Presentation is loading. Please wait.

Presentation is loading. Please wait.

Mary Beth Fontana M.D. Cardiovascular Medicine

Similar presentations

Presentation on theme: "Mary Beth Fontana M.D. Cardiovascular Medicine"— Presentation transcript:

1 Mary Beth Fontana M.D. Cardiovascular Medicine
Diagnostic Utility of Examination of the Carotid Pulse Apex Impulse Jugular Venous Pulse Mary Beth Fontana M.D. Cardiovascular Medicine Examination of the carotid pulse, apex impulse, and jugular venous pulse are essential components of the cardiovascular physical examination. Identified abnormalities can contribute to making many diagnoses of cardiac and pericardial disease. I will include many pearls of physical exam in this discussion, many of which were mentioned in the physical exam demonstration, and which will be useful as you evaluate patients. In cardiac patients the physical examination is particularly valuable in making diagnoses.

2 Block Learning Objectives
Evaluate carotid pulse and auscultate for bruits  Localize and characterize the apex impulse  Identify jugular venous pulse components and assess jugular venous pressure Describe the abnormalities of the carotid pulse, apex impulse, and jugular venous pulse in cardiac and pericardial disease The first 3 objectives have been covered in your physical examination tutorials and during the physical exam session earlier in this block. They will briefly be reviewed here since being able to correctly evaluate them is the foundation for deciding whether they are normal or abnormal. The emphasis in this module will be on abnormal findings and how they relate to specific diagnoses of cardiac and pericardial disease

3 Resources Lilly doesn’t have specific sections on carotid pulse or apex impulse, instead describing them with some specific diagnoses. Jugular venous pulse; Chapter 2, pp.29-30 This module summarizes the abnormalities of all 3 that are pertinent to diagnosis Lilly reports abnormalities of the carotid pulse and apex impulse only with individual diagnoses, primarily in heart failure, valvular disease, and pericardial disease. Ther is a discussion of the jugular venous pulse in Chapter 2 as indicated. This eLearning module has all of the important abnormalities of all 3 in one location.

4 Learning Objectives For the carotid pulse, apex impulse, jugular venous pulse be able to: Describe the normal characteristics Describe the method of examination Explain the pathophysiology causing abnormalities of the components of each The abnormalities described are mentioned in the clinical examination of the individual diagnoses At the completion of this module, for all 3 components, you should be able to * describe the normal characteristics, * describe the method of examination, and * explain the pathophysiology causing the abnormalities that are found on examination. Heart failure has already been addressed and valvular and pericardial disease are discussed concurrent with the availability of this eLearning module.

5 Carotid Pulse Palpate between larynx and sternocleidomastoid muscle
Marker of ventricular systole Rapid upstroke and slower decline The carotid pulse should be palpated at the level of the thyroid cartilage (ye old voice box). Avoid the angle of the jaw or you may find your patient on the floor from inadvertently massaging the carotid sinus which can cause bradycardia and decreased cerebral perfusion. Timing auscultatory events is made easier by simultaneously palpating the carotid since it is a marker of ventricular systole. The upstroke of the carotid is rapid due to high velocity of ventricular ejection. This is important because the internal jugular vein is in the same location with its own pulsations which are described more in detail later in this module.

6 Normal Carotid Pulse Dicrotic notch Rapid upstroke
This phonocardiogram shows heart sound recordings, ECG, and a recording of the carotid pulse with a pressure transducer applied to the neck. The magnitude of the pulse recording is more determined by the recording amplifier settings than the LV stroke volume. Note the very rapid upstroke to the carotid pulse. The dicrotic notch which is synchronous with the aortic closure sound of S2 can be recorded but not felt clinically. Rapid upstroke

7 Abnormal Carotid Pulse
Increased volume, rapid upstrokes Sympathetic stimulation increases stroke volume and upstroke velocity Bradycardia-larger stroke volume per beat Aortic valvular regurgitation Aging stiffens walls – flow is transmitted more rapidly which raises systolic blood pressure and maintains the rapid upstroke Finding the carotid pulse is the first step, but then assessment of its volume and rapidity of the upstrokes is important for diagnostic purposes. Increased magnitude and rapidity of the upstrokes can occur in several normal and abnormal situations * Stimulation of the sympathetic nervous system increases stroke volume and upstroke velocity due to the positive inotropic and chronotropic effects on the heart. *If bradycardia is present, then the stroke volume goes up to maintain cardiac output. *Significant aortic valvular regurgitation increases stroke volume due to blood leaking back into the LV during diastole. More on that diagnosis is in other lectures. * Arterial walls stiffen with aging so pulse wave velocity increases which maintains normal upstrokes even when obstruction of blood flow getting to the carotids is present.

