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Critical Care Nursing Exam 2 > Shock > Flashcards

Shock Flashcards

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1
Q

What is shock defined as?

A

inability of the circulatory system to meet the oxygen and nutrient needs of body tissues

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2
Q

Fill in the blank:

The cause for shock is; ___________ __________ does not meet _________ _________.

A

Tissue 02 supply does not meet 02 demand

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3
Q

what is the conceptual framework of shock?

A

relationship between 02 supply (delivery) and 02 demand (consumption)

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4
Q

What state is the body in during shock?

A

hypermetabolic; the body is using a lot of energy

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5
Q

What does the hypermetabolic state of shock cause?

A

skewed electrolytes

elevated blood glucose

pale and cool skin

decreased capillary refill

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6
Q

what is shock?

A

a condition in which tissue perfusion is inadequate to deliver oxygen and nutrients to support vital organs and cellular function

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7
Q

which body systems does shock effect?

A

ALL OF THEM

Shock effects all body systems

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8
Q

What are some potential causes for shock?

A
  • Ineffective pumping
  • insufficient volume
  • massive vasodilation vascular bed
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9
Q

Physiological changes regarding shock?

A
  • hypoperfusion of tissues
  • hypermetabolism
  • activation of inflammatory response
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10
Q

What is a sign the inflammatory response has been activated?

A

An elevated CRP is the main sign

CRP worsens the metabolic state because it requires steroids to treat; then worsens the hypermetabolic state causing the BG, and electrolytes to be elevated

requires an insulin drip to regulate BG

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11
Q

What is common to all shock states:
A. BP of 90mmHg, HR >100
B. Loss of blood volume
C. Decreased 02 delivery with decreased 02 consumption
D. Inadequate 02 delivery to meet cellular demands

A

The answer is d.

this is the biggest defining trait between all types of shock
With hypermetabolic, you will have increased oxygen consumption

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12
Q

What is the pathophysiology of shock? (4)

A
  • diminished tissue perfusion
  • widespread vasodilation
  • cellular dysfunction
  • compensatory mechanisms
  • multiple organ dysfunction syndromes (MODS)
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13
Q

some major traits related to the pathophysiology of shock? (6)

A
  • inadequate 02 to cells
  • anaerobic metabolism
  • acidotic environment
  • Na-K pump malfunction
  • cell structures damaged
  • cell death
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14
Q

How long does it take MODS to reverse?

A

THIS IS A TRICK QUESTION

MODS IS NON REVERSIBLE BECAUSE TISSUE DEATH IS NON REVERSIBLE

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15
Q

tests to identify that compensatory mechanisms have begun working? (2)

A

ABG’s

Lactic Acid

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16
Q

How much of a window do we have for treating shock?

A

think time=muscle!!!

very narrow window for treatment of shock

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17
Q

signs of shock?

A 
increased temperature
increased HR
low BP
dizzy, cool and pale skin
decreased UOP, and perfusion
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18
Q

What are the cellular effects of shock? (7)

A
  • cellular edema
  • Efflux of K+
  • Increased membrane permeability
  • lysosomal membrane rupture
  • influx of Na and H20
  • cell damage and death
  • mitochondrial damage and swelling
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19
Q

What are cytokines?

A

any number of substances, such as interferon, interleukin, and growth factors, that are secreted by certain cells of the immune system and have an effect on other cells

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20
Q

What is perfusion dependant on?

A

MAP

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21
Q

What is the compensatory mechanism related to cytokines?

A

Cytokines are released by the cells and stimulate vasodilation or vasoconstriction depending on the need for cell oxygen and nutrients

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22
Q

What works together on the cellular level to increase CO?

A

interaction of neural, chemical, and hormonal regulators work together to adjust cardiac output and peripheral resistance

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23
Q

what is cardiogenic shock?

A

the heart is unable to pump enough blood to meet the needs of the body

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24
Q

Common causes of cardiogenic shock?

A
  • Left ventricular failure
  • Myocardial Infarction
  • any condition stressing the myocardium (maybe coronary or noncoronary)
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25
Q

What is hypovolemic shock?

