This article is about the muscular organ. For the human heart, see Human heart. For the radio network, see The Heart Network. For other uses, see Heart (disambiguation).This article needs additional citations for verification.
Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (July 2009)HeartThe heart is a muscular organ found in all vertebrates that is responsible for pumping blood throughout the blood vessels by repeated, rhythmic contractions. The term cardiac (as in cardiology) means "related to the heart" and comes from the Greek καρδιά, kardia, for "heart."
The vertebrate heart is composed of cardiac muscle, an involuntary striated muscle tissue which is found only within this organ. The average human heart, beating at 72 beats per minute, will beat approximately 2.5 billion times during an average lifespan. It weighs on average 250 g to 300 g in females and 300 g to 350 g in males.[1]
Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (July 2009)HeartThe heart is a muscular organ found in all vertebrates that is responsible for pumping blood throughout the blood vessels by repeated, rhythmic contractions. The term cardiac (as in cardiology) means "related to the heart" and comes from the Greek καρδιά, kardia, for "heart."
The vertebrate heart is composed of cardiac muscle, an involuntary striated muscle tissue which is found only within this organ. The average human heart, beating at 72 beats per minute, will beat approximately 2.5 billion times during an average lifespan. It weighs on average 250 g to 300 g in females and 300 g to 350 g in males.[1]
Early developmentMain article: Heart developmentThe mammalian heart is derived from embryonic mesoderm germ-layer cells that differentiate after gastrulation into mesothelium, endothelium, and myocardium. Mesothelial pericardium forms the inner lining of the heart. The outer lining of the heart, lymphatic and blood vessels develop from endothelium. Myocardium develops into heart muscle.[2]
From splanchnopleuric mesoderm tissue, the cardiogenic plate develops cranially and laterally to the neural plate. In the cardiogenic plate, two separate angiogenic cell clusters form on either side of the embryo. Each cell cluster coalesces to form an endocardial tube continuous with a dorsal aorta and a vitteloumbilical vein. As embryonic tissue continues to fold, the two endocardial tubes are pushed into the thoracic cavity, begin to fuse together and are completely fused at approximately 21 days.[3]
At 21 days after conception, the human heart begins beating at 70 to 80 beats per minute and accelerates linearly for the first month of beating.The human embryonic heart begins beating around 21 days after conception, or five weeks after the last normal menstrual period (LMP), which is the date normally used to date pregnancy. It is unknown how blood in the human embryo circulates for the first 21 days in the absence of a functioning heart. The human heart begins beating at a rate near the mother’s, about 75-80 beats per minute (BPM).
The embryonic heart rate (EHR) then accelerates approximately 100 BPM during the first month of beating, peaking at 165-185 BPM during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 BPM per day, or about 10 BPM every three days, an increase of 100 BPM in the first month.[4] After 9.1 weeks after the LMP, it decelerates to about 152 BPM (+/-25 BPM) during the 15th week after the LMP. After the 15th week the deceleration slows reaching an average rate of about 145 (+/-25 BPM) BPM at term. The regression formula which describes this acceleration before the embryo reaches 25 mm in crown-rump length or 9.2 LMP weeks is: Age in days = EHR(0.3)+6. There is no difference in male and female heart rates before birth.[5]
[edit]StructureThe structure of the heart varies among the different branches of the animal kingdom. (See Circulatory system.) Cephalopods have two "gill hearts" and one "systemic heart".
Fish have a two-chambered heart that pumps the blood to the gills and from there it goes on to the rest of the body.
[edit]In double circulatory systemsIn amphibians and most reptiles, a double circulatory system is used, but the heart is not completely separated into two pumps.
In living amphibians, the heart has three chambers, with two separate atria and a single, undivided ventricle. The heart of lungfish also has three chambers, but here, there is a septum extending from the division between the atria part-way into the ventricle. This allows for some degree of separation between the de-oxygenated bloodstream destined for the lungs, and the oxygenated stream that is delivered to the rest of the body. The absence of such a division in living amphibian species may be at least partly due to the amount of respiration that occurs through the skin in such species; thus, the blood returned to the heart through the vena cavae is, in fact, already partially oxygenated. As a result, there may be less need for a clear division between the two bloodstreams than in lungfish or other tetrapods. Nonetheless, in at least some species of amphibian, the spongy nature of the ventricle seems to maintain more of a separation between the bloodstreams than appears the case at first glance.[6]
The heart of most reptiles (except for crocodilians; see below) has a similar structure to that of lungfish, but here, the septum is generally much larger. This divides the ventricle into two halves, but because the septum does not reach the whole length of the heart, there is a considerable gap near the openings to the pulmonary artery and the aorta. In practice, however, in the majority of reptilian species, there appears to be little, if any, mixing between the bloodstreams, so that the aorta receives essentially only oxygenated blood.[6]
[edit]The fully-divided heartHuman heart removed from a 64-year-old male.Surface anatomy of the human heart. The heart is demarcated by:
-A point 9 cm to the left of the midsternal line (apex of the heart)
-The seventh right sternocostal articulation
-The upper border of the third right costal cartilage 1 cm from the rightsternal line
-The lower border of the second left costal cartilage 2.5 cm from the left lateral sternal line.[7]Archosaurs (crocodilians and birds) and mammals show complete separation of the heart into two pumps, for a total of four heart chambers; it is thought that the four-chambered heart of archosaurs evolved independently from that of mammals. In crocodilians, there is a small opening, the foramen of Panizza, at the base of the arterial trunks, and there is some degree of mixing between the blood in each side of the heart. Thus, only in birds and mammals are the two streams of blood - those to the pulmonary and systemic circulations - kept entirely separate by a physical barrier.[6]
In the human body, the heart is usually situated in the middle of thethorax with the largest part of the heart slightly offset to the left (although sometimes it is on the right, see dextrocardia), underneath the sternum. The heart is usually felt to be on the left side because the left heart (left ventricle) is stronger (it pumps to all body parts). The left lung is smaller than the right lung because the heart occupies more of the left hemithorax. The heart is fed by the coronary circulation and enclosed by a sac known as the pericardium and is surrounded by the lungs. The pericardium comprises two parts: the fibrous pericardium, made of dense fibrous connective tissue; and a double membrane structure (parietal and visceral pericardium) containing a serous fluid to reduce friction during heart contractions. The heart is located in the mediastinum, the central sub-division of the thoracic cavity. The mediastinum also contains other structures, such as the esophagus and trachea, and is flanked on either side by the right and left pulmonary cavities, which house the lungs.[8]
The apex is the blunt point situated in an inferior (pointing down and left) direction. A stethoscope can be placed directly over the apex so that the beats can be counted. It is located posterior to the 5th intercostal space just medial of the left mid-clavicular line. In normal adults, the mass of the heart is 250-350 g (9-12 oz), or about twice the size of a clenched fist (it is about the size of a clenched fist in children), but extremely diseased hearts can be up to 1000 g (2 lb) in mass due to hypertrophy. It consists of four chambers, the two upper atria and the two lower ventricles.
[edit]FunctioningIn mammals, the function of the right side of the heart (see right heart) is to collect de-oxygenated blood, in the right atrium, from the body (via superior and inferior vena cavae) and pump it, via the right ventricle, into the lungs (pulmonary circulation) so that carbon dioxide can be dropped off and oxygen picked up (gas exchange). This happens through the passive process of diffusion. The left side (see left heart) collects oxygenated blood from the lungs into the left atrium. From the left atrium the blood moves to the left ventricle which pumps it out to the body (via the aorta). On both sides, the lower ventricles are thicker and stronger than the upper atria. The muscle wall surrounding the left ventricle is thicker than the wall surrounding the right ventricle due to the higher force needed to pump the blood through the systemic circulation.
Starting in the right atrium, the blood flows through the tricuspid valve to the right ventricle. Here it is pumped out the pulmonary semilunar valve and travels through the pulmonary artery to the lungs. From there, blood flows back through the pulmonary vein to the left atrium. It then travels through the mitral valve to the left ventricle, from where it is pumped through the aortic semilunar valve to the aorta. The aorta forks and the blood is divided between major arteries which supply the upper and lower body. The blood travels in the arteries to the smaller arterioles, then finally to the tiny capillaries which feed each cell. The (relatively) deoxygenated blood then travels to the venules, which coalesce into veins, then to the inferior and superior venae cavae and finally back to the right atrium where the process began.
The heart is effectively a syncytium, a meshwork of cardiac muscle cells interconnected by contiguous cytoplasmic bridges. This relates to electrical stimulation of one cell spreading to neighboring cells.
Some cardiac cells are self-excitable, contracting without any signal from the nervous system, even if removed from the heart and placed in culture. Each of these cells has its own intrinsic contraction rhythm. A region of the human heart called the sinoatrial node SA node, or pacemaker, sets the rate and timing at which all cardiac muscle cells contract. The SA node generates electrical impulses, much like those produced by nerve cells. Because cardiac muscle cells are electrically coupled by inter-calated disks between adjacent cells, impulses from the SA node spread rapidly through the walls of the artria, causing both artria to contract in unison. The impulses also pass to another region of specialized cardiac muscle tissue, a relay point called the atrioventricular (AV) node, located in the wall between the right artrium and the right ventricle. Here, the impulses are delayed for about 0.1s before spreading to the walls of the ventricle. The delay ensures that the artria empty completely before the ventricles contract. Specialized muscle fibers called Purkinje fibers then conduct the signals to the apex of the heart along and throughout the ventricular walls. The Purkinje fibres form conducting pathways called bundle branches. The impulses generated during the heart cycle produce electrical currents, which are conducted through body fluids to the skin, where they can be detected by electrodes and recorded as an electrocardiogram (ECG or EKG).[9]
Cardiac arrest is the sudden cessation of normal heart rhythm which can include a number of pathologies such as tachycardia, an extremely rapid heart beat which prevents the heart from effectively pumping blood, fibrillation which is an irregular and ineffective heart rhythm, andasystole which is the cessation of heart rhythm entirely.
