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Manual of Small Animal Emergency and Critical Care Medicine
Manual of Small Animal Emergency and Critical Care Medicine
Manual of Small Animal Emergency and Critical Care Medicine
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Manual of Small Animal Emergency and Critical Care Medicine

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Manual of Small Animal Emergency and Critical Care Medicine, Second Edition presents essential information on common emergencies in small animals using a concise, practical outline format.  Offering a thorough update to this classic reference, the new edition provides new chapters on orthopedic injuries and wound management, significant revisions to the treatment protocols, and expanded toxicology information, as well as new references and drug information. The book retains its logical division into two parts, the first covering initial stabilization and the second offering a systems approach to specific conditions.

As in the previous edition, chapters are extensively indexed and cross-referenced to facilitate ease of use in emergency situations. With many formulas, tables, drug dosages, and illustrations, Manual of Small Animal Emergency and Critical Care Medicine is an indispensable, convenient resource for busy emergency clinicians, whether they are new graduates or seasoned professionals.

 

LanguageEnglish
PublisherWiley
Release dateMay 31, 2012
ISBN9781118351130
Manual of Small Animal Emergency and Critical Care Medicine

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    Manual of Small Animal Emergency and Critical Care Medicine - Douglass K. Macintire

    PART

    I

    Life Support and Initial Stabilization, Monitoring, and Intensive Care of the Critically lll Patient

    CHAPTER

    1

    APPROACH TO THE EMERGENCY PATIENT

    Steve C. Haskins and Douglass K. Macintire

    I. INITIAL PREPARATION AND MANAGEMENT

    A. Life-threatening abnormalities should be stabilized without delay.

    1. A secondary, more exhaustive physical and laboratory examination can be completed once the life-threatening problems have been stabilized.

    2. Semicomprehensive tertiary examinations should be repeated at regular intervals throughout the day and on subsequent days to keep abreast of the progress of the underlying abnormalities and their response to therapy, as well as to identify new problems that may become apparent.

    B. Adequate preparation of the facility, equipment, supplies, and personnel for the array of emergencies likely to be presented, cannot be overemphasized.

    1. The emergency receiving area should be designated and set up in advance with all of the necessary equipment and supplies readily available. There should be easy access to the area for patients on gurneys and stretchers, and there should be enough room for the care-givers to move around and gain easy access to the patient.

    2. Equipment must be immediately available and in good working order. Personnel should be well trained in its use.

    3. Supplies must be immediately available and inventoried daily and after each emergency.

    4. Personnel should be trained and retrained in the job that they will be expected to perform when the emergency arrives. Protocols and procedures are established in advance and placed in an easy-to-access notebook. Wall charts of procedures and dosages are an excellent way to facilitate the conduct of emergency patient resuscitation.

    5. Reference books and sources of information (e.g., poison control hot lines) for situations that were not foreseen should be readily available.

    C. Effective management of the emergent patient begins when the hospital receives the call from the owner stating that there is a problem. The owner may be able to provide some first-aid care that would be beneficial to the animal even though the individual is not medically trained. Owners should be instructed to bring such animals to the nearest veterinary facility.

    1. If the animal is unconscious or seizuring, the owner should place the animal on a blanket and transport it immediately to the hospital.

    2. If the animal is not breathing, owners can be instructed as to how to manually hold the mouth closed, extend the head, and blow into the nose to get the chest to rise slightly.

    3. Animals that have severe respiratory distress should brought immediately to the hospital.

    4. If the animal is conscious and has been hit by a car, owners should be warned that such animals are hurt and scared and may bite when handled. Such animals should be strapped to a flat transport board if possible to prevent further orthopedic or spinal cord injury.

    5. Open wounds should be covered with clean, moist towels prior to transport.

    6. Fractured lower leg bones could be splinted with rolled up newspaper and tape but animals with fractures of the humerus or femur should just be moved onto a blanket and transported to the hospital. Cover open wounds with a clean, moist towel.

    7. Animals that have ingested a poison/toxin should be brought to the hospital along with the container of ingestate. If not contraindicated (see Toxin Chapter) vomition can be induced.

    8. Burn wounds should be covered with a cool, wet compress.

    9. Suspected heat stroke patients should be wet down with cool water before transport.

    10. Counterpressure should be applied to sites of active hemorrhage during transport.

    11. Proptosed eyeballs should be held in place with wet compresses.

    12. Owners should obey all traffic laws during the transport of patients to the hospital.

    II. THE PRIMARY SURVEY: INITIAL EXAMINATION TO IDENTIFY LIFE-THREATENING PROBLEMS (Tables 1.1 and 1.2)

    A. Assess the general demeanor of the animal.

    1. Seizures should be terminated immediately by the administration of anticonvulsants.

    a. Benzodiazepines (diazepam [0.2–0.6 mg/kg IV], midazolam [0.1–0.4 mg/kg IV]) are common choices. Any rapidly acting general anesthetic will also terminate seizure activity.

    b. Phenobarbital (5–25 mg/kg) has anticonvulsant properties in subanesthetic dosages but has a slow onset of action (20 min) making it inconvenient to use in the initial management of seizures but ideal for preventing recurrence (4–6 mg/kg IV, IM q 12 hr).

    c. Seizures in puppies may be due to hydrocephalus, hypoglycemia (glycogen storage disease), infection (distemper), toxemia, portocaval shunt, or may be idiopathic.

    d. Seizures in adults may be idiopathic, infectious, neoplastic, traumatic, ischemic, or thromboembolic, or may be caused by hypoglycemia (insulinoma), hypocalcemia, or granulomatous meningoencephalitis.

    e. Other monitoring/treatment considerations: hyperthermia, airway protection, aspiration, neurogenic pulmonary edema, hypoxemia, hypoventilation, considerations specific to the underlying cause.

    2. Tremors and hyperexcitability are treated symptomatically with benzodiazepines (diazepam, midazolam) or methocarbamol (50–150 mg/kg IV).

        Tremors and hyperexcitability can be caused by amphetamines, herbal ephedra, ma huang, guarana root, methylxanthines (caffeine), pseudoephedrine, LSD, phencyclidine, marijuana, cocaine, benzodiazepines, opioids (large dose), metaldehyde, mycotoxins (penitrem A), blue-green algae, strychnine, 1080, bromethalin, ivermectin, organochlorine insecticides, pyrethrins, permethrins, organophosphates, carbamates, lead, zinc phosphate, tricyclic antidepressants, 4-aminopyridine, 5-fluorouracil, chocolate (large dose).

    3. Severe obtundation and coma have many causes; initial management strategies involve examination, monitoring, and support of cardiopulmonary function.

    a. Apnea? Intubate and ventilate (rate 10–15/min; tidal volume 10–15 ml/kg; proximal airway pressure 10–15 cm H2O).

    b. Cardiac arrest? Institute cardiopulmonary resuscitation.

    c. Traumatic head injury? Prevent hypoxemia, hypoventilation, hyperthermia, hypotension, or induced hypertension (spontaneous hypertension should be allowed) or hypervolemia. Hyperosmotic edema-reducing therapy may be indicated (mannitol, hypertonic saline).

    TABLE 1.1 PROBLEMS IDENTIFIED AT TRIAGE THAT REQUIRE IMMEDIATE ATTENTION

    aDifficult breathing heralded by openmouthed breathing or gasping, extended head and neck, asynchronous chest wall and abdominal movement.

    bDisseminated intravascular coagulation.

    cConsequences depend upon the specific kind of snake.

    dConsequences depend upon the specific poison/toxin.

