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From: Essential Cardiology: Principles and Practice, 2nd Ed.
Edited by: C. Rosendorff © Humana Press Inc., Totowa, NJ
28 Cardiopulmonary Resuscitation
Joseph P. Ornato, MD
INTRODUCTION
Sudden cardiac death (SCD) due to unexpected cardiac arrest in adults claims the lives of an estimated 400,000 to 460,000 adult Americans each year (1). Most episodes of unexpected SCD in adults occur in the home. The most common victim is a male who is 50 to 75 yr of age. The majority of SCD victims have underlying structural heart disease, usually in the form of coronary atherosclerosis and/or cardiomegaly. Although 75% of SCD victims have significant atheroscle- rotic narrowing (>75%) in one or more major coronary artery, fewer than half of all sudden deaths occur during an acute myocardial infarction (AMI).
SCD is usually caused by a chance arrhythmic event that is triggered by an interaction between structural heart abnormalities and transient, functional electrophysiological disturbances. In the majority of cases the initiating event is a ventricular tachyarrhythmia, either pulseless ventricular tachycardia (VT) that degenerates rapidly to ventricular fibrillation (VF) or “primary” VF (2). The majority of neurologically intact survivors of sudden, unexpected cardiac arrest come from a sub- set of patients whose event is initiated by a ventricular tachyarrhythmia. In such cases, the single most important determinant of survival is the time interval from initiation of the cardiac arrest until defibrillation can be provided to terminate the ventricular tachyarrhythmia and restore a more nor- mal rhythm accompanied by effective perfusion of vital organs.
PRINCIPLES OF RESUSCITATION
The American Heart Association (AHA) has introduced the “chain of survival” metaphor to represent the sequence of events that ideally should occur to maximize the odds of successful resuscitation from cardiac arrest in adults (3). Fewer than 5% of all out-of-hospital cardiac arrest victims survive to leave the hospital with neurological functioning intact (3). Survival from in- hospital cardiac arrest is not much better (averaging between 10 and 20%) (4). There is substantial variability in the odds for survival among various geographic locations.
The outcome of resuscitation is influenced strongly by the patient’s initial cardiac rhythm. The likelihood of survival is relatively high if the initial rhythm is VT or VF (particularly if the VF is
“coarse,” the arrest was witnessed, and prompt CPR and defibrillation are provided). The best out- comes from VT/VF in adults occur regularly in the electrophysiology laboratory, where prompt defibrillation (within 20–30 s) results in virtually 100% survival. The next best reported outcomes are in cardiac rehabilitation programs, where defibrillation occurs in 1 to 2 min, and survival is approx 85 to 90%. At Chicago’s O’Hare and Midway airports, 61% of cardiac arrest patients whose initial rhythm was VF survived to hospital discharge (5). Survival from out-of-hospital VT/VF treated by police officers equipped with automated external defibrillators (AEDs) in Rochester, MN has averaged 50% with a median time from collapse to defibrillation of about 5 min (6). Out- comes in many locations with EMS systems that cannot provide defibrilation until 10 min or more
after patient collapse typically yield survival rates of <10%. Thus, survival from cardiac arrest due to ventricular tachyarrhythmias is highly dependent on the time interval from collapse to defibril- lation. For every minute’s delay from the patient’s collapse to defibrillation the chance for sur- vival diminishes by approx 7–10% (3).
If the initial rhythm is not VT or VF, survival is typically <2–3% in most reported series. Asys- tolic patients whose cardiac arrest was unwitnessed rarely survive to hospital discharge neurologi- cally intact, even when they are treated promptly with atropine, epinephrine, and/or an artificial pacemaker. The only common exceptions are witnessed cardiac arrest patients whose initial brady- cardia or asystole (bradyasystole) is due to increased vagal tone or other relatively easily correctible factors (e.g., hypoxia of brief duration).
Pulseless electrical activity (PEA) is, by definition, the presence of an organized rhythm unac- companied by a detectable pulse in an individual who is clinically in cardiac arrest. The latter part of the definition is important for exclusion of conditions in which the rescuer is unable to detect a pulse but there is unmistakable evidence that there is adequate blood pressure and cardiac output to maintain vital organ perfusion (e.g., a conscious patient with profound vasoconstriction due to hypothermia). The underlying physiological cause of PEA in most cases is a marked reduction in cardiac output that is due to either profound myocardial depression or mechanical factors that reduce venous return or otherwise impede the flow of blood through the cardiovascular system.
