Chapter 20 notes (Heart)

From Biol557

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*The mediastinum holds the heart (in the pericardial sac) and the '''great vessels''' as well as the thymus, esophagus, and trachea.
*The mediastinum holds the heart (in the pericardial sac) and the '''great vessels''' as well as the thymus, esophagus, and trachea.
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====The pericardium====
====The pericardium====
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*The sulci also contain the coronary arteries / veins and substantial amounts of fat.
*The sulci also contain the coronary arteries / veins and substantial amounts of fat.
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====The heart wall====
====The heart wall====
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**Sometimes, patients with damage to their right ventricle can survive because of this physiological effect.
**Sometimes, patients with damage to their right ventricle can survive because of this physiological effect.
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=====The heart valves=====
=====The heart valves=====
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*The coronary arteries originate at the aortic sinuses.
*The coronary arteries originate at the aortic sinuses.
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*'''Valvar heart disease''' occurs when a patient's heart valves misfunction to the point that a steady flow of blood cannot be maintained.
*'''Valvar heart disease''' occurs when a patient's heart valves misfunction to the point that a steady flow of blood cannot be maintained.
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*Blood flow to cardiac tissue can increase by 9 or 10 fold at times of greatest exertion.
*Blood flow to cardiac tissue can increase by 9 or 10 fold at times of greatest exertion.
-
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=====The coronary arteries=====
=====The coronary arteries=====
 +
 +
===20-3 Events during a complete heartbeat constitute a cardiac cycle===
 +
 +
====Phases of the cardiac cycle====
 +
 +
====Pressure and volume changes in the cardiac cycle====
 +
 +
=====Atrial systole=====
 +
*Atrial systole occurs to push blood into the ventricle to fill the 30% of the volume that wasn't already filled passively.
 +
**Hence one can live without atrial systole.
 +
*At the end of atrial systole, the ventricle contains all that it will hold for the current cardiac cycle: '''the end diastolic volume'''.
 +
 +
=====Ventricular systole=====
 +
*During ventricular systole, both sides of the heart eject about 70-80 mL of blood: the '''stroke volume'''.
 +
*At rest, the ratio of stroke volume to end diastolic volume is about 60%; this is called the '''ejection fraction'''.
 +
*At the end of ventricular systole, the volume of blood remaining in the ventricle is about 40% of the original end diastolic volume and is called the '''end systolic volume'''.
 +
 +
=====Ventricular diastole=====
 +
*The ventricle relaxes until atrial pressure is greater than ventricle pressure.
 +
*Then the atrioventricular valves open and blood passively passes from the atria to the ventricle until atrial systole begins.
 +
 +
===20-4 Cardiodynamics examines the factors that affect cardiac output===
 +
*Stroke volume is end diastolic volume (EDV) minus end systolic volume (ESV).
 +
*Stroke volume is the most important consideration in cardiodynamics.
 +
*Cardiac output, then is the stroke volume multiplied by the heart rate.
 +
**Cardiac output, essentially, tells us how much blood is flowing through the circulation each minute.
 +
 +
====Overview: Factors affecting cardiac output====
 +
*Heart rate and stroke volume are the two factors that can be adjusted and they are usually adjusted in concert.
 +
*The heart rate can be changed through the autonomic nervous system or through the endocrine system.
 +
*Stroke volume can be changed through the autonomic nervous system or through the endocrine system (which will adjust the EDV and ESV).
 +
 +
====Factors affecting the heart rate====
 +
=====Autonomic nervous system=====
 +
*The autonomic nervous system can control the heart rate from the cardioinhibitory center and cardioacceleratory center of the medulla oblongata.
 +
*The sympathetic system will be controlled by the cardioacceleratory center which will cause the heart to beat faster and with greater contractility.
 +
*These centers in the brain change the heart rate based on information from baroreceptors and chemoreceptors found in arteries and innervated by the cranial nerves.
 +
*The parasympathetic and sympathetic nervous systems change the heart rate by changing ion permeability at the SA node.
 +
**For instance, making them more permeable to K+ will mean that the cell will depolarize less quickly (because K+ will be flowing out more and Na+ will be flowing in the same as before).  This can be achieved through the parasympathetic release of acetylcholine.
 +
**The sympathetic system, on the other hand, can release norepinephrine in order to bind a channel and allow more Na+ to enter the cell, thus depolarizing the SA node at a higher frequency.
 +
*Another way the autonomic nervous system can receive feedback is from cells of the right atrium.
 +
**When they stretch (that is, when venous return is high) they cause increased sympathetic stimulation and thus increased heart rate.
 +
 +
=====Hormones=====
 +
*Just as the sympathetic system uses norepi, hormonal release of norepi or epi can trigger an increase in heart rate.
 +
*Epi increase not only the heart rate but also contractility.
 +
 +
====Factors affecting the stroke volume====
 +
*To affect stroke volume, one must change either EDV or ESV or both.
 +
 +
=====The EDV=====
 +
*The filling time, when increased can increase the EDV and ''vice versa'' when decreased.
 +
**Filling time is directly proportional to the heart rate; increased heart rate means decreased filling time.
 +
*The preload is the amount of stretching experienced by the ventricular muscles.
 +
**Preload is directly proportional to the EDV; the higher the EDV the more stretch (preload).
 +
**The more preload (stretch) the higher the force of contraction by the mycardium (because as mycardial fibers stretch, more of the sarcomere length overlaps).
 +
**Therefore as the mycardiocytes approach optimal sarcomere stretching, they will increase contractile strength and decrease the ESV.
 +
**So we see an increase of EDV and a decrease of ESV which means an increase of stroke volume.
 +
**And so, this relationship of increased EDV leading to increased stroke volume is called the '''Frank-Starling principle'''.
 +
 +
=====The ESV=====
 +
*There are three factors that affect the ESV: preload (as discussed in the EDV section), contractility, and afterload.
 +
 +
*Contractility is the force produced during contraction at a given preload.
 +
**This is usually controlled by the autonomic nervous system and hormones but can also be manipulated with drugs and abnormal ion concentrations in the extracellular fluid.
 +
**Things that increase contractility are said to be '''positively inotropic''' and generally work by increasing Ca+ permeability into the cells such that the force and length of contraction are increased.
 +
**Things that decrease contractility are said to be '''negatively inotropic''' and generally work by blocking Ca++ or by depressing cardiac muscle metabolism.
 +
**The autonomic systems can control contractility through NE, E (sympathetic, increased metabolism) and ACh (parasympathetic, hyperpolarization).
 +
*Hormonal control of contractility:
 +
**Anything that increases metabolism of the cells will increase contractility, including glucagon.
 +
**Negative inotrophs are used as hypertension (high blood pressure) drugs because they can decrease heart contractility and thus decrease blood pressure.
 +
*Afterload:
 +
**Afterload is the amount of pressure the ventricular muscles must generate in order to open the semilunar valves.
 +
**As afterload increases, the isovolumetric stage of ventricular systole increases and thus the duration of ventricular blood ejection decreases.  This means that the ESV will decrease and stroke volume will decrease.
 +
**Anything that increases resistance in the blood vessels will increase the afterload.
 +
**Though reduction of ESV to zero because of afterload is rare in healthy hearts, if the heart tissue is damaged it be the case that it simply cannot reach the necessary afterload needed to pump blood; this is known as heart failure.

