Determination of CVP can be helpful in the overall hemodynamic assessment of the patient. This pressure can be affected by a variety of factors, including those of cardiac, noncardiac, and aifactual origin. Venous tone, right ventricular compliance, intrathoracic pressure, and blood volume all influence CVP. Vasoconstrictor drugs, positive-pressure ventilation (with and without PEEP), mediastinal compression, and hypervolemia all increase CVP. Acute pulmonary embolism, when clinically significant, elevates CVP by causing right ventricular overload and increased right atrial pressure. Sepsis, on the other hand, decreases CVP through both the release of vasodilatory mediators and the loss of intravascular plasma volume due to increased capillary permeability. Trends in CVP measurement are more reliable than isolated readings. CVP, along with other hemodynamic parameters, can also be useful in differentiating septic shock from other etiologies of shock; shock is inadequate tissue perfusion. Septic shock has two phases: (1) a hypodynamic phase that is characterized by hypovolemia and myocardial depression and (2) a hyperdynamic phase that follows fluid resuscitation and is characterized by a normal to increased cardiac output