope secondary to a cardiac arrhythmia - certain antecedent symptoms lasting 10 seconds (darkening vision or tunnel vision or graying vision, lightheadedness, swaying sensation, nausea, sweating, feeling "hot", face and distal limb numbness), especially if preceded by a provocative emotional event and occurring in an upright position suggest vaso-vagal syncope (also called vasodepressor or reflex or neurocardiogenic syncope) (* vasovagal syncope is also more likely to happen in overcrowded social settings where prolonged mandatory standing is a requirement eg. church, military parades in hot weather) - antecedent/accompanying chest pain (AMI or PE) or abdominal pain (ectopic pregnancy) or back pain (ruptured abdominal aortic aneurysm or dissecting aortic aneurysm) or headache (SAH) suggests serious pathology - prominent antecedent/accompanying dyspnea suggests hyperventilation syndrome, pulmonary embolism or pulmonary hypertension - accompanying brainstem symptoms (diplopia or blurred vision, dysarthria, dysphagia, deafness, vertigo, ataxia, limb weakness or hypoesthesia, face pain or hypoesthesia) suggest vertebro-basilar artery insufficiency or basilar artery migraine - the patient's posture at the time of syncope is very important - sudden syncope in a non-erect position signifies serious pathology , while lightheadedness for 30 - 60 seconds after suddenly standing/walking and immediately preceding the syncopal episode suggests underlying orthostatic hypotensive syndromes (autonomic neuropathy and/or volume depletion and/or drug-induced vasodilatation) - sudden syncope related to turning or hyperextending the head (eg. when shaving or while wearing tight constricting neckwear) suggests carotid sinus syncope - sudden syncope during strenuous physical activity (exertional syncope ) suggests potentially serious pathology (HOCM or aortic stenosis, or atrial myxoma or anomalous coronary artery; or a malignant arrhythmia eg. torsade des pointes and VT) - pscyhological triggering events (painful stimuli, sudden bad news) suggest vasovagal syncope (* however sudden stress/excitement in patients with long QT syndrome can trigger torsades des pointes) - evidence of volume loss may precede syncope (vomiting, diarrhea) or accompany syncope (hematemesis or melena) - syncope related to strenuous unilateral upper arm activity suggests subclavian steal syndrome - situational syncope is self-diagnostic - cough syncope, micturition syncope, defecation syncope, hair-grooming syncope, adolescent stretch syncope, deglutition (swallow) syncope, glossopharyngeal syncope and "weight-lifter blackouts" - antecedent "glue-sniffing" or "huffing" suggests a ventricular arrhythmia and/or hypoxia as the cause of the syncope; sympathomimetic drug abuse (cocaine or amphetamines) suggest a tachyarhythmia - recurrent bouts of progressive gradual loss of consciousness over several minutes while walking or standing + NO sweating + NO pallor + fixed heart rate suggest chronic dysautonomic syncope (* patients often also have a history of hypohidrosis, impotence, blurred vision, urinary difficulties, constipation, nocturnal polyuria and " coat-hanger" pain [neck and shoulders ache - present only when standing]) - recent meal ingestion in an elderly patient may suggest post-prandial hypotensive syncope - short-lived myoclonic seizures or twitching are compatible with convulsive syncope, and do not imply a true seizure (* a true seizure is more likely if an aura and/or convulsions precede the fall, tongue biting and/or urinary incontinence occurs, convulsions are generalized and last longer than 30 seconds, prolonged post-ictal confusion-lethargy occurs = see the table in the appendix section for further details) Clinical clue table Clinical clue Suggests Sudden syncope at rest when non-erect Cardiac arrhythmia, atrial myxoma Sudden syncope on exertion Aortic stenosis, HOCM, atrial myxoma, malignant cardiac arrhythmia Preceding "lightheadness" prodrome when erect Vasovagal syncope, orthostatic hypotension Preceding palpitations Cardiac arrhythmia Preceding or accompanying dyspnea Pulmonary embolism, tension