Cardiac Output and Stroke Volume

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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?

  • 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?

  • 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?

  • 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?

<p>By decreasing afterload through the dilation of skeletal muscle blood vessels, which increases SV and COP at a low energy cost. (A)</p> Signup and view all the answers

What is the primary mechanism by which the respiratory pump enhances venous return?

<p>By increasing the pressure gradient between the peripheral veins and the right atrium during inspiration. (D)</p> Signup and view all the answers

Considering a scenario where a patient experiences increased sympathetic stimulation but their cardiac output remains unchanged, what is the most likely underlying compensatory mechanism?

<p>An increase in afterload reduces stroke volume, counteracting the effect of increased heart rate. (A)</p> Signup and view all the answers

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?

<p>It decreases the duration of diastole, potentially reducing ventricular filling and stroke volume if filling time is significantly compromised. (A)</p> Signup and view all the answers

In a patient with chronic hypertension, how does increased afterload typically affect the velocity and duration of left ventricular ejection?

<p>It decreases both the velocity and duration of left ventricular ejection. (C)</p> Signup and view all the answers

Under what conditions would the sympathetic vasoconstrictor tone most contribute to venous return?

<p>During prolonged standing, preventing blood pooling in the lower limbs. (C)</p> Signup and view all the answers

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?

<p>Both HR and SV increase, triggered by vasodilation and increased metabolic demand. (C)</p> Signup and view all the answers

How does the skeletal muscle pump affect venous return from the lower extremities during periods of prolonged standing, and what is the underlying mechanism?

<p>It enhances venous return by intermittent muscle contractions that compress veins and propel blood toward the heart, aided by one-way valves. (C)</p> Signup and view all the answers

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.

<p>The sympathetic system increases heart rate and can increase stroke volume, while the parasympathetic system decreases heart rate and has minimal direct impact on stroke volume. (B)</p> Signup and view all the answers

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?

<p>CVP and RAP are approximately equal, reflecting the pressure in the great veins at their entry to the heart and providing insights into preload. (B)</p> Signup and view all the answers

What is the primary role of the cardiac suction mechanism in facilitating venous return, and under which conditions is this mechanism most significant?

<p>To reduce ventricular pressure during rapid filling allowing blood to move into the ventricles. (D)</p> Signup and view all the answers

Which best describes the relationship between sympathetic stimulation, venous return, and the maintenance of cardiac output during increased metabolic demand?

<p>Sympathetic stimulation increases venous return by enhancing venous tone and promoting vasoconstriction, thus helping to maintain cardiac output. (C)</p> Signup and view all the answers

Mean Systemic Filing Pressure (MSFP) is measured with what process?

<p>MSFP is measured everywhere in the systemic circulation after blood flow has been stopped by clamping large BVs at the heart (C)</p> Signup and view all the answers

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?

<p>By preventing blood from flowing backward during muscle relaxation, thus ensuring unidirectional movement of blood toward the heart. (D)</p> Signup and view all the answers

What are the effects of hormones such as thyroxine on Cardiac Output:

<p>Increases due to it increasing HR (C)</p> Signup and view all the answers

How Does physical and mental activity affect Cardiac Output:

<p>It increasees in anxiety and excitation but does not change in sleep (C)</p> Signup and view all the answers

If a patient increases their EDV, what affect does that have on SV?

<p>It will increase SV according to Frank starling law (&amp;vice versa) (B)</p> Signup and view all the answers

How does the Frank-Starling mechanism intrinsically regulate stroke volume? (Select the best answer)

<p>By increasing the initial length of myocardial fibers (increased EDV), leading to a more forceful contraction and increased stroke volume, within physiological limits. (C)</p> Signup and view all the answers

Which scenario would most likely result in a sustained increase in cardiac output (COP) due to hormonal influence?

<p>Chronic administration of thyroxine, leading to increased metabolic rate and oxygen demand. (A)</p> Signup and view all the answers

How does the respiratory pump mechanism facilitate venous return during the phases of respiration?

<p>By decreasing intra-thoracic pressure during inspiration and increasing intra-abdominal pressure, creating a pressure gradient that favors venous flow towards the heart. (C)</p> Signup and view all the answers

What is the impact of increased afterload on left ventricular function and what compensatory mechanisms are triggered in response to this change?

<p>Decreases stroke volume and increases end-systolic volume (ESV), triggering concentric hypertrophy to maintain normal stroke volume. (D)</p> Signup and view all the answers

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?

<p>Enhanced skeletal muscle pump activity in the lower extremities, alongside compensatory increase in blood volume. (B)</p> Signup and view all the answers

Flashcards

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

The calculated value representing cardiac output adjusted for body size; 3.2 L/m2/min is normal.

Ejection Fraction

The percentage of blood ejected from the ventricle with each contraction: normally 65% or 2/3 of 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)

Volume of blood remaining in the ventricle after ejection, normally 50-70 ml (average 60 ml).

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Preload

The muscle length prior to contraction; dependent on ventricular filling. Venous return is the most important determining factor.

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Afterload

The tension against which the ventricle must contract, or arterial pressure.

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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 in afterload leads to increased stroke volume and cardiac output at a lower energy cost.

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COP and Posture

Cardiac Output decreases by 25% when standing compared to lying down.

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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 such as epinephrine and thyroxine increase COP.

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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

The Autonomic Nervous System (ANS) controls heart function, balancing sympathetic and parasympathetic inputs, affecting HR and SV.

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Starling law

Within limits, increased initial length of heart muscle fibers increases strength of contraction.

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Heterometric Regulation

Relates preload (EDV) with strength of the subsequent contraction. Increase EDV will increase strength of contraction.

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Afterload definition.

The heart has to overcome pressure or resistance to eject blood.

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Sympathetic Nerve

Sympathetic (Accelerator) increases heart rate.

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Vagus Nerve

Parasympathetic (Vagus) decreases heart rate.

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Parasympathetic stimulation

Parasympathetic stimulation inhibits the heart rate, it is regarded as a negative chronotropic effect.

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Sympathetic stimulation

Sympathetic stimulation increases the heart rate; it is regarded as positive chronotropic effect.

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Venous Return

Volume of blood flow returning to heart from veins.

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Venous Return equation

VR = (MSFP - RAP) / RVR

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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

MCP (mean circulatory pressure) is the mean pressure in both systemic & pulmonary circulation. MSFP ≈ MCP.

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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 surround to veins in the lower limbs, and pumps the veins around.

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Muscle relaxation effect

During muscle relaxation: The valves prevent the back flow of blood

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Central Venous Pressure (CVP)

CVP = Central Venous Pressure

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MSFP

7 mmHg is the typical systemic filling pressure

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Study Notes

  • 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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