STUDY - Technical - New Dacian's Medicine
Heart
Murmur (2)
Translation Draft
I'll continue with the presentations on systolic blasts.
A telesystolic blast begins long after the onset of ejection and is usually best heard at the apex of the left ventricle or towards the apex and the left edge of the sternum. When preceded by a click, which is not in the ejection, usually indicates a systolic prolapse of the mitral valve cups in the left atrium.
The click and breath approach S1 after the maneuvers that decrease the volume of the left ventricle (Valsalva orthostatism) and move away from S1 after the volume increases (leg lift, squat position). The intensity of the blast increases with the increase of systemic post-pregnancy (squat position, pressure agents) and decreases with vasodilation (amyl nitrite). Isometric exercises, which also delay the onset of the breath, accentuate its intensity.
Holosystolic blasts, also called pansystolic blasts, start with S1 and continue the whole systole to S2. These are, with rare exceptions, suggestive for a regurgitation through the atrioventricular valves or for a ventricular septal defect. The blast of mitral insufficiency is more intense in the left apex. Its irradiation reflects the direction of the regurgitation jet.
When prolapsed the mitral posterior cuspa, due to a tendon cord rupture, for example, the jet is directed anterosuperiorly and the blast irradiates especially at the base of the heart, where it can be confused with a blast of valvular aortic stenosis, if the carotid pulsations are not carefully examined. Conversely, a prolabation of the anterior cup is associated with a rear-directed jet, which radiates into the axis and back. He can even hit the spine and transmit to the base of the neck.
Severe mitral insufficiency is usually associated with a systolic fret, a soft S3 and a short and strong diastolic blast that is easier to listen to in the left lateral decubit. The holosystolic breath of tricuspid insufficiency is usually less intense (grade I-III/IV) than that of mitral insufficiency, is stronger on the left side of the lower sternum and increases in intensity in breathing.
Associated signs include extensive c-v waves on the recording of the jugular vein pulse, systolic hepatic pulsations and peripheral edema. Among the few causes of tricuspid insufficiency, dilation of the valvular ring with that of the right ventricle, caused by pulmonary arterial hypertension, is the most common.
The ventricular septal defect also causes a holosystolic blast whose intensity varies inversely in proportion to the anatomical size of the defect. It is usually accompanied by a palpable hum along the left edge in the middle portion of the sternum. The breath produced in the ventricular septal defect is stronger than that of tricuspid insufficiency and is not characterized by increased intensity in the breath or associated peripheral signs, like the latter.
The time has come to deal with diastolic heart blasts which, like systolic blasts, can be classified according to the time of their occurrence.
Protodiastolic blasts are produced by the incompetence of the semi-lunar valve and start from the valve closing noise (A2 or P2), thus indicating the place of origin. They generally have high tonality and a decreasing configuration, especially in chronic regurgitation, their duration being a relative indicator of the severity of the lesion. The breath of aortic insufficiency is generally, but not always, best heard in the second intercostal space on the left edge of the sternum.
There is a tendency of the breath associated with a primary valvular pathology (e.g. rheumatic lesion, congenital bicuspid valve, endocarditis) to irradiate especially along the left sternal edge and to be well transmitted to the apex, while the blast associated with a primary pathology of the root of the aorta (e.g. annoaortic ectasis, aorta dissection) irradiates more frequently along the right sternal edge.
It is sometimes necessary for the patient to be examined in the forward bent position and forced exhale to assess the breath, a maneuver that brings the root of the aorta closer to the anterior chest wall. Severe aortic insufficiency may be accompanied by a low-tonality meso or telediastolic blast at the apex (Austin Flint), which is generally assumed to reflect the turbulence in the mitral orifice resulting from the conflict between regurgitation (aortic) and normal (mitral) flow and should be differentiated from mitral stenosis.
In the absence of significant heart failure, severe chronic aortic insufficiency is accompanied by several peripheral signs due to increased diastolic volume, including a large systemic pulse pressure and carotid pulsations as "hammer blows" (Corrigan pulsations). The breath associated with acute aortic insufficiency is obviously shorter in duration, with low tonality and can be difficult to assess in the presence of tachycardia.
