Section I Hemodynamic Data

Cardiac catheterization provides anatomic information through cineangiograms and equally important physiologic information through the recording of hemodynamic data, including pressure measurements, cardiac output (CO) determinations, and blood oximetry.

Pressure Waves in the Heart

Blood within the heart or vessels exerts pressure. A pressure wave is created by cardiac muscular contraction and is transmitted from the vessel or chamber along a closed, fluid-filled column (catheter) to a pressure transducer, which converts the mechanical pressure to an electrical signal that is displayed on a video monitor. Cardiac pressure waveforms are cyclical, repeating the pressure change from the onset of one cardiac contraction (systole) to the onset of the next contraction. The complete description of the physiology of heart function is beyond the scope of this book, but an examination of the diagram of the cardiac cycle and corresponding pressures (Figs. 3-1 and 3-2) provides an understanding of basic hemodynamics in the cardiac catheterization laboratory.

Figure 3-1 A, Normal left ventricular (LV) and aortic (Ao) pressure with electrocardiogram. P, P wave; R, R wave; S₁, S₂, first and second heart sounds; LVEDP, LV end-diastolic pressure. Scale mark indicates 100 mm Hg. B, LV and pulmonary capillary wedge (PCW) pressures on 0 to 40 mm Hg scale. A, A wave; V, V wave corresponding to mitral valve opening and closing; x, X descent; y, Y descent.

Figure 3-2 Normal oxygen saturation, oxygen volume percentage, and pressure ranges in heart chambers and great vessels with pressure tracings in relation to electrocardiogram.

The collection of hemodynamic data is an integral part of every catheterization protocol. Even complex hemodynamic data recording can be accomplished accurately and rapidly if an efficient and consistently used method is established in the laboratory. One measurement sequence used in our laboratory (Tables 3-1, 3-2, and 3-3) is an example of one method. This sequence facilitates simultaneous pressure measurements across the heart, concentrating on the aortic (Ao) and mitral valves, which are the most commonly affected by disease. Of all hemodynamic questions, 90% can be answered by examining data collected in this way. As with most brief formulas this technique is not all-inclusive. Different hemodynamic measurements for specific clinical situations are necessary. Specific examples are included in the case studies.

Table 3-1 Right-Sided Heart Catheterization Protocol

∗ Only 1 to 2 drops of heparin should be aspirated and flushed out of 1- to 3-ml heparinized syringes.

Table 3-2 Left-Sided Heart Catheterization Protocol^∗

∗ Right-sided heart hemodynamic studies often precede left-sided heart studies. Simultaneous pressures of the left and right sides of the heart provide the most precise and accurate information.

† 100 mm/sec sweep speed if aortic valve gradient present.

Table 3-3 Combined Hemodynamic Measurements of the Left and Right Sides of the Heart

The routine collection of hemodynamic data from the right and left sides of the heart with appropriate sampling of blood for oxygen saturations and CO measurements can be accomplished in less than 30 minutes. CO by the thermodilution technique is routine. The Fick CO method using a measured or assumed oxygen consumption calculation is often used for valvular lesions. Arterial, vena caval, right atrial (RA), and pulmonary artery (PA) oxygen saturations are collected routinely throughout the right and left sides of the heart for intracardiac shunt identification.

Right- and Left-Sided Heart Catheterization

The protocol used during right-sided heart catheterization is summarized in Table 3-1. Right-sided heart catheterization is performed for specific indications. Right-sided heart catheterization is indicated for patients with a history of dyspnea, valvular heart disease, or intracardiac shunts. Patients with a history of pulmonary edema occurring on a previous hospital admission often have only dyspnea with no objective evidence of left ventricular (LV) dysfunction (e.g., chest film, echocardiography). Dyspnea caused by lung disease cannot be differentiated from that caused by pulmonary hypertension or LV dysfunction.

Computations for Hemodynamic Measurements

When the hemodynamic data have been obtained, computations are made to quantify cardiac function. In this section only the most common computations and standard formulas are provided. These computations provide measurement of cardiac work, flow resistance, valve areas, and shunts. Specific derivations and applications of these formulas can be found elsewhere.

