Shock Flashcards
1
Q
What is shock defined as?
A
inability of the circulatory system to meet the oxygen and nutrient needs of body tissues
2
Q
Fill in the blank:
The cause for shock is; ___________ __________ does not meet _________ _________.
A
Tissue 02 supply does not meet 02 demand
3
Q
what is the conceptual framework of shock?
A
relationship between 02 supply (delivery) and 02 demand (consumption)
4
Q
What state is the body in during shock?
A
hypermetabolic; the body is using a lot of energy
5
Q
What does the hypermetabolic state of shock cause?
A
skewed electrolytes
elevated blood glucose
pale and cool skin
decreased capillary refill
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
7
Q
which body systems does shock effect?
A
ALL OF THEM
Shock effects all body systems
8
Q
What are some potential causes for shock?
A
- Ineffective pumping
- insufficient volume
- massive vasodilation vascular bed
9
Q
Physiological changes regarding shock?
A
- hypoperfusion of tissues
- hypermetabolism
- activation of inflammatory response
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
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
12
Q
What is the pathophysiology of shock? (4)
A
- diminished tissue perfusion
- widespread vasodilation
- cellular dysfunction
- compensatory mechanisms
- multiple organ dysfunction syndromes (MODS)
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
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
15
Q
tests to identify that compensatory mechanisms have begun working? (2)
A
ABG’s
Lactic Acid
16
Q
How much of a window do we have for treating shock?
A
think time=muscle!!!
very narrow window for treatment of shock
17
Q
signs of shock?
A
increased temperature increased HR low BP dizzy, cool and pale skin decreased UOP, and perfusion
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
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
20
Q
What is perfusion dependant on?
A
MAP
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
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
23
Q
what is cardiogenic shock?
A
the heart is unable to pump enough blood to meet the needs of the body
24
Q
Common causes of cardiogenic shock?
A
- Left ventricular failure
- Myocardial Infarction
- any condition stressing the myocardium (maybe coronary or noncoronary)
25
What is hypovolemic shock?
inadequate volume in the vascular space
26
Causes of hypovolemic shock?
- Blood Loss
- Third Spacing (fluid in extremities)
- Trauma
27
What population are most susceptible to hypovolemic shock?
The elderly
28
What is distributive shock?
abnormal placement or distribution of volume
29
Types of distributive shock?
- Sepsis
- Neurogenic
- Anaphylaxis
30
what two conditions does hypovolemic shock result from?
1. decreased fluid volume in circulation (traumatic blood loss)
2. Internal fluid shift (dehydration, severe edema, ascites)
31
Pathophysiology of hypovolemic shock?
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
32
Examples of fluid shifts causing hypovolemic shock? (5)
- hemorrhage
- burns
- ascites
- Peritonitis
- dehydration
33
Why do burns cause fluid shifts resulting in hypovolemic shock?
third spacing results from the skins inability to keep fluids in; this is why burn patients need drains
34
Examples of fluid losses resulting in hypovolemic shock?? (6)
- trauma
- surgery
- vomiting
- diarrhea
- diuresis
- diabetes insipidus
35
why is it a problem when there is a diminished supply of hemoglobin?
Hemoglobin carries oxygen to tissues; with less hemoglobin comes less oxygen transported to tissues
36
What can a transport shock state lead to? (3)
- carbon monoxide toxicity
- anemia
- hemorrage
37
what might carbon monoxide toxicity look like?
cannot regulate; patient will be sleepy, confused, HA, stewed 02 and H and H
38
Pathophysiology of cariogenic shock?
impaired delivery due to cardiac dysfunction either by the right or left ventricle
39
causes of cardiogenic shock? (9)
- 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
40
What is the number one cause of cardiogenic shock?
