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Physiology > CVS > Flashcards

CVS Flashcards

1
Q

What is the primary function of the CVS?

A

To deliver blood to tissues, providing essential nutrient transport to cells for metabolism and removes waste from cells.

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2
Q

What homeostatic functions is the CVS involved in? (4)

A
  1. regulation of arterial pressure 2. deliver regulatory hormones 3. Participates in thermoregulation 4. Adjusts to altered physiologic sates (hemorrhages, exercise, postural changes)
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3
Q

What is the pathway of blood through the heart in relation to the blood vessels?

A

Heart -> Arteries -> arterioles -> Capillary body -> venules -> veins -> Heart

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4
Q

What occurs in the capillaries?

A

Nutrient, waste, fluid exchange

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5
Q

What percentage of circulation is systemic?

A

84%

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6
Q

What percentage of circulation is pulmonary?

A

9%

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7
Q

What percentage of circulation is of the heart?

A

7%

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8
Q

How much of the circulation goes to the venous system?

A

64%

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9
Q

How much of the circulation goes to the arterial system?

A

13%

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10
Q

How much of the circulation goes to the arterioles and capillaries?

A

7%

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11
Q

Which organs receive 25% of the cardiac output?

A

Renal, GI, Skeletal Muscles

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12
Q

Which organs receive 15% of the cardiac output?

A

cerebral

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13
Q

Which organs receive 5% of the cardiac output?

A

Coronary, Skin

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14
Q

What can change the percentages of cardiac output to organs?

A

Tissue demand

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15
Q

The left side of the heart composes which portion of the CVS?

A

Systemic

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16
Q

The right side of the heart composes which portion of the CVS?

A

Pulmonary

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17
Q

What structure connects the two sides of the heart relative to their atria and ventricles?

A

Arterioventricular valves

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18
Q

What direction is the flow of blood through the AV valves?

A

Unidirectional

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19
Q

True/False: The left and right side function simultaneously to pump blood.

A

False, they function in series (Left side -> systemic circulation -> right side -> pulmonary circulation)

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20
Q

What is the term given to the rate at which blood is pumped from either ventricle?

A

Cardiac output

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21
Q

What term is given to the rate at which blood is returned to the atria from the veins?

A

Venous return

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22
Q

True/False: Increasing venous return decreases cardiac output in steady state.

A

False, they are equal so an increase in one leads to an increase in the other.

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23
Q

What structure(s) delivers blood to and from the tissues?

A

Blood vessels

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24
Q

True/false: Blood vessels are a closed system of active conduits.

A

False, Passive conduits

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25
Q

True/False: Resistance of BVs have no effect on blood flow.

A

False, When resistance is altered, flow is altered.

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26
Q

What are the blood vessel types?

A

Arteries, Arterioles, Venules, Veins, capillaries

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27
Q

Which blood vessel type is the largest?

A

Arteries

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28
Q

Which blood vessel type delivers oxygenated blood to the organs?

A

Arteries

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29
Q

Which blood vessel type is the site for nutrient, gas, water, and solute exchange?

A

Capillaries

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30
Q

Which blood vessel type have walls innervated by alpha-adrenergic receptors that allow for contraction?

A

Arterioles and venules

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31
Q

What do the beta-adrenergic receptors that innervate arterioles and venules allow?

A

Dilation

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32
Q

Which blood vessel type is the least elastic?

A

Venous

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33
Q

What are the walls of veins composed of?

A

Endothelium and modest amount of elastin, smooth muscle, and connective tissue

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34
Q

Which blood vessel type receives the highest pressure (stressed volume)?

A

Arteries

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35
Q

Which blood vessel type receives the unstressed volume?

A

Veins

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36
Q

True/False: Veins have the largest capacitance.

A

True.

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37
Q

Where does blood from the lungs travel to?

A

LA

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38
Q

Where does blood go next from the LA?

A

LV

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39
Q

Through what structure does blood pass through to get to the LA?

A

Pulmonary veins

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40
Q

Through what structure does blood flow through to get from the LA to LV?

A

Mitral valve

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41
Q

Where is blood transported following the fill of the LV?

A

Aorta

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42
Q

Through what structure does blood need to pass through to get to the aorta from the LV?

A

Aortic Valve

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43
Q

Where does blood flow from the aorta?

A

Arterial system

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44
Q

Through what structure(s) does the cardiac output distribute blood to the organs?

A

Parallel arteries

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45
Q

Where does blood go travel through to return to the heart?

A

Veins

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46
Q

Venous return pumps blood into what structure?

A

RA

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47
Q

Where does blood travel to following the fill of the RA?

A

RV

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48
Q

Through what structure must blood flow through to go from the RA to RV?

A

Tricuspid Valve

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49
Q

Where does the blood flow go following fill of the RV?

A

Pulmonary arteries

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50
Q

Through what structure must blood flow through to get to the pulmonary arteries from the RV?

A

Pulmonary valve

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51
Q

Where does blood travel after its release from pulmonary valves?

A

Lungs

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52
Q

Where does the blood flow from the lungs next?

A

Back to the heart via pulmonary veins for new cycle to begin

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53
Q

What are the three mechanisms for achieving blood flow change?

A
  1. CO remains constant but blood flow is redistributed 2. CO increases or decreases but distribution percentage is constant. 3. Both are altered (strenuous activity)
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54
Q

What are the principles that govern blood flow?

A

Hemodynamics

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55
Q

What is the velocity of blood flow?

A

The rate of displacement of blood per unit

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56
Q

What is the primary determinant of velocity of blood flow?

A

The size of the diameter

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57
Q

What is the normal cardiac output?

A

5L/min

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58
Q

What is cross sectional area formula?

A

pi x r^2

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59
Q

What is the formula for velocity of blood flow through a vessel?

A

Velocity = Flow/Cross sectional area

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60
Q

Would a small or large blood vessel at a given flow have a greater velocity?

A

Small

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61
Q

What two factors determine blood flow?

A

Pressure difference and vascular resistance

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62
Q

What gives rise to the determining of the relationship between voltage, resistance, and current?

A

Ohm’s law

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63
Q

What is the formula for flow in relation to pressure and resistance?

A

Pressure Difference/Resistance

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64
Q

How would you rearrange the flow formula to find the resistance of a blood vessel?

A

Resistance = Pressure difference/ Flow

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65
Q

What is the term given to the resistance of the entire systemic vasculature?

A

Total Peripheral Resistance

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66
Q

How do you determine total peripheral resistance?

A

TPR = Change in pressure/CO

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67
Q

What is the name of the equation to determine the relationship between resistance, diameter, and viscosity?

A

Poiseuille equation

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68
Q

What is the poiseuille equation?

A

Total resistance (R) = 8 x viscosity X length / pi x r^4

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69
Q

If a radius decreased by half, how much would resistance increase?

A

16-fold (2^4)

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70
Q

Does greater or lower viscosity have higher resistance?

