CV Anatomy modules 1-9 Flashcards

(127 cards)

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
The difference in these 2 values determine the ability of a cell to depolarize
Difference in RMP and TP
26
When is depolarization easier to achieve
When RMP is closer to TP
27
When is depolarization harder to achieve
When RMP is further from TP
28
What purpose does the Na/K ATPase serve in excitable tissue
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
29
What type of channel is the Na/K ATPase
An active transport channel requiring ATP for energy
30
How does severely elevated potassium affect the heart
It inactivates the Na+ channels and they arrest in their closed-inactive state Cells are unable to repolarize
31
Describe the 5 phases of the myocyte action potential
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
32
How does the cardiac myocyte AP differ from the neuron AP
The myocyte AP has a plateau phase where depolarization is prolonged This allows for contraction
33
Which ions move across the cell membrane during phase 1 (initial repolarization) and how
Na+ channels inactivated K+ out via Ito channels Cl- in via Icl channels
34
Which ions move across the cell membrane during phase 2 (plateau) and how
Ca++ in, via slow voltage-gated Ca++ channels (Ica) Na+ channels inactive state K+ out
35
Which ions move across the cell membrane during phase 3 (final repolarization) and how
K+ out via delayed rectifiers (Ik) | Ca+ in briefly but slow Ca++ channels become deactivated
36
Which ions move across the cell membrane during phase 4 (resting phase) and how
K+ out via leak channels | Na+ removed, K+ replaced via Na/K-ATPase
37
Which ions move across the cell membrane during phase 0 (depolarization) and how
Na+ in via fast voltage-gated Na+ channels (Ina)
38
What makes up the cardiac conduction system, in order from start to finish
SA node -> internodal tracts -> AV node -> bundle of His -> left/right bundle branches -> Purkinje fibers
39
What determines the HR
The intrinsic firing of the SA node, the rate of phase 4 spontaneous depolarization, and autonomic tone
40
How does volatile anesthetics affect SA node automaticity
They depress automaticity explaining why junctional rhythms occur
41
Describe the SA/AV node AP (3 phases)
Phase 4 = spontaneous depolarization; Na+ in (I-f) Ca++ in (T-type) Phase 0 = depolarization; Ca++ (L-type) Phase 3 = repolarization; K+
42
How can we increase HR via the AP phases
Increase the rate of phase 4 spontaneous depolarization | Bring resting membrane potential and threshold potential closer together
43
Which ions move across the cell membrane during SA node phase 4 (spontaneous depolarization) and how
Na+ in, via I-f activated by hyperpolarization | Ca++ in, via T-type channels at -50 mV
44
Which ions move across the cell membrane during SA node phase 0 (depolarization) and how
Ca++ in, via voltage-gated L-type channels
45
Which ions move across the cell membrane during SA node phase 3 (repolarization) and how
K+ out, via open K+ channels and closing Ca++ L-type channels
46
What is the intrinsic firing rate (bpm) for each node SA AV Purkinje fibers
``` SA = 70-80 AV = 40-60 Purkinje = 15-40 ```
47
What CN provides PNS tone to the heart nodes
Vagus nerve (CN 10)- right innervates the SA node, left innervates the AV node
48
What spinal levels provide SNS tone to the heart
T1-T4 via cardiac accelerator fibers
49
What factors can increase heart rate via the AP
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
50
How is phase 4 slope of the SA node AP affected by SNS
The slope is INCREASED because norepinephrine stimulates beta-1 receptors thus increasing Na+ and Ca++ conductance
51
How is phase 4 slope of the SA node AP affected by PNS
The slope is DECREASED because ACh stimulates M2 receptors and slows the HR by increasing K+ conductance Leads to hyperpolarization of SA node
52
``` Normal values for the following CaO2 __ DO2 __ VO2 __ CvO2 __ ```
``` CaO2 = 20 mL/O2/dL DO2 = 1,000 mL/min VO2 = 250 mL/min CvO2 = 15 mL/dL ```
53
What does DO2 tell us
How much O2 is carried in arterial blood and how fast it's being delivered to tissues
54
What is the DO2 equation
CO x [(Hgb x SaO2 x 1.34) + (PaO2 x 0.003)] x10 | or CO x CaO2 x 10
55
What is CaO2
How many grams of O2 are contained in a deciliter of arterial blood
56
What is the CaO2 equation
(Hgb x SaO2 x 1.34) + (PaO2 x 0.003)
57
How much O2 is extracted by the tissues
25%
58
What is VO2
How much O2 is consumed by the tissues
59
What is normal VO2
250 mL/min or 3.5 mL/kg/min
60
What is CvO2
How much O2 is carried in venous blood (15 mL/dL)
61
What portion of the CaO2 equation depicts the amount of O2 carried by hgb
Hgb x SaO2 x 1.34
62
What portion of the CaO2 equation depicts the amount of O2 dissolved in blood
PaO2 x 0.003
63
The amount of O2 dissolved in blood (PaO2) follows what law?
