The Cardiac Catheterization Laboratory

Published on 07/02/2015 by admin

Filed under Anesthesiology

Last modified 07/02/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 3470 times

Chapter 2 The Cardiac Catheterization Laboratory

From its inception until recently, the cardiac catheterization laboratory was primarily a diagnostic unit. In the 21st century, its focus has changed to therapy. As the noninvasive modalities of echocardiography, computed tomography, and magnetic resonance imaging improve in resolution, sensitivity, and specificity, the role of the diagnostic cardiac catheterization will likely decline in the next decade. The diagnosis and treatment of peripheral and cerebral vascular disease are now commonly performed in catheterization laboratories previously restricted to cardiac work. Newer coronary stents, as well as patent foramen ovale (PFO)/atrial septal defect (ASD)/ventricular septal defect (VSD) closure devices, are emerging as alternatives to cardiac surgery for many patients. Percutaneous valve replacement/repair is in development as well. In this arena, the need for more “routine” involvement of anesthesiologists in the catheterization laboratory will be important.

Diagnostic catheterization led to interventional therapy in 1977 when Andreas Gruentzig performed his first percutaneous transluminal coronary angioplasty (PTCA). Refinements in both diagnostic and interventional equipment occurred during the decade of the 1980s, with the 1990s seeing advances in both new device technologies for coronary artery disease (CAD) and the entry of cardiologists into the diagnosis and treatment of peripheral vascular disease. The 2000s will see advances in all of these interventional areas as well as the emergence of percutaneous valve replacement/repair.

This brief historical background serves as an introduction to the discussion of diagnostic and therapeutic procedures in the adult catheterization laboratory. The reader must realize the dynamic nature of this field. Whereas failed percutaneous coronary interventions (PCIs) once occurred in up to 5% of coronary interventions, most centers now report procedural failure rates under 1%. Simultaneously, the impact on the anesthesiologist has changed. The high complication rates of years past required holding an operating room (OR) open for all PCIs, and many almost expected to see the patient in the OR. Current low complication rates lead to complacency, along with amazement and perhaps confusion when a PCI patient comes emergently to the OR. Additionally, the anesthesiologist may find the information in this chapter useful in planning the preoperative management of a patient undergoing a cardiac or a noncardiac surgical procedure based on diagnostic information obtained in the catheterization laboratory. Finally, it is the goal of these authors to provide a current overview of this field so that the collaboration between the anesthesiologist and the interventional cardiologist will be mutually gratifying.


Room Setup/Design/Equipment

The setup and design for the cardiac catheterization laboratory vary from a single room, as seen in a mobile catheterization laboratory or a small community hospital, to a multilaboratory facility, as is found in large tertiary care centers (Box 2-1). In these facilities with multiple laboratories, a central work area is needed to coordinate patient flow to each of the surrounding laboratories and for centralized equipment storage. Patient holding areas are used for observation and evaluation of patients before and after the procedure.

Facility Case Load

All catheterization facilities must maintain appropriate patient volume to assure competence. American College of Cardiology/American Heart Association (ACC/AHA) guidelines recommend that a minimum of 300 adult diagnostic cases and 75 pediatric cases per facility per year be performed to provide adequate care. A case load of at least 200 percutaneous coronary interventions (PCIs) per year, with an ideal volume of 400 cases annually, is recommended.

Facilities performing PCIs without in-house surgical backup are becoming more prevalent. Despite this, national guidelines still recommend that both elective and emergent PCIs be performed in centers with surgical capabilities. Although emergent CABG is infrequent in the stent era, when emergent CABG is required the delays inherent in the transfer of patients to another hospital would compromise the outcomes of these patients.

Although minimal volumes are recommended, no regulatory control currently exists. In a study of volume-outcome relationships published for New York State, a clear inverse relationship between laboratory case volume and procedural mortality and coronary artery bypass graft (CABG) rates was identified. In a nationwide study of Medicare patients, low-volume centers had a 4.2% 30-day mortality, whereas the mortality in high-volume centers was 2.7%. Centers of excellence, based on physician and facility volume as well as overall services provided, may well be the model for cardiovascular care in the future.

