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.
2
Q
How are the systemic and pulmonary circulations arranged?
A
They are in series, and the cardiovascular system is closed.
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).
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).
5
Q
What two factors determine cardiac output (CO)?
A
Heart Rate (bpm) and Stroke Volume (ml).
6
Q
How is cardiac output (CO) calculated?
A
CO = Heart Rate (bpm) × Stroke Volume (ml).
7
Q
In what units is cardiac output measured?
A
Milliliters per minute (ml/min).
8
Q
What are the four factors that can directly affect cardiac output (CO)?
A
Preload, Afterload, Contractility, and Heart Rate.
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.
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.
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.
12
Q
What is preload?
A
The degree of stretch of a ventricle immediately before it contracts.
13
Q
What determines preload?
A
Preload is a function of the end-diastolic volume (EDV).
14
Q
How is preload related to filling pressure?
A
It is related to the filling pressure of the ventricle.
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.
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).
17
Q
What is the normal pressure range associated with preload?
A
3-8 mmHg.
18
Q
What does the venous system do?
A
It collects blood from the microcirculation and brings it back to the heart.
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.
20
Q
What 3 things allow the venous system to accomplish blood return with a small pressure gradient?
A
21
Q
What is CVP a function of?
A
The amount of blood in the veins and the vein capacitance.
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.
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.
24
Q
What is afterload?
A
The force against which a ventricle pumps to eject blood.
25
What primarily determines left ventricular (LV) afterload?
Aortic blood pressure.
26
What 2 factors influence left ventricular afterload?
Total peripheral resistance (TPR).
Aortic stiffness.
27
What primarily determines right ventricular (RV) afterload?
Pulmonary artery pressure.
28
What are the approximate pressures associated with afterload?
Pulmonary circulation: ~15 mmHg.
Systemic circulation: ~95 mmHg.
29
Who demonstrated the effect of altered preload on the heart?
Otto Frank.
30
What did Otto Frank's experiment show?
Isovolumetric pressure development in a frog heart (with a ligated aorta) depended on diastolic volume.
31
What does increased preload do to isovolumetric pressure development?
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.
32
Who demonstrated the effect of altered preload in an intact circulation?
Ernest Starling.
33
What did Ernest Starling's experiment show?
The relationship between preload (filling pressure) and cardiac output is also present in an intact circulation.
34
What device did Ernest Starling use to measure cardiac output?
A bell cardiometer.
35
What is the purpose of the venous reservoir in Starling's setup?
It regulates central venous pressure (CVP) by controlling the volume of blood entering the heart.
36
What role does the Starling resistor (TPR) play in the setup?
It simulates total peripheral resistance, affecting afterload and cardiac output.
37
What does the screw clamp control in the experimental setup?
It adjusts venous return to the heart by modulating the flow from the venous reservoir.
38
What does the Frank-Starling relationship describe?
It describes the relationship between preload (e.g., end-diastolic pressure or volume) and cardiac output or stroke volume.
39
What happens as preload increases within the physiological range?
Cardiac output or stroke volume increases due to greater myocardial stretch, enhancing the force of contraction.
40
What is plotted on the x-axis of the Frank-Starling curve?
Preload-related measures such as EDP, EDV, or venous return.
41
What is plotted on the y-axis of the Frank-Starling curve?
Cardiac work, force of contraction, energy of contraction, tension, stroke volume, or cardiac output.
42
What mechanisms explain how force increases with muscle stretch?
43
What proteins make up the troponin complex?
TnC: Binds calcium.
TnI: Inhibits interaction between actin and myosin.
TnT: Anchors the troponin complex to tropomyosin.
44
What does length-dependent activation refer to in muscle contraction?
The dependence of muscle contraction force on the sarcomere length due to actin-myosin overlap.
45
What is the optimal sarcomere length for maximal tension in cardiac muscle?
Around 2.2 μm.
46
What happens when sarcomere length is too short (e.g., 1.25 μm)?
Overlapping actin filaments interfere with cross-bridge formation, reducing tension.
47
What happens when sarcomere length is too long (e.g., 3.65 μm)?
Actin and myosin filaments are too far apart, reducing the number of cross-bridges and decreasing tension.
48
How does sarcomere length affect calcium sensitivity in cardiac muscle?
Longer sarcomere lengths (e.g., 2.2 microns) increase calcium sensitivity, leading to greater force development at a given intracellular calcium concentration ([Ca²⁺]i).
49
What happens to force development at shorter sarcomere lengths (e.g., 1.8 microns)?
Force development is reduced due to lower calcium sensitivity, even at the same [Ca²⁺]i.
50
According to the Frank-Starling Law, how are the stroke volumes of the left and right ventricles related?
The stroke volumes of the left and right ventricles are perfectly matched, except for very transient differences.
51
What determines cardiac output (CO) at a given heart rate and contractility?
Central venous pressure (CVP) determines cardiac output (CO).
52
How does the Frank-Starling Law help maintain cardiac output?
It helps maintain CO even in the face of increased afterload or decreased contractility.
53
What is another term for cardiac contractility?
Inotropy
54
How is cardiac contractility defined?
The strength of contraction.
