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ICU & ER > Vasopressors, Inodilators, Inopressors, Pure Vasopressors, Methylene Blue, Midodrine > Flashcards

Vasopressors, Inodilators, Inopressors, Pure Vasopressors, Methylene Blue, Midodrine Flashcards

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1
Q

What is the effect of dobutamine on stroke volume?

A

Increases stroke volume

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2
Q

What should be monitored when titrating dobutamine and milrinone?

A

Echocardiogram, urine output, central venous pressure

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3
Q

What happens to beta receptors with prolonged dobutamine use?

A

They undergo desensitization and efficacy decreases.

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4
Q

What is a pro of using dobutamine?

A

It is easily titratable.

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5
Q

What is a downside of dobutamine in patients with atrial fibrillation?

A

It increases heart rate, which may worsen atrial fibrillation.

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6
Q

How does milrinone compare to dobutamine?

A

Milrinone has a greater vasodilatory effect than dobutamine.

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7
Q

What is a downside of milrinone in patients with chronic kidney disease?

A

It can accumulate and cause significant negative effects.

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8
Q

What is a major downside of isoproterenol?

A

It is extremely expensive.

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9
Q

What are inopressors used for?

A

They increase contractility, stroke volume, cardiac output, and blood pressure.

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10
Q

What are some examples of inopressors?

A

Norepinephrine, epinephrine, and dopamine.

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11
Q

What is a concern with using dopamine?

A

It is generally not favored due to its side effects.

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12
Q

What is norepinephrine primarily known for?

A

Strong alpha 1 receptor agonist activity and beta 1 receptor agonist activity.

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13
Q

What type of receptors does epinephrine primarily act on at lower doses?

A

Beta 1 and beta 2 receptors.

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14
Q

What happens to epinephrine’s activity at higher doses?

A

It becomes an alpha 1 receptor agonist while retaining beta agonist activity.

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15
Q

What is the primary activity of dopamine at lower doses (1-4)?

A

Dopamine receptor type activity, leading to mild increase in cardiac output and vasodilatory effects.

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16
Q

What effects does dopamine have at doses of 4-10?

A

Increased beta receptor stimulation, leading to increased heart rate and cardiac output.

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17
Q

What occurs with dopamine at doses of 10-20?

A

Increased alpha receptor activity, raising systemic vascular resistance.

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18
Q

What are the risks associated with dopamine use?

A

Difficult to titrate, higher mortality rates, and potential gut malperfusion.

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19
Q

What is a significant adverse effect of dopamine extravasation?

A

High risk of tissue necrosis.

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20
Q

What is a key indication for using angiotensin II?

A

Septic shock or vasodilatory shock.

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21
Q

What is the effect of stimulating alpha-1 receptors?

A

Increased vascular resistance and blood pressure.

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22
Q

What do alpha-1 receptors stimulate?

A

Norepinephrine and epinephrine stimulate alpha-1 receptors.

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23
Q

Where are alpha-1 receptors present?

A

Alpha-1 receptors are present on arterioles and venules.

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24
Q

What happens when alpha-1 receptors on arterioles are stimulated?

A

It clamps down on arterioles, increasing systemic vascular resistance and blood pressure.

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25
Q

What is the effect of stimulating alpha-1 receptors on venules?

A

It increases venous vasoconstriction, raising preload and cardiac output.

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26
Q

What is the effect of beta-1 receptor stimulation?

A

It increases heart rate and contractility, thus increasing cardiac output.

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27
Q

What does epinephrine act as?

A

Epinephrine is a beta agonist, specifically a strong beta-2 agonist.

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28
Q

What is the effect of epinephrine on the lungs?

A

Epinephrine causes bronchodilation, similar to albuterol.

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29
Q

How does epinephrine affect mast cells?

A

It inhibits mast cells from releasing histamine, reducing bronchospasm.

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30
Q

What effect does epinephrine have on lactate production?

A

Epinephrine increases lactate production in the liver.

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31
Q

What is the relationship between stroke volume and cardiac output?

A

Increasing stroke volume leads to an increase in cardiac output.

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32
Q

What are the primary indications for norepinephrine and epinephrine?

A

Septic shock and cardiogenic shock are primary indications for norepinephrine and epinephrine.

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33
Q

Which drug is considered first-line for septic shock?

