[Objectives 1, 2]
The initial rhythms that may be observed in a cardiac arrest include the following:
1. Pulseless VT (pVT), in which the ECG displays a wide, regular QRS complex at a rate faster than 120 beats per minute (beats/min)
2. VF, in which irregular chaotic deflections that vary in shape and height are observed on the ECG but there is no coordinated ventricular contraction
3. Asystole, in which no cardiac electrical activity is present
4. PEA, in which electrical activity is visible on the ECG but central pulses are absent
VF and pVT are shockable rhythms. This means that delivering a shock to the heart by means of a defibrillator may result in termination of the rhythm. Asystole and PEA are nonshockable rhythms.
Survival when a patient presents in a shockable rhythm is up to 6 times as high as when they have a nonshockable rhythm (Herlitz, et al., 2002; Martinez, 2012).
Ventricular Tachycardia
VT exists when three or more ventricular complexes occur in immediate succession at a rate greater than 100 beats/min. VT may occur with or without pulses, and the patient may be stable or unstable with this rhythm.
When the QRS complexes of VT are of the same shape and amplitude, the rhythm is called mono-morphic VT ( Table 4.1, Fig. 4.1). When the QRS complexes of VT vary in shape and amplitude from beat to beat, the rhythm is called polymorphic VT (PMVT). In PMVT, the QRS complexes appear to twist from upright to negative, or negative to upright, and back. PMVT is a dysrhythmia of intermediate sever-ity between monomorphic VT and VF. If monomorphic VT or PMVT is present without a pulse, the rhythm is treated as VF (discussed later). Monomorphic VT is discussed in more detail in Chapter 5 with wide-QRS tachycardias. PMVT is discussed in Chapter 5 with irregular tachycardias.
Ventricular Fibrillation [Objective 3]
VF is a chaotic rhythm that begins in the ventricles ( Table 4.2). With VF, there is no organized depo-larization of the ventricles. The ventricular muscle quivers, and as a result, there is no effective myocardial contraction and no pulse. The resulting rhythm looks chaotic with deflections that vary in shape and amplitude; no normal-looking waveforms are visible. The amplitude of VF waveforms decreases over
TABLE 4.1 Characteristics of Monomorphic Ventricular Tachycardia
Rhythm Ventricular rhythm essentially regular
Rate 101 to 250 (121 to 250 per some cardiologists) beats/min
P waves Usually not seen; if present, they have no set relationship with the QRS complexes that appear between them at a rate different from that of the VT
PR interval None
QRS duration 0.12 sec or greater; often difficult to differentiate between the QRS and the T wave
TABLE 4.2 Characteristics of Ventricular Fibrillation
Rhythm Rapid and chaotic with no pattern or regularity
Rate Cannot be determined because there are no discernible waves or complexes to measure P waves Not discernible
PR interval Not discernible QRS duration Not discernible
Fig. 4.1 When the QRS complexes of ventricular tachycardia (VT) are of the same shape and amplitude, the rhythm is called monomorphic VT. (From Aehlert B: ECG study cards, St. Louis, 2004, Mosby.)
85
CHAPTER 4 Cardiac Arrest Rhythms
time as myocardial blood flow and energy metabolism diminishes (Li & Tang, 2012). VF with waves that are 3 or more millimeters (mm) high is called coarse VF. VF with low amplitude waves (ie, less than 3 mm) is called fine VF. Survival to hospital discharge increases with VF waveforms of 3 to 4 mm and is best for VF of 5 mm or greater ( Li & Tang, 2012). Fig. 4.2 illustrates a comparison of ventricular dysrhythmias.
Factors that increase the susceptibility of the myocardium to fibrillate include the following:
• Acute coronary syndromes
• Dysrhythmias
• Electrolyte imbalance
• Environmental factors (eg, electrocution)
• Hypertrophy
• Increased sympathetic nervous system activity
• Proarrhythmic effect of antiarrhythmics and other medications
• Severe heart failure
• Vagal stimulation
The patient in VF is unresponsive, apneic, and pulseless. The priorities of care in cardiac arrest because of pVT or VF are high-quality CPR and defibrillation. When pVT or VF persists or recurs after one or more shocks it is called refractory pVT/VF (Link, et al., 2015). Use the memory aids PATCH-4-MD and the Five Hs and Five Ts to recall possible reversible causes of cardiac emergencies (Boxes 4.1, 4.2).
