733
edits
Physical Examination: Difference between revisions
Jump to navigation
Jump to search
→Murmurs categorized by time in cardiac cycle
No edit summary |
|||
| (20 intermediate revisions by 2 users not shown) | |||
| Line 12: | Line 12: | ||
===Family History=== | ===Family History=== | ||
A family history could provide important information not only in atherosclerotic cardiovascular disease but also for many other cardiac diseases. For example, congenital heart diseases are more common in the offspring of parents, family members or siblings. Genetic diseases, such as neuromuscular disorders, connective tissue disorders (eg, Marfan syndrome), lipid metabolism disorders can affect the cardiovascular system as well [ | A family history could provide important information not only in atherosclerotic cardiovascular disease but also for many other cardiac diseases. For example, congenital heart diseases are more common in the offspring of parents, family members or siblings. Genetic diseases, such as neuromuscular disorders, connective tissue disorders (eg, Marfan syndrome), lipid metabolism disorders can affect the cardiovascular system as well [http://www.textbookofcardiology.org/wiki/Chronic_Coronary_Disease]. | ||
==Common Symptoms== | ==Common Symptoms== | ||
| Line 237: | Line 237: | ||
===Syncope and Pre-syncope=== | ===Syncope and Pre-syncope=== | ||
Light-headedness, dizziness, pre-syncope, and syncope are important symptoms, often caused by a reduction in cerebral blood flow. The mentioned symptoms are nonspecific and can be due to a broad caused by a broad range of underlying pathophysiology such as metabolic conditions, dehydration, primary central nervous system disease, or inner-ear problems. Because bradyarrhythmias and tachyarrhythmias are important cardiac causes of these symptoms, they are of importance in the cardiovascular examination. A careful history taking, including preceding symptoms such as palpitations or chest pain, are of great importance. Further information on this topic can be found in | Light-headedness, dizziness, pre-syncope, and syncope are important symptoms, often caused by a reduction in cerebral blood flow. The mentioned symptoms are nonspecific and can be due to a broad caused by a broad range of underlying pathophysiology such as metabolic conditions, dehydration, primary central nervous system disease, or inner-ear problems. Because bradyarrhythmias and tachyarrhythmias are important cardiac causes of these symptoms, they are of importance in the cardiovascular examination. A careful history taking, including preceding symptoms such as palpitations or chest pain, are of great importance. Further information on this topic can be found in [http://www.textbookofcardiology.org/wiki/Syncope]. | ||
===Transient Central Nervous System Deficits=== | ===Transient Central Nervous System Deficits=== | ||
| Line 246: | Line 246: | ||
===Palpitation=== | ===Palpitation=== | ||
Cardiac activity usually cannot be experienced by individuals in normal resting condition. If a patient is aware of its heart activity it is usually referred to as palpitation. Among cultures and patients there is no standard definition for the type of sensation represented by palpitation. It is often very illustrative to ask the patients to tap with their hand the perceived heartbeat. Most commonly palpitations are caused by an unusually forceful heart beat at a normal rate (60–100 bpm). When a patient senses more forceful contractions as usual without a significant increased heart rate, the palpitations are most commonly the result of endogenous catecholamine excretion. A customary cause of this phenomenon is anxiety. Another common experienced feeling is that of the heart stopping transiently and/or the occurrence of isolated forceful beats. The nature of this sensation is usually premature ventricular contractions. The rapid regular or irregular heart rates most linked to the term “palpitations” are the least common sensation reported by individual patients and is usually supraventricular of origin. More information on palpitations caused by arrhythmias can be found in the subsequent chapter [ | Cardiac activity usually cannot be experienced by individuals in normal resting condition. If a patient is aware of its heart activity it is usually referred to as palpitation. Among cultures and patients there is no standard definition for the type of sensation represented by palpitation. It is often very illustrative to ask the patients to tap with their hand the perceived heartbeat. Most commonly palpitations are caused by an unusually forceful heart beat at a normal rate (60–100 bpm). When a patient senses more forceful contractions as usual without a significant increased heart rate, the palpitations are most commonly the result of endogenous catecholamine excretion. A customary cause of this phenomenon is anxiety. Another common experienced feeling is that of the heart stopping transiently and/or the occurrence of isolated forceful beats. The nature of this sensation is usually premature ventricular contractions. The rapid regular or irregular heart rates most linked to the term “palpitations” are the least common sensation reported by individual patients and is usually supraventricular of origin. More information on palpitations caused by arrhythmias can be found in the subsequent chapter [http://www.textbookofcardiology.org/wiki/Cardiac_Arrhythmias]. | ||
