|
Sinus tachycardia : when HR > 100 bpm. The rhythm is regular. The
P:QRS ratio is 1:1, P, QRS, ST and T are normal (or non-specific ST-T
changes)
Etiology : hypoxia, hypercarbia,
pain (light anesthesia), hypovolemia, fever, sepsis, increased metabolism
Treatment : correct underlying
problems first, then medications e.g. beta-blocker, ca-blocker, cholinergic
drugs, etc.
Ref
1. Thomas SJ, Kramer JL. Manual of Cardiac
Anesthesia 2nd ed. Churchill Livingstone 1993.
2. Thys DM, Narang J. Electrocardiographic monitoring in Estafanous
FG, Brash PG, Reves JG : Cardiac Anesthesia ; Principles and
Clinical Practice 2nd ed. Lippincott William & Wilkins 2001 |
SvO2
or Mixed Venous Oxygen saturation is the oxygen saturation of the
venous blood, should be sampled at the last place where the venous
blood is all mixed and the standard sampling place is the blood drawn
from the PA catheter (right before enter the lung for gas exchanges).
Some PA catheter has the fiberoptic channel for continuous SvO2
monitoring. The same fiberoptic device placed in the internal jubular
bulb will read the jugular venous bulb oxygen saturation.
SvO2 varied with CO, Hb, total body oxygen consumption
and SpO2 as the formula :
 |
As the formula
imply, the SvO2 will change as
-Decrease SvO2
: increased O2 consumption e.g. fever, shivering,
exercise, MH, thyroid storm
: decrease O2 delivery e.g. hypoxia, CO,
anemia, abnormal Hb
-Increase SvO2
e.g. Lt. to Rt. shunt, high CO, impair tissue uptake (e.g. CN- toxicity),
decrease O2 consumption e.g. hypothermia, Sepsis,
Sampling error (e.g. wedged PA cath)
CO (Cardiac Output) is a product of stroke volume and heart rate (normal
is 4-6.5 L/min). CO can be measured clinically by many methods. The
most common is using PA catheter and thermodilution technique. The
special PA catheter which allows nearly continuous (every 30 second)
CO monitoring is available. Another method which will be discussed
is Fick method. The commercial available Fick method device for CO
monitoring, using CO2 is NICO which is already
discussed in the forum update.
Fick Equation relationship
Adolph Fick, the German physiologist described the O2
as an indicator dilution for calculation of CO in 1870. The formula
is
 |
To measure CO by
Fick method need the O2 consumption measurement
which is done by collecting patient's exhaled air, respiratory gas
analysis and indirect calorimetry. Some clinicians may use a constant
basal value for O2 consumption (approx 200-250
mL/min).
Ref
Miller RD : Anesthesia 5th Ed. Churchill
Livingstone 2000. |
LV filling occurs in diastole which can be divided into 4 phases
1.)
isovolumic relaxation
2.) rapid
ventricular filling
3.) Diastasis
or slow filling
4.) atrial
systole
Many factors will
affect LV filling, to start the thinking process from phase 1 the
isovolemic relaxation which occurs after the aortic valve closes about
50-60 msec. The LV relaxation will create the pressure relatively
negative, once the pressure in LV chamber below the LA, the mitral
valve will open and allow the 2nd phase. The factor that will afftect
this phase includes the LV compliance (decrease compliance or increase
LV stiffness will reduce LV relaxation). Increase chamber stiffness
may come from the myocardial tissue e.g. concentric hypertrophy or
increase muscle stiffness that found in restrictive cardiomypopathies
e.g. amyloidosis, hemochromatosis.
Mitral valve function is a major contribution to the 2nd phase, mitral
stenosis or impair mitral valve function will impedes the rapid ventricular
filling process.
Atrial systole or atrial kick contributes to LV filling about 20-30%.
The loss of atrial contraction e.g. atrial fibrillation or atrial
flutter will result in loss of atrial systole.
Overall, the heart rate also afffect the LV filling. The faster the
heart rate, the shorter diastolic time and less LV filling.
Ref
Miller RD : Anesthesia 5th Ed. Churchill
Livingstone 2000. |
| |
|
| 4.