Medications that may be used in the treatment of pVT/VF includeepinephrine ( Table 4.3) and amio-darone. Epinephrine is a vasopressor. A vasopressor is administered during cardiac arrest to increase the perfusion pressure of (1) the myocardium, for increased chance of ROSC; and (2) the brain, for increased chance of neurologically intact survival (Sunde & Steen, 2012). Epinephrine is a potent medication that stimulates both alpha- and beta-adrenergic receptors. It should be given by the intravenous (IV) or intraosseous (IO) route in cardiac arrest. Because the effects of epinephrine do not last long, epinephrine should be repeated every 3 to 5 minutes as long as the patient is in cardiac arrest. Although epinephrine has been used in the management of cardiac arrest for more than 40 years, there is some concern that
B
C A
1 sec
Fig. 4.2 Ventricular tachydysrhythmias. A, Rhythm strip showing monomorphic VT. B, Example of polymorphic VT (PMVT).
C, Example of ventricular fibrillation (VF). All tracings are from lead V 1. (From Goldman L, Ausiello DA, Arend W, et al.: Cecil medicine, ed 23, Philadelphia, 2007, Saunders.) Hypoxia—ensure adequate oxygenation and
ventilation
Heat/cold (hyperthermia/hypothermia)— cool-ing/warming methods
Hypokalemia/hyperkalemia (and other electro-lytes)—monitor serum glucose levels closely in concert with correcting electrolyte distur-bances
Myocardial infarction—reperfusion therapy Drug overdose/accidents—antidote/specific
therapy
epinephrine administration during cardiac arrest may negatively affect patient outcomes. In a study that compared patients given epinephrine versus no epinephrine, the investigators concluded that although patients receiving epinephrine experienced ROSC more frequently and had a statistically significant improvement for survival to hospital admission, the final outcome was not significantly affected (Herlitz, et al., 1995). A more recent study found that although the rate of ROSC increased with epi-nephrine, there was no statistically significant difference in hospital discharge rate ( Jacobs, et al., 2011).
After its administration, epinephrine can have unwanted effects including increased myocardial oxygen consumption and postdefibrillation ventricular dysrhythmias ( Attaran & Ewy, 2010). Noting that the value and safety of its beta-adrenergic effects are controversial because they may increase myocardial work
and reduce subendocardial perfusion, current resuscitation guidelines reflect that standard-dose epineph-rine (ie, 1 mg every 3 to 5 minutes) may be reasonable for patients in cardiac arrest ( Link, et al., 2015).
With regard to the timing of epinephrine administration during cardiac arrest, current guidelines state that it may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest associated with an initial nonshockable rhythm (Link, et al., 2015). However, because optimal timing may vary based on patient factors and resuscitation conditions, there is insufficient evidence to make a rec-ommendation as to the optimal timing of epinephrine, particularly in relation to defibrillation, when cardiac arrest is associated with a shockable rhythm (Link, et al., 2015).
TABLE 4.3 Epinephrine (Adrenalin)
Class Natural catecholamine; sympathomimetic; adrenergic agonist Mechanism of
Action
Binds with alpha- and beta-adrenergic receptors, increasing heart rate and force of contraction, causing vasoconstriction, and relaxing bronchial smooth muscle Indications • Cardiac arrest: VF, pVT, asystole, PEA
• Symptomatic bradycardia
• Hypotension Dosage Cardiac arrest
• IV/IO: 1 mg (10 mL) of 1:10,000 solution IV push, follow with 20 mL fluid flush; may repeat 1 mg dose every 3 to 5 min (Link, et al., 2015)
• Tracheal: 2 to 2.5 mg diluted in 5 to 10 mL of sterile water or normal saline
Post –cardiac arrest care: Continuous IV infusion of 0.1 to 0.5 mcg/kg/min (Callaway, et al., 2015)
Symptomatic bradycardia or hypotension: Continuous infusion at 2 to 10 mcg/min (Link, et al., 2015)
Considerations • Epinephrine is available in different concentrations and in different medication containers. Read the label carefully before giving epinephrine to ensure that you are giving the right dose and using the right concentration of the drug.
• Increases myocardial oxygen demand; may cause postresuscitation myocardial dysfunction and ventricular dysrhythmias ( Attaran & Ewy, 2010).
• Administer an epinephrine infusion via an infusion pump.
• Check IV site frequently for evidence of tissue sloughing.
• Should not be administered in the same IV line as alkaline solutions: this inactivates epinephrine.
