Source:

Nursing2015

December 2007, Volume 37 Number 12 , p 56CC1 - 56CC3 [FREE]

Author

  • Kathy Dittrich RN, CCRN, BSN

Abstract

Cardiopulmonary resuscitation moves to the forefront. Read on to find out how drugs now fit into resuscitation efforts.

Cardiopulmonary resuscitation moves to the forefront. Read on to find out how drugs now fit into resuscitation efforts.

 

No matter how experienced you are, few situations can produce as much of an adrenaline rush as patient in cardiac arrest. Within moments you're orchestrating care that may save a person's life, following basic life support and advanced cardiovascular life support (ACLS) algorithms.

 

In recent years the American Heart Association (AHA) has reviewed these guidelines and recommended changes that are being implemented nationwide. In this article, I'll look at changes in the ACLS algorithms affecting the medications we administer.

 

The 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations challenged the Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care and produced the most evidence-based recommendations to date. During the conference, researchers overwhelmingly stressed the need for effective cardiopulmonary resuscitation (CPR), with medication administration assuming a lesser role. According to the AHA guidelines, studies have found that resuscitation drugs don't increase the rate of survival to hospital discharge.

 

Once you've determined that a patient is in cardiac arrest, the updated guidelines direct you to focus on early, high-quality CPR with little interruption and prompt defibrillation when indicated. Next, you'll establish intravenous (I.V.) access, consider drug therapy, and insert an advanced airway. The AHA addresses four routes of administration:

 

* peripheral I.V. To administer medications with little or no interruption in CPR, you can use existing peripheral access or insert a large-gauge peripheral catheter. Although medications take longer to circulate when given peripherally (1 to 2 minutes), compared with central venous administration, the AHA's goal is uninterrupted CPR, as the benefit of continued CPR is significant. When administering a medication peripherally, follow the bolus dose immediately with a 20-mL bolus of I.V. fluid and elevate the arm for 10 to 20 seconds to enhance flow to the central circulation.

 

* intraosseous (IO). An alternative when I.V. access can't be established, IO cannulation (through a venous plexus) achieves delivery similar to central venous administration.

 

* central venous. Although frequently obtained, central venous access isn't needed in most resuscitation attempts. If the patient doesn't have I.V. access, insert a large peripheral venous catheter, which doesn't require interrupting CPR. If the patient's spontaneous circulation doesn't return after defibrillation and peripheral or IO drug administration, consider inserting a central line, unless complications prevent it. For example, a patient on fibrinolytic therapy for acute coronary syndrome may not be a candidate for a central line. Evaluate the risks versus benefits before starting a central line.

 

* endotracheal (ET) tube. Instilling some resuscitation drugs via an ET tube results in lower circulating blood levels of the medication and lower survival rates compared with I.V. administration. Use this method only if I.V. or IO access can't be established. Only naloxone, atropine, vasopressin, epinephrine, and lidocaine can be administered via ET tube. The recommended dosing is two to two and a half times the I.V. dose, although little evidence supports this practice. After diluting the recommended drug dose in 5 to 10 mL of sterile water or 0.9% sodium chloride solution, instill the drug directly into the ET tube, followed by ventilations via a bag-valve-mask device.

 

 

Resuscitation drugs administered in response to cardiac arrest can be attributed to four lethal arrhythmias: ventricular fibrillation (VF), pulseless ventricular tachycardia (VT), asystole, and pulseless electrical activity (PEA). Medications are given to increase coronary and cerebral perfusion. Because directly measuring perfusion in response to CPR and medication administration isn't easy, the updated ACLS guidelines recommend fewer pulse checks during resuscitation efforts. The rationale is that palpable pulses don't tell you if coronary or cerebral flow is adequate.

 

The AHA guidelines tell you to give effective chest compressions (push hard and fast at a rate of 100 compressions/ minute), let the chest fully recoil after each compression, and minimize interruptions in chest compressions. (Interrupt compressions only for defibrillation and rhythm checks.) Medications should be administered during CPR as soon as possible after a rhythm check. Follow this sequence: CPR, rhythm check, CPR with drug administration and defibrillator charging, defibrillation. Now let's look at specific medications and when to give them.

 

If your patient's persistent VF or VT doesn't respond to CPR and one or two shocks, the next step is to administer vasopressors.

