Shock

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Last updated 4:24 PM on 10/1/26
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102 Terms

1
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What is shock

A global state of inadequate oxygen delivery and use, causing poor tissue perfusion.

2
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What is MAP influenced by?

Total blood and intravascular fluid volume, CO, size of vascular bed, and blood flow

3
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What 4 circulation problems can cause shock?

too little fluid volume, a failing cardiac pump, a dilated vascular bed, or blocked blood flow

4
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What are the four classes of shock?

Hypovolemic, cardiogenic, distributive, and obstructive.

5
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What happens to cells when perfusion is inadequate?

They receive too little oxygen, switch toward anaerobic metabolism, and produce lactate.

6
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What is preload?

volume of blood in ventricles at end of diastole (volume returning to the heart)

7
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What is contractility?

Hearts contractile strength

8
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What is afterload?

The resistance the ventricle must pump against

9
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What causes hypovolemic shock?

Too little circulating volume returns to the heart, reducing preload

10
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What are causes of absolute fluid loss?

Hemorrhage, vomiting, diarrhea, excessive diuresis, and other direct fluid losses.

11
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What are causes of relative fluid loss?

Fluid or blood shifting out of effective circulation, such as with burns, ascites, bowel obstruction, or internal bleeding.

12
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What may be the earliest vital-sign changes with fluid loss?

Increased HR and RR

13
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Why can blood pressure stay normal early in hypovolemic shock?

Tachycardia and vasoconstriction temporarily compensate for falling stroke volume.

14
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What happens when there is 15% fluid loss?

Patient may tolerate. early increased HR and RR

15
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What happens when there is 15% - 30% fluid loss?

SNS activated, attempt to boost CO, increasing hr, CO, and RR to try to oxygenate

16
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What happens when there is >30% fluid loss?

Compensatory mechanisms may fail; immediate replacement with blood or fluids

17
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What happens when there is >40% fluid loss?

Irreversible tissue destruction

18
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Why is hypotension a concerning finding in hypovolemic shock?

It can mean compensatory mechanisms are failing.

19
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What is the compensatory mechanism when stroke volume decreases?

Increased HR to maintain CO

20
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What is the compensatory mechanism when CO decreased

Increased HR fails, SNS is activated to vasoconstrict, BP remains the same

21
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What is the compensatory mechanism when increased O2 extraction from hgb

attempt to increased available O2

22
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What is the compensatory mechanism when BP and UOP changes

VERY LATE SIGNS after everything doesnt work

23
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What are common skin findings in hypovolemic shock?

Pale, cool, clammy

24
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What hemodynamic pattern is expected in hypovolemic shock?

Low CVP/PCWP, low stroke volume and CO, high SVR.

25
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What is the main treatment goal?

Stop the loss and restore circulating volume

26
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What interventions might be needed?

Large-bore IV access, fluid or blood replacement as indicated, and a procedure or surgery to stop bleeding.

27
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What findings help evaluate response to resuscitation?

Trends in MAP/BP, mentation, pulses, capillary refill, skin, urine output, and lactate.

28
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What are the fluid resuscitation end points?

CVP of 15 or PCWP 10-12

29
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What causes cardiogenic shock?

Ventricular pump failure prevents the heart from moving enough blood forward.

30
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What is the main cause of cardiogenic shock?

A large myocardial infarction that severely impairs ventricular contractility.

31
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What happens with left ventricular failure?

Blood backs up into the lungs, causing findings such as crackles, hypoxemia, and increasing oxygen needs.

32
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What happens with right ventricular failure?

Blood backs up into the venous system, causing findings such as JVD and peripheral edema.

33
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What is another cause of cardiogenic shock other than MI?

Commotio cordis

34
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How can sympathetic compensation worsen cardiogenic shock?

Faster heart rate and vasoconstriction increase the failing heart's workload and oxygen demand.

35
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What hemodynamic pattern is expected in cardiogenic shock?

Low CO, high SVR, HIGH PCWP and CVP (only shock with elevated preload)

36
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What are common assessment findings in cardiogenic shock?

Hypotension, tachycardia, weak pulses, cool clammy skin, low urine output, and possibly chest pain or pulmonary crackles.

37
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What are the main treatment goals of cardiogenic shock?

Restore blood flow to the myocardium, reduce cardiac workload, and improve CO.

38
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What may restore blood flow when an MI is the cause?

Reperfusion therapy

39
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Why might dobutamine be used for with cardiogenic shock?

It increases contractility and can improve cardiac output.

40
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What is nitroglycerin used for in cardiogenic shock?

IV NTG to reduce preload and afterload

41
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Why must fluids be given cautiously in cardiogenic shock?

The failing heart may be unable to move added fluid forward, worsening congestion

42
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What is the core problem in distributive shock?

Massive vasodilation makes the vascular space too large for the circulating volume, reducing SVR and effective perfusion.

43
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What are the three distributive shock types?

Septic, neurogenic, and anaphylactic

44
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Which distributive types also involve increased capillary permeability?

Septic and anaphylactic shock. Fluid leaks out of the blood vessels.

45
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Does fluid volume change with distributive shock?

No, it is normal but the side of the vascular beds increased and capillary permeability increase

46
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What initiates septic shock?

A dysregulated response to infection causes vasodilation, capillary leak, and impaired tissue perfusion

47
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What is the warm phase of septic shock?

Early vasodilation with low SVR, often high CO, warm flushed skin, and possibly bounding pulses.

48
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What is the cold phase of septic shock?

Later worsening perfusion with cooler or mottled skin, weaker pulses, and potentially lower CO.

49
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Why can septic shock cause organ dysfunction even if CO is initially high?

Blood flow is poorly distributed, and oxygen delivery within the microcirculation is impaired

50
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What neurological changes can occur in septic shock?

