Mdcu Comprehensive Cardio

MD Chula 2010 Comprehensive tutorial y Feb 2010 nl O se U Spectrum of Coronary Heart Disease al rn • Chronic Ischemic Heart Disease – Chronic stable angina te • Acute Coronary Syndromes In – Unstable angina / non ST elevation MI – Acute ST elevation MI • Sudden Cardiac Death • Ischemic Cardiomyopathy • Silent ischemia

MD Chula 2010 Coronary Heart Disease Stable disease Acute Coronary Syndromes (Stable plaque) (Active plaque) • Chronic stable angina • UA / NSTEMI • Ischemic • Acute ST elevation MI y cardiomyopathy • Ischemic sudden cardiac nl • Silent ischemia death O se U ACS and CSA al rn CHEST PAIN te • Angina vs non-angina • Typical vs atypical angina In • Exclude other life threatening non cardiac chest pain • STEMI vs NSTEMI/Unstable vs stable angina • Plaque rupture vs secondary UAE

MD Chula 2010 CHEST PAIN • Angina vs non-angina • Typical vs atypical angina •Location • Exclude other life threatening non cardiac chest y pain ( next slide) •Characteristic nl • STEMI vs NSTEMI/Unstable vs stable angina •Radiation • Plaque rupture vs secondary UAE •Exertion O •relief se U ED Evaluation of Patients With STEMI al Differential Diagnosis of STEMI: rn Other Nonischemic Cardiovascular te • Early repolarization • Pericarditis •Brugada syndrome • Wolff-Parkinson- • Vasospastic angina •Myocarditis White syndrome •Hyperkalemia In • Hypertrophic • Deeply inverted T- cardiomyopathy •Bundle-branch waves suggestive of a blocks • Atypical angina central nervous system lesion or apical hypertrophic cardiomyopathy • LV hypertrophy with strain 6

MD Chula 2010 ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Other Noncardiac Gastroesophageal reflux Cervical disc or neuropathic (GERD) and spasm pain Chest-wall pain Biliary or pancreatic pain Pleurisy Somatization and psychogenic pain disorder y Peptic ulcer disease Panic attack nl O se 7 U CHEST PAIN al rn • Angina vs non-angina • Typical vs atypical angina te In • Exclude other life threatening non cardiac chest pain ( next slide) • STEMI vs NSTEMI/Unstable vs stable angina • Plaque rupture vs secondary UAE

MD Chula 2010 ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Life-Threatening Aortic dissection Pulmonary embolus Perforating ulcer y Tension pneumothorax Boerhaave syndrome nl (esophageal rupture with mediastinitis) O se 9 U ED Evaluation of Patients With STEMI al Differential Diagnosis of STEMI: Life-Threatening rn Aortic dissection Sudden onset te Pulmonary embolus Tearing pain In Perforating ulcer BP Tension pneumothorax Radiate to back Boerhaave syndrome Unequal pulse (esophageal rupture with mediastinitis) Stroke 10

MD Chula 2010 ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Life-Threatening Aortic dissection Sudden onset Pulmonary embolus Dyspnea Perforating ulcer Tension pneumothorax hypoxemia y Boerhaave syndrome tachycardia nl (esophageal rupture with mediastinitis) Lung clear O Pleuritic pain se 11 U ED Evaluation of Patients With STEMI al Differential Diagnosis of STEMI: Life-Threatening rn Aortic dissection te Pulmonary embolus Epigastric pain In Perforating ulcer Guarding Tension pneumothorax of liver dullness Loss Boerhaave syndrome (esophageal rupture with mediastinitis) 12

MD Chula 2010 ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Life-Threatening Aortic dissection Sudden onset Pulmonary embolus Tearing pain Perforating ulcer BP y Tension pneumothorax Radiate to Boerhaave syndrome back nl (esophageal rupture with mediastinitis) Unequal pulse O Stroke se 13 U ED Evaluation of Patients With STEMI al Differential Diagnosis of STEMI: Life-Threatening rn Sudden onset dyspnea Aortic dissection Trachea shift te Pulmonary embolus Hyperresonance on In Perforating ulcer percussion Tension pneumothorax Subcut.emphysema Boerhaave syndrome (esophageal rupture with mediastinitis) 14

MD Chula 2010 ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Other Nonischemic Cardiovascular • Early repolarization • Pericarditis •Brugada syndrome • Wolff-Parkinson- • Vasospastic angina Position syndrome •Myocarditis White related • Hypertrophic •Hyperkalemia • Deeply inverted T- cardiomyopathy Sharp pain waves suggestive of a •Bundle-branch y blocks • Atypical angina Rubcentral nervous system nl lesion or apical hypertrophic cardiomyopathy O • LV hypertrophy with strain se 15 U ACS and CSA al rn CHEST PAIN • Angina vs non-angina te • Typical vs atypical angina In • Exclude other life threatening non cardiac chest pain • STEMI vs NSTEMI/Unstable vs stable angina • UAE : Plaque rupture vs secondary UAE • Risk stratification

MD Chula 2010 Spectrum of Coronary Heart Disease • Chronic Ischemic Heart Disease – Chronic stable angina • Acute Coronary Syndromes • Acute ST elevation MI EKG y – non ST elevation MI nl – Unstable angina • Sudden Cardiac Death O • Ischemic Cardiomyopathy • Silent ischemia • Printzmetal angina se U Spectrum of Coronary Heart Disease al rn • Chronic Ischemic Heart Disease – Chronic stable angina te • Acute Coronary Syndromes – Unstable angina In Cardiac – non ST elevation MI marker – Acute ST elevation MI • Sudden Cardiac Death • Ischemic Cardiomyopathy • Silent ischemia • Printzmetal angina

MD Chula 2010 Spectrum of Acute Coronary Syndromes Presentation Ischemic Discomfort at Rest Emergency No ST-Segment ST- ST-Segment Department Elevation Elevation y nl + + + O In- In-Hospital Unstable Non STEMI STEMI Angina se (Non-Q-wave MI) (⊕ : positive cardiac biomarker) (Q-wave MI) U Further investigations for al “making diagnosis” diagnosis” rn History te Intermediate Low likelihood High likelihood In likelihood - Excluded Need for - Monitor, f/u risk stratification? EST yes no Stress imaging Rx Coronary Angiography

MD Chula 2010 High risk • Prolong pain >20 min • S3 or rale • Hypotension y • Pulmonary edema nl • New or worsening MR O • Dynamic ST change > 1 mm • Troponin positive se U al Intermidiate risk rn • Rest angina >20 min but relief by nitrate te • Nocturnal angina In • Age > 65 yrs • Dynamic T wave change > 1 mm

MD Chula 2010 Low risk • Resting angina < 20 min • Normal or unchange EKG y nl O se U Acute Coronary Syndromes al Management of Unstable Angina: Risk evaluation rn Features Higher risk Lower risk te CAD- CAD- likelihood - Known/suspect - Low History - Prolonged, rest - Effort angina In chest pain - Angina > 2 wk PE - Hemodynamic - Normal instability ECG - Dynamic ST - Normal / near- near- changes normal - Deep inverted T Troponin T or I - Positive - Negative

MD Chula 2010 Acute Coronary Syndromes Management of Unstable Angina: Risk evaluation Unstable Angina y Higher risk Lower risk nl O • Worse outcomes • Good prognosis • CCU admission • Out-patient, ward Out- • Aggressive Rx se • Less aggressive Rx U al rn te F Clinical predictors In F ECG F Cardiac markers

MD Chula 2010 Cardiac markers in UA / NSTEMI • Only useful in appropriate clinical settings (ie. CP suspicious of ACS) • Can be falsely elevated in many other y clinical conditions nl • Typical rise & fall is helpful to make O diagnosis of ACS se U TIMI Risk Score al rn 1. Age > 65 2. Risk factor > 2 0 - 2 = Low risk te 3. Known CAD (>50% stenosis) (>50 % In 4. Prior aspirin use (last 7 d) 3 - 4 = Int. risk 5. (2) Chest pain in the last 24 h 5 - 7 = High risk 6. ST changes on ECG 7. Elevated cardiac markers

MD Chula 2010 Current Management of ACS Plaque rupture Stable Unstable Non-Q Q-wave angina angina wave MI MI y Non-ST elevation ACS ST elevation ACS nl O ECG se U Fibrous Cap al Rupture rn Platelet Tissue Factor Activation Release te In Platelet TF binds & activate Adhesion Factor VII Platelet Extrinsic Coagulation Aggregation Pathway Cascade CLOT

MD Chula 2010 y nl O se U Management of UA / NSTEMI al rn • Prevent death / MI (Keep the artery from closing!) te – Prevent further propagation of thrombus • Antiplatelet In • Anticoagulant – Mechanical opening: revascularization (PCI, CABG) • Relieve ischemia – Anti-anginal agents Anti- – Revascularization (PCI, CABG)

MD Chula 2010 Recent Updates in NSTEMI: What’s New? ESC Guidelines for the Management of NSTE-ACS June 2007 August 2007 y nl O se 33 U Updated Guidelines al Classes of Recommendations rn I IIa IIb III Intervention is useful and effective te Evidence conflicts/opinions differ but In leans towards efficacy Evidence conflicts/opinions differ but leans against efficacy Intervention is not useful/effective and may be harmful

MD Chula 2010 Updated Guidelines Weighing the Evidence n 1994 version was starting point; literature searches added more current reports n Weight of evidence grades: = Data from many large, randomized trials y = Data from fewer, smaller randomized trials, nl careful analyses of nonrandomized studies, O observational registries = Expert consensus se U al rn te Medication In UAE / nonSTEMI