 

* Epinephrine, a natural catecholamine, has alpha- and beta-adrenergic agonist activity and is a potent vasoconstrictor. Epinephrine's alpha-adrenergic properties can increase coronary and cerebral blood flow during CPR. The drug's beta-adrenergic effects, however, can increase myocardial work and reduce subendocardial perfusion. Give 1 mg of epinephrine I.V. or IO every 3 to 5 minutes. The drug also may be administered via ET tube if I.V. or IO access is delayed or can't be established. High-dose and escalating epinephrine aren't routinely recommended under the 2005 guidelines. However, higher doses may be administered for specific problems, such as beta-blocker or calcium channel blocker overdose.

 

* Vasopressin is an alternative to epinephrine. The ACLS guidelines let a health care professional administer epinephrine, the conventional treatment choice, or a onetime dose of vasopressin. Some emergency care providers question the widespread use of epinephrine over vasopressin, saying it's being used out of habit. According to the AHA, no studies have shown that either epinephrine or vasopressin improves rates of patient survival to discharge. Because vasopressin's effects haven't been shown to differ from those of epinephrine in cardiac arrest, one dose of vasopressin (40 units I.V. or IO) may replace either the first or second dose of epinephrine. Vasopressin can be administered via ET tube, but evidence is insufficient to recommend a specific dose.

 

 

Antiarrhythmics should be considered to treat VF or pulseless VT that's unresponsive to CPR, two or three shocks, and a vasopressor.

 

* Amiodarone has been shown to increase short-term survival to hospital admission when compared with placebo or lidocaine. Amiodarone has alpha- and beta-adrenergic blocking properties and affects sodium, potassium, and calcium channels. Its principal effect on cardiac tissue is to delay repolarization by prolonging the action potential duration and effective refractory period. Administer an initial dose of 300 mg (dilute in 20 to 30 mL D5W) I.V. or IO. This can be followed, after 3 to 5 minutes, by one dose of 150 mg I.V. or IO.

 

* Lidocaine controls ventricular dysrhythmias by suppressing automaticity in the His-Purkinje system and by suppressing spontaneous depolarization of the ventricles during diastole. The AHA guidelines state that although lidocaine has no proven short-term or long-term efficacy in cardiac arrest, it's an alternative to amiodarone that has been used for many years, is familiar to clinicians, and causes fewer immediate adverse reactions than other antiarrhythmics.For VF and pulseless VT, administer an initial dose of 1 to 1.5 mg/kg I.V. or IO; subsequent I.V. or IO doses of 0.5 to 0.75 mg/kg may be given at 5- to 10-minute intervals, to a maximum dose of 3 mg/kg. Lidocaine also can be administered via ET tube.

 

* Magnesium sulfate is given to treat magnesium deficiency, which can cause cardiac dysrhythmias. A prolonged QT interval can induce torsades de pointes, an irregular polymorphic VT associated with a prolonged QT interval. To treat VF or pulseless VT associated with torsades de pointes, you may give an I.V. or IO loading dose of 1 to 2 grams of magnesium sulfate diluted in 10 mL of D5W and administered over 5 to 20 minutes. Avoid rapid administration, which can precipitate asystole.

 

 

According to the AHA, despite treatment, survival rates are low for patients in asystole or PEA. Pulseless electrical activity refers to any semiorganized electrical activity seen on the cardiac monitor, although the patient lacks a palpable pulse. This definition excludes VF, VT, and asystole. Because PEA produces myocardial contractions too weak to support adequate organ perfusion, the goal is to identify a precipitating cause and initiate treatment.

 

The key to treating asystole and PEA is high-quality CPR. Make sure you confirm asystole in two leads. To prevent fatigue and enhance CPR efforts, change compressor role every five cycles or 2 minutes. After five cycles of CPR, you can administer epinephrine or vasopressin in the same doses given for VF or pulseless VT.

 

Another option is atropine, given for asystole or slow PEA rate. This parasympatholytic enhances sinus node automaticity and atrioventricular conduction via direct vagolytic action. Administer 1 mg I.V. or IO every 3 to 5 minutes; the maximum is three doses or 3 mg. Remember that giving less than 0.5 mg can produce a paradoxical bradycardia that may precipitate VF.

 

The updated guidelines recommend I.V. fluids during cardiac arrest only for hypovolemic patients. In the past, you may have run I.V. fluids wide open during codes, but no research supports routine administration of I.V. fluids during cardiac arrest.

 

In reviewing its guidelines, the AHA has identified a need to conduct more research in all aspects of emergency care, including medication administration. By following the updated guidelines, you can keep your practice in line with the latest research-based standards of care.

No matter how experienced you are, few situations can produce as much of an adrenaline rush as patient in cardiac arrest. Within moments you're orchestrating care that may save a person's life, following basic life support and advanced cardiovascular life support (ACLS) algorithms.

