Cardiopulmonary Resuscitation

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Chapter 3 Cardiopulmonary Resuscitation

David Shimabukuro, MDCM

Most of the information provided in this chapter can be reviewed in greater detail by referring to specific guidelines published by the American Heart Association (AHA), in conjunction with the International Liaison Committee on Resuscitation. Please visit the AHA’s website at http://www.heart.org and follow the links to Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (CPR & ECC). Also see the Bibliography at the end of this chapter. This chapter focuses on basic life support (BLS) and the management of pulseless arrest (a part of advanced cardiovascular life support [ACLS]).

1 What is meant by cardiopulmonary resuscitation (CPR)?

To most people, CPR refers to BLS, which encompasses closed-chest compressions and rescue breathing. For health care providers, the term can be much broader and can include

image ACLS

image Pediatric advanced life support (PALS)

image Advanced trauma life support (ATLS)

Thus it is very important for the physician to be specific whenever discussing resuscitation with patients and their families.

2 Is iatrogenic cardiopulmonary arrest very common?

It probably occurs much more often than it really should. Without a doubt, errors of omission and commission contribute to the incidence and poor outcome of in-hospital cardiopulmonary arrests. In a study of 562 in-hospital arrests, a major unsuspected diagnosis was present (and proved by autopsy) in 14% of cases. The two most common missed diagnoses were pulmonary embolus and bowel infarction, which together accounted for 89% of all missed conditions. Retrospective reviews indicate that as many as 15% of in-hospital arrests are probably avoidable. These cases can be attributed to respiratory insufficiency and hemorrhage that are often undetected or diagnosed too late, because aberrations in patients’ vital signs and their complaints (especially dyspnea) are frequently ignored.

Direct iatrogenesis also contributes to in-hospital cardiopulmonary arrests. Almost every procedure, including esophagogastroduodenoscopy, bronchoscopy, central venous line placement, and an abdominal computed tomography scan with contrast, has, on occasion, been associated with an arrest. The injudicious use of lidocaine, sedative-hypnotics, and opiates is primarily responsible for these types of arrests throughout the hospital. Careful hemodynamic monitoring, especially pulse oximetry, by a dedicated practitioner can decrease the occurrence of this easily avoidable complication.

3 What are the four major components of BLS?

image Recognition of an unresponsive patient who is not breathing or not breathing in a normal manner

image Activation of the emergency medical system with acquisition of an automated external defibrillator (AED)

image Closed-chest cardiac compressions with ventilations

image Actual defibrillation

4 What is the CAB of resuscitation?

According to all published guidelines, the CAB of resuscitation is compressions, airway, and breathing. This has replaced the old mnemonic of ABCD because initial resuscitation now begins with closed-chest compressions once it has been established that the patient is unresponsive, is not breathing, and has no pulse. After 30 chest compressions, the airway is opened and two breaths are delivered. Thus the sequence is compressions, airway, and breathing (CAB).

5 How is BLS performed?

For any patient in cardiac arrest, the most important steps are to

1. Immediately recognize unresponsiveness

2. Check for lack of breathing or lack of normal breathing

3. Activate emergency response system and retrieve an AED

4. Check for a pulse (no more than 10 seconds)

5. Start cycles of 30 chest compressions followed by two breaths

This applies to all patients, regardless of location (in hospital or out of hospital).

image Responsiveness: A quick check for the presence of breathing or lack of normal breathing should be performed when assessing a patient who may be in cardiac arrest. If the patient is unresponsive, then the emergency response system should be activated and an AED or defibrillator should be quickly retrieved (i.e., call 911 or call a code).

image Compressions: Because a pulse can be very difficult to assess, it may be necessary to use other clues, such as whether the patient is breathing spontaneously or moving. Regardless, the health care provider should take no more than 10 seconds to check for a definitive pulse at either the carotid or femoral artery. If the patient has no pulse or no signs of life, or the rescuer is unsure, chest compressions should be started immediately. The heel of the hand should be placed longitudinally on the lower half of the sternum, between the nipples. The sternum should be depressed at least 5 cm (2 inches) at a rate of at least 100 compressions per minute. Complete chest recoil is necessary to allow for venous return and is important for effective CPR. The pattern should be 30 compressions to two breaths (30:2 equals one cycle of CPR) regardless of whether one or two rescuers are present. Pulse checks and signs of life should be assessed after every five cycles (equivalent to 2 minutes) of CPR. Once the AED or defibrillator arrives, it should be attached without delay so that an electrical shock can be immediately delivered to improve the likelihood of a return of spontaneous circulation (ROSC).

