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Medications
• all regular cardiac medications should be continued to the morning of surgery
(including nitro patch), except:
• Amiodarone – usually continued to prevent A-fib despite potential intraoperative
problems (resistant bradycardia, hypotension, etc.)
• ACE inhibitors – small risk of hypotension perioperatively with these drugs, therefore
stop 24 hours preop (controversial)
• anticoagulants
coumadin: stop 4-5 days prior to surgery; admit and start on IV heparin if high risk of
thrombosis, large left atrium, atrial fibrilation, mitral valve prosthesis
heparin: IV heparin should be stopped on call to OR
ASA/ticlodipine/NSAIDs/clopidogrel – stop 7-10 days preop if possible (new
evidence suggests ASA should be continued to day of surgery and restarted
within 24-48h post-op*)
*Mangano, et al. Aspirin and mortality from coronary bypass surgery. NEMJ 2002, 347(17): 1309-1317.
Intraoperative Monitoring
• standard monitors include:
five-lead ECG monitoring with ST segment analyses (leads II, V5)
noninvasive blood pressure measurement
direct arterial pressure
pulse oximetry
end tidal gas analysis (capnography)
temperature (nasopharyngeal in all patients, also rectal in infants)
urine output via Foley catheter
central venous pressure (CVP) (assess filling of right ventricle)
• commonly used monitors:
Swan-Ganz catheter
monitors central venous pressure (CVP), pulmonary artery pressure,
pulmonary capillary wedge pressure (PCWP), cardiac output
(as needed), and mixed venous gas measurements (as needed)
indications for use: LV dysfunction (EF<40%), poor distal vessels (high
risk of poor revascularization), preoperative hemodynamic instability,
anticipated long cardiopulmonary bypass time, significant coexistent
medical disease (pulmonary, cerebral, renal)
transesophageal echocardiography (TEE)
indications: significant atheromatous disease of aorta, mitral valve
repair/replacement, aortic valve repair/replacement, adult/pediatric
congenital heart disease, ventricular myomectomy, ventricular
remodeling procedures, endocarditis, cardiac tumour resection, heart
transplant, perioperative cardiovascular instability or difficult weaning
from CPB; postoperative applications include evaluation of adequacy of
surgical repair, detection of intracardiac air and management of
hemodynamics
contraindications: esophageal pathology (stricture, tumour, recent
surgical resection), C-spine instability; relative contraindications:
esophageal varices, esophagitis, coagulopathy
• monitors added at conclusion of operation:
pacing wires (atrial on right side and ventricular on left)
mediastinal and pleural chest tubes
Cardiopulmonary Bypassy Bypass
• CPB and cardioplegia provide a still bloodless heart by diverting blood into a
heart-lung machine (extracorporeal circuit)
• an initial dose of 3000 IU/kg of heparin is administered to achieve systemic
anticoagulation (activated clotting time or ACT should be >500 seconds before
initiation of bypass)
Indications
• unstable angina with failed maximal medical therapy
• severe chronic stable angina with multivessel disease, left main stenosis or
proximal LAD stenosis
• severe reversible LV dysfunction (documented by stress thallium
scan or dobutamine echocardiography)
• coronary occlusive complications during PTCA or other endovascular interventions
• patients who develop life-threatening complications after acute MI; including VSD,
ventricular free-wall rupture or acute MR
• to improve survival in patients (even if asymptomatic) with:
left main stenosis >50% (annual mortality 10-15%)
left main equivalent: >70% stenosis of proximal left anterior descending
(LAD) and proximal circumflex artery (PCA)
three vessel disease with ejection fraction (EF) <50%
three vessel disease with EF >50% but significant inducible ischemia
one or two vessel disease with extensive myocardium at risk, not PTCA
candidate
Operative Issues
• isolated proximal disease in large coronary arteries (>1.0 - 1.5 mm) is ideal for
bypass surgery; small, diffusely diseased coronary arteries are not suitable for bypass
surgery
• arteries with severe stenoses (>50% diameter reduction) are bypassed, except those of
small caliber (<1 mm in diameter)
• see Cardiology, C19 for discussion of PTCA vs. surgery