Oxygen consumption is best measured from a metabolic “hood” (this device is no longer widely available); it is more commonly estimated as 3 ml O₂/kg or 125 ml/min/m². Arteriovenous oxygen (AVO₂) difference is calculated from arterial – mixed venous (PA) O₂ content, where O₂ content = saturation × 1.36 × hemoglobin.

For example, if the arterial saturation is 95%, then the O₂ content = 0.95 × 1.36 × 13.0 g = 16.7 ml, PA saturation is 65%, and O₂ consumption is 210 ml/min (70 kg × 3ml/kg) or measured value, and CO would be determined as follows:

where CO = cardiac output; BSA = body surface area.

where HR = heart rate.

Resistance calculations follow the form of Ohm’s law, where

R = resistance; Δp = mean pressure differential across the vascular bed; = blood flow. Resistance units (mm Hg/L/min) are also called Hybrid resistance units or Wood units. To convert Wood units to metric resistance (dynes × s × cm^–5), multiply by 80.

Computations of Valve Areas from Pressure Gradients and Cardiac Output

A pressure gradient is the pressure difference across an area of valvular or vascular obstruction, such as a stenosis or an occlusion or narrowed valve. Figure 3-3 is a diagram of a coronary stenosis with higher pressure proximal to the stenosis and lower pressure beyond the stenosis. The same principle applies for heart valves with higher pressure proximal to the stenotic valve and lower pressure distal to it. There are several methods used to measure transvalvular gradients.

Figure 3-3 Diagram of pressure gradient across a stenosis or narrowing. The pressure gradient is the difference between proximal and distal pressure. The pressure distal to the narrowing shows a systolic and a diastolic pressure gradient.

Techniques to measure LV-Ao pressure gradients include the following in order of least to most accurate:

All pressure gradients are affected by a number of physiologic, anatomic, and artifactual variables. Physiologic variables include (1) rate of blood flow (e.g., CO, coronary blood flow), (2) resistance to flow, and (3) proximal chamber pressure and compliance. Anatomic variables include (1) shape and length of valve orifice, (2) tortuosities of the vessels (for arterial stenosis); folding of coronary artery by guidewire (i.e., pseudostenosis), and(3) multiple or serial lesions (for cardiac valves and arterial stenosis).

Artifactual variables include

Examples of Aortic and Mitral Valve Area Calculations

Most modern physiologic recording systems use computer-generated waveforms and gradient producing valve areas automatically. When using femoral artery and LV pressure, time shifting the femoral artery back to match upstroke of the left ventricle will under-estimate the true Ao valve gradient (Fig 3-4). When calculating from the formula, CO should be converted to milliliters per minute, not liters per minute. When computing flow, the ejection period and filling period are converted to fractions of the period in seconds.

Figure 3-4 Aortic valve area computed by shifted and unshifted femoral artery pressure compared with central aortic pressure. The unshifted gradient area is bigger than the central area overestimating the severity of valve area. The shifted area is smaller than central area under-estimating valve area.

(From Folland ED, Parisi AF, Carbone C: J Am Coll Cardiol 4:1207-1212, 1984.)

Data obtained at catheterization for Ao stenosis (Fig. 3-5):

Figure 3-5 Left ventricular and central aortic pressure measured by transseptal technique. Note immediate upstroke of aortic pressure measured just above aortic valve with no delay as seen with femoral artery pressure. Data for calculating aortic valve area are displayed beneath beat 1.

Use of Valve Resistance for Aortic Stenosis

Valve resistance, a measure of valve obstruction, although not commonly computed has been shown to have clinical value. Valve resistance has not been used because the units of dynes − second − cm⁻⁵ were not well related to clinical outcomes.

Although they have obvious strengths, valve area measurements have practical and theoretical limitations such as three-dimensional (3D) geometric influences on flow, using blood as nonviscous fluid, neglecting turbulence and blood viscosity, and assuming that blood flow is gravity driven rather than pulsatile as in the arterial system.

Valve areas of less than 0.7 cm² are almost always associated with an important clinical syndrome, and areas of greater than 1.1 cm² are usually not associated with significant symptoms, but areas between these two measurements are in a gray zone. One of the most common clinical situations is found in a patient with a valve area of 0.9 to 1.0 cm², a low transvalvular pressure gradient, low CO, and poor LV function. There is uncertainty regarding the outcome after valve replacement, as well as a high mortality rate if ventricular function does not improve after surgery.