pneumothorax, cardiac tamponade, air embolism Preceding or accompanying chest pain AMI, PE, cardiac tamponade, dissecting aneurysm, tension pneumothorax, mitral valve prolapse Preceding or accompanying back pain Dissecting aortic aneurysm, leaking AAA Preceding or accompanying abdominal pain Leaking AAA, ectopic pregnancy Occurring when turning head to side, or looking up Carotid sinus syncope Occurring when exercising upper arm Subclavian steal syndrome Occurring during (or immediately after) coughing, laughing, vomiting, swallowing, urination, defecation, combing hair, stretching Situational syncope Occurring after prolonged standing Vasovagal syncope Occurring after emotional upset Vasovagal syncope, prolonged QT interval and torsade Recent illicit drug use Cardiac arrhythmia, air or foreign body embolism Recent sudden headache SAH Recent neurological symptoms Brain stem stroke, vertebro-basilar artery insufficiency, basilar migraine, carotid or vertebral artery dissection, dissecting aortic aneurysm Recent vaginal insufflation Air embolism Recent black stools GI bleed Recent fluid loss (diarrhea, vomiting, sweating) Orthostatic hypotension, Addisonian crisis Recent meal Postprandial hypotensive syncope Polypharmacy, recent sialdenafil use Orthostatic syncope History of fever or myalgia or arthalgia or rash Atrial myxoma, cardiac tamponade History of known cardiac ischemia or structural heart disease Cardiac arrhythmia, pro-arrhythmia drug effect, valve dysfunction History of mechanical heart valve Thrombosis of valve Recent history of cancer, prolonged immobilization, leg injury or surgery Pulmonary embolism History of autonomic dysfunction (impotence, anhydrosis, sphincter dysfunction) Orthostatic hypotension secondary to autonomic neuropathy History of recurrent syncope Cardiac arrhythmia, carotid sinus syncope, atrial myxoma, aortic stenosis, subclavian steal syndrome, prolonged QT interval - torsade Family history of syncope or sudden death HOCM, prolonged QT syndrome Pacemaker Pacemaker failure Risk factors for syncope Underlying causes of orthostatic hypotension - volume depletion (vomiting, diarrhea, excessive perspiration, diuretic use) - blood loss - adrenal insufficiency - primary or secondary dysautonomias (multiple sclerosis, Guillane-Barre syndrome, spinal cord injury, tabes dorsalis, Parkinsonism, Shy-Drager syndrome, diabetic autonomic neuropathy) - peripheral neuropathy (chronic alcoholism, diabetes) - polypharmacy in elderly patients with impaired baroreceptor reflexes - prolonged recumbency and secondary "cardiac-deconditioning" Drugs predisposing to syncope - vasodilators (alpha blockers, beta blockers, ACEI's, calcium channel blockers, nitrates, phenothiazines) - cardio-inhibitor drugs (beta blockers, digoxin) - psycho-active drugs (anti-convulsants, CNS sedative-depressants, anti-histamines, anti-depressants, anti-psychotics) Conditions predisposing to a prolonged QT interval and torsade des pointes Acquired causes Enviromental and endocrinological causes Medicinal and toxicological causes Congenital causes Neurological causes Ischemic coronary artery disease Hypothermia Class 1A antidysrhythmics - quinidine, procainamide, disopyramide Jervell-Lange-Nielsen syndrome Subarachnoid hemorrhage Congestive heart failure Bulemia, stringent dieting Class 1C antidysrhythmics - flecainide, encainide Romano-Ward sydrome Cerebrovascular occlusive disease Rheumatic heart disease Hypothyroidism Phenothiazine overdose Refsum syndrome Traumatic brain injury Myocarditis Hypokalemia Butyrophenone overdose Mitral valve prolapse Encephalitis Hypocalcemia Tetracyclic/tricyclic antidepressant overdose Hypomagnesemia Organophosphate overdose Macrolide antibiotics + terfenadine or astemizole or cisapride Azole antigungals + terfenadine or astemizole or cisapride Examination - a selective examination can offer clinical clues as to the etiology of the syncope Blood pressure - difference in blood pressure between left and right upper limbs 20mmHg is abnormal (suggests dissecting aortic aneurysm or subclavian steal syndrome) - difference in blood pressure