Preventing Hospital Patients from Arresting
Jennifer J. Devey, DVM, Diplomate ACVECC
Saanichton, British Columbia
Cardiopulmonary arrest is defined as a cessation of spontaneous ventilation and circulation. Prevention of cardiopulmonary arrest is the best way to treat cardiac or respiratory arrest. Of those patients that experience a full cardiac arrest, less than 5-10% will leave the hospital. Part of the reason for this dismal number is that a fair number of patients that arrest have terminal diseases or serious diseases that are difficult, if not impossible, to cure. Part of the reason is that staff are inadequately trained to deal with an arrest, and part of the reason relates to inadequate equipment or drugs available to treat the arrest.
The first goal in the hospitalized patient should be to identify those that are at a high risk for experiencing an arrest, those that are hypoxemic, hypercarbic, acidemic, hypotensive, those with significant electrolyte imbalances (especially involving potassium, magnesium and calcium), and those with diseases that lead to high vagal tone. In the face of hypoxemia, hypercarbia or hyperkalemia, an increase in vagal tone can trigger ventricular asystole.
Cellular hypoxia is a major cause of cardiac arrest. This can be due to inadequate ventilatory or pulmonary function, inadequate hemoglobin to carry the oxygen, or inadequate cardiac output due to cardiac disease or circulatory disease (such has hypovolemic shock). Hypercarbia and acidemia trigger catecholamine release which may, in excess, cause a supraventricular tachycardia to progress to ventricular fibrillation. In addition acidemia lowers the fibrillation threshold.
Patients with increased vagal tone are typically bradycardic and any increase in the vagal tone may lead to an arrest due to insufficient cardiac output and hypoxia. The increase in vagal tone may be due to the disease process or it may be due to interventions by hospital personnel. It is essential this latter category be minimized. A vagally-mediated arrest in the very early stages will be evidenced by a respiratory arrest with a very significant bradycardia. If this bradycardia is reversed rapidly the patient will survive. If the severe bradycardia is not recognized quickly enough or the wrong interventions are provided it may progress from a severe bradycardia to a full cardiac arrest. Survival at this point is significantly decreased.
Diseases with high vagal tone include intrathoracic diseases such as pneumonia, thoracic effusions, cardiac disease and cancer. Patients with laryngeal paralysis and significant chronic lower airway disease may have high resting vagal tone. They include certain intraabdominal diseases especially gastrointestinal abnormalities. Vomiting is a vagal maneuver and can lead to a vagal arrest. Patients at high risk for a vagal arrest should have their vomiting aggressively controlled.
It is very important to have knowledge of the patient’s heart rate prior to taking the patient’s temperature since straining to have a bowel movement or straining against a thermometer can cause a Valsalva-type maneuver where intrathoracic pressure builds up and a vagal arrest may ensue. For the same reason rectal exams and proctoscopic exams can cause vagal arrests. The use of rectal thermometers should be avoided in hypotensive or bradycardic patients. This includes fading puppies and kittens, patients with signs of significant shock, and patients with high-resting vagal tone. Instead, an axillary temperature should be used.
Endotracheal intubation and extubation can cause a vagal arrest. This again becomes extremely important in patients with high resting vagal tone or hypotensive patients. Both veterinarians and veterinary nurses/technicians must be familiar with the use of a laryngoscope. A laryngoscope allows the airway to be visualized and prevents excessive manipulation of the larynx, which can lead to a vagally-mediated arrest. Tracheal suctioning during intubation procedures or during care of tracheostomy patients can significantly increase vagal tone.
Ophthalmic procedures, especially manipulation of the globe, can cause significant vagal input. Manipulation of cervical, thoracic or abdominal structures intraoperatively can lead to a vagal arrest.
Identification of signs of impending arrest help prevent the arrest from actually happening. This requires very close monitoring of those patients determined to be at risk. Critically ill or injured patients cannot be left alone at night. They require round-the-clock monitoring – by staff who are with the patients all the time – and by staff who are trained to recognize and treat the signs of impending arrest. The words “found dead in cage” should no longer be acceptable.