A

greater viscosity

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71
Q

What determines viscosity?

A

Hematocrit

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72
Q

Describe series resistance.

A

BVs within a given organ is supplied by a major artery and drained by a major vein so resistance builds: Total = Rartery+Rarterioles+Rcapillaries+Rvenules+Rvein

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73
Q

Describe parallel resistance.

A

Blood flow among the various major arteries branching off the aorta is a fraction of the total blood flow: = 1/Rtotal = 1/R1 +1/R2+ 1/R3….

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74
Q

What is laminar flow?

A

Smooth, parabolic profile of velocity of blood flow and center of the stream.

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75
Q

What does an irregularity in blood flow due to a defective valve or clot cause?

A

Turbulent flow

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76
Q

What is used to predict whether blood flow will be laminar or turbulent?

A

Reynolds number

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77
Q

What is the formula for Reynolds number?

A

Nr= density of blood x diameter of BV x velocity of BV / viscosity

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78
Q

What value indicated laminar flow? turbulent?

A

<2000, >3000

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79
Q

Turbulent flow causes what to occur in blood pressure?

A

Korotkoff sounds

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80
Q

What can stenosis of BVs causing turbulent flow cause?

A

Audible vibrations = murmur

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81
Q

Ultimately, what happens when narrowing of a BV occurs?

A

decrease diameter = increase velocity = increase Reynolds number

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82
Q

What condition can result in functional murmurs?

A

Anemia (decrease hematocrit)

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83
Q

What does thrombus in a BV cause?

A

(Blood clot in lumen) = narrow diameter = increase velocity = increase reynolds number = turbulence

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84
Q

What does polycthemia do to reynolds number?

A

(increased hematocrit) = increase viscosity = increase resistance (=CO) will be less turbulent

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85
Q

What is the consequence of blood traveling at different velocities within a blood vessels adjacent to others?

A

Shear

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86
Q

Where is shear highest? Lowest?

A

At BV wall, at center of BV

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87
Q

What is the term given for the volume capable of being held at a given pressure?

A

Compliance (capacitance)

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88
Q

What is compliance related to?

A

The distensibility

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89
Q

What is the formula for compliance?

A

C= volume/Pressure

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90
Q

Ultimately, does a higher or lower volume have a greater compliance at a given pressure?

A

Higher

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91
Q

What does changes in compliance result in?

A

Redistribution of blood between the veins and arteries (unstressed and stressed blood)

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92
Q

If compliance decreases, what happens to the ratio of unstressed to stressed volume?

A

Decreases volume = Decreases unstressed volume and increases stressed volume

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93
Q

If compliance increases, what happens to the ratio of unstressed to stressed volume?

A

increases volume = increases unstressed volume and decreases stressed volume

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94
Q

What affects does aging have on BVs?

A

Become stiffer and less distensible, therefore, less compliant

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95
Q

True/False: Blood pressures are equal.

A

False, blood pressures aren’t equal, creating a driving force for blood flow

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96
Q

What is the mean pressure measured in?

A

mm Hg

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97
Q

What are the pressures in the systemic circulation?

A

Aorta, Large arteries, Arterioles, Capillaries, Vena Cava, Right Atrium

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98
Q

What are the pressures in the pulmonary circulation?

A

Pulmonary artery, capillaries, pulmonary vein, left atrium.

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99
Q

Does systemic circulation or pulmonary circulation have higher pressures?

A

Systemic

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100
Q

What is the mean pressure of the aorta?

A

100 mm Hg

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101
Q

What is the mean pressure of the large arteries?

A

100 mm Hg (systole 120, diastole 80)

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102
Q

What is the mean pressure of the arterioles?

A

50 mm Hg

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103
Q

What is the mean pressure of the capillaries of the systemic circulation?

A

20 mm Hg

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104
Q

What is the mean pressure of the vena cava?

A

4 mm Hg

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105
Q

What is the mean pressure of the Right atrium?

A

0-2 mm Hg

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106
Q

What is the mean pressure of the pulmonary artery?

A

15 mm Hg (systole 25, diastole 8)

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107
Q

What is the mean pressure of the capillaries of the pulmonary circulation?

A

10 mm Hg

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108
Q

What is the mean pressure of the of the pulmonary vein?

A

8 mm Hg

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109
Q

What is the mean pressure of the Left atrium?

A

2-5 mm Hg

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110
Q

What exists in the arterial pressure that reflect the activity of the heart?

A

Pulsations/oscillations

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111
Q

What is the lowest arterial pressure measured during a cardiac cycle when no blood is being ejected and ventricles relax?

A

Diastolic pressure

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112
Q

What is the highest arterial pressure measured during a cardiac cycle when the blood is being ejected from the left ventricle?

A

Systolic pressure

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113
Q

What is the blip in the arterial pressure curve produced when the aortic valve closes?

A

Dicrotic notch

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114
Q

Where is the greatest pressure drop and why?

A

Capillaries because of the resistance provided

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115
Q

What is the difference between the systolic pressure and diastolic pressure?

A

Pulse pressure

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116
Q

What are the factors that affect pulse pressure?

A

Stroke volume, arterial compliance

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117
Q

What is stroke volume?

A

the volume of blood ejected from the left ventricle on a single beat

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118
Q

True/False: If all other factors are equal, the magnitude of pulse pressure reflects the stroke volume.

A

True

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119
Q

What is the average pressure completed in a complete cardiac cycle?

A

Mean arterial pressure

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120
Q

What is the formula for finding mean arterial pressure?

A

Diastolic pressure + 1/3 Pulse pressure

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121
Q

Why does damping (decrease of amplitude) of the oscillations other than the large large arteries occur?

A

resistance of blood vessel makes it difficult to transmit pulse pressure and compliance , the more complianr the more volume can be added to it without causing an increase in pressure

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122
Q

What effect does arteriosclerosis have on pressure?

A

Decreases diameter = decreases compliance therefore increasing systolic pressure, pulse pressure, and mean arterial pressure

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123
Q

What affect does aortic stenosis have on pressure?

A

narrows Valve and size of opening = decreases blood ejection = decreased systolic pressure, pulse pressure, and mean arterial pressure

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124
Q

What affect does aortic regurgitation have on pressure?

A

incompetent valve causes back flow and pressure can drop close to zero

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125
Q

What affect does PDA (patient ductus arteriosus) have on pressure?

A

1/2 of blood volume pumped back into aorta causing a decrease in diastolic blood pressure

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126
Q

For the heart to serve as a pump what must be electrically activated and contract?

A

Ventricles

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127
Q

Where does an action potential in the heart generate?

A

SA node

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128
Q

What is the ability of the heart to self excitation?

A

Automaticity

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129
Q

What is the ability of APs to propagate the electrical impulses from one cell to another?

A

Conductivity

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130
Q

What are the two types of cardiac muscle cells?

A

Contractile and conducting

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131
Q

What type of cells make up the atrial and ventricular tissue, functioning as the working cells of the heart?