MD Chula 2010 Hospital Care Anti- Anti-Thrombotic Therapy I IIa IIb III Immediate Aspirin Clopidogrel, if aspirin contraindicated Aspirin + clopidogrel for up to 1 month, y if medical therapy or PCI is planned nl Heparin (IV unfractionated, scLMWH) with antiplatelet agents listed above O Enoxaparin preferred over UFH unless CABG is planned within 24 hours se U Hospital Care al Clopidogrel Therapy rn I IIa IIb III te Aspirin + clopidogrel, for up to 1 month* In Aspirin + clopidogrel, for up to 9 months* Withhold clopidogrel for 5-7 days for CABG * For patients managed with an early conservative strategy, and those who are planned to undergo early PCI hGuidelines do not specify initial approach to using clopidogrel when coronary anatomy is unknown

MD Chula 2010 Hospital Care Platelet GP IIb/IIIa Inhibitors ( 1) (1 I IIa IIb III Any GP IIb/IIIa inhibitor + ASA/Heparin for all patients, if cath /PCI planned Eptifibatide or tirofiban + ASA/Heparin for high-risk* patients in whom early cath/PCI is not planned y nl Any GP IIb/IIIa inhibitor for patients already on ASA + Heparin + clopidogrel, O if cath /PCI is planned se * High-risk: Age > 75; prolonged, ongoing CP; hemodynamic instability; rest CP w/ ST ∆; VT; positive cardiac markers U Hospital Care al Platelet GP IIb/IIIa Inhibitors ( 2) (2 rn I IIa IIb III te Eptifibatide or tirofiban + ASA/Heparin for patients without continuing In ischemia in whom PCI is not planned Abciximab for patients in whom PCI is not planned

MD Chula 2010 Hospital Care Anti- Anti-Ischemic Therapy (1) (1 I IIa IIb III β-blocker (IV→oral) if not contraindicated Non-dihydropyridine Ca2+ antagonist if β- blocker contraindicated and no LV y dysfunction, for recurrent ischemia nl ACE inhibitor if ↑ BP persists with NTG+ β-blocker, for pts with CHF or diabetes O se U Hospital Care al Anti- Anti-Ischemic Therapy (2) (2 rn I IIa IIb III ACE inhibitor for all ACS pts te Extended-release Ca 2+ blocker instead of β-blocker In Immediate-release Ca 2+ blocker with β- blocker Long-acting Ca2+ blocker for recurrent ischemia, if no contraindications and NTG + β-blocker used fully

MD Chula 2010 Early Invasive Strategy Class I l An early invasive strategy is indicated in patients who have refractory angina or hemodynamic or electrical instability (without contraindications). (LOE: B) y l An early invasive strategy is indicated in initially stabilized patients (without contraindications) who have are high nl risk for clinical events. (LOE: A) O l In women with low-risk features, a conservative strategy is recommended. (Level of Evidence: B) se Anderson JL. J Am Coll Cardiol 2007;50:e1-157 U Early Invasive vs Conservative al Strategy rn Class IIb l In initially stabilized patients, an initially conservative te strategy may be considered for patients who have elevated risk including those who are troponin positive. In (LOE: B) l The decision to implement an initial conservative (vs. invasive) strategy in these patients can consider MD and patient preference. (LOE: C) l An invasive strategy may be reasonable in patients with chronic renal insufficiency. (Level of Evidence: C) Anderson JL. J Am Coll Cardiol 2007;50:e1-157

MD Chula 2010 Early Invasive Strategy Not Recommended Class III l An early invasive strategy is not recommended in patients with extensive comorbidities, in whom the risks of revascularization are likely to outweigh the benefits. (LOE: C) y l An early invasive strategy is not recommended in patients with nl acute chest pain and a low likelihood of ACS. (LOE: C) l An early invasive strategy should not be performed in patients who O will not consent to revascularization. (LOE: C) se Anderson JL. J Am Coll Cardiol 2007;50:e1-157 U Hospital Care al Conservative vs. Invasive Strategies (1) (1 I IIa IIb III rn Early invasive strategy in high-risk patients with any of the following: te - Recurrent ischemia, despite meds - Elevated Troponin I or T In - New ST-segment depression ST- - New CHF symptoms - High-risk stress test findings High- - LV dysfunction (EF < 40%) 40%) - Hemodynamic instability, sustained VT - PCI within 6 months, prior CABG

MD Chula 2010 Hospital Care Conservative vs. Invasive Strategies (2) (2 I IIa IIb III Either strategy in low- to moderate-risk patients without contraindications to revascularization y Early invasive strategy for patients with nl repeated ACS presentations, without high-risk features or ongoing ischemia O se U al Biological changes Inflammation, abnormal flow dynamics, rn LDL oxidation, infection?, etc. te Antiplatelets PLAQUE DISRUPTION Anticoagulant In Platelet aggregation, thrombus formation Mechanical obstruction Ischemia PCI Infarction CABG Sudden death

MD Chula 2010 Diagnosis of UA/NSTEMI is Likely Algorithm for an or Definite Initial ASA (Class I, LOE: A) Invasive Clopidogrel if ASA intolerant (Class I, LOE: A) Strategy Select Management Strategy Proceed with an Initial Conservative Strategy Initial Invasive Strategy Initiate Anticoagulant Rx (Class I, LOE: A) Choices: enoxaparin or UFH (Class I, LOE: A) Alternatives: bivalirudin or fondaparinux (Class I, LOE: B) y Prior to Angiography Initiate at least one (Class I, LOE: A) or both (Class IIa, LOE: B) of : nl Clopidogrel IV GP IIb/IIIa inhibitor Factors favoring both include: O Delay to Angiography High Risk Features Early recurrent ischemic discomfort se Proceed to Angiography Anderson JL. J Am Coll Cardiol 2007;50:e1-157. Figure 7 U Algorithm for Initial Conservative Strategy al Diagnosis of UA/NSTEMI is Likely or Definite rn ASA (Class I, LOE: A) te Clopidogrel if ASA intolerant (Class I, LOE: A) Select Management Strategy Proceed with In Invasive Strategy Conservative Strategy Initiate Anticoagulation Rx (Class I, LOE: A): choices: enoxaparin or UFH (Class I, LOE: A) or fondaparinux (Class I, LOE: B), but enoxaparin or fondaparinux are preferable (Class IIA, LOE: B) Initiate clopidogrel (Class I, LOE: A) Consider adding GPIIbIIIa antagonist IV eptifibatide or tirofiban (Class IIb, LOE: B) (Continued) Anderson JL. J Am Coll Cardiol 2007;50:e1-157. Figure 8

MD Chula 2010 Algorithm for Initial Conservative Strategy (Continued) Any subsequent events necessitating angiography? Yes No Evaluate LVEF (Class IIa, (Class I, LOE: B) y EF 0.40 or LOE: B) EF greater less than 0.40 Stress Test nl (Class IIa, LOE: B) Proceed to Dx Not Low Low Risk (Class I, LOE: A) O Angiography (Class I, LOE: A) Risk Cont ASA indefinitely (Class I, LOE A) Cont clopidogrel for at least one month (Class I, LOE A) and ideally up to 1 yr (Class I, LOE B) Anderson JL. J Am Coll Cardiol 2007;50:e1-157. Figure 8 se DC IV GP IIb/IIIa if started previously (Class I, LOE A) DC Anticoagulation Rx (Class I, LOE A) U Conclusions al rn • Invasive strategy appears to be a better strategy for intermediate- and high-risk intermediate- high- te non- non-ST elevation ACS patients In • This can only be accomplished by – Aggressive antithrombotic agents (combined antiplatelets, LMWH) – Use of GPIIbIIIa inhibitors and stents in the cath lab/PCI procedures

MD Chula 2010 Conclusions • For low-risk (and some intermediate- low- intermediate- risk) patients, conservative (selectively invasive) strategy is y appropriate nl • No one should go home without at O least non-invasive stress test non- se U al Discharge/Post- Discharge/Post-Discharge Medications rn I IIa IIb III te ASA, if not contraindicated Clopidogrel, when ASA contraindicated In Aspirin + Clopidogrel, for up to 9 months β-blocker, if not contraindicated Lipid ↓ agents + diet, if LDL >130 mg/dL ACE Inhibitor: CHF, EF < 40%, DM, or HTN

MD Chula 2010 Risk Factor Modification I IIa IIb III Smoking Cessation Counseling Dietary Counseling and Modification y Cardiac Rehabilitation Referral nl HTN Control (BP < 130/85 mm Hg) O Tight Glycemic Control in Diabetics se U Preparation for Discharge After UA/NSTEMI al rn • Antiplatelet Rx – ASA 75 - 162 mg/day – Clopidogrel 75 mg/day te • Beta Blocker • ACEI / ARB – Especially if DM, HF, EF <40%, HTN In • Statin – LDL <100 mg/dL (ideally <70 mg/dL) • Secondary Prevention Measures – Smoking Cessation – BP <140/90 mm HG or <130/80 mm HG for DM or chronic kidney disease – HbA1C <7% – BMI 18.5-24.9 – Physical Exercise 30-60 min at least 5 days/wk

