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Emergency Nursing Mr. Angel M. Rivera, CVT, VTS (ECC) Animal Emergency Center, Glendale, Wisconsin There can be no state of the art medicine, if there is no state of the art nursing.... Introduction The field of veterinary medicine has gone through major changes and advancement in the last four decades. Within the profession, the specialty of Emergency and Critical Care has become an evolving, dynamic and challenging field. Because of the uniqueness and complexity of the emergency patient, emergency nursing is evolving in its own way into a specialty field of veterinary technology. In 1994, a group of technicians and veterinarians in the emergency and critical care field started efforts towards creating a body that would recognize veterinary technicians in this particular field as a specialty and provide a means for advanced skills, education, and evaluate competency of veterinary technicians who work in the area of emergency and critical care. In January of 1996, the North American Veterinary Technician Association (NAVTA) recognized the Academy of Veterinary Emergency and Critical Care Technicians as a specialty in veterinary technology. Successful management of the emergency patient is dependent on several factors: the training and skills of personnel and readiness of facility. The implementation of team approach thorough the use of established policies, protocols and procedures; allows for coordinated resuscitative efforts. By understanding the principles of first aid; triage, primary and secondary survey; basic principles of assessment for shock, trauma and hemorrhage; the technician is able to perform rapid and continuous evaluation, monitoring and assessment of patients. The technician must have a clear understanding of his or her role in cardiopulmonary resuscitation, general principles of fluid and drug therapy. All the above (factor, skills, protocols and principles of patient care) require that the technician have understanding basic of anatomy, physiology and pathophysiology. It is through knowledge and understanding of the body overall functions and disease processes, that appropriate nursing assessment, monitoring and intervention can be achieved. Elements of Emergency Care Personnel The survival of the emergency patient is dependent on the collaborative effort of the veterinarian and the technician. Technicians and veterinarians should work together to resuscitate, stabilize, diagnose, and treat the emergency patient. The emergency patient requires prompt attention and rapid stabilization, thus requiring the technician to assume a more collaborative role with the veterinarian and other members of the team. A collaborative environment exists when there is mutual respect and understanding of the unique contributions that each individual makes to the care of the patient. It is the result of careful planning by the veterinarian and the technician in identifying guidelines that might increase the patientís chance of survival and minimize complications. The success of the team is not only dependent on the knowledge base and skill level of each member, but also on the consistency and repetition of their practice as a team. The predetermined delegation of specific nursing intervention in the emergency setting; such as allowing the technician to initiate basic cardiopulmonary resuscitation (CPR) or intubate a patient that has gone into respiratory arrest, fosters the efficient organization of talents and manpower, which in turn decrease the time between onset of the event or trauma causing the emergency; and the delivery of definitive care. The technician or emergency vet nurse should be skilled at placing intravenous catheters, obtaining blood samples, administering medications through various routes (IV, SQ, IM), performing basic CPR; assisting the veterinarian in advanced CPR, surgery, and anesthesia. The technician should be skilled in patient monitoring based on clinical and physiological parameters; and knowledgeable at utilizing different types of monitoring equipment. He or she should also know how to perform various emergency laboratory tests and be familiar with their normal values. (Fig 1: List Of Recommended Skills For Veterinary Technician Providing Emergency Care) Facility capabilities The receiving area of the veterinary clinic or hospital should be wide, with good lighting, and arranged to facilitate the rapid transport of an injured animal to the emergency or centralized area of the building. Stretchers and gurneys should be easily accessible for transporting non-ambulatory patients. Long boards and various sizes of plastic sheets are also recommended to be available for transport. Duct tape is also needed to secure dogs to theses devices in lateral recumbency. Blankets, towels and sheets of plastic bubble wrap can be used to provide insulation and protection. Resuscitative equipment and drugs should be organized and readily available for use in the emergency area (Fig 2: List Of Recommended Emergency Equipment). A portable cart should be used to store Instruments and equipments if other areas of the hospital share these. The anesthesia induction area is often chosen as the emergency area because key pieces of equipment such as oxygen and endotracheal tubes are readily accessible. The proximity of the operating room can be advantageous because some patients require immediate surgical intervention for stabilization. Clinics that lack enough space to equip a central area can benefit from having a tackle box containing essential emergency materials. A well organized movable resuscitation cart which remains in the emergency area, with several drawers for storage is ideal. Essential equipment such as ECG, blood pressure monitor and suction device are placed on top. The drawers are organized into different sections, such as airway drawer, emergency drug drawer and catheter drawer. The instruments and drugs are held in place by shaping holes into foam pads that fit in the drawer, and each space is labeled. A cardiopulmonary resuscitation sheet is kept within the resuscitation cart for recording the cause and time of arrest, mode of ventilation, and drug dose and route of administration. The airway drawer should contain different sized endotracheal tubes with cuff inflating syringes pre-attached, and a laryngoscope with at least two different size blades. Forrester sponge forceps, for retrieval of airway foreign bodies, and tracheostomy tubes are kept in this drawer. A butterfly catheter (for small patients) and a 18 gauge one and half needle (for larger patients), 3-way stop cock is set up for immediate chest tap. When a chest tube is required, having a sterile chest tube pack on the cart ready to open will expedite placement. The drug drawer should contain atropine, epinephrine and lidocaine with different size syringes preloaded with needles. Other drugs like antibiotics, glucocorticosteroids, dopamine, or dobutamine are kept on an open shelf near by. A wall chart indicating drug dosages per weight and direct current watt-second defibrillation voltages is posted centrally for quick reference during CPR. The catheter drawer should include all materials required for the placement of intravenous and intraosseous catheters. An additional drawer is stocked with bandage materials for use on the patient that is bleeding or has an open wound; sterile gloves for surgical interventions such as chest tube placement, and hair clippers with long extension cords. For the monitoring of heart rhythm and cardiac electrical activity, an ECG with alligator clips is necessary. A defibrillator with internal and external paddles is also kept on the cart ready for use in the patient in ventricular fibrillation. A suction device with different suction tips should be available. Large stiff dental suction tips work well for suctioning pharyngeal fluid; smaller pliable tips will pass through the endotracheal tubes. Hand held and powered by squeezing suction units, should be available if there is no electrical suction system present. All suction units should generate up to 300 mmHg of suction pressure within 4-5 seconds of the suction tip being occluded. Basic laboratory test used in the emergency setting include pack cell volume (PCV), total solids (TS), blood glucose (lab test strips), blood urea nitrogen (lab test strips), serum electrolytes and urine specific gravity and lab dipstick. Different blood collection tubes, micro-centrifuge tubes, a centrifuge, laboratory test strips and a timer are part of this basic emergency laboratory setting and are located in the emergency area. To guarantee constant readiness, each person starting a shift reviews a check-off list of all the instruments and drugs. The instruments should be tested for proper function (e.g. light bulb on the laryngoscope) and the emergency drugs checked for quantity, proper location and expiration date. By reviewing the check-off list, the technician and clinician become familiar with the materials and its location. Policies and procedural protocols Policies, procedural protocols, and guidelines provide consistency and efficiency within and organization. Policies state the organizations belief concerning how certain thing should be done, at what times they are to be done, or under conditions they are to take place. Procedural protocols mandate how to do things in a step by step action plan. In the emergency setting, quick decisions and independent functions are needed; policies and procedural protocols provide the guidance necessary to ensure acceptable response. Established policies and protocols can be used to ensure continuity of care as the patients move from one department to another. As policies and protocols