image Airway: With the new 2010 BLS guidelines, the importance of airway management has taken more of a secondary role. The old mnemonic ABCD (airway, breathing, circulation, and defibrillation) with “look, listen, and feel” has been changed to CAB (compressions, airway, and breathing). This change is due to evidence proving the importance of chest compressions and the need to quickly restore blood flow to improve the likelihood of ROSC. Airway maneuvers should still be attempted, but they should occur quickly and efficiently and minimize interruptions in chest compressions. Opening of the airway can be achieved by a simple head tilt–chin lift technique. A jaw thrust maneuver can be used in patients with suspected cervical spine injury. Simple airway devices, such as nasal or oral airways, can be inserted to displace the tongue from the posterior oropharynx. Definitive airway management, such as placement of an endotracheal tube, is an aspect of ACLS and should never be a part of BLS.

image Breathing: Although several large out-of-hospital studies have demonstrated that chest compression–alone CPR is not inferior to traditional compression-ventilation CPR, health care providers are still expected to provide assisted ventilation. A lone rescuer, outside the hospital setting, should not use a bag-mask for ventilation, but should use mouth-to-mouth or mouth-to-mask. Care should be taken to avoid rapid or forceful breaths. Delivered tidal volumes are given over a 1-minute period and should be just enough to produce visible chest rise. Large tidal volumes should be avoided because they would promote hyperventilation and decrease preload. Hyperventilation in the patient with cardiac arrest receiving closed-chest compressions has been proved to be detrimental for neurologic recovery.

image Defibrillation: An AED or defibrillator should be attached to the patient as soon as possible. Proper electrode pad or paddle placement on the chest wall should be to the right of the upper sternal border below the clavicle and to the left of the nipple with the center in the midaxillary line. If using a portable out-of-hospital AED device, turn the AED on first and then follow the voice commands. If the defibrillator’s electrical output is adjustable, then the initial voltage delivered should be the manufacturer’s recommendation. When this is unknown, 200 J should be used. Immediately after the shock, closed-chest compressions are resumed.

Of note, BLS should ideally be performed only by those persons who have been certified by the AHA, or other similar organization. However, it is not uncommon for 911 operators to provide instruction over the phone when no other qualified individual is nearby. Certification is easily obtained by attending one or two classes taught by qualified instructors. Most communities offer these classes to the general public.

6 How does blood flow during closed-chest compressions?

Two basic models derived from animal studies explain the movement of blood during closed-chest compressions:

image In the cardiac pump model, the heart is squeezed between the sternum and spine. Systole occurs when the heart is compressed; the atrioventricular valves close and the pulmonary and aortic valves open, ensuring ejection of blood with unidirectional, antegrade flow. Diastole occurs with the release of the squeezed heart resulting in a fall in intracardiac pressures; the atrioventricular valves open while the pulmonary and aortic valves close. Blood is subsequently drawn into the heart from the venae cavae and lungs.

image In the thoracic pump model, the heart is considered a passive conduit. Closed-chest compression results in uniformly increased pressures throughout the thoracic cavity. Forward flow of blood occurs with each squeeze of the heart and thorax because of the relative noncompliance of the arterial system (i.e., they resist collapse) and the one-way valves preventing retrograde flow in the venous system. Both of these models probably contribute to blood flow during CPR.

7 What is the main determinant of a successful resuscitation?

Two principal factors can highly influence the outcome of resuscitation.

image The first factor is access to defibrillation. For most adults, the primary cause of sudden, nontraumatic cardiac arrest is ventricular tachycardia (VT) or ventricular fibrillation (VF), for which the recommended treatment is electrical defibrillation.

image The second factor is time—or more specifically, time to defibrillation. Survival from a VF arrest decreases by 7% to 10% for each minute of delay. Defibrillation at the earliest possible moment is vital in facilitating a successful resuscitation.

