Transcript plaque a induction

Anesthesia in Ischemic Heart
Disease for non-cardiac surgery
Dr N.Nasseh
Departmant of Anesthesia of Qazvin University Medical scienses
• The prevalence of vascular disease and ischemic heart
disease in the United States increases significantly with
age.
• By some estimates 30% of patients who undergo surgery
annually in the United States have ischemic heart
disease.
• The first manifestations of IHD
– Angina pectoris,
– acute MI,
– sudden death
• cardiac dysrhythmias are probably the major cause of
sudden death in these patients.
Risk factors for development of ischemic heart disease
• Male gender
• Increasing age
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Hypercholesterolemia
Hypertension
Cigarette smoking
Diabetes mellitus
Obesity
Sedentary lifestyle
Genetic factors/family history
• Patients with ischemic heart disease can have
– chronic stable angina
– acute coronary syndrome
at presentation.
ST elevation myocardial
infarction (STEMI)
unstable angina / non–ST
elevation myocardial
infarction (UA/NSTEMI)
coronary blood flow (supply)
oxygen consumption (demand)
The coronary artery circulation normally supplies sufficient
blood flow to meet the demands of the myocardiumin
response to widely varying workloads.
oxygen consumption (demand)
coronary blood flow (supply)
ischemia
 An imbalance between coronary blood flow (supply) and myocardial
oxygen consumption (demand) can precipitate ischemia, which frequently
manifests as angina pectoris.
 Atherosclerosis is the most common cause of impaired coronary
blood flow resulting in angina pectoris.
oxygen consumption (demand)
coronary blood flow (supply)
ischemia
• Stable angina typically develops in the setting of partial occlusion or
significant (>70%) chronic narrowing of a segment of coronary artery.
• An extreme imbalance
CHF
electrical instability with cardiac dysrhythmias
MI
• Angina pectoris reflects intra cardiac release of
– Adenosine
Stmulation of nociceptive &
Mechanosensitive receptores
– bradykinin
slow atrioventricular nodal conduction
and decrease cardiac contractility,
These substances also which
improves the balance between
myocardial oxygen demand and supply.
afferent neurons converge
with the upper five thoracic
sympathetic ganglia and
somatic nerve fibers in the
spinal cord,
ultimately produce thalamic
and cortical stimulation that
results in the typical chest
pain of angina pectoris.
Diagnosis
Angina pectoris is typically described as
retrosternal chest discomfort , pain, pressure, or heaviness.
The chest discomfort often radiates to the
neck, left shoulder, left arm, or jaw
occasionally to the back or down both arms.
Angina may also be perceived as epigastric discomfort
resembling indigestion.
Some patients describe angina as shortness of breath,
mistaking a sense of chest constriction as dyspnea.
The need to take a deep breath, rather than to breathe rapidly,
often identifies shortness of breath as an anginal equivalent.
Angina pectoris usually lasts several minutes and is
crescendo-decrescendo in nature.
A sharp pain that lasts only a few seconds or a dull ache
that lasts for hours is rarely caused by myocardial
ischemia.
Physical exertion, emotional tension, and cold weather
may
induce angina.
Rest and/or nitroglycerin relieve Angina pectoris .
• Chronic stable angina refers to chest pain or discomfort
that does not change appreciably in frequency or severity
over 2 months or longer.
•
Unstable angina, is defined as angina
– At rest,
– Angina of new onset,
– An increase in the severity or frequency of previously
stable angina
without an increase in levels of cardiac biomarkesr.
• Sharp retrosternal pain exacerbated
– deep breathing,
– coughing,
– or change in body position
suggests pericarditis.
• Noncardiac chest pain is often exacerbated by chest wall movement
and is associated with tenderness over the involved area, which is
often a costochondral junction.
• Esophageal spasm can produce severe substernal pressure that may
be confused with angina pectoris and may also be relieved by
administration of nitroglycerin.
ELECTROCARDIOGRAPHY
• During myocardial ischemia, the standard 12-lead ECG
demonstrates
• ST-segment depression (in 50% of patients)
(characteristic of sub endocardial ischemia) that coincides in time
with anginal chest pain.
– This may be accompanied by transient symmetrical T-wave
inversion.
– Patients with chronically inverted T waves ( previous MI)===>
may manifest pseudonormalizationof the T wave during
myocardial ischemia. (return of the T waves to the normal upright position )
• ST elevation
– Variant angina, angina that results from coronary vasospasm
rather than occlusive coronary artery disease
Exercise ECG
• useful for detecting signs of myocardial ischemia & establishing
their relationship to chest pain.
• provides information about exercise capacity.
• The appearance of a new murmur of mitral regurgitation or
a in BP during exercise adds to the diagnostic value of the test.
• Exercise testing is not always feasible
– inability of a patient to exercise
– the presence of conditions that interfere with interpretation of
the exercise ECG ( paced rhythm , LVH , digitalis administration ,
preexcitation syndrome).
• Contraindications to exercise stress testing include :
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severe aortic stenosis,
severe hypertension,
acute myocarditis,
uncontrolled heart failure,
infective endocarditis
• The Exercise ECG is most likely to indicate myocardial ischemia
when there is at least 1 mm of horizontal or down-sloping
ST-segment depression within 4 minutes after exercise.
• The greater the degree of ST-segment depression, The greater
is the likelihood of significant coronary artery disease.
– When the ST-segment abnormality is associated with angina pectoris
and occurs during the early stages of exercise and persists for several
minutes after exercise, significant CAD is very likely.
•
Exercise ECG is less accurate but more cost effective than imaging tests
for detecting ischemic heart disease.
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A negative stress test result does not exclude the presence of
coronary artery disease, but it makes the likelihood 3VD or left main
coronary disease extremely low.
• Exercise ECG is less sensitive and specific in detecting IHD than nuclear
cardiology techniques .
NUCLEAR CARDIOLOGY TECHNIQUES
Nuclear stress imaging is useful for assessing coronary perfusion.
• It can define vascular regions in which stress-induced coronary blood flow is limited
• It can estimate left ventricular systolic size and function.
• Tracers such as thallium & technetium (obstructive lesion ===> less blood flow
===> less tracer activity)
• Exercise perfusion imaging with simultaneous ECG testing
– coronary blood flow increases markedly with exercise except in those
regions distal to a coronary artery obstruction ===> increases the
difference in tracer activity between normal and underperfused
regions
– Imaging is carried out in two phases:
• immediately after cessation of exercise ===> detect regional ischemia,
• 4 hours later ===> reversible ischemia
– Areas of persistently absent uptake signify an old MI.
• The size of the perfusion abnormality is the most important
indicator of the significance of the coronary artery disease
detected.
• Noninvasive imaging tests for the detection of IHD are
usually recommended when
exercise ECG is not possible or interpretation of ST-segment
changes would be difficult (peripheral vascular or
musculoskeletal disease, deconditioning, dyspnea on exertion
due to pulmonary disease, or prior stroke)
– To create cardiac stress ===>
• administration of atropine,
HR
• infusion of dobutamine,
• institution of artificial cardiac pacing
• (Alternative, administering a coronary vasodilator such
as adenosine or dipyridamole.)
