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61 Cards in this Set
- Front
- Back
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left main coronary artery - left anterior descending
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ant. 2/3 vent septum, anterior L ventricle, apex, R&L bundle branches
anterior wall MI septal/anteroseptal MI |
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left main coronary artery - left circumflex
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40-45% SA node, L atrium, posterior wall
lateral wall MI posterior wall MI (also RCA) |
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right coronary artery
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posterior/superior ventricular septum, L atrium, R atrium,, 55=6-% SA node, AV node, R ventricle, posterior and diaphragmatic L ventricle
inferior wall MI posteroir wall MI ventricular MI (proximal RCA) |
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collateral circulation
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flow redirected, new vessels develop as vessels occluded; compensatory
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MI results from
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CAD, beyond ischemia to irreversible tissue damage and necrosis
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CAD due to
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atherosclerosis (fatty streak, plaque, complicate lesion)
thrombosis spasm inflammation |
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O2 demand exceeds supply =
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aqnaerobic metabolism in cells = lactic acid +acidosis = dysrhythmias, contractility, angina
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necrosis of cells
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decreased contractililty
myocardial irritabillty/altered repolarization release of enzymes |
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3 zones of necrotic tissue
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zone of infarction and necrosis (nonviable)
zone of hypoxic injury (can return to normal) zone of ischemia (reversible) |
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spread of necrosis
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endocardium to epicardium
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transmural MI
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all 3 layers necrosed
dyskinetic or akinetic tissue |
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subendocardial MI
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only one layer
subendocardial (inner) imtramural (middle) subepicardial (outer) |
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inflammatory markers
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risk factor identification
homocysteine, c-reactive proteins |
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external triggers to MI
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circadian variations
seasonal variations physical exertion emotional stress |
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MI pain
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25% silent ischemia
no relieved with NTG |
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classic MI pain
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precordial/sbusternal
crushing, squeezing, constircting, choking, burning, sharp |
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atypical MI pain
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vague - not localized
aching, sore, dull indigestion toothahce radiate to jaw, neck, back, L arm, stomach |
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MI clinical manifestations
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SNS activations (+BP, +HR, diaphoresis
anxiety/denial N/V heart failure sx (elderly) fever |
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12 lead EKG
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ST segement elevated = injury
T wave flat/invered & ST segment depression = ischemia q wave wider/deeper = necrosis |
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creatine kinase (CK) MB
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increased in 3-6 hours, peaks 10-24 hours, returns to normal in 2-4 days
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Troponin T
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normal <.2ng/L
increase in 4-6 hours, peaks 10-24 hours, returns to normal in 10-14 days |
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Troponin I
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<.4 ng/L
increase in 4-6 hours, peaks 10-24 hours, returns to normal in 10-14 days |
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myoglobin
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early detection, nonspecific
increases 2-3 hours, peaks in 6-9 hours, returns to normal in 12 hours |
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lactate dehydrogenase (LDH) M1
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increases in 14-24 hours, peaks in 48-72 hours, normal in 7-14 days
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aspartate aminotransferase (AST)
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increases within several hours, peaks 12-18 hours, normal 3-4 days
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radio nuclide imaging
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camera records gamma rays emitted by radioisotope (thallium 201 = ischemia), technetium 99 = necrosis
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coronary angiography
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visualize arteries and measure function
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creatine kinase (CK) MB
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increased in 3-6 hours, peaks 10-24 hours, returns to normal in 2-4 days
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interventional procedures
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thrombolytics
percutaneous transluminal coronary angioplasty (PTCA) coronary stents athrectomy (rotoblad) CABG |
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Troponin T
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normal <.2ng/L
increase in 4-6 hours, peaks 10-24 hours, returns to normal in 10-14 days |
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emergency interventions
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calm/quiet
elevate HOB |
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Troponin I
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<.4 ng/L
increase in 4-6 hours, peaks 10-24 hours, returns to normal in 10-14 days |
