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First Aid 2014 > CARDIOVASCULAR- PHYSIOLOGY > Flashcards

CARDIOVASCULAR- PHYSIOLOGY Flashcards

1
Q

How are the phases of the cardiac cycle outlined?

A

Each is given a letter

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2
Q

How many phases are there of the cardiac cycle?

A

7

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3
Q

Where does the cardiac cycle begin?

A

Depolarization and contraction of the atria

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4
Q

What does A in the cardiac cycle stand for?

A

Atrial systole

Note that this is the final phase of ventricular filling

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5
Q

What happens prior to atrial systole?

A

P-wave of the ECG (i.e. atrial depolarization)

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6
Q

What happens to left atrial pressure with contraction of the left atrium?

A

Increase in pressure

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7
Q

How is atrial systole reflected in the venous pulse graph?

A

A-wave–increase in atrial pressure is reflected back into the veins

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8
Q

What does a S4 heart sound correspond with?

A
  • Atrial contraction in ventricular hypertrophy

- Atrium is contracting/filling against a stiffened left ventricle

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9
Q

What is B in the cardiac cycle?

A

Isovolumetric ventricular contraction

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10
Q

What part of the ECG corresponds to isovolumetric ventricular contraction?

A

QRS Complex (prior)

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11
Q

What major events occur during isovolumetric ventricular contraction?

A

1) Ventricles contract
2) Ventricular pressure increases without a change in volume

When LV pressure is greater than LA pressure, mitral valve closes

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12
Q

What heart sound is produced in phase B of the cardiac cycle?

A

S1 i.e. closure of the AV valves

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13
Q

In S1 splitting, what’s happening?

A

Mitral valve is closing slightly before tricuspid valve

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14
Q

What is phase C of the cardiac cycle?

A

Rapid Ventricular Ejection

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15
Q

What events happen in phase C of the cardiac cycle?

A

1) Ventricles continue to contract, increasing pressure
2) Ventricular pressure exceeds aortic pressure (reaches maximum)
- Aortic valve opens
3) Blood is ejected into the aorta
- Ventricular volume decreases
4) Aortic pressure increases and reaches maximum value

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16
Q

What part of the ECG corresponds to phase C of the cardiac cycle?

A

ST segment

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17
Q

What is phase D of the cardiac cycle?

A

Reduced ventricular Ejection

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18
Q

What major events occur during phase D of the cardiac cycle?

A

1) Blood continues to eject into the aorta
2) Ventricular volume reach minimum
3) Aortic pressure starts to fall

*Note that at the same time, left atrial pressure increases are blood enters from the pulmonary vein

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19
Q

What part of the ECG corresponds to phase D of the cardiac cycle?

A

T-wave i.e. ventricular repolarization

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20
Q

What is phase E of the cardiac cycle?

A

Isovolumetric Ventricular Relaxation

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21
Q

What are the major events that occur during Isovolumetric Ventricular Relaxation?

A

1) Ventricles relax
2) Ventricular pressure decreases
3) Ventricular volume is constant

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22
Q

What happens in terms of the cardiac valves during phase E?

A

Isovolumetric relaxation, aortic (and pulmonic) valve closes

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23
Q

What heart sound corresponds with aortic and pulmonic valve closing?

A

S2

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24
Q

Why is there normally splitting of S2?

A

Inspiration causes a delay in the closing of the pulmonic valve

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25
Q

What happens to the aortic pressure curve when the aortic valve closes?

A

Blip or dicrotic notch/ incisura

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26
Q

What is phase F of the cardiac cycle?

A

Rapid Ventricular Filling

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27
Q

What major events occur during rapid ventricular filling?

A

1) Ventricles relaxed and pressure falls (AV valves open)
2) Ventricles fill with blood from the atria
3) Volume increases but pressure is constant

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28
Q

What heart sound can be produced in rapid ventricular filling?

A

S3, rapid filling of the ventricles

  • Normal in kids
  • Abnormal in adults
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29
Q

What does S3 in an adult indicate?

A
  • Volume overload e.g. CHF

- AV valve regurgitation

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30
Q

What is the phase G of the cardiac cycle?

A

Reduced Ventricular Filling or “Diastasis”

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31
Q

What major events occur during reduced ventricular filling?

A

1) Ventricles are relaxed

2) Final phase of ventricular filling

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32
Q

What marks the end of diastole?

A

Atrial systole

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33
Q

What physiologic change can reduce diastasis? What are the implications?

A

Increased HR–>decreased SV

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34
Q

What is stroke volume?

A

The volume of blood ejected by the ventricles with each beat

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35
Q

What is the ejection fraction?

A

Fraction of the end diastolic volume ejected with each beat

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36
Q

What is cardiac output?

