Small Animal Critical Care Medicine (Key Critical Care Concepts) PDF

46 PART I • KEY CRITICAL CARE CONCEPTS 144. Ronco C, Tetta C, Mariano F, et al: Interpreting the mechanisms of continuous renal replacement therapy in sepsis: the peak concentration hypothesis, Artif Organs 27:792, 2003. 145. Palevsky PM: Renal replacement therapy in acute kidney injury, Adv Chr...

46 PART I • KEY CRITICAL CARE CONCEPTS 144. Ronco C, Tetta C, Mariano F, et al: Interpreting the mechanisms of continuous renal replacement therapy in sepsis: the peak concentration hypothesis, Artif Organs 27:792, 2003. 145. Palevsky PM: Renal replacement therapy in acute kidney injury, Adv Chronic Kidney Dis 20:76, 2013. 146. Moore FA, Moore EE: The Evolving rationale for early enteral nutrition based on paradigms of multiple organ failure: a personal journey, Nutr Clin Pract 24:297, 2009. 147. Ortiz Leyba C, Montejo Gonzalez JC, Vaquerizo Alonso C: Guidelines for specialized nutritional and metabolic support in the critically-ill patient: update. Consensus SEMICYUC-SENPE: septic patient, Nutr Hosp 26(Suppl 2):67, 2011. 148. van den Berghe G, Wouters P, Weekers F, et al: Intensive insulin therapy in critically ill patients, N Engl J Med 345:1359, 2001. 149. Treggiari MM, Karir V, Yanez ND, et al: Intensive insulin therapy and mortality in critically ill patients, Crit Care 12:R29, 2008. 150. Finfer S, Chittock DR, Su SY, et al: Intensive versus conventional glucose control in critically ill patients, N Engl J Med 360:1283, 2009. 151. Finfer S, Liu B, Chittock DR, et al: Hypoglycemia and risk of death in critically ill patients, N Engl J Med 367:1108, 2012. 152. Kampmeier TG, Ertmer C, Rehberg S: Translational research in sepsis— an ultimate challenge? Exp Transl Stroke Med 3:14, 2011. 153. Hall TC, Bilku DK, Al-Leswas D, et al: The difficulties of clinical trials evaluating therapeutic agents in patients with severe sepsis, Irish J Med Sci 181:1, 2012. 154. Vincent JL: The rise and fall of drotrecogin alfa (activated), Lancet Infect Dis 12:649, 2012. 155. Artigas A, Niederman MS, Torres A, et al: What is next in sepsis: current trials in sepsis, Expert Rev Anti Infect Ther 10:859, 2012. 156. Platt SR, Radaelli ST, McDonnell JJ: The prognostic value of the modified Glasgow Coma Scale in head trauma in dogs, J Vet Intern Med Am Coll Vet Intern Med 15:581, 2001. CHAPTER 8 HYPOTENSION Edward Cooper, VMD KEY POINTS Copyright © 2014. Elsevier. All rights reserved. • Blood pressure is a combination of the effects of various elements. These include heart rate, stroke volume, and systemic vascular resistance. • Hypotension occurs when at least one of the controls of blood pressure is overcome or neutralized. • Treatment of hypotension involves treating the underlying cause and targeting the patient’s normal control mechanisms. Hypotension is a reduction in systemic arterial blood pressure, which results from disruption in normal cardiovascular homeostasis. Because numerous factors contribute to maintenance of normal blood pressure, hypotension only develops secondary to a disease process that has negatively affected this regulation. What follows is a review of the normal physiology and pathophysiology of blood pressure control as they relate to causes of hypotension in critically ill patients. Although covered elsewhere in greater detail, there is also consideration of various treatment options for these assorted disorders. NORMAL DETERMINANTS OF BLOOD PRESSURE Systemic arterial blood pressure provides the hydraulic force that drives blood flow and thereby significantly affects tissue perfusion. More specifically, it is the force exerted by blood against any unit area of the vessel wall.1 Arterial blood pressure varies depending on the phase of the cardiac cycle (systolic vs. diastolic), but it is the mean arterial pressure (MAP) that plays the biggest role in tissue Silverstein, D., & Hopper, K. (2014). Small animal critical care medicine. Elsevier. Created from purdue on 2024-01-16 20:44:02. perfusion.2 Understanding the main cardiovascular elements that determine MAP is essential to understanding the development of hypotension. These factors can be represented by the so-called tree of life (Figure 8-1). True of any fluid that is pumped through a closed system, pressure (in this case MAP) is primarily determined by the product of flow (cardiac output [CO]) and resistance (systemic vascular resistance [SVR]). Cardiac output, in turn, is a function of the volume of blood ejected with each contraction of the heart (stroke volume [SV]) times the number of contractions per minute (heart rate [HR]). The determinants of