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34 Cards in this Set
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Bacteremia SIRS Severe sepsis MODS |
Presence of viable bacteria in blood systemic inflammation response syndrome can be precursor to sepsis (2 or more of the criteria) sepsis associated w/ organ dysfunction -Presence of altered organ function in an acutely ill individual |
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SIRS criteria (2 or more) |
Temp > 38 or < 36 HR > 90 RR >20 or CO2 <32 WBC >12,000 <4,000 or <10% bands |
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Shock septic shock: severe sepsis complicate by persistent hypotension refractory to fluid therapy SPB < 90, ^HR |
syndrome characterized by decreased tissue perfusion and impaired cellular metabolism Results in imbalance between supply and demand for oxygen and nutrients When cells experience hypoperfusion, the demand for oxygen and nutrients exceeds the supply at the microcirculatory level |
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SNS mediated response results in: |
increased HR, CO, RR, depth Decreased PAWP, Stroke volume, and central venous pressure because of decreased circulating blood volume |
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Sepsis |
a systemic inflammatory response to a documented or suspected infection 10-30% of pt with sepsis have unidentified causative organism |
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Severe sepsis |
sepsis complicated by organ dysfunction high mortality rate as high as 28-50% |
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Septic shock |
The presence of sepsis and hypotension despite adequate fluid resuscitation, along with inadequate tissue perfusion resulting in tissue hypoxia |
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Main organisms that can cause sepsis are gm - and gm + bacteria Parasites, fungi, and viruses can also cause sepsis and septic shock |
Microog enters body, normal immune/ inflammatory responses are started in severe sepsis and septic shock, the body's response to the microorganism is exaggerated inflammation and coagulation increase and fibrinolysis decreases |
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Endotoxins from the microorganism cell wall stimulate the release of cytokines, including TNF, interleukin 1, other proinflammatory mediators that act through secondary mediators such as platelet activating factor, and IL |
The release of platelet activating factor results in the formation of microthrombi and obstruction of the microvasculature Combined effects of the mediators result in damage to endothelium, vasodilation, increased cap perm, and neutrophil and platelet aggregation/ adhesion to the endothelium |
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Septic shock has 3 major pathophysiologic effects: |
vasodilation maldistribution of blood flow myocardial depression |
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Pt may be euvolemic, but because of acute vasodilation, relative hypovolemia and hypotension occur |
BF in the microcirculation is decreased, causing poor oxygen delivery and tissue hypoxia |
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Combo of TNF and IL-1 has role in sepsis induced myocardial dysfunction |
Ejection fraction is decreased for first few days after the initial insult Decreased EF, ventricles dilate to maintain stroke volume (EF improves and ventricular dilaton resolves over 7-10 days) |
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Persistence of high CO and low SVR beyond 24 hrs is an ominous finding and associated w/ increased development of hypotension and MODS |
Coronary artery perfusion and myocardial oxygen metabolism are not primarily altered in septic shock |
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Respiratory failure is common in sepsis |
pt initally hyperventilates as a comp mech = respiratory alkalosis -Once pt can no longer compensate, respiratory acidosis develops -Resp failure develops in 85% of pt and 40% develop ARDS -These pt need to be intubated and mechanically ventilated |
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Other clinical signs of septic shock |
Alteration in neurologic status decreased urine output GI dysfunction GI bleed Paralytic illeus |
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Diagnostic criteria for sepsis General variables |
Fever (temp > 38.8) Hypothermia (core temp <36) HR >90 Tachypnea Altered mental status Significant edema Hyperglycemia (bg> 140) in absence of DM |
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Inflammatory variables WBC (4,000-10,000) |
Leukocytosis (WBC > 12,000) Leukopenia (WBC < 4,000) Normal WBC w/ > 10% bands Elevated CRP Elevated procalcitonin |
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Hemodynamic variables |
Arterial hypotension SBP < 90 MAP < 70 decrease in SPB >40 |
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Organ dysfunction variables |
Arterial hypoxemia (PaO2/ FIO2 < 300) Acute oligura (<0.5 mL/kg/hr for atleast 2 hr) Serum creatine increase > 0.5 Coagulation abnormailites (INR>1.5, PTT> 60sec) Ileus (absent bowel sounds) Thrombocytopenia (platelet count <100,000) Hyperbilirubinemia (>4mg) |