Physician Credentialing

The more experience an operator has with a particular procedure, the more likely this procedure will have a good outcome. The American College of Cardiology Task Force has established guidelines for the volume of individual operators in addition to the facility volumes mentioned earlier. The current recommendations for competence in diagnostic cardiac catheterization require a fellow perform a minimum of 300 angiographic procedures, with at least 200 catheterizations as the primary operator, during his or her training.1

In 1999, the American Board of Internal Medicine established board certification for interventional cardiology. To be eligible, a physician has to complete 3 years of a cardiology fellowship, complete a (minimum) of a 1-year fellowship in interventional cardiology, and obtain board certification in general cardiology. In addition to the diagnostic catheterization experience discussed earlier, a trainee must perform at least 250 coronary interventional procedures. Board certification requires renewal every 10 years and initially was offered to practicing interventionalists with or without formal training in intervention. In 2004, the “grandfather” pathway ended, and a formal interventional fellowship is required for board certification in interventional cardiology. After board certification, the physician should perform at least 75 PCIs as a primary operator annually.

The performance of peripheral interventions in the cardiac catheterization laboratory is increasing. Vascular surgeons, interventional radiologists, and interventional cardiologists all compete in this area. The claim of each subspecialty to this group of patients has merits and limitations. Renal artery interventions are the most common peripheral intervention performed by interventional cardiologists, but distal peripheral vascular interventions are performed in many laboratories. Stenting of the carotid arteries looks favorable when compared with carotid endarterectomy. Guidelines are being developed with input from all subspecialties. These guidelines and oversight by individual hospitals will be needed to ensure that the promise of clinical trials is translated into quality patient care.


Indications for Cardiac Catheterization in the Adult Patient

Table 2-1 lists generally agreed on indications for cardiac catheterization. With respect to CAD, approximately 15% of the adult population studied will have normal coronary arteries. Coronary angiography is, for the moment, still consideredthe gold standard for defining CAD. With advances in magnetic resonance imaging and multislice computed tomography, the next decade may well see a further evolution of the catheterization laboratory to an interventional suite with fewer diagnostic responsibilities.

Table 2-1 Indications for Diagnostic Catheterization in the Adult Patient

Coronary Artery Disease
Unstable angina
Postinfarction angina
Angina refractory to medications
Typical chest pain with negative diagnostic testing
History of sudden death
Diagnostic Testing
Strongly positive exercise tolerance test
Early positive, ischemia in > 5 leads, hypotension, ischemia present for > 6 minutes of recovery
Positive exercise testing following after myocardial infarction
Strongly positive nuclear myocardial perfusion test
Increased lung uptake or ventricular dilation after stress
Large single or multiple areas of ischemic myocardium
Strongly positive stress echocardiographic study
Decrease in overall ejection fraction or ventricular dilation with stress
Large single area or multiple or large areas of new wall motion abnormalities
Valvular Disease
Aortic stenosis with syncope, chest pain, or congestive heart failure
Aortic insufficiency with progressive heart failure
Mitral insufficiency or stenosis with progressive congestive heart failure symptoms
Acute orthopnea/pulmonary edema after infarction with suspected acute mitral insufficiency
Diagnostic Testing
Progressive resting LV dysfunction with regurgitant lesion
Decreased LV function and/or chamber dilation with exercise
Adult Congenital Heart Disease
Atrial Septal Defect
Age > 50 with evidence of coronary artery diseaseSeptum primum or sinus venosus defects
Ventricular Septal Defect
Catheterization for definition of coronary anatomy
Coarctation of the Aorta
Detection of collateral vessels
Coronary arteriography if increased age and/or risk factors are present
Acute myocardial infarction therapy—consider primary PCI
Mechanical complication after infarction
Malignant cardiac arrhythmias
Cardiac transplantation
Pretransplant donor evaluation
Post-transplant annual coronary artery graft rejection evaluation
Unexplained congestive heart failure
Research studies with institutional review board review and patient consent

LV = left ventricular.

