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From Wikipedia, the free encyclopedia

Asystole
Other namesCardiac flatline, asystolic arrest
A rhythm strip showing two beats of normal sinus rhythm followed by an atrial beat and asystole
Pronunciation
SpecialtyCardiology Edit this on Wikidata

Asystole (New Latin, from Greek privative a "not, without" + systolē "contraction"[1][2]) is the absence of ventricular contractions in the context of a lethal heart arrhythmia (in contrast to an induced asystole on a cooled patient on a heart-lung machine and general anesthesia during surgery necessitating stopping the heart). Asystole is the most serious form of cardiac arrest and is usually irreversible. Also referred to as cardiac flatline, asystole is the state of total cessation of electrical activity from the heart, which means no tissue contraction from the heart muscle and therefore no blood flow to the rest of the body.

Asystole should not be confused with very brief pauses below 3 seconds in the heart's electrical activity that can occur in certain less severe abnormal rhythms. Asystole is different from very fine occurrences of ventricular fibrillation, though both have a poor prognosis, and untreated fine VF will lead to asystole. Faulty wiring, disconnection of electrodes and leads, and power disruptions should be ruled out.

Asystolic patients (as opposed to those with a "shockable rhythm" such as coarse or fine ventricular fibrillation, or unstable ventricular tachycardia that is not producing a pulse, which can potentially be treated with defibrillation) usually present with a very poor prognosis. Asystole is found initially in only about 28% of cardiac arrest cases in hospitalized patients,[3] but only 15% of these survive, even with the benefit of an intensive care unit, with the rate being lower (6%) for those already prescribed drugs for high blood pressure.[4]

Asystole is treated by cardiopulmonary resuscitation (CPR) combined with an intravenous vasopressor such as epinephrine (a.k.a. adrenaline).[5] Sometimes an underlying reversible cause can be detected and treated (the so-called "Hs and Ts", an example of which is hypokalaemia). Several interventions previously recommended—such as defibrillation (known to be ineffective on asystole, but previously performed in case the rhythm was actually very fine ventricular fibrillation) and intravenous atropine—are no longer part of the routine protocols recommended by most major international bodies.[6] 1 mg epinephrine by IV every 3–5 minutes is given for asystole.[7]

Survival rates in a cardiac arrest patient with asystole are much lower than a patient with a rhythm amenable to defibrillation; asystole is itself not a "shockable" rhythm. Even in those cases where an individual suffers a cardiac arrest with asystole and it is converted to a less severe shockable rhythm (ventricular fibrillation, or ventricular tachycardia), this does not necessarily improve the person's chances of survival to discharge from the hospital, though if the case was witnessed by a civilian, or better, a paramedic, who gave good CPR and cardiac drugs, this is an important confounding factor to be considered in certain select cases.[8] Out-of-hospital survival rates (even with emergency intervention) are less than 2 percent.[9]

YouTube Encyclopedic

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  • Pulseless electrical activity (PEA) and asystole | NCLEX-RN | Khan Academy
  • 10b: Pulseless Electrical Activity and Asystole (2023)
  • 10b: Pulseless Electrical Activity and Asystole (2021) OLD
  • 7c: Pulseless Electrical Activity and Asystole (2024)
  • Cardiac arrest rhythms, VF, VT, Asystole and PEA

