The Cardiac Exam

The cardiac exam does not begin and end with the stethoscope. As with any examination, it begins the moment you see the patient, with simple observation. The following is the approach we like to take:

• General observation
• Identification of the jugular venous pulse with quantitative and qualitative assessments
• Evaluation of the peripheral pulse
• Observation of the precordium, looking for movement
• Inspection and palpation of the point of maximal impulse (PMI, at the cardiac apex)
• Auscultation of the heart

 

Observation allows for the generation of hypotheses that can guide your exam and help you anticipate findings. For example, if your patient has signs of intravenous drug use, such as track marks on their arms, endocarditis should be considered. Your examination will then become more focused, allowing you to recognize findings that you may have otherwise missed. Here are a few things you may notice on first meeting and interviewing a patient:

• Does the patient look sick or well?
• Are they anxious, in distress?
• How is their breathing?
• Do you notice any abnormal coloring?
• Are there signs of a systemic disease in their face, skin, torso or extremities?
  • Look at their hands, chest wall, mouth, toes
  • Endocarditis can present with splinter hemorrhages of the nail beds, Roth spots in the retina, hemorrhages in the conjunctiva, Janeway lesions and Osler nodes on the fingers and toes, and clubbing (see the figures in this article)

 

Does your patient look like this?

This is Jonathan Larson, author of the musical Rent, who died of an aortic dissection the night before his play premiered. No one suspected Marfan’s, despite several trips to the emergency room, but look at his feet!

After this initial inspection, assess the jugular venous pulse for both central venous pressure and to see if there are any unusual waveforms. See the jugular venous pulse section for more information.

Next, feel the pulse – radial is usually adequate, but the carotid is often better as it is more central.

Next, with the patient in a supine position, inspect and palpate the chest wall. See the precordial movement section for more information.

 

The Patient

In order to do get the most accurate information from your examination, it is best to inspect, palpate, and auscultate directly over the patient’s skin, not through clothing. An explanation of this to your patient followed by a request to uncover areas that should be accessed is recommended. When examining any part of the patient, modesty and privacy should be respected. In order to properly examine the heart, you will need to feel and listen in the cardiac apex, an area that is often covered by the left breast. At least one study has shown that the examination of women in this area is inferior to that done on men likely due to physician discomfort.

One approach is to explain to your patient what examination you would like to perform, why it is important, and ask if you can lift their breast (patients may feel more comfortable lifting it themselves).

• Drapes should be positioned by you properly to protect patient modesty
• Expose the minimum amount of skin
• Make sure curtains are drawn and doors are closed
• As you are examining the patient, explain what you are doing and try to allay any fears that may arise as you may be listening longer than what they are used to
• When you are done examining the patient, if you untied or unsnapped their gown, redo what you undid. Always leave a patient’s room in better condition than you found it.

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Jugular Venous Pulse

Our approach to evaluating the jugular venous pulse includes three separate but related components:

1) Identification of the jugular venous pulse

2) Quantitative assessment of the jugular venous pulse 

3) Qualitative assessment of the jugular venous pulse

Section I: Identification of the jugular venous pulse

Identification of the jugular venous pulse is the most important of the three components. Without it, components 2 and 3 cannot even be attempted. Often you will hear from trainees and colleagues that the jugular venous pulse could not be visualized for x or y reason. Usually because of a large neck or beard. In our experience, the jugular venous pulse is visible in the vast majority of patients. So, where do we find the pulse? The best location for viewing the jugular venous pulse, and the one that you should go to first, is the right internal jugular vein (RIJ). It is ideal because of its direct route into the right atrium. If the RIJ is unavailable, the left IJ should be examined next. It is important to note here that we are not actually visualizing the internal jugular vein itself, we are visualizing the movement of the skin that overlies the vessel. If neither IJ is available, then we can use the external jugular veins. If we have exhausted that list and still cannot find the venous pulse, perhaps there are other places to look, which we will explore later in the tutorial.

 

 

This data is from a 1973 study and it demonstrates two things. First, the RIJ is highly reliable for estimating central venous pressure. Second, the LIJ and EJ are nearly as reliable as the RIJ. Right atrial pressure is plotted on the X axis, and the pressure of the blood vessel in question on the Y axis. All measurements were obtained directly. You can see that for the most part, there is a linear relationship between the pressure in the right atrium and the pressure in each of those blood vessels. It should be noted that while the EJ can be used to estimate CVP, it does not transmit the actual waveform very well, so it is less reliable for the purposes of qualitative assessment.

Let us talk about the approach to identifying the jugular venous pulse. The first and most important step is patient positioning. When we walk into a room, the patient is often slouched in bed and their neck is flexed forward. You try to move the back of the bed up and down and it only moves their neck. To address this issue, we recommend flattening the bed and helping the patient slide up so that their head reaches the end of it. Now, when the backboard of the bed is adjusted it will move the angle of the patient’s torso, and not just their neck. You want the patient’s neck and torso to be in the same plane. And you want to make sure the neck is nice and relaxed. You do not want flexion of the sternocleidomastoid muscles getting in your way. Sometimes you have to add or subtract pillows to accomplish this. Step 2 is to observe the neck. The tendency is to look at the neck from a perpendicular perspective. You will miss subtle movement if you do this. In order to pick up the most subtle movement it is best to assume a tangential vantage point. Step 3 is identifying movement in the neck. The traditional “window” for viewing the jugular venous pulse is confined to the region of the neck between the clavicle and the angle of the jaw. Sometimes you have to manipulate the angle of the patient in order to bring the waveform into this window. Finally, the last step in this process is to determine whether the movement you are seeing is venous or arterial.

 

 

There are a host of strategies for determining whether the movement you are seeing is venous or arterial. The waveform itself can be revealing. An arterial pulse has a single peak that is quick and sharp. In contrast, the venous pulse is typically double and undulating in nature. The most striking feature of the arterial pulse is the outward movement. Obviously, what goes out must come back in, but it does so subtly and gradually and it is hardly noticeable. The most striking feature of the venous pulse on the other hand is the inward movement (the x and y troughs). The arterial pulse tends to be pinpoint, involving a small area of the neck. The venous pulse on the other hand is diffuse, often involving a large area of the neck. The arterial pulse does not vary with patient positioning, respiratory cycle, or abdominal pressure. In contrast, the venous pulse is affected by all three actions. As the angle at which the patient is positioned decreases, the venous pulse climbs up the neck, and as the angle is increased, the venous pulse moves downward. The venous pulse is also affected by respiration, normally moving down with inspiration. And with abdominal pressure, the venous pulse will move up the neck. Finally, the arterial pulse is palpable while the venous pulse is almost always non-palpable.

What is the nature of this pulsation in the following video?

 

 

Notice that there is a single outward peak without significant inward movement, and there is one small area in particular that seems to contain most of the movement – it is pinpoint and you can put your finger right on that spot. And if you did, you would feel a pulse. This is a normal carotid pulse. You can follow the synchronized cursor along the arterial tracing.

Compare the arterial pulse with the pulsation demonstrated in the following video:

 

 

Notice that there are two peaks and two troughs, and it is the inward movement that really catches your eye. It is diffuse, stretching over most of the neck. These are all of the characteristics of a venous pulse, and in fact this is the normal jugular venous pulse. You can follow the synchronized cursor along the venous tracing to identify each component in the neck. Remember that the c wave is not visible at the bedside.

The abdominojugular (reflux) test is a physical examination maneuver that is performed by placing firm pressure over the patient’s abdomen with the palm of the hand while observing the effect on jugular venous pressure. This test has several applications. First, it can serve to distinguish a venous pulse (will rise with abdominal pressure) from an arterial pulse (no change with abdominal pressure). Second, a sustained rise in jugular venous pressure of >3 cm lasting more than 10 to 15 seconds while abdominal pressure is continuously applied, is highly suggestive of elevated wedge pressure >15 mm Hg. The following video demonstrates abdominojugular reflux in a patient with elevated wedge pressure:

 

 

As we discussed earlier, we typically first attempt to evaluate the right internal jugular vein. If it is unavailable for any reason, we move to evaluate the left internal jugular vein. The following video is simply a demonstration of the jugular venous pulse on the left side of the neck:

 

 

When the right and left internal jugular veins fail to provide adequate evaluation of the jugular venous pulse, the external jugular vein can be used to estimate central venous pressure. The external jugular is easily recognizable as a visible vein on the surface of the neck (much like the veins on the dorsum of the hand can be visualized). Unlike the internal jugular vein, which provides indirect evaluation of the jugular venous pulse via movement of the overlying skin (the actual vessel itself is not visualized), the external jugular vein provides direct evaluation of the jugular venous pulse. However, the external jugulars often transmit the venous waveform poorly. These veins are therefore suitable for quantitative assessment of the jugular venous pulse, but are not reliable for qualitative assessment. In addition to showing central venous pressure via the external jugular vein, the following video also nicely demonstrates an arterial pulse and venous pulse side by side.

