Emergency Medicine Flashcards
When a man comes into the ED with dyspnea and palpitations, what is the first thing that should be done?
The patient should get an IV and be placed on cardiac and pulse oximetry
monitors.
Causes of Afib (5 Categories)
Cardiac - Hypertension (approximately 80% of cases), coronary artery disease,
cardiomyopathy, valvular heart disease, rheumatic heart disease, congenital
heart disease, myocardial infarction, pericarditis, myocarditis
Pulmonary - Pulmonary embolism, chronic obstructive pulmonary disease (COPD),
obstructive sleep apnea
Systemic disease - Hyperthyroidism, obesity, metabolic syndrome, inflammation
EToh - “Holiday heart syndrome”
Post op - Cardiac surgery, any surgery
Idiopathic Approximately 10% of AF
How does AF lead to poor perfusion of the limbs and the brain?
Acutely, the loss of the “atrial kick” leads to a reduction in cardiac output (CO) by as much as 15%.
Together with the rapid ventricular
response shortening the diastolic filling time, CO may be significantly reduced,
especially in those with already poor left ventricular function
Treatment options for stable patients with AF starts with?
What type of control is prioritized in the ED.?
Rate control and/or
rhythm control, with or without anticoagulation.
In the acute setting such as the emergency department, ventricular rate control is the single most important goal
of therapy.
Two groups of patients with AF who should not receive rate controlling agents.
unstable patients in whom the instability is presumed to be caused by the rhythm, (2) patients with Wolff-Parkinson-White (WPW) syndrome
Name 4 AV Nodal blocking agents
Why shouldnt patients with with WPW should not
receive any AV nodal blocking agents
What should they get instead?
Adenosine, Beta blockers, CCBs and Digoxin
It could lead to accelerated conduction down the accessory pathway and potentially induce ventricular fibrillation and
cardiac arrest.
Give them cardio-version
Drugs for rate control in AFib (x4)
Dilatizem, B-blockers, Digoxim and Amiodarone/Dronedarone
What is the risk of Hypotension with Diltiazem?
lowest risk of
hypotension because it has least negative
inotropic effect compared to other drugs
Why is role digoxin limited in the ED
of its slow onset of action, long half-life, and ineffectiveness
at rate control in the typical high sympathetic tone ED patient
Which drug for Rate Control in Afib has the highest risk of hypotension
Beta blockers - particularly in patients with borderline low blood pressure or poor LV function
What is the major causes of thromobogenesis post cardioversion
dislodging of an existing clot or the
formation of new clot caused by the “atrial stunning.”
Define the 48 hour rule
AF of less
than 48 hours duration does not generally require acute anticoagulation except
when the patient has mitral valve disease, severe left ventricle dysfunction, or prior history of embolic stroke.
Anticoagulation protocol prior to cardioversion with TEE (3 parts)
Screening transesophageal echocardiography
(TEE), if no clot, administer heparin or enoxaparin, get INR of 2-3 and proceed immediately to cardioversion
Warfarin in continue 3-4 weeks, post cardioversion in the context of atrial stunning
Which is the most effective types of cardioversion?
What factors make cardioversion less successful (x4)
Complications of DC Cardioversion
DC is more successful compared to chemical.
hypertension,
an enlarged left atrium, heart failure, or AF for more than a year.
bradycardia, ventricular tachycardia, ventricular stunning with hypotension
Drugs for Cardioversion
Class 1c? x2
Adverse Effects?
Contraindications?
Flecainide
(oral), Can lead to Dizziness and dyspnea; Contraindicated in CAD
Propafenone
(oral) can lead to dizziness, VT; Contraindicated in CAD
Drugs for Cardioversion
Class III? x4
Adverse Effects?
When are they preferred?
Dofetilide (oral) can lead to VT, torsade de pointes Preferred if any structural
heart disease is
present, especially
LV dysfunction
Amiodarone (oral or IV), can lead to Hypotension, bradycardia, pulmonary toxicity, hepatotoxity, hyper/hypothyroidism, photosensitivity, ataxia, peripheral neuropathy, blurry vision. Preferred if any structural heart disease is
present, especially
LV dysfunction
Ibutilide (IV), can lead to VT, torsade de pointes, Specifically for AF and
atrial flutter
Vernakalant (IV) can lead to Hypotension, bradycardia. Rapid conversion, low
proarrhythmic risk
How does Dabigatran compare to warfarin? Positives and Negatives?
+ reduces the rate of
ischemic and hemorrhagic strokes, major bleeding, and overall mortality compared
to warfarin. does not require INR monitoring, is less susceptible to diet and drug interactions
- higher cost, twice daily dosing, need for adjustment in patients with renal failure,
lack of an antidote, and lack of long-term safety data
If some one can not take warfarin or dabigatran, what might you recommend for antiplatlet therapy
Antiplatelet therapy consists of aspirin 75 to 325 mg daily, clopidogrel 75 mg
daily, or both together, knowing its not as good as the other two drugs.
Process for evaluation person with palpitations +/- hypotension
Labs?
ABCs, Stabilize if need be History, including medications and habits, a complete head-to-toe examination, 12-lead ECG, Lytes and CXR
Maybe a DrugScreen or drug level, or TSH
How do you tell the difference between VT and SVT with aberrancy.
What do you do if you cant tell the difference.
Demographics:
VT - ≥50, history of coronary artery disease or congestive heart failure, history
of VT, atrioventricular dissociation, fusion beats, QRS >0.14 second, extreme
left axis deviation, and precordial concordance (QRS complexes either all positive or all negative).
SVT w/ ab - ≤35, history of SVT, preceding ectopic P waves with
QRS complexes, QRS
Sinus tachycardia
ECG findings and treatment?
Atrial rate 100-160 bpm.
1:1 conduction.
Normal sinus P waves and PR intervals
Treat underlying cause
Atrioventricular nodal reentrant
tachycardia (AVNRT)
ECG findings (P waves?) and treatment?
P wave usually buried in QRS complex. 1:1 conduction. Often preceded by premature junctional or atrial contraction.
Rarely >225 bpm
If stable, consider vagal
maneuvers, adenosine, calciumchannel
blockers or β-blockers
Atrioventricular reentrant
tachycardia (AVRT)
ECG findings (P waves?) and treatment?
Inverted retrograde P waves
after QRS complex. Retrograde reentry involving
bypass tract.
consider vagal maneuvers, adenosine, calciumchannel
blockers or β-blockers
Atrial flutter.
ECG findings (P waves?), response to vagal maneuvers? treatment?
Atrial rate 250-350 bpm.
