Obstructive Shock, P

Total Page:16

File Type:pdf, Size:1020Kb

Obstructive Shock, P CHAPTER 10 SHOCK OBJECTIVES KEY TERMS Upon completion of this chapter, the OEC Anaphylactic shock, p. 228 technician will be able to: Anticoagulants, p. 231 10-1 Define shock. Cardiogenic shock, p. 228 10-2 Describe the three primary causes of Distributive shock, p. 228 shock. Fainting, p. 230 10-3 Describe how the body compensates Hypovolemic shock, p. 227 for shock. Neurogenic shock, p. 229 10-4 Define the two stages of shock. Obstructive shock, p. 229 10-5 List the four major types of shock. Perfusion, p. 224 10-6 List the classic signs and symptoms of Peripheral vascular resistance, p. 226 shock. Pulmonary embolism, p. 230 10-7 Describe and demonstrate the Sepsis, p. 228 management of shock. Septic shock, p. 228 Shock, p. 224 Stroke volume, p. 226 Tachycardia, p. 226 Tachypnea, p. 226 HISTORICAL TIMELINE 1964. The NSP adopts the gold cross as its official emblem. © Jones & Bartlett Learning LLC, an Ascend Learning Company. NOT FOR SALE OR DISTRIBUTION. 9781284189599_CH10_223_238.indd 223 4/14/2020 4:37:33 PM 224 Outdoor Emergency Care, Sixth Edition CHAPTER OVERVIEW One of the most serious threats to life is the condition known as shock. Shock is defined as inadequate perfusion or flow of blood to the cells, causing cellular and tissue hypoxia due to reduced oxygen delivery. Perfusion is the circu- lation of blood within an organ or tissue in ade- quate amounts to meet the cells’ current needs for oxygen, nutrients, and waste removal. The body is perfused via the cardiovascular (circulatory) system. Although the potential causes of shock are numerous, shock occurs when one or more com- ponents of the cardiovascular system fail. This Figure 10-1 A patroller assisting with respirations. sets into motion a series of events that, unless © Edward McNamara. corrected, may cause other body systems to fail and death to ensue. Shock is initially reversible but must be recognized and treated immedi- ANATOMY AND PHYSIOLOGY ately to prevent progression to irreversible organ The cardiovascular (circulatory) system, described dysfunction. in detail in Chapter 6, Anatomy and Physiology, in- Shock is one of the most serious problems cludes the heart, blood vessels, and blood. When that OEC technicians will encounter. It is caused functioning properly, the heart pumps oxygenated by various medical and traumatic conditions. Un- blood through arterial vessels to the capillaries, fortunately, the signs and symptoms of shock may where oxygen and carbon dioxide are exchanged not be apparent initially because the body com- at a cellular level. Deoxygenated blood travels pensates, maintaining normal vital signs. The pa- through venous blood vessels to the heart, which tient’s overall health, age, and medications taken pumps the blood on to the lungs. There, carbon may make shock more difficult to recognize at dioxide is excreted into the atmosphere and the first. OEC technicians must be keenly aware of blood is oxygenated and returned to the heart, the causes of shock and the body’s responses to which begins the cycle again. it. Using this information, OEC technicians will be Problems affecting any part of the circulatory better able to recognize shock and initiate appro- system can disrupt this process, resulting in de- priate treatment (Figure 10-1). creased blood flow, cellular hypoxia, and shock. CASE Presentation On a gentle slope, you find an approximately 55-year-old man holding his left side. You identify yourself and ask if you can examine him. While talking to him, you find he fell about 10 minutes ago on his left side. As you begin your assessment, the man says he’s fine and really doesn’t think any examination is necessary. Although he appears a little pale, his radial pulse seems normal, perhaps a little slow. As you gently touch his left upper abdomen and lower chest, he winces slightly. What should you do? © Jones & Bartlett Learning LLC, an Ascend Learning Company. NOT FOR SALE OR DISTRIBUTION. 