A

Contractile cells

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132
Q

What type of cells make up the tissues of the SA node, Atrial internodal tracts, AV node, bundle of His, and purkinje system that can spontaneously generate action potentials and generate them over the myocardium?

A

Conducting cells

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133
Q

What structure initiates the action potential?

A

SA node, serving as the pacemaker

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134
Q

Where does the action potential go after leaving the SA node?

A

Atria via atrial internodal tracts to the AV node

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135
Q

What happens to the AP when it arrives the the AV node?

A

Conduction velocity slows to ensure ventricles have sufficient time to fill before activation and contraction

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136
Q

Where does the AP go from the AV node?

A

Rapidly enters the bundle of His to the purkinje system then rapidly to one ventricular muscle cell to the next via low resistance pathways

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137
Q

Where does the AP end?

A

Ventricle

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138
Q

What is normal sinus rhythm?

A

AP generates from the SA node at rate of 60-100 impulses per minute for activation of myocardium to occur in the correct sequence with correct timing and delays

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139
Q

What determines the membrane potential?

A

Conductance/permeability to ions and the concentration gradients for those ions

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140
Q

What will occur if the cardiac muscle has a high conductance/permeability to an ion?

A

That ion will flow down its gradient and will attempt to drive MP toward equilibrium potential

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141
Q

How is the membrane potential expressed in terms of measure and polarity?

A

mVs and intracellular potential expressed relative to extracellular (-85 mV = 85 mV w/ negative cell interior)

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142
Q

What type of ions does the resting membrane potential of cardiac cells favor?

A

K+

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143
Q

Do cardiac cells utilize Na+ K+ ATPase?

A

Yes, to maintain the concentrations

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144
Q

What causes changes in membrane potential?

A

Flow of ions in or out of the cell due to a change in conductance or in electrochemical gradient

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145
Q

What is the potential difference at which there is a net inward current, where upstroke occurs?

A

Threshold potential

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146
Q

What are the characteristics of action potentials on the ventricles, atria, and purkinje system?

A

Have a long duration ( ~150 ms in atria, ~250 ms in ventricles, ~ 350 ms in Purkinje system), Have a stable RMP, and have a plateau (sustained period of depolarization)

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147
Q

What occurs during phase 0 of the action potential in VAPs?

A

Upstroke - rapid depolarization from Na+ influx

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148
Q

What occurs during phase 1 of the action potential in VAPs?

A

Initial repolarization - brief period of repolarization, Na+ inactivation gates close and K+ efflux occurs.

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149
Q

What occurs during phase 2 of the action potential in VAPs?

A

Plateau - long period (150-200 ms) of stable, depolarized MP by a balance of currents due to efflux of Ca2+ (slow inward current)

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150
Q

What occurs during phase 3 of the action potential in VAPs?

A

Repolarization - gradually at the end of phase 2, speeds up here to RMP by decrease of conductance of K+ and Ca2+

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151
Q

What is the final phase of the action potential in VAPs?

A

RMP/Electrical diastole = MP returns to resting levels of ~ -85 mV. MP is stable again and currents are equal.

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152
Q

Describe the major difference in an AP in the SA node vs VAPs?

A

SA node does not have phase 1 (initial repolarization) or 2 (plateau)

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153
Q

What occurs during phase 0 of an AP in SA node?

A

Upstroke, by increase in conductance and inward current of Ca2+ carried by L-type Ca2+ channels

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154
Q

What occurs during phase 3 of an AP in SA node?

A

Repolarization due to an increase in K+ conductance due to electrochemical driving forces = outward current of K+, which depolarizes the membrane

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155
Q

What occurs during phase 4 of an AP in SA node?

A

Spontaneous depolarization/pacemaker potential - ~65 mV, slow depolarization produced by the opening of Na+ channels and inward current occurs. Once brought back to threshold, Ca2+ channels open for upstroke.

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156
Q

What is the firing rate of the SA node?

A

70-80 impulses/min

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157
Q

What is the firing rate of the AV node?

A

40-60 impulses/min

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158
Q

What is the firing rate of the Bundle of His?

A

40 impulses/min

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159
Q

What is the firing rate of purkinje fibers?

A

15-20 impulses/min

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160
Q

What does the rate of the spontaneous depolarization help determine?

A

The heart rate

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161
Q

What effect does ischemia have on cardiac APs?

A

Heart cannot extract O2, so ATP production decrease, decreasing Na+K+ATPase which increases ECF [K+] and ICF [Na+] so the RMP becomes less negative and Na+ channels remain inactivated and lose phase 0 so AP is slower

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162
Q

How do Ca2+ channel blockers affect the AP?

A

L-type channels are inhibited so Ca2+ prevent the release of Ca2+ so inhibits plateau period

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163
Q

What do calcium channel blockers do to blood pressure?

A

Decrease it

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164
Q

What are the examples of calcium channel blockers?

A

Nifedipine, diltiazem, verapamil, amlodipine

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165
Q

What is a latent pacemaker?

A

Other cells have the capacity to take over the spontaneous phase 4 depolarization

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166
Q

What is the term given for the latent pacemakers being suppressed when the SA node controls the HR?

A

Overdrive suppression

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167
Q

Will the heart beat slower or faster when driven by a latent pacemaker?

A

Slower

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168
Q

What is the term given when the latent pacemaker becomes THE pacemaker?

A

Ectopic pacemaker/ectopic focus

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169
Q

What is the speed at which APs are propagated?

A

Conduction velocity

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170
Q

What is the CV of the atria?

A

1 m/s

171
Q

What is the CV of the AV node?

A

0.01-0.05 m/s

172
Q

What is the CV of His-Purkinje?

A

2-4 m/s

173
Q

What is the CV of Ventricle?

A

1 m/s

174
Q

What is the total time it takes for an action potential to spread through the heart?

A

220 ms

175
Q

In what part of the action potential is there a time delay?

A

Through the AV node

176
Q

In normal rhythm, what is the approximate time it takes the AP to get from the SA node (time zero) to the AV node?

A

~60 ms

177
Q

In normal rhythm, what is the approximate time it takes the AP to get through the AV node to the bundle of His?

A

~100 ms = 160 ms

178
Q

In normal rhythm, what is the approximate time it takes the AP to get from the bundle of his to the bundle branches?

A

~10 ms = 170 ms

179
Q

In normal rhythm, what is the approximate time it takes the AP to get from the bundle branches to the Purkinje fibers?

A

~20 ms = 190 ms

180
Q

In normal rhythm, what is the approximate time it takes the AP to get from the purkinje fibers to the ends of the ventricles?

A

~LV: 20 ms = 210 ms, ~RV: 30 ms = 220 ms.

181
Q

What does conduction velocity depend on most?

A

The size of local currents

182
Q

What refractory period is the majority of the duration of AP in which another AP cannot be generated?

A

Absolute

183
Q

What refractory period includes and extends the coverage of the absolute refractory period?

