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APEX-CV & Respiratory > CV Anatomy modules 1-9 > Flashcards

CV Anatomy modules 1-9 Flashcards

1
Q

What is resting membrane potential of cardiac myocytes

A

-90 mV

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2
Q

How does potassium level affect resting membrane potential of the myocyte

A

hypokalemia = DECREASES RMP (more negative)
-Resistant to depolarization

HYPERkalemia = INCREASES RMP (less negative)
-Depolarizes easier

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3
Q

How much mitochondria do myocytes contain compared to skeletal myocytes

A

MORE mitochondria

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4
Q

What ion regulates resting membrane potential of myocyte

A

Potassium

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5
Q

What is the normal threshold potential of the myocyte

A

-70 mV

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6
Q

What ion regulates threshold potential

A

Calcium

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7
Q

How does calcium level affect threshold potential

A

HYPOcalcemia = DECREASE TP (more negative)
-Easier depolarization

HYPERcalcemia = INCREASES TP (less negative)
-Resistant to depolarization
-

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8
Q

How is depolarization transmitted in the heart

A

Via gap junctions (NOT t-tubules)

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9
Q

Define automaticity

A

The ability to generate an action potential spontaneously

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10
Q

Define excitability in relation to myocardial cells

A

The ability to respond to an electrical stimulus by depolarizing and firing an AP

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11
Q

Define resting membrane potential

A

The difference in electrical potential between the inside and outside of the cell

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12
Q

Define threshold potential

A

It’s the voltage change that must occur to initiate depolarization

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13
Q

Define depolarization

A

It’s the movement of a cell’s membrane potential to a more positive value

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14
Q

Define repolarization

A

It’s the return of a cell’s membrane potential towards a more negative value after depolarization

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15
Q

What is the role of the Na/K ATPase in excitable tissue

A

To restore the ionic balance towards resting membrane potential

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16
Q

What properties make cardiac myocytes unique

A

They have properties of both skeletal and neural tissue
NEURAL properties:
-generate a TMP
-propagate an AP

SKELETAL m properties:
-Contain contractile elements arranged in sarcomeres

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17
Q

What properties are unique to cardiac muscle

A

Myocytes are joined end-to-end by specialized junctional complexes called INTERCALATED DISC to form a functional syncytium

INtercalated discs transfer mechanical force and contain low resistance pathways (gap junctions)that spread the AP

Myocytes contain more mitochondria than skeletal muscle and consume more O2 at rest

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18
Q

How much O2 do cardiac myocytes consume at rest

A

8-10 mL O2/100 g/min

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19
Q 
Is the equilibrium potential for each ion positive or negative in the ECF
K
Ca
Na
Cl
A 
K = negative (-94)
Ca = positive (+132)
Na =  positive (+60)
Cl = negative (-97)
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20
Q

Inotropy definition

A

The force of myocardial contraction during systole

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21
Q

Chronotropy definition

A

heart rate

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22
Q

Dromotropy definition

A

conduction velocity through heart

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23
Q

Lusitropy

A

rate of myocardial relaxation during diastole

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24
Q

What 3 things determine the resting membrane potential

A
  1. Chemical force (concentration gradient)
  2. Electrostatic counterforce
  3. Na/K ATPase
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25
Q

The difference in these 2 values determine the ability of a cell to depolarize

A

Difference in RMP and TP

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26
Q

When is depolarization easier to achieve

A

When RMP is closer to TP

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27
Q

When is depolarization harder to achieve

A

When RMP is further from TP

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28
Q

What purpose does the Na/K ATPase serve in excitable tissue

A

Restoring ionic balance toward resting membrane potential

  • By removing Na+ that enters the cell during depolarization
  • Returns K+ that has left the cell during repolarization
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29
Q

What type of channel is the Na/K ATPase

A

An active transport channel requiring ATP for energy

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30
Q

How does severely elevated potassium affect the heart

A

It inactivates the Na+ channels and they arrest in their closed-inactive state
Cells are unable to repolarize

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31
Q

Describe the 5 phases of the myocyte action potential

A

Phase 0 = depolarization; Na+ in
Phase 1 = initial repolarization; Cl- in, K+ out
Phase 2 = plateau; Ca++ in, K+ out
Phase 3 = repolarization; K+ out
Phase 4 = maintenance of TMP; K+ out, Na/K-ATPase function

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32
Q

How does the cardiac myocyte AP differ from the neuron AP

A

The myocyte AP has a plateau phase where depolarization is prolonged
This allows for contraction

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33
Q

Which ions move across the cell membrane during phase 1 (initial repolarization) and how

