Gabriel Habib, Sr., M.S., M.D., F.A.C.C., F.C.C.P., F.A.H.A.
Her blood pressure was on the low side. I felt her pulse in the carotid artery in her neck; it was weak, difficult to detect. Unlike the usual thumping carotid artery, her pulse rose only reluctantly to the examining finger. At the base of her neck, on the chest wall, there was an easily felt shudder, a rough vibration with each pulse, like a cat’s purr. When I listened to her heart, . . . I heard a gruff,
harsh sound like the clearing of a throat. . . . It was no great Oslerian feat of diagnosis on my part to suspect that she had severe aortic stenosis.
harsh sound like the clearing of a throat. . . . It was no great Oslerian feat of diagnosis on my part to suspect that she had severe aortic stenosis.
John Stone (1936–2008)
“The Long House Calls” from
In the Country of Hearts: Journeys in the Art of Medicine, 1990
PHYSICAL EXAMINATION
1. Explain normal splitting of the second heart sound (S2).
S2 is normally split into aortic (A2) and pulmonic (P2) components caused by the closing of the two respective valves. The degree of splitting varies with the respiratory cycle or physiologic splitting. With inspiration, the negative intrathoracic pressure leads to increased venous return to the right side of the heart and a decrease to the left side. The increased venous return to the right atrium (RA) causes P2 to occur slightly later and A2 to occur slightly earlier, leading to a widening of the S2 split. With expiration, the negative intrathoracic pressure is eliminated and A2 and P2 occur almost simultaneously. The largest contributor
to the physiologic third heart sound (S3) split is the respiratory variation in the timing of
the pulmonic closure sound.
to the physiologic third heart sound (S3) split is the respiratory variation in the timing of
the pulmonic closure sound.
2. What is paradoxical splitting of (S2) ?
A widening of the split of A2 and P2 with expiration and shortening of the split with inspiration
(the opposite of normal).
(the opposite of normal).
3. What causes paradoxical splitting of S2?
It is usually seen with aortic insufficiency, aortic stenosis, and hypertrophic cardiomyopathy (HCM). In paradoxical splitting, P2 precedes A2 during expiration and is usually due to conditions that delay A2 by delaying ejection of blood from the left ventricle (LV) and, therefore, aortic valve closure. Causes include HCM, myocardial infarction (MI), left bundle branch block (LBBB), and a right ventricular (RV) pacemaker.
It is usually seen with aortic insufficiency, aortic stenosis, and hypertrophic cardiomyopathy (HCM). In paradoxical splitting, P2 precedes A2 during expiration and is usually due to conditions that delay A2 by delaying ejection of blood from the left ventricle (LV) and, therefore, aortic valve closure. Causes include HCM, myocardial infarction (MI), left bundle branch block (LBBB), and a right ventricular (RV) pacemaker.
4. What causes fixed and wide splitting of S2?
Atrial septal defects (ASDs), RV dysfunction, or both, resulting in an interval between A2 and P2 that is wider than normal and does not change with the respiratory cycle. The wide and fixed S2 split occurs because:
Atrial septal defects (ASDs), RV dysfunction, or both, resulting in an interval between A2 and P2 that is wider than normal and does not change with the respiratory cycle. The wide and fixed S2 split occurs because:
- A2–P2 is wider than normal owing to shunting of blood from the left atrium (LA) to the RA, resulting in a greater RV filling and a resulting delay in the timing of the pulmonic closure sound P2; and,
- A2–P2 splitting is fixed and does not increase with inspiration. The fixed splitting occurs because the extra filling of the RV that normally occurs during inspiration is small relative to the above-described increase in RV filling due to interatrial shunting and thus does not significantly delay P2.
5. Explain the significance of a loud P2.
It usually indicates the presence of pulmonary hypertension (HTN), whether primary or secondary to chronic pulmonary disease.
It usually indicates the presence of pulmonary hypertension (HTN), whether primary or secondary to chronic pulmonary disease.
6. What is S3?
A low-frequency sound heard just after S2; also called a “ventricular gallop.”
7. What is a physiologic S3?
An S3 found in young patients without cardiac disease.
