Chapter 272 - Diagnostic Cardiac Catheterization and Coronary Angiography Flashcards
Summarize the history of cardiac catheterization and coronary angiography.
“Diagnostic cardiac catheterization and coronary angrioaphy are considered the gold standard in the assessment of the anatomy and physiology of the heart and its associated vasculature. In 1929, Forssmann demonstead the feasibility of cardiac catheterization in humans when he passed a urological catheter from a vein in his arm to his right atrium and documented the catheter’s position in the heart by x-ray. In the 1940s, Cournand and Richards applied this technique to patients with cardiovascular diease to evaluate cardiac function. These three physicians were awarded the Nobel Prize in 1956. In 1958, Sones inadvertently perfomed the first selective coronary angiography when a catheter in the left ventricle slipped back across the aortic valve, engaged the right coronary artery, and power-injected 40 mL of contrast down the vessel. The resulting angiogram provided superb anatomic detail of the artery, and the patient suffered no adverse effects. Sones went on to develop selective coronary catheters, which were modified further by Judkins, who developed preformed catheters and allowed coronary artery angiography to gain widespread use as a diagnostic tool. In the United States, cardiac catheterization is the second most common operative procedure, with more than one million procedures performed annually.”
Which subset of patients might not need cardiac catheterization before cardiac surgery?
“Cadiac catheterization is not mandatory prior to cardiac sugery in some younger patients who have congenital or valvular heart disease that is well defined by noninvasive imaging and who do not have symptoms or risk factors that suggest concomitant coronary artery disease.”
What are the major complications of elective and emergent catheterization?
“the risks associated with elective cardiac catheterization are relatively low, with a reported risk of 0,05% for myocardial infarction, 0,07% for stroke, and 0,08-0,14% for death. These risks increase substantially if the catheterization is performed emergently, during acute myocardial infarction or in hemodynamically unstable patients.”
Besides major complications, name additional risks of catheterization.
“Additional risks of the procedure include tachy- or bradyarrhythmias that require countershock or pharmacologic therapy, acute renal failure leading to transiet or permanent dialysis, vascular complications that necessitate surgical repiair, and significant access-site bleeding. Of these risks, vascular access-site bleeding is the most common complication, occuring in 1,5-2,0% of patients, with major bleeding events associated with a worse short-a nd long-term outcome.”
What are the absolute and relative contraindications of cardiac catheterization?
Absolute: none.
Relative: “Relative contraindications do, however, exist; these include decompensated congestive heart failure; acute renal failure; severe chronic renal insufficiency, unless dialysis is planned; bacteremia; acute stroke; active gastrointestinal bleeding; severe, uncorrected electrolyte abnormalities; a history of an anaphylactic/anaphylactoid reaction to iodinated contrast agents; and a history of allergy/bronchospasm to aspirin in patients for whom progression to a percutaneous coronary intervention is likely and aspirin desensitization has not been performed.”
How many patients have an allergic reaction to contrast agents? How many have a severe reaction?
Less than 5% and 0,1-0,2% of the general population, respectively.
How does one differentiate a mild from a severe anaphylactoid reaction to a contrast agent?
“Mild reactions manifest as nausea, vomiting, and urticaria, while severe anaphylactoid reactions lead to hypotensive shock, pulmonary edema, and cardiorespiratory arrest. Patients with a history of significant contrast allergy should be premedicated with corticosteroids and antihistamines (H1- and H2-blockers) and studies performed with nonionic, low-osmolar contrast agents that have a lower reported rate of allergic reactions.”
How frequently does contrast-induced acute kidney injury occur? How does one define it? Which patients are at greater risk?
“Contrast-induce acute kidney injury, defined as an increase in creatinine >0,5mg/dL or 25% above baseline that occurs 48-72 hours after contrast administration, occurs in ~2-7% of patients with rates of 20-30% reported in high-risk patients, including those with diabetes mellitus, congestive heart failure, chronic kidney disease, anemia, and older age.”
Regarding contrast-induced acute kidney injury, how frequently does a patient require dialysis? What is the meaning of this procedure for in-hospital mortality?
“Dialysis is required in 0,3-0,7% of patients and is associated with a fivefold increase in in-hospital mortality.”
Explain the different procedures do reduce ontrast-induced acute kidney injury.
“For all patients, adequate intravascular volume expansion with intravenous 0,9% saline (1,0-1,5mL/Kg per hour) for 3-12 hours before and continued 6-24 after the procedure limits the risk of contrast-induced acute kidney injury. Pretreatment with N-acetylcysteine (Mucomyst) has not reduced the risk of contrast-induced acute kidney injury consistently and, therefore, is no longer recommended routinely. Diabetic patients treated with metformin should stop the drug 48 hours prior to the procedure to limit the associated risk of lactic acidosis. Other strategies to decrease risk include the administration of sodium bicarbonate (3mL/Kg per hour) 1 hour before and 6 hours after the procedure; use of low- or iso-osmolar contrast agents; and limiting the volume of contrast to less than 100mL per procedure.”
Besides the preventive protocols for contrast-induced acute kidney injury, how should one preparate a patient for cardiac catheterization? Is there any difference in preparation if the patient will be submitted to percutaneous coronary intervention?
“Cardiac catheterization is performed after the patient has fasted for 6 hours and has received intravenous conscious sedation to remain awake but sedated during the procedure. All patients with suspected coronary artery disease are pretreated with 325 mg aspirin. In patients in whom the procedure is likely to progress to a percutaneous coronary intervention, an additional antiplatelet agent should be started: clopidogrel (600-mg loading dose and 75 mg daily) or prasugrel (60-mg loading dose and 10 mg daily) or ticagrelor (180-mg loading and 90 mg twice daily). Prasugrel should not be selected for individuals with prior stroke or transient ischemic attack. Warfarin is held starting 2-3 days prior to the catheterization to allow the internation l normalized ratio (INR) to fall to less than 1,7 and limit access-site bleeding complications. Cardiac catheterization is a sterile procedure, so antibiotic prophylaxis is not required.”
