I. Introduction - Shock (Chapter 11) A. Review of anatomy and physiology B. Pathophysiology Initiation | * Decreased tissue oxygenation * Decreased intravascular volume * Decreased Myocardial contractility (cardiogenic ) * Obstruction of blood flow (obstructive) * Decreased vascular tone (distributive) * Septic (mediator release) * Neurogenic (suppression of SNS) | No observable clinical indications Decreased CO may be noted with hemodynamic monitoring | Compensatory | * Neural compensation by SNS * Increased HR and Contractiliy * Vasoconstriction * Redistribution of blood flow from nonessential to essential organs * Bronchodilation * Endocrine Compensation (RAAS, ADH, glucocorticoid release) * Renal reabsorption of sodium, chloride, and water * Vasoconstriction * Glycogenolysis | * Increased HR (EXCEPT NEUROGENIC) * Narrowed pulse pressure * Rapid, deep respirations causing respiratory alkalosis * Thirst * Cool,moist skin * Oliguria * Diminished bowel sounds * Restlessness progressing to confsion * Hyperglycemia * Increased specific gravity and decreased creatinine clearance. | Progressive | * Progressive tissue hypoperfusion * Anaerobic metabolism wih lactic acidosis * Failure of sodium potassium pump * Cellular edema | * Dysrhythmias * Decreased BP with narrowed pulse pressure * Tachypnea * Cold, clammy skin * Anuria * Absent bowel sounds * Lethargy progressing to coma * Hyperglycemia * Increase BUN, CREATININE, AND POTASSIUM * Respiratory and metabolic acidosis. | Refractory | * Severe tissue hypoxia with ischemia and necrosis * Worsening acidosis * SIRS * MODS | * Lifethreatening dysrhythmias * Severe hypotension despite vasopressors * Respiratory and metabolic acidosis * Acute respiratory failure * Acute respiratory distress syndrome * DIC * Hepatic dysfunction/failure * Acute kidney injury * Myocardial ischemia/ infarction/failure * Cerebral ischemia/infarction |

C. Stages of shock 1. Initiation * hypoperfusion – (inadequate DO2, inadequate extraction of o2, or both). No obvious clinical indication of hypoperfusion are noted - hemodynamic monitoring is used for pt assessment. 2. Compensatory Stage – * sustained reduction in tissue perfusion initiates a set of neural, edocrine, and chemical compensatory mechanisms (to maintain blood flow to vital organs and to restore homeostasis) * symptoms become apparent, but shock may still be reversed with minimal morbidity. a. Neural compensation - * Baroreceptors and chemo receptors (carotid sinus and aortic arch) detect the reduction in arterial blood pressure. Impulses go to vasomotor center in the medulla oblongata, stimulating the sympathetic release epinephrine and norepinephrine (adrenal medulla), both HR and contractility increase to improve CO. * Coronary arteries dilate (increase perfusion to meet demands for o2) * Systemic vasoconstriction (improves blood pressure, venous vasoconstriction increased preload and CO), * Blood is shunted to heart and brain (from the kidneys, gastrointestinal tract, and skin.) * Bronchial smooth muscles relax, (RR and Depth are increased) – improving gas exchange and oxygenation. * Catecholamine -increased blood glucose levels * Liver converts glycogen to glucose for energy production; * Pupils dilate; * Peripheral vasoconstriction * Cool, moist skin - increased sweat gland activity * Endocrine compensation – combat shock by providing the body with glucose for energy and by increasing the intravascular blood volume. * Aldosterone – (in response to reduction in blood pressure, messages are also relayed to the hypothalamus, which stimulates the anterior and posterior pituitary gland. BP (water and sodium reabsorption) is increased from mineralcoricoids. * Hyperglycemia - (cortisol release with gluconeogenesis.) Blood glucose is increased from increased cortisol with gluconeogenesis. * The rass system is activated ADH is actived (get intravascular volume) * Chemical compensation – want to increase supply but cerebral perfusion may decrease * Pulmonary blood flow is reduced - ventilation-perfusion imbalances occur. Initially, alveolar ventilation is adequate, but the perfusion of blood through alveolar capillary bed is decreased. * Chemoreceptors are stimulated (low oxygen tension in the blood). * Hyperventilation leading to respiratory alkalosis - rate and depth of respirations increase. * Low CO2 and alkalosis – vasoconstriction of cerebral blood vessels cerebral hypoxia and ischemia (reduced o2 tension with vasoconstriction). \ 3. Progressive Stage –responds poorly to fluid replacement alone and requires aggressive interventions to be reversed a. Systemic Vasoconstriction. (the decrease in blood flow leads to ischemia in the extremities, weak or absent pulses, and altered body defenses.) b. Decreased capillary blood flow and cellular hypoxia (Prolonged vasoconstriction) c. Lactic acid (anaerobic metabolism metabolic acidosis.) d. Anaerobic metabolism produces less ATP causes failure of the NaK-pump. e. Cellular swelling (Sodium and water accumulate within the cell reduction in cellular function.
The micro circulation - dilation (increase the blood supply). * Arterioles remain constricted (keep vital organs perfused) * Precapillary sphincters relax (blood flow into the capillary bed), * Postcapillary sphincters constricted. (blood flows fin but not out). * Interstitial edema - Fluid is pushed from the capillaries into the interstitial space. (This fluid shift is further aggravated by the release of histamine and other inflammatory mediators that increase capillary permeability, along with the loss of proteins through enlarged capillary pores, which increase capillary oncontic preesure. * Capillary sludging as red blood cells, platelets, and proteins clump together. * Blood becomes more viscous and blood flow is slowed (decrease in intravascular blood volume). * Further decrease in CO and Preload (The loss of intravascular volume and capillary pooling further reduce venous return to the heart and cardiac output) * Decrease in myocardial contractility (Coronary artery perfusion pressure is decreased (MDF – ischemic pancreas) * Cardiac output, blood pressure, and tissue perfusion decrease.(At this point, the patient shows classic signs and symptoms of shock.

4. Refractory Stage – Prolonged inadequate tissue perfusion unresponsive to therapy ultimately contributes to multiple organ dysfunction and death * blood remains pooled in the capillary bed, and arterial blood pressure is too low to support perfusion of vital organs. * Dysrhythmias (failure of the NaK – Pump from decreasd ATP, hypoxemia, ischemia, and acidosis. * Cardiac failure (if ischemia, acidosis, and the effects of MDF) * ARDS (no surfactant production) - Endothelial damage in the capillary bed and precapillary arterioles, damage to the type 2 pneumocytes, which make surfactant) * Hypoxemic vasoconstriction of pulmonary circulation and pulmonary hypertension (Hypoxemia). * Ventilation-perfusion mismatch (disturbances in both ventilation and perfusion). * Pulmonary edema (disruption of the alveolar capillary membrane, ARDS, heart failure, or overaggressive fluid resuscitation. * Cerebral infarction may occur - Loss of auto regulation resulting in brain ischemia. (When cerebral perfusion pressure is significantly impaired). * Massive vasodilation (Sympathetic nervous system dysfunction) * Bradycardia and bradypnea (depression of cardiac and respiratory centers) * Poikilothermism (impaired thermoregulation). * Decreased GFR – (Renal vasoconstriction and hypoperfusion) * ATN (Prolonged ischemia of the kidney) * Worsening metabolic acidosis (lactic acid production during anaerobic metabolism) * The pt is predisposed to sepsis and bacterermia (Hypoperfusion damages the reticulendothlial cells, which recircultate bacteria and cellular debris). * Hypoglycemia -Liver failure/dysfunction -Damage to hepatocytes cuases the lver to be unable to detoxify drugs, toxins, and hormones, conjugate billiruben, or synthesize clotting factors. decreased ability to mobilize carbohydrate, protein, and fat stores * Hyperglycemia (dehydration and electrolyte imbalaances related to osmotic diuresis; impairment of leukocyte function causing increased phagocytosis and increased risk of infection; depression of the immune response; impairment in gastric motility; shifts in substrate availability from glucose to free fatty acids or lactate; negative nitrogen balance; and decreased wound healing * MDF (Pancreatic ischemia causes the release of MDF. Pancreatic enzymes are released by the ischemic and damaged pancreas., which impairs cardiac contractility.. * Stress ulcer (Ischemic and increased gastric acid production caused by glucocorticoids increase the risk of stress ulcer development. * Increased risk for sepsis –(Prolonged vasoconstriction and ischemia lead to the inability of the intestinal wall to act as intact barriers to prevent the migration of bacteria out of the gastrointestinal tract. This may result in the translocation of bacteria from the gastrointestinal tract into the lmphatic and vascular beds. * Microvascular thrombosis - Hypoxia and release of inflammatory cytokines impair blood flow and result. * DIC -Sluggish blod flow, massive tissue trauma, and consumption of clotting factors may cause. * Leukocytosis early and leukopenia. The bone marrow mobilizes the release of white blood cells, depletion of white blood cells in blood and in bone marrow occurs. * Development of SIRS - Massive tissue injury caused by widespread ischemia with a massive release of mediators of the inflammatory process * Fluid shifts – loss of vasomotor tone – hypovolemia (Poor renal function, respiratory failure, and impaired cellular function aggravate the existing state of acidosis. * Low HR, impaired contractility and decreased CO/tissue perfusion. (Alteration in the cardiovascular system and continued acidosis) * Cerebral ischemia (reduction in cerebral blood flow.) sympathetic nervous system is stimulated, an effect that aggravates the existing vasoconstriction, increasing afterload and decreasing cardiac output. P * Vasodilation and bradycardia result (Loss of sympathetic nervous system response, prolonged cerebral ischemia) * Decreasing blood pressure and heart rate (lethal decrease in tissue perfusion, multisystem organ failure that is unresponsive to therapy and ultimately brain death and cardiopulmonary arrest.