    TABLE 1.2 TREATMENT PRIORITIES IN EMERGENCY PATIENT

    B. Evaluate respiratory status

    1. Apnea is a sign of a central nervous system (CNS) lesion or a peripheral problem with the neuromuscular axis.

    a. If there are no breathing efforts, intubate and ventilate with 100% oxygen.

    b. If unable to intubate because of pharyngeal/laryngeal obstructions and the obstruction is not a foreign body that can be removed, try to intubate with a smaller-than-normal endotracheal tube. If unable to intubate with a small endotracheal tube, pass a stiff urinary catheter into the trachea and use it

    1) to insufflate oxygen;

    2) for high-frequency jet ventilation (connect the common outlet tube from an anesthetic machine to the catheter and use very brief flushes with the oxygen flush valve at a rapid rate); or

    3) as a stylet to guide the introduction of an endotracheal tube.

    c. If none of the above techniques work or appear unlikely to work on initial examination, an emergency tracheostomy can be performed (see p. 143) to bypass the obstruction.

    2. Breathing effort without air movement may be caused by complete upper airway obstruction (remove or bypass the obstruction [see II.B.1.b and c above]) or a severe pneumothorax (perform a thoracentesis [see p. 155]).

    3. Minimal breathing effort with little air movement may be caused by intracranial disease (hematoma, neoplasia, edema), spinal cord disease (disc prolapse, fibrocartilaginous embolism, neoplasia, trauma), a neuromuscular junction problem (myasthenia gravis, botulism, polyradiculoneuritis, paralytic tick envenomation, paralytic snake envenomation), or toxin overdose (ivermectin, moxidexin, baclofen, or drug causing respiratory depression).

    a. Intubate and

    b. Ventilate

    4. Increased breathing effort without much air movement may be caused by (Table 1.3):

    a. Upper airway obstruction (inspiratory low-pitched snoring or high-pitched squeaking). Remove or bypass obstruction.

    b. Lower airway obstruction (inspiratory/expiratory midpitched wheezing). Bronchodilators if bronchoconstriction; nebulization if exudate.

    c. Loss of chest wall integrity: flail chest (if severe, anesthetize, intubate, and ventilate); open pneumothorax (place a tube in the hole, squeeze the tissues around tube to make an airtight seal, and aspirate the air; or anesthetize, intubate, and ventilate).

    d. Abdominal filling disease (gastric distension, ascites, neoplasia, pyometra). Evacuate the offending problem.

    e. Pleural space filling disease (muffled lung sounds) may be caused by pneumothorax, hydrothorax, pyothorax, chylothorax, hemothorax. Diagnose and treat with thoracentesis.

        Diaphragmatic hernia: thoracentesis negative, abdomen palpates empty, radiographic evidence. Oxygen support and positive pressure ventilation if necessary until surgical correction.

    f. Pneumonia, edema, contusions, or neoplasia: oxygen therapy or positive pressure ventilation.

    TABLE 1.3 CHARACTERIZATION OF BREATHING NOISES AND PATTERNS

    aExtrathoracic.

    bIn a compensated state; in a crisis, it will be rapid and shallow.

    cFever, metabolic acidosis, hypotension, pain, anxiety, pulmonary thromboembolism.

    5. Blood oxygenation

    a. Cyanosis (blue or grey discoloration of mucous membranes) represents unoxygenated hemoglobin. Cyanosis is usually attributed to hypoxemia and, as such, represents severe hypoxemia. It is a late sign of hypoxemia and may not be manifested in animals that are anemic. It may also be due to sluggish peripheral circulation (severe hypovolemic shock, cardiac arrest) and methemoglobinemia.

    b. Pulse oximetry

    1) Pulse oximeters have to be able to detect a pulse to work and therefore require perfusion to the tissue where the probe is placed.

    2) Pulse oximeters calculate oxyhemoglobin saturation from light absorption in arterial blood. Normal is about 98%; hypoxemia is represented by a value of less than 95%, and severe hypoxemia by a value of 90%.

    3) Pulse oximeters can generate inaccurately low values. The indicated value is more likely to be correct if the indicated pulse rate matches that of the patient. Move the sensor to (several) new positions; record the highest reading. If the indicated values respond positively to increasing the inspired oxygen concentration, they are more likely to be correct. Evaluate other indices of blood oxygenation to corroborate the pulse oximeter-derived value (e.g., arterial blood gas measurement).

    C. Evaluate cardiovascular status

    1. Mucous membrane color

    a. Red = vasodilation (sepsis, hyperthermia), cyanide, carbon monoxide

    b. Pale = vasoconstriction (hypovolemia, heart failure, hypothermia), anemia

    c. Cyanosis = unoxygenated hemoglobin

    d. Brown = methemoglobinemia

    2. Capillary refill time (CRT) (normal = 1–1.5 sec).

    a. Vasoconstriction prolongs CRT: hypovolemia, heart failure, hypothermia, pain, vasoconstrictor drugs. Vasoconstriction may impair perfusion of peripheral tissues.

    b. Vasodilation shortens CRT: sepsis, hyperthermia, vasodilator drugs. Vasodilation may cause hypotension.

    3. Pulse quality is a determination of the height and width of the pulse pressure wave form. It is not a measure of blood pressure and cannot be used to define blood pressure. Pulse quality estimates must be indexed to patient size.

    a. Tall, wide pulse waveforms (bounding pulses) are attributed to large stroke volumes in vasodilated patients (sepsis, hyperthermia)

    b. Tall, narrow pulse waveforms (water-hammer pulses) are attributed to large stroke volumes in patients with very rapid diastolic runoff (patent ductus arteriosus, aortic insufficiency).

    c. Small, narrow pulse waveforms (weak, thready pulses) are attributed to small stroke volumes in vasoconstricted patients (hypovolemia, heart failure, hypothermia).

    d. The term pulse deficit denotes pulses that are intermittently diminished or absent in association with an ausculted heartbeat or ECG depolarization (ventricular arrhythmias, premature atrial depolarization, atrial fibrillation).

    e. Absent palpable pulses associated with an auscultable heartbeat may be caused by thromboembolism or severe hypotension; if there is no auscultable heart beat, it may represent cardiac arrest.

    4. Heart rate

    a. Tachycardia (large-breed dog >160; small-breed dog >180; puppy >200; cat >220) may be caused by hypovolemia, pain, hypoxemia, hypercapnia, hyperthermia, sepsis, anemia, stress, hyperthyroidism, or heart failure.

    b. Bradycardia (dogs <60; cats <80) may be caused by hyperkalemia (urethral obstruction, hypoadrenocorticism, iatrogenic), organophosphate toxicity, hypothermia, hypoxia, and drug overdose (opioids, alpha2-agonists), head trauma, atrioventricular conduction disturbances, and excessive vagal tone.

    5. Hydration status

    a. Dehydration represents a deficit of an extracellular crystalloid (water with variable concentrations of sodium). All dehydrated patients are hypovolemic, but there may be poor correlation between the two (hypovolemia may occur without dehydration) and, therefore, hydration status and volemic status must be evaluated separately. Dehydrated patients usually need crystalloid fluid replacement (see Fig. 1.1).

    b. Edema represents an excess of extracellular crystalloid. Such patients may be hypovolemic (hypoproteinemia; increased vascular permeability) or hypervolemic (heart failure, iatrogenic). Edematous patients do not need any additional crystalloid fluids.

    6. Jugular vein distention is a clinical assessment of venous blood volume and preload pressure to the heart. At normal venous volume, jugular veins are easy to distend by occluding flow at the thoracic inlet. Jugular veins that are distended without occluding flow at the thoracic inlet may represent excessive venous volume (hypervolemia). Jugular veins that are difficult/impossible to distend by occluding flow at the thoracic inlet may represent hypovolemia.

