Cardiopulmonary arrest (CPA) can be defined as a sudden cessation of functional ventilation and systemic perfusion. This will result in reduced O₂ delivery to tissues with decreased removal of CO₂. Cardiac arrest and respiratory arrest can occur at the same time but often respiratory arrest will occur first. This must be quickly treated to prevent cardiac arrest ensuing.

Signs of impending CPA include:

 Changes in the patient's respiratory rate, depth, pattern and effort

 Decreasing end-tidal carbon dioxide

 Hypotension

 Cyanotic, grey or pale mucous membranes

 Capillary refill time may be prolonged

 Weak, irregular pulses, irregular heart sounds, tachycardia, ventricular premature complexes

 Bradycardia

 Sudden, unexplained increases in anaesthetic depth

 Hypothermia despite rewarming efforts

Signs of CPA include:

 No detectable heart sounds on auscultation

 Loss of palpable pulses and flat direct arterial catheter and pulse oximeter traces

 Fixed, dilated pupils

 Absence of ventilation or agonal gasping - may be masked if patient is artificially ventilated

 Pale, grey or cyanotic mucous membranes

 Absence of bleeding at the surgical site, blood may appear dark if the arrest is due to hypoxaemia

 Electrocardiogram (ECG) tracing may be abnormal

 Collapse and loss of consciousness

 Loss of skeletal muscle tone and cranial nerve reflexes

Reasons for arrest include:

 Hypoxaemia

 Hypercarbia

 Hypotension

 Hypoglycaemia

 Hypovolaemia

 Electrolyte imbalances, e.g., hyperkalaemia

 Vagal stimulation

 Overdose of anaesthetic agent

 Hypothermia

 Acid-base abnormalities

 Sensitisation of the heart to circulating catecholamines

 Severe trauma, systemic or metabolic disease

 Severe underlying cardiac or respiratory disease

 Central nervous system (CNS) e.g., herniation or traumatic brain injury

 Sepsis or systemic inflammatory response syndrome (SIRS)

Equipment

An adequately stocked crash trolley or box is essential and should contain equipment for both basic and advanced life support techniques. It should be kept in a central, easily accessed location and be regularly checked and always be immediately restocked after use. This can be encouraged by using a plastic seal or piece of tape which is easily broken in an emergency but identifies that the crash trolley has been used.

An emergency drug chart should be attached to the trolley or box giving the doses in millilitres for different weights of patient, e.g., 2.5 kg, 5 kg, 10 kg etc. for all drugs required in CPCR. This allows drugs to be drawn up quickly in a crash situation.

Cardiopulmonary and Cerebral Resuscitation

Our aim when performing cardiopulmonary and cerebral resuscitation (CPCR) is to achieve a return to spontaneous ventilation and circulation. We are also aiming to maximise perfusion to the heart and brain.

All clinical staff should have training in CPCR with this training being refreshed every 6 months. CPCR will be ineffective if performed by only one person so a well trained team is essential. The use and displaying of CPCR algorithms and drug dosage charts is recommended.

As soon as a CPA occurs turn off the gaseous anaesthetic (if applicable), notify the surgeon and call for help and begin initial basic life support procedure:

 A - Airway

 B - Breathing

 C - Circulation

Also consider perioperative drugs that may have contributed to CPA. Reverse these drugs where possible, e.g., reverse opioids using naloxone, benzodiazepines using flumazenil and medetomidine/dexmedetomidine with atipamezole.

Airway Management (A)

Quickly establish a patent airway. Check existing tubes to ensure they have not become dislodged or blocked. If the patient is not already intubated quickly place an endotracheal tube, secure in place and inflate the cuff if necessary. It may be necessary to suction the airway to remove any mucus, regurgitated ingesta or foreign material present.

If the patient cannot be intubated due to respiratory obstruction then oxygen may be provided in a number of ways until an emergency tracheostomy can be performed:

 An oxygen cannula or urinary catheter may be able to pass the obstruction to allow oxygen administration.

 An over-the-needle catheter can be placed between tracheal rings distal to the obstruction to allow oxygen to be insufflated.

Breathing (B)

Intermittent positive-pressure ventilation (IPPV) should be commenced with 100% oxygen using an appropriate anaesthetic breathing system:

 Initially give the patient two breaths 1–2 seconds in duration and then assess for signs of spontaneous ventilation.