Peripheral signs due to increased diastolic volume may be absent. These characteristics reflect the sudden increase in diastolic pressure in a noncompliant left ventricle, with an appropriate and rapid decline of the left diastolic diastolic aorta-ventricle pressure gradient. The blast of pulmonary failure (Graham Steell) begins with a strong (palpable) closing pulmonary noise (P2) and is best heard in the pulmonary foci, having an irradiation along the left sternal edge. Typically, it has a high tonality with a descending configuration and indicates a significant pulmonary arterial hypertension with a diastolic diastolic right pulmonary-ventricle artery gradient.
Increased intensity in breathing is what can differentiate it from an aortic failure. Signs of load through volume and pressure of the right ventricle are also usually present. When there is a significant mitral stenosis, a descending protodiastolic blast can be encountered along the left sternal edge and is almost always due to aortic rather than pulmonary insufficiency, despite the coexistence of pulmonary arterial hypertension.
Insufficiency of the pulmonary valve, in the absence of pulmonary arterial hypertension, can occur in congenital disorders and rarely in infectious endocarditis. In this case, the protodiastolic blast is sweeter and has a lower tonality than the classic Graham-Steell blast. It starts at or even after P2, which should be easily separable from component A2, thus distinguishing a protodiastolic pause.
Mezodiastolic blasts usually occur due to obstruction and/ or increased flow through the atrioventricular valves. A classic example is mitral stenosis due to a rheumatic injury. In the absence of extensive calcifications, the first cardiac noise (S1) is strong and the blast begins after the opening click (the time interval between S2 and the opening click is inversely proportional to the left ventricle pressure gradient).
The breath has low tonality and is best heard with the stethoscope membrane applied to the area of the apex, especially in the left lateral decubit. If its intensity does not accurately reflect the severity of the obstruction, the duration of the blast indicates to some extent its degree. A longer lasting blast denotes the persistence of a left atrioventricular pressure gradient over a longer period of diastole. The presystolic accentuation of the blast frequently occurs at sinus rhythm and reflects an additional increase in the transmissional flow following the mechanical atrial systole.
The breath of tricuspid stenosis exhibits many of these characteristics, but it is best heard on the lower left sternal edge and, like most right heart disorders, increases in intensity in breathing. The examiner may observe an elongated descending "y" slope on the recording of the jugular venous pulse. Signs of right heart failure may be prevalent.
There are a few other causes of mezodiasistolic blast that are important to differentiate from mitral stenosis. The left atrial mixoma may simulate mitral stenosis, but diastolic blast is not accompanied by an opening click or a presystolic accent. Increased flow into the diastole through the mitral valve, as it occurs in severe mitral insufficiency or in intracardiac left-right broad shuns or large vessels, can produce a short, low-tonality apical mezodiastolic blast.
The blast generally follows a sweet S3, which has a lower tonality and starts later than the opening click. Severe tricuspid insufficiency can also produce increased diastolic flow through tricuspid and a right filling syndrome similar to that accompanying severe mitral insufficiency. The Austin-Flint blast that occurs in severe aortic insufficiency has been described above and occurs in the presence of severe aortic insufficiency.
Let's talk about the continuous blasts now! They begin in the systole, have a maximum intensity close to S2 and continue throughout or part of the diastole. They reflect the persistence of a luxury between two cavities during both phases of the cardiac cycle. Two nonpathological variants are cervical venous murmur and breast blast. The first is heard in healthy children and young adults in the right supralavicolal fossa and can be abolished by compressing the internal jugular vein.
Its diastolic component may be more intense than the systolic component. Breast breath indicates the presence of increased arterial flow through stuned breasts and can be ausculted towards the end of the third trimester of pregnancy and early in postpartum. A firm press with the stethoscope diaphragm can remove the diastolic part of the breath. The breath gradually disappears after birth.
The classic continuous breath is that due to the persistence of the arterial canal after birth. It is best heard in or just above and to the left of the pulmonary foci, but it can also be heard dorsal. Over time, a wide uncorrected shunt can lead to increased pulmonary vascular resistance, resulting in pulmonary arterial hypertension and the decrease or disappearance of the diastolic component.
