Describes coronary blood supply anatomy, myocardial oxygen demand and supply, and basic anesthesia consideration (history taking, special investigation, and optimization)
2. Background
Cardiac anesthesiologist:
Normal and altered cardiac physiology
Cardiovascular and anesthetic medications
pharmacology
Physiologic alterations associated with cardiopulmonary
bypass (CPB)
Surgical procedures.
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3. Coronary blood supply:
RCA – RA, RV and variable
portion of LV( inferior wall)
85% - gives PDA ( dominant)
LCA – LA, Left
interventricular septum, LV
After short course – LAD &
CX artery ( PDA – 15%)
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4. SA node – RCA (60%), LAD(40%)
AV node – RCA(85-90%), CX (10-
15%)
Bundle of His – PDA & LAD
Anterior papillary muscle –
diagonal branch of LAD
margincal branch of CX
Posterior papillary mucle – only
PDA( more vulnerable to
ischaemia)
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5. Myocardial
oxygendemand
Prevention/treatment of MI during CABG
surgery decreases the incidence of
perioperative myocardial infarction.
Avoid factors that increase myocardial oxygen
demand (MV⋅O2)
Vulnerable period - pre-CPB period
It is well recognized that most ischemic events
occur with minimal or no change in MV⋅O2
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6. Myocardial O2
demand
The principal determinants of MV⋅O2
are:
wall tension
contractility.
Explained by Laplace Law
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MVO2 ~ wall
Tension
7. Myocardial O2
Supply
• Myocardial O2 demand only met by increasing
coronary blood flow
Coronary Blood Flow
The critical factors that modify coronary blood
flow are :
Perfusion pressure
vascular tone of the coronary circulation
Time available for perfusion (determined mainly
by heart rate),
Severity of intraluminal obstructions
Presence of (any) collateral circulation.
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8. CoronaryBlood
Flow:
1)Perfusion
pressure
Most vulnerable area – subendocardium of
left ventricle
Directly exposed to intracavitory pressure
Greatest metobolic requirement
Greater systolic shortening time than other
areas of myocardium
LV perfusion – entirely during diastolic
RV – diastolic and systolic
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9. CoronaryBlood
Flow:
1)Perfusion
pressure
LV CPP = AoDP - LVDP
Low LVDP is ideal for improving
perfusion (higher pressure gradient)
and reducing MV⋅O2 (decreased LV
volume and wall tension).
Increasing perfusion pressure by
raising the aortic pressure will
increase MV⋅O2.
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10. CoronaryBlood
Flow:
2)Vasculartone
Autoregulated
Coronary vascular reserve = Basal flow
(autoregulated) - max flow
normally 3-5 times higher than basal flow.
Once perfusion pressure decreases to < 40 mmHg,
autoregulation of subendocardial coronary flow is
lost.
Whenever MV⋅O2 increases above available
reserve, signs, symptoms, and metabolic evidence of
ischemia develop.
Irreversible injury to the myocardium can occur if
coronary blood flow is occluded for longer than 20
minutes, leading to myocardial cell death and
necrosis.
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11. CoronaryBlood
Flow:
2)Vasculartone
In reversible ischemia, the myocardium remains viable
:
• Stunning myocardium:
• to a state of abnormal function that occurs after an
acute, discrete episode of ischemia.
No cell death occurs
but it may take several days or longer for the myocardium
to recover, even though adequate blood flow has been
restored.
Hibernating myocardium :
to a chronic state of reduced coronary blood flow and
abnormal function
usually secondary to a fixed stenosis.
In response to decreased oxygen supply, hibernating
myocardial cells downregulate their metabolism and
oxygen demand to maintain viability.
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12. Haemodynamic
goals
Pry goal:
prevention of myocardial ischemia
prompt identification and
treatment of new ischemic episodes
The anesthetic interventions -
reducing and controlling the factors
that increase MV⋅O2 (heart rate,
contractility, and wall tension).
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15. Preoperative
preparation
Other systems:
Pulmonary- COPD or infection, cigarette
smoking, pulmonary HTN
Renal dysfunction – common in post op
Hepatic dysfunction
Neurologic- Cerebrovascular disease ,
carotid bruits, TIA
Endocrine - diabetes
Hematologic - Conditions predisposing to
bleed
Electrolytes – arrythmia
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16. Preoperative
preparation
The depth and detail of the
explanation should be custom-
tailored to each patient
The anticipated events from
transport to the operating room
until emergence should be
discussed with the patient.
