Cardiopulmonary cerebral resuscitation

Cardiopulmonary cerebral resuscitation (CPCR) is a procedure for maintaining the support of vital functions after a ventilatory and cardiocirculatory arrest, until the circulation and, if possible, spontaneous ventilation can be restored. To optimise CPCR all the staff of the veterinary facility must be fully trained in the procedure and be aware of their own role during such an emergency. To improve the promptness and effectiveness of the procedure, drills must be run with the participation of the entire staff. The goal of CPCR is not only to restore the heart rhythm and an efficient circulation, but also to restore cerebral perfusion to protect the brain from secondary injuries; CPCR should be provided for at least 20 minutes and for not more than 30 minutes.

The most common causes of cardiopulmonary arrest are:_¹

• hypoxia (e.g. lung diseases, pleural space disorders);
• hypotension (e.g. shock);
• systemic diseases that can produce acid-base and electrolyte imbalances;
• drugs (e.g. anaesthetics)
•  chest trauma
•  severe haemorrhages
• severe sepsis and multiple organ failure syndrome
• vagal stimulation (e.g. vomiting, laryngo-pharyngeal diseases, orotracheal intubation, eye surgery)
• status epilepticus
• primary cardiovascular diseases (e.g. arrhythmias, vascular surgery)
• neuromuscular diseases
• anti-arrhythmic drugs

Cardiopulmonary cerebral resuscitation can be divided into three stages: basic life support (BLS), advanced life support (ALS), and prolonged life support (PLS).

BASIC LIFE SUPPORT

The main purpose of BLS is to prevent damage caused by cerebral anoxia. BLS is provided by using the resuscitation procedures designed to restore the patency of the upper airways, ventilating the lungs and supporting the pump function of the heart through direct or indirect cardiac massage. An aspirator should always be available, in order to remove material (e.g. froth, blood, vomit) from the upper airways, as well as large forceps (Klemmer or Durante type) to remove any foreign bodies, such as large fragments of food or blood clots, which may be present. Pulmonary ventilation must be carried out after orotracheal intubation with a suitably sized tube; the emergency trolley must always have an adequate selection of orotracheal tubes in order to treat patients of all sizes. To this end, tracheal tubes of extremely  small diameter (2.0 ID) should also be available, as it is not uncommon to have to perform CPCR on neonates (1-2 days old) and paediatric patients under 4 months of age. A Miller straight blade laryngoscope should always be ready in the emergency trolley for the intubation of patients in which the procedure may be difficult because of the animals’ age, size or laryngeal anatomy.

In the presence of apnoea, the animal must be intubated and given two long insufflations, lasting 1.5-2 seconds each, with 100% oxygen through the resuscitation bag (known as an Ambu bag). If the animal does not resume breathing spontaneously within 5-7 seconds, the ventilation should be continued at a frequency of 10-24 insufflations per minute, making sure that the chest expands well. If the expansion of the chest wall cannot be detected because the patient is overweight, the insufflation must be stopped when the resistance produced by lung compliance can be felt through the bag. It is advisable that inexperienced resuscitators do not cuff the tracheal tube because this might cause barotrauma as a result of aggressive ventilation. 

When a respiratory arrest evolves into a cardio-respiratory arrest and peripheral pulses are no longer perceptible, a cardiac massage should be performed. Having first restored airway patency and ventilation, external cardiac massage is performed  through repeated compression of the chest in the area of the heart (4_^th-5_^th left intercostal space) (Fig. 1), with the patient in right lateral decubitus; if the animal weighs less than 15 kg it is preferable to place it in dorsal decubitus, with the aid of a dog cot or sandbags used to perform X-rays. The compressions aimed at ensuring adequate cardiac output as well as coronary and cerebral perfusion are more difficult to perform in large patients.

When CPCR is performed by a single person, two ventilations are provided every 15 chest compressions. However, when two or more people are present, three to five compressions are performed between one ventilation and the next. In patients with a body weight of up to 7 kg the frequency of the compressions must be around 120 per minute; in patients weighing more than 7 kg, the frequency of the compressions must be around 100 per minute. The pressure exerted on the chest must be such that it deforms the costal arch. In small  patients, compression is performed on the hemithorax in the area of the heart; in dogs weighing more than 7 kg, it can be performed on the most convex portion of the chest wall, exploiting the thoracic pump effect, or better still with the animal in dorsal decubitus (Figs. 2 and 3). Compression of the chest in the most convex area (in large patients) causes compression of both the heart chambers and the large blood vessels, thus moving a larger volume of blood than when only the heart chambers are compressed. Alternating abdominal and chest compression facilitates filling of the large vessels and heart during diastole. Closed-chest resuscitation cannot be performed in the presence of multiple fractures of the chest wall, pleural space disorders (e.g. thoracic haemorrhage, pleural effusion, tension pneumothorax), or cardiac tamponade.

