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APEX > Unit 3 - CV A&P > Flashcards

Unit 3 - CV A&P Flashcards

1
Q

how are myocytes similar to neural & skeletal tissue

A
  • generate RMP
  • can propagate an AP
  • contain contractile elements arranged in sarcomeres
  • have T-tubules
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2
Q

RMP is established by what 3 mechanisms

A
  1. chemical force
  2. electrostatic counterforce
  3. Na/K-ATPase
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3
Q

3 things unique to cardiac muscle (vs. skeletal and neural)

A
  1. joined by intercalated discs
  2. gap junctions
  3. consume a lot of O2 at rest - 8-10 mL O2/100g/min (contain a lot more mitochondria)
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4
Q

what is the purpose of gap junctions in cardiac muscle

A

facilitate spread of cardiac AP through myocardium

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5
Q

why do myocytes consume a lot more O2 at rest vs. skeletal muscle cells

A

contain more mitochondria

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6
Q

what is equilibrium potential?

A

situation where there’s no net movement of an ion across a cell membrane

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7
Q

equation used to predict an ion’s equilibrium potential

A

Nernst equation

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8
Q

what is automaticity

A

ability to generate AP spontaneously

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9
Q

how do cardiac conduction cells display automaticity

A

when they set HR (normally SA node)

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10
Q

what is excitability

A

ability to respond to an electrical stimulus by depolarizing & firing AP

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11
Q

what is conductance

A

ability to transmit electrical current

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12
Q

what is inotropy

A

force of myocardial contraction during systole

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13
Q

what is chronotropy

A

heart rate

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14
Q

what is dromotropy

A

conduction velocity through the heart (velocity = distance/time)

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15
Q

lusitropy

A

rate of myocardial relaxation during diastole

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16
Q

what is RMP?

A

an electrical potential across a cell membrane at rest

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17
Q

what eletrolyte is continuously leaked by nerve cells at rest

A

K+ (loses positive charge)

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18
Q

what is the primary determinant of RMP?

A

K+

increased : RMP more negative
decreased: RMP more positive

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19
Q

what is threshold potential

A

voltage change that must occur to initiate depolarization

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20
Q

what is the primary determinant of threshold potential

A

calcium

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21
Q

how does calcium affect threshold potential

A

decreased serum Ca2+ = TP more negative
increased calcium = TP more positive

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22
Q

what is depolarization

A

movement of a cell’s membrane potential to a more positive value (less difference between inside and outside of cell)

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23
Q

what happens to HR as distance between threshold potential & RMP narrows

A

increases bc myocardial cells reach threshold faster

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24
Q

what is the all or none phenomenon

A

once depolarization starts, it cant be stopped

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25
Q

what determines the ability to depolarize

A

difference of RMP & TP

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26
Q

how does the difference in RMP & TP affect depolarization

A

RMP closer to TP = easier to depolarize
RMP further from TP = harder to depolarize

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27
Q

what happens after depolarization in excitable tissue

A

action potential

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28
Q

what is repolarization

A

return of cells RMP to more negative value after depolarization

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29
Q

what causes cell repolarization?

A

when K+ leaves the cell or Cl- enters the cell

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30
Q

when is the cell resistant to subsequent depolarization

A

refractory period

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31
Q

what is hyperpolarization

A

movement of a cell’s membrane potential to a more negative value beyond baseline RMP

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32
Q

can a hyperpolarized cell be depolarized?

A

it’s more difficult bc RMP is further from TP

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33
Q

2 purposes of Na-K-ATPase

A
  1. removes Na+ that enters cell during depolarization
  2. returns K+ that left cell during depolarization
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34
Q

for every ___ Na+ ions removed by Na-K-ATPase, ____ K+ ions are brought in

A

3 Na
2 K

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35
Q

restores ionic balance towards RMP in excitable tissue

A

Na-K-ATPase

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36
Q

positive inotropic drug that inhibits Na-K-ATPase

A

digoxin

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37
Q

is Na-K-ATPase active or passive transport?

A

active transport - requires energy in the form of ATP

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38
Q

how does hypokalemia affect RMP/TP

A
  • RMP more negative
  • cells more resistant to depolarization
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39
Q

how does hyperkalemia affect RMP

A
  • more positive
  • cells depolarize more easily
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40
Q

how does hypocalcemia affect RMP/TP

A
  • TP becomes more negative
  • cells depolarize more easily
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41
Q

how does hypercalcemia affect RMP/TP

A
  • TP more positive
  • cells more resistant to depolarization
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42
Q

what happens to Na+ channels in severe hyperkalemia

A
  • inactivated
  • channels arrest in closed-inactivated state
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43
Q

how does cardioplegia solution work

A
  • high levels of K+; cells can’t repolarize, Na+ channels locked
  • arrests heart in diastole
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44
Q

why does IV calcium reduce the risk of dysrhythmias in hyperkalemic patients

A

increases the gap between RMP and TP

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45
Q

why is depolarization longer in myocytes vs. neurons

A

AP has a plateau phase - depolarization prolonged

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46
Q

do SA and AV nodes have a plateau phase?