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17. Preoperative
preparation
The depth and detail of the
explanation should be custom-
tailored to each patient
The anticipated events from
transport to the operating room
until emergence should be
discussed with the patient.
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19. Current
medications
Almost all cardiovascular drugs are
continued until the time of surgery
Interactions between these drugs
and anesthetics are more often
beneficial than harmful in
maintaining hemodynamic control
during periods of surgical stress
and reducing morbidity and
mortality
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20. Current
medications
Regular medication:
Beta blockers should be continued in same dosage
Anti platelet medications - stopped at least 1 week prior to
surgery
ACEI may be stopped 24 to 36 hours prior to surgery
(substituted with calcium channel blockers)
For DM patients – conversion to short acting Insulin.
Anti aspiration prophylaxis:
Pantoprazole 40mg, prokinetic -metoclopramide 10mg
Anti anxiety:
Alprazolam 0.5 -1mg, midazolam 0.05 mg/kg
Fentanyl 1mcg/kg IV
30 minutes prior to surgery with supplemental oxygen.
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23. Preparation
Preparation, organization, and attention
to detail permit one to deal more
efficiently with unexpected intraoperative
problems
The anesthesia machine, monitors,
infusion pumps, and blood warmer should
all be checked before the patient arrives.
Drugs —including anesthetic and
vasoactive agents—should be immediately
available.
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24. Preparation
Many clinicians prepare one vasoconstrictor
and one vasodilator infusion before the start
of the procedure.
2 anesthesiologist
Premedication – good monitoring system
In children – induction started at
premedication
Trolley should have monitor together
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25. Monitoring
*** 2 monitors- 1 for surgeon & 1 for
anesthesiologist
Continous ECG monitoring for ST
segments
II, V4 or V5
V4R, V5R – risk of RV ischaemia
SpO2, ETCO2
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28. Monitoring –
Pulmonary artery
catheter(PAC)
Usually placed via the right internal jugular vein
Differs from centers to centers
2011 AHA/ACCF CABG practice guidelines -
hemodynamically compromised patient
Sudden occlusion – LV dysfunction
Use is controversial - ASA Practice Guidelines
Indications:
EF <0.4
Significant abnormality of the left ventricular
wall motion
LVEDP > 18 mm Hg at rest.
Recent MI and unstable angina.
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37. Monitoring–
Labparameter
Lab testing is mandatory in cardiac
surgery
ABG, Hb, K+, ionized Ca+, Glu
report should be immediately
available
ACT / TEG
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38. Selectionof
anesthesia
No ideal anesthesia
The choice of anesthetic should be based
on:
known hemodynamic, pharmacologic, and
pharmacokinetic effects of each drug
Experience of the anesthesiologist
relative cost–benefit of each agent
extent of pre- existing myocardial dysfunction.
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39. Selectionof
anesthesia
Titrated to desired effect
For mild and moderate – some
degree of myocardial depression
is beneficial
Reduces episodes of ischemia by
decreasing oxygen demand
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41. Selectionof
anesthesia–
Opioids
The primary advantages of opioids are:
lack of myocardial depression
maintenance of a stable hemodynamic
state
reduction of heart rate.
Current practice – supplementation of
opioids with benzodiazepine & volatile
agents
Morphine – cardioprotective and anit-
inflammatory
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42. Selection of
anesthesia-
volatile anesthesia
Desirable features:
dose-dependent hemodynamic changes
easy reversibility
titratable myocardial depression
amnesia
suppression of sympathetic responses to surgical
stress and CPB.
Volatile anesthetics protect the myocardium from
ischemia and reperfusion injury and reduce
myocardial infarct size
“anesthetic preconditioning”
“anesthetic postconditioning”
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43. Selection of
anesthesia-
volatile anesthesia
Only volatile based – systemic
hypotension
Balanced technique with opioids
Isoflurane is a coronary vasodilator
other volatile anesthetics - lesser degree
< 1 MAC – no clinical significant
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44. Selection of
anesthesia-
volatile anesthesia
Desflurane –
cardiac profile = isoflurane.
rapid uptake and distribution
useful in cases in which hemodynamic changes
mandate rapid changes in anesthetic depth
Desflurane vs Sufentanil – Sympathetic
activity as outcome
Helman et al – Desflurane has increase
sympathetic activity
Isoflurane + Fenta vs Sevo + Fenta
Similar outcome
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45. IVsedative
hypontics
Shorting acting - Mida, Propofol,
dexmedetomine
Alternative adjunct
Can be continued postop in the ICU
Volatile vs propofol
Propofol:
Less favourable for cardiac function
Higher need for inotropes
elevated plasma troponins after cardiac
surgery in elderly patients
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46. Treatmentof
ischeamia
The use of anesthetics or vasoactive drugs is aimed
at decreasing heart size, decreasing heart rate, and
improving myocardial perfusion pressure.
