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Acs0801 Cardiac Resuscitation
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1. © 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 8 CRITICAL CARE 1 Cardiac Resuscitation — 1 1 CARDIAC RESUSCITATION Terry J. Mengert, M.D. Approach to Cardiovascular Resuscitation Out-of-hospital sudden cardiac arrest claims the lives of more than INITIATION OF CPR 300,000 persons in the United States each year, making it the leading While awaiting the arrival of a deﬁbrillator and advanced help, cause of death.1-4 In fact, approximately 50% of all cardiac deaths are the rescuer assesses the patient’s airway, breathing, and circulation sudden deaths.5 In hospitals, a minimum of 370,000 patients also suf- [see The Primary Survey, below] and initiates CPR [see Table 1]. fer a cardiac arrest, followed by an attempted, but only sometimes When CPR is started within 4 minutes of collapse, the likelihood of successful, resuscitation.6 Although most victims of sudden death patient survival at least doubles.17,18 have underlying coronary artery disease (70% to 80%), sudden death is the ﬁrst manifestation of the disease in half of these persons.2 Other INITIATION OF DEFIBRILLATION causes and contributing factors include abnormalities of the my- When the AED or monitor-deﬁbrillator arrives, attach it appro- ocardium (i.e., chronic heart failure or hypertrophy from any cause), priately to the patient and analyze the patient’s rhythm; if the patient electrophysiologic abnormalities, valvular heart disease, congenital is in VF or pulseless VT, a deﬁbrillatory shock should be rapidly ap- heart disease, and miscellaneous inﬂammatory and inﬁltrative disease plied [see Tables 2 and 3]. If required, two additional shocks may be processes (e.g., myocarditis, sarcoidosis, and hemochromatosis).7-9 administered sequentially.The importance of rapid access to deﬁb- The pathophysiology that culminates in a sudden cardiac death rillation cannot be overemphasized. In a patient who is dying from a is complex and poorly understood. It likely represents a mix of elec- shockable rhythm, the chance of survival declines by 7% to 10% for trical abnormalities combined with acute functional triggers, such every minute that deﬁbrillation is delayed.19 as myocardial ischemia, central and autonomic nervous system ef- fects, electrolyte abnormalities, and even pharmacologic inﬂu- INITIATION OF ADVANCED CARE ences.1 Classically, most sudden deaths that occur in adults in the If the patient remains pulseless despite the steps described above, community are thought to be secondary to ventricular tachycardia resume CPR; establish a deﬁnitive airway, conﬁrm its correct place- (VT) that quickly degenerates into ventricular ﬁbrillation (VF). In a ment, and then secure it; establish intravenous access; then adminis- 10-year study in the Seattle area, the different arrhythmias found in ter appropriate medications as determined by the rhythm and the ar- prehospital cardiac arrest patients presumed to have underlying car- rest circumstances. If the patient is in VF or pulseless VT, repeated diovascular disease were VF (45%), asystole (31%), pulseless elec- attempts at deﬁbrillation are interspersed with delivery of vasoactive trical activity (PEA; 10%),VT (1%), and other arrhythmias (14%).3 and antiarrhythmic drugs [see Table 4]. Studies indicate that the out-of-hospital incidence of VF has de- creased in recent years, probably because of the decrease in mortal- RESUSCITATION OUTCOME ity from coronary artery disease.10 When every link in the chain of survival is quickly and sequen- tially available, the patient is provided an optimal opportunity for return of spontaneous circulation.19-22 In the United States, indi- The Chain of Survival vidual communities report survival rates of 4% to 40% or more in The resuscitation of an adult victim of cases of sudden cardiac death.23-27 Prehospital victims of VF have sudden cardiac arrest should follow an had survival rates to hospital discharge of greater than 50% when orderly sequence, no matter where the an AED was expeditiously used.28 Many other factors also inﬂu- patient’s collapse occurs. This sequence ence patient survival, however; these include whether the patient’s is called the chain of survival.11 It com- collapse was witnessed, the rapidity and effectiveness of bystander prises four elements, all of which must be CPR, the rhythm associated with the cardiac arrest, and underly- instituted as rapidly as possible: activa- ing comorbidities.29,30 With inpatient cardiac arrest, for example, tion of the emergency medical service overall survival rates vary from 9% to 32%,31-37 but in one study, network, cardiopulmonary resuscitation survival to hospital discharge was 30% for patients with primary (CPR), early deﬁbrillation, and provision heart disease, 15% for patients with infectious diseases, and only of advanced care. 8% for patients with other end-stage diseases (e.g., cancer, lung ACTIVATION OF EMERGENCY MEDICAL SERVICES disease, liver failure, or renal failure).38 Such statistics underline the importance of using cardiac resusci- A person in cardiac arrest is unresponsive and pulseless, although tation appropriately and with discrimination. Cardiac resuscitation agonal respirations may last for minutes. Conﬁrm unresponsiveness provides rescuers with powerful tools that save the lives of thou- by speaking loudly and gently shaking the patient. If the patient is sands of people every year.These techniques are capable of return- truly unresponsive, immediately call for help by activating the emer- ing patients who would otherwise die to productive and meaningful gency medical service in the community (in most locales, this lives. However, cardiac resuscitation should not be employed to re- means calling 911); or if the patient is already in the hospital, call a verse timely and natural death. Under those circumstances, it has code (e.g., code blue, code 199). If an automated external deﬁbril- the potential to lengthen the dying process and to increase human lator (AED) is available, have it brought to the resuscitation scene. suffering. All practitioners are well advised to remember that “death AEDs are both easily used and lifesaving.12-16 is not the opposite of life, death is the opposite of birth. Both are as-
© 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 8 CRITICAL CARE 1 Cardiac Resuscitation — 2 Patient is in cardiac arrest Confirm unresponsiveness. If out of hospital, call EMS. If in hospital, activate appropriate code. Approach to Call for a defibrillator. Cardiovascular Resuscitation Primary survey Assess ABCs. Begin CPR; when defibrillator arrives, attach to patient and briefly withhold CPR. Assess rhythm. Pulseless VT or VF Pulseless electrical activity Asystole Immediately administer shock, first at 200 J, Resume CPR. Resume CPR and confirm asystole. then 200–300 J, then 360 J; if patient is already Ensure that patient is appropriately attached to attached to a monitor-defibrillator, begin monitor-defibrillator, that ECG gain control on resuscitation with immediate defibrillation. the defibrillator is at maximum, and that the Resume CPR. rhythm is assessed in several leads. Secondary survey Endotracheally intubate, confirm tube placement, secure tube, establish I.V. access. Concomitantly with preceding steps, identify and correct technical difficulties hampering resuscitation [see Table 6]; initiate emergency therapy for conditions contributing to cardiac arrest [see Table 7]. Pulseless VT or VF Pulseless electrical activity Asystole Subsequent steps assume continuing VT or VF Subsequent steps assume continuing Subsequent steps assume continuing despite interventions; do not interrupt CPR PEA despite interventions; do not asystole despite interventions; do not except as required for rapid performance of interrupt CPR except as required for interrupt CPR except as required for rapid lifesaving procedures. rapid performance of lifesaving performance of lifesaving procedures. Administer vasoactive drugs with ongoing CPR: procedures. Attempt transcutaneous pacing, if Epinephrine, 1 mg I.V. push, repeated every Administer epinephrine, 1 mg I.V. push, available (may be initiated simultaneously 3–5 min throughout CPR with ongoing CPR; repeat every 3–5 with above steps). or min as long as CPR is required. Administer medications with ongoing CPR: Vasopressin, 40 U I.V. push in a single dose; If heart rate as shown on monitor is Epinephrine, 1 mg I.V. push; repeat if no response after 10 min, administer slow, administer atropine, 1 mg I.V. every 3–5 min for as long as patient epinephrine as described above. push, with ongoing CPR; may repeat requires CPR (vasopressin, 40 U I.V. every 3–5 min to a total dose of 3 mg. one time, is a reasonable alternative) Follow medication delivery with a 20 ml and saline bolus and elevation of the Atropine, 1 mg I.V. push; repeat every Administer antiarrhythmic drugs with ongoing CPR: extremity containing the I.V. line. 3–5 min to a total dose of 3 mg Amiodarone, 300 mg I.V. push; if a second dose is Follow medication delivery with a 20 ml needed, 150 mg after 5 min saline bolus and elevation of the or extremity containing the I.V. line. Lidocaine, 1.0–1.5 mg/kg I.V. push; if a second dose is needed, repeat initial dose in 3–5 min. End resuscitation attempt if patient remains in confirmed asystole for > 10 min and Hypomagnesemia or torsade de pointes is suspected: there is no technical problem preventing Magnesium sulfate, 1–2 g I.V. push resuscitation, no imminently treatable Intermittent or recurrent VT/VF after an initial cause, and no extenuating circumstance. response to shocks: Procainamide, 20–50 mg/min I.V. infusion to a total dose of 17 mg/kg. Follow medication delivery with a 20 ml saline bolus; elevate extremity with I.V. line, and continue CPR for 30–60 sec to circulate medication; then administer shock (360 J for up to three shocks).