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Tissue perfusion variables |
Decreased capillary refill or motting Hyperlactatemia (>1 mmol/L) |
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Diagnostic studies |
No dg study Establishing dg starts w/ H&P, hx of recent events (surgery, CP, trauma) Decreased tissue perfusion in shock leads to elevation of lactate and a base deficit ( amount needed to bring the pH back to normal) These changes reflect an increase in anerobic metabolism 12 lead ecg, continuous monitoring chest x-ray continuous pulse ox hemodynamic monitoring |
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Successful management of the pt in shock includes: |
ID of pt at risk for developing shock Integration of pt's h&P, and clinical findings to establish a dg Interventions to control or eliminate the cause of the decreased perfusion Protection of target and distal organs from dysfunction Provision of multisystem supportive care |
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ensure airway, naturally or with ET tube give oxygen or mechanically vent to maintain oxygen sat of 90% or more (PaO2 greater than 60) to avoid hypoxemia MAP and circulating BV are optimized w. fluid replacement and drug therapy |
Oxygen delivery depends on CO, avail hgb, and arterial oxygen sat (SaO2) increase supply by optimizing CO w/ fluid replacement or drug therapy Increasing hgb thu transfusion of whole blood, PRBCs Increasing arterial oxygen sat w/ supplemental O2 and mech vent |
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Cornerstone for therapy in septic shock is to volume expansion w/ admin of appropriate fluid start using 1-2 large bore (14-16 g) Iv caths in AC or CVC 30 mL/kg repeated |
Crystalloids (NS, hypertonic sol) Colloids (albumin) NS used in initial resuscitation Some cases hypertonic saline to expand plasma |
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Nutritional therapy |
Protein calorie malnutirion is one of the main manifestations in hypermetabolism in shock enteral nutrition should be started w/n first 24 hrs PN used if enteral contrandicated start on slow continuous drip (10 mL/h) early feedings increase perfusion to the GI tract and maintain integrity of gut mucosa |
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Pt in septic shock require large amounts of fluid replacement |
Volume resuscitation of 30-50 mL/kg is done w/ isotonic crystalloids to get CVP of 8-12 Albumin 0.5- g/kg/dose added when pt require substantial volumes Hemo monitoring w/ a minimum of CVC is necessary -Overall goals: restore intravascular volume and organ perfusion |
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Once CVP is 8 or more, vasopressors may be added First choice is NE |
VasoD and low CO or VasoD alone can cause low BP in spite of adequate fluid resuscitation Vasopressin used in pt refractory to pressor therapy Exogenous vasopresin is used to replace the physiologic vasporessin that are often depleted in septic shock |
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IV corticosteroids used if pt cant get adequate BP with vasopressor despite fluid resuscitation Pt may start off with a normal or high CO if pt has inadequate CO, unmet oxygen needs, CO needs to be increased using dopamine |
Abx should be started within the first hour of septic shock Obtain blood cultures before abx are started Broad spectrum then specific once causative organism is ID'd |
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Glucose levels should be maintained below: |
Below 180 for pt in shock Intesive BG control (81-108) actually increases mortality |
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Stress ulcer prophylaxis - pantoprazole for pt with bleeding risk factors |
venous thromboembolism prophylaxis (heparin, enoxaparin) also reccomended for these pts |
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At risk for shock |
older immunocompromised chronic illness surgery / trauma |
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Carefully monitor all pts for the development of infection. Progression from an infection to sepsis and septic shock depends on the pt's defense mechanisms Pt who are immunocompromised are at high risk for opportunistic infections |
ways to decrease risk of HAIs Decrease the # of invasive catheters use aseptic technique during invasive procedures strict attention to hand washing all equipt changed, cleaned, discarded btw pt use |
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Sepsis bundle w/n 3 hours |
1) Measure lactate 2) Obtain blood cultures x2 prior to admin of abx Do not delay longer than 45 min, take from central line and sterile percutaneous site, one from each IV if greater than 48 h 3) Administer broad spectrum abx 4) Administer 30 mL/kg crystalloid for hypotension SBP <90 or lactate >4 (16 g IV, preferably central line) may need oxygen |
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within 6 hours |
1) vasopressors; MAP > 65 systemic perfusion NE, Levophed is a vasoC, can cause necrotic toes, very potent, fill the tank and give fluid then give vasopressor 2) Persistent hypotension (SBP <90) *Measure CVP (want > 8, normal 8-10) fluid balance *Measure ScvO2 3) remeasure lactate if initial lactate was elevated |