evolve, the standards for care of patients will also be set. Common emergency problems that benefit from written protocols include initial stabilization of patients with gastric dilatation-volvulus, head trauma, urinary tract obstruction, acute heart failure, stupor and coma; and catastrophic trauma. All team members should be familiar with the protocols, which should be discussed and reviewed at staff meetings. Key Aspect of Emergency Nursing Initial Contact and First Aid Treatment of the critically ill or trauma patient begins at the site of the accident or in the ownerís home. The receptionist or technician usually makes initial contact with the owner on the phone. This person that provides the first contact with the caller is termed ìa first responderî. It is recommended that specific protocols be established on exactly what information and or advice the first responder is to give the caller. These responses can be placed in on 5 x 8 cards and indexed according to callers concerns. The first responder should have some medical knowledge to properly assist the client in first aid, transport and recognition of catastrophic emergencies, (respiratory arrest, upper airway obstruction). Appropriate first aid can prevent further injury at the scene or during transport. The client should be given precise instructions for the most direct and simple route to the hospital. The telephone number for the poison control center should be readily available for reference in case of suspected toxin ingestion. Telephone contact, handling, first aid at the scene, and transport It is important that upon initial telephone contact, vital information such has clientís name, telephone number, patient species, age and gender, the presenting complaint, petís current condition; and expected time of arrival. It is helpful to write this information on the apposite board, to alert the veterinary team and aid in preparing the emergency area accordingly. When answering a call, an assessment must take place so that one is able to prioritize needs. It is important to first determine if a life-threatening condition exist and instruct according to hospital policies and guidelines. Second, determine if first aid advice is needed and offer guidance appropriately using the protocols approved by the hospital administration. All other calls should be handled cautiously without diagnosing and should always end with a recommendation for the caller to seek medical treatment for their pet. (Fig 4: Common historic or observed problems that warrant immediate medical attention) Owners can provide significant medical assistance at the scene of the injury. The first concern is for the ownerís safety. Advise the owner to take a quiet, gentle approach while handling the injured pet. They should use a soft and calm voice and approach very slowly so they don't startle or scare the animal. Ask that they watch for signs of aggression, snarling, growling, or any clues that may have difficulty working with this animal. If the animal is in pain or acting aggressively they may need to muzzle him. If it is a cat a blanket to cover him up will help provide the rescuer with adequate protection while attempting to pick him up or handle him. Callers should always be cautioned that despite theses preventative measures, there is still the possibility of them sustaining an injury. One may be able to gain control by placing a heavy blanket over the animal while an assistant gains control of the head or places a muzzle. When placing a muzzle on the dog a cloth strap or strip of gauze 24" in length is tied around the nose first with a simple overhand knot tied beneath the jaw. The straps are then brought around behind the neck and below the ears where they are snugly tied together. One could improvise and use a tie, a pantyhose or a shoelace to fashion a muzzle if no other material is available. These types of muzzles are not indicated if the animal is bleeding from the nose or the nasal passages appear to be occluded. Cats should be picked up slowly, with one hand supporting the chest while transporting him in a firm, secure manner under the arm. Hold the front legs with one hand and the head and neck with the other. Placing the cat into a cardboard box or pillowcase is another alternative means of immobilization and transport. To avoid further injury care is taken to transport the animal carefully to the veterinarian. Animals suffering from severe illness are often weak and have poor muscle coordination, putting them at a higher risk for developing injuries. Unconscious or stuporous animals are also at risk for developing injuries and are at risk of vomiting and aspirating the contents into their trachea and lower airways. Pressure should not be placed on their neck or chest as this could lead to vagal nerve induced bradycardia, hypotension and in rare instances cardiac arrest. They should be transported in a sternal or lateral position. If an injury leaves the animal unconscious or unable to walk a spinal injury should be suspected. This animal should be immobilized, transported laterally, taped or tied down if possible on a flat wooden, cardboard, or plastic object which becomes an ideal form of transportation as well as allowing X-ray examination of the neck and back without any further mobilization of the pet. When sliding the animal onto a board makes certain that the body remains parallel to the board's surface to prevent excessive manipulation of the head or spine. An animal with a chest wound may have a damaged lung on that side. If possible, and the animal allows it, animals sustaining trauma to one side of the chest should be transported with that side down to allow for full expansion of the lesser traumatized lung on the opposite side. If the animal will not lie down and begins to become agitated it is best not to force him. If the animal continues to struggle upon immobilization on its side, a respiratory problem should be suspected, and he should be allowed to be in a sternal position. Fractures of the long bones below the elbow, hock or stifle (knee) with significant displacement have potential for nerve, muscle, and skin penetration and should be supported during transport. The owner can fashion a splint from a rolled newspaper or magazine, which is then secured in place by a long piece of fabric such as a tie or scarf. Immobilization of the hit by car patient on to a board may be beneficial in preventing further internal bleeding. The Veterinary Technician: Rendering First Aid First aid is the immediate care given to a pet that has been injured or suddenly taken ill as they arrive to the veterinary facility. Knowledge of what to do will improve the pet's overall chance of recovery and possibly save its life. When using first aid always understand one's limitations. A key first aid principle is to seek further medical assistance in all cases of illness or injury. Do not use first aid as the only treatment. As first aid provider's your objectives are to:
When delivering first aid one should conduct an initial assessment of the animal. It is wise to include a quick survey of the scene or area where the animal is currently. The initial response during the early moments of an emergency is critical. In addition to protecting the animal from further injury one of the first rules involved in providing first aid is one must insure the safety of everyone providing care. Following an evaluation of the emergency and the circumstances surrounding the event, the formation of a care plan should follow a three-step approach: Avoiding doing any further harm:
The Initial Assessment should include the standard ABC's of emergency first aid: Check for Airway patency... Is the animal Breathing and if so does it appear rapid, shallow, labored or is it normal? Is there any blood visibly associated with the respiratory system, i.e. is there blood exiting the nasal passages or the mouth. The answers to these questions will be of great benefit to the veterinary team. Next check to evaluate the heart rate and Circulatory competence. Check the heart rate by gently feeling the heart beat by cupping the sternum in your hand midway along the ribcage. In most dogs and cats you should be able to feel the heart beat just behind the sternum between the fourth and sixth ribs. This is known as the Apical Beat. In large chested animals you may have more success feeling for a femoral pulse by using several fingers with light pressure on the inside of the thigh. One can determine the pulse rate by using the femoral pulse. When taken correctly, the absence of a femoral pulse suggests a systolic arterial blood pressure below 60 mmHg (normal is greater than 100) which can occur in shock and other low blood volume situations (such as acute hemorrhaging). Always follow this basic assessment with auscultation with a stethoscope to assess heart tones and breath sounds. Breath sounds should be clear equal bilaterally, and heart sounds should be crisp as a lub-dub-lub-dub, without any murmurs or additional sounds. Completion of the cardiovascular function assessment is done by noting the animals capillary refill time, mucus membranes color, and amount of jugular vein distention. Cardiopulmonary Resuscitation Life-threatening Primary Pulmonary and Cardiovascular Emergency Events Emergency patient are often presented unresponsive without respirations but with palpable pulse. This condition is termed respiratory arrest. However, failure to achieve effective ventilation results in a progressive acidosis and hypoxemia that may lead to cardiovascular dysfunction, hypotension, and eventual circulatory collapse. Initially, hypoxemia enhances the peripheral chemical drive to breathe and stimulates heart rate. Profound hypoxemia, on