Frequently Asked Questions Regarding

Cardiopulmonary Arrest and Resuscitation

In the Dog and Cat

Wayne E. Wingfield, MS, DVM

wwingfie@vth.colostate.edu


1. Define cardiopulmonary arrest and list the three phases.

Cardiopulmonary arrest is defined as the abrupt, unexpected cessation of spontaneous and effective ventilation and systemic perfusion (circulation). Cardiopulmonary arrest (CPR) provides artificial ventilation and circulation until advanced life support can be provided and spontaneous circulation and ventilation can be restored. CPR is divided into three support stages:

RISK FACTORS

1. Which animals are at risk to suffer cardiopulmonary arrest and what are the predisposing factors?

Cardiopulmonary arrest is usually the result of a cardiac dysrhythmia. This arrest may be the result of primary cardiac disease or diseases which affect other organs. In animals, arrest most frequently occurs with diseases of the respiratory system (pneumonia, laryngeal paralysis, neoplasia, thoracic effusions, and aspiration pneumonitis), as a result of severe multisystem disease, trauma, and following cardiac dysrhythmias.

Predisposing causes of cardiopulmonary arrest include the following:

1) cellular hypoxia;

2) vagal stimulation;

3) acid-base and electrolyte abnormalities;

4) anesthetic agents;

5) trauma;

6) systemic and metabolic diseases.

WARNING SIGNS AND DIAGNOSIS OF CARDIOPULMONARY ARREST

1. What are the warning signs of 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.

2. How is cardiopulmonary arrest diagnosed?

The classical description of arrest includes the following:

1) absence of ventilation and cyanosis ("respiratory arrest");

2) absence of a palpable pulse (pulse will disappear when systolic pressure < 60 mm Hg);

3) absence of heart sounds (heart sounds will disappear when systolic pressure < 50 mm Hg);

4) dilatation of the pupils.

PHASES OF CARDIOPULMONARY RESUSCITATION AND GOALS

1. What is involved with each of the phases of cardiopulmonary resuscitation?

Basic Life Support:

A -- Establishment of an Airway.

B -- Breathing support.

C -- Circulation support.

Advanced Life Support:

D -- Diagnosis and Drugs.

E -- Electrocardiography.

F -- Fibrillation control.

Prolonged Life Support:

G -- Gauging a patient's response.

H -- Hopeful measures for the brain

I -- Intensive care.

In order to optimize CPR, one should ASSESS prior to initiating basic, advanced, and prolonged life support. Eg. Assessment Airway support; assessment breathing support; assessment circulation support, etc.

2. Should you keep accurate records for each cardiopulmonary arrest animal?

Yes! Although you won't likely be recording every action during the arrest, it is important to record this information.

BASIC_LIFE_SUPPORT

1. How important is basic life support?

Basic life support is the most important phase of cardiopulmonary resuscitation. This requires practice by your staff. It is easy to develop "simulated" arrests using "stuffed" toy animals in which you can practice the ABC's of CPR. Through these practice sessions the staff can all be trained to rapidly respond to this serious emergency.

2. How do we establish an airway?

The first step is the establishment of the unresponsiveness and assessment of the airway. Quickly check the airway for foreign materials (bones, blood clots, fractured mandible, vomitus). Position the animal in a ventral recumbency in preparation for intubation with an endotracheal tube. Accurately place the endotracheal tube.

3. How do we breathe for the animal?

First, assess that the animal is apneic and requires assisted ventilation. Once you have seen there is no movement to the chest wall, begin to ventilate the animal with two long breaths (1.5 - 2.0 seconds each). If the animal does not begin to breathe within 5 to 7 seconds, begin to ventilate at a rate of 12 - 20 times per minute.

Use of accupuncture to stimulate respirations has been reported. Placing a needle in acupuncture point Jen Chung (GV26) may reverse respiratory arrest under clinical conditions. The technique involves using a small (22 - 28 gauge, 1 - 1.5 inch) needle in the nasal philtrum at the ventral limit of the nares. The needle is twirled strongly and moved up and down while monitoring for improvement in respiration. This is a simple technique and can be employed quickly.