 

 

You can easily appreciate the differences that distinguish them. The arterial pulse is characterized by a single outward peak that is sharp and quick, and occurring over a relatively small area of the neck; the venous pulse is double, diffuse, and undulating.

The traditional “window” for viewing the jugular venous pulse is confined to the region of the neck between the clavicle and the angle of the jaw. However, when central venous pressure is markedly elevated, the jugular venous pulse may not be readily visible within that window, even when the patient is sitting in the upright position. In such circumstances, be sure to look above the jaw as the pulse is often transmitted by veins of the periauricular area, temple, or forehead. The following video demonstrates the unmistakable “inward” movement of the venous pulse in the patient’s periauricular area:

 

 

This video demonstrates the unmistakable “inward” movement of the venous pulse in the patient’s temple:

 

 

Here is another video demonstrating the unmistakable “collapsing” movement of the venous pulse in the patient’s forehead:

 

Carotid Pulse

The jugular venous pulse must be distinguished from the carotid pulse. There are important differences between arterial and venous pulses that allows the examiner to distinguish them at the bedside. The normal carotid arterial pulse is characterized by a single peak that is quick and sharp. Following the peak, the skin subtly recedes back to its former position until the next pulse occurs, but there is no obvious or aggressive inward movement. The pulse is confined to a smaller area of the neck than the jugular venous pulse. The arterial pulse is unaffected by patient positioning, respiratory cycle, or abdominal pressure (abdominojugular reflux). It is easily palpable with a finger (we prefer to use the thumb).

 

Jugular Venous Pulse via the Right Internal Jugular Vein

Because of its direct route to the heart, the right internal jugular vein is the preferred site to evaluate the jugular venous pulse. At the bedside, we do not actually visualize the internal jugular vein itself. Rather, the movement we observe in the neck is within the soft tissue that overly the internal jugular vein. The tissue transmits the pulsation of the internal jugular vein, allowing us to characterize its height (quantitative assessment) and contour (qualitative assessment).

 

Jugular Venous Pulse via the Left Internal Jugular Vein

The right internal jugular vein is the preferred site to evaluate the jugular venous pulse. Sometimes it is unavailable because of thrombosis or the presence of a catheter. In other patients, it is simply not well seen on the right for unknown reasons. In such circumstances, the left internal jugular vein may be used to evaluate the jugular venous pulse. The left internal jugular vein has been shown to be nearly as accurate as the right internal jugular vein for evaluation of central venous pressure.

 

Jugular Venous Pulse via the External Jugular Vein

When the right and left internal jugular veins fail to provide adequate assessment of the jugular venous pulse, the external jugular vein can be used to estimate central venous pressure. The external jugular is easily recognizable as a visible vein on the surface of the neck (much like the veins on the dorsum of the hand can be visualized). Unlike the internal jugular vein, which provides indirect evaluation of the jugular venous pulse via movement of the overlying skin (the actual vessel itself is not visualized), the external jugular vein provides direct evaluation of the jugular venous pulse. However, the external jugulars often transmit the venous waveform poorly. These veins are therefore suitable for quantitative assessment of the jugular venous pulse, but are not reliable for qualitative assessment.

 

Abdominojugular (reflux) Test

The abdominojugular (reflux) test is a physical examination maneuver that is performed by placing firm pressure over the patient’s abdomen with the palm of the hand while observing the effect on jugular venous pressure. This test has several applications. First, it can serve to distinguish a venous pulse (will rise with abdominal pressure) from an arterial pulse (no change with abdominal pressure). Second, a sustained rise in jugular venous pressure of >3 cm lasting more than 10 to 15 seconds while abdominal pressure is continuously applied, is highly suggestive of elevated wedge pressure >15 mm Hg.

Section II: Quantitative Assessment of the Jugular Venous Pulse

Now that we have established how to identify the jugular venous pulse, we are ready to address the second component of the exam: quantitative assessment. This is also known as jugular venous pressure or JVP. When clinicians report a JVP as 8 cm H2O or 16 cm H₂O, they are providing a quantitative assessment.

This is the most frequently applied component of the evaluation of the jugular venous pulse. It’s used on a day-to-day basis.

We should begin by asking the question, what are we measuring? We are measuring right atrial pressure. In order to interpret the significance of the JVP, one must know normal right atrial pressure. When measured in mm Hg, normal RA pressure is <6. When measured in cm H₂O, normal is <8. So why are we measuring JVP? First, it can be helpful in establishing a diagnosis. For example, when a patient presents with dyspnea, the JVP exam is an instrumental part of the workup that can, at best, provide you with the diagnosis, and at worst, narrow the differential diagnosis. In addition to its diagnostic utility, we often use JVP to establish and follow volume status. Pressure in the right atrium is usually a function of volume. As volume goes up, so does pressure.

So how do we measure JVP? We want to measure the height of the column of blood above the middle of the RA. But the RA is in the middle of the chest and we cannot see it. So we must use landmarks to extrapolate to the center of the RA. The angle of Louis represents one such landmark. In the supine position, the Angle of Louis is about 5 cm above the middle of the RA. At 30 degrees or more, that number increases to 8-10 cm. The clavicle is another landmark that we can use, but only in the upright position, where it is 12-16 cm above the middle of the RA. Textbooks teach a method for measuring JVP using a ruler and another straight edge, demonstrated by the following image:

We do not know of any clinicians who actually use this technique at the bedside. Instead, measure the width of your hand. This can be used as the vertical rule straight edge, and you can estimate JVP that way.

The following video demonstrates the jugular venous pulse at the angle of the patient’s jaw:

 

 

The patient is positioned at 45 degrees. If the top of the jugular venous pulse is 14 cm above the angle of Louis, and we assume the angle of Louis to be 8 cm above the middle of the right atrium, then the jugular venous pressure in this case is 14 + 8 = 22 cm H₂O.

When you see abnormal indentations in a patient’s forehead, you should immediately consider longstanding elevated central venous pressure. Here is a photograph of a patient with such indentations:

 

 

Here is the same patient in a more reclined position:

 

 

You can see those veins engorge with blood.

When all else has failed, we have found that the dorsum of the hand can provide fertile ground for estimating central venous pressure. When the internal or external veins are unavailable or when the pressure is extremely elevated, try using the hand veins to estimate central venous pressure. When the hands are at the patient’s side, check for engorgement of the veins. If present, lift the hand high above the patient’s chest until the veins drain and flatten. Then, slowly lower the hands down to find the moment that the veins begin to fill. The distance between the top of the hand and the angle of Louis can be used to estimate central venous pressure (by adding to it the estimated distance between the angle of Louis and center of the right atrium). This technique may also be useful in the setting of severe tricuspid regurgitation, when the average central venous pressure can be difficult to estimate using the veins of the neck.

 

 

Normal Jugular Venous Pressure

The jugular venous pulse can be used to measure right atrial pressure. Normal right atrial pressure is less than 8 cm H₂O (via exam) or less than 6 mm Hg (via direct measurement). The ability to recognize normal right atrial pressure at the bedside is critical in a variety of clinical contexts.

Elevated Jugular Venous Pressure (upper neck)

The jugular venous pulse can be used to measure right atrial pressure. Normal right atrial pressure is less than 8 cm H₂O (via exam) or less than 6 mm Hg (via direct measurement). The ability to recognize elevated right atrial pressure at the bedside is critical in a variety of clinical contexts.

 

Elevated Jugular Venous Pressure (temple)

The traditional “window” for viewing the jugular venous pulse is confined to the region of the neck between the clavicle and the angle of the jaw. However, when central venous pressure is markedly elevated, the jugular venous pulse may not be readily visible within that window, even with the patient sitting in the upright position. In such circumstances, be sure to look above the jaw as the pulse is often transmitted by veins of the periauricular area, temple, or forehead.

