Abstract

The keys to optimize success of CPCR are prompt intervention, adequate CPCR protocol, efficient team work and frequent training. The etiology of the arrest should influence prioritization of CPCR technique. For cardiopulmonary arrest (CPA) the CAB protocol is advocated, Compressions first, followed by Airway and Breathing, whereas, in the respiratory arrest ventilation is mandatory. The new guidelines for CPCR emphasize the importance of providing continuous uninterrupted chest compressions CCCPR, if necessary interruptions should be minimized to <10 seconds. The chest wall should be allowed to completely recoil after being compressed at least 30% of the chest diameter. Chest compressions must never be interrupted but if a second rescuer is available orotracheal intubation is advocated. Each time positive ventilation is on board the intrathoracic pressure increases thus reducing venous return to the heart, coronary perfusion and CPP. Current recommendations include 1 sec. positive inspiration phase followed by complete relaxation at respiratory rate < 10-12bpm. An impedance threshold device (ITD) limits air entry into the lungs during chest recoil thus improving venous return, hemodynamic parameters, CPP, myocardial perfusion and ROSC when used as an adjunct to CPCR in intubated cardiac arrest patients. CCCPR for 60sec before defibrillation and for 2 minutes after a single shock before reassessment of the rhythm by ECG is recommended for ventricular fibrillation. For asystole and pulseless electrical activity resuscitation defibrillation is contraindicated, high-quality CCCPR is indicated. Vasopressin has shown improved outcomes in human asystolic arrests and may show promise in veterinary medicine. In order to prevent stone heart, the current recommended dose for epinephrine is lower than ever 0.01-0.02mg/kg/iv/3-5min. Amiodarone is the medication of choice for treatment of refractory ventricular fibrillation after defibrillation. Excessive IV fluids during CPCR reduce coronary perfusion pressure, shock volumes are contraindicated. Allowing permissive hypothermia post resuscitation has been found to be beneficial and may increase success rate. In the event of cardiopulmonary arrest CPA, cardiopulmonary cerebral resuscitation CPCR provides artificial ventilation and circulation until the return of spontaneous circulation ROSC. The reported survival rate to hospital discharge SRDC for in hospital CPA is approximately 4.1% for dogs and 4.0-9.6% for cats, though discouraging similar outcomes have been described for humans. Recent studies on experimental animals and human reviews for SHDC have shown that even when performed by professionals, CPCR is generally inadequately performed. The main problems found were lack of training, excessive ventilatory rates, low thoracic excursion, low frequency and frequently interrupted chest compressions, as well as ineffective monitoring.

Recognition CPA

The major reasons for unsuccessful resuscitation are delayed recognition of CPA and delayed CPCR initiation. Vigilant monitoring and anticipation of CPA in critical patients are essential. Frequent monitoring of arterial blood pressure, CVP, core and peripheral temperature and critical diagnostic tests and procedures (blood gases, lactate, K⁺, D-dimmer, PT, APTT, chest tap or tubing) may be necessary. Changes in respiratory depth, rate or rhythm may occur and should prompt immediate intervention. Clinical signs of CPA include loss of consciousness, absence of spontaneous ventilation, absence of heart sounds on auscultation (BP<50mmHg) and absence of palpable pulses (MAP<60mmHg).

Initiation of CPCR

Signed directives indicating client's desires about resuscitation attempts must be obtained. All hospitalized patients should be assigned to 1 of 3 groups, do not attempt resuscitation DNAR, external CPCR and open chest CPCR and identified with a color code clearly posted on the patient chart and on the cage door.

To reduce the elapsed time for intervention every essential supply should be on hand and ready to go, including oxygen, an Ambu bag, a crash cart and an ECG monitor. Even non-nursing staff members should be trained on performing CPCR, time is precious and we never know who will be the first-one to advert sudden CPA. They can be easily trained to perform chest compressions, ventilate after intubation or draw up pre-calculated drugs.

