Emergency Medicine Flashcards

1
Q

Define hypothermia?

A
  • A reduction of core body temperature below 35°C (normal 37°C).
  • Core temperature is measured with a rectal probe or through the esophagus
  • Severe hypothermia is a core
    temperature below 30°C.
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2
Q

Describe the clinical presentation for Hypothermia?

A
  • Lethargy, confusion and weakness.
  • Death usually occurs from arrhythmia because the cold alters cardiac conduction.
  • Patients may have metabolic acidosis, respiratory acidosis, kidney injury and hyperkalemia.
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3
Q

How do you diagnose hypothermia?

A
  • EKG shows an arrhythmia, either ventricular fibrillation or ventricular tachycardia.
  • Elevation of the J point, known as Osborne waves.
  • J wave elevation looks like ST-segment elevation
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4
Q

How do you treat hypothermia?

A
  • Warm bed, bath or heated blankets.
  • Warmed IV fluids or warmed humidified oxygen in severe cases.
  • Caution because rapid heating may also cause arrhythmias.
  • If arrhythmia presents, continue resuscitative measures until body temperature is >35°C (95 F)
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5
Q

Name three exertional heat disorders.

A
  • Heat cramps
  • Heat exhaustion
  • Lethal heat stroke
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6
Q

Name two nonexertional heat disorders.

A
  • Malignant hyperthermia

- Neuroleptic malignant syndrome

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7
Q

What are heat cramps and how are they treated?

A
  • Occurs with fluid and electrolyte depletion
  • Develop painful muscle contractions with muscle tenderness
  • Patient is able to sweat normally with no neurological abnormalities.
  • Treat with rest, oral rehydration and salt replacement.
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8
Q

What is heat exhaustion and how do you treat it?

A
  • More severe exertional disorder .
  • Patient is weaker, has systemic symptoms, body temperature is slightly elevated,.
  • Neurologic symptoms include headache, nausea and anxiety.
  • Death is unlikely but can progress to heat stroke if not treated.
  • Patient can still sweat and remove heat from the body.
  • Treatment is oral fluid rehydration and electrolyte replacement, may require IV.
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9
Q

What is a heat stroke and how do you treat it?

A
  • Severe and potentially life threatening.
  • Patients have lost ability to sweat and remove heat from the body.
  • Body temperature may be elevated (>41°C or 105 F) resulting in confusion, disorientation, nausea, blurred vision and seizures.
  • Labs may show hemoconcentration, rhabdomyolysis, elevated BUN, creatinine and white cell count.
  • Anuria, DIC and lactic acidosis may develop.
  • Treat with IV fluid replacement and rapid cooling off of the body such as placing in a cool environment and spraying with water and fanning to evaporate the fluid.
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10
Q

What is malignant hyperthermia?

A

Occurs as an idiotsyncratic reaction to the use of anesthetic agents such as halothane or succinylcholine (paralytic)

  • May be caused by any anesthetic.
  • Rhabdomyolysis may develop
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11
Q

How do you treat malignant hyperthermia?

A

Dantrolene
- Depresses excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor 1 and decreases intracellular calcium concentration.

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12
Q

What is neuroleptic malignant syndrome?

A
  • Idiosyncratic reaction to a wide variety of phenothiazines or butyrophenones such as haloperidol.
  • Muscular rigidity and rhabdomyolysis may occur.
  • Treat with bromocriptine, stimulates dopamine receptors, specifically in the nigrostriatal pathway.
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13
Q

What is asystole?

A
  • Complete absence of electrical activity in the heart
  • Does not necessarily mean a flat line
  • Usually due to ischemia
  • Presents as unresponsive person with no pulse
  • Treatment
    1. CPR, obtain IV access and prepare for intubation
    2. 1 mg epinephrine via IV push every 3-5 minutes
    3 Reevaluate for atypical clinical features
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14
Q

Most common causes of asystole and other arrhythmias

A
Hypoxia
Hypo/Hyperkalemia
Hypothermia
Hypoglycemia
Hypovolemia
Trauma
Toxins (Includes overdose)
Tamponade
Tension Pneumothorax
Thrombosis (coronary and pulmonary)
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15
Q

When is bicarbonate helpful in asystole?

A
When due to:
Pre-existing acidosis:
Tricyclic antidepressant (amitriptyline)
Aspirin
Hyperkalemia
Diabetic Ketoacidosis
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16
Q

What is the recommended treatment for a patient that presents to the ED within 12 hours of an MI?

A
  1. Percutaneous coronary intervention (PCI)
    - Preferred choice
    - Lower rates of intracerebral hemorrhage and recurrent MI
  2. Fibrinolysis
    - Only if PCI not available
    - Use tenecteplase or alteplase
    - Contraindicated if GI bleeding or recent surgery
    - It binds fibrin in the thrombus and converts entrapped plasminogen to plasmin
    - Plasmin causes clot lysis and restores coronary flow
    - Hemorrhage is most adverse therapy
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17
Q

Clinical signs that a patient has an intracranial hemorrhage?

A
  • Decreased level of consciousness
  • Asymmetric pupils
  • Irregular breathing
18
Q

Clinical signs of intraventricular septum perforation

A
  • Presents with chest pain, dyspnea, cardiogenic shock and a harsh holosystolic murmur on the left sternal border
  • Results in a left to right shunt and symptoms of acute heart failure
19
Q

Clinical presentation of pulmonary embolism?