4. How is circulation supported during CPR?

Assessment is necessary to determine the pulselessness of the animal prior to initiating external cardiac compression. Currently there are two theories to explain the mechanism of forward blood flow during CPR: 1) Cardiac pump theory and 2) thoracic pump theory. The cardiac pump theory is likely most important in the smaller animals (< 7 Kg) and the thoracic pump most important in larger animals (> 7 Kg). It is believed that both the cardiac and thoracic pump are interactive and each contributes to the pressure gradients responsible for blood flow during CPR.

5. What is the "cardiac pump theory"?

The original hypothesis, suggests that blood flow to the periphery during external cardiac compression of the heart results from direct compression of the heart between the sternum and vertebrae (dorsal recumbency) or between the right and left thoracic wall (lateral recumbency) of the dog and cat. According to this concept, thoracic compression ("artificial systole") is similar to internal cardiac massage, and will result in blood being squeezed from both ventricles into the pulmonary arteries and aorta as the pulmonary and aortic valves open. Retrograde flow of blood is prevented by closure of the left and right atrioventricular valves. During the relaxation phase of thoracic compression ("artificial diastole"), the ventricles recoil to their original shape and fill by a suction effect, while elevated arterial pressure closes the aortic and pulmonic valves.

6. What is the "thoracic pump theory"?

As pressure is applied to the animal's thorax, it has been noted there is a correlation between the rise in intrathoracic pressure during compression and the apparent magnitude of carotid artery blood flow and pressure. For brain blood flow to occur during resuscitation, a carotid arterial-to-jugular pressure gradient must be present during chest compression. Experimental studies in large dogs have shown that thoracic compression during CPR results in an essentially equal rise in central venous, right atrial, pulmonary artery, aortic, esophageal, and lateral pleural space pressures with no transcardiac gradient being developed. Aortic pressure is efficiently transmitted to the carotid arteries, but retrograde transmission of intrathoracic venous pressure into the jugular veins is prevented by valves at the thoracic inlet and possibly by venous collapse. Thus, during "artificial systole" a peripheral arterial venous pressure gradient appears, and blood flow occurs consequent to this gradient. In such a system, there is no pressure gradient across the heart and thus the heart acts mearly as a passive conduit. Cineangiographic studies in large dogs confirm these observations by demonstrating partial right atrioventricular valve closure, collapse of the venae cavae, and opening of the pulmonary, left atrioventricular and aortic valves during thoracic compression. When thoracic compression is released ("artificial diastole"), intrathoracic pressures fall toward zero, and venous flow to the right heart and lungs occur. During "diastole", a modest gradient also develops between the intrathoracic aorta and the right atrium providing coronary (myocardial) perfusion.

In small dogs receiving vigorous chest compressions, intrathoracic vascular pressures are much higher than recorded pleural pressures. In these animals, the rise in vascular pressures likely is a result of compression of the heart during chest compression and is likely not a result of rising intrathoracic pressure.

7. What are the determinants of vital organ perfusion during CPR?

Cerebral blood flow is dependent on the gradient between the carotid artery and the intracranial pressure during systole (thoracic compression). Myocardial blood flow is dependent on the gradient between the aorta and right atrium during diastole (release phase of thoracic compression). During conventional CPR, cerebral and myocardial flow are less than 5% of prearrest values. Below the diaphagm, renal and hepatic blood flow during CPR is 1% to 5% of prearrest values.

8. What are the determinants of improved vital organ perfusion during CPR?

Force, rate, and duration of chest compression during CPR will determine the effectiveness of organ perfusion during CPR. Irrespective of the mechanism of forward blood flow during CPR, increasing the force of chest compressions increases arterial pressures. At pressures >400 newtons (about 40 Kg), bone and tissue trauma are more likely. Increasing the rate of chest compressions will significantly increase the arterial pressure.

GENERAL GUIDELINES FOR CPR IN ANIMALS

1. What is the optimal position for maximizing blood flow?

A lateral recumbency (with the sternum parallel to the table top) is used for animals < 7 Kg and, ideally, a dorsal recumbency for animals > 7 Kg. As we all know, it is extremely difficult to maintain a dog in dorsal recumbency without special "V"-shaped troughs or other techniques. However, the doral recumbency will provide maximal changes in intrathoracic pressure and thus forward blood flow. When no peripheral pulse is felt during CPR, consider changing the animal's position and your technique.

