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CC Quiz Study Guides > Electrophysiology & Vasoactive Agents Quiz > Flashcards

Electrophysiology & Vasoactive Agents Quiz Flashcards

1
Q

What is a cation?

A

Positively charged Ions that have lost electrons

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2
Q

What is an anions?

A

Negatively charged ions that have gained electrons

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3
Q

H+ is what Ion?

A

Hydrogen

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4
Q

Na+ is what Ion?

A

Sodium

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5
Q

K+ is what Ion?

A

Potassium

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6
Q

Ca++ is what Ion?

A

Calcium

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7
Q

Cl- is what Ion?

A

Chlorine

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8
Q

PO₄³⁻ is what Ion?

A

Phosphate

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9
Q

What is an Ion?

A

Any atom or molecule that has a charge

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10
Q

What are Cardiac Muscle Cells called?

A

Myocytes

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11
Q

What is a positively charge particles located in nucleus?

A

Protons

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12
Q

What is are neutral particles that are located in the nucleus called?

A

Neutrons

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13
Q

What are negatively charged particles orbiting the nucleus called?

A

Electrons

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14
Q

How many particles are atoms composed of?

A

3 particles

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15
Q

What are the 3 particles that make up an atom?

A

Protons, Neutrons, and electrons

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16
Q

What is an ionic bond?

A

When cations and anions bond together they create a

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17
Q

The division of ionic bonds causes the formation of?

A

Electrolytes

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18
Q

What are the two cardiac cells called?

A

Myocytes and Pacemaker (nodal) cells

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19
Q

What are Nodal Cells?

A

They are pacemaker cells

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20
Q

How many phases of the cardiac cycle are there?

A

There are 5 phases.

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21
Q

What phase is the resting phase of the cardiac cycle?

A

Phase 4

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22
Q

What phase is the depolarization phase of the cardiac cycle?

A

Phase 0

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23
Q

What phase of the cardiac cycle is the repolarization (notch waveform)?

A

Phase 1

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24
Q

What phase of the cardiac cycle is the Plateau Phase?

A

Phase 2

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25
Q

What phase of the cardiac cycle is the repolarization (complete) phase?

A

Phase 3

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26
Q

What ion channels open in phase 0 of the cardiac cycle?

A

Sodium Channels open allowing sodium in.

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27
Q

What Ion Channels close and open in Phase 1 of the cardiac cycle?

A

Sodium Channels close and Potassium Channels open allowing potassium out of the cell.

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28
Q

What Ion Channels open in phase 2 of the cardiac cycle?

A

Potassium channels are still open allowing potassium out, but calcium channels open to allow calcium into the cell.

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29
Q

What ion channels open and close during phase 3 of the cardiac cycle?

A

Potassium channels are still open and calcium channels close.

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30
Q

What channels close during phase 4 of the cardiac cycle?

A

All channels are closed allowing rest

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31
Q

What do cardiac pacemaker cells make up and are responsible for?

A

They make up the conductive network and are responsible for the propagation of electrochemical signaling

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32
Q

What do cardiac Myocytes make up and responsible for?

A

Make up the heart muscle and are responsible for the contraction and movement of blood

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33
Q

What is a concentration gradient?

A

A variance between the number of ions on either side of the cell membrane

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34
Q

What creates an electrical form of potential energy?

A

The difference in ion concentrations in and out of the cell

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35
Q

What is Unique to the heart, long thin cells capable of shortening, composted of smaller fibrils, large number of mitochondria for increased ATP production and resistant to fatigue?

A

Cardiac Myocytes

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36
Q

What is able to generate impulses spontaneously, unique to the heart, transmits impulses through the heart?

A

Pacemaker cells

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37
Q

What phase of the cardiac cycle is at -90mv?

A

Phase 4. The resting phase

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38
Q

What are the Phases of the pacemaker cycle?

A

Phases 4, 0, and 3

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39
Q

What is phase 4 of the pacemaker cycle called?

A

Phase 4 resting phase

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40
Q

What is the depolarization phase of the pacemaker cycle called?

A

Phase 0

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41
Q

What is the repolarization phase of the pacemaker cycle called?

A

Phase 3

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42
Q

At what mv is depolarization triggered in the pacemaker cycle?

A

-40mv

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43
Q

What mv is the resting phase of the pacemaker cycle?