Valve resistance is calculated using the same variables for valve area measurement. In contrast to valve area, the mean pressure gradient is considered to be a linear variable rather than taken as a square root term. The contribution of pressure gradient to the magnitude of valve resistance is greater. Resistance has also been shown to be more constant than valve area under conditions of changing CO. Figure 3-6 shows resistance and area calculated in a group of patients before and after balloon Ao valve dilation. Resistance rises sharply above a valve area of 0.7 cm². The shoulder of this curve is 0.7 to 1.1 cm², which is the common area of indeterminate significance of Gorlin Ao valve area. Some patients in this gray zone tend to have higher valve resistance than others. It has been shown in this setting that patients with resistance greater than 250 dynes − sec − cm⁻⁵ are more likely to have significant obstruction than patients with resistance less than 200 dynes − sec − cm⁻⁵. There is also a gray zone in using this index, and some patients may have resistance less than 250 dynes − sec − cm⁻⁵ despite a planar valve area of 0.7 to 0.8 cm².

Figure 3-6 Comparison of valve area by Gorlin formula versus valve resistance before (pre) and after (post) aortic valvuloplasty. Valve resistance less than 200 dynes − sec − cm⁻⁵ is associated with minimal obstruction; greater than 250 dynes − sec − cm⁻⁵ with significant obstruction. This measure complements and refines valve area decision making.

(From Feldman T, Ford L, Chiu YC, et al: J Heart Valve Dis 1:55-64, 1992.)

Resistance is a complementary index, not a replacement for valve area. Valve resistance is not expected to remain consistent. As with peripheral resistance, valve resistance is interpreted in the context of the clinical conditions under which it is measured. A peripheral resistance of 1000 dynes − sec − cm⁻⁵ has a different significance in a patient with presumed sepsis than it does in a patient with LV failure. Similarly, we can expect valve resistance to vary as CO changes.

Data from Catheterization Laboratory for Calculation of Mitral Valve Area

Figure 3-7 is a hemodynamic tracing to calculate mitral valve area.

1. Cardiac output = 3.5 L/min = 3500 ml/min

2. Heart rate = 80 beats/min

3. Scale factor = 1 cm = 3.9 mm Hg (40 mm Hg full scale)

4. Tracing of LV-PCW pressure at 100 mm/sec paper speed = (10 cm/sec paper speed) (align PCW v wave with down stroke of LV pressure)

Figure 3-7 Hemodynamic tracing used to calculate mitral valve area. The shaded area is the diastolic mitral valve gradient surrounded by the diastolic filling period (DFP). CF, Correction factor or scale factor; LA, left atrial pressure; LV, left ventricular pressure (scale 0 to 40 mm Hg); MVG, mean value gradient. See text for details.

Step 1: Planimeter 5 LV-PCW areas (10 if in atrial fibrillation).

Area = 9.46 cm²

Step 2: Measure diastolic filling period (DFP).

Step 3: Convert planimetered area to mean diastolic pressure gradient.

Step 4: Compute mitral valve flow.

For the mitral gradient, similar to Ao valve areas, DFP is in centimeters at this point owing to scale factor.

Step 5: Compute mitral valve area (MVA).

Notes on Mitral Valve Gradient

Obtaining an accurate PCW pressure is crucial. PCW pressure overestimates LA pressure in patients with prosthetic mitral valves. Overestimation is caused in part by the phase delay and worse pressure transmission making correction and alignment of pressure tracings difficult.

Use of direct LA pressure from transseptal measurement is the most accurate method. Transseptal catheterization should be performed to confirm pressure gradients, especially for suspected prosthetic mitral stenosis. However, if the PCW pressure-LV pressure tracings show no significant gradients, transseptal catheterization is unnecessary. A worksheet for valve area calculation is shown in Figure 3-8.

Figure 3-8 Worksheet for determination of valve areas.

(Modified from Grossman W: Cardiac catheterization and angiography, ed 3, Philadelphia, 1986, Lea & Febiger.)