A

Effective Refractory Period

184
Q

What occurs at the end of the ERP?

A

Na+ channels start to recover

185
Q

Can another AP generate during the ERP?

A

It COULD but it would not conduct, meaning there is not enough inward current to move the AP to the next site

186
Q

What refractory period begins at the end of the ERP and continues until the cell membrane has almost fully repolarized?

A

Relative Refractory Period

187
Q

What occurs in the RRP?

A

Na+ channels have recovered to the closed but available state

188
Q

Could a second AP generate in the RRP?

A

It could but it would require a greater-than-normal stimulus

189
Q

What would happen to the second AP if it were to generate in the RRP?

A

will be abnormal in configuration and shortened plateau phase

190
Q

What refractory period follows the RRP while the MP is at ~-75 until it returns back to normal ~-85 mV?

A

Supranormal period

191
Q

Could a second AP generate during the supranormal period?

A

Yes, The cell’s excitability prior to MP makes it easier to fire an AP than if it were at RMP.

192
Q

What parts of the heart receive sympathetic innervation?

A

All parts

193
Q

What parts of the heart receive parasympathetic innervation?

A

Via Vagus nerve stimulated SA and AV nodes, and slight atria

194
Q

What is the term given to the effects of the ANS on heart rate?

A

Chronotropic effects

195
Q

What type of chronotropic effects increase heart rate?

A

Positive chronotropic effects

196
Q

What type of chronotropic effects decrease heart rate?

A

Negative chronotropic effects

197
Q

What type of stimulation mostly effects the increase in heart rate?

A

sympathetic stimulation

198
Q

What type of stimulation mostly effects decreases in heart rate?

A

parasympathetic stimulation

199
Q

Describe the mechanism behind increasing heart rate by sympathetic stimulation.

A

Norepinephrine released by beta1 receptors at the SA node couple with adenylyl cyclase through Gs protein which produces an increase in spontaneous depolarization which increases Heart rate

200
Q

Describe the mechanism behind decreasing heart rate by parasympathetic stimulation.

A

Ach released from PNS fibers activated muscarnic (M2) receptors in SA node couple with Gk which inhibits adenylyl cyclase which decreases the rate of spontaneous depolarization and increases the conductance K-ACH Channels producing outward current of K+ leading to hyperpolarization therefore decreasing heart rate

201
Q

What autonomic effects effect conduction velocity?

A

Dromotropic effects

202
Q

In what part of the heart are dromtropic effects more important?

A

AV nodes which alter the rate at which APs are conducted

203
Q

Which ANS system increases conduction velocity?

A

SNS

204
Q

How does the SNS work to increase conduction velocity?

A

Increases the Ica, which causes upstroke in the AV node which directly increases inward current and CV

205
Q

Which ANS system decreases conduction velocity?

A

PNS

206
Q

How does the PNS work to decrease conduction velocity?

A

Decreases the Ica and increases Ik-ach which decreases the rate of AP conduction

207
Q

What can occur if no production can be conducted at all from overstimulation of the PNS?

A

Heart block

208
Q

What are the effects that alter contractility?

A

Inotropic effects

209
Q

Which inotropic effects increase contractility?

A

Positive

210
Q

Which inotropic effects decrease contractility?

A

Negative

211
Q

What ion is primarily responsible for the changes in contractility?

A

Ca2+, more release = larger inward current = more contractility

212
Q

What type of ANS stimulation have a positive inotropic effect on the myocardium?

A

SNS

213
Q

How does the SNS increase contractility?

A

Beta1 receptors, coupled w/ Gs protein to adenylyl cyclase which leads to the production of cAMP and protein kinase A, and phosphorylates Sarcolemmal Ca2+ channels and Phospholamban (regulates SERCA) to increase contractility.

214
Q

What type of SNS stimulation have a negative inotropic effect on the atria?

A

PNS

215
Q

How does the PNS decrease contractility?

A

Muscarinic receptors coupled with Gk to adenylyl cyclase which is inhibits by Ach decreasing the inward current of Ca2+ during the plateau phase and increasing the Ik-ach shortening the duration of AP and indirectly decreasing the Ca2+ current which produces a decrease in contractility

216
Q

What substances also act as positive inotropic agents?

A

Cardiac glycosides

217
Q

Name a few examples of cardiac glycosides.

A

Digoxin, digitoxin, oubain

218
Q

What are the functions of cardiac glycosides?

A

To treat CHF

219
Q

How do cardiac glycosides increase contractility?

A

By inhibiting the Na+ K+ Pump, increasing the intracellular [Na+] which alters the Na+ gradient the and Ca2+ Na+ exchanger decreasing the amount of Ca2+ released so intracellular [Ca2+] increases producing an increase in tension which increases contractility

220
Q

True/False: As heart rate increases or decreases, contractility increases or decreases the opposite way.

A

False, a decrease in one leads to a decrease in the other and same for increase

221
Q

How would increasing HR increase contractility?

A

Increasing HR increases the AP propagation which will increase the total amount of Ca2+ that enters the cell during the plateau phases which increases tension therefore increasing contractility

222
Q

What type of effect best shows the HR and tension relationship?

A

Staircase Effect/Bowditch staircase/Treppe Staircase

223
Q

What is a measurement of tiny potential differences on the surface of the body that reflect the electrical activity of the heart?

A

Electrocardiogram

224
Q

On an EKG, what does the P wave represent?

A

The depolarization of the atria

225
Q

On an EKG, what does the QRS complex represent?

A

Collectively, Depolarization of the ventricles

226
Q

On an EKG, what does the T wave represent?

A

Repolarization of the ventricles

227
Q

On an EKG, what does the QT interval represent?

A

the time of the first ventricular depolarization to the last

228
Q

On an EKG, what does the ST segment represent?

A

Isoelectric portion of the QT interval that corresponds with the plateau period of ventricular AP

229
Q

How is HR measured?

A

Counting the number of QRS complexes per minute

230
Q

what can occur because of the relationship between HR and refractory periods?

A

Arryhthmias

231
Q

What is bradycardia?

A

Decreased HR

232
Q

What is tachycardia?

A

Increased HR

233
Q

True/False: overall, myocardial contractile machinery is similar to skeletal muscle.

A

True, composed of actin/myosin, sarcomeres, t tubules, etc

234
Q

What does the excitation-contraction coupling in cardiac muscle translate the AP into?

A

Tension

235
Q

Describe the mechanism behind ECC in cardiac muscle.

A
  1. Ap is initiated and depolarization spreads to the cell interior via T-tubules. Plateau period results in an increase in Gca and an inward current flows through dihydropyridine receptors from ECF to ICF. 2. Entry of Ca2+triggers CICR from ryanodine receptors. 3/4. Ca2+ bind to troponin c, tropomyosin moves and actin and myosin cross bridge cycling occurs, producing tension. This continues until Ca2+ levels drop below levels for it to unbind from troponin c. (the magnitude of tension developed is proportional to intracellular [Ca2+], 5. Relaxation occurs when Ca2+ is reaccumulated in SR by SERCA. [Ca2+] falls to resting levels and it dissociated from troponin, actin-myosin interaction is blocked and relaxation occurs.
236
Q

What is the basis for the length-tension relationship?