A continuous blast may also indicate the presence of a congenital aneurysm of ruptured Valsalva sinus, which occurs either spontaneously or as a complication of infectious endocarditis. In this case, a high-pressure fistula is created between the aorta and a cardiac cavity, usually the right atrium or ventricle. The breath is stronger along the right or left sternal edge and is frequently accompanied by a fret.
To emphasize, the diastolic component is stronger than the systolic component. It may be difficult to differentiate continuous breaths from the systolic and diastolic blasts, separated over time, of an aortic valve disease or severe isolated aortic insufficiency. The difference is given by the enveloping of S2 by the continuous breath and the break between the blasts in aortic valvular disease.
A variety of other injuries can cause continuous blasts. A coronary arteriovenous fistula sometimes produces a continuous, weak blast with a stronger diastolic component on the left sternal edge or on the left ventricle apex. Severe atherosclerotic disease of a large systemic artery can cause a continuous noise, the presence of which signifies very large obstruction of the fence.
Patients with stenosis of peripheral lung branches or with extensive pulmonary and pulmonary collateral atresia may also experience continuous breathing, which can best be heard dorsal or on the side of the chest. similar clinical signs are present in patients with severe aorta coarctation, a lesion to be diagnosed on the basis of weak and delayed pulse in the lower limbs and hypertension in the upper limbs. Continuous breath is produced in enlarged collateral (intercostal) arteries.
To complete this may there is something more to be said about the patient's approach. in many patients the cause of the heart rate breath can be easily elucidated by the correct assessment of the breath itself taking into account the history, general physical examination and other data provided by the cardiac examination. When there is doubt about the diagnosis or additional anatomological and physiological data are needed to evaluate the patient and plan treatment, performing Doppler transthoracic echocardiography has great value in determining not only the etiology of the breath, but also the severity of the responsible lesion.
Most heart blasts are mesosystolic and less intense (grade I or II/IV). When such a blast occurs in a child or a young adult without any evidence of heart disease after the clinical examination, it is usually benign and in general echocardiography is not indicated. On the other hand, cardiac ultrasound is recommended in patients with intense systolic blasts (greater than or equal to III/IV), especially holosystolic, as in most patients with diastolic or continuous blasts.
Done!!! From tomorrow we move to hypertension...
I'll continue with the presentations on systolic blasts.
A telesystolic blast begins long after the onset of ejection and is usually best heard at the apex of the left ventricle or towards the apex and the left edge of the sternum. When preceded by a click, which is not in the ejection, usually indicates a systolic prolapse of the mitral valve cups in the left atrium.
The click and breath approach S1 after the maneuvers that decrease the volume of the left ventricle (Valsalva orthostatism) and move away from S1 after the volume increases (leg lift, squat position). The intensity of the blast increases with the increase of systemic post-pregnancy (squat position, pressure agents) and decreases with vasodilation (amyl nitrite). Isometric exercises, which also delay the onset of the breath, accentuate its intensity.
Holosystolic blasts, also called pansystolic blasts, start with S1 and continue the whole systole to S2. These are, with rare exceptions, suggestive for a regurgitation through the atrioventricular valves or for a ventricular septal defect. The blast of mitral insufficiency is more intense in the left apex. Its irradiation reflects the direction of the regurgitation jet.
When prolapsed the mitral posterior cuspa, due to a tendon cord rupture, for example, the jet is directed anterosuperiorly and the blast irradiates especially at the base of the heart, where it can be confused with a blast of valvular aortic stenosis, if the carotid pulsations are not carefully examined. Conversely, a prolabation of the anterior cup is associated with a rear-directed jet, which radiates into the axis and back. He can even hit the spine and transmit to the base of the neck.
Severe mitral insufficiency is usually associated with a systolic fret, a soft S3 and a short and strong diastolic blast that is easier to listen to in the left lateral decubit. The holosystolic breath of tricuspid insufficiency is usually less intense (grade I-III/IV) than that of mitral insufficiency, is stronger on the left side of the lower sternum and increases in intensity in breathing.
Associated signs include extensive c-v waves on the recording of the jugular vein pulse, systolic hepatic pulsations and peripheral edema. Among the few causes of tricuspid insufficiency, dilation of the valvular ring with that of the right ventricle, caused by pulmonary arterial hypertension, is the most common.
