Cardiovascular System Physical Examination Objectives

Medex Objectives Fall 2002

MEDEX Northwest Physician Assistant Objectives Home: http://faculty.washington.edu/alexbert/MEDEX/

Last updated 7 Dec 2003

Cardiovascular System Physical Examination Objectives

Goal: After learning the prescribed information, learning the prescribed cardiovascular exam and practicing it frequently, the student should be able to identify and describe pathology associated with cardiovascular system in any given patient.

1. Be able to describe the components of the Cardiovascular Exam, and when and why portions are done.

Norm

This question pertains to the cardiovascular branching exam in our syllabus. Use this with Baldwigs book, pages 208 and 218-221 to get a better understanding for what we have been taught. The answer would be too long to type for this question.

Vince B

refer to cardio branching exam.

2. Review the anatomy and physiology of the cardiovascular (CV) system. Note in particular the following points:

location of the apical impulse (aka: P.M.I.)

tracing the circulation through the heart

events in the cardiac cycle: systole and diastole, the timing and causes of S₁, S₂, opening snap, S₃, and S₄

normal splitting of S₂ and S₁

locations on the chest wall for sounds and murmurs from the four heart valves

concepts of cardiac output, stroke volume, preload and afterload

relation of internal jugular veins to right atrial pressure

changes with age

Zen Seeker

	Diastolic	Systolic
Aortic	Regurgitation	Stenosis
Mitral	Stenosis	Regurgitation

Norm

Location of the apical pulse (aka PMI) is located at the 5th intercostal space Mid-clavicular line.

The circulation of the heart goes as follows. Blood enters from the superior vena cava into the R atrium, through the tricuspid valve into the R ventricle. From there it travels through the pulmonary valve into the pulmonary artery then to the lungs. From the lungs it enters via the pulmonary veins into the L atrium. From there the blood goes through the mitral valve into the L ventricle where it is then squeezed through the Aortic valve into the aorta and into systemic circulation. Swartz pg. 246

Systole: Is the period when the heart contracts and the fibers shorten, forcing blood out of the heart. Tabers

Diastole: Is the relaxation phase of the heart when the heart dilates and fills with blood. Tabers

S1: Is the closure of the semi-lunar valves, S-2 is the sound of the aortic and the pulmonic valves closing. Swartz pg350

Opening snap: Is heard only when the valves are damaged such as with stenotic or narrowed valves. The sound of a damaged atrioventricular valve. Swartz pg 350

S3: Is an abnormal heart sound in people over the age of 30. It is the sound following S2 that signifies volume overload of the ventricle, regurgitation, valve lesions or CHF. Swartz pg 350

S4: Is an abnormal heart sound that occurs before the S1 sound. It can signify noncompliant or stiff ventricle that may have resulted from hypertrophy of the ventricle. Swartz pg 352

Normal S1-S2 splitting: During inspiration more blood is drawn into the right heart causing a longer ejection into the pulmonary artery and the pulmonary vein remaining open longer. This is the cause of the physiologic split of S2. Swartz pg 352

Location on the chest for sounds and murmurs from the four heart valves. Swartz pg 349

Aortic: 2nd intercostal space, R sternal border

Pulmonic: 2nd intercostal space, L sternal border

Tricuspid: L lower sternal boarder

Mitral: Cardiac apex, 5th intercostal space mid-clavicular line.

Cardiac Output: The amount of blood discharged from the L or R ventricle

per minute. Calculated by multiplying the stroke volume X heart rate. Tabers

Stroke volume: The amount of blood ejected from the left ventricle at each heartbeat. Tabers

Preload: The end diastolic stretch of the cardiac muscle fiber. It is influenced by venous return and the compliance of the ventricles. (The greater the volume the greater the stretch) Tabers

Afterload: The stress or tension that develops in the ventricular wall during systole. The force the ventricles must overcome to eject their blood volume. Tabers

Relation of the Jugular veins to the R atrial pressure: The jugular veins are provide direct information about the right side of the heart due to the fact that they drop their blood into the R atrium and the R ventricle. If there are stenotic changes of the pulmonic or mitral valves as may occur with age jugular venous distension may occur.

Vince B Bates. 8th ed. Review the anatomy and physiology of the cardiovascular (CV) system. Note in particular the following points:

246-location of the apical impulse (aka: P.M.I.) -located in 5th IC and 7-9 cm lateral to midsternal line.

247-tracing the circulation through the heart- Blood enters through the superior/inferior vena cava to Right atrium. through tricuspid valve into Right ventricle and out through pulmonic valve into pulmonary artery to lungs. Returns through pulmonary veins into Left atrium. Passes though Mital valve into Left ventricle, then out through Aortic valve into aorta and system.

events in the cardiac cycle:

248-systole and diastole-

during systole, the aoric valve is open, allowing ejection of bleed from left ventricle into aorta- mitral valve is closed.

During diastole, the aortic valve is closed to prevent blood from backflowing into left ventricle- mitral valve is open. First and second heart sounds are duration of systole and diastole

249-the timing and causes of S₁, S_2-

during systole, LV starts to contrast and ventricular pressure exceeds left atrial pressure closing the mitral valve producing the first heart sound (S1).

When LV pressure drops below aortic pressure, aortic valve shuts producing second heart sound (S2).

250-opening snap-

in diastole, LV pressure drops and falls below LA pressure and the mitral valve opens. This is usually a silent event, but may be audible as a pathologic opening snap (OS) if valve leaflet motion is restricted, as in mitral stenosis.

250- S₃, and S_4-

In children and young adults, a third sound may be heard (S3) and arises from deceleration of column of blood against the ventricular wall. In older adults an S3 (S3 gallop) usually indicates a pathologic change in ventricular compliance.

251-normal splitting of S₂ and S₁ -

second heart sound-come from closing of aortic (A2) and pulmonary valve (P2). During expiration, these two are fused together into a single sound S2, but during inspiration they separate slightly and S2 spits into its two audible components.

252-locations on the chest wall for sounds and murmurs from the four heart valves

Sounds and murmurs arising from mitral valve are best heard at and around the cardiac apex. Tricuspid- at or near the lower left sternal border. Murmurs arising from Pulmonic valve- 2^nd or 3^rd left intercostals space close to sternum, but may be heard higher or lower. Aortic valve- anywhere from right 2^nd intercostals to apex.

254-concepts of cardiac output-

the amount of blood ejected from each ventricle during one minute. Cardiac output= heart rate+ stroke volume.

254-stroke volume-

amount of blood ejected with each heartbeat.

254-preload and after load-

preload- the load that stretches the cardiac muscle prior to contraction. after load- vascular resistance against which the ventricle must contract.

256-relation of internal jugular veins to right atrial pressure

pressure in the jugular veins reflects right atrial pressure.

258-changes with age-

age may affect the location of apical impulse, pitch of heart sounds and murmurs, stiffness of arteries, and BP.

3. Identify the potential significance of small, weak pulses and large, bounding pulses.

Anonymous Table 9-3, Bates, p. 322

The pulse pressure is diminished, and the pulse feels weak and small. The upstroke may feel slowed, the peak prolonged. Causes include (1) decrease stroke volume, as in heart failure, hypovolemia, and severe aortic stenosis, and (2) increased peripheral resistance, as in exposure to cold and severe congestive heart failure.

The pulse pressure is increased and the pulse feels strong and bounding. The rise and fall may feel rapid, the peak brief. Causes include (1) an increased stroke volume, a decreased peripheral resistance, or both, as in fever, anemia, hyperthyroidism, aortic regurgitation, arteriovenous fistulas, and patent ductus arteriosus, (2) an increased stroke volume due to slow heart rates, as in bradycardia and complete heart block, and (3) decreased compliance (increased stiffness) of the aortic walls, as in aging or atherosclerosis.

Anonymous

Small, weak pulses- Causes include:

*Decreased stroke volume, as in heart failure, hypovolemia, and severe aortic stenosis.

*Increased peripheral resistance, as in exposure to cold and severe CHF.

Large, bounding pulses- Causes include:

*An increased stroke volume, a decreased peripheral resistance, or both, as in fever, anemia, hyperthyroidism, aortic regurgitation, arteriovenous fistulas, and patent ductus arteriosus.

*An increased stroke volume due to slow heart rates, as in bradycardia and complete heart block.

*Decreased compliance (increased stiffness) of the aortic walls, as in aging or atherosclerosis.

Norm (I could not find a resource for this info, this came from my head and prior cardiovascular studies. Take heed.)

A small weak pulse can signify cardiogenic shock related to cardiomyopathy, hypovolemic shock, or septicemia. Large bounding pulse can indicate fluid overload (CHF), cardiac dysrythmias.

Vince B Bates.270

Identify the potential significance of small, weak pulses- and large, bounding pulses. Small, thready, or weak pulse in cardiogenic shock; bounding, large pulse in aortic insufficiency (pg 90).

4. Be able to properly auscultate for a carotid bruit.

Anonymous

During palpation of the carotid artery, you may detect humming vibrations that feel like the throat of a purring cat. These are termed a thrill. If you feel them, listen over the area with the diaphragm of the stethoscope (or bell which may fit better in the neck) for a bruit, a murmurlike sound of vascular rather than cardiac origin.

You should also listen for bruits over the carotid arteries if the patient is middle-aged or elderly or if you suspect cerebrovascular disease. Heart sounds alone do not constitute a bruit.

A carotid bruit with or without a thrill in a middle-aged or older person suggests but does not prove arterial narrowing. An aortic murmur may radiate to the carotid artery and sound like a bruit.

Anonymous

A carotid bruit with or without a thrill in a middle-aged or older person suggests but does not prove arterial narrowing. An aortic murmur may radiate to the carotid artery and sound like a bruit.

5. Identify common potential errors of blood pressure measurement.

Anonymous Bates, pp. 294-296

To measure blood pressure accurately, you must carefully choose a cuff of appropriate size. Cuffs that are too short or too narrow may give falsely high readings. Using a regular-size cuff on an obese arm may lead to a false diagnosis of hypertension.

If the brachial artery is much below heart level, blood pressure appears falsely high. The patient’s own effort to support the arm may raise the blood pressure.

A loose cuff or a bladder that balloons outside the cuff leads to falsely high readings.

An unrecognized auscultatory gap may lead to serious underestimation of systolic pressure or overestimation of diastolic pressure. If you find an auscultatory gap, record your findings completely (e.g. 200/98 with an auscultatory gap from 170 to 150).

Anonymous Bates: pgs. 294 & 295

1. Cuffs that are too short or too narrow may give falsely high readings.

2. Using a regular-sized cuff on an obese arm may lead to a false diagnosis of hypertension.

3. If the brachial artery is much below the heart level, BP appears falsely high.

4. The patients own effort to support the arm may rise the BP.

5. A loose cuff or a bladder that balloons outside the cuff leads to falsely high readings.

Paul, Bates pg 294-298:

Improperly sized blood pressure cuff. Cuffs that are too short or too narrow may give falsely high readings. Using a regular size cuff on an obese arm may lead to a false diagnosis of hypertension
Patient should not have ingested caffeine or smoked for 30 minutes and should rest for at least 5 minutes
Room should be quiet and comfortably warm
Arm should be resting and free of clothing
Arm should be free of fistulas, scarring from brachial cutdowns, and lymphedema
Position the arm is at heart level. If the brachial artery is much below heart level, blood pressure appears falsely high.
A loose cuff or a bladder that balloons outside the cuff leads to falsely high readings.
An unrecognized auscultatory gap (silent interval that may be present between the systolic and diastolic pressures) may lead to serious underestimation of systolic pressure or overestimation of diastolic pressure
Avoid slow or repetitive inflations of the cuff, because the resulting venous congestion can cause false readings.

Norm Bates, 8th Ed., p. 255; Swartz p. 353, 367

Level of recent physical activity, emotional state, noise, body temperature, coffee, tobacco, drugs, time of day,
Inspiratory increase: BP increases up to 10 mm Hg upon inspiration during quiet respiration.
Cuff error: is +/- 3 mm Hg.
Cuff size: If too small, will increase BP reading. Cuff should fit snugly, with lowest edge 1” above antecubital fossa.
Arm position: Support pt arm at heart level. If pt has to support own arm, will increase reading.
Stethoscope technique: If you push too hard on the diaphragm, the diastolic reading will decrease, with no change in systolic.
Auscultatory gap: This is the disappearance of Korotkoff sounds after the initial appearance and then reappearance at a lower BP. (Korotkoff sounds are the turbulent pulse sounds heard when auscultating BP). This gap is present when there is a decreased blood flow to the extremities, as found in HTN and aortic stenosis. An error can occur if the SBP is mistaken for the lower, reappearance of Korotkoff sounds after the gap.

