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Cardiac catheterization techniques: Normal hemodynamics

Cardiac catheterization techniques: Normal hemodynamics
Literature review current through: Jan 2024.
This topic last updated: Jun 13, 2022.

INTRODUCTION — Hemodynamic data have always been, and remain, an integral part of all cardiovascular observations. Significant advances in both surgical and nonsurgical techniques for heart disease have been established in the last decade, in large part due to innovations both within and outside the cardiac catheterization laboratory. Many difficult forms of heart disease can now be readily confirmed with the improvement in two-dimensional and Doppler echocardiographic techniques. However, given the nature of clinical testing, there will always be suboptimal noninvasive examinations or patients in whom such testing cannot be performed. Thus, the catheterization laboratory remains critical to accurate measurements and the establishment of diagnoses. The presence of coexisting hemodynamic abnormalities in patients with coronary artery disease, myocardial infarction, cardiomyopathy, or peripheral arterial disease cannot be established without direct information.

VASCULAR ACCESS AND SPECIAL CATHETERIZATION TECHNIQUES FOR OBTAINING HEMODYNAMIC DATA — Routine catheter access is obtained from either the radial or femoral artery and a convenient vein in most situations. The radial artery approach has gained wide acceptance and demonstrated reduced bleeding complications relative to femoral artery access. Many laboratories now use radial access as the default approach for routine cardiac catheterization [1-4]. Use of in-lab portable echocardiography facilitates access for both radial and femoral arteries with reduced complications [5,6]. An antecubital vein on the same arm is often used for right heart catheterization when using the radial approach for arteriography and left ventricular (LV) hemodynamics.

In addition to standard arterial and venous vascular access, there are a variety of special access techniques that may be required for optimal hemodynamic assessment (table 1) [7-9].

Transseptal access to the left atrium or ventricle is most often employed when prosthetic valves are located either in the aortic or mitral positions. Direct left atrial pressure measurement via the transseptal approach is also highly desirable, if not critical, to accurate decision making in conditions such as mitral stenosis (image 1), in which the pulmonary capillary wedge pressure is unreliable as a surrogate for the left atrial pressure. Under fluoroscopic guidance the transseptal access is obtained using a Brockenbrough catheter that is passed through the atrial septum over a long needle that is used to puncture the septum at the fossa ovalis. This technique is commonly used for accurate assessment of mitral valve disease and as access for mitral balloon valvuloplasty and a clip technique for percutaneous repair of secondary mitral regurgitation.

Direct LV puncture through the LV apex via the fifth intercostal space using echo-guided needle positioning is applied for transapical aortic valve replacement. This method carries significant risk of bleeding and potential coronary artery damage. The transapical approach is also needed in patients with both aortic and mitral prosthetic valves blocking entrance to the LV. This technique is rarely used for diagnostic purposes.  

Access to the pericardium using long needles or specialized curved tip needles permits introduction of catheters into the pericardial space when pericardial effusion requires evacuation. Pericardial catheters can measure pericardial pressure for the assessment of clinical tamponade or congestive heart failure symptoms or hypotension of unexplained etiology in the setting of echocardiographic evidence of pericardial fluid. Pericardial access has been used for treatment of arrhythmias and left atrial appendage occlusion.

ROUTINE HEMODYNAMIC MEASUREMENTS — Routine hemodynamic measurements are obtained from the aorta (Ao), left ventricle (LV), right ventricle (RV), right atrium (RA), pulmonary artery (PA), and the pulmonary artery wedge position (for pulmonary capillary wedge pressure or PCWP); the last is usually equivalent to the left atrial (LA) pressure (figure 1) [10].

Historically, systemic or aortic pressure was often accepted from the side arm pressure of a femoral arterial sheath. However, femoral artery pressure does not precisely represent central aortic pressure; systole may be higher because of the summation effect of reflected waves within the arterial system and the time delay in upstroke as the pressure reaches the femoral artery. In general, an overshoot of <20 mmHg relative to central aortic pressure is common and satisfactory for most clinical situations (waveform 1). When this overshoot is excessive (as may occur in young patients or aortic insufficiency), or when there is evidence of peripheral vascular disease (with marked reduction of the overshoot), measurement of central aortic pressure above the aortic valve (and simultaneous LV pressure) should be obtained with either a second arterial catheter or a dual lumen catheter [9]. Other options for two simultaneous pressure measurements include a 6F guide catheter with a 4F pigtail in the LV or a 0.014 pressure sensor wire.