A

nope

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47
Q

5 phases of myocyte AP

A
  1. depolarization
  2. initial repolarization
  3. plateau
  4. final repolarization
  5. resting phase
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48
Q

what part of EKG tracing reflects depolarization

A

Q wave

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49
Q

which phase of myocyte AP reflects Na+ in

A

depolarization

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50
Q

electrolyte movement during initial repolarization phase of myocyte AP

A

Cl- in
K+ out

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51
Q

electrolyte movement in final repolarization phase of myocyte AP

A

K+ out

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52
Q

part of EKG tracing that corresponds with final repolarization phase of myocyte AP

A

T wave

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53
Q

during which phase of myocyte AP is the EKG isoelectric

A

resting phase

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54
Q

electrolyte movement during resting phase of myocyte AP

A

K+ out
Na/K-ATPase function (K+ leak)

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55
Q

part of EKG wave that corresponds with plateau phase of myocyte AP

A

ST segment

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56
Q

electrolyte movement during plateau phase of myocyte AP

A

Ca2+ in
K+ out

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57
Q

threshold potential at myocyte depolarization

A

-70 mV

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58
Q

what counters loss of K+ ions to maintain depolarized state in plateau of myocyte AP

A

activation of slow voltage-gated Ca2+ channels

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59
Q

transmembrane resting potential of myocytes

A

-90 mV

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60
Q

purpose of K+ leak channel open in resting phase of myocyte AP

A

maintains transmembrane resting potential

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61
Q

order of normal cardiac conduction

A

SA node - internodal tracts - AV node - bundle of His - L/R bundle branches - Purkinje fibers

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62
Q

how many phases involved in SA node AP

A

3 (no phase 1 or 2)

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63
Q

3 phases of SA node AP

A

spontaneous depolarization
depolarization
repolarization

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64
Q

electrolyte movement during spontaneous depolarization of SA node

A
  • Na+ in
  • Ca2+ in (T-type)
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65
Q

electrolyte movement during depolarization phase of SA node AP

A

Ca2+ in (L-type)

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66
Q

what is the “funny current” in SA node AP and why is it called that?

A
  • at the end of repolarization (MP about -60 mV), ion channels open that conduct slow depolarizing currents
  • initiates phase 4 depolarization
  • called “funny” bc it’s activated by hyperpolarization, not depolarization
  • abbreviated I-f
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67
Q

events that occur in spontaneous depolarization of SA node myocytes

A
  • Na+ enters cell progressively, making it more positive
  • at -50 mV, transient Ca2+ channels open (T-type) to further depolarize cell
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68
Q

what causes depolarization in SA node myocytes

A

Ca2+ entry via voltage-gated calcium channels (L-type)

(T-type calcium channels close)

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69
Q

events that occur during repolarization of SA node conduction tissue

A
  • K+ channels open, K+ exits cell making it more negative
  • K+ efflux = repolarization, return of phase 4
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70
Q

what happens to calcium channels during repolarization of SA node

A

L-type Ca2+ channels close, Ca2+ conductance decreased

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71
Q

what 2 things determine heart rate

A
  1. intrinsic rate of dominant pacemaker (usually SA node)
  2. autonomic tone
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72
Q

intrinsic firing rates of SA, AV, and purkinje fibers

A

SA = 70-80
AV = 40-60
purkinje = 15-40

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73
Q

where does the SA node reside

A

right atrium

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74
Q

what determines the intrinsic rate of SA node firing

A

the rate of spontaneous phase 4 depolarization of SA node

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75
Q

how do volatiles affect SA node

A

depress SA node automaticity - can cause junctional rhythm

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76
Q

why is a junctional rhythm slow and without a P wave?

A

disease or hypoxia impairs SA node’s ability to function as dominant pacemaker - cells with next highest rate of spontaneous phase 4 depolarization assumes as pacemaker

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77
Q

responsible for SNS tone

A

cardiac accelerator fibers (T1-T4)

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78
Q

responsible for PNS tone

A

CN 10 (vagus)

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79
Q

what 3 variables can be manipulated to change the sinus node rate

A
  1. rate of spontaneous phase 4 depolarization
  2. threshold potential
  3. RMP
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80
Q

3 situations that can increase HR and reach threshold potential faster

A
  1. slope of phase 4 depolarization increases
  2. slope of phase 4 remains constant but TP becomes more negative
  3. slope of phase 4 remains constatnt but RMP becomes less negative
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81
Q

how does more negative threshold potential affect HR

A

shorter distance between RMP and TP - cells reach threshold faster

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82
Q

how does SNS affect HR

A

NE stimulates beta-1 receptor, increases HR by Na+ and Ca2+ conductance

increases rate of spontaneous phase 4 depolarization

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83
Q

how does PNS affect HR

A

ACh stimulates M2 receptor - slows HR by increased K+ conductance, hyperpolarizing SA node

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84
Q

how does PNS affect RMP

A

decreases - reduced slope of spontaneous phase 4 depolarization

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85
Q

oxygen delivery calculation

A

DO2 = CO x [(hgb x SaO2 x 1.34) + (PaO2 x 0.003)] x 10

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86
Q

equation for O2 carrying capacity

A

(Hgb x SaO2 x 1.34) + (PaO2 x 0.003)

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87
Q

what is CaO2

A

O2 carrying capacity

tells us how many grams of O2 are contained in a dL of arterial blood

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88
Q

what happens to HR if the distance between threshold potential and resting potential narrows?

