Dr jeevraj cabg management

Anaesthesia for cabg
DR JEEVRAJ RAJAWAT
UNMCRC

LAD or Circumflex
Most commonly affected; proximal areas
ECG changes in Anterior & lateral leads
LMCA , TVD, Prox LAD are high risk
RCA
Proximal or distal areas
ECG changes in Inferior leads
Status of collateral circulation and microcirculation,
diffuse distal distal dis.

Subendocardial Region of LV
More prone to ischemic damage due to:
Ventricular contraction
Compression of subendocardial vessels
LV subendocardial blood flow is intermittent and occurs
only during the diastolic portion of the cardiac cycle.
Of the total LV coronary flow, 85% occurs during
diastole and 15% occurs in systole (primarily in the
epicardial region

coronary perfusion pressure
• Coronary blood flow is seen to be constant
• (autoregulated) over coronary perfusion pressures
from 60–140 mmHg.
• When coronary perfusion pressure
• reaches 60 mmHg, there will be maximal
autoregulatory vasodilation to maintain coronary
blood flow.
• Further decreases in coronary perfusion pressure
will result in decreases in coronary blood flow.
• At pressures higher than 60 mmHg, maximal
autoregulatory vasodilation will provide
autoregulatory vasodilator reserve.
• This reserve provides the increased coronary blood
flow necessary to meet increases in myocardial
oxygen consumption such as those induced by
exercise

Determinants of myocardial oxygen supply
• In broad terms, the supply of oxygen to the myocardium is determined by the arterial
oxygen content of the blood and the blood flow in the coronary arteries.
1.Determinants of arterial oxygen content
O2content = (hemoglobin) (1.34) (% saturation) + (0.003) (PO2)
• Ensuring maximal O2 content therefore involves having a high
hemoglobin level, highly saturated blood, and a high PO2.
2.Determinants of blood flow in normal coronary arteries.
• CBF varies directly with the pressure difference across the
coronary bed [coronary perfusion pressure (CPP)] and
inversely with coronary vascular resistance (CVR)
CBF = CPP/CVR

PREDICTIVE RISK FACTOR IN CABG
• Risk factors for increased morbidity and mortality
are -
• Poor LV function
- h/o CHF or EF<30%
- h/o DM, HTN etc.
- obesity
- redo procedures
- emergency procedures
- advanced age

Classification of Patients
1. Good LV function
CI > 2.5 L/min; EF > 55%
LVEDP < 12 mmHg
No chest pain
2. Poor LV function
CI < 2.0 L/min; EF < 40%
LVEDP > 18 mmHg
CHF symptoms

PRE OP INVESTIGATION
• CBC
• Coagulation profile
• Lipid profile
• Electrolytes
• Blood grouping and serology
• Renal and liver function tests
• CXR
• ECG
• Echo
• USG n carotid doppler
• Abdomen (elderly males)
• PFT

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
• To alley anxiety related to the procedure
• CAROTID DOPPLER Preoperative assessment of the
carotid arteries

• Co-morbidities requiring combined procedure
carotid artery stenosis, peripheral vascular
disease (PVD) should be assessed by Doppler
examination. A patient with carotid stenosis
>70% has a higher peri-operative neurological
morbidity and mortality and may require carotid
endarterectomy alone or as a combined
procedure with OPCAB/CPB based CABG
• Similarly a patient with PVD will contraindicate
the passage of IABP by femoral route if required

•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
• Angiography defines location and degree of occlusion and
coronary artery spasm
•Myocardial perfusion scans using thallium-201 or Tc 99m locate
and quantitate ischemic areas
•Contrast ventriculography shows areas of hypokinesia, akinesia
and dyskinesia

PRE OP MEDICINE
 β-Adrenergic blockers: Should be continued perioperatively in patients
already on β-blocker therapy. Consider β-blockers in high-risk patients
with heart rate greater than 60 beats/min(contraindications: hypotension,
third-degree heart block, bronchospasm
 Statins: Should be continued perioperatively in patients already on statin
therapy. Consider statins in all patients with CAD because of emerging
data that the complex effects of statins, including lipid-stabilizing effects
and anti-inflammatory properties, improve outcome, including in patients
undergoing CABG surgery.
 Calcium channel blockers: Should be continued perioperatively;
greater incidence of heart block or need for pacing.
 Angiotensin-converting enzyme inhibitor: Perioperative use
controversial; possible increased risk for hypotension during
induction, vasoplegic syndrome, and mortality.
 Diuretics: No firm recommendations; ensure adequate serum
potassium levels.

• Heparin: Regimen is often surgeon specific.
Usually discontinued 4 hours before for stable
patients, continued up to and through pre-
CPB period for critical left main disease or
acutely unstable angina patients.

• Oral hypoglycemic agents: Data suggest that
oral antidiabetic drugs may abolish the
preconditioning effect of potent inhalation
anesthetics. No firm recommendations;
consider holding administration. However,
glucose control has to be ensured.

ANTIPLATELET DRUGS
 ASPRIN : Irreversibly inhibits platelet cyclo-oxygenase (COX).
Increases bleeding and transfusions in patients who have undergone cardiac
surgery, especially in “hyper-responders.”
Implications: desirable to discontinue if possible, but not necessary, especially
in patients with CABG, because it reduces complications of angina, MI,
transient ischemic attack (TIA), atrial fibrillation (AF), and stroke
 Ticlopidine and Clopidogrel:
Irreversibly inhibit adenosine diphosphate (ADP)-mediated aggregation,
thereby inhibiting activation of the glycoprotein (GP) IIb/IIIa receptor
complex.
Oral use only; biotransforms to active metabolite, which persists in serum.
Implications: Delay surgery by 4 to 6 days if possible.