2. What is the optimal compression/relaxation ratio for administering external cardiac compression?

Studies have shown the best ratio of cardiac compression to ventilation is 1:1 (simultaneous compression-ventilation) in animals. This means you will breathe for the animal each time you compress the thoracic wall.

3. At what rate should you compress and ventilate when two persons are available to do CPR?

In animals weighing less than 7 Kg the recommended rate of ventilation and compression is 120 times per minute. In animals weighing > 7 Kg, the rate of compression and ventilation is 80 - 100 times each minute.

4. What is "interposed abdominal compression"?

To improve venous return and to decrease arterial run-off during external thoracic compression, have one person press upon the cranial abdomen between each compression of the chest. In humans, this has shown to improve hospital discharge rates as much as 33%. No comparable studies are yet available in animals.

5. What if there is only one person available to do CPR?

One person CPR in animals is very ineffective. The ratio of ventilation to chest compression is 15:2. Give 15 chest compressions and then 2 long ventilations. Use a rate of 120 chest compressions per minute when the animal weighs less than 7 Kg and 80 - 100 times per minute when the animal weighs > 7 Kg.

6. Is ventilation really necessary during CPR?

For more than 30 years, emergency ventilation has been considered an essential component of basic life support CPR. It would seem logical that ventilation has the potential to improve the success of resuscitation from cardiac arrest by improving tissue oxygenation and acidosis, but this benefit has only recently been studied.

When blood flow stops, ventilation does not affect tissue conditions. Ventilation does affect oxygenation, CO2, and pH of arterial and venous blood and may affect intracellular environment in the presence of low rates of blood flow. Ventilation may be unnecessary during the first few minutes of CPR, but under conditions of prolonged untreated cardiac arrest, it affects return of spontaneous circulation and is important for survival. Chest compression alone and spontaneous gasping provides some pulmonary ventilation and gas exchange. However, blood oxygenation can be improved with supplemental oxygen.

A recent report in experimentally induced cardiopulmonary resuscitation in swine has shown an excellent resuscitation rate through providing only cardiac compression. In fact, the researchers were unable to detect a difference in hemodynamics, 48-hour survival , or neurological outcome when CPR was applied with or without ventilatory support. With this in mind, if inadequate numbers of professional staff are available, apply only cardiac compressions if cardiopulmonary arrest is present.

7. When should I open the chest and do CPR?

Chest compressions raise the venous (right atrial) pressure peaks almost as high as arterial pressure peaks and increase intracranial pressure, thus causing low cerebral and myocardial perfusion pressures. Open chest CPR does not raise atrial pressures, provides better cerebral and coronary perfusion pressures and flows than external CPR in animals. When applied promptly in operating room arrests, open chest CPR, which was introduced in the 1880's until 1960 yielded good clinical results in people. The switch from external to open-chest CPR has not yet improved outcome in human patients, probably because its initiation was too late. There are no comparable studies available for clinically-employed open chest CPR in animals. Currently, open-chest CPR should be restricted to the operating room and in selected instances of penetrating thoracic injury.

8. How can one monitor the effectiveness of my external thoracic compressions?

Traditionally, the presence of a pulse during thoracic compression has been the hallmark of effective compression. More recently, while monitoring peripheral pulses using quantitative Doppler techniques have shown the pulse generated during compression was in fact from venous flow and not arterial. In veterinary medicine, monitoring the pulse will be the most commonly employed monitoring for effectiveness.

Using pulse oximetry can provide information on hemoglobin saturation. During CPR you should see an improvement of oximetry values and mucous membrane color. End-tidal carbon dioxide monitoring has proven to be the most effective means for measuring the effectiveness of CPR. This device fits in-line with the endotracheal tube and will measure carbon dioxide levels. With effective CPR you should see an increased end-tidal CO2.

9. What can you do if there is no pulse, change in oximetry or end-tidal CO2?

As mentioned above, consider changing the position of the animal, the force or the rate of thoracic compression.

