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Shock, SIRS, MODS
DONNA-lewis ch.67 (1772-1786,1794-1795
| Question | Answer |
|---|---|
| Shock definition: | not a disease but a syndrome; effect of many different disease conditions; abnormal physiologic state |
| what is shock characterized by? | decreased tissue perfusion and impaired cellular metabolism **** |
| With shock, what is imbalanced? | the supply for and the demand of O2 and nutrients to cells |
| what happens to the demand for O2 when there is hypoperfusion: | demand exceeds supply |
| What are the 2 low blood flow types of shock? | cardiogenic, hypovolemic |
| what are the 3 maldistribution of blood flow types of shock: | neurognic, anaphylaxis, and septic shock |
| what are the preciptitating factors of shock: | myocardial dysfunction, dysrhythmias, structural alterations |
| what are the myocardial dysfunctions associated with shock: | MI, cardiomyopathy, blunt cardiac injury, sever systemic of pulmonary HTN |
| what kind of cardiac structural issue is associated with shock: | valvular abnormality |
| Cardogenic shock defined: | systolic or diastolic dysfunction of the pumptin action of hte heart. |
| is there compromised cardiac output with cardiogenic shock? | yep1 |
| systolic cardiogenic shock problem: | impaired forward flow |
| diastolic cardiogenic shock problem: | impaired filling |
| what can a cardiogenic shock problem look like? | acute decompensated heart failure |
| what are the S/S of cardiogenic shock? | L C.O., ^ myocardial O2 consumption, Na and H20 retained, crackles, tachypnea,tachycardia, hypotension, cyanosis, anxiety, confusion and agitation, decreased U.O. |
| wwhat is the skin of a person with cardiogenic shock like: | cyanotic, pallor, cool & clammy |
| what is the PAWP with a cardiogenic shock problem: | increased |
| what is the pulmonary vascular resistance (PVP) with a cardiogenic shock problem: | increased |
| what is the septemic vascular resistance (SVR)with a cardiogenic shock problem: | increased |
| what is used to diagnose cardiogenic shock: | cardiac enzymes, Troponin, ECG, CXR, echocardiogram |
| what is troponin? | Troponins are specific proteins found in heart muscle |
| hypovolemic shock: | impaired tissue perfusion resulting from severely diminished circulating volume-loss of intravascular volume |
| absolute hypovolemia: | fluid is lost via hemmorrhage, GI loss, drainage, diuresis, or diabetes |
| relative hypovolemia: | internal, extravascular loss into the interstitial spaces or the intracavitory space (third spacing) |
| If I'm hypovolemic d/t my fluid being in my tissues, what kind of shock is that? | relative hypovolemic |
| If i'm hypovolemic d/t a GI bleed, what kind of shock is that | absolute hypovolemic |
| what are the products of cell metabolism: | CO, water, heat, energy |
| hypovolemic shock: S/S depend on what? | extent of injury, age and general health |
| hypovolemic shock:how much blood does the average 150 lb person have? | 5 L |
| hypovolemic shock, how much blood loss can the body compensate for? | the loss of 15% of the blood or 750 mL |
| hypovolemic shock, at what point are Sx present | when there is a 15-30% loss of blood (1500 mL) |
| hypovolemic shock, what provides a mediated response: | sympathetic nervous system |
| hypovolemic shock: what is the sypathetic response: | increased HR,^C.O., ^RR rate and depth |
| what is decreased with hypovolemic shock | stroke volume, PAWP, and urin output |
| what pyschosocial sx is present with hypovolemic shock: | anxiety |
| is the tissue dysfxn of hypovolemic shock reversible: | yes, with crystalloid fluid replacement |
| hypovolemic shock, greater than __% must be immediately replaced with blood or blood products: | 30% |
| what happens with hypovolemic shock after a while? | compensatory mechanisms begin to fail |
| what percentage of blood loss will result in permanant damage? | 40% or > 2,000 mL |
| hypovolemic shock diagnosis, what is used: | HCT/HGB, urine specific gravity, serum electrolytes, blood gasses, lactic acid |
| hypovolemic shock-is urine specific gravity up or down: | up |
| Neurogenic shock: what point on the spine is this common: | T5 or above |
| what are the preciptiating factors of Neurogenic shock: | spinal injury T5 or above, spinal anesthesia, vasomotor center depression |
| neurogenic shock is not the same thing as: | spinal cord shock |
| Neurogenic shock: | massive vasodilation without compensation d/t loss of sympathetic nervous system vasonstriction tone |
| what does Neurogenic shock lead to: | pooling of blood in BV, tissue hypoperfusion and impaired cellular metablolism. |