A

inadequate volume in the vascular space

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26
Q

Causes of hypovolemic shock?

A
  • Blood Loss
  • Third Spacing (fluid in extremities)
  • Trauma
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27
Q

What population are most susceptible to hypovolemic shock?

A

The elderly

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28
Q

What is distributive shock?

A

abnormal placement or distribution of volume

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29
Q

Types of distributive shock?

A
  • Sepsis
  • Neurogenic
  • Anaphylaxis
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30
Q

what two conditions does hypovolemic shock result from?

A
  1. decreased fluid volume in circulation (traumatic blood loss)
  2. Internal fluid shift (dehydration, severe edema, ascites)
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31
Q

Pathophysiology of hypovolemic shock?

A

decreased intravascular volume leads to decreased venous return to right atrium, decreases ventricular filling decreases cardiac output
decreased BP leads to decreased tissue perfusion which causes cell death

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32
Q

Examples of fluid shifts causing hypovolemic shock? (5)

A
  • hemorrhage
  • burns
  • ascites
  • Peritonitis
  • dehydration
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33
Q

Why do burns cause fluid shifts resulting in hypovolemic shock?

A

third spacing results from the skins inability to keep fluids in; this is why burn patients need drains

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34
Q

Examples of fluid losses resulting in hypovolemic shock?? (6)

A
  • trauma
  • surgery
  • vomiting
  • diarrhea
  • diuresis
  • diabetes insipidus
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35
Q

why is it a problem when there is a diminished supply of hemoglobin?

A

Hemoglobin carries oxygen to tissues; with less hemoglobin comes less oxygen transported to tissues

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36
Q

What can a transport shock state lead to? (3)

A
  • carbon monoxide toxicity
  • anemia
  • hemorrage
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37
Q

what might carbon monoxide toxicity look like?

A

cannot regulate; patient will be sleepy, confused, HA, stewed 02 and H and H

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38
Q

Pathophysiology of cariogenic shock?

A

impaired delivery due to cardiac dysfunction either by the right or left ventricle

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39
Q

causes of cardiogenic shock? (9)

A
  • MI (especially anterior wall MI)
  • mechanical complications (valve failure)
  • cardiomyopathy (contractility)
  • myocardial contusion (damage to heart)
  • pericardial tamponade (fluid surrounding the heart, causing the heart to pump ineffectively)
  • ventricular rupture
  • arrhythmias
  • valvular dysfunction (leaky valves)
  • end stage HF
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40
Q

What is the number one cause of cardiogenic shock?

A

Anterior wall MI

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41
Q

Vulnerable populations for cardiogenic shock? (4)

A
  • elderly
  • diabetic
  • anterior MI
  • history of MI
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42
Q

pathophysiology of cardiogenic shock state?

A

decreased cardiac contractility

decreased stroke volume and CO

causes pulmonary congestion, decreased systemic tissue perfusion, and decreased coronary artery perfusion

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43
Q

how does necrosis effect the heart muscle?

A

impairs contractility and CO

cannot go back once the tissue is dead

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44
Q

effects of Infarction in LV? (6)

A
  • necrosis in heart
  • oxygenated blood not moved forward into systemic circulation
  • tissues have decreased 02
  • decreased SV
  • decreased CO
  • decreased BP
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45
Q

effects of infarction in RV? (5)

A
  • ejects too little blood into the LV
  • tissues have decreased 02
  • decreased SV of LV
  • decreased CO
  • decreased BP
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46
Q

what is an obstructive shock state?

A

mechanical barrier to blood flow blocks 02 delivery to tissues

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47
Q

examples of obstructive shock causes? (3)

A
  • pulmonary embolism
  • tension pneumothorax
  • cardiac tamponade
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48
Q

true or false:

You can only have one type of shock at a time

A

FALSE!

you can have more than one type of shock

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49
Q

characteristics of distributive (circulatory) shock?

A
  • blood volume pools in peripheral vessels
  • result of either loss of sympathetic tone or release of biochemical mediators from cells
  • massive arterial and venous dilation cause peripheral pooling
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50
Q

3 types of distributive shock?

