Cardiopulmonary resuscitation: a review (Proceedings)

Objectives

-To discuss current thoughts and techniques in cardiopulmonary resuscitation.

Cardiopulmonary Arrest (CPA)

Cardiopulmonary arrest and resuscitation are not practice-builders! The success rate of cardiopulmonary cerebral resuscitation (CPCR) for animals or humans is disappointingly low. For example, one retrospective investigation of intensive care patients at Colorado State University found that only 4.1% of the dogs and 9.6% of the cats which suffered cardiopulmonary arrest survived to discharge (Wingfield et al.1992). However, animals which experienced respiratory arrest alone were much more likely to be successfully resuscitated. Studies in human hospital patients indicate that ~21-29% will survive to discharge.

Anesthetic-related cardiopulmonary arrest and mortality is a concern for owners and veterinarians alike. In 2006, Broadbelt and co-workers reported that the risk of anesthesia and sedation-related death to be 0.17% and 0.24% in dogs and cats, respectively. Interestingly, the postoperative time period was the most common time period for perianesthetic death (within 3 hours of termination of the procedure) in this study. A variety of investigations have identified factors that increase or decrease anesthetic risk for mortality. Poor health status (increasing ASA classification), breed (brachycephalic), old age, small size, xylazine, trauma, urgency of procedure, and length of procedure have all been associated with increased risk of death associated with anesthesia in recent studies. Premedication with acepromazine was identified as a factor that decreased the risk associated with general anesthesia in one study (Brodbelt et al. 2007), and the presence of technician monitoring reduced risk in another (Dyson et al. 1998). Pulse oximetry was identified as a monitoring tool associated with decreased mortality in cats (Brodbelt et al. 2007).

Anesthetized patients suffering CPA may have improved outcome as compared to the general population. Presumably this is because those patients are intubated, breathing 100% O2, and have a peripheral catheter in place. Moreover, recognition of CPA will most likely occur more rapidly in the anesthetized patient. Indeed, one investigation (Kass, J Vet Emerg Crit Care, 1992) observed that all survivors of CPA were those animals whose arrest was associated with anesthetic drug administration Similarly, Hofmeister and co-workers (2009) evaluated cardiopulmonary arrest in a teaching hospital and showed that CPCR was more likely to be successful in dogs that had cardiopulmonary arrest while anesthetized.

Anesthesia-related CPA may be due to equipment failure, respiratory or cardiovascular problems, or human error. Cooper and co-workers (2002) reported that 82% of preventable anesthetic mishaps were associated with human error. Although the majority of mishaps in this study did not result in patient mortality, the findings highlight the importance of training, checklists, communication, and preparation in preventing anesthetic-related mortality. Indeed, due to the low rate of successful resuscitation and significant morbidity in survivors, prevention of CPA should be one of the most important goals of any anesthesia management plan.

Four factors are generally believed to be related to poor outcome of CPA: 1) Long arrest time prior to initiation of CPR. 2) Prolonged ventricular fibrillation. 3) Inadequate coronary or cerebral perfusion during CPR. 4) Pre-existing disease. Early recognition and appropriate intervention are the keys to successful resuscitation.

The following is a summary of the latest recommendations in CPCR:

Airway and Breathing:

Airway and breathing: Rapid placement of a cuffed endotracheal tube is an important first step in CPCR. It is important to confirm correct placement of the tube within the trachea as capnography will not necessarily indicate proper tube placement when cardiac output is low or nonexistent (That is, ventilation through a properly-placed endotracheal tube may not necessarily result in a detectable exhaled CO2). Manual ventilation should be initiated as soon as possible and at a rate of 10-12/min, inspiratory pressure less than 20 cm H2O and with an inspiratory time of ~ 1 second. The inspired gas mixture should include supplemental oxygen whenever possible.

Circulation:

External cardiac massage can be expected to generate less than 50% of pre-arrest blood flow (and flow generally decreases over time with external cardiac massage). In small animals (<15 kg) external cardiac massage probably evokes blood flow by direct compression of the heart (cardiac pump theory). The A-V valves, as a result of increased intraventricular pressure during systole, close and prevent retrograde blood flow. External cardiac compression in larger animals (>15 kg) probably does not result in direct compression of the heart. In these animals, blood flow is the result of increased thoracic pressure (thoracic pump theory). Retrograde blood flow is prevented because, in addition to causing blood flow out of the chest, increased thoracic pressure collapses the relatively compliant thoracic veins. Forward flow of blood occurs because extra thoracic pressure is less than intrathoracic pressure during chest compression, and maximization of intrathoracic pressure results in optimal blood flow.

