Show Summary Details
Page of

Cardiac catheterization and angiography 

Cardiac catheterization and angiography
Chapter:
Cardiac catheterization and angiography
Author(s):

Edward D. Folland

DOI:
10.1093/med/9780199204854.003.160304_update_002

Update:

March 2014 – chapter reviewed; no significant changes required.

Updated on 27 Nov 2014. The previous version of this content can be found here.
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2015. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy).

Subscriber: null; date: 18 October 2017

Essentials

Cardiac catheterization/angiography is indicated for evaluation of patients with coronary, valvular, and congenital heart disease in whom diagnostic or therapeutic decisions cannot be made on the basis of noninvasive tests. Most patients presenting for cardiac catheterization have coronary artery disease: catheterization and coronary angiography are integral parts of interventional treatments for patients experiencing ischaemic coronary syndromes.

Technique and diagnostic utility—vascular access is usually obtained percutaneously from the femoral, radial, or brachial artery (for the left heart), or the femoral, internal jugular, or brachial/antecubital vein (for the right heart). Key information that can be obtained by cardiac catheterization/angiography include (1) pressures within cardiac chambers; (2) cardiac output; (3) quantitative estimation of left ventricular function; (4) diagnosis and quantitation of intracardiac shunts; (5) calculation of systemic and pulmonary vascular resistances; (6) assessment of cardiac valves; and (7) details of coronary arterial anatomy and function.

Therapeutic utility—cardiac catheterization/angiography permits interventions, particularly coronary angioplasty/stenting (see Chapters 16.13.5 and 16.13.6), that are of great and increasing therapeutic importance.

Introduction

Invasive cardiac diagnosis by means of catheterization and angiography developed hand in hand with cardiac surgery throughout the 20th century. It answered the need for precise information about cardiac physiology and anatomy, which arose in the 1940s when surgical techniques for the treatment of congenital and rheumatic heart disease first became available. A few years earlier, in 1929, Werner Forsman of Germany successfully and safely passed a filiform urinary catheter from a median basilic vein into the right atrium of his own heart and documented it on X-ray film. Although this feat cost him his own job, it enabled Andre Cournand and Dickenson Richards a decade later to use catheters for sampling blood, measuring pressure and flow, and injecting radio-opaque contrast medium (angiography) into the intact, beating human heart, ushering in the era of invasive cardiac diagnosis. Cournand, Richards, and Forsman later won the Nobel Prize for their important work. This chapter reviews the diagnostic applications of cardiac catheterization and angiography.

Indications for cardiac catheterization and angiography

Catheterization entails some degree of risk and discomfort, and is expensive, hence patients should be carefully selected. In broadest terms, it is indicated for detailed evaluation of those with coronary, valvular, and congenital heart disease, once they have been identified as candidates for surgery or other forms of intervention. It may also be indicated for patients whose diagnosis is uncertain from noninvasive evaluation.

Coronary artery disease

Most patients presenting for cardiac catheterization have coronary artery disease. Angiography of the coronary arteries performed during cardiac catheterization is essential for patients in whom revascularization is indicated. In spite of the limitations discussed later in this chapter, no other imaging modality, including MRI and CT (see Chapter 16.3.3), can as yet provide the detailed anatomy of the entire coronary circulation that is needed for planning revascularization procedures such as coronary artery bypass surgery and percutaneous intervention.

Coronary angiography is indicated for patients with chronic stable angina that persists in spite of reasonable efforts at pharmacological therapy. It is also indicated for patients whose survival would be improved by revascularization, regardless of symptoms. Such patients are those with severe stenosis of the main left coronary artery and those with severe two- and three-vessel coronary artery disease in combination with impaired left ventricular function. These patients may be identified by the following features of stress testing: ischaemia at low workload (especially in stage 1 of the Bruce protocol), marked depression of the electrocardiographic ST segment (>2 mm), failure to augment systolic blood pressure during exercise, and large exercise-induced defects or increased lung uptake during radionuclide perfusion imaging (see Chapters 16.3.1 and 16.3.3). In addition, patients with high-risk clinical presentations such as acute myocardial infarction, unstable angina, and post-myocardial infarction ischaemia are candidates for angiography. Patients having acute myocardial infarction are best served by immediate percutaneous coronary intervention if this is available in a timely manner (see Chapters 16.13.5 and 16.13.6). Finally, catheterization is sometimes indicated to obtain a definitive diagnosis when noninvasive testing has yielded equivocal or inconsistent results.

Valvular disease

Catheterization was once considered essential prior to the surgical treatment of valvular heart disease. This is no longer the case because of advances in noninvasive testing using ultrasound and Doppler techniques. Nevertheless, catheterization is frequently helpful for gathering the information needed to properly select patients for surgical therapy, and to guide the surgeon in providing optimum treatment, the most common issue being to assess the need for coronary artery revascularization, particularly among those with aortic stenosis, who commonly have coronary artery disease. Haemodynamic studies may also be necessary in cases where noninvasive diagnostic data are limited or equivocal. By contrast, it is often possible to avoid catheterization in young patients in whom noninvasive studies yield unequivocal conclusions and there is no evidence of coronary artery disease.

Congenital disease

Most patients with congenital heart defects can be definitively diagnosed by transthoracic or transoesophageal ultrasound, CT, or MRI (see Chapters 16.3.2 and 16.3.3). As in valvular disease, catheterization is most useful in cases where the abnormality is unusually complex, the noninvasive data are incomplete, or the patient is suspected of having coronary artery disease. Catheterization is particularly useful in quantifying shunt flow and pulmonary vascular resistance, both of which are important considerations in the treatment of intracardiac defects. The physical passage of a systemic venous catheter across the atrial septum into a pulmonary vein or the left ventricle is diagnostic of an atrial septal defect.

