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Coronary Artery Disease

Patients with coronary artery disease (CAD) are often


identified during the history and physical
examination. When identified preoperatively, CAD
should prompt risk stratification following the
ACC/AHA algorithm. Patients with acute coronary
syndromes should not undergo noncardiac surgery.
Tests to consider include:
■ Chest radiograph to evaluate for cardiomegaly,
pulmonary edema, or pleural effusion.
■ ECG to evaluate for left ventricular hypertrophy,
ST segment changes, inverted T waves, Q waves, and
arrhythmias.
■ Transthoracic Doppler echocardiography for wall
motion abnormalities, ejection fraction, and chamber
pressures.
■ Stress test to assess for functional cardiac ischemia.
This can be combined with echocardiography.
■ Perfusion nuclear imaging to assess cardiac
perfusion at
rest and with function.
■ Cardiac angiography.
Asymptomatic patients with CAD may, however,
develop
symptoms in the perioperative period. Risk factors for
CAD are DM, HTN, smoking, hypercholesterolemia,
and a family history. CAD may result in stable angina
or one of the acutecoronary syndromes (ACSs). Stable
angina often presents with precordial pain radiating to
the left arm, neck, and jaw upon exertion. It is relieved
by rest or the use of sublingual nitroglycerin. ACSs
include unstable angina, non–STelevated MI, and ST-
elevated MI. Symptoms are similar to stable angina
but occur with less exertion than is usual, or at rest,
and do not abate with further rest. The history
surrounding the onset of chest pain has a diagnostic
sensitivity of 90% when the symptoms are classic. An
ECG may show ST segment depression or inverted T
waves indicating ischemia. ST
segment elevation indicates frank MI. The treatment
of any patient suspected of having ACS begins with
the correct diagnosis. The diagnosis can be confirmed
with:
■ A 12-lead ECG (ST elevation, inverted T waves, Q
waves).
■ Cardiac enzymes (CK-MB [MB isoenzyme of
creatine
kinase], troponins).
The initial treatment should include a standardized
approach to reduce morbidity and mortality. All of the
following should be instituted concurrently:
■ Oxygen via facemask.
■ Nitrates administered sublingually (or
intravenously).
■ Morphine for pain and to decrease sympathetic
output.
■ Aspirin 325 mg administered sublingually.
Additional treatment may include intravenous heparin
and/or platelet glycoprotein IIa/IIIb antagonists to
impair clotting and beta blockers to decrease
myocardial oxygen demand.
Definitive treatment may include the administration of
thrombolytic agents, percutaneous angioplasty with
stenting, or coronary artery bypass grafting.
The use of perioperative beta blockers has been shown
to
reduce the likelihood of cardiac events including MI.
Patients with a recent MI may be at risk for re-
infarction following the initial infarct. This has led to
the historical suggestion of avoiding elective surgery
for a period of 6 months. The current management of
MI has radically changed since the early 1990s and,
given the number of possible cardiac interventions
after an MI, the risk of re-infarction may be much less
than was originally thought. This may allow elective
surgery to be performed within a much shorter period
of time after an infarction, perhaps after only 6 weeks.
NEW TOPIC
Ischemic Heart Disease (IHD)
• Disease process secondary to stenotic coronary
arteries that leads to ischemic sequelae
from a myocardial oxygen supply and demand
imbalance.
• Myocardial oxygen is dependent on oxygen
supply and coronary blood flow. Myocardial
oxygen demand is determined by wall stress,
heart rate and contractility. Consequences of IHD
Stable Angina Transient chest discomfort due
to a fixed atheromatous plaque secondary to a
myocardial oxygen supply and demand
imbalance.
• Symptoms include dyspnea on exertion,
retrosternal chest pain that may radiate to the
arm or jaw. Patients will often describe the
symptoms as a pressure or an elephant sitting
on their chest. Patients may place a clenched
fist over the sternum (Levine’s sign). Symptoms
normally appear when a vessel is at least 70%
stenotic. The symptoms normally cease after
5–10 minutes with rest.
• Diagnostic workup – EKG may show ST
depression or T wave inversion. Stress testing
is done (bike, treadmill, or pharmacologic) to
assess cardiac reserve. Pharmacologic testing
may be carried out with dipyridamole thallium
in persons unable to exercise. Echocardiogram
is used to assess wall function, ejection fraction, and
valvular function. Coronary angiography is used to
assess stenotic coronary arteries (gold standard).
Acute Coronary Syndrome Disease processes
along a continuum secondary to a ruptured
atherosclerotic plaque with subsequent formation of
a thrombus within the coronary vessel.
• Unstable angina – occurs secondary to a coronary
thrombus that is partially occlusive.
Patients have chest pain that is not relieved by
rest. Can see signs of ischemic changes on an
EKG with negative cardiac enzymes.
• Non-ST segment elevation MI – due to partially
occlusive thrombus that results in a subendocardial
infarction. Patients present with chest pain, nausea,
dyspnea, and diaphoresis. EKG shows ST depression
or T wave inversion. Will see elevated serum
biomarkers such as troponins and CK-MB. (CK-MB is
used to assess for early reinfarction due to its shorter
half-life in comparison to troponins.)
• ST segment elevation MI – due to an occlusive
thrombus that results in a transmural infarct.
Will see ST segment elevations and serum biomarkers.
Symptoms similar to NSTEMI.
Complications of MI (STEMI or NSTEMI) –
may lead to fatal arrhythmias, conductions blocks,
cardiogenic shock, ventricular wall rupture, and
heart failure.
Treatment of IHD
• Nitrates – cause venodilation, which decreases
preload (determinant of wall stress) and dilates
coronary arteries.
• Beta-blockers and calcium channel blockers –
decrease oxygen demand by decreasing heart
rate and contractility.
• Ranolazine – inhibits sodium channels in
myocardial cells, which leads to less intracellular
calcium and decreased contractility.
• Percutaneous coronary intervention – balloontipped
catheter is placed in a peripheral artery
and maneuvered into the stenotic coronary
vessel. A bare metal or drug eluting stent iis
then deployed to increase the patency of the
coronary vessel. Patients are placed on antiplatelet
drugs to decrease coronary thrombosis, as the stents
are thrombogenic (drug-eluting
stents are more thrombotic than bare metal
stents). Drug-eluting stents decrease the rate of
epithelialization.
• Coronary artery bypass grafting (CABG) –
grafting done to bypass obstructive coronary
vessels. Preferred for multivessel disease. Treatment of
MI
• Morphine – used for analgesia and
anxiolysis.
• Oxygen – increases oxygen supply to the
myocardium.
• Nitrates – improve coronary flow.
• Aspirin – decreases platelet aggregationBeta-
blockers – decrease myocardial oxygen
demand.
• Transfer to hospital (remember time is myocardium)
for PCI with stent deployment or
fibrinolytic therapy if the hospital does not
have interventional cardiology capabilitiesA

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