Hemodynamics 2 Flashcards
(205 cards)
1
Q
What is shock?
A
Systemic hypoperfusion and cardiovascular collapse
2
Q
3 causes of shock?
A
- Decreased circulating blood volume
- Decreased cardiac output
- Sepsis
3
Q
3 other causes of shock (much less common)?
A
- Anaphylaxis
- SIRS
- Neurogenic causes
4
Q
Hypovolemic shock (decreased circulating blood volume) is due to?
A
- Bleeding
- Fluid loss from vomiting
- Diarrhea
- Extensive burns
* All these things would lead to loss of fluid!
5
Q
Cardiogenic shock (decreased cardiac output) is due to?
A
- MI
- Arrhythmia
- Pulmonary embolism
- Hemopericardium
6
Q
When a hemopericardium (hemmorhage in the heart) is squeezing the cardiac filling chambers and obstructing filling, what is this called?
A
Cardiac tamponade
7
Q
Shock due to widespread vasodilation, where not enough blood is returned to the heart and lungs?
A
Septic shock
8
Q
Can a patient have more than one type of shock at a given time?
A
Of course, Hickam’s dictum
9
Q
What blood pressure defines “shock”?
A
None, shock is a syndrome, not a number
10
Q
First symptoms of shock?
A
Agitation… Nervous, fidgety, irritable
11
Q
Clinical manifestations of shock?
A
Decreased mental status, eventually coma
12
Q
A patient has a weak rapid (“thready”) pulse, with cool, clammy, cyanotic skin. What kind of shock do they have?
A
Hypovolemic or cardiogenic shock
13
Q
Patient has warm, flushed skin. What type of shock?
A
Septic shock
14
Q
7.6% increase in mortality unless an antibiotic is given is a characteristic of?
A
Septic shock
15
Q
Should you rely on vital signs to indicate shock?
A
No, vital signs are late responders to shock
16
Q
Why should you be weary of a young trauma or post-op patient with regards to shock?
A
Young ppl are better at compensating. One minute, they fine. The next, cardiac arrest due to painless bleeding into the abdomen or retroperitoneum
17
Q
Least common of the three major types of shock?
A
Cardiogenic shock
18
Q
Failure of heart as a pump due to intrinsic heart disease is what type of shock?
A
Cardiogenic
19
Q
Bleeding into pericardial sac (hemopericardium) prevents the heart from filling and can lead to cardiogenic shock. This is known as?
A
Cardiac tamponade
20
Q
How do you treat cardiac tamponade?
A
remove the blood from the pericardial sac
21
Q
A large pulmonary thromboembolus has obstructed the pulmonary trunk. What type of shock are you concerned about?
A
Cardiogenic
22
Q
Some would put shock from pulmonary embolism or cardiac tamponade into a fourth category of shock known as?
A
Obstructive shock
23
Q
Explain septic shock?
A
Systemic vasodilation leads to too much blood “pooled” in the periphery and not enough returning to the heart for adequate perfusion
24
Q
Anaphylactic shock has the same feature as septic shock and these two are sometimes put into a broad group of shock called?
A
Vasogenic shock
25
Should the ever changing fashion in the terminology of shock come as a shock to you?
No, no Nichols, it shouldn't. Thanks
26
A type of vasogenic shock due to spinal cord injury or spinal anesthesia causing acute loss of sympathetic nervous system maintenance of normal levels of vasoconstriction?
Neurogenic shock
27
Trauma patients can have shock that is partly hemorrhagic and partly more like septic shock. Why?
Increased production of pro inflammatory cytokines such as TNF, IL-1, IL-6
28
Most common of the three major types of shock?
Hypovolemic shock
29
Is it important to categorize shock? Why?
Very important! The type of shock determines the treatment
30
How much blood loss causes hemorrhagic shock?
25-30%
31
Life threatening shock if not immediately diagnosed and treated?
35-45%
32
Dividing line between life and death?
