Hemodynamics II Flashcards
(142 cards)
1
Q
Shock:
A
state of systemic (total body) hypoperfusion, cardiovascular collapse
2
Q
Severe sepsis:
A
sepsis with acute organ dysfunction
3
Q
Septic shock:
A
severe sepsis with refractory arterial hypotension
4
Q
AKI :
A
acute (reversible) renal injury due to hypoperfusion or hypoxemia
5
Q
ATN :
A
AKI severe enough to cause (reversible) necrosis of renal tubules
6
Q
ALI :
A
acute non-cardiogenic pulmonary edema and alveolar hyaline membranes
7
Q
ARDS:
A
acute non-cardiogenic bilateral lung infiltrates and severe hypoxemia
8
Q
What are the 3 most common causes of shock?
A
(1) decreased circulating blood volume,
(2) decreased cardiac output
(3) sepsis
9
Q
Other than the 3 most common causes of shock, what else can cause it?
A
anaphylaxis,
systemic inflammatory response syndrome (SIRS)
neurogenic causes.
10
Q
What are the most common types of shock?>
A
- hypovolemic shock
- cardiogenic shock
- septic shock
11
Q
What can cause hypovolemic shock?
A
bleeding or fluid loss from vomiting, diarrhea, extensive burns
12
Q
What can cause cardiogenic shock?
A
MI
cardiac arrhythmia messing up signaling mechanism for adequate pump,
pulmondary embolism obstructing output of the right heart
cardiac tamponade=> hemopericardium squeezing cardiac filling chambers, obstructing filling
13
Q
Septic shock is generally mixed with anaphylaxis to be termed distributive shock. What is a feature of this type?
A
all feature widespread vasodilation
maldistributes the available blood volume diffusely throughout the body in too many places, returning too little to the heart and lungs to oxygenate and pump it to where it is needed.
14
Q
A patient who suffered a MI and also a ruptured gastric ulcer will have what type of shock?
A
cardiogenic
hypovolemic
15
Q
How is shock measured?
A
it cannot be measured with a value. It depends on numerous amounts of signs and symptoms to total body hypoperfusion
it affects the patient as a whole person
16
Q
What is one of the earliest symptoms of shock?
A
agitation
17
Q
The clinical manifestations of shock include what?
A
- decreasing mental status,
- progressing from confusion to lethargy,
- delirium (sometimes)
- coma
18
Q
Patients in hypovolemic or cardiogenic shock have what type of heart rate? skin?
A
a weak rapid (“thready”) pulse
cool, clammy, sometimes cyanotic skin.
19
Q
Patients in septic shock have what type of skin?
A
warm flushed skin
20
Q
The importance of differentiating septic shock from other forms of shock is what?
A
every hour of delay in starting effective antibiotic therapy for septic shock was associated with a 7.6% increase in mortality for each of the six hours after the first hour.
21
Q
Patients in all forms of shock have what sign?
A
decreasing urine output.
22
Q
T/F vital signs are a good indicator of shock
A
false, they are usually late responders and considerable injury to cells and tissues have occurred
23
Q
Who should be examined closer, the young trauma patient or the old postoperative patient? why?
A
young trauma patient because of seemingly normal vital signs and physiologic functioning until limits are reached beyond ability to compensate causing a sudden crash that can be irretrievable
24
Q
How should you treat hemorrhagic hypovolemic shock? septic shock? cardiogenic shock?
A
Hemorrhagic shock needs treatment with blood transfusion.
Septic shock needs treatment with antibiotic therapy.
Cardiogenic shock needs treatment that assists the heart.