“Sawtooth” flutter wave (best seen in II, III, aVF, V1-V2). 2:1 conduction common (although
may be any ratio)
Will not convert to sinus with vagal maneuvers or adenosine
calcium channel
blockers, β-blockers.
Treat underlying cause
Junctional tachycardia
Patholophysiology? and Causes (5x)
increased automaticity in the AV node coupled with decreased automaticity in the sinus node.
Digoxin toxicity (= the classic cause of AJR) Beta-agonist, Myocardial ischaemia, Myocarditis, Cardiac surgery
Junctional tachycardia
ECG findings (P waves?), response to vagal maneuvers? treatment?
Inverted P wave before or after QRS or buried in QRS
complex. Rate >100 bpm
Will not convert to sinus with vagal maneuvers or adenosine. If stable, consider diltiazem, β-blockers. Treat underlying
cause
Ventricular tachycardia
ECG findings (P waves?),treatment?
Wide QRS-complex
Dissociated P wave (if present). 100-250 bpm
If stable, consider amiodarone,
procainamide, or sotalol.
Lidocaine as second-line agent
Antidromic AVRT
ECG findings (P waves?),treatment?
Retrograde P waves may or may not be visible, may be obscured by ventricle depoilarization
Avoid β-blockers, calcium channel blockers, and adenosine
Narrow complex tachycardia
with aberrancy
ECG findings (P waves?, QRS? Axis),treatment?
Preceding ectopic P waves with
QRS complexes.
QRS usually
Pharm therapy for non sustained VTach (lasting less than 30 secs
None. F/u with Cardiologist for workup for structural or congenital heart disease. e
Treatment of Hypovolemic Shock in DM type 1, Adults vs Kids
Maintainence fluids?
Adults with clinical shock should receive an initial
2-L bolus of normal saline with frequent reassessment. In children, shock is treated
with boluses of 20 mL/kg of normal saline.
continue an infusion of half normal
saline at two to three times maintenance
An insulin dose DM type 1
For how long?
0.1 U/kg/h (5-10 U/h in the adult) is adequate for almost all clinical situations.
when the serum glucose falls to 200 to 300 mg/dL and the person’s anion gap is normal.
If the initial serum K is normal or low in DKA then…..
Potassium replacement can be started immediately.
What is the single most common underlying cause of DKA in young people
UTIs
SIRS Criteria (4 parts)
At least 2 of the following
Temperature >38°C or 20 breaths per minute or Paco2 12,000 cells/mL or 10% bands
Definition of severe sepsis (8 Points)
Sepsis in conjunction with at least one sign of organ failure or
hypoperfusion, such as lactic acidosis (lactate ≥4 mmol/L), oliguria (urine output
≤0.5 mL/kg for 1 hour), abrupt change in mental status, mottled skin or delayed
capillary refill, thrombocytopenia (platelets ≤ 100,000 cells/mL) or disseminated
intravascular coagulation, or acute lung injury/acute respiratory distress syndrome
Definitions of septic Shock
Multiorgan Dysfunction Syndrome?
Severe sepsis with hypotension (or requirement of vasoactive
agents, eg, dopamine or norepinephrine) despite adequate fluid resuscitation in the
form of a 20- to 40-cc/kg bolus
MODS is the far end of the spectrum that begins with SIRS. It is defined as dysfunction of two or more organ systems such that homeostasis cannot be maintained without intervention.
Common Pathogens causing infection of unknown source.
Empiric Antibiotic Recommendations?
Escherichia coli, Staphylococcus aureus, Streptococcus pneumoniae, Enterococcus spp, Klebsiella spp, Pseudomonas aeruginosa
Vancomycin plus antipseudomonal penicillin (eg, piperacillin/tazobactam) Or antipseudomonal cephalosporin (eg, ceftazadine, cefepime) plus fluoroquinolone (eg, levofloxacin, ciprofloxacin) Or aminoglycoside (eg, gentamicin, amikacin)
Common Pathogens causing Pneumonia
Empiric Antibiotic Recommendations?
Streptococcus pneumoniae, Mycoplasma pneumoniae, Haemophilus influenza,, Chlamydophila pneumoniae, Legionella
Antipseudomonal cephalosporin (eg, ceftazadine, cefepime), plus macrolide (eg, azithromycin Or fluoroquinolone (eg, levofloxacin, moxifloxacin)
Common Pathogens causing UTI
Empiric Antibiotic Recommendations?
Escherichia coli, Klebsiella spp
Enterococcus spp
Fluoroquinolone (eg, levofloxacin)
Or third-generation cephalosporin
(eg, ceftriaxone)
Empiric Therapy for an Abdominal infection
Ampicillin ( if Listeria is suspected)
plus
Cefazolin, cefuroxime, ceftriaxone,
cefotaxime, ciprofloxacin, or levoflox-
acin,
plus
metronidazole
How do Infants and the elderly present with sepsis differently than adults and adolescents?
What other nonspecific sign can one look for?
they may present
with hypothermia rather than hyperthermia, leukopenia rather than leukocytosis,
and they may not be able to mount a tachycardia (as in elderly patients on β- or
calcium-channel blockers) or they may have a tachycardia attributed to other
causes (as in anxious infants
vomiting, fatigue, behavioral changes—should prompt concern
for sepsis
Parts of the Sepsis Bundle for a patient coming into the ED. Access? Labs? Imaging? Drugs?
How Quickly should Abx be started in the context of sepsis.
cardiac and pulse-oxygenation monitor and ECG, nasal canula or facemask should be titrated to keep oxygen saturation >93%
Access: two large-bore, peripheral IVs with 20 to 40 mL/kg (2-4 L in adults) crystalloid unless, they have heart or renal failure
Labs: Lactic acid, CBC, CMP, Blood cultures from two sites, Urinalysis with culture, Pregnancy test in women of childbearing age
Imaging: CXR
Drugs: Broad-spectrum intravenous antibiotics
Broad-spectrum intravenous antibiotics should be started rapidly —ideally after
the cultures have been drawn, but antibiotic infusion should not be delayed if cultures cannot be obtained in a timely fashion (
What is goal-directed therapy (EGDT) and whne should it be initiated? (2 criteria)
Early Goal-Directed Therapy
If the patient continues to be hypotensive or has a lactate level greater than 4 mmol/dL or has other signs of continued hypoperfusion,
then early goal-directed therapy (EGDT) should be initiated.
Goal 1 of EGDT: central venous pressure (CVP) at… what if mechanically ventilated?
How often can you give saline to option this goal?
8-12 mm Hg
> 12 mm Hg if mechanically ventilated
500 cc of normal saline can be bolused every
15 to 30 minutes until the CVP goal is met.
