STUDY - Technical - New Dacian's Medicine
Chest
Discomfort and Palpitations (1).
Translation Draft
The time has come to address a new signal from our body about the presence of diseases... Chest discomfort is one of the most common problems for which patients seek help, and is instinctively considered a more important manifestation than pain.
Among the causes of chest discomfort, the one that requires our attention, due to its frequency of manifestation, is the discomfort caused by myocardial ischemia that occurs when oxygen intake to the heart is deficient than necessary (the heart receives less oxygen than it should).
Blood flow through the coronary arteries (those that irrigate the heart muscle) is directly proportional to the pressure gradient between the aorta and the ventricular myocardium (during systole - contraction of the heart muscle) or the ventricular cavity (during diastole - relaxation of the heart muscle).
However, in the presence of critical stenosis, it is also proportional to the (mathematical) square of the coronary artery radius. A relatively insignificant alteration in the diameter of coronary lumens below a critical level may produce a significant decrease in coronary flow, provided that these factors remain constant. Coronary blood irrigation occurs mainly during diastole, when blood flow is not prevented by systolic myocardial compression of coronary vessels.
When the epicardial coronary arteries are critically narrowed (more than 70% stenosis of the luminal diameter - by far, the most common cause of myocardial ischemia is organic narrowing of the coronary arteries, secondary to coronary atherosclerosis, acute thrombosis formed on an atherosclerotic plaque being frequently the cause of unstable angina and acute myocardial infarction), intramyocardial coronary arterioles expand in an effort to maintain total flow at a level that will avoid resting myocardial ischemia and , thus, the subsequent dilation that normally occurs during physical exertion becomes impossible.
Therefore, any situation that increases heart rate, blood pressure or myocardial contractility and occurs in the presence of coronary obstruction tends to precipitate the angina crisis, by increasing myocardial oxygen requirements, in the situation where only a fixed amount of oxygen can be provided.
With the exception of conditions that shrink the lumen of the coronary arteries, the only common causes of myocardial ischemia are conditions such as valvular aortic stenosis or hypertrophic cardiomyopathy, which produce a marked disproportion between coronary infusion pressure and the oxygen needs of the heart.
Under these conditions, the increase in systolic pressure in the left ventricle is not, as in hypertensive states, balanced by a similar increase in aortic infusion pressure. The thoracic discomfort of myocardial ischemia, most commonly due to coronary arterial disease, but occasionally having other causes of the aforementioned ischemia, is angina pectoris. Myocardial ischemia in coronary atherosclerosis is usually more common in adults, especially elderly people who have hypercholesterolemia, diabetes, hypertension, obesity or are smokers.
So let's get to the description of what 'feels'!
Angina is a sensation usually described as a weight, pressure, compression or as a sensation of tightening or tightness in the thorax, but can also be described as a living pain, burning or even indigestion.
Some patients deny pain but describe discomfort or unusual sensation (often associated with fear, foreboding, etc.) or complain of difficulty breathing. Typically, angina develops gradually during exertion, after copious meals, anger, agitation, frustration or other emotional states and is not precipitated by coughing, respiratory movements or other movements (beware of those who think they have such a problem when embarrassment occurs to cough, breathing, movement with thoracic "touch" that have entirely other problems).
When angina is determined by walking, it often forces the patient to stop or reduce the speed, but the typical angina pain passes within 5 to 30 minutes. If it does not pass it should be taken into account that a more prolonged myocardial ischemia frequently represents myocardial infarction, while prolonged pain without further evidence of myocardial ischemia suggests a noncoronary etiology.
Increased heart rate is especially harmful for those with coronary atherosclerosis or aortic stenosis, as in both cases it increases myocardial oxygen consumption and shortens the diastola (which must be greater than the systole) and thereby decreases the total infusion available.
Tachycardia, low blood pressure, thyrotoxicosis and decreased arterial oxygen content (as happens in anemia or arterial hypoxia) are rather precipitating or aggravating factors of angina.
Angina occurs most frequently in the retrosternal region, in the anterior mediothoracic region and may irradiate to the interscapular region, in the arms, shoulders, sometimes teeth and abdomen (rarely occurring only in these irradiation regions) and less often irradiates in the subombilical region, in the region of the neck or suboccipital.
