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82 Cards in this Set

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what is the definition of shock?
syndrome involving poor perfusion, normally presenting as hypotension
what is the end sequela of shock?
muliple organ failure and death
how is tissue perfusion clinically measured? what is this factor dependent on?
clinically measured by MAP
MAP depends on CO and SVR
which shock type involves intravascular volume loss?
hypovolemic
which shock type involves pump failure?
cardiogenic
which shock type involves peripheral vasodilation and increase in vascular permeability?
septic (distributive)
describe the clinical presentation of shock
hypotension: SBP < 90 or MAP <65 mmHg
tachycardia: HR > 90
tachypnea: RR >20
altered mental status
decreased organ perfusion (decrease urinary output)
metabolic acidosis
the following clinical situation indicates which type of shock:
decreased MAP
decreased PCWP
decreased CO
increased SVR
hypovolemic
the following clinical situation indicates which type of shock:
decreased MAP
increased PCWP
decreased CO
increased SVR
cardiogenic
the following clinical situation indicates which type of shock?
decreased MAP
decreased or normal PCWP
decreased or normal CO
decreased SVR
septic
what are the two types of hypovolemic shock and what are some causes of each?
hemorrhagic:
trauma/surgery
internal bleeding (aortic aneurysm rupture, retroperitoneal bleed, GI bleed)
non-hemorrhagic:
dehydration
intravascular fluid shift (ascites)
fluid loss (burns, heat stroke)
describe the hemodynamics of hypovolemic shock?
decreased venous return (SV) leads to decreased PCWP and CO; to maintain MAP there is an increase in SVR
what are the goals of treatment for hypovolemic shock?
PCWP 6-15
CVP 2-6
CI 2.8-4.5
What is the effect of giving fluids in the treatment of hypovolemic shock?
increase tissue perfusion and oxygen delivery:
BP
HR
organ function
what is the first line treatment of hypovolemic shock?
fluids
true of false: there is no convincing data to support the superiority of colloids
true
which type of fluid it 1st line in treating hemorrhagic hypovolemic shock?
crystalloid
when are colloids indicated in the treatment of hemorrhagic hypovolemic shock?
in conjunction with crystalloids prior to blood products (only if needed!!!)
when colloids are indicated, which type is preferred? protien or non-protein
non-protein (hetastarch)
when are blood products indicated for hemorrhagic hypovolemic shock?
if O2 carrying capacity is reduced or there is a need for clotting factors or platelets (Hgb <10?)
which type of fluid is 1st line in treating non-hemorrhagic hypovolemic shock?
crystalloid
when are colloids indicated for the treatment of non-hemorrhagic shock
capillary leak w/ pulmonary/peripheral edema, administration of >2L of crystalloids w/o effect
what are some treatments used for hypovolemic shock (excluding fluids)
Oxygen
PRBC
other blood products: platelets (if <30,000), fresh frozed plasma (if INR is increased), cryoprecipitate (clotting factors)
inotropes
vasopressors
what is the definition of cardiogenic shock?
inadequate tissue perfusion due to cardiac dysfunction
decreased CO and evidence of tissue hypoxia in the presence of adequate intravascular volume
what are the hemodynamic criteria associated with cardiogenic shock?
sustained hypotension (SBP <90 for at least 30 minutes)
reduced CI (<2.2) in the presence of elevated PCWP (>15 mmHg)
what hemodynamic changes occur w/ cardiogenic shock?
decreased CO leads to increased pulmonary congestion and increased PCWP; to maintain MAP there is an increase in SVR
what are some causes of cardiogenic shock?
acute mitral regurgitation
rupture of interventricular septum
acute MI***
myocarditis
end-stage cardiomyopathy***
septic shock w/ severe myocardial depression
myocardial dysfunction after prolonged cardiopulmonary bypass
valvular heart disease
hypertrophic obstructive cardiomyopathy***
myocardial contusion
what goals are associated with the treatment of cardiogenic shock?