5. Systemic Inflammatory Response Syndrome – widespread inflammation. It may result from or lead to MODS. SIRS is most frequently associated wih sepsis. Sepsis is an infection associated with SIRS.
The inflammatory cascades maintain homeostasis through a balance between proinflammatory and intiinflammatory processes. Inflammation is normally a localized process; SIRS is a systemic response associated with the release of mediators. These mediators cause an increase in the permeability of the endothelial wall, shifting fluid from the intravascular space into extravascular spaces, including the interstitial space. Intravascular volume is reduced, resulting in a condition of relative hypovolemia. Other mediator cause micro vascular clotting, impaired fibrinolysis, and widespread vasodilation.

6. Effects of Aging – * left ventricular wall thickens, * ventricular compliance decrease * calcification and fibrosis of the heart valves occur. * Stroke volume, cardiac output are reduced. * Decreased sensitivity of the baroreceptors and a diminished heart rate response to sympathetic nervous system stimulation in the early stage of shock. * More likely to be prescribed BB, which also decrease the heart rate response. * Increased SVR - Arterial walls lose elasticity. Increases the myocardial oxygen demand and decreases the responsiveness of the arterial system to the effect of catecholamines. * decreased lung elasticity, * decreased alveolar perfusion,surface area, and thickening of the alveolar capillary membrane. * These changes limit the body’s ability to increase blood oxygen levels during shock states. * Decreased urine concentration -which limits the body’s ability to conserve water when required. * immunosenescenceThe immune system loses effectiveness with age, increases the risk of infection and sepsis, especially with illness, injury, or surgery. * Greater risk for anaphylaxis since they have been exposed to more antigens and therefore have antibodies to more antigens.

II. Assessment A. Clinical presentation – Change in vital signs, hemodynamic parameters, sensorium | Secondary to decreased tissue perfusion and initation of compensatory mechanisms | Decreased urine otput, risin BUN and creatinine levels | Secondary to initation of compensatory mechanisms and decreased renal perfusion | Tachypnea, ypoxemia, worsening chest xray | Related to development of acute respiratory ditress syndrome secondary to hypoperfusion | Petechiae, ecchymosis, blooding from puncture sites overt or occult blood in urine, stool, gastric aspirate, tracheal aspirate | Related to development of disseminated intravascular coagulation secondary to shock, SIRS | Hypoglycemia, increase in liver enxymes | Related oto hepatic dysfunction secondary o hypoperfusion |

B. Central Nervous System – First system affected in cellular perfusion. Most sensitive to changes in the supply of O2 and nutrients..
Initial responses include: restlessness, agitation, and anxiety. As shock progresses, confuse and lethargic As shock progresses, unresponsive. C. Cardiovascular System –assesssment is blood pressure. Know the patient’s baseline blood pressure. a. Compensatory stage, increase in myocardial contractility and vasoconstriction (innervation of the sympathetic nervous system) normal or lightly elevated systolic pressure, an increased diastolic pressure, and a narrowed pulse pressure. b. As the shock state progresses systolic blood pressure decreases, but the diastolic remains normal resulting in a narrowed pulse pressure. this narrowed pulse pressure may preceed changes in heart rate. c. 90 mm Hg is hypotensive. ---If the patient is hypertensive, a decrease in systolic pressure of 40 mm Hg from usual systolic pressure is hypotensive. d. Use intraarterial monitoring. Auscultated blood pressure in shock maybe inaccurate (peripheral vasoconstriction.). If he brachial pulse is readily palpable, 80 mm Hg. (femoral and carotid pulses is 70 and 60). * Palpate pulses -In shock, the pulse is often weak and thready. The pulse rate is increased, (over 100 beats ), through stimulation of the sympathetic nervous systm as a compensatory response to the decreased cardiac output and increased demand of the cells for oxygen. * In later stages of shock, the pulse slows, possibly from release of MDF. * Medications -Negative inotropic agents, (propranolol and metropolol) are widely used in the treatment of angina, hypertension, and dysrhythmias - cause a decrease in heart rate and cardiac output. A patient who is taking these medications has an altered ability to respond to the stress of shock and may not exhibit the typical signs and symptoms such as tachycardia and anxiety. * JVD (assesses CVP) (distended inobstructive or cardiogenic shock Flat in hypovolemic shock) * Capillary refill assesses perfusion. vasoconstriction (Delay). Not reliable in a patient who is hypothermic or has peripheral circulatory problems. * CVP – decreased in hypovolemia, vascular capacitance (distributive shock) * CVP increased when cardiogenic shock (heart inability to contract forcefully) and obstructive shock (tension pneumothrox). A central venous catheter (to aid in differential diagnosis of shock, administer and monitor therapies, evaluate the preload of the heart.) * A PA catheter. (caution insertion infections) The PA catheter can give information regarding cardiac dynamics, fluid balance,a nd effects of vasoactive agents. Preload (RAP – right ventricle PAOP – left ventricle) CO index, afterload, and stroke work indices can also be assessed with a PA catheter. Use a oximetric PA catheter to measure SvO2. * If SvO2 is less than 60% either the DO2 inadequate or the VO2 is excessive. The SvO2 is decreased in all forms of shock except in early septic shock, (poor oxygen extraction causes SvO2 to be high). The SvO2 is useful in identifying the type of shock and in evaluating the effectiveness of treatment.. ScvO2 correlates to SvO2 and is easier to obtain in emergent situations. D. Respiratory System – early shock, RR are rapid and deep (shock and metabolic acidosis to eliminate CO2. * Stimulation of the medulla by chemoreceptors. As shock progresses, metabolic wastes accumulate and cause generalized muscle weakness, shallow breathing with poor gas exchange. * Pulse ox can be wrong from decreased perfusion to the skin and extremities. * ABG is GOLD Standard E. Renal System –oliguria (<.5 ml/kg/hr) hypoperfusion and decreased GFR. * Sodium and water reabsorption (The RAAS system is active – promotes retention of sodium and the reabsorption of water in the kidneys, further decreasing urinary output. * Concentrated urine, increased BUN, serum creatinine is normal. (pre-renal cause of acute kidney injury) * Creatinine levels increase when decreased persusion is prolonged and acute tubular necrosis (intrarenal failure) occurs F. Gastrointestinal System – * decreased bowel sounds, distention, nausea, and constipation (hypoperfusion slowing of intestinal activity). * Paralytic ileus and ulceration with bleeding may occur with prolonged hypoperfusion. * Translocation of bacteria from GI tract to lympatic and systemic circulation. (Damage to microvilli) Increasing the risk of infection and sepsis in the already compromised critically ill patient.
Liver – decreased function and alterations in liver enzyme levels such as LDH and AST. If decreased perfusion persists, the lver is not able to produce coagulation factors, detoxify drugs, or neutralize invading microorganisms. Clotting disorders, drug toxicity concerns, and increased susceptibility for infection occur. G. Hematological System – * clotting in the microcirculatory system and bleeding (inflammation and coagulation enhances clotting and inhibits fibrinolysis). * consumptive coagulopathy (increased consumption of platelets and clotting factors occurs) The inability of the Liver to manufacture clotting factors also contributes to the coagulopathy. A decreased platelet count, decreased clotting factors, and prolonged clotting times are seen with coagulopathy. * Petchiae and ecchymosis, blood in the urine, stool, gastric aspirate, and or tracheal secretions. * peripheral ischemia manifested by acrocyanosis and necrosis of digits and extremities. (clotting in the microcircultation). Leukocytosis frequently occurs, especially in early septic shock. Leukopenia occurs later because of consumption of white blood cells.

H. Integumentary System – skin color, temperature, texture, turgor,and moisture level are evaluated. * Cyanosis (late and unreliable sign.) * central cyanosis (mucous membranes of the mouth and nose; or peripheral cyanosis, evident in the nails and earlobes. * Turgor is frequently used to determine the presence of interstitial dehydration, elderly adults have decreased skin elasticity, making this evaluation misleading.

I. Laboratory Studies (see box, “Laboratory Alert”) Glucose | <70 >100 | Increased early shockIncrease impairs immune response Decreased late shock | BUN | >20 | Increased – hypoperfusion (prerenal) Increased – gastrointestinal bleeding and catabolism | Creatinine | >1.2 | Increased acute kidney injury | Sodium | <136 or >145 | Decreased Hemodilution from replacement of excessive hypotonic fluid | Chloride | >108 | Increased Hemoconcentratino from fluid loss Increased excess infusion of normal saline; may cause hyperchloremic acidosis | K | <3.5 or >5.3 | Decreased excessive loss of K Increased impaired elimination from acute kidney injury Observe for cardiac dysrhythmias | Lactate | >2.2 | Increased hypoxia leading to anaerobic metabolism and production of lactic acid | AST | >20 | Increased hepatic impairment | LDH | >102 | Increased hepatic impairment, renal impairment, intestinal ischemia, or MI | WBC | <4500 or >11,000 | Increased Stress response; significant increased indicated infection Decreased late shock due to consumption of WBC | HGB | <12 | Decreased blood loss | HCT | <35 | Decreased blood loss Increased dehydration and hemoconcentration | PH | | Increased : early shock – respiratoy alkalosis due to hyperventilation Decreased late shock – metabolic acidosis due to lactic acidosis | PaCO2 | | Decreased early shock – respiratory alkalosis due to hyperventilation | PaO2 | <80 | Decreased; may indicate pulmonary edema or ARDS | HCO3 | <22 | Decreased late shock – metabolic acidosis caused by hypoxia, anaerobic metabolism and lactic acidosis. | | | |

J. QSEN Exemplar – Quality Improvement – central line associated blood stream infection and VP are common causes of morbidity and mortality in critically ill patients. Interventions to prevent blood stream infections include handwashing, full barrier precautions during central line insertion, chlorhexidine skin cleansing, avoidance of femoral insertion sites, and timely removal of unnecessary central line catheters. Head of the bed elevated, DVT prophylaxis, gastric ulcer prophylaxis, daily assessment for weaning appropriateness, and appropriate management of sedation comprised VAP preventive strategies. Additionally, a comprehensive safety program was implemented in each participating unit. In an effort to promote a culture of safety, practitioners were empowered to stop procedures where safety was potentially compromised. K. Hemodynamic Alterations in Shock States – Table 11-3 III. Management – treat the cause as rapidly as possible. Correcting or revering the altered circulatory compent and reversing tissue hypoxia. Manintain tissue perfusion and improve oxygen delivery. Increase the CO and CI, HGB, arterial o2 saturation. Minimize o2 consumption.

