Vet Clin Exot Anim 10 (2007) 275–291

Shock and Cardiopulmonary-CerebralResuscitation in Small Mammals

and Birds

Marla Lichtenberger, DVM, DACVECC11015 North Mequon Square Drive, Mequon, WI 53092, USA

Increasing numbers of exotic animals are being kept as pets, and ownerswant to receive high-quality medical care for these pets. Treatment of hypo-volemic shock and cardiopulmonary arrest in exotic small mammals andbirds is complicated by small patient size, physiologic diversity, and lackof research and clinical data on their response to therapy. Despite these im-pediments, the same principles and techniques of monitoring used in domes-tic animals can be applied to the bird and small mammal patient. The goalof this article is to provide an overview on the principles of shock, shock re-suscitation methods, and cardiopulmonary-cerebral resuscitation (CPCR) inrabbits, ferrets, small mammals, and birds (pet birds and raptors).

Shock pathophysiology

Shock is defined as poor tissue perfusion from either low blood flow orunevenly distributed flow. This results in an inadequate delivery of oxygento the tissues. This definition applies to all species of animals. Although thereare many types of shock (eg, cardiogenic, distributive, or septic), this articleconcentrates on the pathophysiologic characteristics of hypovolemic shock.

Hypovolemic shock is caused by either an absolute or a relative inade-quate blood volume. Absolute hypovolemia occurs as a result of actualloss of blood by arterial bleeding, gastrointestinal ulcers, or coagulopathies.In relative hypovolemia, there is no direct blood loss (hemorrhage) from theintravascular space. Examples of relative hypovolemia include severe dehy-dration from gastrointestinal tract loss, significant loss of plasma (burns), orextensive loss of intravascular fluids into a third body space, such as the

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276 LICHTENBERGER

peritoneal cavity. When a small mammal or bird begins hemorrhaging orthere is significant loss of body fluid, there is a decrease in blood volumeand a decrease in venous return to the right side of the heart. This causesa decrease in return to the left side of the heart and therefore a decreasein cardiac output. With a substantial hypovolemia (ie, greater than 30%blood or plasma volume), blood pressure decreases below a mean arterialpressure of 60 mm Hg or a systolic pressure of less than 90 mm Hg. The ca-rotid and aortic artery baroreceptors detect a decrease in stretch caused bythe decrease in cardiac output. This sends a neural signal to the vasomotorcenter in the medulla oblongata, which results in inhibition of the vagalparasympathetic center and stimulation of the sympathetic center. Thiscauses vasoconstriction of the veins and arterioles throughout the peripheralcirculatory system and increases heart rate and strength of heart contrac-tion. The humoral response, an increase in adrenal circulating catechol-amines, stimulates renin release by way of adrenergic receptors on cells ofthe juxtaglomerular apparatus (specialized smooth muscle cells in theafferent arterioles). The release of rennin stimulates activation of the ren-nin-angiotensin-aldosterone system [1]. These combined effects lead to a res-toration of blood pressure, increased cardiac performance, and maximalvenous return in the face of blood loss.

Hypovolemic shock: three phases

Early or compensatory phase

The early or compensatory stage of shock occurs as a result of the baro-receptor-mediated release of catecholamines. Blood pressure increasesbecause of the increase in cardiac output and systemic vascular resistance.This is the stage seen commonly in birds (as in dogs) with blood loss lessthan 20% of their total body weight. Small mammals, as is true in cats,rarely present with this stage of shock. Clinical signs in the bird includean increase in heart rate, normal or increased blood pressure, and normalor increased flow (bounding pulses and capillary refill less than 1 second).The increased heart rate and normal or increased blood pressure are key in-dicators of compensatory shock. Volume replacement at this stage is usuallyassociated with a good outcome. This phase is rarely seen in small mammalsand cats, as discussed later.

Early decompensatory phase

The second stage of shock is called the middle or early decompensatorystage of shock. This stage occurs when fluid losses continue. There is a reduc-tion in the blood flow to the kidneys, gastrointestinal tract, skin, andmuscles. There is an uneven distribution of blood flow.

Clinical signs of early decompensatory shock in birds and small mammalsinclude hypothermia, cool limbs and skin, tachycardia, normal or decreased

277SHOCK AND CPCR IN SMALL MAMMALS AND BIRDS

blood pressure, pale mucous membranes, prolonged capillary refill time, andmental depression. This stage of shock is seen in birds with a blood volumeloss of greater than 25% to 30% of their total blood volume. In the author’sexperience, rabbits, ferrets, and other small mammals commonly present inearly decompensatory stage of shock. Signs of early decompensatory shockin the small mammal patient (as in the cat) are bradycardia, hypothermia,and hypotension. Signs seen in the avian patient are increased heart rateand hypotension. Aggressive fluid therapy using crystalloids and colloidsto support blood pressure and heart rate is required in this stage.

