Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
History of present illness—detailed account of symptom chronology: acute versus chronic
Angina—stable or unstable, arrhythmia, congestive heart failure
Timing of recent intervention
Dyspnea: New York Heart Association (NYHA) functional classification for heart failure
Class I: no limitations during ordinary activity, asymptomatic
Class II: slight limitation during ordinary activity
Class III: marked limitation of ordinary activity
Class IV: no physical activity without symptoms
Arrhythmia, palpitations, peripheral edema
Medical and surgical history—detailed
Prior sternotomy
Recent percutaneous coronary intervention (PCI)
Medications and allergies—detailed list and dosages
Current anticoagulation use; clopidogrel should be stopped 5 days before surgery
Social history, including tobacco, ethyl alcohol, and drug use
Family history
Review of symptoms
Neurologic—cranial nerves, strength, and motor bilaterally
Pulmonary—rales, rhonchi, wheezing (pneumonia, congestive heart failure, chronic obstructive pulmonary disease)
Cardiovascular
Signs or symptoms of congestive heart failure—jugular venous distention, rales, S3 gallop
Arrhythmias, presence of a pacemaker, and/or defibrillator
Previous sternotomy/thoracotomy incisions, chest tubes
Vascular examination
Documentation of peripheral pulses—radial, ulnar, femoral, dorsalis pedis
Evidence of tissue loss or ischemic extremities
Evaluation of carotid disease, bruits
Evaluation of neck/groin for potential internal jugular/femoral cannulation
Evaluation of conduit suitability (radial arteries, saphenous veins, blood pressure in both arms)
Heart murmurs
Systolic ejection: aortic stenosis (AS) (radiates to carotids), pulmonary stenosis, atrial septal defect (ASD), innocent flow murmurs
Pansystolic: mitral regurgitation (MR) (radiates to axilla), tricuspid regurgitation, ventricular septal defect (VSD), patent ductus arteriosus (PDA)
Early diastolic: aortic insufficiency (AI), pulmonary regurgitation
Gastrointestinal—old incisions, hernia
Musculoskeletal—strength, sensation, gait, among others
Electrocardiogram—arrhythmias, ischemic changes, conduction delays, chamber enlargement
Laboratory—complete blood cell count, electrolytes, coagulation profile, type and crossmatch for 2 units of packed red blood cells
Posteroanterior and lateral chest radiograph—visualize plane between sternum and heart on lateral
Nuclear perfusion testing
Myocardial reserve—hibernating myocardium that may benefit from revascularization
Functional significance of coronary lesion
Cardiac catheterization and echocardiogram
Distribution of coronary artery disease
Evaluation of ventricular wall motion and ejection fraction function and wall motion
Presence of valvular dysfunction
Risk calculator (STS, EuroScore, Seattle Heart Failure Models)
Accurate height and weight recorded in chart to calculate body surface area
Twelve-lead electrocardiogram
Posteroanterior and lateral chest radiograph (recent)
Hibiclens scrub and clipper prep to chest the night before surgery
Nothing by mouth (NPO) after midnight
Antibiotics on call—cefuroxime 1.5 g intravenous (IV) on call or use vancomycin 1 g IV for reoperative/valve patients
Medications
In general, medications are continued until surgery, especially antianginal agents, antihypertensive agents with the exception of angiotensin-converting enzyme (ACE) inhibitors, nitroglycerin, and heparin drips (hold hours before surgery).
Continue all antiarrhythmic agents.
Perioperative steroid and insulin coverage is per routine.
Ensure appropriate discontinuation of anticoagulants.
Perioperative monitors generally placed immediately before operation
Right radial/brachial radial/brachial arterial line
Swan-Ganz catheter (some institutions omit this step for straightforward procedures)
Indications
Chronic stable angina unrelieved by medication/asymptomatic angina—left main disease, left main equivalent disease (proximal left anterior descending [LAD] and proximal circumflex arteries), three-vessel disease
Unstable angina despite treatment/stable angina—left main disease, left main equivalent, three-vessel disease, two-vessel disease with proximal LAD and reduced ventricular function (left ventricular ejection fraction [LVEF] <50%)
Acute myocardial infarction—if significant coronary disease exists beyond the area of infarction, ongoing angina after infarction, or unstable hemodynamic status. Controversy exists on the timing of surgical intervention. Unstable angina/non–ST elevation myocardial infarction (NSTEMI)—left main, left main equivalent disease
Ventricular arrhythmias with coronary disease/ST elevation myocardial infarction (STEMI)—failed PCI or anatomically not a PCI candidate
Failed percutaneous transluminal coronary angioplasty/poor LV function—left main disease, left main equivalent, proximal LAD and two-vessel disease
Life-threatening ventricular arrhythmias—left main, three-vessel disease
Failed PCI—shock with ongoing ischemia
Coronary artery bypass grafting (CABG) has been shown to be superior to medical treatment of coronary disease in the following situations:
In patients with asymptomatic or mild angina and the following conditions:
Significant left main disease (Veterans Affairs Cooperative Study 1972–74)
Three-vessel coronary artery disease with proximal left anterior descending disease or double-vessel disease in conjunction with left main disease (European Coronary Surgery Study Group 1973–76)
Three-vessel disease and ventricular dysfunction (Coronary Artery Surgery Study 1975–79)
In patients with chronic moderate-to-severe angina
Unstable angina despite full medical therapy
Failed percutaneous transluminal coronary angioplasty with reasonable targets
Persistent ventricular arrhythmias in patients with coronary artery disease
Patients with diabetes with double-vessel disease—reduced ventricular function
There is no difference in rates of myocardial infarction in CABG and medically treated patients.
