An arrhythmia is an abnormal heart sound usually detected using a sphygmomanometer

Summary

History and general examination

History [1]

Dyspnea
Chest pain [see “Cardiovascular causes of chest pain”]
Palpitations: an unpleasant awareness of one's own heartbeat; can feel like a fluttering or pounding in the chest
Syncope
Hemoptysis
Edema
Fatigue
Claudication

General examination [1]

Appearance

Level of consciousness
Syndromic features [e.g., in trisomy 21, trisomy 18; associated with congenital heart defects]
Features of rheumatic fever: migrating polyarthritis, erythema marginatum, subcutaneous nodules
Features of left-sided heart failure
Features of right-sided heart failure

Skin and mucous membranes

Color changes
- Central cyanosis [see features of “Cyanotic congenital heart defects” and “Congestive heart failure”]
- Pallor [anemia]
- Plethora [polycythemia]
Xanthomas [dyslipidemia]
Dehydration
Temperature

Hands

Perfusion
- Temperature
- Capillary refill time
- Peripheral cyanosis
Palms: Osler nodes, Janeway lesions [see “Clinical features of infective endocarditis”]
Nails: clubbing, splinter hemorrhages

Face

General
- Malar flush
- Swollen face
Eyes
- Xanthelasmas, arcus lipoides corneae [dyslipidemia]
- Hypertensive retinopathy [ophthalmologic examination]
Mouth
- Poor dental health
- High arched palate [Marfan syndrome]

Neck

Other

Lung bases: pulmonary edema
Lower limbs
- Peripheral edema
- Signs of venous insufficiency
Signs of stroke

Blood pressure

The patient should sit for several minutes before blood pressure is measured.

Use the correct cuff size.

Ask the patient to rest the arm on a horizontal surface at the level of the heart.

Record the pressure in both arms and note any differences.

Determine the systolic and diastolic blood pressure value [e.g., auscultatory method using Korotkoff sounds over the brachial artery].

Repeat measurement.

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

Interpretation

Korotkoff sounds
- Definition: sounds heard when auscultating over the brachial artery during sphygmomanometry
- Origin: turbulent blood flow through a brachial artery that is partially compressed by the inflated arm cuff of a sphygmomanometer
- Interpretation: When deflating the cuff, the pressure at which Korotkoff sounds appear marks systolic BP, and the pressure at which Korotkoff sounds disappear marks diastolic BP.
Normal blood pressure
- Systolic blood pressure < 120 mm Hg and diastolic blood pressure < 80 mm Hg [1]
- See also “Normal vital signs at rest” for all age groups.
Hypotension
Hypertension
- Systolic blood pressure ≥ 130 mm Hg and/or a diastolic blood pressure ≥ 80 mm Hg [3]
- See “Diagnosis of hypertension.”

Jugular venous pressure

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

Approach [1]

Interpretation [1]

Height

Elevated JVP: > 4 cm filling level of the internal jugular vein above the sternal notch
Signs of an elevated JVP
- Jugular venous distention
- Kussmaul sign: distention of the jugular veins during inspiration due to the negative intrathoracic pressure that attempts to pull blood into the right heart, which is restricted by noncompliant pericardium or myocardium [e.g., constrictive pericarditis, restrictive cardiomyopathy, right atrial tumors, ventricular tumors, right HF, massive PE] [6]
- Hepatojugular reflux
Causes of elevated JVP
- Right heart failure
- Fluid overload
- Tricuspid valve dysfunction
- Pericardial effusion
- Constrictive pericarditis
- Cardiac tamponade
- SVC syndrome
- Pulmonary hypertension

Character

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

JVP waves and abnormalities [1]WaveDescriptionAbnormalitiesa wavec wavex descentv wavey descent

The first peak caused by atrial contraction	Absent in atrial fibrillation
The second peak caused by tricuspid valve closure, contraction of the right ventricle, and bulging of the tricuspid valve into the right atrium	cv wave : severe tricuspid valve regurgitation
A drop in JVP caused by atrial relaxation	Absent in: Tricuspid valve regurgitation Right heart failure
The third peak caused by venous refilling of the right atrium against the closed tricuspid valve	Prominent in: Tricuspid valve regurgitation Right heart failure
A drop in JVP caused by decreased right atrial pressure as blood flows into the right ventricle after opening of the tricuspid valve	Prominent in: [7] Tricuspid valve regurgitation Constrictive pericarditis Absent in: Cardiac tamponade Tricuspid valve stenosis

Pulses

A pulse wave is produced by ventricular contraction during systole.