Goal 2 of EGDT mean arterial pressure at….
what can you use to obtain to this goal, if fluids arent working?
greater than 65 mm Hg
vasopressors should be initiated, with either norepinephrine or dopamine
Goal 3 of EGDT: central venous oxygen saturation at …..
what does it mean when the o2 sat is less than 70 percent
How can you correct this issue? What it that does not work
greater than 70%:
the tissues are extracting as much oxygen as possible from the blood, and therefore that tissue demand is not being met
Transfusing packed red blood cells to a hematocrit ≥30%. If that does not work, dobutamine infusion should be started to
boost cardiac output.
Glucose is reccommended to be at what level in sepsis?
A patient’s glucose goals should be between 140 and 180 mg/dL.
When should platlets be be started in a patient with DIC. Other medications?
platelets may be given if the platelet count is
Complications associated with sepsis 5 systems
Cardiac failure ALI and ARDS DIC (disseminated intravascular coagulation) Hepatic failure Renal failure
Shock is divided into three stages….
Compensated, progressive, and irreversible.
How does the body get to progressive shock?
What happens to blood in low flow states?
What fluid shift occur in context to progressive shock?
Arterial pressure falls. This leads to
cardiac depression from decreased coronary blood flow, and, in turn, further decreases
arterial pressure.
In the microvasculature,
low blood flow causes the blood to sludge, amplifying the inadequate delivery of oxygen
to the tissues.
Ischemia results in increased microvascular permeability, and
large quantities of fluid and protein move from the intravascular space to the extravascular
compartment, which exacerbates the already decreased intravascular volume
What is the definition of irreversible shock?
any therapeutic
efforts become futile. Despite transiently elevated arterial pressures and cardiac output,
the body is unable to recover, and death becomes inevitable.
Where are the five sources of bleeding one should focus on in a trauma patient?
Labs to be obtained in the context of Hemorrhagic shock.
1) external
bleeding (eg, scalp/extremity lacerations); (2) thorax (eg, hemothorax, aortic injury);
(3) peritoneal cavity (eg, solid organ lacerations, large vessel injury); (4) pelvis/
retroperitoneum (eg, pelvic fracture); and (5) soft-tissue compartments (eg, longbone fractures)
hemoglobin, hematocrit, base deficit, and lactate levels.
When is a blood transfusion indicated for a trauma patient? (x 2 reasons)
Other blood products?
A blood transfusion is indicated if the patient persists in shock despite the rapid infusion of 2 to 3 L of crystalloid solution, or if the patient has had such severe
blood loss that cardiovascular collapse is imminent.
Crystalloids, fresh-frozen
plasma (FFP), and/or platelets may need to be transfused if massive blood volumes
have been given. Transfusion protocols differ by institution regarding the ratio of
FFP to platelets to PRBCs that should be administered.
Definition of pemissive hypotension and why do we think it is effective?
blood pressure is allowed to remain low (mean arterial pressures of
60-70 mm Hg or a systolic blood pressure of 80-90 mm Hg).
Permissive hypotension
is thought to be effective in hemorrhagic shock because it is thought that post-hemorrhage, the artificially increased blood pressure by aggressive fluid
resuscitation may disrupt endogenous clot formation and promote further bleeding
What effects can large amount of crystalloid have on outcomes.
crystalloid is often administered at room temperature, which is actually colder than the body temperature and can result in hypothermia.
also dilute the endogenous clotting factors and erythrocyte concentration, resulting in poorer control of bleeding and also
diminished oxygen carrying capacity
Contraindications to permissive hypotension.
patients with traumatic brain injuries who require maintenance of their cerebral perfusion pressure; patients with a history
of hypertension, congestive heart failure, or coronary artery disease, in whom
hypotension will be poorly tolerated and may produce other medical problems
such as strokes or myocardial infarctions.
What type of excess is necessary for a patient with pentrating trauma.
1) large-bore IV access at two sites
Complications of penetrating Chest injuries?
Signs and symptoms
Further Studies/ Interventions? (Imaging and Procedures)
Pericardial effusion/tamponade
Pneumothorax or hemothorax
Distant heart sounds, hypotension, JVD Decreased breath sounds, low oxygen saturation, hypotension
CXR may detect air or fluid in the pleural cavity. FAST is sensitive in detecting fluid within the pericardial sac ED ultrasound is useful in detecting an occult pneumothorax Chest tube thoracostomy may yield a rush of air or blood
Complications of penetrating Abdomen or
pelvis injuries?
Signs and symptoms
Further Studies/ Interventions? (Imaging and Procedures)
Hollow viscus injury, Liver laceration, Splenic laceration, Vascular injury
Peritonitis, Shock (hypotension, altered mental status), Bowel evisceration
Local wound exploration, CT scan may reveal path of, injury and grading of solid, organ injuries
Angiography may be useful, for both diagnosis and treatment
FAST—free intraperitoneal fluid, Exploratory laparotomy
Complications of penetrating back and flank injuries?
Signs and symptoms
Further Studies/ Interventions? (Imaging and Procedures)
Retroperitoneal, hematoma, Urinary tract injury
Hematuria, Hypotension
CT is the best diagnostic tool
for evaluating retroperitoneal
bleeding. CT with delayed imaging and intravenous pyelography.
Complications of penetrating injuries to the extremities?
Signs and symptoms
Further Studies/ Interventions? (Imaging and Procedures)
Vascular injury, Nerve damage, Tendon disruption
6 Ps (pain, pulselessness, poikilothermia, paresthesias, pallor, paralysis
Ankle-brachial indexes (ABIs), CT angiography, Angiography, Wound exploration in the OR
In a high risk mechanism of chest injury, what do you do with a CXr that is negative for pneumothorax
What is an occult pnemothorax
Why is local wound exploration of the chest injury no recommended
It should be confirmed by a repeat upright CXR in 4 to
6 hours or by computed tomography (CT).
A small pneumothorax visualized by CT and missed by
CXR is referred to as an “occult pneumothorax.” An occult pneumothorax should
be reevaluated for progression in 4 to 6 hours by CXR
because the procedure itself can penetrate the pleura and cause a pneumothorax.
When should operative tracheotomy be indicated?
How does one evalute injuries to the cardiac box?
When can Resuscitative (or so-called emergency department) thoracotomy be performed
tube. Considerations for operative thoracotomy include initial output of 1500 mL of blood, or 200 mL/h over the next 4 hours.
With FAST Scan
It is reserved for patients who are in extremis or who have lost vital signs in the ED or within a few
minutes prior to arrival. Outcomes are generally poor with mortality of 97 percent
How must thoracoabdomial injuries be evaluated?
What are the risk of untreated injuries to the diaphragm.