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myoglobin
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early detection, nonspecific
increases 2-3 hours, peaks in 6-9 hours, returns to normal in 12 hours |
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lactate dehydrogenase (LDH) M1
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increases in 14-24 hours, peaks in 48-72 hours, normal in 7-14 days
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aspartate aminotransferase (AST)
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increases within several hours, peaks 12-18 hours, normal 3-4 days
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radio nuclide imaging
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camera records gamma rays emitted by radioisotope (thallium 201 = ischemia), technetium 99 = necrosis
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coronary angiography
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visualize arteries and measure function
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interventional procedures
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thrombolytics
percutaneous transluminal coronary angioplasty (PTCA) coronary stents athrectomy (rotoblad) CABG |
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emergency interventions
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calm/quiet
elevate HOB apply oxygen, IV inserted, cardiac monitor ASA at scene CPR as needed |
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thrombolytic therapy selection criteria
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onset of pain <6 hrs
ST segment elevation ischemic pain no condition predisposing to hemorhaging complications* bleeding |
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thrombolytic therapy
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streptokinase (streptase)
urokinase (abbokinase) tissue plasminogen activator (t-PA, ateplase) anisoylated plasminogen-streptokinase activator complex (APSAC, anistreplace) recombinant plasminogen activator (rPA, reteplase) |
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complications d/y myocardial necrosis
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ventricular aneurysm (vent. dysrhythmias)
ventricular septal rupture (new murmur, CHF, l to r shunt) paillary muscle rupture (acute mitral valave insufficiency and heart failure) cardiac rupture (cardiac tamponade) |
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dressler's syndrome
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late pericarditis
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paricarditis
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inflamed tissue rubs against pericardial surface
precordial pain, intensified with cough, deep breathing, movement, treat with anti-inflammatory agents |
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nonmodifiable risk factors
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age
gender (men > wmen until 65 years) ethnicity (white > african maericans genetic predisposition and family history of heart disease |
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modifiable risk factors
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serum lipids
blood pressure >140/90 DM tobacco use physical inactivity obesity |
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nitrate action
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promote peripheral vasodilation; decreases preload and afterload
coronary artery vasodilation |
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ex. of nitrates
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sublingual nitroglycerin
translingual spray nitroglycerin ointment transdermal nitroglycerin extended-release buccal tablets isosorbide dinitrate IV nitro |
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beta-blockers action
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inhibit parasympathetic nervous stimulation of the heart
reduce heart rate, contractilitiy, and BP decrease afterload |
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ex. of beta blockers
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-lol
atenolol (ternormin) carvedilol (coreg) metoprolol (Lopressor) nalodol (Corgard) propanolol (Inderal) |
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calcium channel blockers action
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prevent Ca entry into vascular smooth muscle and myocytes
coronary and peripheral vasodilation reduce HR, contractility, BP |
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ACE inhibitors action
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prevent conversion of angiotensin I to II = vasodilation
decrease endothelial dysfunction for HF, tachy, MI, HTN, DM, CKD |
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ACE inhibitors examples
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-pril
catopril (capoten) enapril (Vasotec) |
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Angiotensin II receptor blockers action
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inhibit binds of angiotensin II to AT receptors = vasodilation
patients intolerant of ACE inhibitors |
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Angiotensin II receptor blockers examples
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losarten (Cozaar)
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heparin action
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prevent conversion of fibrinogen to fibrin and prothrombin to thrombin
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fibrinolytic therapy action
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breaks of fibrin meshwork in clots
used only in ST-segment elevation MI |
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morphine
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opioid analgesics
analgesic and sedative vasodilation to reduce preload and myocardial oxygen consumption |
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managing rt. ventricular infarcts
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inferior of posteriod wall MIs
JVD, clear lungs, hypotension increase preload to improve contractility |
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heart failure - potential complication
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PCWP >18. CI <2.2
decrease preload and afterload, improve contraciltiy |
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cardiogenic shock - potential complication
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decreased BP, tachy, restless, acidosis, cool-clammy skin, decreased UO, PCWP >18, CI <2.2
goal: improve tissue perfusion and decrease cardiac workload |
