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Current Thoughts on Cardiopulmonary Arrest and Resuscitation

Andrea L. Looney, DVM
MSPCA/Rowley Memorial Animal Hospital
Springfield, MA

Cardiopulmonary arrest (CPA) is defined as the abrupt and unexpected cessation of spontaneous, effective ventilation and circulation. Cardiopulmonary resuscitation (CPR), often now known as cardiopulmonary cerebral resuscitation (CPCR) (just what we needóanother acronym!!!) is the collective processes by which artificial ventilation and circulation are provided until advanced life support or spontaneous cardiopulmonary function are restored. Todayís seminar will discuss classic basic concepts to help us identify patients likely to benefit from cardiopulmonary resuscitation, recognize causes of arrest, understand principles in various levels of therapeutic support, and discuss important treatment issues in CPA/CPR throughout basic and advanced life support.

CPR had its beginnings in the late nineteenth century and early twentieth centuries in experiments performed by physicians using animal models. In the early 1960ís, following a series of experiments at Johns Hopkins University describing artificial ventilation, external cardiac compression, and electrical defibrillation, CPR was gradually adopted as a medical intervention following CPA. Since many of the guidelines for CPR in humans have been drawn from experimental animal studies, they are directly relevant to veterinary medicine and are included in current recommendations. Sadly though, success rates, which range from 0-22% over the past two decades, have not changed even though many of the actual treatment recommendations have changed. The area of post-resuscitation disease prevention has shed new light on many of the theories and recommendations around how we deal with an arrested animal or person. Postresuscitation disease includes reperfusion failure, reoxygenation injury, extracerebral derangements, and possible post arrest inflammatory processes. Most clinicians would agree that the defining factor determining the success of resuscitation is not the treatments provided, but the chance of intact neurologic survival.

Who should be resuscitated? The purpose of cardiopulmonary resuscitation is to reverse sudden unexpected death resulting from REVERSIBLE disease processes or iatrogenic complications. Although difficult to determine the REVERSIBILITY of the event in a veterinary situation, signalment and brief history, especially with respect to current pharmacy intake of patient, adds much to the probability. Frank and disturbing as it may sound, performing resuscitation procedures on all patients, especially those critically ill, is unwarranted and intrusive, let alone costly and time/staff inefficient. The definition of futile enters a gray zone in many subsets of patients, and decision making for these individuals should be discussed with the family preemptively whenever possible. Patients with diffusely metastatic/terminal cancer, progressive cardiac failure, end-stage renal failure, sepsis, multiple organ failure, and massive tissue damage frequently arrest due to unknown causes; statistics have shown that survival from such arrests is exceedingly rare and costly.

Levels of therapeutic support should be clearly noted on records and cages (although color coding may suffice) along with a discussion explaining the rationale in the record. "No-CPR" orders do not mean that the patient is not to be treatedóit means the patient should continue treatment up until/if it codes. Likewise, patients and their families should not be emotionally or physically abandoned at times of arrest. This is why it is so critical that clinicians should discuss the possibility of CPA, prognosis, and associated expenses, so that owners of terminally ill animals can be actively involved in the decision making process ahead of time instead of at the time of acute problems.

Documentation and communication between hospital staff as to problem listing, pharmacy orders, changes in treatments, sedations, etc., help the staff know exactly how to proceed should an arrest occur, especially unexpectedly. As stated earlier, although patients with primary respiratory arrest are associated with a higher resuscitation rate than those with cardiac arrest, few animals that undergo CPA are resuscitated and even fewer leave the hospital as normal pets. The major reasons for unsuccessful resuscitation include a delay in the diagnosis of CPA and a subsequent delay in administering appropriate therapy. By recognizing animals at increased risk of CPA, training of both technical and support staff in early recognition, and the use of a team approach in treating the arrest patient, CPR can be initiated in a timely and coordinated manner.