Pericardial disease

Pericardial tamponade and constriction lend themselves particularly well to diagnosis by catheterization. Although ultrasonography has superseded catheterization as a rapidly available method of confirming the clinical diagnosis of tamponade, it is usually inconclusive for patients with pericardial constriction. At catheterization, patients with both conditions usually demonstrate equalization of all intracardiac diastolic pressures, with unique pressure waveforms exhibited in the right atrium and right ventricle usually distinguishing the two diagnoses (Fig. 16.3.4.1).

Fig. 16.3.4.1 Pericardial constriction. This is a tracing of simultaneous left ventricular (LV) and right ventricular (RV) pressure in a patient with pericardial constriction. Generally, the diastolic pressure of the left ventricle is higher than that of the right ventricle. For patients with a constriction, the pericardium determines the diastolic compliance of both chambers, causing the diastolic pressures to be equal. Note also the typical ‘dip–plateau’ pattern or ‘square-root sign’ of both chambers in diastole. Although diastolic ventricular pressures are also equal for patients having tamponade, the dip–plateau pattern is usually absent.

Fig. 16.3.4.1
Pericardial constriction. This is a tracing of simultaneous left ventricular (LV) and right ventricular (RV) pressure in a patient with pericardial constriction. Generally, the diastolic pressure of the left ventricle is higher than that of the right ventricle. For patients with a constriction, the pericardium determines the diastolic compliance of both chambers, causing the diastolic pressures to be equal. Note also the typical ‘dip–plateau’ pattern or ‘square-root sign’ of both chambers in diastole. Although diastolic ventricular pressures are also equal for patients having tamponade, the dip–plateau pattern is usually absent.

Congestive heart failure

The aetiology and pathophysiology of congestive heart failure are readily elucidated by catheterization. States of pressure and volume overload as well as systolic and diastolic dysfunction of the ventricles can be easily identified, as explained in detail later in this chapter. Furthermore, catheterization is uniquely suited for identifying transient or reversible causes of left ventricular dysfunction caused by ischaemia or myocardial hibernation due to underlying coronary artery disease. Sometimes exercise or other interventions are performed during a catheter study to elicit transient abnormal haemodynamic function. Myocardial biopsy performed during catheterization can sometimes identify the aetiology of primary myocardial dysfunction.

Pulmonary vascular disease

Patients with primary pulmonary hypertension (see Chapter 16.15.2) should undergo catheterization to measure pulmonary vascular pressure and resistance. Certain vasodilating drugs may or may not benefit the patient, depending upon their effect on pressure and resistance during acute administration. Pulmonary angiography performed during right heart catheterization is traditionally regarded as the most definitive test for pulmonary embolism, although in most cases the diagnosis can be secured by CT angiography or radioisotope lung scanning.

Practicalities of cardiac catheterization

Preparing the patient

Precatheterization evaluation should consist of a careful history and examination, particularly aimed at eliciting details of prior cardiac procedures, reactions to contrast medium, renal function, peripheral vascular status, and haemostatic function. The patient should be carefully advised of the indications, alternatives, risks, discomforts, and expected benefits of the procedure. The skilled clinician does this while building the patient’s confidence and avoids creating undue alarm. Following an uncomplicated diagnostic catheterization the patient should usually expect to go home the same day and to resume customary physical activities within a day or two.

Vascular access

The traditional approach to vascular access is via a cut-down near the antecubital fossa, with isolation and mobilization of the brachial or antecubital vein and the brachial artery for right and left heart catheterization thereby allowing arterial and venous access. After the procedure the arterial entry site is repaired by suture and the vein is usually tied off. However, although this approach has the advantage of enabling early postprocedure ambulation and the security of direct arterial closure in anticoagulated patients, it has the disadvantage of being time-consuming for most physicians and less cosmetic for the patient. Hence the cut-down approach is now seldom used, with percutaneous arterial catheterization becoming increasingly popular.

Percutaneous vascular access is achieved by direct puncture with a needle through which a flexible spring guide wire is passed into the vessel. Catheters may then be passed into the vessel over the guide wire. Following the procedure haemostasis is achieved by applying pressure over the puncture site until bleeding stops. Percutaneous access is frequently employed at the femoral site, although it may also be used at brachial, axillary, internal jugular, and radial locations. It has the advantage of speed, simplicity, and—when performed from the femoral vessels—frees the upper body and arms during angiographic filming. However, it has the disadvantage of sometimes requiring several hours’ immobilization of the catheterization site following the procedure. Nevertheless, the femoral approach remains popular, especially when smaller catheters (4 and 5 French) and arterial closure devices enable earlier ambulation. In recent years the percutaneous approach to the radial artery has become the preferred choice of many physicians because it is associated with fewer bleeding complications and shortens hospital time.

Right heart catheterization

Right heart catheterization can be performed from any of the approaches described above. Although traditionally performed with a stiff, woven Dacron, end-hole catheter, it is often done with a flexible, balloon-tip, flow-directed catheter (Swan–Ganz) because this is safer and enables the measurement of cardiac output by thermodilution.

Catheterization of the right heart is indicated by itself for the study of pulmonary vascular disease and haemodynamic response to exercise or drug administration. It is indicated in combination with left heart catheterization for patients requiring haemodynamic study of valvular, congenital, or myocardial disease, and for patients being studied primarily for coronary artery disease who also have heart failure, valvular, or pulmonary disease.