• According to the Institute for Safe Medication Practices, ratio expressions no longer appear on single entity drug products as of May 1, 2016. Epinephrine 1:1000 is displayed as 1 mg/mL and epinephrine 1:10,000 is displayed as 0.1 mg/mL.
ECG, electrocardiogram; IO, intraosseous; IV, intravenous; PEA, pulseless electrical activity; pVT, pulseless ventricular tachycardia; VF, ventricular fibrillation
BOX 4.2 Five Hs and Five Ts
Hypovolemia Tamponade, cardiac
Hypoxia Tension pneumothorax
Hypothermia Thrombosis: lungs (ie, massive pulmonary embolism)
Hypokalemia/Hyperkalemia Thrombosis: heart (ie, acute coronary syndromes) Hydrogen ion (acidosis) Tablets/toxins: drug overdose
87
CHAPTER 4 Cardiac Arrest Rhythms
ACLS Pearl ACLS Pearl
An
An agonist agonist is a drug or substance that produces a predictable response (ie, stimulates action). An is a drug or substance that produces a predictable response (ie, stimulates action). An antagonist
antagonist isis anan ageagentnt thathatt exeexertsrts anan actactionion oppopposiositete toto anoanothetherr (i(ie,e, bloblockscks actactionion).). A A chronotropechronotrope isis aa substance that affects the heart rate: positive chronotrope
substance that affects the heart rate: positive chronotrope¼¼ "" heart rate; negative chronotrope heart rate; negative chronotrope¼¼ ## hea
heartrt ratrate.e. A A dromotropedromotrope isis aa subsubstastancence thathatt affaffectectss AVAV conconducductiotionn velvelociocity:ty: pospositiitiveve drodromotmotropropee¼¼ ""
AV
AV conductionconduction velocity;velocity; negativenegative dromotropedromotrope¼¼ ## AV AV conductionconduction velocity.velocity. AnAn inotrope inotrope isis aa subsubstastancence that affects myocardial contractility: positive inotrope
that affects myocardial contractility: positive inotrope¼¼ "" force of contraction; negative inotrope force of contraction; negative inotrope¼¼ ## force of contraction.
force of contraction.
ACLS Pearl ACLS Pearl
Sympathetic (ie, adrenergic) receptors are located in different organs and have different physiologic Sympathetic (ie, adrenergic) receptors are located in different organs and have different physiologic act
actionionss whewhenn stistimulmulateated.d. AdrAdreneenergirgicc recrecepteptorsors havhavee beebeenn catcategoegoririzedzed intintoo thethe folfollowlowiningg maimainn typtypes:es:
alpha
alpha11,, alpalphaha22,, bebetata11,, bebetata22,, anandd bebetata33.. AlpAlphaha11recrecepteptorsors areare foufoundnd inin theeyes,theeyes, perperiphipheraerall smasmallll artarter- er-ies
ies andand arterarteriolesioles,, bladdbladder,er, gastrgastrointeointestinstinalal sphisphincterncters,s, andand malemale reprreproductoductiveive organorgans.s. StimStimulatiulationon of of alpha
alpha11recepreceptortor sitessites primprimarilarily y causescauses constconstrictrictionion ofof vascuvascularlar smootsmoothh musclmuscle.e. AlphAlphaa22recepreceptortor sitessites are found on platelets, blood vessels, and both presynaptically and postsynaptically on neurons in are found on platelets, blood vessels, and both presynaptically and postsynaptically on neurons in the brain (
the brain ( Wecker, et al., 2010Wecker, et al., 2010 ). Stimulation results in suppression of ). Stimulation results in suppression of further norepinephrine release.further norepinephrine release.
Bot
Bothh alpalphaha11 and alpha and alpha22 receptors have been found in the myocardium but their physiologic function receptors have been found in the myocardium but their physiologic function remains more clearly defined in the peripheral blood vessels than in the heart (
remains more clearly defined in the peripheral blood vessels than in the heart ( Opie & Hasenfuss,Opie & Hasenfuss, 2012
2012 ). ). Beta Beta receptor receptor sites sites are are divided divided into into betabeta1,1, beta beta22, and beta, and beta33. Beta. Beta11 receptors are found in receptors are found in the heart and kidneys. In the heart, stimulation of beta
the heart and kidneys. In the heart, stimulation of beta11 receptor sites results in an increase in heart receptor sites results in an increase in heart rate
rate (ie,(ie, positpositiveive chronchronotropotropy),y), anan incrincreaseease inin thethe strenstrengthgth ofof cardicardiacac contrcontractioactionn (ie,(ie, positpositiveive inotrinotropy),opy), and, ultimately, irritability of cardiac cells. Beta
and, ultimately, irritability of cardiac cells. Beta22 receptor sites are found in several locations in receptor sites are found in several locations in the body. In the lungs, stimulation of these receptors causes bronchodilation. Beta
the body. In the lungs, stimulation of these receptors causes bronchodilation. Beta22 receptors have receptors have also been found in the heart and account for about 20% of beta receptors in the left ventricle and also been found in the heart and account for about 20% of beta receptors in the left ventricle and about 40% in the atria (
about 40% in the atria ( Opie & Hasenfuss, 2012Opie & Hasenfuss, 2012 ). Beta ). Beta33 receptors are localized in fat cells. receptors are localized in fat cells.
