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Original Contribution

Prehospital Heart Sounds

September 2005

EMS providers are generally not educated to evaluate more than gross differences in heart sounds. In fact, heart sounds are rarely included in prehospital patient assessment guidelines. In addition, fire/EMS agencies supply inexpensive stethoscopes not suited for good heart sound interpretation. In spite of these issues, EMS providers can make a positive impact in patient outcome by taking time to acquire the skill of interpreting heart sounds.

Case Study

Medic Ambulance 310 is sent to a private residence for a sick person. You are directed to a 75-year-old male sitting in a chair. His daughter, who stopped by to visit, tells you he is weak, not eating well, and she is concerned that he is not bouncing back to baseline after suffering the flu for the past few days. You have been on more than 100 flu calls in the past couple of months and recognize the familiar story.

You approach the patient, who is alert and oriented. He adamantly tells you he doesn't want to go to the hospital, but his daughter won't leave him alone. He simply has the flu and is slow to recover. After all, he tells you, he's not 20 years old anymore. While he is weaker than normal, he says he is still able to get around, but he mentions one incident of near-syncope and some dyspnea on exertion. He now feels like he is improving and denies chest pain. Food and liquid intake are reported to be normal, with no nausea or vomiting. You see adequate food in plain view, and the apartment looks clean and orderly. The patient has a history of hypertension, with no medications and no known allergies. His last visit to a physician was over five years ago. He dislikes the whole concept of visiting doctors and avoids hospitals, particularly emergency departments, under all circumstances.

His BP is 150/92, PR 86, RR 16, PO2 97%, NSR in lead II, skin slightly pale, warm and dry. Pupils are PEARL, grips and speech are normal, with no JVD or peripheral edema.

Given the plethora of flu cases you have seen in the last two months, you agree that transport to the emergency department is not necessary, although follow-up with a physician would be a good idea considering his age and lack of recent medical care. You recommend transport to the ED and, as you expect, he still refuses transport for "a simple case of the flu." Except for that one case of near-syncope and dyspnea on exertion, which is not that typical for flu, you tend to agree with his analysis, although you are concerned about his lack of routine healthcare. Knowing he is going to wait at least six hours before getting past the triage nurse, you make one more attempt to get him to go, but he again refuses. As you are thinking "what now?" and your EMT partner is looking in your clipboard for your list of clinic referrals, you realize you were distracted by your initial conversation with the patient and his daughter and neglected to listen to his lung sounds. You listen and find them clear, with normal tidal volume. You then move to auscultate the heart and are surprised to hear a harsh crescendo systolic ejection murmur, with no radiation to the neck or axilla. You know this could be many things, but, considering his history, you begin to suspect aortic valve stenosis or hypertrophic cardiomyopathy, which would account for his symptoms beyond the simple flu. In the prehospital setting and this particular case, the exact diagnosis is not the issue. You now have evidence to convince him to go to the ED to diagnose a heart problem beyond your capability. He listens to your concern and, with the help of his daughter, your patient reluctantly consents to transport. His gait is more unsteady than he admitted as you assist him to your gurney. The patient is later diagnosed with left ventricular outflow tract obstruction and, after surgical resection of the subaortic membrane, recovery is uneventful.

The Medic's Role

An EMS provider is often the first person a patient encounters in the healthcare system, and your role as patient advocate can make a difference in patient outcome. Systems with 12-lead EKG capability can direct a patient with ST elevation myocardial infarction (STEMI) to a hospital capable of percutaneous coronary intervention (PCI) rather than a community hospital not capable of PCI, where the inevitable delay will exceed the 90-minute ACC/AHA recommended window for transport to a higher level of care.1 Paramedics can direct a symptomatic stroke patient with specific acceptance criteria to a "stroke center" rather than simply the closest facility, or alert the appropriate agency to elder abuse and neglect and make a significant difference in a person's quality of life. Heart sound evaluation is another tool in your arsenal that can be used to make a difference in patient outcome.

Auscultation of the Heart

Approach heart sounds in a systematic manner. One method is to auscultate the right upper sternal border, then the left upper sternal border and proceed down the left sternal border to the apex of the heart. Another method is to start at the apex and work in the reverse direction. The goal is to listen to four areas corresponding to valve locations as illustrated in Figure 1. The right second intercostal space corresponds to the aortic valve; the left second intercostal space corresponds to the pulmonic valve; the fourth intercostal space, left sternal border corresponds to the tricuspid valve; and the fifth left intercostal space, midclavicular line, or slightly medial to that line, corresponds to the mitral valve. 2 For practical purposes, the latter location corresponds to the apex of the heart. Listen with both the bell and diaphragm: the bell for low-frequency and the diaphragm for higher-frequency sound. If you have a tunable stethoscope, you can listen to both ranges by simply altering the pressure on the tunable diaphragm.

Listening to the apex of the heart, you hear the normal lub dub, which corresponds to the sounds of valves closing, called S1 and S2 heart sounds. Basic heart sounds are identified as S1, S2, S3 and S4.

S1 corresponds to the closure of mitral and tricuspid valves. If you listen at the left sternal border, you can sometimes hear a normal S1 split where the mitral valve closes prior to the tricuspid valve. An abnormally loud S1 generally indicates mitral valve stenosis, while a softer sound could indicate mitral valve regurgitation.

S2 corresponds to closure of the aortic and pulmonary valves. This sound can split normally on increasing respiration when the aortic valve closes before the pulmonic valve. This sound can also split pathologically and can at times be diagnostic, as shown in Table I.