Current revision as of 14:10, 17 March 2010

Contents

[edit] Chapter 20: The heart

[edit] An introduction to the cardiovascular system

  • There is a pulmonary circuit and a systemic circuit.
  • Efferent vessels = arteries = away from the heart.
  • Afferent vessels = veins = toward the heart.
  • Capillaries = exchange vessels.
  • The heart pumps 100k times per day, moving 8k liters!
  • The right atrium receives blood from the systemic circuit; the left atrium receives blood from the pulmonary circuit.
  • The ventricles pump at the same time and move the same volume of fluid into each circuit.

ch20-01.jpg

[edit] The heart is a four-chambered organ, supplied by the coronary circulation, that pumps oxygen-poor blood to the lungs and oxygen-rich blood to the rest of the body

  • The heart lies slightly to the left of center, behind the sternum.
  • The inferior tip of the heart is called the apex.
  • The mediastinum is the region between the two pleural cavities.
  • The mediastinum holds the heart (in the pericardial sac) and the great vessels as well as the thymus, esophagus, and trachea.

ch20-02.jpg

[edit] The pericardium

  • The pericardial sac is like a balloon in which one's heart is depressed.
  • The pericardial sac has two tissue layers:
    • The visceral pericardium (epicardium) covers and adheres to the surface of the heart.
    • The parietal pericardium lines the inner surface of the sac.
  • Between the membranes, there is pericardial fluid which serves to reduce friction between the membranes and to protect the heart.
    • Pericarditis is the reduction of pericardial fluid and thus presents with a scratching noise that can be heard via stethoscope.
    • Cardiac tamponade occurs when fluid builds up in the pericardial sac (from infection or wounding, perhaps) and thus restructs the movements of the heart.
      • Tampon means plug in latin.

