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Approach to the Patient with Shock: Introduction Shock is the clinical syndrome that results from inadequate tissue perfusion. Irrespective of cause, the hypoperfusion-induced imbalance between the delivery of and requirements for oxygen and substrate leads to cellular dysfunction. The cellular injury created by the inadequate delivery of oxygen and substrates also induces the production and release of damage-associated molecular patterns (DAMPs or “danger signals”) and inflammatory mediators that further compromise perfusion through functional and structural changes within the microvasculature. This leads to a vicious cycle in which impaired perfusion is responsible for cellular injury that causes maldistribution of blood flow, further compromising cellular perfusion; the latter ultimately causes multiple organ failure (MOF) and, if the process is not interrupted, leads to death. The clinical manifestations of shock are also the result, in part, of autonomic neuroendocrine responses to hypoperfusion as well as the breakdown in organ function induced by severe cellular dysfunction (Fig. T-1). When very severe and/or persistent, inadequate oxygen delivery leads to irreversible cell injury; only rapid restoration of oxygen delivery can reverse the progression of the shock state. The fundamental approach to management, therefore, is to recognize overt and impending shock in a timely fashion and to intervene emergently to restore perfusion. This often requires the expansion or reexpansion of intravascular blood volume. Control of any inciting pathologic process (e.g., continued hemorrhage, impairment of cardiac function, or infection), must occur simultaneously. Clinical shock is usually accompanied by hypotension (i.e., a mean arterial pressure (MAP) <60 mmHg in previously normotensive persons). Multiple classification schemes have been developed an attempt to synthesize the seemingly dissimilar processes leading shock. Strict adherence a scheme may be difficult from clinical standpoint because of frequent combination two or more causes shock any individual patient, but shown Table T-1 provides useful reference point which discuss and further delineate underlying processes. Table T–1. Classification Shock 1. Distributive a) Septic Shock b) Pancreatitis c) Severe Burns d) Anaphylactic Shock e) Neurogenic Shock f) Endocrine Shock Adrenal Crisis 2. Cardiogenic Shock a) Myocardial Infarction b) Myocarditis c) Arrhythmia d) Valvular i) aortic valve insufficiency ii) mitral insufficiency 3. Obstructive a) Tension pneumothorax b) Cardiac tamponade c) Constrictive pericarditis d) Pulmonary embolism e) Aortic dissection 4. Hypovolemic a) Hemorrhagic i) Trauma ii) GI bleeding iii) Ruptured ectopic pregnancy b) losses c) Polyuria i) Diabetic ketoacidosis ii) Diabetes insipidus Pathogenesis Organ Response Microcirculation Normally when cardiac output falls, systemic vascular resistance rises maintain level pressure that is adequate for perfusion heart brain at expense other tissues such as muscle, skin, especially gastrointestinal (GI) tract. Systemic determined primarily by luminal diameter arterioles. The metabolic rates are high, their stores energy substrate low. These organs critically dependent on continuous supply oxygen nutrients, neither tolerates severe ischemia than brief periods (minutes). Autoregulation (i.e., maintenance blood flow over wide range pressures), critical sustaining cerebral coronary despite significant hypotension. However, MAP drops ≤60 mmHg, these function deteriorates. Arteriolar smooth muscle has both α- β-adrenergic receptors. α1 receptors mediate vasoconstriction, while β2 vasodilation. Efferent sympathetic fibers release norepinephrine, acts one most fundamental compensatory responses reduced pressure. Other constrictor substances increased forms include angiotensin II, vasopressin, endothelin 1, thromboxane A2. Both norepinephrine epinephrine released adrenal medulla, concentrations catecholamines bloodstream rise. Circulating vasodilators prostacyclin [prostaglandin (PG) I2], nitric oxide (NO), and, importantly, products local metabolism adenosine match tissue’s needs. balance between various vasoconstrictors influences acting upon microcirculation determines perfusion. Transport cells depends microcirculatory flow; capillary permeability; diffusion oxygen, carbon dioxide, through interstitium; exchange across cell membranes. Impairment central pathophysiologic late stages all shock, results derangement cellular ultimately responsible organ failure. The endogenous response mild moderate hypovolemia restitution intravascular volume alterations hydrostatic osmolarity. Constriction arterioles leads reductions number beds perfused, thereby limiting