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Chest Pain and Shortness of Breath: Pattern Recognition and Treatment of Potential Emergencies

Chest Pain and Shortness of Breath: Pattern Recognition and Treatment of Potential Emergencies. James Hoekstra, MD, FACEP Wake Forest University. Atraumatic Chest Pain: Differential Dx. Acute Coronary Syndrome (STEMI, UA, NSTEMI) Pulmonary Embolus Thoracic Aortic Dissection

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Chest Pain and Shortness of Breath: Pattern Recognition and Treatment of Potential Emergencies

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  1. Chest Pain and Shortness of Breath:Pattern Recognition and Treatment of Potential Emergencies James Hoekstra, MD, FACEP Wake Forest University

  2. Atraumatic Chest Pain: Differential Dx • Acute Coronary Syndrome (STEMI, UA, NSTEMI) • Pulmonary Embolus • Thoracic Aortic Dissection • Borehaave’s Syndrome • Pneumothorax • Pneumonia/Bronchitis • Musculoskeletal CP/Costochondritis • Pleurisy • GERD • Cancer

  3. Classic History and Physical Patterns • Quality of Pain • Location • Radiation • Duration/Chronology • Exacerbating/Alleviating Factors • Associated Symptoms • Risk Factors

  4. Case #1 • 56 yo male presents with midline chest tightness for one hour, constant. • Radiates to jaw, left arm • SOB, diaphoresis, nausea • Intermittent, exertional in past • Hx of HTN, Cholesterol, FH AMI • BP 150/90, P 100, exam normal, nontender • ECG with NSST changes

  5. Acute Coronary SyndromesSTEMIUA/NonSTEMIPresumed ACS

  6. Chest Pain History, Physical EKG Definite Non-Cardiac STEMI UA/NSTEMI/ High Risk Mod Risk Low Risk Initial Risk Stratification Scheme

  7. ED Risk Stratification Tools • Clinical History • Initial ECG • Continuous or Serial ECG • Serum Markers of AMI • Provocative Testing/Imaging

  8. Serum Markers • Myoglobin: Early peak in serum after MI, nonspecific, good negative predictive value for MI. • CKMB: Gold standard for many years. False elevation in muscle damage, renal failure. Must take relative index into account. Good risk stratifier • TnI, TnT: Peaks at same time as CKMB, prolonged elevation in serum after MI, more sensitive and specific for MI than CKMB, but low levels (<1.0) can still be false positives. Best predictor of increased risk for bad outcomes

  9. TIMI Risk Score For ACS TIMI > 4 is high risk Antman et al JAMA 2000;284: 835 Download  www.timi.org

  10. Non STE ACS Features • High Risk Features • Accelerated pattern of angina • Ongoing rest pain > 20 min • Signs of CHF • Hemodynamic instability • Arrhythmias - Atrial or ventricular • Advanced age (> 75 years) • Ischemic ECG changes • Elevated cardiac markers

  11. ACS Risk Stratification Levels • Level 1: STEMI: ST segment elevation MI • Level 2: NSTE ACS: ST depression, positive markers (objective findings) • Level 3: Moderate Risk: No ECG or marker changes but high risk of UA by history, risk factors, known CAD, high TIMI risk • Level 4: Low: No ECG or marker changes and possibility of UA (atypical story, low TIMI risk) • Level 5: Noncardiac Pain

  12. Class I ED Treatment of STEMI(ST Elevation, BBB, Pain<12 Hours) • Targeted ED Protocol, Door to Needle <30 minutes • O2, IV, monitor • ASA immediately • Nitrates, beta blockers • Heparin weight based dosing (max 4000/1000) • Clopidogrel 300 mg • Thrombolytics in less than 30 minutes or PCI less than 90 minutes • PCI should be utilized with IIb/IIIa therapy • Treatment of Complications

  13. Thrombolytic Therapy Inclusions • Symptoms >30 minutes<12 hours • ECG ST elevation >2mm in 2 contiguous precordial leads or >1mm in 2 contiguous limb leads, or ST depression >2mm in precordial leads with reciprocal ST elevation in II, AVF, V6 • New BBB • Patient Consent

  14. Active Bleeding Altered Mental Status Major CNS Surgery <6 weeks PTA CVA <2 yrs PTA Bleeding Diathesis SBP >180, DBP >110 CNS AVM, Aneurysm, Tumor AAA Hemorrhagic Pancreatitis Thrombolytic Therapy Exclusions

  15. Recent Surgery or Trauma <2 wks Pericarditis Coumadin Use Liver Disease Presumed SBE Diabetic Retinopathy Cardiogenic Shock Peptic Ulcer Disease Recent GI/GU bleed Pregnancy Thrombophlebitis Thrombolytic Therapy Relative Contraindications

  16. Facilitated PCI • Primary angioplasty or stent placement is the gold standard treatment of STEMI in cath lab centers. • ASA, NTG, Heparin weight based dosing • Abciximab either prior to or at the same time as PCI decreases reocclusion and has some fibrinolytic effects equal to streptokinase. • Benefits of cath over thrombolytics lost if time from door to cath lab greater than 90 minutes.