| what are the S/S of Neurogenic shock: | hypotension, bradycardia,not able to regulate temperature, Poikilothermia-takes temp of environment, skin is dry |
| anaphylactic shock: | acute life-threatening hypersensitivity (allergy) reaction to a sensitizing substance |
| with anaphylactic shock, has there been a previous exposure to the allergen? | yes-you have built antibodies to that exposure |
| what causes anaphylactic shock: | peanut butter, chemicals, vaccines, food, insect venom, drugs |
| what med route is most likely to cause anaphylactic shock: | IV |
| what does anaphylactic shock cause: | massive vasodilation, release of vasoactive mediators and increased capillary permability; fluid leads from vessels into interstitial spaces |
| how fast does anaphylactic shock come on: | fast |
| what are the S/S of anaphylactic shock: | resp. distress, laryngeal edema, sever bronchospasm, wheezing, stridor, circulatory faiure, chest pain, dizziness, swollen lips/tongue, hives, flushing, itching, angioedema, anxiety, confusion, impending doom |
| infectious septic shock: | microbial phenomenon characterized by an inflammatory response to the presence of microorganisms or by the invasion of a normally sterile host tissue by organisms. |
| bacteremia septic shock: | presence of viable bacteria in the blood |
| Sepsis: | systemic inflammatory response ot infection, documented or suspected |
| sepsis is manifested by ? | 2 or more conditions that define SIRS |
| what are the criteria for SIRS: | T-^100.9 or less than 97.0, HR >90, RR > 20, PaCO2 < 32, WBC greater than 12,000 or less than 4,000 or >10% bands |
| WBC for sepsis: | >12,000, <4,000 |
| RR for sepsis | >20 |
| PaCO2 in sepsis: | < 32 |
| severe sepsis: | sepsis complicated by organ dysfunction, HYPOTENSION or hypoperfusion |
| septic shock: | sepsis induced state with hypotension, DESPITE adequate fluid resucitation, along with the presence of tissue perfusion abnormalities (missing pulse***) |
| what is the primary shock Sx: | hypotension**** |
| Manifestations of sepsis: | lactic acidosis, oliguria, acute mental status changes, respiratory failure, ARDS, decreased UO, GI bleeding, and parlytic illeus |
| are all septic pts. hypotensive: | no, if they are recieving intropic or vasopressor agents, they might not be the time it is measured |
| MODS: | multiple organ dysfunction syndrome-presence of progressive physiologic dysfunction in two or more organ systems after an acute threat to homeostasis |
| what is the defining symptomatic picture of sepsis: | there is not, complex-no single sign or group of signs that define this |
| what is an ominous finding with septic shock: | persistantly high C.O. and a low SVR beyond 24 hrs. |
| Hypotension and MODS are signs of what: | septic shock |
| what are the stages of shock: | initial, compensatory, progressive, refractory |
| what is the outcome of shock dependant on: | extent of injury, host condition, age, ability to compensate |
| what happens in the initial stage of shock: | no outward signs, but the body is beginning to respond |
| in the initial stages of shock, what happens with the lactic acid: | it builds up d/t anaerobic cellular metabolism-the liver is supposed to remove this, but it requires O2 supply to remove it from the body-liver may not be recieving sufficient O2 |
| compensitory stage of shock, why is it activated: | to overcome the the anaerobic metabolism and maintain homeostasis |
| what are types of compensation in the compensitory stage of shock | Neural, hormonal and biochemical |
| compensitory stage of shock: what does the sympathetic nervous system respond to? | the decrease in cardiac output (hypotension) |
| what is released in a neural compensitory stage of shock | epinephrine and norepinephrine |
| what is the effect of epinephrine and norepinephrine in the compensitory stage of shock: | blood flow is shunted to the most vital organs (brain and heart) while it is diverted from other places (kidneys, GI, skin, lungs) |
| what happens when glucocorticoids are released in the compensitory stage of shock: | ^BS |
| what happens when mineral corticoids are released in the compensitory stage of shock: | aldosterone causes the Na+ and H20 to be retained |
| compensitory stage of shock:what activates the renin-angiotensin system- | the decreased blood flow to the kidneys |
| what enhances venous return resulting in increased blood pressure with compensitory stage of shock: | vasoconstriction |
| Na respirations and K+ excretion are enhanced in compensitory stage of shock, this triggers the release of: | ADH |