Elevated Jugular Venous Pressure (forehead)

The “window” for viewing the jugular venous pressure is typically confined to the region of the neck between the clavicle and jaw. However, when central venous pressure is markedly elevated, the jugular venous pulse may not be readily visible within that window, even with the patient sitting in the upright position. In such circumstances, be sure to look above the jaw as the pulse is often transmitted by veins of the periauricular area, temple, or forehead.

Hand Vein Assessment

We have found that the dorsum of the hand can provide fertile ground for estimating central venous pressure. When the internal or external veins are unavailable, try using the hand veins to estimate central venous pressure. When the hands are at the patient’s side, check for engorgement of the veins. If present, lift the hand high above the patient’s chest until the veins drain and flatten. Then, slowly lower the hands down to find the moment that the veins begin to fill. The distance between the top of the hand and the angle of Louis can be used to estimate central venous pressure (by adding to it the estimated distance between the angle of Louis and center of the right atrium). This technique may also be useful in the setting of severe tricuspid regurgitation, when the average central venous pressure can be difficult to estimate using the veins of the neck

Section III: Qualitative Assessment of the Jugular Venous Pulse

Now that we have discussed the first two components of the jugular venous pulse examination, identification and quantitative assessment, we are ready to move into the third and slightly more sophisticated component: qualitative assessment.

Evaluation of the jugular venous waveform can provide a host of useful information about the heart, beyond simply measuring right atrial pressure. To illustrate this point, ask yourself how you define Mobitz I heart block. Most would define the condition as periodically dropped QRS complexes on an electrocardiogram, that are preceded by progressively lengthening PR intervals. When did Wenckebach describe Mobitz I heart block? It was the year 1893. When was the electrocardiogram clinically available? 1895. How is this possible? Wenckebach used the jugular venous waveform to describe the type of heart block that now bears his name. The way he did it will become clear as we proceed in the tutorial.

To be able to perform a qualitative assessment of the jugular venous pulse, one must be able to understand the normal waveform, and the cardiac events that cause each of its components to occur. It is helpful to orient yourself to the cardiac cycle.

 

 

Let us start with the first peak in the waveform, the a wave, which is caused by right atrial contraction. When the atrium contracts, pressure inside the atrium increases, and this is seen as a positive deflection in the jugular venous waveform. Atrial contraction occurs at the very end of diastole, when the atrium is squeezing the last bit of blood into the right ventricle. Next, during early systole, isovolumetric ventricular contraction triggers closure of the tricuspid valve, which bulges into the right atrium, producing the c wave. In mid-systole, the combination of atrial relaxation and descent of the atrial floor during ventricular contraction results in the x descent. The third peak, the v wave, occurs as a result of atrial filling during late systole. Finally, passive ventricular filling in early diastole produces the y descent.

Every aspect of the cardiovascular examination should be performed together when possible. We often look at the jugular venous pulse while simultaneously ausculting the heart or palpating the peripheral pulse. This allows the examiner to establish the cardiac cycle and understand whether events are occurring in systole or diastole. One can identify components of the jugular venous waveform by simultaneously ausculting the heart. We know that the c wave occurs in the middle of the x descent. And the c wave occurs as a result of tricuspid valve closure, which is the same event that produces S1. So, the x descent should occur at the same time as S1. S2 occurs on the upstroke of the v wave. What causes an S4 gallop? It occurs when blood is squeezed into a stiff ventricle at the end of diastole. It corresponds to the a wave. What causes an S3 gallop? It occurs during the initial rush of blood into a dilated ventricle during passive ventricular filling. It corresponds to the y descent.

 

 

Let us reexamine the following video:

 

 

Take a look at the jugular venous pulse via the external jugular vein. There is one dominant descent demonstrated by the video. Is it the x or the y descent? How could you tell? You could auscult the heart. Or, in this case, you happen to have a visible arterial pulse that can serve as a nice frame of reference. The arterial pulse should occur, of course, during the x descent. If you time it, you will see that the arterial pulse does occur at the same time as the dominant descent in the venous waveform, indicating that it is indeed the x descent.

Now that we can recognize the normal jugular venous waveform and the cardiac events that cause each of its components, we are ready to discuss various abnormalities. What is the abnormality in the following tracing?

 

 

There is no a wave, a very small x descent (remember that normally the x descent is more prominent than the y descent), and the waveform is occurring in an irregular rhythm. This is all indicative of atrial fibrillation. Because atrial fibrillation does not allow for coordinated atrial contraction, the a wave disappears. Similarly, since there is no atrial relaxation in the setting of atrial fibrillation, the x descent is smaller than normal.

What is the abnormality in the following tracing?

 

 

The a wave is more pronounced than usual. These are giant a waves. As you now know, the a wave occurs as a result of right atrial contraction. When there is resistance to right ventricular filling, right atrial contraction generates increased pressure, resulting in large a waves. Giant a waves occur with every beat, unlike cannon a waves, which usually occur intermittently. Causes of giant a waves include tricuspid stenosis and increased right ventricular end-diastolic pressure from any cause (e.g., pulmonary hypertension). Listen for an associated right-sided S4 gallop.

What is the abnormality in the following tracing?

 

 

The a wave is even more pronounced compared to the giant a wave, and it occurs intermittently between normal waveforms. These are cannon a waves. Cannon a waves usually occur intermittently, unlike giant a waves, which occur with every beat. The cannon a wave occurs as a result of atrial contraction against a closed tricuspid valve, which occurs sporadically as a result of atrioventricular dissociation.

What is the abnormality in the following tracing?

 

 

The x descent has been replaced by a large cv fusion wave. This is known as Lancisi’s sign, and is a physical finding of tricuspid regurgitation. In the setting of severe tricuspid regurgitation, retrograde blood flow into the right atrium during ventricular systole results in loss of the x descent, creating a fused cv wave that appears as a large pulsation within the internal jugular vein. This wave is typically followed by an augmented y descent, which is the consequence of an increased pressure gradient between the right atrium and right ventricle. The often palpable cv fusion wave is one of the exceptions to the rule that the jugular venous waveform is nonpalpable. Listen for an associated holosystolic murmur over the left lower sternal border that augments with inspiration.

What is the abnormality in the following tracing?

 

 

The y descent is sharper and deeper than usual. This is known as Friedreich’s sign, and is a physical finding of constrictive pericarditis and restrictive cardiomyopathy. The y descent occurs as a result of passive ventricular filling during early diastole. In constrictive pericarditis, the characteristic sharp and deep y descent reflects rapid filling in early diastole which occurs when the unyielding pericardium elevates atrial pressure and limits ventricular filling to the early diastolic period. Listen for an associated pericardial knock.

What is the abnormality in the following tracing?

 

 

Here we have sharp x and y descents, known as the “W” sign. In a subset of patients with constrictive pericarditis, the prominent y descent occurs in combination with a prominent x descent, creating two steep troughs known as the “W” sign. This sign is more specific for constrictive pericarditis than Friedreich’s sign, and can therefore be helpful in distinguishing constrictive pericarditis from restrictive cardiomyopathy. As before, listen for an associated pericardial knock.

What is the abnormality in the following tracing?

 

 

The jugular venous pressure paradoxically increases with inspiration. This is known as Kussmaul’s sign. Decreased intrathoracic pressure during inspiration normally leads to an increase in venous return to the right side of the heart, with an associated decrease in jugular venous pressure. When there is impaired filling of the right ventricle, the jugular veins instead become engorged. Causes of Kussmaul’s sign include right ventricular infarction, severe right ventricular failure, restrictive cardiomyopathy, constrictive pericarditis, and tricuspid stenosis.

Normal Jugular Venous Waveform

The normal jugular venous pulse is best evaluated via the right internal jugular vein, and is characterized by three peaks and two troughs. The first peak, called the a wave, results from atrial contraction during late diastole. Next, during early systole, ventricular contraction triggers closure of the tricuspid valve, producing the c wave (not visible at the bedside). In mid-systole, a combination of atrial relaxation and descent of the atrial floor during ventricular contraction results in the x descent. The third peak, the v wave, occurs as a result of atrial filling during late systole. Finally, passive ventricular filling in early diastole produces the y descent. The most conspicuous features of the venous pulse are the troughs, which generate obvious, aggressive inward movements of the skin. In the normal jugular venous waveform, the x descent is deeper than the y descent. Compared to the arterial pulse, the venous pulse involves a more diffuse area of the neck. It varies with patient positioning, respiratory cycle, and abdominal pressure (abdominojugular reflux). The normal venous pulse is not palpable. 