Consider administration of an antiarrhythmic if pVT/VF continues despite CPR, defibrillation, and Consider administration of an antiarrhythmic if pVT/VF continues despite CPR, defibrillation, and giving
giving aa vasoprvasopressoressor. Although some antiar. Although some antiarrhythmrhythmicsics have been assochave been associated with increiated with increased rates ofased rates of ROSCROSC and
and hoshospitpital aal admisdmissiosion,n, nonnonee hashas proprovedved toto incincreareasese lonlong-tg-termerm sursurvivavivall oror sursurvivavivall witwithh aa googoodd neuneurolorologicgic outcome (
outcome (Link, et al., 2015Link, et al., 2015). Further, the ideal sequence and timing of antiarrhythmic administration). Further, the ideal sequence and timing of antiarrhythmic administration during c
during cardiaardiac arrec arrest inst in relatrelation to theion to the delivedelivery ofry of shockshocks is nots is not known (known (Link, eLink, ettal., 20al., 201515). Ami). Amiodaroodaronene isis an antiarrhythmic that blocks sodium channels, inhibits sympathetic stimulation, and blocks potassium an antiarrhythmic that blocks sodium channels, inhibits sympathetic stimulation, and blocks potassium ch
chanannenelsls asas wewellll asas cacalcilciumum chchanannelnelss (( Table Table4.44.4).). ThThee adadmiminisnistrtratatioionn ofof lidlidococainainee mamayy bebe coconsnsididerereded asas anan alternative to amiodarone for pVT/VF that is unresponsive to CPR, defibrillation, and vasopressor alternative to amiodarone for pVT/VF that is unresponsive to CPR, defibrillation, and vasopressor ther-apy(
apy(LiLinknk,,etetalal.,.,20201515).). LiLidodocacaineine isis aa ClClasasss 1B1B anantitiararrhrhytythmhmicic ththatat ininhihibibitsts ththee ininflufluxx ofof sosodidiumum ththrorougughh the fast channels of the myocardial cell membrane and decreases conduction in ischemic cardiac tissue the fast channels of the myocardial cell membrane and decreases conduction in ischemic cardiac tissue without
without adversely affecting adversely affecting normal conduction normal conduction (( Table 4.5 Table 4.5). Although the routine use of lidocaine after ). Although the routine use of lidocaine after cardiac arrest is not supported by current resuscitation guidelines, the initiation or continuation of cardiac arrest is not supported by current resuscitation guidelines, the initiation or continuation of lido-caine may be considered immediately after ROSC from cardiac arrest associated with pVT/VF ( caine may be considered immediately after ROSC from cardiac arrest associated with pVT/VF ( Link,Link, et al., 2015
Asystole, which which is is also also calledcalled ventricular asystole, ventricular asystole, is a total absence of ventricular electrical activity is a total absence of ventricular electrical activity (( Table 4.6 Table 4.6,, Fig. 4.3 Fig. 4.3). There is no ventricular rate or rhythm, no pulse, and no cardiac output. Some atrial). There is no ventricular rate or rhythm, no pulse, and no cardiac output. Some atrial electrical activity may be evident. If atrial electrical activity is present, the rhythm is called
electrical activity may be evident. If atrial electrical activity is present, the rhythm is called “ “ P-wave P-wave ” ” asystole
asystole or or ventricular standstill ventricular standstill ( (Fig. 4.4Fig. 4.4).).
The memory aids PATCH-4-MD and the Five Hs and Five Ts may be used to recall possible The memory aids PATCH-4-MD and the Five Hs and Five Ts may be used to recall possible revers-ible causes of asystole. In addition, ventricular asystole may occur temporarily after termination of a ible causes of asystole. In addition, ventricular asystole may occur temporarily after termination of a tachycardia with medications, defibrillation, or synchronized cardioversion.
tachycardia with medications, defibrillation, or synchronized cardioversion.
