Authors: Ahmed Elsherif 1 ; Michelle Wyatt 2
Peer Reviewers: Stanley Oiseth 3 ; Joseph Alpert 4
Affiliations: 1 Suez Canal University; 2 Medical Editor at Lecturio; 3 Chief Medical Editor at Lecturio; 4 Tucson University, Arizona
The cardiovascular examination consists of assessing the vital signs, jugular venous pulse (JVP), chest inspection, palpation of the chest and peripheral pulses, and auscultation of the heart. It should also include a fundoscopic exam to evaluate for retinopathy in patients with diabetes or hypertension. A complete cardiovascular examination takes time to master and is critical in diagnosing cardiac pathology. 
For further review of this topic, including links to lectures by specialists in the field, follow this link: https://app.lecturio.com/#/course/c/47869
This article is not intended to be a substitute for professional medical advice and should not be relied on as health or personal advice. Always seek the guidance of your doctor or other qualified health professional with any questions you may have regarding your health or a medical condition.
Vital signs are necessary for every patient you clinically examine, including heart rate (HR), respiratory rate (RR), and blood pressure (BP). In most situations, these are measured with basic equipment (a watch, a sphygmomanometer, and a stethoscope) and are part of a physician’s basic skills.
It is essential to learn how to perform these examinations correctly and the basic rules associated with each measurement. Even if the hospital or clinic staff provide the patient’s BP readings, most physicians in clinical practice will repeat some of the vital sign measurements. Automated and validated oscillometric BP monitors are preferred to stethoscope-based manual methods.
The patient should be resting comfortably, lying supine (for hospitalized patients in bed), or sitting in any other situation (at home or in the clinic).  Before checking their BP, the patient should have rested for 3 to 5 minutes (not run in from the parking lot or just had a blood draw). Wash your hands and explain to the patient what you are doing. Do not perform the exam through clothing—use a bare arm. Do not use an arm with a medical problem or on the same side as a mastectomy.
With the anterior chest exposed, observe your patient’s thorax and the rest of their body. Look at the eyes, upper and lower extremities, and neck veins as well.
- Scars from prior cardiac surgery. A vertical scar on the sternum is an indication of prior open-heart surgery.
- Chest deformities include pectus excavatum (a sunken sternum and ribs may be a sign of a connective tissue disease such as Marfan syndrome) and pectus carinatum (“pigeon chest,” a protrusion of the sternum and ribs).
- Yellow plaques around the eyes and eyelids, called xanthelasmas, may signify hypercholesterolemia. Although sometimes seen in patients without hyperlipidemia, xanthelasmas can be a sign of a risk factor for cardiovascular disease.
- Roth spots are observed on the retina with an ophthalmoscope and appear as a red ring surrounding a white center. These are only seen in about 2% of patients with infective endocarditis but are a classic sign that medical students are often tested on. 
Upper and Lower Extremities
Clubbing of the fingers or toes manifests with the distal part of the digit appearing flatter and broader. This is a sign of lung disease or chronic hypoxemia but may occasionally be seen in individuals without these conditions.
Cyanosis, a bluish discoloration of the skin and mucous membranes, implies poor perfusion. The presence of at least 3 g/dL of reduced or deoxygenated hemoglobin (Hb) corresponds to an O2 saturation of < 85% if the patient is not anemic. The lower the Hb level, the lower the O2 saturation needed before cyanosis can be appreciated. Cyanosis does not appear at a Hb level of 10 g/dL until the O2 saturation is ~ 70%. If you see cyanosis in a severely anemic patient, this means that the concentration of Hb is very low, and the patient is critically ill. Cyanosis can be detected in the extremities (peripheral cyanosis) or the lips (central cyanosis, which is more serious). 
Infective endocarditis lesions on the hands and feet
Osler nodes are raised, painful, red lesions on the hands and feet. They are caused by immune complex deposition. Janeway lesions are small, red, and painless. They are caused by microemboli. Splinter hemorrhages manifest as short dark lines beneath the nails and are also caused by microemboli.
Jugular Venous Distention
The cardiovascular exam includes observing the right internal jugular vein (IJV). This test helps evaluate right heart function and central venous pressure.
- Elevate the patient’s head between 15° and 30° while lying supine.