A

HR will increase because myocardial cells will reach treshold faster

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89
Q

current that’s responsible for spontaneous phase 4 depolarization in SA node?

A

I-f

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90
Q

primary determinant of the pacemaker’s intrinsic HR

A

I-f current (sets the rate of spontaneous phase 4 depolarization)

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91
Q

expected oxygen delivery in a 70 kg adult

A

1,000 mL/min

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92
Q

expected CaO2 in 70 kg adult

A

20 mL/O2/dL

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93
Q

expected VO2 (oxygen consumption) in 70 kg adult

A

250 mL/min

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94
Q

expected CvO2 (venous oxygen content) in 70 kg adult

A

15 mL/dL

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95
Q

solution coefficient for dissolved oxygen

A

0.003

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96
Q

body extraction ratio

A

EO2 = 25%

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97
Q

how to calculate MAP using Ohm’s law

A

MAP = (CO x SVR / 80) + CVP

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98
Q

what are the flow, pressure gradient, and resistance factors of blood pressure?

A
  • flow = CO
  • pressure gradient = MAP - CVP
  • resistance = SVR
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99
Q

primary determinant of vascular resistance

A

radius of arterioles

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100
Q

used to predict if flow will be laminar or turbulent

A

Reynold’s number

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101
Q

Reynold’s number that will predict if flow will be laminar, turbulent, or transitional

A
  • laminar: Re < 2,000
  • turbulent: Re > 4,000
  • transitional: Re = 2,000 - 4,000
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102
Q

2 possible assessment findings when there’s turbulent flow

A

vibrations can cause a murmur (valve disease) or bruit (stenosis)

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103
Q

what is viscosity the result of

A

friction from intermolecular forces as fluid passes through a tube

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104
Q

what determines viscosity

A
  • Hct
  • body temp
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105
Q

relationship between blood viscosity and temperature

A

inversely related

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106
Q

how does saline dilution improve flow when giving PRBCs

A

decreases Hct

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107
Q

what 2 factors determine EDV (Preload)

A
  • filling pressures
  • compliance
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108
Q

what 2 factors determine ESV

A
  • afterload
  • contractility
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109
Q

what 2 factors determine stroke volume

A
  • EDV (preload)
  • ESV
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110
Q

determinants of CO

A
  • HR
  • SV
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111
Q

determinants of MAP

A
  • CO
  • SVR
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112
Q

determinants of tissue blood flow

A
  • MAP
  • local vascular resistance
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113
Q

determinants of O2 delivery

A
  • tissue blood flow
  • CaO2
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114
Q

normal CO in adult

A

5-6 L/min

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115
Q

cardiac index calculation & normal values

A

CO/BSA
2.8-4.2 L/min per m^2

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116
Q

stroke volume calculation & normal values

A

EDV - ESV or CO x 1000/HR
50-110 mL/beat

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117
Q

stroke volume index calculation & normal values

A

SV/BSA
30-65 mL/beat per m^2

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118
Q

ejection fraction calculation & normal values

A

(EDV - ESV / EDV) * 100 or (SV/EDV) * 100
60-70%

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119
Q

MAP calculation & normal values

A

(1/3 x SBP) + (2/3 x DBP) or (COxSVR /80) + CVP
70-105 mmHg

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120
Q

amount of oxygen dissolved in blood (PaO2) follows what law

A

Henry’s

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121
Q

flow is directly proportional to what 2 factors

A
  1. vessel radius
  2. arteriovenous pressure difference
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122
Q

flow is inversely proportional to what 2 factors

A
  1. viscosity
  2. length of tube
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123
Q

what are the 5 components of Poiseuille’s law

A
  1. Q - blood flow
  2. R - radius
  3. △P - arteriovenous pressure gradient
  4. n - viscosity
  5. L - length of tube
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124
Q

how much more flow occurs when the radius of a tube is quadrupled?

