This patient is normotensive but tachycardic, which together with her physical findings suggests a compensated shock state. This is confirmed by her low CO and high calculated systemic vascular resistance (SVR) (Table 12.5). The differential diagnoses for low SV include hypovolemia, impaired LV systolic and diastolic function and/or RV contractility, and obstruction of the heart or great vessels by pericardial fluid or embolism. PAC data can assist in narrowing the diagnosis, although changes in measured pressures do not always translate to changes in intracardiac volume.

The patient's CVP is markedly elevated, which can be a result of potential intracardiac or extracardiac pathology. In the absence of significant tricuspid valve stenosis or regurgitation, intracardiac causes include hypervolemia (unlikely, given this patient's clinical presentation) and RV dysfunction from ischemia or outflow obstruction. This dysfunction increases RV end-diastolic pressure (EDP) and leads to a corresponding rise in venous filling pressures. Extracardiac causes of elevated CVP include extrinsic cardiac compression by pericardial or intrapleural conditions, including cardiac tamponade, large pleural effusion(s) and tension pneumothorax. It is important to note that in cases of extrinsic compression, the CVP is measuring the intracardiac pressure and the pressure applied to the RA (eg, a hypovolemic patient with a transmural right atrial pressure of 3 mm Hg can have a measured CVP of 23 mm Hg once 20 mm Hg of pressure is applied to the RA, creating a false impression of the patient's true filling pressures).

The patient's PA pressure is elevated. A PAOP less than 15 mm Hg and elevated diastolic pulmonary gradient points to a precapillary cause, and is confirmed by the elevated calculated pulmonary vascular resistance (PVR) (Table 12.5). In this patient, the most likely causes are long-standing pulmonary vascular remodeling from chronic mitral disease and pulmonary atelectasis from dyspnea and altered respiratory mechanics.

The PAOP is a surrogate measure for left atrial pressure (LAP) and can inform about LV filling as well as LV and mitral valve function. This patient's PAOP is normal and makes prosthetic mitral valve dysfunction from obstruction or regurgitation unlikely. As with CVP, caveats apply in the interpretation of PAOP and LAP concerning LV volume status. Furthermore, any alteration in the thick-walled LV compliance will affect the degree to which LAP represents LV preload, which is ultimately represented by LV end-diastolic volume (EDV). For example, acute ischemia will decrease LV compliance, which would result in a higher EDV for the same EDP.

Taken together, the patient's clinical and hemodynamic findings suggest a low CO state due to cardiac tamponade and/or RV dysfunction from ischemia or increased RV afterload due to embolism. Concurrent LV dysfunction cannot be excluded based on PAC data alone. Echocardiography can assist with further refinement of the differential diagnoses by defining RV and LV function, relative atrial pressures, and the presence of pericardial fluid.

Note the absence of "equalization of pressures" in this patient, that is CVP, PA diastolic, and PAOP are not within 5 mm Hg of each other. This does not exclude a diagnosis of cardiac tamponade, as the pericardium is often left open in cardiac surgery patients. Equalization of pressures presumes that intrapericardial pressure is equally distributed through the pericardial sac. This is usually a late finding when compensatory mechanisms are almost exhausted in patients with an intact pericardium, and might not be seen at all in patients where the pericardium is not intact.

References

• Goldstein JA. Introduction to Pericardial Disease. In: Kern MJ, Lim MJ, Goldstein JA, eds. Hemodynamic Rounds: Interpretation of Cardiac Physiology From Pressure Waveform Analysis. 4th ed. Wiley-Blackwell; 2018:269.
• Magder S. Invasive hemodynamic monitoring. Crit Care Clin. 2015;31:67-87.
• Opitz CF, Hoeper MM, Gibbs SR, et al. Pre-capillary, combined, and post-capillary pulmonary hypertension: a pathophysiological continuum. J Am Coll Cardiol. 2016;68:368-378.