A
  • Acute onset of dyspnea, pleuritic chest pain and possible hemoptysis
  • Tachycardia, hypotension, cyanosis and loss of consciousness can occur if severe.
20
Q

What is the mechanism of action of etoposide and podophyllin?

A
  • Inhibit Topoisomerase II’s ability to seal the strand breaks it induces, cause chromosomal breaks to accumulate and eventual cell death.
  • Used for testicular cancer and small cell lung cancer.
  • Podophyllin is used for genital warts
21
Q

ER migraine cockdtail?

A
Phenergan 50 mg
Benadryl 50 mg
Ativan 2 mg
Caffeine 200 mg
Normal Saline .9% 1000 ml
22
Q

Scorpion Sting treatment and labs

A
Lipase
UA without micro
CMP
CBC
Give:
- Normal Saline
- Zofran 4-8 mg IVP
- Ativan 1-2 mg IVP
- Dilauted 1-2 mg 
Check for tongue fasciculations
23
Q

Patient comes in with chest pain/tightness and SOB, what do you do?

A
  1. Prescribe 325 mg of aspirin
  2. EKG and Continous Cardiac Monitoring
  3. Labs
    - EKG
    - CBC
    - CMP
    - D-Dimer
    - Troponin
    - Creatine Kinase
24
Q

What is ventricular fibrillation?
What are the causes?
How does it present?
How do you treat?

A
  • Significant electrical activity with no signs of an organized pattern
  • Due to ischemia, myocadial infarction, cardiomyopathy and severe underlying cardiac disease
  • Dead person with ventricular fibrillation on EKG
  • Treat with defibrillation, a single unsynchronized shock
25
Q

What is ventricular tachycardia?
What is the cause?
How does it present?

A
  • A wide complex tachycardia with an organized, uniform pattern on EKG
  • No visible p waves
  • Due to ischemia, MI and anotomic cardiac disease
  • It originates from ectopic focus in the myocardium or from AV node due to reentry
  • The slowness of the conduction produces slower and wider complexes
  • Short bursts < 30 seconds may produce no symptoms.
  • > 30 seconds is referred to as sustained tachycardia and may produce lightheadedness, hypotension, CHF, syncope and death
  • Treat with amiodarone or lidocaine and cardioversion
26
Q

What is torsade de pointes?

A

A form of VT where the morphology varies with an undulating amplitude , making it seem as it twists around a point
- May be associated with hypomagnesemia and preceded by long QT interval

27
Q

What medications can prolong QT interval? What other causes?

A
TCAs
Antipsychotics
Erythromycin
Methadone
Fluoroquinolones
Amiodarone
Quinidine
Sotolol
Flecainide
Procainamide
Mg
K 
Ca
28
Q

What do leads I and aVL look at?

A

The left lateral ventrical

29
Q

What do leads II, III and aVF look at?

A

The inferior wall of the heart

30
Q

What does leads aVR look at?

A
  • It is unipolar, determines if the electrical activity is traveling in the correct direction
  • The wave should be inverted
31
Q

What do leads V1 and V2 look at?

A

The interventricular septum

32
Q

What do leads V3 and V4 look at?

A

The anterior left ventrical

33
Q

What do leads V5 and V6 look at?

A

The left lateral ventricle along with leads I and aVL

34
Q

What are the 6 steps when examining an EKG?

A
  1. General impression
  2. Calibration
  3. Rhythm Determination
  4. QRS Assesment
  5. Hypertrophy
  6. Ischemic Infarction
35
Q

What is step 1 when examining an EKG?

A
  • The general impression
  • Does anything stick out?
    1. Are there fast rhythms?
    2. Are there slow rhythms?
    3. Is anything ugly?
    Jot down what you see quickly?
36
Q

What is step 2 when examining an EKG?

A

Check if its standard, 2x or 1/2 amplitude?

  1. Standard calibration
    - 1mV standard is 10 mm tall and .2mm wide (5mm)
  2. 2X amplitude is 20 mm tall .2mm wide (5mm)
  3. 1/2 amplitude is 5mm tall and .2 mm wide
37
Q

What is step 3 when examining an EKG?

A

Rhythm interpretation

  1. Rate
  2. Regularity
  3. P-wave
  4. PR-interval
  5. QRS-complex
  6. Interpretation
38
Q

What is step 4 when examining an EKG?

A

QRS assesment

  1. R wave progression (RWP)
    - Is it good RWP or poor RWP
  2. QRS axis
    - Is the axis normal, right, left or indeterminant?
  3. Bundle branch block and fascicular block
    - Is it RBBB or LBBB?
    - Is it LAFB or LPFB?
39
Q

What is step 5 when examining an EKG?

A

Is there hypertrophy?

  1. Atrial enlargement
    - Look at the P waves
  2. Ventricular rhypertrophy
    - Look at the QRS complex
40
Q

What is step 6 when examining an EKG?

A

Is there ischemia or infarction?
Is there ST segment elevation?
Is there ST segment depression?
Are there pathological q waves?

41
Q

What is the treatment of choice when a patient ingests rodenticide that contains brodifacoum (long acting 4- hydroxycoumarin derivative) that cause coagulopathy and abnormal bleeding?

A
  • Requires immediate treatment with fresh frozen plasma in addition to vitamin K
  • Similar to warfarin toxicity
42
Q

When conducting an emergency Cricothyrotomy, what structures do you have to cut through?

A
  1. The skin
  2. Superficial cervical fascia (including subcutaneous fat and platysma)
  3. Investing and pretracheal layers of the deep cervical fascia
  4. Cricothyroid membrane