surface area filtration occurs. When oncotic remains constant rises, there net reabsorption fluid into bed, accord with Starling’s law interstitial liquid exchange. Metabolic changes (including hyperglycemia elevations glycolysis, lipolysis, proteolysis) raise extracellular osmolarity, osmotic gradient increases intracellular volume. Cellular Responses Interstitial transport nutrients impaired decline high-energy phosphate stores. Mitochondrial dysfunction uncoupling oxidative phosphorylation likely decreased amounts triphosphate (ATP). As consequence, accumulation hydrogen ions, lactate, anaerobic metabolism. progresses, vasodilator metabolites override vasomotor tone, causing hypotension hypoperfusion. Dysfunction membranes thought represent common end-stage pathway Normal transmembrane potential associated increase sodium water, swelling interferes microvascular perfusion. In preterminal event, homeostasis calcium via membrane channels lost flooding intracellularly concomitant hypocalcemia. There also evidence widespread selective apoptotic (programmed cell-death) loss cells, contributing immune failure. Neuroendocrine Response Hypovolemia, hypotension, hypoxia sensed baroreceptors chemoreceptors contribute autonomic attempts restore volume, perfusion, mobilize substrates. Hypotension disinhibits center, resulting adrenergic vagal activity. Release neurons induces peripheral splanchnic major contributor activity rate output. Loss recognized upregulate innate immunity inflammatory response. effects circulating medulla largely metabolic, glycogenolysis gluconeogenesis pancreatic insulin release. inhibits production mediators stimulation cells. Severe pain stresses cause hypothalamic adrenocorticotropic hormone (ACTH). This stimulates cortisol secretion contributes uptake glucose amino acids, enhances gluconeogenesis. Increased glucagon during stress accelerates hepatic elevates concentration. hormonal actions act synergistically tissue volume. Many ill patients recently exhibit low plasma levels ACTH stimulation, linked decrease survival. importance illustrated profound circulatory collapse occurs cortical insufficiency . Renin discharge juxtaglomerular apparatus kidney. Renin formation I then converted extremely potent vasoconstrictor stimulator aldosterone cortex vasopressin posterior pituitary. Aldosterone enhancing renal tubular sodium, excretion low-volume, concentrated, sodium-free urine. Vasopressin direct action distal tubules enhance water reabsorption. Cardiovascular Response Three variables—ventricular filling (preload), ventricular ejection (afterload), myocardial contractility—are paramount controlling stroke . output, determinant product rate. Hypovolemia preload turn reduces An limited mechanism A shock-induced reduction compliance frequent, reducing end-diastolic hence given Restoration return normal only elevated pressures. pressures stimulate natriuretic peptide (BNP) secrete relieve heart. Levels BNP correlate outcome following stress. addition, sepsis, ischemia, infarction (MI), trauma, hypothermia, general anesthesia, prolonged acidemia impair contractility reduce significantly influenced resistance, depressed early hyperdynamic stage septic neurogenic initially allowing maintained elevated. The venous system contains nearly two-thirds total small veins, serves dynamic reservoir autoinfusion blood. Active venoconstriction consequence α-adrenergic important therefore On hand, dilation, potentially output. Pulmonary Response The pulmonary bed parallels relative particularly exceed right failure. Shock-induced tachypnea tidal dead space minute ventilation. Relative subsequent induce respiratory alkalosis. Recumbency involuntary restriction ventilation secondary functional residual capacity lead atelectasis. Shock particular, resuscitation-induced oxidant radical generation, acute lung injury distress syndrome (ARDS). disorders characterized noncardiogenic edema diffuse endothelial alveolar epithelial injury, hypoxemia, bilateral infiltrates. Hypoxemia underventilated nonventilated alveoli. surfactant compliance. work breathing requirements muscles increase. Renal Response Acute kidney , serious complication hypoperfusion, less frequently heretofore aggressive repletion. Acute necrosis now seen result interactions administration nephrotoxic agents (such aminoglycosides angiographic contrast media), rhabdomyolysis; latter skeletal trauma. physiologic hypoperfusion conserve salt water. addition flow, afferent arteriolar accounts diminished glomerular (GFR) together urine formation. Toxic epithelium obstruction debris back leak filtrate. depletion ATP impairment function. Metabolic Derangements During disruption cycles carbohydrate, lipid, protein Through citric acid cycle, alanine conjunction pyruvate