A

-60mv

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44
Q

What ion influx causes depolarization of the pacemaker cycle?

A

Ca++

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45
Q

What Ion channels open to normalize the concentration gradient during repolarization of the pacemaker cycle?

A

K+

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46
Q

The pacemaker cycle occurs at the rate of what in the SA nodal cells, AV nodal cells, and Purkinje system?

A

SA: 60-100
AV: 40-60
Purkinje: <40

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47
Q

What is our pro-dominant extracellular ion?

A

Na+ (sodium)

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48
Q

What is the pro-dominant intracellular ion?

A

K+ (Potassium)

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49
Q

What ion channels do Cardizem effect?

A

Calcium Channels

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50
Q

What Ion channels does Amiodarone effect?

A

Potassium Channels

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51
Q

What Ion channels does lidocaine effect?

A

Sodium Channels

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52
Q

Nodal cells are leaky to what Ion?

A

Calcium

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53
Q

Beta 1 agonists increase the permeability of what ion?

A

Calcium

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54
Q

Unstable myocardium sign is?

A

A wide QRS complex

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55
Q

What are the 3 stages to stabilize Hyperkalemia?

A

Stabilize myocardium, shift intracellular, and elimination of K+

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56
Q

How doe you stabilize the myocardium in hyperkalemia?

A

Treat with CaCl (Calcium Chloride) and/or NaHCO₃ (sodium bicarbonate)

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57
Q

How do you shift the potassium intracellularly in Hyperkalemia?

A

Treat with insulin 0.1 units/kg

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58
Q

How do you eliminate K+ in Hyperkalemia?

A

Cause the patient to urinate or have bowel movements to help get rid of it or dialysis. For example lasix to urinate and Kayexalate.

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59
Q

Sodium Channel Blocker toxicity treatment?

A

Sodium Bicarbonate, possibly seizure control, and airway management

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60
Q

Hypokalemia and Hyperkalemia can lead to torsades de pointes because?

A

Of the widening QRS interval.

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61
Q

A QTC >500 is more likely to?

A

Lead to torsades de pointes

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62
Q

What drug has the least effect on QTC interval?

A

Lidocaine

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63
Q

What drug has the most QTC prolongation effects?

A

Amiodarone

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64
Q

Sympathetic stimulation releases?

A

Adrenergic neurotransmitters (Epi and NorEpi)

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65
Q

What drug stimulates Beta 1 receptors?

A

Epinephrine

66
Q

Stimulation of the Beta 1 receptors releases what?

A

Intracellular cAMP

67
Q

cAMP is what?

A

Cyclic adenosine monophosphate

68
Q

Increased cAMP levels reduce what and promote what?

A

Reduce time for action potential to occur.
Promotes a more complete contraction of the Myocyte.

69
Q

Parasympathetic stimulation releases what?

A

Antagonistic neurotransmitters (Acetylcholine)

70
Q

Acetylcholine binds to what? Which causes what?

A

Muscanaric receptors and causes decreased cAMP levels intracellular

71
Q

Decreased cAMP levels intracellular causes what?

A

A reduce in heart rate, force of contraction, and conduction velocity

72
Q

Stimulation of the vagus nerve increases?

A

Parasympathetic activity.

73
Q

Sodium Channel Blockade effects what phase of the cardiac cycle?

A

Phase 0, Depolarization phase

74
Q

Signs and symptoms of a Na+ channel blockade?

A

Depolarization is prolonged, QRS widened, QT prolonged, heart rate reduced, reduced membrane excitability, and refractory period is prolonged.

75
Q

Higher extracellular Na+ levels allow?

A

The body to tolerate a greater fluctuation in serum levels

76
Q

What can cause a sodium channel blockade?

A

TCA overdose, Cocaine toxicity, Diphenhydramine overdose.

77
Q

Minor variations of what Ion can cause significant ECG changes?

A

K+

78
Q

Ion that has a very prominent role in the cardiac cycle?

A

K+

79
Q

What ECG sign is the most common with HyperK?

A

Peaked T waves

80
Q

Sign wave is a sign of?

A

Impending death due to potassium increase outside the cell

81
Q

First treatment rendered if a sign wave is notable on ECG?

A

Treat with Calcium Chloride or Sodium Bicarbonate

82
Q

HyperK treatments?

