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Asystole - Causes, Symptom And Treatment of Asystole
What is Asystole? Asystole is a state of no cardiac electrical activity, hence no contractions of the myocardium and no cardiac output or blood flow. Asystole or bradyasystole follows untreated VF and commonly occurs after unsuccessful attempts at defibrillation. Causes of Asystole Asystole is usually caused by ventricular fibrillation. Primary asystole develops when cellular metabolic functions are no longer intact and an electrical impulse cannot be generated. With severe ischemia, pacemaker cells cannot transport the ions necessary to effect the transmembrane action potential. Implantable pacemaker failure may also be a cause of primary asystole. Treatment of Asystole There are no specific treatment for asystole. Primary asystole may be prevented by the appropriate use of a permanent pacemaker in those patients who have high-grade heart block or sinus arrest.The only 2 drugs recommended by the American Heart Association (AHA) for adults in asystole are epinephrine and atropine.Transcutaneous pacing (TCP), even when used immediately, has not altered meaningful survival (ie, functional lifestyle) significantly. Transcutaneous pacing (TCP), even when used immediately, has not altered meaningful survival significantly. The H’s and T’s of ACLS is a mnemonic used to help recall the major contributing factors to pusleless arrest including PEA, Asystole, Ventricular Fibrillation, and Ventricular Tachycardia. These H’s and T’s will most commonly be associated with PEA, but they will help direct your search for underlying causes to any of arrhythmias associated with ACLS. Each is discussed more thoroughly below. The H’s include: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hyper-/hypokalemia, Hypoglycemia, Hypothermia. The T’s include: Toxins, Tamponade(cardiac),Tension pneumothorax, Thrombosis (coronary and pulmonary), and Trauma. Hypovolemia Hypovolemia or the loss of fluid volume in the circulatory system can be a major contributing cause to cardiac arrest. Looking for obvious blood loss in the patient with pusleless arrest is the first step in determining if the arrest is related to hypovolemia. After CPR, the most import intervention is obtaining intravenous access/IO access. A fluid challenge or fluid bolus may also help determine if the arrest is related to hypovolemia. Hypoxia Hypoxia or deprivation of adequate oxygen supply can be a significant contributing cause to cardiac arrest. You must ensure that the patient’s airway is open, and that the patient has chest rise and fall and bilateral breath sounds with ventilation. Also ensure that your oxygen source is connected properly. Hydrogen ion (acidosis) To determine if the patient is in respiratory acidosis, an arterial blood gas evaluation must be performed. Prevent respiratory acidosis by providing adequate ventilation. Prevent metabolic acidosis by giving the patient sodium bicarbonate. Hyper-/hypokalemia Both a high potassium level and a low potassium level can contribute to cardiac arrest. The major sign of hyperkalemia or high serum potassium is taller and peaked T-waves. Also, a widening of the QRS-wave may be seen. This can be treated in a number of ways which include sodium bicarbonate (IV), glucose+insulin, calcium chloride (IV), Kayexalate, dialysis, and possibly albuterol. All of these will help reduce serum potassium levels. The major signs of hypokalemia or low serum potassium are flattened T-waves, prominent U-waves, and possibly a widened QRS complex. Treatment of hypokalemia involves rapid but controlled infusion of potassium. Giving IV potassium has risks. Always follow the appropriate infusion standards. Never give undiluted intravenous potassium. Hypoglycemia Hypoglycemia or low serum blood glucose can have many negative effects on the body, and it can be associated with cardiac arrest. Treat hypoglycemia with IV dextrose to reverse a low blood glucose. Hypothermia If a patient has been exposed to the cold, warming measures should be taken. The hypothermic patient may be unresponsive to drug therapy and electrical therapy (defibrillation or pacing). Core temperature should be raised above 86 F (30 C) as soon as possible. The T’s include: Toxins Accidental overdose of a number of different kinds of medications can cause pulseless arrest. Some of the most common include: tricyclics, digoxin, betablockers, calcium channel blockers, and erythromycin). Street drugs and other chemicals can precipitate pulseless arrest. Cocaine is the most common street drug that increases incidence of pulseless arrest. ECG signs of toxicity