between upper and lower limbs 20mmHg when recumbent is abnormal (suggests a dissecting aortic aneurysm) Pulse volume - decreased and delayed upstoke (aortic stenosis/hypertrophic obstructive cardiomyopathy) - positive pulsus paradoxus (cardiac tamponade, massive pulmonary embolism) - absent pulses (dissection of the aorta, cardiac emboli) Neck bruits - suggests great artery stenosis eg. subclavian steal syndrome or carotid artery dissection Jugular venous pressure - increased in heart failure or pulmonary embolism or cardiac tamponade (positive Kussmaul's sign) - 'cannon' a waves suggests AV conduction block Apex beat - displaced and forceful (LVH), forceful (RVH) Heart sounds - decreased (pericardial tamponade) - 3rd/4th heart sounds (ventricular failure or LV overload) - loud second heart sound (pulmonary embolism or pulmonary hypertension) - ejection systolic murmurs (aortic stenosis or hypertrophic cardiomyopathy - increased murmur when standing, decreased when squatting) - machinary murmur (air embolism) - "tumor plop" or diastolic murmur (atrial myxoma) - varying heart sounds/murmurs (thrombotic occlusion of a prosthetic valve) Abdomen - pulsatile masses (abdominal aneurysm) - rectal exam for melena or heme-occult positive stools (gastro-intestinal bleeding) - absent/decreased femoral pulses (dissection of the aorta) Neuro exam - signs of vertebro-basilar artery TIA/CVA or neuropathy or myelopathy Diagnostic testing Cardiac monitoring - immediate and continuous monitoring during the ED evaluation period is highly recommended - arrhythmias may be etiologically significant (* no study has determined the ideal duration of ED cardiac monitoring ECG - an abnormal ECG may be etiologically significant, although the 'definitive' diagnostic yield is low ( 5%) - ECG abnormalities include:- previous or acute cardiac ischemic changes signs of pericarditis or electrical alternans (cardiac tamponade) LVH (hypertension, aortic stenosis, HOCM) RVH (PE or pulmonary hypertension) classical/non-specific ECG signs of PE WPW syndrome LBBB or bifasicular block (conducting system disease) bradyarrythmias or tachyarrhythmias long QT interval Brugada syndrome (partial RBBB with elevated ST segments in leads V1-3 and peculiar downsloping of the elevated ST segments + inverted T waves in those leads) arrhythmogenic right ventricular dysplasia (RBBB, QRS complex 110 msec in leads V 1-3, inverted T wave or epislon wave Pulse oximetry - a low reading may suggest a possible etiology (cyanotic congenital heart disease, pulmonary embolism, pulmonary hypertension Blood testing - not generally useful - Hb/Hct helpful in establishing baseline in bleeding patients - glucose and electrolytes have no/little utility (* hyponatremia + hyperkalemia may rarely suggest Addison's disease; hypoglycemnia rarely produces syncope without ongoing symptoms of hypoglycemia) - serum HCG rarely helpful in reproductive age female patients (* very rare patient with an ectopic pregnancy presenting as syncope without any abdominal pain/vaginal bleeding) Carotid sinus massage - may be useful in diagnosing carotid sinus syncope in elderly patients - first performed on the right side for a minimum of 5 seconds (preferably 15 seconds) = measure pulse rate and blood pressure = wait 120 seconds = repeat test on the left side - positive response = longer than 3 seconds of asystole, and/or systolic blood pressure drop of 50 mmHg when supine - borderline positive response = slowing of heart rate 30 - 40% and/or systolic blood pressure drop of 30mmHg when supine - 90% of positive-test patients have the cardio-inhibitory or combined response, while only 10% have the vaso-depressor response - up to 10% of elderly patients have carotid sinus hypersensitivity to some degree, however only 5 - 20% of these patients have carotid sinus syndrome (carotid sinus syncope etiologically related to carotid artery hypersensitivity) - carotid sinus syncope can only be definitively diagnosed when syncope or near-syncope occurs during carotid massage (* carotid sinus massage is contra-indicated in patients with a history of a CVA, a recent