CHAPTER 28– CARDIOLOGY Flashcards
Canadian cardiovascular scale
class 1 = angina with strenuous or protracted activity Class II =occasional angina with normal daily activities EG climbing stairs Class III =marked limitation of activities and pain with everyday activities Class IV =symptoms at rest
unstable angina
= non-ST elevation myocardial infarction
–Generally due to formation of nonocclusive thrombus at site of rupture of surface or of atherosclerotic plaque
–Thrombus progresses until includes blood cell vessel or embolizes to distal vessels
–Sudden onset unrelated to precipitating event is Hallmark
acute myocardial infarction with ST segment elevation
–abrupt onset of unremittent chest pain
–Usually with dyspnea diaphoresis and sense of doom
–Usually caused by abrupt occlusion of coronary artery I thrombus at site of ruptured atherosclerotic plaque
–EKG shows ST elevation in 2 or more leads the territory of the artery
–if not treated within 6-12 hours, suffers significant myocardial damage
Prinzmetal angina
–uncommon
–coronary spasm, usually at site atherosclerotic lesion
–transient chest pain with ST elevation
–Often occurs at rest
syndrome X
patients with –Angina –Evidence of exercise-induced ischemia –Normal epicardial coronary arteries –70% female –Average age = 50 years –etiology not understood
differential diagnosis of angina
–multiple causes of similar pain
Response to nitroglycerin seen in
–Esophageal spasm
–Diastolic dysfunction
diagnoses mimicking angina or MI
–esophageal spasm –Peptic ulcer –Asthma –Aortic dissection –Mitral valve prolapse –Pulmonary embolus –Exertional hypertension –Cholecystitis –Musculoskeletal syndromes –Panic attack –pericarditis –Pleuritis –Congestive heart failure –Diastolic dysfunction –Costochondritis
diagnosing chronic stable angina
–physical exam not uses a helpful
–+/- S1 or S4.. Systolic or diastolic dysfunction
–EKG usually normal
–May have a prior myocardial infarction or ischemia with ST depression
–Exercise treadmill will show EKG changes with exercise
–post exercise echocardiogram also helpful
–64 slice CAT scan can image coronary arteries
–Coronary angiography is gold standard
acute coronary syndrome definition
–unstable angina
–Non-ST elevation myocardial infarction
–ST elevation myocardial infarction
EKG changes in various ST elevation myocardial infarction
–anterior MI = V1–V4
–Lateral MI = V1, V6, 1, aVL
–Inferior MI = II, III, aVF
CK–MB and cardiac troponins occurred when
CK–MB and cardiac troponins do not elevated for the first 8 hours after an MI
other name for statin
=HCM–CoA
= Hydroxy methyl Glutaryl coenzyme A
medications to treat angina and MI symptoms without improvement in survival
nitrates and calcium channel blockers
–Avoid amlodipine and felodipine if left ventricular dysfunction
symptoms seen in MI
–substernal chest pain –Radiation to either arm, neck, jaw, epigastrium –diaphoresis –Nausea or vomiting –Palpitations –Weakness –Lightheadedness
–Atypical symptoms often an elderly and/or diabetic
–more than 40% presented with sudden cardiac death as first symptom of MI
differential diagnosis of possible MI
AORTIC DISSECTION
– stabbing ripping chest pain radiating to the back
–different blood pressures between left and right arm
– wide mediastinum x-ray
–new diastolic murmur of aortic regurgitation
PULMONARY EMBOLUS –Dyspnea –Pleuritic chest discomfort –Hemoptysis –Low oxygen saturation
PERICARDITIS
–Sharp pleuritic pain
–Positional, better sitting up or leaning forward
–Friction rub or pulsus paradoxus
EKG evidence for reperfusion therapy
–new Left bundle-branch block
–New ST segment elevation greater than 0.1 mV in 2 or more continuous leads
–Also useful in posterior MIwith ST depression in V1–6
conditions that obscure EKG diagnosis of MI
–known left bundle branch block –Paced rhythm –Left ventricular hypertrophy with strain –Wide complex tachycardia –Wolff-Parkinson-White syndrome
biomarkers of MI onset and peak
CK-MB –elevated in 4 hours –Peaks 12-24 hours –Duration 36-48 hours –low sensitivity and specificity
TROPONINS
–begins in 3-6 hours
–Elevated 7-14 days
–Worse prognosis than MB CK elevation
which artery involved in various MI
anterior infarct =
–left proximal anterior descending artery (LAD)
Anterolateral infarct=
– left circumflex, or diagonal branch of left anterior descending artery
Diaphragmatic =
–inferior infarct = right coronary artery
True posterior infarct =
–distal circumflex artery posterior descending artery
–Distal right coronary artery
percent reduction in early MI mortality with aspirin
24%
direction of P wave in various leads
–positive in lead 1, 2, V5, V6
–negative in aVR
–Up, down, or biphasic in V1
Ectopic foci may be normal if close to the sinus node
direction of P wave in PR interval
–includes P wave and PR segment
–Encompasses atrial repolarization and depolarization AV node and His-Purkinje system
–Prolonged by slow AV node conduction
––Decreased sympathetic tone
––Increased vagal tone