Management of patients with PEA is directed at identifying and treating the underlying cause(s).
There are two fundamental goals in resuscitating an adult from cardiac arrest. First, a rhythm must be restored with a rate that is potentially capable of generating an adequate cardiac output and per- fusion pressure. This may involve defibrillating a patient out of VF or speeding up a bradyasystolic rhythm with atropine or an artificial pacemaker. Once an acceptable rhythm has been restored, atten- tion should be focused on optimizing cardiac output and perfusion pressure.
CPR
The technique and quality of CPR can affect critical organ perfusion pressure and blood flow dramatically. Maintenance of both the systolic and diastolic arterial pressure is even more vital for optimizing critical organ perfusion during CPR than in nonarrest conditions. Since flow to most vital organs (except the heart) occurs during the downstroke of closed chest compression (systole), a minimal systolic arterial pressure of 50 to 60 mmHg is usually required to resist arteriolar collapse.
Diastolic pressure is particularly important during CPR because it is a critical determinant of the coronary perfusion pressure (CPP = aortic diastolic pressure right atrial pressure). CPP is one of the best hemodynamic predictors of return of spontaneous circulation (ROSC) in both animal models and humans. A minimal threshold CPP gradient of approx 15 mmHg (usually correspond- ing to an aortic diastolic pressure of 30–40 mmHg) provides enough myocardial blood flow to meet minimum metabolic needs of the arrested myocardium and to achieve ROSC. Uninterrupted, or minimally interrupted, chest compressions appear to be helpful in maintaining an optimal CPP and improving ROSC in animal models and humans.
Understanding the mechanisms of blood flow during closed-chest CPR and real-time monitor- ing of hemodynamic parameters allows rescuers to modify chest compression techniques (the force of compression and the downstroke:upstroke ratio) when appropriate to optimize perfusion pressure and blood flow. It is now known that there are at least two major mechanisms of blood flow during closed-chest CPR: the “cardiac pump” and the “thoracic pump.”
It was initially believed that blood flow during CPR was caused by direct compression of the heart between the sternum and the spine (“cardiac pump”). In the mid-1970s, the cardiac-pump theory began to be challenged by investigators who observed that increased intrathoracic pressure alone (without precordial compression) is capable of generating blood flow. A sudden increase in the intrathoracic pressure causes air trapping in the alveoli and small bronchioles during chest compression, creating a pressure gradient between the intrathoracic and extrathoracic cavities. In the thoracic-pump theory, the heart functions as a passive conduit. Pressurization of the thorax
collapses veins at the thoracic inlet, preventing venous backflow. Forward flow occurs because the more muscular arteries remain open, particularly if epinephrine is administered.
Transesophageal echocardiography studies demonstrate that both mechanisms are operative during CPR (7). Physiological studies in experimental models and humans suggest a strong, prob- ably dominant, role for the thoracic pump during closed chest compression in adults. In addition, active decompression of the chest by application of negative pressure or suction to the sternum may further enhance cardiac output by improving venous inflow and/or by increasing the intrathoracic pressure difference between the upstroke and downstroke phase of chest compression (active com- pression-decompression CPR, also known as ACD-CPR). Unfortunately, ACD-CPR did not im- prove survival compared to standard CPR in a recent large, well-controlled, randomized clinical trial (8). Other experimental techniques, such as interposing an abdominal compression between chest compressions (IAC-CPR) (9) or phased chest and abdominal compression (10,11) are designed to simulate the physiological effects of intraaortic balloon counterpulsation. Use of an inspiratory resistance valve in patients in cardiac arrest increases the efficiency of CPR and, when combined with other efficient forms of chest compression, can increase the diastolic arterial pressure to >50 mmHg (12–15). It is not clear whether any of these techniques is clinically superior to well-per- formed standard CPR.
Chest compression delivers blood and oxygen to the myocardium, allowing a buildup of high- energy phosphates intracellularly. Interrupting chest compressions causes the coronary perfusion pressure and flow to fall precipitously, forcing cells to expend their high-energy phosphate reserves (16). Even brief (i.e., 10–15 s) pauses or delays in performing chest compressions can decrease the probability of successful defibrillation and return of spontaneous circulation in animal models (17) and humans (18).