• left ventricular function is an important determinant of outcome of all heart diseases
• patients with severe LV dysfunction usually have poor prognosis, but surgery can
sometimes dramatically improve LV function; patients with severe LV dysfunction and
easily bypassable coronaries usually do very well whereas those with bad ventricles
and marginally graftable coronary arteries are usually poor surgical candidates
• assess viability of non-functioning myocardial segments using thallium and sestamibi
myocardial imaging, PET scanning or MRI (see Cardiology, C9)
• surgically correcting volume overloading conditions (e.g. AI/MR) may not change the
prognosis due to irreversibly damaged myocardium but symptoms can be improved;
however depressed ventricular function caused by AS almost always improves
following relief of obstruction
• the Surgical Treatment for Ischemic Heart Failure (STICH) Trial is a RCT comparing
medical treatment with CABG and/or surgical ventricular restoration among patients
with CHF, LVEF <35%, and coronary disease suitable for revascularization; it should be
completed by 2008 (http://www.stichtrial.org)
Surgical Options
• balloon valvuloplasty (rarely done)
reserved for critically ill patients with end-stage AS as a “bridge” to aortic valve
replacement or other therapeutic procedures; also considered in pregnancy
50% recurrence of AS in 6 months
• decalcification/debridement
in patients with mild to moderate AS in whom the primary indication for
surgery is coronary artery disease
• commissurotomy
useful in a small percentage of patients with aortic rheumatic valve disease with
a trileaflet valve and minimal to no calcification
• valve replacement
practically all patients with severe AS require aortic valve replacement
Aortic Regurgitation (AR)
Indications for Surgery
• acute AR with CHF
• NYHA class III-IV symptoms
• endocarditis with hemodynamic compromise or recurrent emboli
• evidence of LV decompensation in the asymptomatic patient
EF <55%, end-diastolic dimension > 70 mm, end-systolic dimension > 55 mm
Surgical Options
• valve repair
partial resection of valve leaflets with reapproximation to improve leaflet
coaptation (especially for bicuspid valves), often with a suture annuloplasty
useful in younger patients
• valve replacement
most patients with AR require aortic valve replacement
• Bentall procedure
valved conduit used when an ascending aortic aneurysm (annuloaortic ectasia)
is also present
Mitral Stenosis (MS)
Indications for Surgery
• MV area < 1.5 cm2 (normal is 4-6 cm2)
• NYHA classes III-IV
• NYHA class II when MV area < 1 cm2 (critical mitral stenosis)
• history of atrial fibrillation and/or systemic emboli (from LA thrombus)
• worsening pulmonary hypertension
Surgical Options
• percutaneous balloon mitral valvuloplasty
useful in young rheumatic patients with MS and good leaflet pliability,
minimal chordal thickening and intact subvalvular mechanism
considered in pregnant patients with critical MS
contraindicated if left atrial thrombus present
• open mitral commisurotomy
for patients with mild calcification and mild leaflet/chordal thickening ± other
coexistent diseased valves (e.g. aortic and/or tricuspid)
technique involves incision of both commissures, incision/resection of fused
chordae, and occasionally incision into papillary muscle to increase mobility (if
evidence of chordae shortening from scarring and fibrosis)
50% of patients will require reoperation 8 years following initial
commisurotomy due to restenosis
• valve replacement
for moderate to severe calcification with severely scarred valve leaflets or subvalvular
apparatus
Mitral Regurgitation (MR)
Indications for Surgery
• acute MR associated with CHF, cardiogenic shock, or papillary muscle rupture
• acute endocarditis with hemodynamic compromise or recurrent emboli
• NYHA class III-IV
• NYHA class I-II symptoms with onset of atrial fibrillation or evidence of deteriorating
LV function
EF < 55%, end-diastolic dimension > 75 mm, end-systolic dimension > 45 mm
Surgical Options
• valve repair
applicable to more than 75% of patients with MR
myxomatous degeneration of the MV is ideal for repair
techniques include annuloplasty rings, leaflet repairs, patch repair (for
endocarditis), and chordal transfers, shortening or replacement