    7. Arterial blood pressure is the most important determinant of cerebral and coronary perfusion. Normal values: systolic 100–160 mmHg, mean 80–120 mmHg, and diastolic 60–100 mmHg.

    a. Hypotensive values of concern: systolic <80–100 mmHg, mean <60–80 mmHg, and diastolic <40–60 mmHg. Mean pressure is the most important when available. Excessive hypotension may be associated with inadequate cerebral and coronary perfusion. Hypotension should be treated first with preload volume augmentation (fluids)(Fig 1.1)(p. 10) and, if necessary, sympathomimetics (p. 32).

    b. Hypertensive values of concern: systolic pressure >180 mmHg, mean pressure >140 mmHg. Excessive hypertension may be associated with edema, hemorrhage (epistaxis, retinal, intracranial, intrapulmonary), retinal detachment. Hypertension that is not compensatory for increased intracranial pressure should be treated with vasodilators (p. 92).

    D. Evaluate intracranial status

    1. Mentation should be evaluated at entry and periodically thereafter to assess the progress of the disease and treatment.

    a. Bright and alert

    b. Mildly obtunded (the animal is spontaneously aware of environmental events but may sleep if there are no environmental stimuli). The judicious administration of tranquilizer drugs (phenothiazine, benzodiazepines) may, for example, produce this state.

    c. Moderately obtunded (the animal mostly sleeps but will wake up and respond to loud noises or gentle physical stimulation). The judicious administration of sedative drugs (opioids) may, for example, produce this state.

    d. Severely obtunded (the animal will only awaken to strong physical stimulation).

    e. Comatose (the animal is unconscious and does not mentally respond to even the strongest of physical stimulations; withdrawal and hemodynamic reflexes may still be present).

    f. Decreased mentation can be attributed to intracranial or extracranial causes. Intracranial causes are often associated with abnormal, localizing or lateralizing, cranial nerve signs. Extracranial causes are often associated with reduced cranial nerve signs, which are usually bilaterally symmetrical.

    2. Is there external evidence of trauma (skin abrasions or lacerations, epistaxis, cerebrospinal fluid (CSF) or blood in the external ear canal (hyphema or other hemorrhages, fractures)?

    3. Eye signs: nystagmus, strabismus, bilateral miosis or mydriasis, anisocoria, hippus, menace reflex, palpebral reflex, pupillary light reflex, dazzle reflex?

    4. Head tilt, torticollis, circling, head pressing, reluctance to be placed in some particular positions, positional nystagmus?

    5. Sneeze reflex, gag reflex?

    6. Brain stem involvement is characterized by unconsciousness; bilateral light-unresponsive miotic or mydriatic pupils; strabismus; absent physiologic nystagmus but present spontaneous or positional nystagmus, absent gag, swallow, and laryngeal reflexes; irregular breathing rhythms or apnea, decerebrate rigidity (extensor rigidity in all four appendages).

    a. Cerebellar injury may also be associated with extensor rigidity but these animals are not comatose. Decerebellate rigidity carries a better prognosis than decerebrate rigidity.

    b. Shiff-Sherrington syndrome is characterized by extensor rigidity of the forelimbs and flaccid paralysis of the rear limbs and denotes a severe spinal cord lesion between T2 and L4.

    7. Treatment should be for the underlying disease process. Mannitol should be administered if the cranial nerve signs worsen or if the history suggests an event known to be associated with cerebral edema (hypoxia, hypoglycemia, trauma, prolonged seizures, neoplasia).

    FIG. 1.1 Deciding which fluids to administer.

    E. Evaluate spinal cord function

    1. Check for pain or misalignment of vertebral column, spontaneous movement of front and hind legs, and tail. Evaluate front and hind pain perception, front and hind appendage reflexes (withdrawal, crossed-extensor), panniculus reflex, and anal tone and reflexes.

    2. Animals with suspected traumatic spinal injuries should be taped to a solid transport stretcher suitable for radiographic imaging so that they cannot move or be moved prior to assuring an intact vertebral column.

    F. Temperature

    1. Hyperthermia

    a. Fevers up to 40°C (104°F) could be an appropriate response to infection and should not be treated specifically. Hyperthermia in excess of 41°C (106°F) can be self-perpetuating and should be symptomatically treated. Hyperthermia in excess of 42°C (108°F) can be tissue damaging.

    b. Common causes include infection, inflammation, excessive muscular activity (seizures or respiratory distress), and environmental (hot car, hot day, forced exercise, iatrogenic).

    c. Active cooling is necessary in hyperthermia. Usually, wetting the animal down with room-temperature water (augments evaporative heat loss) and a fan (augments convective heat loss) is sufficient, along with room-temperature IV fluids. Stop active cooling when the temperature is about 1–1.5°C (2–3°F)above the desired goal. (Usually, stop cooling efforts when body temperature reaches 103°F.)

    2. Hypothermia

    a. Mild hypothermia (down to 35°C [95°F]) is of little medical concern although it may cause some discomfort and shivering for patients with normal mentation. It is usually adequate to cover the animal with blankets to prevent further heat loss, allowing the animal to warm itself. Moderate hypothermia (33–35°C [91–95°F]) may depress mentation (additive to drug sedative effects) and may require active rewarming. Severe hypothermia (30–33°C [86–91°F]) is associated with significant obtundation and requires active rewarming; such patients do not have sufficient metabolic activity to warm themselves. Very severe hypothermia (<30°C [<86°F])may be associated with coma, arrhythmias, and coagulopathies.

    b. Hypothermia is due to either excessive heat loss (environmental), insufficient heat production (impaired hypothalamic thermostasis in any critically ill patient), or both (general anesthesia).

    c. Active rewarming applies a heat source to the patient.

    1) Forced hot-air blankets

    2) Circulating warm-water blankets

    3) Infrared heat lamps (do not place too close to the patient because they will cause excessive skin heating)

    4) Hot-water bottles placed around the patient (do not allow contact with the patient if water temperature exceeds 42°C [108°F]). Cover the patient and bottle to make a heat tent.

    G. Stop or minimize external hemorrhage

    1. Manual counterpressure should be applied immediately.

    2. Compression bandages may work, but may only hide the hemorrhage until the bandage soaks through

    3. Tourniquets, applied for too long, can cause ischemic damage of the appendage.

    4. Pulsating arterial bleeders generally require surgical ligation to stop the hemorrhage.

    H. Evaluate blood glucose

    1. Hypoglycemia is life threatening because the normal brain lives on glucose.

    a. Common causes include sepsis, glycogen storage diseases in toy breeds, insulinoma, iatrogenic.

    b. Severely hypoglycemic patients should receive a glucose bolus—0.5 g/kg diluted and given IV. Such patients may require a glucose infusion (0.1–0.25 g/kg/h or 2.5–5% added to IV fluids) to maintain acceptable blood glucose concentrations.

    2. Hyperglycemia is not, per se, life threatening but some human studies suggest that glycemic control (to near-normal levels) reduces septic complications and improves survival.

    a. Common causes include stress, diabetes mellitus, iatrogenic.

    b. Most important treatment consideration is effective management of the underlying disease process. Insulin may be necessary if the hyperglycemia does not respond to treatment of the underlying disease.

    I. Packed cell volume

    1. Anemia reduces oxygen carrying capacity of the blood. In general, a packed cell volume of 20% has been used as a trigger for blood transfusion in animals with acute hemorrhage. Lower trigger thresholds can be used in animals with normal cardiac reserve, capable of increasing cardiac output to support oxygen delivery in the face of anemia (e.g., immune mediated anemia). Higher trigger thresholds should be used in animals with reduced cardiac reserve and reduced ability to increase cardiac output (sepsis, general anesthesia).

    2. Polycythemia increases blood viscosity and reduces cardiac output and tissue perfusion. Values above 60–70% in dehydrated patients should be treated with crystalloid fluid administration to rehydrate the patient and dilute the red blood cells. Values above 60–70% in nondehydrated patients should also receive clear fluids but a preemptive removal of whole blood may be necessary to prevent hypervolemia.