ECHOCARDIOGRAPHY
• Wall motion analysis can be performed immediately after
stressing the heart either pharmacologically or with exercise.
• Localizing obstructive coronary lesions stress correspond to sites
of myocardial ischemia ===>New ventricular wall motion abnormalities
• It can visualize global wall motion under baseline conditions
and under cardiac stress. (stress echocardiography)
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Valvular function can be assessed as well.
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Limitations ===> poor visualization
STRESS CARDIAC MAGNETIC RESONANCE IMAGING
• Pharmacologic stress imaging with cardiac MRI compares
favorably with other methods and is being used clinically in
some centers, especially when other modalities cannot be
used effectively.
ELECTRON BEAM COMPUTED TOMOGRAPHY
• Calcium deposition occurs in atherosclerotic vessels.
• Coronary artery calcification can be detected by electron beam
computed tomography.
• High sensitivity but, it is not a very specific test and yields
many false-positive results.
• Its routine use is not recommended.
CORONARY ANGIOGRAPHY
• provides the best information about the condition of
the coronary arteries.
• It is indicated in patients with
– known or possible angina pectoris
– who have survived sudden cardiac death,
– who continue to have angina pectoris despite maximal
medical therapy,
– who are being considered for coronary revascularization
– for the definitive diagnosis of coronary disease for
occupational reasons (e.g., in airline pilots).
– diagnosis of nonatherosclerotic coronary artery disease
such as coronary artery spasm,
• Kawasaki's disease,
• radiation-induced vasculopathy,
• primary coronary artery dissection.
• Among patients with chronic stable angina:
– 25% will have significant single-, double-, or triple-vessel
coronary artery disease,
– 5% to 10% will have left main coronary artery disease,
– 15% will have no flow-limiting obstructions.
• The important prognostic determinants in patients with CAD are
Anatomic extent of the atherosclerotic disease,
– Ejection Fraction of left ventricular
– The stability of the coronary plaque.
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• Left main coronary artery disease is the most dangerous anatomic
lesion and is associated with an unfavorable prognosis when managed
with medical therapy alone.
– ≥50% stenosis of the LM ===> with a mortality rate of 15% per year.
• Vulnerable plaques, which are most likely to rupture and
form an occlusive thrombus, have
– A thin fibrous cap
– A large lipid core containing
– A large number of macrophages.
• The presence of vulnerable plaque predicts a greater risk of
MI regardless of the degree of coronary artery stenosis.
• Acute MI most often results from rupture of a plaque that had
produced less than 50% stenosis of a coronary artery.
Treatment
Comprehensive management of ischemic heart disease has five
aspects:
(1) Identification & treatment of diseases that can precipitate or
worsen ischemia
(2) Reduction of risk factors for coronary artery disease
(3) Lifestyle modification
(4) Pharmacologic management of angina
(5) Revascularization
– coronary artery bypass grafting (CABG)
– percutaneous coronary intervention (PCI) with or without placement
of intracoronary stents.
The goal of treatment of patients with chronic stale angina is to
achieve complete or almost complete elimination of anginal chest
pain and a return to normal activities with minimal side effects.
TREATMENT OF ASSOCIATED DISEASES
• Conditions that increase oxygen demand or decrease oxygen
delivery may contribute to an exacerbation of previously
stable angina or worsen existing angina.
• These conditions include fever, infection, anemia, tachycardia,
thyrotoxicosis, heart failure, and cocaine use.
• Treatment of these conditions is critical to the management
of stable ischemic heart disease.
REDUCTION OF RISK FACTORS AND LIFESTYLE
MODIFICATION
The progression of atherosclerosis may be slowed by
– Cessation of smoking
– Maintenanc of an IBW (low-fat, low-cholesterol diet)
– Regular aerobic exercise
– Rx of Hypertension.
– Lowering the low-density lipoprotein (LDL) cholesterol level
( diet and/or drugs such as statins )
• Drug treatment ===> when the LDL levels ≥130 mg/dL.
• The goal of treatment ===> The LDL < 100 mg/dL.
In Pts with IHD even lower
LDL levels (<70 mg/dL)
• Hypertension
direct vascular injury
LV Hypertrophy
↑the risk of coronary events
↑ myocardial
oxygen demand
Control of HTN to normal levels of BP
↓the risk of MI, congestive heart failure, stroke.
• If LV dysfunction + hypertension ===> ACE inhibitor /an ARB is
recommended.
MEDICAL TREATMENT OF MYOCARDIAL ISCHEMIA
• Antiplatelet drugs, nitrates, β-blockers, calcium channel
blockers, and ACE inhibitors are used in the medical
treatment of angina pectoris.
• Three classes of antiplatelet drugs are widely used in the
management of ischemic heart disease:
1. aspirin
2. Thienopyridines (clopidogrel and prasugrel)
3. platelet glycoprotein IIb/IIIa inhibitors (eptifibatide,
tirofiban, and abciximab).
– Dipyridamole ,affects platelet cyclic adenosine
monophosphate , is not widely used.
– A new class of short-acting, reversible platelet inhibitors
(cangrelor & ticagrelor) is currently under development.
Aspirin inhibits the enzyme cyclooxygenase-1 (COX-1) ===>
inhibition of thromboxane A2 (an important role in platelet
aggregation).
• This inhibition of COX-1 :
– is irreversible
– lasts for the duration of platelet life span (around 7 days)
– can be produced by low dosages of Aspirin.
• Low-dose aspirin therapy (75 to 325 mg/day) is
recommended for all patients with ischemic heart disease.
• Clopidogrel inhibits the adenosine diphosphate (ADP) receptor
P2Y12 (piunergic receptor) and inhibits platelet aggregation in
response to ADP release from activated platelets
• This inhibition of ADP receptors :
– is irreversible
– lasts for the duration of the platelet's life span.
– Seven days after cessation of this drug 80% of platelets will have
recovered normal aggregation function.
• Clopidogrel is a prodrug that is metabolized into an active compound in
the liver.
•
Due to genetic differences in the enzymes that metabolize clopidogrel to the active
drug, significant variability in its activity has been observed.
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Approximately, 10% to 20% of patients taking aspirin & clopidogrel
demonstrate hyporesponsiveness (resistance) or hyperresponsiveness.
• proton pump inhibitors ( PPIs) ===> ↓the effectiveness of clopidogrel.
• Clopidogrel can be used in patients who have a contraindication to or are
intolerant of Aspirin.
Prasugrel also
• inhibits the ADP P2Y12 receptor irreversibly.
• The more predictable pharmacokinetics than clopidogrel
– rapidly absorbed,
– faster onset action,
– less interindividual variability in platelet responses compared with
clopidogrel.
• higher risk of bleeding than clopidogrel
Platelet glycoprotein IIb/IIIa receptor antagonists (abciximab,
eptifibatide, tirofiban)
• inhibit platelet adhesion, activation, and aggregation.
Nitrates
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decrease the frequency, duration, and severity of angina pectoris
increase the amount of exercise required to produce ST-segment depression.
in combination with β-blockers or Ca Channel blockers ===> ↑ The antianginal
effects
dilate coronary arteries and collateral blood vessels ===> improve coronary
blood flow.
decrease PVR ===> ↓ LV afterload & myocardial oxygen consumption.
