STUDY - Technical - New Dacian's Medicine
Heart
Murmur (1)
Translation Draft
Here I was on my first day (since I started this post marathon) when I didn't even have time to hold a job as a debt. So, even if it's May 16th, I'm going to do the post with the mention of May 15th. That's what it is. I hope it doesn't happen again.
Cardiac auscultation is the last stage of the examination of the cardiovascular system and, for many patients with a suspected or diagnosed heart disease, represents the defining moment of the relationship with the doctor-patient.
The doctor should carry out this examination by an integrative approach containing relevant information from several sources. The auscultator data should be interpreted in the context of the general history and physical examination and should be consistent with observations on the forms of venous waves and major arterial pulses. In this way, anomalies of cardiac noises, added noises and breaths can be placed in a correct perspective.
In many patients, the heart rate is the only or valuable sign obtained through the physical examination. Recognition of a cardiac blast generally leads to additional tests, such as electrocardiogram, chest X-ray and echocardiography, and at the request of a cardiologist.
Differential diagnosis of a cardiac blast should begin correctly with a careful and systematic assessment of its major characteristics: the time of occurrence and disappearance, duration, intensity, tonality, frequency, configuration, localization, irradiation and response to maneuvers. Further, laboratory tests may be carried out to remove any remaining question marks and to provide additional anatomical and physiological information useful in the patient's approach.
Heart blasts are defined after the time of occurrence and the final one in the cardiac cycle. Systolic blasts begin with the first cardiac noise (S1) and end at or before the T2 or P2 component of the second heart noise (S2) corresponding to the place of origin of the blast ("left or right heart").
Diastolic blasts begin at or after the associated component of S2 and end at or before the next S1. Continuous breaths are not limited to a specific phase of the cardiac cycle, but usually begin in the systole and continue after S2 all or part of the diastola. Proper evaluation of the occurrence and end of cardiac blasts is the first essential step in identifying them.
The distinction between S1 and S2 and, consequently, between systole and diastole, is usually a simple process, but it can be difficult when there is a tachyarrhythmia, in this case the noises of the heart can be recognized by simultaneous palpation of the carotid arterial pulse. The pulse wave must closely follow S1.
Systolic cardiac blasts occur as a result of increased turbulence associated with: 1. increased or associated flow through a normal semi-lunar valve or in a large dilated vessel, 2. flow through a semi-lunar valve with abnormal structure or through a narrow ventricular trajectory and 4. flow through the interventional septum. A differential diagnostic approach catlasts these flows according to the time of occurrence and duration in the systolic phase of the cardiac cycle.
Protosystolic blasts start with S1 and last for a variable period of time, ending well before S2. Their causes are relatively few. Severe acute mitral insufficiency in a normal left atrium in volume, but relatively non-compliant, produces a attenuated protosistolic blast, decreasing in configuration and which is usually heard best medial of or in the apex shock area.
These characteristics reflect the rapid increase in pressure in the left atrium, caused by the sudden filling of an undilated chamber and clearly contrast with the auscultatory characteristics of the blast of chronic mitral insufficiency.
The clinical situations in which this breath occurs are: 1. rupture of the papillary muscle complicating acute myocardial infarction, 2. infectious endocarditis, 3. rupture of tendon cords and 4. trauma by contusion of the chest wall. Acute mitral insufficiency caused by rupture of the papillary muscle usually accompanies a lower, posterior or lateral infarction.
In almost half of the cases, the blast is accompanied by a precordial hum and must be differentiated from that associated with the postinfarct rupture of the interventional septum. In the latter situation, the breath is accompanied much more frequently (90%) of a hum on the left edge of the sternum, is holosystolic and complicates the anterior infarctions and to the same extent the infero-posterior ones.
Diagnosing any of these mechanical defects requires aggressive medical stabilization and emergency surgery. Other causes of severe acute mitral insufficiency can be differentiated on the basis of associated clinical data. Spontaneous rupture of cords usually occurs due to a mixomatous degeneration, as with most of the underlying forms of mitral valve prolapse.
This lesion may be part of a larger process, as in Marfan syndrome or Ehlers-Danlos, or it may be an isolated phenomenon. Infectious endocarditis is accompanied by fever, peripheral embolic lesions and positive blood cultures and occurs most frequently on an affected valvular apparatus. Trauma is usually obvious, but it can be disarmingly banal. It can cause contusion and rupture of papillary muscles, rupture of cords, perforation or avulsion of the valvular cups.