Pressures in two or more chambers are simultaneously measured to establish the presence of pressure gradients across various structures (eg, valves, LV outflow tract). As examples, simultaneous Ao and LV pressures are obtained to establish a gradient across the aortic valve, while simultaneous LV and LA (or PCWP) pressures will establish a gradient across the mitral valve (image 1). In some situations, high fidelity pressure recordings are necessary for accurate diagnosis. As an example, in the assessment of aortic stenosis, high fidelity manometer-tipped pressure catheters (or pressure sensor guidewire) are available to record small differences between aortic and left ventricular pressure (waveform 4B). A 0.014 pressure wire through a diagnostic or guide catheter also produces high-fidelity recordings. This technique can identify aortic gradients with improved precision when compared with fluid-filled transducer systems. Double lumen catheters are preferred for best clinical measurements of aortic stenosis or left ventricular outflow tract gradients.

NORMAL WAVEFORMS — Analysis of waveforms from the different cardiac chambers, large arteries, and veins is essential for the understanding of normal hemodynamics and to detect and quantify valvular, myocardial, and pericardial abnormalities. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults".)

Right atrium — The right atrial pressure waveform consists of two major positive deflections, the "a" and "v" waves (waveform 4B).

The "a" wave represents atrial systole resulting from right atrial contraction. Electrical activity triggers mechanical activity, with the “a” wave immediately following the P wave on the surface electrocardiogram (ECG).

Following the “a” wave and right atrial contraction, atrial diastole produces right atrial pressure reduction, defining the "x" descent. Coincident with ventricular contraction as the atrioventricular valves are closed and pulled downward, a small positive deflection, known as the "c" wave, may be seen reflecting closure of the tricuspid valve. Right atrial pressure declines over the remaining part of systole and increases as atrial filling increases from the beginning of diastole.  

After full atrial relaxation and the nadir of the "x" descent, right atrial pressure rises due to increased volume from peripheral venous return. With right ventricular systole and the rapid increase in right ventricular pressure, the tricuspid valve closes. The increasing right atrial pressure during right ventricular systole culminates in the "v" wave, reaching maximal amplitude just prior to the opening of the tricuspid valve. When the pressure in the right ventricle falls below that of the right atrium the tricuspid valve opens.

After tricuspid valve opening, at the beginning of right ventricular diastole, the pressure in the right atrium rapidly falls, defining the "y" descent. After the "y" descent, the pressure in the right atrium equals the right ventricular end diastolic pressure since the tricuspid valve is opened; it slowly increases as the right ventricle fills. Similar physiology is present for the left atrium and mitral valve hemodynamics.

The normal mean right atrial pressure is between 1 and 8 mmHg.

Jugular venous pulsations — The jugular venous pulse closely reflects changes in right atrial pressure, and also parallels changes observed in the vena cavae [11,12]. The variations in pressure within the right atrium are reflected principally by a change in volume for the venous system.

It is thought that the pulse wave transmission from the right atrium to the jugular veins has the least disparity for pressure waves that are positive and conducted more rapidly, as compared to negative more slowly conducted pressure waves [13]. The venous pulse "a" and "c" waves have an average delay from the right atrium of approximately 60 msec, while the "v" wave delay is 80 msec; by comparison, the "y" trough delay is 90 msec, and the "x" trough 110 msec [13]. It also requires 60 msec for the right atrial "a" wave to reach the right ventricle and cause a positive defection in this chamber. These delays should be considered when examining the jugular venous pulse, as well as inferior vena caval pressure waves as a reflection of right atrial pressure [14].

Carotid arterial pressure waves may induce artifact in jugular vein pulsations. This artifact can be recognized by an irregular pulsation that often obscures the "x" descent. The irregular wave shows a carotid-like contour with the dichrotic notch recognized in the middle of the "x" descent [14].

Right ventricle — The right ventricular waveform consists of systole, a result of right ventricular contraction, and diastole occurring with right ventricular relaxation (waveform 2). During right ventricular systole, the pressure rapidly rises; when it is higher than that of the right atrium, the tricuspid valve closes. When the pressure exceeds that of the pulmonary artery, the pulmonic valve opens. The systolic waveform is rapid in upstroke and similar in pattern to that of the left ventricle; it occurs immediately after the QRS complex on the surface ECG. The peak or maximal amplitude of this waveform is the right ventricular systole pressure.