 If spontaneous ventilation does not occur then ventilations should continue at a rate of 10–12 breaths/min.

Peak inspiratory pressure should be kept below a maximum of 20 cmH₂0 with tidal volume being approximately 10–15 ml/kg in patients with normal lungs.

Cats, neonates and patients with restrictive lung disease, e.g., pneumonia and diaphragmatic hernia, will require smaller tidal volumes of 6–10 ml/kg at higher respiratory rates of 12–15 breaths/min to avoid potential complications.

Doxapram administration is contraindicated in patients with respiratory arrest as it decreases cerebral perfusion and increases cerebral oxygen consumption and requirement.

Circulation (C)

Pulses should be assessed following intubation and initial commencement of ventilation. If the patient is in cardiac arrest then compressions should be started immediately and continued until spontaneous circulation returns or a decision is made to stop.

Closed cardiac compressions:

 Cardiac pump mechanism. This method is employed in patients weighing less than 15 kg, i.e., cats and small, narrow-chested dogs. The chest is compressed directly over the heart. This action directly compresses the ventricles to create blood flow. The patient should be positioned in right lateral recumbency with a sandbag placed under the opposite chest wall. The heel of one or both hands is used to compress the chest at the fifth intercostal space directly over the heart. In smaller patients the heart is compressed using the thumb and forefingers either side of the chest. Compress the chest by approximately one-third and avoid excessive pressure, which may lead to intrathoracic trauma.

 Thoracic pump mechanism. This method is suitable for larger patients, over 15 kg, or barrel-chested breeds such as the bulldog. The patient can be placed in either lateral or dorsal recumbency. If the patient is placed in right lateral recumbency, a sandbag should be placed under the opposite chest wall. Again compress the chest by approximately one-third but this time at its widest point. If the patient is in dorsal recumbency, sandbags can be used to secure the patient in position. The chest is compressed over the sternum.

Simultaneous ventilation and chest compression create positive intrathoracic pressure. The increase in thoracic pressure causes forward blood flow into the arteries. Back flow into the venous system is prevented by the atrioventricular valves and the collapsing of the great veins due to the pressure. This increased arterial flow will promote cerebral and myocardial perfusion. The relaxation of the chest following compression and the subsequent drop in pressure facilitates venous return.

For both mechanisms the person performing compressions should be situated so that they are above the patient's chest.

Interposed abdominal compressions can be performed if there are enough personnel and may increase venous return.

Chest compressions should be performed at a rate of approx 100–120 compressions per minute, depending on the size of the patient, with a 1:1 ratio of compression to relaxation to allow full chest recoil.

The effectiveness of the chest compressions can be monitored by a person with their finger on a pulse. Effective compressions should produce a palpable pulse and pink mucous membranes. To monitor pulmonary perfusion a capnograph should be utilised. If there is adequate delivery of blood to the lungs due to effective chest compressions then gaseous exchange will occur due to artificial ventilation resulting in increasing end-tidal CO₂ levels being displayed on the capnograph. An end-tidal CO₂ level above 14 mmHg is a sign of good CPCR technique. Assessment of cerebral blood flow can be made using a Doppler ultrasound transducer placed on the cornea.

Open-chest CPCR. Indications for open chest CPCR include:

 If the chest cavity or abdominal cavity are already exposed, e.g., thoracotomy or laparotomy

 Pneumothorax

 Haemothorax

 Severe chest trauma including penetrating chest wounds

 Fractured ribs

 Diaphragmatic hernia

 Flail chest

 Pericardial tamponade

 Severe hypovolaemia

 Deep-chested dogs and obese patients where closed chest CPCR will not create high intrathoracic pressure

 Coagulopathies

 Septic, anaphylactic or distributive shock

 Other primary thoracic diseases, e.g., neoplasia, foreign body

 If closed chest CPCR is not effective within 2–5 minutes (controversial and the subject of much debate)

A strip of hair should be quickly clipped over the fourth intercostal space and antiseptic solution quickly applied. The vet will make an incision at the fourth intercostal space. The fourth and fifth ribs are spread apart using rib retractors and the lungs displaced to expose the pericardium. The pericardium is torn at the apex of the heart and the heart directly compressed. The compression rate remains the same as with closed compressions at approximately 100 per minute.

