JVP Explain the significance of the JVP. What does the JVP reflect?

In normal circumstances, the maximal pressure in the right atrium is 8cm H2O. Thus, if a

person is sitting vertically, the pressure will go up to 8cm above the middle of
the right atrium. The distance from the angle of Luis (sterno-manubrial angle) to the right atrium is approximately 5cm.

So in a normal person we would expect the JVP to be about 3cm above the angle of Luis.

JVP = vertical height of blood column (jugular venous pulsations) present in the venous system above the angle of Luis. A JVP of more than 4cm is abnormal.

CLINICAL APPROACH TO JVP How is the JVP taken from a patient? Look from side at patients neck between the ear lobe and the bottom of the neck, with patients head turned to side and relaxed. JVP can be taken with patient lying at 45 degrees or sitting upright. Measure with a ruler from the angle of Luis to the top of the venous pulsation. Normally it should be 3-4cm. If the JVP is higher than 3-4cm, it is pathological. We also should look for the pulse pattern in the JVP (this can be difficult to appreciate).

What are the different waves in the JVP during one cardiac cycle? In summary, in one cardiac cycle there are three positive pressure waves the a wave, c wave and v wave; and there are two negative descents the x wave and y wave.

Explain in detail the different parts of the cardiac cycle that each of the JVP waves represent?

The a wave represents atrial systole. As the right atrium contracts, pressure in the right atrium increases (there is a back pressure) and this is transferred to the jugular vein, with the jugular venous pulsations moving upwards. The c wave As soon as right atrium begins relaxing, the JVP column moves downwards (beginning the x descent). At the onset of ventricular systole, rising intraventricular pressure causes the tricuspid valve to close. The closure of the tricuspid valve causes a slight bulge into the atrium and a brief rise in atrial pressure. This produces the spike in the JVP known as the c wave. It is usually not visible in the neck. The x descent Relaxation of the right atrium (atrial diastole) causes the pressure in the atrium to begin to decrease, which marks the beginning of the x descent. The x descent is momentarily disrupted by the closure of the tricuspid valve, which causes a spike in pressure and cuts off communication between the right atrium and ventricle. The atrium continues to relax, allowing the atrium to accommodate more blood and causing pressure to fall the x descent. The v wave After the atrium has become filled, which occurs at the bottom of the x descent, the continued accumulation of venous return in the right atrium and caval system causes an increase in JVP, known as the v wave. The y descent Onset of ventricular diastole causes the tricuspid valve to open, allowing the accumulated blood to rapidly flow from the atrium to the ventricle. Right atrial pressure falls quickly causing the y descent.

Clinically, what distinguishes the JVP from arterial pulsations?

Differentiating between arterial and venous pulsations: o Venous pulsations move up and down (suction pulsations), while arterial pulsations move in and out (expansile pulsations). o During one cardiac cycle, an arterial pulsation occurs once, whereas venous pulsations occur twice during each cardiac cycle. o Arterial pulsations are palpable, whereas venous pulsations are not palpable (unless there is severe tricuspid regurgitation). o Pressing gently at the root of neck will cause venous pulsations to disappear , while it will not affect arterial pulse. o Pressing the right upper quadrant of the patients abdomen will increase venous return, causing an increased JVP. Arterial pulsations will not be affected by pressing the right upper abdomen.

Describe pathological JVP patterns and their pathophysiology Normal pattern, but with elevated pressures can be caused by fluid overloading. This occurs in congestive heart failure, where blood backs up through the right heart. Raised JVP without pulsations (just static no clearcut waveform) vena caval obstruction (mass lesion), causing pulsations from the right atrium not to be able to be transmitted to the jugular system. JVP rises due to the blockage of blood from moving as easily from the vena caval system into the right atrium. Large a waves pulmonary stenosis, pulmonary hypertension, right ventricular hypertrophy, tricuspid stenosis all cause the atrium to contract more forcefully than normal to overcome the high pressures in the right ventricle. This causes a waves to become heightened.

Cannon waves (EXTREMELY large a waves) atrium is contracting against a CLOSED tricuspid valve causing extreme increases in atrial pressure with atrial systole. This can occur in complete heart block (when the atrial electrical impulses are not transferred to the ventricular electrical system). The atrium may be beating according the sinus node control (e.g. at 80 beats per minute), while the ventricle is following stimulation from an ectopic focus (e.g. at 40 beats per minute). It can also occur in ventricular tachycardia, where a tachycardic focus may be driving the ventricle at 160 bpm, while the atrium is beating at 60 bpm. The normal sequence of contraction is dissociated so cannon waves will occur when the atrium happens to contract against a closed tricuspid valve.

Fused c-v wave this occurs soon as ventricular wave), blood begins to flow

in tricuspid regurgitation. As contraction begins (at the c back pathologically from the

ventricle into the atrium, causing venous pressure to rise abnormally after the c wave (instead of the normal x descent).

NOTE: We should observe the JVP while palpating the carotid on the other side. Any wave that comes before the carotid pulse will be the a wave (occurring before ventricular systole). Any wave that occurs just after feeling the carotid pulse is the v wave (occurring during ventricular systole due to filling of the atrium). If we see a wave that occurs simultaneously with the carotid pulse it is a fused c-v wave.

CONSTRICTIVE PERICARDITIS What is constrictive pericarditis? Constrictive pericarditis = Severe and prolonged inflammation of the pericardial sac, causing fibrosis of the pericardium. The fibrosed pericarditis constricts around the ventricles preventing proper ventricular relaxation and filling. Steep fall of y descent and steep rise (of a wave?) What JVP abnormalities are associated with constrictive pericarditis? Constrictive pericarditis is associated with a steeper than normal fall of the y descent and a steep rise of the a wave. Because fibrosis of the pericardium limits total filling of the ventricles, the right atrium overaccumulates blood. The over-accumulation of blood in the right atrium results in high right atrial pressures. As soon as the right ventricle relaxes, blood very rapidly moves from the right atrium (where it has over-accumulated) into the right ventricle. The right atrium rapidly empties and JVP rapidly decreases (causing a steep y descent). Expansion of the right ventricle is abruptly stopped by the constrictive pericarditis. This correlates to an abrupt stoppage in the falling JVP and it begins to rapidly rise again (steep a wave).

Under normal physiological conditions, what variations occur in JVP during inspiration and expiration? During inspiration, the diaphragm contracts and the thoracic cavity expands in size, causing negative intrathoracic pressure. The negative intrathoracic pressure not only causes air to flow in to the lungs, it also causes blood to flow in to the thorax. Thus, venous return to the right heart is increased during inspiration. Thus, JVP decreases slightly during inspiration (blood empties from the external jugular veins into the right heart). During expiration, the diaphragm relaxes and the thorax decreases in volume, causing positive intrathoracic pressure. The positive intrathoracic pressure causes air to be expelled, and also decreases inflow of blood into the thorax. As a result, venous return to the right heart is decreased during expiration. Hence, JVP increases slightly during inspiration (as less blood empties from the external jugular veins).

Kussmauls sign For patients with constrictive pericarditis, there is a paradoxical increase in JVP during inspiration, known as Kussmauls sign. This is caused by the presence of the constrictive fibrotic pericardial band causing reduced ventricular compliance (particularly reduced right ventricular compliance, as the pressures in the right heart are lower than the left). During inspiration the tight fibrotic pericardial band is pulled downwards by the diaphragm as it contracts, causing it to exert a tighter pressure on the ventricles. As a result, ventricular filling is reduced during inspiration and the blood backs up into the right heart and vena cava. This causes the paradoxical increase in JVP during inspiration in constrictive pericarditis.