A

Total volume of blood ejected from the heart per unit of time

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37
Q

What is the equation for stroke volume?

A

EDV- ESV= SV

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38
Q

What is a normal SV?

A

70 mL

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39
Q

What is the equation for EF?

A

SV/EDV

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40
Q

What is a normal EF?

A

0.55 or 55%

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41
Q

What is the equation for CO?

A

CO= SV x HR

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42
Q

What is a normal CO?

A

5,000 mL/min

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43
Q

Describe the Frank-Starling Relationship.

A

1) Volume of blood ejected by the ventricle is dependent on the volume of blood in the ventricle at the end of diastole (EDV)
2) EDV is dependent on the volume of blood returned to the heart i.e. venous return

Thus, the volume ejected in systole equals the volume the heart receives in venous return

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44
Q

What happens to EDV, RAP, and SV with increased venous return?

A

EDV, RAP, and SV all increase

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45
Q

What happens to SV with a positive ionotrope?

A

SV and CO increase for a given EDV

A larger fraction of the EDV is ejected per beat

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46
Q

Draw the ventricular pressure volume loop. Label points 1, 2, 3, and 4.

A

N/A (p.147)

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47
Q

What happens between points 1 and 2 in the ventricular pressure volume loop?

A

Isovolumetric contraction

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48
Q

Describe what happens during isovolumetric contraction.

A
  • Isovolumetric contraction starts at the end of diastole–the ventricle is relaxed but filled with blood
  • It CONTRACTS
  • PRESSURE INCREASES but VOLUME remains CONSTANT
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49
Q

What happens between points 2 and 3 on the ventricular pressure volume curve?

A

Ventricular ejection

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50
Q

Describe what happens during ventricular ejection.

A
  • Point 2, ventricular pressure exceeds aortic pressure–AORTIC VALVE OPENS
  • Ventricle continue to contract–increasing pressure–as blood volume is ejected (volume goes down)
  • Point 3, contraction ends with some volume of blood remaining in the ventricle– the ESV
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51
Q

What is the width of the ventricular pressure-volume curve?

A

Volume ejected from the ventricle in one beat: the SV

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52
Q

What happens between points 3 and 4 in the ventricular pressure volume curve?

A

Isovolumetric relaxation

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53
Q

Describe what happens during isovolumetric relaxation.

A
  • Ventricle relaxes, dropping its pressure rapidly
  • Ventricular pressure drops below aortic pressure, closing the aortic valve

All valves are closed; thus, NO CHANGE IN VOLUME

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54
Q

What happens between points 4 and 1 on the ventricular pressure-volume curve?

A

Ventricular filling

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55
Q

Describe ventricular filling.

A
  • Ventricular pressure falls to a point less than left atrial pressure, MITRAL VALVE OPENS
  • Ventricle fills with blood
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56
Q

What is preload?

A

Venous return or end diastolic volume (EDV)

57
Q

Draw what happens to the ventricular pressure-volume curve with increased preload.

A

N/A p. 148

58
Q

What happens to the ventricular pressure-volume curve with increased preload?

A

Increased SV i.e. width of the curve increases

59
Q

What is afterload?

A

Aortic pressure

60
Q

Draw what happens to the ventricular pressure-volume curve with increased afterload.

A

N/A p.148

61
Q

What happens to the ventricular pressure-volume curve with increased afterload?

A
  • SV decreases

- End systolic volume (ESV) increases

62
Q

Draw what happens to the ventricular pressure-volume curve with increased contractility.

A

N/A p. 148

63
Q

What happens to the ventricular pressure-volume curve with increased contractility?

A
  • SV increases

- ESV decreases

64
Q

What is cardiac minute work?

A

CO x aortic pressure

65
Q

What does myocardial oxygen consumption correlate directly with?

A

Cardiac minute work (CO x aortic pressure)

66
Q

What are the two types of cardiac work? Which is more “costly?”

A

1) Volume work i.e. cardiac output
2) Pressure work i.e. aortic pressure*

*More costly = disproportionate myocardial oxygen consumption is directed toward pressure work

67
Q

How does aortic stenosis affect myocardial oxygen consumption?

A

1) Increased aortic pressure
2) Increased pressure work

= Increased myocardial oxygen consumption

68
Q

Which ventricle works harder?

A

Left ventricle b/c is has the “work” against the relatively higher aortic pressure vs. pulmonary pressure

69
Q

How does systemic HTN impact cardiac work? What compensatory mechanism follows?

A
  • Increases pressure work required of the left ventricle

- LVH= compensation

70
Q

What is the Law of Laplace?

A

P= 2HT/r

Pressure is directly correlated with T, tension and H, wall thickness; inversely correlated with radius of the sphere.

71
Q

What principle is used to measure cardiac output?

A

Fick Principle

72
Q

What is the Fick Principle?