If closed chest resuscitation has not been successful after 2-5 minutes, or has not been able to generate a pulse and peripheral perfusion (detected by means of a Doppler examination of the vessels), an emergency thoracotomy and open-chest, direct cardiac massage may be performed. Direct cardiac massage is recommended in the following cases: multiple rib fractures, disorders of the pleural space, pulmonary haemorrhage, diaphragmatic hernia, gastric dilatation-torsion and abdominal surgery. The thoracotomy should be performed at the 5^th-6^th intercostal space, preparing the surgical field as well as possible, shaving the intercostal space and irrigating the area with a disinfectant. The incision is made with a scalpel blade whereas the thoracotomy is carried out with blunt-ended scissors. After reaching the heart, this should be lifted out to perform a pericardiotomy along its major axis, in order to externalise the heart in toto. The heart chambers must be emptied by rhythmically compressing the heart from the apex to base. When resuscitation is effective the pulse can be felt in the femoral artery. To increase flow to the brain and heart, the descending aorta can be clamped with haemostatic forceps or with a Rummel tourniquet. Generation of a pulse during resuscitation signifies that the cardiac compression is being performed properly.

Open-chest resuscitation is more effective at generating cardiac output, blood pressure and peripheral, coronary and cerebral perfusion. The lack of restoration of blood circulation within 15 minutes leads to brain damage; cardiac arrest causes cerebral hypoxia after 10 seconds, while the ATP stores in the brain become depleted in 4-5 minutes. When resuscitation is successful, the state of consciousness returns to normal after about 15-30 minutes. In some cases consciousness may be recovered but in the absence of vision. This deficit is not necessarily permanent and vision may be recovered in 2-4 days.

During this first phase, the following arrhythmias can be found:

• Asystole: characterized by the absence of electrical and mechanical activity of the myocardium.
• ventricular fibrillation: this appears when the myocardial cells contract in a haphazard and random manner and fail to create an effective mechanical event.
• electromechanical dissociation: in this case, the electrocardiogram (ECG) tracing is normal, the heart chambers do not contract and the pulse is absent. Possible treatments include high-dose atropine, naloxone hydrochloride (0.03 mg/kg) and adrenaline.

ADVANCED LIFE SUPPORT

After starting the resuscitation manoeuvres, ECG electrodes must be connected to the patient and continuous ECG monitoring maintained until the patient is discharged or vital functions are stable. An ECG is essential for evaluating the recovery of normal cardiac function or the presence of abnormalities of cardiac rhythm. If the internal cardiac massage is ineffective and the animal has ventricular fibrillation, or even in the absence of this tachyarrhythmia, intrathoracic or extrathoracic defibrillation can be performed, with a power of 0.5-1 J/kg in the former case, or 2-5 J/kg in the latter. Three additional shocks, with the power increased by 50%, are also possible.

In order to support blood circulation with fluid therapy and to be able to administer drugs, it is important to establish a venous access in a central or peripheral blood vessel. Should this not be possible, an intraosseous infusion is very rapid and effective for the administration of fluids and medications. All the drugs used during CPCR can be administered by the intraosseous route. In patients which were euvolaemic before the arrest, the infusion rate of crystalloid fluids during CPCR is 10-40 ml/kg in dogs and 10-20 ml/kg in cats. The volume of colloids is 10 ml/kg. In cats the colloid bolus must not exceed 5 ml/kg and must be infused slowly.

Numerous beta-agonists and sympathomimetic drugs are available to facilitate the recovery of cardiac function and to restore systolic blood pressure. These can be injected or administered parenterally by an intravenous, intraosseous, intratracheal, intracardiac, intramuscular or sublingual route. When opting for intratracheal administration, dosages must be doubled and after the drug has been given, the tracheal tube should be flushed with 2-5 ml of saline solution.

