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Shock
5. SHOCK Ronald S. Walton, D.v.M.
1. Define shock in small animals. Shock is a critical imbalance between the delivery of oxygen and nutrients to the cell and utilization of oxygen and nutrients by the cell. Inadequate tissue perfusion and removal of cellular waste products lead to a failure of oxidative metabolism that can involve deficits of oxygen delivery, transport, utilization, or a combination of all three. Shock may be any syndrome, disease state, or injury that results in a critical decrease in effective blood flow. Lack of effective blood flow leads to derangement in cellular metabolism and ultimately cell death. When left unchecked, shock results in global cellular dysfunction, leading to entire organ dysfunction, progressing to multiple organ dysfunction and failure, and culminating with death. 2. What are the immediate concerns for a patient in shock? The three most important concepts in dealing with shock are summarized in the acronym VIP: V = Ventilation to ensure a patent airway and maximize oxygenation and oxygen carrying capacity of the blood. I = Infusion of fluids to restore vascular volume. P = Maintenance of myocardial pumping function to restore cardiac output and blood flow. 3. Name the four pathophysiologic classifications of shock. 1. Hypovolemic 3. Distributive 2. Cardiogenic 4. Traumatic 4. Give an example of each of the four classifications of shock, and note which is most commonly seen in small animals. Blood volume, vascular resistance, vascular capacitance, and pump function determine the pattern of blood flow. Each of the four pathophysiologic classifications can be related to one or more of these determinants. Hypovolemic shock is the most common form of shock in small animals. A typical patient has volume loss due to hemorrhage, severe volume loss, third spacing of fluids, or volume loss due to diuresis, as in severe diabetic ketoacidosis. Cardiogenic shock is a form of shock seen in heart failure characterized by pump failure and high central venous pressures. Pump failure may be related to cardiomyopathy, arrhythmias, and valvular abnormalities. The key features of cardiogenic shock are systemic hypotension, elevated heart rate, increased central venous pressure, increased oxygen extraction, and decreased cardiac output. The pump failure may be related to valvular and/or myocardial incompetence. In some classifications, obstructive forms of shock, such as heartworm disease, pericardial tamponade, and pulmonary thromboembolism, are also classified as cardiogenic shock because of a general failure of forward blood flow. Distributive shock is a form of vasogenic shock seen with sepsis, anaphylaxis, neurogenic causes, and adverse pharmacologic/toxic reactions. Traumatic shock is a form of shock associated with extensive tissue trauma. Hypovolemic shock is often a component of traumatic shock. A traumatic insult causes extensive capillary damage with extensive plasma loss in the tissues. Extensive tissue injury also initiates an inflammatory response by the body due to release of endogenous mediators of inflammation. Pain associated with extensive injury can result in inhibition of the vasomotor center and interfere with the normal vasoconstriction response.
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5. During the course of the physical examination, how do you determine the classification of shock? A patient with hypovolemic, cardiogenic, or obstructive shock typically has cool extremities, pallor of the mucous membranes, hypotension, and tachycardia. A patient with distributive shock also may present in this manner during the late stages. Typically, a patient with distributive shock has warm extremities, hyperemic mucous membranes, normotension to hypertension, and tachycardia. 6. What constitutes a minimal database before initiation of therapy in an emergent patient with clinical signs of shock? Most patients present with some form of hypovolemic shock. Before initiation of fluid therapy, hematocrit (packed-cell volume [PCY]), total solids, blood glucose, blood urea nitrogen (BUN; Azostick), and urine specific gravity (USG) should be considered the minimal database. All of the tests except USG (2 drops of urine) can be performed on the blood remaining in the hub of the catheter as it is placed in the patient (4-5 drops of blood). This small amount of information provides a good idea about patient status at the beginning of therapy. If possible, one should draw a sample large enough to provide adequate evaluation beyond these basic parameters to understand the physiologic status of the animal. 7. Describe the changes seen in measurement of packed-eell volume (hematocrit) immediately after significant acute hemorrhage. What changes occur with time? PCY immediately after a hemorrhagic episode may appear normal. With time the PCY falls as a result of loss of red cell mass and redistribution of interstitial and intracellular volumes to the vascular space. Once the hemorrhagic episode is stabilized, the final change in PCY can take hours to develop. Early overinterpretation of values can underestimate the severity of the hemorrhagic episode. Classically, the PCY change is 14-36% by the end of 2 hours, 36-50 % by the end of 8 hours, and only 63-77% by the end of 24 hours. Always expect that the actual red-cell mass is lower than measured in an acute hemorrhagic shock patient in the first day or two of therapy. 8. What is the core-to-toe-web temperature gradient? How is it used? Toe web temperature is typically :5: 4°C less than core temperature. Use of the gradient between core temperature and toe web temperature gives an approximation of peripheral perfusion. As perfusion decreases, toe web temperature decreases and the gradient between core and toe web increases. Similarly, as perfusion improves, the gradient decreases. Core temperature - toe web temperature = gradient
9. What two parameters are used to evaluate the amount of oxygen available to an animal? Which is the more important? Why? Partial pressure of oxygen in arterial blood (Pa02) and arterial oxygen content (Ca0 2) are used to evaluate available oxygen. Ca02 is more important because it represents the total amount of oxygen contained in a sample of blood. Oxygen content represents both oxygen bound to hemoglobin and oxygen dissolved in plasma. The measured amount of oxygen bound to hemoglobin is the primary determinant of oxygen content; oxygen dissolved in plasma plays a very small role. Pa02 measures only the amount of oxygen dissolved in plasma and does not depend on hemoglobin concentration. Therefore, a severely anemic animal may have a normal Pa02 but considerable oxygen debt due to low Ca02' 10. What is the basic premise of oxygen delivery? Why is it so important? Oxygen delivery is the product of cardiac output, oxygen-carrying capacity of the blood, and arterial saturation. The product of these factors is crucial, and each parameter warrants careful attention. Although we tend to focus our efforts on cardiovascular volume resuscitation to improve output, we cannot forget the critically important role that correction of hemoglobin concentration and oxygen saturation plays in the overall outcome. High-volume resuscitation with non-oxygencontaining fluid temporarily improves oxygen delivery by mechanically enhancing cardiac output. This effort eventually fails as oxygen content continues to decrease.
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11. What is central venous pressure? How is it measured? Central venous pressure (CVP) is the measure of the luminal blood pressure in the intrathoracic jugular vein as it enters the right atrium. The CVP represents a measure of the relative ability of the heart to pump the venous return. Measurement of CVP can be expressed in centimeters of water (cmH 20) or millimeters of mercury (mmHg). Typically, CVP is measured with a water column manometer in veterinary patients. An imaginary line is drawn from the estimated region of the right atrium and the manometer to serve as the zero reference mark. The difference between the meniscus of the water column and the zero point is the measured CVP (cmH 20). However, a standard mechanical pressure transducer can be applied to the central venous catheter to measure the CVP directly (mmHg). Most published values in dogs and cats are expressed as cmHzO. To convert mmHg to cmHzO, multiply the value by 1.36. Note: In cats, caudal vena caval pressures can serve as an accurate indicator of CVP when a jugular catheter cannot be placed.