S3 heard mid-diastolic at the apex is a low- pitched gallop or blowing sound sometimes called a ventricular gallop2 and is a common sign of left ventricular failure or distension. This sound is normal in children, but can be an indication of pericarditis, mitral regurgitation, tricuspid regurgitation or right ventricular failure in adults. Instead of hearing the normal lub da, you will hear a lub-da-da in rapid succession.

S4 heard late diastolic (just before S1) at the apex is also low-pitched gallop-sounding, always pathologic and can indicate hypertension, coronary artery disease or hypertrophic cardiomyopathy. This may accompany a loud S2 when hypertension is a factor. 2, 3

S3 and S4, best heard with the bell rather than the diaphragm of your stethoscope, are sometimes difficult to hear, especially in the less-than-optimal prehospital setting, and it requires mentoring, as well as practice, to distinguish the subtle nature of the sounds.

Clicks and Snaps

These pathologic sounds, whether they are called clicks or snaps, are associated with valve openings. A high-pitched click, heard soon after S1, indicates sudden opening of a stiff aortic valve, usually due to aortic stenosis. A high-pitched click heard soon after S2 is frequently the sudden opening of a stiff mitral valve due to mitral stenosis.4

The sound of an artificial valve is probably the easiest and most obvious heart sound because it is so atypical. Unlike other heart sounds, this sound is obviously mechanical and is easily differentiated from any other sound you will ever hear from your stethoscope on a human subject.

Heart Murmurs

Abnormal heart sounds, typically called murmurs, are graded 1 through 6, from very faint to very loud. EMS providers in their less-than-optimal environment can generally hear them when they are at least grade 3 or 4, and even grade 2 in a quiet environment. Murmurs are classified as systolic and diastolic, and are classified by intensity, frequency, configuration, timing, duration and radiation. Higher-graded murmurs are associated with a thrill, which is a sensation of vibration felt during examination.

Grade 1: A very soft murmur detected after careful auscultation.

Grade 2: A soft murmur that is readily evident in an optimum environment.

Grade 3: A moderately intense murmur not associated with a palpable thrill (vibration).

Grade 4: Loud murmur; a palpable thrill is not present, or is intermittent.

Grade 5: A loud cardiac murmur associated with a palpable thrill; the murmur is not audible when the stethoscope is lifted from the thoracic wall.

Grade 6: A loud cardiac murmur associated with a palpable thrill and audible even when the stethoscope is lifted from the thoracic wall.

Systolic murmurs, which can be caused by outflow obstruction, are called ejection murmurs and constitute a crescendo-decrescendo sound. If you plotted this sound over time, it would be diamond-shaped. It typically results from aortic stenosis, pulmonic stenosis and/or hypertrophic cardiomyopathy. 2 This was the sound noted during the initial case presentation.

Diastolic murmurs are classified as regurgitant (retrograde flow across the aortic or pulmonic valve) or diastolic filling (turbulent flow across the mitral or tricuspid valve). 2 Both are difficult to distinguish and will not be considered further.

Specific Murmurs

Aortic stenosis, a defect in which the aortic valve is more narrow than normal, is a systolic ejection murmur and is a harsh sound. As the stenosis worsens, it results in valve closure delay and a decrease in intensity. Initially, the sound peaks early in systole. These late changes result in what is called paradoxical splitting of S2. On inspiration, closure of the valves is near simultaneous, while on expiration, the pulmonic valve closes prior to the aortic valve, resulting in a split S2 sound.2

Hypertrophic cardiomyopathy, enlargement of the cells of the heart and therefore the heart itself, is an outflow obstruction that results in turbulent ejection of blood from the left ventricle during systole. This murmur is usually best heard at the left sternal border near the ventricle. Valsalva's maneuver usually results in increased loudness.5 Have the patient hold his breath to quantify loudness and then perform Valsalva's maneuver to note any difference.

Mitral regurgitation generates a murmur when blood flows from the left ventricle to the left atrium. This is a blowing sound vs. the harsh sound of stenosis and is best heard at the apex of the heart. The sound tends to radiate to the axilla. If the mitral valve also prolapses, you may be able to hear the click when this occurs.

Tricuspid regurgitation generates a murmur when blood flows from the right ventricle to the right atrium and sounds very similar to mitral valve regurgitation. This murmur increases on inspiration and radiates to the right side of the sternum.

Murmurs are also generated by both atrial and ventricular septal defects. Although they are a concern and can be heard as an abnormal murmur, they are difficult to distinguish.

Conclusion

Auscultation of the heart is an acquired skill and requires mentoring and practice. Google the Internet with the term "heart sounds" and you will find several websites that offer a good sampling of the most common heart sounds discernable in the field. Buy a quality stethoscope, start listening and, when you hear something unusual, compare your impression with that of the emergency department staff.

References

  1. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. Executive summary: A report of the ACC/AHA Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines on the Management of Patients with Acute Myocardial Infarction). Circulation 110:5--7, 2004.
  2. Karmath B, Thornton W. Auscultation of the heart. Hospital Physician, pp. 39--43, Sept 2002.
  3. Piekert T, Asher CR, Griffin BP. Systolic ejection murmur presenting with dyspnea on exertion. Cleveland Clinic Journal of Medicine 68:809--814, Sept 2001.
  4. Lester SJ, Herlbron B, Gin K, et al. The natural progression of aortic stenosis. Chest 113:1109--1114, 1998.
  5. Maron BJ. Hypertrophic cardiomyopathy. Lancet 350:127--133, 1997.

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