Decompensatory shock

When a large blood volume is lost (greater than 60% in avian species and40% in small mammals) the neuroendocrine responses to hypovolemiabecome ineffective, and irreversible organ failure begins [1]. The late decom-pensatory stage of shock is the final common pathway of all forms of shockin all species.

The pathophysiologic profile of terminal shock is a continuum of thatdescribed for the early decompensatory stage, except that the damage hasoverwhelmed the body’s natural protective mechanisms and multiple organfailure has occurred. The clinical signs are bradycardia with low cardiac out-put, severe hypotension, pale or cyanotic mucous membranes, absent capil-lary refill time, weak or absent pulses, hypothermia, oliguria to anuric renalfailure, pulmonary edema, and a stupor to comatose state. Cardiopulmo-nary arrest commonly occurs.

Fluid resuscitation plan

A fluid therapy plan involves the type, quantity, and rate of fluid to beadministered. Fluid therapy is used to correct life-threatening abnormalitiesin volume, electrolyte, and acid–base status. The primary goal is to give theleast amount of fluids possible to reach the desired end points of resuscita-tion. Clinical markers are the most frequently used end points of resuscita-tion. The markers used are those parts of the initial survey that suggesta patient is in shock and include the following: altered mentation, prolongedcapillary refill time (CRT), weak and thready pulse/hypotension, tachycar-dia/bradycardia, tachypnea, cold extremities, weakness, reduced urine out-put, and pale mucous membranes.

The fluid therapy plan typically has a resuscitation (correction of perfu-sion deficits), a rehydration (correction of interstitial deficits), and a mainte-nance phase [2]. Resuscitation implies an urgent need to restore tissueperfusion and oxygenation. Intravascular volume must be replaced first.The type, quantity, and rate of fluid administration required to reach the de-sired resuscitation end points are determined based on the phase of shock

278 LICHTENBERGER

[2]. Re-evaluation of hydration status after the resuscitation phase is neces-sary before planning the rehydration phase.

Interstitial volume deficits are typically associated with a decrease in skinturgor and dry mucous membranes. Rehydration of the interstitial compart-ment is best accomplished using an isotonic replacement fluid. The rate offluid administration depends primarily on the rate of fluid losses and clinicalstatus of the animal, as indicated by the physical examination and labora-tory parameters. For animals with evidence of interstitial dehydration onphysical examination but stable cardiovascular parameters, fluid deficitscan be replaced over 12 to 24 hours. If the interstitial volume is rapidlylost, then the interstitial fluid deficit should be rapidly replaced (4–6 hours).Isotonic replacement fluids are administered according to the patient’s esti-mated dehydration, maintenance needs, and anticipated ongoing losses. Themaintenance phase provides fluids and electrolytes to replace ongoing losses,meet metabolic demands, and restore intracellular water balance until thepatient is eating and drinking on its own. Maintenance requirements arehigher in small mammals and birds because of their high metabolic rate.

Types of fluids

Individual characteristics of fluids influence type and volume of fluid ad-ministered. Crystalloid solutions are commonly used together with colloidsin the resuscitation phase. The four basic groups of fluids (ie, crystalloids,synthetic colloids, hemoglobin-based oxygen carriers, and blood products)are discussed.

Crystalloids

Isotonic crystalloid solutions can be used together with colloids duringthe resuscitation phase. Crystalloids are the mainstay of the rehydrationand maintenance phases of fluid therapy. Crystalloids (also called replace-ment fluids) are fluids containing sodium chloride and other solutes thatare capable of distributing to all body fluid compartments. The most com-monly used replacement fluids are 0.9% saline (Baxter; Deerfield, IL), lac-tated Ringer’s solution (Abbott Laboratory; North Chicago, IL), andNormosol-R (CEVA Laboratories; Overland Park, KS) or Plasmalyte-A(Baxter).

Hypertonic saline is a hyperosmolar crystalloid fluid used for resuscita-tion of hypovolemia. It is usually given as a 7.5% solution (2600 mOsm/L).The hyperosmolarity leads to rapid intravascular volume expansion bydrawing fluids from the interstitial and intracellular spaces into the intra-vascular space. Synthetic colloids (hetastarch) provide a synergistic effectwhen added to hypertonic saline resuscitation, as the duration (in excess of3 hours) and extent of volume resuscitation (improvement of cardiac outputand blood pressure) are greater than would be achieved with either agent

279SHOCK AND CPCR IN SMALL MAMMALS AND BIRDS

alone [2,3]. It is administered in small volumes at 3–5 mL/kg over 10 minutes.The animal can be given 3–5 mL/kg of hetastarch with 3–5 mL/kg of 7.5%hypertonic saline (not mixed in the same syringe) each given over 10 minutes.The advantage is that rather than infusing three times the shed volume of iso-tonic crystalloids (eg, 90 mL/kg in a dog and bird and 60 mL/kg in smallmammals), only a limited portion of the volume deficit needs to be adminis-tered when using hypertonic saline [3,4]. Recent research focuses on the ef-fects that hypertonic saline has on the microcirculation, inflammatoryresponse, and cellular function. These findings are intriguing evidence forits use in the veterinary patients that have hypovolemic/hemorrhagic shock,septic shock, and traumatic brain injury [3,4]. Potential side effects includehypernatremia, hyperchloremia, hypokalemia, and dehydration. This move-ment of intracellular fluid points to one of the feared complications of hyper-tonic saline resuscitation: cell dehydration. Hypertonic saline should beavoided in dehydrated patients, because the extravascular fluid compartmentis volume-depleted before therapy.