Anterior wall MI
41
Vulnerable populations for cardiogenic shock? (4)
- elderly
- diabetic
- anterior MI
- history of MI
42
pathophysiology of cardiogenic shock state?
decreased cardiac contractility
decreased stroke volume and CO
causes pulmonary congestion, decreased systemic tissue perfusion, and decreased coronary artery perfusion
43
how does necrosis effect the heart muscle?
impairs contractility and CO
cannot go back once the tissue is dead
44
effects of Infarction in LV? (6)
- necrosis in heart
- oxygenated blood not moved forward into systemic circulation
- tissues have decreased 02
- decreased SV
- decreased CO
- decreased BP
45
effects of infarction in RV? (5)
- ejects too little blood into the LV
- tissues have decreased 02
- decreased SV of LV
- decreased CO
- decreased BP
46
what is an obstructive shock state?
mechanical barrier to blood flow blocks 02 delivery to tissues
47
examples of obstructive shock causes? (3)
- pulmonary embolism
- tension pneumothorax
- cardiac tamponade
48
true or false:
You can only have one type of shock at a time
FALSE!
you can have more than one type of shock
49
characteristics of distributive (circulatory) shock?
- 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
50
3 types of distributive shock?
- septic
- neurogenic
- anaphylactic
51
what is septic shock caused by?
widespread infection
52
s/s r/t septic shock
- tachycardia, fever, flushed skin, bounding pulses, tachypnea, change in UOP, and GI function
53
what are two signs of hyper-metabolism?
increased blood sugar and insulin resistance
54
what does a high CRP indicate?
infection and the presence of long term diseases
55
what does CRP show?
inflammation in the body
56
treatment for CRP?
```
steroids:
solumedrol
prednisone
cortisone
dexamethasone
```
57
what is neurogenic shock?
loss of balance between sympathetic and parasympathetic
sympathetic nervous system unable to respond to body stressors
predominant parasympathetic response resulting vasodilation
58
causes of neurogenic shock? (5)
- spinal cord injury
- spinal anesthesia
- nervous system damage
- depressant action of a medication
- hypoglycemic
59
s/s of neurogenic shock?
dry and warm skin
hypotension
bradycardia
60
What is anaphylactic shock?
- severe allergic reaction with systemic antigen-antibody reaction
- sudden onset of HoTN, near compromise, respiratory distress and cardiac arrest
61
what type of cells release potent vasoactive substances in anaphylactic shock?
mast cells release histamine and bradykinin
62
what does anaphylactic shock cause throughout the body?
widespread vasodilation and capillary permeability
63
What occurs in the initial stage of shock?
no signs or symptoms yet
64
what occurs in the compensatory stage of shock?
attempt to compensate for decreased CO and adequate oxygen and nutrients -- neural, hormonal and chemical responses
65
what occurs in the progressive stage of shock?
end organ failure due to cellular damage, usually GI and renal first then cardiac, with loss liver and cerebral function
66
What occurs in the refractory stage of shock?
irreversible damage (necrosis, tissue death)
67
What does the SNS cause in the compensatory stage of shock?
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
68
what occurs in the compensatory stage of shock as a result of anaerobic metabolism?
acidosis
69
what increases r/t acidosis and what can it cause?
RR; may cause a compensatory respiratory alkalosis
70
What is anaerobic metabolism
creation of energy through the combustion of carbs in the absence of 02
71
what organ causes anaerobic metabolism?
the lungs; they cannot put enough 02 into the bloodstream to keep up with the demands from your muscles for energy
72
What is the main occurrence in the progressive shock stage?
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
What occurs in the progressive stage related to the lungs?
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
Fill in the blank:
| Inadequate perfusion fo the heart causes _______ and _______.
dysrhythmias and ischemia
75
# Fill in the blank:
as MAP falls below __; ___ cannot be maintained causing _____ _____ _______.
70; GFR; acute renal failure
76
What functions are affected by decreased MAP?
Liver function, GI function, and hematologic function are all affected
77
What Is DIC?
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
What happens in the refractory stage of shock?
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
What is the HR in the intial stage of shock?
less than or equal to 100
80
what is the HR in the compensatory stage of shock ?
over 100
81
what Is the HR in the progressive stage of shock?
greater than or equal to 120
82
what is the HR in the refractory stage of shock?
greater than or equal to 140
83
what stages of shock is BP normal in?