Cardiac Tamponade is a condition in which the fibrous sac surrounding the heart fills with excess fluid or blood, suppressing the heart's ability to beat properly. Tamponade is treated by pericardiocentesis, the gentle insertion of the needle of a syringe into the pericardial sac (avoiding the heart itself) on an angle, usually from just below the sternum, and gently withdrawing the tamponading fluids.
[edit]History of discoveriesA human heart with a visible gun shot woundThe valves of the heart were discovered by a physician of the Hippocratean school around the 4th century BC. However, their function was not properly understood then. Because blood pools in the veins after death, arteries look empty. Ancient anatomists assumed they were filled with air and that they were for transport of air.
Philosophers distinguished veins from arteries but thought that the pulse was a property of arteries themselves. Erasistratos observed that arteries that were cut during life bleed. He ascribed the fact to the phenomenon that air escaping from an artery is replaced with blood that entered by very small vessels between veins and arteries. Thus he apparently postulatedcapillaries but with reversed flow of blood.
The 2nd century AD, Greek physician Galenos (Galen) knew that blood vessels carried blood and identified venous (dark red) and arterial (brighter and thinner) blood, each with distinct and separate functions. Growth and energy were derived from venous blood created in the liver fromchyle, while arterial blood gave vitality by containing pneuma (air) and originated in the heart. Blood flowed from both creating organs to all parts of the body where it was consumed and there was no return of blood to the heart or liver. The heart did not pump blood around, the heart's motion sucked blood in during diastole and the blood moved by the pulsation of the arteries themselves.
Galen believed that the arterial blood was created by venous blood passing from the left ventricle to the right by passing through 'pores' in the inter ventricular septum, air passed from the lungs via the pulmonary artery to the left side of the heart. As the arterial blood was created 'sooty' vapors were created and passed to the lungs also via the pulmonary artery to be exhaled.
The first major scientific understanding of the heart was put forth by the medieval Arab polymath Ibn Al-Nafis, regarded as the father of circulatory physiology.[10] He was the first physician to correctly describe pulmonary circulation,[11] the capillary[12] and coronary circulations.[13] Prior to this, Galen`s theory was widely accepted, and improved upon by Avicenna. Al-Nafis rejected the Galen-Avicenna theory and corrected many wrong ideas that were put forth by it, and also adding his new found observations of pulse and circulation to the new theory. His major observations include (as surmised by Dr. Paul Ghalioungui):[12]
1. "Denying the existence of any pores through the interventricular septum."
2. "The flow of blood from the right ventricle to the lungs where its lighter parts filter into the pulmonary vein to mix with air."
3. "The notion that blood, or spirit from the mixture of blood and air, passes from the lung to the left ventricle, and not in the opposite direction."
4. "The assertion that there are only two ventricles, not three as stated by Avicenna."
5. "The statement that the ventricle takes its nourishment from blood flowing in the vessels that run in its substance (i.e. the coronary vessels) and not, as Avicenna maintained, from blood deposited in the right ventricle."
6. "A premonition of the capillary circulation in his assertion that the pulmonary vein receives what comes out of the pulmonary artery, this being the reason for the existence of perceptible passages between the two."
Ibn Al-Nafis also corrected Galen-Avicenna assertion that heart has a bone structure through his own observations and wrote the following criticism on it:[14]
"This is not true. There are absolutely no bones beneath the heart as it is positioned right in the middle of the chest cavity where there are no bones at all. Bones are only found at the chest periphery not where the heart is positioned."
For more recent technological developments, see Cardiac surgery.
[edit]Healthy heartObesity, high blood pressure and high cholesterol can increase the risk of developing heart disease. However, fully half the amount of heart attacks occur in people with normal cholesterol levels. Heart disease is a major cause of death (and the number one cause of death in theWestern World).
Of course one must also consider other factors such as lifestyle and overall health (mental and social as well as physical).[15][16][17][18]
[edit]See also
From splanchnopleuric mesoderm tissue, the cardiogenic plate develops cranially and laterally to the neural plate. In the cardiogenic plate, two separate angiogenic cell clusters form on either side of the embryo. Each cell cluster coalesces to form an endocardial tube continuous with a dorsal aorta and a vitteloumbilical vein. As embryonic tissue continues to fold, the two endocardial tubes are pushed into the thoracic cavity, begin to fuse together and are completely fused at approximately 21 days.[3]
At 21 days after conception, the human heart begins beating at 70 to 80 beats per minute and accelerates linearly for the first month of beating.The human embryonic heart begins beating around 21 days after conception, or five weeks after the last normal menstrual period (LMP), which is the date normally used to date pregnancy. It is unknown how blood in the human embryo circulates for the first 21 days in the absence of a functioning heart. The human heart begins beating at a rate near the mother’s, about 75-80 beats per minute (BPM).
The embryonic heart rate (EHR) then accelerates approximately 100 BPM during the first month of beating, peaking at 165-185 BPM during the early 7th week, (early 9th week after the LMP). This acceleration is approximately 3.3 BPM per day, or about 10 BPM every three days, an increase of 100 BPM in the first month.[4] After 9.1 weeks after the LMP, it decelerates to about 152 BPM (+/-25 BPM) during the 15th week after the LMP. After the 15th week the deceleration slows reaching an average rate of about 145 (+/-25 BPM) BPM at term. The regression formula which describes this acceleration before the embryo reaches 25 mm in crown-rump length or 9.2 LMP weeks is: Age in days = EHR(0.3)+6. There is no difference in male and female heart rates before birth.[5]
[edit]StructureThe structure of the heart varies among the different branches of the animal kingdom. (See Circulatory system.) Cephalopods have two "gill hearts" and one "systemic heart".
Fish have a two-chambered heart that pumps the blood to the gills and from there it goes on to the rest of the body.
[edit]In double circulatory systemsIn amphibians and most reptiles, a double circulatory system is used, but the heart is not completely separated into two pumps.
In living amphibians, the heart has three chambers, with two separate atria and a single, undivided ventricle. The heart of lungfish also has three chambers, but here, there is a septum extending from the division between the atria part-way into the ventricle. This allows for some degree of separation between the de-oxygenated bloodstream destined for the lungs, and the oxygenated stream that is delivered to the rest of the body. The absence of such a division in living amphibian species may be at least partly due to the amount of respiration that occurs through the skin in such species; thus, the blood returned to the heart through the vena cavae is, in fact, already partially oxygenated. As a result, there may be less need for a clear division between the two bloodstreams than in lungfish or other tetrapods. Nonetheless, in at least some species of amphibian, the spongy nature of the ventricle seems to maintain more of a separation between the bloodstreams than appears the case at first glance.[6]
The heart of most reptiles (except for crocodilians; see below) has a similar structure to that of lungfish, but here, the septum is generally much larger. This divides the ventricle into two halves, but because the septum does not reach the whole length of the heart, there is a considerable gap near the openings to the pulmonary artery and the aorta. In practice, however, in the majority of reptilian species, there appears to be little, if any, mixing between the bloodstreams, so that the aorta receives essentially only oxygenated blood.[6]
[edit]The fully-divided heartHuman heart removed from a 64-year-old male.Surface anatomy of the human heart. The heart is demarcated by:
-A point 9 cm to the left of the midsternal line (apex of the heart)
-The seventh right sternocostal articulation
-The upper border of the third right costal cartilage 1 cm from the rightsternal line
-The lower border of the second left costal cartilage 2.5 cm from the left lateral sternal line.[7]Archosaurs (crocodilians and birds) and mammals show complete separation of the heart into two pumps, for a total of four heart chambers; it is thought that the four-chambered heart of archosaurs evolved independently from that of mammals. In crocodilians, there is a small opening, the foramen of Panizza, at the base of the arterial trunks, and there is some degree of mixing between the blood in each side of the heart. Thus, only in birds and mammals are the two streams of blood - those to the pulmonary and systemic circulations - kept entirely separate by a physical barrier.[6]
In the human body, the heart is usually situated in the middle of thethorax with the largest part of the heart slightly offset to the left (although sometimes it is on the right, see dextrocardia), underneath the sternum. The heart is usually felt to be on the left side because the left heart (left ventricle) is stronger (it pumps to all body parts). The left lung is smaller than the right lung because the heart occupies more of the left hemithorax. The heart is fed by the coronary circulation and enclosed by a sac known as the pericardium and is surrounded by the lungs. The pericardium comprises two parts: the fibrous pericardium, made of dense fibrous connective tissue; and a double membrane structure (parietal and visceral pericardium) containing a serous fluid to reduce friction during heart contractions. The heart is located in the mediastinum, the central sub-division of the thoracic cavity. The mediastinum also contains other structures, such as the esophagus and trachea, and is flanked on either side by the right and left pulmonary cavities, which house the lungs.[8]
The apex is the blunt point situated in an inferior (pointing down and left) direction. A stethoscope can be placed directly over the apex so that the beats can be counted. It is located posterior to the 5th intercostal space just medial of the left mid-clavicular line. In normal adults, the mass of the heart is 250-350 g (9-12 oz), or about twice the size of a clenched fist (it is about the size of a clenched fist in children), but extremely diseased hearts can be up to 1000 g (2 lb) in mass due to hypertrophy. It consists of four chambers, the two upper atria and the two lower ventricles.