Patient Evaluation before Cardiac Catheterization

Diagnostic cardiac catheterization in the 21st century is universally considered an outpatient procedure except for the patient at high risk. Therefore, the precatheterization evaluation is essential for quality patient care. Evaluation before cardiac catheterization includes diagnostic tests that are necessary to identify the high-risk patient. An ECG must be performed on all patients shortly before catheterization. Necessary laboratory studies before catheterization include a coagulation profile (prothrombin time [PT], partial thromboplastin time [PTT], and platelet count), hemoglobin, and hematocrit. Electrolytes are obtained along with a baseline determination of blood urea nitrogen (BUN) and creatinine to assess renal function. Urinalysis and chest radiograph may provide useful information but are no longer routinely obtained by all operators. Prior catheterization reports should be available. If the patient had prior PCI or coronary artery bypass surgery, this information must also be available.

Patient medications must be addressed. On the morning of the catheterization, antianginal and antihypertensive medications are routinely continued while diuretic therapy is held. Diabetic patients are scheduled early, if possible. Because breakfast is held, no short-acting insulin is given. Patients on oral anticoagulation should stop warfarin sodium (Coumadin) therapy 48 to 72 hours before catheterization (INR ≤ 1.8). In patients who are anticoagulated for mechanical prosthetic valves, the patient may best be managed with intravenous heparin before and after the procedure, when the warfarin effect is not therapeutic. Low-molecular-weight heparins (LMWHs) are used in this setting, but this is controversial. LMWHs vary in their duration of action, and their effect cannot be monitored by routine tests. This effect needs to be considered, particularly with regard to hemostasis at the vascular access site. Intravenous heparin is routinely discontinued 2 to 4 hours before catheterization, except in the unstable angina patient. Aspirin therapy for angina patients or in patients with prior CABG is often continued, particularly in patients with unstable angina.


Whether the procedure is elective or emergent, diagnostic or interventional, coronary or peripheral, certain basic components are relatively constant in all circumstances.

Patient Monitoring and Sedation

Standard limb leads with one chest lead are used for ECG monitoring during cardiac catheterization. One inferior and one anterior ECG lead are monitored during diagnostic catheterization. During an interventional procedure, two ECG leads are monitored in the same coronary artery distribution as the vessel undergoing PTCA. Radiolucent ECG leads improve monitoring without interfering with angiographic data.

Cardiac catheterization laboratories routinely monitor arterial oxygen saturation by pulse oximetry (SpO2) on all patients. Utilizing pulse oximetry, Dodson and associates demonstrated that 38% of 26 patients undergoing catheterization had episodes of hypoxemia (SpO2 < 90%) with a mean duration of 53 seconds. Variable amounts of premedication were administered to the patients.

Sedation in the catheterization laboratory, either from preprocedure administration or subsequent intravenous administration during the procedure, may lead to hypoventilation and hypoxemia. The intravenous administration of midazolam, 1 to 5 mg, with fentanyl, 25 to 100 μg, is common practice. Institutional guidelines for conscious sedation typically govern these practices. Light to moderate sedation is beneficial to the patient, particularly for angiographic imaging and interventional procedures. Deep sedation, in addition to its widely recognized potential to cause respiratory problems, poses distinct problems in the catheterization laboratory. Deep sedation often requires supplemental oxygen, and this complicates the interpretation of oximetry data and may alter hemodynamics. Furthermore, deep sedation may exacerbate respiratory variation, altering hemodynamic measurements.

