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Responses To Multisystem Problem > Shock > Flashcards

Shock Flashcards

1
Q

When cardiovascular system fails to perfuse tissues adequately

A

Shock

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2
Q

Initiated by subclinical hypoperfusion

A

Stage I (Initiation)

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3
Q

Sustained reduction in tissue perfusion initiates a set of neural, endocrine, and chemical compensatory mechanisms

A

Stage II (Compensatory Stage)

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4
Q

During this stage, symptoms become apparent but shock may still be reversed.

A

Stage II (Compensatory Stage)

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5
Q

Baroreceptors and chemoreceptors located in the carotid sinus and aortic arch detect the reduction in arterial blood pressure.

A

Neural Compensation

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6
Q

Heart rate and contractility increase to improve cardiac output.

A

Catecholamine Release

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7
Q

To increase perfusion to the myocardium to meet the increased demands for oxygen.

A

Dilation of the coronary artery

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8
Q

Improves blood pressure

A

Arterial vasoconstriction

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9
Q

Augments venous return to the heart, increasing preload and cardiac output.

A

Venous vasoconstriction

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10
Q

Messages relayed to the hypothalamus, which stimulates the anterior and posterior pituitary gland.

A

Endocrine Compensation

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11
Q

Activates the adrenal cortex to release aldosterone.

A

Angiotensin II

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12
Q

Attempt to combat shock by providing the body with glucose for energy and by increasing the intravascular blood volume.

A

Endocrine Compensation

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13
Q

Profound hypoperfusion results with further patient deterioration.

A

Stage III (Progressive Stage)

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14
Q

Reduces the energy available for cellular metabolism.

A

Anaerobic metabolism

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15
Q

Causes failure of the sodium-potassium pump.

A

Lack of ATP

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16
Q

Exerts opposite effect and dilates to increase the blood supply to meet local tissue neds

A

Microcirculation

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17
Q

Attempts to keep vital organs perfused.

A

Constriction of arterioles

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18
Q

Allowing blood to flow into the capillary bed.

A

Postcapillary sphincters

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19
Q

Caused by increased capillary hydrostatic pressure, and pushed fluid from the capillaries into the interstitial space.

A

Interstitial Edema

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20
Q

Prolonged inadequate tissue perfusion that is unresponsive to therapy.

A

Stage IV (Refractory Stage)

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21
Q

Decreases the glomerular filtration rate.

A

Renal vasoconstriction and hypoperfusion

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22
Q

Massive vasodilation, depression of cardiac and respiratory centers, and impaired thermoregulation.

A

Systemic Nervous System Dysfunction

23
Q

Damages the reticuloendothelial cells, which recirculate bacteria and cellular debris, thereby predisposing the patient to bacteremia and sepsis.

A

Hypoperfusion

24
Q

Causes the liver to be unable to detoxify drugs, toxins, and hormones, conjugate bilirubin, or synthesize clotting factors.

A

Damage to hepatocytes.

25
Q

May occur because of the endogenous corticosteroids, exogenous corticosteroids, or insulin resistance.

A

Hyperglycemia

26
Q

Impair blood flow and result in microvascular thrombosis

A

Hypoxia and release of inflammatory cytokines

27
Q

Cause a reduction in heart rate, impaired myocardial contractility

A

Alterations in the CVS

28
Q

Occurs because of the reduction in cerebral blood flow

A

Cerebral Ischemia

29
Q

Pulmonary blood flow is reduced, ventilation-perfusion imbalances occur.

A

Chemical compensation

30
Q

Attempt to combat shock by increasing oxygen supply.

A

Chemical compensation

31
Q

Ineffective pumping of the heart.

A

Cardiogenic shock

32
Q

Insufficient volume of circulating blood.

A

Hypovolemic shock

33
Q

Massive vasodilation of the vascular bed causing maldistribution of blood.

A

Distributive shock

34
Q

Obstruction of blood flow.

A

Obstructive shock

35
Q

Caused by loss of whole blood (hemorrhage), plasma (burns), or interstitial fluid (diaphoresis, DM, DI, emesis, diarrhea, or diuresis) in large amount.

A

Hypovolemic shock

36
Q

Decreased output and evidence of tissue hypoxia in the presence of adequate intravascular volume.

A

Cardiogenic shock

37
Q

Caused by obstruction in the heart or great vessels that either impeded venous return or prevents effective cardiac pumping action.

A

Obstructive shock

38
Q

Result from widespread vasodilation and decreased peripheral resistance.

A

Distributive shock

39
Q

Imbalance between parasympathetic and sympathetic stimulation of vascular smooth muscle.

A

Neurogenic shock

40
Q

Widespread hypersensitivity; Release of large amount of histamine, producing marked vasodilation.

A

Anaphylactic shock

41
Q

Sepsis-induced shock with hypotension requiring vasopressors to maintain blood pressure.

A

Septic shock

42
Q

Features common to all shock states.

A

Hypoperfusion, hypercoagulability, and activation of the inflammatory response.

43
Q

To provide optimal oxygenation.

A

Supplemental oxygen/mechanical ventilation

44
Q

To restore intravascular volume.

A

Fluid replacement

45
Q

To restore vasomotor tone and improve cardiac function.

A

Vasoactive medications

46
Q

To address the metabolism.

A

Nutritional support

47
Q

Given in all types of shock.

A

Fluid replacement (Resuscitation)

48
Q

Best fluid to be given.

A

Fluid that is readily available

49
Q

Contains dextrose and electrolytes dissolved in water.

A

Crystalloids

50
Q

Often selected crystalloid because they contain the same concentration of electrolytes as the extracellular fluid.

A

Isotonic crystalloid solutions

51
Q

Contain substances that should not diffuse through capillary walls.

A

Colloids (Plasma expanders)

52
Q

Given due to hemorrhage; infusion of blood and blood products

A

Blood products

53
Q

To improve the patient’s hemodynamic stability when fluid therapy cannot maintain adequate MAP.

A

Vasoactive medication

54
Q

Recommended positioning for hypovolemic shock

A

Modified Trendelenburg

Responses To Multisystem Problem (1 decks)

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