The drugs most commonly used during CPCR are listed below._^2,3

• Adrenaline. This is a beta-stimulating and, to a lesser degree, an alpha-stimulating  catecholamine that increases heart rate, myocardial excitability and conduction and cardiac output. It has inotropic activity and induces peripheral vasoconstriction. The dose is 0.01 to 0.02 mg/kg (low dose) by the intravenous, intratracheal or intraosseous route and can be repeated after 3-5 minutes. When a high dose is preferred, 0.1 to 0.2 mg/kg  can be given; a high dose is recommended only if a low dose has been ineffective, as it may cause excessive vasoconstriction, arrhythmia and ventricular fibrillation;
• Atropine. This is an antimuscarinic drug which competitively antagonizes the acetylcholine receptors at post-ganglionic parasympathetic sites. Its effect is dose-dependent and it is used in the course of bradycardia, asystole and to increase parasympathetic tone. It is administered at a dose of 20-40 mg/kg by an intravenous, intraosseous or intramuscular route, using the lowest effective dose;
• Sodium bicarbonate. Administered 5-10 minutes after the arrest to correct metabolic acidosis:  the dose is 0.5 mEq/kg every 5 minutes of arrest.
• Magnesium hydrochloride. An intravenous bolus dose of 0.15- 0.3 mEq/kg c
• an be given (in refractory arrhythmias, such as flutters and fibrillations, or in unresponsive arrest).
• Lidocaine. The dose is 1-3 mg/kg as an intravenoous bolus (in dogs), 60-100 mg/kg/min as a constant rate intravenous infusion, or 1-2 mg/kg intravenously (in cats). There is a risk of bradycardia and hypotension when this drug is administered at high doses and in a rapid infusion.
• Vasopressin. 0.4-0.8 U/kg intravenously.
• Crystalloid solutions.
  • 10-40 ml/kg intravenous/intraosseous (in dogs)
  • 10-20 ml/kg intravenous/intraosseous (in cats)
• Hypertonic crystalloids (e.g. sodium chloride 7.5%); 4-5 ml/kg/day intravenously, to effect.
• Colloids. 10 ml/kg intravenously, to effect, if hypovolaemic (in cats, slow boluses of 5 ml/kg).

In addition to ECG monitoring, blood gases (oxygen and carbon dioxide) should be monitored. The partial oxygen pressure (PaO₂) should stabilise above 80 mmHg, oxygen saturation must be greater than 95% while CaO₂ must not exceed 45 mmHg.

Whereas the first two stages of cerebral cardiopulmonary resuscitation are meant to support and restore the vital functions of the animal, the purpose of the third and final phase is to support the restored vital functions.        

PROLONGED LIFE SUPPORT

Particular attention should be paid to the vital signs in the 4 hours following cardio-respiratory arrest, as it is precisely in this period that the patient could suffer another cardiac arrest. During this phase, mechanical ventilation must be provided until recovery of spontaneous respiration. Mean arterial pressure (MAP) must be maintained above 60 mmHg;  when it is not possible to measure MAP, systolic blood pressure must be kept  higher at 90 mmHg or higher. MAP should be kept within 60-150 mmHg.  It is advisable to take a blood sample to check the acid-base status, electrolytes, glycaemia, haematocrit and total proteins. Any electrolyte abnormalities, hypoxia, or hypovolaemia should be promptly corrected to avoid complications when circulation has been restored._⁴

The patient should be monitored closely for at least 4-6 hours throughout the entire post-arrest period. This means that, in addition to monitoring the heart rate with an ECG, as a minimum the following parameters must be checked: heart rate, pulse rate and characteristics, blood pressure, mucous membrane colour, capillary refilling time, respiratory rate and characteristics, body temperature and urine output. A chest X-ray should also be performed to check for rib fractures and pulmonary oedema.

 References

1) Santilli R., PF Ferrieri, S. Poggiagliolmi. Emergenze cardiovascolari. Medicina d’urgenza e terapia Intensiva, in Vigano’ F. ed. Medicina d’urgenza e terapia intensiva del cane e del gatto. Milano: EV s.r.l. Masson/EV s.r.l.; 2004, pp 135-175.
2) Crowe DT, Fox RF, Devey JJ, Spreng D. Cardiopulmonary and cerebral resuscitation, in    Fox PR, Sisson D, Moise NS ed. Textbook of canine and feline Cardiology. Philadelphia: Saunders; 1999, pp 427-441.
3) Cole SG, Otto Cm, Hughes D. Cardiopulmonary cerebral resuscitation in small animal a clinical practice review Part II. J Vet Emerg Crit Care, 2003;13(1): 13-23.
4) Boller M, Kellet-Gregory L, Shofer FS, Rishniw M. The clinical practice of CPCR in small animals: an internet-based survey. J Vet Emerg Crit Care, 2010: DOI:10.1111/j.1476-4431.2010.00571.