CI >2.5
PCWP <18
MAP >65
UO >0.5 mL/kg/hr
what are the initial diagnostic steps for cardiogenic shock?
directed history and physical examination
electrocardiography
echocardiography
lab tests
CXR
pulmonary artery catheterization
what are the initial therepeutic steps in managing cardiogenic shock?
supplemental O2/mechanical ventilation
venous access
monitoring by electrocardiography
pain relief
hemodynamic support: fluid challange in pts w/o pulmonary edema; vasopressors for hypotension unresponsive to fluid
if, after initial therapeutic management of cardiogenic shock, tissue perfusion remains inadequate, what are the subsequent treatment options?
inotropic agents (dobutamine, milrinone, medium dose dopamine)
IABP (intra-aortic ballooon pump)
if, after initial therapeutic management of cariogenic shock, tissue is adequately perfused but there is still pulmonary congestion, what are the subsequent treatment options?
diuretics
vasodilators (if BP is normal)
what are the three inotropes used to treat cardiogenic shock, and how does each work?
dobutamine: increases contractility and HR, causes peripheral vasodilation (careful in pts w/ low BP)
milrinone: increases contractility, casues peripheral vasodilation
dopamine: incraease contractility and heart rate, causes peripheral vasodilation (medium dose range, vasoconstriction doesn't occur until high dose)
how are vasopressors used to treat cardiogenic shock? which pressors are commonly used?
vasopressors increase MAP
norepinephrine
dopamine
how are diuretics used to treat cardiogenic shock? which are commonly used?
diuretics decrease PCWP
furosemide
bumetanide
no difference in effectiveness; use continuous IV infusion carefully- can cause too much fluid loss or ARF
how are vasodilators used to treat cardiogenic shock? which are commonly used?
vasodilators are used to decreased SVR
sodium nitroprusside (careful in pts w/ renal failure - cyanide toxicity)
nitroglycerin
hydralazine
what are the indications for an IABP?
LV compromise in septic shock
severe myocardial contusion
drug-induced failure
CPR
what are the contraindications for an IABP
irreversible brain damage
chronic end stage heart disease
dissecting arotic or thoracic aneurysms
what are some complications of using an IABP
vasular - limb ischemia throbectomy, surgery, amputation
aortic dissection
hemorrhage
infection
thrombocytopenia
renal insufficiency
what are the types of ventricular assist devices used to treat cardiogenic shock?
electric and pneumatic LVAD (only works for 2-3 weeks)
bi-ventricular assist device (only works for about 1 week)
what are some mechanical options for treating cardiogenic shock?
intra-aortic balloon pump
ventricular assist devices
what are some causes of septic (distributive) shock?
infections
anaphylaxis
neurogenic
drug-induced
acute adrenal insufficiency
true or false: sepsis related deaths equals the number of acute MI related deaths
true
which type of organism causes the most cases of sepsis?
gram positive bacteria
(not too sure about this, one graph showed g+ as being higher, another showed g-)
what are the criteria for systemic inflammatory response syndrome (SIRS)
2 (3?) or more of the following:
temp >38 C or <36
HR>90
RR>20 or PaCO2 <32 mmHg
WBC >12,000 or <4,000/mm3 or >10% immature bands
what is the criteria for sepsis?
3 of 4 criteria for SIRS + presence of infection
what is the criteria for severe sepsis?
sepsis + organ dysfunction, hypoperfusion or hypotension
(organ dysfx defined by MODS or SOFA)
what are the organ dysfunction criteria?
MAP < or = to 70mmHg or SBP < or = to 90 for at least 1 hour despite adequate fluid resuscitation
UO < 0.5 mL/kg/h for at least 1 hour despite adequate fluid resuscitation
PaO2/FiO2 < or = 250 or 200 if primary organ dysfx???
platelets < or = 80,000/mm3 or decrease of 50% in 3 days
metabolic acidosis pH < or = 7.3 with a base deficit of > or = 5 mmol/L plus lactate level >1.5 times the upper limit
what is the criteria for septic shock?
sepsis + hypotension despite adequate volume resuscitation
SBP < 90 or MAP < 60 or a decrease in SBP of >40 from baseline
(septic shock indicates that severe sepsis has already occured)
what are some risk factors associated with sepsis?