A

Na+ channels inactivated
K+ out via Ito channels
Cl- in via Icl channels

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34
Q

Which ions move across the cell membrane during phase 2 (plateau) and how

A

Ca++ in, via slow voltage-gated Ca++ channels (Ica)
Na+ channels inactive state
K+ out

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35
Q

Which ions move across the cell membrane during phase 3 (final repolarization) and how

A

K+ out via delayed rectifiers (Ik)

Ca+ in briefly but slow Ca++ channels become deactivated

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36
Q

Which ions move across the cell membrane during phase 4 (resting phase) and how

A

K+ out via leak channels

Na+ removed, K+ replaced via Na/K-ATPase

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37
Q

Which ions move across the cell membrane during phase 0 (depolarization) and how

A

Na+ in via fast voltage-gated Na+ channels (Ina)

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38
Q

What makes up the cardiac conduction system, in order from start to finish

A

SA node -> internodal tracts -> AV node -> bundle of His -> left/right bundle branches -> Purkinje fibers

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39
Q

What determines the HR

A

The intrinsic firing of the SA node, the rate of phase 4 spontaneous depolarization, and autonomic tone

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40
Q

How does volatile anesthetics affect SA node automaticity

A

They depress automaticity explaining why junctional rhythms occur

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41
Q

Describe the SA/AV node AP (3 phases)

A

Phase 4 = spontaneous depolarization; Na+ in (I-f) Ca++ in (T-type)
Phase 0 = depolarization; Ca++ (L-type)
Phase 3 = repolarization; K+

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42
Q

How can we increase HR via the AP phases

A

Increase the rate of phase 4 spontaneous depolarization

Bring resting membrane potential and threshold potential closer together

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43
Q

Which ions move across the cell membrane during SA node phase 4 (spontaneous depolarization) and how

A

Na+ in, via I-f activated by hyperpolarization

Ca++ in, via T-type channels at -50 mV

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44
Q

Which ions move across the cell membrane during SA node phase 0 (depolarization) and how

A

Ca++ in, via voltage-gated L-type channels

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45
Q

Which ions move across the cell membrane during SA node phase 3 (repolarization) and how

A

K+ out, via open K+ channels and closing Ca++ L-type channels

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46
Q

What is the intrinsic firing rate (bpm) for each node
SA
AV
Purkinje fibers

A 
SA = 70-80
AV = 40-60
Purkinje = 15-40
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47
Q

What CN provides PNS tone to the heart nodes

A

Vagus nerve (CN 10)- right innervates the SA node, left innervates the AV node

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48
Q

What spinal levels provide SNS tone to the heart

A

T1-T4 via cardiac accelerator fibers

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49
Q

What factors can increase heart rate via the AP

A
  1. The slope of phase 4 depolarization increases
  2. The TP becomes more negative and shortens the distance between RMP and TP
  3. The RMP becomes less negative and shortens the distance between RMP and TP
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50
Q

How is phase 4 slope of the SA node AP affected by SNS

A

The slope is INCREASED because norepinephrine stimulates beta-1 receptors thus increasing Na+ and Ca++ conductance

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51
Q

How is phase 4 slope of the SA node AP affected by PNS

A

The slope is DECREASED because ACh stimulates M2 receptors and slows the HR by increasing K+ conductance
Leads to hyperpolarization of SA node

52
Q 
Normal values for the following
CaO2 \_\_
DO2 \_\_ 
VO2 \_\_
CvO2 \_\_
A 
CaO2 = 20 mL/O2/dL
DO2 = 1,000 mL/min
VO2 = 250 mL/min
CvO2 = 15 mL/dL
53
Q

What does DO2 tell us

A

How much O2 is carried in arterial blood and how fast it’s being delivered to tissues

54
Q

What is the DO2 equation

A

CO x [(Hgb x SaO2 x 1.34) + (PaO2 x 0.003)] x10

or CO x CaO2 x 10

55
Q

What is CaO2

A

How many grams of O2 are contained in a deciliter of arterial blood

56
Q

What is the CaO2 equation

A

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

57
Q

How much O2 is extracted by the tissues

58
Q

What is VO2

A

How much O2 is consumed by the tissues

59
Q

What is normal VO2

A

250 mL/min or 3.5 mL/kg/min

60
Q

What is CvO2

A

How much O2 is carried in venous blood (15 mL/dL)

61
Q

What portion of the CaO2 equation depicts the amount of O2 carried by hgb

A

Hgb x SaO2 x 1.34

62
Q

What portion of the CaO2 equation depicts the amount of O2 dissolved in blood

A

PaO2 x 0.003

63
Q

The amount of O2 dissolved in blood (PaO2) follows what law?