A

Norepinephrine is the first-line drug for septic shock.

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34
Q

How do norepinephrine and epinephrine affect cardiac output in cardiogenic shock?

A

They can increase heart rate and contractility, improving cardiac output in cardiogenic shock.

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35
Q

Which drug provides more beta-1 activity in cardiogenic shock?

A

Epinephrine provides more beta-1 activity compared to norepinephrine in cardiogenic shock.

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36
Q

What is a common add-on treatment for cardiogenic shock?

A

Dobutamine or milrinone are common add-on treatments for cardiogenic shock.

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37
Q

What role does epinephrine play in bradycardia?

A

Epinephrine can help increase heart rate in patients with bradycardia.

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38
Q

What is a preferred treatment for severe bradycardia?

A

Transcutaneous pacing and atropine are preferred treatments for severe bradycardia.

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39
Q

What is push-dose epinephrine used for?

A

Push-dose epinephrine is used to stabilize patients who are becoming bradycardic or in asystole.

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40
Q

What is a potential drug for bradycardic periarrest patients?

A

Epinephrine infusion or push-dose epi.

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41
Q

What is the dose of intramuscular epinephrine for anaphylaxis?

A

0.5 milligrams every five minutes, up to three doses.

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42
Q

What is the acceptable MAP goal in shock patients?

A

Greater than or equal to 65 mmHg.

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43
Q

What does MAP stand for?

A

Mean Arterial Pressure.

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44
Q

How is MAP calculated?

A

Diastolic BP + one third of pulse pressure.

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45
Q

What effect does epinephrine have on the bronchioles?

A

Causes bronchodilation.

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46
Q

What is the mechanism of epinephrine in anaphylactic shock?

A

Inhibits mast cell degranulation and causes vasoconstriction.

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47
Q

What is a significant response of epinephrine in anaphylactic shock?

A

Increases heart rate and blood pressure.

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48
Q

What should be monitored when titrating epinephrine?

A

Blood pressure, specifically MAP.

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49
Q

What is the target MAP for titrating epinephrine?

A

Greater than or equal to 65 mmHg

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50
Q

What heart rate can be targeted when titrating epinephrine?

A

Greater than 50 beats per minute

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51
Q

What is norepinephrine primarily used for?

A

First line treatment for septic shock

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52
Q

What is a potential downside of norepinephrine in patients with atrial fibrillation?

A

It may increase heart rate, worsening rapid AFib

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53
Q

What is epinephrine effective for?

A

Septic shock and cardiogenic shock

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54
Q

What effect can epinephrine have on patients with lung disease?

A

Bronchodilation effect

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55
Q

What should clinicians monitor when administering epinephrine?

A

Lactate levels

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56
Q

What does a lactate level greater than or equal to 4 indicate?

A

Possible lactic acidosis due to tissue perfusion issues

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57
Q

What does epinephrine do to lactate production?

A

It increases lactate production

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58
Q

What might indicate a patient could respond well to angiotensin II?

A

Being on a pre-illness ACE inhibitor.

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59
Q

What should be considered when giving epinephrine to a patient with AFib?

A

It can worsen AFib due to increased beta-1 stimulation

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60
Q

What does an increase in lactate levels indicate regarding tissue perfusion?

A

An increase in lactate does not necessarily mean poor tissue perfusion; it may be due to beta-2 receptor effects on the liver increasing lactate production.

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61
Q

What are pure vasopressors primarily used for?

A

Pure vasopressors primarily function to clamp down on peripheral blood vessels.

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62
Q

Name three drugs classified as pure vasopressors.

A

Phenylephrine, vasopressin, and angiotensin II.

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63
Q

What type of receptor does phenylephrine primarily stimulate?

A

Phenylephrine primarily stimulates alpha-1 receptors.

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64
Q

How does vasopressin function in the body?

A

Vasopressin works by stimulating V1 receptors on systemic arterioles and V2 receptors in the kidneys.

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65
Q

What are V1 and V2 receptors associated with?

A

V1 receptors are associated with peripheral vessels; V2 receptors are associated with kidney tubules.

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66
Q

What is the significance of angiotensin II in vasopressor therapy?

A

Angiotensin II acts on angiotensin II receptors in arterioles, causing vasoconstriction, but data on its efficacy is still limited.