9781284189599_CH10_223_238.indd 224 4/14/2020 4:37:51 PM Chapter 10 Shock 225 Review of the anatomy and physiology of the cir- culatory system will help you understand shock. Table 10-1 The Progression of Shock If the pump (heart), blood vessels (arteries and Progression Signs and Symptoms veins), or blood is affected, tissue will not receive oxygen and nutrients, resulting in shock. Compensated • Agitation shock • Anxiety • Restlessness CAUSES OF SHOCK • Feeling of impending doom There are different types of shock, resulting from • Altered mental status three basic causes. Any of these three conditions • Weak, rapid (thready), or results in decreased perfusion, with insufficient absent pulse oxygen or nutrients reaching vital organ tissue. • Clammy (pale, cool, moist) When two or more of these conditions occur to- skin gether, shock develops rapidly. • Pallor, with cyanosis about 1. Pump failure. If the heart cannot pump the lips correctly (i.e., the heart fails), then cardiac • Shallow, rapid breathing output decreases and blood is not pumped to • Air hunger (shortness of the body adequately to sustain life. breath), especially if there 2. Failure of blood vessels to respond properly. is a chest injury In this condition, the veins and arteries • Nausea or vomiting expand too much, pooling blood in them. • Capillary refill of longer The smooth muscle in the arteries and veins than 2 seconds in infants does not constrict these tubes during some and children pathological conditions. • Marked thirst 3. Low fluid volume. In this condition, there is not • Narrowing pulse pressure enough blood to pump through the system. Decompensated • Falling blood pressure Blood can be lost through internal or external shock (systolic blood pressure of bleeding, or a medical condition can decrease 90 mm Hg or lower in an the amount of healthy blood. Also, body adult) fluids can be lost due to dehydration, from • Labored or irregular causes such as diarrhea or vomiting, burns, or breathing excessive intake of diuretics (fluid pills). • Ashen, mottled, or cyanotic skin • Thready or absent periph- STAGES OF SHOCK eral pulses Shock is a progressive disorder that can be divided • Dull eyes, dilated pupils into two stages: compensated shock and decom- • Poor urinary output pensated shock (Table 10-1). Compensated Shock KEY POINT The human body can compensate to maintain homeostasis even during times of stress or harm. The body’s systems have built-in redundancy and Blood Pressure and Shock flexibility that correct adverse conditions with- During the early stages of shock, the out incurring a total shutdown of body systems patient’s blood pressure is maintained. or long-term organ damage. In times of increased metabolic demand, the body activates various compensatory mechanisms that help restore ho- If the body detects a decrease in the amount meostasis, but those mechanisms can function of blood being circulated or a sudden decrease in only for a while unless the problem is corrected. the amount of oxygen reaching the cells, the brain © Jones & Bartlett Learning LLC, an Ascend Learning Company. NOT FOR SALE OR DISTRIBUTION. 