PCI is acceptable treatment option for single-vessel disease or two-vessel disease. CABG has been shown to be superior to drug-eluting stent (DES) PCI in patients with complex coronary disease, such as left main or three-vessel disease. CABG has been shown to have lower incidence of revascularization and myocardial infarction (MI) in the Synergy Between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) trial.
Internal mammary artery grafts are the conduit of choice because of superior patency rates compared with saphenous vein grafts (in situ and free grafts) (90%–95% vs. 50%–60% at 10 years). Patency rates for the internal mammary artery compared with the great saphenous vein graft at 10 and 15 years are 95% and 88% and 61% and 32%, respectively. Radial artery and less commonly gastroepiploic artery may be used as conduit.
Off-pump CABG is an approach used to minimize aortic manipulation and avoid the systemic effects of cardiopulmonary bypass. On-pump versus off-pump CABG shows no difference in outcomes, with off-pump surgery conferring a lower initial stroke risk that was not clinically significant and a trend toward lower number of target vessels grafted.
AS
It is commonly caused by bicuspid valve, rheumatic disease, or calcific/degenerative AS.
Symptoms include triad of dyspnea, angina, and syncope.
AS severity
Mild AS: aortic valve area greater than 1.5 cm 2 , mean pressure gradient less than 25 mm Hg, peak jet velocity less than 3.0 m/s
Moderate AS: aortic valve area 1.0–1.5 cm 2 , mean pressure gradient 25–40 mm Hg, peak jet velocity 3.0–4.0 m/s
Severe AS: aortic valve area less than 1.0 cm 2 , mean pressure gradient greater than 40 mm Hg, peak jet velocity greater than 4.0 m/s
Indications for surgery
Symptomatic patients with severe AS valve gradient of greater than 50 mm Hg or valve area less than 0.8 cm 2 /m 2
Asymptomatic patients with significant stenosis and left ventricular hypertrophy should be considered who are undergoing CABG.
Asymptomatic patients with evidence of decreased systolic function should also be considered.
Coronary angiography is performed before surgery because of high rate of concomitant coronary artery disease.
AI
Causative factors include rheumatic disease, annular ectasia, endocarditis, aortic dissection, and aortitis.
Frequently asymptomatic unless acute or decompensated
Acute AI presents with syncope, pulmonary edema, classic “water hammer” pulse, and Austin Flint murmur (late diastolic) from blood flow regurgitant jet hitting the anterior mitral valve leaflet.
Indications for surgery
Symptomatic patients
Patients with cardiomegaly or deteriorating systolic function as assessed by echocardiography asymptomatic; patients with severe AI and reduced systolic function less than 50% as assessed by echocardiography
Asymptomatic patients and left ventricular diameter at end diastole (LVEDD) greater than 75 mm or left ventricular diameter at end systole (LVESD) greater than 55 mm
Mitral stenosis
Primarily rheumatic—leaflet thickening with calcification and fusion
Symptoms—dyspnea, orthopnea, and paroxysmal nocturnal dyspnea, atrial fibrillation. Loud S1, opening snap. Radiographs may demonstrate left atrial enlargement and pulmonary venous hypertension.
Indications for surgery—presence of chronic symptoms or acute episodes of pulmonary venous hypertension. Mitral valve area less than 1.5 cm 2 and NYHA class III–IV symptoms
Chronic atrial fibrillation—a complication of progressive left atrial enlargement
Mitral regurgitation
Causative factors—rheumatic disease, myxomatous valve structure, endocarditis, ischemia or papillary muscle dysfunction, and congenital structural defects
Severity and development of symptoms—varies with causative factor; rheumatic disease is more insidious in onset, whereas ischemic mitral regurgitation is often acute in onset.
Carpentier classification
Type I—normal leaflet motion: endocarditis, dilated cardiomyopathy with annular dilation
Type II—excessive leaflet motion: prolapse, chordal rupture, papillary muscle rupture
Type III—restricted leaflet motion
IIIa: restricted opening: rheumatic disease
IIIb: restricted closing: ischemic MR
As with mitral stenosis, indications for surgery depend on the severity of symptoms. Indications for surgery:
Symptomatic severe MR and NYHA class II–IV LV dysfunction
Asymptomatic severe MR with normal LV if repair greater than 90% likely, or new atrial fibrillation, or pulmonary artery pressure (PAP) greater than 50 mm Hg at rest
Ischemic mitral regurgitation is usually corrected at the time of coronary bypass, with either valve replacement or annuloplasty. Often mild ischemic mitral regurgitation may improve by coronary bypass only.