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
What is Henry's law and how does it relate to PaO2
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
How is blood flow related to hematocrit
Inversely proportional. Hct indicates viscosity Increased Hct = decreased BF Decreased Hct = increased BF
66
How is Ohm's law applied to the circulatory system
It describes flow related to pressure and resistance - flow directly proportional to pressure - flow inversely proportional to resistance
67
What is Poiseuille's law
An adaptation of Ohm's law that incorporates vessel diameter, viscosity, and tube length
68
What is best method to impact blood flow described by Poiseuille's law
Increase radius Flow is directly proportional to radius to the 4th power radius increase then flow increase 4 fold
69
What is the primary determinant of vascular resistance
The radius of the arterioles
70
When turbulent flow is present, what may be assessed
Bruit (carotid stenosis) or murmur (valvular heart disease)
71
How is blood viscosity related to Hct and body temperature
Hct - directly proportional | Body temp - inversely proportional
72
What is Ohm's law
Flow = (pressure gradient)/resistance
73
How do the variables of ohm's law correlate with CV hemodynamics
Flow = CO Pressure gradient = MAP-CVP Resistance = SVR
74
What are the components of Poiseuille's equation
Q = flow Top: R = radius dP = AV pressure gradient Bottom: n = viscosity L = length of tube
75
According to Poiseuille's equation, when radius is tripled how much does flow increase
81-time increase of flow
76
What are 3 types of blood flow
Laminar flow Turbulent flow Transitional flow
77
What is laminar flow
Molecules travel in a parallel path through the tube
78
What is turbulent flow
Molecules travel in a non-linear path and will create eddies
79
What is transitional flow
laminar flow along the vessel walls with turbulent flow in the center
80
What are consequences of turbulent blood flow
1. A lot of energy is lost to heat and vibration | 2. Viscosity increases from intermolecular friction
81
How does adding warm saline to PRBCs during transfusion affect flow
Dilution by NS decreases Hct and the increased temperature decreases viscosity
82
Equation for stroke volume when CO and HR are known
CO x (1,000/HR)
83
Equation for EF
[(EDV-ESV)/EDV] x 100
84
Equation for systemic vascular resistance
[(MAP - CVP)/CO] x 80
85
MAP equation when CO, SVR, and CVP are known
[(CO x SVR)/80] + CVP
86
``` Normal hemodynamic values for CO __ SV __ EF __ MAP __ SVR __ PVR __ ```
``` 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
How do cardiac index and stroke volume index compensate for CO and SV respectively
They are divided by BSA
88
How is the Frank-Starling mechanism applied to the heart
It relates ventricular volume to ventricular output
89
Which variables are related by the Frank-Starling mechanism
``` PAOP (ventricular volume) Stroke volume (ventricular output) ```
90
What is the Frank-Starling law
The heart will eject a larger stroke volume if it's filled to a higher volume at the end of diastole
91
What is another word for end-diastolic volume
Preload
92
What are clinical indices of ventricular preload
CVP, PAD, PAOP, LAP, LVEDP, PVEDV, RVEDV
93
What are clinical indices of ventricular output
CO, SV, LV stroke work, RV stroke work
94
How much does atrial contraction contribute to cardiac output
20-30%
95
What are 4 conditions associated with reduced myocardial compliance? What are consequences if A-Fib is present
- Myocardial hypertrophy - Heart failure with preserved EF (diastolic HF) - Fibrosis - Aging HYPOTENSION, because they are dependent on preload
96
How is the tension a sarcomere generates related to contraction
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