Resuscitation of hypovolemic shock is performed using crystalloids alongwith colloids. This is because 80% of the volume of crystalloid fluid infusedre-equilibrates and leaves the intravascular space within 1 hour of adminis-tration. On a short-term basis crystalloids expand the intravascular space,but this effect is short-lived. Crystalloids thus should be thought of as inter-stitial rehydrators, not intravascular volume expanders. This increase in in-terstitial fluid can lead to tissue edema (thus decreasing the ability of oxygento diffuse to the cells). Interstitial edema may be extremely detrimental incases of cerebral edema and pulmonary edema.

Colloids

Colloids are fluids containing large molecular-weight substances that gen-erally are not able to pass through capillary membranes. Colloids can beconsidered intravascular volume expanders. The three types of colloidsare natural colloids (ie, blood products as whole blood), synthetic colloidsincluding hetastarch (Braun Medical Inc.; Irvine, CA), and hemoglobin-based oxygen carriers (ie, Oxyglobin, Biopure; Cambridge, MA).

HetastarchThis synthetic colloid fluid contains large molecular-weight particles that

effectively increase the colloid osmotic pressure (COP) beyond what can beobtained with blood product infusion alone. They maintain intravascularosmotic pressure because their molecular size is too large to pass throughthe normal capillary pores. They expand volume by approximately 1.4 timesthe volume actually infused. Synthetic colloids are administered with iso-tonic crystalloids to reduce interstitial volume depletion. The dose of crystal-loid administered is only 40% to 60% of what it would be if crystalloidswere used alone during resuscitation.

280 LICHTENBERGER

The standard daily dose of hetastarch is 20 mL/kg. The dose is given asan intravenous bolus (more slowly in small mammals over 10 minutes) forshock resuscitation, titrated in doses of 5 mL/kg to the desired effect.When used for COP support the dose should be administered over 24 hours.

OxyglobinOxyglobin is a hemoglobin-based oxygen carrier (HBOC). HBOC are in-

dicated during resuscitation when increased oxygen delivery to tissues is de-sired. Although HBOC are colloids, they have the added advantage ofcarrying oxygen to the tissues. Oxyglobin is a purified, polymerized bovinehemoglobin that is in a modified lactated Ringer’s solution approved for usein dogs [5].

Oxyglobin can be administered by way of intravenous administrationsets, and standard intravenous infusion pumps can be used for delivery.Because it contains no antigens, cross-matching is not required and thereis no possibility of transfusion reactions. Filters are not required. It canbe kept at room temperature and has a 3-year shelf life, which makes it use-ful for hospitals that cannot keep blood products readily available. Onceopened, the bag must be discarded within 24 hours because of the produc-tion of methemoglobin. The disadvantage to its use is that availability islimited.

Oxyglobin is up to 10 times more effective than blood when given duringfluid resuscitation to animals in hemorrhagic shock [5]. For this reason, lowvolumes of Oxyglobin can be used effectively to treat hemorrhagic shock. Inhypovolemic ferrets, rabbits, and small mammals, Oxyglobin is infused at2 mL/kg over 10 to 20 minutes as a bolus (as in the cat). This is in contrastto the bird, in which Oxyglobin has been infused by the author as a rapidbolus at 5 mL/kg over a few minutes.

Blood transfusion (natural colloids)If promoting cardiac output is the first priority in the management of

acute hemorrhage, then blood is not the ideal resuscitation fluid for acuteblood loss, because blood products do not promote blood flow as well assome acellular fluids (eg, hetastarch). Blood is rarely used for initial resusci-tation unless the patient is exsanguinating or there is excessive loss of clot-ting factors secondary to warfarin toxicity. The density of erythrocytesimpedes the ability of blood products to promote blood flow (a viscosityeffect). The availability of blood products in sufficient quantities to meetthe needs of exotic patients is often the limiting factor in survival. Most hos-pitals do not have readily available donors and commercial blood banks donot carry exotic pet blood products except for ferret blood.

Blood products are administered when albumin, antithrombin, coagula-tion factors, platelets, or red blood cells are required. Most fluid-responsiveshock patients tolerate acute hemodilution to a hematocrit of 20%. Mostanimals can tolerate an acute blood loss of 10% to 15% of their blood

281SHOCK AND CPCR IN SMALL MAMMALS AND BIRDS

volume without requiring a blood transfusion. Acute hemorrhage exceeding20% of the blood volume often requires transfusion therapy in addition toinitial fluid resuscitation. In animals that have acute blood loss requiringtransfusion therapy, fresh whole blood or packed red blood cells shouldbe used in an attempt to stabilize the clinical signs of shock, maintain thehematocrit at greater than 25%, and sustain the clotting times within thenormal range. Whole blood can be administered at 10–20 mL/kg intrave-nously or intraosseously.

