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Historical Perspective of Cardiac Catheterization

In 1844, Claude Bernard passed a catheter into both the right and left ventricles of a horse's heart via a retrograde approach from the jugular vein and carotid artery. He was the first to perform a scientific study of cardiac physiology, and he set the stage for cardiac catheterization as it is known today.

In 1929, in Eberswalde, Germany, a 25-year-old surgical trainee named Werner Forssmann was the first to pass a catheter into the heart of a living person—his own. He passed the catheter into his right atrium via the left antecubital vein under fluoroscopic guidance and then climbed the stairs to the radiology department to undergo a chest radiograph. His efforts were not rewarded but, rather, stimulated considerable opposition and bitter criticism; however, in 1956, he shared the Nobel Prize in medicine with other pioneers of invasive cardiology.

Further developments in invasive cardiology were slow until the work of Andre Cournand and Dickenson Richards, who performed the first comprehensive studies of right heart physiology in humans.

In 1947, Louis Dexter expanded the clinical use of right heart catheterization with studies in patients with congenital heart disease and identified the pulmonary capillary wedge pressure as a useful clinical measurement. By this point, the value of hemodynamic measurements was being fully realized, and further developments came rapidly.

Cardiac catheterization and coronary angiography

Although the technique and accuracy of noninvasive testing continues to improve, cardiac catheterization remains the standard for the evaluation of hemodynamics. Cardiac catheterization helps provide not only intracardiac pressure measurements, but also measurements of oxygen saturation and cardiac output.1 Hemodynamic measurements usually are coupled with a left ventriculogram for the evaluation of left ventricular function and coronary angiography.

Coronary angiography remains the criterion standard for diagnosing coronary artery disease and is the primary method used to help delineate coronary anatomy.2 In addition to defining the site, severity, and morphology of lesions, coronary angiography helps provide a qualitative assessment of coronary blood flow and helps identify collateral vessels. Correlation of the coronary angiogram and left ventriculogram findings permits identification of potentially viable areas of the myocardium that may benefit from a revascularization procedure. Left ventricular function can be further evaluated during stress using atrial pacing, dynamic exercise, or pharmacologic agents.


Preparation of the Patient for Cardiac Catheterization

Before the procedure, the responsible cardiologist should fully explain the risks and benefits to the patient, should obtain written consent, and should answer questions asked by the patient or family. A close physician-patient relationship is important to reduce fears about the procedure. Before the procedure, a complete history, physical examination, complete blood count, blood chemistries, chest radiograph, and ECG should be obtained.

Special attention should be given to identifying patients with insulin-dependent diabetes mellitus, renal insufficiency, peripheral vascular disease, contrast allergy, or long-term anticoagulation use because these conditions are associated with a higher risk of procedure-related complications. Appropriate therapies before the procedure can minimize these risks. For example, adequate hydration before the contrast load will minimize the risk of contrast-induced nephropathy3 and pretreatment with corticosteroids will diminish the likelihood of an allergic reaction to contrast. Evidence is strong that pretreatment with sodium bicarbonate, theophylline, and acetylcysteine are nephroprotective.4

Patients should fast for at least 8 hours before the procedure. Premedication with a mild sedative is common, and some operators administer diphenhydramine or a narcotic.


Catheters and Associated Equipment

Numerous items of disposable equipment are used for the procedure, including various catheters, wires, needles, syringes, introducer sheaths, and stopcocks. Frequently, a Swan-Ganz catheter is used for measuring right heart pressures, collecting blood to measure oxygen saturation in various chambers, and determining cardiac output. Pressure measurements within the left ventricle usually are obtained using a pigtail catheter, and this same catheter is used for left ventricular and aortic angiography. A wide variety of preformed catheter shapes exist for coronary and bypass graft angiography. The outer diameter of a catheter is measured in French units (F); 1 F is 0.33 mm. The inner diameter of the catheter is smaller than the outer diameter because of the thickness of the catheter material.

Decisions about which catheter to use are based on several factors, including (1) the vascular and heart anatomy, (2) the necessity to adequately opacify the coronary arteries and cardiac chambers in different clinical situations, (3) the extent to which the catheter must be manipulated and the desire to limit vascular injury and complications, and (4) whether arterial access is obtained via the femoral artery or via an upper extremity artery. Larger-diameter catheters (7-10F) allow for greater catheter manipulation and excellent visualization, but they have a higher potential for trauma to the coronary or peripheral vasculature. In contrast, smaller catheters (4-6F) are less traumatic and permit earlier ambulation after catheterization, but contrast delivery may be limited in certain situations, thus compromising the quality of the procedure. The 6F diagnostic catheter is used widely for routine angiography because it has a good balance of the necessary requirements.

Although not a necessity, a short vascular access sheath often is used to facilitate arterial access and multiple catheter exchanges, which often are necessary. All catheters and sheaths are advanced over a guidewire to diminish the chance of trauma to the vasculature. A commonly used wire is a 150-cm, 0.035-in J-tipped guidewire.

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Cardiac catheterization sites.

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Pig tail catheter. Image courtesy of Olurotimi Badero, MD and

Indications and Contraindications

Cardiac catheterization is a procedure undertaken for the diagnosis of a variety of cardiac diseases. As with any invasive procedure that is associated with important complications, the decision to recommend cardiac catheterization must be based on a careful evaluation of the risks and benefits to the patient.

General indications for cardiac catheterization

Indications for cardiac catheterization are as follows:

  • Identification of the extent and severity of coronary artery disease and evaluation of left ventricular function
  • Assessment of the severity of valvular or myocardial disorders such as aortic stenosis and/or insufficiency, mitral stenosis and/or insufficiency, and various cardiomyopathies to determine the need for surgical correction
  • Collection of data to confirm and complement noninvasive studies
  • Determination of the presence of coronary artery disease in patients with confusing clinical presentations or chest pain of uncertain origin

Contraindications to cardiac catheterization

With the exception of patient refusal, cardiac catheterization has no absolute contraindications. Clearly, the risk-to-benefit ratio must be considered because a procedure associated with some risk should be contraindicated if the information derived from it is of no benefit to the patient. Relative contraindications are as follows:

  • Severe uncontrolled hypertension
  • Ventricular arrhythmias
  • Acute stroke
  • Severe anemia
  • Active gastrointestinal bleeding
  • Allergy to radiographic contrast
  • Acute renal failure
  • Uncompensated congestive failure (patient cannot lie flat)
  • Unexplained febrile illness and/or untreated active infection
  • Electrolyte abnormalities (eg, hypokalemia)
  • Severe coagulopathy

Note that many of these factors can be corrected before the procedure, thereby lowering the risk. This always should be considered unless the procedure is being performed in an emergency situation.

Technique and Approach

In the early days of cardiac catheterization, access to the arterial system was obtained by direct exposure of the brachial artery and insertion of the catheters under direct visualization. After the procedure, the arteriotomy and then the skin were sutured closed. Although this classic brachial approach still is used by some operators, the majority of procedures now are performed using a percutaneous approach from the femoral, radial, brachial, or axillary artery. Right heart catheterization now is commonly performed from the femoral, internal jugular, or subclavian veins using percutaneous access methods.

Arterial access from the upper extremity (modified Sones method)

The classic brachial artery technique was developed by Mason Sones, MD and thus often is referred to as the Sones method. Although surgical exposure of the brachial artery still is used by some operators, percutaneous access now is used commonly. A 5F or 6F sheath is inserted into the brachial artery, and catheters are maneuvered through the axillary and subclavian arteries into the ascending aorta. Coronary angiography is performed using either a Sones catheter, which requires deflection of the catheter tip off the aortic valve cusps, or a variety of preformed catheter shapes.

Alternatively, access can be obtained from the axillary artery or radial artery. Access from the axillary artery avoids the potential for injury to the median nerve and provides a better platform for compression of the artery against the humerus to obtain hemostasis. Obtaining access from the radial artery is increasing in popularity. Performing an Allen test before the procedure is necessary to insure continuity of the arterial arch in the hand should the radial artery occlude during or after the procedure. Standard catheters may be used from the radial approach, and several new shapes have been developed to facilitate easy cannulation of the coronary arteries. The main advantage of the radial approach is a low incidence of serious vascular complications and the ability to mobilize the patient quickly after the procedure. The disadvantages of the radial approach are a longer learning curve for the operator and occasional severe arterial spasm, which impairs manipulation of the catheter.

In general, arterial access from the upper extremity is preferred if the patient has important iliac or femoral artery atherosclerosis, prior bypass grafting of these same vessels, or severe obesity rendering the normal landmarks for access difficult to appreciate.

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Cardiac catheterization sites.

Arterial access from the lower extremity

The common femoral artery is the only access site used in the lower extremity. Catheters used for performing coronary angiography via the femoral artery were developed by Melvin Judkins, MD, and thus, the method often is referred to as the Judkins technique. This widely used method requires separate preformed catheters for the right and left coronary arteries. A pigtail catheter frequently is used for measuring left heart pressures and performing a left ventriculogram.

Proper access to the common femoral artery is critical for this technique. Vascular complications are increased if the arterial puncture is made either above or below the common femoral artery. The main advantages to this method are its ease and substantial safety record. The main disadvantage is the need for an extended (2-6 h) period of bedrest after completion of the procedure. Several types of arterial closure devices now are available that provide rapid hemostasis and shorten the period of bedrest considerably. However, complication rates with these closure devices are similar to conventional manual compression.

Because of the smaller-diameter arteries in the upper extremity and thus the more occlusive nature of the catheters, anticoagulation is required for the procedure and unfractionated heparin is used frequently. Many operators also administer heparin when access is from the femoral artery, especially if the procedure is prolonged and several catheter exchanges are required.

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Femoral access. Image courtesy of Olurotimi Badero, MD and

Additional vascular approaches used for cardiac catheterization

Rarely, severe atherosclerotic disease may affect both the upper and lower extremities and preclude vascular access at the usual sites. Access to the descending aorta can be obtained via a translumbar approach, and coronary angiography can be performed using the standard catheter shapes.

Catheterization of the left atrium and left ventricle can be performed using a transseptal approach. This technique involves puncture of the intra-atrial septum with a needle followed by advancement of a catheter into the left atrium and left ventricle. Transseptal catheterization is used in patients with mechanical aortic valves or if obtaining a true left atrial pressure is necessary. This technique requires a firm understanding of cardiac radiographic anatomy to avoid puncturing adjacent structures such as the free wall of the right atrium, the coronary sinus, or the aortic root. If left ventricular hemodynamics are necessary in patients with mechanical valves in both the aortic and mitral position, a direct left ventricular puncture may be the only option.




Intraprocedure Complications


Transient hypotension may occur when large volumes of ionic contrast agents are administered and often is more prominent if the ventricular filling pressures are low. This usually requires no treatment. Other causes of important hypotension require quick investigation and treatment. Ventricular filling pressures can be quickly measured and corrected by volume administration if low. Concurrent drug therapies, such as intravenous nitroglycerin, should be considered and regulated if necessary. Occult blood loss from a retroperitoneal hematoma should be evaluated if hypotension persists, and a vasopressor agent should be administered if central perfusion is critically compromised.5

Congestive heart failure

Due to the osmotic effects of the contrast agents and fluid administration during the procedure, congestive heart failure may develop, especially in patients with marginal left ventricular function. This may require aborting the procedure and instituting treatment with oxygen, diuretics, and nitroglycerin.

Chest pain

Chest pain may occur, especially during coronary angiography. Some patients are sensitive to the vasodilator effects of the contrast and may experience mild chest discomfort during each dye injection, even in the absence of underlying coronary artery disease. However, in patients with important coronary artery disease, myocardial ischemia with pain and ST-segment changes may occur. This frequently resolves with sublingual or intravenous nitroglycerin, but persistent pain with evidence of myocardial ischemia may indicate the need for urgent revascularization.6


Minor arrhythmias (eg, atrial or ventricular premature beats, brief episodes of supraventricular tachycardia) are common and usually resolve without treatment. Ventricular tachycardia or fibrillation is a rare occurrence but requires prompt defibrillation.

Major Complications

The risk of a major complication during diagnostic cardiac catheterization is less than 1-2%. The risk-to-benefit ratio strongly favors performance of this procedure as part of the evaluation and treatment of potentially fatal or lifestyle-limiting cardiac disease in appropriately selected patients. In a large series reported from the Society of Cardiac Angiography and Interventions Registry, the multivariate predictors of complications were shock, acute myocardial infarction (MI) within the past 24 hours, renal insufficiency, cardiomyopathy, aortic and mitral valve disease, poorly compensated congestive heart failure, severe hypertension, and unstable angina.


Death rates from cardiac catheterization have declined steadily over the past 15 years. The incidence of procedure-related death is now approximately 0.08%. A high-risk subgroup can be defined based on characteristics identified in multiple large series. The risk of death varies with age; patients older than 60 years and younger than 1 year have an increased mortality rate from catheterization. New York Heart Association functional class IV is associated with nearly a 10-fold increase in mortality compared with classes I and II. A similar increase in risk is observed in those with severe narrowing of the left main coronary artery and poor left ventricular function (ie, left ventricular ejection fraction <30%).

Patients with valvular heart disease, renal insufficiency, insulin-dependent diabetes mellitus, peripheral vascular disease, cerebrovascular disease, or pulmonary insufficiency also have an increased incidence of death and major complications from left heart catheterization. Mortality is especially high in those with preexisting renal insufficiency who have further deterioration of renal function within 48 hours after the procedure, particularly when dialysis is required.

Myocardial infarction

The current risk rate for procedure-related myocardial infarction (MI) is less than 0.03%. The risk of precipitating an MI is influenced by patient-related and technique-related variables. Risk factors that predispose patients to an MI during the procedure include (1) recent unstable angina or non–Q-wave infarction, (2) severe of coronary artery disease, and (3) the presence of important comorbidities.

In high-risk patients, serial ECGs and cardiac enzyme measurements may be considered following the procedure.


The procedure-related stroke rate was as high as 0.23% in 1973, but it has decreased to 0.06% in contemporary registries. Although incidence of stroke has decreased, it is one of the most devastating complications of cardiac catheterization. A stroke may not always be apparent during the procedure. The first symptoms may develop hours after the procedure is completed when atherosclerotic debris loosened from plaques in the proximal aorta finally break free and embolize. Maintain a very high level of suspicion, and evaluate patients after the procedure to assess any neurologic changes.6

High-osmolar contrast agents in the carotid arteries may cause transient neurologic deficits.


Cardiac catheterization is a sterile procedure, thus, the incidence of infections is very low. The American College of Cardiology/American Heart Association task force does not mandate full surgical scrubbing and attire for the femoral approach, but it does recommend it for the brachial approach, which has a 10-fold higher infection risk (0.62% vs 0.06%). Special care should be used in patients with femoral bypass grafts because these patients are prone to life-threatening infections. To eliminate the risk of patient-to-patient infection, the laboratory should be cleaned between procedures and multiuse drug vials should be avoided. Fever occurring after the procedure usually is not due to infection, but rather, it is due to phlebitis or often is unexplained. Pyrogen reactions as a cause for fever are now very uncommon because almost all of the catheters used are single-use disposable devices.