Rapid auscultation for audible heart sounds is performed while simultaneously palpating for the presence of peripheral pulse. If heart sounds and pulses are absent, continuous external chest compressions are begun and the remainder of the CPCR team is alerted to begin the chain of organized and trained responses. Now-a-days in the event of CPA the CAB protocol is advocated, Compressions first, followed by Airway and Breathing. Chest compressions will provide circulation as well as some gas exchange, thus simultaneous treating both circulatory and ventilatory failure. Nevertheless, the etiology of the arrest should influence prioritization of CPCR technique. In the respiratory arrest ventilation is mandatory. In an asphyctic animal model CPCR without ventilation resulted in 100% mortality, whereas 100% survived in the group with ventilation.

Chest compressions are performed with the patient in right lateral recumbence with the rescuer standing above the patient's chest, so that the whole upper body rather than just the arms are involved in performing the compressions. Even pressure to the chest wall is applied with straight arms and hands parallel one on top of the other. Compressions are performed over the widest part of the thorax for patients >10kg, whereas for those between 7-10kg the hands should be placed over the 4th-6th intercostal spaces at the costochondral junction. For smaller dogs and cats, fingers of on hand are placed on one side of the chest and the thumb on the other. Compressions rate should be 80-100/min, with a 1:1 compression to relaxation ratio.

The main priorities of CPCR are to maximize myocardial and cerebral perfusion pressure CPP. CPP is determined by the difference between MAP and intracranial pressure ICP, whereas the difference between aortic diastolic pressure and right atrial pressure determines myocardial perfusion. The chest wall should completely recoil after being compressed at least 30% of the chest diameter. The degree of chest compression directly affects cardiac output CO and arterial forward movement. Meanwhile, the degree of chest wall recoil has a tremendous impact on the amount of venous return, cardiac preload and on cerebrospinal fluid drainage thus favoring CPP. Compression interruptions allow a decrease in intrathoracic differential pressure, MAP, CPP and coronary perfusion, thus every effort should be made to provide continuous chest compression CCCPR and to minimize the number and the duration of interruptions to <10sec. The person performing chest compressions should change every 2 minutes to reduce rescuer's fatigue and maintain adequate force and rate. CCCPR have shown a significant difference on SHDC if compared to 15:2 CPR when performed by one rescuer (10.4% vs. 14.6%). The same have proven truth in animal models. Therefore, chest compressions must never be interrupted but if a second rescuer is available orotracheal intubation is advocated. Sometimes manual or vacuum cleaning of secretions, blood and debris is required. Proper placement should be confirmed by direct visualization and appropriate chest wall excursions during ventilation. Some cases may require a cricothyroideal puncture or a cricothyroidectomy to place a tracheostomy tube. The patient is given 2 breaths 1-2sec in duration, using 100%FiO₂ and then evaluated for spontaneous ventilation. Reversal agents for anesthetic drugs that may cause apnea are administered. Doxapram is contraindicated because it decreases cerebral blood flow and increases cerebral oxygen demands. If spontaneous ventilation does not return, ventilations are begun. Each time positive ventilation is on board the intrathoracic pressure increases thus reducing venous return to the heart, coronary perfusion and CPP. Current recommendations include 1 sec. positive inspiration phase at <20cmH₂O airway pressures followed by complete relaxation at respiratory rate of 10-12bpm. Pediatric Ambu bags are recommended because they have shown to reduce esophageal and gastric insufflation.

Several assist devices are available for CPCR in humans. The active compression-decompression device can increase venous return to the heart by extra-expanding the chest cavity during decompression. However, it may be difficult to use in most veterinary patients. An impedance threshold device (ITD) is a valve that limits air entry into the lungs during chest recoil thus improving venous return. In animal models, the ITD can improve hemodynamic parameters, increase CPP by lowering ICP, improve myocardial perfusion and ROSC when used as an adjunct to CPCR in intubated cardiac arrest patients.

Internal cardiac massage should be considered for penetrating chest wounds, chest wall trauma, pleural space disease, pericardial effusion and lack of ROSC after 3-5min of external compressions. During CPCR ETCO₂ is more dependent on CO than on minute ventilatory volume and it has proven to be the best tool to monitor the effectiveness of CPCR, providing almost immediate detection of ROSC (ETCO₂ increases to 18-24mmHg).