- Identify the right IJV. This may take some practice. It crosses deep to the sternocleidomastoid muscle and anterior to the right ear. Ask the patient to turn their head to the left or perform a Valsalva maneuver. The hepatojugular reflux maneuver can also help find the internal jugular vein. Apply firm pressure to the right upper quadrant of the liver for a few seconds, and the IJV will fill with blood. A penlight can be very useful while trying to find the IJV.
- Measure the top of the IJV fluid level in cm above the Angle of Louis (sternal angle). A normal measurement is a vertical height 3 cm above the sternal angle.
The palpation portion of the cardiovascular exam includes evaluating the peripheral pulses in the neck (for carotid pulses) and extremities; it also palpation of the point of maximum impulse (PMI) on the anterior chest wall. A relatively strong vibration is created when the ventricles contract, transmitted down the apex of the heart and into the chest wall. The PMI is located at the 5th intercostal space in the left midclavicular line in a healthy individual.
Evaluation of the Extremities
Evaluate the extremities for temperature. Gently touch the hands and feet and note their temperatures. A well-perfused extremity will be slightly warm or at body temperature. A cold extremity indicates poor perfusion or blood being shunted away from the skin. A warm extremity suggests a reduction of vascular resistance and may be a sign of septic shock in a patient with severe hypotension.
There are a variety of pulse points with which you should be familiar. Some are regularly used (radial pulse, carotid pulse), and some are infrequently used (femoral pulse). A thorough cardiac exam requires an evaluation of all peripheral pulses. Always compare the pulses on both sides of the body to detect differences in strength.
- Carotid artery
- Radial artery
- Femoral artery
- Popliteal artery
- Posterior tibial artery
- Dorsalis pedis artery
Palpating the extremities is the preferred method for quantifying peripheral edema. The two types of edema are pitting and non-pitting edema.
Pitting edema refers to the depressed or indented area that results from pressure applied over an area of swollen/edematous tissue. It is caused by the displacement of thin, watery, protein-poor (transudative) interstitial fluid. Although it can affect any part of the body, pitting edema usually occurs in the legs, feet, and ankles due to venous insufficiency caused by congestive heart failure. Edema associated with decreased plasma oncotic pressure (e.g., low serum albumin associated with liver failure or malnutrition) does not change with dependency.
Non-pitting or “brawny” edema is observed when applied pressure does not leave an indentation. It is usually caused by compression or compromise of lymphatic drainage (lymphedema) and can also be seen in myxedema of hypothyroidism. The non-compressible subcutaneous tissue contains proteinaceous and possibly organizing collagenous substances.
Pitting edema refers to the depressed or indented area that results from pressure applied over an area of swollen/edematous subcutaneous tissue. It is caused by the displacement of thin, watery, protein-poor (transudative) interstitial fluid. Although it can affect any part of the body, pitting edema usually occurs in the legs, feet, and ankles when due to venous insufficiency caused by congestive heart failure. Edema associated with decreased plasma oncotic pressure (e.g., low serum albumin associated with liver failure or malnutrition) does not change with dependency. Non-pitting or “brawny” edema is observed when applied pressure does not leave an indentation. It is usually caused by compression or compromise of lymphatic drainage, and can also be seen in myxedema of hypothyroidism. The non-compressible subcutaneous tissue contains proteinaceous and possibly organizing collagenous or myxomatous substances.
Procedure: Press firmly on the affected area for 5 seconds—usually the lower leg (on the medial ankle or anterior tibia). Pitting is measured by the table below:
|Trace||Barely detectable impression when a finger is pressed into the skin|
|1+||Mild pitting edema, disappears rapidly|
|2+||Moderate indentation, persists for more than a few seconds|
|3+||Moderately severe pitting, more profound and persists longer than 2+|
|4+||Severe pitting that persists for over a minute|
Although all clinicians use this scale, there is no agreed-upon definition of these grades. Some sources use 0.5 cm to 2 cm for 1+ to 4+, others use 2mm to 8 mm, and some use times for rebound from 15 seconds to 2 minutes. However, this scale is still useful because it documents relative changes in edema on repeat exams. [7,8]
Point of Maximal Impulse (PMI)
- Place the palm of your right hand on the chest. With the heel of your palm at the left lower sternal border, your fingers should wrap around the patient’s ribs laterally.
