Chapter 41 Cardiopulmonary Resuscitation
1. What is cardiopulmonary resuscitation (CPR)? What is basic life support (BLS)? What is advanced cardiac life support (ACLS)?
2. Who developed the Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care?
Basic life support (BLS)
3. What are the four major components of BLS? What major change was recommended in 2010 regarding the sequence of attention to airway, breathing, and circulation during BLS?
Closed-Chest (External) Cardiac Compressions
4. Where should the rescuer’s hands be placed on the adult patient to maximize blood flow when performing closed-chest cardiac compressions? What are some risks to the patient when the rescuer’s hands are placed incorrectly?
5. How should the rescuer be positioned relative to the patient when performing closed-chest cardiac compressions? By how much is the sternum of an adult patient depressed during each compression?
6. What is the minimum rate (number of compressions per minute) for adult BLS? What is the ratio of cardiac compressions to ventilation during one-rescuer CPR? What is the ratio of cardiac compressions to ventilation during two-rescuer CPR?
7. What are the two proposed mechanisms for blood flow during closed-chest cardiac compressions? Which of these is thought to be the most important?
8. How can the effectiveness of closed-chest cardiac compressions be verified? What should the goal be for end-tidal CO2 if an end-tidal CO2 monitor is available?
External Defibrillation
11. What is the definitive treatment for pulseless ventricular tachycardia (VT) and ventricular fibrillation (VF)? What is the most important determinant of return of spontaneous circulation in a patient with VT/VF when performing external defibrillation?
12. How many joules of electricity should be delivered during an initial attempt at external defibrillation? How many joules should be delivered in subsequent defibrillation attempts, provided they are necessary?
13. Where on the chest is the appropriate placement of paddles/pads for external defibrillation?
14. What is the risk of external defibrillation in the patient with a cardiac pacemaker?
Advanced cardiac life support
15. What are the three advanced cardiac life support (ACLS) algorithms most likely to be used in the operating room?
Drug therapy
32. What is the goal of initial drug therapy during CPR? What are the mainstays of treatment for the patient in cardiac arrest?
33. What actions of epinephrine are thought to be responsible for its beneficial effects during cardiac arrest?
34. What actions of vasopressin are thought to be responsible for its beneficial effects during cardiac arrest?
35. When is amiodarone administered during cardiac arrest?
36. What is the advantage of the delivery of drugs by a centrally placed intravenous catheter during CPR? How long should the rescuers wait for drug administered via a peripheral vein to reach the central circulation?
37. What are two alternatives for drug delivery when vascular access is not available?
Resuscitation of infants and children
38. Where should the pulse be palpated in infants up to 1 year of age? Where should it be palpated in children?
39. How should closed-chest cardiac compressions be performed in infants?
40. How should closed-chest cardiac compressions be performed in children?
41. What energy setting, in joules, should be applied for optimal success for a return of spontaneous circulation when using an external defibrillator? If the initial attempt at defibrillation is unsuccessful, what energy setting should be used for the subsequent attempts?
Special perioperative considerations
44. What are some of the more common drugs used in the operating room that can precipitate an anaphylactic reaction? In addition to removing or stopping the inciting agent, what is the primary treatment for anaphylaxis?
45. What is the treatment for an intraoperative venous gas embolism?
46. What is the primary treatment for local anesthetic toxicity? How long should the resuscitation continue in the event of complete cardiovascular collapse?
