12.6 A Flashcards

(45 cards)

1
Q

What are the three types of shock?

A

hypovolemic, cardiogenic, and distributive

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2
Q

What are some conditions that cause hypovolemic shock?

A
  • hemorrhage
  • dehydration
  • burns
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3
Q

What are some conditions that cause distributive shock?

A
  • sepsis

- anaphylaxis

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4
Q

What are some conditions that cause cardiogenic shock?

A
  • cardiac tamponade
  • heart failure
  • myocardial infarction
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5
Q

Hypovolemic shock is a problem with _____ while distributive shock is a problem with _____ and cardiogenic shock is an issue with _____.

A
  • blood volume
  • arterioles
  • pump
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6
Q

What is the inciting event for distributive shock?

A

generalized systemic vasodilation

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7
Q

Central venous pressure is high in what kind of shock?

A

cardiogenic

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8
Q

Central venous pressure is low in what kind of shock?

A

hypovolemic

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9
Q

Which type of shock is characterized by warm skin?

A

distributive

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10
Q

How can you distinguish hypovolemic shock due to hemorrhage from that due to dehydration?

A

in hemorrhagic shock, plasma osmolality will be nearly normal, it won’t be in dehydration shock

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11
Q

Why is someone’s pulse typically weak or thready when experiencing hypovolemic shock?

A

because stroke volume is reduced and stroke volume is directly proportional to pulse pressure

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12
Q

Arterial pressure doesn’t significantly drop until CO drops by how much?

A

roughly 20%

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13
Q

Describe the changes seen on a Starling curve beginning at the onset of hypovolemic shock.

A
  • first EDV will decrease along the curve

- then baroreflex will kick in and increase inotropic state, shifting the curve upward a little

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14
Q

Why does sympathetic firing not increase EDV despite triggering venoconstriction and thus increases venous return?

A

because it also increases heart rate, decreasing filling time

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15
Q

Describe the steps that put one in a state of distributive shock.

A
  • systemic release of inflammatory mediators
  • increased iNOS expression by endothelial cells
  • excessive NO production
  • generalized arteriolar vasodilation
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16
Q

What happens to arterial diastolic pressure in those with distributive shock?

A

it decreases because vasodilation allows for increased runoff into the venous system

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17
Q

Why do vasoconstrictors not effectively treat distributive shock?

A

because there is so much NO that the vascular smooth muscle does not contract normally

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18
Q

How can leukocyte adherence occur during septic shock with so much NO in the circulation?

A

because NO is a single anti-adherence molecule and the overall balance is still towards an inflammatory response and leukocyte adherence

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19
Q

Neurogenic shock is what type of shock?

20
Q

What are some possible causes of neurogenic shock?

A
  • deep anesthesia
  • pain reflex from deep trauma
  • vasovagal syncope
21
Q

How does neurogenic shock occur?

A

one of the triggers like deep anesthesia results in decreased sympathetic activity and thus arteries are allowed to vasodilate

22
Q

CO is decreased in what types of shock?

A
  • hypovolemic

- cardiogenic

23
Q

How does cardiac tamponade result in cardiogenic shock?

A

the fluid accumulation in the pericardial sac impairs heart filling, decreasing stroke volume, decreasing cardiac output, decreasing MAP

24
Q

What happens to the passive filling curve (ventricular pressure v. ventricular volume) in someone experiencing cardiac tamponade-related cardiogenic shock?

A

the curve is shifted upward given that less volume is needed to increase the pressure within the ventricle since it is having a hard time relaxing

25
What is a paradoxical pulse?
a greater than normal decline in systolic arterial pressure during inspiration
26
Why does someone experiencing cardiac tamponade experience a paradoxical pulse?
- upon inspiration, the right ventricle fills more than it otherwise would - this causes the interventricular septum to bulge into the left ventricle - this limits filling even more than would be expected, reducing stroke volume and systolic arterial pressure
27
What is the major change seen on an EKG in someone with cardiac tamponade?
the magnitude of the electrical events would be reduced
28
Beta-1 receptors have what cardiovascular effects?
increase heart rate and inotropic state
29
Alpha-1 receptors have what cardiovascular effects?
they vasoconstrict systemic arteries (except in skeletal muscle)
30
Beta-2 receptors have what cardiovascular effects?
they vasodilate arteries in skeletal muscle and in the lungs
31
If reduced CO is the cause of shock, the baroreflex will work to increase what?
TPR
32
If reduced TPR is the cause of shock, the baroreflex will mainly work by trying to increase what?
CO
33
What is the most significant secondary complication of cardiogenic shock?
pulmonary edema
34
What is the most significant secondary complication of hypovolemic shock?
the increase in vascular permeability
35
What is the most significant secondary complication of distributive shock?
the increase in vascular permeability
36
Why is distributive shock life threatening?
- because although some organs are now getting higher than normal blood flow, others are getting less and there is no distributive regulation - one of these is the heart which is also working harder during shock to maintain CO
37
How does microcirculation change to compensate for shock?
with hypotension there is less filtration and more resorption than normal so there is a net increase in plasma volume
38
What happens to hematocrit during shock?
with increased resorption and decreased filtration in the capillaries, RBC concentration falls
39
How is hypovolemic shock best treated?
with volume resuscitation
40
How is cardiogenic shock best treated?
with treatment of the underlying condition (e.g. removal of blood from the pericardial sac)
41
How is distributive shock best treated?
with alpha-1 agonists and antihistamines for anaphylaxis or with antibiotics and fluid for sepsis
42
Why can't we give L-NAME to treat distributive shock?
because it will block iNOS and NO synthase, leading to massive leukocyte adhesion and microvascular injury
43
What changes occur to induce the transition to irreversible shock?
- impaired organ blood flow leads to cell injury and therefore the release of toxic factors which impair heart contractility - local accumulation of vasodilator metabolites increase lactic acid production, impairing cell function - the vasodilator metabolites overcome the sympathetic NS response, leading to widespread vasodilation
44
What is myocardial depressant factor?
a toxic factor released by injured cells during shock which reduce cardiac contractility
45
Why is a blood transfusion often harmful in the case of prolonged hemorrhagic shock?
because it is like a reperfusion injury and factors are produced that increase vascular permeability