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Questions and Answers
A patient's end-diastolic volume (EDV) is 150 ml, and their end-systolic volume (ESV) is 60 ml. If their heart rate is 75 beats per minute, what is their cardiac output?
A patient's end-diastolic volume (EDV) is 150 ml, and their end-systolic volume (ESV) is 60 ml. If their heart rate is 75 beats per minute, what is their cardiac output?
- 11.25 L/min
- 6.75 L/min (correct)
- 4.5 L/min
- 7.5 L/min
How does increased venous return affect cardiac function, according to the Frank-Starling law, within physiological limits?
How does increased venous return affect cardiac function, according to the Frank-Starling law, within physiological limits?
- It decreases heart rate, which reduces cardiac output despite an increase in stroke volume.
- It decreases preload, which subsequently reduces stroke volume.
- It increases afterload, making it harder for the ventricle to eject blood, decreasing stroke volume.
- It increases end-diastolic volume (EDV), leading to increased myocardial stretch and a stronger contraction, thereby increasing stroke volume. (correct)
If a patient's ejection fraction (EF) decreases while their end-diastolic volume (EDV) remains constant, what compensatory mechanism would the left ventricle likely undergo over time?
If a patient's ejection fraction (EF) decreases while their end-diastolic volume (EDV) remains constant, what compensatory mechanism would the left ventricle likely undergo over time?
- Increased production of ANP (atrial natriuretic peptide) to reduce blood volume.
- Left ventricular hypertrophy to increase its work and maintain normal stroke volume. (correct)
- Atrial fibrillation to maintain cardiac output.
- Downregulation of adrenergic receptors to reduce heart rate and myocardial oxygen demand.
During exercise, how does the body ensure an increase in both stroke volume (SV) and cardiac output (COP) efficiently, minimizing energy consumption?
During exercise, how does the body ensure an increase in both stroke volume (SV) and cardiac output (COP) efficiently, minimizing energy consumption?
What is the primary mechanism by which the respiratory pump enhances venous return?
What is the primary mechanism by which the respiratory pump enhances venous return?
Considering a scenario where a patient experiences increased sympathetic stimulation but their cardiac output remains unchanged, what is the most likely underlying compensatory mechanism?
Considering a scenario where a patient experiences increased sympathetic stimulation but their cardiac output remains unchanged, what is the most likely underlying compensatory mechanism?
How would an increase in heart rate due to sympathetic stimulation affect the duration of diastole, and what implications would this have on ventricular filling and stroke volume?
How would an increase in heart rate due to sympathetic stimulation affect the duration of diastole, and what implications would this have on ventricular filling and stroke volume?
In a patient with chronic hypertension, how does increased afterload typically affect the velocity and duration of left ventricular ejection?
In a patient with chronic hypertension, how does increased afterload typically affect the velocity and duration of left ventricular ejection?
Under what conditions would the sympathetic vasoconstrictor tone most contribute to venous return?
Under what conditions would the sympathetic vasoconstrictor tone most contribute to venous return?
If a patient's Cardiac Output (CO) increases by 40% due to being in a hot, humid climate, what adjustments do the cardiac parameters likely exhibit and why?
If a patient's Cardiac Output (CO) increases by 40% due to being in a hot, humid climate, what adjustments do the cardiac parameters likely exhibit and why?
How does the skeletal muscle pump affect venous return from the lower extremities during periods of prolonged standing, and what is the underlying mechanism?
How does the skeletal muscle pump affect venous return from the lower extremities during periods of prolonged standing, and what is the underlying mechanism?
In the context of cardiac function, differentiate between the roles of the sympathetic and parasympathetic nervous systems in regulating heart rate and stroke volume, while considering their potential interactions.
In the context of cardiac function, differentiate between the roles of the sympathetic and parasympathetic nervous systems in regulating heart rate and stroke volume, while considering their potential interactions.
How does central venous pressure (CVP) relate to right atrial pressure (RAP), and what does this relationship imply for assessing a patient's fluid status?
How does central venous pressure (CVP) relate to right atrial pressure (RAP), and what does this relationship imply for assessing a patient's fluid status?
What is the primary role of the cardiac suction mechanism in facilitating venous return, and under which conditions is this mechanism most significant?
What is the primary role of the cardiac suction mechanism in facilitating venous return, and under which conditions is this mechanism most significant?