Surgical consultation should be obtained when diaphragmatic injury is suspected because
the definitive diagnostic study is surgical evaluation by laparoscopy or thoracoscopy.
herniation of intra-abdominal contents into the chest may eventually occur due to the presence of negative intrathoracic pressure.
Indications for laparotomy include
If there is no indication for laparotomy, how can one continue to evaluate the wound?
evidence of shock (hypotension, tachycardia, cold and clammy skin, or diaphoresis), peritonitis,
gun-shot wound with a suspected course through the abdominal cavity, or evisceration of abdominal contents
With Wound exploration under local anesthesia and sterile technique.
What is the most sign of retroperiteneal injury. How do FAST Scan, DPL, and Physical Exam compare?
Imaging of the back for penetrating trauma includes?
Hematuria is the most reliable sign of injury to the kidneys, ureters, and bladder. physical examination, FAST, and DPL are insensitive in diagnosing
injuries to the retroperitoneum, including the colon, kidneys, and ureters. CT with delayed images, intravenous pyelography (IVP), and perhaps retrograde cystography
How can evaluate a pulse in the extremities if the pulse is weak or non palpable.
Doppler can be used to identify
arterial flow.
NEXUS LOW-RISK CRITERIA 5 parts
(1) No posterior midline
cervical tenderness. (2) No evidence intoxication. (3) Normal level of alertness.
(4) No focal neurologic deficits. (5) No painful distracting injuries. The major
limitation of this approach is that no precise definition for painful distracting injuries
was provided.
Asymptomatic patients with neck injury sholud be assessed with which screen criteria.
temporarily non-assessable patients? (intoxicated or patient with significant distracting injury
Symptomatic patients?
Asymptomatic patients can
be approached using the CCR, which has been shown to lead to the reduction in
unnecessary radiography and has been demonstrated to be superior in comparison to
the NEXUS criteria
assess the patient as an obtunded
patient with CT and/or MRI or reassess the individual after treatments of distracted injuries or return of
normal mentation.
evaluated with either 3-view C-spine x-rays or preferably CT; symptomatic patients with negative CT who are suspected of having ligamentous injuries need to be further evaluated with MRI of the C-spine, and if both CT and MRI are negative, then the patients can be discharged with a collar for comfort
What is done is a patient post neck injury has persistent neck pain after 2 weeks?
flexion/extension
films are recommended to assess C-spine stability.
Why dont patients with compromised ventilation secondary to C-spine injuries generally exhibit any
external signs of respiratory distress?
What is the most reliable why to assess the oxygenation
most of the respiratory
accessory muscles receive their motor innervations from the thoracic level, and the diaphragm receives its innervations from C3-C5
most of the respiratory
accessory muscles receive their motor innervations from the thoracic level,
and the diaphragm receives its innervations from C3-C5;
In the context of spinal cord injury it is always
preferable to maintain a mean arterial pressure where?
what can be done about low pressures? Bradycardia?
85 to 90 mm Hg to maximize spinal cord perfusion
Initiation of vassopressors such as dopamines or norepinephrine.
Bradycardia
associated with neurogenic shock can be addressed with atropine.
At what point does the administration of steroid in the context of cord injury seen to be helpful.
Within 3 hours of the injury.
Three Diagnostic Criteria for dx of Anaphylaxis
Acute onset (minutes to hours) with reaction of the skin and/or mucosal tissue in addition to respiratory symptoms or hypotension.
Two or more of the following occurring rapidly (minutes to hours) after exposure
to a likely allergen: involvement of the skin-mucosal tissue, respiratory symptoms,
hypotension, or gastrointestinal symptoms. Gastrointestinal symptoms
include abdominal pain, cramping, and diarrhea.
Hypotension occurring rapidly (minutes to hours) after exposure to known
allergen for that patient. Hypotension may present as faintness or altered mental
status.
Epi dosing for anaphalaxis
IV single dose? IV infusion, IM?
IV single dose: 100 μg over
5-10 min; 1:100,000 dilution given
as 0.1 mg in 10 mL at 1 mL/min
IV infusion: 1-4 μg/min (this can be given as 1 amp of 1:1000 epi placed in a 1000 ml bag of saline, titrated to a rate of 1-4 cc/min)
IM: 0.3-0.5 mg (0.3-0.5 mL of
1:1000 dilution)
Dosing of Albuterol in the context of Anaphalaxis
Single treatment: 2.5-5.0 mg nebulized (0.5-1.0 mL of 0.5% solution)
Continuous nebulization:
5-10 mg/h
How long will it take for steroid to take effect in the context in anaphalaxis
When should steroid be stopped?
How much Methylpred can be administered in the context of Anaphalaxis
Prednisone?
6 hours, but will blunt the effects of the inflammatory mediators
Steroids should be continued for days after the reaction
and gradually tapered
125 mg IV
40-60 mg/day PO divided bid or qd (for outpatients: 3-5 days;
tapering not required)
How fluids should be administered in the context of anaphalaxis?
How can Histamine be controlled
1-2-L bolus
with H1 and H2 blockers, like diophenhydramine and ranitidine.
Indication for ABG in context of Asthma?
CXR?
ECG?
To determine degree of hypercapnea or assess degree of deterioration in tiring patient not yet
sick enough to warrant endotracheal intubation.
Temp >38°C, Unexplained chest pain, Leukocytosis, Hypoxemia, Comorbidities/alternative diagnosis
Persistent tachycardia
Comorbidities/alternative diagnosis
Oxygen should be provided to maintain a pulse oximetry reading of at least ______ in
adults and at least _____in infants, pregnant women, and patients with coexisting
heart disease
What is the advantage of Heliox?
90 percent, 95%
Heliox mixtures produce a more laminar airflow and potentially deliver nebulized
particles to more distal airways, but they have not been shown to consistently lead to improved ED outcomes for all asthmatic patients
Dosing Albuterol in asthma
for Severe Asthma?
2.5 to 5 mg of albuterol is intermittently nebulized every 15 to 20 minutes for the first hour of therapy and then repeated every 30 minutes thereafter for 1 to 2 more hours.
Continuous nebulization with higher doses (10-20 mg/h) of albuterol benefits severe
asthmatics.
Significance of Fusobacterium necrophorum pharyngitis?
causes pharyngitis at a rate similar to GABS in young adults and if not treated is implicated
in causing Lemierre syndrome
Centor criteria (5 points)
Presence of tonsillar exudates: 1 point
Tender anterior cervical adenopathy: 1 point
Fever by history: 1 point
Absence of cough: 1 point
Age less than 15 y,a add 1 point to total score
Age more than 45 y,a subtract 1 point from total score
Centor criteria algorithm
4 points - Abx, no testing needed
2-3 if RAT is positive, Abx, if negative get throat culture.
