Hemodynamics 2 (Word Doc) Flashcards
1
Q
3 Most common causes of shock:
A
(1) decreased circulating blood volume (2) decreased cardiac output (3) sepsis
2
Q
Causes of hypovolemic shock:
A
bleeding or fluid loss from
vomiting
diarrhea
extensive burns
3
Q
Cause of cardiogenic shock:
A
- myocardial infarction
- arrhythmia (compromises pumping)
- pulmonary embolism (obstructing right heart -output)
- hemopericardium (obstructing filling)
4
Q
What is cardiac tamponade?
A
Blood (hemopericardium) pressing downon the chambers of the heart, limiting filling
5
Q
Why does septic shock cause hypoperfusion?
A
Systemic vasodilation–sends too much blood out, and too little comes back to the heart/lungs
6
Q
Shock is not a number, but a _____
A
Syndrome
7
Q
Characterized by the signs and symptoms of systemic hypoperfusion
A
Shock
8
Q
Progressing cognitive symptoms of shock:
A
Agitation (earliest) –> decreasing mental status –> lethary –> coma
9
Q
What is an obvious way to distinguish septic shock from cardiogenic/hypovolmic shock?
A
Warm verus cool/clammy skin
10
Q
Patients in all form of shock have decreased:
A
Urine output
11
Q
What are two late signs of shock? (When noticed, injury has already occurred)
A
Elevated heart rate (>100) and low blood pressure (<90 systolic or 40mmHg lower than usual)
12
Q
T/F: A sudden, profound crash is characteristic of old people.
A
F: Young people crash crash suddenly and profoundly and (often) irretrievably because they can compensate longer, thus their vitals are okay
13
Q
Accurate categorization of shock is important because:
A
treatments are different
14
Q
Treatment for hemorrhagic shock:
A
Blood transfusion
15
Q
Treatment for septic shock:
A
Abx
16
Q
Cardiogenic shock usually results from
A
Pump failure
17
Q
What are 3 symptoms of cardiac tamponade?
A
shock
distant heart sounds
jugular venous distention
18
Q
What is the treatment for cardiac tamponade?
A
removing the blood from the pericardial sac
19
Q
What two conditions are sometimes considered obstructive shock?
A
cardiac tamponade and pulmonary thromboembolus that blocks the pulmonary trunk
20
Q
What two conditions are sometimes considered vasogenic shock?
A
Anaphylactic shock and septic shock
21
Q
Condition in which vasodilatation increases the capacitance of the vascular system so much that the too much blood pools in the periphery and too little returns to the heart (for oxygenation and repumping)
A
Septic and Anaphylactic shock
22
Q
Vasogenic shock associated with spinal cord injury or spinal anesthesia; causes acute loss of sympathetic nervous system maintenance of normal vasoconstriction
A
Neurogenic shock
23
Q
Why do trauma patients experience shock that is partially hemorrhagic and partially septic?
A
increased production of proinflammatory cytokines (TNF, IL-1 and IL-6)
24
Q
The dividing line between lethal and non-lethal hemorrhage
A
loss of 50% of blood volume
25
Percentage of blood loss causing symptoms of compensation
15-20%
26
Percentage of blood loss causing shock
25-30%
27
Percentage of blood loss causing life-threatening shock
35-45%
28
In a healthy person, 50% blood loss can be tolerated if:
It occurs over days-weeks ("The more slowly a hemorrhage takes place, the greater a hemorrhage a person can survive")
29
T/F: A person's general health partially determines the amount of blood loss that can be tolerated.