A

Henry’s law
At a constant temperature, the amount of gas that dissolves in solution is directly proportional to the partial pressure of that gas

64
Q

What is Henry’s law and how does it relate to PaO2

A

At a constant temperature, the amount of gas that dissolves in solution is directly proportional to the partial pressure of that gas

Dissolved O2 in blood follows henry’s law

65
Q

How is blood flow related to hematocrit

A

Inversely proportional. Hct indicates viscosity
Increased Hct = decreased BF
Decreased Hct = increased BF

66
Q

How is Ohm’s law applied to the circulatory system

A

It describes flow related to pressure and resistance

  • flow directly proportional to pressure
  • flow inversely proportional to resistance
67
Q

What is Poiseuille’s law

A

An adaptation of Ohm’s law that incorporates vessel diameter, viscosity, and tube length

68
Q

What is best method to impact blood flow described by Poiseuille’s law

A

Increase radius

Flow is directly proportional to radius to the 4th power

radius increase then flow increase 4 fold

69
Q

What is the primary determinant of vascular resistance

A

The radius of the arterioles

70
Q

When turbulent flow is present, what may be assessed

A

Bruit (carotid stenosis) or murmur (valvular heart disease)

71
Q

How is blood viscosity related to Hct and body temperature

A

Hct - directly proportional

Body temp - inversely proportional

72
Q

What is Ohm’s law

A

Flow = (pressure gradient)/resistance

73
Q

How do the variables of ohm’s law correlate with CV hemodynamics

A

Flow = CO
Pressure gradient = MAP-CVP
Resistance = SVR

74
Q

What are the components of Poiseuille’s equation

A

Q = flow
Top:
R = radius
dP = AV pressure gradient

Bottom:
n = viscosity
L = length of tube

75
Q

According to Poiseuille’s equation, when radius is tripled how much does flow increase

A

81-time increase of flow

76
Q

What are 3 types of blood flow

A

Laminar flow
Turbulent flow
Transitional flow

77
Q

What is laminar flow

A

Molecules travel in a parallel path through the tube

78
Q

What is turbulent flow

A

Molecules travel in a non-linear path and will create eddies

79
Q

What is transitional flow

A

laminar flow along the vessel walls with turbulent flow in the center

80
Q

What are consequences of turbulent blood flow

A
  1. A lot of energy is lost to heat and vibration

2. Viscosity increases from intermolecular friction

81
Q

How does adding warm saline to PRBCs during transfusion affect flow

A

Dilution by NS decreases Hct and the increased temperature decreases viscosity

82
Q

Equation for stroke volume when CO and HR are known

A

CO x (1,000/HR)

83
Q

Equation for EF

A

[(EDV-ESV)/EDV] x 100

84
Q

Equation for systemic vascular resistance

A

[(MAP - CVP)/CO] x 80

85
Q

MAP equation when CO, SVR, and CVP are known

A

[(CO x SVR)/80] + CVP

86
Q 
Normal hemodynamic values for 
CO \_\_
SV \_\_
EF \_\_
MAP \_\_
SVR \_\_ 
PVR \_\_
A 
CO 5-6 L/min
SV 50-100 mL/beat
EF 60-70%
MAP 70-105 mmHg
SVR 800-1,500 dynes*sec*cm^-5
PVR 150-250 dynes*sec*cm^-5
87
Q

How do cardiac index and stroke volume index compensate for CO and SV respectively

A

They are divided by BSA

88
Q

How is the Frank-Starling mechanism applied to the heart

A

It relates ventricular volume to ventricular output

89
Q

Which variables are related by the Frank-Starling mechanism

A 
PAOP (ventricular volume)
Stroke volume (ventricular output)
90
Q

What is the Frank-Starling law

A

The heart will eject a larger stroke volume if it’s filled to a higher volume at the end of diastole

91
Q

What is another word for end-diastolic volume

92
Q

What are clinical indices of ventricular preload

A

CVP, PAD, PAOP, LAP, LVEDP, PVEDV, RVEDV

93
Q

What are clinical indices of ventricular output

A

CO, SV, LV stroke work, RV stroke work

94
Q

How much does atrial contraction contribute to cardiac output

95
Q

What are 4 conditions associated with reduced myocardial compliance?
What are consequences if A-Fib is present

A
  • Myocardial hypertrophy
  • Heart failure with preserved EF (diastolic HF)
  • Fibrosis
  • Aging

HYPOTENSION, because they are dependent on preload

96
Q

How is the tension a sarcomere generates related to contraction

A

The amount of tension each sarcomere can generate is directly r/t the number of cross-bridges that can form before contraction
increased tension = increased contraction (to a point)