A

Degree of overlap of thick and thin filaments and the number of possible sites for it to cross bridge

237
Q

In myocardial cells where does maximal tension occur? (Lmax)

A

2.2 microunits

238
Q

What other two things (aside from degree of overlap) alter tension development?

A

Increasing muscle length increases Ca2+ sensitivity of Troponin C AND it increases Ca2+ release from SR.

239
Q

What component of the length-tension relationship corresponds with the LV end-diastolic volume?

A

Length (the length of a muscle fiber just prior to contraction

240
Q

What component of the length-tension relationship corresponds with the pressure developed by the entire LV?

A

Tension

241
Q

Check out ventricular pressure curve ppt!

A

Check out ventricular pressure curve ppt!

242
Q

What is preload for the left ventricular end-diastolic volume?

A

the resting length from which the muscle contracts

243
Q

What is afterload for the left ventricle?

A

Aortic pressure.

244
Q

The velocity of shortening of cardiac muscle is maximal when afterload is _ and velocity of shortening _ as afterload _.

A

zero, decreases, increases

245
Q

What is stroke volume?

A

The amount of blood ejected by the ventricle on each beat.

246
Q

What is the “formula” for stroke voluma?

A

End-diastolic volume - end-systolic volume

247
Q

What is ejection fraction?

A

a fraction of the end-diastolic volume ejected in each stroke volume

248
Q

What is cardiac output?

A

The total volume ejected by ventricle per time unit

249
Q

What is the normal stroke volume?

A

~70 mL

250
Q

What is the normal ejection fraction?

A

55%

251
Q

What is the “formula” for ejection fraction?

A

SV/ End diastolic volume

252
Q

What is the formula for cardiac output?

A

CO = SV + HR

253
Q

What is the normal cardiac output?

A

5000 mL/min in a 70 kg man

254
Q

What is the Frank-Starling Relationship?

A

The volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole (CO=VR)

255
Q

What occurs during isovolumetric contraction?

A

LV has filled with blood from LA and its volume is the end-diastolic volume, 140 mL. Ventricle is activated, it contracts, and ventricular pressure increases dramatically. Valves are closed

256
Q

What occurs during ventricular ejection?

A

Ventricular pressure is higher than aortic so aortic valve opens and blood rapidly ejects from LV. LV pressure remains high due to ventricular contraction but volume decreases to ~70 mL (=SV)

257
Q

What occurs during isovolumetric relaxation?

A

systole ends and ventricle relaxes. Ventricular pressure decreases below aortic pressure so aortic valve closes so volume remains constant at ~70 mL.

258
Q

What occurs during ventricular filling?

A

Ventricular pressure has fallen to a level that is now less than left atrial pressure causing the mitral valve to open and blood flows into LV. LV vol increases back to 140 mL and is relaxed and there is only a slight pressure increase, waiting for the next cycle.

259
Q

What affect does increased preload have on the ventricular cycle?

A

VR increased = increase preload = increase SV due to increased VR but contractility remains constant

260
Q

What affect does increases afterload have on the VC cycle?

A

(or, increased aortic pressure) LV must eject blood against greater than normal pressure so ventricular pressure must rise to compensate. Less blood is ejected, decreasing SV so more blood stays in LV increasing end-systolic volume.

261
Q

What affect does increasing contractility have on the ventricular cycle?

A

Increased contractility = greater tension and pressure and can eject a larger volume so, SV increases so less blood remains in LV at the end of systole thus end-systolic volume decreases

262
Q

What two components alter SV?

A

End-diastolic volume, end systolic volume

263
Q

What factors alter end diastolic volume?

A

Filling pressure, filling time, ventricular compliance

264
Q

What factors alter the end systolic volume?

A

HR, Preload, afterload, contractility

265
Q

What two components alter HR?

A

Intrinsic and extrinsic regulation

266
Q

What factors alter intrinsic regulation?

A

Threshold potential, max diastolic potential, slope of diastolic depolarization

267
Q

What factors alter extrinsic regulation?

A

ANS, Humoral Factors

268
Q

What is work defined as?

A

Force x distance

269
Q

What is stroke work defined as?

A

The work the heart performs on each beat

270
Q

What is cardiac minute work?

A

cardiac output x aortic pressure

271
Q

What are the two components of cardiac minute work?

A

Pressure work and volume work

272
Q

What correlates directly with cardiac minute work?

A

Myocardial O2 consumption

273
Q

Which work is more costly for O2 consumption?

A

Pressure work

274
Q

What affect does aortic stenosis have on O2 consumption?

A

Greatly increased because the LV must develop extremely high pressures to pump blood

275
Q

Does O2 consumption increase or decrease in conditions when a larger-than-normal percentage of total cardiac work being pressure work?

A

Increases

276
Q

When CO is very high and volume work contributes a greater-than-normal percentage of total cardiac work what happens to O2 consumption?

A

O2 consumption will increase just a little

277
Q

What affect does systemic hypertension on cardiac work?

A

Requires LV to perform more pressure work than normally so LV wall will hypertrophy as compensation for increased workflow

278
Q

What is the Law of Laplace?

A

for a sphere, pressure correlates directly with tension and wall thickness and inversely with radius

279
Q

What is the formula for pressure regarding the law of laplace?

A

P = 2 x thickness x tension / radius

280
Q

Ultimately, the _the thickness of the wall, the _ the pressure that can be developed.

A

greater, greater

281
Q

What will happen as a compensatory mechanism that happens when wall thickness increases?

A

Ventricle has to pump harder so atrial pressure is increased

282
Q

Pulmonary hypertension can cause what to happen?

A

RV Hypertrophy

283
Q

What can be used to measure CO?

A

Fick principle

284
Q

What does the fick principle state regarding the heart?

A

in steady state, CO of LV and RV are equal

285
Q

How is the fick principle applied to O2 consumption?

A

In steady state, O2 consumption rate must equal the amount of air leaving the lungs in the pulmonary vein minus the amount of O2 returning to the lungs in the pulmonary artery

286
Q

What is the “equation” for O2 consumption?

A

(CO x [O2] pulm vein) - (CO x [O2] pulm artery)

287
Q

How would you solve for cardiac output in relation to O2 consumption?

A

CO = O2 consumption/ ([O2]pulm vein - [O2]pulm artery)

288
Q

What is the typical total O2 consumption?

A

~250 mL/min in a 70 kg man

289
Q

What is the first phase of the cardiac cycle?

A

Atrial systole

290
Q

What part on an EKG indicates atrial systole?

A

P wave, PR interval

291
Q

What are the major events of atrial systole?

A

Atrial contraction marks the depolarization of the atria. Final phase of ventricular filling, Mitral valve is open so ventricle fills with blood from atrium.

