Cardiopulmonary resuscitation (Proceedings)

Definition

Cardiopulmonary arrest (CPA) is the cessation of functional ventilation and effective circulation. Apneustic gasps may occur, but do not produce effective ventilation. Similarly, cardiac electrical or muscle activity may persist, but effective tissue perfusion does not occur. Clinical signs of CPA include absence of auscultable heartbeat, lack of palpable pulse, apnea or agonal gasping, absence of bleeding, loss of consciousness, and pupillary dilation.

Predisposing Factors

When possible, the clinician should anticipate CPA in critical patients and eliminate predisposing factors. Electrolyte and acid-base imbalances should be identified and corrected. Animals with respiratory distress should be observed closely with minimal stress and receive supplemental oxygen. Shock, trauma, sepsis, hypothermia, and cardiac arrhythmias may all result in CPA if not treated aggressively. In anesthetized patients, anesthetic overdose, hypoventilation, inadequate fluid volume, and extreme hypothermia should be avoided.

Successful Resuscitation

The patients most likely to be successfully resuscitated are those which were normal prior to the incident resulting in CPA and those in which CPR techniques were initiated immediately. It is important to have a "CPR station" at the hospital which is kept in a state of continual readiness. A crash cart should contain an assortment of endotracheal tubes, catheters, syringes, gauze, and cardiac drugs already drawn up in appropriate sized syringes. In addition, sterile instruments should be available. The station must be near an oxygen source, an electrocardiogram, and a defibrillator with internal and external paddles. It is often helpful to have a list of cardiac drugs with dosages posted in this area.

When an arrest occurs, the clinician must respond with urgency, but not with panic. The approach is methodical and deliberate, but efficient. The clinician needs to remember to proceed in an orderly fashion though the "ABC's" of CPR, and not to jump out of sequence.

"A" is for Airway

The first step of CPR may very well be the most important, since subsequent efforts are futile if the animal is not receiving oxygen. As soon as the clinician has determined that CPA has occurred (no palpable pulse, no auscultable heartbeat), the animal should be intubated. Due to the importance of this step, the clinician must make SURE that the endotracheal tube is in the trachea. This can be done by 1) direct visualization of the tube entering the glottis or 2) palpation of the tube in proper position between the arytenoid cartilages. The cuff should be inflated and the tube secured in place.

Some animals with upper airway obstruction cannot be intubated orally. In these animals, an emergency slash tracheostomy should be performed to establish an airway.

"B" is for Breathing

Once the airway is established, the animal should be ventilated several times with 100% oxygen and then quickly checked for return of the heartbeat. If there is no heartbeat, some clinicians, including this author, recommend immediate defibrillation. This technique will be discussed in a later section.

Artificial ventilation is administered by intermittent positive pressure breathing (IPPB) using either an Ambu-bag with 100% oxygen or an anesthetic machine (anesthetic gas turned off; tubing and bag flushed or replaced). Animals should be ventilated at least 12 times per minute. Popular ratios include 1 breath per 5 compressions with 2 rescuers, or 2 breaths per 15 compressions for a single rescuer, with the breaths interposed between compressions. Recent recommendations, however, call for more rapid ventilations which are timed simultaneously with cardiac compressions. The increased ventilatory rate tends to off-set metabolic acidosis that invariably develops with CPA, and will help to remove CO2 which can build up to very high levels, especially if sodium bicarbonate is administered. Simultaneous ventilations and external chest compressions have been associated with increased blood flow and cardiac output due to the effect of generalized increased intrathoracic pressure on the thoracic pump mechanism. At our hospital, ventilations are administered simultaneously to external chest compressions at the rate of 40-60 breaths per minute.

Recommended inspiratory pressures for IPPB are 20 cm water (dog) and 15 cm water (cat). When ventilations are simultaneous with compressions, higher pressures (20-30 cm water) may be required. Animals with pleural fluid, pulmonary edema, hemorrhage, or pneumonia may also require higher pressures to obtain lung expansion. Inspiratory time should be less than 1.5 seconds to allow for adequate venous return as the intrathoracic pressure drops. It is also important that expiratory pressure be allowed to fall to 0 cm H20 between forced inspirations. Generally, positive-end-expiratory-pressure (PEEP) is not indicated in CPA because it diminishes venous return, cardiac output, and the effectiveness of the thoracic pump mechanism.