Having the chest open allows direct visualisation of ventricular filling and heart rhythm, accurate intracardiac drug administration and occlusion of the aorta if required.

Open-chest CPCR will require a surgical team on standby, if the patient is not already in theatre, to repair the thorax post resuscitation. There is a risk of sepsis with this technique. Other complications associated with excessive force during direct myocardial compression are cardiac trauma, cardiac dysrhythmias and ventricular fibrillation.

Advanced Life Support

This includes further steps with the aim to establishing and maintaining spontaneous ventilation and circulation via the administration of drugs, appraisal of the ECG and further interventional techniques such as defibrillation.

Drugs (D)

 Atropine: Anticholinergic, parasympatholytic agent that can be used to treat vagally induced bradycardias and in the treatment of ventricular asystole. It is effective at reducing the effects of parasympathetic stimulation and cholinergic responses and acts to increase heart rate, control hypotension and increase systemic vascular resistance. Excessive doses may produce sinus tachycardia and can predispose the myocardium to ventricular dysrhythmias.

 Adrenaline (epinephrine): Adrenaline is a mixed adrenergic agonist and a catecholamine. It is the first-choice drug for treatment of severe bradycardia that is unresponsive to atropine/glycopyrrolate, severe hypotension and cardiac arrest. During CPCR adrenaline is administered for its α-2 agonist effects which cause peripheral vasoconstriction, thus increasing coronary and cerebral perfusion. It is believed that adrenaline is less effective in hypoxic, acidotic states. Adrenaline increases myocardial oxygen demand and may lead to ventricular dysrhythmias if overdosed.

 Vasopressin: Vasopressin is a nonadrenergic pressor that causes vasoconstriction. Unlike adrenaline it is not affected by acidosis and may be effective in cases where adrenaline fails. It works by stimulating receptors in the smooth muscle of vessel walls and appears to cause more vasoconstriction in peripheral tissues than in the coronary and renal vasculature promoting perfusion of these areas. It is also thought to provide a dilatory effect in the vessels supplying the brain resulting in increased perfusion to this area. Vasopressin is indicated for use with or instead of adrenaline in treatment of ventricular tachycardia, ventricular fibrillation and pulseless electrical activity (PEA).

 Lidocaine: A class 1b antiarrhythmic (sodium channel blocker) indicated for use in cases of atrial fibrillation, some forms of supraventricular tachycardia, ventricular tachycardia and refractory ventricular fibrillation unresponsive to CPCR techniques (including defibrillation and pressor therapy). Largely superseded by amiodarone in human medicine.

Routes of Drug Administration During CPCR

The routes are listed in order of preference:

 Central venous route: A cranial vena cava or jugular catheter is the route of choice for administration of resuscitation drugs as the drugs are deposited in close proximity to the heart

 Peripheral venous route: Often the most convenient route as many patients will already have a peripheral intravenous catheter. It can take up to 2 minutes for the administered drugs to reach the central circulation during CPCR. A flush of sterile saline and raising of the extremity can increase the drug's ability to reach the central circulation. Chest compressions should be continued for 2 minutes following administration of drugs via a peripheral vein before evaluating the ECG

 Intraosseous route: If vascular access is limited an intraosseous or spinal needle may be placed into the medullary cavity of the wing of the ilium, tibial crest, humerus or femur. The medullary cavity does not collapse during CPA, uptake is rapid and large volumes of fluid can be administered via this route if necessary. This is a valuable technique in small mammals and neonates where vascular access may be difficult

 Intratracheal route: Some drugs may be administered via this route - NAVAL, i.e., naloxone, atropine, vasopressin, adrenaline and lidocaine. A sterile urinary catheter is passed down through the endotracheal tube to administer the drug into the distal trachea. The drug dose for administration via this route should be 2–2.5 times that of the intravenous dose, except adrenaline which should be increased by 3–10 times. Dilution of each drug in sterile water, 5–10 ml, is necessary when administered by this route

 Intralingual: Useful technique for small mammals and neonates. The base of the tongue has a rich vascular supply and drugs are absorbed readily from this area

 Intracardiac: Should be avoided during closed-chest CPCR as potential complications include coronary and pulmonary laceration, myocardial trauma, arrhythmias and cardiac tamponade. Intracardiac injections may be indicated when open-chest compressions are being performed. This method is employed to hasten the delivery of drugs to the coronary arteries and myocardium. The dose for intracardiac administration is generally half that of the intravenous dose.

