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Keywords:

  • Amiodarone;
  • Cardiac arrest;
  • Epinephrine;
  • Lidocaine;
  • Vasopressin

Abstract

  1. Top of page
  2. Abstract
  3. History of CPCR
  4. Recognition of CPA
  5. Basic Life Support
  6. Arrhythmias
  7. Advanced Cardiac Life Support (ACLS)
  8. Monitoring the Effectiveness of CPCR
  9. Care of the Patient After Successful Resuscitation
  10. Conclusion
  11. References

In December 2005, the American Heart Association published new guidelines for cardiopulmonary cerebral resuscitation (CPCR) in humans for the 1st time in 5 years. Many of the recommendations are based on research conducted in animal species and may be applicable to small animal veterinary patients. One important change that may impact how CPCR is performed in veterinary medicine is the recommendation to avoid administration of excessive ventilatory rates because this maneuver severely decreases myocardial and cerebral perfusion, decreasing the chance of survival. The new guidelines also emphasize the importance of providing well-executed, continuous, uninterrupted chest compressions. Interruption of chest compressions should be avoided and, if necessary, should be minimized to <10 seconds. During defibrillation, immediate resumption of chest compressions for 2 minutes after a single shock, before reassessment of the rhythm by ECG, is recommended. This recommendation replaces previous recommendations for the delivery of 3 defibrillatory shocks in rapid succession. Allowing permissive hypothermia postresuscitation has been found to be beneficial and may increase success rate. Medications utilized in cardiopulmonary resuscitation, including amiodarone, atropine, epinephrine, lidocaine, and vasopressin, along with the indications, effects, routes of administration, and dosages, are discussed. The application of the new guidelines to veterinary medicine as well as a review of cardiopulmonary resuscitation in small animals is provided.

In December 2005, the American Heart Association (AHA) published new guidelines for cardiopulmonary cerebral resuscitation (CPCR) in humans for the 1st time in 5 years.1 The International Liaison Committee on Resuscitation, an international consortium of representatives from many resuscitation councils, reviewed the current science, developed a worldwide evidence-based guide for resuscitation practice, and collaborated to develop the guidelines. The consensus statements were published in December 2005 in the journal Circulation.1 These guidelines are available without charge online at the website http://www.circulationaha.org.

Highlights of the new guidelines include a greater emphasis on chest compressions, avoidance of excessive ventilation rates, and immediate resumption of compressions after a single defibrillation. Many of the recommendations are based on small animal research and may be pertinent to the veterinary patient. The revised recommendations particularly applicable to the pet population as well as an overview of CPCR will be discussed in more detail in this article.

History of CPCR

  1. Top of page
  2. Abstract
  3. History of CPCR
  4. Recognition of CPA
  5. Basic Life Support
  6. Arrhythmias
  7. Advanced Cardiac Life Support (ACLS)
  8. Monitoring the Effectiveness of CPCR
  9. Care of the Patient After Successful Resuscitation
  10. Conclusion
  11. References

The 1st scientific references to artificial ventilation appeared in the 16th century.2 Andreas Vesalius, often referred to as the father of resuscitation, described the use of bellows for apnea in 1530.2 Tossach documented the administration of mouth-to-mouth ventilation in 1732.2 Various methods have been utilized to attempt to save the life of the apparently deceased. Modern cardiopulmonary resuscitation had evolved by 1960 to include endotracheal intubation, artificial ventilation, and cardiac compressions. Since 1960, little improvement has been made in the success rate of CPCR in humans.2,3

Approximately 330,000 people in the United States die every year from sudden cardiac arrest, according to the Center for Disease Control and Prevention.4 The survival rate for out-of-hospital sudden cardiac arrest in people, defined by survival to discharge from the hospital, is <6.4% for the United States and Canada.5–10 In dogs and cats that undergo cardiopulmonary arrest (CPA) in the hospital, the reported survival rate to discharge was approximately 4% for dogs and between 4 and 9.6% for cats.11,12

Recognition of CPA

  1. Top of page
  2. Abstract
  3. History of CPCR
  4. Recognition of CPA
  5. Basic Life Support
  6. Arrhythmias
  7. Advanced Cardiac Life Support (ACLS)
  8. Monitoring the Effectiveness of CPCR
  9. Care of the Patient After Successful Resuscitation
  10. Conclusion
  11. References

In veterinary medicine, there are several elements of CPCR that should be in place before CPA occurs to optimize success, including essential supplies, oxygen, and a crash cart with up-to-date medications to perform CPCR. Communication with the client, including verification of a telephone number where the client can be reached, is essential. Clients frequently have false expectations regarding the success of CPCR. Utilization of the term “do not attempt resuscitation” (DNAR) with the client may be beneficial, because it indicates that an attempt will be made, rather than a guarantee of success. The decision to attempt CPCR should be based on the client's desires. The decision to terminate CPCR should be based on the patient's disease process, the original prognosis, and the client's desires. In most cases, continued CPCR efforts are ended by 20 minutes after arrest.13 All hospitalized patients should be assigned to 1 of 3 groups, depending on the extent of CPCR to be provided: patients with DNAR orders, external CPCR, and those patients for whom everything possible should be attempted, including open chest CPCR.

The most successful CPCR is the one avoided. In small animal practice, there are many predisposing causes for CPA, including sepsis, cardiac failure, pulmonary disease, neoplasia, coagulopathies, anesthesia, toxicities, multisystem trauma, traumatic brain injury, and systemic inflammatory response syndrome.12–16 Anticipation of CPA and vigilant monitoring for deterioration in critical patients are essential. Frequent reevaluation and repetition of critical diagnostic tests and procedures may be necessary.

Before CPA, several changes may be observed, including obtundation, hypothermia, bradycardia, hypotension, and dilated, unresponsive pupils. Changes in respiratory depth, rate, or rhythm may occur, progressing to gasping and finally agonal breaths at death.17–20 Mucous membrane color and capillary refill time should not be used to assess the patient for CPA because they may remain normal for several minutes after arrest. The definitive clinical signs of CPA include loss of consciousness, absence of spontaneous ventilation, absence of heart sounds on auscultation, and absence of palpable pulses.16

Basic Life Support

  1. Top of page
  2. Abstract
  3. History of CPCR
  4. Recognition of CPA
  5. Basic Life Support
  6. Arrhythmias
  7. Advanced Cardiac Life Support (ACLS)
  8. Monitoring the Effectiveness of CPCR
  9. Care of the Patient After Successful Resuscitation
  10. Conclusion
  11. References

Performing chest compressions, providing ventilatory breaths, and administering a defibrillatory shock for ventricular fibrillation are the only aspects of CPCR proven to be effective treatment for CPA.1 Only manual chest compressions with manual ventilation and the use of a defibrillator for the treatment of ventricular fibrillation or pulseless ventricular tachycardia have consistently improved long-term survival from CPA.1 All veterinary team members should be trained and efficient in providing CPCR.

Airway

Establishment of an airway is performed, ideally by placement of a well-fitting, low-pressure, high-volume, cuffed endotracheal tube. If the ideal endotracheal tube is not available or does not fit, other options include placement of any hollow tube that fits into the trachea via the orotracheal route or via an emergency tracheostomy. The surgical approach for a tracheostomy is documented elsewhere.21,22 A laryngoscope should be utilized to place the endotracheal tube and avoid vagal-induced bradycardia from excessive manipulation of the epiglottis.23,24 Suctioning of blood or fluid from the caudal oropharynx may be necessary in some patients. Proper placement should be confirmed by visualization, appropriate chest wall excursions during ventilation, and palpation of the tube in the trachea rather than palpation of “two tracheas,” which indicates the endotracheal tube is in the esophagus.

End-tidal carbon dioxide (ETCO2) monitoring has been helpful to confirm endotracheal tube placement in anesthetized animals.25–27 A positive reading for exhaled CO2 is usually a reliable indicator of proper tube placement within the trachea in animals with normal circulation. However, in the patient with CPA, ETCO2 initially may read near zero because of lack of perfusion and therefore may not be a reliable indicator of proper tube placement in these patients.25,28,29

Breathing

The veterinary patient is given 2 breaths 1–2 seconds in duration, with positive pressure ventilation using 100% inspired oxygen, and then evaluated for spontaneous ventilation.30 If the patient resumes spontaneous ventilation, a full CPA situation may have been avoided. If the patient has only respiratory arrest, acupuncture of the Jen Chung (GV26) point should be considered. This technique is performed by twirling a 25-G, 5/8-in. needle inserted to the bone in the nasal philtrum at the ventral aspect of the nares.16,31 This technique has been effective at increasing the ventilation rate in dogs.16,31 Reversal agents are administered for medications that may cause apnea. Doxapram administration is contraindicated because it decreases cerebral blood flow and increases cerebral oxygen consumption and requirement.32–34

If spontaneous ventilation does not return in the veterinary patient, ventilations are begun at a rate of 10–12 breaths per minute (bpm) at airway pressures of ≤20 cmH2O.25,35 All breaths should be given over 1 second with sufficient volume to cause a visual rise in the chest wall, and then allow normal relaxation of the chest wall.36 The ventilations delivered to the patient should be neither too large nor too forcefully administered, or barotrauma of the lungs may occur.14,37 An ambu bag or rebreathing bag on an anesthetic machine with the inhalant anesthetic turned off should be used.36

In patients with pre-existing hypoxia or severe pulmonary disease, higher ventilation rates, 12–15 bpm, may be beneficial.22,37 Previous recommendations for veterinary patients were to provide a ventilatory rate of 20–24 bpm.22,30 Lower ventilation rates are an essential part of the new guidelines.1 In humans, a ventilatory rate of 8–12 bpm is recommended for adults and 12–20 bpm for pediatric patients and neonates.1,35,38 Delivery of an excessive ventilatory rate should be avoided, because an excessive rate has been shown to lower coronary perfusion pressure and decrease the success rate of CPCR in human and in animal models.38–40 Excessive ventilatory rates cause decreased coronary perfusion pressure, decreased cardiac preload, decreased cardiac output, decreased right ventricular function, increased intrathoracic pressure, and decreased venous return to the heart.38

Although ventilatory rates are currently controversial, a recent study published in the medical literature found that providing chest compressions alone in resuscitation for out-of-hospital witnessed cardiac arrest resulted in a higher survival rate than no CPCR at all.41 In instances in which 1 person is available or during transport, it may be appropriate to administer chest compressions only while awaiting assistance.41

Circulation

Standard manual CPCR was developed to pump blood from the chest to the vital organs during chest compression and enhance venous return into the chest during relaxation of the chest wall. The goal is to maximize cerebral and myocardial perfusion.42–45 The difference between mean arterial pressure and intracranial pressure is cerebral perfusion pressure. Maintenance of cerebral blood flow and function depends on adequate cerebral perfusion pressure.46,47 The difference between aortic diastolic pressure and right atrial pressure determines myocardial perfusion. Studies in humans and animals have shown that successful return of spontaneous circulation (ROSC) corresponds with maintenance of sufficiently high myocardial perfusion pressures.46,48

Compression of the chest wall causes an increase in intrathoracic pressure and direct compression of the heart. The degree of recoiling of the chest wall has a tremendous impact on the amount of blood flow back to the chest. With each chest wall decompression, venous return of blood to the right heart increases and intracranial pressure decreases transiently.42,49–52 The decrease in intracranial pressure is the result of direct transfer of pressure through the thoracic spine to the cerebrospinal fluid and increased venous drainage of the nonvalvular veins of the paraspinal plexuses, resulting in increased venous return to the heart via the jugular veins.50,53–55

External Chest Compressions

The new guidelines for people emphasize the importance of continuous, uninterrupted chest compressions.1 Every effort should be made to minimize the number and the duration of interruptions to <10 seconds, because interruptions allow a decrease in intrathoracic pressure, intravascular pressure, and coronary perfusion pressure.1,56–60 According to recent studies in humans, interruptions for attempted defibrillation, securing and checking the airway, placement of IV catheters, drug administration, ECG evaluation, and CPCR assessment resulted in cessation of chest compressions 40–50% of the time and were associated with increased mortality.56,57,59–61

Rapid auscultation of the chest for audible heart sounds is performed while simultaneously palpating for the presence of a peripheral pulse. If heart sounds and pulses are absent, continuous external chest compressions are begun. The thoracic pump theory, the mechanism thought to be in effect in humans and medium to large dogs, suggests that the application of pressure to the chest wall in a rhythmic manner creates blood flow by increasing intrathoracic pressure that is transmitted to arteries and veins, with a pressure gradient causing forward blood flow, and also by compressing the heart directly.22,62 The cardiac pump theory is the method thought to be responsible for forward blood movement from external chest compressions in cats and in dogs <15 kg. According to the cardiac pump theory, arterial flow is thought to be caused by direct compression of the ventricles.22 External chest compressions that are correctly performed in humans can generate systolic arterial pressure peaks of 60–80 mmHg and cardiac output between 25 and 40% of prearrest values.46,63

The patient should be placed on a firm surface in right lateral recumbency. Ideally, the person administering chest compressions (the compressor) should be above the patient's chest.64,65 Placement of the compressor's hands varies depending on the shape of the patient's chest. For medium and large dogs (thoracic pump), the compressor's hands should be placed over the widest part of the chest and 1 hand should be placed on top of the other hand with the hands parallel, applying even pressure to the chest wall with the palm of the hand. For animals weighing 7–10 kg, the compressor should place his or her hands directly over the apex of the heart, which lies between the 4th and the 6th intercostal spaces at or slightly dorsal to the costochondral junction. Hands should be placed slightly more dorsal in animals weighing >10 kg. For smaller dogs (<7 kg) and cats, the fingers of 1 hand should be placed on 1 side of the chest and the thumb on the other side. Compressions with the fingertips should be avoided.22,30,66–68 The person performing chest compressions should change every 2 minutes to maintain adequate force and rate.1,69,70

Chest compressions for veterinary patients should be provided at 80–100 compressions per minute with a 1 : 1 compression to relaxation ratio (compression time should equal relaxation time).13,22 The currently recommended chest compression rate for humans is 100 compressions per minute for adult and pediatric patients and 90 compressions per minute for neonatal patients. The chest wall should be allowed to completely recoil after being compressed approximately 30% of the chest wall diameter; otherwise, decreased coronary and cerebral perfusion and increased intrathoracic pressure occur, leading to decreased survival to discharge from the hospital.57,59,71–73

Chest compressions should be continuous, with no pauses during administration of ventilatory breaths, placement of IV catheters, endotracheal intubation, ECG assessment, palpation of pulses, or administration of medications.1,51,56,57,66 For witnessed out-of-hospital cardiac arrest, a study in humans showed no improvement in neurological outcome by adding mouth-to-mouth ventilation to external chest compressions.41 Although some studies have shown that the technique of interposed abdominal compression with chest compressions may increase venous return to the heart, other studies have not shown any survival advantage.67,68 Evidence for or against the use of interposed abdominal compression is lacking in the new CPCR guidelines.1

Compression Assist Devices

There are several compression assist devices available for CPCR in humans. The theory of the active compression-decompression device is that venous return to the heart can be increased during decompression by expanding the chest cavity and decreasing intrathoracic pressure. The results of studies utilizing these devices have been inconsistent.69,70,74 Such a device may be difficult to use in most veterinary patients because of the hair coat.