AMI or when a neck bruit is present Orthostatic vital signs - the patient should be recumbent for at least 5 minutes prior to performing the test and the patient should stand for at least 2 minutes - a positive test is defined as a systolic blood pressure decrease of 20 - 30mmHg, a diastolic decrease of 10 - 15mmHg and/or heart rate increase of greater than 30 bpm when standing - the test is non-dependable, often inconsistent and has a low specificity - a significant drop in blood pressure + fixed heart rate suggests dysautonomia - a significant drop in blood pressure + increased heart rate suggests volume depletion and/or excessive vasodilatation - an insignificant drop in blood pressure + marked increase in heart rate suggests postural tachycardia syndrome, which is a heterogenous entity (history of frequent fainting, symptoms of autonomic overactivity - palpitations, diaphoresis, tremulousness, visual blurring, non-anginal chest pain, "spaced-out" feelings, inability to concentrate, inability to breathe, sensations of impending doom) Echocardiography - diagnostic yield low in the absence of historical or physical signs of organic heart disease - only definitely indicated in patients with exertion-related syncope, in all patients who have a prosthetic heart valve, or when the clinical suspicion of organic heart disease is high (eg. strong clinical suspicion of obstructive cardiac lesions - HOCM, AS or atrial myxoma) -some conservative physicians believe that organic heart disease cannot be fully excluded prior to performing echocardiography (unsuspected findings are found in 5 - 10% of unselected patients) and that echocardiograph should routinely be performed in all patients, or definitely in patients 50 years Exercise-stress testing - indicated for patients with exertion-related syncope or suspected CAD - should always be preceded by echocardiography to first rule-out cardiac obstructive pathology eg. HOCM, aortic stenosis, atrial myxoma Signal-averaged electrocardiography - not usually helpful with many false-positives - may be useful in selecting patients for electrophysiological studies when CAD is present and secondary VT suspected Intracardiac electrophysiologic studies - expensive, invasive and with low yield - not indicated in patients with clinically normal hearts and a normal ECG - most useful in patients with known organic heart disease (patients with a history of a MI or CHF - especially if the ejection fraction 40%) and/or an abnormal ECG - usefulness is mainly based on the ability of EPS testing to induce malignant arrhythmias eg. sustained monomorphic ventricular tachycardia - induction of non-sustained VT, polymorphic VT and VF during testing is of no/uncertain clinical usefulness - less useful for detecting bradyarrhythmias - sinus node recovery time 3 seconds may reflect sinus node disease requiring a pacemaker - an HV interval exceeding 100 msec or infranodal block induced by pacing suggest AV nodal disease and a bradycarrhythmic cause of the syncope Neurological testing - EEG, CT scan, transcranial/carotid Dopplers - not indicated unless there is substantial reason to suspect a seizure or other significant neuropathology Medical decision-making An overriding concern and uncertainty about what may happen to the patient in the near future may cause an emergency physician to unnecessarily admit too many patients Patients who can clearly be discharged include those with a classical presentation of vasovagal syncope (irrespective of age), those with situational syncope, those with mild, reversible orthostatic syncope (including polypharmacy syndrome in the elderly patient) and patients with hysterical conversion syncope Indications for admission of patients presenting with syncope include: new clinical evidence of structural heart disease significant antecedent/associated chest pain or ECG evidence of cardiac ischemia history of previous CHF or myocardial ischemia history of a previous malignant arrhythmia sudden syncope preceded by and/or associated with palpitations or an irregular heart beat significant malignant arrhythmia detected in the