Eugene Yevstratov MD

Sustained Ventricular Tachycardia No pulse Pulse present UnstableStable O 2 and IV access 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 Consider

Eugene Yevstratov MD Asystole Continue CPR Epinephrine 1: , 0.5 – 1.0mgIV push Intubate when possible Atropine, 1.0 mg IV push ( repeated in 5 min ) Consider bicarbonate Consider pacing 20 min

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.

Eugene Yevstratov MD Cardiac Arrest 3 Serum osmolality should be adjusted to a normal value of 280 to 295 mOsm/kg H 2 O 4 Normal temperature should be controlled and shivering prevented 5 Seizure activity should be controlled with phenobarbital, phenitoin or diazepam

Eugene Yevstratov MD 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.

Eugene Yevstratov MD 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.

Eugene Yevstratov MD 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.

Eugene Yevstratov MD 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.

Eugene Yevstratov MD 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

Eugene Yevstratov MD 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

Eugene Yevstratov MD Syncope caused by postural Hypotension Functional (venous pooling and depletion of blood volume) Mastocytosis Organic

Eugene Yevstratov MD Syncope caused by excessive vagal reflexes Carotid sinus syncope Syncope due to other vagal reflexes

Eugene Yevstratov MD