Myocardial Protection and Cardiopulmonary Bypass

Myocardial Protection and Cardiopulmonary Bypass
1. Myocardial Perfusion
A. Normally, subendocardial flow exceeds subepicardial flow
B. Myocardial perfusion, however, is altered by cardiopulmonary bypass
C. Narrow pulse pressure and variable mean pressure affects coronary perfusion pressure
D. Wall tension is increased in the empty, smaller heart
E. Ventricular fibrillation also increases wall tension
F. Regulatory and inflammatory factors are released which affect coronary resistance
G. Microemboli from the circuit and hemodilution impair oxygen delivery
H. Endothelial and myocardial edema further affect perfusion
I. Subendothelial vulnerability is increased by hypertrophy, coronary disease, fibrillation, cyanosis, shock, and chronic heart failure
J. The acutely ischemic heart may have poor reflow to the injured area
2. Myocardial Ischemic Injury
A. Acute ischemic dysfunction
1) Global myocardial ischemia
2) Reversible contractile failure, mostly from change in perfusion pressure
3) Immediate recovery as oxygen supply is restored
B. Stunning
1) Reversible systolic and diastolic dysfunction, no myocardial necrosis
2) Begins in subendothelium and progresses outward
3) May be accompanied by endothelial dysfunction
4) Results from ischemia-reperfusion insult, mediated by increased intracellular calcium accumulation
5) Recovery occurs within hours to weeks
C. Hibernation
1) Reversible chronic contractile depression
2) Related to poor myocardial blood flow
3) Recovery occurs within weeks to months
D. Necrosis
1) Irreversible ischemic injury with myocardial necrosis
2) Hypercontracture occurs first in the subendothelium and is more rapid in the hypertrophied heart
3) Typically results in contraction band necrosis, rarely "stone heart"
4) Osmotic and ionic dysregulation produce membrane injury and myocyte lysis
3. Cardioplegia
A. Studies in animals have inconsistent correlation with clinical results due to species differences, extent of disease, and perioperative events that precipitate, extend, or enhance myocardial damage
B. The goals of cardioplegia are to protect against ischemic injury, provide a motionless and bloodless field, and allow for effective post-ischemic myocardial resuscitation
C. Cardioplegic techniques vary according to perfusate (blood vs. crystalloid), duration (continuous vs. intermittent), route (antegrade vs. retrograde), temperature (warm vs. cold), and additives
D. Special consideration is required for the acutely ischemic heart and the neonate
4. Mechanisms of Cardioplegic Protection
A. Mechanical arrest (potassium-induced) will reduce oxygen consumption by 80%
B. Hypothermia will reduce consumption by another 10-15%
C. Aerobic metabolism can be maintainted with oxygenated cardioplegia
D. Hypothermic arrest is sustained with readministration every 15-30 minutes
E. Retrograde delivery protects the left ventricle more completely than the right ventricle
F. Prevent myocardial rewarming with systemic hypothermia, aortic and ventricular vents, and caval occlusion
G. In acute ischemia, use warm induction with substrate enhancement (glutamate, aspartate)
H. Reperfusion should be controlled, using warm, hypocalcemic alkaline cardioplegia
I. This approach combats intracellular acidosis and rapid calcium infusion injury
J. Retrograde or low-pressure antegrade perfusion is preferred for reperfusion
K. Ensure uniform warming
5. Neonates and Children
A. Children older than 2 months have similar myocardial physiology to adults
B. The neonatal myocardium, however, is different in several ways
C. Hypoxia is more easily tolerated
D. There are greater glycogen stores and more amino acid utilization
E. ATP breakdown is slower due to deficiency in 5' nucleotidase
F. Multidose cardioplegia is disadvantageous