AIDS
immunosuppressant and cytotoxic agents
malnutrition
alcoholism
malignancy
DM
elderly (>65)
increased number of resistant organisms
of the following, which are increased and which are decreased in the coagulation pathway associated w/ septic shock:
TF: tissue factor
PAF: platelet activating factor
thrombin
TFPI: tissue factor pathway inhibitor
APC: activated protien C
ATIII: antithrombin III
increased: PAF, thrombin, TF
decreased: TFPI, APC, ATIII
of the following, which are increased and which are decreased leading to a decrease in the fibrinolytic pathway during sepsis?
PAI-1: plasminogin activator inhibitor 1
TAFI: thrombin activatable fibrinolysis inhibitor
t-PA: tissue plasminogen activator
u-PA
increased: PAI-1, TAFI
decreased: t-PA, u-PA
which inflammatory mediators contribute to the inflammation that occurs during sepsis?
IL-1B
TNF-a
describe the pathophysiology associated with septic shock?
1. inflammation: from inflammatory cytokines in response to infection
2. thrombosis: activation of the coagulation cascade
3. supressed fibrinolysis: depletion of the fibrinolytic pathway factors
describe the hemodynamics associated w/ septic shock
SVR is DECREASED*** leading to an increase in CO to maintain MAP; CO is only increased for short term, then ultimately decreases, leading to hypotension
describe the presentation of both early and late sepsis
early: hyperthermia/hypothermia, hyperglyc/hypoglyc, myopathy/myalgia, tachycardia, hypoxia, MS changes, leukocytosis, tachypnea, rigor, chills, proteinuria, N/V, lethargy/malaise, hyperbilirubinemia
late: lactic acidosis, oliguria/anuria, leukopenia, disseminated intravascular coagulopathy (DIC), myocardial depression, pulmonary edema, hypotension (shock), hypoglyc, azotemia, thrombocytopenia, ARDS, coma
which scenario is associated with higher mortality rates: high temperature with increased WBC or low temperature w/ decreased WBC
low temp w/ decreased WBC
what is the definition of MODS (multi-organ dysfunction syndrome)
the presence of altered organ fx in an acutely ill patient such that homeostasis cannot be maintained w/o intervention
what are the most common failed organs in septic shock?
lungs
cardiovascular
renal
hematologic
hepatic
how does pulmonary failure present in a pt w/ severe sepsis?
PaO2:FiO2 <250 or < 200 if lungs are the sole organ
acute respiratory distress syndrome (ARDS): inflammatory response ---> endothelial injury ---> hypoxemia
how does cardiovascular failure present in a pt w/ sever sepsis?
SBP <90 or MAP <65 that is unresponsive to fluids and requires vasopressors ("hypotension")
inflammatory response ---> endothelial injury and vasodilation (increased NO and decreased vasopressin), both of which contribute to hypotension
how does renal failure present in a patient with severe sepsis?
oliguria w/ UO < 0.5 mL/kg/hr despite adequate fluid resuscitation
inflammatory response ---> both endothelial injury and hypotension, both of which contribute to oliguria
how does hematologic failure present in a pt w/ severe sepsis?
platelet count <80,000/mm3 or a 50% decrease over 3 days
DIC: coagulation response--> platelet activation/aggregation---> thrombocytopenia
which pts are more likely to survive ARDS: pts w/ trauma induced or infection?
trauma induced ARDS
describe the "surviving sepsis campaign" for sepsis management
initial resuscitation
abx therapy
vasopressors
inotropes
steriods (if adrenal insufficient?)