Allergic reaction

Allergic reactions during cardiac catheterization may be precipitated by local anesthetics, iodinated contrast agents, protamine sulfate, and latex exposure. Allergies to local anesthetic usually occur with the older agents (eg, procaine) rather than the newer agents. These reactions actually may be vasovagal in origin, caused by preservatives in the older ester agents. Some centers perform skin testing prior to the procedure to avoid reactions.

Reactions to iodinated contrast agents occur in approximately 1% of patients. This reaction is not a true anaphylactic reaction but, rather, the result of direct complement activation and thus is an anaphylactoid reaction. Symptoms include sneezing, urticaria, angioedema, bronchospasm, and profound hypotension. The risk of a contrast reaction is increased in patients with other atopic disorders, multiple other allergies, or history of a prior reaction to contrast agents.

To decrease the risk of contrast reactions, high-risk patients should be premedicated with corticosteroids and a nonionic contrast agent should be used. Some physicians also administer H1 and H2 receptor blockers. Severe reactions usually are reversed by an intravenous injection of dilute epinephrine.

Protamine sulfate is now rarely given to reverse the anticoagulant effect of heparin. However, if it is used, serious allergic reactions with profound hypotension can occur. Such reactions are reported to be more frequent in patients with diabetes who previously received neutral protamine Hagedorn (NPH) insulin. The prior long-term exposure to protamine is thought to sensitize the patient to protamine.

Latex-induced allergic reactions are being recognized more frequently. They usually are local, although systemic reactions may occur. These can be avoided by the use of latex-free materials in sensitive patients.

Renal dysfunction

Renal dysfunction is a potential complication of any angiographic procedure. Approximately 5% of patients experience a transient rise in plasma creatinine concentration (>1 mg/dL) after contrast exposure. Patients with preexisting renal insufficiency, multiple myeloma, dehydration, or those taking nephrotoxic medications are at an increased risk. The risk of contrast-induced nephropathy is not increased in patients with diabetes who have normal renal function, but patients with diabetes who have impaired renal function are at high risk. Creatinine levels usually begin to rise 2-3 days after contrast exposure and slowly return to baseline within 7 days. Contrast-induced renal failure usually is nonoliguric, but dialysis occasionally is necessary. Approximately 1% of patients eventually require long-term dialysis.

Contrast nephropathy can be avoided by limiting contrast volume to the minimum required for completion of the procedure. Low-osmolar contrast agents should be used because these appear to have less renal toxicity than high-osmolar agents.

Although many therapies have been tried, the mainstay of prevention is adequate hydration with normal or half-normal saline before and after the procedure. A recent study demonstrated that premedication with N -acetylcysteine (Mucomyst) may prevent worsening of renal function in patients with renal insufficiency.

Systemic cholesterol embolization is another cause of renal failure after cardiac catheterization. This occurs in approximately 0.15% of patients, mostly in those with severe atherosclerosis. Renal failure in these patients tends to develop slowly over weeks compared with contrast-induced nephropathy, which develops over several days. The hallmark of cholesterol embolization is peripheral embolization resulting in livedo reticularis, foot pain, and purple toes. Episodic hypertension, transient eosinophilia, and hypocomplementemia usually precede the signs of embolization. Treatment is purely supportive, and approximately half of these patients progress to renal failure.


Arrhythmias and conduction disturbances can occur during cardiac catheterization. Most are of little clinical significance except for asystole or ventricular fibrillation. Atrial fibrillation usually is well tolerated but may provoke hemodynamic decompensation in patients with severe coronary disease, hypertrophic cardiomyopathy, aortic stenosis, or severe systolic dysfunction.

Prompt treatment by cardioversion prevents progressive decompensation due to the arrhythmia. Ventricular tachycardia and/or fibrillation occurs in approximately 0.4% of patients. These arrhythmias may result from catheter manipulations or the injection of contrast directly into a coronary artery or bypass graft. Vigorous contrast injection into the conus branch of the right coronary artery, which supplies the right ventricular outflow tract, has a high likelihood of provoking ventricular fibrillation.

Bradycardia occurs commonly at the end of a right coronary artery injection performed using high-osmolar agents. Forceful coughing usually helps clear the contrast from the coronary arteries, supports aortic pressure, and restores normal cardiac rhythm. Bradycardia and hypotension also may occur during a vasovagal reaction. Other symptoms of a vasovagal reaction are yawning, nausea, sweating, and hypotension. The 2 most common times for this to develop are during the administration of local anesthesia in the groin and after the application of pressure to obtain femoral artery hemostasis. Intravenous fluids and atropine are the treatments for a vasovagal reaction.

For related information, see Medscape's Atrial Fibrillation and Cardiac Rhythm Management Resource Centers.

Vascular Complications

Complications at the catheter insertion site are among the most common problems observed after cardiac catheterization. These include acute thrombosis, distal embolization, arterial dissection, pseudoaneurysm, or bleeding.

Predisposing factors for arterial thrombosis include a small vessel lumen, peripheral vascular disease, diabetes mellitus, and female sex. Arterial thrombosis is a greater concern with brachial access, and thus, heparin is a requirement. Consultation with a vascular surgeon is necessary in case paresthesia or reduced distal pulses occur following catheterization.


Bleeding is the most common vascular complication. This may simply result in a local hematoma of little clinical significance. However, severe blood loss may develop if bleeding occurs in the retroperitoneal space. Unexplained hypotension and a decreasing hematocrit level should suggest the possibility of a retroperitoneal hematoma. Abdominal sonography or CT scanning usually is diagnostic.

Pseudoaneurysm is another potential cause of important groin bleeding and must be recognized. A pseudoaneurysm develops if a connection persists between a hematoma and the arterial lumen. It presents as a pulsatile mass, sometimes with a systolic bruit. The diagnosis is confirmed by duplex ultrasonography. Management often is conservative, using prolonged compression or thrombin injection in selected patients. Surgical correction is necessary for large pseudoaneurysms with a wide connection to the parent artery.

Bleeding from the arterial puncture may track into the adjacent venous puncture, forming an arteriovenous fistula and a continuous bruit. Many of these are small and resolve spontaneously. Surgical repair is required to fix enlarging fistulae before hemodynamic compromise develops.

Hemodynamic Data

Mitral and Aortic Stenosis

Determining the severity of a valvular stenosis based on the pressure gradient and flow across the valve is an important aspect of the evaluation in patients with valvular heart disease. The measurement of the pressure gradient alone often is insufficient to distinguish significant from insignificant valvular stenosis. In patients with aortic stenosis, a true transvalvular pressure gradient should be obtained whenever possible. Although measuring the gradient between the left ventricle and the femoral artery is convenient, downstream augmentation of the pressure signal and delay in pressure transmission between the proximal aorta and femoral artery may alter the pressure waveform and introduce errors. This is especially important in patients with a low pressure gradient and cardiac output.

In many patients, left ventricular-femoral artery pressure gradients may suffice as an estimate of the severity of aortic stenosis, especially if the gradient is high and the cardiac output is preserved. The normal aortic valve area is 2.6-3.5 cm2 in adults. Valve areas of 0.8 cm2 or smaller represent severe aortic stenosis.

In patients with mitral stenosis, the valve gradient usually is measured using the left ventricular and pulmonary capillary wedge pressure. The pulmonary wedge pressure tracing must be realigned with the left ventricular tracing for accurate mean gradient determination. However, the most accurate method uses the left atrial and left ventricular pressure. This requires a transseptal catheterization approach.

The normal mitral valve area is 4-6 cm2, and severe mitral stenosis is present with valve areas smaller than 1.0-1.2 cm2.

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Aortic stenosis tracings. Image courtesy of Olurotimi Badero, MD and

Left Ventriculography

This technique is used to define the anatomy and function of the left ventricle and related structures in patients with congenital, valvular, coronary, and myopathic heart disease.7 It provides valuable information about global and segmental left ventricular function, mitral regurgitation, ventricular septal defect, and hypertrophic cardiomyopathy. The ventriculogram findings can be analyzed qualitatively and quantitatively. The analysis should use a normal sinus beat if possible because ectopic and postectopic beats yield inaccurate information about ventricular function. The ejection fraction may be estimated visually or computed using the area-length method to derive actual end-diastolic and end-systolic volume estimates. Segmental wall motion also can be visually graded as normal, hypokinetic, akinetic, or dyskinetic or quantified using several computer algorithms.

Mitral regurgitation

The severity of mitral regurgitation can be graded based on the amount of contrast regurgitation from the left ventricle through the incompetent mitral valve into the left atrium, using the opacification of the left atrium as a guide. The opacification is graded as follows:

  • Grade 1+ (mild): Regurgitation essentially clears with each beat and never opacifies the entire left atrium.
  • Grade 2+ (moderate): Regurgitation does not clear with 1 beat and opacifies the entire left atrium after several beats.
  • Grade 3+ (moderately severe): The left atrium is opacified completely and achieves equal opacification to the left ventricle.
  • Grade 4+ (severe): The entire left atrium is opacified within 1 beat and becomes denser with each beat, with associated refluxing into the pulmonary veins during systole.


Acute severe mitral regurgitation. Image courtesy of Olurotimi Badero, MD and

Regurgitant fraction

An estimate of the degree of valvular regurgitation may be obtained by computing the regurgitant fraction (RF). The difference between the angiographic stroke volume and the forward stroke volume is the regurgitant volume. Angiographic stroke volume is computed from the left ventriculogram findings, and forward stroke volume is derived from cardiac output as determined by the Fick or thermodilution method and the heart rate. The RF is that portion of the angiographic stroke volume that does not contribute to the net cardiac output. RF is computed as the regurgitant stroke volume divided by angiographic stroke volume.

  • An RF of 20% is approximately equivalent to grade 1+ regurgitation described visually.
  • An RF of 21-40% is equivalent to grade 2+ regurgitation.
  • An RF of 41-60% is equivalent to grade 3+ regurgitation.
  • An RF of 60% or more is equivalent to grade 4+ regurgitation.



Click to see larger picture Media file 1: The heart catheterization.

The heart catheterization.

Click to see larger picture Media file 2: Acute severe mitral regurgitation. Image courtesy of Olurotimi Badero, MD and

Acute severe mitral regurgitation. Image courtesy of Olurotimi Badero, MD and

Click to see larger picture Media file 3: Cardiac catheterization sites.

Cardiac catheterization sites.

Click to see larger picture Media file 4: Femoral access. Image courtesy of Olurotimi Badero, MD and
Click to see larger picture Media file 5: Mitral stenosis tracings. Image courtesy of Olurotimi Badero, MD and
Click to see larger picture Media file 6: Left main coronary artery dissection from catheter. Image courtesy of Olurotimi Badero, MD and

Left main coronary artery dissection from catheter. Image courtesy of Olurotimi Badero, MD and

Click to see larger picture Media file 7: Pig tail catheter. Image courtesy of Olurotimi Badero, MD and


left heart cardiac catheterization, left cardiac catheterization, coronary angiography, coronary angiogram, left ventriculogram, Judkins technique, heart catheter, Sones method, intracardiac pressure measurement, oxygen saturation, cardiac output, coronary artery disease, myocardial disorders, aortic stenosis, aortic insufficiency, mitral stenosis, mitral insufficiency, cardiomyopathy



Percutaneous Transluminal Coronary Angioplasty

Robert Vincent Kelly, MD, Consulting Staff, Division of Interventional Cardiology, University of North Carolina Hospital
George A Stouffer III, MD, Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center; Jeb Burchenal, MD, Assistant Professor of Medicine, University of Colorado School of Medicine; Consulting Staff, South Denver Cardiology Associates; James Maddux, MD, Consulting Staff, Department of Cardiology, International Heart Institute
Contributor Information and Disclosures

Updated: Aug 23, 2006

Overview and Historical Perspective

Since the first human percutaneous transluminal coronary angioplasty (PTCA) procedure was performed in 1977, the use of this procedure has increased dramatically, becoming one of the most common medical interventions performed. The technique, originally developed in Switzerland by Andreas Gruentzig, has transformed the practice of revascularization for coronary artery disease (CAD). Initially used in the treatment of patients with stable angina and discrete lesions in a single coronary artery, coronary angioplasty has multiple indications today, including unstable angina, acute myocardial infarction (MI), and multivessel CAD. With the combination of sophisticated equipment, experienced operators, and modern drug therapy, coronary angioplasty has evolved into an effective nonsurgical modality for treating patients with CAD.

In 2000, more than 500,000 percutaneous coronary interventions (PCIs) were performed in the United States. By 2004, the number exceeded 650,000 in the United States with rapid growth in other developed countries. Worldwide, the number of PCIs continues to increase annually.

Clinical indications and contraindications to PTCA

  • Indications
    • Stable angina
    • Unstable angina
    • Anginal equivalent (eg, dyspnea, arrhythmia, dizziness/syncope)
    • Acute myocardial infarction
    • Objective evidence of reversible ischemia on the following:
      • Resting electrocardiogram
      • Positive result on exercise stress test
      • Positive result on exercise or pharmacologic scintigraphy
      • Stress echocardiography
      • Holter monitoring
  • Contraindications - Significant comorbidities (relative contraindication)

Angiographic indications and contraindications to PTCA

  • Indications - Hemodynamically significant lesion in a vessel serving viable myocardium (vessel diameter >1.5 mm)
  • Relative contraindications
    • Left main stenosis or left main equivalent stenosis (Coronary artery bypass graft [CABG] surgery is still the preferred treatment for left main stenosis. However, this area is rapidly evolving toward safe and feasible PCI options.)
    • Chronic total occlusion (CTO) with the following:
      • No proximal stump visible
      • Extensive bridging collaterals present
    • Diffusely diseased small-caliber artery or vein graft
    • Other coronary anatomy not amenable to percutaneous intervention

Recent advances in guidewires, stents, and devices to cross chronically occluded arteries are evolving so that more patients with CTOs are now being successfully treated percutaneously.

Improvements in catheter technique and the development of new devices, wires, stents, drug-eluting stents, and medications have occurred parallel to advances in the understanding of cardiovascular physiology, the pathogenesis of atherosclerosis, and the body's response to vascular injury. Intracoronary stents and atherectomy devices were developed to increase the success rate of, and decrease the complications associated with, conventional balloon dilation and to expand the indications for revascularization. These devices have enabled the interventionalist to safely treat more complex coronary lesions and restenosis. Now, stents have evolved to a level where the problems of restenosis seen with bare metal stents are a less frequent occurrence after drug-eluting stents are implanted. At the same time, advances in imaging techniques, including intravascular ultrasonography (IVUS), fractional flow reserve evaluation, and Doppler flow analysis, have improved the understanding of coronary plaquemorphology,

plaque vulnerability, and coronary physiology. Furthermore, many of these technologies are able to help identify those patients who will benefit most from PCI or from medical therapy. Adjunctive pharmacologic therapies aimed at preventing acute reocclusion have also improved the safety and efficacy of coronary angioplasty.

The growth of PCIs has been remarkable and will likely continue as new technologies have resulted in improved outcomes. Since 1994, the use of intracoronary stents has risen dramatically, and now with drug-eluting stents, stents are used in more than 80% of PCI cases in the United States. Innovations in PCIs over the last 2 decades have been paralleled by a dramatic reduction in 30-day death, MI, and target vessel revascularization rates.