47. How should one manage cardiovascular collapse in a patient who has received neuraxial anesthesia?
Answers*
1. CPR is the institution of artificial circulation and ventilation until spontaneous cardiopulmonary function returns, extracorporeal life support is initiated, or resuscitation efforts are discontinued. It consists of BLS and ACLS. BLS is the rapid evaluation of an unresponsive individual with the activation of the emergency medical system and the acquisition of an automated external defibrillator (AED) or a regular defibrillator. Artificial circulation is achieved through closed-chest cardiac compressions and ventilation is performed via mouth-to-mouth, mask-to-mouth, or bag-valve mask. Any individual (including nonhealth care personnel) who has had the appropriate training and certification can perform BLS. ACLS, based on BLS, can only be performed by health care workers and adds advanced airway management, cardiovascular drugs, cardiac rhythm analysis, and postresuscitation management. ACLS also includes recognition, diagnosis, and initial treatment of acute myocardial infarction and acute stroke. (715)
2. The International Liaison Committee on Resuscitation publishes the guidelines based on evidence from the medical and basic science literature. This multinational committee, primarily represented by the American Heart Association and European Resuscitation Council, meets every few years to evaluate and/or revise the guidelines. (715)
Basic life support (bls)
3. The four major components of BLS are the recognition of an unresponsive patient that is not breathing, activation of the emergency medical system and acquisition of an AED, closed-chest cardiac compressions with ventilations, and actual defibrillation. In 2010 a major change occurred in the recommendation for the sequence of attention by the rescuer in airway, breathing, and circulation. The old mnemonic of ABCD (airway, breathing, circulation, and defibrillation) was changed to CAB (compression, airway, breathing). In the hospital setting, ventilation is expected in cardiopulmonary resuscitative efforts, although large out-of-hospital studies have shown no difference in outcome between patients who had chest compression alone CPR versus those who had chest compression and ventilation CPR. (716, Figure 44-1)
Closed-Chest (External) Cardiac Compressions
4. For closed-chest cardiac compressions in the adult patient, the rescuer’s hands should be placed in the middle of the patient’s sternum. This provides for maximum compression to the underlying cardiac ventricles and optimizes blood flow produced by the compressions. If the rescuer’s hands are placed incorrectly during closed-chest cardiac compression, not only is blood flow not optimized, but the patient may suffer from internal injury as well. For example, pressure over the xiphoid process or rib cage can result in damage to abdominal organs, especially the liver, or cause rib fractures. Rib fractures can result in damage to the heart and lungs. (716, Figure 44-2)
5. During closed-chest cardiac compressions, the rescuer’s upper body should be directly over the patient’s chest. The shoulders are positioned directly over the hands and the elbows are kept straight. This position enables the rescuer to use the weight of his or her upper body for compression and may prevent fatigue. The sternum of an adult patient should be depressed at least 2 inches (5 cm) during closed-chest cardiac compression. (716, Figure 44-2; 725, Table 44-3)
6. The rate for closed-chest compressions for an adult is at least 100 compressions per minute. The rescuer needs to push hard and push fast, but allow for full chest recoil. The ratio of cardiac compressions to ventilation during CPR is 30:2, regardless of the number of rescuers. (716, Figure 44-1; 725, Table 44-3)
7. There are two proposed mechanisms for blood flow during closed-chest cardiac compression: (1) the cardiac pump mechanism and (2) the thoracic pump mechanism. The cardiac pump mechanism theorizes that the direct compression of the cardiac ventricles between the sternum and the spine results in an increase in intracardiac pressures, closure of the tricuspid and mitral valves, and the forward flow of blood into the pulmonary arteries and aorta. During relaxation, the aortic and pulmonary valves close to ensure unidirectional movement of blood. The second proposed thoracic pump mechanism for forward blood flow revolves around the alternating increase in intrathoracic pressure that accompanies closed-chest compressions and decrease in intrathoracic pressure during relaxation. During compressions, the increase in intrathoracic pressure ejects blood out of the chest; during relaxation, the drop in intrathoracic pressure promotes venous return back into the thoracic cavity. Evidence for the thoracic pump mechanism can be seen with forceful coughing, which can sustain consciousness for as long as 1.5 minutes. The dominant mechanism for forward blood flow during closed-chest compression is unclear, but most believe it to be the cardiac pump mechanism. However, heart size, the anterior-to-posterior chest distance, and thoracic compliance are believed to influence which of these mechanisms eventually dominates.