the other hand, depresses neural function and produces bradycardia refractory to atropine. At this point, cardiovascular function is usually severely disturbed, because cardiac and vascular smooth muscles function poorly under conditions of hypoxia and acidosis. In addition, there is also reduced cardiac output due to decreased stroke volume and heart rate. The heart may abruptly fail to achieve an effective output because of an arrhythmia or a suddenly impaired pump function resulting from diminished preload (volume of blood returning to the heart), excessive after-load (volume of blood being pumped by the heart), or decreased contractility. The normal heart compensates for changes in heart rate over a wide range through the Starling mechanism which states that; the more the heart is filled during diastole (within certain physiologic limits), the greater the quantity of blood it will pump. Thus, patients with dilated or stiff heart, lose this reserve and are highly sensitive to changes in heart rate. For this reason, patients with congestive heart failure poorly tolerate bradycardia. Animals that are sick or injured may also loss their normal ability to overcome or for sympathetic override the bradycardia. Decreases in preload sufficient to result in cardiovascular collapse are usually due to reflex vasodilation, massive hemorrhage, pericardial effusion/tamponade, or tension pneumothorax. Abrupt increase in after-load sufficient to cause catastrophic cardiovascular collapse usually affect the right ventricle and can be due to embolism to the pulmonary circuit by a clot or air. Cardiac muscle dysfunction can result from hypoxemia, acidosis, electrolyte imbalance, or myocardial infarction. The ABCs of Basic Life Support The main purpose of basic life support is to maintain organ function by promoting perfusion of the two major organs, the brain and the heart. Several conditions are considered life threatening, but three in particular require immediate attention: respiratory arrest, circulatory failure and severe bleeding. Respiratory arrest and/or circulatory failure can set off a chain of events that will lead to death. Severe uncontrolled bleeding can lead to irreversible state of shock in which death is inevitable. Thus, first aid priorities that demand rapid and accurate assessment can be grouped as those that compromise: Airway, Breathing, and or Circulation (cardiovascular to include bleeding), after which other injuries may be addressed. Airway Any interference with breathing produces oxygen depletion (anoxia) throughout the entire body. Therefore your first priority is to ensure that there is a patent airway and be able to maintain its patency. A partial obstruction can become a total airway obstruction resulting in unconsciousness and respiratory arrest. Total or partial airway obstruction may occur due to foreign body (bone, meat chunk, ball or stick), large blood clots, vomitus, thick saliva, or a direct blow to the larynx/trachea causing hemorrhage or spasm. During the summer some dogs will develop laryngeal edema due to over exertion and heat induced illness. Signs one can observe in a partially airway obstructed animal are: difficulty breathing upon inspiration, exaggerated airway sounds (usually, by this time 75% of the airway is compromised), accessory muscles of the face and neck are being utilized and eventually (and this is a very late sign) cyanosis (blue coloration of the gums, and tongue). Partial airway obstruction: First aid measures in the partially obstructed airway victim consist of removing any visible object from the mouth that may be causing the obstruction. Precautions should be taken not to get bitten by the animal. Remember partial obstructions can turn into total obstructions, as the victim struggles for more air, they become more distressed, frantic and non responsive to commands even form their owners. If one has witnessed or has an idea of what type of material is causing the obstruction, the rescuer can attempt to dislodge the object via abdominal thrust compressions similar to those used in the Heimlich maneuver in people. It is important that these patients be rushed to the veterinarian. If the patient is 30 minutes away, but there is a clinic closer to them , have the owner take the victim to the nearest veterinary facility. Signs seen in the total airway obstruction victim are; no airway sounds can heard, most often the victim is unconscious or near unconsciousness, cyanotic, no movement or expansion of chest wall. First aid measure to consider in these patients, especially the unconscious ones are:
Breathing is an act which is automatic and one over which the individual (human or animal) exerts only a certain degree of control. Breathing consist of two separate acts; inhalation, the enlarging the chest cavity so air is driven into the lungs, and exhalation, the decreasing the size of the chest cavity so air is driven out. The diaphragm provides most of the power for the act of inspiration and exhalation is passive normally. Providing artificial ventilation (rescue breathing) : When there is absence of respiration the rescuer should commence artificial ventilation. While extending the neck, hold the tongue out, close the jaws over the tongue (so the incisor teeth hold the tongue from moving back in the mouth and occlude the airway) and proceed to breath through both nostrils using your mouth, (or your mouth over the animal's nose and mouth in small patients) giving 12 to 20 breaths. In bradycephalic animals (animals with short, flat faces) it is best to hold down the upper fleshy lip over the lower jaw to aid in creating a seal. One should be able to observer the chest wall rise and fall with every breath. If the patient does not start breathing on its own, provide a few more breaths and assess the victim for a pulse or heartbeat. Lack of spontaneous breathing and the absence of a pulse or heart beat are indications to proceed to the "C" of basic life support while still performing artificial ventilation. This is best achieved by recruiting another person to assist. An animal can stop breathing for several reasons, including; electrical shock, drowning, suffocation/choking, head injuries, congestive heart failure, severe hypovolemic shock, various toxicities, vagally influence and cardiac arrhythmias. Symptoms of suffocation in the unconscious victim include dark blue (cyanotic) colored mucus membranes, lips, nail beds and insides of earflaps. The pulses may become weak and rapid initially but later become weak and slow before stopping. The pupils may become dilated. Over a few minutes as hypoxemia to the brain occurs. The cause of a suffocation episode is often due to an obstructed airway preventing air from getting into the lungs and artificial ventilation is of no value until blockage is removed. Along with airway obstructions due to the presence of objects in the airway, suffocation may occur when a victim gets tangled with a leash or collar. Any head injury that produces swelling of the brain and/or hemorrhage into the skull can cause the automaticity of breathing to be compromised. Animals with known heart disease can develop (pulmonary edema) or the accumulation fluid in their lungs which affects their ability to exchange oxygen and carbon dioxide and hinders the lungís capability to expand. Certain abnormal heart rhythms can cause an animal to collapse and stop breathing (syncopal episodes). Circulation/Cardiac compressions Cardiopulmonary arrest can be defined as the cessation of functional ventilation (breathing) and effective circulation. For example, during shock, as the victim's condition progressively worsens, the brain and heart begin to decompensate. Reduced blood flow to the heart muscle (coronary blood flow) leads to damage of the heart muscle itself resulting in heart failure (myocardial failure). The resulting reduced blood flow to the brain causes depression of respiratory and cardiovascular centers that control heart rate and respiratory rate. During this stage the blood vessels dilate in the muscles, skin, and abdominal organs causing blood to pool in these tissues. All these alterations feed a vicious cycle of changes that eventually precipitate cardiopulmonary arrest. Signs observed in the cardiopulmonary arrest victim are: absence of an auscultable or palpable apex heart beat, lack of palpable pulses (due to arterial hypotension), apnea (cessation of breathing) or agonal breathing (ineffective breaths taken prior to death), absence of bleeding even in the presence of a wound or laceration of considerable size (this will occur with blood loss of more than 40-55% blood volume), loss of consciousness (10-15 seconds following arrest), and pupillary dilatation (30-45 seconds following arrest). If the animal has not responded to artificial ventilation and an apex heartbeat or pulse is not detectable commence rhythmical chest compressions consisting of 60 to 140 compressions per minute, should be done IF IT IS DETERMINED THAT RESUSCITATION IS INDICATED. Artificial ventilation (rescue breathing) should be provided at 12-20 breaths per minute . In cases where significant restriction to lung expansion is observed then rescue breathing should be increased 30 to 60 breaths per minute. Ventilatory and CPR rates are dependant upon size of the animal, with the larger animals requiring slower rates. In medium to large dogs compress the chest wall with one or two hands depending on the size of the animal and rescuer. Place the hand(s) on the side of the chest wall where it is the widest, at or within 2-3 inches of the point of the elbow, or on the sternum with the dog laying on its back (fig. 4). Depress the rib cage 1.5-3 inches. Do this 80-100 times per minute. Continue providing artificial ventilations at least 12 times per minute in large dogs if you have no help (single rescuer technique). Chest compressions and ventilations should be coordinated to give breaths during the compressions if this can be performed. When both ventilations and compressions cannot be performed together (as in larger dogs) two quick breaths should be given right after every 15 compressions. When two rescuers are working together artificial ventilation should be given during heart compressions with every 2nd to 5th compression, depending on the size of the animal. The table in figure 6 will assist the rescuer in determining the rate of providing ventilation and CPR to an arrested animal. (Fig 6: Rate guide for delivering artificial rescue ventilation and CPR based on an animal's weight). CPR should continue until:
It is recommended to use clear plastic tubes with inflatable cuffs that are high volume and low pressure. A clear tube allows visualization of any fluid or exudate coming from the trachea or lungs. A high volume-low pressure cuff helps reduce the incidence of pressure necrosis of the trachea when the tube is maintained for extended periods. If the arrest is of pulmonary origen, and the heart is still beating but at a very slow rate; the initial ventilations may be enough to reestablish breathing and increase heart rate. If the patient continues to breathe on its own; supplemental oxygen should be provided via nasal cannula, oxygen hood or transtracheally. It is very important to observe the patient's respiratory pattern. If it is unusually slow or shallow or unstable - then these patients will need continued ventilatory support. Patients with respiratory arrest should be intubated on lateral or dorsal recumbency to avoid manipulation of the head or neck in case of hypotension or a cervical lesion. Using 100% oxygen, ventilate and make sure the lungs expand well. Use a stethoscope to listen for bilateral lung sounds while the patient is being ventilated. Failure to hear lung sound bilaterally can indicate an endotracheal tube placement in one side of the main pulmonary tree or a unilateral pleural space disease. If there is a pressure gauge available, ventilation should achieve inspiratory pressures of 20 cm of water in the dog and 10-15 cm in the cat. Patients with suspected pleural or lung parenchymal disease will require greater inspiratory pressures. Overzealous inflation of the lungs will interfere with venous return, as well as cause a rupture of the pulmonary tree, leading to free air in the thoracic cavity. In the absence of a pressure gauge, provide enough inspiratory pressure to see movement of the chest wall. When attempts to ventilate are met with an increasing resistance; one should suspect a pneumothorax and a larger needle or tube should be inserted into the pleural space to evacuate it of the air. In the vast majority of cases in veterinary medicine respiratory arrest is the principle inciting factor that leads to cardiac arrest. One exceptions maybe the Doberman Pincher that has been observed to have sudden onsets of ventricular fibrillation prior to respiratory arrest. Another exception is in pets that under go a vaso-vagal reflex with sudden stoppage of the heart due to a vagus nerve stimulation. This is observed in animals most commonly after or in conjunction with micturation, defecation, vomiting or other manipulations that can stimulate parasympathetic nerve discharge in the face of ongoing sympathetic reasons, such as that seen postoperatively or post traumatically. It is more prone to occur in out experience with animals that are hypoxemic and acidemic. In very weak and older animals a vaso-vagal induced arrest may also occur with insertion of the rectal thermometer for temperature taking and laryngeal manipulation as occurs with intubation. If the patient is deemed to have a respiratory arrest, ventilations should occur at a rate of 12-20 times per/minute, and if associated with a cardiac arrest then done with each 2 or 3 chest compressions. Performing the ventilations during the compressions increases the airway pressures within the chest, which has been associated with improved aortic pressures generated with the chest compressions. This simultaneous compressions and ventilations cannot be done without a cuffed ET tube in place. Compression of the chest should be done at least 80 times per minute. In between chest compressions, one can deliver abdominal compressions (termed abdominal pump) similar to those of the chest; to aid in increasing oxygen delivery, coronary blood flow and cerebral blood flow. ABDOMINAL COMPRESSIONS should only be done with a cuffed ET tube in place. Small animals can have chest compressions done laterally over the heart to utilize what is termed cardiac pump. However, in small animals (<10 kg), the chest should be compressed at the widest part of their chest. Deep chest animals (Standard Poodles, Borzois etc...) should have chest compressions applied from the sternum to the vertebral column while on dorsal recumbency. To monitor the results of compressions it is recommended to use a doppler flow probe on the patient's eye. The doppler will detect Blood flow generated in the external ophthalmic vessels IF FLOW is EFFECTIVLY being generated. If a doppler is not available then palpation of the femoral or brachial artery for a pulse with each compression is recommended. IF NO FLOW IS DETECTED with basic life support skills then advanced skills that involved epinephrine delivery, and possibly performing a resuscitative thoracotomy and aortic cross -clamping (encircling and occluding the thoracic aorta just distal to the arch) using a feeding tube could be required. Using a laryngoscope with the patient in right lateral position is recommended for intubation to avoid lifting the patient's head, which could decrease the blood flow to his brain, cause vomitus to migrate into the trachea, and cause a vagal response that may lead to a cardiac arrest if one had not yet occurred. Use of a laryngoscope with a good light will allow actual visualization of the larynx for either removal of foreign bodies or the placement of an endotracheal tube. It is recommend that an AMBU bag and reservoir be used over that of an anesthetic machine and rebreathing bag to ventilate emergency near arrested or arrested patients. This is because with the former no attention has to be paid to a pop-off valve and the compliance of the lung can be assessed more accurately with compressions of the bag. By-standers can also be shown how to use the AMBU bag to assist in resuscitation attempts if this is necessary. much easier than the anesthetic machine. Hemorrhage Catastrophic hemorrhage is life-threatening due to the massive volume of blood that may be lost (internally, externally, or both). Bleeding internally into areas that surround vital organs such as heart and brain can create increased pressure that compromises vital organ function. Internal hemorrhage can occur in other areas such as the chest, abdomen and osseofascial compartments like the pelvic area, around the humerus and femur. Bleeding into the chest and the abdomen requires a veterinarian's skills and assessment tools. Some specific signs to look for in the animal with abdominal hemorrhage are a red circular discoloration with its center at the umbilicus caused by an accumulation of red cells under the skin, and/or abdominal distention from blood accumulation, although this usually requires a blood loss of 40ml or more of blood per kilogram of body weight (one kilogram is equivalent to 2.2 pounds of weight). Bleeding into an osseofascial compartment is generally due to blunt trauma and one can expect to see signs such as swelling of area, bruises, wounds and lacerations. The immediate goal in any hemorrhage event is to stop, or at least slow down bleeding, restore volume to prevent vascular collapse (decreased volume of blood in veins and arteries), and avoid irreversible damage to organs. Shock in these patients is a result of lack of circulating blood volume, secondary to vascular collapse and hypoxia (lack of oxygen). Restoring volume to these patients becomes a major priority and can only be done by a trained professional in a veterinary facility. These patients require rapid intravenous fluids consisting of crystalloid, colloids and transfusions with blood components such as whole blood or packed red cells in order to maintain sufficient pressure to perfuse vital organs such as the heart, brain and kidneys, and to restore red cells to serve as oxygen carrying vehicles. ADVANCE CPR or Advanced Life Support (ALS) The goal of advanced cardiac life support is to intervene with appropriate pharmacological agents, restore an ECG rhythm, achieve adequate acid base balance, and diminish neurologic impairment. Advanced life support begins where basic life support left. Chaos often surrounds initial attempts at CPR. A prompt, and well directed resuscitative effort is critical to achieve adequate cardiopulmonary and neurological function. Resuscitative equipment should be close at hand, there should be established protocols and a predetermined team. A single person must be in charge of the resuscitation team. This person should integrate all pertinent information and establish priorities for response. The team leader, should monitor the ECG, order medications, and direct the actions of the other team members, but should not be distracted from the leadership role by performing procedures. The hallmarks of advanced CPR are:
Establishing effective ventilation: Basic support of the airway, breathing and circulation should not be interrupted for long periods to perform adjunctive procedures. These patients require intubation by the most experienced person to achieve definitive control. Intubation attempts should not interrupt ventilation or chest compressions for more than 15 seconds. Therefore, all materials including laryngoscope, endotracheal tubes, and suction equipment should be assembled and tested before any attempt at intubation. When neither intubation nor effective ventilation can be accomplished because of abnormalities of the upper airway, restricted cervical motion, or patient agitation, sedation or paralysis should be considered. The patient with a total upper airway obstruction should have a tracheostomy performed to allow effective ventilation. In the patient with a partial airway obstruction, emergency aid can be delivered by insufflation of oxygen via a large bore needle/catheter puncture at the cricothyroid membrane; thus providing adequate oxygenation until a more definitive airway is established. During CPR, ventilation should normalize arterial pH and provide adequate oxygenation. The cornerstone of pH correction is adequate ventilation; not bicarbonate administration. Venous blood gases can be used to assess the effectiveness of the compressions. High pC02 is seen with poor blood flow generation. End-tidal CO2 monitoring can also be used to determine effectiveness. A valve above 12 mmHg has been associated with increased brain survival in experimental studies. Clinical studies in humans seem to also substantial this. Establishing effective circulation: Blood flow during CPR is theorized to occur by two mechanisms: cardiac pumping, and thoracic pumping. Cardiac compressions theory proposes that chest compressions generate positive intraventricular pressure, stimulating cardiac muscles to contract, making the heart valves function to achieve forward blood flow with each compression. Unfortunately, in most dogs over 20 Kg in weight the direct compression cardiac pump is not very effective due to the large size of the chest and the space taken up by lung tissue as compared to humans or pigs. In animals less than 10 Kg in size some cardiac pumping is done, particularly if the chest can be compressed from both sides with hands or fingers/thumb; the later for very small patients. The thoracic pump theory proposes that the heart serves as a passive conduit for blood flow. Chest compressions create a positive pressure relative to extrathoracic structures, and flow is valved at the thoracic inlet. Retrograde vena cava flow is prevented by jugular venous valves and functional compression of the inferior vena cava at the diaphragmatic hiatus. Binding of the caudal abdomen and rear limbs using bandage materials, towels or commercially produced MAST (military antishock trousers), can aid in decreasing blood flow to nonessential areas, and increasing the blood supply to the anterior portion of the body. They also can be used to splint, stabilize and control hemorrhage of the lower extremities. Because close chest CPR, is only one third effective, the team should be prepared to perform open-chest CPR, IF SPONTANEOUS CARDIAC CONTRACTIONS DOES NOT BEGIN WITHIN 5 MINUTES. Electrocardiogram and administration of drugs: The EKG allows for characterization of any existing arrhythmia and determination of defibrillation or drugs to be administered. There are five major arrhythmias that are frequently associated with cardiac arrest: Asystole, ventricular flutter, ventricular fibrillation, pulseless idioventricular rhythm, and electrical mechanical dissociation. Asystole: Any rhythm is better than asystole, which is defined as the complete absence of electrical activity (a flat line EKG). Therefore, the aim in CPR when encountered with this EKG, is to stimulate electrical activity and then modify the rhythm to one with a pulse. Asystole usually indicate extended interruption of perfusion and carries a grave prognosis. An important point to remember is that low-amplitude ventricular fibrillation may go unrecognized or mistakenly called asystole. Because of this, it is recommended to administer epinephrine and defibrillate the suspected asystole patient. Ventricular flutter: This is a more chaotic wave than ventricular fibrillation. It represents an extreme type of ventricular tachycardia that is about to convert to ventricular fibrillation within a few seconds. Lidocaine is the first drug of choice used to block the excited foci. If ineffective after several boluses, defibrillation may be required. Ventricular fibrillation: This rhythm implies multiple foci within the ventricles firing rapidly and independently, resulting in no coordinated mechanical activity. It is an uncoordinated depolarization of the ventricle muscle, resulting in abrupt cessation of effective blood flow. This arrhythmia occurs only when the heart is severely damaged by ischemia, drugs, trauma, or contact with high voltage electricity. The goal is to abruptly stop the electrical activity and allow one strong focus to take over (coarse fibrillation), rather than multiple weak foci (fine fibrillation). When fibrillation is fine, epinephrine is administered; if there is no change, lidocaine is administered, prior to defibrillation. Pulseless idioventricular rhythm: This electrical activity originates from an ectopic ventricular focus producing insufficient pressure to generate a peripheral pulse. It is important not to suppress these slow ventricular rhythms, lidocaine is not to be used. Electrical mechanical dissociation: This arrhythmia is characterized by the inability to detect pulsatile activity in response to coordinated EKG complexes. When cardiac in origen, EMD carries a dismal prognosis because it is usually associated with massive pump destruction or free wall rupture. In the administration of drugs during CPR, the goal is to deliver this agent to myocardium via the coronary vessels as quickly as possible. Oxygen is the first and most important drug of CPR, and should have been addressed during the management of the airway and breathing. Cardiopulmonary arrest patient should by intubate and ventilated using a system such as an ambu-bag, capable of delivering 100% oxygen. Most CPR cases, will have an endotracheal tube as a means of establishing an airway. Certain drugs such as Atropine, Epinephrine and Lidocaine can be administered via endotracheal tube, directly to the pulmonary tree where they are rapidly absorbed and placed into the circulation. An important point to remember is that the dose of these drugs must be doubled with an equal amount of sterile saline to add sufficient volume to allow for the delivery of the drug at the end of the endotracheal tube followed by one or two ventilation. Other means of delivering drugs during CPR are intralingual, intraosseous, and intravenously via peripheral or central lines. Administration of drugs into the venous sinuses of the tongue provides rapid drug uptake into the systemic circulation when chest compressions and ventilations are employed. If an intraosseous catheter is in place prior to the arrest, drugs can be administered by this route. There is rapid uptake and distribution, most likely faster than via peripheral. Administration of cardiac drugs is best accomplished through a long centrally placed catheter (jugular catheter). However, most patients resuscitated also require that large volumes of fluids be delivered into the intravascular space rapidly; most central line are of small in diameter, thus limiting the amounts of fluids required. Establishing and maintaining intravenous access: The heart simply cannot pump, that which is not returned to it. In CPR, a variety of condition produce either relative or absolute hypovolemia, and therefore; provision of adequate circulating volume must be accomplished. The choice of catheters used for fluid bolus administration is not mundane matter. It is worth understanding that the rate of flow is directly related to the fourth power of the diameter and inversely related to the length of the catheter (Pouiselleís Law). Therefore, short large bore catheters connected to a pressure device or infusion pump are preferable. In al emergency patients showing signs of shock, at least one large bore catheter IV line (18 gauge in cats and small dogs; and 14 and 16 gauge in medium/larger breeds), should be placed and crystalloids, colloids and or blood products administered as needed. Several hematocrit tubes should be obtained from the blood seated in the hub of the catheter. Theses samples can be used to obtain base line values for PVC, TS, blood glucose, and BUN. Special procedures Although the veterinary technician is not going to be performing a resuscitative thoracotomy or aortic cross-clamping to increase blood flow to the heart and brain during CPR it is recommended that these procedures be at least understood and be familiar with. In some veterinary emergency centers technician are part of the team perform open-chest and aortic cross-clamp. They are also expected to be able to assist in the procedure and perform cardiac compressions. Other special techniques associated with CPR also include defibrillation and the delivery of drugs down the airway for rapid uptake in the arrested patient, being resuscitated. Physiological Parameters Assessed in the Emergency Patient Urine Output Pathophysiology The main function of the kidneys is to excrete metabolic wastes and reabsorb vital electrolytes and water. The volume and contents of the urine produced is a result of the function of the population of nephrons, made up of the glomerulus and renal tubules. The volume of urine produced is dependent upon the glomerular filtration rate (GFR) and ability of the renal tubules to reabsorb sodium and water. The factors governing the GFR are the size of the glomerular capillary bed, the permeability of the capillaries, and