T
30
Patient-as-a-whole syndrome that occurs in response to infection
Sepsis
31
Definition of sepsis:
systemic inflammatory response syndrome (SIRS) due to infection, proven or highly suspected
32
SIRS Criteria (4):
1. Fever (>38 C [100.4F]) or hypothermia (90/minute)
| 3. Tachypnea (RR >20/minute) or hyperventilation (arterial pCO2 12,000/cu mm) or leukopenia (WBC 10% bands)
33
Severe sepsis includes:
acute organ dysfunction (aka malfunction such that a person cannot maintain homeostasis without intervention)
34
Refractory arterial hypotension that only adequately responds to fluid replacement
septic shock
35
Oliguria
low urine output
36
If blood pressure normalizes when fluids are given, it suggests that shock is:
hypovolemic
37
T/F: Severe sepsis is a subset of septic shock
F: Septic shock is a subset of severe sepsis
38
Most people with sepsis have _____ blood cultures
Negative
39
T/F: Altered mental status is a sepsis/SIRS symptom
T
40
In sepsis/SIRS: CRP is (elevated/decreased)
Elevated (>2 standard deviations)
41
In sepsis/SIRS: procalcitonin is (elevated/decreased)
Elevated (>2 standard deviations)
42
Less than what oxygen saturation % constitutes SIRS?
<70%
43
In sepsis/SIRS: creatinine is (elevated/decreased)
elevated
44
In sepsis/SIRS: PTT is (elevated/decreased)
Elevated (>60 seconds)
45
In sepsis/SIRS: thromobocytopenia is (elevated/decreased)
Decreases (<100,000)
46
In sepsis/SIRS: bilirubin is (elevated/decreased)
Elevated (>4)
47
In sepsis/SIRS: Fever is defined as
>38.3 degrees
48
What are two SIRS symptoms you would quickly notice after inspecting a patients arms/legs?
Mottling and "significant" edema
49
In sepsis/SIRS: heart rate is (elevated/decreased)
Elevated (>2 standard deviations)
50
Microbial cell wall and internal elements (lipoproteins and LPS, fungal wall components, nucleic acids)
pathogen-associated molecular patterns (PAMPs)
51
What receptors bind PAMPs (3)?
Toll-like, NOD1/2, GPCR
52
What type of receptors react with intercellular pathogens?
NOD
53
What types of receptors are located on macrophages, neutrophils and endothelial cells?
Toll like reeptors
54
Binding of PAMPs activates inflammatory cells, which produce: (8)
TNF, IL-1, IL-6, IL-8, IL-12, IL-18, IFN-G, HMGB1
55
How do cytokines direct leukocytes to the site of infection?
Upregulation of the expression of endothelial cell adhesion molecules which bind leukocytes
56
State of systemic (total body) hypoperfusion + cardiovascular collapse
Shock
57
What type of cell membrane enzyme produces PAF in response to SEPSIS?
phospholipase A2
58
What types of cells produce PAF?
platelets, endothelial cells, neutrophils, monocytes
59
What does PAF do?
vasodilation, increased vascular permeability, activates/promotes platelet aggregation, promotes leukocyte migration/degranulation
60
How do microbes activate the fibrinolytic system?
Plasmin
61
What do CD4 cells secrete in response to antigen and costimulation?
IFN-Gamma
62
What so APC secrete to sustain the expression of costimulatory molecules?
IL12
63
What APC costimulation molecule binds to CD28?
CD80
64
Why was TGN1412 so toxic to the volunteers?
anti-CD28
65
What occurs in response to IL-1 and IL-8?
mast cells in the connective tissue adjacent to blood vessels to release large quantities of histamine from granules in their cytoplasm
66
Histamine causes...
dilation of arterioles and increased permeability of venule
67
What types of cells synthesized prostaglandin?
Activated macrophages, neutrophils, endothelial cells and mast cells
68
PGD2, PGE1 and PGE2 cause
vasodilation
69
PGD2 and PGE2 cause
increased vascular permeability
70
How do activated endothelial cells and activated macrophages/neutrophils use NO differently?
activated endothelial cells: potent vasodilator
| Activated macrophages and neutrophils: kills microbes by combining with reactive oxygen species
71
Extracellular ROS (in small amounts) can increase expression of:
IL8 and endothelial cell leukocyte adhesion molecules
72
Extracellular ROS (in large amounts) will:
Damage endothelial cells, which increases vascular permeability and allows fluid to leak out into the tissues--this deceases blood volume
73
T/F: Sepsis leads to shock by a phenomenal number of redundant pathways
T
74
2 ways in which NO contributes to sepsis
Vasodilation, decreased blood volume (due to increased vascular permeability from endothelial cell damage)
75
Activated Hageman factor initiates what 4 systems?