[edit]FunctioningIn mammals, the function of the right side of the heart (see right heart) is to collect de-oxygenated blood, in the right atrium, from the body (via superior and inferior vena cavae) and pump it, via the right ventricle, into the lungs (pulmonary circulation) so that carbon dioxide can be dropped off and oxygen picked up (gas exchange). This happens through the passive process of diffusion. The left side (see left heart) collects oxygenated blood from the lungs into the left atrium. From the left atrium the blood moves to the left ventricle which pumps it out to the body (via the aorta). On both sides, the lower ventricles are thicker and stronger than the upper atria. The muscle wall surrounding the left ventricle is thicker than the wall surrounding the right ventricle due to the higher force needed to pump the blood through the systemic circulation.
Starting in the right atrium, the blood flows through the tricuspid valve to the right ventricle. Here it is pumped out the pulmonary semilunar valve and travels through the pulmonary artery to the lungs. From there, blood flows back through the pulmonary vein to the left atrium. It then travels through the mitral valve to the left ventricle, from where it is pumped through the aortic semilunar valve to the aorta. The aorta forks and the blood is divided between major arteries which supply the upper and lower body. The blood travels in the arteries to the smaller arterioles, then finally to the tiny capillaries which feed each cell. The (relatively) deoxygenated blood then travels to the venules, which coalesce into veins, then to the inferior and superior venae cavae and finally back to the right atrium where the process began.
The heart is effectively a syncytium, a meshwork of cardiac muscle cells interconnected by contiguous cytoplasmic bridges. This relates to electrical stimulation of one cell spreading to neighboring cells.
Some cardiac cells are self-excitable, contracting without any signal from the nervous system, even if removed from the heart and placed in culture. Each of these cells has its own intrinsic contraction rhythm. A region of the human heart called the sinoatrial node SA node, or pacemaker, sets the rate and timing at which all cardiac muscle cells contract. The SA node generates electrical impulses, much like those produced by nerve cells. Because cardiac muscle cells are electrically coupled by inter-calated disks between adjacent cells, impulses from the SA node spread rapidly through the walls of the artria, causing both artria to contract in unison. The impulses also pass to another region of specialized cardiac muscle tissue, a relay point called the atrioventricular (AV) node, located in the wall between the right artrium and the right ventricle. Here, the impulses are delayed for about 0.1s before spreading to the walls of the ventricle. The delay ensures that the artria empty completely before the ventricles contract. Specialized muscle fibers called Purkinje fibers then conduct the signals to the apex of the heart along and throughout the ventricular walls. The Purkinje fibres form conducting pathways called bundle branches. The impulses generated during the heart cycle produce electrical currents, which are conducted through body fluids to the skin, where they can be detected by electrodes and recorded as an electrocardiogram (ECG or EKG).[9]
Cardiac arrest is the sudden cessation of normal heart rhythm which can include a number of pathologies such as tachycardia, an extremely rapid heart beat which prevents the heart from effectively pumping blood, fibrillation which is an irregular and ineffective heart rhythm, andasystole which is the cessation of heart rhythm entirely.
Cardiac Tamponade is a condition in which the fibrous sac surrounding the heart fills with excess fluid or blood, suppressing the heart's ability to beat properly. Tamponade is treated by pericardiocentesis, the gentle insertion of the needle of a syringe into the pericardial sac (avoiding the heart itself) on an angle, usually from just below the sternum, and gently withdrawing the tamponading fluids.
[edit]History of discoveriesA human heart with a visible gun shot woundThe valves of the heart were discovered by a physician of the Hippocratean school around the 4th century BC. However, their function was not properly understood then. Because blood pools in the veins after death, arteries look empty. Ancient anatomists assumed they were filled with air and that they were for transport of air.
Philosophers distinguished veins from arteries but thought that the pulse was a property of arteries themselves. Erasistratos observed that arteries that were cut during life bleed. He ascribed the fact to the phenomenon that air escaping from an artery is replaced with blood that entered by very small vessels between veins and arteries. Thus he apparently postulatedcapillaries but with reversed flow of blood.
The 2nd century AD, Greek physician Galenos (Galen) knew that blood vessels carried blood and identified venous (dark red) and arterial (brighter and thinner) blood, each with distinct and separate functions. Growth and energy were derived from venous blood created in the liver fromchyle, while arterial blood gave vitality by containing pneuma (air) and originated in the heart. Blood flowed from both creating organs to all parts of the body where it was consumed and there was no return of blood to the heart or liver. The heart did not pump blood around, the heart's motion sucked blood in during diastole and the blood moved by the pulsation of the arteries themselves.
Galen believed that the arterial blood was created by venous blood passing from the left ventricle to the right by passing through 'pores' in the inter ventricular septum, air passed from the lungs via the pulmonary artery to the left side of the heart. As the arterial blood was created 'sooty' vapors were created and passed to the lungs also via the pulmonary artery to be exhaled.
The first major scientific understanding of the heart was put forth by the medieval Arab polymath Ibn Al-Nafis, regarded as the father of circulatory physiology.[10] He was the first physician to correctly describe pulmonary circulation,[11] the capillary[12] and coronary circulations.[13] Prior to this, Galen`s theory was widely accepted, and improved upon by Avicenna. Al-Nafis rejected the Galen-Avicenna theory and corrected many wrong ideas that were put forth by it, and also adding his new found observations of pulse and circulation to the new theory. His major observations include (as surmised by Dr. Paul Ghalioungui):[12]
1. "Denying the existence of any pores through the interventricular septum."
2. "The flow of blood from the right ventricle to the lungs where its lighter parts filter into the pulmonary vein to mix with air."
3. "The notion that blood, or spirit from the mixture of blood and air, passes from the lung to the left ventricle, and not in the opposite direction."
4. "The assertion that there are only two ventricles, not three as stated by Avicenna."
5. "The statement that the ventricle takes its nourishment from blood flowing in the vessels that run in its substance (i.e. the coronary vessels) and not, as Avicenna maintained, from blood deposited in the right ventricle."
6. "A premonition of the capillary circulation in his assertion that the pulmonary vein receives what comes out of the pulmonary artery, this being the reason for the existence of perceptible passages between the two."
Ibn Al-Nafis also corrected Galen-Avicenna assertion that heart has a bone structure through his own observations and wrote the following criticism on it:[14]
"This is not true. There are absolutely no bones beneath the heart as it is positioned right in the middle of the chest cavity where there are no bones at all. Bones are only found at the chest periphery not where the heart is positioned."
For more recent technological developments, see Cardiac surgery.
[edit]Healthy heartObesity, high blood pressure and high cholesterol can increase the risk of developing heart disease. However, fully half the amount of heart attacks occur in people with normal cholesterol levels. Heart disease is a major cause of death (and the number one cause of death in theWestern World).
Of course one must also consider other factors such as lifestyle and overall health (mental and social as well as physical).[15][16][17][18]
[edit]See also
Atrial systoleAtrial systoleAtrial systole is the contraction of the heart muscle (myocardia) of the left and right atria. Normally, both atria contract at the same time. The term systole is synonymous with contraction (movement or shortening) of a muscle. Electrical systole is the electrical activity that stimulates the myocardium of the chambers of the heart to make them contract. This is soon followed by Mechanical systole, which is the mechanical contraction of the heart.
As the atria contract, the blood pressure in each atrium increases, forcing additional blood into the ventricles. The additional flow of blood is called atrial kick.
70% of the blood flows passively down to the ventricles, so the atria do not have to contract a great amount.[2]
Atrial kick is absent if there is loss of normal electrical conduction in the heart, such as during atrial fibrillation,atrial flutter, and complete heart block. Atrial kick is also different in character depending on the condition of the heart, such as stiff heart, which is found in patients with diastolic dysfunction.
[edit]Detection of atrial systoleElectrical systole of the atria begins with the onset of the P wave on the ECG. The wave of bipolarization (or depolarization) that stimulates both atria to contract at the same time is due to sinoatrial node which is located on the upper wall of the right atrium. 30% of the ventricles are filled during this phase
[edit]Ventricular systoleVentricular systoleVentricular systole is the contraction of the muscles (myocardia) of the left and right ventricles.
At the later part of the ejection phase, although the ventricular pressure falls below the aortic pressure, the aortic valve remains patent because of the inertial energy of the ejected blood.[3]
The graph of aortic pressure throughout the cardiac cycle displays a small dip which coincides with the aortic valve closure. The dip in the graph is immediately followed by a brief rise then gradual decline. The small rise in the graph is known as the "dicrotic notch" or "incisure", and represents a transient increase in aortic pressure. Just as the ventricles enter into diastole, the brief reversal of flow from the aorta back into the left ventricle causes the aortic valves to shut. This results in the slight increase in aortic pressure caused by the elastic recoil of the semilunar valves and aorta.[4] [5] [6]
[edit]Detection of ventricular systole[edit]Heart soundsMain article: Heart soundsThe closing of the mitral and tricuspid valves (known together as the atrioventricular valves) at the beginning of ventricular systole cause the first part of the "lub-dub" sound made by the heart as it beats. Formally, this sound is known as the First Heart Tone, or S1. This first heart tone is created by the closure of mitral and tricuspid valve and is actually a two component sound, M1, T1.
The second part of the "lub-dub" (the Second Heart Tone, or S2), is caused by the closure of the aortic and pulmonary valves at the end of ventricular systole. As the left ventricle empties, its pressure falls below the pressure in the aorta, and the aortic valve closes. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary valve closes. The second heart sound is also two components, A2, P2. The aortic valve closes earlier than the pulmonary valve and they are audibly separated from each other in the second heart sound. This "splitting" of S2 is only audible during inhalation.