8. How is S3 best heard?
With the stethoscope bell. Unlike a physiologically split A2–P2, the A2–S3 interval does not change during respiration. Associated physical findings of congestive heart failure (CHF), such as pulmonary rales, distended neck veins, or edema are usually present along with an S3.
9. What is a pathologic S3?
An S3 occurring in a variety of pathologic conditions including CHF, mitral valve prolapse (MVP), thyrotoxicosis, coronary artery disease (CAD), cardiomyopathies, pericardial constriction, mitral or aortic insufficiency, and left-to-right shunts.
10. Describe the mechanism behind an S3.
The mechanism behind an S3 is controversial, but it may be due to an increase in the velocity of blood entering the ventricles (rapid ventricular filling). When present, an S3 usually represents myocardial decompensation associated with heart disease.
The mechanism behind an S3 is controversial, but it may be due to an increase in the velocity of blood entering the ventricles (rapid ventricular filling). When present, an S3 usually represents myocardial decompensation associated with heart disease.
11. What is the fourth heart sound (S4)?
A sound occurring just before S1; also called an “atrial gallop.” An S4 reflects decreased ventricular compliance (a stiff ventricle) and is associated with CAD, pulmonic or aortic valvular stenosis, HTN, and ventricular hypertrophy from any cause.
A sound occurring just before S1; also called an “atrial gallop.” An S4 reflects decreased ventricular compliance (a stiff ventricle) and is associated with CAD, pulmonic or aortic valvular stenosis, HTN, and ventricular hypertrophy from any cause.
12. What is an opening snap (OS)?
A high-frequency early diastolic sound associated with mitral or tricuspid valve opening.
A diastolic rumble at the apex confirms the physical diagnosis of mitral stenosis.
13. Summarize the pathophysiology and significance of an OS in patients with mitral stenosis.
An OS is typically present only when the mitral valve leaflets are pliable, and it is, therefore, usually accompanied by an accentuated first heart sound (S1). Diffuse calcification of the mitral valve can be expected when an OS is absent. If calcification is confined to the tip of the mitral valve, an OS is still commonly present. The interval between the aortic closure sound and the OS (A2–OS) is inversely related to the mean LA pressure. A short A2–OS interval is a reliable indicator of severe mitral stenosis; however, the converse is not necessarily true.
An OS is typically present only when the mitral valve leaflets are pliable, and it is, therefore, usually accompanied by an accentuated first heart sound (S1). Diffuse calcification of the mitral valve can be expected when an OS is absent. If calcification is confined to the tip of the mitral valve, an OS is still commonly present. The interval between the aortic closure sound and the OS (A2–OS) is inversely related to the mean LA pressure. A short A2–OS interval is a reliable indicator of severe mitral stenosis; however, the converse is not necessarily true.
14. What is the differential diagnosis of an abnormal early diastolic sound heard at the apex and lower left sternal border?
& Loud P2
& S3 gallop
& Loud P2
& S3 gallop
& OS
& Pericardial knock
& Tumor plop (atrial myxoma)
An early diastolic sound may be due to wide splitting of S2, with or without a loud pulmonic closure sound. An ASD causes wide and fixed splitting of S2.
& Pericardial knock
& Tumor plop (atrial myxoma)
An early diastolic sound may be due to wide splitting of S2, with or without a loud pulmonic closure sound. An ASD causes wide and fixed splitting of S2.
15. What causes a pericardial knock?
The sudden slowing of LV filling in early diastole associated with the restriction of a rigid pericardium acting as a “rigid shell” such as in chronic constrictive pericarditis.
The sudden slowing of LV filling in early diastole associated with the restriction of a rigid pericardium acting as a “rigid shell” such as in chronic constrictive pericarditis.
16. What is a tumor plop?
The sound heard with cardiac auscultation caused by obstruction of blood flow by an atrial myxoma protruding through the mitral valve during diastole leading to sudden cessation of LV filling. Cardiac auscultation in various positions helps to detect a tumor plop; likewise, cardiac symptoms in these patients are often related to body position.