1-0 no abx or further test. Reconsider in the event of sick contact with confirmed GAS infections
Tx and length of therapy for GABS pharyngitis
Dosing?
Pencillin for 10 days
500mg BID for adults, or shot of IM pencillin G
Dx of Epiglottis
Treatment?
Lateral cervical radiograph (thumb-printing sign)
Urgent ENTconsultation for airway management, Helium-O2 mixture,
Cefuroxime antibiotic
therapy
Ludwigs angina Presentation?
Dx?
Tx?
Submaxillary, sublingual, or submental mass with elevation of tongue, jaw swelling, fever, chills,
trismus
Lateral cervical
radiograph or CT
imaging
Stabilize airway
Surgical drainage
Antibiotics (penicillin and
metronidazole)
Peritonsillar
abscess Presentation?
Dx?
Tx?
Swelling in the peritonsillar region with uvula deviation, fever, sore throat, dysphagia, trismus
Cervical radiograph
or CT imaging
Aspiration of the
region with pus
Abscess drainage
Antibiotic therapy (penicillin
and metronidazole)
indications for immediate reperfusion therapy?
ST elevation >1 mV (1 mm) in 2 contiguous leads and
how fast should an indiviudal with suspected STEMI be obtaining an ECG?
How do you deal with a ECG that is non-diagnostic or normal, in a person with STEMI symptoms
What Rheumatologic conditions increase the risk of MI.
Within 10 mins
Comparing the current ECG to old tracings is crucial,
Serial ECGs performed at 15- to 30-minute intervals, continuous ST-segment monitoring.
Rheumatoid arthritis, systemic lupus erythematous
THERAPIES OF PROVEN BENEFIT FOR MI? (x8)
Aspirin (162 mg, chewed immediately, then continued daily for life)
Primary percutaneous coronary intervention (angioplasty or stenting the blocked artery)
Thrombolysis (if primary PCI not available; most regimens require heparin therapy)
β-blockers (immediate IV use and started orally within 24 h; if no contraindications then
continued daily)
Angiotensin-converting enzyme inhibitor (started within 1-3 d, continued for life)
Cholesterol-lowering drugs (started within 1-3 d and continued daily for life)
Enoxaparin (dosage given prior to thrombolysis or PCI, for patients less than 75 y of age)
Clopidogrel (75 mg daily with or without reperfusion therapy)
TIMI Score? x7
Age >65 y
Prior documented coronary artery stenosis >50%
Three or more CHD risk factors
Use of aspirin in the preceding 7 d
Two or more anginal events in the preceding 24 h
ST-segment deviation (transient elevation or persistent depression)
Increased cardiac markers
One point is assigned to each of the seven components. Risk of death, MI, or revascularization at 2 wk by score: 1, 5%; 2,
8%; 3, 13%; 4, 20%; 5, 26%; 6, 41%.
Minimal therapy in the context of NSTEMI
When are Beta blockers added?
Aspirin and nitroglycerin, maybe morphine.
B-blockers, such as IV metoprolol, are usually added in cases
presenting with hypertension or tachycardia
High risk therapy in UA/NSTEMI?
What makes a person high risk?
When do you go for Intravenous glycoprotein IIB/IIIA inhibitors?
molecular-weight heparin and oral clopidogrel + min therapy
Ischemic ECG changes, elevated cardiac markers, or if the TIMI risk score is 3 or greater.
It is reserved for the subset of high-risk patients who will undergo early angiography and PCI, in whom these agents have been shown to reduce subsequent
CHD morbidity.
When do you go for Intravenous glycoprotein IIB/IIIA inhibitors?
It is reserved for the subset of high-risk patients who will undergo early angiography and PCI, in whom these agents have been shown to reduce subsequent
CHD morbidity.
What is the early
invasive strategy in the context of NSTEMI
When is it indicated?
high-risk patients with UA and NSTEMI are taken for
angiography and PCI within 24 to 36 h
refractory angina, hemodynamic instability, signs of heart failure,
ventricular tachycardia, ST depressions on ECG, or elevated cardiac enzymes.
Artery and ECG leads involved in a Anteroseptal infarct?
Anterior?
Lateral?
Inferior?
Right ventricular?
Posterior?
LAD, Anteroseptal V1, V2, V3
LAD Anterior V2-V4
LCA Lateral I, aVL, V4-V6
RCA Inferior II, III, aVF
RCA Right ventricular V4R (also II, III, aVF)
RCA, LCA Posterior R waves in V1, V2
most frequently encountered MI complications in the
ED and prehospital setting? (x2)
Consequences of anterior MI taking out the His-purkinje system?
Inferior MI?
ventricular tachycardia and ventricular fibrillation
(sudden death)
Heart Block
arteriovenous (AV) node dysfunction and second-degree block that is transient and
may respond to atropine.
Right ventricular infarction Consequences, dx, and tx
presents as hypotension without pulmonary congestion.
diagnosis is confirmed by ST elevation in lead V4 on a right-sided ECG,
primary treatment is aggressive volume loading. Nitroglycerine and high-dose
morphine should be avoided in these patients.
Late consequences of MIs
Late complications of MI that tend to occur in the intensive care unit several hours to days after presentation include left ventricular free wall rupture causing
tamponade, ventricular septal defect, pericarditis, left ventricular aneurysm, and thromboembolism
How doanticholinergic agents lead to improvement in pulmonary functional biochemically speaking
Dosing for ipratropium bromide
Anticholinergics decrease intracellular cyclic guanosine
monophosphate (cGMP) concentrations, which reduce vagal nerve-mediated
bronchoconstriction on medium- and larger-sized airways. Additionally, anticholinergic
agents may have some minor anti-inflammatory properties that help to
stabilize capillary permeability and inhibit mucous secretion.
Two puffs from a MDI with spacer device, or 0.5 mL of the
0.02% solution.
Dosing of Prednisone and methylpred in the context of Asthma exacerbation?
Preferences in the ED?
When do you use IV medications
Oral administration of prednisone (dose 40-60
mg) is usually preferred to intravenous methylprednisolone (dose 125 mg) is less invasive and the effects are equivalent.
Intravenous steroids, however, should
be administered to patients with severe respiratory distress who are too dyspneic
to swallow, patients who are vomiting, or patients who are agitated or drowsy.
In which population of asthmatics has magnesium been shown to be effective.
At what dose?
Side Effects and Contraindications?
Although no benefit has been shown in mild to moderate asthmatics, magnesium
sulfate given intravenously at dosages of 2 to 4 g benefits asthmatics with severe
airway obstruction.
The
dose of magnesium is 2 to 4 g IV in adults and 30 to 70 mg/kg IV in children given
over 10 to 15 minutes.
