1. What is the meaning of a slow rate of rise of the carotid arterial pulse?
A carotid arterial pulse that is reduced (parvus) and delayed (tardus) argues for aortic valvular stenosis. Occasionally this also may be accompanied by a palpable thrill. If ventricular function is good, a slower upstroke correlates with a higher transvalvular gradient. In left ventricular failure, however, parvus and tardus may occur even with mild aortic stenosis (AS).
2. What is the significance of a brisk carotid arterial upstroke?
It depends on whether it is associated with normal or widened pulse pressure. If associated with normal pulse pressure, a brisk carotid upstroke usually indicates two conditions: & Simultaneous emptying of the left ventricle into a high-pressure bed (the aorta) and a lower pressure bed: The latter can be the right ventricle (in patients with ventricular septal defect [VSD]) or the left atrium (in patients with mitral regurgitation [MR]). Both will allow a rapid left ventricular emptying, which, in turn, generates a brisk arterial upstroke. The pulse pressure, however, remains normal. & Hypertrophic cardiomyopathy (HCM): Despite its association with left ventricular obstruction, this disease is characterized by a brisk and bifid pulse, due to the hypertrophic ventricle and its delayed obstruction. If associated with widened pulse pressure, a brisk upstroke usually indicates aortic regurgitation (AR). In contrast to MR, VSD, or HCM, the AR pulse has rapid upstroke and collapse.
3. In addition to aortic regurgitaiton, which other processes cause rapid upstroke and widened pulse pressure?
The most common are the hyperkinetic heart syndromes (high output states). These include anemia, fever, exercise, thyrotoxicosis, pregnancy, cirrhosis, beriberi, Paget’s disease, arteriovenous fistulas, patent ductus arteriosus, aortic regurgitation, and anxiety—all typically associated with rapid ventricular contraction and low peripheral vascular resistance.
4. What is pulsus paradoxus?
Pulsus paradoxus is an exaggerated fall in systolic blood pressure during quiet inspiration. In contrast to evaluation of arterial contour and amplitude, it is best detected in a peripheral vessel, such as the radial artery. Although palpable at times, optimal detection of the pulsus paradoxus usually requires a sphygmomanometer. Pulsus paradoxus can occur in cardiac tamponade and other conditions.
5. What is pulsus alternans?
Pulsus alternans is the alternation of strong and weak arterial pulses despite regular rate and rhythm. First described by Ludwig Traube in 1872, pulsus alternans is often associated with alternation of strong and feeble heart sounds (auscultatory alternans). Both indicate severe left ventricular dysfunction (from ischemia, hypertension, or valvular cardiomyopathy), with worse ejection fraction and higher pulmonary capillary pressure. Hence, they are often associated with an S3 gallop.
6. What is Duroziez’s double murmur?
Duroziez’s is a to-and-fro double murmur over a large central artery—usually the femoral, but also the brachial. It is elicited by applying gradual but firm compression with the stethoscope’s diaphragm. This produces not only a systolic murmur (which is normal) but also a diastolic one (which is pathologic and typical of AR). Duroziez’s has 58% to 100% sensitivity and specificity for AR.
7. What is the carotid shudder?
Carotid shudder is a palpable thrill felt at the peak of the carotid pulse in patients with AS, AR, or both. It represents the transmission of the murmur to the artery and is a relatively specific but rather insensitive sign of aortic valvular disease.
8. What is Corrigan’s pulse?
Corrigan’s is one of the various names for the bounding and quickly collapsing pulse of aortic regurgitation, which is both visible and palpable. Other common terms for this condition include water hammer, cannonball, collapsing, or pistol-shot pulse. It is best felt for by elevating the patient’s arm while at the same time feeling the radial artery at the wrist. Raising the arm higher than the heart reduces the intraradial diastolic pressure, collapses the vessel, and thus facilitates the palpability of the subsequent systolic thrust.
9. How do you auscultate for carotid bruits?
By placing your bell on the neck in a quiet room and with a relaxed patient. Auscultate from just behind the upper end of the thyroid cartilage to immediately below the angle of the jaw.