10. How can you train your staff in CPR?

Periodic training sessions in basic life support should be conducted in each veterinary practice. This is not a time-consuming activity and the benefits are tremendous when your "team" can respond quickly and efficiently. An effective means to provide training is to develop an inexpensive "CPR Animal". These teaching aids were developed by simply taking some old corregated anesthetic tubing ("trachea"), an anesthetic Y-piece ("tracheal bifercation"), two anesthetic rebreathing bags ("lungs"), and then "implanting" them in the chest of a commercially available stuffed animal purchased at any retail outlet. These devices can then be used to practice CPR techniques with your staff. One can place foreign materials in the "mouth", can practice "Gen Chung" manuveurs, palpate for pulses, see the thorax expand with each breath, and feel the expanding "lungs" as you apply chest compression. Someone in your practice can manufacture this model and practice sessions can be called at any time to simulate the sudden, unexpected occurrence of an arrest.

ADVANCED LIFE SUPPORT

1. What drugs should one have available in the "crash cart"?

Drugs considered "necessary drugs" for cardiopulmonary arrest are as follows:

1) Epinephrine

2) Atropine

3) Magnesium chloride

4) Naloxone

5) Lidocaine

6) Sodium bicarbonate

7) Methoxamine

8) Bretylium tosylate.

2. What other drugs should be available?

Drugs which are important in the post-resuscitation phase of CPR include:

1) Dobutamine

2) Mannitol

3) Furosemide

4) Lidocaine

5) Verapamil

6) Sodium bicarbonate

7) Dopamine

8) Crystalloid fluids.

3. What are the indications for emergency drug use during CPR?

4. What is the best route for administration of drugs during CPR?

There are four commonly used routes for drug administration during CPR, each of them having their own advantages and disadvantages.

1) Intravenous (IV)-The preferred route for drug administration during CPR is the IV route. With central venous catheters drugs can be given rapidly and these drugs will be rapidly delivered to their site of action via the coronary arteries. When giving IV drugs during CPR it is important to follow each drug with a bolus of saline or water for injection to encourage the transport of the drug towards the heart. This is important as cardiopulmonary arrest usually results in hypotension, vasoconstriction, and hypovolemia. At present there are no conclusive data to support the use of a central venous rather than a peripheral venous route.

2) Intratracheal (IT)-The IT route has the advantages of accessibility, close proximity to the left side of the heart via the pulmonary veins, and a large surface area for drug absorption. The disadvantages of this route are the increased dosage required for many of the drugs (often 10 times the dosage given IV!), the decreased efficacy in the presence of pulmonary disease, and the fact some drugs cannot be given IT (ie, sodium bicarbonate).

3) Intraosseous (IO) or Intramedullary-The bone marrow cavity represents a large venous access to the cardiovascular system. Drugs normally given via the intravenous route may be given via the bone marrow cavity. The bone marrow cavity is most commonly accessed either through the trochanteric fossa of the femur or the distal cranial femur during CPR.

4) Intracardiac (IC)-Drugs can be delivered directly to the heart when given via the intracardiac route. When using the IC route, the difficulty comes with the inability of personnel to inject the drugs into the heart. Without the apex beat normally present, many find this technique to be most difficult in animals. Additionally, there are problems with the delivery of drugs into the myocardium instead of the ventricular chambers. This may result in dysrhythmias, laceration of coronary arteries, and will require you to discontinue basic life support while attempting the IC injections.

5. What are the common cardiac rhythms of cardiopulmonary arrest?

Remember, the only way you can distinguish between the various dysrhythmias of arrest is with the use of an electrocardiogram.

1) Ventricular Asystole-There is an absence of both mechanical and electrical activity on the electrocardiogram.

Ventricular Asystole

Treatment: Epinephrine, Atropine

2) Nonperfusing Rhythm-(Generally referred to as electromechanical dissociation or EMD). With this rhythm one will see 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.

Electromechanical Dissociation

Treatment: Naloxone, Epinephrine, Megadosage Atropine

3) Ventricular Fibrillation-Chaotic, disorganized, ectopic ventricular activity resulting in sustained ventricular systole. Remember, the coronary arteries perfuse the myocardium during diastole and therefore there is no perfusion taking place as long as the animal has ventricular fibrillation.

Ventricular Fibrillation

Treatment: Electrical DC countershock is the treatment of choice for ventricular fibrillation. If ventricular fibrillation is the first rhythm encountered, sequential attempts at electrical defibrillation should be performed. If ventricular fibrillation is not the first rhythm encountered, or if countershock results in persistent ventricular fibrillation or another nonperfusing spontaneous cardiac rhythm, endotracheal intubation should be performed, chest compressions initiated, and an intravenous line established in preparation for subsequent management of the observed rhythm.