25
Cardiogenic shock usually results from what?
the failure of the heart as a pump due to intrinsic heart disease,
bleeding into the pericardial sac can prevent the heart from filling, with resultant shock
26
What is cardiac tamponade?
distant heart sounds
jugular venous distention
bleeding into pericardial sac can prevent heart from filling
27
Cardiac tamponade due to hemoperidcardium needs urgent treatment. How should you treat?
remove blood from pericardial sac
28
A large pulmonary thromboembolus can obstruct pulmonary trunk. How would this cause shock?
preventing outflow from the right heart
29
Septic shock is due to what?
vasodilatation increasing the capacitance of the vascular system
this is done so much that the amount of blood pooled in the periphery leaves too little returning to the heart for adequate perfusion of the body as a whole.
30
What form of shock is neurogenic shock? What causes neurogenic shock?
vasogenic shock
vasodilatation due to spinal cord injury or spinal anesthesia causing acute loss of sympathetic nervous system maintenance of a normal level of vasoconstriction.
31
What type of shock would you expect a trauma patient with a long bone fracture to have? why?
hemorrhagic and septic shock
due to increased production of proinflammatory cytokines such as TNF, IL-1 and IL-6
32
T/F hypovolemic shock is most common of 3 types in surgery and trauma patients
true
33
Other than hemorrhagic shock, what else can cause hypovolemic shock?
**fluid loss (dehydration)** caused by severe diarrhea or extensive burns
**severe bleeding** (especially retroperitoneum, abdominal cavity, chest or intestines)
34
What % of blood volume is the threshold for shock? name specifically
25% for an older person,
30% for a young one
35
At what point does blood loss cause life threatening shock?
35-45% of person's blood volume
36
What is the common dividing line between lethal and non-lethal hemrrhage?
50% of one's blood volume
37
What is the ultimate factor when dealing with blood loss?
time
a 50% decrease over time has a better chance of living than one that is quickly lossed
38
What is sepsis?
patient-as-a-whole syndrome of response to infection
39
SIRS must meet 2 of the 4 criteria. Name all 4
1. **Fever** (temperature over 38 degrees C [100.4 degrees F]) or **hypothermia** (temperature less than 36 degrees [96.8 degrees F])
2. **Elevated heart rate** (over 90/minute)
3. **Tachypnea** (respiratory rate over 20/minute)
or **hyperventilation** (arterial pCO2 [partial pressure of dissolved CO2 in the blood] less than 32 mm Hg)
4. **Leukocytosis** (white blood cell count over 12,000/cu mm) or **leukopenia** (white blood cell count less than 4,000/cu mm) or **bandemia** (over 10% bands).
40
What are the 2 critical subsets of sepsis?
severe sepsis
septic shock
41
What is severe sepsis?
sepsis with acute organ dysfunction
42
What is septic shock wrt sepsis?
sepsis with refractory arterial hypotension
43
acute organ dysfunction qualifying a patient for the category of severe sepsis is what?
malfunction such that a person cannot maintain homeostasis without intervention.
44
What are examples of severe sepsis?
acute alteration in mental status
oliguria (low urine output)
lactic acidosis
45
What is the definition septic shock?
sepsis-induced hypotension with systolic BP less than 90 mm Hg or \>40 mm Hg lower than baseline,
refractory to adequate fluid resuscitation,
together with acute organ dysfunction.
46
If you are able to normalize a patients blood pressure with fluid resuscitation. What type of shock do you expect?
hypovolemic shock
47
FACT: Septic shock is a subset of severe sepsis and severe sepsis is a subset of sepsis.
48
SIRS was altered wrt to many ways. name them (haha)
* HR\>2 SDs above normal value for age
* significant edema
* positive fluid balance \>20mL/kg over 24hrs
* hyperglycemia in absence of diabetes
* CRP \>2SDs above normal
* procalcitonin \>2 SDs above normal
* mixed venous O2 saturation \<70%
* cardiac index \> 3.5
* arterial hypoxemia
* acute oliguria
* creatinine increase \>0.5mg/dL
* INR \>1.5
* partial thromboplastin time \>60secs
* ileus, thrombocytopenia (\<100,000/cu mm)
* bilirubin\>4mg/dL
* lactate \>1mmol/L
* decreased capillary refeal
* cutaneous mottling
* 38.3 C
49
Describe the molecular mechanisms of sepsis and septic shock
1. PAMPS =\> TLRs on macs, neutro, ECs or GCPR or NODs bind pamps
2. Binding activates inflamm cells=\> produce TNF, IL-1, IL-6, IL-8, IL-12, IL-18, IFN-y, HMGB1
3. cytokines upregulate expression of EC adhesion moleucles that bind leukocytes to direct to infection
50
What does sepsis cause in the cell membranes of platelets, ECs, neutrophils, monocytes? what will this do?
