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International Journal of Clinical Cardiology

DOI: 10.23937/2378-2951/1410019

Physical Examination of the Cardiovascular System

John P. Higgins*

Chief of Cardiology, Lyndon B. Johnson General Hospital, University of Texas Health Science Center at Houston, USA

*Corresponding author: John P. Higgins MD, MBA (Hons), MPHIL, FACC, FACP, FAHA, FACSM, FASNC, FSGC, Associate Professor of Medicine, The University of Texas Health Science Center at Houston (UTHealth), LBJ General Hospital, 5656 Kelley St, UT Annex-Room 104, Houston, TX 77026-1967, USA, Tel: 713-500-6836; Fax: 713-500-5912; E-mail:
Int J Clin Cardiol, IJCC-2-019, (Volume 2, Issue 1), Review Article; ISSN: 2378-2951
Received: October 13, 2014 | Accepted: January 23, 2015 | Published: January 27, 2015
Citation:Higgins JP (2015) Physical Examination of the Cardiovascular System. Int J Clin Cardiol 2:019. 10.23937/2378-2951/1410019
Copyright: © 2015 Higgins JP. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


The physical examination, while frequently not performed well, is critical to the diagnosis and management of cardiovascular disorders. This paper describes a basic cardiovascular physical examination and explains findings, with the goal of improving skills in this area.


Physical examination, Murmurs, Clicks, Valsalva maneuver


Cardiac physical examination skills have waned [1]. While portable ultrasound can aid in the accuracy of the bedside cardiovascular evaluation, the cardiac physical is cheap, of diagnostic value, and establishes rapport between patient and physician [2].

First, it is important to be systematic. Second, form a differential diagnosis before you start, so the physical will help rule in/out the possible diagnoses. In addition, try to correlate all information e.g. if the patient has an Electrocardiogram (ECG) with a right-bundle-branch block, you should hear a wide split second heart sound (S2). Thus, accuracy in the examination is best achieved by evaluating the physiologic variables that characterize cardiac function (pulse amplitude, blood pressure, jugular venous pressure, and makers of neurohumoral activation), and the identification of which cardiac chambers are involved using precordial motion and the electrocardiogram [3]. Finally, innocent murmurs in childhood are not normally found in adults, except for pregnant women whose blood viscosity and velocity resemble children's; when significant murmurs are found in nonpregnant adults, echocardiography is prudent [4].

An important issue that arises during the physical examination is how to distinguish physiological signs from similar pathological signs. For example, in an asymptomatic patient with a 1/6-2/6 short early- or mid-peaking systolic murmur at the left sternal border, this is usually benign and simply represents a physiological flow murmur [5]. In contrast, holosystolic and long systolic murmurs are more significant [6].

In addition, the effect of Valsalva, squatting, and hand grip maneuvers on different physiological parameters influencing preload, afterload, chamber dimensions, and pressure gradients will have specific and predictable effects on true pathological murmurs [5]. Another important aspect of helping to distinguish pathological murmurs is their sound distribution on the chest wall. A recent study noted that when diagnosing systolic murmurs, the most important physical finding may also be the distribution of sound on the chest wall with respect to the 3rd left parasternal space [6]. For instance, aortic valve murmurs radiate symmetrically above and below the 3rd left parasternal space, in an oblique direction to both sides of the sternum, in a pattern sometimes resembling a sash worn over the right shoulder ("broad apical-base" pattern) [6]. In other words, the radiation pattern of the murmur may provide additional clues to its etiology. Learning this will take much time and practice in order to distinguish normal distribution from abnormal radiation suggesting true pathology.

Also, a patient with pericardial effusions, even if small, will result in a diminishing of the frequency of all murmur patterns [6].

Finally, additional classic cardiovascular findings can aid one in refining their differential diagnosis, but these findings are sometimes absent, thus illustrating both the value of the bedside examination and its limits [6].

The reader is recommended to several excellent online training sites including: Heart Sounds - Easy Auscultation (, Heart Sounds and Murmurs - Practical Clinical Skills (, The Auscultation Assistant (, and Blaufuss Multimedia - Heart Sounds and Cardiac Arrhythmias (

Cardiovascular Physical Examination

After initial inspection, I recommend the following order: hands, head, neck, heart, chest, abdomen, & lower limbs; for auscultation, start supine, then left lateral decubitus position, and finally sit or stand the patient up. The core findings and their associations are listed in Tables 1- 8, while a brief explanation follows.