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67
Q

What happens when alpha-1 receptors are stimulated?

A

Stimulation of alpha-1 receptors leads to vasoconstriction, increasing systemic vascular resistance.

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68
Q

What is the effect of phenylephrine on arterial and venous vessels?

A

Phenylephrine binds to receptors on both arterioles and venules, causing them to clamp down and increase systemic vascular resistance.

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69
Q

What happens when you clamp down on the arterials?

A

Decreases diameter, increases systemic vascular resistance, increases blood pressure, and increases afterload.

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70
Q

How does increasing preload affect stroke volume?

A

Increasing preload increases stroke volume.

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71
Q

What is the effect of phenylephrine?

A

Stimulates alpha-1 receptors, causing vasoconstriction and increasing blood pressure.

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72
Q

What receptor does vasopressin stimulate for vasoconstriction?

A

V1 receptor.

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73
Q

What is the effect of stimulating V2 receptors by vasopressin?

A

Increases aquaporins in kidney tubules, enhancing water reabsorption.

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74
Q

How does vasopressin increase blood pressure?

A

By retaining more water from kidneys and causing vasoconstriction.

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75
Q

What does angiotensin II do when it binds to its receptors on systemic arterioles?

A

Causes vasoconstriction, increasing systemic vascular resistance and blood pressure.

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76
Q

What is the effect of increased aldosterone?

A

Increases sodium and water reabsorption, raising blood volume and blood pressure.

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77
Q

What role does ADH play in blood pressure regulation?

A

Stimulates water reabsorption to increase blood volume and blood pressure.

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78
Q

What happens when blood volume increases?

A

It increases blood pressure and stimulates ADH release.

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79
Q

What does ADH do when released?

A

It reabsorbs more water, increasing blood volume and blood pressure.

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80
Q

What is the effect of increasing ADH and aldosterone?

A

It effectively increases blood volume and blood pressure.

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81
Q

What is a common type of vasodilatory shock?

A

Septic shock.

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82
Q

What is the first-line agent for vasodilatory shock?

A

Norepinephrine.

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83
Q

What is a second-line agent for vasodilatory shock?

A

Vasopressin.

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84
Q

What is angiotensin II used for?

A

It is a last-ditch effort in treatment when other vasopressors fail.

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85
Q

What condition can vasopressin treat in neuro ICU?

A

Central diabetes insipidus.

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86
Q

What happens when ADH is not released in impending herniation?

A

Kidneys do not hold water, leading to significant urine output and decreased blood volume.

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87
Q

What can result from excessive dilute urine output?

A

It can significantly lower blood volume and blood pressure.

88
Q

What is the effect of producing a lot of dilute urine?

A

It lowers blood volume and blood pressure significantly.

89
Q

What does vasopressin do in the body?

A

It acts on V2 receptors to reabsorb water in the kidneys.

90
Q

What condition can vasopressin help with in cirrhosis patients?

A

Hepatorenal syndrome.

91
Q

How does vasopressin benefit patients with hepatorenal syndrome?

A

It causes vasoconstriction of efferent arterioles, increasing glomerular pressure and urine output.

92
Q

When is angiotensin II particularly beneficial?

A

In patients with septic shock and high renin levels (≥200).

93
Q

What is a potential response of patients on renal replacement therapy to angiotensin II?

A

They may experience increased urine output.

94
Q

What is the appropriate MAP goal for titration of vasopressin?

A

Greater than or equal to 65 mmHg

95
Q

When can vasopressin be beneficial?

A

In septic shock and central diabetes insipidus or hepatorenal syndrome

96
Q

What is the titration goal for phenylephrine?

A

MAP greater than or equal to 65 mmHg

97
Q

What is a pro of phenylephrine in patients with AFib with RVR?

A

It can cause reflex bradycardia, which is beneficial

98
Q

What is a potential con of using phenylephrine in patients with low ejection fraction?

A

It may increase afterload, making it harder to push blood out

99
Q

What MAP goal should angiotensin II be titrated to?

A

Greater than or equal to 65 mmHg

100
Q

What should be monitored when titrating angiotensin II?

A

Heart function, urine output, MAP, and clinical status

101
Q

What is the effect of phenylephrine on blood vessels?

A

It causes vasoconstriction, increasing blood pressure

102
Q

What is a benefit of phenylephrine for patients with aortic stenosis?

