Ischemic heart disease: Angina pectoris, acute MI and sudden death are often the 1st

manifestations of this dease.

a. Risk factors for ischemic heart disease:
i. Male gender
ii. Increasing age
II.
Stable myocardial ischemia (ANGINA PECTORIS): occurs when there is a mistmacthch of
O2 delivered to the myocardium (supply) and myocardial oxygen consumption (demand).
When this becomes bad CHF, MI or dysrhythmias happen.
a. s/s described as retrosternal chest pain pressure that radiates somewhere.
b. Diagnosis:
i. ECG:
1. SUB ENDOCARDIAL ISCHEMIA= ST depression.
2. Variant angina (angina that results from coronary vasospasm) = ST
elevation during angial pain.
3. T-wave inversion
4. pseudonormalization= T waves go back to normal.
ii. Electrocardiography
iii. Nuclear cardiology techniques
iv. Echocardiography
v. Stress cardiac magnetic resonance imaging
vi. Electron beam computed tomography
vii. Coronary angiography
c. Treatment:
i. LIFE STYLE MODIFICATION.
1. Stop smoking
2. Work out
3. LDL <100
ACUTE CORONARY SYNDROMES: hypervoagulable state because plaque is released. And is a
partial or complete obstruction.
STEMI: St elevations
NSTEMI: ST depressions with + biomarkers.
UA: with ST depressions with biomarkers.
III.
STEMI: Occurs when BF decreases due to a clot after a plaque ruptures.
a. Plaque ruptures and creates and clot environment with collagen, ADP, epi, to
accumulate platelet aggregation, vasoconstriction occurs and thromboxane A2 is
released
b. Diagnosis:
i. Ischemic symptoms
ii. Q waves
iii. ECG changes indicating ST elevation or depression
iv. Imaging evidence of a new loss of viable myocardium or new regional wall
motion abnormality.
v. LABORATORY:
1. Trops rise within 3 hours after MI and remain elevated for 7 to 10 days.
vi. TX:
1. MONAB
2. 30-60 minutes TPA
3. within 90 minutes coronary angioplasty
IV.
UNSTABLE/NSTEMI: angina at rest and feels worse than ur previous stable angina.
a. s/s : presents in 3 days: angina at rest lasting for more than 20 minutes
b. chronic angina pectoris that becomes more frequent and more easilty provoked,
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VIII.

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X.

i. new-onset angina that is severe, prolonged or disabling.

ii. *****sharp retrosternal pain exacerbated by deep breathing, coughing, or
chang in body position suggests pericarditis.
c. TX: is the same MONAB
COMPLICATIONS OF MI
a. Dysrhthymia
b. Pericarditis
c. Mitral regurgitation (PAP muscle rupture) treat quick
PERIOPERATIVE IMPLICATIONS OF PERCUTATNEOUS CORONARY INTERVENTION:
a. PCI includes percutaneous transluminal coronary angioplasty (PTCA) wit and
without placement of a coronary stent.
b. Two types of stents: pt at risk of thrombosis
i. Bare metal stent: 12 weeks after BMS risk for clot
1. Wait for 6 weeks and preferably 90 days after stent placemnt
ii. Drugeluciting stent: >1 year risk for clot formation
1. Wait for electevice sx for at least a year
c. STOP CLOPIDOGREL 7-10 days befpre sx
PERIOPERATIVE MI: occur 24-48 hours after surgery
a. Because of increased myocardial oxygen demand relative to supply
b. Thrombosis associated with vulnerable plaque rupture.
c. Diagnosis of at least two :
i. Ischemic chest pain
ii. Changes on ECG
iii. Increase and decrease in cardiac biomarker levels
d. Delay sx for more than 30 days after acute MI
e. Elective noncardiac sx should be delayed for more than 4 to 6 weeks after
coronary angioplasty.
i. 6 weeks after CABG
Intraoperative
a. Goals are to prevent MI by optimizing myocardial oxygen supply and reducing
myocardial oxygen deman
b. And to monitor for and treat ischemia.
Cardiac transplant:
a. Indicated for
i. Dilated cardiomyopathy
ii. IHD
b. MANAGEMENT OF ANESTHESIA:
i. Etomidate is preffered
ii. Responsds to epi and dobutamine
iii. With severe hypotension vasopressin is good
c. PREOPERATIVE EVALUATION:
i. KEEP preload good they depend on it!!!
MANAGEMENT OF ANESTHESIA
a. Denervated heart is unable to respond to fluid shifts in blood volume with an
increase in heart rate