12. What is normal CVP in dogs and cats? The normal CVP for dogs and cats ranges from 0-10 cmH 2 0. Values < 0 cmH 20 indicate relative hypovolemia and values> 10 cmH 20 indicate relative hypervolemia.
13. What are the four determinants of CVP? Intrathoracic pressure, intravascular volume, right ventricular function, and venous tone.
14. What are the body's initial hemodynamic responses to volume loss? The loss of effective circulating volume leads to a decrease in arterial systolic, diastolic, and pulse pressure along with an increase in pulse rate and a decrease in cardiac stroke volume, which leads to a decrease in cardiac output. Reflex tachycardia ensues in an attempt to maintain blood pressure. In response 10 decreasing cardiac output, baroreceptor-mediated initiation of the sympathoadrenal reflex occurs. This reflex initiates the release of norepinephrine, epinephrine, and cortisol from the adrenal gland, leading to increased cardiac output. Increases in contractility, heart rate, and venous lone are responsible for the initial increase in cardiac output. Arteriolar vasoconstriction in skin, muscle, kidney, and gastrointestinal tract allows blood to be shunted centrally to the heart and brain. Decreased renal blood flow secondary to activation of the renin-angiotensinaldosterone system reduces urinary output and fluid loss and increases retention of sodium and water. The release of antidiuretic hormone and aldosterone also promotes volume conservation. Cortisol and catecholamines promote release, mobilization, and conversion of energy substrates to help meet metabolic demands. The diagram below illustrates these initial steps.
Compensatory responses to volume loss.
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15. Blood flow to which organ is the most highly preserved of all organ systems in shock? The brain.
16. What are the main consequences of the cellular energy deficit in patients with shock? Lack of oxygen delivery leads to a general failure of energy-dependent functions of the cell. The end result is cell swelling and death. Adenosine triphosphate (ATP) is the primary "currency" of metabolism, and failure to deliver adequate oxygen and nutrients to the cell slows and stops the production of this vital chemical. Life itself depends on continual production and availability of ATP to run the energy-dependent mechanisms of cell function. Normal aerobic metabolism yields the highest amount of energy (ATP) per gram of nutrients, whereas anaerobic metabolism yields the least. Anaerobic metabolism also increases the yield of metabolic waste products, especially pyruvate and lactate. The switch of global energy production from oxygendependent (aerobic) to oxygen-independent (anaerobic) metabolism results in only a short-term solution for inadequate energy product. As the shock episode is prolonged, so are the deleterious changes. The energy-dependent sodium-potassium-ATPase pump of the cell membrane evenutally fails, leading to ionic gradient failure and loss of transmembrane potential. As a result of ionic pump failure, intracellular accumulations of ions and water occur. These cells swell in response, leading to cell membrane disruption and cell death.
17. What laboratory parameter can be used to assess tissue perfusion in shock? Lactate. Mild systemic hypoperfusion has been associated with lactate levels of 3-5 mmoUL; moderate hypoperfusion with values of 5-10 mmoVL and severe hypoperfusion states often demonstrate values greater than 10 mmoUL. Plasma lactate concentration generally falls with adequate volume resuscitation. While not universally available, plasma lactate levels can be a useful guide in directing therapy. 18. What is GI PiCO z? GI PiCO z is gastrointestinal intraluminal partial pressure of carbon dioxide. Monitoring involves placement of a tonometry catheter into the lumen of the 01 tract (colon, stomach, or small intestine). Measurements of GI PiC0 2 reflect the energy status of the 01 mucosa. The 01 mucosa is at high risk for inadequate perfusion during shock and resuscitation. Measurement of this parameter can help guide adequacy of resuscitation. 19. Define systemic inflammatory response syndrome (SIRS). The systemic inflammatory response is a generalized inflammatory response to a variety of severe systemic insults. Current defining criteria for SIRS include two or more of the following: • Temperature> 103.5°F or < IOO.O°F • Heart rate> 160 beats/min (dog) or > 250 beats/min (cat) • Respiratory rate> 20 breaths/min or PaC02 < 32 mmHg • White blood cell count> 12,000 or < 4,000 cells or> 10% nucleated cells/band neutrophils 20. Describe the basic inflammatory components of shock. Inflammatory changes, which develop during shock, vary greatly. To some degree, however, all forms of shock have an aspect of inflammation. Ischemia and reperfusion are components of every form of shock state, regardless of etiology. In evaluating the ischemia-reperfusion aspect of shock, successful hemodynamic resuscitation initiates proinflammatory mediators, chemotactic cytokines, and activation of leukocytes. Once the animal is reperfused, we seldom recognize an inflammatory response, because rapid hemodynamic correction of hypovolemic and cardiogenic shock episodes results in a minimal inflammatory response. However, prolonged hypoperfusion and significant tissue trauma exhibit profound inflammatory changes during reperfusion. A systemic inflammatory response then results in elevated levels of proinflammatory mediators such as cytokines, eicosanoids, kinins, and complement. These substances activate endothelial cells and leukocytes. Activated endothelial cells and leukocytes can upregulate the expression of cellular adhesion molecules, integrins, and selectins, resulting in adhesion of activated leukocytes to
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endothelial cells. Activated endothelial cells also can release nitric oxide, which may induce substantial vasodilatation and exacerbate efforts to improve resuscitation. The activated leukocytes release destructive oxygen free radicals, which cause further damage to tissues and microcirculation. Although the hemodynamic components of shock are readily reversible, the systemic inflammatory components often are not. 21. What is septic shock? A form of distributive shock secondary to the systemic inflammatory response caused by severe infection. Bacteria or bacterial toxins cause the classic form. Other microorganisms that can initiate septic shock include fungal, protozoal, and viral organisms. The characteristic findings are hypotension and perfusion abnormalities that persist despite adequate fluid therapy. By definition, patients with clinical evidence of infection and signs of shock are in septic shock. 22. When should you suspect septicemia or septic shock? When patients present with tachycardia, hypotension, hypovolemia, fever or hypothermia, high or low white blood cell count, and signs of multiple organ involvement. In such patients, perfusion and cardiac output often fail to improve despite adequate fluid therapy. 23. What are the classic changes in systemic vascular resistance (SVR) and cardiac output in early septic shock? In early septic shock (hyperdynamic phase), SVR is decreased and cardiac output is increased. The increase in cardiac output is a compensatory response to the falling SVR. 24. What are the indications for sympathomimetic therapy in the treatment of septic shock? Sympathomimetic therapy is appropriate when aggressive fluid therapy (high CVP or high pulmonary wedge pressure [PWPj) has failed to restore tissue perfusion, pulse quality, arterial blood pressure, or cardiac output. The goals of therapy are to restore cardiac output and tissue perfusion, to increase oxygen delivery, to maintain systemic blood pressure in vital circulation, and to limit excessive vasoconstriction or vasodilatation. 