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52 Cards in this Set
- Front
- Back
epidemiology of CHD
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-Coronary heart disease (CHD) caused ~ 1/5 US deaths in 2005
~ 1/2 of men and 2/3 of women who die suddenly of CHD have no previous symptoms (FHS/NHLBI)!! |
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risk factors
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1. age
2. gender 3. FH 4. genetics 5. hx of DM 6. hx of vascular dz 7. HTN 8. glucose control 9. lipid profile 10. smoking 11. obesity 12. sedentary lifestyle |
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etiology
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1. coronary atherosclerosis (over 90%)
-Underlying cause in > 90% of patients -Acute surge in arterial pressure or sudden vasoconstriction causes plaque to fissure, rupture, or ulcerate=> 2. thrombosis 3. coronary vasospasm- more commonly with stimulants (cocaine) 4. Other: vasculities, coronary ostial occlusion, congenital, trauma, metabolic |
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vulnerable plaque
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-large lipid pool
-younger, less stenotic -located at branch point -infiltrated with macrophages -more likely to rupture! |
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2 distinct types of clots
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1. platelet rich- unstable angina/ NSTEMI
2. fibrin rich- completely occlude the vessel; STEMI |
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pathophysiology
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-affected by distribution of coronary artery anatomy/ collaterals
-oxygen demand exceeds supply -progression over time ischemi --> injury --> infarct |
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pathophysiologic gender differences
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-CAD is manifested earlier in men
-women have smaller hearts -coronary vessels are smaller in women -Women commonly have microvascular ischemia than cannot be detected by angiography |
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goals in pts with ACS
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- identify early
-Treat to save muscle based on pathophysiology -prevent early death from: arrhythmias, LV failure -prevent recurrence |
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Factors That Affect Prehospital Delay
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Sociodemographic characteristics
-Increase: Older age, Female, Lower educational level, Black or Latino, Low socioeconomic status Clinical characteristics: -Increase: History of angina, Prior MI ( no difference in some studies), Diabetes, Hypertension, Heart failure, Hyperlipidemia Social: -decrease: Consultation with a nonrelative Cognitive and emotional: -decrease:Correct attribution of symptom origin |
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history: chest pain
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Location: usually substernal
Quality: pressure, crushing, squeezing, can resemble indigestion Radiation: shoulders, arms, neck, jaw, epigastrium, scapulae, back Duration: 15 minutes to several hours |
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features not characteristic of MI
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1. pleuritic pain
2. Primary or sole location of discomfort in the middle or lower abdominal region 3. Pain that may be localized at the tip of 1 finger, particularly over the LV apex 4. Pain reproduced with movement or palpation 5. Episodes of pain that last a few seconds or less 6. pain that radiates into the lower extremities |
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history: associated sx
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1. dyspnea
2. diaphoresis 3. weakness 4. nausea/vomiting 5 dizziness/syncope 6. angor animi (profound sense of impending doom) |
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how presentations vary
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-Women present with more co-morbidities at a later age, with different types of complaints
-The elderly (esp. > 75 yo) and diabetics often present without “chest pain” |
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circadian pattern of onset of ischemic events
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-in the morning more common
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physical exam
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-appearance: anxious, restless, pallor, diaphoresis
-vital signs: pulse, BP variable; fever within 24-48 hrs -pulmonary: inc rate, cough, rales, wheeze -JVD/edema -Cardiac exam: ? muffled sounds, SEM (systolic ejection murmur), rub, paradoxical split S2 (LBBB), S3, S4 |
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diagnostic tests
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1. CBC, plts, ESR, coag profile
2. electrolytes, BUN, creatinine 3. ABG or pulse oximetry 4. CXR -SHOULD NOT DELAY EKG! |
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EKG
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-Classic: ST elevation, T wave inversion, Q waves ("transmural"). DON’T WAIT FOR Q!!
-non‑Q wave with ST elevation ("subendocardial") “STEMI” -Other ST-T wave changes with chest pain: Unstable Angina/Non-ST elevation MI (UA/NSTEMI) |
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Unstable angina
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1. Rest angina: Angina occurring at rest and usually prolonged >20 minutes occurring within a week of presentation.
2. New onset angina: Angina of at least CCSC III severity with onset within 2 months of trial presentation*. 3. increasing angina: Previously diagnosed angina that isdistinctly more frequent, longer in durationor lower in threshold. |
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features not characteristic of MI
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1. pleuritic pain
2. Primary or sole location of discomfort in the middle or lower abdominal region 3. Pain that may be localized at the tip of 1 finger, particularly over the LV apex 4. Pain reproduced with movement or palpation 5. Episodes of pain that last a few seconds or less 6. pain that radiates into the lower extremities |
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Localization of infarct
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Anterior: I, V2‑4
Anterolateral: I, aVL, V5‑6 Inferior: II, III, aVF Posterior: large R wave and upright T wave V1 |
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Serum markers
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1. AST, LDH
2. CK-MB 3. myoglobin- goes up first 4. troponin-I 5. troponin- T -slide 58 |
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history: associated sx
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1. dyspnea
2. diaphoresis 3. weakness 4. nausea/vomiting 5 dizziness/syncope 6. angor animi (profound sense of impending doom) |
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how presentations vary
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-Women present with more co-morbidities at a later age, with different types of complaints
-The elderly (esp. > 75 yo) and diabetics often present without “chest pain” |
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circadian pattern of onset of ischemic events
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-in the morning more common
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physical exam
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-appearance: anxious, restless, pallor, diaphoresis
-vital signs: pulse, BP variable; fever within 24-48 hrs -pulmonary: inc rate, cough, rales, wheeze -JVD/edema -Cardiac exam: ? muffled sounds, SEM (systolic ejection murmur), rub, paradoxical split S2 (LBBB), S3, S4 |
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diagnostic tests
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1. CBC, plts, ESR, coag profile
2. electrolytes, BUN, creatinine 3. ABG or pulse oximetry 4. CXR -SHOULD NOT DELAY EKG! |
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EKG
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-Classic: ST elevation, T wave inversion, Q waves ("transmural"). DON’T WAIT FOR Q!!