In recent years the American Heart Association (AHA) has reviewed these guidelines and recommended changes that are being implemented nationwide. In this article, I'll look at changes in the ACLS algorithms affecting the medications we administer.

Medications take a backseat

The 2005 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations challenged the Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care and produced the most evidence-based recommendations to date. During the conference, researchers overwhelmingly stressed the need for effective cardiopulmonary resuscitation (CPR), with medication administration assuming a lesser role. According to the AHA guidelines, studies have found that resuscitation drugs don't increase the rate of survival to hospital discharge.

Once you've determined that a patient is in cardiac arrest, the updated guidelines direct you to focus on early, high-quality CPR with little interruption and prompt defibrillation when indicated. Next, you'll establish intravenous (I.V.) access, consider drug therapy, and insert an advanced airway. The AHA addresses four routes of administration:

 
Figure. No caption a... - Click to enlarge in new windowFigure. No caption available.

* peripheral I.V. To administer medications with little or no interruption in CPR, you can use existing peripheral access or insert a large-gauge peripheral catheter. Although medications take longer to circulate when given peripherally (1 to 2 minutes), compared with central venous administration, the AHA's goal is uninterrupted CPR, as the benefit of continued CPR is significant. When administering a medication peripherally, follow the bolus dose immediately with a 20-mL bolus of I.V. fluid and elevate the arm for 10 to 20 seconds to enhance flow to the central circulation.

* intraosseous (IO). An alternative when I.V. access can't be established, IO cannulation (through a venous plexus) achieves delivery similar to central venous administration.

* central venous. Although frequently obtained, central venous access isn't needed in most resuscitation attempts. If the patient doesn't have I.V. access, insert a large peripheral venous catheter, which doesn't require interrupting CPR. If the patient's spontaneous circulation doesn't return after defibrillation and peripheral or IO drug administration, consider inserting a central line, unless complications prevent it. For example, a patient on fibrinolytic therapy for acute coronary syndrome may not be a candidate for a central line. Evaluate the risks versus benefits before starting a central line.

* endotracheal (ET) tube. Instilling some resuscitation drugs via an ET tube results in lower circulating blood levels of the medication and lower survival rates compared with I.V. administration. Use this method only if I.V. or IO access can't be established. Only naloxone, atropine, vasopressin, epinephrine, and lidocaine can be administered via ET tube. The recommended dosing is two to two and a half times the I.V. dose, although little evidence supports this practice. After diluting the recommended drug dose in 5 to 10 mL of sterile water or 0.9% sodium chloride solution, instill the drug directly into the ET tube, followed by ventilations via a bag-valve-mask device.

How medications fit in

Resuscitation drugs administered in response to cardiac arrest can be attributed to four lethal arrhythmias: ventricular fibrillation (VF), pulseless ventricular tachycardia (VT), asystole, and pulseless electrical activity (PEA). Medications are given to increase coronary and cerebral perfusion. Because directly measuring perfusion in response to CPR and medication administration isn't easy, the updated ACLS guidelines recommend fewer pulse checks during resuscitation efforts. The rationale is that palpable pulses don't tell you if coronary or cerebral flow is adequate.

The AHA guidelines tell you to give effective chest compressions (push hard and fast at a rate of 100 compressions/ minute), let the chest fully recoil after each compression, and minimize interruptions in chest compressions. (Interrupt compressions only for defibrillation and rhythm checks.) Medications should be administered during CPR as soon as possible after a rhythm check. Follow this sequence: CPR, rhythm check, CPR with drug administration and defibrillator charging, defibrillation. Now let's look at specific medications and when to give them.

Vasopressors for VF or pulseless VT

If your patient's persistent VF or VT doesn't respond to CPR and one or two shocks, the next step is to administer vasopressors.

* Epinephrine, a natural catecholamine, has alpha- and beta-adrenergic agonist activity and is a potent vasoconstrictor. Epinephrine's alpha-adrenergic properties can increase coronary and cerebral blood flow during CPR. The drug's beta-adrenergic effects, however, can increase myocardial work and reduce subendocardial perfusion. Give 1 mg of epinephrine I.V. or IO every 3 to 5 minutes. The drug also may be administered via ET tube if I.V. or IO access is delayed or can't be established. High-dose and escalating epinephrine aren't routinely recommended under the 2005 guidelines. However, higher doses may be administered for specific problems, such as beta-blocker or calcium channel blocker overdose.