The cardiac response to countershock is largely time-dependent (Figure 1). If countershock can be performed within 3 minutes of the onset of ventricular fibrillation, 70 to 80 percent of patients will convert to a rhythm associated with adequate perfusion (human data!). After 5 minutes of ventricular fibrillation, countershock rarely results in a spontaneous perfusing rhythm; asystole, EMD, or persistent ventricular fibrillation are the usual results.

Figure 1. Curves showing estimated success of defibrillation versus delivered energy after 1, 5, and 9 minutes of fibrillation in dogs receiving closed chest cardiac massage and artificial ventilation with epinephrine. (After Yakaitis et al, 1980).

If countershock fails to convert the ventricular fibrillation, epinephrine should be given (IV or IT). The beneficial effects of epinephrine depend primarily on its alpha1-adrenergic effects, which include arterial vasoconstriction and selective redistribution of cardiac output. Epinephrine increases the CPR diastolic aortic-to-right-atrial myocardial perfusion gradient (coronary perfusion pressure) by increasing aortic diastolic pressure and improves the cerebral perfusion gradient by increasing carotid arterial pressure. Chemical defibrillating drugs have unproven efficacy in clinical veterinary medicine. Unfortunately, many veterinarian do not have electrical defibrillators and thus the chemical defibrillating drugs may be the only option. Drugs which may be tried in ventricular fibrillation include: Bretylium tosylate or Magnesium Chloride. There are reports where these drugs have been effective in terminating ventricular fibrillation when electrical countershock has failed.

6. When using an electrical defibrillator, what are some of the important things to keep in mind?

The electrical defibrillator is the treatment of choice for ventricular fibrillation. It is also a very dangerous instrument which can cause injury to your patient and death to you if improperly used. The optimal delivered energy to the myocardium is roughly 2 - 4 joules/Kg. When delivering this countershock to the myocardium, it is only necessary to "hit" about 28% of the myocardial cells to defibrillate. Thus, paddle position is not as important as once believed. One should make every effort to reduce transthoracic impedance during electrical defibrillation. Factors which influence impedance are as follows:

1) Use large surface area paddles.

2) Countershocks applied close together may be most effective.

3) Use an electrode-skin interface material such as electrolyte paste or gel. DO NOT use alcohol!

4) Apply pressure to the electrodes.

5) Defibrillate during expiration.

Be careful!! Always announce "ALL CLEAR!" and look around to be sure nobody is in contact with the animal, table or instruments.

7. Is there anything different between a cat and dog in ventricular fibrillation?

In normal cats, the heart is generally small enough that it may spontaneously convert from ventricular fibrillation to a sinus rhythm. Unfortunately, sick cats may also have enlarged hearts. In these cases, electrical defibrillation should be attempted.

8. Which drugs should be used with caution during advanced life support?

1) Calcium will enhance ventricular excitability (thus increasing myocardial oxygen requirements!), it will decrease sinus nodal impulse formation, blood flow to the brain is reduced to nearly zero following calcium administration during CPR, it will cause coronary artery vasospasm, and is an important mediator in the formation of arachidonic acid and oxygen-free radical formation.

Currently, use of calcium during CPR is not routinely recommended except under conditions of hyperkalemia, hypocalcemia, or where calcium channel blocking agents have been previously used. CaCl2 will result in the longest and most predictable increase in plasma ionized calcium.

2) Isoproterenol is a pure B-agonist drug. It will produce increased myocardial oxygen demands and is shown to reduce cerebral blood flow during CPR. Currently, isoproterenol is reserved for patients with atropine-resistant bradycardias.