Clinical signs of impending arrest include deterioration in mentation, changes in respiratory rate or effort, significant decrease or increase in heart rate, development of life-threatening arrhythmias such as ventricular tachycardia with R-on-T phenomenon, high grade second degree heart block or third degree heart block, significant sinus arrest, and changes in blood pressure. Laboratory values that may indicate impending arrest include significant hypoxia, hypercarbia, anemia, electrolyte imbalances, and acidemia
Everyone must have the skills to be able to recognize these episodes and to be able to treat them hopefully before the patient experiences a full arrest. Patients who have high resting tone should be identified to all staff. This can be done through verbal communication or a sign on the patient’s cage. Precautions should be taken to ensure procedures causing an increase in vagal tone are minimized. If the patient requires the procedures (such as tracheal suctioning) then the heart rate should be closely monitored throughout the procedure. At the first sign of a decrease in the heart rate the procedure should be stopped and treatment instituted as necessary. If the patient with high vagal tone is noted to be vomiting it should be monitored extremely closely – ideally by checking the heart rate. If the patient collapses after a vomiting episode it should be assumed a vagal arrest has occurred. Treatment includes providing oxygen immediately. The heart rate should be checked to ensure it is truly low and if this is confirmed the patient should be treated with atropine intravenously at high doses. Low doses of atropine can lead to a second degree heart block. The patient’s head MUST NOT be elevated during a vagal arrest. Brain blood flow is already very low. If the head is raised this will lower brain blood flow even further and potentially trigger a full cardiac arrest. Intubation should be accomplished with the patient in lateral recumbency and the patient's head held as level with the heart as possible.
Patients who are at high risk for arresting should have a laryngoscope and appropriate-sized endotracheal tube beside their cage. A drug chart with doses of emergency drugs (with volumes to be drawn up) should be posted on the patient’s cage (or top of the patient’s record if the record is kept close to the patient). Oxygen and airway suctioning equipment must be readily available. Intravenous catheters should be placed in case drugs are needed on an emergent basis.
Patients who are being maintained on oxygen should be monitored to ensure they are receiving the oxygen and that the oxygen tanks have not run out of oxygen. If the patient is receiving oxygen by hood or oxygen cage overheating and overhumidification can occur and must be prevented. If the patient is not responding to oxygen supplementation, intubation and positive pressure ventilation should be considered since exhaustion from struggling to breathe can lead to respiratory failure. Arrhythmias should be treated appropriately. If the arrhythmia is life-threatening it should be treated aggressively until the potential for an arrest has been resolved. Patients with identified abnormalities that could lead to an arrest should have lab work performed as frequently as it is indicated. Patients who may be actively hemorrhaging may need packed cell volumes checked every 15 to 30 minutes. Blood gases, electrolytes, glucose should be checked on as needed basis. Hypotension should be reversed.
Patients under anesthesia are the third major category of patient that may experience a cardiopulmonary arrest. This is more true of the critical patient but can just as easily happen in a routine spay or neuter. The same causes as discussed above can lead to an increased likelihood of arrest. Every anesthetized patient needs a complete physical exam. Ideally lab work should be checked to ensure lack of anemia, hypoxia, hypercarbia, electrolyte imbalances and hypoglycemia. An electrocardiogram and blood pressure is also ideal preanesthesia.
Someone should be monitoring the patient under anesthesia at all times. In order to prevent arrests it is essential that the use and limitations of monitoring equipment be understood. Measured vital signs should be recorded on an anesthetic flow sheet to ensure trends of change are not overlooked. There are a variety of methods of monitoring patients but nothing totally replaces the human being. Checking mucous membrane colour, tongue pulse rate and quality, respiratory rate and effort are all essential. An esophageal stethoscope can allow the anesthetist to monitor for arrhythmias, murmurs, and changes in lungs sounds. Respiratory monitors monitor breathing but do not indicate anything about the effectiveness of the breath or cardiovascular status of the patient. Pulse oximetry is extremely useful if the patient is not on 100% oxygen but if the patient is breathing 100% oxygen the patient is in severe trouble by the time the oximeter shows desaturation. Doppler monitors allow blood pressure to be monitored as well as flow, heart rate and arrhythmias. Oscillometric monitors allow blood pressure and heart rates to be monitored but do not allow flow or arrhythmias to be assessed and provides no audible sound for the surgeon. Capnometers are the only means of assessing adequacy of ventilation (and therefore the presence of hypercarbia or hypocarbia) without the use of blood gases. In severely hypotensive patients, very low end-tidal carbon dioxide measurements indicate lack of pulmonary blood flow. An electrocardiogram allows assessment of rhythm but does not indicate anything about the effectiveness of the cardiac contractions.
References available on request.