An impedance threshold device (ITD) is a valve that limits air entry into the lungs during chest recoil between chest compressions to improve venous return to the heart by increasing negative intrathoracic pressure during the decompression phase of CPCR without affecting exhalation.42,75–77 In animal models, the ITD can improve hemodynamic parameters, increase cerebral perfusion by lowering intracranial pressure, improve myocardial perfusion when intrathoracic pressure becomes increasingly negative, and improve ROSC when used as an adjunct to CPCR in intubated cardiac arrest patients.42,50–52 Although ITDs have been used in animals in research, their use is not yet reported in veterinary practice.

Internal Cardiac Massage

The indications for internal cardiac massage include penetrating chest wounds, thoracic trauma with rib fractures, pleural space disease, diaphragmatic hernia, pericardial effusion, hemoperitoneum, intraoperative sudden cardiac arrest, and failure to achieve adequate circulation within 2–5 minutes of external chest compressions, especially in dogs weighing >20 kg.30,78–80 The surgical approach for internal cardiac massage has been described elsewhere.79,81 It has been suggested previously to place a cross-clamp around the descending aorta, caudal to the heart, to increase coronary and cerebral blood flow.21,81,82 An alternative is to gently apply digital pressure to the descending aorta, caudal to the heart, with 1 finger while cardiac compression is performed with the remaining part of the hand.30,79 If a cross-clamp tourniquet or digital pressure is applied, it should be utilized for <10 minutes and slowly withdrawn.81

Arrhythmias

  1. Top of page
  2. Abstract
  3. History of CPCR
  4. Recognition of CPA
  5. Basic Life Support
  6. Arrhythmias
  7. Advanced Cardiac Life Support (ACLS)
  8. Monitoring the Effectiveness of CPCR
  9. Care of the Patient After Successful Resuscitation
  10. Conclusion
  11. References

Although rhythm analysis is important and ECG assessment should occur early in CPA, it should be carried out as briefly as possible to avoid impeding chest compressions. There are only 4 rhythms that can cause a pulseless cardiac arrest: asystole, ventricular tachycardia, ventricular fibrillation, and pulseless electrical activity (PEA). Another arrhythmia of importance is sinus bradycardia (a heart rate <40–60 bpm in dogs and <120–140 bpm in cats with a normal sinus rhythm on ECG). Increased vagal tone, hypothermia, increased intracranial pressure, and medications can cause sinus bradycardia.83,84

Asystole and Pulseless Electrical Activity

In humans, the survival rate from cardiac arrest with asystole is very low.1 Asystole is the most common arrest rhythm in dogs and cats.83,84 It can result from numerous serious disease processes, trauma, and increased vagal tone.1,83 Evaluation of all leads of an ECG is important, because fine ventricular fibrillation can mimic asystole.85,86 Administration of a defibrillation shock to a patient in asystole may prove detrimental to survival.87–91 Resuscitation efforts should be directed at performing high-quality CPCR with minimal interruptions and to identify and treat reversible causes or complicating factors. No medications have been shown to be effective in the treatment of asystole.1

Pulseless electrical activity is the condition in which, despite a normal heart rate and rhythm on ECG, there is an absence of myocardial contractility. Pulseless electrical activity was referred to previously as electrical mechanical dissociation and has been combined with asystole under the new 2005 guidelines for humans.1 Under the new guidelines, many rhythms are grouped in the PEA category, including idioventricular rhythms and ventricular escape rhythms.1 No medications have proven effective in the treatment of PEA (ie defibrillation is not beneficial), and resuscitation should focus on performing high-quality CPCR and treatment of reversible causes or complicating factors.1 The prognosis is poor for successful resuscitation.1

Ventricular Tachycardia

Ventricular tachycardia results from repetitive firing of an ectopic focus or foci in the ventricular myocardium or Purkinje system and can precipitate ventricular fibrillation.83 Causes of ventricular tachycardia include hypoxia, pain, ischemia, sepsis, electrolyte changes, trauma, pancreatitis, gastric dilatation and volvulus, primary cardiac disease, and other conditions.84,92 Treatment of the underlying cause should be addressed.83

Ventricular Fibrillation

Ventricular fibrillation is unorganized ventricular excitation resulting in poorly synchronized and inadequate myocardial contractions that cause cardiac pump failure. Sudden loss of cardiac output leads to global tissue ischemia, with the brain and myocardium being most susceptible. Ventricular fibrillation may be either fine, with lower amplitude and complete lack of organization, or coarse, with higher amplitude and more orderly appearance.83,84 Orthogonal leads (lead I and aVF, lead II and aVL) should be checked to verify fine ventricular fibrillation, which can mimic asystole on the ECG. Fine ventricular fibrillation may be more difficult to convert to sinus rhythm than coarse ventricular fibrillation.85,86

Defibrillation

Defibrillation is defined as termination of ventricular fibrillation for at least 5 seconds after delivery of an electric shock that depolarizes myocardial cells and eliminates ventricular fibrillation. It is an electrophysiologic event that occurs 300–500 ms after delivery of a defibrillatory shock.93–95 Ventricular fibrillation should be identified as early as possible because it is more responsive to defibrillation if detected early. There are 2 types of defibrillators, monophasic and biphasic, referring to the type of current used. Newer defibrillators are usually biphasic and are effective at terminating ventricular fibrillation in humans at lower energy levels (120–200 J) than are monophasic defibrillators (360 J). It is important to know the type of defibrillator available and the energy level proven by the manufacturer to be effective at terminating ventricular fibrillation.96–98

Chest compressions should be performed while the defibrillator is being connected and charged. With a manual defibrillator, the defibrillator operator selects the shock energy (in joules); however, it is the amplitude of current flow (in amperes) that causes depolarization of the myocardium and results in defibrillation.99 Alcohol, ultrasound gel, or other nonconductive gels should not be used on electrode paddles.1,36 Conductive paste should be applied liberally to the paddles or self-adhesive pads should be used. The largest electrode paddles or pad that will fit on the patient's chest should be used because small electrodes may cause myocardial necrosis.100–102 The patient should be placed in dorsal recumbency and the paddles should be placed with pressure on opposite sides of the chest.

When the defibrillator is charged, the word “clear” should be shouted to warn personnel to cease contact with the patient and anything connected to the patient, and then 1 shock should be administered as quickly as possible. The person administering the shock must avoid contact with the patient's limbs, the table, the ECG leads, and everything connected to the patient. Doing so can be difficult with the patient in dorsal recumbency. Alternatively, the patient can remain in right lateral recumbency, a flat paddle can be placed under the patient's chest on the down side, and a standard paddle can be used on the upper side of the chest. The initial counter shock energy for external defibrillation is 2–5 J/kg.103,104 Other dosage recommendations for external defibrillation are to administer 50 J for small dogs and cats, 100 J for medium dogs, and 200 J for large dogs or to administer 7 J/kg to patients <15 kg and 10 J/kg to patients >15 kg. For internal defibrillation, saline-soaked sponges should be placed between the paddles and the heart. The energy of the counter shock for internal defibrillation is 1/10 of the dosage used for external defibrillation (0.2–0.5 J/kg).104

Under the 2005 guidelines, to minimize the interruption in chest compressions, 1 shock should be administered rather than the 3 successive shocks recommended previously.56,71,105,106 Chest compressions should immediately be resumed for 2 minutes before reassessing the cardiac rhythm and administration of an additional shock.1 Assessment of an ECG immediately after defibrillation rarely is helpful and delays resumption of postshock chest compressions.59,72,107–109 After successful defibrillation, a short period of a nonperfusing rhythm, either asystole or pulseless electrical activity, is common before returning to normal sinus rhythm.96,110,111 Immediate chest compressions after attempted defibrillation increase myocardial perfusion and are more likely to make conversion successful than the administration of a 2nd shock.56,71,98,105,106,110–115

In an unwitnessed, out-of-hospital arrest, the 2005 CPCR guidelines recommend the administration of external chest compressions first for approximately 2 minutes, followed by 1 defibrillatory shock, regardless of the type of defibrillator used, with immediate resumption of chest compressions for 2 minutes before reassessing the cardiac rhythm.116,117 In these situations, a clinically relevant period of no perfusion may have occurred. The responsiveness of ventricular fibrillation to defibrillation may be enhanced by previous chest compressions and epinephrine administration.71,106

When CPA occurs in a human hospital, immediate defibrillation is recommended. If ventricular fibrillation continues after 1 or 2 shocks plus compression, epinephrine should be administered every 3–5 minutes, or a dose of vasopressin may be substituted for the 1st or the 2nd dose of epinephrine. If ventricular fibrillation continues after 2 or 3 shocks, compressions and administration of a vasopressor, followed by amiodarone, are recommended.108,118–120

The likelihood of ROSC proportionately decreases with delays in cardiac compressions from repeated defibrillation, rhythm assessment, and other interruptions.56,57,60,105,113,115 A precordial thump is no longer recommended because research has shown that it can lead to deterioration of cardiac rhythm, increased rate of ventricular tachycardia, conversion of ventricular tachycardia to ventricular fibrillation, complete heart block, or asystole.121–123

Automated external defibrillators (AEDs) are computerized devices that use voice and visual prompts to guide safe defibrillation. They are useful for out-of-hospital sudden cardiac arrest in public access areas such as airports and sports venues.124–127 Microprocessors in the AED analyze features of the surface ECG. The voice and visual prompts along with diagrams guide the rescuer and will not send a defibrillating shock unless the automated ECG rhythm analysis determines that administration of a shock is indicated.57,61,124–127

Although manual defibrillators with dose adjustment capabilities are recommended for children, AEDs equipped with pediatric attenuator systems are available for children 1–8 years of age.128–130 If an AED is to be used on a small animal patient, studies in swine show that it is advisable to use an AED equipped with a pediatric dose attenuation system.103,131

Advanced Cardiac Life Support (ACLS)

  1. Top of page
  2. Abstract
  3. History of CPCR
  4. Recognition of CPA
  5. Basic Life Support
  6. Arrhythmias
  7. Advanced Cardiac Life Support (ACLS)
  8. Monitoring the Effectiveness of CPCR
  9. Care of the Patient After Successful Resuscitation
  10. Conclusion
  11. References

Pharmacologic support of circulation and placement of an advanced airway are some of the treatments considered to be a part of ACLS. These measures are provided in addition to basic life support to increase the likelihood of successful resuscitation and survival to discharge from the hospital.

Routes of Administration for Medications and Fluid Therapy

A central line is the preferred route for administration of medication during CPCR. Unfortunately, one rarely is in place before CPA, and a central line should not be placed during CPCR because of the time-consuming nature of placement.132,133 A peripheral IV catheter is the next most preferred route, followed by intraosseous (IO) administration and finally the intratracheal (IT) route.36,134 Because of the rapid access to the IT route and delays in placing peripheral catheters during CPA, some prefer the IT route. Intracardiac injections should be avoided, except possibly during open chest CPCR, when the heart is directly observed. In addition to the difficulty of injecting blindly into the left ventricle, intracardiac injections can result in numerous complications, including coronary vessel laceration, myocardial ischemia, hemorrhage, arrhythmia, and pneumothorax.16,135,136 Medication administered via a peripheral catheter should be given as a bolus injection, followed by 0.9% NaCl IV and raising of the extremity for 10–20 seconds.1,137,138 It usually takes 1–2 minutes for medication administered via a peripheral vein to reach the central circulation. The new guidelines recommend chest compressions be administered for 2 minutes after drug administration via a peripheral vein before checking the ECG.132,133 The sites for IO administration include the tibial crest, the femoral trochanteric fossa, and the proximal humerus, and the technique has been described elsewhere.139

The medications found to be well absorbed and safe for administration via the IT route are atropine, epinephrine, lidocaine, naloxone, and vasopressin (see Table 1).140–145 IT administration of sodium bicarbonate should be avoided because it inactivates the surfactant and irritates tissues.16,140,146–151 Medications to be administered via the IT route should be diluted in 5–10 mL of sterile water, which is absorbed better than 0.9% NaCl.146–149 If sterile water is not available, 0.9% NaCl should be utilized.146,148 For IT administration, the dosage of most drugs should be increased 2–2.5 times their IV dosage, except for epinephrine, which should be increased by 3–10 times the IV dosage (0.03–0.1 mg/kg).149,152–155 In studies of humans and animals, lower dose epinephrine administered via the IT route caused hypotension and decreased cerebral perfusion pressure because of transient β-adrenergic effects.153,154,156–160

Table 1.   Medications and shock energy doses used in CPCR.
MedicationCanineFelineDetails
  • a

    All medications administered IT should be diluted in 5–10 mL of sterile water.

