Cardiac Catheterization of Left Heart Technique

Updated: Apr 13, 2016
  • Author: Roger B Olade, MD, MPH; Chief Editor: Karlheinz Peter, MD, PhD  more...
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Technique

Approach Considerations

In the early days of cardiac catheterization, access to the arterial system was obtained by means of 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 is still used by some operators, most left-heart catheterization procedures are now performed via a percutaneous approach from the femoral, radial, brachial, or axillary artery (see the image below). Right-heart catheterization is commonly performed via a percutaneous approach from the femoral, internal jugular, or subclavian vein.

Cardiac catheterization sites. Cardiac catheterization sites.
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Left-Heart Catheterization

Arterial access from upper extremity (modified Sones method)

The classic brachial artery technique was developed by Mason Sones, MD, and often is referred to as the Sones method.

Insert a 5- or 6-French sheath into the brachial artery. Maneuver the catheters through the axillary and subclavian arteries into the ascending aorta. Perform coronary angiography using either a Sones catheter, which requires deflection of the catheter tip off the aortic valve cusps, or any of a variety of preformed catheter shapes.

Alternatively, access can be obtained from the axillary artery or the 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 (see the images below) is increasing in popularity: the transradial approach is used in approximately 50% of coronary angiograms in Asia and 40% of those in Europe. In the United States, however, this approach is used in only 7% of coronary angiograms, possibly because of the inability to introduce larger equipment and intra-aortic balloon pumps through the radial artery, the incidence of arterial spasm, and the need for additional training with the technique.

Image showing catheter advancing into the ascendin Image showing catheter advancing into the ascending aorta via the right radial artery in the transradial approach. Note the tortuous aorta. Image courtesy of Tak W. Kwan, MD
Transradial cardiac angiogram showing pigtail cath Transradial cardiac angiogram showing pigtail catheter in the ascending aorta via a retro-esophageal subclavian artery (arteria lusoria). Image courtesy of Olurotimi Badero, MD, FACP.

Radial artery spasm complicates transradial catheterizations in 2-6% of cases. [6, 7] Difficulty in accessing the relatively narrow radial artery and increased need for catheter manipulation for coronary engagement on the part of less experienced operators can also result in longer procedure times.

An Allen test must be performed before the procedure to ensure the continuity of the arterial arch in the hand should the radial artery become occluded during or after the procedure.

Standard catheters may be used for the transradial approach, and several new shapes have been developed to facilitate easy cannulation of the coronary arteries. The main advantages of this approach are a low incidence of serious vascular complications and the ability to mobilize the patient quickly after the procedure. The disadvantages are a longer learning curve for the operator and occasional severe arterial spasm, which impairs manipulation of the catheter.

Not all patients are ideal candidates for a radial artery approach to cardiac catheterization. The ideal patient will have the following characteristics:

  • Pannus or poor body habitus
  • Severe peripheral vascular disease or fibrosis
  • Elevated international normalized ratio (prosthetic valves and atrial fibrillation on anticoagulation)
  • Inability to lie supine or remain still
  • Large abdominal aortic aneurysms
  • Back pain
  • Probable normal coronary status
  • A preference for the procedure

In general, arterial access from the upper extremity is preferred if the patient has clinically significant iliac or femoral artery atherosclerosis or has severe obesity that renders the normal landmarks for access difficult to appreciate.

Arterial access from 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; 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 (see the images below). A pigtail catheter is frequently used for measuring left heart pressures and performing left ventriculography.

Judkins left 4 (JL4) catheter in place. Image cour Judkins left 4 (JL4) catheter in place. Image courtesy of Olurotimi Badero, MD, FACP.
Judkins right 4 (JR4) catheter in place. Image cou Judkins right 4 (JR4) catheter in place. Image courtesy of Olurotimi Badero, MD, FACP.

Proper access to the common femoral artery is critical for this technique (see the image below). 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 period (2-6 hours) of bed rest after completion of the procedure.

Femoral access. Image courtesy of Olurotimi Badero Femoral access. Image courtesy of Olurotimi Badero, MD, FACP and www.tctmd.com.

Several types of arterial closure devices are now available that provide rapid hemostasis and shorten the period of bed rest considerably. However, complication rates with these closure devices are similar to those of 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 obtained from the femoral artery, especially if the procedure is prolonged and several catheter exchanges are required.

Additional vascular access approaches

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

Catheterization of the left atrium and the left ventricle can be performed via a transseptal approach. Transseptal catheterization is useful if the patient has a mechanical aortic valve or if obtaining a true left atrial pressure is necessary. The intra-atrial septum is punctured with a needle, and the catheter is advanced into the left atrium and ventricle. The operator must have a firm understanding of cardiac radiographic anatomy to avoid puncturing adjacent structures (eg, the free wall of the right atrium, the coronary sinus, or the aortic root).

