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APEX-CV & Respiratory > CV Anatomy modules 10-18 > Flashcards

CV Anatomy modules 10-18 Flashcards

1
Q

When is the mitral valve open and aortic valve closed

A

During:
Rapid ventricular filling
Diastasis
Atrial systole

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2
Q

What valve is open when LA pressure is greater than LV pressure

A

Mitral valve

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3
Q

What valve is open when LV pressure is greater than aortic pressure

A

Aortic valve

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4
Q

What happens to the aortic valve when aortic pressure exceeds LV pressure

A

It closes (producing the second heart sound), then causes retrograde flow from aorta toward aortic valve (Dicrotic notch)

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5
Q

What happens to the mitral valve when LV pressure exceeds LA pressure

A

It closes producing the 1st heart sound

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6
Q 
Identify the status of the mitral valve during each phase of the cardiac cycle:
Atrial systole
Ventricular ejection
Isovolumetric ventricular relaxation
Isovolumetric ventricular contraction
Rapid ventricular filling
A

Atrial systole-MV open
Ventricular ejection-MV closed
Isovolumetric ventricular relaxation-MV closed
Isovolumetric ventricular contraction-MV closed
Rapid ventricular filling-MV open

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7
Q 
Identify the status of the aortic valve during each phase of the cardiac cycle
Atrial systole
Ventricular ejection
Isovolumetric ventricular relaxation
Isovolumetric ventricular contraction
Rapid ventricular filling
A

Atrial systole-AV closed
Ventricular ejection-AV open
Isovolumetric ventricular relaxation-AV closed
Isovolumetric ventricular contraction-AV closed
Rapid ventricular filling-AV closed

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8
Q 
What does each element represent in the cardiac PV loop
Height
Width
Corners
Area of PV loop
A

Height = ventricular pressure
Width = ventricular volume
Corners = where valves open and close
Area of PV loop = myocardial workload

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9
Q

What happens to myocardial external workload if the volume axis widens or the pressure axis increases heaight

A

Each will increase workload

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10
Q 
Determine the severity of cardiac dysfunction based on EF
>50%
41-49%
26-40%
<25%
A 
>50% = normal
41-49% = mild dysfunction
26-40% = moderate dysfunction
<25% = severe dysfunction
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11
Q

What alterations affect the morphology of the cardiac PV loop

A

Preload
Contractility
Afterload

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12
Q

How does preload change the cardiac PV loop

A 
Increased = wider PV loop
Decreased = narrower loop
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13
Q

How does a change in contractility affect the cardiac PV loop

A 
Increased = PV loop is wider, taller, and shifts LEFT
Decreased = PV loop is narrower, shorter, and shifts RIGHT
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14
Q

How do changes to afterload affect the PV loop

A 
Increased = PV loop is narrower, taller, and shifts ESV to right
Decreased = PV loop is wider, shorter, and shifts ESV left
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15
Q

What arteries arise from the LCA

A

Left anterior descending

circumflex arteries

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16
Q

What does the left anterior descending artery perfuse

A

Anterolateral and apical wall of LV

Anterior 2/3 of interventricular septum

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17
Q

Perfusion changes caused by the left anterior descending will be seen in which lead

A

EKG V1-V4

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18
Q

What does the circumflex artery supply?

A

Left atrium

Lateral and posterior walls of ventricle

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19
Q

Perfusion changes caused by the circumflex artery will be seen in which leads

A

Leads I, aVL, V5 - 6

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20
Q

What does the right coronary artery perfuse

A

Right atrium
Right ventricle
Interatrial septum
Posterior third of interventricular septum

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21
Q

Perfusion changes caused by the right coronary artery are seen in which leads

A

Leads II, III, aVF

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22
Q

What does the posterior descending artery perfuse

A

Inferior wall

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23
Q

Where is the coronary sinus

A

The heart’s posterior surface

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24
Q

Where does the coronary sinus return blood

A

To the right atrium

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25
Q

How is the coronary sinus used during bypass

A

It can be cannulated to administer retrograde cardioplegia solution

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26
Q

Describe the unique properties of the Thebesian circulation

A

It returns deoxygenated blood to the left side of the heart

Contributes to small amount of anatomic shunt

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27
Q

When using TEE/TTE, what is the best view for diagnosing myocardial ischemia

A

Midpapillary muscle level in short-axis

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28
Q

Where do the left and right coronary arteries originate

A

The aortic root

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29
Q

How is PDA coronary dominance defined

A

Defined by origin:
right dominance = RCA gives rise to PDA
Left dominance = circumflex
Codominance = RCA and circumflex

