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CardioPulm > 12.6 A > Flashcards

12.6 A Flashcards

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?

A

distributive

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
Q

What is a paradoxical pulse?

A

a greater than normal decline in systolic arterial pressure during inspiration

26
Q

Why does someone experiencing cardiac tamponade experience a paradoxical pulse?

A
  • 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
Q

What is the major change seen on an EKG in someone with cardiac tamponade?

A

the magnitude of the electrical events would be reduced

28
Q

Beta-1 receptors have what cardiovascular effects?

A

increase heart rate and inotropic state

29
Q

Alpha-1 receptors have what cardiovascular effects?

A

they vasoconstrict systemic arteries (except in skeletal muscle)

30
Q

Beta-2 receptors have what cardiovascular effects?

A

they vasodilate arteries in skeletal muscle and in the lungs

31
Q

If reduced CO is the cause of shock, the baroreflex will work to increase what?

A

TPR

32
Q

If reduced TPR is the cause of shock, the baroreflex will mainly work by trying to increase what?

A

CO

33
Q

What is the most significant secondary complication of cardiogenic shock?

A

pulmonary edema

34
Q

What is the most significant secondary complication of hypovolemic shock?

A

the increase in vascular permeability

35
Q

What is the most significant secondary complication of distributive shock?

A

the increase in vascular permeability

36
Q

Why is distributive shock life threatening?

A
  • 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
Q

How does microcirculation change to compensate for shock?

A

with hypotension there is less filtration and more resorption than normal so there is a net increase in plasma volume

38
Q

What happens to hematocrit during shock?

A

with increased resorption and decreased filtration in the capillaries, RBC concentration falls

39
Q

How is hypovolemic shock best treated?

A

with volume resuscitation

40
Q

How is cardiogenic shock best treated?

A

with treatment of the underlying condition (e.g. removal of blood from the pericardial sac)

41
Q

How is distributive shock best treated?

A

with alpha-1 agonists and antihistamines for anaphylaxis or with antibiotics and fluid for sepsis

42
Q

Why can’t we give L-NAME to treat distributive shock?

A

because it will block iNOS and NO synthase, leading to massive leukocyte adhesion and microvascular injury

43
Q

What changes occur to induce the transition to irreversible shock?

A
  • 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
Q

What is myocardial depressant factor?

A

a toxic factor released by injured cells during shock which reduce cardiac contractility

45
Q

Why is a blood transfusion often harmful in the case of prolonged hemorrhagic shock?

A

because it is like a reperfusion injury and factors are produced that increase vascular permeability

CardioPulm (31 decks)

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