Left atrial pressure can be measured indirectly via right heart catheterization by wedging the tip of the catheter in a pulmonary arteriole, or by occluding a pulmonary artery branch with the inflated balloon at the tip of a Swan–Ganz catheter. In either case, this creates a static column of blood from the tip of the catheter, through the pulmonary capillary bed, to the left atrium. This static column of blood has the effect of extending the tip of the catheter to the left atrium for pressure-measuring purposes. The resulting pressure is identical to the directly measured left atrial pressure, except that it is delayed temporally by approximately 80 ms. This pressure, commonly known as the pulmonary (artery) capillary wedge (PCW) pressure, is very useful in the management of left heart failure and shock, and for estimating the diastolic gradient across the mitral valve in patients with mitral stenosis.

Left heart catheterization

Left heart catheterization is generally performed in conjunction with coronary angiography, but is specifically required for the assessment of left ventricular function and assessment of stenosis or regurgitation of the left-sided valves (mitral and aortic). It is most often accomplished by femoral, radial, or brachial arterial access, and by retrograde crossing of the aortic valve to enter the left ventricle. Left heart catheterization may also be achieved by controlled puncture of the interatrial septum with a catheter originating from the right femoral vein (trans-septal left heart catheterization): this can then be used to measure left atrial pressure directly, and be passed antegradely through the mitral valve to measure pressure and perform angiography of the left ventricle. Retrograde access of the left atrium from the left ventricle is technically difficult and seldom done.

The left ventricle may also be entered via transthoracic needle puncture. This approach, known as direct left ventricular puncture, is occasionally necessary for studying patients who have both mitral and aortic mechanical prosthetic valves. The passage of the needle into the left ventricle from the cardiac apex is facilitated by echocardiographic guidance.

Information obtained from cardiac catheterization and angiography

Intracardiac pressures

Methodology

Pressure at the tip of the catheter is transmitted through the fluid inside the catheter (usually saline) to a transducer, which converts the pressure signal to an electrical signal that can then be amplified, displayed on a screen, and stored as a digital time recording. Once calibrated, the pressure at the tip of the catheter can be read graphically from the recording screen and analysed electronically. The fidelity of recording depends upon the physical characteristics of the fluid-filled catheter, stopcocks, connecting tubing, and the pressure transducer itself. A fluid-filled system is usually capable of responding to transient pressure changes up to 20 or occasionally 30 Hz, which is of sufficient fidelity to reproduce diagnostically useful pressure waveforms from the heart. However, it is not responsive enough to accurately reproduce the rate of rise of left ventricular pressure during the isovolumic phase of systole (dP/dt). This requires responsiveness to transient pressure changes of at least 60 Hz, of which fluid-filled catheter systems are not capable. For such applications catheter-tip manometers are available (Millar catheters) in which the transducer is placed at the catheter tip, eliminating the need for an intervening column of fluid. These devices are expensive and are used only when such fidelity is required, usually in research applications.

Normal intracardiac pressures

The upper limits of all normal intracardiac pressures measurable from a right heart catheter are approximate multiples of six, hence they are easily remembered by the ‘rule of sixes’ (Table 16.3.4.1). For example, the mean right atrial pressure is 6 mmHg or less, mean left atrial pressure is 12 mmHg or less. A further aid to remembering normal pressures is the ‘corollary of continuity’, which means that contiguous chambers have a common pressure when the intervening valve is open. For example, the right ventricle and right atrium are essentially a common chamber when the tricuspid valve is open in diastole, therefore the upper limit of right ventricular end-diastolic pressure is the same as the upper limit of the normal right atrial pressure, or 6 mmHg. This assumes there is no significant stenosis or regurgitation across the tricuspid valve, and that the right ventricle has normal compliance. The same condition applies to the mitral valve in diastole and the pulmonic and aortic valves in systole. Another practical rule is that the pulmonary artery diastolic and pulmonary artery capillary pressures approximate each other in the absence of severe pulmonary vascular disease. Once this has been established for any given patient, the pulmonary artery diastolic pressure can be followed as a surrogate for pulmonary capillary wedge pressure in situations where a pulmonary artery catheter is used for intensive-care monitoring.

Table 16.3.4.1 Normal intracardiac pressuresa

Location

Phasic pressure (mmHg)

Mean pressure (mmHg)

Right atrium

3 ± 2

  • Right ventricle

  • Systole

  • Diastole

  • 24 ± 4

  • 5 ± 3

  • Pulmonary artery

  • Systole

  • Diastole

  • 24 ± 6

  • 13 ± 5

13 ± 5

  • Pulmonary capillary

  • Wedge

9 ± 3

Left atrium

9 ± 3

  • Left ventricle

  • Systole

  • Diastole

  • 120 ± 18

  • 10 ±5

a These values are derived from 100 consecutive catheterization studies of patients proven to have no evidence of heart disease at the West Roxbury Veterans Administration Hospital from 1955 to 1980. An easy way to remember the upper limits of normal values (≤2 standard deviations above mean) is that they are generally multiples of the number 6.

All intracardiac pressures rise and fall phasically with breathing due to transmission of shifting intrapleural pressure during respiratory effort. Usually this variation is no more than a few mmHg from inspiration to expiration, but it can be quite marked in patients with obstructive lung disease. Standards of normal pressure are based upon measurements taken during resting respiration, averaging several respiratory cycles. Pressures in the catheterization laboratory should be similarly measured: asking a patient to hold their breath may generate misleading data.