-non‑Q wave with ST elevation ("subendocardial") “STEMI” -Other ST-T wave changes with chest pain: Unstable Angina/Non-ST elevation MI (UA/NSTEMI) |
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Unstable angina
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1. Rest angina: Angina occurring at rest and usually prolonged >20 minutes occurring within a week of presentation.
2. New onset angina: Angina of at least CCSC III severity with onset within 2 months of trial presentation*. 3. increasing angina: Previously diagnosed angina that isdistinctly more frequent, longer in durationor lower in threshold. |
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Localization of infarct
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Anterior: I, V2‑4
Anterolateral: I, aVL, V5‑6 Inferior: II, III, aVF Posterior: large R wave and upright T wave V1 |
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Serum markers
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1. AST, LDH
2. CK-MB 3. myoglobin- goes up first 4. troponin-I 5. troponin- T -slide 58 |
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CK-MB
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Twice normal in six hours, peaks 12-24 hours, gone in 4-5 days
Useful in ruling out AMI in ED Prognostic utility in predicting complications >90% sensitive three hour s/p presentation problems: also in s. muscle, bone, brain; wide range of nmls; requires sig damage to raise levels |
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myogobin
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Twice nl. in two hours, peaks 4-6 hours, gone by 12 hours
91% sensitivity one hour after presentation 99% NPV within one hour after presentation problem: found in all types of muscle |
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troponin
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Regulates tropomyosin's interaction with actin/myosin
Samples left sitting may lose detectable troponin Presence in even small amounts suggests injury Twice nl. in six hours peak 12-24 hours Elevated up to 14 days |
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Acute Cardiac Imaging When Dx. Unclear
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1. 2D echo
wall motion LV function aneurysm MR, VSD, etc. 2. Radionucleotide imaging -perfusion, ventriculography studies. Non-specific 3. CT/CTA, MRI/MRA, PET |
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slide 74
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slide 74
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morphine
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-(2 - 4 mg IV with increments of 2 - 8 mg IV, repeated at 5 - 15 minute intervals) is the analgesic of choice for STEMI-associated pain management
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beta blockers
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-Oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have the following:
1. signs of HF 2. inc risk for cardiogenic shock 3. inc time since onset of sx |
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C/I to bblocks
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1. PR interval >.24 sec
2. sec or 3rd degree heart block 3. active asthma or reactive airway dz |
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STEMI <12 hrs duration- reperfusion options
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-invasive (PCI) (within 90 min)- angioplasty or stenting
-fibrinolytics (door to needle 30 min) Choice based on: time, risk, availability |
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Fibrinolytics
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-non-selective plasmin produces: ? higher incidence of bleeding. Lower risk of ICH (stop heparin): Streptokinase
-relatively clot-selective cont low-dose heparin: rt-PA |
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Reteplase
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-recombinant protein derivative of human tissue plasminogen activator
-catalyzes conversion of plasminogen to plasmin -10 U IV bolus, repeated 30 min later |
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contraindications to fibrinlytic therapy
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Any prior intracranial hemorrhage
Known structural cerebral vascular lesion (eg, AVM) Known malignant intracranial neoplasm Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours Suspected aortic dissection Active bleeding or bleeding diathesis (x menses) Significant closed head trauma or facial trauma within 3 months |
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finbrinolytics- complications
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1. bleeding
2. arrhythmias 3. hypotension 4. nausea, vomiting, fever, chilld, rash |
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STEMI <12 hrs- adjunctive therapies
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1. ACEs
2. ARBs 3. Statins |
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UA/NSTEMI or STEMI >12 hrs
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1. No fibrinolytics!
2. Glycoprotein IIb/IIa inhibitor 3. Risk Stratify 4. Early Invasive Strategy if High Risk |
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AHA high risk indicators
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1. New ST-segment depression and positive troponin
2. persistent or recurrent sx 3. hemodynamic instability or VT 4. depressed LV function (ejection fraction <40%) 5. ECG or functional study that suggest multivessel CAD |
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common arrhythmias after MI
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PVCs
Bradycardias 2nd degree Type I AV block (Inferior MI) 2nd degree Type II AV block (Anteroseptal MI) 3rd degree AV block (Inferior/Anterior MI) Tachycardias |
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post-hospital discharge care
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A Aspirin & Anticoagulants
ACEI if CHF, ST elev., LBBB B Beta blockers and BP C Cholesterol/ Cigarettes D Diet and Diabetes E Education and Exercise ERT (HRT) not to be initiated p MI, but should be continued in women already on it |
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intra-aortic balloon pump (IABP)
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-inflates during diastole to support coronary vessel perfusion
-deflates during systole to allow flow through the aorta to systemic circulation -significantly decreases afterload, and therefore myocardial wall stress |
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secondary prevention
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1. stop smoking, no exposure to enviornmental tobacco smoke
2. control BP <140/90 or <130/80 if pt has DM or chronic kidney disease 3. physical activity: 30 min, 7 days/week 4. wt mgmt: BMI 18.5-24.9 and waist circumferance <40 in men and <35 in women 5. HbA1c < 7% 6 flu vaccine |
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reperfusion strategies for STEMI
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-PLan A: PCI
-Plab B: thrombolytics |
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barriers to timely reperfusion
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1. the pt: failure to recognize sx, hesitate to seek med attention
2. time to transport 3. decision process on arrival 4. time to implement treatment strategy |