Of interest, only 15% to 20% of patients who have an out-of-hospital arrest survive to discharge; the percentage is even lower for those who have an in-hospital event.

8 What is the role of pharmacologic therapy during ACLS?

The immediate goals of pharmacologic therapy are to improve myocardial blood flow, increase ventricular inotropy, and terminate life-threatening arrhythmias, thereby restoring and/or maintaining spontaneous circulation. Combined α/β-adrenergic agonists, such as epinephrine, and smooth-muscle V1 agonists, such as vasopressin, augment the mean aortic-to-ventricular end-diastolic pressure gradient (coronary perfusion pressure) by increasing arterial vascular tone. Phenylephrine and norepinephrine also increase arterial pressure and myocardial blood flow, but neither has been shown to be superior to epinephrine. Of note, recent data have shown that vasopressin plus epinephrine may be advantageous over epinephrine alone when comparing patients’ survival rates to hospital discharge and residual neurologic deficits. None of the studies reached statistical significance.

In addition to improving or maintaining myocardial blood flow, pharmacologic therapy during ACLS is also aimed at terminating or preventing arrhythmias, which can further damage an already severely ischemic heart. VT and VF markedly increase myocardial oxygen consumption at a time when oxygen supply is tenuous because of poor delivery. Intracellular acidosis only causes the myocardium to be more dysfunctional and irritable, which makes the heart more vulnerable to arrhythmias. Amiodarone, a class III antiarrhythmic agent, has become the drug of choice for the treatment of the majority of life-threatening arrhythmias.

9 Is sodium bicarbonate indicated in the routine management of cardiopulmonary arrest?

No! The primary treatment of metabolic acidosis from tissue hypoperfusion and hypoxia during a cardiac arrest is adequate chest compressions and ventilations. The metabolic acidosis is usually unimportant in the first 15 to 18 minutes of resuscitation. If appropriate ventilation can be maintained, the arterial pH usually remains above 7.2. Some argue that, during CPR, ventilation is at best suboptimal, leading to a combined metabolic and respiratory acidosis, dropping the pH well below 7.2. Studies have shown that severe acidosis leads to depression of myocardial contractile function, ventricular irritability, and a lowered threshold for VF. In addition, a markedly low pH interferes with the vascular and myocardial responses to adrenergic drugs and endogenous catecholamines, reducing cardiac chronotropy and inotropy. Although it is appealing to administer sodium bicarbonate in this situation, the clinician must keep in mind that the bicarbonate ion, after combining with a hydrogen ion, generates new carbon dioxide. Cell membranes are highly permeable to carbon dioxide (more so than bicarbonate), and therefore administration of sodium bicarbonate causes a paradoxic intracellular acidosis. The resultant intramyocardial hypercapnia leads to a profound decline in cardiac contractile function and failure of resuscitation. The generated carbon dioxide also needs to be eliminated to prevent worsening of an already present respiratory acidosis. Given the poor cardiac output during CPR and probable suboptimal ventilation, this may be quite difficult.

Because the optimal acid-base status for resuscitation has not been established and no buffer therapy is needed in the first 15 minutes, the routine administration of sodium bicarbonate for acidosis resulting from a cardiac arrest is not recommended. Only restoration of the spontaneous circulation with adequate tissue perfusion and oxygen delivery can reverse this ongoing process.