The ventricular septal defect also causes a holosystolic blast whose intensity varies inversely in proportion to the anatomical size of the defect. It is usually accompanied by a palpable hum along the left edge in the middle portion of the sternum. The breath produced in the ventricular septal defect is stronger than that of tricuspid insufficiency and is not characterized by increased intensity in the breath or associated peripheral signs, like the latter.
The time has come to deal with diastolic heart blasts which, like systolic blasts, can be classified according to the time of their occurrence.
Protodiastolic blasts are produced by the incompetence of the semi-lunar valve and start from the valve closing noise (A2 or P2), thus indicating the place of origin. They generally have high tonality and a decreasing configuration, especially in chronic regurgitation, their duration being a relative indicator of the severity of the lesion. The breath of aortic insufficiency is generally, but not always, best heard in the second intercostal space on the left edge of the sternum.
There is a tendency of the breath associated with a primary valvular pathology (e.g. rheumatic lesion, congenital bicuspid valve, endocarditis) to irradiate especially along the left sternal edge and to be well transmitted to the apex, while the blast associated with a primary pathology of the root of the aorta (e.g. annoaortic ectasis, aorta dissection) irradiates more frequently along the right sternal edge.
It is sometimes necessary for the patient to be examined in the forward bent position and forced exhale to assess the breath, a maneuver that brings the root of the aorta closer to the anterior chest wall. Severe aortic insufficiency may be accompanied by a low-tonality meso or telediastolic blast at the apex (Austin Flint), which is generally assumed to reflect the turbulence in the mitral orifice resulting from the conflict between regurgitation (aortic) and normal (mitral) flow and should be differentiated from mitral stenosis.
In the absence of significant heart failure, severe chronic aortic insufficiency is accompanied by several peripheral signs due to increased diastolic volume, including a large systemic pulse pressure and carotid pulsations as "hammer blows" (Corrigan pulsations). The breath associated with acute aortic insufficiency is obviously shorter in duration, with low tonality and can be difficult to assess in the presence of tachycardia.
Peripheral signs due to increased diastolic volume may be absent. These characteristics reflect the sudden increase in diastolic pressure in a noncompliant left ventricle, with an appropriate and rapid decline of the left diastolic diastolic aorta-ventricle pressure gradient. The blast of pulmonary failure (Graham Steell) begins with a strong (palpable) closing pulmonary noise (P2) and is best heard in the pulmonary foci, having an irradiation along the left sternal edge. Typically, it has a high tonality with a descending configuration and indicates a significant pulmonary arterial hypertension with a diastolic diastolic right pulmonary-ventricle artery gradient.
Increased intensity in breathing is what can differentiate it from an aortic failure. Signs of load through volume and pressure of the right ventricle are also usually present. When there is a significant mitral stenosis, a descending protodiastolic blast can be encountered along the left sternal edge and is almost always due to aortic rather than pulmonary insufficiency, despite the coexistence of pulmonary arterial hypertension.
Insufficiency of the pulmonary valve, in the absence of pulmonary arterial hypertension, can occur in congenital disorders and rarely in infectious endocarditis. In this case, the protodiastolic blast is sweeter and has a lower tonality than the classic Graham-Steell blast. It starts at or even after P2, which should be easily separable from component A2, thus distinguishing a protodiastolic pause.
Mezodiastolic blasts usually occur due to obstruction and/ or increased flow through the atrioventricular valves. A classic example is mitral stenosis due to a rheumatic injury. In the absence of extensive calcifications, the first cardiac noise (S1) is strong and the blast begins after the opening click (the time interval between S2 and the opening click is inversely proportional to the left ventricle pressure gradient).
The breath has low tonality and is best heard with the stethoscope membrane applied to the area of the apex, especially in the left lateral decubit. If its intensity does not accurately reflect the severity of the obstruction, the duration of the blast indicates to some extent its degree. A longer lasting blast denotes the persistence of a left atrioventricular pressure gradient over a longer period of diastole. The presystolic accentuation of the blast frequently occurs at sinus rhythm and reflects an additional increase in the transmissional flow following the mechanical atrial systole.
The breath of tricuspid stenosis exhibits many of these characteristics, but it is best heard on the lower left sternal edge and, like most right heart disorders, increases in intensity in breathing. The examiner may observe an elongated descending "y" slope on the recording of the jugular venous pulse. Signs of right heart failure may be prevalent.