9781284189599_CH10_223_238.indd 225 4/14/2020 4:37:54 PM 226 Outdoor Emergency Care, Sixth Edition sends signals that stimulate the release of epi- to vital tissues under adverse conditions. If left un- nephrine, a hormone that causes tachycardia (the corrected, shock would inevitably lead to death heart to beat faster) and the ventricles to contract (Figure 10-2). It is important to keep in mind that more forcefully. Both changes increase the stroke the body’s ability to compensate for shock early can volume (amount of blood pumped out of the left mask a gravely serious uncorrected condition, giv- ventricle into the aorta during one heartbeat), ing you the false impression that the patient is less which enables more blood, oxygen, and nutrients sick or less injured than is in fact the case. to reach the body’s tissues and organs. The first signs of shock are tachycardia, In addition, the central nervous system controls tachypnea (respiratory rate greater than 20 breaths smooth muscles in the blood vessels, contracting per minute), delayed capillary refill (greater than the vessels (decreasing their diameter) or dilat- 2 seconds), cool skin, anxiety or restlessness, ing them (increasing their diameter). Peripheral and a normal blood pressure. Treated early, this vascular resistance refers to the tightening of the form of shock is correctable and generally has no smaller-diameter blood vessels in the extremities. long-term adverse effects. Untreated, however, By increasing resistance of blood flow to the ex- shock will progress until the body is no longer able tremities, blood flow to the vital organs increases, a to compensate. Treatment involves correcting the key compensation in the early phases of shock. condition causing shock. At the same time, the brain sends signals to increase the rate and depth of respirations to bring more oxygen into the body and expel more Decompensated Shock carbon dioxide. This combination of tachycardia, If the body’s compensatory mechanisms are un- increased stroke volume by the heart, increased able to restore blood perfusion to the tissues, cel- peripheral vascular resistance, and increased ox- lular hypoxia will worsen, and the body’s organs ygen, by faster breathing, helps to stabilize the in- and systems will fail. Heart rate will continue to ternal environment, at least temporarily. rise, systolic blood pressure will now begin to fall Compensated shock, therefore, is the body’s (to below 90 mm Hg),
Recommended publications
  • Suplento1 Volumen 71 En
    S1 Volumen 71 Mayo 2015 Revista Española de Vol. 71 Supl. 1 • Mayo 2015 Vol. Clínica e Investigación Órgano de expresión de la Sociedad Española de SEINAP Investigación en Nutrición y Alimentación en Pediatría Sumario XXX CONGRESO DE LA SOCIEDAD espaÑOLA DE CUIDADOS INTENSIVOS PEDIÁTRICOS Toledo, 7-9 de mayo de 2015 MESA REDONDA: ¿HACIA DÓNDE VAMOS EN LA MESA REDONDA: EL PACIENTE AGUDO MONITORIZACIÓN? CRONIFICADO EN UCIP 1 Monitorización mediante pulsioximetría: ¿sólo saturación 47 Nutrición en el paciente crítico de larga estancia en UCIP. de oxígeno? P. García Soler Z. Martínez de Compañón Martínez de Marigorta 3 Avances en la monitorización de la sedoanalgesia. S. Mencía 53 Traqueostomía, ¿cuándo realizarla? M.A. García Teresa Bartolomé y Grupo de Sedoanalgesia de la SECIP 60 Los cuidados de enfermería, ¿un reto? J.M. García Piñero 8 Avances en neuromonitorización. B. Cabeza Martín CHARLA-COLOQUIO SESIÓN DE PUESTA AL DÍA: ¿ES BENEFICIOSA LA 64 La formación en la preparación de las UCIPs FLUIDOTERAPIA PARA MI PACIENTE? españolas frente al riesgo de epidemias infecciosas. 13 Sobrecarga de líquidos y morbimortalidad asociada. J.C. de Carlos Vicente M.T. Alonso 68 Lecciones aprendidas durante la crisis del Ébola: 20 Estrategias de fluidoterapia racional en Cuidados experiencia del intensivista de adultos. J.C. Figueira Intensivos Pediátricos. P. de la Oliva Senovilla Iglesias 72 El niño con enfermedad por virus Ébola: un nuevo reto MESA REDONDA: INDICADORES DE CALIDAD para el intensivista pediátrico. E. Álvarez Rojas DE LA SECIP 23 Evolución de la cultura de seguridad en UCIP. MESA REDONDA: UCIP ABIERTAS 24 HORAS, La comunicación efectiva.