Blood groups have not been identified in ferrets. Repeated attempts toidentify naturally occurring erythrocyte antibodies or to experimentally in-duce erythrocyte antibodies were unsuccessful [6,7]. Blood groups have notbeen studied in rabbits, but transfusions have been administered successfullyfrom donor rabbits in the author’s clinic. A cross-match is recommended [6].Blood groups have not been studied in birds. Homologous transfusions withspecies-specific blood is recommended [6,7]. Until controlled studies are per-formed, it is valid to assume that homologous transfusions are preferable toheterologous transfusions. A cross-match is recommended before transfu-sion [6,7].

Blood should be warmed at least 15 minutes before administration to pre-vent hypothermia. Warming can be done in a warm-water bath (42�C). Theblood-administration set must include a filter to remove most of the aggre-gated debris. Administer the donor blood by slow bolus or by infusion witha syringe pump (Infusion Pump, Baxter Health Care; Deerfield, IL) intoa catheter placed in the jugular, saphenous, or cephalic vein, or into an in-traosseous catheter. Blood transfusions should be administered within 4hours to prevent the growth of bacteria, according to standards set by theAmerican Association of Blood Banks [10]. In cases of massive hemorrhage,blood can be given within minutes.

Fluid therapy plan for the avian patient

The avian patient with a blood volume loss of greater than 25% to 30%of their total blood volume presents in early decompensatory shocksimilarly to the dog. The heart rate is elevated, mucous membranes arepale, and hypotension is present.

Any sick, debilitated bird presenting for emergency care should immedi-ately be placed in a warm incubator (temperature at 85�F–90�F [29.4�C–32.1�C]) with oxygen supplementation for 8 to 12 hours. When activeexternal hemorrhage is present, this must be stopped immediately. Mostbirds benefit from the administration of warmed crystalloids at 3 mL/100 gbody weight intravenously, intraosseously, or subcutaneous (SQ). Birdsshould be offered food and water during this time. When the bird seems sta-ble (alert, responsive) and can be safely anesthetized with mask isoflurane(Abbott Laboratory) or sevoflurane (Abbott Laboratory), diagnostics andtreatment for hypovolemia and dehydration can be performed. Blood

282 LICHTENBERGER

pressure monitoring using Doppler and an ECG should be used during theseprocedures. External heat should be provided throughout, using a heatingpad or forced warm heating blanket.

The Doppler cuff can be placed on the distal humerus or femur and theDoppler probe on the medial surface of the proximal ulna or tibiotarsus, re-spectively. The blood pressures of various avian species under isoflurane orsevoflurane anesthesia at the author’s clinic is 90 to 140 mm Hg systolic.When blood pressures are less than 90 mm Hg systolic, birds are treatedfor hypovolemia as described below. Bolus administration of crystalloids(10 mL/kg) and colloids (hetastarch (HES) or Oxyglobin at 5 mL/kg) canbe given intravenously or intraosseously until blood pressure is greater than90 mm Hg systolic. In the author’s experience, one or two bolus infusionsare usually required. When hypotension cannot be corrected after using threeboluses of hetastarch and isotonic crystalloids, the author recommends thatthe clinician use Oxyglobin at 5 mL/kg intravenously or intraosseously. Usu-ally one to two boluses are required to increase the blood pressure in refrac-tory cases. Oxyglobin has oxygen-carrying capacity and vasoconstrictionproperties.WhenOxyglobin is not available, the author has used 7.5%hyper-tonic saline at 5mL/kg bolus given slowly over 10minutes to refractory hypo-tensive birds.

Blood pressure monitoring helps the veterinarian identify cardiovascularproblems in patients under anesthesia earlier than when using an ECG only.Immediate correction of hypotension (systolic blood pressure less than90 mm Hg) with a fluid bolus helps correct hypovolemia and prevents car-diovascular collapse and death.

Fluid therapy for the surgical patient is necessary to replace losses duringthe surgical procedure. After mask anesthesia induction using isoflurane orsevoflurane, the patient is intubated. An intraosseous or intravenous cathe-ter is placed during surgical induction and the patient is maintained ona crystalloid infusion at 5 to 10 mL/kg/h. The patient is placed on an exter-nal heat source during the surgery. Doppler blood pressure and ECG mon-itoring should be used. Blood pressure is recorded every 5 minutes. If theblood pressure decreases to less than 90 mm Hg systolic, the patient is givena bolus of crystalloids at 10 mL/kg and colloids at 5 mL/kg. These bolusesare repeated until the blood pressure is greater than 90 mm Hg systolic. Thisprotocol helps identify hypotension and allows correction early. Dehydra-tion deficits are calculated after correction of perfusion deficits.