There are a few other causes of mezodiasistolic blast that are important to differentiate from mitral stenosis. The left atrial mixoma may simulate mitral stenosis, but diastolic blast is not accompanied by an opening click or a presystolic accent. Increased flow into the diastole through the mitral valve, as it occurs in severe mitral insufficiency or in intracardiac left-right broad shuns or large vessels, can produce a short, low-tonality apical mezodiastolic blast.
The blast generally follows a sweet S3, which has a lower tonality and starts later than the opening click. Severe tricuspid insufficiency can also produce increased diastolic flow through tricuspid and a right filling syndrome similar to that accompanying severe mitral insufficiency. The Austin-Flint blast that occurs in severe aortic insufficiency has been described above and occurs in the presence of severe aortic insufficiency.
Let's talk about the continuous blasts now! They begin in the systole, have a maximum intensity close to S2 and continue throughout or part of the diastole. They reflect the persistence of a luxury between two cavities during both phases of the cardiac cycle. Two nonpathological variants are cervical venous murmur and breast blast. The first is heard in healthy children and young adults in the right supralavicolal fossa and can be abolished by compressing the internal jugular vein.
Its diastolic component may be more intense than the systolic component. Breast breath indicates the presence of increased arterial flow through stuned breasts and can be ausculted towards the end of the third trimester of pregnancy and early in postpartum. A firm press with the stethoscope diaphragm can remove the diastolic part of the breath. The breath gradually disappears after birth.
The classic continuous breath is that due to the persistence of the arterial canal after birth. It is best heard in or just above and to the left of the pulmonary foci, but it can also be heard dorsal. Over time, a wide uncorrected shunt can lead to increased pulmonary vascular resistance, resulting in pulmonary arterial hypertension and the decrease or disappearance of the diastolic component.
A continuous blast may also indicate the presence of a congenital aneurysm of ruptured Valsalva sinus, which occurs either spontaneously or as a complication of infectious endocarditis. In this case, a high-pressure fistula is created between the aorta and a cardiac cavity, usually the right atrium or ventricle. The breath is stronger along the right or left sternal edge and is frequently accompanied by a fret.
To emphasize, the diastolic component is stronger than the systolic component. It may be difficult to differentiate continuous breaths from the systolic and diastolic blasts, separated over time, of an aortic valve disease or severe isolated aortic insufficiency. The difference is given by the enveloping of S2 by the continuous breath and the break between the blasts in aortic valvular disease.
A variety of other injuries can cause continuous blasts. A coronary arteriovenous fistula sometimes produces a continuous, weak blast with a stronger diastolic component on the left sternal edge or on the left ventricle apex. Severe atherosclerotic disease of a large systemic artery can cause a continuous noise, the presence of which signifies very large obstruction of the fence.
Patients with stenosis of peripheral lung branches or with extensive pulmonary and pulmonary collateral atresia may also experience continuous breathing, which can best be heard dorsal or on the side of the chest. similar clinical signs are present in patients with severe aorta coarctation, a lesion to be diagnosed on the basis of weak and delayed pulse in the lower limbs and hypertension in the upper limbs. Continuous breath is produced in enlarged collateral (intercostal) arteries.
To complete this may there is something more to be said about the patient's approach. in many patients the cause of the heart rate breath can be easily elucidated by the correct assessment of the breath itself taking into account the history, general physical examination and other data provided by the cardiac examination. When there is doubt about the diagnosis or additional anatomological and physiological data are needed to evaluate the patient and plan treatment, performing Doppler transthoracic echocardiography has great value in determining not only the etiology of the breath, but also the severity of the responsible lesion.
Most heart blasts are mesosystolic and less intense (grade I or II/IV). When such a blast occurs in a child or a young adult without any evidence of heart disease after the clinical examination, it is usually benign and in general echocardiography is not indicated. On the other hand, cardiac ultrasound is recommended in patients with intense systolic blasts (greater than or equal to III/IV), especially holosystolic, as in most patients with diastolic or continuous blasts.
Done!!! From tomorrow we move to hypertension...
Don't forget to have a
good day and that the weekend is coming that must be the one to
be woner!
Dorin, Merticaru