"C" is for Circulation/Cardiac Compressions

As soon as an airway has been secured and CPA persists despite 3-4 rapid ventilations, immediate defibrillation should be considered. In humans, defibrillation within 1 minute of CPA has a 98% chance of conversion, within 4 minutes a 50% chance, and within 10 minutes a 1% chance. Because of the rapid decline in effectiveness over time, defibrillation should be attempted as soon as possible — before drugs are administered, before compressions are initiated, even before the electrocardiogram in some instances. Ventricular fibrillation is the most common arrhythmia in CPA and some cases of asystole may actually be fine fibrillation. The benefits of immediate defibrillation outweigh the potential hazards of unnecessary defibrillation. The harmful effects of a single direct current countershock on the non-fibrillating myocardium are thought to be minimal.

External cardiac compressions are accomplished by applying pressure directly over the animal's heart at the rate of 80-120 times per minute. In cats and dogs less than 6 kg, the thorax can be compressed between the thumb and forefingers of one hand. According to the "cardiac pump theory" the AV valves remain functional, and when the heart is compressed blood moves out of the ventricles into systemic circulation.

In larger animals, closed chest compressions are performed with the animal in lateral recumbency with its back towards the clinician. The veterinarian stands above the animal and, with arms extended, applies pressure over the heart with the palms of one or both hands. The diameter of the chest should be compressed by 25-30% and the pressure fully released between each compression.

According to the "thoracic pump theory", it is not direct compression of the heart but changes in intrathoracic pressure which result in circulation of the blood. Since veins are thin-walled, they tend to collapse with increased intra-thoracic pressure, and blood flows into the arteries. Venous valves also help to prevent retrograde blood flow.

In large or obese dogs > 25 kg, it may be difficult or impossible to obtain adequate cardiac output with closed chest compressions. Therefore, if there is no improvement in mucous membrane color or peripheral pulses within 3-5 minutes after instituting closed chest compression, internal cardiac massage should be implemented.

For internal massage, the right side of the chest is rapidly clipped and an incision is made over the fifth intercostal space. A stab incision is made into the thorax and is widened by inserting the curved blade of Metzenbaum scissors and running them dorsally and ventrally along the length of the rib. The pericardial sac should be opened, avoiding the phrenic and vagus nerves. The heart is compressed from the ventricles toward the base of the heart.

Other conditions which require internal cardiac massage include tension pneumothorax, diaphragmatic hernia, flail chest/rib fractures, pericardial effusion, and pleural effusion.

"D" is for Drugs and Defibrillate

Table I lists the drugs most commonly used in CPR.

There are 5 routes which can be used to administer drugs during CPR. Intravenous may be used if a catheter is already in place. If there is no venous access, a venous cut down should be done over the jugular vein. In cats, the medial saphenous vein is often the most accessible. When there is no venous access, drugs can be given via the sublingual route. The injection is made into the ventral meaty part of the tongue and is rapidly absorbed due to the preferential circulation to the head and brain. Drugs such as epinephrine, atropine, lidocaine, and dexamethasone can also be administered by the intratracheal route. The intravenous dosage is doubled and the drugs are diluted with 5-10 ml diluent and administered into the lower airway with a catheter passed through the endotracheal tube. Drug administration should be followed by several deep insufflations. The intraosseous route is useful in neonatal and very small animals. A spinal needle can be placed through the trochanteric fossa to the medullary cavity of the femur. All drugs, including shock dose fluids and/or blood transfusions, can be administered via this route. Intracardiac injections are not recommended routinely because of the potential hazards involved, including lung laceration, coronary vessel lacerations, and refractory ventricular fibrillation resulting from intramuscular injection into the myocardium. In addition, intracardiac injection necessitates cessation of external cardiac compressions. Intracardiac injections can still be effective during internal cardiac massage, since the likelihood of coronary vessel or lung damage is greatly reduced.

The importance of early defibrillation has already been stated. The recommended dosage for shock therapy ranges from 4-20 joules/kg (external) and 1-2 joules/kg (internal). Since excessive energy can damage the myocardium, it is best to start at lower dosages and increase as needed. To prevent burning and tissue damage, electrode gel must be applied to the paddles generously, and good contact made on either side of the chest opposite the heart (left 6th intercostal space and right 4th intercostal space). For persistent ventricular fibrillation, the animal is defibrillated (three times, increasing dosages), then given epinephrine, then repeat defibrillation, then lidocaine, then repeat defibrillation. This cycle can be repeated with increasing electrical charges, substituting bretylium for lidocaine the second time. Sodium bicarbonate can be administered at the clinician's discretion after 10 minutes.

"E" is for Electrocardiogram and Evaluation

There are 5 different arrhythmias seen with CPA.