Fluid therapy for shock in small mammals

In the author’s experience, rabbits, ferrets, and other small mammalswith hypovolemia commonly present in the early decompensatory stage ofshock. The earlier compensatory stages of shock commonly seen in thedog and bird are not seen in the cat and the small mammal patient. Signs

283SHOCK AND CPCR IN SMALL MAMMALS AND BIRDS

of early decompensatory shock in the small mammal patient (as in the cat)are bradycardia, hypothermia, and hypotension.

The blood volume in the ferret and rabbit is 50 to 60 mL/kg, in contrastto 90 mL/kg in the dog. When intravascular volume deficits result in poorperfusion, it has been recommended in the past that crystalloids be admin-istered quickly in volumes equivalent to the animal’s blood volume. Resus-citation with crystalloids alone, however, can result in significant pulmonaryand pleural fluid accumulation. The resultant hypoxemia contributes to theshock pathophysiology.

Rabbits, ferrets, and small mammals are difficult to resuscitate from hy-potensive episodes. In the rabbit, when baroreceptors have detected inade-quate arterial stretch, it has been found that vagal fibers are stimulatedsimultaneously with sympathetic fibers [5,8–12]. As a result, the heart ratemay be normal or slow instead of the typical tachycardia demonstratedby the dog. This baroreceptor response may be similar in the ferret and inother small mammals. In the author’s experience, normal ferrets and rabbitshave heart rates between 180 and 240 beats per minute (bpm), systolic bloodpressures between 90 and 120 mm Hg, and temperatures between 100�F and102�F (37.7�C–38.8�C).

Most ferrets, rabbits, and small mammals presented for hypovolemicshock demonstrate heart rate lower than 200 bpm, hypotension (systolicblood pressure less than 90 mm Hg), and hypothermia (temperature lessthan 98.0�F [36.6�C]). Because cardiac output is a function of contractilityand rate, the compensatory response to shock normally seen in dogs andbirds is most likely blunted in ferrets, rabbits, and small mammals. The hy-perdynamic signs of shock seen in the dog and bird are not typically seen inthe cat, ferret, rabbit, and small mammals. Shock in the cat, rabbit, ferret,and small mammal is most commonly decompensatory, manifested by nor-mal heart rate or bradycardia (less than 180 bpm), hypothermia (tempera-ture lower than 98.0�F [36.6�C]), weak or nonpalpable pulses withhypotension, and profound mental depression. The mucous membranesare gray or white and capillary refill is not evident. The bradycardia andlow cardiac output contribute to hypothermia, and hypothermia accentu-ates the bradycardia.

Resuscitation from hypovolemic shock can be safely accomplished witha combination of crystalloids, colloids, and rewarming procedures. In thehypovolemic ferret, rabbit, and small mammal, a bolus infusion of isotoniccrystalloids is administered at 10 to 15 mL/kg. Hetastarch is administered at5 mL/kg intravenously over 5 to 10 minutes. The blood pressure is checked,and once it is greater than 40 mm Hg systolic, only maintenance crystalloidsare given while the patient is aggressively warmed. The warming should bedone within 1 to 2 hours with warm water bottles, forced air heating blan-kets, and warming the intravenous fluids. Intravenous fluid warmers facili-tate core temperature warming (Elltec Warmel WL-1, Gaymar IndustriesInc.; Oakland Park, NY).

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Once the rectal temperature approaches 98.0�F, it seems that the adren-ergic receptors begin to respond to catecholamines and fluid therapy. Tem-peratures during this rewarming phase must be checked frequently in allexotic species (especially ferrets) to prevent hyperthermia. Once the animal’srectal temperature has increased to 98.0�F, the blood pressure is rechecked,and crystalloid (10 mL/kg) with hetastarch at 5 mL/kg increments can berepeated over 15 minutes until the systolic blood pressure increases togreater than 90 mm Hg (systolic). The rectal temperature must be main-tained as needed by a warm incubator and warmed fluids. When the systolicblood pressure is greater than 90 mm Hg, the rehydration phase of fluid re-suscitation begins. A continuous rate infusion (CRI) of hetastarch at 0.8mL/kg/h is continued during the rehydration phase. If end point parameters(normal blood pressure, heart rate, mucous membrane color, and CRT) arestill not obtained, the animal is evaluated and treated for causes of nonre-sponsive shock (eg, excessive vasodilation or vasoconstriction, hypoglyce-mia, electrolyte imbalances, acid–base disorder, cardiac dysfunction,hypoxemia).