===Cough=== | ===Cough=== | ||
| Line 256: | Line 256: | ||
====General appearance in severe disease==== | ====General appearance in severe disease==== | ||
*Signs of acute life threatening disease which need acute intervention to avert death. First important symptom is the colour of the face and skin which could be pallor or cyanotic as a sign of diminished circulation and/or respiration. Furthermore, the respiratory pattern and rate should be assessed for severe signs such as slow and irregular pattern, an audible rasp breathing with foam around the mouth, or in some cases a very fast and superficial breathing pattern. Additionally, the absence or a very weak pulsation could also be a sign of an acute life threatening disease. (For more detailed assessment of the pulse please notice the paragraph on this topic [ | *Signs of acute life threatening disease which need acute intervention to avert death. First important symptom is the colour of the face and skin which could be pallor or cyanotic as a sign of diminished circulation and/or respiration. Furthermore, the respiratory pattern and rate should be assessed for severe signs such as slow and irregular pattern, an audible rasp breathing with foam around the mouth, or in some cases a very fast and superficial breathing pattern. Additionally, the absence or a very weak pulsation could also be a sign of an acute life threatening disease. (For more detailed assessment of the pulse please notice the paragraph on this topic [http://www.textbookofcardiology.org/wiki/Physical_Examination#Pulse]) Be aware that these symptoms can be apparent, but there absence does not rule out an acute life threatening disease. | ||
*Signs of severe diseases which are life threatening demands a similar approach with special attention to face colour, respiration and pulse. The face colour can be pallor, cyanotic or red. Respiration can be fast and superficial, often a sign of severe disease. The pulse is also important in case of severe disease, for more information see [ | *Signs of severe diseases which are life threatening demands a similar approach with special attention to face colour, respiration and pulse. The face colour can be pallor, cyanotic or red. Respiration can be fast and superficial, often a sign of severe disease. The pulse is also important in case of severe disease, for more information see [http://www.textbookofcardiology.org/wiki/Physical_Examination#Pulse]. Furthermore it is important to assess signs of lowered degree of consciousness, emaciation, high body temperature and agitation. | ||
====Body position==== | ====Body position==== | ||
| Line 338: | Line 338: | ||
====Pulse==== | ====Pulse==== | ||
[[Image:Circulatory System.svg|thumb|right|400px|'''Figure 1.''' Body locations for examining the pulse.]] | |||
The peripheral pulsations should be assed by both palpitation of the pulse and auscultation for bruits. Pulse abnormalities and bruits increase the likelihood of peripheral arterial disease. Pulsations should be assessed and documented in several arteries in the body in order to get an idea of the state of peripheral vasculature. Easily and fast palpable pulses in healthy individuals include the brachial, radial, and ulnar arteries of the upper extremities and the femoral, popliteal, dorsalis pedis, and posterior tibial arteries of the lower extremities. Minor or absent pulsations suggest a severe stenotic lesion proximal of the palpation site. To asses the cardiac (dys)function through the pulse generally an artery close to the heart should be selected, such as the carotid. Bounding high-amplitude carotid pulses suggest an increase in stroke volume and should be accompanied by a wide pulse pressure on the blood pressure measurement. A weak carotid pulse suggests a reduced stroke volume. [Figure 1] | The peripheral pulsations should be assed by both palpitation of the pulse and auscultation for bruits. Pulse abnormalities and bruits increase the likelihood of peripheral arterial disease. Pulsations should be assessed and documented in several arteries in the body in order to get an idea of the state of peripheral vasculature. Easily and fast palpable pulses in healthy individuals include the brachial, radial, and ulnar arteries of the upper extremities and the femoral, popliteal, dorsalis pedis, and posterior tibial arteries of the lower extremities. Minor or absent pulsations suggest a severe stenotic lesion proximal of the palpation site. To asses the cardiac (dys)function through the pulse generally an artery close to the heart should be selected, such as the carotid. Bounding high-amplitude carotid pulses suggest an increase in stroke volume and should be accompanied by a wide pulse pressure on the blood pressure measurement. A weak carotid pulse suggests a reduced stroke volume. [Figure 1] | ||