    [Show full text]
  • Fluid Resuscitation Therapy for Hemorrhagic Shock
    CLINICAL CARE Fluid Resuscitation Therapy for Hemorrhagic Shock Joseph R. Spaniol vides a review of the 4 types of shock, the 4 classes of Amanda R. Knight, BA hemorrhagic shock, and the latest research on resuscita- tive fluid. The 4 types of shock are categorized into dis- Jessica L. Zebley, MS, RN tributive, obstructive, cardiogenic, and hemorrhagic Dawn Anderson, MS, RN shock. Hemorrhagic shock has been categorized into 4 Janet D. Pierce, DSN, ARNP, CCRN classes, and based on these classes, appropriate treatment can be planned. Crystalloids, colloids, dopamine, and blood products are all considered resuscitative fluid treat- ment options. Each individual case requires various resus- ■ ABSTRACT citative actions with different fluids. Healthcare Hemorrhagic shock is a severe life-threatening emergency professionals who are knowledgeable of the information affecting all organ systems of the body by depriving tissue in this review would be better prepared for patients who of sufficient oxygen and nutrients by decreasing cardiac are admitted with hemorrhagic shock, thus providing output. This article is a short review of the different types optimal care. of shock, followed by information specifically referring to hemorrhagic shock. The American College of Surgeons ■ DISTRIBUTIVE SHOCK categorized shock into 4 classes: (1) distributive; (2) Distributive shock is composed of 3 separate categories obstructive; (3) cardiogenic; and (4) hemorrhagic. based on their clinical outcome. Distributive shock can be Similarly, the classes of hemorrhagic shock are grouped categorized into (1) septic; (2) anaphylactic; and (3) neu- by signs and symptoms, amount of blood loss, and the rogenic shock. type of fluid replacement. This updated review is helpful to trauma nurses in understanding the various clinical Septic shock aspects of shock and the current recommendations for In accordance with the American College of Chest fluid resuscitation therapy following hemorrhagic shock.
    [Show full text]
  • 20Mg Spironolactone I.P…..50Mg
    For the use only of a Registered Medical Practitioner or Hospital or a Laboratory. This package insert is continually updated: Please read carefully before using a new pack Frusemide and Spironolactone Tablets Lasilactone® 50 COMPOSITION Each film coated tablet contains Frusemide I.P. …….. 20mg Spironolactone I.P…..50mg THERAPEUTIC INDICATIONS Lasilactone® contains a short-acting diuretic and a long-acting aldosterone antagonist. It is indicated in the treatment of resistant oedema where this is associated with secondary hyperaldosteronism; conditions include chronic congestive cardiac failure and hepatic cirrhosis. Treatment with Lasilactone® should be reserved for cases refractory to a diuretic alone at conventional doses. This fixed ratio combination should only be used if titration with the component drugs separately indicates that this product is appropriate. The use of Lasilactone® in the management of essential hypertension should be restricted to patients with demonstrated hyperaldosteronism. It is recommended that in these patients also, this combination should only be used if titration with the component drugs separately indicates that this product is appropriate. POSOLOGY AND METHOD OF ADMINISTRATION For oral administration. The dose must be the lowest that is sufficient to achieve the desired effect. Adults: 1-4 tablets daily. Children: The product is not suitable for use in children. Elderly: Frusemide and Spironolactone may both be excreted more slowly in the elderly. Tablets are best taken at breakfast and/or lunch with a generous amount of liquid (approx. 1 glass). An evening dose is not recommended, especially during initial treatment, because of the increased nocturnal output of urine to be expected in such cases.