8. Verification of the effectiveness of closed-chest cardiac compressions can be estimated by the palpation of peripheral pulses and, if an arterial line is present, a diastolic blood pressure of at least 20 mm Hg. If an endotracheal tube is in place, a capnogram should be used to guide the effectiveness of closed-chest cardiac compression. When ventilation and CO2 production are constant, alterations in the end-tidal CO2 are reflective of alterations in pulmonary blood flow and cardiac output. When end-tidal CO2 monitors are available during closed-chest cardiac compression, an end-tidal CO2 of 20 mm Hg or more suggests effective CPR. Conversely, an end-tidal CO2 of 10 mm Hg or less is suggestive of poor CPR or a grave prognosis. (718-720, Figure 44-5)
Provision of a Patent Upper Airway
9. Upper airway obstruction in an unconscious patient is due to the tongue falling against the posterior pharynx. The head-tilt/jaw thrust maneuver involves extension of the head and displacement of the mandible to an anterior position thereby moving the tongue forward away from the posterior pharynx. For many individuals, this is adequate to provide a patent airway. For patients with suspected neck trauma, the rescuer needs to modify the head-tilt/jaw thrust maneuver to avoid exacerbating a potential spinal cord injury. The head-tilt should be excluded from the maneuver and only the jaw thrust performed in these patients. (717, Figure 44-3)
Specialized Equipment to Maintain the Airway
10. There are several advantages of a cuffed endotracheal tube for ventilation of the lungs in a patient receiving CPR. First, it allows for proper ventilation and end-tidal carbon dioxide (ETCO2) monitoring. Second, compressions and ventilations are no longer synchronous. Compressions are performed non-stop, while breaths are given once every 6 to 8 seconds. This allows for more time with an adequate perfusion pressure. Third, it also allows for the addition of supplemental oxygen in a reliable manner. Finally, a cuffed endotracheal tube provides the lungs with some protection against the aspiration of gastric contents. (718-720, Figure 44-5)
External Defibrillation
11. The definitive treatment for pulseless VT and VF is external defibrillation. The most important determinant of the success of external defibrillation is the duration of the time lapse between cardiopulmonary arrest and external defibrillation. For this reason, the current recommendation is to apply external defibrillation as soon as possible in these patients. (718-719, Figures 44-1 and 44-5)
12. The initial, and subsequent, attempts at external defibrillation require a shock of 120 to 200 J (biphasic) for adult patients. If the amount of energy needed to terminate VF is not known for the specific device, then 200 J (biphasic) should be used. (718-719, Figure 44-5)
13. The paddles/pads should be applied to the chest with firm pressure ensuring good skin contact in a position that will reduce impedence or resistance and maximize the flow of electrical current through the myocardium. The standard placement is with one paddle/pad below the right clavicle and to the right of the sternum; the second paddle/pad is applied at the level of the apex of the heart in the midaxillary line. Poor skin contact can lead to an increase in the resistance or impedence to current flow during shock delivery or arcing of the current. (718, Figure 44-4)
14. The risk of external defibrillation in the patient with a cardiac pacemaker is the malfunction of the pacemaker. It is recommended that the paddles/pads be placed 1 to 2 cm away from the pacemaker generator. (718)
Advanced cardiac life support
15. Every anesthesiologist should be familiar with pulseless arrest, bradycardia, and tachycardia algorithms.
Ventricular Fibrillation/Pulseless Ventricular Tachycardia
16. Possible causes of VF/pulseless VT include hypovolemia, hypoxia, hydrogen ion (acidosis), hypokalemia/hyperkalemia, hypothermia, tension pneumothorax, cardiac tamponade, toxins, thrombosis (pulmonary), and thrombosis (coronary). (719, Figure 44-5, 723, Table 44-2)
17. Patients in VF/pulseless VT should receive immediate defibrillation of 120 to 200 J with a biphasic defibrillator. Good quality CPR should also be instituted and maintained throughout the resuscitation. Vasoactive medications, such as epinephrine and vasopressin, are to be given at the appropriate times. Amiodarone, an antiarrhythmic, should be considered as well. (718-722, Figure 44-5 and Table 44-1)
18. Torsades de pointes is an atypical form of VT with a characteristic twisting of the QRS around the baseline such that it appears as a sine wave. Causes of torsades de pointes include drugs that prolong the QT interval, such as quinidine, procainamide, disopyramide, phenothiazines, and tricyclic antidepressants; other causes include bradycardia, hypokalemia, hypomagnesemia, and acute myocardial ischemia or infarction.
19. The treatment for torsades de pointes may include overdrive pacing of the cardiac atria or ventricles and/or treatment with magnesium sulfate for stable patients. Patients whose condition is unstable should undergo defibrillation.