- Apply some pressure to the chest wall until you feel the heartbeat in your palm.
- Identify the point of maximum impulse on the chest wall. It will be a small area, no larger than 2–3 cm wide.
Obesity will make this part of the exam difficult. The PMI of a healthy person with a normal and healthy heart will be located near the 5th intercostal space, along the midclavicular line. The PMI of a dilated or hypertrophied left ventricle will be displaced laterally.
A thrill–a vibration associated with turbulent blood flow– may be detected if valvular disease is present. This is through a damaged or malformed valve. Thrills are located near the area in which the valves are auscultated.
The detection and recognition of heart sounds play an important role in diagnosing various cardiac and valvular conditions. Because familiarity with heart sounds has such profound and practical importance, students undertaking the USMLE are expected to have a good understanding of their pathophysiology and their clinical applications.
Auscultation is best performed on bare skin. Always be sure to maintain your patient’s modesty while examining on the chest.
On auscultation, 2 heart sounds are heard from a normal heart, known as “S1” and “S2,” or the first and second heart sounds. They reflect the turbulence created when the heart valves close. Two extra heart sounds may also be heard, called the third and fourth heart sounds, “S3” and “S4” may be heard in both normal and abnormal conditions.  A murmur consists of a blowing, whooshing, or rasping sound heard during a heartbeat as blood flows through the heart’s chambers and valves or blood vessels near the heart. It can be a sign of a benign/physiologic or pathologic condition.
A murmur is a sound that is produced by turbulent blood flow across a heart valve. The turbulent flow can occur for two reasons; blood flowing across an abnormal heart valve or increased blood flowing across a normal heart valve. Heart murmurs may be classified as physiological or innocent murmurs or pathologic murmurs based on their etiology. 
- A physiological or innocent murmur is heard when there is increased turbulent blood flow across a normal valve, as can happen in patients with fever, thyrotoxicosis, or anemia and during exercise. The key features of innocent murmurs can be summarized by the “Seven S’s”:
- Sensitive (changes with body position or with respiration)
- Short duration (not holosystolic)
- Single (no associated clicks or gallops)
- Small (murmur limited to a small area and not radiating away from this area)
- Soft (low amplitude)
- Sweet (not harsh sounding)
- Systolic (occurs during and is limited to systole)
- A pathologic murmur occurs when there is turbulent blood flow across an abnormal valve. This can be due to either stenosis or insufficiency.
Stenosis is the abnormal narrowing of a valve orifice, commonly seen when age-related calcific deposits (“degenerative calcification”) occur in the aortic valve. Stenosis is also seen in a mitral valve damaged by scar tissue from healed rheumatic heart disease (RHD), mostly seen in developing countries, or by myxomatous disease and fibroelastic deficiency, more common in developed countries.
Regurgitation refers to the abnormal backward flow of blood from a high-pressure chamber to a low-pressure chamber, often due to an incompetent valve (i.e., a valve that cannot close properly). An example is valvular aortic regurgitation (AR), most commonly due to congenital or degenerative abnormalities of the aortic leaflets, aortic root, and ascending aorta in developed countries. At the same time, RHD remains the most common cause of severe AR worldwide. [10.11]
Origins and Timing of the Heart Sounds
First and Second Heart Sounds
The closure of the heart valves produces vibrations that are picked up as the two heart sounds.
The first heart sound, S1, corresponds to the closure of the atrioventricular valves—the tricuspid and mitral valves of the heart. S1 represents the start of ventricular systole. The closure of the mitral valves precedes the closure of the tricuspid valves, but this is only minimally different so that S1 is usually heard as a single sound. S1 is best heard at the apex of the heart, which points to the left of the body and is located near the PMI in a healthy individual).
The second heart sound, S2, corresponds to the closure of the semilunar valves—the aortic and pulmonary valves of the heart. S2 signifies the end of ventricular systole and the beginning of diastole. S2 is shorter, softer, and slightly higher pitched than the first heart sound. A reduced or absent S2 indicates pathology due to an abnormal aortic or pulmonic valve.
The pulmonary component of S2 is called P2, and the aortic component is called A2.