CARDIOVASCULAR ASSESSMENT DURING RESUSCITATION Echocardiography
Conventional transthoracic echocardiography is of value during CPR but is sometimes limited because it is difficult to image the heart when the chest wall is in motion. Transesophageal echo- cardiography provides high-resolution, real-time images during CPR and can be used to (1) better define the mechanism of blood flow during chest compression; (2) determine the presence of peri- cardial effusion, intracardiac tumor or clot, chamber enlargement or hypertrophy, severe volume depletion, pneumothorax, or thoracic aortic dissection; (3) better define the cause of PEA; (4) eval- uate global and regional wall motion after ROSC; and (5) provide a visual guide for positioning intra- cardiac catheters and pacemaker wires.
Capnography
The percentage of carbon dioxide (CO2) contained in the last few milliliters of gas exhaled from the lungs with each breath is termed the end-tidal carbon dioxide concentration (PetCO2). During normal respiration and circulation, the PetCO2 averages 4 to 5%. Two units of measure are popu- larly used in reporting the PetCO2: percentage and mmHg (1% is approx 7 mmHg). The PetCO2 can be used to confirm endotracheal (ET) tube airway placement, particularly in the noncardiac-arrest patient who has a pulse and an adequate blood pressure (where the sensitivity and specificity of the PetCO2 for detecting correct ET tube placement approach 100% and 90%, respectively) (19).
Ventilation through an ET tube that has been properly inserted in the trachea yields a PetCO2 of 4 to 5% in a patient with a normal cardiac output and no significant ventilation–perfusion gradient.
Ventilation through an ET tube that has been inadvertently inserted into the esophagus results in a PetCO2 of <0.5%.
There is a logarithmic relationship between the PetCO2 and the cardiac output (20). At normal or elevated levels of cardiac output, ventilation is the rate-limiting factor responsible for eliminat- ing the large amount of CO2 passing through the pulmonary circuit (e.g., hyperventilation lowers,
and hypoventilation raises, the PetCO2). In this range, the PetCO2 closely approximates arterial CO2 tension (PaCO2) and can be used as a “real-time” guide to the adequacy of ventilation. At low levels of cardiac output (below approx 50% of normal in animal models), ventilation has much less effect on the PetCO2. If ventilation is kept relatively constant in this range, an increase or a decrease in the cardiac output will usually be reflected by a rise or fall in the PetCO2, respectively.
During CPR the PetCO2 is typically between one quarter and one third of normal, paralleling the low cardiac output and pulmonary blood flow (20,21). As CO2 builds up in venous blood, hyper- ventilation cleanses the reduced quantity of venous blood traversing the lungs of CO2, resulting in a low arterial (PaCO2) and a high central venous (PcvCO2) CO2 concentration (a venoarterial CO2 and pH gradient). Within seconds following ROSC, the improved cardiac output delivers large quantities of CO2-rich venous blood to the lungs and the PetCO2 climbs suddenly to normal or above-normal levels (21–23). The dramatic change from a low to a high PetCO2 due to venous CO2 washout is often the first clinical indicator that ROSC has occurred.
Monitoring the PetCO2 during CPR can be used as a guide to the patient’s hemodynamic status.
Inadequate chest compression is usually accompanied by a very low (i.e., <1%) PetCO2 that increases linearly with increasing sternal compression depth and force (24). Administration of sodium bicar- bonate intravenously causes a transient rise in PetCO2 as the substance dissociates into water and CO2. Disorders that cause significant ventilation–perfusion mismatch (e.g., pulmonary emboliza- tion), or decrease in production of CO2 (e.g., hypothermia) are accompanied by a low PetCO2. The initial PetCO2 also has prognostic value. An end-tidal CO2 level of 10 mmHg measured 20 min after the initiation of ACLS accurately predicts death in patients with cardiac arrest associated with electrical activity but no pulse. Cardiopulmonary resuscitation may be terminated in such patients (25).
ADVANCED AIRWAY MANAGEMENT Endotracheal Intubation
One of the most important goals early in resuscitation is to establish a definitive airway that will allow delivery of oxygen in high concentrations, protect the airway from aspiration, and permit administration of aerosolized medications. Intubation of the trachea with an endotracheal (ET) tube serves all of these purposes and is generally considered to be the airway of choice during CPR.