[edit]ElectrocardiogramIn an electrocardiogram, electrical systole of the ventricles begins at the beginning of the QRS complex.
[edit]DiastoleCardiac diastoleCardiac Diastole is the period of time when the heart relaxes after contraction in preparation for refilling with circulating blood. Ventricular diastole is when the ventricles are relaxing, while atrial diastole is when the atria are relaxing. Together they are known as complete cardiac diastole.
During ventricular diastole, the pressure in the (left and right) ventricles drops from the peak that it reaches insystole. When the pressure in the left ventricle drops to below the pressure in the left atrium, the mitral valveopens, and the left ventricle fills with blood that was accumulating in the left atrium. Likewise, when the pressure in the right ventricle drops below that in the right atrium, the tricuspid valve opens, and the right ventricle fills with blood that was accumulating in the right atrium. During diastole the pressure within the myocardium is lower than that in aorta, allowing blood to circulate in the heart itself via the coronary arteries.
[edit]Regulation of the cardiac cycleCardiac muscle has automaticity, which means that it is self-exciting. This is in contrast with skeletal muscle, which requires either conscious or reflex nervous stimuli for excitation. The heart's rhythmic contractions occur spontaneously, although the rate of contraction can be changed by nervous or hormonal influences, exercise and emotions. For example, the sympathetic nerves to heart accelerate heart rate and the vagus nerve decelerates heart rate.
The rhythmic sequence of contractions is coordinated by the sinoatrial (SA) and atrioventricular (AV) nodes. The sinoatrial node, often known as the cardiac pacemaker, is located in the upper wall of the right atrium and is responsible for the wave of electrical stimulation that initiates atrial contraction by creating an action potential. Once the wave reaches the AV node, situated in the lower right atrium, it is delayed there before being conducted through the bundles of His and back up the Purkinje fibers, leading to a contraction of the ventricles. The delay at the AV node allows enough time for all of the blood in the atria to fill their respective ventricles. In the event of severe pathology, the AV node can also act as a pacemaker; this is usually not the case because their rate of spontaneous firing is considerably lower than that of the pacemaker cells in the SA node and hence is overridden.
As the atria contract, the blood pressure in each atrium increases, forcing additional blood into the ventricles. The additional flow of blood is called atrial kick.
70% of the blood flows passively down to the ventricles, so the atria do not have to contract a great amount.[2]
Atrial kick is absent if there is loss of normal electrical conduction in the heart, such as during atrial fibrillation,atrial flutter, and complete heart block. Atrial kick is also different in character depending on the condition of the heart, such as stiff heart, which is found in patients with diastolic dysfunction.
[edit]Detection of atrial systoleElectrical systole of the atria begins with the onset of the P wave on the ECG. The wave of bipolarization (or depolarization) that stimulates both atria to contract at the same time is due to sinoatrial node which is located on the upper wall of the right atrium. 30% of the ventricles are filled during this phase
[edit]Ventricular systoleVentricular systoleVentricular systole is the contraction of the muscles (myocardia) of the left and right ventricles.
At the later part of the ejection phase, although the ventricular pressure falls below the aortic pressure, the aortic valve remains patent because of the inertial energy of the ejected blood.[3]
The graph of aortic pressure throughout the cardiac cycle displays a small dip which coincides with the aortic valve closure. The dip in the graph is immediately followed by a brief rise then gradual decline. The small rise in the graph is known as the "dicrotic notch" or "incisure", and represents a transient increase in aortic pressure. Just as the ventricles enter into diastole, the brief reversal of flow from the aorta back into the left ventricle causes the aortic valves to shut. This results in the slight increase in aortic pressure caused by the elastic recoil of the semilunar valves and aorta.[4] [5] [6]
[edit]Detection of ventricular systole[edit]Heart soundsMain article: Heart soundsThe closing of the mitral and tricuspid valves (known together as the atrioventricular valves) at the beginning of ventricular systole cause the first part of the "lub-dub" sound made by the heart as it beats. Formally, this sound is known as the First Heart Tone, or S1. This first heart tone is created by the closure of mitral and tricuspid valve and is actually a two component sound, M1, T1.
The second part of the "lub-dub" (the Second Heart Tone, or S2), is caused by the closure of the aortic and pulmonary valves at the end of ventricular systole. As the left ventricle empties, its pressure falls below the pressure in the aorta, and the aortic valve closes. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary valve closes. The second heart sound is also two components, A2, P2. The aortic valve closes earlier than the pulmonary valve and they are audibly separated from each other in the second heart sound. This "splitting" of S2 is only audible during inhalation.
[edit]ElectrocardiogramIn an electrocardiogram, electrical systole of the ventricles begins at the beginning of the QRS complex.
[edit]DiastoleCardiac diastoleCardiac Diastole is the period of time when the heart relaxes after contraction in preparation for refilling with circulating blood. Ventricular diastole is when the ventricles are relaxing, while atrial diastole is when the atria are relaxing. Together they are known as complete cardiac diastole.
During ventricular diastole, the pressure in the (left and right) ventricles drops from the peak that it reaches insystole. When the pressure in the left ventricle drops to below the pressure in the left atrium, the mitral valveopens, and the left ventricle fills with blood that was accumulating in the left atrium. Likewise, when the pressure in the right ventricle drops below that in the right atrium, the tricuspid valve opens, and the right ventricle fills with blood that was accumulating in the right atrium. During diastole the pressure within the myocardium is lower than that in aorta, allowing blood to circulate in the heart itself via the coronary arteries.
[edit]Regulation of the cardiac cycleCardiac muscle has automaticity, which means that it is self-exciting. This is in contrast with skeletal muscle, which requires either conscious or reflex nervous stimuli for excitation. The heart's rhythmic contractions occur spontaneously, although the rate of contraction can be changed by nervous or hormonal influences, exercise and emotions. For example, the sympathetic nerves to heart accelerate heart rate and the vagus nerve decelerates heart rate.
The rhythmic sequence of contractions is coordinated by the sinoatrial (SA) and atrioventricular (AV) nodes. The sinoatrial node, often known as the cardiac pacemaker, is located in the upper wall of the right atrium and is responsible for the wave of electrical stimulation that initiates atrial contraction by creating an action potential. Once the wave reaches the AV node, situated in the lower right atrium, it is delayed there before being conducted through the bundles of His and back up the Purkinje fibers, leading to a contraction of the ventricles. The delay at the AV node allows enough time for all of the blood in the atria to fill their respective ventricles. In the event of severe pathology, the AV node can also act as a pacemaker; this is usually not the case because their rate of spontaneous firing is considerably lower than that of the pacemaker cells in the SA node and hence is overridden.
Cardiac cycle is the term referring to all or any of the events related to the flow or blood pressure that occurs from the beginning of oneheartbeat to the beginning of the next.[1] The frequency of the cardiac cycle is the heart rate. Every single 'beat' of the heart involves five major stages: First, "Late diastole" which is when the semilunar valves close, the Av valves open and the whole heart is relaxed. Second, "Atrial systole" when atria is contracting, AV valves open and blood flows from atrium to the ventricle. Third, "Isovolumic ventricular contraction" it is when the ventricles begin to contract, AV valves close, as well as the semilunar valves and there is no change in volume. Fourth, "ventricular ejection", Ventricles are empty, they are still contracting and the semilunar valves are open. The fifth stage is: "Isovolumic ventricular relaxation", Pressure decreases, no blood is entering the ventricles, ventricles stop contracting and begin to relax, semilunars are shut because blood in the aorta is pushing them shut. Throughout the cardiac cycle, the blood pressureincreases and decreases. The cardiac cycle is coordinated by a series of electrical impulses that are produced by specialized heart cells found within the sino-atrial node and the atrioventricular node. The cardiac muscle is composed of myocytes which initiate their own contraction without help of external nerves (with the exception of modifying the heart rate due to metabolic demand). Under normal circumstances, each cycle takes approximately o
heart pressure:
Blood pressure (BP) is the pressure exerted by circulating blood on the walls of blood vessels, and is one of the principal vital signs. During each heartbeat, BP varies between a maximum (systolic) and a minimum (diastolic) pressure. The mean BP decreases as the circulating blood moves away from the heart througharteries, has its greatest decrease in the small arteries and arterioles, and continues to decrease as the blood moves through the capillaries and back to the heart through veins.[1]
The term blood pressure usually refers to the pressure measured at a person's upper arm. It is measured on the inside of an elbow at the brachial artery, which is the upper arm's major blood vessel that carries blood away from the heart. A person's BP is usually expressed in terms of the systolic pressure and diastolic pressure, for example 115/75.
BP is sometimes measured at other places, for instance at an ankle. The ratio of the BP measured at the main artery of an ankle, to the BP measured at the brachial artery of an upper arm, gives the Ankle Brachial Pressure Index (ABPI).
Blood pressure (BP) is the pressure exerted by circulating blood on the walls of blood vessels, and is one of the principal vital signs. During each heartbeat, BP varies between a maximum (systolic) and a minimum (diastolic) pressure. The mean BP decreases as the circulating blood moves away from the heart througharteries, has its greatest decrease in the small arteries and arterioles, and continues to decrease as the blood moves through the capillaries and back to the heart through veins.[1]
The term blood pressure usually refers to the pressure measured at a person's upper arm. It is measured on the inside of an elbow at the brachial artery, which is the upper arm's major blood vessel that carries blood away from the heart. A person's BP is usually expressed in terms of the systolic pressure and diastolic pressure, for example 115/75.
BP is sometimes measured at other places, for instance at an ankle. The ratio of the BP measured at the main artery of an ankle, to the BP measured at the brachial artery of an upper arm, gives the Ankle Brachial Pressure Index (ABPI).