The sound heard with cardiac auscultation caused by obstruction of blood flow by an atrial myxoma protruding through the mitral valve during diastole leading to sudden cessation of LV filling. Cardiac auscultation in various positions helps to detect a tumor plop; likewise, cardiac symptoms in these patients are often related to body position.
17. What is a hyperdynamic precordial impulse?
A thrust of exaggerated height that falls away immediately from the palpating fingers and is typically found in patients with a large stroke volume. The clinical conditions with a large stroke volume include thyrotoxicosis, anemia, beriberi, atrioventricular (AV) shunts or grafts, exercise, or mitral regurgitation (MR). (Stroke volume is the amount of blood ejected with each contraction.) A hyperdynamic precordial impulse should be differentiated from the sustained apical impulse, a graphic equivalent of a heave, detected in the presence of LV hypertrophy due to HTN or aortic stenosis.
A thrust of exaggerated height that falls away immediately from the palpating fingers and is typically found in patients with a large stroke volume. The clinical conditions with a large stroke volume include thyrotoxicosis, anemia, beriberi, atrioventricular (AV) shunts or grafts, exercise, or mitral regurgitation (MR). (Stroke volume is the amount of blood ejected with each contraction.) A hyperdynamic precordial impulse should be differentiated from the sustained apical impulse, a graphic equivalent of a heave, detected in the presence of LV hypertrophy due to HTN or aortic stenosis.
18. What are the classifications of and physical findings associated with heart murmurs?
See Table 4-1. Systolic murmurs are classified from grade 1 to grade 6. Diastolic murmurs are classified from grade 1 to grade 4. Murmurs rarely exceed grade 4. Systolic murmurs grade 3 or greater are more likely to be clinically significant.
19. What is the likely cause of a systolic ejection murmur, best heard at the second right intercostal space, in an 82-year-old asymptomatic man?
Aortic sclerosis, not aortic stenosis. Aortic sclerosis is characterized by thickening and/or calcification of the aortic valve and, unlike valvular aortic stenosis, is typically not associated with any significant transvalvular systolic pressure gradient.
Aortic sclerosis, not aortic stenosis. Aortic sclerosis is characterized by thickening and/or calcification of the aortic valve and, unlike valvular aortic stenosis, is typically not associated with any significant transvalvular systolic pressure gradient.
20. How is aortic stenosis differentiated from aortic sclerosis by physical examination?
The following clinical findings are present in patients with aortic stenosis but absent with aortic sclerosis:
& Diminished carotid arterial upstroke (i.e., the rate of rise of the carotid pulse is less steep)
& Diminished peripheral arterial pulses (a finding consistent with moderate-to-severe aortic stenosis)
& Late peaking of systolic murmur (as aortic stenosis worsens in severity, the systolic murmur peak becomes more delayed)
& Loud or audible (or both) S4
& Syncope, angina, or heart failure signs or symptoms
& Loud systolic murmur associated with a systolic thrill
21. How do standing, squatting, and leg-raising affect the intensity and duration of the systolic murmur heard on dynamic auscultation in a patient with HCM?
Standing increases the murmur intensity, and leg-raising and squatting decrease the murmur intensity. In HCM, a decrease in the size of the LV increases the dynamic LV outflow obstruction, leading to an increased intensity of the murmur. A decrease in LV volume occurs on standing. In contrast, leg-raising and squatting increase venous return and thereby increase LV volume, decreasing the dynamic LV obstruction and the murmur intensity.
22. What are the physical examination findings in MR?
& An apical holosystolic murmur with variation of intensity and radiation depending on the cause and severity of the MR
& S3
& Quick upstroke and short duration of peripheral pulses
& Widened pulse pressure
& Hyperdynamic precordium
22. What are the physical examination findings in MR?
& An apical holosystolic murmur with variation of intensity and radiation depending on the cause and severity of the MR
