About heart murmur,
Murmurs are extra heart sounds that are produced as a result of turbulent blood flow that is sufficient to produce audible noise. Most murmurs can only be heard with the assistance of a stethoscope ("on auscultation").
A functional murmur or "physiologic murmur" is a heart murmur that is primarily due to physiologic conditions outside the heart, as opposed to structural defects in the heart itself. Functional murmurs may be benign (an "innocent murmur"), mildly troublesome, or serious.
Murmurs may also be the result of various problems, such as narrowing or leaking of valves, or the presence of abnormal passages through which blood flows in or near the heart. Such murmurs, known as pathologic murmurs, should be evaluated by an expert.
Heart murmurs are most frequently organized by timing, into systolic heart murmurs and diastolic heart murmurs. However, continuous murmurs cannot be directly placed into either category.
Classification
Murmurs can be classified by seven different characteristics: timing, shape, location, radiation, intensity, pitch and quality.
Timing refers to whether the murmur is a systolic or diastolic murmur.
Shape refers to the intensity over time; murmurs can be crescendo, decrescendo or crescendo-decrescendo.
Location refers to where the heart murmur is usually auscultated best. There are six places on the anterior chest to listen for heart murmurs; each of the locations roughly corresponds to a specific part of the heart. The first five of the six locations are adjacent to the sternum. The six locations are:
the 2nd right intercostal space
the 2nd to 5th left intercostal spaces
the 5th mid-clavicular intercostal space.
Radiation refers to where the sound of the murmur radiates. The general rule of thumb is that the sound radiates in the direction of the blood flow.
Intensity refers to the loudness of the murmur, and is graded on a scale from 0-6/6.
Pitch can be low, medium or high and is determined by whether it can be auscultated best with the bell or diaphragm of a stethoscope.
Quality refers to unusual characteristics of a murmur, such as blowing, harsh, rumbling or musical.
Interventions that change murmur sounds
Inhalation will increase the amount of blood filling into the right ventricle, thereby prolonging ejection time. This will affect the closure of the pulmonary valve. This finding, also called Carvallo's Maneuver,has been found by studies to have a sensitivity of 100% and a specificity of 80% to 88% in detecting murmurs originating in the right heart.
abrupt standing
squatting
valsalva maneuver. One study found the valsalva maneuver to have a sensitivity of 65%, specificity of 96% in detecting Hypertrophic obstructive cardiomyopathy (HOCM).
hand grip
post ectopic potentiation
amyl nitrite
methoxamine
positioning of the patient. ie. positioning patients in the left lateral position will allow a murmur in the mitral valve area to be more pronounced.
Examples of anatomic source of murmur
Stenosis of Bicuspid aortic valve
Symptoms tend to present between 40 and 70 years of age.
Stenosis of Tricuspid Aortic Valve
Symptoms more likely to present after 80 years of age.
Hypertrophic subaortic stenosis
Symptoms are a harsh murmur in mid-systole, often accompanied by S4, Brisk Bifid Carotid upstroke. Murmur increases with standing and valsalva maneuver.
Ventral septal defect
Symptoms are holosystolic, heard best at left lower sternal border.
Wednesday, June 16, 2010
What Is Afterload?
Some info about afterload,
Afterload is used to measure the tension produced by a chamber of the heart in order to contract. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
However, the strict definition of the term afterload relates to the properties of a single cardiomyocyte. It is therefore only of direct relevance in the laboratory; in the clinic, the term end-systolic pressure is usually more appropriate, although not equivalent.
Afterload can also be described as the pressure that the chambers of the heart have to generate in order to eject blood out of the heart and thus is a consequence of the aortic pressure and pulmonic pressure, since the pressure in the left and right ventricles must be greater than the systemic and pulmonary pressure in order to open the aortic valve and pulmonic valve, respectively. Study of pressure gradients across the aortic and pulmonic valves are well documented with the AoV and PV open in Systole and closed in Diastole. Everything else held equal, as afterload increases, cardiac output decreases.
Mathematical definition of afterload remains elusive to contemporary medical imaging. Cardiac imaging is a somewhat limited modality in defining Afterload because it is greatly incumbent upon interpretation of volumetric data. Prior work defining End Diastolic Volume (EDV) is mathematically close to Afterload but is better matched to Preload.
