Vasopressors & Inotropic Agents Flashcards

1
Q

Definition of shock?

A

Syndrome initiated by acute systemic hypoperfusion, leading to tissue hypoxia and organ dysfunction

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2
Q

How is perfusion affected in hypovolemic shock?

A

Perfusion is decreased everywhere

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3
Q

How is perfusion affected in sepsis?

A

Perfusion is just maldistributed

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4
Q

Common conditions that affect hemodynamics?

A

PE, Ischemic conditions (L or R ventricular infarct), shock states (sepsis, hypovolemia, cardiogenic shock)

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5
Q

What is mean arterial pressure (MAP)?

A

Average arterial pressure throughout one cardiac cycle

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6
Q

How is mean arterial pressure (MAP) calculated?

A

MAP = [(SBP-DBP)/3] + DBP

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7
Q

Normal value for MAP?

A

80-100 mmHg

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8
Q

Clinical use of MAP is for rapid assessment of what?

A

Circulatory status

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9
Q

Normal values for systemic vascular resistance (SVR)?

A

800-1200 dyne*sec/cm^5

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10
Q

Clinical use of SVR is for estimation of what?

A

Vascular tone (constriction vs. dilation)

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11
Q

SVR is a major determinant of what?

A

Afterload

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12
Q

How can SVR be regulated?

A

Autonomic Nervous System (ANS) or pharmacological intervention

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13
Q

Normal value for cardiac output (CO)?

A

4-7 L/min

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14
Q

Determinants of cardiac output?

A

HR and stroke volume

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15
Q

How to calculate cardiac output?

A

CO = HR x SV

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16
Q

Clinical use for CO is used to determine the rate of what?

A

Rate of blood flow pumped by heart

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17
Q

CO is a major determinant of what?

A

Oxygen delivery (DO2)

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18
Q

How to calculate Cardiac Index (CI)?

A

CI = CO/BSA

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19
Q

Normal value for CI?

A

2.5-4 L/min/m^2

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20
Q

Clinical use for CI is used as a more accurate account of what?

A

Blood flow adjusting for the size of a person

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21
Q

Normal value for central venous pressure (CVP)?

A

0-4 cm H2O

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22
Q

Normal value for pulmonary arterial pressure (PAP)?

A

15-25/5-10 mmHg

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23
Q

What does continuous venous oxygen saturation (SvO2) reflect?

A

Total body balance between O2 delivery (DO2) and O2 consumption (VO2)

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24
Q

Normal value for SvO2?

A

68-77%

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25
Q

Low values for SvO2 that indicate inadequate DO2 and/or increased O2 consumption?

A

55-65%

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26
Q

Low values for SvO2 that suggest anaerobic metabolism?

A

<55%

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27
Q

High values for SvO2?

A

80-95%

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28
Q

Possible causes of high SvO2?

A

Increased CO, L to R shunting (back-leak from systemic to pulmonary circulation), inadequate O2 consumption

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29
Q

Monitoring parameters for shock?

A

HR, BP, Temp, Urine output, Pulse oximetry

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30
Q

What is a common heart rate finding in shock?

A

Tachycardia (more common due to body trying to compensate/ deliver more O2 to make up for lack of perfusion)

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31
Q

What is a common BP finding in shock?

A

Hypotension most common

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32
Q

What does temperature help distinguish in shock?

A

If infection is involved (sepsis)

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33
Q

What is one of the first signs of inadequate perfusion?

A

Oliguria (abnormally small amounts of urine)
*shows up even before BP or HR changes

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34
Q

What does pulse oximetry measure?

A

% of hemoglobin in the blood that is saturated w/ O2

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35
Q

Hemorrhagic causes of hypovolemic shock?

A

Internal bleeding, trauma

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36
Q

Nonhemorrhagic causes of hypovolemic shock?

A

GI and renal loss, burns, pancreatitis

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37
Q

“Pump failure” causes of cardiogenic shock?