A

It is suitable due to their fixed afterload

103
Q

What is a key consideration when using vasopressin?

A

Expect changes in urine output

104
Q

What effect does phenylephrine have on preload?

A

It increases preload, which can increase stroke volume and cardiac output.

105
Q

In which condition might increasing preload not help?

A

In severe systolic heart failure with low ejection fraction.

106
Q

What is a key characteristic of phenylephrine compared to norepinephrine?

A

Phenylephrine lacks beta-1 activity unlike norepinephrine.

107
Q

What is a benefit of vasopressin on the efferent arteriole?

A

It causes vasoconstriction, increasing glomerular hydrostatic pressure and urine output.

108
Q

How does vasopressin affect pulmonary vessels?

A

It can cause vasodilation, lowering pulmonary artery pressure.

109
Q

What is a major risk of extravasation of vasopressin?

A

It can cause tissue necrosis and digital ischemia.

110
Q

What potential con is associated with angiotensin II?

A

It may increase thrombosis and coagulation cascade activity.

111
Q

What is a potential risk of angiotensin II?

A

Increased risk of thrombosis and pro-thrombotic state.

112
Q

What does interleukin-6 contribute to?

A

Cytokine storm and multi-organ system dysfunction.

113
Q

What happens when the angiotensin II gene is knocked out in studies?

A

Lower mortality rates observed.

114
Q

What type of shock is methylene blue used for?

A

Refractory vasoplegic shock of any etiology.

115
Q

Where does methylene blue primarily act?

A

In vascular smooth muscle.

116
Q

How does methylene blue affect nitric oxide synthase?

A

It inhibits nitric oxide synthase, decreasing nitric oxide levels.

117
Q

What is the effect of low nitric oxide levels on cyclic GMP?

A

Less nitric oxide leads to lower cyclic GMP levels.

118
Q

What is the result of low cyclic GMP levels?

A

Increased calcium levels in the cytoplasm.

119
Q

What does methylene blue inhibit?

A

Nitric oxide synthase

120
Q

What is the effect of methylene blue on cyclic GMP?

A

It inhibits the conversion of GTP to cyclic GMP

121
Q

What happens to calcium levels in the cytoplasm when methylene blue is administered?

A

Calcium levels in the cytoplasm increase

122
Q

What does increased calcium in the cytoplasm lead to?

A

Increased contraction of smooth muscle

123
Q

What is the result of smooth muscle contraction due to methylene blue?

A

Vasoconstriction

124
Q

What happens to systemic vascular resistance with vasoconstriction?

A

It increases

125
Q

How does methylene blue affect blood pressure?

A

It increases blood pressure

126
Q

In which condition is methylene blue beneficial?

A

Refractory vasoplegic shock

127
Q

What is the typical dosage of methylene blue?

A

2 mg/kg

128
Q

What MAP goal should be targeted when titrating methylene blue?

A

Greater than or equal to 65

129
Q

What is a potential negative effect of methylene blue?

A

Increased pulmonary vascular resistance

130
Q

How does methylene blue affect pulmonary vessels?

A

Causes vasoconstriction

131
Q

What can increased pulmonary vascular resistance lead to?

A

Increased right ventricular stress

132
Q

What effect can methylene blue have on oxygen saturation readings?

A

It can lower oxygen saturation

133
Q

What unusual reading might a pulse oximeter show after administering methylene blue?

A

A pulse ox of 52

134
Q

What effect does methylene blue have on pulse oximeter readings?

A

It can cause inaccurate readings, showing low oxygen saturation despite proper oxygenation.

135
Q

What condition can methylene blue potentially cause due to its role as a monoamine oxidase type A inhibitor?

A

Serotonin syndrome, which can increase blood pressure and heart rate.

136
Q

How does methylene blue affect patients with G6PD deficiency?

A

It acts as an oxidating agent, increasing hemolytic anemia and Heinz body production.

137
Q

What impact does methylene blue have on the cytochrome P450 system?

A

It inhibits the system, increasing drug concentrations of other medications.

138
Q

Is it safe to administer vasopressors through a peripheral IV in a crashing patient?

A

Yes, it is safe for a short period of time, but monitoring is essential.

139
Q

What should be monitored when administering vasopressors through a peripheral IV?

A

The peripheral IV site and patient parameters to prevent complications.

