Most times, luckily, anesthesia is a routine procedure. However, patients can and do arrest, even in a previously healthy patient.
Most times, luckily, anesthesia is a routine procedure. However, patients can and do arrest, even in a previously healthy patient. This talk is aimed at allowing technicians to recognize the causes of cardiopulmonary arrest, the signs of impending arrest, and what to actually do if it happens.
Causes of arrest
Cardiopulmonary arrest is almost always caused by decreased delivery of oxygen to the brain and heart. A number of causes can contribute.
Hypoxia occurs when tissues are not receiving enough oxygen. This can be caused by either not enough oxygen in the blood or not enough red blood cells. Anemia will contribute greatly to decreased carrying capacity of oxygen. A rapid decrease in PCV can be more serious than a lower (i.e., mid-20s) PCV that is stable. Consider blood transfusions if the PCV is less than 18-20%. Hypoxemia during anesthesia is the result of either poor oxygen exchange (i.e., pulmonary disease) or more commonly, hypoventilation. Hypoventilation occurs when tidal volume is too low. It will increase PaCO2, but without much increase in the ETCO2.
Reduced cardiac output
Occurs when the heart is not putting enough blood forward. This can be due to several causes. Hypovolemia can occur from blood loss, dehydration, or third space losses. IV fluid boluses can be given to correct hypovolemia. Decreased cardiac contractility occurs with many anesthetic agents such as Dexdomitor (dexmedetomidine), isoflurane, halothane, and Propofol. Arrhythmias contribute to poor forward flow. These may be due to primary cardiac disease, electrolyte disturbances, or can be disease related. Sinus bradycardia is one of the most common anesthetic complications. In many patients, it is related to excessive anesthetic depth, hypothermia and hypoxia. Simply turning down the inhalant concentration and administering atropine can prevent an arrest.
Is defined as a systolic BP < 90 or MAP < 60 mmHg. This is another serious and common complication of anesthesia. When under anesthesia, the patient lacks normal compensatory responses to hypotension. This can be caused by hyperventilation, which will cause decreased catecholamine response. Additionally, many anesthetic drugs will most commonly cause hypotension. Acepromazine, Dexdomitor (late), Propofol and inhalants will cause vasodilation and blunt the normal response to hypotension. Fluid boluses are frequently used to expand vascular volume.
This is an extremely common consequence of anesthesia. Small patient size, open body cavities, convective losses and the cool temperatures common in the operating room contribute to development of hypothermia. As hypothermia worsens, the decreased metabolic rate will lessen amount of anesthetic drug needed. This makes it much easier to overdose the patient or create a too deep plane of anesthesia.
Signs of impending arrest
Usually, arrest is preceded by a number of clinical signs. The anesthetist paying close attention to the patient can detect these signs and take action prior to arrest occurring. Hypotension is often one of the first signs noted. A reflex tachycardia may occur. Tachycardia alone also signals that something is wrong. Tachycardia can also indicate that the patient is too light, so further investigation is necessary. Bradycardia is a more serious sign and should be promptly addressed. The onset of cardiac dysrhythmias (such as ventricular premature contractions) signals that the myocardium is not receiving enough oxygen.
Falling end-tidal CO2 is an excellent indicator of impending arrest. As blood flow to the lungs decreases sharply, the patient will breathe off the remaining CO2 and the ET CO2 will decrease. Poor oxygenation (pulse oximeter < 90%) is often a late sign, and may not actually decrease much (and sometimes not at all) until after arrest has occurred.
What to do if you don't have lots of monitoring equipment?
Even without equipment, an observant anesthetist is the best defense against anesthetic arrest. The following parameters should be monitored no more than every 5 minutes, and more frequently in sick patients. Respiratory rate should be carefully monitored. Make sure that the patient is breathing, but also make sure that it is taking adequate breaths. Surgical manipulation in the abdomen can cause minor movements of the rebreathing bag, so ensure that chest excursions are adequate. Heart rate and rhythm should be assessed, either through taking pulses, ausculting the chest, or by placement of an esophageal stethoscope. Mucus membranes can indicate cardiovascular status. Pale mucous membranes indicate anemia or poor perfusion (either vasoconstriction or poor cardiac output). If a patient with a normal PCV becomes pale, hypotension should be suspected. Cyanosis occurs at PaO2 < 40 mmHg or if > 5g/dl unsaturated Hgb. This change will occur very late in patients breathing 100% oxygen. Finally the patient should be monitored carefully for inappropriate anesthetic depth. Eyes that are central indicate that the patient is either too light or too deep. Always err on the side of caution and assume that the patient is too deep. Eyes that are positioned ventromedial indicate an appropriate plane of anesthesia.
What do you do if you suspect an arrest?
The goal of CPCR is to maximize myocardial and cerebral circulation. First, do not panic. You can only help. As we discuss the steps below, remember that CPCR runs in cycles lasting 2-3 minutes each. During a cycle, compressions should not be stopped for any reason (including assessing for return of spontaneous circulation - ROSC). At the end of each cycle, you may stop for a few seconds to auscult the patient or check the ECG.
Begin compressions first! Adequate chest compressions will effect an adequate tidal volume, meaning that unless the animal died for hypoxemic reasons, you may not need to breathe for them. With that said, the animal should be intubated as CPCR progresses (if not already intubated), but it is not the top priority.
