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Cardiac Tamponade 

Cardiac tamponade is a medical emergency as a cause of obstructive shock. It is defined as a decompensated cardiac compression caused by pericardial fluid accumulation and rising intrapericardial pressure. The good news here is that we can make the diagnosis of tamponade based on focused cardiac ultrasound (FoCUS).

   Physiology recap. 

During spontaneous ventilation the negative intrathoracic pressure generated increases RV preload. The blood in the RV restricts full expansion of the LV limiting LV preload. The pulmonary veins also receive less blood as a consequence of the negative intrathoracic pressure. This also causes less LV preload. As a consequence stroke volume and CO drops to lower levels on inspiration when breathing spontaneously. This is the paradoxical pulse. The opposite occurs in a patient undergoing mechanical ventilation as the inspiration causes a drop of RV preload. Under normal circumstances the respirophasic differences of BP due to inspiration is less than 10mmHg as seen on figure 1. 



Figure 1. Diagram showing normal respirophasic changes in volumes of the ventricles. On inspiration the RV has more preload due to the negative intrathoracic pressure. There is less return of blood from the pulmonary veins plus the interventricular septum gets displaced to the left. The cardiac output thus is lower on inspiration. During expiration the preload of the RV decreases, more blood gets returned on the LV via the pulmonary veins and the preload of the LV which result in LV cardiac output. Blue and red representing RV and LV chambers respectively. Image modified from Patrick J Lynch and Carly Jaffe MD. 

Cardiac Tamponade Features

Pericardial fluid accumulates around the heart but it is not the volume per se but the change in pressure that is important that impairs filling of the heart. The right sided heart structures normally operate at a lower pressure than those on the left to keep fluid moving forward. With pericardial fluid, the pressure differential between the right sided chambers and the pericardial fluid restricts movement of flow into the RV. In essence once the pericardial sack generates more pressure than the pressure needed to deliver preload to the RV we have tamponade. The RV then receives less preload which ultimately results in hemodynamic compromise. Keep in mind that a pericardium that accumulates blood slowly has more time to adapt to the changes in pressure than one that does so fast. The importance here is that the volume in the pericardium is not as important as its physiologic effect on the heart and cardiac ultrasound can help us with this. 


Patients with tamponade have thus exaggerated respirophasic features. As mentioned, the increased intrapericardial pressure restricts flow to the right sided structures. On inspiration thus the RV tries to accommodate this restriction of flow by invaginating the interventricular septum into the LV. This ultimately results in a lower stroke volume and cadiac output and clinically seen as a drop in BP greater than 10mm Hg. This is called pulsus paradoxus.