include prolongation of the QT interval. Physical signs include bradycardia, pupil symptoms, and other neurological changes. Support of circulation while an antidote or reversing drug is obtained is of primary importance. Poison control can be utilized to obtain information about toxins and reversing agents. Tamponade Cardiac tamponade is an emergency condition in which fluid accumulates in the pericardium (sac in which the heart is enclosed). The buildup of fluid results in ineffective pumping of the blood which can lead to pulseless arrest. ECG symptoms include narrow QRS complex and rapid heart rate. Physical signs include jugular vein distention (JVD), no pulse or difficulty palpating a pulse, and muffled heart sounds due to fluid inside the pericardium. The recommended treatment for cardiac tamponade is pericardiocentesis. Tension Pneumothorax Tension pneumothorax occurs when air is allowed to enter the plural space and is prevented from escaping naturally. This leads to a build up of tension that causes shifts in the intrathroacic structure that can rapidly lead to cardiovascular collapse and death. ECG signs include narrow QRS complexes and slow heart rate. Physical signs include JVD, tracheal deviation, unequal breath sounds, difficulty with ventilation, and no pulse felt with CPR. Treatment of tension pneumothorax is needle decompression. Thrombosis (heart: acute, massive MI) Coronary thrombosis is an occlusion or blockage of blood flow within a coronary artery caused by blood that has clotted within the vessel. The clotted blood causes an Acute Myocardial Infarction which destroys heart muscle and can lead to sudden death depending on the location of the blockage. ECG signs indicating coronary thrombosis are 12 lead ECG with ST-segment changes, T-wave inversions, and/or Q waves. Physical signs include: elevated cardiac markers on lab tests, and chest pain/pressure. Treatments for coronary thrombosis include use of fibrinolytic therapy, PCI (percutaneous coronary intervention). The most common PCI procedure is coronary angioplasty with or without stent placement. Thrombosis (lungs: massive pulmonary embolism) Pulmonary thrombus or pulmonary embolism (PE) is a blockage of the main artery of the lung which can rapidly lead to respiratory collapse and sudden death. ECG signs of PE include narrow QRS Complex and rapid heart rate. Physical signs include no pulse felt with CPR. distended neck veins, positive d-dimer test, prior positive test for DVT or PE. Treatment includes surgical intervention (pulmonary thrombectomy) and fibrinolytic therapy. Trauma The final differential diagnosis of the H’s and T’s is trauma. Trauma can be a cause of pulseless arrest, and a proper evaluation of the patients physical condition and history should reveal any traumatic injuries. Treat each traumatic injury as needed to correct any reversible cause or contributing factor to the pulseless arrest. Shockable Pulseless Arrest Rhythms Pulseless arrest rhythms are divided into shockable and nonshockable. Shockable rhythms are VF or ventricular tachycardia (VT). If VT/VF persists after the first shock and 5 cycles or 2 minutes, then give another shock, resume CPR, and obtain intravenous (IV) access. The IV access should be obtained and should be peripheral or interosseous (IO) and not interfere with chest compressions. Central lines do provide better peak drug concentrations and shorter circulation times, but also are more difficult to obtain and result in longer interruptions in CPR. Drugs may also be given endotracheally but should be diluted with 5-10 cc of water or normal saline.[4,8] If VT/VF persists, give a vasopressor. Drugs may be given immediately before or after the shock. Epinephrine 1 mg may be given IV or IO and repeated every 3-5 minutes. Vasopressin 40 IU may be given as an alternate to the first or second dose of epinephrine. Resume CPR for 5 cycles or 2 minutes; check the rhythm; shock; and resume CPR. Should VT/VF persist, then give an antiarrhythmic. Amiodarone 300 mg IV/IO followed by 150 mg IV/IO is first-choice. Lidocaine 1-1.5 mg/kg IV/IO first dose followed by 0.5-0.75 mg/kg IV/IO up to a total of 3 doses or 3 mg/kg may also be given. If torsades de pointes is present, then give magnesium 1-2 g diluted in 10 mL D5W IV/IO push, typically over 5-20 minutes (Class IIa for torsades). Continue CPR followed by 1 shock and additional CPR/medications for 5 cycles or 2 minutes. If the rhythm becomes nonshockable, then practitioners should follow the algorithm for nonshockable rhythms.