The venodilating effect ===> ↓ venous return ===> ↓ LV preload &
myocardial oxygen consumption.
Nitrates are contraindicated in the presence of hypertrophic CMP or severe
Aortic Stenosis
Nitrates should not be used within 24 hours of sildenafil, tadalafil, or
vardenafil (may produce severe hypotension)
The most common side effect of nitrate treatment is headache.
– Hypotension may occur in hypovolemic patients.
•
development of tolerance (To avoid nitrate tolerance, a daily 8- to 12-hour
interval free of nitrate exposure is recommended.)
β-Blockers
• They are the principal drug treatment for patients with stable angina
pectoris.
• They have antiischemic, antihypertensive, and antidysrhythmic properties.
• Long-term administration of β-blockers
– ↓ the risk of death
– ↓ re- MI in patients who have had an MI, (even in patients in whom βblockers were traditionally thought to be contraindicated, such as those with
CHF , pulmonary disease, or advanced age)
• β1-adrenergic receptors blocker (atenolol, metoprolol, acebutolol, bisoprolol)
===> ↓HR & ↓ myocardial contractility
↓ in myocardial
oxygen demand
↑ the length of diastole ===> ↑ coronary perfusion time
↓ in ischemic events
during exertion.
• β2-Adrenergic blockers (propranolol, nadolol) can increase the risk of
bronchospasm in patients with reactive airway disease.
• All β-blockers (β1 and β2 ) seem to be equally effective in the treatment of
angina pectoris.
• The most common side effects of β-blocker therapy are fatigue & insomnia.
– Heart failure may be intensified.
• β-Blockers are contraindicated in the presence of :
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severe bradycardia,
sick sinus syndrome,
severe reactive airway disease,
second- or third-degree atrioventricular heart block,
uncontrolled CHF
Diabetes mellitus is not a contraindication to β-blocker therapy, although
these drugs may mask signs of hypoglycemia.
• Abrupt withdrawal of β-blockers after prolonged administration can
worsen ischemia in patients with chronic stable angina.
Calcium channel blockers
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They are uniquely effective in decreasing the frequency and severity of angina
pectoris due to coronary artery spasm (Prinzmetal's or variant angina).
They are not as effective as β-blockers in ↓ the incidence of re-MI.
• The effectiveness of Ca channel blockers is due to:
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decrease vascular smooth muscle tone,
dilate coronary arteries,
decrease myocardial contractility and oxygen consumption,
decrease systemic blood pressure.
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They are potent vasodilators and are useful in treating both HTN & Angina.
(amlodipine, nicardipine, isradipine, felodipine, and longacting nifedipine)
Long-acting Ca channel blockers are comparable to β-blockers in relieving anginal
pain. However, short-acting calcium channel blockers such as Verapamil and
Diltiazem are not.
Common side effects ===> hypotension, peripheral edema & headache.
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Ca channel blockers are contraindicated ===> severe CHF or severe AS
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They must be used cautiously if given in combination with β-blockers (both classes of
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drugs have significant depressant effects on HR & myocardial contractility)
ACE Inhibitors
Excessive Angiotensin II can lead to
• development of
– myocardial hypertrophy
– interstitial myocardial fibrosis
– increased coronary vasoconstriction
– endothelial dysfunction
• promotes inflammatory responses & atheroma formation.
• ACE inhibitors are recommended for patients with
– coronary artery disease, especially with HTN
– left ventricular dysfunction
– diabetes
• Angiotensin Receptor Blockers offer similar benefits.
• Contraindications to ACE inhibitor use include :
– documented intolerance or allergy,
– hyperkalemia,
– bilateral renal artery stenosis, and renal failure.
REVASCULARIZATION
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Revascularization by CABG or PCI with or without placement of intracoronary
stents is indicated
– when optimal medical therapy fails to control angina pectoris.
– Left main coronary artery stenosis > 50%
– ≥70% or greater stenosis in an epicardial coronary artery.
– Significant CAD with Ejection Fraction of <40%
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Extensive myocardial fibrosis from a prior MI is unlikely to be improved by
revascularization.
patients with IHD have chronically impaired myocardial function (hibernating
myocardium) that demonstrates improvement in contractility following surgical
revascularization.
In patients with stable angina pectoris and one- or two-vessel CAD, ===> PCI ± stent
placement, or CABG
CABG is preferred over PCI in patients with :
– significant left main artery disease
– 3VD
– DM patients who have 2/3Vsssel CAD
•
Operative mortality rates for CABG surgery currently range from 1.5% to 2%.
ACUTE CORONARY SYNDROME
• ACS represents a hypercoagulable state.(Focal disruption of an atheromatous
plaque triggers the coagulation cascade ===> generation of thrombin ===> partial
or complete occlusion of the coronary artery by a thrombus)
•
Imbalance of myocardial oxygen supply & demand ===> ischemic chest
pain
Patients with ST Elevation (STEMI)
Patients with ST-segment depression or nonspecific
changes on the ECG ===> levels of cardiac-specific
Troponins or (CK-MB)
UA
NSTEMI
ST Elevation Myocardial Infarction
• The short-term mortality rate of patients with STEMI
– receive aggressive reperfusion therapy ===> about 6.5%.
– not received reperfusion therapy ===> 15% to 20%
– Advanced age ===> ↑ early mortality
•
Nearly all STEMIs are caused by thrombotic occlusion of a coronary artery.
• The long-term prognosis after an Acute MI is determined principally by:
– the severity of residual LV dysfunction,
– the presence and degree of residual ischemia
– the presence of malignant ventricular dysrhythmias.
• Most deaths ===> during the first year & within the first 3 months after
hospital discharge.
• Ventricular function can be substantially improved during the first few
weeks after an acute MI, particularly in patients in whom early reperfusion was
achieved.
• measurement of ventricular function 2 to 3 months after an MI is a more
accurate predictor of long term prognosis
STEMI Pathophysiology
• Atherosclerosis ===> recognized as an inflammatory disease.
– ↑Serum markers of inflammation, such as CRP & fibrinogen,
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Vulnerable plaques (rich lipid cores and thin fibrous caps) ===> rupture ===> A
platelet monolayer forms at the site of ruptured plaque ===> various chemical
mediators (collagen, ADP, Epi, serotonin) ===> stimulate PLT aggregation +
Thromboxane A2 (potent vasoconstrictor ) ===> further compromises
coronary blood flow.
Activated GP IIb/IIIa receptors on the PLTs ===> ↑ the ability of PLTs to
interact with adhesive proteins and other PLTs ===> causes growth and
stabilization of the thrombus ===> activation of coagulation ===>
strengthening of the clot by fibrin deposition ===> more resistant to
thrombolysis.
• plaques that rupture ===> rarely of a size that causes significant coronary
obstruction
• flow-restrictive plaques that produce angina pectoris ===> stimulate
development of collateral circulation ===> less likely to rupture.