Perioperative digoxin toxicity : management |
back
to top |
Digoxin toxicity in awake patients presents with N-V, diarrhea, yellow
vision, arrhythmia, gynaecomastia, etc
With the anesthetized patients, only a wide variety of arrhythmias
can be observed. The most common is PVCs (unifocal and multifocal,
oftens with bigeminy or trigeminy), A-V junctional escape rhythms,
nonparoxysmal junctional tachycardia, paroxysmal atrial tachycardia
with A-V block, 2nd degree A-V block, VT and VF. Hypokalemia will
enhance digoxin effects.
Recommended Treatment includes
| |
T
maintain normal to high K level, repleted to 4.5 mEq/L.
T
Lidocaine may be useful for ventricular ectopy, phenytoin can
reverse the high degree AV block (central mechanism)
T
Concomitant given drugs that will elevate digoxin level e.g.
quinidine, verapamil and B-blocker should be discontinued.
T
Temporary pacemaker may be required for severe bradycardia or
advanced heart block that is non-responsive to pharmacologic
approaches.
T
Mg should be administered 1-2 gm empirically unless patient
who has hypermagnesimia or impaired renal function.
T
Specific treatment to reduce the absorption e.g. gastric emptying
and activated charcoal should be considered in acute toxicity.
Generally, most of the patients have been taking digoxin chronically
and the toxicity aggravated by the elctrolytes derangement.
Digoxin-specific Fab antibody fragments are the definitive treatment
for hemodynamic significant arrhythmias.
T
Digoxin level may be measured to follow the trend. However,
in the patient who recieves Digoxin-Fab Ab, the level may increase
due to the increase in Fab-bound digoxin and indistinguishable
from free digoxin. The clinical improvement in arrhythmias during
the treatment can be observed. If the clinical improvement is
not manifested, the serum free digoxin can be measured by rapid
ultrafiltration assays |
Ref
1.
Lionel H. Opie. Drugs For the Heart 3rd ed. W.B. Saunders 1991
2 . Thomas SJ, Kramer JL. Manual of Cardiac Anesthesia 2nd ed.
Churchill Livingstone 1993. |
50% of patients have right dominant coronary circulation while 25%
have left dominant and 25% are clasfied as indeterminant (angiographically).
The right dominant means that a large part of posterior wall of LV
is supplied by the post. descending branch of Rt. coronary artery
and the A-V node is usually supplied by the right coronary artery.
For the left dominant, the posterior LV wall is supplied by a posterior
descending branch of the circumflex coronary artery and the A-V node
is also usually supplied from the left coronary artery.
Ref
1. Dinardo JA. Anesthesia for Cardiac
Surgery 2nd Ed. Appleton & Lange 1998
2. Miller RD : Anesthesia 5th Ed. Churchill Livingstone 2000. |
| |
|
| 6.
Complication of brachial artery cannulation |
back
to top |
Brachial artery cannulation is not recommended
*1 because of the potential for thrombosis and ischemia
of the lower arm and hand. Alternative sites such as the radial, femoral,
or axillary artery should be chosen.*
Special concerns for brachial artery cannulation are - lack of collateral
blood supply (compare to radial-ulnar system), needs a longer catheter,
biceps tendon injury is possible, elbow flexion will interfere with
monitoring, upper extremity compartment syndrome following brachial
a. cannulation has been reported. However, Bazaral
et al, reported over 3000 brachial artery cannulation with
safety. Another concern with brachial a. cannulation (and also axillary
a. cannulation) is the tip of the catheter may be close to the innominate
or lt. carotid a. branch in the aortic arch, the automatic flushing
with accidental air injection may cause cerebral embolisms. (more
common with axilllary a. cannulation)
Other complications in general for arterial cannulation includes hematoma,
arterial injury, thromboembolism, infection, nerve injury, AV malformation,
loss of limbs, etc.
Ref
1. *American
Heart Association. Chapter 12 p 12-5-12-6 Adjuncts for artificial
Circulation in Advanced Cardiac Life Support 1994-1997
2. Miller RD : Anesthesia 5th Ed. Churchill Livingstone 2000. |
-The
correct paddle size, the correct position, the correct energy used.
-Early defibrillation allows more success or the longer period of
VF, the less success of defibrillation.
-Course (high voltage) VF is easier to defib than fine (low voltage)
fibrillation.
-Epinephrine is generally accepted to give for next defibrillation.