SV are preload (stretching of the ventricle before contraction, largely a function of venous return), contractility (force of ventricular contraction), and afterload (the force needed to overcome LOCAL CO2 PGs NO Histamine MAP  CO × SVR SV × HR Preload Afterload Contractility SYSTEMIC Vasopressin Angiotensin II SNS SNS vs. PNS FIGURE 8-1 The “tree of life” representing the key physiologic factors that determine mean arterial pressure. CO, Cardiac output; CO2, carbon dioxide; HR, heart rate; PGs, prostaglandins; PNS, parasympathetic nervous system; MAP, mean arterial pressure; NO, nitric oxide; SNS, sympathetic nervous system; SV, stroke volume; SVR, systemic vascular resistance. CHAPTER 8 • aortic pressure and achieve left ventricular outflow). SV is directly related to preload and contractility, whereas it is inversely related to afterload. Heart rate, the other major contributor to CO, is dictated by the relative balance between input from the sympathetic nervous system (SNS) and parasympathetic nervous system (PNS). Regulation of SVR is another major factor that serves to determine MAP. Vascular tone, and thereby SVR, is affected by both systemic and local mediators, which cause either vasoconstriction or vasodilation. Catecholamines released by the SNS are primarily responsible for basal systemic vascular tone, as well as minute-tominute regulation of blood pressure.1 Angiotensin II and vasopressin, also having vasoconstrictive effects, play more of a role in long-term regulation of vascular tone. In addition to these systemic mediators, local factors can also serve to affect blood flow in response to changes in metabolic demand, muscle activity, and vascular injury and to circumvent systemic vascular control. Examples include vasodilatory substances such as nitric oxide (NO), histamine, prostacyclin, and carbon dioxide, as well as vasoconstrictive agents such as endothelin, thromboxane, and thrombin.1 Although their effects are to meant to alter local vascular tone, excessive/systemic release can result in significant changes to SVR. POTENTIAL CAUSES OF HYPOTENSION Significant alterations in any of the previously described components of the “tree of life” could result in a reduction in MAP and lead to the development of hypotension. A categorical approach to causes of hypotension can be helpful in recognizing the pathophysiology involved and thereby aid in recognition and treatment (Table 8-1). Reduction in Preload Reduction in preload is a common cause of hypotension and can result from a number of different disease processes. As a reflection of venous return, preload will be affected by any cause of significant fluid loss from the vascular space, including hemorrhage, gastrointestinal or urinary losses leading to severe dehydration, edema, or Hypotension cavitary effusions (hypovolemic shock; see Chapter 5). For patients experiencing acute bleeding, it is typically necessary to have greater than 30% loss of vascular volume before hypotension will develop.3 Another important (and sometimes overlooked) cause of relative hypovolemia and preload reduction is venodilation. Veins have a significant capacity for volume; relaxation results in pooling and diminished venous return (see Reduction in Systemic Vascular Resistance later in this chapter). In addition to hypovolemia, any major obstruction in venous return will result in a preload reduction and the potential for hypotension to develop (obstructive shock). A classic example is gastric dilation/volvulus, whereby gastric distention results in compression of the vena cava and impedes return of blood from caudal circulation. Further, twisting of the stomach itself results in venous congestion and trapping of vascular volume away from effective circulation. Through similar mechanisms, caval or portal venous thrombosis, severe pneumothorax, mesenteric volvulus, and massive pulmonary thromboembolism could all be placed in this category. Another specific cause of obstruction is pericardial effusion with cardiac tamponade. Although there is sometimes a tendency to consider this a primary cardiogenic issue, the main pathogenesis involves collapse of the right atrium from increased pericardial pressure and failure of right-sided filling (i.e., preload). This becomes particularly important when considering therapeutic options, as will be discussed later. Reduction in Cardiac Function Diseases originating in the heart (primary) or externally affecting the heart (secondary) can also cause hypotension (cardiogenic shock; see Chapter 39). Myocardial dysfunction can occur as a primary disease with dilated cardiomyopathy, characterized