    III. BRIEF HISTORY

    A brief history should be obtained once initial lifesaving procedures have been implemented.

    A. Obtain the reason for bringing the animal to the hospital. Ascertain (preferably in writing) whether the bringing person is the owner of the animal or not, and whether this person is willing to assume financial responsibility.

    B. Upon completion of the primary survey, the owner should be informed of the current status of the animal, the immediate resuscitation plan, the expected outcome, and the estimated costs. Once informed, the owner must give consent to either continue or terminate the endeavor (preferably in writing).

    C. Does the owner know what happened (what the owner knows for sure v. what the owner imagines might have happened)?

    D. What signs have been manifested and how long have they existed?

    E. Are any other animals showing similar clinical signs?

    F. Are there any known medical conditions or medications?

    G. To what poisons/toxins has the animal had access?

    IV. THOROUGH SECONDARY SURVEY

    Once initial life-saving procedures have been implemented, a more thorough secondary survey of the patient should be obtained. First, repeat the primary survey to determine what changes may have occurred as a consequence of the underlying disease process and the treatments so far implemented.

    A. Respiratory

    1. Arterial partial pressure of oxygen (PaO2) is a measure of blood oxygenation. Normal is 80–110 mmHg when the animal is breathing room air.

    a. Hyperoxemia is caused by enriched oxygen breathing.

    b. Hypoxemia is caused by low inspired oxygen (when attached to a malfunctioning anesthetic machine or breathing circuit), global hypoventilation (defined by PaCO2), or lung dysfunction. Hypoxemia below about 60 mmHg should be treated.

    1) Hypoxemia is first treated symptomatically with oxygen. If oxygen therapy alone does not alleviate the hypoxemia, add positive pressure ventilation (PPV), positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP).

    2) Once the hypoxemia has been alleviated, institute effective therapy of the underlying disease process. (See Mechanical ventilation, p. 185.)

    2. Central venous partial pressure of oxygen (PvO2) is a measure of tissue oxygenation. Peripheral venous PvO2 is not reflective of central PvO2 and cannot be interpreted in the context of this discussion. Central PvO2 is determined by the balance between oxygen delivery and oxygen consumption. Normal is 40–50 mmHg.

    a. Values above 60 mmHg may indicate reduced oxygen consumption (hypothermia, sepsis) but may also occur with 100% oxygen breathing and general anesthesia.

    b. Values below 30 mmHg may indicate reduced oxygen delivery (poor cardiac output, low oxygen content).

    3. Arterial partial pressure of carbon dioxide (PaCO2) is a measure of alveolar minute ventilation. Normal is 35–45 mmHg (dog).

    a. Hypoventilation causes an increase in PaCO2. Values above 60 mmHg should be treated with positive pressure ventilation.

        Hypercapnia causes cerebral vasodilation, which increases intracranial blood volume and intracranial pressure. In patients with intracranial disease, the PaCO2 should be maintained below 45 mmHg.

    b. Hyperventilation causes a decrease in PaCO2. Hypocapnia is usually not treated specifically; therapy is aimed at the underlying disease.

    c. PvCO2 can be used as a surrogate marker of PaCO2 because it is usually about 5 mmHg higher than PaCO2. Although, PvCO2 can be much higher than PaCO2 in instances of poor tissue perfusion. Normal values are 40–50 mmHg.

    d. End-tidal PCO2 can be used as a surrogate marker of PaCO2 because it is usually about 5 mmHg lower than PaCO2. Although end-tidal CO2 values can be much lower with hypovolemia, hypotension, or pulmonary thromboembolism. Normal values are 30–40 mmHg.

    4. Imaging procedures can be performed to further characterize abnormalities (radiography, computed tomography [CT], magnetic resonance imaging [MRI]).

    5. Thoracentesis can be diagnostic or therapeutic. Cytologic examination should be performed on all aspirates.

    6. Tracheal fluid aspiration when appropriate

    a. Cytologic examination will help differentiate exudates from transudates.

    b. Comparing total protein concentration or colloid osmotic pressure of undiluted samples with that of plasma may help differentiate a hydrostatic pulmonary transudate (congestive heart failure, volume overload) from a permeability pulmonary transudate (ARDS, sepsis, electric shock, noncardiogenic pulmonary edema).

    B. Cardiovascular

    1. Arterial blood pressure (ABP), if it was not done as part of the primary survey, should be done as part of the secondary survey.

    a. Indirect blood pressure can be measured using a circumferential cuff applied around an appendage to occlude blood flow, an aneroid manometer to measure the pressure in the cuff, and a blood flow detection device to measure blood flow beyond the cuff as the cuff pressure is decreased. The detection device could be a finger to palpate a pulse or a Doppler blood flow detector. Oscillometric devices interpret changes in intracuff pressure as the cuff is deflated and then display a value for systolic, diastolic, mean blood pressure, and heart rate.

    b. Direct blood pressure involves catheterization of an artery (dorsal metatarsal, femoral, tail, ear, ulnar, humeral), either percutaneously or via surgical exposure, which is then attached to a commercial transducer and a physiologic patient monitor.

    c. Normal values: systolic 100–160 mmHg, mean 80–120 mmHg, and diastolic 60–100 mmHg. The most important pressure is mean, which is the average area under the pulse pressure waveform and represents the average driving pressure to tissue perfusion.

    1) The primary determinants of systolic pressure are stroke volume and arterial compliance. The primary determinants of diastolic pressure are vascular resistance and heart rate.

    2) Directly measured systolic and diastolic pressures can be blunted by an overdamped measuring system (a partial occlusion), and exaggerated by an underdamped measuring system (the harmonics of the measuring system match that of the patient’s arterial system).

    2. Central venous pressure (CVP) is a measure of preload pressure to the right heart. It is a surrogate marker of preload, which is end-diastolic (or presystolic) ventricular muscle stretch or end-diastolic ventricular volume.

    a. Normal CVP is 0–10 cm H2O.

    b. The CVP can be up to midnormal range in a hypovolemic patient (representing venoconstriction around a reduced blood volume).

    c. A high-normal range CVP is a common endpoint of fluid loading; a high pressure being generally associated with a high preload.

    d. The CVP can be high in association with low preload in a heart with low compliance (hypertrophic cardiomyopathy, pericardial tamponade, endo/myo/epicardial fibrosis).

    3. The base deficit/excess describes the metabolic component of the acid-base balance. Normal is 0 ± 4 mM/L.

    a. Surrogate markers of base deficit/excess include decreased standard bicarbonate concentration (bicarbonate concentration indexed to a PCO2 of 40 mmHg), bicarbonate concentration, and total carbon dioxide concentration (most of which is bicarbonate).

    b. Metabolic acidosis can be caused by lactic acid (anaerobic glycolysis), ketoacids (insulin deficiency), phosphoric and sulfuric acids (renal failure), glycolic acid (ethylene glycol), bicarbonate losses (duodenal vomition, diarrhea), hypoadrenocorticism, renal tubular acidosis.

    c. Metabolic alkalosis can be caused by gastric vomition, furosemide administration, hypochloremia, hypokalemia, and metabolism of organic anions (lactate, acetate, gluconate, citrate).

    4. Electrocardiogram should be obtained if arrhythmias (including bradycardia and tachycardia) were detected on the physical exam.

    5. Ultrasound evaluation of cardiac and valvular performance.

    C. Neurologic

    1. Determine the animal’s ability to stand or walk (after spinal damage has been ruled out).

    2. Assess proprioception, and for lameness or abnormal gait.

    3. Serial neurologic exams should be performed on all animals with acute head or spinal cord injuries.

    4. Imaging procedures can be performed to further characterize abnormalities (radiography, computed tomography [CT], magnetic resonance imaging [MRI]).