––Drugs e.g. digitalis and beta adrenergic blocking agents
PR interval shortened one pulses Risa ventricles to AV node bypass tract as in Wolff-Parkinson-White
direction of QRS wave
–ventricles depolarized simultaneously
–Left ventricle is 3 times larger than the right therefore overshadows electrically
–Upright in lead 1, V5, V6, left side, posterior leads
–Negative in aVR and V1, right-sided and more anterior leads
–Abnormal in bundle branch blocks, fascicular blocks
–
factors affecting amplitude of QRS complex
–thickness of ventricular wall
–Presence of pleural or pericardial fluid
–Affected by age, sex, race
–Younger patients have greater QRS voltages
–Men have greater QRS voltages
ST segment and T-wave
–represent ventricular repolarization
–T wave results of sequential repolarization of ventricular cells
–Abnormalities and repolarization shown by elevation or depression of ST segments and changes in polarity of T wave
–T-wave amplitude should be at least 10% of QRS complex
–Inverted T waves in lead 1 her always abnormal
–Flat or inverted T waves often occur with rapid ventricular rates. Her nonspecific
–Most common cause of ST segment elevation includes
––Acute transmural ischemia
––Pericarditis
––High potassium
––Acute myocarditis
U-wave
–precise etiology not clear
–May increase with hypokalemia
QT abnormalities
–QT = onset of Q-wave to end of T-wave
––Includes QRS, ST segment, T-wave
–Interval is rate-dependent
–Affected by ––Temperature ––Drugs ––Electrolyte abnormalities ––Genetic factors ––Neurogenic factors ––Ischemia
–Low potassium,or low calcium prolonged QT
–high potassium or high calcium lengthens QT
significant of peaked or tented T-wave
high potassium
acute ischemia and infarction on EKG
characterized by changes in ST segment, QRS complex, T-wave
–
sequence of EKG changes with ischemia and infarction
- Peaking of the T-wave
- ST segment elevation or depression
- Development of abnormal Q waves
- T-wave inversion
incidence of peripheral artery disease
10-30% of adults over age 50
–Marker for coronary and cerebrovascular disease
–60% of patients with PAD have CAD cerebrovascular disease or both
–Patient with PAD 3 times greater risk for CVA and MI
etiology of PAD
–starts early in life
–Plavix start in endothelial tissue
–Expanded increments on to subclinical episodes of plaque rupture
–TriCor is surrounded by complex fibrotic Composed of calcium, connective tissue and smooth muscle cells
–Plaque rupture exposes highly thrombogenic core to circulating blood elements resulting in platelet activation and aggregation along with activation fibrinogen
–Strongest risk factor the cigarettes
main symptoms of claudication
–cramping pain and lower extremities were by Dr.,
–Reliably produced by threshold level of exercise
–Relieved by a few minutes of rest
–Elevation of limb worsening claudication
–Classic symptoms occur in only one third of patients
–Symptoms may be mild
PAD symptoms and location of stenosis
calf claudication = femoral artery stenosis
–Foot claudication suggests popliteal or proximal tibial peroneal stenosis
–Thigh and buttock pain suggests aortoiliac involvement
–Critical limb ischemia usually requires multiple sites of severe obstruction
physical findings in PAD at rest
–cool skin –Pallor –Dependent rubor –Atrophic skin and nails Delayed capillary refill Ischemic ulcers
–Ischemic ulcers tend to be painful and occur at the lateral malleolus, tips of the toes, metatarsal heads, bunion area
In contrast venous stasis ulcers are usually painless and occur over medial malleolus
Lack of bruits reduce his likelihood of significant PAD
differential diagnosis of PAD like–symptoms
pseudo-claudication (symptom of spinal stenosis)
–Less reproducible on specific effort level
–Not relieved by rest
–Only relief with sitting or lumbar flexion
Claudication pain improves when standing still, but not was pseudo-claudication
interpreting ABI
ratio of brachial blood pressure to dorsalis pedis and posterior tibial artery pressure
–ABI of 0.9 has 95% sensitivity and 100% specificity
–ABI <0.4 consistent with severe PAD
–Extremities with ischemia at rest generally associated with a ABI <0.20
treatment of PAD
–risk factor reduction –Glycemic control –ACE inhibitor's –Diuretics –Beta blockers –Antiplatelet the agents, aspirin –Statins –clopidogrel slightly superior to aspirin but minimal difference –Exercise
guidelines for prevention of infective endocarditis in the presence of vvalvular or congenital heart disease
–optimal oral health and hygiene
–Antibiotic prophylaxis only for those at highest risk
––History of previous infective endocarditis
Test test prosthetic heart valves
––Cardiac transplant recipient’s with valvulopathy
––Unrepaired cyanotic congenital heart disease
–Completely repaired congenital heart disease with prosthetic materials are devices during the first 6 months of after the procedure
–Those with residual defects at or adjacent to site of a prosthetic patch should be treated indefinitely