[edit] Superficial anatomy of the heart

  • The atria have thin, muscular walls that are highly expandable.
  • The atria have auricles that go limp and wrinkle after contracting blood out of the atria.
  • The coronary sulcus is a deep grove that marks the boundary between the atrium and the ventricle.
  • The anterior / posterior interventricular sulci are shallower depressions that mark the boundary between the left and right ventricles.
  • The sulci also contain the coronary arteries / veins and substantial amounts of fat.

ch20-03.jpg

[edit] The heart wall

  • There are three layers to the wall of the heart:
    • The epicardium is the same as the visceral pericardium and has two sub layers: the exposed mesothelium and the areolar tissue which is connected to the myocardium.
      • Areolar: "Areolar tissue known as areis exhibits interlacing, loosely organized fibers, abundant blood vessels, and significant empty space. Its fiber run in random directions and are mostly collagenous, but elastic and reticular fibers are also present." [1]
    • The myocardium contains nerves, blood vessles, and muscle tissue that intricately wraps around the great vessels, the atria, and the ventricles with a figure-eight pattern. The myocardium has multiple layers of muscle fibers.
    • The endocardium is a simple squamous epithelium that covers the inside of the heart, including the valves, and is continuous with the endothelium of the vasculature.
      • Squamous: "In anatomy, squamous epithelium (from Latin squama, "scale") is an epithelium characterised by its most superficial layer consisting of flat, scale-like cells called squamous cell". [2]

ch20-04.jpg

[edit] Cardiac muscle tissue
  • Cardiac muscle fibers are connected with intercalated discs where the membranes of adjacent muscle cells interlock and are held together by desmosomes and gap junctions.
  • These junctions allow for the fast propagation of action potentials.
  • Note that cardiac muscle fibers can be differentiated in histological slides by:
    • their smaller size,
    • their single, centrally located nucleus,
    • their branching interconnections, and
    • the presence of intercalated discs.

table-20-01.jpg

ch20-05.jpg

[edit] Internal anatomy and organization

  • The muscular interatrial and interventricular septums separate the atriums and the ventricles.
  • The atrioventricular valves keep blood from flowing from the ventricle to the atrium.

