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Pharmacology > 1D4 > Flashcards

1D4 Flashcards

1
Q

what is cardiac output

A

the amount of blood ejected from the heart in liters/min

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2
Q

what is the normal cardiac output

A

4-8 L/min

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3
Q

what are the determinants of cardiac output

A
  1. heart rate

2. stroke volume

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4
Q

what are the determinants of stroke volume

A

a. preload
b. afterload
c. contractility

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5
Q

what is the equation for cardiac output

A

CO = HR x SV

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6
Q

what is the cardiac index

A

a more accurate determinant of heart function

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7
Q

what does cardiac index take into account

A

the pt’s body surface area (m^2)

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8
Q

what is CI determined by

A

HR, SV, height, weight

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9
Q

what is HR

A

of beats per minte

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10
Q

what does optimal heart rate balance

A

coronary blood flow with cardiac output

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11
Q

when does coronary blood flow take place

A

mainly during diastole

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12
Q

what is the optimal heart rate b/m

A

80-100

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13
Q

normal sinus rhythm ensures ______ ______ and maximizes _____ ______

A

ensures atrioventricular synchrony and maximizes cardiac efficiency

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14
Q

what is stroke volume

A

the amount of blood which is ejected from the heart with each beat

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15
Q

what can stroke volume be manipulated by

A

fluids, inotropes, vasopressors and vasodilators

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16
Q

what is preload

A

pressure or stretch exerted on the walls of the ventricle by blood filling at end diastole

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17
Q

what is the saying for Starling’s law of the heart

A

“the heart will pump what it receives”

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18
Q

the frank starling mechanism describes the ability fo the heart to change its force of _____ (and hence ___ ____) in response to changes in ____ ____

A

its force of contractility (and hence stroke volume) in response to changes in venous return

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19
Q

if the end diastolic volume increases, there is a corresponding _____ in stroke volume

A

increase

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20
Q

preload reflects

A

volume status

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21
Q

preload increases with

A

hypervolemia

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22
Q

preload decreases with

A

hypovolemia

may result from bleeding, fluid loss, or vasodilation

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23
Q

what is afterload

A

resistance to left ventricular contraction

end systolic wall stress or resistance

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24
Q

how is after load assessed

A

by measuring systemic vascular resistance (SVR)

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25
Q

after load is the degree of ____ or _____ of the arterial circulation

A

constriction or dilatation

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26
Q

high after load increases what and decreases what

A

increases myocardial work and oxygen demand

decreases cardiac output

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27
Q

after load increases with (5)

A
  • hypothermia
  • aortic valve stenosis
  • history of hypertension
  • increase in SVR
  • vasoconstriction
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28
Q

contractility

A

the ability of the myocardial muscle fiber to shorten independent of preload and afterload

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29
Q

Contractility is the ability of the heart to ____ and the ____ at which it does so

A

heart to contract and the force at which it does so

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30
Q

force of contraction is determined by

A

the concentration of calcium ions in the cell

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31
Q

increase contractility can be increase by

A

flooding cell with more calcium (beta agonist) or by keeping more calcium in the cell and not letting it escape

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32
Q

when do you give calcium

A

after cross clamp

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33
Q

myocardial contractility is enhanced by using what

A

isotrope pharacological agents such as adrenaline, dobutamine, milronone and levosimendan

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34
Q

the central nervous system consists of the

A

brain and spinal cord

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35
Q

the central nervous system is responsible for

A

processing and interpreting information

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36
Q

the peripheral nervous system includes

A

all of the nervous tissue outside of the brain and spinal cord

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37
Q

what is the PNS comprised of what nervous systems

A

the autonomic nervous system and the somatic nervous system

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38
Q

what is the ANS

A

motor system that receives and conducts information from the brain and spinal cord to the effector cells

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39
Q

the ANS can be further divided into the

A

sympathetic and parasympathetic divisions

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40
Q

SNS is stimulated by what and where

A

acetylcholine at the preganglionic site
&
norepinephrine at the postganglionic site

