INTRODUCTION
“There is already plenty of evidence to show that we are in danger of losing our clinical heritage, and of pinning too much faith in figures thrown up by machines. Medicine must suffer if this tendency is not checked.”1
Paul Wood expressed this apprehension in 1950. Since then, around seven decades have passed. And now, justifying his apprehension, bedside cardiology has become a heritage science! Most importantly, evidence-based medicine is asking and demanding evidences in favor of bedside cardiology.
DYSPNEA
In a study2 to evaluate symptoms as predictor of heart failure or chronic obstructive pulmonary disease (COPD), dyspnea on effort predicted depressed left ventricular systolic function with a sensitivity of 100% and specificity of 20%. Orthopnea predicted heart failure with a sensitivity and specificity of 71% and 65% and paroxysmal nocturnal dyspnea (PND) with the sensitivity and specificity of 47% and 75%, respectively. All these symptoms had a likeli hood ratio (LR) of 2 or less. In Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial, orthopnea requiring two or more pillows independently predicted pulmonary capillary wedge pressure (PCWP) >30 mm Hg with an odd ratio of 3.6.3
In acute heart failure, exertional dyspnea is a poor predictor for diagnosis with a LR+ of 1.3 and LR− of 0.48. Orthopnea and PND are better predictors. The former has a LR+ of 2.2 and LR− of 0.65. The later has a LR+ of 2.6 and LR− of 0.7.4 In chronic heart failure, dyspnea on exertion is more sensitive (72–100%) and less specific (17–44%) symptom to diagnose heart failure. PND and orthopnea are less sensitive (27–40%) and more specific (80–99%).
CHEST PAIN4
In acute coronary syndrome (ACS), nature of chest pain has mixed predictive value. Pressure-type chest pain has LR+ of 1.3 only. Radiation down to arm 2has a better predictive value with LR+ of 2.3–4.7. A stabbing or pleuritic chest pain, with tenderness has lesser predictive value with LR– of 0.2–0.3. Chest pain responding to nitrate is not a predictive feature for chest pain in ACS. For stable patient, typical angina bears a high predictive value for coronary artery disease (CAD) with LR+ of 5.8, whereas nonanginal chest pain shows least predictive value for CAD, with a LR of 0.1.
PALPITATION
From history of palpitation, arrhythmic palpitation is more likely, when the age of the patient is >60 years with a LR+ of 1.70, male gender with a LR+ of 1.70, and sleep disturbances due to palpitation with a LR+ of 2.29.
JUGULAR VENOUS PRESSURE
In one study,5 central venous pressure was determined clinically from jugular venous pressure (JVP) and by central venous catheter. The sensitivity of JVP at identifying low (<0 mm Hg), normal (0–7 mm Hg), or high (>7 mm Hg) central venous pressure was 33%, 33%, and 49%, respectively. The specificity was 73%, 62%, and 76%, respectively. In another study,6 clinically detected central venous pressure was compared to pulmonary artery pressure by catheter. Clinical prediction was correct in 55% cases. It has been shown7 that a raised JVP increases the probability, that the monitored central venous pressure will be four times higher.
When the clinically measured JVP is low, there is least possibility (LR 0.2) of a higher monitored central venous pressure. A normal JVP (LR 1), however, does not increase or decrease the probability of abnormal central venous pressure. Hepatojugular reflux8 is a more specific test. It is suggestive of increased right atrial and ventricular end-diastolic pressure and increased PCWP of >15 mm Hg with a LR+ of 6.7 and LR− of 0.08.
PULSE
“Is the pulse in atrial fibrillation irregularly irregular?”9 In this excellent study, it has been shown that nonrandom sequence of R-R interval is found in 30% cases and pulsus alternans in 46% cases of atrial fibrillation. Thus, a particular pattern of regularity is common in atrial fibrillation, rather than irregular irregularity. Detection of transient pulse irregularity has a LR+ of 3.3 of atrial fibrillation in ECG, whereas persistent pulse irregularity has a LR+ of 24.1. Absence of any irregularity in pulse indicates a negative LR of 0.1 for having atrial fibrillation.
Hill sign recently has been challenged.10 Intra-arterial pressure tracing has shown that there is no major difference between upper and lower limb pressure in aortic regurgitation and Hill sign is a sphygmomanometric artifact! Pulse pressure has a good predictive value on severity of aortic regurgitation and a pulse pressure >80 mm Hg has a LR+ of 10.9 for the presence of moderate to severe aortic regurgitation.3
Presence of femoral bruit, even in asymptomatic patient, bears a good predictive value for the presence of peripheral artery disease with a LR+ of 4.80. Presence of renal bruit with both systolic and diastolic component enhances the likelihood of renal artery stenosis with a sensitivity of 39% and specificity of 99%. Similarly, a carotid bruit increases the likelihood of significant carotid artery stenosis with a sensitivity of 53% and specificity of 83%.
APICAL IMPULSE
In one study,11 left ventricular enlargement, as determined by the site of the impulse and its diameter, was compared with echocardiographic left ventricular enlargement. Sensitivity and specificity of apical impulse outside left midclavicular line as an indicator of left ventricular enlargement was 100% and 18%, respectively with a LR of 1.2. When midsternal line was taken as reference point in place of midclavicular line, apical impulse situated >10 cm outside, indicated left ventricular enlargement with a sensitivity of 100% and specificity of 33%. An increased diameter of apical impulse was a good indicator of left ventricular enlargement with a sensitivity of 92% and specificity of 75%.