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30
Q

What coronary supplies the SA node

A

RCA

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31
Q

The RCA supplies which cardiac node

A

SA node

AV node in 80% pts

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32
Q

What coronary artery supplies the AV node

A

RCA in ~80% of patients

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33
Q

What coronary supplies the Bundle of His

A

LCA in 75% of pts

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34
Q

What nodes does the LCA supply

A

Bundle of His

Left and right bundle branches

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35
Q

What coronary supplies the left and right bundle branches

A

LCA

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36
Q

What are the 3 main coronary veins

A

Great cardiac vein
Middle cardiac vein
Anterior cardiac vein

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37
Q

What blood drains into the coronary sinus

A

Most of the blood returning from the LV

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38
Q

Which veins carry most of the blood returning from the right ventricle

A

Anterior cardiac vein

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39
Q

What type of coronary vessels are the RCA, LAD, and CxA

A

Epicardial vessels

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40
Q

Describe the function of collateral vasculature in the heart

A

They provide redundancy of blood flow to poorly perfused areas

They develop from different branches of the same coronary artery or between 2 different coronary arteries

Single fed vessels are at risk if occlusion develops proximal to collateral branch

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41
Q

Lateral leads

A

I, aVL, V5, V6

42
Q

Inferior leads

A

II, III, aVF

43
Q

Septal leads

44
Q

What is coronary blood flow at rest? What percent of CO?

A

225-250 mL/min

4-7% of CO

45
Q

What are the variables in the equation for coronary blood flow?

A

Coronary BF = (Coronary perfusion pressure)/(Coronary vascular resistance)

46
Q

What range is coronary BF MAP autoregulated?

A

MAP between 60-140 mmHg

47
Q

What is the most important determinant of coronary vessel diameter

A

Local metabolism

48
Q

How does cardiac metabolism impact coronary vessels

A

It affects the coronary vessel diameter

49
Q

What percent of O2 is consumed by myocardium in coronary blood flow

50
Q

Definition = To ensure constant amount of blood flow over a wide range of perfusion pressures

A

Autoregulation

51
Q

What is coronary BF autoregulation?

A

The constant amount of blood flow over a wide range of perfusion pressures

MAP 60-140 mmHg

Allows for constant coronary BF over a wide range of BPs

52
Q

How is coronary BF affected when out of autoregulation range

A

BF is dependent on CPP

53
Q

What is coronary reserve

A

The difference between coronary BF at rest and maximal dilation

Coronary reserve = resting coronary BF - Maximal dilation BF

54
Q

What is the difference between resting coronary BF and coronary BF at maximal dilation

A

Coronary reserve

55
Q

What does coronary reserve allow for during stress

A

Allows CBF to increase in times of hemodynamic stress or exercise

56
Q

Describe coronary reserve in the patient with atherosclerosis

A

When O2 demand increases, atherosclerotic vessels are maximally dilated at rest and can’t dilate further

Patient has DECREASED coronary reserve

57
Q

What is autoregulation of coronary BF affected by

A

Local metabolism
Myogenic response
Autonomic nervous system

58
Q

What metabolic byproducts cause coronary vasodilation

A

Adenosine, a byproduct of ATP metabolism

59
Q

What are some mediators of coronary vasodilation

A 
Nitric oxide
PGs
Hydrogen (decreased pH, increased CO2)
Potassium
CO2
60
Q

What are the effects of vasodilation on coronary blood flow (3)

A
  1. Decreases vascular resistance
  2. Increases coronary perfusion
  3. Flushes out products of metabolism
61
Q

How does hypocarbia affect coronary blood flow

A

It causes vasoconstriction, decreasing CBF

62
Q

What muscarinic mediators cause coronary artery vasodilation

A

Nitric oxide

63
Q

Which receptors lead to coronary artery vasodilation

A

Beta-2
Histamine-2
Muscarinic

64
Q

What receptors lead to coronary artery vasoconstriction

A

Alpha

Histamine-1

65
Q

What 2 pressures determine coronary perfusion pressure

A

CPP = Aortic DBP - LVEDP

66
Q

What 3 responses are responsible for autoregulation of coronary BF

A
  1. Local metabolism
  2. Myogenic response
  3. Autonomic nervous system
67
Q

Why does LCA endocardial vessel flow decrease dramatically during systole

A

LV contraction compresses the endocardial vessels during systole due to the large mass of the LV

68
Q

Describe the coronary flow via the RCA during the cardiac cycle

A

Flow remains relatively constant throughout the cardiac cycle

69
Q

Why is the RV coronary flow more constant versus the LV coronary flow

A

RV has a thinner wall that doesn’t generate high enough pressures to occlude blood supply during systole

70
Q

How does P50 affect myocardial O2 consumption

A

Left shift means less O2 is released to myocardium

Decreases supply

71
Q

How does end-diastolic volume affect myocardial O2 consumption

A

Decreased EDV reduces wall stress

Decreased demand

72
Q

How does heart rate affect myocardial O2 consumption

A

Reduces supply and increases demand

Increased heart rate decreases DIASTOLIC filling time

73
Q

How does aortic diastolic BP affect myocardial O2 consumption

A

Decreased DBP means decreased supply and reduced CPP

74
Q

What 2 components maintain myocardial O2 balance

A

Supply and demand

75
Q

What are 3 determinants of O2 delivery (supply)

A

Coronary BF
CaO2
O2 extraction

76
Q

What are 4 determinants of O2 demand

A

Preload
Afterload
Contractility
Wall stress

77
Q

How is tachycardia detrimental to the ischemic heart?