50%
33
This 50% number comes with caveats. If a very slow hemorrhage occurs in a healthy person, will losing 50% of their blood kill them?
No
34
If someone with MI and narrowing of several large coronary arteries loses 5% of their blood through hemorrhage will they die?
Possibly
35
How is sepsis defined?
SIRS with suspected infection
36
What are the two subsets of sepsis?
Severe sepsis and septic shock
37
Define SIRS
2 or more of the following criteria:
1. Temp above 38 or below 36
2. HR > 90
3. Tachypnea > 20 or arterial pCO2 12000 or <4000
38
Of the three: sepsis, severe sepsis, septic shock, which is most likely to have a positive blood culture?
Septic shock: 69% For the others, a positive blood culture is in the minority
39
A new conference in 2003. Lots of docs made a new list of what qualifies as "sepsis" and "SIRS". What did they add to the list?
About 15 new things.. altered mental status, HR >2 st dev above normal, "significant edema", positive fluid balance >20ml/kg, lots of others...
40
What can we take from the fact that tons of doctors couldn't agree on a concise list of symptoms and signs for sepsis?
In diagnosis, there is no substitute for experience
41
General, overall view of the molecular mechanism of sepsis?
PRR's (on TLR's, NOD's and others) bind PAMPs (bacterial cell wall lipoproteins, lipopolysacs). This activates inflammatory cells which release cytokines (TNF, IL-1, 6, 8, 12, 18, INF, HMGB-1). Cytokines upregulate endothelial adhesion molecules that bind leukocytes directing them to site of infection
42
What molecule is 100-1000 times more potent at inducing vascular dilation and increasing vasc perm than histamine?
Platelet activating factor (PAF)
43
Other functions of PAF?
1. Promotes leukocyte adhesion to endothelial cells
2. Chemotaxis
3. Degranulation
4. Oxidative burst that enables microbial killing in leukocytes
44
What components of the complement system increase vasc perm and cause vasodilation by inducing mast cells to release histamine?
C3a and C5a
45
According to Nichols (who suuuucks at teaching Immunology), what results in T-cell activation and proliferation?
Binding of CD80 (on APC's) to CD28 (on T-cells)
46
What sustains expression of CD80 on the surface of APC's?
The release of IL-12 from Th1 cells that have been activated by the APC
47
Which interleukins (IL) causes release of histamine from mast cells?
IL-1 and IL-8
48
Histamine is released from mast cells and basophils, but also from ?
Platelets
49
What cells can do the arachidonic acid pathway and create prostaglandins?
Activated macrophages, neutrophils, mast cells, and endothelial cells
50
What are prostaglandins?
Short lived lipid mediators that bind to G-coupled receptors on many cell types and have a variety of effects.
51
Which prostaglandins cause vasodilation?
1. PGI2 (prostacyclin)
2. PGD2
3. PGE1
4. PGE2
52
Which prostaglandins cause an increase in vascular permeability?
PGD2 and PGE2
53
What cells can release PAF?
macrophages, neutrophils, mast cells, endothelial cells, platelets
54
What does PAF do?
Increases vascular permeability
55
What chemical that is a potent vasodilator is released from activated endothelial cells?
Nitric oxide (NO)
56
What cells can produce NO?
Endothelial cells, macrophages, neutrophils
57
How can too much NO cause problems?
It would cause too much vasodilation which would damage endothelial cells. Damaged endothelial cells would lead to increased vascular permeability which would allow fluid to leak out of the blood vessels. This would decrease blood volume leading to septic shock
58
What activates Hagaman factor (XII)?
Activated platelets, basement membrane, collagen
59
Hageman factor is the king activator of what pathways?
Kinin, Clotting, Fibrinolytic, Complement
60
What does activated factor X do?
Causes increased vascular permeability and leukocyte emigration from blood vessels
61
Who is the king of clotting?
Thrombin
62
What does Thrombin generate that causes increased vascular permeability and is chemotactic for leukocytes?
Fibrinopeptides
63
How does Thrombin link the clotting and complement cascades?