ED high-grade conduction block or high-grade carotid sinus syncope sudden onset syncope without premonitory symptoms, especially if occurring when non-erect and associated with injury exercise-induced syncope (irrespective of age) syncope associated with moderate/severe orthostatic hypotension resistant to ED treatment or due to life-threatening pathology eg. ectopic pregnancy syncope associated with any significant neurological symptoms/signs syncope suggestive of pulmonary embolism or pulmonary hypertension strong family history of sudden syncope/sudden death syncope in a patient with an abnormal ECG - long QT interval or Brugada syndrome or WPW syndrome age 60 years with no evidence of vasovagal syncope or readily reversible chronic-or-benign orthostatic causes syncope due to cardiac tamponade or active internal bleeding patient taking pro-arrhythmia medications that may potentially cause malignant arrhythmias eg. quinidine, sotalol, amiodarone ACEP task force recommendations for admission include: Admit patients with syncope and any of the following: 1. A history of congestive heart failure or ventricular arrhythmias 2. Associated chest pain or other symptoms compatible with acute coronary syndrome 3. Evidence of significant congestive heart failure or valvular heart disease on physical examination 4. ECG findings of ischemia, arrhythmia, prolonged QT interval, or bundle branch block Consider admission for patients with syncope and any of the following: 1. Age older than 60 years 2. History of coronary artery disease or congenital heart disease 3. Family history of unexpected sudden death 4. Exertional syncope in younger patients without an obvious benign etiology for the syncope 24-hour Holter (continuous ambulatory electrocardiographic) monitoring - traditional approach to syncope of unknown etiology with low yield - 4% true positives (symptoms correlate with arrhythmia) and 15% false positives (symptoms without any arrhythmia); 14% of patients have an asymptomatic arrhythmia which may suggest a cause for the syncope (sinus pauses, non-sustained VT, Mobitz type II block) - extending the continuous ambulatory electrocardiograhic monitoring to 72 hours results in a slightly higher yield - if no symptoms/arrhythmias are detected, arrhythmogenic syncope cannot be excluded = further testing is required for patients with recurrent syncope, or if there is a strong clinical suspicion of malignant cardiac arrythmias eg. known severe structural heart disease +/- history of recurrent palpitations Long-term event and memory loop recorders - provide continuous ambulatory electrocardiographic recordings for prolonged periods (weeks) - useful for patients who have recurrent syncope ( 1x/4 weeks) Implantable loop recoders - latest development based on a loop-based memory system capable of providing continuous ambulatory electrocardiographic recording for up to 18 months - indicated for patients with recurrent syncope with no definite organic heart disease Tilt table testing - used to confirm neurocardiogenic syncope in a patient, who does not have a classical history of vaso-vagal (vasodepressor) syncope; has also been useful in diagnosing neurally-mediated syncope, which manifests as post-exertional syncope - used to investigate recurrent syncope in elderly patients with probable autonomic neuropathy - some cardiologists reserve tilt testing for patients with unexplained, recurrent syncope in whom cardiac causes of syncope, including arrhythmias, have been excluded by echocardiography and Holter monitoring and EPS testing - can also be used to differentiate convulsive syncope from true seizures Psychiatric evaluation - may be indicated in young patients who faint frequently for no apparent reason, especially when symptoms are suggestive of postural tachycardia syndrome Appendix Causes of syncope Vasomotor/vascular Hypovolemia dehydration fluid loss "third" spacing osmotic/iatrogenic diuresis Hemorrhage ruptured abdominal aortic aneurysm ectopic pregnancy GIT bleeding trauma-induced Vasomotor insufficiency Postural orthostasis Vasodepressor (vaso-vagal) syncope Glossopharyngeal