DIAGNOSIS
Dx of Acute MI===>the typical ↑ and then ↓in
plasma levels of biochemical markers of
myocardial necrosis in combination with at
least one of the following:
(1) ischemic symptoms,
(2) pathologic Q waves on the ECG,
(3) ECG changes indicative of ischemia (STsegment elevation or depression),
(4) new loss of viable myocardium or new
Regional WMlA
-R/O pulmonary embolism, aortic dissection,
spontaneous PNX pericarditis, cholecystitis
About quarter of patients, especially the elderly
and those with diabetes, have no or only mild
pain at the time of MI.
On physical examination
•anxious, pale, and diaphoretic.
•Sinus tachycardia ( usually ).
•Hypotension or cardiac dysrhythmias
•Rales signal CHF
•ischemic MR
Laboratory Studies
• Troponin (T or I) is a cardiac-specific protein and biochemicalmarker for
acute MI. (3 Hour after MI ↑-----> 7- 10 day)
• Magnitude of the infarction by measuring the cardiac biomarker level
Imaging Studies
• Echocardiography
• Patients with typical ECG evidence of acute MI do not require evaluation
with echocardiography.
• useful in patients with
– LBBB
– an abnormal ECG in whom the diagnosis of acute MI is uncertain
– in patients with suspected aortic dissection.
• Demonstrate RWMA in most patients with acute MI
• Radionuclide imaging
• The time required to perform myocardial perfusion imaging
• Inability to differentiate between new and old MI the
limits utility of
radionuclide
imaging in the
early diagnosis
of acute MI.
TREATMENT
Initial steps of Rx of Acute MI include
• evaluating hemodynamic stability,
• 12-lead ECG,
• oxygen
• Pain relief( ↓catecholamine release )===> IV morphine and/or SL Nitroglycerin
• Aspirin (or clopidogrel for those intolerant of aspirin) ===> ↓further thrombus
formation.
• β-Blockers ===> in Pts with hemodynamically stable condition who are
not in heart failure, in a low cardiac output state, or at risk of cardiogenic
shock. & not given to those with heart block.
• In management of STEMI ===> Reperfusion therapy
coronary angioplasty ± placement of stent (as soon as possible)
Reperfusion Therapy
• Thrombolytic therapy
– SK, tissue plasminogen activator, reteplase, or tenecteplase
– should be initiated within 30 to 60 minutes of hospital arrival, and
within 12 hours of symptom onset.
– The most feared complication ===> ICH
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in elderly patients (>75 years of age)
uncontrolled HTN
GI Bleeding
recently undergone surgery
• Percutaneous Coronary Intervention
– Angioplasty should be performed within 90 minutes of hospital
arrival & within 12 hours of symptom onset.
– It is the modality of choice in patients with
• contraindication to thrombolytic therapy
• severe heart failure and/or pulmonary edema.
• About 5% of patients who undergo immediate PCI require emergency
cardiac surgery
Coronary Artery Bypass Graft Surgery
• Emergency CABG is usually reserved for patients in whom:
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failed angioplasty,
evidence of Post MI VSD or MR
STEMI who develop cardiogenic shock,
LBBB
posterior wall MI within 36 hours of an acute STEMI
• Mortality from CABG is significant during the first 3 to 7 days after
an Acute MI.
Adjunctive Medical Therapy
• IV Heparin therapy is commonly administered for 48 hours after
thrombolytic therapy to decrease the risk of thrombus regeneration.
– Low Molecular- Weight Heparin ===> alternative to unfractionated heparin.
– Bivalirudin (direct thrombin inhibitors ) ===> in patients with a Hx of HIT .
• Administration of β-blockers is associated with a significant decrease
in early (in-hospital) and long-term mortality & Re-MI
– In the absence of specific contraindications ===> as early as possible after
acute MI.
– β-Blocker therapy should be continued indefinitely.
• ACE inhibitors, or ARBs (if they are intolerant of ACEIs) in patients with
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A large anterior wall MI,
Left ventricular failure,
EF < 40%
Diabetes
• Statins have strong immune-modulating effects and should be started as
soon as possible after MI
• Glycemic control
• prophylactic administration of lidocaine or other anti dysrhythmic drugs is
not recommended in the absence of ventricular dysrhythmias, .
•
Calcium channel blockers should not be administered routinely but
should be reserved for patients with persistent myocardial ischemia
despite optimal use of aspirin, β-blockers, nitrates, and heparin.
• Routine administration of Magnesium is not recommended,( unless Tdp
VT)
Unstable Angina/Non–ST Elevation Myocardial Infarction
Pathophysiologic processes may contribute to UA/NSTEMI:
• (1) Nonocclusive thrombosis (rupture or erosion of a coronary plaque )
• (2) Dynamic obstruction due to vasoconstriction (Prinzmetal's variant
angina, cold, cocaine use);
• (3) worsening coronary luminal narrowing due to progressive
atherosclerosis, in-stent restenosis, or narrowing of coronary artery bypass grafts;
• (4) inflammation (vasculitis);
• (5) ↑oxygen demand (sepsis, fever, tachycardia, anemia).===> myocardial
Ischemia
• Most culprit arteries have less than 50% stenosis.
• Embolization of PLTs and clot fragments into the coronary microvasculature
===> microcirculatory ischemia & infarction ===> ↑ cardiac biomarker
levels without elevation of the ST segments on a 12-lead ECG.
DIAGNOSIS
• UA/NSTEMI has three principal presentations:
– Angina at Rest (usually lasting > 20 minutes without anti anginal
medication),
– Change in frequency / intensity of chronic angina pectoris
– New-onset Angina that is severe, prolonged, or disabling.
• Other presentations ===>
– Hemodynamic instability
– CHF (S3 gallop, jugular venous distention, rales, peripheral
edema)
– Acute MR ( ischemia induced papillary muscle dysfunction)
– Significant ECG abnormalities (in 50% of Pts) ===> transient
ST elevation, ST depression, T-wave inversion.
• Elevated levels of cardiac biomarkers establish the diagnosis of
Acute MI.
TREATMENT of U/A & NSTEMI
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↓ myocardial oxygen demand & limiting thrombus formation
– Bed rest, supplemental oxygen, analgesia, and β-blocker (Ca C blockers can
also be used)
– SL or IV TNG ===> improve myocardial oxygen supply.
– Aspirin, clopidogrel, prasugrel & 48 hours of Heparin therapy ===> ↓further
thrombus formation ( GP IIb/IIIa agents are as an alternative)
• Thrombolytic therapy is not indicated in UA/NSTEMI and has been shown
to increase mortality.
• High risk Patients for ↑ mortality include:
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Elderly,
Ischemic symptoms in the preceding 48 hours,
prolonged chest pain (>20 minutes),
Heart failure or hemodynamic instability,
Sustained ventricular dysrhythmias,
PCI within the past 6 months / prior CABG surgery,
↑ Troponin levels,
Angina at low-level activity
– Mild to Mod Renal insufficiency
(creatinine clearance of >30 mL/min)
early invasive
evaluation
coronary angiography &
revascularization
(PCI or CABG)
COMPLICATIONS OF ACUTE MYOCARDIAL INFARCTION
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Cardiac Dysrhythmias
Pericarditis
Mitral Regurgitation
Ventricular Septal Rupture
Congestive Heart Failure and Cardiogenic Shock
Myocardial Rupture
Right Ventricular Infarction
Stroke
Post MI Cardiac Dysrhythmias
.
