Cardiovascular | Cardiac Output

Name: Cardiovascular | Cardiac Output
Uploaded: 2017-08-03T20:33:46.000Z
Duration: 1 h 28 min 59 s

Cardiac Output

In this section, we will discuss cardiac output, which is defined as the product of heart rate and stroke volume. We will explore the units of heart rate and stroke volume and calculate the normal cardiac output.

Cardiac Output Calculation

Cardiac output (CO) is equal to heart rate (HR) multiplied by stroke volume (SV).

Heart rate is measured in beats per minute, while stroke volume is the total volume of blood ejected by the ventricles with each beat.

By canceling out the beats, we are left with milliliters per minute as the unit for cardiac output.

The average heart rate falls between 60 to 80 beats per minute, and the average stroke volume is around 70 milliliters.

Multiplying these values gives us a normal cardiac output of approximately 5 liters per minute or 5000 milliliters per minute.

Factors Affecting Cardiac Output

Cardiac output can be significantly increased during exercise or decreased due to parasympathetic innervation or other factors.

Heart Rate Regulation

In this section, we will delve into heart rate regulation and discuss factors that influence heart rate.

Heart Rate Range

The normal range for heart rate is typically between 60 to 100 beats per minute. When it exceeds 100 beats per minute, it is considered tachycardia.

The SA node sets the sinus rhythm and determines the average heart rate within this range. It generates intrinsic action potentials that spread throughout the heart.

Sympathetic Nervous System Influence

The sympathetic nervous system plays a role in increasing heart rate. It releases neurotransmitters such as norepinephrine and epinephrine, which act on beta-1 adrenergic receptors to stimulate the heart.

These chemicals have a positive effect on heart rate, meaning they increase it.

The transcript is already in English, so there is no need to translate it.

New Section

This section discusses the regulation of heart rate and the role of different factors such as acetylcholine, sympathetic nervous system, parasympathetic nervous system, hormones, body temperature, ions (calcium and potassium), and their effects on heart rate.

Regulation of Heart Rate

Acetylcholine, released by the parasympathetic nervous system, acts on muscarinic type 2 receptors to decrease heart rate. It hyperpolarizes the cell and inhibits cyclic GMP production.

The sympathetic nervous system, with the presence of epinephrine and norepinephrine, acts as a positive chronotropic agent to increase heart rate.

Thyroid hormones (T3 and T4) are powerful regulators that can increase heart rate and basal metabolic rate.

Increased body temperature stimulates an increase in heart rate by increasing metabolic rate.

Calcium levels play a role in regulating heart rate. High calcium levels tend to speed up the heart rate (positive chronotropic effect), while low calcium levels slow down the heart rate (negative chronotropic effect).

Potassium levels also influence heart rate. High potassium levels in the blood (hyperkalemia) can affect potassium movement into cells and impact heart rate.

New Section

This section continues discussing factors that influence heart rate regulation, including body temperature and ions like calcium and potassium.

Body Temperature

Body temperature is a significant regulator of heart rate. Increasing body temperature stimulates an increase in metabolic rate and speeds up the heart rate.

Ions

Calcium is a crucial regulator of heart rate. High calcium levels tend to speed up the heart rate (positive chronotropic effect), while low calcium levels slow down the heart rate (negative chronotropic effect).

Potassium also influences heart rate. High potassium levels in the blood (hyperkalemia) can affect potassium movement into cells and impact heart rate.

The transcript is already in English, so there is no need to translate it.

Effects of Imbalances in Potassium and Calcium Levels

This section discusses the effects of imbalances in potassium and calcium levels on the heart.

Imbalance in Potassium Levels

Low potassium levels can cause the heart to send action potentials less effectively, leading to cardiac arrest.

Low potassium levels can also result in arrhythmias.

High potassium levels act as an inhibitor for the heart.

Imbalance in Calcium Levels

High calcium levels act as a stimulator for the heart.

Low calcium levels act as an inhibitor for the heart.

Chemoreceptors and their Role in Heart Rate Regulation

This section explains the role of chemoreceptors in regulating heart rate.

Chemoreceptors are specialized cells located at specific points, such as the bifurcation point of the common carotid artery.

Chemoreceptors are stimulated when there is low oxygen, high CO2, or low pH in the blood.

The information from chemoreceptors is carried to the central nervous system, specifically to the medulla.