A

Calcium Chloride, Sodium Bicarbonate, Insulin infusion, dextrose infusion, albuterol, diuretics, hemodialysis

83
Q

What is Hypokalemia commonly caused by?

A

Diuretics, diarrhea, dialysis

84
Q

Signs of hypokalemia?

A

A delay in repolarization, prolonged QT segments, ST segment depression, T wave inversion with the “U” wave, PR prolongation

85
Q

Treatment for Hypokalemia?

A

Administration of LR, comfort measures for pain and muscle spasms. Sometimes IV potassium.

86
Q

What is primarily caused by hyperparathyroidism?

A

Hypercalcemia

87
Q

Hypercalcemia effects was phase of the cardiac cycle? What does it do to the phase?

A

Phase 2 (plateau phase.) shortens which means a shortened QT segment.

88
Q

Calcium plays a crucial role in what?

A

Both myocardial contraction and signal conduction

89
Q

Common target for pharmaceutical intervention do dysrhythmias and management of cardiac output?

A

Calcium channels

90
Q

The primary cation for initiation of impulses in the SA node?

A

Calcium

91
Q

What functions very similar to calcium?

A

Magnesium

92
Q

Primarily caused by hypoparathyroidism?

A

Hypocalcemia

93
Q

What phase is effected by hypocalcemia?

A

Phase 2 (Plateau phase) prolongs and causes prolonged QT segment

94
Q

Hypocalcemia increases?

A

Contraction and excitability of non-cardiac muscle cells

95
Q

Treatment for Torsades De Pointes?

A

Mag Sulfate 1-2 grams IVP, cardioversion

96
Q

Calcium channel blockade effects what phase?

A

Phase 2 (Plateau phase) causes an extension of the action potential

97
Q

What are the 2 major kinds of calcium channel blockers?

A

dihydropyrodines, non-dihydropyrodines

98
Q

Signs and symptoms of an overdose on a Non-dihydropyridine calcium channel blockers?

A

Hypotension, Bradydysrhythmias (Esp AV blockers), Ventricular Dysrhythmias, Junctional Dysrhythmias, Asystole

99
Q

Signs and symptoms of a Dihydropyridine calcium channel blocker?

A

Tachycardia and vasodilatory shock.

100
Q

What will calcium channel blocker toxicity typically result in?

A

Hyperglycemia

101
Q

Beta blocker toxicity signs and symptoms?

A

Hypotension, bradydysrhythmias (es. AV blocks), Junctional Dysrhythmias, and ventricular Dysrhythmias

102
Q

Beta blockers bind to what and and block what?

A

Beta receptor sites and block stimulation from catecholamines

103
Q

Cardioselective beta blocking agents target what beta receptor?

A

Beta 1

104
Q

Beta blockers do what?

A

Reduce SA node firing rate. Conduction through AV node is slowed and arterial repolarization is prolonged

105
Q

ECG findings of beta blocker overdose?

A

P wave activity is reduced, PR segment is prolonged, QRS width depend on origin of impulse, and QT segment is prolonged

106
Q

Treatment of a beta blocker overdose?

A

Glucagon 2-5mg IVP (Recent evidence shows to be ineffective) High dose insulin therapy, Pacing can be attempted but reduced success rate.

107
Q

4 major classes of Vasoactive drugs?

A

Inopressor, Inodilator, Vasopressor, Vasodilator

108
Q

Right ventricle is a

A

Low pressure circuit

109
Q

Left ventricle is a

A

High pressure circuit

110
Q

Central venous pressure (think preload)

A

Right side

111
Q

Diastolic pressure (Think afterload)

A

Left side

112
Q

Alpha 1 receptors target?

A

Venal and arterial system

113
Q

Beta 1 receptors target?

A

Ventricles

114
Q

Beta 2 receptors target?

A

Bronchioles

115
Q

Ino means?

A

Targets heart in some form

116
Q

Inopressors do what?

A

Increases contraction of heart and increases vasoconstriction

117
Q

What drugs are inopressors?

A

NorEpi, Epi, Dopamine

118
Q

Norepinephrine’s common name?

A

Levophed

119
Q

Does for norepi?

A

2-20 mcg/min

120
Q

NorEpi is

A

The frontline agent for most shock states especially sepsis

121
Q

NorEpi stimulates what receptors and how?

