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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
Q

initial phase of shock

A

decreased cardiac output
decreased perfusion
decreased oxygenation = anaerobic metabolism -> lactic acidosis

26
Q

compensatory phase of shock

A

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
Q

progressive phase of shock

A

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
Q

refractory phase of shock

A

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
Q

4 categories of shock management

A

optimize oxygen delivery to hypoxic tissue
fluid resuscitation
perfusion and pressure support
perfusion and oxygenationi

30
Q

shock management: interventions to optimize oxygen delivery to hypoxic tissue

A

patient may require intubation
close assessment of arterial blood gases
optimize gas exchange
assess for hyperoxemia

31
Q

shock management: interventions for fluid resuscitation

A

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
Q

shock management: interventions for perfusion and pressure support

A

vasopressors
epinephrine, dopamine, phenylephrine, vasopressin, norepinephrine

33
Q

shock management: interventions for perfusion and oxygenation

A

ECMO: extracorporeal membrane oxygenation

34
Q

shock priorities

A

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
Q

components to assess what kind of shock it is

A

patient history
physical exam
diagnostics

36
Q

components of patient history

A

recent illness
fever
chest pain
traumatic injury
toxins/ingestions
recent hospitalization
environmental exposure

37
Q

components of physical exam

A

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
Q

components of diagnostic exams for shock

A

physical exam
EKG
CXR
CT
infectious source?
labs:
CBC
blood culture
UA, UDS, urine HCG
CMP
lactate and procal
coagulation
ABG
lumbar puncture

39
Q

compensatory mechanisms of shock

A

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
Q

hypovolemic shock

A

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
Q

clinical manifestations of hypovolemic shock

A

tachycardia
narrowed pulse pressure
hypotension
increased respiratory rate
decreased urine output
pale, cool, clammy skin
delayed cap refill

42
Q

pathophysiology of hypovolemic shock

A

decreased circulating volume
decreased venous return
decreased stroke volume
decreased cardiac output
decreased cellular oxygen supply
impaired tissue perfusion
impaired cellular metabolism

43
Q

neurogenic shock

A

disruption of autonomic nervous system

44
Q

neurogenic shock etiology

A

spinal cord injury
spinal anesthesia
anoxic brain injury
depressive drugs

45
Q

clinical manifestations of neurogenic shock

A

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
Q

anaphylactic shock

A

allergic response

47
Q

anaphylactic shock clinical manifestations

A

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
Q

anaphylactic treatment

A

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
Q

septic shock

A

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
Q

septic shock clinical manifestations

A

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
Q

sepsis related organ failure

A

lungs, heart, kidneys, liver, and coagulation factors

52
Q

obstructive shock etiology

A

tension pneumothorax: compresses the heart, needs emergent chest tube
cardiac

53
Q

cardiogenic shock etiology

A

pump failure
acute MI
cardiomyopathy
myocardial contusion
myocarditis

54
Q

cardiogenic shock clinical manifestations

A

tachycardic, dysrhythmias
decreased cardiac output
tachypnea
crackles
weak and thready pulses
diminished heart sounds
decreased urine output

55
Q

etiology of MODS

A

injury or infection

56
Q

MODS results in…

A

hypoxia
anaerobic metabolism
lactic acidosis
unregulated apoptosis due to inflammation
disrupted blood flow -> microvascular coagulopathy

57
Q

MODS

A

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
Q

MODS clinical manifestations

A

abnormals in all system assessments

59
Q

Becks triad

A

hypotension
increased CVP (JVD)
muffled heart tones

NURS 470 (28 decks)

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