Because of size-related differences in CPR physiology, recommendations for external chest compression are also different. In animals less than 15 kg body weight, where direct cardiac compression is likely, external chest compression is done with the animal in right lateral recumbence. Compression is directed over the heart (4th-5th intercostal space).

Larger animals (>15 kg) should be positioned in lateral recumbence and direct thoracic compression over the widest part of the lateral thorax. The rate of compression for external cardiac massage is 80-100/min with a 1:1 compression: relaxation ratio. Some clinicians recommend dorsal recumbence for large dogs or dogs with barrel shaped chests (i.e., bulldogs) as greater intrathoracic pressures may be generated, at least one study (Hofmeister 2009) has shown that survival from CPA was greater in those positioned in lateral recumbence for CPCR. Moreover, it is often difficult to maintain dorsal recumbence during CPCR without troughs or v-boards.

Internal cardiac massage is associated with higher cardiac output and arterial blood pressure, increased myocardial and cerebral blood flow, and most importantly, improved survival and neurological outcome when compared to external cardiac massage. The technique allows the rescuer to evaluate diastolic filling and visualize organization and strength of myocardial contraction. Internal cardiac massage should be considered when external techniques do not generate adequate pulse quality or tissue perfusion (ie, in large dogs), when pre-existing chest trauma (i.e., broken ribs) is present or when pneumothorax is present. The success of internal cardiac massage is dependent upon the time of initiation. Most clinicians recommend that internal massage is instituted quickly after initial resuscitation (i.e., 2-5 minutes). Rate of compression for internal massage is generally 80-100/min but should be guided by cardiac filling.

When emergency thoracotomy and internal massage are used, it is essential that adequate personnel and facilities be present to allow for appropriate patient care. Briefly, the technique is as follows: 1) Hair is removed with clippers at the 5th intercostal space and the skin is washed once with an antiseptic solution (my preference!) 2) A scalpel is used to incise skin and muscle layers. Care should be taken to avoid the intercostal vessels that run along the caudal border of each rib. 3) The pleural cavity is entered using a blunt instrument (i.e., hemostat) and scissors are used to extend the incision. Care must be exercised to avoid the internal thoracic artery, which runs in a cranial to caudal direction approximately one cm lateral to the sternum. 4) The pericardial sac is then incised (avoid the phrenic nerve), and the heart visualized. 5) The heart should be gently grasped and internal massage may be initiated. The heart must not be rotated on its base as this will result in occlusion of the great vessels. The descending aorta can be manually occluded during internal cardiac massage to increase myocardial and cerebral perfusion. 6) If the resuscitation is successful, the patient should be moved to a sterile operating suite, the thorax lavaged with warm isotonic saline solution, a chest tube placed, and the thoracotomy closed. Should cardiopulmonary arrest occur during an abdominal surgery, internal cardiac massage may also be instituted through a diaphragmatic incision.

Regardless of whether internal or external massage is used, it is important to perform cardiac massage without interruption. The general recommendation is to begin cardiac massage and to avoid any interruption of greater than 10 seconds.

Determining the effectiveness of cardiac massage is often difficult. Palpation of a peripheral pulse is a simple and rapid method for determining the effectiveness of CPR. Direct measurement of arterial and venous pressures is desirable, but often impossible to do in the patient suffering from CPA. End-tidal CO2 (mm Hg) can be measured quickly and noninvasively using a capnometer or capnograph. We normally use a capnograph to measure effective ventilation during anesthesia. However, end-tidal CO2 is dependent upon blood flow during CPR. Thus, capnography can be used to measure the effectiveness of CPR. Indeed, end-tidal CO2 has been shown to correlate well with patient hemodynamics (i.e., cardiac output, coronary perfusion pressure) and survival. Palpation of arterial pulses and detection of peripheral blood flow using a Doppler flow transducer are two other methods used to assess blood flow. Rapid and inexpensive measurement of blood flow and pressure may become possible in the future as a result of application of new technologies to medicine.

Acid-Base Management: Rapidly changing metabolic rate, local tissue perfusion, and total blood flow, and altered efficiency of gas exchange may complicate interpretation of acid base status during CPA and CPCR. The most common acid-base abnormality seen during CPCR is acidosis. Acidosis lowers the fibrillation threshold, attenuates the response to catecholamines and alters the function of enzymes. During cardiopulmonary arrest, CO2 is produced in tissues, but is not excreted efficiently because of dramatically decreased total and regional blood flows. Consequently, CO2 produced by cellular metabolism accumulates in tissues and venous blood (i.e., a tissue and venous respiratory acidosis exists). In contrast, respiratory alkalosis and mild metabolic acidosis may be observed on the arterial side of the circulation.