Waveforms

The shape of intracardiac pressure waveforms carries useful diagnostic information. Atria and ventricles have characteristic waveforms, the left-sided chambers normally demonstrating similar patterns at relatively higher pressures than right-sided chambers. The state of volume loading and the relative compliance or ‘stiffness’ of the respective ventricles during diastolic filling determines pressures in the right and left atria. The left ventricle is generally thicker, stiffer, and less compliant to the stretch of increasing volume than the right ventricle; hence the left atrial and left ventricular diastolic pressures are higher than the respective pressures in the right heart. Conditions such as pericardial constriction and tamponade alter this normal relationship (see Fig. 16.3.4.1).

Cardiac flow and output

Measurement of cardiac output was one of the earliest applications of catheterization. Most methods entail application of the indicator dilution theory (the Fick principle), summarized graphically in Fig. 16.3.4.2, which can be stated simply as follows: the rate of flow can be measured if an indicator substance is added to the moving vehicle (e.g. blood) at a known rate, and the concentration of the indicator is also known proximal and distal to the point where the indicator is added. The indicator can be any readily measured substance such as oxygen, indocyanine green dye, or saline, the temperature of which is known and different from that of the bloodstream.

Fig. 16.3.4.2 The Fick principle. The flow rate (F) through a vessel (cardiac output, in this case) can be measured if an indicator is added to the flowing liquid at a known rate (q/min) and the concentration (q/L) of the indicator is measured after complete mixing has occurred.

Fig. 16.3.4.2
The Fick principle. The flow rate (F) through a vessel (cardiac output, in this case) can be measured if an indicator is added to the flowing liquid at a known rate (q/min) and the concentration (q/L) of the indicator is measured after complete mixing has occurred.

Cardiac output by oximetry

In this method, commonly called the Fick method, the indicator is oxygen that is carried physiologically by the blood. The method requires that the subject be in a metabolic steady state where the use of oxygen is constant. Such a steady state exists at rest and also during exercise, provided that the workload is constant for at least 3 min. As seen in Fig. 16.3.4.3, the pulmonary blood flow can be calculated when the oxygen consumption rate is known and the oxygen contents of blood in systemic and pulmonary arteries are known. In the absence of intracardiac shunts the pulmonary blood flow equals the systemic blood flow, or cardiac output.

Fig. 16.3.4.3 Cardiac output measured by oximetry. This is an application of the Fick principle in which oxygen is the indicator carried by flowing blood. The patient’s metabolism must be at steady state, a condition where oxygen consumption and utilization are matched. It requires three measurements: oxygen consumption rate (Qo2), systemic arterial oxygen content (SAo2), and pulmonary arterial oxygen content (PAo2). Ao, aorta; cc, volume in ml; CO, cardiac output; LV, left ventricle; PV, pulmonary vein; RV, right ventricle; VC, vena cava.

Fig. 16.3.4.3
Cardiac output measured by oximetry. This is an application of the Fick principle in which oxygen is the indicator carried by flowing blood. The patient’s metabolism must be at steady state, a condition where oxygen consumption and utilization are matched. It requires three measurements: oxygen consumption rate (Qo2), systemic arterial oxygen content (SAo2), and pulmonary arterial oxygen content (PAo2). Ao, aorta; cc, volume in ml; CO, cardiac output; LV, left ventricle; PV, pulmonary vein; RV, right ventricle; VC, vena cava.

Dye dilution

This method entails the rapid injection of a known quantity of indocyanine dye into the pulmonary artery. Blood is then sampled by withdrawal at a constant rate from a systemic artery. The sampled blood passes through a spectrophotometer, which is calibrated to measure the concentration of dye. A concentration curve is inscribed when the injected bolus of dye passes the sampling point (Fig. 16.3.4.4). Dividing the quantity of dye injected by the area of the time–concentration curve (corrected for recirculation) yields the cardiac output. This method is now seldom used.

Fig. 16.3.4.4 Cardiac output measured by dye curve. The concentration curve of indocyanine green dye generated by sampling distal to an injection point can be analysed to yield cardiac output. See text for more details. Thermodilution cardiac output employs the same principle, except that temperature is the measured indicator. F, flow or cardiac output; Q, quantity of indicator injected.

Fig. 16.3.4.4
Cardiac output measured by dye curve. The concentration curve of indocyanine green dye generated by sampling distal to an injection point can be analysed to yield cardiac output. See text for more details. Thermodilution cardiac output employs the same principle, except that temperature is the measured indicator. F, flow or cardiac output; Q, quantity of indicator injected.

Thermodilution

Measurement of cardiac output by thermodilution uses the same principle as dye dilution, with the indicator being ‘negative calories’ (the difference between the caloric content of the injected bolus of cool saline and the caloric content of the same quantity of the subject’s blood). The downstream ‘concentration’ of injected negative calories is measured as a transient drop in temperature by a thermistor at the tip of the injection catheter several centimetres from the point of injection. Dividing the negative calories injected by the area of the distal time–temperature curve yields cardiac output. The advantages of speed, automaticity, and repeatability of this method make it particularly suitable for serial measurements during different haemodynamic states.

Angiographic output

This is the only commonly used method that does not employ the indicator dilution or Fick principle. The left ventricular stroke volume calculated from quantitative angiography is multiplied by the heart rate to yield the left ventricular output. In the absence of valvular regurgitation this is the same as cardiac output. As explained in greater detail later in the chapter, this method is particularly useful in assessing mitral and aortic valvular regurgitation.