Inspection - general

Cyanosis is a bluish discoloration of the skin and mucous membranes resulting from abnormal perfusion by either an increased amount of reduced hemoglobin or abnormal hemoglobin. Peripheral cyanosis is commonly due to cutaneous vasoconstriction secondary to exposure to cold air or water, or from hyperadrenergic states including severe heart failure; the later leads to pallor and coldness of the extremities, and cyanosis of the digits when severe. In contrast, central cyanosis is characterized by decreased arterial oxygenation (in Caucasians arterial saturation < = 85%) [7]. It is the absolute amount of reduced hemoglobin that produces the blue discoloration; hence patients with polycythemia vera become cyanotic at higher levels of arterial saturation, whereas those with anemia may not manifest cyanosis despite marked arterial desaturation until it is severe [7] (Table 1).

Table 1: General inspection View Table 1

Inspection - focused

Enlargement of the aorta may stretch the left recurrent laryngeal nerve as it passes around the ligamentum arteriosum (the embryonic remnant of the ductus arteriosus, located between the pulmonary artery and distal aortic arch), resulting in hoarseness.

Clubbing refers to the swelling of the soft tissue of the terminal phalanx of a digit with subsequent loss of the normal angle between the nail and the nail bed [8] (Table 2).

Table 2: Focused inspection View Table 2

Palpation - extremities

Inspiration causes the intrathoracic pressure to become more negative, facilitating venous return to the right heart, transiently increasing right ventricular volume; this causes a leftward bulging of the interventricular septum, which slightly limits left ventricular filling, resulting in a small decline in left ventricular output and systolic blood pressure. Many variables influence heart rate [9]. In cardiac tamponade, because the high pressure in the surrounding pericardial fluid limits the total volume shared by the two ventricles, this normal physiological response is exaggerated (pulsus paradoxus), and is a relatively sensitive finding [10]. This biventricular interdependence (series and parallel) plays an important role in the inspiratory decrease in left ventricular stroke volume that results in this physical finding [11]. Further, early recognition of pulsus paradoxus in the emergency room can help to rapidly diagnose and manage cardiac tamponade [11] (Table 3).

Table 3: Palpation of extremities View Table 3

Jugular venous pulse

The right internal jugular vein is best for examining the jugular venous pulse (JVP) waveform and estimating central venous pressure. A JVP >8cm is elevated; however, many physicians cannot diagnose heart failure by examining the JVP [12] (Table 4).

Table 4: Jugular Venous Pulse (JVP) View Table 4

Kussmaul's sign reflects an inability of the right sided chambers to accept additional volume, typical of constrictive pericarditis. In diastole, as the blood passes from the right atrium to the right ventricle, the right ventricle size expands and quickly reaches the limit imposed by the rigid constricting pericardium. At that point, further filling is suddenly arrested, venous return to the right heart ceases, and systemic venous pressure rises. In addition, the impaired filling of the left ventricle causes a reduction in stroke volume, cardiac output, and blood pressure falls [13].

It is easier to see the x, y descents in the neck than the positive pressure a, c, v waves, because the former produce larger excursions [2]. Palpation of the left carotid artery while examining the right JVP helps adjudicate which pulsations are venous & their timing in the cardiac cycle.

The a wave just precedes S1 and represents venous distention due to right atrial contraction near the end of diastole.

The a wave becomes more prominent in conditions that in which the right atrium is contracting against increased resistance. Amplified or cannon a waves are evident when the right atrium contracts against a closed tricuspid valve.

The c wave corresponds to tricuspid valve closure & bulging into the right atrium with onset of right ventricular systole.

The x descent is from right atrial relaxation & the downward descent of the base of the atrium & tricuspid valve during right ventricular systole.

The v wave is produced by right atrial filling during right ventricular systole when the tricuspid valve is closed, and almost coincides with the S2.

The y descent is rapid and deep since opening of the tricuspid valve in early diastolic right ventricular filling is unimpeded. Constrictive pericarditis occasionally has prominent x descent in addition to the rapid y descent which leads to a "W" shaped JVP. A slow y descent suggests an obstruction to tricuspid valve filling.

In cardiac tamponade, the intracardiac diastolic pressures are elevated and equal, ventricular filling is impaired, and cardiac output declines. The pericardial fluid compresses the right ventricle, and prevents its rapid expansion. The right atrium cannot empty quickly, and the y descent is blunted or absent [10]. Thus, the x descent is most prominent.

Palpation - chest and abdomen

The most inferolaterally palpable beat with the patient supine and in the left lateral position is the apex beat or impulse. It's usually at or medial to the left midclavicular line in the fourth or fifth intercostal space and is a tapping, early systolic outward thrust localized to a point about 2 finger tips in size. It is primarily due to recoil of the heart as blood is ejected (Table 5).