10 What are the arrhythmias associated with most cardiopulmonary arrests?

Most sudden nontraumatic cardiopulmonary arrests in adults are caused by VF or VT from myocardial ischemia or infarct from coronary artery disease. Electrolyte disturbances (hypokalemia or hypomagnesemia), prolonged hypoxemia, and drug toxicity can also be important inciting factors in patients with multiple medical problems. Also not uncommon are bradyasystolic arrests (as many as 50% of in-hospital arrests). One cause of this arrhythmia could be unrecognized hypoxemia or acidemia. Other causes include heightened vagal tone precipitated by medications, an inferoposterior myocardial infarction (Bezold-Jarisch reflex), or invasive procedures. A third common arrest rhythm seen is pulseless electrical activity (PEA). A common etiology is prolonged arrest itself. Typically, after 8 minutes or more of VF, electrical defibrillation induces a slow, wide-complex PEA that tends to be terminal and is known as a pulseless idioventricular rhythm. On most occasions of an unsuccessful resuscitation, VF degrades to pulseless idioventricular rhythm before the patient becomes asystolic. The rhythm of PEA can also be narrow and fast, which accompanies other reversible life-threatening conditions, rather than just representing a terminal rhythm. Examples are cardiac tamponade, hypovolemia, pulmonary embolus, or tension pneumothorax. These are discussed later in some detail.

11 What are the most common, immediately reversible causes of cardiopulmonary arrest?

An alert clinician should recognize, at the patient’s bedside, the following treatable causes of cardiopulmonary arrest:

image Hypovolemia: This should be suspected in all cases of arrest associated with rapid blood loss. This absolute hypovolemia occurs in settings such as trauma (pelvic fractures), gastrointestinal hemorrhage, or rupture of an abdominal aortic aneurysm. A relative hypovolemia can occur with sepsis or anaphylaxis resulting from extensive capillary leak. Regardless of the type, a large amount of fluid (crystalloid, colloid, blood) should be rapidly administered and the cause of the hypovolemia corrected (e.g., by taking the patient to the operating room or administering antibiotics).

image Hypoxia: Hypoxia from a variety of causes can lead to a cardiac arrest. Tracheal intubation with the delivery of a high concentration of oxygen is the treatment of choice while the cause of the hypoxia is determined and definitive management instituted.

image Hydrogen ions (acidosis): These can lead to myocardial failure resulting in cardiogenic shock and arrest. The high hydrogen ion concentration also increases myocardial irritability and arrhythmia formation. A known preexisting severe acidosis can be partially compensated for by hyperventilation, but sodium bicarbonate may still need to be administered. The underlying cause of the acidosis should be diagnosed and corrected.

image Hyperkalemia: This condition is encountered in patients with renal insufficiency, diabetes, and profound acidosis. Peaked T waves and a widening of the QRS complex, with the electrical activity eventually deteriorating to a sinus-wave pattern, herald hyperkalemia. Treatment includes the administration of calcium chloride, sodium bicarbonate, insulin, and glucose. Hypokalemia and other electrolyte disturbances leading to a cardiac arrest are much less common. Treating the abnormality should help restore spontaneous circulation.

image Hypothermia: This condition should be easily detected on examination of the patient. The electrocardiogram (ECG) may reveal Osborne waves that are pathognomonic. All resuscitation efforts should be continued until the patient is euthermic.

image Tablets or toxins: Ingestion of these items should be considered in those patients with an out-of-hospital cardiac arrest. Some of the more common intoxications include carbon monoxide poisoning after prolonged exposure to smoke or exhaust fumes from incomplete combustion, cyanide poisoning during fires involving synthetic materials, and drug overdoses (intentional or unintentional). High-flow, high-concentration, and, if possible, hyperbaric oxygen, along with the management of acidosis, are the cornerstones of treatment for carbon monoxide and cyanide poisonings. In addition, intravenous (IV) sodium nitrite and sodium thiosulfate can be used to help remove cyanide from the circulation. Tricyclic antidepressant drugs act as a type Ia antiarrhythmic agent and cause slowing of cardiac conduction, ventricular arrhythmias, hypotension, and seizures. Aggressive alkalinization of blood and urine, in addition to seizure control, should aid in controlling toxicity. An opiate overdose causes hypoxia from hypoventilation, whereas an overdose of cocaine can lead to myocardial ischemia. Naloxone reverses the effects of opioids and should be administered immediately if an opioid overdose is suspected.

image Cardiac tamponade: Cardiac tamponade presents with hypotension, a narrowed pulse pressure, elevated jugular venous pressure, distant and muffled heart sounds, and low-voltage QRS complexes on the ECG. Trauma patients and patients with malignancies are at greatest risk. Pericardiocentesis or subxiphoid pericardiorrhaphy can be lifesaving.