  • IO, intraosseous; IT, intratracheal; CPCR, cardiopulmonary cerebral resuscitation.

Amiodarone5.0 mg/kg IV, IO over 10 minutes Repeat dose 2.5 mg/kg IV, IO over 10 minutesSameOnly 1 repeat dose, after 3–5 minutes, is recommended. Do not administer IT
Atropine0.04 mg/kg IV, IO 0.08–0.1 mg/kg ITaSameCan repeat every 3–5 minutes for a maximum of 3 doses
Calcium gluconate 10%0.5–1.5 mL/kg IV slowlySameDo not administer IT
Epinephrine0.01 mg/kg IV, IO 0.03–0.1 mg/kg ITa Repeat dose 0.1 mg/kg IV, IO, ITaSame Initial dose Repeat doses should be administered every 3–5 minutes
Lidocaine2.0–4.0 mg/kg IV, IO 4.0–10 mg/kg ITa0.2 mg/kg IV, IO, ITUse cautiously in cats
Magnesium sulfate0.15–0.3 mEq/kg IV slowly over 10 minutesSameCan repeat to a maximum of 0.75 mEq/kg Do not administer IT
Naloxone0.02–0.04 mg/kg IV 0.04–0.10 mg/kg ITaSameOpioid reversal agent
Sodium bicarbonate0.5 mEq/kg IV, IO 0.08 × BW (kg) × base deficit =# of mEq to administerSameDo not administer IT. Administer cautiously after 10–15 minutes of CPA; can repeat every 10 minutes
Vasopressin0.2–0.8 U/kg IV, IO 0.4–1.2 U/kg ITaSameRepeat every 3–5 minutes or alternate with epinephrine
External defibrillation shock energy (J)2–5 J/kg Or 50 J for small dogs, 100 J for medium dogs, and 200 J for large dogs Or 7 J/kg if <15 kg and 10 J/kg if >15 kg2–5  J/kg Or 50 J Or 7 J/kg if <15 kg 
Internal defibrillation shock energy (J)0.2–0.5 J/kgSame 

IV Fluid Therapy

The 2005 guidelines for humans state that IV fluids should be administered if the patient is hypovolemic.1 IV fluids should not be administered at shock dosages (90 mL/kg for dogs and 45 mL/kg for cats) unless the patient was hypovolemic before CPA. In the euvolemic CPA patient, the recommended dosage for crystalloid IV fluids is a 20 mL/kg bolus for dogs and a 10 mL/kg bolus for cats, as rapidly as possible. The administration of excessive volumes of IV fluids to euvolemic patients during CPCR in animal studies decreased coronary perfusion pressure because of an increase in right atrial pressure relative to aortic pressure.12,161,162 If colloids are necessary, the IV dosage of hetastarch or plasma is 20 mL/kg/day for dogs and 5–10 mL/kg/day for cats. Hetastarch may be administered as an IV bolus during CPCR at a dosage of 5 mL/kg for dogs and 2–3 mL/kg for cats.163–167 Hypertonic saline has been shown to improve survival from ventricular fibrillation when compared with 0.9% NaCl in animal studies.168,169 Although the concentrations and dose recommendations are variable, the authors recommend 3% hypertonic saline, at a dosage of 4–6 mL/kg IV, slowly over 5 minutes.168,169 If hypertonic saline is administered too rapidly, it can cause vagal-induced bradycardia and hypotension.168,169

Epinephrine

Epinephrine hydrochloride is a mixed adrenergic agonist, acting on α- and β-receptors.170,171 It possesses both β1-agonist (increased myocardial contractility, increased heart rate, increased myocardial automaticity, and increased myocardial oxygen consumption) and β2-agonist (smooth muscle relaxation, peripheral vasodilatation, systemic hypotension, and bronchial dilatation) effects.172,173 Epinephrine is administered during CPCR mainly for its α2-adrenergic receptor-stimulating effects, including peripheral arteriolar vasoconstriction, which leads to increased coronary and cerebral perfusion pressure.174,175 The α2-agonist effect of increased peripheral arteriolar vasoconstriction overrides the β2-agonist–induced hypotension and causes an increase in systemic vascular resistance and increased arterial blood pressure, which result in the shunting of blood to the brain, heart, and lungs.174,176 The α1-agonist effects can be detrimental to the myocardium by increasing myocardial oxygen demands and causing intramyocardial coronary arteriolar vasoconstriction and enhancing the reduction in myocardial perfusion.174–184

The optimal dosage of epinephrine is not known. In veterinary patients, epinephrine (1 : 1,000) should be administered initially at 0.01 mg/kg IV, unless it is being administered IT, in which case the dosage is 0.03–0.1mg/kg.149,174,185,186 Epinephrine administration should be repeated every 3–5 minutes if indicated. In veterinary medicine, if repeated doses are not successful, vasopressin can be administered instead or the epinephrine dosage can be increased to 0.1 mg/kg IV.171,185–188 Many protocols in human medicine now call for 1 dose of epinephrine, followed by a dose of vasopressin IV before repeating or increasing the dose of epinephrine.171,187,188 There have been no randomized clinical studies comparing an epinephrine dosage of 0.01 mg/kg with placebo in cardiac arrest.189 Placebo was shown to be superior to an epinephrine dosage of 0.1 mg/kg in survival to discharge in humans with CPCR.189–191 Although epinephrine 0.1 mg/kg IV appears to be superior for maximizing cerebral blood flow and the aortic diastolic-right atrial gradient, it is also associated with a higher refibrillation rate and a lower survival rate.190–192

Vasopressin

Vasopressin is a nonadrenergic endogenous pressor peptide that causes peripheral, coronary, and renal vasoconstriction.193,194 At a dosage of 0.2–0.8 U/kg IV or 0.4–1.2 U/kg IT, vasopressin stimulates specific V1A receptors in the smooth muscle of the vasculature, leading to nonadrenergic vasoconstriction.171,195–201 Vasopressin may improve cerebral perfusion by causing dilatation of cerebral vasculature. It causes less constriction in coronary and renal blood vessels than in peripheral tissue, resulting in preferential shunting of blood to the central nervous system and heart.171,196,198,202

Because the outcome from pulseless cardiac arrest did not differ in humans treated with vasopressin compared with those treated with epinephrine, the 2005 guidelines state that vasopressin can be used with or instead of epinephrine in the treatment of ventricular fibrillation, ventricular tachycardia, and PEA.1 In humans with asystole, vasopressin was superior to epinephrine in survival to discharge from the hospital in some studies, and it is recommended in the treatment of asystole.1,89,91,203 The utilization of vasopressin in CPCR of companion animals is increasing because asystole is the most common arrest arrhythmia.90,204 Several studies in animals with ventricular fibrillation showed that vasopressin was superior to both epinephrine and placebo for ROSC.87,89,193,205 The responses of the V1A receptors remain intact in an acidotic environment, as encountered in cardiac arrest, allowing vasopressin to function, whereas epinephrine and other catecholamines lose much of their vasopressor effects in hypoxic and acidotic environments.171,195 According to a recent report in human medicine, the initial dosage of vasopressin can be repeated every 3–5 minutes or vasopressin can be alternated with epinephrine every 3–5 minutes.188

Atropine

Atropine sulfate is an anticholinergic parasympatholytic that is effective at muscarinic receptors.206,207 During cardiac arrest, ventricular vagal tone is suspected to be high, suppressing automaticity.207 Atropine reverses cholinergic-mediated responses and parasympathetic stimulation and acts to increase heart rate, control hypotension, and increase systemic vascular resistance.207 As a vagolytic, it is most effective in the treatment of vagal-induced asystole.207 It increases automaticity of the sinoatrial node and conduction of the atrioventricular node.208,209 Although there are no prospective controlled studies supporting the use of atropine in asystole or PEA cardiac arrest, the 2005 guidelines recommend atropine in these instances.1 The recommended dosage for atropine during CPCR in dogs and cats is 0.04 mg/kg IV.104 If there is no effect, the dose can be repeated every 3–5 minutes for a maximum of 3 doses.210,211

Amiodarone

Amiodarone is a class III antiarrhythmic agent with several effects, including prolongation of myocardial cell action potential duration and refractory period by affecting sodium, potassium, and calcium channels, and noncompetitive α- and β-adrenergic inhibition.119,212 It is the medication of choice for treatment of refractory ventricular fibrillation after defibrillation, according to the 2005 guidelines.1,118,120,213 Although numerous studies in humans and animals showed improvement in response to defibrillation in patients treated with amiodarone compared with patients treated with lidocaine, other studies dispute these findings.214 It should also be noted that the rate of survival to hospital discharge did not improve with the administration of amiodarone.1 Lidocaine and amiodarone are indicated for the treatment of atrial fibrillation, narrow-complex superventricular tachycardia, ventricular tachycardia, wide-complex tachycardia of uncertain origin, and refractory ventricular fibrillation that is unresponsive to compressions, defibrillation, and vasopressor administration.118,120,212–214 The dosage of amiodarone is 5.0 mg/kg IV or IO over 10 minutes. One repeated dose of amiodarone, at a dosage of 2.5 mg/kg IV, may be administered after 3–5 minutes.119,215

Lidocaine

Lidocaine is a class Ib antiarrhythmic agent that stabilizes cell membranes by sodium channel blockade and also acts as a local anesthetic. In clinical trials, in comparison with amiodarone, lidocaine resulted in decreased ROSC and increased incidence of asystole after defibrillation.118,216 Because it has no proven efficacy in cardiac arrest, the 2005 guidelines state that lidocaine should be considered an alternative treatment to amiodarone.1 Lidocaine is not recommended for treatment of ventricular fibrillation if defibrillation is planned, because it may make electrical defibrillation more difficult by increasing the defibrillation threshold and decreasing myocardial automaticity.217,218 For ventricular arrhythmias after resuscitation, lidocaine may be beneficial and should be considered if amiodarone is not available.118,213,214 The dosage of lidocaine in dogs is 2.0–4.0 mg/kg IV or IO.12,25 For IT administration in dogs, the lidocaine dosage is increased 2–2.5 times and it is diluted in sterile water.12,25,143,144 Lidocaine should be used cautiously, if at all, in cats at a dosage of 0.2 mg/kg IV, IO, or IT.219,220

Sodium Bicarbonate

Sodium bicarbonate was recommended previously for the treatment of severe acidosis during CPCR. Evidence for its efficacy is lacking and the new guidelines recommend it only in the treatment of tricyclic antidepressant overdose, severe pre-existing metabolic acidosis, and severe hyperkalemia.221–227 For these conditions, sodium bicarbonate may be administered at a dosage of 0.5mEq/kg IV.221–227 The best treatment for the respiratory acidosis and nonrespiratory (metabolic) acidosis that occur during CPA is to maximize ventilation and perfusion.1,153,228,229 Sodium bicarbonate may inactivate catecholamines that are administered simultaneously and can cause hypernatremia, hyperosmolality, extracellular alkalosis, decreased systemic vascular resistance, left shift of the oxyhemoglobin curve, and decreased release of oxygen from hemoglobin.23

Calcium

Calcium was thought to be useful for increasing cardiac contractility during CPCR, but there is no proven benefit for the administration of calcium during CPCR.230–232 Calcium is currently recommended for the treatment of calcium channel blocker toxicity, hyperkalemia, and documented ionized hypocalcemia, rather than routine use during CPCR.231 When indicated, the dosage of 10% calcium gluconate is 0.5–1.5mL/kg slowly IV.233 In critically ill patients, serum total calcium concentration is an inadequate reflection of serum ionized calcium concentration, which is affected by interactions of serum pH, individual serum protein-binding capacity and affinity, and serum protein concentration.232,234–236

Magnesium Sulfate

Magnesium sulfate is an essential enzyme cofactor with numerous roles in cellular metabolism. A deficiency of magnesium may result in altered depolarization, repolarization, and pacemaker activity because of abnormalities of potassium and sodium homeostasis from decreased sodium, potassium-adenosinetriphosphatase (Na+, K+-ATPase) activity. Magnesium also affects vascular tone.237–240 The administration of magnesium sulfate may be beneficial in the treatment of refractory ventricular arrhythmias, including ventricular fibrillation and torsades de pointes (a life-threatening, polymorphic form of ventricular tachycardia).1,241–243 Decreased intracellular concentrations of magnesium increase myocardial excitability, potentially resulting in ventricular arrhythmias.241–244 The dosage of magnesium sulfate during cardiac arrest is 0.15–0.3 mEq/kg administered slowly IV over 10 minutes, repeated to a maximum dosage of magnesium sulfate of 0.75 mEq/kg/day.215

Glucose

Glucose administration is not recommended during CPCR unless the patient has documented hypoglycemia. Neurologic outcome after resuscitation is worse in patients with hyperglycemia.228,245–248

Bretylium Tosylate

Bretylium tosylate is a type III antiarrhythmic agent with both direct myocardial and adrenergic effects. It is no longer recommended because of its hypotensive effects, antiadrenergic effects, and lack of proven efficacy.36,249,250

Reversal Agents

If CPA is associated with sedation or anesthesia, administration of a reversal agent if one is available and appropriate is recommended. Reversal agents include α2-adrenergic antagonists (yohimbine or atipamezole, 0.1–0.2 mg/kg IV slowly), benzodiazepam antagonists (flumazenil, 0.02 mg/kg IV), and opioid antagonists (naloxone, 0.02–0.04 mg/kg IV).251 The administration of inhalation anesthetics should be stopped and the breathing circuit should be evaluated before CPCR is initiated.