 

Atrial Fibrillation

The jugular venous pulse can provide a clue to the diagnosis of atrial fibrillation. The a wave of the jugular venous waveform occurs as a result of right atrial contraction. Because atrial fibrillation does not allow for coordinated atrial contraction, the a wave disappears. Similarly, since there is no atrial relaxation in the setting of atrial fibrillation, the x descent is smaller than normal.

 

Giant a Wave

The a wave of the jugular venous waveform occurs as a result of right atrial contraction. When there is resistance to right ventricular filling, right atrial contraction generates increased pressure, resulting in giant a waves. These waves occur with every beat, unlike cannon a waves, which usually occur intermittently. Causes of giant a waves include tricuspid stenosis and increased right ventricular end-diastolic pressure from any cause (e.g., pulmonary hypertension).

 

Cannon a Wave

The a wave of the jugular venous waveform occurs as a result of right atrial contraction. When there is resistance to right ventricular filling, right atrial contraction generates increased pressure, resulting in large a waves. Cannon a waves usually occur intermittently, unlike giant a waves, which occur with every beat. The cannon a wave occurs as a result of atrial contraction against a closed tricuspid valve, which occurs sporadically as a result of atrioventricular dissociation. When cannon a waves occur with every beat, it indicates atrioventricular dissociation with retrograde atrial activation from supraventricular tachycardia (e.g., junctional rhythm).

Lancisi’s Sign

In the setting of severe tricuspid regurgitation, retrograde blood flow into the right atrium during ventricular systole results in loss of the x descent, creating a fused cv wave that appears as a large pulsation within the internal jugular vein. This wave is typically followed by an augmented y descent, which is the consequence of an increased pressure gradient between the right atrium and right ventricle. The often palpable cv fusion wave is one of the exceptions to the rule that the jugular venous waveform is nonpalpable. Listen for an associated holosystolic murmur over the left lower sternal border that augments with inspiration.

 

Friedreich’s Sign

The normal jugular venous waveform contains two descents, x and y. The x descent, which corresponds to the combination of right atrial relaxation and depression of the atrial floor during ventricular contraction, is normally dominant. The y descent occurs as a result of passive ventricular filling during early diastole. A sharp and deep y descent that becomes more dominant than the x descent is known as Friedreich’s sign. It is associated with constrictive pericarditis and restrictive cardiomyopathy.

The W Sign

The normal jugular venous waveform contains two descents, x and y. Under normal conditions, the x descent is more prominent than the y descent. In constrictive pericarditis, the unyielding pericardium causes elevated atrial pressure and limits ventricular filling to the early diastolic period, resulting in a sharp and deep y descent, known as Friedreich’s sign. In some patients, the prominent y descent occurs in combination with a prominent x descent, creating two steep troughs known as the “W” sign. This finding is helpful in distinguishing constrictive pericarditis from restrictive cardiomyopathy, in which the x descent is typically diminished.

 

Kussmaul’s Sign

The jugular venous pulse can provide a clue to the presence of abnormal right ventricular filling. This video demonstrates a paradoxical rise in jugular venous pressure during inspiration, known as Kussmaul’s sign. Decreased intrathoracic pressure during inspiration normally leads to an increase in venous return to the right side of the heart, with an associated decrease in jugular venous pressure. When there is impaired filling of the right ventricle, the jugular veins instead become engorged. Causes of Kussmaul’s sign include right ventricular infarction, severe right ventricular failure, restrictive cardiomyopathy, constrictive pericarditis, and tricuspid stenosis.

 

The Jugular Venous Pressure of Lung Disease

The jugular venous pulse can provide a clue to the presence of lung disease. This video demonstrates striking normal respiratory variation in the jugular venous pressure. Decreased intrathoracic pressure during inspiration normally leads to an increase in venous return to the right side of the heart, with an associated decrease in jugular venous pressure. In patients with lung disease, the “normal” inspiratory drop and expiratory rise in jugular venous pressure is amplified. This most likely occurs as a result of the exaggerated drop in inspiratory intrathoracic pressure and rise in expiratory intrathoracic pressure that occurs as a result of altered lung mechanics.

Cardiac Tamponade

In the setting of cardiac tamponade, the jugular venous pulse is elevated. Qualitatively, the y descent is diminutive or absent.

 

View Lecture On Jugular Venous Pulse

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Cardiac Auscultation

 

The Stethoscope

• The ear pieces should be pointing forward.
• If you have a choice between hard ear pieces and soft ones, we recommend the hard ones. The soft ones, while more comfortable, may collapse in your ear canal and impair sound transmission.
• Most stethoscope heads have 2 sides, the flat diaphragm and the concave bell, while others have a single head that functions as a bell with light pressure and a diaphragm with firm pressure.
• While the human ear is capable of hearing sounds over a wide range of frequencies (20-20,000 Hz) we hear best at the frequency of our spoken voice (roughly 300-3000 Hz), and many cardiac sounds are below this optimal range.
• The diaphragm is useful for most heart, lung, and abdominal sounds, but filters out sounds below 300 Hz.
• Low pitched cardiac sounds (gallops, mitral stenosis murmur) are in the 40-150 Hz range, and are often only heard with the bell. On a boards exam, if they are using a bell to listen to the heart, the answer is either a gallop or mitral stenosis. 
• When you use the diaphragm, you may need to press firmly to get the best sound conduction, but with the bell you should only apply enough pressure to generate a seal. if you push too hard, the patient’s skin may then act as a diaphragm and filter out the low pitched tones you are trying to hear – this phenomenon can be used to differentiate low pitched from high pitched sounds by varying pressure on the bell. 

 

Auscultation

In order to improve your skills, practice whenever you can, and pay careful attention to what you hear. When listening to the heart, try to ignore other sounds (like respiratory and bowel sounds) and just listen to the heart sounds, much like when you listen to a piece of music and only pay attention to the bass or the drums while mentally filtering out the other instruments. Try to do so in as quiet an environment as you can, and try to be quiet when someone else is listening to a patient in the room with you. Have a systematic approach, listening in the same order each time. Pay careful attention to the heart sounds and try to describe how they sound and even mimic them with your voice.

Here is an x-ray from the New England Journal of Medicine website showing the location of 4 artificial valves. However, when we listen to the heart, the different sounds are usually best heard away from the anatomic location of the valves. The aortic valve is usually heard best just to the right of the sternum, between the 2^nd and 3rd ribs (2^nd intercostal space), the pulmonic valve in the left 2^nd intercostal space, the tricuspid in left 5^th intercostal space next to the sternum, and the mitral in the 5^th intercostal space in the mid clavicular line (an imaginary line from the middle of the clavicle). Since S1 is made by closure of the mitral and tricuspid valves, you will hear those sounds better in the lower portions of the heart, known as the apex, whereas the S2 sounds, from the aortic and pulmonic valves, are heard in the upper portion, known as the base. As noted above, develop a consistent approach and do it the same way every time. Some like to start at the apex and listen to S1 first, working their way back to tricuspid, pulmonic and then aortic, while others go in the opposite order. Patients are usually examined lying in bed at 30-45 degrees, with the examiner to their right.

• Listen first with the diaphragm, paying attention to S1 – is it loud or soft? Single or split?
• Do the same with S2. Then listen just to systole – is it quiet or do you hear a murmur?
• Do the same with diastole. Is it silent (as it should be) or do you hear any extra sounds?
• Now listen with the bell at the apex for extra sounds (gallops or low-pitched murmurs).
• Gallops are best heard in the left lateral decubitus position, and some murmurs may be heard better with the patient sitting upright (aortic regurgitation, mitral valve prolapse).
• If you hear sounds that you are not sure about, listen to them carefully not just in the 4 cardinal locations, but slowly slide or inch your stethoscope between those sites to see how the sound changes.

 

Differentiating S1 and S2        

• By timing and cadence. Diastole (from S2 to S1) is longer than systole (from S1 to S2) at heart rates below around 110 bpm.
• By location. Listen over different parts of the chest and see where these sounds are loudest. S2 is heard best over the base and S1 over the apex.
• By simultaneously evaluating the peripheral pulse. In a normal, healthy person, the pulse can be felt at the same time you hear the S1. However, this can be misleading as the peripheral pulse can sometimes be delayed. One of our favorite texts (Marriott) cautions that in differentiating systole from diastole, the pulse is a “refuge for those who are otherwise destitute.”

Transient Heart Sounds

Transient sounds are short in duration, like S1 and S2. This is in contrast to sounds of longer duration, such as murmurs.