In response to this information, the medulla integrates it and increases respiration rate.

The medulla can also stimulate the cardiac accelerator, resulting in an increase in heart rate through sympathetic effect.

Stimulation of Peripheral Chemoreceptors and Heart Rate Increase

This section discusses how stimulation of peripheral chemoreceptors can lead to an increase in heart rate.

Situations with hypoxia (low oxygen), increased CO2 partial pressure, or decreased pH can activate peripheral chemoreceptors.

Stimulation of peripheral chemoreceptors due to these factors leads to an increase in heart rate.

However, this effect on heart rate is not as significant as the effect on respiration rate.

Heart Rate Variations with Age and Gender

This section explores heart rate variations based on age and gender.

Fetus and infants have extremely high heart rates, ranging from 120 to 140 beats per minute.

Adults generally have heart rates ranging from 60 to 100 beats per minute.

Females tend to have slightly faster heart rates compared to males.

Heart Rate and Age

This section discusses the relationship between heart rate and age, with specific ranges for different age groups.

Heart Rate Variation with Age

The heart rate varies depending on age.

Fetus and infants have a higher heart rate compared to adults.

Adults generally aim for a heart rate of 60 to 80 beats per minute (bpm).

Males typically have a heart rate of 64 to 72 bpm, while females tend to have a slightly faster heart rate of 72 to 80 bpm.

Factors Affecting Heart Rate

This section explores various factors that can affect heart rate.

Factors Affecting Heart Rate

Heart rate can fluctuate due to various factors.

Some factors include age, certain drugs, and endurance activities.

Endurance runners may have lower heart rates due to their strong myocardium and increased stroke volume.

Cardiac output is dependent on both heart rate and stroke volume.

Bradycardia and Tachycardia

This section defines bradycardia and tachycardia and discusses their potential causes.

Bradycardia and Tachycardia

Bradycardia refers to a heart rate less than 60 bpm.

Causes of bradycardia can include vagal stimulation, certain drugs, or endurance activities in athletes.

Endurance runners may have lower heart rates due to their strong myocardium and increased stroke volume compensating for cardiac output.

Tachycardia refers to a heart rate greater than 100 bpm.

Causes of tachycardia can include sympathetic nervous system activity, high T3 and T4 levels, certain drugs, or anxiety.

Stroke Volume and Endurance Activities

This section explains the relationship between stroke volume and endurance activities.

Stroke Volume in Endurance Activities

Stroke volume is the amount of blood pumped out of the ventricles per beat.

Endurance runners have high stroke volumes due to their strong myocardium, good preload, and contractility.

The increased stroke volume allows for a lower heart rate during exercise.

Cardiac output is dependent on both heart rate and stroke volume.

Summary of Heart Rate Variations

This section summarizes the variations in heart rate discussed earlier.

Summary of Heart Rate Variations

Heart rate varies with age, with higher rates in fetuses and infants.

Adults aim for a heart rate of 60 to 80 bpm.

Males typically have a heart rate of 64 to 72 bpm, while females tend to have a slightly faster heart rate of 72 to 80 bpm.

Bradycardia refers to a heart rate less than 60 bpm and can be caused by various factors such as vagal stimulation or certain drugs.

Tachycardia refers to a heart rate greater than 100 bpm and can be caused by factors like sympathetic nervous system activity or anxiety.

Endurance runners may have lower resting heart rates due to their strong myocardium and increased stroke volume compensating for cardiac output.

Definition of EDV (End Diastolic Volume)

In this section, the speaker defines EDV as End Diastolic Volume.

Definition of EDV

EDV stands for End Diastolic Volume.

It refers to the volume of blood in the heart before ventricular contraction.

It can be thought of as the pre-pumping volume.

Definition of ESV (End Systolic Volume)

The speaker explains the definition of ESV, which stands for End Systolic Volume.

Definition of ESV

ESV refers to the volume of blood remaining in the heart after ventricular contraction or systole.

After contraction, blood is ejected into either the pulmonary trunk and lungs or into the aorta and systemic circulation.

The remaining blood volume is called ESV.

On average, ESV is about 50 milliliters but can range from 50 to 70 milliliters.

Relationship between ESV and Stroke Volume

This section discusses the relationship between ESV and stroke volume.

Relationship between ESV and Stroke Volume

Stroke volume is calculated by subtracting ESV from EDV.