10. What is the correlation between symptomatic carotid bruit and high-grade stenosis?
It’s high. In fact, bruits presenting with transient ischemic attacks (TIAs) or minor strokes in the anterior circulation should be evaluated aggressively for the presence of high-grade (70%–99%) carotid stenosis, because endarterectomy markedly decreases mortality and stroke rates. Still, although presence of a bruit significantly increases the likelihood of high-grade carotid stenosis, its absence doesn’t exclude disease. Moreover, a bruit heard over the bifurcation may reflect a narrowed external carotid artery and thus occur in angiographically normal or completely occluded internal carotids. Hence, surgical decisions should not be based on physical examination alone; imaging is mandatory.
11. What is central venous pressure (CVP)?
The pressure within the right atrium/superior vena cava system (i.e., the right ventricular filling pressure). As pulmonary capillary wedge pressure reflects left ventricular end-diastolic pressure (in the absence of mitral stenosis), so central venous pressure reflects right ventricular end-diastolic pressure (in the absence of tricuspid stenosis).
12. Which veins should be evaluated for assessing venous pulse and CVP?
13. Can the external jugulars be used for evaluating central venous pressure?
Theoretically not, practically yes. Not because:
- While going through the various fascial planes of the neck, they often become compressed.
- In patients with increased sympathetic vascular tone, they may become so constricted as to be barely visible.
- They are farther from the right atrium and thus in a less straight line with it. Yet both internal and external jugular veins can actually be used for estimating CVP because they yield comparable estimates. Hence, if the only visible vein is the external jugular, do what Yogi Berra recommends you should do when coming to a fork in the road: take it.
14. What is a ‘‘cannon’’ A wave?
A ‘‘cannon’’ A wave is the hallmark of atrioventricular dissociation (i.e., the atrium contracts against a closed tricuspid valve). It is different from the other prominent outward wave (i.e., the presystolic giant A wave) insofar as it begins just after S1, because it represents atrial contraction against a closed tricuspid valve.
15. How do you estimate the CVP?
By positioning the patient so that you can get a good view of the internal jugular vein and its oscillations. Although it is wise to start at 45 degrees, it doesn’t really matter which angle you will eventually use to raise the patient’s head, as long as it can adequately reveal the vein. In the absence of a visible internal jugular, the external jugular may suffice.
By identifying the highest point of jugular pulsation that is transmitted to the skin (i.e., the meniscus). This usually occurs during exhalation and coincides with the peak of ‘‘A’’ or ‘‘V’’ waves. It serves as a bedside pulsation manometer.
By finding the sternal angle of Louis (the junction of the manubrium with the body of the sternum). This provides the standard zero for jugular venous pressure. (The standard zero for central venous pressure is instead the center of the right atrium.)
By measuring in centimeters the vertical height from the sternal angle to the top of the jugular pulsation. To do so, place two rulers at a 90-degree angle: one horizontal (and parallel to the meniscus) and the other vertical to it and touching the sternal angle. The extrapolated height between the sternal angle and meniscus represents the jugular venous pressure (JVP).
By adding 5 to convert jugular venous pressure into central venous pressure. This method relies on the fact that the zero point of the entire right-sided manometer (i.e., the point where central venous pressure is, by convention, zero) is the center of the right atrium. This is vertically situated at 5 cm below the sternal angle, a relationship that is present in subjects of normal size and shape, regardless of their body position. Thus, using the sternal angle as the external reference point, the vertical distance (in centimeters) to the top of the column of blood in the jugular vein will provide the JVP. Adding 5 to the JVP will yield the CVP.
16. What is the significance of leg swelling without increased central venous pressure?
It reflects either bilateral venous insufficiency or noncardiac edema (usually hepatic or renal). This is because any cardiac (or pulmonary) disease resulting in right ventricular failure would manifest itself through an increase in central venous pressure. Leg edema plus ascites in the absence of increased CVP argues in favor of a hepatic or renal cause (patients with cirrhosis do not have high CVP). Conversely, a high CVP in patients with ascites and edema argues in favor of an underlying cardiac etiology.
