What to do about a code blue


How often do you perform CPR in your practice? If discomfort with the process is your concern, here are some guidelines to help.

Because of the gravity of the presenting situation, no one wants to deal with cardiopulmonary resuscitation (CPR). The prognosis is never “good” after cardiopulmonary arrest (CPA), but if CPR is performed correctly, you can increase your chances of stabilizing that patient in front of you.1 Your crash cart is stocked and ready. What do you do with everything in it? Guidelines have been updated. Here's a quick look at what to do.

CPA is associated with a poor prognosis, with a less than 6% survival rate reported in the literature.1,2 Moreover, most of the protocols previously used in veterinary medicine were extrapolated from human guidelines from the American Heart Association.

The Reassessment Campaign on Veterinary Resuscitation (RECOVER) recently completed a systematic review of the literature relevant to veterinary CPR and developed the first evidence-based, consensus CPR guidelines for small animals.3 The RECOVER initiative is one of the first in veterinary medicine to evaluate and create guidelines for CPR.


Basic life support consisting of performing chest compressions, securing a patent airway and providing ventilation should be initiated as quickly as possible after CPA is diagnosed. While we were all previously taught basic cardiopulmonary resuscitation should follow the ABC rule-airway (A), breathing (B), circulation (C)-the new CPR guidelines emphasize the importance of CAB resuscitation-first initiate chest compressions (C), then obtain an airway (A) and finally start respirations or breathing (B).

Circulation: Chest compressions

Patients with CPA have no forward blood flow out of the heart. The resulting lack of delivery of oxygen to the tissues and removal of waste products from the tissues increases the risk for hypoxemia, ischemic organ injury and reperfusion injury if tissue blood flow is reinstituted. The goals of chest compressions are to provide pulmonary blood flow for oxygen uptake and waste elimination and tissue perfusion for oxygen delivery to restore cellular metabolic activity. There are two theories when initiating closed-chest CPR.

Cardiac pump theory. This method is most often considered in cats, small dogs and keel-chested larger dogs (e.g. greyhounds, Doberman pinschers). With this theory, the heart is the true heart of the matter. The heart is compressed between the ribs, which manually opens the pulmonic and aortic valves, leading to the forceful delivery of blood from the ventricles through the pulmonic and aortic valves, leading to the forceful delivery of blood from the ventricles through the pulmonic and aortic valves. Retrograde flow is prevented via the closing of both atrioventricular valves followed by artificial diastole (rest and recoil), which refills the ventricles.

Guidelines for this method:

• Apply compression directly over the heart (the ventral one-third of the thorax over the fourth through sixth intercostal spaces) with the patient in lateral recumbency.

• Use a rate of 100 to 120 compressions/minute.

• Perform ventilation at a rate of 10 breaths/minute throughout the compression cycle.

• Allow adequate recoil of the chest between compressions.

Thoracic pump theory. This method is most often considered in medium, large and giant round-chested breeds (e.g. Labrador retrievers, Rottweillers). The heart is a secondary not the primary element of this theory. The goal is to have the forceful compressions change the intrathoracic pressure, resulting in opening and closing of the heart valves and movement of blood flow. Retrograde blood flow is prevented by the increase in intrathoracic pressure collapsing the thoracic vasculature.

Guidelines for this method:

• With the patient in lateral recumbency, apply compression at the widest part of the thorax, generally between the seventh and eighth intercostal spaces.

• Depress the thorax by one-third.

• Use of a rate of 100 to 120 compressions/minute.

• Perform ventilation at a rate of 10 breaths/minute throughout the compression cycle.

• Aim for a compression-to-relaxation ratio of 1:1.

• Allow adequate recoil of the chest between compressions.

While most patients will benefit from CPR performed in lateral recumbency, broad-chested dogs such as bulldogs may benefit from CPR performed in dorsal recumbency, similar to humans. When CPR is performed in dorsal recumbency, compressions should depress the sternum 1.5 to 2 inches.

Chest compressions should be delivered without interruption in cycles of two minutes. A new compressor should begin chest compressions after each cycle to decrease the likelihood of fatigue blunting the effectiveness of CPR. Be sure to minimize interruption in chest compressions to decrease the likelihood of a drop in coronary perfusion pressure (CPP). CPP is a critical determinant of myocardial blood flow and the likelihood of return of spontaneous circulation. 

Airway and breathing: Ventilation

I know I just said to minimize any delay in chest compressions, but during CPR the patient should be intubated for airway control, oxygenation and ventilation as soon as possible. Although not conventional for most veterinarians, intubation can be performed in lateral recumbency to lessen the need for cessation of chest compressions during endotracheal tube placement.

