Cardiovascular examination

Last updated: October 30, 2023

Summarytoggle arrow icon

The cardiovascular examination is an essential cardiological tool that comprises the assessment of vital signs and jugular venous pulse, chest inspection and palpation, and, most importantly, auscultation of the heart. For specific auscultatory findings in valvular heart disease, see “Auscultation in valvular defects.” For specific auscultatory findings of heart defects, see “Congenital heart defects.” Details regarding the specific signs and symptoms of cardiovascular disease can be found via the links provided below.

History and general examinationtoggle arrow icon

History [1]

General examination [1]


Skin and mucous membranes





Blood pressuretoggle arrow icon

Approach [1]

  1. The patient should sit for several minutes before blood pressure is measured.
  2. Use the correct cuff size.
  3. Ask the patient to rest the arm on a horizontal surface at the level of the heart.
  4. Record the pressure in both arms and note any differences.
  5. Determine the systolic and diastolic blood pressure value (e.g., auscultatory method using Korotkoff sounds over the brachial artery).
  6. Repeat measurement.

24-hour ambulatory blood pressure measurement can be helpful in establishing the average and peak blood pressure values during daily activities.


Sources of errors in blood pressure measurement [4]

  • Incorrect positioning
  • White coat hypertension
  • Mönckeberg arteriosclerosis [5]
  • Incorrect cuff size
  • Auscultatory gap
    • Korotkoff sounds between systolic and diastolic blood pressures sometimes diminish or disappear, presumably due to increased arterial stiffness in hypertensive patients.
    • When the cuff is insufficiently pumped (i.e., below systolic blood pressure), the first appearance of Korotkoff sounds is misinterpreted as systolic blood pressure (a falsely low reading).
    • The falsely low reading can be prevented by simultaneously palpating the radial pulse on the arm in which blood pressure is measured.

Jugular venous pressuretoggle arrow icon

Jugular venous pressure (JVP) can be used to estimate central venous pressure (CVP) and provides information about fluid status and cardiac function.

Approach [1]

  • The patient should be in the supine position, torso elevated to 45°, with the head extended backward and turned to the left.
  • Identify the venous pulsation of the internal jugular vein and evaluate the following:
    • The height of the internal jugular venous filling pressure, by measuring it from the sternal angle
    • Estimation of the CVP, obtained by adding 5 cm to the JVP height
    • The character of the JVP, by assessing JVP waves
  • Hepatojugular reflux should be tested if JVP cannot be assessed properly.

Interpretation [1]



A normal JVP waveform consists of three waves (a, c, v) and two descents (x, y).

JVP waves and abnormalities [1]
Wave Description Abnormalities
a wave
  • The first peak caused by atrial contraction
c wave
x descent
  • A drop in JVP caused by atrial relaxation
v wave
y descent

Pulsestoggle arrow icon

A pulse wave is produced by ventricular contraction during systole.

Approach [1]

The thumb of the examiner should never be used to take the pulse because its own strong pulse might be mistaken for the patient's pulse.

Palpation [1]

The pulse should be assessed for rate, rhythm, character, volume, the speed of upstroke, and delay.

Palpation of the arterial pulse

Pulse characteristics

Description Possible causes
  • Regular: the interval between individual pulse waves remains consistent
  • Physiological (normal)
  • Regularly irregular pulse: the interval between individual pulse waves varies in a consistent pattern, i.e., there is a pattern to the irregularity
  • Irregularly irregular pulse: a pulse in which the interval between individual pulse waves varies with no consistent pattern
  • Pulsus bigeminus: a regularly irregular rhythm in which two heartbeats occur in rapid succession followed by a gap (the usual pattern is: high-volume pulse, low-volume pulse, delay, repeat)

Volume (amplitude)

  • Reverse pulsus paradoxus: pulse volume increases with inspiration
  • Pulsus bisferiens: a pulse wave with two peaks, i.e., a rapid, short pulse followed by a slower, broader pulse
Speed of pulse upstroke (wave contour)
  • Radiofemoral delay: a delay in palpation of the femoral arterial pulse when compared with the radial arterial pulse

Auscultation [1]

Chest inspectiontoggle arrow icon

Approach [1]

The patient is asked to undress from the waist up and the physician evaluates for the following:

Cardiac palpationtoggle arrow icon

Apex beat [1]

The apex beat (apex impulse) is the outermost and lowermost palpable cardiac impulse on the chest wall.