Mechanisms and Devices of Angioplasty


Mechanism of angioplasty

The original description of angioplasty by Dotter and Judkins described enlargement of the vessel lumen through a mechanism of atheromatous plaque compression. Plaque compression is now understood to account for very little of the observed improvement following balloon angioplasty. Most of improvement in luminal diameter following balloon angioplasty results from stretching of the vessel wall by the balloon. Balloon inflation actually results in overstretching of the vessel wall and partial disruption of not only the intimal plaque but also the media and adventitia, resulting in enlargement of the lumen and the outer diameter of the vessel. Axial redistribution of plaque material also contributes to improvements in lumen diameter. Atherectomy devices and, subsequently, intracoronary stents were developed, in part, to decrease the early and late loss in luminal diameter observed with conventional balloon angioplasty.

Devices for coronary interventions

Balloon angioplasty

The primary device for balloon angioplasty is the balloon-tipped catheter. Several different balloon catheter designs exist (over-the-wire, monorail, fixed wire) with balloon materials that have different compliance characteristics allowing various degrees of expansion with increasing pressure.

Irrespective of the balloon design, a steerable guidewire precedes the balloon into the artery and allows navigation through a considerable portion of the coronary tree. The development of balloon catheters that bend, allowing easy advancement through tortuous vascular segments (trackability), and that have increased shaft stiffness (pushability), allowing the catheter to be forced through stenotic lesions, has increased their versatility significantly. Another evolving feature of catheter design has been a reduction in the diameter of the deflated balloon, allowing easier passage through very stenotic lesions. Over the last decade, improvements in catheter design have been partially responsible for the improved success rates of PCIs. The balloon catheter also serves as an adjunctive device for many other interventional therapies, including atherectomy and coronary stents.

Atherectomy devices and coronary stents

As a result of technical challenges, as described above, suboptimal clinical outcomes, and the significant rates of restenosis following percutaneous coronary artery balloon angioplasty, 2 innovative types of devices were developed and studied in large-scale clinical trials. The idea behind atherectomy devices was to physically remove atheroma, calcium, and excess cellular material from the site of a coronary occlusion or stenosis. Mechanical and laser-based approaches are described below. An alternative approach developed at about the same time was intracoronary stent placement, based on the notion that permanent implantation of a scaffold to hold open the coronary artery at the site of an intervention would improve outcomes.

As is discussed below, long-term outcomes from atherectomy alone have been disappointing and little better than balloon angioplasty in most cases. Stents, particularly stents coated with materials to reduce inflammatory and cell growth responses, have resulted in greatly improved outcomes. Atherectomy is still used for specific, niche indications, but the most common intracoronary device used today is a stent.

Rotational atherectomy

The rotational atherectomy catheter (Rotablator) is a device designed for the removal of plaque from coronary arteries. This device, which has a diamond-studded burr at its tip, rotates at about 160,000 rpm and is particularly well suited for ablation of calcific or fibrotic plaque material (see Image 1).

Unlike other atherectomy devices that rely on tissue cutting, the rotational atherectomy device relies on plaque abrasion and pulverization. Rotational atherectomy is successful in 92-97% of these cases, with a low incidence of major complications. It causes dislodgement of particles into the microcirculation, which occasionally may lead to infarction and no reflow. Currently, the use of rotational atherectomy is largely confined to fibrotic or heavily calcified lesions that can be wired but not crossed by a balloon catheter.

The Excimer Laser, Rotational Atherectomy, and Balloon Angioplasty Comparison (ERBAC) Study showed rotational atherectomy was associated with a higher short-term success rate than balloon angioplasty (90% vs 80%), but major ischemic complications and repeat revascularization were higher 6 months after treatment (46% vs 37%).

In a recent meta-analysis that compared rotational atherectomy, cutting balloon angioplasty, and laser atherectomy failed to show any significant difference in mortality, major adverse cardiovascular events (MACE), or revascularization rates in patients treated with either rotational atherectomy, laser, or cutting balloon angioplasty when compared with balloon angioplasty alone. In some cases, rotational atherectomy was actually associated with an increase in periprocedural MI. However, none of these trials compared stent-related outcomes. In fact, many of these devices may be used to facilitate stent delivery in complex lesions, especially when balloon angioplasty alone has failed.

Directional coronary atherectomy/laser atherectomy

Since 1987, directional coronary atherectomy (DCA) has been used to debulk coronary plaques. A steel fenestrated cage housing a cup-shaped blade is positioned against the coronary lesion by a low-pressure positioning balloon, allowing any protruding plaque to be removed. Atherectomy is typically followed by balloon dilation and stenting. The acute gain, therefore, is a combination of the removal of atheromatous plaque and radial displacement of plaque from dilation. Major complication rates associated with directional atherectomy are low and similar to conventional balloon angioplasty. Other complications (eg, distal embolization of plaque, transient side-branch occlusion, coronary vasospasm, the no reflow phenomenon, non–Q-wave MI) are greater with DCA than with balloon angioplasty. Because of the increased complication rates and the greater technical demands of DCA compared with balloon angioplasty or stenting, the use of DCAs has greatly decreased in recent years.

Although initial excitement about the development of laser atherectomy was considerable, it is not used widely because of the technical demands of this device and no clear improvements in outcome over therapy with other devices.

Intracoronary stents

Intracoronary stents have been used widely since the early 1990s. Many different stents are available and differ in composition (eg, stainless steel, tantalum, chromium cobalt), architectural design (slotted tube vs coiled wire), and mode of implantation (balloon expandable vs self-expanding). In the last 3 years, the development of drug-eluting stents (DESs) has revolutionized coronary intervention to the extent that balloon angioplasty and bare metal stents did in the 1980s and 1990s.

Today, multiple types of DESs are available, with the 2 most commonly used in the United States being the sirolimus (Cypher) stent (SES) and the paclitaxel (Taxus) stent (PES). These stents comprise a metal stent with a polymer that elutes a drug that reduces neointimal hyperplasia. Newer stent platforms are evolving with more uniform drug delivery systems and with the ability for some stents to store different drugs for local intracoronary delivery (eg, to improve coronary artery blood flow and myocardial perfusion during primary angioplasty). SES and PES have both been extensively tested in a wide spectrum of coronary lesions, all of which have demonstrated significant reductions in restenosis and target lesion revascularization (TLR) rates when compared with bare metal stents. Any differences between the SES and PES appear to be small, with some registries and meta-analyses suggesting fewer Q wave MIs and subacute thromboses with SES than PES.

Studies with SES, PES, and many newer DESs are ongoing and include efforts to improve stent technology and drug deliverability and to define outcomes in every range of PCI setting: stable and unstable lesions, small vessels, vein grafts, CTOs, primary PCI, and comparing DES technologies with CABG in left main and diabetes patients with multivessel CAD.

Intracoronary imaging techniques

Coronary angiography provides a display of luminal narrowing in multiple planes and is useful in guiding coronary interventions. However, angiography cannot provide information about the vessel wall, which is where the atherosclerotic process resides. IVUS was developed to provide information about the plaque and the vessel wall in addition to the degree of luminal narrowing. IVUS provides a tomographic cross-section of the vessel, allowing operators to gather significant qualitative and quantitative information that is potentially valuable in assessing stenosis severity and the true extent of atherosclerotic involvement (see Image 5).
Identification of the lumen border and the media-adventitia interface form the key landmarks during interpretation. Plaque can be distinguished from the lumen by differences in echogenicity. In addition to providing information about the amount and distribution of plaque, IVUS can identify features ofplaque composition, such as calcification and lipid collections, that may not be appreciated by angiography alone. Frequent uses of IVUS include the assessment of indeterminate lesions and the evaluation of adequate stent deployment. Recent developments in ultrasonography (virtual histology) and other technologies (optical coherence tomography, plaque thermography) have led to ways of characterizing and identifying vulnerable segments of plaque, which may pose a risk for future cardiac events. This is being examined in the ongoing PROSPECT trial.

Intracoronary Doppler flow wires are able to characterize coronary physiology and to estimate the impact of lesion severity on coronary blood flow. This technology measures the ratio of maximal myocardial flow in a stenotic area to the maximum myocardial flow in the same territory if the stenosis were absent. (This is performed during a period of maximal hyperemia induced by an injection of intravenous or intracoronary adenosine).

Comparison of pressure distal to a lesion with aortic pressure enables determination of fractional flow reserve (FFR). FFR measurement below 0.75 during maximal hyperemia is consistent with a hemodynamically significant lesion and this may help determine whether to perform PCI in an angiographic intermediate lesion. Clinical data, namely the DEFER study, support using this approach, with a low event rate seen in medically managed patients with angina and an FFR measurement greater than 0.75. This form of physiologic lesion assessment is also useful for defining optimal stenting, assessing the angiographic severity of jailed side branch lesions, helping guide the decision for mutivessel PCI or CABG in multiple intermediate lesions, and assessing the severity of instant restenosis (see Image 6). FFR measurements have excellent correlation with IVUS analysis, especially when determining lesion severity, such as in ambiguous left mainartery anatomy.



Early registries of balloon angioplasty results showed complication rates that were much higher than those typically observed today. With advancements in technique, devices, and adjuvant medical therapy, percutaneous transluminal coronary intervention is now associated with mortality and emergency bypass rates of less than 1%. The rate of nonfatal MI following coronary angioplasty ranges from 5-15%, whereas the rate following stent placement is 2-5%. Restenosis after balloon angioplasty requiring a second revascularization procedure is a major limitation occurring in about 30-50% of patients, depending on the definition of restenosis applied. However, with drug-eluting stents (DESs), restenosis rates are now less than 10%.

Reduction in the complications of balloon angioplasty has been complemented by improvements in the acute success rate. Registries, such as the National Heart, Lung, and Blood Institute (NHLBI) Coronary Angioplasty Registry from the early 1980s, reported primary success rates of 61%. Today, success rates are as high as 95% following conventional balloon angioplasty and are even higher with the use of DESs and adjunctive pharmacotherapy.

Acute complications

The mechanism by which balloon angioplasty or stenting improves luminal diameter is associated with significant local trauma to the vessel wall, which can in turn lead to occlusive complications in a minority of patients. Coronary artery dissection typically results from the vessel injury secondary to balloon expansion. Animal and postmortem studies have shown that localized dissection at the site of balloon expansion is a common occurrence detected angiographically in as many as 50% of patients immediately following the procedure. Such small dissections probably are necessary to obtain adequate lumen expansion, rarely interfere with antegrade blood flow, and rarely are important. Angiographic follow-up typically shows no residual evidence of a dissection as early as 6 weeks after angioplasty in most of the cases studied. However, larger dissections can lead to complications.

Abrupt vessel closure may occur in as many as 5% of balloon angioplasty cases and typically develops when compression of the true lumen by a large dissection flap occurs, thrombus formation, superimposed coronary vasospasm, or a combination of these processes. The presence of large coronary dissections immediately after balloon angioplasty is associated with a 5-fold increase in the risk of abrupt closure. This underscores the importance of a good postprocedure angiographic result on clinical outcomes.

Today, the use of intracoronary stents and new antiplatelet drugs has decreased the incidence of abrupt closure significantly (to <1%). Microembolization of plaque debris or adherent thrombus may also cause acute complications during angioplasty and may contribute to postprocedure cardiac enzyme elevation and chest pain in some patients. In less than 1% of patients undergoing angioplasty, microembolization of the platelet-rich thrombus may cause diffuse distal arteriolar vasospasm secondary to the release of vasoactive agents, resulting in the phenomenon of no-reflow. This complication is difficult to treat but may respond to intracoronary calcium channel antagonists, adenosine, or nitroprusside. Patients undergoing balloon angioplasty of saphenous vein graft lesions and primary angioplasty in the setting of acute MI with a large amount of adherent thrombus are at greatest risk of distal embolization.

Coronary perforation or rupture following balloon angioplasty is very rare (<1%) and typically is associated with the use of ablative devices or oversized balloons.


Following balloon angioplasty or stent implantation, the vessel wall undergoes a number of changes. Platelets and fibrin adhere to the site within minutes of vessel injury. Within hours to days, inflammatory cells infiltrate the site and vascular smooth muscle cells begin to migrate toward the lumen.

The vascular smooth muscle cells then hypertrophy and excrete an extensive extracellular matrix. During this period of vascular smooth muscle cell proliferation, endothelial cells colonize the surface of the lumen and regain their normal function. Over the course of several weeks to months, multiple forces interact to cause remodeling of the vessel wall with either a decrease in lumen diameter (negative remodeling) or an increase in lumen diameter (positive remodeling). The amount of late loss in lumen diameter is dependent on the amount of neointimal proliferation and the degree of remodeling following intervention. After 6 months, the repair process stabilizes and the risk of restenosis decreases significantly (see Image 7).

Several studies have shown that the lumen diameter or area after treatment is one of the major predictors of restenosis. The use of coronary artery stents has decreased the rate of restenosis by improving the acute gain achieved and by minimizing negative remodeling. Depending on the definition used, angiographic restenosis has been reported in as many as 50% of patients within 6 months after balloon angioplasty, necessitating repeat target vessel revascularization (TVR) in approximately 20-30% of patients. Today, DESs have reduced restenosis rates to less than 10%. Poststent lumen diameter and lesion complexity are still the major predictors of restenosis with these newer stents.

While DESs have significantly reduced restenosis events, concerns of stent thrombosis with these newer stents still exist. In fact, the rate of thrombosis with DES is virtually identical to that for bare metal stent (BMS) (0.4-1.5%). The biggest factor contributing to stent thrombosis is interruption of antiplatelet therapy. Another important factor is final stent diameter and area. Underdeployment or incomplete apposition of the DES may also increase the risk for stent thrombosis. This is extremely important because acute and subacute stent thrombosis often have a fatal outcome. Late stent thrombosis is another consideration. DES may take up to 4 years to endothelialize on the coronary vessel wall and discontinuing antiplatelet therapy may expose these patients to an increased risk for sent thrombosis over time.

In some clinical situations (such as before urgent noncardiac surgery where antiplatelet therapy may have to be discontinued and in patients with known or potential medicine compliance issues), implanting a BMS may be preferred during PCI rather than using a DES.


Comparison of Angioplasty With Other Treatments

Stable angina (PCI vs medical therapy)

Early trials (VA, ACME, RITA II, ACIP) demonstrated the benefit of percutaneous transluminal coronary angioplasty (PTCA) over medical therapy for symptomatic angina in single and multivessel coronary artery disease (CAD), with improvements in symptoms, reduction in need to take antianginal medications, improvement in exercise duration, and similar survival rates to medical therapy.

In the Randomized Intervention in the Treatment of Angina (RITA-II) study, 1018 patients with stable angina were randomized to balloon angioplasty or medical therapy, and their cases were followed for a mean of 2.7 years. Death or definite myocardial infarction (MI) occurred in 6.3% of the balloon angioplasty patients compared with 3.3% of the medical patients (P =0.02), but only 44% of the deaths were actually due to heart disease. Angina improved in both groups, but a 16.5% absolute excess of grade 2 or worse angina occurred in the medical group 3 months following randomization.