© 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 8 CRITICAL CARE 1 Cardiac Resuscitation — 3 in the laboratory, an arterial pressure wave occurred.42 Further Table 1 Initial Resuscitation Steps in the study and reﬁnements led to the technique of closed-chest CPR, the careful description of which was published in 1960.43 The ﬁrst Unresponsive Patient report of the use of this technique in patients was in 1961.44 Since Confirm unresponsiveness those early days, the fundamentals of closed-chest CPR have re- Activate the emergency medical system mained relatively unchanged. Mouth-to-mouth, mouth-to-mask, In most community locales, call 911 or bag-valve-mask ventilation oxygenates the blood. Chest com- In the hospital, activate the appropriate code response pressions produce forward blood ﬂow.This ﬂow appears to result Call for an automatic external defibrillator (AED) from a combination of direct compression of the heart and in- Begin basic life support (CPR) trathoracic pressure changes.45,46 Open airway CPR in isolation does not deﬁbrillate the heart. Its main beneﬁt Check breathing; if not breathing, deliver two initial breaths is to extend patient viability until a deﬁbrillator and advanced inter- Check for a carotid pulse; if pulseless, do the following: ventions become available and, one hopes, succeed in restoring Begin chest compressions at the rate of 100 compressions/min, de- pressing the sternum 4–5 cm per compression in patients older than spontaneous circulation in the patient. CPR is not nearly as effec- 8 yr tive as a contracting heart; systolic arterial pressure peaks of 60 to Intersperse ventilations with chest compressions: in nonintubated pa- 80 mm Hg may be generated, but diastolic blood pressure remains tients, deliver 15 compressions, pause for two breaths, then repeat; in intubated patients, deliver one breath every 5 sec, with no pause low, and a cardiac output of only 25% to 30% of normal can be in compressions achieved even under optimal conditions.47 Still, effective CPR is Reassess for return of spontaneous circulation every 1–3 min critical to keeping the patient alive. It is worth remembering that When defibrillator arrives, immediately analyze and treat arrhythmia the most important rescuers at a cardiac resuscitation are those Attach patient to AED [see Table 2] or the monitor-defibrillator who are performing expert CPR, because it is only through their ef- [see Table 3] Analyze arrhythmia and treat as appropriate forts that the patient’s heart and brain are kept viable until deﬁbril- lation and other advanced interventions can restore spontaneous circulation. After unresponsiveness is conﬁrmed, the emergency medical pects of life.”39 It is untimely death that requires immediate inter- system is activated and an AED is called for; the primary survey vention with cardiac resuscitation. (A, B, C, and D) proceeds as described (see below) until the AED arrives. The Primary and Secondary Surveys of Cardiac Airway Optimization Resuscitation Open the patient’s mouth and optimize the airway in the non- A cardiac resuscitation is a stressful event for everyone involved. trauma patient by use of the head-tilt and chin-lift maneuver. A Too often, clinic and inpatient cardiac arrests and their manage- jaw-thrust maneuver should be used instead of the head-tilt tech- ment are episodes of chaos in the busy lives of resident and attend- nique if cervical spine injury is suspected. In patients with suspect- ing physicians.Yet, it has been eloquently stated that a good resusci- ed spine injury, proper spine alignment must be maintained tation team should function like a ﬁne symphony orchestra.40 Such throughout all phases of the resuscitation. In such circumstances, as skill levels require dedicated individual and team practice and care- ful code-team organization. Mastery in cardiac resuscitation is in fact a lifelong pursuit that requires training and retraining in ad- vanced cardiac life support (ACLS); regular practice and review; and leadership and team skill development. Its key elements in- Table 2 Using an Automatic External clude not only the resuscitation itself but the response to the an- Defibrillator in Patients Older than 8 Years nouncement of a code, postresuscitation stabilization of the patient, notiﬁcation of the family and primary care provider, and code cri- Automatic external defibrillator (AED) arrives (CPR is in progress) Place AED beside patient. tique and debrieﬁng.To help practitioners learn and apply some of Turn on the AED. the most essential techniques used in cardiac resuscitation more Attach the electrodes to the AED (they may be preattached). easily and effectively, the American Heart Association (AHA) has Attach the electrode pads to the patient (as diagrammed on the pads). developed the concepts of primary and secondary surveys of a pa- AED analyzes patient’s rhythm tient in atraumatic cardiac arrest.41 Stop CPR (and ensure no one is touching the patient). Press the Analyze button on the AED (some devices analyze the rhythm THE PRIMARY SURVEY automatically as soon as the pads are placed on the patient). The primary survey for the victim of AED instructs rescuers (via an audible voice prompt and/or on-screen instructions) sudden cardiac arrest consists of the ap- Shock is indicated: clear the patient (ensure no one is touching the propriate assessment of the patient’s air- patient) and push the Shock button. way (A), breathing (B), and circulation After delivering shock, press the Analyze button again; the sequence of (C) and the simultaneous application of analysis followed by shock (if so indicated) may be performed a total of three times. expert CPR until deﬁbrillation (D) be- or comes possible (assuming the patient is Shock not indicated: reassess the patient for signs of circulation; if pres- in VF or pulseless VT).Thus, the primary ent, assess the adequacy of breathing; if there are no signs of circula- survey includes the second and third tion, resume CPR for 1–2 min. After 1 min of CPR, assess the patient again for signs of circulation; if present, assess the adequacy of links in the chain of survival (see above). breathing. If the patient is still pulseless, repeat analysis, followed In 1958, Kouwenhoven noted that when his research fellow (if indicated) by shock steps. forcefully applied external deﬁbrillating electrodes on a dog’s chest