MD Chula 2010 Acute STEMI y nl O se U al rn te In

MD Chula 2010 ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Life-Threatening Aortic dissection Tension pneumothorax Pulmonary embolus Boerhaave syndrome Perforating ulcer (esophageal rupture with mediastinitis) y nl O se 59 U ED Evaluation of Patients With STEMI al Differential Diagnosis of STEMI: Other Cardiovascular and rn Nonischemic te Pericarditis LV hypertrophy with strain Atypical angina Brugada syndrome In Early repolarization Wolff-Parkinson-White Myocarditis syndrome Hyperkalemia Deeply inverted T-waves Bundle-branch blocks suggestive of a central nervous system lesion Vasospastic angina or apical hypertrophic Hypertrophic cardiomyopathy cardiomyopathy 60

MD Chula 2010 ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Other Noncardiac Gastroesophageal reflux Cervical disc or neuropathic (GERD) and spasm pain Chest-wall pain Biliary or pancreatic pain Pleurisy Somatization and psychogenic pain disorder y Peptic ulcer disease Panic attack nl O se 61 U al Ischemic myocardium potentially salvageable by reperfusion rn 100 te 80 Ischemic myocardium potentially salvageable In 60 by intervention 40 20 Necrotic myocardium 1 2 3 4 5 6 12 18 24 3 6 9 12 6 Reversible Irreversible injury injury Hours Days Wks

MD Chula 2010 Options for Transport of Patients With STEMI and Initial Reperfusion Treatment • Patients receiving fibrinolysis should be risk-stratified to identify need for further revascularization with percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG). • All patients should receive late hospital care and secondary prevention of STEMI. Noninvasive Risk Fibrinolysis Stratification y Not Late Rescue Ischemia Hospital Care PCI Capable nl driven and Secondary PCI Capable Prevention O PCI or CABG Primary PCI se 63 U ACC/AHA Guideline for AMI al rn Step 1 Access time and risk te • Time since onset of symptoms In • Risk of STEMI • Risk of fibrinolysis • Time required for transport to a skill PCI lab.

MD Chula 2010 ACC/AHA Guideline for AMI Fibrinolysis is generally prefered • Early presentation • Invasive strategy is not an option • Delay to invasive strategy y • Prolong transport (door to balloon – door to nl neddele time > 60 minutes) O • Medical contact to balloon or door to balloon time is > 90 minutes. se U Reperfusion Options for STEMI Patients Step 2: Select Reperfusion Treatment. al If presentation is < 3 hours and there is no delay to an invasive strategy, rn there is no preference for either strategy. Invasive strategy generally preferred § Skilled PCI lab available with surgical backup te § Door-to-balloon < 90 minutes § Door to balloon – door to neddele time < 1 hour In § High Risk form STEMI § Cardiogenic shock, Killip class ≥ 3 § Contraindications to fibrinolysis, including increased risk of bleeding and ICH § Late presentation § > 3 hours from symptom onset § Diagnosis of STEMI is in doubt 66

MD Chula 2010 Contraindications and Cautions for Fibrinolysis in STEMI Absolute • Any prior intracranial hemorrhage Contraindications • Known structural cerebral vascular lesion (e.g., arteriovenous malformation) • Known malignant intracranial neoplasm (primary or metastatic) y • Ischemic stroke within 3 months EXCEPT nl acute ischemic stroke within 3 hours O NOTE: Age restriction for fibrinolysis has been removed compared with prior guidelines. se 67 U Contraindications and Cautions for Fibrinolysis in STEMI al rn Absolute • Suspected aortic dissection Contraindications • Active bleeding or bleeding diathesis te (excluding menses) • Significant closed-head or facial trauma In within 3 months 68

MD Chula 2010 Contraindications and Cautions for Fibrinolysis in STEMI Relative • History of chronic, severe, poorly controlled Contraindications hypertension • Severe uncontrolled hypertension on presentation (SBP > 180 mm Hg or DBP > 110 mm Hg) • History of prior ischemic stroke greater than y 3 months, dementia, or known intracranial pathology not covered in contraindications nl • Traumatic or prolonged (> 10 minutes) CPR or major surgery (< 3 weeks) O se 69 U Contraindications and Cautions for Fibrinolysis in STEMI al rn Relative • Recent (< 2 to 4 weeks) internal bleeding Contraindications • Noncompressible vascular punctures te • For streptokinase/anistreplase: prior exposure (> 5 days ago) or prior allergic In reaction to these agents • Pregnancy • Active peptic ulcer • Current use of anticoagulants: the higher the INR, the higher the risk of bleeding 70

MD Chula 2010 pitfall Diagnosis • Do not serial EKG • Do not do EKGàDelay in Dx (atypical y presentation) nl • Miss Dx (aortic dissection ) O se U al pitfall rn Management te • Use too much time to Dx In • Delay treatment after Dx • Do not beware of thrombolysis contraindication • Do not reassess sign of reperfusion

MD Chula 2010 Summary of Pharmacologic Rx: Ischemia 1st During Hosp DC + 24 h Hosp Long Term Aspirin 162-325 mg 75-162 75-162 chewed mg/d p.o. mg/d p.o. Fibrinolytic tPA,TNK, rPA, SK y 60U/kg (4000) aPTT nl UFH 12 U/kg/h (1000) 1.5 - 2 x C aPTT 1.5 - 2 x C O Beta-blocker Oral daily Oral daily Oral daily JACC 2004;44: 671 Circulation 2004;110: 588 se 73 U Summary of Pharmacologic Rx: LVD, Sec. Prev., al 1st During Hosp Hosp DC + 24 h Long Term rn ACEI Anterior MI, Oral Pulm Cong., EF < 40 Oral Daily te ARB ACEI intol., Daily Indefinitely HF, EF < 40 In Aldo No renal dysf, Same as Blocker K+ < 5.0 mEq/L during On ACEI, Hosp. HF or DM Statin Start w/o lipid Indefinitely, profile LDL << 100 JACC 2004;44:671 2004;44: Circ 2004;110:588 2004;110: 74

MD Chula 2010 This slide set was adapted from the 2007 Focused Update of the ACC/AHA Guidelines for Management of Patients With ST-Elevation Myocardial Infarction (Journal of the American College of Cardiology published ahead of print on December 10, 2007, available at http://content.onlinejacc.org/cgi/content/full/j.jacc .2007.10.001. y The full-text guidelines are also available on the nl Web sites: ACC (www.acc.org) and, O AHA (www.americanheart.org) se ACC/AHA 2007 STEMI Guidelines Focused Update U al rn te Thienopyridines In ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 CLARITY-TIMI 28 Primary Endpoint: Occluded Artery (or D/MI thru Angio/HD) 36% Odds Ratio 0.64 Occluded Artery or Death/MI (%) 25 21.7 Odds Reduction (95% CI 0.53-0.76) 20 P=0.00000036 15.0 15 y 10 nl 5 O n=1752 n=1739 0.4 0.6 0.8 1.0 1.2 1.6 0 Clopidogrel Placebo Clopidogrel Placebo better better LD 300 mg MD 75 mg se STEMI, Age 18-75 Sabatine N Eng J Med 2005;352:1179. ACC/AHA 2007 STEMI Guidelines Focused Update U COMMIT: Effect of CLOPIDOGREL on al Death In Hospital Placebo + ASA: rn 1,846 deaths (8.1%) Clopidogrel + ASA: 1,728 deaths (7.5%) te 0.6% ARD 7% RRR Dead In (%) P = 0.03 N = 45,852 No Age limit ; 26% > 70 y Lytic Rx 50% No LD given Chen ZM, et al. Lancet. 2005;366:1607. Days Since Randomization (up to 28 days) ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Summary of Pharmacologic Rx: Ischemia 1st During Hosp DC + 24 h Hosp Long Term Aspirin 162-325 mg Clopidogrel 75-162 75-162 chewed mg/d p.o. mg/d p.o. Fibrinolytic tPA,TNK, rPA, SK y 60U/kg (4000) aPTT nl UFH 12 U/kg/h (1000) 1.5 - 2 x C aPTT 1.5 - 2 x C O Beta-blocker Oral daily Oral daily Oral daily JACC 2004;44: 671 Circulation 2004;110: 588 se 79 U al rn te Anticoagulants In ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Anticoagulants I IIa IIb III Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours (Level of Evidence: C) and preferably for the duration of the index hospitalization, up to 8 days I IIa IIb III (regimens other than unfractionated heparin [UFH] are recommended if anticoagulant therapy is given for more than 48 hours because of the risk of heparin-induced y thrombocytopenia with prolonged UFH treatment). nl (Level of Evidence: A) O Anticoagulant regimens with established efficacy include: ♥ UFH (LOE: C) ♥ Enoxaparin (LOE:A) ♥ Fondaparinux (LOE:B) se ACC/AHA 2007 STEMI Guidelines Focused Update U Unfractionated Heparin al Advantages Disadvantages rn § Immediate anticoagulation § Indirect thrombin inhibitor so does not inhibit clot-bound § Multiple sites of action in te thrombin coagulation cascade § Nonspecific binding to: § Long history of successful ― Serine proteases In clinical use ― Endothelial cells (can lead to variability in level of § Readily monitored by aPTT and anticoagulation) ACT § Reduced effect in ACS ― Inhibited by PF-4 § Causes platelet aggregation § Nonlinear pharmacokinetics § Risk of HIT Hirsh J, et al. Circulation. 2001;103:2994-3018. aPTT = activated partial thromboplastin time; ACT = activated coagulation time; PF-4 = platelet factor 4; HIT = heparin-induced thrombocytopenia. ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Low-Molecular-Weight Heparin Advantages Disadvantages § Increased anti-Xa to anti-IIa activity → § Indirect thrombin inhibitor inhibits thrombin generation more § Less reversible effectively § Difficult to monitor § Induces ↑ release of TFPI vs UFH (no aPTT or ACT) § Not neutralized by platelet factor 4 § Renally cleared § Less binding to plasma proteins (eg, § Long half-life acute -phase reactant proteins) → more § Risk of HIT consistent anticoagulation y § Lower rate of HIT vs UFH § Lower fibrinogen levels nl § Easy to administer (SC administration) § Long history of clinical studies and experience, FDA-approved indications O § Monitoring typically unnecessary SC = subcutaneous; aPTT = activated partial thromboplastin time; ACT = activated coagulation time. se Hirsh J, et al. Circulation. 2001;103:2994-3018. TFPI = tissue factor pathway inhibitor; UFH = unfractionated heparin; ACC/AHA 2007 STEMI Guidelines Focused Update U ExTRACT-TIMI 25: Primary End Point (ITT) al Death or Nonfatal MI rn 15 UFH 12.0% te 12 Primary End Point (%) 17% RRR 9.9% In 9 Enoxaparin Relative Risk 6 0.83 (95% CI, 0.77 to 0.90) P<.001 3 Lost to follow-up = 3 0 0 5 10 15 20 25 30 Days after Randomization Adapted with permission from Antman EM, et al. N Engl J Med. 2006;354:1477-1488. ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Anticoagulants For patients undergoing PCI after having received an anticoagulant regimen, the following dosing recommendations should be followed: a. For prior treatment with UFH: administer additional boluses of UFH as needed to support y I IIa IIb III the procedure taking into account whether GP nl IIb/IIIa receptor antagonists have been administered. (Level of Evidence: C) Bivalirudin O may also be used in patients treated previously with UFH. (Level of Evidence: C) se Recommendation continues on the next slide. ACC/AHA 2007 STEMI Guidelines Focused Update U Anticoagulants al rn I IIa IIb III b. For prior treatment with enoxaparin: if the last SC dose was administered within the prior 8 hours, te no additional enoxaparin should be given; if the last SC dose was administered at least 8 to 12 hours earlier, an IV dose of 0.3 mg/kg of In enoxaparin should be given. I IIa IIb III c. For prior treatment with fondaparinux: administer additional intravenous treatment with an anticoagulant possessing anti-IIa activity taking into account whether GP IIb/IIIa receptor antagonists have been administered. ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Anticoagulants I IIa IIb III Because of the risk of catheter thrombosis, fondaparinux should not be used as the sole anticoagulant to support PCI. An additional anticoagulant with anti-IIa activity should be administered. y nl O se ACC/AHA 2007 STEMI Guidelines Focused Update U Summary of Pharmacologic Rx: Ischemia al 1st During Hosp DC + rn 24 h Hosp Long Term Aspirin 162-325 mg Clopidogrel 75-162 75-162 te chewed mg/d p.o. mg/d p.o. Fibrinolytic tPA,TNK, In rPA, SK 60U/kg (4000) aPTT UFH LMWH > 12 U/kg/h (1000) UFH 2 x C 1.5 - aPTT 1.5 - 2 x C Beta-blocker Oral daily Oral daily Oral daily JACC 2004;44: 671 Circulation 2004;110: 588 88