Initial and compensatory
84
what does the BP look like n the progressive stage of shock?
70-90mmHg
85
What does BP look like in the refractory stage of shock?
<50-60mmHg
86
what does the RR look like in the initial stage of shock?
normal
87
what does the RR look like in the compensatory stage of shock?
20-30
88
what does the RR look like in the progressive stage of shock?
30-40
89
what does the RR look like in the refractory stage?
>40
90
what does UOP look like in the initial stage?
>30mL/hr
91
what does UOP look like in the compensatory stage?
20-30mL/hr
92
what does UOP look like in the progressive stage?
5-20mL/hr
93
what does UOP look like in the refractory stage?
negligible- no UOP
94
What does skin look like in initial stage?
cool, pink, and dry
95
what does skin look like in the compensatory stage?
cool/pale, dry moist
96
what does skin look like in progressive stage?
cold, pale, moist
97
what does skin look like in refractory stage?
cold, mottled, cyanotic, dry
98
what does cap refill look like in initial stages
normal
99
what does cap refill look like in compensatory stage?
slight delay
100
what does cap refill look like in progressive stage?
delay
101
what does cap refill look like in refractory stage?
not noted
102
four most important things for all types of shock?
- early identification
- identify and treat the underlying cause
- sequence of events can vary
- management and care of the patient will vary
103
treatments for all types of shock?
- 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
What is a normal serum lactate?
less than 2 mMol/L
105
what is serum lactate evidence of?
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
what does metabolic acidosis result from?
hyperlactatemia
107
what is base deficit?
amount of base required to titrate 1L of arterial blood to normal pH
108
what is base deficit calculated from?
ABG
109
what is a normal base deficit?
(+)3 mMol to (-)3mMol
110
what are 3 ways to optimize 02 delivery?
- supplemental 02
- IV fluids
- inotropic drugs
111
what is a crystalloid?
IV fluids such as lactated ringer, NS, D5, normosol
112
what is a colloid?
blood related products; PRBC's, FFP, plasma, platelets
113
what is the goal of crystalloids?
restore interstitial and IV volume, increase preload (CVP) and CO
114
what is the goal of colloids?
enhance bloods oxygen carrying capacity
115
What is the effect of inotropic drugs?
increase the force of the hearts contraction
116
example of inotropic drugs?
dopamine, dobutamine, milrinone, digoxin
117
what are the go to drugs for cardiogenic shock?
dobutamine and milrinone
118
what type of drug is dobutamine?
beta 1 receptor and beta 2 adrenergic
- increases cardiac contractility and CO without increasing the HR
- decreases SVR
- vasodilates
119
What type of drug is milrinone?
phosphodiesterase inhibitor
- increases cardiac contractility and CO
- decrease SVR
120
what are the four primary vasoactive drugs? (pressors)
- epinephrine
- norepinephrine (levophed)
- High dose dopamine
- vasopressin
121
what is the first line agent for HoTN?
Levophed (Norepinephrine)
122
examples of vasodilators? (2)
Nipride
| Nitroglycerin
123
what effect do vasodilators have?
increased CO, SV, and decreased SVR
| reducing the afterload
124
What is Nipride?
a systemic vasodilator
125
what is nitroglycerin?
a cardiac vasodilator; decreases o2 consumption and can worsen heart damage. DO NOT USE UNLESS NECESSARY
126
what is the go to vasodilator?
Nipride (nitropresside)
127
What do we need to watch for with Nipride?
cyanide toxicity
| -s/s: odor of almonds on breath, acidosis, tachycardia, mental status changes, and death
128
what is the tx for cyanide toxicity?
theosulfate
129
why does nipride have a bag covering it?
exposure to light can increase the chances of the medication giving you cyanide toxicity
130
what is the risk when putting a patient in modified trendelenburg?
may increase afterload to LV and decrease SV
131
ways to decrease total body work? (5)
1. mechanical ventilation
2. Neuromuscular blocking agents
3. Sedation
4. minimize pain and anxiety
5. maintain body temperature
132
examples of neuromuscular blocking agents? (4)
- pavulon (panacuronium)
- norcuron (vecuronium)
- Rocuronium
- succinylcholine
133
examples of sedation?
propofol, fentanyl
134
why is it important to prevent the patient of shivering?
the more they shiver, the more energy they use up
135
what is the window for treatment for shock?