25. Briefly discuss the sympathomimetic drugs commonly used to treat septic shock. Dobutamine is the drug of choice. It restores cardiac output and oxygen delivery more reliably than dopamine. Although it is a potent beta) and beta2 agonist, dobutamine has fewer alpha effects than dopamine. The usual dosage range is 5-l511glkg/min. Dopamine is also a potent beta agonist, but in addition it has strong alpha) and alpha2 effects as well as dopaminergic properties. Constant-rate infusion (CRI) at l-3llglkglmin enhances perfusion to renal and visceral circulation via dopaminergic effects. If dopamine is used for cardiovascular and blood pressure support, the dose is increased to 3-10 Ilglkg/min. This and higher doses of dopamine increase cardiac output and blood pressure. However, the renal and visceral perfusion-enhancing properties are often blunted or overridden at higher dosages. Other sympathomimetic drugs include epinephrine, norepinephrine, phenylephrine, dopexamine, and ephedrine. The first three agents cause profound vasoconstriction and tend to be reserved for the most refractory cases of hypotension. Dopexamine is principally a beta2 and dopaminergic agonist without alpha agonist activity. The usual dosage range is 5-20 Ilglkg/min by CRI. Dopexamine increases cardiac output, decreases peripheral vascular resistance, and improves visceral perfusion without the peripheral vasoconstriction effects of dopamine. 26. What is meant by the term ''vicious cycle of shock"? Prolonged shock triggers a cascade of events. Decreased cardiac output leads to decreased blood pressure. As the driving pressure decreases, so do peripheral perfusion and microcirculatory response. Poor venous return leads to decreased filling pressure for the heart. The resultant increase in myocardial work can lead 10 further failure of myocardial function secondary to decreased coronary perfusion. Prolonged tissue perfusion deficit leads to microcirculatory damage, cellular aggregation, microcirculatory obstruction, and cellular hypoxia. Loss of cellular ionic gradients due to
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energy-dependent ionic pump failure and increased intracellular accumulation of ions and fluid cause cell swelling and membrane disruption, which lead to loss of intracellular fluids and ions. An overall metabolic acidosis and accumulation of toxic mediators further destroy the metabolic machinery. Normal compensatory mechanisms fail, resulting in decreased cardiac function and failure to maintain sympathetically induced arterial and venous vasoconstriction. As the metabolic machinery of the cell is destroyed and regulatory mechanisms meant to preserve homeostasis fail, no manner of resuscitation effort can restore the failing system and death results.
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27. How can septic shock and cardiogenic shock appear similar? In the hypodynamic (late) phases of septic shock, cardiac index is decreased and pulmonary capillary resistance is increased. Combined, these factors can markedly decrease cardiac output and increase CVP, appearing quite similar to right heart failure. Patients typically have cool extremities due to decreased perfusion and tachycardia. The prognosis is poor.
28. What are the primary goals of treatment for septic shock? The primary goals are to maximize tissue oxygen delivery because of the increased oxygen demand. You must improve the hemodynamic status and correct the underlying metabolic abnormalities. Then you must aggressively seek and eliminate the source of infection.
29. What are the primary goals of treating hemorrhagic shock? Stop continued loss, restore volume, and restore oxygen-carrying capacity.
30. What are the key factors in the treatment of cardiogenic shock? Reduction of preload and/or afterload, improvement of myocardial contractility, and control of serious arrhythmias.
31. What is neurogenic shock? Neurogenic shock results from acute loss of sympathetic vascular tone, which leads to arteriolar and venous dilatation. Neurogenic shock may result from spinal cord injury and even excessive
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administration of general anesthetics. This form of vasogenic or distributive shock may be refractory to standard fluid therapy. An alpha agonist may be needed to treat refractory hypotension.
32. What is anaphylactic shock? A type of vasogenic shock characterized by an antigen-antibody reaction that occurs immediately after a sensitized patient is exposed to the antigen. The resulting reaction is a decrease in venous return due to venous dilation, which pools blood in capacitance vessels. Accompanying venous dilation is systemic arterial dilation, which decreases systemic blood pressure. Capillaries become increasingly permeable, and hypovolemia results from the capillary leak of plasma into tissues. Angioedema, laryngeal edema, bronchospasm, and urticaria also may be seen.
33. What type of shock is pericardial tamponade? Obstructive, pericardial tamponade physically compresses the heart within the pericardial sac. This compression limits the amount of blood that can enter the heart during diastole and subsequently limits the stroke volume, leading to a decrease in cardiac output.
34. What happens to the GI tract in shock? What protective methods can be used? The GI tract is prone to mucosal ulceration and sloughing during periods of shock when visceral blood flow is reduced. The mechanism of GIT damage is complex and multifactorial, ranging from loss of normal protective barriers and self-destruction due to hydrogen ions, pancreatic proteases, and bile acids to mucosal cell death due to hypoxia. Ultimately, mucosal permeability is increased, and tissue penetration of acid, bacteria, and endotoxin exacerbates the condition. Protective efforts are focused on ensuring or reestablishing adequate visceral perfusion and oxygenation. Monitoring perfusion can be instituted with a GI tonometry catheter (GI-PiCO z; see question 18). The protective actions of Hz blockers, proton pump inhibitors, mucosal patching, and mucous stimulatory drugs are controversial, but all can aid in the treatment and amelioration of signs and symptoms. Pharmacologic manipulations alone, however, cannot take the place of adequate restoration of visceral circulation, perfusion, and oxygen delivery.
35. Briefly discuss the development of acute renal faDure in shock. Renal failure is commonly seen in shock patients. Depending on the stage and degree of renal injury, patients may present with any of the following: initial high urine output, low tubule pressure and sodium retention, damage to renal parenchyma, renal dysfunction, fulminant failure, and/or anuria. During shock, glomerular filtration rate falls and renal cortical blood flow is reduced. Renal hypoperfusion leads to ischemic damage, causing tubular necrosis and edema, which often obstructs tubules. Loss of renal tubular function leads to increasing metabolic acidosis, hyperkalemia, and impaired clearance of drugs and other compounds. As the renal perfusion pressure continues to decline, further releases of renin, angiotensin, and aldosterone magnify the problem. Urine output typically is used as an index of adequate renal perfusion. When in doubt, a urinary catheter should be placed to measure urine output. The goal of treatment should be 1-2 ml/kglhr of urine. Fluid therapy is the hallmark of treatment. If volume therapy alone fails to restore urine output, aggressive efforts with diuretics and dopamine are indicated.
36. What does the term "shock lung" mean? Because they receive the entire cardiac output, the lungs are involved in the inflammatory components of shock more than any other system. Acute respiratory distress syndrome (ARDS) is the term used to describe lung injury caused by the systemic inflammatory response. Inflammatory mediators and activated leukocytes from throughout the body target the pulmonary vascular endothelium and cause an activation of the pulmonary vascular endothelium. Pulmonary capillaries can then become plugged by leukocytes. Activated leukocytes directly damage the capillary endothelium, exacerbating the inflammatory process. This exacerbation can lead to ventilation-perfusion mismatching, increased shunt fraction, and increased capillary leak.