A
  • septic
  • neurogenic
  • anaphylactic
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51
Q

what is septic shock caused by?

A

widespread infection

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52
Q

s/s r/t septic shock

A
  • tachycardia, fever, flushed skin, bounding pulses, tachypnea, change in UOP, and GI function
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53
Q

what are two signs of hyper-metabolism?

A

increased blood sugar and insulin resistance

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54
Q

what does a high CRP indicate?

A

infection and the presence of long term diseases

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55
Q

what does CRP show?

A

inflammation in the body

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56
Q

treatment for CRP?

A 
steroids:
solumedrol
prednisone
cortisone
dexamethasone
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57
Q

what is neurogenic shock?

A

loss of balance between sympathetic and parasympathetic

sympathetic nervous system unable to respond to body stressors

predominant parasympathetic response resulting vasodilation

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58
Q

causes of neurogenic shock? (5)

A
  • spinal cord injury
  • spinal anesthesia
  • nervous system damage
  • depressant action of a medication
  • hypoglycemic
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59
Q

s/s of neurogenic shock?

A

dry and warm skin
hypotension
bradycardia

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60
Q

What is anaphylactic shock?

A
  • severe allergic reaction with systemic antigen-antibody reaction
  • sudden onset of HoTN, near compromise, respiratory distress and cardiac arrest
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61
Q

what type of cells release potent vasoactive substances in anaphylactic shock?

A

mast cells release histamine and bradykinin

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62
Q

what does anaphylactic shock cause throughout the body?

A

widespread vasodilation and capillary permeability

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63
Q

What occurs in the initial stage of shock?

A

no signs or symptoms yet

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64
Q

what occurs in the compensatory stage of shock?

A

attempt to compensate for decreased CO and adequate oxygen and nutrients – neural, hormonal and chemical responses

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65
Q

what occurs in the progressive stage of shock?

A

end organ failure due to cellular damage, usually GI and renal first then cardiac, with loss liver and cerebral function

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66
Q

What occurs in the refractory stage of shock?

A

irreversible damage (necrosis, tissue death)

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67
Q

What does the SNS cause in the compensatory stage of shock?

A

vasoconstriction
- increased HR and contractility
Maintains BP and CO
body shunts blood from skin, kidneys, and GI tract
- causing cool and clammy skin; hypoactive bowel sounds and decreased UOP, and perfusion of tissues is inadequate

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68
Q

what occurs in the compensatory stage of shock as a result of anaerobic metabolism?

A

acidosis

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69
Q

what increases r/t acidosis and what can it cause?

A

RR; may cause a compensatory respiratory alkalosis

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70
Q

What is anaerobic metabolism

A

creation of energy through the combustion of carbs in the absence of 02

71
Q

what organ causes anaerobic metabolism?

A

the lungs; they cannot put enough 02 into the bloodstream to keep up with the demands from your muscles for energy

72
Q

What is the main occurrence in the progressive shock stage?

A

mechanisms that regulate BP can no longer compensate and BP and MAP decrease

  • all organs suffer from hypo perfusion
  • vasoconstriction continues, compromising the cellular perfusion
  • mental status deteriorates r/t decreased cerebral perfusion and hypoxia
73
Q

What occurs in the progressive stage related to the lungs?

A

the lungs begin to fail and decreased pulmonary blood flow causes further hypoxemia and carbon dioxide levels increase; alveoli collapse and pulmonary edema occurs

74
Q

Fill in the blank:

Inadequate perfusion fo the heart causes _______ and _______.

A

dysrhythmias and ischemia

75
Q

Fill in the blank:

as MAP falls below __; ___ cannot be maintained causing _____ _____ _______.

A

70; GFR; acute renal failure

76
Q

What functions are affected by decreased MAP?

A

Liver function, GI function, and hematologic function are all affected

77
Q

What Is DIC?

