Circulatory System Anatomy, Diagram, & Function | Study Guides, Projects, Research Electronic Circuits Analysis

BIO 208 Heart Notes

Turner

THE CARDIOVASCULAR SYTEM: HEART

I. General Anatomy

A. Location

1. Located in the mediastinum

2. Apex – directed anteriorly, inferiorly and to the left.

3. Base – directed posteriorly, superiorly and to the right

4. Superior right point – superior border of the 3rd costal cartilage

5. Superior left point – inferior border of the 2nd costal cartilage, 3 cm left of the midline.

6. Inferior left point – 5th intercostal space, 9cm from midline

7. Inferior right point – superior border of 6th costal cartilage, 3 cm from midline.

B. Pericardium

1. Fibrous Pericardium

a. Outer layer of dense connective tissue.

b. It protects and anchors the heart, prevent the heart from overstretching.

2. Serous Pericardium

a. Inner layer of simple squamous epithelium that forms a thin, delicate membrane.

b. It is a double folded membrane consisting of the parietal and visceral pericardium

c. Pericardial fluid (serous fluid) is found between the layers in the pericardial cavity.

3. Heart Wall

a. Epicardium is the visceral pericardium that clings to heart forming the most

superficial surface.

b. Myocardium is the middle layer composed of cardiac muscle.

c. Endocardium is the inner surface of the heart formed by simple squamous epithelium

over a connective tissue layer.

4. Chambers and Sucli

1. There are four chambers.

a. Atria are the superior chambers and are less muscular.

b. Ventricles are the inferior, more muscular chambers.

2. Valves

a. Atrioventricular Valves

Tricuspid – between right atrium and ventricle; 3 cusps

Biscupid or Mitral – between left atrium & ventricle; 2 cusps

Chordae Tendineae – “heart strings” that assist the valves from prolapsing

Papillary Muscles – attach to the chordae tendineae; when valves close these

muscle contract to tighten the chordae tendineae.

b. Semilunar Valves

Pulmonic – between the right ventricle and pulmonary trunk

Aortic – between the left ventricle and aorta

3. Sulci are the grooves on the surface that accommodate coronary vessels.

a. The coronary sulcus is the boundary between the atria and ventricles.

b. The anterior interventricular sulcus is located between the ventricles anteriorly.

c. The posterior interventricular sulcus is located between the ventricles

posteriorly.

II. Blood Circulation

A. Systemic Circulation

1. The left side of the heart pumps blood through the body.

2. The left ventricle pumps oxygenated blood into the aorta.

3. The aorta branches into many arteries.

Partial preview of the text

Download Circulatory System Anatomy, Diagram, & Function and more Study Guides, Projects, Research Electronic Circuits Analysis in PDF only on Docsity!

BIO 208 Heart Notes Turner

THE CARDIOVASCULAR SYTEM: HEART

I. General Anatomy A. Location

Located in the mediastinum
Apex – directed anteriorly, inferiorly and to the left.
Base – directed posteriorly, superiorly and to the right
Superior right point – superior border of the 3rd^ costal cartilage
Superior left point – inferior border of the 2nd^ costal cartilage, 3 cm left of the midline.
Inferior left point – 5th^ intercostal space, 9cm from midline
Inferior right point – superior border of 6th^ costal cartilage, 3 cm from midline. B. Pericardium
Fibrous Pericardium a. Outer layer of dense connective tissue. b. It protects and anchors the heart, prevent the heart from overstretching.
Serous Pericardium a. Inner layer of simple squamous epithelium that forms a thin, delicate membrane. b. It is a double folded membrane consisting of the parietal and visceral pericardium c. Pericardial fluid (serous fluid) is found between the layers in the pericardial cavity.
Heart Wall a. Epicardium is the visceral pericardium that clings to heart forming the most superficial surface. b. Myocardium is the middle layer composed of cardiac muscle. c. Endocardium is the inner surface of the heart formed by simple squamous epithelium over a connective tissue layer.
Chambers and Sucli
There are four chambers. a. Atria are the superior chambers and are less muscular. b. Ventricles are the inferior, more muscular chambers.
Valves a. Atrioventricular Valves  Tricuspid – between right atrium and ventricle; 3 cusps  Biscupid or Mitral – between left atrium & ventricle; 2 cusps  Chordae Tendineae – “heart strings” that assist the valves from prolapsing  Papillary Muscles – attach to the chordae tendineae; when valves close these muscle contract to tighten the chordae tendineae. b. Semilunar Valves  Pulmonic – between the right ventricle and pulmonary trunk  Aortic – between the left ventricle and aorta
Sulci are the grooves on the surface that accommodate coronary vessels. a. The coronary sulcus is the boundary between the atria and ventricles. b. The anterior interventricular sulcus is located between the ventricles anteriorly. c. The posterior interventricular sulcus is located between the ventricles posteriorly. II. Blood Circulation A. Systemic Circulation
The left side of the heart pumps blood through the body.
The left ventricle pumps oxygenated blood into the aorta.
The aorta branches into many arteries.