Clotting, fibrinolytic, complement, kinin
76
Activated factor X causes:
Increased vascular permeability and leukocyte emigration from blood vessels
77
Fibrinopeptides are generated by ______ and function in (2):
Thrombin
| Increase vascular permeability, leukocytes chemotaxis
78
How does thrombin affect the complement cascade?
Cleaves C5 to release C5a (links clotting and the complement cascade)
79
A decrease in these indirectly promotes clotting in sepsis by decreasing fibrinolysis: (3)
tissue factor pathway inhibitor, thrombomodulin and protein C
80
An increase in these promotes clotting in sepsis: (3)
tissue factor, plasminogen activator inhibitor-1 (inhibits fibrinolysis)
81
Sepsis-related clotting seen in 50% of patients with sepsis
disseminated intravascular coagulation
82
Major function of IL10:
Down-regulate the responses of activated macrophages ("calm them down")
83
Counter-regulate the pro-inflammatory effects of complement activation: (3)
C1 inhibitor, factor H (limits convertase formation) and decay-accelerating factor
(limits of convertase formation)
84
How do lipoxins counter inflammation?
inhibit neutrophil adhesion to endothelial cells and chemotaxis
85
Blocks TNF
Soluble tumor necrosis factor receptor (sTNFR)
86
Mixed antagonistic response syndrome (MARS):
Alternation of pro-inflammatory response syndrome and a compensatory anti-inflammatory response syndrome
87
What are 3 counter-regulatory mechanisms causing immunosuppression?
- apoptosis of CD4 and CD8 lymphocytes
- apoptosis of gastro-intestinal epithelial cells
- expression of ligands for inhibitory receptors on lung epithelial cells
88
What results from CARS immunosuppression?
opportunistic infections, reactivation of latent infections and GI hemorrhage
89
To treat autoimmune disease, Infliximab (Remicade), etanercept (Enbrel) and adalimumab (Humira) block:
TNF-alpha
90
To treat autoimmune disease, Tocilizumab blocks
IL6 receptors
91
Why do burns, acute pancreatitis and multi-organ ischemic necrosis cause SIRS?
tissue death
92
Tissue death (necrosis) elicits an:
inflammatory response
93
Extensive necrosis elicits a:
SYSTEMIC inflammatory response
94
Superantigens
Molecules that promote T cell mitosis in a nonspecific way, bypassing antigen receptor specificity
95
Toxin that can bind to any TCR with a V-beta 2 segment (activates 5-20% of T cells instead of the 0.001%)
toxic shock syndrome toxin-1 (TSST-1)
| "covers 1/2 of the flanking MHC alpha-helices of HLA-DR1"
96
What is a toxic shock storm?
An abnormally large number of T cells are activated by TSST1; these release mass quantities of cytokines, such as IL-1 and TNF (cytokine storm)
97
Nonspecific immunologic over-reaction to a bacteria-secreted exotoxin
Toxic Shock Syndrome
98
What bacteria are most associated with Toxic Shock Syndrome?
staphylococci or streptococci
99
Toxic Shock Syndrome
Nonspecific immunologic over-reaction to a bacteria-secreted exotoxin
100
T/F: Menstrual toxic shock syndrome is an infection caused by Staph aureus.
F: colonization by the bacteria; When Staph aureus overgrows in a tampon, numerous T cells are exposed to the exotoxin (eliciting the reaction)
101
Almost all menstrual cases (and 50% of nonmenstrual cases) of toxic shock syndrome are associated with:
TSST-1
102
T/F: TSS can be caused by a group A strep infection of the skin or pharynx, with strains of Strep pyogenes producing streptococcal pyrogenic exotoxin A and acting as a superantigen.
T (sorry, didn't know how else to include this)
103
What influences the likelihood of a patient experiencing a cytokine storm?
Their genetics (90% TSS occurs in whites)
104
What makes sepsis or SIRS "severe"?
Acute organ dysfunction
105
What causes skeletal muscle dysfunction in severe SIRS/sepsis?