_VF
_VT
_AF
_A Flutter
_Sinus Bradycardiais
_2/3 AVHB
• Ventricular fibrillation ( VF) ===>
– in 3% to 5% of Pts with acute MI,
– usually during the first 4 hours after the event.
– Rapid defibrillation with 200 to 300 J of energy is necessary
– Prophylactic Lidocaine is not necessary if DC shock can be promptly
accomplished
– Amiodarone ===> one of the most effective antidysrhythmic drugs for
control of ventricular tachydysrhythmias, especially after MI.
– Hypokalemia is a risk factor for VF.
– VF is often fatal ===>with co-existing HOTN and/or CHF
• Ventricular tachycardia (VT) ===>
– Non-sustained VT
• do not predispose a patient to sustained VT or Vf
– Sustained / Hemodynamically significant VT
• must be treated promptly with electrical cardioversion.
– Asymptomatic VT
• can be treated with Intravenous Lidocaine OR Amiodarone.
– Recurrent VT or VF
• Implantation of a cardioverter-defibrillator (ICD)
Atrial Fibrillation & Atrial Flutter
• AF and Atrial flutter are the most common atrial dysrhythmias seen with
acute MI.
• They occur in about 20% of patients.
• Precipitating factors ===>
– hypoxia, acidosis, heart failure, pericarditis, sinus node ischemia
– AF may also result from Atrial ischemia
pressure (as a result of LV dysfunction )
OR from an acute ↑ in LA
• patients who receive thrombolytic therapy ===> ↓incidence of AF
•
If AF is hemodynamically significant, ===> cardioversion is necessary.
•
If AF is well tolerated, ===> β-blockers or Ca C blockers are indicated to
control the ventricular response.
Sinus bradycardia
• common after acute MI, particularly inferior wall MI.
– acute ischemia of the sinus node or AV node.
• Treatment with
– Atropine and/or a temporary cardiac pacemaker (if
hemodynamic compromise from the bradycardia)
Second- or third-degree atrioventricular heart block occurs in:
• about 20% of patients with inferior wall MI.
• Complete heart block requires temporary cardiac pacing.
Pericarditis
• Acute pericarditis is a common complication that occurs 1 to 4 days after
MI in 10% to 15% of patients.
•
It may cause chest pain ===> The pain of pericarditis is pleuritic, gets worse
with inspiration or lying down
• Pericardial friction rub ===> often transient and positional.
• Diffuse ST-segment and T-wave changes ===> on the ECG.
•
Treatment ====> In the absence of a significant pericardial effusion
===> relieving the chest pain.===> Aspirin or Indomethacin
– Corticosteroids can relieve symptoms dramatically but are usually
reserved for refractory cases, ( it is recommended that steroid therapy
be deferred for at least 4 weeks after an Acute MI.
– Dressler's syndrome (post–MI syndrome) ===> pericarditis several
weeks to months after an Acute MI.(may be immune mediated)
Mitral Regurgitation
• Mitral regurgitation due to ischemic injury to the papillary muscles and/or
the ventricular muscle to which the papillary muscles
•
Severe MR is rare and usually results from partial or complete rupture of
a papillary muscle.
• After an Inferior wall MI sever MR is 10 times more likely than Anterior
wall MI.
• Severe Acute MR ===> Pulmonary Edema & Cardiogenic shock.
• Total papillary muscle rupture ===> Death within 24 hours.
• Prompt surgical repair is required.
• Treatments until surgery can be accomplished :
↓ LV afterload & ↑coronary perfusion ===> IABP or Nitroprusside IV
===> ↓ the regurgitant volume and ↑ forward flow & cardiac output.
Ventricular Septal Rupture
• VSD is more likely after Anterior wall MI rather than inferior wall MI.
• The characteristic holosystolic murmur (may be difficult to distinguish from the
murmur of severe MR)
•
The Diagnosis ===> by Echocardiography.
• As soon as the Dx of ventricular septal rupture ===> IABP
•
•
Emergency surgical repair ===> VSD with Hemodynamic compromise.
The mortality rate associated with surgical repair of a post-MI VSD is
about 20%.
• In Hemodynamically stable condition ===> It is better to wait at least 1
week before surgical repair is undertaken
• If the defect is left untreated, mortality approaches 90%.
Congestive Heart Failure and Cardiogenic Shock
Cardiogenic shock ===>
• this term restricted to Acute heart failure in which the cardiac output is
insufficient to maintain adequate perfusion of the brain, kidneys, and
other vital organs. ===> Hypotension and oliguria persist after relief
of anginal pain, abatement of excess sympathetic nervous system
activity, correction of hypovolemia, and treatment of dysrhythmias.
• ↓Systolic BP, ± pulmonary edema & arterial
hypoxemia.
• Cardiogenic shock is usually a manifestation of infarction of more than
40% of the left ventricular myocardium.
• Mortality of cardiogenic shock >50%. (In the setting of an acute MI,)
• Management of cardiogenic shock ===> Diagnosis + prompt treatment of
potentially reversible mechanical complications of MI.
– These include (1) rupture of the LV free wall, septum, or papillary muscles;
(2) cardiac tamponade;
(3) acute, severe MR
• Echocardiography is extremely helpful in diagnosing and
quantifying these pathologic conditions.
• Treatment of cardiogenic shock
– Norepinephrine, Vasopressin, Dopamine, Dobutamine ===> to
improve BP and cardiac output.
– If the BP is adequate, ===> Nitroglycerin can be used
– Concomitant Pulmonary Edema ===> Morphine, Diuretics,
mechanical ventilation.
– Thrombolytic therapy, PCI, or surgical revascularization may be
indicated.
– Circulatory assist devices can help sustain viable myocardium and support
cardiac output until revascularization can be performed. ===> LV assist devices
improve cardiac output much more than IABP
– Infusion of a combination of inotropic & vasodilator drugs
may serve as a pharmacologic alternative to mechanical
counterpulsation
Myocardial Rupture
• Myocardial rupture usually causes acute cardiac tamponade.
• This typically occurs within the first week after an MI and presents with
sudden hemodynamic collapse or sudden death.
• In an extremely small percentage of cases, it is possible to have time for
medical stabilization and emergency surgery
Right Ventricular Infarction
• RV infarction occurs in about 1/3 of patients with Acute inferior wall MI.
•
The RV has a more favorable oxygen supply/demand ratio than the left ventricle (smaller muscle
mass and its improved oxygen delivery, which results from delivery of CBF during both systole &
diastole.)
•
The pathognomonic clinical triad of RV infarction:
•
•
•
•
•
HOTN ,↑JVP , clear lung fields in a patient with an inferior wall MI
Kussmaul's sign (distention of the jugular vein on inspiration) is often seen.
Echocardiography ===> RV dilation, RV asynergy, abnormal interventricular septal motion
Treatments for LV failure may worsen RV failure. (vasodilators & diuretics are very
undesirable.)
Initial therapy for right ventricular failure consists of ;
– Intravenous fluids.
If HOTN persists,===> inotropic support, with or without IABP
Complication of RV infarction:
– Cardiogenic shock, ===> uncommon, but it is the most serious complication
– About 1/3 of patients ===> AF.