© 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 8 CRITICAL CARE 1 Cardiac Resuscitation — 4 nal thrusts are then applied, followed by a ﬁnger sweep of the 52,89 oropharynx to relieve suspected obstruction, and then ventilation Table 3 Using a Manual Defibrillator attempts are repeated. Deﬁnitive intervention for an obstructed air- Defibrillator arrives (CPR is in progress) way in the hospital setting may involve laryngoscopic visualization Place defibrillator beside patient. of the cause of obstruction and foreign-body removal. If an ade- Turn defibrillator on (initial energy level setting is typically 200 J).* quate airway cannot be established by less invasive means, cricothy- Set Lead Select switch to Paddles. Alternatively, if patient is already at- rotomy may be required. tached to monitor leads, set Lead Select switch to lead I, II, or III; en- sure all three leads are correctly attached to the patient and the defib- CPR Initiation rillator: white to right shoulder, black to left shoulder, red to ribs on left side. The health care rescuer next checks for a carotid pulse in the un- Apply gel to paddles or place conductor pads on patient’s chest. Some responsive patient but should allow no more than 10 seconds to do devices use disposable electrode patches that are prepasted with a conducting gel. In either case, the appropriate positions of the pad- so. (The AHA no longer recommends pulse checks for rescuers who dles with applied gel, conductor pads, or disposable paddles are as are not health care providers.49 Instead, lay rescuers should initiate follows: sternal paddle is placed to the right of the sternum, just below chest compressions if the patient is not breathing, coughing, or mov- the right clavicle; apex paddle is placed to the left of the left breast, centered in the left midaxillary line at the fifth intercostal space. ing after the initial two breaths.) If the patient has no carotid pulse, Analyze rhythm begin chest compressions.The patient should be on a ﬁrm surface, Briefly withhold CPR and the heel of the rescuer’s hand should be in the center of the infe- If using paddles to assess rhythm, apply paddles as described with firm rior half of the patient’s sternum (but cephalad to the xiphoid pressure (25 lb of pressure to each paddle) and visually assess rhythm on monitor (if using leads, briefly withhold CPR and assess rhythm in process). The rescuer’s other hand is placed on top of the lower leads I, II, or III). If rhythm is either pulseless VT or VF, proceed as fol- hand, with the ﬁngers interlocked. lows: The rescuer’s arms are held straight, with the force of each com- Defibrillate, then reassess pression coming from the rescuer’s trunk. In patients older than 8 Announce to resuscitation team, “Charging defibrillator, stand clear!” and press Charge button on either paddles or defibrillator (initial years, the sternum is smoothly compressed by 1.5 to 2.0 inches, energy, 200 J, not synchronized).* then released.The duration of the compression-release cycle is di- Warn resuscitation team that a defibrillatory shock is coming: vided equally between compression and release. The rate of chest “I am going to shock on three! ONE, I’m clear; TWO, you’re clear, compression is 100 compressions/min in patients older than 8 THREE, everybody’s CLEAR!” Simultaneously with these statements, visually ensure that no resuscitation team member is in contact with years.The chest should be allowed to rebound to its precompres- patient. sion dimensions between compressions, but the resuscitator’s palm Press the Discharge buttons on both paddles simultaneously to deliver a closest to the patient should remain in contact with the sternum. defibrillatory shock. Reassess rhythm on monitor; if patient is still in VT or VF, recharge defib- In nonintubated patients, chest compressions are regularly inter- rillator (now 300 J)* and repeat process of loudly informing team mem- rupted for the delivery of ventilations.The sequence is the same, re- bers by giving the warning statements as above, and then apply defib- gardless of whether one-rescuer or two-rescuer CPR is being per- rillatory shock. formed: the rescuer delivers 15 compressions, pauses for two Reassess rhythm on monitor; if patient is still in VT or VF, recharge defib- rillator (now 360 J)* and repeat process of loudly informing team mem- breaths (each given over 2 seconds), then resumes compressions. In bers by giving the warning statements as above, and then apply defib- endotracheally intubated patients, no pause for ventilation is neces- rillatory shock. sary; every 5 seconds, one ventilation is delivered over a period of 1 Reassess rhythm on monitor; if patient is still in VT or VF, resume CPR and continue with resuscitation sequence. to 2 seconds, while compressions continue.18 The optimal timing and ratio of ventilations to compressions in *Note: if using a biphasic defibrillator, a lower initial defibrillatory energy level (< 200 J) CPR is an ongoing area of research, which may lead to changes in without energy escalation on subsequent shocks is acceptable. VF—ventricular fibrillation VT—ventricular tachycardia the current recommendations. In the porcine model, for example, optimal neurologic outcome was achieved with the use of only com- pressions for the ﬁrst 4 minutes, followed by a compression-ventila- tion ratio of 100:2.50 In the prehospital setting, when rapid advanced equipment becomes available, the patient’s spine requires immobi- care is available within minutes, bystander-initiated mouth-to- lization with a padded backboard, hard cervical collar, appropriate mouth ventilation combined with chest compressions offers no ad- bolstering around the patient’s head to prevent movement, and vantage over chest compressions alone.51 strapping of the patient to the backboard.48 Good technique is critical throughout CPR delivery.The patient should have carotid pulses with chest compressions and should Breathing Assessment have appropriate breath sounds and chest movement with ventila- To assess breathing, the rescuer places his or her cheek close to tions. Interestingly, femoral pulsations with CPR do not necessarily the patient’s mouth and looks, listens, and feels for patient respira- indicate effective CPR; these pulsations often are venous rather tions. If the respirations are agonal or the patient is apneic, the res- than arterial. Quantitative end-tidal carbon dioxide levels can be cuer then delivers two initial breaths. Each breath is delivered over monitored, if practical. Higher levels correlate with more effective 1.5 to 2.0 seconds.The patient’s chest should rise with each deliv- CPR and increased survival.52 The patient should be reassessed for ered breath, and exhalation is allowed for between breaths. Breaths return of spontaneous circulation every 1 to 3 minutes [see Table 1]. may be delivered using the mouth-to-mouth technique with appro- priate barrier precautions (the patient’s nose should be pinched if Deﬁbrillation the mouth-to-mouth technique is used) or mouth-to-mask tech- When the monitor-deﬁbrillator or AED arrives, it is attached to nique.The ideal device, if available, is a bag-valve-mask device at- the patient; the rhythm is analyzed, and if the patient is in VF or tached to high-ﬂow oxygen; this allows the delivery of a substantial- pulseless VT, deﬁbrillation is provided [see Tables 2 and 3]. ly higher oxygen concentration to the patient. If the patient cannot Deﬁbrillation is thought to work by simultaneously depolarizing a be ventilated, the rescuer repositions the airway and attempts the sufﬁcient mass of cardiac myocytes to make the cardiac tissue ahead technique again. If the airway is still obstructed, up to ﬁve abdomi- of the VT or VF wavefronts refractory to electrical conduction. Subse-