Pulseless Electrical Activity
20. Causes of PEA are identical to those of VF or pulseless VT. (719, Figure 44-5 and 723, Table 44-2)
21. PEA is a term used to describe the presence of a normally perfusing cardiac rhythm on the electrocardiogram with little or no cardiac output. In patients with PEA, there is an absence of peripheral pulses or systemic blood pressure. Cardiac rhythms that may be present include organized electrical activity, idioventricular rhythms, and/or ventricular escape rhythms. PEA should be treated with closed-chest compressions and the rapid administration of epinephrine and/or vasopressin. There should also be a search for, and correction of, possible causes. (719-723, Figure 44-5 and Table 44-1)
Cardiac Asystole
22. Causes of cardiac asystole are identical to those of PEA, VF, or pulseless VT. It is treated identically to PEA. (719, Figure 44-5 and 723, Table 44-2)
Bradycardia
23. Typically, bradycardia is defined as a heart rate of less than 60 beats/min. (720, Figure 44-6)
24. Treatment for bradycardia depends on symptoms and underlying rhythm. Asymptomatic patients can be monitored and observed. Symptomatic patients or those with a high degree block need more definitive pharmacologic therapy (atropine, dopamine infusion, epinephrine infusion) or cardiac pacing. (720,Figure 44-6, 722, Table 44-1, 723)
Narrow-Complex Tachycardias
25. The factor that determines the appropriate method of treatment for narrow-complex tachycardias is the amount of hemodynamic compromise that occurs as a result of the cardiac dysrhythmia. Patients who are hemodynamically unstable should undergo immediate synchronized cardioversion. The amount of energy used is dependent upon the regularity of the QRS complex and likelihood of a type of dysrhythmia. The treatment of patients with narrow-complex tachycardias whose condition is stable includes vagal maneuvers, adenosine, β-blockers, calcium channel blockers, and amiodarone. (721, Figure 44-7, 722, Table 44-1, 723)
26. Side effects of the administration of adenosine include flushing, dyspnea, chest pain, and bronchospasm.
27. The risk of cardioversion that is not synchronized is VF. VF results if the cardioversion shock occurs on the relative refractory period of the cardiac cycle. (723)
Wide-Complex Tachycardias
28. The appropriate treatment for wide-complex tachycardias is determined by the hemodynamic stability of the patient. Pulseless patients should receive immediate defibrillation of 120 to 200 J with a biphasic defibrillator. Hemodynamically unstable patients with evidence of acute myocardial ischemia or infarction, who have acute pulmonary edema, or who have other evidence of end-organ hypoperfusion should undergo immediate synchronized or unsynchronized cardioversion with a shock of 100 to 200 J (biphasic) depending on the regularity of the QRS complex and the likelihood of the type of dysrhythmia. Sedation will likely be needed in awake patients. Hemodynamically stable patients can undergo drug treatment. Drug therapy includes amiodarone, sotalol, or procainamide. A cardiologist should be consulted before starting any of these drug therapies in a stable patient. (721, Figure 44-7, 722, Table 44-1, 723)
29. Adenosine should only be administered in a wide-complex tachycardia when the rate is regular and the QRS complex is monomorphic in nature. Adenosine has no effect on monomorphic VT. β receptor blockers and calcium channel blockers should be administered very cautiously and only if it is clear that the tachyarrhythmia is supraventricular in origin. (721, Figure 44-7, 722, Table 44-1, 723)
30. In a wide-complex tachycardia, the main risk of unsynchronized cardioversion is a change in rhythm to VF. However, with rapid ventricular rates, synchronization may not be possible and the defibrillator will fail to discharge.
Precordial Thump
31. A precordial thump is the delivery of a single, forceful blow by the rescuer with a closed fist to the middle portion of the patient’s sternum. A precordial thump is recommended in adult patients for the initial treatment of VF or VT when a defibrillator is not immediately available. Immediate external defibrillation should not be delayed for a precordial thump. A precordial thump is not recommended in pediatric patients.