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37. What are the characteristics of an ''ideal'' resuscitative fluid for patients in shock? The ideal fluid would be safe, readily available, reasonable in cost, and easy to administer; it would require no special handling, provide volume and vascular retention, and have the capability of oxygen carriage and delivery. 38. What is the fluid of choice for treating patients in shock? Fluid administration is the cornerstone of effective therapy for patients with noncardiogenic shock. Although the exact fluid may be controversial, depending on the author, the basic principle is the same. Crystalloids (containing sodium) are the initial fluid of choice. They are easy to administer, readily available, inexpensive, and effective. Shock initially should be treated aggressively with fluid containing an adequate amount of sodium because of the relatively high concentration of sodium in extracellular fluid. Readily available and commonly used isotonic solutions include 0.9% sodium chloride, lactated Ringer's solution, Plasmalyte, and Normosol-R. 39. Why may Plasmalyte or Normosol-R have an advantage over Ringer's lactate solution for patients in shock? Ringer's lactate solution uses lactate as its primary buffer, which depends on active hepatic metabolism for conversion to bicarbonate. In shock patients, hepatic metabolism can be markedly impaired. Normosol-R and Plasmalyte contain acetate and gluconate as their primary buffers. Acetate and gluconate are metabolized primarily by the skeletal muscle to bicarbonate. Although blood cell flow to skeletal muscle is decreased in shock, acetate and gluconate can be converted to bicarbonate easily as circulation is restored. As the circulatory system and peripheral perfusion are reestablished, the liver is presented with an excess of lactate to metabolize (lactic acidosis) and may not be able to do so adequately. 40. What is hypertonic saline? When is it used? Hypertonic saline is a crystalloid fluid with a supraphysiologic amount of sodium. The typical sodium concentration is 3-7%. A dose of 4-5 ml/kg of 7% hypertonic saline has been shown to be an effective acute volume expander in dogs. It acts by drawing water from the intracellular and interstitial spaces into the vascular compartment. These changes cause a rapid but transient increase in intravascular volume. When combined with a synthetic colloid such as dextran 70, the volume-expanding effects can be prolonged. The contraindications for hypertonic saline are hypernatremia, hyperosmolality, cardiogenic shock, and renal failure. Hypertonic saline is used only for the rapid emergency restoration of volume and must be followed with definitive treatment, because the effects of hypertonic saline are only temporary. 41. What volume of crystalloid fluid is used to resuscitate a shock patient? The volumes for cats and dogs are different in the published literature. In dogs, shock volumes of fluid are reported at 50-90 mllkg/hr or up to complete blood volume per hour. In cats, volumes are reported at 40-60 ml/kg/hr or approximately complete plasma volume per hour. The difference between cat and dog resuscitation volume is unclear in the literature. Typically these volumes should be regarded as indicators of volume "to be prepared to deliver" in an hour, but treatment should be titrated to the volume needed by the individual patient. A highly effective method is to deliver shock fluid volumes in one-fourth shock volume increments. One-fourth of the calculated shock volume is delivered every 15 minutes with monitoring of the deviation from the baseline packed cell volume and total protein. Few patients require 90 mllkg/hr using this method, and volume overload is unlikely. 42. What is a standard volume of infusion for a synthetic colloid solution in patients in shock? The standard volume of colloid, whether synthetic or natural, is generally 10-20 ml/kg/day. This volume is typically given over 4-6 hours but may be given faster if needed.
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Often the infusion of a synthetic colloid in the fluid therapy program allows a reduction in the crystalloid fluid requirement by 40-60%.
43. What is oxyglobin? When is it used in a shock patient? Oxyglobin is a member of a group of compounds know as hemoglobin-based oxygen carriers (HBOC). The molecule is polymer of bovine hemoglobin that recently was approved for use in dogs in the United States. The HBOCs have evolved from more than 50 years of research into acelluar blood replacement solutions. The oxygen-carrying characteristics of this product are similar to those of blood with several important differences. Oxyglobin binds and releases oxygen more readily than whole blood, requires no typing or cross-matching, requires no special administration set or filter, does not depend on levels of 2,3-diphosphoglycerate to regulate its oxygen-binding site, and is shelf-stable for more than I year at room temperature. Oxyglobin has demonstrated its effectiveness in restoring oxygen delivery in anemic dogs or dogs in hemorrhagic shock. Recent research has demonstrated that Oxyglobin administered at low doses improves oxygen delivery to tissues by increasing the transfer of oxygen across the interstitial fluid barrier and by reaching tissues that red blood cells cannot. Label directions must be followed closely. Oxyglobin has significant colloidal osmotic properties and can induce circulatory overload if administered too rapidly or in excess of recommended dosages.
44. What is the rationale behind low-volume resuscitation in hemorrhagic shock? The rationale is simple: administration of small volumes of fluids during traumatic or hemorrhagic shock reduces the risk of disrupting clotted vasculature and exacerbating hemorrhage until definitive care is available. Although this concept recently has been popularized based on one paper, no currently available data determine how low or for how long a patient can be maintained before irreversible shock will result. The efficacy and safety of this theory are unproved in the clinical setting and warrant further study. BIBLIOGRAPHY I. Aldrich J: Shock. In King L, Hammond R (eds): Manual of Canine and Feline Emergency and Critical Care. Cheltenham, UK, BSAVA, 1999, pp 23-36. 2. Astiz ME, Rackow EC, Weil MH: Pathophysiology and treatment of circulatory shock. Crit Care Clin 9: 183-203, 1993. 3. Crystal MA, Cotter SM: Acute hemorrhage: A hematologic emergency in dogs. Compend Cont Educ Pract Vet 14:60-68, 1992. 4. Ford SL, Schaer M: Shock syndrome in cats. Compend Cont Educ Pract Vet 15: 120-125, 1993. 5. Hansen B: Fluid therapy in the shock patient. Proceedings IVECCS VI, San Antonio, TX, 1998, pp 216-221 6. Haskins SC: Therapy for shock. In Bonagura JD (ed): Current Veterinary Therapy, vol. XIII. Philadelphia, wn. Saunders, 2000, pp 140-146. 7. Hughes D: Lactate measurement: Diagnostic, therapeutic, and prognostic implications. In Bonagura JD (ed): Current Veterinary Therapy, vol. XIII. Philadelphia, WB. Saunders, 2000, pp 140-146. 8. Kirby R: Septic shock. In Bonagura JD (ed): Current Veterinary Therapy, vol XII. Philadelphia, WB. Saunders, 1995, pp 139-146. 9. Kline lA. Shock. In Rosen D (ed): Emergency Medicine: Concepts and Clinical Practice, vol I. SI. Louis, Mosby, 1998 pp 86-106. 10. Rackow Ee. Astiz ME: Mechanisms and management of septic shock. Crit Care Clin 9:219-237, 1993. I I. Schertel ER, Muir WW: Shock: Pathophysiology, monitoring, and therapy. In Kirk RW (ed): Current Veterinary Therapy, vol X. Philadelphia, wn. Saunders, 1989, pp 316-330. 12. Walley KR, Wood LD: Shock. In Hall JB (ed): Principles of Critical Care. New York, McGraw-Hill, 1998, pp 277-301. 13. Ware WA: Shock. In Murtaugh RJ, Kaplan PM (eds): Veterinary Emergency and Critical Care Medicine. Chicago, Mosby-Year Book, 1992, pp 163-175. 14. Wingfield WE. How much fluid should you administer? Proceedings VECCS, 1997, pp 17-19.