Readiness in the form of staff, area, and training are essential to resuscitate those potentially reversible problems! For the benefits of patients with potential for resuscitation, hospitals should have a fully stocked, readily positioned, frequently checked "crash cart" available, and all staff should be trained in basic life support (BLS). All hospital staff can assist in managing an arrest. For example, nontechnical staff can learn to ventilate, record drugs administered and times of events for later review. Advanced life support (ALS) using drug administration and electrical defibrillation also involves advanced planning. Calculating these drug dosages in the environment of an arrest is difficult. This is why computer programs, clinical algorithms, and pre-prepared charts giving routes and amounts per body weight, can be invaluable in an arrest. Having regular CPR drills can help emphasize the team approach, not only to CPR, but also to health care in general. Staff meetings can serve as an ideal time to practice basics in a low stress environment.

The assembly of a crash cart or box is not as difficult as thought. In fact, it can be managed in a small practice very similarly to that in a large referral or academic setting. To assemble the necessary components, think of your ABCís and the items necessary for the first steps. Multiple lists have been compiled, but in case you lack one, here are some of the essentials: mouth gags, cuffed endotracheal tubes, laryngoscope working with appropriate blades, Ambu bags and means of supplying oxygen, oxygen masks, syringes and needles (paired and ready to go), gauze and tape, catheters, chest tubes, three way stopcocks, gauze pads, fluids and administration sets, butterflies, long red rubber or polyethylene urinary catheters, drugs (Atropine, Epinephrine, Lidocaine, at minimum), sterile surgical emergency pack, blades, scrub, saline, alcohol, and means of assessment and monitoring (Doppler, Pulse oximeter, End tidal capnometer, ECG, blood pressure equipment). Suction equipment and oxygen masks are extremely valuable if affordable.

Cardiopulmonary arrest can have multiple etiologies. In veterinary medicine, arrest most frequently occurs with diseases of the respiratory system, as a result of severe multisystemic disease or trauma, or following cardiac arrhythmias. Exact causes of the arrest include, but are not limited to, the following: electrolyte and acid-base disturbances (potassium, calcium, magnesium); cellular hypoxia; vagal stimulation; and anesthetic/pharmacologic agents. The field of intensive care medicine and point of care medicine for both human and veterinary patients has made monitoring of high-risk patients cost efficient, timely, practical and necessary to diagnose and treat CPA in a timely manner. Nowhere is the adage "an ounce of prevention is worth a pound of cure" more applicable than in critically ill patients. It has been said, "patients donít suddenly deteriorate, but healthcare professionals suddenly notice theyíve deteriorated." Monitoring allows for early recognition of this deterioration and appropriate intervention.

Vital signs are VITAL! Arterial lines with blood pressure alarm limits provide a more direct assessment of cardiovascular performance than most other monitoring means. However, they are not practical and their use is often limited to more seriously ill patients. Noninvasive, intermittent blood pressure monitors are useful for ongoing assessment and recognition of ominous trends. However, hypotensive, vasoconstricted patients cannot be adequately monitored with these devices. Likewise, an electrocardiogram may be normal in a quickly deteriorating or worse yet, dead patient. Frequent or continuous monitoring of vital signs (TPR/neuro q. hourly) can provide early clues to physiologic decompensation. For example, patients developing acute respiratory failure typically develop tachypnea and tachycardia long before more serious signs of decompensation, such as bradyasystolic arrest, occur. Patients with increasing cerebral edema develop altered mental status and bradycardia rate changes as their decompensation occurs. Fever or hypothermia may be signs of impending deterioration in septic patients.

The Doppler flow probe, which provides continuous monitoring of pulse activity, and the pulse oximeter, which allows visualization of a pulse waveform, may be of great value in the patient suspected of having an arrest situation. Capillary refill time is a poor indicator of the circulatory status of an animal. Normal refill times may be observed in a dead animal. Likewise, the absence of any heartbeat on auscultation may indicate inadequate cardiac output, but not necessarily cardiopulmonary arrest. The absence of a continuous pulse usually indicates cardiopulmonary arrest. Pupillary dilation begins within 20 seconds of arrest and is maximal at 45 seconds of arrest, but is not a reflection of irreversible neurologic damage unless it remains throughout the resuscitation period.