Echocardiography should be performed in all suspected cases of severe acute mitral insufficiency in order to detect the mechanism responsible, estimate its severity and provide preliminary information on the chances of a surgical valve repair (versus its replacement) to be successful.
Another cause of protosystolic blast is the small congenital ventricular septal defect. The duration of the blast is reduced by closing the defect during systolic contraction. The breath is located on the left edge of the sternum and usually has grade IV/VI or V/VI intensity. Signs of pulmonary hypertension or just volume overload of the ventricle are absent.
Tricuspid insufficiency with normal pulmonary arterial pressure, such as that caused by infectious endocarditis of intravenous drug users, can produce a protosystolic blast. The breath is sweet, best audible on the lower left edge of the sternum and can be accentuated by the inspiration (Carvallo sign). The regurgitation waves that you can be visible on the recording of the jugular venous pulse.
Mesosystolic blows begin at a short interval after S1, end before S2, and usually have a crescendo-decrescendo configuration. Semi-lunar valve stenosis is the classic prototype. In aortic valve stenosis the blow is generally stronger in the second right intercostal space (aortic focus) and radiates along the carotid arteries.
The intensity of the blast varies in direct correlation with cardiac flow, valvular aortic stenosis associated with severe heart failure can cause a deceptive low-intensity systolic blast. When cardiac output is normal, the presence of a systolic fret usually indicates severe stenosis with a peak gradient in excess of 50-60 mmHg.
A protosystolic click of associated elective can be heard in young patients with a bicuspid valve, its presence locating obstruction at the valvular level (as opposed to the sub or supravalvular one). The mesosystolic blow of aortic stenosis can be transmitted to the apex, especially in the elderly, to which it becomes less harsh and of slightly higher tonality (The Gallavardin effect). The breath of aortic stenosis should increase in intensity after a premature beating, while the blast of mitral insufficiency should not change in intensity.
Aortic valve sclerosis produces a blast with similar localization, irradiation and configuration, but not accompanied by the usual signs with hemodynamic significance. The carotid pulse wave is preserved, the breath has a maximum mesosystolic intensity and is not accompanied by the hum, and the peak gradient, estimated by Doppler ultrasound, is small.
Non-critical sclerodegenerative thickening of the aortic valve cups is probably the most common etiology of the mesosystolic blast that occurs in the elderly. A similar mesosystolic blast is found in pulmonary valve stenosis, usually introduced by an ejection click, and is best audible in the second and third left intercostal spaces (pulmonary focus).
The duration of the breath and the intensity of the P2 component decreases with the increase in the degree of stenosis. A mesosystolic blast in the aortic foci, without any functional significance, can also be detected in hyperdynamic states (fever, thyrotoxicosis, pregnancy, anemia) and in the presence of isolated aortic regurgitation with increased flow through a dilated proximal aorta.
Mesosystolic crescendo-decresendo blasts of Grade II/IV or III/IV intensity, heard in the pulmonary foci, may be nonpathological (sufful still), unless accompanied by signs of heart disease in children and young adults, or may suggest increased flow in a normal pulmonary artery in hyperkinetic states or increased flow in a dilated pulmonary artery.
The last situation occurs when there is an atrial septal defect, in this case the S2 duplication being abnormal (fixed). Mesosystolic breath in hypertrophic cardiomyopathy is generally more intense between the left sternal edge and apex, grade II/IV to III/VI in intensity and crescendo-decresendo in configuration.
Unlike valvular aortic stenosis, the breath does not radiate to the neck vessels and the carotid pulsations are rapid and extensive, and may even be bifid. The intensity of the blast associated with hypertrophic cardiomyopathy increases after the maneuvers that decrease the volume of the left ventricle (the phase of exhale with the closed glot of the Valsalva maneuver, orthostatism, amyl nitrite) or increase myocardial contractility (positive inotropic therapy). Conversely, the intensity of the mesosistolic breath decreases after the maneuvers that increase the ventricular volume (squat position, passive lifting of the legs), decrease contractility (blocking beta-adrenergic receptors) or increase pre-pregnancy and systemic post-pregnancy (squat position).
Between these maneuvers, auscultation in orthostatism and squat position, if possible, is the most sensitive technique to determine a dynamic change in the intensity of the blast associated with obstructive hypertrophic cardiomyopathy.
Let's move on to the next post (today's, really)!