The first rule of compressions is to “keep it physiologic”. That means matching the animals' normal heart rate. In the dog, aim for 80-120 compressions per minute (more on this in a moment), and in the cat, 180 compressions per minute. Yes, it is possible to meet these rates easily. You can sing of the following songs and do compressions to the beat
Dog: “Stayin' Alive” by the BeeGees – 103 bpm
“Another One Bites the Dust” by Queen – 100 bpm
Cat: “Footloose” by Kenny Loggins – 175 bpm
“Livin' La Vida Loca” by Ricky Martin – 180bpm
The second rule of compressions is to make your compressions count. Use appropriate technique. In medium-large breed dogs, the patient should be lateral recumbency. The hands should be placed flat or in a fist over the heart (where the elbow meets the costochondral junction). Keep your elbows straight and use your back muscles to compress. If you are using your upper arm muscles, you will fatigue much more rapidly and your compressions will be less effective. Unless you have a lift table, you will likely need to stand on a stool to effectively “put your back into it”. In the cat or small breed dog, the hand should be wrapped around the chest over the heart and the chest compressed between the flats of the fingers (not just the fingertips). For any size animal, you should compress the chest by 25-35% of thoracic width. Allow for complete chest recoil, as this improves venous return to the heart. Studies have shown that compressions become less effective after just 2 minutes. Switch compressors at the end of each cycle.
The third rule of compressions, and the most important, is to NOT interrupt compressions. Every time you halt compressions, the cardiac output is zero. The most common reasons for interrupting compressions are: intubation, catheter placement, drug administration and attempted defibrillation. There is no reason to stop compressions for any of these. Wait until the end of the cycle to briefly (few seconds) halt compressions.
Airway and breathing
Once compressions have started, an airway can be established and ventilation begun. Place an appropriately sized endotracheal tube, and remember to tie it in place and inflate the cuff. The only rule of ventilation is to “keep it physiologic”. Ventilation rates should be 8-12 bpm. Higher ventilation rates are associated with worse outcome. Avoid barotrauma by not ventilating to pressures > 20 cmH2O. If the patient died from hypoxemic causes or you suspect alveolar disease (pneumonia, pulmonary contusions, heart failure), consider providing positive end-expiratory pressure (PEEP). To do this, partially close the pop-off valve and hold pressure on the bag so that the manometer does not drop below 5 cmH2O. This will help to prevent alveolar collapse at end expiration from dilution of surfactant with alveolar fluid. Ambu-bags are unable to deliver PEEP.
Asystole is the most common arrest rhythm. It is a complete cessation of electrical and mechanical activity, and is the least likely to convert. The treatment of choice is epinephrine, even though epinephrine has not been proven to be helpful in asystole. The dose of epinephrine is controversial. High dose epinephrine (1:1000) 0.1ml/kg IV (or 1ml per 10 kg or 20 lbs) is associated with a higher rate of ROSC, but also a higher rate of re-arrest. Low dose epinephrine (1:10,000) is associated with a lower rate of ROSC, but a lower rate of re-arrest. Overall, there is no evidence that one dose is better than the other; however, most human emergency departments have switched to low dose epinephrine. You can either purchase 1:10,000 epinephrine, or dilute 1:1000 epi at a 1:10 dilution in bacteriostatic saline.
If the animal fails to convert after one cycle with epinephrine, consider use of vasopressin. Vasopressin is a powerful vasoconstrictor mediated through V1 receptors in the vascular smooth muscle, and has the added benefit of not causing post-resuscitative tachycardia like epinephrine. Currently, there is no evidence that vasopressin is superior to epinephrine for treatment of asystole. The dose of vasopressin is 0.8 u/kg IV.
Atropine is also considered controversial for treatment of asystole. It has a clear benefit for bradycardia, but does not increase rate in the non-beating heart. Its use is associated with post-resuscitative tachycardia, similar to high dose epinephrine. The bottom line is that if the animal did not arrest from a vagal cause (vomiting, coughing, defecation), then atropine is not likely to be useful and may be harmful. The dose of atropine is 0.02-0.04 mg/kg IV, or 1 ml per 10kg or 20 lbs.
If IV access is not available, the following drugs can be given via the intratracheal route: naloxone, atropine, vasopressin, epinephrine and lidocaine (NAVEL). The dose for IT administration should be doubled or tripled. A long red rubber catheter should be used for drug delivery into the lungs rather than the drug being trickled down the endotracheal tube. IV administration is preferred if available. Remember that circulation during CPCR is very sluggish with even the best compressions, so it will take the entire 2-3 minute cycle for it to reach the heart. Do not stop compressions to administer drugs or to gauge effectiveness until the end of the cycle. Large (6-30ml, depending on patient size) flush volumes may be used to help improve drug return to the heart. It the drug is injected into a cephalic or saphenous catheter, elevate the limb to improve flow time.
The only treatment for ventricular fibrillation is defibrillation. Defibrillation does not start the heart, but instead, stuns it and allows normal electrical activity to take over. With that said, it is possible to shock the heart into asystole. Defibrillation is more likely to be successful if at least one cycle of CPCR has taken place prior to defibrillation. To defibrillate, place the patient in dorsal recumbency and apply the paddles firmly to either side of the thorax. Electrical conducting gel should be used to improve contact with the skin, and hair can be clipped if time allows. Do not use alcohol. Administer ONE shock of 2-4 J/kg (monophasic) or 1-2J/kg (biphasic), and resume compressions immediately. Do not stop to see if the defibrillation has been successful until the end of the cycle.
Will it work?
Out of all causes of arrest, anesthetic death has the best recovery rate. However, one study showed that CPCR lasting longer than 15 minutes was unsuccessful in almost all cases. Severe neurological deficits were seen in dogs with CPCR lasting greater than 12 minutes. No cats survived if CPCR was > 17 min. Faster resuscitation = better outcome.