Approach [1]

Three-finger method: palpation with tips of the 2nd, 3rd, and 4th fingers
Palpate the common carotid artery, radial artery, abdominal aorta, femoral artery, popliteal artery, tibialis posterior artery, and dorsalis pedis artery.
The carotid artery pulse should never be palpated at the same time bilaterally. [8]

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

DescriptionPossible causesRateRhythm

Volume [amplitude]

Speed of pulse upstroke [wave contour]Delay

Bradycardia: < 60 bpm Tachycardia: > 100 bpm See also “Normal vital signs at rest” for all age groups.	Physiological variations Bradyarrhythmias Tachyarrhythmias
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	Atrial tachyarrhythmias [e.g., atrial flutter] with a fixed AV block Respiratory sinus arrhythmia
Irregularly irregular pulse: a pulse in which the interval between individual pulse waves varies with no consistent pattern	Atrial fibrillation Atrial tachyarrhythmias [e.g., atrial flutter] with a varying AV block Ventricular ectopics [premature ventricular contractions]
Pulse deficit: the difference between the pulse rate [measured by cardiac auscultation] and the peripheral pulse rate [obtained by palpating the radial artery for 1 minute]	Pulse deficit > 10/min: atrial fibrillation Pulse deficit < 10/min: premature ventricular contractions Hypertrophic obstructive cardiomyopathy [HOCM]
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]	Severe left heart failure Digoxin toxicity
Hyperkinetic pulse [pulsus altus]: bounding pulse Water hammer pulse Bounding pulse with a rapid upstroke followed by a prompt collapse of the vessel Referred to as Corrigan pulse when present in the carotid artery Traube sign: pistol shot-like sounds that are heard over the femoral artery upon compression	Aortic regurgitation Arterial hypertension Hyperdynamic circulation: anemia, sepsis Patent ductus arteriosus Ventricular septal defect [VSD]
Hypokinetic pulse [pulsus parvus]: soft pulse with a low amplitude	Low blood pressure
Pulsus paradoxus: pathological decrease in the pulse wave amplitude and systolic blood pressure > 10 mm Hg during inspiration Decrease of intrathoracic pressure during inspiration → expansion of vena cava and right atrium → ↑ venous return → ↑ RV filling ↓ Pericardial compliance [e.g., due pericardial rigidity in constrictive pericarditis] → ↑ bowing of the ventricular septum into the left ventricle → ↓ LV ejection volume → ↓ systolic blood pressure	Constrictive pericarditis Cardiac tamponade Severe obstructive airway disease [asthma, COPD] Obstructive sleep apnea Croup Tension pneumothorax Superior vena cava syndrome
Reverse pulsus paradoxus: pulse volume increases with inspiration	HOCM AV dissociation Intermittent positive pressure ventilation [IPPV]
Pulsus alternans: alternation of strong and weak pulses caused by alterations in the stroke volume [cardiac output] Dicrotic pulse: two peaks in the pulse wave occurring in systole and diastole	Congestive heart failure
Pulsus bisferiens: a pulse wave with two peaks, i.e., a rapid, short pulse followed by a slower, broader pulse	HOCM Aortic regurgitation Aortic stenosis
Fast-rising pulse [pulsus celer]: rapid upstroke of the pulse	Aortic regurgitation
Slow-rising pulse [pulsus tardus]: delayed peak pressure of the carotid artery	Aortic stenosis
Radiofemoral delay: a delay in palpation of the femoral arterial pulse when compared with the radial arterial pulse	Coarctation of the aorta Vascular obstruction [atherosclerosis] Aneurysms

Auscultation [1]

Chest inspection

Cardiac palpation

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]

Abnormalities of the apex beat [1]AbnormalityEtiologyPositionCharacter

Lateral and downward displacement	Left ventricular enlargement
Displacement to the right hemithorax	Dextrocardia
Lateral displacement	Right ventricular hypertrophy Right tension pneumothorax Large right-sided pleural effusion Chest wall deformities
Hyperdynamic impulse: a brief, forceful impulse palpable over a diffuse area [> 3 cm2]	High cardiac output [e.g., thyrotoxicosis, anemia, sepsis, beriberi] Volume overload: aortic regurgitation, mitral regurgitation, VSD, patent ductus arteriosus
Heaving impulse: a prolonged, forceful impulse	Pressure overload: hypertension, HOCM, aortic stenosis
Hypodynamic impulse: a weak or absent apex impulse	Myocardial infarction Conditions that impair transmission of the apex impulse to the chest wall: obesity, pericardial effusion, left-sided pleural effusion, pneumothorax, COPD
Tapping apex beat: palpable first heart sound	Mitral stenosis
Dyskinetic apex beat: uncoordinated impulse over a diffuse area	Left ventricular dysfunction, e.g., anterior myocardial infarction