Abciximab , Tirofiban (Aggrastat), Eptifibatide
(Integrilin):
 Inhibits platelet membrane glycoprotein IIb/IIIa receptor.
 Abciximab: if possible, delay emergency or urgent CABG for
12 hours or elective CABG for 1 to 2 days. Prophylactic or
antecedent platelet transfusion is required. Full loading and
maintenance heparin doses are required for CPB;
abciximab prolongs the activated clotting time (ACT) by 35
to 85 seconds. Use hemoconcentration during CPB to help
eliminate abciximab. Transfuse platelet if excessive
bleeding is present after protamine reversal.
 Tirofiban and eptifibatide: No delay in emergency or
urgent CABG is necessary. Delay elective surgery by 2 to 4
hours. No prophylactic platelet transfusion is necessary

GOALS OF ANESTHETIC MGMT
 Provision of safe anaesthesia using a technique that offers
maximum cardiac protection and stability
 Maintaining haemodynamics in the intraoperative period by
physical and pharmacological methods
 Allowing early emergence, ambulation
 Providing adequate pain relief in the postoperative period.
 Avoid increases in myocardial oxygen consumption.
 Avoid tachycardia; it compromises oxygen delivery at any
MAP.
“Appreciate that the patient’s baseline ischemic pattern will
continue into the preoperative and intraoperative periods;
these episodes must be treated when recognized “
•

• Optimize the determinants of myocardial O2
supply and demand.
• Select anesthetics and adjuvant agents and
techniques according to their effects on O2
supply and demand.
• Monitor for ischemia to detect its occurrence
early and intervene rapidly.

Premedication
- Anti aspiration prophylaxis
- Anti anxiety: tab Alprazolam 0.5-1mg oral in night before
surgery
 Benzodiazepines, opioids and anticholinergic medications.
 0.05mg.kg-1 of midazolam and 1µg.kg -1 of fentanyl are
administered intramuscularly thirty minutes prior to surgery.
 provide supplemental oxygen.
 Before insertion of intravenous and arterial cannulae
administer additional midazolam and fentanyl.
 Patients with low cardiac output secondary to CHF sedation
should be performed judiciously to avoid myocardial
depression and resultant hypotension

INTRA OP MONITORING
• ECG – Simultaneous observation of an inferior lead
[II, III, aVF ] and anterior lead [V4,V5] detects
approximately 90% of events.
• SpO2,
• ETCO2
• Temperature monitoring
• Neurophysiologic monitoring: eg. cerebral oximetry
- Urinary output monitoring
- Invasive blood pressure (IBP) monitoring -
- By radial or femoral artery
- Dominant hand radial art preffered
- The cannulation of the femoral artery not only permits access to
the central arterial tree but provides access to quick insertion of
an intra aortic balloon pump.

Pulmonary artery catheter (PAC)
Indications:
 Ejection fraction <0.4
 Significant abnormality of the left ventricular wall motion.
 LVEDP > 18 mm Hg at rest.
 Recent MI and unstable angina.
 Post MI complications
 VSD
 LV aneurysm
 Mitral regurgitation
 Congestive cardiac failure
 Emergency surgery
 Combined procedures
 Reoperations

ROLE OF TEE IN CABG
• Intraoperative TEE: Recommendations
• Class I
– Intraoperative TEE should be performed for evaluation of
acute, persistent, and life-threatening hemodynamic
disturbances that have not responded to treatment(Level of
Evidence: B)
– Intraoperative TEE should be performed in patients undergoing
concomitant valvular surgery. (Level of Evidence: B)
• Class IIa
– Intraoperative TEE is reasonable for monitoring of
hemodynamic status, ventricular function, regional wall
motion, and valvular function in patients undergoing
CABG. (Level of Evidence: B)

• The main considerations in choosing an
induction technique for patients undergoing
CABG are
LV function
Coronary pathology.
Patients eligible for fast-tracking and early
extubation

Myocardial oxygen demand
The three major determinants of myocardial O2 demand are heart rate,
contractility, and wall stress.
1. Heart rate. O2 demand per minute increases with heart
rate increase.
2. Contractility. More O2 is used by a highly contractile heart
compared with a more relaxed heart.
3. Wall stress depends on the pressure in the ventricle during
contraction (afterload), the chamber size (preload), and the
wall thickness.
Wall stress= pressure x radius / 2 (wall thickness)

Induction and Maintenance of General
Anesthesia
• Induction of anesthesia should take place in a calm and
relaxed manner,
• Ambient room temperature or warm blankets placed on
the patient because entry into an excessively cold operating
room can elicit an unwanted sympathetic response with
increases in blood pressure and HR increasing oxygen
demand.
• Preoxygenation should be used and invasive continuous
blood pressure monitoring should be in place before
induction
• Goal is to avoid undue hypotension and to attenuate
hemodynamic response to laryngoscopy and intubation

• Avoid hypertension and tachycardia which is commonly seen in
patients with normal ventricular function, a history of arterial
hypertension, and left ventricular hypertrophy.
• Hypotension and excessive myocardial depression, in a patient with
depressed entricular function or with severe flow-dependent
stenoses (e.g., left main or proximal LAD disease, coexisting severe
valvular stenosis).
• 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 BP >20% of baseline needs
use of inotropes
• Fast-track anesthetic protocols aiming for early extubation favored
in most patients (restrict a high-dose opioid technique for patients
at very high risk who do not tolerate inhalation anesthetics

•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.

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

MIXED INTRAVENOUS/INHALATION ANESTHESIA-
Propofol 0.5-1.5 mg/kg or thiopentone 2-3 mg/kg or etomidate.
(0.2 to 0.3 mg/kg and midazolam 0.05 to 0.1 mg/kg plus Fentanyl 5
mcg /kg
Muscle relaxation with vecronium 0 .1 mg /kg and controlled
ventilation ensures adequate oxygenation and prevents
hypercapnia
• Opioids are given intermittently and total dose of fentanyl and
remifentanil should not exceed 15 and 5 mcg/kg respectively.
• Selected agent should be given in small incremental doses and titrated first
against loss of consciousness then to an acceptable fall in BP.
• Maintenance of anesthesia. Anesthesia is maintained with a combination of
volatile agents, {Isoflurane or sevoflorane ) low-dose narcotics, and IV
hypnotic agents

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
• The ultra-short-acting opioid remifentanil is associated
with good hemodynamic stability, adequate attenuation
of the neurohumoral stress response, and early
awakening. However, due to its short half-life, it requires
supplemental analgesia in the postoperative period.