Medications that are commonly administered via the ET tube during resuscitation include epineph- rine, lidocaine, atropine, and naloxone. Epinephrine should be given in higher dosages endotrach- eally (at least double the iv dosage).
Laryngeal Mask Airway and Combitube™ Airway
In the past several years, the laryngeal mask airway (LMA) has become a highly accepted alter- native to endotracheal tube insertion for many elective operative procedures as well as for use dur- ing resuscitation. The device is easy to use, even in the hands of nurses and paramedics, and can generally be inserted much more quickly than an endotracheal tube. Insertion is performed blindly without the need for a laryngoscope. The Combitube airway is another suitable alternative that can permit minimally trained rescuers to ventilate adult cardiac arrest victims effectively.
Confirmation of Correct Airway Placement
The PetCO2 can be used to confirm whether an ET tube or LMA has been positioned in the trachea or the esophagus in the cardiac-arrest patient. If the PetCO2 during CPR is very low (below 0.5%) on at least the seventh breath following intubation, it is highly likely that inadvertent esophageal insertion of the ET tube has occurred. Conversely, a moderately low (above 0.5% but below 2.0%) PetCO2 does not necessarily indicate esophageal placement of the ET tube, as there are many other causes for this finding during CPR (Table 1). An alternative to the measurement of PetCO2 for confirmation of airway placement is the use of an aspiration syringe or bulb device.
Such devices are attached to the ET tube immediately after it is inserted. Suction is applied to the
ET tube using an aspiration syringe or bulb. If the tip of the ET tube is in the trachea, air is aspirated readily since the cartilage-containing trachea does not collapse. If the tip of the ET tube is in the esophagus, application of suction causes the esophagus to collapse. In such a case, there is resistance to the flow of air during aspiration.
USE OF VASOPRESSORS AND INOTROPIC AGENTS Epinephrine
Epinephrine is the vasopressor of choice for use during CPR. It improves coronary and cerebral blood flow by increasing peripheral vasoconstriction. By enhancing coronary perfusion pressure, epinephrine facilitates the resynthesis of high-energy phosphates in myocardial mitochondria and enhances cellular viability and contractile force.
The optimal dose of epinephrine to augment aortic diastolic blood pressure in humans during CPR has been controversial. However, recent prospective, randomized clinical trials have not shown improved outcome with “high dose” (e.g., >1 mg in adults) compared to standard dose (0.5–1 mg) epinephrine (26–29). The AHA currently recommends an adult iv dose of 0.5 to 1.0 mg at intervals that do not exceed 3 to 5 min. The use of higher doses of epinephrine after the initial 1-mg dose during resuscitation is neither recommended nor discouraged. If the dose is given by peripheral injection, it should be followed by a 20-mL flush of iv fluid to ensure drug delivery into the central compartment.
During cardiac arrest epinephrine also may be administered by continuous iv infusion (add 30 mL of a 1:1000 solution to 250 mL of normal saline or D5W, infused at 100 mL/h and titrating to the desired hemodynamic endpoint). Continuous infusions of epinephrine should be administered centrally to reduce the risk of extravasation. Epinephrine should not be added to infusion bags or bottles that contain alkaline solutions.
Dopamine
Dopamine is less effective than epinephrine with respect to improving blood flow to vital organs during CPR. During resuscitation, treatment with dopamine is usually reserved for patients with hypotension and shock that occurs after return of spontaneous circulation. When used to treat shock, norepinephrine should be added if more than 20 μg/kg/min of dopamine is needed to maintain an adequate blood pressure.
Dobutamine
Dobutamine may be the ideal agent to use after ROSC, particularly if congestive heart failure rather than hypotension is present. In animal models, dobutamine that is initiated within 15 min
Table 1
Common Causes of Low (<2%) PetCO2 During CPR Inadequate ventilation
Unrecognized esophageal intubation Airway obstruction
Inadequate blood flow
Inadequate chest compression Hypovolemia
Tension pneumothorax Pericardial tamponade Ventilation–perfusion mismatch
Pulmonary embolism
Decreased metabolic production of carbon dioxide Hypothermia
of successful resuscitation can successfully overcome the global systolic and diastolic left ventric- ular dysfunction resulting from prolonged cardiac arrest and CPR (30). At present, the AHA rec- ommends giving 2.0 to 20 μg/kg/min of dobutamine (500 mg mixed in 250 mL of D5W or normal saline), using the smallest effective dose needed to improve hemodynamics. The maximum dose is 40 μg/kg/min.