MeasurementA medical student checking blood pressure using a sphygmomanometer and stethoscope.Arterial pressure is most commonly measured via a sphygmomanometer, which historically used the height of a column of mercury to reflect the circulating pressure.[2] Today BP values are still reported in millimetres of mercury (mmHg), though aneroid and electronic devices do not use mercury.
For each heartbeat, BP varies between systolic and diastolic pressures. Systolic pressure is peak pressure in the arteries, which occurs near the end of the cardiac cycle when the ventricles are contracting. Diastolic pressure is minimum pressure in the arteries, which occurs near the beginning of the cardiac cycle when the ventricles are filled with blood. An example of normal measured values for a resting, healthy adult human is 115 mmHg systolic and 75 mmHg diastolic (written as 115/75 mmHg, and spoken [in the US] as "one-fifteen over seventy-five"). Pulse pressure is the difference between systolic and diastolic pressures.
Systolic and diastolic arterial BPs are not static but undergo natural variations from one heartbeat to another and throughout the day (in a circadian rhythm). They also change in response to stress, nutritional factors, drugs, disease, exercise, and momentarily from standing up. Sometimes the variations are large.Hypertension refers to arterial pressure being abnormally high, as opposed to hypotension, when it is abnormally low. Along with body temperature, respiratory rate, and pulse rate, BP measurements are the most commonly measured physiological parameters.
Arterial pressures are usually measured non-invasively, without penetrating skin or artery. Measuring pressure invasively, by penetrating the arterial wall to take the measurement, is much less common, and usually restricted to a hospital setting.
[edit]Noninvasive measurementThe noninvasive auscultatory and oscillometric measurements are simpler and quicker than invasive measurements, require less expertise in fitting, have virtually no complications, and are less unpleasant and painful for the patient. However, noninvasive methods may yield somewhat lower accuracy and small systematic differences in numerical results. Non-invasive measurement methods are more commonly used for routine examinations and monitoring.
[edit]Palpation methodA minimum systolic value can be roughly estimated without any equipment by palpation, most often used in emergency situations. Palpation of a radial pulse indicates a minimum BP of 80 mmHg, a femoral pulse indicates at least 70 mmHg, and a carotid pulse indicates a minimum of 60 mmHg. However, one study indicated that this method was not accurate enough and often overestimated patients' systolic BP.[3] A more accurate value of systolic BP can be obtained with a sphygmomanometer and palpating for when a radial pulse returns.[4] The diastolic blood pressure can not be estimated by this method.[5] Sometimes palpation is used to get an estimate before using the auscultatory method.
[edit]Auscultatory methodAuscultatory method aneroid sphygmomanometer with stethoscopeMercury manometerThe auscultatory method (from the Latin for listening) uses a stethoscope and a sphygmomanometer. This comprises an inflatable (Riva-Rocci) cuff placed around the upper arm at roughly the same vertical height as the heart, attached to a mercury or aneroid manometer. The mercury manometer measures the height of a column of mercury, giving an absolute result without need for calibration, and consequently not subject to the errors and drift of calibration which affect other methods. The use of mercury manometers is often required in clinical trials and for the clinical measurement of hypertension in high risk patients, such aspregnant women.
A cuff of appropriate size is fitted smoothly and snugly, then inflated manually by repeatedly squeezing a rubber bulb until the artery is completely occluded. Listening with the stethoscope to the brachial artery at the elbow, the examiner slowly releases the pressure in the cuff. When blood just starts to flow in the artery, the turbulent flow creates a "whooshing" or pounding (first Korotkoff sound). The pressure at which this sound is first heard is the systolic BP. The cuff pressure is further released until no sound can be heard (fifth Korotkoff sound), at the diastolic arterial pressure.
The auscultatory method has been predominant since the beginning of BP measurements but is gradually being replaced by other noninvasive techniques better suited to being automated.[6]
[edit]Oscillometric methodThe Oscillometric method was first demonstrated in 1876 and involves the observation of oscillations in the sphygmomanometer cuff pressure[7] which are caused by the oscillations of blood flow, i.e. the pulse.[8] The electronic version of this method is sometimes used in long-term measurements and general practice. It uses a sphygmomanometer cuff like the auscultatory method, but with an electronic pressure sensor(transducer) to observe cuff pressure oscillations, electronics to automatically interpret them, and automatic inflation and deflation of the cuff. The pressure sensor should be calibrated periodically to maintain accuracy.
Oscillometric measurement requires less skill than the auscultatory technique, and may be suitable for use by untrained staff and for automated patient home monitoring.
The cuff is inflated to a pressure initially in excess of the systolic arterial pressure, and then reduces to below diastolic pressure over a period of about 30 seconds. When blood flow is nil (cuff pressure exceeding systolic pressure) or unimpeded (cuff pressure below diastolic pressure), cuff pressure will be essentially constant. It is essential that the cuff size is correct: undersized cuffs may yield too high a pressure, whereas oversized cuffs yield too low a pressure. When blood flow is present, but restricted, the cuff pressure, which is monitored by the pressure sensor, will vary periodically in synchrony with the cyclic expansion and contraction of the brachial artery, i.e., it will oscillate. The values of systolic and diastolic pressure are computed, not actually measured from the raw data, using an algorithm; the computed results are displayed.
Oscillometric monitors may produce inaccurate readings in patients with heart and circulation problems, that include arterial sclerosis,arrhythmia, preeclampsia, pulsus alternans, and pulsus paradoxus.
In practice the different methods do not give identical results; an algorithm and experimentally obtained coefficients are used to adjust the oscillometric results to give readings which match the auscultatory results as well as possible. Some equipment uses computer-aided analysis of the instantaneous arterial pressure waveform to determine the systolic, mean, and diastolic points. Since many oscillometric devices have not been validated, caution must be given as most are not suitable in clinical and acute care settings.
The term NIBP, for Non-Invasive Blood Pressure, is often used to describe oscillometric monitoring equipment.
[edit]White-coat hypertensionFor some patients, BP measurements taken in a doctor's office may not correctly characterize their typical BP.[9] In up to 25% of patients, the office measurement is higher than their typical BP. This type of error is called white-coat hypertension (WCH) and can result from anxiety related to an examination by a health care professional.[10] The misdiagnosis of hypertension for these patients can result in needless and possibly harmful medication. WCH can be reduced (but not eliminated) with automated BP measurements over 15 to 20 minutes in a quiet part of the office or clinic.[11]
Debate continues regarding the significance of this effect.[citation needed] Some reactive patients will also react to many other stimuli throughout their daily lives, and require treatment. In some cases a lower BP reading occurs at the doctor's office.[12]
[edit]Home monitoringAmbulatory blood pressure devices that take readings every half hour throughout the day and night have been used for identifying and mitigating measurement problems like white-coat hypertension. Except for periods during sleep, home monitoring could be used for these purposes instead of ambulatory blood pressure monitoring.[13] Home monitoring may also be used to improve hypertension management and to monitor the effects of lifestyle changes and medication related to BP.[14] Compared to ambulatory blood pressure measurements, home monitoring has been found to be an effective and lower cost alternative.[13][15][16]
Aside from the white coat effect, BP readings outside of a clinical setting are usually slightly lower in the majority of people. The studies that looked into the risks from hypertension and the benefits of lowering BP in affected patients were based on readings in a clinical environment.
When measuring BP, an accurate reading requires that one not drink coffee, smoke cigarettes, or engage in strenuous exercise for 30 minutes before taking the reading. A full bladder may have a small effect on BP readings, so if the urge to urinate exists, one should do so before the reading. For 5 minutes before the reading, one should sit upright in a chair with one's feet flat on the floor and with limbs uncrossed. The BP cuff should always be against bare skin, as readings taken over a shirt sleeve are less accurate. During the reading, the arm that is used should be relaxed and kept at heart level, for example by resting it on a table.[17]
Since BP varies throughout the day, measurements intended to monitor changes over longer time frames should be taken at the same time of day to ensure that the readings are comparable. Suitable times are:
[edit]Invasive measurementArterial blood pressure (BP) is most accurately measured invasively through an arterial line. Invasive arterial pressure measurement with intravascular cannulae involves direct measurement of arterial pressure by placing a cannula needle in an artery (usually radial, femoral, dorsalis pedis or brachial). This procedure can be done by any licensed doctor or a Respiratory Therapist.
The cannula must be connected to a sterile, fluid-filled system, which is connected to an electronic pressure transducer. The advantage of this system is that pressure is constantly monitored beat-by-beat, and a waveform (a graph of pressure against time) can be displayed. This invasive technique is regularly employed in human and veterinary intensive care medicine, anesthesiology, and for research purposes.
Cannulation for invasive vascular pressure monitoring is infrequently associated with complications such as thrombosis, infection, and bleeding. Patients with invasive arterial monitoring require very close supervision, as there is a danger of severe bleeding if the line becomes disconnected. It is generally reserved for patients where rapid variations in arterial pressure are anticipated.
Invasive vascular pressure monitors are pressure monitoring systems designed to acquire pressure information for display and processing. There are a variety of invasive vascular pressure monitors for trauma, critical care, and operating room applications. These include single pressure, dual pressure, and multi-parameter (i.e. pressure / temperature). The monitors can be used for measurement and follow-up of arterial, central venous, pulmonary arterial, left atrial, right atrial, femoral arterial, umbilical venous, umbilical arterial, and intracranial pressures.