These systemic arteries branch into arterioles in the tissue.
Arterioles then branch into capillaries. The capillaries are the site of nutrient, gas, and waste exchange.
Capillaries merge into venules that bring oxygen poor blood away from the organ and send it toward the heart.
The venules merge into larger vessels, called veins, which ultimately empty the oxygen poor blood into the right atrium. B. Pulmonary Circulation
The right side of the heart pumps deoxygenated blood to the lungs.
The right ventricle pumps blood into the pulmonary trunk.
The pulmonary trunk splits into left and right pulmonary arteries , which carry blood to the lungs.
The blood passes through capillaries in the lungs where it receives oxygen.
The blood returns to the left side of the heart through pulmonary veins. C. Coronary Circulation
This is the blood supply that feeds the heart.
Cardiac muscle has a high oxygen demand.
The first branches of the aorta are the right and left coronary arteries. a. Arise from the base of the ascending aorta b. Left Coronary Artery divides into the Anterior Interventricular Branch and the Circumflex Branch  Anterior Interventricular supplies O 2 to both ventricles and the interventricular septum  Circumflex Artery supplies O 2 to the left atrium and left ventricle. c. Right Coronary Artery supplies small branches to the right atrium and then divides into the Posterior Interventricular Branch and the Marginal Branch  Posterior Interventricular Branch supplies both ventricles  Marginal Branch supplies the right ventricle
Coronary Veins a. Coronary Sinus – a venous space with no smooth muscle to alter diameter  Collects the returned deoxygenated blood  Empties into the right atrium b. Great Cardiac Vein and Middle Cardiac Vein carry blood to the coronary sinus
Blood is returned to the right atrium through the coronary sinus. III. Electrical Activity of the Heart A. Types of Cardiac Cells
Autorhythmic Cells a. These do not contract. b. They are specialized for initiating and conducting the action potentials for contraction. c. Two important functions  They act as the pacemaker (set the rhythm)  They form the conduction system of the heart.
Contractile Cells a. 99% of the cardiac muscle cells are contractile. b. They mechanically work in pumping. c. They do not initiate their own action potential.

a. Atrial excitation and contraction should be complete before the onset of ventricular contraction.  80% of ventricular filling occurs passively as blood flows from the atria to the ventricles.  The last 20% occurs during atrial contraction.  In order for all of the blood to make it through the circulation, the atria need to contract before the ventricles. b. Excitation of cardiac muscle fibers should be coordinated to ensure that each heart chamber contracts as a unit to accomplish efficient pumping.  Uncoordinated excitation and contraction is known as Fibrillation.  V-Fib causes death because the heart cannot pump blood. D. Normal Spread of Cardiac Excitation

Atrial Excitation a. The action potential spreads from the SA node throughout both atria via gap junctions. b. Interatrial Pathway – this extends from the SA node within the right atrium to the left atrium. This ensures both atria become depolarized to contract simultaneously. c. Internodal Pathway – extends from the SA node to the AV node.  AV node is the only electrical contact point between the atria and ventricles.  There is a direct spread of an action potential from the SA node to the AV node to ensure sequential contraction of the ventricles following atrial contraction.
Transmission between Atria and Ventricles a. This is a relatively slow transmission through the AV node b. It allows for complete ventricular filling. c. The impulse delay is 0.1 second. Known as AV delay.
Ventricular Excitation a. The impulse rapidly travels down the bundle of His, and throughout the ventricular myocardium via Purkinje fibers. b. Not every cell is directly stimulated. The other cells receive the action potential via gap junctions, which are in abundance around the Purkinje fibers. IV. Action Potential of Contractile Cardiac Muscle Cells A. Contractile Fibers
These are “working” atrial and ventricular muscle fibers.
The action potential travels along the conduction system and spreads out to excite these fibers. B. Resting Membrane Potential & Depolarization
In cardiac muscle RMP is close to -90mV (contractile cells)
Na+^ channels open rapidly when the fibers are brought to threshold. a. The membrane potential rapidly becomes reversed to +30mV. b. The opened channels increase the permeability of the sarcolemma to Na+.
Inflow of Na+^ along the electrochemical gradient. a. The cytosol becomes positive. b. There is a rapid depolarization. c. Within a few milliseconds fast Na+^ channels are inactivated. C. Plateau
The action potential is prolonged near its peak.
This occurs because of the activation of “slow” Ca2+^ channels.
The opening of the Ca2+^ channels results in a slow, inward diffusion of Ca2+. a. Ca2+^ is in the greatest concentration in the ECF.