In this case, stroke volume would be equal to 120 mL minus 50 mL, resulting in a stroke volume of 70 mL per beat.

Subcategories of Stroke Volume

The speaker explains that stroke volume can be divided into three subcategories.

Subcategories of Stroke Volume

Stroke volume can be further divided into three categories:

Preload

Contractility

Afterload

Definition of Preload

The speaker defines preload and its effect on stroke volume.

Definition of Preload

Preload refers to the degree of stretch of the cardiac muscle.

It is a measure of how much the myocardium stretches when filled with blood.

Increasing preload leads to increased stretch of the heart, resulting in an increase in stroke volume.

Increasing End Diastolic Volume (EDV)

This section discusses ways to increase end diastolic volume (EDV).

Increasing End Diastolic Volume (EDV)

One way to increase EDV is by increasing venous return.

Venous return can be increased through activities such as muscular milking and changes in thoracic and abdominal pressures during breathing.

Muscular Milking and Breathing for Increased Venous Return

The speaker explains how muscular milking and breathing can help increase venous return.

Muscular Milking and Breathing for Increased Venous Return

Muscular milking refers to the contraction of muscles surrounding veins, which helps pump blood upwards.

Breathing also affects venous return. When breathing, changes in abdominal and thoracic pressures compress veins, aiding in blood flow towards the heart.

Pressure Changes during Breathing

This section discusses pressure changes during breathing and their impact on venous return.

Pressure Changes during Breathing

During inhalation, abdominal cavity pressure increases while thoracic cavity pressure decreases.

These pressure changes result in increased abdominal pressure and decreased thoracic pressure above the diaphragm.

The high abdominal pressure pushes blood towards the heart, while low thoracic pressure facilitates blood flow into the thoracic cavity.

Pressure Differences and Venous Return

The speaker explains how pressure differences affect venous return.

Pressure Differences and Venous Return

The pressure difference between the abdominal cavity (high pressure) and thoracic cavity (low pressure) helps increase venous return.

This pressure difference, along with muscular milking and other factors, contributes to increased end diastolic volume (EDV) and preload.

The transcript is already in English.

Respiratory Pump and Sympathetic Nervous System

This section discusses the respiratory pump and the role of the sympathetic nervous system in regulating venous return.

Respiratory Pump

The respiratory pump refers to the mechanism by which breathing increases abdominal cavity pressure, decreases thoracic cavity pressure, and helps to increase venous return.

The respiratory pump acts like a vacuum, sucking blood upwards and aiding in venous return.

Sympathetic Nervous System Control

The sympathetic nervous system has control over vasoconstriction in the smooth muscle of veins.

Release of chemicals such as norepinephrine and epinephrine by the sympathetic nervous system stimulates smooth muscle contractility, leading to increased blood flow and venous return.

Venoconstriction

Venoconstriction refers to the constriction of veins, which can be considered a positive regulator of venous return.

Venoconstriction helps squeeze blood upwards, aiding in venous return.

Filling Time

Adequate filling time is important for allowing the heart to fill with blood and stretch.

Insufficient filling time due to increased heart rate can decrease preload (the amount of blood filling the heart during diastole), which is not beneficial for cardiac function.

Impaired Stretchability

Myocardial infarctions (heart attacks) can lead to fibrous tissue replacing heart muscle.

Fibrous tissue does not stretch well, impairing preload and affecting cardiac function negatively.

Frank-Starling Law

This section explains Frank-Starling Law, which describes the relationship between stretch and force of contraction in the heart.

Frank-Starling Law

Frank-Starling Law states that an increased stretch on the heart leads to a greater force of contraction.

Increased stretching allows for more cross-bridge connections and optimal length, resulting in increased preload and stroke volume.

Contractility and Sympathetic Nervous System

This section discusses the importance of contractility in cardiac function and its dependence on the sympathetic nervous system.

Contractility

Contractility refers to the ability of the heart muscle to contract forcefully.

It is highly dependent on the sympathetic nervous system.

Chemicals like epinephrine and norepinephrine released by the sympathetic nervous system act on beta-1 adrenergic receptors, increasing calcium levels in cardiac cells.

Increased calcium levels enhance contractility by increasing cross bridge connections, leading to more frequent contractions and increased stroke volume.