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41
Q

the receptors of the SNS are also called ____ receptors

A

adrenergic

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42
Q

what are the 3 main adrenergic receptors

A

alpha
beta
dopaminergic

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43
Q

what is acetylcholine

A

the neurotransmitter at both pre and post sites in the PNS

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44
Q

PNS receptors are refereed to as _____ receptors

A

cholinergic receptors

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45
Q

what are the two major types of cholinergic receptors

A

nicotinic and muscarinic

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46
Q

where are nicotinic receptors found

A

at neuromuscular junctions

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47
Q

where are muscarinic receptors found

A

throughout the body on many target tissues

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48
Q

what are the two type of alpha receptors

A

Alpha 1

Alpha 2

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49
Q

which alpha receptor is a postsynaptic receptor that elicits peripheral vasoconstriction

A

Alpha 1

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50
Q

which alpha receptor is a presynaptic receptor that decreases the release of NE at sympathetic nerve terminals

A

Alpha 2

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51
Q

alpha 1 location and actions

A

location: vascular smooth muscle
action: vasoconstriction

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52
Q

alpha 2 location and actions

A

location: presynaptic neurons
action: decrease NA release, decrease Act release, decrease insulin release

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53
Q

what are the the three subtypes of beta receptors

A

beta1
beta 2
beta 3

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54
Q

what are beta one receptors

A

postsynaptic receptors that when activated INCREASE HR and contractility, increase AV node conduction, and increase renin release

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55
Q

what are beta 2 receptors

A

postsynaptic receptors cause vasodilation, insulin release, bronchodilator, and glycogenolysis

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56
Q

what is beta 3 receptors

A

postsynaptic receptors cause increased lipolysis

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57
Q

B1 location and actions

A

location: heart
actions: increase rate, force, and automaticity

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58
Q

B2 location and actions

A

location: smooth muscle
action: relaxation

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59
Q

B3 location and actions

A

location: adipose tissue
action: increase lipolysis

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60
Q

what are the two subtypes of dopaminergic receptors

A

dopamine 1

dopamine 2

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61
Q

what is dopaminergic 1 receptors

A

postsynaptic receptors that cause renal and mesenteric vasodilation

62
Q

what is dopaminergic 2 receptors

A

presynaptic receptors that inhibit NE release

63
Q

what receptors act on brain Parkinson’s disease, schizophrenia

A

D2

64
Q

what part of the cardiopulmonary system express D1, D2, D4 receptors?

A

the pulmonary artery

65
Q

what effect does D1, D2, and D4 receptors have on the pulmonary artery?

A

cause vasodilatory effects of dopamine in the blood vessels

66
Q

what dopamine receptors does the heart have and what does it do

A

D4

increase CO and increase contractility without increasing HR

67
Q

what dopamine receptors does the kidney have and what does it do

A

D1

affects diuresis and natriuresis

68
Q

what are the mechanisms that regulate CO

A

ANS
PNS
SNS

69
Q

how does the autonomic nervous system regulate cardiac output

A

alter the HR, contractility, preload and afterload

70
Q

how does the parasympathetic nervous system regulate cardiac output

A

by slowing down the HR

-operates to conserve the energy expenditure of the body

71
Q

how does the sympathetic nervous system regulate the cardiac output

A

innervates the conduction system of the heart, the arterioles, and veins

-regulates energy expenditure and is operative during stressful situations

72
Q

what does stimulation of the SNS produce

A

an increase in HR, contractility, preload (venous constriction) and after load (arterial vasoconstriction)

73
Q

what are inotropes

A

medicines that change the force of your heart’s contractions

74
Q

what is the main goal of inotropic drug therapy

A

to improve myocardial function and end-organ perfusion

75
Q

how do you increase CO

A

by increasing stroke volume and/or heart rate

76
Q

what does increasing diastolic pressure increase

A

MAP

77
Q

what are the two kind of inotropes

A

positive inotropes

negative inotropes

78
Q

what do positive inotropes strengthen and help

A

strengthen the force of the heartbeat and help the heart pump more blood with fewer heartbeats

-for congestive heart failure or cardiomyopathy

79
Q

what do negative inotropes weaken and help

A

weaken the force of the heartbeat

-include beta-blockers, calcium channel blockers, anti arrhythmic medicines

80
Q

what do negative inotropes treat

A

treat hypertension, chronic heart failure, arrhythmias, and angina

81
Q

all positive inotropic drugs work by

A

increasing calcium entry into the myocyte increasing the physiologic response of “calcium induced - calcium release”

82
Q

when the increase of “calcium induced - calcium release”, what is the result?