Vascular pressure parameters are derived in the monitor's microcomputer system. Usually, systolic, diastolic, and mean pressures are displayed simultaneously for pulsatile waveforms (i.e. arterial and pulmonary arterial). Some monitors also calculate and display CPP (cerebral perfusion pressure). Normally, a zero key on the front of the monitor makes pressure zeroing extremely fast and easy. Alarm limits may be set to assist the medical professional responsible for observing the patient. High and low alarms may be set on displayed temperature parameters.
[edit]ClassificationThe following classification of blood pressure applies to adults aged 18 and older. It is based on the average of seated BP readings that were properly measured during 2 or more office visits.[14][18]
Classification of blood pressure for adultsCategorysystolic, mmHgdiastolic, mmHgHypotension< 90< 60 Normal 90 – 11960 – 79 Prehypertension120 – 13980 – 89 Stage 1 Hypertension140 – 15990 – 99 Stage 2 Hypertension≥ 160≥ 100 [edit]Normal valuesWhile average values for arterial pressure could be computed for any given population, there is often a large variation from person to person; arterial pressure also varies in individuals from moment to moment. Additionally, the average of any given population may have a questionable correlation with its general health, thus the relevance of such average values is equally questionable. However, in a study of 100 subjects with no known history of hypertension, an average blood pressure of 112/64 mmHg was found,[19] which is in the normal range.
Various factors influence a person's average BP and variations. Factors such as age and gender[20] influence average values. In children, the normal ranges are lower than for adults and depend on height.[21] As adults age, systolic pressure tends to rise and diastolic tends to fall.[22] In the elderly, BP tends to be above the normal adult range,[23] largely because of reduced flexibility of the arteries. Also, an individual's BP varies with exercise, emotional reactions, sleep, digestion and time of day.
Differences between left and right arm BP measurements tend to be random and average to nearly zero if enough measurements are taken. However, in a small percentage of cases there is a consistently present difference greater than 10 mmHg which may need further investigation, e.g. for obstructive arterial disease.[24][25]
The risk of cardiovascular disease increases progressively above 115/75 mmHg.[26] In the past, hypertension was only diagnosed if secondary signs of high arterial pressure were present, along with a prolonged high systolic pressure reading over several visits. In the UK, patients’ readings are considered normal up to 140/90 mmHg.[27]
Clinical trials demonstrate that people who maintain arterial pressures at the low end of these pressure ranges have much better long term cardiovascular health. The principal medical debate concerns the aggressiveness and relative value of methods used to lower pressures into this range for those who do not maintain such pressure on their own. Elevations, more commonly seen in older people, though often considered normal, are associated with increased morbidity and mortality.
[edit]PhysiologyThe physics of the circulatory system is very complex. That said, there are many physical factors that influence arterial pressure. Each of these may in turn be influenced by physiological factors, such as diet, exercise, disease, drugs or alcohol, stress, obesity, and so-forth.
Some physical factors are:
[edit]Mean arterial pressureThe mean arterial pressure (MAP) is the average over a cardiac cycle and is determined by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (CVP),[29]
MAP can be approximately determined from measurements of the systolic pressure and the diastolic pressure while there is a normal resting heart rate,[29]
[edit]Pulse pressureThe up and down fluctuation of the arterial pressure results from the pulsatile nature of the cardiac output, i.e. the heartbeat. The pulse pressureis determined by the interaction of the stroke volume of the heart, compliance (ability to expand) of the aorta, and the resistance to flow in thearterial tree. By expanding under pressure, the aorta absorbs some of the force of the blood surge from the heart during a heartbeat. In this way the pulse pressure is reduced from what it would be if the aorta wasn't compliant.[30]
The pulse pressure can be simply calculated from the difference of the measured systolic and diastolic pressures,[30]
[edit]Vascular resistanceThe larger arteries, including all large enough to see without magnification, are low resistance conduits (assuming no advanced atheroscleroticchanges) with high flow rates that generate only small drops in pressure.
[edit]Vascular pressure waveModern physiology developed the concept of the vascular pressure wave (VPW). This wave is created by the heart during the systole and originates in the ascending aorta. Much faster than the stream of blood itself, it is then transported through the vessel walls to the peripheralarteries. There the pressure wave can be palpated as the peripheral pulse. As the wave is reflected at the peripheral veins it runs back in a centripetal fashion. Where the crests of the reflected and the original wave meet, the pressure inside the vessel is higher than the true pressure in the aorta. This concept explains why the arterial pressure inside the peripheral arteries of the legs and arms is higher than the arterial pressure in the aorta,[31][32][33] and in turn for the higher pressures seen at the ankle compared to the arm with normal ankle brachial pressure index values.
[edit]RegulationThe endogenous regulation of arterial pressure is not completely understood. Currently, three mechanisms of regulating arterial pressure have been well-characterized:
[edit]Pathophysiology[edit]High arterial pressureMain article: HypertensionOverview of main complications of persistent high blood pressure.Arterial hypertension can be an indicator of other problems and may have long-term adverse effects. Sometimes it can be an acute problem, for example hypertensive emergency.
All levels of arterial pressure put mechanical stress on the arterial walls. Higher pressures increase heart workload and progression of unhealthy tissue growth (atheroma) that develops within the walls of arteries. The higher the pressure, the more stress that is present and the more atheroma tend to progress and the heart muscle tends to thicken, enlarge and become weaker over time.
Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysms, and is the leading cause of chronic renal failure. Even moderate elevation of arterial pressure leads to shortened life expectancy. At severely high pressures, mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated.[35]
In the past, most attention was paid to diastolic pressure; but nowadays it is recognised that both highsystolic pressure and high pulse pressure (the numerical difference between systolic and diastolic pressures) are also risk factors. In some cases, it appears that a decrease in excessive diastolic pressure can actually increase risk, due probably to the increased difference between systolic and diastolic pressures (see the article on pulse pressure).
[edit]Low arterial pressureMain article: HypotensionBlood pressure that is too low is known as hypotension. The similarity in pronunciation with hypertension can cause confusion. Hypotension is a medical concern only if it causes signs or symptoms, such as dizziness, fainting, or in extreme cases, shock.[18]
When arterial pressure and blood flow decrease beyond a certain point, the perfusion of the brain becomes critically decreased (i.e., the blood supply is not sufficient), causing lightheadedness, dizziness, weakness or fainting.
Sometimes the arterial pressure drops significantly when a patient stands up from sitting. This is known as orthostatic hypotension (postural hypotension); gravity reduces the rate of blood return from the body veins below the heart back to the heart, thus reducing stroke volume and cardiac output.
When people are healthy, the veins below their heart quickly constrict and the heart rate increases to minimize and compensate for the gravity effect. This is carried out involuntarily by the autonomic nervous system. The system usually requires a few seconds to fully adjust and if the compensations are too slow or inadequate, the individual will suffer reduced blood flow to the brain, dizziness and potential blackout. Increases in G-loading, such as routinely experienced by aerobatic or combat pilots 'pulling Gs', greatly increases this effect. Repositioning the body perpendicular to gravity largely eliminates the problem.
Other causes of low arterial pressure include:
If there is a significant difference in the pressure from one arm to the other, that may indicate a narrowing (for example, due to aortic coarctation, aortic dissection, thrombosis or embolism) of an artery.
[edit]Other sitesBlood pressure generally refers to the arterial pressure in the systemic circulation. However, measurement of pressures in the venous system and the pulmonary vessels plays an important role in intensive care medicine but requires an invasive central venous catheter.
[edit]Venous pressureVenous pressure is the vascular pressure in a vein or in the atria of the heart. It is much less than arterial pressure, with common values of 5 mmHg in the right atrium and 8 mmHg in the left atrium.
[edit]Pulmonary pressureNormally, the pressure in the pulmonary artery is about 15 mmHg at rest.[36]
Increased BP in the capillaries of the lung cause pulmonary hypertension, with interstitial edema if the pressure increases to above 20 mmHg, and to frank pulmonary edema at pressures above 25 mmHg.[37]
[edit]Fetal blood pressureFurther information: Fetal circulation#Blood pressureIn pregnancy, it is the fetal heart and not the mother's heart that builds up the fetal BP to drive its blood through the fetal circulation.
The BP in the fetal aorta is approximately 30 mmHg at 20 weeks of gestation, and increases to ca 45 mmHg at 40 weeks of gestation.[38]
The average BP for full-term infants:
Systolic 65–95 mm Hg
Diastolic 30–60 mm Hg [39]
[edit]See also
For each heartbeat, BP varies between systolic and diastolic pressures. Systolic pressure is peak pressure in the arteries, which occurs near the end of the cardiac cycle when the ventricles are contracting. Diastolic pressure is minimum pressure in the arteries, which occurs near the beginning of the cardiac cycle when the ventricles are filled with blood. An example of normal measured values for a resting, healthy adult human is 115 mmHg systolic and 75 mmHg diastolic (written as 115/75 mmHg, and spoken [in the US] as "one-fifteen over seventy-five"). Pulse pressure is the difference between systolic and diastolic pressures.
Systolic and diastolic arterial BPs are not static but undergo natural variations from one heartbeat to another and throughout the day (in a circadian rhythm). They also change in response to stress, nutritional factors, drugs, disease, exercise, and momentarily from standing up. Sometimes the variations are large.Hypertension refers to arterial pressure being abnormally high, as opposed to hypotension, when it is abnormally low. Along with body temperature, respiratory rate, and pulse rate, BP measurements are the most commonly measured physiological parameters.
Arterial pressures are usually measured non-invasively, without penetrating skin or artery. Measuring pressure invasively, by penetrating the arterial wall to take the measurement, is much less common, and usually restricted to a hospital setting.