A

disseminated intravascular coagulation

  • condition in which blood clots form throughout the body small vessels. these blood clots can reduce or block blood flow through the bloods vessels and damage the bodies organs
78
Q

What happens in the refractory stage of shock?

A

organ damage is so severe that the patient does not respond to treatment and cannot live.

  • BP remains low
  • renal and liver functions fail
  • anaerobic metabolism worsens acidosis
  • multiple organ dysfunction progresses to complete organ failure
79
Q

What is the HR in the intial stage of shock?

A

less than or equal to 100

80
Q

what is the HR in the compensatory stage of shock ?

A

over 100

81
Q

what Is the HR in the progressive stage of shock?

A

greater than or equal to 120

82
Q

what is the HR in the refractory stage of shock?

A

greater than or equal to 140

83
Q

what stages of shock is BP normal in?

A

Initial and compensatory

84
Q

what does the BP look like n the progressive stage of shock?

A

70-90mmHg

85
Q

What does BP look like in the refractory stage of shock?

A

<50-60mmHg

86
Q

what does the RR look like in the initial stage of shock?

A

normal

87
Q

what does the RR look like in the compensatory stage of shock?

A

20-30

88
Q

what does the RR look like in the progressive stage of shock?

A

30-40

89
Q

what does the RR look like in the refractory stage?

A

> 40

90
Q

what does UOP look like in the initial stage?

A

> 30mL/hr

91
Q

what does UOP look like in the compensatory stage?

A

20-30mL/hr

92
Q

what does UOP look like in the progressive stage?

A

5-20mL/hr

93
Q

what does UOP look like in the refractory stage?

A

negligible- no UOP

94
Q

What does skin look like in initial stage?

A

cool, pink, and dry

95
Q

what does skin look like in the compensatory stage?

A

cool/pale, dry moist

96
Q

what does skin look like in progressive stage?

A

cold, pale, moist

97
Q

what does skin look like in refractory stage?

A

cold, mottled, cyanotic, dry

98
Q

what does cap refill look like in initial stages

A

normal

99
Q

what does cap refill look like in compensatory stage?

A

slight delay

100
Q

what does cap refill look like in progressive stage?

A

delay

101
Q

what does cap refill look like in refractory stage?

A

not noted

102
Q

four most important things for all types of shock?

A
  • early identification
  • identify and treat the underlying cause
  • sequence of events can vary
  • management and care of the patient will vary
103
Q

treatments for all types of shock?

A
  • supplemental o2 ( if not on vent)
  • fluid replacement to restore IV volume
  • vasoactive medications to restore vasomotor tone and improve cardiac function
  • nutritional support
104
Q

What is a normal serum lactate?

A

less than 2 mMol/L

105
Q

what is serum lactate evidence of?

A

anaerobic metabolism

the by product of anaerobic metabolism is lactate; showing that there is not enough oxygen to meet the oxygen demand

lactate indicates hypoprofusion

106
Q

what does metabolic acidosis result from?

A

hyperlactatemia

107
Q

what is base deficit?

A

amount of base required to titrate 1L of arterial blood to normal pH

108
Q

what is base deficit calculated from?

A

ABG

109
Q

what is a normal base deficit?

A

(+)3 mMol to (-)3mMol

110
Q

what are 3 ways to optimize 02 delivery?

A
  • supplemental 02
  • IV fluids
  • inotropic drugs
111
Q

what is a crystalloid?

A

IV fluids such as lactated ringer, NS, D5, normosol

112
Q

what is a colloid?

A

blood related products; PRBC’s, FFP, plasma, platelets

113
Q

what is the goal of crystalloids?

A

restore interstitial and IV volume, increase preload (CVP) and CO

114
Q

what is the goal of colloids?

A

enhance bloods oxygen carrying capacity

115
Q

What is the effect of inotropic drugs?

A

increase the force of the hearts contraction

116
Q

example of inotropic drugs?

A

dopamine, dobutamine, milrinone, digoxin

117
Q

what are the go to drugs for cardiogenic shock?

A

dobutamine and milrinone

118
Q

what type of drug is dobutamine?

