Cardiopulmonary Arrest and Resuscitation:
Basic Life Support
In the Dog and Cat

Wayne E. Wingfield, MS, DVM

wwingfie@vth.colostate.edu

http://www.cvmbs.colostate.edu/clinsci/wing/cpr/blsnotes.htm
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Table of Contents:
Introduction
       Risk Factors
        Warning Signs and Diagnosis of Cardiopulmonary Arrest
        Phases of Cardiopulmonary Resuscitation and Goals
            Basic Life Support
        General Guidelines for CPR in Animals
        Selected References


INTRODUCTION

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 resuscitation (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:

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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.

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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.

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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.

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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 (cerebral perfusion pressure) is dependent on the gradient between the carotid artery and the intracranial pressure during systole (thoracic compression). Myocardial blood flow (myocardial perfusion pressure) 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.

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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.

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SELECTED REFERENCES

1. Babbs CF. Interposed abdominal compression-CPR: A case study in cardiac arrest research. Ann Emer Med 1993;22:24-32.

2. Babbs CF. New versus old theories of blood flow during CPR. Crit Care Med 1980;8:191-196.

3. Babbs CF. Effect of thoracic venting on arterial pressure, and flow during external cardiopulmonary resuscitation in animals. Crit Care Med 1981;9:785-788.

4. Berg RA, Wilcoxson D, Hilwig RW, et al. The need for ventilatory support during bystander CPR. Ann Emer Med 1995;26(3): 342 - 350.

5. Chandra NC. Mechanisms of blood flow during CPR. Ann Emer Med 1993;22:281- 288.

6.. Haskins SC. Internal cardiac compression. JAVMA 1992;200:1945-1946.

10. Henik RA. Basic life support and external cardiac compression in dogs and cats. JAVMA 1992;200:1925-1930.

11. Janssens L, Altman S, Rogers PAM. Respiratory and cardiac arrest under general anesthesia: Treatment by accupuncture of the nasal philtrum. Vet Rec. Sept.22, 1979:273-276.

12. Kass PH and Haskins SC. Survival following cardiopulmonary resuscitation in dogs and cats. Vet Emer Crit Care 1993;2:57-65.

13. Neimann JT, Rosborough JP, Hausknecht M, et al. Pressure synchronized cineangiography during experimental cardiopulmonary resuscitation. Circulation 1981;64:985.

14. Niemann JT. Cardiopulmonary resuscitation. NEJM 1992;327:1075-1080.

15. Rudikoff MT, Maughan WL, Effron M, et al. Mechanisms of flow during cardiopulmonary resuscitation. Circulation 1980;61:345-351.

16. Ward KR, Sullivan RJ, Zelenak RR, et al. A comparison of interposed abdominal compression CPR and standard CPR by monitoring end-tidal CO2. Ann Emerg 1989;18:831-837.

17. Wingfield WE, Van Pelt DR. Respiratory and cardiopulmonary arrest in dogs and cats: 65 cases (1986 - 1991). JAVMA 1992; 200:1993-1996.

18. Wingfield, WE. Cardiopulmonary arrest and resuscitation in small animals. Part I. Basic life support. Emerg Science Technol 2:21-26, 1996.

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Copyright, 1998.  Wayne E. Wingfield, DVM, Colorado State University.  All Rights Reserved.
This page was last edited:  07/19/01