Magnesium has minimal side effects. The most commonly reported are hypotension, a flushing sensation, and malaise. It is contraindicated
in renal failure and in cases of hypermagnesemia as it can cause significant muscle
weakness.
What should be tried before intubation in the the event of severe asthma exacerbation?
Settings?
When do you decide to intubate
PPV usually done with BiPAP.
inspiratory pressure 8 to 15 cm H2O and expiratory pressure 3 to
5 cm H2O.
Patients who fail to improve over 30 to 60 minutes will likely require
intubation.
Steps in the intubation process of a conscious patient.
Drugs of Choice and Advantages?
Dosing of Ketamine
In an awake patient,
an appropriate induction agent (eg, ketamine) and paralytic agent (eg, succinylcholine)
should be used prior to intubation.
Ketamine is the induction agent of choice
because it stimulates the release of catecholamines and causes relaxation of bronchial
smooth muscle, leading to bronchodilation.
Intravenous bolus of
1 mg/kg, followed by a continuous infusion of 0.5 to 2 mg/kg/h.
Suggest initial setting for the ventilator in the context of Asthma. plateau pressures, PEEP, flow rate
How can you confirm sucess of the ventalation in maintaining oxygenation
Assist Control mode at a respiratory rate of 8 to 10 breaths per minute, tidal volume
6 to 8 mL/kg, no extrinsic PEEP, inspiratory-to-expiratory (I/E) ratio of 1:4, and an
inspiratory flow rate of 80 to 100 L/min. To prevent barotrauma, plateau pressures
should not exceed 30 cm H2O. Following initiation of PPV, blood-gas analysis can
be used to modify ventilator or BiPAP settings.
blood-gas analysis can
be used to modify ventilator or BiPAP settings.
When should you consider hospital admisision in an asthma patient?
Hospital admission should be considered in patients that fail to
respond to therapy (ie, PEFR or FEV1
Discharge medications for Asthma, length of therapy, steroid taper?
Asthmatics who are discharged from the ED should receive albuterol, an MDI
spacer device, and a 5- to 10-day course of oral steroids.
Benefits of wound irrigation?
Choices of Irrigants , device, method of irrigation?
Proper irrigation can significantly reduce the risk of wound infection.
High-pressure and large-volume irrigation remains the gold standard to reduce or
eliminate particulate matter and bacterial loads from the wound. This is usually
established with a 35- to 60-mL syringe and 16- to 19-gauge catheter using constant
hand pressure. This generates a pressure of 5 to 8 psi, which is adequate to irrigate a
wound. Sterile saline is the most commonly used irrigant
Amide Local Anesthetics
Onset speed, duration of Action and maximal doses of
Bupivacaine
Ropivacaine
Mepivacaine
Lidocaine
all are with epi
Bupivacaine
Slow Onset.
last for 4-5h (2mg/kg)
7-8h (3mg/kg)
Ropivacaine
Medium Onset.
last for 3-4h (3mg/kg)
6-7h (3mg/kg)
Mepivacaine
Rapid Onset.
last for 2-3h (5mg/kg)
5-6h (7mg/kg)
Lidocaine
Rapid Onset.
last for 1-2 (5mg/kg)
2-4h (7mg/kg)
Ester Local Anesthetics
Onset speed, duration of Action and maximal doses of
Procaine
Tetracaine
Prilocaine
Chloroprocaine
all are with epi
Procaine
Slow Onset.
last for .5-1h (8mg/kg)
1-1.5h (10mg/kg)
Tetracaine
Slow Onset.
last for 3-4 (8mg/kg)
9-10 (2.5mg/kg)
Prilocaine
Medium Onset.
last for .5-1 (5mg/kg)
5-6 (7.5mg/kg)
Chloroprocaine
Rapid Onset.
last for .5-1 (10mg/kg)
1-1.5 (15mg/kg)
What methods can be used to reduce the amount of pain with the injection. (x7)
Benefit of adding epi to anesthetic solutions.
smaller gauge needles, injecting
at a slow rate, infiltrating the wound edge instead of surrounding skin, adding
sodium bicarbonate to the anesthetic solution at a 1:10 dilution, and warming the
solution. Lidocaine gel is also use often in the pediatric population.
It augments homeostasis
and prolongs the duration of action of the anesthetic by decreasing systemic absorption
through local vasoconstriction
What goes into the inspection of the a scalp laceration.
Closure of the scalp involves what type of suture?
When can they be removed?
How should the galea be closed if ruptured? Benefits?
Palpation for depressed skull fractures, and assess the integrity of the galea aponeurosis, which covers the periosteum.
4-0 monofilament suture of different color than the
patient’s hair or staples
7 to 10 days
it should be repaired with long-lasting absorbable suture material (eg, Vicryl,
Monocryl). Closing the galea helps to control heavy bleeding associated with scalp
wounds and limits the spread of potential infection.
Repair of forehead lacerations should be done with what sutures and removed when?
6-0 nonabsorbable
interrupted sutures, and removed after 5 days
What might be the best option for the ED physican in the context of a lacerations to upper and lower lid margins and those
involving the lacrimal duct?
What must be consider in the event of injury to the eye medial to the puncta
an oculoplastic specialist or ophthalmologist.
Injury to the canicular system. Staining the laceration with fluorescein
dye can be used to determine damage to the canaliculus
How does injury to the levator palpebrae superioris muscle manifest in the ED?
Repair ofEyelid lacerations should be done with what sutures and removed when?
This commonly manifests as ptosis
6-0 or 7-0 interrupted sutures, with care to stay superficial; the
suture is removed after 3 to 5 days.
What can be the result from septal trauma of the defect is no repaired.
Treatment and Anesthesia?
Repair of Cartilage laceration should be done with what sutures and removed when? How about the skin
Can be done about lacerations to the nasal alae?
Septal trauma may lead to hematoma formation,
which can lead to necrosis of the septum or chronic obstruction of the nasal passageway.
Septal hematomas require drainage.
Anesthesia in this area is difficult because of the tightness of skin over the cartilage,
but can be obtained via a dorsal nerve block
4-0 or 5-0 absorbable sutures, and the skin closed with
6-0 nonabsorbable suture for 3 to 5 days.
They usually
complex and difficult to anesthetize; these wounds often require consultation of a
plastic or ear, nose, and throat (ENT) surgeon.
Lacerations involving the lip that do not cross the vermilion border can be closed in layers with….
Considerations in the repair if the laceration crosses the vermillion border.
Anesthesia?
Infection prophalaxis?