* Vasopressin is an alternative to epinephrine. The ACLS guidelines let a health care professional administer epinephrine, the conventional treatment choice, or a onetime dose of vasopressin. Some emergency care providers question the widespread use of epinephrine over vasopressin, saying it's being used out of habit. According to the AHA, no studies have shown that either epinephrine or vasopressin improves rates of patient survival to discharge. Because vasopressin's effects haven't been shown to differ from those of epinephrine in cardiac arrest, one dose of vasopressin (40 units I.V. or IO) may replace either the first or second dose of epinephrine. Vasopressin can be administered via ET tube, but evidence is insufficient to recommend a specific dose.

Antiarrhythmics for VF or pulseless VT

Antiarrhythmics should be considered to treat VF or pulseless VT that's unresponsive to CPR, two or three shocks, and a vasopressor.

* Amiodarone has been shown to increase short-term survival to hospital admission when compared with placebo or lidocaine. Amiodarone has alpha- and beta-adrenergic blocking properties and affects sodium, potassium, and calcium channels. Its principal effect on cardiac tissue is to delay repolarization by prolonging the action potential duration and effective refractory period. Administer an initial dose of 300 mg (dilute in 20 to 30 mL D5W) I.V. or IO. This can be followed, after 3 to 5 minutes, by one dose of 150 mg I.V. or IO.

* Lidocaine controls ventricular dysrhythmias by suppressing automaticity in the His-Purkinje system and by suppressing spontaneous depolarization of the ventricles during diastole. The AHA guidelines state that although lidocaine has no proven short-term or long-term efficacy in cardiac arrest, it's an alternative to amiodarone that has been used for many years, is familiar to clinicians, and causes fewer immediate adverse reactions than other antiarrhythmics.For VF and pulseless VT, administer an initial dose of 1 to 1.5 mg/kg I.V. or IO; subsequent I.V. or IO doses of 0.5 to 0.75 mg/kg may be given at 5- to 10-minute intervals, to a maximum dose of 3 mg/kg. Lidocaine also can be administered via ET tube.

* Magnesium sulfate is given to treat magnesium deficiency, which can cause cardiac dysrhythmias. A prolonged QT interval can induce torsades de pointes, an irregular polymorphic VT associated with a prolonged QT interval. To treat VF or pulseless VT associated with torsades de pointes, you may give an I.V. or IO loading dose of 1 to 2 grams of magnesium sulfate diluted in 10 mL of D5W and administered over 5 to 20 minutes. Avoid rapid administration, which can precipitate asystole.

Medications for asystole and PEA

According to the AHA, despite treatment, survival rates are low for patients in asystole or PEA. Pulseless electrical activity refers to any semiorganized electrical activity seen on the cardiac monitor, although the patient lacks a palpable pulse. This definition excludes VF, VT, and asystole. Because PEA produces myocardial contractions too weak to support adequate organ perfusion, the goal is to identify a precipitating cause and initiate treatment.

The key to treating asystole and PEA is high-quality CPR. Make sure you confirm asystole in two leads. To prevent fatigue and enhance CPR efforts, change compressor role every five cycles or 2 minutes. After five cycles of CPR, you can administer epinephrine or vasopressin in the same doses given for VF or pulseless VT.

Another option is atropine, given for asystole or slow PEA rate. This parasympatholytic enhances sinus node automaticity and atrioventricular conduction via direct vagolytic action. Administer 1 mg I.V. or IO every 3 to 5 minutes; the maximum is three doses or 3 mg. Remember that giving less than 0.5 mg can produce a paradoxical bradycardia that may precipitate VF.

The updated guidelines recommend I.V. fluids during cardiac arrest only for hypovolemic patients. In the past, you may have run I.V. fluids wide open during codes, but no research supports routine administration of I.V. fluids during cardiac arrest.

More research for practice

In reviewing its guidelines, the AHA has identified a need to conduct more research in all aspects of emergency care, including medication administration. By following the updated guidelines, you can keep your practice in line with the latest research-based standards of care.

RESOURCES

 

2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 112(22, Suppl.):III1-III136, November 29, 2005.

 

Kern K, et al. New guidelines for cardiopulmonary resuscitation and emergency cardiac care. JAMA. 285(10):1267-1269, March 14, 2001.

 

Sanders A, Ewy G. Cardiopulmonary resuscitation in the real world: When will the guidelines get the message? JAMA. 293(3):363-365, January 19, 2005.

 

Wenzel V, et al. A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. The New England Journal of Medicine. 350(2):105-113, January 8, 2005.