97
Q

What is the definition of preload

A

the ventricular wall tension (stretch) at the end of diastole
Or the volume that returns to the heart during diastole which causes end-diastolic tension

98
Q

What are 7 factors that influence preload

A 
Blood volume
Atrial kick
Venous tone
Intrapericardial pressure
Intrathoracic pressure
Body position
Valvular regurgitation
99
Q

What measures of ventricular filling pressures

A

CVP, PAD, PAOP, LAP, LVEDP

100
Q

What are measures of end-diastolic volume

A

RVEDV

LVEDV

101
Q

What can alter ventricular compliance

A

myocardial ischemia

hypertrophy

102
Q

What are the two measures of ventricular compliance

A

volume and pressure

103
Q

How does contractility (inotropy) affect ventricular output

A

At a given preload:
increased contractility increases ventricular output
decreased contractility reduces ventricular output

104
Q

Which metabolic conditions alter inotropy

A

Hypoxia (acidosis)
Hyperkalemia
Hypercapnia

105
Q

What is inotropy

A

Contractility

The ability of the myocardial sarcomeres to perform work and produce force

106
Q

What are factors that increase inotropy

A

SNS stimulation
Catecholamines
Digitalis
PDE inhibitors

107
Q

What are factors that decrease contractility

A 
Myocardial depression:
Myocardial ischemia
Severe hypoxia
Acidosis
Hypercapnia
Hyperkalemia
Hypocalcemia
Volatile anesthetics
Propofol
Beta-blockers
CCBs
108
Q

How does hyperkalemia impair contractility

A

Locks voltage-gated Na channels in their closed-inactive state
This prevents cells from depolarizing

109
Q

What role does Ca++ play in the myocardium

A

Ca++ is a second messenger that plays a role in excitation-contraction coupling

110
Q

How does Ca++ affect contractility

A

It increases contractility by binding to troponin C, stimulating cross-bridge formation and contractility

111
Q

Where is Ca++ stored inside the myocyte

A

Inside the sarcoplasmic reticulum bound to calsequestrin

112
Q

How does beta-1 stimulation affect contractility? How?

A

Stimulation increases contractility

  • Activation of adenylate cyclase converting ATP to cAMP activating PKA.
    1. Activates more L-type Ca++ channels
    2. Stimulates ryanodine 2 receptors to release Ca+
    3. Stimulate SERCA2 pump to increase Ca++ uptake
113
Q

What cardiac effects does beta-1 receptor stimulation have

A

Positive inotropy = more forceful contraction over shorter time
Positive lusitropy = enhanced relaxation between beats

114
Q

Define afterload

A

The force that the ventricle must overcome to eject its stroke volume

115
Q

Describe the difference in afterload between the left and right ventricles

A

Left ventricle must overcome a much higher afterload than the right ventricle

116
Q

What measure is used as a surrogate for afterload? Normal value

A

SVR 800-1500 dynesseccm^-5

117
Q

What determines a portion of afterload

A

Arteriolar tone aka SVR

118
Q

Aside from arterioles, what conditions can alter afterload

A

Aortic stenosis
hypertrophic cardiomyopathy
coarctation of the aorta

119
Q

What other factors, besides SVR, determine afterload (3)

A

Blood viscosity
Blood density
Ventricular wall tension

120
Q

What are the variable to measure SVR

A

[(MAP-CVP)/CO] x 80

121
Q

What are the variable to measure PulmVR

A

[(MPAP-PAOP)/CO] x 80

122
Q

How is the Law of Laplace applied to the mechanics of afterload

A

Wall stress = (intraventricular pressure * radius)/ventricular thickness

123
Q

What variables are used when apply the Law of Laplace to afterload effects on myocardial wall stress

A

Intraventricular pressure = force that pushes the heart apart
Wall stress = force that holds the heart together
Wall thickness/radius

124
Q

How does wall stress relate to intraventricular press, radius, and myocardial wall thickness

A

Directly proportional to intraventricular pressure and radius:
if IVP and radius decrease, so does wall stress

Inversely proportional to wall thickness:
If wall thickness increase, wall stress decreases

125
Q

How is oxygen consumption affected by myocardial wall stress

A

Increased stress = increased myocardial O2 consumption

Decreased wall stress improves O2 supply and demand

126
Q

MAP equation

A

(1/3 x SBP) + (2/3 x DBP)

[(CO x SVR)/80] + CVP

127
Q

What effect would be seen on a pressure-volume loop when phenylephrine is given

A

ESV shifts right

Loop width reduced

APEX-CV & Respiratory (8 decks)

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