| Term 
 
        | Shock from any  cause can progress to....   (2) |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | What is multiple organ dysfunction syndrome? |  | Definition 
 
        | progressive   often involves the ultimate failure of 2 or more organ systems after a severe illness or injury. |  | 
        |  | 
        
        | Term 
 
        | How can shock be classified? (3) |  | Definition 
 
        | type prinicipal pathophys process clinical manifestations |  | 
        |  | 
        
        | Term 
 
        | What causes the following: 
 
cardiogenic:  neurogenic or vasogenic:  anaphylactic:  septic:  hypovolemic: traumatic shock:  |  | Definition 
 
        | cardiogenic: caused by heart failure neurogenic or vasogenic: caused by alterations in vascular smooth muscle tone anaphylactic: caused by hypersensitivity septic: caused by infection hypovolemic: caused by insufficient intravascular fluid volume traumatic shock: components of hypovolemic and septic shock |  | 
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        | Term 
 
        | What are common signs of symptoms of pt experiencing shock? |  | Definition 
 
        | feel sick weak cold hot neauseated dizzy confused afraid thirsty  SOB |  | 
        |  | 
        
        | Term 
 
        | What is the common pathway in all types of shock? |  | Definition 
 
        | impairment of cellular metabolism |  | 
        |  | 
        
        | Term 
 
        | Explain the impairment of oxygen use in:   cardiogenic shock hypovolemic shock neurogenic, anaphylactic and septic shock |  | Definition 
 
        | cardiogenic shock: CO is too low to deliver adequate oxygen to the cell   hypovolemic shock: O2 delivery is impaired by inadequate numbers of red cells or inadeq volume of intrvascular fluid.   Neurogenic, anaphylactic, septic shock: systemic vascular resistance is too low and perfusion pressure in the capillaries is inadequate to drive O2 across cell membranes   Septic shock: hypoxia is made worse by fever, which increases the cell's oxygen consumption rate and by endotoxic and inflammatory chemical disruption of cell metabolism, which impairs the cells' ability to use oxygen |  | 
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        | Term 
 
        | What happens when a cell doesn't have oxygen? |  | Definition 
 
        | it shifts from aerobic to anaerobic metabolism   anaerobic metabolism is less efficient method of extracting energy from carbon bonds and cell begins to use adenosine triphosphate faster than it can be replaced |  | 
        |  | 
        
        | Term 
 
        | What happens when a cell doesn't have ATP? |  | Definition 
 
        | without ATP, cell loses its ability to maintain an electrochemical gradient across its selectively permeable membrane (ie. can't work the Na/K pump) |  | 
        |  | 
        
        | Term 
 
        | What happens if the Na and K pump doesn't work bc of lack of O2? |  | Definition 
 
        | sodium and chloride builds up in the cell and K exits |  | 
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        | Term 
 
        | How do you get decreased circulatory volume when there is impairment of oxygen use? |  | Definition 
 
        | As sodium moves into the cell, water follows. Throughout the body, the water drawn from the interstitium into the cells is "replaced" by water that is in turn drawn out of the vascular space, often called "third spacing" of fluid |  | 
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        | Term 
 
        | What 3 positive feedback loops further impair oxygen use: |  | Definition 
 
        | 1. activation of the clotting cascade 2. decreased circulatory volume 3. lysosomal enzyme release |  | 
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        | Term 
 
        | What activates the clotting cascade in the positive feedback loop?   What are complications of clotting cascade in shock? |  | Definition 
 
        | sluggish capillary flow decreases tissue perfusion further and activates the clotting cascade.   Complications: acute tubular necrosis, ARDS, DIC |  | 
        |  | 
        
        | Term 
 
        | What amplifies intravascular fluid loss? |  | Definition 
 
        | when serum protein and other plasma proteins are consumed for fuel which results in decreased intravascular osmotic pressure, shift of fluid to the interstitial or extracellular spaces and decreased circulation volume |  | 
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        | Term 
 