How do we recognize oncoming cardiopulmonary arrest? Changes in the respiratory rate, depth, or pattern; a weak or irregular pulse; bradycardia; hypotension; unexplained changes in the depth of anesthesia; cyanosis; and hypothermia. What are the more obvious signs that an arrest has occurred? The absence of ventilation, or the absence of a pulse; fainting or collapsing are less common signs but indeed have been seen in cases of cardiac arrest in cats and dogs.

Where do we begin in the resuscitation process? Certain steps must be followed in the same order every time in order for the process to become efficient. The scene for the resuscitation always should be surveyed to ensure that it is safe (water, wires, contaminated material). Gloves should be worn at all times if possible, especially if there is noticeable blood on the patient. Humans may be injured in the process of transporting or assisting the animal and blood may carry infectious agents from them as well as from animals. It should be confirmed that the animal is truly unconscious before someone tries to intubate. Knowledge of rabies status also cannot be overemphasized.

The assessment phases of BLS are crucial. No patient should undergo any of the phases of CPR until the need for it has been established by appropriate assessment. Each of the ABCís of CPR, airway, breathing, and circulation, begins with an often forgotten, yet much needed ASSESSMENT phase: for A, is there a lack of responsiveness; for B, is the patient breathless, for C, is the patient pulseless? There was a recent thought in veterinary medicine that the ABCís of CPR should be changed to CABís. In the Netherlands, the algorithm CAB has been adopted for human emergency care. Why? Well, in humans, severe dysrhythmias, particularly ventricular fibrillation, is the most common cause of cardiac arrest. Hence, the "A and B" of ABC may not be essential during the first several minutes of CPR when ventricular fibrillation occurs in the absence of asphyxia. This of course is the case for the severe, sudden dysrhythmia of myocardial infarction in human beings. However, asystole, not ventricular fibrillation, is the most common form of cardiac arrest in animals. Hypoxia is its most common cause. The provision of "A and B" as such seems very important in these patients, and to delay such therapy courts failure. As such, there seems to be little impetus currently to change our acronym. Now lets examine the "ABCís" in finer detail.

A=AIRWAY

Once it has been established that the patient is not breathing, mouth-to-mouth or mouth-to-nose ventilation should be provided until an airway can be established. Open the airway (mouth) to determine its patency. Clean any foreign material or blood from the mouth and pharynx utilizing a mouth gag. A simple suction device can help remove fluid or blood from the upper airways. As soon as a laryngoscope is available, the animal should be intubated via the orotracheal route. A laryngoscope should be used to ensure the arytenoid cartilages are visualized and the patient is accurately intubated. In addition, atraumatic intubation prevents bradycardia secondary to stimulation of the laryngeal nerve and may prevent an arrest from occurring.

If the patient is too awake to intubate, providing oxygen via a facemask is appropriate. Oxygen is a great therapy! If you cannot intubate, donít throw away the idea of providing supplemental oxygen, just find another means of providing it! If you cannot orotracheally intubate, perform a tracheostomy. Once intubated, the patient should be ventilated with 100% oxygen to full lung inflation 2-3 times. The chest should be ausculted bilaterally to ensure airway sounds and absence of a pneumothorax and to confirm tracheal intubation. If you are unable to get the animal intubated or pass a tracheostomy tube, continuous flow insufflation through a plastic catheter whose tip is placed at or above the corina will suffice if oxygen is allowed to flow at 0.2 L/kg/min.