If assessment of left ventricular hemodynamics is necessary in patients with mechanical valves in both the aortic and mitral position, a direct left ventricular puncture may be the only option. This approach has been used in ablation therapy in atrial fibrillation; transseptal guide wires (TSP-GW) have been used in cases of resistant atrial septum that did not allow the standard needle. [8]

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Complications

Intraprocedural 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. It 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 (eg, intravenous [IV] nitroglycerin) should be assessed 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. [9]

Congestive heart failure may develop as a consequence of the osmotic effects of the contrast agents and fluid administered during the procedure, especially in patients with marginal left ventricular function. In such cases, it may be necessary to abort the procedure and institute treatment with oxygen, diuretics, and nitroglycerin.

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 (CAD). However, in patients with important CAD, myocardial ischemia with pain and ST-segment changes may occur. This frequently resolves with sublingual or IV nitroglycerin, but persistent pain with evidence of myocardial ischemia may be an indication for urgent revascularization. [10]

Minor arrhythmias (eg, atrial or ventricular premature beats or 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 that a major complication will occur during diagnostic cardiac catheterization is lower 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 preceding 24 hours, renal insufficiency, cardiomyopathy, aortic and mitral valve disease, poorly compensated congestive heart failure, severe hypertension, and unstable angina.

Death

Death rates from cardiac catheterization have declined steadily over the past 15 years. The incidence of procedure-related mortality is now approximately 0.08%. A high-risk subgroup can be defined on the basis of 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 from catheterization. New York Heart Association (NYHA) functional class IV is associated with nearly a 10-fold increase in mortality as 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 lower than 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 experience 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 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 the following:

  • Recent unstable angina or non–Q-wave infarction
  • Severe CAD
  • The presence of significant comorbidities

In high-risk patients, serial electrocardiography (ECG) and cardiac enzyme measurement may be considered after the procedure.

Stroke

The procedure-related stroke rate was as high as 0.23% in 1973 but has fallen to 0.06% in contemporary registries. Nevertheless, stroke remains one of the most devastating complications of cardiac catheterization.

A stroke may not always be apparent during the procedure. The first symptoms may not develop until hours after the procedure is completed, when atherosclerotic debris loosened from plaques in the proximal aorta finally breaks free and embolizes. Maintain a very high level of suspicion, and evaluate patients after the procedure to assess any neurologic changes. [10] High-osmolar contrast agents in the carotid arteries may cause transient neurologic deficits. There have also been some instances of cognitive dysfunction, but this has not been found to be associated with microemboli. [11]

Infection

Because cardiac catheterization is a sterile procedure, the incidence of infections is very low. The American College of Cardiology (ACC)/American Heart Association (AHA) task force does not mandate full surgical scrubbing and attire for the femoral approach, [12] but it does recommend these 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; it is more often due to phlebitis and is sometimes unexplained. Pyrogen reactions are now a very uncommon cause for fever, because almost all of the catheters currently 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 before the procedure to avoid reactions.

Reactions to iodinated contrast agents occur in approximately 1% of patients. Such reactions are not true anaphylactic reaction; rather, they result from direct complement activation and thus are considered anaphylactoid reactions. 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 a history of a previous reaction to contrast agents.

To reduce the risk of contrast reactions, high-risk patients should be premedicated with corticosteroids, and a nonionic contrast agent should be used. Data from the TRUST trial (N=17,513) suggest that the nonionic agent iopromide carries only a very low risk of adverse drug reactions in the setting of cardiac catheterization. [13] Some physicians also administer H1 and H2 receptor blockers. Severe reactions can usually be reversed with an IV injection of dilute epinephrine.

Protamine sulfate is now rarely given to reverse the anticoagulant effect of heparin. 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. Previous long-term exposure to protamine is thought to sensitize the patient to protamine.

Latex-induced allergic reactions are being recognized more frequently. Such reactions are usually local, though systemic reactions may occur. They may be avoided by using latex-free materials in sensitive patients.

Renal dysfunction

Renal dysfunction is a potential complication of any angiographic procedure. [14] About 5% of patients experience a transient rise in plasma creatinine concentration (>1 mg/dL) after contrast exposure. Patients who have preexisting renal insufficiency, multiple myeloma, or dehydration or are taking nephrotoxic drugs are at 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. [15]

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 [16] ; however, optimal hydration regimens remain to be determined. [17]  Premedication with N-acetylcysteine may prevent worsening of renal function in patients with renal insufficiency.

Systemic cholesterol embolization is another cause of renal failure after cardiac catheterization. [18, 19] 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; in contrast, contrast-induced nephropathy 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

Arrhythmias and conduction disturbances can occur during cardiac catheterization. With the exception of asystole and ventricular fibrillation, most of these abnormalities are of little clinical significance. Atrial fibrillation usually is well tolerated but may provoke hemodynamic decompensation in patients with severe CAD, hypertrophic cardiomyopathy, aortic stenosis, or severe systolic dysfunction.