– Heart block ===> 50% of these Pts (3 ed AVHB ===> temporary A-V sequential
pacing, (the value of atrioventricular synchrony in maintaining ventricular filling in the ischemic, and
noncompliant, RV.)
Stroke
•
The possibility of an ischemic stroke are very significant ===> In about 1/3 of
patients with Anterior wall & Apex MI of the Left Ventricle results in
thrombus formation
• Echocardiography is used to detect a left ventricular thrombus.
•
The presence of LV thrombus is an indication for immediate anticoagulation
with Heparin & then warfarin. for 6 months
• Thrombolytic therapy is associated with hemorrhagic stroke in 0.3% to 1%
of patients. The stroke is usually evident within the first 24 hours after
treatment and is associated with a high mortality rate.
PERIOPERATIVE IMPLICATIONS OF PERCUTANEOUS
CORONARY INTERVENTION
• Percutaneous coronary angioplasty (PTCA) was introduced as an
alternative to CABG to mechanically open stenosed coronary
arteries.
• It was effective, but restenosis of the angioplast site occurred in
15% to 60% of patients. ===> Bare metal stents were introduced.
• coronary restenosis due to neointimal hyperplasia was observed in
10% to 30% of patients with Bare metal stents.
• Stents coated with drugs (drug-eluting stents) were then
introduced to reduce neointimal hyperplasiaand subsequent
stenosis.
• The drugs in these stents prevent cell division and hence reduce
neointimal hyperplasia.
Percutaneous Coronary Intervention and Thrombosis
•
Mechanically opening a blood vessel by angiography causes vessel injury, especially
destruction of the endothelium. ===>prone to thrombosis.
• Reendothelialization after
Balloon angioplasty ===> about 2 to 3 weeks
After bare metal stent placement, ===> up to 12 weeks
After Drug-eluting stent ===> even after 1 year may not be
completely endothelialized
• Thus, thrombosis after angioplasty and stent placement is a major concern.
• Stent thrombosis ===>
–
–
–
–
•
Acute (within 24 hours),
Subacute (between 2 and 30 days),
Late (between 30 days and a year),
Very late (after a year)
Early stent thrombosis ===> mechanical in origin
and due to coronary artery dissection or under expansion of the stent
• Late stent thrombosis ===>
Stent malposition , Abnormal reendothelialization , Hypersensitivity.
• Dual antiplatelet therapy (aspirin with clopidogrel) is better in preventing
stent thrombosis compared with aspirin alone.
• Clopidogrel discontinuation is the most significant independent predictor
of stent thrombosis
• Current recommendations for Dual antiplatelet therapy :
– at least 2 weeks after balloon angioplasty without stenting,
– at least 6 weeks after bare metal stent placement,
– at least 1 year after drug-eluting stent placement.
• Patients at risk for stent thrombosis include:
Pts with acute coronary syndrome, low ejection fraction, diabetes, renal
impairment, advanced age, cancer.
• Elective surgery and emergency surgery both increase the risk of stent
thrombosis because of the prothrombotic state during the perioperative
period.
Surgery and Risk of Stent Thrombosis
The frequency of major adverse cardiovascular events (death,MI, stent
thrombosis, or the need for repeat revascularization) after noncardiac
surgery
– within 4 weeks of PCI===> 10.5%.
– between 31 and 90 days after PCI ===> 3.8%
– >90 days after PCI ===> 2.8%
– within 6 weeks of bare Metal stent placement ===> 5% to 30%
– within 1 year of Drug-eluting stent placement ===> > 30% (is higher
after placement of a Drug-eluting stent)
• emergency surgery ===> Higher risk of adverse events
– bare metal stents, >>> 3 fold ↑ in adverse events.
– drug-eluting stents, >>>> 3.5-fold ↑ in adverse events.
Risk of Bleeding with Antiplatelet Agents
• The risk of spontaneous bleeding increases in patients who are receiving
antiplatelet agents.
• The risk of bleeding:
– continuing Aspirin therapy ===> ↑ the risk of bleeding by a factor of
1.5, but the severity of adverse events is not increased.
– Clopidogrel ===> in non-cardiac surgery risk of bleeding has not been
extensively studied.
– Clopidogrel + Aspirin ===> ↑ the relative risk of bleeding by 50%.
• So far no increase in mortality has been noted except for intracranial
surgery.
Bleeding Vs Stent Thrombosis in the Peri-op Period
•
Discontinuing antiplatelet therapy causes a significant increase in coronary,
cerebrovascular, and peripheral vascular events.
1. In situations the risk of coronary thrombosis is high & the consequence of
thrombosis could be catastrophic; &, although the risk of bleeding is increased,
bleeding could be manageable & does not contribute to significant morbidity
and mortality ===> may be prudent to continue antiplatelet therapy.
2. individuals are more prone to bleeding or need to undergo procedures in
which bleeding can have severe consequences.
–
These include neurosurgery, spinal cord decompression, aortic aneurysm
surgery, prostatectomy
– The risk of bleeding > the risk of thrombosis ===> antiplatelet therapy should
be stopped before these operations (at least 5 to 7 days before surgery for
clopidogrel) and resumed as soon as feasible postoperatively.
3.
Antiplatelet therapy for secondary prevention of cardiovascular events.
– These Pts have no stents ===> risk of bleeding > risk of cardiovascular events.
– Antiplatelet drugs can be temporarily withheld for high-risk surgery.
Management of Patients with Stents
CONTINUATION OF DUAL ANTIPLATELET THERAPY
•
Dual antiplatelet therapy should be continued for at least
– 6 weeks in patients with bare metal stents
– 1 year in patients with drug-eluting stents.
•
•
•
If dual antiplatelet therapy needs to be stopped, at least aspirin therapy
should be continued.
Aspirin should be stopped before elective surgery only when absolutely
indicated.
In a bleeding patient, platelets can be administered to counteract the effects
of antiplatelet drugs,
– effectiveness of the platelet infusions will depend on the timing of the last
dose of clopidogrel.
– Platelet transfusions can be administered as soon as 4 hours after
•
discontinuation of clopidogrel, but they will be most effective 24 hours
after the last dose of clopidogrel.
Intraoperative continuous ECG monitoring with ST analysis is very helpful
monitoring ===> Any angina in a patient with a stent ===>should prompt R/O
acute MI===>urgent cardiology evaluation
ANESTHETIC TECHNIQUE
Use of Neuraxial anesthetic
techniques
•The American Society of
Regional Anesthesia and
the European Society of
Anaesthesiologists have
adopted a conservative
approach in this matter.
•Use of neuraxial blockade
is not encouraged in
patients who are receiving
dual antiplatelet therapy.
IMMEDIATE AVAILABILITY OF AN INTERVENTIONAL
CARDIOLOGIST
• Any angina in a patient with a stent should prompt evaluation to rule out
acute MI, and an urgent cardiology evaluation should be sought.
• Once the diagnosis of acute MI or acute stent thrombosis is made or
considered, triage to interventional cardiology within 90 minutes is
strongly recommended.
• Ambulatory surgical facilities, endoscopy suites, and other non–hospitalbased operating locations without these resources on site should develop
a relationship with interventional cardiologists that can facilitate rapid
transfer if needed.