b. The inflow prolongs the positivity inside of the cells. c. This is primarily responsible for the plateau phase of the action potential. D. Mechanism for Contraction from an Action Potential

It is similar to skeletal muscle.
The presence of local action potentials within the T-tubules triggers Ca2+^ release into the sarcoplasm from the sarcoplasmic reticulum.
There is diffusion of Ca2+^ also into the cytosol across the sarcolemma from the ECF. a. This is different from skeletal muscle. b. The triggers even further release of Ca2+^ from the SR. c. The extra Ca2+^ is responsible for the prolongation of the cardiac action potential and lengthening the period of cardiac contraction.  The contraction last about 3 times longer than skeletal muscle.  It ensures adequate time to eject the blood. E. Repolarization
K+^ channels open and K+^ diffuses out of the cell.
Ca2+^ channels are in the process of closing.
As more K+^ leaves and fewer Ca2+^ enters, the fiber returns to RMP of -90mV.
Role of Calcium is the same as in skeletal muscle. a. Ca2+^ binds to the tropin-tropomyosin complex b. This allows for cross-bridge attachment of myosin to actin.
Some drugs alter cardiac function by influencing Ca2+^ movement across the myocardial sarcolemma. a. Verapmil (Ca2+^ blocking agent) blocks Ca2+^ influx during an action potential. This reduces the force of contraction. b. Digitalis increases cardiac contractility by inducing an accumulation of cytosolic Ca2+. F. Refractory Period
Responsiveness to an action potential is completely gone. a. It is impossible for another action potential to be generated.
Cardiac muscle has a longer refractory period than skeletal muscle. a. It is about 250 msec. b. It is almost as long as the period of contraction initiated by the action potential (300msec).
Another contraction cannot happen until relaxation is well under way.
Therefore, it cannot undergo tetani. a. If tetani occurred then blood flow would stop. b. The chambers could not be filled and emptied again, and the result is fatal. V. Electrocardiogram (ECG or EKG) – Record of electrical activity of the heart. A. What it represents
It is a recording of the electrical activity induced in the body fluids by the cardiac impulse reaching the body surface. {it is not a direct recording of the actual electrical activity}
It represents the overall spread of activity throughout the heart during depolarization and repolarization. a. It is not a recording of a single action potential in a single cell at a single point in time. b. It represents the sum of the electrical acidity in all of the cardiac muscle cells.
It represents comparisons in voltage detected by electrodes at two different points on the body surface. B. Pattern of Electrical Activity Recorded

c. Isovolumetric Relaxation is a brief interval corresponding to the AV valves and semilunar valves being closed. The ventricular blood volume does not change. d. Ventricular pressure continues to fall as the space inside expands. When the pressure drops below the atrial pressure, the AV valves open.