Although irradiation of chest discomfort to the left arm increases the likelihood of myocardial ischemia or infarction, impulses in the skin and in visceral structures, such as the esophagus and heart, converge to a common trunk of neurons in the posterior horn of the spinal cord and their origin may be confused in the cerebral cortex. People with significant right ventricular hypertension may experience pain of exertion which is absolutely similar to that of angina.
Myocardial infarction is usually accompanied by similar discomfort in characteristics and distribution to that of angina, but is longer lasting (usually 30 minutes) and usually has a higher intensity. In contrast to angina, the pain of myocardial infarction is not rapidly relieved by rest or by coronarodilating drugs and may require high doses of narcotics (may be accompanied by diaphoresis, nausea and hypotension).
Chest pain due to (associated) pericarditis is believed to be caused by inflammation of the adjacent parietal pleura. The visceral surface of the pericardium is usually insensitive to pain, as is the parietal surface, except for the lower portion, which has a relatively small number of nociceptors that reach the frenic nerves.
These observations explain why non-infectious pericarditis (such as that associated with uremia or myocardial infarction) and cardiac tamponade with mild inflammation are usually painless or accompanied only by mild pain, as long as pericarditis, being almost always more intense and stretching towards the pleura in the vicinity, is usually accompanied by pain.
Pericarditis can cause pain in a few localizations. Because the central part of the diaphragm receives the sensory nerve endings in the frenic nerve (which originates from the third to the fifth cervical segment of the spinal cord), the pain in the lower parietal pericardium and the central pillar of the diaphragm is characteristically felt in the shoulder, edge of the trapezium and neck.
Involvement of the lateral portion of the diaphragmatic pleura, which receives fibers from the intercostal nerves, from the sixth to the ninth, causes pain not only in the anterior part of the chest, but also in the upper abdomen or corresponding region of the back, sometimes simulating pain from acute or pancreatic cholecystitis.
Pericardial pain usually also has a pleuritic component, being proportional to respiratory movements and aggravated by coughing and/ or deep breathing due to pleural irritation. In some cases it is caused even by swallowing, because the esophagus is located right behind the posterior region of the heart and is often intensified by a change in the position of the body, becoming sharper and localizing on the left side in the lying position and reducing when the patient sits, leaning forward.
In some patients, however, pericardial pain can be described as persistent retrosternal discomfort, which can mimic the pain of acute myocardial infarction. The mechanism of this persistent retrosternal pain is not certain, but may be due to marked inflammation of the inner parietal surface of the pericardium, relatively insensitive, or irritation of the related cardiac nerve fibers located in the periadventicial layers of the superficial coronary arteries. Occasionally, pleuritic and persistent pain may be present simultaneously.
Vascular causes of chest pain are mainly due to aortic dissection. It develops as a result of a subtimdal hematoma, which may be due to a crack in the intimate aorta or due to bleeding in the vasa vasorum.
Anterograde displacement of this hematoma may compromise the main branches of the aorta, while retrograde displacement may block a coronary aorta, damage the aortic valve ring or rupture in the pericardial space. Pain caused by acute dissection of the aorta or an aortic expanding aortic aneurysm results from stimulation of nerve endings in the advent.
Pain usually starts suddenly, quickly reaches a maximum limit and is felt in the center of the chest and/ or back, depending on the location of the dissection, lasts for hours and usually requires large amounts of painkillers to reduce it. Patients usually report real pain, rather than vague discomfort that is sometimes described in cases of myocardial ischemia and is not aggravated by changes in position or respiratory movements.
Chest pain due to pulmonary embolism is generally the result of massive pulmonary embolism but appears to be associated with pulmonary hypertension and pulmonary artery distension. Infarction of a segment of the lung adjacent to the pleura usually irritates the surface of the pleura and causes chest discomfort, hours or even days later.
Pain resulting from pulmonary embolism can be similar to that of acute myocardial infarction, and in massive embolism is localized retrosternal. In individuals with small embolisms, pain is caused by focal pulmonary infarction and is usually located more laterally, is of a pleuritic nature and can sometimes be associated with hemoptysis.
And I will complete this post with other causes of chest discomfort because a variety of lung diseases can cause chest discomfort. Pleural pain is usually short, sharp, like a stab and is precipitated by inspiration or cough, is very common and generally results from the extent of the parietal pleura, inflamed by fibrinous pleurisy or any pneumonic process.