    D. The abdomen should be inspected for contusions, lacerations. It should be palpated for pain (which should be localized in so far as possible), fluid accumulation, and normal (urinary bladder, kidneys, spleen, liver, intestines) and abnormal masses (hematomas, neoplasias, GI foreign bodies, hernias).

    1. A diagnostic paracentesis (single site, four-quadrant thoracentesis, or a diagnostic peritoneal lavage) is indicated if free abdominal fluid is detected.

    a. If available, ultrasound guidance can be used to detect fluid pockets and obtain a diagnostic sample.

    b. If ultrasound is not available, the following procedure can be performed:

    1) Single site paracentesis (p. 227): Insert a 20/22 ga needle perpendicularly into the abdominal cavity at about the level of the midabdominal midline; gently aspirate.

    2) Four-quadrant paracentesis: If the single site paracentesis does not obtain a sample of fluid, one could attempt multiple site paracentesis, but avoid the area of the liver, stomach, spleen, and urinary bladder.

    3) Peritoneal lavage paracentesis (p. 228): If the multiple site paracentesis does not obtain a sample of fluid, one could instill approximately 20 ml/kg of a warmed isotonic crystalloid into the abdominal cavity via a preplaced intravenous catheter; role the animal to wash the peritoneal cavity; gently aspirate.

    2. All aspirates should be examined cytologically and cultured if infection is possible.

    a. High specific gravity and cell count suggest exudates.

    b. High neutrophil counts suggest inflammation.

    c. Intracellular bacteria denote septic peritonitis.

    d. Bile salts and high bilirubin concentration suggest gall bladder/bile duct rupture.

    e. High lactate and low glucose (compared to plasma) suggest sepsis.

    f. High creatinine, urea nitrogen, potassium (compared to plasma) suggest urine.

    3. Imaging procedures can be performed to further characterize abnormalities (radiography, ultrasound, computed tomography [CT], magnetic resonance imaging [MRI]).

    E. Internal hemorrhage into a body cavity (hemothorax, hemoabdomen), into muscle or subcutaneous tissues (hematoma), or into organs (brain, lung contusions) may occur secondary to ruptured vessels or to coagulopathy.

    1. Recognition of internal hemorrhage depends upon the site of hemorrhage.

    a. Pleural space: increasing breathing effort; decreasing lung sounds; hypovolemia, which is poorly/transiently responsive to fluid therapy; decreasing hemoglobin concentration; decreasing blood oxygenation; increasing blood carbon dioxide. Diagnostics: auscultation, thoracentesis (p. 155), ultrasound, radiography. Therapy: chest drainage (p. 158), blood transfusions as necessary.

    b. Abdomen: increasing abdominal girth and pressure; hypovolemia, which is poorly/transiently responsive to fluid therapy; decreasing hemoglobin concentration. Diagnostic paracentesis, ultrasound, and radiography may be indicated. Blood can be removed from the abdominal cavity if it has accumulated in sufficient quantity to cause impaired ventilation, if abdominal pressure exceeds 20–25 cm H2O, or if the blood is needed for autotransfusion.

    c. Hematoma: palpable enlarging mass. Therapy: apply counterpressure.

    d. Brain contusion: deteriorating intracranial signs

    e. Lung contusion: deteriorating pulmonary function

    2. In all cases of hemorrhage, fluid therapy should be conservative but sufficient to reestablish a modest arterial blood pressure (60–80 mmHg mean) and tissue perfusion (decreasing lactate concentration or metabolic acidosis, capillary refill time of about 2 seconds). It is not necessary that cardiovascular parameters be normalized at this point. Aggressive fluid therapy could worsen the hemorrhage.

    3. Coagulopathies should be ruled in or out in all cases of hemorrhage. Clotting problems can occur secondary to abnormalities of platelets, coagulation factors, and fibrinolysis.

    a. Platelet counts are determined as part of a complete blood count and can be estimated from a blood smear by multiplying the number counted per high power field by 15,000. Bleeding secondary to thrombocytopenia is not expected until platelet numbers are far below 30,000.

    b. Platelet function is determined by the presence or absence of petechiae or ecchymoses, by bleeding time, or by a commercial platelet function analyzer.

    c. Problems within the coagulation cascade are determined by prolongation of prothrombin time, activated partial thromboplastin time, activated coagulation time, or whole blood coagulation time.

    d. Fibrinolysis is assessed by D-dimer analysis. Primary fibrinolysis is thought to be very rare; it is normally associated with, and secondary to, activated coagulation.

    e. Disseminated intravascular coagulation is a thrombotic syndrome heralded by thrombocytopenia, prolonged coagulation tests, and elevated fibrin degradation products and D-dimers.

    F. Miscellaneous

    1. Rectal examination to check for pelvic fractures, anal tone, or hemorrhage.

    2. Debris should be removed from open wounds by copious lavage with sterile saline. Swabs for bacterial culture should be procured. Povidone iodine (1:9) or chlorhexidine (1:40) can be added to the lavage solution to aid decontamination. Dead or devitalized tissue should be removed from the wound as soon as possible to prevent further bacterial growth and contamination. Pack the wound with gauze pads moistened with one of the above solutions until definitive repair under general anesthesia can be accomplished.

    3. Limb fractures should be immobilized to prevent further injury. Temporary splints can be made of rolled up magazines or newspaper, or cardboard in the absence of more suitable materials. Heavily padded compressive bandages can be used for fractures below the elbow or stifle. A splint that extends over the shoulder or hip can be used to help stabilize a humeral or femoral fracture.

    4. A ruptured urinary system (ureter, bladder, urethra) may be revealed by detection of free urine in the abdomen.

    a. A palpable bladder or a bladder visualized by radiography or ultrasound reinforces, but does not prove, the absence of a rupture.

    b. An excretory urogram (p. 272) or a positive contrast cystogram (p. 271) or urethrogram (p. 272) helps rule in/out rupture of a ureter, bladder, or urethra.

    c. Monitor urine output, patient demeanor, and plasma creatinine/BUN. A ruptured urinary system will be associated with abnormalities in 1–3 days.

    G. Chemistry panel, complete blood count, and urinalysis should be measured as indicated.

    CHAPTER

    2

    EMERGENCY ROOM READINESS

    Steve C. Haskins and Douglass K. Macintire

    I. BEING PREPARED

    In order to expeditiously process an emergency patient, the room, the equipment, the supplies, and the people need to be ready to spring into action at a moment’s notice.

    A. A designated area of the hospital should be set up to receive emergency patients.

    B. The equipment necessary to manage the array of patient problems likely to be presented should be present and in good working order.

    C. The supplies and drugs necessary to manage the array of patient problems likely to be presented must be readily available.

    D. Personnel likely to be utilized in the management of emergency patients should be trained to be a functional part of the resuscitation team.

    II. EQUIPMENT RECOMMENDATIONS

    A. Penlight, stethoscope, ophthalmoscope, and otoscope

    B. A means of providing oxygen therapy

    1. An oxygen source and flow meter

    2. To improve the efficiency of flow-by oxygen therapy, an enclosure such as a face mask or plastic bag can be used to minimize dispersion of the oxygen and maximize inspired oxygen concentration.

    3. A breathing circuit such as a nonrebreathing circuit or circle system (an anesthetic machine)could be used to further increase the inspired oxygen concentration.