Transcription

-[Voiceover] Ventricular asystole and pulseless electrical activity are two types of cardiac arrest, meaning the heart has stopped. In both of these, a patient doesn't have a pulse, meaning that they're not pumping blood to the rest of the body, and that's why both of these conditions are absolutely fatal unless they're corrected immediately. So in ventricular asystole, there's no electrical activity in the heart. That there's no electrical activity, that means that the ventricle walls aren't contracting. And that's what asystole basically means. A means no, and systole implies ventricular contractions. So no ventricular contractions. Again, no electrical activity means no ventricular contractions, means no cardiac output, or in other words, there's no blood flowing to the rest of the body. So there's no cardiac output. And without cardiac output, you're not going to have a pulse. So anybody who has ventricular asystole will not have a pulse. On an EKG, this looks like a flat line because there's no electrical activity to cause any movement on an EKG. And this is the flat line that you hear about on movies and TV shoes, and they say, "The patient's flatlining!" It's asystole. And then there's pulseless electrical activity. And this is known as PEA. In PEA, there is electrical activity on EKG. However, it doesn't result in a pulse. And the electrical activity you see on an EKG could be something that normally produces a pulse, such as normal sinus rhythm, or even heart block, or sinus bradycardia, but for some reason there's not a pulse. Now how could this be? Well, in a normal heart, the heart's electrical activity causes the muscle cells to contract. So you have action potentials that propagate or went through the heart, and they'll lead to muscle contraction. And this relationship between electrical activity and mechanical contraction is called electro-mechanical coupling. However, when the heart is under extreme stress, so say the heart's been deprived of oxygen for a long time, the system gets disconnected. So, even though there's electrical activity, it's not going to lead to contractions. Because we've disconnected the system, and this is called electro-mechanical uncoupling. So despite the fact that cells can undergo and propagate action potentials, the action potentials don't result in muscle contraction. Another reason why you could have electrical activity without a pulse is because there could be something blocking the heart. Now the heart has a sac outlining it called the pericardium. And in some cases, this might be full of blood. And if it is full of blood, it's going to press down on the heart, and the heart is not going to have any room to pump. This is called tamponade, or cardiac tamponade. And again, this is the condition where the heart is constricted by this fluid filled sac around the heart, and the heart can't pump. So even though you can have action potentials and electrical activity in the heart, you're not going to be able to pump, and you won't have a pulse. Okay, so I'm sure you've seen in movies or TV shows, when someone flat lines or has asystole, and someone else comes running into the room, puts paddles on the chest, and yells, "Clear!" In this case, they're defibrillating the patient, meaning they're providing electrical shock to the heart, hopefully to convert the heart back to a normal rhythm. However, this is a common misconception. We never shock asystole or PEA for that matter. Defibrillation only works on very specific abnormal cardiac rhythms that can potentially be reversed with an electric shock, and these are called shockable rhythms. Shockable rhythms include ventricular fibrillation, where the walls of the ventricles are spasming, and therefore they can't contract, and they're not going to circulate blood to the rest of the body, and pulseless ventricular tachycardia, meaning that there's some sort of abnormal conduction in the ventricles that cause the ventricles to pump at a dangerously high rate. So neither of these has a pulse. And just a side note, we never shock anyone with a pulse. Something else to note is that even though ventricular fibrillation and pulseless v tach meet the criteria for PEA, and that there's electrical activity but no pulse, we don't typically classify them as PEA. These two arrhythmias are a class of their own because we treat them differently. They're shockable rhythms. PEA is considered electric activity without a pulse. That's not v fib or pulseless v tach. Now how do we treat asystole and PEA? Asystole and PEA are considered nonshockable rhythms, meaning providing a shock won't likely restore a normal rhythm. How do we treat nonshockable rhythms? We start with cardiopulmonary resuscitation, or CPR, where we alternate chest compressions with some sort of artificial breathing for the patient, whether that be mouth-to-mouth, or doing oxygen through some sort