PERIOPERATIVE MYOCARDIAL INFARCTION
• The risk of peri-op death due to cardiac causes is <1% in patients without
IHD
• The incidence of perioperative MI :
– Elective High-risk vascular surgery ===> 5% -15%. (even higher for
emergency surgery)
– Urgent hip surgery ===> 5% - 7%
– Elective total hip or knee arthroplasty ===> <3%
• Perioperative MIs ===> 20% mortality.
• The most perioperative MIs occur in the first 24 to 48 hours after surgery.
• Many post-op MIs are NSTEMIs ===>
– Can be diagnosed by release of cardiac biomarkers and/or ECG changes.
– These MIs are usually preceded by tachycardia and ST depression and are
often silent.
Factors that can contribute to perioperative MI
Diagnosis
• In the peri-op period, ischemic episodes often are not associated with
chest pain.
• Many post-op ECGs are non diagnostic. (newonset dysrhythmias)
• An acute increase in troponin levels should be considered to indicate MI in
the peri-operative setting.
• There is a significant association between increased troponin levels and
short- and long-term morbidity and mortality in surgical patients.
• An increase in troponin level postoperatively, even in the absence of clear
cardiovascular signs and symptoms, is an important finding that requires
careful attention and referral to a cardiologist for further evaluation and
management.
PREOPERATIVE ASSESSMENT OF PATIENTS WITH
Known OR Suspected IHD
History
•
•
It should focus on determining the presence of major, intermediate, minor clinical
risk factors (next slide)
Angina and dyspnea may be absent at rest ===> Evaluating the patient's response
to physical activities (walking or climbing stairs).
– Limited exercise tolerance in the absence of significant lung disease ===>
↓ cardiac reserve.
– Climbing two to three flights of stairs without symptoms, ===> it is likely
that cardiac reserve is adequate.
• Dyspnea after the onset of angina pectoris ===> Acute LV dysfunction
caused by myocardial ischemia.
• Silent myocardial ischemia usually occurs at a HR & BP < exercise-induced
ischemia.
–¾ of ischemic episodes ===> without angina pectoris
– 10% to 15% of acute Mis ===> silent
overt
CHF
stresses of
anesthesia,
surgery, fluid
replacement,
post-op pain
• The highest risk of myocardial ischemia ,re-MI , cardiac death
It is common practice to delay
during the peri-op period:
–
Acute MI (1 to 7 days previously)
– Recent MI (8 to 30 days previously)
– Unstable angina
elective surgery for at least 30 days
following MI.
• It is prudent to delay Elective non cardiac surgery for:
– 6 weeks after PCI with bare metal stent placement
– 12 months after drug-eluting stent placement.
– 6 weeks after coronary bypass surgery
• Aortic Stenosis ===>2-3 fold ↑ risk of peri-op cardiac morbidity & mortality.
• Renal insufficiency (creatinine >2.0 mg/dL) ↑ risk of peri-op cardiac events.
MANAGEMENT OF ANESTHESIA
IN PATIENTS WITH Known OR Suspected IHD
undergoing NONCARDIAC SURGERY
Risk Stratification
Lee Revised Cardiac Risk Index ===>
• In patients with stable condition undergoing Elective Major noncardiac
surgery,
• Predictors of Major cardiac complications (cardiac death, cardia carrest or
ventricular fibrillation, complete heart block, acute MI, pulmonary edema)
1. High-risk surgery
2. Hx of ischemic heart disease
3. Hx of congestive heart failure
4. Hx of cerebrovascular disease
5. Preoperative insulin-dependent DM
6. Preoperative serum Cr > 2.0 mg/dL.
• The higher the number of risk factors present, the greater the probability of
perioperative cardiac complications
• These risk factors have been incorporated into the ACC/AHA guidelines for
perioperative cardiovascular evaluation for noncardiac surgery.
Risk Stratification
• An intervention is indicated or not indicated irrespective of the need for
surgery.
• Pre-op testing should be performed only if it the result is likely to
influence Peri-op management.
• The ACC/AHA guidelines provide a multistep algorithm for determining the
need for preoperative cardiac evaluation.
• The first step ===> assesses the urgency of the surgery.
• Subsequent steps
Clinical risk factors ===> from the Hx , Ph Ex, review of the ECG
(1) Major clinical risk factors
(2) Moderate clinical risk factors
(3) Minor clinical risk factors
The surgery-specific risk factors graded as :
– High
−Intermediate
− Low
Risk Stratification
(1) Major clinical risk factors
U/A , decompensated HF, significant dysrhythmias, severe VHD ===> may
require delay of elective surgery & cardiologic evaluation ===> if urgent or
emergent surgery ===> Intensive pre-op management is necessary
(2) Moderate clinical risk factors
stable angina pectoris, previous MI (by Hx or pathologic Q waves), compensated
or previous HF, IDDM, renal insufficiency ===>
well-validated markers of ↑risk of peri-op cardiac complications
(3) Minor clinical risk factors
HTN, LBBB, nonspecific ST-T wave changes, Hx of stroke ===> markers of
CAD that have not been proven to independently ↑ peri-op cardiac risk.
• Functional capacity/exercise tolerance ===> expressed in metabolic
equivalent of the task (MET) units.
• The O2 consumption of a 70-kg, 40-yrs man in a resting state is
3.5 mL/kg/min or 1 MET
• Patients <4-MET demand during normal daily activities ===> ↑Peri-op
cardiac risk
• These individuals may be able to perform some activities, such as baking,
slow ballroom dancing, golfing (riding in a cart), or walking at a speed of
approximately 2 to 3 mph, but are unable to perform more strenuous
activity without developing chest pain or significant shortness of breath.
• The surgery-specific risk of noncardiac surgical procedures is graded as
– High
– Intermediate
– Low
High-risk surgery ===> cardiac risk > 5%.
– Emergency major surgery
– Aortic and other major vascular surgery
– Peripheral vascular surgery
– Prolonged surgery associated with large fluid shifts and/or blood loss
Intermediate-risk surgery ===> cardiac risk < 5%.
–
–
–
–
–
–
Endovascular aortic surgery
CEA
Head & Neck surgery
Intraperitoneal & Intrathoracic surgery
Orthopedic surgery
Prostate surgery
Low-risk procedures ===> cardiac risk < 1%
–
–
–
–
–
endoscopic surgery
superficial surgery
cataract surgery
breast surgery
ambulatory surgery
Patients require cardiology consultation, workup, &
optimization of care before Elective surgery
• Major clinical risk factors
• Elective High-risk surgery & low exercise tolerance & ≥ 3 Moderate clinical
risk factors
• Intermediate-risk surgery & low exercise tolerance & ≥ 3 Moderate clinical
risk factors
• Intermediate-risk surgery & low exercise tolerance & 1-2 Moderate
clinical risk factors ===> may be considered for further evaluation if it will
affect perioperative management
• Nuclear imaging can better detect myocardium at risk.
• Preoperative coronary angiography is most suitable in a patient with a
positive stress test result.
• In nonoperative settings,
– treatment strategies such as PCI (± stenting), CABG surgery, and
medical therapy have proven efficacious in improving long-term
morbidity and mortality.