Thrombin cleaves C5 which releases C5a
64
Can a medical student memorize all the interconnections of these pathways in a month?
No
65
Will we have to memorize all the interconnections of these pathways in a month if we want to do well on the test?
Yes
66
Endothelial cells, when activated by sepsis, promote what?
Increased vascular permeability, dilation, and thrombosis
67
Does sepsis cause clotting?
Yes, it indirectly inhibits fibrinolysis
68
How does sepsis indirectly inhibit fibrinolysis?
1. Increases plasminogen activator inhibitor-1
2. Decreases tissue factor pathway inhibitor
3. Decreases thrombomodulin
4. Decreases protein C
69
What is a common complication (50%) in sepsis patients?
Unlocalized disseminated intravascular coagulation (DIC)... Septic patients are DICs haha (but it helps doesn't it...)
70
Is lipoxin inflammatory or anti-inflammatory?
Anti-inflammatory
71
How is lipoxin anti-inflammatory? What does it do?
inhibits neutrophil adhesion to endothelial cells
72
What is lipoxin generated from ?
Arachidonic acid
73
What are the anti-inflammatory molecules of the complement system?
Factor H, DAF, C1 inhibitor, lipoxins
74
What is anti-inflammatory for macrophages?
IL-10
75
What makes IL-10
Macrophages.. It "calms" itself down
76
What blocks the inflammatory actions of TNF?
sTNFR (soluble TNF receptor)
77
What do you call the anti-inflammatory mechanism that leads to apoptosis of lymphocytes and GI epithelial cells that leads to immunosuppression?
Counter-regulatory mechanism
78
What are some results of immunosuppression?
Opportunistic infections, reactivation of latent infections, GI hemorrhage
79
Can sepsis be fatal due to the counter-regulatory mechanism "overshooting"?
You betcha
80
Whats the acronym for the counter-regulatory mechanism?
CARS: compensatory anti-inflammatory response syndrome
81
When a patient swings back and forth between pro-inlfammatory response and anti-inflammatory response what do you call that?
MARS: mixed antagonistic response syndrome
82
Infliximab (Remicade), etanercept (Enbrel), and adalimumab (Humira) block what cytokine?
TNF-alpha
83
What drug blocks IL-6 receptors?
Tocilizumab
84
What have these cytokine blocking drugs been used to treat?
Autoimmune diseases
85
Extensive trauma or burns, acute pancreatitis, extensive multi-organ ischemic necrosis, and infection can all cause?
SIRS
86
Antigens that promote T lymphocyte mitosis in a nonspecific way, bypassing antigen receptor specificity
Superantigens
87
Toxic shock syndrome toxin-1 (TSST-1) activates what percentage of T cell clones?
5-20% (the normal is 0.001%)
88
Give the generalized steps going from super antigen to toxic shock syndrome
Superantigens activate tons of T-cells. T-cells release tons of cytokines (IL-1 and TNF). Cytokine storm ensues leading to SIRS and toxic shock
89
Toxic shock is due to a nonspecific immunologic over-reaction to a bacterial product produced by?
Staphylococci or streptococci
90
Staph aureus has overgrown in a superabsorbent tampon. What is this called?
Menstrual toxic shock syndrome
91
First step in treating menstrual toxic shock syndrome?
Remove the tampon containing overgrown bacteria. Then give antibiotics
92
Is menstrual toxic shock syndrome due to infection?
No, its due to bacteria
93
An infection of what bacteria in the skin or pharynx produces streptococcal pyrogenic exotoxin A (SPEA) acting as a superantigen?
Streptococcus pyogenes
94
Is disease racist? Give 2 examples
Yes, 90% of toxic shock syndrome occurs in whites. Chinese are more likely to get severely ill with influenza
95
How is severe sepsis/SIRS different from sepsis/SIRS?
ACUTE ORGAN DYSFUNCTION!!
96
What's MOF?
Multiple organ failure
97
Can hypovolemic and cardiogenic shock also cause MOF?
