Some Considerations

1
Some Considerations in Emergency Treatment
2
Sustained Ventricular Tachycardia
Pulse present
No pulse
Unstable
Stable
O2 and IV access
Consider
Treat as VF
Lidocaine 1mg/kg Consider sedation Lidocaine
0.5mg/kg Cardiovert 50J Every 8
min.untill VT resolves
or up to 3mg/kg if not
Cardiovert 100J Procainamide 20mg/min until
VT resolve
or up to 1gr If not
Cardiovert up to 360J
3
Asystole

• Continue CPR
• Epinephrine 1 10 000 , 0.5 1.0mgIV push
• Intubate when possible
• Atropine, 1.0 mg IV push
  ( repeated
  in 5 min )
• Consider bicarbonate
• Consider pacing 20 min
• 
  

4
Cardiac Arrest

• 1 Endotracheal intubation as well as
  hyperventilation should be performed to maintain
  a PaCo2 between 25 to 30mm Hg and a Pa O2 of
  approximately 100mm Hg
• 2 Cerebral perfusion pressure should be
  maintained between 80 and 100 mm Hg by
  maintaining mean arterial pressure and reducing
  intracranial pressure, if it is elevated.
  (Cerebral perfusion pressure is the mean arterial
  pressure minus intracranial pressure) Reduction
  in intracranial pressure can be produced by
  hyperventilation and the administration of
  osmotic and loop diuretics.

5
Cardiac Arrest

• 3 Serum osmolality should be adjusted to a normal
  value of 280 to 295 mOsm/kg H2O
• 4 Normal temperature should be controlled and
  shivering prevented
• 5 Seizure activity should be controlled with
  phenobarbital, phenitoin or diazepam

6
Cardiac Arrest

• 6 Cerebral edema after cardiac arrest can be
  treated with methylprednisolone sodium succinate
  in doses of 60 to 100 mg, or dexamethasone sodium
  phosphate, 12 to 20 mg IV every 6 hours. However,
  it is not certain if corticosteroids are
  effective in decreasing cerebral edema after
  cardiac arrest. Shock lung, aspiration
  pneumonitis, or cardiogenic shock can be treated
  with these or similar corticosteroids.

7
Cardiac Arrest

• 7 Limit IV fluids to approximately 1,500 ml daily
  to prevent water excess, hyponatremia, and
  further edema of the brain.
• 8 The head should be elevated to 30º to increase
  venous drainage.
• 9 Tracheal suctioning should be performed
  carefully because it produces an increased
  itracranial pressure.

8
When a patient with cardiac arrest has been
resuscitated, the EEG may be helpful in
determining prognosis. Adverse prognostic EEG
sings include regular recurrence of any
particular EEG pattern (the slower the repetition
rate the worse the prognosis), paroxysmal
activity, consistently low amplitude, episodic
reductions in amplitude, lack of theta and alpha
activity, and absence of an EEG response to
painful or auditory stimulation.
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Syncope, or fainting, is a transient loss of
consciousness. It is most commonly caused by
cerebral hypoxia secondary to inadequate cerebral
blood flow. Syncope is discussed here in the
context of cardiac emergencies because it may be
an important clue to cardiac disease, and early
treatment of patients with syncope may avert
future cardiac emergencies. However, who faint do
not have underlying cardiac problems.
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Classification of Syncope

• Vasodepressor (vasovagal) syncope
• Syncope of cardiac origin
• Syncope caused by postural Hypotension
• Syncope caused by excessive vagal reflexes
• Syncope caused by cerebral factors

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Syncope of cardiac origin

• Aortic stenosis
• Hypertrophic cardiomyopathy
• Acute pulmonary embolism
• Malfunction of a prosthetic valve
• Primary pulmonary hypertension
• Left atrial myxoma
• Cardiac tamponade
• Complete AV block
• Tachiarrhytmias
• Runaway pacemaker

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Syncope caused by postural Hypotension

• Functional (venous pooling and depletion of
  blood volume)
• Mastocytosis
• Organic

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Syncope caused by excessive vagal reflexes

• Carotid sinus syncope
• Syncope due to other vagal reflexes

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Eugene Yevstratov MD
ostlandfox_at_medscape.com