Simplified Mitral Valve Gradient Calculation by Cui et al

Cui simplified the estimation of the mitral valve gradient (MVG) and thus simplified the calculation of mitral valve area from the hemodynamic tracings. Because the mean MVG is the pressure difference between the mean left atrial pressure (MLAP) and mean left ventricular pressure during diastole (MLVP) (i.e., MLVG = MLAP – MLVP), the computation of the mean MVG is simply knowing the MLVP. The MLAP is easily obtained from the electronically meaned LA signal on the hemodynamic recorder. The area under the LV pressure during diastole is roughly a triangle with the three corners formed from the intersections of the diastolic filling period (DFP) starting and ending points (mitral valve closure and opening) marking the vertical lines intersecting with the LV pressure line (rising diagonally across diastole, see Figure 3-9). This triangular area can be estimated from the rectangular area LVEDP × DFP divided by 2. Thus the MLVP is equal to the LVEDP/2. From this key calculation, the mean valve gradient is therefore simplified as

Figure 3-9 Cui method to calculate mean valve gradient from hemodynamic tracings. Left ventricular (LV) and left atrial (LA) pressures are superimposed. The LV-LA gradient is triangular in shape, representing half of the rectangle delineated by A-B (diastolic filling period, DFP), C (left ventricular end-diastolic pressure [LVEDP]). D, mitral value closing; E, mitral value opening.

(From Cui W, Dai W, Zhang G: Cathet Cardiovasc Intervent 70:754-757, 2007.)

There is strong correspondence between the mitral valve areas calculated by the Gorlin and Hakki formulas, both before and after mitral balloon valvuloplasty with an error of estimates at 1.6 mm Hg. The Cui MVG slightly overestimated MVG before but not after mitral valvuloplasty. Hakki significantly under-estimated MVGs after mitral balloon valvuloplasty. Unlike Hakki, the Cui MVG was not affected by mitral regurgitation, Ao insufficiency, atrial fibrillation, or heart rate.

Although simple, the Cui MVG still has potential problems. Heart rate changes will change the shape of the triangular area under the LV pressure curve, and thus tachycardia may cause a potential overestimation of valve severity. There is one very interesting advantage for this simplified method. The MVG can be estimated easily from a pressure pullback from left ventricle to the left atrium without necessarily making simultaneous two-chamber tracings. Mitral valve area could be calculated without entering the left ventricle.

Pulmonic Valve Stenosis

A pulmonary valvular stenosis gradient (Fig. 3-10) can be obtained by catheter “pullback,” continuously measuring pressure during catheter withdrawal across the stenotic valve. Two catheters, multiple-lumen balloon-tipped catheters, or double-lumen Cournand catheters are more precise, however, and can record simultaneous PA and RV pressures in the manner used for Ao valve stenosis. There is no validated formula for pulmonary valve area. Prognostic data are based on RV pressure and gradient alone.

Figure 3-10 Hemodynamic tracings from a patient with pulmonary stenosis. The shaded area is pulmonary stenosis gradient (scale 0 to 50 mm Hg; time lines are 1 second). PA, Pulmonary artery pressure; RA, right atrial pressure, RV, right ventricular pressure.

Measurement of Cardiac Output

In the cardiac catheterization laboratory, CO is determined by one of two techniques: (1) measurement of oxygen consumption (Fick technique) or (2) indicator dilution technique (thermodilution using a PA catheter).

Fick Principle for Measurement of Cardiac Output

The Fick principle states that uptake or release of a substance by any organ is the product of the arteriovenous concentration difference of the substance and the blood flow to that organ. Pulmonary blood flow (which is equal to systemic blood flow in the absence of an intracardiac shunt) is determined by measuring the arteriovenous difference of oxygen across the lungs and the uptake of oxygen from room air by the lungs. CO is calculated as oxygen consumption divided by the arteriovenous oxygen concentration difference. The arteriovenous oxygen consumption difference is calculated (in milliliters of oxygen) as the difference in LV oxygen content (1.36 × hemoglobin × LV O₂ saturation x 10) minus the PA (mixed venous) oxygen content (1.36 × hemoglobin × PA O₂

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

1. Introduction to the Catheterization Laboratory
2. The Electrophysiology Laboratory and Electrophysiologic Procedures
3. Peripheral Artery Disease and Peripheral Artery Angiography
4. Angiographic Data

Stay updated, free articles. Join our Telegram channel

Join