© 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 8 CRITICAL CARE 1 Cardiac Resuscitation — 5 Table 4 Drugs Useful in Cardiac Arrest3,90 Drug and Doses Indications in Category Adult Dosage Comments Supplied Cardiac Arrest I.V. boluses of epinephrine (1 mg) are appropriate only in 1 mg I.V. push; may repeat every 3–5 min pulseless cardiac arrest patients; if continued epinephrine Epinephrine, 1 mg in 10 ml Pulseless VT or VF unre- for as long as patient is pulseless; can is required after resuscitation, a continuous infusion should emergency syringe; sponsive to initial de- Vasopressors also be given via the endotracheal route: be started (1–10 µg/min). 1 mg/ml (1 ml and 30 ml fibrillatory shocks; PEA; 2–2.5 mg diluted with normal saline (NS) High-dose epinephrine (up to 0.2 mg/kg I.V. per dose) does vials) asystole to 10 ml total volume not improve survival to hospital discharge in cardiac arrest patients and is no longer recommended in adults. Vasopressin, Pulseless VT or VF unre- 40 IU I.V. push, single dose only; can also be If no response after 10 min of continued resuscitation, ad- 20 IU/ml (1 ml vial) sponsive to initial de- given via endotracheal tube: same dose, minister epinephrine, as above. fibrillatory shocks diluted with NS to 10 ml total volume Pulseless VT or VF unre- VT/VF: 300 mg diluted in 20–30 ml; NS or sponsive to initial de- D5W rapid I.V. push; a repeat dose of Amiodarone, Side effects may include hypotension and bradycardia in the fibrillatory shocks and 150 mg may be given if required in 5 50 mg/ml (3 ml vial) postresuscitation phase. epinephrine plus min; maximum dose in 24 hr should not shock(s) exceed 2,200 mg Initial dose: 1–1.5 mg/kg I.V.; for refractory If lidocaine is effective, initiate continuous I.V. infusion at 2–4 Lidocaine, 50 mg or Pulseless VT or VF unre- VF or unstable VT, may repeat 1–1.5 mg/min when patient has return of a perfusing rhythm (but 100 mg in 5 ml emer- sponsive to initial de- mg/kg I.V. in 3–5 min; maximum dose, do not use if this rhythm is an idioventricular rhythm or gency syringes; pre- fibrillatory shocks and 3 mg/kg third-degree heart block with an idioventricular escape mixed bag, 1 g/250 ml epinephrine plus May also be given endotracheally: rhythm). or 2 g/250 ml shock(s) 2–4 mg/kg diluted with NS to 10 ml total Continuous infusion should begin at 1 mg/min in congestive volume heart failure or chronic liver disease or in elderly patients. Antiarrhythmics Pulseless VT or VF un- Administer 1–2 g diluted in 100 ml D5W Measured magnesium levels correlate only approximately responsive to initial de- I.V. over 1–2 min Magnesium sulfate, with the actual level of deficiency. fibrillatory shocks and Total body magnesium deficits should be 500 mg/ml (2 ml and Patients with renal insufficiency are at risk for dangerous epinephrine plus replaced gradually after initial therapy 10 ml vials), or 10 ml hypermagnesemia; use appropriate caution. shock(s) if suspected has stabilized the emergency: adminis- emergency syringe hypomagnesemic ter 0.5–1 g/hr for 3–6 hr, then reassess Side effects may include bradycardia, hypotension, generalized state continued need weakness, and temporary loss of reflexes. 20–30 mg/min I.V. (up to 50 mg/min if sit- uation is critical); maximum dose is 17 Administer procainamide during a perfusing rhythm. Procainamide, 100 mg/ml Recurrent or intermittent mg/kg over time (but maximum dose is Stop procainamide administration when arrhythmia is ade- (10 ml injection); pulseless VT or VF reduced to 12 mg/kg in setting of car- quately suppressed, hypotension occurs, QRS widens to 500 mg/ml (2 ml vial) diac or renal dysfunction) > 50% of original duration, or maximum dose is administered. Maintenance infusion is 1–4 mg/min For asystole or PEA: 1 mg I.V. every 3–5 Atropine, 1 mg in 10 ml Asystole or PEA (if rate of min up to 3 mg Minimal adult dose is 0.5 mg. Anticholinergic Avoid use in type II second-degree heart block or third- emergency syringe rhythm is slow) May be given via ET tube: 2–3 mg diluted with NS to 10 ml degree heart block. Significant hyperkalemia In non–dialysis-dependent hyperkalemic patients, bicarbon- Significant metabolic aci- Hyperkalemia therapy: 50 mEq I.V. ate is most useful if metabolic acidosis is also present; bi- dosis unresponsive to Metabolic acidosis: 1 mEq/kg slow I.V. carbonate is less effective in dialysis-dependent renal fail- Bicarbonate, 50 mEq optimal CPR, oxygena- push; may repeat half initial dose in 10 in 50 ml emergency ure patients. The use of bicarbonate in metabolic acidosis tion, and ventilation min; ideally, ABGs should help guide fur- management in cardiac arrest patients is controversial. syringe ther therapy Certain drug overdoses, in- Side effects may include sodium overload, hypokalemia, and Miscellaneous cluding tricyclic anti- Use in overdose: discuss with toxicologist metabolic alkalosis. depressants and aspirin Significant hyperkalemia Do not use if suspected cause of hyperkalemia is acute In hyperkalemia: 5–10 ml slow I.V. push; Calcium chloride, Calcium channel blocker digoxin poisoning. may repeat if required 100 mg/ml in 10 ml drug overdose Do not combine in same I.V. with sodium bicarbonate. prefilled syringe In calcium channel blocker overdose: dis- Profound hypocalcemia of cuss with toxicologist Calcium chloride is not a routine medication in cardiac other causes arrest. Note: All medications used during cardiac arrest, when given via a peripheral venous site in an extremity, should be followed by a 20 ml I.V. saline bolus and elevation of the extremity for 10 to 20 sec. ABG—arterial blood gases D5W—5% dextrose in water ET—endotracheal PEA—pulseless electrical activity VF—ventricular fibrillation VT—ventricular tachycardia quently, the sinus node or another appropriate pacemaker region of charge was 74% for patients who received their ﬁrst deﬁbrillation no the heart with inherent automaticity can resume orderly depolariza- later than 3 minutes after a witnessed collapse.28 In this study, deﬁb- tion-repolarization, with return of a perfusing rhythm.15,53 The sooner rillation was delivered via an AED operated by casino security ofﬁcers. deﬁbrillation occurs, the higher the likelihood of resuscitation.When Early deﬁbrillation is so critical that if a deﬁbrillator is immediately deﬁbrillation is provided immediately after the onset of VF, its suc- available, its use traditionally takes precedence over CPR for patients cess rate is extremely high.54 In a study of sudden cardiac arrest pa- in VF or pulseless VT of recent onset. If CPR is already in progress, it tients in Nevada gambling casinos, the survival rate to hospital dis- should of course be halted while deﬁbrillation takes place. Newer de-
© 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 8 CRITICAL CARE 1 Cardiac Resuscitation — 6 ﬁbrillators can compensate for thoracic impedance, ensuring that the selected energy level is in fact the energy that is delivered to the my- Table 5 Confirmation of Endotracheal ocardial tissue. In addition, deﬁbrillators that deliver biphasic deﬁbril- Tube Placement lation waveforms instead of the standard monophasic damped sinu- soidal waveforms allow effective deﬁbrillation at lower energy levels Intubation process (< 200 joules) and without the need for energy-level escalation during Vocal cords are visualized by intubator subsequent shocks.15,55-58 In the Optimized Response to Cardiac Ar- Tip of ET tube is seen passing between the cords rest (ORCA) study, which involved 115 patients with prehospital VF, Cuff of ET tube also passes cords by 1 cm the 150-joule biphasic-shock AED was more effective than the tradi- Postintubation checks tional high-energy monophasic-shock AED in four respects: it was Esophageal detector device or end-tidal CO2 detector confirms ET tube placement in trachea more successful in producing deﬁbrillation with the ﬁrst shock (96% Breath sounds are symmetrical (auscultate over lateral anterior chest versus 59%); it led to a higher rate of ultimate success with deﬁbrilla- and in midaxillary line bilaterally) tion (100% versus 84%); it had a better rate of return of spontaneous No gurgling with auscultation over epigastrium circulation (76% versus 54%); and its use was associated with a high- Patient’s chest rises and falls