Vince B Bates. 75-79

Identify common potential errors of blood pressure measurement. include improper size, bladder or stethoscope not over artery, malfunctioning meter, pt not at rest.

6. Identify the potential significance of BP differences between the two arms.

Anonymous

Normal difference is 5mm Hg to 10mm Hg

Pressure difference of more than 10-15 mm Hg suggests arterial compression or obstruction on the side with the lower pressure.

Anonymous Bates: pg. 297

BP should be taken in both arms at least once. Normally, there may be a difference in pressure of 5mm Hg and sometimes up to 10mm Hg. Subsequent readings should be made on the arm with the higher pressure.

Brent K Swartz p. 369

A BP difference between arms can be a result of supravalvular aortic stenosis.

Norm

Could mean supravalvular aortic stenosis: the R. arm would be hypertensive, the L. arm hypotensive. Swartz, p. 369
Aortic stenosis: An impairment of blood flow from the L. ventrical to the aorta, as a result of aortic valvular disease or gunk just above or below the aortic valve. Taber’s

7. Describe the blood pressure findings seen in orthostatic hypotension.

Anonymous

A fall in systolic pressure of 20 mm Hg or more, especially when accompanied by symptoms, indicates hypotension.

Anonymous

A fall in systolic pressure of 20mm Hg or more, especially when accompanied by symptoms indicates orthostatic (postural) hypotension. Causes include drugs, loss of blood, prolonged bed rest, and diseases of the autonomic nervous system.

Brent K Swartz p. 368

Once the patient has been a recumbent position for at least 5 minutes, measure BP and P. Then have patient stand and repeat immediately. A drop in systolic BP of 20mm Hg or more in addition to associated Sx’s such as dizziness or syncope, would be characterized as orthostatic hypotension.

Norm Swartz, p. 368-369

To take orthostatic BP/P, the pt will lie down for 5 min., and a recumbent BP and pulse will be taken. The pt. will then stand, and a standing BP and pulse will be taken immediately.
If the standing BP is 20 mm Hg lower than the recumbent BP, and the pt is symptomatic (dizziness, syncope upon standing), then the pt has orthostatic hypotension.
The heart rate would probably undergo a compensatory increase upon standing.

8. Identify the blood pressure standards for stating that a patient has hypertension or isolated systolic hypertension.

* Optimal blood pressure: systolic <120 and diastolic <80

* Normal blood pressure: systolic 120-129 and diastolic 80-84

* High-normal blood pressure: systolic 130-139 or diastolic 85-89

* Hypertension:

Stage 1: systolic 140-159 or diastolic 90-99

Stage 2: systolic 160-179 or diastolic 100-109

Stage 3: systolic 180 or diastolic 110

ISH SBP > 160 with a DBP < 90

Zen Seeker

Classification and Management of Blood Pressure for Adults
				Initial Drug Therapy
BP Classification	*SBP, mm Hg**	*DBP, mm Hg**	Lifestyle modifications	Without Compelling Indications	With Compelling Indications
Normal	<120	And <80	Encourage
Prehypertension	120-139	Or 80-89	Yes	No antihypertensive drug indicated	Drug(s) for compelling indications†
Stage 1 Hypertension	140-159	Or 90-99	Yes	Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination	Drug(s) for the compelling indications.‡ Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed
Stage 2 Hypertension	> 160	Or >100	Yes	Two-drug combination for most† (usually thiazide-type diuretic and ACEI or ARB or BB or CCB)
DBP=diastolic blood pressure, SBP=systolic blood pressure. Drug abbreviations: ACEI=angiotensin converting enzyme inhibitor; ARB=angiotensin receptor blocker; BB=beta-blocker; CCB=calcium channel blocker * Treatment determined by highest blood pressure category † Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension. ‡ Treat patients with chronic kidney disease or diabetes to blood pressure goal of <130/80 mmHg. Adapted from JNC VII

AMA1998 - Old School

Blood Pressure Classifications For People Age 18 and Older*
CATEGORY	SYSTOLIC	DIASTOLIC
Normal blood pressure	Lower than 130 mm Hg	Lower than 85 mm Hg
High-normal blood pressure	130 to 139 mm Hg	85 to 89 mm Hg
Hypertension:
Stage 1 (mild)	140 to 159 mm Hg	90 to 99 mm Hg
Stage 2 (moderate)	160 to 179 mm Hg	100 to 109 mm Hg
Stage 3 (severe)	180 to 209 mm Hg	110 to 119 mm Hg
Stage 4 (very severe)	210 mm Hg or higher	120 mm Hg or higher
*A diagnosis of hypertension is based on two or more blood pressure readings taken at separate visits to the doctor's office. If your systolic blood pressure falls into one category and your diastolic pressure into another, the higher reading will be used to classify your blood pressure status. For example, a blood pressure reading of 160/92 mm Hg would be classified as stage 2 (moderate) hypertension, and a reading of 180/120 mm Hg would be classified as stage 4 (very severe) hypertension. For people who have isolated systolic hypertension, a reading of 170/85 mm Hg would be classified as stage 2 (moderate) hypertension.

Anonymous

Hypertension= mild-140-159/90-99

Mod-160-179/100-109

Severe-180+/110+

Isolated systolic hypertension= 140/90

Anonymous

HYPERTENSION	SYSTOLIC(mm Hg)	DIASTOLIC(mm Hg)
Stage 3 (severe)	> 180	> 110
Stage 2 (moderate)	160-179	100-109
Stage 1 (mild)	140-159

Hypertension is diagnosed when a higher than normal level has been found on at least 2 or more visits after initial screening. Either the diastolic blood pressure (DBP) or the systolic blood pressure (SBP) may be considered high. In isolated systolic hypertension, systolic pressure is 140mm Hg or more and diastolic pressure is less than 90mm Hg

Brent K answer provided in objectives

BP Standards:

Optimal BP S<120 and D<80

Normal BP S120-129 and D 80-84

High-normal BP S130-139 and D 85-89

Hypertension Standards:

Stage 1: S140-159 or D90-99

Stage 2: S160-179 or D100-109

Stage 3: S>180 or D>110

Isolated systolic HTN: S³160 with a D£90

Norm

- Optimal BP: SBP<120 DBP<80

- Normal BP: SBP 120-129 DBP 80-84

- High-normal BP: SBP 130-139 DBP 85-89

- HTN: Stage 1: SBP 140-159 DBP 90-99

Stage 2: SBP 160-179 DBP 100-109

Stage 3: SBP >180 or DBP > 110

- Isolated systolic HTN: SBP > 160 DBP < 90

9. Identify the significance of a femoral pulse that is smaller and later than the radial pulse.

Anonymous

A femoral pulse that is later and smaller than a radial pulse coarctation of the aorta or occlusive aortic disease. Blood pressure is lower in the legs than in the arms in these conditions.

Anonymous

This suggests coarctation of the aorta or occlusive aortic disease. Blood pressure is lower in the legs than in the arms in these conditions.

Brent K Bates Pocket Guide p.66

The significance of a smaller and later femoral pulse compared to the radial pulse can be indicative of an arterial occlusion or arteriosclerosis obliterans.

Norm

Radial and femoral pulses should peak at either the same time or with the femoral pulse first.
Any delay or weakness in the femoral pulse should raise suspicion of coarctation of the aorta, esp. in a hypertensive individual.
This technique need be performed on only one side.
To support Dx: Compare leg and arm systolic BP. With coarctation of the aorta, leg SBP < arm SBP. (Normal: leg SBP > arm SBP.) Swartz, p. 369, 399
Coarctation of the aorta: A localized congenital malformation resulting in the narrowing of the aorta, often resulting in HTN. Taber’s

10. Identify the potential significance of increased jugular venous pressure.

Anonymous

Increased pressure suggest right-sided heart failure, or less commonly, constrictive pericarditis, tricuspid stenosis, or superior vena cava obstruction.

Anonymous

This suggests right-sided heart failure, or less commonly, constrictive pericarditis, tricuspid stenosis, or superior vena cava obstruction.

In patients with obstructive lung disease, venous pressure may appear elevated on expiration only; the veins collapse on inspiration. This finding does not indicate congestive heart failure.

Brent K Swartz p. 371

Increased jugular venous pressure is a sign of right-sided heart failure. If the right side of the heart becomes inefficient, for whatever reason, the venous system backs up causing increased venous pressure and distention.

Bill

The raised pressure in the superior vena cava can be observed in the neck in the form of jugular vein engorgement (raised jugular venous pressure). Pathology book, page 174.

The jugular venous pulse provides direct information about the pressures in the right side of the heart, because the jugular system is in direct continuity with the right atrium. Swartz book, page 354.

11. Describe the technique for checking the hepatojugular reflux and its potential significance.

Anonymous

Hopefully, I will find more on this but I think that you press upward and hold the liver for about 30 sec. And watch the jugulars for distension.

This could potentially indicate CHF.

Michelle Swartz pg. 374

-Useful test for assessing high jugular venous pressure, also known as abdominal compression.

-By applying pressure over the liver, the examiner can grossly assess right ventricular function. Patients with right ventricular failure have dilated sinusoids

in the liver.

-The procedure is performed with the patient lying in bed, mouth open, breathing normally; this presents a Valsalva maneuver. The examiner places the right hand

over the liver in the right upper quadrant and applies a firm, progressive pressure. Compression is maintained for 10 seconds. The normal response is for the internal and external jugular veins to show a transient increase in distention during the first few cardiac cycles, which is followed by a fall to baseline levels during the later part of the

compression. In patients with right ventricular failure or elevated pulmonary artery wedge pressure, the neck veins remain distended during the entire period of compression; this distention falls rapidly (at least 4 cm) on sudden release of the compressing hand.

Sung K, Swartz, p.374

A useful test in assessing high jugular venous pressure. By applying pressure over the liver, the examiner can grossly assess right ventricular function. Patients with R. ventricular failure have dilated sinusoids in the liver. Pressure on the liver pushes blood out of these sinusoids and into the inferior vena cava and right heart, causing further distention of the neck veins. The procedure is performed with the patient lying down at a 30 degree angle, mouth open, breathing normally; this prevents a Valsalva maneuver. The examiner places the right hand over the liver in the right upper quadrant and applies a firm, progressive pressure that is maintained for 10 seconds (30 seconds per Randy). The normal response is for the internal and external jugular veins to show a transient increase in distention during the first few cardiac cycles, which is followed by a fall to baseline levels during the later part of the compression. In patients with R. VENTRICULAR FAILURE or ELEVATED PULMONARY ARTERY WEDGE PRESSURE, the neck veins remain distended during the entire period of compression; this distention falls rapidly (at least 4 cm) on sudden release of the compressing hand.

Bill

This procedure is performed with the patient lying in bed, mouth open, breathing normally; this prevents a Valsava maneuver. The examiner places the right hand over the liver in the right upper quadrant and applies a firm, progressive pressure. Compression is maintained for 10 seconds. The normal response is for the internal and external jugular veins to show a transient increase in distention during the first few cardiac cycles, which is followed by a fall to baseline levels during the later part of the compression. In patients with right ventricular failure or elevated pulmonary artery wedge pressure, the neck veins remain distended during the entire period of compression; this distention falls rapidly (at least 4 cm) on sudden release of the compressing hand. Swartz book, page 374.

12. Describe how you can tell S₁ from S₂ – by timing and by loudness of the sounds at the apex and the base.

Anonymous

S1 is the first of the paired heart sounds, S2 is the second, and the relatively long diastolic interval separates one pair from the next.

S1 is usually louder than S2 at the apex; more reliable S2 is usually louder than S1 at the base.

Anonymous

When listening to heart sounds through the stethoscope, S1 is the first of the paired heart sounds and S2 is the second sound. The relatively long diastolic interval separates one pair from the next.