A

It decreases O2 SUPPLY and increases O2 DEMAND

78
Q

How does afterload affect coronary perfusion pressure

A

it INCREASES CPP

79
Q

When do most perioperative myocardial infarctions occur

A

within 24-48 hours of surgery

80
Q

What is normal coronary sinus O2 saturation?

81
Q

What does the amount of myocardial O2 extraction mean for myocardial O2 delivery/demand

A

The heart cannot meaningfully increase O2 extraction ratio when O2 demand increases

82
Q

What 2 factors must increase to meet myocardial O2 demand

A

Coronary BF or CaO2

83
Q

List factors that increase myocardial O2 demand (7)

A 
Tachycardia
HTN
SNS stimulation
INC wall tension
INC LV EDV
INC afterload
INC contractility
84
Q

List factors that decrease myocardial O2 delivery

A

Decreased coronary flow

  • Tachycardia
  • DEC aortic pressure
  • DEC vessel diameter (hypocapnia, spasm)
  • INC LV EDV

Decreased CaO2

  • Hypoxemia
  • Anemia

Decreased O2 extraction

  • DEC P50 (left shift)
  • DEC capillary density
85
Q

How does tachycardia affect myocardial O2

A

It can decrease supply by
-decreasing diastolic filling time

Increase demand
-increasing cardiac contraction and cycles requires more energy/ATP and O2 utilization

86
Q

How does increased aortic diastolic pressure affect myocardial O2

A

Increased supply

  • It increases coronary artery perfusion
  • INC aortic DBP - LVEDP = INC CPP

Increased demand

  • Increased wall tension to overcome afterload
  • Myocardium requires higher pressures to overcome AV
87
Q

How does increased preload affect myocardial O2

A

Decreased supply
-Increased EDV decreases CPP

Increased demand
-higher preload increases wall stress (pressure)

88
Q

Describe the relationship between nitric oxide and hgb

A

NO is inactivated by hgb, which is why it has a short half-life (5 seconds)
It is inactivated before entering systemic circulation

89
Q

What 4 responses regulate vascular smooth muscle tone

A

Autonomic nervous system
Renin-angiotensin-aldosterone system
Local metabolism
Myogenic response

90
Q

How does Ca++ affect vessel diameter

A

INCREASED CA++ = vasoconstriction

DECREASED Ca++ = vasodilation

91
Q

List the second messenger systems that modulate vascular tone by altering Ca++ concentrations

A 
G-protein cAMP
-Increased cAMP = vasodilation
Nitric oxide cGMP
-Increased cGMP = vasodilation
Phospholipase C
-Increased IP3 and DAG = vasoconstriction
92
Q

Describe the process of the G-protein cAMP pathway to vasodilation

A

Norepi => beta-2 receptor => G-protein => adenyl cyclase => cAMP increase => PKA => decreased Ca++ => vasodilation

93
Q

How does PKA affect excitation-contraction coupling

A

Leads to vasodilation via

  • Inhibition of voltage-gated Ca++ channels in sarcolemma
  • Inhibition of SR release of Ca++ release
  • Myofilament reduced Ca++ sensitivity
  • Ca++ reuptake into SR via SERCA2 pumps facilitated

DECREASES available Ca++ in sarcolemma, from SR, sequesters Ca in SR and decreases myofilament Ca sensitivity

94
Q

What mediators increase nitric oxide production (8)

A 
ACh
Substance P
Bradykinin
Serotonin
Vasoactive intestinal peptide
Thrombin
Shear stress
95
Q

What is the role of NOS in the nitric oxide pathway

A

NOS is an enzyme that catalyzes conversion of L-arginine to NO

96
Q

How does NO travel into smooth muscle

97
Q

What activates guanylate cyclase?

Role of activated guanylate cyclase?

A

nitric oxide

converts guanosine triphosphate to cyclic guanosine monophosphate (cGMP)

98
Q

How does phosphodiesterase (PDE) contribute to vessel diameter

A

It deactivates cGMP to guanosine monophosphate (Ca++ availability increases?)

99
Q

What mediators activated the PLC pathway? The result?

A

Mediators = phenylephrine, norepinephrine, angiotensin 2, endothelin-1

Result = vasoconstriction

100
Q

Describe the PLC pathway to vasoconstriction

A

Angiotensin 2 etc => ATII receptor => Gq G-protein => PLC => IP3, DAG => Increased Ca++ => vasoconstriction

101
Q

What 2 second messengers are activated by PLC

APEX-CV & Respiratory (8 decks)

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