It is important to clearly identify S1 and S2 because it helps distinguish systolic from diastolic murmurs and other events in the cardiac cycle. Here are three clues to help distinguish them: the time between S1 and S2 (systole) is shorter than the time between S2 and the next S1 (diastole); S1 is usually louder than S2 (useful if tachycardia interferes with the interpretation), and S1 is synchronized with the carotid pulse. [12, 13]
Splitting of the Second Heart Sound
Physiologic Splitting of S2:
Both the aortic and pulmonic valves will close when the pressure above them is higher than the pressure in the ventricle below. The pulmonic valve closes later than the aortic valve because of two main factors. The first is that the vascular resistance in the pulmonary artery is lower than that in the aorta, so blood continues flowing into the pulmonary artery after the aortic valve closes. In 70% of normal adults, this difference can be heard as splitting of the second heart sound. Additionally, during inspiration, more blood fills the right ventricle leading to a slightly longer ejection time of the right ventricle, adding to the delayed pulmonic valve closure and to the length of the S2 split. A2 is heard widely all over the chest. P2 is usually soft and only heard at the pulmonic region (second intercostal space, left sternal border), but even here, A2 is louder.
Abnormal (Pathologic) Splitting of S2:
- Wider-than-normal splitting of S2 is an exaggerated (persistent) physiological split that is more pronounced during inspiration. Wide splitting is caused by delayed pulmonic valve closure, such as in patients with pulmonic stenosis or right bundle branch block, or early closure of the aortic valve caused by mitral regurgitation.
- Fixed splitting of S2: wide splitting that does not vary with respiration, often due to prolonged right ventricular systole, seen in atrial septal defect or advanced right ventricular failure.
- Reversed or paradoxical splitting of S2: Aortic valve closure delayed due to aortic stenosis) or conduction disease (left bundle branch block). Normal inspiratory delay of P2 usually makes the split disappear.
Absent normal/physiologic splitting of S2 can be seen in patients with:
- Severe aortic stenosis (seen most often in older adults)
- Ventricular septal defect (VSD) with Eisenmenger syndrome (in pediatric patients)
Extra Heart Sounds
Third Heart Sound (S3)
“Extra” heart sounds include the third and fourth heart sounds called S3 and S4. S3 is a mid-diastolic, low-pitched sound that occurs after S2 during the rapid passive filling of the ventricle. When there is an audible S3, the heart sounds are described as having a gallop rhythm, resembling a galloping horse, especially at rapid heart rates, which sounds like the word “Kentucky.” S3 is also called a ventricular gallop.
A physiologic S3 is produced when there is rapid filling during diastole, as can happen in conditions that increase cardiac output, such as thyrotoxicosis and pregnancy. It is also sometimes seen as a normal finding in children. On the other hand, a pathologic S3 is produced when there is decreased compliance of the ventricle (dilatation or overload), arising from high left ventricular filling pressures and abrupt deceleration of blood as it flows into the ventricle at the end of the rapid filling phase of diastole. Causes include decreased myocardial contractility, heart failure, ventricular volume overload from aortic or mitral regurgitation, hypertrophic cardiomyopathy, and left-to-right shunts (e.g., patent ductus arteriosus, ventricular septal defect). Reduced right ventricular compliance can also cause a pathologic S3, including right ventricular failure and constrictive pericarditis. [14,15]
Fourth Heart Sound (S4)
The fourth heart sound (S4) is a late diastolic sound. It is a bit higher-pitched than S3. An S4 sound can produce a gallop rhythm but with a cadence that matches the word “Tennessee.” It is never heard when there are no atrial contractions (it is absent in atrial fibrillation). S4 is caused by decreased ventricular compliance; the most common causes of a left-sided S4 include hypertensive heart disease, aortic stenosis, and ischemic and hypertrophic cardiomyopathy. As in pulmonary hypertension and pulmonary stenosis, reduced right ventricular compliance can also cause a right-sided S4.
It is possible for the third and fourth heart sounds to co-exist, which is called a quadruple rhythm. This indicates significantly impaired ventricular function. If S3 and S4 are superimposed when tachycardia is present, it produces a summation gallop. 
