The Dip Sign is a specific pattern observed during the assessment of heart function, providing a powerful clue for identifying a particular cardiac condition. This sign relates directly to the mechanical process of how the heart chambers fill with blood during diastole, the resting phase of the cardiac cycle. It indicates a serious problem where the heart’s ability to relax and take in blood is severely compromised.
Defining the Dip Sign
The Dip Sign, also termed the “square root sign” (√) or “dip and plateau” pattern, is a characteristic pressure waveform measured within the heart’s ventricles. It is a graphic representation of abnormal ventricular filling mechanics during diastole, defined by two distinct phases. The first phase is the “dip,” which occurs as the ventricle rapidly relaxes and begins to fill with blood from the atrium, causing a quick pressure drop. This initial filling is unimpeded. The second phase is the “plateau,” which immediately follows the dip and involves an abrupt halt in the pressure drop, resulting in a sustained high pressure throughout the rest of diastole. This transition is caused by the heart chamber quickly reaching the limit of its expansion, restricted by an external force. The overall shape—a rapid drop followed by a sustained, high-pressure line—resembles the square root symbol, giving the sign its alternative name.
The Disease Behind the Finding
The Dip Sign is the classic hemodynamic signature of Constrictive Pericarditis, a condition where the sac surrounding the heart, the pericardium, becomes stiff and unyielding. The pericardium is a two-layered membrane that normally allows for full expansion during the filling phase. In this disease, chronic inflammation causes the pericardium to become thickened, fibrotic, and often calcified, forming a rigid shell around the heart muscle. This non-compliant shell physically prevents the ventricles from expanding fully. The restriction imposed by the rigid pericardium creates the Dip Sign’s unique pressure pattern: the initial rapid filling (the dip) stops abruptly when the ventricle hits the limit set by the scarred sac, causing the pressure to spike and remain high (the plateau). Common causes include previous heart surgery, radiation therapy to the chest, and infections such as tuberculosis, which remains a leading cause in many regions. Other triggers can involve viral infections, autoimmune disorders, and idiopathic causes.
Diagnostic Methods Used
Identifying the Dip Sign and confirming constrictive physiology relies on a combination of non-invasive and invasive diagnostic tools. The primary non-invasive tool is Doppler Echocardiography, which uses sound waves to visualize the heart’s structure and measure blood flow velocities. Echocardiography cannot directly measure the pressure curve, but it detects indirect effects, such as pronounced respiratory variation in blood flow. In constrictive pericarditis, the flow across the mitral and tricuspid valves changes drastically, often showing a greater than 25% variance in peak velocity between inspiration and expiration. Echocardiography may also reveal “septal bounce,” where the wall between the ventricles shifts dramatically with the respiratory cycle due to the external restriction. Cardiac Catheterization, an invasive procedure, remains the definitive method for directly observing the actual Dip Sign. This procedure involves inserting a catheter to measure pressure within the heart chambers, allowing the physician to plot the ventricular pressure curve and physically see the characteristic “square root sign” pattern. Advanced imaging techniques, such as Cardiac Magnetic Resonance Imaging (MRI) and Computed Tomography (CT), are also used to visualize the pericardium, often revealing thickening or calcification that supports the diagnosis.
When the Dip Sign is Suspected
Physicians suspect constrictive pericarditis when a patient presents with symptoms of impaired venous return and right-sided heart failure. These symptoms occur because the restricted heart cannot adequately take in blood returning from the body, causing fluid backup in the systemic circulation. Common complaints include chronic, persistent swelling (edema), particularly in the legs and ankles. Patients often experience a swollen abdomen (ascites) and significant shortness of breath, especially with exertion. General weakness and profound fatigue are also frequently reported, stemming from the heart’s reduced pumping efficiency. The combination of these symptoms prompts the investigation that leads to the detection of the underlying constrictive physiology.