    4. Nasal catheters or cannulas for extended oxygen therapy along with flow meters, bubble humidifiers, tubing, and staplers or superglue

    5. A way to humidify the oxygen for prolonged use

    6. (Optional) An enclosed, environmentally controlled, oxygen chamber

    C. A means of endotracheal intubation

    1. Laryngoscope and assortment of blades

    2. An assortment of endotracheal tubes

    3. Tracheostomy tubes

    D. A means of providing positive pressure ventilation

    1. Self-reinflating resuscitation bag

    2. A rebreathing bag on a nonrebreathing circuit

    3. An anesthetic machine

    4. (Optional) A mechanical ventilator

    E. Electrocardiograph, defibrillator with internal and external paddles

    F. A means of controlling fluid administration rates

    1. Fluid pumps

    2. A pressure bag for rapid fluid administration

    3. A syringe pump

    G. Pulse oximeter

    H. End-tidal CO2 monitor

    I. Indirect blood pressure measuring equipment

    1. An assortment of cuff sizes

    2. A cuff inflator and aneroid manometer

    3. A Doppler blood flow detector, or

    4. An oscillometric blood pressure measuring device

    J. Mouth speculum and an assortment of gastric tubes

    K. Ability to monitor and correct body temperature

    1. Thermometers

    2. Circulating warm-water blankets or

    3. Forced-air warming blankets

    4. Heat lamps

    5. Source of tap water to wet patients

    6. Source of ice for ice packs

    L. Microhematocrit centrifuge and capillary tubes

    M. Refractometer

    N. Microscope, slides, stains

    O. Glucometer

    P. Hemoglobinometer

    Q. A means of imaging thorax and abdomen

    1. Radiography

    2. Ultrasound

    R. Hair clippers and backup blades; vacuum for hair removal

    S. The means to do sterile emergency surgical procedures

    1. Antiseptic prep solutions

    2. Surgical caps, masks, gowns; sterile gloves

    3. Sterile minisets of basic surgical instruments; suture material

    4. Surgical lights

    5. Sterile retractors for open-chest CPR

    6. Anesthetic machine

    7. Surgical table

    8. Instrument stand

    9. Sterile towels and drapes

    T. Suction apparatus, collection bottles, tubing, and suction tips and catheters

    U. Culture swabs and broth

    1. Aerobic and anaerobic

    2. Blood culture vials

    3. Portable culture swabs and media

    V. A means of in vitro coagulation testing with known normals

    1. Activated clotting time

    2. Partial thromboplastin time; prothrombin time

    3. Buccal mucosal bleeding time lancet

    W. Defibrillator with small and large external and internal paddles

    X. Trash containers and biomedical/sharps waste containers

    Y. Ability to perform in-house chemistry analyses and complete blood counts

    Z. A pH and blood gas, and electrolyte analyzer

    AA. Lactate analyzer

    BB. Osmometer; colloid osmometer (desirable)

    CC. Fluid warmer

    DD. Nebulizer (ultrasonic)

    EE. Stomach tubes and stomach pumps

    FF. Forceps to retrieve foreign objects from the pharynx, trachea, and external ear canals

    GG. Weight scales

    HH. Endoscope, bronchoscope

    II. Neonatal incubator

    III. RECOMMENDED SUPPLIES

    A. Full assortment of syringes and needles, spinal needles, bone marrow biopsy (intraosseous) needles

    B. A full assortment of peripheral and central venous catheters (14–24 ga)

    C. A full assortment of fluid administration sets, extension sets, three-way stopcocks, injection ports, graduated burettes, T-ports

    D. Catheters/cannulas for thoracentesis and chest drainage; a means of collecting chest fluid secretions

    E. Wide selection of fluids

    1. Extracellular replacement solution (such as lactated Ringer’s or Plasmalyte 148 or Normosol R, and 0.9% saline)

    2. 5 and 50% dextrose in water

    3. A low-sodium maintenance solution (such as Plasmalyte 56, or Normosol M, or 0.45% NaCl and 2.5% dextrose)

    F. Sterile and nonsterile lubricating jelly

    G. Tongue depressors and cotton-tipped applicators

    H. Wide selection of concentrates (potassium chloride, potassium phosphate, 7.5% sodium chloride, sodium bicarbonate, mannitol)

    I. A colloid solution such as voluven or hetastarch

    J. Source of hemoglobin and plasma products; a means of blood typing or cross-matching

    K. Administration sets (regular and pediatric) and supplies for fluids and blood products

    1. (Desirable) Calibrated burettes

    2. Extension sets

    3. Three-way stopcocks

    4. Injection ports (catheter caps)

    5. T-port connectors

    L. An assortment of urinary catheters (for dogs and cats) and closed urine collection bags

    M. Nasal and nasoesophageal catheters

    N. Tape, cotton, gauze, and other bandaging materials

    O. Cage padding

    P. Splint/casting material

    Q. Sandbags for patient positioning

    R. An assortment of suture material;(desirable) quick-attach options: superglue; staple gun and staples

    S. Sterile gloves, latex examination gloves, and surgical scrub solutions, alcohol

    T. Test kits for FeLV/FIV; ethylene glycol, parvoviral enteritis, cPLI for pancreatitis, BNP to differentiate cardiac from respiratory disease

    U. Supplies for dipstick analyses (urinalysis, glucose, Azostix, lactate)

    V. Blood collection tubes; culture swabs and growth media

    IV. RECOMMENDED DRUGS

    A. Sympathomimetics, cardiotonics, and vasoactive agents

    1. Epinephrine

    2. Dopamine

    3. Dobutamine

    4. Norepinephrine

    5. Phenylephrine

    6. Hydralazine

    7. Nitroprusside

    8. Digitalis

    9. Calcium-channel blocker (nifedipine, amlodipine, diltiazem, verapamil)

    10. Nitroglycerine ointment

    11. Vasopressin

    B. Parasympatholytic (atropine or glycopyrrolate)

    C. Sodium bicarbonate

    D. Calcium (gluconate)

    E. Heparin

    F. Antiarrhythmics

    1. Sodium-channel blockers (lidocaine and procainamide

    2. Calcium-channel blockers (diltiazem or verapamil)

    3. Beta-blockers (propanolol and esmolal)

    4. Mixed-mechanism antiarrhythmics (amiodarone and sotalol)

    G. Anesthetic agents

    1. Ketamine

    2. Propofol

    3. Thiopental

    4. Inhalational (isoflurane or sevoflurane)

    5. Etomidate

    6. Pentobarbital

    H. Analgesic agents

    1. Agonists (oxymorphone or hydromorphone or methadone or morphine or fentanyl)

    2. Agonist-antagonists (butorphanol or buprenorphine or nalbuphine)

    3. Naloxone

    4. Fentanyl patches

    5. Tramadol

    6. Antiprostaglandins (meloxicam or deracoxib or carprofen)

    I. Anxiolytics (acepromazine and benzodiazepine [diazepam or midazolam]; benzodiazepine reversal agent (flumazenil)

    J. Alpha2 agonist (medetomidine or dexmedetomidine) and reversal agent (atipamezole)

    K. Antiemetics (metoclopramide, prochlorperazine, and maropitant)

    L. Antacids

    1. H2-blockers (cimetidine, ranitidine, or famotidine)

    2. Proton pump blockers (omeprazole, pantoprazole)

    M. Emetic (apomorphine)

    N. Eye lubricant

    O. Antiseizure drugs (phenobarbital, benzodiazepine, levetiracetam [Keppra], potassium bromide)

    P. Doxapram

    Q. Glucocorticoids (dexamethasone phosphate, prednisolone sodium succinate, methylprednisolone sodium succinate)

    R. Diuretics (furosemide and mannitol)

    S. Hydrogen peroxide

    T. Activated charcoal and kaolin pectate

    U. Antitoxins

    1. Pralidoxime (for organophosphates)

    2. Calcium-EDTA (for heavy metals: lead, zinc, mercury, cadmium)

    3. Dimercaprol (for heavy metals)

    4. Sodium nitrite and sodium thiosulfate (for arsenic)

    5. Succimer (for lead)

    6. Vinegar (for neutralizing alkalis)

    7. Vitamin K (for vitamin K antagonist rodenticides)

    8. Ethanol (for ethylene glycol)

    9. Antivenin (for snakebite)

    10. Yohimbine or atipamezole (for amitraz)

    11. 4-methylpyrazole (for ethylene glycol)