B=BREATHING

entilation should begin with 100% oxygen at a rate of 12-30 breaths per minute. Ambu bags are inexpensive, easy to use, and most come with positive-end expiratory valves that can be very useful in improving oxygenation in cases of long-term ventilation. Ventilation with an anesthetic machine is no longer recommended because of the possibility of residual CO2 or anesthetic being ventilated into an already hypercapneic or depressed individual, as well as the time required to open and close a pop-off valve for intermittent ventilation. The use of acupuncture to stimulate respirations has been reported. Needling the point GV26 may reverse respiratory arrest under clinical conditions. The technique involves using a small needle, placing it at a perpendicular angle into the lower nasal philtrum level at the ventral limit of the nares, to a depth of 10-20mm, and using it in a hen-pecking motion, while monitoring for improvement in respiration.

End-tidal carbon dioxide monitoring has been useful not only to confirm tracheal intubation, but also to gauge effectiveness of CPR. The concentration of exhaled carbon dioxide changes when blood flow to the lungs changes, and is an indirect indicator of cardiac output and systemic blood flow. When ventilation is controlled, end-tidal carbon dioxide is linearly related to cardiac output even during low blood flow rates as would occur during CPR. In a recent study, where respiratory variables were controlled and ventilation was adequate, dogs with the highest rate of survival from arrest also had the highest levels of expired carbon dioxide, probably indicative of better tissue perfusion during CPR. Increasing carbon dioxide levels means a decrease in minute ventilation, allowing a way to evaluate effectiveness of ventilation.

The force on "bags" which one uses to ventilate an animal should depend upon the problem that resulted in the arrest. In general, however, inspiratory pressure should not exceed 20 cmH2O. One must be very careful in ventilating cats especially because it is so easy to overventilate and create pneumothorax situations. Overventilation will result in loss of carbon dioxide and in dangerously low levels of PaCO2, the latter of which can easily result in cerebral vasodilation. Tidal volume remains at the 10-15 ml/kg level. Active compression-decompression devices, marketed for human CPR, allow a chest re-expansion via the use of a suction cup. This provides greater negative pressure and as a result, greater inspiratory airflow and tidal volume. Though currently not practical for animal models, in the near future, these may prove indispensable for resuscitation of dogs.

Assessing adequacy of ventilation at the cellular level can be done through the use of mixed venous blood gases, which are not as affected by changes in minute ventilation as are the arterial blood gases. Changes in pH and oxygen tension in venous blood have been shown to correlate strongly with tissue lactate levels.

C=CARDIAC/CIRCULATION

The heart should be ausculted and femoral pulses should be simultaneously palpated for 10 seconds to ensure that no heartbeat is present. Pulses can be palpated in several areas; the most commonly used areas in small animal medicine are the carotid and femoral/dorsal pedal arteries. Chest compressions are then started immediately if there is no heartbeat or if the heartbeat is below 20-30 beats per minute. Chest compressions are provided at a rate of 60-120 beats per minute. Chest compressions in cats and small dogs (<7kg) are best accomplished in lateral recumbency. Compression is applied directly over the heart, and the chest wall is compressed 25-30% of its dimension. Thoracic compression in dogs over 7 kg is performed with the patient in dorsal recumbency, which maximizes the increase in intrathoracic pressure and the return of blood flow to the central organs. When two persons are available to do CPR, simultaneous compression and ventilation will also maximize intrathoracic pressure, resulting in increased venous return to the central compartment and increased cardiac output.

A report in 1976 described a method of improving standard CPR by which abdominal compressions were alternated with chest compressions. Blood flow was increased in the coronary and carotid arteries. Several mechanisms have been proposed to explain this increase in cardiac output. The abdominal compressions may increase retrograde aortic blood flow and pressure, resulting in higher coronary flow. Second, because the diaphragm is forced toward the chest, the abdominal compressions may also increase intrathoracic pressure. The incidence of trauma to abdominal organs during this type of CPR in humans has been reported to be minimal.