When examining the peripheral arterial pulsations by palpitation three important aspects should be noticed: | When examining the peripheral arterial pulsations by palpitation three important aspects should be noticed: | ||
*The amplitude of the pulse, which correlates with the pulse pressure | *The amplitude of the pulse, which correlates with the pulse pressure | ||
| Line 363: | Line 362: | ||
Ideally the patient is positioned into the semi-upright posture, with an elevation of the head of the bed to 30°, that permits visualization of the top of the right internal jugular venous blood column. A venous arch may be used to measure the JVP more accurately. The JVP is the elevation at which the highest oscillation point of the jugular venous pulsations is usually seen in euvolemic patients. The height of the column of blood seen in the internal jugular vein, vertically from the sternal angle, is added to 5 cm of blood (the presumed distance to the centre of the right atrium from the sternal angle) to obtain an estimate of central venous pressure in centimetres of blood. In patients who are hypovolemic, you may anticipate that the jugular venous pressure will be low. Likewise, in hypervolemic patients, you may anticipate that the JVP will be high. As a result, in hypovolemic patients the head should be in a lowered position (up to 0°), while in a hypervolemic state the head should be subsequently raised of the bed. | Ideally the patient is positioned into the semi-upright posture, with an elevation of the head of the bed to 30°, that permits visualization of the top of the right internal jugular venous blood column. A venous arch may be used to measure the JVP more accurately. The JVP is the elevation at which the highest oscillation point of the jugular venous pulsations is usually seen in euvolemic patients. The height of the column of blood seen in the internal jugular vein, vertically from the sternal angle, is added to 5 cm of blood (the presumed distance to the centre of the right atrium from the sternal angle) to obtain an estimate of central venous pressure in centimetres of blood. In patients who are hypovolemic, you may anticipate that the jugular venous pressure will be low. Likewise, in hypervolemic patients, you may anticipate that the JVP will be high. As a result, in hypovolemic patients the head should be in a lowered position (up to 0°), while in a hypervolemic state the head should be subsequently raised of the bed. | ||
Additionally, the characteristics of the right internal jugular pulse should be assessed, because they can be reveal clinical signs of right-heart function and rhythm disturbances. The distinctive waves of the jugular vein are summarized in Table 7 and visualized in Figure | Additionally, the characteristics of the right internal jugular pulse should be assessed, because they can be reveal clinical signs of right-heart function and rhythm disturbances. The distinctive waves of the jugular vein are summarized in Table 7 and visualized in Figure 2. | ||
[[Image:Jugular Venous Pulse.svg|right|thumb|300px|'''Figure 2.''' Jugular venous pulse waveform.]] | |||
{| class="wikitable" border="0" cellspacing="0" cellpadding="0" width="600px" | {| class="wikitable" border="0" cellspacing="0" cellpadding="0" width="600px" | ||
| Line 382: | Line 383: | ||
The " y " descent corresponds to the rapid empt'''Y'''ing of the atrium into the ventricle following the opening of the tricuspid valve. | The " y " descent corresponds to the rapid empt'''Y'''ing of the atrium into the ventricle following the opening of the tricuspid valve. | ||
|} | |} | ||
An elevated JVP is the classic sign of venous hypertension, typically in right sided heart failure. JVP elevation can be visualized as jugular venous distension, whereby the JVP is visualized at a level of the neck that is higher than normal. The paradoxical increase of the JVP with inspiration (instead of the expected decrease) is referred to as the Kussmaul sign, and indicates impaired filling of the right ventricle. The differential diagnosis of Kussmaul's sign includes constrictive pericarditis, restrictive cardiomyopathy, pericardial effusion, and severe right-sided heart failure. | An elevated JVP is the classic sign of venous hypertension, typically in right sided heart failure. JVP elevation can be visualized as jugular venous distension, whereby the JVP is visualized at a level of the neck that is higher than normal. The paradoxical increase of the JVP with inspiration (instead of the expected decrease) is referred to as the Kussmaul sign, and indicates impaired filling of the right ventricle. The differential diagnosis of Kussmaul's sign includes constrictive pericarditis, restrictive cardiomyopathy, pericardial effusion, and severe right-sided heart failure. | ||