VALVULAR HEART DISEASE:

Cardiac valve lesions produce: pressure overload: ( mitral stenosis, aortic stenosis)
Volume overload= MR, AR,
I. PreOPERATIVE EVALUATION: of patients with valvular heart disease includes assessment
of
a. Severity of the cardiac disease

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V.

b. The degree of impaired myocardial contractility

c. Presence of associated major organ system disease
d. History and physical: need to know if they can tolerate exercise and if they have
CHFif they do we need to get it under control first and postpone sx.
e. Complications: endocarditis and valve thrombosis or systemic embolization
f. Labs:
i. ECG: Broad notched P waves
ii. ChestXRay: heart excees 50%
iii. Cardiac catheterization: will demonstrate the presence and severity of
valvular stenosis and regurgitation, CAD, shunting, pressure gradients and
pulmonary HTN, and presence of RHF
Mitral stenosis: MV orifice 4-6 cm2 and symptoms develop when orifice is less than 1.5
a. Results in increase in left atrial pressure and volume.
b. s/s: opening snap that occurs in early diastole and rumbling diastolic murmur at
apex or axilla. BLOOD STASIS in LA.
c. TX:
i. Diuretics to reduce left atrial pressure
ii. HR control
iii. Anticoagulation
iv. Sx correction
d. Diagnostics :Echocardiography: Pulmonary HTN if LAP is above 25 mmhg
e. Anesthesia: we want to decrease SVR
f. Post operative management: at risk for pulmonary edema and right sided HF. Pain
and hypoventilation can cause increased HR and increased Pulmonary vascular
resistance.
Mitral regurgitation: MR is characterized by decreases in forward left ventricular stroke
volume and CO associated with increased LAP. Volume and pressure overload of LA
are increased.
a. s/s holosytolic murmur, V wave in a pulmonary artery occlusion pressure
waveform
b. tx: Decrease SVR and PVR
Mitral valve prolapse: is the prolapse of one or both mitral leaflets into the left atrium
during systeole with or without MR. Can cause Infective endocarditis. Dysrhythmias
respond well to BB. SVT VT
a. Dx: prolapse of 2 mm above annulus.
b. Management of anesthesia: we want to decrease SVR
c. Drugs: phenylephrine, etomidate are good.
Aortic stenosis: Obstruction to ejection of blood into the aorta caused by decreases in the
aortic valve area necessitates an increase in left ventricular pressure to maintain forward
SV. Transvalvular pressure is greater than 50 mmHg and valve area of less than 0.8
a. s/s angina pectoris, syncope, CHF, SYSTOLIC MURMUR
b. anesthesia: avoid brady or tachy, maintain NSR, avoid hypotension,
i. DO NOT DECREASE SVRneraxial is no good causes decrease in SVR
ii. If you see a junctional rhythm or brady treat it fast with glycopyrrolate,
atropine, or ephedrine.
iii. SVT terminate with cardioversion
Aortic regurgitation: regurgitation of some of the ejected SV from the aorta back into the
right ventricle during diastole results in a combined pressure and volume overlaod on the
left ventricle. The magnitude of the regurgitant volume depends on 1. The duration of
diastole, which is determined by HR, and 2. Pressure gradient across the aortic valve
which is depending on SVR. Magnitude of AR is decreased by Tachycardia and peripheral

vasodilation. SEVERE LEFT VENTIRCULAR VOLUME OVERLOAD. CAUSING HEART FAILURE

AND CORONARY ISCHEMIA.
a. S/S: diastolic murmur heart at right sternal boarder.
b. Can have bradycardia and junctional rhythm.
VI.