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PCRS > Control of cardiac output and blood pressure > Flashcards

Control of cardiac output and blood pressure Flashcards

1
Q

What must cardiac output (CO) be adjusted to meet?

A

The metabolic needs of the body’s tissues.

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2
Q

How are the systemic and pulmonary circulations arranged?

A

They are in series, and the cardiovascular system is closed.

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3
Q

What must be equal between the left and right ventricles over time?

A

The outputs of the left and right ventricles must be the same over time (COlv = COrv).

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4
Q

What must venous return equal?

A

Venous return must be the same as cardiac output, although transient differences can occur (e.g., when you stand up).

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5
Q

What two factors determine cardiac output (CO)?

A

Heart Rate (bpm) and Stroke Volume (ml).

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6
Q

How is cardiac output (CO) calculated?

A

CO = Heart Rate (bpm) × Stroke Volume (ml).

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7
Q

In what units is cardiac output measured?

A

Milliliters per minute (ml/min).

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8
Q

What are the four factors that can directly affect cardiac output (CO)?

A

Preload, Afterload, Contractility, and Heart Rate.

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9
Q

What is preload, and how does it affect stroke volume?

A

Preload is the filling pressure of the right ventricle and affects stroke volume by influencing ventricular filling during diastole.

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10
Q

What is afterload, and how does it affect stroke volume?

A

Afterload is the resistance to outflow from the left ventricle and affects stroke volume by increasing the workload on the heart to pump blood.

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11
Q

What is contractility, and how does it affect cardiac output?

A

Contractility refers to the heart’s pumping function or strength of contraction, directly impacting stroke volume and cardiac output.

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12
Q

What is preload?

A

The degree of stretch of a ventricle immediately before it contracts.

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13
Q

What determines preload?

A

Preload is a function of the end-diastolic volume (EDV).

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14
Q

How is preload related to filling pressure?

A

It is related to the filling pressure of the ventricle.

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15
Q

What is the filling pressure for the left ventricle (LV)?

A

LVEDP (Left Ventricular End-Diastolic Pressure) = Left atrial pressure = Pulmonary venous pressure.

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16
Q

What is the filling pressure for the right ventricle (RV)?

A

RVEDP (Right Ventricular End-Diastolic Pressure) = Right atrial pressure (RAP) = Central venous pressure (CVP).

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17
Q

What is the normal pressure range associated with preload?

A

3-8 mmHg.

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18
Q

What does the venous system do?

A

It collects blood from the microcirculation and brings it back to the heart.

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19
Q

What pressure gradient allows blood flow to the right heart?

A

A small pressure gradient of 5-10 mmHg between the microcirculation and the right heart.

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20
Q

What 3 things allow the venous system to accomplish blood return with a small pressure gradient?

A
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21
Q

What is CVP a function of?

A

The amount of blood in the veins and the vein capacitance.

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22
Q

What happens when veins are constricted (e.g., by the SNS)?

A

Venous capacitance decreases, and CVP increases.

Example: Venoconstriction during exercise increases CVP, allowing the right and left ventricles to output more blood to meet muscle demands.

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23
Q

How do changes in blood volume affect CVP?

A

Decrease in blood volume:
- Example: Hemorrhage decreases CVP (as ~65% of blood is in systemic veins), reducing cardiac output (CO).
- Example: Sustained exercise causes fluid loss (sweating), reducing CVP and exercise capacity.

Increase in blood pooling (orthostasis):
- Example: Pooling in the lower extremities decreases CVP, CO, and blood pressure.

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24
Q

What is afterload?

A

The force against which a ventricle pumps to eject blood.

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25
Q

What primarily determines left ventricular (LV) afterload?

A

Aortic blood pressure.

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26
Q

What 2 factors influence left ventricular afterload?

A

Total peripheral resistance (TPR).
Aortic stiffness.

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27
Q

What primarily determines right ventricular (RV) afterload?

A

Pulmonary artery pressure.

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28
Q

What are the approximate pressures associated with afterload?

A

Pulmonary circulation: ~15 mmHg.

Systemic circulation: ~95 mmHg.

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29
Q

Who demonstrated the effect of altered preload on the heart?

A

Otto Frank.

