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.

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....

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

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

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

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

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

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

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

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