Preload best describes the maximum viscous blood volume/mass of end Diastole while Afterload better describes the maximum tension/compliance state of the semisolid myocardial muscle mass in end Systole. Precise mathematical labeling of Afterload and Preload is a further challenge since both maximum measurements (volume/tension) occur simultaneously in the late Time phase of Systole. More simply stated, Preload is well addressed by computational interpretation of imaging-derived blood volumetric data. Afterload remains beholden to definition of myocardial muscle work and is perhaps still better illustrated on a chalkboard.
Pathology
Disease processes that increase the left ventricular afterload include elevated blood pressure and aortic valve disease.
Systemic hypertension (HTN) (elevated blood pressure) increases the left ventricular afterload because the left ventricle has to work harder to eject blood into the aorta. This is because the aortic valve won't open until the pressure generated in the left ventricle is higher than the elevated blood pressure in the aorta.
Pulmonary Hypertension (PH) is increased blood pressure within the right heart leading to the lungs. PH indicates a regionally applied increase in Afterload dedicated to the right side of the heart, divided and isolated from the left heart by the intraventricular Cardiac Septum.
Aortic stenosis increases afterload because the left ventricle has to overcome the pressure gradient caused by the stenotic aortic valve in addition to the blood pressure in order to eject blood into the aorta. For instance, if the blood pressure is 120/80, and the aortic valve stenosis creates a trans-valvular gradient of 30 mmHg, the left ventricle has to generate a pressure of 110 mmHg in order to open the aortic valve and eject blood into the aorta.
Aortic insufficiency increases afterload because a percentage of the blood that is ejected forward regurgitates back through the diseased aortic valve. This leads to elevated systolic blood pressure. The diastolic blood pressure would fall, due to regurgitation. This would result in an increase pulse pressure.
Mitral regurgitation decreases the afterload. During ventricular systole, regurgitant blood flows backwards through a leaking mitral valve in addition to blood that is properly ejected through the aortic valve. With an extra pathway for blood flow through the mitral valve, the left ventricle does not have to work as hard to eject its blood, i.e. there is a decreased afterload. Afterload is largely dependent upon aortic pressure.
Afterload is used to measure the tension produced by a chamber of the heart in order to contract. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
However, the strict definition of the term afterload relates to the properties of a single cardiomyocyte. It is therefore only of direct relevance in the laboratory; in the clinic, the term end-systolic pressure is usually more appropriate, although not equivalent.
Afterload can also be described as the pressure that the chambers of the heart have to generate in order to eject blood out of the heart and thus is a consequence of the aortic pressure and pulmonic pressure, since the pressure in the left and right ventricles must be greater than the systemic and pulmonary pressure in order to open the aortic valve and pulmonic valve, respectively. Study of pressure gradients across the aortic and pulmonic valves are well documented with the AoV and PV open in Systole and closed in Diastole. Everything else held equal, as afterload increases, cardiac output decreases.
Mathematical definition of afterload remains elusive to contemporary medical imaging. Cardiac imaging is a somewhat limited modality in defining Afterload because it is greatly incumbent upon interpretation of volumetric data. Prior work defining End Diastolic Volume (EDV) is mathematically close to Afterload but is better matched to Preload.
Preload best describes the maximum viscous blood volume/mass of end Diastole while Afterload better describes the maximum tension/compliance state of the semisolid myocardial muscle mass in end Systole. Precise mathematical labeling of Afterload and Preload is a further challenge since both maximum measurements (volume/tension) occur simultaneously in the late Time phase of Systole. More simply stated, Preload is well addressed by computational interpretation of imaging-derived blood volumetric data. Afterload remains beholden to definition of myocardial muscle work and is perhaps still better illustrated on a chalkboard.
Pathology
Disease processes that increase the left ventricular afterload include elevated blood pressure and aortic valve disease.
Systemic hypertension (HTN) (elevated blood pressure) increases the left ventricular afterload because the left ventricle has to work harder to eject blood into the aorta. This is because the aortic valve won't open until the pressure generated in the left ventricle is higher than the elevated blood pressure in the aorta.
Pulmonary Hypertension (PH) is increased blood pressure within the right heart leading to the lungs. PH indicates a regionally applied increase in Afterload dedicated to the right side of the heart, divided and isolated from the left heart by the intraventricular Cardiac Septum.
Aortic stenosis increases afterload because the left ventricle has to overcome the pressure gradient caused by the stenotic aortic valve in addition to the blood pressure in order to eject blood into the aorta. For instance, if the blood pressure is 120/80, and the aortic valve stenosis creates a trans-valvular gradient of 30 mmHg, the left ventricle has to generate a pressure of 110 mmHg in order to open the aortic valve and eject blood into the aorta.