An ECG monitor should be attached to the patient in order to diagnose cardiac arrhythmias. For asystole and pulseless electrical activity resuscitation, treatment of reversible causes (K⁺, hypovolemia, tamponade) and high-quality CCCPR is indicated. Defibrillation shock to treat asystole is contraindicated. Vasopressin, epinephrine and atropine alone or in alternation can be used to try to recover an electrical cardiac rhythm. Unlike other drugs, vasopressin (0.8U/kg/iv/3-5min) maintains its effectiveness in an acidotic, hypoxemic environment and has shown improved outcomes in human asystolic arrests. The recommended dose for epinephrine is lower than ever, 0.01-0.02mg/kg/iv/3-5min or 0.03-0.1mg/kg/IT (diluted in 5-10ml of sterile water or 0.9% NaCl). Atropine 0.04 mg/kg/IV/3-5min for a maximum of 3 doses may halt the progression of unstable bradycardia to asystole or treat vagal-induced asystole.

Ventricular fibrillation can be the cause of CPA or the result of a minor success from the treatment of asystole. CCCCPR for at least 60 seconds before defibrillation have shown to improve myocardial perfusion, ATP storage and ROSC. Only one shock should be delivered, immediately followed by CCCPR for at least 2 minutes prior to reassessing the ECG rhythm. The dose for a monophasic defibrillator is 2-4joules/kg and 1-2joules/kg for a biphasic defibrillator. Amiodarone 5.0 mg/kg/iv-io over 10 minutes is the drug of choice for refractory ventricular fibrillation, 2.5 mg/kg/IV may be administered after 3-5min. Lidocaine may increase the defibrillation threshold and it is not recommended for ventricular fibrillation. For ventricular arrhythmias after resuscitation, lidocaine may be beneficial. The dosage of lidocaine in dogs is 2.0-4.0 mg/kg/IV-IO or 4-10mg/kg/IT. Lidocaine should be used cautiously, if at all, in cats (0.2mg/kg/iv, IO or IT). The best treatment for acidosis during CPA is to optimize perfusion and ventilation, NaHCO₃ is not recommended because it paradoxically reduces intracellular pH thus further impairing mitochondrial work and myocardial response to CPCR.

The decision to terminate CPCR should be based on the original prognosis of the disease process and the client's desires. In most cases, continued CPCR efforts are ended after 20 min. Respiratory or CPA commonly recur after successful CPCR, close monitoring is essential. Common complications that can be seen after CPCR include cerebral edema, hypoxemia, reperfusion injury, abnormal hemostasis, acute renal failure, sepsis, multiple organ dysfunction syndrome. In addition, treatment is needed to address the underlying disease process that resulted in the initial CPA.

Supplemental oxygen at a FiO₂ <50% to avoid oxygen toxicity and ventilatory support if necessary should be provided. Permissive hypothermia (33-34°C) reduces metabolic O₂ demands, neurologic impairment and may increase the success rate from CPCR. Glucocorticoids are contraindicated, they may worsen neurologic injury secondary to ischemia by causing hyperglycemia. Due to increased right atrial pressure relative to aortic pressure excessive IV volumes during CPCR reduce coronary perfusion pressure. Dobutamine 2.0-20.0μg/kg/min/CRI is the drug of choice to treat normotensive decreased contractility. Dopamine 1.0-10.0μg/kg/min/CRI may work if dobutamine does not, but may cause excessive vasoconstriction. In the hypotensive patient with normal cardiac contractility, a CRI of a vasopressor is indicated but cautious administration is necessary because excessive vasoconstriction may occur. The dosage for CRI of epinephrine is 0.1-1.0 μg/kg/min, for vasopressin it is 0.01-0.04 U/min, whereas for norepinephrine it is 0.5-1.0 μg/kg/min IV as a CRI, titrated to effect.

Nutritional support should be instituted as soon as possible depending on the patient's mentation after resuscitation, original disease process, and underlying clinical status. A nasogastric tube and microenteral fluid therapy can be started very soon after resuscitation, the placement of a feeding tube should be considered later.