G. Cyanosis may worsen resistance to ischemia
H. Amino acid substrate enhancement is beneficial
6. Cardioplegia Composition
A. Blood has the advantage of oxygen carrying capacity, histidine and hemoglobin buffers, free radical scavengers in RBCs, and metabolic substrates
B. Blood also has improved rheologic and oncotic properties, which may lessen myocardia edema
C. Buffers such as THAM, histidine, and NaHCO3 form a slightly alkaline solution for reperfusion that can counteract intracellular acidosis
D. Small amounts of calcium (0.1-0.5 mM/L) restores calcium that has been chelated by citrate
E. Potassium concentrations range from 10-25 mM/L, with the first dose being the highest
F. Other substrates are being evaluated, including allopurinal, SOD, deferoxamine, adenosine, nucleoside transport inhibitors, and potassium-channel openers
CARDIOPULMONARY BYPASS
1. The Circulatory Environment
A. Cardiopulmonary bypass is an abnormal circulatory state
B. Non-pulsatile flow, hemolysis, hemodilution, foreign surface exposure, general stress response, and the inflammatory response all contribute
C. Mechanial components
1) Roller pumps are slightly non-occlusive, resistance-independent, and may cause less blood trauma
2) Centrifugal pumps are dependent on inflow or outflow resistance; will cease flow at very low inflow resistance and very high outflow resistance
3) Venous drainage can be active or siphoned
4) Active drainage requires vacuum through the venous reservoir or negative pressure from the pump
B. Heat exchanger
1) The cooling or warming gradient is usually within 10-14 degrees of the patient's temperature
2) This minimizes the tendency for gas to come out of solution and risk of air embolism
3) Mixed blood temperature should be less than or equal to 38.5C
4) The water bath should stay between 15 and 42C to prevent organ damage (too cold) and hemolysis (too warm)
C. Oxygenator
1) Largest foreign surface contact area
2) Membrane oxygenators can be microporous, hollow fiber, or silastic (true membrane)
3) Gas flow is titrated to maintain PaO2 between 85 and 250mmHg to avoid O2 toxicity
4) PCO2 is regulated by gas and blood flow through the membrane
5) pH is controlled by adjusting the PaCO2
6) alpha stat adjusts the pH to 37C, with the goal of providing optimal enzymatic function during hypothermia
7) pH stat corrects the pH to the temperature of the patient's blood, with the goal of relative hypercarbia to increase cerebral blood flow
2. Mechanisms of Injury
A. Mechanical
1) The foreign surfaces of the bypass circuit (boundary layer of oxygenator, heat exchanger, filters, tubing) interact with the blood
2) Shear stresses include the pump, cardiotomy suction, and cannulae
3) Microemboli can form as particles from the oxygenator, platelet aggregate, or fibrin aggregates, and are greatest within the first 15 minutes of bypass
B. Humoral
1) Factor XII (Hageman factor), the alternative complement cascade (C3a), kallekrein, and plasminogen are activated in various degrees
2) Other factors interrelate and amplify the inflammatory reaction, including the arachidonic acid cascade, interleukins, TNF, and PAF
C. Cellular
1) Neutrophils play a major role in humoral activation and are sequestered in the lung, releasing cytotoxin and free radicals which increase vasoreactivity and vascular permeability
2) Monocytes and mast cells also participate, although their role is unclear
3) Lymphocytes have a minor role, if any
4) Platelets are activated and elaborate GPIB, IIB, and IIIA
5) Absolute number of platelets is reduced by 40% by the end of bypass, and the number of receptors is also decreased
6) Endothelial cells are affected by abnormal flow, humoral factors, and local ischemia