S1 is softer than S2 at the base (R and L 2^nd interspaces). S2 is usually louder than S1 at the base.

S1 is often, but not always, louder than S2 at the apex.

Michelle Swartz pg 350

S1= the first heart sound made by the closing of the AV values, the tricuspid and mitral valves. This is heard loudest at the cardiac apex.

S2= the second heart sound, made by the closure of the semilunar valves, the aortic and the pulmonic. This is heard loudest at the base.

Sung K, Swartz, p.378-9

The most reliable way of identifying S₁ and S₂ is to time the sounds by palpating the carotid artery. While the examiner’s right hand is positioning the stethoscope, the left hand is placed on the patient’s carotid artery. The sound that comes before the carotid pulse is the S₁. The S₂ follows the pulse. The carotid, not the radial pulse, must be used. Also S₁ is heard louder at the apex and S₂ is heard louder at the base.

Bill Swartz book, page 378-379, with pictured demonstration.

The most reliable way of identifying S1 and S2 is to time the sounds by palpating the carotid artery. While the examiners right hand is positioning the stethoscope, the left hand is place on the patient’s carotid artery. The sound that precedes the carotid pulse is the S1. The S2 follows the pulse. The carotid, no the radial pulse, must be used.

13. Define "thrill" as it is used in cardiovascular exam, and identify its significance.

Anonymous

Thrill is a vibration accompanying a cardiac or vascular murmur that can be palpated.

Thrills may accompany loud, harsh, or rubbing murmurs as those of aortic stenosis, patent ductus arteriousus, ventricular septal defect, and less commonly, mitral stenosis.

Anonymous

During palpation of the carotid artery, you may detect humming vibrations that feel like the throat of a purring cat. These are termed a thrill. If you feel them, listen over the area with the diaphragm of the stethoscope for a bruit, a murmurlike sound of vascular rather than cardiac origin.

Thrills may accompany loud, harsh, or rumbling murmurs such as those of aortic stenosis, patent ductus arteriosus, ventricular septal defect, and less commonly mitral stenosis.

A carotid bruit with or without a thrill in a middle-aged or older person suggests but does not prove arterial narrowing. An aortic murmur may radiate to the carotid artery and sound like a bruit.

Michelle Swartz pg. 374

-Thrill- low-frequency cutaneous vibrations associated with loud heart murmurs.

-These are superficial vibratory sensations felt on the skin overlying an area of turbulence. The presence of thrill indicates a loud murmur.

Sung K, Swartz, p.376

Thrills are the superficial vibratory sensations felt on the skin overlying an area of turbulence through the heart or a major artery (sensation is like placing a hand over the neck of a purring cat). The palpation of thrills is generally of little importance. It may signify a murmur after auscultation over the same area which may or may not have a pathological cause.

Bill Swartz book, page 376.

Thrills are the superficial vibratory sensations felt on the skin overlying an area of turbulence. The presence of a thrill indicates a loud murmur.

14. Identify the significance of a cardiac impulse felt lateral to the midclavicular line.

Anonymous

They suggest cardiac enlargement or displacement.

Anonymous

Cardiac impulses lateral to midclavicular line suggests cardiac enlargement or displacement. The apical impulse may be displaced upward into the left by pregnancy or a high left diaphragm. It may also be displaced by deformities of the thorax, by a mediastinal shift, or by enlargement of the heart.

Michelle Swartz pg.375

-If the PMI is laterally displaced you can suspect cardiomegaly.

Sung K, Swartz, p.375

May suggest cardiomegaly

Bill

A PMI that is laterally displaced or is felt in two interspaces during the same phase of respiration suggests cardiomegaly.

15. Identify the potential significance of increased amplitude or sustained contraction of the apical impulse.

Anonymous Bates pg. 307

This could mean there is Left Ventricular Hypertrophy, (Hypertension) or an increased after load to the heart.

Anonymous

Increased amplitude (hyperkinetic impulse) may reflect hyperthyroidism, severe anemia, pressure overload of the left ventricle (e.g. aortic stenosis), or volume overload of the left ventricle (e.g. mitral regurgitation).

Hyperkinetic impulse is normal in younger persons and after exercising.

Anonymous

Increased amplitude may also reflect hyperthyroidism, severe anemia, pressure overload of the left ventricle (e.g., Aortic stenosis), or why am overload of the left ventricle (e.g., mitral regurgitation).

A sustained, high amplitude impulse that is normally located suggests left ventricular hypertrophy from a pressure overload (as in hypertension). If such an impulse is displaced laterally, consider volume overload.

Michelle Swartz pg.

Left blank by Michelle

Sung K, Barkauskas, p.359

The amplitude of the apical impulse may seem to be increased in normal individuals with thin chest walls. In patients with high cardiac output states, such as anemia, anxiety, fever, or hyperthyroidism, the apical impulse often increases in amplitude and duration. Left ventricular hypertrophy and/or dilatation displaces the apical impulse downward and to the left, and may also increase the size of the impulse.

MIKE Bates pg. 286 There is a little info on pg 374-375 of Swartz

This could mean there is Left Ventricular Hypertrophy, (Hypertension) or an increased after load to the heart.

16. Identify which sounds and murmurs are best heard with the diaphragm and the bell of the stethoscope.

Anonymous Bates pg. 310

Diaphragm-S1 and S2 sounds. High pitched sounds. Aortic and Mitral regurgitations, pericardial friction rubs,

Bell- S3 and S4 sounds. Low pitched sounds. Mitral stenosis. Use on heart apex and lower sternal borders.

Anonymous

Throughout the precordium use the diaphragm of your stethoscope, press it firmly to the chest. The diaphragm is more appropriately used to hear high-pitched sounds, such as S1 and S2, the murmurs of aortic and mitral regurgitation, and pericardial friction rubs.

The bell of your stethoscope is more sensitive for low2-pitched sounds such as S3

and S4, and the murmur of mitral stenosis. Also use the bell at the apex and more medially along the lower sternal borders. Apply lightly, with enough pressure to produce a seal with its full rim: rest the heel of your hand on the chest to maintain this light pressure. (Bates pg.310)

Anonymous

The diaphragm is better for picking up relatively high pitched sounds such as S1, S2, the murmurs of Aortic and mitral regurgitation, and pericardial friction rubs.

The bell is more sensitive to low pitched sounds such as S3, S4, and the murmur of mitral stenosis.

Tim Schwartz, Ch. 13, pg.377

Diaphragm; used for high frequency sounds such as valve closure, systolic events and regurgitant murmurs. Should be applied tightly to the skin.

Bell; used for lower frequency sounds such as gallop rhythms and murmurs of AV stenosis. Should be applied lightly to the skin.

MIKE Bates pg 278 and a little in Swartz 377-378

The diaphragm is better for picking up relatively high pitched sounds such as S1, S2, the murmurs of Aortic and mitral regurgitation, and pericardial friction rubs.

The bell is more sensitive to low pitched sounds such as S3, S4, and the murmur of mitral stenosis.

17. Describe the two additional positions (besides supine) which you should use to listen for heart sounds, and what sounds and murmurs are best heard with each one.

Zen Seeker

	Sitting Up, Leaning Forward tends to bring out the murmurs of aortic and pulmonic regurgitation, in addition to the murmur of aortic stenosis. diaphragm Exhale + stop breathing left sternal border and apex.
	The Left Semilateral Position can be used to accentuate the mitral opening snap and mitral regurgitation murmurs, in addition to the left-sided S3 and S4. bell lightly apical impulse.
	The Recumbent Position often accentuates the murmurs of mitral and tricuspid stenosis.
	Exercise is associated with an increased heart rate, shorter diastole, elevated left atrial pressure, more abrupt closure of the heart valves, and increased blood velocity. These changes help account for the increased intensity of S1, S2, the mitral opening snap, the left-sided S3 and S4, the right-sided S4, and the murmurs of mitral regurgitation, mitral stenosis, and patent ductus arteriosus, noted in normal patients immediately following exercise.
	Prompt Standing shifts blood to the lower extremities and reduces left ventricle filling and size. This maneuver can often be used to accentuate the mitral and tricuspid clicks.
	Sitting Up tends to accentuate the tricuspid valve opening snap.

Anonymous

Sitting leaning forward, after full expiration. Listen along the left sternal border and at the apex. Can hear soft decrescendo murmur of aortic insufficiency.

Anonymous (Bates pg. 311: pictures shown to demonstrate)

Listen to the entire precordium with the patient in the supine position.

Ask the patient to roll onto their left side, bringing the left ventricle closer to the chest wall. In this position mitral murmurs, especially the murmur of mitral stenosis. Place the bell of the stethoscope lightly on the apical impulse.

Ask the patient to sit up, lean foreword, exhale completely, and stop breathing in expiration. With the diaphragm press on the chest, listening to the left sternal border and at the apex, pause periodically so the patient can take a breath. Aortic murmurs are best heard in this position, as well as aortic regurgitation.

Anonymous

Listen to the entire precordium with the patient in the supine position. Ask the patient to roll onto their left side, bringing the left ventricle closer to the chest wall. In this position mitral murmurs, especially the murmur of mitral stenosis. Place the bell of the stethoscope lightly on the apical impulse. Ask the patient to sit up, lean foreward, exhale completely, and stop breathing in expiration. With the diaphragm press on the chest, listening to the left sternal border and at the apex, pause periodically so the patient can take a breath. Aortic murmurs are best heard in this position, as well as aortic regurgitation. (Bates pg. 311: pictures shown to demonstrate)

Tim Schwartz, Ch. 13, pg. 379

Upright; S1 in all areas, S2 in all areas, systolic and diastolic sounds and murmurs in all areas.

Left lateral decubitus; Diastolic events at the apex with bell of stethoscope.

Upright, leaning forward; Diastolic events at the base with diaphragm of stethoscope.

MIKE

18. Describe what you will listen for at each auscultatory area.

Anonymous Bates, pp. 312

S₁ Intensity, any apparent splitting. (splitting normal along lower L sternal border)

S₂ Intensity

Split S2 splitting in 2^nd and 3^rd left interspaces. More detail in Bates, pp. 312

Width of split

Timing of split

Split disappear during exhalation?

Intensity of A2 and P2

extra sounds

in systole ejection sounds or systolic clicks: note location, timing, intensity, pitch, & effect of respiration on sound

extra sounds

in diastole S₃, S₄ or opening snap: note location, timing, intensity, pitch, & effect of respiration on sound (S₃ or S₄ is normal finding in athletes)

systolic/

diastolic

murmurs murmurs are differentiated from heart sounds by their longer duration

Anonymous Bates pg. 312: Ausculatory Sounds

S1: Note intensity, and apparent splitting, (normal splitting can be heard along the left sternal border.

S2: Note intensity

Split S2: Listen for splitting of this sound in the 2nd and 3rd left interspaces. Ask the pt. to breathe quietly, and then slightly more deeply than normal. Does S2 split into its two components, as it normally does? If not ask the pt. to (1) breathe more deeply, or (2) sit up. Listen again. A thick chest wall may make the pulmonic component of S1 inaudible.

Width of split: How wide is the split? It is normally quite narrow.

Timing of split: When in the respiratory cycle do you hear the split? It is normally heard late in inspiration. Does the split disappear as it should, during exhalation? If not, listen again with the pt. sitting up.

Intensity of A2 and P2: Compare intensity of the two components, A2 and P2. A2 is usually louder.

Extra Sounds in Systole: Such as ejection sounds or systolic clicks.

Extra Sounds in Diastole: Such as S3, S4, or an opening snap. Note their Location, timing, intensity, pitch, and the effects of respiration on the Sounds. (An S3 or S4 in athletes is a normal finding).

Systolic and Diastolic Murmurs: Murmurs are differentiated from heart sounds by their longer duration.

Tim Schwartz, Ch.13, pg. 377+379

Upright Position

Aortic, pulmonic, tricuspid and mitral areas are the primary auscultatory areas however, examiner should inch along both sternal borders as well.

Each area correlates to the valve it is named for so at the aortic area you are listening for the aortic valve, pulmonic area the pulmonic valve, etc.

In addition to individual areas, the examiner should listen at all areas for S1, S2, systolic (clicks) and diastolic (snaps) and murmurs. In all areas S3 and S4 are abnormal and should be noted. There are too many other intricacies involved to list here.

