ASP Medical Clinic sept 2012 ACLS Brief Overview

ASP Medical Clinic/ sept 2012

ACLS Brief Overview & 2010 AHA ECC Guidelines Dr. M. Hajikarimi interventional cardiologist

WHAT IS ACLS? Advanced Cardiac Life Support An extension of BLS (Basic Life Support) Implementation of advanced life support is not intended to suggest an abrupt cessation of basic life support activities but rather a merging and transition from one level of activity to the next.

ACLS More specialized In field or in hospital Monitor, Defib. , Cardioversion, Proper Airway, I/V Access, Drugs Continuing CPR.

Excellent basic life support & its importance in ACLS

BLS (Basic Life Support)

Every effort be made NOT to interrupt CPR In the past, clinicians frequently interrupted CPR to check for pulses, perform tracheal intubation, or obtain venous access. The 2010 ACLS Guidelines strongly recommend that every effort be made NOT to interrupt CPR; other less vital interventions (eg, tracheal intubation or administration of medications to treat arrhythmias) are made either while CPR is performed or during the briefest possible interruption.

Chest compressions are often performed incorrectly Studies in both the in-hospital & prehospital settings demonstrate that chest compressions are often performed incorrectly, inconsistently, & with excessive interruption. Chest compressions must be of sufficient depth (at least 5 cm, or 2 inches) & rate (at least 100 per min), & allow for complete recoil of the chest between compressions, to be effective.

Airway Management During ACLS Ventilation is performed during CPR to maintain adequate oxygenation & eliminate carbon dioxide. Nevertheless, during the first few minutes following sudden cardiac arrest (SCA), oxygen delivery to the brain is limited primarily by reduced blood flow. Therefore, in adults, the performance of excellent chest compressions takes priority over ventilation during the initial period of basic life support. In settings with multiple rescuers or clinicians, ventilations & chest compressions are performed simultaneously.

Good ventilations A 30 to 2 compression to ventilation ratio (one cycle) is recommended in patients without advanced airways. According to the 2010 ACLS Guidelines, asynchronous ventilations at 8 to 10 per minute are administered if an endotracheal tube or extraglottic airway is in place, while continuous chest compressions are performed simultaneously. We believe that 6 to 8 ventilations per minute are sufficient in the low-flow state of cardiac resuscitation & help to prevent over-ventilation.

Although research has yet to identify the preferred parameters for ventilation (eg, respiratory rate, tidal volume, inspired oxygen concentration), it is widely believed that a lower minute ventilation is needed for patients in cardiac arrest. Therefore, lower respiratory rates are used (the 2010 ACLS Guidelines recommend 8 to 10 breaths per minute with an advanced airway in place; we believe 6 to 8 breaths are adequate). In addition, we know that hyperventilation is harmful, as it leads to increased intrathoracic pressure, which decreases venous return & compromises cardiac output. Tidal volumes of approximately 600 m. L delivered in a controlled fashion such that chest rise occurs over no more than one second is recommended in the 2010 ACLS Guidelines.

If rescuers decide that tracheal intubation is necessary during CPR, an experienced intubator should perform the procedure. Ideally, intubation is performed while excellent chest compressions continue uninterrupted. However, if the operator is unable to intubate during the performance of chest compressions, further attempts should be deferred to the two minute interval (after a complete cycle of CPR) when defibrillation or patient reassessment is performed. This approach minimizes loss of perfusion. Attempts at intubation should last no longer than 10 seconds.

Taking these principles into account, the 2010 ACLS Guidelines support the use of a bag-mask device or a blindly placed supraglottic airway for ventilation during the initial management of SCA, deferring placement of an endotracheal tube, unless intubation can be performed without interrupting chest compressions. A blindly inserted supraglottic airway (eg, laryngeal mask airway, Combitube™, laryngeal tube) can be placed without interrupting chest compressions, provides adequate ventilation in most cases, & reduces the risk of aspiration compared to bag-mask ventilation. Therefore, clinicians may prefer to ventilate with a supraglottic device while CPR is ongoing, rather than performing tracheal intubation.