Sparse data exist regarding the effect of sedation on hemodynamic variables and respiratory parameters in the cardiac catheterization laboratory. One study examined the cardiorespiratory effects of diazepam sedation and flumazenil reversal of sedation in patients in the cardiac catheterization laboratory. A sleep-inducing dose of diazepam was administered intravenously in the catheterization laboratory; this produced only slight decreases in mean arterial pressure (MAP), pulmonary capillary wedge pressure, and left ventricular (LV) end-diastolic pressure (LVEDP), with no significant changes in intermittently sampled arterial blood gases. Flumazenil awakened the patient without significant alterations in either hemodynamic or respiratory variables.

More complex interventions have resulted in longer procedures. Although hospitals require conscious sedation policies, individual variation in the type and degree of sedation is common. Although general anesthesia is rarely required for adult patients, it is needed more frequently for pediatric procedures. In the future, more complex adult interventions may well require the presence of an anesthesiologist in the catheterization laboratory, similar to the early days of adult coronary intervention.

Right-Sided Heart Catheterization

Clinical applications of right-sided heart hemodynamic monitoring changed greatly in 1970 with the flow-directed, balloon-tipped, pulmonary artery (PA) catheter developed by Swan and Ganz. This balloon flotation catheter allowed the clinician to measure PA pressure (PAP) and pulmonary capillary wedge pressure (PCWP) without fluoroscopic guidance. It also incorporated a thermistor, making the repeated measurement of cardiac output feasible. With this development, the PA catheter left the cardiac catheterization laboratory and entered both the operating room and intensive care unit.

In the cardiac catheterization laboratory, right-sided heart catheterization is performed for diagnostic purposes. The routine use of right-sided heart catheterization during standard left-sided heart catheterization was studied by Hill and coworkers. Two hundred patients referred for only left-sided heart catheterization for suspected CAD underwent right-sided heart catheterization. This resulted in an additional 6 minutes of procedure time and 90 seconds of fluoroscopy. Abnormalities were detected in 35% of the patients. However, management was altered in only 1.5% of the patients. With this in mind, routine right-sided heart catheterization cannot be recommended. Box 2-2 outlines acceptable indications for right-sided heart catheterization during left-sided heart catheterization.

Diagnostic Catheterization Complications

Complications are related to multiple factors, but severity of disease is important. Mortality rates are shown in Table 2-2. Complications are specific for both right- and left-heart catheterization (Table 2-3). Although advances in technology continue, these complication rates are still present today, most likely due to the higher risk patient undergoing catheterization.


Table 2-2 Cardiac Catheterization Mortality Data

Rights were not granted to include this table in electronic media. Please refer to the printed book.

From Pepine CJ, Allen HD, Bashore TM, et al: ACC/AHA guidelines for cardiac catheterization and cardiac catheterization laboratories. Circulation Nov, 84(5): 2213–2247

Definition of Pressure Waveforms—Cardiac Cycle

Right-Sided Heart Pressures

The right-sided heart pressures, as measured in the cardiac catheterization laboratory, consist of the central venous pressure (CVP) or right atrial (RA) pressure (RAP), right ventricular (RV) pressure (RVP), PAP, and PCWP. The CVP consists of three waves and two descents (Fig. 2-1, Box 2-3). The A wave occurs synchronously with the Q wave of the ECG and accompanies atrial contraction. Next, a smaller C wave appears, which results from tricuspid valve closure and bulging of the valve into the right atrium as the right ventricle begins to contract. After this, with the tricuspid valve in the closed position, the atrium relaxes, resulting in the X descent. This is followed by the V wave, which corresponds to RA filling that occurs during RV systole with a closed tricuspid valve. As the RV relaxes, the RVP then becomes less than the RAP, the tricuspid valve opens, and the atrial blood rapidly empties into the ventricle. This is signified by the Y descent.