The time has come to address a new signal from our body about the presence of diseases... Chest discomfort is one of the most common problems for which patients seek help, and is instinctively considered a more important manifestation than pain.
Among the causes of chest discomfort, the one that requires our attention, due to its frequency of manifestation, is the discomfort caused by myocardial ischemia that occurs when oxygen intake to the heart is deficient than necessary (the heart receives less oxygen than it should).
Blood flow through the coronary arteries (those that irrigate the heart muscle) is directly proportional to the pressure gradient between the aorta and the ventricular myocardium (during systole - contraction of the heart muscle) or the ventricular cavity (during diastole - relaxation of the heart muscle).
However, in the presence of critical stenosis, it is also proportional to the (mathematical) square of the coronary artery radius. A relatively insignificant alteration in the diameter of coronary lumens below a critical level may produce a significant decrease in coronary flow, provided that these factors remain constant. Coronary blood irrigation occurs mainly during diastole, when blood flow is not prevented by systolic myocardial compression of coronary vessels.
When the epicardial coronary arteries are critically narrowed (more than 70% stenosis of the luminal diameter - by far, the most common cause of myocardial ischemia is organic narrowing of the coronary arteries, secondary to coronary atherosclerosis, acute thrombosis formed on an atherosclerotic plaque being frequently the cause of unstable angina and acute myocardial infarction), intramyocardial coronary arterioles expand in an effort to maintain total flow at a level that will avoid resting myocardial ischemia and , thus, the subsequent dilation that normally occurs during physical exertion becomes impossible.
Therefore, any situation that increases heart rate, blood pressure or myocardial contractility and occurs in the presence of coronary obstruction tends to precipitate the angina crisis, by increasing myocardial oxygen requirements, in the situation where only a fixed amount of oxygen can be provided.
With the exception of conditions that shrink the lumen of the coronary arteries, the only common causes of myocardial ischemia are conditions such as valvular aortic stenosis or hypertrophic cardiomyopathy, which produce a marked disproportion between coronary infusion pressure and the oxygen needs of the heart.
Under these conditions, the increase in systolic pressure in the left ventricle is not, as in hypertensive states, balanced by a similar increase in aortic infusion pressure. The thoracic discomfort of myocardial ischemia, most commonly due to coronary arterial disease, but occasionally having other causes of the aforementioned ischemia, is angina pectoris. Myocardial ischemia in coronary atherosclerosis is usually more common in adults, especially elderly people who have hypercholesterolemia, diabetes, hypertension, obesity or are smokers.
So let's get to the description of what 'feels'!
Angina is a sensation usually described as a weight, pressure, compression or as a sensation of tightening or tightness in the thorax, but can also be described as a living pain, burning or even indigestion.
Some patients deny pain but describe discomfort or unusual sensation (often associated with fear, foreboding, etc.) or complain of difficulty breathing. Typically, angina develops gradually during exertion, after copious meals, anger, agitation, frustration or other emotional states and is not precipitated by coughing, respiratory movements or other movements (beware of those who think they have such a problem when embarrassment occurs to cough, breathing, movement with thoracic "touch" that have entirely other problems).
When angina is determined by walking, it often forces the patient to stop or reduce the speed, but the typical angina pain passes within 5 to 30 minutes. If it does not pass it should be taken into account that a more prolonged myocardial ischemia frequently represents myocardial infarction, while prolonged pain without further evidence of myocardial ischemia suggests a noncoronary etiology.
Increased heart rate is especially harmful for those with coronary atherosclerosis or aortic stenosis, as in both cases it increases myocardial oxygen consumption and shortens the diastola (which must be greater than the systole) and thereby decreases the total infusion available.
Tachycardia, low blood pressure, thyrotoxicosis and decreased arterial oxygen content (as happens in anemia or arterial hypoxia) are rather precipitating or aggravating factors of angina.
Angina occurs most frequently in the retrosternal region, in the anterior mediothoracic region and may irradiate to the interscapular region, in the arms, shoulders, sometimes teeth and abdomen (rarely occurring only in these irradiation regions) and less often irradiates in the subombilical region, in the region of the neck or suboccipital.
Although irradiation of chest discomfort to the left arm increases the likelihood of myocardial ischemia or infarction, impulses in the skin and in visceral structures, such as the esophagus and heart, converge to a common trunk of neurons in the posterior horn of the spinal cord and their origin may be confused in the cerebral cortex. People with significant right ventricular hypertension may experience pain of exertion which is absolutely similar to that of angina.