3) Sodium bicarbonate in the past has been a routine drug during CPR. There are many potential problems with the empirical use of this drug. The following list provides insight to some of these problems:

a. Increased serum osmolality (8.5% solution = 1500 mOsm).

b. The metabolism of sodium bicarbonate will result in the formation of increased PCO2

(HCO3- + H+ <===> H2CO3 <===> CO2 + H2O)

c. With inadequate ventilation, paradoxical cerebral spinal fluid (CSF) acidosis will result (HCO3- crosses the blood-brain barrier more slowly than CO2).

d. Sodium bicarbonate will shift the oxyhemoglobin dissociation curve to the left (decreased amounts of oxygen will be released to the tissues).

e. Direct myocardial depression will result with alkalosis (decreasing cardiac output).

f. Metabolic alkalosis (pH > 7.55) predisposes to cardiac dysrhythmias which may be unresponsive to antiarrhythmic therapy.

g. Before giving sodium bicarbonate, be sure the animal has adequate ventilation.

h. Ideally, administration of sodium bicarbonate should be based upon pH and PCO2.

Use of buffer therapy depends upon the duration of arrest and CPR times. Metabolic acidemia (base deficit) should be corrected, as proper acid-base balance improves cardiovascular resuscitability and cerebral recovery in dogs. After ventricular fibrillation no flow of five minutes in dogs, metabolic acidemia is mild and transient, and early empirical NaHCO3 administration is not harmful to the heart and may benefit the brain. After longer arrest or CPR times, evidence in animals of improved cardiovascular and cerebral recovery supports the recommendation to accompany epinephrine with an empirical dose of 1 mEq/kg of IV NaHCO3 during CPR, to be followed by correction of monitored base deficit greater than 5 mEq/kg NaHCO3. This may produce a transient CO2 load that worsens the arrest-induced myocardial hypercarbia, which can depress cardiac resuscitability. This NaHCO3-induced hypercarbia is usually mild, transient, correctable with hyperventilation, and harmless for the heart when used with epinephrine and was not apparently harmful to the brain.

4. Intravenous fluids are only administered during CPR when hypovolemia is the cause of the arrest. Fluid loading during CPR will result in decreased cerebral blood flow, increasing right atrial pressures (resulting in decreased coronary perfusion pressures) and therefore decreased coronary blood flow.

5. Doxapram hydrochloride is a central respiratory stimulant. Its use during CPR is not advised. Often the stimulation of the respiratory center will result in a transient hyperventilation followed by apnea.

9. What is the dilution of epinephrine during CPR?

Epinephrine is no longer diluted. The concentration of 1:1000 as it is packaged is what is used with IV, IT, IO, and IC routes.

PROLONGED LIFE SUPPORT

1. What are the main complications seen following resuscitation?

Recurrence of either respiratory or cardiopulmonary arrest is the biggest concern following resuscitation. In most cases the reoccurrence of arrest will occur within the first 4 hours of the first episode (Figures 4 and 5).

Figure 4. Cardiopulmonary arrest in the dog. (Wingfield WE, Van Pelt DR. 1992. Respiratory and cardiopulmonary arrest in dogs and cats: 265 cases (1986-1991). JAVMA. 200(12):1993-1996.)

Figure 5. Cardiopulmonary arrest in the cat. (Wingfield WE, Van Pelt DR. 1992. Respiratory and cardiopulmonary arrest in dogs and cats: 265 cases (1986-1991). JAVMA. 200(12):1993-1996.)

Following arrest cerebral resuscitation becomes the next most important complication. Due to the low flow state to the brain during CPR, ischemia and hypoxia will lead to cerebral edema.

As the heart begins to reperfuse tissues there may be significant injury products released to the systemic circulation.

2. What are some of the cerebral complications expected following cardiac arrest?

In normal brain, autoregulation will maintain a global cerebral brain flow of about 50 ml/100 g brain per minute, despite cerebral perfusion pressures (CPP) (ie, mean arterial pressure minus intracranial pressure) between 50 and 150 mm Hg. When CPP drops below 50 mm Hg, CBF decreases and the viability of normal neurons seems threatened by CPP less than 30 mm Hg, global cerebral blood flow less than 15 ml/100 g per minute, or cerebral venous oxygen partial pressures (PO2) of less than 20 mm Hg.

During complete cerebral ischemia, calcium shifts, brain tissue lactic acidosis, and increases in the brain free acids, osmolality and extracellular concentration of excitatory amino acids (particularly glutamate and aspartate) set the stage for reoxygenation injury.