Quantitative angiography

Quantitative left ventricular angiography enables the measurement of left ventricular volume at instants throughout the cardiac cycle. Radiographic contrast medium is injected rapidly into the left ventricle and the shadow image of the opacified ventricle captured electronically at a particular frame rate in any chosen projection. The most common projection is 30° right anterior oblique at a framing rate of 30 images/s. In this view the image of the left ventricle is parallel to its long axis, resembling an ellipse. Arvidsson and Greene first suggested that the volume of the left ventricle could be calculated from the volume formula for an ellipsoid, the three-dimensional structure created by rotating an ellipse on its long axis. Dodge and Sandler improved upon this concept by deriving the minor hemi-axes from an idealized ellipse of the same length and area as the projected image of the ventricle. This method is still commonly used and is often referred to as the area–length method. Images captured at end diastole and end systole are analysed and corrected for magnification to yield end-diastolic and end-systolic volumes, the difference between these volumes being the stroke volume and the product of the stroke volume and heart rate, the angiographic left ventricular output. These indices are useful in the assessment of left ventricular function and valvular regurgitation as discussed later in this chapter.

Intracardiac shunts

The same methods of oximetry and indicator dilution used in measuring cardiac output can be employed for the detection and quantitation of intracardiac shunts. Under normal resting conditions, blood is approximately 75% saturated as it returns from the body to the right heart and pulmonary artery. As it leaves the lungs in the pulmonary veins blood is 99% saturated. Intracardiac shunts can be detected, localized, and quantified by measuring the oxygen saturation in various locations. Left-to-right shunts will cause a step-up in the saturation of the blood at the location of the shunt; for example, in a patient with an atrial septal defect the saturation will rise in the right atrium, whereas with a ventricular septal defect the saturation will rise in the right ventricle. A patient with Eisenmenger’s syndrome (pulmonary hypertension and right-to-left shunting) will exhibit a drop in saturation at the location of the shunt, namely at the left atrium or ventricle in the case of atrial and ventricular septal defects, respectively. The degree of the change in saturation is proportional to the size of the shunt, and enables calculation of the shunt flow in either direction in litres/min. Figure 16.3.4.5 presents a scheme and formulae for calculating shunt volume.

Fig. 16.3.4.5 Quantitation of intracardiac shunts. Shunts between the left and right sides of the heart due to septal defects can be quantified by oximetry using this scheme. EPBF, effective pulmonary blood flow, i.e. that part of the systemic venous return that actually passes through the lungs and is oxygenated; PBF, pulmonary blood flow; mixed VO2, mixed systemic venous oxygen content; PAO2, pulmonary artery oxygen content; PVO2, pulmonary vein oxygen content; SAO2, systemic artery oxygen content; SBF, systemic blood flow.

Fig. 16.3.4.5
Quantitation of intracardiac shunts. Shunts between the left and right sides of the heart due to septal defects can be quantified by oximetry using this scheme. EPBF, effective pulmonary blood flow, i.e. that part of the systemic venous return that actually passes through the lungs and is oxygenated; PBF, pulmonary blood flow; mixed VO2, mixed systemic venous oxygen content; PAO2, pulmonary artery oxygen content; PVO2, pulmonary vein oxygen content; SAO2, systemic artery oxygen content; SBF, systemic blood flow.

Vascular resistance

Blood flow through the pulmonary and systemic circulations can be compared to the flow of an electric current through a circuit. Pressure is the driving force analogous to voltage, flow rate is analogous to current, and the impediment to flow through the vascular bed is resistance. Pressure, flow, and resistance relate to each other in a fashion analogous to Ohm’s law:

resistance=pressure/flow

In the above formula ‘pressure’ is the difference in mean pressure across the systemic vascular bed (systemic arterial pressure − right atrial pressure) or the pulmonary vascular bed (pulmonary artery pressure − left atrial pressure). In the absence of intracardiac shunts ‘flow’ is the same for both circulations and is measured as cardiac output by methods already described. In cases of intracardiac shunting the systemic and pulmonary flows will differ according to the degree of shunting, and can be calculated as described under the section on cardiac shunts and in Figure 16.3.4.5. Normal values for pulmonary vascular and systemic vascular resistance are expressed either in dyne s cm–5 or Wood units and are shown in Table 16.3.4.2. Total pulmonary resistance is a useful concept for expressing the total resistance against which the right ventricle must work, and includes not only the pulmonary vascular resistance but also the resistance engendered by the static pressure in the left atrium. Hence, pulmonary vascular disease, left heart failure, or both, can increase the total pulmonary resistance.

Table 16.3.4.2 Normal vascular resistancea

Location

Resistance (dynes s cm–5)b

Total systemic resistance

1276 ± 371

Total pulmonary resistance

185 ± 57

Pulmonary vascular resistance

55 ± 18

a The values are derived from 100 consecutive catheterization studies of patients proven to have no evidence of cardiac disease at the West Roxbury Veterans Administration Hospital during the years 1955–1980.

b Divide these values by 10 to obtain values in MPa s m−3.

Measurement of resistance is useful for assessing the state of the pulmonary circulation in congenital heart disease with intracardiac shunting: high pulmonary vascular resistance may preclude the safe correction of an intracardiac shunt, particularly if the shunt is from right to left. It is also useful in diagnosing the relative contribution of left heart failure and pulmonary vascular disease in patients with pulmonary hypertension, and is the best indicator of the effectiveness of vasodilating drugs for patients with pulmonary hypertension.

