Cardiopulmonary-cerebral resuscitation (Proceedings)

Cardiopulmonary arrest (CPA) is defined as the cessation of functional ventilation and effective circulation. Factors predisposing to CPA may include respiratory or cardiovascular abnormalities (hypoxia, hypercarbia, hypotension, cardiac arrhythmias, or severe anemia); acid-base, electrolyte, or metabolic abnormalities (acidosis, hyperkalemia, hypoglycemia); or hypothermia. Cardiopulmonary-Cerebral Resuscitation (CPCR) is the combination of basic life support and advanced life support techniques, as well as post-resuscitation care.

Reports on the rate of return of spontaneous rhythm vary from 30% to 60%. However, reported rate of survival to discharge is only 2-14% in human patients. A study in veterinary patients showed 1-week survival post CPCR to be only 4%.

The prognosis improves if the patient has a reversible underlying disease process. These conditions can include anesthetic overdose, vagally mediated arrest, upper airway obstruction, hemorrhage, and electrolyte abnormalities. Successful resuscitation from arrests secondary to these reversible conditions may lead to long-term survival, so aggressive resuscitation efforts are warranted.

A grave prognosis exists for patients with severe predisposing conditions such as sepsis, SIRS, neoplasia, or severe cardiac, pulmonary or neurologic disease. In these instances, the clinician and owner need to consider carefully whether or not to institute resuscitative efforts.

Regardless of cause, a better prognosis is associated with CPCR instituted immediately after witnessed CPA. The sooner the CPCR is instituted following CPA, the better the prognosis for return to spontaneous rhythm, therefore it is very important to closely monitor patients with predisposing conditions.

Once CPCR is instituted, a grave prognosis exists if there is no return of spontaneous rhythm within 20 minutes. In patients that do respond to CPCR, re-arrest rates are reported to be 68% in dogs and 37.5% in cats following initial resuscitation.

Basic Life Support is the ABC's. A = Airway. Check for and relieve any obstructions to breathing such as pharyngeal or tracheal foreign bodies. Suction any blood or fluid from the airway. The patient should be intubated immediately. If intubation is impossible, an emergency tracheostomy may be necessary. Verify placement of the tracheal tube, inflate the cuff, and tie securely in place.

B = Breathing. Positive pressure ventilation should be instituted with 100% oxygen. The rate should be 10-24 breaths/min, depending on the size of animal. Inspiratory pressure should reach approximately 15 cmH2O in the cat or approximately 20 cmH2O in the dog. Monitor for adequate chest wall movement with each breath. If chest movements are inadequate, search for the cause: tube malposition, occlusion, or pleural space diseases (pneumothorax, pleural effusion, diaphragmatic hernia). Always allow complete exhalation before beginning the next inhalation.

Hyperventilation should be avoided, as this is associated with a poor outcome. This is due to increased intrapleural pressure, which, in turn, decreases coronary perfusion pressures and blood pressure.

C = Circulation. Our most important goal in CPCR is to maximize myocardial and cerebral perfusion. Myocardial perfusion pressure is determined by the difference between aortic diastolic pressure and right atrial pressure. Cerebral perfusion pressure is determined by the difference between mean arterial pressure and intracranial pressure.

External chest compressions should be initiated first. Apply pressure to compress the chest a minimum of 25-30% at a rate of 100-120 compressions per minute. The animal can be in lateral or dorsal recumbency, depending on the body type. Allow the chest to fully recoil between compressions. It is extremely important to limit any interruptions in chest compressions, as continuous, properly performed chest compressions is the one component of CPCR that has been associated with an improved outcome.

Hand position for chest compressions depends on the size of the patient, as there are two different theories behind the use of chest compressions to improve circulation. The heart pump theory is employed in cats, small exotic species, small dogs, and neonates 9<10kg). This theory assumes direct compression of the heart ventricles causes blood to flow out of the ventricle into the aorta. These chest compressions should be performed directly over the heart using one or two hands.