MD Chula 2010 Beta-Blockers y nl O se ACC/AHA 2007 STEMI Guidelines Focused Update U Beta-Blockers al rn II IIa IIb III Oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) te increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive In airway disease). I IIa IIb III It is reasonable to administer an IV beta blocker at the time of presentation to STEMI patients who are hypertensive and who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease). ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Beta-Blockers I IIa IIb III IV beta blockers should not be administered to STEMI patients who have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd- y degree heart block, active asthma, or reactive nl airway disease). O se ACC/AHA 2007 STEMI Guidelines Focused Update U al rn te Primary PCI In ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Primary PCI I IIa IIb III STEMI patients presenting to a hospital with PCI capability should be treated with primary PCI within 90 min of first medical contact as a systems goal. I IIa IIb III STEMI patients presenting to a hospital without PCI y capability, and who cannot be transferred to a PCI nl center and undergo PCI within 90 min of first medical contact, should be treated with fibrinolytic O therapy within 30 min of hospital presentation as a systems goal, unless fibrinolytic therapy is contraindicated. se ACC/AHA 2007 STEMI Guidelines Focused Update U al rn te Rescue and Late PCI In ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Rescue PCI A strategy of coronary angiography with intent to perform PCI (or emergency CABG) is recommended in patients who have received fibrinolytic therapy and have: I IIa IIb III a. Cardiogenic shock in patients < 75 years who are y suitable candidates for revascularization nl I IIa IIb III b. Severe congestive heart failure and/or pulmonary O edema (Killip class III) I IIa IIb III c. Hemodynamically compromising ventricular arrhythmias. se ACC/AHA 2007 STEMI Guidelines Focused Update U al Rescue PCI rn A strategy of coronary angiography with intent to I IIa IIb III perform rescue PCI is reasonable for patients in te whom fibrinolytic therapy has failed (ST-segment elevation < 50% resolved after 90 min following In initiation of fibrinolytic therapy in the lead showing the worst initial elevation) and a moderate or large area of myocardium at risk [anterior MI, inferior MI with right ventricular involvement or precordial ST-segment depression]. ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Rescue PCI A strategy of coronary angiography with intent to I IIa IIb III perform PCI in the absence of any of the above Class I or IIa indications might be reasonable in moderate- or high-risk patients, but its benefits and risks are not well established. The benefits y of rescue PCI are greater the earlier it is initiated after the onset of ischemic discomfort. nl O se ACC/AHA 2007 STEMI Guidelines Focused Update U al Rescue PCI rn A strategy of coronary angiography with intent to I IIa IIb III perform PCI (or emergency CABG) is not te recommended in patients who have received fibrinolytic therapy if further invasive In management is contraindicated or the patient or designee do not wish further invasive care. ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Late PCI after Fibrinolysis or for Patients Not Undergoing Primary Reperfusion I IIa IIb III PCI of a hemodynamically significant stenosis in a patent infarct artery > 24 hours after STEMI may be considered as part of a invasive strategy. PCI of a totally occluded infarct artery > 24 hours y II IIa IIb III after STEMI is not recommended in asymptomatic nl patients with 1- or 2-vessel disease if they are hemodynamically and electrically stable and do O not have evidence of severe ischemia. se ACC/AHA 2007 STEMI Guidelines Focused Update U al rn te Hospital Care In ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Anticoagulants I IIa IIb III It is reasonable for patients with STEMI who do not undergo reperfusion therapy to be treated with anticoagulant therapy (non-UFH regimen) for the duration of the index hospitalization, up to 8 days. y I IIa IIb III Convenient strategies that can be used include those with LMWH (Level of Evidence: C) or nl fondaparinux (Level of Evidence: B) using the same O I IIa IIb III dosing regimens as for patients who receive fibrinolytic therapy. se ACC/AHA 2007 STEMI Guidelines Focused Update U Emergency Management of Complicated STEMI Clinical signs: Shock, hypoperfusion, congestive heart failure, acute pulmonary edema al Most likely major underlying disturbance? Hypovolemia Low Output - Arrhythmia Acute Pulmonary Edema Cardiogenic Shock rn Administer Bradycardia Tachycardia First line of action Administer • Furosemide IV 0.5 to 1.0 mg/kg • Morphine IV 2 to 4 mg • Fluids • Oxygen/intubation as needed • Blood transfusions • Nitroglycerin SL, then 10 to 20 mcg/min IV if SBP • Cause-specific Check Blood Pressure te greater than 100 mm Hg interventions See Section 7.7 • Dopamine 5 to 15 mcg/kg per minute IV if SBP 70 to Consider vasopressors in the ACC/AHA Guidelines for 100 mm Hg and signs/symptoms of shock present Patients With ST-Elevation • Dobutamine 2 to 20 mcg/kg per minute IV if SBP 70 Myocardial Infarction to 100 mm Hg and no signs/symptoms of shock In Check Blood Pressure Systolic BP Systolic BP Systolic BP Systolic BP Second line of action Greater than 100 mm Hg 70 to 100 mm Hg 70 to 100 mm Hg less than 70 mm Hg NO signs/symptoms Signs/symptoms Signs/symptoms of shock Systolic BP of shock of shock Greater than 100 mm Hg and not less than 30 mm Hg below baseline Nitroglycerin Dobutamine Dopamine Norepinephrine 10 to 20 mcg/min IV 2 to 20 5 to 15 0.5 to 30 mcg/min IV mcg/kg per mcg/kg per ACE Inhibitors minute IV minute IV Short-acting agent such as captopril (1 to 6.25 mg) Third line of action Further diagnostic/therapeutic considerations (should be considered in nonhypovolemic shock) Circulation 2000;102(suppl I):I-172-I-216. Diagnostic Therapeutic ♥ Pulmonary artery catheter ♥ Intra-aortic balloon pump ♥ Echocardiography ♥ Reperfusion/revascularization ♥ Angiography for MI/ischemia ♥ Additional diagnostic studies 102