If cardiac function is normal, and glucose, acid–base, and electrolyte ab-normalities have been corrected, treatment for nonresponsive shock is con-tinued. Oxyglobin has not been approved for use in the cat, ferret, rabbit, orsmall mammal, but it has been used successfully at the author’s hospitalwhen given in small-volume boluses. Titrate 2-mL/kg boluses given over10 to 15 minutes until normal heart rate and blood pressure (systolic bloodpressure greater than 90 mm Hg) are obtained. This is followed by a contin-uous-rate infusion of Oxyglobin at 0.2 to 0.4 mL/kg/h. When Oxyglobin isnot available the author has used the vasopressor dopamine at 5 to 10 mcg/kg/min. When Oxyglobin is not available for treatment of refractory hypo-tension, the author has used 7.5% hypertonic saline at 5 mL/kg bolus givenslowly over 10 minutes. Vasopressors such as dopamine or norepinephrinecan be used to treat refractory hypotension; however, when using the pro-tocol mentioned, the author has never had to use these drugs in smallmammals.

Dehydration deficits are assessed when perfusion parameters are normal.Replacement of dehydration deficits is done with the use of isotonic crystal-loids. This is discussed in the rehydration section that follows.

Glucocorticoids in shock

The use of glucocorticoids in the treatment of shock is controversial.These drugs have been extensively investigated in the shock syndrome. Al-though they have repeatedly shown promise in some experimental studies,they have not shown consistent efficacy in clinical shock syndromes. Theside effects of immunosuppression, increased risk for infection, hyperglyce-mia, and gastric ulceration, may outweigh their benefits. Their use in hem-orrhage and hypovolemia is not currently recommended.

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Sodium bicarbonate in shock

The most important method of correction of severe metabolic acidosis isaimed at increasing the pH through increasing the extracellular fluid pH.Crystalloid fluids containing lactate, acetate, and gluconate (eg, Plasma-Lyte, Normasol R, lactated ringers solution (LRS)) are considered animportant means of increasing the alkalinity of the extracellular fluid. Cor-rection of acidemia initially begins with correction of the patient’s perfusionand hydration status through the use of fluid therapy.

When faced with severe acidemia resulting from lactic acidosis and whenaggressive measures to improve oxygen delivery and reverse tissue hypoxiahave already been initiated without improvement (ie, optimal fluid resuscita-tion), cautious use of sodium bicarbonate may be used. Blood gas parametersshould be carefully monitored if bicarbonate therapy is deemed necessary.

Fluid therapy for dehydration deficits in small mammals and birds

Once immediate life-threatening perfusion deficits are corrected, provideadditional fluid based on estimated percentage of dehydration and mainte-nance needs. The percentage of dehydration can be subjectively estimatedbased on the presence and degree of loss of body weight, mucous membranedryness, decreased skin turgor, sunken eyes, and altered mentation. Theseparameters are largely subjective because they can also be affected by de-creased body fat and increased age. Four percent to 6% dehydration is es-timated based on increased skin tenting, dry oral mucous membranes, andnormal pulses. Ten percent dehydration is evidenced by severe skin tenting,very dry mucous membranes, and dry eyes. Greater than 10% dehydrationis also accompanied by signs of hypovolemic shock.

To determine the volume of fluid required for rehydration, use the for-mula: Volume (L) ¼ hydration deficit � body weight (kg) � 1000 mL.For example, a 2-kg rabbit that is 10% dehydrated requires 0.1 � 2 �1000 mL, or 200 mL of fluids for rehydration. Dehydration deficits areadded to daily maintenance fluid requirements; then estimate ongoing los-ses. Maintenance requirements for the small mammal and bird are higherthan those required for dogs and cats because of their high metabolicrate, and are estimated at 3 to 4 mL/kg/h. The small mammal and bird re-quire larger maintenance volumes because of their high metabolic rates.Eighty percent of the calculated fluid deficit can be replaced in the first 24hours. Usually acute losses are replaced over 6 to 8 hours and chronic lossesover 12 to 24 hours. After successfully treating hypovolemic shock and re-placing fluid deficits estimated based on the percentage of dehydration,one should administer maintenance fluids until the mammal or bird canmaintain hydration on its own, provided no ongoing losses are present.The adage, ‘‘As soon as the gut works, use it,’’ is recommended for early en-teral feeding. Enteral feeding decreases intestinal cellular death and

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subsequent bacterial translocation leading to sepsis. Enteral feedingamounts can be used as part of the animal’s maintenance requirementsand should be included in the calculation of fluid volumes required. Enteralfeeding is discussed in the articles in this issue for each species.

Cardiopulmonary-cerebral resuscitation

The goal of cardiopulmonary resuscitation (CPR) is the restoration ofspontaneous circulation. In the 2000s, the American Heart Associationchanged the guidelines to include the preservation of neurologic functionas a goal of successful resuscitation. The term cardiopulmonary-cerebral re-suscitation was adopted. The most recent International Heart Associationguidelines for CPCR and emergency cardiac care in humans were publishedin 2004. Basic life support consists of the ABC approach (airway, breathing,circulation). Advanced life support consists of electrocardiographic identifi-cation of the arrest rhythm, defibrillation, fluid and drug administration,and postresuscitative care. A crash cart should be readily available with sup-plies (ie, drugs on Table 1) to maximize the chances of a successful outcome.There are anatomic differences in avian species and small mammals, andtherefore guidelines for CPCR are discussed for each species. This sectionreviews the American Heart Association’s CPCR guidelines of 2000 and ex-trapolates these principles to small mammals and birds.