• valve replacement
indicated only when satisfactory repair cannot be accomplished
patients with MR due to ischemic heart disease, rheumatic heart disease or
advanced myxomatous disease are more likely to need MV replacement
replacement usually required if heavily calcified annulus or if papillary
muscle rupture
• the advantages of repair vs. replacement are the low rate of endocarditis, lack of need
for long-term anticoagulation, and less chance of re-operation
Aortic Dissection
Definition
• spontaneous tear in aortic intima allowing blood to be driven between the aortic
intima and media; acute < 2 weeks, chronic > 2 weeks
Classification
• DeBakey:
Type I – involves ascending and descending aorta
Type II – ascending aorta only (stops at the innominate artery)
Type IIIA – descending thoracic aorta only (distal to left subclavian artery and
proximal to diaphragm)
Type IIIB – Type IIIA plus abdominal aorta
• Stanford
Type A – ascending aorta and aortic arch; requires emergency surgery
Type B – aorta distal to subclavian artery; emergency surgery only if
complications of dissection (requires long-term follow-up to assess aneurysm
size)
Etiology
• most common: damage to aortic media (smooth muscle and elastic tissue), leading to
degenerative/cystic changes due to hypertension
• other: cystic medial necrosis, atherosclerosis, connective tissue disease (Marfan’s,
Ehlers-Danlos), congenital conditions (coarctation of aorta, bicuspid aortic valves,
PDA), infection, trauma, arteritis (Takayasu’s)
Epidemiology
• incidence of 5.2 in 1,000,000
• male:female = 3.2:1.0
• small increased incidence in African-Canadians (related to higher incidence of
hypertension)
• lowest incidence in Asians
Clinical Features
• sudden onset searing chest pain that radiates to back with:
hypertension (75-85% of patients)
asymmetric BPs and pulses between arms
ischemic syndromes due to occlusion of aortic branches: coronary (MI),
carotids (ischemic stroke, Horner’s syndrome), splanchnic (ischemic gut)
“unseating” of aortic valve cusps (new diastolic murmur in 20-30%)
rupture into pleura (dyspnea, hemoptysis) or peritoneum (hypotension, shock)
or pericardium (cardiac tamponade)
renal insufficiency
lower limb ischemia (cold legs)
Investigations
• CXR:
Pleural cap
Widened mediastinum
Left pleural effusion with extravasation of blood
• TEE: user dependent, cannot visualize abdominal aorta
• ECG: LVH (90%), ± MI, pericarditis, heart block
• CT, aortography, MRI
• Blood work: LDH (R/O ischemic gut), amylase (R/O pancreatitis)
Treatment
• Pharmacologic
sodium nitroprusside and β-blocker to lower BP and decrease cardiac
contractility
• Surgical
resection of intimal tear, reconstitution of flow through true lumen, replacement
of the affected aorta with prosthetic graft, correction of any pred13sposing factors
(e.g. bicuspid aortic valve, PDA, etc)
post-operative complications: renal failure, intestinal ischemia, stroke,
paraplegia, persistent leg ischemia, and death
Type A: requires emergent surgery with CPB, may require hypothermic
circulation for transverse arch dissections, valve replacement and coronary
re-implantation for aortic root involvement
Type B: initially managed medically – 10-20% require urgent operation for
complications (expansion, rupture, compromise of branch arteries,
refractory HTN, or ongoing pain)
Aortic Aneurysm
Definition
• localized dilatation of an artery that is beyond its normal diameter (2X diameter)
true aneurysm: involving all vessel wall layers (intima, media and adventitia)
false aneurysm: disruption of the aortic wall or the anastomotic site between
vessel and graft with containment of blood by fibrous capsule made of
surrounding tissue
• aneurysms can rupture, thrombose, embolize or erode and fistulize
Classification
• thoracic: ascending, transverse arch, descending
• thoracoabdominal
• abdominal
Etiology
• medial degeneration, atherosclerosis, expansion of chronic dissections,
metabolic/endocrine, mycotic (gram-ve salmonella, gram+ve staphylococcus, usually
suprarenal), neoplastic, cystic medial necrosis, trauma, aortitis (vasculitis), connective
tissue disease (Marfan syndrome, Ehlers-Danlos)
Epidemiology
• incidence 4.7 to 31.9 per 100,000 for AAA and 5.9 per 100,000 for TAA
• high risk groups:
65 years and older
male:female = 3.8:1
peripheral vascular disease, CAD, CVD
family history of AAA
Clinical Features
• common presentation: due to acute expansion or disruption of wall
syncope, pain (chest, abdominal, flank, back)
hypotension
palpable mass above the umbilicus, pulsatile mass in two directions
airway or esophageal obstruction, hoarseness (left recurrent nerve paralysis),
hemoptysis, or hematemesis
bounding femoral pulses
distal pulses may be intact
• 75% asymptomatic (discovered incidentally)
• uncommon presentation
partial bowel obstruction
ureteric obstruction and hydronephrosis
GI bleed (duodenal mucosal hemorrhage, aortoduodenal fistula)
aortocaval fistula
distal embolization (blue toe)
• associated diseases
hypertension, PVD, CAD, COPD, renal insufficiency
Investigations
• abdominal U/S (100% sensitive, up to ± 0.6 cm accuracy in size determination)
• CT (accurate visualization, size determination)
• MRI (accurate visualization, limited access)
• aortogram (not for diagnosis because false negative normal lumen size due to
thrombus formation; indicated for associated renovascular HTN, peri-renal AAA,
visceral angina, iliac disease)
• doppler/duplex (r/o vascular tree aneurysms elsewhere)
Treatment
Conservative
• cardiovascular risk factor reduction: smoking cessation*, HTN control*, DM and
hyperlipidemia control (*most important)
• regular exercise
• watchful waiting, U/S q 6 months
Surgical
• when risk of rupture greater than or equal to risk of surgery
• risk of rupture depends on:
1. size 1-year rupture risk
< 4 cm 0%
4-4.99 cm 1%
5-5.99 cm 11%
6-6.99 cm 25%
2. rate of enlargement > 0.4 cm/yr
3. symptomatic, co-morbidities (HTN, COPD, dissection), smoking
• elective AAA repair mortality: 2-5%, elective TAA repair mortality < 10% (highest
with proximal aortic and thoracoabdominal repairs)
• consider revascularization for patients with CAD before elective repair of aneurysm
• indications:
general: ruptured, symptomatic, mycotic, associated with acute Type A
dissection or complicated Type B dissection or when risk of rupture
is greater than risk of surgery (size > 5.5 cm or > 2x normal lumen size)
ascending thoracic aortic aneurysms
symptomatic, enlarging, diameter > 5.5 cm or > 2x normal lumen
size, > 4.5 cm + aortic regurgitation (annuloaortic ectasia)
• contraindications: life expectancy < 1 year, terminal disease (cancer), significant
co-morbidities (recent MI, unstable angina), decreased mental acuity, advanced age
• surgical options:
open surgery (laparotomy) with graft replacement (see Figure 5)
possible complications
– early: renal failure, spinal cord injury (paraparesis or
paraplegia), impotence, arterial thrombosis, anastomotic rupture
or bleeding, peripheral emboli
– late: graft infection/ thrombosis, aortoenteric fistula,
anastomotic (pseudo) aneurysm
endoluminal graft placement under image guidance
newer procedure, no long term data
high success rates in patients with suitable anatomy and experienced
centres
advantages: decreased morbidity and mortality, procedure time, need
for transfusion, ICU admissions, length of hospitalization, and
recovery time
disadvantages: endoleak rates as high as 20-30%, device failure
increasing as longer follow-up periods are achieved, re-interventions
rates 10-30%, cost-effectiveness is an issue (devices are very expensive)
complications
– early: immediate conversion to open repair, groin hematoma,
arterial thrombosis, iliac artery rupture, and thromboemboli
– late: endoleak, severe graft kinking, migration, thrombosis,
rupture of aneurysm
Chronic Arterial Occlusion/Insufficiency
Etiology
• predominantly due to atherosclerosis; primarily a disease of the lower extremities with
symptoms related to the location and number of obstructions
Risk Factors
• major: smoking, DM, hyperhomocysteinemia
• minor: HTN, hyperlipidemia, family history, obesity, sedentary lifestyle, male gender
Clinical Features
• claudication: 3 components
pain with exertion: usually in calves or any exercising group
relieved by short rest: 2 to 5 minutes, and no postural changes necessary
reproducible: same distance to illicit pain, same location of pain, same amount
of rest to relieve pain
• pulses may be absent at some locations
• signs of poor perfusion: hair loss, hypertrophic nails, atrophic muscle, skin ulcerations