Palpation of the apex beat [1]

  • Approach
    • Performed in the supine position with the torso elevated to 45°
    • The examiner places a flat hand on the cardiac apex to locate the apex beat, and further localizes and assesses the beat by palpating with 2–3 fingers.
    • If the apex beat is not initially palpable, the patient should be positioned on the left lateral side and the cardiac apex palpated during expiration.
  • Normal findings
Abnormalities of the apex beat [1]
Abnormality Etiology
  • Lateral and downward displacement
  • Displacement to the right hemithorax
  • Hyperdynamic impulse: a brief, forceful impulse palpable over a diffuse area (> 3 cm2)
  • Heaving impulse: a prolonged, forceful impulse
  • Hypodynamic impulse: a weak or absent apex impulse
  • Dyskinetic apex beat: uncoordinated impulse over a diffuse area

Other impulses [1]

Chest percussiontoggle arrow icon

Although cardiac percussion can provide some information about the size and shape of the heart, it is very unreliable and dependent on the examiner and is thus of limited clinical use.

Cardiac auscultationtoggle arrow icon

Approach [1]

  • The patient should be in a supine position with the torso elevated to 45°.
  • Ask the patient to refrain from speaking while the heart sounds are being assessed.
  • The radial pulse should be palpated while auscultation is performed.
  • If heart sounds are weakly audible, ask the patient to hold their breath after exhaling.
  • Assess the following:

Auscultatory locations [1]

"All Physicians Earn Too Much" (Aortic, Pulmonary, Erb point, Tricuspid, Mitral)

Heart soundstoggle arrow icon

Normal heart sounds [1]

  • The first (S1) and second (S2) heart sounds are physiological sounds heard in all healthy individuals.
  • The third (S3) and fourth (S4) heart sounds may be physiological (particularly in young adults, pregnant women, and the elderly) or pathological.
Normal heart sounds
Sound Origin Location Timing
First heart sound (S1)
  • At the onset of systole
  • Heard just before the carotid pulsation is felt
Second heart sound (S2) Aortic component of the second heart sound
  • Heard best in the aortic area at the right upper sternal border
Pulmonary component of the second heart sound

Extra heart sounds [1]

Extra heart sounds (gallops)
Sound Origin Timing Occurrence
Third heart sound (S3)
  • Due to rapid ventricular filling and sudden deceleration of blood when the ventricle reaches its elastic limit
  • Heard best with the bell of the stethoscope in the mitral area with the patient in a left lateral position
Fourth heart sound (S4)
  • Due to late diastolic contraction of the atria (atrial kick) against high ventricular pressure
  • Heard best with the bell of the stethoscope in the mitral area with the patient lying in a left lateral position
  • Late diastolic (presystolic) sound heard immediately before S1
  • S1 rapidly follows S4, resembling the cadence of the word “Tennessee” (Ten-nes: S4, S1, see: S2) on auscultation.

Gallops that originate from the left side of the heart (the most common) become softer with inspiration, while those that originate from the right side become louder.

Changes in intensity [9]

Increased or decreased intensity (loudness) of the heart sounds may indicate certain pathologies.

S1 intensity

S2 intensity

Splitting of heart sounds [1]

If the aortic and pulmonary valves do not close simultaneously, an apparent splitting of S2 can be heard upon auscultation.

Splitting of heart sounds
Type of split Description Causes
Split S1
  • Conduction disorders
  • Hemodynamic cause

Split S2

Physiological split
  • Especially pronounced among young individuals

Wide split

Fixed split

  • Does not change with respiration and tends to be wide, i.e., the split is also audible during expiration
  • Left-to-right shunt in ASD RV volume overload → delay in the closure of the pulmonary valve

Paradoxical split (reversed split)

  • Audible during expiration but not inspiration
    • Expiration: A2 is heard after P2 during expiration due to delayed closure of the aortic valve (split reversal)
    • Inspiration: the closure of the pulmonary valve is also delayed, resulting in A2 and P2 occurring simultaneously (i.e., a paradoxical decrease in the split during inspiration)
Absent split

Additional sounds [1]