A. Maintenance of Circulating Blood Volume and Adequate Hemoglobin Level –hypovolemia (hypovolemic shock) or relative (distrubitive shock) * administration of IV fluids to restore intravascular volume, * maintain oxygen carrying capacity , * establish hemodynamic stability.

Cardiogenic shock managed parimarily with medications that reduce both preload and afterload.
Fluid administration is adjusted based on blood pressure, urine output, hemodynamic values, diagnostic test results, and the clinical picture of the patient’s response to treatment. Values obtained from hemodynamic monitoring also assist in monitoring effects of treatment. * MAP (65 to 70) * Improved LOC, UO, Peripheral perfusion(evidence of end organ tissue perfusion is reestabilished),
Severe shock: rapid rapid volume replacement. (blood pump to administer fluids under pressure, by using large-bore insusion tubing,) * a rapid-infusion device. * Large volumes of room temperature and cause hypothermia (alteration in cardiac contractility and coagulation) * Large volumes of fluids should be infused through warming devices. B. Intravenous Access – IV access is needed to administer fluids and medicaions.

* 2 IV catheters (peripheral and central 14 or 16). Establishing IV in a pt in shock is difficult (peripheral vasoconstriction and venous collapse).
Multilumen catheters, which provide multiple access ports, and blood products. * A PA catheter may be inserted to monitor hmodynamic pressures and guide fluid replacement. C. Fluid Challenge – to assess the pt’s hemodynamic response to fluid administration. Rapid infusion of 250 ml (up to 2L) of a crystalloid solution. Nursing responsibilities: obtaining the baseline hemodynamic measurements, administering the fluid challenge, and assessing the pt’s response.

D. Types of Fluids – blood, blood products, crystalloids, and colloids are used alone, or in combo, to restore intravascular volume. Crystalloids until diagnostic testing and blood typing and crossmatching are completed.

* Colloids are avoided in sepsis and septic shock, anaphylactic shock and burns (increase in capillary permeability). Don't give albumin if critically ill patients with hypovolemia – higher risk of death.
Crystalloids are classified by tonicy. Isotonic solutions have approximately the same tonicty as plasma (osmolarity, 250 to 350 mOsm/L). LR solution and .9% NS are isotonic solutions (move freely from the intravascular space into the tissues) * 3 mL crystalloid to replace each 1 mL of blood loss. * LR solution (resembles plasma and may be the only fluid replacement required if blood loss is < 1500 ml). * LR contains lactate, (liver converts to bicarbonate) counteracts metabolic acidosis if the liver function is normal. * LR should not be infused in pt with impaired liver function or severe lactic acidosis. * .9% NS (isotonic solution), its side effects hypernatremia, hypokalemia, and hyperchloremic metabolic acidosis. * 5% dextrose in water and .45% normal saline (hypotonic and are not used for fluid resuscitation.) Hypotonic solutions rapidly leave the intravascular space, causing interstitial and intracellular edema. * Large volumes of crytalloids are infused, the pt is at risk of developing hemodilution of RBC and plasma proteins. * Impairs o2 delivery if the HCT value is decreased and the CO cannot increase enough to compensate. * Pulmonary edema. Hemodilution of plasma proteins decreases colloid osmotic pressure. Eldery pt are at increased risk of developing pulmonary edema and may require invasive hemodynamic monitoring to guide fluid resuscitation. * Colloids contain protein that increase osmotic pressure. * Colloids remain in the intravascular space longer than crystalloids, (give smaller volumes of colloids are given in shock states). * BURN, peritonitis, bowel obstruction- give albumin and plasma protein fraction (plasmanate) when the volume loss is caused by a loss of plasma rather than blood, Typing and crossmaticng of albumin and plasma protein fraction are not required. * Pulmonary edema is a potential complication, (increased pulmonary capillary permeability or increased capillary hydrostatic pressure in the pulmonary vasculature created by rapid plasma expansion.)
Hetastarch (synthetic colloid) acts as a plasma expander but carries less risk for pulmonary edema. Side effects include altered prothrombin time and activated partial thromboplastin time and the potential for circulatory overload. No more than 1L should be administered in a 24 HR period.

Blood products, PRBC, FFP, and platelets are administered to treat major blood loss. Typing and crossmatching. In extreme emergencies, the pt may be transfused with type-specific or O-neg blood (universal doner blood type.) * Transfusions require (at least a 20 gauge, preferably an 18 gauge or larger, catheter (22 ok for adults with small veins). * Solutions other than .9% NS are not infused with blood because they cause red blood cells to aggregate, swell and burst. * Never give IV medication in the same port with blood. * Blood filter to trap debris with infusions and clots. * In the event of a reaction, the transfusion is stopped, disconnected from IV site, keep open with 9%NS, assess pt and notify physicial and laboratory. All transfusion eq and any blood or urine specimens obtained are sent to the laboratory according to hospital policy. * Document interventions
. Documentation of the transfusion includes the blood product administered, baseline vital signs, start and completion time of the transfusion, volume of blood and fluid, assessment of the patient during the transfusion, and any nursing actions taken. * PRBC increase the blood volume (provide more o2 carrying capability). One unit of PRBC increase the hematocrit by 3% and the HBG 1. * Typing and crossmatching of PRBC are required. * RBC tend to aggregate because of the fibrinogen coating; therefore, washed rbc may be given. Acidosis, hyperkalemia, and coagulation problems are associated with transfusions of banked blood older than 24 hr. * Massive transfusion (10 units) is assoiated with a decreased 2,3-DPG cuasing a shift to the LEFT.

* FFP (GIVE TO CLOT) (replace all clotting factors except platelets). One unit of FFP for every 4 – 5 units of PRBC transfused. Typing and crossmatching is required. * Platelets (TYPING is REQUIRED but not crossmatching) given rapidly to help control bleeding from low platelets ( <50,000).

E. Maintenance of Arterial Oxygen Saturation and Ventilation – airway is TOP PRIORITY. * HOB elevated, oral or nasopharyngeal airways, * intubation (depending on pt condition). * Suctioning and CPT (facilitate secretion removal -maintain a patent airway). * O2 (elevate the arterial o2 tension, thereby improving tissue oxygenation.) * O2 (nasal canula to mechanical ventilation, depending) * Mechanical ventilation (ventilation as reflected by a normal partial pressure of arterial carbon dioxide level. )Decrease WOB and o2 consumption * Low Tidal volumes (6 – 8ml/kg) and inspiratory pressures (<30 cm) (kept low to prevent ventilator-induced lung injury. and inspiratory plateau pressures are maintained at less than 30 cm H20. * PEEP (maintain alveolar recruitment and may protect against ventilator modes, - the pressure-regulated volume-controlled mode, aid in keeping inspiratory pressures low.) * Sedation or neuromuscular blockade ( reduce o2 consumption) Arteral blood gases, pulseoximetry and demodynamic monitoring aid in the evauation of o2 consumption and delivery. F. Pharmacological Support (Medications Commonly Used in Shock Table 11-4) G. Cardiac Output – low/high HR and dysrhythmias decrease cardiac output. * neurognic shock, sinus bradycarida from cervical spinal cord injury does not usually require therapy. * bradycardia is significant = decreased perfusion atropine or temporary pacemaker may be required. 1. Preload – hypovolemic and distributive shock, FLUID ADMINISTRAION IS PRIMARY TREATMENT TO INCREASE PRELOAD. * In cardiogenic shock give vasodilators or diuretics, the myofibrils are overstretched and the preload needs to be reduced. 2. Afterload –
Distributive shock (anaphylaxis, neurogenic, septic) low GIVE VASOCONSTRICTOS (-prine and vasopressin) (increase vascular tone and tissue perfusion pressure.). These drugs increase blood pressure and SVR. * A negative effect of drugs = increase in the myocardial o2 demand. * Use PA catheter - measurement/calculation of SVR and PVR

Hypovolemic shock - give fluids not vasopressors further diminishes tissue perfusion – they need volume..
Cardiogenic shock, -use IABP. Arterial vasodilators to reduce afterload may be limited by the pt’s BP. When hypotension prevents the use of arterial vasodilators,

3. Contractility – dobutamine may be administered in cardiogenic shock. Although drugs that decrease contractility (BB) may be used to decrease myocardial o2 consumption in pt in shock. H. Other Medications –sedatives, analgesics, insulin, corticosteroids, and antibiotics. Increase DO2. Although respiratory acidosis is treated by improving ventilation, metabolic acidosis caused by lactic acidosis is best treated by improving the aspects of DO2: SaO2, hemoglobin level, and cardiac output. * ABG analysis and serum lactate levels are used to guide treatment. * Hyperglycemia – give INSULIN to keep under 150 (common in shock pt esp with septic shock.) * LMW heparin (DVT) * –tideine or PPI (peptic ulcer prophylaxis)