the hydrostatic and oncotic pressure gradients across the capillary walls. The factors governing the function of the tubular cells include: oxygen utilization, glucose availability, and integrity of the cellular enzyme systems. Variations in these factors have predictable results. For example, should the mean arterial blood pressure falls below 60 mmHg, the hydrostatic pressure gradient declines across the glomerular capillary beds and glomerular filtration almost stops (oliguria). Severe prolonged hypoxia can cause the dysfunction or death of the glomerular and tubular cells, leading to inadequate urine production. In addition, interruption of the tubular cell ability to reabsorb sodium results in high urine sodium and an increased urine production. Procedure Accurate and frequent measurement of urine output requires bladder catheterization. A sterile soft red rubber or polyurethane feeding tube is used in the male dog and a Foley catheter in the female. Open-ended tom cat catheters or 3.5 French soft red rubber feeding tubes are used in cats. Aseptic technique, utilizing sterile gloves, minimizes iatrogenic urinary tract infections. The catheter is lubricated and advanced slowly through the urethra into the neck of the urinary bladder and sutured to the vulva or prepuce. A closed urinary collection system utilizing a sterile collection bag and IV line is attached with the bag maintained off the floor and below the level of the catheter. The bladder is immediately emptied and the time recorded as the 0 time (start of collection). The frequency of measuring UO is determined by the rate of onset and the severity of the disease. In general, UO is measured every 2 hours. Daily examination of urine sediment is performed to monitor for infection. Urinary catheters should be flushed with sterile saline and inspected for kinks and clots in the line at least every 8 hours or if there is a sudden decline in urine collected. An indirect method of estimating UO is to place diaper sheets (under-pads or chucks) in the patient's cage to collect the urine. The weight of a dry diaper is subtracted from the weight of a urine soaked diaper. Each1mg increase in weight equals 1ml of urine. An alternate method is to place the animal on a grate elevated off the cage floor. Urine is then collected and measured. Fluid input and UO are recorded, including any fluids administered by enteral or parental routes. Quantities of fluid lost through vomiting and diarrhea are estimated and recorded. Assessment Normal UO is 1-2 ml/kg/hour. Oliguria is defined as UO <0.27 ml/kg/hr and anuria is <0.08 ml/kg/hr. However, as urine falls below 1 ml/kg/hr, oliguria is anticipated. Oliguria can be from prerenal, renal, or postrenal causes. Prerenal conditions such as hypovolemia, cardiac failure, hypotension, excessive vasoconstriction or hypercalcemia can lead to reduced GFR. Dehydration and hypotension will decrease UO (prerenal) until adequate intravascular volume has been restored. Renal changes affect the glomeruli and/or tubular cell function, with sepsis, trauma, toxins (such as aminoglycosides, amphotericin), radiocontrast agents, infections (polynephritis) as potential etiologies. Postrenal problems cause interruption of the flow of urine through the ureters, bladder or urethra and include renal calculi, blood clots, neoplasia or trauma. True oliguria in an animal receiving IV fluid will result in a decreased PCV/TS due to hemodilution. The CVP will increase and harsh or wet lung sounds may develop. The body weight will increase rapidly as fluid accumulates. Increasing blood levels of urea nitrogen, creatinine and potassium suggests renal failure or postrenal obstruction and warrants immediate veterinary attention. Excessive urine production is called polyuria and can be due to IV fluid overload or impaired renal tubular absorption of sodium and water. Other conditions such as medullary wash out, post obstructive diuresis and sepsis can causes polyuria and require large amounts of IV fluids. Intervention The technician must evaluate the UO in relation to the hematocrit, total solids, central venous pressure (CVP), blood pressure, heart rate, and body weight. Any decrease in UO in an adequately hydrated and perfused animal warrants immediate notification of the veterinarian. The IV fluid rate is reduced and the urinary collection system examined for postrenal causes of urine outflow obstruction. If the origen of the condition is determined to be renal the veterinarian will administer either mannitol or furosemide and dopamine to stimulate urine production. A polyuric animal will require a greater quantity of intravenous fluids for maintenance of normal hydration. Medullary washout often occurs and requires a slow tapering from IV fluids onto oral fluids to avoid significant dehydration. Potassium is commonly low in these animals and required aggressive supplementation. Blood Pressure Pathophysiology Arterial blood pressure is a product of cardiac output (heart rate and stroke volume) and peripheral vascular resistance. Systolic pressure is the pressure exerted by the blood as a result of contraction of the left ventricle. Diastolic pressure is the pressure exerted by the blood within the vessel when the ventricle is at rest. The difference between the diastolic and the systolic pressure is called the pulse pressure. Mean arterial pressure (MAP) is the diastolic pressure plus one-third the pulse pressure. Any factor that alters cardiac output or peripheral vascular resistance will alter the blood pressure. Procedure Blood pressure can be measured by either direct or indirect methods. Direct (invasive) blood pressure measurement requires the insertion of a catheter into an artery (e.g. femoral or dorsal pedal artery) and connecting a transducer linked to a monitor. The direct arterial pressure is demonstrated in waveform on an oscilloscope with the high point being the systolic and the low point the diastolic pressures. Though direct measurement provides the most accurate pressure values, expensive and sophisticated monitoring equipment is required. A surgical approach is often necessary for arterial catheter placement in hypotensive or obese animals. Indirect (noninvasive) blood pressure measurements, though less accurate, are more easily obtained utilizing affordable equipment. Blood pressure cuffs can be placed around the distal portion of a leg or around the tail. The two most common methods used for indirect blood pressure instruments in veterinary medicine are oscillometric and Doppler. Systolic pressure should be above 100 mmHg. Systolic pressure below 80 mmHg is significant, and below 60 mmHg may be associated with poor renal perfusion and oliguria. Cerebral circulation is compromised when systolic pressure falls below 50 mmHg, with brain ischemia occurring when systolic pressures are below 30-35 mmHg for 2 hours. Coronary perfusion is best maintained when systolic pressures are higher than 70 mmHg. Hypertension with systolic pressures above 2OO mmHg can be associated with a hyperdynamic stage of shock, excessive endogenous production of renin, chronic renal failure, and excessive sympathetic stimulation. Oscillometric measurement involves the use of a microprocessor and cuff that determines systolic and diastolic pressure from oscillations detected from the blood vessel as the cuff is automatically inflated and deflated. The optimal width of the cuff bladder is 40-60% of the circumference of the limb to which it is applied. It is important when using an automated oscillometric unit to obtain five consecutive readings, discarding the lowest and highest values and averaging the remaining three. The doppler flow probe emits ultrasonic signals and detects these signals as they are reflected by from the moving column of blood in the vessel. The reflected wave is shifted slightly from the transmitted wave, and the difference is converted into an audible signal. The frequency varies directly with blood velocity. The flow probe is lubricated with ultrasonic gel, and secured to the shaved skin over an artery (e.g. the digital or dorsal metatarsal artery). The flow probe is attached to an amplifier, which produces the sound of blood moving through the vessel. A blood pressure cuff with sphygmomanometer is secured to the limb proximal to the probe. The optimal width of the cuff bladder is 40-60% of the circumference of the extremity to which it is applied. The cuff is inflated until the swishing sound is not heard. The valve on the manometer is gradually opened to slowly allow the cuff to deflate. The point at which the swishing sound is first heard again is the systolic pressure. The point where the swishing sound changes from its short pulsatile character to a more continous swishing, longer lasting sound, is the approximate diastolic pressure. Assessment The normal blood pressure in the dog and cat averages 120 mmHg systolic and 80 mmHg diastolic. The mean arterial pressure is normally 80-90 mmHg. Increases in blood pressure can be caused by any condition that increases cardiac output, such as fever, exercise, and septic shock. Decreases in blood pressure can be caused by cardiac failure, hypovolemic shock, drugs (such as sedatives, opioids, and anesthetics). Blood pressure should be evaluated together with the animal's perfusion parameters, UO, and disease state. As with any other monitoring parameter, repeated measurements are needed to detect a trend in change. Renal perfusion over the short term is considered adequate if BP is maintained above 60 mmHg. Shivering, trembling, struggling, vasoconstriction, and inappropriate cuff size are common causes erroneous measurements when utilizing the oscillometric method. There is also a decreased reliability