Lacerations involving the lip that do not cross the vermillion
border can be closed in layers with 6-0 nonabsorbable suture and left in place for
5 days.
the first stitch in repair should exactly
approximate the border using 6-0 nonabsorbable suture. even a 1-mm discrepancy is noticeable
Regional anesthesia is helpful, because
local anesthetic infiltration can obscure the anatomy
Regional anesthesia is helpful, because
local anesthetic infiltration can obscure the anatomy
Two other injuries that must be considered in the event of ear trauma
Anesthesia considerations?
Types suture used in the repair of superficial lacerations and how long before they can be removed?
When does make the referral to Plastics or ENT?
basilar skull fracture or tympanic membrane rupture
Regional
auricular block is effective, and again, epinephrine should be avoided.
Superficial
lacerations should be repaired with 6-0 nonabsorbable sutures, and removed in 5 days.
Auricular hematoma, avulsed tissue, or crushed cartilage is probably best
handled by a plastic surgeon or otolaryngologist
What should be done first before the repair of a facial or cheek laceration?
Types suture used in the repair of lacerations and how long before they can be removed?
What lacerations dont need closure and how can they be treated
investigation the vital
structures in the region such as the facial nerve and parotid duct
6-0 monofilament interrupted suture technique is appropriate for repair.
Sutures are removed after 5 days.
Simple lacerations (
What is done about lacerations to the buccal cavity larger than 2cm
How are they fixed? what other medication must be used?
buccal cavity greater than 2 cm have the propensity
to collect food, which can lead to infection. These typically require closure.
Absorbable 5-0 sutures are preferred. As stated above, all intraoral wounds are
dirty and are at high risk for infection. Therefore, prophylactic penicillin or clindamycin
is indicated
How long does C.Tetani spores take to incubate in the human body?
Where should patients with tetenus be directed, with what therapeutic interventions?
When is Tetunus booster given
The usual incubation period varies from 7 to
21 days, but can extend from 3 to 56 days.
admitted to the intensive care unit. Wound debridement, respiratory support as needed
The dose of tetanus toxoid (TT) or diphtheria/tetanus toxoid (dT) is
0.5 mL IM regardless of age, in the presence of dirty and/or major wound when has be less then 10 year since the last booster or when the date of the last booster can not be remembered.
When is Tetanus immunoglobulin (TIG) is given?
In patients
with a possible tetanus exposure and have incomplete tetanus immunization
(
Management of a bite wound starts with…
Medications?
Physical examination
should focus on the patient’s neurovascular status, the potential for tendon
involvement, any evidence of cellulitis, and the potential for joint space violation.
The wound should be irrigated, tetanus booster updated if more than 5 years has
elapsed since the last administration. and antibiotics administered
if the bite is high risk for infection or already infected
Why should radiographs be obtained in animal bites.
What is does in the context of tendon injury 2/2 to animal bite.
Timeframe for closure of simple bites of the trunk and extremities (except for hands and feet)
A radiograph should also be
obtained to evaluate for a fracture and retained teeth.
For bites with potential tendon
injury, the involved extremity should be splinted.
splinted. Simple bites of the trunk and
extremities (except for hands and feet) less than 6 hours old can generally be closed
primarily.
Handling of simple bites of the head and neck…
puncture wounds, bites of the hand or foot, wounds more than 12 hours old…..
Simple bites of the head and neck area less than 12 hours old also can be repaired primarily
puncture wounds, bites of the hand or foot, wounds
more than 12 hours old, and infected tissues, are usually left open
Who should be contacted in the event of a bite wound?
With any bite injury, the appropriate authorities should be notified to find the
animal and observe it for abnormal behavior.
How are “Fight Bites handled
What is evaulation is delayed?
The wound should be
irrigated, the tendons examined, and antibiotics administered
One should look for signs of infection including cellulitis, abscess formation, or
tenosynovitis. Due to the high risk of infection, these cases typically require admission to the hospital for IV antibiotics or surgery
Antibiotic choice for bite wounds
How long for established infections vs prophylaxis.
amoxicillin–clavulanic acid, ticarcillin–clavulanic acid, ampicillin–sulbactam, or a second-generation cephalosporin.
Duration of administration
for established infections is 10 to 14 days and 3 to 5 days for prophylaxis.
Type of virus of Rabies. Target tissue
Length of incubation
Length of Prodrome and features
Rabies is a single-stranded ribonucleic acid (RNA) rhabdovirus attacks the
central nervous system causing an encephalomyelitis that is almost always fatal
averaging 1 to 2 months, but may be as short as
7 days or as long as 1 year.
1- to 4-day prodrome fever, headache, malaise, nausea, emesis, and a productive cough.
Features of the Encephalitic Phase of Rabies
hyperactivity, excitation, agitation, and confusion. Brain
stem dysfunction follows with cranial nerve involvement, excessive salivation, followed
by coma and respiratory failure. Hydrophobia (the violent contraction of
respiratory, diaphragmatic, laryngeal, and pharyngeal muscles initiated by consumption
of liquids) is a late sign of infection.
Parts of PEP for Rabies and how long it will last?
Rabies immunoglobulin can give a rapid, passive immunity that
will last for 2 to 3 weeks. It should be injected around the wound site as soon as possible
Active Vaccines, should be administered on days 0, 3, 7, and 14.
What is meant by dry bites?
Nature of Pit viper envenomation
Nature of Coral Snake bites.
Not every snakebite results in the release of venom into the victim; “dry bites”
occur up to 20% of the time.
ranges from minor local swelling and discomfort at the injection site
to marked swelling, pain, blisters, bruising, and necrosis at the incision site; and
systemic symptoms such as fasiculations, hypotension, and severe coagulopathy
usually begins as minor pain at the incision with a
delayed serious systemic reaction that may lead to respiratory distress secondary to
neuromuscular weakness.
Treatment of Snake Bites.
Labs in the context of Snake bites.
Has does giving blood product in the context of bite treat the hemotological problems.
Find out what type of snake it was, administer the appropriate anti-venom
clotting studies, liver enzymes,
and complete blood counts with platelets are necessary.
Giving blood products to an
envenomated patient with a coagulopathy will not correct the problem. The circulating
venom responsible for the coagulopathy is still present and will likely inactivate
the blood products.
Most commonly available Antivenom for pit viper bites (Crotalidae)
When should Surgical debridement of fasciotomy be done
Neurological features of bites….
How long should these patient be observed if they are asymptomatic
Crotalidae polyvalent immune Fab CroFab.
Surgical debridement
or fasciotomy in the setting of envenomation should not be done
weakness, paresthesia, paralysis,
confusion, and respiratory depression
Asymptomatic patients who were bit by a
pit viper should be observed for 8 to 12 hours after the bite
Three different types of strokes and the demographics of each type?
