Angina - Stable and Unstable
8
a. Major detriments of myocardial oxygen supply and demand 1. Refers to lack of O2 due to inadequate perfusion a. Ischemia occurs if O2 demands are increased (LVH due to AS, AS can cause angina indistinguishable from coronary atherosclerosis) b. Ischemic occurs if O2 carrying capacity of blood is low (severe anemia, carboxyhemoglobin) c. Ischemia 2. Inadequate perfusion leads to disturbances in mechanical, biochemical, and electrical function a. HF (LVF or RVF or both) i. Angina, if ischemia is prolonged or develop coronary occlusion, may lead to myocardial necrosis ii. Segmental akinesis bulging (dyskinesis) iii. Mechanical b. FA cant be oxidized i. Increased lactate production ii. Reduced pH with metabolic acidosis iii. Biochemical c. Inversion of T wave i. Transient displacement of ST segment ii. Depres sion - sube ndocar dial iii. Elevation - sube picardial iv. Electrical instability: VT or VF v. Electrical d. Effects of Ischemia 3. Most common cause of ischemia a. Decreased perfusion and limited increase when demand is needed i. Supply/demand ii. Decreased CA lumen b. Constriction of vessel (spasm) i. Clot formation (thrombi, emboli) ii. Risk factors that contribute t o altered function of vascular endothelium. c. Atherosclerosis 4. Angina - Stable and Unstable Friday, January 20, 2012 9:03 AM CPII Pa e 1
Transcript of Angina - Stable and Unstable
8/3/2019 Angina - Stable and Unstable
http://slidepdf.com/reader/full/angina-stable-and-unstable 1/8
a.
Major detriments of myocardial oxygen supply and demand1.
Refers to lack of O2 due to inadequate perfusiona.
Ischemia occurs if O2 demands are increased (LVH due to AS, AS can cause
angina indistinguishable from coronary atherosclerosis)
b.
Ischemic occurs if O2 carrying capacity of blood is low (severe anemia,
carboxyhemoglobin)
c.
Ischemia2.
Inadequate perfusion leads to disturbances in mechanical, biochemical,
and electrical function
a.
HF (LVF or RVF or both)i.Angina, if ischemia is prolonged or develop coronary occlusion, may
lead to myocardial necrosis
ii.
Segmental akinesis bulging (dyskinesis)iii.
Mechanicalb.
FA cant be oxidizedi.
Increased lactate productionii.
Reduced pH with metabolic acidosisiii.
Biochemicalc.
Inversion of T wavei.
Transient displacement of ST segmentii.
Depression - subendocardialiii.
Elevation - subepicardialiv.
Electrical instability: VT or VFv.
Electricald.
Effects of Ischemia3.
Most common cause of ischemiaa.
Decreased perfusion and limited increase when demand is neededi.
Supply/demandii.
Decreased CA lumenb.
Constriction of vessel (spasm)i.
Clot formation (thrombi, emboli)ii.
Risk factors that contribute to altered function of vascular endothelium.c.
Atherosclerosis4.
Angina - Stable and UnstableFriday, January 20, 2012
9:03 AM
CPII Pa e 1
8/3/2019 Angina - Stable and Unstable
http://slidepdf.com/reader/full/angina-stable-and-unstable 2/8
Contribute to subintimal collection of fat1)
Abnormal interaction with plts/monocytesiii.
Stenosis of 75-80% is sig1)
Leads to reduction in cross sectional area (stenosis)iv.
Reduces CA flow, worsens ischemia, leads to necrosisi.
Location of atherosclerosis will determine the amount of
myocardium that is vulnerable.
ii.
Plaques are subject to endothelial instability with fissuring, hemorrhage,
and thrombosis.
d.
NCEP Guideline III. Stricter target lipid levelsi.
LDL - less than 70 mg/dL1)
HDL low is greater than 60 mg/dL2)
TG high is 150 mg/dL3)
1% decrease in TC = 3% decrease risk of CADa)
Total cholesterol is less than 200 mg/dL4)
For patients with prior events and a 10 year risk of CHD (20% or
greater):
ii.
Hyperlipidemiaa.
Smokingb.
Hypertensionc.
Insulin resistance1)
Hypertension2)
High TG, low HDL3)
Hyperuricemia4)
Hypercoaguable5)
Recognized by AHA as major risk factor (metabolic syndrome)i.
DMd.
Obese - BMI >30i.
Overweight - BMI 25-30ii.
Men <.9a)
Women <.8b)
Desirable waist/hip ratio:1)Desirable - BMI 21-25iii.
Or Kg/Ht(m)^21)
BMI = (lbs*705)/Ht (inches)^2iv.
Obesitye.
Need 45-60 min of moderate intensity 5-7x/wki.
Physical Inactivityf.
Male - >45 y/oi.
Female - >55y/oii.
Age, Genderg.
Premature IHDi.
1st degree men relatives, <45 y/o (55)ii.
1st degree women relatives, <55 y/o (65)iii.
Family Historyh.
Risk Factors of Atherosclerosis5.
Over 25% of US adults have metabolic syndromea.
Obesity - abdomen over 40'' (men) or 35'' (women)i.
Low HDL - men <40 and women <50ii.
High TG, >150iii.