image Tension pneumothorax: This condition must be recognized immediately. Most often it occurs in patients who have had trauma or in patients receiving positive-pressure ventilation. The signs of a tension pneumothorax are rapid-onset hypotension, hypoxia, and an increase in airway pressures. Subcutaneous emphysema and reduced breath sounds on the affected side with tracheal deviation toward the unaffected side are commonly noted. The placement of a 14- or 16-gauge IV catheter into the second intercostal space at the midclavicular line or into the fifth intercostal space at the anterior axillary line for immediate decompression is imperative for restoration of circulation. A chest tube can be placed after the tension pneumothorax is converted to a simple pneumothorax.

image Thrombosis of a coronary artery: This condition can lead to myocardial ischemia and infarct. Reperfusion is a vital determinant for eventual outcome. Cardiac catheterization is the primary choice if it is immediately available; thrombolysis is a good alternative.

image Thrombosis of the pulmonary artery: Thrombosis of the pulmonary artery can be devastating. Some patients may be seen initially with dyspnea and chest pain, similar to acute coronary syndromes, but those who are seen in cardiac arrest have a minimal chance of survival. Therapy would include immediate thrombolysis to unload the right ventricle while restoring pulmonary blood flow.

12 How should VF be treated?

Early defibrillation with a single nonsynchronized electrical shock at an energy level of 360 J for a monophasic waveform defibrillator or the manufacturer’s recommendation (see later) for a biphasic waveform defibrillator is recommended to minimize myocardial damage. A single subsequent shock, after five cycles (2 minutes) of CPR, should continue if the patient remains in pulseless VT or VF. If using a biphasic waveform defibrillator, the energy level equivalent to a 360-J monophasic waveform shock, as determined by the manufacturer, should be used. If this energy level is not known and it is firmly established that one is using a biphasic waveform defibrillator, it is recommended that a single shock of 200 J be administered.

If the initial single shock is not successful at terminating the VF, according to ACLS guidelines, epinephrine or vasopressin should be given while CPR continues. After five cycles, or 2 minutes of CPR, the rhythm should be reevaluated. If the patient remains in VF or pulseless VT, the defibrillator should be charged while CPR continues (if the charge time is more than 5-10 seconds; most standard hospital defibrillators charge within 5 seconds). When ready, the patient should be cleared and the shock delivered; CPR should be immediately reinstituted and rhythm analysis delayed for 2 minutes. After five cycles, or 2 minutes of CPR, the patient should once again be reevaluated by a pulse check and a rhythm check. If this process continues to be unsuccessful, an antiarrhythmic agent, amiodarone, should be administered. Venous access and a definitive airway should be obtained during periods of patient reevaluation. CPR is not to be interrupted unless absolutely necessary. The sequence should always be five cycles of CPR, patient evaluation, charge of defibrillator with CPR in progress (if long charge time), defibrillation, immediate resumption of five cycles of CPR with drug administration and patient evaluation.

13 Is pulseless idioventricular rhythm treatable?

Delayed electrical defibrillation or prolonged VF frequently results in a pulseless idioventricular rhythm or asystole. In the majority of cases, the idioventricular rhythm is not amenable to treatment and results in death. In animal experiments, high-dose epinephrine (0.1-0.2 mg/kg) has helped to restore cardiac contractility and pacemaker activity; however, several clinical studies have shown no benefit in long-term survival or neurologic outcome. It is not recommended.

14 How is asystole treated?

Asystole is treated identically to PEA. These two rhythms do not require defibrillation (asystole has no electrical activity whereas PEA is an organized electrical rhythm). However, given the grim prognosis for successful resuscitation, the clinician should rapidly determine whether any evidence exists that resuscitation should not be attempted when approaching a patient in asystole. If resuscitation is appropriate, perform CPR for 2 minutes and then reconfirm the absence of electrical cardiac activity (a flatline in an ECG may be due to technical mistakes). Rotate the monitoring leads 90 degrees (if using paddles), and maximize the amplitude to detect fine VF (if present, defibrillation should be performed immediately). If using the pads and ECG leads, cycle through the various leads (I, III, III). Verify the absence of pulses at the carotid or femoral artery. Epinephrine 1 mg is administered every 5 minutes; vasopressin 40 U can replace the first or second dose. The use of atropine is not recommended. Throughout the resuscitation, the clinician should always consider stopping resuscitative efforts.