Monitoring the Effectiveness of CPCR

  1. Top of page
  2. Abstract
  3. History of CPCR
  4. Recognition of CPA
  5. Basic Life Support
  6. Arrhythmias
  7. Advanced Cardiac Life Support (ACLS)
  8. Monitoring the Effectiveness of CPCR
  9. Care of the Patient After Successful Resuscitation
  10. Conclusion
  11. References

To assess the effectiveness of CPCR efforts, the patient's ETCO2 level should be monitored as an indication of perfusion.25,29,252 If ventilation during CPCR is relatively constant, changes in cardiac output are reflected by changes in ETCO2 levels.25 In studies of humans, patients who could not be resuscitated had significantly lower ETCO2 levels than those who were successfully resuscitated.245,252–255 The presence of a palpable carotid or femoral pulse may not be a reliable indicator of successful CPCR, because venous pulses may be felt in the absence of adequate arterial blood flow during CPCR because of backflow of blood from the caudal vena cava.256,257 Assessment of cerebral blood flow can be performed by placement of a Doppler ultrasound transducer on the lubricated cornea.258,259 Assessment of oxygenation at the tissue level during CPCR can be achieved by monitoring central venous blood gases from a pulmonary artery catheter sample.25 Evaluation of central venous blood gases provides a more accurate assessment of tissue acid-base status during CPCR because it takes into consideration the effects of low peripheral blood flow and the resulting tissue hypoxia, hypercarbia, and acidosis that occur during CPA.1,25,260 Studies have shown that evaluation of arterial blood gases during CPCR does not adequately reflect the effectiveness of ventilation or the severity of tissue acidosis or tissue hypoxemia.260–263 Pulse oximetry is not helpful because peripheral pulsatile blood flow is inadequate.1,245

Care of the Patient After Successful Resuscitation

  1. Top of page
  2. Abstract
  3. History of CPCR
  4. Recognition of CPA
  5. Basic Life Support
  6. Arrhythmias
  7. Advanced Cardiac Life Support (ACLS)
  8. Monitoring the Effectiveness of CPCR
  9. Care of the Patient After Successful Resuscitation
  10. Conclusion
  11. References

Respiratory or CPA commonly recur after successful CPCR in veterinary patients.12 A “sepsis-like syndrome” characterized by coagulopathy, immunologic dysfunction, and multiple organ failure has been documented after successful resuscitation in people because of the presence of global ischemia and reperfusion injury.264–266 The following parameters should be monitored: pulse rate, rhythm and character, mental status, ECG, pulse oximetry, body temperature, lung sounds, mucous membrane color, capillary refill time, urine output, electrolytes, blood gases, PCV and total solids, blood glucose concentration, serum lactate concentration, central venous pressure, neurologic function, and patient comfort.228,245,246

Supplemental oxygen should be provided via ventilatory support if inadequacies in spontaneous ventilation are present, or via a nasal catheter, a hood, or an oxygen kennel.36 Initially, the patient should be ventilated with 100% oxygen, but the oxygen concentration should be decreased to <60% as quickly as possible to avoid oxygen toxicity.108,267–271 If continued ventilation is required, arterial blood gases and direct arterial blood pressure or indirect systolic blood pressure should be monitored continuously.

If the animal has mild hypothermia or becomes hypothermic during CPCR, permissive hypothermia should be allowed.272,273 Permissive hypothermia is the term used when hypothermia is allowed to continue without taking steps to rewarm the patient to a normal body temperature. This term differs from induced hypothermia, in which the human patient is manipulated via medical treatment and external devices to a body temperature of 32–34 °C and maintained at this low body temperature for 12–24 hours.272–274 Although induced hypothermia may be useful in human patients, it requires advanced monitoring and medical devices not typically available in veterinary practice. Complications of hypothermia include arrhythmias and coagulopathy.1,272–275 The target temperature for dogs and cats is 33–34 °C.276,277 Permissive hypothermia diminishes the oxygen demands of tissues, reduces neurologic impairment after CPA, and may increase the success rate from CPCR.272–280

IV fluid therapy should be administered cautiously. Crystalloids should not be administered at shock fluid dosages unless the patient was hypovolemic before CPA. To improve peripheral perfusion and cardiac output, it may be beneficial to administer an IV bolus of a colloid such as hetastarch (5–10 mL/kg IV for dogs and 2–3mL/kg IV slowly over 15 minutes for cats.)166,281 If the colloid bolus does not improve cardiac output, blood pressure, and peripheral perfusion, it may be beneficial to administer a positive inotrope or vasopressor.

After an adequate IV fluid bolus, if the patient is normotensive, with decreased perfusion and decreased cardiac contractility as evaluated by echocardiography, administration of a positive inotrope (eg dobutamine or dopamine) may be indicated. Peripheral perfusion can be evaluated by assessing serum lactate concentration, urine output, capillary refill time, and rectal and peripheral temperatures. Dobutamine is usually the drug of choice to improve cardiac output without causing excessive vasoconstriction. The dosage of dobutamine for infusion is 2.0–20.0 μg/kg/min IV as a constant rate infusion (CRI) titrated to effect.282,283

The administration of dopamine may be beneficial if dobutamine does not produce the desired response. Dopamine has a greater impact on systemic arterial blood pressure but may cause excessive vasoconstriction without an additional increase in cardiac output. The dosage of dopamine to produce a positive inotropic effect is 1.0–10.0 μg/kg/min IV as a CRI titrated to effect.282,283 The following formula may be used to calculate a dobutamine or dopamine CRI: 6 × body weight in kilograms = the number of milligrams of dobutamine or dopamine added to a total volume of 100 mL 0.9% NaCl. When this preparation is delivered at 1.0 mL/h IV, 1.0 μg/kg/min is administered. The CRI solution should be protected from light.284

After an adequate IV fluid bolus, if the patient is hypotensive, with normal cardiac contractility as evaluated by echocardiography, the administration of a vasopressor (eg epinephrine, vasopressin, or norepinephrine) IV as a CRI titrated to effect may be beneficial to increase systemic arterial blood pressure and cardiac output, but cautious administration is necessary because excessive vasoconstriction may occur.282,285 The dosage of epinephrine (1 : 1,000) for infusion is 0.1–1.0 μg/kg/min IV as a CRI titrated to effect.283 The following formula may be useful to calculate an epinephrine CRI: 0.6 × body weight in kilograms = the number of milligrams of epinephrine added to a total volume of 100 mL 0.9% NaCl. When this preparation is delivered at 1.0 mL/h IV, 0.1 μg/kg/min is administered. The CRI solution should be protected from light.284 The dosage of vasopressin for infusion is 0.01–0.04 U/min IV as a CRI titrated to effect.286,287

Norepinephrine is a potent vasoconstrictor and inotropic agent with mixed α- and β-adrenergic receptor action that may be indicated in the patient who remains hypotensive despite adequate volume replacement and treatment with other, less potent, inotropes such as dopamine.1,288,289 Cardiac contractility, cardiac oxygen demand, heart rate, and stroke volume increase after the administration of norepinephrine.1,284 Renal, splanchnic, and pulmonary vasoconstriction also occurs.1,290,291 Norepinephrine is available in 2 forms. Norepinephrine, 1 mg, is equivalent to 2 mg of norepinephrine bitartate. Norepinephrine, 4 mg, or 8 mg of norepinephrine bitartate, should be diluted in 250 mL of 5% dextrose in water or 5% dextrose in normal saline before administration. The dosage of norepinephrine is 0.5–1.0 μg/kg/min IV as a CRI, titrated to effect.1,284

Neurologic dysfunction occurs commonly after CPCR. Often, the clinical abnormalities resolve over 24–48 hours. The patient should be allowed a minimum of 48 hours before a prognosis is made regarding neurologic abnormalities.73,84,292,293 To avoid increasing the brain's oxygen requirements, hyperthermia should be avoided and antiepileptic treatment should be administered to a patient with seizures. Situations that cause increased intracranial pressure such as sneezing caused by nasal oxygen cannulas and neck wraps for jugular catheters or esophagostomy tubes should be avoided. Glucocorticoid administration is contraindicated in these patients and may worsen neurologic injury secondary to ischemia by causing hyperglycemia.248,294 Nutritional support should be instituted as soon as possible depending on the patient's mentation after resuscitation, original disease process, and underlying clinical status. If oral enteral nutritional support is not possible, placement of a feeding tube or parenteral nutritional support should be considered.

Studies in humans identified 4 clinical signs that correlate with poor neurologic outcome when observed 24 hours after resuscitation: absent corneal reflex, absent pupillary response, absent withdrawal response to pain, and absent motor response.73,292

Common complications that can be seen after CPCR include cerebral edema, hypoxemia, reperfusion injury, abnormal hemostasis, acute renal failure, sepsis, multiple organ dysfunction syndrome, and recurrent CPA. In addition, treatment is needed to address the underlying disease process that resulted in the initial CPA.264,265,278,280,295–297

Conclusion

  1. Top of page
  2. Abstract
  3. History of CPCR
  4. Recognition of CPA
  5. Basic Life Support
  6. Arrhythmias
  7. Advanced Cardiac Life Support (ACLS)
  8. Monitoring the Effectiveness of CPCR
  9. Care of the Patient After Successful Resuscitation
  10. Conclusion
  11. References

The goal of resuscitation is survival to hospital discharge, and hopefully continued quality of life after discharge. Many of the experimental studies of CPCR have been conducted on dogs, providing useful information for veterinarians. The new AHA guidelines for humans have many applications to small animal veterinary medicine. These new guidelines should be instituted in the protocol for CPCR of dogs and cats where practical and applicable. The new recommendations for humans that are applicable to veterinary patients include the administration of chest compressions continually throughout CPCR, keeping interruptions as brief and few as possible, avoiding excessive ventilatory rates, application of 1 defibrillation shock, followed immediately by chest compressions rather than 3 successive shocks, the utilization of amiodarone in preference to lidocaine for the treatment of refractory ventricular tachycardia or fibrillation after defibrillation, and allowance of mild permissive hypothermia in the postarrest period.