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30
Q

What did Otto Frank’s experiment show?

A

Isovolumetric pressure development in a frog heart (with a ligated aorta) depended on diastolic volume.

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31
Q

What does increased preload do to isovolumetric pressure development?

A

It increases the pressure generated during contraction.

The relationship between preload (diastolic volume) and pressure development over time, showing that higher preload results in greater pressure generation.

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32
Q

Who demonstrated the effect of altered preload in an intact circulation?

A

Ernest Starling.

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33
Q

What did Ernest Starling’s experiment show?

A

The relationship between preload (filling pressure) and cardiac output is also present in an intact circulation.

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34
Q

What device did Ernest Starling use to measure cardiac output?

A

A bell cardiometer.

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35
Q

What is the purpose of the venous reservoir in Starling’s setup?

A

It regulates central venous pressure (CVP) by controlling the volume of blood entering the heart.

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36
Q

What role does the Starling resistor (TPR) play in the setup?

A

It simulates total peripheral resistance, affecting afterload and cardiac output.

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37
Q

What does the screw clamp control in the experimental setup?

A

It adjusts venous return to the heart by modulating the flow from the venous reservoir.

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38
Q

What does the Frank-Starling relationship describe?

A

It describes the relationship between preload (e.g., end-diastolic pressure or volume) and cardiac output or stroke volume.

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39
Q

What happens as preload increases within the physiological range?

A

Cardiac output or stroke volume increases due to greater myocardial stretch, enhancing the force of contraction.

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40
Q

What is plotted on the x-axis of the Frank-Starling curve?

A

Preload-related measures such as EDP, EDV, or venous return.

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41
Q

What is plotted on the y-axis of the Frank-Starling curve?

A

Cardiac work, force of contraction, energy of contraction, tension, stroke volume, or cardiac output.

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42
Q

What mechanisms explain how force increases with muscle stretch?

A
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43
Q

What proteins make up the troponin complex?

A

TnC: Binds calcium.
TnI: Inhibits interaction between actin and myosin.
TnT: Anchors the troponin complex to tropomyosin.

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44
Q

What does length-dependent activation refer to in muscle contraction?

A

The dependence of muscle contraction force on the sarcomere length due to actin-myosin overlap.

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45
Q

What is the optimal sarcomere length for maximal tension in cardiac muscle?

A

Around 2.2 μm.

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46
Q

What happens when sarcomere length is too short (e.g., 1.25 μm)?

A

Overlapping actin filaments interfere with cross-bridge formation, reducing tension.

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47
Q

What happens when sarcomere length is too long (e.g., 3.65 μm)?

A

Actin and myosin filaments are too far apart, reducing the number of cross-bridges and decreasing tension.

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48
Q

How does sarcomere length affect calcium sensitivity in cardiac muscle?

A

Longer sarcomere lengths (e.g., 2.2 microns) increase calcium sensitivity, leading to greater force development at a given intracellular calcium concentration ([Ca²⁺]i).

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49
Q

What happens to force development at shorter sarcomere lengths (e.g., 1.8 microns)?

A

Force development is reduced due to lower calcium sensitivity, even at the same [Ca²⁺]i.

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50
Q

According to the Frank-Starling Law, how are the stroke volumes of the left and right ventricles related?

A

The stroke volumes of the left and right ventricles are perfectly matched, except for very transient differences.

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51
Q

What determines cardiac output (CO) at a given heart rate and contractility?

A

Central venous pressure (CVP) determines cardiac output (CO).

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52
Q

How does the Frank-Starling Law help maintain cardiac output?

A

It helps maintain CO even in the face of increased afterload or decreased contractility.

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53
Q

What is another term for cardiac contractility?

A

Inotropy

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54
Q

How is cardiac contractility defined?

A

The strength of contraction.

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55
Q

What 2 factors reflect cardiac contractility?

A

The amount and rate of cardiac tension development.

The ability of the heart to eject a stroke volume at a given preload and afterload.

56
Q

What regulates cardiac contractility?

A

Intracellular calcium (Ca²⁺) in cardiac myocytes, influenced by sympathetic nervous system (SNS) stimulation.

Other factors such as pH and partial pressure of oxygen (pO₂).