& S3
& Quick upstroke and short duration of peripheral pulses
& Widened pulse pressure
& Hyperdynamic precordium
23. List the peripheral arterial signs of chronic aortic regurgitation (AR).
& de Musset’s sign: bobbing of the head with each heartbeat
& Corrigan’s pulse: abrupt distention and quick collapse of femoral pulses (also called “water-hammer pulse”)
& Traube’s sign: booming, “pistol-shot” systolic and diastolic sounds heard over the femoral pulse
& Muller’s sign: systolic pulsations of the uvula
& Duroziez’s sign: systolic murmur over the femoral artery when compressed proximally and diastolic murmur when compressed distally
& Quincke’s sign: capillary pulsations of the fingertips
& Hill’s sign: popliteal cuff systolic pressure exceeding brachial cuff pressure by > 60 mmHg
24. How do you measure the jugular venous pulse (JVP) as an estimate of central venous pressure (CVP) at the bedside?
& Elevate the head of the bed until the patient’s chest is at the point at which the venous
pulsations are maximally visualized (usually 30–45°).
& Measure the height of this oscillating venous column above the sternal angle (angle of Louis) (Fig. 4-1).
& Estimate the CVP by adding 5 cm to the measurement.
The sternal angle is about 5 cm from the RA regardless of the elevation angle.
Normal CVP is 5–9 cmH2O.
25. Name the three waves composing the JVP.
& A wave: produced by RA contraction, occurring just before S1
& C wave: caused by bulging upward of the closed tricuspid valve during RV contraction (often difficult to see)
& V wave: caused by RA filling just before opening of the tricuspid valve
26. What are “cannon” A waves?
Very large and prominent A waves occurring when the atria contract against a closed tricuspid valve. Irregular “cannon” A waves are seen in AV dissociation or ectopic atrial beats.
Regular “cannon” A waves are seen in a junctional or ventricular rhythm in which the atria are depolarized by retrograde conduction.
27. Define “pulsus paradoxus.”
A decrease of > 10 mmHg in the systolic blood pressure (BP) during normal inspiration, first described by Adolf Kussmaul in 1873. Kussmaul originally described the disappearance of the pulse during inspiration, though.
28. Describe the mechanism of a pulsus paradoxus.
Pulsus paradoxus can occur when the fall in intrathoracic pressure during inspiration is rapidly transmitted through a pericardial effusion, resulting in an exaggerated increase in venous return to the right side of the heart. The increased venous return causes bulging of the interventricular septum toward the LV, resulting in a smaller LV volume and a smaller LV stroke volume. The decreased LV stroke volume results in a lower cardiac output and lower systolic BP during inspiration. A drop in systolic BP is a normal physiologic finding as long as this drop does not exceed 10 mmHg. In contrast, an exaggerated drop in systolic BP> 10 mmHg is a pathologic finding characteristic of cardiac tamponade.
29. What medical diseases present with pulsus paradoxus?
& Cardiac tamponade (classic finding but may be absent with severe volume contraction, dehydration, or hypotension)
& Severe chronic obstructive pulmonary disease (COPD)
& Chronic constrictive pericarditis (very rarely)
30. Describe the Y descent of the JVP waveform tracing in chronic constrictive pericarditis.
The Y descent of the JVP waveform tracing corresponds to the rapid early RA emptying phase or the rapid early ventricular filling phase. In patients with chronic constrictive pericarditis, early ventricular filling is unimpeded. During the very early filling, the RV is very small and its filling is enhanced by the sudden “pouring” of blood as the tricuspid valve opens. During this early filling phase, the ventricle is too small and has not yet “perceived” the constricting effect of the calcified or thickened pericardium and, thus, filling is unimpeded. Once the ventricle meets the thick or calcified “noncompliant” pericardium, ventricular filling suddenly slows and corresponds to the “pericardial knock” sound. Although found in chronic constrictive pericarditis, the steep Y descent rarely occurs in cardiac tamponade. At the same time that the steep Y descent occurs, the RV early filling occurs and there is a “dip” or sudden decrease in RV pressure. Once the ventricular filling is suddenly slowed or halted by the thick or calcified noncompliant pericardium, the RV pressure rises to a plateau. The “dip-and-plateau” RV pressure waveform, just like the steep Y descent of the RA pressure waveform, is a distinctive finding in chronic constrictive pericarditis and helps to differentiate chronic constrictive pericarditis from cardiac tamponade.