Here I was on my first day (since I started this post marathon) when I didn't even have time to hold a job as a debt. So, even if it's May 16th, I'm going to do the post with the mention of May 15th. That's what it is. I hope it doesn't happen again.
Cardiac auscultation is the last stage of the examination of the cardiovascular system and, for many patients with a suspected or diagnosed heart disease, represents the defining moment of the relationship with the doctor-patient.
The doctor should carry out this examination by an integrative approach containing relevant information from several sources. The auscultator data should be interpreted in the context of the general history and physical examination and should be consistent with observations on the forms of venous waves and major arterial pulses. In this way, anomalies of cardiac noises, added noises and breaths can be placed in a correct perspective.
In many patients, the heart rate is the only or valuable sign obtained through the physical examination. Recognition of a cardiac blast generally leads to additional tests, such as electrocardiogram, chest X-ray and echocardiography, and at the request of a cardiologist.
Differential diagnosis of a cardiac blast should begin correctly with a careful and systematic assessment of its major characteristics: the time of occurrence and disappearance, duration, intensity, tonality, frequency, configuration, localization, irradiation and response to maneuvers. Further, laboratory tests may be carried out to remove any remaining question marks and to provide additional anatomical and physiological information useful in the patient's approach.
Heart blasts are defined after the time of occurrence and the final one in the cardiac cycle. Systolic blasts begin with the first cardiac noise (S1) and end at or before the T2 or P2 component of the second heart noise (S2) corresponding to the place of origin of the blast ("left or right heart").
Diastolic blasts begin at or after the associated component of S2 and end at or before the next S1. Continuous breaths are not limited to a specific phase of the cardiac cycle, but usually begin in the systole and continue after S2 all or part of the diastola. Proper evaluation of the occurrence and end of cardiac blasts is the first essential step in identifying them.
The distinction between S1 and S2 and, consequently, between systole and diastole, is usually a simple process, but it can be difficult when there is a tachyarrhythmia, in this case the noises of the heart can be recognized by simultaneous palpation of the carotid arterial pulse. The pulse wave must closely follow S1.
Systolic cardiac blasts occur as a result of increased turbulence associated with: 1. increased or associated flow through a normal semi-lunar valve or in a large dilated vessel, 2. flow through a semi-lunar valve with abnormal structure or through a narrow ventricular trajectory and 4. flow through the interventional septum. A differential diagnostic approach catlasts these flows according to the time of occurrence and duration in the systolic phase of the cardiac cycle.
Protosystolic blasts start with S1 and last for a variable period of time, ending well before S2. Their causes are relatively few. Severe acute mitral insufficiency in a normal left atrium in volume, but relatively non-compliant, produces a attenuated protosistolic blast, decreasing in configuration and which is usually heard best medial of or in the apex shock area.
These characteristics reflect the rapid increase in pressure in the left atrium, caused by the sudden filling of an undilated chamber and clearly contrast with the auscultatory characteristics of the blast of chronic mitral insufficiency.
The clinical situations in which this breath occurs are: 1. rupture of the papillary muscle complicating acute myocardial infarction, 2. infectious endocarditis, 3. rupture of tendon cords and 4. trauma by contusion of the chest wall. Acute mitral insufficiency caused by rupture of the papillary muscle usually accompanies a lower, posterior or lateral infarction.
In almost half of the cases, the blast is accompanied by a precordial hum and must be differentiated from that associated with the postinfarct rupture of the interventional septum. In the latter situation, the breath is accompanied much more frequently (90%) of a hum on the left edge of the sternum, is holosystolic and complicates the anterior infarctions and to the same extent the infero-posterior ones.
Diagnosing any of these mechanical defects requires aggressive medical stabilization and emergency surgery. Other causes of severe acute mitral insufficiency can be differentiated on the basis of associated clinical data. Spontaneous rupture of cords usually occurs due to a mixomatous degeneration, as with most of the underlying forms of mitral valve prolapse.
This lesion may be part of a larger process, as in Marfan syndrome or Ehlers-Danlos, or it may be an isolated phenomenon. Infectious endocarditis is accompanied by fever, peripheral embolic lesions and positive blood cultures and occurs most frequently on an affected valvular apparatus. Trauma is usually obvious, but it can be disarmingly banal. It can cause contusion and rupture of papillary muscles, rupture of cords, perforation or avulsion of the valvular cups.