recombinant activated protein C
blood products
glycemic products
describe the process of resuscitation and the goals during treatment of septic shock
fluid and more fluids during first 6 hours
crystalloid (500-1000 ml) or colloid (300-500 ml) boluses
goals:
MAP: >65
CVP: 8-12mmHg
ScvO2: >70% or Hgb >7
UO: >0.5 mL/kg/min(I think this is supposed to be per hour, not minute)
describe the use of Abx in the treatement of septic shock
culture susptected sites
start abx w/in 1 hr of diagnosis
abx must have activity against likely pathogens and have adequate penetration
re-assess after 24-48 hrs when cultures are available
initiate w/ empirical abx that will cover for expected pathogens
double cover for pseudomonas: b-lactam (pip/tazo) + aminoglycoside (if kidneys are OK) or FQ
use vano or linezolid if susptected resistent pathogen
what is the most common source of infection in sepsis?
respiratory infection
what are the most common organisms associated w/ septic shock?
g(-): e.coli, klebsiella, pseudomonas
g(+): staph, enterococci, strept
when are vasopressors indicated for septic shock, which are used 1st line, and what are the goals of vasopressor treatment?
start pressors if adequate MAP not achieved w/ fluid resuscitation; Norepinephrine*** or dopamine are used first line
goal is to maintain MAP > 65
when is vasopressin used for septic shock?
used for refractory shock w/ adequate fluid resuscitation and high dose pressors
used additively to NE or DA tx, may be able to decrease doses of other pressors
will cause a decrease in CO
dose(physiologic): 0.01-0.04 units/min
when are inotropes indicated for the treatement of septic shock? which are commonly used? what are the goals of inotrope tx?
indicated for pts w/ low (<2.2) CI despite adequate fluid resuscitation or w/ a ScvO2 <70% despite adequate blood transfusion during 1st 6 hrs of resuscitaion
dobutamine is used, or milrinone if SBP<100 (dobutamine is C/I)
goal: goal CI not recommended; achieve adequate ScvO2
inotropes are usually LAST LINE, must weight the risks and benefits (at this point, most pts will not live)
when are corticosteriods indicated in the treatment of septic shock?
in pts w/ adrenal insufficiency
what is the dose of hydrocortisone used for septic shock?
200-300mg/day, tid-qid for 7 days w/ vasopressor requirements
? use of fludricortisone 50mcg/day
describe the ACTH test and what it is used for
used to asses adrenal insufficiency; if pts random cortisol level is >25, they are NOT adrenal insufficien; if it is <18, they ARE adrenal insufficient; ACTH test used for pts with random level between 18-25
250 mcg ACTH administered, measure cortisol change after 30-60min. >9mg/dL increase indicates that there is NO adrenal insufficiency
how does recombinant human activated protein C (drotecogin alfa, Xigris) help treat septic shock?
in septic shock, sepsis is due to inflammation and coagulation (low levels of activated protein C); Xigris inhibits Va and VIIIa leading to a decrease in thrombin production; it is also an anti-inflammatory and a pro-fibrinolytic; targets all three mechanisms of sepsis
what is the dose of Xigris used to treat septic shock?
24 mcg/kg/hr continuous infusion for 96 hours
what are the ADRs associated w/ Xigris?
bleeding, many contraindications
what are some disadvantages to using Xigris?
high cost ($8-10,000 per dose)
efficacy is controversial in pts who do not fit into the orginal study criteria
what pts (barring any of the 38 exclusion criteria) are candidates for xigris?
pts w/ 3 or more SIRS criteria and 1 or more organ dysfunction that lasted no longer than 24 hours
therapy must be started w/in 24-48 hours
describe blood product management for pts w/ septic shock: when is it indication, what are the goals?
transfusion is indicated when Hgb < 7 or ScvO2 <70% despite adequate fluid resuscitation and pressor tx during 1st six hours of resuscitation.
goals: Hgb: 10, Hct 30% during first 6 hours
describe glycemic control for pts w/ septic shock: what is the advantage, what are the goals?
tight glycemic control is associated w/ improved survival, decrease LOS, and time on ventilator
goal: glucose 70-110 mg/dL
glucose monitoring q30-60min w/ initiation then q 4 h when normalized
blood glucose levels <60 are associated w/ an increase in mortality