I. Maintenance of Body Temperature – pt temperature is monitored frequently.. Hypothermia (depresses cardiac contractility and impairs CO and o2 delivery, impairs the coagulation pathway, - significant coagulopathy) Hypothermia anticipated when fluids are infused rapidly, (FLUID WARMER). Excessive warmth increases the o2 demand on an already stressed CV system. J. Nutritional Support –initiate enteral intake ASAP and maintain sufficient caloric intake to assist in the healing process.(Early enteral feeding decreases hypermetabolism, minimizes bacterial translocation, decreases diarrhea, and decreases length of stay.). Enteral feeding preferred method, and immune-bosting formulas may be prescribed. Admin of enteral nutrition may be limited by paralytic ileus, gastric dilation or both, which are common in shock. TPN is given if pt are unable to tolerate enteral feeding. K. Maintenance of Skin Integrity – * The pt is turned at frequent intervals, and lotion is applied. * Pressure relieving decides (therapeutic beds/matresses) do not substitute for the pressure relief afforded by manual turning and positioning. * Float heels with (pillows or with pressure relief boots. ) L. Psychological Support – Provide information (important for the psychological well-being of the pt and the family, and may help to give them a sense of understanding and control of the situation. M. Nursing Diagnosis 1. Nursing Care Plan for the Patient in Shock IV. Specific Classifications of Shock A. Summary of Classifications of Shock 1. Hypovolemic Shock – low blood volume. caused by external or internal losses of either blood or fluid. - unable to transport o2 and nutrients to tissues.
External volume deficits include loss of blood plasma, or body fluids. HEMORRHAGE. * External loss of blood (traumatic injury, surgery, or obstetrical delivery or with coagulation alterations (hemophilia, thrombocytopenia, DIC and anticoagulant med). * External plasma losses may be seen in pt with burn injuries who have significant fluid shift from the intravascular space to the interstitial space. * Excessive external loss of fluid from GI tract via suctioning, upper GI bleeding, vomiting, diarrhea, reduction in oral flid intake, or fistulas; through the genitourinary tract as a result of excessive diuresis, DM with polyuria, DI, Addisons; or though the skin secondary to diaphoresis without fluid and electrolyte replacement. * Blood or body fluid may be sequestered within the body outside the vascular bed.
Internal sequestration of blood may be seen in pt with a ruptured spleen or lvier, hemothorax, hemorrhagic pancreatitis, fractures of the femur or pelvis, and dissecting aneurysm. * Internal seqestrat in of the fluids include ascites, peritonitis, and peripheral edema. Fluids sequestration is also seen in pt with intestinal obstruction , which causes fluid to lead from the intestinal capillaruies into the lumen of the intestine. * Fluid losses may be obvious or suble. Assessment includes: * weighing dressings; measuring drainage from chest or ng tubes; monitoring potential sites for bleeding, such as surgical wounds, or IV or intra arterial catheter sites after removal; and considering insensible lossess, such as perspiration. * ABD girth is measured periodically in pt in whom occult bleeding may be suspected or in those with ascites. * Daily weights same scale with pt wearing the same clothing at approximately the same time each day. * Evaluation of the hct determining whether blood or fluid was lost. * In a pt with blood loss, the HCT will be DECREASED, pt with fluid loss, the HCT will be increased. * Reduction of intravascular volume and a decrease in venous return, * Reduction of ventricular filling pressures - decrease in stroke volume and cardiac output. As the CO decreases, blood pressure decreases and tissue perfusion decreases. Pt with hypovolemic shock present with signs and symptoms: (poor organ perfusion) * altered mentation ranging from lethargy to unresponsiveness * rapid, deep respirations; * cool, clammy skin * weak, thread pulses; tachycardia; and oliguria.

* HEMORRHAGING Hypovolemic shock resulting blood lost and the resultant effects on the level of consciousness, vial signs, and urine output.

Increase in abd girth means abd bleeding or fluid loss into the abdomen. ULTRASOND to determine which. CT can pinpoint sources of bleeding, (hypovolemic shock) or locate possible abscess, which cause sepsis. Management of hypovolemic shock: identifying, treating, and eliminating the cause of the hypovolemia and replacing lost fluid. * Examples of treating the cause include : * surgery, * antidiarrheal (diarrhea) * insulin (hyperglycemia) * Isotonic crystalloids such as normal saline are genereally used first, * blood and blood products IF THE PT IS BLEEDING. - The 3 for 1 rule is used (300 ml of isotonic solution for every 100 ml of blood lost.) use Hemodynamic to guide fluid replacement. * Blood replacement require less than 3 times the lost volume. * Hypertonic saline expands the intravascularr volume (osmotic effect that displaces water from the intracellular space). * hypertonic saline for trauma pt because less volume is required. 2. Cardiogenic Shock –heart fails to act as an effective pump. A decrease in myocardial contractility decreased cardiac output and impaired tissue perfusion. (high mortality rate) The most common extensive left ventricular myocardial infarction. If 40% or more of the left ventricle is damaged, cardiogenic shock increases. Other dysrhythmias, cardiomyopathy, myocarditis, valvular dysfunction, severe heart failure, and structural disorders.
When damage to the myocardium occurs, contractile force is reduced and stroke volume decreases.. Cardiac output and ejection fraction decrease causing hypotension. Hypotension reflex compensatory peripheral vasoconstriction and increased afterload, Backup of blood into the pulmonary circulation decreased o2 perfusion across the alveolar membranes, reducing the o2 tension in the blood and decreased cellular metabolism. An increased demand is on myocardium as it attempts to increase perfusion. The heart rate increases (compensatory mechanism) increased o2 demand on an overworked myocardium. In pts with cardiogenic shock secondary to acute myocardial infarction, the increased demand may increase infarction, the increased demand may increase infarction size.
The clinical presentation of cardiogenic shock is manifestation of: * left ventricular failure (S3, crackles, dyspnea, hypoxemia) * right ventricular failure (JVD, peripheral edema, hepatomegaly). * A PA catheter. * In cardiogenic Shock, cardiac output and cardiac index decrease; however RAP, PAP, and PAOP increase as pressure and volume back up into the pulmonary circulation and the right side of the heart. * Prevention and treatment: * promoting myocardial contractility, * decreasing the myocardial o2 demand, * increasing the o2 supply to the damaged tissue * percutaneous coronary interventions, * stent, * fibrinolyitic agents when primary percutaneous coronary is not available, * glycoprotein IIb/IIIa inhibitors, * BB to limit the size of the infarction. * Pain relief and rest reduce the workload of the heart and infarct size. * O2 administration increases o2 delivery to the ischemic muscle and may help save myocardial tissue.

* Diuretics and vasodilators reduce preload and venous return to the heart. * nitroglycerin at low doses cause venous vasodilation to decrease preload. * - used cautiously because they may cause hypotension, thereby contributing to further cellular hypoperfusion. * Positive inotropic agents increase the contractile force of the heart. As contractility increases, ventricular emptying improves, filling pressures decrease, and stroke volume improves. the improved stroke voume increases cardiac output and improves tissue perfusion. * However, positive inotropic agents also increase myocardial o2 demand and must be used cautiously in pt with MI.

* Afterload reduction - cautionsly administer arterial vasodilators to decrease SVR, increase stroke volume, and increase cardiac index. * BP to keep MAP above 65 to ensure organ perfusion. * Significant hypotension may limit the use of arterial vasodilators, as coronary artery perfusion pressure may be reduced and worsen MI. * IABP - The balloon is inserted percutaneously at the pt bedside or under fluoroscopy. The tip is positioned just distal to the left subclavian artery. Correct placement is verified by chest x-ray. The balloon is inflates during diastole when the aortic valve is closed. The inflation cycle displaces blood backward and forward simultaneously. The backward flow increases perfusion to the coronary arteries, and the forward flow increases perfusion to vital organs. Balloon inflation occurs during diastole, reduces the pressure in the aorta and decreases afterload and myocardial o2 demand. Desired outcomes during diastole, reduces the pressure in the aorta and decreses afterload and myocardial o2 demand. Desired outcomes for a pt in cardiogenic shock with an IABP include decreased SVR, diminished symptoms of myocardial ischemia (chest pain, st elevation), and increased stroke volume and cardiac output.
Counterpulsation therapy with an IABP requires a high decree of nursing skill because of the complexity of the eq and the need for frequent monitoring. * Potential complications Limb ischemia and embolism, dissection of the aorta, infection, ineffective pumping, and technical problems. * Use of the IABP is contraindicated in p with aortic valve insufficiency or aortic aneurysm.
Ventricular assest devices are temporary to support a failing ventricle that has not responded to IABP therapy and pharmacological therapy. VADs allow the ventricle to recover or to support the pt awaiting cardiac transplant as a bridge to transplant. In general, they consist of an external pump, which diverts blood from the failing ventricle or ventricles and pumps it back into the aorta, the pulmonary artery, or both great vessels. The use of VAD requires extensive training and advanced nursing care. These devices are not typically available in community hospitals.

3. Obstructive Shock –physical impairment to adequate circulatory blood flow. Causes: impaired diastolic filling (cardiac tamponade, tension pneumothorax, constrictive pericarditis, compression of the great veins), increased right ventricular afterload (pulmonary embolism, severe pulmonary hypertension, increased intrathoracic pressures), and increased left ventricular afterload (aortic dissection, systemic embolization, aortic stenosis) obstruction of the heart or great vessels either impedes venous return to the right side of the heart or prevents effective pumping action of the hart. This results in decreased cardiac output, hypotension, decreased tissue perfusion, and impaired cellular metabolism. Clinical findings: chest pain, dyspnea , JVD, and hypoxia. Cardiac tampnoade is manifested by muffled heart sounds (filling problem), hypotension, and pulsus paradox (decrease in systolic blood pressure of more than 10 mm Hg during inspiration.) Tension Pneumothorax ( diminished breath sounds on the affected side and tracheal shift away from the affected side.) * Massive PE is manifested: right ventricular failure (JVD, peripheral edema, hepatomegaly). * Aortic dissection is manifested: by complaints of ripping chest pain that radiates to the back, pulse differences between the left and right side, and a widened mediastinum on chest x-ray, echocardiogram, or CT scan.
Obstructive shock may be prevente/ treated :Cardiac tamponade (pericardiocentesis or thoracocentesis) , PE - (SCD, ROM exercises , anticoagulants) early surgical reduction of the long bone fractures, devices to enhance circulation in immobile pts (scd) range of motion exercises, and prophylactic anticoaglat therapy.