    [Show full text]
  • Severe Sepsis and Septic Shock Antibiotic Guide
    Stanford Health Issue Date: 05/2017 Stanford Antimicrobial Safety and Sustainability Program Severe Sepsis and Septic Shock Antibiotic Guide Table 1: Antibiotic selection options for healthcare associated and/or immunocompromised patients • Healthcare associated: intravenous therapy, wound care, or intravenous chemotherapy within the prior 30 days, residence in a nursing home or other long-term care facility, hospitalization in an acute care hospital for two or more days within the prior 90 days, attendance at a hospital or hemodialysis clinic within the prior 30 days • Immunocompromised: Receiving chemotherapy, known systemic cancer not in remission, ANC <500, severe cell-mediated immune deficiency Table 2: Antibiotic selection options for community acquired, immunocompetent patients Table 3: Antibiotic selection options for patients with simple sepsis, community acquired, immunocompetent patients requiring hospitalization. Risk Factors for Select Organisms P. aeruginosa MRSA Invasive Candidiasis VRE (and other resistant GNR) Community acquired: • Known colonization with MDROs • Central venous catheter • Liver transplant • Prior IV antibiotics within 90 day • Recent MRSA infection • Broad-spectrum antibiotics • Known colonization • Known colonization with MDROs • Known MRSA colonization • + 1 of the following risk factors: • Prolonged broad antibacterial • Skin & Skin Structure and/or IV access site: ♦ Parenteral nutrition therapy Hospital acquired: ♦ Purulence ♦ Dialysis • Prolonged profound • Prior IV antibiotics within 90 days ♦ Abscess
    [Show full text]
  • When the Heart Kills the Liver: Acute Liver Failure in Congestive Heart Failure
    December 14, 2009 Eu Ro PE an JouR nal oF MED I cal RE sEaRcH 541 Eur J Med Res (2009) 14: 541-546 © I. Holzapfel Publishers 2009 WHEn tHE HEaRt KIlls tHE lIvER: acutE lIvER FaIluRE In congEstIvE HEaRt FaIluRE F. H. saner1, M. Heuer1, M. Meyer1, a. canbay2, g. c. sotiropoulos1, a. Radtke1, J. treckmann1, s. Beckebaum1, c. Dohna-schwake2, s. W. oldedamink3, 4, a. Paul1 1Department of general-, visceral- and transplant surgery, university Hospital Essen, germany, 2Department of Pediatric Medicine, university Hospital Essen, germany, 3Department of surgery, university of Maastricht, netherlands, 4Department of surgery, university college london Hospital, ucl, uK Abstract gestive heart failure may be absent [5, 18]. Both, congestive heart failure as a cause of acute liver fail- chronic and acute congestive heart failure can lead to ure is rarely documented with only a few cases. hepatic dysfunction [10, 17]. although there is no although the pathophysiology is poorly under- classic pattern of abnormalities, a cholestatic bio- stood, there is rising evidence, that low cardiac output chemical profile is common, with a mild elevation in with consecutive reduction in hepatic blood flow is a total bilirubin (usually 3 g/dl), a mild elevation in al- main causing factor, rather than hypotension. In the kaline phosphatase and only occasional elevations in setting of acute liver failure due to congestive heart transaminases. another common observation is an in- failure, clinical signs of the latter can be absent, which crease in InR. the presumed causes of hepatic dys- requires an appropriate diagnostic approach. function in congestive heart failure are hepatic con- as a reference center for acute liver failure and liver gestion from venous outflow obstruction and result- transplantation we recorded from May 2003 to De- ing hypertension and decreased oxygen delivery from cember 2007 202 admissions with the primary diag- an impaired cardiac output [10].
