anaesthesia for cpb is complex to understand...

2. “ provide a non beating bloodless heart with flow
temporarily diverted to an extra-corporeal circuit that
functionally replaces heart and lung ”
“ boldest and most decisive feats of man’s mind ”
Introduction:

3. An Overview –
1. basic circuitry.
2. Pre-operative evaluation
3. Intra-op monitoring
4. Anaesthetic delivery
• Premedication
• Induction
5. Pre-cardiopulmonary bypass period
6. Maintenance of bypass
7. Myocardial protection
8. Preparation from weaning
7. Weaning from the bypass.
8. Events in Post bypass period.

4. CPB is a technique that diverts venous blood away from
the heart (most often from one or more cannulas in the
right atrium), adds oxygen, removes CO 2 , and returns the
blood through a cannula in a large artery (usually the
ascending aorta or a femoral artery). As a result, nearly
all blood bypasses the heart and lungs.

5. Surgical procedures requiring cardiopulmonary bypass
1. Coronary artery bypass surgery
2. Cardiac valve repair and/or replacement (aortic valve, mitral valve,
tricuspid valve, pulmonic valve)
3. Repair of large septal defects (atrial septal defect, ventricular septal
defect, atrio-ventricular septal defect)
4. Repair and/or palliation of congenital heart defects (Tetralogy of
Fallot, Transposition of the great vessels)
5. Transplantation (heart transplantation, lung transplantation, heart–
lung transplantation)
6. Repair of some large aneurysms (aortic aneurysms, cerebral
aneurysms)
7. Pulmonary thromboendarterectomy and thrombectomy.

6. 1.Basic circuit:
The typical CPB machine has six basic components:
1.venous reservoir,
2.an oxygenator,
3. heat exchanger,
4.main pump,
5.an arterial filter,
6.Tubing-conducts venous blood to the venous reservoir,
and
7.tubing that conducts oxygenated blood back to the patient .
Modern machines use a single disposable unit that includes
the reservoir, oxygenator, and heat exchanger

9. Heart lung machine

10. Venous cannula
Arterial
cannula
Venous
reservoirs

11. Membrane oxygenator bubble oxygenator heparin coated
blood oxygenator

12. Roller pumps
Centrifugal
pump

13. Arterial
filter
Cardioplegic
pump

14. Perfusionist and their roles
1. The perfusionist is a highly trained member of
the cardiothoracic surgical team.
2. The perfusionist is solely responsible for the
management of the physiological and metabolic
needs of the patient so that the cardiac
surgeon may operate on a still, unbeating heart.
3. management of circulatory and respiratory
functions of the patient.
4. autologous blood collection and processing,
implementation and management of the intra-
aortic balloon pump, adult and
infant extracorporeal membrane
oxygenation(ECMO) as well as monitoring of
anticoagulation, electrolyte, acid-base balance
and blood-gas composition.
5. Informs surgeon about the time lapsed in surgery
at frequent intervals(2mins).

15. Priming
•Prior to its use, the CPB machine must be primed with fluid
(1200-1800 mL) that is devoid of bubbles.
•Usually a balanced salt solution is used to flush the machine, but
sometimes Albumin or Hespan is added.
•Blood is also used as a priming solution for small pediatric
patients or for anemic adult patients.
•At the onset of bypass, hemodilution usually decreases the
hematocrit to about 22-25% in most patients.
•That is why in the more critically ill or anemic patients, blood is
used for priming the CPB machine to avoid too drastic a drop in
hematocrit and consequently compromising O2 delivery and
leading to Ischemia.

16. Hypothermia
• Intentional hypothermia is routinely used following initiation
of CPB
• Core body temp. Is usually reduced to 20-32 degrees C
• Metabolic O2 demands are generally cut in half with each
reduction of 10 degrees C in body temp
• Profound hypothermia to 15-18 degrees C allows total
circulatory arrest for complex repairs of the aorta for up to 60
min.
• During that time, both the heart and cpb pump are stopped

17. • Hypothermia is NOT w/o its problems
• profound hypothermia can be associated with:
1) Platelet dysfunction
2) Reduced serum ionized calcium
3) Reversible coagulopathy
4) Depression of myocardial contractility

18. Myocardial Preservation
• Optimal surgical results depend on prevention of myocardial
damage and maintenance of normal cellular integrity and
function during CPB
• Nearly ALL patients sustain some myocardial damage during
CPB
• Proper preservation techniques can keep this damage to a
minimum

19. Myocardial Preservation
• Inadequate myocardial preservation usually manifests at the
end of CPB as a persistently LOW CO, EKG signs of
ischemia, or cardiac arrhythmias
• Aortic cross-clamping during CPB completely cuts off
coronary blood flow
• Although no studies have really been done to determine an
optimal time for cross-clamping, it is believed that cross-clamp
times GREATER than 120 min. Are generally considered as
undesirable

20. Myocardial Preservation
• The most widely used method or arresting the myocardium
and decreasing O2 demand is through the use of a solution
high in K+ called “cardioplegia”
• Following initiation of CPB, induction of hypothermia and
cross-clamping of the aorta, the coronary circulation is
periodically perfused with cold cardioplegia

21. Myocardial protection-
• To provide a motionless field for surgery, heart
is stopped in diastole by administering a
potassium rich cardioplegia soln.
• It interrupts myocardial electromechanical
activity, reduces oxygen consumption by 90%
and cold cardioplegia soln. Reduces it by 97%.

22. • For most complete cardioplegia , both antegrde (through
aortic root) and retrograde(through coronary sinus)
approach is used
• Arrest can be reversed by reperfusing heart by warm
normokalemic blood(hot shot)

23. potassium cardioplegic solutions
BASIC COMPONENTS REMARKS
1.POTASSIUM (10-40 mEq/L) Decreases transmembrane potential
2.SODIUM <140 mEq/l (conc<plasma) Ischemia increases intracellular sodium
3.CALCIUM 0.7-1.2 mmol/l Maintain cellular integrity
4.MAGNESIUM 1.5-15 mmol/l control excessive intracellular influxes of
calcium
5.BUFFERS- BICARBONATE, HISTIDINE,
TROMETHAMINE(THAM)
prevent excessive buildup of acid
metabolites
6.HYPERTONIC AGENTS-MANNITOL control cellular edema
7. LIGNOCAINE AND GLUCOCORTICOIDS MEMBRANE STABILIZING AGENTS
8.GLUCOSE, GLUTAMATE, ASPARTATE ENERGY SUBSTRATES
9.VEHICLE/SOLVENTS CRYSTALLOIDS OR BLOOD(MORE COMMON)

24. Cardioplegia
• Since the cardioplegia cannot reach areas of the heart that are
distal to the coronary artery obstructions, many surgeons also
administer cardioplegia retrograde through a coronary sinus
catheter and back through the venous system
• Some studies have reported that the combination of antegrade
and retrograde cardioplegia is FAR superior at protecting the
myocardium as compared to only antegrade administration

25. Cardioplegia
• Cardioplegia is usually administered every 20-30 minutes
while the patient is on CPB
• Excessive cardioplegia can result in an absence of electrical
activity, AV conduction blockade, or a poorly contracting heart
at the conclusion of CPB
• There is often a period of “wash out” needed after long cases
at which time the heart is allowed to return beating while still
on partial CPB to allow excess cardioplegia and cellular
byproducts to become eliminated and allow the myocardium to
contract fully and without any depression

26. IV Access
• In the preop suite prior to induction, place AT LEAST an 18g,
preferably a 16g, IV cath.
• Once the IV cath is placed, premedication can be given and
then the arterial-line is placed.
• This is the minimum needed prior to induction
• In sicker patients, an introducer and an SwanGanz catheter
need to be placed as well ALL prior to induction of anesthesia.

27. PREOPERATIVE EVALUATION-
• History and physical examination to evaluate LV dysfunction
and LV/RV failure, respiratory disease, prior cardiac surgery
• Chest radiograph to detect resp. disease, CHF, abnormal
cardiothoracic ratio etc.
• Resting ECG to detect rhythm disturbances, conduction
defects, decision of intra-op lead selection

28. •Exercise ECG showing significant ST segment changes in
early stages, sustained changes, abnormal changes in HR or
BP, development of angina or arrythmia indicate severe CAD
•ECHO shows segmental wall motion abnormality
•Stress ECHO with exercise or dobutamine and contrast
ECHO detect abnormal areas of perfusion
•Myocardial perfusion scans using thallium-201 or tc 99m
locate and quantitate ischemic areas

29. •Angiography defines location and degree of occlusion
and coronary artery spasm
•Contrast ventriculography shows areas of
hypokinesia, akinesia and dyskinesia
•Ejection fraction= edv-esv/edv [n-50-75%]
25-50%- symptoms on exercise
<25% - LVF symptoms at rest

30. Monitoring
• The following monitors are usually used during a CABG procedure:
1) EKG (at least a minimum of 2 leads, II and V5)
2) O2 sat
3) BP cuff
4) Temp
5) Etco2
6) A-line (for abg’s and continuous BP; placed PREOP)
7) SG cath (with or without fiberoptics to calculate CO and to sample
mixed venous blood or to get a continuous readout of MVO2 sat)
8) TEE
9) BIS

31. INTRA-OP MONITORING-
•IBP- dominant hand radial art prefered .
•ECG- ST segment changes or new T wave changes are
diagnostic of ischemia
•Simultaneous observation of an inferior lead [II, III,
avf ] and anterior lead [V4,V5] detects approximately
90% of events.
•Posterior heart ischemia is difficult to detect

32. •Cvp – internal jugular vein
• PA CATHETER- appearance of new V wave in
pulmonary artery pressure waveform indicates
development of Mitral Valve Reguegitation due to
ischemic papillary muscle dysfunction
Imp in post-op period where TEE can not be used
Intra-op monitoring may require frequent balloon
inflations

33. TRANSESOPHAGEAL ECHOCARDIOGRAPHY –
can assess regions supplied by all three major coronary arteries
•Regional wall motion abnormality can precede ECG and PA
wave form changes
•Intra-op stress TEE with low dose dobutamine can
demonstrate myocardial contractile reserve and helps
revascularize myocardium that will be benefited from increased
blood supply
•Contrast TEE [using microbubbles] also avoids needless
therapeutic intervention

34. Anticoagulation
• Anticoagulation must be established prior to CPB to prevent
acute DIC and formation of clots in the CPB pump.
• The adequacy of anticoagulation MUST be confirmed by a test
called an ACT (activated clotting test).
• An ACT longer than 400-480 sec is considered SAFE at most
centers.
• Anticoagulation is achieved by heparinization.

35. Heparinization-
• Heparin 300-400u/kg is administered through a central
vein targeting ACT level min of 480s
• ACT is the time from adding whole blood to a tube
containing a contact phase activator (celite or kaolin) up
to the time when first clot appears.
• Repeat act is measured after 5 mins and if it is less,
100u/kg is to be administered again.

36. Bleeding prophylaxis
• Bleeding prophylaxis with antifibrinolytic agents may be initiated
before or after anticoagulation , preferably after.
• The antifibrinolytic agents : ε-aminocaproic acid and Tranexamic
acid, not affect the ACT and only rarely induce allergic reactions.
• Ε-aminocaproic acid = as 50–75 mg/kg( loading dose )
• 20–25 mg/kg/h (maintenance infusion)
• some clinicians use a standard 5–10 g loading dose followed by1 g/h)
• Tranexamic acid is often dosed at 10 mg/kg followed by 1 mg/kg/h,
• Intraoperative collection of platelet-rich plasma by pheresis prior to
CPB is employed by some centers; reinfusion following bypass may
decrease bleeding and reduce transfusion requirements.

37. PREMEDICATION
• Pain and anxiety :narcotic or anxiolytic agent or both.
• Supplemental intra-venous drugs- commonly midazolam and
fentanyl- are often necessary during radial artery cannulation
before induction of anesthesia.
• Patients with low cardiac output secondary to CHF sedation
should be performed judiciously to avoid myocardial
depression and resultant hypotension.
• Patients with an EF <40% should be given preop medications
slowly and carefully since they are much more sensitive to the
hypotensive effects of the meds

38. Induction-
Goal is to avoid undue hypotension and to attenuate
hemodynamic response to laryngoscopy and
intubation
Hypotension may be due to hypovolemic state and
reduction in sympathetic tone in response to inducing
agents particularly in patients with poor lv function.
Fall in B.P >20% of baseline needs use of inotropes.

39. •Hypertension may be due to pre-induction
anxiety and sympathetic stimulation.
•All anesthetic agents except ketamine cause
decreased blood pressure by
• decreasing sympathetic tone ,
• systemic vascular resistance ,
•inducing bradycardia or
•directly depressing myocardial function.

40. •Selected agent should be given in small incremental
doses and titrated first against loss of consciousness
then to an acceptable fall in BP.
•Muscle relaxation and controlled ventilation ensures
adequate oxygenation and prevents hypercapnia.

41. High dose narcotics-
•Fentanyl 50-100 mcg/kg or sufentanil 15-25mcg/kg
•Produces prolonged post-op respiratory depression,
high incidence of awareness, rigidity, fail to control
hypertensive response to stimulation

42. Total intravenous anesthesia-
•Infusion of PROPOFOL,0.5-1.5 mg/kg f/b 25-100
mcg/kg/min and
•REMIFENTANIL 1 mcg/kg bolus f/b 0.25-1 mcg/kg
infusion.
•Total dose of fentanyl should be 5-7 mcg/kg
•Use of short acting agents results in early extubation and
lesser hospital stay
•Drugs are costlier and remifentanil should be supplemented
by morphine at the end for post operative pain relief.

43. Mixed intravenous
• Midazolam 0.05 mg/kg for sedation.
• Propofol 0.5-1.5 mg/kg or Etomidate(0.1-0.3 mg/kg) for
induction.
• Opioids are given intermittently and total dose of fentanyl
and remifentanil should not exceed 15 and 5 mcg/kg
respectively (fast track management).

44. INHALATION ANESTHESIA-
• Volatile agents{0.5-1.5 MAC for maintenance of anesthesia
and sympathetic response suppression(MACBAR)}
• Isoflurane , sevoflurane or desflurane are used for
maintenance.
• It results in easy control of depth of anesthesia and
hemodynamic stability and early extubation.
Others-
• In frail patients, combination of ketamine and midazolam
provides hemodynamic stability, good amnesia, analgesia
and minimal respiratory depression.

45. 1. Pre cardio-pulmonary bypass period-
1. Check bilateral breath sounds
2. Adjust fresh gas flow
3. Check pressure points
4. Protect eyes
5. Check all monitors and tubings after final position
6. Administer antibiotics
7. Check baseline ACT
8. Check baseline blood gas parameters, electrolytes and hematocrit
by doing ABG

46. 9. Skin incision can cause sympathetic stimulation, so adequate depth of
anesthesia is necessary
10. 10. Sternal incision and splitting accompanies high level of sympathetic
stimulation
11. Sternal splitting can cause:
a. Awareness and recall, so amnesic agents like benzodiazepines or propofol is
to be used
b. Tachycardia & raised BP can be treated by nitroglycerine boluses or by
esmolol
c. Pain --high doses of fentanyl can be use
12. Lungs are to be deflated during sternal splitting to avoid damage.
• Sternal splitting can cause kinking or mal-positioning of PA cath.
• Dissection of post -ganglionic sympathetic fibres from aorta to cannulate it
can cause intense stimulation

47. Hemodynamic changes
Hypotension-may be due to
 Hypovolemia
 Decreased venous return due to increased airway pressure ,
tension pneumothorax , handling of heart and great vessels
 Impaired myocardial contractility
 Ischemia
 Dysarrythmia
 Measurement error due to kinked catheter, wrist positioning error
etc.

48. T/T of hypotension-
• Rule out technical and mechanical factors
• Check for dysarrythmia
• Use of inotropes
• Fluid loading
• Decrease inhalational agents

49. Hypertension-
may be due to
 Light anesthesia
 Hypercapnia
 Hypoxia
 Hypervolemia
T/T of hypertension-
• Increasing anesthetic depth
• Vasodilator agents like nitroglycerine, nitroprusside
• Using b-blockers

50. SINUS BRADYCARDIA-
may be due to
 Vagotonic effects of narcotics
 Use of b-blockers
 Hypoxia
 Ischemia
• T/t of bradycardia
• is indicated if there is fall in bp or hr<40 even with no fall
in bp
• Atropine 0.4-0.6 mg i.v is indicated.

51. SINUS TACHYCARDIA-
may be due to
 Light anesthesia
 Hypovolemia, anemia
 Inotropic drugs , pancuronium , isoflurane
 Hypoxia
 Hypercapnia
 Ischemia
Management of tachycardia includes
• Checking ventilation abnormalities
• Increasing depth of anesthesia
• Volume loading
• Using b-blockers

52. DYSRYTHMIAS
may be due to-
 Mechanical stimulation of heart
 Pre-existing dysrythmia
 Electrolyte imbalance
 Increased catecholamines
 Ischemia
These can be treated by treating underlying causes, using
lidocaine , b-blockers and by synchronized cardioversion.

53. •PRIMING of circuit is to be done by balanced salt
solution(1200-1800ml for adults)
•Other components like albumin or hetastarch, mannitol,
heparin and bicarbonate are added
•It decreases hematocrit to 22-25%
•In patients who are severely anemic or pediatric patients
blood is used as prime
•In patients with sufficient hemoglobin auto transfusion is
done after termination of cpb

54. Benefits of hemodilution-
•Decreased viscosity improves microcirculation and
compensates for increased viscosity due to
hypothermia
Risks-
•Decreased SVR decreases BP
•Dilution of drugs and coagulation factors
•Low oncotic pressure increases fluid shifts and edema
formation
•Decreased oxygen carrying capacity

55. • Whole blood heparin conc. Of about 3-4u/ml is
sufficient for CPB.
• Heparin resistance is seen in cases of at-iii
deficiency which can be treated with infusion of 2-3
units of ffp , at-iii concentrates , recombinant at-iii etc.

56. Cannulation-
•Aortic cannula is inserted first to allow rapid
volume infusion in cases of hemorrhage during
venous cannulation
•SBP is lowered to avoid risk of dissection and PEEP
applied to avoid air entrainment by increasing
intracardiac pressure

57. Complications during aortic cannulation can be
•Aortic dissection
•Bleeding
•Embolisation of atheromatous plaque
•Dysrythmia
•Hypotension
Venous cannulation of major veins or right atrium
follows aortic cannulation

58. Prebypass checklist-
•Anticoagulation (min ACT of 480sec) is needed
•Position of cannulae is to be checked by checking waveforms
•Urine noted and urobag is to be emptied
•Equality of carotid pulse is to be checked
•Supplemental doses of anesthetic agents are to be administered
to compensate for dilution
•All i.V lines are to be closed to avoid hemodilution

59. Initial bypass checklist-
•Face is to be checked for colour , edema , conjunctival
chemosis
•PA pressure should be less than 15 mm hg
•Arterial blood pressure should be mean 30-40 mm hg
•CVP should be<5 mm hg
•Cardiac contractility and distensibility is to be checked

60. Maintenance of bypass-
• ACT repeated every 30-60 mins, if less supplemental
heparin is added
• Blood gas values to be evaluated every 30-60 mins
• Pao2 maintained between 100-300 mm hg & paco2
between 35-40 mm hg.
• Blood glucose and hematocrit is measured every 30-60
min

61. • Sufficient anesthetic depth is maintained to prevent
awareness, spontaneous movement, hypertensive and
tachycardic responses
• Depth maintained by adding anesthetic agents and
muscle relaxants directly into the circuit and adding
volatile agents by connecting vapouriser to oxygenator

62. • Intra operative awareness may be due to underdosing ,
dilution or absorption of drugs and increased
requirement during rewarming .
• It can be prevented monitoring bis and supplementing
drug.
• Ventilation should cease when total bypass begins.

63. • Pump flow rate is to be maintained at 50-70 ml/kg/min
or 2.2-3.1 l/min/square mt
• Urine output should be at least 0.5ml/kg/hr
• Core temp. Is to be monitored at nasopharynx or
tympanic membrane( jugular bulb temp is gold
standard)
• De-airing of heart is to be done before weaning from
CPB by increasing venous pressure by inflating lungs

64. Preparation for weaning-
(elements of romanoff and royster’s)
Pneumonic is CVP
• COLD- patient’s temp. Should be 36-37 degrees,
hyperthermia is deleterious.
• Conduction- hr of 80-100 bpm is optimal, bradycardia
may need epicardial pacing wire for av pacing or
inotropes, tachycardia needs t/t of cause, av block may
need av pacing and supraventricular tachycardia needs
pharmacotherapy and cardioversion

65. • CONTRACTILITY is estimated by TEE and CO by
PA catheter
• Cells-hb should be at least 7-8g%
•COAGULATION- long bypass period and extreme
hypothermia increase risk, PT,PTT,PC should be
normal
•VENTILATION OF LUNGS- must be established
after PA blood flow is restored

66. •VISUALISATION of heart and TEE for regional and
global contractility
•VOLUME expansion-if necessary
•PACER AND PRESSOR AGENTS should be readily
available
•POTASSIUM must be corrected as hypokalemia can
cause dysrythmias and hyperkalemia can cause
conduction blocks

67. Weaning from bypass-
• Before termination, patient should be rewarmed, heart is
de-aired, regular cardiac electrical activity confirmed or
supported by pacemaker, lab values confirmed and
corrected
• Ventilation of lungs is established, venous drainage is
slowly reduced and cardiac filling volume is gradually
increased
• Vasopressors or inotropic support may be needed

68. • When patient becomes hemodynamically stable,
protamine is administered to reverse anticoagulation
• 1-1.3mg of protamine per 100 units of heparin is
administered slowly over 10-15 mins
• ACT should be brought to baseline values
• When pre-loading is optimal and contractility is
adequate, aortic inflow line is clamped to separate
from bypass

69. • Elevated BP should be avoided to prevent stress on
suture lines
• If CO is not optimal, preload can be increased in
100ml increments as rewarming is associated with
vasodilation
• Increase in hemodynamic instability and use of
inotropes may need reinstitution of CPB

70. Events in post bypass period-
1.Cardiovascular decompensation-
Ischemia and infarction may be due to
• Thrombosis or particulate or air emboli in graft
• Kinking or spasm of graft
• Incomplete revascularization due to distal disease
• Inoperable vessels

71. LV dysfunction is amenable to combination of inotropes and
vasodilators to increase CO
RV dysfunction may be due to inadequate protection, ischemia,
infarction, pulmonary air emboli, preexisting pulmonary
HTN
RV failure needs inotropic support as well as pulmonary
vasodilation nitroglycerin, nitroprusside, prostaglandin E1
(PGE1), b-type natriuretic peptide (e.G., Nesiritide),
sildenafil, or inhaled agents such as nitric oxide and
prostacyclin (prostaglandin I2 [PGI2, epoprostenol]).

72. Hypotension may be due to low svr, severe anemia, low
viscosity, acid-base disturbances and is treated with
vasoconstrictors
DYSRYTHMIAS - AF is most common and converted to
sinus rhythm by synchronized cardioversion, amiodarone
etc.
Vf or flutter needs defibrillation and drugs like
amiodarone and lidocaine
Bradycardia and heart block need AV sequential pacing
by epicardial pacing wires

73. 2.Bleeding and coagulopathy-
• Inadequate surgical hemostasis is most common
cause
• Platelet dysfunction due to hemodilution,
hypothermia, contact activation, adhesion and
sequestration.
• Activation of coagulation cascade by contact factors
• Fibrinolysis by release of t-pa from damaged
endothelium

74. • Consumption of factors
• Treated by FFP and platelet concentrates
•Thrombo-elastography is routinely done in some
centres to identify the causes of bleeding after CPB.

75. 3.Pulmonary complications-
• Atelectasis causing decreased oxygenation, lungs are
to be reinflated by hand before machine ventilation
• Hemothorax, pneumothorax may need chest tube
insertion

76. • Cardiogenic pulmonary edema due to fluid overload
in patients with preexisting HF
• Noncardiogenic pulmonary edema due to
inflammatory response, multiple emboli, increased
permeability, transfusion reaction

77. 4.Metabolic disturbances-
•Hypokalemia due to diuretics, mannitol, hyperglycemia
treated with insulin :- treated with kcl @ 10-20 meq/hr
•Hyperkalemia due to cardioplegia, blood products,
impaired renal function: - treated with hyperventilation,
calcium, diuretics, glucose and insulin infusion

78. Hypocalcemia due to citrate in blood products, hemodilution,
alkalosis:- treated with 10% calcium chloride 5-10mg/kg
Hypomagnesemia due to hemodilution:- treated with 2-4 g of
magnesium
Hyperglycemia is deleterious and is due to stress of surgery
and inflammatory response, glucose level > 200mg/dl:- should
be treated with insulin

79. 6.Effect on CNS-
• MC complication is transient neuropsychiatric
dysfunction, strokes are uncommon
• Causes are micro and macro emboli, global
hypoperfusion, cerebral hyperthermia, cerebral edema,
inflammation, BBB disruption
• Intra-op awareness should be avoided

80. Temperature regulation-
• Hypothermia causes increase in SVR, shivering
increasing oxygen consumption and coagulopathy
• So normothermia should be achieved at end of bypass
• Rewarming should be gradual
•Hyperthermia should be avoided as it delays neuronal
metabolic recovery, increases excitotoxic
neurotransmitter release, oxygen free radical
production, intracellular acidosis, increased BBB
permeability.

81. Renal effects-
•Fluid loss, myocardial depression and vasodilation by
anesthetic agents, long term use of aceis, inflammatory
response, loss of pulsatile flow decrease renal perfusion
•Fluid replacement, vasoconstrictors, frusemide 10-20
mg or mannitol 0.5-1mg/kg can be used

83. Transport from OT
Complications during transport-
•Inadvertent extubation
•Pull off of monitors
•Loss of i.V lines
•Injury to body parts
•Disconnection of pacemaker wires
•Chest tube, foleys dislodgement
•Removal of arterial line and PA catheter

84. Transport to icu-
•Portable monitoring equipment,
•infusion pumps,
•full oxygen cylinder with a self-inflating bag for
ventilation should be ready
•Upon arrival to icu patient is attached to ventilator,
•breath sounds checked,
• orderly transfer of monitors and infusions should
follow

85. Care in icu-
•Most patients require mechanical ventilation for 2-12 hrs,
sedation and analgesia should be continued
•Hypertension unresponsive to sedation and analgesics
should be aggressively treated with vasodilators
•Extubation is considered when patient becomes conscious,
muscle paralysis has worn off, blood gas values are
acceptable, surgical hemostasis is adequate and the
patient is hemodynamically stable

86. OFF PUMP CABG
Candidates-
• Pts with anterior lesions,single /double vessel ds.
•Pts with high risk of stroke, renal failure ,pulmonary
dysfunction, severe valvular ds.
•Surgeon employed
•Institute
Hypothermia is avoided throughout.

87. Major differences from onpump
•Following sternotomy , goal of heparin anticoagulation
achived is – > 2 times of baseline ACT or > 300 sec or
same as onpump(>400 secs).
• Only focal area of heart is stablized via epicardial
stablizers. Distal anastmosisis done then aorta is
partially clamped to perform proximal anastmosis .(BP
kept <100 mmhg).
•Hemodynamic disturbances & arrhythmias more
frequent and need to be adderssed.

88. • CABG procedures relieve chest pain and angina, enable
patients to resume a healthy life style, lower the risk of
further heart attack and its consequences
•They do not prevent coronary disease from recurring,
hence medications along with appropriate lifestyle
changes are strongly recommended to reduce the risk of
recurrence.

89. Thank you