Beginning in early diastole, the RV waveform reaches its minimum pressure shortly before or as the tricuspid valve opens. During the rapid filling phase of diastole, the ventricular pressure rises slowly and usually an A wave, which signifies atrial contraction, is seen just before the onset of ventricular systole. As ventricular contraction occurs, peak systolic pressure is rapidly reached. Just before the onset of contraction, and after the A wave, the RV end-diastolic pressure (RVEDP) can be determined.

The PAP is usually greater than the RVP during the time the pulmonic valve is closed, during ventricular relaxation and filling. During systole, RVP crosses over PAP by a small margin, causing the pulmonic valve to open, and the ventricle ejects blood into the PA. It is not uncommon for a 5-mm gradient to exist between the RV and PA during peak systolic contraction. The minimal PA diastolic pressure can also be measured just before the onset of contraction, as an estimate of the PCWP; however, the presence of increased pulmonary vascular resistance will invalidate this correlation. With an inflated balloon, the tip of the PA catheter is protected from pulsatile pressures and “looks forward” to the pressure in the pulmonary venous system and the left atrium. This “wedge” pressure shows many of the characteristics of the left atrial (LA) pressure (LAP). The differences between these two waves are considered in the discussion of LAP below.

Left-Sided Heart Pressures

The LA, LV, aortic, and peripheral pressures are commonly measured in the cardiac catheterization laboratory. The LAP can be measured directly if a transseptal catheter is placed. Because this is not commonly done, the PCWP is used to estimate LAP. The LAP has a very similar appearance (A, C, V waves; X, Y descent) to that in the RA, although the pressures seen are about 5 mm Hg higher. The A wave in the RA tracing is normally larger than the V wave whereas the opposite is true in the LA (or PCWP). The PCWP provides reasonable estimations of the LAP, although the waveform is often damped and also delayed in time compared with the LAP (Fig. 2-2).

LV pressure also has many similar characteristics to the RVP, although because this is a thick-walled chamber, the generated pressures are higher than those reached in the RV. The central aortic pressure displays a higher diastolic pressure than that seen in the ventricle due to the properties of resistance in the arterial tree and the presence of a competent aortic valve. The dicrotic notch, which signifies the aortic valve closure, is a prominent feature of the aortic pressure wave in the central aorta. As the site of pressure measurement moves more distally in the arterial tree, there is a progressive distortion of the arterial waveform, usually demonstrated as an increase in systolic pressure. This is thought to be due to the addition of the pressure wave of reflected waves from the elastic arterial wall. Summation of reflected pressure waves has been postulated as a contributing factor in aneurysm formation. Additionally, the rapid propagation of reflected waves along stiff arteries has been advanced as an explanation of the systolic hypertension seen in the elderly. Table 2-4 displays the range of normal pressures on the right and left side of the heart.

Valvular Pathology

Each type of valvular pathology has its own particular hemodynamic “fingerprint,” the character of which depends on the severity of the pathology, as well as its duration.

Stenotic Lesions

To assess the severity of stenotic lesions, the transvalvular gradient as well as the transvalvular flow must be quantified. For a given amount of stenosis, hydraulic principles state that as flow increases, so also will the pressure drop across the orifice. Both the CO and the HR determine flow; it is during the systolic ejection period that flow occurs through the semilunar valves and during the diastolic filling period for the atrioventricular (AV) valves.

Gorlin and Gorlin derived a formula from fluid physics to relate valve area with blood flow and blood velocity:


In general, as a valve orifice becomes increasingly stenotic, the velocity of flow must progressively increase if total flow across the valve is to be maintained. To estimate valve area, flow velocity can be measured by the Doppler principle; however, in the catheterization laboratory, this is not as practical as measuring blood pressures on either side of the valve.

As described by Gorlin, the velocity of blood flow is related to the square root of the pressure drop across the valve:


Stated another way, for any given orifice size, the transvalvular pressure gradient is a function of the square of the transvalvular flow rate. For example, with mitral stenosis, as the valve area progressively decreases, a modest increase in the rate of flow across the valve causes progressively larger increases in the pressure gradient across the valve (Fig. 2-3).