periphery presence deprivation glucose. With availability breakdown pyruvate, represents inefficient cycling minimal production. lactate ratio preferable alone measure reflects inadequate Decreased clearance exogenous triglycerides coupled lipogenesis rise serum triglyceride concentrations. catabolism substrate, negative nitrogen balance, if process prolonged, wasting. Inflammatory Responses Activation extensive network proinflammatory mediator systems plays role progression importantly development multiple (MOD), failure (MOF) (Fig. T-2). those surviving insult, counterregulatory “turn off” excessive If restored, patient does well. excessive, adaptive suppressed highly susceptible nosocomial infections, drive delayed MOF. Multiple humoral activated injury. complement cascade, classic alternate pathways, generates anaphylatoxins C3a C5a Direct fixation injured can progress C5-C9 attack complex, damage. Activation coagulation cascade thrombosis, fibrinolysis repeated episodes reperfusion. Components (e.g., thrombin), expression adhesion molecules activation neutrophils, Coagulation activates kallikrein-kininogen hypotension. Eicosanoids vasoactive immunomodulatory arachidonic cyclooxygenase-derived prostaglandins (PGs) A2, well lipoxygenase-derived leukotrienes lipoxins. Thromboxane A2 hypertension PGI2 PGE2 permeability cysteinyl LTC4 LTD4 pivotal sequelae anaphylaxis, states sepsis LTB4 neutrophil chemoattractant secretagogue reactive species. Platelet-activating factor, ether-linked, arachidonyl-containing phospholipid mediator, bronchoconstriction, vasodilation, permeability, priming macrophages neutrophils produce enhanced mediators. Tumor factor α (TNF-α), produced macrophages, reproduces many components state, including lactic acidosis, Interleukin 1β (IL-1β), originally defined “endogenous pyrogen” tissue-fixed immediately trauma IL-6, predominantly macrophage, slightly peak best single predictor recovery MOF Chemokines IL-8 chemoattractants activators aggregation, adherence, damage endothelium. While endothelium normally produces NO, inducible isoform NO synthase (iNOS), overexpressed toxic nitrosyl- oxygen-derived free radicals cardiovascular sepsis. Multiple platelets, contributors inflammation-induced Margination pathologic finding due radicals, lipases, PLA2, proteases. high intermediates species (ROI ROS) rapidly consumes essential antioxidants Newer efforts control reperfusion treatment monoxide, sulfide, Tissue-fixed virtually orchestrate duration source monocyte macrophage conserved toll-like (TLRs) recognize DAMPs HMGB-1, pathogen-associated molecular patterns (PAMPs) endotoxins pathogenic microbial organisms, respectively. Toll-like appear chronic inflammation Crohn’s disease, ulcerative colitis, transplant rejection. variability genetic predisposition that, part, nucleotide polymorphisms (SNPs) sequences affecting mediators. Treatment: Shock Monitoring Patients require care ICU. Careful assessment status necessary. Arterial indwelling line, pulse, should monitored continuously; Foley catheter inserted follow mental assessed frequently. Sedated allowed awaken (“drug holiday”) daily assess neurologic shorten ventilator support. There ongoing debate indications using flow-directed artery (PAC, Swan-Ganz catheter). Most ICU safely managed without use PAC. loss, shifts, dysfunction, PAC useful. placed percutaneously subclavian jugular vein circulation artery. ports proximal atrium provide access infusions measurements. Right atrial (PAPs) measured, wedge (PCWP) approximation left hemodynamic parameters 230-2 T-2. Table T–2. Hemodynamic Parameters Parameter Calculation Normal Values Cardiac (CO) SV x HR 4–8 L min Cardiac index (CI) CO BSA 2.6–4.2 (L min) m2 Stroke (SV) CO HR 50–100 mL beat Systemic (SVR) [(MAP – RAP) CO] 80 700–1600 dynes · s cm5 Pulmonary (PVR) [(PAPm PCWP) 80 20–130 cm5 Left (LVSW) SV(MAP 0.0136 60–80 g-m beat Right (RVSW) SV(PAPm RAP) 10–15 beat Abbreviations: BSA, body area; HR, rate; MAP, mean arterial pressure; PAPm, pressure—mean; PCWP, RAP, pressure. Cardiac thermodilution technique, high-resolution thermistors used determine monitor resuscitation. oximeter port offers additional advantage on-line monitoring mixed saturation, overall resistances calculated drop Determinations content blood, hemoglobin concentration, allow calculation delivery, consumption, oxygen-extraction (Table T-3). T-4. Table T–3. Oxygen Transport Calculations Parameter Calculation Normal Values Oxygen-carrying hemoglobin 1.39 g Plasma O2 concentration PO2 0.0031 Arterial concentration (CaO2) 1.39 SaO2 + 0.0031 PaO2 20 vol% Venous (CvO2) 1.39 SvO2 PvO2 15.5 vol% Arteriovenous difference (CaO2 CvO2) 1.39 (SaO2 SvO2) (PaO2 PvO2) 3.5 vol% Oxygen delivery (DO2) CaO2 CO 10 (dL L) 1.39 10 800–1600 min Oxygen (VO2) (CaO2 CvO2) 10 1.39 10 150–400 (DO2 I) DO2 BSA 520–720 (mL m2 Oxygen (VO2I) VO2 BSA 115–165 extraction (O2ER) [1 (.VO2 .DO2)] 100 22–32% Abbreviations: CO, output; PO2, partial oxygen; PaO2, blood; PvO2, SaO2, saturation SvO2, blood. Table T–4. Physiologic Characteristics Various Forms Shock Type Shock CVP PCWP Cardiac Output Systemic Vascular Resistance Venous Saturation Hypovolemic ↓ ↓ ↑ ↓ Cardiogenic ↑ ↓ ↑ ↓ Septic Hyperdynamic ↓↑ ↓ ↑ Hypodynamic ↓↑ ↓ ↑ ↑↓ Traumatic ↓ ↓↑ ↑↓ ↓ Neurogenic ↓ ↓ ↓ ↓ Hypoadrenal ↓↑ ↓ =↓ ↓Abbreviations: CVP, pressure. In resuscitation it optimize hemodynamics, rapidly. reasonable goal therapy achieve oxygen-saturation arteriovenous ratio. To red mass, augmented singly simultaneously. not accompanied consumption implies dependent. Conversely, elevation was inadequate. cautious interpretation required link among work, consumption. accompanying indicates vasoconstriction reversing improved determination stepwise expansion performance allows identification optimum (Starling’s law). algorithm Fig. T-3. Fig. T-3 : *Monitor SVO2, SVRI, RVEDVI markers correction hypovolemia. Consider age-adjusted CI. index; RVEDVI, right-ventricular index. CI, per m2; ECHO, echocardiogram; Hct, hematocrit; PAC, catheter; mmHg; SBP, systolic VS, vital signs; W U, up. Specific Shock Hypovolemic Shock This form either mass hemorrhage extravascular sequestration GI, urinary, insensible losses. signs symptoms nonhemorrhagic hypovolemic same hemorrhagic although they insidious onset. attempting effective activity, hyperventilation, capacitance vessels, hormones, replace recruitment output. Mild (≤20% volume) tachycardia relatively few external signs, supine young T-5). (~20–40% volume), becomes increasingly anxious tachycardic; position, postural tachycardia. (≥40% appear; declines unstable even develops marked tachycardia, oliguria, agitation confusion. Perfusion nervous until severe. Hence, obtundation ominous sign. transition rapid. reversed rapidly, elderly comorbid illnesses, death imminent. very narrow time frame separates derangements found progressive decompensation irreversible injury. Table T–5. Hypovolemic Shock Mild (<20% Blood Volume) Moderate (20–40% Volume) Severe (>40% Blood Volume) Cool extremities Increased capillary refill time Diaphoresis Collapsed veins Anxiety Same, plus: Tachycardia Tachypnea Oliguria Postural changes Same, plus: Hemodynamic instability Marked tachycardia Hypotension Mental status deterioration (coma) Diagnosis Hypovolemic shock is readily diagnosed when there are signs of hemodynamic instability and the source of volume loss is obvious. The diagnosis is more difficult when the source of blood loss is occult, as into the GI tract, or when plasma volume alone is depleted. Even after acute hemorrhage, hemoglobin and hematocrit values do not change until compensatory fluid shifts have occurred or exogenous fluid is administered. Thus, an initial normal hematocrit does not disprove the presence of significant blood loss. Plasma losses cause hemoconcentration, and free water loss leads to hypernatremia. These findings should suggest the presence of hypovolemia. It is essential to distinguish between hypovolemic and cardiogenic shock because, while both may respond to volume initially, definitive therapy differs significantly. Both forms are associated with a reduced cardiac output and a compensatory sympathetic mediated response characterized by tachycardia and elevated systemic vascular resistance. However, the findings in cardiogenic shock of jugular venous distention, rales, and an S3 gallop distinguish it from hypovolemic shock and signify that ongoing volume expansion is undesirable and may cause further organ dysfunction. Treatment: Hypovolemic Shock Initial resuscitation requires rapid reexpansion of the circulating intravascular blood volume along with interventions to control ongoing losses. In accordance with Starling’s law , stroke volume and cardiac output rise with the increase in preload. After resuscitation, the compliance of the ventricles may remain reduced due to increased interstitial fluid in the myocardium. Therefore, elevated filling pressures are frequently required to maintain adequate ventricular performance. Volume resuscitation is initiated with the rapid infusion of either isotonic saline (although care must be taken to avoid hyperchloremic acidosis from loss of bicarbonate buffering capacity and replacement with excess chloride) or a balanced salt solution such as Ringer’s lactate (being cognizant of the presence of potassium and potential renal dysfunction) through large-bore intravenous lines. Data, particularly on severe traumatic brain injury (TBI), regarding benefits of small volumes of hypertonic saline that more rapidly restore blood pressure