MD Chula 2010 Secondary Prevention and Long-Term Management y nl O se ACC/AHA 2007 STEMI Guidelines Focused Update U Secondary Prevention al rn • Stop smoking – I (B) • Clopidogrel 75 mg daily: te – PCI – I (B) – no PCI – IIa (C) In • Statin goal: – LDL-C < 100 mg/dL – I (A) – consider LDL-C < 70 mg/dL – IIa (A) • Daily physical activity 30 min 7 d/wk, minimum 5 d/wk – I (B) • Annual influenza immunization – I (B) ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Secondary Prevention and Long Term Management Goals Class I Recommendations Antiplatelet agents/ For all post-PCI STEMI stented patients without anticoagulants: aspirin resistance, allergy, or increased risk of Aspirin bleeding, aspirin 162 to 325 mg daily should be y given for at least 1 month after bare-metal stent implantation, 3 months after sirolimus-eluting nl stent implantation, and 6 months after paclitaxel- eluting stent implantation, after which long-term O aspirin use should be continued indefinitely at a dose of 75 to 162 mg daily. CHANGED TEXT se ACC/AHA 2007 STEMI Guidelines Focused Update U Secondary Prevention and Long Term Management al Goals Class I Recommendations rn Antiplatelet te agents/ For all post-PCI patients who receive a drug-eluting anticoagulants: stent (DES), clopidogrel 75 mg daily should be In given for at least 12 months if patients are not at Clopidogrel high risk of bleeding. For post-PCI patients receiving a bare metal stent (BMS), clopidogrel should be given for a minimum of 1 month and ideally up to 12 months (unless the patient is at increased risk of bleeding; then it should be given for a minimum of 2 weeks). CHANGED TEXT ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Secondary Prevention and Long Term Management Goals Recommendations Antiplatelet For all STEMI patients not undergoing stenting agents/ (medical therapy alone or PTCA without stenting), anticoagulants: treatment with clopidogrel should continue for at Clopidogrel least 14 d. (Class I; LOE: B) y Long-term maintenance therapy (e.g., 1 year) with nl clopidogrel (75 mg per day orally) is reasonable in STEMI patients regardless of whether they O undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. (Class IIa; NEW LOE: C) se RECS ACC/AHA 2007 STEMI Guidelines Focused Update U Secondary Prevention and Long Term Management al Goals Class I Recommendations rn Antiplatelet Managing warfarin to INR = 2.0 to 3.0 for te paroxysmal or chronic atrial fibrillation or flutter is agents/ recommended, and in post-STEMI patients when anticoagulants: clinically indicated (e.g., atrial fibrillation, left In Warfarin ventricular thrombus). CHANGED TEXT Use of warfarin in conjunction with aspirin and/or NEW clopidogrel is associated with increased risk of REC bleeding and should be monitored closely. In patients requiring warfarin, clopidogrel, and aspirin therapy, an INR of 2 to 2.5 is recommended NEW REC with low dose aspirin (75 to 81 mg) and a 75 mg dose of clopidogrel. ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Stepped Care Approach To Pharmacologic Therapy for Musculoskeletal Symptoms with Known Cardiovascular Disease or Risk Factors for Ischemic Heart Disease • Acetaminophen, ASA, tramadol, narcotic analgesics (short term) • Nonacetylated salicylates • Non COX-2 selective NSAIDs Select patients at low risk y of thrombotic events nl • NSAIDs with some • Regular monitoring for sustained Prescribe lowest dose COX-2 activity hypertension or worsening of prior required to control symptoms blood pressure control), edema, worsening renal function, or O gastrointestinal bleeding. Add ASA 81 mg and PPI to patients • COX-2 Selective at increased risk of thrombotic • If these events occur, consider events * NSAIDs reduction of the dose or discontinuation of the offending drug, a different drug, or alternative * Addition of ASA may not be sufficient protection against thrombotic events Antman EM, et al. J Am Coll Cardiol 2008. Published ahead of print se therapeutic modalities, as dictated by clinical circumstances. ACC/AHA 2007 STEMI Guidelines Focused Update on December 10, 2007. Available at http://content.onlinejacc.org/cgi/content/full/j.jacc.2007.10.001 . U Secondary Prevention and Long Term Management al Goals Class I Recommendations rn Renin- ACE inhibitors should be started and continued indefinitely in all Angiotensin- patients recovering from STEMI with LVEF ≤ 40% and for those te Aldosterone with hypertension, diabetes, or chronic kidney disease, unless System contraindicated. CHANGED TEXT Blockers: ACE In Inhibitors ACE inhibitors should be started and continued indefinitely in patients recovering from STEMI who are not lower risk (lower risk defined as those with normal LVEF in whom cardiovascular NEW REC risk factors are well controlled and revascularization has been performed), unless contraindicated. Among lower risk patients recovering from STEMI (i.e., those NEW with normal LVEF in whom cardiovascular risk factors are well REC controlled and revascularization has been performed) use of ACE inhibitors is reasonable. (Class IIa; LOE: B) ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Secondary Prevention and Long Term Management Goals Class I Recommendations Renin- Use of ARBs is recommended in patients who are Angiotensin- intolerant of ACE inhibitors and have HF or have had Aldosterone a STEMI with LVEF ≤ 40%. CHANGED System TEXT Blockers: ARBs y It is beneficial to use ARB therapy in other patients nl NEW who are ACE-inhibitor intolerant and have REC hypertension. O NEW Considering use in combination with ACE inhibitors REC in systolic dysfunction HF may be reasonable. se ACC/AHA 2007 STEMI Guidelines Focused Update U Secondary Prevention and Long Term Management al Goals Class I Recommendations rn Renin- Angiotensin- Use of aldosterone blockade in post-STEMI te Aldosterone patients without significant renal dysfunction or System hyperkalemia is recommended in patients who In Blockers: are already receiving therapeutic doses of an ACE Aldosterone Blockade inhibitor and beta blocker, have an LVEF of ≤ 40% and have either diabetes or HF. CHANGED TEXT ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Secondary Prevention and Long Term Management Goals Class I Recommendations Beta- It is beneficial to start and continue beta- Blockers blocker therapy indefinitely in all patients who have had MI, acute coronary y syndrome, or left ventricular dysfunction with or without HF symptoms, unless nl contraindicated. O CHANGED TEXT se ACC/AHA 2007 STEMI Guidelines Focused Update U Secondary Prevention and Long Term Management al rn Goals Class I Recommendations te Influenza Patients with cardiovascular disease Vaccination should have an annual influenza In vaccination. NEW REC ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010 Post MI medical Rx y nl O se U al rn te Chronic stable angina In

MD Chula 2010 Risk stratification yes High probability of Clinical Assessment - co-morbid co- severe CAD - Patient’s preference Patient’ no no Suitable for EST yes Exercise ECG Test Intermediate-risk Stress Imaging Study y High-risk Low-risk Low-risk Intermediate-risk High-risk nl O Medical Treatment Failure se Coronary Angiography U al rn te Stress test In

MD Chula 2010 Treatment Ø Treatment that prevents death / MI (should be highest priority) l Antiplatelet agents l Lipid lowering agents l Beta-blocker in post MI patients Beta- y l CABG in patients with left main or nl mulitvessels disease and LV dysfunction l (ACE-inhibitors) (ACE- O Ø Treatment that improves quality of life l Antianginal therapy se U Treatment al rn Ø Pharmacologic treatment that prevents te death / MI l Antiplatelet agents In l Lipid lowering agents Ø Antianginal therapy Ø Treatment of risk factors Ø Myocardial revascularization

MD Chula 2010 Revascularization in patients with chronic stable angina Ø Severe or limiting symptoms l Despite maximal medical treatments l Intolerable to medical treatment Ø Large area of ischemia or high-risk noninvasive high- y tests Ø Malignant coronary anatomy: nl l Left main disease O l Triple vessels disease, esp. with abnormal LV function l Proximal LAD disease Ø se Survivor of sudden cardiac death U CAUSES OF ANGINAL CHEST PAIN al rn CORONARY ARTERIAL DISEASE Fixed obstructive coronary disease te Coronary disease with dynamic flow limitation Microvascular angina (Syndrome X) In VASCULAR DISORDERS Variant angina Coronary vasospasm (see Printzmetal angina) Syndrome X (without obstructive vascular disease)

MD Chula 2010 CAUSES OF ANGINAL CHEST PAIN • CORONARY ARTERIAL DISEASE • VASCULAR DISORDERS OTHER CARDIAC DISORDERS Aortic stenosis Hypertrophic cardiomyopathy Hypertensive heart disease and left ventricular hypertrophy y Mitral valve prolapse nl Severe pulmonary hypertension and right ventricular hypertrophy O SYSTEMIC DISORDERS PRECIPITATING ANGINA Anaemia Thyrotoxicosis High-output states (e.g., arterio-venous shunts) se U al rn te In

MD Chula 2010 y nl O se U CARDIOGENIC SHOCK: DIFFERENTIAL DX al rn • Complications of acute MI Extensive LV infarction and ischemia te Extensive RV infarction and ischemia VSR In Acute, severe MR Tamponade With free wall rupture Without free wall rupture Arrhythmia (electrical complication)

MD Chula 2010 CARDIOGENIC SHOCK: DIFFERENTIAL DX • Complications of acute MI • Other conditions • Acute MI with Ischemic/infarcted bowel Ruptured abdominal aortic aneurysm y Sepsis nl Hemorrhage Anaphylaxis O Excessive β- or calcium channel blockade se U CARDIOGENIC SHOCK: DIFFERENTIAL DX al • Complications of acute MI rn • Other conditions Aortic dissection te Myocarditis PE Critical aortic or mitral stenosis In Hypertrophic cardiomyopathy with outflow obstruction Acute aortic or MR Pericarditis with tamponade LV apical ballooning/Takostubo cardiomyopathy Metabolic/toxic Calcium channel or β-blocker overdose Acidosis, hyperkalemia, hypoxemia Thyroid storm, myxedema coma

MD Chula 2010 y nl O se U al Aortic dissection rn te In

MD Chula 2010 Types of Aortic Dissection y nl O se U al rn te In

In te rn al U MD Chula 2010 se O nl y

MD Chula 2010 y nl O se U al Cardiac tamponade rn te In

MD Chula 2010 • BECK TRIAD • Pulsus paradoxus y nl O se U al rn te In

MD Chula 2010 y nl O se U A ETIOLOGY OF ACUTE PERICARDITIS al • Idiopathic rn • Infectious Bacterial, Tuberculous, Viral: Coxsackie, Influenza, HIV, etc. Fungal, Rickettsial, Mycoplasma, Leptospira, Listeria, Parasitic, Other te • Vasculitis/Connective Tissue Disease: Rheumatoid Arthritis, Rheumatic Fever, SLE, Scleroderma Sjögren's Syndrome, Reiter Syndrome, Ankylosing Spondylitis, In Wegener's Granulomatosis, Giant Cell Arteritis, Polymyositis (Dermatomyositis), Behcet Syndrome, Familial Mediterraneun Fever, Dermatomyositis, Polyarteritis, Churg-Strause Syndrome, TTP, Leukoclastic Vasculitis, Other • Diseases in Adjacent Structures: myocardial infarction, aortic dissection, pneumonia, pulmonary embolism, empyema • Metabolic Disorders: Uraemic, Dialysis-Related, Myxoedema, Gout, Scurvy • Hypereosinophilic Syndromes, Acute Pancreatitis, etc.