References

  1. Top of page
  2. Abstract
  3. History of CPCR
  4. Recognition of CPA
  5. Basic Life Support
  6. Arrhythmias
  7. Advanced Cardiac Life Support (ACLS)
  8. Monitoring the Effectiveness of CPCR
  9. Care of the Patient After Successful Resuscitation
  10. Conclusion
  11. References
  • 1
    ECC Committee, Subcommittees and Task Force of the American Heart Association. 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2005;112:IV1IV203.
  • 2
    Chamberlain D. Never quite there: A tale of resuscitation medicine. Clin Med 2003;3:573577.
  • 3
    Hurt R. Modern cardiopulmonary resuscitation—Not so new after all. J R Soc Med 2005;98:327331.
  • 4
    Zheng ZJ, Croft JB, Giles WH, Mensah GA. Sudden cardiac death in the United States, 1989 to 1998. Circulation 2001;104:21582163.
  • 5
    DeMaio V, Stiell IG, Wells GA, Spaite DW. Optimal defibrillation response intervals for maximum out-of-hospital cardiac arrest survival rates. Ann Emerg Med 2003;42:242250.
  • 6
    DeVos R, Koster RW, De Haan RJ, et al. In-hospital cardiopulmonary resuscitation: Prearrest morbidity and outcome. Arch Intern Med 1999;159:845850.
  • 7
    Doig CJ, Boiteau PJ, Sandham JD. A 2-year prospective cohort study of cardiac resuscitation in a major Canadian hospital. Clin Invest Med 2000;23:132143.
  • 8
    Fedoruk JC, Paterson D, Hlynka M, et al. Rapid on-site defibrillation versus community program. Prehospital Disaster Med 2002;17:102106.
  • 9
    Olson DW, LaRochelle J, Fark D, et al. EMT-defibrillation: The Wisconsin experience. Ann Emerg Med 1989;18:806811.
  • 10
    Stiell IG, Wells GA, Field B, et al. Advanced cardiac life support in out-of-hospital cardiac arrest. N Engl J Med 2004;351:647656.
  • 11
    Kass KH, Haskins S. Survival following cardiopulmonary resuscitation in dogs and cats. J Vet Emerg Crit Care 1992;2:5765.
  • 12
    Wingfield WE, Van Pelt DR. Respiratory and cardiopulmonary arrest in dogs and cats: 265 cases (1986–1991). J Am Vet Med Assoc 1992;200:19931996.
  • 13
    Wingfield WE. Cardiopulmonary arrest. In: WingfieldWE, RaffeMR, eds. The Veterinary ICU Book. Jackson Hole, WY: Teton New Media; 2002:421452.
  • 14
    Cole SG, Otto CM, Hughes D. Cardiopulmonary cerebral resuscitation in small animals—A clinical practice review (part I). J Vet Emerg Crit Care 2002;12:261267.
  • 15
    Gilroy BA, Dunlop BJ, Shapiro HM. Outcome from cardiopulmonary resuscitation: Laboratory and clinical experience. J Am Anim Hosp Assoc 1987;23:133139.
  • 16
    Hackett TB, Van Pelt DR. Cardiopulmonary resuscitation. In: BonaguraJ, ed. Kirk's Current Veterinary Therapy XII. Philadelphia, PA: WB Saunders Co; 1995:167175.
  • 17
    Gozal D, Torres JE, Gozal YM, Nuckton TJ. Characterization and developmental aspects of anoxia-induced gasping in the rat. Biol Neonate 1996;70:280288.
  • 18
    Menegazzi JJ, Check BD. Spontaneous agonal respiration in a swine model of out-of-hospital cardiac arrest. Acad Emerg Med 1995;2:10531056.
  • 19
    St-John WM, Paton JF. Respiratory-modulated neuronal activities of the rostral medulla which may generate gasping. Respir Physiol Neurobiol 2003;135:97101.
  • 20
    Xie J, Weil MH, Sun S, et al. Spontaneous gasping generates cardiac output during cardiac arrest. Crit Care Med 2004;32:238240.
  • 21
    Crowe DT Jr. Cardiopulmonary resuscitation in the dog: A review and proposed new guidelines (Part I). Semin Vet Med Surg (Small Anim) 1988;3:321327.
  • 22
    Henik RA. Basic life support and external cardiac compression in dogs and cats. J Am Vet Med Assoc 1992;200:19251931.
  • 23
    Crowe DT, Fox PR, Devey JJ, Spreng D. Cardiopulmonary and cerebral resuscitation. In: FoxPR, SissonD, MoisseN, eds. Textbook of Canine and Feline Cardiology, Principles and Clinical Practice, 2nd ed. Philadelphia, PA: WB Saunders Co; 1999:427445.
  • 24
    Crowe DT. Triage and trauma management. In: MurtaughRJ, KaplanPM, eds. Veterinary Emergency and Critical Care. St Louis, NO: Mosby-Year Book; 1992:77121.
  • 25
    Evans AT. New thoughts on cardiopulmonary resuscitation. Vet Clin North Am Small Anim Pract 1999;29:819829, viii.
  • 26
    Johnson PA, Mann FA, Dodam J, et al. Capnographic documentation of nasoesophageal and nasogastric feeding tube placement in dogs. J Vet Emerg Crit Care 2002;12:227233.
  • 27
    White SJ, Slovis CM. Inadvertent esophageal intubation in the field: Reliance on a fool's “gold standard.” Acad Emerg Med 1997;4:8991.
  • 28
    Bhende MS, Karasic DG, Menegazzi JJ. Evaluation of an end-tidal CO2 detector during cardiopulmonary resuscitation in a canine model for pediatric cardiac arrest. Pediatr Emerg Care 1995;11:365368.
  • 29
    Kern KB, Sanders AB, Voorhees WD, et al. Changes in expired end-tidal carbon dioxide during cardiopulmonary resuscitation in dogs: A prognostic guide for resuscitation efforts. J Am Coll Cardiol 1989;13:11841189.
  • 30
    Rieser TM. Cardiopulmonary resuscitation. Clin Tech Small Anim Pract 2000;15:7681.
  • 31
    Davies A, Janse J, Reynolds GW. Acupuncture in the relief of respiratory arrest. N Z Vet J 1984;32:109110.
  • 32
    Dani C, Bertini G, Pezzati M, et al. Brain hemodynamic effects of doxapram in preterm infants. Biol Neonate 2006;89:6974.
  • 33
    Ebihara S, Ogawa H, Sasaki H, et al. Doxapram and perception of dyspnea. Chest 2002;121:13801381.
  • 34
    Roll C, Horsch S. Effect of doxapram on cerebral blood flow velocity in preterm infants. Neuropediatrics 2004;35:126129.
  • 35
    Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation 2004;109:19601965.
  • 36
    Haldane S, Marks SL. Cardiopulmonary cerebral resuscitation: Techniques (part I). Comp Cont Ed Pract Vet 2004;26:780790.
  • 37
    Kruse-Elliott KT. Cardiopulmonary resuscitation: Strategies for maximizing success. Vet Med 2001;16:5158.
  • 38
    Aufderheide TP, Lurie KG. Death by hyperventilation: A common and life-threatening problem during cardiopulmonary resuscitation. Crit Care Med 2004;32:S345S351.
  • 39
    Fewell JE, Abendschein DR, Carlson CJ, et al. Continuous positive-pressure ventilation decreases right and left ventricular end-diastolic volumes in the dog. Circ Res 1980;46:125132.
  • 40
    Sykes MK, Adams AP, Finlay WE, et al. The effects of variations in end-expiratory inflation pressure on cardiorespiratory function in normo-, hypo- and hypervolaemic dogs. Br J Anaesth 1970;42:669677.
  • 41
    SOS-KANTO Study Group. Cardiopulmonary resuscitation by bystanders with chest compression only (SOS-KANTO): An observational study. Lancet 2007;369:920926.
  • 42
    Aufderheide TP, Lurie KG. Vital organ blood flow with the impedance threshold device. Crit Care Med 2006;34:S466S473.
  • 43
    Becker LB, Ostrander MP, Barrett J, Kondos GT. Outcome of CPR in a large metropolitan area—Where are the survivors? Ann Emerg Med 1991;20:355361.
  • 44
    Eisenberg MS, Horwood BT, Cummins RO, et al. Cardiac arrest and resuscitation: A tale of 29 cities. Ann Emerg Med 1990;19:179186.
  • 45
    Niemann JT. Cardiopulmonary resuscitation. N Engl J Med 1992;327:10751080.
  • 46
    Paradis NA, Martin GB, Goetting MG, et al. Simultaneous aortic, jugular bulb, and right atrial pressures during cardiopulmonary resuscitation in humans. Insights into mechanisms. Circulation 1989;80:361368.
  • 47
    Shaffner DH, Eleff SM, Brambrink AM, et al. Effect of arrest time and cerebral perfusion pressure during cardiopulmonary resuscitation on cerebral blood flow, metabolism, adenosine triphosphate recovery, and pH in dogs. Crit Care Med 1999;27:13351342.
  • 48
    Niemann JT, Criley JM, Rosborough JP, et al. Predictive indices of successful cardiac resuscitation after prolonged arrest and experimental cardiopulmonary resuscitation. Ann Emerg Med 1985;14:521528.
  • 49
    Yannopoulos D, Sigurdsson G, McKnite S, et al. Reducing ventilation frequency combined with an inspiratory impedance device improves CPR efficiency in swine model of cardiac arrest. Resuscitation 2004;61:7582.
  • 50
    Yannopoulos D, McKnite S, Aufderheide TP, et al. Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model of cardiac arrest. Resuscitation 2005;64:363372.
  • 51
    Yannopoulos D, Tang W, Roussos C, et al. Reducing ventilation frequency during cardiopulmonary resuscitation in a porcine model of cardiac arrest. Respir Care 2005;50:628635.
  • 52
    Yannopoulos D, Aufderheide TP, McKnite S, et al. Hemodynamic and respiratory effects of negative tracheal pressure during CPR in pigs. Resuscitation 2006;69:487494.
  • 53
    Guerci AD, Shi AY, Levin H, et al. Transmission of intrathoracic pressure to the intracranial space during cardiopulmonary resuscitation in dogs. Circ Res 1985;56:2030.
  • 54
    Marino BS, Yannopoulos D, Sigurdsson G, et al. Spontaneous breathing through an inspiratory impedance threshold device augments cardiac index and stroke volume index in a pediatric porcine model of hemorrhagic hypovolemia. Crit Care Med 2004;32:S398S405.
  • 55
    Yannopoulos D, Metzger A, McKnite S, et al. Intrathoracic pressure regulation improves vital organ perfusion pressures in normovolemic and hypovolemic pigs. Resuscitation 2006;70:445453.
  • 56
    Abella BS, Sandbo N, Vassilatos P, et al. Chest compression rates during cardiopulmonary resuscitation are suboptimal: A prospective study during in-hospital cardiac arrest. Circulation 2005;111:428434.
  • 57
    Abella BS, Alvarado JP, Myklebust H, et al. Quality of cardiopulmonary resuscitation during in-hospital cardiac arrest. JAMA 2005;293:305310.
  • 58
    Babbs CF, Kern KB. Optimum compression to ventilation ratios in CPR under realistic, practical conditions: A physiological and mathematical analysis. Resuscitation 2002;54:147157.
  • 59
    Berg RA, Cobb LA, Doherty A, et al. Chest compressions and basic life support-defibrillation. Ann Emerg Med 2001;37:S26S35.
  • 60
    Valenzuela TD, Kern KB, Clark LL, et al. Interruptions of chest compressions during emergency medical systems resuscitation. Circulation 2005;112:12591265.
  • 61
    Wik L, Kramer-Johansen J, Myklebust H, et al. Quality of cardiopulmonary resuscitation during out-of-hospital cardiac arrest. JAMA 2005;293:299304.
  • 62
    Guerci AD, Halperin HR, Beyar R, et al. Aortic diameter and pressure-flow sequence identify mechanism of blood flow during external chest compression in dogs. J Am Coll Cardiol 1989;14:790798.
  • 63
    Andreka P, Frenneaux MP. Haemodynamics of cardiac arrest and resuscitation. Curr Opin Crit Care 2006;12:198203.
  • 64
    Handley AJ, Handley JA. Performing chest compressions in a confined space. Resuscitation 2004;61:5561.
  • 65
    Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-chest cardiac massage. JAMA 1960;173:10641067.
  • 66
    Yannopoulos D, Aufderheide TP, Gabrielli A, et al. Clinical and hemodynamic comparison of 15:2 and 30:2 compression-to-ventilation ratios for cardiopulmonary resuscitation. Crit Care Med 2006;34:14441449.
  • 67
    Mateer JR, Stueven HA, Thompson BM, et al. Pre-hospital IAC-CPR versus standard CPR: Paramedic resuscitation of cardiac arrests. Am J Emerg Med 1985;3:143146.
  • 68
    Waldman PJ, Walters BL, Grunau CF. Pancreatic injury associated with interposed abdominal compressions in pediatric cardiopulmonary resuscitation. Am J Emerg Med 1984;2:510512.
  • 69
    Malzer R, Zeiner A, Binder M, et al. Hemodynamic effects of active compression-decompression after prolonged CPR. Resuscitation 1996;31:243253.
  • 70
    Orliaguet GA, Carli PA, Rozenberg A, et al. End-tidal carbon dioxide during out-of-hospital cardiac arrest resuscitation: Comparison of active compression-decompression and standard CPR. Ann Emerg Med 1995;25:4851.
  • 71
    Berg RA, Hilwig RW, Kern KB, Ewy GA. Precountershock cardiopulmonary resuscitation improves ventricular fibrillation median frequency and myocardial readiness for successful efibrillation from prolonged ventricular fibrillation: A randomized, controlled swine study. Ann Emerg Med 2002;40:563570.
  • 72
    Berg RA, Hilwig RW, Kern KB, et al. Automated external defibrillation versus manual defibrillation for prolonged ventricular fibrillation: Lethal delays of chest compressions before and after countershocks. Ann Emerg Med 2003;42:458467.
  • 73
    Kern KB, Ewy GA, Sanders AB, et al. Neurologic outcome following successful cardiopulmonary resuscitation in dogs. Resuscitation 1986;14:149155.
  • 74