[edit]Noninvasive measurementThe noninvasive auscultatory and oscillometric measurements are simpler and quicker than invasive measurements, require less expertise in fitting, have virtually no complications, and are less unpleasant and painful for the patient. However, noninvasive methods may yield somewhat lower accuracy and small systematic differences in numerical results. Non-invasive measurement methods are more commonly used for routine examinations and monitoring.
[edit]Palpation methodA minimum systolic value can be roughly estimated without any equipment by palpation, most often used in emergency situations. Palpation of a radial pulse indicates a minimum BP of 80 mmHg, a femoral pulse indicates at least 70 mmHg, and a carotid pulse indicates a minimum of 60 mmHg. However, one study indicated that this method was not accurate enough and often overestimated patients' systolic BP.[3] A more accurate value of systolic BP can be obtained with a sphygmomanometer and palpating for when a radial pulse returns.[4] The diastolic blood pressure can not be estimated by this method.[5] Sometimes palpation is used to get an estimate before using the auscultatory method.
[edit]Auscultatory methodAuscultatory method aneroid sphygmomanometer with stethoscopeMercury manometerThe auscultatory method (from the Latin for listening) uses a stethoscope and a sphygmomanometer. This comprises an inflatable (Riva-Rocci) cuff placed around the upper arm at roughly the same vertical height as the heart, attached to a mercury or aneroid manometer. The mercury manometer measures the height of a column of mercury, giving an absolute result without need for calibration, and consequently not subject to the errors and drift of calibration which affect other methods. The use of mercury manometers is often required in clinical trials and for the clinical measurement of hypertension in high risk patients, such aspregnant women.
A cuff of appropriate size is fitted smoothly and snugly, then inflated manually by repeatedly squeezing a rubber bulb until the artery is completely occluded. Listening with the stethoscope to the brachial artery at the elbow, the examiner slowly releases the pressure in the cuff. When blood just starts to flow in the artery, the turbulent flow creates a "whooshing" or pounding (first Korotkoff sound). The pressure at which this sound is first heard is the systolic BP. The cuff pressure is further released until no sound can be heard (fifth Korotkoff sound), at the diastolic arterial pressure.
The auscultatory method has been predominant since the beginning of BP measurements but is gradually being replaced by other noninvasive techniques better suited to being automated.[6]
[edit]Oscillometric methodThe Oscillometric method was first demonstrated in 1876 and involves the observation of oscillations in the sphygmomanometer cuff pressure[7] which are caused by the oscillations of blood flow, i.e. the pulse.[8] The electronic version of this method is sometimes used in long-term measurements and general practice. It uses a sphygmomanometer cuff like the auscultatory method, but with an electronic pressure sensor(transducer) to observe cuff pressure oscillations, electronics to automatically interpret them, and automatic inflation and deflation of the cuff. The pressure sensor should be calibrated periodically to maintain accuracy.
Oscillometric measurement requires less skill than the auscultatory technique, and may be suitable for use by untrained staff and for automated patient home monitoring.
The cuff is inflated to a pressure initially in excess of the systolic arterial pressure, and then reduces to below diastolic pressure over a period of about 30 seconds. When blood flow is nil (cuff pressure exceeding systolic pressure) or unimpeded (cuff pressure below diastolic pressure), cuff pressure will be essentially constant. It is essential that the cuff size is correct: undersized cuffs may yield too high a pressure, whereas oversized cuffs yield too low a pressure. When blood flow is present, but restricted, the cuff pressure, which is monitored by the pressure sensor, will vary periodically in synchrony with the cyclic expansion and contraction of the brachial artery, i.e., it will oscillate. The values of systolic and diastolic pressure are computed, not actually measured from the raw data, using an algorithm; the computed results are displayed.
Oscillometric monitors may produce inaccurate readings in patients with heart and circulation problems, that include arterial sclerosis,arrhythmia, preeclampsia, pulsus alternans, and pulsus paradoxus.
In practice the different methods do not give identical results; an algorithm and experimentally obtained coefficients are used to adjust the oscillometric results to give readings which match the auscultatory results as well as possible. Some equipment uses computer-aided analysis of the instantaneous arterial pressure waveform to determine the systolic, mean, and diastolic points. Since many oscillometric devices have not been validated, caution must be given as most are not suitable in clinical and acute care settings.
The term NIBP, for Non-Invasive Blood Pressure, is often used to describe oscillometric monitoring equipment.
[edit]White-coat hypertensionFor some patients, BP measurements taken in a doctor's office may not correctly characterize their typical BP.[9] In up to 25% of patients, the office measurement is higher than their typical BP. This type of error is called white-coat hypertension (WCH) and can result from anxiety related to an examination by a health care professional.[10] The misdiagnosis of hypertension for these patients can result in needless and possibly harmful medication. WCH can be reduced (but not eliminated) with automated BP measurements over 15 to 20 minutes in a quiet part of the office or clinic.[11]
Debate continues regarding the significance of this effect.[citation needed] Some reactive patients will also react to many other stimuli throughout their daily lives, and require treatment. In some cases a lower BP reading occurs at the doctor's office.[12]
[edit]Home monitoringAmbulatory blood pressure devices that take readings every half hour throughout the day and night have been used for identifying and mitigating measurement problems like white-coat hypertension. Except for periods during sleep, home monitoring could be used for these purposes instead of ambulatory blood pressure monitoring.[13] Home monitoring may also be used to improve hypertension management and to monitor the effects of lifestyle changes and medication related to BP.[14] Compared to ambulatory blood pressure measurements, home monitoring has been found to be an effective and lower cost alternative.[13][15][16]
Aside from the white coat effect, BP readings outside of a clinical setting are usually slightly lower in the majority of people. The studies that looked into the risks from hypertension and the benefits of lowering BP in affected patients were based on readings in a clinical environment.
When measuring BP, an accurate reading requires that one not drink coffee, smoke cigarettes, or engage in strenuous exercise for 30 minutes before taking the reading. A full bladder may have a small effect on BP readings, so if the urge to urinate exists, one should do so before the reading. For 5 minutes before the reading, one should sit upright in a chair with one's feet flat on the floor and with limbs uncrossed. The BP cuff should always be against bare skin, as readings taken over a shirt sleeve are less accurate. During the reading, the arm that is used should be relaxed and kept at heart level, for example by resting it on a table.[17]
Since BP varies throughout the day, measurements intended to monitor changes over longer time frames should be taken at the same time of day to ensure that the readings are comparable. Suitable times are:
- immediately after awakening (before washing/dressing and taking breakfast/drink), while the body is still resting,
- immediately after finishing work.
[edit]Invasive measurementArterial blood pressure (BP) is most accurately measured invasively through an arterial line. Invasive arterial pressure measurement with intravascular cannulae involves direct measurement of arterial pressure by placing a cannula needle in an artery (usually radial, femoral, dorsalis pedis or brachial). This procedure can be done by any licensed doctor or a Respiratory Therapist.
The cannula must be connected to a sterile, fluid-filled system, which is connected to an electronic pressure transducer. The advantage of this system is that pressure is constantly monitored beat-by-beat, and a waveform (a graph of pressure against time) can be displayed. This invasive technique is regularly employed in human and veterinary intensive care medicine, anesthesiology, and for research purposes.
Cannulation for invasive vascular pressure monitoring is infrequently associated with complications such as thrombosis, infection, and bleeding. Patients with invasive arterial monitoring require very close supervision, as there is a danger of severe bleeding if the line becomes disconnected. It is generally reserved for patients where rapid variations in arterial pressure are anticipated.
Invasive vascular pressure monitors are pressure monitoring systems designed to acquire pressure information for display and processing. There are a variety of invasive vascular pressure monitors for trauma, critical care, and operating room applications. These include single pressure, dual pressure, and multi-parameter (i.e. pressure / temperature). The monitors can be used for measurement and follow-up of arterial, central venous, pulmonary arterial, left atrial, right atrial, femoral arterial, umbilical venous, umbilical arterial, and intracranial pressures.
Vascular pressure parameters are derived in the monitor's microcomputer system. Usually, systolic, diastolic, and mean pressures are displayed simultaneously for pulsatile waveforms (i.e. arterial and pulmonary arterial). Some monitors also calculate and display CPP (cerebral perfusion pressure). Normally, a zero key on the front of the monitor makes pressure zeroing extremely fast and easy. Alarm limits may be set to assist the medical professional responsible for observing the patient. High and low alarms may be set on displayed temperature parameters.
[edit]ClassificationThe following classification of blood pressure applies to adults aged 18 and older. It is based on the average of seated BP readings that were properly measured during 2 or more office visits.[14][18]
Classification of blood pressure for adultsCategorysystolic, mmHgdiastolic, mmHgHypotension< 90< 60 Normal 90 – 11960 – 79 Prehypertension120 – 13980 – 89 Stage 1 Hypertension140 – 15990 – 99 Stage 2 Hypertension≥ 160≥ 100 [edit]Normal valuesWhile average values for arterial pressure could be computed for any given population, there is often a large variation from person to person; arterial pressure also varies in individuals from moment to moment. Additionally, the average of any given population may have a questionable correlation with its general health, thus the relevance of such average values is equally questionable. However, in a study of 100 subjects with no known history of hypertension, an average blood pressure of 112/64 mmHg was found,[19] which is in the normal range.
Various factors influence a person's average BP and variations. Factors such as age and gender[20] influence average values. In children, the normal ranges are lower than for adults and depend on height.[21] As adults age, systolic pressure tends to rise and diastolic tends to fall.[22] In the elderly, BP tends to be above the normal adult range,[23] largely because of reduced flexibility of the arteries. Also, an individual's BP varies with exercise, emotional reactions, sleep, digestion and time of day.
