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NURS 470 > Shock and MODS > Flashcards

Shock and MODS Flashcards

1
Q

definition of shock

A

state of cellular ad tissue hypoxia due to either reduced oxygen delivery, increased oxygen consumption, inadequate oxygen utilization, or a combination of these processes

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2
Q

oxygen delivery (DO2)

A

total amount of oxygen delivered to the tissues per minutes

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3
Q

factors that affect oxygen delivery

A

hemoglobin
cardiac output
arterial oxygen saturation

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4
Q

oxygen consumption (VO2)

A

total amount of oxygen removed from the blood due to aerobic metabolism

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5
Q

factors that affect how oxygen is consumed

A

fever
inflammation
hyperthyroidism
adrenergic drugs
increased muscular activity
seizures
pain
vent weaning
shivering

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6
Q

oxygen extraction

A

how cells extract oxygen from blood
based upon energy needs
the amount of oxygen uploaded into tissues

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7
Q

oxygen extraction ratio (O2ER)

A

ratio of O2 consumption
(VO2)/(DO2)

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8
Q

cardiac O2ER

A

> 60%

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9
Q

hepatic O2ER

A

45-55%

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10
Q

renal O2ER

A

<15%

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11
Q

venous oxygen saturation (SVO2)

A

measures the amount of oxygen returned to the right side of the heart after the organs/tissues have extracted O2
measured from the pulmonary artery

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12
Q

what does low SVO2 indicate

A

the supply of O2 is not meeting tissue or cellular demands
increased oxygen consumption

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13
Q

what does high SVO2 indicate

A

inadequate oxygen extraction from the tissues

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14
Q

SVO2 of a healthy body

A

70%

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15
Q

contributors to low SVO2

A

low hemoglobin
low cardiac output
heart failure
pulmonary emboli
increased oxygen demand

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16
Q

contributors to high SVO2

A

sepsis (high CO, low extraction)
acidosis
hypothermia
excessive use of vasoactive drugs

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17
Q

central venous oxygen saturation (ScvO2)

A

measures blood return from the upper body (head and upper extremities)
from the jugular or subclavian vein
values slightly lower than mixed SVO2

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18
Q

normal range of ScvO2

A

65-75%

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19
Q

activities that increase VO2 consumption

A

nursing assessment
positioning
dressing change
bed bath
restlessness and agitation
weighing patient on sling bed scale
visitors

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20
Q

causes of abnormally high O2ER

A

decreased oxygen delivery or increased consumption
hypoxia
anemia
shock states
shivering
MODS

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21
Q

what does a low O2ER suggest

A

increased oxygen delivery but decreased oxygen consumption
malnutrition
hyperventilation
hypometabolism
sedation
hypothyroidism
paralysis

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22
Q

objective parameters of shock

A

arterial pH (7.35-7.45)
serum lactate (>2 mmol/L)
base deficit: the amount of base required to titrate 1 liter of arterial blood back to normal
procalcitonin for septic shock and MODS

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23
Q

4 shock classifications

A

cardiogenic
hypovolemic
obstructive
distributive: septic, neurogenic, anaphylactic