A

MI, cardiomyopathy

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38
Q

Mechanical causes of cardiogenic shock?

A

Aortic or mitral valve stenosis, mitral regurg, ventricular septal defect

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39
Q

What is distributive shock?

A

Maldistribution of blood flow and volume

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40
Q

Causes of distributive shock?

A

Sepsis, severe sepsis (sepsis + acute organ dysfunction), anaphylactic shock

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41
Q

Cardiogenic shock presentation?

A

Decrease in CO/CI w/ hypotension not responding to fluid resuscitation

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42
Q

Cardiogenic shock is most likely due to what?

A

MI/ACS

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43
Q

Septic shock is usually secondary to what?

A

Infection

44
Q

Septic shock is driven by what?

A

Inflammatory response/chemicals

45
Q

What can occur in septic shock that can cause acute organ failure?

A

Hypercoagulation

46
Q

Therapeutic goals for oxygenation in shock?

A

-Keep hematocrit above 30
-SvO2 >70%

47
Q

How to keep hematocrit above 30 in shock?

A

Supplemental O2 via blood transfusions and respiratory assistance (face mask, intubation, etc.)

48
Q

How to keep SvO2 > 70% in shock?

A

Blood transfusions/volume, inotropic agents

49
Q

Therapeutic goals for perfusion in shock?

A

-SBP > 90 mmHg
-HR < 100 bpm
-CI w/in normal range, prefer if elevated
-Urinary output > 0.5 ml/kg/hr

50
Q

Reason for keeping HR > 100bpm in shock?

A

Maintain appropriate BP

51
Q

How to increase CI during shock to maintain normal levels?

A

Increase CO w/ inotropic agents, afterload reducers (as long as patient is not hypotensive)

52
Q

How to keep SBP > 90 mmHg in shock?

A

Volume, vasopressors, inotropic agents

52
Q

Administering vasopressors before fluid resuscitation could lead to what?

A

Profound tissue ischemia and necrosis: compare bn cardiogenic shock vs septic shock ???????

53
Q

How to keep urinary output > 0.5 ml/kg/hr during shock?

A

Volume, diuretics, vasopressin, vasopressors (i.e. maintaining adequate BP)

54
Q

Types of crystalloid fluid used for resuscitation/BP?

A

Normal saline, lactated ringers

55
Q

Types of colloid fluid used for resuscitation/BP?

A

Blood/blood products (Packed RBCs, platelets, fresh frozen plasma), Albumin, Hetastarch (Hespan)

56
Q

Which is better: colloid or crystalloid fluid for resuscitation?

A

Data shows no difference in outcomes

57
Q

Which is used more commonly for resuscitation: crystalloid or colloid fluid? Why?

A

Crystalloids (20 ml/kg bolus good starting point) - less expensive, no risk of infections as opposed to colloids (ex. hepatitis)
*blood still used to maintain hematocrit/restore any blood loss

58
Q

Where are V1 receptors found?

A

Arteries

59
Q

Where are B1 receptors found?

A

Cardiac tissue

60
Q

Where are a1 receptors found?

A

Arteries

61
Q

Where are dopamine receptors found?

A

Arteries

62
Q

Ratio of receptor agonism for NE?

A

Predominantly equal balance between a1 and b1 receptors

63
Q

What is the 1st pharmacological choice to restore pressure after attempts w/ fluids?

A

NE

64
Q

Goal systolic pressure w/ NE use?

A

> 90 mmHg

65
Q

Start at 1 mcg/min of NE and titrate up to what?

A

Goal MAP

66
Q

What are limiting features to NE uptitration?

A

MC limiting factor: tachycardia
goal MAP vs. comfortability w/o tachycardia
*clinical decision

67
Q

What is the ratio of receptor agonism of dopamine?

A

Dopamine R’s (liver metabolizes dopamine into NE –> vasoconstricts)

68
Q

What is the second pharmacological choice to restore pressure after attempts w/ fluids?