55
What 2 factors reflect cardiac contractility?
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
What regulates cardiac contractility?
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
How does noradrenaline (norepinephrine) increase contractility?
By stimulating β₁ (and to a lesser extent β₂) adrenergic receptors.
58
What does the graph show about contractility?
Increased contractility (e.g., due to sympathetic stimulation) raises stroke volume for a given end-diastolic pressure (EDP).
59
How does the Frank-Starling mechanism compensate for decreased cardiac contractility?
By increasing end-diastolic pressure (EDP) or volume to maintain stroke volume and cardiac output (CO).
60
What is heart failure (HF)?
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
in what 2 ways can heart failure occur?
Acutely: During a myocardial infarction (MI).
Chronically: In long-term heart failure.
62
How is heart failure characterized on a function curve?
By a lower function curve compared to normal cardiac function, indicating reduced stroke volume for a given EDP.
63
What happens to renal excretion of fluid when cardiac output (CO) falls in heart failure?
Renal excretion of fluid is reduced, increasing blood volume, especially in the veins.
64
What 2 systems are activated due to reduced blood pressure in heart failure?
Sympathetic Nervous System (SNS): Increases contractility, heart rate, and venoconstriction.
Renin-Angiotensin-Aldosterone System (RAAS): Promotes fluid retention and venoconstriction.
65
How do venous blood volume and venoconstriction affect central venous pressure (CVP)?
They increase CVP, which equals right ventricular end-diastolic pressure (RVEDP).
66
What would a graph show about heart failure compensation?
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
How does compensated heart failure differ from normal cardiac function on a graph?
Compensated HF has higher EDP but lower stroke volume compared to normal cardiac function.
68
What is the direct effect of increased afterload on cardiac output?
To reduce stroke volume due to decreased ejection time.
69
How can cardiac contractility be affected by increased blood pressure (BP)?
It may fall due to the baroreceptor reflex.
70
What secondary effect compensates for reduced stroke volume when afterload increases?
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
What is the effect of afterload on cardiac output within the normal range of blood pressures?
Afterload has little effect on cardiac output in the normal range of blood pressures.
72
What happens to cardiac output when afterload exceeds the normal range?
Cardiac output decreases significantly as mean arterial pressure increases beyond the normal range.
73
What condition can significantly increase afterload and reduce cardiac output?
Aortic valve stenosis.
74
What does the term "blood pressure" (BP) refer to?
The pressure in the large arteries.
75
How does blood pressure behave during the cardiac cycle?
It oscillates, rising and falling with systole and diastole.
76
What are the two key components of blood pressure?
Systolic Blood Pressure (SBP): The peak pressure during ventricular contraction.
Diastolic Blood Pressure (DBP): The lowest pressure during ventricular relaxation.
77
What causes pressure and flow waves in the arteries?
Blood from the heart hitting the blood in the aorta, propagating waves down the vascular system.
78
How does the pressure wave change as it moves down the arterial tree?
It becomes larger due to greater arterial stiffness.
79
What happens to the pressure wave as it reaches the arterioles and microcirculation?
It progressively dies out.
80
How does blood flow change as it moves into the arterioles and microcirculation?
Flow becomes progressively smoothed out.
81
Why does the pressure wave grow larger in the arterial tree before it dies out?
Due to the increasing stiffness of the arteries, which amplifies the wave.
82
What happens to arterial blood pressure (ABP) and blood flow during systole?
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
What is the role of the elastic walls of large arteries during systole?
They store energy and volume, helping to maintain blood flow during diastole.
84
How does total peripheral resistance (TPR) affect blood flow?
TPR, primarily determined by resistance arteries and arterioles, controls blood flow to different regions like the skin, muscle, brain, and gut.
85
What happens to arterial blood pressure (ABP) and blood flow during diastole?
Stored energy in the elastic walls of the arteries maintains blood flow during diastole by arterial recoil, pushing blood into smaller arteries
86
What is the role of arterial recoil during diastole?
Arterial recoil pushes blood forward into smaller arteries, ensuring continuous blood flow despite the heart being in the relaxation phase.
87
What happens to the stored pressure during diastole?
The stored pressure gradually falls as blood flows through the tissues.
88
What is diastolic pressure?
The minimum pressure reached in the arteries before the next systole.
89
How does total peripheral resistance (TPR) affect blood flow during diastole?
TPR, mainly due to arterioles, regulates how blood is distributed to various tissues like the skin, muscles, brain, and gut.
90
What is the relationship between pressure, flow, and resistance?
ΔPressure = Flow × Resistance.
91
what is p1 and p2 in this diagram
p1 = Arterial Blood Pressure (ABP).
p2 = Central Venous Pressure (CVP).
92
Where does the steepest drop in pressure occur in the vascular system?
Across the resistance arteries and arterioles (R2), due to their high resistance.
93
What is the mean arterial pressure (MAP) at the aorta?
Approximately 95 mmHg (with a range of 120/80 mmHg for systolic/diastolic pressures).
94
What is the pressure in the veins?
Around 5–10 mmHg, dropping to 0–5 mmHg as blood returns to the heart.