Valvular stenosis

Valvular stenosis is assessed by measuring the transvalvular pressure gradient and by calculating the valvular orifice area using a formula introduced in the late 1940s by cardiologist Richard Gorlin and his father, an engineer. The Gorlin formula for valve area was initially developed for patients with rheumatic mitral stenosis. It is based upon a study which utilized data from right heart catheterization alone, validated by relatively crude intraoperative estimates of valve area using the index finger of surgeon Dwight Harken during closed mitral commissurotomy operations at the Peter Bent Brigham Hospital in Boston, Massachusetts. Although its validation was relatively crude, the formula has stood the test of time and remains the standard for the haemodynamic assessment of valvular stenosis. In its generalized form it is expressed as follows:

valve area=TFR/(Km)

where K is a constant unique to mitral or aortic valve analysis (38 and 44.5, respectively), TFR is the transvalvular flow rate, and m is the mean pressure gradient in mmHg during the time when the valve is open.

In aortic valve applications TFR (i.e. cardiac output normalized for the time that the valve is actually open) is the cardiac output divided by the product of heart rate and systolic ejection period. In mitral valve applications it is the cardiac output divided by the product of heart rate and diastolic filling period. Cardiac output is the effective systemic blood flow as determined by Fick, thermodilution, or dye dilution methods, unless there is associated valvular regurgitation, in which case it is the total left ventricular output as determined by quantitative left ventricular angiography.

Figure 16.3.4.6 shows tracings that demonstrate typical gradients from patients with aortic and mitral stenosis. The ranges of calculated valve area associated with various levels of stenosis for both aortic and mitral valves are displayed in Table 16.3.4.3. In general, procedures performed for the relief of anatomical stenosis are expected to be beneficial in symptomatic patients with severe valvular obstruction. However, many factors enter into such a decision and individual clinical judgement is required. Although patients with large transvalvular gradients generally experience the best result from intervention, the gradient by itself can be misleading due to its exponential relationship to cardiac output.

Fig. 16.3.4.6 Pressure gradients associated with valvular stenosis. The upper panel shows simultaneous tracings of left ventricular (LV) and ascending aortic (Ao) pressure in a patient with severe aortic stenosis. The mean systolic gradient across the aortic valve is 60 mmHg. The lower panel shows simultaneous tracings of left ventricular (LV) and pulmonary capillary wedge (PCW) pressure in a patient with severe mitral stenosis. The mean diastolic pressure gradient across the valve is 16 mmHg. The respective valvular gradients are cross-hatched.

Fig. 16.3.4.6
Pressure gradients associated with valvular stenosis. The upper panel shows simultaneous tracings of left ventricular (LV) and ascending aortic (Ao) pressure in a patient with severe aortic stenosis. The mean systolic gradient across the aortic valve is 60 mmHg. The lower panel shows simultaneous tracings of left ventricular (LV) and pulmonary capillary wedge (PCW) pressure in a patient with severe mitral stenosis. The mean diastolic pressure gradient across the valve is 16 mmHg. The respective valvular gradients are cross-hatched.

Table 16.3.4.3 Calculated valve areas associated with various degrees of mitral and aortic stenosis

Severity

Valve area (cm2)

Aortic

Mitral

Mild

>1.2

>2.0

Moderate

0.8–1.2

1.1–2.0

Severea

< 0.8

≤1.0

a ‘Severe’ stenosis is generally considered to be sufficient to warrant surgical correction.

Valvular regurgitation

Qualitative assessment

Regurgitation of all four cardiac valves can be qualitatively assessed by angiography. The downstream side of the valve in question is opacified by a rapid injection of radiographic contrast medium. Regurgitation is visualized as upstream leakage of contrast across the closed valve. In the case of mitral regurgitation systolic opacification of the left atrium occurs during injection of the left ventricle. In aortic regurgitation diastolic opacification of the left ventricle occurs during supravalvular injection of the aorta. The degree of regurgitation is graded on an arbitrary scale from mild (1+) to severe (4+).

Quantitative assessment

Aortic and mitral regurgitation can be quantified in terms of regurgitant flow in litres/min or regurgitant fraction as a percentage of left ventricular output. Regurgitant flow is the difference obtained by subtracting the effective forward flow (Fick method described earlier) from the total left ventricular output (angiographically derived). It is the best method for measuring the severity of regurgitation, provided that the left ventricular angiogram, which itself may change cardiac output, is performed soon after the Fick measurement. Furthermore, both measurements must be made with considerable care to ensure accuracy. Regurgitation is considered clinically severe when 50% or more of the total left ventricular output is simply shuttling or regurgitating across the defective valve. The ability to quantify regurgitation across either valve is lost when both mitral and aortic valves are leaky.

Left ventricular function

Global function

Global function of the left ventricle is broadly described by its ability to generate pressure and flow under particular conditions of preload and afterload. Plotting the pressure and volume of the left ventricle at instants in time for a single cardiac cycle generates a pressure–volume loop displayed in Fig. 16.3.4.7. Most of the commonly used indices of left ventricular function can be derived from such a loop, including end-diastolic volume, end-systolic volume, stroke volume, ejection fraction, end-diastolic pressure, and dP/dt. Of these, the ejection fraction is most useful because it correlates with prognosis in a variety of cardiac diseases.