when attached to animals less than 15 pounds. Erroneous results can occur with the doppler method due to malpositioning of transducer, inappropriate cuff size, poor contact with coupling gel, and flexion of the limb. Intervention Any blood pressure outside the normal value must be reported to the veterinarian. Intervention by the veterinary team is performed after complete patient assessment including LOC, CVP, perfusion and UO. Hypotension may be treated by hemostasis, crystalloid or colloid infusion, and potentially positive inotropes or vasopressors. Hypertension can be treated by pain relieve, diuretics or possibly vasodilators. Central Venous Pressure Pathophysiology Central venous pressure (CVP) is a function of four independent forces: volume and flow of blood in the vena cava, distensability and contractility of the right chambers during filling, venomotor activity in the vena cava, and intrathoracic pressure. When right heart function and intrathoracic pressure are normal, CVP can be used as a reflection of intravascular volume. Changes in blood volume will result in pressure changes in the vena cava and are reflected by the CVP. Procedure Central venous pressure monitoring set-up : Central venous pressure measurement requires placement of a central catheter into the cranial vena cava with the tip lying near the base of the heart (i.e. right atrium). The catheter is attached to IV extension tubing, which is connected at right angles to a water manometer by a three way stopcock. Across from the IV extension tubing on the stopcock is an IV line and fluids. The zero on the water manometer should be at the level of the right atrium. A horizontal line drawn between the thoracic inlet and the manometer establishes the zero reference level. The stopcock is off to the manometer when the patient is receiving intravenous fluids. To measure CVP, the manometer is filled with fluid from the IV bag and then the stopcock is turned off to the bag leaving a column of fluid within the manometer. The stopcock is then opened towards the patient, allowing the fluid in the manometer to access the patient. The fluid level in the manometer is allowed to equilibrate with the pressure in the jugular vein. The fluid level may oscillate a few millimeters with each respiration or heart beat. Three values or readings are obtained to ensure consistent readings. Assessment Normal CVP measurements are reported as -1 to 5 cmH2O. However, critical animals are resuscitated to supra-normal values and the CVP is optimally maintained between 5-8 cmH2O. Values less than 5 are suggestive of insufficient intravascular volume. Values over 14 cmH2O are of concern for right heart failure or significant volume overload. Factors unrelated to right heart function and volume overload (such as pleural, pericardial or mediastinal pressure, and increases in pulmonary hypertension) can also raise the CVP. If readings do not fluctuate with respiration, the readings are inaccurate. Note what side the animal is positioned and, future reading should be made with the animal lying on the same side. Always use the same zero point reference (thoracic inlet), so that readings are comparable. Always obtain three or five consecutive reading at a time. Each reading should be approximately close in measurement. Huge discrepancies in readings should alert the nurses to trouble shoot the CVP set-up for kinks, clogs or changes in catheter or patient position. Intervention The CVP can be used to guide aggressive intravascular fluid resuscitation. When the CVP is low in a hypotensive animal, crystalloids and colloids are rapidly administered until the CVP is between 5-8 cmH2O. At that time if hypotension persists, positive inotropes or pressor agents are administered. High CVP measurements warrant examination of the system for occlusion of the catheter. If the system is patent, then fluid overload or right heart failure are suspected. The fluid rate is lowered and the veterinarian will opt to administer diuretics or drugs specific for the cardiac condition. Any CVP measurements outside of the target values set by the veterinary team should be reported to the attending veterinarian. Pulse Oximetry Pathophysiology Pulse oximetry is a quick and reliable noninvasive method of measuring arterial oxygen saturation (SaO2). Oxygen saturation is the percentage of hemoglobin sites that are chemically combined with oxygen. Oxygen saturation and pulse rate are determined by passing two wavelengths of light, one red and one infrared, through body tissue to a photo detector. The signal strength resulting from each light source determines the SaO2. Pulse oximetry can be affected by the color and thickness of body tissues, the probe placement, the intensity of the light source, and the absorption of the arterial and venous blood in the body tissue. Procedure There are several types of probes that can be placed. The probes that are clamps can be placed on the tongue or on a shaved, nonpigmented skin surface. The rectal probe is placed against the rectal mucosa, which has been cleared of feces. The oximeter is turned on and the SaO2 and pulse rate is digitally reported. Assessment Animals requiring oxygen therapy or under anesthesia should have their SaO2 monitored as well as monitoring for physical signs of hypoxia (e.g. decreased LOC, tachycardia, arrhythmias, restlessness, altered blood pressure, increased respiratory rate, and changes in MM color). The use of pulse oximetry for monitoring oxygen saturation and pulse rate can provide early warning of pulmonary or cardiovascular deterioration before it is clinically apparent. Normal SaO2 is 98%. Values below 90% are correlated with PaO2 <60 mmHg and cyanosis is eminent. It is of most value when the arterial oxygen saturation is between 90% and 95%. Limitations of pulse oximetery include its inability to differentiate carboxyhemoglobin (seen with carbon monoxide poisoning) from hemoglobin. The pulse oximeter can not distinguish a declining PaO2 that is above 100mmHg (e.g. a fall from 330 mmHg to100 mmHg will still report an SaO2 of 100%) or the presence of methemoglobin. Results can be erroneous in animals with poor peripheral perfusion, heavily pigmented skin, hypothermia, icterus, and anemia. Intervention Any sudden decrease in the oxygen saturation with proper probe placement requires immediate notification of the veterinarian and rapid assessment of the animal's cardiopulmonary function. The oxygen concentration may need to be increased or the method of ventilation improved. Pathophysiology, Clinical Signs and Therapy Shock may accompany many emergency situations; thus an understanding of it pathophysiology, assessment and therapy is essential for those providing emergency care. Shock can be defined as ineffective circulation and failure to provide adequate oxygen-rich blood to organs throughout the body. Shock is usually due to a failure of the patientís circulatory system to function properly causing a deficit known as ìinadequate tissue perfusionî. Circulation depends on the proper balance of the following: an adequate blood volume, and efficient heart pump (effective cardiac output), and a healthy vascular bed (vascular resistance). The vascular bed maintains the peripheral resistance necessary to distribute blood and maintain venous return. The vascular bed is composed of arteries, vein and capillary network or microcirculation (composed of arterioles and venules). All of theses anatomical structures normally work together in a state of dynamic equilibrium. But the heart, arteries and vein function some what independent of the microcirculation. Impulses from the sinoatrial node induce myocardial contraction. The heart, arteries and veins, are also subject to direct stimulation of the sympathetic nervous system. The microcirculation, in contrast is primarily responsive to local tissue needs. It delivers body fluid and solutes such as nutrients, electrolytes and oxygen to the interstitium and removes waste. It also helps regulate total blood volume and adjust and direct blood flow by constricting and relaxing pre-capillary sphincters. The ability of some vessels in the capillary network to dilate and constrict permits the micro-circulation to selectively supply undernourished tissue while temporarily bypassing tissues with no immediate need. The microcirculation includes over 90% of the body's blood vessels and at any given time only 6%-7% of capillary vessels are perfused with blood. If too many capillary bed vessels dilate and fill with blood, the rest of the circulatory system becomes depleted and blood pressure drops precipitously. At the cellular level Shock can be due to various causes, but the overall effect of cellular damage or death is the same regardless of the precipitating factor. Shock is a progressive process, with an initial systemic compensatory reaction, but if adequate intervention is not instituted at this time; decompensation and eventually an irreversible stage of shock will ensue. Shock regardless of the type or cause, produces circulatory insufficiency that reduces blood flow through the microcirculation. Inside the cell, the mitochondria is responsible for producing the cells energy supply. By oxidizing glucose and other nutrients, the mitochondria manufactures adenosine triphosphate (ATP) the fuel for all cellular activity. The mitochondria use 90% of all oxygen entering the cell oxygen to make ATP, this process is called aerobic metabolism. Eventually tissue cells supplied by the microcirculation become so deprived of oxygen that they no longer can maintain aerobic metabolism and other normal activities. The cell mitochondrion adapts to an anaerobic metabolism (metabolism without oxygen). This process permits the cell to