8 Pulsus Parvus Reduced stroke volume Left ventricular failure
Severe fixed LV outflow obstruction Blood volume depletion Reduction of stroke volume from any cause can cause small volume carotid pulses, called pulsus parvus (Latin for small pulse). Common causes are *low output LV failure* severe fixed obstruction to outflow from the LV such as valvular aortic stenosis* and blood volume depletion as from dehydration or blood loss.

9 Pulsus Tardus Slow upstrokes
Obstruction to flow between heart and carotid Most common is valvular aortic stenosis Turbulent flow in carotid is audible—called a BRUIT and can cause a palpable vibration of the arterial wall – called a THRILL Slow upstrokes signify obstruction to flow between the heart and the carotid, usually from severe valvular aortic stenosis. In severe AS turbulent flow is transmitted to the carotid producing a bruit, which is the same as a murmur over the heart, and the artery may actually vibrate which is called a thrill. This is a new definition of a thrilling experience!! You can simulate a thrill by feeling over your larynx while talking.

10 Pulsus Parvus &Tardus Valvular Aortic Stenosis
This phonocardiogram illustrates a small volume carotid with slow upstrokes from a young patient with severe valvular AS. Note also the loud ejection murmur (SM) and no recordable aortic component of the second sound—the arrow indicates where it should be. A soft murmur of aortic regurgitation(DM) is also recorded, but AS clearly predominates because of the carotid pulse findings. Slow upstroke Small volume carotid ECG

11 Bisferiens or Bifid Carotid
Two systolic peaks Rapid ejection of a large stroke volume as in severe aortic valvular regurgitation. The elastic artery reverberates Initial rapid ejection followed by slow ejection in the same systole. Seen in dynamic muscular subvalvular aortic obstruction, called hypertrophic obstructive cardiomyopathy. Only the initial spike is palpable Sometimes 2 systolic peaks are palpable in the carotid pulse, called a bisferiens or bifid carotid pulse. Causes are *severe valvular aortic regurgitation, where the stroke volume is so large that the elastic arterial wall reverberates resulting in 2 systolic peaks that are palpable. *In hypertrophic obstructive cardiomyopathy (known as HOCM), initial ejection is very rapid until the muscle gets in its own way and flow out of the LV is diminished later in systole. Recordings are show next.

12 Bisferiens Carotid Pulse Aortic Regurgitation
2 systolic peaks The 2 systolic peaks are well shown in this recording of a patient with severe aortic regurgitation. Note the systolic and diastolic murmurs consistent with stenosis and regurgitation. Regurgitation is the predominant lesion here because of the bisferiens pulse and very rapid upstrokes.

13 Bisferiens Carotid Pulse Hypertrophic Obstructive Cardiomyopathy
spike The distinctive spike and dome carotid of hypertrophic obstructive cardiomyopathy is well shown. It is a bisferiens pulse, but in the clinical real world, the dome is usually not palpable. Note the systolic ejection murmur which is similar to valvular AS. The characteristics of the carotid pulse help you differentiate the 2 diagnoses. dome Dicrotic notch

14 Pulsus Alternans Sign of severe left ventricular failure
Aortic pressure Strong beat from larger LV diastolic volume Weak beat from smaller LV diastolic volume The presence of pulsus alternans (alternating weak and strong beats) is an indicator of severe LV muscle failure. It can be palpable or detectable when measuring a patients blood pressure when the Korotkof sounds suddenly double in frequency as you lower the mercury column. This is reflecting Frank Starling forces in which more muscle cells contract when the diastolic volume of the LV is larger producing the strong beat, but the enhanced emptying then leaves less volume to stretch the sarcomeres on the next beat resulting in a smaller stroke volume. More blood is then left in the ventricle for the next beat so the stroke volume increases on the next beat--- and so the pattern keeps repeating.

15 Paradoxical Pulse Sign of fluid under pressure in the pericardial space-- tamponade inspiration expiration 15mmHg drop Aortic pressure This is a recording of the aortic pressure in a patient with cardiac tamponade which occurs when fluid in the pericardial space exerts so much pressure on the heart that any increase in right heart filling during inspiration decreases LV stroke volume. A decrease of greater that 10mm of mercury in systolic pressure with inspiration defines paradoxical pulse. There is more on this in the pericardial diseases lecture. It really should be called pulsus exaggeratus not paradoxical pulse, since hyperventilation in a normal subject or marked intrathoracic pressure swings in COPD/Asthma can cause the same phenomenon.This is another example where considering all of the findings on history and physical examination is important to arrive at the correct diagnosis!! Greater than 10 mmHg fall in systolic pressure with inspiration

16 LV Apex Impulse Recording of the apex impulse- usually only the E is palpable Systolic contraction of LV contacting the chest wall is palpable– the E point A wave may be palpable at time of S4 Rapid filling wave may be palpable at time of an S3 Locating the apex impulse of the left ventricle is done by palpation. It is usually a single impulse designated in the above drawing as the E point which represents the impact of the LV apex with the chest wall during contraction.Filling of the ventricle occurs in early diastole and after atrial contraction. When there is pathology resulting in increased filling during those times and/or if ventricular compliance is reduced these events may be palpable. Sometimes gallops are better felt than heard!!!