CARIAC ARREST 2005 vs 2010

HIGH QUALITY CPR Ø Adequate Rate; 100/min Ø Adequate Depth: Adults & Children; 2 inches Infants; 1 ½ inches Ø Allow complete chest recoil Ø Minimizing Interruptions Ø Avoid excessive ventilation Ø Multiple rescuers -----Rotate task every 2 mins

Key principles in the performance of ACLS Excellent CPR is crucial. • Excellent chest compressions must be performed throughout the resuscitation without interruption, using proper timing (100 compressions per minute) and force (≥ 5 cm depth), and allowing for complete chest recoil. • Do not stop compressions until the defibrillator is fully charged. • Anything short of excellent CPR does not achieve adequate cerebral and coronary perfusion. • Excellent chest compressions take priority over ventilation. If a second rescuer is present, ventilations must be performed using proper timing (6 to 8 breaths per minute in the intubated patient; ratio of 30 compressions to 2 ventilations if not intubated) and force (each breath delivered over a full 1 to 2 seconds); avoid hyperventilation. Defibrillate VF and pulseless VT as rapidly as possible. Rapidly identify and treat causes of non-shockable arrest (PEA, asystole). • Important causes include the 5 H's and 5 T's: • Hypoxia, Hypovolemia, Hydrogen ions (acidosis), Hyper/Hypo-kalemia, Hypothermia; • Tension pneumothorax, Tamponade-cardiac, Toxins, Thrombosis-coronary (MI), Thrombosispulmonary (PE). • If reversible causes are not corrected rapidly, the patient has little chance of survival.

Management Of Specific Arrhythmias

Ventricular fibrillation & pulseless ventricular tachycardia VF & pulseless VT are nonperfusing rhythms emanating from the ventricles, for which early rhythm identification, defibrillation, & CPR are the mainstays of treatment. Early defibrillation is the most critical action in the resuscitation effort, followed by the performance of excellent CPR. Manage potentially treatable underlying causes as appropriate. Begin performing excellent chest compressions as soon as SCA is recognized & continue while the defibrillator is being attached. If a defibrillator is not immediately available, continue CPR until one is obtained. As soon as a defibrillator is available, attach it to the patient, charge it, assess the rhythm, & treat appropriately (eg, defibrillate VF or pulseless VT; continue CPR if asystole or PEA). Resume CPR immediately after any shock is given.

Ventricular fibrillation

VT

In the case of a witnessed cardiac arrest, perform defibrillation as quickly as possible. Decreased time to defibrillation improves the likelihood of successful conversion to a perfusing rhythm & of patient survival. Biphasic defibrillators are recommended because of their increased efficacy at lower energy levels. The 2010 ACLS Guidelines recommend that when employing a biphasic defibrillator clinicians use the initial dose of energy recommended by the manufacturer (120 to 200 J). If this dose is not known, the maximal dose may be used. We suggest a first defibrillation using 200 J with a biphasic defibrillator or 360 J with a monophasic defibrillator for VF or pulseless VT. It should be noted that many automated external defibrillators (AEDs) do not allow for adjustment of the shock output.

The 2010 ACLS Guidelines recommend the resumption of CPR immediately after defibrillation without rechecking for a pulse. CPR should not be interrupted to assess the rhythm & additional shocks should be considered no more frequently than every two minutes. If VF or pulseless VT persists after at least one attempt at defibrillation & two minutes of CPR, give epinephrine (1 mg IV every 3 to 5 min) while CPR is performed continuously. Vasopressin (40 units IV) may replace the first or second dose of epinephrine.

Evidence suggests that antiarrhythmic drugs provide little survival benefit in refractory VF or pulseless VT. Nevertheless, the current ACLS Guidelines state that they may be used in certain situations. The timing of antiarrhythmic use is not specified. We suggest that antiarrhythmic drugs be considered after a second unsuccessful defibrillation attempt in anticipation of a third shock. Amiodarone (300 mg IV with a repeat dose of 150 mg IV as indicated) may be administered in VF or pulseless VT unresponsive to defibrillation, CPR, & epinephrine. Lidocaine (1 to 1. 5 mg/kg IV, then 0. 5 to 0. 75 mg/kg every 5 to 10 min) may be used if amiodarone is unavailable. Magnesium sulfate (2 g IV, followed by a maintenance infusion) may be used to treat polymorphic ventricular tachycardia consistent with torsade de pointes.