1. Electromechanical Dissociation (EMD) occurs when the electrical activity of the heart appears normal on the electrocardiogram tracing, but mechanical activity of the heart is absent. It is believed to result from a failure of the calcium transport system, which is necessary for electrical depolarization to result in mechanical contraction. EMD is associated with significant pump failure and carries a grave prognosis. Epinephrine is the drug of choice. Calcium is no longer recommended by the American Heart Association as treatment for EMD because retrospective studies showed no benefit from its use. Instead, calcium may contribute to impaired neurologic recovery caused by adverse metabolic effects of calcium salts. Calcium administration is only recommended in cases of known hypocalcemia, life-threatening hyperkalemia, or calcium channel blocking agent overdose.

2. Pulseless Idioventricular Rhythm (PIVR) appears as slow, wide bizarre QRS complexes on the ECG tracing and is due to progressive failure of the conduction system. Dexamethasone can help to stabilize membranes and may cause release of ATP from the mitochondria. Dexamethasone administration was associated with improved resuscitation rate in people with PIVR. Atropine may also be helpful by reducing parasympathetic tone. Epinephrine is also given to improve myocardial and cerebral perfusion by peripheral vasoconstriction resulting from alpha adrenergic stimulation.

3. Ventricular Asystole is characterized by complete absence of ventricular activity. Treatment recommendations include immediate defibrillation, followed by atropine and epinephrine. A sharp blow to the chest (precordial thump) may also be attempted, although results of 1 study in dogs showed no benefit with this technique. The precordial thump should not be used in dogs with ventricular tachycardia, as it may result in ventricular fibrillation.

4. Ventricular flutter is a very rapid form of ventricular tachycardia which, if not treated, usually degenerates into ventricular fibrillation. The treatment of choice is synchronized cardioversion. If equipment is not available, lidocaine, procainamide or bretylium may be successful in converting the arrhythmia.

5. Ventricular Fibrillation appears as disorganized chaotic waves on the electrocardiogram. Immediate defibrillation is indicated. In the absence of a defibrillator, chemical defibrillation (1 mg potassium chloride and 6 mg acetylcholine/kg, followed by 1 ml/10 kg 10% calcium chloride) may be attempted, but it is rarely effective. Fine fibrillation should be converted to coarse fibrillation with epinephrine before countershock is attempted. The American Heart Association guidelines recommend 3 rapid consecutive attempts at defibrillation followed by epinephrine in refractory cases. After repeat defibrillation, lidocaine may also be given before repeating defibrillation at increasing shock dosages.

After completing the previous steps of CPR, the patient should be evaluated. Favorable prognostic signs include spontaneous breathing, attempts to swallow, return of palpebral reflex, responsive pupils, normal sinus rhythm, and strong pulses. Lack of response to CPR within 30 minutes generally warrants a poor prognosis and resuscitative efforts are discontinued.

Post-Resuscitative Care

If an animal survives internal cardiac massage, the chest should be lavaged and closed under sterile conditions and broad spectrum systemic antibiotics administered.

Complications to anticipate in the post-resuscitative patient include cardiac arrhythmias, neurologic deficits (including temporary or permanent blindness), cerebral edema, pulmonary edema, gastrointestinal mucosal sloughing, renal failure, hypothermia, and shock. Patient monitoring should include CNS signs, heart rate, peripheral pulses, blood pressure, electrocardiogram, urine output, capillary refill time, mucous membrane color, temperature, respiration, and acid-base/electrolyte status. Low dose dopamine (2-3 μg/kg/min) infusion will dilate renal arteries and may stimulate urine output. Higher doses of dopamine (5-10 μg/kg/min) increase cardiac output and raise blood pressure by peripheral vasoconstriction. Dobutamine (5-10 μg/kg/min) is a positive inotrope with less vasoconstrictor and chronotropic effects than dopamine. Epinephrine can also be administered as a continuous infusion to maintain blood pressure and cardiac output.

Drug Therapy for Cardiopulmonary Resuscitation

I. Drugs to Increase Blood Pressure or Cardiac Output

Pressor agents should be tapered off as soon as possible, or irreversible renal damage may occur. Furosemide (1-2 mg/kg) and mannitol (1-2 g/kg) may promote urine output and reduce cerebral edema. Steroids may also be useful in the treatment of shock and cerebral edema. Other drugs such as iron chelators (desferroxamine) and oxygen radical scavengers (DMSO, allopurinol, mannitol) may be beneficial in preventing reperfusion-induced cellular injury. At the present time, much research is being conducted in this area. Definitive recommendations await the results of these on-going studies.

Drug Therapy for Cardiopulmonary Resuscitation

II. Drugs to Increase Contractility

III. Anti-arrhythmic drugs

IV. Drugs for supportive care.