But defibrillation should not be delayed for epinephrine administration.
-Transthoracic impedance plays an important role for external defibrillation.
The resistance decreases with the larger paddle and the use of saline-soaked
gauze pads or gels/creams and also successive shocks. Transthoracic
impedance is slightly (significantly) higher during inspiration.
-Serum K of 5 mEq/L decreases the defibrillation threshold.
-After CPB, aortic perfusion pressure and duration of reperfusion
after aortic cross-clamp removal ( should have mean BP at least
50 mmHg for > 5 min ). The reason is the anaerobic metabolism
that occured in the subendocardial region need a longer period of
washout of anaerobic products.
-myocardial temperature should be > 30 °C. (spontaneous fibrillation
occurs at 28 °C)
-Patients with valvular heart disease are more difficult to obtain
success defibrillation compare to patients with normal valvular
functions.
-Lidocaine has been shown to reduce the number and energy needed
for DC shocks but prophylactic lidocaine is not necessary.
Ref
1.
Dinardo JA. Anesthesia for Cardiac Surgery 2nd Ed. Appleton
& Lange 1998
2. American Heart Association. Advanced Cardiac Life Support
1994-1997 |
The cardiac output
(CO) curves that we use in general clinical setting is from thermodilution
(TD) technique. TDCO measurement is the modification of indicator
(dye) dilution method which flow is determined from
 |
Picture
from Peter R. Lichtenthal. Quick guide to Cardiopulmonary Care.
Baxter |
In clinical settings, the dilution is the temperature of the known
amount of injectate (usually 10 cc of 5%DW or NSS). The thermister
will detect changes of temperature at the tip of the PA catheter and
calculate the flow as CO (L/min).
 |
Picture
from Peter R. Lichtenthal. Quick guide to Cardiopulmonary Care.
Baxter |
Important points
1. TDCO is a measure of pulmonary blood flow, which in the
absence of shunting, is equal to forward right heart output
2. CO is inversely proportional to the area under the PA temp-time
curve
3. The injectate volume can vary from 1 to 10 ml but for adults,
uses of 3-5 ml results in more within-patient variation than
a 10 ml volume. (volume 1,2 and 3 ml have been shown to produce
reliable results in infants and small children)
4. Injectate temp from 0 c to room temperature can be used.
The accuracy and variability in adults is similar with either
room temperature or iced injectate. (SB and A.fib have been
reported with iced injectate)
5. There are large cyclical variations during different phases
of mechanical ventilation due to variations in pulmonary blood
flow.
|
TDCO are inaccurate in the presence of :
-low
CO. CO is overestimated because low flows allows the injectate
to get warm and reduces the area under curve.
-Lt. to Rt. intracardiac shunts (ASD, VSD) , often impossible
for computer analysis due to the recirculation which results
in a prolonged, flat deflection and interruption of exponential
down slope of the curve.
-TR ; regurgitation of the injectate results in delayed clearance
of the indicator from the Rt. heart. The curve is broad and
low in amplitude which results in inaccurate assessment of
forward CO.
-Rapid infusion of volume via peripheral line can results
in variations of up to 80% in TDCO. The rapid infusions should
be terminated or held at a constant rate for at least 30 seconds
before measurement.
|
Ref
Dinardo JA. Anesthesia for Cardiac Surgery 2nd Ed. Appleton
& Lange 1998 |
Five letter system for permanent pacemaker, 3 letter is the former
system and also used for the transport or intraop pacemaker.
|
First
letter
|
Second
letter
|
Third
letter
|
Fourth
letter
|
Fifth
letter
|
|
Chamber
paced
|
Chamber
sensed
|
Response
(of pacemaker)
|
Programmability
|
Anti-tachycardia
function
|
|
A
(atrium)
|
A
|
T
(triggered)
|
P
(programmable)
|
O
(none)
|
|
V
(ventricle)
|
V
|
I
(inhibited)
|
M
(multiprogrammable)
|
P (pacing)
|
|
D
(dual/both)
|
D
|
D
(both T and I)
|
C
(communicating)
|
S
(shock)
|
|
|
O
(none)
|
O
(none)
|
R
(rate modulation)
|
D
(both)
|
|
The common modes of pacemaker are :
VOO
: this is a fix asynchronous mode, just pace the ventricle regardless
of intrinsic R wave. This is the most common mode used in the
OR to disregard the electrical interference from the ESU. Ventricular
fibrillation has been reported. The magnet that used in the
OR will turn some models of pacemaker into this mode.