Asystole & pulseless electrical activity

Asystole & pulseless electrical activity Asystole is defined as a complete absence of demonstrable electrical & mechanical cardiac activity. Pulseless electrical activity (PEA) is defined as any one of a heterogeneous group of organized electrocardiographic rhythms without sufficient mechanical contraction of the heart to produce a palpable pulse or measurable blood pressure. By definition, asystole & PEA are non-perfusing rhythms requiring the initiation of excellent CPR immediately when either is present.

After initiating CPR, treat reversible causes as appropriate & administer epinephrine (1 mg IV every three to five minutes). The 2010 ACLS Guidelines state that vasopressin may be given (40 units for the first 10 minutes of resuscitation) in place of the first or second epinephrine dose. Neither asystole nor PEA responds to defibrillation. Atropine is no longer recommended for the treatment of asystole or PEA. Cardiac pacing is ineffective for cardiac arrest & not recommended in the 2010 ACLS Guidelines.

CARIAC ARREST 2005 vs 2010

Bradycardia

Bradycardia is defined conservatively as a heart rate below 60 beats per minute, but symptomatic bradycardia generally entails rates below 50 beats per minute. The 2010 ACLS Guidelines recommend that clinicians not intervene unless the patient exhibits evidence of inadequate tissue perfusion thought to result from the slow heart rate. Signs & symptoms of inadequate perfusion include hypotension, altered mental status, signs of shock, ongoing ischemic chest pain, & evidence of acute pulmonary edema. Hypoxemia is a common cause of bradycardia; look for signs of labored breathing (eg, increased respiratory rate, retractions, paradoxical abdominal breathing) & low oxygen saturation. Mild symptoms may not warrant treatment.

Tachycardia is defined as a heart rate above 100 beats per minute, but symptomatic tachycardia generally involves rates over 150 beats per minute, unless underlying ventricular dysfunction exists. Management of tachyarrhythmias is governed by the presence of clinical symptoms & signs caused by the rapid heart rate. The fundamental approach is as follows: First determine if the patient is unstable (eg, manifests ongoing ischemic chest pain, acute mental status changes, hypotension, signs of shock, or evidence of acute pulmonary edema). Hypoxemia is a common cause of tachycardia; look for signs of labored breathing (eg, increased respiratory rate, retractions, paradoxical abdominal breathing) & low oxygen saturation.

VT

POST-RESUSCITATION CARE The 2010 ACLS Guidelines recommend a combination of goal-oriented interventions provided by an experienced multidisciplinary team for all cardiac arrest patients with return of spontaneous circulation. Important objectives for such care include: Optimizing cardiopulmonary function & perfusion of vital organs Managing acute coronary syndromes Implementing strategies to prevent & manage organ system dysfunction & injury

TERMINATION OF RESUSCITATIVE EFFORTS Determining when to stop resuscitation efforts in cardiac arrest patients is difficult, & little data exist to guide decision-making. Physician survey data & clinical practice guidelines suggest that factors influencing the decision to stop resuscitative efforts include: Duration of resuscitative effort >30 min without a sustained perfusing rhythm Initial electrocardiographic rhythm of asystole Prolonged interval between estimated time of arrest & initiation of resuscitation Patient age & severity of comorbid disease Absent brainstem reflexes

More objective endpoints of resuscitation have been proposed. Of these, the best predictor of outcome may be the end tidal CO 2 level following 20 min of resuscitation. End tidal CO 2 values are a function of CO 2 production & venous return to the right heart & pulmonary circulation. A very low end tidal CO 2 (<10 mm. Hg) following prolonged resuscitation (>20 min) is a sign of absent circulation & a strong predictor of acute mortality. It is crucial to note that low end tidal CO 2 levels may also be caused by a misplaced (esophageal) endotracheal tube, & this possibility needs to be excluded before the decision is made to terminate resuscitative efforts.

ACLS Drugs

V F & Pulseless VT Epinephrine Vasopressin Amiodarone Lidocaine Magnesium

PEA & A Systole Epinephrine Vasopressin

Tachycardia Medications Adenosine Diltiazem Beta Blockers Amiodarone Digoxin Verapamil Magnesium Sulphate

Bradycardia Medications Atropine Epinephrine Dopamine

Acute Coronary Syndrome Treatment Oxygen Aspirin Nitroglycerine Morphine Heparin Beta Blockers Fibrinolytic Therapy

Adenosine First drug of choice for all stable marrow QRS Complex tachycardia. Half life is 5 seconds. 3 mg/ml in 2 ml per each vial. 6 mg rapid bolus IV/IO initially over 1 – 3 seconds. 12 mg rapid bolus, observed 1 – 2 minutes. Repeat another 12 mg if not successful

Amiodarone Indication Recurrent VF. Unstable VT. Shock refractory VF/VT after epinephrine. Dose for cardiac arrest (VF/VT), 300 mg rapid infusion diluted in 20 -30 ml of D. W 5 % over 10 – 20 minutes, then 900 mg over 24 hours as post resuscitation. for stable VT/ Wide QES Complex Tachycardia, 300 mg IV infusion over 20 – 60 minutes, then 900 mg over 24 hours in CCU.