19. List the 9 attributes of heart murmurs that you should identify and describe, if a murmur is present.

Anonymous I found seven so far Bates, pp. 312

Timing

Shape

Location of maximal intensity

Radiation or transmission from this location

Intensity

Pitch

quality

Anonymous Bates pg. 312

1. timing

2. shape

3. location and maximal intensity

4. radiation or transmission from its location

5. intensity

6. pitch

7. quality

Anonymous Bates pg. 312

1. timing

2. shape

3. location and maximal intensity

4. radiation or transmission from its location

5. intensity

6. pitch

7. quality

Tim Schwartz, Ch. 13, pg. 379

1. timing

2. location

3. radiation

4. duration

5. intensity

6. pitch

7. quality

8. relationship to respiration

9. relationship to position

MIKE Swartz pg 379

1. timing 1. Timing in cardiac cycle

2. shape 2. Location

3. location and maximal intensity 3. Radiation

4. radiation or transmission from its location 4. Duration

5. intensity 5. Intensity

6. pitch 6. Pitch

7. quality 7. Quality

Bates pg 280 8. Relationship to respiration

9. Relationship to body position

20. Identify the usual significance of diastolic murmurs versus systolic murmurs.

Anonymous Bates, pp. 313

Diastolic murmurs usually indicate valvular heart disease. Systolic murmurs may indicate valvular disease, but often occur when the heart is entirely normal.

Anonymous Bates pg. 313

Diastolic murmurs usually indicate valvular heart disease. Systolic murmurs may indicate valvular disease, but often occur when the heart is entirely normal.

Tim Bates, pg. 313

Diastolic murmurs usually indicate valvular heart disease. Systolic murmurs may indicate valvular disease, but often occur when the heart is entirely normal.

Dawn Bates – p. 313, 331 7^th ed

Diastolic murmurs almost always indicate valvular heart disease. There are two basic types. Early decrescendo diastolic murmurs signify regurgitant flow through an incompetent semilunar valve, more commonly the aortic. Rumbling diastolic murmurs in mid- or late diastole suggest stenosis of an atrioventricular valve, more often the mitral. They occur between S₂ and S₁. Systolic murmurs may indicate valvular disease, but often occur when the heart is entirely normal. They occur between S₁ and S₂.

21. Define (or draw) the following terms used in describing the timing or shape of murmurs, and identify their typical significance:

midsystolic murmur

pansystolic (or holosystolic) murmur

late systolic murmur

early diastolic murmur

middiastolic murmur

late diastolic (or presystolic) murmur

continuous murmur

crescendo murmur

decrescendo murmur

crescendo-decrescendo murmur

Zen Seeker

	Early Systolic Murmur - begins with S1 and ends before or about the middle of systole.
	Mid Systolic Murmur - begins after S1 and ends before S2.
	Late Systolic Murmur - begins at about the middle of systole and ends at the time of S2.
	Holosystolic Murmur - begins with S1 and ends with, or continues somewhat beyond, S2.
	Early Diastolic Murmur - begins with S2.
	Mid Diastolic Murmur - begins after S2.
	Late Diastolic Murmur - occurs immediately prior to S1.
	Continuous Murmur - has both systolic and diastolic components.
	Crescendo - the loudness of the murmur increases progressively. The systolic component of a patent ductus arteriosus murmur is of this type.
	Decrescendo - the loudness of the murmur decreases progressively. The murmurs of aortic and pulmonic regurgitation are examples of this type.
	Crescendo-Decrescendo - the loudness of the murmur increases and then decreases. This configuration is typical of systolic ejection murmurs.
	Plateau - the loudness of the murmur remains relatively constant. Holosystolic murmurs are representative of this type.

Anonymous

Terms for timing:

midsystolic murmur: Most often related to blood flow across the semilunar (aortic and

pulmonic) valves. Begins after S1 and stops before S2. Brief gaps are audible between the murmur and the heart sounds: listen carefully before S2. Most common type of murmur. May be (1) pathologic (2) physiologic, or (3) innocent.

Bates pgs. 313, 328-329.

pansystolic (or holosystolic)murmur: Starts with S1 and stops at S2 without a gap

between murmur and heart sounds. Often occurs with regurgitation flow across

the atrioventricular valves. A pathologic murmur: they are heard when blood

flows from a chamber of high pressure to one of lower pressure through a valve

or other structure that should be closed.

Bates pgs. 313,330

late systolic murmur: Usually starts in mid- or late systole and persists up to S2. This is

the murmur of mitral valve prolapse and is often, but not always, preceded by a

systolic click.

Bates pg. 313

early diastolic murmur: Starts right after S2, without a discernable gap, and then usually

fades into silence before the next S1. Early diastolic murmurs typically

accompany regurgitation flow across incompetent semilunar valves.

Bates pg. 313

middiastolic murmur: Starts a shor time after S2. It may fade away or merge into a late

diastolic murmur. Middiastolic and presystolic murmurs are related to turbulent

flow across the atrioventricular valves. Diastolic murmurs almost always indicate

heart disease.

Bates pgs. 313, 331.

late diastolic (or presystolic) murmur: Starts late in diastole and typically continues

up to S1.

continuous murmur: An occasional murmur that is caused by a patent ductus arteriosus,

starts in systole and continues without pause through S2 into but not necessarily

throughout diastole. Bates pg. 314

crescendo murmur: This type grows louder. The presystolic murmur of mitral stenosis

in normal sinus rhythm. Bates 314

decrescendo murmur: This murmur grows softer. The early diastolic murmur of aortic

regurgitation. Bates pg. 314

crescendo-decrescendo murmur: This murmur first rises in intensity, then falls. The

midsystolic murmur of aortic stenosis and innocent flow murmurs.

plateau murmur: Has same intensity throughout. The pansystolic murmur of mitral

regurgitation. Bates pg. 314

Anonymous

midsystolic murmur: begins after S1 and stops before S2 w/ brief gaps between the murmur and the heart sounds; crescendo-decrescendo shape. Most often related to blood flow across the semilunar valves (ex. aortic stenosis).

pansystolic (or holosystolic) murmur: starts with S1 and stops at S2; no gap; plateau shape. Often occur with regurgitant (backflow) across the atrioventricular valves.

late systolic murmur: usually starts in mid- or late systole, persists up to S2; crescendo shape. Mitral valve prolapse; often preceded by a systolic click.

early diastolic murmur: starts at S2 (no gap), may fade away (decrescendo) before S1 or merge into a late diastolic murmur. Typically regurgitant flow across semilunar valves.

middiastolic murmur: starts a short time after S2 (gap), may fade away (decrescendo) before S1 or merge into a late diastolic murmur. Turbulent flow across atrioventricular valves.

late diastolic (or presystolic) murmur: starts late in diastole, typically continues to S1; crescendo shape. Turbulent flow across atrioventricular valves (ex. mitral stenosis).

continuous murmur: starts in systole, continues w/o pause through S2, not necessarily throughout diastole. Ex. patent ductus arteriosus.

Terms for shape (intensity of sound over time):

crescendo murmur: grows louder.

decrescendo murmur: grows softer.

crescendo-decrescendo murmur: first rises in intensity, then falls.

plateau murmur: same intensity throughout.

Stephen. Suggest reading the section in Shwartz on murmurs pg. 386. I don’t have a Bates, but it looks like I need one.

Janelisa see Bates’ Pocket 202-203 for diagrams; Harrison’s 12^th ed. 848-849

midsystolic murmur – are often crescendo-decrescendo in shape, occur when blood is ejected across the aortic or pulmonic outflow tracts. Starts shortly after S₁ when the ventricular pressure rises sufficiently to open the semilunar valve. Ejection then begins and with it the onset of the mumur ;as ejection increases, the murmur is augmented, and as ejection declines, it diminishes. The murmur ends before the ventricular pressure falls enough to permit closure of the aortic or pulmonic leaflets. Most benign, functional murmurs are midsystolic and originate from the pulmonary outflow tract.

pansystolic (or holosystolic) murmur – are generated when there is a flow between 2 chambers which have widely different pressures throughout systole, such as the left ventricle and either the left atrium or right ventricle. The pressure gradient is established early in contraction and lasts until relaxation is almost complete. At the area of maximal intensity, they begin with S₁ and end after S₂. Associated with mitral or tricuspid regurgitation, ventricular septal defect, and aortopulmonary shunts.

late systolic murmur – are faint or moderately loud high-pitched apical murmurs, which start well after ejection and do not mask either heart sound. They are probably related to papillary muscle disfunction caused by infarction or ischemia. Late systolic murmurs following midsystolic clicks are associated with late systolic mitral regurgitation caused by prolapse of the mitral valve into the left atrium.

early diastolic murmur – begin with or shortly after the 2^nd heart sound as soon as the corresponding ventricular pressure falls sufficiently below that in the aorta or pulmonary artery. Usually decrescendo and associated with aortic or pulmonic regurgitation

middiastolic murmur – usually arise from the AV valves, occur during early ventricular filling, and are due to disproportion between valve orifice size and flow rate. May be loud even if slight stenosis is present and blood flow is normal or increased. Conversely, the murmur may be soft or absent when stenosis is severe if cardiac output is markedly reduced. Middiastolic murmurs may be generated across the mitral valve in ventricular sepral defect, patent ductus arteriosus, or mitral regurgitation, and across the tricuspid valve in atrail septal defect or tricuspid regurgitation.

late diastolic (or presystolic) murmur – begin during the period of ventricular filling that follows atrial contraction and therefore occur in sinus rhythm. They are usually due to AV valve stenosis and have the ssame quality as the middiastolic filling rumble but are usually crescendo, reaching peak intensity at the time of a loud S₁. It is most characteristic of tricuspid stenosis and sinus rhythm.

continuous murmur – begin in systole, peak near S₂, and continue into all or part of diastole. A patent ductus arteriosus causes a continuous murmur as long as the pressure in the pulmonary artery is much below that in the aorta. A continuous murmur in the back may be present in coarctation of the aorta; pulmonary embolism may cause continuous murmurs in partially occluded vessels.

crescendo murmur –Bates’ Pocket 202 late systolic, example is mitral valve prolapse

decrescendo murmur – Bates’ Pocket 202 early systolic, example is aortic regurgitation

crescendo-decrescendo murmur – Bates’ Pocket 202 midsystolic murmurs, examples are innocent murmurs, aortic or pulmonic stenosis

Dawn

Midsystolic murmur: Begins after S₁ and stops before S₂. Brief gaps are audible between the murmur and the heart sounds. Listen carefully for the gap just before S₂. This usually confirms the murmur as midsystolic, not pansystolic. Also called an ejection murmur is the most common kind of heart murmur. It may be (1) pathologic: secondary to structural cardiovascular abnormality), (2) physiologic: secondary to physiologic alteration in the body, and (3) innocent: not associated with any detectable physiologic or structural abnormality. Midsystolic murmurs tend to peak near midsystole, and usually stop before S₂. The crescendo-decrescendo shape is not always obvious to the ear, but the gap between the murmur and S₂ helps to distinguish midsystolic from pansystolic murmurs. Bates- p. 313, 328 7^th ed
Pansystolic (or holosystolic) murmur: these murmurs are pathologic. They are hear when blood flows from a chamber of high pressure to one of lower pressure through a valve or other structure that should be closed. The murmur begins immediately with S₁ and continues up to S₂. There is no gap between murmur and hearts sounds. Bates – p. 313, 330 7^th ed and Swartz – p. 380
Late systolic murmur: this usually represents mitral regurgitation (mitral valve prolapse) – a flow of blood from left ventricle to left atrium. This is often, but not always, preceded by a systolic click. The murmur usually crescendos up to S₂. This starts in mid – or late systole and persists up to S₂. Bates – p. 313, 326
Early diastolic murmur: Starts right after S₂, without a discernible gap, and then usually fades into silence before the next S₁. Usually decrescendo murmurs which signify regurgitant flow through an incompetent semilunar valve, more commonly the aortic. Bates – p. 313, 331
Middiastolic murmur: Starts a short time after S_2.It may fade away, or merge into a late diastolic murmur. It is seen in mitral stenosis. The mitral valve fails to sufficiently open in diastole. The resulting murmur of mitral stenosis has two components: (1) middiastolic: during rapid ventricular filling and (2) presystolic: see below Bates – p. 313, 331
Late diastolic (or presystolic) murmur: Starts late in diastole and typically continues up to S₁. seen in mitral stenosis. Occurs during atrial contraction. Presystolic disappears if atrial fibrillation develops, leaving only a middiastolic rumble. Bates – p. 313, 331
Continuous murmur: begins in systole and continues through the second sound into all or part of diastole. It need not continue through diastole. (ie: patent ductus arteriosus may be classified as continuous. Bates – p. 314, 332
Crescendo murmur: A murmur that grows louder. Seen in the presystolic murmur of mitral stenosis in normal sinus rhythm. Bates – p. 314
Decrescendo murmur: A murmur that grows softer. Seen in the early diastolic murmur of aortic regurgitation. Bates – p. 314
Crescendo-decrescendo murmur: A murmur which first rises in intensity, then falls. Seen in the midsystolic murmur of aortic stenosis and innocent flow murmurs. Bates – p. 314

22. Describe the importance of location of maximum intensity and radiation in determining the probable cause of a murmur.