Yes
98
Does the MOF become its own syndrome with a life of its own?
Yes
99
What are the 3 stages of shock?
1. Non-progressive
2. Progressive
3. Irreversible
100
Which stage has manifestations of decompensating organ function?
Progressive
101
Which stage has reflex compensatory mechanisms that maintain perfusion of vital organs?
Non-progressive
102
Which stage of shock causes death even if the cause of shock is reversed?
Irreversible
103
What are the compensatory responses to shock?
1. Sympathetic nervous system responses
2. Fluid shifts within the body
3. Neuroendocrine stress responses
104
Does the sympathetic nervous system and neuroendocrine system response increase or decrease the heart rate?
Increase
105
What are the molecular mediators to neuroendocrine response to shock?
Epinepherine/norepinepherine (from adrenal medulla), vasopressin (from pituitary), and renin (from kidneys)
106
Describe the fluid shift response
Movement of water from extravascular compartment to the blood. This dilutes the blood, but it keeps the blood pressure up
107
Continue the fluid shift response...
Kidneys stop making urine. Body shuts down perfusion to periphery (last to go is heart and brain)
108
Last to go if cerebral shutoff is slow enough?
Deeply emotional memories and central "tunnel" vision
109
Cells are deprived of adequate oxygen so they resort to anaerobic metabolism generating lactic acid. What stage of shock are we in?
Progressive
110
What are the biomarkers for the "point of no return"?
Blood levels of TNF-alpha, IL-1, and IL-6
111
Pathology of shock in brain?
Cerebral necrosis with red (dead) neurons and cerebral edema
112
Pathology of shock in intestines?
Hemorrhagic ischemic enteritis
113
Pathology of shock in kidneys?
Renal acute tubular necrosis
114
Pathology of shock in adrenals?
Adrenal cortical lipid depletion and necrosis
115
Pathology of shock in liver?
Centrilobular hepatic necrosis
116
Pathology of shock in lungs?
Pulmonary diffuse alveolar damage
117
Pathology of shock in heart?
Myocardial necrosis
118
Are cerebral necrosis and edema common outcomes of shock?
Yes
119
How long after death do the neurons in the brain develop condensed cytoplasm rendered hypereosinophilic?
12 hours
120
What is the name for these hypereosinophilic (in the cytoplasm) neurons?
Red neurons
121
The dead red neurons shrink and their nuclei become shrunken and condensed and hyper basophilic. What is this clumping of the nucleus called?
Pyknosis
122
People that are resuscitated from shock or cardiac arrest can have return of all organ function except the brain. Why?
Neurons do not regenerate
123
Shutting off the bowel can convert hypovolemic shock to?
Septic shock
124
Ischemic bowel mucosa becomes?
Leaky and sticky
125
What all leaks into the bowel/mucosa during bowel ischemia/necrosis?
Bile pigment, fibronectin (which causes stool to stick to bowel linings), blood
126
Whats the pathologic appearance of ischemic bowel?
Dusky
127
How do you cure septic shock from ischemic bowel?
Remove the portion of ischemic bowel
128
Acute kidney injury (AKI) caused by shock is irreversible? T/F
False, it is reversible
129
Gross pathology of AKI?
swollen kidney with pale cortex and congested medulla
130
AKI "hits" primarily in the?
Tubules
131
What does AKI do to the tubules?
Loss of proximal tubule epithelial cell brush borders, then epithelial cell swelling and vacuolization. Finally, epithelial cell necrosis and sloughing into tubular lumen
132
What are the two possible elements of tubular obstruction in the case of AKI?
1. Eosinophilic hyaline material (Tamm-Horsfall protein)
2. If shock has resulted in rhabdomyolysis (skeletal muscle breakdown), then myoglobin casts may also obstruct the tubules
133
Leukocytes in the vasa recta (small blood vessels of adrenal medulla) is associated with?
AKI
134
What does shock initially do to the adrenal glands?