There are 8 possible features of heart murmurs to describe and document after auscultating a patient’s heart to formulate a diagnosis. The characteristics of a heart murmur are intensity (grade), quality, pitch, timing, configuration (shape), location, and whether they are affected by maneuvers such as hand grip, Valsalva, or squatting. For example, after examining a patient, a student may present this information: “The patient has a 2/6, harsh, low-pitched, systolic crescendo-decrescendo murmur heard loudest at the right upper sternal border that radiates to the neck into both carotids,” which lets us know this patient most likely has valvular aortic stenosis.
Timing, Pitch, and Quality
Systolic murmurs are produced during systole (contraction) of the ventricles, which is the period between S1 and S2. These murmurs can be midsystolic (ejection), late systolic, or pansystolic. Systolic murmurs can be either normal or abnormal.
Midsystolic ejection murmurs have their highest intensity in the middle of systole. They are often described as having a “crescendo-decrescendo” configuration or shape. This could be a physiological murmur caused by an increased flow through a normal valve or indicate various pathologic conditions, such as aortic stenosis or pulmonary stenosis. In cases of congenital aortic or pulmonary stenosis, an early high-pitched systolic ejection click may also be heard, representing the sudden opening of these valves, which are still mobile.
A late systolic murmur is when there is a gap between hearing S1 and the murmur. This can be caused by mitral regurgitation, as in the case of papillary muscle dysfunction or mitral valve prolapse.
A pansystolic (holosystolic) murmur extends from S1 to S2. The pitch and loudness of this murmur stay the same during systole. The murmur is caused by leakage from a high-pressure chamber to a low-pressure chamber. Causes of pansystolic murmurs include mitral or tricuspid regurgitation and ventricular septal defect.
A mid-systolic murmur in an asymptomatic individual is most likely physiological, unlike diastolic murmurs, which are always pathological.
It is usually easier to auscultate a systolic murmur than a diastolic one because it tends to be louder, with a harsher sound, and does not require a special maneuver to accentuate it.
Diastolic murmurs, as their name implies, occur during ventricular diastole. They are always pathological. They are less common, softer, and more challenging to hear than systolic murmurs. There are two basic types in adults. Early decrescendo (meaning the sound decreases in intensity from the beginning to the end of the murmur) diastolic murmurs are caused by regurgitant flow through an incompetent semilunar valve, usually the aortic. Rumbling diastolic murmurs in mid- or late diastole are most often caused by mitral stenosis.
An early diastolic murmur starts with S2 and is a decrescendo murmur that is loudest at its commencement. It produces a high-pitched sound. Causes of an early diastolic murmur include aortic regurgitation or pulmonary regurgitation. The decrescendo quality mirrors the peak in aortic and pulmonary pressures at the start of diastole.
Compared to early diastolic murmurs, mid-and late diastolic murmurs are lower-pitched and can be mitral or tricuspid stenosis or atrial myxoma (rare). They may be described as “rumbling” in quality. In patients with mitral stenosis, the diastolic murmur may be preceded by a high-pitched opening snap which represents the abrupt opening of the stenosed mitral valve.
Continuous murmurs occur during both systole and diastole without a pause. The sound is created by unidirectional flow when there is communication between a high-pressure and a low-pressure source. The constant pressure gradient results in a continuous flow. The most common causes are nonvalvular and include patent ductus arteriosus, an arteriovenous fistula, and coarctation of the aorta. A venous hum is also a continuous sound that is benign, common in children, and produced by turbulence of blood in the jugular veins.
If a murmur is heard, various dynamic maneuver tests are required to characterize it further. These maneuvers alter circulatory hemodynamics and, in doing so, change the emphasis with different murmurs.
- Grade 1: Murmur is very soft and is initially not heard.
- Grade 2: Murmur is soft but can be readily heard by a skilled examiner.
- Grade 3: Murmur is easy to hear.
- Grade 4: Murmur is slightly loud and accompanied by a palpable thrill (these murmurs are always pathological).
- Grade 5: Murmur is very loud, and the accompanying thrill is easily palpable.
- Grade 6: Murmur is so loud that it is audible even without directly placing the stethoscope on the chest.
The intensity of the murmur doesn’t always correlate to the severity of the lesions, as a smaller VSD produces louder murmurs than a larger VSD.
- Murmurs of grade III and above are usually pathological.
- Thrills are palpable murmurs and only can be felt in murmurs of grade IV and above.