VVI : this mode paces
the ventricle and senses the intrinsic R waves. If the pacemaker
senses an intrinsic R wave, it turns off or inhibited.
DDD : The pacemaker senses
P waves and R waves, paces the atrium and ventricle and has
both inhibited and triggered activity - tatally automatic. |
|
Ref
1. Thomas SJ, Kramer JL. Manual of Cardiac
Anesthesia 2nd ed. Churchill Livingstone 1993.
2. Estafanous FG, Brash PG, Reves JG : Cardiac Anesthesia
; Principles and Clinical Practice 2nd ed. Lippincott William
& Wilkins 2001
|
After the institution of CPB, all venous return should be diverted
to the CPB through the venous cannula (or cannulae) but there
is still some blood returns that not going to the CPB machine.
The blood return to the Rt. heart is mostly from coronay blood
flow. The blood that returns to the left heart includes Thebesian
vein, Bronchial veins, extracardiac Lt. to Rt. shunts e.g. BT
shunt, imcompetent Ao valve |
 |
Ref
Dinardo JA. Anesthesia for Cardiac Surgery 2nd Ed. Appleton
& Lange 1998 |
The major causes of hypotension at initiation of bypass is the hemodilution
which cause a great reduction in SVR and the loss of pulsatile flow.
During CPB, the most serious possible cause of hypotension is the
aortic dissection. Others includes
-measurement
errors e.g. transducer problem, kinked artrial catheter
-reduced pump flow from
a.
Inadequate venous return e.g. obstruction, air lock, venous
cannulae kink, etc, Insuficient pump volume, Hypovolemia,
Operating table is too low
b. Incomplete occlusion of
pump heads
c. High aortic line pressure
(reflecting distal obstruction e.g. kinking, etc) |
-Vasodilation
from e.g. volatile anesthetics, temperature, hemodilution
|
|
Ref
Thomas SJ, Kramer JL. Manual of Cardiac
Anesthesia 2nd ed. Churchill Livingstone 1993.
|
-Pulmonary ; this is the most
serious side effect and may be dose related. Amiodarone can cause
pneumonitis which further develop to pulmonary fibrosis (1-10%).
-Cardiac ; inhibition of SA or
AV node
-CNS ; proximal muscle weakness,
peripheral neuropathy, others e.g. headache, ataxia, tremors, impaired
memory, insomnia, dreams, etc. (variable incidence)
-Thyroid : at a low dose (200-400
mg) 3-5 % of patients may develop hypothyroidism or hyperthyroidism.
10% may have silent alterations in thyroid function.
-GI ; nausea 50% (even with dose
200 mg daily), increased liver enzymes in 10-20%. These side effects
usually resolve with dose reduction.
-Others ; corneal microdeposits
(nearly all adult patients with prolonged treatment) which may cause
impairment of visual acuity, Macular degeneration (rarely), 10 % of
patients develop photosensitive slate-gray or bluish skin discoloration
(after prolonged treatment .. 18 months).
Ref
1.
Lionel H. Opie. Drugs For the Heart 3rd ed. W.B. Saunders 1991
p. 202-203
2 . Thomas SJ, Kramer JL. Manual of Cardiac Anesthesia 2nd ed.
Churchill Livingstone 1993. |
Capnometry shows promise as a noninvsive measure of CO generated during
ongoing CPR. Blood flow to the lungs depends on CO. In most patients
in cardiac arrest, the CO2 that reaches the
lungs diffuses out. Capnometry measures CO2
excretion through the endotracheal tube. In experimental models, end-tidal
CO2 concentration during ongoing CPR correlated
with CO, perfusion pressures, and successful resuscitation from cardiac
arrest. Clinical studies have demonstrated that patients who were
succesfully resuscitated from cardiac arrest had significantly higher
end-tidal CO2 levels than patients who could
not be resusciated. Capnometry can also be used as an early indicator
of return of spontaneous circulation. Despite these promising studies,
a number of factors must be considered. Large changes in the MV will
affect the end-tidal CO2 reading. Thus, ventilation
must be held relatively constant during the resuscitation effort.