Which best describes the relationship between sympathetic stimulation, venous return, and the maintenance of cardiac output during increased metabolic demand?
Which best describes the relationship between sympathetic stimulation, venous return, and the maintenance of cardiac output during increased metabolic demand?
Mean Systemic Filing Pressure (MSFP) is measured with what process?
Mean Systemic Filing Pressure (MSFP) is measured with what process?
How does the role of the venous valves contribute to the effectiveness of the skeletal muscle pump in promoting venous return from the lower extremities?
How does the role of the venous valves contribute to the effectiveness of the skeletal muscle pump in promoting venous return from the lower extremities?
What are the effects of hormones such as thyroxine on Cardiac Output:
What are the effects of hormones such as thyroxine on Cardiac Output:
How Does physical and mental activity affect Cardiac Output:
How Does physical and mental activity affect Cardiac Output:
If a patient increases their EDV, what affect does that have on SV?
If a patient increases their EDV, what affect does that have on SV?
How does the Frank-Starling mechanism intrinsically regulate stroke volume? (Select the best answer)
How does the Frank-Starling mechanism intrinsically regulate stroke volume? (Select the best answer)
Which scenario would most likely result in a sustained increase in cardiac output (COP) due to hormonal influence?
Which scenario would most likely result in a sustained increase in cardiac output (COP) due to hormonal influence?
How does the respiratory pump mechanism facilitate venous return during the phases of respiration?
How does the respiratory pump mechanism facilitate venous return during the phases of respiration?
What is the impact of increased afterload on left ventricular function and what compensatory mechanisms are triggered in response to this change?
What is the impact of increased afterload on left ventricular function and what compensatory mechanisms are triggered in response to this change?
In a scenario involving a patient with autonomic neuropathy experiencing diminished sympathetic vasoconstrictor tone, what compensatory mechanism is most likely to maintain adequate venous return?
In a scenario involving a patient with autonomic neuropathy experiencing diminished sympathetic vasoconstrictor tone, what compensatory mechanism is most likely to maintain adequate venous return?
Flashcards
Cardiac Output (CO)
Cardiac Output (CO)
The amount of blood pumped by each ventricle per minute, typically around 5.5 L/min and is equal in both ventricles.
Cardiac Index
Cardiac Index
The calculated value representing cardiac output adjusted for body size; 3.2 L/m2/min is normal.
Ejection Fraction
Ejection Fraction
The percentage of blood ejected from the ventricle with each contraction: normally 65% or 2/3 of EDV.
End Diastolic Volume (EDV)
End Diastolic Volume (EDV)
Volume of blood in the ventricle at the end of diastole, normally 110-140 ml (mean 130 ml).
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End Systolic Volume (ESV)
End Systolic Volume (ESV)
Volume of blood remaining in the ventricle after ejection, normally 50-70 ml (average 60 ml).
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Preload
Preload
The muscle length prior to contraction; dependent on ventricular filling. Venous return is the most important determining factor.
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Afterload
Afterload
The tension against which the ventricle must contract, or arterial pressure.
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Afterload and Ventricles
Afterload and Ventricles
Increased arterial pressure leads to increased afterload; afterload determined by pulmonary artery pressure for the right ventricle.
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Decrease Afterload
Decrease Afterload
Decrease in afterload leads to increased stroke volume and cardiac output at a lower energy cost.
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COP and Posture
COP and Posture
Cardiac Output decreases by 25% when standing compared to lying down.
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COP and Physical/Mental Activity
COP and Physical/Mental Activity
Exercise increases COP significantly; in anxiety and excitation, but no change in quiet sleep.
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Hormones that Increases Cardiac Output
Hormones that Increases Cardiac Output
Hormones such as epinephrine and thyroxine increase COP.
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Diseases affecting COP
Diseases affecting COP
Cardiac output is increased anemia, fevers and thyrotoxicosis. It decreases in heart failure, rapid arrhythmias and valve disease.
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ANS Control of COP
ANS Control of COP
The Autonomic Nervous System (ANS) controls heart function, balancing sympathetic and parasympathetic inputs, affecting HR and SV.
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Starling law
Starling law
Within limits, increased initial length of heart muscle fibers increases strength of contraction.
