An 81-year-old patient presented to the emergency room complaining of weakness and fatigue. His family had noted mild disorientation. Physical exam revealed blood pressure (BP) 113/73, temperature 100°F, and heart rate (HR) 130. The lungs were clear. He was given 2 liters of intravenous normal saline. The chest x-ray subsequently showed pulmonary congestion, and the patient was found to have a cardiomyopathy and markedly reduced ejection fraction.
Doctors at all levels of training and experience make errors in diagnosis. Every doctor has made many mistakes for a variety of reasons; many of these are unavoidable. Failure to recognize heart failure when physical findings are present is not a rare occurrence. I believe this also applies to other common cardiovascular disorders. Did the doctor in this hypothetical narrative know how to evaluate the venous pressure and how to listen for a third heart sound? These are skills that, with practice, can be learned at an early stage of training.
Accordingly, the emphasis in this section will be limited to physical findings that I think a trainee should know in detail in order to evaluate the following diseases. Many findings discussed in a standard textbook of medicine are not covered. The focus will be on physical findings in common diseases and conditions that demand early recognition because of their serious nature, such as the following:
Congestive heart failure and left ventricular dysfunction
Acute and chronic pulmonary hypertension
Complications of myocardial infarction
Cardiac tamponade
Mitral aortic (pulmonic) and tricuspid valve disease
Innocent murmurs
Dilated and hypertrophic cardiomyopathy
Atrial septal defect (ASD) and ventricular septal defect (VSD)
HEART SOUNDS
Normal First and Second Heart Sounds
Intensity of the first heart sound is related to the rapidity of closure of the mitral valve, which is dependent on the left ventricular-left atrial pressure gradient in late diastole, the position of the mitral valve immediately before complete closure, and left ventricular dp/dt.
The first heart sound is best appreciated at the apical impulse in the left decubitus position.
Narrow splitting of the S1 representing tricuspid and mitral closure sounds may be heard in normals.
A2 and P2 refer to the two components of the second heart sound.
The intensity of the A2 or P2 is related to the pressures against which aortic and pulmonary valves close. Because aortic diastolic pressure is normally significantly higher than the pulmonary artery diastolic pressure, A2 is much louder than the P2 (for abnormal intensity of heart sounds, see Table 1-1).
Splitting of S2 is usually heard best at the left sternal border in the second and third interspace using the diaphragm of the stethoscope.
Normally, P2 occurs later than A2 because pulmonary artery “hang out time” is longer than the aortic “hang out time.” The pulmonary hang out normally is about 60 msec and that of the aorta is about 20 to 30 msec. The difference between these two hang out times explains why P2 follows A2 and also the differences in normal splitting of the second heart sound. The hang out times are primarily determined by pulmonary artery and aortic compliance, pulmonary and aortic pressures and right and left ventricular stroke volumes.1
During inspiration, P2 is further delayed as a result of further prolongation of the pulmonary artery hang out time due to transient increase in right ventricular stroke volume during inspiration. (Note that decreased impedance decreases ventricular ejection time, and increased impedance prolongs ventricular ejection time. Normal earlier electrical activation of the left ventricle causes a minor contribution for earlier A2, and higher LV dp/dt similarly also contributes, to a rather small extent, to the normal A2-P2 interval.)
The normal second heart sound is thus usually split with inspiration and single with expiration in children and younger adults. In older adults (over age 50) it is commonly single in all phases of respiration.2 (for abnormal splitting of heart sounds, see Table 1-2).
A2 is louder than P2 when listening in the second left interspace in 70% of normal subjects under age 20, and it is always louder than P2 in subjects over age 20.2
“Normal children, young adults, and trained athletes, may have persistent splitting of S2 when examined supine, which disappears when they sit or stand owing to decreased venous return. By contrast, S2 remains audibly split during expiration in pathologic conditions, even when the patient is examined sitting or standing.”3
TABLE 1-1 Abnormal intensity of heart sounds
Soft
Loud
S1
•
First degree A-V block
•
Hyperkinetic circulation as in children, hyperthyroidism, anemia, fever, etc.