The thoracic pump theory is employed in dogs greater than 10-15kg. In these patients, compressions are performed over the widest part of the chest. These compressions cause a generalized increase in thoracic pressure, causing blood to move out of the heart and aorta. The pressure-induced collapse of the great veins prevents backward flow of blood; so oxygenated blood is pumped out of the heart into the arteries.

Several augmentation techniques have been variably recommended to increase the success of closed chest compressions. Interposed abdominal compressions involve a second compressor. In this technique, the abdomen is compressed during the relaxation phase of the chest compression. This results in blood flow back into the chest during the relaxation of the heart, and thereby augments blood pressure, cardiac output, and myocardial and cerebral blood flow. The danger of this technique is that it can lead to damage to abdominal organs.

A second augmentation technique is the use of simultaneous ventilation and compression. This results in a greater intrathoracic pressure during the compression phase, thereby increasing systolic and diastolic blood pressure and cerebral blood flow. However, this technique is very difficult to achieve and can cause lung damage, therefore it is not recommended at this time.

Internal heart compression (Open Chest CPR) is associated with better cardiac output, arterial blood pressure, cerebral and coronary perfusion, myocardial perfusion, and peripheral tissue perfusion, higher survival and improved neurologic outcome. Indications for open chest include failure of closed chest compression to return an effective heart beat within 2-5 minutes; un-witnessed arrests; inadequacy of closed chest compression to create effective circulation (i.e. giant breeds); pneumothorax, rib fractures, diaphragmatic hernia, and pericardia or pleural effusions. When using this technique, consider aortic cross clamping which helps direct essential blood flow to the brain and heart. If indicated, internal defibrillation can be performed on an exposed heart.

The technique for performing internal chest compressions begins with a quick clipping of hair along the line of the intended incision. A quick swab with antiseptic solution should substitute for a full surgical scrub. An incision is made midway between ribs down to the thoracic pleura. Penetrate the pleura with a finger or hemostat (not during inspiration) then extend the incision dorsally and ventrally with scissors, avoiding the internal thoracic artery.

Once the chest is open, break the sternopericardial ligament ventral to the heart, gently lift the heart, and open the pericardial sac. Compress the heart between flats of the fingers and palm of the hand. Dog studies show that compressing the heart with two hands is superior to one hand. Higher rates—up to 150 compressions/min are associated with higher vital organ perfusion pressures. Compress from apex to base, allowing filling between compressions.

Advanced Life Support includes drugs, defibrillation, and electrocardiography. Intravenous fluid therapy should be carefully considered during CPCA. It is very important to avoid causing hypervolemia, so fluids may not be necessary for every CPA patient. Rapid intravenous isotonic crystalloid at 10-40ml/kg may be administered if the animal has a pre-existing hypovolemia or significant ongoing losses that may have led to the arrest. Other fluids to consider include hypertonic saline (4-6ml/kg), mannitol (5-10ml/kg of 20-25%), or colloids (5-10ml/kg) IV bolus. These fluids require a smaller volume and may remain in the vascular space longer than crystalloids.

Electrocardiography is essential to CPCR. There are five heart rhythms commonly associated with cardiac arrest. Ventricular asystole is the cessation of all electrical or mechanical activity. Ventricular fibrillation appears as chaotic electrical activity with no associated mechanical contraction. On visualization, the heart is rippling but not effectively contracting. Pulseless electrical activity (PEA) may appear as a normal EKG but is associated with no mechanical activity. Bradycardia is caused by increased vagal tone and appears as a slow EKG rhythm with mechanical contractions present. Cardiovascular collapse (respiratory arrest, severe hypotension) may have a normal EKG with mechanical contractions present.

Pharmacological agents are commonly used in CPCR to help increase blood pressure and cardiac contractility, increase heart rate, or convert an arrhythmic rhythm. Route of administration of drugs is an important consideration, as many of these patients may not have intravenous access, and none of these patients have normal or effective circulation to deliver these drugs to the intended organ (heart).

The peripheral venous route provides the easiest access, however the ineffective circulation creates a time delay in delivering the drug to the heart. The anterior vena cava may be accessed via a jugular catheter. This is the ideal route, as it is close to heart. Consider performing a cut down to access the jugular vein.