31. What is cardiac tamponade?
The sudden accumulation of fluid within the pericardial sac under pressure. When the clinical triad of cardiac tamponade was first described by Claude Beck in 1935, he noted hypotension, elevated systemic venous pressure, and a small, quiet heart. The condition was commonly due to penetrating cardiac injuries, aortic dissection, or intrapericardial rupture of an aortic or cardiac aneurysm. Today, the most common causes are neoplastic disease, idiopathic pericarditis, acute MI, and uremia.
32. Summarize the physical examination findings in cardiac tamponade.
& Jugular venous distention: Almost universally present except in patients with severe hypovolemia.
& Pulsus paradoxus: Defined as a decrease in systolic BP > 10 mmHg during quiet inspiration. Pulsus paradoxus is difficult to elicit in volume-depleted patients.
& Tachycardia with a thready peripheral pulse: Sometimes severe cardiac tamponade may restrict LV and RV filling enough to cause hypotension, but a thready and rapid pulse is almost invariably present.
33. What is Kussmaul’s sign?
An inspiratory increase in systemic venous pressure commonly present in chronic constrictive pericarditis but rarely detected in acute cardiac tamponade.
The following clinical findings are present in patients with aortic stenosis but absent with aortic sclerosis:
& Diminished carotid arterial upstroke (i.e., the rate of rise of the carotid pulse is less steep)
& Diminished peripheral arterial pulses (a finding consistent with moderate-to-severe aortic stenosis)
& Late peaking of systolic murmur (as aortic stenosis worsens in severity, the systolic murmur peak becomes more delayed)
& Loud or audible (or both) S4
& Syncope, angina, or heart failure signs or symptoms
& Loud systolic murmur associated with a systolic thrill
21. How do standing, squatting, and leg-raising affect the intensity and duration of the systolic murmur heard on dynamic auscultation in a patient with HCM?
Standing increases the murmur intensity, and leg-raising and squatting decrease the murmur intensity. In HCM, a decrease in the size of the LV increases the dynamic LV outflow obstruction, leading to an increased intensity of the murmur. A decrease in LV volume occurs on standing. In contrast, leg-raising and squatting increase venous return and thereby increase LV volume, decreasing the dynamic LV obstruction and the murmur intensity.
22. What are the physical examination findings in MR?
& An apical holosystolic murmur with variation of intensity and radiation depending on the cause and severity of the MR
& S3
& Quick upstroke and short duration of peripheral pulses
& Widened pulse pressure
& Hyperdynamic precordium
22. What are the physical examination findings in MR?
& An apical holosystolic murmur with variation of intensity and radiation depending on the cause and severity of the MR
& S3
& Quick upstroke and short duration of peripheral pulses
& Widened pulse pressure
& Hyperdynamic precordium
23. List the peripheral arterial signs of chronic aortic regurgitation (AR).
& de Musset’s sign: bobbing of the head with each heartbeat
& Corrigan’s pulse: abrupt distention and quick collapse of femoral pulses (also called “water-hammer pulse”)
& Traube’s sign: booming, “pistol-shot” systolic and diastolic sounds heard over the femoral pulse
& Muller’s sign: systolic pulsations of the uvula
& Duroziez’s sign: systolic murmur over the femoral artery when compressed proximally and diastolic murmur when compressed distally
& Quincke’s sign: capillary pulsations of the fingertips
& Hill’s sign: popliteal cuff systolic pressure exceeding brachial cuff pressure by > 60 mmHg
24. How do you measure the jugular venous pulse (JVP) as an estimate of central venous pressure (CVP) at the bedside?
& Elevate the head of the bed until the patient’s chest is at the point at which the venous
pulsations are maximally visualized (usually 30–45°).
& Measure the height of this oscillating venous column above the sternal angle (angle of Louis) (Fig. 4-1).
& Estimate the CVP by adding 5 cm to the measurement.
The sternal angle is about 5 cm from the RA regardless of the elevation angle.
Normal CVP is 5–9 cmH2O.