Electrocardiography (E)

It is essential to monitor the heart rhythm immediately following CPA and during CPCR, this is achieved through use of an ECG. It allows monitoring of response to treatment and evaluation of the appropriate drug therapy and/or treatment to be delivered according to the rhythm. Note: a normal ECG appearance is not indicative of contractile function of the myocardium or peripheral perfusion.

Spirit must NOT be used when placing an ECG on a CPA patient as defibrillation may be required. Spirit, if it does not evaporate, is flammable and there is a risk that the patient may be set on fire.

The common arrest rhythms in veterinary patients are asystole, ventricular fibrillation and pulseless electrical activity (PEA):

 Asystole: A flat line will be seen on the ECG indicating the absence of mechanical and electrical activity. Always check the patient's pulses and ECG connections before you assume your patient is asystolic! Treatment requires rapid basic life support measures - ABC with minimal interruptions. No medications have been shown to be effective in the treatment of asystole. However, atropine/glycopyrrolate and adrenaline/ vasopressin remain the drug treatments of choice for this condition

 Ventricular fibrillation: An irregular quivering of the ventricles with no effective cardiac output. The ECG will demonstrate fibrillation waves with no QRS complexes. There will be no palpable pulse. All leads should be checked as fine ventricular fibrillation can mimic asystole in some leads. This is the least common arrest rhythm seen in veterinary patients

 Direct current cardioversion to defibrillate the heart is the recommended treatment. Chest compressions should be performed whilst the defibrillator is being prepared. Defibrillation may be attempted externally with paddles which must be covered with conductive gel to prevent burning of the patient. The paddles are placed either side of the chest avoiding contact with each other and the table. No personnel should be in contact with the patient, ECG leads or the table and the operator of the defibrillator should give clear instructions for personnel to 'stand clear' before releasing the charge. The initial countershock is delivered at 2–5 J/kg. One shock should be administered then chest compressions should immediately be resumed for 2 minutes before reassessing the cardiac rhythm and administration of an additional shock. Power settings are selected according to patient size and response to previous attempts. A chart can be attached to the defibrillator showing appropriate settings for different patient body weights for both internal and external cardioversion techniques

 Adrenaline is generally administered every 3–5 minutes if ventricular fibrillation continues after the initial countershock and subsequent 2 minutes of compressions. Adrenaline is reported to convert fine ventricular fibrillation to coarse ventricular fibrillation, which is reportedly easier to convert. Vasopressin can be given as an alternative to adrenaline

 Lidocaine cannot convert the heart from ventricular fibrillation to normal sinus rhythm but is used to help control ventricular dysrhythmias following defibrillation

 Pulseless electrical activity (PEA): PEA is used to describe patients which have ECG evidence of cardiac rhythm but with an absent or very weak pulse. The waveform can range from having relatively normal QRS complexes to wide and bizarre complexes. Treatment involves correction of the underlying cause if possible and rapid commencement of basic life support techniques

 ABC. Again no medications have been shown to be effective and the prognosis is poor for successful resuscitation. However, adrenaline/ vasopressin is still administered in PEA cases.

Fluid Therapy (F)

If CPA is due to hypovolaemia then aggressive fluid therapy may be necessary. Shock rate fluids are generally not administered unless the patient was hypovolaemic prior to CPA. Fluid resuscitation should be approached cautiously in patients whose volume status was normal prior to arrest especially those with pre-existing lung/cardiac disease.

References

1.  Bryant S. Anaesthesia for Veterinary Technicians. Iowa: Blackwell Publishing, 2010.

2.  King LG, Boag A, eds. BSAVA Manual of Canine and Feline Emergency and Critical Care. 2nd ed. Gloucester: British Small Animal Veterinary Association, 2007.

3.  Plunkett SJ, McMicheal M. Cardiopulmonary resuscitation in small animal medicine: an update. Veterinary Internal Medicine 2008;22:9–25.

4.  Seymour C, Duke-Novakovski T, eds. BSAVA Manual of Canine and Feline Anaesthesia and Analgesia. 2nd ed. Gloucester: British Small Animal Veterinary Association, 2007.

5.  www.acvecc-recover.org