Table 5: Palpation of chest and abdomen View Table 5

With a left parasternal lift, the pulsation occurs distinctly later than the left ventricular apex beat, is synchronous with the v wave in the left atrial pressure curve, and is due to anterior displacement of the right ventricle by an enlarged, expanding left atrium. In right parasternal lift, there is a similar impulse to the left one, it occurs to the right of the sternum in some patients with severe tricuspid regurgitation and a massive right atrium.

Thrills are palpable, low-frequency vibrations felt when your hand touches the chest wall, usually associated with heart murmurs.

Auscultation - heart sounds

Most acoustic stethoscopes have a (1) diaphragm or plastic disc: the underlying sound waves vibrate the diaphragm, creating acoustic pressure waves which travel up the tubing to the listener's ears; best for higher frequency sounds >200Hz; & (2) bell or hollow inverted cup: the vibrations of the skin directly produce acoustic pressure waves; best for low frequency sounds (< 200 Hz) [14] (Table 6).

Table 6: Auscultation - heart sounds View Table 6

Regarding timing, at a resting heart rate of 75beats/minute, ventricular systole lasts 0.30 seconds and diastole 0.50 seconds. Depending on the frequency and amplitude of the sound, the human ear may not distinguish separate sounds that are 0.01-0.02 seconds or less apart [15].

First heart sound "the lub": The first heart sound (S1) consists of a first component of mitral valve closure and a second component from tricuspid valve closure, and is heard the loudest between the left lower sternal border and apex with the stethoscope diaphragm firmly pressed. During systolic contraction, when the left ventricular pressure exceeds that in the left atrium, the mitral valve closes. Physiological splitting of the two high-pitched components of S1 by up to 0.03 seconds exists mainly in early youth according to some published articles is a normal phenomenon, but is not always distinguished [15].

Wide audible splitting of S1 (up to 0.06 seconds) is usually abnormal, and may occur due to delay in the onset of the right ventricular pressure pulse and thus delay in closure of the tricuspid valve, which may occur in in patients with right bundle branch block, Ebstein's anomaly, or right atrial myxoma.

In reversed splitting of S1, the mitral component follows the tricuspid component.

S1 is louder if diastole is shortened (tachycardia), if atrioventricular flow is increased (high cardiac output), prolonged (mitral stenosis), or if atrial contraction precedes ventricular contraction by an unusually short interval (short PR interval).

A soft S1 may be due to poor conduction of the sound through the chest wall, a slow rise of the left ventricular pulse, a long PR interval, or imperfect closure of the mitral valve due to reduced valve substance, as in mitral regurgitation. S1 is also soft when the anterior mitral leaflet is immobile because of rigidity, even in the presence of predominant mitral stenosis.

Second heart sound "the dup": The second heart sound (S2) is split into audibly distinct aortic (A2) and pulmonic (P2) components. Normal physiologic splitting widens with inspiration because the increased right heart volume takes longer to empty, the maximal split being 0.03 seconds. Splitting is heard best at the base of the heart (left/right upper sternal border) with the stethoscope diaphragm firmly pressed.

Splitting that persists with expiration is usually abnormal when the patient is in the upright position. Fixed splitting of S2 occurs in atrial septal defect due to delayed closure of the pulmonic valve. Since the capacitance of the pulmonary bed is greatly increased, right ventricular stroke volume is not appreciably influenced by respiration. Upon inspiration, augmentation of the systemic venous return is counterbalanced by a reciprocal decrease in the volume of the left-to-right shunt, such that right ventricular filling and the timing of P2 relative to A2 does not change, resulting in a fixed split.

Third heart sound: The third heart sound (S3) or ventricular gallop arises from the sudden termination of excessive early rapid diastolic filling & stretching of the left ventricle at the time of the atrioventricular valve opening, with timing like the "-ky" in "Ken-tuc-ky." [2]. An S3 is a dull thud lower in pitch than S1 or S2, and is best heard in the left lateral position with the bell at the apex during expiration (left-sided S3) or at the left sternal border/sub-xiphoid during inspiration (right-sided S3).

The S3 is a barometer of heart failure decompensation: its presence indicates high filling pressures, its absence reflecting improved filling pressures [16].

Fourth heart sound: The fourth heart sound (S4) or atrial gallop is a low-pitched short thud (but higher pitched than S3), presystolic sound produced in sinus rhythm during atrial systole with ejection of a jet of blood against a stiff or non-compliant ventricle, usually having elevated ventricular end-diastolic pressure [17]. It precedes S1 & S2 like "Ten-" in "Ten-nes-see," and is best heard at apex using the bell and with patient in left lateral decubitus position [2]. It is accentuated by mild isotonic or isometric exercise in the supine position.