Atropine First drug of choice for treating bradycardia. can be given by IV, IO and through Endotracheal Tube. doses: Ø 500 microgram / ml/ IV every 3 – 5 minutes as needed, the maximum total dosages is 3 mg (6 ampules)

Vasopressin can be given through (IV, IO, ETT). 40 Units IV/IO push, may be given for once only as a replacement for the first or second dose of epinephrine.

Diltiazem Used for control the ventricular response rate in patients with Atrial Flutter or Atrial Fibrillation. 15 – 20 mg IV over 2 minutes. can repeat 20 – 25 mg over 2 – 5 minutes.

Dopamine Second line drug for symptomatic Bradycardia when Atropine is not effective. 2 – 10 microgram / kg/ min infusion

Lidocaine Indications Wide QRS Complex. Cardiac Arrest from VF/ Pulseless VT

Lidocaine Doses Cardiac arrest from VF/ Pulseless VT: Initial dose, 1 – 1. 5 mg / kg/IV Stable VT, Wide QRS Tachycardia From 0. 5 – 0. 75 mg / kg and up to 1 – 1. 5 mg/ kg. Repeat 0. 5 – 0. 75 mg / kg every 5 – 10 minutes with maximum total dose of 3 mg / kg.

Epinephrine Indications VF. VT. PEA. Cardiac Arrest. A Systole. Bradycardia.

Dose IV 1 mg (10 ml of 1: 10, 000) followed by 20 ml Flush, At intervals of 3 - 5 min Infusion : 1 mg (1 ml of 1: 1000 Solution) added to 500 ml N/S or 5% D/W, run at 2 – 10 mcg/min. Titrate to 2 - 10 mcg/min. can be given by IV, IO and ETT.

Defibrillation: Advanced Cardiac Life Support

Chain of Survival Early Recognition and Assessment • Early Access • Early CPR • Early Defibrillation • Early Advanced Cardiac Life Support

Indications Pulseless VT • VF

How does it work? Electronic counter-shock between to paddles or pads Depolarises all cardiac cells and interrupts arrhythmia Allows SA node to recommence its dominant role Defibrillation is the most time critical intervention in a patient with a shockable rhythms

How does it work? Thoracic Impedance is the natural resistance to the flow of electrical current, measured in Ohms. Impedance is determined by a number of factors, such as: Underlying structures and pathology Paddle or adhesive pad position

How does it work? Monophasic Defibrillation Delivers ‘shock’ in one phase Adult: 200 J, 360 J, all subsequent shocks at 360 J Child: 2 J/Kg, 4 J/Kg, all subsequent shocks at 4 J/Kg

How does it work? Biphasic Defibrillation Two phases to the delivery of the ‘shock’ Adjusts ‘shock’ according to thoracic impedance Adult: 150 J, 150 J Child: 1– 2 J/Kg

How does it work? Monophasic v Biphasic Defibrillation Peak current decreased resulting in less myocardial damage

How does it work? Semi-Automatic External Defibrillation Primarily used by laypersons in the pre-hospital setting Survival rate increased to ~ 70% pre-hospital and 80% in-hospital Considered BLS “a udib prom le and v the d pt to dis isual c deliv efibrillat harge or a er a n reco s gnis hock w d h e rhyt hm” s a sho en it ckab le

Transcutaneous Pacing Early asystole with reversible cause Attach adhesive pad anterior / posterior Set rate Set Milliamps until capture is achieved

Transcutaneous Pacing Temporary Consider other pacing options Sedate patient

Safety Operator Safety Assertive Announce: CHARGING, ALL CLEAR / STAND CLEAR (Visual Check of Area), SHOCKING Check rhythm Discharge Shock Continue as per algorithm