25. Name the three waves composing the JVP.
& A wave: produced by RA contraction, occurring just before S1
& C wave: caused by bulging upward of the closed tricuspid valve during RV contraction (often difficult to see)
& V wave: caused by RA filling just before opening of the tricuspid valve
26. What are “cannon” A waves?
Very large and prominent A waves occurring when the atria contract against a closed tricuspid valve. Irregular “cannon” A waves are seen in AV dissociation or ectopic atrial beats.
Regular “cannon” A waves are seen in a junctional or ventricular rhythm in which the atria are depolarized by retrograde conduction.
27. Define “pulsus paradoxus.”
A decrease of > 10 mmHg in the systolic blood pressure (BP) during normal inspiration, first described by Adolf Kussmaul in 1873. Kussmaul originally described the disappearance of the pulse during inspiration, though.
28. Describe the mechanism of a pulsus paradoxus.
Pulsus paradoxus can occur when the fall in intrathoracic pressure during inspiration is rapidly transmitted through a pericardial effusion, resulting in an exaggerated increase in venous return to the right side of the heart. The increased venous return causes bulging of the interventricular septum toward the LV, resulting in a smaller LV volume and a smaller LV stroke volume. The decreased LV stroke volume results in a lower cardiac output and lower systolic BP during inspiration. A drop in systolic BP is a normal physiologic finding as long as this drop does not exceed 10 mmHg. In contrast, an exaggerated drop in systolic BP> 10 mmHg is a pathologic finding characteristic of cardiac tamponade.
29. What medical diseases present with pulsus paradoxus?
& Cardiac tamponade (classic finding but may be absent with severe volume contraction, dehydration, or hypotension)
& Severe chronic obstructive pulmonary disease (COPD)
& Chronic constrictive pericarditis (very rarely)
30. Describe the Y descent of the JVP waveform tracing in chronic constrictive pericarditis.
The Y descent of the JVP waveform tracing corresponds to the rapid early RA emptying phase or the rapid early ventricular filling phase. In patients with chronic constrictive pericarditis, early ventricular filling is unimpeded. During the very early filling, the RV is very small and its filling is enhanced by the sudden “pouring” of blood as the tricuspid valve opens. During this early filling phase, the ventricle is too small and has not yet “perceived” the constricting effect of the calcified or thickened pericardium and, thus, filling is unimpeded. Once the ventricle meets the thick or calcified “noncompliant” pericardium, ventricular filling suddenly slows and corresponds to the “pericardial knock” sound. Although found in chronic constrictive pericarditis, the steep Y descent rarely occurs in cardiac tamponade. At the same time that the steep Y descent occurs, the RV early filling occurs and there is a “dip” or sudden decrease in RV pressure. Once the ventricular filling is suddenly slowed or halted by the thick or calcified noncompliant pericardium, the RV pressure rises to a plateau. The “dip-and-plateau” RV pressure waveform, just like the steep Y descent of the RA pressure waveform, is a distinctive finding in chronic constrictive pericarditis and helps to differentiate chronic constrictive pericarditis from cardiac tamponade.
31. What is cardiac tamponade?
The sudden accumulation of fluid within the pericardial sac under pressure. When the clinical triad of cardiac tamponade was first described by Claude Beck in 1935, he noted hypotension, elevated systemic venous pressure, and a small, quiet heart. The condition was commonly due to penetrating cardiac injuries, aortic dissection, or intrapericardial rupture of an aortic or cardiac aneurysm. Today, the most common causes are neoplastic disease, idiopathic pericarditis, acute MI, and uremia.
32. Summarize the physical examination findings in cardiac tamponade.
& Jugular venous distention: Almost universally present except in patients with severe hypovolemia.
& Pulsus paradoxus: Defined as a decrease in systolic BP > 10 mmHg during quiet inspiration. Pulsus paradoxus is difficult to elicit in volume-depleted patients.
& Tachycardia with a thready peripheral pulse: Sometimes severe cardiac tamponade may restrict LV and RV filling enough to cause hypotension, but a thready and rapid pulse is almost invariably present.
33. What is Kussmaul’s sign?
An inspiratory increase in systemic venous pressure commonly present in chronic constrictive pericarditis but rarely detected in acute cardiac tamponade.
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