MD Chula 2010 A ETIOLOGY OF ACUTE PERICARDITIS • Neoplastic • Secondary (Metastatic, or Direct Spread): Carcinoma, Lymphoma, Carcinoid, Other • Primary Mesothelioma, Sarcoma, Fibroma, Lipoma, Other • Trauma Direct: y • 1. Pericardial Perforation: Penetrating Injury, Esophageal or Gastric Perforation 2. Cardiac Injury: Cardiac Surgery, Percutaneous Procedures nl Indirect: Radiation, Non-Penetrating Chest Injury • Association with Other Syndromes O Post-Myocardial and Pericardial Injury Syndromes, Inflammatory Bowel Disease, Loffler Syndrome, Stevens-Johnson Syndrome, Giant Cell Aortitis, Hypereosinophilic Syndromes, Acute Pancreatitis, etc. se U al rn te In

MD Chula 2010 IE y nl O se U DEFINITION OF IE ACCORDING TO al THE MODIFIED DUKE CRITERIA rn te In

MD Chula 2010 y nl O se U Indications for Surgery for al Native Valve Endocarditis rn • Surgery of the native valve is indicated in patients who present te with heart failure. In • Surgery of the native valve is indicated in patients with infective endocarditis caused by fungal or other highly resistant organisms.

MD Chula 2010 Indications for Surgery for Native Valve Endocarditis • complicated by – heart block, annular – aortic abscess – destructive penetrating lesions • (e.g., sinus of Valsalva to right atrium, right y ventricle, or left atrium fistula; mitral leaflet perforation with aortic valve endocarditis; or nl infection in annulus fibrosa ) • recurrent emboli and persistent vegetations O despite appropriate antibiotic therapy. se U al IE prophylaxis rn te In

MD Chula 2010 Patients and Procedures for Which Antibiotic Prophylaxis Is Recommended • Patient-Specific Risk – High risk – Moderate risk – Low risk y • Procedure-Specific Risk nl – Prophylaxis recommended O – Prophylaxis not recommended se U CARDIAC CONDITIONS AND THE NEED FOR ENDOCARDITIS PROPHYLAXIS al rn • ENDOCARDITIS PROPHYLAXIS RECOMMENDED High risk te • Prosthetic cardiac valves, including bioprosthetic and homograft valves In • Previous bacterial endocarditis, even in the absence of heart disease • Complex cyanotic congenital heart disease (e.g., single ventricle states, transposition of the great arteries, tetralogy of Fallot) • Surgically constructed systemic–pulmonary shunts or conduits

MD Chula 2010 Moderate risk Low risk • Mitral valve prolapse • Mitral valve prolapse with significant without evidence of regurgitation, or regurgitation or leaflet thickening myxomatous leaflets • Hypertrophic • Physiologic murmurs cardiomyopathy • Isolated secundum ASD • Acquired valvular • 6 months after surgical heart disease repair of including stenosis, ASD/VSD/PDA y regurgitation and • Cardiac pacemakers or rheumatic nl ICDs • Other congenital • Previous CABG malformations O • Hx of rheumatic fever (ostium primum ASD, or Kawasaki disease VSD, PDA, bicuspid without evidence of aortic valve, se valvular dysfunction coarctation) U Prophylaxis recommended al Dental rn • Extractions te • Periodontal procedures • Initial placement of bands In • Intraligamentary local anesthesia • Dental implants • Root canal

MD Chula 2010 y nl O se U Valvular heart al disease rn te In

MD Chula 2010 Loud S1 OS DRM y RV heaving /P2 nl O se U al rn te In

MD Chula 2010 y nl O se U al Physical examination rn te In

MD Chula 2010 Cardiac examination • Inspection • Palpation • Percussion • Auscultation y nl O se U Inspection al • Cyanosis rn – Clubbing ( upper /lower) te • Neck vein • Carotid artery In • Pale • Edema • Tachypnea • Clinical syndrome

MD Chula 2010 y nl O se B:Anacrotic pulse with slow initial upstroke and delayed peak indicate fixed aortic stenosis. U al rn te In •C:Pulsus bisferiens with increased amplitude of percussion and tidal waves occurs during systole. • observed in patients with significant Aortic regurgitation.

MD Chula 2010 ALTERED CHARACTERS OF THE ARTERIAL PULSE AND THEIR CLINICAL SIGNIFICANCE • Pulsus alternans—suspect acute or chronic reduction in left ventricular ejection fraction y • Pulsus paradoxus—suspect nl tamponade, emphysema O se U ALTERED CHARACTERS OF THE ARTERIAL PULSE AND THEIR CLINICAL SIGNIFICANCE al • Anacrotic pulse, delayed upstroke, palpable thrill, rn delayed peak—suspect fixed left ventricular outflow tract obstruction such as aortic valve stenosis te • Pulsus biferiens—suspect aortic regurgitation, aortic stenosis with dominant aortic regurgitation, In dynamic left ventricular outflow tract obstruction (obstructive hypertrophic cardiomyopathy), large patent ductus arteriosus with left-to-right shunt, complete heart block, hyperkinetic heart syndrome (e.g., in hyperthyroidism) • Dicrotic pulse—suspect low-output syndrome with increased systemic vascular resistance, high output with low systemic resistance (e.g., in septic shock), postaortic valve replacement with depressed left ventricular ejection fraction

MD Chula 2010 ABNORMALITIES OF THE VENOUS PRESSURE AND PULSE AND THEIR CLINICAL SIGNIFICANCE • Positive hepatojugular reflux—suspect CHF, particularly left ventricular systolic dysfunction • Elevated systemic venous pressure without obvious ‘x’ or ‘y’ descent and quiet precordium and pulsus paradoxus—suspect cardiac tamponade • Elevated systemic venous pressure with sharp ‘y’ y descent, Kussmaul sign, and quiet precordium— suspect constrictive pericarditis nl • Elevated systemic venous pressure with a sharp, brief ‘y’ descent, Kussmaul sign, and evidence of O pulmonary hypertension and tricuspid regurgitation—suspect restrictive cardiomyopathy se U Distinguishing Pulsations al rn Internal Jugular Pulsations Carotid Pulsations • Rarely palpable • Palpable • Soft, rapid undulating te • A more vigorous quality—two elevations thrust with a single and troughs per pulse outward component In beat • Pulsations not • Eliminated by light pressure on the vein just eliminated by this above the sternal end of pressure the clavicle • Level of pulsations • Level changes with does not change with position or respiration position or respiration

MD Chula 2010 Auscultation • Bell and Diaphragm • Area – Valve area ( pic) – Radiation : Neck Axilla Back • Position y – Supine nl – Left lateral decubitus – Sitting leaning forward ( expire) O • Maneuver se U S1 al • Decrease : MR rn • Increase : te – shorten diastolic ( tachycardia ) – short PR In – MS • Split – Wide split : RBBB ( M>>T ) – Reverse split : LBBB ,severe MS, Lt atrial myxoma

MD Chula 2010 S2 • Increase P2 : pulmonary HT • Decrease A2 : AS Split y • Wide split ( A2 P2à): nl – RBBB – Increase RV pressure : PE, PS O – Increase RV volume : ASD , RV failure se U S2 al Split rn • Wide split ( ßA2 P2 ): te – MR – VSD In • Wide fixed split S2 : ASD • Paradoxical split S2 ( P2 A2 ): – Severe AS – LBBB

MD Chula 2010 Extra heart sound Diastole Systole • OS: MS ,TS • SEC : – Usually confuse with – Semilunar valve P2 stenosis – Duration A2-OS – Dilated Ao, PA • K • MSC y • T – MVP nl • S3 O se U Murmur al • Systolic rn – Pan /holo : • Atrioventricular valve (MR,TR) te • VSD – SEM ( early/mid/late ) : In • Semilunar ( AS, PS ( ASD), HCOM) • Diastolic – Early diastolic blowing : AR,PR – Mid diastolic rumbling : MS ,TS – Pre systolic accentuation

MD Chula 2010 Mitral valve prolapse y nl O se U describe al • Systolic vs diastolic rn • Grade I –VI te • Area of maximum intensity • Radiation In • Quality • maneuver

MD Chula 2010 Systolic murmur • Pansystolic : – MR – VSD – TR • SEM : y – AS nl – HCOM – ASD O – PS se U Diastolic murmur al • AR rn • MS te In