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Heterometric Regulation
Heterometric Regulation
Relates preload (EDV) with strength of the subsequent contraction. Increase EDV will increase strength of contraction.
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Afterload definition.
Afterload definition.
The heart has to overcome pressure or resistance to eject blood.
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Sympathetic Nerve
Sympathetic Nerve
Sympathetic (Accelerator) increases heart rate.
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Vagus Nerve
Vagus Nerve
Parasympathetic (Vagus) decreases heart rate.
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Parasympathetic stimulation
Parasympathetic stimulation
Parasympathetic stimulation inhibits the heart rate, it is regarded as a negative chronotropic effect.
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Sympathetic stimulation
Sympathetic stimulation
Sympathetic stimulation increases the heart rate; it is regarded as positive chronotropic effect.
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Venous Return
Venous Return
Volume of blood flow returning to heart from veins.
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Venous Return equation
Venous Return equation
VR = (MSFP - RAP) / RVR
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Mean Systemic Filling Pressure
Mean Systemic Filling Pressure
MSFP (mean systemic venous pressure) is the pressure measured everywhere in the systemic circulation after blood flow has been stopped by clamping large BVs at heart.
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Mean Circulatory Pressure
Mean Circulatory Pressure
MCP (mean circulatory pressure) is the mean pressure in both systemic & pulmonary circulation. MSFP ≈ MCP.
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Respiratory pump
Respiratory pump
Respiratory pump: During inspiration, the intra-thoracic pressure becomes more negative. So, the intermittent inspiration functions as an intermittent suction pump
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Skeletal muscles pump:
Skeletal muscles pump:
Skeletal muscles surround to veins in the lower limbs, and pumps the veins around.
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Muscle relaxation effect
Muscle relaxation effect
During muscle relaxation: The valves prevent the back flow of blood
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Central Venous Pressure (CVP)
Central Venous Pressure (CVP)
CVP = Central Venous Pressure
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MSFP
MSFP
7 mmHg is the typical systemic filling pressure
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- Intended learning outcomes include defining cardiac output, explaining intrinsic regulation of stroke volume and listing factors that affect venous return
Cardiac Output (COP)
- COP is the amount of blood pumped by each ventricle per minute
- Normal value is 5.5 L/min and is equal in both ventricles
- Equals minute volume
- Calculated as Heart Rate (HR) x Stroke Volume (SV)
- Not an actual volume, but a calculated volume
- COP can be expressed as L/min, with a normal value of ~5 L/min
- Cardiac Index = COP / m^2 of body surface area = 3.2 L/m2/min
Stroke Volume (SV)
- SV is the amount of blood pumped around the body by the left ventricle in one contraction
- SV = End Diastolic Volume (EDV) - End Systolic Volume (ESV)
- SV is a real volume
- Normal SV is 60-90 ml with a mean of 80 ml
- Calculated as 130 ml (EDV) - 50 ml (ESV) = 80 ml
End Diastolic Volume (EDV)
- EDV is the volume of blood in the ventricles at the end of diastole
- Normal EDV ranges from 110-140 ml with a mean of 130 ml
- Increased venous return increases EDV which increases preload, that consequently increases SV according to Frank Starling law
End Systolic Volume (ESV)
- ESV is the volume remaining in the ventricle after the end of ejection
- Normal ESV ranges from 50-70 ml, with an average of 60 ml
Heart Rate (HR)
- Heart Rate (HR) is the number of beats per minute
- Normal resting HR is 60-90 bpm, with a mean of 70 bpm
- Increased HR (up to 150 bpm) occurs by sympathetic stimulation which increases COP, provided SV is not decreased
Ejection Fraction
- Ejection Fraction is the fraction of EDV that is ejected during each contraction
- Normal is around 50-65%
- Ejection fraction is calculated as SV/EDV x 100, normally equals 65% which is 2/3 EDV
Cardiac Vocabulary
- Preload is the muscle length prior to contractility that is dependent on ventricular filling or end diastolic volume (EDV)
- Preload is influenced by venous return and is the fiber length or tension from which the heart contracts
- Venous return is the most important determining factor for preload
- The value of preload is related to right atrial pressure
- Afterload is the tension/arterial pressure against which the ventricle must contract
- If arterial pressure increases, afterload also increases
- Afterload for the left ventricle is determined by aortic pressure
- Afterload for the right ventricle is determined by pulmonary artery pressure
- An Increase in afterload results in decreased strength, velocity and duration of LV ejection, decreasing SV and increasing ESV
- The LV ms will become thicker (LV hypertrophy) to maintain normal SV against high resistance at low costs of oxygen consumption
- Decrease in afterload results in increased SV and COP at a low cost of energy and oxygen consumption.