| When ADH is released in the compensitory stage of shock, what changes | increased C.O. and BP |
| what does the skin feel like in compensitory stage of shock: | cool, moist skin |
| what happens with the lungs in the compensitory stage of shock: | decreased perfusion to the lungs and decreased arterial O2 levels, increased rate and depth. Decreased arterial O2 levels |
| what happens with the heart in the compensitory stage of shock: | myocardium requires more O2 d/t ^ HR,watch the MI pt. If the perfusion deficit is not corrected here it will enter the progressive stage |
| Progressive stage of shock, when does it begin | when compensitory mechanisms fail |
| what happens in the cappillaries in the progressive stage of shock: | capillary permeability increases, allowing fluid and proteins to leak from the intravascular space into the interstitial space. (3rd spacing, anasarca) |
| what happens with circulating volume of blood in Progressive stage of shock | it is depleted |
| Progressive stage of shock: pulmonary effect: | pulmonary arterial constriction, capillary leaks, alveolar edema and decreased surfactant, vasoconstriction and bronchoconstriction, tachypnea, crackles, increased WOB, very likely to develop ARDS |
| Progressive stage of shock: Cardiovascular effect: | CO falls, L perfusion, L coronary perfusion, decreased BP, increased risk for arrythmias and MI, peripheral edema and ischemia |
| what chan the increased peripheral edema and ischemia result in with the Progressive stage of shock: | tissue necrosis, compartment syndrome |
| Progressive stage of shock: sustained hypoperfusion results in what: | ischemia of distal extremities and weak peripheral pulses |
| Progressive stage of shock, hemotological sx | DIC-disseminated intravascular coagulation (clots in microstructure), significant bleeding from orifices |
| refractory stage of shock: | final stage, profound hypotension and hypoxemia, multisystem organ failure, recovery very unlikely. |
| what are the diagnostic studies used for ? | Labs, chest x-rays(ARDS), 12 lead (arrythmias), pt. specific |
| what labs are checked in shock pt.: | CBC, HGB, HCT, WBC, DIC screening, electrolytes, BUN, creatinine, liver panel, ABG, lactate, blood cultures |
| HCT relates to: | volume of water lost-volume lab |
| what is important to collaborative care for shock: | identify at risk pt. , PMH, exam, clinical findings, control or eliminate cause, protect target/distal organs, multisystem support care |
| general mgmt of shock: | airway, o2/ventilation, fluid resusitation, drug therapy, nutritional therapy |
| how can the nurse optimize oxygen delivery: | increase cardiac output with drugs or fluids, increase HGB with transfusions, O2 saturation with additional O2, intubation, mechanical ventilation, O2 concerving measures |
| SVO2: | mixed venous oxygenation |
| SCVO2: | central venous O2 |
| ex. colloids: | hespan, albumin |
| ex crystalloid: | NS, LR |
| what types of shock should not be fluid resusuitated? | neurogenic and cardiogenic shock |
| fluid resusicitation, how many IV's-what size | 2 IV's, 14 or 16 |
| what to monitor during fluid resusicitation: | pulmonary status, U.O. BP, hypothermia, bleeding tendancy |
| what electrolytes does LR have in it? | Ca+, Cl+ |
| In shock, what is the goal MAP (mean arterial pressure) | 60-65 |
| vasodilator agents: | NTG, or nipride used in cardiogenic, nitroprusside in non cardiogenic shock |
| what is the goal of treatment for shock: | to correct decreased tissue perfusion. |
| sympathomimetic agent: | epinephrine |
| what are the nutritional interventions to take with shock pt: | Providep CHON/calories, daily weights, enteral or perenteral feeding |
| what is the advantage of enteral feeding of the shock pt: | enhances perfusion of the GI tract |
| SIRS: | systemic inflammatory response to an insult (infection, injury, ischemia, infarct)-characterized by inflmmation of organs remote from initial insult |
| what happens with the inflammatory cells in SIRS: | they are activated causing the release of mehypermetabolismdialators, damage to endotherlium and vasodilation and permeablility |
| MODS: | failure of more than one organ system in an acutely ill pt. |
| Primary MODS: | occurs early as a result of a well defined illness or injury |
| secondary MODS: | result of uncontrolled systemic inflammation with resultant organ dysfunction |
| MODS homeostasis can't be maintained w/o | intervention |
| MODS results from _____ | SIRS |
| how does the transition happen from SIRS to MODS? | not in a clear cut manner |
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