by impaired myofibril contraction, decreased contractility, and progressive ventricular dilation (see Chapter 42). Secondary myocardial dysfunction can arise associated with severe acidosis or alkalosis, toxin exposure, drug administration, or systemic inflammatory response syndrome (SIRS)/sepsis. Numerous theories have been advanced to explain the occurrence of cardiomyopathy in patients with SIRS/sepsis, including Table 8-1 Causes of Hypotension and Recommended Treatment Cause Reduction in Preload Hypovolemia Copyright © 2014. Elsevier. All rights reserved. Obstructive Sample Diseases Treatments Hemorrhage Severe dehydration Edema/cavitary effusions Gastric dilation-volvulus Mesenteric volvulus Caval/portal venous occlusion Pericardial effusion Severe pleural space disease Pulmonary thromboembolism Address underlying problem. Provide fluid resuscitation. Relieve the obstruction if possible, with surgery, pericardiocentesis, or thoracentesis; administration of thrombolytics; or thrombectomy as needed. Provide fluid resuscitation. Reduction in Cardiac Function Primary Cardiomyopathy Valvular disease Tachyarrhythmia or bradyarrhythmia Secondary Systemic inflammatory response syndrome/sepsis Electrolyte abnormalities Severe hypoxia Severe acidosis or alkalosis Administer positive inotrope. Administer antiarrhythmics. Provide supportive measures for congestive heart failure Address the underlying cause. Administer positive inotrope. Reduction in Systemic Vascular Resistance SIRS/sepsis Electrolyte abnormalities Severe hypoxia Severe acidosis or alkalosis Drug or toxins Address the underlying cause. Provide fluid resuscitation. Administer vasopressors. Silverstein, D., & Hopper, K. (2014). Small animal critical care medicine. Elsevier. Created from purdue on 2024-01-16 20:44:02. 47 48 PART I • KEY CRITICAL CARE CONCEPTS myocardial ischemia, microcirculatory dysregulation, impact of various cytokines (tumor necrosis factor α [TNF-α], interleukin 1β [IL-1β], IL-6), impaired calcium transport, catecholamine insensitivity, and mitochondrial dysfunction function, among others.4,5 No single mechanism has been identified; it is likely a combination of these factors. Severe mitral regurgitation is another potential cause of cardiogenic hypotension. As the majority of the left ventricular volume moves backward into the atrium, rather than forward into arterial circulation, there is a significant reduction in effective stroke volume and thereby cardiac output (see Chapter 42). Severe tachyarrhythmias (ventricular or supraventricular) and bradyarrhythmias (thirddegree AV block, sick sinus syndrome, hyperkalemia) are also potential causes of decreased cardiac output and hypotension (see Cardiac Disorders section below). Reduction in Systemic Vascular Resistance Diseases that cause hypotension through a decrease in SVR share a common mechanism of inappropriate vasodilation resulting in maldistribution of blood flow (maldistributive or vasodilatory shock). The cardiovascular changes brought about by SIRS and sepsis best exemplify this process (see Chapters 6 and 91). Vasodilation associated with SIRS/sepsis is related to excessive production of nitric oxide from upregulation of induced nitric oxide synthase by assorted cytokines (e.g., TNF-α, IL-1β, IL-6) and direct vasoactive properties of various other inflammatory mediators.6 Additional factors implicated include upregulation of adenosine triphosphate (ATP)–sensitive potassium channels, depletion of vasopressin stores, and vascular insensitivity to catecholamines.6 In the early stages of SIRS/sepsis, the afterload reduction brought about by arterial vasodilation actually results in an increase in CO and a hyperdynamic state during which blood pressure is sustained. However, progressive vasodilation, along with myocardial dysfunction, eventually leads to a hypodynamic state and hypotension. It is important to remember that concurrent venodilation and associated pooling of blood volume, especially in the splanchnic circulation, causes decreased venous return (preload) and further contributes to cardiovascular collapse. Anaphylaxis represents another example of reduced SVR through systemic release of vasoactive substances (see Chapter 152). In susceptible patients, immunoglobulin E (IgE) produced in response to allergen exposure binds to mast cells and basophils. This binding triggers release of histamines, leukotrines, and other substances that promote vasodilation and increased vascular permeability.7 Finally, disruption of sympathetic outflow, from either severe brain or spinal cord injury, can result in systemic vasodilation. Because