The treatment of acidosis with NaHCO3 is generally not recommended during the initial stages of CPCR. The acidosis initially observed during CPA/CPCR is the result of increased CO2 concentrations. NaHCO3 is only an effective buffer when volatile acid (i.e., CO2) can be effectively eliminated by the lungs. The low flow state that is present during cardiopulmonary arrest and resuscitation prevents elimination of CO2. Indeed, when NaHCO3 is administered to an animal that cannot eliminate CO2, intracellular and CNS acidosis may worsen.

Metabolic acidosis and lactic acid accumulation do occur during CPA/CPCR. Some research has indicated that bicarbonate therapy immediately after CPR is associated with not benefit, or, in some cases, worsened outcome. Vumir et al (Crit Care Med 23:515-522, 1995) examined the effects of sodium bicarbonate in a canine model of ventricular fibrillation cardiac arrest (5 or 15 minute arrest period) and found beneficial effects associated with sodium bicarbonate administration. They observed that dogs arrested for 15 min and treated with NaHCO3 had improved coronary perfusion pressure, systemic perfusion pressure, and rate of return to spontaneous circulation. Moreover, bicarbonate-treated animals had improved neurologic outcome compared to controls. NaHCO3 treatment did not substantially improve these parameters in dogs arrested for 5 min prior to CPR, but neither was bicarbonate therapy detrimental in these animals. In human beings, the use of sodium bicarbonate during CPCR has not been shown to be beneficial. Thus, the general recommendation is to use it only in patients with pre-existing acidosis or with hyperkalemia. Ideally, acid-base therapy should be guided by blood-gas measurements-and mixed venous samples are usually the most beneficial.

Assessment of cardiac rhythm is an essential part of treating CPA. Asystole, ventricular fibrillation, and pulseless electrical activity (formerly electromechanical dissociation) are considered the three primary arrest rhythms (although profound bradycardia is considered by some to be a fourth arrest rhythm). Unlike human beings, where ventricular fibrillation is the most common rhythm disturbance seen with CPA, the distribution of arrest rhythms is more homogeneous, and with asystole as being the most common in dogs.

Ventricular defibrillation is the therapy of choice in patients with ventricular fibrillation. When utilized, personnel safety is of utmost importance and all personnel must avoid physical contact with the patient or anything connected to/touching the patient (table, monitoring equipment etc.). The instrument is designed to electrically induce a synchronous myocardial contraction after which normal beats may follow. Defibrillators may be synchronized with the electrocardiogram to treat certain arrhythmias (i.e., ventricular tachycardia). Current may be applied directly to the heart (internal defibrillation) or through the thoracic wall (external defibrillation). Electrode paste should be used to provide increased electrode contact for external defibrillation. Sterile saline solution may be used to improve contact with internal defibrillation. Alchohol-containing solutions should not be used prior to defibrillation. When used, one shock should be given followed by 2 minutes of cardiac massage. The energy required for internal defibrillation is approximately 1/10 of that required for external defibrillation.

Crystalloid fluids (i.e., lactated Ringer's solution, 0.9% sodium chloride solution) are frequently used during CPCR. Care must be taken to avoid over hydration of the patient as this may result in pulmonary edema, cerebral edema, decreased cerebral blood flow, and increased neuronal injury. Thus, most animals should receive a rapid bolus 10-20 ml/kg of a crystalloid fluid initially unless pre-existing hypovolemia was evident. Colloidal fluids (i.e., dextrans, hydroxyethyl starch) have also been used during CPR. Intravascular volume may be expanded more rapidly and with a smaller volume than with crystalloid fluids. In addition, plasma volume is increased for a longer time after colloidal fluid therapy compared to crystalloid therapy. However, colloidal fluids are more expensive than crystalloid fluids and may be associated with coagulopathies and pulmonary edema when given at high doses. Hypertonic solutions (i.e., hypertonic saline solution) also require relatively small volumes for resuscitation, and have been shown to expand plasma volume, reduce intracranial pressure and promote urine output. However, effects of hypertonic saline administration are relatively short-lived. The safety and efficacy of hypertonic saline solution during CPR have yet to be clearly defined. The shock dose of crystalloid solution has been reported to be 90 ml/kg/h in the dog and 50 ml/kg/h in the cat, and is approximately equal to one blood volume.