17 LV Apex Impulse Midclavicular line 5th intercostal space in the supine and upright position Palpable in 50% Quarter size or smaller Marker of ventricular systole Size of impulse, duration, and magnitude can be assessed in left lateral position The normal LV apex impulse is usually at or inside of the midclavicular line in the 5th intercostal space with the patient in the supine or sitting position. It is only palpable in about ½ of patients– no conclusions can be drawn if it is not palpable. If it is palpable it should be no larger than a quarter in size and is a good marker of ventricular systole for timing events. Rolling the patient into the left lateral decubitus position moves the apex closer to the chest wall, making it more likely to be felt so that size, duration, and magnitude can be assessed. The size of the heart by chest wall landmarks can no longer be used, however. The RV impulse is rarely palpable if normal in size. Enlargement can produce a palpable impulse along the left sternal border. The RV cannot displace the sternum anteriorly so the heart rotates clockwise(as seen from below) and the RV becomes palpable.

18 Abnormal Apex Enlarged LV - displaced toward left axilla
Prominent heave- ejection of large stroke volume Sustained- Poor LV systolic function, prolongation of ejection time from obstruction to LV outflow Double or triple apex impulses - palpable gallop(s) Abnormalities of the apex impulse that are helpful diagnostically are: * displacement of the apex to the left of the midclavicular line toward the axilla when supine or upright usually indicates enlargement of LV volume. The LV dilates when it fails and when volume overload occurs in valvular and congenital heart disease. * The apex usually appears and recedes quickly. If it is very prominent, ejecting a large stroke volume and/or hypertrophy of the chamber could be present. When it is prolonged or sustained, it can indicate poor LV contraction or prolonged ejection time due to obstruction to outflow, as in aortic stenosis. *You can feel up to 3 impulses per cardiac cycle if gallop sounds are palpable.

19 Normal JVP - RA a = atrial contraction C=upward thrust of T valve
x =atrial relaxation, emptying v = atrial filling with T valve closed during ventricular systole y descent = atrial emptying in early diastole This recording shows the wave forms in the right atrium which will be the same in the jugular veins since there are no valves between them. The heart sounds are also recorded so that timing of events can be seen. The different components of the JVP are shown along with the events in the cardiac cycle that occur with each wave and descent. Examination of the jugular veins is one of the most difficult parts of the cardiovascular physical examination because the pressure is normally very low at 0 to 8 mm. Hg

20 Carotid artery and internal jugular vein anatomy
The common carotid artery and internal jugular vein being beside each other in the neck can make differentiation of the two difficult. This is especially true since carotid artery pressure is high ( /60-90) and jugular venous pressure is low (not greater than 8 mm Hg mean pressure in normal people). You can feel the carotid pulse in any position, but the jugular veins are visible upright only with extreme elevations of right atrial pressure. The proper technique for examining the jugular vein and differentiating it from the carotid pulse are described in the next slide.

21 JVP Examination Elevate head degrees to see waves and estimate pressure. If JVP visible at 45 degrees, RA pressure is abnormally high Measure vertical distance above manubrial-sternal junction and add 5 to get RA pressure. Time events by feeling carotid pulse on opposite side of neck; a is before carotid, v peak is after. The c is not seen Descents are more rapid than ascents of waves JVP normally goes down with inspiration The patients head should be elevated about degrees above the horizontal so that you can see the tops of the a and v waves. In this drawing the head is probably up 30 degrees, whereas the examining table is up to about 45 degrees. Patients don’t always bend where the table is, often sliding down so that they are more horizontal. *Find the manubrial sternal juction, measure the vertical distance above that of the top of the jugular venous columns and add 5 to get right atrial pressure. * If pulsations are seen, they can be timed by palpating the carotid pulse on the other side of the neck. The A precedes the carotid, the V peaks after the carotid. The C wave is generally not seen. * The x and y descents are more rapid than the ascent of the a and v waves so they are easier to see. * The jugular venous pressure normally goes down with inspiration due to negative intrathoracic pressure increasing right heart filling.