A

256x

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125
Q

pulse pressure calculation & normal values

A

SBP - DBP

(stroke volume output / arterial tree compliance)

40 mmHg

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126
Q

normal SVR

A

800-1500 dynes x sec x cm-5

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127
Q

SVR index calculation & normal values

A

(MAP-CVP / CI) x 80

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128
Q

PVR calculation & normal values

A

(MPAP - PAOP / CO) x 80
150-250 dynes x sec x cm-5

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129
Q

PVR index calculation & normal values

A

(MPAP - PAOP / CI) x 80
250-400 dynes x sec x cm-5 per m^2

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130
Q

functional unit of the contractile tissue in the heart

A

sacromere

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131
Q

amount of tension each sarcomere can generate is directly related to:

A

number of cross-bridges that can be formed before contraction

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132
Q

what is preload

A

ventricular wall tension at the end of diastole just before contraction
(the volume that returns to the heart during diastole)

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133
Q

how does A-fib affect preload

A

loss of atrial kick = reduced preload

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134
Q

how does venous tone affect preload

A

decreased tone (sympathectomy) = decreased preload

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135
Q

how does valvular regurgitation affect preload

A

aortic or mitral regurg increase preload

136
Q

illustrates the relationship between ventricular volume and output

A

ventricular function curve

137
Q

what is the Frank Starling mechanism

A

increased ventricular volume produces a larger CO up to the plateau, after which additional volume overstretches sarcomeres, decreases # cross-bridges that can be formed, and decreases CO

138
Q

commonly used as a surrogate for ventricular volume

A

filling pressure

139
Q

how is ventricular volume measurement obtained

A

TEE

140
Q

3 surrogate measures of LVEDV

A
  • LVEDP
  • LAP
  • PAOP
141
Q

x and y axis of ventricular function curve

A
142
Q

measurement of ventricular volume

A

PAOP

143
Q

relates ventricular volume to ventricular output

A

Frank starling mechanism

144
Q

terms that can be used on the y axis of Frank Starling curve

A
  • CO
  • SV
  • LVSW
  • RVSW

(ventricular output)

145
Q

terms that can be used on x axis of Frank Starling curve

A

filling pressures:
- CVP
- PAD
- PAOP
- LAP
- LVEDP

EDV:
- RVEDV
- LVEDV

146
Q

ability of myocardial sarcomeres to perform work (shorten & produce forece)

A

contractility

147
Q

reflects ventricular output for given EDV

A

contractility

148
Q

atrial contraction = ____% of final LDEDV & CO

A

20-30%

149
Q

why does CO usually decrease in A fib

A

loss of atrial kick, which contributes 20-30% of final LDEDV & CO

150
Q

why is a non-compliant ventricle more dependent on well-timed atrial kick to fill ventricle & generate SV

A

ventricle is stiff

151
Q

patients more likely to experience a decreased CO with cardiac rhythm disturbances like A-fib or a junctional rhythm?

A

patients with decreased ventricular compliance: hypertrophy, diastolic failure (preserved EF), fibrosis, aging

152
Q

how do most meds increase or decrease contractility

A

alter amount of calcium available to bind to myofilaments or impair sensitivity of myocardium to calcium

153
Q

5 things that increase contractility

A
  1. SNS stimulation
  2. catecholamines
  3. calcium
  4. digitalis
  5. PDE inhibitors
154
Q

how does hypercapnia affect contractility

A

decreases

155
Q

how do hyperkalemia and hypocalcemia affect contractility

A

decrease

156
Q

how do volatiles affect contractility

A

decreases

157
Q

2nd messenger in the myocardium

A

calcium

158
Q

primary substance that determines contractility

A

calcium

159
Q

action that opens voltage-gated L-type Ca2+ channels in the myocyte

A

depolarization of T-tubule

160
Q

what results in activation of RyR2 in the myocyte

A

influx of calcium

161
Q

what stimulates cross-bridge formation and causes myocardial contraction in the myocyte

A

calcium binds to troponin C (Tnc)

162
Q

what causes myocardial relaxation in the myocyte

A

calcium unbinds from troponin C (Tnc)

163
Q

how is most calcium returned to sarcoplasmic reticulum

A

SERCA2 pump (ATP-dependent)

164
Q

once inside the SR, what does calcium bind to

A

storage protein called CSQ (calsequestrin)

165
Q

how is some calcium removed from the myocyte

A

Na+-Ca2+ exchange pump (NCK)

166
Q

what determines the duration of myocyte contraction?

A

action potential duration

167
Q

restores RMP in myocyte

A

Na/K-ATPase

168
Q

what happens to the myocyte if RMP increases to a level that exceeds a level of normal repolarization

A

voltage-gated Na+ channels can’t fire and get stuck in closed-inactive state

169
Q

3 ways beta-1 receptor stimulation modulates calcium in the myocyte

A
  1. activation of L-type calcium channels
  2. stimulation of ryanodine 2 receptor to release more calcium
  3. stimulation of SERCA2 pump to increase calcium uptake
170
Q

how does beta-1 stimulation in the myocyte affect PKA?

A

activates AC - converts ATP to cAMP - increases PKA activation

171
Q

normally inhibits SERCA2 activity

A

phospholamban (PLN)

172
Q

net effect of beta-1 stimulation in myocyte

A

more forceful contraction over a shorter time (positive inotropy) with enhanced relaxation (positive lusitropy) between beats

173
Q

what is afterload

A

force the ventricle must overcome to eject its stroke volume

174
Q

3 factors that decrease stroke volume

A
  • decreased preload
  • decreased contractility
  • increased afterload
175
Q

what determines the majority of afterload

A

SVR (arteriolar tone)

176
Q

why is the LV thicker than the right?