    12. N-acetylcysteine (for acetaminophen)

    13. D-pencillamine (for heavy metals: lead, zinc, copper, cadmium, inorganic mercury)

    14. Silybin phytosome (for mushroom toxicity)

    15. Calcitonin-salmon (for vitamin D rodenticide toxicity)

    16. Diphenhydramine (for transfusion/allergic reactions)

    17. Methocarbamol (muscle relaxant for tetanus, snail bait, strychnine, tremors)

    18. Naloxone (for narcotic overdose)

    19. S-adenosylmethionine (for hepatotoxicity)

    20. Cyproheptadine (antiserotonin drug for serotonin syndrome)

    21. 20% lipid solution (for use in fat-soluble toxins—ivermectin, baclofen)

    V. Methocarbamol

    W. Broad-spectrum antibiotics effective for Gram-negative and Gram-positive aerobes and anaerobes

    X. H1-blockers (diphenhydramine)

    Y. Bronchodilators

    1. Aminophylline

    2. Beta2-agonists (terbutaline or albuterol)

    Z. B-complex vitamins, thiamine

    AA. Regular Insulin

    BB. Antiparasitic agents: ivermectin, capstar, imidocarb, fenbendazole, pyrentel pamoate, droncit, flea and tick products

    CC. Euthanasia solution

    CHAPTER

    3

    CARDIOPULMONARY-CEREBRAL RESUSCITATION (CPCR)

    Steve C. Haskins

    I. CAUSE

    Cardiac arrest may be caused by any disease that interferes with myocardial oxygenation, electrical depolarization, or mechanical contraction.

    A. Hypoxemia

    B. Anemia

    C. Hypovolemia

    D. Acid-base and electrolyte (potassium, calcium, magnesium) imbalances

    E. Excessive sympathetic or parasympathetic stimulation

    F. Adverse drug reactions

    G. Myocardial infiltrative or inflammatory disease

    H. Myocardial failure or arrhythmias

    I. Blunt or penetrating trauma

    J. Thromboembolism

    II. CLINICAL SIGNS

    A. Prevention of cardiac arrest is always more successful than treatment of it. Signs of impending arrest include:

    1. Severe bradypnea or dyspnea and hypoxemia

    2. Cyanotic or white mucous membranes

    3. Weak, barely auscultable heart beat or palpable pulse

    4. Severe hypotension, bradycardia, or tachycardia

    B. Signs of a cardiac arrest include:

    1. Apnea or agonal gasping

    2. Cyanotic or white mucous membranes

    3. Dilated, non-light-responsive pupils

    4. Absence of an auscultable heart beat or palpable pulse

    5. Lack of bleeding at the surgical site

    III. THE NATURE OF CELL INJURY DURING CARDIAC ARREST

    A. Lack of perfusion injury: the lack of oxygen and other cellular metabolic substrates disables the cell’s ability to maintain energy stores for essential cellular functions.

    1. Such cells initially lose the ability to pump sodium out and, as a result, develop intracellular edema.

    2. If the process continues unabated, such cells will die.

    B. Reperfusion injury: it has been observed that organ systems may function reasonably well in some patients immediately after resuscitation but then deteriorate in the ensuing hours. There are several possible mechanisms:

    1. Reactive oxygen intermediate metabolites

    2. Leukocyte activation, sequestration, and cytokine liberation

    3. Intravascular thrombosis

    IV. PROGNOSIS/GENERAL RECOMMENDATIONS

    A. Resuscitation can generate a return of spontaneous heart beat rate of 30%–50%. Long-term survival in dogs and cats ranges between 2 and 10%; in humans, it is about 6% (inclusive of all neurological status).

    B. Resuscitation is not recommended in all instances of cardiac arrest. The decision to resuscitate or not should be made in advance on the merits of each individual case, and in consultation with the owner.

    C. A cardiopulmonary resuscitation (CPR) flow sheet or checklist should be posted at the CPR station for the practice to ensure that essential components are not omitted from the resuscitation endeavor.

    A CPR record should also be readily available and filled out with each resuscitation.

    D. An ECG should be monitored before, during, and after the arrest, if possible. Common initial arrest rhythms include asystole, pulseless electrical activity, sinus bradycardia, and ventricular fibrillation. The rhythm can change during CPR and may warrant a change in therapy. Return to spontaneous circulation should be recognized when it occurs so that it can be managed appropriately.

    E. Resuscitation rates approach zero after about 30 minutes.

    V. TREATMENT

    Procedure for witnessed cardiopulmonary arrest is set out in Table 3.1.

    A. Airway: Secure the airway by endotracheal intubation.

    B. Breathing: Institute positive-pressure ventilation with 100% oxygen.

    1. One ventilation should be delivered between approximately every 8–12 chest compressions (without a pause in the chest compressions).

    2. Previous recommendations advocated a higher respiratory rate (1 per 5 compressions), but hyperventilation reduces forward blood flow, hence the newer recommendations for a slower respiratory rate.

    a. Simultaneous ventilation and chest compression is a maneuver used to augment circulation and should not be considered ventilation.

    b. If the resuscitation is being conducted by one person, two ventilations should be delivered approximately every 15 chest compressions.

    c. Inspiratory pressure should be about 15–20 cm H2O (dog or cat), although higher pressure may be required with reduced thoracic compliance (diffuse pulmonary disease, pleural space filling disorders).

    d. Inspiratory time should be brief (<1 sec) and airway pressure must fall to 0 cm H2O between ventilations.

    e. Animals with preexisting hypoxia or severe pulmonary disease may require higher rates (12–20 bpm).

    C. Circulation

    1. External chest compression is accomplished by applying pressure directly over the heart in animals less than 10 kg, and at the widest part of the chest in medium to large dogs (thoracic pump mechanism) at a rate of 80–120 times per minute.

    a. The chest is compressed by 25%–30%.

    b. This may be done in lateral or dorsal recumbency.

    c. The optimal duty time (compression to release ratio) is 50:50.

    d. Compression should be held for a brief time to maximize the elimination of blood from the heart and the chest.

    e. The pressure must be fully released between compressions.

    f. Frequent or prolonged interruptions in compressions should be avoided because interruptions reduce survival and lower the chances of return to spontaneous circulation.

    g. If possible, persons performing compressions should be rotated out after several minutes to prevent rescuer fatigue. The switch should be made in <5 seconds.

    h. The specific technique that will cause effective forward blood flow varies markedly from patient to patient.

    2. The effectiveness of the external chest compression technique must be evaluated.

    a. Palpable pulses (femoral, dorsal pedal, lingual) associated with each chest compression

    b. Audible blood flow (Doppler blood flow detector) in a peripheral artery or over the eyeball

    c. An improvement in mucous membrane color

    d. Detection of peripheral pulses with a pulse oximeter

    e. Detection of carbon dioxide in the end-tidal gases. End-tidal CO2 levels drop to 0 with cardiac arrest, but will begin to rise with restoration of circulation and expulsion of carbon dioxide from the lungs. The goal is to achieve the highest possible ETCO2.

    TABLE 3.1 PROCEDURE FOR WITNESSED CARDIOPULMONARY ARREST

    3. If the external chest compression technique is not effective, the compression technique should be changed (in no particular order):

    a. The rate of compression or the amount of force could be increased or decreased.

    b. The duration of systole could be increased slightly.

    c. The position of the hands or the animal could be changed.

    d. The compressor could be changed.