7) A wide variety of substances are expressed by the endothelium, including prostaglandins, thromboxanes, leukotrienes, and interleukins
3. Miscellaneous
A. Circulatory arrest with profound hypothermia (18-20C) is generally safe up to 45 minutes
B. Over 60 minutes is associated with increased incidence of neurologic deficit
C. The period between 45 and 60 minutes is unclear, as histologic injury seems to be greater than functional injury
D. Maintain a gradient of 4-6C, as rapid cooling produces uneven cerebral cooling
E. Retrograde and low flow cerebral perfusion are currently being evaluated
F. Pulsatile flow has not been shown to be superior to non-pulsatile flow
G. Lower ACT of 300-350 seconds is not associated with greater complications compared to standard ACT of 450
H. Aprotinin will elevate the ACT (600-800), neutralizes the kallikrein cascade, and protects platelet receptors
I. Protamine reactions occur through the classical component pathway and cause direct myocardial depression

























Minimally Invasive Cardiac Surgery
1. History
A. Beating heart anastomosis
1) Alexsis Carrell on dog
2) Kolessov 1967 first LIMA to LAD (6 pts)
3) Banned/ Buffalo 1990/1991
4) Subramanian/Acuff/Mack/Calafiore - MIDCAB
2. Port Access Cardiac Surgery
A. CABG -- Stevens 1996 (Stanford)
B. MVR -- Schwartz, Ribakove (NYU)
C. MIDCAB --
D. Exposure thru 4th ICS
E. 1 or 2 vessel bypass
F. 5-20% stenosis rate
G. Anterior wall revascularization only
H. Less use of resources
I. Eliminates CPB and sternotomy
3. OPCAB
A. Exposure median sternotomy
B. Bypass multiple targets
C. Patency unknown
D. No CPB
E. Port access
F. 4th ICS
G. Femoral cannulation CPB
H. Still heart
I. Total revascularization
J. Can use SVG for proximals
K. Over 2000 cases done similar results as open
4. Endoscopic CABG
A. LIMA taken down with scope only
B. Then conventional MIDCAB or Port Access
5. MIDCAB or OPCAB
A. Use in patients you might not want to use CPB
B. Calcified aorta, poor LVEF, severe PVD
C. Severe COPD, CRF, coagulopathy
D. Transfusion issues, i.e., Jehovahs witness
E. Good target vessels not diffuse disease
F. Anterior/lateral wall revascularzation
G. Target revascularzation in older sicker patients
6. Port Access
A. More universal use
B. Multi-vessel revascularization
C. Redo cases
D. Where sternum healing is problem
E. Obese, DM, steroids
7. Aortic Valve surgery
A. Approach
1) Right parasternal first used by Cosgrove 2nd and 3rd costal cartilages
removed try to preserve RIMA
2) Mini sternotomy (Gundry) upper sternotomy T off to the right 3rd or 4th
ICS better for homograft root replacement
3) Transected sternum (Cosgrove) transect at 3rd ICS level both RIMA and LIMA divided
8. Mitral Valve Surgery
A. Approach
B. Right parasternal
C. Lower mini sternotomy
D. Right anterior lateral thoracotomy
E. CPB has been accomplished with Heartport system
F. Fem-fem CPB
G. Direct cannulation of aorta and atrium
9. Advantages
A. Decreased length of stay (average 4 days)
B. Decreased blood transfusions (Cohn, et al)
C. Return to activity sooner
D. Less atrial fibrillation (5-10% incidence vs 20-30% open CPB)
10. Pediatric Cardiac Surgery
A. Ligation of PDA and division of vascular rings via thorascopic technique (Burke)
B. Open procedures VSD, Tetralogy via mini-sternotomy (Gundry)
C. ASD closure with Heartport port access
Mini L-Shaped Sternotomy
Mini T-sternotomy
Mini- Parasternal & Mini-Thoracotomy
D. Graphs
AF Incidences
Patency Rates
Long-Term Results
Angiographic Results
Postoperative AF
Decision Grid
Sternotomy vs No Sternotomy
Off-Pump Indications
11. Future robotics
A. 3-D imaging
B. Total closed chest still experimental
C. What to do?
D. All will become tools to be used
E. Each will find a niche
F. How to define role for each tool
G. Balance co-morbidities with complete revascularization

