Myocardial infarction is usually accompanied by similar discomfort in characteristics and distribution to that of angina, but is longer lasting (usually 30 minutes) and usually has a higher intensity. In contrast to angina, the pain of myocardial infarction is not rapidly relieved by rest or by coronarodilating drugs and may require high doses of narcotics (may be accompanied by diaphoresis, nausea and hypotension).
Chest pain due to (associated) pericarditis is believed to be caused by inflammation of the adjacent parietal pleura. The visceral surface of the pericardium is usually insensitive to pain, as is the parietal surface, except for the lower portion, which has a relatively small number of nociceptors that reach the frenic nerves.
These observations explain why non-infectious pericarditis (such as that associated with uremia or myocardial infarction) and cardiac tamponade with mild inflammation are usually painless or accompanied only by mild pain, as long as pericarditis, being almost always more intense and stretching towards the pleura in the vicinity, is usually accompanied by pain.
Pericarditis can cause pain in a few localizations. Because the central part of the diaphragm receives the sensory nerve endings in the frenic nerve (which originates from the third to the fifth cervical segment of the spinal cord), the pain in the lower parietal pericardium and the central pillar of the diaphragm is characteristically felt in the shoulder, edge of the trapezium and neck.
Involvement of the lateral portion of the diaphragmatic pleura, which receives fibers from the intercostal nerves, from the sixth to the ninth, causes pain not only in the anterior part of the chest, but also in the upper abdomen or corresponding region of the back, sometimes simulating pain from acute or pancreatic cholecystitis.
Pericardial pain usually also has a pleuritic component, being proportional to respiratory movements and aggravated by coughing and/ or deep breathing due to pleural irritation. In some cases it is caused even by swallowing, because the esophagus is located right behind the posterior region of the heart and is often intensified by a change in the position of the body, becoming sharper and localizing on the left side in the lying position and reducing when the patient sits, leaning forward.
In some patients, however, pericardial pain can be described as persistent retrosternal discomfort, which can mimic the pain of acute myocardial infarction. The mechanism of this persistent retrosternal pain is not certain, but may be due to marked inflammation of the inner parietal surface of the pericardium, relatively insensitive, or irritation of the related cardiac nerve fibers located in the periadventicial layers of the superficial coronary arteries. Occasionally, pleuritic and persistent pain may be present simultaneously.
Vascular causes of chest pain are mainly due to aortic dissection. It develops as a result of a subtimdal hematoma, which may be due to a crack in the intimate aorta or due to bleeding in the vasa vasorum.
Anterograde displacement of this hematoma may compromise the main branches of the aorta, while retrograde displacement may block a coronary aorta, damage the aortic valve ring or rupture in the pericardial space. Pain caused by acute dissection of the aorta or an aortic expanding aortic aneurysm results from stimulation of nerve endings in the advent.
Pain usually starts suddenly, quickly reaches a maximum limit and is felt in the center of the chest and/ or back, depending on the location of the dissection, lasts for hours and usually requires large amounts of painkillers to reduce it. Patients usually report real pain, rather than vague discomfort that is sometimes described in cases of myocardial ischemia and is not aggravated by changes in position or respiratory movements.
Chest pain due to pulmonary embolism is generally the result of massive pulmonary embolism but appears to be associated with pulmonary hypertension and pulmonary artery distension. Infarction of a segment of the lung adjacent to the pleura usually irritates the surface of the pleura and causes chest discomfort, hours or even days later.
Pain resulting from pulmonary embolism can be similar to that of acute myocardial infarction, and in massive embolism is localized retrosternal. In individuals with small embolisms, pain is caused by focal pulmonary infarction and is usually located more laterally, is of a pleuritic nature and can sometimes be associated with hemoptysis.
And I will complete this post with other causes of chest discomfort because a variety of lung diseases can cause chest discomfort. Pleural pain is usually short, sharp, like a stab and is precipitated by inspiration or cough, is very common and generally results from the extent of the parietal pleura, inflamed by fibrinous pleurisy or any pneumonic process.
It's
been another month... I wish you a new month full of spores
and a year full of achievements (the real new year, from the
ancestral estates begins on March 1st, hence the custom of
tomorrow's march)!
Dorin, Merticaru