1. Define shock in small animals. Shock is a critical imbalance between the delivery of oxygen and nutrients to the cell and utilization of oxygen and nutrients by the cell. Inadequate tissue perfusion and removal of cellular waste products lead to a failure of oxidative metabolism that can involve deficits of oxygen delivery, transport, utilization, or a combination of all three. Shock may be any syndrome, disease state, or injury that results in a critical decrease in effective blood flow. Lack of effective blood flow leads to derangement in cellular metabolism and ultimately cell death. When left unchecked, shock results in global cellular dysfunction, leading to entire organ dysfunction, progressing to multiple organ dysfunction and failure, and culminating with death. 2. What are the immediate concerns for a patient in shock? The three most important concepts in dealing with shock are summarized in the acronym VIP: V = Ventilation to ensure a patent airway and maximize oxygenation and oxygen carrying capacity of the blood. I = Infusion of fluids to restore vascular volume. P = Maintenance of myocardial pumping function to restore cardiac output and blood flow. 3. Name the four pathophysiologic classifications of shock. 1. Hypovolemic 3. Distributive 2. Cardiogenic 4. Traumatic 4. Give an example of each of the four classifications of shock, and note which is most commonly seen in small animals. Blood volume, vascular resistance, vascular capacitance, and pump function determine the pattern of blood flow. Each of the four pathophysiologic classifications can be related to one or more of these determinants. Hypovolemic shock is the most common form of shock in small animals. A typical patient has volume loss due to hemorrhage, severe volume loss, third spacing of fluids, or volume loss due to diuresis, as in severe diabetic ketoacidosis. Cardiogenic shock is a form of shock seen in heart failure characterized by pump failure and high central venous pressures. Pump failure may be related to cardiomyopathy, arrhythmias, and valvular abnormalities. The key features of cardiogenic shock are systemic hypotension, elevated heart rate, increased central venous pressure, increased oxygen extraction, and decreased cardiac output. The pump failure may be related to valvular and/or myocardial incompetence. In some classifications, obstructive forms of shock, such as heartworm disease, pericardial tamponade, and pulmonary thromboembolism, are also classified as cardiogenic shock because of a general failure of forward blood flow. Distributive shock is a form of vasogenic shock seen with sepsis, anaphylaxis, neurogenic causes, and adverse pharmacologic/toxic reactions. Traumatic shock is a form of shock associated with extensive tissue trauma. Hypovolemic shock is often a component of traumatic shock. A traumatic insult causes extensive capillary damage with extensive plasma loss in the tissues. Extensive tissue injury also initiates an inflammatory response by the body due to release of endogenous mediators of inflammation. Pain associated with extensive injury can result in inhibition of the vasomotor center and interfere with the normal vasoconstriction response.
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5. During the course of the physical examination, how do you determine the classification of shock? A patient with hypovolemic, cardiogenic, or obstructive shock typically has cool extremities, pallor of the mucous membranes, hypotension, and tachycardia. A patient with distributive shock also may present in this manner during the late stages. Typically, a patient with distributive shock has warm extremities, hyperemic mucous membranes, normotension to hypertension, and tachycardia. 6. What constitutes a minimal database before initiation of therapy in an emergent patient with clinical signs of shock? Most patients present with some form of hypovolemic shock. Before initiation of fluid therapy, hematocrit (packed-cell volume [PCY]), total solids, blood glucose, blood urea nitrogen (BUN; Azostick), and urine specific gravity (USG) should be considered the minimal database. All of the tests except USG (2 drops of urine) can be performed on the blood remaining in the hub of the catheter as it is placed in the patient (4-5 drops of blood). This small amount of information provides a good idea about patient status at the beginning of therapy. If possible, one should draw a sample large enough to provide adequate evaluation beyond these basic parameters to understand the physiologic status of the animal. 7. Describe the changes seen in measurement of packed-eell volume (hematocrit) immediately after significant acute hemorrhage. What changes occur with time? PCY immediately after a hemorrhagic episode may appear normal. With time the PCY falls as a result of loss of red cell mass and redistribution of interstitial and intracellular volumes to the vascular space. Once the hemorrhagic episode is stabilized, the final change in PCY can take hours to develop. Early overinterpretation of values can underestimate the severity of the hemorrhagic episode. Classically, the PCY change is 14-36% by the end of 2 hours, 36-50 % by the end of 8 hours, and only 63-77% by the end of 24 hours. Always expect that the actual red-cell mass is lower than measured in an acute hemorrhagic shock patient in the first day or two of therapy. 8. What is the core-to-toe-web temperature gradient? How is it used? Toe web temperature is typically :5: 4°C less than core temperature. Use of the gradient between core temperature and toe web temperature gives an approximation of peripheral perfusion. As perfusion decreases, toe web temperature decreases and the gradient between core and toe web increases. Similarly, as perfusion improves, the gradient decreases. Core temperature - toe web temperature = gradient
9. What two parameters are used to evaluate the amount of oxygen available to an animal? Which is the more important? Why? Partial pressure of oxygen in arterial blood (Pa02) and arterial oxygen content (Ca0 2) are used to evaluate available oxygen. Ca02 is more important because it represents the total amount of oxygen contained in a sample of blood. Oxygen content represents both oxygen bound to hemoglobin and oxygen dissolved in plasma. The measured amount of oxygen bound to hemoglobin is the primary determinant of oxygen content; oxygen dissolved in plasma plays a very small role. Pa02 measures only the amount of oxygen dissolved in plasma and does not depend on hemoglobin concentration. Therefore, a severely anemic animal may have a normal Pa02 but considerable oxygen debt due to low Ca02' 10. What is the basic premise of oxygen delivery? Why is it so important? Oxygen delivery is the product of cardiac output, oxygen-carrying capacity of the blood, and arterial saturation. The product of these factors is crucial, and each parameter warrants careful attention. Although we tend to focus our efforts on cardiovascular volume resuscitation to improve output, we cannot forget the critically important role that correction of hemoglobin concentration and oxygen saturation plays in the overall outcome. High-volume resuscitation with non-oxygencontaining fluid temporarily improves oxygen delivery by mechanically enhancing cardiac output. This effort eventually fails as oxygen content continues to decrease.
30
Shock
11. What is central venous pressure? How is it measured? Central venous pressure (CVP) is the measure of the luminal blood pressure in the intrathoracic jugular vein as it enters the right atrium. The CVP represents a measure of the relative ability of the heart to pump the venous return. Measurement of CVP can be expressed in centimeters of water (cmH 20) or millimeters of mercury (mmHg). Typically, CVP is measured with a water column manometer in veterinary patients. An imaginary line is drawn from the estimated region of the right atrium and the manometer to serve as the zero reference mark. The difference between the meniscus of the water column and the zero point is the measured CVP (cmH 20). However, a standard mechanical pressure transducer can be applied to the central venous catheter to measure the CVP directly (mmHg). Most published values in dogs and cats are expressed as cmHzO. To convert mmHg to cmHzO, multiply the value by 1.36. Note: In cats, caudal vena caval pressures can serve as an accurate indicator of CVP when a jugular catheter cannot be placed.