At the end of systole and the beginning of diastole, right ventricular relaxation produces a rapid fall in pressure back to baseline. When the pressure in the right ventricle falls below that of the pulmonary artery, the pulmonic valve closes. As the right ventricular pressure falls further, lower than that of the right atrium, the tricuspid valve opens.

Diastole consists of three periods generating three waveforms:

The first period, occurring at the onset of tricuspid valve opening, produces an early rapid filling wave during which approximately 60 percent of ventricular filling occurs.

Following this event is a slow filling period, accounting for approximately 15 percent of ventricular filling.

Right atrial systole, which accounts for approximately 25 percent of right ventricular diastolic filling, produces an "a" wave that is simultaneous with and identical in morphology and amplitude to the "a" wave on the right atrial pressure tracing, since the tricuspid valve is opened and creates essentially one chamber. The pressure at the end of the "a" wave is termed the right ventricular end-diastolic pressure (RVEDP).

The right ventricular pressure tracing is similar to that generated by the left ventricle except that the pressures are lower.

The normal right ventricular diastolic pressure is 1 to 8 mmHg and the peak systolic pressure is 15 to 30 mmHg.

Pulmonary artery — The pulmonary artery waveform reflects systolic pressure resulting from rapid flow of blood into the pulmonary artery from the right ventricle during right ventricular systole. Since the pulmonic valve is opened, the waveform in systole is identical in morphology and amplitude to that of right ventricular systole.

As right ventricular ejection ends, the pressure in the pulmonary artery falls in similar fashion to that in the right ventricle. However, as right ventricular pressure falls below that of the pulmonary artery, the pulmonic valve closes, resulting in an incisura, or dichrotic notch, on the downslope of the pressure tracing. Pressure in the pulmonary artery continues to fall gradually as blood flows through the pulmonary arteries and veins into the left side of the heart, reaching a nadir or the end-diastolic pulmonary artery pressure.

The waveform of the pulmonary artery is similar in morphology to that of the aorta, but the pressure is lower.

The normal pulmonary artery systolic pressure is 15 to 30 mmHg and the pulmonary artery diastolic pressure is 4 to 12 mmHg.

Pulmonary capillary wedge and left atrium — The pulmonary capillary wedge pressure (PCWP) has a waveform and amplitude that is similar to that of the left atrial pressure wave, but it is damped and delayed because of transmission through the capillary vessels (waveform 3 and waveform 4B). The normal "wedge" and left atrial waveforms are similar in morphology to those of the right atrial pressure tracing, although the pressure is higher.

The normal waveform consists of an "a" wave due to atrial contraction, a "v" wave reflecting left atrial filling during left ventricular contraction, a "c" wave (which may not be apparent on the PCWP tracing) due to mitral valve closure, and an "x" and "y" descent due to left atrial relaxation and left ventricular diastole, respectively. In the normal situation, the mean PCWP and end-diastolic pulmonary artery pressure are approximately equal.

The normal mean left atrial pressure (and pulmonary capillary wedge pressure) is between 4 and 12 mmHg.

Left ventricle — The components of the left ventricular pressure waveform are similar to that of the right ventricular waveform except the systolic and diastolic pressures are appropriately higher (waveform 4A and waveform 4B).

Left ventricular systole causes a rapid increase in left ventricular pressure. Following the QRS signal on the ECG, isovolumetric contraction increases left ventricular pressure. When it becomes higher than that of the left atrium, the mitral valve closes. The pressure continues to rise; when it exceeds that of the aorta, the aortic valve opens.

After the peak systolic pressure, which is coincident with the T wave on the ECG, left ventricular diastole begins with a rapid fall in left ventricular pressure. When the left ventricular pressure falls below that of the aorta, the aortic valve closes. As the left ventricular pressure continues to fall (during isovolumetric relaxation) below that of the left atrium, the mitral valve opens, resulting in left atrial emptying into the left ventricle and beginning of the diastolic filling period of the left ventricle (waveform 5).