Zen Seeker

	Diastolic	Systolic
Aortic	Regurgitation	Stenosis
Mitral	Stenosis	Regurgitation

Events related to the heart valves are best heard not over their anatomic locations, but in the auscultatory areas bearing their names. Although a loud murmur may be heard over the entire precordium, there are specific areas in which particular murmurs will usually be loudest:

	Aortic Area - located in the second intercostal space at the right sternal margin. The systolic murmurs of Aortic Stenosis and Increased Aortic Valve flow.
	Pulmonic Area - located in the second intercostal space at the left sternal border. The systolic murmur of Pulmonic Stenosis and the diastolic murmur of Pulmonic Regurgitation.
	Tricuspid Area - located at the lower left sternal border (LLSB). The diastolic murmur of Tricuspid Stenosis.
	Mitral Area - located about the apex beat, which is usually in the fifth intercostal space. It is also called the apical, or the left ventricular area. The systolic murmur of Mitral Regurgitation and the diastolic murmurs of Mitral Stenosis and Increased Valvular Flow.

Anonymous Bates pg. 314

Determined by the site where the murmur originates. Location is found by exploring the are where the murmur can be heard, and wherever it is heard best is the location of maximum of intensity. Describe in terms of interspace, and its relationship to the sternum, the apex, or the midsternal, the midclavicular, or one of the axillary lines.

(Eg.: Murmur can be best heard in the 2nd right interspace usually originates at or near the aortic valve.)

Anonymous

Location on chest of maximum intensity of murmur provides clue of anatomical origin of murmur. Ex. max. intensity over 2nd right intercostal space usually aortic valve (or nearby) origin.

Find location by exploring area over which you hear the murmur; describe location of maximum intensity in terms of the intercostal space and relation to the sternum, the apex, or the midsternal, midclavicular, or one of the axillary lines.

Radiation of the sound from the point of maximal intensity (i.e., where else can you hear it?) reflects intensity of murmur and direction of blood flow. Ex. loud murmur of aortic stenosis often radiates into neck (direction of arterial flow).

Janelisa Harrison’s 12^th ed. 847 The location on the chest wall where the murmur is best heard and the areas to which it radiates can be helpful in identifying the cardiac structure from which the murmur originates. For example, the murmur of aortic valve stenosis is loudest usually in the 2^nd right IC space and radiates to the carotid arteries. By contrast, the murmur of mitral regurgitation is most often loudest at the cardiac apex and may radiate to the left sternal border and base of the heart when the posterior mitral leaflet is predominantly involved or to the axilla and back when the anterior leaflet is more severely affected.

Dawn

Location of maximum intensity will determine where the murmur originates. Explore the area in which you can hear the murmur, and describe where you hear it best in terms of the interspace and its relation to the sternum, the apex, or the midsternal, the midclavicular, or one of the axillary lines. (ie: a murmur best heard in the 2^nd right ICS usually originates at or near the aortic valve.) Radiation or Transmission from the PMI will reflect not only the site of origin but also the intensity of the murmur and the direction of blood flow. Explore the area around a murmur and determine where else you can hear it. (ie: a loud murmur of aortic stenosis often radiates into the neck: in the direction of arterial flow.) Bates- p. 314

23. Be able to use correctly or understand the 6-point scale used to describe the intensity (loudness) of a murmur.

Zen Seeker

Murmur Grades
Grade	Volume	Thrill
1/6	very faint, only heard in ideal circumstances	No
2/6	loud enough to be generally heard	No
3/6	louder then grade 2	No
4/6	louder then grade 3	Yes
5/6	heard with stethoscope partially off chest	Yes
6/6	heard with stethoscope entirely off chest	Yes

Anonymous Bates pgs. 314-315

The intensity of a murmur is graded on a 6-point scale and expressed as a fraction. The numerator describes the intensity of the murmur wherever it is loudest, and the denominator indicates the scale you are using. Intensity is influenced by the thickness of the chest wall and the presence of intervening tissue.

Grade 1: Very faint, heard only after listener has "tuned in"; may not be heard in all positions.

Grade 2: Quiet, but heard immediately after placing the stethoscope on the chest.

Grade 3: Moderately loud.

Grade 4: Loud.

Grade 5: Very loud. May be heard when the stethoscope is partly off the chest.

Grade 6: May be heard when the stethoscope is entirely off the chest.

Anonymous

Grade 1 Very faint, heard only after listener has ‘tuned in’; may not be heard in all positions

Grade 2 Quiet, but heard immediately after placing the stethoscope on the chest

Grade 3 Moderately loud

Grade 4 Very loud. May be heard when the stethoscope is partly off the chest.

Grade 6 May be heard when stethoscope entirely off the chest.

Janelisa Swartz 380 I. lowest intensity, often not heard by inexperienced listeners. II. Low intensity, usually audible by inexperienced listeners. III. Medium intensity without a thrill. IV. Medium intensity with a thrill. V. Loudest murmur that is audible when the stethoscope is placed on the chest, associated with a thrill. VI. Loudest intensity, audible when stethoscope is removed from chest, also associated with a thrill.

Dawn

I lowest intensity, often not heard by inexperienced listeners; very faint,

heard only after listener has “tuned in”; may not be heard in all positions

II low intensity, usually audible by inexperienced listeners; quiet, but heard

Immediately after placing the stethoscope on the chest

III medium intensity without a thrill; moderately loud

IV medium intensity with a thrill; loud

V loudest murmur that is audible when the stethoscope is placed on the chest. Associated with a thrill. Very loud. May be heard when the stethoscope is partly off the chest.

VI loudest intensity: audible when stethoscope is removed from chest.

Associated with a thrill.

Murmurs can be described for example “grade II/VI” or “grade II-III/VI”. The “/VI” is used because there is another less common grading system using only 4 categories. The higher number of the murmur, the more turbulence. Intensity is influenced by the thickness of the chest wall and the presence of intervening tissue. Swartz – p. 380 and Bates – p. 315

24. Given a patient or a sound recording be able to identify normal and abnormal examples of:

The "First Heart Sound"

The "Second Heart Sound"

Extra heart sounds heard in systole

Extra heart sounds heard in diastole

Cardiovascular sounds heard in systole and diastole

Anonymous

Table 9-5 Variations in the First Heart Sound: Bates pg. 324

Normal Variations: S1 is softer than S2 at the base (right and left 2nd interspace). S1 is often but not always louder than S2 at the apex.

Accentuated S1: S1 is accentuated in (1) tachycardia, rhythms with a short PR interval, and high cardiac output states (eg. exercise, anemia, hyperthyroidism), and (2) mitral stenosis. In these conditions, the mitral valve is still open wide at the onset of ventricular systole, and then closes quickly.

Diminished S1: S1 diminished in first-degree heart block (delayed conduction from atria to ventricles). Here the mitral valve has had time after atrial contraction to float back into an almost closed position before ventricular contraction shuts it. It closes less loudly. S1 is also diminished (1)when the mitral valve is calcified and relatively immobile, as in mitral regurgitation, and (2) when left ventricular contractility is markedly reduced, as in CHF or coronary artery disease.

Varying S1: S1 varies in intensity (1) in complete heart block, when atria and ventricles are beating independently of each other, and (2) in any totally irregular rhthm (eg. a-fib). In these situations, the mitral valve is in varying positions before being shut by ventricular contraction. Its closure sound, therefore, varies in loudness.

Split S1: S1 may be split normally along the lower left sternal border where the tricuspid component, often to fain to be heard, becomes audible. May be heard at the apex, but consider an S4, an aortic ejection sound, and an early systolic click. Abnormal splitting of both heart sounds may be heard in right bundle branch block and in premature ventricular contractions.

Table 9-6 Variations in the Second Heart Sound: Bates pg. 325

Physiologic Splitting: The second heart sound can usually be detected in the 2nd or 3rd left interspace. The pulmonic component of S2 is usually too faint to be heard at the apex or aortic area, where S2 is a single and derived from aortic valve closure alone. (Normal splitting is accentuated by inspiration and and usually disappears on expiration. S2may not become completely single on expiration in younger children, or when the pt. sits up.)

Pathologic Spitting: Can be caused by a delayed closure of the pulmonic valve.

Fixed Splitting: Wide splitting that does not vary with respiration. It occurs in atrial septal defect and right ventricular failure.

Paradoxical or Reversed Splitting: Appears on expiration and disappears on inspiration. Closure of the aortic valve is abnormally delayed so that A2 follows P2 in expiration. Most common reason is a left bundle branch block.

Increased Intensity of A2 (Rt. 2nd interspace): Occurs in systemic HTN, because of the increased pressure. Also when the aortic root is dialated.

Decreased or Absent A2 (Rt. 2nd interspace): Noted in calcific aortic stenosis because the valve is immobile.

Increased Intensity of P2: Whe it is equal or louder than A2, pulmonary HTN may be suspected. Other causes include: dialated pulomonary artery and atrial septal defect.

Decreased or Absent P2: Most commonly due to increased anteroposterior diameter of the chest associated with aging. Can also result from pulmonic stenosis.

Table 9-7 Extra Heart Sounds in Systole: Bates pg. 326

Early systolic Ejection Sounds: Occur shortly after first heart sound, coincident with the opening of the aortic and pulmonic valves. Relatively high pitched, have a sharp-clicking quality, and are heard better with the diaphragm of the stethoscope. Indicates CVD.

Aortic Ejection: heard at both base and apex, and may be more loud at the apex. Dosen't vary with respiration. Indicates: dialated aorta or aortic valve disease (congenital stenosis, or bicuspid valve)

Pulmonic Ejection: Heard best at 2nd and 3rd left interspaces. When the first heart sound, usually relatively soft in this area, appears to be loud, you may instead hear this sound.

Systolic Clicks: Usually due to mitral valve prolapse (an abnormal systolic ballooning of part of the valve into the lt. Atrium). Occur mild to late systolic. More than one click may be heard. The click is often followed by a late systolic murmur.

Table 9-8 Extra Heart Sounds in Diastole: Bates pg. 327

Opening Snap: Very early diastolic sound usually produced by the opening of a stenotic mitral valve.

Physiological Third Heart Sound: Frequently heard in children, and may persist till the age of 35 or 40. Common during late trimester of pregnancy. Occurs early diastole during rapid ventricular filling, later than an opening snap, dull and low in pitch. Use bell with very light pressure.

Table 9-9 Midsystolic Murmurs: Bates pg. 328: I'm only giving brief descriptions on this section, otherwise I would be typing several pages, which we could not possible remember)

Innocent Murmur: Result from a turbulent blood flow. No CVD. Common in children, young adults, and older adults.

Physiologic Murmurs: Turbulence due to temporary increase in blood flow. Predisposing conditions include: anemia, pregnancy, fever, an hyperthyroidism.

Pathologic Murmurs: Stenosis of the pulmonic valve is impairs flow across the valve, and increases the afterload on the rt. Ventricle. It is congenital, and most often found in children. May mimic a murmur of pulmonic stenosis. (See Bates pgs. 328-329 for a lot more information on murmurs)

Table 9-10 Pansystolic/Holosystic Murmurs: Bates pgs. 330-331

Mitral Regurgitation: When the mitral valve fails to close fully in systole, blood regurgitates from left ventricle to left atrium, causing a murmur. A volume overload is created on the left ventricle with subsequent dilation and hypertrophy. At the apex, a soft to loud blowing-sound with a medium to high-pitch could be present that is unlike a murmur, and does not become louder on inspiration.