of mask. We'll also administer vasoconstrictive medications. Now, vasoconstrictive means that we're constricting the vasos, or the vessels. So these drugs constrict the blood vessels. And equally important with any patient who is pulseless, we have to consider any factors that could be reversed that might be contributing to the cardiac arrest. And you can remember which factors to consider by the mnemonic Hs and Ts, which we're going to go over in just one second. So what are the Hs and Ts? Remember, they're potentially reversible conditions that could be causing or even contributing to the cardiac arrest. So, if any patient in cardiac arrest has any of these factors, we want to try to reverse it, or fix it, to help save them. Now, something to note is that a lot of these Hs and Ts are conditions where there's some sort of lack of adequate blood circulating through the body, or adequate oxygen delivery to the body, including the heart. Heart cells need oxygen to function properly. So if there's not enough oxygen getting to the heart, then the heart cells aren't happy, and they quit working properly. The first H we're going to talk about is hypovolemia, so hypo means low, and volemia refers to volume. So this basically means low blood volume. Usually, from excessive bleeding. In hypovolemia, not enough blood is circulating, so not enough oxygen is getting around. The next H is hypoxia. That means that there's inadequate oxygen supplied to the body. And hypoxia can be due to many things, such as drowning or even a heart attack. So there's inadequate oxygen getting to the body, to the heart, and to the brain. The next H is hydrogen ions. And hydrogen ions basically means acidosis, meaning that the body's PH is too low. And acidosis often results from long periods of hypoxia. We also need to consider a person's potassium level, because hypo and hyperkalemia can lead to cardiac arrest. Now, hypokalemia means that there's too low potassium, and hyperkalemia means the potassium level is too high. Potassium plays a really important role in maintaining normal electrical conduction in the heart. So you can imagine that if the levels are too high or too low, this will disrupt the heart's electrical conduction system. In anyone with cardiac arrest that comes in, we're going to check their glucose level, because hypoglycemia, or low blood glucose, can lead to cardiac arrest, and this is something that's easily fixed. And the last H we're going to talk about is hypothermia, or low body temperature. And typically, we think of hypothermia as a temperature less than 95 degrees Fahrenheit or 35 degrees Celsius. So as a person's core temperature drops, the heart's pacemaker cells fire less and less, and eventually, the heart can stop. Okay, so those are the Hs. Now, let's move on to the Ts. We need to consider toxins, and toxins include both prescription medications and street drugs. If someone comes in because of cardiac arrest due to a toxin, there might be a reversible agent that will help reverse the effects of the toxins, and can help save the patient. The second T is tamponade, and that's something we just talked about. And we're referring to cardiac tamponade. Like we said, this is a condition where blood fills the space that lines the heart, or the pericardial sac, and this constricts the heart and makes it a lot harder for the heart to pump, and sometimes the heart can't even pump at all. And if the heart's not pumping, no blood circulating. And one way I like to think about it is to think about doing a jumping jack. Now, imagine doing that jumping jack underwater. It's a lot harder to do a jumping jack underwater because all this pressure's around your arms and legs. Likewise, it's harder for the heart to pump with all the added pressure surrounding it. And the next T is something called tension pneumothorax. So in the chest wall, the lungs are surrounded by a plural lining. So there's a space created called the plural space between the lungs and the chest wall. In a tension pneumothorax, air can somehow enter this plural space. And this is usually because of some sort of trauma to the chest. And what happens is, air enters this plural space, but it can't leave, and as more and more air enters the space, it crushes the lung, and even pushes the lung and the heart to the side. A crushed or collapsed lung is not going to be able to move oxygen very easily, and the heart can stop. And the last T we're going to talk about is thrombosis, basically meaning blood clot. In the case of cardiac arrest, we're concerned about a blood clot to the coronary artery, or an artery that supplies the heart with oxygenated blood, or we're concerned about a clot in the lungs, and that's known as a pulmonary embolism. So a pulmonary embolism is a clot in the lung. So clots in either the heart or the lungs can lead to severe oxygen depletion, and eventually lead to cardiac arrest.