Ventricular filling a. This occurs just after the AV values open. b. The blood from the atria rushes into the ventricles. c. 70% of the ventricles fills during this period. d. Atrial systole contributes about 20-30% of the blood filling the ventricles, as it is squeezed out of the atria. e. Atrial systole corresponds to depolarization (P wave).
Ventricular systole (contraction) a. This occurs near the end of atrial systole.  The impulse from the SA node has passed through the AV node and into the ventricles.  The ventricles depolarize (QRS complex) b. Ventricular contraction begins c. Blood is pushed up against the AV valves and forces them shut. d. Isovolumetric Contraction is a period of about 0.05 sec when all valves are shut while the ventricles are contracting. e. The pressure rises in the ventricles as the contraction continues.  The left ventricle pressure surpasses the aortic pressure of about 80 mm Hg.  The right ventricle pressure surpasses the pulmonary trunk pressure of 15- mm Hg.  Both semilunar valves open and eject blood. F. Heart Sounds
Auscultation – the act of listening to sounds within the body
Lubb (S 1 ) a. Sound of AV valves closing b. Signifies onset of systole when ventricular pressure rises above atrial pressure c. Tend to be louder, longer, more resonant
Dupp (S 2 ) a. Sound of semilunar valves snapping shut b. Short, sharp sound c. Beginning of ventricular systole
Possible to listen at four specific regions of the thorax and distinguish individual valve sounds a. Mitral valve closes slightly before tricuspid b. Aortic semilunar valve generally snaps shut just before the pulmonic semilunar valve
Murmurs a. Abnormal or unusual heart sound b. Flow noise heard after, before, between the lubb-dupp c. Generally is not a problem, however sometimes indicates a valve problem.  Mitral Stenosis – narrowing of mitral valve  Mitral Valve Prolapse – inherited disorder in which part of the mitral valve is pushed back too far during ventricular contraction. VII. Mean Arterial Blood Pressure and Cardiac Output

A. Cardiac output is the amount of blood pumped out by each ventricle in 1 min, and therefore is also known as the minute volume. B. The formula for calculating Cardiac Output

Stroke Volume (SV) x Heart Rate (HR) = Cardiac Output (CO)
Factors that increase or decrease stroke volume or heart rate affect cardiac output.
The entire blood volume flows through the pulmonary and systemic circulation about once a minute.
Cardiac reserve is the difference between cardiac output at rest and maximum cardiac output. a. The greater a person’s cardiac reserve the greater capacity for exercise. b. Cardiovascular disease and lack of exercise can reduce cardiac reserve and affect the quality of life. C. Mean Arterial Pressure (MAP) is a little less than the average of the systolic and diastolic pressure of the aorta. It is the Cardiac Output times the Peripheral Resistance. D. Regulation of Stroke Volume by Intrinsic Regulation
Preload: Effect of Stretching - this is the extent to which the ventricular walls are stretched. a. Increase in preload, causes an increased cardiac output and vice versa. b. There is a relationship between changes in the pumping effectiveness and changes in preload. c. Frank-Starling Law of the Heart.  The more the heart is filled during diastole, the greater the force of contraction during systole. This is because the muscle is stretched to its maximum.  If the heart rate exceeds 160 beats/min stroke volume declines because the heart is beating too fast to adequately fill. d. Frank-Starling equalizes output of the left and right ventricles and keeps the same volume of blood flowing to both systemic and pulmonary circulations.
Contractility – the strength of contraction at any given period
Afterload – the pressure to overcome the pressure in the aorta and move blood into the aorta. a. This is the pressure that must be overcome before the semilunar valves will open. b. When the blood pressure increases or arteries narrow, more blood remains in the ventricles and the stroke volume decreases. E. Heart Failure
Inability of the cardiac output to keep pace with the body’s demands for supplies and removal of wastes.
Either or both ventricles may fail. a. The result is an inability to pump out all of the blood returned to it. b. The veins behind the failing ventricle become congested with blood.
Reasons for failure. a. Damage to the heart muscle such as from a myocardial infarction (MI) or impaired coronary circulation to the cardiac muscle, or AV valve problems. b. Prolonged pumping against a chronically high blood pressure.
The Frank-Starling Curve is shifted downward and to the right. A failing heart will pump out a smaller stroke volume.
Compensatory measures to restore stoke volume to normal. a. Positive Feedback Mechanisms b. Sympathetic activity to the heart is reflexively increased; increases the contractility of the heart toward normal. However, this is limited because the heart becomes less responsive over time.

 This enhances the heart’s pumping efficiency  Increases heart rate and contractility. b. Thyroid hormone also enhances cardiac contractility and increases heart rate

