Angina, Unstable Angina, ACS, and testing Flashcards
Risk factors for atherosclerosis
o Hyperlipidemia – high LDL, low HDL, high TG, high lipoprotein (a)
o Smoking
o DM – major risk factor
o HTN
o Family hx of coronary heart disease, ischemic stroke, or peripheral vascular disease
o Obesity
o Physical inactivity (need 30-60 min medium intensity 4-7 days/week)
o Psychosocial stress – causes catecholamine release
o Sleep disturbances – arrhythmias, hypoxia due to OSA
o Age and gender (males >55, females >65)
Metabolic Syndrome
o Insulin resistant o HTN o High TG, low HDL o Hyperuricemia o Hyper coagulable o Obese, overweight (need to get back to desirable weight)
Mechanical complications of ischemia
- HF – LVF or RVF or both
- Angina – prolonged ischemia or develop coronary occlusion, may lead to nyocardial necrosis
- Segmental akinesis bulging (dyskinesis
Biochemical consequences of ischemia
- Fatty acids can’t be oxidized
- Increased lactate production
- Reduced pH with metabolic acidosis (higher lactic acid, higher mortality)
Electrical consequences of ischemia
- Inversion of T wave
- Transient displacement of ST segment
- Depression – subendocardial portion of heart
- Elevation – subepicardial portion or transmural injury of the heart
- Electrical instability – VT, VF
LAD distribution
Anterior wall infarction
Most of septum and anterior portion of the heart
Leads V1-V6
RCA distribution
inferior wall infarction
• Most of inferior of heart and part of RV
• Leads II, III, AVF; V3R – V6R
Circumflex A distribution
– lateral wall
• I, AVL, V5, V6
Posterior Descending A distribution
posterior wall infarction
• Reciprocal changes anteriorly - V1-V3
Non CP symptoms of chronic ischemic heart disease
o Dyspnea o Non chest locations of discomfort – exertion or rest o Mid-epigastric or abdominal o Diaphoresis o Excessive fatigue and weakness o Dizziness and syncope
Chronic stable angina
consequence of imbalance between oxygen supply demand
• Low risk of plaque rupture – small lipid core and thick fibrous cap
Supply angina
- Decrease O2 deliver to tissue lead to ischemia
- Coronary vasoconstriction, stenosis, platelets release serotonin, TxA2
- Tx: aspirin to inhibit COX to inhibit platelet aggregation
Demand angina
- Increase myocardial O2 requirements, workload can lead to ischemia
- Exercise, stress, emotion, fever, thyrotoxicosis
- LVH due to AS
- Anemia – low O2 carrying capacity
ECG findings in angina
- Initial (early) may be normal, or nonspecific half the time – look at hx
- During angina attack, may have displaced ST segment, most commonly depression
- Subendocardial injury-ischemia
- May show old MI
Classic hx for angina pectoris
• Chest discomfort brought on by exertion/emotion/excitement
• Relief by rest usually predictable, stable, not occurring more often, not lasting longer
• Men 50-60; Women 60-70
Fx: premature IHD
Physical exam findings in angina pectoris
- Often normal
- Xanthelasma – soft, yellowish spots on eyelids
- Xanthomas
- Diabetic skin lesions
- Nicotine stains
- Pale
- Absent peripheral pulses
- Abnormal cardiac impulse (LV dyskinetic)
- Bruits – carotid, abdominal aorta, femorals
- Gallop – S3, S4, or both
- Systolic murmur of MR if papillary muscle is dysfunctional
- Associated with inferior or inferior-posterior ischemia due to RCA disease
DDX for angina pectoris
• Aortic valve disease, pulmonary HTN, hypertrophic cardiomyopathy
Discomfort experienced in angina pectoris
o Varies – heavy, pressure, squeezing tightness, smothering, choking, dullness, ache, sharp, heart burn, indigestion, gas
o Substernal, clenched fist – Levine’s sign
o Crescendo/decrescendo pattern lasts 15-20 min
o May radial into L shoulder, down ulnar surface of forearm/hand; both arms
o May radiate or arise in neck, jaw, teeth, epigastric, or back
o May be precipitated by heavy meal, cold exposure
Anginal equivalent
o Causes dyspnea, fatigue, faintness, gastric eructation’s (belching)