Variations in Cardiac Output (COP)
- Varies in different individuals and in the same individual under different conditions
- Posture affects venous return and COP
- COP decreases 25% from its level during standing after recumbency
- Physical and mental activity
- Exercise increases COP up to 25L/min in sedentary and 35 L/min in athletes
- Increases in anxiety and excitation
- It does not change in quiet sleep only in dreams of exercise or stressful conditions.
- Temperature
- Hot humid climate increases COP 40%
- Low body temperature as in hypothermic cardioplegia & open heart surgery decreases COP
- Eating increases COP, especially with a heavy meal
- During Pregnancy, COP increases 10% in late pregnancy due to increased metabolism of fetus and mother
- Hormones and drugs increase COP (E, NE, thyroxine, histamine)
- Pathological conditions
- Anemia, fevers, thyrotoxicosis increase COP
- Heart failure, rapid arrhythmias & valve disease decrease COP
Regulation of Cardiac Output
- The COP is regulated extrinsically and intrinsically
- Extrinsic factors affecting SV and HR, include
- ANS [symp* →↑ COP (↑HR & ↑ SV) and parasympath →↓ COP (↓HR & ↓ SV).
- Hormones such has CA & thyroxine
- Glucagon (positive inotropic)
- Intrinsic factors affect the SV only and include
- Heterometric regulation
- Factors affecting SV include Preload
- Increased initial length of myocardium (↑ EDV) by increasing in VR, increasing contraction & SV
- According to Starling law: within limit, Preload, cardiac suction, and nervous and hormonal compensation all help the heart function.
Factors Affecting Heart Rate
- Parasympathetic stimulation inhibits the heart rate; negative chronotropic effect
- Sympathetic stimulation increases the heart rate; positive chronotropic effect
- Epinephrine hormone (released from the adrenal medulla) increases the heart rate; positive chronotropic effect
- The nervous system controls heart rate
- Two nerves link the cardiovascular center in the medulla oblongata of the brain with the SA node of the heart
- Accelerator nerve: sympathetic NS, when stimulated releases neurotransmitter at the SA node to INCREASE heart rate
- Vagus nerve: parasympathetic NS, when stimulated releases neurotransmitter at the SA node to DECREASE heart rate
Venous Return
- Represents volume of blood flow returning to heart from veins
- The skeletal muscle pump involves muscle contraction & valves
- The respiratory pump moves blood into the right atrium
- Lower thoracic pressure increases abdominal pressure during inhalation
- VR = (MSFP - RAP)/RVR, where
- MSFP = Mean systemic filling pressure
- RAP= Right atrial pressure
- RVR = Resistance to venous return
- MSFP (mean systemic venous pressure) is the pressure measured everywhere in the systemic circulation after blood flow has been stopped by clamping large BVs at heart
- MCP (mean circulatory pressure) is the mean pressure in both systemic & pulmonary circulation; MSFP MCP (pulmonary circulation with little contribution)
- CVP equals central venous pressure
- MCP= 7 mmHg is the systemic filling pressure in the living, peripheral venous pressure (6-8 mmHg)
- Central venous = 0-5 mmHg is the pressure in great veins at their entry to the heart = RAP
Physiological Factors Helping Venous Return Against Gravity
- Respiratory pump
- During inspiration, the intra-thoracic pressure becomes more negative
- The intermittent inspiration functions as an intermittent suction pump
- During inspiration, the intra-abdominal pressure becomes more positive i.e. intermittent pressure pump.
- Skeletal muscle pump
- Skeletal muscles surround the veins in the lower limbs
- During muscle contraction, the veins are squeezed & the blood is shifted toward the heart
- During muscle relaxation, the valves prevent the back flow of blood
- Cardiac suction
- Refers to the rapid filling phase, during which the rapid expansion of the ventricles decreases Ventricular pressure & blood is sucked into the ventricles
- The sympathetic vasoconstrictor tone
- It prevents the shift of blood to the veins of lower limbs (being constricted)
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