neuralgia Trigeminal neuralgia Autonomic/peripheral neuropathy Subclavian steal syndrome Anaphylactic shock Cardiac Dysrhythmias tachyarrhythmias bradyarrhythmias Carotid sinus hypersensitivity Pacemaker malfunction Myocardial ischemia Dissection of the aorta Mechanical outflow obstruction or venous return impedance aortic stenosis hypertrophic obstructive cardiomyopathy pulmonary stenosis pulmonary embolus primary pulmonary hypertension atrial myxoma prosthetic valve malfunction/thrombosis pericardial tamponade tricuspid stenosis mitral stenosis retrictive cardiomyopathy tension pneumothorax Congenital heart disease anomalous origin of the left coronary artery Eisenmenger's syndrome Tetralogy of Fallot Situational cough (post-tussive) micturition defecation swallowing postprandial weight-lifters adolescent stretch hair grooming trumpet player's Metabolic "hypoglycemia" addisonian crises pheochromocytoma hypothyroidism Central nervous system subarachnoid hemorrhage "seizures" basilar migraine posterior circulation TIA's vertebral artery dissection carotid artery dissection Miscellaneous air embolism amniotic fluid embolism foreign body embolism asphyxia/hypoxia carbon monoxide poisoning breath-holding attacks hyperventilation syndrome conversion disorder pro-arrhythmic drugs polypharmacy "glue sniffing or huffing" postural tachycardia syndrome Differentiating syncope from seizure Feature Syncope Seizure Aura Absent Rarely present Antecedent "dizziness-prodrome" prior to event Sometimes present Absent Color at onset of event Sometimes pale Sometimes florid/purple Jerking movements Infrequent and short-lived (seconds) Common and longer-lasting (minutes) Pattern of convulsions Uncoordinated myoclonic jerks and twitches - after LOC Generalized tonic and/or clonic movements - coincident with LOC Upturning of eyes Common Uncommon Forced conjugate deviation of eyes Absent Common Tongue biting - lateral Absent Common Urinary incontinence Rare Common Duration of event Seconds Minutes Prolonged disorientation or sleepiness after event Absent-rare Present-common Increase in CK enzyme or lactate Absent Present Suggested algorithm for workup of syncope Disclaimer : My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use. On Fri, 19 Sep 2003 13:02:00 GMT, "V35B" wrote: Of course if you place mothers milk in an IV line it can kill you too. The point is N20 is arguably safer than local anesthetics, when used within its therapeutic realm. No chance of anaphylactic hypersensitivity reaction... etc. The point also is that the two are not interchangable... "Joel M. Eichen D.D.S." wrote in message .. . There have been accidental deaths from N2O. One hospital case happened where the plumbers couldn't figure out the mismatched pipe sizes and cut them off and incorrectly rematched them. **The mismatch PREVENTS people from mixing up the hoses ~ normally it is impossible to crank up the N2O/O2 ratio past 80/20. The 20% O2 is required for life. After the plumbers did their work the tragedy happened. The docs thought there were on 100% O2 but it was really 100% N2O. Tragic. Joel On Fri, 19 Sep 2003 13:43:27 +0200, Mxsmanic wrote: V35B writes: Nitrous Oxide is not potent enough to induce a state of general anesthesia ... That's one of the reasons why it is dangerous for that purpose. Still, it is a general anesthetic in its mechanism of action (i.e., it's not a local anesthetic by any means). General anesthetics require greater caution than local anesthetics. -- Joel M. Eichen, . Philadelphia PA STANDARD DISCLAIMER applies: You fill it in -- Joel M. Eichen, . Philadelphia PA STANDARD DISCLAIMER applies: You fill it in |
Thread Tools | |
Display Modes | |
|
|
Similar Threads | ||||
Thread | Thread Starter | Forum | Replies | Last Post |
At what age should a child start going to dentist | Cherie | General | 11 | July 28th 04 02:20 PM |
Dentist and breastfeeding | Nancy | Pregnancy | 3 | January 14th 04 03:48 PM |
parents in the dentist's room | Denise | General | 33 | December 12th 03 11:07 PM |
Dentist uses Nitrous Oxide? | Wendy Marsden | General | 255 | October 2nd 03 09:44 PM |