4. Distributive Shock - widespread vasoliation and decreased SVR. Vasodilation increases the vascular capacity; however, the blood volume is unchanged, in a relative hypovolemica (decrease in venous return and ventricular filling pressures) * Anaphylactic shock and septic shock are also complicated by increase in capillary permeability, (decreases intravascular volume, further compromising venous return) * All forms of distributive shock: stroke volume, cardiac output, and blood pressure decrease, in decreased tissue perfusion and impaired cellular metabolism.

a. Neurogenic shock – disturbance in the nervous system affect the vasomotor center in the medulla. In healthy persons, the vasomotor center initiates sympathetic stimulation of nerve fibers that travel down the spinal cord and out to the perihphery. There, they innervate the smooth muscles of the blood vessels to cause vasoconstriction. In neurogenic shock, there is an interruption of impulse transmission or a lockage of sympathetic outflow resulting in vasodilation, inhibition of baroreceptor response, and impaired thermoregulation. Consequently, these reactions create vasodilation with decreased SVR, venous return, preload, and cardiac output and a relative hypovolemia. * Causes: injury or disease of the upper spinal cord, spinal anesthesia, nervous system damage, administration of gangionic and adrenergic bloacking agents, and vasomotor depression. Pts who have a cervical spinal cord injury may experience a permanent or temporary interruption in sympathetic nerve stimulation. Spinal anesthesia may extend up the spinal cord and may block sympathetic nerve impulses from the vasomotor center. * Vasomotor depression – deep general anesthesia, and injury to the medulla, administration of drugs, severe pain, and hypoglycemia. * The most profound features of neurogenic shock are bradycardia with hypotension from the decreased sympathetic activity. * The skin frequently warm, dry, and flushed. * Hypothermia develops from uncontrolled heat loss. * Venous pooling in the lower extremities promotes the formation of DVT, resulting PE. * Management – treat the cause, reversal of offending drugs or glucose administration for hypoglycemia. * Immobilization of spinal injuries with traction devices (halo brace to maintain alignment) or surgical intervention to stabilize the injury assists in preventing severe neurogenic shock. * Elevate HOB -spinal anesthesia, (prevent the progression of the spinal blockade up the cord.) * IV fluids for hypotension; however, give cautiously to prevent fluid overload and cerebral or spinal cord edema. * Vasopressors. Alpha and Beta adrenergic agents (dopamine or norepinephrine) are preferred because pure alpha adrenergic agents (phenylephrine) - persistent bradycardia. * Hypothermia - REWARMED SLOWLY (rapid rewarming cause vasodilaion and worsen the pt’s hemodynmic staus.) * Atropine is used for symptomatic bradiacardia but temporary or permanent pacemaker may be required.

Anaphylactic shock - a severe allergic reaction can precipitate a second form of distributive shock. Antigens, initiate an antigen antibody response. Once an antigen enters the body, antibodies (IgE) are producd that attach to mast cells and basophils. The greatest concentrations of mast cells are found in the lungs, around the blood vessels, in connective tissue, and in the uterus. Mast cells are also found to a lesser extent in the kidney, heart, skin, liver, and spleen and in the omentum of the GI tract. Basophils circulate in the blood. Both mast cells and basophils contain histamina n histamine – like substances, which are potent vasodilator
The initial exposure (primary immune response) to the antigen does not usually cause any harmful effects; however, subsequent exposures to the antigen may cause an anaphylactic reaction.
The antigen antibody reaction causes cellular breakdown and the release of powerful vasoactive mediators from the mast cells and basophils. these mediator cause bronchoconstriction, excessive mucus secretion, vasodilation, increased capillary permeability, inflammation, GI cramps, and cutaneous reactions that stimulate nerve endings, causing itching and pain. The combined effects result in decreased blood pressure, relative hypovolemia caused by the vasodilation and fluid shifts, and symptoms of anaphylaxis that primarily affect the skin, respiratory, and GI systems. Injecting small amounts before the entire dose is given (assist in detecting a possible reaction) monitor for reactions during blood transfusions.. The clinical presentation includes: flushing, pruritus, urticarial, and angioedema. Cough, runny nose , nasal congestion, hoarseness, dysphonia, and dyspnea are common because of upper airway obstruction from edema of the larynx, epiglottis, or vocal cords. Stridor may occur as a result of larynegeal edema. Lower airway obstruction and causes wheezing and chest tightness. Tachycardia and hypotension occur. Neurological symptoms include lethargy and decrease consciousnesss. Elevated levels of IgE are seen on laboratory analysis. Goals of therapy: remove the antigen, reverse the effects of the mediators, and promote adequate tissure perfusion. * If the anaphylactic reaction results from meds, contrast dye, bloo or bloo products, the infusion is immediately stopped. * Airway, ventilation, and circulation are supported. * Laryngeal edema (may require intubation/ or cricothrotomy if swelling is so severe that an endotracheal tube cant be placed.) * O2 is administered to keep the SpO2 greater than 90%. * Removal of the offending agent removing the stinger, administering anti-venom, stopping the drug, performing gastric lavage, or flushing the skin. * EPINEPHRINE is a drug of choice. (promotes bronchodilation and vasoconstriction.) For mild reactions, epinephrine .1 to .25 mg is administered intramuscular or subq. The nose may be repeated at 20 – 30 min intervals until anaphylaxis is resolved. * Diphenhydramine (To block histamine release), * Second line: h1 antagonist or h2 antagonist decrease some of the cutaneous symptoms of anaphylaxis,. * Cortiocosteriods such as methylprednisolone are used to reduce inflammation. * Fluid replacement, positive inotropic agens and vasopresors may be required.

b. Septic shock . Invasion of the host by microorganism or an infection begins the process that may progress to sepsis, followed by severe sepsis and septic shock, which progresses to MODS.
Once the microorganism has invaded a host, inflammatory response (restore homeostasis.) Sirs ( release of inflammatory mediator or cytokines, which are produced by the WBC. SIRS can also occur as a result of trauma, shock, pancreatitis, or ischemia. SIRS may progress to septic shock and MODS. * Proinflammatory cytokines including tumor nerosis factor, interleukin-1alpha and beta produce pyrogenic responses and initiate the hepatic response to infection. * Antiinflammaory cytokines including nitric oxide, lipopolysaccharide, and interleukin 1 receptor antagonist are compensatory, ensuring that the effect of the proinflammatory mediators does not become destructive.

* In sepsis, continued activation of proinflammatory cytokines overwhelms the anti-inflammatory cytokines and excessive systemic inflammation results. * A state of enhanced coagulation (stimulation of the coagulation cascade, reduction in the levels of activated protein C and antihromnin III generation of thrombin and the formation of microemboli (impair blood flow and organ perfusion) * Fibrinolysis is activated (from activation of the coagulation cascade to promote clot blockdown) However, activation is followed by inhibition, further promoting coagulopathy. This imbalance among inflammation, coagulation , and fibrolysis results in systemic inflammation, widespread coagulopathy, and microvascular thrombi that impair tissue perfusion, leading to MODS.
These inflammatory mediators damage the endothelial cells that line blood vessels, producing profound vasodilation and increased capillary permeability. * Initially, this results in tachycardia, hypotension, and low SVR. Although Norepi and RAAS are unable to enter the cells, hypotenstion and vasodilation persist. * Low levels of the ADH (or vasopressin) are low despite hypotension. The exact mechanism that creates this low concentration is not known; however, administering a continuous vasopressin infusion significantly increases blood pressure in septic shock.
Sepsis can progress to septic shock. (Septic shock is sepsis + hypotension that is unresponsive to fluid resuscitation along with signs of inadequate organ perfusion such as metabolic acidosis, acute encephalopathy, oliguria, hypoxemia, or coagulation disorders. This clinical course of septic shock is frequently differentiated between that early (warm, hyperdynmaic) phase and the late (cold, hypodymic)
Factors that increase the risk of developing sepsis are categorized as immunosuppression or significant bacteremia. Sepsis is infection with SIRS and is the systemic response to infection. SIRS is present if two or more (what are manifestations of SIRS). Sepsis can advance to severe sepsis with hypotension, chills, decreased urine output, decreased skin perfusion, poor capillary refill, skin mottling , decreased platelets, petechiae, hyperglycemia, and unexplained chages in mental status.

Prevention of sepsis: preventing infections, including proper hand washing, use of aseptic technique, and awareness of the patitent at risk. The critically ill patient is debilitated and has many potential portals of entry for bacterial invasion. Meticulous technique is required during procedures such as suctioning, dressing changes, and wound care and when handling catheers or tubes. Frequent assessment of temperature, wound, and laboratory results including white blood cell count, differential counts, and cultures is important for the identification of infection.

Gram negative bacteria (E.coli, Klebsiella species, or pseudomonas) are cause of infections in adults. Common sites include: the pulmonary system, urinary tract, gastrointestinal system, and wounds. UTI is often overlooked case of secondary blood stream infections. Minimizing the use of indwelling catheters by assessing daily their need and promptly removing unnecessary catheters is recommended.
Gram positive bacteria (staphylococcus aureus). These bacteria release a potent toxin that enters its effects within hours. Infection has been associated with the use of tampons in menstruating women (tss) it is also seen after vaginal and cesarean delivery and in patients with surgical wounds, abscesses, infected burns, abrasions, insect bites, herpes zoster cellulitis, septic abortion, and osteomyelitis. In addition, the bacteria may be transmitted from mother to newborn. * Management includes antimicrobial therapy, removal of the source of infection if one is found, fluid resuscitation, and vasoactive medication to improve cardiac performance.