        | Impair oxygen use causes lysosomal enzymes to be released from cells...what is the impact? |  | Definition 
 
        | the enzymes not only damage the cell that released them but also injures adjacent cells.   By damaging the mechanisms of surrounding cells, lysosomal enzymes extend areas of impaired metabolism and cellular injury. |  | 
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        | Term 
 
        | WHen you don't have oxygen for cells, the cells go into anaerobic metabolism. This has an effect on the pH. Explain. |  | Definition 
 
        | it causes metabolic acidosis   cardiac and skeletal muscle use lactic acid as fuel sources, but only for a limited time |  | 
        |  | 
        
        | Term 
 
        | What are consequences of decreasing pH of a cell? |  | Definition 
 
        | Enzymes necessary for cellular function dissociate under acid conditions.   Enzyme dissociation stops cell function, repair and division.   As lactic acid is released systemically- blood pH drops, reducing the oxygen-carrying capacity of the blood; THEREFORE LESS OXYGEN IS DELIVERED TO THE CELLS!   further acidosis triggers the release of more lysosomal enzymes because the low pH disrupts lysosomal membrane integrity |  | 
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        | Term 
 
        | What prevents glucose uptake? |  | Definition 
 
        | vasoactive toxins, endotoxins, histamine and kinins |  | 
        |  | 
        
        | Term 
 
        | What can influence glucose metabolism to be increased or disrupted? (2) |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | What are the effects of high serum levels of cortisol, growth hormone, and catecholmines?   5 |  | Definition 
 
        | cause hyperglycemia and insulin resistance tachycardia increased SVR increased cardiac contractility |  | 
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        | Term 
 
        | When cells are not getting the glucose that they need, for example, due to a shock state- how do they compensate? |  | Definition 
 
        | glycogenolysis, gluconeogenesis and lipolysis |  | 
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        | Term 
 
        | True or False:   The depletion of fat and glycogen stores is the cause of organ failure. |  | Definition 
 
        | False   The energy costs of glycogenolysis and lipolysis are considerable and contribute to the cells' failure. |  | 
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        | Term 
 
        | What is a cause of organ failure in shock?   why? |  | Definition 
 
        | depletion of protein is a cause   why? Gluconeogensis causes proteins to be used for fuel soo these proteins are no longer available to maintain cellular structure, function, repair and replication. |  | 
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        | Term 
 
        | During anaeorobic metabolism,   protein breakdown liberates ____, which is converted to ___ acid. IN sepsis this ____ acid is changed into lactic acid and positive feedback loop is formed. |  | Definition 
 
        | 
 
During anaeorobic metabolism,   protein breakdown liberates alanine, which is converted to pyruvic acid. IN sepsis this pyruvic acid is changed into lactic acid and positive feedback loop is formed. |  | 
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        | Term 
 
        | what is the byproduct of proteins broken down during anaerobic metabolism--aka what is produced?   2 |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | In septic shock plasma protein breakdown includes ____, thereby impairing immune system function when it is most needed. |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | what is considered a final outcome of impaired cellular metabolism? |  | Definition 
 
        | build up of metabolic end products in the cell and interstitial spaces.    Waste products are toxic to the cells and further disrupt cellular function and membrane integrity.   Ex. in septic shock- a deficiency isn cellular metabolism and the buildup of toxins may precede and cause decreased tissue perfusion. |  | 
        |  | 
        
        | Term 
 
        | The inability of the heart of pump adequate blood to tissues and end organs from any cause, the most common being within hours of an acute MI or severe epidsode of myocardial ischemia.   What is this called? |  | Definition 
 | 
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        | Term 
 