3. What is the pathophysiology of the cerebral injury following resuscitation?

Postresuscitation cerebral injury appears to consist of four components: 1) Perfusion failure (ie, inadequate oxygen delivery, 2) reoxygenation chemical cascades to cerebral necrosis, 3) extracerebral derangements, including intoxication from postanoxic viscera, and 4) blood derangements due to stasis.

Perfusion failure seems to progress through four stages: 1) multifocal no reflow occurs immediately and seems to be readily overcome by normotensive or hypertensive reperfusion, 2) transient global "reactive" hyperemia, which lasts 15 to 30 minutes, 3) delayed, prolonged global and multifocal hypoperfusion, event from about 2 to 12 hours postarrest; global cerebral blood flow is reduced to about 50% of baseline, while global O2 uptake returns to or above baseline levels and cerebral venous PO2 decreases to less than 20 mm Hg, reflecting mismatching of O2 delivery to O2 uptake, and finally 4) after 20 hours, either normal global cerebral blood flow and global oxygen uptake are restored or both remain low (with coma), or there is a secondary hyperemia, postulated to be associated with reduced O2 uptake, followed by brain death.

Reoxygenation, while essential, also might provoke chemical cascades (involving free iron, free radical, calcium shifts, acidosis, excitatory amino acids, and catecholamines) that result in lipid peroxidation of membranes.

Extracerebral derangements can worsen cerebral outcome. Studies in dogs have shown a delayed reduction in cardiac output following cardiac arrest despite controlled normotension. Pulmonary edema can be prevented by prolonged controlled ventilation.

Blood derangements include aggregates of polymorphonuclear leukocytes and macrophages that might obstruct capillaries, release free radicals, and damage endothelium.

4. How do we manage the postresuscitation patient to reduce the adverse complications of cardiopulmonary resuscitation?

Careful monitoring is most important during the first 4 hours post-arrest. All patients require oxygen administered via an oxygen cage, nasal insufflation, or via facemask. If cardiopulmonary resuscitation was successful, one needs to support the heart during the post-resuscitation phase. This support is directed to inotropic support (dobutamine or dopamine), possibly using vasodilator drugs (sodium nitroprusside), and antiarrhythmic drugs (lidocaine). These drugs will be useful in reducing the pulmonary edema usually seen following arrest. Additionally, furosemide is usually administered to further reduce pulmonary edema.

Cerebral hypoxia and ischemia result during cardiopulmonary resuscitation. The end result is cerebral edema. Treatment for cerebral edema includes mannitol and usually corticosteroids. Additional drugs which may be tried to improve cerebral resuscitation include the following drugs:

-Calcium channel blocking drugs: Reverse cerebral vasospasm prevents the lethal intracellular calcium influx.

-Barbiturates: Mild calcium antagonists, decrease arachidonic acid and free fatty acid levels in neurons, decrease metabolic demands of the brain. To date, there is no conclusive evidence to support the use of barbiturates. Additionally, the sedation which results makes sequential neurological assessment impossible.

-Iron chelating drugs: Free radical scavengers. Experimental at this point but very hopeful results for the future.

5. How do you know the cerebral outcome of your patient following cardiopulmonary resuscitation.

One should always be concerned about irreversible cerebral injury following arrest. Daily neurological evaluations and assessment are required. Record your findings each day to note the progress of your patient.

Clinical features to observe following arrest include the following:

6. Are there patients that are unlikely to be resuscitated?

No studies are currently available in animals but studies in humans indicate that certain groups of patients do not survive. Such patients include those with oliguria, metastatic cancer, sepsis, pneumonia, and acute stroke. Very likely animals with these conditions also will not survive.

7. When do we employ do-not-resuscitate orders?

Do-not-resuscitate orders must be initiated by the pet owner. Good client communications will be useful anytime an animal is hospitalized. It is probably wise to advise owners that arrest occurs suddenly and unexpectantly. Ask the owner "how far should we go if the pet arrests". Record the response and abide by the owner's wishes.

The decision to stop cardiopulmonary resuscitation must be tempered with common sense, client communication, and experience of the resuscitators. Our experience suggests that the mean duration of CPR is generally about 20 minutes.

After more than 30 years of widespread use of CPR, the reevaluation of its benefits in terms of survival and the quality of life shows it to be a desperate effort that will help only a limited number of patients. For most, CPR is unsuccessful.

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