140
Q

Is it okay to run vasopressors through peripheral IVs?

A

Yes, but ensure the IV is easily monitored and avoid deep ultrasound guided IVs.

141
Q

What should you monitor for when using peripheral IVs for vasopressors?

A

Surrounding tissue necrosis and signs of extravasation.

142
Q

What counteracting agent can be used for extravasation of vasopressors?

A

Phentolamine can be used against catecholamine vasopressors.

143
Q

Which vasopressors should be used cautiously with peripheral IVs?

A

Vasopressin and dopamine should not be used for long periods.

144
Q

What is the gold standard for administering high-dose vasopressors?

A

Central venous catheters are the gold standard for high-dose vasopressors.

145
Q

Which veins are commonly used for central venous access?

A

Internal jugular, subclavian, and femoral veins are used.

146
Q

When is it appropriate to use arterial lines with vasopressors?

A

To get accurate mean arterial pressure measurements in certain patients.

147
Q

What conditions may warrant the use of arterial lines?

A

Subclavian stenosis, aortic dissection, or issues with cuff pressures.

148
Q

Can peripheral IVs be used for low-dose vasopressors?

A

Yes, using peripheral IVs for low-dose vasopressors is acceptable.

149
Q

What is an arterial line used for?

A

To provide a better representation of mean arterial pressure, especially in hypotensive patients.

150
Q

What is the primary mechanism of action of Midodrine?

A

It is primarily an alpha-1 receptor agonist causing vasoconstriction.

151
Q

What does Midodrine increase in the body?

A

Systemic vascular resistance, blood pressure, preload, stroke volume, and potentially cardiac output.

152
Q

What are the indications for using Midodrine?

A

To wean off IV vasopressors and in patients with hepatorenal syndrome.

153
Q

What did the MIDAS trial conclude about Midodrine?

A

It is not very effective in weaning off vasopressors, but is still used due to its alpha-1 activity.

154
Q

What are the cons of using Midodrine?

A

It is renally excreted and may accumulate in renal dysfunction; can cause reflex bradycardia.

155
Q

How is Midodrine administered?

A

Typically started at 10 mg every 8 hours, with titration as needed.

156
Q

What is a medication to consider when weaning off IV vasopressors?

A

Metoprolol, starting at 10 mg q8 hours.

157
Q

What is the maximum dosage of Metoprolol when weaning off vasopressors?

A

Up to 40 mg q8 hours.

158
Q

What should be monitored when weaning off vasopressors?

A

The patient’s underlying renal function.

159
Q

What risk is associated with Metoprolol in patients with low ejection fraction?

A

It may stress the heart.

160
Q

What condition may not respond to an increase in preload?

A

Severe systolic heart failure.

161
Q

What topic was discussed in the video?

A

Vasopressors.

162
Q

What is the first step in treating severe bradycardia in a patient at risk of cardiac arrest?

A

Transcutaneous pacing.

163
Q

What is the goal when starting medications for shock management?

A

To titrate against specific clinical parameters, not just blood pressure.

164
Q

What is the potential issue with titrating shock medications against blood pressure?

A

They have variable effects on blood pressure.

165
Q

What should dobutamine and milrinone be titrated against?

A

Cardiac output

166
Q

What is a common method to measure cardiac output?

A

Echocardiogram (echo)

167
Q

What can indicate an increase in cardiac output?

A

Increased urine output

168
Q

What is the primary use of isoproterenol?

A

To increase heart rate

169
Q

What is a benefit of dobutamine?

A

Short half-life, easily titratable

170
Q

What is a downside of long-term dobutamine use?

A

Beta receptor desensitization

171
Q

What surrogate measurements can help assess cardiac output?

A

Central venous pressure, Svo2, lactate levels

172
Q

How does increased perfusion to the kidneys relate to cardiac output?

A

It should increase urine output

173
Q

What is unique about milrinone’s mechanism of action?

A

It does not involve catecholamines or adrenergic receptors.

174
Q

What enzyme converts ATP into cyclic AMP?

A

Adenylate cyclase

175
Q

What does cyclic AMP stimulate in muscle tissue?

A

Protein kinase A

176
Q

What effect does protein kinase A have on cardiac muscle?

A

Stimulates contraction

177
Q

What effect does protein kinase A have on smooth muscle?