A

has to overcome a much higher afterload

177
Q

what is wall stress in the heart

A

force that holds the heart together

178
Q

things that reduce myocardial wall stress

A
  • decreased intraventricular pressure
  • decreased radius
  • increased wall thickness
179
Q

what explains why pt with HTN compensates with LVH?

A

increased wall stress

180
Q

what is intraventricular pressure

A

force that pushes the heart apart

181
Q

wall stress =

A

(intraventricular pressure x radius) / ventricular thickness

182
Q

during what part of the cardiac cycle are all 4 valves closed

A

isovolumetric contraction & relaxation

183
Q

valves open and closed during ventricular ejection

A
  • mitral closed
  • aortic opened
184
Q

valves open/closed during atrial systole

A
  • open: mitral
  • closed: aortic
185
Q

what valve is open during rapid ventricular filling

A

mitral

186
Q

3 events that occur during systole

A
  1. isovolumetric contraction
  2. rapid ejection
  3. reduced ejection
187
Q

equation for law of laplace as it relates to the LV?

A

wall stress = (intraventricular pressure / radius) / ventricular thickness

188
Q

3 phases of the cardiac cycle assoc. with open mitral valve and closed aortic valve

A
  1. rapid ventricular filling
  2. atrial systole
  3. diastasis
189
Q

3 events that occur during diastole

A
  1. isovolumetric relaxation
  2. rapid filling
  3. reduced filling
190
Q

4 events that occur between Q wave & end of T wave

A
  1. rapid ventricular ejection
  2. LV systole
  3. aortic valve opens
  4. stroke volume
191
Q

valves open/closed during ventricular ejection

A
  • mitral closed
  • aortic open
192
Q

what causes first heart sound

A

during isovolumetric contraction, LV pressure > LA pressure and mitral valve closes

193
Q

phases of cardiac cycle that occur during systole

A
  1. isovolumetric contraction
  2. ventricular ejection
194
Q

phases of cardiac cycle that occur during diastole

A
  1. isovolumetric ventricular relaxation
  2. rapid ventricular filling
  3. reduced ventricular filling (diastasis)
  4. atrial systole
195
Q

what causes aortic valve to open during ventricular ejecion

A

LV pressure > aortic pressure

196
Q

during what phase of the cardiac cycle is SV ejected into aorta

A

ventricular ejection

197
Q

when is most SV ejected from LV

A

first 1/3 of systole

198
Q

what causes the 2nd heart sound

A

aortic pressure > LV pressure, aortic valve closes

199
Q

what happens to LV pressure and volume during isometric ventricular relaxation

A

LV pressure decreases, volume constant

200
Q

what does the dicrotic notch represent

A

onset of aortic valve closure causes a short period of retrograde flow from aorta towards valve, followed by complete termination of retrograde flow upon complete valve closure

201
Q

required to pump Ca2+ back into sarcoplasmic reticulum

A

ATP

202
Q

what causes the mitral valve to open

A

LA pressure > LV pressure

203
Q

during what parts of cardiac cycle is mitral valve open

A
  • rapid ventricular filling
  • reduced ventricular filling
  • atrial systole
204
Q

when does 80% of LV filling occur

A

during ventricular filling

205
Q

what contributes to last 20% of LV filling

A

atrial kick

206
Q

the end of atrial systole correlates with:

A

EDV

207
Q

what does height measure in a cardiac pressure volume loop

A

ventricular pressure

208
Q

what does width measure in a cardiac pressure volume loop

A

ventricular volume

209
Q

what do corners measure in a cardiac pressure volume loop

A

where valves open & close

210
Q

what does net external work output measure in a cardiac pressure volume loop

A

myocardial work

211
Q

what 2 events measured by pressure volume loop occur in systole

A

isovolumetric contraction
ejection

212
Q

phases of ventricular pressure volume loop

A
  1. ventricular filling (diastole)
  2. isovolumetric contraction (systole)
  3. ventricular ejection (systole)
  4. isovolumetric contraction (diastole)
  5. ejection
  6. isovolumetric relaxation
213
Q

normal LV volume and pressure at the beginning of diastole

A

volume ~50 mL (ESV)
pressure 2-3 mmHg

214
Q

net gain during ventricular filling

A

70 mL

215
Q

which is greater during isovolumetric contraction: LV pressure or LA pressure?