Pneumonia is a common trigger for sepsis. VAP is a significant risk factor for the development of sepsis. Several strategies have been identified that reduce the risk for VAP are easily implemented. These include provided regular oral care with chlorhexidine to intubated pts, and reducing the number of ventilator circuit changes. VAP prevention measures also include VTE prophylaxis, stress ulcer prophylaxis, and ventilator weaning trials. * sedation vacation to evaluate the pts ability to wean from the ventilator. * endotracheal tube with a dorsal lumen to allow continuous suction of secretions from the subglottic area.
Timely identification of the causative organism and the initiation of appropriate antibiotics improve survival of patients with sepsis or septic shock. * Any catheter suspected to be a source of infection should be removed. * Surgery may be required to locate the source of infection, drain an abcess, and/or debride necrosis.
Before antibiotic therapy is initiated, culture and sensitivity tests of blood, urine, sputum, wound, tip of catheter, and any suspicious site are obtained. This helps to id the source of th infection, the type of organism, and which the source of th infection, they type of organisms, and which antibiotic should be used. However, the need for early administration of antibiotic, preferabily within 1 hour , requires the initial antibiotic selection be directed toward the most likely organism, and frequently, empirical and broad spectrum antibiotics are iniated. Antibiotics may be changed after Gram stain results (4 hrs) or culture and sensitivity results (72 hrs) are available. Antibiotics are discounted if the cause of the sepsis is not bacterial. Unfortunately, abo do not acto on the immune response to infection and do not directly tissue perfusion.
Early goal directed therapy has been shown to derese mortality in pts with severe sepsis and septic shock and is advocated for the first 6 hours of sepsis resuscitation. Early goal directed theapy includes administration of IV fluids to keep the CVP at 8 or greater but no more that 15. And the RH at less that 110, administration of vasopressors to keep the MAP at 65 or greater, and administration of dobutamine, PRBC or both to keep the ScvO2 at 70% or greater.
Isotonic crystalloid solutions are infused for fuid resuscitation. Colloids are likely to lead out of the vascular bed into the interstitium because of increased capillary permeability. Vasopressors, frequently norepi or dopamine, are used to increase SVR ann map, Vasopressin may be added to norepi esp when high doses of norepinephrine are quired. Advantages of vasopressin include decreaseing exogenous catecholamines and increase the release of cortisol and ACTH. In addition, vasopressin causes vasoconstriction without the adverse effects of tachycardia and ventricular ectopy seen with catecholamines such as dopamine or norepi. Dobutamine may be used to increase the myocardial contractility and improve the CI and DO2 in pt with a decrease ScvO2
Elevated cardiac troponin levels and elevated BNP indicated LEFT ventricular dysfunction and a poor prognosis in a patient with sepsis and septic shock. ACTH stimulated cortisol levels may be measured because poor ACTH cortisol responses are associated with a high mortality. Corticosteroids have ben shown to reduce mortality for thsose patients with sepsis or septic shock who have an inadequate response o the ACTH stimulation test. Routine use of corticosteroids however, is not recommended because of the effects on glucose homeostasis, the risk for infection, and the potential for myopathy.
In severe sepsis, the patient has excessive coagulation, inflammation, and impaired fibrolsis. Recombant human activated protein C (drotrecogin alfa (Xigris)) is an intiinflammatory, antithrombotic, and profibrinolytic agent that reduces the inflammatory, clotting, andbleeding responses to spsis. It has been shown to reduce mortality in patients with severe sepsiss with dysfunction of two organ systems . continued evaluation has failed to show a survival benefit for pateitns with severe severe sepsis and septic shock. The manufacturer announced a voluntary recall from the market in October 2011.
Hyperglycemia and insulin resistance are common in the pt with sepsis. The effect is evern more significant in patients with MODS casued by sepsiss. Guidelines pulished in 2008 recommend frequent glucose testing and intensive IV insulin protocols to maintain blood glucose levels at less than 150. Data from the NICe Sugar sugget that the target be less than 180. On the basis of those results, normal blood glucose levels ma not be the clinical goal.
Although pyrogens (polypeptides that produce fever) aid in activation of the immune response, temperature reduction is considered for core body temperatures at 41 C or higher because of the significant increase in o2 consumption. Treatment of fever includes physiologica cooling (ice pack, tepid baths, cooling blanket, or misting) along with administration of antipyretics (acetaminophen, ibuprofen, or aspirin). Care must be taken to avoid overcooling because hypothermia adversely affects o2 delivery and may result in shivering, which increases o2 consumption.
May experimental therapies have been advocated for sepsis and septic shock. Plasmapheresis may remove endotoxin and other harmful substances produced byeither the infective organism or the inflammatory process. Immunoglobulins may be also be prescribed, especially in patiens who are immunocompromised.

MODS - progressive dysfunction of 2 or more organ syystems as a result of an unrolled inflammatory response to severe illness or injury. Organ dysfunction can progress to organ failure and death. The most common cause of MODS are sepsis and septic shock; however, MODS can occure after any severe injury or disease process that activates a massive systemic inflammatory response including any classification of shock. The immune system and the body’s response to stress can cause maldistribution of circulating volume, globacl tissue hypoxia, and metabolic alterations that result in damage to organs. Failure of tow or more organs is associated with an estimated 45 to 55 motality, 80% mortality when three or more organ systems fail, and 100 % mortality of three or more organs may be primary or secondary. In primary MODS there is direct injury to an organ from shock, trauma, urn injury, or infection with impaired perfusion that results in dysfunction. Decreased perfusion may be localized or systemic. As a result of this insult, the stress response and inflammatory resonse are activated with the release of catecholamines and activation of mediators that affect celloular activity. Seconday MODS is a consequence of widespread systemic inflammation that results in dysfunction of organs not involved with the initial insult. It occurs in response to altered regulation of the acute immune and inflammatory responses. Failure to control the inflammatory response leads to excessive production of inflammatory cells and biochemical mediators that casue widespread damage to vascular endothelium and orgnandamage. The interaction of injured organs then leads to self perpentuating inflammation wih maldistriution of blood flow and hypermetabolism. Maldistribution of blood flow refers to the uneven distribution of flow to various organs and between the large vessels and capillary beds. It is caused vasodilation, increased capillary permeability, selective casoconstriction, and impaired microvascular circulation. This impaored bloow flow leads to impaired tissue perfusionand decreased o2 suppl to the cells. The organs most severly affected are the lungs, splanchnic beds, liver, and kidneys. Hypermetabolism with altered carbohydrate, fat, and lipid metabolism is initially compensatory to meet the body;s increased demands for energy. Eventually, hypermeatbolism becomes detrimental, placing tremendous demands on the heart as cardiac output increases up to twice the normal value. Hyperglycema occur as gluconeogenesis by the liver increases and glucose use by the cells decreases. The decreases o2 deliver to the cells and increase do2 needs of the cells (mypermetabolism) create an imbalance in o2 supply and demand. In MODS, the amount of 2o consumed becomes dependent on the amount of o2 that con be delivered to the cells. Hypoxemia, cellular acidosis, and impaired cellular function results with the development of multiple organ failure. The clinical presentation of MODS is cuased by inflammatory mediator damage, tissue hypoxia, and hypermetabolism. Damage to the organs is useually sequential rather than simultaneous. The first system frequently affected is the pulmonary system, with acute ARDS developing within 12 to 24 hrs after the initial insult. Coagulopathy frequently develops, followed by renal, hepatic, and intestinal impairment. Failure of the cardiovascular system, neurological system, or both, are frequently fatal evelts. MODS progresses from minor dysfunction of one or multiple organs to multiple organs requiring support. Criteria used in the diagnoses of organ dysfunction…. Pulmonary dysfunction is manifested by tachypnea, hypoxemia (despite high levels of o2) and CXR changes. Hematological dysfunction is manifested by petechiae, bleeding, thrombocytopenia, prolonged PT and aPTT, increased fibrin split products, and a positive D-dimer. The earliest sign of hepatic dysfunction is hypoglycemia, which is followed by jaundice, increased liver enzymes and bilirubin, prolonged PT, and decreased albumin. The first indication of intestinal dyfunction is frequently intolerance of enteral feedings with abdominal distension and increased retention volumes. Renal dysfunction is evidenced by oliguria to anuria, increased BUN and Creatineine, and fluid and electrolyte imbalance. Tachycardia, hypotension, and hemodynamic alteraltion indicate cardiovascular dysfunction. Finally, cerebral dyscunction is manifested by a change in level of onsciousness, confusion, and focal neurological signs such as hemiparesis. The final response to MODS is hypotension that is unresponsive to fluids and vaopressors, and cardiac arrest. Management of Mods focuses on PREVENTION and support. The initial source of inflammation must be elimated or controlled. A secondary insult must be avoided. Potential sites of infection are removed, including debriding necrotic tissue, draining abcesses, reducing the number of invasive procedures performed, and removing hematomas. Golas are to control infection, provide adequate tissue oxygenation, restore intravascular volume, and support organ fuction. Antiiotics are administered . SpO2 is maintained between 99 and 92, hgb legels should be above 7- 9 , and SvO2 greater than 70% is desired. Aggressive fluid therapy with isotonic crystalloid solutions is initiated early during systemic vasodilation to promote o2 delivery to the tissues. Support for each organ must be provided. Respiratory failure is managed with mechanical ventilation with low tidal volumes, high o2 concentrations, and PEEP. Adequate nutrition and metabolic support is provided iwith enteral feedings. Acute kidney injury is managed with continuous renal replacement therapies or HD. Inotropic drugs (low dose dopamine or dobutamine) or vasopressors may be needed to maximize cardiac contractility and maintain CO. V. Patient Outcomes – improved tissue perfusion. AAO, normotension, warm, dry skin, adequate UO; hemodynamic and lab values WNL; absence of infection, and intat skin. Resting quietly.