Aortic insufficiency increases afterload because a percentage of the blood that is ejected forward regurgitates back through the diseased aortic valve. This leads to elevated systolic blood pressure. The diastolic blood pressure would fall, due to regurgitation. This would result in an increase pulse pressure.
Mitral regurgitation decreases the afterload. During ventricular systole, regurgitant blood flows backwards through a leaking mitral valve in addition to blood that is properly ejected through the aortic valve. With an extra pathway for blood flow through the mitral valve, the left ventricle does not have to work as hard to eject its blood, i.e. there is a decreased afterload. Afterload is largely dependent upon aortic pressure.
What is preload???
Another facts about physiology of heart.
In cardiac physiology, preload is the pressure stretching the ventricle of the heart, after passive filling of the ventricle and subsequent atrial contraction. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
Preload is theoretically most accurately described as the initial stretching of a single cardiomyocyte prior to contraction. This cannot be measured in vivo and therefore other measurements are used as estimates. Estimation is inaccurate, for example in a chronically dilated ventricle new sarcomeres may have formed in the heart muscle allowing the relaxed ventricle to appear enlarged. The term end-diastolic volume is better suited to the clinic, although not exactly equivalent to the strict definition of preload.
Calculation
Quantitatively, preload can be calculated as
where LVEDP=Left ventricular end diastolic pressure, LVEDR= Left ventricular end diastolic radius (at the ventricle's midpoint), and h=thickness of the ventricle. This calculation is based on the Law of Laplace.
Factors affecting preload
Preload is affected by venous blood pressure and the rate of venous return. These are affected by venous tone and volume of circulating blood.
Preload is related to the ventricular end-diastolic volume; a higher end-diastolic volume implies a higher preload. However, the relationship is not simple because of the restriction of the term preload to single myocytes.
Mathematical expression of a titrated Preload is then (narrowly) volumetrically suggested by the inexpensive echocardiographic measurement end diastolic volume or EDV. Extrapolation to performance of a single cardiomyocyte is a worthy endeavor but subject to shading study of the overall performance of the myocardium to the trees rather than the forest.
Preload increases with exercise (slightly), increasing blood volume (overtransfusion, polycythemia) and neuroendocrine excitement (sympathetic tone).
An arteriovenous fistula can increase preload.
In cardiac physiology, preload is the pressure stretching the ventricle of the heart, after passive filling of the ventricle and subsequent atrial contraction. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
Preload is theoretically most accurately described as the initial stretching of a single cardiomyocyte prior to contraction. This cannot be measured in vivo and therefore other measurements are used as estimates. Estimation is inaccurate, for example in a chronically dilated ventricle new sarcomeres may have formed in the heart muscle allowing the relaxed ventricle to appear enlarged. The term end-diastolic volume is better suited to the clinic, although not exactly equivalent to the strict definition of preload.
Calculation
Quantitatively, preload can be calculated as
where LVEDP=Left ventricular end diastolic pressure, LVEDR= Left ventricular end diastolic radius (at the ventricle's midpoint), and h=thickness of the ventricle. This calculation is based on the Law of Laplace.
Factors affecting preload
Preload is affected by venous blood pressure and the rate of venous return. These are affected by venous tone and volume of circulating blood.
Preload is related to the ventricular end-diastolic volume; a higher end-diastolic volume implies a higher preload. However, the relationship is not simple because of the restriction of the term preload to single myocytes.
Mathematical expression of a titrated Preload is then (narrowly) volumetrically suggested by the inexpensive echocardiographic measurement end diastolic volume or EDV. Extrapolation to performance of a single cardiomyocyte is a worthy endeavor but subject to shading study of the overall performance of the myocardium to the trees rather than the forest.
Preload increases with exercise (slightly), increasing blood volume (overtransfusion, polycythemia) and neuroendocrine excitement (sympathetic tone).
An arteriovenous fistula can increase preload.
What Is Stroke Volume?
In cardiovascular physiology, stroke volume (SV) is the volume of blood pumped from one ventricle of the heart with each beat. It is calculated by subtracting the volume of the blood in the ventricle at the end of a beat (called end-systolic volume) from the volume of blood just prior to the beat (called end-diastolic volume). The term stroke volume applies equally to both left and right ventricles of the heart. These two stroke volumes are generally equal, both approximately 70 ml in a healthy 70-kg man.
