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77 Cards in this Set
- Front
- Back
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when does shock begin? |
when CV system fails to function properly because of an alteration in blood volume, myocardial contractility, vascular resistance |
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basic premise of shock/bottom line? |
impaired tissue perfusion - O2 supply does not meet O2 demands |
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how do hemostatic mechanisms attempt to compensate? |
sympathetic NS (fight or flight) activation aldosterone and ADH released (sodium and water volume increase); RAA increase angiotensin II & aldosterone (water and sodium held and increased; hyperventilation to perfuse tissues; increase in lactic acid because tissues not perfusing adequately (anaerobi metabolism) |
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what do you look at when questioning tissue perfusion? |
pulses, capillary refill, skin temp/color, LOC, UO |
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major focus of all types of shock? |
improve tissue perfusion- adequate supply of o2, adequate CO and hemoglobin (fluid, blood, meds) |
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hypovolemic shock |
loss of intravascular fluid volume (third spacing) |
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what things can cause hypovolemic shock? Response to acute volume loss depends on what? |
bleeding, severe dehydration (MC), liver issues, pancreatitis, burn extent of injury/insult, age (young and old do not handle well at risk) general state of health |
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Stages of hypovolemic shock |
initial stage: fluid loss up to 15%; insufficient oxygen delivery- begin to utilize anaerobic metabolism second stage: (compensatory) 15-30% loss, CO decreases enough to see compensatory responses start (increased resp rate, UO decreased to hold more volume, signs of decreased blood flow (weak pulses, skin doesn't look good) Third stage (progressive): 30-40% loss, fluid loss too much for compensatory mechanisms to handle major organ dysfunction results fourth stage (refractory: very unlikely to be responsive to treatment- severe hypotension, hypoxic regarldess of o2 admin, unresponsive |
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hemodynamic findings in hypovolemic shock |
decreased CO & cardiac index, decreased CVP, increased SVR
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Why is there increased systemic vascular resistance? |
because of the volume loss, vasoconstriction occurs to compensate |
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hypovolemic shock management |
FLUIDS: crystalloids (NS or LR) to restore intravascular fluid volume
colloids (albumin) provide intravascular volume AND have oncotic abilities (pull fluid back in)
blood products if absolute blood loss |
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What fluid do you stay away from with hypovolemic shock? |
dextrose- you are giving a lot of volume to restore status and glycemic index will be out of control |
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colloid (albumin) is given to patients with what? |
liver damage, pancreatitis, burns- brings third spacing fluids back into intravascular space |
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through what do you restore fluids? |
two large-bore IVs |
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fluid replacement process |
1-2 liters of fluid then assess response
titrate (measure) amount and type of fluid to patients situation & response
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fluid resuscitation in trauma victims |
if someone is actively bleeding, the more fluids you give them the more they will bleed - so give enough volume to perfuse organs but not so much to cause bleeding to continue
you want to resuscitate to SBP of 70-90mmHg (enough to perfuse organs) until reach the OR |
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patient positioning with hypovolemic shock |
head low (increases preload) and limbs SLIGHTLY elevated -if elevated high it will decrease after load
recumbent with extremities elevated 30-45 degrees unless contraindicated |
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nutrition with hypovolemic shock |
initiate enteral nutrition within first 24 hours if this in contraindicated or fails to meet at least 80% of caloric needs initiate parenteral
maintain blood glucose within acceptable parameters |
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what is the problem with enteral feedings during hypovolemic shock? |
gut isn't working well because of inadequate perfusion, so feeding will sit there |
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why monitor blood glucose? |
likely to have issues with this when in a state of stress and while receiving nutrition delivery |
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cardiogenic shock |
failure of the heart to pump blood - can't deliver adequate amount of blood to the body -decreased perfusion -SV decreases -CO & CI decrease -preload increases |
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why does preload increase with cardiogenic shock? |
the heart is unable to pump effectively |
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what type of MI is more likely to lead to cardiogenic shock & why? |
left sided heart MI - blood left in the ventricle |
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Risk factors for cardiogenic shock |