17. What is Kussmaul’s sign?
Kussmaul’s sign is the paradoxical increase in JVP that occurs during inspiration. Jugular venous pressure normally decreases during inspiration because the inspiratory fall in intrathoracic pressure creates a ‘‘sucking effect’’ on venous return. Thus, Kussmaul’s sign is a true physiologic paradox. This can be explained by the inability of the right side of the heart to handle an increased venous return.
Disease processes associated with a positive Kussmaul’s are those that interfere with venous return and right ventricular filling. The original description was in a patient with constrictive pericarditis. (Kussmaul’s is still seen in one third of patients with severe and advanced cases, in whom it is often associated with a positive abdominojugular reflux.) Nowadays, however, the most common cause is severe heart failure, independent of etiology. Other causes include cor pulmonale (acute or chronic), constrictive pericarditis, restrictive cardiomyopathy (such as sarcoidosis, hemochromatosis, and amyloidosis), tricuspid stenosis, and right ventricular infarction.
18. What is the ‘‘venous hum’’?
Venous hum is a functional murmur produced by turbulent flow in the internal jugular vein. It is continuous (albeit louder in diastole) and at times strong enough to be associated with a palpable thrill. It is best heard on the right side of the neck, just above the clavicle, but sometimes it can become audible over the sternal/parasternal areas, both right and left. This may lead to misdiagnoses of carotid disease, patent ductus arteriosus, or AR/AS. The mechanism of the venous hum is a mild compression of the internal jugular vein by the transverse process of the atlas, in subjects with strong cardiac output and increased venous flow. Hence, it is common in young adults or patients with a high output state. A venous hum can be heard in 31% to 66% of normal children and 25% of young adults. It also is encountered in 2.3% to 27% of adult outpatients. It is especially common in situations of arteriovenous fistula, being present in 56% to 88% of patients undergoing dialysis and 34% of those between sessions.
19. Which characteristics of the apical impulse should be analyzed?
Location: Normally over the fifth left interspace midclavicular line, which usually (but not always) corresponds to the area just below the nipple. Volume loads to the left ventricle (such as aortic or mitral regurgitation) tend to displace the apical impulse downward and laterally. Conversely, pressure loads (such as aortic stenosis or hypertension) tend to displace the impulse more upward and medially—at least initially. Still, a failing and decompensated ventricle, independent of its etiology, will typically present with a downward and lateral shift in point of maximal impulse (PMI). Although not too sensitive, this finding is very specific for cardiomegaly, low ejection fraction, and high pulmonary capillary wedge pressure. Correlation of the PMI with anatomic landmarks (such as the left anterior axillary line) can be used to better characterize the displaced impulse.
Size: As measured in left lateral decubitus, the normal apical impulse is the size of a dime. Anything larger (nickel, quarter, or an old Eisenhower silver dollar) should be considered pathologic. A diameter greater than 4 cm is quite specific for cardiomegaly.
Duration and timing: This is probably one of the most important characteristics. A normal apical duration is brief and never passes midsystole. Thus, a sustained impulse (i.e., one that continues into S2 and beyond—often referred to as a ‘‘heave’’) should be considered pathologic until proven otherwise and is usually indicative of pressure load, volume load, or cardiomyopathy.
Amplitude: This is not the length of the impulse, but its force. A hyperdynamic impulse (often referred to as a ‘‘thrust’’) that is forceful enough to lift the examiner’s finger can be encountered in situations of volume overload and increased output (such as aortic regurgitation and ventricular septal defect) but may also be felt in normal subjects with very thin chests. Similarly, a hypodynamic impulse can be due to simple obesity but also to congestive cardiomyopathy. In addition to being hypodynamic, the precordial impulse of these patients is large, somewhat sustained, and displaced downward/laterally.
Contour: A normal apical impulse is single. Double or triple impulses are clearly pathologic.
Hence, a normal apical impulse consists of a single, dime-sized, brief (barely beyond S1), early systolic, and nonsustained impulse, localized over the fifth interspace midclavicular line.
20. What is a thrill?
A palpable vibration associated with an audible murmur. A thrill automatically qualifies the murmur as being more than 4/6 in intensity and thus pathologic.