Drug therapy
32. The goal of initial drug therapy during CPR is the increasing of coronary and cerebral perfusion pressures. The mainstay for treatment of the patient in cardiopulmonary arrest is the administration of oxygen and epinephrine. (718-723, Figure 44-5, Table 44-1)
33. Epinephrine is a nonspecific α receptor and β receptor agonist. During a resuscitation, its action on α1 receptors is probably the most important. As mediated through the α receptor, there is an increase in cerebral and coronary perfusion pressure, intense arterial vasoconstriction in other vascular beds, and a selective redistribution of cardiac output. There is some evidence that epinephrine administered early in the resuscitative effort in a patient with cardiac arrest can possibly improve outcome. (723)
34. Vasopressin is a potent peripheral and mesenteric vasoconstrictor, yet a potent pulmonary artery and cerebral artery vasodilator. Its effects are mediated via the vasopressin receptor. Blood is redirected from the peripheral to the central circulation, thus, increasing blood to the brain and heart. (723-724)
35. Amiodarone, a class III antiarrhythmic, is used in the treatment of VF and VT (with and without a pulse). An initial dose of 300 mg IV push can be followed by a subsequent single dose of 150 mg IV push, if there has been no return of spontaneous circulation and resuscitation continues. In patients with stable VT with a pulse, 150 mg IV over 10 minutes can be administered in an effort to terminate the VT with conversion into sinus rhythm. (724)
36. The advantage of the administration of drugs by a centrally placed catheter during CPR is the rapid delivery of drugs to the heart. When a peripheral intravenous site is used for the administration of drugs during cardiopulmonary arrest, a period of 1 to 2 minutes should be allowed for drugs to reach the central circulation. In addition, drug administration should always be followed by at least 20 mL of normal saline. CPR should not be interrupted for placement of central venous access unless peripheral access and intraosseous access cannot be obtained. (720)
37. Two alternatives for drug delivery when vascular access is not available include an endotracheal tube or the placement of an intraosseous line. Drugs that can be absorbed across the alveolar epithelium include epinephrine and vasopressin. The intraosseous line should be treated as any other peripherally or centrally inserted intravenous line. (720)
Resuscitation of infants and children
38. In infants up to 1 year of age, the best location to check for a pulse is the brachial artery in the mid-upper arm. In children older than 1 year of age, the carotid artery is the preferred location for pulse palpation. (725, Table 44-3)
39. The heart in infants and children is positioned below the lower sternum, as in adults. Hand placement during closed-chest cardiac compressions in infants is with the rescuer’s one hand to support the back while compressions are performed with two fingers of the other hand. Closed-chest cardiac compression in the infant should be performed at a rate of at least 100 per minute. The sternum of the infant patient during closed-chest cardiac compressions should be depressed by at least one third of the anterior-posterior diameter or 1.5 inches (4 cm). (724-725, Table 44-3)
40. Closed-chest cardiac compressions in children can be accomplished with the heel of one hand directly over the midsternum. The recommended rate of closed-chest cardiac compressions in children is at least 100 per minute, identical to infants and adults, and depression of the sternum should also be one third to one half the anterior-posterior diameter or 1.5 to 2 inches (4 to 5 cm). (724-725, Table 44-3)
41. The energy setting that should be used for the optimal success of external defibrillation of children is directly related to their body weight. The recommended initial energy setting is 2 to 4 J/kg. If the initial attempt at defibrillation is unsuccessful, the subsequent attempt should be made with at least 4 J/kg, but no more than 10 J/kg. (724-725)
Postresuscitation Care
42. The management of the cardiac arrest patient after the return of spontaneous circulation should follow the algorithm for postresuscitation life support. Postresuscitation management should include close monitoring, supplemental oxygen to maintain an adequate oxygen saturation, and vasopressor drug therapy as needed to maintain an adequate perfusion pressure. Mild hypothermia should be immediately started and continued for the first 12 to 48 hours in comatose patients after resuscitation from cardiopulmonary arrest. (725-727, Figure 44-8)
43. In the postresuscitation phase, hypoglycemia and hyperglycemia have been shown to be deleterious for optimal neurologic outcome. Both hypoglycemia and hyperglycemia should be avoided. There is no evidence correlating specific values of the arterial partial pressure of carbon dioxide (PaCO2) to neurologic outcome. Hyperventilation is not recommended and may be harmful due to its effects on cerebral blood flow. The goal is normocapnia. (727)
Special perioperative considerations
44. Common medications used in the operating room and associated with anaphylaxis are antibiotics and muscle relaxants. Intravenous contrast agents and latex may also be associated with intraoperative anaphylactic reactions. The main pharmacologic treatment for an anaphylactic reaction is epinephrine. (727, Table 44-4)
45. The treatment for intraoperative gas embolism is to stop insufflation, if it is being used, occlude open veins, and/or flood the field with saline. The patient should also be placed in a Trendelenburg position with the left side down. In case of cardiac arrest, CPR and ACLS need to be performed. (727)
46. The primary treatment for local anesthetic toxicity is the administration of intralipid. In the event of complete cardiac collapse, resuscitation should be continued for at least 60 minutes. (727-728, Table 44-5)
47. Cardiac arrest from neuraxial anesthesia is a rare event. Should it occur, it should be managed with CPR and ACLS. (728)