Tricuspid Regurgitation: The tricuspid valve fails to close fully in

Systole, blood regurgitates from right ventricle to right atrium, producing a murmur. Most common cause is right ventricular failure and dilation, with resulting enlargement of the tricuspid orifice. Initiating causes are pulmonary HTN, or left ventricular failure. On the lower left sternal border, a medium blowing sound is present may increase with inspiration.

Ventricular Septal Defect: A congenital abnormality, in which blood flows from the relatively high-pressure left ventricle into the losw-pressure right ventricle through a hole. An often very loud, harsh high-pitch sound with the presence of a thrill. Located at the 3rd, 4th , or 5th left sternal border.

Table 9-11 Diastolic Murmurs:

Aortic Regurgitation: The leaflets of the aortic valve fail to close completely during diastole, and blood regurgitates from the aorta back into the left ventricle. A volume overload on the left ventricle results. Two other murmurs may be associated: (1) midsystolic, or (2) mitral systolic (Austin Flint murmur). The latter is attributed to diastolic impingement of the regurgitant flow on the anterior leaflet or the mitral valve. Located at the 2nd to 4th left intercostals. Grade 1 to 3. Pitch is high with a blowing quality (may sound like breath sounds), heard best with patient sitting, leaning foreward, and with breath held in on exhalation.

Mitral Stenosis: When the leaflets of the mitral valve thicken, stiffen, and become distorted from the effects of rheumatic fever, the valve fails to open sufficiently in diastole. Two components are the result of the murmur: (1) middiastolic, and (2) presystolic during atrial contraction. The location is the apex. Grade 1 to 4. Pitch is low, and is heard better on exhalation.

Table 9-12 Cardiovascular Sounds With Both Systolic and Diastolic Components:

Pericardial Friction Rub:

Timing: May have 3 short components, each associated with cardiac movement: (1) atrial systole, (2) ventricular systole, and (3) ventricular diastole. Usually the first tow are present; all three make diagnosis easy; only one (usually systolic) invites confusion with a murmur.

Location: Usually heard best in the 3rd interspace to the left of the sternum.

Radiation: Little.

Intensity: Variable. May increase when the patient leans forward and exhales.

Quality: Scratchy, scraping.

Pitch: High (use bell)

Patent Ductus Arteriosis:

Timing: Continuous murmur in both systole and diastole, often with a silent interval late in diastole.

Location: Left 2nd interspace.

Radiation: Toward the left ventricle.

Intensity: Usually loud, sometimes associated with a thrill.

Quality: Harsh, machinerylike.

Pitch: Medium.

Venous Hum:

Timing: Continuous murmur without a silent interval. Loudest in diastole.

Location: Above the medial 3rd of the clavicles, especially on the right.

Radiation: 1st to 2nd interspace.

Intensity: Soft to moderate. Can be obliterated by pressure on the jugular veins.

Quality: Humming, roaring.

Pitch: Low

Janelisa Swartz 350, Bates 4^th ed. 301-302

The "First Heart Sound" is noted as S₁ and is the closure of the tricuspid and mitral AV valves

The "Second Heart Sound" is noted as S₂ and is the closure of the aortic and pulmonic semilunar valves

Extra heart sounds heard in systole

1. There are 2 types of early systolic ejection sounds which occur shortly after the 1^st heart sound, are high in pitch, and have a sharp, clicking quality. Aortic ejection is heard at both base and apex and may be louder at the apex. It usually doesn’t vary with respiration. Pulmonic ejection is best heard in the 2^nd and 3^rd left interspaces. When the 1^st heart sound, usually relatively soft in this area appears to be loud, you may be hearing this instead. Decreased intensity during inspiration will be a clue.

2. Systolic clicks are usually due to mitral valve prolapse and are usually heard mid- or late systolic. The click is usually single and high-pitched, but more than one can be heard. It is best heard at or medial to the apex. Findings vary from time to time and with position.

Extra heart sounds heard in diastole

1. An opening snap is a very early diastolic sound, high-pitched, best heard just medial to the apex and along the lower LSB. When it is loud, it radiates to the apex and to the pulmonic area.

2. A physiologic 3^rd heart sound is frequently heard in children and may persist until 40. It is common during the last trimester of pregnancy. Occurring early in diastole during rapid ventricular filling, it is later than an opening snap, dull and low-pitched, and best heard at the apex in the left lateral decubitus position. The bell of the stethoscope should be used.

3. A pathologic S₃ or ventricular gallop in a person over 40 is almost certainly pathologic. It sounds just like a physiologic S₃. and is louder on inspiration.

4. An S₄ or atrial gallop occurs just before S₁, is low-pitched, dull, and better heard with the bell. It often increases with inspiration.

Cardiovascular sounds heard in systole and diastole Bates 4^th ed. 310

1. A pericardial friction rub is high, scratchy, scraping and usually best heard in the 3^rd IC to the left of the sternum. May increase when the patient leans forward and exhales.

2. Patent ductus arteriosus is medium in pitch, harsh, machinery-like, heard at the left 2^nd IC. Usually loud and sometimes associated with a thrill.

Venous hum is low, best heard with the bell; humming, roaring sound; heard above the medial third of the clavicles, especially on the right.

25. Given a heart-sound recording be able to identify and describe abnormalities present .

26. Given a patient be able to identify and describe any abnormalities present in a cardiac examination.

Deb B. Swartz, Chapter 13

There are various abnormalities to include splitting of heart sounds (S1, S2), hearing murmurs, clicks, or snaps. Also, look for dependent edema, cyanosis, syncope, dyspnea, palpitations, neck vein distention

Greg R. Swartz p. 382-389. Bates’ p. 251-295. There is much in these two to review.

27. Review the anatomy and physiology of the peripheral vascular system.

Anonymous See Bates ch. 16, pgs.461-482

Deb B./Swartz pg.391-392

PVS involves arteries, veins, or lymphatics. Peripheral arterial system- cause ischemia of extremities ( when body at rest, collateral blood vessels may provide adequate circulation, but during exercise O2 demand increases, then the collateral vessels above may not be adequate compensation—leads to ischemia)

Venous system- series low-pressure capacitance vessels(little resistance, have valves that aid in return of blood to rt. Side of heart) When upright, venous pressure in lower extremity is highest, over years, dilatation of veins occurs as result weakening of walls. As walls dilate, veins unable close adequately, and reflux of blood occurs------leads to venous stasis, complications of which are cellulites, thrombus formation, ulceration.

Lymphatic system- extensive vascular network and responsible for returning tissue fluid (lymph) back to venous sys. Important symptom lymphatic obstruction= lymphedema and lymphangitis.

Greg R. Bates’ p. 441-446. Good review with photos.

28. Describe normal changes with age in the peripheral vascular system .

Anonymous Bates, p. 466

Children and younger adolescents normally have larger lymph nodes relative to body size than do adults. Aging adults have relatively few clinically important changes. The arteries lengthen and become tortuous and stiff with or without atherosclerosis.

Anonymous

The aorta and large arteries stiffen with age and become arteriosclerotic. Peripheral arteries tend to lengthen, become tortuous, and feel harder and less resilient. A tortuous aorta occasionally raises the pressure in the jugular veins on the left side of the neck by impairing their drainage within the thorax. In western societies, systolic blood pressure tends to rise from childhood through old age. Diastolic blood pressure stops rising, however, when people enter their sixties. Elderly people develop an increased tendency toward postural hypotension—a sudden drop in blood pressure when they rise to a sitting or standing position. Elderly people are also more likely to have abnormal heart rhythms.

Deb B./ Bates pg. 446

Age lengthens arteries, makes them tortuous, and stiffens their walls. Skin may get thin and dry, nails may grow more slowly, and hair on legs often becomes scant.

Greg R. Bates’ p. 446.

Aging itself brings relatively few clinically important changes to the peripheral vascular system. Although arterial & venous disorders, especially atherosclerosis, do afflict older people more frequently, they probably cannot be considered part of the aging process. Age lengthens arteries, makes them tortuous, and typically stiffens their walls, but these changes develop with or without atherosclerosis and therefore lack diagnostic specificity. Loss of arterial pulsations is not a part of normal aging, however, and demands careful evalutation.

Dawn Bates – p. 466

Age lengthens the arteries, makes them tortuous, and typically stiffens their walls, but these changes develop with or without atherosclerosis and therefore lack diagnostic specificity. Skin may get thin and dry with age, nails may grow more slowly, and hair on the legs often becomes scant.

29. Identify the potential significance of each of the following:

edema of an arm

lymphedema of the arm and hand

Raynaud's disease

enlarged epitrochlear node

local vs. generalized lymphadenopathy

decrease or absence of the arterial pulses in the legs

decreased or absent foot pulses

Anonymous

Lymphedema of the arm and hand: may follow axillary node dissection and radiation therapy.

Raynaud’s disease: wrist pulses are typically normal but spasms of more distal arteries cause episodes of sharply demarcated pallor of the fingers.

Enlarged epitrochlear node: may be secondary to a lesion in its drainage area or may be associated with generalized lymphadenopathy.

Local vs. generalized lymphadenopathy: refers to enlargement of nodes with or without tenderness. Local – causative lesion in drainage area; generalized – enlarged nodes in at least 2 other non-contiguous regions.

Decrease or absence of the arterial pulses in the legs: indicates partial or complete arterial occlusion proximally. Femoral – disease at aortic or iliac level. Arteriosclerosis obliterans.

Decreased or absent of foot pulses: occlusive disease in the lower popliteal artery or its branches; associated w/ DM.

Anonymous Kraytman pg 56-57

EDEMA OF AN ARM: localized edema in UE signifies a possible superior vena cava obstruction, bronchogenic CA, mediastinal lymphoma or aneurysm of the aorta.

LYMPHADEMA OF ARM AND HAND: May follow axillary node dissection and radiation therapy Lymphedema can signify tumor, fibrosis or inflammation.

RAYNAUD’S DZ: a vascular dz. Wrist pulses are typically normal but and episodic spasms of more distal arteries and arterioles cause episodes of sharply demarcated pallor of the fingers without organic occlusion. If the syndrome is SECONDARY to other conditions, occlusion may occur.

ENLARGED EPITROCHLEAR NODE: lymph from the ulnar surface of the forearm and hand, the little finger and ring finger and the adjacent surface of the middle finger. Enlargement may be secondary to a lesion in its drainage area or may be associated w/ generalized lymphadenopathy.

LOCAL AND VS GENERALIZED LYMPHADENOPATHY: refers to enlargement of nodes with or without tenderness. LOCAL- causative lesion in drainage area. GENERALIZED- enlarged nodes in at least 2 other non-contiguous areas.

DECREASED OR ABSENCE OF ARTERIAL PULSES IN THE LEGS: Femoral dz at the aortic or iliac level.

Arteriosclerosis Obliterans-most commonly obstructs arterial circulation in the thigh. Femoral pulse normal, popliteal decreased or absent.

Sudden Arterial Occlusion- as by embolism or thrombosis, causing pain, numbness or tingling. Emergency treatment is required.

DECREASED OR ABSENT FOOT PULSES:

Congenital absence – dorsalis pedis artery may be absent or may branch higher in the ankle.

Occlusive Dz in Lower Popliteal Artery or branches: decreased or absent foot pulses w/ normal femoral and popliteal pulses. A pattern often associated w/ diabetes mellitus

Deb B./Bates

edema of an arm - *couldn’t find this*

lymphedema of the arm and hand – may be signif of axillary node dissection and radiation therapy pg. 450

Raynaud's disease – episodic spasm of small arteries and arterioles; no vascular occlusion pg. 460

enlarged epitrochlear node- may be secondary to lesion in its drainage area or may be assoc. with generalized lymphadenopathy pg.451

local vs. generalized lymphadenopathy –local= find causative lesion in drainage area/ generalized= enlarged nodes in at least 2 other noncontiguous lymph node regionspg. 452

decrease or absence of the arterial pulses in the legs- indicates partial or complete occlusion proximally, chronic arterial occlusion causes intermittent claudicationpg.452

decreased or absent foot pulses – occlusive disease in lower popliteal artery or its branches, pattern often assoc. with DMpg. 454

Greg R.

edema of an arm - Bates’ p. 450. Prominent veins in an edematous arm suggest venous obstruction.

lymphedema of the arm and hand – Bates’ p. 450. may follow axillary node dissection and radiation therapy.