57
Q

How does noradrenaline (norepinephrine) increase contractility?

A

By stimulating β₁ (and to a lesser extent β₂) adrenergic receptors.

58
Q

What does the graph show about contractility?

A

Increased contractility (e.g., due to sympathetic stimulation) raises stroke volume for a given end-diastolic pressure (EDP).

59
Q

How does the Frank-Starling mechanism compensate for decreased cardiac contractility?

A

By increasing end-diastolic pressure (EDP) or volume to maintain stroke volume and cardiac output (CO).

60
Q

What is heart failure (HF)?

A

When CO falls to insufficient levels to meet the body’s metabolic needs or when CO can only be maintained by elevated EDP/volume.

61
Q

in what 2 ways can heart failure occur?

A

Acutely: During a myocardial infarction (MI).
Chronically: In long-term heart failure.

62
Q

How is heart failure characterized on a function curve?

A

By a lower function curve compared to normal cardiac function, indicating reduced stroke volume for a given EDP.

63
Q

What happens to renal excretion of fluid when cardiac output (CO) falls in heart failure?

A

Renal excretion of fluid is reduced, increasing blood volume, especially in the veins.

64
Q

What 2 systems are activated due to reduced blood pressure in heart failure?

A

Sympathetic Nervous System (SNS): Increases contractility, heart rate, and venoconstriction.

Renin-Angiotensin-Aldosterone System (RAAS): Promotes fluid retention and venoconstriction.

65
Q

How do venous blood volume and venoconstriction affect central venous pressure (CVP)?

A

They increase CVP, which equals right ventricular end-diastolic pressure (RVEDP).

66
Q

What would a graph show about heart failure compensation?

A

Compensated HF: Stroke volume is partially restored due to fluid retention and venoconstriction.

Decompensated HF: Stroke volume fails to improve significantly, leading to worsening heart function.

67
Q

How does compensated heart failure differ from normal cardiac function on a graph?

A

Compensated HF has higher EDP but lower stroke volume compared to normal cardiac function.

68
Q

What is the direct effect of increased afterload on cardiac output?

A

To reduce stroke volume due to decreased ejection time.

69
Q

How can cardiac contractility be affected by increased blood pressure (BP)?

A

It may fall due to the baroreceptor reflex.

70
Q

What secondary effect compensates for reduced stroke volume when afterload increases?

A

Frank-Starling Mechanism: As ejection fraction decreases, more blood remains in the heart at the end of systole, increasing preload and improving subsequent stroke volume.

Anrep Response: Stretch caused by increased LVEDV triggers the release of Angiotensin II (Ang 2) and endothelin, enhancing calcium transients over 10–15 minutes, increasing contractility and stroke volume.

71
Q

What is the effect of afterload on cardiac output within the normal range of blood pressures?

A

Afterload has little effect on cardiac output in the normal range of blood pressures.

72
Q

What happens to cardiac output when afterload exceeds the normal range?

A

Cardiac output decreases significantly as mean arterial pressure increases beyond the normal range.

73
Q

What condition can significantly increase afterload and reduce cardiac output?

A

Aortic valve stenosis.

74
Q

What does the term “blood pressure” (BP) refer to?

A

The pressure in the large arteries.

75
Q

How does blood pressure behave during the cardiac cycle?

A

It oscillates, rising and falling with systole and diastole.

76
Q

What are the two key components of blood pressure?

A

Systolic Blood Pressure (SBP): The peak pressure during ventricular contraction.

Diastolic Blood Pressure (DBP): The lowest pressure during ventricular relaxation.

77
Q

What causes pressure and flow waves in the arteries?

A

Blood from the heart hitting the blood in the aorta, propagating waves down the vascular system.

78
Q

How does the pressure wave change as it moves down the arterial tree?

A

It becomes larger due to greater arterial stiffness.

79
Q

What happens to the pressure wave as it reaches the arterioles and microcirculation?

A

It progressively dies out.

80
Q

How does blood flow change as it moves into the arterioles and microcirculation?

A

Flow becomes progressively smoothed out.

81
Q

Why does the pressure wave grow larger in the arterial tree before it dies out?