Vasopressin
Vasopressin produces significantly higher coronary perfusion pressure and myocardial blood flow than epinephrine during closed-chest CPR in a pig model of ventricular fibrillation (31). Both vasopressin and adrenocorticotropin concentrations are higher during CPR in patients in whom resuscitation is successful compared to those in whom it fails (32). Because of these observations, there has been considerable interest in the use of vasopressin for supporting coronary perfusion pressure during CPR in humans.
In a small, blinded, randomized clinical study, 40 patients with out of hospital VF resistant to electrical defibrillation were treated with either epinephrine (1 mg iv; n = 20) or vasopressin (40 U iv; n = 20) during resuscitation (33). Seven (35%) patients in the epinephrine group and 14 (70%) in the vasopressin group survived to hospital admission (p = 0.06). At 24 h, 4 (20%) epinephrine- treated patients and 12 (60%) vasopressin-treated patients were alive (p = 0.02). Three (15%) patients in the epinephrine group and eight (40%) in the vasopressin group survived to hospital discharge (p = 0.16). Neurological outcomes were similar in both groups.
Unfortunately, survival to hospital discharge did not differ for patients receiving either epineph- rine or vasopressin during resuscitation in the emergency department, intensive care unit, or hospi- tal inpatient units in a large, well-controlled, Canadian randomized clinical trial (34). This finding has been explained by some to possibly represent the lack of difference between the two vasocon- strictors early in resuscitation. This leaves open the possibility that vasopressin might be superior to epinephrine later in resuscitation when adrenergic agents typically become less effective due to downregulation of receptors. Further study will be needed to determine whether vasopressin has advantages over epinephrine late in resuscitation. In addition, there is increasing evidence that the combination of vasopressin and epinephrine may be more effective than either alone (35–37).
ACID-BASE MANAGEMENT
The marked fall in cardiac output during CPR reduces tissue oxygen delivery to critically low levels. Cells shift to anaerobic metabolism, causing a gradual building up of lactic acid. The PCO2 level begins to increase inside cells, including heart muscle cells in which the concentration of CO2 may reach very high levels (>400 mmHg), at which point PEA develops (38).
There is a dynamic equilibrium between intracellular CO2 and the blood traversing each capil- lary bed in the body. As CO2 diffuses into capillary blood in exchange for oxygen, the CO2 is trans- ported to the heart and lungs in venous blood. Because of this, central (mixed) venous blood during closed chest compression is acidotic (pH approx 7.15) and hypercarbic (PvCO2 approx 74 mmHg).
CO2 is removed from the lungs during ventilation. During well-performed closed-chest compres- sion, arterial blood pH is usually normal, slightly acidotic, or mildly alkalotic. Early in resuscita- tion, arterial blood can be slightly alkalotic while the venous blood is acidotic. Severe arterial acido- sis early during closed chest compression is usually due to inadequate ventilation or other forms of acidosis (e.g., lactic acidosis). The best solution is usually to improve the technique of closed- chest compression and to increase ventilation, if possible. If severe acidosis is present despite con- firmed proper endotracheal intubation, hyperventilation, and acceptably performed external chest compression, an alternate method for providing assisted circulation (e.g., open chest compressions or venoarterial bypass) should be considered.
In the past, administration of sodium bicarbonate was recommended for use early during closed- chest compression because of the belief that bicarbonate would buffer the H+ ion produced during
anaerobic metabolism. However, sodium bicarbonate itself contains a large amount of CO2 (260–
280 mmHg). In plasma, the CO2 is released and diffuses into cells more rapidly than HCO3, causing a paradoxical rise in intracellular PCO2 and a fall in intracellular pH. The increases in intracellu- lar PCO2 in heart muscle cells decrease cardiac contractility, cardiac output, and blood pressure.
Sodium bicarbonate causes other potentially harmful effects, including paradoxical acidosis of cerebrospinal fluid, hyperosmolality, alkalemia, and sodium overload.