[8] Nonshockable Pulseless Arrest Rhythms Nonshockable rhythms include asystole and pulseless electrical activity. If these rhythms result after a shock, give a vasopressor. Epinephrine 1 mg IV/IO every 3-5 minutes or vasopressin 40 IU IV/IO instead of the first or second dose of epinephrine may be given. If there is no response and pulseless electrical activity or asystole persists, give atropine 1 mg IV/IO, which may be repeated every 3-5 minutes. HCPs should search for and treat possible reversible causes for cardiac arrest ( Table 1 ).[4,8] Symptomatic Bradycardia Bradycardia is defined as a heart rate < 60 beats/minute, which may be normal for some individuals. However, if the individual has symptoms, such as hypotension, altered mental status, chest pain, syncope, or other signs of shock, then treatment is warranted.[9] Practitioners should provide basic treatment, including oxygen, airway maintenance and breathing assistance, electrocardiographic (ECG) monitoring, and IV access, and prepare for transcutaneous pacing. If there is a high-degree atrioventricular (AV) block, such as Mobitz II or third-degree AV bock, consider giving medications as a bridge to pacing. Atropine 0.5 mg IV (up to 3 mg maximum), an epinephrine infusion 2-10 micrograms (mcg)/minute, or a dopamine infusion 2-10 mcg/minute may be given. Begin transcutaneous pacing if these medications are ineffective and prepare for transvenous pacing with expert consultation.[4,9] Symptomatic Tachycardia Although tachycardia is defined as a heart rate > 100 beats/minute, patients are usually symptomatic with rates > 150 beats/minute. Patients with symptoms of shock should be treated. Basic treatment is the same as for symptomatic bradycardia; however, sedation may be considered. Immediate synchronized cardioversion is performed for unstable supraventricular tachycardia (SVT) due to reentry, unstable atrial fibrillation, unstable flutter, and unstable monomorphic VT. An unstable patient with polymorphic VT should receive immediate high-energy unsynchronized shock ( Table 2 ).[9] Further treatment for stable patients is based on classification of the rhythm into narrow-complex or wide-complex tachycardia and regular or irregular. Regular narrow-complex tachycardias (QRS < 0.12 seconds) include sinus tachycardia and SVT. There is no specific drug treatment for sinus tachycardia. HCPs should search for and treat the underlying cause, such as fever, anemia, or shock. Initial treatment for SVT is vagal maneuvers, which terminate 20% to 25% of reentry SVT, and adenosine.[9] Give adenosine 6 mg IV over 1-3 seconds followed by 20 mL of saline flush and arm elevation. If the rhythm persists after 1-2 minutes, give 12 mg IV. If the rhythm doesn't convert, give a second 12-mg bolus 1-2 minutes later. Side effects are transient and include flushing, shortness of breath, and chest pain.[9] If the rhythm persists after adenosine, then second-line drugs, such as a calcium channel blocker (verapamil or diltiazem) or a beta blocker, may be used. Verapamil 2.5-5 mg IV over 2 minutes and repeat doses of 5-10 mg may be given at 15-minute intervals to a total dose of 20 mg. For diltiazem, the dose is 15-20 mg IV over 2 minutes, and if there is no response in 15 minutes, then 20-25 mg may be given followed by a maintenance infusion of 5-15 mg/hour. These drugs should not be used for Wolff-Parkinson-White syndrome. HCPs should use the beta blocker with which they are most familiar. Side effects include bradycardias, hypotension, and AV conduction delays.[9] Regular wide-complex tachycardias (QRS ≥ 0.12 seconds) include VT, SVT with aberrancy, and those associated or mediated by accessory pathways. Adenosine is recommended for wide-complex tachycardias that are believed to be SVT. If VT and the patient are stable, then an antiarrhythmic drug may be given. Amiodarone 150 mg IV may be given over 10 minutes and may be repeated to a maximum dose of 2.2 g IV every 24 hours. Other drugs include procainamide 20 mg/minute as an infusion until the rhythm is converted, the QRS is widened by 50%, or a total of 17 mg/kg has been given. Maintenance is 1-4 mg/minute. Sotalol 1-1.5 mg/kg may be given at a rate of 10 mg/minute.[9] If the rhythm is wide or narrow and irregular, then it may be atrial fibrillation with an uncontrolled ventricular response. Expert consultation is advised. Consultation is also advised for polymorphic VT or torsades de pointes; however, if the patient is unstable, then provide high-energy unsynchronized shock and begin CPR following the steps for a pulseless cardiac arrest.[9] http://equimedcorp.com/rhythms/topic/51/ http://www.learnekgs.com/learnecgrules.htm http://cal.vet.upenn.edu/projects/anestecg/Basics/smartrev.htm http://www.medicinenet.com/sudden_cardiac_death/article.htm |