    4. If the external chest compression technique is still deemed ineffective, the following augmentation techniques may prove useful:

    a. Abdominal counterpressure splints the abdomen, preventing the caudal movement of the diaphragm, and augments the increased intrathoracic pressure when the chest is compressed. Abdominal counterpressure can be applied by the hands of an assistant or a sandbag or a large book.

    b. Interposed (between chest compressions) abdominal compressions increase venous return to the chest by alternating abdominal compressions with chest compressions.

    c. Antishock trousers (inflatable pants) return a small amount of blood from the peripheral pool to the central circulation and prevent the runoff of arterial blood into the periphery.

    1) Antishock trousers can be simulated by wrapping the hind legs and caudal abdomen with elastic bandaging material.

    2) Do not wrap too far forward on the abdomen because it will cause anterior displacement of the liver. Thoracic compression is then likely to fracture the liver, resulting in hemorrhage.

    3) A single abdominal tourniquet is a surrogate for shock trousers. A rope or belt can be placed tightly around the lower abdomen, sufficiently tight to compress the descending aorta.

    4) Such wraps and tourniquets can be slowly removed 10–20 minutes after restarting the heart; after hemodynamics have had a chance to stabilize.

    5. Internal heart compression is associated with better cardiac output, arterial blood pressure, cerebral and coronary perfusion, myocardial perfusion, peripheral tissue perfusion, and higher survival rates with improved neurologic recovery compared to external techniques. A thoracotomy is indicated when:

    a. There is an open pneumothorax, a closed pneumothorax, chest trauma with broken ribs, diaphragmatic hernia, pleural effusion, or pericardial effusion, or when the size or shape of the thorax precludes effective external chest compression.

    b. There is no evidence of effective artificial circulation and tissue perfusion after 5 minutes.

    c. There is no return of a spontaneous heart beat after 10 minutes.

    d. Additional advantages of a thoracotomy include:

    1) The adequacy of diastolic refilling can be assessed between each heart compression. The heart should fill as rapidly as it is released. If this does not occur, a fluid bolus or a vasoconstrictor is indicated.

    2) An accumulation of fluids or blood within the pericardial sac can be observed and drained. The pericardial sac can be opened to prevent pericardial tamponade during or after resuscitation.

    3) The descending aorta can be depressed with the index finger of the opposite hand or clamped, directing essential blood flow to the brain and heart. This compression should remain for the duration of the resuscitation. Aortic compression can be slowly removed 10–20 minutes after restarting the heart, after hemodynamics have had a chance to stabilize.

    4) Fibrillation can be diagnosed by direct observation and internal defibrillation efforts may be more effective than external.

    5) Myocardial flaccidity can be assessed by direct visualization.

    6) Direct intracardiac injections are safer than blind sticks of the heart.

    e. A thoracotomy should only be done in a fully equipped hospital by properly trained personnel.

    f. Time is limited, so the procedure should be performed rapidly and yet must be done carefully with due consideration to anatomical structures.

    1) Thoracotomy is facilitated by clipping a strip of hair along the line of the intended incision at the fifth intercostal space.

    2) Hair and loose dirt can be removed with a quick swab with an antiseptic solution (or water).

    3) The incision is made midway between the ribs (to avoid the big intercostal vessels at the caudal edge of the rib) down to, but not through, the pleura.

    4) Pleural penetration should be accomplished with a finger or a blunt instrument.

    5) The incision is then extended dorsally and ventrally with scissors, taking care to avoid the internal thoracic artery, which runs longitudinally just lateral to the sternum. The intercostal artery, which runs just caudal to the rib, should also be avoided.

    6) The heart should be compressed between the flats of the fingers and the palm of the hand, taking care not to shift or rotate the natural position of the heart.

    a) Small hearts can be compressed between two fingers and the thumb.

    b) Large hearts can be compressed between the palm and the opposite chest wall.

    c) Do not use the fingertips, which can easily penetrate the wall of an atrium or ventricle.

    TABLE 3.2 AGONISTS USEFUL DURING CARDIOPULMONARY RESUSCITATION

    D. After the first several minutes of cardiac arrest, tissue anoxia causes peripheral vasodilation. This increasing blood volume capacity must be filled with exogenous fluids to maintain an effective central circulating volume.

    1. The type of fluid used is not as important as the volume derived from its administration.

    a. Isotonic extracellular replacement crystalloid fluid (with a near-sodium concentration) can be rapidly administered in aliquots of approximately 20 mL/kg for a dog and 10 mL/kg for a cat.

    b. Artificial colloids can be administered in aliquots of approximately 5 ml/kg for a dog and 2.5 ml/kg for a cat.

    c. A 7.5% hypertonic saline can be administered as a single dose of 6 ml/kg for a dog and 3 ml/kg for a cat (administered over 5 minutes).

    d. Mannitol (20%–25%) can be administered as a single dose of 5 ml/kg for a dog or 2.5 ml/kg for a cat.

    2. Fluid boluses may need to be repeated periodically throughout the resuscitation endeavor in quantities sufficient to maintain an effective circulating volume.

    3. Excessive fluid volumes to these heart failure patients can cause pulmonary edema.

    E. Sympathomimetics

    1. Arterial constriction increases arterial blood pressure and diminishes the loss of arterial blood volume into the periphery.

    2. Venoconstriction redistributes blood from the venous capacitance vessels into the active arterial circulation.

    3. Epinephrine is the most efficacious catecholamine in cardiac arrest (see Table 3.2). The standard dose is 0.01 mg/kg (low dose epinephrine). Larger dosages (up to 0.1 mg/kg high dose) may be more effective in inducing a spontaneous heart beat but are also associated with a higher incidence of ventricular fibrillation.

    4. Catecholamines with primarily alpha-agonist activity—norepinephrine (0.02–0.2 mg/kg), phenylephrine(0.1–1.0 mg/kg) and methoxamine (40–80 mcg/kg IV—are almost as efficacious as epinephrine.

    5. Vasopressin (0.8 U/kg IV) is an effective vasoconstrictor in refractory cardiac arrest especially under conditions of severe acidosis when epinephrine is not effective.

    6. Isoproterenol, dopexamine, and dobutamine are not recommended because of their vasodilating properties.

    F. There are four routes by which small volume emergency drugs can be administered:

    1. Peripheral venous routes are the most commonly available and include (in order of closeness to the heart) cephalic, saphenous, intraosseous, and sublingual.

    a. A long jugular catheter (with the tip of the catheter near the right atrium) shortens the time delay between injection and delivery of the drug to the coronary circulation, but can only be used if it is already in place at the time of the arrest.

    b. Venous cut down may be necessary to place the catheter if percutaneous access is unsuccessful after a couple of attempts.

    2. Intracardiac injections deliver the drug very close to the heart but are associated with a number of problems that decrease the desirability of this method.

    a. The compression technique must be stopped in order to deliver the intracardiac injection.

    b. Blind intracardiac injections may be associated with lung laceration, coronary artery laceration, and atrial or right ventricular laceration.

    c. Intramyocardial deposition of epinephrine may cause refractory ventricular fibrillation.

    d. Multiple myocardial injections cause trauma and may predispose to ventricular ectopic beats or ventricular fibrillation.

    3. Capillary bed techniques include intratracheal, sublingual, intralingual, conjunctival, and intrapulmonary injections.

    While uptake of drugs from such locations is exceptionally good in an animal with a beating heart, uptake during CPR is sporadic and undependable.

    4. Intraosseous administration can be used in pediatric patients or exotic animals with very small peripheral veins.

    G. Anticholinergics may be indicated; excessive vagal tone can stop a heart and keep supraventricular pacemakers subdued. Lacking an idioventricular (escape) rhythm in such patients is asystole.

        The dose of atropine for asystole is 0.04 mg/kg IV (1 ml per 20 lb).

    1. Although a low dose may cause

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