Similar to pressure changes in the right ventricle, left ventricular diastole consists of three periods: rapid filling, slow filling, and atrial contraction (figure 2). The pressure immediately after left atrial contraction, the "a" wave, is the left ventricular end-diastolic pressure (LVEDP). Since the mitral valve is opened, the "a" wave is identical to that seen on the left atrial waveform.

The normal LVEDP is 4 to 12 mmHg.

Left ventricular end-diastolic pressure — Left ventricular end-diastolic filling pressure (LVEDP) is often indicative of the hemodynamic health of the left ventricle [15]. Left ventricular pressure is available for examination from nearly every catheterization.

Coincident with the R wave on the corresponding ECG, the LVEDP immediately precedes the beginning of isovolumetric ventricular contraction on the left ventricular pressure waveform. This point, also known as the "Z" point, is situated on the downslope of the left ventricular "a" wave and marks the crossing over of left atrial and left ventricular pressures. (waveform 4A-B).

Identification of the true LVEDP can at times be difficult. There may be several different inflection points of the LVEDP; the "a" wave can show a changing pressure since the multiple-holed pigtail catheter that is usually placed into the left ventricle for pressure measurements and radiographic contrast media injection may move across the aortic valve with inspiration or heart motion, thereby causing the LVEDP to be artifactually higher. This artifact can be detected by the pressure waveform and identification of the lowest left ventricular pressure at the initiation of diastole. Thus, stability of the catheter and acquisition of a reliable pressure wave is required for the accurate interpretation of LVEDP.

Interpretation of the LVEDP waveform has contributed to our understanding of left ventricular contraction and relaxation (waveform 4A) and (figure 3). The pressure wave is a reflection of ventricular compliance and therefore indirectly represents the clinical conditions that affect ventricular performance. As an example, early clinical studies of hypertrophic cardiomyopathy emphasized the intraventricular gradient, while echocardiographic information has documented abnormal diastolic function with prolonged left ventricular isovolumetric relaxation phases and impaired diastolic filling. Diastolic function and systolic performance can be improved in patients with hypertrophic cardiomyopathy with a calcium channel blocker [16]. The substantial hemodynamic and clinical improvement corresponds to normalization of the left ventricular diastolic pressure curve. The LVEDP is normally <12 mmHg. (See "Hypertrophic cardiomyopathy: Morphologic variants and the pathophysiology of left ventricular outflow tract obstruction".)

Abnormal left ventricular end-diastolic filling pressure — The LVEDP is a function of chamber compliance and may be elevated when the left ventricle experiences excessive diastolic volume overload, as occurs, for example, with mitral or aortic valvular regurgitation or high-volume shunting at or distal to the ventricular septum. Impairment of myocardial contractility also alters the diastolic pressure-volume relationship and shifts the end-diastolic pressure point upward. Conditions of concentric hypertrophy due to hypertension or valvular stenosis, restrictive or infiltrative cardiomyopathy, or other diseases of the ventricular muscle produce a stiffer chamber and thus alter the pressure-volume curve, thereby elevating the LVEDP (waveform 6).

In the routine examination of the LVEDP, careful inspection of the waveform in diastole provides important information about left ventricular diastolic function. Myocardial relaxation abnormalities may be suggested by observing the trend of pressure during diastasis. As an example, a low LVEDP with a continuing decline of pressure over the mid-diastolic period, with the pressure nadir occurring midway through the diastolic period, suggests impaired myocardial relaxation that may be found in patients with severe left ventricular hypertrophy. In addition, with left ventricular hypertrophy and a "stiff" ventricle, an abnormally tall "a" wave resulting in a marked elevation of LVEDP may occur, although the diastolic pressure prior to atrial contraction can be normal (figure 3 and waveform 6).

Patients with an inducible obstructive LV outflow tract gradient due to hypertrophic cardiomyopathy may have an abnormal LVEDP waveform that resembles that seen in LV hypertrophy due to hypertension. An abnormal LVEDP waveform may develop with a Valsalva maneuver or induced premature ventricular contractions that result in the development of an intraventricular gradient (waveform 7). (See "Hypertrophic cardiomyopathy: Morphologic variants and the pathophysiology of left ventricular outflow tract obstruction" and "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".)