Cause

Possible underlying causes, which may be treatable and reversible in certain cases, include the Hs and Ts.[10][11][12]

While the heart is asystolic, there is no blood flow to the brain unless CPR or internal cardiac massage (when the chest is opened and the heart is manually compressed) is performed, and even then it is a small amount. After many emergency treatments have been applied but the heart is still unresponsive, it is time to consider pronouncing the patient dead. Even in the rare case that a rhythm reappears, if asystole has persisted for fifteen minutes or more, the brain will have been deprived of oxygen long enough to cause severe hypoxic brain damage, resulting in brain death or persistent vegetative state.[13]

See also

References

  1. ^ Harper, Douglas. "asystole". Online Etymology Dictionary.
  2. ^ συστολή. Liddell, Henry George; Scott, Robert; A Greek–English Lexicon at the Perseus Project.
  3. ^ Baldzizhar, Aksana; Manuylova, Ekaterina; Marchenko, Roman; Kryvalap, Yury; Carey, Mary G. (September 2016). "Ventricular Tachycardias". Critical Care Nursing Clinics of North America. 28 (3): 317–329. doi:10.1016/j.cnc.2016.04.004. PMID 27484660.
  4. ^ Kutsogiannis, Demetrios J.; Bagshaw, Sean M.; Laing, Bryce; Brindley, Peter G. (4 October 2011). "Predictors of survival after cardiac or respiratory arrest in critical care units". CMAJ: Canadian Medical Association Journal. 183 (14): 1589–1595. doi:10.1503/cmaj.100034. PMC 3185075. PMID 21844108.
  5. ^ Kempton, Hannah; Vlok, Ruan; Thang, Christopher; Melhuish, Thomas; White, Leigh (March 2019). "Standard dose epinephrine versus placebo in out of hospital cardiac arrest: A systematic review and meta-analysis". The American Journal of Emergency Medicine. 37 (3): 511–517. doi:10.1016/j.ajem.2018.12.055. PMID 30658877. S2CID 58580872.
  6. ^ Neumar, R. W.; Otto, C. W.; Link, M. S.; Kronick, S. L.; Shuster, M.; Callaway, C. W.; Kudenchuk, P. J.; Ornato, J. P.; McNally, B.; Silvers, S. M.; Passman, R. S.; White, R. D.; Hess, E. P.; Tang, W.; Davis, D.; Sinz, E.; Morrison, L. J. (17 October 2010). "Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 122 (18_suppl_3): S729–S767. doi:10.1161/CIRCULATIONAHA.110.970988. PMID 20956224.
  7. ^ Jordan, Matthew; Lopez, Richard; Morrisonponce, Daphne (2022). Asystole. Treasure Island, Florida (US): StatPearls Publishing. PMID 28613616.
  8. ^ Thomas, Andrew; Newgard, Craig; Fu, Rongwei; Zive, Dana; Daya, Mohamud (2013). "Survival in Out-of-Hospital Cardiac Arrests with Initial Asystole or Pulseless Electrical Activity and Subsequent Shockable Rhythms". Resuscitation. 84 (9): 1261–1266. doi:10.1016/j.resuscitation.2013.02.016. PMC 3947599. PMID 23454257.
  9. ^ "Medical Futility in Asystolic Out-of-Hospital Cardiac Arrest". Survey of Anesthesiology. 52 (5): 261–262. October 2008. doi:10.1097/01.SA.0000318635.97636.a6.
  10. ^ Mazur G (2004). ACLS: Principles And Practice. Dallas: American Heart Association. pp. 71–87. ISBN 978-0-87493-341-3.
  11. ^ Barnes TG, Cummins RO, Field J, Hazinski MF (2003). ACLS for experienced providers. Dallas: American Heart Association. pp. 3–5. ISBN 978-0-87493-424-3.
  12. ^ ECC Committee, Subcommittees and Task Forces of the American Heart Association (December 2005). "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care – Part 7.2: Management of Cardiac Arrest". Circulation. 112 (24 Suppl): IV1–203 (7.2 IV58–66). doi:10.1161/CIRCULATIONAHA.105.166550. PMID 16314375.
  13. ^ Shah, Sandy (16 October 2021). "Asystole: Background, Pathophysiology, Etiology". eMedicine.

External links

This page was last edited on 30 March 2024, at 07:52
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