12. What is normal CVP in dogs and cats? The normal CVP for dogs and cats ranges from 0-10 cmH 2 0. Values < 0 cmH 20 indicate relative hypovolemia and values> 10 cmH 20 indicate relative hypervolemia.
13. What are the four determinants of CVP? Intrathoracic pressure, intravascular volume, right ventricular function, and venous tone.
14. What are the body's initial hemodynamic responses to volume loss? The loss of effective circulating volume leads to a decrease in arterial systolic, diastolic, and pulse pressure along with an increase in pulse rate and a decrease in cardiac stroke volume, which leads to a decrease in cardiac output. Reflex tachycardia ensues in an attempt to maintain blood pressure. In response 10 decreasing cardiac output, baroreceptor-mediated initiation of the sympathoadrenal reflex occurs. This reflex initiates the release of norepinephrine, epinephrine, and cortisol from the adrenal gland, leading to increased cardiac output. Increases in contractility, heart rate, and venous lone are responsible for the initial increase in cardiac output. Arteriolar vasoconstriction in skin, muscle, kidney, and gastrointestinal tract allows blood to be shunted centrally to the heart and brain. Decreased renal blood flow secondary to activation of the renin-angiotensinaldosterone system reduces urinary output and fluid loss and increases retention of sodium and water. The release of antidiuretic hormone and aldosterone also promotes volume conservation. Cortisol and catecholamines promote release, mobilization, and conversion of energy substrates to help meet metabolic demands. The diagram below illustrates these initial steps.
Compensatory responses to volume loss.
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31
15. Blood flow to which organ is the most highly preserved of all organ systems in shock? The brain.
16. What are the main consequences of the cellular energy deficit in patients with shock? Lack of oxygen delivery leads to a general failure of energy-dependent functions of the cell. The end result is cell swelling and death. Adenosine triphosphate (ATP) is the primary "currency" of metabolism, and failure to deliver adequate oxygen and nutrients to the cell slows and stops the production of this vital chemical. Life itself depends on continual production and availability of ATP to run the energy-dependent mechanisms of cell function. Normal aerobic metabolism yields the highest amount of energy (ATP) per gram of nutrients, whereas anaerobic metabolism yields the least. Anaerobic metabolism also increases the yield of metabolic waste products, especially pyruvate and lactate. The switch of global energy production from oxygendependent (aerobic) to oxygen-independent (anaerobic) metabolism results in only a short-term solution for inadequate energy product. As the shock episode is prolonged, so are the deleterious changes. The energy-dependent sodium-potassium-ATPase pump of the cell membrane evenutally fails, leading to ionic gradient failure and loss of transmembrane potential. As a result of ionic pump failure, intracellular accumulations of ions and water occur. These cells swell in response, leading to cell membrane disruption and cell death.
17. What laboratory parameter can be used to assess tissue perfusion in shock? Lactate. Mild systemic hypoperfusion has been associated with lactate levels of 3-5 mmoUL; moderate hypoperfusion with values of 5-10 mmoVL and severe hypoperfusion states often demonstrate values greater than 10 mmoUL. Plasma lactate concentration generally falls with adequate volume resuscitation. While not universally available, plasma lactate levels can be a useful guide in directing therapy. 18. What is GI PiCO z? GI PiCO z is gastrointestinal intraluminal partial pressure of carbon dioxide. Monitoring involves placement of a tonometry catheter into the lumen of the 01 tract (colon, stomach, or small intestine). Measurements of GI PiC0 2 reflect the energy status of the 01 mucosa. The 01 mucosa is at high risk for inadequate perfusion during shock and resuscitation. Measurement of this parameter can help guide adequacy of resuscitation. 19. Define systemic inflammatory response syndrome (SIRS). The systemic inflammatory response is a generalized inflammatory response to a variety of severe systemic insults. Current defining criteria for SIRS include two or more of the following: • Temperature> 103.5°F or < IOO.O°F • Heart rate> 160 beats/min (dog) or > 250 beats/min (cat) • Respiratory rate> 20 breaths/min or PaC02 < 32 mmHg • White blood cell count> 12,000 or < 4,000 cells or> 10% nucleated cells/band neutrophils 20. Describe the basic inflammatory components of shock. Inflammatory changes, which develop during shock, vary greatly. To some degree, however, all forms of shock have an aspect of inflammation. Ischemia and reperfusion are components of every form of shock state, regardless of etiology. In evaluating the ischemia-reperfusion aspect of shock, successful hemodynamic resuscitation initiates proinflammatory mediators, chemotactic cytokines, and activation of leukocytes. Once the animal is reperfused, we seldom recognize an inflammatory response, because rapid hemodynamic correction of hypovolemic and cardiogenic shock episodes results in a minimal inflammatory response. However, prolonged hypoperfusion and significant tissue trauma exhibit profound inflammatory changes during reperfusion. A systemic inflammatory response then results in elevated levels of proinflammatory mediators such as cytokines, eicosanoids, kinins, and complement. These substances activate endothelial cells and leukocytes. Activated endothelial cells and leukocytes can upregulate the expression of cellular adhesion molecules, integrins, and selectins, resulting in adhesion of activated leukocytes to
32
Shock
endothelial cells. Activated endothelial cells also can release nitric oxide, which may induce substantial vasodilatation and exacerbate efforts to improve resuscitation. The activated leukocytes release destructive oxygen free radicals, which cause further damage to tissues and microcirculation. Although the hemodynamic components of shock are readily reversible, the systemic inflammatory components often are not. 21. What is septic shock? A form of distributive shock secondary to the systemic inflammatory response caused by severe infection. Bacteria or bacterial toxins cause the classic form. Other microorganisms that can initiate septic shock include fungal, protozoal, and viral organisms. The characteristic findings are hypotension and perfusion abnormalities that persist despite adequate fluid therapy. By definition, patients with clinical evidence of infection and signs of shock are in septic shock. 22. When should you suspect septicemia or septic shock? When patients present with tachycardia, hypotension, hypovolemia, fever or hypothermia, high or low white blood cell count, and signs of multiple organ involvement. In such patients, perfusion and cardiac output often fail to improve despite adequate fluid therapy. 23. What are the classic changes in systemic vascular resistance (SVR) and cardiac output in early septic shock? In early septic shock (hyperdynamic phase), SVR is decreased and cardiac output is increased. The increase in cardiac output is a compensatory response to the falling SVR. 24. What are the indications for sympathomimetic therapy in the treatment of septic shock? Sympathomimetic therapy is appropriate when aggressive fluid therapy (high CVP or high pulmonary wedge pressure [PWPj) has failed to restore tissue perfusion, pulse quality, arterial blood pressure, or cardiac output. The goals of therapy are to restore cardiac output and tissue perfusion, to increase oxygen delivery, to maintain systemic blood pressure in vital circulation, and to limit excessive vasoconstriction or vasodilatation. 25. Briefly discuss the sympathomimetic drugs commonly used to treat septic shock. Dobutamine is the drug of choice. It restores cardiac output and oxygen delivery more reliably than dopamine. Although it is a potent beta) and beta2 agonist, dobutamine has fewer alpha effects than dopamine. The usual dosage range is 5-l511glkg/min. Dopamine is also a potent beta agonist, but in addition it has strong alpha) and alpha2 effects as well as dopaminergic properties. Constant-rate infusion (CRI) at l-3llglkglmin enhances perfusion to renal and visceral circulation via dopaminergic effects. If dopamine is used for cardiovascular and blood pressure support, the dose is increased to 3-10 Ilglkg/min. This and higher doses of dopamine increase cardiac output and blood pressure. However, the renal and visceral perfusion-enhancing properties are often blunted or overridden at higher dosages. Other sympathomimetic drugs include epinephrine, norepinephrine, phenylephrine, dopexamine, and ephedrine. The first three agents cause profound vasoconstriction and tend to be reserved for the most refractory cases of hypotension. Dopexamine is principally a beta2 and dopaminergic agonist without alpha agonist activity. The usual dosage range is 5-20 Ilglkg/min by CRI. Dopexamine increases cardiac output, decreases peripheral vascular resistance, and improves visceral perfusion without the peripheral vasoconstriction effects of dopamine. 26. What is meant by the term ''vicious cycle of shock"? Prolonged shock triggers a cascade of events. Decreased cardiac output leads to decreased blood pressure. As the driving pressure decreases, so do peripheral perfusion and microcirculatory response. Poor venous return leads to decreased filling pressure for the heart. The resultant increase in myocardial work can lead 10 further failure of myocardial function secondary to decreased coronary perfusion. Prolonged tissue perfusion deficit leads to microcirculatory damage, cellular aggregation, microcirculatory obstruction, and cellular hypoxia. Loss of cellular ionic gradients due to
Shock
33
energy-dependent ionic pump failure and increased intracellular accumulation of ions and fluid cause cell swelling and membrane disruption, which lead to loss of intracellular fluids and ions. An overall metabolic acidosis and accumulation of toxic mediators further destroy the metabolic machinery. Normal compensatory mechanisms fail, resulting in decreased cardiac function and failure to maintain sympathetically induced arterial and venous vasoconstriction. As the metabolic machinery of the cell is destroyed and regulatory mechanisms meant to preserve homeostasis fail, no manner of resuscitation effort can restore the failing system and death results.