phospholipase A2
generate platelet activating factor (acetyl glycerol ether phosphocholine)
51
T/F PAF is more potent than histamine. explain
true
* induces vasodilation and increased vascular permeability
* activates platelets and promotes aggregation
52
Other than inducing vasodilation and increasing vascular permeability, what else does PAF do?
promote leukocyte adhesion to ECs
chemotaxis
degranulation and oxidative burst that allows killing in leukocytes
53
Microbial components activate the complement cascade. How?
both directly and indirectly through the activity of plasmin from the fibrinolytic system.
54
Activation of the complement cascade yields C3a and C5a. What do these do?
increase vascular permeability and cause vasodilation by inducing mast cells to release histamine.
55
antigen presenting cells present microbial antigens to what cells?
T lymphocytes
56
If these microbial antigens are presented in conjunction with CD3 on the T cell surface and with costimulatory molecules, what is the result?
CD4-positive effector T-cells secrete interferon-gamma that activates phagocytic cells to kill intracellular bacteria,
upregulate their own expression of CD40 ligand,
binds to CD40 on the antigen presenting cells,
releases IL-12
sustains the expression of costimulatory molecules.
57
The costimulatory molecule CD80 binds to CD28 that results in what?
T cell activation and proliferation.
58
What will the cytokines IL-1 and IL-8 cause mast cells to do?
degranulate
mast cells in the connective tissue adjacent to blood vessels to release large quantities of histamine from granules in their cytoplasm.
59
What all can histamine be released from? what does histamine cause?
platelets, mast cells
dilation of arterioles and increased permeability of venules.
60
Activated macrophages, neutrophils, endothelial cells and mast cells rapidly convert arachidonic acid in their cell membranes into what? and what do they bind to?
prostaglandins, which are short-lived lipid mediators that bind to G-coupled receptors on many cell types and have a variety of effects.
61
Which prostaglandins cause vasodilation?
PGI2 (also called prostacyclin), but also PGD2, PGE1 and PGE2
62
Which prostaglandins cause an increased vascular permeability?
PGD2 and PGE2
63
PAF is a phospholipid derived mediator. What releases it and what does it do?
activated macrophages, neutrophils, mast cells, endothelial cells and platelets themselves,
increases vascular permeability.
64
activated endothelial cells increase their expression of what molecule? what is the purpose of this?
inducible nitric oxide synthetase and production of nitric oxide (NO).
** potent vasodilator.**
65
Activated macrophages and neutrophils also produce NO. What is the action of NO in this regard?
kills microbes by combining with reactive oxygen species.
66
Extracellular release of small amounts of reactive nitrogen species and reactive oxygen species can increase the expression of what?
IL-8 and other cytokines
endothelial cell leukocyte adhesion molecules.
too much NO or ROS is damaging to ECs
67
If too much NO or ROS is released then ECs are damaged. What is the result?
damage increases vascular permeability.
Increased vascular permeability allows fluid to leak out of the blood into inflamed tissues, decreasing the circulating blood volume.
68
decreased blood volume combined with vasodilatation increasing vascular capacitance causes what?
septic shock
69
What activates blood clotting?
Exposure of clotting factor XII (Hageman factor) to activated platelets, basement membrane or collagen activates it
70
Activated Hageman factor activates what?