Stroke volume is an important determinant of cardiac output, which is the product of stroke volume and heart rate. Because stroke volume decreases in certain conditions and disease states, stroke volume itself correlates with cardiac function.
Calculation
Its value is obtained by subtracting end-systolic volume (ESV) from end-diastolic volume (EDV) for a given ventricle.
SV = EDV − ESV
In a healthy 70-kg man, EDV is approximately 120 mL and ESV is approximately 50 mL, giving a difference of 70 mL for the stroke volume.
"Stroke work" refers to the work, or pressure of the blood ("P") multiplied by the stroke volume.
Determinants
Men, on average, have higher stroke volumes than women due to the larger size of their hearts. However, stroke volume depends on several factors such as heart size, contractility, duration of contraction, preload (end-diastolic volume), and afterload.
Exercise
Prolonged aerobic exercise training may also increase stroke volume, which frequently results in a lower (resting) heart rate. Reduced heart rate prolongs ventricular diastole (filling), increasing end-diastolic volume, and ultimately allowing more blood to be ejected.
Preload
Stroke volume is intrinsically controlled by preload (the degree to which the ventricles are stretched prior to contracting). An increase in the volume or speed of venous return will increase preload and, through the Frank-Starling law of the heart, will increase stroke volume. Decreased venous return has the opposite effect, causing a reduction in stroke volume.
Afterload
Elevated afterload (commonly measured as the aortic pressure during systole) reduces stroke volume. Though not usually affecting stroke volume in healthy individuals, increased afterload will hinder the ventricles in ejecting blood, causing reduced stroke volume. Increased afterload may be found in aortic stenosis and arterial hypertension.
Stroke volume is an important determinant of cardiac output, which is the product of stroke volume and heart rate. Because stroke volume decreases in certain conditions and disease states, stroke volume itself correlates with cardiac function.
Calculation
Its value is obtained by subtracting end-systolic volume (ESV) from end-diastolic volume (EDV) for a given ventricle.
SV = EDV − ESV
In a healthy 70-kg man, EDV is approximately 120 mL and ESV is approximately 50 mL, giving a difference of 70 mL for the stroke volume.
"Stroke work" refers to the work, or pressure of the blood ("P") multiplied by the stroke volume.
Determinants
Men, on average, have higher stroke volumes than women due to the larger size of their hearts. However, stroke volume depends on several factors such as heart size, contractility, duration of contraction, preload (end-diastolic volume), and afterload.
Exercise
Prolonged aerobic exercise training may also increase stroke volume, which frequently results in a lower (resting) heart rate. Reduced heart rate prolongs ventricular diastole (filling), increasing end-diastolic volume, and ultimately allowing more blood to be ejected.
Preload
Stroke volume is intrinsically controlled by preload (the degree to which the ventricles are stretched prior to contracting). An increase in the volume or speed of venous return will increase preload and, through the Frank-Starling law of the heart, will increase stroke volume. Decreased venous return has the opposite effect, causing a reduction in stroke volume.
Afterload
Elevated afterload (commonly measured as the aortic pressure during systole) reduces stroke volume. Though not usually affecting stroke volume in healthy individuals, increased afterload will hinder the ventricles in ejecting blood, causing reduced stroke volume. Increased afterload may be found in aortic stenosis and arterial hypertension.
Systemic Circulation
Here are some facts about systemic circulation,
Systemic circulation is the portion of the cardiovascular system which carries oxygenated blood away from the heart, to the body, and returns deoxygenated blood back to the heart. The term is contrasted with pulmonary circulation.
In the systemic circulation, arteries bring oxygenated blood to the tissues. As blood circulates through the body, oxygen diffuses from the blood into cells surrounding the capillaries, and carbon dioxide diffuses into the blood from the capillary cells. Veins bring deoxygenated blood back to the heart.
Arteries
Oxygenated blood enters the systemic circulation when leaving the left ventricle, through the hi aortic semilunar valve. The first part of the systemic circulation is the artery aorta, a massive and thick-walled artery. The aorta arches and gives off major arteries to the upper body before piercing the diaphragm in order to supply the lower parts of the body with its various branches.