The administration of bicarbonate will increase CO2
excretion for several minutes before it returns to baseline measurements.
High doses of pressor agents such as epinephrine will increase myocardial
perfusion pressure but decrease CO. CO2 excretion
will decrease with decreased blood flow to the lungs. Finally, for
capnometry to be a truly useful prognostic indicator of successful
resuscitation, clinical studies must be demonstrate that strategies
that improve end-tidal CO2 levels will result
in improved outcome from cardiac arrest. In summary, end tidal CO2
monitoring during cardiac arrest can be useful as a noninvasive indicator
of cardiac output generated during CPR. Further research needs to
be done to determine its use as a prognostic inidicator in clinical
practice.
Ref
American
Heart Association. Chapter 12 p 12-5-12-6 Adjuncts for artificial
Circulation in Advanced Cardiac Life Support 1994-1997 |
EMD or Electromechanical Dissociation is a term that is recently called
by the ACLS as a PEA (Pulseless Electrical Activity). EMD is a state
which organized elctrical depolarization occurs throughout the myocardium
but no synchronous shortening of the myocardial fiber occurs. Mechanical
contraction are absent. The term pseudo-EMD is called when there is
an electrical activity associated with mechanical contractions, only
these contractions do not produce a blood pressue detectable by the
usual methods of palpation or sphygmomanometer. The most common causes
of PEA is hypovolemia, the other possible causes are cardiac tamponade,
tension pneumothorax, massive PE, massive MI, Hypothermia, hypoxia,
durg overdoses [ tricyclics, digoxin, b-blockers,
Ca channel blockers], Hyperkalemia, preexisting acidosis, etc. The
Algorithm for PEA is as shown below.
Ref
American
Heart Association. Chapter 1p 1-21-1-25 Essentials of ACLS in
Advanced Cardiac Life Support 1994-1997 |
The cerebral injury has been recognized as a complication asssociated
with open heart surgery with CPB. The incidence of various types of
neurologic injuries in CABG compare to peripheral vascular surgery
is shown in this table.
| New
Neurologic Findings |
CABG
(n=308)
|
Peripheral
Vascular Surgery(n=49)
|
| Fatal
cerebral injury |
1
(0.3%)
|
0
|
| Depressed
consciousness > 24 hrs |
10
(3%)
|
0
|
| Stroke |
15
(5%)
|
0
|
| Reversible
ischemic deficit |
9
(3%)
|
0
|
| Ophthalmological
abnormalities |
78
(25%)
|
0
|
| Primitive
reflexes |
123
(39%)
|
2
(4%)
|
| Psychosis |
4
(1%)
|
0
|
| Peripheral
neuropathy |
37
(12%)
|
7
(14%)
|
 |
|
|
| Data
from : Shaw P, Bates D, Cartlidege NEF, et al: Early neurological
complications of coronary artery bypass surgery. BMJ 1985; 291:1384-1376;
and Shaw PJ, Bates D, Cartlidge NEF, et al : neurologic and
neurophyschological morbidity following major surgery : Comparison
of coronary artery bypass and peripheral vascular surgery. Stroke
1987; 18:700-707) |
The risk factors of neurologic
injury.
-Age >
75 yr or < 1 mo
-Previous neurologic injury or stroke
-Ascending Aortic Atherosclerosis
-Genetic predisposition : APOEepsilon 4 allele
-DM
-Hypertension
-Peripheral vascular disease
-Three-vessel coronary artery disease
-poor preop LV function or LV thrombi
-prolonged CPB associated with poor neurologic outcome, membrane
oxygenator produce fewer numbers of microscopic gas emboli
-DHCA |
Controversies in perioperative management
1.
Glucose management : the
evidence of studies in the dogs shows the hyperglycemic CPB
results in poor neurologic outcome but the clinical studies
cannot confirm this.
2. Mild and moderate hypothermia
: Hypothermia has long been considered to provide a "cerebral
protection" during CPB. However the concepts of normothermic
cardioplegia (warm) started iin the early 1990s has been great
interest and many studies still show controversies. The conclusion
: current evidence suggest that sustained normothermia during
CPB is associated with less favorable outcomes.