o Pathogenesis: ischemia causing elevated LV filling pressure leading to pulmonary edema
o Seen in diabetics, elderly, women
Unstable angina (Acute coronary syndrome)
o New or worsening chest pain
o Tempo has changed, more severe, prolonged more frequent
o May occur at rest, awaken from sleep
o Pain lasting longer than 20 min
o Using more medication for relief
o Less effort to provoke symptoms
o No evidence of myocyte necrosis (no elevation of troponin I or CK-MB)
Non-ST elevation MI
o CP with elevation of cardiac enzymes (troponin I or CK-MB) and WITHOUT ST elevation
o Ddx
• PE – ECG changes, elevated troponin
• RBBB, sinus tach, afib, S1Q3T3
• Nonspecific
• Aortic dissection
• VHD – AS, AI, hypertrophic cardiomyopathy
• Huge QRS voltage
• Myocarditis – pericarditis
• Stress cardiomyopathy – takotsubo syndrome – deeply inverted T wave
Unstable Angina and NSTEMI patients
o Atherosclerotic plaque rupture or erosion with platelet aggregation and thrombus leading to a PARTIAL occlusion of the coronary artery
o ECG:
• Magnitude of ST segment depression correlates with prognosis
• 1mm or greater in 2 or more leads – 4x likely to die within 1 year
• 2 mm or greater – 6x more likely to die within 1 year
• 2 mm or greater in more than 1 region of ECG – mortality is 10 fold
Labs for Acute Coronary Syndrome
o Cardiac enzymes – Troponin I – detected in 2-4 hrs in NSTEMI
o Increased CK-MB – after 3-6 hours
o BNP – increased BNP associated with increased mortality in NSTEMI
• Marker for ventricle stretching
o CRP – inflammatory biomarker
o CMP, BUN, Cr, liver panel, electrolytes, CBC
o FLP (fasting lipid profile), TSH
Signs of risk for coronary event
o Positive stress test at low work load
o ST depression greater than 5 min after completion of test
o Decreased BP – systolic fall > 10mmHg during exercise
o VT during exercise
o Reduced EF during exercise (stress echo)
Variant Angina or Prinzmetal Angina
o Transient ST segment elevation during CP in absence of severe CAD
o Spasm of coronary arteries
o CP predominantly at rest, awaken from sleep
o Relieved by Nitro
o Rx: dihydropyridine CCB (amlodipine)
Stress test contraindications
• Recent MI or acute MI, unstable arrhythmias, acute PE, aortic dissection, unstable angina, severe AS, decompensated HF, endocarditis, DVT
Pharmacologic stress test
- Use adenosine/regadenosine
- Vasodilators increase HR
- Dobutamine increase HR
Nuclear myocardial perfusion imaging
- SPECT – single proton emission CT
* Useful in LBBB, LVH, digitalis effect
Stress Echocardiogram
- With exercise or dobutamine
* Defect wall motion abnormality and EF
Cardiac CT Angiography (CCTA)
- Detect coronary calcification
* Specificity 50% in identifying obstructive CAD
CXR
usually normal unless hx of HI, HF, VHD
• Cardiomegalia in HTN, VHD, cardiomyopathy, pericardial effusion
Coronary Angiography
(cardiac catherization)
• Gold standard
• Percutaneous coronary intervention (PCI) – stent insertion – 1 or 2 vessels
• Criteria for CABG – L main disease or 3 vessel disease
Aspirin
- Blocks platelet aggregation
* Inhibits cyclooxygenase
Beta Blockers
- Slow everything – decrease HR, workload, O2 consumption
- Contraindicated if decompensated HF, hypotension, advanced AV block (higher than 1st degree)
- Get them out of HF first
- Symptoms initiating drug – fatigue “wearing them out”
- Lower mortality
Nitro/Nitrates
- Decrease preload
* Need 8-12 hour free interval to prevent tolerance
CCBs
- Not shown to decrease mortality
* Caution with verapamil in impaired LV function – negative inotropic effect
Aggravating conditions in Angina
o Obesity – weight loss if obese, consult dietitian o HTN – treat to goal o Hyperthyroid – meds, RAI o Anemia – find cause and tx o Smoking – cease o Hyperlipidemia – statins • Goals: • LDL-C less than 70 mg/dL • HDL-C greater than 60 mg/dL • TG below 150 mg/dL • Total Cholesterol less than 200 mg/dL o 1% decrease in TC yields 3% decrease in risk of CAD o Diabetes – ADA diet, oral agents, insulin