A

Due to the increasing stiffness of the arteries, which amplifies the wave.

82
Q

What happens to arterial blood pressure (ABP) and blood flow during systole?

A

Approximately 75% of the stroke volume (SV) is transiently stored in the elastic walls of the aorta and large arteries.

About 25% of the stroke volume is pushed forward into smaller arteries.

83
Q

What is the role of the elastic walls of large arteries during systole?

A

They store energy and volume, helping to maintain blood flow during diastole.

84
Q

How does total peripheral resistance (TPR) affect blood flow?

A

TPR, primarily determined by resistance arteries and arterioles, controls blood flow to different regions like the skin, muscle, brain, and gut.

85
Q

What happens to arterial blood pressure (ABP) and blood flow during diastole?

A

Stored energy in the elastic walls of the arteries maintains blood flow during diastole by arterial recoil, pushing blood into smaller arteries

86
Q

What is the role of arterial recoil during diastole?

A

Arterial recoil pushes blood forward into smaller arteries, ensuring continuous blood flow despite the heart being in the relaxation phase.

87
Q

What happens to the stored pressure during diastole?

A

The stored pressure gradually falls as blood flows through the tissues.

88
Q

What is diastolic pressure?

A

The minimum pressure reached in the arteries before the next systole.

89
Q

How does total peripheral resistance (TPR) affect blood flow during diastole?

A

TPR, mainly due to arterioles, regulates how blood is distributed to various tissues like the skin, muscles, brain, and gut.

90
Q

What is the relationship between pressure, flow, and resistance?

A

ΔPressure = Flow × Resistance.

91
Q

what is p1 and p2 in this diagram

A

p1 = Arterial Blood Pressure (ABP).

p2 = Central Venous Pressure (CVP).

92
Q

Where does the steepest drop in pressure occur in the vascular system?

A

Across the resistance arteries and arterioles (R2), due to their high resistance.

93
Q

What is the mean arterial pressure (MAP) at the aorta?

A

Approximately 95 mmHg (with a range of 120/80 mmHg for systolic/diastolic pressures).

94
Q

What is the pressure in the veins?

A

Around 5–10 mmHg, dropping to 0–5 mmHg as blood returns to the heart.

95
Q

How is total vascular resistance
(Rtotal) calculated?

A

R1 = resistance of arteries

R2 = resistance of arterioles

R3 = resistance of veins

96
Q

What limits the extent of blood pressure (BP) changes?

A

The baroreceptor reflex.

97
Q

What is the role of the arterial baroreflex?

A

It helps maintain a relatively constant BP, regulating blood flow to some organs while ensuring constant flow to others.

98
Q

What does the BP set point refer to?

A

The baseline BP level that can adjust to meet physiological needs, such as increasing during exercise to accommodate higher cardiac output.

99
Q

How does the body prioritize blood flow via the baroreflex?

A
100
Q

What type of receptors are baroreceptors?

A

Mechanoreceptors with fine nerve endings sensitive to stretch.

101
Q

What happens to baroreceptor firing when pressure decreases?

A

Decreased pressure causes decreased firing.

102
Q

Within what blood pressure range are baroreceptors most sensitive?

A

Between 80-150 mmHg.

103
Q

How does pulse pressure affect baroreceptor sensitivity?

A

Sensitivity increases with larger pulse pressures, making baroreceptors more responsive to rapid changes in pressure.

104
Q

What is baroreceptor adaptation?

A

Baroreceptors reset to a new pressure if it is sustained for a few hours, such as in chronic hypertension.

105
Q

Where are baroreceptors located in the cardiovascular system?

A

Carotid sinus

Aortic arch

106
Q

Which cranial nerves are involved in the baroreceptor reflex pathway?

A

IX (Glossopharyngeal nerve)
X (Vagus nerve)

107
Q

Where are signals from baroreceptors processed in the brain?

A

In the nucleus tractus solitarius (NTS) of the brainstem.

108
Q

What triggers the baroreceptor reflex?

A

A decrease in blood volume or mean arterial pressure (MAP), which reduces baroreceptor firing.

109
Q

How does the baroreceptor reflex restore MAP?

A

By increasing sympathetic drive and decreasing parasympathetic drive, leading to increased cardiac output (CO) and total peripheral resistance (TPR).