Anaerobic metabolism and lactic acid build up
106
Stages of pathophysiological stock: (3)
1) nonprogressive, with compensation
2) progressive, with manifestations of decompensating organ function
3) irreversible, with resultant death even if the cause of shock is reversed
107
Compensatory mechanisms for shock:
| How does the brainstem respond to the blood loss signaled by baroreceptors?
Decreases the level of inhibition of arteriolar vasoconstriction
108
Compensatory mechanisms for shock:
| Why do the sympathetic nervous system and neuroendocrine response increase heart rate?
Since there is less blood to carry oxygen and other nutrients, it needs to be pumped faster
109
Molecular mediators of the neuroendocrine response to shock: (4)
1. epi (adrenal medulla)
2. norepinephrine (adrenal medulla)
3. vasopressin or ADH (pituitary)
4. renin (kidneys)
110
How does the fluid shift response to hypovolemic shock restore volume?
moves water from the extravascular compartment into the blood (it's dilute, but at least it's there)
111
Compensatory mechanisms for shock:
| How do the kidneys respond to hypovolemia?
Stop making urine
112
Compensatory mechanisms for shock:
| How does blood perfusion change as shock worsens?
Body shuts down perfusion of less vital organs: toes -> feet -> legs -> pelvic organs -> organs below diaphragm -> arms -> heart/brain
113
Why does shock induce lactic acidosis?
cells deprived of adequate oxygen resort to anaerobic metabolism, generating lactic acid
114
What blood level provides a measure of the degree of tissue hypoxia?
Lactate
115
Biomarkers of the irreversible stage of shock:
TNF-alpha
IL-1
IL-6
116
T/F: Shock is irreversible only when the patient is dead.
F: Shock has a point of no return after which nothing will save a patient’s life
117
Cerebral pathology of shock:
necrosis with red (dead) neurons and cerebral edema
118
Neurons begin dying ___ minutes after their blood supply stops.
4
119
Dead neurons with condensed (hypereosinophilic) cytoplasm contains denatured, closely-packed proteins.
Red neurons (occurs after 12 hours)
120
Pyknosis
Nuclei shrinking and condensation (hyperbasophilic)
121
Why do resuscitated patients often regain all organ function but not brain function ("anoxic encephalopathy")?
neurons are the cells most rapidly killed by ischemia (by a wide margin) and they do not regenerate
122
What is a possible result of shutting off perfusion of the bowel (a compensatory mechanism)?
hypovolemic shock can convert into septic shock
123
Describe the process of bowel ischemia. (4)
1. Bile enters through the leaky, ischemic bowel
2. Stool sticks to the walls (probably due to some of the proteins that leaked in)
3. As ischemia worsens, blood leaks into the mucosa and then deeper layers
4. Intestina mucosa breaks down, and the bacteria from the lumen can invade
124
What does the serosal surface of ischemic bowel look like?
"Dusky", dark red
125
The only way to cure septic shock from ischemic bowel:
Resection (removal of the ischemic portion)
126
A particularly common site of ischemic bowel
cecum
127
When resuscitating a patient, refractory lactic acidosis should tell you to go looking for...
Dusky bowel
128
Gross pathology of AKI: (3 characteristics)
1. swollen
2. pale cortex
3. congested medulla
129
T/F: Acute kidney injury is always irreversible.
F: reversible
130
Rhabdomyolysis
skeletal muscle breakdown
131
In AKI, where may leukocytes be found?
vasa recta--the small straight blood vessels of the renal medulla
132
What portion of the kidney is the most affected by AKI?
Tubules
133
Manifestation of AKI: (3)
1. Attenuation/loss of proximal tubule epithelial cell brush borders
2. Epithelial cell swelling and vacuolization
3. Epithelial cell necrosis and sloughing into the tubular lumen
134
Two causes of tubular obstruction:
1. Myoglobin resulting from shock-induced rhabdomyolysis
2. Eosinophilic hyaline material (mostly Tamm-Horsfall protein, a urinary glycoprotein normally secreted by parts of the tubules)
135
Pathologic manifestations of shock in the adrenal glands:
| What causes cortical lipid depletion?