Table 1

Quick reference chart for avian and small mammal CPCR drugs

Drug (conc.)

Weight (g)

Weight (kg) Dose 25 mL 50 100 1 2

Epi low (1:10,000)

(0.1 mg/mL)

0.01 mg/kg 0.0025 0.005 0.01 0.1 0.2

Epi high (1:1000)

(1 mg/mL)

0.1 mg/kg 0.0025 0.005 0.01 0.1 0.2

Atropinea

(0.54 mg/mL)

0.02 mg/kg 0.001 0.002 0.004 0.037 0.074

Glycopyrrolate

(0.2 mg/mL)

0.01 mg/kg 0.0025 0.005 0.01 0.1 0.2

Glucose (50%) 1 mL/kg dilute

50% with saline

0.025 0.05 0.1 1 2

Calcium

(100 mg/mL)

50 mg/kg 0.01 0.025 0.05 0.5 1

Doxapram

(20 mg/mL)

2 mg/kg 0.0025 0.005 0.01 0.1 0.2

Vasopressin

(20 U/mL)

0.8 u/kg 0.001 0.002 0.004 0.04 0.08

External defib 2–10 J/kg n/a n/a 1 2 4

a Atropine (onset of action, 15–30 s) is not recommended in rabbits, because many possess

serum atropinesterase and dose is unpredictable. Increasing the dose of atropine increases the

risk for severe tachycardia and increases the risk for ventricular arrhythmias. Use glycopyrro-

late (onset of action, 30–45 s) in rabbits.

287SHOCK AND CPCR IN SMALL MAMMALS AND BIRDS

Effectiveness of cardiopulmonary-cerebral resuscitation

The presence of palpable pulses is not an indication of adequate bloodflow. Although palpable pulses may evaluate the response to CPR, theydo not indicate the adequacy of organ perfusion during CPR. Two measure-ments described in the article by Lichtenberger and Ko in this issue on mon-itoring, end-tidal CO2 and blood gas measurements, can provide a moreaccurate assessment of organ perfusion.

The excretion of carbon dioxide in exhaled gas is a function of pulmonaryblood flow (cardiac output), and thus the level of CO2 in exhaled gaschanges in direct proportion to changes in cardiac output. End-tidal CO2

should be used to monitor cardiac output during CPR. A steady increasein end-tidal CO2 during CPR is more likely to be associated with a successfuloutcome. When end-tidal CO2 does not increase to greater than 10 mm Hgafter a resuscitation time of 15 to 20 minutes, the resuscitative effort is un-likely to be successful [13]. The common practice of monitoring arterialblood gases during CPR should be abandoned in favor of monitoring ve-nous blood gases. Venous blood gases represent the oxygenation andacid–base status of the peripheral tissues [13–17]. Arterial blood can showa respiratory alkalosis, whereas venous blood shows a metabolic acidosisduring CPR [13–17].

Failure to regain consciousness in the first few hours after CPR is nota harbinger of prolonged or permanent neurologic impairment [13–17].Coma that persists longer than 4 hours after CPR, however, carriesa poor prognosis for full neurologic recovery.

Several brainstem reflexes can have prognostic value in patients that donot regain consciousness after CPR, but none can match the predictive valueof the papillary light reflex (PLR). Absence of the PLR after 1 or more daysof coma indicates little or no chance for neurologic recovery. This reflex hasno prognostic value in the first 6 hours after CPR, because it can be tran-siently lost and then reappear [13–17]. Finally, the resuscitation drugs atro-pine and epinephrine can produce papillary dilation, but these agents do notinterfere with the pupillary response to light [13–17].

Cardiopulmonary-cerebral resuscitation in birds

The prognosis for respiratory arrest, especially when caused by isofluraneanesthesia overdose, is good. Cardiac arrest in birds carries a poor progno-sis, because direct compression of the heart is not possible because of theoverlying sternum. Because birds do not have a diaphragm, closed-chestcompressions cannot use the thoracic pump mechanism to increase overallnegative intrathoracic pressure. Anesthetized birds should always be moni-tored using an electrocardiogram and Doppler blood pressure (BP) mea-surement. Early recognition of cardiovascular instability is imperative inavian species. If cardiopulmonary arrest occurs when a bird is anesthetized,administration of anesthesia should be stopped immediately. If the bird is

288 LICHTENBERGER

masked, intubate and initiate positive-pressure ventilation with 100% oxy-gen. Alternatively, positive-pressure ventilation can be achieved by way ofplacement of an air sac cannula. Administer doxapram (0.2 mL for a largebird and 0.1 mL for a small bird intramuscularly) to stimulate the respira-tory centers. In the author’s experience, birds commonly become bradycar-dic before a cardiac arrest.