A

LV

216
Q

which is greater during ventricular ejection: LV pressure or aortic pressure

A

LV

217
Q

when are DBP and SBP measured via AL waveform

A

DBP when aortic valve opens
SBP at peak of ejection curve

218
Q

which is greater during period of isovolumetric relaxation: aortic pressure or LV pressure

A

aortic

219
Q

what is ejection fraction

A

percentage of how much blood is pumped by the heart during each beat

220
Q

EF values:
- normal
- mild dysfunction
- moderate dysfunction
- severe dysfunction

A
  • normal > 50%
  • mild dysfunction 41-49%
  • moderate 26-40%
  • severe < 25%
221
Q

what is external work

A

amount of work the ventricle must do to eject SV

222
Q

how is external work estimated

A

multiply SV x mean aortic pressure

223
Q

2 factors that increase workload of heart

A
  • ventricle accepts increased volume
  • ventricle has to generate more pressure to open aortic valve
224
Q

what happens to pressure volume loop with increased or decreased preload

A
  • increased: gets wider but returns to original ESV
  • decreased: gets narrower but returns to original ESV
225
Q

what happens to ESV with increased contractility

A

decreases

226
Q

what happens to pressure volume loop with increased contractility

A

loop gets wider, taller, & shifts to left

227
Q

what happens to pressure-volume loop with decreased contractility

A

loop gets narrower, shorter, shifts to right

228
Q

pressure volume loop with increased afterload

A

loop gets narrower, taller, and shifts ESV to the right

229
Q

pressure volume loop with decreased afterload

A

loop gets wider, shorter, shifts ESV to the left

230
Q

where do LCA & RCA arise from

A

aortic root (sinus of Valsalva)

231
Q

where does the left coronary artery emerge from

A

behind pulmonary trunk, divides into LAD and circumflex arteries

232
Q

what artery divides to form LCA & circumflex arteries

A

left coronary

233
Q

what artery perfuses the anterolateral and apical walls of LV and anterior 2/3 of interventricular septum

A

left anterior descending artery

234
Q

what does the circumflex artery supply

A

LA and lateral/posterior walls of LV

235
Q

what perfuses the RA, RV, interarterial septum, and posterior 1/3 of interventricular septum

A

right coronary

236
Q

perfuses inferior wall of LV

A

posterior descending artery
(RCA)

237
Q

the origin of which vessel defines coronary dominance

A

posterior descending artery

238
Q

what gives rise to posterior descending artery in 70-80% of patients

A

RCA (right dominance)

239
Q

what is it called if the circumflex artery gives rise to the posterior descending artery

A

left dominance

240
Q

what is it called when the RCA supplies the PDA

A

co-dominance

241
Q

where does SA node receive blood supply from in ~70% of patient?

where is it received from in remaining population?

A

RCA

circumflex

242
Q

where does the AV node receive blood supply from in ~80% of patients

A

RCA

243
Q

what perfuses the bundle of His in ~75% of patients

A

LCA

244
Q

what almost exclusively supplies the right and left bundle branches

A

LCA

245
Q

4 main components of coronary venous circulation

which coronary artery do they run along

A
  1. great cardiac vein (LAD)
  2. middle cardiac vein (PDA)
  3. anterior cardiac vein (RCA)
  4. coronary sinus
246
Q

where is the coronary sinus located

A

posterior aspect of RA just superior to tricuspid

247
Q

where does blood returning to coronary circulation from LV drain?

A

coronary sinus

248
Q

what is cannulated to admin retrograde cardioplegia during CPB

A

coronary sinus

249
Q

how does blood returning from RV empty directly into RA

A

anterior cardiac veins carry bypass coronary sinus and go directly to RA

250
Q

small amount of blood empties directly into all 4 cardiac chambers via:

A

thebesian veins

251
Q

how does adenosine affect coronaries

A

causes vasodilation

252
Q

how does hypocapnia affect coronaries

A

causes vasoconstriction

253
Q

what 2 pressures determine coronary perfusion pressure

A

aortic DBP - LVEDP

254
Q

3 epicardial vessels

A
  1. RCA
  2. LAD
  3. CxA
255
Q

what provides majority of coronary vascular resistance

A

coronary arterioles

256
Q

how does muscarinic stimulation affect coronaries

A

cause coronary vasodilation

257
Q

how does histamine-2 activation affect coronary circulation

A

causes coronary vasodilation

258
Q

how does histamine-1 activation affect coronary circulation

A

causes coronary vasoconstriction

259
Q

which myocardial arterial bed is most susceptible to ischemia

A

endocardial blood vessels of the myocardium

260
Q

what area of the LV does lead I monitor

A

lateral

261
Q

biploar leads & what they monitor

A

I - lateral LV (circumflex artery)
II - inferior LV (RCA)
III - inferior LV (RCA)

262
Q

limb leads and what they monitor

A

aVR
aVL - lateral LV (circumflex artery)
aVF - inferior LV (RCA)

263
Q

precordial leads and what they monitor

A

V1 - septum (LAD)
V2 - septum (LAD)
V3 - anterior (LAD)
V4 - anterior (LAD)
V5 - lateral (circumflex)
V6 - lateral (circumflex)

264
Q

best TEE view for diagnosing LV ischemia

2nd best view?