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27. How can septic shock and cardiogenic shock appear similar? In the hypodynamic (late) phases of septic shock, cardiac index is decreased and pulmonary capillary resistance is increased. Combined, these factors can markedly decrease cardiac output and increase CVP, appearing quite similar to right heart failure. Patients typically have cool extremities due to decreased perfusion and tachycardia. The prognosis is poor.
28. What are the primary goals of treatment for septic shock? The primary goals are to maximize tissue oxygen delivery because of the increased oxygen demand. You must improve the hemodynamic status and correct the underlying metabolic abnormalities. Then you must aggressively seek and eliminate the source of infection.
29. What are the primary goals of treating hemorrhagic shock? Stop continued loss, restore volume, and restore oxygen-carrying capacity.
30. What are the key factors in the treatment of cardiogenic shock? Reduction of preload and/or afterload, improvement of myocardial contractility, and control of serious arrhythmias.
31. What is neurogenic shock? Neurogenic shock results from acute loss of sympathetic vascular tone, which leads to arteriolar and venous dilatation. Neurogenic shock may result from spinal cord injury and even excessive
34
Shock
administration of general anesthetics. This form of vasogenic or distributive shock may be refractory to standard fluid therapy. An alpha agonist may be needed to treat refractory hypotension.
32. What is anaphylactic shock? A type of vasogenic shock characterized by an antigen-antibody reaction that occurs immediately after a sensitized patient is exposed to the antigen. The resulting reaction is a decrease in venous return due to venous dilation, which pools blood in capacitance vessels. Accompanying venous dilation is systemic arterial dilation, which decreases systemic blood pressure. Capillaries become increasingly permeable, and hypovolemia results from the capillary leak of plasma into tissues. Angioedema, laryngeal edema, bronchospasm, and urticaria also may be seen.
33. What type of shock is pericardial tamponade? Obstructive, pericardial tamponade physically compresses the heart within the pericardial sac. This compression limits the amount of blood that can enter the heart during diastole and subsequently limits the stroke volume, leading to a decrease in cardiac output.
34. What happens to the GI tract in shock? What protective methods can be used? The GI tract is prone to mucosal ulceration and sloughing during periods of shock when visceral blood flow is reduced. The mechanism of GIT damage is complex and multifactorial, ranging from loss of normal protective barriers and self-destruction due to hydrogen ions, pancreatic proteases, and bile acids to mucosal cell death due to hypoxia. Ultimately, mucosal permeability is increased, and tissue penetration of acid, bacteria, and endotoxin exacerbates the condition. Protective efforts are focused on ensuring or reestablishing adequate visceral perfusion and oxygenation. Monitoring perfusion can be instituted with a GI tonometry catheter (GI-PiCO z; see question 18). The protective actions of Hz blockers, proton pump inhibitors, mucosal patching, and mucous stimulatory drugs are controversial, but all can aid in the treatment and amelioration of signs and symptoms. Pharmacologic manipulations alone, however, cannot take the place of adequate restoration of visceral circulation, perfusion, and oxygen delivery.
35. Briefly discuss the development of acute renal faDure in shock. Renal failure is commonly seen in shock patients. Depending on the stage and degree of renal injury, patients may present with any of the following: initial high urine output, low tubule pressure and sodium retention, damage to renal parenchyma, renal dysfunction, fulminant failure, and/or anuria. During shock, glomerular filtration rate falls and renal cortical blood flow is reduced. Renal hypoperfusion leads to ischemic damage, causing tubular necrosis and edema, which often obstructs tubules. Loss of renal tubular function leads to increasing metabolic acidosis, hyperkalemia, and impaired clearance of drugs and other compounds. As the renal perfusion pressure continues to decline, further releases of renin, angiotensin, and aldosterone magnify the problem. Urine output typically is used as an index of adequate renal perfusion. When in doubt, a urinary catheter should be placed to measure urine output. The goal of treatment should be 1-2 ml/kglhr of urine. Fluid therapy is the hallmark of treatment. If volume therapy alone fails to restore urine output, aggressive efforts with diuretics and dopamine are indicated.
36. What does the term "shock lung" mean? Because they receive the entire cardiac output, the lungs are involved in the inflammatory components of shock more than any other system. Acute respiratory distress syndrome (ARDS) is the term used to describe lung injury caused by the systemic inflammatory response. Inflammatory mediators and activated leukocytes from throughout the body target the pulmonary vascular endothelium and cause an activation of the pulmonary vascular endothelium. Pulmonary capillaries can then become plugged by leukocytes. Activated leukocytes directly damage the capillary endothelium, exacerbating the inflammatory process. This exacerbation can lead to ventilation-perfusion mismatching, increased shunt fraction, and increased capillary leak.