appropriately with ventilation er rate of good cerebral performance in the survivors (87% versus ET tube depth is appropriate: 21 cm at the corner of the mouth in women, 23 cm in men 53%).59 There were no differences, however, in terms of survival to Secure the ET tube to prevent dislodgment hospital admission or discharge, and replication of the ORCA ﬁnd- Reassess the adequacy of oxygenation and ventilation throughout the re- ings is lacking at this time. Current AHA guidelines state that lower- suscitation (bedside patient assessment; also obtain ABGs when feasible) energy biphasic waveform deﬁbrillators are safe and have equivalent After resuscitation, obtain a portable chest radiograph or higher efﬁcacy for termination of VF, as compared with the stan- dard monophasic waveform deﬁbrillator.15,49 ABG—arterial blood gas ET—endotracheal Ongoing research suggests that the duration of VF is a consider- ation in deciding whether to deﬁbrillate immediately and as soon as a deﬁbrillator is available or to perform CPR for a brief period ﬁrst to “prime the pump” before proceeding to deﬁbrillation. In the theless, oral endotracheal intubation is generally the preferred ad- porcine model in the setting of prolonged VF (> 10 minutes), CPR vanced airway technique for cardiac resuscitation, especially in the before countershock provides several physiologic beneﬁts.60 Studies hospital setting, where experienced intubators are generally present; have found that patients with VF of longer than 5 minutes’ duration in the prehospital setting, the evidence supporting endotracheal in- had better return of spontaneous circulation, survival to hospital tubation remains inconsistent. Endotracheal intubation isolates the discharge, and 1-year survival if ambulance personnel provided 3 airway, maintains airway patency, helps protect the trachea from the minutes of CPR before performing deﬁbrillation than if ambulance ever-present risk of aspiration, helps permit optimal oxygenation personnel performed deﬁbrillation immediately after arriving at the and ventilation of the patient, allows for tracheal suctioning, and scene; however, some experts question the validity of these results, even provides a route for delivery of some medications to the sys- on the basis of study design.61,62 temic circulation (via the pulmonary circulation) if intravenous ac- cess is unobtainable or lost.63 THE SECONDARY SURVEY The secondary survey for a victim of Optimization of Breathing and Ventilation persistent cardiac arrest takes place after When a cardiac arrest patient undergoes endotracheal intuba- completion of the primary survey. Like tion, correct positioning of the ET tube must be immediately con- the primary survey, the secondary survey ﬁrmed and regularly reconﬁrmed during and after the resuscitation follows an ABCD format, which in this [see Table 5]. Routine use of an esophageal detector device or end- case consists of advanced airway inter- tidal CO2 detector is recommended, along with careful patient ex- ventions (A); optimized oxygenation and amination. Caution is necessary with qualitative colorimetric end- ventilation by conﬁrmation of endotra- tidal CO2 detectors because both false positive and false negative cheal (ET) tube placement and repeated results have been documented during cardiac arrests.65 Breath reassessment of the adequacy of deliv- sounds should be present during auscultation over the anterior and ered breaths (B); intravenous access and appropriate medication lateral chest walls, and the patient’s chest should rise and fall with delivery to the patient’s circulation (C); and deﬁnitive therapy (D), delivered ventilations. No gurgling should be heard when the epi- based on a differential diagnosis that considers the speciﬁc disease gastrium is auscultated.The ET tube should be inserted to the ap- processes thought to be responsible for, or contributing to, the car- propriate depth marking: for average-sized adults, this is 21 cm at diac arrest. The secondary survey includes the fourth link in the the corner of the mouth in a woman and 23 cm in a man.The pa- chain of survival, rapid advanced care (see above). tient’s skin color should be reasonable (i.e., not dusky or cyanotic), provided that the patient’s pigmentation allows such assessment. Placement of an Advanced Airway Once correct positioning is conﬁrmed, the ET tube is then appro- Patients who remain in cardiac arrest after completion of the pri- priately secured to prevent its dislodgment.When feasible, an arteri- mary survey require placement of an advanced airway. Depending al blood gas (ABG) measurement will help further conﬁrm the ade- on the setting and the experience of the rescuers, this advanced air- quacy of oxygenation and ventilation as the resuscitation proceeds. way may be a laryngeal mask airway, an esophageal-tracheal Com- bitube (a tracheal tube bonded side by side with an esophageal ob- Establishment of Circulation Access turator), or an ET tube.36,63,64 The laryngeal mask airway and the Access to the patient’s venous circulation is mandatory; such ac- Combitube can be placed by personnel with less training than that cess may be achieved by a code-team member or members simulta- required for endotracheal intubation, and they do not require addi- neously while other resuscitators pursue steps A and B of the sec- tional special equipment or visualization of the vocal cords. Never- ondary survey. Ideally, a large intravenous cannula is placed in a
© 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 8 CRITICAL CARE 1 Cardiac Resuscitation — 7 Table 6 Technical Problems That May Prevent a Successful Resuscitation Problem Patients at Risk Recommendations Ensure technically perfect CPR. Confirm carotid pulses with CPR. Ineffective CPR All cardiac arrest If arterial line was in place before cardiac arrest, confirm adequate arterial waveform with CPR on arterial line monitor. patients Monitor end-tidal CO2 if available (higher levels correlate with better CPR and improved patient survival). Confirm adequate oxygenation with an ABG when feasible. Ensure optimal airway positioning and control. Have suction immediately available to manage pharyngeal and airway secretions. Ensure use of properly fitting, tightly sealed face mask for bag-valve mask (BVM) ventilation until a definitive airway is established. Inadequate Apply cricoid pressure to prevent gastric distention during BVM ventilation until a definitive airway is established. oxygenation All cardiac arrest Ensure that supplemental oxygen is flowing to BVM at 15 L/min. and ventilation patients Deliver an appropriate tidal volume per breath (6–7 ml/kg if oxygen is available) at the rate of 12–15 breaths/min. Confirm bilateral and equal breath sounds with ventilation. Confirm that patient’s chest rises with each ventilation. Allow adequate time for exhalation between breaths. Confirm optimal oxygenation and ventilation with an ABG when feasible. Allow ≤ 20–30 sec/intubation attempt. Intubator should see tip of ET tube and cuff pass between vocal cords at time of intubation. All patients intubated After intubation, immediately confirm correct ET tube placement; regularly reconfirm ET tube placement throughout ET tube difficulties resuscitation. with ET tube Confirm adequacy of oxygenation and ventilation with an ABG. After intubation, consider nasogastric tube placement to decompress stomach and optimize diaphragmatic excur- sions with ventilation. Place one or more 18-gauge or larger