Eighty percent of strokes are ischemic—due to the blockage of a blood vessel
secondary to thrombosis or embolism. They are generally seen in patients older than
the age of 50 and present with the sudden onset of focal neurologic deficits.
Hemorrhagic
strokes are typically seen in younger patients and are due to intraparenchymal
or subarachnoid cerebral vessel bleeding.
Ischemic stroke Syndromes Presentations of Stroke:
Dominant hemisphere? Nondominant hemisphere? Anterior cerebral artery? Middle cerebral artery? Posterior cerebral artery?
Contralateral numbness Dominant hemisphere - and weakness, contralateral visual
field cut, gaze preference, dysarthria, aphasia
Nondominant hemisphere - Contralateral numbness and weakness, visual field cut, contalateral neglect, dysarthria
Anterior cerebral artery - Contralateral weakness (leg > arm); mild sensory
deficits; dyspraxia.
Middle cerebral artery - Contralateral numbness and weakness (face, arm > leg); aphasia (if dominant hemisphere
Ischemic stroke Syndromes Presentations of Stroke:
Posterior cerebral artery?
Vertebrobasilar syndrome?
Basilar artery occlusion?
Lacunar infarct?
Posterior cerebral artery - Lack of visual recognition; altered mental status with
impaired memory; cortical blindness
Vertebrobasilar syndrome - Dizziness, vertigo; diplopia; dysphagia; ataxia; ipsilateral
cranial nerve palsies; contralateral weakness
(crossed deficits)
Basilar artery occlusion - Quadriplegia; coma; locked-in syndrome (paralysis except upward gaze)
Lacunar infarct - Pure motor or sensory deficit
Hemorrhagic stroke Syndromes Presentations of Stroke:
Intracerebral hemorrhage
Cerebellar hemorrhage
Intracerebral hemorrhage - May be clinically indistinguishable from infarction; contralateral numbness and weakness; aphasia, neglect (depending on hemisphere); headache,
vomiting, lethargy, marked hypertension more common
Cerebellar hemorrhage - Sudden onset of dizziness, vomiting, truncal instability, gaze palsies, stupor
Why is it critical to find out the exact time of onset of stroke symptoms?
Risk factors for Stroke. Demographics? PMH? Heart Conditions? Lifestyle?
Thrombolytics can only be given within a 4.5-hour window from the onset of
symptoms?
Male, African Americans, Stroke include a history of transient ischemic attack (TIA) or previous stroke, hypertension, atherosclerosis, cardiac
disease (eg, atrial fibrillation, myocardial infarction, valvular disease), diabetes,
carotid stenosis, dyslipidemia, hypercoagulable states, tobacco and alcohol use.
What is the NIH Stroke Scale (NIHSS) and what and what areas does it focus on (x6)
At what score is a severe stroke indicated?
At what score is tPA indicated?
3), a standardized system that measures the level of impairment caused by stroke. It measures several aspects of brain function such as consciousness, vision, sensation, movement, speech, and language.
A score above 20 to the maximal score
of 42 represents a severe stroke. They have increased ncreased risk of hemorrhagic conversion with tPA
Current guidelines allow strokes with scores above
4 to be treated with tPA.
What is the time frame for evaulation and imaging established by the National Institute of Neurological Disorders and Stroke (NINDS) for the treatment of stroke
What diagnostics studies are needed in the evaluation of a stroke.
physician evaluation within 10 minutes of arrival, specialist/neurologist notification within 15 minutes, CT of head within
25 minutes and CT interpretation within 45 minutes
An oxygen saturation - to exclude hypoxia,
ECG - cardiac abnormalities are common among stroke
patients like AF
POC Glucose - Hypoglycemia is a known mimicker of acute stroke and this condition
can be rapidly ruled out with a normal glucose level
CBC - platelets
should also be above 100,000 per mm3 to administer thrombolytics
INR - if the patient is on anticogulation and a risk for for bleeding
Imaging need in the context of stroke
Signs of stroke on CT, grey/white matter, vessels
non-contrast head CT scan.
An early CT
finding in ischemic stroke is loss of the grey-white differentiation due to increased water concentration in ischemic tissues. Another early CT finding is increased density within the occluded vessel, which represents the thrombus.
DDx for stroke in the ED
Neurologic Entities?
Toxic/metabolic abnormalities?
Infectious etiologies?
Cardiac or vascular causes?
Psychiatric/Neoplastic/Hemotologic/?
Neurologic - seizure/Todd’s paralysis, complicated migraine headaches, nonconvulsive status epilepticus, flares of demyelinating disorders such as multiple sclerosis, or spinal cord lesions
Toxic - hypo- and hyperglycemia, hypo- or hypernatremia,
drug overdose, and botulism.
Infectious etiologies - systemic infection, Bell palsy, meningitis/encephalitis,
Rocky Mountain spotted fever, and brain abscess
Other - tumor, sickle cell cerebral crisis, depression or psychosis,
and heat stroke.
Dosing of Atelplase during stroke therapy.
What should be done if the patient has had Aspirin or heparin?
How do you handle a patient with an elevated BP? Drugs?
If the BP is to be lower, what level can it be lower to?
rtPa is
usually administered 0.9 mg/kg with a maximum dose of 90 mg with 10% of the
dose administered as an IV bolus and the remainder infused over 60 minutes
neither heparin nor aspirin is used during the initial 24 hours. However,
thrombolytics should not be withheld from a patient who has recently taken
aspirin.
Elevated blood pressures are generally left untreated to maintain cerebral perfusion pressure. However, systolic blood pressure >220 mm Hg and diastolic blood pressures >120 mm Hg are best treated with easily titratable agents such as IV labetalol
and nitrates
If the BP is to be lower during strokes, what level can it be lower to? If rTa is to be given?
How does the treatment of hemorrhagic stroke differ from the treatment of ischemic strokes. What if anticogulation is present?
The blood pressure should not be lowered more than 25 percent of the presenting mean arterial blood pressure. The treated blood pressure should be
below 185/110 mm Hg for rTPA administration.
Treatment of hemorrhagic stroke is different and includes blood pressure control with anti-hypertensives such as nimodipine. nimodipine, possibly reversing any anticoagulation
with cryoprecipitate or platelets, and consultation with a hematologist and
neurosurgeon.
At what level of B-HCG is methotrexate most likely to be successful in induce an ectopic pregnancy? what size of fetus.
5000 mIU/mL, if the fetus is smaller than 3.5 cm, and if there is no detectable fetal cardiac activity
Why is morphine no longer reccommeded for the treatment of CHF
Morphine
is no longer recommended as standard therapy for CHF due to an association
with increased rates of intubation and ICU admission.