If an endotracheal tube is not readily available, mouth-to-snout ventilation is an alternative to improve oxygenation and waste product (carbon dioxide) removal. To perform mouth-to-snout ventilation, hold the patient's mouth closed firmly with one hand and extend the neck to align the snout with the spine. This allows opening of the airway to achieve the best oxygenation and ventilation. Then place your mouth over the patient's nares and blow firmly into the nares to inflate the chest.

Again, chest compressions should not be delayed during intubation or ventilation by the mouth-to-snout technique but rather performed simultaneously during ventilation. Intubated patients should be ventilated at a rate of 10 breaths/minute with an inspiratory time of approximately one second. The tidal volume can be assessed by using a spirometer, with the goal of approximately 10 ml/kg for each breath. Hyperventilation should be avoided as this may lead to hypocapnia and cerebral vasoconstriction, ultimately leading to decreased perfusion. 



Once basic life support has been initiated, the CPR team should initiate advanced life support, which focuses on drug therapy and electrical defibrillation.

Depending on the arrest rhythm, drug therapy may include the use of vasopressors, anticholinergics or anti-arrhythmics, reversal agents, intravenous fluids and alkalinizing drugs. Thus, placement of a peripheral or central intravenous or intraosseous catheter is recommended.


Vasopressors are recommended to increase peripheral vasoconstriction and improve cardiac output since even the most forceful chest compressions will not mimic the cardiac function of a healthy patient.4 It is up to the clinician to then consider medications to improve perfusion to the vital organs including the heart, lungs and brain.

Epinephrine causes peripheral vasoconstriction by stimulating alpha1-adrenergic receptors as well as beta1- and beta2-adrenergic receptors. Low doses (0.01 mg/kg) are recommended initially. After prolonged CPR, a higher dose may be considered (0.1 mg/kg). While intravenous or intraosseous administration is recommended, epinephrine may also be diluted 1:1 with isotonic (0.9%) saline solution and given via a long catheter through an endotracheal tube (double the dose-0.02 mg/kg low dose; 0.2 mg/kg high dose).5

Vasopressin exerts its vasoconstrictive effects by activating the peripheral V1 receptors. This can be used in combination or in place of epinephrine at a dose of 0.8 U/kg intravenously or intraossesously. The potential benefits of vasopressin include efficacy in acidic environments in which alpha1-adrenergic receptors may become unresponsive to epinephrine. However, vasopressin lacks beta1-adrenergic effects, which may cause increased myocardial oxygen consumption and worsened myocardial ischemia upon return of spontaneous circulation. Vasopressin may also be administered via an endotracheal tube by using the technique described for epinephrine above. 


Atropine is the most common anticholinergic considered in CPR and is a parasympatholytic medication. A dosage of 0.04 mg/kg intravenously or intraossesously is considered during CPR in dogs and cats when the cause is considered a result of asystole or pulse electrical activity associated with increased vagal tone. Atropine may also be administered via an endotracheal tube (0.08 mg/kg).


Ventricular fibrillation, or pulseless ventricular tachycardia, should be treated as early as possible with electrical defibrillation. If electrical defibrillation is not corrective, drug therapy may be warranted. Consider amiodarone, dosed at 2.5 to 5 mg/kg intravenously or intraossesously.3 If amiodarone is not available, lidocaine at a dosage of 2 mg/kg slowly intravenously or intraossesously is an alternative.

When should I consider open-chest CPR?

As compared with closed-chest CPR, open-chest CPR results in improved output. But open-chest CPR is more invasive and expensive and requires significant planning after the return of spontaneous circulation. Indications for open-chest CPR include pericardial disease, pleural space disease and thoracic wall defects such as numerous rib fractures or a flail chest. If the patient has been anesthetized for an abdominal procedure, direct cardiac massage can be performed with an incision into the diaphragm. Finally, giant-breed and very large chested dogs may not respond to closed-chest CPR, so open-chest CPR should be considered for these patients. 

Side effects of amiodarone may include anaphylactic reactions, hypotension, peripheral vasodilation, wheals or hives. Treatment with diphenhydramine (2 mg/kg intramuscularly), anti-inflammatory corticosteroids (0.1 mg/kg dexamethasone sodium phosphate intravenously), or both is recommended if these signs are seen following return of spontaneous circulation.

Reversal agents

Reversal agents are considered when reversible anesthetic drugs were recently administered. Naloxone (0.01 mg/kg intravenously or intraossesously) may be used to reverse opioids, flumazenil (0.01 mg/kg intravenously or intraossesously) for benzodiazepines and atipamezole (0.1 mg/kg intravenously or intraossesously) or yohimbine (0.1 mg/kg intravenously or intraossesously) for alpha2 agonists.