Fig. 16.3.4.7 Pressure–volume loops. Simultaneously plotting the instantaneous pressure and volume of the left ventricle throughout a single cardiac cycle produces these loops. The loop is a synthesis of most information relevant to left ventricular function. In this figure a loop from a normal patient is contrasted with those from patients with pressure load (hypertension or aortic stenosis), volume load (aortic or mitral regurgitation), and cardiomyopathy. Point A represents mitral valve closure; segment A–B, isovolumic contraction; point B, aortic valve opening; segment B–C, systolic ejection; point C, aortic valve closure; segment C–D, isovolumic relaxation; point D, mitral valve opening; and segment D–A, diastolic filling.

Fig. 16.3.4.7
Pressure–volume loops. Simultaneously plotting the instantaneous pressure and volume of the left ventricle throughout a single cardiac cycle produces these loops. The loop is a synthesis of most information relevant to left ventricular function. In this figure a loop from a normal patient is contrasted with those from patients with pressure load (hypertension or aortic stenosis), volume load (aortic or mitral regurgitation), and cardiomyopathy. Point A represents mitral valve closure; segment A–B, isovolumic contraction; point B, aortic valve opening; segment B–C, systolic ejection; point C, aortic valve closure; segment C–D, isovolumic relaxation; point D, mitral valve opening; and segment D–A, diastolic filling.

Grading angiographic wall motion in various segments of the left ventricle as normal, hypokinetic, akinetic, or dyskinetic assesses the regional function of the left ventricle. Regions of abnormal function generally correspond to locations of infarcted or ischaemic myocardium.

Contractility

This parameter is difficult to assess in the intact heart because all pressure and volume indices are dependent upon preload and afterload. Although ejection fraction is clinically useful it can be misleading in situations of high afterload (e.g. severe aortic stenosis) and low afterload (e.g. severe mitral regurgitation). The concept of ‘elastance’ has gained favour as a useful index of intrinsic contractility because it is relatively independent of loading conditions. Elastance is the slope of the line generated by plotting the end-systolic left ventricular pressure from a series of pressure–volume loops generated at differing afterloads created by the infusion of pressor or vasodilator drugs. The method is laborious and generally reserved for research applications.

Diastolic function

Diastolic function of the left ventricle is best appreciated from the slope of the pressure–volume loop during the period from mitral valve opening to its closure at the onset of systole. The curve becomes steeper as the left ventricle becomes less compliant due to the effects of hypertrophy, ischaemia, or infiltrative disease. In general, left ventricular end-diastolic pressure (LVEDP) rises as diastolic compliance falls, accounting for the high left atrial pressure and heart failure seen in diastolic left ventricular dysfunction.

Assessment of coronary arterial anatomy and function

Disease of the coronary arteries can be characterized at catheterization by both anatomical and functional assessment. Coronary angiography images the lumen of the vessel, which has been rendered radio-opaque by injection of radiographic contrast medium. It is a shadowing technique that displays the impact of the lesion on the arterial lumen but does not image the plaque per se. Intracoronary ultrasonography provides a tomographic image of the vessel wall and is capable of demonstrating the thickness and sonic density of the vessel wall and any associated plaque, hence angiography and intravascular ultrasonography are complementary methods of assessing vascular anatomy. To learn the haemodynamic importance of a coronary lesion it may be necessary to analyse its effect on function by measuring pressure and flow in the affected vessel. All these anatomical and functional modalities may be accomplished by catheterization.

Coronary arteriography or angiography

Coronary arteriography or angiography is presently the single most essential application of cardiac catheterization. The anatomy of coronary arteries in living, conscious humans was first demonstrated by nonselective injection of the aortic root. In the early 1960s David Littmann developed a loop catheter that enabled the injection of contrast medium preferentially in the outer circumference of the aortic root, opacifying the left and right coronary arteries simultaneously. At the time it was commonly believed that selective injection of contrast material into a coronary artery would have fatal consequences. This changed when Mason Sones accidentally performed the first selective coronary angiogram without harm. He was intending to inject the left ventricle, but the catheter recoiled across the aortic valve and into the right coronary artery. Sones, a cardiologist by training, went on to develop a safe method of selective coronary angiography from the brachial artery cut-down approach using the flexible-tip catheter bearing his name. At the same time Melvin Judkins, a radiologist by training, was perfecting his own method of selective coronary angiography, using preshaped catheters, from a percutaneous femoral artery approach. Both methods have continued to be practised, although the percutaneous femoral, or Judkins’ approach, has become most popular because of its speed and simplicity. However—as stated previously—in recent years there has been a return to the arm approach using percutaneous catheterization of the radial artery, which enables more rapid patient ambulation, and the radial artery approach is also associated with fewer serious access site complications.

Normal coronary anatomy is demonstrated in Fig. 16.3.4.8. A patient’s anatomy is considered to be right (80%)- or left (20%)-dominant, depending upon whether the posterior descending artery arises from the right or left coronary artery, respectively.

Fig. 16.3.4.8 Normal coronary anatomy. Left coronary angiogram showing main stem, left anterior descending, and left circumflex arteries from right anterior oblique view (a) and left anterior oblique view (b). Right coronary angiogram showing right coronary and posterior descending arteries from right anterior oblique view (c) and left anterior oblique view (d).

Fig. 16.3.4.8
Normal coronary anatomy. Left coronary angiogram showing main stem, left anterior descending, and left circumflex arteries from right anterior oblique view (a) and left anterior oblique view (b). Right coronary angiogram showing right coronary and posterior descending arteries from right anterior oblique view (c) and left anterior oblique view (d).