extensive MI mechanical problems MI with existing myocardial damage advanced age (compensatory mechanisms don't work well) |
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clinical manifestations of cardiogenic shock |
decreased CO due to pump failure pt. looks like they would with acute HF -pulmonary issues, crackles (if left side is the culprit) - if right side is the culprit peripheral signs, edema |
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are compensatory mechanisms helpful in cardiogenic shock? |
no. the body increases volume to compensate and we do not want this - it is not a true lack of volume that is causing this
HR still increases |
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cardiogenic shock management: goals |
IMPROVE TISSUE PERFUSION treat underlying cause enhance pump effectiveness -decrease workload of heart, improve contractility |
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how do we do this? |
positive inotropes -increase contractility (dobutamine, milrinone) vasopressors (vasoconstrictors) -increase contractility vasodilators- reduce afterload (nitro glycerine, nitro puriside) |
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what is a risk when using positive inotropes? |
they increase oxygen consumption (still use them) |
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risk when using vasopressors (vasoconstrictors)? |
vasoconstriction may not be helpful, and make heart irritable |
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Intraaortic balloon pump |
balloon attached to end of catheter inserted into femoral artery & advanced up through aorta -inflates on diastole & deflates on systole |
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purpose of intraaortic balloon pump? two things to remember with this? |
decreases afterload (workload) and improves coronary blood flow
inflates during diastole & causes regurgitation of blood to send more blood to coronary arteries systole deflates and decreases resistance at which blood has to come out |
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complications with this pump
what to assess at bedside? |
emboli formation infection aortic rupture or dissection compromised distal circulation improper balloon placement or timing
frequent pulse checks -if something bad happens to balloon this is where you will see first signs |
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septic shock |
hypotension d/t massive vasodilation- reduction in SVR
'relative hypovolemia' d/t increased capillary permeability (same amount of volume but hose is bigger) -third spacing
maldistribution of circulating blood volume |
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can you be septic and not develop septic shock? |
yes |
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risk factors for septic shock |
very young & very old impaired immune system (cancer, chemo, AIDS, organ transplant) wounds/injuries (trauma, burns, pressure ulcers) substance abusers invasive treatments (IVs, catheters)
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what is the culprit of septic shock? |
infection |
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SIRS - criteria |
systemic inflammatory response syndrome -must have 2 or more of these 4 criteria temp > 100 or < 96.8 HR > 90 resp rate >20 or PCO2 < 32 WBS >12000 or <4000 or >10% bands |
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Sepsis criteria |
>/= 2 SIRS criteria plus infection sepsis is NOT the infection- it is the systemic response to infection
patient with infection without SIRS is not septic |
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if a patient has SIRS and the cause is infection |
they are septic |
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initiating events of SIRS |
pancreatitis trauma aspiration major surgery burns |
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sepsis = Severe sepsis = septic shock = |
SIRS + infection
sepsis + organ hypoperfusion or hypotension
sepsis + organ hypoperfusion & hypotension |
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classic signs of organ hypoperfusion |
decreased mental status decreased UO lactic acidosis (tells us we aren't perfusing tissues well)
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when do we start questioning adequate perfusion? |
when SBP is below 90 |
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the sepsis cascade |
some type of infection, increased inflammation and coagulation, decreased fibromyolysis hypoperfusion & ischemia |
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the process of the sepsis cascade |
organisms release endotoxins that invade bloodstream where they release cytokines -leads to vasodilation & increased cap permeability
injured endothelial cells and activated monocytes secrete tissue factor (thromboplstin) activated factor VII & factor X induces thrombin generation, fibrin formation
third spacing results in intravascular volume losses, massive vasodilation, clotting issues, increased permeability |
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sepsis cascade clinical manifestations |
low volume and vasodilation- BP tries to compensate at first but will be hypotensive skin warm pink and flush CO drops bc body cannot compensate (increased at first) decreased CVP & SVR resps increased lactate levels increased crackles altered LOC UO decreased
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sepsis management |
identify & treat infection provide fluids vasoactive drugs: positive inotropes, vasopressors or vasoconstrictors
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sepsis resuscitation bundle |