Auscultation - other sounds

Ejection sounds are sharp, high-pitched click(s) occurring in early systole and closely following S1. They may be aortic or pulmonic in origin, require a mobile valve for their generation, and begin at the time of maximal valve opening. Frequently, the valve is abnormal, and the ejection sound is valvular; this sound is generated by the halting of the doming of the valve. If the valve associated with the ejection sound is normal, it is called a vascular ejection sound. The pulmonic ejection sound, loudest in the 2nd left intercostal space, is the only right-sided sound that is softer during inspiration. With inspiration, increased venous return augments right atrial systole, resulting in partial opening of the pulmonic valve before right ventricular systole commences [18] (Table 7).

Table 7: Auscultation - other sounds View Table 7

Midsystolic clicks may be single or multiple, and probably result from chordae tendineae that are functionally unequal in length on either or both atrioventricular valves and are heard best along the lower left sternal border and at the left ventricular apex [2].

The opening snap (OS) is a brief, crisp, high-frequency, early diastolic sound, due to stenosis of an atrioventricular valve, most often the mitral valve. It is generated when the systolic "bowed" anterior mitral leaflet suddenly changes direction toward the left ventricle during diastole "dome" secondary to the high left atrial pressure. It is heard best with the stethoscope diaphragm at the lower left sternal border and radiates well to the base of the heart. With severe mitral stenosis, greater left atrial pressure causes the mitral valve leaflets to dome sooner, allowing less distance for the leaflets to move in early diastole, and so the opening snap occurs earlier (shorter S2-OS interval); this corresponds with left ventricular isovolumic relaxation time. In general, the longer the diastolic murmur lasts, the more severe the mitral stenosis; this corresponds to a longer duration of the diastolic pressure gradient across the mitral valve [19].

When a large atrial myxoma moves into the region of the mitral or tricuspid valve orifice and obstructs atrioventricular flow during diastole, a tumor plop may be heard in up to 50% of cases [20]. The tumor plop has the same timing as the mitral OS, but differs in that it is a low frequency sound, heard best with the stethoscope bell.

A pericardial knock is a discrete and loud high pitched sound heard in early-mid diastole, occurring slightly earlier than S3 [13]. It is produced when the rapid early diastolic filling of the left ventricle suddenly halts due to the restrictive effect of the rigid pericardium [13].

Auscultation - murmurs

Murmurs are caused by rapid, turbulent blood flow, usually through damaged valves, which causes vibrations which are then acoustically transmitted as sound [21]. During stenosis, blood is forced through a narrow opening, at high speed, causing substantial turbulence and associated murmur. During regurgitation, the valve is prevented from closing fully, which allows blood to spurt backward, and a blowing or hissing sound is heard [21] (Table 8).

Table 8: Auscultation - murmurs View Table 8


Early systolic murmurs begin with S1 and end in midsystole.

Holosystolic (pansystolic) murmurs begin before aortic ejection (early in contraction) at S1 and end when relaxation is almost complete after S2, and are generated when there is flow between two chambers that have widely different pressures throughout systole, such as the ventricle and either its atrium or the other ventricle (ventricular septal defect, VSD). Carvallo's sign, an increase in the intensity of the pansystolic murmur of tricuspid regurgitation during or at the end of inspiration, in found in most patients with severe tricuspid regurgitation [22]. The murmur of VSD does not vary with respirations and does not radiate to the axilla so can be differentiated from tricuspid regurgitation (Carvallo's sign) and mitral regurgitation, respectively.

Midsystolic (ejection systolic) murmurs starts shortly after S1 and occur when the ventricular pressure becomes high enough to exceed the outflow tract pressure thus forcing the semilunar valve open [23,24]. Most benign (innocent) functional murmurs are midsystolic and originate from the pulmonary outflow tract.

Late systolic murmurs are faint or moderately loud, high-pitched apical murmurs that start well after ejection and do not mask either heart sound, and are probably related to papillary muscle dysfunction caused by ischemia/infarction of these muscles or to their distortion by left ventricular dilation.

Early diastolic murmurs begin with S2. In severe acute aortic regurgitation, the murmur often is lower pitched and shorter in duration than the murmur of chronic aortic regurgitation because the lower pressure difference between the aorta and the left ventricle in diastole. When pulmonic regurgitation develops in the setting of pulmonary hypertension, the murmur begins with a loud P2 and may last throughout diastole (Graham Steell murmur) [25].