A

increase of the number of cross bridges that can form thus increasing contraction

83
Q

in diastolic dysfunction, there may be an increase and decrease in what, and it leads to what?

A

increase in sarcomere Ca2+ sensitivity and a decrease in the rate of Ca2+ reuptake via SERCA2a and NCX

leads to state of Ca2+ overload

84
Q

in diastolic dysfunction, the state of Ca2+ overload leads to and what does it cause?

A

a slow or incomplete relaxation of the ventricles and causes pulmonary edema and hypertension

85
Q

what happens when augmenting diastolic function

A
  • inotropes increase filling time
  • lower LVEDP
  • decrease. LA pressure
  • decrease oxygen demand
86
Q

which vasopressors-inotropes are given after lung transplant

A

Beta2: bronchial dilation and vasodilation of coronary arteries

87
Q

what are sympathomimetics

A

substances that mimic or modify the actions of endogenous catecholamines (NE, E, dopamine) of the SNS

88
Q

direct agonists directly activate

A

adrenergic receptors

89
Q

indirect agonists enhance the

A

actions of endogenous catecholamines

90
Q

what is epinephrine (adrenaline) considered

A

both a hormone and medication

91
Q

where does Epinephrine act?

A

Direct acting catecholamine agonist at alpha1, alpha2, beta1, beta2 receptors

92
Q

what kind of response is called from epinephrine dose?

A

“balanced response”

93
Q

response at various receptors is

A

dose dependent

94
Q

what are the advantages of Epinephrine? (4)

A
  1. direct acting response not dependent on NE stores
  2. balanced alpha and beta response
  3. effective bronchodilator
  4. Systole is shortened allowing for increased diastolic filling as long as no tachycardia
95
Q

what are the disadvantages of epinephrine?

A

dose dependent

  1. potential for tachycardia
  2. increased oxygen demand
  3. PVR may increase in higher doses potentiating RV failure
96
Q

Norepinephrine directly acts on

A

alpha, apha2, and beta1 agonist

97
Q

what does norepinephrine not act on

A

beta2

98
Q

actions of norepinephrine

A 
increase contractility (minimal) 
increases CO (may decrease due to SVR) 
increase BP 
increase SVR 
increase PVR
99
Q

advantages of norepinephrine

A

very effective alpha1 effect

may be effective when phenylephrine is not due to increased potency

100
Q

disadvantages of norepinephrine

A
  • reduced end organ perfusion
  • risk of ischemic bowel
  • increase PVR
101
Q

what is dopamine

A

catecholamine precursor to NE and E that has both direct and indirect actions that are dose dependent

102
Q

direct actions of dopamine

A

alpha1
beta1
beta2
D1 agonist

103
Q

indirect actions of dopamine

A

increase endogenous NE

does dependent

104
Q

what is dopamine metabolized by

A

MAO and COMT

105
Q

advantages of dopamine

A

increased renal flow

easy to titrate response

106
Q

at low doses, what is dopamine useful as

A

vasodilator

107
Q

how much is a “renal dose” of dopamine

A

1-3 ug/kg/min

-works primarily at D1 receptors to increase renal and mesenteric flow

108
Q

at 3-10 ug/kg/min, where does dopamine work

A

at beta1 and beta2

increased HR and CO , decreased SVR

109
Q

at > 10 ug/kg/min, where does dopamine work and what does it do

A

alpha1 starts to dominate response

  • increased SVR and SVR
  • decreased renal flow
  • increased in HR
110
Q

what is a disadvantage of dopamine

A

an increase in after load may decrease CO and increase oxygen demand

111
Q

where does dobutamine directly act

A

beta1 synthetic agonist with little alpha1 and beta2 effects

112
Q

what does dobutamine increase

A

HR
CO
contractility

113
Q

what does dobutamine decrease

A

LVEDP
SVR slightly
PVR (beta2)