of unchallenged vagal tone, bradycardia can also accompany and further potentiate the associated hypotension. Copyright © 2014. Elsevier. All rights reserved. RESPONSE TO DECREASES IN BLOOD PRESSURE Given the importance of MAP in tissue perfusion, especially to vital organ systems, all effort is made to preserve normal blood pressure and prevent the development of hypotension. To that end there are a number of mechanisms in place, both immediate and delayed, that respond to a decrease in blood pressure. The main moment-to-moment regulator of blood pressure is the baroreceptor reflex system. With a fall in blood pressure, and thereby stretch of the baroreceptors (especially in the carotid sinus and aortic arch), stimulus to the vasomotor center of the medulla is decreased. The result is in an increase in sympathetic and a decrease in parasympathetic outflow. This shift in autonomic balance and release of catecholamines then leads to vasoconstriction (increase in SVR) and increased HR and contractility (and thereby CO), all functioning to Silverstein, D., & Hopper, K. (2014). Small animal critical care medicine. Elsevier. Created from purdue on 2024-01-16 20:44:02. raise blood pressure back to normal. Although most emphasis is placed on arterial vasoconstriction, a significant increase venous tone also occurs. This will cause decreased capacitance and promote venous return, thereby supporting preload. Another important contributor is the chemoreceptor reflex. This reflex, originating in chemoreceptor organs (such as the carotid and aortic bodies), responds to a decrease in tissue oxygen tension, increase in carbon dioxide, or decrease in pH. These changes reflect a decrease in blood flow or oxygen delivery rather than a change in blood pressure per se. Also unlike the baroreceptors, these changes cause increased signaling from the chemoreceptors and serve to excite the vasomotor center and promote sympathetic outflow. Acute decreases in blood volume or pressure will also promote the movement of fluid from the interstitium into the vascular space. Associated decreases in capillary hydrostatic pressure cause a shift in the net balance of Starling’s forces toward the vascular compartment. The resulting internal fluid resuscitation helps to maintain blood volume, preload, and MAP. Through a number of mechanisms, decreased blood pressure and blood flow to the kidneys result in activation of the renin-angiotensinaldosterone (RAA) system. Renin is released by juxtaglomerular cells in response to decreased baroreceptor activity, sympathetic activation, or decreased tubular chloride as sensed by the macula densa. The associated generation of angiotensin II exerts a number of effects to help return blood pressure to normal. Angiotensin II causes vasoconstriction by both direct (triggering vascular smooth muscle contraction) and indirect actions (stimulation of sympathetic activity and release of vasopressin). The RAA system also plays a major role in expanding blood volume. Angiotensin II promotes sodium and water retention in the proximal tubule and alters glomerular filtration rate through preferential constriction of the efferent arteriole. In addition, aldosterone release from the adrenal cortex drives sodium reabsorption and potassium excretion in the cortical collecting duct. Release of vasopressin (also called antidiuretic hormone [ADH]) from the anterior pituitary is primarily regulated by changes in blood osmolarity. However, in the face of significant hypovolemia/ hypotension (and with further input from the SNS and RAA system), release of vasopressin can increase significantly, independent of osmolarity (also known as nonosmotic stimulation of ADH). Through activation of V1 receptors, vasopressin causes vasoconstriction and an increase in SVR. Further, ADH-mediated activation of V2 receptors in the renal collecting duct promotes water retention to help support blood volume and preload. These compensatory mechanisms are in place to maintain MAP at all costs, which is the reason for its central location in the “tree of life.” It is only when these efforts are overwhelmed that blood pressure will significantly decrease. As such it is important to note that there can be significant disruption of the cardiovascular system before hypotension develops (as the patient is still in the compensated stages of shock). Once blood pressure drops, the patient has developed “decompensated shock” and the body can no longer keep up with the severity of the cardiovascular insult. If left unchecked, the compensatory mechanisms are not just overwhelmed but become exhausted. Tissue reserves and