        | Name 3 things that can lead to cardiogenic shock. |  | Definition 
 
        |  pathologic conditions that:   1. reduce contractility: AMI, cardiomyopathy, sepsis,  myocarditis, dysarrythmias, metabolic abnormalities, papillary muscle reputure   2. impair diastrolic filling: related to arrythmias   3. cause obstruction: due to PE, cardiac tamponade, valvular disorders and wall rupture or defects |  | 
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        | Term 
 
        | What are some compensatory mechanisms that kick in when CO decreases? |  | Definition 
 
        | RAA system neurohormoanal and sympathetic nervous system   BP mainted through vasoconstriction in response to catecholmine release from adrenals; catecholmines also increase HR and contractility   Increases in blood volume and vascular resistance normalize blood pressure and increase cardiac performance |  | 
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        | Term 
 
        | What progressively deteriorates the mycocardium? |  | Definition 
 
        | increased coronary, tissue and cellular ischemia   pg. 1700 |  | 
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        | Term 
 
        | Tachycardia tachypnea hypotension JVD low measured CO |  | Definition 
 
        | hallmarks of cardiogenic shock |  | 
        |  | 
        
        | Term 
 
        | What are signs of end organ failure in cardiogenic shock? |  | Definition 
 
        | cyanosis, skin mottling, rapid, faint or irregular pulses, low urine output and occasional peripheral edema |  | 
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        | Term 
 
        | Name causes of hypovolemic shock. |  | Definition 
 
        | whole blood (hemorrhage) plasma (burns) interstitial fluid (diaphoresis, DM, diabetes insipidus, emesis or diuresis)   |  | 
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        | Term 
 
        | How do the liver and spleen try to assist in hypovolemic shock? |  | Definition 
 
        | add to blood volume by disgorging stored red blood cells and plasma |  | 
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        | Term 
 
        | How do the kidneys assist in hypovolemic shock? |  | Definition 
 
        | renin stimulates aldosterone relase and retention of sodium (and hence water), whereas ADH, or vasopressin, from the posterior pituitary gland increases water retention |  | 
        |  | 
        
        | Term 
 
        | high SVR poor skin turgor thirst oliguria low systemic and pulmonary preloads and rapid heart rate |  | Definition 
 | 
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        | Term 
 
        | Widespread and massive vasodilation that results from an imbalance between parasympathetic and sympathetic stimulation of vascular smooth muscle.   what is this describing? |  | Definition 
 
        | neurogenic or vasogenic shock |  | 
        |  | 
        
        | Term 
 
        | Explain the process of impaired cellular metabolism as it related to neurogenic shock |  | Definition 
 
        | blood volume has not changed, but the amt of space containing the blood has increased, so the SVR decreases drastically; thus pressure in the vessels is inadequate to drive nutrients across capillary membranes, and nutrient delivery to the cells is impaired. |  | 
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        | Term 
 
        | parasympathetic stimulation automatically ___ sympathetic activity and vice versa |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Normally, sympathetic stimulation maintain ____.   If the stimulation is interrupted or inhibited- this causes... |  | Definition 
 
        | muscle tone   causes vasodilation |  | 
        |  | 
        
        | Term 
 
        | WHat are ways to interrupt sympathetic activity causing neurogenic shock? |  | Definition 
 
        | trauma to the spinal cord or medulla   conditions that interrupt the supply of oxygen to the medulla, or conditions that deprive the medulla of glucose   Other: depressive drugs, anesthetic agents, severe emotional stress and pain |  | 
        |  | 
        
        | Term 
 
        | low SVR bradycardia ejection fraction remains high (indicates healthy myocardium) fainting |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | True or False   Most  episodes of fainting are NOT shock |  | Definition 
 | 
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        | Term 
 
        | widespread hypersensitivity reaction |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | What is the inflammatory response to allergen in anaphylactic shock? |  | Definition 
 
        | vasodilation and increased vascular permeability, resulting in peripheral pooling and tissue edema   Extravascular effects: constriction of extravascular smooth muscle--often causes respiratory difficulty bc it tends to affect smooth muscle layers in the airways walls |  | 
        |  | 
        
