Jugular venous pulse

Published on 02/04/2015 by admin

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15 Jugular venous pulse

Instruction

Examine this patient’s neck.

Examine this patient’s cardiovascular system.

Salient features

History

• Shortness of breath

• Symptoms of right heart failure (leg oedema, ascites).

Examination

• The JVP is measured ….. cm above the angle of Louis (manubriosternal angle). Remember that the distance between the angle of Louis and the mid-right atrium can be varied and the JVP may be measured as high as at the level of the ear lobes.

• Comment on the waveform (timing it with the carotid pulse):

• ‘v’ waves of tricuspid regurgitation
• Cannon waves of heart block
• Absent ‘a’ waves in atrial fibrillation (irregular carotid pulse)
• Large ‘a’ waves of pulmonary hypertension, pulmonary stenosis, tricuspid stenosis.

• Check the hepatojugular reflex.

• Tell the examiner that you would like to look for other signs of heart failure:

• Basal crackles and pleural effusion
• Dependent oedema (ankle and sacral oedema)
• Tender hepatomegaly.

Diagnosis

This patient has raised jugular venous pulse with ‘v’ waves (lesion) caused by tricuspid regurgitation (see Case 19) and is in heart failure (functional status).

Questions

What are the causes of a raised jugular venous pulse?

• Congestive cardiac failure (N Engl J Med 2001;345:574–81)

• Cor pulmonale

• Tricuspid regurgitation (prominent ‘v’ waves)

• Tricuspid stenosis (prominent ‘a’ waves)

• Complete heart block (cannon waves)

• Non-pulsatile neck veins seen in superior venal caval obstruction (p. 796).

How do you differentiate jugular venous pulsations from carotid artery pulsations?

Unlike the arterial pulse, the venous pulse has a definite upper level which falls during inspiration and changes with posture. The venous pulse is seen to have a dominant inward motion, towards the midline (the ‘y’ descent), whereas the arterial pulse exhibits a dominant outward wave. The venous pulse is better seen than felt, whereas the arterial pulse is readily felt by very slight pressure of the clinician’s finger.

What do you know about the hepatojugular reflux?

A positive hepatojugular (abdominojugular) reflux is a feature of left ventricular systolic failure with secondary pulmonary hypertension. It is elicited by upper abdominal compression for ~10 s and an abnormal response is one where there is an increase followed by an abrupt fall. The hepatojugular manoeuvre is often useful in eliciting venous pulsations when not readily visible.

Advanced-level questions

What do you know about the waveforms in the jugular pulse?

There are two outward moving waves (‘a’ and ‘v’ wave) and two inward moving waves (the ‘x’ and ‘y’ descent) (Fig 15.1):

• The ‘a’ wave is caused by atrial contraction and is presystolic. It can be identified by simultaneous auscultation of the heart and the examination of the jugular venous pulse. The ‘a’ wave occurs at about the first heart sound.

• The ‘c’ wave is caused by closure of the tricuspid valve and is not readily visible.

• The ‘v’ wave is caused by venous return to the right heart (not from ventricular contraction) and occurs nearer to the second heart sound.

• The ‘x’ descent is caused by atrial relaxation (sometimes referred to as systolic collapse).

• The ‘y’ descent is produced by opening of the tricuspid valve and rapid inflow of blood into the RV.

image

Fig. 15.1 Normal jugular venous pulse.

What is Kussmaul’s sign?

Normally there is an inspiratory decrease in JVP. In constrictive pericarditis, there is an inspiratory increase in JVP. Kussmaul’s sign is also seen in severe right heart failure regardless of aetiology. It is caused by the inability of the heart to accept the increase in right ventricular volume without a marked increase in the filling pressure.

What is the prognostic value of raised JVP in heart failure?

Raised JVP and third heart sounds are associated with adverse outcomes, including subsequent hospitalization for heart failure, progression of heart failure as defined by death from pump failure and by the composite end-point of death or hospitalization for heart failure, and death from all causes (N Engl J Med 2001;345:574–81).

What is the mechanism of anaemia in heart failure?

The aetiology and pathophysiology of anaemia in heart failure is also multifactorial and is caused by a complex interaction between cardiac function, renal dysfunction, neurohormonal and inflammatory responses, haemodilution, iron deficiency, impaired ability to utilize available iron stores, bone marrow suppression caused by cytokines (e.g. tumour necrosis factor α (TNF-α), interleukin-1, interleukin-6 (IL-6) and C-reactive protein), blunted bone marrow responsiveness to erythropoietin, impaired iron mobilization and effects of medications. Aspirin and ACE inhibitors contribute to the anaemia potentially through the actions of haematopoiesis inhibitor N-acetyl-seryl-aspartyl-lysyl-proline. IL-6 stimulates the production of hepcidin in the hepatic cells, which blocks absorption of iron in duodenum and downregulates ferroprotein expression; this, in turn, prevents release of iron from total body stores. TNF-α (and IL-6) inhibits erythropoietin production in the kidney by activating the GATA-binding protein GATA2 and nuclear factor-κB and it also inhibits proliferation of bone marrow erythroid progenitor cells.

Adolf Kussmaul (1822–1902) was Professor of Medicine successively at Heidelberg, Enlargen, Freiburg and Strasbourg, and coined the term polyarteritis nodosa (Berl Klin Wochnschr 1873;10:433). Kussmaul breathing is deep sighing respiration seen when the arterial pH is low.

In 1867, Potain described the waveforms of the internal jugular vein.

In 1902, James Mackenzie championed that the jugular venous pulse is an essential part of the cardiovascular physical examination.

In 1928, Carl Wiggers wrote that the jugular venous pulse might have utility in the interpretation of dynamic events in the heart.

In 1956, Paul Wood wrote, ‘Precise analysis of the cervical venous pulse and measurement of the height of each individual wave with reference to the sternal angle is not only possible at the bedside but highly desirable’.

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