First Heart Sound (S1)

S1 is generated by the closure of the mitral and tricuspid valves, marking the beginning of systole. It is a high-pitched sound best heard over the apex of the heart. It usually coincides with the peripheral pulse and the x descent of the jugular venous waveform. 

Loud S1

 

Causes of Loud S1
Condition	Mechanism
Short P-R interval (0.08-0.12 second)	Valve wide open from recent atrial contraction
Premature beats, tachycardia	Valves wide open from rapid early diastolic filling
Mitral stenosis, tricuspid stenosis, atrial myxoma	Texture of valve; valve maximally open from prolonged ventricular filling
Exercise, fever, anemia, thyrotoxicosis, epinephrine, anxiety, pregnancy, A-V fistula	Forcible ventricular contraction (plus tachycardia)
Thin chest wall, child	Minimal damping effects

Soft S1

The common causes of a soft S1 include weak ventricular contractions, long PR interval, emphysema, obesity, and pericardial effusion.

Split S1

S1 is generated by closure of the mitral and tricuspid valves. These paired left- and right-sided valves do not close at exactly the same time, but the human ear cannot distinguish sounds that are 0.02-0.03 seconds apart as 2 separate sounds. When conditions further delay tricuspid valve closure, a split S1 can be appreciated. One of the most common causes of delayed tricuspid valve closure is a right bundle branch block.

 

Mechanical S1

A mechanical S1 is generated by closure of a prosthetic heart valve (virtually always in the mitral position). It has a “metallic” quality. The presence of a sternotomy scar can provide a clue to the history of valve replacement.

 

Second Heart Sound (S2)

S2 is generated by the closure of the aortic and pulmonic valves, marking the end of systole. It is a high-pitched sound best heard over the base of the heart. It usually coincides with the last third of the upstroke of the v wave of the jugular venous waveform.

Loud S2

The common causes of a loud S2 include high systemic (A2) or pulmonary (P2) pressures and closure of a prosthetic valve (usually in the aortic position). If the S2 is split, try to decipher which component is loudest. A2 should always be louder than P2, except over the pulmonic area where they may be equal. If P2 is louder than A2 anywhere in the chest, pulmonary hypertension should be suspected. Look for other signs of pulmonary hypertension, such as giant a waves in the jugular venous waveform or the presence of a right ventricular heave.

Soft S2

The common causes of a soft S2 include aortic or pulmonic stenosis, emphysema, obesity, and pericardial effusion.

Split S2

S2 is generated by closure of the aortic and pulmonic valves. These paired left- and right-sided valves do not close at exactly the same time, but the human ear cannot distinguish sounds that are 0.02-0.03 seconds apart as 2 separate sounds. When conditions further delay pulmonic valve closure, a split S2 can be appreciated. There are four varieties of S2 splitting: physiologic, persistent, fixed, and paradoxical.

 

 

In the figure above (from Marriott), normal depicts a physiologically split S2, RBBB depicts a persistently split S2, ASD depicts a fixed split S2, and LBBB depicts a paradoxically split S2

Physiologically Split S2

Normally the higher pressure left-sided valves close first (mitral before tricuspid, aortic before pulmonic). This discordance is exaggerated by inspiration, allowing the human ear to perceive two distinct sounds. During inspiration, intrathoracic pressure drops and augments RV filling. As a result, more time is required for the RV to pump the higher volume of blood into the pulmonary artery, thus delaying pulmonic valve closure.

Persistently Split S2

A persistently split S2 describes the presence of a split S2 on expiration that widens further upon inspiration. The most common cause of a persistently split S2 is a right bundle branch block, but it can occur whenever there is prolonged right ventricular ejection, such as outflow obstruction, pulmonary hypertension, or increased RV output.

Fixed Split S2

A fixed split S2 describes the presence of a split S2 that does not vary significantly (<0.01 second) between expiration and inspiration. The classic cause of a fixed split S2 is an atrial septal defect. Other causes include anomalous pulmonary venous return, pulmonic stenosis, ventricular septal defect, mitral regurgitation with RV failure, bundle branch block (either right or left) with RV failure, and cardiomyopathy.

Paradoxically Split S2

A paradoxically split S2 describes the presence of a split S2 during expiration only (the opposite of a physiologically split S2). This is caused by any condition that delays aortic valve closure. During expiration, the aortic valve closes after the pulmonary valve, creating a split. During inspiration, the increase in RV filling causes pulmonic valve closure to become “as delayed as” aortic valve closure, such that the two sounds become single. The most common cause of paradoxically split S2 is a left bundle branch block. Other causes of delayed aortic valve closure include aortic stenosis, systemic hypertension, aortic regurgitation, and LV failure.

 

Mechanical S2

A mechanical S2 is generated by closure of a prosthetic heart valve (usually in the aortic position). It has a “metallic” quality. Mechanical aortic valves can often be heard with the naked ear.

 

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Extra Sounds Near S1

S4 Gallop

Gallop sounds are extra transient sounds that can be heard in certain cardiac conditions during filling of the left ventricle. They are low pitched sounds, and should be listened for with the bell of the stethoscope, not the diaphragm. When using the bell, put just enough pressure to create a seal, but no more than that, otherwise you will convert it into a diaphragm and filter out the low-pitched sounds. Gallops are best heard over the apex of the heart. Sometimes the frequency of a gallop is below the threshold for human hearing (20-100 Hz). In such cases, it may be palpable but not audible.

The S4 occurs in late diastole, just before S1, coinciding with atrial contraction (the a wave in the jugular venous waveform). It is generally present when the heart is so stiff that it is reliant upon a significant amount of filling via atrial contraction. Like the split S1, the S4 gallop is best heard over the apex of the heart. However, unlike the split S1, it is best heard with the bell of the stethoscope because of its low pitch.

• S4s may be heard in conditions that make the heart so stiff that is depends upon vigorous atrial contraction, including longstanding systemic hypertension, diastolic heart failure, and myocardial infarction.
• S4s are NOT heard in atrial fibrillation as the atrium does not contract effectively.

 

It is classically taught that the S3 gallop is associated with dilated/systolic/eccentric heart failure, while the S4 is associated with restrictive/diastolic/concentric heart failure. In our experience, preserved systolic function produced only the S4 gallop, while reduced systolic function can produce either the S3 or the S4 or sometimes both (while listening to the same patient for an extended period of time, we have observed the sound switching from an S4 to an S3 and vice versa).

Ejection Click

An ejection click is an early systolic sound, and occurs during the opening of an abnormal aortic or pulmonic valve (eg, bicuspid aortic valve), or from ejection of blood into a dilated great vessel (aorta or pulmonary artery, such as in pulmonary hypertension). The sound is close to S1 and can sound like an S1 split. However, an ejection click is best appreciated over the aortic and pulmonic valves (base of the heart), as opposed to the split S1 which is best heard toward the apex of the heart. 

 

Tumor Plop

The tumor plop is a high-pitched sound best heard with the diaphragm of the stethoscope. The classic tumor plop originates from an atrial tumor obstructing the mitral orifice, resulting in an early diastolic sound from either 1) tumor tensing, 2) valve obstruction, or 3) tumor impact against the chamber walls. It is often confused for an opening snap. Depending on the anatomic location of the tumor, the tumor plop can sometimes be heard in systole rather than early diastole.

 

Extra Sounds Near S2

S3 Gallop

Gallop sounds are extra transient sounds that can be heard in certain cardiac conditions during filling of the left ventricle. They are low pitched sounds, and should be listened for with the bell of the stethoscope, not the diaphragm. When using the bell, put just enough pressure to create a seal, but no more than that, otherwise you will convert it into a diaphragm and filter out the low-pitched sounds. Gallops are best heard over the apex of the heart. Sometimes the frequency of a gallop is below the threshold for human hearing (20-100 Hz). In such cases, it may be palpable but not audible.

The S3 occurs during the rapid filling phase of early diastole (the y descent of the jugular venous waveform), 0.14-0.22 seconds after S2 (farther from S2 than a widely split S2). Unlike the split S2, the S3 is best heard over the apex of the heart using the bell of the stethoscope.

• S3 gallops may be heard in 3 situations, all characterized by vigorous early ventricular filling:
  • • Young (< age 40) healthy patients with athletic hearts may have what is called a physiologic S3
    • Systolic heart failure
    • Valvular regurgitation and cardiac shunts
• The finding of an S3 has a positive likelihood ratio of 3-4 for a depressed ejection fraction, and the finding in a preoperative patient predicts postoperative pulmonary edema with a likelihood ratio of 14.6.