95
How is total vascular resistance
(Rtotal) calculated?
R1 = resistance of arteries
R2 = resistance of arterioles
R3 = resistance of veins
96
What limits the extent of blood pressure (BP) changes?
The baroreceptor reflex.
97
What is the role of the arterial baroreflex?
It helps maintain a relatively constant BP, regulating blood flow to some organs while ensuring constant flow to others.
98
What does the BP set point refer to?
The baseline BP level that can adjust to meet physiological needs, such as increasing during exercise to accommodate higher cardiac output.
99
How does the body prioritize blood flow via the baroreflex?
100
What type of receptors are baroreceptors?
Mechanoreceptors with fine nerve endings sensitive to stretch.
101
What happens to baroreceptor firing when pressure decreases?
Decreased pressure causes decreased firing.
102
Within what blood pressure range are baroreceptors most sensitive?
Between 80-150 mmHg.
103
How does pulse pressure affect baroreceptor sensitivity?
Sensitivity increases with larger pulse pressures, making baroreceptors more responsive to rapid changes in pressure.
104
What is baroreceptor adaptation?
Baroreceptors reset to a new pressure if it is sustained for a few hours, such as in chronic hypertension.
105
Where are baroreceptors located in the cardiovascular system?
Carotid sinus
Aortic arch
106
Which cranial nerves are involved in the baroreceptor reflex pathway?
IX (Glossopharyngeal nerve)
X (Vagus nerve)
107
Where are signals from baroreceptors processed in the brain?
In the nucleus tractus solitarius (NTS) of the brainstem.
108
What triggers the baroreceptor reflex?
A decrease in blood volume or mean arterial pressure (MAP), which reduces baroreceptor firing.
109
How does the baroreceptor reflex restore MAP?
By increasing sympathetic drive and decreasing parasympathetic drive, leading to increased cardiac output (CO) and total peripheral resistance (TPR).
110
What are the effects of increased sympathetic drive on the heart?
Increased heart rate (HR) via β₁ receptors.
Increased stroke volume (SV) via enhanced contractility and venous return
111
How does the baroreceptor reflex affect blood vessels?
Venoconstriction increases venous return via α₁ receptors.
Systemic arteriole constriction increases TPR via α₁ receptors.
112
What type of feedback does the baroreceptor reflex use?
Negative feedback to restore MAP.
113
What triggers the renin-angiotensin-aldosterone system (RAAS)?
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
What is the role of renin in the RAAS?
Renin converts angiotensinogen (produced by the liver) into angiotensin I in the blood.
115
What enzyme converts angiotensin I into angiotensin II?
Angiotensin-Converting Enzyme (ACE).
116
What are the effects of angiotensin II?
117
What is the role of aldosterone in the RAAS?
It increases sodium reabsorption in the kidneys, which leads to water retention and increased blood volume.
118
What is pressure diuresis?
The increase in water excretion by the kidneys in response to elevated arterial pressure.
119
What is pressure natriuresis?
The increase in sodium excretion by the kidneys in response to elevated arterial pressure.
120
How does increased mean arterial pressure (MAP) affect renal perfusion?
It increases renal perfusion pressure, enhancing water (diuresis) and sodium (natriuresis) excretion.
121
What substances decrease due to increased renal perfusion pressure?
Angiotensin II levels decrease.
122
what substances increase with elevated renal perfusion pressure?
Nitric oxide, prostaglandins, and renal kinins.
123
How does increased medullary blood flow influence natriuresis?
It increases renal interstitial hydrostatic pressure, reducing tubular sodium reabsorption and promoting sodium excretion.
124
What is the relationship between arterial pressure and urine output?
Urine output increases exponentially as arterial pressure rises, demonstrating pressure diuresis and natriuresis.
125
What role does renal interstitial hydrostatic pressure play in sodium excretion?
It opposes tubular sodium reabsorption, promoting natriuresis.
126
What is the primary mechanism for long-term regulation of arterial blood pressure (BP)?
Maintenance of a constant extracellular fluid volume, including plasma volume.
127
What determines extracellular fluid volume?
Sodium (Na⁺) concentration.
128
What hypothesis explains the prevalence of diseases like hypertension and type 2 diabetes in modern society?
The thrifty genotype hypothesis.
129
What is the thrifty genotype hypothesis?
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
Why might humanity have evolved to crave salt?
Early humans emerged in hot and dry environments, where salt was scarce, making salt retention critical for survival.
131
How does the abundance of salt in modern diets relate to health issues?
Excess salt intake, driven by evolutionary programming, contributes to diseases like hypertension.
132
Is renal sodium (Na⁺) excretion the only factor that stabilizes blood pressure (BP) over the long term?
No, other factors such as the sympathetic nervous system (SNS) and vascular tone also contribute.
133
What happens to the baroreceptor reflex over time?
The baroreceptor reflex doesn’t remain active indefinitely; it adjusts and diminishes over time.
134
What role does vascular tone play in long-term blood pressure control?
Regulation of vascular tone, influenced by the SNS or calcium (Ca²⁺) inhibitors, can contribute to blood pressure control.
135
Na excretion can occur without changes in BP - why does this matter?
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.