Additional sounds on cardiac auscultation
Sound Origin Timing Etiology
Aortic ejection click
  • Opening of a stiff aortic valve
  • Heard best with the diaphragm of a stethoscope at the aortic region with the patient seated and leaning forward
  • Early systolic sound (immediately after S1)
Mitral valve prolapse click
  • Midsystolic sound
Mitral valve opening snap
Mechanical valve clicks
  • S1 and S2 sound like clicks.
  • Heard best with the diaphragm of a stethoscope
  • Coincides with a normal S1 and S2
Pericardial friction rub
  • Scratching sound due to friction between the visceral and parietal pericardium
  • Heard best over the left sternal border during expiration with the patient sitting upright and leaning forward
Pericardial knock

The presence of an aortic ejection click can be used to differentiate a pathological systolic murmur of aortic stenosis from a flow murmur. When the click is present, the murmur is pathological.

The absence of a click in patients with prosthetic valves may indicate valve failure.

Heart murmurstoggle arrow icon

Overview [1]

Functional and pathological murmurs

Murmurs may be functional or pathological.

Difference between functional and pathological murmurs

Functional heart murmur (physiological or innocent)

Pathological murmur
  • Caused by structural defects (valvular disease or heart defects)


  • Soft (grade < 3/6 without a thrill)
  • Typically grade > 3/6
  • Thrill may be present
  • Most commonly midsystolic or continuous
Position change
  • Position-dependent; varies in intensity or disappears
  • Rarely disappears

Location and radiation [1]

Timing [1]

Timing of heart murmurs [11]
Murmur Timing Occurrence
Functional Pathological
Systolic murmur
  • During ventricular contraction (i.e., occurs with or after S1 and before S2)
  • Can be classified as:
    • Early systolic murmur
    • Midsystolic murmur
    • Late systolic murmur
    • Holosystolic murmur
Diastolic murmur
  • During ventricular relaxation (i.e., occurs with or after S2 and before S1)
  • Can be classified as:
    • Early diastolic murmur
    • Middiastolic murmur
    • Late diastolic murmur
    • Holodiastolic murmur
  • Does not occur physiologically
Continuous murmur

Diastolic murmurs are almost always pathological.

Diastolic murmurs may require certain maneuvers to make them more apparent, e.g., letting the patient sit and lean forward to intensify the murmur of aortic regurgitation.

Intensity [1]

The intensity refers to the loudness of the murmur on auscultation (grades I–VI).

Grading of murmur intensity [12]
Levine grading scale Intensity

Grade I

Grade II

  • Faint murmur, but can be detected almost immediately

Grade III

Grade IV

Grade V

  • Very loud murmur with an easily palpable thrill
  • Audible with just the rim of the stethoscope touching the chest

Grade VI

  • Loudest possible murmur
  • Audible with the stethoscope hovering above the chest

While most grade III and above murmurs are pathological, the intensity of a murmur does not always correlate to the severity of the underlying lesion. For example, a larger VSD produces a softer murmur than a small VSD, and a murmur of severe aortic stenosis may disappear if a patient develops left heart failure.

All diastolic murmurs and any grade II and above systolic murmurs require further echocardiographic evaluation.

Configuration [1]

The configuration describes the change in intensity (loudness) of a murmur, which is determined by the pressure gradient driving the turbulent flow.

  • Types
    • Uniform: unchanging intensity
    • Crescendo: increasing intensity
    • Decrescendo: decreasing intensity
    • Crescendo-decrescendo: initial increase followed by a decrease in intensity

Frequency (pitch) [1]

The frequency of a murmur is determined by the velocity of turbulent flow, which is in turn affected by the pressure gradient.

  • High pitch: high-pressure gradient and high-velocity flow (e.g., VSD)
  • Low pitch: low-pressure gradient and low-velocity flow (e.g., mitral stenosis)

Maneuvers [1]

Certain maneuvers may be performed to elicit a change in the intensity of a murmur.

Maneuvers and their effect on murmurs
Maneuver Effect on cardiac parameters Effect on murmurs


  • ↑ Intensity of murmurs arising from the right side of the heart
  • ↓ Intensity of murmurs arising from the left side of the heart (see “Exceptions to maneuvers” below)

Valsalva maneuver/standing

Squatting/lying down quickly/raising the legs

Hand grip

Sitting and leaning forward

  • No effect

Lying down in the left lateral position

  • No effect

Exceptions to maneuvers

In the following conditions, maneuvers that increase preload decrease the intensity of the murmur and vice versa.

