ACLS- Cardiac arrest: VF/Pulseless VT Case

Purpose of defibrillation

*Does not restart the heart* -Defibrillation stuns the heart and briefly terminates all electrical activity, including VT and pVT -If heart is still viable, its normal pacemakers may eventually resume electrical activity After the first minutes of successful defibrillation, any spontaneous rhythm is typically slow and may not create pulses or adequate perfusion --Pt needs CPR for several minutes until adequate heart function resumes

Physiologic monitoring during CPR: PETCO2

*End-tidal CO2 (PETCO2)*: main determinant of this during CPR is blood delivery to lungs --<10 mmHg during CPR in intubated patients suggests ROSC is unlikely (try to improve chest compressions and vasopressor therapy) --If abruptly increases to a normal value (35-40 mmHg) it is reasonable to consider this an indicator of ROSC

Ultrasound use in cardiac arrest

*For VF/pVT/Asystole/PEA* Helps assess myocardial contractility and to help identify potentially treatable causes of cardiac arrest (hypovolemia, pneumothorax, pulmonary thromboembolism, or pericardial tamponade)

Extracorporeal CPR (ECPR)

*For VF/pVT/Asystole/PEA* Venoarterial extracorporeal membrane oxygenation during cardiac arrest Requires adequate vascular access and specialized equipment

Magnesium sulfate during cardiac arrest

*ONLY for torsades de pointes associated with a long QT interval* -1-2 g IV/IO diluted in 10 mL (D5W, normal saline) given as IV/IO bolus, typically over 15-20 minutes Sodium/potassium pump agonist Suppresses atrial L-and T-type calcium channels, and ventricular after-depolarizations *pVT is treated with high energy shock, magnesium sulfate is an adjunctive agent used to PREVENT recurrent or treat persistent VT associated with torsades de pointes*

Lidocaine during cardiac arrest

*Used if amiodarone is not available* *1-1.5 mg/kg IV/IO first dose, then 0.5-0.75 mg/kg IV/IO at 5- to 10-minute intervals; max dose 3 mg/kg* Suppresses automaticity of conduction tissue in the heart, by increasing electrical stimulation threshold of the ventricle, His-Purkinje system, and spontaneous depolarization of the ventricles during action on tissues

Biphasic defibrillators shock energy

120-200J Manufacture recommendation (e.g. initial dose of 120-200J) If unknown, use maximum available Second and subsequent doses should be equivalent, and higher doses may be considered

Monophasic defibrillators shock energy

360J

Nonshockable rhythms

Asystole PEA

Antiarrhythmic use in ACLS

Can give either before or after a shock *Amiodarone*= first line antiarrhythmic in cardiac arrest because it has been clinically demonstrated that it improves the rate of ROSC and hospital admission in adults with refractory VF/ pulseless VT

Physiologic monitoring during CPR: Central venous oxygen saturation

Changes in SCVO2 reflect changes in oxygen delivery due to changes in CO -Can be measured continuously by using oximetric tipped central venous catheters placed in the superior vena cava or pulmonary artery (Normal 60%-80%) ----If <30% improve chest compressions and vasopressor therapy

Treatment of VF/pVT in Hypothermia

Defibrillation is appropriate for the cardiac arrest patient in VF/pVT who has severe hypothermia and a body temp of <30 C (<86F) -Can do more than one shock Hypothermic patients can have reduced rate of drug metabolism (concern that drugs may accumulate to toxic levels)- space meds at longer intervals

How to determine appropriate energy dose for shockable rhythms

Determined by the identity of the defibrillator- *monophasic or biphasic*

Most effective way to treat VF

Electrical defibrillation -For every minute that passes between collapse and defibrillation, the chance of survival declines 7%-10% per minute if no by stander CPR is provided ---With CPR, decline is 3%-4%/minute

Drugs for VF/ Pulseless VT

Epinephrine Norepinephrine Amiodarone Lidocaine Magnesium sulfate Dopamine Oxygen Other medications depending on cause

Amiodarone during cardiac arrest

For VF or pVT unresponsive to shock, CPR, and vasopressor *300 mg IV/IO bolus, then consider additional 150 mg IV/IO once in 3-5 minutes* -Blocks sodium channels at rapid pacing frequencies -Exerts a noncompetitive antisympathetic action One of the main effects of prolonged use= lengthening of cardiac action potential

When should you give Epinephrine during persistent/pulseless VT

Give 1 shock and resume CPR immediately for 2 minutes after the shock *When IV/IO access is available, give epinephrine during CPR after the second shock as follows* --1 mg IV/IO, repeat every 3-5 minutes

Giving epinephrine if IV/IO access cannot be obtained

Give epinephrine 2-2.5 mg diluted in 5-10 mL sterile water or normal saline, and inject into ET tube

How should you administer a drug peripherally?

Give the drug by bolus unless otherwise specified Follow with a 20mL bolus of IV fluid Elevate extremity for about 10-20 seconds to facilitate delivery of the drug to the central circulation

Endotracheal route of drug administration

IV and IO are preferred over ET -Optimal dose of most drugs given by ET route is unknown -The typical dose of drugs given through ET is 2-2.5 times the IV route -CPR will need to be stopped transiently so drug does not regurgitate up the ET tube Epinephrine, lidocaine, and vasopressin are absorbed into circulatory system after ET route -Dilute dose in 5-10 mL sterile water or normal saline

Intraosseous route of drug administration

If IV access is not readily available Can be established in all age groups Access can be achieved in 30-60 seconds Preferred over the ET route and may be easier to establish in cardiac arrest Any ACLS drug or fluid that can be administered IV can also be given IO

Physiologic monitoring during CPR: Coronary Perfusion Pressure or Arterial Relaxation Pressure

Increased CPP correlates with both myocardial blood flow and ROSC A reasonable surrogate for CPP during CPR is arterial relaxation (diastolic) pressure (can be measured with an intra-arterial catheter) --If arterial relaxation pressure <20mmHg, it is reasonable to try to improve chest compressions and vasopressor therapy

Do you need central line access during resuscitation?

No- not necessary to have unless a central line has already been placed and is usable Inserting a central line during cardiac can cause complications --Interruptions in CPR --vascular laceration --hematoma --bleeding Inserting a peripheral IV line does not require interruption of CPR, but drugs require 1-2 minutes to reach the central circulation when given peripherally

Vasopressors during cardiac arrest

Optimize cardiac output and blood pressure *Epinephrine* 1 mg IV/IO every 3-5 minutes

Chest compression fraction (CCF)

The proportion of time during cardiac arrest resuscitation when chest compressions are performed -Should be as high as possible (at least 60% and ideally 80%)

Fluid administration during cardiac arrest

Titrate fluid administration and vasoactive drugs or inotropic agents as needed to optimize blood pressure, cardiac output, and systemic perfusion *Hypovolemic patients*: Use NS or LR. *Avoid D5W* because it will reduce serum sodium too fast

Optimal post-cardiac arrest blood pressure

Unknown, but a MAP of 65 or greater is reasonable

Epinephrine

Used during resuscitation primarily for its B-adrenergic effects (vasoconstriction) -Vasoconstriction increases cerebral and coronary blood flow during CPR by increasing MAP and aortic diastolic pressure -*produces vasoconstriction, increases BP and HR, and improves perfusion pressure to brain and heart* Escalating and high-dose epinephrine did not improve survival to discharge or neurologic outcome Does not increase survival rate, just improves aortic diastolic BP, coronary artery perfusion pressure, and the rate of ROSC

Shockable rhythms

Vfib Pulseless Vtach