| Line 470: | Line 468: | ||
'''Pathological causes:''' | '''Pathological causes:''' | ||
*<span style="color: #00CCFF;">'''P'''</span>ericardial effusion | *<span style="color: #00CCFF;">'''P'''</span>ericardial effusion | ||
*<span style="color: # | *<span style="color: #00CCFF;">'''O'''</span>besity and thick chest wall | ||
*<span style="color: #00CCFF;">'''P'''</span>leural effusion (left sided) | *<span style="color: #00CCFF;">'''P'''</span>leural effusion (left sided) | ||
*<span style="color: #00CCFF;">'''E'''</span>mphysema | *<span style="color: #00CCFF;">'''E'''</span>mphysema | ||
| Line 492: | Line 490: | ||
===Cardiac Auscultation=== | ===Cardiac Auscultation=== | ||
[[Image:Gray1216 modern locations.svg|thumb|right|400px|'''Figure 3.''' Locations for cardiac auscultation]] | |||
The acceleration and deceleration of blood and the subsequent vibration of the cardiac structures during the phases of the cardiac cycle are causing heart sounds. In healthy adults, there are two normal heart sounds often described as a lub and a dub (or dup), that occur in sequence with each heart beat. These are the first heart sound (S1) and second heart sound (S2), produced by the closing of the atroventricular valves and semilunar valves respectively. In addition to these normal sounds, a variety of other sounds may be present including heart murmurs, adventitious sounds, and gallop rhythms S3 and S4.To hear cardiac sounds, use a stethoscope with a bell and a tight diaphragm. The bell is best used to hear low-frequency sounds which are associated with ventricular filling. The diaphragm is best used to appreciate the medium-frequency sounds that are associated with valve opening and closing. Cardiac murmurs are caused due to turbulent blood flow and are usually high-to-medium frequency. In most cases the diaphragm is best used to hear cardiac murmurs. An important exception to this is the low-frequency atrioventricular valve inflow murmurs, such as that produced by mitral stenosis, which are best heard with the bell. Murmurs may be physiological or pathological. Abnormal murmurs can be caused by stenosis restricting the opening of a heart valve, resulting in turbulence as blood flows through it. Abnormal murmurs may also occur with valvular insufficiency (or regurgitation), which allows backflow of blood when the incompetent valve closes with only partial effectiveness. | The acceleration and deceleration of blood and the subsequent vibration of the cardiac structures during the phases of the cardiac cycle are causing heart sounds. In healthy adults, there are two normal heart sounds often described as a lub and a dub (or dup), that occur in sequence with each heart beat. These are the first heart sound (S1) and second heart sound (S2), produced by the closing of the atroventricular valves and semilunar valves respectively. In addition to these normal sounds, a variety of other sounds may be present including heart murmurs, adventitious sounds, and gallop rhythms S3 and S4.To hear cardiac sounds, use a stethoscope with a bell and a tight diaphragm. The bell is best used to hear low-frequency sounds which are associated with ventricular filling. The diaphragm is best used to appreciate the medium-frequency sounds that are associated with valve opening and closing. Cardiac murmurs are caused due to turbulent blood flow and are usually high-to-medium frequency. In most cases the diaphragm is best used to hear cardiac murmurs. An important exception to this is the low-frequency atrioventricular valve inflow murmurs, such as that produced by mitral stenosis, which are best heard with the bell. Murmurs may be physiological or pathological. Abnormal murmurs can be caused by stenosis restricting the opening of a heart valve, resulting in turbulence as blood flows through it. Abnormal murmurs may also occur with valvular insufficiency (or regurgitation), which allows backflow of blood when the incompetent valve closes with only partial effectiveness. | ||
Auscultation should take place in areas that correspond to the location of the heart and great vessels. Such placement will, of course, need to be modified for patients with unusual body habitus or an unusual cardiac position. When no cardiac sounds can be heard over the precordium, they can often be heard in either the subxiphoid area or the right supraclavicular area. The body positions for the placement of the stethoscope are shown in Figure 3. | Auscultation should take place in areas that correspond to the location of the heart and great vessels. Such placement will, of course, need to be modified for patients with unusual body habitus or an unusual cardiac position. When no cardiac sounds can be heard over the precordium, they can often be heard in either the subxiphoid area or the right supraclavicular area. The body positions for the placement of the stethoscope are shown in Figure 3. | ||