1. activates blood clotting,
2. kallikrein and the kinin cascade,
3. via both the clotting and kinin cascades, the fibrinolytic system and the complement cascade.
71
Within the clotting system, activated factor X causes what?
increased vascular permeability
leukocyte emigration from blood vessels.
72
Thrombin, the king of clotting, generates fibrinopeptides that cause what?
increase vascular permeability and are chemotactic for leukocytes.
73
What is the link between the clotting and complement cascades? How?
cleaves complement C5 to release C5a
74
How do activated and injured ECs cause shock?
if activated/injured by sepsis then they promote vasodilation
increase vascular permeability (decrease vascular volume)
promote thrombosis
75
Sepsis causes increased tissue factor. What is its action?
tissue factor promotes clotting.
76
How does sepsis inhibit fibrinolysis?
Sepsis causes increased plasminogen activator inhibitor-1, which indirectly promotes clotting by inhibiting fibrinolysis
decreased tissue factor pathway inhibitor,
decreased thrombomodulin
decreased protein C
77
In up to 50% of patients with sepsis, what is the result wrt clotting?
unlocalized disseminated intravascular coagulation (DIC) in small blood vessels.
lead to bleeding because of the consumption of clotting factors and platelets in so many blood vessels.
78
Lipoxins are generated from arachidonic acid. What is their role?
inhibit neutrophil adhesion to endothelial cells and chemotaxis
79
In the complement system, what do C1 inhibitor (factor H) and DAF (limiter of convertase) serve as?
serve to counter-regulate the pro-inflammatory effects of complement activation
80
How do activated macrophages down regulate responses of other activated macrophages?
secrete IL-10
81
What anti-inflammatory actions of the immune system cause immunosuppression and can lead to opportunistic infections, GI bleeding, and reactivation of latent infections?
poptosis of CD4 and CD8 lymphocytes,
apoptosis of gastro-intestinal epithelial cells
expression of ligands for inhibitory receptors on lung epithelial cells.
82
What is CARS?
compensatory anti-inflammatory response syndrome that is a counter regulatory mechanism of sepsis leading to immuno suppression
83
What is MARS?
patients swing back and forth between pro-inflamm and CARS
84
There are some therapies against cytokines. What blocks TNF-a?
Infliximab (trade name Remicade),
etanercept (trade name Enbrel)
adalimumab (trade name Humira)
85
What does Tocilizumab block?
IL-6 receptors
86
How do targeted therapies against some cytokines help treat sepsis and septic shock?
they are not helpful due to the redundancy of the pathways involved
87
What is a superantigen?
antigen elicits an acquired immune response from multiple clones of lymphocytes
88
What does a superantigen do?
promote T lymphocyte mitosis in a nonspecific way, bypassing antigen receptor specificity.
89
How does toxic shock syndrome toxin-1 work?
covers MHC helices and allows binding to any TCR thus activating 5-20% of T cell clones instead of proceeding with normal antigen processing
the clones create a cytokine storm leading to SIRS resulting in toxic shock syndrome
90
Toxic shock syndrome is due to what?
nonspecific immunologic over-reaction to a secreted bacterial product, an exotoxin, produced by staphylococci or streptococci,
most notoriously when Staphylococcus aureus has overgrown in a superabsorbent tampon and numerous T lymphocytes are exposed to the exotoxin, eliciting the reaction.
91
Describe mentrual toxic shock syndrome
represents a colonization by the bacteria rather than an infection
92
Other than menstral toxic shock syndrome, how else can the syndrome be caused?
group A streptococcal infection of the skin or pharynx with strains of Streptococcus pyogenes producing streptococcal pyrogenic exotoxin A (SPEA) acting as a superantigen.
93
FACT: cytokine storm is associated with immunological over-reactions
94
T/F genetics plays a role in determining which patients will get a cytokine storm
true
95
Multiple organ failure can be from overt shock, what specific types of shock can cause MOF?
hypovolemic
cardiogenic
96
Describe the 3 stages of shock
1) **non-progressive,** with reflex compensatory mechanisms that maintain perfusion of vital organs,
2) **progressive**, with manifestations of decompensating organ function,
3) **irreversible,** with resultant death even if the cause of shock is reversed.