MD Chula 2010 Diastolic murmur • AR Rhythm? ( sinus or AF) • MS RV heaving ( pul HT ) S1 increase OS P2 increase ( pul HT ) DRM ( mid diastole) y left lat.decubitus nl Presystolic accentuation murmur ( sinus ) O TR ( pul HT ) se U al 2nd Prevention Lesion Symptom Control and Natural Hx rn Mitral Diuretics for HF Penicillin stenosis 2o prophylaxis te for atrial fibrillation : against recurrent Digoxin, B-blockers episodes of In rheumatic fever; non dihydro CCB Anticoagulants to prevent systemic thromboembolism MR for heart failure No proven Diuretics and treatment vasodilators (usually ACE inhibitors)

MD Chula 2010 2nd Prevention and Lesion Symptom Control Natural Hx Aortic for HF; lipid lowering stenosis Diuretics therapy may slow progression of calcific aortic for angina : stenosis nitrates and B-blockers y Aortic for heart failure Vasodilators nl regurgit Diuretics and (nifedipine or ation vasodilators ACE inhibitors) to protect the O (usually ACE inhibitors) left ventricular myocardium se U REVISED JONES CRITERIA FOR THE DIAGNOSIS al OF ACUTE RHEUMATIC FEVER, 1992 rn Major criteria Carditis te Polyarthritis Chorea Erythema marginatum In Subcutaneous nodules Minor criteria • Arthralgia • Fever • Elevated erythrocyte sedimentation rate • Elevated C-reactive protein levels • First-degree atrioventricular block

MD Chula 2010 SYNCOPE y nl O se U SYNCOPE: DIAGNOSTIC CLASSIFICATION al NEURALLY MEDIATED REFLEX SYNCOPE Vasovagal faint rn Carotid sinus syncope Cough/swallow syncope and related disorders Gastrointestinal, pelvic, or urologic origin (swallowing, defecation, postmicturition status) te ORTHOSTATIC SYNCOPE Primary autonomic failure Secondary autonomic failure (e.g., diabetic and alcoholic In neuropathy, drug effects) CARDIAC ARRHYTHMIAS AS A PRIMARY CAUSE OF SYNCOPE Sinus node dysfunction (including bradycardia/tachycardia syndrome) Atrioventricular conduction system disease Paroxysmal supraventricular tachycardias Paroxysmal ventricular tachycardia (including torsade de pointes) Implanted pacing system malfunction, “pacemaker syndrome” Brugada syndrome, long/short QT syndrome

MD Chula 2010 SYNCOPE: DIAGNOSTIC CLASSIFICATION • NEURALLY MEDIATED REFLEX SYNCOPE • ORTHOSTATIC SYNCOPE • CARDIAC ARRHYTHMIAS AS A PRIMARY CAUSE OF SYNCOPE STRUCTURAL CARDIOVASCULAR OR CARDIOPULMONARY DISEASE Cardiac valvular disease/ischemia Acute myocardial infarction Obstructive cardiomyopathy Subclavian steal syndrome y Pericardial disease/tamponade Pulmonary embolus nl Primary pulmonary hypertension Acute aortic dissection CEREBROVASCULAR O Intracerebral steal, migraine, vertebrobasilar transient ischemic attack se U al rn te In

MD Chula 2010 CHEST PAIN SYNCOPE y nl O se U SYNCOPE: DIAGNOSTIC CLASSIFICATION al • NEURALLY MEDIATED REFLEX SYNCOPE rn • ORTHOSTATIC SYNCOPE • CARDIAC ARRHYTHMIAS AS A PRIMARY CAUSE OF SYNCOPE STRUCTURAL CARDIOVASCULAR OR CARDIOPULMONARY te DISEASE Cardiac valvular disease/ischemia Acute myocardial infarction In Obstructive cardiomyopathy Subclavian steal syndrome Pericardial disease/tamponade Pulmonary embolus Primary pulmonary hypertension Acute aortic dissection CEREBROVASCULAR Intracerebral steal, migraine, vertebrobasilar transient ischemic attack

MD Chula 2010 HT y nl O se U al HT rn • Primary( essential HT) vs Secondary • Severity ( grade) te • TOD In • Associated atherosclerosis risks ( DM,dyslipidemia,metabolic syndrome, smoking,family Hx) • Co-morbid disease considerate for anti-HT ( compelling indication)

MD Chula 2010 • Primary or essential hypertension (90- 95%) • Secondary hypertension: (2-10%) – Renal (2.5-6%) – Renovascular hypertension (0.2-4%) – Vascular y – Endocrine (1-2%) nl – Pregnancy-induced hypertension – Drugs and toxins O se U al – Renal (2.5-6%) • Renal parenchymal disease rn • Polycystic kidney disease • Urinary tract obstruction te • Renin-producing tumor • Liddle syndrome In – Renovascular hypertension (0.2-4%) 0.2-4% – Vascular • Coarctation of aorta • Vasculitis

MD Chula 2010 Endocrine (1-2%) - Adrenal • Primary aldosteronism • Cushing syndrome • Pheochromocytoma • Congenital adrenal hyperplasia – Hyperthyroidism and hypothyroidism y – Hypercalcemia nl – Hyperparathyroidism O – Acromegaly se U al Pregnancy-induced hypertension rn Drugs and toxins te • Oral contraceptives • Alcohol In • Cocaine • Cyclosporin • Erythropoietin • Adrenergic medications

MD Chula 2010 • A Hx of sweating, labile hypertension, and palpitations suggests of pheochromocytoma • A history of cold or heat tolerance, sweating, lack of energy, and y bradycardia or tachycardia may nl indicate hypothyroidism or hyperthyroidism O se U al • A history of weakness suggests hyperaldosteronism rn te • Abdominal bruit suggests the possibility of renal artery stenosis In • Absence of femoral pulses suggests coarctation of aorta.

MD Chula 2010 • Kidney stones raise the possibility of hyperparathyroidism • A history of drug ingestionoral – contraceptives – Licorice y – sympathomimetics nl O se U Class of Medication When to Use When Not to Use al Loop diuretics Renal insufficiency Gout (additional therapy) rn Potassium-sparing Primary Renal insufficiency hyperaldosteronism (additional therapy te in combination with thiazide diuretics) In Thiazides Uncomplicated Gout, dyslipidemia hypertension (high-dose) (preferred therapy), systolic hypertension in elderly people (preferred therapy), for older diabetic patients without nephropathy

MD Chula 2010 Class of Medication When to Use When Not to Use Beta-adrenergic Post–myocardial Asthma, peripheral antagonists infarction, vascular disease uncomplicated (severe) hypertension (preferred therapy), diabetes (without nephropathy) ACE inhibitors Diabetes, post– Bilateral renovascular myocardial infarction, disease, pregnancy heart failure, renal disease, y uncomplicated nl hypertension (preferred therapy) ) Angiotensin II Diabetes (alternative Bilateral renovascular O antagonists therapy), heart disease, pregnancy failure (alternative therapy), se uncomplicated hypertension (preferred therapy) U Class of Medication When to Use When Not to Use al Nondihydropyridine Uncomplicated Heart block, heart CCB hypertension failure (alternative rn therapy) dihydropyridines Systolic Heart failure te CCB hypertension (preferred therapy), ) In uncomplicated therapy (alternative therapy) Alpha-adrenergic Uncomplicated Autonomic antagonists/central hypertension dysfunction acting agents (alternative therapy)

MD Chula 2010 Risk Preferred Therapy Alternative Avoid Factor/Disease Therapy Therapy Low-dose thiazidelike Combinations diuretics, of first-line Uncomplicated beta-blockers, drugs hypertension ACE inhibitors, (<60 y) long-acting dihydropyridine CCB Low-dose thiazidelike Combinations y diuretics, of first-line Uncomplicated ACE inhibitors, drugs hypertension nl long-acting (>60 y) dihydropyridine CCB O As for uncomplicated Dyslipidemia hypertension se U Risk Preferred Alternative Avoid Therapy Factor/Disease Therapy Therapy al ACE inhibitors Angiotensin High-dose Diabetes II receptor diuretics and rn mellitus blockers centrally acting with agents (in the nephropathy setting of te autonomic neuropathy) In Diabetes ACE inhibitors mellitus or without beta-blockers nephropathy Low-dose Diabetes thiazidelike mellitus diuretics without or nephropathy , with systolic long-acting hypertension dihydropyridine CCB

MD Chula 2010 Risk Preferred Alternative Avoid Therapy Factor/Disease Therapy Therapy Beta-blockers Long-acting (ACE inhibitors CCB Angina as add-on therapy) Prior Beta-blockers, myocardial ACE inhibitors infarction y ACE inhibitors Angiotensin II Nondihydropyr nl (thiazide or receptor idine calcium loop diuretics, blockers, channel Systolic beta-blockers, blockers O dysfunction spironolactone hydralazine/iso (diltiazem, is additive sorbide verapamil) therapy) dinitrate, se amlodipine U Risk Preferred Alternative Avoid Therapy al Factor/Disease Therapy Therapy Most Hydralazine, rn Left antihypertensi minoxidil ventricular ves reduce hypertrophy LVH te As for As for Beta-blockers Peripheral In uncomplicated uncomplicated (with severe arterial hypertension hypertension disease) disease ACE inhibitors Dihydropyridi ACE inhibitors in (diuretics as ne calcium cases of additive channel bilateral renal Renal disease therapy) blockers artery stenosis

MD Chula 2010 CHF y nl O se U al rn te In

MD Chula 2010 y nl O se U Stage C Therapy (Reduced LVEF with Symptoms) al Implantable Cardioverter- rn Defibrillators (ICDs) An ICD is recommended as secondary prevention to te prolong survival in patients with current or prior symptoms of HF and reduced LVEF who have a history of cardiac arrest, ventricular fibrillation, or hemodynamically In destabilizing ventricular tachycardia. ICD therapy is recommended for primary prevention to reduce total mortality by a reduction in sudden cardiac death in patients with ischemic heart disease who are at least 40 days post-MI, have an LVEF less than or equal to 30%, with NYHA functional class II or III symptoms while undergoing chronic optimal medical therapy, and have reasonable expectation of survival with a good functional status for more than 1 year.