Echocardiography should be performed in all suspected cases of severe acute mitral insufficiency in order to detect the mechanism responsible, estimate its severity and provide preliminary information on the chances of a surgical valve repair (versus its replacement) to be successful.
Another cause of protosystolic blast is the small congenital ventricular septal defect. The duration of the blast is reduced by closing the defect during systolic contraction. The breath is located on the left edge of the sternum and usually has grade IV/VI or V/VI intensity. Signs of pulmonary hypertension or just volume overload of the ventricle are absent.
Tricuspid insufficiency with normal pulmonary arterial pressure, such as that caused by infectious endocarditis of intravenous drug users, can produce a protosystolic blast. The breath is sweet, best audible on the lower left edge of the sternum and can be accentuated by the inspiration (Carvallo sign). The regurgitation waves that you can be visible on the recording of the jugular venous pulse.
Mesosystolic blows begin at a short interval after S1, end before S2, and usually have a crescendo-decrescendo configuration. Semi-lunar valve stenosis is the classic prototype. In aortic valve stenosis the blow is generally stronger in the second right intercostal space (aortic focus) and radiates along the carotid arteries.
The intensity of the blast varies in direct correlation with cardiac flow, valvular aortic stenosis associated with severe heart failure can cause a deceptive low-intensity systolic blast. When cardiac output is normal, the presence of a systolic fret usually indicates severe stenosis with a peak gradient in excess of 50-60 mmHg.
A protosystolic click of associated elective can be heard in young patients with a bicuspid valve, its presence locating obstruction at the valvular level (as opposed to the sub or supravalvular one). The mesosystolic blow of aortic stenosis can be transmitted to the apex, especially in the elderly, to which it becomes less harsh and of slightly higher tonality (The Gallavardin effect). The breath of aortic stenosis should increase in intensity after a premature beating, while the blast of mitral insufficiency should not change in intensity.
Aortic valve sclerosis produces a blast with similar localization, irradiation and configuration, but not accompanied by the usual signs with hemodynamic significance. The carotid pulse wave is preserved, the breath has a maximum mesosystolic intensity and is not accompanied by the hum, and the peak gradient, estimated by Doppler ultrasound, is small.
Non-critical sclerodegenerative thickening of the aortic valve cups is probably the most common etiology of the mesosystolic blast that occurs in the elderly. A similar mesosystolic blast is found in pulmonary valve stenosis, usually introduced by an ejection click, and is best audible in the second and third left intercostal spaces (pulmonary focus).
The duration of the breath and the intensity of the P2 component decreases with the increase in the degree of stenosis. A mesosystolic blast in the aortic foci, without any functional significance, can also be detected in hyperdynamic states (fever, thyrotoxicosis, pregnancy, anemia) and in the presence of isolated aortic regurgitation with increased flow through a dilated proximal aorta.
Mesosystolic crescendo-decresendo blasts of Grade II/IV or III/IV intensity, heard in the pulmonary foci, may be nonpathological (sufful still), unless accompanied by signs of heart disease in children and young adults, or may suggest increased flow in a normal pulmonary artery in hyperkinetic states or increased flow in a dilated pulmonary artery.
The last situation occurs when there is an atrial septal defect, in this case the S2 duplication being abnormal (fixed). Mesosystolic breath in hypertrophic cardiomyopathy is generally more intense between the left sternal edge and apex, grade II/IV to III/VI in intensity and crescendo-decresendo in configuration.
Unlike valvular aortic stenosis, the breath does not radiate to the neck vessels and the carotid pulsations are rapid and extensive, and may even be bifid. The intensity of the blast associated with hypertrophic cardiomyopathy increases after the maneuvers that decrease the volume of the left ventricle (the phase of exhale with the closed glot of the Valsalva maneuver, orthostatism, amyl nitrite) or increase myocardial contractility (positive inotropic therapy). Conversely, the intensity of the mesosistolic breath decreases after the maneuvers that increase the ventricular volume (squat position, passive lifting of the legs), decrease contractility (blocking beta-adrenergic receptors) or increase pre-pregnancy and systemic post-pregnancy (squat position).
Between these maneuvers, auscultation in orthostatism and squat position, if possible, is the most sensitive technique to determine a dynamic change in the intensity of the blast associated with obstructive hypertrophic cardiomyopathy.
Let's move on to the next post (today's, really)!
I hope yesterday was a
good day for you!
Dorin, Merticaru