Capillaries
Blood passes from arteries to arterioles and finally to capillaries, which are the thinnest and most numerous of the blood vessels. These capillaries help to join tissue with arterioles for transportation of nutrition to the cells, which absorb oxygen and nutrients in the blood. Peripheral tissues do not fully deoxygenate the blood, so venous blood does have oxygen, but in a lower concentration than in arterial blood. In addition, carbon dioxide and wastes are added. The capillaries can only fit one cell at a time.
Venules
The deoxygenated blood is then collected by venules, from where it flows first into veins, and then into the inferior and superior venae cavae, which return it to the right heart, completing the systemic cycle. The blood is then re-oxygenated through the pulmonary circulation before returning again to the systemic circulation.
Veins
The relatively deoxygenated blood collects in the venous system which coalesces into two major veins: the superior vena cava (roughly speaking from areas above the heart) and the inferior vena cava (roughly speaking from areas below the heart). These two great vessels exit the systemic circulation by emptying into the right atrium of the heart. The coronary sinus empties the heart's veins themselves into the right atrium.
Advantages
Because the systemic circulation is powered by the left ventricle (which is very muscular), one advantage of this form of circulation - as opposed to open circulation, or the gill system that fish use to breathe - is that there is simultaneous high-pressure oxygenated blood delivered to all parts of the body.
Summary
From the lungs, the blood goes back to the heart through the pulmonary veins. The oxygenated blood now enters the left atrium. The blood then goes down into the left ventricle through the mitral valve. This valve also closes as the left ventricle starts to pump blood to all parts of the body through the aortic semi-lunar valve to the aorta. The aorta is where the oxygenated blood passes on its way to the head, arms, hands, chest, and down to the waist, legs, and feet. At the different body parts, blood delivers nutrients and oxygen, picks up waste materials and flows back to the heart again. The movement of the blood from the left part of the heart to the various parts of the body and back to the heart is commonly called as the systemic circulation.
Systemic circulation is the portion of the cardiovascular system which carries oxygenated blood away from the heart, to the body, and returns deoxygenated blood back to the heart. The term is contrasted with pulmonary circulation.
In the systemic circulation, arteries bring oxygenated blood to the tissues. As blood circulates through the body, oxygen diffuses from the blood into cells surrounding the capillaries, and carbon dioxide diffuses into the blood from the capillary cells. Veins bring deoxygenated blood back to the heart.
Arteries
Oxygenated blood enters the systemic circulation when leaving the left ventricle, through the hi aortic semilunar valve. The first part of the systemic circulation is the artery aorta, a massive and thick-walled artery. The aorta arches and gives off major arteries to the upper body before piercing the diaphragm in order to supply the lower parts of the body with its various branches.
Capillaries
Blood passes from arteries to arterioles and finally to capillaries, which are the thinnest and most numerous of the blood vessels. These capillaries help to join tissue with arterioles for transportation of nutrition to the cells, which absorb oxygen and nutrients in the blood. Peripheral tissues do not fully deoxygenate the blood, so venous blood does have oxygen, but in a lower concentration than in arterial blood. In addition, carbon dioxide and wastes are added. The capillaries can only fit one cell at a time.
Venules
The deoxygenated blood is then collected by venules, from where it flows first into veins, and then into the inferior and superior venae cavae, which return it to the right heart, completing the systemic cycle. The blood is then re-oxygenated through the pulmonary circulation before returning again to the systemic circulation.
Veins
The relatively deoxygenated blood collects in the venous system which coalesces into two major veins: the superior vena cava (roughly speaking from areas above the heart) and the inferior vena cava (roughly speaking from areas below the heart). These two great vessels exit the systemic circulation by emptying into the right atrium of the heart. The coronary sinus empties the heart's veins themselves into the right atrium.
Advantages
Because the systemic circulation is powered by the left ventricle (which is very muscular), one advantage of this form of circulation - as opposed to open circulation, or the gill system that fish use to breathe - is that there is simultaneous high-pressure oxygenated blood delivered to all parts of the body.
Summary
From the lungs, the blood goes back to the heart through the pulmonary veins. The oxygenated blood now enters the left atrium. The blood then goes down into the left ventricle through the mitral valve. This valve also closes as the left ventricle starts to pump blood to all parts of the body through the aortic semi-lunar valve to the aorta. The aorta is where the oxygenated blood passes on its way to the head, arms, hands, chest, and down to the waist, legs, and feet. At the different body parts, blood delivers nutrients and oxygen, picks up waste materials and flows back to the heart again. The movement of the blood from the left part of the heart to the various parts of the body and back to the heart is commonly called as the systemic circulation.