Angioplasty patients had a greater improvement in exercise duration compared with the medically treated group, and 23% of the medical group required revascularization during follow-up. During follow-up, 7.9% of the angioplasty patients required bypass surgery, compared with 5.8% of the medically treated patients. Although the patients in RITA-II were asymptomatic or mildly symptomatic, emphasizing that most had severe anatomic CAD is important; 62% had multivessel CAD, and 34% had important disease of the proximal left anterior descending artery. Thus, RITA-II demonstrated that balloon angioplasty results in better control of ischemic symptoms and improves exercise capacity compared with medical therapy, but balloon angioplasty is associated with an increased incidence of the combined end point of death and MI.

The Asymptomatic Cardiac Ischemia Pilot (ACIP) study suggested that revascularization either by surgery or by angioplasty compares favorably with medical therapy in patients with myocardial ischemia with or without angina.

In the Atorvastatin Versus Revascularization Treatment (AVERT) trial, 341 patients with stable CAD symptoms, normal left ventricle (LV) function, and class I or II angina were assigned randomly to balloon angioplasty or medical therapy with atorvastatin. After 18 months of follow-up, 13% of the medically treated group had ischemic events compared with 21% of the angioplasty group (P =0.048), suggesting that, in low-risk patients with stable CAD, aggressive lipid-lowering therapy may be as effective as balloon angioplasty in reducing ischemic events. Based on the limited data available from randomized trials comparing medical therapy with balloon angioplasty, considering medical therapy seems prudent for the initial management of most patients with Canadian Cardiovascular Society Classification Class I and II symptoms and reserving percutaneous or surgical revascularization is appropriate for patients with more severe symptoms and ischemia.

Overall, medical therapy is recommended as first-line therapy in stable angina patients unless the following occur: a change in symptom severity, early positive stress test result, failed medical therapy, coronary anatomy, and/or LV dysfunction or patient age concerns that provide an indication for cardiac catheterization and percutaneous coronary intervention (PCI) of coronary artery bypass graft (CABG).

Stable angina (PCI vs surgical revascularization)

Two prospective clinical trials have evaluated balloon angioplasty versus surgery for revascularization of isolated left anterior descending coronary artery disease. Using a combined endpoint (cardiac death, MI, or refractory angina requiring revascularization by surgery), the Medicine, Angioplasty, or Surgery Study (MASS) showed, after 3 years of follow-up, that endpoint events occurred in 24% of angioplasty patients, 17% of medical patients, and 3% of surgical patients. However, overall survival was similar among the 3 groups.

The other trial compared balloon angioplasty versus bypass surgery with an internal mammary artery graft to the left anterior descending artery and also showed no difference in survival during follow-up. Although 94% of the angioplasty patients and 95% of the bypass patients were free of limiting symptoms, those treated by angioplasty required more antianginal drugs. At median follow-up of 2.5 years, 86% of the surgery patients versus 43% of angioplasty patients were free from late events (P <0.01), and this difference primarily was due to restenosis requiring a second revascularization procedure. Emphasizing that balloon angioplasty was used in these trials rather than stent placement is important; thus, current rates of restenosis with stenting should be lower.

Five large (>300 patients) randomized trials comparing balloon angioplasty with bypass surgery in patients with multivessel CAD have been conducted (see Table 1). The major findings from these trials have a consistent theme. In appropriately selected patients with multivessel CAD, the incidence of death or MI is similar whether balloon angioplasty or bypass surgery is used, but more patients treated with angioplasty require a second revascularization procedure. In the Bypass Angioplasty Revascularization Investigation (BARI), 5-year survival was 86.3% for those assigned to angioplasty versus 89.3% for those assigned to surgery (P= 0.19), and 5-year freedom from Q-wave MI was 78.7% and 80.4%, respectively. However, after 5-years of follow-up, 54% of those assigned to angioplasty required an additional revascularization procedure compared with only 8% of those assigned to surgery.

Table 1. Comparison of Surgical Therapy and Coronary Angioplasty

Open table in new window

End Point Pocock et al* Pocock et al BARI Study
Death (%) 0.3 1.9 2.8 3.1 10.7 13.7
Death or MI 4.5 7.2 8.5 8.1 11.7 10.9
Repeat CABG 1.4 16.0II 0.8 18.3II 0.7 20.5II
Repeat CABG or PTCA 3.6 30.5II 3.2 34.5II 8.0 54.0II
More than mild angina 6.5 14.6II 12.1 17.8II
End Point Pocock et al* Pocock et al BARI Study
Death (%) 0.3 1.9 2.8 3.1 10.7 13.7
Death or MI 4.5 7.2 8.5 8.1 11.7 10.9
Repeat CABG 1.4 16.0II 0.8 18.3II 0.7 20.5II
Repeat CABG or PTCA 3.6 30.5II 3.2 34.5II 8.0 54.0II
More than mild angina 6.5 14.6II 12.1 17.8II

*Meta-analysis of the results of 3 trials at 1 year: Patients with single-vessel disease were studied (Pocock, 1995).

† Meta-analysis of the results of 3 trials at 1 year: Patients with multivessel disease were studied (Pocock, 1995).

‡Reported results are for the 5-year follow-up. Patients with multivessel disease were studied.

§ Coronary artery bypass graft

II P <0.05

In a similar manner, the 3-year follow-up of the Argentine Randomized Trial of Percutaneous Transluminal Coronary Angioplasty Versus Coronary Artery Bypass Surgery in Multivessel Disease (ERACI) showed that freedom from combined cardiac events was significantly better for bypass surgery (77% vs 47%, P <0.001) compared with angioplasty. However, no differences occurred in overall and cardiac mortality rates or in the frequency of MI between the 2 groups. Patients who had bypass surgery were free of angina more frequently (79% vs 57%) and had fewer additional revascularization procedures (6% vs 37%) than patients treated with angioplasty.

An exception to equivalent mortality rate results of balloon angioplasty and bypass surgery in multivessel disease exists for patients with diabetes mellitus. Among diabetic patients in the BARI trial, 5-year survival was 65.5% in those treated by balloon angioplasty compared with 80.6% for those having bypass surgery (P =0.003). The improved survival with surgery was due to a reduced cardiac mortality rate (5.8% vs 20.6%, P =0.0003) and was confined to those receiving at least 1 internal mammary artery graft. Better survival among diabetic patients with multivessel disease treated with bypass surgery rather than angioplasty also was observed in a large retrospective study.

The major limitations of balloon angioplasty have been acute vessel closure and restenosis. Early studies with intracoronary stents showed that these devices were highly effective for treating or preventing acute or threatened vessel closure and, thus, avoiding emergency bypass surgery. In 1994, 2 randomized trials, STRESS and BENESTENT, demonstrated that coronary stenting of de novo lesions in native vessels reduced angiographic restenosis by approximately 30% compared with conventional balloon angioplasty. Stenting produces a larger lumen diameter than conventional balloon angioplasty immediately following the procedure (acute gain) and at follow-up (net gain), resulting in less restenosis.

The use of stenting, instead of balloon angioplasty, was compared with bypass surgery for the treatment of multivessel CAD in the Arterial Revascularization Therapies Study (ARTS). After 1 year of follow-up, no difference was noted between the groups in the rate of death, stroke, or MI. Event-free survival was better in the surgery group compared with the stent group (87.8% vs 73.8%), and only 3.5% in the surgery group required a second revascularization procedure.

In comparison, 16.8% in the stent group needed a second revascularization procedure, but this was considerably lower than the 37% and 54% who needed a second revascularization when treated by balloon angioplasty in the ERACI and BARI trials, respectively. Overall, patients with diabetes and those who received incomplete surgical revascularization did worse. The cost of the initial revascularization procedure was $4212 less for those treated by stent placement, but, because of the need for more repeat revascularization procedures in the stent group, the cost advantage for stenting was reduced to $2973 after 1 year.

The stent or surgery (SoS) trial compared BMS and CABG in similar patients and reported a 21% 2-year target vessel revascularization (TVR) rate in stent patients versus 6% in CABG patients, with a similar death and MI rate in both groups. However, the SoS trial had a higher noncardiac death rate in the PCI arm, thought to be attributed to a type II error that may have affected the study results. Few stent patients in the SoS trial received glycoprotein (GP) IIb/IIIa receptor inhibitors. Still, this and the ARTS study do point to the safety of PCI treatment in multivessel disease. Mortality risk is low (discounting the noncardiac deaths) and the rates of need for repeat TVR have been halved.

Drug-eluting stents and coronary artery bypass graft

The use of DES was compared with CABG in stable angina populations in the ARTS II trial, which was a registry comparing sirolimus (Cypher) stent (SES) with the PTCA and CABG arms of the ARTS I trial. SESs were associated with an 8% MACE rate (13% for CABG in ARTS I) and an 8.5% TVR rate (4% for CABG and 21% for PTCA in ARTS I). The 1-year MACE rate was 10.5% for SES patients. Overall, DESs are equivalent to CABGs except in patients with diabetes where conflicting data exist. DES data show similar outcomes in the ARTS and AWESOME trials for patients with diabetes mellitus. The ongoing FREEDOM trial will compare DES and CABG in patients with diabetes and multivessel CAD. The SYNTAX trial is currently comparing paclitaxel (Taxus) stent (PES) and CABG in multivessel CAD that includes left main disease. COMBAT is a similar trial design using SES.

Acute coronary syndromes

The management of patients with non–Q-wave MI and unstable angina has changed considerably over the past 5 years. Before the widespread use of stents and GP IIb/IIIa receptor inhibitors, conventional balloon angioplasty in this subgroup of patients was associated with substantial risks, including MI (as much as 9%), restenosis (as much as 50%), need for emergency coronary bypass surgery (as much as 12%), and death (as much as 5%). The optimal strategy in patients presenting with acute coronary syndromes remains a controversial issue in contemporary cardiology. Several studies have investigated the use of a conservative strategy versus an early invasive strategy of revascularization for patients with unstable coronary syndromes.

The Veterans Affairs Non–Q-Wave Infarction Strategies in Hospital (VANQWISH) trial compared an invasive strategy with conservative medical treatment in patients with non–Q-wave MI. The rates of death or nonfatal MI were higher in the invasive strategy group than in the conservative strategy group before hospital discharge, at 1 month, and at 1 year. Criticisms of this study include the following: (1) the exclusion of patients at very high risk, (2) the lack of current aggressive medical therapies, (3) a high rate of crossover to angiography in the conservative arm, (4) a higher surgical mortality rate than expected compared with contemporary standards, and (5) the observation that most of the complications at 30 days occurred in patients who underwent coronary artery bypass surgery and very few occurred in patients who underwent balloon angioplasty.

In contrast to the VANQWISH trial, 3 randomized studies found that an early invasive approach in patients with acute coronary syndromes was associated with improved outcomes.

The Thrombolysis in Myocardial Infarction (TIMI) IIIb study showed less ischemia, shorter hospital stays, fewer readmissions, and fewer symptoms in patients treated by an early invasive approach. The Fragmin and Fast Revascularization during Instability in Coronary artery disease (FRISC) II trial prospectively randomized 2457 patients to an early invasive treatment versus a noninvasive treatment strategy and used intracoronary stenting. At 6 months, the composite endpoint of death or MI was higher in the noninvasive treatment group than in patients undergoing an early invasive approach to management. Additionally, symptoms of angina and hospital readmissions in the noninvasive arm were twice that observed using the invasive treatment strategy. More recently, the Randomized Intervention in the Treatment of Angina (RITA-III) study reported improved outcomes with early invasive therapy.

Data from the Treat angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy-Thrombolysis in Myocardial Infarction (TACTICS-TIMI) 18 trial showed that the primary endpoint of death, MI, or rehospitalization at 6 months occurred in 19.4% of the conservative group versus 15.9% of the invasive group (P =0.0025) with the incidence of death and/or MI occurring in 9.5% versus 7.3%, respectively (P <0.05). Patients who had a positive troponin, who had ST segment changes, who were older than age 65 years, and especially women with elevated brain natriuretic peptide (BNP) and C-reactive protein (CRP) levels did particularly better from an early invasive strategy.

Based on these results, the American Heart Association/American College of Cardiology (AHA/ACC) guidelines recommended that an early (within 48 h) invasive approach be used to treat patients presenting with chest pain who have positive cardiac biomarkers or abnormal ECG. The guidelines have also included patients with unstable angina, worsening heart failure and/or mitral regurgitation, LV systolic dysfunction, ventricular tachycardia (VT), prior PCI and/or CABG, and a high-risk positive stress test result as indications for early catheterization. In lower-risk patients, invasive or medical therapy provides similar outcomes.

Acute myocardial infarction

The recognition that intracoronary thrombosis is the primary mechanism of vessel occlusion in acute MI and that prompt restoration of vessel patency provides significant clinical benefit has lead to the development of aggressive new treatments for this disorder.

Thrombolytic therapies, such as front-loaded tissue plasminogen activator (t-PA), reteplase (r-PA), and tenecteplase (TNK), open approximately 80% of infarct-related vessels within 90 minutes, but only 50% will have normal (TIMI grade 3) flow. In addition, 10% of vessels opened by thrombolysis either reocclude or are the source for recurrent symptoms of angina. Because of these limitations to thrombolytic therapy, several randomized trials have evaluated mechanical revascularization, so-called primary angioplasty, in the setting of acute MI.

A recent analysis of 23 trials confirms the superiority of primary angioplasty over fibrinolytic therapy in terms of adverse event and mortality reduction both in the short and long term. Overall, primary PCI was associated with significant reductions in death (P =0.0002), recurrent MI (P <0.0001), reinfarction (P <0.0001), and the combined end point of death, MI, and stroke.

In the situation where patients are transferred from outside hospitals, primary angioplasty is often preferred to on-site fibrinolytic therapy for patients with the following: expected door-to-balloon time less than 90 minutes and symptom duration less than 3 hours, symptom duration more than 3 hours, cardiogenic shock, contraindications to fibrinolytic therapy, and age older than 75 years. The use of thrombolytic therapy and then referral for intentional PCI (facilitated PCI) has not been shown to be superior to primary PCI and may actually worsen outcomes with increased risk of stroke and bleeding (ASSENT 4).

Recent data suggest that early use of GP IIb/IIIa inhibitors may help to achieve earlier infarct vessel patency and better outcomes during PCI. Whether this is so for all of these agents is being assessed in several studies. A recent meta-analysis has shown that abciximab is associated with a 46% reduction in death and reinfarction in primary PCI patients and the AHA/ACC STEMI guidelines currently recommend early use of abciximab in these patients. When fibrinolytic therapy is given but fails to produce ST resolution, then immediate PCI (rescue PCI) is recommended.

Some of the most important considerations in providing effective primary PCI relate to the logistic issues and barriers that are known to exist: the PCI system or network, ambiguity of leadership and organization, protocols/care, pathways/interfacility transfer, and reimbursement issues are the main areas of contention. Studies of the US primary PCI sites that are considered the best (those sites who deliver door-to-balloon times consistently within 90 minutes, which is currently in about 5% of the US MI population) have identified the key determinants of shorter door-to-balloon times as the following: ECG being performed within 10 minutes, the ED independently making the decision to engage the catheterization laboratory team, and interdisciplinary teamwork.