• Patients with significant IHD who come for noncardiac surgery
– candidates for one or more of these therapies (PCI ,CABG) regardless
of their need for surgery
– Optimal medical management can improve peri-op outcomes.
– Coronary intervention should be guided by the patient's cardiac
condition and by the potential consequences of delaying surgery for
recovery from the revascularization
• The indications for pre-op surgical coronary revascularization are the same
as those in the nonoperative setting.
• In view of the serious limitations of current PCIs and lack of utility of
CABG and PCI in patients with stable coronary artery disease, very few
patients with stable coronary artery disease will undergo revascularization
before surgery.
Pharmacological Rx
– patients with stable CAD and/or risk factors for CAD
– patients with significant IHD & Emergent or urgent surgery.
• Nitroglycerin ===> for Active peri-op ischemia. (prophylactic use of TNG has
•
not been shown to be efficacious)
β-blockers ===> ↓peri-op cardiac morbidity &mortality in high-risk patients
undergoing vascular surgery.
– continue β-blocker use in patients who are already receiving β-blockers.
– vascular surgery & multiple risk factors ===> pre-op β-blockers
– β-blockers should be initiated at least a week before elective surgery, for
prophylactic purposes & acute administration of high-dose β-blockers in
high-risk populations is not recommended(European & the AHA guidelines)
– longer-acting β-blockers ( Atenolol or Bisoprolol) may be more
efficacious
•
•
•
•
Statins ===>1 to 4 weeks before High-risk surgery & be continued peri-op
α2-Agonists ===> in patients who cannot tolerate β-blockers.
Glycemic Control ===> peri-op glucose level <180 mg/dL.
Pre-op anxiety reduction
Intraoperative Management
• The basic challenges during induction and maintenance of anesthesia in
patients with IHD are :
– (1) prevent myocardial ischemia (optimizing myocardial oxygen supply & ↓
myocardial oxygen demand)
•
•
•
•
– (2) monitor for ischemia,
– (3) treat ischemia if it develops.
Hyperventilation must be avoided (hypocapnia may cause coronary artery
vasoconstriction)
Maintenance of the balance between myocardial oxygen supply and
demand is more important than which specific anesthetic technique or
drugs are selected to produce anesthesia and muscle relaxation.
Isoflurane may decrease coronary vascular resistance, predisposing to
coronary steal syndrome, there is no evidence that this drug increases the
incidence of intra-op myocardial ischemia.
To keep the HR & BP within 20% of the normal awake value for that patient
INDUCTION OF ANESTHESIA
• Ketamine is not a likely choice, because the associated increase in heart
rate and blood pressure transiently increases myocardial oxygen
requirements.
• Muscle relaxant ===> by administration of Sux or NDMR for intubation
• Short duration of direct laryngoscopy (≤15 seconds) is useful in minimizing
the magnitude and duration of the circulatory changes associated with tracheal
intubation.
–
–
–
–
–
Laryngo tracheal lidocaine,
Intravenous lidocaine,
Esmolol,
fentanyl,
Dexmedetomidine
have all been shown to be useful
for blunting the increase in heart
rate evoked by tracheal intubation.
MAINTENANCE OF ANESTHESIA
• Volatile anesthetics
• may be beneficial in patients with IHD
– ↓ myocardial oxygen requirements
– precondition the myocardium to tolerate ischemic
events,
• may be detrimental because they lead to a ↓ in BP ===> ↓
coronary perfusion pressure.
• The AHA guidelines ===> can be beneficial to use volatile
anesthetic agents during noncardiac surgery ,in patients in
hemodynamically stable condition at risk for myocardial
ischemia.
• Nitrous oxide ===> may have harmful effects (↑in PVR , ↑ diastolic
dysfunction)
• Patients with severely impaired LV function
– Opioids ( ± N2o, BDZ , a low-dose VA )
MAINTENANCE OF ANESTHESIA
• Regional anesthesia is an acceptable technique in patients with IHD
(Prompt treatment of HOTN that exceeds 20% of the pre block BP is
necessary)
– benefits include ===> excellent pain control, ↓ incidence of DVT
– incidence of peri-op cardiac morbidity & mortality does not appear to
be significantly different for GA & RA .
• Muscle relaxants with minimal or no effect on HR and systemic BP
pressure (vecuronium , rocuronium, cisatracurium) are attractive choices
for patients with IHD.
• Reversal of neuromuscular blockade (anticholinesterase + anticholinergic
===> safe in patients with IHD (glycopyrrolate ===> is preferred )
MONITORING
Type of perioperative monitoring is influenced by
– the complexityof the operative procedure
– the severity of the IHD
• The simplest, most cost-effective method for detecting peri-op myocardial
ischemia is Electrocardiography
• Dx of myocardial ischemia ===> focuses on changes in the ST segment
(elevation or depression of at least 1 mm and T-wave inversions)
• The degree of ST-segment depression parallels the severity of myocardial
ischemia .
– monitoring of two leads (leads II and V5) has been the standard
– monitoring three leads (leads II, V4, and V5, or V3, V4, and V5)
improves the ability to detect ischemia.
• Other causes of ST segment abnormalities include:
– Cardiac dysrhythmias
– Digitalis therapy
– Hypothermia
− Cardiac conduction disturbances
− Electrolyte abnormalities
• The occurrence & duration of intra-op ST-segment changes
in high-risk patients ===> ↑incidence of peri-op MI and
adverse cardiac events.
• pulmonary artery catheter is a relatively insensitive method of
monitoring for myocardial ischemia.
Other manifestation of Intra-op myocardial ischemia:
• ↑acute PAOP (due to changes in LV compliance & LV systolic performance)
– V waves PAOP tracing (if global myocardial ischemia or papillary muscle
involvement)
• The development of new regional ventricular wall motion abnormalities
INTRAOPERATIVE MANAGEMENT OF MYOCARDIAL ISCHEMIA
• Treatment of myocardial ischemia should be instituted when there are 1mm ST-segment changes on the ECG.
• Nitroglycerin
• β-blocker (esmolol) ===> ↑ HR & normal or high BP
• Hypotension ===> sympathomimetic drugs & fluid infusion
• In an unstable hemodynamic situation, circulatory support with inotropes
or an IABP may be necessary.
• It may also be necessary to plan for early postoperative cardiac
catheterization.
POSTOPERATIVE PERIOD
• Avoiding of shivering on awakening, (leading to abrupt and dramatic
increases in myocardial oxygen requirements)
• Pain, hypoxemia, hypercarbia, sepsis, hemorrhage ===> increased
myocardial oxygen demand ===> oxygen supply/demand imbalance ===>
precipitate myocardial ischemia, infarction, or death
• Most adverse cardiac events occur within the first 48 hours post-op
• Delayed cardiac events ===> within the first 30 days and can be the result
of secondary stresses.
• Prevention of hypovolemia & HOTN is necessary postoperatively, (with
adequate intravascular volume & adequate Hb concentration )
• Early extubation is possible and desirable in many patients as long as they
fulfill the criteria for extubation.
• Continuous ECG monitoring (post-op myocardial ischemia is often silent)
Reference :
Stoelting's Anesthesia and Co-existing Disease,
6th Edn.