Chest percussion

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 auscultation

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 sounds

Normal heart sounds [1]

Extra heart sounds [1]

Extra heart sounds [gallops]SoundOriginTimingOccurrenceThird heart sound [S3]Fourth heart sound [S4]

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	Early diastolic sound that is heard immediately after S2 Ventricular gallop: S1 is followed by S2 and S3 in close succession, resembling the cadence of the word “Kentucky” [Ken-TUC-ky] on auscultation.	Physiological: young individuals [< 40 years of age], athletes, or pregnant women Pathological Chronic mitral regurgitation Aortic regurgitation Heart failure Dilated cardiomyopathy Thyrotoxicosis
Due to late diastoliccontraction 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-SEE] on auscultation.	Physiological: advanced age Pathological if palpable Ventricular hypertrophy [e.g., hypertension, aortic stenosis, cor pulmonale] Ischemic cardiomyopathy Acute myocardial infarction

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

Loud S1
- Mitral stenosis
- Tachycardia
- Hyperdynamic states [e.g., left-to-right shunts ]
- Short PR interval [e.g., AVRT]
Soft S1
Variable intensity

S2 intensity

Loud A2: arterial hypertension, coarctation of the aorta
Loud P2: pulmonary hypertension , atrial septal defects [10]

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 soundsType of splitDescriptionCausesSplit S1

Split S2

Physiological split

Wide split

Fixed split

Paradoxical split [reversed split]

Absent split

Occurs when the closure of the tricuspid valve is delayed [e.g., due to an RBBB], resulting in the sound of tricuspid valve closure heard shortly after mitral valve closure	Conduction disorders Hemodynamic cause
The sound of aortic valve closure [A2] precedes the sound of pulmonary valve closure [P2] during inspiration Inspiration → fall in intrathoracic pressure → increase in venous return to the right side of the heart → prolonged right ventricular systole → delayed closure of P2 Pooling of blood in pulmonary circulation → shortened left ventricular systole → premature A2	Especially pronounced among young individuals
An exaggerated physiological split, which is more pronounced during inspiration [A2 precedes P2] Caused by any condition that increases right ventricular afterload or decreases left ventricular preload Increased right ventricular afterload → prolonged right ventricular systole Decreased left ventricular preload → shortened left ventricular systole	Pulmonary hypertension Pulmonary valve stenosis RBBB Massive pulmonary embolism Severe mitral regurgitation Wolff-Parkinson-White syndrome Constrictive pericarditis
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	Atrial septal defect [ASD] Severe RV failure
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]	Aortic stenosis Left bundle branch block HOCM [LV outflow tract obstruction] Early excitation of the right ventricle [e.g., RV pacing, Wolff-Parkinson-White syndrome]
No splitting of S2	Severe aortic stenosis [geriatric] VSD with Eisenmenger syndrome [pediatric]

Additional sounds [1]

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 murmurs

Overview [1]

Murmurs are blowing or whooshing sounds that occur as a result of turbulent blood flow.
They are described according to the location, radiation, timing, intensity, configuration, frequency, and response to dynamic maneuvers.
For specific auscultatory findings in valvular heart disease, see “Auscultation in valvular defects.”
For specific auscultatory findings of heart defects, see “Congenital heart defects.”

Functional and pathological murmurs

Murmurs may be functional or pathological.

Location and radiation [1]

Location: see “Auscultatory locations.”
Radiation
- Aortic stenosis: a systolic murmur radiates to carotid arteries
- Mitral regurgitation: a systolic murmur radiates to the left axilla [in the left lateral recumbent position]
- Pulmonary stenosis: a systolic murmur radiates to the interscapular region

Timing [1]

Timing of heart murmurs [11]MurmurTimingOccurrenceFunctionalPathologicalSystolic murmurDiastolic murmurContinuous 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	Children Pregnancy During states of excitement or strenuous activity Anemia Fever, sepsis Thyrotoxicosis Beriberi Arteriovenous fistula Still murmur Most common innocent murmur in children Grade 1–3 midsystolic murmur heard best at the left midsternal border or between the left lower sternal border and the apex Louder when the patient is supine and softer when the patient is upright Unknown etiology	Aortic stenosis Pulmonary stenosis Mitral regurgitation Tricuspid regurgitation VSD Coarctation of the aorta HOCM
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	Mitral stenosis Aortic regurgitation Tricuspid stenosis Pulmonary regurgitation
During systole and diastole	Hyperdynamic state Cervical venous hum Common benign finding in children due to turbulent flow in internal jugular veins Heard best at the infraclavicular and supraclavicular regions [more common on the right side] Becomes softer or disappears with flexion of the head, compression of the jugular vein, or in the supine position May radiate to the 1st and 2nd ICS	PDA Arteriovenous fistulas

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].