The effectiveness of CPR should be assessed by palpating pulses, or with the use of a flow detection device, such as a Doppler ultrasound transducer. If the compressions are not generating adequate blood flow, the resuscitation technique should be altered to increase intrathoracic pressure, or open-chest cardiac compression should be considered. A number of studies clearly indicated that open-chest direct cardiac compression produces greater cardiac output and higher cerebral and coronary perfusion gradients than does closed-chest CPR. Closed-chest CPR relies on compression of the thorax or the thoracic pump mechanism. Open-chest CPR relies on the cardiac pump mechanism. The rate of survival decreases rapidly if open-chest CPR is delayed beyond 15 minutes. Current recommendations suggest that if closed-chest CPR shows no flow within 2 minutes or no return of spontaneous circulation within 10 minutes that open-chest CPR should be attempted.

Inherent in the connotation of C=cardiac/circulation is the fact that usually we lump the attachment of the electrocardiogram and the delivery of fluids into this third step. What is the appropriate fluid choice for resuscitation? Shock should be treated aggressively with fluids containing an adequate amount of sodium because of the relatively high concentration of sodium in extracellular fluid. Isotonic solutions readily available and commonly used are 0.9% sodium chloride, lactated Ringerís, Plasmalyte, and Normosol-R. Shock doses are 50-90ml/kg/hour for dogs and 40-60ml/kg/hour for cats. A highly effective method is to deliver shock fluid volumes in one-fourth increments. One-fourth of the calculated shock volume is delivered every 15 minutes with monitoring of the deviation from the packed cell volume and total protein. Few patients require the 90ml/kg/hour using this method and volume overload is unlikely. Synthetic colloids can be used and the standard volume is 10-20ml/kg/day--if needed, this can be delivered in parcel with the crystalloids, allowing a reduction in the latter by 40-60%. The total dose of the colloid can be delivered over 4-6 hours, depending upon the cause of fluid loss.

Drug administration is essential during CPR in order to maximize brain and coronary blood flow, optimize blood pressure, treat arrhythmias, and help correct acidosis. The most effective means of delivering drugs during CPR is via a central catheter. The second route of choice is intratracheal, the third, a peripheral catheter, and the fourth is intraosseous and sublingual. Intracardiac injections may cause laceration of the heart and coronary vessels. In addition, cardiac compressions must be stopped while the drug is given. For these reasons, cardiac injections are not recommended unless the site of the injection can be visualized. Medications given peripherally should be followed by large amounts of saline to rapidly carry the agent to the heart. Intratracheal administration of drugs is advocated in cases without a central line. Drugs delivered to the lungs will be absorbed and rapidly carried to the left heart, where these agents can reach the coronary circulation. Sodium bicarbonate should not be given by this route, as it destroys alveolar surfactant and may potentially worsen respiratory distress. By and large, a peripheral catheter is almost always placed first, followed by a central or second peripheral line.

The most commonly encountered arrhythmias during CPA in veterinary medicine include sinus bradycardia, supraventricular tachyarrhythmias, ventricular aystole, electromechanical dissociation, and ventricular fibrillation. Without an ECG, differentiation is impossible. Despite the number and variety of both cardiac and noncardiac illnesses and trauma that can result in cardiac arrhythmias, therapeutic decisions (i.e., should I treat or not treat?) always depend on the clinicianís answers to two basic questions regarding the patient and the arrhythmia:

1)  Is there reason to believe that the arrhythmia is compromising the patientís hemodynamic status or contributing substantially to the pathogenesis of the clinical signs?

2)  Considering the patientís clinical situation, is it likely that the arrhythmia increases the risk of sudden death?

Ventricular asystole appears as a straight line on an ECG, or as P-waves without QRS complexes. Usually the result of severe myocardial ischemia from prolonged period of inadequate coronary perfusion, it carries a grave prognosis. Treatment includes administration of atropine and epinephrine. Nonperfusing (electromechanical dissociation EMD) results in electrical activity without sufficient mechanical activity to cause adequate cardiac output or pulses. The failure of contractility is likely due to depletion of myocardial oxygen stores and may be perpetuated by endogenous endorphins. Treatment with the opiate antagonist naloxone may be associated with improved responsiveness of the heart to catecholamines. Ventricular fibrillation is chaotic, disorganized ventricular electrical activity resulting in sustained ventricular systole. Since the coronary arteries perfuse the myocardium during diastole, no coronary perfusion occurs. The cardiac response to defibrillation or countershock is largely time-dependent. After extended ventricular fibrillation (5-7 minutes), countershock rarely results in spontaneous perfusing rhythm; asystole, EMD, or persistent fibrillation are the usual results.