responsiveness to the various mediators become diminished, which, in conjunction with severe acidemia, leads to vasodilation, venous pooling, bradycardia, and ultimately complete cardiovascular collapse. Therefore early recognition and treatment are paramount in the management of impending or existing hypotension. DIAGNOSIS OF HYPOTESION Diagnosis of hypotension is largely related to the history, presenting clinical picture, and progression of signs through the course of CHAPTER 8 • treatment, including aspects of physical examination and blood pressure measurement. Physical Examination Indicators of hypotension found on physical examination are largely related to the systemic reflection of compensatory mechanisms and, for the most part, occur regardless of the underlying cause. These include clinical signs such as tachycardia (sympathetic stimulation of HR), as well as pale mucous membranes, prolonged capillary refill time (CRT), weak peripheral pulses, cool distal extremities, and altered mentation (all reflecting peripheral vasoconstriction or impaired perfusion). It is important to note that cats may also demonstrate bradycardia in shock states (especially cardiogenic and vasodilatory). As another exception to this, patients that are in the early (hyperdynamic) stages of vasodilatory shock may have bounding pulses, red mucous membranes, and shortened CRT to reflect the reduction in SVR and increase in peripheral perfusion. As described earlier, many of these signs will develop before a decrease in blood pressure (i.e., during compensation) but should definitely be present once the patient is hypotensive. Aside from disruption of these perfusion parameters, other clinical signs related to the specific underlying disease may be present (e.g., internal/external bleeding, abdominal distention, murmur/arrhythmias, and respiratory distress). Measurement of Blood Pressure By definition, a diagnosis of hypotension can only be made after obtaining a blood pressure measurement that is below the normal range (Table 8-2).8 Because they are more reflective of tissue perfusion and less variable with peripheral measurement, MAP values are generally preferred.2 In dogs and cats, hypotension could be considered when the MAP is below 80 mm Hg, although concern for impaired tissue perfusion, especially renal, generally does not occur until MAP gets below 60 to 65 mm Hg. Recognizing the limitations, in circumstances where MAP is not available (e.g., when using Doppler ultrasonography), a systolic blood pressure of less than 90 to 100 mm Hg could also be considered to reflect hypotension. Numerous methodologies can be used to measure blood pressure, including direct and indirect techniques (see Chapter 183). Direct blood pressure monitoring Hypotension sampling to monitor acid-base status and blood gas parameters in critically ill patients. Use of direct blood pressure is not without its drawbacks, risks, and complications. Obtaining arterial access can be challenging and invasive, the equipment can be very expensive, and there are potential complications from catheter placement (e.g., bleeding, infection, thrombosis). Despite these limitations, direct blood pressure monitoring is generally preferred in the management of a critically ill or hypotensive dog. Direct blood pressure monitoring is less commonly used in cats, except for temporary monitoring (e.g., during anesthesia) because secondary thrombosis and failure to establish collateral circulation are common in this species. Indirect blood pressure measurement Indirect methods of blood pressure measurement (including Doppler ultrasonography and oscillometric sphygmomanometry) are generally less invasive, less expensive, less technically challenging, and more readily available when compared with direct. Therefore for practical considerations these methods are often used as the initial, if not only, means of obtaining a patient’s blood pressure. In many clinical circumstances they can provide useful information to guide diagnosis and clinical decision making, but it is important to be aware of their limitations. The accuracy of indirect methods is less than direct measurement, with a general tendency to overestimate blood pressure in hypotension and underestimate in hypertension.10 In addition, there are other limiting aspects related to either methodology that should be considered. Doppler ultrasonography Doppler blood pressure measurement is relatively sensitive in small patients (<10 kg) or patients in low-flow states and is readily available in most veterinary settings. However, there are a number of potential limitations. This method