Anesthetic effects on myocardial oxygen supply and
demandA. Intravenous nonopioid agents
1. Thiopental
– Decrease SVR and cardiac contractility
– Increase heart rate
So, the net effect on myocardial O2 balance is not easily predicted.
2. Ketamine
• increase sympathetic tone leading to increases in SVR, filling
pressures, contractility, and heart rate
• Myocardial O2 demand is strongly increased, whereas O2 supply
may be only slightly augmented, thus producing ischemia. Ketamine
is not recommended for routine use in patients with ischemic heart
disease. It is, however, sometimes used in the setting of tamponade
physiology because of its ability to preserve heart rate, contractility,
and SVR.

3. Etomidate.
• Induction doses (0.2 to 0.3 mg/kg)
• do not alter heart rate or cardiac output,
• although mild peripheral vasodilation may lower BP slightly.
• As such, it is an ideal drug for rapid induction of anesthesia in
patients with ischemic heart disease.
• offers little protection from the increases in heart rate and
blood pressure that accompany intubation. It usually is
necessary to supplement etomidate with other agents (e.g.,
opioids, BZD, volatile agents, β-blockers, NTG) in order to
control the hemodynamic profile and prevent myocardial O2
supply/demand inequality.
• An induction dose will block adrenal steroidogenesis for 6 to 8
hours.

Etomidate : limitations
• High concentrations of etomidate inhibit influx of
extracellular calcium but had no effect on availability of
intracellular calcium required for excitation-contraction
coupling.
• It is known to inhibit adrenal mitochondrial
hydroxylase activity, resulting in reduced
steroidogenesis even after a single bolus dose,
• Postoperative nausea and vomiting are other potential
adverse effects seen with etomidate administration.
• Myoclonic jerking can be observed in the absence of
muscle relaxation

PROPOFOL
• propofol exerts a direct negative inotropic effect in nonfailing and
failing human myocardium, but only at concentrations larger than
typical clinical concentrations.
• Negative inotropic effects are reversible with β-adrenergic
stimulation, suggesting that propofol does not alter the contractile
reserve but may shift the dose responsiveness to adrenergic
stimulation.
• propofol,enhance antioxidant activity in the heart and thus may
prevent lipid peroxidation after ischemia/reperfusion, offering a
potential protective effect on the heart
• The negative inotropic effect of propofol is at least partially
mediated by decreased Ca++ uptake into the SR; however, the net
effect of propofol on contractility is insignificant at clinical
concentrations because of a simultaneous increase in the sensitivity
of the myofilaments to activator Ca+

VOLATILE VS IV ANAESTHETICS
• Propofol has antioxidant properties of potential value in subjects
with reperfusion injury.
• The salutary properties of volatile anesthetics during myocardial
ischemia are well known. Their negative inotropic and chronotropic
effects are considered to be beneficial, particularly in the setting of
elevated adrenergic tone that is common with surgical stimulation.
• Volatile agents have some degree of coronary arterial vasodilation
(with isoflurane considered the most potent), the role of a “steal
phenomena” in the genesis of ischemia is considered to be trivial
• In comparison to propofol/opioid infusions, volatile agents seem to
reduce troponin release, preserve myocardial function, and improve
resource utilization (ie, ICU or hospital lengths of stay) and 1-year
outcome.

• Patients who had sevoflurane preconditioning during the
first 10 minutes of CPB had lower levels of biochemical
markers of myocardial and renal impairment.
• Brain natriuretic peptide level as an indicator of myocardial
dysfunction is significantly decreased in the sevoflurane .
• Conzen et al studied randomized patients undergoing
OPCAB surgery with a propofol infusion versus a continuous
inhalation-based anesthetic technique with sevoflurane.
Patients in the sevoflurane group had significantly lower
troponin I levels, as well as better LV function

The PROTECT II (PROpofol
cardioproTECTion for type II diabetics)
• Diabetic myocardium is resistant to physical or pharmacologic
preconditioning stimulus.
• Experimental studies have detected corrupted protective signal
transduction pathways and enhanced mitochondrial permeability
transition, which could explain the increased susceptibility to injury in
ischemia-reperfused diabetic myocardium
• Effective antioxidant intervention during ischemia–reperfusion appears
important for preserving myocardial function; thus, alleviating oxidant-
mediated post-ischemic injury by increasing antioxidant defenses
(cardioprotection) is an alternative to preconditioning

Benzodiazepines.
• Midazolam (0.2 mg/kg) maintain hemodynamic stability,
• BP may decrease more with midazolam owing to more
potent peripheral vasodilation.
• Negative inotropic effect
• Blood pressure and filling pressures decrease with
induction, whereas heart rate remains essentially
unchanged. combination with a narcotic to induce
anesthesia for CABG
• Contractility is depressed by midazolam, although
afterload was reduced simultaneously, resulting in no net
change in cardiac index.