1. SIRS- Chapter 11, Systemic Inflammatory Response Syndrome – widespread inflammation that can occur in patients with diverse disorders such as infection, trauma, shock pancreatitis, or ischemia. It may result from or lead to MODS. SIRS is most frequently associated wih sepsis. Sepsis is defined as infection associated with SIRS.
The inflammatory cascades maintains homeostasis through a balance between proinflammatory and intiinflammatory processes. Inflammation is normally a localized process; SIRS is a systemic response associated with the release of mediators. These mediators cause an increase in the permeability of the endothelial wall, shifting fluid from the intravascular space into extravascular spaces, including the interstitial space. Intravascular volume is reduced, resulting in a condition of relative hypervolemia. Other mediator cause micro vascular clotting, impaired fibrinolysis, and widespread vasodilation. I. a. Review the Inflammatory process (See Chapter 16, Inflammation and Phagocytosis, p468) – the second line of defense involves the processes of inflammation and phagocytosis. Inflammation is initated by cellular injury, is necessary for tissue repair, and is harmful when uncrolled. When both a mediator and neutrophil response. Mediator substances ( histamine, serotonin, kinins, llysosomal enzymes, prostaglandin, platelet – activating factor, clotting factors, and complement proteins) are released at the site of injury. These mediators cause vaso dilation, increase blood flow, induce capillary permeability, and promote chemotaxis and phagocytoss by neutrophils. Inflammatory symptoms such as redness, heat pain, and swelling are sequelae of these responses. Complement proteins enhance the antibody activity, phagocytosis, and inflammation.
Neutrophils are attracted to and migrate to areas of inflammation or bacterial invasion, where they injest and kill invading microorganisms by phagocytosis. The inflammatory response is a rapid process initiated by granulocytes and cellular injury. Once phagocytes have been attracted to an area by the release of mediators, a process called opsonization occurs, in which antibody and complement proteins attach to the target cell and enhance the phagocyte’s ability to engulf the target cell. Once the bacteria have been engulfed, they are killed and digested within the cell by lysosomal enzymes. Exudate formation at the inflammatory site has three functions: dilute the toxins produced, deliver proteins and leukocytes to the site, and carry away toxins and debris.
When infectious organisms escape the local phagocytic responses, they may be engulfed and destroyed in a similar fashion by the tissue macrophages within they lymphoreticular organs. The portal circulation of the spleen and liver filters the majority of blood, where infectious organisms can be removed before infecting the tissues. In the lmphatic system, pathogenic substances are filtered by the lymph nodes and are phagocytized by tissue macrophages. Here they may also stimulate immune responses by the lymphoid cells.
Other nonspefic defenses – another nonspecific defensive activity is the release of cytokines and chmokines from BC, and are either proinflammatory, anti-inflammatory, or both. These naturally occurring biological response modifiers, which include interleukins, tumor necrosis factor, colony- stimulating factors, monocoloal antibodies, interferons, mediate various interactions between immune system cells. At least 30 human IL have been identified. An example of interleukin is IL-1, which is a proinflammatory cytokine that increases body temperature in infection, thereby inhibiting the growth of temperature-ensitive pathogens. IL- 1 also activates phagocyte and lymphocytes, and acts as a growth factor for may cells. The IFN have antitumor and antiviral activity and include 20 subtypes of IFN alpha, 2 subtypes of IFN beta, and IFN gamma. Through recombinant DNA technology, IFN and other naturally occurring substances can be produced synthetically for the treatment fof may disorders. IFNs colony stimulating factors and monoclonal antibodies are some examples of biological therapies currently approved for the treatment of certain malignant dsisorders. II. Septic Shock- Chapter 11, p272 & pp278-283 b. Summary of Shock classifications, Table 11-5, p272 – Septic Shock only c. Dx. Criteria & Management in the Continuum of Sepsis, Tables 11-7 & 11-8 d. Pathophysiology of Sepsis & Septic Shock, Fig. 11-13 III. MODS- Chapter 11, pp283-285 e. Fig. 11-14 f. Stages of Septic Shock, Table 11-8 IV. Bleeding Disorders- Chapter 16, pp492-501 g. The Bleeding Patient – also known as coagulopathies, disorders are considered inherited (hemophilia, von willebrand disease) or acquired (vit K deficiency, DIC) . A patient with abnormal bleeding requires a careful medical and social history. It is important to assess for medical disorders and medications known to interfere with platelets, coagulation proteins, or fibrinolysis. Disruptions in hemostasis commonl occur with renal disease, hepatic or GI disorders, mal nutrition. Medications that may altoer hemostasis include aminoglycosides, anticoagulatns, anti platelet agents, cephalosporins, histamine blockers, nitrates, sulfonamides, sympathomimetics, and vasodilators.
The physical exam is extremely important. Although many patients with bleeding disorders demonstrate active bleeding from body orifices, mucous membranes, and open lesions or IV line sites, equal numbers of pts have less obvious bleeding. The most susceptible sites for bleeding are existing openings in the epithelial surfaces. Mucous membranes have a low threshold for bleeding because the capillaries lie close to the membrane surface, and minor injury may damage and expose vessels. Substantial blood loss can occur in any coagulopathy, resulting in hypovolemic shock.
Diagnostic tests are performed to evaluate the casue of the bleeding disorder and the extent of blood loss. The CBC provides quantitative values for RBC and platelets. When the disorder arises from coagulation protein or clot lysis abnormailites, screening coagulation test of fibrinogen level, protrombin time, and partial thromboplastin time are usually ordered. Point of care tests for hemoglobin, hematocrit, and partial thrombopastin time are important resources to obtain immediate feedback regarding the patient’s status. In certin disease states. Additional pspecialized tests such as bleeding time and levels of fibrin degradation products are monitored.
Medical interventions – depends on the cause. Component specific replacement transfusions are preferred over whole blood because they provide more targeted treatment of the bleeding disiorder. Transfusion threshods are established based on laboratory values and patient specific variables. In general, a threshold for RBC transfusion is considered a hematrocrit of 28% to 31%, based on the patient’s cardiovascular tolerance. If angina or orthostasis is present, a high threshold may be maintained. The threshold for transfusing platelets is usually between 20,000 and 50, 000. Cryoprecipitate is usually infused if the fibrinogen level is less than 100 mg/dl. FFP is used to coret a prolonged prothrombin time and partial thromboplastin time or a specific factor defiency. Table 16-11. When the cause of bleeding is unknown or mulitifactorial, nonspecific interventions aimed at stopping bleeding are used. Thes include local and systemic procoagulant medication and therapies. Local therapies to stop bleeding are used when systemic anticoagulation is necessary for treatment of another health condiation (myocardial infarction, ischemic stroke, or pulmonary emboim) local procoagulations act by direct tissue contact and initiation of surface clot.
Nursing interventions - administration of fluids and blood products is a priority that depends on the pts situation. . when the pts blood does not clot because of thrombocytopenia, administration of RC before platelets will result in RBC losss from disrupted vascular structures.
Additionally : weigh dressings to assess blood loss, assess fluids for occult blood, observe for oozing and bleeding from skin and mucous membranes, and leave clots undisturbed. Precautions such as limiting invasive procedures, including indwelling urinary catheters or rectal temperature measurement.
D
i. Nursing Care plan p493 ii. EBP box, p493 – massive transfusion substantially reduced the risk of death in the trauma population. However when massive transfusion was not needed (surgery), transfusion was associated with an increased risk for death and a three fold increased risk of developing acue lung injury. They found restrictive transfusions based on triggers significantly reduced the risk for infection, and no differences between groups on mortality, complications, and lengths of stay. They didn't support transfusion if the hGB was 10 or higher. Most supported transfusion when the HGN fell below 8. Transfusion when the hemoglobin is between 8 – 10 needs to be based on comorbidities of the pt. 1. Imp for nursing - with the exception of the trauma pt who needs massive transfusion, administration of RBC is associated with a higher risk for acute lung injury and mortality. more restrictive use of transfusion unless the hemoglobin falls below 8g/dl. The pt underlying comorbidities must be considered in decision making nrses must monitor serial hemoglobin levels and assess patients fir signs and symptoms related to lower HGB and HCT. If transfusion is suggested at a higher threshold, nurses should discuss rationale with the physician iii. Summary of blood products, Table 16-11 h. Thrombocytopenia (See supplemental Chart via Moodle)
A deficiency of platelets - thrombocytopenia. A platelet count of less than 150, 000. If less than 30,000 – critically low and spontaneous bleeding may occur. Fatal hemorrhage is a great risk when the count is less than 10,000. The pathophysiology may be related to decreased production of platelets by the bone marrow, increased destruction of platelets, or sequestration of platelets. Presents with petechiae, purpura, and echymoses, and oozing from mucous membranes. The patient may also have melena, hematuria, epitaxis.
Medical interventions – infusions of platelets. Pts who require multiple platelet transfusion should be evaluated for single-donor platelet products, ehich permit administration of 6 -10 units of platelets with exposure to the antigens of only one person. For every unity of single donor platelets, the platelet count should increase by 5000, to 10000. Pts who receive many platelet transfusions can become refractory, or allimmunized , to the may different platelet antigens and may only benefit from receiving platelets that are a match. After multiple platelet transfusions, febrile nad allergic transfusion reactions are common but can be reduced by administration of acetaminophen and diphenhydramine before transfusion. Thrombopoietin, platelet stimulating cytokine, is neing investigated as an alternative to platelet transfusion. Some Thrombocytopenias are autoimmune b induced and may resond to filtration of antibodies via plasmapheresis or immune suppression with corticosteroids. When the speen is enlarged and tender and these other supportive therapies are unsuccessful, splenectomy can alleviate the autoimmune reaction.
NURSING – must recognize and limit factors that can deplete or shorten the life span of platelets. (high fever and high metabolic activity (seizure) prematurely destroy platelets. Desired outcomes – adequate tissue perfusion, skin integrity, prompt recognition and treatment of bleeding, and absence of pain.