Aortic Aneurysm
1. Morphology
A. Atherosclerotic (degenerative) aneurysm: most common cause (1/2) of localized aortic enlargement
B. Chronic aortic dissection: persistent false channel of outer media and adventitia gradually enlarges
C. Chronic traumatic aortic transection: false aneurysm contained only by aortic adventitia
D. Annulo-aortic ectasia: aneurysmal dilation of sinuses of Valsalva (Marfan, cystic medial necrosis)
E. Aortitis: granulomatous or syphilis
2. Location
Ascending aorta 45%
Arch 10%
Descending thoracic 55%
Thoracoabdominal 10%
3. Symptoms
A. Usually asymptomatic
B. Pain implies sudden extension or rupture of aneurysm
1) Ascending aorta - neck, jaw
2) Descending aorta - back, inter-scapular
3) Thoracoabdominal aorta - low back
C. Compression of adjacent structures
1) SVC syndrome
2) Hoarseness, laryngeal nerve
4. Associated Atherosclerotic Disease
Coronary arteries 16%
Cerebrovascular 10%
Peripheral vascular 10%
Abdominal aortic aneurysm 10%
5. Diagnosis
A. Chest X-ray - enlarged aortic shadow
B. Aortography - most valuable for assessment of aorta proximal and distal to aneurysm
C. Echocardiography - is useful in the assessment of aortic valve function and can demonstrate an intimal flap.
D. Computed axial tomography - real size of aneurysm and relation to adjacent structures
E. Magnetic resonance imaging - multiple planes possible, cine loop
6. Natural History
A. Aortic aneurysms enlarge, eventually rupture (74%)
B. Large aneurysms(>6 cm) tend to rupture
C. Symptoms herald rupture (2 years)
D. Aneurysm with chronic dissection have worst prognosis
7. Operations - Ascending Aorta and Arch
A. Conventional cardiopulmonary bypass is utilized
B. Aortic valve replacement with valved conduit (Bentall procedure)or repair/resuspension if feasible
C. Arch anastomosis by tailoring or arch vessel reimplantation
D. Reimplant the coronary arteries as buttons
E. Do not cover the graft, as this will increase the risk of false aneurysm
F. Elephant trunk
G. Cerebral perfusion antegrade ? retrograde
H. Deep hypothermia - circulatory arrest
8. Operation - Descending Thoracic Aorta
A. Clamp and go is the traditional method
B. Incise the aneurysm to work inside
C. There are many approaches to protect the spinal cord and kidneys, including:
1) NTP and spinal fluid drainage are somewhat controversial
2) LV or ascending aorta to descending aorta shunt (Gott)
3) LA to femoral artery bypass
4) Femoral-femoral cardiopulmonary bypass
5) Deep hypothermia and circulatory arrest may be the most controlled approach
D. The proximal anastomosis should be precisely matched to the aorta
E. Reattach the intercostal arteries as an island; this is particularly important in the distal portion of the repair
F. The distal anastomosis may be fashioned either end-to-end or as an elephant trunk
9. Operation - Thoracoabdominal Aorta
A. Spinal cord and renal protection are essential
B. Hemorrhage remains a challenging problem
C. Thoracoabdominal incision with a retroperitoneal approach
D. There are also various approaches to these aneurysms:
1) Clamp and go with or without heparinization
2) Deep hypothermia with circulatory arrest
E. Reimplant the visceral and intercostal-lumbar arteries when involved
10. Results
Death (hospital) - bleeding, neuro, MI
Ascending aorta 4-10%
Arch 5-50%
Descending 5-15%
Thoracoabdominal up to 50%
Survival - new aneurysm, CHF, renal
5 years 60%
10 years 40%




Acute Aortic Dissection
Definition
Dissection of the aorta is an event that results in the separation of the layers of the media by blood, producing a false channel with variable proximal and distal extension.
1. Etiology
A. Cystic medial necrosis - 20%
B. Marfan syndrome - 20-40%
C. Other causes: hypertension, bicuspid aortic valve/aortic stenosis, atherosclerosis, coarctation, pregnancy, trauma, aortic cannulation, aortic cross-clamping, cardiac catheterization
2. Morphology
A. Blood leaves the normal aortic channel through intimal tear, rapidly dissecting through the media to produce a false channel
B. The intimal tear is sometimes absent; possible rupture of vasa vasorum with medial hemorrhage
C. Usually the dissection proceeds distally; 38% dissect proximally and 10% in the transverse arch
D. Dissection may shear off or extend into branch arteries
E. False channel characteristics:
1) Thickens and gradually enlarges with time
2) May interrupt blood supply of branches by ext ernal compression
3) Outer wall thin - media + adventitia
4) May rupture to pericardium or pleural space
5) May thrombose
3. Classification
A. Acute = less than 2 weeks, chronic = greater than 2 weeks
DeBakey I Ascending + arch Stanford A
DeBakey II Ascending only Stanford A
DeBakey IIIa Descending only Stanford B
DeBakey IIIb Descending + abdom Stanford B
4. Clinical Features
A. Severe pain - tearing, interscapular, precordial, neck, migrating, persisting
B. Signs of occlusion of major vessel
1) Arch - stroke, syncope
2) Intercostal - paraplegia
3) Renal - oliguria-anuria
4) Iliac - ischemic leg
C. Sudden death
1) Rupture to pericardium, pleural, peritoneal space
2) Shear off coronary artery
D. Hypovolemic Shock
1) Blood in periaortic tissues
2) Acute aortic valve insufficiency
3) Cardiac tamponade
5. Diagnosis
A. Imaging
1) Chest X-ray - widened mediastinum, cardiomegaly, pleural effusion, intimal calcification separated more than 6mm from the edge
2) Echo - identifies intimal flap/false channel, noninvasive, no contrast media, performed at bedside