Maneuvers that decrease LV preload (e.g., inspiration, Valsalva maneuver) usually decrease the intensity of murmurs arising from the left side of the heart, except in HOCM and MVP, in which a decrease in LV preload increases the intensity of the murmur.

Audio clip examples of murmurs

Diagnosticstoggle arrow icon

Imaging [13]

Chest x-ray (heart)

The heart shadow can be viewed on a chest x-ray.


Invasive tests [13]

Referencestoggle arrow icon

  1. Talley NJ, O’Connor S. Clinical Examination. Elsevier Health Sciences ; 2013
  2. Feather A, Randall D, Waterhouse M. Kumar and Clark's Clinical Medicine. Elsevier ; 2020
  3. Doherty JU, Kort S, Mehran R, Schoenhagen P, Soman P. ACC/AATS/AHA/ASE/ASNC/HRS/SCAI/SCCT/SCMR/STS 2017 Appropriate Use Criteria for Multimodality Imaging in Valvular Heart Disease. J Am Coll Cardiol. 2017; 70 (13): p.1647-1672.doi: 10.1016/j.jacc.2017.07.732 . | Open in Read by QxMD
  4. Holler JG, Bech CN, Henriksen DP, Mikkelsen S, Pedersen C, Lassen AT. Nontraumatic Hypotension and Shock in the Emergency Department and the Prehospital setting, Prevalence, Etiology, and Mortality: A Systematic Review. PLoS ONE. 2015; 10 (3): p.e0119331.doi: 10.1371/journal.pone.0119331 . | Open in Read by QxMD
  5. Whelton, PK, Carey, RM et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. Hypertension. 2017; 71 (6): p.e13–e115.doi: 10.1161/hyp.0000000000000065 . | Open in Read by QxMD
  6. Hall WD. Pitfalls in the Diagnosis and Management of Systolic Hypertension. South Med J. 2000; 93 (3): p.256-260.
  7. Sahoo J, Patil M, Kamalanathan S, Vivekanandan M. Pseudo hypertension: Clue from Osler sign. J Family Med Prim Care. 2016; 5 (3): p.743.doi: 10.4103/2249-4863.197277 . | Open in Read by QxMD
  8. Gurdjian ES, Webster JE, Martin FA, Hardy WG. Observations On Unilateral Compression And Palpation Of The Carotid Bifurcation. J Neurosurg. 1957; 14 (2): p.160-170.doi: 10.3171/jns.1957.14.2.0160 . | Open in Read by QxMD
  9. Johnson SK, Naidu RK, Ostopowicz RC, et al. Adolf Kussmaul: distinguished clinician and medical pioneer. Clin Med Res. 2009; 7 (3): p.107-12.doi: 10.3121/cmr.2009.850 . | Open in Read by QxMD
  10. Pittenger B, Sullivan PD, Mansoor AM. Friedreich’s sign. BMJ Case Reports. 2018: p.bcr-2018-226820.doi: 10.1136/bcr-2018-226820 . | Open in Read by QxMD
  11. Walker HK, Hall WD, Hurst JW. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition.. Butterworths ; 1990
  12. Colman R, Whittingham H, Tomlinson G, Granton J. Utility of the Physical Examination in Detecting Pulmonary Hypertension. A Mixed Methods Study. PLoS ONE. 2014; 9 (10): p.e108499.doi: 10.1371/journal.pone.0108499 . | Open in Read by QxMD
  13. Mikrou P, Ramesh P. General paediatric evaluation of heart murmurs. Paediatrics and Child Health. 2017; 27 (2): p.90-92.doi: 10.1016/j.paed.2016.09.004 . | Open in Read by QxMD
  14. Silverman ME, Wooley CF. Samuel A. Levine and the History of Grading Systolic Murmurs. Am J Cardiol. 2008; 102 (8): p.1107-1110.doi: 10.1016/j.amjcard.2008.06.027 . | Open in Read by QxMD

Icon of a lockAccess full content

Sign up and get unlimited access.
 Evidence-based content, created and peer-reviewed by physicians. Read the disclaimer