    [Show full text]
  • National Cardiogenic Shock Initiative
    EXCLUSION CRITERIA NATIONAL CARDIOGENIC SHOCK INITIATIVE Evidence of Anoxic Brain Injury Unwitnessed out of hospital cardiac arrest or any cardiac arrest in which ROSC is not ALGORITHM achieved in 30 minutes IABP placed prior to Impella Septic, anaphylactic, hemorrhagic, and neurologic causes of shock Non-ischemic causes of shock/hypotension (Pulmonary Embolism, Pneumothorax, INCLUSION CRITERIA Myocarditis, Tamponade, etc.) Active Bleeding Acute Myocardial Infarction: STEMI or NSTEMI Recent major surgery Ischemic Symptoms Mechanical Complications of AMI EKG and/or biomarker evidence of AMI (STEMI or NSTEMI) Cardiogenic Shock Known left ventricular thrombus Hypotension (<90/60) or the need for vasopressors or inotropes to maintain systolic Patient who did not receive revascularization blood pressure >90 Contraindication to intravenous systemic anticoagulation Evidence of end organ hypoperfusion (cool extremities, oliguria, lactic acidosis) Mechanical aortic valve ACCESS & HEMODYNAMIC SUPPORT Obtain femoral arterial access (via direct visualization with use of ultrasound and fluoro) Obtain venous access (Femoral or Internal Jugular) ACTIVATE CATH LAB Obtain either Fick calculated cardiac index or LVEDP IF LVEDP >15 or Cardiac Index < 2.2 AND anatomy suitable, place IMPELLA Coronary Angiography & PCI Attempt to provide TIMI III flow in all major epicardial vessels other than CTO If unable to obtain TIMI III flow, consider administration of intra-coronary ** QUALITY MEASURES ** vasodilators Impella Pre-PCI Door to Support Time Perform Post-PCI Hemodynamic Calculations < 90 minutes 1. Cardiac Power Output (CPO): MAP x CO Establish TIMI III Flow 451 Right Heart Cath 2. Pulmonary Artery Pulsatility Index (PAPI): sPAP – dPAP Wean off Vasopressors & RA Inotropes Maintain CPO >0.6 Watts Wean OFF Vasopressors and Inotropes Improve survival to If CPO is >0.6 and PAPI >0.9, operators should wean vasopressors and inotropes and determine if Impella can be weaned and removed in the Cath Lab or left in place with transfer to ICU.
    [Show full text]
  • Septic Shock V9.0 Patient Flow Map
    Septic Shock v9.0 Patient Flow Map Approval & Citation Summary of Version Changes Explanation of Evidence Ratings Patient presents to the ED with fever and/or concern for infection and ED sepsis score ≥ 6 ! BPA fires Use the ED Suspected Septic Shock RN and Well-appearing patients should be placed pathway for all ill on the appropriate ED CSW pathway for Provider appearing patients their underlying condition (e.g. ED No including HemOnc/BMT, Huddle: HemOnc BMT Suspected Infection, ED Central Line Infection Is the patient ill Suspected Central Line Infection, ED and Neonates appearing? Neonatal Fever) Yes ED Septic Shock Pathway • Use ED Suspected Septic Shock Plan • Antibiotics and blood cultures for specific populations included Inpatient Admit Criteria Does NOT meet Inpatient Admit Minute criteria • Resolution of hypotension and no • Admit to ICU ongoing signs of sepsis after ≤ 40 ml / 60 Huddle: YES NO • Follow ICU Septic Shock Pathway kg NS bolus Does patient meet • Use PICU/CICU Septic Shock Admit • First dose antibiotics administered Inpatient admit Plan • RISK to follow criteria? • Antibiotics, blood cultures for specific populations included in sub plans Previously healthy > 30 days RISK RN to follow all • Admit to General Medicine patients admitted with • Follow Admit from ED Septic Shock concern for sepsis Pathway • Use Inpatient Septic Shock Plan ! Concern for evolving sepsis Previously healthy < 30 days Any • Admit to General Medicine admitted • Call RRT or Code Blue • Follow Neonatal Fever Pathway patient with • Follow Inpatient
    [Show full text]
  • Evaluation and Management of the Polytraumatized Patient in Various Centers
    World J. Surg. 7, 143-148, 1983 Wor Journal of Stirgery Evaluation and Management of the Polytraumatized Patient in Various Centers S. Olerud, M.D., and M. Allg6wer, M.D. The Akademiska Sjukhuset Uppsala, Sweden, and the Department of Surgery, Kantonsspital, Basel, Switzerland A questionnaire was sent to the following 6 trauma centers: Paris: Two or more peripheral, visceral, or com- University Hospital for Accident Surgery, Hannover, Fed- plex injuries with respiratory and circulatory fail- eral Republic of Germany (Prof. H. Tscherne); University ure. (This excludes patients who only have sus- of Munich, Department of Surgery, Klinikum Grossha- tained fractures.) dern, Munich, Federal Republic of Germany (Prof. G. Dallas: Multiply injured patient presenting le- Heberer); Akademiska Sjukhuset Uppsala, Sweden (Prof. sions to 2 cavities, associated with 2 or more long S. Olerud); University Hospital, Department of Surgery, bone failures; lesions to 1 cavity associated with 2 Basel, Switzerland (Prof. M. Allgiiwer); H6pital de la Piti~, or more long bone failures; or lesions to multiple Paris, France (Prof. R. Roy-Camille); and University of extremities (at minimum, 3 long bone failures). Texas Southwestern Medical School, Dallas, Texas, U.S.A. (Prof. B. Claudi). Their answers have been summarized in a few short paragraphs where tabulation was not possible, Do You Grade Polytrauma, and If So, How? and then mainly in tabular form for convenient comparison among the various centers. There seems to be considerable international agreement on the main points of early aggres- Hannover: Yes, with our own grading system along sive cardiopulmonary management to prevent multiple with ISS and AIS.