At present, there are no convincing data indicating that treatment with sodium bicarbonate is of benefit during closed-chest compression and it does not improve survival in experimental ani- mals. The AHA no longer recommends routine administration of sodium bicarbonate during resus- citation because it provides minimal, if any, benefit and adds significant risk. If used at all, bicarbonate should not be given until proven interventions such as defibrillation, cardiac compression, support of ventilation including intubation, and pharmacological therapies such as epinephrine and anti- arrhythmic agents have been employed. If used, the initial recommended dose of sodium bicar- bonate is 1 mEq/kg. No more than half of the original dose should be given every 10 min thereafter.
There are a small number of “special situations” in which sodium bicarbonate is indicated for use early and, in some cases, repeatedly during resuscitation. Such circumstances include severe hyper- kalemia, known severe metabolic acidosis, and certain toxicological conditions (e.g., tricyclic anti- depressant or barbiturate overdose). Alternate buffer agents do not appear to improve survival dur- ing cardiac resuscitation.
MANAGEMENT OF VENTRICULAR TACHYARRHYTHMIAS
Electrical countershock is the treatment of choice for VF and pulseless VT. If three initial coun- tershocks at increasing energies (200, 200–300, and 360 J), intubation, epinephrine, and a fourth countershock (360 J) fail to terminate the arrhythmia (refractory VF or VT) or if, as in many cases, the arrhythmia rapidly recurs, antiarrhythmic drug therapy is usually recommended. Until recently, the agents most commonly used for this purpose included lidocaine, bretylium tosylate, procain- amide, -blockers, and magnesium sulfate. With one recent exception, there are no randomized, placebo-controlled clinical trials confirming whether these agents are any better than just repeat- ing electrical countershocks, continuing CPR, and administering intermittent epinephrine.
Lidocaine Hydrochloride
For refractory VF and pulseless VT, the AHA guidelines suggest an initial lidocaine dosage of 1.5 mg/kg for all adult patients. After restoration of spontaneous circulation, lidocaine is con- tinued as an iv infusion at a rate of 30 to 50 μg/kg/min (2–4 mg/min). The need for additional bolus doses of lidocaine is usually guided by clinical response and/or by plasma lidocaine concentra- tions. A recent European out-of-hospital cardiac arrest clinical trial showed no benefit from the use of lidocaine over placebo (which included repeated defibrillation attempts and epinephrine) for patients with recurrent and/or refractory VF (39).
Procainamide
Procainamide is a Type 1 antiarrhythmic agent with presynaptic ganglionic blocking, vasodilat- ing, and modest negative inotropic properties. During resuscitation procainamide is usually given in a dosage of 1 gm administered at a rate of 20 to 30 mg/min, followed by a maintenance infusion of 1 to 4 mg/min. An alternative regimen that achieves therapeutic levels faster (in some patients in only 15 min) includes a loading dose of 17 mg/kg given over 1 h followed by a maintenance infusion of 2.8 mg/kg/h. In patients who might clear the agent slowly, the loading dose is reduced to 12 mg/kg and the infusion rate is reduced to 1.4 mg/kg/h. The rate of drug administration should be reduced or stopped temporarily if hypotension occurs or there is prolongation of the QT interval or QRS complex by 50% or more.
Other Antiarrhythmic Agents and Treatments
Other conventional antiarrhythmic agents that may be tried in patients with recurrent and/or refractory VT/VF include iv -blockers or magnesium sulfate. Unfortunately, -blockers have not been formally studied during cardiac arrest and recent randomized, placebo-controlled clinical trials have not shown benefit from IV magnesium sulfate (40,41).
Recently there has been considerable interest in the use of iv amiodarone to treat patients with recurrent life-threatening ventricular arrhythmias. Studies on hospitalized patients have confirmed that this agent is active within minutes after iv administration. It is at least as effective as bretylium in terminating refractory and/or recurrent, life-threatening ventricular tachyarrhythmias but causes fewer side effects.
In a recent randomized, controlled clinical prehospital trial conducted on 504 cardiac arrest patients with recurrent and/or refractory ventricular tachyarrhythmias, the administration of a sin- gle 300-mg bolus of IV amiodarone at the time of the first IV epinephrine administration resulted in 26% greater survival to hospital admission compared to standard ACLS therapy (42). The study was inadequately powered to answer the question of whether IV amiodarone increases survival to hospital discharge. Dorian et al. conducted a randomized, controlled, clinical trial in Toronto, Canada comparing IV amiodarone and lidocaine in 347 patients with out-of-hospital cardiac arrest.
