Unexpected cardiovascular collapse and death most often result from ventricular fibrillation in pts withunderlying coronary artery disease, with or without acute MI. Other common causes are listed in Table. The arrhythmic causes may be provoked by electrolyte disorders (primarily hypokalemia), hypoxemia, acidosis, or massive sympathetic discharge, as may occur in CNS injury. Immediate institution of cardiopulmonary resuscitation (CPR) followed by advanced life support measures (see below) are mandatory. Ventricular fibrillation, or asystole, without institution of CPR within 4–6 min usually causes death.
Management of Cardiac Arrest
Basic life support (BLS) must commence immediately (Fig. 13-1):
• Open mouthof patient and remove visible debris or dentures. If there is respiratory stridor, consider aspiration of a foreign body and perform Heimlich maneuver.
• Tilt head backward, lift chin, and begin mouth-to-mouth respiration if rescue equipment is not available (pocket mask is preferable to prevent transmission of infection). The lungs should be inflated twice in rapid succession for every 15 chest compressions.
• If carotid pulse is absent, perform chest compressions (depressing sternum 3–5 cm) at rate of 80–100 per min. For one rescuer, 15 compressions are performed before returning to ventilating twice.
• As soon as resuscitation equipment is available, begin advanced life support withcontinued chest compressions and ventilation.
• Although performed as simultaneously as possible, defibrillation takes highest priority (Fig. 13-2A), followed by placement of intravenous access and in tubation. 100% O2 should be administered by endotracheal tube or, if rapid intubation cannot be accomplished, by bag-valve-mask device; respirations should not be interrupted for more than 30 s while attempting to intubate.
• Initial intravenous access should be through the antecubital vein, but if drug administration is ineffective, a central line (internal jugular or subclavian) should be placed. Intravenous NaHCO3 should be administered only if there is persistent severe acidosis (pH < 7.15) despite adequate ventilation. Calcium is not routinely administered but should be given to pts with known hypocalcemia, those who have received toxic doses of calcium channel antagonists, or if acute hyperkalemia is thought to be the triggering event for resistant ventricular fibrillation.
• The approach to cardiovascular collapse caused by bradyarrhythmias, asystole, or pulseless electrical activity is shown in Fig. 13-2B.
• Open mouthof patient and remove visible debris or dentures. If there is respiratory stridor, consider aspiration of a foreign body and perform Heimlich maneuver.
• Tilt head backward, lift chin, and begin mouth-to-mouth respiration if rescue equipment is not available (pocket mask is preferable to prevent transmission of infection). The lungs should be inflated twice in rapid succession for every 15 chest compressions.
• If carotid pulse is absent, perform chest compressions (depressing sternum 3–5 cm) at rate of 80–100 per min. For one rescuer, 15 compressions are performed before returning to ventilating twice.
• As soon as resuscitation equipment is available, begin advanced life support withcontinued chest compressions and ventilation.
• Although performed as simultaneously as possible, defibrillation takes highest priority (Fig. 13-2A), followed by placement of intravenous access and in tubation. 100% O2 should be administered by endotracheal tube or, if rapid intubation cannot be accomplished, by bag-valve-mask device; respirations should not be interrupted for more than 30 s while attempting to intubate.
• Initial intravenous access should be through the antecubital vein, but if drug administration is ineffective, a central line (internal jugular or subclavian) should be placed. Intravenous NaHCO3 should be administered only if there is persistent severe acidosis (pH < 7.15) despite adequate ventilation. Calcium is not routinely administered but should be given to pts with known hypocalcemia, those who have received toxic doses of calcium channel antagonists, or if acute hyperkalemia is thought to be the triggering event for resistant ventricular fibrillation.
• The approach to cardiovascular collapse caused by bradyarrhythmias, asystole, or pulseless electrical activity is shown in Fig. 13-2B.
Follow-up
If cardiac arrest was due to ventricular fibrillation in initial hours of an acute MI, follow-up is standard post-MI care. For other survivors of a ventricular fibrillation arrest, extensive assessment, including evaluation of coronary anatomy, left ventricular function, and invasive electrophysiologic testing, is often recommended. In absence of a transient or reversible cause, ICD placement usually indicated.
Salam
Source: Manual of Medicine
Image: hana.com
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