What is the definition of preload
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
What are 7 factors that influence preload
``` Blood volume Atrial kick Venous tone Intrapericardial pressure Intrathoracic pressure Body position Valvular regurgitation ```
99
What measures of ventricular filling pressures
CVP, PAD, PAOP, LAP, LVEDP
100
What are measures of end-diastolic volume
RVEDV | LVEDV
101
What can alter ventricular compliance
myocardial ischemia | hypertrophy
102
What are the two measures of ventricular compliance
volume and pressure
103
How does contractility (inotropy) affect ventricular output
At a given preload: increased contractility increases ventricular output decreased contractility reduces ventricular output
104
Which metabolic conditions alter inotropy
Hypoxia (acidosis) Hyperkalemia Hypercapnia
105
What is inotropy
Contractility | The ability of the myocardial sarcomeres to perform work and produce force
106
What are factors that increase inotropy
SNS stimulation Catecholamines Digitalis PDE inhibitors
107
What are factors that decrease contractility
``` Myocardial depression: Myocardial ischemia Severe hypoxia Acidosis Hypercapnia Hyperkalemia Hypocalcemia Volatile anesthetics Propofol Beta-blockers CCBs ```
108
How does hyperkalemia impair contractility
Locks voltage-gated Na channels in their closed-inactive state This prevents cells from depolarizing
109
What role does Ca++ play in the myocardium
Ca++ is a second messenger that plays a role in excitation-contraction coupling
110
How does Ca++ affect contractility
It increases contractility by binding to troponin C, stimulating cross-bridge formation and contractility
111
Where is Ca++ stored inside the myocyte
Inside the sarcoplasmic reticulum bound to calsequestrin
112
How does beta-1 stimulation affect contractility? How?
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
What cardiac effects does beta-1 receptor stimulation have
Positive inotropy = more forceful contraction over shorter time Positive lusitropy = enhanced relaxation between beats
114
Define afterload
The force that the ventricle must overcome to eject its stroke volume
115
Describe the difference in afterload between the left and right ventricles
Left ventricle must overcome a much higher afterload than the right ventricle
116
What measure is used as a surrogate for afterload? Normal value
SVR 800-1500 dynes*sec*cm^-5
117
What determines a portion of afterload
Arteriolar tone aka SVR
118
Aside from arterioles, what conditions can alter afterload
Aortic stenosis hypertrophic cardiomyopathy coarctation of the aorta
119
What other factors, besides SVR, determine afterload (3)
Blood viscosity Blood density Ventricular wall tension
120
What are the variable to measure SVR
[(MAP-CVP)/CO] x 80
121
What are the variable to measure PulmVR
[(MPAP-PAOP)/CO] x 80
122
How is the Law of Laplace applied to the mechanics of afterload
Wall stress = (intraventricular pressure * radius)/ventricular thickness
123
What variables are used when apply the Law of Laplace to afterload effects on myocardial wall stress
Intraventricular pressure = force that pushes the heart apart Wall stress = force that holds the heart together Wall thickness/radius
124
How does wall stress relate to intraventricular press, radius, and myocardial wall thickness
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
How is oxygen consumption affected by myocardial wall stress
Increased stress = increased myocardial O2 consumption | Decreased wall stress improves O2 supply and demand
126
MAP equation
(1/3 x SBP) + (2/3 x DBP) [(CO x SVR)/80] + CVP
127
What effect would be seen on a pressure-volume loop when phenylephrine is given
ESV shifts right | Loop width reduced