After treatment with amiodarone, 22.8% of 180 patients survived to hospital admission, as compared with 12.0% of 167 patients treated with lidocaine (p = 0.009; odds ratio, 2.17; 95% CI, 1.21–3.83).
Thus, as compared with lidocaine, amiodarone leads to substantially higher rates of survival to hospital admission in patients with shock-resistant out-of-hospital ventricular fibrillation. The principal side effects of iv amiodarone are hypotension and bradycardia, which usually respond readily to therapy (volume infusion and vasopressors; atropine and/or electrical pacing).
Other treatment strategies and troubleshooting checklists should be considered when the patient develops refractory or recurrent VT/VF. Underlying metabolic derangements, such as hypokale- mia and/or hypomagnesemia, should be sought and corrected. Arterial hypoxemia and acidosis should be reversed or minimized by endotracheal intubation, ventilation with 100% oxygen, and proper CPR technique. Proarrhythmic drug effects, hypokalemia, and/or hypomagnesemia can induce ventricular arrhythmias such as torsade de pointes. Although magnesium sulfate can be tried, torsade de pointes is best managed with electrical pacing (or other forms of overdrive suppression such as with isoproterenol until pacing is available).
MANAGEMENT OF BRADYASYSTOLIC CARDIAC ARREST
Survival is poor regardless of therapy for cardiac arrest patients who present with bradyasystole.
It is always important to exclude disconnection of a lead or monitor electrode prior to concluding that a “flat line” is the patient’s rhythm, as some patients with such a tracing may have VF (a rhythm more amenable to treatment) masquerading as asystole. Whenever there is any doubt, the monitor lead should be switched quickly to another lead to confirm the diagnosis prior to treatment. Treat- ment with atropine sulfate may improve outcome in patients with bradyasystolic cardiac arrest that is due to excessive vagal stimulation, but atropine is less effective when asystole or pulseless idio- ventricular rhythms are the result of prolonged ischemia or mechanical injury in the myocardium.
For patients with bradyasystolic cardiac arrest, a 1-mg dose of atropine is administered iv and is repeated every 3 to 5 min if asystole persists. Three milligrams (0.04 mg/kg) given intravenously is a fully vagolytic dose in most adults patients. The administration of a total vagolytic dose of atro- pine should be reserved for patients with bradyasystolic cardiac arrest. Endotracheal atropine (1–
2 mg diluted in 10 mL of sterile water or normal saline) produces a rapid onset of action similar to that observed with iv injection.
Pacing (transvenous, transthoracic, or transcutaneous) rarely influences survival in the unwit- nessed cardiac arrest patient who is initially found with asystole or bradycardia without a pulse.
However, pacing is extremely useful for bradycardic patients with a pulse and in selected patients
in whom a pacemaker can be placed immediately after the development of the conduction distur- bance. In such cases, a precordial thump can also stimulate ventricular complexes and a pulse (“fist pacing”).
Endogenous adenosine released during myocardial hypoxia and ischemia relaxes vascular smooth muscle, decreases atrial and ventricular contractility, depresses pacemaker automaticity, and impairs AV conduction. The cellular electrophysiological effects of adenosine can be compe- titively antagonized by methylxanthines, but not by atropine. Aminophylline, a competitive non- specific adenosine antagonist, has been shown to restore cardiac electrical activity within 30 s in 12 of 15 in-hospital, bradyasystolic cardiac arrest patients who were refractory to atropine and epi- nephrine (43). Another small randomized clinical pilot study found that adenosine blockade may restore normal sinus rhythm in some bradyasystole patients who do not respond to conventional ther- apy (44). Although further clinical research will be necessary to determine the potential value of adenosine blockade for bradyasystolic cardiac arrest, adenosine blockade should not be used when VF is present because use of this agent may make it more difficult to terminate this arrhythmia.
MANAGEMENT OF PULSELESS ELECTRICAL ACTIVITY
PEA is present when there is organized electrical activity on the electrocardiogram but no effec- tive circulation, as manifest by a lack of a detectable pulse. There are many underlying potential causes, but the most common denominator may involve myocardial ischemia and dysfunction due to intramyocardial increases in CO2. Prognosis is generally poor unless a discrete and treatable etiol- ogy for PEA can be discerned and corrected. Efforts should be directed toward detecting causes such as hypovolemia, hypoxemia, acidosis, tension pneumothorax, and pericardial tamponade.
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