 

It is classically taught that the S3 gallop is associated with dilated/systolic/eccentric heart failure, while the S4 is associated with restrictive/diastolic/concentric heart failure. In our experience, preserved systolic function produced only the S4 gallop, while reduced systolic function can produce either the S3 or the S4 or sometimes both (while listening to the same patient for an extended period of time, we have observed the sound switching from an S4 to an S3 and vice versa).

Pericardial Knock

The pericardial knock is a loud, high pitched sound in early diastole that occurs in patients with constrictive pericarditis. It is the result of rapid deceleration of blood due to the inelastic pericardium. It occurs farther from S2 than a split S2 and the opening snap of mitral stenosis, but not as far from S2 as an S3. In patients with suspected constrictive pericarditis, try to identify a constellation of supportive physical findings, including Kussmaul’s sign, Friedreich’s sign, the W sign, and the pericardial knock.

Opening Snap

The opening snap is a high-pitched sound in early diastole that occurs in the vast majority of patients with mitral stenosis. It coincides with the opening of the mitral valve. It generally occurs closer to S2 than the pericardial knock and the S3 gallop. It is best heard in the “supramammary area” – just above and slightly to the left of the nipple (or between the apex and the left sternal border).

Tumor Plop

The tumor plop is a high-pitched sound best heard with the diaphragm of the stethoscope. The classic tumor plop originates from an atrial tumor obstructing the mitral orifice, resulting in an early diastolic sound from either 1) tumor tensing, 2) valve obstruction, or 3) tumor impact against the chamber walls. It is often confused for an opening snap. Depending on the anatomic location of the tumor, the tumor plop can sometimes be heard in systole rather than early diastole.

 

Vegetation Plop

The vegetation plop is similar to the tumor plop, but occurs as a result of large vegetation from endocarditis.

 

Mid-to-Late Systolic Click

The mid-to-late systolic click is a high-pitched sound that occurs in patients with mitral valve prolapse. Listen for a plateau-shaped murmur that follows the click. The timing of this sound can be influenced by a variety of maneuvers. Any maneuver that increases left ventricular volume (eg, standing to squatting) will move the click later into systole; any maneuver that decreases left ventricular volume (eg, Valsalva) will move the click earlier into systole.

Summation Gallop

The summation gallop is a loud, lower pitched sound in diastole that occurs under certain circumstances in patients who have both an S3 and an S4. Tachycardia or prolonged P-R interval can cause the timing of the S3 and S4 to be so similar that the two sounds coincide and augment one another.

Sounds with Duration

Murmurs are audible sounds of some duration (not a transient clicking or popping sound) from turbulent blood flow and may reflect pathology of one or more of the valves such as valvular stenosis or regurgitation. When the valves are calcified, scarred, or malformed, impairing blood flow because they don’t open fully, they are said to be stenotic; whereas if they don’t close all the way and cause leakage they are said to be regurgitant or insufficient. Pericardial friction rubs are also considered in this section.

 

Important Characteristics of Murmurs:

 

• Timing
  • In systole the aortic and pulmonic valves are opened, the tricuspid and mitral are closed; so valvular murmurs in systole are from either stenosis of the aortic/pulmonic valves or regurgitation of the mitral/tricuspid valves.
  • If a valve is stenotic, the murmur won’t start right after S1 (if systolic, like AS) or S2 (if diastolic, like MS) because the valve has to open first.
  • If a valve is regurgitant, the murmur can occur right away, as leaky valves leak when there is a pressure gradient across them.
  • Early or late in systole or diastole?
  • Late systolic murmurs are mitral valve prolapse and hypertrophic obstructive cardiomyopathy, both of which are heard when the ventricular volume is lower
  • Late diastolic murmurs are usually caused by mitral stenosis
    • Mitral stenosis cannot start right at S2, as the mitral valve does not open until isovolumetric relaxation has occurred first.
    • In mitral stenosis, the diastolic murmur crescendos right before S1 (“presystolic accentuation”) as a result of increased turbulence from atrial contraction.

 

• Location
  • There are 4 cardinal areas of auscultation: the right upper sternal border (aortic area), left upper sternal border (pulmonic area), left lower sternal border (tricuspid area), and the apex (mitral area). The classic mnemonic “Al Pacino The Man” can help you remember these areas.
  • Note: “Al Pacino The Man” can be helpful, but some murmurs like aortic stenosis or regurgitation can travel widely across the chest (imagine a sash from the right clavicle down to the apex).

 

• Intensity of the Murmur
  • A 6-point scale:
    • 1 = soft murmur, not immediately audible.
    • 2 = audible immediately but quiet.
    • 3 = loud but no thrill palpable.
    • 4 = thrill palpable.
    • 5 = Audible with the edge of the stethoscope (and a thrill).
    • 6 = Audible with the stethoscope off the chest (and a thrill).
  • The intensity of the murmur may correlate with the severity of the valve disease but not always. In severe AS, severe stenosis may cause a soft murmur, and in severe congestive heart failure all heart sounds, even severe valvular disease, may be inaudible.
    • Some use a 4-point scale for diastolic murmurs
    • The intensity of a murmur can be helpful in distinguishing between right- and left-sided lesions. Usually left-sided pressures are significantly higher than right-sided pressures, which means that left-sided murmurs tend to be louder than right-sided murmurs. However, if right-sided pressures are significantly elevated (eg, pulmonary hypertension), then the intensity of a right-sided murmur can match that typical of the left.

• Shape
  • Crescendo/decrescendo (diamond shaped) murmurs are classically from stenosis of the aortic or pulmonic valve.
  • Plateau murmurs are classically from regurgitant valves (mitral, tricuspid) or VSD.

 

• Radiation
  • AS murmurs radiate to the right clavicle or the neck. We prefer to listen over the clavicle because when listening over the neck breath sounds can impair the heart sounds and carotid bruits can sound like murmurs.
  • Mitral regurgitation radiates to the axilla.

 

• Maneuvers
  • Some maneuvers can be helpful such as
    • Inspiration can make right-sided murmurs louder (you are increasing flow to the right side of the heart when you breathe in)
      • This is known as Carvallo’s sign, after Jose Manuel Rivero Carvallo, a Mexican cardiologist who published his findings in 1946.
    • Standing or Valsalva both REDUCE preload, and can make 2 unusual murmurs (mitral valve prolapse and HOCM) louder or longer.
    • Increasing afterload (via isometric hand grip or by using BP cuffs as tourniquets) will make left sided regurgitant murmurs (MR, VSD, AR) louder, while it will make the murmur of AS softer.

 

Systolic Murmurs:

 

Flow Murmur

• Flow murmurs may also be referred to as innocent, physiologic, benign, and systolic flow related.
• They are typically systolic, short, soft (usually <3/6), crescendo-decrescendo in shape (early-peaking), and heard best over the base of the heart.
• Flow murmurs in adults are usually the result of hyperdynamic circulation. An increase in blood flow across a structurally normal valve will cause turbulence and an associated murmur.
  • Common causes of hyperdynamic circulation include anemia, fever, exercise, pregnancy, and sepsis.
• Flow murmurs are not caused by structural abnormalities, do not have any hemodynamic repercussions, and require no further workup.
• Flow murmurs are almost always associated with a well-preserved S2 with normal split. The presence of a diminished or absent S2 should raise concern for pathologic murmur.
• In trying to differentiate a flow murmur from a pathologic one, there is an old medical adage: judge a murmur by the company it keeps. Murmurs that are associated with symptoms, extra transient sounds, thrills, or other abnormalities (eg, abnormal EKG) should be considered pathologic until proven otherwise.

Aortic Stenosis

• One of the most common murmurs, especially in the older population.
• An important cause of syncope, CHF and death.
• Murmur is systolic, crescendo-decrescendo in shape.
• Harsh in quality.
• Located in the sash distribution (clavicle to apex).
• Radiates to clavicle or neck.
• Causes are usually calcification in older (age > 50) patients, congenital bicuspid valve in younger (age < 50).
• If the etiology is a bicuspid valve you may hear an ejection click shortly after S1 (attributed to the abnormal valve opening).
• Pulses weak and delayed (pulsus parvus et tardus).
• Murmur is louder after a long pause, as after a premature ventricular contraction.
• Delayed pulse distally compared to proximally. Normally, if you palpate the brachial artery and radial artery the pulses occur simultaneously; in patients with aortic stenosis, you may be able to detect a palpable delay between the two. In this paper, a palpable delay was felt in all patients with severe AS, and rarely felt in patients without severe AS.