3. Acid-Base management : it has been unclear which
hypothermia acid-base strategy (pH stat vs alpha-stat) might
be most appropriate for humans during hypothermic CPB because
humans are neither poikilotherms (alpha-stat) nor hibernators
(pH stat) and normally do not become hypothermic. The conclusions
: there seems to be no neurologic disadvantage to alpha-stat
management during continuous CPB at moderate hypothermia, and
probably a slight advantage. However, the neurologic outcome
differences between alpha-stat are not detectable until CPB
durations are prolonged.
4. Systemic arterial Pressure : CMRO2 are decreased
during CPB (hypothermia, anesthesia) but the cerebral O2
delivery is reduced (hemodilution, hypothermia-induced CBF reduction).
Therefore, the safe lower limit of MAP have been controversial.
Conclusions : it may be particularly true that hypotension,
low CO is clearly associated with adverse neurologic outcome.
Increasing MAP increases CBF and may preserve viability of a
region that would have died otherwise. Therefore, it makes perfect
sense that hemodynamic instability post-CPB should contribute
to neurologic morbidity.
5. Barbiturates :
Barbiturates have been considered to be "cerebral protective"
agents. Many studies show controversies and lead to conclusion
that under usual CPB conditions that cerebral embolization is
small (use of membrane oxygenator, arterial filter) and/or hypothermic
protection is already present, barbiturates are very unlikely
to provide substantive brain protection. The most rational (but
unproved) use of thiopental (or etomidate or propofol) might
be those settings in w hich, under normothermia, a shower of
emboli is anticipated (such as resumption of ejection after
an open chamber procedure).
6. Pulsatile perfusion : to date, no clinical evidence
of superior neurologic outcome with pulsatile perfusion (animal
stuides in the 1970s and 80s indicated that nonpulsatile flow
unfavorably influenced cerebral perfusion). As practically achievable,
it seems that pulsatile CPB has little effect on the brain or
the processes resulting in brain injury during cardiac surgery
7. Hemodilution and postop. Anemia : both human and
animal studies indicate brain oxygenation is adequate with hematocrit
(Hct) levels in the mid-20s during CPB at 27 °c. There was
a study (Savagaeu et al., 1982) that report the neurologic impairment
was associated with Hct levels < 30% in the first 12 hr after
surgery. ASA guidelines for blood component therapy stated that
"transfusion is rarely indicated when the Hb >10 g/dL
and is almost always indicated when it is < 6 g/dL, especially
when the anemia is acute." |
Ref
Dinardo JA. Anesthesia for Cardiac Surgery 2nd Ed. Appleton
& Lange 1998 |
AVR surgery is mostly performed for aortic valve stenosis (AS) more
than aortic insufficiency. The pathophysiology of these 2 diseases
are different. In AS, the global systolic LV function is well preserved
until a very late and severe form of AS occurs. The gradient across
the valve need to be maintain and acute decrease in systemic BP, particularly
diastolic BP can be detrimental. Hemodynamic goals for AS and AR can
be reviewed as follow.
| |
AS
|
AR
|
| Preload |
inc
|
inc
|
| Afterload |
-/inc
|
-/dec
|
| Contractility |
-
|
-
|
| Rate |
avoid
extremes
|
-/inc
|
| Rhythm |
maintain
sinus
|
-
|
| MvO2 |
potential
problem
|
-
|
|
There are many
causes of hypertension. During general anesthesia, an adequate anesthesia
must be achieved before the antihypertensive treatment. Narcotic analgesics
or potent inhalation anesthetic agent may be used. To reduce the BP
in severe AS is very critical. The pressure gradient across the valve
may drop and the diastolic pressure which determine the coronary perfusion
may be too low against the increase in wall tension for subendocardial
perfusion. The cardiac arrest that occur in severe AS has a very poor
prognosis in term of resuscitation. The treatment plan can be formulated
from the fact that BP = CO x SVR. In AS, to reduce the afterload is
unfavorable. However, if necessary, the rapid onset and titratable
drug e.g. Sodium Nitroprusside would be an ideal choice 2.
To maintain the gradient across the valve, the only factor that can
be altered to reduce the BP is to decrease the CO. In this case, the
CO should be measured before and after treatment. The CO that is too
low is also an unfavorable condition. The CO can be reduced by decrease
the SV or heart rate or contractility. Decreased preload in AS is
not suggested, the volume needed to be adequate to pass the stenotic
valve. The heart rate can be reduced by b-blocker,
the short acting and titratable drug like esmolol is an ideal choice.
