Advance Directives and Advance Care Planning: Ensuring Patient Voices Are Heard
8.myocardial protection during cpb
1. MYOCARDIAL PROTECTION
GOAL
TO PROTECT THE
MYOCARDIUM FROM
INTRAOPERATIVE DAMAGES
MYOCARDIAL PROTECTION
GOAL
TO PROTECT THE
MYOCARDIUM FROM
INTRAOPERATIVE DAMAGES
3. Determinants of ishemic injury
Accumilation of tissue
metabolites(lactate,co2 and hydrogen ions)
Duration of ishemia
Baseline health of tissue
Distinction b/w Global and regional ishemia
4. Mechanisms of myocardial ischemic
injury
Depletion of high energy phosphates
Intracellular acidosis.
Alteration in intracellular calcium.
Direct myocellular injury from ischemia.
Oxygen derived free radicals generation
upon reperfusion.
Myocardial edema from ischemia and
reperfusion.
5. Cessation of Myocardial Blood
Flow
mitochondria
cellular pO2 < 5mmHg within
seconds
oxidative phosphorilation
stops
cytosol
anaerobic glycolysis
glycogen
glucose-6-phosphate
pyruvate
lactate
cellular acidosis
depletion of ATP
6. Depletion of ATP < 50% of Normal
Level-
irreversible lethal cell injury
glycolysis is blocked
increasing cellular acidity
protein denaturation
structural, enzymatic, nuclear changes
7. Severity and duration of ischemia
The potential for myocardial injury related to
duration of warm ischemia
To reduce the severity of postischemic injury
1. Rapid arrest
2. Venting LV to decrease O2 requirements
3. Imposing cardiac hypothermia
• Safe period 15 to 45 mts. Up to 4hrs with
hypothermic intermittant cardioplegia
13. How to minimize reperfusion injury ?
Decrease extracellular calcium
Addition of antioxidants like superoxide
dismutase,glutathione
Controlled reperfusion
mannitol
14. Myocardium, Coronary Flow
coronary blood flow: 250 ml/min
entirely during diastole
~ aortic diastolic pressure minus LVDP
~ duration of diastole
pressure < 150 mmHg
oxygenated by superb membrane
oxygenator-”the lungs”
15. Myocardial Protection
encompass all the strategies employed during
cardiac surgery
preoperative phase
operative phase
– global myocardial ischaemic time
– reperfusion
postoperative phase
16. Myocardial oxygen cosumption
Reduction Oxygen Demand
Normothermic Arrest (37ο
C) 1mL/100g/min 90%
Hypothermic Arrest (22ο
C) 0.30 mL/100g/min
Hypothermic Arrest (10ο
C) 0.14 mL/100g/min ~ 97%
17. Myocardial oxygen consumption
contd.,
Normal working myocardium consumes
8ml/100gm of oxygen/minute.
Empty beating heart consumes
5.6ml/100gm/minute.
Potassium arrested heart consumes
1.1ml/100gm/mt
Myocardial cooling reduces the consumption
to .3ml/100gm/mt of myocardium
18. HYPOTHERMIA
lowers metabolic rate
decrease myocardial energy requirements
promoting electromechanical quiescence
every 10 0C in temperature, VO2 halved
25. Antegrade Cardioplegia
Advantages
Produces prompt arrest.
Simple
Mimics normal coronary
flow
pitfalls
poor distribution in coronary
patients unless delivered
through the vein grafts
poor distribution in patients
with aortic regurgitation
risk of ostial injury from direct
perfusion (during AVR)
interruption of procedure
during mitral surgery
27. Retrograde Cardioplegia
advantages
distribution of CP to
regions supplied by
occluded or stenosed
vessels
improved subendocardial
CP delivery
flushing of air and/or
atheromatous debris
Does not impede surgery
pitfalls
shunting of CP into
ventricular cavities via
Thebesian channels
perfusion defects especially
right ventricle and posterior
septal regions
Catheter placement can be
difficult
complex
28. Blood Cardioplegia
1980’s
improved oxygen carrying capacity and delivery until
electromechanical quiescence developed
enhanced myocardial oxygen consumption
preserved high-energy phosphate stores
buffering changes in pH
use of free radical scavengers (superoxide dismutase,
catalase, and glutathione)
provide appropriate osmotic environment for myocardial
cells and lessen the myocardial oedema
29. “The heart takes up oxygen over time
rather than by dose,
so that blood cardioplegic solutions must
be delivered over a time interval, rather
than by volume”
31. Microplegia
A cardioplegia technique that mixes blood
from CPB circuit with small quantities of
concentrated additives.(Pottssium)
Relies on precision pumps to deliver
accurate quantities of additives.
Minimizes crystalloid quantity of cardioplegia
solution.
32. Warm Induction
“resuscitation of the heart”
severe left ventricular dysfunction
cardiogenic shock
preischaemic depletion of energy stores
warm induction showed improved aerobic
metabolism and LV function in dogs
33. Warm Reperfusion (hot-shot)
early myocardial metabolic recovery while
maintaining electro-mechanical arrest
repletion of energy stores
maintenance of unnecessary contractile activity
34. Continuous Warm Cardioplegia
avoidance of direct myocellular injury
inflicted by any cold solution or
environment
increased rate of perioperative stroke and
neurological events
36. Myocardial monitoring technique
Temperature
Pros
Ease of use
Cons
Location dependent
Temp not equivalent to
protection
Ph
Pros
Potential to alter
surgical conduct and
improve protection.
Cons
Specialized equipment
Efficacy unclear
37. Cardioplegia Additives
Drug Advantage Dis adv
Nicorandil Less plegia/Kcl Cost
requirement
reduced periop
coronary spasm
preconditioning
reduced need of
catacolamines post op
43. Ventricular Fibrillation with
Intermittent Aortic Cross-clamping
induces global ischaemia with fibrillation,
followed by anoxic arrest and electrical silence
on the ECG
44. Ventricular Fibrillation with
Intermittent Aortic Cross-clamping
Advantages
cumulative cross-clamp times are less than with
cardioplegia
the myocardium is intermittently perfused with oxygenated
blood
increasing areas of myocardium are reperfused during the
course of the procedure
Disadvantages
Repeated aortic clamping
Anastomotic time limited