For left cardiac catheterization, how should one choose between femoral and radial site-of-access?
“The radial artery (or brachial artery) may also be used as an arterial access site in patients, particularly those with peripheral arterial disease that involves the abdominal aorta, iliac, or femoral vessels; severe iliac artery tortuosity; morbid obesity; or preference for early postprocedure ambulation. Use of radial-artery access is gaining popularity due to a lower rate of access-site bleeding complications.”
Allen’s test should be performed before using radial artery as an access for cardiac catheterization.
True or False?
True.
If one wants to acces the right heart through catheterization but the patient has an inferior vena cava filter, which other accesses should be considered?
Internal jugular or antecubital veins.
In which conditions might be reasonable to perform a right heart catheterization?
Unexplained dyspnea, valvular heart disease, pericardial disease, right and/or left ventricular dysfunction, congenital heart disease, and suspected intracardiac shunts.
How does one measure left atrial pressure while performing right heart catheterization?
It cannot be measured directly but a surrage, pulmonary wedge pressure, is measured.
How should one access the left ventricle in patients with a tilting-disc prosthetic aortic valve?
“In patients with a tilting-disc prosthetic aortic valve, corssing the valve with a catheter is contraindicated, and the left heart may be accessed via a transseptal technique from the right atrium using a needle-tipped catheter to puncture the atrial septum at the fossa ovalis. Once the catheter crosses from the right to the left atrium, it can be advanced across the mitral valve to the left ventricle. This technique is also used for mitral valvuloplasty.”
Is there a need to anticoagulate patients during left heart catheterization? If so, how does one anticoagulate them?
“Heparin is given for prolonged procedures to limit the risk of stroke from embolism of clots that may form on the catheter. For patients with heparin-induced thrombocytopenia, the direct thrombin inhibitors bivalirudin (0,75mg/Kg bolus, 1,75mg/Kg per hour for the duration of the procedure) or agatroban (350μg/Kg bolus, 15μg/Kg per minute for the duration of the procedure) may be used.”
While performing left cardiac catheterization, which indicators help one distinguish between aortic stenosis and hypertrophic obstructive cardiomyopathy?
“Hemodynamic measurements also discriminate between aortic stenosis and hypertrophic obstructive cardiomyopathy where the asymmetrically hypertrophied septum creates a dynamic intraventricular pressure gradient during ventricular systole. The magnitude of this bostruction is measured using an end-hole catheter positioned at the left ventricular apex that is pulled back while recording pressure; once the catheter has passed the septal obstruction and is positioned in the apex of the left ventricle, a gradient can be measured between the left ventricular apex and the aorta. Hypertrophic obstructive cardiomyopathy is confirmed by the Brockenbough-Braunwald sign: following a premature ventricular contraction, there is an increase in the left ventricular-aorta pressure gradient with a simultaneous decrease in the aortic pulse pressure. These findings are absent in aortic stenosis.”
Which hemodynamic measurements help one differentiate between cardiac tamponade, constrictive pericarditis, and restrictive cardiomyopathy?
“In cardiac tamponade, right atrial pressure is increased with a decreased or absent “y” descent, indicative of impaired right atrial emptying in diastole, and there is diastolic equalization of pressures in all cardiac chambers. In constrictive pericarditis, right atrial pressure is elevated with a prominent “y” descent, indicating rapid filling of the right ventricle during early diastole. A diastolic dip and plateau or “square root sign”, in the ventricular waveforms due to an abrupt halt in ventricular filling during diastole; right ventricular and pulmonary artery pressures are elevated; and discordant pressure changes in the right and left ventricles with inspiration (right ventricular systolic pressure increases while left ventricular systolic pressure decreases) are observed. The latter hemodynamic phenomenon is the most specific for constriction. Restrictive cardiomyopathy may be distinguished from constrictive pericarditis by a marked increase in right ventricular and pulmonary artery systolic pressures (usually >60mmHg), a separation of the left and right ventricular diastolic pressures by >5mmHg (at baseline or with acute volume loading), and concordant changes in left and right ventricular diastolic filling pressures with inspiration (both increase).”
How does one calculate cardiac output using catheterization? Which method is more reliable?
“Cardiac output is measured by the Fick methoed or the thermodilution techcnique. Typically, the Fick method and thermodilution technique are both performed during cardiac catheterization, although the Fick method is considered more reliable in the presence of tricuspid regurgitation and in low-output states.”
What is the formula for Fick’s method?
"The Fick method uses oxygen as the indicator substance and is based on the principle that the amount of a substance taken up or released by an organ (oxygen consumption) is equal to the product of its blood flow (cardiac output) and the difference in the concentration of the substance in the arterial and venous circulation (arterial-venous oxygen diffrence)." Cardiac output (L/min) = (oxygen consumpion[mL/min]/(arterial-venous oxygen difference[mL/L])
Which drugs might reduce pulmonary vascular resistance and might be useful during catheterization?
“Pulmonary vascular resistance is lowered by oxygen, nitroprusside, calcium channel blockers, prostacyclin infusions, and inhaled nitric oxide; these therapies may be administered during catheterization to determine if increased pulmonary vascular resistance is fixed or reversible.”
Which formulas does one use to calculate the following: (i) cardiac output; (ii) vascular resistance; (iii) valve area.
(i) Fick’s method formula.
(ii) Extrapolation from Ohm’s law of electrical resistance.
(iii) Grolin formula.