The contractility may be as well reduced by b-blocker
or Ca channel blocker.
In AI, because the reduced afterload is preferable. The drugs that
reduce SVR e.g. a adrenergic blocker, hydralazine,
potent vasodilating anesthetic agent, ACEI, peripheral acting Ca Channel
blocker, sodium nitroprusside, etc can be used.
Ref
1.
Jackson JM. Valvular Heart Disease in Thomas SJ, Kramer JL :
Manual of Cardiac Anesthesia 2nd ed. Churchill Livingstone 1993
2. Dinardo JA. Anesthesia for Vavle Replacement in Patients
With Acquired Valvular Heart Disease. Dinardo JA : Anesthesia
for Cardiac Surgery 2nd ed. Appleton & Lange 1998 |
There are 3 terms regarding to actue coronary syndrome which are 3Is
- Myocardial Ischemia, Myocardial
Injury and Myocardial Infarction
Myocardial Ischemia occurs
with a mismatch between the amount of blood flowing to a section of
the heart and the amount of oxygen needed by that section of the haert.
Usually desieased and narrow coronary arteries cause ischemia when
they cannot carry enough blood to an area of the actively beating
heart. Patients usually experience ischemia as chest pain and discomfort
or angina. Ischemia can quickly resove by either reducing the oxygen
needs of the heart (resting, slowing the rate with b-blockers) or
increasing the blood flow (vasodilatation with nitroglycerin).
In awake patients, the presenting symptoms include chest pain, dysrhythmias,
signs of ventricular failure. Some patients may be asymptomatic or
the anesthetized patients, these symptoms can not detected. The EKG
is still the gold standard for diagnosis of myocardial ischemia. The
appropriate leads are leads II and V5 which are commonly used simultatneously.
These combination has a high sensitivity but will not detect true
posterior ischemia (esophageal ECG may be used). The changes in PCWP
and PCWP waveform may be used intraoperatively but have poor sensitivity
and specificity, so they canot be relied upon as the sole indicator
of ischemia. The regional wall motion abnormalities (RWMA) from TEE
are very helpful and numerous studies have shown it to be more sensitive
than EKG changes and to be capable of detecting myocardial ischemia
before EKG changes. But recent data show a lack of concordance between
ischemia detected by EKG and that detected by TEE. There are both
TEE-detected ischemia that not detected by TEE and EKG-detected ischemia
which is not detected by TEE.
EKG
changes
The typical
EKG changes of ischemia are ST depression > 1 mm. The upsloping
ST segment is often a nonspecific finding while the horizontal
is more specific for ischemia and the down-sloping is most indicative
of ischemia. The T-wave changes are less specific either T-wave
inversion or tall, peaked, asymetrical T. However, Giant, hyperacute
T are sometimes the only changes seen early in an AMI and these
changes can be an indication for thrombolytic therapy. Some
clinical conditions that can cause ST depression and T changes
are digoxin, LVH, early repolarization, LBBB and pre-excitation. |
Myocardial Injury
occurs if the period of ischemia is prolonged more than just a few
minutes and Infarction
refers to the actual death of injured myocardial cells. The hallmark
of EKG changes in myocardial injury areST elevation (significant when
ST segment measures > 1 mm above the PT baseline at a point 0.04
second (1 mm) past the J point. And the hallmark of EKG changes associated
with infarction is the presence of abnormal Q waves. Q waves are considered
abnormal if they are > 1 mm (0.04 sec) wide and the height greater
than 25% of the height of the R wave in that lead. Q waves that are
similar in width and height may indicate normal septal depolarization.
Q waves indicate infarcted myocardial tissue. They can appear within
hours after occlusion but usually not before 2 hours of onset of symptoms.
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Ref
1.
Dinardo JA. Anesthesia for Myocardial Revascularization p.83-91
in Anesthesia for Cardiac Surgery. 1998, 2nd editon. Appleton
& Lange
2.American
Heart Association. Chapter 9 p 9-23-9-24 The Acute Coronary
Syndrome in Advanced Cardiac Life Support 1994-1997
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