ch20-06.jpg

[edit] The right atrium
  • The right atrium receives blood from the superior and inferior vena cava and coronary sinus.
  • The superior vena cava delivers blood from the head, neck, upper limbs, and chest.
  • The inferior vena cava delivers blood from the rest of the trunk, the viscera, and the lower limbs.
  • The coronary sinus delivers blood from the coronary veins.
  • The foramen ovale allows blood to pass from the right atrium to the left atrium until birth when it closes.
  • The formen ovale is generally permanently closed by three months of age leaving only the fossa ovalis.
  • When the foramen ovale doesn't close, there are serious cardiovascular problems.
  • The posterior side of the right atrium has a smooth surface while the anterior side and the auricle have muscular ridges called pectinate muscles.
[edit] The right ventricle
  • Blood flows from the right atrium to the right ventricle via the right atrioventricular valve which is also called the tricuspid valve because there are three cusps made of fibrous tissue.
  • There are chordae tendinae that are attached to the papillary muscles inside the ventricle that keep the cusps from being forced backward into the atrium when the ventricle contracts and blood pressure increases.
  • There is a band called the moderator band that connects the internal conduction system to the papillary muscles so that the papillary muscles will be contracted before the rest of the heart flexes.
  • The blood in the right ventricle is pumped through the pulmonary valve (also called the pulmonary semilunar valve) and into the pulmonary trunk and then into the left and right pulmonary arteries.
[edit] The left atrium
  • The left atrium receives blood from the four pulmonary veins.
  • Like the right atrium, the left atrium has an auricle.
  • The right atrium has an atrioventricular valve, called the bicuspid valve or the mitral valve.
  • Remember that you "tri (sic) to be right when remembering where the tricuspid valve is located."
[edit] The left ventricle
  • The left ventricle is similar to the right ventricle:
    • It has chrodae tendinae that support the atrioventricular valve (the mitral valve) to prevent backflow.
    • There are large muscular ridges.
    • The two ventricles hold the same volume of blood.
  • The left ventricle has much thicker walls than the right ventricle, however, so that it can generate the increased pressure needed to circulate blood throughout the entire body.
  • Blood leaves the left ventricle via the aortic semilunar valve (also called the aortic valve) to enter the ascending aorta and then the aortic arch and the descending aorta.
  • In the fetus, the pulmonary branch of the circulatory system is linked to the systemic branch through a blood vessel that later deteriorates into a fibrous ligament called the ligamentum arteriosum.
[edit] Structural differences between the left and right ventricles
  • The function of the atria are almost identical and thus they look almost identical; the ventricles, however, are different because they have different duties.
  • The right ventricle only has to push blood through the short pulmonary circuit which has relatively wide vessels and is therefore able to be effective which much lower pressures. Therefore, it has developed into a bellow-like compartment that compresses into the wall of the left ventricle.
    • Bellows: "A bellows (AKA Bagpipe) is a device for delivering pressurized air in a controlled quantity to a controlled location. Basically, a bellows is a deformable container which has an outlet nozzle. When the volume of the bellows is decreased, the air escapes through the outlet." ref
  • The right ventricle has a circular cross section and concentric muscular form.
  • When contracting, the right ventricle both narrows its diameter and shortens the chamber and can thus generate 4-6 times as much pressure as the right ventricle.
  • The contraction of the left ventricle causes it to bulge into the chamber of the right ventricle and thus helps pump blood into the pulmonary system as well.
    • Sometimes, patients with damage to their right ventricle can survive because of this physiological effect.

ch20-07.jpg

[edit] The heart valves
[edit] The atrioventricular valves
  • Backflow of blood is also called regurgitation.
[edit] The semilunar valves
  • The semilunar valves (those that lead from ventricles to either the systemic or pulmonary circuits) don't need supporting chordae because there is no pressure on the blood in the circuit trying to get back into the ventricle.
  • When the semilunar valves close, the three flaps support each other like the three legs of a tripod.
  • At the aortic valve, there are aortic sinuses (sacs) that keep the cusps of the valve from sticking to the walls of the aorta as blood is flowing outward.
  • The coronary arteries originate at the aortic sinuses.

ch20-08.jpg

  • Valvar heart disease occurs when a patient's heart valves misfunction to the point that a steady flow of blood cannot be maintained.
    • Often VHD develops after carditis (an inflammation of the heart tissue) which can be caused by infections.
    • Rheumatic fever, an autoimmune inflammatory response to an infection is often the cause of carditis.

[edit] STUFF MISSING!

[edit] The Blood Supply to the Heart

  • Blood flow to cardiac tissue can increase by 9 or 10 fold at times of greatest exertion.

ch20-09.jpg

[edit] The coronary arteries

[edit] 20-3 Events during a complete heartbeat constitute a cardiac cycle

[edit] Phases of the cardiac cycle

[edit] Pressure and volume changes in the cardiac cycle

[edit] Atrial systole
  • Atrial systole occurs to push blood into the ventricle to fill the 30% of the volume that wasn't already filled passively.
    • Hence one can live without atrial systole.
  • At the end of atrial systole, the ventricle contains all that it will hold for the current cardiac cycle: the end diastolic volume.
[edit] Ventricular systole
  • During ventricular systole, both sides of the heart eject about 70-80 mL of blood: the stroke volume.
  • At rest, the ratio of stroke volume to end diastolic volume is about 60%; this is called the ejection fraction.
  • At the end of ventricular systole, the volume of blood remaining in the ventricle is about 40% of the original end diastolic volume and is called the end systolic volume.
[edit] Ventricular diastole
  • The ventricle relaxes until atrial pressure is greater than ventricle pressure.
  • Then the atrioventricular valves open and blood passively passes from the atria to the ventricle until atrial systole begins.