The key factor for effective primary PCI is timely reperfusion therapy. Recent studies from the National Registry of Myocardial Infarction (NRMI) data have shown that shortening door-to-balloon time to less than 90 minutes is associated with a reduction in mortality. In certain situations, timely reperfusion may be best achieved with fibrinolytic therapy if delays are likely in accessing primary PCI.

From a procedural perspective, because primary PCI involves a thrombotic plaque, the potential risk of more complications exists, especially no reflow and distal embolization. These patients should achieve final TIMI 3 flow. Stenting plus GP IIb/IIIa inhibition has been shown to improve outcomes, reducing TVR and MI rates in comparison with balloon angioplasty. The use of adjunctive antithrombotic approaches, including early GP IIb/IIIa inhibition use and mechanical thrombectomy or embolic protection devices, is the subject of ongoing debate. Important issues remain as to which type of stent to use (DES or BMS), timing of antiplatelet therapy (both IV and oral), and whether a facilitated approach (using fibrinolytic therapy or GP IIb/IIIa inhibition) in a shorter time frame might provide better outcomes for certain patients.


Adjunctive Therapies in the Catheterization Laboratory

Aspirin and heparin have been the traditional adjunctive medical therapies for patients undergoing coronary angioplasty and have been shown to decrease complications following the procedure. Since 1994, several new antithrombotic drugs have been developed that have advantages over standard heparin therapy. Although an effective anticoagulant, heparin has several limitations, including variable pharmacokinetics requiring careful monitoring, inhibition by substances released from activated platelets, and an inability to inhibit fibrin-bound thrombin.

To address these limitations, several direct thrombin inhibitors have been developed. Hirudin and bivalirudin (Angiomax) were evaluated in 2 multicenter trials. Both were found to be slightly better than heparin in preventing ischemic complications during balloon angioplasty, but they had no effect on restenosis rates. Low molecular weight heparins are also being substituted for standard heparin in some centers in patients with acute coronary syndromes and during coronary interventions. Newer factor IX and factor Xa inhibitors are being evaluated as potential alternative anticoagulants. However, recent trials have failed to show a significant difference in efficacy of factor Xa inhibition compared with unfractionated heparin (UFH).

In the early days of stenting, multiple antiplatelet agents and warfarin were used in an attempt to prevent stent thrombosis, but thrombosis continued to occur in approximately 6% of patients.

With an improved understanding of how stents should be deployed, warfarin is no longer necessary. Patients receiving stents are now treated with a combination of aspirin and clopidogrel, and, with this therapy, the incidence of subacute thrombosis is approximately 1%. Today, this combination is given to all stent patients for 4 weeks after a bare metal stent (BMS) and 6-12 months when a drug-eluting stent (DES) was used. Issues remain as to whether the duration of aspirin and clopidogrel should be longer in DES patients. The authors advocate that aspirin should be maintained for life unless bleeding contraindications restrict its use. Other considerations with antiplatelet therapy during PCI include the cost of clopidogrel, the proper loading dose, and timing of the initial dose relative to cardiac catheterization.

In elective situations, clopidogrel is most effective when given prior to PCI. In acute situations, this may not be practical and clopidogrel is often given after PCI. Concerns still exist in relation to risk of bleeding and platelet transfusion requirements in patients taking clopidogrel who require urgent CABG. However, as emergent CABG is rare, there may be time to risk-stratify patients and to give clopidogrel before cardiac catheterization. If CABG is required, the effect of clopidogrel usually diminishes within 5 days.

Another important consideration is the dose of clopidogrel. If given 2 hours prior to PCI, 600 mg is recommended; if given more than 2 hours prior to PCI, then 300 mg is recommended. Some centers have even given 900 mg instead of 600 mg. At present, the ACC/AHA guidelines recommend giving 300 mg up to 6 hours prior to PCI. Development of newer intravenous antiplatelet therapies with shorter half lives may help to overcome these issues. Aspirin 325 mg should be given prior to all PCI and then maintained at 81 mg daily.

All types of percutaneous coronary interventions result in disruption of the coronary endothelium, which leads to platelet activation. Activated platelets bind to the vessel wall (adhesion) and to each other (aggregation) and release numerous vasoactive compounds. Aspirin blocks the cyclooxygenase pathway and reduces thrombotic complications after balloon angioplasty. However, despite heparin and aspirin therapy, thrombotic complications are not eliminated. Further studies identified the importance of the GP IIb/IIIa receptor, which binds fibrinogen and mediates the cross-linking of platelets and platelet aggregation.

The introduction of GP IIb/IIIa receptor inhibitors has had a major influence on current treatment strategies in the catheterization laboratory. Abciximab, tirofiban, and eptifibatide have all been shown to reduce ischemic complications in patients undergoing balloon angioplasty and coronary stenting. In primary PCI, GP IIb/IIIa receptor inhibitors have also been shown to improve flow and perfusion and to reduce adverse events. Abciximab may improve outcomes in patients when given prior to their arrival in the catheterization lab for primary PCI. A recent meta-analysis of GP IIb/IIIa inhibitor trials showed a significant reduction in early mortality rates when these agents are used during coronary intervention. The combined end point of death or MI was also reduced significantly at 30 days. Thus, these agents are effective at reducing ischemic complications of PCIs. However, they have not been shown to improve outcome in saphenous vein graft (SVG) PCI.



Click to see larger picture Media file 1: Percutaneous transluminal coronary angioplasty (PTCA). The rotational atherectomy catheter (Rotablator) is a device designed for the removal of plaque from coronary arteries. This device, which has a diamond-studded burr at its tip, rotates at about 160,000 rpm and is particularly well suited for ablation of calcific or fibrotic plaque material.

Percutaneous transluminal coronary angioplasty (PTCA). The rotational atherectomy catheter (Rotablator) is a device designed for the removal of plaque from coronary arteries. This device, which has a diamond-studded burr at its tip, rotates at about 160,000 rpm and is particularly well suited for ablation of calcific or fibrotic plaque material.

Click to see larger picture Media file 2: Percutaneous transluminal coronary angioplasty (PTCA). TRISTAR stent.

Percutaneous transluminal coronary angioplasty (PTCA). TRISTAR stent.

Click to see larger picture Media file 3: Percutaneous transluminal coronary angioplasty (PTCA). NIR stent.

Percutaneous transluminal coronary angioplasty (PTCA). NIR stent.

Click to see larger picture Media file 4: Percutaneous transluminal coronary angioplasty (PTCA). Wallstent.

Percutaneous transluminal coronary angioplasty (PTCA). Wallstent.

Click to see larger picture Media file 5: Example of an intravascular ultrasound (IVUS) image in percutaneous transluminal coronary angioplasty (PTCA).

Example of an intravascular ultrasound (IVUS) image in percutaneous transluminal coronary angioplasty (PTCA).

Click to see larger picture Media file 6: Mechanism of restenosis following percutaneous transluminal coronary angioplasty (PTCA).

Mechanism of restenosis following percutaneous transluminal coronary angioplasty (PTCA).

Click to see larger picture Media file 7: Fractional flow ratio (FFR). Pressure wire is advanced across left anterior descending (LAD) stenosis and intracoronary adenosine is given. FFR ratio is recorded at baseline and then after adenosine push is given. Here, LAD lesion and FFR postadenosine is shown.

Fractional flow ratio (FFR). Pressure wire is advanced across left anterior descending (LAD) stenosis and intracoronary adenosine is given. FFR ratio is recorded at baseline and then after adenosine push is given. Here, LAD lesion and FFR postadenosine is shown.


percutaneous transluminal coronary angioplasty, PTCA, coronary artery disease, CAD, bare metal stent, BMS, coronary artery bypass surgery, CABG, unstable angina, drug-eluting stents, DES, myocardial infarction, MI, percutaneous coronary interventions, PCI, target vessel revascularization, TVR, rotational atherectomy, directional coronary atherectomy, laser atherectomy, balloon angioplasty, intracoronary stents, stable angina, surgical revascularization, coronary angioplasty, fibrinolytic therapy, primary angioplasty, primary PCI



Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA)
Ravi H Dave, MD, Associate Professor of Medicine, University of California at Los Angeles David Geffen School of Medicine; Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Contributor Information and Disclosures

Updated: Jan 28, 2009



Percutaneous pericardiocentesis was introduced during the 19th century.FrankSchuhfirst described this procedure in 1840. By the 20th century, percutaneous pericardiocentesis became a preferred technique for the treatment of patients with pericardial effusion or for diagnostic purposes.

Before the advent of 2-dimensional echocardiography, the procedure used a blind-subxiphoid approach. Serious complications were not uncommon (eg, injury to liver, myocardium, coronary arteries, lungs). Because 2-dimensional echocardiography permits direct visualization of cardiac structures and adjacent vital organs, the procedure now is performed with minimal risk. Since 1979, echo-guided pericardiocentesis has been the preferred initial procedure for the diagnosis and treatment of most pericardial effusions. The technique has been modified and refined in the past 22 years. Percutaneous pericardiocentesis now is the procedure of choice for the safe removal of pericardial fluid. Whenever possible, this procedure should be performed by a surgeon or cardiologist trained in invasive techniques.


An increase in production or a decrease in drainage of pericardial fluid can cause pericardial effusion. Increased production can be due to inflammation of the pericardium, usually the visceral pericardium. Typically, the amount of pericardial effusion is larger when caused by lymphatic or venous obstruction. Accumulation of more than 20-30 mL of fluid in the pericardial sac is usually abnormal, and an increase in the pericardiac/cardiac silhouette is detectable when at least 250 mL of fluid accumulates in the pericardial cavity.

The rate of pericardial fluid accumulation is critical. As the pericardium stretches, a large effusion that develops slowly produces no hemodynamic effects until it is massive. A case of subacute cardiac tamponade with 2000 mL of pericardial fluids has been reported with no significant hemodynamic effect because of the gradual accumulation of pericardial fluid.1 Hemodynamic instability can result from rapid collection of fluid.

Hemopericardium can occur as a result of coagulation abnormalities, postsurgical complications, anticoagulation therapy, dissecting aortic aneurysm, or myocardial rupture (eg, in acute myocardial infarction [MI] or traumatic injury). Chylopericardium is a pericardial effusion of chyle, which is often associated with irritation of the pericardium as well (acute or chronic pericarditis). The primary form is rare, and the secondary chylopericardium may be due to radiation, subclavian thrombosis, infections (eg, tuberculosis), mediastinal tumors, following cardiac and aortopulmonary surgeries, or any process that damages the thoracic ducts. Chylopericardium has been reported even following minimally invasive mitral valve repair.2

Pneumopericardium is a rare finding, which has very broad etiologies such as chest trauma, following medical interventions, fistula formation, and a variety of gas-forming infections. Tension pneumopericardium is associated with tamponade and hemodynamic instability and needs immediate attention.


United States

The common etiologic factors are acute idiopathic pericardial effusion, iatrogenic (eg, postsurgical, drug-induced), chronic idiopathic pericardial effusion, malignancy, post – myocardial infarction (Dressler syndrome), uremia, infection, and radiation.


In some of the developing countries tuberculosis may be the most common cause (generally an extrapulmonary presentation in HIV positive patients) and may account for 70% of all cases.3  


Since the advent of 2-dimensional echocardiography, the morbidity and mortality rates have been reduced. A review of 1127 echocardiography-guided pericardiocentesis that were performed during more than 20 years at a major tertiary care center showed a procedural success rate of 97% overall, with a total complication rate of 4.7% (major, 1.2%; minor, 3.5%). This rate may be different from one institute to another, but echocardiographic-guided pericardiocentesis is considered an overall safe procedure with minimal complication and mortality rates.



The signs and symptoms depend on the amount of pericardial fluid present and the duration of disease. A patient can be asymptomatic when fluid accumulates very slowly or symptomatic when it accumulates very rapidly (eg, trauma, rupture of myocardium after myocardial infarction). An incidental finding of effusion may be found on 2-dimensional echocardiography images, chest CT scans, chest MRIs, or other imaging results. Symptoms of pericardial effusion include the following:

  • Chest pain is a presenting symptom when inflammation is the cause or when effusion is severe. Patients with diseases such as malignancy or chronic renal failure may be pain free.
  • Dyspnea commonly occurs with cardiac tamponade.
  • Cough usually occurs with bronchial encroachment of the pericardium.
  • Fever is associated with infectious or inflammatory causes.
  • Hoarseness of the voice can occur from compression of the recurrent laryngeal nerve by the enlarging pericardial sac.
  • Hiccups generally occur from esophageal compression or irritation of the vagus or phrenic nerves.



Findings upon physical examination depend on the size of the effusion and the accumulation rate of pericardial fluid. Generally, no physical findings exist if the effusion is very small. Large effusions can cause significant hemodynamic instability by impairing ventricular filling. Patients may have generalized discomfort from a large effusion. Other findings include the following:

  • Tachycardia usually occurs due to increased venous pressure and decreased blood pressure, which indicates hemodynamically significant pericardial effusion.
  • Tachypnea may develop in acute situations (eg, cardiac tamponade).
  • Jugular venous distention is visible in large pericardial effusion and loculated effusion compressing the right atrium or ventricle.
  • Narrow pulse pressure can occur in patients with significant pericardial effusion.
  • Although pulsus paradoxus is a classic finding in patients with pericardial effusion, pulsus paradoxus also can occur in patients with obstructive lung diseases.
  • Pericardial friction rub with a small effusion is most suggestive of pericarditis with secondary effusion.
  • Elevated central venous pressure occurs from increased pressure in the pericardial space and the ventricles. This condition usually is associated with hypotension.
  • The Ewart sign is another potential finding. In the late 1800s,WilliamEwartdescribed a different method of identifying pericardial effusion by physical examination. Pericardial fluid compresses the adjacent lung, producing dullness to percussion, tactile fremitus, and egobronchophony at the angle of the left scapula. This is termed the Ewart sign. Massive cardiomegaly and left pleural effusion can produce a similar finding with dullness in the left axillary area. Most clinicians use chest radiographs and 2-dimensional echocardiography findings for diagnosis of pericardial effusion and to differentiate between pericardial effusion and massive cardiomegaly and left pleural effusion. This sign is only of historic importance.
  • Of note, posterior pericardial effusions can occur following cardiothoracic surgery and can be difficult to detect clinically (see Imaging Studies).
  • In a retrospective literature analysis of patients with pericardial effusion, the presence of cardiac tamponade was associated with 5 features: (1) symptoms of dyspnea, (2) tachycardia, (3) pulsus paradoxus of greater than 10 mm Hg, (4) elevated jugular venous pressure, and (5) cardiomegaly on chest radiograph.4



A small asymptomatic effusion may be found incidentally in 8-15% of patients and in as many as 43% of healthy pregnant women. In general, most of the causes of pericarditis can also cause the accumulation of fluid in the pericardial sac. In addition to these etiologies, other conditions, such as rupture of a left ventricular (LV) aneurysm, may give a large pericardial effusion with minimal or no inflammation of the pericardium.

In the Mayo Clinic registry with 1127 echocardiography-guided pericardiocenteses, cardiothoracic surgery together with malignancy and perforation from catheter-based procedures accounted for nearly 70% of all therapeutic pericardiocenteses performed.5 Obviously, this pattern can be different at other institutes depending on the number of cardiothoracic surgeries performed at the institute, number and type of cancer patients, and many other factors. The pattern of etiologies of moderate-to-large pericardial effusion is not the same as pericarditis. For example, hypothyroidism is not a common cause of pericarditis, but it is a known etiology of large chronic pericardial effusion.6 The etiology of pericarditis is idiopathic, viral, or autoimmune in most cases.