•
Decreased left ventricular contractility
•
Acute severe aortic insufficiency with
•
A short P-R interval
premature closure of the mitral valve
•
Mitral stenosis when the valve cusps
•
Thickening and calcification of the mitral valve resulting in reduced mobility
are mobile. This is believed to be as a result of prolongation of diastolic flow providing a large excursion of the valve leaflets and a loud sound as they strike the valve ring
•
Variability of intensity of S1 occurs when the rhythm is irregular due to variations in excursion of the mitral valve
•
Variability of intensity of S1, in the presence of regular rhythm, suggests the presence of A-V dissociation as in complete heart block or ventricular tachycardia
S2
•
A soft P2 in comparison to A2 may be heard in valvular pulmonary stenosis due to valve deformity and decreased pulmonary artery diastolic pressure
•
A loud A2 may be heard in systemic hypertension or in hyperkinetic states such as thyrotoxicosis or aortic regurgitation
•
Similarly, A2 is often soft in severe valvular aortic stenosis because of relative reduction of aortic diastolic pressure
•
A P2 equal in loudness or louder than A2 is heard in pulmonary hypertension, either chronic such as in primary pulmonary hypertension, or acute as in pulmonary embolism
•
Since this latter condition occurs frequently in older adults where the second heart sound is often single, a single soft second heart sound may be heard or the second heart sound may be absent
•
In the elderly patients with aortic stenosis with history of arterial hypertension, the intensity of A2 may be preserved or even louder
TABLE 1-2 Abnormal splitting of heart sounds
Persistent
Fixed
Paradoxical
Wide on expiration and wider on inspiration
No (or only slight) phasic variation in the splitting during the respiratory cycle in all positions
During inspiration, P2 becomes delayed and occurs simultaneously with A2 or after A2. This results in splitting in expiration (A2 follows P2) and a single S2 in inspiration (A2 and P2 occur simultaneously). This is referred to as paradoxical splitting
Type A Wolff-Parkinson-White syndrome presumably as a result of delayed activation
pulmonary vascular capacitance and increased pulmonary blood flow as a result
activation of the left ventricle, A2 may be delayed and occur after P2 in expiration
of the right ventricle
of the shunt. This results in a delayed P2 and
•
Other causes of paradoxical splitting of S2
•
Left ventricular pacing as during biventricular pacing
wide splitting of the second heart sound. Inspiration does not further increase
include left ventricular outflow tract obstruction such as hypertrophic obstructive cardiomyopathy
•
In valvular pulmonary artery stenosis the second heart sound is widely split and the degree of splitting is directly related to the severity of the right ventricular out-flow obstruction. The splitting of the second heart sound is not usually fixed until the right ventricular stroke volume is also fixed
pulmonary blood flow and there is redistribution of pulmonary and systemic blood flow and hence the duration of splitting is relatively fixed
and severe aortic valvular stenosis. Right ventricular PVCs, and right ventricular pacing may also cause paradoxical splitting due to electrical delay in left ventricular activation, significant aortic regurgitation due to the selective increase in left ventricular stroke volume1
The Third Heart Sound (S3 or Ventricular Gallop)
This sound may normally be heard in children and young adults, pregnant women, and trained athletes.
In the context of other evidence of heart disease, an S3 correlates with elevated ventricular end diastolic pressure and also to elevated B-type natriuretic peptide (BNP) in patients with systolic heart failure.
It is best timed by focusing on the second heart sound followed by a brief interval after S2, followed by S3. The interval is longer than the A2-P2 interval and longer than the S2 opening snap interval. It may be faint and best heard when focusing on the instant when it is expected; that is to say, “tuning in.”3
It is a low-frequency sound, best heard with soft application of the bell over the apical impulse, with the patient lying on the left side. An outward movement of the apex may be noted that is synchronous with the S3 (visible and audible). This is further confirmation that the sound is an S3.
The most practical way to recognize the S3 or S4 is by listening with the bell of the stethoscope, which is useful to appreciate these lower frequency sounds, and then to listen with the diaphragm of the stethoscope, which cuts off the lower frequency sounds. Thus the S3 or S4 becomes muffled or cannot be appreciated.
This description applies to a left ventricular gallop. A right ventricular S3 gallop is best heard over the lower left sternal border or rarely below the xiphoid process. It is best heard with the bell and may be heard as the patient inspires. It is heard in patients with right ventricular systolic or diastolic failure and indicates elevated right ventricular diastolic pressure.
The Fourth Heart Sound (S4 or Atrial Gallop)
This sound results from forceful atrial contraction against a ventricle with decreased compliance. “This change in compliance may be related to ventricular hypertrophy, ischemia, infarction, fibrosis, or increased afterload as in systemic or pulmonary hypertension.”3
It is a low-frequency sound occurring just before S1 and best heard with the bell. A left ventricular S4 is best heard at the apex with the patient lying on the left side and may be accompanied by a presystolic outward movement of the apex, which is palpable and visible. A right ventricular S4 may be heard at the left sternal border.
It may also be heard in first degree A-V block. It is also commonly heard in acute mitral insufficiency following rupture of a chorda tendinea. “An Audible S4 is an unusual finding in the normal heart in patients under fifty years of age except in the presence of A-V block.”3
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