Shock
35
37. What are the characteristics of an ''ideal'' resuscitative fluid for patients in shock? The ideal fluid would be safe, readily available, reasonable in cost, and easy to administer; it would require no special handling, provide volume and vascular retention, and have the capability of oxygen carriage and delivery. 38. What is the fluid of choice for treating patients in shock? Fluid administration is the cornerstone of effective therapy for patients with noncardiogenic shock. Although the exact fluid may be controversial, depending on the author, the basic principle is the same. Crystalloids (containing sodium) are the initial fluid of choice. They are easy to administer, readily available, inexpensive, and effective. Shock initially should be treated aggressively with fluid containing an adequate amount of sodium because of the relatively high concentration of sodium in extracellular fluid. Readily available and commonly used isotonic solutions include 0.9% sodium chloride, lactated Ringer's solution, Plasmalyte, and Normosol-R. 39. Why may Plasmalyte or Normosol-R have an advantage over Ringer's lactate solution for patients in shock? Ringer's lactate solution uses lactate as its primary buffer, which depends on active hepatic metabolism for conversion to bicarbonate. In shock patients, hepatic metabolism can be markedly impaired. Normosol-R and Plasmalyte contain acetate and gluconate as their primary buffers. Acetate and gluconate are metabolized primarily by the skeletal muscle to bicarbonate. Although blood cell flow to skeletal muscle is decreased in shock, acetate and gluconate can be converted to bicarbonate easily as circulation is restored. As the circulatory system and peripheral perfusion are reestablished, the liver is presented with an excess of lactate to metabolize (lactic acidosis) and may not be able to do so adequately. 40. What is hypertonic saline? When is it used? Hypertonic saline is a crystalloid fluid with a supraphysiologic amount of sodium. The typical sodium concentration is 3-7%. A dose of 4-5 ml/kg of 7% hypertonic saline has been shown to be an effective acute volume expander in dogs. It acts by drawing water from the intracellular and interstitial spaces into the vascular compartment. These changes cause a rapid but transient increase in intravascular volume. When combined with a synthetic colloid such as dextran 70, the volume-expanding effects can be prolonged. The contraindications for hypertonic saline are hypernatremia, hyperosmolality, cardiogenic shock, and renal failure. Hypertonic saline is used only for the rapid emergency restoration of volume and must be followed with definitive treatment, because the effects of hypertonic saline are only temporary. 41. What volume of crystalloid fluid is used to resuscitate a shock patient? The volumes for cats and dogs are different in the published literature. In dogs, shock volumes of fluid are reported at 50-90 mllkg/hr or up to complete blood volume per hour. In cats, volumes are reported at 40-60 ml/kg/hr or approximately complete plasma volume per hour. The difference between cat and dog resuscitation volume is unclear in the literature. Typically these volumes should be regarded as indicators of volume "to be prepared to deliver" in an hour, but treatment should be titrated to the volume needed by the individual patient. A highly effective method is to deliver shock fluid volumes in one-fourth shock volume increments. One-fourth of the calculated shock volume is delivered every 15 minutes with monitoring of the deviation from the baseline packed cell volume and total protein. Few patients require 90 mllkg/hr using this method, and volume overload is unlikely. 42. What is a standard volume of infusion for a synthetic colloid solution in patients in shock? The standard volume of colloid, whether synthetic or natural, is generally 10-20 ml/kg/day. This volume is typically given over 4-6 hours but may be given faster if needed.
36
Shock
Often the infusion of a synthetic colloid in the fluid therapy program allows a reduction in the crystalloid fluid requirement by 40-60%.
43. What is oxyglobin? When is it used in a shock patient? Oxyglobin is a member of a group of compounds know as hemoglobin-based oxygen carriers (HBOC). The molecule is polymer of bovine hemoglobin that recently was approved for use in dogs in the United States. The HBOCs have evolved from more than 50 years of research into acelluar blood replacement solutions. The oxygen-carrying characteristics of this product are similar to those of blood with several important differences. Oxyglobin binds and releases oxygen more readily than whole blood, requires no typing or cross-matching, requires no special administration set or filter, does not depend on levels of 2,3-diphosphoglycerate to regulate its oxygen-binding site, and is shelf-stable for more than I year at room temperature. Oxyglobin has demonstrated its effectiveness in restoring oxygen delivery in anemic dogs or dogs in hemorrhagic shock. Recent research has demonstrated that Oxyglobin administered at low doses improves oxygen delivery to tissues by increasing the transfer of oxygen across the interstitial fluid barrier and by reaching tissues that red blood cells cannot. Label directions must be followed closely. Oxyglobin has significant colloidal osmotic properties and can induce circulatory overload if administered too rapidly or in excess of recommended dosages.
44. What is the rationale behind low-volume resuscitation in hemorrhagic shock? The rationale is simple: administration of small volumes of fluids during traumatic or hemorrhagic shock reduces the risk of disrupting clotted vasculature and exacerbating hemorrhage until definitive care is available. Although this concept recently has been popularized based on one paper, no currently available data determine how low or for how long a patient can be maintained before irreversible shock will result. The efficacy and safety of this theory are unproved in the clinical setting and warrant further study. BIBLIOGRAPHY I. Aldrich J: Shock. In King L, Hammond R (eds): Manual of Canine and Feline Emergency and Critical Care. Cheltenham, UK, BSAVA, 1999, pp 23-36. 2. Astiz ME, Rackow EC, Weil MH: Pathophysiology and treatment of circulatory shock. Crit Care Clin 9: 183-203, 1993. 3. Crystal MA, Cotter SM: Acute hemorrhage: A hematologic emergency in dogs. Compend Cont Educ Pract Vet 14:60-68, 1992. 4. Ford SL, Schaer M: Shock syndrome in cats. Compend Cont Educ Pract Vet 15: 120-125, 1993. 5. Hansen B: Fluid therapy in the shock patient. Proceedings IVECCS VI, San Antonio, TX, 1998, pp 216-221 6. Haskins SC: Therapy for shock. In Bonagura JD (ed): Current Veterinary Therapy, vol. XIII. Philadelphia, wn. Saunders, 2000, pp 140-146. 7. Hughes D: Lactate measurement: Diagnostic, therapeutic, and prognostic implications. In Bonagura JD (ed): Current Veterinary Therapy, vol. XIII. Philadelphia, WB. Saunders, 2000, pp 140-146. 8. Kirby R: Septic shock. In Bonagura JD (ed): Current Veterinary Therapy, vol XII. Philadelphia, WB. Saunders, 1995, pp 139-146. 9. Kline lA. Shock. In Rosen D (ed): Emergency Medicine: Concepts and Clinical Practice, vol I. SI. Louis, Mosby, 1998 pp 86-106. 10. Rackow Ee. Astiz ME: Mechanisms and management of septic shock. Crit Care Clin 9:219-237, 1993. I I. Schertel ER, Muir WW: Shock: Pathophysiology, monitoring, and therapy. In Kirk RW (ed): Current Veterinary Therapy, vol X. Philadelphia, wn. Saunders, 1989, pp 316-330. 12. Walley KR, Wood LD: Shock. In Hall JB (ed): Principles of Critical Care. New York, McGraw-Hill, 1998, pp 277-301. 13. Ware WA: Shock. In Murtaugh RJ, Kaplan PM (eds): Veterinary Emergency and Critical Care Medicine. Chicago, Mosby-Year Book, 1992, pp 163-175. 14. Wingfield WE. How much fluid should you administer? Proceedings VECCS, 1997, pp 17-19.