A 10-year prospective survey from France reported on 114 patients requiring emergency drainage for cardiac tamponade, showed that malignant disease was the primary cause of medical tamponade (74 patients [65%]), followed by viral history (11 patients [10%]) and intrapericardial bleeding due to anticoagulation treatment (4 patients [3%]). One-year mortality was 76.5% in patients with malignant disease and 13.3% in those without malignant disease.7

Most of the causes of pericardial effusion are as follows:

  • Idiopathic
  • Infectious
    • Bacteria (eg, staphylococci, streptococci, pneumococci, Haemophilus influenzae, Mycoplasma species, Neisseria species, Borrelia burgdorferi, Chlamydia species, Legionella species, Salmonella species, Mycobacterium tuberculosis, Mycobacterium avium).
    • Viral (eg, coxsackievirus, adenovirus, Epstein-Barr virus, echovirus, cytomegalovirus, infectious mononucleosis, parvovirus B19, influenza, mumps, varicella, hepatitis B, HIV)
    • Fungal (eg, histoplasmosis, aspergillosis, blastomycosis, coccidioidomycosis, Candida species, Nocardia species)
    • Rickettsial organisms
    • Parasitic (toxoplasmosis, amebiasis)
  • Neoplasm
    • Metastatic (eg, lung or breast carcinoma, lymphoma, leukemia, melanoma)
    • Primary (eg, rhabdomyosarcoma, lipoma, teratoma, fibroma, fibrosarcoma, angioma, angiosarcoma, mesothelioma)
    • Early and late post – myocardial infarction, rupture of ventricular aneurysm, dissecting aortic aneurysm
  • Drugs
    • Procainamide
    • Hydralazine
    • Warfarin
    • Heparin
    • Thrombolytics
    • Methysergide
    • Isoniazid
    • Cyclosporine
  • Autoimmune disorders
  • Trauma
    • Blunt
    • Penetrating
    • Iatrogenic (eg, perforation caused by catheter insertion or pacemaker implantation, status post cardiopulmonary resuscitation)
  • Other
    • Hypothyroidism
    • Amyloidosis and autoimmune diseases
    • Chylopericardium
    • Uremia
    • Radiation
    • Pneumopericardium
    • Post cardiothoracic surgery
    • Idiopathic thrombocytopenic purpura
    • Postpericardiotomy syndrome


Pulmonary Artery Catheterization

Bojan Paunovic, MD, Assistant Professor, Department of Internal Medicine, Section of Critical Care, University of Manitoba; Medical Director of Critical Care, Grace Hospital, Canada
Sat Sharma, MD, FRCP(C), FCCP, FACP, DABSM, Program Director, Associate Professor, Department of Internal Medicine, Divisions of Pulmonary and Critical Care Medicine, University of Manitoba; Site Director of Respiratory Medicine, St Boniface General Hospital
Contributor Information and Disclosures

Updated: Dec 20, 2007


The flow-directed balloon-tipped pulmonary artery catheter (PAC) (also known as the Swan-Ganz or right heart catheter) has been in clinical use for more than 30 years. Initially developed for the management of acute myocardial infarction (AMI), it gained widespread use in the management of a variety of critical illnesses and surgical procedures. This article covers both the clinical and technical aspects of its use.


In 1929, Werner Forssmann was the first to demonstrate that a catheter could be advanced safely into the human heart (in this case, his own). His primary purpose was to develop a technique for direct delivery of drugs to the heart. With the advent of the PAC, pressure measurements and blood sampling from the cardiac chambers and PA became possible outside of the cardiac catheterization laboratory. This transformed the procedure from one that was labor and resource intensive to one that could be performed rapidly at the bedside of a critically ill patient.

Although the concept of using a balloon-assisted catheter had been published 15 years earlier, a serendipitous observation by a noted cardiologist led to its further development. During a day at the beach, Dr H. J. Swan noticed a sailboat moving quickly despite the calm weather. This led to the initial idea of devising a catheter with a parachutelike or sail-like device attached.

Initial testing was conducted with a balloon-tipped catheter because it was easier to fabricate. It proved so successful that the original parachute idea was abandoned. At the same time, the work of William Ganz on the thermodilution method of measuring cardiac output (CO) was incorporated into the catheter's use. This basic design remains in use today. Interestingly, despite the widespread use of their names for the flow-directed balloon-tipped PA catheter, neither the physicians nor the original manufacturer could obtain a patent.

Indications and Contraindications

Despite widespread use of the PAC for more than 3 decades, no validated indications exist for its general use. Some publications present only authors' suggestions for indications and contraindications for the use of the PAC. Various association and subspecialty guidelines exist as consensus statements. For example, in 1998 the American College of Cardiology published a consensus statement regarding the use of the PAC in patients with cardiac disease. The following are general guidelines for clinical use of PAC:

  • Indications
    • Diagnostic
      • Diagnosis of shock states
      • Differentiation of high- versus low-pressure pulmonary edema
      • Diagnosis of primary pulmonary hypertension (PPH)
      • Diagnosis of valvular disease, intracardiac shunts, cardiac tamponade, and pulmonary embolus (PE)
      • Monitoring and management of complicated AMI
      • Assessing hemodynamic response to therapies
      • Management of multiorgan system failure and/or severe burns
      • Management of hemodynamic instability after cardiac surgery
      • Assessment of response to treatment in patients with PPH
    • Therapeutic - Aspiration of air emboli
  • Contraindications

    • Tricuspid or pulmonary valve mechanical prosthesis
    • Right heart mass (thrombus and/or tumor)
    • Tricuspid or pulmonary valve endocarditis

Technical Considerations

Pulmonary artery catheter

Although variations of the PAC exist, the typical version is a multilumen catheter, 110 cm long, with extra connecting tubes for attachment to the pressure transducer (see Media file 1).

At the tip is the PA lumen, or distal lumen. A 1.5-cc balloon is located just proximal to the tip. Approximately 4 cm proximal to the balloon is the thermistor used to measure temperature changes for calculation of CO. Two additional lumens usually are present at 19 cm and 30 cm from the tip. Depending on the degree of right heart enlargement and the position of the catheter (ie, distance advanced into the patient), these lumina reside within the right ventricle (RV), right atrium (RA), or the superior vena cava (SVC). Some catheters are coated with heparin to reduce thrombogenicity and have connections for temporary ventricular pacing. The former is important to remember in case the patient develops heparin-induced thrombocytopenia, because only a small amount of heparin is necessary to sustain this process.

Necessary equipment

Proper attachment of the PAC to the monitoring equipment is essential for accurate measurements. Transmission of pressures from the body to the display system is accomplished via semirigid, noncompliant tubing filled with fluid, usually isotonic saline with a small amount of heparin. This, in turn, is connected to a fluid-filled pressure transducer. Often, a constant infusion or "interflow" device is placed into the connecting pressure line. This device does not alter the pressure and provides a small constant infusion of fluid through the catheter to prevent backup of blood. Because the fluid is incompressible and the tubing noncompliant, this system fairly accurately transmits intracardiac pressures to the transducer, causing small amounts of movement in the transducer membrane. Deformation of this membrane generates a proportional electric current that is amplified and transmitted to the monitor.

Zero reference

Any independent vertical movement of the transducer or the patient will affect the hydrostatic column of this fluid-filled system and thus alter the pressure measurements. At some time before or after PAC insertion, the system must therefore be zeroed to ambient air pressure. The reference point for this is the midpoint of the left atrium (LA), estimated as the fourth intercostal space in the midaxillary line with the patient in the supine position. With the transducer at this height, the membrane is exposed to atmospheric pressure, and the monitor is then adjusted to zero.


Once zeroed, the monitoring system must be calibrated for accuracy. Currently, most monitors perform an automated electronic calibration. Two methods are used to manually calibrate and check the system. If the catheter has not been inserted, the distal tip of the PAC is raised to a specified height above the LA. For example, raising the tip 20 cm above the LA should produce a reading of approximately 15 mm Hg if the system is working properly (1 mm Hg equals 1.36 cm H2 0). Alternatively, pressure can be applied externally to the transducer and adjusted to a known level using a mercury or aneroid manometer. The monitor then is adjusted to read this pressure, and the system is calibrated.

Dynamic tuning

Central pressures are dynamic waveforms (ie, they vary from systole to diastole) and thus have a periodic frequency. To monitor these pressures accurately, the system requires an appropriate frequency response. A poorly responsive system produces inaccurate pressure readings, and differentiating waveforms (eg, PA from pulmonary capillary wedge pressure [PCWP]) can become difficult. When signal energy is lost, the pressure waveform is dampened. Common causes of this are air bubbles (which are compressible), long or compliant tubing, vessel wall impingement, intracatheter debris, transducer malfunction, and loose connections in the tubing. A qualitative test of the frequency response is performed by flicking the catheter and observing a brisk high-frequency response in the waveform.

After insertion, the system can be checked by using the rapid flush test. When flushed, an appropriately responsive system shows an initial horizontal straight line with a high-pressure reading. Once the flushing is terminated, the pressure drops immediately, which is represented by a vertical line that plunges below the baseline. A brief and well-defined oscillation occurs, followed by return of the PA waveform. A dampened system will not overshoot or oscillate, and causes a delay in returning to the PA waveform.


The PAC is inserted percutaneously into a major vein (jugular, subclavian, femoral) via an introducer sheath. The actual venous access techniques are not described here, but the following points are important. Preference considerations for cannulation of the great veins are as follows:

  • Right internal jugular vein (RIJ) - Shortest and straightest path to the heart
  • Left subclavian - Does not require the PAC to pass and course at an acute angle to enter the SVC (compared to the right subclavian or left internal jugular [LIJ])
  • Femoral veins - These access points are distant sites, from which passing a PAC into the heart can be difficult, especially if the right-sided cardiac chambers are enlarged. Often, fluoroscopic assistance is necessary, but these sites are compressible and may be preferable if the risk of hemorrhage is high.

As with any catheterization procedure, sterile technique is essential. The total length of a PAC is approximately 150 cm; extra sterile towels around the head, shoulders, and chest ensure that aseptic technique is not compromised.

While the Trendelenburg position is used for venous access (internal jugular [IJ] and subclavian routes), passage of the PAC is easier when the patient subsequently is placed flat or slightly upright.

Before insertion, check the PAC for cracks and kinks. Then, check balloon function (see Media file 2), connect all lumens to stopcocks, and flush them to eliminate air bubbles. Flick the PAC tip to check frequency response. Finally, the PAC is threaded through a sterile sleeve (be sure to check orientation) to ensure sterility of the PAC after insertion and allow some adjustment of position.

The packaging of the PAC causes it to have a preformed curve. This can be used to facilitate passage into the PA. The direction in which the curl is inserted into the introducer depends on which vein is cannulated. For instance, from the head of the bed using the RIJ approach, the curl should be in the direction of the patient's left shoulder (concave-cephalad). Once the PAC is in the RV, a clockwise quarter turn moves the tip anteriorly to allow easier passage into the PA.

After inserting the PAC as far as the 20-cm mark (30-cm mark if the femoral route used), the balloon is inflated with air. Inflation should be slow and controlled (1 mL/s) and should not surpass the recommended volume (usually 1.5 mL). Always inflate the balloon before advancing the PAC, and always deflate the balloon before withdrawing the PAC.

Always use continuous pressure monitoring from the distal lumen. Watch the monitor for changes in the waveform and abnormal cardiac rhythms. From the RIJ approach, the RA is entered at approximately 25 cm, the RV at approximately 30 cm, and the PA at approximately 40 cm; the PCWP can be identified at approximately 45 cm.

If an RV waveform still present approximately 20 cm after the initial RV pattern appears, the catheter may be coiling in the RV. If withdrawal is necessary, always proceed slowly to decrease the risk of knotting the catheter upon itself. If the catheter is knotted, fluoroscopy may be necessary to visualize the catheter and remove the knot. As a last resort, slowly withdraw the PAC to the point where it catches on the introducer tip. From this point, the PAC and introducer can be removed as one unit. Apply prompt pressure for a minimum of 5 minutes. If bleeding persists, suturing the site may be necessary.

Once the PCWP is obtained and the catheter sleeve secured, make sure the PCWP pattern is reproducible before removing the sterile field. Also, determine the volume of air in the balloon required to obtain a PCWP waveform. Volumes less than half the balloon maximum may indicate that the tip is too far distal. Some clinicians advocate that, after establishing that the PA diastolic pressure is equal to the PCWP pressure, further balloon inflations are unnecessary and the PA diastolic pressure should be used as the parameter to assess left ventricular (LV) filling; this relationship may not hold if the clinical situation changes.

Once the procedure is complete, obtain a chest radiograph to check the position of the PAC and to assess for central venous access complications (eg, pneumothorax).


Passage of the PAC is difficult in certain disease states. When right-sided pressures are elevated, the air-filled balloon actually may hinder proper positioning. In such cases, filling the balloon with 1 mL of sterile saline and placing the patient in a more upright position allows gravity to cause the PAC to fall into position. Once the catheter is in position, aspirate the saline and replace it with air to ensure reproducible PCWP tracings. Insertion with a noninflated balloon may also allow passage into the PA. Neither of these techniques are advocated by PAC manufacturers and the techniques have the potential for adverse events. These techniques should only be used in extenuating circumstances and should only be attempted by experienced practitioners under the guidance of fluoroscopy.

The presence of large V waves can make discriminating a PA tracing from a PCWP tracing difficult. Look for subtle signs of waveform differences, such as loss of the dicrotic notch in the PA tracing (see Media file 3). Determining the oxygen saturation of a blood sample obtained from the distal lumen while the balloon is inflated also can confirm that the waveform is a true PCWP. After aspirating enough volume (5-7 mL) to clear the blood from the PA distal to the inflated balloon, the oxygen saturation should be similar to that measured by arterial blood gas or pulse oximetry, thus confirming that the catheter is in the correct position to measure PWCP.

Fluoroscopy may be required for proper placement of the PAC in difficult situations.

The following table shows the normal range of pressures for the RA, RV, PA, and PCWP.

Open table in new window

Circulatory Pressures (mm Hg)
  Systolic Diastolic Mean
AO 120 80 100
LV 120 8 -
LA* 7 10 4
PA 15 7 12
RV 15 2 -
RA* 4 4 0
PCW* 7 10 4
* A wave V wave  
Circulatory Pressures (mm Hg)
  Systolic Diastolic Mean
AO 120 80 100
LV 120 8 -
LA* 7 10 4
PA 15 7 12
RV 15 2 -
RA* 4 4 0
PCW* 7 10 4
* A wave V wave  

Other important information provided by a PAC catheter includes the CO, mixed venous oxygen saturation (SaO2), and oxygen saturations in the right heart chambers to assess for the presence of an intracardiac shunt.

Using these measurements, other variables can be derived, including pulmonary or systemic vascular resistance and the difference between arterial and venous oxygen content (see Media files 4-5). Obtaining CO and PCWP measurements is the primary reason for inserting most PACs; therefore, understanding how they are obtained and what factors alter their values is of prime importance.