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

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

Maneuvers [1]

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

Maneuvers and their effect on murmursManeuverEffect on cardiac parametersEffect on murmurs

Inspiration

Valsalva maneuver/standing

Squatting/lying down quickly/raising the legs

Hand grip

Sitting and leaning forward

Lying down in the left lateral position

↑ RV preload ↓ LV preload No effect on LV afterload	↑ 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]
↓ RV preload ↓ LV preload ↓ LV afterload	↑ Intensity of MVP [with early midsystolic click] and hypertrophic cardiomyopathy [HCM] murmurs ↓ Intensity of murmurs arising from the left side of the heart [see “Exceptions to maneuvers” below]
↑ RV preload ↑ LV preload No effect on LV afterload [afterload may increase with squatting]	↑ Intensity of all murmurs [see “Exceptions to maneuvers” below] ↓ Intensity of MVP [with late midsystolic click] and HCM murmurs Tetralogy of Fallot: The severity of tet spells and the associated murmurs decrease with squatting. MVP: click occurs later in systole
No effect on RV preload No effect on LV preload ↑ LV afterload	↑ Intensity of murmurs resulting from backward flow of blood in the left side of the heart [e.g., aortic regurgitation, mitral regurgitation, VSD, MVP] ↓ Intensity of murmurs associated with forward flow of blood in the left side of the heart [e.g., mitral stenosis, aortic stenosis, HCM] MVP: click occurs later in systole
No effect	↑ Intensity of murmurs at or near the aortic valve [e.g., aortic stenosis, aortic regurgitation, coarctation of the aorta, HOCM]
No effect	↑ Intensity of murmurs at or near the mitral valve [e.g., mitral stenosis, mitral regurgitation, MVP]

Exceptions to maneuvers

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

HOCM
MVP

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

Diagnostics

Imaging [13]

Chest x-ray [heart]

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

Echocardiography

Transthoracic echocardiography [TTE]
- A noninvasive ultrasonographic examination of the heart in which a transducer is placed on the anteriorchest wall and the epigastrium
- Recommended for initial evaluation of pathological murmurs [e.g., diastolic murmur, late systolic murmur, all symptomatic murmurs] [14]
- Used to assess valvular function by determining the following:
- Used to assess myocardial contractility [e.g., decreased contractility in heart failure, cardiac wall motion abnormalities in myocardial infarction, right ventricular hypokinesia in pulmonary embolism]
- Used to evaluate for other pathologies [e.g., septal defects, aneurysms, thrombi, vegetations, pericardial effusions]
Transesophageal echocardiography [TEE]

References

Talley NJ, O’Connor S. Clinical Examination. Elsevier Health Sciences ; 2013
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
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
Hall WD. Pitfalls in the Diagnosis and Management of Systolic Hypertension. South Med J. 2000; 93 [3]: p.256-260.
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
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
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
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
Feather A, Randall D, Waterhouse M. Kumar and Clark's Clinical Medicine. Elsevier ; 2020
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
Walker HK, Hall WD, Hurst JW. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition.. Butterworths ; 1990
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
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
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

Summary

History and general examination

History [1]

General examination [1]

Appearance

Skin and mucous membranes

Hands

Face

Neck

Other

Blood pressure

Interpretation

Jugular venous pressure

Approach [1]

Interpretation [1]

Height

Character

Pulses

Approach [1]

Palpation [1]

Auscultation [1]

Chest inspection

Cardiac palpation

Apex beat [1]

Palpation of the apex beat [1]

Chest percussion

Cardiac auscultation

Approach [1]

Auscultatory locations [1]

Heart sounds

Normal heart sounds [1]

Extra heart sounds [1]

Changes in intensity [9]

S1 intensity

S2 intensity

Splitting of heart sounds [1]

Additional sounds [1]

Heart murmurs

Overview [1]

Functional and pathological murmurs

Location and radiation [1]

Timing [1]

Intensity [1]

Configuration [1]

Maneuvers [1]

Exceptions to maneuvers

Audio clip examples of murmurs

Diagnostics

Imaging [13]

Chest x-ray [heart]

Echocardiography

References

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