A

CO= O2 consumption/ [O2Pv] - [O2Pa]

73
Q

What is the cardiac function curve?

A

Plot of the relationship between

1) Cardiac output
2) RAP

74
Q

What happens to CO with increased EDV or RAP?

A

Increased CO

75
Q

When does CO no longer increase with EDV or RAP?

A

When RAP reaches 4mm/Hg

At this pressure, or with this much venous return, cardiac output can no longer keep up and eject all of the blood each cycle

76
Q

What is the vascular function curve?

A

Plot of the relationship between:

1) venous return
2) RAP

77
Q

Describe the relationship between venous return and RAP?

A

1) Venous return is driven by a pressure gradient: high systemic pressure and low RAP
2) As RAP increases the pressure gradient DECREASES, and venous return DECREASES

78
Q

What is the mean systemic pressure?

A

RAP at which venous return is zero

Think of this as the pressure that would be measured throughout the CV system if the heart were stopped

79
Q

What is the difference between unstressed and stress volume in the CV system?

A

Unstressed= volume the veins can hold (does not produce pressure)

Stressed= volume the arteries can hold (produces pressure)

80
Q

What does an increased in blood volume cause? What does this do to the vascular function curve?

A

Increase in mean systemic pressure

Shifts the x-intercept to the right

81
Q

What does a decrease in the compliance of the veins cause? What does this do to the vascular function curve?

A

Increase in mean systemic pressure (vasoconstriction= less unstressed volume and a redistribution of blood into the stressed volume, generating pressure)

Shifts the x-intercept to the right

82
Q

What determines the slope of the vascular function curve?

A

TPR (resistance of the arterioles)

83
Q

How will a decrease in TPR shift the vascular function curve?

A

CLOCKWISE rotation of the vascular function curve

84
Q

How will an inrease in TPR shift the vascular function curve?

A

COUNTER-CLOCKWISE rotation of the vascular function curve

85
Q

Draw the combined cardiac and vascular function curves.

A

p. 154

86
Q

What is the intersection of the cardiac and vascular function curves?

A

Steady state i.e. CO = venous return

87
Q

In the combined cardiac and vascular function curves, how will inotropic effects be reflected?

A

Change in the CARDIAC function curve

88
Q

In the combined cardiac and vascular function curves, how will changes in blood volume/ venous compliance be reflected?

A

Change in the VASCULAR function curve

89
Q

In the combined cardiac and vascular function curves, how will changes in TPR be reflected?

A

Change in BOTH curves

90
Q

Draw the effects of an inotropic agent on the combined cardiac and vascular function curves.

A

p. 156

91
Q

How will the steady state change with the addition of a positive inotropic agent?

A

Upward and to the left, which indicates:

  • Cardiac output INCREASED
  • RAP DECREASED
92
Q

How will the steady change with a negative inotropic agent?

A

Downward and to the right, which indicates:

  • CO DECREASED
  • RAP INCREASED
93
Q

Draw the effects of an increased in blood volume on the combined cardiac and venous function curves.

A

p. 157

94
Q

How will the steady state change with an increase in blood volume?

A

Upward and rightward shift, which indicates:

  • CO INCREASED
  • RAP INCREASED

Note the Mean Systemic Pressure increase as well

95
Q

How will the steady state change with an decrease in blood volume?

A

Downward and leftward shift, which indicates:

  • CO DECREASED
  • RAP DECREASED
96
Q

How are changes in venous compliance reflected in the combined cardiac and venous function curves?

A
  • Decreased compliance is similar to increased volume

- Increased compliance is similar to decreased volume

97
Q

Draw the effects of increased and decreased TPR on the combined cardiac and vascular function curves.

A

p. 158

98
Q

What is the “a” wave on the jugular venous pressure curve?

A

Atrial systole

99
Q

What would cause an absent “a” wave on the jugular venous pressure curve?

A

A-fib

100
Q

What would cause a large “a” wave on the jugular venous pressure curve?

A

Increased RV pressure e.g. Tricuspid Stenosis

101
Q

What would cause a “cannon a-wave” on the jugular venous pressure curve?

A

Closed tricuspid valve e.g. complete heart block

102
Q

What is the “c” wave on the jugular venous pressure curve?

A

Corresponds to RV isovolumetric contraction; tricuspid valve balloons into the RA, increased RAP

103
Q

What is the “x” wave on the jugular venous pressure curve?

A

Atrial relaXation

104
Q

What will cause an absent “x” wave on the jugular venous pressure curve?

A

Tricuspid regurgitation

105
Q

What will cause a rapid “x” wave on the jugular venous pressure curve?

A

Constrictive percarditis or cardiac tamponade

106
Q

What does the “v” wave correspond to on the jugular venous pressure curve?