Rheumatic or myxomatous valve disease may be corrected by valve repair or replacement. The advantages of repair versus replacement are the low rate of endocarditis and lack of need for long-term anticoagulation. Mitral valve repair is associated with favorable outcomes over replacement.
Incidence 6.2 per 100,000 people per year
Etiology—indwelling catheters, IV drug use in the setting of damaged cardiac endothelium results in platelet and fibrin deposition and allows bacteria or fungus to adhere
Mitral > aortic > tricuspid (most common in IV drug users), may also have prosthetic valve endocarditis
Microbiology
Streptococcus viridans , Staphylococcus aureus , Staphylococcus epidermidis , enterococci
Clinical findings
Fevers, new murmur, Roth spots, Osler nodes, Janeway lesions, petechiae
Duke criteria
Major criteria (2): positive blood cultures ( S. viridans , Streptococcus bovis , HACEK [ Haemophilus species, Aggregatibacter species, Cardiobacterium hominis , Eikenella corrodens , and Kingella species], enteroccoci, S. aureus ), evidence for endocardial involvement on echocardiogram
Minor criteria (5): fever less than 38°C, vascular phenomena, immunologic phenomena, positive blood culture not previous meeting requirement, new-onset heart failure, new conduction disturbances, predisposing heart condition or IV drug use
Echocardiography—Transesophageal is 90% specific and 95% sensitive for detecting endocardial vegetations or lesions, versus transthoracic (90% specific and 50% sensitive).
Indications for surgery—new-onset heart failure, new heart block, continued sepsis despite optimal medical management, valve dehiscence, and fungal infection
Causative factors—hypertension, atherosclerosis, connective tissue disorders, cystic medial necrosis (e.g., Marfan syndrome, Ehlers-Danlos, Turner syndrome), infections, trauma, pregnancy, age greater than 60 years are risk factors.
Clinical considerations
Dissections diagnosed within 2 weeks from onset of symptoms are acute.
Mortality secondary to acute dissection ranges from 30% to 40%.
Clinical presentation—sudden sharp tearing chest pain that radiates to the back; other symptoms can include stroke, MI, hemopericardium/tamponade, severe AI, renal/mesenteric ischemia, limb ischemia, paraplegia
DeBakey classification
Type I—intimal disruption of ascending aorta that extends to involve the entire descending thoracic aorta and abdominal aorta
Type II—involves the ascending aorta only (stops at the innominate artery)
Type III—involves the descending thoracic and abdominal aorta only (distal to left subclavian artery)
Stanford classification
Type A—any dissection that involves the ascending aorta
Type B—any dissection that involves only the descending aorta, distal to the left subclavian artery
Diagnosis is usually made by aortogram, chest computed tomography scan, or echocardiogram (transesophageal echocardiogram [TEE] or transthoracic echocardiogram [TTE]). Preoperative control of hypertension with nitroprusside and beta-blockers is an essential part of management.
Initial management
Start beta-blockade first to decrease heart rate and aortic wall d P /d t.
Nitroprusside can then decrease the blood pressure (if sodium nitroprusside [SNP] given first, it actually increases cardiac work and the d P /d t ; this theoretically can increase propagation of the dissection).
Dissection may advance proximally, disrupting coronary blood flow or inducing aortic valve incompetence, or distally, causing stroke, renal failure, paraplegia, or intestinal ischemia.
Indications for emergent operative repair
Acute type A dissection
Operative repair involves replacement of the affected aorta with a prosthetic graft.
Cardiopulmonary bypass is required, and hypothermic circulatory arrest is often used for transverse arch dissections.
Aortic valve replacement (AVR) and coronary reimplantation may be required for type A aneurysms that involve the aortic root.
Type B dissection with failed medical therapy such as hypertension, inadequate pain control, progressive dissection by radiographic studies, impaired organ perfusion, or impending aortic rupture
Type B dissections can be medically managed unless expansion, rupture, or compromise of branch arteries develops or hypertension becomes refractory.
Postoperative complications include renal failure, intestinal ischemia, stroke, and paraplegia.
This injury results from deceleration injury and usually occurs just distal to the left subclavian artery, at the level of the ligamentum arteriosum.
Chest radiograph findings include widened mediastinum, pleural capping, associated first and second rib fractures, loss of the aortic knob, hemothorax, deviation of the trachea or nasogastric tube, and associated thoracic injuries (scapular and clavicular fractures).
Definitive diagnosis is made by aortogram, but chest computed tomography and transesophageal echocardiography also aid in the diagnosis.
Imperative that immediate life-threatening injuries (e.g., positive diagnostic peritoneal lavage) be treated before repair.
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