The principal vasoactive drugs are:
nitrates,
β-blockers,
peripheral vasoconstrictors
calcium entry blockers.
Volatile anesthetics can also be used to control
blood pressure and reduce contractility.
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47. Treatmentof
ischeamia-
Nitrates
Nitroglycerin(TNG) –
Drug of choice in acute MI
Dose - 0.5 to 3 μg/kg/min
( reduced in hepatic & renal failure)
Higer dose – hypotension
Methemoglobin
Role of prophylaxis in intra or post ?
No evidence
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48. Treatmentof
ischeamia-
Nitrates
Sodium Nitroprusside (SNP)–
Decreases peripheral vascular resistance
Improves ventricular compliance in the ischemic
myocardium.
Dose - 0.5 to 3 μg/kg/min
( reduced in hepatic & renal failure)
cyanide and thiocyanate toxicity,
Triad - elevated mixed venous O2 (SVO2),
tachyphylaxis and metabolic acidosis
Other drugs should not be infused in the same
solution as SNP.
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49. Treatmentof
ischeamia-
Vasoconstrictor
Phenylephrine, norepinephrine, Vasopressin
Adjuncts in the prevention and treatment of
ischemia :
increase systemic blood pressure
Improves coronary perfusion pressure,
(at the expense of increasing afterload and perhaps MV⋅O2 )
Venoconstriction – increases preload
(TNG added to counteract)
No one vasoconstrictor is superior
Combination may be needed
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50. Treatment of
ischeamia -β-
Blockers
Metoprolol, Labetalol, Esmolol,
propranolol(rarely)
Improves myocardial oxygen balance by
decreasing the chronotropic and inotropic state
Propranolol - nonselective β-blocker, t1/2 4 to 6
hours
Metoprolol - β1- selectivity, less likely to trigger
bronchospasm
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51. Treatment of
ischeamia -β-
Blockers
Labetalol – β and α- blockade, useful in
treating hyperdynamic and hypertensive
situations
Esmolol –
Short-acting β1-blocker (half-life of - 9.5
minutes)
Cardio selective
Useful in treating transient increases in heart
rate owing to episodic sympathetic stimulation.
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52. Treatment of
ischeamia -Calcium
channel blockers
Depresses contractility
Reduces coronary and systemic vascular tone
Decreases SA firing rate
Impede AV conduction at a remarkably variable
degree.
CCB have been found to have cardioprotective
effects during reperfusion
Negative inotropic effect:
Verapamil > nifedipine > diltiazem >nicardipine
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53. Treatment of
ischeamia -Calcium
channel blockers
Verapamil – Atrial fibrillation/flutter
Diltiazem- preferred in myocardial function
Nicardipine - coronary antispasmodic and
vasodilatory effects more than systemic arterial
vasodilatory effects.
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54. Treatment of
ischeamia -Calcium
channel blockers
Nifedipine & Nicardipine - postoperative
hypertension in cardiac surgical patients
(prominent systemic arterial dilators )
Clevidipine was a better antihypertensive agent
than SNP or TNG and was equivalent to nicardipine
Aronson S et al. The ECLIPSE trials (2008)
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55. Treatment of
ischeamia -
Magnesium
Coronary arterial dilating properties
Reduces the size of myocardial infarction
in the setting of acute ischemia
Decreases mortality associated with
infarction
Antiarrhythmic
minimizes myocardial reperfusion injury
Garcia LA et al. Magnesium reduces free radicals in an in
vivo coronary occlusion-reperfusion model. J Am Coll
Cardiol. 1998;32:536–539.
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56. Treatment of
ischeamia -
Magnesium
Although magnesium was found to
prevent atrial fibrillation in
coronary artery surgery, in patients
treated with β-blockers, the
addition of prophylactic IV
magnesium did not reduce the
incidence of atrial arrhythmias
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57. Summary
Blood supply of the heart
Avoid factors that increase myocardial oxygen demand
(MV⋅O2)
Anesthetic goal - reducing and controlling the factors
that increase MV⋅O2 (heart rate, contractility, and wall
tension).