Intracardiac administration of drugs is no longer recommended during CPCR, as a blind injection may cause lung laceration, coronary artery laceration, or atrial or right ventricular laceration. Cardiac trauma may also lead to refractory ventricular fibrillation.

The intratracheal route is easily accessible, however there is variable and unpredictable drug uptake. Therefore, when using this route, double the intravenous drug dosage and dilute in 5-6mL of saline to promote absorption. Drugs that can be delivered via the intratracheal route included epinephrine, atropine, vasopressin, and lidocaine. Epinephrine should be given at the high dose (0.1-0.2mg/kg) if given via this route.

The intraosseous route may be useful, especially in neonates. Sites for intraosseous injections include the trochanteric fossa of the femur, proximal humerus, or tibial crest. The sublingual route allows rapid reabsorption due to preferential circulation to the head and may be useful if other routes are unavailable.

Sympathomimetics are commonly employed during CPCR. Epinephrine is recommended for use in the management of asystole, PEA, refractory VF, or pulseless VT. Epinephrine possesses both α-adrenergic and β-adrenergic activity. Alpha effects are of primary importance during CPR as α-agonism leads to arterial and venous constriction. This redistributes blood from venous capacitance vessels into the arterial circulation and increases arterial blood pressure. β-agonism stimulates pacemaker activity and enhances cardiac contractility. Deleterious beta effects include peripheral vasodilation, chronotropy, and inotropy that may increase cardiac work and myocardial oxygen demand. There are two dose recommendations for epinephrine. The low dose is 0.01-0.02 mg/kg, and the high dose is 0.2mg/kg. The high dose is associated with a higher incidence of ventricular arrhythmias and fibrillation and in humans is shown to have no benefit and is associated with worse 24-hour survival. Therefore, it is currently recommended to start with the low dose and repeat at 3-5 min intervals. The high dose may then be given if there is no effect.

Vasopressin is a potent vasopressor that exerts its effects by directly stimulating V1 receptors in vascular smooth muscle. The response to vasopressin is not blunted in the face of acidosis, an advantage over epinephrine. Vasopressin lacks β activity, and therefore is not associated with increased myocardial oxygen demand. The dose is 0.8 U/kg IV once. Some studies have shown that vasopressin is more effective than epinephrine at increasing myocardial blood flow and restoring spontaneous cardiovascular function.

Anticholinergics are indicated for asystole, PEA, or sinus bradycardia, as excessive vagal tone and lack of an escape rhythm may maintain asystole. Atropine is used at a dose of 0.04mg/kg. Lower doses (0.004-0.01 mg/kg) may be recommended if sinus bradycardia is the primary rhythm. Low doses may increase vagal tone and cause temporary worsening of bradycardia and high doses may cause sinus tachycardia or ventricular fibrillation.

Sodium bicarbonate is another consideration during CPCR, as patients develop a moderate to severe metabolic acidosis during cardiac arrest. Alkalinization may help to speed resuscitative efforts and neurologic recovery. However, the use of sodium bicarbonate is controversial, as several potential side effects can occur. These may include metabolic alkalosis, intracellular or CSF acidosis, hypokalemia, hypocalcemia, hypernatremia and hyperosmolality. The dose is 0.5-1 mEq/kg IV per 5 minutes. Indications for consideration of sodium bicarbonate can include prolonged CPCR (>10min), severe hyperkalemia, or a severe pre-existing metabolic acidosis.

Calcium is not used routinely during CPCR as it may worsen already high intracellular calcium. However, calcium may be indicated if a life-threatening hyperkalemia exists, or if there is a severe hypocalcemia or an overdose of calcium channel blockers. Calcium may also be considered if all other efforts have failed. The recommended dose is 0.2ml/kg of 10% CaCl or 0.6ml/kg of 10% Ca gluconate IV.

Magnesium may be considered if there are refractory arrhythmias such as ventricular flutter, ventricular fibrillation, or non-responsive cardiac arrest. The recommended dosage is 0.15-0.3mg/kg IV slowly.

