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PULMONARY ARTERY CATHETER-DERIVED HEMODYNAMIC VARIABLES

The cardiovascular system is often modeled as an electrical circuit, with the relationship between cardiac output, blood pressure, and resistance to flow related in a manner similar to Ohm's law. The electrical version of this relationship is familiar as Equation 7.

V = I · R (7)

where V = voltage
I = current
R = resistance

The analogous formulas for determining SVR and PVR rearrange Ohm's law and replace voltage with blood pressure and current with blood flow.









where SVR = systemic vascular resistance
PVR = pulmonary vascular resistance
MAP = mean arterial pressure (mm Hg)
CVP = mean central venous pressure (mm Hg)
MPAP = mean pulmonary artery pressure (mm Hg)
PAWP = mean pulmonary artery wedge pressure (mm Hg)
CO = cardiac output (L/min)

Multiplying by 80 corrects SVR and PVR values from Wood units (mm Hg/L/min) to standard metric units (dynes · sec · cm-5 ).

Normal values for SVR and PVR are given in Table 32-14 . Note that these calculations of SVR and PVR are based on a hydraulic fluid model that assumes continuous, laminar flow through a series of rigid pipes. [709] [710] These calculations also use atrial pressure as the downstream pressure for systemic or pulmonary flow, with CVP used for right atrial pressure in the SVR calculation and PAWP used for left atrial pressure in the PVR calculation. Alternative methods to calculate resistance ignore the effect of these downstream pressures. For the systemic circulation, total resistance may be calculated from mean arterial pressure and cardiac output alone, and for the pulmonary circulation,


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total pulmonary resistance describes the ratio of mean pulmonary artery pressure and cardiac output.

All these resistance formulas oversimplify the behavior of the cardiovascular system. A more physiologic model of the systemic circulation considers the vasculature to be a series of collapsible vessels with intrinsic tone. This model, also called the vascular waterfall, describes a critical closing pressure in the downstream end of the circuit that exceeds right atrial pressure and serves to limit flow—an effective downstream pressure that is higher than the right atrial pressure used in the SVR formula. Detailed consideration of these issues is beyond the scope of this discussion and is available in other sources.[711] [712] The important issue for clinicians is that therapy focused on the fine adjustment of SVR may be very misleading and should be avoided.

Additional problems arise when considering the pulmonary vasculature and using the formulas just presented as a measure of resistance to flow through the lung. The pulmonary vasculature is more compliant than the systemic vasculature, and marked increases in pulmonary blood flow may not produce any significant increase in PAP. In addition, flow usually ceases at end-diastole in the low-resistance pulmonary circuit.[443] [713] Thus, changes in PVR may result from intrinsic alterations in pulmonary vascular tone (constriction or dilation), vascular recruitment, or rheologic dynamics.[710] [713] [714] For the pulmonary circuit, a better approach to evaluating changes in PVR may be to examine the end-diastolic gradient between pulmonary artery diastolic and wedge pressure (see Fig. 32-51 ).[714] Alternatively, more complex calculations of impedance rather than resistance will better describe these vascular properties of the pulmonary circuit.[715]

Another set of common calculations derived from standard hemodynamic variables adjusts these measurements for the patient's body surface area (BSA) in an attempt to normalize these measurements for patients of different size. BSA is generally determined from standard nomograms based on height and weight. The most commonly indexed variables are the cardiac index (cardiac index = cardiac output/BSA) and stroke volume index (stroke volume index = stroke volume/BSA). On occasion, SVR and PVR are indexed as well. Note, however, that indexed resistances are higher than nonindexed values because the cardiac index term is in the denominator of these equations. The appropriate formulas are SVR index = SVR × BSA and PVR index = PVR × BSA.

In theory, normalizing hemodynamic values through "indexing" should help clinicians determine appropriate normal physiologic ranges to assist in guiding therapy. Unfortunately, there is little evidence that these additional calculations provide valid normalizing adjustments. BSA is a biometric measurement with an obscure relationship to blood flow, and it does not adjust for variations between individuals based on age, sex, body habitus, or metabolic rate.[716] Although it is important to be aware of a patient's size and medical history when interpreting and treating changes in any of the measured or calculated hemodynamic variables, it is not appropriate to target therapy solely at achieving normal indexed values.

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