Hemodynamics II Flashcards

(49 cards)

1
Q

What is shock?

A

Total body hypoperfusion; cardiovascular collapse.

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2
Q

What is severe sepsis?

A

Sepsis with acute organ dysfunction.

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3
Q

What is septic shock?

A

Severe sepsis with refractory arterial hypotension.

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4
Q

What is acute kidney injury (AKI)?

A

Acute, reversible renal injury due to hypoperfusion or hypoxemia.

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5
Q

What is acute tubular necrosis (ATN)?

A

AKI severe enough to cause necrosis of renal tubules.

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6
Q

What is acute lung injury (ALI)?

A

Acute, non-cardiogenic pulmonary edema with damage to alveolar hyaline membranes.

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7
Q

What is acute respiratory distress syndrome (ARDS)?

A

Acute, non-cardiogenic bilateral lung infiltrates and severe hypoxemia.

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8
Q

What are the 3 most common types of shock?

A
  1. Septic
  2. Hypovolemic
  3. Cardiogenic
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9
Q

T or F. Shock is a syndrome, NOT a number.

A

T.

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10
Q

What are the 4 clinical manifestations of shock?

A
  1. Decreasing mental status
  2. Decreasing urine output
  3. Pulse
  4. Skin characteristics
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11
Q

What is the pulse and skin like in a patient in either hypovolemic or cardiogenic shock?

A

Pulse: weak, rapid, thready. Skin: cool, clammy, cyanotic.

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12
Q

What is the skin like in a patient in septic shock?

A

Warm, flushed skin.

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13
Q

T or F. The vital signs are late responders to shock, especially in young people.

A

T.

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14
Q

Why is it important to figure out what type of shock a patient is in?

A

Different types require different treatment.

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15
Q

Shock caused by bleeding is treated how?

A

Blood transfusion and stopping the bleed.

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16
Q

What percentage of a patient’s blood volume is the dividing line between lethal and non-lethal hemorrhage?

A

50%.

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17
Q

T or F. Septic shock is a subset of severe sepsis which is a subset of sepsis.

A

T.

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18
Q

Septic shock is severe sepsis with addition of what?

A

Refractory hypotension.

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19
Q

Is sepsis a positive blood culture?

A

Helllllllllllllllllllllllllllllllllllllllllllllllllll NO!

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20
Q

What stimulates the release of inflammatory mediators that cause vasodilation and leaky blood vessels in septic shock?

A

PAMPs bind TLRs and other receptors on immune cells which activates them stimulating release.

21
Q

What are the 3 initial major cytokines in sepsis and septic shock? Others?

A

TNF, IL-1, and IL-6. IL-8, -12, -18, IFN-gamma, HMGB-1.

22
Q

What other molecules play a role in sepsis and septic shock?

A

PAF, C3a, C5a, PGI2, PGD2, PGE1, PGE2.

23
Q

What clotting factor is activated in sepsis that activates both the kinin and clotting cascades?

A

Factor X11a (Hageman factor).

24
Q

What protein activates the fibrinolytic system?

A

Kallikrein, a product of the kinin cascade.

25
What fibrinolytic protein activates the complement cascade?
Plasmin.
26
Kallikrein also activates what factor resulting in autocatalytic amplification of cascades in sepsis?
Factor XII.
27
How do sepsis, severe sepsis, and septic shock lead to disseminated clotting in small vessels throughout the body?
Since they are pro-coagulant states, many clotting factors are activated.
28
What is Disseminated Intravascular Coagulation (DIC)?
Widespread fibrin thrombi in arterioles, capillaries, and venules.
29
DIC is a complication of what 4 things?
1. Severe infection 2. Advanced malignancies 3. Massive trauma 4. Various obstetric crises
30
Where is DIC the worst?
Brain, heart, lungs, and kidneys.
31
How does DIC sometimes lead to bleeding?
Thrombi consume clotting factors resulting in consumptive coagulopathy.
32
Counter-regulatory mechanisms of sepsis lead to what 2 things?
1. Immunosuppression | 2. Compensatory Anti-inflammatory Response Syndrome (CARS)
33
What 5 things can result in a syndrome that closely resembles sepsis?
1. Extensive burns 2. Extensive trauma 3. Acute pancreatitis 4. Extensive tissue necrosis 5. Toxic shock syndrome
34
What are the 3 stages of shock? Describe each of them.
1. Non-progressive: reflex compensatory mechanisms maintain perfusion of vital organs 2. Progressive: worsening lactic acidosis, etc. 3. Irreversible: death results even if cause of shock is reversed
35
What is the histological manifestation of shock in the brain?
Red dead neurons.
36
When do red neurons become visible histologically? What do they look like?
After 12 hours. Shrunken and hypereosinophilic.
37
In the early phase (first day) of ALI, what is present?
Alveolar edema: bubbly white fluid.
38
In the intermediate phase (first week) of ALI, the edema is condensed into what?
Alveolar hyaline membranes.
39
What is seen histologically in shock heart?
Myocardial coagulation necrosis or contraction band necrosis.
40
What causes contraction band necrosis?
Reperfusion allows calcium in the cell which causes sarcomeres to hypercontract.
41
Histologically, myocytes lack what 2 things after an acute MI?
1. Striations | 2. Nuclei
42
What is the earliest finding of AKI?
Tubular epithelial edema.
43
In later stages of a worse injury to the kidney, what is seen histologically?
Acute tubular necrosis.
44
Can tubular epithelial cells regenerate and be replaced?
Yes.
45
What 3 things are associated with shock liver?
1. Centrilobular necrosis 2. Sinusoids leak blood 3. High ALT and AST levels
46
What 3 things are associated with shock bowel?
1. Hemorrhagic ischemic enteritis 2. Serosa appears dusky 3. High lactate and amylase levels
47
What happens to adrenal glands in shock?
Cortical lipid depletion.
48
If a patient is in septic shock due to meningococcus complicated with DIC, hemorrhage can do what to the adrenal glands? What does this do?
Completely wipe out adrenals. Massively contribute to shock b/c there is no source of epinephrine, cortisol, etc.
49
What is Waterhouse-Friderichsen Syndrome?
When the adrenal glands are wiped out.