A

Dopamine (second to NE)

69
Q

Is dopamine a strong or weak vasoconstrictor?

A

Weak

70
Q

Evidence has shown increased risk of what in dopamine when compared to NE?

A

Side effects

71
Q

Start dopamine low at 5 mcg/kg/min and titrate up to what?

A

10 mcg/kg/min
Medium doses are target (don’t typically use low doses)

72
Q

With dopamine, as the dose increases, what also increases?

A

Risk of proarrhythmic effects

73
Q

What is the ratio of receptor agonism of epi?

A

a and b adrenergic R’s

74
Q

Evidence suggests that what agent is preferred over epi to restore pressure?

A

NE

75
Q

The pharmacology of epi is similar to that of what drug?

A

NE

76
Q

What is the drug of choice for anaphylactic shock?

A

Epi

77
Q

Which drugs are inotropic and vasopressor agents?

A

NE, dopamine, epi

78
Q

Which drugs are vasopressor agents?

A

Vasopressin, phenylephrine

79
Q

Which drugs are inotropic agents?

A

Dobutamine, phosphodiesterase inhibitors,

80
Q

Mechanism of action of vasopressin is devoid of what?

A

Adrenergic pharmacology

81
Q

Vasopressin has no risk of what?

A

Arrhythmias, tachycardia, etc.

82
Q

Vasopressin is also known as what?

A

ADH (Anti-diuretic hormone)

83
Q

Vasopressin works on what receptors?

A

V1 R’s

84
Q

Vasopressin has good effects with increasing what?

A

Increasing MAP, SVR, & urine output

85
Q

What is the ratio of receptor agonism for Phenylephrine?

A

Primarily a-1 R agonist, minimal to no beta-adrenergic activity

86
Q

What kind of agonist is phenylephrine?

A

Selective alpha agonist

87
Q

Phenylephrine has little to no effect on what?

A

HR

88
Q

Phenylephrine has no increase in what?

A

Myocardial oxygen demand

89
Q

What is usually the last line agent for shock?

A

Phenylephrine

90
Q

Is phenylephrine a mild or profound vasoconstrictor?

A

Profound

91
Q

What is the ratio of receptor agonism for Dobutamine?

A

Directly stimulates B-1 R’s of heart
Also a-1
(little activity on B-2, a-2)

92
Q

What does dobutamine increase?

A

Cardiac contractility, CO, DO2, and VO2 w/o changing MAP
*Used to increase CI

93
Q

What can dobutamine cause if fluids aren’t properly resuscitated?

A

Hypotension (has vasodilatory properties)

94
Q

Dobutamine is often combined with what other medication?

A

NE

95
Q

Which medications are phosphodiesterase inhibitors (class of inotropic agents)?

A

Milrinone and Amrinone

96
Q

Phosphodiesterase inhibitors increase cAMP, which has what effect?

A

Positive inotropic effect, some afterload reduction

97
Q

Phosphodiesterase inhibitors are commonly used in the setting of what kind of shock?

A

Cardiogenic shock

98
Q

In order to be treated with phosphodiesterase inhibitors, what must be at adequate values in patients?

A

BP

99
Q

What is the pharmacotherapy approach of the “sepsis bundle”?

A

Abx + fluid, vasopressors for pressure resuscitation if necessary

100
Q

When should the sepsis bundle be administered?

A

Within 1 hour (as opposed to 3/6 hour bundle)
*amplifies urgency and need of care

101
Q

Stress ulcer prophylaxis?

A

H2RA or PPI

102
Q

DVT prophylaxis?

A

heparin or lovenox (enoxaparin)

103
Q

If BP is still low (MAP<65) despite fluid and vasopressors, what can be used ?

A

Physiological replacement doses of hydrocortisone

104
Q

Glucose control is necessary in sepsis if the levels are greater than what value?

A

> 180mg/dl