Hyperglycemia has been shown to be associated with increased incidence of postischemic brain injury and death in experimental studies in animals and clinical studies in humans. On the basis of these studies, glucose-containing fluids should be avoided during CPR unless hypoglycemia was present prior to arrest.

Epinephrine is a catecholamine with alpha and beta adrenergic effects and is commonly used during CPR. The beta effects of epinephrine (which mediate increased cardiac contractility and heart rate) are not responsible for its effectiveness during CPR. Evidence for this was shown in investigations which demonstrated that beta agonists (i.e., dobutamine and isoproterenol) did not improve the success of resuscitation during cardiopulmonary arrest. Similarly, beta blockers do not decrease the effectiveness of initial resuscitation with epinephrine. The alpha effects of epinephrine cause peripheral vasoconstriction and increased arterial diastolic pressure and coronary perfusion pressure. These changes are important to restoration of spontaneous circulation. Epinephrine administration should be repeated every 3-5 minutes, or the drug may be given as a continuous infusion. Because progressive ischemia and acidosis may decrease the responsiveness to catecholamines, higher doses of epinephrine may be necessary during prolonged CPCR. Thus, epinephrine administration may be initiated at the low dose, and the dose progressively increased with time. However, the trend in human medicine is to substitute vasopessin for epinephrine when the latter has not been successful at re-establishing spontaneous circulation.

Arginine vasopressin is an endogenous hormone that may be administered during CPR to increase coronary blood flow and venous return during CPR. The drug is less likely to precipitate ventricular dysrythmias or tachycardia than epinephrine. Arginine vasopressin has been used similarly to increase venous return and coronary perfusion during CPR. The American Heart Association has recently included this drug in their CPR algorithm, and has been shown to be superior to epinephrine in human beings with asystole. (The recommended dose in small animals is 0.2-0.8 U/kg IV and repeated every 3-5 min).

Atropine is a parasympatholytic drug that may restore normal electrical activity and AV nodal conduction during asystole. The anticholinergic drug is also used to treat symptomatic bradycardia. The usual emergency dose is 0.02-0.04 mg/kg IV, with lower doses used to treat bradycardia.

Lidocaine is a class Ib anti arrhythmic drug (sodium channel blocker) used to control ventricular ectopic contractions, which commonly occur post resuscitation. Historically, the drug has also been used during ventricular fibrillation, presumably to improve the chance for successful electrical defibrillation. Recent research has shown lidocaine actually increased the energy necessary to defibrillate the myocardium. Thus, the use of lidocaine prior to initiation of spontaneous organized electrical activity is probably not warranted. Cats are more sensitive than dogs to the toxic effects of lidocaine. (Canine dose: 1-2 mg/kg IV; feline dose: 0.2 mg/kg IV). Recent evidence in human beings suggests that amiodarone (5 mg/kg IV) is more effective lidocaine for the treatment of VF or VT. This drug will has replaced lidocaine in some veterinary hospitals for CPCR.

Bretylium tosylate (class III anti arrhythmic) in combination with KCl and acetylcholine has been reported as a chemical defibrillatory protocol. However, the efficacy of this combination appears to be minimal. Electrical defibrillation is the method of choice for treating ventricular fibrillation.

Calcium chloride or gluconate were routinely used in CPCR in the recent past. Today, it is only indicated in patients with decreased ionized serum calcium concentration, calcium channel blocker toxicity, or hyperkalemia. Magnesium sulfate may be administered to animals with refractory ventricular arrhythmias.

Ideally, each arrested patient should be instrumented with a central venous catheter to allow rapid administration of therapeutic agents close to the heart. Peripheral venous catheters allow drugs to be administered directly into the blood stream, but at a site distant from the heart. Thus, there is often significant delay in delivery of drug to the heart when drugs are administered via peripheral venous catheter during CPR. Because it is difficult to obtain venous access during cardiopulmonary arrest, other routes of administration must be considered: Intratracheal drug administration may be accomplished by injecting drugs through the lumen of the endotracheal tube and into the small airways/alveoli using a syringe and urinary catheter. Uptake of drug from airway mucosa is dependent upon blood flow, and absorption into the blood stream may be erratic during CPR.

Intracardiac injections should be avoided. Improper needle placement may result in damage to the coronary vasculature, pericardial tamponade, lung laceration, or myocardial damage and arrhythmias. Some clinicians will use intracardiac, luminal injections after thoracotomy, as needle placement can then be visually confirmed. Drugs and fluids may also be administered via the intraosseous route

Resources:

Plunkett SJ, McMichael M. Cardiopulmonary resuscitation in small animal medicine: an update. J Vet Internal Med 22:9-25, 2008.