CONTENTS:
Page
1.
CARDIAC PHYSIOLOGY REVISION
2. MYOCARDIAL PROTECTION
DURING CPB [No X-clamp]
3. MYOCARDIAL PROTECTION
DURING CPB [X-clamp]
9. BLOOD VERSUS CRYSTALLOID
CARDIOPLEGIA
10. COLD & INTERMITTENT
CARDIOPLEGIA
11. MYOCARDIAL REPERFUSION
INJURY
13. COLD OXYGENATED
CRYSTALLOID
15. DRUG CALCULATIONS IN
BUCKBERG SYSTEM
1. CARDIAC PHYSIOLOGY REVISION
Wigger’s Graph Note that 90% of MvO2
occurs during isovolumetric contraction Action potential of
cardiac cells ·
Depolarisation is
associated with fast sodium channel opening ·
Refractory period is
associated with slow calcium channel opening ·
Repolarisation is
associated with potassium channel opening
Adapted from Mora
Note that
1.1 the
potassium arrested heart has the lowest MvO2 at any temperature
1.2 the
nonworking (empty) beating heart at normothermia uses only one third of the
MvO2 of the working heart
1.2.1 Therefore
CPB itself, by minimising afterload can reduce MvO2 substantially
1.3 The empty fibrillating heart at £ 32°C has a lower MvO2 then an
empty but still beating heart
1.4 Oxygen
consumption doubles with fibrillation (normothermia not decompressed)
1.5 Significant
reductions in MvO2 by arresting heart and minimal reductions in MvO2 by cooling
heart
1.6 Normal
adult heart weighs 300g; hypertrophy can triple the weight
2. MYOCARDIAL PROTECTION DURING CPB [No X-clamp]
2.1 Reduce
MvO2
2.1.1 Note
that 90% of MvO2 occurs during isovolumetric contraction of heart
2.1.2 Reduce
Preload [chamber distension]
2.1.2.1 Left
heart
2.1.2.1.1 Venting
2.1.2.2 Right
heart
2.1.2.2.1 Adequate
decompression with venous cannulae
2.1.3 Reduce
Chronotropy [heart rate]
2.1.3.1 Cardioplegia
2.1.3.2 Turn
off pacemakers
2.1.3.3 Turn
off chronotropic drugs
2.1.3.4 Hypothermia
2.1.4 Reduce
Inotropy [contractility]
2.1.4.1 Hypothermia
2.1.4.1.1 Systemic
2.1.4.1.2 Topical
2.1.4.2 Reduce
catecholamines
2.1.4.2.1 Turn off
inotropes
2.1.4.2.2 Reduce
endogenous stress response
2.1.4.2.2.1 Anaesthetic drugs
2.1.5 Reduce
Afterload
2.1.5.1 Reduce
systemic vascular resistance [= systemic vascular hinderence (SVH) times
viscosity]
2.1.5.1.1 Reduce
SVH
2.1.5.1.1.1 arteriolar vasodilation
2.1.5.1.1.2 IABP
2.1.5.1.2 Reduce
viscosity by haemodilution
2.2 Increase
MDO2
2.2.1 MDO2
= CaO2 ´ Coronary blood flow
2.2.2 CaO2
= Oxygen combined with haemoglobin ´ oxygen dissolved in plasma
2.2.2.1 Increase
haemoglobin
2.2.2.1.1 Left
ventricular hypertrophy &/or CAD
2.2.2.1.1.1 Hct ³ 22
2.2.2.1.2 No LVH
or CAD
2.2.2.1.2.1 Hct ³ 18
2.2.2.2 Increase
PaO2
2.2.3 Increase
coronary blood flow
2.2.3.1 Note:
Coronary perfusion pressure = Diastolic blood pressure — left ventricular end
diastolic pressure
2.2.3.2 Increase
coronary perfusion pressure
2.2.3.2.1 Left
ventricular hypertrophy &/or CAD
2.2.3.2.1.1 CPP > 60 mmHg
2.2.3.2.2 No LVH
or CAD
2.2.3.2.2.1 CPP ³ 50 mmHg
2.2.3.3 Reduce
LVEDP
2.2.3.3.1 Venting
2.2.3.4 Avoid
ventricular fibrillation
2.2.3.5 Dilate
coronary arteries
2.2.3.5.1 Glycerol
trinitrate
2.2.3.6 Use
of IABP when weaning
3. MYOCARDIAL PROTECTION DURING CPB [X-clamp]
3.1 Reduce
MvO2
3.1.1 Note
that 90% of MvO2 occurs during isovolumetric contraction of heart
3.1.2 Reduce
Preload [chamber distension]
3.1.2.1 Left
heart
3.1.2.1.1 Venting
3.1.2.2 Right
heart
3.1.2.2.1 Adequate
decompression with venous cannulae
3.1.3 Reduce
Chronotropy [heart rate]
3.1.3.1 Cardioplegia
3.1.3.2 Hypothermia
3.1.4 Reduce
Inotropy [contractility]
3.1.4.1 Cardioplegia
3.1.4.2 Hypothermia
3.1.4.2.1 Systemic
