DO 2 > VO 2. The amount of oxygen delivered is a product of cardiac output (L/min) and the amount of oxygen in the arterial blood (ml/dl).

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1 Shock (Part 1): Review and Diagnostic Approach Jeffrey M. Todd, DVM, DACVECC University of Minnesota, St. Paul, MN Overview Shock is the clinical presentation of inadequate oxygen utilization, typically from a form of circulatory failure. Patients that succumb to shock, do not die of shock per se, but secondary to the inflammatory response of cellular hypoxia. Therefore, early diagnosis of the correct classification of shock, followed by appropriate and aggressive treatment minimizes the damage associated with this inflammatory state. Understanding cardiovascular physiology, and subsequent pathophysiology in shock, will increase the odds of a successful outcome. Perfusion Blood flow throughout cardiovascular system is maintained by cardiac work and pressure gradients. This system allows for appropriate flow to reach the microcirculation (arterioles, capillaries, venules) where nutrients and oxygen can be delivered. Appropriate tissue perfusion requires both blood flow and adequate oxygen delivery. Oxygen Delivery Cardiovascular oxygen delivery (DO2) for cellular consumption (VO2) with resultant ATP energy production is the primary purpose of breathing. In health, the cardiovascular system constantly adjusts to deliver oxygen in amounts that are greater than is required at the tissue level: DO 2 > VO 2 DO2 (oxygen delivery): the supply of oxygen to a tissue/organ/body over a period of time VO2 (oxygen consumption): the consumption of oxygen by a tissue/organ/body over a period of time The amount of oxygen delivered is a product of cardiac output (L/min) and the amount of oxygen in the arterial blood (ml/dl). DO2 = CO x CaO2 CO (cardiac output): the amount of blood pumped out of the left ventricle in one minute SV (stroke volume): the amount of blood pumped out of the left ventricle per beat (preload, contractility, afterload) CO = HR x SV SV = EDV- ESV

2 The total amount of oxygen provided within a volume of blood (CaO2) is the sum of the oxygen bound to hemoglobin and that dissolved within the plasma. CaO2 = (Hgb x 1.34 x SaO2) + (PaO2 x 0.003) DO2 = HR x (EDV-ESV) x (Hgb x 1.34 x SaO2) + (PaO2 x 0.003) Therefore, the amount of oxygen that can be delivered to the tissues is dependent upon: Cardiac Output Stroke Volume Preload Contractility Afterload Heart rate Oxygen in arterial blood Oxygen Saturation Hemoglobin concentration Oxygen Consumption Oxygen consumption (VO2) is the amount of oxygen that is utilized by the cells for energy generation. It is the energy expenditure (amount of energy consumed from carbohydrates, lipids and amino acids) that determines the need for additional oxygen. As oxygen demand increases, so does oxygen delivery (via increased HR and CO) as well an increased oxygen extraction ratio. This compensation allows cells to be efficient in energy production via continued aerobic respiration. Once delivery and extraction of oxygen can no longer provide enough energy, the cells begin to produce energy inefficiently via anaerobic respiration. This point is called the DO2 critical point. O2ER = VO2 / DO2 = (CaO2-CvO2) / CaO2