Contrary to asystole, PEA has a more favorable outcome. However, the underlying cause needs to be addressed for the resuscitation to be successful. Reversible causes of cardiopulmonary arrest were reviewed earlier (see Question 11).

15 What are the appropriate routes of administration of drugs during resuscitation?

The preferred choice is by the IV route. If a central venous catheter is in place, this should be used over a peripheral venous line. Administration of drugs through a peripheral venous line will result in a slightly delayed onset of action, although the peak drug effect is similar to that achieved via the central route. Drugs administered peripherally should be followed with at least 20 mL of normal saline solution to ensure central delivery. Intracardiac administration should not be performed.

Virtually every resuscitation drug can be administered in conventional doses via the intraosseous (IO) route. Because of the ease of insertion via readily available kits, this method is preferred in all patients when an IV line cannot be readily obtained.

The NAVEL drugs (i.e., naloxone, atropine, vasopressin, epinephrine, lidocaine) are absorbed systemically after endotracheal administration. Although pulmonary blood flow, and hence systemic absorption, is minimal during CPR, recent animal studies suggest that comparable hemodynamic responses can occur. At this time, two to three times the standard IV doses are recommended for the endotracheal route. Of note, the endotracheal administration of drugs should only be considered when attempts on obtaining an IV or IO line have failed.

16 What is the usual outcome of in-hospital CPR?

Most patients who receive CPR in the hospital do not survive. In fact, only 5% to 20% of patients live to be discharged home. Furthermore, many patients who do survive have severe impairments of independence and cognition. Unfortunately, it is not yet possible to confidently predict the outcome of in-hospital resuscitation.

Key Points Cardiopulmonary Resuscitationimage

1. Iatrogenic cardiopulmonary arrests can occur during procedures; extra care needs to be taken to monitor patients during procedures.

2. Compressions, Airway, and Breathing (C-A-B); NOT airway, breathing, and circulation (A-B-C).

3. Remember the reversible causes of cardiac arrest: hypovolemia, hypoxia, hydrogen ions (acidosis), hyperkalemia, toxins, tamponade, tension pneumothorax, coronary thrombosis, pulmonary thrombosis.

4. If IV access is not readily available, then move to the IO route.

5. Only 5% to 20% of inpatients will undergo CPR and survive their hospitalization.

Bibliography

1 Bedell S.E., Fulton E.J. Unexpected findings and complications at autopsy after cardiopulmonary resuscitation (CPR). Arch Intern Med. 1986;146:1725–1728.

2 Brown C.G., Martin D.R., Pepe P.E., et al. A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital. N Engl J Med. 1992;327:1051–1055.

3 Dorian P., Cass D., Schwartz B., et al. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med. 2002;346:884–890.

4 Field J.M., Hazinski M.F., Sayre M.R., et al. Part 1: executive summary: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(3 Suppl):S640–S656.

5 Gueugniaud P.Y., David J.S., Chanzy E., et al. Vasopressin and epinephrine vs. epinephrine alone in cardiopulmonary resuscitation. N Engl J Med. 2008;359:21–30.

6 McGrath R.B. In-house cardiopulmonary resuscitation—after a quarter of a century. Ann Emerg Med. 1987;16:1365–1368.

7 Paradis N.A., Martin G.B., Rivers E.P., et al. Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. JAMA. 1990;263:1106–1113.

8 Shimabukuro D.S., Liu L.L. Cardiopulmonary resuscitation. In: Miller R.D., Pardo M.Jr. Basics of Anesthesia. 6th ed. Philadelphia: Saunders; 2011:715–728.

9 SOS-KANTO Study Group. Cardiopulmonary resuscitation by bystanders with chest compression only (SOS-KANTO): an observational study. Lancet. 2007;369:920–926.

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