A

midpapillary muscle level in short axis

2nd - apical segment in short axis

265
Q

supplies oxygenated blood to the myocardium

A

left and right coronaries

266
Q

normal coronary blood flow

A

225-250 mL/min or 4-7% of CO

267
Q

myocardial O2 consumption and extraction ratio at rest

A

8-10 mL/min/100g with extraction ratio of ~70%

268
Q

coronary blood flow =

A

coronary perfusion pressure / coronary vascular resistance

269
Q

coronary blood flow is autoregulated between at what MAP?

A

between ~60-140 mmHg

270
Q

autoregulation of coronary flow is a net effect of what 3 things

A
  1. local metabolism
  2. myogenic response
  3. ANS
271
Q

what is coronary blood flow dependent on at a MAP < 60 or > 140

A

coronary perfusion pressure

272
Q

how do coronary vascular resistance or LVEDP affect coronary blood flow

A

anything that increases resistance or LVEDP can decrease coronary blood flow

273
Q

most important determinant of coronary vessel diameter

A

local metabolism

274
Q

byproduct of ATP metabolism & potent coronary vasodilator

A

adenosine

275
Q

how does the coronary endothelium react to increased MvO2

A
  • releases adenosine and a variety of other vasodilators (NO, PGs, hydrogen, K+, CO2) to increase blood flow
276
Q

how does vasodilation affect coronary perfusion

A

increases

277
Q

refers to a vessel’s innate ability to maintain a constant vessel diameter

A

myogenic response

278
Q

myogenic response when coronary vessel diameter increases

A

tendency to contract

279
Q

myogenic response to coronary vessel diameter decrease

A

tendency to dilate

280
Q

times when ANS effects prevail over products of local metabolism to affect coronary vascular tone

A

Prinzmetal angina (vasospastic myocardial ischemia) - overactive coronary alpha receptors can cause intense chest pain at rest

281
Q

how does endocardial beta-2 stimulation affect the coronaries

A
  • increases cAMP
  • decreases MLCK sensitivity to Ca2+
  • results in coronary vasodilation
282
Q

what is the difference between coronary blood flow at rest and maximal dilation

A

coronary reserve

283
Q

allows coronary flow to increase in times of HD stress or exercise

A

coronary reserve

284
Q

coronary reserve in patients with atherosclerotic vessels and increased O2 demand

A

vessels may be maximally dilated at rest and unable to dilate further

decreased coronary reserve

285
Q

what happens to flow through LCA during ventricular systole

A

greatly diminished

286
Q

what happens to flow through RCA throughout cardiac cycle

A

remains relatively constant

287
Q

what happens to endocardial vessels during myocardial contraction

A

dramatically reduced flow during systole d/t mass of LV

288
Q

why can’t the RV occlude it’s blood supply during systole

A

doesn’t generate a high enough pressure

289
Q

myocardial O2 consumption at rest

A

consumes ~70% of the O2 delivered to it

290
Q

normal coronary sinus O2 sat

A

~30%

291
Q

what must happen to satisfy increased myocardial O2 demand

A
  • coronary blood flow and/or CaO2 must increase
  • heart can’t meaningfully increase its extraction ratio when O2 demand increases
292
Q

contributes to perception of chest pain during ischemia

A

lactic acid production (r/t anaerobic metabolism)

293
Q

4 things that decrease coronary blood flow and in turn decrease myocardial O2 supply

A
  • tachycardia
  • decreased aortic pressure
  • decreased vessel diameter (spasm, hypocapnia)
  • increased LVEDP
294
Q

2 things that decrease CaO2 and myocardial O2 delivery

A
  1. hypoxemia
  2. anemia
295
Q

2 things that cause decreased O2 extraction and myocardial O2 delivery

A
  • L shift of hgb dissociation curve (decreased P50)
  • decreased capillary density
296
Q

how does increased HR affect myocardial O2 supply and demand

A

decreases O2 supply while increasing demand

297
Q

how does EDV affect myocardial O2 demand

A

decreased EDV reduces wall stress and decreases demand

298
Q

how does aortic DBP affect myocardial O2 supply

A

decreased aortic DBP = decreased coronary perfusion pressure = decreased O2 supply

299
Q

3 circumstances that affect both sides of the myocardial O2 delivery/demand equation

A
  • changes in HR
  • aortic DBP
  • preload
300
Q

when is the LV best perfused

A

during diastolic filling time

301
Q

how does diastolic filling time affect myocardial O2 supply

A

shorter time = less time to deliver O2 to LV = decreased supply

302
Q

usually unaffected by tachycardia, well-perfused throughout cardiac cycle

A

RV

303
Q

how does increased aortic DBP affect myocardial O2 supply

A

increases pressure that perfuses coronaries and increases supply

304
Q

how does increased aortic DBP increase both myocardial o2 supply and demand

A
  • supply: increases pressure that perfuses coronaries
  • demand: increases wall tension and afterload
305
Q

how does increased preload affect myocardial supply and demand

A
  • supply: increased EDV = dec coronary perfusion pressure = dec supply; increased LVEDP decreases coronary perfusion pressure and decreases supply
  • demand: increased wall stress = increased demand
306
Q

when do most perioperative MIs occur

A

24-48 hours following surgery

307
Q

what is regulation of vascular smooth muscle tone dependent on?