    Shultz JJ, Coffeen P, Sweeney M, et al. Evaluation of standard and active compression-decompression CPR in an acute human model of ventricular fibrillation. Circulation 1994;89:684693.
  • 75
    Lurie KG, Mulligan KA, McKnite S, et al. Optimizing standard cardiopulmonary resuscitation with an inspiratory impedance threshold valve. Chest 1998;113:10841090.
  • 76
    Plaisance P, Lurie KG, Payen D. Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation: A randomized evaluation in patients in cardiac arrest. Circulation 2000;101:989994.
  • 77
    Wolcke BB, Mauer DK, Schoefmann MF, et al. Comparison of standard cardiopulmonary resuscitation versus the combination of active compression-decompression cardiopulmonary resuscitation and an inspiratory impedance threshold device for out-of-hospital cardiac arrest. Circulation 2003;108:22012205.
  • 78
    Crowe DT Jr. Cardiopulmonary resuscitation in the dog: A review and proposed new guidelines (Part II). Semin Vet Med Surg (Small Anim) 1988;3:328348.
  • 79
    Haskins SC. Internal cardiac compression. J Am Vet Med Assoc 1992;200:19451946.
  • 80
    Wittnich C, Belanger MP, Saberno TA, et al. External vs internal cardiac massage. Comp Cont Ed Pract Vet 1991;13:5059.
  • 81
    Barton L, Crowe DT. Open chest resuscitation. In: BonaguraJ, ed. Kirk's Current Veterinary Therapy XIII. Philadelphia, PA: WB Saunders Co; 2000:147149.
  • 82
    Heller MB. Open-chest cardiac massage. The possible rebirth of an old procedure. Postgrad Med 1990;87:189194.
  • 83
    Rush JE, Wingfield WE. Recognition and frequency of dysrhythmias during cardiopulmonary arrest. J Am Vet Med Assoc 1992;200:19321937.
  • 84
    Waldrop JE, Rozanski EA, Swank ED, et al. Causes of cardiopulmonary arrest, resuscitation management, and functional outcome in dogs and cats surviving cardiopulmonary arrest. J Vet Emerg Crit Care 2004;14:2229.
  • 85
    Bonvini RF, Camenzind E. Pacemaker spikes misleading the diagnosis of ventricular fibrillation. Resuscitation 2005;66:241243.
  • 86
    Callaway CW, Menegazzi JJ. Waveform analysis of ventricular fibrillation to predict defibrillation. Curr Opin Crit Care 2005;11:192199.
  • 87
    Guyette FX, Guimond GE, Hostler D, Callaway CW. Vasopressin administered with epinephrine is associated with a return of a pulse in out-of-hospital cardiac arrest. Resuscitation 2004;63:277282.
  • 88
    Martin DR, Gavin T, Bianco J, et al. Initial countershock in the treatment of asystole. Resuscitation 1993;26:6368.
  • 89
    Wenzel V, Lindner KH, Prengel AW, et al. Endobronchial vasopressin improves survival during cardiopulmonary resuscitation in pigs. Anesthesiology 1997;86:13751381.
  • 90
    Wenzel V, Lindner KH, Prengel AW, et al. Vasopressin improves vital organ blood flow after prolonged cardiac arrest with postcountershock pulseless electrical activity in pigs. Crit Care Med 1999;27:486492.
  • 91
    Wenzel V, Krismer AC, Arntz HR, et al. A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med 2004;350:105113.
  • 92
    Fox PR, Sisson D, Moisse N. Textbook of Canine and Feline Cardiology, Principles and Clinical Practice, 2nd ed. Philadelphia, PA: WB Saunders Co; 1999.
  • 93
    Cummins RO, Chamberlain DA, Abramson NS, et al. Recommended guidelines for uniform reporting of data from out-of-hospital cardiac arrest: The Utstein Style. A statement for health professionals from a task force of the American Heart Association, the European Resuscitation Council, the Heart and Stroke Foundation of Canada, and the Australian Resuscitation Council. Circulation 1991;84:960975.
  • 94
    Gliner BE, White RD. Electrocardiographic evaluation of defibrillation shocks delivered to out-of-hospital sudden cardiac arrest patients. Resuscitation 1999;41:133144.
  • 95
    White RD. External defibrillation: The need for uniformity in analyzing and reporting results. Ann Emerg Med 1998;32:234236.
  • 96
    Carpenter J, Rea TD, Murray JA, et al. Defibrillation waveform and post-shock rhythm in out-of-hospital ventricular fibrillation cardiac arrest. Resuscitation 2003;59:189196.
  • 97
    Morrison LJ, Dorian P, Long J, et al. Out-of-hospital cardiac arrest rectilinear biphasic to monophasic damped sine defibrillation waveforms with advanced life support intervention trial (ORBIT). Resuscitation 2005;66:149157.
  • 98
    Van Alem AP, Chapman FW, Lank P, et al. A prospective, randomised and blinded comparison of first shock success of monophasic and biphasic waveforms in out-of-hospital cardiac arrest. Resuscitation 2003;58:1724.
  • 99
    Yoon RS, DeMonte TP, Hasanov KF, et al. Measurement of thoracic current flow in pigs for the study of defibrillation and cardioversion. IEEE Trans Biomed Eng 2003;50:11671173.
  • 100
    Dahl CF, Ewy GA, Warner ED, Thomas ED. Myocardial necrosis from direct current countershock. Effect of paddle electrode size and time interval between discharges. Circulation 1974;50:956961.
  • 101
    Kerber RE, Grayzel J, Hoyt R, et al. Transthoracic resistance in human defibrillation. Influence of body weight, chest size, serial shocks, paddle size and paddle contact pressure. Circulation 1981;63:676682.
  • 102
    Stults KR, Brown DD, Cooley F, Kerber RE. Self-adhesive monitor/defibrillation pads improve prehospital defibrillation success. Ann Emerg Med 1987;16:872877.
  • 103
    Berg RA, Chapman FW, Berg MD, et al. Attenuated adult biphasic shocks compared with weight-based monophasic shocks in a swine model of prolonged pediatric ventricular fibrillation. Resuscitation 2004;61:189197.
  • 104
    Cole SG, Otto CM, Hughes D. Cardiopulmonary cerebral resuscitation in small animals—A clinical practice review (part II). J Vet Emerg Crit Care 2003;13:1323.
  • 105
    Cammarata G, Weil MH, Csapoczi P, et al. Challenging the rationale of three sequential shocks for defibrillation. Resuscitation 2006;69:2327.
  • 106
    Yakaitis RW, Ewy GA, Otto CW, et al. Influence of time and therapy on ventricular defibrillation in dogs. Crit Care Med 1980;8:157163.
  • 107
    Kern KB, Hilwig RW, Berg RA, et al. Importance of continuous chest compressions during cardiopulmonary resuscitation: Improved outcome during a simulated single lay-rescuer scenario. Circulation 2002;105:645649.
  • 108
    Rea TD, Eisenberg MS, Sinibaldi G, White RD. Incidence of EMS-treated out-of-hospital cardiac arrest in the United States. Resuscitation 2004;63:1724.
  • 109
    Yu T, Weil MH, Tang W, et al. Adverse outcomes of interrupted precordial compression during automated defibrillation. Circulation 2002;106:368372.
  • 110
    Hess EP, White RD. Ventricular fibrillation is not provoked by chest compression during post-shock organized rhythms in out-of-hospital cardiac arrest. Resuscitation 2005;66:711.
  • 111
    White RD, Russell JK. Refibrillation, resuscitation and survival in out-of-hospital sudden cardiac arrest victims treated with biphasic automated external defibrillators. Resuscitation 2002;55:1723.
  • 112
    Bain AC, Swerdlow CD, Love CJ, et al. Multicenter study of principles-based waveforms for external defibrillation. Ann Emerg Med 2001;37:512.
  • 113
    Eftestol T, Sunde K, Steen PA. Effects of interrupting precordial compressions on the calculated probability of defibrillation success during out-of-hospital cardiac arrest. Circulation 2002;105:22702273.
  • 114
    Koster RW, Walker RG, Van Alem AP. Definition of successful defibrillation. Crit Care Med 2006;34:S423S426.
  • 115
    Sato Y, Weil MH, Sun S, et al. Adverse effects of interrupting precordial compression during cardiopulmonary resuscitation. Crit Care Med 1997;25:733736.
  • 116
    Cobb LA, Fahrenbruch CE, Walsh TR, et al. Influence of cardiopulmonary resuscitation prior to defibrillation in patients with out-of-hospital ventricular fibrillation. JAMA 1999;281:11821188.
  • 117
    Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: A randomized trial. JAMA 2003;289:13891395.
  • 118
    Dorian P, Cass D, Schwartz B, et al. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med 2002;346:884890.
  • 119
    Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med 1999;341:871878.
  • 120
    Levine JH, Massumi A, Scheinman MM, et al. Intravenous amiodarone for recurrent sustained hypotensive ventricular tachyarrhythmias. Intravenous Amiodarone Multicenter Trial Group. J Am Coll Cardiol 1996;27:6775.
  • 121
    Gertsch M, Hottinger S, Hess T. Serial chest thumps for the treatment of ventricular tachycardia in patients with coronary artery disease. Clin Cardiol 1992;15:181188.
  • 122
    Morgera T, Baldi N, Chersevani D, et al. Chest thump and ventricular tachycardia. Pacing Clin Electrophysiol 1979;2:6975.
  • 123
    Weihui L, Kohl P, Trayanova N. Myocardial ischemia lowers precordial thump efficacy: An inquiry into mechanisms using three-dimensional simulations. Heart Rhythm 2006;3:179186.
  • 124
    Cummins RO, Eisenberg M, Bergner L, Murray JA. Sensitivity, accuracy, and safety of an automatic external defibrillator. Lancet 1984;2:318320.
  • 125
    Davis EA, Mosesso VN Jr. Performance of police first responders in utilizing automated external defibrillation on victims of sudden cardiac arrest. Prehosp Emerg Care 1998;2:101107.
  • 126
    White RD, Vukov LF, Bugliosi TF. Early defibrillation by police: Initial experience with measurement of critical time intervals and patient outcome. Ann Emerg Med 1994;23:10091013.
  • 127
    White RD, Hankins DG, Bugliosi TF. Seven years' experience with early defibrillation by police and paramedics in an emergency medical services system. Resuscitation 1998;39:145151.
  • 128
    Atkins DL, Jorgenson DB. Attenuated pediatric electrode pads for automated external defibrillator use in children. Resuscitation 2005;66:3137.
  • 129
    Jorgenson D, Morgan C, Snyder D, et al. Energy attenuator for pediatric application of an automated external defibrillator. Crit Care Med 2002;30:S145S147.
  • 130
    Samson RA, Berg RA, Bingham R, et al. Use of automated external defibrillators for children: An update: An advisory statement from the pediatric advanced life support task force, International Liaison Committee on Resuscitation. Circulation 2003;107:32503255.
  • 131
    Berg RA, Samson RA, Berg MD, et al. Better outcome after pediatric defibrillation dosage than adult dosage in a swine model of pediatric ventricular fibrillation. J Am Coll Cardiol 2005;45:786789.
  • 132
    Barsan WG, Levy RC, Weir H. Lidocaine levels during CPR: Differences after peripheral venous, central venous, and intracardiac injections. Ann Emerg Med 1981;10:7378.
  • 133
    Kuhn GJ, White BC, Swetnam RE, et al. Peripheral vs central circulation times during CPR: A pilot study. Ann Emerg Med 1981;10:417419.
  • 134
    Banerjee S, Singhi SC, Singh S, Singh M. The intraosseous route is a suitable alternative to intravenous route for fluid resuscitation in severely dehydrated children. Indian Pediatr 1994;31:15111520.
  • 135
    Jespersen HF, Granborg J, Hansen U, et al. Feasibility of intracardiac injection of drugs during cardiac arrest. Eur Heart J 1990;11:269274.
  • 136
    Sabin HI, Coghill SB, Khunti K, McNeill GO. Accuracy of intracardiac injections determined by a post-mortem study. Lancet 1983;2:10541055.
  • 137
    Emerman CL, Pinchak AC, Hancock D, Hagen JF. The effect of bolus injection on circulation times during cardiac arrest. Am J Emerg Med 1990;8:190193.
  • 138
    Emerman CL, Pinchak AC, Hagen JF, Hancock DE. Dye circulation times during cardiac arrest. Resuscitation 1990;19:5360.
  • 139
    Otto C, Crowe D. Intraosseous resuscitation techniques and applications. In: KirkRW, BonaguraJD, eds. Kirk's Current Veterinary Therapy XI. Philadelphia, PA: WB Saunders Co; 1992:107112.
  • 140
    Hasegawa EA. The endotracheal use of emergency drugs. Heart Lung 1986;15:6063.
  • 141
    Jasani MS, Nadkarni VM, Finkelstein MS, et al. Effects of different techniques of endotracheal epinephrine administration in pediatric porcine hypoxic-hypercarbic cardiopulmonary arrest. Crit Care Med 1994;22:11741180.
  • 142
    Johnston C. Endotracheal drug delivery. Pediatr Emerg Care 1992;8:9497.
  • 143
    Prengel AW, Lindner KH, Hahnel J, Ahnefeld FW. Endotracheal and endobronchial lidocaine administration: Effects on plasma lidocaine concentration and blood gases. Crit Care Med 1991;19:911915.
  • 144
    Prengel AW, Lindner KH, Hahnel JH, Georgieff M. Pharmacokinetics and technique of endotracheal and deep endobronchial lidocaine administration. Anesth Analg 1993;77:985989.