Wave Form Analysis in Healthy States


Cardiac pressures

Right- and left-sided heart pressure waveforms share many physiologic similarities, but, in the healthy individual, the waves are of different magnitudes.

Right-sided pressures

The central venous pressure (CVP) and right atrial pressure (RAP) are nearly equal to the diastolic RV pressure in the absence of heart or lung disease (see Media file 6). The mean CVP and RAP normally range from 0-5 mm Hg, and vary as intrathoracic pressure changes with respiration (see Media file 7).

RA contraction creates pressure changes, which are influenced strongly by the patient's volume status. Atrial contraction produces an increase in pressure called the A wave. The C wave is a small convexity noted on the initial descent of the A wave and is thought to be secondary to closure of the tricuspid valve. The initial descent after the A wave is called the X descent. This decline in RAP is secondary to RA relaxation and downward movement of the tricuspid valve. Following this is the V wave, which is somewhat smaller than the A wave, and reflects RA filling during ventricular systole. The Y descent occurs after the V wave and represents rapid filling of the RV after opening of the tricuspid valve (see Media file 8).

CVP is most commonly elevated in the setting of biventricular heart failure. Other causes of RAP elevation are tricuspid regurgitation or stenosis, pulmonary hypertension, volume overload, constrictive pericarditis, and cardiac tamponade. Large, so-called cannon A waves occur when the RA contracts against a closed tricuspid valve. Cannon A waves are detected in certain cardiac rhythm disturbances, including junctional rhythms and ventricular tachycardia, and in some patients with ventricular pacemakers. Large V waves may occur in the presence of tricuspid regurgitation, with their magnitude affected by the size and compliance of the RA.

Pulmonary arterial pressure

In the pulmonary artery pressure (Ppa) tracing, an initial positive upstroke secondary to RV systole occurs, and a dicrotic notch is formed on the downstroke when the pulmonary valve closes. A normal PA systolic pressure ranges from 20 to 30 mm Hg and is equal to the RV systolic pressure. Ppa is elevated in some high-flow states (eg, hypervolemia), left ventricular failure, and high-resistance states (eg, pulmonary hypertension, mitral valve disease) (see Media file 9).

Pulmonary artery occlusion pressure (wedge pressure)

Understanding the theory and required assumptions behind PCWP measurement and conditions that alter it are essential for proper use of this often misunderstood measurement. When the PAC tip is positioned properly and the balloon is inflated, the PAP tracing disappears. This occurs because inflation of the balloon causes distal migration (approximately 2 cm) of the tip into a smaller branch of the PA, where it occludes blood flow. The resulting nonpulsatile pressure tracing is called the PCWP (or pulmonary artery occlusion pressure [Ppao]) (see Media file 10).

Under the proper circumstances, this pressure reflects the mean left atrial pressure (LAP) (see Media file 11). The assumption is that a static column is created between the PAC tip and the LA. This assumption is correct only if the tip is in the proper lung zone and no vascular obstruction, such as pulmonary vein stenosis, occurs downstream. When the PAC catheter balloon is inflated, the balloon stops antegrade blood flow and allows an uninterrupted column of blood to exist between the catheter tip and the LA (see Media files 12-13). The PCWP waveform reflects events in the LA. The A, C, and V waves have origins similar to those that appear in the RAP waveform (see Media file 14). The waveforms can be discerned by using simultaneous ECG monitoring (see Media file 15).

The 3 lung zones of West

The lung can be divided into 3 vertical zones with varying pressure changes (see Media file 16).
In zone 1 (apex), alveolar pressure (Palv) exceeds both mean Ppa and pulmonary venous pressures (Ppv). Flow depends on Palv. In zone 2 (central), Ppa is greater than Palv, which is greater than Ppv, and flow depends on a balance between Ppa and Palv. Because capillary collapse is present, neither zone 1 nor zone 2 allows a direct connection with the LA. In zone 3 (lung bases), Palv is less than Ppa and Ppv. Flow is not interrupted, and a direct column of blood extends to the LA. Fortunately, the actual practice of placing the tip in zone 3 to ensure more accurate measurements of LAP is not complicated. In the supine patient, most of the lung is considered zone 3. Blood flow to this area is increased, making balloon flotation easier. In critically ill patients who require positive end expiratory pressure (PEEP) levels greater than 10 cm H2 O, the zone 3 area can be reduced.

To assess proper location, a supine chest radiograph showing the tip below the level of the LA is sufficient, although occasionally a lateral chest radiograph is required. If the tip position remains questionable, blood can be aspirated from the distal port during balloon inflation.

Preload (left ventricular end-diastolic pressure)

PCWP is a reflection of LAP, which, in the absence of mitral valve disease, is an indication of LV diastolic pressure. Often, the inference is made that PCWP reflects left ventricular end-diastolic volume (LVEDV) or end-diastolic pressure (LVEDP). Numerous conditions in critically ill patients preclude this assumption.

PCWP is the measurement by which changes in lung water (pulmonary capillary hydrostatic pressure [PCHP]) can be assessed. This concept holds true only if the resistance of the pulmonary venous system is assumed to be zero. In fact, the small pulmonary veins and capillaries account for approximately 40% of the total pulmonary vascular resistance. This value may be even higher in critically ill patients in whom pulmonary venoconstriction is common secondary to conditions such as hypoxemia and acute respiratory distress syndrome (ARDS). PCHP is always greater than PCWP. PCWP can be used to estimate the contribution of PCHP to lung edema if evidence of chronically elevated Ppv, permeability, pleural pressure, and osmotic pressure are considered.

Effect of respiration

The final critical concept in PCWP interpretation is the effect of the respiratory cycle on PCWP measurements. The timing of PCWP measurement is critical because intrathoracic pressures can vary widely with inspiration and expiration and are transmitted to the pulmonary vasculature. During spontaneous inspiration, the intrathoracic pressures decrease (more negative); during expiration, intrathoracic pressures increase (more positive). Positive pressure ventilation (eg, in an intubated patient) reverses this situation. To minimize the effect of the respiratory cycle on intrathoracic pressures, measurements are obtained at end-expiration, when intrathoracic pressure is closest to zero.

In patients with severe respiratory distress, end-expiration can be difficult to determine. In these situations, sedation, or even paralysis, may be necessary to remove the transmission of respiratory efforts to the pressure tracings.

Positive end-expiratory pressure

PEEP (intrinsic or extrinsic) also transmits pressure to the vascular space. Lung compliance is the main determinant of the amount of pressure transmission. For example, in disease states (eg, ARDS) associated with low compliance (ie, stiff lungs), pressure transmission is minimal. Debate exists over how to correct PCWP in the presence of PEEP. Although previously advocated, temporary discontinuation of PEEP may have adverse effects, such as cardiovascular collapse or hypoxemia, that are difficult to reverse. For PEEP greater than 10 cm H2 O, the following general rule can be applied: Corrected PCWP equals measured PCWP minus one half the quotient of PEEP divided by 1.36. If available, an intraesophageal balloon can be used. Esophageal pressure equals pleural pressure, so corrected PCWP equals measured PCWP minus esophageal pressure.


Wave Form Analysis in Pathologic States



Shock has been defined as inadequate perfusion to meet the metabolic demands of body tissues. The most common forms of shock are hypovolemic, cardiogenic, septic, and obstructive. PACs are used frequently in the management of various forms of shock, as described in this section (see Media file 17).

Hypovolemic shock

Hypovolemic shock is due to a reduction in circulating blood volume resulting from either hemorrhage or fluid depletion. Preload is markedly decreased, leading to inadequate ventricular filling. The patient with hypovolemic shock manifests hypotension and tachycardia. Systemic, venous, and intracardiac pressures are abnormally low. The overall PAC pressure tracing has a damped appearance.

Cardiogenic shock

Cardiogenic shock is the result of severe depression in cardiac performance. Cardiogenic shock is characterized by systolic blood pressure less than 80 mm Hg, cardiac index less than 1.8 L/min/m2, and PCWP greater than 18 mm Hg. This form of shock can occur from a direct insult to the myocardium (eg, large AMI, severe cardiomyopathy) or from a mechanical problem that overwhelms the functional capacity of the myocardium (eg, acute severe mitral regurgitation, acute ventricular septal defect).

Common causes of acute mitral regurgitation in critical care units are ruptured papillary muscles secondary to AMI, myocardial ischemia leading to papillary muscle dysfunction, bacterial endocarditis, ruptured chordae, and trauma. Other causes are rheumatic fever and myxomatous degeneration of the mitral valve. With acute mitral regurgitation, large volumes of blood regurgitate into a poorly compliant LA, raising Ppv and causing pulmonary edema.

Large V waves usually are observed in the PCWP pressure tracing (see Media files 18-20). The PA waveform appears falsely elevated because of the large V wave reflected back from the LA through the compliant pulmonary vasculature. The Y descent is quite rapid as the overdistended LA quickly empties. Care must be exercised to distinguish a large V wave from a systolic PA waveform. Failure to recognize a large V wave may cause the PAC to be advanced further in an attempt to record a PCWP pressure, increasing the risk of perforation.

In chronic mitral regurgitation, an equivalent volume of blood may regurgitate, but this volume is better tolerated by a markedly dilated LA. Compared with acute mitral regurgitation, LA pressure may be less and large V waves may be absent.

Septic shock

Septic shock is the most common cause of death in intensive care units in the United States. Septic shock is an example of distributive shock, a form of shock characterized by profound peripheral vasodilation. Although the CO may be normal or even elevated in this type of shock, organ and tissue perfusion are inadequate. Other types of distributive shock include anaphylaxis, neurogenic shock, and adrenal insufficiency. Swan-Ganz catheter measurements frequently demonstrate low filling pressures.

Extracardiac obstructive shock

Pericardial tamponade is an example of this form of shock. Cardiac tamponade results from abnormal rapid fluid accumulation in the pericardial sac. The increased pericardial pressure impairs ventricular diastolic filling, decreasing preload, stroke volume, and CO. This may occur secondary to viral infections, malignancy, trauma, or myocardial rupture. As little as 50 mL of fluid accumulation can begin to impair cardiac filling during systole, leading to a severe reduction in CO. Ventricular filling is impaired throughout all of diastole, thereby causing equalization of all diastolic pressures.

The RAP approximates the RV diastolic pressure, which approximates the PA diastolic pressure, and also approximates PCWP (see Media file 21). The RA waveform shows a minimal X and small and/or absent Y descent, and the mean RAP is elevated. Ppa loses its usual respiratory variation. In pericardial tamponade, the systemic arterial pressure shows evidence of pulsus paradoxus (see Media file 22). Other causes of extracardiac shock include massive PE and tension pneumothorax.

Hemodynamics of other cardiac abnormalities

Constrictive pericarditis

Thickening of the pericardial sac creates an indolent process that may lead to constrictive pericarditis. This can occur in patients with rheumatic diseases, tuberculosis, metastatic cancer, or prior chest radiation or open-heart surgery. Idiopathic cases also occur. Early diastolic filling is normal until limited by the rigid pericardial shell. Once this occurs, ventricular filling is stopped abruptly, creating a plateau in the RV pressure, which is typical of constrictive pericarditis. This is called the "dip and plateau" pattern or square root sign; the RAP waveform has a characteristic configuration suggestive of an M or W. A and V waves are accentuated with rapid X and Y descents, in contrast to pericardial tamponade, above. PCWP may be as high as 20-25 mm Hg, and usually appears similar to the RA waveform. Pulsus paradoxus is present much less commonly with constrictive pericarditis than with pericardial tamponade (see Media files 23-24).

Mitral stenosis

In severe mitral stenosis, LAP, and thus PAWP, is elevated. Pulmonary hypertension also develops as the severity of the valve lesion progresses. This leads to increase in RV systolic pressure and in the RA A wave. RV diastolic pressure may increase if RV failure or important tricuspid regurgitation develops. Atrial fibrillation is a common complication in mitral stenosis and results in loss of A waves in both the RA and PCWP pressure tracings.

Aortic stenosis

Aortic stenosis can be supravalvular, valvular, or subvalvular in origin. The RA, RV, and PA waveforms usually are normal unless congestive heart failure is present. PCWP may show large A waves in severe cases because of poor LV compliance.

Aortic regurgitation

The hemodynamic abnormalities are different in acute and chronic aortic regurgitation. Acute regurgitation is observed most often in bacterial endocarditis, chest trauma, ascending aortic dissection, and degeneration of valve leaflets. The hemodynamics in acute aortic regurgitation include modestly elevated RAP and elevated RV systolic and diastolic pressures. PA systolic and diastolic pressures also are elevated, as is PCWP. A widened and elevated systemic arterial pressure without a dicrotic notch is sometimes observed. Acute and chronic aortic regurgitation often present with contrasting manifestations; a wide pulse pressure usually is not observed in acute regurgitation.


Other Hemodynamic Measurements Made by the Pulmonary Artery Catheter

Cardiac output

CO can be determined via the PAC by several methods. It can be determined by using the Fick principle, which is a variation of the law of conservation and states that consumption of a substance must equal the product of blood flow to the organ and the difference between the arterial and venous concentrations of the substance. In this circumstance, the substance is oxygen, and CO is determined by the following formula:

CO equals oxygen consumption per minute (VO2) divided by arterial oxygen content (CaO2) minus mixed venous oxygen content (CvO2)

CO is determined by using systemic arterial and PA blood samples, and by measuring or estimating VO2. The Fick method is most accurate when the CO is low and the arterial-venous oxygen difference is high. Unfortunately, in critically ill patients, establishing a steady-state and estimating or measuring VO2 is difficult; thus, the reliability of this technique is poor.

The indicator-dilution technique is more accurate and reproducible. A known amount of dye (indocyanine green) is injected into the PA. Arterial blood is withdrawn from the aorta as the dye circulates, and a concentration-versus-time curve is derived. The first-pass curve is used to determine CO, which is calculated by dividing the initial mass of the injectate by the average concentration. This value then is corrected (60 s/time of the curve) to obtain CO. This procedure requires considerable blood sampling and is time consuming, because recirculation of the dye complicates the calculation.

Many PACs also allow CO to be measured by using a variation of the indicator-dilution method known as the thermodilution method. This method is more efficient because the injectate does not recirculate to a significant degree and no blood sampling is necessary. A saline bolus of known volume (5-10 mL) and temperature (usually £ 25 º C) is injected through the proximal (RA) lumen. The thermistor at the end of the PAC monitors the change in blood temperature, and a temperature-versus-time curve is generated (see Media file 25). The change in temperature as warm venous blood dilutes the injectate is inversely proportional to the derived CO. The Stewart-Hamilton formula shows this relationship:

CO equals the volume of injectate multiplied by blood temperature minus injectate temperature multiplied by computation constants, and divided by change of blood temperature as a function of time (area under the curve)

Understanding this formula allows discernment of artifact errors that can lead to underestimation or overestimation. Loss of injectate or inadvertent administration of a volume lower than required results in a low-amplitude temperature-versus-time curve that produces a falsely elevated CO value. Causes of this are system leak, right-to-left intracardiac shunts, inappropriately rapid injection, and a poorly positioned PAC. Conversely, too much injectate or too slow an injection leads to a falsely low CO reading. Temperature errors can occur when continuous infusions are used. Thrombus or vessel wall impingement can alter the thermistor function.