α2-Agonists (e.g., dexmedetomidine
and clonidine
• These agent reduces stress-mediated neurohumoral response and
therefore are associated with decreases in heart rate and blood pressure.
• These agents typically are used during maintenance of anesthesia or
postoperatively.
• Pre op use of oral clonidine may be associated with a reduced incidence
of perioperative myocardial ischemia in patients undergoing CABG surgery.
• Dexmedetomidine is associated with a greater relative α2 selectivity than
clonidine.
• Dexmedetomidine is approved for use as a postoperative sedative and is
administered as an infusion (0.2 to 0.7 μg/kg/hour
• Use of α 2-adrenergic agonists is associated with a reduced opioid
requirement. Additionally, α 2-adrenergic agonists do not result in
respiratory depression

Off pump vs on pump cabg
• The course of patients in the early postoperative period is
usually improved with OPCAB surgery compared with on
pump surgery. The duration of ventilatory support, ICU
length of stay, and hospital length of stay are significantly
diminished myocardial enzymes and troponin I release are
reduced after off-pump surgery
• Avoiding CPB eliminates aortic cannulation and cross-
clamping, and is expected to reduce systemic inflammatory
response, coagulation disorders, multiple organ
dysfunction and reduce the incidence of embolic events
from the atheromatous Aorta

Contraindications of beating heart
cabg
Presence of intracavitary thrombi
Malignant ventricular arrhythmias
Deep intramyocardial vessels
Procedures combined with valve replacement or
ventricular aneurysmectomy.
 Very small arteries ( <1mm)
Calcified arteries.
Poor conduits.
Hemodynamic Instability/Ischemia.

HEPARIN in BEATING CABG
• At the time of harvesting the left internal mammary artery, half
dose of heparin (100 u/kg) can be given
• Prior to commencement of grafting either proximal or distal, ‘full
heparinization’ is achieved by administering 200-300 U.kg-1 of
heparin intravenously.
- ACT performed 3 minutes after administration.
- The goal is to keep the ACT between 250 - 300 seconds.
- ACT repeated hourly and repeat bolus of 5000 units Heparin is
essential if ACT <250 seconds.
- Heparin is reversed with protamine sulfate (1 mg/1mg of heparin. )
- Acceptable ACT – upto 140 seconds after protamine administration.
- A high ACT will require additional protamine in a dose of 25 to 50
mg.

Temperature homeostasis
• heat preservation is critically important when early
extubation is anticipated because hypothermia will
• delay respiratory weaning and
• may be associated with postoperative arrhythmias and
• coagulopathy.
• Additionally, hypothermia may precipitate shivering, which
significantly raises myocardial oxygen consumption.
• IV fluid warmers may be of great clinical utility, especially
when there are large transfusion requirements.
• Forced hot-air convective warming is the best means of
preserving body temperature during off-bypass
revascularization.

Problem in off pump cabg
• Severe haemodynamic alterations
• Transient deterioration of cardiac pump
function
• Acute intraoperative myocardial ischaemia.
• Conversion to CPB in case of sustained
ventricular FIbrillation or cardiovascular
collapse

sequence of anastomosis of coronary
arteries
• The more stenotic vessel is anastomosed first because of the presence of good
collateral circulation because less stenosed vessel will maintain supply to the area
of more stenosed vessel initially during anastomosis
• The coronary arteries should be grafted in order of increasing cardiac
displacement, i.e. anterior wall vessels followed by inferior wall vessels and finally
lateral wall vessels. The guiding principle that more cardiac displacement is
tolerated with increasingly complete revascularization.
• The LIMA to LAD graft is usually first, the inferior wall grafts (PDA, RCA)
are usually next and the lateral wall grafts (OM) are usually last.
• The proximal anastomoses can be performed before or after the distal
anastomoses. The advantage of completing the proximal anastomosis first is
immediate perfusion through the graft after the completion of the distal
anastomosis.

Positioning
• Exposure of the vessels during distal grafting requires heart tilting manoeuvres
using swabs, pericardial stitches and suction devices by the surgeon which
typically cause hemodynamic derangement.
• Enucleation consists of enucleating the heart by aspiration by a suction device or
by pulling the pericardium with single/multiple stitches placed in the oblique
sinus.
•
• Displacement: Positioning the heart for exposure of the LAD and its branches
(diagonals) requires just a slight traction on pericardial stitches with or without
placement of a pericardial swab, and this is not expected to lead to significant
haemodynamic derangement. However placement of stabilizer device on the
actively contracting anterior wall does decrease the SV and cardiac output (CO).
The haemodynamic compromise is more with anterior and lateral wall
compression than with posterior and inferior wall compression

Verticalization:
• Verticalization of the heart causes haemodynamic
derangement by two mechanisms: firstly the
atria get below the ventricles and thus require
higher filling pressure tofill the corresponding
ventricle.
• Diastolic dysfunction has been reported during
verticalization which again requires higher filling
pressures. Secondly, verticalization distorts the
mitral and the tricuspid annuli leading to an
increase in severity of valvular regurgitation
especially in patients with pre-existing lesions

Management of hemodynamic
compromise
• Trendelenberg position: preload augmentation
• Judicious fluid boluses also augment the preload.
• Vasopresors(norepinephrine, phenylephrine, vasopressin)
increase mean arterial pressure by vasoconstriction, with a small
increase (10 to 15%) in cardiac output and stroke volume. These
drugs are used in OPCAB as low dose boluses or infusion
• Inotropes(epinephrine) are usually not required unless the LVEF is
poor OR in hemodynamic compromise not amenable to fluid
boluses and vasopressors especially during grafting Left circumflex
and its obtuse marginal branches

• For Lateral LV wall presentation (Obtuse Marginals,
Posterolateral branches of right coronary artery) the
OR table is placed in steep Trendelenburg position and
the table is raised and rotated toward the right .
• This will allow gravity to displace heart to the right and
apex anteriorly. Suspensory sutures on the right side of
the pericardium are removed. The right pleural space is
opened and the right pericardial incision is extended
towards the inferior vena cava. These maneuvers allow
the heart to move toward the right pleural space.