3) TEE is best for the descending aorta; TTE best for the ascending aorta and arch
4) Aortography - conventional method of diagnosis (gold standard), shows origin of arteries from true or false lumen
5) CT Scan - identifies intimal flap rapidly, requires contrast media
6) MRI - multiple planes, cine for AI
B. Main points of interest
1) Involvement of the ascending aorta
2) Location of the intimal tear
3) Status of perfusion in the major branches
4) Size of the aorta and presence of AI
5) Extent of the false lumen
6) Pericardial effusion
6. Treatment Overview
A. Type A and complicated type B dissections are managed surgically
B. Uncomplicated type B dissections are managed medically
C. The goals of surgical therapy are to prevent extension, excise the intimal tear, and replace the segment of aorta which is susceptible to rupture
D. The goals of medical therapy are to prevent extension, control blood pressure, and relieve pain
7. Treatment - Ascending Aorta
A. Immediate operation is indicated because rupture is likely
B. Contraindications: ? advanced age, incurable coexisting disease, paraplegia
C. Note: new stroke may resolve, not a contraindication
D. Replace ascending aorta and the aortic valve if insufficient; the valve may be worth preserving if normal
E. Replace arch if false channel leaking or site of tear
F. Operative strategy (elephant trunk)
1) Use circulatory arrest if indicated
2) Incise in a longitudinal fashion, avoiding the phrenic and recurrent nerves
3) Follow the dissection from inside the aorta to determine extent and remove damaged intima and media
4) Invert the graft into the distal aorta and approximate only the aortic adventitia to the inside of the graft
5) Pull the graft out and anastomose the arch vessels as a group
6) Once the distal repair is completed, the proximal repair can be performed with the graft clamped in a fashion that allows reperfusion and rewarming of the body while the proximal aspect of the repair is completed (with continued protection of the heart with cardioplegia)
8. Treatment - Descending Aorta
A. Medical treatment indicated unless complications of dissection have occurred
1) NTP + beta-blocker to maintain normal blood pressure
2) 80% survive 1 year
3) Close follow-up required, 50% die in 3-5 years
B. Complications dictate immediate operation (interposition graft or fenestration)
1) Hemothorax, persisting pain, limb ischemia, acute renal failure, paraparesis (malperfusion syndrome)
2) Paraplegia NOTan indication for operation because not likely to resolve
9. Results After Operation
A. Early (hospital) death
1) Ascending aorta - 5-10% (up to 30%)
2) Arch - 10-25% (up to 50%)
3) Descending - 10% (up to 25-60%)
B. 10 year survival - 46%
1) 1/3 late death related to residual old false channel or redissection
C. Aneurysm of false channel
1) Uncontrolled hypertension - 50%
2) Controlled blood pressure - 10-20%
D. Redissection - 10% (Marfan higher)









































































































Selection of Prostheses
1. Mechanical valves
A. Selection
1) <70 yo 2) no h/o bleeding B. Survival - over ½ of late deaths are related to valve complications C. Hemodynamics 1) Tilting disc and bileaflet are “low-profile” a) Tilting disc - 6-7mmHg gradient 2) Caged ball is “high-profile” D. Thromboembolism 1) Highest risk is in first 14 months 2) Steady level after - 0.5%/pt-yr 3) INR 2.5 = therapeutic 4) Coumadin for all - antiplatelet agent for high-risk (a-fib, h/o embolus, etc.) 5) Thrombolytic therapy - never for patients in a low-output state E. Hemorrhage 1) Incidence the same for aortic and mitral position 2) Associated w/high anticoagulation levels (INR >4.5)
3) At INR 2.5-3.5, anticoagulation-related death = 0.2%/pt-yr
F. Endocarditis
1) PVE - mortality = 23-69%
2) Most commonly in first several months
3) After initial period = 0.17%/pt-yr
G. Periprosthetic leakage (see Table 122-2)
1) Predisposing factors
a) Annular calcification
b) Infection
c) Annuloprosthetic mismatch
d) Excessive tension on sutures, annulus or both
e) Technique
f) Abnormal annulus tissue
H. Structural valve degeneration
1) Rare
2) Leaflet fracture - may be due to mishandling à scratches
I. Nonstructural valve degeneration
1) Pannus formation
2. Bioprosthetic Cardiac Valves
A. Features
1) No indication for anticoagulation
2) Survival
B. Glutaraldehyde-preserved porcine valves
C. Hemodynamics
1) Central unimpeded flow
2) In aortic position, small (19-21mm) valves are stenotic
3) Supraannular bioprosthesis improves flow
D. Thromboembolism
1) INR 2.0-3.0 for a-fib
E. Hemorrhage-see Table 122-4
F. Structural valve dysfunction
1) Progressive degeneration
2) Reasons
a) Calcification
b) Collagen degeneration-associated cuspal defect
c) Time-dependent - accelerated failure after 8-10 years
d) Valve failure and calcification accelerated in childrenàyoung adults
e) Mitral > aortic failure
G. Endocarditis
H. Periprosthetic leak
3. Pericardial Valves
A. Better flow (than porcine bioprostheses)
B. Newer designs more durable
4. Homograft Valve Prostheses
A. Patient survival 85-90% @ 7.5yr // 71% @ 14yr
B. Durability
1) Early homografts - calcification & cusp rupture
2) Cryopreservation (vs irradiation & chemical processes)
a) 95-98% freedom from structural deterioration (10yr)
C. Thromboembolism
1) ? Role of endothelium
D. Endocarditis
1) S. aureus a major player
2) Many respond to Abx
3) Failure to respond to Abx = surgical indication