Middiastolic murmurs begin at a clear interval after S2 during early ventricular filling, usually arise from the mitral or tricuspid valves, and are due to a mismatch between a decreased valve orifice size and an increased flow rate. The Austin-Flint murmur is a murmur of relative mitral stenosis caused by narrowing of the mitral orifice by the severe aortic regurgitation stream hitting the anterior mitral valve leaflet [26]. The Carey Coombs murmur is a soft blubbering apical middiastolic murmur occurring in the acute stage of rheumatic mitral valvulitis, arising from inflammation of the mitral valve cusps or excessive left atrial blood flow secondary to mitral regurgitation [2].

Presystolic (late diastolic) murmurs begin immediately before S1 during the period of ventricular filling that follows atrial contraction. They are usually due to atrioventricular valve stenosis and have the same quality as the middiastolic filling rumble, but they are usually crescendo, reaching peak intensity at the time of a loud S1. The presystolic murmur corresponds to the atrioventricular valve gradient, which is minimal until the moment of right or left atrial contraction.

Continuous murmurs begin in systole, peak near S2, and continue without interruption through S2 into part or all of diastole. These murmurs result from continuous flow due to a communication between high and low pressure areas that persist through the end of systole and the beginning of diastole. The prototype continuous murmur is patent ductus arteriosus, which is 'machinery-like' & peaks just before or after S2, decreases in late diastole, and may be soft or absent prior to S1.

Modulation (shape)

Modulation refers to the pattern that a murmur makes on a phonocardiogram in or electronic stethoscope display.


The location of the stethoscope on the chest where sounds are loudest can aid in diagnosis.

When the murmur of aortic regurgitation radiates selectively to the right sternal border (3rd & 4th intercostal spaces), it suggests that aortic root dilatation is the cause.


Initially, stenotic murmurs get louder as the stenosis gets worse; when the ventricle starts to fail and/or the leaflet motion becomes significantly reduced, the murmur quietens. Paradoxically, with regurgitant murmurs, small high pressure regurgitation may be intense, whereas a wide open regurgitation (less turbulence) may be faint.

Frequency (pitch)

The murmur of acquired pulmonary regurgitation is a high-frequency diastolic blow along the left sternal border. The murmur of congenital pulmonary regurgitation is a low- to medium-pitched, decrescendo murmur heard along the left sternal border, which peaks shortly after P2.


The direction of the high velocity jet of blood may transmit sound to certain locations which help diagnosing the sources.


A Pericardial rub (scratchy) is best appreciated with the patient upright and leaning forward and may be accentuated during inspiration. It has three components related to (1) atrial systole, (2) ventricular systole, and (3) ventricular diastole (with an approximate timing around S3). A friction rub that had been present during the acute phase of pericarditis may disappear if a large effusion separates the inflamed layers from one another.

Maneuvers making murmur louder

I recommend regularly performing and becoming familiar with those maneuvers that increase the intensity of the murmur.

The valsalva maneuver, deep inspiration followed by forced expiration against a closed glottis for 20 seconds, reduces the intensity of most murmurs by diminishing both right and left ventricular filling (ventricular preload). Specifically, during the strain phase, intrathoracic pressure increases leading to decreased venous return to the right heart, which leads to decreased left ventricular filling, resulting in a decreased cardiac output, so most murmurs decrease in intensity [27].

In mitral valve prolapse, when end-diastolic volume is decreased such as with standing or valsalva maneuver, the critical volume is achieved earlier in systole and the click-murmur complex occurs more quickly after the first heart sound.

In hypertrophic obstructive cardiomyopathy, actions that reduce the left ventricular size, such as standing or the Valsalva maneuver, bring the anterior mitral leaflet and the interventricular septum into closer proximity, thus obstructing the left ventricular outflow tract and intensifying the murmur.

Inspiration increases systemic venous return to right heart and increases right sided murmurs.

Extra Signs

These are all the other clues that together lend credence to your diagnosis. For instance, one might expect to see the constellation of pulsatile liver, prominent jugular venous v waves, and a pansystolic murmur that increases with inspiration (Carvallo sign) in a patient with severe tricuspid regurgitation [22].


Basic cardiovascular physical examination is a skill that is improved with training and practice. This skill has numerous benefits including establishing a bond between patient and physician, following and managing a patients clinical condition, as well as being very cost effective when done well. Using a systematic manner, and constantly reviewing the possible diagnosis while hunting for clues, the physical examination can become an exciting and elucidating part of clinical medicine.

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