6 hours of diagnosis
136
when would you use a paralytic?
post code hypothermia
post code
shivering
combative and pulling lines/bucking
137
how do they diagnose septic shock?
- 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
when do you hang antibiotics for septic shock?
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
most common causes of sepsis:(3)
catheter
PICC
CVL
140
what is a fluid challenge?
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
what is the goal of vasopressors?
maintain a MAP over 65mmHg
142
true or false:
| you can give dopamine and levophed through the peripheral IV site for 24 hours maximum
FALSE
you can do 12 hours MAX
preferred through a CVL or PICC d/t the harmful effects
143
what is the problem with steroids?
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
what is the target tidal volume?
6mL/kg of body weight
145
what is the expected PEEP for a patient with ARDS?
10-12
146
what angle should the patient be sitting at with a dx of ARDS?
30-45 degrees
147
what is ARDS caused by?
sepsis
148
what is the target BG for a patient in shock?
150mg/dL because they are hypermetabolic, going within a "normal" range would cause the same effects as hypoglycemia on these patients
149
methods of renal replacement?
intermittent dialysis- CRRT (short term)
150
what is CRRT?
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
methods of DVT prophylaxis? (3)
- UFH (un-fractioned heparin)
- LMWH (low molecular weight heparin) AKA enoxaparin
- SCDs
152
Methods of stress ulcer prophylaxis?
H2 blocker - ranitidine/ famotidine
| Proton pump inhibitor- protonix/prilosec
153
why are shock patients at risk for stress ulcers?
- the body is already hyper-metabolic and body is stressed out
- decreased peristalsis
- aspiration r/t ventilator
154
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
restore fluid volume and increase preload
155
what is SIRS?
systemic inflammatory response syndrome
- inflammatory syndrome
- affects the whole body
- response to infection
- related to sepsis
156
what are the criteria for SIRS diagnosis?
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
complications of SIRS? (5)
- Acute lung injury
- ARDS
- AKI
- Shock
- MODS
158
what is MODS?
multiple organ dysfunction syndrome
159
criteria for dx of MODS
- 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
how many stages are there in MODS?
four
161
Describe stage 1 of MODS?
- increased volume requirements
| - mild respiratory alkalosis - oliguria, hyperglycemia, increased insulin requirements (hypermetabolic)
162
Describe stage 2 of MODS?
- tachypneic
- hypocapneic
- hypoxemic
- moderate liver dysfunction
163
describe stage 3 of MODS?
azotemia - (high levels of nitrogen containing compounds such as; urea, and creatinine)
acid base disturbances
significant coagulation abnormalities (DIC)
164
describe stage 4 of MODS?
- vasopressor dependent
- oliguric/anuria
- ischemic colitis (hypoactive BS x4)
- lactic acidosis (lactic 2+)
165
the cardiovascular system during MODS
Systolic BP- <90
MAP- <70
requires pressor support
166
the respiratory system during MODS
Pa02/Fi02 <250
PEEP >7.5
requires mechanical ventilation
167
the renal system during MODS
UOP <0.5ml/kg/hr
increased creatinine (>50% over baseline)
requires CRRT
168
the hematologic system during MODS
platelets <100,000/mm3
| PT/PTT> upper limit of normal
169
the metabolic system during MODS
```
low pH (<7.30)
high plasma lactate
```
170
the hepatic system during MODS
Liver enzymes >2x upper limit of normal
| very jaundice
171
the CNS during MODS
altered consciousness
confused
LOC
decreased GCS
172
What does MODS always follow?
SIRS!!!!
173
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
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
what med is best for clearing high ammonia?
lactulose