are variable, but tend to show improved survival thought to be linked to immunomodulation. No distinct benefit from the use of colloid has been demonstrated, and in trauma patients it is associated with a higher mortality, particularly in patients with TBI. The infusion of 2–3 L of salt solution over 20–30 min should restore normal hemodynamic parameters. Continued hemodynamic instability implies that shock has not been reversed and/or there are significant ongoing blood or other volume losses. Continuing acute blood loss, with hemoglobin concentrations declining to ≤100 g/L (10 g/dL), should initiate blood transfusion, preferably as fully cross-matched recently banked (<14 days old) blood. Resuscitated patients are often coagulopathic due to deficient clotting factors in crystalloids and banked packed red blood cells (PRBCs). Early administration of component therapy during massive transfusion [fresh-frozen plasma (FFP) platelets] approaching a 1:1 ratio PRBC FFP appearsimprove survival. In extreme emergencies, type-specific or O-negative may be transfused. Following severe prolonged hypovolemia, inotropic support with norepinephrine, vasopressin,dopamine required maintain adequate ventricular performance but only after volume has been restored. Increases peripheral vasoconstriction inadequate resuscitation leads tissue loss organ failure. Once hemorrhage is controlled the patient stabilized, transfusions should not continued unless hemoglobin <~7g dL. Studies have demonstrated an increased survival treated this restrictive protocol. Successful also requires respiratory function. Supplemental oxygen always provided, endotracheal intubation necessary arterialoxygenation. from isolated hemorrhagic shock, end-organ damage frequently less than following septic traumatic shock. This absence activation inflammatory innate immune response consequent nonspecific injury failure. Traumatic Shock Shock trauma is, large measure, hemorrhage. However, even when controlled, can continue suffer into interstitium injured tissues. These fluid losses compounded by injury-induced responses that which contribute secondary microcirculatory injury. Proinflammatory mediators induced DAMPs released recognized highly conserved membrane receptors TLR family (see “Inflammatory Responses” above). on system, particularly circulating monocyte, tissue-fixed macrophage, dendritic cell, potent activators excessive proinflammatory phenotype cellular causes maldistribution flow, intensifying ischemia leading multiple system addition, direct structural heart, chest, head For example, pericardial tamponade tension pneumothorax impairs filling, while myocardial contusion depresses contractility. Treatment: Traumatic Shock Inability systolic pressure ≥90 mmHg trauma-induced hypovolemia associated mortality rate up –50%. To prevent decompensation homeostatic mechanisms, must promptly administered. The initial management seriously attention “ABCs” resuscitation: assurance airway (A), ventilation (breathing, B), establishment circulation (C). Control ongoing immediate attention. stabilization fractures, debridement devitalized contaminated tissues, evacuation hematomata all reduce subsequent insult minimize damaged-tissue release diffuse Supplementation depleted endogenous antioxidants reduces failure mortality. Cardiogenic Shock See cardiogenic shock chapter Compressive Cardiogenic Shock With extrinsic compression, heart surrounding structures compliant, therefore normal filling pressures generate diastolic stroke volume. Blood within poorly distensible sac cause . Any intrathoracic such as pneumothorax, herniation abdominal viscera through diaphragmatic hernia, positive-pressure pulmonary function, compressive simultaneously impeding venous return preload. Although initially responsive produced expansion, compression increases, recurs. The window opportunity gained loading very brief until irreversible Diagnosis intervention occur urgently. The diagnosis most based clinical findings, chest radiograph, echocardiogram. cardiac more difficult establish setting present simultaneously. classic findings include triad hypotension, neck vein distention, muffled sounds Pulsus paradoxus (i.e., inspiratory reduction>10 mmHg), may also be noted. The diagnosis is confirmed by echocardiography, and treatment consists of immediate pericardiocentesis or open subxiphoid pericardial window. A tension pneumothorax produces ipsilateral decreased breath sounds, tracheal deviation away from the affected thorax, and jugular venous distention. Radiographic findings include increased intrathoracic volume, depression of the diaphragm of the affected hemithorax, and shifting of the mediastinum to the contralateral side. Chest decompression must be carried out immediately, and, ideally, should