Auscultation in various positions is recommended to appreciate sounds and murmurs at maximally. For the first examination the patient should be in a suspine position. Furthermore, the patient should be asked to roll partly onto the left side into the left lateral decubitus position. This position brings the left ventricle close to the chest wall. In this position accentuates or brings out a left-side S3 and S4 an mitral murmurs. The other important position is sitting and forward leaning. The patient should be asked to completely exhale and stop breathing in expiration. The stethoscope diaphragm should be pressed along the left sternal border and at the apex. This position accentuates or brings out aortic murmurs maximally. | Auscultation in various positions is recommended to appreciate sounds and murmurs at maximally. For the first examination the patient should be in a suspine position. Furthermore, the patient should be asked to roll partly onto the left side into the left lateral decubitus position. This position brings the left ventricle close to the chest wall. In this position accentuates or brings out a left-side S3 and S4 an mitral murmurs. The other important position is sitting and forward leaning. The patient should be asked to completely exhale and stop breathing in expiration. The stethoscope diaphragm should be pressed along the left sternal border and at the apex. This position accentuates or brings out aortic murmurs maximally. | ||
| Line 544: | Line 541: | ||
{| class="wikitable" border="0" cellspacing="0" cellpadding="0" width="600px" | {| class="wikitable" border="0" cellspacing="0" cellpadding="0" width="600px" | ||
|- | |- | ||
|colspan="2" align="center"|Table 8. Graduation of Murmurs | |colspan="2" align="center"|'''Table 8. Graduation of Murmurs''' | ||
|- | |- | ||
!Grade | !Grade | ||
!Description | !Description | ||
|- | |- | ||
|width=" | |width="50px"|Grade 1 | ||
|Very faint, heard only after listener has "tuned in"; may not be heard in all positions. Only heard if the patient "bears down" or performs the Valsalva manoeuvre. | |Very faint, heard only after listener has "tuned in"; may not be heard in all positions. Only heard if the patient "bears down" or performs the Valsalva manoeuvre. | ||
|- | |- | ||
| Line 567: | Line 564: | ||
|Very loud, with thrill. May be heard with stethoscope entirely off the chest. | |Very loud, with thrill. May be heard with stethoscope entirely off the chest. | ||
|} | |} | ||
[[Image:P1.svg|thumb|right|400px|'''Figure 4.''' Murmur sound shapes.]] | |||
*Timing in the cardiac cycle – Murmurs could be heard early, mid or late in systole, throughout systole (holosystolic), early, mid or late in diastole or continuous. See below for more detail. | *Timing in the cardiac cycle – Murmurs could be heard early, mid or late in systole, throughout systole (holosystolic), early, mid or late in diastole or continuous. See below for more detail. | ||
*Shape – Several shapes can be distinguished as shown in Figure 4. | *Shape – Several shapes can be distinguished as shown in Figure 4. | ||
*Radiation – Some of the underlying pathologic disease cause murmurs to radiate. The distinctive pattern follows the blood flow from the point of maximal intensity: | *Radiation – Some of the underlying pathologic disease cause murmurs to radiate. The distinctive pattern follows the blood flow from the point of maximal intensity: | ||
**Aortic regurgitation – From the aortic valve area into the apex | **Aortic regurgitation – From the aortic valve area into the apex | ||
| Line 585: | Line 581: | ||
**Lateral decubitis – In this manoeuvre the patient rolls partly onto the left side and the apex should be auscultated. By bringing the left ventricle closer tot the chest, left-sided murmurs an generally louder. | **Lateral decubitis – In this manoeuvre the patient rolls partly onto the left side and the apex should be auscultated. By bringing the left ventricle closer tot the chest, left-sided murmurs an generally louder. | ||
**Vasalva manoeuvre – During this manoeuvre the patient bears down and expires against a closed glottis (hold the breathe and strain hard for 10 seconds). A increasing intrathoracic pressure and markedly reducing venous return to the heart will be caused by this manoeuvre. Almost all cardiac murmurs decrease in intensity, however during strain the murmur of hypertrophic obstructive cardiomyopathy may become louder because and the murmur associated with mitral regurgitation from mitral valve prolapse may become longer and louder because of the earlier occurrence of prolapse during systole. After release of the strain the murmur will decrease and most other murmurs will increase in intensity. | **Vasalva manoeuvre – During this manoeuvre the patient bears down and expires against a closed glottis (hold the breathe and strain hard for 10 seconds). A increasing intrathoracic pressure and markedly