Aorta — The waveform generated in the aorta is similar to that seen in the pulmonary artery except that the systolic and diastolic pressures are significantly higher. The systolic wave is similar to that of the left ventricular systolic wave as the aortic valve is opened and the two structures are in direct communication. When left ventricular pressure falls to a level below that of the aorta, the aortic valve closes and produces the dichrotic notch on the aortic pressure tracing. A gradual fall in aortic pressure continues as blood flows from the aorta to the peripheral vessels, until the end-diastolic pressure is reached (waveform 1 and figure 4 and figure 1).

There are gender differences in the central aortic pressure waveform. One study reported that women had a prominent secondary late systolic peak in the aortic pressure wave and as a result had a higher augmentation index (the difference between early and late pressure peaks divided by the pulse pressure), an index of pulsatile afterload (figure 5) [17]. Women also had a lower subendocardial viability index (the ratio of diastolic to systolic time integral), reflecting a reduction in subendocardial blood flow; this was largely the result of a higher heart rate and shorter diastolic period. These differences may explain the greater degree of age-related left ventricular hypertrophy and the higher incidence of congestive heart failure after myocardial infarction despite smaller infarctions in women compared to men.

Body height also alters the aortic waveform. Short stature is associated with a faster heart rate, shortened return times for reflected waveforms, and increased augmentation of the primary systolic pulse, but no change in mean blood pressure [18]. These factors cause a stiffening of the aorta in late systole (which increases the stroke and minute work of the left ventricle) and a reduction in diastolic pressure and duration (which reduces coronary artery blood flow). These findings may explain the association between short stature and an increased risk for coronary heart disease [19].

SIMULTANEOUS LEFT VENTRICULAR AND RIGHT VENTRICULAR END-DIASTOLIC PRESSURES — Insights into the diagnosis of left ventricular dysfunction may be appreciated by examination of simultaneously displayed left and right ventricular (LV and RV) pressure waveforms. Abnormalities of ventricular contraction and relaxation, ventricular conduction abnormalities, and restrictive/constrictive pathophysiologic states are often evident (waveform 6).

Simultaneous LV and RV systolic pressures normally move together in respiration. However, dynamic respiratory variation with discordant systolic ventricular pressures can distinguish between restrictive and constrictive pathology (waveform 8 and figure 6). (See "Differentiating constrictive pericarditis and restrictive cardiomyopathy".)

Abnormalities of cardiac rhythm can produce marked distortions in the timing relationship between left ventricular and right ventricular pressures (waveform 9 and waveform 10 and figure 7). As an example, a paced rhythm from a right ventricular endocardial pacemaker delays and skews the relaxation period of left ventricle pressure, resulting in overlap of the LV pressure downslope with that of the RV pressure, an unusual alignment of the diastolic pressures (waveform 9).

LEFT VENTRICULAR COMPLIANCE — The curvilinear relationship between stroke work and left ventricular end-diastolic pressure (LVEDP) has been commonly called the LV function curve; it is a measure of the performance of ventricular activity. The ventricular function curves are shifted upward by positive inotropic interventions and downward by those impairing inotropic activity. Afterload also may significantly influence the elevation or decline of the ventricular function curve.

Compliance of the LV is probably the major determinant of the LVEDP. Compliance is defined as the change in volume divided by the change in ventricular pressure (figure 8). Both ventricular volume and pressure must be measured simultaneously to compute compliance. The slope of the compliance curve is called stiffness, which is the inverse of compliance.

Compliance tends to decrease in chronic conditions involving myocardial hypertrophy, restrictive cardiomyopathy, or other infiltrative processes (figure 9). In patients with cardiac disease, LVEDP may be altered as myocardial ischemia is provoked. As an example, one study of normal subjects and patients with coronary artery disease with and without angina reported the LVEDP at rest, during rapid atrial pacing, and upon immediate termination of pacing [20]. In contrast to normal individuals, LV pressure was elevated in patients with pacing-induced myocardial ischemia, while patients without pacing-induced ischemia had a smaller change in LVEDP. The compliance shift due to ischemia altered the LVEDP (figure 8).

Although information about ventricular performance, especially diastolic function, can be gleaned from careful examination of the LVEDP waveform, artifacts of pressure waveforms should be identified to avoid confusion with true pathophysiologic responses.