occur based on clinical findings rather than awaiting a chest radiograph. Release of air and restoration of normal cardiovascular dynamics are both diagnostic and therapeutic. Septic Shock See in septic shock chapter Neurogenic Shock Interruption of sympathetic vasomotor input after a high cervical spinal cord injury, inadvertent cephalad migration of spinal anesthesia, or devastating head injury may result in neurogenic shock. In addition to arteriolar dilation, venodilation causes pooling in the venous system, which decreases venous return and cardiac output. The extremities are often warm, in contrast to the usual sympathetic vasoconstriction-induced coolness in hypovolemic or cardiogenic shock. Treatment involves a simultaneous approach to the relative hypovolemia and to the loss of vasomotor tone. Excessive volumes of fluid may be required to restore normal hemodynamics if given alone. Once hemorrhage has been ruled out, norepinephrine or a pure α-adrenergic agent (phenylephrine) may be necessary to augment vascular resistance and maintain an adequate mean arterial pressure. Hypoadrenal Shock The normal host response to the stress of illness, operation, or trauma requires that the adrenal glands hypersecrete cortisol in excess of that normally required. Hypoadrenal shock occurs in settings in which unrecognized adrenal insufficiency complicates the host response to the stress induced by acute illness or major surgery. Adrenocortical insufficiency may occur as a consequence of the chronic administration of high doses of exogenous glucocorticoids. In addition, recent studies have shown that critical illness, including trauma and sepsis, may also induce a relative hypoadrenal state. Other, less common causes include adrenal insufficiency secondary to idiopathicatrophy, use of etomidate for intubation, tuberculosis, metastatic disease, bilateral hemorrhage, and amyloidosis. The shock produced by adrenal insufficiency is characterized by loss of homeostasis with reductions in systemic vascular resistance, hypovolemia, and reduced cardiac output. The diagnosis of adrenal insufficiency may be established by means of an ACTH stimulation test but is inconsistent. Treatment: Hypoadrenal Shock In the persistently hemodynamically unstable patient, dexamethasone sodium phosphate, 4 mg, should be given intravenously. This agent is preferred if empiric therapy is required because, unlike hydrocortisone, it does not interfere with the ACTH stimulation test. If the diagnosis of absolute or relative adrenal insufficiency is established as shown by nonresponse to corticotropin stimulation (cortisol ≤9μg/dL change poststimulation), the patient has a reduced risk of death if treated with hydrocortisone, 100 mg every 6–8 h, and tapered as the patient achieves hemodynamic stability. Simultaneous volume resuscitation and pressor support are required. The need for simultaneous mineralocoid is unclear. Adjunctive Therapies The sympathomimetic amines dobutamine, dopamine, and norepinephrine are widely used in the treatment of all forms of shock. Dobutamine is inotropic with simultaneous afterload reduction, thus minimizing cardiac-oxygen consumption increases as cardiac output increases. Dopamine is an inotropic and chronotropic agent that also supports vascular resistance in those whose blood pressure will not tolerate peripheral vascular dilation. Norepinephrine primarily supports blood pressure through vasoconstriction and increases myocardial oxygen consumption while placing marginally perfused tissues such as extremities and splanchnic organs, at risk for ischemia or necrosis, but it is also inotropic without chronotropy. Arginine-vasopressin (antidiuretic hormone) is being used increasingly to increase afterload and may better protect vital organ blood flow and prevent pathologic vasodilation. Rewarming Hypothermia is a frequent adverse consequence of massive volume resuscitation . The infusion of large volumes of refrigerated blood products and room temperature crystalloid solutions can rapidly drop core temperatures if fluid is not run through warming devices. Hypothermia may depress cardiac contractility and thereby further impair cardiac output and oxygen delivery/utilization. Hypothermia, particularly temperatures <35°C (<95°F), directly impairs the coagulation pathway, sometimes causing a significant coagulopathy. Rapid rewarming to >35°C (>95°F) significantly decreases the requirement for blood products and produces an improvement in cardiac function. The most effective method for rewarming is endovascular countercurrent warmers through femoral vein cannulation. This process does not require a pump and can rewarm from 30° to 35°C (86° to 95°F) in 30–60 minutes.
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