3.1.4.2.2 Topical
3.1.4.2.3 Cardioplegia
3.2 Increase
MDO2
3.2.1 MDO2
= CaO2 ´ Coronary blood flow rate
3.2.1.1 CaO2
= Oxygen combined with haemoglobin ´ oxygen dissolved in plasma
3.2.1.1.1 Oxygenated
blood cardioplegia
3.2.1.1.2 Oxygenated
crystalloid cardioplegia
3.2.1.2 Increase
coronary blood flow
3.2.1.2.1 Note:
Coronary perfusion pressure = Diastolic blood pressure — left ventricular end
diastolic pressure
3.2.1.2.2 Increase
coronary perfusion pressure
3.2.1.2.2.1 Adequate cardioplegia pressure & flows
3.2.1.2.3 Reduce
LVEDP
3.2.1.2.3.1 Venting
3.2.1.2.4 Avoid
ventricular fibrillation
3.2.1.2.5 Dilate
coronary arteries
3.2.1.2.5.1 Magnesium
3.2.1.2.5.2 Procain
3.2.1.2.5.3 Calcium channel blockers
3.2.1.2.6 Deliver
continuous blood cardioplegia
4. AORTIC ROOT
4.1 Technique
4.1.1 Cardioplegia
cannula in aortic root
4.1.1.1 Require
patent aortic valve
4.1.1.1.1 Minor
aortic regurgitation may be aortic root pleged by the surgeon gripping the
heart and manipulating it to minimise regurgitation
4.1.2 Pressures
4.1.2.1 Induction
[aortic root]
4.1.2.1.1 100 mmHg
4.1.2.2 Maintenance
4.1.2.2.1 50-80
mmHg
4.1.2.3 Terminal
warm dose
4.1.2.3.1 50 mmHg
4.1.2.4 Issues
4.1.2.4.1 Dilemma
of increased pressures resulting in better perfusion distal to stenosed
coronaries but increased oedema in overperfused regions [especially associated
with reduced endothelial integrity seen with ischaemia]
4.1.2.4.2 Line
pressures may exceed aortic root
pressures by > 50 mmHg
4.1.3 Flows
4.1.3.1 250 -
400 ml/min
4.1.3.1.1 Low
4.1.3.1.1.1 Severe widespread coronary artery disease
4.1.3.1.1.2 Small patient
4.1.3.1.1.3 Intimal infusion
4.1.3.1.2 High
4.1.3.1.2.1 Lack of coronary artery disease
4.1.3.1.2.2 Large patient [ie large heart]
4.1.3.1.2.3 Aortic incompetence
4.1.3.1.2.4 Cross clamp malposition
4.1.3.1.3 Issues
4.1.3.1.3.1 Normal coronary perfusion is 5 - 8 % of cardiac output
4.1.4 Times
4.1.4.1 Induction
4.1.4.1.1 3.5 min
4.1.4.2 Maintenance
4.1.4.2.1 1.5 min
4.1.4.3 Duration
of infusion is dependent on:
4.1.4.3.1 Extent
of coronary artery disease
4.1.4.3.2
Cessation of ECG activity
4.1.4.3.3 Degree
of myocardial hypertrophy
4.1.4.3.4 Cooling
of heart
4.2 Advantages
4.2.1 Easy
to set up and monitor
4.2.2 Physiological
antegrade flow
4.2.3 Prompt
arrest
4.2.3.1 Both
left & right coronary arteries simultaneously infused
4.2.4 Aortic
root tolerates higher pressures
4.3 Disadvantages
4.3.1 Contraindicated:
4.3.1.1 Aortic
regurgitation
4.3.2 Compromised
perfusion distal to stenosed coronary arteries
4.3.3 Poor
subendocardial perfusion
4.3.3.1 Concern
for hypertrophic heart
4.3.4 Distension
of right atrium if have snared bicaval vena cava
5. RETROGRADE CORONARY SINUS
5.1 Technique
5.1.1 Cardioplegia
infused via coronary sinus
5.1.2 Usually
blood cardioplegia
5.1.3 Aortic
root usually vented
5.1.4 Coronary
sinus cannula:
5.1.4.1 3
lumens: plegia infusion, balloon inflation, sinus pressure
5.1.4.2 Inserted
via right atrial wall into coronary sinus
5.1.4.2.1 Prior to
commencement CPB [atrium is full]
5.1.4.2.2 Soon after
commencement CPB [are able to rotate heart to insert coronary sinus cannula],
note: must maintain a positive pressure in right atrium to prevent air
entrapment
5.2 Pressures
5.2.1 Coronary
sinus pressures 34 - 40 mmHg
5.2.2 Cardioplegia
delivery line pressures < 100 mmHg
5.2.3 Concerns
5.2.3.1 Important
to keep coronary sinus pressures mid 30’s mmHg as too low pressures may
compromise cardioplegia distribution, while too high pressures may rupture the
coronary sinus
5.3
Flows
5.3.1
150 - 400 ml/min
5.3.1.1
Low
5.3.1.1.1 Overinflated balloon
5.3.1.1.2 Too deep insertion of cannula into coronary sinus
5.3.1.1.3 Rotation of heart
5.3.1.2
High
5.3.1.2.1 Inadequate cardioplegia distribution
5.3.1.2.2 Leakage of blood around inadequately filled balloon
5.3.1.2.3 Ruptured coronary sinus
5.4 Times
5.4.1 Induction
5.4.1.1 7 min
5.4.2 Maintenance
5.4.2.1 3.5
min
5.4.3 Issues
5.4.3.1 Duration
of infusion is dependent on:
5.4.3.1.1 Extent
of coronary artery disease
5.4.3.1.2
Cessation of ECG activity
5.4.3.1.3 Degree
of myocardial hypertrophy
5.4.3.1.4 Cooling
of heart
5.4.3.2 Adequacy
of perfusion is further monitored by presence of desaturated blood in aortic
root via coronary ostia
5.4.3.3 Importance
of adequate flows, pressures & durations especially in hypertrophic heart
5.5 Advantages
5.5.1 Alternate
to ostial cardioplegia in aortic valve regurgitation
5.5.2 Cardioplegia
distribution to post stenotic coronary artery regions
5.5.2.1 Coronary
veins do not become stenosed by coronary artery disease
5.5.3 Good
distribution to subendocardium - relevance to hypertrophic heart
5.5.3.1 Subendocardium
is the distal distribution of the coronary arteries
5.5.4 Ability
to retrogradely flush coronary arteries of emboli
5.5.4.1 Redo
CABG with atherosclerotic vein grafts
5.5.4.2 Aortic
root opening - deair root prior to closure
5.5.5 Ability
to run warm continuous cardioplegia
5.5.6 Can
be run with minimal interference to surgeon
5.6 Disadvantages
5.6.1 Technical
skill in insertion & operation
5.6.2 Delay
in initiation of arrest
5.6.2.1 Increased
ischaemic duration
5.6.3 Impaired
heart protection
5.6.3.1 Impaired
right heart protection
5.6.3.1.1 Only
coronary veins draining the left side of the heart enter the coronary sinus
5.6.3.1.2 Delayed
recovery of right ventricle not unusual
5.6.3.2 Too
far insertion of cannula/ variations in anatomy may limit retrograde flow via
small cardiac vein & middle cardiac veins
5.6.3.3 Presence
of a left SVC [0.5% ‘normal’ adults] - cardioplegia may preferentially enter
left SVC at expense of myocardium
6. CORONARY OSTIA
6.1 Technique
6.1.1 Surgeon
held cannula into coronary ostia
6.2 Pressures
6.2.1 250
- 300 mmHg cardioplegia delivery line pressure
6.2.1.1 The
small bore of the cardioplegia cannula results in high line pressures for
relatively moderate flow rates
6.3 Flows
6.3.1 150
- 250 ml/min
6.3.2 Issues
6.3.2.1 Normal
coronary perfusion is 5 - 8 % of cardiac output
6.3.2.2 For
right dominant hearts [70 - 80%], left & right coronary ostial blood flow
proportions are equivalent.
6.4 Times
6.4.1 Induction
6.4.1.1 3.5
min
6.4.2 Maintenance
6.4.2.1 1.5
min
6.4.3 Duration
of infusion is dependent on:
6.4.3.1
Extent of coronary artery disease
6.4.3.2
Cessation of ECG activity
6.4.3.3
Degree of myocardial hypertrophy
6.4.3.4
Cooling of heart
6.5 Advantages
6.5.1 Ability
to cardioplege antegradely despite aortic regurgitation or aortic root opening
6.5.2 Physiological
antegrade flow
6.6 Disadvantages
6.6.1 Myocardial
ischaemia interval from cross-clamping, opening the aortic root to positioning
the coronary ostial cannula and cardiopleging both left and right ostia
6.6.2 Ostia
are (usually) pleged sequentially
6.6.3 Time
consuming and disruptive to surgeon
6.6.4 Dependent
on surgical adeptness and technique
6.6.5 Compromised
perfusion distal to stenosed coronary arteries
6.6.6 Poor subendocardial perfus