• Communicate with the surgeon assertively to lift the stabilizer after
applying suction based stabilizers rather than compressing it.
• Opening the right pleura helps in getting some volume in right ventricle
during Verticalization and grafting on RCA and PDA
• Anastomosing the proximal RCA may lead to arrhythmias and complete
heart block and therefore a pacemaker should be available in the
operating room
• A CO2 blower is crucial for beating heart surgery but has to be used VERY
sparingly at a flow rate not > 5 L /min, to prevent damage to the coronary
endothelium. Avoid directing the gas jet directly into the vessel lumen to
prevent gas embolization

Proximal grafting
• It requires controlled hypotension using
reverse trendelenberg position, NTG, and
judicious timely doses of opioids and
benzodiazepines.
• In patients with carotid artery disease MAP
shouldn’t fall below 65 mm hg so as to
maintain the cerebral perfusion

Incidence of perioperative ischemia
• Efforts to prevent myocardial ischemia usually target control of the
hemodynamic determinants of myocardial oxygen demand such as
HR and blood pressure (BP).
• Approximately 40% of cardiac surgical patients will experience ST-
segment evidence of ischemia sometime in the 48 hours prior to
elective cardiac surgery.
• Approximately Half of intraoperative ischemic events are unrelated
to changes in HR and BP. This suggests that decreases in myocardial
oxygen supply may be important in the genesis of intraoperative
ischemia.
• Less than one-fourth of these episodes are preceded by a HR
increase of 20% or more. In addition, most of these episodes are
clinically silent

Mechanism of intra op MI
• The endocardial region of the heart faces higher wall stresses and consumes
approximately 20% more oxygen per unit mass than the epicardium.
• Myocardial flow and metabolism are coupled over a wide range of coronary
perfusion pressures, resulting in relatively constant values of 70% and 30% for
oxygen extraction ratio and coronary sinus oxygen saturation, respectively.
• The difference between basal coronary blood flow and maximal attainable blood
flow, for any given level of myocardial metabolism, is termed the "coronary
vascular reserve“ . This reserve is accomplished by coronary dilation and is
available to satisfy the increased myocardial oxygen demands of stress and
exercise.
• In patients with a stenotic coronary artery, the coronary vasculature distal to the
lesion may already be maximally dilated at rest. Coronary vascular reserve is
therefore exhausted, and flow distal to the obstruction becomes pressure-
dependent.
• In this situation, increasing myocardial oxygen demand precipitates ischemia,
starting in the vulnerable subendocardium. On the other hand, a fall in myocardial
metabolic requirements restores coronary vascular reserve, and flow once again
becomes autoregulated

Peri op mi
• The presence of new persistent Q waves of at least
0.03-second duration broadening of preexisting Q
waves, or new QS deflections on the postoperative ECG
have been considered evidence of perioperative AMI.
• Signs of non–Q-wave MI, such as ST-T wave changes,
are even less reliable signs of AMI after cardiac surgery
in the absence of biochemical evidence.
• ST-segment changes are even less specific for
perioperative MI because they can be caused by
changes in body position, hypothermia, transient
conduction abnormalities and electrolyte imbalances

Diagnosing myocardial ischemia
The gold standard for diagnosis of myocardial
ischemia is the presence of ECG changes.
Unfortunately, ECG changes occur relatively late
in the temporal sequence of myocardial ischemia
after deterioration of ventricular diastolic and
systolic function.
Simultaneous monitoring of leads II and V5 is
commonly used because of the high sensitivity of
this combination in detecting myocardial
ischemia.

USE of PA catheter in CABG
 Changes in PCWP and the PCWP waveform have poor sensitivity and
specificity in detecting episodes of myocardial ischemia.because
 PCWP does not necessarily reflect LVEDP
 When only a small region of LV wall develops diminished compliance with
an ischemic episode,overall LV function may be only minimally affected.
This will reduce the observed changes in LVEDP as reflected by the PCWP.
 The quantitative change in PCWP and the qualitative change in the PCWP
waveform necessary to define an ischemic event have not been
systematically defined.
 Acute elevations in afterload in the absence of ischemia can produce
elevations in PCWP. This may lead to a false positive interpretation of the
PCWP tracing.
 Appearance of a new V wave on the pulmonary capillary occlusion
pressure waveform indicates functional mitral regurgitation, which is due
to “new” ischemic papillary muscle dysfunction It may occur before or
even in the absence of ECG changes.

TEE in off pump CABG
• TEE is highly sensitive but not specific for myocardial ischemia.
• LV diastolic dysfunction detected with TEE is one of the earliest changes
identified after coronary artery occlusion, and it often precedes the
development of abnormal systolic function (RWMAs ). They occur within
seconds of inadequate blood flow or oxygen supply.
• The transgastric short-axis midpapillary muscle view, commonly used
because of its inclusion of myocardium supplied by the three major
coronary arteries, may entirely miss RWMAs occurring in the basal or
apical portions of the heart
• Myocardial ischemia or repositioning the heart during OPCAB can be the
cause of a sudden onset of mitral regurgitation or worsening of preexisting
mitral regurgitation, both of which can be detected with TEE monitoring

TEE VS ECG for detection of MI
 Ischemic episodes may be missed because qualitative wall motion analysis
is difficult for patients with preexisting wall motion abnormalities.
 Some RWMA (particularly in areas tethered to scar) may not be ischemic
in origin. Changes in afterload may unmask areas of previous scarring.
 Ventricular pacing or a bundle-branch block may make detection of
RWMA more difficult because of asynchronous contraction.
 Stunned myocardium may exhibit continued RWMA despite adequate
perfusion.
 The ECG may detect ischemia with small areas of subendocardial ischemia
undetectable by TEE
“Numerous studies have shown intraoperative TEE qualitative analysis of
regional wall excursion and thickening to be a more sensitive detector of
myocardial ischemia than ECG changes and to be capable of detecting
ischemia before ECG changes”

MYOCARDIAL PROTECTION DURING
OFF PUMP CABG
• Maintaining myocardial oxygendemand and
supply balance
• Use of an intracoronary shunt
• Ischaemic/pharmacological preconditioning

MYOCARDIAL PROTECTION DURING
OFF PUMP CABG
• Myocardial oxygen demand is reduced with
decrease in heart rate (HR ~ 50-60/min in
patients with preserved LV function and
around 80-90/min in patients with severe LV
dysfunction) and contractility.
• This can be achieved by using intraoperative
beta-blockers, TEA or calcium channel blockers
• Reduction in preload :Using NTG

• Oxygen supply is maintained by maintaining
coronary perfusion pressure (CPP). A mean BP
>65-70 mmHg or CPP >50 mmHg by use of a
vasoconstrictor such as phenylephrine or nor-
epinephrine, and volume loading, is usually
sufficient to maintain oxygen supply and thus
avoid myocardial ischemia.
• Use of an intracoronary shunt: They maintain
coronary blood flow in the period during
anastomosis. Also, it provides a bloodless field for
the surgeon

• Mixed venous oxygen saturation should be of at
least 60% or more is suggestive of adequate
tissue perfusion
• If the wedge pressure is low, administration of
boluses of intravenous fluid andTrendelenburg
position
• Avoid bradycardia it may decrease cardiac output
electrically pacing the patient.Bradycardia may
commonly be seen during grafting of right
coronary artery

Acute Treatments for Suspected
Intraoperative
Myocardial Ischemia

Need for IABP in OPCAB
• Inadequate hemodynamics:
• SYSTOLIC BLOOD PRESSURE LESS THAN 80 mm. Hg.
• Cardiac index Less than 2.0 L/min/sq.
M
• LA PREESSURE MORE THAN 20 mm.Hg.
• Vascular resistance More than 2500
dynes/sec/cm-5
• Large doses of multiple inotropic drugs
• Continued refractory ventricular arrhythmias

WHEN TO CONVERT TO ON-PUMP
CABG
• Conversion to on-pump CABG should be done as per
the suggestions by Chassot et al
• Persistence of the following for >15 min despite
aggressive therapy:
• Cardiac index <1.5 litre min-1 m-2
• SvO2<60%
• MAP <50 mm Hg
• ST-segment elevation >2 mV
• Large new RWMA or deterioration of LV
function assessed by TOE
• Sustained malignant arrhythmias

•Skin incision can cause sympathetic stimulation, so adequate
depth of anesthesia is necessary
•Sternal incision and splitting accompanies high level of
sympathetic stimulation
• Sternal splitting can cause awareness and recall, so amnesic
agents like benzodiazepines or propofol is to be used
• Tachycardia and raised BP can be treated by nitroglycerine
boluses or by B blocker
• High doses of fentanyl can reduce response to pain
• Lungs are to be deflated during sternal splitting to avoid damage
• Sternal spread can cause kinking or malpositioning of PA cath.

HEPARIN IN CPB
• Heparin is administered in a dose of 300-400u/kg for uncoated
circuits with monitoring of its anticoagulant effect by the activated
clotting time (ACT).
• A blood sample is drawn 3–5 minutes after heparin administration
and should achieve an ACT >480 seconds
• For heparin-coated circuits, a level of >350 seconds is generally
acceptable
• 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.
• Repeat ACT is measured after 5 mins and if it is less, 100u/kg is to
be administered again

CANNULATION-
•Aortic cannula is inserted first to allow rapid volume
infusion in cases of hemorrhage during venous
cannulation
•Dissection of post ganglionic sympathetic fibres from
aorta to cannulate it can cause intense stimulation
•SBP is lowered to avoid risk of dissection and PEEP
applied to avoid air entrainment by increasing
intracardiac pressure

initiation of CPB
Systemic arterial hypotension (MAP = 30 to
40 mm Hg) is relatively common
MAP increases with initiation of
hypothermia-induced vasoconstriction,
 The hemodilution also results in the loss of
NO binding by hemoglobin; the excess free
NO can lead to vasodilation.
 Treatment with α-agonists usually is not
necessary if the hypotension is brief (< 60
seconds

Conti.
• Until the aortic cross-clamp is applied, the coronary arteries are perfused with
hemodiluted, nonpulsatile blood.
• If the aortic cross-clamp is applied within 1–2 minutes after the start of CPB, a
MAP greater than 30mmHg with a pump flow of 2.0–2.4 L/min/m2 is acceptable
for patients without cerebrovascular disease.
• For patients with known cerebrovascular disease, a MAP in excess of 50mmHg may
be required .
• A MAP of atleast 50 mmHg should be maintained for perfusion of the beating,
empty heart.
 subendocardial ischemia occurred in the distribution of critical coronary stenosis
when MAP was less than 80 mm Hg in the normothermic empty beating heart.
 If placement of the aortic cross-clamp is delayed, MAP should be maintained in
the range of 60 to 80 mm Hg to support myocardial perfusion, especially in the
presence of severe coronary stenosis or ventricular hypertrophy.

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
• 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

• 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
• 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.

MYOCARDIAL OXYGEN DEMAND
• Compared with the oxygen
uptake of a normally
beating heart, eliminating
cardiac work by venting the
beating heart during bypass
reduces oxygen demand by
30% to 60%.
• Arresting the heart reduces
demands by another 50%,
producing a total reduction
of approximately 90%.
• Hypothermia extends the
reductions in oxygen
demand.

MYOCARDIAL PROTECTION-
• low-risk CABG appear to do equally well with crystalloid or blood cardioplegic protection
• More critically ill patients, including those with “energy-depleted” hearts (e.g., cardiogenic shock,
AMI before CPB), have improved outcomes using blood cardioplegia.
• Patients at high risk also appear to have better recovery using a combination of antegrade and
retrograde blood cardioplegia delivery, when compared with antegrade administration alone
• Hypothermia results in a leftward shift in the oxygen hemoglobin dissociation curve, inhibiting the
release of oxygen into tissues. The myocardium is relatively ischemic during this initial induction
phase of cardioplegia
• Infusion of a single, warm (37° C) reperfusion dose of cardioplegia (so-called hot shot) containing
metabolic substrates (i.e., glucose,glutamate, and aspartate) just before aortic cross-clamp removal
is preferred) this normothermia maximally enhances myocardial aerobic metabolism and recovery
after an ischemic period

Hypothermia
• . Hypothermia reduces coronary vasodilator
reserve capacity and potentially limits myocardial
oxygen delivery.
• Therefore, despite the fact that hypothermia
reduces myocardial oxygen consumption ,
subendocardial ischemia develops in the beating,
empty heart when MAP is lower than 50mmHg at
28◦C due to attenuated coronary vasodilator
reserve

HEMATOCRIT
• In the presence of coronary stenoses or
concentric hypertrophy, Hct values in the 20–
30% range may be needed to prevent
ischemia during normothermic CPB.

Neuroprotection IN ON PUMP CABG
 Early and aggressive control of hemodynamic instability
 Perioperative euglycemia between 100 and 180 mg/dL
 Routine epiaortic scanning before manipulation of ascending Aorta
 Avoidance of manipulation of ascending aorta in severe atheromatosis
 Maintenance of adequate cerebral perfusion pressure
(neuromonitoring/cerebral oximetry)
 Monitoring of cerebral venous pressure via a proximal central venous
pressure catheter or the introducer port of a pulmonary artery catheter
 Alpha-stat pH management during moderate hypothermic
cardiopulmonary bypass (CPB)
 Avoidance of arterial inflow temperature greater than 37°C
 Use of CPB circuitry incorporating membrane oxygenator and 40-μm
arterial line filter
 Use of surface-modified and reduced-area CPB circuitry
 Use of cerebral oximetry

WEANING FROM BYPASS-
• Oxygenation and ventilation must begin before discontinuation of
bypass. The lungs should be manually reinflated and visually
inspected to document bilateral reinflation and elimination of
atelectasis.
• volatile anesthetic agents induce vasodilation and
facilitate rewarming and may be continued if rewarming is
slow but should be discontinued approximately 10
minutes before termination of bypass.
• Patients with chronic lung disease may sometimes require positive
end-expiratory pressure (PEEP), pressure controlled ventilation, or
bronchodilators.

Rewarming
• When systemic hypothermia is used, body temperature is restored to
normothermia by gradually increasing perfusate temperature with the
heat exchanger.
• Time required for rewarming (i.e., heat transfer) varies with arterial
perfusate temperature, patient temperature, and systemic flow.
• Excessive perfusate heating is not advisable for at least three reasons:
 Possible denaturation of plasma proteins,
 Possible cerebral hyperthermia,
 Dissolved gas can come out of solution and coalesce into bubbles if
the temperature gradient is too great.
• Because small increases (0.5° C) in cerebral temperature exacerbate
ischemic injury in the brain, it is critical to perfuse the patient with blood
temperatures at or below 37° C.

DEAIRING
• Intracardiac air may be present in 10% to 30% of closed cardiac cases as
well (e.g., CABG)
• During aortic cross-clamping, air may enter the aorta and left ventricle
retrograde through native coronary arteries opened in the course of
CABG surgery, particularly when suction is applied to vent the left side
of the heart or aortic root.
• Studies reported that air ejected from the left ventricle also can travel
to the coronary arteries, resulting in sudden and sometimes extreme
myocardial ischemia and failure after separation from CPB.
• mobilization of air by positive chamber filling, stretching of the atrial
wall, and repeated chamber ballottement; removal of mobilized air by
continuous ascending aortic venting; and proof of elimination by TEE.
• Manuals ventilation of lungs to promote clearance of air from the
pulmonary veins
• Before removal of the aortic cross-clamp, the patient is placed head
down so that bubbles will float away from the dependent carotid
arteries

SEPARATION FROM CPB
• Separation is accomplished by gradual occlusion of the venous
cannula,. Arterial inflow from the pump is then gradually reduced.
• Hemodynamics and ventricular function are assessed by visual
inspection of the heart and by TEE.
• Venous cannula clamping can be increased, arterial inflow
decreased, and hemodynamics reassessed.
• This process is repeated until separation from CPB is complete.
• Hemodynamic management focuses on regulating four primary
determinants of cardiac function:
 Rate and rhythm,
 Arterial pressure,
 Preload or ventricular volume (ventricular filling pressure),
 Contractility (stroke volume).

Heart Rate and Rhythm
• After the aortic cross clamp is released and coronary reperfusion
commences, cardiac electrical activity returns. This may be in the
form of ventricular fibrillation, which is likely a reperfusion
arrhythmia due to calcium overload of ischemic myocardium.
• Lidocaine is often given before the cross clamp is released or in the
cardioplegia and is effective at preventing ventricular fibrillation.
• Ventricular fibrillation during CPB may result in ventricular
distension and irreversible myocardial damage. The heart should be
electrically defibrillated as soon as possible.
• Electrolytes should be treated if abnormal. Recurrent ventricular
fibrillation should be treated with amiodarone and repeat
defibrillation.
• β-Adrenergic blockers are also remarkably effective for facilitating
defibrillation in resistant cases

CONTI.
• Return of cardiac electrical activity is in the form of a junctional bradycardia or
sinus bradycardia with atrioventricular conduction block.
• Sinus bradycardia is easily treated with atrial pacing when normal A-V conduction
is present.
• Sequential atrioventricular pacing is indicated for atrioventricular conduction block
or significant first-degree heart block. This preserves the atrial contribution to
ventricular filling, which is a significant advantage in the presence of a
noncompliant hypertrophied ventricle (hypertension, or enlarged ventricle)
• If second- or third-degree heart block is present, pacing in the DVI or DDD mode is
appropriate
• Ventricular pacing (VVI ) should be used only when atrial or atrioventricular pacing
is not feasible (e.g., atrial fibrillation or flutter with a very slow ventricular
response) or in a backup demand mode when the patient is in sinus rhythm.
• In patients with low ejection fractions and preoperative conduction system
abnormalities, temporary biventricular pacing may improve postoperative
hemodynamics and prevent left ventricular dyssychrony

CONTI.
• . Transient ST-segment elevation is common during emergence from CPB but
usually resolves shortly thereafter (. Persistent ST-segment elevation suggests
myocardial ischemia, which may require surgical treatment (i.e., revision of a graft
or placement of an additional graft).
• Intracoronary air embolism usually involves the right coronary artery and resolves
after a period of increased perfusion pressure.
• Coronary artery or internal mammary artery spasm responds to treatment with
intravenous nitroglycerin or to elevation of the perfusion pressure.
• Causes of tachycardia, including hypoxemia, hypercapnia, anemia, inadequate
anesthesia, and effects of vasoactive drugs.
• Once these causes are eliminated and if myocardial function is determined to be
adequate, then give appropriate doses of β-adrenergic receptor or calcium
channel blocking drugs.
• Refractory supraventricular tachycardia, atrial fibrillation, or flutter is best treated
intraoperatively with electrical cardioversion

HEMODYNAMIC MANAGEMENT AFTER
CPB SEPARATION
• After CPB, the clinical management goal is to have a systolic arterial
pressure of 90 to 100 mm Hg, a normal cardiac index (>2.0 L/min/m2) and
a normal or low ventricular filling pressures of 10 to 15 mm Hg
• Additional volume can be infused directly from the pump through the
aortic cannula until the cannula is removed usually after protamine
reversal.
• The need for additional volume infusion can be judged by evaluating the
arterial pressure and filling pressure responses.
• Adequate filling of the heart is assessed by direct inspection of the RV,
hemodynamic measurement, and TEE.
• The pulmonary artery occlusion or pulmonary diastolic pressure is
frequently used to guide volume infusion at the conclusion of CPB. A
pulmonary artery diastolic pressure of 10 to 15 mm Hg is almost always
adequate in patients after isolated coronary artery bypass surgery.

Conti.
• Pulmonary artery wedge or diastolic pressure correlates poorly with
left ventricular end-diastolic volume after coronary artery bypass
surgery secondary to acute decreases in left ventricular compliance
.
• TEE clearly provides the best available clinical intraoperative
estimate of ventricular volumes
• In case of mild hypotension with measured filling pressures that
are slightly high with a TEE which reveals an underfilled ventricle
shortly after terminating CPB is common.
• These patients can be temporarily supported with vasoconstrictor
to raise the coronary perfusion pressure and nitroglycerin to
decrease the filling pressures. Additional volume may then be
necessary to maintain cardiac index

• Pure α receptor agonists are useful in the treatment of
hypotension in patients with good ventricular function.
The beneficial increase in coronary perfusion pressure
usually outweighs the negative effects of decreased
cardiac output and increased filling pressures in the
patient with coronary artery disease or ventricular
hypertrophy.
• In general, the use of pure α agonists to increase
arterial blood pressure in patients with poor
ventricular function or pulmonary hypertension is best
avoided because increased afterload without a
compensatory increase in contractility results in a
decreased stroke volume

CONTI.
• Systemic vascular resistance progressively decreases
with rewarming and continues to decrease during the
period after CPB.
• Pronounced vasodilation at the termination of CPB can
be related to the duration of rewarming, comorbid
diseases which can cause peripheral neuropathy such
as diabetes, chronic drug therapy such as angiotensin-
converting enzyme (ACE) inhibitors.
• This condition is manifested by hypotension with low
filling pressures, a normal to high cardiac index and
good ventricular function on TEE.

CONTI.
• If refractory arterial vasodilation is present or if
vasodilation is combined with mildly reduced left
ventricular function, norepinephrine may be
appropriate to counteract the vasodilation while
providing some degree of inotropic support to
meet the increased afterload.
• In patients receiving ACE inhibitors who are
refractory to phenylephrine and norepinephrine,
vasopressin should be considered

Myocardial dysfunction after cpb
• Inadequate myocardial protection during the procedure will
adversely affect LV systolic function.
• This is particularly likely if the patient has suffered a
preoperative ischemic event or has poor preoperative
ventricular function
• Optimization of preload and HR are necessary first steps in
obtaining hemodynamic stability
• Ionotropic agent can given with vasopressor like norad
• Dobutamine reduce myocardial oxygen consumption in the
failing heart. Although dobutamine increases contractility,
it reduces LV radius and end-diastolic pressure while
increasing arterial pressure and maintaining HR. DOSE

• Levosimendan is a myofilament calcium sensitizer
that increases myocardial contractility by
stabilizing the calcium bound conformation of
troponin C.
• The drug causes vasodilation and an increase in
HR. Finally, levosimendan stimulates ATP-
sensitive potassium channels, which improves
coronary blood flow, reduces preload and
afterload, and may have relevant anti-ischemic
actions

Blood Transfusion
• For patients on CPB with risk of critical end-
organ ischemia/injury, hemoglobin levels
above 7g/dl is recommended
• . In the setting of hemoglobin values
exceeding 6g/dl while on CPB, transfusion of
red cells were based on the patient’s risk for
complications of inadequate oxygenation.

• Fresh frozen plasma (FFP) were given for correction of
microvascular bleeding in the pre-sence of elevated (> 1.5
times normal) PT or PTT, for correction of Microvascular
bleeding secondary to coagulation factor deficiency in
patients transfused with more than one blood volume and
when PT and PTT cannot be obtained in a timely fashion.
• Cryoprecipi- tate transfusions were recommended in
bleeding patients with hypofibrinogenemia
• Platelet transfusion was recommended after
cardiopulmonary bypass in patients with normal coagula-
tion values and platelet counts below 100 x 109/l when
major unexplained bleeding occurs

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
• 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

COMPELTION OF CPB
• At the time of arterial decannulation, the systolic pressure should be between 85
and 100 mm Hg to minimize the risk for dissection or tearing of the aorta.
• The head of the bed may be raised, or small boluses of a short-acting vasodilator
(e.g., nitroglycerin, nitroprusside) may be given to lower the systemic blood
pressure as necessary.
• Tight control of the arterial blood pressure may be needed for a few minutes until
the cannulation site is secure.
• When patient becomes hemodynamically stable, protamine is administered to
reverse anticoagulation
• When the arterial cannula has been removed, the heparin effects are reversed with
protamine,( 1-1.3mg of protamine per 100 units of heparin is administered slowly
over 10-15 mins) ACT should be brought to baseline values

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