Intravenous fluids

Administering intravenous fluids in euvolemic or hypervolemic patients is not recommended during CPR as it will increase right atrial pressure, resulting in decreased perfusion of the brain and heart. Conversely, in hypovolemic patients intravenous fluids are recommended to restore adequate circulating volume and increase the efficacy of chest compressions with improved perfusion.


The use of corticosteroids during CPR in dogs and cats is not recommended. No body of evidence shows significant benefit from the use of corticosteroids during CPR. Moreover, side effects of corticosteroid use include gastric ulceration, suppression of the immune system and reduced prostaglandin production in the kidney.

Alkalinization therapy

In patients with prolonged CPA (greater than 10 to 15 minutes), consider alkalinization therapy with sodium bicarbonate dosed at 1 mEq/kg (diluted intravenously). The rationale for this therapy is that prolonged CPA results in severe acidemia (lactic acid, uremic acids and venous respiratory acidosis) due to poor perfusion and accumulation of carbon dioxide. The acidemia ultimately results in vasodilation and inhibition of normal enzymatic and metabolic activity.6,7

Electrical defibrillation

Electrical defibrillation is considered in patients with ventricular fibrillation or pulseless ventricular tachycardia. Defibrillators may be either monophasic (delivering a current in one direction across the paddles) or biphasic (delivering a current in one direction and then reversing and delivering a current in the opposite direction). The use of biphasic defibrillators is recommended because a lower current is required to successfully defibrillate the patient, decreasing the likelihood of myocardial injury.

Monophasic defibrillators are used at an initial dose of 4 to 6 J/kg, while biphasic defibrillation should initially be used at 2 to 4 J/kg. If the first defibrillation is unsuccessful, a second attempt can be tried by increasing the dose by 50%. After defibrillation, resume chest compressions immediately. Interruptions of basic life support and chest compressions during defibrillation and monitoring should be very brief . A complete two-minute CPR cycle should be performed before reassessing the ECG following defibrillation to determine if the patient requires additional defibrillation for continued ventricular tachycardia. Signs of return of spontaneous circulation following defibrillation may include palpable heart beats during compressions, more appropriate ECG complexes and improved femoral pulses.

Additional monitoring

Commonly used monitoring devices for CPR include pulse oximetry, direct and indirect blood pressure monitors, continuous electrocardiography and end-tidal carbon dioxide monitoring (ETCO2).

Electrocardiographic monitoring during CPR is used to diagnose the arrest rhythm:

• Asystole

• Pulseless electrical activity

• Ventricular fibrillation

The ECG is also used to determine if there is a change in the cardiac rhythm during and following therapy.

ETCO2 monitoring during CPR has several indications. One is to determine if endotracheal intubation was successful. If the endotracheal tube was placed mistakenly in the esophagus, there will be little to no reading. If there is measureable carbon dioxide by ETCO2, this would be supportive of correct placement of the endotracheal tube. Importantly, if there is return of spontaneous circulation, ETCO2 will rapidly increase due to the rapid increase in circulation. It is therefore used as an early indicator of return of spontaneous circulation during CPR. 


1. Hofmeister EH, Brainard BM, Egger CM, et al. Prognostic indicators for dogs and cats with cardiopulmonary arrest treated by cardiopulmonary cerebral resuscitation at a university teaching hospital. J Am Vet Med Assoc 2009;235(1):50-57.

2. Boller M, Fletcher DJ. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 1: evidence analysis and consensus process: collaborative path toward small animal CPR guidelines. J Vet Emerg Crit Care 2012;22(Suppl 1):S4–S12.

3. Fletcher DJ, Boller M, Brainard BM, et al. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 7: Clinical guidelines. J Vet Emerg Crit Care 2012;22(Suppl 1):S102-S131.

4. Maier GW, Tyson GS Jr, Olsen CO, et al. The physiology of external cardiac massage: high-impulse cardiopulmonary resuscitation. Circulation 1984;70(1):86-101.

5. Naganobu K, Hasebe Y, Uchiyama Y, et al. A comparison of distilled water and normal saline as diluents for endobronchial administration of epinephrine in the dog. Anesth Analg 2000;91(2):317-321.

6. Leong EC, Bendall JC, Boyd AC, et al. Sodium bicarbonate improves the chance of resuscitation after 10 minutes of cardiac arrest in dogs. Resuscitation 2001;51(3):309-315.

7. Vukmir RB, Bircher NG, Radovsky A, et al. Sodium bicarbonate may improve outcome in dogs with brief or prolonged cardiac arrest. Crit Care Med 1995;23(3):515-522.

Dr. Pachtinger is an emergency and critical care clinician and the trauma center medical director at Veterinary Specialty and Emergency Center in Levittown, Pennsylvania, and Philadelphia, Pennsylvania. He is the House Officer Program Director for BluePearl Veterinary Partners and as well as the chief operating officer for VETgirl.

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