Meticulous preparation, organization & monioting
No ideal anesthesia in cardiac surgery
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59. Refeences
3/11/2022 59
Barash et al. 8th edition
Morgan 6th edition
2011 AHA/ACCF practice guideline
(https://www.ahajournals.org/doi/pdf/10.1161/CIR.0b013
e31823c074e)
Editor's Notes
The prevention or treatment of myocardial ischemia during coronary artery bypass graft (CABG) surgery decreases the incidence of perioperative myocardial infarction.
The hemodynamic management should avoid factors that increase myocardial oxygen demand (MV⋅O2), particularly during the vulnerable pre-CPB period, while optimizing oxygen delivery to the myocardium, since it is well recognized that most ischemic events occur with minimal or no change in MV⋅O2
According to Laplace law, wall tension is directly proportional to intracavitary pressure and radius and inversely proportional to wall thickness
Therefore, MV⋅O2 can be reduced by interventions that decrease intraventricular pressure and prevent or promptly treat ventricular distention.
According to Laplace law, wall tension is directly proportional to intracavitary pressure and radius and inversely proportional to wall thickness
Therefore, MV⋅O2 can be reduced by interventions that decrease intraventricular pressure and prevent or promptly treat ventricular distention.
A low LVDP is ideal for improving perfusion (higher pressure gradient) and reducing MV⋅O2 (decreased LV volume and wall tension).
On the other hand, increasing perfusion pressure by raising the aortic pressure will increase MV⋅O2.
However, this is not as important, when one considers that tachycardia is the most important cause of intraoperative and perioperative ischemia.
The difference between auto regulated (basal) flow, and blood flow available under conditions of maximal vasodilation is termed coronary vascular reserve and is normally three to five times higher than basal flow.
Coronary vascular reserve = Basal flow - max flow
In reversible ischemia, the myocardium remains viable and can be differentiated into stunned or hibernating myocardium.
Stunning refers to a state of abnormal function that occurs after an acute, discrete episode of ischemia.
No cell death occurs in stunning, but it may take several days or longer for the myocardium to recover, even though adequate blood flow has been restored.
Hibernating myocardium refers to a chronic state of reduced coronary blood flow and abnormal function usually secondary to a fixed stenosis.
In response to decreased oxygen supply, hibernating myocardial cells downregulate their metabolism and oxygen demand to maintain viability.
The primary goal of any successful cardiac anesthetic is prevention of myocardial ischemia and prompt identification and treatment of new ischemic episodes.
The anesthetic interventions are geared at reducing and controlling the factors (Table 39-1) that increase MV⋅O2 (heart rate, contractility, and wall tension).
The first intervention is to optimize coronary blood flow, that is, maintain coronary perfusion pressure, while keeping in mind that the peripheral arterial systolic pressure is different (usually higher) than the aortic root pressure, and to increase diastolic time.
Thus, the cardiac goals for patients with coronary artery disease are slow (heart rate), small (ventricular size), and well perfused (adequate blood pressure).
Preoperative medications that may benefit coronary patients include statins and angiotensin-converting enzyme inhibitors (to stabilize the atherosclerotic plaque) as well as β-blockers (to control heart rate).
TEE permits assessment of:
ventricular volume
global and regional function
estimation and quantitation of valvular pathology
measurement of valve gradients and calculation of filling pressures
visualization of the thoracic aorta
detection of intracardiac air.
TEE permits assessment of:
ventricular volume
global and regional function
estimation and quantitation of valvular pathology
measurement of valve gradients and calculation of filling pressures
visualization of the thoracic aorta
detection of intracardiac air.
TEE permits assessment of:
ventricular volume
global and regional function
estimation and quantitation of valvular pathology
measurement of valve gradients and calculation of filling pressures
visualization of the thoracic aorta
detection of intracardiac air.
TEE permits assessment of:
ventricular volume
global and regional function
estimation and quantitation of valvular pathology
measurement of valve gradients and calculation of filling pressures
visualization of the thoracic aorta
detection of intracardiac air.
TEE permits assessment of:
ventricular volume
global and regional function
estimation and quantitation of valvular pathology
measurement of valve gradients and calculation of filling pressures
visualization of the thoracic aorta
detection of intracardiac air.
TEE permits assessment of:
ventricular volume
global and regional function
estimation and quantitation of valvular pathology
measurement of valve gradients and calculation of filling pressures
visualization of the thoracic aorta
detection of intracardiac air.
TEE permits assessment of:
ventricular volume
global and regional function
estimation and quantitation of valvular pathology
measurement of valve gradients and calculation of filling pressures
visualization of the thoracic aorta
detection of intracardiac air.