and infections, slow capillary refill, prolonged pallor with elevation and rubor on
dependency, venous troughing (collapse of superficial veins of foot)
• other manifestations of atherosclerosis: CVD, CAD, impotence, splanchnic ischemia
• differential diagnosis:
osteoarthritis (OA): worse at night and varies from day-to-day
neurogenic claudication: due to spinal stenosis or radiculopathy; pain very
similar but relieved by longer rest and postural changes
varicose veins: localized pain, typically less severe, after exercise and never
at rest; related to the presence and site of varices
inflammatory processes: Buerger’s disease, Takayasu’s arteritis
other: popliteal entrapment (e.g. tumour, Baker’s cyst), radiation injury, remote
trauma
Investigations
• non-invasive
ankle-brachial index (ABI): measure brachial and ankle pressures bilaterally
(use highest value) generally, ABI < 0.90 abnormal, rest pain appears at < 0.3
Prognosis
• conservative therapy: 60-80% improve, 20-30% stay the same, 5-10% deteriorate,
5% will require intervention within 5 years, <4% will require amputation
Varicose Veins
Definition
• distended torturous superficial veins due to incompetent valves in the deep, superficial
or perforator systems
• distribution: greater saphenous vein and tributaries (most common), esophagus,
anorectum, scrotum
Etiology
• primary
main factor: inherited structural weakness of valves
contributing factors: age, female, OCP use, occupations requiring long hours of
standing, pregnancy, obesity
• secondary
deep-venous valvular insufficiency and incompetent perforating veins
malignant pelvic tumours with venous compression
• congenital anomalies – arteriovenous fistulae
Epidemiology
• most common form of venous disorder of lower extremity
• 10-20% of population
Clinical Features
• diffuse aching, fullness/tightness, nocturnal cramping
• aggravated by prolonged standing (end of day), premenstrual
• visible long, dilated and tortuous superficial veins along thigh and leg
• ulceration, hyperpigmentation, and induration (secondary varicosities)
• esophageal varices (GI bleed), hemorrhoids, varicocele
• Brodie-Trendelenberg test (valvular competence test)
with patient supine, raise leg and compress saphenous vein at thigh; have
patient stand; if veins fill quickly from top down then incompetent valves; use
multiple tourniquets to localize incompetent veins
Complications
• recurrent superficial thrombophlebitis
• hemorrhage: external or subcutaneous
• ulceration, eczema, lipodermatosclerosis, and hyperpigmentation
Treatment
• largely a cosmetic problem
• conservative: elevation of leg and/or elastic stockings
• surgical: high ligation and stripping of the long saphenous vein and its tributaries,
image-guided injection sclerotherapy, endovenous laser therapy (EVLT) – a newer
technique that offers a minimally invasive approach to ablation of the long or short
saphenous veins
Prognosis
• natural history benign, slow with predictable complications
• almost 100% symptomatic relief if varicosities are primary
• good cosmetic results
• significant post-operative recurrence, especially with sclerosing agent injection
Chronic Venous Insufficiency
Definition
• chronic elevation of deep venous pressure and blood pooling in lower extremeties
Etiology
• calf muscle pump dysfunction and valvular incompetence (valvular reflux) due to
phlebitis, varicose veins or DVT
• venous obstruction
• AV fistulas, venous malformations
Clinical Features
• pain (most common), ankle and calf edema – relieved by foot elevation
• pruritis, brownish hyperpigmentation (hemosiderin deposits)
• stasis dermatitis
• ulceration: shallow, above medial malleolus, weeping (wet), painless, irregular outline
• positive Brodie-Trendelenberg test, varicose veins
Investigations
• ambulatory venous pressure measurement (gold standard)
• Doppler U/S
• photoplethysmography
Treatment
• conservative
elastic compression stockings, leg elevation, avoid prolonged sitting/standing
ulcers: zinc-oxide wraps, split-thickness skin grafts, antibiotics, debridement
• surgical
if conservative measures fail, or if recurrent/large ulcers
surgical ligation of perforators in region of ulcer, greater saphenous vein
stripping
venous bypass if short segment obstruction