A

Alpha 1 agonist by vasoconstriction, has mild beta effects but minimal on heart rate. Lower doses can cause venoconstriction which augments preload.

122
Q

How do you mix levophed and what is the concentration?

A

4mg in a 250mL D5W. concentration is 16 mcg/mL

123
Q

Epinephrine is the?

A

Frontline agent in anaphylaxis

124
Q

Epi effects what receptors and how?

A

Alpha 1 and Beta 1 and 2 agonism. Effects vasoconstriction, inotropy, and heart rate. Can be proarrhythmic due to the beta agonism

125
Q

What is the dose to Epi?

A

2-20 mcg/min

126
Q

How do you mix Epi and what is the concentration?

A

1mg of 1:1 Epi in 100mL of D5W. Concentration is 10 mcg/mL

127
Q

Dopamines concentration?

A

800mg/250mL of D5W

128
Q

Dose to Dopamine?

A

2-20 mcg/kg/min

129
Q

Why is dopamine not primarily used anymore?

A

It’s difficult to use effectively as its effects change as you increase dosage

130
Q

What receptors does dopamine effect?

A

Alpha 1, beta 1, beta 2 agonism.

131
Q

What’s the dosage of dopamine to effect Alpha 1 receptors?

A

Up to 10 mcg/kg/min

132
Q

What’s the dosage of Dopamine to get Beta receptor effects?

A

10 mcg/kg/min and higher

133
Q

What drugs are vasopressors?

A

Phenylephrine (Neosynephrine) and Vasopressin (ADH)

134
Q

What does phenylephrine effect and cause?

A

Strong alpha 1 agonism and causes potent vasoconstriction without effect on the heart

135
Q

What dos vasopressin effect and cause?

A

Targets V receptors and causes potent vasoconstriction. Also stimulates the retention of solute-free water.

136
Q

What drugs are inodilators?

A

Dobutamine and Milrinone (primacor)

137
Q

Dosage of dobutamine?

A

2-10 mcg/kg/min

138
Q

Milrinone dosage?

A

0.375-0.75 mcg/kg/min

139
Q

Dobutamine effects what receptor and causes what?

A

Very strong beta 1 agonism, increases heart rate, force of contraction and causes vasodilation.

140
Q

When is dobutamine indicated?

A

Heart failure and cardiogenic shock

141
Q

What does Milrinone do and effect?

A

Phosphodiasterase inhibitor and increases force of contraction and vasodilation

142
Q

When is Milrinone indicated?

A

Indicated in heart failure and cariogenic shock (Mainly seen with pediatrics)

143
Q

What drugs are vasodilators?

A

Nitroglycerin, Nicardipine, and Nitroprusside

144
Q

What does Nitro do?

A

Strong venodilator and mild arterial dilation. Effects arteries with increased dosages.

145
Q

What’s the dosage for Nitro?

A

5-400 mcg/min

146
Q

What does nicardipine effect and do?

A

Arterial selective calcium channel blocker. Strong arterial dilator

147
Q

Dosage of Nicardipine?

A

5-15 mg/hr must titrate cautiously

148
Q

Common name for nicardipine?

A

Cardene

149
Q

Common name for nitropprusside?

A

Nitropress

150
Q

What does nitroprusside do?

A

Very potent arterial dilator

151
Q

What does nitroprusside breakdown to and what to watch for?

A

Breaks down to nitric oxide. Watch for cyanide toxicity

152
Q

With this medication a arterial line placed is highly recommended

A

Nitropress

153
Q

How many Anti arrhythmic drug classes are there?

A

4

154
Q

What is class 1 effect? antiarrythmics

A

Na+ (Lidocaine, Procainmide)

155
Q

What does class 2 effect? Antiarrythmics

A

Beta blockers (Metoporol, Esmolol, Labetalol)

156
Q

What does class 3 effect? Antiarrythmics

A

K+ (Amiodarone)

157
Q

What does class 4 effect? Antiarrythmics

A

Ca++ (Cardizem, verapamil)

158
Q

Hyperkalemia is seen in patients with?

A

Rhabdomyolysis, Burns, Profound acidosis, Crush patients for compartment syndrome.

159
Q

Nitro dose to cause venodilation?

A

5-50 mcg/min

160
Q

Nitro to cause arterial dilation?

A

50-100 mcg/min starting range.

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