The Anatomy of Human Heart
Here are some facts about human heart.
The heart is basically a hollow muscular pump, which pushes the blood through out the body via the blood vessels. A normal sized healthy heart is roughly the same size as a fist. It is located between the lungs and slightly to the left of center. The heart is an involuntary muscle that has approximately seventy to ninety contractions per minute during a restful state. It begins to pump early in the life of a fetus and will continue unceasingly until death.
A hollow organ, the heart’s walls are made up by three distinct layers. They are as follows:
1. Endocardium (en-do-kar’de-um) this is a very smooth layer of cells that form the interior membrane of the heart. The endocardium tissue is also the type of tissue that makes up the valves of the heart.
2. Myocardium (mi-o-kar’de-um) is the actual muscle tissue of the heart and is by far the thickest layer.
3. Pericardium (per-I-kar’de-um) is the outermost layer of the heart and is also the tissue that serves as the lining of the pericardial sac.
The main portion of the heart is split into two different sides with an actual partition called the septum. Each side of the heart works as a separate pump and have two chambers apiece or as a whole, the heart has four distinct chambers.
1. Right atrium is the thin-walled area that receives the venous or “used” blood returning to the body by the veins.
2. Right ventricle is the “pump” area of the heart’s right side. The atrium dumps the blood into the ventricle where it is then pumped out the pulmonary arteries and to the lungs.
3. Left atrium receives the oxygenated blood returning from the lungs.
4. Left ventricle has the thickest walls of all. It is from this chamber the blood is pumped out of the heart, into the aorta and out to the rest of the body.
Since blood flow needs to be a one-way affair, there are valves at the entrance and exit of each ventricle. The entrance valves are called atrioventricular (a-tre-o-ven-trik’u-lar) and the exit valves are semilunar (sem-e-lu’nar). Each of the actual valves has it’s own specific name though.
1. Tricuspid valve is the one located at the entrance of the right ventricle. It prevents the blood from washing back into the right atrium. It gets its name from the three “cusps” or flaps that make up the valve.
2. Pulmonary semilunar valve is located between the right ventricle and the pulmonary artery.
3. Mitral valve is made of very heavy cusps and is located at the entrance of the left ventricle. This is a powerful valve that closes as the left ventricle begins each of its contractions to ensure the oxygenated blood doesn’t re-enter the left atrium.
4. Aortic valve is located, as its name would imply, between the left ventricle’s exit and the aorta itself.
Even though the heart is split up into two distinct halves, these two must work together to function properly.
When the heart starts to contract, it begins in the upper (atrium), thin-walled chambers and causes the blood to be squeezed out into the lower (ventricle) chambers. As the upper chamber finishes its squeeze, the lower chamber begins its work. The active action of these two chambers working together is called systole (sis’to-le). Each of these active periods will be followed by a short resting period known as diastole (di-as’to-le) although the heart never actually stops.
As the walls of the atrium complete their contraction, the ventricle begins its active stage. As the ventricle has been contracting the atrium has been filling up with blood so the entire process begins anew.
The sound of a normal heartbeat has often been described as “lubb” and “dupp”. The “lubb” period is the longer and deeper sounding of the two and is made as the ventricle is in its systole period. It is thought the sound is a result of the thick muscled walls of the ventricle contracting and the atrioventricular valves slamming shut. The “dupp” sound is shorter and has a distinctively sharper pitch. It occurs during the ventricle’s diastole period and is made as the semilunar valves close.
When these valves are not functioning normally there is a “swooshing” sound that can be heard. These are caused by the blood backwashing into the various chambers of the heart and are one of the possibilities when health care professionals are speaking of “murmurs.”
If a spinal or some other type of injury occurs and the nerves to voluntary muscles are cut, that muscle ceases to work and the area becomes paralyzed. Amazingly, if the nerves to the heart are cut it will continue to beat. The reason for this is that even though the heart is controlled by the nervous system, the heart’s muscles can actually contract rhythmically on its own. Unfortunately the nervous system is required for the heart to beat rapidly enough to maintain proper blood flow. If the nerves were to be cut, the heart’s rate could drop below 40 beats per minute and even if activity is increased, the heart’s rate would not.
The human heart is a fascinating organ that many, if given the chance, would love to exam. For most this possibility will never become a reality but for the really curious, there is an adequate substitute. This substitute is the heart of the common cow and can usually be obtained by visiting a local meat market and asking for one.