Atherosclerotic disease is manifest by lesions that encroach upon the opacified lumen of the coronary artery (Fig. 16.3.4.9). Various approaches are used to grade the severity of these lesions. Most commonly a visual estimate of the percentage of the stenotic reduction in luminal diameter is given to each lesion, with severity quantified by comparing the minimal lumen diameter within a lesion to the diameter of the nearest normal segment of artery. This can be done manually using callipers or automatically using computer-based systems for edge detection and contrast densitometry. Quantitative coronary angiography is a complex subject because it requires attention to many variables, such as selection of view and frame, and choice made from among several analytical techniques.

Fig. 16.3.4.9 Atherosclerotic coronary artery disease. The constrictions and blunt terminations seen in this patient’s coronary angiogram represent atherosclerotic lesions.

Fig. 16.3.4.9
Atherosclerotic coronary artery disease. The constrictions and blunt terminations seen in this patient’s coronary angiogram represent atherosclerotic lesions.

Early work by Lance Gould determined that a lesion must impair coronary blood flow to be clinically important. Although flow at rest is not usually reduced until stenosis reduces vessel diameter by 90%, flow under stress may be impaired when the diameter is reduced by 70%. The clinical impact of a stenosis of any given severity is also dependent upon the degree of collateral flow into the vascular bed distal to the stenosis.

Coronary physiological measurements (pressure and flow)

Flow and pressure may be directly measured in the coronary artery by means of special guide wires that have pressure transducers or Doppler flow transducers mounted near their tips. As mentioned above, the flow at rest may be normal across a particular coronary artery stenosis. Coronary flow normally increases after maximal vasodilatation induced by local vasodilators. The quotient of the vasodilated flow divided by the resting flow, which is called the coronary flow reserve, is normally greater than 2. If not, the lesion in question is considered to be haemodynamically important. Pressure can be measured in the coronary artery at a location distal to a lesion using a guide wire with a transducer at its tip. The quotient of pressure distal to a lesion compared to the proximal pressure during maximal vasodilatation is called the fractional flow reserve. A quotient less than 0.75 is considered to be clinically important. The measurement of fractional flow reserve has proven useful in selecting vessels in need of revascularization.

Intravascular ultrasonography (IVUS)

IVUS is accomplished by advancing a catheter over a guide wire previously placed into a coronary artery. The catheter has a miniature ultrasound transducer near its tip, which enables rotational Doppler imaging of the vessel wall in a plane perpendicular to its axis. IVUS is particularly useful for assessing the nature of angiographically questionable lesions, determining the true size of the vessel prior to stent deployment, and assessing the completeness of stent deployment. It is also probably the best method for serial studies of coronary anatomy during drug treatment trials, because it is able to image the plaque itself and is therefore a more sensitive method than angiography.

Complications of cardiac catheterization

Although cardiac catheterization is a relatively safe procedure, it is nevertheless important for both the patient and the referring physician to recognize the nature and likelihood of potential complications. Table 16.3.4.4 lists the complications of bilateral heart catheterization, including coronary, left ventricular, and aortic angiography, in a prospective study of valvular heart disease from the United States Veterans Administration. Even though these data were collected over 30 years ago from a particularly high-risk group of patients, the frequency of complication is a realistic estimate of what should currently be expected. The rate of each particular complication will vary with the age and general health of the patient. For example, the risk of vascular complication is considerably increased by the presence of vascular disease, and the risk of renal failure due to contrast medium is particularly high in diabetic patients with pre-existing renal dysfunction. Access site complications (bleeding, haematoma, arteriovenous fistula, pseudoaneurysm, and occlusion) have received particular attention in recent years because of the use of aggressive anticoagulation and antiplatelet treatments during percutaneous coronary intervention. Use of smaller gauge catheters and careful location of arterial puncture site is important. Vascular closure devices enable earlier ambulation of patients having femoral procedures.

Table 16.3.4.4 Complications of cardiac catheterization from a prospective study of 1559 procedures performed on 1483 United States veterans having valvular heart disease during the years 1977–1982a

Type of complication

Frequency (%)

Death within 24 h

0.1

Death between 24 h and 30 days

0.1

Stroke

0.3

Transient cerebral ischaemia

0.1

Myocardial infarction

0.2

Peripheral arterial embolism

0.1

Access site complications

1.7

Cardiac tamponade

0.3

Ventricular fibrillation

0.5

Arrhythmia other than ventricular fibrillation

1.5

Primary hypotension

0.5

Reaction to contrast medium (allergic and renal)

1.8

Arterial perforation or dissection

0.3

Miscellaneous complications

1.4

Patients having one or more of the above complications

6.9

a Although this is a high-risk group of patients undergoing extensive study, the rates are very comparable to what should be expected today. In fact, some complications, especially bleeding, are now more frequent because of aggressive anticoagulation and antiplatelet treatments given to many patients before and during catheterization.

In counselling the patient regarding the likelihood of untoward events it is important to give individualized advice based on the patient’s particular circumstances. The decision to recommend catheterization must be based on the anticipation that its benefits justify its risk and cost.

Further reading

De Bruyne B, et al. (2012). Fractional flow reserve guided-PCI versus medical therapy in stable coronary disease. N Engl J Med, 367, 991–1001.Find this resource:

    Kern M (2011). The cardiac catheterization handbook, 5th edition. Elsevier, Philadelphia, PA.Find this resource:

      Moscucci M (2013). Grossman and Baim’s cardiac catheterization, angiography and intervention, 8th edition. Lippincott Williams and Wilkins, Baltimore, MD.Find this resource:

        Tonino PA, et al. (2009). Fractional flow reserve versus angiography for guiding percutaneous coronary intervention. N Engl J Med, 360, 213–24.Find this resource: