Approach to anaesthesia for
adult cardiac patient
Monitoring during cardiac
surgeries
Heart and vascular system
ELECTROCARDIOGRAPHY:
Standard monitoring involves 5 lead electrode system.
One electrode for each extremity and a standard precordial lead
At V5 position- left axillary line at 5th ICS.
Ischaemia detection- lead II and V5.
When combined with V4, sensitivity is 100 percent.
Invasive BP monitoring
Provides continuous beat to beat assessment of arterial perfusion pressure.
Also enables frequent drawing of blood for lab purposes.
Radial artery - m/c
Others- femoral,brachial,ulnar,dorsalis pedis,posterior tibial, axillary
If the radial artery graft is to be harvested for CABG, it is usually taken from non
dominant hand.
Hence arterial line has to be secured in dominant hand.
CENTRAL VENOUS PRESSURE MONITORING (CVP
line)
- Monitoring central venous pressure
- Access for IV volume replacement, drugs
- Access for the insertion of PA catheters.
M/C - IJV- ease of approach and optimal distance from operative field.
Femoral- inappropriate if femoral bypass cannula is used or femoral vein is
harvested.
Subclavian- risk of catheter obstruction during sternal retraction.
Pulmonary artery catheterization
Central nervous system
The patients undergoing cardiothoracic surgery are at greater risk of
developing
Stroke
Post op cognitive dysfunction.
2 main reasons: Emboli - particulate or microgaseous
hypoperfusion
Monitoring of CNS
1.Trans esophageal echo and epiaortic echo
2.cerebral oximetry
3.transcranial doppler
4.EEG and BIS
Cerebral oximetry
Measures the cerebral oxygen saturation by near infrared spectroscopy.
rSO2 < 80% of preop values or
Absolute rSO2 <50%
Transcranial doppler
Measures the blood flow velocity across middle cerebral and common
carotid arteries.
Can detect emboli but couldn’t differentiate gaseous and solid emboli.
Highly user dependent.
EEG and BIS
EEG measures only the cortical activity. Any ischaemia or emboli below the level
of cortex cannot be detected.
The Multichannel EEG monitoring is converted to Dual channel processed EEG
termed BISPECTRAL INDEX.
BIS is widely used for detecting intraop awareness and its use is still
controversial in fast tracking.
RENAL SYSTEM- CSA AKI
GLYCAEMIC MONITORING
CPB increases the stress response to surgery to manyfold.
Degree of hyperglycaemia depends on
1. Pump prime fluid
2. Degree of hypothermia induced
3. Use of epinephrine and other inotropic drugs.
SOCIETY OF THORACIC SURGEONS- guidelines state that blood glucose levels
to be kept lower than 180mg/dl throughout the periop period.
Thyroid hormone
Both increased and decreased level of thyroid hormone can occur during or
immediately after CPB.
FT3 - biologically active form can decrease because of decreased activity of
the enzyme 5- monodeiodinase.
Coagulation monitoring
HEPARIN- thrombin-Anti thrombin 3 complex
ACTIVATED CLOT FORMATION TIME- ACT
Baseline ACT- normal range is 80 to 120 seconds.
For extracorporeal circulation targeted ACT is 400 to 480 seconds- can be
achieved by IV administration of 300 to 400 units per kg of heparin.
Maintenance dose- 50 to 100 units per kg (administered anywhere between 30
minutes to 2 hour)
Bank blood- heparinized with 2500 to 5000 units/ unit of blood.
Current practice:
1.Administer heparin 300 units per kg
2. Draw an arterial sample for act in 3 to 5 minutes
3.Give additional heparin to achieve ACT >300 secs during normothermic CPB
and >400 secs for hypothermic <30 deg celsius.
4.Prime the extracorporeal circuit with 3units /ml heparin.
5.Monitor ACT every 30 minutes during CPB.
6.If ACT decreases below desired value, repeat dose of 50 to 100 units per kg is
given.
Limitations of ACT:
ACT values can be prolonged due to:
1.hypothermia
2.hemodilution
3.APOTININ : a serine protease inhibitor used for blood conservation
during open heart surgery.Maintain ACT values of more than 750 when apotinin is
used.
Protamine- Heparin neutralization
A polycationic protein derived from the sperm of salmon fish.
Binds with heparin to form stable precipitate which has no anticoagulation
property.
Has got mild anticoagulant effect independent of heparin.
Dose- 1 to 1.3mg of protamine is given for every 100 units of heparin.
Protamine reaction
Myocardial ischaemia and
protection strategies
Myocardial ischaemia during cpb
2 mechanisms:
1.Hypoxia ( 0xygen saturation, Hb content of blood)
2.Ischaemia- inadequate coronary blood flow
MYOCARDIAL ISCHAEMIA
Myocardial 02 supply is rapidly depleted
Acceleration of glycolysis and depletion of ATP
Switch to Anaerobic metabolism- lactic acidosis.
Structural damage to myocardium occurs- manifested by low CO following CPB.
Atrial and ventricular dysrrhythmias -subtle manifestation of myocardial damage.
Stunned myocardium
Atransient and reversible myocardial dysfunction that completely recovers after 48
to 72 hours.
Usually caused by ischaemia of limited duration.
No structural and biochem evidence of tissue injury.
Events during CPB leading to myocardial injury:
1. Aortic cross clamping
2. Ventricular fibrillation
3. Ventricular distension
4. Coronary embolism
5. Low perfusion pressure
6. Catecholamines
7. reperfusion
Aortic cross clamping
Aortic cross clamping was done to obtain bloodless operating field.
During aortic cross clamping coronary perfusion is completely stopped.
Earlier days- continuous coronary perfusion and frequent VF was practiced.
But these mechanisms didn’t prevent the myocardial damage.
Intermittent cross clamping with periods of
reperfusion
In this Aorta is cross clamped and VF is induced with fibrillator.
Fibrillation continued for period of 10 minutes
f/b heart is defibrillated and reperfused for 3 to 5 minutes.
This reperfusion period allows partial regeneration of high energy
metabolites and allows the washout of metabolic end products.
Operative procedure is performed only when the aorta is cross clamped.
Proximal anastamosis of grafts- done when the aorta is unclamped and the heart
is beating.
Distal anastamosis- done when the aorta is cross clamped and the heart is
fibrillating.
MYOCARDIAL PROTECTION STRATEGIES
CPB- reduce the contractile work
Cardioplegia - eliminates the electromechanical activity of the heart
Hypothermia- reduces the basal metabolism
Left ventricular vent- decompression of heart
cardioplegia
Solution to produce temporary cessation of heart during cardiac surgery.
Contains high potassium.
Arrests the heart at diastole.
Reduces the transmembrane potential from -85mv to -65mv
The voltage dependant fast Na channels are blocked.
The cardiac action potential is blocked at phase 0.
Depolarized arrest.
Goals of cardioplegia
Provide bloodless operating field
Reduce myocardial oxygen demand- Limits myocardial damage
Prevents the reperfusion injury
Prevents calcium paradox
Calcium paradox
Massive cellular destruction that occurs when myocardium is perfused with
calcium containing solution after a period of calcium free perfusion.
CARDIOPLEGIA SOLUTION
St.Thomas cardioplegia:
Short periods of asystole- 20mins
Del Nido cardioplegia:
Longer periods- 40 mins
Custodial:
Currently mainly used for perfusing and flushing organs from organ
donors.
Anterograde cardiplegia
Administered into the aortic root or coronary ostia via 14 guage cannulaafter
aortic cross clamping at a pressure of 80 to 100mm Hg.
Surgeons has to ensure that LV is not distending due to aortic valve incompetence
Retrograde cardioplegia
Cardioplegic solution is administered into coronary sinus
Via a triple lumen catheter.
1.administration of cardioplegic soln- 100ml/min
2.distending the balloon with saline
3. Pressure monitoring -40 mm Hg.
Aortic root should be vented
Ensures homogenous distribution of cardioplegia beyond the coronary artery
occlusion.
Eliminates the need for coronary artery cannulation during aortic valve surgery
Based on temperature
Warm cardioplegia: delivered at 37 degree celsius.
Metabolic req and O2 consumption is high.Hence administered
continuously.
Crystalloid based cardioplegia is unable to meet metabolic requirements
hance blood is essential for warm cardioplegia.
Cold cardioplegia: delivered at 4 degree Celcius.
Cools the myocardium to 15 to 16 degree Celcius.
Can be given intermittently
Tepid cardioplegia: Delivered at 29 degree Celcius
Provides the benefit of warm cardioplegia and refuses
myocardial hypothermia.
TIMING OF DELIVERY
INTERMITTENT CARDIOPLEGIA:
Initially high K+ (20 to 30 mEq/L) 1 to 1.5 litres delivered
Then low k+ (10 to 20 mEq/L) 200 to 500ml infused at 20 to 40 mins
interval.
CONTINUOUS CARDIOPLEGIA:
Delivery at low flow.
Used for longer surgeries.
COMPOSITION ( mmol/L)
K+ 20 to 30 diastolic arrest
Na+ 109
Cl- 114
Calcium 1
Bicarbonate 27 buffers acidic metabolites
Glucose- 28 energy substrate
Mannitol 54 controls myocardial edema, free radical scavenger.
Substrate enriched cardioplegia
Adenosine: potent coronary vasodilator and arresting agent.
L-arginine
Magnesium
Insulin
Normal myocardial O2 consumption in a full beating heart
is 10mlO2 /100gm/min.
LV vent
Ischaemia reperfusion injury
Reperfusion of myocardium following an extended period of ischaemia usually for
>45 minutes results in ischaemia reperfusion injury.
Approach to anaesthesia for adult cardiac patient (1).pdf
Approach to anaesthesia for adult cardiac patient (1).pdf

Approach to anaesthesia for adult cardiac patient (1).pdf

  • 1.
    Approach to anaesthesiafor adult cardiac patient
  • 2.
  • 3.
    Heart and vascularsystem ELECTROCARDIOGRAPHY: Standard monitoring involves 5 lead electrode system. One electrode for each extremity and a standard precordial lead At V5 position- left axillary line at 5th ICS. Ischaemia detection- lead II and V5. When combined with V4, sensitivity is 100 percent.
  • 4.
    Invasive BP monitoring Providescontinuous beat to beat assessment of arterial perfusion pressure. Also enables frequent drawing of blood for lab purposes. Radial artery - m/c Others- femoral,brachial,ulnar,dorsalis pedis,posterior tibial, axillary
  • 6.
    If the radialartery graft is to be harvested for CABG, it is usually taken from non dominant hand. Hence arterial line has to be secured in dominant hand.
  • 7.
    CENTRAL VENOUS PRESSUREMONITORING (CVP line) - Monitoring central venous pressure - Access for IV volume replacement, drugs - Access for the insertion of PA catheters. M/C - IJV- ease of approach and optimal distance from operative field. Femoral- inappropriate if femoral bypass cannula is used or femoral vein is harvested. Subclavian- risk of catheter obstruction during sternal retraction.
  • 8.
  • 11.
    Central nervous system Thepatients undergoing cardiothoracic surgery are at greater risk of developing Stroke Post op cognitive dysfunction. 2 main reasons: Emboli - particulate or microgaseous hypoperfusion
  • 13.
    Monitoring of CNS 1.Transesophageal echo and epiaortic echo 2.cerebral oximetry 3.transcranial doppler 4.EEG and BIS
  • 16.
    Cerebral oximetry Measures thecerebral oxygen saturation by near infrared spectroscopy. rSO2 < 80% of preop values or Absolute rSO2 <50%
  • 17.
    Transcranial doppler Measures theblood flow velocity across middle cerebral and common carotid arteries. Can detect emboli but couldn’t differentiate gaseous and solid emboli. Highly user dependent.
  • 18.
    EEG and BIS EEGmeasures only the cortical activity. Any ischaemia or emboli below the level of cortex cannot be detected. The Multichannel EEG monitoring is converted to Dual channel processed EEG termed BISPECTRAL INDEX. BIS is widely used for detecting intraop awareness and its use is still controversial in fast tracking.
  • 20.
  • 23.
    GLYCAEMIC MONITORING CPB increasesthe stress response to surgery to manyfold. Degree of hyperglycaemia depends on 1. Pump prime fluid 2. Degree of hypothermia induced 3. Use of epinephrine and other inotropic drugs.
  • 24.
    SOCIETY OF THORACICSURGEONS- guidelines state that blood glucose levels to be kept lower than 180mg/dl throughout the periop period.
  • 25.
    Thyroid hormone Both increasedand decreased level of thyroid hormone can occur during or immediately after CPB. FT3 - biologically active form can decrease because of decreased activity of the enzyme 5- monodeiodinase.
  • 27.
  • 28.
    ACTIVATED CLOT FORMATIONTIME- ACT Baseline ACT- normal range is 80 to 120 seconds. For extracorporeal circulation targeted ACT is 400 to 480 seconds- can be achieved by IV administration of 300 to 400 units per kg of heparin. Maintenance dose- 50 to 100 units per kg (administered anywhere between 30 minutes to 2 hour) Bank blood- heparinized with 2500 to 5000 units/ unit of blood.
  • 29.
    Current practice: 1.Administer heparin300 units per kg 2. Draw an arterial sample for act in 3 to 5 minutes 3.Give additional heparin to achieve ACT >300 secs during normothermic CPB and >400 secs for hypothermic <30 deg celsius. 4.Prime the extracorporeal circuit with 3units /ml heparin. 5.Monitor ACT every 30 minutes during CPB. 6.If ACT decreases below desired value, repeat dose of 50 to 100 units per kg is given.
  • 30.
    Limitations of ACT: ACTvalues can be prolonged due to: 1.hypothermia 2.hemodilution 3.APOTININ : a serine protease inhibitor used for blood conservation during open heart surgery.Maintain ACT values of more than 750 when apotinin is used.
  • 31.
    Protamine- Heparin neutralization Apolycationic protein derived from the sperm of salmon fish. Binds with heparin to form stable precipitate which has no anticoagulation property. Has got mild anticoagulant effect independent of heparin. Dose- 1 to 1.3mg of protamine is given for every 100 units of heparin.
  • 32.
  • 34.
  • 35.
    Myocardial ischaemia duringcpb 2 mechanisms: 1.Hypoxia ( 0xygen saturation, Hb content of blood) 2.Ischaemia- inadequate coronary blood flow
  • 36.
    MYOCARDIAL ISCHAEMIA Myocardial 02supply is rapidly depleted Acceleration of glycolysis and depletion of ATP Switch to Anaerobic metabolism- lactic acidosis. Structural damage to myocardium occurs- manifested by low CO following CPB. Atrial and ventricular dysrrhythmias -subtle manifestation of myocardial damage.
  • 37.
    Stunned myocardium Atransient andreversible myocardial dysfunction that completely recovers after 48 to 72 hours. Usually caused by ischaemia of limited duration. No structural and biochem evidence of tissue injury.
  • 38.
    Events during CPBleading to myocardial injury: 1. Aortic cross clamping 2. Ventricular fibrillation 3. Ventricular distension 4. Coronary embolism 5. Low perfusion pressure 6. Catecholamines 7. reperfusion
  • 39.
  • 40.
    Aortic cross clampingwas done to obtain bloodless operating field. During aortic cross clamping coronary perfusion is completely stopped. Earlier days- continuous coronary perfusion and frequent VF was practiced. But these mechanisms didn’t prevent the myocardial damage.
  • 41.
    Intermittent cross clampingwith periods of reperfusion In this Aorta is cross clamped and VF is induced with fibrillator. Fibrillation continued for period of 10 minutes f/b heart is defibrillated and reperfused for 3 to 5 minutes. This reperfusion period allows partial regeneration of high energy metabolites and allows the washout of metabolic end products. Operative procedure is performed only when the aorta is cross clamped.
  • 42.
    Proximal anastamosis ofgrafts- done when the aorta is unclamped and the heart is beating. Distal anastamosis- done when the aorta is cross clamped and the heart is fibrillating.
  • 43.
    MYOCARDIAL PROTECTION STRATEGIES CPB-reduce the contractile work Cardioplegia - eliminates the electromechanical activity of the heart Hypothermia- reduces the basal metabolism Left ventricular vent- decompression of heart
  • 44.
    cardioplegia Solution to producetemporary cessation of heart during cardiac surgery. Contains high potassium. Arrests the heart at diastole. Reduces the transmembrane potential from -85mv to -65mv The voltage dependant fast Na channels are blocked. The cardiac action potential is blocked at phase 0. Depolarized arrest.
  • 45.
    Goals of cardioplegia Providebloodless operating field Reduce myocardial oxygen demand- Limits myocardial damage Prevents the reperfusion injury Prevents calcium paradox
  • 46.
    Calcium paradox Massive cellulardestruction that occurs when myocardium is perfused with calcium containing solution after a period of calcium free perfusion.
  • 47.
    CARDIOPLEGIA SOLUTION St.Thomas cardioplegia: Shortperiods of asystole- 20mins Del Nido cardioplegia: Longer periods- 40 mins Custodial: Currently mainly used for perfusing and flushing organs from organ donors.
  • 50.
    Anterograde cardiplegia Administered intothe aortic root or coronary ostia via 14 guage cannulaafter aortic cross clamping at a pressure of 80 to 100mm Hg. Surgeons has to ensure that LV is not distending due to aortic valve incompetence
  • 51.
    Retrograde cardioplegia Cardioplegic solutionis administered into coronary sinus Via a triple lumen catheter. 1.administration of cardioplegic soln- 100ml/min 2.distending the balloon with saline 3. Pressure monitoring -40 mm Hg. Aortic root should be vented
  • 52.
    Ensures homogenous distributionof cardioplegia beyond the coronary artery occlusion. Eliminates the need for coronary artery cannulation during aortic valve surgery
  • 53.
    Based on temperature Warmcardioplegia: delivered at 37 degree celsius. Metabolic req and O2 consumption is high.Hence administered continuously. Crystalloid based cardioplegia is unable to meet metabolic requirements hance blood is essential for warm cardioplegia.
  • 54.
    Cold cardioplegia: deliveredat 4 degree Celcius. Cools the myocardium to 15 to 16 degree Celcius. Can be given intermittently Tepid cardioplegia: Delivered at 29 degree Celcius Provides the benefit of warm cardioplegia and refuses myocardial hypothermia.
  • 55.
    TIMING OF DELIVERY INTERMITTENTCARDIOPLEGIA: Initially high K+ (20 to 30 mEq/L) 1 to 1.5 litres delivered Then low k+ (10 to 20 mEq/L) 200 to 500ml infused at 20 to 40 mins interval. CONTINUOUS CARDIOPLEGIA: Delivery at low flow. Used for longer surgeries.
  • 56.
    COMPOSITION ( mmol/L) K+20 to 30 diastolic arrest Na+ 109 Cl- 114 Calcium 1 Bicarbonate 27 buffers acidic metabolites Glucose- 28 energy substrate Mannitol 54 controls myocardial edema, free radical scavenger.
  • 57.
    Substrate enriched cardioplegia Adenosine:potent coronary vasodilator and arresting agent. L-arginine Magnesium Insulin
  • 58.
    Normal myocardial O2consumption in a full beating heart is 10mlO2 /100gm/min.
  • 59.
  • 61.
    Ischaemia reperfusion injury Reperfusionof myocardium following an extended period of ischaemia usually for >45 minutes results in ischaemia reperfusion injury.