I.V. cannulas in an antecubital or external jugular vein site. Check for I.V. infiltration regularly throughout the resuscitation. Follow all medications administered through a peripheral I.V. site with a 20 ml saline bolus and elevation of the extremity containing the I.V. for 10–15 sec (if possible). Consider central line placement if the resuscitation is prolonged. Intravenous line All cardiac arrest Be aware of all I.V. infusions the patient is receiving. difficulties patients Stop all nonessential medications that had been started before the cardiac arrest. During the resuscitation, the only infusions the patient should receive are normal saline, blood products (if clinically indicated), and pertinent medications necessary to assist with return of spontaneous circulation. Pulmonary artery catheters and central lines occasionally act as an arrhythmogenic focus within the right ventricle. If applicable, deflate all relevant balloons on the catheter and withdraw the catheter to a superior vena cava position. Make sure Synchronization Mode button is in the off position when defibrillating patients in pulseless VT or VF. Make sure electricity is not arcing over the patient’s chest because of perspiration or smeared conducting gel; dry patient’s chest with a towel except for areas directly beneath pads or paddles. Do not administer shock through nitroglycerin paste or patches. If the patient has an internal cardioverter-defibrillator (ICD) or a pacemaker, the patient may still be manually defibrillat- Monitor defibrillator All cardiac arrest ed, but do not shock directly over the internal device. Under these circumstances, place the pads or paddles at difficulties patients least 2.5 cm away from the patient’s internal device. If the ICD is intermittently firing but not defibrillating the patient and if the ICD is thought to be compromising the resuscitation, turn the device off with a magnet so that manual defibrillation may take place without interference. Maximize the gain or electrocardiography “size” and check the rhythm in several leads (or change the axes of the paddles if reading the rhythm in Paddles mode) to confirm asystole when the initial rhythm appears to be asystole. ABG—arterial blood gas ET—endotracheal VF—ventricular fibrillation VT—ventricular tachycardia prominent upper-extremity vein or the external jugular vein to opti- the arrest arrhythmia is asystole or PEA is slow), and miscellaneous mize delivery of needed medications. If a peripheral line is not drugs used to treat speciﬁc problems contributing to the arrest achievable, additional access possibilities include central line place- state, such as sodium bicarbonate (for severe metabolic acidosis, hy- ment via the internal jugular, subclavian (via the supraclavicular ap- perkalemia, and certain drug overdoses), and calcium chloride (for proach), or, less ideally, femoral vein; even intraosseous access is pos- hyperkalemia, calcium channel blocker drug overdose, or severe sible (intraosseous access is a common emergency vascular access hypocalcemia) [see Table 4]. site in pediatric patients, but it is an unusual route of access in adults). Persons in cardiac arrest (which can result from pulseless VT,VF, It is useful to remember, as already noted, that some important re- PEA, or asystole) require a vasopressor for as long as they remain suscitation medications can be delivered via the ET tube in cases of pulseless.Typically, this consists of 1 mg of epinephrine intravenously failed intravenous access; such medications include naloxone, atropine, every 3 to 5 minutes. Epinephrine stimulates adrenergic receptors, vasopressin, epinephrine, and lidocaine (mnemonic: NAVEL). which leads to vasoconstriction and optimization of CPR-generated The commonly used medications in cardiac resuscitation may be blood ﬂow to the heart and brain.Vasopressin (40 units I.V. once only) grouped into the following general categories: vasopressors (epi- is a reasonable alternative to epinephrine, at least initially.Vasopressin nephrine or vasopressin), antiarrhythmics (amiodarone, lidocaine, in the recommended dose is a potent vasoconstrictor. It also has the magnesium, and procainamide), anticholinergic agents (atropine, if theoretical advantage over epinephrine of not increasing myocardial
© 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 8 CRITICAL CARE 1 Cardiac Resuscitation — 8 Table 7 Potentially Treatable Conditions That May Cause or Contribute to Cardiac Arrest3 Condition Clinical Setting Diagnostic and Corrective Actions Obtain stat ABG. Preexisting acidosis, diabetes, Reassess technical quality of CPR, oxygenation, and ventilation. Acidosis diarrhea, drugs, toxins, prolonged Confirm correct endotracheal tube placement. resuscitation, renal disease, shock Hyperventilate patient (PaCO2 of 30–35 mm Hg) to partially compensate for metabolic acidosis. If pH < 7.20 despite above interventions, consider I.V. sodium bicarbonate, 1 mEq/kg I.V. slow push. Initiate large-volume I.V. crystalloid resuscitation. Hemorrhagic diathesis, malignancy, Confirm diagnosis with emergency bedside echocardiogram, if available. Cardiac tamponade pericarditis, post cardiac surgery, Perform pericardiocentesis. post myocardial infarction, trauma Immediate surgical intervention is appropriate if pericardiocentesis is unhelpful but cardiac tamponade is known or highly suspected clinically. Adrenal insufficiency, alcohol abuse, Consider clinical setting and obtain finger-stick glucose or stat blood glucose measurements (may be obtained on aspirin overdose, diabetes, drugs, ABG specimen). Hypoglycemia toxins, liver disease, renal disease, sepsis, certain tumors If glucose < 60 mg/dl, treat: 50 ml = 25 g of D50W I.V. Follow glucose levels closely post treatment.* Alcohol abuse, burns, diabetic ketoacidosis, severe diarrhea, Obtain stat serum magnesium level. diuretics, drugs (e.g., cisplatin, Hypomagnesemia Treat: 1–2 g magnesium sulfate I.V. over 2 min. cyclosporine, pentamidine), malabsorption, poor intake, Follow magnesium levels over time, because blood levels correlate poorly with total body deficit. thyrotoxicosis Alcohol abuse, burns, central ner- vous system disease, debilitated Obtain core body temperature. and elderly patients, drowning, If severe hypothermia (< 30° C), limit initial shocks for pulseless VT/VF to three, initiate active internal rewarming and † Hypothermia drugs, toxins, endocrine disease, cardiopulmonary support, and hold further resuscitation medications or shocks until core temperature > 30° C . exposure history, homelessness, If moderate hypothermia (30°–34° C), proceed with resuscitation (space medications at intervals greater than usual), poverty, extensive skin disease, passively rewarm, and actively rewarm truncal body areas. spinal cord disease, trauma Initiate large-volume I.V. crystalloid resuscitation. Obtain stat hemoglobin level on ABG specimen. Major burns, diabetes, gastrointesti- Emergently transfuse packed red blood cells (O negative if type-specific blood not available) if hemorrhage or pro- Hypovolemia, hemor- nal losses, hemorrhage, hemor- found anemia is contributing to arrest. rhage, anemia rhagic diathesis, malignancy, preg- nancy, shock, trauma Emergently consult necessary specialty for definitive care. Emergency thoracotomy with open cardiac massage is a consideration if experienced providers are available for the patient with penetrating trauma and cardiac arrest. Reassess technical quality of CPR, oxygenation, and