97
The compensatory mechanisms for shock include what 3 things?
sympathetic nervous system responses,
fluid shifts within the body
neuroendocrine stress responses
98
How do tissues with inadequate blood perfusion maintain their BP and perfusion?
constrict their arterioles
99
How does blood loss decrease the level of inhibition of arteriolar vasoconstriction?
Blood loss causes decreased baroreceptor stimulation in large arteries
sends a reflex neural signal to the brainstem
decrease the level of inhibition of arteriolar vasoconstriction.
100
Molecular mediators of the neuroendocrine response to shock include what? name source too
epinephrine and norepinephrine from the adrenal medulla,
vasopressin (also called antidiuretic hormone [ADH]) from the pituitary
renin from the kidneys.
101
Describe the fluid shift response to hypovolemic shock
moves water from the extravascular compartment into the blood, which makes it dilute, but restores the volume
kidney stops making urine.
102
Describe the lactate present In the progressive stage of shock,
it is worse (higher concentration) due to cells deprived of adequate oxygen resort to anaerobic metabolism, generating lactic acid.
103
The level of lactate in the blood provides a measure of what?
measure of the degree of tissue hypoxia
104
gross and microscopic pathologic manifestations of shock include
* cerebral necrosis with red (dead) neurons and cerebral edema,
* hemorrhagic ischemic enteritis,
* renal acute tubular necrosis,
* adrenal cortical lipid depletion and necrosis,
* centrilobular hepatic necrosis,
* pulmonary diffuse alveolar damage
* myocardial necrosis.
105
How long does it take neurons to start dying after losing their blood supply?
Neurons begin dying as soon as **4 minutes** after losing their blood supply.
106
Starting approximately 12 hours after they die, dead neurons develop what?
condensed cytoplasm rendered hypereosinophilic by the denatured, closely packed cytoplasmic proteins.
referred to as "red neurons"
107
Describe what cells undering pyknosis means
the cells shrink and their nuclei become shrunken, condensed, hyperbasophilic
108
What cells are most rapidly killed by ischemia?
neurons
109
What is anoxic encephalopathy?
patients who are resuscitated from shock or cardiac arrest from other causes to have return of all organ functions except those of the brain.
110
T/F The body's compensatory mechanism of shutting off perfusion of the bowel can convert hypovolemic shock into septic shock.
true
111
During septic shock, why does the bowel turn green?
Ischemic bowel mucosa becomes leaky and sticky.
Bile pigment leaks into the intestinal lining, turning it green,
stool sticks to the lining, presumably due to proteins such as fibronectin that have leaked into the bowel lumen.
112
What is the only way to cure septic shock from ischemic bowel?
surgically resect it
113
Why does a septic bowel turn dark red in appearance?
As the ischemia worsens, blood leaks into the mucosa and then deeper layers.
The intestinal mucosa breaks down, allowing bacteria from the lumen to invade.
The serosal surface of such ischemic bowel takes on a dusky (dark red) appearance.
114
T/F acute kidney injury (AKI) is caused by shock and is reversible
true
115
The gross pathology of AKI is what?
swollen kidney with pale cortex and congested medulla.
116
AKI is primarily seen in what part of the kidney? What is it manifested by?
primarily to the tubules
1. attenuation and loss of proximal tubule epithelial cell brush borders,
2. epithelial cell swelling and vacuolization,
3. epithelial cell necrosis and sloughing into the tubular lumen
117
AKI is also associated with leukocytes where?
in the vasa recta (the small straight blood vessels of the renal medulla).
118
The pathologic manifestations of shock in the adrenal glands progress how?
from cortical lipid depletion to necrosis and hemorrhage
119
What does shcok stimulate the adrenal cortical cells to do?
deplete their cholesterol making these stress hormones, which are then secreted into the bloodstream.