110
Q

What are the effects of increased sympathetic drive on the heart?

A

Increased heart rate (HR) via β₁ receptors.
Increased stroke volume (SV) via enhanced contractility and venous return

111
Q

How does the baroreceptor reflex affect blood vessels?

A

Venoconstriction increases venous return via α₁ receptors.
Systemic arteriole constriction increases TPR via α₁ receptors.

112
Q

What type of feedback does the baroreceptor reflex use?

A

Negative feedback to restore MAP.

113
Q

What triggers the renin-angiotensin-aldosterone system (RAAS)?

A

Various stimuli such as low blood pressure, low sodium levels, or sympathetic nervous system activation, leading to renin release from juxtaglomerular (JG) cells in the kidney.

114
Q

What is the role of renin in the RAAS?

A

Renin converts angiotensinogen (produced by the liver) into angiotensin I in the blood.

115
Q

What enzyme converts angiotensin I into angiotensin II?

A

Angiotensin-Converting Enzyme (ACE).

116
Q

What are the effects of angiotensin II?

A
117
Q

What is the role of aldosterone in the RAAS?

A

It increases sodium reabsorption in the kidneys, which leads to water retention and increased blood volume.

118
Q

What is pressure diuresis?

A

The increase in water excretion by the kidneys in response to elevated arterial pressure.

119
Q

What is pressure natriuresis?

A

The increase in sodium excretion by the kidneys in response to elevated arterial pressure.

120
Q

How does increased mean arterial pressure (MAP) affect renal perfusion?

A

It increases renal perfusion pressure, enhancing water (diuresis) and sodium (natriuresis) excretion.

121
Q

What substances decrease due to increased renal perfusion pressure?

A

Angiotensin II levels decrease.

122
Q

what substances increase with elevated renal perfusion pressure?

A

Nitric oxide, prostaglandins, and renal kinins.

123
Q

How does increased medullary blood flow influence natriuresis?

A

It increases renal interstitial hydrostatic pressure, reducing tubular sodium reabsorption and promoting sodium excretion.

124
Q

What is the relationship between arterial pressure and urine output?

A

Urine output increases exponentially as arterial pressure rises, demonstrating pressure diuresis and natriuresis.

125
Q

What role does renal interstitial hydrostatic pressure play in sodium excretion?

A

It opposes tubular sodium reabsorption, promoting natriuresis.

126
Q

What is the primary mechanism for long-term regulation of arterial blood pressure (BP)?

A

Maintenance of a constant extracellular fluid volume, including plasma volume.

127
Q

What determines extracellular fluid volume?

A

Sodium (Na⁺) concentration.

128
Q

What hypothesis explains the prevalence of diseases like hypertension and type 2 diabetes in modern society?

A

The thrifty genotype hypothesis.

129
Q

What is the thrifty genotype hypothesis?

A

Evolution shaped humans to crave and conserve nutritional resources (e.g., salt) to survive during scarcity, but in modern times, this leads to overconsumption.

130
Q

Why might humanity have evolved to crave salt?

A

Early humans emerged in hot and dry environments, where salt was scarce, making salt retention critical for survival.

131
Q

How does the abundance of salt in modern diets relate to health issues?

A

Excess salt intake, driven by evolutionary programming, contributes to diseases like hypertension.

132
Q

Is renal sodium (Na⁺) excretion the only factor that stabilizes blood pressure (BP) over the long term?

A

No, other factors such as the sympathetic nervous system (SNS) and vascular tone also contribute.

133
Q

What happens to the baroreceptor reflex over time?

A

The baroreceptor reflex doesn’t remain active indefinitely; it adjusts and diminishes over time.

134
Q

What role does vascular tone play in long-term blood pressure control?

A

Regulation of vascular tone, influenced by the SNS or calcium (Ca²⁺) inhibitors, can contribute to blood pressure control.

135
Q

Na excretion can occur without changes in BP - why does this matter?

A

If sodium excretion were the sole determinant of BP, vasodilators wouldn’t lower BP. However, many effective anti-hypertensive drugs are vasodilators, showing the importance of vascular tone.

PCRS (11 decks)

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