Prompt treatment with cardioversion prevents progressive decompensation due to the arrhythmia. Ventricular tachycardia or fibrillation occurs in approximately 0.4% of patients. These arrhythmias may result from manipulation of the catheter or from 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 commonly occurs at the end of a right coronary artery injection involving high-osmolar agents. Forceful coughing usually helps clear the contrast material 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 two most common times for such a reaction to develop are (1) during the administration of local anesthesia in the groin and (2) after the application of pressure to obtain femoral artery hemostasis. IV fluids and atropine are the treatments for a vasovagal reaction.

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, and 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; consequently, heparin is a requirement. Consultation with a vascular surgeon is necessary in case paresthesia or reduced distal pulses occur after catheterization.

Bleeding is the most common vascular complication. It may simply result in a local hematoma of little clinical significance; however, it may result in severe blood loss if it occurs in the retroperitoneal space. Unexplained hypotension and a falling hematocrit should suggest the possibility of a retroperitoneal hematoma. Abdominal ultrasonography or computed tomography (CT) is usually diagnostic.

Pseudoaneurysm is another potential cause of important groin bleeding that 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 means of 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 fistulas before hemodynamic compromise develops.

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Hemodynamic Assessment

Mitral and aortic stenosis

Determining the severity of a valvular stenosis on the basis of 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 valvular stenosis from insignificant valvular stenosis.

In patients with aortic stenosis (see the image below), 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 the femoral artery may alter the pressure waveform and introduce errors. This is especially important in patients with a low pressure gradient and cardiac output (see the Cardiac Output calculator).

Aortic stenosis tracings. Image courtesy of Olurot Aortic stenosis tracings. Image courtesy of Olurotimi Badero, MD, FACP, and www.tctmd.com.

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 (see the image below), the valve gradient is usually determined by measuring the left ventricular and pulmonary capillary wedge pressures. 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 pressures. [20] This requires a transseptal catheterization approach.

Mitral stenosis tracings. Image courtesy of Olurot Mitral stenosis tracings. Image courtesy of Olurotimi Badero, MD, FACP, and www.tctmd.com.

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.

Left ventriculography

Left ventriculography 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. [21] It provides valuable information about global and segmental left ventricular function, mitral regurgitation, ventricular septal defect, and hypertrophic cardiomyopathy (see the image below).

Left ventriculogram showing mid cavity obliteratio Left ventriculogram showing mid cavity obliteration in hypertrophic cardiomyopathy (HOCM). Image courtesy of Olurotimi Badero, MD, FACP.

The findings from ventriculography 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 according to the area-length method to derive actual end-diastolic and end-systolic volume estimates.

The components of the left ventricular pressure waveform are similar to those of the right ventricular waveform, except that the systolic and diastolic pressures are higher.

Left ventricular systole causes a rapid increase in left ventricular pressure. When it becomes higher than that of the left atrium, the mitral valve closes. The pressure continues to rise; when it exceeds that of the aorta, the aortic valve opens. Left ventricular diastole begins after the peak systolic pressure and there is a rapid fall in pressure. When the left ventricular pressure falls to a level below that of the aorta, the aortic valve closes. As the left ventricular pressure continues to fall, it becomes lower than that of the left atrium and the mitral valve opens, resulting in left atrial emptying into the left ventricle, or ventricular diastole.

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

Segmental wall motion also can be visually graded as normal, hypokinetic, akinetic, or dyskinetic or quantified by using one of several computer algorithms.

Mitral regurgitation

The severity of mitral regurgitation can be graded on the basis of the amount of contrast regurgitation from the left ventricle through the incompetent mitral valve into the left atrium, with the opacification of the left atrium used as a guide. Grading is determined 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 (see the image below)
Acute severe mitral regurgitation. Image courtesy Acute severe mitral regurgitation. Image courtesy of Olurotimi Badero, MD, FACP and www.tctmd.com.

Regurgitant fraction

An estimate of the degree of valvular regurgitation may be obtained by computing the regurgitant fraction (RF). The RF is the portion of the angiographic stroke volume that does not contribute to the net cardiac output.

The RF is computed as regurgitant stroke volume divided by angiographic stroke volume. Regurgitant stroke volume is the difference between angiographic stroke volume and the forward stroke volume. Angiographic stroke volume is computed from the left ventriculography 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 correlated with the severity of mitral regurgitation as follows:

  • 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 higher is equivalent to grade 4+ regurgitation

Timing with ECG

Hemodynamic data require examination not only of individual pressure waves, but also their timing to events on the ECG, particularly the QRS complex. Correct interpretation of normal right-sided heart pressure waveforms and careful examination reveal unanticipated pathophysiologic mechanisms.

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

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