Agitation, confusion, altered mental status, and eventually decreased responsiveness

51
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What respiratory changes can occur in septic shock?

Early tachypnea; later hypoxemia, respiratory failure, or ARDS

52
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What are the hemodynamic changes in septic shock?

Early: ↓ SVR, ↑ CO. Later: ↑ SVR, ↓ CO. Capillary leak causes ↓ preload.

53
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What are the main treatment priorities for septic shock?

Support perfusion with fluids as appropriate, identify and treat the infection promptly, use vasopressors when needed, and monitor for organ dysfunction.

54
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Why do we obtain cultures for septic shock?

To help identify the infectious organism and guide antimicrobial treatment.

55
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Which vasopressor is first line for septic shock?

Norepiniphrine

56
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When might vasopressin be added in septic shock?

When hypotension persists despite initial treatment.

57
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What does a rising lactate suggest in septic shock?

Worsening tissue hypoperfusion or impaired lactate clearance; interpret it with the whole clinical picture.

58
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What causes neurogenic shock?

Loss of sympathetic vascular tone (something happens to SNS), commonly after a high spinal cord injury, causes activation of PSNS and widespread vasodilation.

59
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What finding makes neurogenic shock stand out from most other shock types?

Bradycardia with hypotension

60
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Why is heart rate low in neurogenic shock?

Sympathetic input is disrupted, leaving parasympathetic effects relatively unopposed.

61
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What skin finding may appear early in neurogenic shock?

Warm, dry skin from vasodilation and altered temperature regulation

62
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What hemodynamic pattern is expected in neurogenic shock?

Low SVR, reduced venous return and preload, and low CO.

63
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What are the treatment goals for neurogenic shock?

Requires emergency treatment; reverse vasodilation, support organ perfusion, and treat bradycardia and the underlying cause.

64
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What meds do we give for neurogenic shock?

vasopressor (phenylephrine) and atropine

65
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Why give fluids cautiously in neurogenic shock?

Its not a fluid problem, we want to constrict vasculature

66
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What causes anaphylactic shock?

Severe allergic reaction

67
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What two immediate threats must you assess with anaphylactic shock?

Airway obstruction from swelling or bronchospasm and circulatory collapse from vasodilation

68
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What respiratory findings can occur in anaphylactic shock?

Tongue or throat swelling, wheezing, stridor, dyspnea, and severe air hunger.

69
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What is the first-line medication for anaphylaxis?

Epinpehrine

70
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Why is epinephrine effective with anaphylactic shock?

It supports blood pressure, reduces airway swelling, and helps relieve bronchoconstriction.

71
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What additional treatments might be needed with anaphylactic shock?

Airway support, oxygen, IV fluids, bronchodilators, and adjunct medications such as antihistamines.

72
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What should a patient with a serious allergy be taught?

Avoid known triggers, tell healthcare providers about allergies, carry prescribed epinephrine, and know when and how to use it

73
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What hemodynamic profile is observed during anaphylactic shock?

decreased CVP, decreased PCWP, decreased SVR, and decreased CO.

74
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What causes obstructive shock?

A physical obstruction prevents the heart from filling or prevents blood from flowing forward.

75
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what are some examples that cause obstructive shock?

Cardiac tampnade, tension pneumothorax, pulmonary embolism

76
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How can a pulmonary embolism cause obstructive shock?

It blocks blood flow out of the right ventricle through the lungs, reducing return to the left heart and lowering CO.

77
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How can tamponade or tension pneumothorax cause obstructive shock?

Pressure on the heart or great vessels impairs filling and lowers CO.

78
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What is the main treatment for obstructive shock?

Relieve the specific obstruction

79
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Hypovolemic shock

too little preload (FLUID PROBLEM)

80
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Cardiogenic shock

Too little contractility (pump problem)

81
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Distributive shock

Too little afterload (redistributed intravascular volume problem)

82
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Obstrictive shock

blood flow problem

83
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What happens in the initial stage of shock?

Tissue perfusion begins to fall; anaerobic metabolism and lactate production begin, but signs may be subtle.

84
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What happens in the compensatory stage?

The body raises heart rate and tightens blood vessels to keep blood flowing to vital organs.

85
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What happens in the progressive stage?

Compensation fails, capillary leak and hypotension worsen, and vital organs receive inadequate oxygen.

86
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What happens in the refractory stage?

Severe, persistent hypoperfusion leads to multiple organ failure; recovery becomes unlikely.

87
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What early neurological changes may signal poor perfusion?

Restlessness, anxiety, agitation, or confusion.

88
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Why monitor mental status closely?

A change may be an early sign of reduced cerebral perfusion.

89
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What respiratory changes should be monitored?

RR, depth, work of breathing, SpO₂, oxygen needs, breath sounds, and ABGs.

90
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What cardiovascular trends should be monitored?

HR and rhythm, BP/MAP, pulses, capillary refill, and hemodynamic values if available.

91
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What renal finding signals worsening perfusion?

low UOP, high creatinine

92
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Which patients generally need substantial fluid resuscitation?

Patients with hypovolemic shock and many patients with septic or anaphylactic shock

93
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Which shock types call for particular caution with fluids?

Cardiogenic and neurogenic shock.

94
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What do vasopressors do?

Constrict blood vessels to raise vascular resistance and support blood pressure and organ perfusion.

95
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What do inotropes do?

increase contractility

96
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When do we use vasodilators?

cardiogenic shock, (IV nitroglycerine, dobutamine)

97
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Whats first line vasopressor in septic shock

Norepinephrine

98
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What vasopressor do we use with cardiogenic shock?

Dopamine

99
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What is a useful vasopressor in phenylephrine?

Neurogenic shock

100
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How do we want to give a vasopressor?

Through a central line