Makes them deplete their cholesterol making stress hormones which enter the bloodstream
135
Adrenal necrosis is frequently accompanied by?
Hemorrhage
136
What is a big infectious concern in children that can lead to massive adrenal hemorrhage and necrosis?
Neisseria meningitidis
137
Adrenal hemorrhage and necrosis (most commonly due to Neisseria meningitidis) is known as?
Waterhouse-Friderichsen syndrome
138
Gross path of shock liver?
Nutmeg liver
139
Microscopic pathology of shock liver?
Coagulative necrosis of hepatocytes in the center of hepatic lobules
140
Vulnerability of hepatocytes to ischemia is directly proportional to their proximity to?
Hepatic lobular central veins
141
What is the popular thing to call shock lung?
ALI (acute lung injury)
142
Gross path of shock lung (ALI)?
Firn, edematous, congested, beefy, red organ
143
Microscopic path of ALI?
Increased neutrophils in the capillaries in the septa between alveoli
144
Whats the chemotactic for the neutrophils that invade the lung after ALI? What produces these chemokines?
IL-8, produced by macrophages
145
What kind of damage do the neutrophils do to the lung?
Release substances (oxidants, proteases, PAF, leukotrienes) that damage alveolar epithelial cells and increase permeability of air/blood barrier
146
With typical ALI, alveolar adema fluid condenses into eosinophilic hyaline membranes lining the airspaces. What does this cause?
Can block diffusion of oxygen resulting in hypoxemia (decreased oxygen loading of the blood passing thru the lungs)
147
Severe end of ALI?
ARDS (acute respiratory distress syndrome)
148
Acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in absence of evidence for cardiogenic pulmonary edema?
ARDS
149
Is disease racist? Give 2 examples
Yes, 90% of toxic shock syndrome occurs in whites. Chinese are more likely to get severely ill with influenza
150
How is severe sepsis/SIRS different from sepsis/SIRS?
ACUTE ORGAN DYSFUNCTION!!
151
What's MOF?
Multiple organ failure
152
Can hypovolemic and cardiogenic shock also cause MOF?
Yes
153
Does the MOF become its own syndrome with a life of its own?
Yes
154
What are the 3 stages of shock?
1. Non-progressive
2. Progressive
3. Irreversible
155
Which stage has manifestations of decompensating organ function?
Progressive
156
Which stage has reflex compensatory mechanisms that maintain perfusion of vital organs?
Non-progressive
157
Which stage of shock causes death even if the cause of shock is reversed?
Irreversible
158
What are the compensatory responses to shock?
1. Sympathetic nervous system responses
2. Fluid shifts within the body
3. Neuroendocrine stress responses
159
Does the sympathetic nervous system and neuroendocrine system response increase or decrease the heart rate?
Increase
160
What are the molecular mediators to neuroendocrine response to shock?
Epinepherine/norepinepherine (from adrenal medulla), vasopressin (from pituitary), and renin (from kidneys)
161
Describe the fluid shift response
Movement of water from extravascular compartment to the blood. This dilutes the blood, but it keeps the blood pressure up
162
Continue the fluid shift response...
Kidneys stop making urine. Body shuts down perfusion to periphery (last to go is heart and brain)
163
Last to go if cerebral shutoff is slow enough?
Deeply emotional memories and central "tunnel" vision
164
Cells are deprived of adequate oxygen so they resort to anaerobic metabolism generating lactic acid. What stage of shock are we in?
Progressive
165
What are the biomarkers for the "point of no return"?
Blood levels of TNF-alpha, IL-1, and IL-6
166
Pathology of shock in brain?
Cerebral necrosis with red (dead) neurons and cerebral edema
167
Pathology of shock in intestines?
Hemorrhagic ischemic enteritis
168
Pathology of shock in kidneys?
Renal acute tubular necrosis
169
Pathology of shock in adrenals?
Adrenal cortical lipid depletion and necrosis
170
Pathology of shock in liver?
Centrilobular hepatic necrosis
171
Pathology of shock in lungs?