120
Wrt the adrenals and progressive shock, what occurs and what accompanies it?
adrenal cells die and this adrenal necrosis is frequently accompanied by hemorrhage.
121
What is the Waterhouse-Friderichsen syndrome?
Septic shock, especially when due to Neisseria meningitidis infection in children, can lead to massive adrenal hemorrhage and necrosis,
obliterating the important adrenal contribution to counteracting shock.
122
Shock liver features a pattern of what?
alternating red and brown (or tan or yellow or green) tissue resembling the cut surface of a nutmeg
123
Grossly visible nutmeg liver usually shows what?
hemorrhagic necrosis spanning multiple lobules alternating with steatotic areas.
124
In mild cases of nutmeg liver, there is coagulative necrosis of hepatocytes in the center of hepatic lobules. Why?
both the oxygen-rich arterial blood and nutrient-rich portal venous blood diffuse through the lobules from the portal tracts around the periphery.
125
Outflow of venous blood with oxygen and nutrients extracted and toxic metabolites added for a trip to the kidney starts where?
at the lobular central veins,
126
vulnerability of hepatocytes to ischemia is directly proportional to what?
their proximity to the hepatic lobular central veins.
127
Shock lung or ALI is characterized by what?
diffuse alveolar damage
128
Grossly, How would shock lung present?
enlarged and a firm, solidified, edematous, congested, beefy red organ.
129
Microscopically, what is the earliest finding of shock lung?
increased numbers of neutrophils in the capillaries in the septa (walls) between alveoli.
130
About how long does it take pulmonary alveolar macrophages to produce IL-8? What wll the result be?
as quickly as 30 minutes
IL-8 is a strong neutrophil chemotactic and activating agent
IL-8 and other pro-inflammatories activate ECs and lead to sequestration of neutrophils in small pulmonary blood vessels
131
Neutrophils activated by IL-8 and TNF do what wrt ECs?
upregulate their expression of adhesion molecules that bind to receptors on activated endothelial cells (ECs)
132
Activated neutrophils release a variety of substances that do what to the lung?
damage the alveolar epithelial cells
increase the permeability of the barrier between the airspaces and the bloodstream
133
With severe injury, breakdown of the alveolar-capillary barrier allows what action?
allows whole blood to leak into the alveoli.
hemorrhage
134
With less severe (more typical) injury, the alveolar edema fluid does what?
condenses into eosinophilic hyaline membranes lining the airspaces.
135
How does alveolar edema and hyaline membrane result in hypoxemia? what is hypoxemia?
pose a block to the diffusion of oxygen
decreased oxygen loading of the blood passing through the lungs
136
How can ALI be viewed on x rays? severe cases?
pulmonary infiltrates
severe=\> complete dense opacification of lungs (white out)
137
What is acute respiratory distress syndrome (ARDS)?
an acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence for **cardiogenic pulmonary edema**.
138
Subendocardial myocytes begin dying as early as how long after blood supply is absent?
20 minutes after their blood supply has been cut off
139
If a person in shock sustains a subendocardial myocardial infarction, but is successfully resuscitated, they tend to have what?
a circumferential infarct involving the anterior left ventricle (left anterior descending coronary artery territory),
lateral left ventricle (left circumflex coronary artery territory)
posterior left ventricle (right coronary artery territory).
140
The resuscitation may be reflected in hemorrhage from reperfusion of the infarct via what 2 things?
broken-down blood vessels
in the contraction band form of necrosis.
141
coagulation necrosis of the myocytes produces what microscopically?
diffusely dense hypereosinophilia of the cytoplasm
142
The hypercontraction of the sarcomeres is thought to be due to what?
influx of calcium brought in by reperfusion, causing the sarcomeres to make one last extreme contraction from which they cannot relax since they have no energy source.