TEE permits assessment of:
ventricular volume
global and regional function
estimation and quantitation of valvular pathology
measurement of valve gradients and calculation of filling pressures
visualization of the thoracic aorta
detection of intracardiac air.
The current practice is to supplement the opioid with benzodiazepines and volatile agents.
The planned time of extubation is now one of the major factors determining the selection and dosage of opioid.
Shorter-acting opioids (sufentanil and remifentanil) produce equally rapid extubation, similar ICU stay, and similar costs to fentanyl.
Thus, any of these opioids can be used for fast-track cardiac surgery.
The beneficial cardioprotective and anti- inflammatory effects of morphine have been reconsidered recently, bringing back into the foray the opioid that reinvigorated the practice of cardiac anesthesia.
This beneficial effect has been shown when volatile anesthetics are administered before a period of prolonged ischemia (“anesthetic preconditioning”) as well as during reperfusion (“anesthetic postconditioning”).
However, it is difficult to ascertain whether these laboratory-proven benefits have contributed to improved myocardial protection in clinical practice.
Clinical studies using isoflurane to clinical rather than pharmacologic end points have not shown increased episodes of ischemia or a worsened outcome.
Desflurane and sevoflurane have the fastest recovery of all volatile anesthetics.
Desflurane has a rapid uptake and distribution, allowing it to be useful in cases in which hemodynamic changes mandate rapid changes in anesthetic depth. It has a cardiac profile similar to that of isoflurane.
When studying sympathetic nervous system activity, Helman et al. found an increase in sympathetic activity and myocardial ischemia in patients anesthetized with desflurane as the sole anesthetic agent for coronary artery bypass surgery compared with patients anesthetized with sufentanil.
Clinical studies using isoflurane to clinical rather than pharmacologic end points have not shown increased episodes of ischemia or a worsened outcome.
Desflurane and sevoflurane have the fastest recovery of all volatile anesthetics.
Desflurane has a rapid uptake and distribution, allowing it to be useful in cases in which hemodynamic changes mandate rapid changes in anesthetic depth. It has a cardiac profile similar to that of isoflurane.
When studying sympathetic nervous system activity, Helman et al. found an increase in sympathetic activity and myocardial ischemia in patients anesthetized with desflurane as the sole anesthetic agent for coronary artery bypass surgery compared with patients anesthetized with sufentanil.
Its action is via systemic venodilation that decreases LV preload, wall tension, MV⋅O2, and coronary arterial dilation, which is operative in both stenosed coronaries and collateral beds.
adjuncts in the prevention and treatment of ischemia because they increase systemic blood pressure, thereby improving coronary perfusion pressure, albeit at the expense of increasing afterload and perhaps MV⋅O2
adjuncts in the prevention and treatment of ischemia because they increase systemic blood pressure, thereby improving coronary perfusion pressure, albeit at the expense of increasing afterload and perhaps MV⋅O2
adjuncts in the prevention and treatment of ischemia because they increase systemic blood pressure, thereby improving coronary perfusion pressure, albeit at the expense of increasing afterload and perhaps MV⋅O2
adjuncts in the prevention and treatment of ischemia because they increase systemic blood pressure, thereby improving coronary perfusion pressure, albeit at the expense of increasing afterload and perhaps MV⋅O2
adjuncts in the prevention and treatment of ischemia because they increase systemic blood pressure, thereby improving coronary perfusion pressure, albeit at the expense of increasing afterload and perhaps MV⋅O2
adjuncts in the prevention and treatment of ischemia because they increase systemic blood pressure, thereby improving coronary perfusion pressure, albeit at the expense of increasing afterload and perhaps MV⋅O2
Magnesium has coronary arterial dilating properties, reduces the size of myocardial infarction in the setting of acute ischemia, and decreases mortality associated with infarction.62 In addition, it is an antiarrhythmic and minimizes myocardial
2686
reperfusion injury. Although magnesium was found to prevent atrial fibrillation in coronary artery surgery,63 in patients treated with β-blockers, the addition of prophylactic IV magnesium did not reduce the incidence of atrial arrhythmias
Magnesium has coronary arterial dilating properties, reduces the size of myocardial infarction in the setting of acute ischemia, and decreases mortality associated with infarction.62 In addition, it is an antiarrhythmic and minimizes myocardial
2686
reperfusion injury. Although magnesium was found to prevent atrial fibrillation in coronary artery surgery,63 in patients treated with β-blockers, the addition of prophylactic IV magnesium did not reduce the incidence of atrial arrhythmias