Location, Radiation, and Dynamic Maneuvers
There are four locations on the chest that the stethoscope is placed over to listen to heart sounds and any abnormal findings. Auscultation can be carried out clockwise, starting with the aortic, then the pulmonic and mitral areas, followed by the tricuspid area.
To identify the difference between the two heart sounds on auscultation, palpation of the pulse (carotid or radial) while listening to the heart can be helpful. The pulse indicates systole, therefore corresponding to the first heart sound S1. Knowing when systole and diastole occur is essential if an additional heart sound is heard for its timing in the cardiac cycle to be accurately described. 
The aortic area is located in the second intercostal space, at the right sternal border. The diaphragm of the stethoscope can be placed at this site to listen for aortic stenosis.
The pulmonic area is opposite the aortic area t the left second intercostal space, at the left sternal border. The diaphragm is placed here to listen for P2 and pulmonary flow murmurs.
The mitral area is also referred to as the apex of the heart. It is located in the fifth intercostal space, in the midclavicular line. This area should be auscultated with both the bell and the diaphragm of the stethoscope. Low-pitched sounds, such as the diastolic murmur of mitral stenosis and the third heart sound, can be better appreciated with the bell. The diaphragm can be used to detect high-pitched sounds, such as the fourth heart sound and mitral regurgitation.
The tricuspid area is located at the left sternal border in the fourth and fifth intercostal spaces. The diaphragm is placed at this site to listen for tricuspid regurgitation.
Erb’s point is located at the third intercostal space along the left sternal border, one intercostal space below the pulmonic area. It is the midpoint between the base and apex of the heart. Both the S1 and S2 sounds can be heard here, and all other heart sounds. It is often used to quickly assess heart rate and determine if there is a pulse deficit (when not all heartbeats reach the periphery, e.g., in atrial fibrillation, detected by simultaneously palpating the radial pulse). Aortic regurgitation is also heard best here (if not due to aortic root dilatation).
Know that even when a murmur is heard more clearly in a specific location, it might not always help determine its origin because a murmur can radiate away its site of origin. For example, a mitral regurgitation (MR) murmur is best heard in the mitral area, but it may also be heard anywhere else on the chest. The murmur of MR is also characterized by its radiation to the left axilla. The systolic ejection murmur of aortic valve origin characteristically radiates to the neck/carotid arteries.
Performing dynamic maneuvers means altering heart sounds by changing circulatory hemodynamics. These can distinguish the clinical cause of similar auscultatory findings and are frequently tested on board exams. It is essential to understand the physiologic alterations produced by certain maneuvers.
If a murmur is heard, various dynamic maneuver tests can characterize it further. These maneuvers alter circulatory hemodynamics and, in doing so, change the emphasis with different murmurs.
Respiration can be used to differentiate between right-sided and left-sided murmurs. Inspiration has the effect of increasing venous return, and as there is an increase in blood flow to the right side of the heart, right-sided murmurs are accentuated. On the other hand, expiration causes left-sided murmurs to become louder.
Another respiratory maneuver is deep expiration. As the patient leans forward and is in deep expiration, the base of the heart is brought closer to the chest wall. In this maneuver, the murmur of aortic regurgitation, not caused by a dilated aortic root, can be appreciated at Erb’s point, which is the point between the base and the apex of the heart.
- 1. The Valsalva Maneuver
This is a well-known and often-used dynamic maneuver involving forcible exhalation against a closed glottis after full inspiration for 10-20 seconds, causing increased intrathoracic pressure.The normal systolic blood pressure (SBP) response follows four phases (two phases while the glottis is closed and two after the start of breathing normally):
Phase I (onset of the strain phase) is a very short phase at the start of the maneuver. The intrathoracic pressure increases, causing an increase in cardiac output and blood pressure (due to compression). There is also a pressure increase in the chest and abdomen blood vessels (including the superior and inferior vena cavae) and the cardiac chambers. This increase in pressure is associated with a reciprocal decrease in heart rate due to the baroreceptor reflex.
Phase II (continued strain): SBP decreases to below baseline due to decreased venous return as the strain is maintained. Most murmurs become softer, but the systolic murmur of hypertrophic cardiomyopathy increases and the murmur of mitral valve prolapse is heard. Heart rate increases due to the baroreceptor response (reflex) to a decreased SBP.