A

beta 1 receptor and beta 2 adrenergic

  • increases cardiac contractility and CO without increasing the HR
  • decreases SVR
  • vasodilates
119
Q

What type of drug is milrinone?

A

phosphodiesterase inhibitor

  • increases cardiac contractility and CO
  • decrease SVR
120
Q

what are the four primary vasoactive drugs? (pressors)

A
  • epinephrine
  • norepinephrine (levophed)
  • High dose dopamine
  • vasopressin
121
Q

what is the first line agent for HoTN?

A

Levophed (Norepinephrine)

122
Q

examples of vasodilators? (2)

A

Nipride

Nitroglycerin

123
Q

what effect do vasodilators have?

A

increased CO, SV, and decreased SVR

reducing the afterload

124
Q

What is Nipride?

A

a systemic vasodilator

125
Q

what is nitroglycerin?

A

a cardiac vasodilator; decreases o2 consumption and can worsen heart damage. DO NOT USE UNLESS NECESSARY

126
Q

what is the go to vasodilator?

A

Nipride (nitropresside)

127
Q

What do we need to watch for with Nipride?

A

cyanide toxicity

-s/s: odor of almonds on breath, acidosis, tachycardia, mental status changes, and death

128
Q

what is the tx for cyanide toxicity?

A

theosulfate

129
Q

why does nipride have a bag covering it?

A

exposure to light can increase the chances of the medication giving you cyanide toxicity

130
Q

what is the risk when putting a patient in modified trendelenburg?

A

may increase afterload to LV and decrease SV

131
Q

ways to decrease total body work? (5)

A
  1. mechanical ventilation
  2. Neuromuscular blocking agents
  3. Sedation
  4. minimize pain and anxiety
  5. maintain body temperature
132
Q

examples of neuromuscular blocking agents? (4)

A
  • pavulon (panacuronium)
  • norcuron (vecuronium)
  • Rocuronium
  • succinylcholine
133
Q

examples of sedation?

A

propofol, fentanyl

134
Q

why is it important to prevent the patient of shivering?

A

the more they shiver, the more energy they use up

135
Q

what is the window for treatment for shock?

A

6 hours of diagnosis

136
Q

when would you use a paralytic?

A

post code hypothermia
post code
shivering
combative and pulling lines/bucking

137
Q

how do they diagnose septic shock?

A
  • blood cultures from 2 or more areas
  • one or more should be percutaneous
  • one from each vascular access device that has been in place 48 hours
138
Q

when do you hang antibiotics for septic shock?

A

within one hour of diagnosis; ideal to hang broad spectrum antibiotics if even suspected sepsis; since there is such a narrow window, and progresses to fatal so fast. Once blood cultures are back; then can use specific antibiotics

139
Q

most common causes of sepsis:(3)

A

catheter

PICC

CVL

140
Q

what is a fluid challenge?

A

500mL bolus over 30 minutes to evaluate if the patient is able to tolerate fluids to increase the CVP or if the patient requires pressors

141
Q

what is the goal of vasopressors?

A

maintain a MAP over 65mmHg

142
Q

true or false:

you can give dopamine and levophed through the peripheral IV site for 24 hours maximum

A

FALSE
you can do 12 hours MAX
preferred through a CVL or PICC d/t the harmful effects

143
Q

what is the problem with steroids?

A

in shock, the patient is already hypermetabolic because of inflammation AEB high CRP levels; they need steroids to help with the inflammation; and steroids are known to increase BG; therefore the patient will need an insulin drip

144
Q

what is the target tidal volume?

A

6mL/kg of body weight

145
Q

what is the expected PEEP for a patient with ARDS?

A

10-12

146
Q

what angle should the patient be sitting at with a dx of ARDS?

A

30-45 degrees

147
Q

what is ARDS caused by?

A

sepsis

148
Q

what is the target BG for a patient in shock?

A

150mg/dL because they are hypermetabolic, going within a “normal” range would cause the same effects as hypoglycemia on these patients

149
Q

methods of renal replacement?

A

intermittent dialysis- CRRT (short term)

150
Q

what is CRRT?