    [Show full text]
  • Preventing Dehydration
    State of New Jersey Department of Human Services Division of Developmental Disabilities DDDDDD PREVENTIONPREVENTION BULLETINBULLETIN Dehydration Dehydration is a loss of too much fluid from the body. The body needs water in order to maintain normal functioning. If your body loses too much fluid - more than you are getting from your food and liquids - your body loses electrolytes. Electrolytes include important nutrients like sodium and potassium which your body needs to work normally. A person can be at risk for dehydration in any season, not just the summer months. It is also important to know that elderly individuals are at heightened risk for dehydration because their bodies have a lower water content than younger people. Why people with Common Causes and a developmental Risk Factors for disability may be Dehydration: at a higher risk for dehydration. v Diarrhea v Vomiting v People with physical limitations may v Excessive sweating not be able to get something to drink on their own and will need the assistance of v Fever others. v Burns v People who cannot speak or whose v Diabetes when blood sugar is too high speech is hard to understand may have a v hard time telling their support staff that Increased urination (undiagnosed diabetes) they are thirsty. v Not drinking enough water, especially on warm and hot days v Some people may have difficulty swal- lowing their food or drinks and may v Not drinking enough during or after exercise refuse to eat or drink. This can make v Some medications (diuretics, blood pressure them more susceptible to becoming meds, certain psychotropic and anticonvul- dehydrated.
    [Show full text]
  • Shock and Hemodynamic Monitoring
    Shock and Hemodynamic Monitoring Matthew Bank, MD, FACS Assistant Professor Hofstra North Shore‐LIJ School of Medicine Director, Surgical Intensive Care Unit North Shore University Hospital I do not have any financial conflicts of interest to disclose for this presentation Shock • Multiple different strategies for classifying shock, but all forms of shock result in impaired oxygen delivery secondary to either one or both: – reduced cardiac output (cardiogenic, septic) OR – loss of effective intravascular volume (hypovolemic, neurogenic, anaphylactic, septic). Septic Shock –Gram Negative • Gram negative septic shock: —Very studied well studied in animal models —Lipopolysaccharide (LPS) in bacterial cell wall binds to LPS binding protein. —LPS‐LBP complex then binds to cell surface CD14 receptors on monocytes and macrophages. —The LPS‐LBP‐CD14 complex then activates cells via Toll‐like receptor‐4 (TLR4). —TLR4 then “activates” cells which produce a cytokine “cascade” of proinflamatory mediators. Septic Shock –Gram Negative • Tumor Necrosis Factor (TNF) – First cytokine produced in response to gram negative sepsis – Principal mediator for acute response to gram negative bacteria – Major source of TNF is from activated macrophages – High levels of TNF predict mortality and can cause apoptosis. Septic Shock –Gram Negative • Interleukin‐1 (IL‐1) – Levels of IL‐1 increase soon after TNF production in gram negative sepsis (second cytokine to be elevated) – IL‐1 produced by macrophages, neutrophils and endothelial cells – IL‐1 increases levels of next proinflammatory cytokines in cascade, IL‐2 and IL‐12. – IL‐1 does NOT cause apoptosis Septic Shock –Gram Negative • Interleukin‐10 – Anti‐inflammatory cytokine – Inhibits production of IL‐12 – Inhibits T‐cell activation Septic Shock –Gram Positive • Gram positive sepsis – Gram positive cell wall components are also known to be involved in septic response – Peptidoglycans – Teichoic Acid – Likely act in a similar manner as LPS, but less potent on a weight bases.