Supraventricular tachycardias have some evidence of a P-wave, either before, during, or after the QRS depending on the location of the pacemaker. It is therefore reasonable to select an intervention such as a vagal maneuver, a beta blocker, or a calcium channel blocker. Sinus bradycardia is often defined as a sinus rate of less than 60 beats per minute in the dog, but using this definition, most healthy sleeping dogs would be bradycardic. The first principle of bradyarrhythmia management then, is to judge the arrhythmia by the company it keeps. Electrolyte abnormalities should be ruled out prior to treatment, as should drug (sedative) therapy. Chronic conditions including hypothyroidism, bronchitis, and some GI diseases are associated with high vagal tone and bradycardia. In general, no treatment is necessary for sinus bradycardia with rates down to 40 beats per minute. Rates below 40 can be managed with anticholinergics.

Early electrical DC defibrillation is the treatment of choice for ventricular fibrillation. Care must be exercised, as the defibrillator is a very dangerous instrument that can cause injury to all involved. The optimal delivered energy to the myocardium for external defibrillation is roughly 2-4 J/kg. When delivering the countershock to the myocardium, it is only necessary to "hit" about 28% of the myocardial cells to defibrillate the heart. Thus paddle position is not as important as once believed. The following guidelines have been suggested to reduce transthoracic impedance during electrical defibrillation: use large surface area paddles, countershocks applied close together may be most effective, use an electrolyte paste or gel, and apply pressure to the electrodes. Chemical defibrillators have unproven efficacy in clinical veterinary medicine. Drugs used in chemical defibrillation include bretylium tosylate and magnesium chloride. Lidocaine may prevent the recurrence of malignant ventricular arrhythmias but is of questionable value in the treatment of ventricular defibrillation.

The four cardioactive drugs used most commonly during CPR include epinephrine, atropine, lidocaine, and sodium bicarbonate. Administration of these drugs encompasses what is commonly known as advanced life support. The mixed (alpha and beta) agonist epinephrine has withstood the test of time and is still considered to be the best adrenergic agent to administer during the treatment of cardiac arrest. Adrenergic agonists like epinephrine are administered to increase arterial pressure and increase blood flow to vital organs. The mechanism of action of adrenergic agonists is vasoconstriction, resulting in greater arterial pressure, especially during the relaxation phase. The alpha component is thought to be more important in producing the higher arterial pressure that is significant in successful CPR. The recommended dose is 1mg per 10 kg body weight, with additional suggestion that successive doses be increased. The sooner you treat an arrest situation, the less epinephrine should be used. The use of vasopressors is particularly useful in cases of systemic inflammatory response syndrome vasculature dilation and weakness in order to redistribute fluid to the central compartment.

Other vasopressors such as methoxamine, phenylephrine, and norepinephrine have been considered, but only dopamine is essentially equal to epinephrine in treatment success rate. Another group of vasoactive agents that employ a different system of producing vasoconstriction has been recently studied for their potential in the treatment of cardiac arrest. The second messenger system of angiotensin II and vasopressin involves activation of phospholipases, leading to increased inositol phosphates. This is different than the adrenergic system. The use of angiotensin II or vasopressin alone or with epinephrine may improve the current poor survival rates. Atrial natriuretic peptide, which is released during atrial distension, and nitric oxide, a vasodilatory agent released by endothelial cells, could inhibit the effectiveness of the vasoconstricting agents used during the treatment of cardiac arrest. Antagonists to either or both of these substances may improve the response to vasoconstricting agents.