ventilation. Hypoxia All cardiac arrest patients are at risk Confirm correct ET tube placement. Obtain stat ABG to confirm adequate oxygenation and ventilation. Consider in all cardiac arrest patients, especially those with risk factors Review prearrest clinical presentation and ECG. Myocardial for coronary artery disease, a his- Continue resuscitation algorithm; proceed with definitive care as appropriate for the immediate circumstances (e.g., infarction tory of ischemic heart disease, or thrombolytic therapy, cardiac catheterization/coronary artery reperfusion, circulatory assist device, emergency prearrest picture consistent with cardiopulmonary bypass). an acute coronary syndrome (continued) oxygen consumption or lactate production in the arrested heart.66 De- quired when spontaneous circulation does not return despite appro- spite its potential advantages, however, in a study of 200 inpatient car- priate initial interventions.This situation poses a critical question to diac arrest patients, vasopressin did not provide a better survival rate the resuscitators:Why is this patient dying right now? The intellectu- than epinephrine.67 Vasopressin was also found to be comparable to al challenge of that question, which the resuscitators must try to an- epinephrine in out-of-hospital cardiac arrests when the rhythm was VF swer expeditiously and at the bedside, is compounded by the emo- or PEA but superior to epinephrine for patients in asystole.68,69 tional intensity that pervades most cardiac resuscitations. During resuscitation with ongoing CPR, medication delivery The solvable problems that may interfere with resuscitation can through an intravenous cannula needs to be followed by a 20 ml be grouped into three broad categories: technical [see Table 6], phys- saline bolus; if the cannula is in a peripheral vein, the extremity con- iologic, and anatomic [see Table 7]. Technical problems consist of taining the cannula should then be elevated for 10 to 15 seconds to difﬁculties with the resuscitators’ equipment or skills; such difﬁcul- augment delivery of the medication to the central circulation.This is ties include ineffective CPR, inadequate oxygenation and ventila- especially important because of the low-ﬂow circulatory state with tion, ET tube complications, intravenous access difﬁculties, and closed-chest CPR. monitor-deﬁbrillator malfunction or misuse. The physiologic and anatomic problems consist of life-threatening but potentially treat- Differential Diagnosis and Deﬁnitive Care able conditions that may have led to the cardiac arrest in the ﬁrst The most challenging part of the secondary survey, as well as car- place.This differentiation between physiology and anatomy is ad- diac resuscitation management in general, is the problem-solving re- mittedly artiﬁcial, given that physiology is always involved in a car-
© 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 8 CRITICAL CARE 1 Cardiac Resuscitation — 9 Table 7 (continued) Condition Clinical Setting Diagnostic and Corrective Actions Alcohol abuse, bizarre or puzzling be- Consider clinical setting and presentation; provide meticulous supportive care. havioral or metabolic presentation, Emergently consult toxicologist (through regional poison center) for resuscitative and definitive care advice, in- classic toxic syndrome, occupational Poisoning cluding appropriate antidote use. or industrial exposures, history of in- gestion, polysubstance abuse, psychi- Prolonged resuscitation efforts are appropriate. If available, immediate cardiopulmonary bypass should be atric disease considered. Metabolic acidosis, excessive administra- Obtain stat serum potassium level on ABG specimen. tion, drugs and toxins, vigorous exercise, hemolysis, renal disease, rhabdomyoly- Treatment: calcium chloride 10% (5–10 ml I.V. slow push [do not use if hyperkalemia is secondary to digitalis Hyperkalemia sis, tumor lysis syndrome, significant tis- poisoning]), followed by glucose and insulin (50 ml of D50W and 10 U regular insulin I.V.); sodium bicarbonate sue injury (50 mEq I.V.); albuterol (15–20 mg nebulized or 0.5 mg I.V. infusion).‡ Alcohol abuse, diabetes, diuretic use, drugs and toxins, profound gastroin- Obtain stat serum potassium level on ABG specimen. Hypokalemia testinal losses, hypomagnesemia, ex- If profound hypokalemia (K+ < 2–2.5 mEq/L) is contributing to cardiac arrest, initiate urgent I.V. replacement cess mineralocorticoid states, meta- (2 mEq/min I.V. for 10–15 mEq) then reassess.§ bolic alkalosis Hospitalized patients, recent surgical pro- Review prearrest clinical presentation; initiate appropriate volume resuscitation with I.V. crystalloid and augment cedure, peripartum, known risk factors with vasopressors as necessary. for venous thromboembolism (VTE), Attempt emergency confirmation of diagnosis, depending on availability and clinical circumstances; consider Pulmonary history of VTE, prearrest presentation emergency cardiopulmonary bypass to maintain patient viability. embolism consistent with acute pulmonary Continue resuscitation algorithm; proceed with definitive care (thrombolytic therapy, embolectomy via interven- embolism tional radiology, or surgical thrombectomy) as appropriate for immediate circumstances and availability. Post central line placement, mechanical Tension ventilation, pulmonary disease (includ- Consider risks and clinical presentation (prearrest history, breath sounds, neck veins, tracheal deviation). pneumothorax ing asthma, COPD, necrotizing pneu- Proceed with emergency needle decompression, followed by chest tube insertion. monia), post thoracentesis, trauma *Unrecognized hypoglycemia can cause significant neurologic injury and can be life threatening, but caution with I.V. glucose is appropriate in the setting of cardiac arrest. Available evidence indicates that hyperglycemia may contribute to impaired neurologic recovery in cardiac arrest survivors. †Active internal or core rewarming includes warm (42˚–46˚ C) humidified oxygen delivered through the endotracheal tube; warm I.V. fluids; peritoneal lavage; esophageal rewarming tubes; bladder lavage; and extracorporeal rewarming if immediately available. Active external rewarming includes warming beds, hot-water bottles, heating pads, and radiant heat sources applied externally to the patient. ‡Glucose is not necessary initially if patient is already hyperglycemic, but glucose levels should be followed closely after administration of I.V. insulin because of the risk of hypoglycemia (especially in patients with renal failure, because of the long duration of action of I.V. insulin in such patients). Sodium bicarbonate is most helpful in patients with concomitant metabolic aci- dosis; it is less effective in lowering serum potassium in dialysis-dependent renal failure patients. High-dose nebulized albuterol should lower serum potassium by 0.5 to 1.5 mEq/L within 30 to 60 min, but administration during cardiac arrest may be difficult. §In a non–cardiac arrest situation, usual I.V. potassium replacement guidelines for patients requiring parenteral therapy are generally 10 to 20 mEq/hr with continuous electrocardiographic monitoring. If profound hypokalemia is contributing to cardiac arrest, however, these usual replacement rates are not timely enough, given the critical nature of the situation. Under these circumstances, potassium chloride, 2 mEq/min I.V. for 10 to 15 mEq, is reasonable, but reassessment and careful attention to changing levels, redistribution, and