measure serum lactate (tells how bad perfusion compromise is) blood cultures prior to antibiotic admin broad spectrum antibiotics within 1 hour of admission treat hypotension or elevated lactate with fluids vasopressors for ongoing hypotension maintain adequate CVP (give volume they need) adequate CV oxygen saturation |
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sepsis resuscitation bundle goals |
CVP: 8-12 mmHg MAP: >/= 65 UO: >/= 0.5 ml/kg/hr SCVO2 >/= 70% (idea of what their O2 reserve is) |
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treat hypotension or elevated lactate with what? |
fluid challenge over 30 min NS or LR volume expanders (albumin, blood products) repeat based on response/tolerance
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if you give fluid and BP still goes down what should you give? |
vasopressors |
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if they have enough fluid but their status doesn't change do you still give fluid? when would you give more fluid? |
no
if CVP and BP still low |
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you decrease organ failure as you decrease the number of what? |
microemboli |
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do corticosteroids work in decreasing inflammation? |
not very well but not devastation drip keeps contant glycemic index |
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Xigris |
first med to treat sepsis but no longer out |
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MODS |
progressive and potentially reversible dysfunction of 2 or more organs/organ systems |
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MODS is a result of |
any insult that initiates inflammatory response (SIRS, sepsis) |
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Primary MODS |
direct consequence of an initiating event such as injury, hypoxemia, hemorrhage decreased o2 delivery to cells leads to cell death then organ dysfunction
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secondary MODS |
d/t second insult following previous insult that initiated inflammatory response |
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explanations for pathologic changes in MODS |
uncontrolled systemic inflammation tissue hypoxia unregulated apoptosis (cell death) cell death greater than normal and regeneration not as good as should be microvascular coagulopathy: microemboli form and leads to dysfunction |
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what shows first signs of dysfunction in MODS |
lungs ARDS |
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cardiovascular system in MODS |
become hypotensive, give fluids but don't respond well prone to arrhythmias edema -no good blood flow
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Neurological system in MODS |
alterations in LOC, confusion, psychosis glascow coma scale used to measure functioning peripheral neuropathy
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changes in MS may be result of |
hypoperfusion microvascular coagulopathy cerebral edema
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renal system in MODS |
toxic or ischemic insults to renal tubule cells dysfunction tends to develop later in MODS loss of function evident by rise in serum levels of BUN & decrease in GFR |
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Hepatic system in MODS |
manifests in high levels of serum bilirubin albumin & clotting factors affected |
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GI system in MODS |
Gi bleed from acute stress ulceration of stomach no reliable measures of Gi function in MODS ileus, intolerance to enteral tube feedings normal barrier of gut may be affected allowing bacteria adn endotoxins into systemic circulation and extending septic response |
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hematologic system in MODS |
thrombocytopenia (decreased platelets) most common dysfunction DIC |
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Disseminate intravascular coagulation |
widespread intravascular clotting with bleeding |
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conditions associated with DIC |
sepsis trauma (esp. neuro trauma) malignancy severe transfusion reactions obstetric complications |
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patho of DIC |
systemic activation of coagulation system -excessive generation & deposition of fibrin leading to microvascular thrombi formation in addition to exhaustion of platelets due to ongoing activation of coagulation system -may induce severe bleeding complications |
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DIC manifestations |
bleeding from 3 unrelated sites microthrombi formation -signs of organ dysfunction skin necrosis -circumscribed ecchymosis and symmetrical gangrene |
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DIC lab studies |
PT & APTT prolonged decreased fibrinogen levels (using so much fibrin as part of clot issue) elevated d-dimer -tells us our body is trying to break down a clot somewhere in our body exhausted platelets |
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DIC management |
treat underlying cause replace blood and components -FFP, platelets, PRBCs heparin |
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heparin controversial why? when can you give it? |
heparin prevents clot formation but causes more bleeding have to give FFP and platelets to counteract it |
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MODS management |
no definitive treatment suport organ function |