[edit] 20-4 Cardiodynamics examines the factors that affect cardiac output

  • Stroke volume is end diastolic volume (EDV) minus end systolic volume (ESV).
  • Stroke volume is the most important consideration in cardiodynamics.
  • Cardiac output, then is the stroke volume multiplied by the heart rate.
    • Cardiac output, essentially, tells us how much blood is flowing through the circulation each minute.

[edit] Overview: Factors affecting cardiac output

  • Heart rate and stroke volume are the two factors that can be adjusted and they are usually adjusted in concert.
  • The heart rate can be changed through the autonomic nervous system or through the endocrine system.
  • Stroke volume can be changed through the autonomic nervous system or through the endocrine system (which will adjust the EDV and ESV).

[edit] Factors affecting the heart rate

[edit] Autonomic nervous system
  • The autonomic nervous system can control the heart rate from the cardioinhibitory center and cardioacceleratory center of the medulla oblongata.
  • The sympathetic system will be controlled by the cardioacceleratory center which will cause the heart to beat faster and with greater contractility.
  • These centers in the brain change the heart rate based on information from baroreceptors and chemoreceptors found in arteries and innervated by the cranial nerves.
  • The parasympathetic and sympathetic nervous systems change the heart rate by changing ion permeability at the SA node.
    • For instance, making them more permeable to K+ will mean that the cell will depolarize less quickly (because K+ will be flowing out more and Na+ will be flowing in the same as before). This can be achieved through the parasympathetic release of acetylcholine.
    • The sympathetic system, on the other hand, can release norepinephrine in order to bind a channel and allow more Na+ to enter the cell, thus depolarizing the SA node at a higher frequency.
  • Another way the autonomic nervous system can receive feedback is from cells of the right atrium.
    • When they stretch (that is, when venous return is high) they cause increased sympathetic stimulation and thus increased heart rate.
[edit] Hormones
  • Just as the sympathetic system uses norepi, hormonal release of norepi or epi can trigger an increase in heart rate.
  • Epi increase not only the heart rate but also contractility.

[edit] Factors affecting the stroke volume

  • To affect stroke volume, one must change either EDV or ESV or both.
[edit] The EDV
  • The filling time, when increased can increase the EDV and vice versa when decreased.
    • Filling time is directly proportional to the heart rate; increased heart rate means decreased filling time.
  • The preload is the amount of stretching experienced by the ventricular muscles.
    • Preload is directly proportional to the EDV; the higher the EDV the more stretch (preload).
    • The more preload (stretch) the higher the force of contraction by the mycardium (because as mycardial fibers stretch, more of the sarcomere length overlaps).
    • Therefore as the mycardiocytes approach optimal sarcomere stretching, they will increase contractile strength and decrease the ESV.
    • So we see an increase of EDV and a decrease of ESV which means an increase of stroke volume.
    • And so, this relationship of increased EDV leading to increased stroke volume is called the Frank-Starling principle.
[edit] The ESV
  • There are three factors that affect the ESV: preload (as discussed in the EDV section), contractility, and afterload.
  • Contractility is the force produced during contraction at a given preload.
    • This is usually controlled by the autonomic nervous system and hormones but can also be manipulated with drugs and abnormal ion concentrations in the extracellular fluid.
    • Things that increase contractility are said to be positively inotropic and generally work by increasing Ca+ permeability into the cells such that the force and length of contraction are increased.
    • Things that decrease contractility are said to be negatively inotropic and generally work by blocking Ca++ or by depressing cardiac muscle metabolism.
    • The autonomic systems can control contractility through NE, E (sympathetic, increased metabolism) and ACh (parasympathetic, hyperpolarization).
  • Hormonal control of contractility:
    • Anything that increases metabolism of the cells will increase contractility, including glucagon.
    • Negative inotrophs are used as hypertension (high blood pressure) drugs because they can decrease heart contractility and thus decrease blood pressure.
  • Afterload:
    • Afterload is the amount of pressure the ventricular muscles must generate in order to open the semilunar valves.
    • As afterload increases, the isovolumetric stage of ventricular systole increases and thus the duration of ventricular blood ejection decreases. This means that the ESV will decrease and stroke volume will decrease.
    • Anything that increases resistance in the blood vessels will increase the afterload.
    • Though reduction of ESV to zero because of afterload is rare in healthy hearts, if the heart tissue is damaged it be the case that it simply cannot reach the necessary afterload needed to pump blood; this is known as heart failure.
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