292
Q

What heart sound is made during atrial systole?

A

Fourth (S4) not audible in normal adults

293
Q

What is phase two of the cardiac cycle?

A

Isovolumetric Ventricular Contraction

294
Q

What part on an EKG indicates isovolumetric ventricular contraction?

A

QRS complex

295
Q

What are the major events of isovolumetric ventricular contraction?

A

Electrical activation of ventricles, ventricle pressure increases but volume is constant, mitral vvalve closes

296
Q

What heart sound is made during isovolumetric ventricular contraction?

A

First (s1)

297
Q

What occurs during the third phase of the cardiac cycle?

A

Rapid ventricular ejection

298
Q

What part on an EKG indicates the rapid ventricular ejection?

A

ST segment

299
Q

What are the major events of Rapid ventricular ejection?

A

Ventricle continues to contract, ventricle pressure reaches highest value, blood is ejected rapidly into aorta, atrial pressure increases due to large volume, aortic valve opens

300
Q

What is the fourth phase of the cardiac cycle?

A

Reduced Ventricular Ejection

301
Q

What part on an EKG indicated the reduced ventricular ejection phase?

A

T wave

302
Q

What major events occur during reduced ventricular ejection?

A

Ventricles begin to repolarize, ventricular pressure falls, blood continues to eject into aorta (at a reduced rate), aortic pressure falls, L arterial pressure continues to increase as blood returns to the left heart from the lungs

303
Q

What is the fifth phase of the cardiac cycle?

A

Isovolumetric ventricular relaxation

304
Q

What part on an EKG indicates the isovolumetric ventricular relaxation phase?

A

end of T wave

305
Q

What majors events occur during the isovolumetric ventricular relaxation phase?

A

Ventricles are fully repolarized, LV pressure decreases below aortic pressure, ventricular volume is constant ,aortic valve closes

306
Q

What heart sound is made during isovolumetric ventricular relaxation phase?

A

Second (S2)

307
Q

What is the sixth phase of the cardiac cycle?

A

Rapid ventricular filling

308
Q

What major events occur during Rapid ventricular filling?

A

Ventricular pressure is minimal so mitral valve opens and ventricles fill and volume increases, ventricular pressure remains low, aortic pressure decreases

309
Q

What heart sound is made during Rapid ventricular filling?

A

Third (S3)

310
Q

What is the seventh and final phase of the cardiac cycle?

A

Reduced ventricular filling (Diastasis)

311
Q

What are the major events that occur during reduced ventricular filling?

A

Final portion of ventricular filling but at a slower rate, atrial systole marks the end of diastole, ventricular volume is end diastolic volume.

312
Q

What does changes in HR alter the time available for?

A

Diastasis

313
Q

What can be used to plot the relationship between CO of the LV and the right atrial presure?

A

Cardiac Function Curve

314
Q

What can be used to plot the relationship between VR and right atrial pressure?

A

Vascular function curve

315
Q

What determines the slop of the VF Curve?

A

TPR

316
Q

What will a decrease in TPR do to the VF Curve?

A

causes a clockwise rotation of it

317
Q

What will an increase in TPR do to the VF Curve?

A

Causes a counterclockwise rotation of it

318
Q

What is the mean systemic pressure?

A

the pressure that would be measured throughout the CVS if the heart stopped

319
Q

When VR is zero and Pa is maximal, what would the MSP look like?

A

Equal to the pressure through the vasculature, so no blood will flow

320
Q

What is the volume that the veins can hold (under no pressure)?

A

Unstressed volume

321
Q

What is the volume in the arteries (produces BP by stretching of walls)?

A

Stressed volume

322
Q

If the blood volume is 0-4 L, what does the distribution of the blood volume look like?

A

All unstressed

323
Q

If the blood volume rises above 4 L, what does the distribution of blood volume look like?

A

some of the blood will move to stressed volume

324
Q

what will happen to the MSP if stressed volume is added?

A

Quick increase

325
Q

What effect does decreasing compliance have on the blood volume distribution?

A

decreases the amount of blood it can hold = Decreases the unstressed volume to stressed volume, so MSP increases

326
Q

What effect does increasing compliance have on the blood volume distribution?

A

veins can hold more blood = unstressed vol will increase and stressed will decrease = decrease MSP

327
Q

Combining the cardiac function curve and vascular curve causes an intersection which indicates what?

A

Steady state - Where CO and VR are equal

328
Q

What effect will a positive inotropic effect have on the CVF Curve?

A

will increase contractility, SV, and CO for a given R atrial pressure so the Cardiac Curve will have an upward shift and the new steady state will be at a higher CO but lower atrial pressure

329
Q

What effect will a negative inotropic effect have on the CVF Curve?

A

A negative inotropic effect decreases contractility, which decreases CO for any given atrial pressure. CF Curve shifts downward, VF Curve remains constant and a new steady state = CO decrease and atrial pressure increased.

330
Q

What effect does a increasing blood volume have on the CV-F Curve?

A

Increasing the blood volume increases stressed volume therefore increases Mean Systemic Pressure (MSP) [where VR=0]. This shifts the intersection point to the right so the shift is parallel in manner. New steady state = CO increased and R atrial pressure increased.

331
Q

What effect does decreasing blood volume have on the CVF Curve?

A

Decreasing the blood volume decreases stressed volume therefore decreases Mean Systemic Pressure (MSP) [where VR=0]. This shifts the intersection point to the left, parallel in manner. New steady state = CO decreased and R atrial pressure decreased.

332
Q

What effect does increasing TPR have on the CVF Curve?

A

Increasing TPR constricts the arterioles so increases atrial pressure. This increases afterload which decreases CO. The CF Curve shifts downward and VF Curve rotates counterclockwise. New steady state = both CO and VR are decreased.

333
Q

What effect does increasing TPR have on the CVF curve?

A

Decreasing TPR dilates the arterioles so decreases atrial pressure. This decreases afterload which increases CO. The CF Curve shifts upward and VF Curve rotates clockwise. New steady state = both CO and VR are increased.

334
Q

When changes in TPR occur, why does it appear as if Pa is unaffected?

A

Because the effect of changing TPR can not be easily predicted, as magnitude of effects can either increase, decrease, or unchange the Atrial pressure

335
Q

What is Mean Arterial Pressure (Pa)?

A

driving force from difference in arterial and venous pressures ~100 mm Hg.

336
Q

True/False: The Pressure in the major artery serving each organ is equal to Pa due to the parallel arrangement of the arteries off the aorta.

A

True

337
Q

What is the formula for Pa?

A

Pa = CO x TPR

338
Q

What change will occur to Pa if TPR doubles?

A

It will also double (and CO will 1/2 to compensate)

339
Q

What change will occur to Pa if CO halves?

A

A compensatory increase in TPR will decrease Pa only slightly.

340
Q

What two major systems regulate Pa?

