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Pulseless electrical activity3/2/2023 ![]() Cardiac arrest and sudden cardiac deathĬardiac arrest ensues when ventricular contractions cease or are meaningless. ![]() Ventricular fibrillation is treated according to the resuscitation algorithm. By Bagnall et al: BMC Medical Genetics 15 (2014): 99. ECG showing ventricular tachycardia degenerating into ventricular fibrillation. This is pathognomonic (unique) to ventricular fibrillation and must not be confused with any other arrhythmia.įigure 2. No P-wave, QRS complex or T-wave can be seen. The ECG shows irregular waves with varying morphology and amplitude. Electrolyte disorders, acidosis, hypoxemia and ischemia all aggravate the risk of developing ventricular fibrillation, in any situation. Other common causes are cardiomyopathy (hypertrophic or dilated), arrhythmogenic right ventricular cardiomyopathy, Brugada syndrome, early repolarization. Most of these have atherosclerotic heart disease (coronary artery disease) as the underlying cause. The prognosis is very poor, with the majority of patients dying.Īpproximately 80% of individuals who suffer a sudden cardiac arrest have ventricular fibrillation prior to the cardiac arrest. The mechanisms in ventricular fibrillation are, as in atrial fibrillation, the existence of multiple re-entry circuits which cause chaotic ventricular depolarization. The patient dies if the rhythm is not restored. The absence of contractions causes syncope and circulatory collapse. Ventricular fibrillation means that the ventricles do not produce any meaningful contractions, they merely fibrillate. These arrhythmias lead to death if cardiopulmonary resuscitation is not started immediately. This article will focus on ventricular fibrillation, pulseless electrical activity and sudden cardiac arrest. You have completed Chapter XI.Ventricular fibrillation, pulseless electrical activity (PEA) and sudden cardiac arrest To ensure the best outcome for PEA it is vital to have uninterrupted, high quality CPR and to quickly figure out the reversible causes. The following is an algorithm shows management of cardiac arrest due to asystole/PEA (left side of chart) If not shockable, continue CPR for 2 minutes and try to treat the reversible causes Maintain advanced airway and capnography if needed.Epinephrine 1 mg IV/IO and repeat every 3 to 5 minutes.Once IV/IO access is obtained give the following drugs:.Attach monitor and check for shockable rhythm, if no shockable rhythm present, the patient is in asystole or PEA, continue CPR for 2 mins and obtain IV/IO access Management: Initiate the cardiac arrest algorithm on the right if the patient still has no pulse and does not respond to BLS.Once team is in place, one person will be responsible for the compressions and one for breaths using a BVM. If no pulse, immediately start compressions at a rate of 100 compressions per minute and allow chest to recoil.Call a code and get the code team in place.Check carotid pulse and note no pulse is present Check for responsiveness – Tap and shout “Are you alright?” and look at chest for movement.Scenario: You are the physician on duty and are called to the ER to see a patient who was involved in a motorcycle accident and is now unresponsive. Thrombosis (coronary) –formation of a blood clot which blocks a blood vessel in heart Hypothermia – core temp is less than 96.8 F, and severe is less than 86 F Thromobosis (pulmonary) – formation of a blood clot which blocks a blood vessel in lungs Hyper-/hypokalemia –abnormally high or low potassium concentration in the blood Hydrogen ion (acidosis) – Increase in the concentration of H ions in blood Tamponade – compression of the heart produced by excess fluid surrounding the heart Hypoxia- decreased partial pressure of oxygen in blood Tension pneumothorax – air in the pleural space around the lung (lung collapses) PEA can be caused by many factors and are represented as H’s and T’s: H’s ![]()
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