A

Causes relaxation

178
Q

What enzyme does cyclic AMP phosphorylate in smooth muscle?

A

Myosin light chain kinase

179
Q

What is the effect of vasodilation on systemic vascular resistance?

A

Lowers systemic vascular resistance

180
Q

What enzyme inhibits cyclic AMP?

A

Phosphodiesterase type 3 (PDE3)

181
Q

What drug inhibits PDE3 to increase cyclic AMP levels?

A

Milrinone

182
Q

What is the effect of milrinone on cardiac output?

A

Increases cardiac output

183
Q

What condition can be treated with dobutamine and milrinone?

A

Cardiogenic shock

184
Q

What is the effect of vasodilation on blood pressure?

A

Lowers blood pressure

185
Q

What happens to the afterload when smooth muscle relaxes?

A

It lowers the afterload

186
Q

What is the effect of vasodilation of peripheral vessels on afterload?

A

It lowers afterload, which can be beneficial.

187
Q

What condition is characterized by vasodilation and increased capillary permeability?

A

Septic shock.

188
Q

What happens to effective arterial blood volume in septic shock?

A

It is low.

189
Q

Which drugs are used to increase cardiac output in septic shock with low ejection fraction?

A

Dobutamine and milrinone.

190
Q

What is a potential drawback of using dobutamine or milrinone in septic shock?

A

They may worsen vasodilation and drop blood pressure.

191
Q

What type of medications are dobutamine and milrinone considered in septic shock management?

A

Add-ons to vasopressors.

192
Q

What is isoproterenol used for in patients with bradycardia?

A

To increase heart rate and stabilize patients before pacing.

193
Q

What are vasopressors?

A

Medications that constrict blood vessels and increase blood pressure.

194
Q

What is the first category of vasopressors discussed?

A

Inodilators.

195
Q

What does ‘inotropic’ refer to in inodilators?

A

Increase in contractility of the heart.

196
Q

What does ‘dilator’ refer to in inodilators?

A

Causes vasodilation of peripheral vessels.

197
Q

What is the primary drug in the inodilator category?

A

Dobutamine.

198
Q

What type of receptor does dobutamine primarily act on?

A

Beta receptors.

199
Q

What is the primary action of dobutamine?

A

It is a beta agonist that increases heart contractility.

200
Q

What is the secondary drug mentioned in the inodilator category?

A

Milrinone.

201
Q

What enzyme does milrinone inhibit?

A

Phosphodiesterase type 3.

202
Q

What is the third drug mentioned in the inodilator category?

A

Isoproterenol.

203
Q

What type of agonist is isoproterenol?

A

A strong beta agonist.

204
Q

What effect does stimulating beta 1 receptors have on the heart rate?

A

Increases heart rate (chronotropic activity).

205
Q

What is the effect of increased heart rate on cardiac output?

A

It potentially increases cardiac output.

206
Q

What is the relationship between cardiac output and stroke volume?

A

Cardiac output equals heart rate times stroke volume.

207
Q

Where are beta 1 receptors located in the heart?

A

On the contractile myocardium, not on the nodal cells.

208
Q

What effect does stimulating contractile myocardial cells have?

A

Increases contractility, which increases stroke volume.

209
Q

How does dobutamine primarily work?

A

Increases conductive activity, heart rate, and cardiac output.

210
Q

What is the effect of dobutamine on contractile cells?

A

Stimulates contractile cells, increasing calcium and contraction.

211
Q

What type of receptor activity does dobutamine have?

A

Very little alpha activity and more beta activity.

212
Q

What happens when alpha 1 receptors are stimulated on peripheral vessels?

A

Causes vasoconstriction of the blood vessel.

213
Q

What is the effect of dobutamine on systemic vascular resistance?

A

It decreases systemic vascular resistance and blood pressure.

214
Q

What is the effect of beta 2 receptor stimulation by dobutamine?

A

Causes vasodilation, lowering systemic vascular resistance.

215
Q

What is afterload in cardiac physiology?

A

The stress on the heart to pump blood out.

216
Q

What is isoproterenol primarily used for?

A

It is a beta agonist that increases heart rate and contractility.

217
Q

What effect does isoproterenol have on blood pressure?

A

It may cause a decrease in afterload and blood pressure.

ICU & ER (2 decks)

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