When asystole
When asystole is observed is observed on a on a cardiac monitor, cardiac monitor, confirm that confirm that the patient ithe patient is unresponsive s unresponsive and has and has nono pulse, and then begin high-quality CPR. Additional care includes establishing vascular access, pulse, and then begin high-quality CPR. Additional care includes establishing vascular access, consid-ering possible reversible causes of the arrest, administconsid-ering epinephrine, and possibly inserting an ering possible reversible causes of the arrest, administering epinephrine, and possibly inserting an advanced airway. For intubated patients, use continuous end-tidal carbon dioxide (EtCO
advanced airway. For intubated patients, use continuous end-tidal carbon dioxide (EtCO22) monitoring ) monitoring to assess the quality of compressions during the resuscitation effort and to monitor the ROSC.
to assess the quality of compressions during the resuscitation effort and to monitor the ROSC.
TABLE 4.4
TABLE 4.4 Amiodarone Amiodarone (Cordarone)(Cordarone)
C
• DirectlDirectly depresses the automay depresses the automaticity of the SA ticity of the SA and AV nodesand AV nodes
•
• Slows conducSlows conduction through the AV node and in tion through the AV node and in the accessorthe accessory pathway of y pathway of patienpatients withts with Wolff-Parkinson-White preexcitation pattern
Wolff-Parkinson-White preexcitation pattern
•
• InhibitInhibits alpha- and beta-adrenergs alpha- and beta-adrenergic receptorsic receptors
•
• PossesPossesses both vagolytic and calcium channses both vagolytic and calcium channel blocking propertiesel blocking properties
•
• Coronary and peripCoronary and peripheral vasodilheral vasodilatorator
•
• Mild decrease in myocardial contractility; however, cMild decrease in myocardial contractility; however, cardiac output may actually incardiac output may actually increaserease becau
because se of of decreadecreased afterloadsed afterload Indications
Indications •• pVT/VpVT/VF (after CPR, F (after CPR, defibrildefibrillation, and a vasopressor)lation, and a vasopressor)
•
• Stable narrow-Stable narrow-QRS tachycardQRS tachycardias if ias if the rhythm persists despitthe rhythm persists despite vagal maneuvers ore vagal maneuvers or adenosine, or the tachycardia is recurrent
adenosine, or the tachycardia is recurrent
•
• To control ventTo control ventricular rate in atrial fibrillricular rate in atrial fibrillationation
•
• To control ventricuTo control ventricular rate lar rate in preexcited atrial dysrhin preexcited atrial dysrhythmias with conductythmias with conduction over anion over an accessory pathway
Dosage •• pVT/VF: Initial bolus of 300 mg IV/IO; pVT/VF: Initial bolus of 300 mg IV/IO; can be followed by 1 can be followed by 1 dose of 150 mg (dose of 150 mg (Link, et al.,Link, et al., 2015
2015). If ROSC, can consider continuous IV infusion (1 mg/min infusion for 6 hours and). If ROSC, can consider continuous IV infusion (1 mg/min infusion for 6 hours and then a 0.5
then a 0.5 mg/min mainmg/min maintenance infutenance infusion over 18 sion over 18 hourshours). Maximum daily dose 2.2 g ). Maximum daily dose 2.2 g IV IV per 24 hours.
per 24 hours.
•
• Other indicOther indications: Loaations: Loading dose of 150 mg IV over 10 min. May repeat every 10 min if ding dose of 150 mg IV over 10 min. May repeat every 10 min if needed
needed.. AfterAfter converconversion,sion, follow wifollow with a 1 mg/min th a 1 mg/min infusioinfusionn forfor 6 hour6 hours and ts and then a hen a 0.5 mg/ 0.5 mg/
min maintenance infusion over 18 hours. Maximum cumulative dose 2.2 g IV per min maintenance infusion over 18 hours. Maximum cumulative dose 2.2 g IV per 24 hours (
24 hours (Link, et al., 2015Link, et al., 2015).).
Considerations
Considerations •• In the United States, amiodarIn the United States, amiodarone is available in two one is available in two formulaformulations. One formutions. One formulationlation
Considerations •• In the United States, amiodarIn the United States, amiodarone is available in two one is available in two formulaformulations. One formutions. One formulationlation