MD Chula 2010 Stage C Therapy (Reduced LVEF with Symptoms) ICDs (cont’d) ICD therapy is recommended for primary prevention to reduce total mortality by a reduction in sudden cardiac death in patients with nonischemic cardiomyopathy who have an LVEF less than or equal to 30%, with NYHA functional class II or III symptoms while undergoing chronic optimal medical therapy, and who have y reasonable expectation of survival with a good functional status for more than 1 year. nl Placement of an ICD is reasonable in patients with LVEF of 30% to 35% of any origin with NYHA functional class II O or III symptoms who are taking chronic optimal medical therapy and who have reasonable expectation of survival with good functional status of more than 1 year. se U Stage C Therapy (Reduced LVEF with Symptoms) al Cardiac Resynchronization rn te Patients with LVEF less than or equal to 35%, sinus rhythm, and NYHA functional class III or ambulatory class IV symptoms despite recommended, optimal In medical therapy and who have cardiac dyssynchrony, which is currently defined as a QRS duration greater than 120 ms, should receive cardiac resynchronization therapy unless contraindicated.

MD Chula 2010 Stage C Therapy (Reduced LVEF with Symptoms) Exercise Testing and Training Maximal exercise testing with or without measurement of respiratory gas exchange is recommended to facilitate prescription of an appropriate exercise program for patients presenting with HF. y Exercise training is beneficial as an adjunctive nl approach to improve clinical status in ambulatory patients with current or prior symptoms of HF and O reduced LVEF. se U Stage C Therapy (Reduced LVEF with Symptoms) al Unproven/Not Recommended rn Drugs and Interventions for HF te • Nutritional Supplements • Hormonal Therapies In • Intermittent Intravenous Positive Inotropic Therapy

MD Chula 2010 Stage D Therapy Discussion of Options for End-of-Life Care Options for end-of-life care should be discussed with the patient and family when severe symptoms in patients with refractory end-stage HF persist despite application of all y recommended therapies. nl O se U Stage D Therapy al Surgical Therapy rn Referral for cardiac transplantation in te potentially eligible patients is recommended for patients with refractory end-stage HF. In The effectiveness of mitral valve repair or replacement is not established for severe secondary mitral regurgitation in refractory end-stage HF.

MD Chula 2010 Stage D Therapy Device Use Consideration of an LV assist device as permanentor “destination” therapy is reasonable in highly selected patients with refractory end-stage HF and an estimated 1-year mortality over 50% with medical therapy. y Pulmonary artery catheter placement may be nl reasonable to guide therapy in patients with refractory end-stage HF and persistently severe O symptoms. se U Stage D Therapy al Medical Therapy rn Continuous intravenous infusion of a positive te inotropic agent may be considered for palliation of symptoms in patients with refractory end-stage HF. In Routine intermittent infusions of positive inotropic agents are not recommended for patients with refractory end-stage HF.

MD Chula 2010 Differential Diagnosis in Patient with HF and Normal LVEF with Symptoms • Incorrect diagnosis of HF • HF associated with high • Inaccurate measurement of metabolic demand (high- LVEF output states) • Primary valvular disease • Anemia, thyrotoxicosis, • Restrictive (infiltrative) arteriovenous fistulae cardiomyopathies • Chronic pulmonary • Amyloidosis, sarcoidosis, disease with right HF hemochromatosis • Pulmonary hypertension y • Pericardial constriction associated with pulmonary vascular nl • Episodic or reversible LV disorders systolic dysfunction • Atrial myxoma • Severe hypertension, O myocardial ischemia • Diastolic dysfunction of uncertain origin • Obesity se U al rn • Digitalis intoxication te • Warfarin overdose • Drug - drug interaction In • Drug in pregnancy &lactation • Anti HT • Inotropic drug

MD Chula 2010 Digitalis Toxicity Essentials of Diagnosis • Intoxication may result from – Acute single exposure – Chronic accumulation from accidental y overmedication or renal insufficiency nl • Hyperkalemia common after acute O overdose • Many different arrhythmias can se occur U al Digitalis intoxication rn • CVS te – SA node – Nodal block In – Irritability ( trigger activity DAD ) • Atrial tachycardia • Junctional tachycardia • Ventricular tachycardia – ST-T effect +short QT

MD Chula 2010 y nl O se U al Digitalis Toxicity rn Medications • Emergency measures te Ventricular arrhythmias: initially lidocaine, 2–3 mg/kg IV, or In phenytoin, 10–15 mg/kg IV slowly over 30 min if digoxin-specific antibodies are not immediately available (see below) Bradycardia: initially atropine, 0.5–2.0 mg IV, or transcutaneous external cardiac pacemaker

MD Chula 2010 Digitalis Toxicity Increased susceptibility • elderly • heart disease, • renal dysfunction, • hepatic dysfunction, • hypothyroidism, y • chronic obstructive pulmonary disease • electrolyte disturbances nl • (e.g., hypoK, hypoMg, and hypercal ) • hypoxia. O • Drug interactions, – most notably class IA antidysrhythmics, – calcium channel blockers, and B -blockers, potentiate se digitalis toxicity U al Warfarin rn te In

MD Chula 2010 Anti HT side effect • Depression – B-blocker – Methydopa – Hydralazine y • Drug induce SLE : Hydralazine nl • Hemolytic O anemia:Methydopa,Hydralazine • Dysguesia : ACEI se U • 55 y-o man SOB 6 mths . • He has new dyspnea on exertion and orthopnea. al • JVP is 14 cmH20 rn • Lung : rales 2/3 bilaterally. • lower extremity :2+ pitting edema. te • CXR: pulmonary infiltrates,enlarged cardiac silhouette. • EKG: low-voltage in the precordial and limb leads. In • Echo:dilated left ventricle, LVEF= 20%, mild MR, a small pericardial effusion. Which finding on cardiac examination would be consistent with this patient's diagnosis? A. Absent S2 B. Narrow pulse pressure C. Paradoxical splitting of S2 with inspiration D. Pulsus bisferiens

MD Chula 2010 • 55 y-o man SOB 6 mths . • He has new dyspnea on exertion and orthopnea. • JVP is 14 cmH20 • Lung : rales 2/3 bilaterally. • lower extremity :2+ pitting edema. • CXR: pulmonary infiltrates,enlarged cardiac silhouette. • EKG: low-voltage in the precordial and limb leads. • Echo:dilated left ventricle, LVEF= 20%, mild MR, a y small pericardial effusion. nl Which finding on cardiac examination would be consistent with this patient's diagnosis? O A. Absent S2 B. Narrow pulse pressure C. Paradoxical splitting of S2 with inspiration D. Pulsus bisferiens se U al rn te In

MD Chula 2010 Constrictive Pericarditis y nl O se U al rn te In

MD Chula 2010 y nl O se U al D/Dx vs Rx rn te In

MD Chula 2010 HOCM y nl O se U al rn te In

MD Chula 2010 y nl O se U al Marfan rn te In

MD Chula 2010 y nl O se U al CHF rn te In

MD Chula 2010 y nl O se U al Syncope rn te In

MD Chula 2010 y nl O se U al CAD rn te In

MD Chula 2010 y nl O se U al Streptokinase (SK) rn • is a single-chain protein produced by alfa - hemolytic streptococci. te • allergic reactions are possible • Hypotension with infusion usually responds to In fluids and a decreased infusion rate • SK is given as a 1.5 million U intravenous infusion • rate of intracranial hemorrhage of approximately 0.5% • SK produces coronary arterial patency approximately 50% to 60% • decrease mortality rate by 18% compared with placebo.

MD Chula 2010 • Alteplase and its derivatives are fibrin-specific plasminogen activators, • streptokinase, anistreplase, and y urokinase are nonspecific agents nl O se U al rn te In

MD Chula 2010 y nl O se U al RVI rn • Right ventricular infarction occurs in up to 30% of patients with inferior infarction and is clinically significant in 10%. te • clear chest radiogram with jugular venous distention in a patient with an inferior wall MI • ST-segment elevation (V3R to V5R) or by In • right heart catheterization (elevated right atrial and right ventricular end-diastolic pressures with normal to low pulmonary artery occlusion pressure and low cardiac output). • Echocardiography can demonstrate depressed right ventricular contractility. • cardiogenic shock on the basis of right ventricular infarction have a better prognosis than do those with left-side pump failure.

MD Chula 2010 RVI • avoid hypovolemia • Continued fluid loading can compromise left ventricular filling and cardiac output: right ventricular overdistention • Inotropic therapy with dobutamine is often more effective y • atrioventricular synchrony to optimize nl right ventricular filling. • IABP may be useful O • Reperfusion of the occluded coronary artery is also crucial. se U al rn te In

MD Chula 2010 Aortic dissection y nl O se U al rn te In

Mdcu Comprehensive Cardio

by vora kun

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