A

Increased RAP in ventricular systole

107
Q

What is the “y” wave on the jugular venous pressure curve?

A

Atrial emptYing

108
Q

What is Pa?

A

Mean Arterial Pressure

109
Q

What is the equation for Pa?

A

CO x TPR

110
Q

What are the two major systems that regulate Pa?

A

1) Baroreceptor reflex (neural)

2) Renin-angiotensin-aldosterone (hormonal)

111
Q

Where are baroreceptors located? How do these receptors differ?

A

1) Carotid sinus
- Responds to both increases and decreases in pressure
2) Aortic arch
- Responds to increases in pressure

112
Q

Where do baroreceptors relay information?

A

Cardiovascular vasomotor centers in the brainstem

113
Q

What happens at the baroreceptor when there is increased pressure?

A
  • Stretch of the receptor and INCREASED afferent firing

- v.s DECREASED afferent firing for a decreased in pressure/stretch

114
Q

What type of stimuli do baroreceptors respond the strongest to?

A

Changes in pressure

115
Q

What cranial nerves are the afferents from the carotid sinus and aortic arch to the brainstem?

A

Carotid sinus= CN IX (carotid sinus nerve - joins glossopharyngeal)

Aortic arch= CN X (vagus)

116
Q

Specifically, where are brainstem cardiovascular centers located?

A

Medulla and lower 1/3 of the pons

117
Q

What nucleus integrates incoming afferent information about blood pressure?

A

Nucleus tractus solitarius (Medulla)

118
Q

Where does the Nucelus Tractus Solitarius direct changes to alter blood pressure?

A

Cardiovascular centers in the Medulla:

1) Cardiac decelerator
2) Cardiac accelerator
3) Vasoconstrictor

119
Q

What cardiac center is the PNS associated with?

A

Cardiac decelerator

120
Q

What cardiac centers is the SNS associated with?

A

Cardiac accelerator and vasoconstrictor

121
Q

What happens when the cardiac decelerator is stimulated?

A

Increased vagal tone on the SA node to DECREASE heart rate

122
Q

What will be influenced by the cardiac accelerator and the SNS?

A

1) SA node

2) Contractility

123
Q

What will be influenced by the vasoconstrictor center and SNS?

A

1) Arterioles

2) Veins

124
Q

Outline the sequence of events that transpires when there is a decrease in Pa, in the Renin-Angiotensin II- Aldosterone System.

A

1) Decreased Pa= decreased renal perfusion, PRORENIN is converted to RENIN
2) Renin catalyzes the conversion of ANTIOTENSINOGEN to ANGIOTENSIN I
3) In the lungs and kidneys, ANGIOTENSIN I is converted to ANGIOTENSIN II by ANGIOTENSIN-CONVERTING ENZYME (ACE)
4) Angiotensin II activates ANGIOTENSIN II RECEPTORS (AT1) on target tissues

125
Q

What are the major target organs of Angiotensin II?

A

1) Adrenal cortex
2) Vascular smooth muscle
3) Kidneys
4) Brain

126
Q

What if the effect of Angiotensin II binding to AT1 receptors on the adrenal cortex?

A

Stimulation of the synthesis/secretion of ALDOSTERONE

127
Q

What does Aldosterone do?

A

1) Acts on “principal cells” in the renal distal tubule to increase Na+ reabsorption
2) Water follows and blood volume increases

128
Q

What if the effect of Angiotensin II binding to AT1 receptors on the kidney?

A

1) Stimulates Na+/H+ exchange in the RENAL PROXIMAL TUBULE

2) Increases Na+ and HCO3- absorption

129
Q

What if the effect of Angiotensin II binding to AT1 receptors on the brain (hypothalamus)?

A

1) Increased thirst

2) Stimulates secretion of antidiuretic hormone (ADH)

130
Q

What does ADH do?

A

Increases water reabsorption in the collecting ducts of the nephron

131
Q

What if the effect of Angiotensin II binding to AT1 receptors on the arterioles?

A

Vasoconstriction that increases TPR

132
Q

What is the normal pressure of the IVC and RA?

A

Less than 5 mmHg

133
Q

What is the normal pressure of the RV?

A

25/5 mmHg

134
Q

What is the normal mean pulmonary artery pressure?

A

10-14 mmHg

135
Q

What is the definition of pulmonary HTN?

A

Mean pulmonary artery pressure greater than 25 mmHg

136
Q

What is a normal Pulmonary Capillary Wedge Pressure (PCWP)?

A

Less than 12 mmHg

137
Q

What is the normal LA pressure?

A

Less than 12 mmHg

138
Q

What is the normal LV pressure?

A

130/10 mmHg

139
Q

What is the normal aortic pressure?

A

130/90 mmHg

First Aid 2014 (8 decks)

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