3 O2ER (oxygen extraction ratio): the percentage of oxygen delivered that is actually consumed Oxygen Demand: the theoretical amount of oxygen required for normal function in a given state O2 Debt: the difference between the oxygen delivered to the oxygen demand Shock occurs when DO2 < VO2 and cellular hypoxia occurs. Tissue hypoxia Once this oxygen debt is present, the cells will continue to produce ATP for cellular processes via anaerobic respiration. This compensatory mechanism is short lived and is associated with tissue injury and eventually cell death. The consequences of this tissue ischemia is an increase in lactate production,decreased protein synthesis and complications of metabolic acidosis. While these may be reversible when corrected early, they will lead to irreversible tissue damage when unchecked. This causes cellular membrane damage and activation of inflammation (cytokine, complement, leukocyte), production of reactive oxygen species and eventually lysosomal cellular digestion. Shock Response Regardless of the underlying cause of cellular hypoxic state, the homeostatic response is to increase oxygen delivery. As acidosis is recognized by chemoreceptors, activation of the sympathetic response causes an increase in cardiac output (increased contractility, heart rate, and vasoconstriction). This compensated shock can be difficult to discern in the early stages, as the body attempts to maintain homeostasis. At this stage the blood pressure would be normal and the typical perfusion parameters (mm, crt, hr) may all still be in the normal range, although hyperdynamic pulses may be noted. Progression of the shock state occurs when the body is no longer able to provide the DO2 needed for continued cellular functions. At this point, exhaustion of endogenous responses leads to the classic presentation of pale mm, tachycardia, prolonged CRT, decreased blood pressure, decreased mentation/weakness and hypodynamic pulse quality. This stage is called early decompensated shock. Additional endogenous responses include activation of reninangiotensin aldosterone system and vasopressin to increase cardiac output. At this stage, without intervention, the patient will likely die. The final stage is late decompensated shock, complete failure of the circulatory autoregulatory functions will be unresponsive to resuscitative measures and patient death ensues. Classification of Shock

4 The underlying causes of the shock state are typically classified as individual pathophysiologic conditions. While these classifications are helpful to understand the basic concepts, it is important to recognize that in actual patients, it is usually some combination of them. Primary mechanism Cardiac output DO2 Hypovolemic Decreased circulating blood volume Cardiogenic Decreased forward blood flow from the heart Distributive Decreased systemic vascular resistance Altered oxygen extraction, normal, high Metabolic Abnormal cellular function Normal Normal Hypoxemic Decreased CaO2 Normal

5 Diagnostics The diagnostics performed in a patient presenting in shock can be divided into those of macrocirculation (central) from those of microcirculation (tissue). While simple blood pressure measurements can assess a patient that has already progressed to an uncompensated state, it is a poor indicator of tissue oxygenation. Additionally, once we therapeutically manage a patient, and the blood pressure returns to normal, the patient may still be in occult shock. Therefore, diagnostics that assess the delivery and utilization of oxygen are better indicators of

6 shock. As new techniques and methods are developed to validate and standardize evidence of oxygen debt, we can use some diagnostics to give us an idea of this global tissue perfusion. Blood Pressure Information obtained Evidence of cardiovascular instability Usage Use alongside tests of tissue perfusion Lactate Severity of cellular hypoxia Use serially Base excess Severity of cellular hypoxia Use serially ScvO2 Evidence of oxygen debt Use to rapidly assess response Shock Index Early recognition of shock Potential use to more rapidly identify non-clinical shock Central venous pressure Indicator of blood volume Use as therapy guide StO2 (research stage) OPS/SDF (research stage) Direct measure of global perfusion Direct monitoring of microcirculation Future use Future use References Silverstein DC, Hopper K. Small Animal Critical Care Medicine, 2nd ed. St. Louis, MO: Elsevier Saunders; 2015 Ettinger SJ, Feldman EC. Textbook of Veterinary Internal Medicine, 7th ed. St. Louis, MO: Saunders Elsevier; 2010 Gutierrez J, Theodorou AA. Oxygen delivery and oxygen consumption in pediatric critical care. Lucking SE, Pediatric Critical Care Study Guide, Springer; 2012 Young BC, et al. Decreased central venous oxygen saturation despite normalization of heart rate and blood pressure post shock resuscitation in sick dogs. JVECC 24(2) 2014 Vincent JL, DeBacker D. Circulatory shock. NEJM 369(18) 2013 Walley KR. Use of central venous oxygen saturation to guide therapy. Am J Respir Crit Care Med 2011 Prittie J. Optimal endpoints of resuscitation and early goal-directed therapy. JVECC 16(4) 2006 Silverstein D, Pruett-Saratan, et al. Measurements of microvascular perfusion in healthy anesthetized dogs using orthogonal polarization spectral imaging. JVECC 2009 Porter AE, Rozanski EA, et al. Evaluation of the shock index in dogs presenting as emergencies. JVECC 23(5) 2013