A

Baroreceptor reflex and Renin-Angiotensin-Aldosterone System (RAAS)

341
Q

What does the baroreceptor reflex attempt to do?

A

restore Pa to set pint value in a matter of seconds

342
Q

What does the RAAS attempt to do?

A

regulated Pa but more slowly, primarily by its effect on blood volume

343
Q

Where are baroreceptors located?

A

in the walls of the carotid sinus and aoritc arch

344
Q

Where do baroreceptors relay information about blood pressure changes to?

A

Cardiovascular vasomotor centers in the brain stem (medulla)

345
Q

What stimulates a baroreceptor?

A

Stretch/pressure

346
Q

What does the stretch on baroreceptors cause to happen?

A

increase the firing rate of afferent nerves

347
Q

What cranial nerve sends the information from the baroreceptor on the carotid sinus nerve to the brain stem?

A

CN IX (Glossopharyngeal)

348
Q

What cranial nerve sends the information from the baroreceptor on the aortic arch nerve to the brain stem?

A

CN X (Vagus nerve)

349
Q

Afferent serves send the information to what structure for directing the changes in activity of the CVS centers?

A

Nucleus tractus solitarius

350
Q

What effects does PNS outflow have?

A

effect of vagus nerve on SA node to decrease HR

351
Q

What effects does SNS outflow have?

A

increase HR, contractility, and SV; arterioles vasoconstrict and increases TPR, veins venoconstrict and decreased unstressed volume.

352
Q

An increase in Pa will cause a(n) _ in SNS activity and a(n) _ in PNS activity.

A

decrease, increase

353
Q

An decrease in Pa will cause a(n) _ in SNS activity and a(n) _ in PNS activity.

A

increase, decrease

354
Q

So describe the baroreceptor reflex as an compensatory mechanism for an increase in Pa.

A

Baroreceptor is stretched by the added pressure and this information is sent to the brain centers via the nucleus tractus solitarius which sends the integration for change: increase PNS = decrease HR. decreases SNS = decreased contractility, CO, TPR (which increased unstressed volume) = Pa back to set point

355
Q

What is the baroreceptor reflex like during the valsalva maneuver?

A

VM increases intrathoracic pressure which decreases VR, therefore reducing CO, causing a decrease in Pa. so baroreceptors have a decreased stretch which is sent to the brain center which causes decreased PNS to decrease HR and increased SNS outflow = to increase CO, VR, and Pa to decrease HR.

356
Q

What substance(S) are responsible for regulating blood volume by the RAAS?

A

Hormones

357
Q

In RAAS, what is stimulated by a change in pressure?

A

mechanoreceptors

358
Q

What does a decrease in Pa cause to [first] happen during the RAAS?

A

Prorenin to convert to renin in the juxtaglomerular cells.

359
Q

What increases renin secretion? What decreases it?

A

Beta-agonists (isoproterenol), B-antagonists (Propanolol)

360
Q

Renin catalyzes what conversion?

A

angiotensinogen to angiotension I

361
Q

Where does the conversion of angiotensin I to angiotensin II occur?

A

lungs and kidneys

362
Q

What enzyme catalyzes the conversion of angiotensin I to II?

A

ACE

363
Q

What does the production of AGTII cause? [4 things]

A
  1. acts on zona glomerulosa cells of the adrenal cortex to stimulate the synthesis and secretion of Aldosterone which increases Na+ reabsorption to increase ECF and blood volume
  2. stimulates Na+H+ exchange in the renal proximal tubule to increase the reabsorption of Na+ and HCO3-
  3. acts on hypothalamus to increase thirst and water intake therefore stimulating the secretion of ADH which increases water reabsorption, complementing the increase in Na+ absorption
  4. bind to AT1 receptors to activate IP3/Ca2+ second messenger system to cause vasoconstriction and increase TPR which leads to an increase in Pa.
364
Q

Why is the RAAS mechanism a slower response?

A

Synthesis of aldosterone requires transcription which can tale hours-days

365
Q

What two substances can block the actions of AGTII?

A

ACE inhibitor (captopril) and AT1 receptor inhibitor (losartan)

366
Q

Renal artey stenosis causes an early rise in MAP due to what three things?

A

vasoconstriction, renin secretion normalized, second rise in MAP due to Na+, H2O retention of the RAAS system

367
Q

What compensatory mechanism is in place for decreases in O2 (increasing CO2, and decreashing pH)?

A

Peripheral chemoreceptors

368
Q

Peripheral chemoreceptors sense the decrease in Po2 and cause what to occur?

A

increase firing rate of afferent nerves to activate sympathetic vasoconstriction centers to cause arteriolar vasoconstriction AND increase PNS outflow to decrease HR, this decrease in Po2 causes increase in ventilation to counter the PNS decrease in HR

369
Q

What compensatory mechanism is in place for changes in Pco2 and pH?

A

Central Chemoreceptors

370
Q

What happens if the brain becomes cerebral ischemic?

A

cerebral Pco2 increases and pH decreases

371
Q

How do central chemoreceptors work to counter cerebral ischemia?

A

increases SNS outflow = intense arteriolar vasoconstriction and increase TPR so blood flow is redirected to the brain to maintain its perfusion.

372
Q

What is a consequence of the vasoconstriction by central chemoreceptors?

A

dramatic increase in Pa, even to life threatening levels

373
Q

What illustrates the role of the cerebral chemoreceptors?

A

Cushing reaction

374
Q

What role does ADH play in regulation?

A

regulated body fluid osmolarity and participates in the regulation of arterial blood pressure

375
Q

How does ADH work to regulate?

A

When activated, vasoconstriction of arterioles occurs which increases TPR

376
Q

Where are low pressure baroreceptors located?

A

veins, atria, and pulmonary arteries

377
Q

What are low pressure baroreceptors sensitive to?

A

changes in blood volume

378
Q

Primarily, How do low pressure baroreceptors regulate an increase in blood volume?

A

by excretion of Na+ and water

379
Q

What are the four responses to incresing blood volume by low pressure baroreceptors?

A
  1. increased secretion of ANP which binds to ANP receptors to cause vasodilation and decreased TPR. This vasodilation increases Na+ and H20 excretion which decreases total body Na+ content, ECF volumes, and blood volume.
  2. Decreased secretion of ADH = decreased water reabsorption = increased water excretion.
  3. inhibition of SNS vasoconstriction in renal arteries which leads to dilation and increased Na+ and H2o excretion
  4. bainbridge reflex- the baroreceptors send info to the brain and it works to increase venous low-pressure receptors to increase heart rate, increasing CO leading to increased renal profusion and increased excretion
380
Q

In what ways may obesity contribute to HTN?

A

increase CO, decreasing baroreceptor activity which increases SNS activity and RAAS activity; impairment of renal pressure natriuresis; adipocyte dysfunction = increase inflammatory mediators and vascular remodeling and endothelial dysfunction

381
Q

What are the three types of capillaries? describe them.