114
Q

advantages of dobutamine

A

decreases after load while increasing contractility, therefore decreasing how hard heart has to work

no MAO metabolism, COMT only

115
Q

what are the disadvantages of dobutamine

A
  1. tachycardia

2. non-selective vasodilator which may increase shunting

116
Q

what is ephedrine

A

plant derived non-catecholamine with mild direct beta1 and beta2 effects

117
Q

ephedrine is primarily an _____ effect via ___ release

A

an indirect effect via NE release

118
Q

is ephedrine metabolized by MAO or COMT

A

no

119
Q

length of action of ephedrine

A

5-10 min

120
Q

what are the physiological effects of ephedrine

A

-increased HR slightly, CO, contractility, BP, SVR slightly, preload increased (vasoconstriction)

121
Q

what is the dose of ephedrine

A

5-10 mg bolus IV

max dose: 60 mg

122
Q

advantages of ephedrine

A
  1. short duration of action

2. not likely to cause tachycardia

123
Q

ephedrine is used in pregnancy. why

A

does not reduce placental blood flow because it doesn’t cross placenta

safe to give

124
Q

disadvantages of ephedrine

A
  • little or no effect if NE stores are depleted

- MAo inhibitors indirectly effect ephedrine

125
Q

what is phenyephrine

A

direct acting on alpha1

non-catecholamine

126
Q

what are the beta effects on phenylephrine

A

none

127
Q

actions of phenylephrine

A

decrease HR
increase BP
increase SVR
increase coronary perfusion pressure w/o increase MVO2

128
Q

what is a bad action of phenyelphrine

A

increase PVR

129
Q

how long and what dose of phenyelphrine

A

<5 minutes

IV infusion = 100-500 ug/min
bolus 50-200 ug (on CPB usually 100 ug)

130
Q

what is methoxamine

A

synthetic non-cathecholamine

131
Q

what does methoxamine directly affect

A

direct alpha1 agonist

132
Q

actions of methoxamine

A

increase systolic and increase diastolic BP
increase SVR
decrease HR

133
Q

what is the difference between methoxamine and phenyelphrine

A

methoxamine has a long duration of action

134
Q

on CPB, you give 1 cc bolus of what

A

methoxamine

135
Q

1 cc bolus =

A

100 mcg/ml

136
Q

what does phosphodiesterase inhibitors do

A

prevents breakdown of cAMP by enzyme phosphodiesterase

137
Q

causes of phosphodiesterase inhibitors

A

increase in intracellular Ca+ in myocytes

augments catecholamines at B1 B2 receptors

138
Q

actions of phosphodiesterase inhibitors

A
  • inodilation: Increase rate and increase force of contraction
  • peripheral vasodilation in skeletal muscle (B1)
  • bronchodilation (B2)
139
Q

indications of PDE3

A
  • aminophylline: asthma, cardiac failure
  • enoximone: cardiac surgery, pt failing to respond to dobutamine
  • inocor
  • primacor
140
Q

what is the most common vasopressor

A

milrinone

141
Q

what is milrinone

A

PDE III inhibitor

142
Q

what does milrinone inhibit

A

cAMP breakdown

143
Q

actions of milrinone

A

increase CO
decrease SVR and decrease PVR
decrease Preload

144
Q

onset and offset of milrinone

A

max effect within 15-20 min

half life varies b/w 30-60 min

145
Q

advantages of milrinone

A
  • more dependable in states where receptors may be compromised like CHF
  • improves RV function due to PVR effects
146
Q

disadvantages of milrinone

A

vasodilation with loading dose (20-50 ug/kg over 10 min)

147
Q

what are the cardiac glycosides (digitalis)

A

digoxin

digitoxin

148
Q

what are the actions of cardiac glycosides

A

increase force and increase rate of contractions by action on the cellular sodium potassium ATPase pump

-increase inotropy
increase ejection fraction
decrease preload
decrease pulmonary congestion/edema

149
Q

what is cardiac glycosides used for

A
  1. low output heart failure - CHF
  2. atrial fibrillation and flutter
  3. paroxysmal atrial tachycardia
150
Q

what is digitalis toxicity

A

occurs with plasma concentration >2.0 ng/ml

-can cause life-threatening arrhythmias

Pharmacology (3 decks)

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