        | Term 
 
        | What is often the first manifestation of anaphylactic shock? |  | Definition 
 
        | anxiety, difficulty in breathing, GI cramps, edema, hives, and sensations of burning or iteching of the skin |  | 
        |  | 
        
        | Term 
 
        | Why do you give EPI in anaphylactic shock? |  | Definition 
 
        | decrease mast cell and basophil degranulation, cause vasoconstriction and reverse airway constriction |  | 
        |  | 
        
        | Term 
 
        | How does septic shock happen? (ie progression) |  | Definition 
 
        | begins with systemic inflammation response syndrome (SIRS) ↓ Sepsis ↓ severe sepsis ↓ septic shock   |  | 
        |  | 
        
        | Term 
 
        | What are the most common infection sites associated with sepsis in the ICU? |  | Definition 
 
        | pneumonia bloodstream intravascular catheter intra-abdominal urosepsis surgical wound infection |  | 
        |  | 
        
        | Term 
 
        | What is the leading cause of sepsis? |  | Definition 
 
        | gram pos bacteria   (used to be gram neg but abx have helped lower) |  | 
        |  | 
        
        | Term 
 
        | How does bacteria enter the blood to form bacteremia?   2 |  | Definition 
 
        | 1. directly from the stie of infection   2. from toxic substances released by the bacteria directly into the blood stream |  | 
        |  | 
        
        | Term 
 
        | What are the toxic substances released that lead to septic shock? |  | Definition 
 
        | gram neg: endotoxins gram pos: lipoteichoic acids and peptidoglycan |  | 
        |  | 
        
        | Term 
 
        | What are the proinflammatory cells released during septic shock?   what are proinflammatory mediators? |  | Definition 
 
        | cells: polymorphonuclear leukocytes macrophages monocytes platelets   mediators: cytokines TNF kinin   pg. 1704 |  | 
        |  | 
        
        | Term 
 
        | Proinflammatory cytokines enhance tissue factors which initiates ______. |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | What is the end result of septic shock? |  | Definition 
 
        | mixed antagonistic response syndrome as proinflammatory and anti-flammatory mediators respond, intensify and lead the host into MODS |  | 
        |  | 
        
        | Term 
 
        | Septic shock and states of proglonged shock cause.....   |  | Definition 
 
        | tissue hypoxia with lactic acidosis increase NO synthesis, activate ATP sensitive and calcium regulated K channels in vascular smoothmuscle and lead to depletion of ADH.   tachycardia causes cardiac output to remain normal or become elevated, although myocardial contractility is reduced.   Pt could be hyperthermic or hypothermic |  | 
        |  | 
        
        | Term 
 
        | What can help prevent evolution of severe sepsis and shock? |  | Definition 
 
        | ABX and identifiying sepsis in early stages |  | 
        |  | 
        
        | Term 
 
        | What should be included in initial resuscitation in septic shock? |  | Definition 
 
        | initial resuscitation within the first 6 hrs to include fluids, (crystalloids or colloids) ABX |  | 
        |  | 
        
        | Term 
 
        | What are the most common causes of multiple organ dysfunction syndrome? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Who is at the greatest risk for developing MODS? |  | Definition 
 
        | older adults and persons with significant tissue injury or preexisting disease |  | 
        |  | 
        
        | Term 
 
        | What causes secondary MODS? |  | Definition 
 
        | the result of an excessive inflammatory reaction, after a latent period following the initial injury, in organs distant from the site of the original injury |  | 
        |  | 
        
        | Term 
 
        | What organs are most severely affected by MODS? |  | Definition 
 
        | lungs, splanchnic bed, liver and kidneys |  | 
        |  | 
        
        | Term 
 
        | What is an early indicator of progression of sepsis to MODS? |  | Definition 
 
        | shunting caused by loss of autoregulation in some organs     |  | 
        |  |