reducing venous return to the heart will be caused by this manoeuvre. Almost all cardiac murmurs decrease in intensity, however during strain the murmur of hypertrophic obstructive cardiomyopathy may become louder because and the murmur associated with mitral regurgitation from mitral valve prolapse may become longer and louder because of the earlier occurrence of prolapse during systole. After release of the strain the murmur will decrease and most other murmurs will increase in intensity. | ||
**Isometric hand grip – The patient has to relax his body while squeezing both fists. The manoeuvre increases arterial and left ventricular pressure, thus increasing afterload and flow gradient for mitral regurgitation, ventricular septal defect, and aortic regurgitation; the murmurs should then increase in intensity. The manoeuvre is in particular useful in distinguishing the increasing murmur of mitral regurgitation from a similar or lowering pitch aortic stenosis. | **Isometric hand grip – The patient has to relax his body while squeezing both fists. The manoeuvre increases arterial and left ventricular pressure, thus increasing afterload and flow gradient for mitral regurgitation, ventricular septal defect, and aortic regurgitation; the murmurs should then increase in intensity. The manoeuvre is in particular useful in distinguishing the increasing murmur of mitral regurgitation from a similar or lowering pitch aortic stenosis. | ||
====Murmurs categorized by time in cardiac cycle==== | ====Murmurs categorized by time in cardiac cycle==== | ||
[[Image:Phonocardiograms from normal and abnormal heart sounds.svg|thumb|right|500px|'''Figure 5.''' Representation of the sound waves of murmurs associated with heart disease.]] | |||
A schematic scheme of the heart sounds and heart murmurs are shown in Figure 5. | A schematic scheme of the heart sounds and heart murmurs are shown in Figure 5. | ||
'''Systolic murmurs''' are very common and do not always imply cardiac disease. Most murmurs fall in the 1–3 audible intensity range, however murmurs in the 4–6 range are almost always due to pathologic conditions. Again, severe disease can exist with grades 1–3 or no cardiac murmurs. Distinguishing benign from pathologic systolic flow murmurs is one of the major challenges of clinical cardiology. Benign flow murmurs are heard in 80% of children with a declining incidence with increasing age. Other physical conditions known for benign heart systolic murmurs are pregnancy or thin adults or athletic adults. The murmur is usually benign in a patient with a soft flow murmur that diminishes in intensity in the sitting position and neither a history of cardiovascular disease nor other cardiac findings. The physiological flow murmurs are usually heard in grades 1–2 and occur very early in systole. These murmurs have a vibratory quality and are usually less apparent when the patient is in the sitting position (when venous return is less). If an ejection sound is heard, there is usually some abnormality of the aortic or pulmonary valve. The most common systolic murmur is the becoming stronger and fading (crescendo/decrescendo) murmur. This murmur increases in intensity as blood flows early in systole and diminishes in intensity through the second half of systole. This murmur can be caused by a strong flow in a normal heart or to obstructions of flow, as occurs with a stenotic semilunar valve, or hypertrophic cardiomyopathy. | '''Systolic murmurs''' are very common and do not always imply cardiac disease. Most murmurs fall in the 1–3 audible intensity range, however murmurs in the 4–6 range are almost always due to pathologic conditions. Again, severe disease can exist with grades 1–3 or no cardiac murmurs. Distinguishing benign from pathologic systolic flow murmurs is one of the major challenges of clinical cardiology. Benign flow murmurs are heard in 80% of children with a declining incidence with increasing age. Other physical conditions known for benign heart systolic murmurs are pregnancy or thin adults or athletic adults. The murmur is usually benign in a patient with a soft flow murmur that diminishes in intensity in the sitting position and neither a history of cardiovascular disease nor other cardiac findings. The physiological flow murmurs are usually heard in grades 1–2 and occur very early in systole. These murmurs have a vibratory quality and are usually less apparent when the patient is in the sitting position (when venous return is less). If an ejection sound is heard, there is usually some abnormality of the aortic or pulmonary valve. The most common systolic murmur is the becoming stronger and fading (crescendo/decrescendo) murmur. This murmur increases in intensity as blood flows early in systole and diminishes in intensity through the second half of systole. This murmur can be caused by a strong flow in a normal heart or to obstructions of flow, as occurs with a stenotic semilunar valve, or hypertrophic cardiomyopathy. | ||