 

Pulmonic Stenosis

• Pulmonic stenosis is virtually always congenital. However, it may occur as a result of acquired conditions such as rheumatic disease and carcinoid syndrome.
• The systolic murmur of pulmonic stenosis is best heard over the left upper sternal border, is crescendo-decrescendo in shape, and radiates to the neck, left shoulder, and back.
• With increasing severity, the murmur peaks later and lasts longer.
• Like all right-sided murmurs, it augments with inspiration (Carvallo’s sign). Most patients with pulmonic stenosis have an associated ejection click, best heard over the left upper sternal border. Unlike all other sounds originating from the right-side of the heart, the pulmonic ejection click becomes quieter with inspiration. 
• Patients with pulmonic stenosis usually have an abnormally widely split S2.
• Also look for giant a waves in the jugular venous waveform.

 

Mitral Regurgitation

• On inspection, patients may have a visible and palpable heave.
• Blood from high pressure LV ejected into low pressure LA may lift up chest wall in systole.
• PMI may be inferiorly and laterally displaced.
• S3 may be heard and felt, often mistaken for S2.
• Pulses are strong, not weak, so long as EF is normal.
• The MR Murmur:
• Classically holosystolic (from S1 all the way to S2), plateau-shaped.
• AS cannot be holosystolic as the aortic valve does not open with S1, there is a slight pause for isovolumetric contraction.
  • Murmur has more of a blowing, musical quality compared to AS.
  • Louder with increased afterload (hand grip or BP cuffs).
  • Loudest at the apex, radiates to the axilla (except in isolated posterior leaflet MR, where it radiates anteriorly to the tricuspid area).

 

Mitral Valve Prolapse

• Mitral valve prolapse is a variant of MR in which some part of the mitral apparatus is too long, so that the valve does not function well at low volumes. At higher volumes, the valve leaflet may coapt normally. At low volumes, the leaflet may prolapse into the atrium during mid-to-late systole, causing a click or murmur or both.
• On examination, patients with mitral valve prolapse may have a click, a mid-to-late systolic murmur, or both.
• As with HOCM, under filling the heart leads to prolapse earlier in systole, so standing from squatting makes the murmur louder and longer.
• Unlike HOCM, Valsalva does not make the murmur louder, but it does make the click move earlier and the murmur is longer.
• Sometimes mitral valve prolapse causes a “honk” murmur (like the cry of a goose).

 

Tricuspid Regurgitation

• Tricuspid regurgitation is a fairly common lesion in the 21^st century, likely due to the large number of patients who are surviving longer after bouts of endocarditis, pulmonary hypertension, severe left heart disease, etc.
• The murmur is usually soft, heard along the lower left sternal border, and gets louder with inspiration (Carvallo’s sign).
• Tricuspid murmurs are quiet unless pulmonary hypertension is present as RV pressure is normally low.
• The jugular venous waveform in TR demonstrates CV fusion (Lancisi’s sign).
  • The CV fusion wave is so strong it is often confused with carotid artery pulsations.
• Palpable pulsations may be felt in the liver (pulsatile liver).

 

Hypertrophic Obstructive Cardiomyopathy (HOCM)

• Hypertrophic obstructive cardiomyopathy (HOCM) is a condition in which a portion of the myocardium is hypertrophied.
• Patients may develop dynamic aortic outflow obstruction due to narrowing of the outflow tract from septal hypertrophy.
• This can cause turbulent flow in the subaortic area and can also create the Venturi effect, which sucks the anterior leaflet of the mitral valve anteriorly causing mitral regurgitation.
• The HOCM murmur is louder when the ventricular volume is low, as the outflow tract is narrower, so you can make this murmur louder by having the patient Valsalva or go from squatting to standing.
  • In this classic paper, Valsalva increased the murmur of HOCM 65% of the time, and an increase in murmur with Valsalva had a specificity of 96% for HOCM.
• The murmur will become softer by increasing preload, such as with squatting or passive leg raise.

 

Ventricular Septal Defect

• The VSD murmur is classically a holosystolic murmur similar to mitral regurgitation but located along the lower left sternal border, often with a palpable thrill.
• Flow is left to right (as pressure is higher on the left) but over time this can lead to pulmonary hypertension and reversal of flow, called Eisenmenger’s syndrome.
• We have observed a “reverse Carvallo’s sign” phenomenon, whereby the intensity of the murmur lessens during inspiration. We have reasoned that this occurs because the left –> right pressure gradient lessens during inspiration as a result of increased RV blood flow.

 

Diastolic Murmurs:

Aortic Regurgitation

• Soft, decrescendo murmur that starts right at S2 and trails off (turbulence is highest in early diastole when the pressure gradient between the aorta and LV is highest).
• Also can be associated with a systolic flow murmur, due to an increase in blood flow across the aortic valve.
• Murmur may be best heard with the patient leaning forward, holding their breath after a full exhalation.
• This murmur is classically associated with a wide pulse pressure, due to the larger than normal cardiac output (blood coming from both the left atrium and the blood leaking back from the aorta). The diastolic pressure is lower as blood is running off in both directions, and the vasculature peripherally is open to accommodate the increased forward flow (autoregulation). This causes the classic water hammer pulse, which can be felt in the radial pulse, and the Corrigan’s pulse (a large, bounding carotid pulse).
• There are numerous eponyms (signs named after physicians or patients) in aortic regurgitation as various parts of the body may bob and move.
  • De Musset’s sign.
    • Forward and back head bob
  • Traube’s sign.
    • Pistol shot sounds heard on auscultation over arterial pulse.
  • Quincke’s pulse.
    • Pulsation of nail beds.
  • Lighthouse sign.
    • Blanching/flushing of forehead.
  • Duroziez’s sign.
    • Femoral artery compression with diaphragm of stethoscope causing systolic and diastolic murmurs.
  • Muller’s sign.
    • Bobbing of the uvula.
• Austin Flint murmur – Aortic Regurgitation any be associated with a low-pitched, “blubbering”, mid-to-late diastolic murmur heard over the apex, known as the Austin Flint murmur. The mechanism is thought to be distortion and early closure of the anterior leaflet of the mitral valve caused by the regurgitant aortic jet, resulting in functional mitral stenosis.

 

Pulmonic Regurgitation

• There are a variety of causes of pulmonic regurgitation, including pulmonary hypertension (so-called Graham-Steell murmur), infective endocarditis, and congenital abnormalities of the cusps (eg, bicuspid valve).
• The diastolic murmur of pulmonic regurgitation is similar in quality to aortic regurgitation in that it is early and decrescendo. It is best heard in the left upper sternal border, but like AR, may be loudest over the 4^th intercostal space. Unlike AR, the intensity increases with inspiration (Carvallo’s sign).
• Associated findings include pulmonary artery pulsation, pulmonic ejection click, and an ejection murmur, all of which are best appreciated over the left upper sternal border.

Mitral Stenosis

• Mitral stenosis is a rare but potentially catastrophic condition.
• Like aortic regurgitation, it is a diastolic murmur, but sounds much different.
  • Aortic regurgitation starts right after S2, is soft, decrescendo.
  • Mitral stenosis starts after a pause, when the mitral valve snaps open, and is low pitched, rumbling, with presystolic accentuation.
• Most cases are from the sequelae of rheumatic fever, so rarely seen in the US except in patients raised in other countries.
• Time from episode of rheumatic fever to onset of symptoms is about 15 years.
• Symptoms are from obstruction of the left atrium, leading to elevated LA pressure, pulmonary hypertension and elevated right heart pressures.
• Atrial fibrillation, embolic disease, SOB, hemoptysis are classic symptoms.
• The hallmarks of the examination are a loud S1 (from the thickened mitral valve closing under high pressure), quiet systole, a high pitched opening snap (loud opening of the mitral valve, after S2) and a low pitched, rumbling, diastolic murmur after the opening snap that continues through diastole and gets louder (presystolic accentuation) just before S1 due to atrial contraction best heard with the bell at the apex.

 

Tricuspid Stenosis

• Tricuspid stenosis was historically caused by rheumatic heart disease, virtually always in association with mitral stenosis and/or aortic stenosis. However, in our modern-day experience, we have observed this valvular lesion far more often in patients with bioprosthetic tricuspid valves.
• The diastolic murmur is similar in quality to mitral stenosis, but is best heard over the left lower sternal border, or between the left lower sternal border and the apex. It also becomes louder with inspiration (Carvallo’s sign).
• Associated findings include a giant a wave in the jugular venous waveform (accentuated with inspiration), as well as a diminished y descent.

 

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View Lecture On Valvular Heart Disease

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Other

Pericardial Friction Rub

• A pericardial friction rub is the sound that is generated as a result of an inflamed pericardium.
• Rubs consist of one to three sounds that may be mistaken for murmurs. However, the quality of the sound(s) is different and distinctive, often scratchy or creaky.
• Classically there are three components to a pericardial rub that correlate with atrial contraction (so you may hear it just before S1), during ventricular systole (between S1 and S2) and during the rapid filling phase of diastole (right after S2).
• A rub is diagnosed exclusively through physical examination.

Starr-Edwards Prosthetic Valve

• The old “ball-in-cage” prosthetic valve was designed by Albert Starr and Lowell Edwards and implanted into a patient for the first time in 1960.
• Look here for an image of the structure of the valve: https://www.nejm.org/doi/full/10.1056/NEJMicm071210
• The design of the prosthetic valve is unique in that increased pressure either forces the ball to descend to the base of the cage (“closed” position) or ascend inside the cage, exposing the hollow walls of the cage and allowing for blood to flow through (“open”) position.
• When blood flows through the valve it causes the ball to “rattle” at the top of the cage, creating a unique sound.
• The Starr-Edwards “rattle” is listed in the category of continuous sounds, but in reality it is made up of several transient sounds.

Venous Hum

• Often heard in children.
• Etiology is thought to be compression of the internal jugular vein by the transverse process of the atlas.
• The sound is continuous, loudest in diastole.
• Best heard in the neck, in the anterior triangle, on the right side.
• Louder when the patient is upright, inspires, or turns away from the stethoscope (to the left).
• Quieter when lying down or by turning the head towards the stethoscope or with light pressure on the internal jugular vein.
• It can also be heard in adults with high output states, and is of no clinical significance except that it can be mistaken for a PDA or AV fistula.

Caverno-Carotid Fistula

Carotid-cavernous fistula describes the abnormal communication between the carotid artery and the cavernous sinus. It is most often a complication from head trauma resulting in a basilar skull fracture. A continuous bruit can often be auscultated over the patient’s temple.

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Precordial Movement

• Inspect and palpate the precordium with the patient in a supine position.
• Can you see and feel the apical impulse (also known as the apex beat, and often used synonymously with the point of maximum impulse, or PMI)? As the name suggests, it is an outward pulsation in the cardiac apex.

• • It cannot be seen and felt in all patients, but if you do detect it, it should be around the 5^th  intercostal space (located between the 5^th and 6^th ribs) on the left  in the midclavicular line (an imaginary line running down the chest from the center of the clavicle) and it should be about the size of a quarter (2.5 cm) – an apical impulse further inferior or lateral suggest cardiac enlargement.
  • In the left lateral decubitus position the apical impulse may be more easily palpated and the size assessed and will feel larger – apical impulses > 4cm suggest cardiac dilation. This is a difficult exam – do not worry if you cannot feel the PMI in most patients, keep trying (especially in young, thin patients).

• There are other visible or palpable impulses (known as heaves/lifts). These may be from a variety of causes such as valvular regurgitation, pressure overload, or cardiac aneurysms.
• Feel over the valve areas for thrills, which are vibratory sensations (they feel like the purring of a cat). Ask your dialysis patients if you can feel the skin overlying their fistula, and you will feel a prominent thrill. The presence of a thrill signifies that a murmur is at least a grade 4 out of 6.

 

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Peripheral Pulses

Carotid Pulse

At the bedside, the carotid pulse should be inspected and palpated. It can be useful in timing cardiac events. Abnormalities of the carotid pulse can provide clues to a diagnosis. For example, an abnormally vigorous carotid pulse can be suggestive of aortic regurgitation or aortic coarctation. A dampened and prolonged carotid pulse can be suggestive of aortic stenosis.

Brisk carotid upstroke in aortic coarctation

Coarctation of the aorta is a common congenital condition, accounting for 7% of all congenital heart lesions. An augmented carotid pulse – “carotid swell” – can be a clue to the diagnosis. A sustained systolic arterial wave can be visualized in the suprasternal fossa; it travels outwards along the subclavian arteries and up the carotids, where it is most easily observed.

Pulsus bisferiens

Pulsus bisferiens describes the presence of an exaggerated “double pulsation” in the arterial pulse. While the arterial pulse is normally dicrotic, consisting of a percussion wave and a tidal wave, the individual waves are not typically visible or palpable at the bedside. The pulse looks and feels like a single wave. When the two waves are discernable at the bedside, it is known as pulsus bisferiens. It is most often associated with the combination of aortic stenosis and aortic regurgitation, but is sometimes seen in patients with pure aortic regurgitation.

 

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Other

Superior Vena Cava

Superior vena cava (SVC) syndrome occurs when obstruction of the SVC results in impaired cardiac filling, giving rise to a constellation of characteristic symptoms and signs. Dyspnea is one of the most frequent symptoms; orthopnea occurs in around one-half of patients. Distended neck veins, distended superficial chest veins, and edema of the face, neck, and arms are among the most common signs.

 

Frank’s Sign

Diagonal earlobe crease, associated with coronary artery disease.

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Sources and Further Reading

• Jonathan Larson: A diagnosis too late
• Leier, C. V. (2010). “Examining the jugular vein is never in vain.” Circ Heart Fail 3(2): 175-177.
• Merideth, J. and R. D. Pruitt (1973). “Cardiac arrhythmias. 5. Disturbances in cardiac conduction and their management.” Circulation 47(5): 1098-1107.
• Briscoe, C. E. (1973). “A comparison of jugular and central venous pressure measurements during anaesthesia.” Br J Anaesth 45(2): 173-178
• Seth, R., et al. (2002). “How far is the sternal angle from the mid-right atrium?” J Gen Intern Med17(11): 852-856
• Leier, C. V. and K. Chatterjee (2007). “The physical examination in heart failure–Part I.” Congest Heart Fail 13(1): 41-47.
• Salvatore Mangione. Physical Diagnosis Secrets. 2nd Edition. Mosby, 2008
• Devine, P. J., et al. (2007). “Jugular venous pulse: window into the right heart.” South Med J 100(10): 1022-1027; quiz 1004.
• Mansoor, A. M. and S. P. Karlapudi (2015). “Images in clinical medicine. Kussmaul’s sign.” N Engl J Med372(2): e3.
• Burgess, T. E. and A. M. Mansoor (2017). “Giant a waves.” BMJ Case Rep 2017.
• Mansoor, A. M. and S. E. Mansoor (2016). “IMAGES IN CLINICAL MEDICINE. Lancisi’s Sign.” N Engl J Med 374(2): e2.
• Devine PJ, Sullenberger LE, Bellin DA, Atwood JE. Jugular venous pulse: window into the right heart. South Med J. 2007;100(10):1022-7; quiz 04.
• Mangione S. Physical Diagnosis SECRETS. Second ed. Philadelphia, PA: Elsevier; 2008. 702 p.
• Mansoor AM, Mansoor SE. IMAGES IN CLINICAL MEDICINE. Lancisi’s Sign. N Engl J Med. 2016;374(2):e2
• Pittenger B, Sullivan PD, Mansoor AM. Friedreich’s sign. BMJ Case Rep. 2018;2018.
• Mansoor AM, Karlapudi SP. Images in clinical medicine. Kussmaul’s sign. N Engl J Med. 2015;372(2):e3
• Marriott HJL. Bedside Cardiac Diagnosis. Philadelphia, PA: Lippincott Company; 1993.
• Oehler AC, Sullivan PD, Mansoor AM. Mitral stenosis. BMJ Case Rep. 2017;2017
• Burgess, et al. Pericardial Knock. BMJ Case Rep. 2019;2019.
• Cleland WP, et al. Coarctation of the aorta. Br Med J 1956;2:379.
• Cheng S. Superior vena cava syndrome: a contemporary review of a historic disease. Cardiol Rev. 2009;17(1):16-23.
• Sharma, I., et al (2019). “Jugular venous pulse in constrictive pericarditis.” BMJ Case Rep 2020.
• Mansoor AM, Mansoor SE. Images in clinical medicine. Quincke’s pulse. N Engl J Med. 2013;369(7):e8.