Differences between left and right arm BP measurements tend to be random and average to nearly zero if enough measurements are taken. However, in a small percentage of cases there is a consistently present difference greater than 10 mmHg which may need further investigation, e.g. for obstructive arterial disease.[24][25]
The risk of cardiovascular disease increases progressively above 115/75 mmHg.[26] In the past, hypertension was only diagnosed if secondary signs of high arterial pressure were present, along with a prolonged high systolic pressure reading over several visits. In the UK, patients’ readings are considered normal up to 140/90 mmHg.[27]
Clinical trials demonstrate that people who maintain arterial pressures at the low end of these pressure ranges have much better long term cardiovascular health. The principal medical debate concerns the aggressiveness and relative value of methods used to lower pressures into this range for those who do not maintain such pressure on their own. Elevations, more commonly seen in older people, though often considered normal, are associated with increased morbidity and mortality.
[edit]PhysiologyThe physics of the circulatory system is very complex. That said, there are many physical factors that influence arterial pressure. Each of these may in turn be influenced by physiological factors, such as diet, exercise, disease, drugs or alcohol, stress, obesity, and so-forth.
Some physical factors are:
- Rate of pumping. In the circulatory system, this rate is called heart rate, the rate at which blood (the fluid) is pumped by the heart. The volume of blood flow from the heart is called the cardiac output which is the heart rate (the rate of contraction) multiplied by the stroke volume (the amount of blood pumped out from the heart with each contraction). The higher the heart rate, the higher the arterial pressure, assuming no reduction in stroke volume.
- Volume of fluid or blood volume, the amount of blood that is present in the body. The more blood present in the body, the higher the rate of blood return to the heart and the resulting cardiac output. There is some relationship between dietary salt intake and increased blood volume, potentially resulting in higher arterial pressure, though this varies with the individual and is highly dependent on autonomic nervous system response and the renin-angiotensin system.
- Resistance. In the circulatory system, this is the resistance of the blood vessels. The higher the resistance, the higher the arterial pressure upstream from the resistance to blood flow. Resistance is related to vessel radius (the larger the radius, the lower the resistance), vessel length (the longer the vessel, the higher the resistance), as well as the smoothness of the blood vessel walls. Smoothness is reduced by the build up of fatty deposits on the arterial walls. Substances called vasoconstrictors can reduce the size of blood vessels, thereby increasing BP. Vasodilators (such as nitroglycerin) increase the size of blood vessels, thereby decreasing arterial pressure. Resistance, and its relation to volumetric flow rate (Q) and pressure difference between the two ends of a vessel are described by Poiseuille's Law.
- Viscosity, or thickness of the fluid. If the blood gets thicker, the result is an increase in arterial pressure. Certain medical conditions can change the viscosity of the blood. For instance, low red blood cell concentration, anemia, reduces viscosity, whereas increased red blood cell concentration increases viscosity. Viscosity also increases with blood sugar concentration—visualize pumping syrup. It had been thought that aspirin and related "blood thinner" drugs decreased the viscosity of blood, but studies found[28] that they act by reducing the tendency of the blood to clot instead.
[edit]Mean arterial pressureThe mean arterial pressure (MAP) is the average over a cardiac cycle and is determined by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (CVP),[29]
MAP can be approximately determined from measurements of the systolic pressure and the diastolic pressure while there is a normal resting heart rate,[29]
[edit]Pulse pressureThe up and down fluctuation of the arterial pressure results from the pulsatile nature of the cardiac output, i.e. the heartbeat. The pulse pressureis determined by the interaction of the stroke volume of the heart, compliance (ability to expand) of the aorta, and the resistance to flow in thearterial tree. By expanding under pressure, the aorta absorbs some of the force of the blood surge from the heart during a heartbeat. In this way the pulse pressure is reduced from what it would be if the aorta wasn't compliant.[30]
The pulse pressure can be simply calculated from the difference of the measured systolic and diastolic pressures,[30]
[edit]Vascular resistanceThe larger arteries, including all large enough to see without magnification, are low resistance conduits (assuming no advanced atheroscleroticchanges) with high flow rates that generate only small drops in pressure.
[edit]Vascular pressure waveModern physiology developed the concept of the vascular pressure wave (VPW). This wave is created by the heart during the systole and originates in the ascending aorta. Much faster than the stream of blood itself, it is then transported through the vessel walls to the peripheralarteries. There the pressure wave can be palpated as the peripheral pulse. As the wave is reflected at the peripheral veins it runs back in a centripetal fashion. Where the crests of the reflected and the original wave meet, the pressure inside the vessel is higher than the true pressure in the aorta. This concept explains why the arterial pressure inside the peripheral arteries of the legs and arms is higher than the arterial pressure in the aorta,[31][32][33] and in turn for the higher pressures seen at the ankle compared to the arm with normal ankle brachial pressure index values.
[edit]RegulationThe endogenous regulation of arterial pressure is not completely understood. Currently, three mechanisms of regulating arterial pressure have been well-characterized:
- Baroreceptor reflex: Baroreceptors detect changes in arterial pressure and send signals ultimately to the medulla of the brain stem. The medulla, by way of the autonomic nervous system, adjusts the mean arterial pressure by altering both the force and speed of the heart's contractions, as well as the total peripheral resistance. The most important arterial baroreceptors are located in the left and right carotid sinuses and in the aortic arch.[34]
- Renin-angiotensin system (RAS): This system is generally known for its long-term adjustment of arterial pressure. This system allows thekidney to compensate for loss in blood volume or drops in arterial pressure by activating an endogenous vasoconstrictor known asangiotensin II.
- Aldosterone release: This steroid hormone is released from the adrenal cortex in response to angiotensin II or high serum potassium levels. Aldosterone stimulates sodium retention and potassium excretion by the kidneys. Since sodium is the main ion that determines the amount of fluid in the blood vessels by osmosis, aldosterone will increase fluid retention, and indirectly, arterial pressure.
[edit]Pathophysiology[edit]High arterial pressureMain article: HypertensionOverview of main complications of persistent high blood pressure.Arterial hypertension can be an indicator of other problems and may have long-term adverse effects. Sometimes it can be an acute problem, for example hypertensive emergency.
All levels of arterial pressure put mechanical stress on the arterial walls. Higher pressures increase heart workload and progression of unhealthy tissue growth (atheroma) that develops within the walls of arteries. The higher the pressure, the more stress that is present and the more atheroma tend to progress and the heart muscle tends to thicken, enlarge and become weaker over time.
Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysms, and is the leading cause of chronic renal failure. Even moderate elevation of arterial pressure leads to shortened life expectancy. At severely high pressures, mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated.[35]
In the past, most attention was paid to diastolic pressure; but nowadays it is recognised that both highsystolic pressure and high pulse pressure (the numerical difference between systolic and diastolic pressures) are also risk factors. In some cases, it appears that a decrease in excessive diastolic pressure can actually increase risk, due probably to the increased difference between systolic and diastolic pressures (see the article on pulse pressure).
[edit]Low arterial pressureMain article: HypotensionBlood pressure that is too low is known as hypotension. The similarity in pronunciation with hypertension can cause confusion. Hypotension is a medical concern only if it causes signs or symptoms, such as dizziness, fainting, or in extreme cases, shock.[18]
When arterial pressure and blood flow decrease beyond a certain point, the perfusion of the brain becomes critically decreased (i.e., the blood supply is not sufficient), causing lightheadedness, dizziness, weakness or fainting.
Sometimes the arterial pressure drops significantly when a patient stands up from sitting. This is known as orthostatic hypotension (postural hypotension); gravity reduces the rate of blood return from the body veins below the heart back to the heart, thus reducing stroke volume and cardiac output.
When people are healthy, the veins below their heart quickly constrict and the heart rate increases to minimize and compensate for the gravity effect. This is carried out involuntarily by the autonomic nervous system. The system usually requires a few seconds to fully adjust and if the compensations are too slow or inadequate, the individual will suffer reduced blood flow to the brain, dizziness and potential blackout. Increases in G-loading, such as routinely experienced by aerobatic or combat pilots 'pulling Gs', greatly increases this effect. Repositioning the body perpendicular to gravity largely eliminates the problem.
Other causes of low arterial pressure include:
- Sepsis
- Hemorrhage - blood loss
- Toxins including toxic doses of BP medicine
- Hormonal abnormalities, such as Addison's disease
If there is a significant difference in the pressure from one arm to the other, that may indicate a narrowing (for example, due to aortic coarctation, aortic dissection, thrombosis or embolism) of an artery.
[edit]Other sitesBlood pressure generally refers to the arterial pressure in the systemic circulation. However, measurement of pressures in the venous system and the pulmonary vessels plays an important role in intensive care medicine but requires an invasive central venous catheter.
[edit]Venous pressureVenous pressure is the vascular pressure in a vein or in the atria of the heart. It is much less than arterial pressure, with common values of 5 mmHg in the right atrium and 8 mmHg in the left atrium.
[edit]Pulmonary pressureNormally, the pressure in the pulmonary artery is about 15 mmHg at rest.[36]
Increased BP in the capillaries of the lung cause pulmonary hypertension, with interstitial edema if the pressure increases to above 20 mmHg, and to frank pulmonary edema at pressures above 25 mmHg.[37]
[edit]Fetal blood pressureFurther information: Fetal circulation#Blood pressureIn pregnancy, it is the fetal heart and not the mother's heart that builds up the fetal BP to drive its blood through the fetal circulation.
The BP in the fetal aorta is approximately 30 mmHg at 20 weeks of gestation, and increases to ca 45 mmHg at 40 weeks of gestation.[38]
The average BP for full-term infants:
Systolic 65–95 mm Hg
Diastolic 30–60 mm Hg [39]
[edit]See also