    [Show full text]
  • What Is Sepsis?
    What is sepsis? Sepsis is a serious medical condition resulting from an infection. As part of the body’s inflammatory response to fight infection, chemicals are released into the bloodstream. These chemicals can cause blood vessels to leak and clot, meaning organs like the kidneys, lung, and heart will not get enough oxygen. The blood clots can also decrease blood flow to the legs and arms leading to gangrene. There are three stages of sepsis: sepsis, severe sepsis, and ultimately septic shock. In the United States, there are more than one million cases with more than 258,000 deaths per year. More people die from sepsis each year than the combined deaths from prostate cancer, breast cancer, and HIV. More than 50 percent of people who develop the most severe form—septic shock—die. Septic shock is a life-threatening condition that happens when your blood pressure drops to a dangerously low level after an infection. Who is at risk? Anyone can get sepsis, but the elderly, infants, and people with weakened immune systems or chronic illnesses are most at risk. People in healthcare settings after surgery or with invasive central intravenous lines and urinary catheters are also at risk. Any type of infection can lead to sepsis, but sepsis is most often associated with pneumonia, abdominal infections, or kidney infections. What are signs and symptoms of sepsis? The initial symptoms of the first stage of sepsis are: A temperature greater than 101°F or less than 96.8°F A rapid heart rate faster than 90 beats per minute A rapid respiratory rate faster than 20 breaths per minute A change in mental status Additional symptoms may include: • Shivering, paleness, or shortness of breath • Confusion or difficulty waking up • Extreme pain (described as “worst pain ever”) Two or more of the symptoms suggest that someone is becoming septic and needs immediate medical attention.
    [Show full text]
  • Pediatric Shock
    REVIEW Pediatric shock Usha Sethuraman† & Pediatric shock accounts for significant mortality and morbidity worldwide, but remains Nirmala Bhaya incompletely understood in many ways, even today. Despite varied etiologies, the end result †Author for correspondence of pediatric shock is a state of energy failure and inadequate supply to meet the metabolic Children’s Hospital of Michigan, Division of demands of the body. Although the mortality rate of septic shock is decreasing, the severity Emergency Medicine, is on the rise. Changing epidemiology due to effective eradication programs has brought in Carman and Ann Adams new microorganisms. In the past, adult criteria had been used for the diagnosis and Department of Pediatrics, 3901 Beaubien Boulevard, management of septic shock in pediatrics. These have been modified in recent times to suit Detroit, MI 48201, USA the pediatric and neonatal population. In this article we review the pathophysiology, Tel.: +1 313 745 5260 epidemiology and recent guidelines in the management of pediatric shock. Fax: +1 313 993 7166 [email protected] Shock is an acute syndrome in which the circu- to generate ATP. It is postulated that in the face of latory system is unable to provide adequate oxy- prolonged systemic inflammatory insult, overpro- gen and nutrients to meet the metabolic duction of cytokines, nitric oxide and other medi- demands of vital organs [1]. Due to the inade- ators, and in the face of hypoxia and tissue quate ATP production to support function, the hypoperfusion, the body responds by turning off cell reverts to anaerobic metabolism, causing the most energy-consuming biophysiological acute energy failure [2].
    [Show full text]