PULMONARY CAPILLARY WEDGE PRESSURE — The pulmonary artery wedge pressure has been commonly accepted as an accurate reflection of left atrial pressure; it is often used in the assessment of mitral valve disease. The normal pulmonary capillary wedge pressure (PCWP) is obtained with an 5-8F balloon-tipped pulmonary artery catheter that is passed through the right heart and pulmonary artery with the balloon inflated after appropriate flushing of the fluid filled transducer system.

Normal left atrial pressure wave timing precedes PCWP by 40 to 120 msec and often has a slightly higher pressure due to damped transmission of pressure backward through the pulmonary capillaries. The two tracings are nearly identical in waveform [21] (waveform 3).

Simultaneous recording of the left ventricular pressure and Doppler mitral inflow velocity illustrate the early and late filling phases of flow through the mitral valve, corresponding to the "v" and "a" waves, respectively (waveform 5). Peak early filling represents the early ventricular filling "v" wave of the left atrial and pulmonary capillary wedge pressures. The peak atrial filling, producing the "a" wave, is the flow velocity increase due to atrial contraction. The timing of these flow velocities corresponds to the pressure changes, which are important for the hemodynamic assessment of mitral valve disease [9].

Pulmonary capillary wedge pressure fidelity — Although the PCWP is generally accepted as a measurement of left atrial pressure in the examination of mitral valve hemodynamics, pulmonary capillary wedge pressure fidelity is at times not satisfactory. An overly damped pulmonary wedge pressure may provide an equivalent mean pressure to left atrial pressure; however, the phasic wave forms may obscure the precise diagnosis of mitral stenosis (waveform 11). If a diagnosis and accurate measurement is necessary and catheter manipulation and flushing of the transducer system does not improve the quality of the waveform, direct left atrial pressure should be measured with a transseptal catheter.

TIMING OF HEMODYNAMICS WITH THE ECG — Hemodynamic data require examination not only of individual pressure waves, but also their timing to events on the electrocardiogram (ECG), particularly the QRS complex [15]. Correct interpretation of normal right heart pressure waveforms and careful examination of the unusual right heart hemodynamics and their timing in the cardiac cycle may reveal unanticipated pathophysiologic mechanisms.

Abnormalities of the waveforms can occur in the presence of arrhythmia or ventricular pacing [9]. This must be considered when interpreting hemodynamic data.

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

Basics topic (see "Patient education: Cardiac catheterization (The Basics)")

SUMMARY — Hemodynamic data may be required to assess either the cause or severity of a particular clinical presentation attributable to a cardiac abnormality. Echocardiographic evaluation of the heart has replaced and decreased the role of invasive hemodynamic evaluation. However, periodically there are suboptimal noninvasive examinations, as well as cases in which the noninvasive data are felt to be potentially erroneous. Thus, hemodynamic evaluation in the catheterization laboratory remains an important resource.

The following are normal hemodynamic findings:

The normal mean right atrial pressure is between 1 and 8 mmHg. (See 'Right atrium' above.)

The normal right ventricular diastolic pressure is 1 to 8 mmHg and the peak systolic pressure is 15 to 30 mmHg. (See 'Right ventricle' above.)

The normal pulmonary artery systolic pressure is 15 to 30 mmHg and the pulmonary artery diastolic pressure is 4 to 12 mmHg. (See 'Pulmonary artery' above.)

The normal mean left atrial pressure (and pulmonary capillary wedge pressure) is between 4 and 12 mmHg. (See 'Pulmonary capillary wedge and left atrium' above.)

The normal left ventricular end-diastolic pressure (LVEDP) is 4 to 12 mmHg. (See 'Left ventricle' above.)

In the presence of a normal pulmonic valve, the peak right ventricular and pulmonary artery systolic pressures are the same. (See 'Pulmonary artery' above.)

In the presence of a normal aortic valve, the peak left ventricular and aortic systolic pressures are the same. (See 'Aorta' above.)

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  2. The Cardiac Catheterization Handbook, 6th ed, Kern MJ (Ed), Elsevier, Philadelphia 2015.
  3. Interventional cardiac catheterization handbook, 3rd ed, Kern MJ (Ed), Mosby, St. Louis 2011.
  4. Moscucci M. Grossman and Baim’s Cardiac Catheterization, Angiography, and Intervention, 8th ed, Wolters Kluwer/Lippincott Williams & Wilkins, Philadelphia 2013. p.223.
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Topic 1515 Version 19.0

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