Raynaud's disease – Bates’ p. 450-451. wrist pulses are typically normal but spasm of more distal arteries causes episodes of sharply demarcated pallor of the fingers. Bates’ p. 460. Episodic spasm of the small arteries and arterioles; no vascular occlusion.

enlarged epitrochlear node – Bates’ p. 451. An enlarged epitrochlear node may be secondary to a lesion in its drainage area or may be associated with generalized lymphadenopathy. Swartz p. 401. Acute infections of the ulnar aspect of the forearm and hand may be responsible for epitrochlear adenopathy. Epitrochlear nodes are also seen in non-Hodgkin’s lymphoma.

local vs. generalized lymphadenopathy – Swartz p. 401. Generalized lymphadenopathy is the presence of palpable lymph nodes in three or more lymph node chains. Lymphoma, leukemia, collagen vascular disorders, and systemic bacterial, viral, and protozoal infections may be responsible. Localized lymphadenopathy is usually the result of localized infection or neoplasm.

decrease or absence of the arterial pulses in the legs – Bates’ p. 452. A diminished or absent pulse indicates partial or complete occlusion proximally; e.g., at the aortic or iliac level, all pulses distal to the occlusion are typically affected. Chronic arterial occlusion, usually from atherosclerosis, causes intermittent claudication, postural color changes, and trophic changes in the skin.

decreased or absent foot pulses – Bates’ p. 454. Decreased or absent foot pulses (assuming a warm environment) with normal femoral and popliteal pulses suggest occlusive disease in the lower popliteal artery or its branches-a pattern often associated with diabetes mellitus.

Mary

edema of an arm- localized infection, neoplasm, or deep vein thrombosis. Swartz p.401, 404

lymphedema- cancer or infection, see local vs. generalized below.

Raynaud’s disease- a common peripheral vascular problem classically presenting as episodic color changes in the distal fingers and or toes. During arteriospasm, the digits blanche (pallor). Then, as available oxygen is depleted, cyanosis occurs. Finally, as arteriospasm subsides, blood returns (rubor) and the patient may describe a burning parasthesis. p. 404

Enlarged epitrochlear nodes- these nodes, located in the fossa 3 cm proximal to the medial epicondyle of the humerus, are rarely palpable; but, if present, may represent acute infection of the hand or ulnar aspect of the forearm- or are also seen in non-Hodgkin’s lymphoma p.401.

Local vs. generalized lymphadenopathy- generalized lymphadenopathy is the presence of palpable lymph nodes in three or more lymph chains and is associated with lymphoma, leukemia, collagen vascular disorder, or systemic viral, bacterial, or protozoan infections p401. Local lymphadenopathy is indicative of neoplasm-as in breast cancer p.395 or infection in the part of the body drained by the particular lymph node chain involved.

Decreased or absent arterial pulse in legs- may represent occlusive arterial disease – or, if femoral pulse is delayed during simultaneous palpation of the radial and femoral pulse, coarctation (stenosis or stricture) of the aorta should be considered, especially in the hypertensive patient. p.399

Decreased or absent foot pulses- the dorsalis pedis pulse may best be felt by dorsoflexion of the foot, and its absence may indicate occlusive arterial disease, too much edema to palpate, or trauma p.400

30. Describe typical signs of each of the following:

sudden arterial occlusion

deep venous thrombosis

superficial thrombophlebitis

varicose veins

chronic arterial insufficiency

chronic venous insufficiency

Anonymous Bates, p. 470-479

Sudden arterial occlusion: pain and numbness/tingling, limb distal to occlusion becomes cold, pale, pulseless.

Deep venous thrombosis: The extent of edema suggest location – the calf when lower leg or ankle is swollen, the iliofemoral veins when the entire leg is swollen. Painful, pale, swollen leg with tenderness of the femoral vein suggests deep iliofemoral thrombosis. Tenderness and cords deep in the calf suggests its there.

Superficial thrombophlebitis: local swelling, redness, warmth, and a subcutaneous cord.

Varicose veins: dilated, thickened, tortuous veins (usually seen in legs)

Chronic arterial insufficiency Table 16-1 and 16-2 and p. 478-479: intermittent claudication, progressing to pain at rest. Decreased or absent pulses. Paleness, especially on elevation; dusky red on dependency. Cool temp., absent or mild edema, trophic changes: thin, shiny, atrophic skin; loss of hair over the foot and toes; nails thickened and rigid. If ulceration is present, it usually involves the toes or points of trauma on feet. May develop gangrene.

Chronic venous insufficiency Table 16-1 and 16-2: may have no pain, or have aching pain on dependency. Normal pulses, though may be difficult to palpate through edema. Normal color, or cyanotic on dependency. Petechiae and then brown pigmentation appear with chronicity. Normal temp. Edema often present and marked. Often brown pigmentation around the ankle, stasis dermatitis, and possible thickening of the skin and narrowing of the leg as scarring develops. If ulceration is present, it develops at the sides of the ankle, especially medially.

Anonymous

Sudden arterial occlusion: Acute limb ischemia secondary to thrombosis or embolism is a true emergency requiring immediate therapy to salvage the limb. Acute limb ischemia will exhibit one or more of the 6 “P’s” pain, pallor, polar (for cold), pulselessness, parasthesis and paralysis.

Deep Vein Thrombosis (DVT): The formation of venous clots is related to at least one of the Virchows triad of factors: venous stasis, injury to vessel wall and hypercoagulable state. In DVT the extent of the edema suggests the location of the clot. Swelling and tenderness in the involved extremity are the most common findings. Other signs & symptoms include pain, redness, warmth and fever. Pain in the calf with forced dorsiflexion of the ankle and leg straight (Homan’s sign) is not reliable for DVT. The clinical exam is unrel;iable for the detection or exclusion of DVT. Assessment of risk factors may be a stronger predictor (Note the memory aid spells THROMBOSIS). T – Trauma H – Hypercoagulable R – Recreational Drugs O – Old (age > 40) M – Malignancy B – Birth control Pill O – Obesity & Obstetrics S – Surgery or smoking I – Immobilization S – Sickness.

Superficial Thrombophlebitis: Local pain, swelling, redness, warmth and tenderness of a subcutaneous cord along the course of the involved vein are typical findings. Bruising and bleeding may also be noted at the involved site.

Varicose veins: Can be seen as dilated, tortuous and somewhat thickened veins. Most patients with varicose veins have no symptoms wheras others complain of fatigue or aching in the lower part of of the leg or swelling at the end of the day. There may be pitting edema. An itchy, inflamed, scaly rash above or below the medial malleolus, followed by brown pigmentation of the area and finally ulceration. The brown pigmentation occurs from the inflammatory reaction and deposition of hemoglobin.

Chronic arterial insufficiency: Causes intermittent claudication, postural color changes and trophic changes in the skin. Much less common in the arms then in the legs. As the severity of the occlusion worsens, blood flow becomes inadequate for tissue needs even at rest, resulting in the manifestations of more severe arterial insufficiency: ischemic rest pain and tissue necrosis may occur. Peripheral gangrene and erectile impotence may e other signs.

Chronic venous insufficiency: Also called the postphlebitic syndrome, is common chronic disorder that is particularly disabling if stubborn venous ulcers develop. Venous insufficiency accounts for 80-90% of leg ulcers. The presenting complaints center around swelling or ulceration of the lower leg. Chronic recurrent swellingcauses a sensation of tightness or bursting and heaviness or aching of the limb. This is often worst at the end of the day and may largely disappear overnight. With chronicity, brawny induration, hyperpigmentation, and skin ulceration may ensue.

Deb B./Bates, pg. 460-461:

sudden arterial occlusion- distal pain, involving foot and leg, coldness, numbness, weakness, absent distal pulses

deep venous thrombosis- Pain, if present, usually in calf, but often painless, possibly swelling of foot and calf and local calf tenderness, often nothing.

superficial thrombophlebitis-pain in a local area along course of superficial vein, most often in saphenous sys., local redness, swelling, tenderness, a palpable cord, possibly fever.

varicose veins –pg. 456 are dilated and tortuous, (couldn’t find anyother specifics)

chronic arterial insufficiency- pg. 458 see postural color changes, (raise both legs to about 60 degrees until maximal pallor of feet develops, then have pt. sit up with legs dangling down, compare feet) not unusual dusky redness (rubor), increased timing of color return and venous filling (longer than 10 sec. for color/15 sec. for filling of veins)

chronic venous insufficiency-diffuse aching of leg(s), chronic edema, pigmentation, possibly ulceration.

Greg R.

sudden arterial occlusion – Swartz p. 402. The signs of an acute arterial occlusion are the five p’s: pain, pallor, paresthesia, paralysis, and pulselessness. Bates’ p. 454. Sudden arterial occlusion, as by embolism or thrombosis, causes pain and numbness or tingling. The limb distal to the occlusion becomes cold, pale, and pulseless. Emergency treatment is required. If collateral circulation is good, only numbness and coolness may result.

deep venous thrombosis – Swartz p. 403-4. Deep venous thrombosis of a lower extremity is diagnosed when there is unilateral marked swelling, venous distention, erythema, pain, increased warmth, and tenderness. There is often resistance to dorsiflexion of the ankle. Calf swelling is present in most patients with femoral or popliteal venous involvement, whereas thigh swelling occurs with iliofemoral thrombosis.

superficial thrombophlebitis – Bates’ p. 456. Local swelling, redness, warmth, and a subcutaneous cord suggest superficial thrombophlebitis.

varicose veins – Bates’ p. 456. Varicose veins are dilated and tortuous. Their wall may feel somewhat thickened. Many varicose veins can be seen in the leg on

chronic arterial insufficiency – Swartz p. 392. Chronic arterial insufficiency produces a cool and pale extremity.

chronic venous insufficiency – Swartz p. 392. Chronic venous insufficiency produces a warmer than normal extremity. The leg becomes erythematous, and erosions produced by excoriation result. With chronic insufficiency, stasis changes produce increased pigmentation, swelling, and an “aching” or “heaviness” in the legs. These changes characteristically occur in the lower third of the extremity and are more prominent medially. When venous insufficiency occurs, edema of dependent areas results.

Mary

sudden arterial occlusion- patients will present with the 5 p’s: Pain, Pallor, Parasthesia, Paralysis, and Pulselessness. p.402

deep venous thrombosis- pts. will present with marked uni-lateral swelling, venous distention, redness, pain, and often, a resistance to dorsoflexion of the ankle. p 403-4

superficial thrombophlebitis- secondary to deep vein thrombosis. Often the examiner will be able to palpate the indurated vein or cord in the groin or medial thigh p404. *an estimated 45% of patients with thrombophlebitis suffer assymptomatic pulmonary emboli.

varicose veins- may indicate right sided heart failure p 396.

Chronic arterial insufficiency- claudication, then painful ulcers, and then gangrene.p.394

Chronic venous insufficiency- leads to venous stasis, pitting edema, brown or darkly pigmented skin of the lower legs, painless ulceration of dependent area. p. 395

31. Distinguish between common ulcers of the heel and ankles

Anonymous Bates, p. 479

Arterial insufficiency – found on toes, feet, or possibly in areas of trauma; no callus or excess of pigment, may be atrophic; pain is often severe, unless neuropathy masks it; associated gangrene may be present; decreased pulses, trophic changes, pallor of the foot on elevation, dusky rubor on dependency.

Chronic venous insufficiency – located on inner or sometimes outer ankle; skin is pigmented, sometimes fibrotic; pain is not severe; gangrene absent; edema, pigmentation, stasis dermatitis, and possibly cyanosis of the foot on dependency.

Neuropathic ulcer – located on pressure points in areas w/ diminished sensation, as in diabetic polyneuropathy; skin around ulcer is calloused; pain is absent; associate gangrene in uncomplicated neuropathic ulcer, absent; decressed sensation, absent ankle jerks.