High BP - Systolic >130 or Diastolic >85iv.
Need 3 out of 5 to have metabolic syndromeb.
Metabolic Syndrome6.
CPII Pa e 2
8/3/2019 Angina - Stable and Unstable
http://slidepdf.com/reader/full/angina-stable-and-unstable 3/8
High fasting glucose - >110v.
Due to ischemia, usually caused by an increase in myocardial O2 demanda.
Produces ischemia b/c of increased O2 demand1)
Why? Fixed CA stenosis/fixed O2 supplyi.
Thresholds vary; certain levels of activity may provoke angina attackb.
HRi.
Afterloadii.Contractilityiii.
Wall Tensioniv.
Factors that control MVO2 (myocardial O consumption)c.
Angina7.
Men 50-60 yo, Women 60-70 yoa.
Relief on rest usually predictable, stable, not occurring more often,
not last longer
i.
Chest discomfort brought on by exertion/emotion, excitementb.
Can occur at rest - unstable anginai.
Can occur at night - recumbent or angina decubitusii.
Anginac.
Typical history8.
Heavy, pressure, squeezing, smothering, choking, dullness, ache,
sharp, heart burn, indigestion, gas
i.
Description varies;a.
Substernal, clinched fist - levine's Signb.
Lasts 1-30 mini.
Crescendo/decrescendo patternc.
Down ulnar surface of forearm/hand; both armsi.
May radiate into L shoulderd.
May radiate or arise in neck, jaw, teeth, epigastric or backe.
Heavy meal, cold exposurei.
May be precipitated byf.
15-20 minsi.
Longer suggests UA or MIii.
Durationg.
Discomfort9.
a.
Differential Diagnosis10.
Ischemia, but described as dyspnea, fatigue, faintnessa.
Diabetics, elderly, women, S/P CABG or transplants are more1)
Ischemia causing elevated LV filling pressure that leads to pul edemai.
Pathogenesisb.
Anginal Equivalent11.
CPII Pa e 3
8/3/2019 Angina - Stable and Unstable
http://slidepdf.com/reader/full/angina-stable-and-unstable 4/8
likely to experience this than classic angina
Premature IHDi.
Family Historya.
Previously mentionedi.
Risk Factorsb.
Typically normali.
PEc.
Soft yellowish spots on eyelids1)
Xanthelasmai.
Xanthomasii.
Diabetic skin lesionsiii.
Nicotine stainsiv.
Palev.
Absent peripheral pulsesvi.
LV dyskinetic1)
Abnormal cardiac impulsevii.
Carotid, abdominal aorta, femorals1)
Bruitsviii.
S3, S4, both1)
Gallopix.
Systolic murmur of MR if papillary muscle is dysfunctionalx.
AS,1)
AI2)
Pul hypertension3)
Hypertrophic cardiomyopathy4)
Rememberxi.
Signs of Risk Factorsd.
Angina12.
Check for DM - HbA1C, fasting glucose, 2hr pp glucosea.
BUN, creatininei.
Check for renal diseaseb.
Fasting lipid profilec.
CBCd.
Check thyroid status - TSHe.
Troponin 1, CK total, CK-MBi.
Cardiac enzymesf.
Labs13.
Normal in 50% of patientsa.
During anginal attack may have displaced ST segmentb.
May show old MIc.
ECG14.
Stress Tests (contraindications)15.
CPII Pa e 4
8/3/2019 Angina - Stable and Unstable
http://slidepdf.com/reader/full/angina-stable-and-unstable 5/8
a.
Patient being considered for revascularization (CABG or PCI -
percutaneous coronary intervention)
i.
Indicationa.
Successful 90%i.
Maintains revascularization of myocardium to prevent re-
stenosis
1)
Stent insertionii.
Restenosis occurs in 30-45% of patients in 6 monthsiii.
.5-1% b; need for emergency coronary1)
Mortalityiv.
PCI - PTCAb.
Cardiac Cauterization16.
17.
Identify aggravating conditionsa.
Treat risk factorsb.
Dietc.
Treatment of CAD/Angina18.
CPII Pa e 5
8/3/2019 Angina - Stable and Unstable
http://slidepdf.com/reader/full/angina-stable-and-unstable 6/8
i.
Exercise regularlyd.
Statins for hyperlipidemiae.
ACS - acute coronary syndromei.
New onset angina or pre-existing angina that progresses to point
where patient cannot perform less than ordinary activity
ii.
Tempo has changed; higher number of episodes, lasting longer,
more severe intensity symptoms at rest, awaken from sleep, using
more medications, a decrease in amount of effort to provide
symptoms
iii.
Unstable Anginaf.
Rupture of atherosclerotic plaque from inflammation/mediators
released. Activation of platelets, clotting factors, thrombus
i.
Pathophysiology (UA, ACS)g.
a.
b.
Pharmacological Treatment of Angina and CAD19.
CPII Pa e 6
8/3/2019 Angina - Stable and Unstable
http://slidepdf.com/reader/full/angina-stable-and-unstable 7/8
c.
i.
d.
e.
CPII Pa e 7
8/3/2019 Angina - Stable and Unstable
http://slidepdf.com/reader/full/angina-stable-and-unstable 8/8
f.
g.