Ions a. Differences between intracellular and extracellular concentrations are critical to action potential production. b. Elevated K+^ or Na+^ decreases heart rate and contractility  Increased K+^ blocks generation of action potential  Increased Na+^ blocks Ca2+^ inflow and decreases force of contraction  Moderate increase in Ca2+^ speeds heart rate & strengthens heartbeat
Other Factors a. Heat increases HR by enhancing the metabolic rate of cardiac cells  When you have a fever, you have a rapid pounding heart beat  Cold decreases heart rate b. Emotions can cause changes c. Age and Gender  Fetus (140-160 beats/min)  Adult Female (72-80 beats/min)  Adult male (64-72 beats/min)
Abnormalities a. Tachycardia – abnormally fast heart rate. >100 beats/min b. Bradycardia - <60 beats/min IX. Heart Homeostasis A. Effect of Blood Pressure
Baroreceptor reflexes detect changes in blood pressure which results in changes to heart rate and the force of contractions. a. Baroreceptors are stretch receptors that measure blood pressure. b. They are located in the walls of large arteries such as the aorta and internal carotid arteries.
Cardioregulatory center in the medulla receives sensory information from the baroreceptors via the glossopharyngeal (IX) and vagus (X) nerves. a. The cardioacceleratory center increases heart rate, while the cardioinhibitory center decreases heart rate. b. Efferent or motor action potentials travel from the cardioregulatory center to the heart through sympathetic and parasympathetic fibers.
Action potential frequency from baroreceptors is sent to the medulla at a relative constant frequency with normal blood pressure. a. Elevated blood pressure results in increased stretching of the arteries and in turn afferent action potentials being sent at a greater frequency. b. A decrease in the blood pressure in turn results in a decrease in afferent action potentials.
The baroreceptor reflex in response to elevated blood pressure is to decrease sympathetic stimulation and increase parasympathetic stimulation of the heart, resulting in the heart rate to slow.
The baroreceptor reflex in response to a decreased blood pressure is to decrease parasympathetic stimulation and increase sympathetic stimulation of the heart, resulting in the heart rate to speed. B. Effect of pH, CO 2 , and O 2
Chemoreceptors reflexes assist in regulation of heart activity through monitoring of pH and blood gases.

With a drop in pH and rise in CO 2 , there is an increase in sympathetic stimulation and a decrease in parasympathetic stimulation. This results in increased heart rate and force of contraction. a. The increase in Cardiac Output allows for a greater amount of blood to flow through the lungs so the CO 2 can be eliminated. b. The decrease in CO 2 helps to raise the blood pH. C. Effects of Extracellular Ion Concentration
The major ions which affect the cardiac muscle are K+, Na+, and Ca2+.
Excess K+^ will cause the heart rate and stroke volume to decrease. a. If the K+^ increases by 2 times the normal amount the result is heart block. b. The excess K+^ can lead to ectopic action potentials and if enough ectopic action potentials are produce fibrillation results.
A reduction in extracellular K+^ may cause the resting membrane potential to become hyperpolarized. a. This result in longer time for the membrane to depolarize. b. The ultimate result is a decrease in heart rate.
Elevated Ca2+^ produces greater force of cardiac contraction. a. The reason is from a higher influx of Ca2+^ in the sarcoplasm. b. Elevated levels have an indirect effect on heart rate since they reduce the frequency of action potentials. c. Overall a Ca2+^ increase results in lower heart rate.
Low Ca2+^ levels increase heart rate, but not noticeable until the level has fallen to 1/10 of the normal level. D. Effect of Body Temperature
Small increases in cardiac muscle temperature result in the heart rate accelerating.
Decreases in temperature cause the heart rate to slow. X. Risk Factors in Heart Disease A. Five risk factors that can be modified by life style.
High blood cholesterol level  HDL – high density lipoprotein; removes cholesterol from circulation  LDL – low density lipoprotein; associated with fatty plaque formation.  VLDL – very low density lipoprotein; contributes to increased fatty plaque formation. a. Desirable levels  Total Triglyceride should be less than 200 mg/dL  HDL should be greater than 40 mg/dL  LDL should be less than 130 mg/dL b. Low fat diet c. Exercise – increases heart demand for oxygen (benefits from aerobic exercise)  Increased cardiac output  Increased HDL and lower TC (total cholesterol)  Better lung function  Decreased BP  Loss in weight
High Blood Pressure – can be reduced the exercise, diet and medication.
Cigarette Smoking a. Nicotine is a vasoconstrictor which increases blood pressure. b. Stimulates adrenal glands to release NE and epinephrine. c. Heart rate along with blood pressure are increased.
Obesity a. Development of extra capillaries in adipose tissue.

Circulatory System Anatomy, Diagram, & Function, Study Guides, Projects, Research of Electronic Circuits Analysis

Related documents

Partial preview of the text

Download Circulatory System Anatomy, Diagram, & Function and more Study Guides, Projects, Research Electronic Circuits Analysis in PDF only on Docsity!

THE CARDIOVASCULAR SYTEM: HEART