HEART SOUND
A loud S2 (P2) is a strong predictor of pulmonary hypertension. When P2 is audible at the apex, systolic pulmonary artery pressure may be assumed >50 mm Hg.12
The S3 was first described, long back, in 1856. It is taken as a hallmark of left ventricular dysfunction. Its predictive value was studied, which quantitated the interobserver variability of S3.13 In that study, it was found that if one observer heard S3, the probability that a second observer would, was between 34–38%. When, on the other hand, one observer found S3, the chance that a second observer would agree was between 69 and 79%. Auscultatory findings were verified by phonocardiogram and the positive and negative predictive value to identify S3 was 71% and 64%, respectively. When this and few other studies cast doubt about the clinical usefulness of S3, Studies of Left Ventricular Dysfunction (SOLVD) trial14 strongly established its usefulness. In patients with heart failure, clinical detection of S3 increased the risk of hospitalization or death due to pump failure by 50%.
MURMUR
Clinical skill to detect murmur was compared with echocardiogram in several studies. Murmur of mitral regurgitation is detected clinically in 13–56% cases and that of tricuspid regurgitations in 28–33% cases.15,16 Aortic stenosis murmur can be identified clinically better than other murmurs, ranging from 20% to 88%.17 Clinical identification of aortic regurgitation and mitral stenosis murmur are poorer. Sensitivity to diagnose diastolic murmur was only in 5–24% cases.18The sensitivity and specificity to detect a functional murmur are 67% and 91%, respectively and for an organic murmur, the sensitivity and specificity are raised to 79% and 93%.4
CONCLUSION (Box 1)
May evidence-based medicine is casting shadow on bedside cardiology, its survival as a science depends upon the process of its filtration through the stringent criteria of evidence-based medicine. Clinician should remember that the paradigm is shifting from “intuition, unsystemic clinical experiences, and pathophysiologic rationale as sufficient grounds for clinical decision making” to evidence from clinical research.19
REFERENCES
- Wood PH. Disease of the Heart and Circulation. Philadelphia, PA: Lippincott; 1950.
- Zema MJ, Masters AP, Margouleff D. Dyspnoea: the heart or the lungs? Differentiation at bedside by use of the simple valsalva maneuver. Chest. 1984;85:59.
- Drazner MH, Hellkamp AS, Leier CV, et al. Value of clinician assessment of hemodynamics in advanced heart failure: the ESCAPE trial. Circ Heart Fail. 2008;1:170–7.
- Japp AG, Sumpson L, Pettit S, et al. Chapter 1.2 Cardiovascular symptom. In: Camm AJ, Serruys PW, Maurer G. The ESC Textbook of Cardiovascular Medicine. Oxford University Press; 2019. p. 11.
- Connors AF, McCaffree DR, Gray BA. Evaluation of right heart catheterization in the critically ill patient without acute myocardial infarction. N Eng J Med. 1983;308:263.
- Eisenberg PR, Jaffe AS, Schuster DP. Clinical evaluation compared to pulmonary artery catheterization in the hemodynamic assessment of critically ill patients. Crit Care Med. 1984;12:549.
- Cook DJ. The clinical assessment of central venous pressure. Am J Med Sci. 1990;299:175.
- Cook DJ, Simel DL. Does this patient have abnormal central venous pressure? JAMA. 1996;275:630.
- Rawles JM, Rowland E. Is the pulse in atrial fibrillation irregularly irregular? Br Heart J. 1986;56:4.
- Kutryk M, Fitchett D. Hill's sign in aortic regurgitation: enhanced pressure wave transmission or artifact? Can J Cardiol. 1997;13(3):237.
- Eilen SD, Crawford MH, O'Rourke RA. Accuracy of precordial palpation for detecting increased left ventricular volume. Ann Intern Med. 1983;99:628.
- Gaine SP, Rubin LJ. Primary pulmonary hypertension. Lancet. 1998;352(9129):719.
- Drazner MH, Rame JE, Phil M, et al. Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure. N Engl J Med. 1983;308:263.
- Mangione S, Nieman LZ, Gracely E. The teaching and practice of cardiac auscultation during internal medicine and cardiology training. Ann Intern Med. 1993;119:47.
- Attenhofer Jost CH, Turina J, Mayer K, et al. Echocardiography in the evaluation of systolic murmurs of unknown cause. Am J Med. 2000;108:614.
- Spencer KT, Allen S, Anderson AS, et al. Physician-performed point-of-care echocardiography using a laptop platform compared with physical examination in the cardiovascular patient. J Am Coll Cardiol. 2001;37:2013.
- Roldan CA, Shively BK, Crawford MH. Value of the cardiovascular physical examination for detecting valvular heart disease in asymptomatic subjects. Am J Cardiol. 1996;77:1327.
- Evidence-based medicine working group. Evidence-based medicine, a new approach to teaching the practice of medicine. JAMA. 1992;268:2420.
FURTHER READING
- McGee S. Evidence-based Physical Diagnosis, 3rd edition. Philadelphia, PA: Elsevier Saunders; 2012.
- Yusuf S, Cairns JA, Camm AJ, et al. Evidence-based Cardiology, 2nd edition. London: BMJ Books; 2003.