iv. Causes of Thrombocytopenia, Box 16-4 v. ITP vi. HIT 2. HIT, Box 16-5 vii. TTP i. DIC viii. Pathophys. Of DIC, Fig. 16-7 – disorder of hemostasis by exaggerated microvascular coagulation, depletion of clotting factors, and subsequent bleeding. Because of clotting factors are used up in the abnormal coagulation process, this disorder is also termed consumption coagulopathy. The clinical course of DIC ranges from an acute, life threatehning process to a chonic, low grade condition. Sepsis is the most common cause of acute DIC. Acute DIC develops rapidly and is the most serious from of acquired coagulopathy. With chronic DIC, Procoagulatns that cause diffuse, uncrontrolled clotting are release. The intrinsic or extrinsic pathways are activated by release of tissue factor, from either endothelial damage or direct tissue damage. Large amounts of thrombin are produced, resulting in the deposition of fibrin in the microvasculature, the consumption of available clotting factors, and the stimulation of fibrinolysis. Clotting in the microvasculature of the pt wit DIC causes organ ischemia and necrosis. The skin, lungs, and kidneys are most often dmaged. Thrombophlebitis, pulmonary embolism, CVA, GIB, and renal failure may result from thrombosis. Microvsculature thrombosis may result in cyanosis of the finters and toes, purpura fulminans, or infarction and gangrene of the digits or tip of the nose and penis.
The fibrinoluysiss that ensues results in the release of fibrin degration products, which are potent anticoagulants that interfere with thrombin, fibrin, and platelet activity. RBC are damaged as they try to apss through the blocked capillary beds; the damage to RBC cuases excess hemolysis. The lack of available clotting factors coupled with the anticoagulant forces results in an inability to fomr clots when needed and predisposes the patient with DIC to Hemmorrhage.
Assessment – DIC is always a secondary complication of excessive clotting stimuli and may be triggered by vessel injury caused by disease states, tissue injury, or foreign body in the blood stream. Sepsis, multisystem trauma, and burns are the main risk factors for DCI and also provide the most significant stimuli for the clotting cascade. Recognition of potential risk factors and conscientious monitoring of the high risk patient can permit early intervention. Clinically, the pt with DIC first develops microvascular thrombosis. Thrombosis leads to organ ischema and necrosis that may be manifested as changes in mental status, angina, hypoxemia, oliguria, or nonspecific hepatitis. Cyanosis and infarction of the finers and toes as well as infarction of the nose may occur if the DIC is severe. After a thrombotic phase of hours to a few dyas, depletion of cloting factors and clo lysis cause excessive bleeding. Early signs may include occult blood in the stool, emesis, and urine. Capillary fragility and depleted cloting factors often appear early as mucosal or subcutaneous tissue bleeding seen as gingival bleeding, petechiae, or ecchymoses. Overt bleeding ranges from mild ozzing from venipuncture sites to massive hemorrhage from all body orifices. Occult bleeding into body cavities, such as the peritoneal and retroperitoneal spaces, may be detected by vital sign changes or other classic signs of blood loss Diagnosis of DIC is made on recognition of pertinent risk factors, clinical symptoms, and the results of laboratory studies. Evidence of factor depletion in the form of thrombocytopenia and low fibrinogen levels is seen in the early phase; however, definitive diagnosiss is made by evidenc e of excess fibrinolysis detectable by elevated fibrin degradation products, an increased D – dimer level, or a decreased antithrombin III level.altered lab values in DIC are noted. Medical interventions – identifying and treating the underlying cause , stopping the abnormal coagulation, and controlling the bleeding. Correction of hpotension, hypoxemia, and acidosis is vital, as is treatment of infection if it is the triggering factor. If the cause of obstretrical, evacuation of the uterus for retained fetal tissue or other tissue must be performed. Blood volume expanders and crystalloid intravenous fluids, such as lactated ringers solution or NS are given to counteract hypovolemia caused by blood loss. Blood component therapy is used in DIC to replace deficient platelets and clotting factors and to treat hemoohage. Platelet infusions are ussally necessary cuase of consumptive thrombocytopenia. Administration of platelets is the highest priority for transfusion because they provide the clotting factors needed to establish an intial platelet plug from any bleeding site. FFP is administered for fibrinogen repalement. It contains all clotting factors and antithrombin III;however, factor VIII is often inactivated by the freezing process, thus necessitating administration of Concentrated factor VIII in the form of cryoprecipitate. Transfusion of packed RBC are gived to replace cells lost in hemorrhage. Heparin is potent thrombin inhibitor and may be administered, in low dosess, to block the clotting processs that initiates dIC. Haparin is given to preent further clotting and thrombosis that may lead to organ ischemia and necrosis. Slthough heparin’s antithrombin activity prevents further clotting, it may increase the risk of bleeding and may cause futher problems. It use is controversical when it is administered to pt with DIC. Other pharmacological therapy in DIC includes the administration of synthetictic antihtrombin III, which also inhibits thrombin. Antithrombin II conetrates amy ashoten the course of the diseae and my incrase the survival rate. Adminsitraion of aminocaproic adid inhibits fibrinolysis by interfering with plamin activity. Fibrinolytics should be give only if other treatments ve been unsuccessful and hemorrhage is life threatinging, as there is no clear evidence of the risk vs benefit with their use.
NURSING INTERVENTIONS - prevention and recognition of thrombotic and hemorrhagic events. Continuous assessment for comoplications facilitates prompt and aggressive interventions. Psycoschoal support of the pt and family is very importan. Few pt who survive DIC are without some functional deficits casued by isshemia o hemorrhage. Pain relief and promotion of comfort are important nursing priorities. The location, intensity, and quality of the pt pain are assessed, along with the pt response o discomfort. The nurse is conscientiorus not the enhance vasoconstriction, because it contributes to tissue ischemia and its associated discomfort. Relief of discomfort also reduces o2 concumption, which is important for these pt with limited circulatory flow. Pain medication is offered as ordered and before painful procedures. Positioning, with support and proper body alignment and frequent changes, also enhances the pts level of comfort.
Conagulation laboratory studies are carefully monitored for evidence of disease resolution. As fewer clots are created, the platelet count and fibrinogen level are amond the first laboratory tests to return to normal. The fibrin degradation products and D dimer levels fall, and antithrombin III levels rise, as fibrinolysis slows. Other coagulation test are less sensitive and are not usually assessed. The main desired outcomes for the patient with DIC include adequate o2, adequate tissue perfusion, absence of bleeding, and skin integrity. Absence of pain an defective coping are additional expected outcomes.

DIC TEST | NORMAL VALUE | ALTERATION | Platelet | 150,000 – 450,000 | Decreased | Prothrombin | 11 – 16 sec | Prolonged | Activated partial thromboplastin time | 30 – 45 sec | Prolonged | Thrombin Time | 10 – 15 seconds | Prolonged | Fibrinogen | 150 – 400 | Decreased | Fibrin degradation products | Less than 10 | Increased | Antithrombin III | Less than 50% of control (plasma)) | Decreased | D-dimer | <100 | Increased | Protein C | 71% - 142% | Decreased | Protein S | 61 % - 130% | Decreased |

Causes of DIC, Table 16-12 Infections | Bacterial (Gnegative) fungal, viral, mycobacterial protozoan, rickettsial | Trauma | Burns, crush or multiple injuries; snakebite’s severe abortion | Obstetrical | Abruption placentae, placenta previa, amniotic fluid embolism, retained dead fetus, missed abortion, exlampsia, hydatidiform mole, septic abortion. | Hematological/immunological disorders | Transfusion reaction, transplant rejections, anaphylaxis, acute hemolysiss, transfusion of mismatched blood products, autoimmune disorders, sickle cell crisis | Oncologicl disorders | Carcinomas, leukemias, metastic cancer | Miscellaneous | Extracorporal circulation, pulmonary or fat embolism, anozia, acidosis, hyperthermia or hypothermia, hypovolemic shock, ards, sustained hypotension, shock | | |

ix. Lab Alert, p499 x. Coagulation Studies, Table 16-7, p476

Required Readings:
Sole, M. L., Klein, D. G., & Moseley, M. J. (2013). Introduction to Critical Care Nursing, 6th Ed. Saunders, St. Louis, MO. * Recommended Readings: * Inflammation and Phagocytosis, p468 * Coagulation Pathway & Antagonists/Clot Lysis, pp469-471

Handout – 3 Types of Thrombocytopenia Compared (Provided per Moodle)

(Rev. 8/5/13 lhf)

I. AKI (Review pp432-434, not required reading but is review of previous content taught) a. Pathophysiology b. Etiology i. Pre-Renal Causes 1. Prerenal Causes of AKI, Box 15-2, p436 ii. Post-Renal Causes 2. Postrenal Causes of AKI, Box 15-3, p436 iii. Intra-Renal Causes 3. Intrarenal Causes of AKI, p437 4. Schematic of loss of GFR, Fib. 15-5 5. Contrast-induced nephropathy a. EBP: AKI r/t Contrast Media, p439 c. Phases of AKI d. Assessment iv. History 6. Common Nephrotoxic Meds, Box 15-5, p440 v. Vitals vi. Physical Assessment 7. Systematic Manifestations of AKI, Table 15-2 vii. Labs (You will not need to know how to calculate Creatinine Clearance) 8. Clinical Alert e. Management viii. Geriatric Considerations, p443 ix. Diagnostic Procedures x. Nsg. Dx 9. Nsg. Care Plan, p445 & 446 xi. Nsg. Interventions 10. Clinical Alert 11. Measures to Prevent Acute Kidney Injury, Box 15-6, p447 xii. Medical Management xiii. Pharmacological Management xiv. Dietary Management xv. Manage of Fluid, Electrolyte, and Acid-Base Imbalances 12. Lab Alert, p449 13. EKG changes in hyperkalemia, Fig. 15-6, p450 14. Meds to Treat Hyperkalemia, Table 15-5, p451 15. Metabolic Acidosis in AKI, Table 15-8, p451 xvi. RRT (exclude peritoneal dialysis (pp456-457) 16. Hemodialysis 17. CRRT 18. Complications of Dialysis, Box 15-9, p454 19. Case Study