only provides a systolic pressure, although there is evidence that Doppler blood pressure may be more reflective of MAP in cats.10 Accurate measurement can be affected by cuff size, which should be approximately 40% of the limb circumference. If the cuff is too large or too small, measurements may underestimate or overestimate the actual blood pressure, respectively. Doppler measurements also require patient handling, which may stimulate a stress response and “artificially” elevate the patient’s blood pressure. Oscillometric sphygmomanometry Direct measurement through use of an arterial catheter (typically dorsopedal or femoral) and pressure transducer is considered the gold standard for assessment of arterial blood pressure. In addition to being more accurate than indirect methods, direct measurement provides continuous reporting of systolic, diastolic, and mean pressures, as well as display of the arterial waveform. As such, this information can be used to detect and treat hypotension (e.g., with resuscitation fluid therapy, titration of vasopressors) on a minute-tominute basis. Furthermore, the catheter can be used for arterial blood Oscillometric methods carry the advantage of being more automated and providing information about systolic pressure, diastolic pressure, and MAP. Unlike Doppler ultrasonography, oscillometric readings do not require patient manipulation after cuff placement, and many devices are easily set to cycle for repeated pressure readings. Oscillometric measurements are affected by cuff size in a fashion similar to the Doppler technique. Other limitations that can affect accuracy include small patient size (especially cats), significant motion, lowperfusion states, and arrhythmias. Copyright © 2014. Elsevier. All rights reserved. Additional Diagnostics Table 8-2 Normal Arterial Blood Pressure Values in Dogs and Cats Dogs Cats Systolic arterial pressure 110 to 190 mm Hg 120 to 170 mm Hg Diastolic arterial pressure 55 to 110 mm Hg 70 to 120 mm Hg Mean arterial pressure 80 to 130 mm Hg 60 to 130 mm Hg FromWadell LS: Direct blood pressure monitoring, Clin Tech Small Anim Pract 15(3):111, 2000. Silverstein, D., & Hopper, K. (2014). Small animal critical care medicine. Elsevier. Created from purdue on 2024-01-16 20:44:02. Diagnostic evaluation in the hypotensive patient is largely geared toward determining the underlying cause and assessing the extent of systemic compromise. Initial emphasis is placed on point-of-care diagnostics until the patient is stable for transport or a more involved workup. Preliminary laboratory analysis might include packed cell volume/total protein (PCV/TP), blood glucose, arterial or venous blood gas analysis, blood smear, and lactate measurement, with eventual submission of complete blood cell count, chemistry profile, and coagulation profile. The presence of fluid or air in the pleural or peritoneal cavity is easily assessed with ultrasound examination and can be performed at the bedside; thoracic/abdominal radiographs and complete abdominal ultrasound should be performed as indicated. Cardiac assessment can be achieved with electrocardiography 49 50 PART I • KEY CRITICAL CARE CONCEPTS (ECG) and echocardiography. Bedside echocardiogram can be very useful for early detection of pericardial effusion, qualitative assessment of systolic function, and monitoring of relative volume status (cardiac underfilling or overfilling). Studies have demonstrated that some of these assessments can be performed accurately without extensive cardiology training.11 TREATMENT OF HYPOTENSION The key to successful management of hypotension is early detection and swift therapeutic intervention. Whenever possible, therapy should be initiated at the earliest indication of cardiovascular instability (e.g., alteration of perfusion parameters), even if hypotension has not yet developed; once it does, the need to intervene becomes even more critical. Ultimately, addressing the underlying cause is the most essential aspect of treating hypotension. In the immediate sense, stabilization is largely geared toward supporting the affected components of the “tree of life”—preload, cardiac function, and SVR (see Table 8-1). Fluid Resuscitation Fluid administration is often the cornerstone of resuscitative efforts, especially if a reduction in preload is suspected. This includes causes of absolute (e.g., hemorrhage) or relative (e.g., obstruction or vasodilation) hypovolemia and typically not primary causes of cardiac dysfunction. A complete discussion of resuscitation fluid therapy is beyond the scope of this chapter (see Chapter 60, as well as suggested references), but