ongoing clinical circum- stances are essential to prevent life-threatening hyperkalemia from developing. ABG—arterial blood gas COPD—chronic obstructive pulmonary disease D50W—50% dextrose in water ET—endotracheal VF—ventricular fibrillation VT—ventricular tachycardia diac arrest, but it has some usefulness as a teaching and problem- ECG showed prominent ST segment elevation in leads V1 through solving tool. Physiologic problems classically include hypoxia, aci- V4 consistent with a large anterior myocardial infarction, if the pa- dosis, hyperkalemia, severe hypokalemia, hypothermia, hypoglycemia, tient’s resuscitation is failing despite appropriate interventions, and and drug overdose. Anatomic problems are hypovolemia/hemor- if there appear to be no technical problems hampering the resusci- rhage, tension pneumothorax, cardiac tamponade, myocardial in- tation, a working diagnosis of massive myocardial infarction can be farction, and pulmonary embolism.41 made; intravenous thrombolytic therapy may then be a reasonable Whenever possible, the patient’s medical and surgical history and and needed step in such a resuscitation.70 the circumstances and symptoms immediately before the cardiac Thoughtful consideration of the possible reasons why a resuscita- arrest should be sought from family members, bystanders, or hospi- tion is failing will regularly push the code-team captain’s and resus- tal staff as the resuscitation proceeds.This information may contain citation team’s expertise and clinical skills to the limits. Neverthe- important clues to the principal arrest problem and how it may be less, the failure to consider these formidable issues will deprive the expeditiously treated. For example, a patient who presents to an patient of an optimal opportunity to survive the cardiac arrest. emergency department with chest pain and then suffers a VF car- diac arrest is probably dying of a massive myocardial infarction, pul- monary embolism, or aortic dissection, with tension pneumothorax Cardiac Resuscitation Based on Rhythm Findings or cardiac tamponade also being possibilities. When a monitor-deﬁbrillator arrives at the scene of a cardiac ar- Speciﬁc questions to consider include the following: Does the pa- rest, the patient’s rhythm is immediately analyzed.This step consti- tient have risk factors for heart disease, pulmonary embolism, or tutes the beginning part of the deﬁbrillation stage, or step D, of the aortic disease? What was the quality of the patient’s pain and its ra- AHA’s primary survey.There are four rhythm possibilities [see Figure diation before the cardiac arrest? What were the prearrest vital signs 1]: (1) pulseless VT; (2) VF; (3) organized or semiorganized electrical and physical examination ﬁndings? What did the prearrest ECG activity despite the absence of a palpable carotid pulse, which deﬁnes show (if available)? Can any of this information be used now, at the PEA; and (4) asystole.The detailed management of these different bedside, to dictate the needed resuscitation interventions during the cardiac resuscitation scenarios is based on the recommendations of D phase of the secondary survey? For example, if the prearrest the AHA49 and the International Liaison Committee on Resuscita-
© 2005 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 8 CRITICAL CARE 1 Cardiac Resuscitation — 10 tion.71 In following these guidelines, the clinician should remember volved, it is exceptionally difﬁcult to perform high-quality research that, with the exception of early CPR and early deﬁbrillation for VF in cardiac resuscitation. and pulseless VT, many of the recommendations that form the foundation of modern resuscitation are evidence supported or con- PULSELESS VENTRICULAR TACHYCAR- sensus based (rather than evidence based, as would be ideal). Be- DIA OR VENTRICULAR FIBRILLATION cause of the nature of cardiac arrest and the multiple variables in- The appearance of either VF or pulseless VT on the rhythm monitor in a a patient with ongoing CPR is a rela- tively favorable ﬁnding, because there is reasonable hope for a successful out- come with these rhythms. In addition, the interventions and medications se- quentially used in the resuscitation are plainly delineated, and the initial course b of action is clear.VF and pulseless VT are managed identically. Initiation of Deﬁbrillation Deﬁbrillation with 200 joules should be attempted immediately. However, if the time from onset of arrest to CPR to the availability of deﬁbrillation is estimated to be longer than 5 minutes, it may be reasonable to continue CPR for another 3 minutes before initiating c deﬁbrillation [see Deﬁbrillation, above]. If the VF or VT persists after the initial shock, subsequent attempts should be made with 200 to 300 joules and then 360 joules. A lower, nonescalating equivalent biphasic energy level is accept- able, if the deﬁbrillator offers this option. Manually checking the patient’s carotid pulse between shocks is no longer recommended, but the displayed rhythm on the monitor must be carefully assessed after each deﬁbrillation attempt. If there are any doubts concerning d the rhythm or if there is suspicion of a dysfunctional lead or paddle cable, then a manual pulse check would be appropriate. If VF or pulseless VT persists, CPR is resumed, the patient endotracheally intubated, correct ET tube placement conﬁrmed, and the tube se- cured. Simultaneously, intravenous access should be established. Initiation of Drug Therapy e In patients with ongoing VF, drug therapy begins with the ad- ministration of a vasoconstrictor (either epinephrine or vaso- pressin) [see Table 4]. If there is no intravenous access, the drug can be given endotracheally. After each intravenous dose, drug delivery is followed by a 20 ml saline bolus and the extremity containing the I.V. line is elevated. Rescuers continue CPR for 30 to 60 seconds to allow the drug to reach the heart, then attempt deﬁbrillation again f with one to three shocks at 360 joules each. As long as the patient remains pulseless, epinephrine is administered every 3 to 5 min- utes, with each dose followed by one to three attempts at deﬁbrilla- tion.When vasopressin is the chosen initial drug, only a single dose is given; if the resuscitation continues 10 minutes or longer after vaso- pressin is administered, epinephrine should be substituted for vaso- pressin for the remainder of the code. If VF or pulseless VT persists g despite the initial administration of a vasoconstrictor and repeated deﬁbrillation attempts, parenteral antiarrhythmic drug therapy is added; amiodarone or lidocaine is an appropriate agent [see Choice of Antiarrhythmic Drugs, below].Throughout all of these steps, the code-team leader is also actively looking for and correcting any technical and physiologic or anatomic problems that may be pre- venting a successful resuscitation [see Tables 6 and 7]. Figure 1 The sudden cardiac arrest arrhythmias. (a) Ventricular tachy- Emergency Laboratory Tests cardia. (b) Ventricular ﬁbrillation. Pulseless electrical activity encompasses any of several forms of organized electrical activity in the pulseless patient; If spontaneous circulation does not return after the ﬁrst round of these include (c) normal sinus rhythm, (d) junctional rhythm, (e) bradycardic antiarrhythmic drug therapy, the resuscitation team must also en- junctional rhythm, and (f) idioventricular rhythm. (g) Asystole. deavor to identify and treat the clinically relevant conditions causing