A

successful integration of ANS, RAAS, local metabolism, myogenic response

308
Q

which electrolyte plays a critical role in regulation of peripheral vessel diameter

A

calcium

309
Q

as a general rule, how does calcium affect vascular smooth muscle tone

A

increased calcium = vasoconstriction

decreased calcium = vasodilation

310
Q

3 important pathways that affect intracellular calcium

A
  1. G-protein cAMP pathway (vasodilation)
  2. NO cGMP pathway (vasodilation)
  3. PLC pathway (vasoconstriction)
311
Q

how does the G-protein cAMP pathway affect vascular smooth muscle tone

A
  • in vascular muscle cells, increased PKA = decreased intracellular calcium
  • results in vasodilation
312
Q

how does PKA affect excitation-contraction coupling

A
  • inhibits voltage gated calcium channels in sarcolemma
  • inhibits calcium release from SR
  • reduces sensitivity of myofilaments to calcium
  • facilitates calcium reuptake into SR via SERCA2 pump
313
Q

things that decrease NO production

A
  • ACh
  • substance P
  • bradykinin
  • serotonin
  • VIP
  • thrombin
  • shear stress
314
Q

6 steps in NO cGMP pathway leading to vasodilation

A
  1. NOS catalyzes conversion of L-arginine to NO
  2. NO diffuses from endothelium to smooth muscle
  3. NO activates GC
  4. GC converts GTP to cGMP
  5. inc. cGMP reduces intracellular calcium and causes smooth muscle relaxation
  6. PDE5 deactivates cGMP to guanosine monophosplate
315
Q

activators of PLC pathway

A
  • phenylephrine
  • NE
  • AT2
  • endothelin-1
316
Q

how does angiotensin II receptor activation lead to vasoconstriction

A

Gq G-protein stimulated = PLC = IP3 & DAG = increased calcium = vasoconstriction

317
Q

PLC activation increases production of what 2 second messengers

A

IP3 & DAG

318
Q

effects of increased IP3 & DAG production in vascular smooth muscle

A
  • IP3: augments calcium release from SR
  • DAG: activates PKC
  • opens voltage-gated calcium channels in sarcolemma
  • increases calcium influx
319
Q

how does iNO affect vascular smooth muscle

A

increases cGMP = reduced intracellular calcium = pulmonary vasodilation

decreased PVR, decreased RV afterload

320
Q

inactivates iNO

A

hemoglobin

321
Q

why doesn’t iNO cause hypotension

A

inactivated before entering systemic circulation

322
Q

phenylephrine stimulates what effector to ultimately cause vasoconstriction

A

PKA

323
Q

in which phase of ventricular AP is conductance greatest for:
- Cl-
- K+
- Na+
- Ca2+

A
  • Na+ conductance greatest in phase 0
  • Cl- conductance greatest in phase 1
  • Ca2+ conductance greatest in phase 2
  • K+ conductance greatest in phase 3
324
Q

3 things that cause SA node to increase firing rate

A
  1. increased slope of spontaneous phase 4 depolarization
  2. TP more negative
  3. RMP more positive
325
Q

what causes SR to release calcium

A

when calcium stimulates RyR2 receptor

326
Q

what is calcium-induced-calcium release

A

calcium activates RyR2 receptor, which causes large quantities of calcium to be released from SR

327
Q

variables to describe x axis of frank starling curve

A

Filling pressures or EDV
- filling pressures: CVP, PAD, PAOP, LAP, LVEDP
- EDV: RVEDV, LVEDV

328
Q

variables to describe y axis of frank starling curve

A

ventricular output:
- CO
- SV
- LVSW
- RVSW

329
Q

2 conditions that set afterload proximal to systemic circulation

A

aortic stenosis
coarctation of aorta

330
Q

which region of the heart is most susceptible to ischemia? why?

A

LV subendocardium

best perfused during diastole
- as aortic pressure inc. LV tissue compresses its own blood supply
- compression + decreased coronary flow during systole = increased coronary vascular resistance, predisposed to ischemia

331
Q

how does PNS stimulation affect HR

A

slows HR via increased K conductance (hyperpolarizes SA node)

332
Q

how much of CO does the myocardium receive at rest?

A

5% (~225 mL/min)

333
Q

most potent vasodilator released by cardiac myocytes

A

adenosine

334
Q

how does increased preload affect coronary O2 supply and demand

A

increased demand
decreased supply

decreases the supply of oxygen to the myocardium by increasing LVEDV, which in turn decreases CPP.

334
Q

how does increased preload affect coronary O2 suply and demand

A

increased demand
decreased supply

decreases the supply of oxygen to the myocardium by increasing
LVEDV, which in turn decreases CPP.

335
Q

how does increased preload affect coronary O2 suply and demand

A

increased demand
decreased supply

decreases the supply of oxygen to the myocardium by increasing
LVEDV, which in turn decreases CPP.

APEX (54 decks)

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