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ACLS Algorithms

ACLS Algorithms

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Published by: monickams on Mar 14, 2011
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In addition to high-quality CPR, the only rhythm-specifictherapy proven to increase survival to hospital discharge isdefibrillation of VF/pulseless VT. Therefore, this interventionis included as an integral part of the CPR cycle when therhythm check reveals VF/pulseless VT. Other ACLS inter-ventions during cardiac arrest may be associated with anincreased rate of ROSC but have not yet been proven toincrease survival to hospital discharge. Therefore, they arerecommended as considerations and should be performedwithout compromising quality of CPR or timely defibril-
Figure 1.
ACLS Cardiac Arrest Algorithm.
S736 Circulation
November 2, 2010
 by on October 18, 2010circ.ahajournals.orgDownloaded from
lation. In other words, vascular access, drug delivery, andadvanced airway placement should not cause significantinterruptions in chest compression or delay defibrillation.There is insufficient evidence to recommend a specifictiming or sequence (order) of drug administration andadvanced airway placement during cardiac arrest. In mostcases the timing and sequence of these secondary inter-ventions will depend on the number of providers partici-pating in the resuscitation and their skill levels. Timingand sequence will also be affected by whether vascularaccess has been established or an advanced airway placedbefore cardiac arrest.Understanding the importance of diagnosing and treatingthe underlying cause is fundamental to management of allcardiac arrest rhythms. During management of cardiac arrestthe provider should consider the H’s and T’s to identify andtreat any factor that may have caused the arrest or may becomplicating the resuscitative effort (Table 1).It is common for the arrest rhythm to evolve during thecourse of resuscitation. In such cases management shouldshift smoothly to the appropriate rhythm-based strategy. Inparticular, providers should be prepared to deliver a timelyshock when a patient who presented with asystole or PEAis found to be in VF/pulseless VT during a rhythm check.There is no evidence that the resuscitation strategy for anew cardiac arrest rhythm should necessarily be alteredbased on the characteristics of the previous rhythm. Med-ications administered during resuscitation should be mon-itored and total doses tabulated to avoid potential toxicity.If the patient achieves ROSC, it is important to beginpost–cardiac arrest care immediately to avoid rearrest andoptimize the patient’s chance of long-term survival withgood neurologic function (see Part 9). Finally, the reality isthat the majority of resuscitative efforts do not result inROSC. Criteria for ending unsuccessful resuscitative ef-forts are addressed briefly below (see “When ShouldResuscitative Efforts Stop?”) and in more detail in Part 3:“Ethics.”
Rhythm-Based Management of Cardiac Arrest
In most cases of witnessed and unwitnessed cardiac arrest thefirst provider should start CPR with chest compressions andthe second provider should get or turn on the defibrillator,place the adhesive pads or paddles, and check the rhythm.Paddles and electrode pads should be placed on the exposedchest in an anterior-lateral position. Acceptable alternative
Figure 2.
ACLS Cardiac Arrest Circular Algorithm.
Table 1. Treatable Causes of Cardiac Arrest: The H’s and T’s
Hs TsHypoxia ToxinsHypovolemia Tamponade (cardiac)Hydrogen ion (acidosis) Tension pneumothoraxHypo-/hyperkalemia Thrombosis, pulmonaryHypothermia Thrombosis, coronaryFor further explanation of the H’s and T’s, see Part 12: “Special Resusci-tation Situations.”
Neumar et al Part 8: Adult Advanced Cardiovascular Life Support
 by on October 18, 2010circ.ahajournals.orgDownloaded from
inadequate or the patient shows signs of increased work of breathing, provide supplementary oxygen. Attach a monitorto the patient, evaluate blood pressure, and establish IVaccess. If possible, obtain a 12-lead ECG to better define therhythm. While initiating treatment, evaluate the patient’sclinical status and identify potentially reversible causes.The provider must identify signs and symptoms of poorperfusion and determine if those signs are likely to be causedby the bradycardia (Figure 3,
Box 3
). If the signs andsymptoms are not due to bradycardia, the provider shouldreassess the underlying cause of the patient’s symptoms.Remember that signs and symptoms of bradycardia may bemild; asymptomatic or minimally symptomatic patients donot necessarily require treatment (Figure 3,
Box 4
) unlessthere is suspicion that the rhythm is likely to progress tosymptoms or become life-threatening (eg, Mobitz type IIsecond-degree AV block in the setting of acute myocardialinfarction [AMI]). If the bradycardia is suspected to be thecause of acute altered mental status, ischemic chest discom-fort, acute heart failure, hypotension, or other signs of shock,the patient should receive immediate treatment.Atrioventricular (AV) blocks are classified as first-, second-,and third-degree. Blocks may be caused by medications orelectrolyte disturbances, as well as structural problems resultingfromAMIorothermyocardialdiseases.Afirst-degreeAVblock is defined by a prolonged PR interval (
0.20 second) and isgenerally benign. Second-degree AV block is divided intoMobitz types I and II. In Mobitz type I block, the block is at theAV node; the block is often transient and asymptomatic. InMobitz type II block, the block is usually below the AV nodewithin the His-Purkinje system; this block is often symptomatic,with the potential to progress to complete (third-degree) AVblock. Third-degree AV block may occur at the AV node,bundle of His, or bundle branches. When third-degree AV block is present, no impulses pass between the atria and ventricles.Third-degree AV block can be permanent or transient, depend-ing on the underlying cause.
Therapy (Figure 3, Box 5)
Atropine remains the first-line drug for acute symptomaticbradycardia (Class IIa, LOE B). Clinical trials in adults
showed that IV atropine improved heart rate, symptoms, andsigns associated with bradycardia. Atropine sulfate reversescholinergic-mediated decreases in heart rate and should beconsidered a temporizing measure while awaiting a transcu-taneous or transvenous pacemaker for patients with symp-tomatic sinus bradycardia, conduction block at the level of theAV node, or sinus arrest.
The recommended atropine dose for bradycardia is 0.5 mgIV every 3 to 5 minutes to a maximum total dose of 3 mg.Doses of atropine sulfate of 
0.5 mg may paradoxicallyresult in further slowing of the heart rate.
Atropine admin-istration should not delay implementation of external pacingfor patients with poor perfusion.Use atropine cautiously in the presence of acute coronaryischemia or MI; increased heart rate may worsen ischemia orincrease infarction size. Atropine will likely be ineffective in
Figure 3.
Bradycardia Algorithm.
Neumar et al Part 8: Adult Advanced Cardiovascular Life Support
 by on October 18, 2010circ.ahajournals.orgDownloaded from

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