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24
Q

4 shock phases

A

initial
compensatory
progressive
refractory

25
initial phase of shock
decreased cardiac output decreased perfusion decreased oxygenation = anaerobic metabolism -> lactic acidosis
26
compensatory phase of shock
neuroendocrine begins to augment cardiac output and blood flow to restore blood volume glucocorticoids: increased glucose catecholamines: increased HR, RR, BP vasopressin: increased fluid retention
27
progressive phase of shock
compensatory changes not working, hyporesponsive to catecholamines poor perfusion low blood flow metabolic waste MODS persistent hypotension imbalanced oxygen delivery and consumption increasing lactic acid levels hypoxia cellular death
28
refractory phase of shock
cellular destruction and ischemia not responsive to vasopressors hypoxemic despite oxygen therapy circulatory failure impending death significant vascular volume loss tissue death oxygen delivery and consumption not corrected with interventions multiple organ failure (MOF) DIC
29
4 categories of shock management
optimize oxygen delivery to hypoxic tissue fluid resuscitation perfusion and pressure support perfusion and oxygenationi
30
shock management: interventions to optimize oxygen delivery to hypoxic tissue
patient may require intubation close assessment of arterial blood gases optimize gas exchange assess for hyperoxemia
31
shock management: interventions for fluid resuscitation
restore preload and cardiac output start with crystalloids (NS or LR) 20-30mL/kg IV rapid infusion RBCs restore interstitial and intravascular volume: colloids, albumin, starches, dextrans
32
shock management: interventions for perfusion and pressure support
vasopressors epinephrine, dopamine, phenylephrine, vasopressin, norepinephrine
33
shock management: interventions for perfusion and oxygenation
ECMO: extracorporeal membrane oxygenation
34
shock priorities
CAB: circulation (stop bleeding), airway, breathing D: disability (neuro, alert and oriented, PERRLA) E: environment (temp control) E: expose patient (look for bleeding or injury) F: five adjuncts/focused assessment (Xray, ABD, NG/OG, labs, monitor, family) G: give comfort H: history I: inspect (head to toe)
35
components to assess what kind of shock it is
patient history physical exam diagnostics
36
components of patient history
recent illness fever chest pain traumatic injury toxins/ingestions recent hospitalization environmental exposure
37
components of physical exam
vital signs neuro skin: color, temp, rashes, moisture, sores cardiovascular: JVD, heart sounds respiratory: lung sounds, skin, cap refill, ABG GI: abd pain, rigidity, guarding, rebound renal: urine output
38
components of diagnostic exams for shock
physical exam EKG CXR CT infectious source? labs: CBC blood culture UA, UDS, urine HCG CMP lactate and procal coagulation ABG lumbar puncture
39
compensatory mechanisms of shock
increased heart rate (except in neurogenic) increased respiratory rate increased glycolysis decreased urine output decreased flow to internal organs decreased peristalsis (ischemic bowel) cool skin diaphoresis
40
hypovolemic shock
profound dehydration plasma loss related to increased capillary permeability as in the case of burn injury blood loss: traumatic injury, GI bleed, intracranial hemorrhage
41
clinical manifestations of hypovolemic shock
tachycardia narrowed pulse pressure hypotension increased respiratory rate decreased urine output pale, cool, clammy skin delayed cap refill
42
pathophysiology of hypovolemic shock
decreased circulating volume decreased venous return decreased stroke volume decreased cardiac output decreased cellular oxygen supply impaired tissue perfusion impaired cellular metabolism
43
neurogenic shock
disruption of autonomic nervous system
44
neurogenic shock etiology
spinal cord injury spinal anesthesia anoxic brain injury depressive drugs
45
clinical manifestations of neurogenic shock
decreased blood pressure bradycardia, no reflexive tachycardia increased respirations warm dry skin decreased cardiac output poikilothermia: inability to regulate core body temperature, takes on temp of room
46
anaphylactic shock
allergic response
47
anaphylactic shock clinical manifestations
tachycardia wheezing/stridor rash/hives/swelling vomiting decreased cardiac output hypotension confusion, headache, loss of consciousness wheezing, cough, or difficulty getting air swollen eyes, lips, tounge fast heart rate hives abdominal pain or vomiting
48
anaphylactic treatment
airway and breathing epinephrine, IM, IV vasopressors (possibly) diphenhydramine H2 blocker, famotidine solumedrol or dexamethasone IV NS or LR bolus continuous monitoring for rebound
49
septic shock
elevated temp, HR, RR, WBCs severe sepsis progresses into septic shock hypoperfusion hypotension lactic acidosis oliguria fluid shifting from vascular space (relative hypovolemia/endotoxins)
50
septic shock clinical manifestations
tachycardia and hypotension high cardiac output with low systemic vascular resistance wide pulse pressures bounding pulses fever or hypothermia increased SVO2 decreased CVP (decreased preload)
51
sepsis related organ failure
lungs, heart, kidneys, liver, and coagulation factors
52
obstructive shock etiology
tension pneumothorax: compresses the heart, needs emergent chest tube cardiac
53
cardiogenic shock etiology
pump failure acute MI cardiomyopathy myocardial contusion myocarditis
54
cardiogenic shock clinical manifestations
tachycardic, dysrhythmias decreased cardiac output tachypnea crackles weak and thready pulses diminished heart sounds decreased urine output
55
etiology of MODS
injury or infection
56
MODS results in...
hypoxia anaerobic metabolism lactic acidosis unregulated apoptosis due to inflammation disrupted blood flow -> microvascular coagulopathy
57
MODS
control infection enhance perfusion consider steroids consider RBCs mechanical ventilation sedation glucose control and enteral feeds initiate renal replacement therapy heparin educate family prognosis 40-80% mortality
58
MODS clinical manifestations
abnormals in all system assessments
59
Becks triad
hypotension increased CVP (JVD) muffled heart tones

NURS 470 (28 decks)

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