Atropine and glycopyrolate are parasympathetic agents, which have been recommended for use during CPR because there is often a rapid progression of unstable bradycardia to asystole. Inherent in the use of these agents is the fact that if heart rate is to increase, oxygen tension and vasculature volume must be maximized to maintain appropriate coronary circulation at a time when most likely the myocardium cannot sustain increased workload. Thus, 100% oxygen should be in use, either nasally or tracheally, and fluid volume must be maintained to avoid development of shock. Dogs or cats that have received anticholinergics prior to the administration of catecholamines should be monitored for what is known as "frozen myocardium", a stiffened arrested heart, or development of supraventricular or ventricular arrhythmias. Recent recommendations include the use of lidocaine as an antifibrillator and cell membrane stabilizer in between the use of atropine and epinephrine or other vasopressor.

Lidocaine, in addition to being a potent antiarrhythmic, is an adjunct analgesic and has been shown to help prevent programmed cell death (apoptosis) in experimental models. Its use in resuscitation protocols stems from human CPR, where ventricular fibrillation is a much more common fatal arrhythmia. Since in dogs and cats, electrical mechanical dissociation is apparently a much more common arrest arrhythmia, the use of lidocaine has frequently been reserved to help prevent rebound tachycardias (in between use of atropine and epinephrine) and in the treatment of postresusciation dysrhythmias. Serum potassium should be within the reference range for lidocaine to be effective. Hyperkalemia intensifies its depressant effects on cardiac membranes, whereas hypokalemia diminishes its effectiveness.

The administration of bicarbonate for the treatment of cardiac arrest acidosis is probably best reserved for resuscitation attempts lasting greater than 20 minutes. It has traditionally been recommended during CPR to combat the metabolic acidosis generated by anaerobic metabolism in hypoxic tissues. Its efficacy is controversial. When administered liberally, it causes severe metabolic alkalosis and no respectable heart will start beating at an alkaline pH. The administration of such an agent is associated with the generation of carbon dioxide (via carbonic acid) resulting in hypercapnia if the patient is not well ventilated. Carbon dioxide rapidly diffuses into an intracellular compartment and into the CSF. Once inside the cell, it re-equilibrates across the carbonic acid equilibrium generating an excess of hydrogen ion. Intracellular acidosis may be associated with myocardial and CNS depression. Thus, it is imperative that with its use, ventilation be accomplished.

There exist alternative alkalinizing agents. Tromethamine (THAM) binds directly with hydrogen ion, which decreases rather than increases carbon dioxide levels. Dichloroacetate enhances activity of pyruvate dehydrogenase and the metabolism of lactic acid. Carbicarb is an equimolar combination of sodium carbonate and sodium bicarbonate. All of these agents have been tested in animal models, with some degrees of success. Yet, the use of these has not been established as superior to the use of bicarbonate, nor has bicarbonate been proven to lack efficacy. What seems to be the case is that in the short term, all of these agents MAY be efficacious, but changes in survival rates in the long term are not outstanding.

Corticosteroids have been shown to "improve membrane stability" in models of tissue ischemia. However, they have fallen into disfavor because they have not been shown to improve survival from septic shock in several large human studies. In cases of arrest from septic shock, monoclonal antibodies directed against endotoxin, as well as monoclonal antibodies against tumor necrosis factor and interleukin 1 can decrease mortality in experimental sepsis. Calcium used to be administered as a matter of routine. However, when the efficacy of calcium was evaluated in human clinical trials, it was found to be ineffective because it increased coronary and cerebral vasoconstriction. However, it is still considered to be one of the specific treatments for life-threatening hyperkalemia and severe hypocalcemia. It is also recommended if the chest is open and the heart is observed to be dilated, flabby and atonic. Naloxone has been shown to be useful in reversing electromechanical dissociation. It is a narcotic antagonist, which reverses the effects of both endogenously and exogenously administered narcotic agents. Intravenous administration has been associated with increased heart rate, increased cardiac output, and increased mean blood pressure.

References available upon request from author


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