Pulmonary diffuse alveolar damage
172
Pathology of shock in heart?
Myocardial necrosis
173
Are cerebral necrosis and edema common outcomes of shock?
Yes
174
How long after death do the neurons in the brain develop condensed cytoplasm rendered hypereosinophilic?
12 hours
175
What is the name for these hypereosinophilic (in the cytoplasm) neurons?
Red neurons
176
The dead red neurons shrink and their nuclei become shrunken and condensed and hyper basophilic. What is this clumping of the nucleus called?
Pyknosis
177
People that are resuscitated from shock or cardiac arrest can have return of all organ function except the brain. Why?
Neurons do not regenerate
178
Shutting off the bowel can convert hypovolemic shock to?
Septic shock
179
Ischemic bowel mucosa becomes?
Leaky and sticky
180
What all leaks into the bowel/mucosa during bowel ischemia/necrosis?
Bile pigment, fibronectin (which causes stool to stick to bowel linings), blood
181
Whats the pathologic appearance of ischemic bowel?
Dusky
182
How do you cure septic shock from ischemic bowel?
Remove the portion of ischemic bowel
183
Acute kidney injury (AKI) caused by shock is irreversible? T/F
False, it is reversible
184
Gross pathology of AKI?
swollen kidney with pale cortex and congested medulla
185
AKI "hits" primarily in the?
Tubules
186
What does AKI do to the tubules?
Loss of proximal tubule epithelial cell brush borders, then epithelial cell swelling and vacuolization. Finally, epithelial cell necrosis and sloughing into tubular lumen
187
What are the two possible elements of tubular obstruction in the case of AKI?
1. Eosinophilic hyaline material (Tamm-Horsfall protein)
2. If shock has resulted in rhabdomyolysis (skeletal muscle breakdown), then myoglobin casts may also obstruct the tubules
188
Leukocytes in the vasa recta (small blood vessels of adrenal medulla) is associated with?
AKI
189
What does shock initially do to the adrenal glands?
Makes them deplete their cholesterol making stress hormones which enter the bloodstream
190
Adrenal necrosis is frequently accompanied by?
Hemorrhage
191
What is a big infectious concern in children that can lead to massive adrenal hemorrhage and necrosis?
Neisseria meningitidis
192
Adrenal hemorrhage and necrosis (most commonly due to Neisseria meningitidis) is known as?
Waterhouse-Friderichsen syndrome
193
Gross path of shock liver?
Nutmeg liver
194
Microscopic pathology of shock liver?
Coagulative necrosis of hepatocytes in the center of hepatic lobules
195
Vulnerability of hepatocytes to ischemia is directly proportional to their proximity to?
Hepatic lobular central veins
196
What is the popular thing to call shock lung?
ALI (acute lung injury)
197
Gross path of shock lung (ALI)?
Firn, edematous, congested, beefy, red organ
198
Microscopic path of ALI?
Increased neutrophils in the capillaries in the septa between alveoli
199
Whats the chemotactic for the neutrophils that invade the lung after ALI? What produces these chemokines?
IL-8, produced by macrophages
200
What kind of damage do the neutrophils do to the lung?
Release substances (oxidants, proteases, PAF, leukotrienes) that damage alveolar epithelial cells and increase permeability of air/blood barrier
201
With typical ALI, alveolar adema fluid condenses into eosinophilic hyaline membranes lining the airspaces. What does this cause?
Can block diffusion of oxygen resulting in hypoxemia (decreased oxygen loading of the blood passing thru the lungs)
202
Severe end of ALI?
ARDS (acute respiratory distress syndrome)
203
Acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in absence of evidence for cardiogenic pulmonary edema?
ARDS
204
Subendocardial myocyte blood supply is cut off, how long until they begin dying?
20 minutes
205
Person sustains a subendocardial MI but is resuscitated they tend to have?
A circumferential infarct involving anterior left ventricle, left lateral ventricle, and posterior left ventricle