  • 145
    Vaknin Z, Manisterski Y, Ben-Abraham R, et al. Is endotracheal adrenaline deleterious because of the beta adrenergic effect? Anesth Analg 2001;92:14081412.
  • 146
    Hahnel JH, Lindner KH, Schurmann C, et al. Plasma lidocaine levels and PaO2 with endobronchial administration: Dilution with normal saline or distilled water? Ann Emerg Med 1990;19:13141317.
  • 147
    Hahnel JH, Lindner KH, Schurmann C, et al. What is the optimal volume of administration for endobronchial drugs? Am J Emerg Med 1990;8:504508.
  • 148
    Naganobu K, Hasebe Y, Uchiyama Y, et al. A comparison of distilled water and normal saline as diluents for endobronchial administration of epinephrine in the dog. Anesth Analg 2000;91:317321.
  • 149
    Paret G, Vaknin Z, Ezra D, et al. Epinephrine pharmacokinetics and pharmacodynamics following endotracheal administration in dogs: The role of volume of diluent. Resuscitation 1997;35:7782.
  • 150
    Paret G, Mazkereth R, Sella R, et al. Atropine pharmacokinetics and pharmacodynamics following endotracheal versus endobronchial administration in dogs. Resuscitation 1999;41:5762.
  • 151
    Redding JS, Asuncion JS, Pearson JW. Effective routes of drug administration during cardiac arrest. Anesth Analg 1967;46:253258.
  • 152
    Hornchen U, Schuttler J, Stoeckel H, et al. Endobronchial instillation of epinephrine during cardiopulmonary resuscitation. Crit Care Med 1987;15:10371039.
  • 153
    Manisterski Y, Vaknin Z, Ben-Abraham R, et al. Endotracheal epinephrine: A call for larger doses. Anesth Analg 2002;95:10371041, table.
  • 154
    McCrirrick A, Monk CR. Comparison of i.v. and intra-tracheal administration of adrenaline. Br J Anaesth 1994;72:529532.
  • 155
    Ralston SH, Tacker WA, Showen L, et al. Endotracheal versus intravenous epinephrine during electromechanical dissociation with CPR in dogs. Ann Emerg Med 1985;14:10441048.
  • 156
    Efrati O, Ben-Abraham R, Barak A, et al. Endobronchial adrenaline: Should it be reconsidered? Dose response and haemodynamic effect in dogs. Resuscitation 2003;59:117122.
  • 157
    Efrati O, Barak A, Ben-Abraham R, et al. Should vasopressin replace adrenaline for endotracheal drug administration? Crit Care Med 2003;31:572576.
  • 158
    Goetting MG, Paradis NA. High-dose epinephrine improves outcome from pediatric cardiac arrest. Ann Emerg Med 1991;20:2226.
  • 159
    Keeley SR, Bohn DJ. The use of inotropic and afterload-reducing agents in neonates. Clin Perinatol 1988;15:467489.
  • 160
    McCrirrick A, Kestin I. Haemodynamic effects of tracheal compared with intravenous adrenaline. Lancet 1992;340:868870.
  • 161
    Ditchey RV, Lindenfeld J. Potential adverse effects of volume loading on perfusion of vital organs during closed-chest resuscitation. Circulation 1984;69:181189.
  • 162
    Gentile NT, Martin GB, Appleton TJ, et al. Effects of arterial and venous volume infusion on coronary perfusion pressures during canine CPR. Resuscitation 1991;22:5563.
  • 163
    Maruyama M, Pieper GM, Kalyanaraman B, et al. Effects of hydroxyethyl starch conjugated deferoxamine on myocardial functional recovery following coronary occlusion and reperfusion in dogs. J Cardiovasc Pharmacol 1991;17:166175.
  • 164
    Oz MC, Zikria BA, McLeod PF, Popilkis SJ. Hydroxyethyl starch macromolecule and superoxide dismutase effects on myocardial reperfusion injury. Am J Surg 1991;162:5962.
  • 165
    Prough DS, Whitley JM, Taylor CL, et al. Small-volume resuscitation from hemorrhagic shock in dogs: Effects on systemic hemodynamics and systemic blood flow. Crit Care Med 1991;19:364372.
  • 166
    Rudloff E, Kirby R. Colloids: Current recommendations. In: BonaguraJ, ed. Kirk's Current Veterinary Therapy XIII. Philadelphia, PA: WB Saunders Co; 2000:131136.
  • 167
    Zikria BA, Subbarao C, Oz MC, et al. Hydroxyethyl starch macromolecules reduce myocardial reperfusion injury. Arch Surg 1990;125:930934.
  • 168
    Breil M, Krep H, Sinn D, et al. Hypertonic saline improves myocardial blood flow during CPR, but is not enhanced further by the addition of hydroxy ethyl starch. Resuscitation 2003;56:307317.
  • 169
    Fischer M, Dahmen A, Standop J, et al. Effects of hypertonic saline on myocardial blood flow in a porcine model of prolonged cardiac arrest. Resuscitation 2002;54:269280.
  • 170
    Pellis T, Weil MH, Tang W, et al. Evidence favoring the use of an alpha2-selective vasopressor agent for cardiopulmonary resuscitation. Circulation 2003;108:27162721.
  • 171
    Zhong JQ, Dorian P. Epinephrine and vasopressin during cardiopulmonary resuscitation. Resuscitation 2005;66:263269.
  • 172
    Niemann JT, Haynes KS, Garner D, et al. Postcountershock pulseless rhythms: Response to CPR, artificial cardiac pacing, and adrenergic agonists. Ann Emerg Med 1986;15:112120.
  • 173
    Wright M, Heath RB, Wingfield WE. Effects of xylazine and ketamine on epinephrine-induced arrhythmia in the dog. Vet Surg 1987;16:398403.
  • 174
    Michael JR, Guerci AD, Koehler RC, et al. Mechanisms by which epinephrine augments cerebral and myocardial perfusion during cardiopulmonary resuscitation in dogs. Circulation 1984;69:822835.
  • 175
    Yakaitis RW, Otto CW, Blitt CD. Relative importance of alpha and beta adrenergic receptors during resuscitation. Crit Care Med 1979;7:293296.
  • 176
    Schleien CL, Dean JM, Koehler RC, et al. Effect of epinephrine on cerebral and myocardial perfusion in an infant animal preparation of cardiopulmonary resuscitation. Circulation 1986;73:809817.
  • 177
    Ditchey RV, Lindenfeld J. Failure of epinephrine to improve the balance between myocardial oxygen supply and demand during closed-chest resuscitation in dogs. Circulation 1988;78:382389.
  • 178
    Ditchey RV, Rubio-Perez A, Slinker BK. Beta-adrenergic blockade reduces myocardial injury during experimental cardiopulmonary resuscitation. J Am Coll Cardiol 1994;24:804812.
  • 179
    Duncker DJ, Zhang J, Crampton MJ, Bache RJ. Alpha 1-adrenergic tone does not influence the transmural distribution of myocardial blood flow during exercise in dogs with pressure overload left ventricular hypertrophy. Basic Res Cardiol 1995;90:7383.
  • 180
    Grupp IL, Lorenz JN, Walsh RA, et al. Overexpression of alpha1B-adrenergic receptor induces left ventricular dysfunction in the absence of hypertrophy. Am J Physiol 1998;275:H1338H1350.
  • 181
    Ishibashi Y, Duncker DJ, Bache RJ. Endogenous nitric oxide masks alpha 2-adrenergic coronary vasoconstriction during exercise in the ischemic heart. Circ Res 1997;80:196207.
  • 182
    Landzberg JS, Parker JD, Gauthier DF, Colucci WS. Effects of myocardial alpha 1-adrenergic receptor stimulation and blockade on contractility in humans. Circulation 1991;84:16081614.
  • 183
    Otto CW, Yakaitis RW, Blitt CD. Mechanism of action of epinephrine in resuscitation from asphyxial arrest. Crit Care Med 1981;9:364365.
  • 184
    Otto CW, Yakaitis RW. The role of epinephrine in CPR: A reappraisal. Ann Emerg Med 1984;13:840843.
  • 185
    Mazkereth R, Paret G, Ezra D, et al. Epinephrine blood concentrations after peripheral bronchial versus endotracheal administration of epinephrine in dogs. Crit Care Med 1992;20:15821587.
  • 186
    Raymondos K, Panning B, Leuwer M, et al. Absorption and hemodynamic effects of airway administration of adrenaline in patients with severe cardiac disease. Ann Intern Med 2000;132:800803.
  • 187
    Krismer AC, Wenzel V, Stadlbauer KH, et al. Vasopressin during cardiopulmonary resuscitation: A progress report. Crit Care Med 2004;32:S432S435.
  • 188
    Wenzel V, Lindner KH. Vasopressin combined with epinephrine during cardiac resuscitation: A solution for the future? Crit Care 2006;10:125.
  • 189
    Biondi-Zoccai GG, Abbate A, Parisi Q, et al. Is vasopressin superior to adrenaline or placebo in the management of cardiac arrest? A meta-analysis. Resuscitation 2003;59:221224.
  • 190
    Paradis NA, Wenzel V, Southall J. Pressor drugs in the treatment of cardiac arrest. Cardiol Clin 2002;20:6178, viii.
  • 191
    Stiell IG, Hebert PC, Weitzman BN, et al. High-dose epinephrine in adult cardiac arrest. N Engl J Med 1992;327:10451050.
  • 192
    Hilwig RW, Kern KB, Berg RA, et al. Catecholamines in cardiac arrest: Role of alpha agonists, beta-adrenergic blockers and high-dose epinephrine. Resuscitation 2000;47:203208.
  • 193
    Lindner KH, Prengel AW, Pfenninger EG, et al. Vasopressin improves vital organ blood flow during closed-chest cardiopulmonary resuscitation in pigs. Circulation 1995;91:215221.
  • 194
    Oyama H, Suzuki Y, Satoh S, et al. Role of nitric oxide in the cerebral vasodilatory responses to vasopressin and oxytocin in dogs. J Cereb Blood Flow Metab 1993;13:285290.
  • 195
    Asfar P, Hauser B, Radermacher P, Matejovic M. Catecholamines and vasopressin during critical illness. Crit Care Clin 2006;22:131, viii.
  • 196
    Gessner P. The effects of vasopressin on the renal system in vasodilatory shock. Dimens Crit Care Nurs 2006;25:110.
  • 197
    Holmes CL, Patel BM, Russell JA, Walley KR. Physiology of vasopressin relevant to management of septic shock. Chest 2001;120:9891002.
  • 198
    Wakatsuki T, Nakaya Y, Inoue I. Vasopressin modulates K(+)-channel activities of cultured smooth muscle cells from porcine coronary artery. Am J Physiol 1992;263:H491H496.
  • 199
    Schwartz J, Reid IA. Characteristics of the receptors which mediate the stimulation of ACTH secretion by vasopressin in conscious dogs. Neuroendocrinology 1986;42:9396.
  • 200
    Angstwurm M. Vasopressin: A tool as rescue therapy? Take care of dosages and adverse effects! Crit Care Med 2005;33:27132714.
  • 201
    Efrati O, Barak A, Ben-Abraham R, et al. Hemodynamic effects of tracheal administration of vasopressin in dogs. Resuscitation 2001;50:227232.
  • 202
    Asfar P, Radermacher P, Hauser B. Vasopressin and splanchnic blood flow: Vasoconstriction does not equal vasoconstriction in every organ. Intensive Care Med 2006;32:2123.
  • 203
    Salam AM. The therapeutic potential of vasopressin in cardiopulmonary resuscitation. Expert Opin Pharmacother 2005;6:517520.
  • 204
    Schmittinger CA, Astner S, Astner L, et al. Cardiopulmonary resuscitation with vasopressin in a dog. Vet Anaesth Analg 2005;32:112114.
  • 205
    Prengel AW, Lindner KH, Keller A. Cerebral oxygenation during cardiopulmonary resuscitation with epinephrine and vasopressin in pigs. Stroke 1996;27:12411248.
  • 206
    Dhingra RC, Amat YL, Wyndham C, et al. Electrophysiologic effects of atropine on human sinus node and atrium. Am J Cardiol 1976;38:429434.
  • 207
    Kent KM, Epstein SE, Cooper T, Jacobowitz DM. Cholinergic innervation of the canine and human ventricular conducting system. Anatomic and electrophysiologic correlations. Circulation 1974;50:948955.
  • 208
    Schweitzer P, Mark H. The effect of atropine on cardiac arrhythmias and conduction. Part 2. Am Heart J 1980;100:255261.
  • 209
    Schweitzer P, Mark H. The effect of atropine on cardiac arrhythmias and conduction. Part 1. Am Heart J 1980;100:119127.
  • 210
    Blecic S, Chaskis C, Vincent JL. Atropine administration in experimental electromechanical dissociation. Am J Emerg Med 1992;10:515518.
  • 211
    DeBehnke DJ, Swart GL, Spreng D, Aufderheide TP. Standard and higher doses of atropine in a canine model of pulseless electrical activity. Acad Emerg Med 1995;2:10341041.
  • 212
    Williams ML, Woelfel A, Cascio WE, et al. Intravenous amiodarone during prolonged resuscitation from cardiac arrest. Ann Intern Med 1989;110:839842.
  • 213
    Somberg JC, Bailin SJ, Haffajee CI, et al. Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia. Am J Cardiol 2002;90:853859.
  • 214
    Rea RS, Kane-Gill SL, Rudis MI, et al. Comparing intravenous amiodarone or lidocaine, or both, outcomes for inpatients with pulseless ventricular arrhythmias. Crit Care Med 2006;34:16171623.
  • 215
    Mathews KA. Veterinary Emergency and Critical Care, 2nd ed. Guelph, ON: Lifelearn Inc; 2006.
  • 216
    Weaver WD, Fahrenbruch CE, Johnson DD, et al. Effect of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation. Circulation 1990;82:20272034.
  • 217
    Dorian P, Fain ES, Davy JM, Winkle RA. Lidocaine causes a reversible, concentration-dependent increase in defibrillation energy requirements. J Am Coll Cardiol 1986;8:327332.
  • 218