Phase III (“release phase” = normal breathing starts): Very short phase characterized by a rapid drop in SBP and decreased left ventricular volume due to decreased intrathoracic pressure, which may cause syncope or pre-syncope/dizziness. Right-sided murmurs are louder for a short interval. The heart rate increases due to the baroreceptor reflex.
Phase IV (recovery or “overshoot” phase): SBP increases due to reflex sympathetic activation and increased stroke volume. Heart rate decreases due to the baroreceptor reflex.
The Valsalva maneuver accentuates the murmurs of hypertrophic cardiomyopathy and mitral valve prolapse when listening at the left sternal edge.
Squatting is another dynamic maneuver that causes an increase in venous return. The patient quickly moves from a standing position to a squat in this test. This makes the murmurs of aortic stenosis and mitral regurgitation louder, but the murmurs of hypertrophic cardiomyopathy and mitral valve prolapse become softer and shorter. When the patient does the opposite and stands quickly from a squatting position, then the opposite changes in murmurs occur.
- Isometric Exercise
Isometric exercise can also be used for eliciting certain types of murmurs. For this exercise, the patient sustains a handgrip for half a minute. This exercise increases afterload (or peripheral resistance). The murmur of mitral regurgitation is accentuated. The murmur of aortic stenosis and hypertrophic cardiomyopathy becomes softer, while the murmur of mitral valve prolapse becomes shorter.
|Normal Heart Sounds|
|First heart sound (S1)||Closure of the mitral and tricuspid valves|
|Second heart sound (S2)||Closure of the aortic and pulmonary valves|
|Extra Heart Sounds|
|Third heart sound (S3)||A physiological S3 is caused by rapid diastolic filling (e.g., pregnancy, thyrotoxicosis, and sometimes in children). A pathological S3 is caused by reduced compliance of the left ventricle (e.g., left ventricular failure, aortic regurgitation, mitral regurgitation, patent ductus arteriosus, and a ventricular septal defect) or reduced compliance of the right ventricle (right ventricular failure, constrictive pericarditis).|
|Fourth heart sound (S4)||Decreased ventricular compliance of the left ventricle (aortic stenosis, mitral regurgitation, hypertension, angina, myocardial infarction) or the right ventricle (pulmonary hypertension, pulmonary stenosis)|
|Midsystolic murmur||Increased flow through a normal valve (physiologic or innocent murmur), aortic stenosis, pulmonary stenosis, hypertrophic cardiomyopathy, atrial septal defect|
|Late systolic murmur||Mitral regurgitation (MR), due to papillary muscle dysfunction, mitral valve prolapse, or infective endocarditis|
|Pansystolic murmur||Mitral regurgitation, tricuspid regurgitation, ventricular septal defect (VSD), aortopulmonary shunts|
|Early diastolic murmur||Aortic regurgitation, pulmonary regurgitation|
|Mid-diastolic murmur||Mitral stenosis, tricuspid stenosis, atrial myxoma (rare), acute rheumatic fever murmur (Carey Coombs murmur of mitral valvulitis)|
|Presystolic murmur||Mitral stenosis, tricuspid stenosis, atrial myxoma|
|Continuous murmur||Patent ductus arteriosus, arteriovenous fistula, venous hum|
- Where is the murmur of aortic regurgitation heard best?
- At the left lower sternal border, with the patient in the left lateral decubitus position, after a short period of exercise
- At the right upper sternal border during systole and in the carotid arteries to assess for radiation
- At the left lower sternal border, with the patient sitting up, leaning forward, and holding their breath after expiration
- At the left lower sternal border, augmented by Valsalva maneuver
- What distinguishes a grade 6 murmur from other grades in the Levine System?
- It is a murmur that is soft and difficult to hear.
- It can be heard without direct placement of the stethoscope.
- It has a palpable thrill accompanying it.
- It can only be heard by someone experienced in auscultation.
- What is the cause of the physiological splitting of the second heart sound?
- Closure of the mitral and tricuspid valves just before ventricular systole.
- Increase in venous return during inspiration, causing the aortic valves to remain open for longer.
- Aortic regurgitation with retrograde leakage through the valve during diastole
- Delayed closure of the pulmonic valve due to lower pressures in the pulmonary circulation and increased venous return during inspiration.
Answers: 1C, 2B, 3D