Physiologic causes for CO measurement discrepancies include tricuspid and pulmonary regurgitation, which may produce recirculation peaks and thus increase the area under the curve, resulting in a falsely low CO estimate. Arrhythmias alter steadiness of PA flow and may cause difficulty in obtaining a consistent CO.

CO alterations occur during the respiratory cycle and are accentuated by respiratory distress and positive pressure ventilation. Proper timing of the injection to the same phase of respiration (preferably end-expiration) provides more consistent measurements. Averaging the values of 3 injections is recommended to minimize sampling errors.

While CO is one of the most important measurements that the PAC provides, the absolute value should be normalized for the size of the patient. To account for this, the cardiac index (CI), which equals CO divided by body surface area [BSA], is calculated. The physician should keep in mind that, as independent variables, CO and CI are of limited use for assessing tissue perfusion because these must be interpreted along with other clinical data.


Complications of Pulmonary Artery Catheterization

Complications associated with PAC use relate to the initial venous access, insertion of the PAC, and maintenance of the catheter in the PA. The reported incidence of complications varies on the basis of operator skill and patient status. Significant venous access complications include arterial puncture (2-16%), which may manifest immediately (eg, carotid artery hematoma if inserted via the IJ route) or insidiously (eg, hemothorax via subclavian route). Pneumothorax (incidence 2-4%) also relates to choice of access route and occurs more often in the subclavian than in the IJ. In ventilated patients, tension pneumothorax can develop rapidly from a punctured lung.

Arrhythmias constitute the most common complication associated with PAC insertion. More than 80% of these are premature ventricular contractions (PVCs) or nonsustained ventricular tachycardia (VT). These resolve either with advancement of the catheter from the RV into the PA, or with prompt withdrawal of the catheter into the RA. Significant VT or ventricular fibrillation requiring treatment occurs in fewer than 1% of patients, usually those with concurrent cardiac ischemia.

Right bundle-branch block (RBBB) occurs in 5% of PAC insertions and usually is transient after positioning the catheter into the PA. The presence of a preexisting left bundle-branch block (LBBB) puts the patient at risk for complete heart block should RBBB occur. In these patients, temporary pacing equipment should be kept nearby on standby. The incidence of knotting of the PAC on itself or on intracardiac structures is less than 1%. This risk is increased in patients with dilated cardiac chambers. A persistent RV tracing despite advancement of the PAC further than 20 cm into the patient should alert the physician to this possibility.

Of the complications associated with maintenance of the PAC, PA rupture is most catastrophic, with a mortality rate of 50%. Fortunately, it is a rare occurrence (<1%). Patients at risk are those who have pulmonary hypertension, are older than 60 years, or are receiving anticoagulation therapy. The sudden onset of hemoptysis (especially after inflation of the PAC balloon) indicates this possibility. Immediate management includes lateral decubitus positioning (bleeding side down), intubation with a double-lumen endotracheal tube (ETT), and increasing PEEP. Embolization via bronchoscopy or angiography or lobectomy may be necessary if bleeding continues or is massive.

PAC related infection is a fairly common complication. The incidence of positive catheter tip culture result is 45% in some series. Fortunately, the risk for clinical sepsis is less than 0.5% per day of catheter use.

The incidence of pulmonary infarction is less than 7%. Unintentional distal migration of the PAC tip is the usual cause. Some evidence indicates that catheter-related thrombi also may be a significant cause. While postmortem studies have shown that rate of endocardial lesions (eg, thrombi, hemorrhage, vegetations) related to PAC use is significant, correlation with clinical events has not been established.


Recommendations for Clinical Practice and Future Research


Over 1 million PACs are used annually in North America. Given the frequency and duration of their use, it is surprising that only recently were quality randomized clinical trials published. Initially, observational studies from the 1980s and 1990s indicated a greater mortality rate in patients who underwent placement of a PAC than in those who did not. The major criticism of these studies is that the more acutely ill (and therefore at greatest risk of death initially) are more likely to receive a PAC.

However, since then a number of randomized clinical trials were published:

  • Sandham et al enrolled nearly 2000 surgical patients (ASA class 3 or 4) aged 60 years or older. The treatment group received a PAC and a guided therapy protocol while the control group received a central venous catheter and therapy based on physician discretion. No difference was noted in the 2 groups in mortality rate (8%), length of stay, or organ dysfunction.1
  • Richard et al randomized almost 700 patients with early shock, ARDS, or both to use of PAC or not. Treatment was left to physician discretion. No significant difference in mortality or morbidity was noted.2
  • Rhodes et al randomized 201 patients and found no difference in 28-day mortality, ICU, or hospital length of stay in patients with or without a PAC. A formal management protocol was not used.3
  • The PACMAN trial enrolled more than 1000 patients to management with or without a PAC. The timing of insertion and management were at the discretion of the treating physician. No difference in hospital mortality (primary outcome) was noted.4
  • The ESCAPE trial enrolled more than 400 patients who were admitted with severe heart failure. Patients were randomized to having therapy guided by clinical assessment and PAC or clinical assessment alone. No difference was noted in overall mortality or hospitalization.5
  • Shah et al published a large meta-analysis that consisted of 13 randomized clinical trials and more than 5000 patients (including the above mentioned trials). Neither an increase in mortality or length of hospital stay nor a significant benefit could be attributed to the use of a PAC.6
  • In 2006, the ARDSNET group looked at the role of the PAC in acute lung injury patients. Patients were randomized to protocolized hemodynamic management with either a PAC or a central venous catheter (CVC). No difference in mortality (primary outcome), ICU length of stay, or lung function was appreciated.7
  • As well, even in the hallowed ground of PAC use in cardiac surgery patients, Djaiani et al showed that the use of PAC derived data lead to more interventions but no overall clinical benefit.8
  • Unfortunately, a recent Cochrane Review of 12 studies was only able to support the need for "efficacy studies... to determine optimal management protocols and patient groups who could benefit from management with a PAC."9

Overall, the literature does not show a positive effect on patient outcome with PAC use. However, a criticism of the current available research is that patient groups potentially benefit from the use of a PAC but this effect is lost in studies that also include patient groups that gain little or no benefit. Chittock et al published an observational cohort study showing that PAC use was associated with increased mortality in less acutely ill patients but associated with decreased mortality in more acutely ill patients.10 

As well, the use of a monitoring tool such as the PAC itself is unlikely to show a significant treatment effect. Some criticize the current literature because a number of studies did not use a predefined treatment protocol. The lack of defined specific treatment based on measured PAC-derived variables could contribute more to patient outcome than merely the presence or absence of a PAC.

Contention also exists that PACs do not harm people; people harm people. In other words, operator competence may be the root cause of the mortality difference. Reviews have shown deficiencies in both nursing-dependent information derived from the PAC as well as physician-dependent interpretation and subsequent management.


The PAC should not be thought of as a treatment but as a tool for aiding in diagnosis and  evaluation of response to treatment. Knowledge of its capabilities and limitations is essential to minimize potential deleterious effects and maximize potential benefits. However, a rigorous randomized controlled trial has yet to show a definitive indication for its widespread application.



Media file 1: A pulmonary artery catheter is shown here.

A pulmonary artery catheter is shown here.

Media file 2: The balloon of the catheter should be checked prior to insertion.

The balloon of the catheter should be checked prior to insertion.

Media file 3: Pulmonary artery catheter being introduced from pulmonary artery in to wedge position.

Pulmonary artery catheter being introduced from pulmonary artery in to wedge position.

Media file 4: Normal hemodynamic parameters.

Normal hemodynamic parameters.

Media file 5: Calculation of various hemodynamic parameters.

Calculation of various hemodynamic parameters.

Media file 6: Central venous pressure (CVP) measured in superior vena cava (SVC) is identical to right atrial pressure (RAP).

Central venous pressure (CVP) measured in superior vena cava (SVC) is identical to right atrial pressure (RAP).

Media file 7: Respiratory variation is easily identified on the right atrial waveform.

Respiratory variation is easily identified on the right atrial waveform.

Media file 8: Various waveforms of central venous pressure (CVP) monitoring are shown here.

Various waveforms of central venous pressure (CVP) monitoring are shown here.

Media file 9: Pulmonary arterial pressure (Ppa) waveform.

Pulmonary arterial pressure (Ppa) waveform.

Media file 10: Pulmonary artery wedge pressure (PAWP) waveform can be distinguished easily from the pulmonary arterial waveform in most clinical scenarios.

Pulmonary artery wedge pressure (PAWP) waveform can be distinguished easily from the pulmonary arterial waveform in most clinical scenarios.

Media file 11: Pulmonary artery wedge pressure (PAWP) reflects left atrial pressure (LAP).

Pulmonary artery wedge pressure (PAWP) reflects left atrial pressure (LAP).

Media file 12: Inflated balloon obstructs arterial flow and reflects pressures at J point. Redrawn from Principles of Critical Care by Jesse B. Hall, Gregory A. Schmidt, Lawrence D. H. Wood, 2000, McGraw-Hill, Inc.

Inflated balloon obstructs arterial flow and reflects pressures at J point. Redrawn from Principles of Critical Care by Jesse B. Hall, Gregory A. Schmidt, Lawrence D. H. Wood, 2000, McGraw-Hill, Inc.

Media file 13: Having an inflated balloon in a proximal vessel is better because a vessel branch is likely to reflect left atrial pressure (LAP) accurately. Redrawn from Principles of Critical Care by Jesse B. Hall, Gregory A. Schmidt, Lawrence D. H. Wood, 2000, McGraw-Hill, Inc.

Having an inflated balloon in a proximal vessel is better because a vessel branch is likely to reflect left atrial pressure (LAP) accurately. Redrawn from Principles of Critical Care by Jesse B. Hall, Gregory A. Schmidt, Lawrence D. H. Wood, 2000, McGraw-Hill, Inc.

Media file 14: Right or left atrial pressure waveform.

Right or left atrial pressure waveform.

Media file 15: Timing of the pulmonary artery waveforms in relation to electrocardiographic monitoring is shown here. An A wave follows the QRS wave on ECG, whereas V wave follows the T wave on ECG.

Timing of the pulmonary artery waveforms in relation to electrocardiographic monitoring is shown here. An A wave follows the QRS wave on ECG, whereas V wave follows the T wave on ECG.

Media file 16: Physiologic lung zones. For pulmonary capillary wedge pressure (PCWP) to be reliable, the catheter tip must lie in zone 3. Pulmonary artery pressure (Ppa) is greater than pulmonary venous pressure (Ppv), which is greater than alveolar pressure (Palv) at end-expiration. In zones 1 and 2, Ppw reflects Palv if Palv is greater than Ppv. Redrawn from Principles of Critical Care by Jesse B. Hall, Gregory A. Schmidt, Lawrence D. H. Wood, 2000, McGraw-Hill, Inc.

Physiologic lung zones. For pulmonary capillary wedge pressure (PCWP) to be reliable, the catheter tip must lie in zone 3. Pulmonary artery pressure (Ppa) is greater than pulmonary venous pressure (Ppv), which is greater than alveolar pressure (Palv) at end-expiration. In zones 1 and 2, Ppw reflects Palv if Palv is greater than Ppv. Redrawn from Principles of Critical Care by Jesse B. Hall, Gregory A. Schmidt, Lawrence D. H. Wood, 2000, McGraw-Hill, Inc.

Media file 17: Hemodynamic parameters in different pathologic states.

Hemodynamic parameters in different pathologic states.

Media file 18: Tall V waves presented here on pulmonary arterial and wedge pressure waveforms are characteristic of severe mitral regurgitation.

Tall V waves presented here on pulmonary arterial and wedge pressure waveforms are characteristic of severe mitral regurgitation.

Media file 19: Large V waves in a case of mitral regurgitation.

Large V waves in a case of mitral regurgitation.

Media file 20: Simultaneous recording of ECG helps identify V waves in mitral vale regurgitation; V waves correspond to T waves on ECG.

Simultaneous recording of ECG helps identify V waves in mitral vale regurgitation; V waves correspond to T waves on ECG.

Media file 21: Hemodynamic monitoring can confirm the diagnosis of pericardial tamponade. Equalization of diastolic pressures on the left and right sides of the heart, elevated right atrial pressure, and Kussmaul sign (ie, increase in right atrial pressure with inspiration) are noted.

Hemodynamic monitoring can confirm the diagnosis of pericardial tamponade. Equalization of diastolic pressures on the left and right sides of the heart, elevated right atrial pressure, and Kussmaul sign (ie, increase in right atrial pressure with inspiration) are noted.

Media file 22: In cardiac tamponade, systemic arterial pressure (Pa) reflects pulsus paradoxus. Right atrial pressure (RAP) is elevated. Pulmonary artery (PA) diastolic pressure equals mean right atrial (RA), right ventricular (RV) diastolic, and wedge pressures.

In cardiac tamponade, systemic arterial pressure (Pa) reflects pulsus paradoxus. Right atrial pressure (RAP) is elevated. Pulmonary artery (PA) diastolic pressure equals mean right atrial (RA), right ventricular (RV) diastolic, and wedge pressures.

Media file 23: Simultaneous recordings of pulmonary capillary wedge pressure and left ventricular pressure waveforms in a patient with constrictive pericarditis. Note the equalization of diastolic pressures and "square root sign" or "dip and plateau sign" of the left ventricular waveforms, which are confirmatory of the diagnosis of constrictive pericarditis.

Simultaneous recordings of pulmonary capillary wedge pressure and left ventricular pressure waveforms in a patient with constrictive pericarditis. Note the equalization of diastolic pressures and "square root sign" or "dip and plateau sign" of the left ventricular waveforms, which are confirmatory of the diagnosis of constrictive pericarditis.

Media file 24: Right atrial pressure waveform of a patient with constrictive pericarditis. Please note rapid X and Y descents, and elevated A and V waves. This gives an impression of the letter "M" or "W" and is confirmatory of the diagnosis of constrictive pericarditis.

Right atrial pressure waveform of a patient with constrictive pericarditis. Please note rapid X and Y descents, and elevated A and V waves. This gives an impression of the letter "M" or "W" and is confirmatory of the diagnosis of constrictive pericarditis.

Media file 25: Principle of cardiac output measurement.

Principle of cardiac output measurement.


swan-ganz catheterization, pulmonary artery catheterization, PAC, SGC, right heart catheterization, hemodynamic monitoring, pulmonary artery catheter, PA catheter, acute myocardial infarction, AMI, flow-directed balloon-tipped pulmonary artery catheter, primary pulmonary hypertension, PPH, valvular disease, intracardiac shunts, cardiac tamponade, pulmonary embolus, PE, multiorgan system failure, severe burns, aspiration of air emboli, heart pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, wedge pressure, left ventricular end-diastolic pressure, positive end-expiratory pressure

hypovolemic shock, cardiogenic shock, cardiomyopathy, acute mitral regurgitation, acute ventricular septal defect, septic shock, pericardial tamponade, cardiac tamponade, constrictive pericarditis, mitral stenosis, aortic stenosis, aortic regurgitation, cardiac output