    Echt DS, Gremillion ST, Lee JT, et al. Effects of procainamide and lidocaine on defibrillation energy requirements in patients receiving implantable cardioverter defibrillator devices. J Cardiovasc Electrophysiol 1994;5:752760.
  • 219
    Fox PR, Kaplan PM. Feline arrhythmias. Contemp Issues in Small Animal Practice 1987;7:251.
  • 220
    Papich M. Saunders Handbook of Veterinary Drugs. Philadelphia, PA: Saunders Co; 2002.
  • 221
    Arieff AI. Indications for use of bicarbonate in patients with metabolic acidosis. Br J Anaesth 1991;67:165177.
  • 222
    Bradberry SM, Thanacoody HK, Watt BE, et al. Management of the cardiovascular complications of tricyclic antidepressant poisoning: Role of sodium bicarbonate. Toxicol Rev 2005;24:195204.
  • 223
    Hoffmann AC, Scheidegger D. Pharmacology of cardiopulmonary resuscitation. Ann Fr Anesth Reanim 1990;9:204207.
  • 224
    Kamel KS, Wei C. Controversial issues in the treatment of hyperkalaemia. Nephrol Dial Transplant 2003;18:22152218.
  • 225
    Kim HJ. Acute therapy for hyperkalemia with the combined regimen of bicarbonate and beta(2)-adrenergic agonist (salbutamol) in chronic renal failure patients. J Korean Med Sci 1997;12:111116.
  • 226
    Kim HJ, Han SW. Therapeutic approach to hyperkalemia. Nephron 2002;92 (Suppl 1):3340.
  • 227
    Redman J, Worthley LI. Antiarrhythmic and haemodynamic effects of the commonly used intravenous electrolytes. Crit Care Resusc 2001;3:2234.
  • 228
    Angelos MG, DeBehnke DJ, Leasure JE. Arterial blood gases during cardiac arrest: Markers of blood flow in a canine model. Resuscitation 1992;23:101111.
  • 229
    Graf H, Leach W, Arieff AI. Evidence for a detrimental effect of bicarbonate therapy in hypoxic lactic acidosis. Science 1985;227:754756.
  • 230
    Hughes WG, Ruedy JR. Should calcium be used in cardiac arrest? Am J Med 1986;81:285296.
  • 231
    Ramoska EA, Spiller HA, Winter M, Borys D. A one-year evaluation of calcium channel blocker overdoses: Toxicity and treatment. Ann Emerg Med 1993;22:196200.
  • 232
    Urban P, Scheidegger D, Buchmann B, Barth D. Cardiac arrest and blood ionized calcium levels. Ann Intern Med 1988;109:110113.
  • 233
    Plumb DC. Veterinary Drug Handbook, 4th ed. Ames, IA: Iowa State University Press; 2002.
  • 234
    Cardenas-Rivero N, Chernow B, Stoiko MA, et al. Hypocalcemia in critically ill children. J Pediatr 1989;114:946951.
  • 235
    Mischke R, Hanies R, Lange K, Rivera Ramirez PA. The effect of the albumin concentration on the relation between the concentration of ionized calcium and total calcium in the blood of dogs. Dtsch Tierarztl Wochenschr 1996;103:199204.
  • 236
    Schenck PA, Chew DJ. Prediction of serum ionized calcium concentration by use of serum total calcium concentration in dogs. Am J Vet Res 2005;66:13301336.
  • 237
    Altura BT, Altura BM. Endothelium-dependent relaxation in coronary arteries requires magnesium ions. Br J Pharmacol 1987;91:449451.
  • 238
    Dubey A, Solomon R. Magnesium, myocardial ischaemia and arrhythmias. The role of magnesium in myocardial infarction. Drugs 1989;37:17.
  • 239
    Roden DM. Magnesium treatment of ventricular arrhythmias. Am J Cardiol 1989;63:43G46G.
  • 240
    Shattock MJ, Hearse DJ, Fry CH. The ionic basis of the anti-ischemic and anti-arrhythmic properties of magnesium in the heart. J Am Coll Nutr 1987;6:2733.
  • 241
    Keren A, Tzivoni D, Gavish D, et al. Etiology, warning signs and therapy of torsade de pointes. A study of 10 patients. Circulation 1981;64:11671174.
  • 242
    Tzivoni D, Keren A, Stern S. Torsades de pointes versus polymorphous ventricular tachycardia. Am J Cardiol 1983;52:639640.
  • 243
    Tzivoni D, Keren A. Suppression of ventricular arrhythmias by magnesium. Am J Cardiol 1990;65:13971399.
  • 244
    Curry P, Fitchett D, Stubbs W, Krikler D. Ventricular arrhythmias and hypokalaemia. Lancet 1976;2:231233.
  • 245
    Abraham E, Fink S. Conjunctival oxygen tension monitoring in emergency department patients. Am J Emerg Med 1988;6:549554.
  • 246
    Kliegel A, Losert H, Sterz F, et al. Serial lactate determinations for prediction of outcome after cardiac arrest. Medicine (Baltimore) 2004;83:274279.
  • 247
    Nakakimura K, Fleischer JE, Drummond JC, et al. Glucose administration before cardiac arrest worsens neurologic outcome in cats. Anesthesiology 1990;72:10051011.
  • 248
    Steingrub JS, Mundt DJ. Blood glucose and neurologic outcome with global brain ischemia. Crit Care Med 1996;24:802806.
  • 249
    Heissenbuttel RH, Bigger JT Jr. Bretylium tosylate: A newly available antiarrhythmic drug for ventricular arrhythmias. Ann Intern Med 1979;91:229238.
  • 250
    Koch-Weser J. Drug therapy: Bretylium. N Engl J Med 1979;300:473477.
  • 251
    Thurmon JC, Tranquilli WJ, Benson GJ. Preanesthetics and anesthetic adjuncts. In: ThurmonJC, TranquilliWJ, BensonGJ, eds. Lumb & Jones' Veterinary Anesthesia, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1996:183209.
  • 252
    Sanders AB, Atlas M, Ewy GA, et al. Expired PCO2 as an index of coronary perfusion pressure. Am J Emerg Med 1985;3:147149.
  • 253
    Callaham M, Barton C. Prediction of outcome of cardiopulmonary resuscitation from end-tidal carbon dioxide concentration. Crit Care Med 1990;18:358362.
  • 254
    Grmec S, Klemen P. Does the end-tidal carbon dioxide (EtCO2) concentration have prognostic value during out-of-hospital cardiac arrest? Eur J Emerg Med 2001;8:263269.
  • 255
    Sanders AB, Ewy GA, Bragg S, et al. Expired PCO2 as a prognostic indicator of successful resuscitation from cardiac arrest. Ann Emerg Med 1985;14:948952.
  • 256
    Connick M, Berg RA. Femoral venous pulsations during open-chest cardiac massage. Ann Emerg Med 1994;24:11761179.
  • 257
    Cummins RO, Hazinski MF. Cardiopulmonary resuscitation techniques and instruction: When does evidence justify revision? Ann Emerg Med 1999;34:780784.
  • 258
    Allen CH, Ward JD. An evidence-based approach to management of increased intracranial pressure. Crit Care Clin 1998;14:485495.
  • 259
    Crowe DT, Spreng D. Doppler assessment of blood flow & pressure in surgical and critical care patients. In: BonaguraJ, ed. Kirk's Current Veterinary Therapy XII. Philadelphia, PA: WB Saunders Co; 1992:113117.
  • 260
    Weil MH, Rackow EC, Trevino R, et al. Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med 1986;315:153156.
  • 261
    Adrogue HJ, Rashad MN, Gorin AB, et al. Assessing acid-base status in circulatory failure. Differences between arterial and central venous blood. N Engl J Med 1989;320:13121316.
  • 262
    Kette F, Weil MH, Gazmuri RJ, et al. Intramyocardial hypercarbic acidosis during cardiac arrest and resuscitation. Crit Care Med 1993;21:901906.
  • 263
    Tucker KJ, Idris AH, Wenzel V, Orban DJ. Changes in arterial and mixed venous blood gases during untreated ventricular fibrillation and cardiopulmonary resuscitation. Resuscitation 1994;28:137141.
  • 264
    Adrie C, Dib-Conquy M, Laurent I, et al. Successful cardiopulmonary resuscitation after cardiac arrest as a “sepsis-like” syndrome. Circulation 2002;106:562568.
  • 265
    Adrie C, Laurent I, Monchi M, et al. Postresuscitation disease after cardiac arrest: A sepsis-like syndrome? Curr Opin Crit Care 2004;10:208212.
  • 266
    Mayr V, Luckner G, Jochberger S, et al. Arginine vasopressin in advanced cardiovascular failure during the post-resuscitation phase after cardiac arrest. Resuscitation 2007;72:3544.
  • 267
    Bezzant TB, Mortensen JD. Risks and hazards of mechanical ventilation: A collective review of published literature. Dis Mon 1994;40:581638.
  • 268
    Carvalho CR, De Paula Pinto SG, Maranhao B, Bethlem EP. Hyperoxia and lung disease. Curr Opin Pulm Med 1998;4:300304.
  • 269
    Johnston AJ, Steiner LA, Balestreri M, et al. Hyperoxia and the cerebral hemodynamic responses to moderate hyperventilation. Acta Anaesthesiol Scand 2003;47:391396.
  • 270
    Lowe GJ, Ferguson ND. Lung-protective ventilation in neurosurgical patients. Curr Opin Crit Care 2006;12:37.
  • 271
    Sinclair SE, Altemeier WA, Matute-Bello G, Chi EY. Augmented lung injury due to interaction between hyperoxia and mechanical ventilation. Crit Care Med 2004;32:24962501.
  • 272
    Hypothermia After Cardiac Arrest Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549556.
  • 273
    Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557563.
  • 274
    Arrich J. Clinical application of mild therapeutic hypothermia after cardiac arrest. Crit Care Med 2007;35:10411047.
  • 275
    Bernard S, Buist M, Monteiro O, Smith K. Induced hypothermia using large volume, ice-cold intravenous fluid in comatose survivors of out-of-hospital cardiac arrest: A preliminary report. Resuscitation 2003;56:913.
  • 276
    Nozari A, Safar P, Stezoski SW, et al. Critical time window for intra-arrest cooling with cold saline flush in a dog model of cardiopulmonary resuscitation. Circulation 2006;113:26902696.
  • 277
    Safar P, Xiao F, Radovsky A, et al. Improved cerebral resuscitation from cardiac arrest in dogs with mild hypothermia plus blood flow promotion. Stroke 1996;27:105113.
  • 278
    Holzer M, Bernard SA, Hachimi-Idrissi S, et al. Hypothermia for neuroprotection after cardiac arrest: Systematic review and individual patient data meta-analysis. Crit Care Med 2005;33:414418.
  • 279
    Sterz F, Holzer M, Roine R, et al. Hypothermia after cardiac arrest: A treatment that works. Curr Opin Crit Care 2003;9:205210.
  • 280
    Zeiner A, Sunder-Plassmann G, Sterz F, et al. The effect of mild therapeutic hypothermia on renal function after cardiopulmonary resuscitation in men. Resuscitation 2004;60:253261.
  • 281
    Haldane S, Marks SL. Cardiopulmonary cerebral resuscitation: Emergency drugs and postresuscitation care (part 2). Comp Cont Ed Pract Vet 2004;26:791799.
  • 282
    Haskins SC. Therapy for shock. In: BonaguraJ, ed. Kirk's Current Veterinary Therapy XIII. Philadelphia, PA: WB Saunders Co; 2000:140147.
  • 283
    Macintire DK. The practical use of constant-rate infusions. In: BonaguraJ, KirkR, eds. Kirk's Current Veterinary Therapy XII. Philadelphia, PA: WB Saunders Co; 1995:184188.
  • 284
    Zaritsky AL. Catecholamines, inotropic medications, and vasopressor agents. In: ChernowB, ed. Essentials of Critical Care Pharmacology, 2nd ed. Baltimore, MD: Williams & Wilkins; 1994:255272.
  • 285
    Wohl JS, Murtaugh RJ. Use of catecholamines in critical care patients. In: BonaguraJD, KirkR, eds. Kirk's Current Veterinary Therapy XII. Philadelphia, PA: WB Saunders Co; 1995:188193.
  • 286
    Hall LG, Oyen LJ, Taner CB, et al. Fixed-dose vasopressin compared with titrated dopamine and norepinephrine as initial vasopressor therapy for septic shock. Pharmacotherapy 2004;24:10021012.
  • 287
    Tsuneyoshi I, Yamada H, Kakihana Y, et al. Hemodynamic and metabolic effects of low-dose vasopressin infusions in vasodilatory septic shock. Crit Care Med 2001;29:487493.
  • 288
    Astiz ME, Tilly E, Rackow ED, Weil MH. Peripheral vascular tone in sepsis. Chest 1991;99:10721075.
  • 289
    Sibbald WJ, Fox G, Martin C. Abnormalities of vascular reactivity in the sepsis syndrome. Chest 1991;100:155S159S.
  • 290
    Greenway CV, Stark RD. Hepatic vascular bed. Physiol Rev 1971;51:2365.
  • 291
    Insel PA, Snavely MD. Catecholamines and the kidney: Receptors and renal function. Annu Rev Physiol 1981;43:625636.
  • 292
    Booth CM, Boone RH, Tomlinson G, Detsky AS. Is this patient dead, vegetative, or severely neurologically impaired? Assessing outcome for comatose survivors of cardiac arrest. JAMA 2004;291:870879.
  • 293
    Mattana J, Singhal PC. Prevalence and determinants of acute renal failure following cardiopulmonary resuscitation. Arch Intern Med 1993;153:235239.
  • 294
    Bass E. Cardiopulmonary arrest. Pathophysiology and neurologic complications. Ann Intern Med 1985;103:920927.
  • 295
    Adrie C, Monchi M, Laurent I, et al. Coagulopathy after successful cardiopulmonary resuscitation following cardiac arrest: Implication of the protein C anticoagulant pathway. J Am Coll Cardiol 2005;46:2128.
  • 296
    Holzer M, Behringer W, Schorkhuber W, et al. Mild hypothermia and outcome after CPR. Hypothermia for Cardiac Arrest (HACA) Study Group. Acta Anaesthesiol Scand 1997;111 (Suppl):5558.
  • 297
    Laurent I, Monchi M, Chiche JD, et al. Reversible myocardial dysfunction in survivors of out-of-hospital cardiac arrest. J Am Coll Cardiol 2002;40:21102116.