Use atropine (see Table 1) for a vagolytic effect to increase the heart rate.Epinephrine (0.01 mg/kg 1:10,000 solution ¼ 0.1 mg/mL) and atropine (0.02mg/kg) can be given intravenously, intraosseously, or by way of the endotra-cheal route (using a tom cat catheter inserted down the endotracheal tubeand doubling the dose used for intravenous administration). Also dilutethe drug with sterile saline to a volume of 1 mL per 100 g body weight.). In-tracardiac injections are no longer recommended by the American Heart As-sociation because of the risk for lacerating coronary vessels, causinghemopericardium or intractable arrhythmias [18].

Vasopressin is a nonadrenergic agent that causes pronounced vasocon-striction by way of direct stimulation of vasopressin (V1) receptors on vas-cular smooth muscle [18]. It has been suggested that a single dose ofvasopressin (see Table 1) may be considered in veterinary CPCR for pulse-less electrical activity or asystole. Although the pharmakinetics of this drughave been explored in mammals, there are currently no data available forthe avian species. Fluids should be administered to hypovolemic patientsbut avoided in euvolemic patients. There are no studies documenting the ef-ficacy of electrical defibrillation, and therefore it must be used with caution.An electrocardiogram and Doppler BP measurement help determine rhythmand pulse quality, respectively.

Intracardiac injections should be avoided because of the risk for lacerat-ing coronary vessels. An electrocardiogram, Doppler BP measurement, andend-tidal CO2 levels can be used to evaluate the effectiveness of cardiopul-monary resuscitation (Fig. 1).

Cardiopulmonary-cerebral resuscitation in small mammals

Anesthesia-related arrests represent one of the more treatable causes ofarrest in veterinary patients. Doxapram is given as a respiratory stimulantwith respiratory arrest.

In the author’s experience, most small mammals become bradycardic be-fore respiratory arrest while under inhalant anesthesia. The inhalant anes-thesia should be turned off and the animal should be intubated or ifintubated, start ventilating with 100% oxygen. Most small mammals otherthan the ferret are difficult to intubate (see intubation methods in anotherarticle by Lichtenberger and Ko in this issue), and therefore the author rec-ommends the following considerations:

1. If you are unable to intubate, consider forced high-flow oxygenventilation using a tight-fitting mask over the nose and mouth.

289SHOCK AND CPCR IN SMALL MAMMALS AND BIRDS

Positive-pressure ventilation should be provided using 100% oxygen ata rate of 20 to 30 breaths per minute. The disadvantage of this techniqueis accumulation of gastric air and bloating that can limit diaphragmmovement.

Fig. 1. Cardiopulmonary-cerebral resuscitation in birds and small mammals.

290 LICHTENBERGER

2. The second technique is to perform a tracheotomy. This procedure issimilar to that described in dogs and cats [19].

Cardiac arrest involves cessation of effective circulation and is recognizedby the loss of consciousness and collapse. A palpable pulse is not felt, themucous membranes are pale or cyanotic, and respirations commonly cease(ie, cardiopulmonary arrest). Immediate basic life support principles (ie,ABCs) should be initiated. The animal is intubated and ventilated with100% oxygen. The chest compressions of 80 to 100 times per minute directlycompress the myocardium, which leads to increased cardiac output. It is im-portant that both hands be placed on each side of the chest with compres-sions done at the widest portion of the chest. The duration of thecompression should take up half of the total compression–release cycle.

The team should continually assess their efforts at CPR. Check to see ifthe efforts are generating a palpable pulse. If no pulse is felt, increase theforce of chest compressions and assess the electrocardiogram. Different car-diac arrhythmias may require specific treatments. During cardiac arrest andresuscitation, progressive ischemia and acidosis are present. Epinephrine hasroutinely been the vasopressor of choice for ventricular fibrillation, asystole,and pulseless electrical activity (PEA); however, epinephrine and other cat-echolamines lose much of their effectiveness as vasopressors in the hypoxicand acidotic body state. Successful resuscitation depends on coronary perfu-sion being adequate. Coronary perfusion pressure greater than 15 mm Hg isbelieved to be a predictor of return of spontaneous circulation. The use ofvasopressin is today used as a possible consideration for asystole, PEA,and ventricular fibrillation. The addition of vasopressin is first given duringthe acidotic state and then epinephrine is added soon after. This may im-prove rates of restoration of spontaneous circulation and survival. Vaso-pressin is inexpensive. The use of vasopressin in the treatment of shockstates and for CPCR should be considered in the veterinary patient. The au-thor has used the drug in small-animal CPCR during asystole in a case ofcardiac arrest in a rabbit. There was an immediate return of a heart beatand blood pressure. One dog lived to discharge. The rabbit did eventuallydie from other chronic disease processes. The author recommends that theclinician consider administering vasopressin during asystole in small mam-mals and birds. Consider vasopressin use during CPCR with other rhythms(ventricular fibrillation, PEA) refractory to epinephrine, defibrillation, andatropine.

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