22 Elevated Jugular Venous Pressure
Increased blood volume- pregnancy, heart failure Obstruction to atrial emptying- pericardial disease, tricuspid valve obstruction, noncompliant RV Absent wave forms- SVC obstruction Further elevation with inspiration- Kussmaul’s sign-constrictive pericarditis The mean jugular venous pressure will elevate if there is a significant increased in total blood volume. Physiologically that occurs in the last trimester of pregnancy when the blood volume is increased about 50%. In heart failure the JVP goes up due to mechanisms discussed in the heart failure part of this curriculum. * Increasing resistance to right atrial emptying by tricuspid stenosis, pericardial constriction or tamponade, or when the RV is noncompliant will raise JVP to maintain cardiac output (Q=P/R revisited again!!!)* IF the SVC is obstructed the JVP will be high but no wave forms will be seen. * If the JVP goes up with inspiration, which is called Kussmaul’s sign, then pericardial constriction should be suspected.

23 Abnormal A Wave, Attenuated Y Descent
Large a wave due to stenosis of tricuspid valve Attenuated y descent The next few recordings will show examples of alterations of different components of the JVP. They generally al are associated with an increase of the mean JVP as well. In this example the a wave is accentuated and the y descent (heavy arrow) is attenuated due to obstruction to atrial emptying due to tricuspid valve stenosis. A presystolic murmur (ASM) and tricuspid opening snap (TOS) are also recorded. A large A wave can also be seen if the RV is noncompliant as with hypertrophy from any cause. Also seen when the RV muscle has reduced compliance

24 Large V wave-tricuspid valve regurgitation
No a wave – loss of atrial contraction, atrial fibrillation V In severe regurgitation of the tricuspid valve the V wave will accentuate due to the increase of right atrial filling during ventricular systole. The y descent is rapid due to increased volume filling the ventricle. The a wave is absent due to atrial fibrillation. A murmur of tricuspid regurgitation increasing with inspiration is also well shown. The murmur vibrations are seen in the pressure recording due to the special catheter used which records sound and pressure simultaneously. Y The RA is filling from the vena cavae and from the RV during ventricular systole when the T valve should be closed. The Y descent is rapid from emptying a large volume into the RV

25 AV Dissociation – Cannon A waves
P waves and QRS’s occur independently due to complete block of conduction at the AV node A A Atrial contraction when tricuspid valve is closed In this case of complete heart block the P waves are dissociated from the QRS's so that atrial contraction sometimes occurs during ventricular contraction when the tricuspid valve is closed. The a waves are accentuated when that occurs and are called cannon a waves. Cannon a waves are seen whenever the atrium contracts against a closed tricuspid valve which can also occur during ventricular tachycardia, using a pacemaker to pace the ventricle only, or during PVC's. P P

26 RA – JVP Tamponade Fluid under pressure in the pericardial space prevents passive ventricular filling in early diastole 20mm. Hg Good X descent Attenuated Y descent This recording is a little more difficult to interpret since the LV pressure is being recorded simultaneously with the RA pressure. The RA pressure is markedly elevated at 20 mm HG. , the X descent is preserved and the Y descent is blunted. Fluid under pressure in the pericardial space markedly attenuates the early diastolic filling of the ventricles. The ventricles only fill as a result of atrial contraction so the x descent is preserved and in fact accentuated.

27 JVP – RA Accentuated Y Descent Constrictive Pericarditis
In this case of constrictive pericarditis the Y descent is particularly prominent, but the x descent is still also preserved. The jugular venous pressure is high and filling on the ventricles is very rapid once the AV valves open until the rigid pericardium prevents further ventricular expansion and filling. An early diastolic sound called pericardial knock (PK) can be heard at this time. The pressure also appears to increase on the right hand side of the recording which is during inspiration. This is Kussmaul's sign and when present suggests constriction. Constriction raises RA pressure, early diastolic filling is rapid until constricting pericardium limits filling

28 Summary & Advice This concluded this eLearning module. The content that has been reviewed should be helpful to you in making diagnoses by physical examination and most certainly will appear in your evaluation of this block. You will not be required to interpret a phonocardiogram such as those used for teaching purposes in this block, but should recognize descriptions when they appear in the evaluation of patients. No this is not my summer home. However, I would recommend visiting the Biltmore Estate in Asheville, NC at some point on a break from your career in medicine.

29 Carotid Pulse Apex Impulse JVP Quiz

30 Thank you for completing this module
I hope that I was able to teach the subject clearly. If you have any questions, write to me:

31 Survey We would appreciate your feedback on this module. Click on the button below to complete a brief survey. Your responses and comments will be shared with the module’s author, the LSI EdTech team, and LSI curriculum leaders. We will use your feedback to improve future versions of the module. The survey is both optional and anonymous and should take less than 5 minutes to complete. Survey

Download ppt "Mary Beth Fontana M.D. Cardiovascular Medicine"

Similar presentations

Ads by Google