The heart is basically a hollow muscular pump, which pushes the blood through out the body via the blood vessels. A normal sized healthy heart is roughly the same size as a fist. It is located between the lungs and slightly to the left of center. The heart is an involuntary muscle that has approximately seventy to ninety contractions per minute during a restful state. It begins to pump early in the life of a fetus and will continue unceasingly until death.
A hollow organ, the heart’s walls are made up by three distinct layers. They are as follows:
1. Endocardium (en-do-kar’de-um) this is a very smooth layer of cells that form the interior membrane of the heart. The endocardium tissue is also the type of tissue that makes up the valves of the heart.
2. Myocardium (mi-o-kar’de-um) is the actual muscle tissue of the heart and is by far the thickest layer.
3. Pericardium (per-I-kar’de-um) is the outermost layer of the heart and is also the tissue that serves as the lining of the pericardial sac.
The main portion of the heart is split into two different sides with an actual partition called the septum. Each side of the heart works as a separate pump and have two chambers apiece or as a whole, the heart has four distinct chambers.
1. Right atrium is the thin-walled area that receives the venous or “used” blood returning to the body by the veins.
2. Right ventricle is the “pump” area of the heart’s right side. The atrium dumps the blood into the ventricle where it is then pumped out the pulmonary arteries and to the lungs.
3. Left atrium receives the oxygenated blood returning from the lungs.
4. Left ventricle has the thickest walls of all. It is from this chamber the blood is pumped out of the heart, into the aorta and out to the rest of the body.
Since blood flow needs to be a one-way affair, there are valves at the entrance and exit of each ventricle. The entrance valves are called atrioventricular (a-tre-o-ven-trik’u-lar) and the exit valves are semilunar (sem-e-lu’nar). Each of the actual valves has it’s own specific name though.
1. Tricuspid valve is the one located at the entrance of the right ventricle. It prevents the blood from washing back into the right atrium. It gets its name from the three “cusps” or flaps that make up the valve.
2. Pulmonary semilunar valve is located between the right ventricle and the pulmonary artery.
3. Mitral valve is made of very heavy cusps and is located at the entrance of the left ventricle. This is a powerful valve that closes as the left ventricle begins each of its contractions to ensure the oxygenated blood doesn’t re-enter the left atrium.
4. Aortic valve is located, as its name would imply, between the left ventricle’s exit and the aorta itself.
Even though the heart is split up into two distinct halves, these two must work together to function properly.
When the heart starts to contract, it begins in the upper (atrium), thin-walled chambers and causes the blood to be squeezed out into the lower (ventricle) chambers. As the upper chamber finishes its squeeze, the lower chamber begins its work. The active action of these two chambers working together is called systole (sis’to-le). Each of these active periods will be followed by a short resting period known as diastole (di-as’to-le) although the heart never actually stops.
As the walls of the atrium complete their contraction, the ventricle begins its active stage. As the ventricle has been contracting the atrium has been filling up with blood so the entire process begins anew.
The sound of a normal heartbeat has often been described as “lubb” and “dupp”. The “lubb” period is the longer and deeper sounding of the two and is made as the ventricle is in its systole period. It is thought the sound is a result of the thick muscled walls of the ventricle contracting and the atrioventricular valves slamming shut. The “dupp” sound is shorter and has a distinctively sharper pitch. It occurs during the ventricle’s diastole period and is made as the semilunar valves close.
When these valves are not functioning normally there is a “swooshing” sound that can be heard. These are caused by the blood backwashing into the various chambers of the heart and are one of the possibilities when health care professionals are speaking of “murmurs.”
If a spinal or some other type of injury occurs and the nerves to voluntary muscles are cut, that muscle ceases to work and the area becomes paralyzed. Amazingly, if the nerves to the heart are cut it will continue to beat. The reason for this is that even though the heart is controlled by the nervous system, the heart’s muscles can actually contract rhythmically on its own. Unfortunately the nervous system is required for the heart to beat rapidly enough to maintain proper blood flow. If the nerves were to be cut, the heart’s rate could drop below 40 beats per minute and even if activity is increased, the heart’s rate would not.
The human heart is a fascinating organ that many, if given the chance, would love to exam. For most this possibility will never become a reality but for the really curious, there is an adequate substitute. This substitute is the heart of the common cow and can usually be obtained by visiting a local meat market and asking for one.
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