A

continuous - endothelial cells closely joined together by intracellular junctions w/ tiny coated pits
Fenestrated - endothelial cells contain fenestra (pores) that allow the passage of some solutes
Discontinuous(sinusoidal) - endothelial cells contain large fenestrations and gaps = very leaky

382
Q

What are the most predominant type of capillaries?

A

Continuous

383
Q

Which type can you find in skeltal muscle tissue and brain? Liver? Small intestine?

A

continuous, discontinuous, fenestrated

384
Q

What affects the blood flow through the capillaries?

A

Degree of constriction or relaxation

385
Q

What structure function to open and close to allow blood flow?

A

Precapillary sphincters

386
Q

Gases/solutes exchange occurs across the capillary wall by what type of transport?

A

Simple diffusion

387
Q

What substances can pass through the capillary wall?

A

Lipid-soluble (O2, CO2)

388
Q

What substances can pass between endothelial cells by clefts?

A

Water soluble (H2O, ions, glucose, amino acids)

389
Q

How could protein cross the capillary wall?

A

Vesicles

390
Q

What is the most important mechanism for fluid transfer?

A

osmosis

391
Q

What forces drive fluid movement in the capillaries?

A

hydrostatic and osmotic pressures (Starling forces)

392
Q

What is the Starling equation?

A

Jv (fluid movement) = Hydraulic conductance[(Capillary-interstitial hydrostatic pressure) - (capillary - interstitial oncotic pressure)]

393
Q

What is hydraulic conductance? (Kf)

A

the water permeability of the capillary wall

394
Q

What is capillary hydrostatic pressure? (Pc)

A

force favoring filtration out of the capillary, determined by arterial and venous pressures ~17 mm Hg

395
Q

What is interstitial hydrostatic pressure? (Pi)

A

force opposing filtration, normally ~0 or may be slightly negative

396
Q

What is capillary oncotic pressure? (PIc)

A

Force opposing filtration determined by protein concentration

397
Q

Does increasing or decreasing protein concentration increase filtration?

A

Decreasing

398
Q

What is interstitial oncotic pressure? (PIi)

A

Force favoring absorption determined by protein concentration, usually quite low due to low loss of protein from capillaries

399
Q

What are the primary two proteins to affect oncotic pressure?

A

Albumin and Globulins

400
Q

What is the function of the lymphatic system?

A

returns interstitial fluid and proteins to vasculature

401
Q

Describe the flow of lymph.

A

IF and proteins flow to lymphatic capillaries via one way flap valves. then to lymphatic vessels to the thoracic ducts to large veins

402
Q

What type of muscle makes up the walls of lymph vessels and what is the benefit?

A

Smooth muscle to aid in intrinsic contractile activity (propel substances)

403
Q

What is the amount of total daily lymph?

A

2-3L

404
Q

What effect does edema have on circulation of lymph?

A

increases interstitial fluid by increased filtration or impaired drainage

405
Q

What is left sided edema called? Right sided?

A

pulmonary, peripheral

406
Q

If pressure increases, what will happen to lymph flow?

A

It will plateau ~2 mm Hg due to excess pressure compressing the outside surfaces of the larger lymphatics and impedes flow

407
Q

What happens to lymph flow during exercise?

A

increases 10-30 fold

408
Q

What alters to change blood flow to an organ?

A

Arteriolar resistance

409
Q

What are the two mechanisms that regulate blood flow to various organs?

A

Local control and neural/hormonal regulation

410
Q

What occurs during local control?

A

Direct action of local metabolites on arteriolar resistance (autoregulation)

411
Q

What occurs during active hyperemia?

A

blood flow is proportional to its metabolic activity = increase in one increases the other

412
Q

What occurs during reactive hyperemia?

A

an increase in blood flow occurs in response to a prior period of decreased blood flow

413
Q

What are the two mechanisms that explain local control?

A

Myogenic hypothesis, metabolic

414
Q

Which hypothesis states that when vascular smooth muscle is stretched, it contracts?

A

Myogenic

415
Q

Which hypothesis states that 02 delivery can be matched by its consumption by altering resistance of the arterioles to alter blood flow?

A

Metabolic hypothesis

416
Q

Describe how myogenic hypothesis acts on regulation.

A

If Pa is suddenly increased, arterioles are stretched anc contract hich leads to constriction which increases resistance to maintain a constant flow. (If decrease Pa = relaxation = decrease resistance)

417
Q

Describe how metabolic hypothesis acts on regulation.

A

As a result of metabolic activity, tissues produce vasodilator metabolites = vasodilation of arterioles which decreases resistance and increases flow to meet demand.

418
Q

Describe the extrinsic mechanism for regulation.

A

(Neural/hormonal control) Increases of decreases SNS innervation to either vasodilate or vasocontrict

419
Q

In which two circulations is sympathetic control the most important and how do they work?

A

Skin (vasoconstriction by alpha1 receptors) and skeletal muscle (vasconstrict by alpha1 receptors or vasodilate by beta2 receptors)

420
Q

What are some other vasoactive substances that control regulation and how do they work?

A

Histamine, Bradykinin (both released in response to trauma which produces dilation of arterioles and constriction of venules to increase filtration and local swelling), serotonin (release in response to BV damage - local vasoconstriction attempts to reduce blood flow and loss), and prostoglandins (Vasodilators = Prostacyclin and Prostaglandin E series; vasoconstrictors = Thromboxane A2 and porstoglandin F series; AGTII and vasosupressin = potent vasoconstrictors that increase TPR; ANP = vasodilator hormone secreted by atria in response to increases in Pa)

421
Q

What are the overall CVS responses to exercise?

A

Exercise stimulates local responses to increase vasodilator metabolites which decreases TPR. It also increases SNS outflow to increase contractility, CO, constriction of arterioles, and constriction of veins to decrease unstressed volume to increase VR and decreases PNS outflow to increase heart rate to increase blood flow to skeletal muscle

422
Q

What are the overall CVS responses to Hemorrhage?

A

Hemorrhage decreases Pa which stimulates the barorecptor reflex to increase SNS outflow to increase HR, contractility, and CO and constriction of arterioles which increases TPR, and constriction of veins which decreases unstressed volume to increase VR. It also stimulated the RAAS system to increase AGTII secretion to increase TPR and secrete aldosterone which increases Na+ reabsorption to increase blood volume. It also stimulates the capillaries to decrease capillary hydrostatic pressure to increase fluid absorption to increase blood volume. all to increase Pa back toward normal

423
Q

What are the overall CVS responses to moving from supine to standing?

A

Stand = blood pooling in veins = decrease Pa so baroreceptor reflex to increase SNS outflow to increase HR, contractility, and CO, constriction of arterioles to increase TPR and constriction of veins to decrease stressed volume to increase VR, all to increase Pa back toward normal

424
Q

What is orthostatic hyoptension?

A

a decrease in arterial blood pressure upon standing which may cause lightheadesness and possibly fainting

Physiology (11 decks)

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