A

slow continuous dialysis that mimics the kidneys and is performed over 24 hours; it is used to remove fluid and clear solutes and waste products

gives the kidneys a rest

151
Q

methods of DVT prophylaxis? (3)

A
  • UFH (un-fractioned heparin)
  • LMWH (low molecular weight heparin) AKA enoxaparin
  • SCDs
152
Q

Methods of stress ulcer prophylaxis?

A

H2 blocker - ranitidine/ famotidine

Proton pump inhibitor- protonix/prilosec

153
Q

why are shock patients at risk for stress ulcers?

A
  • the body is already hyper-metabolic and body is stressed out
  • decreased peristalsis
  • aspiration r/t ventilator
154
Q

why do crystalloid solutions do in the treatment of shock?

  1. increase Hct by 2-3%
  2. supplement Hgb concentrations
  3. restore fluid volume and increase preload
  4. restore fluid volume and decrease CO
A

restore fluid volume and increase preload

155
Q

what is SIRS?

A

systemic inflammatory response syndrome

  • inflammatory syndrome
  • affects the whole body
  • response to infection
  • related to sepsis
156
Q

what are the criteria for SIRS diagnosis?

A

temp: >100.4 or <96.8
HR >90bpm
RR: >20breaths/minute
WBC: >12,000/mm3 or 4,000/mm3 or >10% immature neutrophils

TWO OR MORE OF THESE TO QUALIFY FOR DIAGNOSIS OF SIRS

157
Q

complications of SIRS? (5)

A
  • Acute lung injury
  • ARDS
  • AKI
  • Shock
  • MODS
158
Q

what is MODS?

A

multiple organ dysfunction syndrome

159
Q

criteria for dx of MODS

A
  • altered function of 2 or more organs
  • acutely ill patient (not chronic)
  • homeostasis cannot be maintained without medical intervention (pressors, maxed ventilator)
  • is irreversible
160
Q

how many stages are there in MODS?

A

four

161
Q

Describe stage 1 of MODS?

A
  • increased volume requirements

- mild respiratory alkalosis - oliguria, hyperglycemia, increased insulin requirements (hypermetabolic)

162
Q

Describe stage 2 of MODS?

A
  • tachypneic
  • hypocapneic
  • hypoxemic
  • moderate liver dysfunction
163
Q

describe stage 3 of MODS?

A

azotemia - (high levels of nitrogen containing compounds such as; urea, and creatinine)
acid base disturbances
significant coagulation abnormalities (DIC)

164
Q

describe stage 4 of MODS?

A
  • vasopressor dependent
  • oliguric/anuria
  • ischemic colitis (hypoactive BS x4)
  • lactic acidosis (lactic 2+)
165
Q

the cardiovascular system during MODS

A

Systolic BP- <90
MAP- <70
requires pressor support

166
Q

the respiratory system during MODS

A

Pa02/Fi02 <250
PEEP >7.5
requires mechanical ventilation

167
Q

the renal system during MODS

A

UOP <0.5ml/kg/hr
increased creatinine (>50% over baseline)
requires CRRT

168
Q

the hematologic system during MODS

A

platelets <100,000/mm3

PT/PTT> upper limit of normal

169
Q

the metabolic system during MODS

A 
low pH (<7.30)
high plasma lactate
170
Q

the hepatic system during MODS

A

Liver enzymes >2x upper limit of normal

very jaundice

171
Q

the CNS during MODS

A

altered consciousness
confused
LOC
decreased GCS

172
Q

What does MODS always follow?

A

SIRS!!!!

173
Q

when caring for a patient with cardiogenic shock and possible MODS, which of the following helps confirm the dx of MODS?
A) crackles throughout both lungs
B) 8/10 crushing chest pain
C) elevated ammonia level and confusion
D) cool extremities and weak pedal pulses

A

C is the best answer because ammonia is a thing that cannot be cleared during MODS, and confusion is a common symptom- change in LOC

174
Q

what med is best for clearing high ammonia?

A

lactulose

Critical Care Nursing Exam 2 (2 decks)

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