Anonymous

	Arterial Insufficiency	Chronic Venous Insufficiency	Neuropathic Ulcer
Location	Toes, feet areas of trauma (shin)	Inner or sometimes outer ankle	Pressure points in areas with diminished sensation, as in diabetic polyneuropathy
Skin around the ulcer	No callus or excess of pigment, may be atrophic	Pigmented, sometimes fibrotic	Calloused
Pain	Often severe, unless neuropathy masks it	Not severe	Absent (and therefore the ulcer may go unnoticed)
Associated Gangrene	May be present	Absent	In uncomplicated neuropathic ulcer, absent
Associated Signs	↓ Pulses, trophic changes, pallor of the foot on elevation, dusky rubor on dependency	Edema, pigmentation, stasis dermatitis, and possibly cyanosis of the foot on dependency	↓ sensation, absent ankle jerks

EChing, Bates 3^rd Ed, P318-319

	Ulcer of Feet	Ulcer of Ankles
	Arterial Insufficiency	Chronic venous insufficiency
Skin surrounding the ulcer	No callus or excess of pigment, may be atrophic	Pigmented, sometimes fibrotic
Pain	Often severe, unless neuropathy masks it	Not severe
Associated gangrene	May be present	Absent
Associated signs	Atrophic skin w/ decreased hair, pallor of foot on elevation, dusky or cyanotic rubor on dependency	Static dermatitis, pigmentation, edema, & possibly, cyanosis of the foot on dependency
	Chronic arterial insufficiency	Chronic venous insufficiency
Pulse	Decreased or absent	Normal, though may be difficult to feel through edema
Color	Pale, especially on elevation; dusky red on dependency	Normal, or cyanotic on dependency
Temp	Cool	Normal
Skin changes	Thin, shiny, atrop0hic skin, loss of hair over foot & toes; nails thickened & ridged	May show brown pigmentation around ankles, stasis dermatitis
Ulceration	If present, involves toes or points of trauma on feel	If present, develops at sides of ankle
Gangrene	May develop	Does not develop

A.T. Swartz p. 383- Feet- Arterial Insufficiency, toe and heel, Painful, have discrete borders “punched out appearance” and can be covered in crust. When infected the tissue is erythematous.

Ankles- Venous- ulceration which is painless, occurs in the ankle or lower leg just above the medial malleolus, cobblestone appearance, ulceration occurs with slight trauma. Development is usually result of venous insufficiency.

Mary p.393-4

Rapidly developing ulcers of the foot and ankles are associated with arterial insufficiency and lead to painful ulcerations and gangrene. Slowly developing ulcers of the foot and ankle are usually the result of chronic venous insufficiency and are usually marked by discoloration of the skin prior to a relatively painless ulceration-a condition called stasis dermatitis.

32. Describe the mechanisms and patterns associated with edema caused by:

right-sided congestive heart failure

hypoalbuminemia

venous stasis

lymphatic stasis

orthostatic edema

Anonymous Bates, p. 480-481

Right sided congestive heart failure – decreased ability of the heart to pump venous blood forward increases hydrostatic pressure. Edema first appears in feet/legs. Pressure in veins and capillaries causes congestion and loss of fluid into tissues.

Hypoalbuminemia – decreased colloid pressure in plasma - cirrhosis, nephritic syndrome, and severe malnutrition. Edema seen in eyelids, feet, and legs.

Venous stasis – thrombophlebitis; hydrostatic pressure increased in veins and and capillaries causing excess fluid loss into tissues. Edema seen in area of blockage.

Lymphatic stasis – congenitally abnormal lymph channels or blockage by tumor, fibrosis, or inflammation. Local swelling in one or both legs.

Orthostatic edema – prolonged sitting/standing without sustained muscular activity – increased pressure in veins. Edema seen in dependent areas.

Anonymous

Right-sided congestive heart failure-decreased ability of the heart to pump venous blood forward increases the hydrostatic pressure in the veins and capillaries, producing congestion and loss of fluid into the tissues. Edema first appears in the dependent areas of the body where hydrostatic pressure is highest , ie, the feet and the legs. When the patient is bedridden, the low back is dependent and becomes edematous.

Hypoalbuminemia-decreased colloid osmotic pressure in the plasma allows excessive fluid to escape into the interstitial space and remain there. Causes include cirrhosis, the nephritic syndrome, and severe malnutrition. Edema may appear first in the loose subcutaneous tissues of the eyelids, especially after the patient lies down at night, but may also show first in the feet and legs. In cirrhosis, ascites often appears first. When cirrhosis is more advanced, edema may become generalized.

Venous stasis-Thrombophlebitis may block venous drainage. Venous valves may be damaged by thrombophlebitis or become incompetent because of varicose veins. Less commonly, veins may be compressed from the outside, as by a tumor or fibrosis. In any case, hydrostatic pressure rises in the veins and capillaries, producing excessive loss of fluid into the tissues. Edema is limited to the area of blockage, often one leg or, less commonly, both legs or an arm. A blocked superior vena cava may cause edema in the entire upper part of the body.

Lymphatic stasis-Lymph channels may be congenitally abnormal, or may be obstructed by tumor, fibrosis, or inflammation. Local, often involving one or both legs. Lymphedema of an arm may follow axillary node dissection and radiation therapy.

Orthostatic edema-Prolonged sitting or standing, without sufficient muscular activity to promote venous flow, increases the pressure in the veins and capillaries and thus increases the flow of fluid into the interstitial spaces. Edema occurs at eh dependent areas (e.g., the legs) Bates, p480-481

Anonymous

Hypoalbuminemia-decreased colloid osmotic pressure in the plasma allows excessive fluid to escape into the interstitial space and remain there. Causes include cirrhosis, the nephritic syndrome, and severe malnutrition. Edema may appear first in the loose subcutaneous tissues of the eyelids, especially after the patient lies down at night, but may also show first in the feet and legs. In cirrhosis, ascites often appears first. When cirrhosis is more advanced, edema may become generalized.

EChing, Bates 3^rd Ed, P320-321

	Mechanisms of edema	Distribution of edema
R. sides congestive heart failure	Decreased ability of the heart to accept venous blood increases the hydrostatic pressure in the veins & capillaries, producing congestion & loss of fluid into the tissues	Edema first appears in the dependent areas of the body where hydrostatic pressure is highest (feet & legs). When the pt is bedridden, the low back is dependent
Hypoalbuminemia	Decreased colloid osmotic pressure in the plasma allows excessive fluid to escape into the interstitial space. Causes: cirrhosis, nephrotic syndrome, and severe malnutrition.	Edema may appear first in the loose subcutaneous tissues of the eyelids, especially after the pt lies down at night, but may also show first in the feet & legs. In cirrhosis, ascites often appears first. When cirrhosis is more advanced, edema may become generalized
Venous stasis (secondary to obstruction or insufficiency)	Thrombophlebitis may block venous drainage. Venous valves may be damaged by thrombophlebitis or become incompetent because of varicose veins. Less commonly, veins may be compressed from the outside, as by a tumor or fibrosis. In any case, hydrostatic pressure rises in the veins & capillaries, producing excessive loss of fluid into the tissues.	Limited to the area of blockage, often one leg, or less commonly, both legs or an arm. A blocked superior vena cava may cause edema in the entire upper part of the body.
Lymphatic stasis (lymphedema)	Lymph channels may be congenitally abnormal or they may be obstructed by tumor, fibrosis, or inflammation.	Local, often involves one or both legs. Lymphedema of an arm may follow radical mastectomy.
Orthostatic edema	Prolonged sitting or standing, without sufficient muscular activity to promote venous flow, increases the pressure in the veins & capillaries & thus increases the flow of fluid into the interstitial spaces.	The dependent areas (legs).

A.T.

right-sided congestive heart failure - Stevens p. 175. In right sided heart failure there is poor perfusion of the lungs and increased pressure in the venous system. Causes edema of the jug. Veins, liver, and subcutaneous edema.

Hypoalbuminemia-Bates 8^th ed. p. 445- In the blood the albumin protein assist in holding the fluid in the vasculature. In malnutrition there is insuffienct protein in the vasculature. Therefore, there is a decrease in colloid osmotic pressure of plasma proteins.

venous stasis-Swartzp. 392. In venous stasis the upright position the venous pressure increases, dilatation occurs, the vessels dilate and the wall are unable to close inadequately and ineffiecent in returning blood to the heart and pooling uccurs.

lymphatic stasis-Swartz 393 primary abnormality in development or an obstruction in flow. Firm non-pitting edema. Over years the skin becomes rough pigskin like.

Mary

Rt. sided heart failure- inability of the right ventricle to keep up with the volume of venous return causing increase in hydrostatic pressure in the legs and other dependent areas with subsequent movement of fluid into the interstitial space. Bates p.480 same for all…

Hypoalbuminemia- not enough protein in the plasma (malnutrition) which causes excess fluid to escape to interstitial spaces causing eyelid swelling at night or ascites (as in cirrhosis).

Venous stasis- venous insufficiency or localized thrombosis causing edema, skin discoloration, and painless ulceration in its chronic form.

Lymphatic stasis- localized edema obstruction of lymph node chain due to neoplasm, excision, or inflammation.

Orthostatic- prolonged sitting or standing causing increased swelling to dependent an area that is relieved by a change in position. Table/Bates p.480-81

33. Describe the process and physical findings associated with peripheral edema caused by:

orthostatic edema

lymphedema

chronic venous insufficiency

Anonymous Bates, p. 482

Orthostatic edema – edema from prolonged sitting/standing, edema of feet (bilat.), soft pits on pressure.

Lymphedema – lymphatic obstruction with marked skin thickening, rare ulceration, foot edema including toes (often bilat.) that is soft early but becomes hard (no pits).

Chronic venous insufficiency – chronic obstruction or valvular incompetence of the deep veins, skin thickening may be present especially near the ankle, ulceration is common as is pigmentation, foot edema is often present – occasionally bilat. Edema is soft with pits on pressure; later may become hard.

EChing, Bates 3^rd Ed, P322

	Orthostatic edema	Lymphedema	Chronic venous insufficiency
Process	Edema from prolonged sitting or standing	Lymphatic obstruction	Deep venous obstruction or valvular incompetence.
Nature of edema	Soft, pits on pressure	Soft early, becomes hard & nonpitting	Soft, pits on pressure, later may become brawny
Skin thickening	Absent	Marked	Occasional
Ulceration	Absent	Rare	Common
Pigmentation	Absent	Absent	Common
Foot involvement	Present	Present	Present
Bilaterality	Always	Often	Occasionally

Mary

orthostatic edema- swelling in the legs after prolonged sitting or bed rest as evidenced by pitting edema that is relieved by a change in position. Bates 481

lymphedema- presents as marked swelling of the affected area, and, except in early stages is characterized by nonpitting. This can be the result of dissection as in radical mastectomy after breast CA. Bates 481/ Swartz 395

chronic venous insufficiency- presents with discoloration-usually of legs, and gradual onset of painless ulcers or stasis dermatitis. Bates 479

34. Given a patient be able to identify and describe abnormalities present on a vascular examination.

EChing, Swartz, P392-402

Many pts with peripheral vascular disease are asymptomatic. When pts are symptomatic, vascular disease can causes: Pain, Changes in skin temp & color, Edema, Ulceration, Emboli, Stroke, Dizziness.

Evaluation of the peripheral vascular system includes:

Inspection:

Symmetry of the extremities, Lower extremities, Assess the skin temp, Assess

varicosities.

Examination of the arterial pulses:

Palpate the radial pulse, Palpate the brachial pulse, Auscultate the carotid artery,

Palpate the abdominal aorta, Rule out abdominal bruits, Palpate the femoral pulse,

Rule out coarctation of the aorta (especially in a hypertensive pt), Palpate Popliteal pulse, Palpate the Dorsalis Pedis pulse, Palpate the posterior Tibial pulse, Grading of pulses (0=absent, 1=diminished, 2=normal 3=increased, 4=bounding).

Examination of the lymphatic system:

Palpate for epitrochlear nodes (flex elbow 90 degree, rarely palpable).

Other special techniques:

Evaluate arterial supply in the upper & lower extremity, Evaluate capillaries refill time in the lower extremity, Test for incompetent saphenous veins, & test for retrograde filling.