Antiarrhythmics may be necessary during CPCR. Lidocaine (1-3mg/kg) may be considered in cases of VF or VT, however caution should be used as the ventricular rhythm may be the patient's only rhythm, so stopping it may lead to complete loss of cardiac rhythm. Lidocaine has rarely been associated with an improved outcome, so it is rarely used.

Amiodarone is the first line antiarrhythmic for VT/VF in humans. It has been shown to increase return of spontaneous circulation and improve early survival in humans. However, animal studies have not been performed, and this drug is less likely to be helpful in the animal patients, as VT/VF is rarely the underlying rhythm.

Corticosteroids have no real evidence supporting their use in CPCR, so they are not recommended at this time.

Defibrillation is indicated as soon as ventricular fibrillation is identified, even before drugs are administered. Place a paddle under the animal in lateral recumbency and a paddle on the upper side. Start with a lower dosage and increase as needed. The starting dosage for external defibrillation is 3-5 joules/kg and for internal is 0.5-1 joules/kg. For refractory ventricular fibrillation defibrillate three times in rapid succession, increasing dose by 50% each time.

Monitoring the efficacy of resuscitation can be accomplished using multiple methods. Physical exam findings, including femoral pulse palpation, may be misleading, as they do not necessarily correlate with perfusion.

Blood gas analysis can be performed but should be interpreted with caution. The arterial pO2, pCO2, and pH may be normal or near normal, but tissue perfusion can still be very low. Venous blood gases are a more accurate reflection of tissue acid-base status.

End-tidal capnography is linearly related to cardiac output at a constant rate of ventilation. A higher end-tidal CO2 reflects greater delivery of CO2 and therefore greater blood flow from the periphery to the pulmonary capillaries. Studies have shown a correlation between increased EtCO2 and cardiac output, coronary perfusion pressure, and successful resuscitation.

Post-resuscitative care is essential to the long-term success once return of spontaneous circulation is accomplished. Rapidly search for and correct any underlying causes of the CPA.

Intensive monitoring and aggressive supportive care are required to prevent re-arrest and significant tissue/organ damage. It is essential to optimize cardiac output, blood pressure, oxygenation, ventilation and vital organ perfusion.

Pulmonary care should include positive-pressure ventilation if the patient is apneic or bradypneic. The lungs should be evaluated for pneumothorax, pulmonary edema, or pulmonary contusions. Radiographs and arterial blood gases may help determine the animal's ability to oxygenate adequately. Oxygen therapy should be provided post-CPCR to increase oxygenation of the tissues.

Evaluating the patient's blood pressure, urine output, blood gas, and central venous pressure should monitor tissue perfusion. Echocardiography may be considered to evaluate myocardial function. Administer catecholamines (dopamine, dobutamine) as needed to support arterial blood pressure and correct any hypovolemia.

Neurologic recovery post-CPA is vital. Cardiac arrest results in cerebral hypoxia, depletes glucose and glycogen stores, and depletes ATP stores. Energy-deficient cells accumulate sodium, calcium, and iron, resulting in cell death. Post-arrest consciousness should begin to return within 15-30 minutes, if no return, assume there is significant cerebral damage.

Avoid hypervolemia or hypertension, hypovolemia or hypotension, hypercapnea or hypocapnea, hypoxia, hyperthermia, or any excess activity. Avoid venous outflow obstruction and drugs such as ketamine, inhalational anesthetics, and xylazine. Mannitol (0.5 g/kg slow IV) may decrease cerebral edema and scavenges hydroxyl radicals. Furosemide (0.5-1 mg/kg) redistributes blood away from the brain and removes excess fluids from the body. Avoid hyperthermia, and err on side of hypothermia for 24-hours post CPA.

Conclusion

Adequate understanding of and preparation for CPCR is vital to its success. Many patients can recover fully from an arrest if the clinician and hospital are trained and fully prepared to deliver prompt, appropriate CPCR when indicated.

References available on request.