continue manufacturing ATP but far less efficiently. As a result, the cell uses up ATP faster than it can replenish its supply, and eventually runs out of fuel for other cell functions such as membrane maintenance. Anaerobic metabolism also produces lactic acid. Normally, only muscle tissue produces lactic acid, which is then metabolized by the heart and liver. However, in shock, lactic acid pours out through the debilitated cell membranes of hypoxic cells in other tissues. The liver and the heart can not accommodate this excess, which then accumulates in the blood, resulting in a metabolic acidosis. The alterations in the cellular metabolism and the oxidative energy production of ATP eventually leads to failure of the sodium-potassium pump, causing redistribution of cellular ions and fluid shifts. It is important to remember that the cell is surround by the interstitial fluid compartment. The cell membrane, by means of passive and active transport to move oxygen and nutrients into the cells and waste products out. In passive transport, osmosis and diffusion move a substance (e.g. water, oxygen) through the cell membrane without any energy expenditure by the cell. Diffusion is the tendency of molecules and particles to spread throughout a medium until molecule and particle concentration is equal throughout. Osmosis maintains a balance between fluid and dissolved particles inside and outside of the cells. Active transport requires energy expenditure by the cell. This transport mechanism handles molecules and particles (glucose, potassium, sodium) that can not easily pass through the cell's pores. Hypoxia, a key finding that accompanies shock, debilitates the cell membrane; causing these transport mechanism to malfunction. Increased amounts of sodium and fluid enter the cell, the cell becomes swollen, and eventually blebs or blisters develop on the cell surface. Potassium exits from the intracellular compartment into the extracellular spaces leading to hyperkalemia. Calcium within the cellular mitochondria contracts the mitochondrial compartment, changing the cell shape. This leads to mitochondrial membrane damage. Lysosomes membrane (the cytoplasmic organelles containing proteolytic enzymes), deteriorates and releases enzymes into the cytoplasma of the cell. Cellular acidosis enhances their activity and they begin to digest the cytoplasma. If the cycle is not interrupted, cellular hypoxia (oxygen deficiency) leads to cell and tissue death, the final stage shocks progression. As more cells are compromised or destroyed, the tissues and organs they constitute begin to fail. In most instances, oxygen restoration within several minutes can return the cell function and energy production to normal. In conclusion, the decompensatory stage of shock ensues as a result of tissue oxygen supply not being equal to oxygen demand at the cellular level, resulting in an oxygen debt. In shock, the cellular oxygen debt, along with cellular damage, and poor removal of waste products; occurs because of inadequate perfusion or inadequate oxygen delivery to tissue structures. Clinical characteristic of shock Clinical signs of shock develop in a specific order. Patients in shock will demonstrate different clinical signs depending on what stage of shock they are experiencing at the time the assessment is made. The stage of shock also determines the patientís acuity level. Decompensatory stage of shock: cyanotic, ashen, white mm, cold skin, decrease rectal temperature, absent or weak femoral pulses, oliguric (due to pressure <60), prolonged or absent CRT, unconscious, stuporous, or losing consciousness. Substantial hemorrhage- may have seized due to low blood pressure. These patients are categorized as Class 1 or "catastrophic". (multiple injuries, shock, or bleeding but with adequate airway function). Mild stage of shock: pale or ashen mm, cool skin, low rectal temperature, weak femoral pulses, tachycardia, decrease urine out put, prolonged CRT., altered mentation (depressed, seizures, uncontrolled hyperexcitability). Hemorrhage- active or slow trickles. These patients are categorized as Class 2 or very severe/ critical. Compensatory stage of shock(false stability): slightly rapid or labored breathing or normal respiration, red or pale mm, normal skin and rectal temperature, normal or bounding pulses, tachycardia, normal urine out put, CRT <1 second or normal. Mentally alert/conscious (aware of surroundings, mildly depressed to excited). Hemorrhage- slight to absent. These are termed Class 3, and are considered serious or urgent. Early compensatory shock: or Class IV patients are less serious but still pressing and require action within 24 hours. Clinical signs observed are: breathing pattern is outwardly normal, normal perfusion or early compensatory shock, red or pink mm, normal skin and rectal temperature, normal or bounding pulses, normal or rapid heart rate, normal urine out put, normal or rapid CRT, mentally normal or excited. Therapy in the Shock The main goal of therapy is to restore and maintain tissue perfusion and to correct the underlying physiological abnormality. This is accomplished by replacing intravascular volume with a combination of crystalloids (lactated Ringers, Plasmalyte), colloids (albumin, dextran or hetastarch), as well as blood. Initially, the lost volume is replaced quickly through more than one peripheral catheter until the state of shock is corrected, as evidenced by achieving predetermined endpoints in heart rate, arterial blood pressure, lactate clearance, urine output. Crystalloid solutions are used most of the time as the primary fluid for acute intravascular volume expansion. When care is taken to titrate total amount of fluid infusion volume to physiologic endpoint, resuscitation can be successful, without the development of pulmonary edema. A concern with isotonic fluids is the large volume often required for resuscitation. This usually results in peripheral and pulmonary edema. Intravenous colloid solutions have in common the presence of large molecules that are relatively impermeable to the capillary membrane. Following acute massive blood loss, red blood cell transfusions are indicated for the restoration of the bloods oxygen carrying capacity. The development of blood component therapy has made it possible to reduce the number of whole blood transfusions to patients. Component therapy consists of fractionation of whole blood at the time of collection into red blood cells (packed red blood cell unit), platelets (platelet rich plasma), and plasma. Autotransfusion, the collection of the patient's own blood from a body cavity (abdomen or thorax) and its readministration is an accepted method in trauma and emergency patient as a resuscitative measure. antishock garments may also be used for patients in profound states of shock as a means of increasing venous return. Pharmacological agents such as vasoactive drugs are frequently required, either because of myocardial depression or persistent hypotension following fluids resuscitation efforts. Dobutamine is a B1, B2 adrenergic agent possessing inotropic and vasodilatory properties used to augment cardiac output when persistent evidence of hypotension exist. Dopamine administered at low dosages improves renal blood flow in patients receiving other pressors. At higher dosages, dopamine improves contractility and increases cardiac output and peripheral vascular resistance, causing renal and mesenteric arterial vasoconstriction. Concluding Remarks Emergency nursing is an integral and important part of the veterinary medicine team. Should the technician be inadequate or incompetent, the effectiveness of the team diminishes or fails, resulting in the patient suffering unnecessary complication or death. Once we accept the responsibility of providing emergency care, we must constantly prepare, educate, and train ourselves to be ready for it. Without highly skilled and trained emergency technicians, the emergency service cannot serves its patients in a way that both the patient and their owners have a right to expect from the veterinary profession. Fig 1: List Of Recommended Skills For Veterinary Technician Providing Emergency Care
Recommended Emergency Equipment
Fig 3: FUS Protocol Protocol developed by Dr. Rebecca Kirby, and used at the Veterinary Institute of Trauma, Emergency and Critical Care. This protocol sets the standard of care for the critically ill blocked cat. Modifications are made to it when treating the less critical patient. Feline Urethral Obstruction Protocol
Fig 6: Rate guide for delivering artificial rescue ventilation and CPR based on an animal's weight. Courtesy Animal Health Foundation, North Stonington, CT Animal Size Rescue Breathing Rate CPR Rate Breaths/Compression ratio < 5 Lbs. 25 Breaths per minute 120-140 compression/min 1 breath per 2 compressions 6-20 Lbs. 20 Breaths per minute 100-120 compression/min 1 breath per 3 compressions 21-60 Lbs. 15 Breaths per minute 80-100 compression/min 1 breath per 5 compressions 61+ Lbs. 12 Breaths per minute 60 compression/min 1 breath per 5 compressions Fig 7: Triage parameter / Normal Vital Sign Parameters
* beats per minute ** size and breed dependent *** breaths per minute **** Mean Arterial Pressure Fig 9: Interpretation of Mucous Membrane Color
* Hemoglobin concentration ** Disseminated intravascular coagulation *** Systemic inflammatory response syndrome Fig 8: Recommended Primary Survey for Emergency Care Professionals
General rules and statements (proverbial "pearls of wisdom") for trauma resuscitation have been developed to help prevent the rescuer from making serious mental mistakes and loosing valuable time in the treatment of injured patients.
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