Shock stimulates the synthesis of cortisol, aldosterone and other steroid hormones
136
Pathologic manifestations of shock in the adrenal glands:
| What typically follows adrenal cell necrosis?
hemorrhage
137
Waterhouse-Friderichsen syndrome
Septic shock due to Neisseria meningitidis infection in kids; can lead to adrenal hemorrhage and necrosis, which eliminates the adrenal contribution to counteracting shock
138
Nutmeg liver looks like...
Tissue with alternating red and brown (or tan or yellow or green)
139
The grossly colored regions in nutmeg liver reflect:
Hemorrhagic necrosis and steatosis
140
Why is there coagulative necrosis of hepatocytes in the center of hepatic lobules?
Both the oxygen-rich arterial blood and nutrient-rich portal venous blood diffuse through the lobules, starting from the portal tracts around the periphery;
The venous blood headed for the kidneys (with oxygen and nutrients extracted and toxic metabolites added) starts at the lobular central veins
141
T/F: The peripherally located hepatocytes are more likely to become ischemic.
F: "The vulnerability of hepatocytes to ischemia is directly proportional to their proximity to the hepatic lobular central veins"
142
Shock lung is typically:
enlarged and firm
143
In ALI, the earliest finding is:
increased numbers of neutrophils in the capillaries, in the septa between alveoli
144
Half an hour after the lung insult, what do pulmonary alveolar macrophages produce?
Increased amounts of IL8 (strong neutrophil chemotactic and activating agent)
145
What results from the increase of proinflammatory cytokines in the lungs?
1. Activation of endothelial cells (leads to sequestration of neutrophils in small pulmonary blood vessels)
2. Up-regulation of adhesion molecules on neutrophils
3. Water and plasma proteins (vascular) leak into the interstitium and airspaces
146
What causes damage the alveolar epithelial cells, and what is the result?
Oxidants, proteases, PAF and leukotrienes from activated neutrophils; increase the permeability of the barrier between the airspaces and bloodstream
147
In severe injury, what leaks into alveoli?
Whole blood
148
Where does fluid collect in less severe ALI?
Alveolar edema fluid condenses into eosinophilic hyaline membranes lining the airspaces
149
What causes ALI-related hypoxemia?
alveolar edema and hyaline membranes block the diffusion of oxygen
150
In ALI, this will be seen in a chest XR:
pulmonary infiltrates
151
Bilateral pulmonary infiltrates and severe hypoxemia (no evidence of cardiogenic pulmonary edema)
acute respiratory distress syndrome (ARDS)
152
Subendocardial myocytes begin dying as early as _____ after their blood supply has been cut off.
20 minutes
153
What causes hypercontraction of sarcomeres in reperfused cardiac cells?
Influx of calcium brought in by reperfusion; since they do not have an energy source, they are unable to relax
154
If a person in shock has a subendocardial MI but is successfully resuscitated, where will the "circumferential infarct" be?
anterior left ventricle (L anterior desc coronary artery)
lateral left ventricle (left circumflex coronary artery)
posterior left ventricle (right coronary artery)
155
Why will hemorrhage occur in the heart after resuscitation?
blood vessels have broken-down
156
Coagulation necrosis of the myocytes produces ______ cytoplasm.
Hypereosinophilic
157
Contraction band necrosis features transverse bands of dense eosinophilic _______ ________ separated by relatively cleared spaces of cytoplasm.
contracted sarcomeres
158
Hypovolemic shock, combined with an MI, "adds an element of":
Cardiogenic shock
159
T/F: If a patient has low urine output, order a diuretic.
F: Go look at the patient first, so you don't kill him/her in the same way Dr. Nichols tried to kill those dogs.
160
ALI
acute non-cardiogenic pulmonary edema and alveolar hyaline membranes
161
ARDS
acute non-cardiogenic bilateral lung infiltrates and severe hypoxemia
162
ATN
AKI severe enough to cause (reversible) necrosis of renal tubules
163
ALI
acute non-cardiogenic pulmonary edema and alveolar hyaline membranes
164
ARDS
acute non-cardiogenic bilateral lung infiltrates and severe hypoxemia
165
ATN
AKI severe enough to cause (reversible) necrosis of renal tubules