a few points bear mentioning. The classic approach to fluid resuscitation involves application of “shock doses” of crystalloids or colloids, titrated to effect based on resolution hypotension and abnormal perfusion parameters. However, there continues to be significant controversy regarding the optimal approach, especially with regard to volumes administered, use of synthetic colloids, and administration of blood products.12-14 It is also important to recognize that once a “reasonable” amount has been administered but the hypotension has not resolved, additional fluids are unlikely to provide benefit and may be harmful. The challenge lies in determining what constitutes “reasonable.” Measurement of central venous pressures or bedside echocardiography may provide some guidance but are not without limitations. Certainly if a full “shock dose” has been administered without improvement, measures to address cardiac dysfunction or vasodilatory processes should be considered. Copyright © 2014. Elsevier. All rights reserved. Positive Inotropes A positive inotrope should be used in cases of documented (through echocardiography) or highly suspected (based on clinical picture) myocardial/systolic dysfunction. This includes causes that are both primary (e.g., dilated cardiomyopathy) and secondary (e.g., sepsis associated). In these cases application of a β-adrenergic agonist is indicated, with dobutamine generally the preferred agent (see Chapter 157). Drawbacks to use of positive inotropes include increased myocardial oxygen demand and the potential to cause arrhythmias. Silverstein, D., & Hopper, K. (2014). Small animal critical care medicine. Elsevier. Created from purdue on 2024-01-16 20:44:02. Vasopressor Agents Patients with an inappropriate vasodilatory process may benefit from administration of a vasopressor agent. It is often challenging to make this determination. Signs consistent with early/hyperdynamic vasodilation (bounding pulses, red mucous membranes, shortened CRT) may be more obvious; however, once progressed to the hypodynamic stage it can be difficult to distinguish from other causes of hypotension. The associated clinical picture (e.g., sepsis, anesthesia, etc.) may also help guide the decision. Because fluid loading is often attempted first, failure to respond might suggest that vasoconstriction is needed. For this purpose an α1 agonist or vasopressin may be used (see Chapters 157 and 158, respectively). Although dopamine has long been considered a first-line vasopressor, current human guidelines recommend use of norepinephrine with vasopressin added second, if needed, in septic patients.12 SUMMARY Hypotension is a common and life-threatening occurrence in critically ill patients. Understanding the normal mechanisms of blood pressure regulation, the main factors that can result in disruption of cardiovascular hemostasis, and the body’s compensatory responses are essential to timely recognition and appropriate therapy. REFERENCES 1. Guyton AC, Hall JE, editors: The textbook of medical physiology, ed 12, Philadelphia, 2000, Saunders. 2. Marino PL: Arterial blood pressure. In Marino P, editor: The ICU book, ed 3, Philadelphia, 2006, Lippincott, Williams & Wilkins. 3. Garrioch MA: The body’s response to blood loss, Vox Sanguinis 87(S1):S74, 2004. 4. Romero-Bermejo FJ, Ruiz-Bailen M, Gil-Cebrian J, Huertos-Ranchal MJ: Sepsis-induced cardiomyopathy, Curr Cardiol Rev 7(3):163, 2011. 5. Costello MF, Otto CM, Rubin LJ: The role of tumor necrosis factor-α (TNF-α) and the sphingosine pathway in sepsis-induced myocardial dysfunction, J Vet Emerg Crit Care 13:25, 2003. 6. Bridges EJ, Dukes S: Cardiovascular aspects of septic shock: pathophysiology, monitoring, and treatment, Crit Care Nurse 25(2):14, 2005. 7. Simons FE: Anaphylaxis, J Allergy Clin Immunol 125(Suppl 2):S161, 2010. 8. Wadell LS: Direct blood pressure monitoring, Clin Tech Small Anim Pract 15(3):111, 2000. 9. Reference deleted in pages. 10. Caulkett NA, Cantwell SL, Houston DM: A comparison of indirect blood pressure monitoring techniques in the anesthetized cat, Vet Surg 27:370, 1998. 11. Tse YC, Rush JE, Cunningham SM, et al: Evaluation of a training course in focused echocardiography for noncardiology house officers, J Vet Emerg Crit Care 23(3):268, 2013. 12. Driessen B, Brainard B: Fluid therapy for the traumatized patient, J Vet Emerg Crit Care 16(4):276, 2006. 13. Dellinger RP, Levy MM, Rhodes A, et al: Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012, Crit Care Med 41(2):580, 2013. 14. Kobayashi L, Costantini TW, Coimbra R: Hypovolemic shock resuscitation, Surg Clin North Am 92(6):1403, 2012.