Hormonal Influence

Thyroid hormones T3 and T4 also play a role in enhancing contractility.

The mechanism by which they do so is explained further in another video.

The transcript provided does not cover all aspects of cardiovascular physiology.

New Section

This section discusses the different types of proteins and drugs that can increase the expression of beta-1 adrenergic receptors, leading to increased responsiveness to certain hormones.

Proteins and Drugs that Increase Expression of Beta-1 Adrenergic Receptors

Certain proteins, such as T3 and T4, can increase the expression of beta-1 adrenergic receptors on myocardial cells. This allows for a greater response to norepinephrine and epinephrine.

Glucagon is another protein that can increase the expression of beta-1 adrenergic receptors, leading to increased contractility.

Various drugs, including digitalis, dopamine, and epinephrine, also have this effect. These drugs stimulate an increase in contractility by increasing calcium levels inside the cell or through other mechanisms.

Other drugs like beta blockers (e.g., metoprolol), calcium channel blockers (e.g., verapamil), and atropine act as inhibitors of contractility. They block certain channels or neurotransmitters to decrease contractile function.

New Section

This section explores how ions can affect contractility in the heart.

Ions and Their Effects on Contractility

Calcium plays a stimulatory role in contractility. Increased calcium levels inside the cell enhance contractile function, while hypocalcemia inhibits it.

High levels of potassium or sodium act as inhibitors of contractility. Hyperkalemia (high potassium) or hypernatremia (high sodium) reduce cardiac contractile function.

Protons, such as those present during acidosis, also have a negative effect on contractility. High levels of protons inhibit the heart's ability to contract effectively.

New Section

This section discusses positive and negative inotropic agents that affect contractility.

Positive and Negative Inotropic Agents

Substances that stimulate contractility are called positive inotropic agents. Examples include calcium, epinephrine, T3 and T4 hormones, glucagon, digitalis, dopamine, and dobutamine.

On the other hand, substances that decrease contractility are referred to as negative inotropic agents. Beta blockers (e.g., metoprolol), calcium channel blockers (e.g., verapamil), high potassium levels (hyperkalemia), high sodium levels (hypernatremia), and acidosis all act as negative inotropic agents.

New Section

This section explains afterload and its clinical relevance.

Afterload Definition and Clinical Relevance

Afterload is defined as the amount of resistance that must be overcome for ventricles to eject blood into the aorta or pulmonary trunk. It has significant clinical relevance, especially in conditions like hypertension where there is increased afterload.

Increased resistance due to stenotic valves or other factors makes it harder for the heart to pump blood effectively against this resistance.

New Section

This section discusses the factors that contribute to increased resistance in blood flow and how it affects the pressure within the aorta.

Factors Affecting Resistance and Pressure

Increased resistance in blood flow, such as due to plaque buildup or vasoconstriction, impedes blood flow through vessels and increases pressure.

Arterioles play a crucial role in regulating resistance by responding to vasoconstrictors like epinephrine and norepinephrine.

Contraction of smooth muscle in arterioles due to vasoconstrictors further impedes blood flow and increases pressure within the aorta.

Increased pressure within the aorta makes it harder for blood to be pushed out from the ventricles, affecting stroke volume.

Higher afterload (pressure against which the heart must pump) decreases stroke volume, while higher preload (ventricular filling pressure) increases stroke volume.

Plaque buildup, valve stenosis or sclerosis, and high systemic vascular resistance can contribute to increased afterload.

New Section

This section explains how increased systemic vascular resistance affects pressure and stroke volume.

Effects of Systemic Vascular Resistance

Contraction of arterioles increases systemic vascular resistance, leading to increased pressure within vessels.

Increased pressure can contribute to decreased stroke volume when there is an increase in afterload.

Factors such as valve dysfunctions (stenosis or sclerosis), plaque buildup, or hypertension can inhibit afterload regulation.

New Section

This section emphasizes the relationship between preload, contractility, and stroke volume.

Preload, Contractility, and Stroke Volume

Increased preload (ventricular filling pressure) leads to increased stroke volume.

Increased contractility also results in increased stroke volume.

Afterload is inversely proportional to stroke volume.

The atrial Bainbridge reflex can stimulate the heart rate by increasing venous return and stretch.

New Section

This section concludes the video by encouraging viewers to leave comments and subscribe if they found the information helpful.

Conclusion

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