  17. WFU Treatment of STEMI(ST Elevation, BBB, Pain<12 Hours) • IV, O2, Monitor • ASA 325 mg po • Nitrates, beta blockers, MS as indicated • Clopidogrel 600 mg po • Heparin 40 U/kg IVP (max 4000), 7 U/kg/hr infusion • Abciximab 0.25 mg IVP, 0.125 mcg/kg/min (max 10 mcg/min) infusion prior to PCI started in the ED • Call Cardiology for PCI FAST

  18. ED Treatment of NSTE ACS(ST Depression, Transient ST elevation, or +Markers) • O2, IV, monitor • ASA immediately • Nitrates/BB/Pain relief • Clopidogrel 600 mg po • LMWH (better than heparin) • PCI in high risk, continued symptoms • IIb/IIIa therapy, initiated in the ED

  19. Dosing • ASA 325 mg PO on arrival • Clopidogrel 300 mg po and • Enoxaparin 1mg/kg Subq q 12 hr or Heparin 60 U/kg IVP, 12 U/kg/hr infusion and • Eptifibatide 180 mcg/kg IVP, 2 mcg/kg/min infusion (preferred) or Tirofiban 0.4mcg/kg/min for 30 min, then 0.1mcg/kg/min infusion or Abciximab 0.25 mg/kg IVP, 10mcg/min infusion (only if going to cath immediately, heparin reduced to 7 U/kg/hour)

  20. ED Treatment of Moderate Risk CP(High or Moderate Risk UA, Nonspecific ECG and -Markers) • O2, IV, monitor • ASA immediately • Nitrates/BB/Pain relief • Enoxaparin Subq • Clopidogrel 300 mg • Admit to Telemetry Bed • Serial enzymes • Protocol driven care • Angiogram versus provocative testing prior to discharge • Any positive enzymes or ECG leads to Level 2 Treatment

  21. ED Treatment of Low Risk CP: Day Hospital Chest Pain EvaluationIntermediate RiskChest Pain Resolved, Neg ECG, Neg Enzymes • ECG, CK, CKMB, TnI on arrival • Day Hospital Admission • Serial ECGs as indicated • CK, CKMB, TnI at 0,4, and 8 hours • Stress Thallium or Dobutamine Echo • Admit if positive stress, enzymes, or ECG changes • D/C if negative

  22. Negative (Low/Moderate Risk) Positive Negative TreatAccordingly Discharge CPC Flow Summary Non ST-elevation patients suspicious for ACS Risk Stratification • History and age • ECG/ECG criteria • Serum markers Chest Pain Center Negative • Serial markers • Serial ECGs • ST-trend monitoring • GXT • Radionuclide • Stress Echo Positive(High Risk) Admit Positive

  23. Case #2 • 44 year old female presents with sharp, left sided chest pain, no radiation • Acute onset • Pleuritic • Short of breath, apprehensive, cough, no sputum • Recent surgery on left knee • Family history of DVT • BP 110/60, P 115, Pulse Ox 98% • Normal exam, not reproduceable

  24. Pulmonary Embolism:DVT and PE

  25. Previous VTE Malignancy Age > 70 Obesity Prolonged bed rest Severe medical illness Pregnancy / postpartum Stroke Myocardial infarction Varicose veins Oral contraceptives Antipsychotic drugs? Travel* VTE/PE Risk Stratification: Patient Factors: Clinical *“Economy class syndrome”

  26. Antithrombin III deficiency Protein C deficiency Protein S deficiency Heparin cofactor 2 deficiency Activated protein C resistance Prothrombin G20210A mutation Hyperhomocysteinemia Elevated factor XI levels Elevated Factor VIII levels Myeloproliferative disease Hyperhomocysteinemia Antiphospholipid antibodies lupus anticoagulant Anticardiolipin Abs VTE/PE Risk Stratification:Patient Factors: Molecular Inherited Acquired

  27. Dyspnea 73% Pleuritic CP 66% Cough 37% Leg swelling 28% Leg pain 26% Hemoptysis 13% Palpitations 10% Syncope <10% Wheezing 9% “Anginal” CP 4% Sudden death ? Pulmonary Embolism: Patient History*† *PIOPED (JAMA 1990;263:2753-9) †No previous cardiopulmonary disease

  28. Tachycardia 70% Tachypnea 30% Crackles 51% Loud P2 23% Diaphoresis 11% Hypotension 8% Fever 7% Wheezing 5% RV lift 4% Homans’ 4% Pleural rub 3% Cyanosis 1% Pulmonary Embolism:Physical Examination*† * From PIOPED (JAMA 1990;263:2753-9) †No previous cardiopulmonary disease

  29. Suspected PE: A Simple Clinical Model and D-dimer to Assess Pretest Probability(n=946 patients) Specific FactorsPoints Clinical DVT (objective swelling, tenderness) 3.0 Heart rate > 100 beats/ min 1.5 Immobilization > 3 days or surgery in previous 4 wks 1.5 Previous DVT/PE 1.5 Hemoptysis 1.0 Malignancy 1.0 PE as likely, or more likely than alternative dx 3.0 Pretest probability of PE: Low: <2.0 Moderate: between 2.0 and 6.0 High: >6.0 Wells PS et al. Ann Intern Med 2001;135:98-107.

  30. Pulmonary Embolism:Laboratory Tests • D-dimer • ELISA D-dimer very sensitive for DVT/ PE • Very nonspecific! (Commonly positive in other settings!) • ELISA most sensitive (latex agglutination not sensitive) • Newer D-dimer tests are more rapid bedside assays • Most useful if negative and pretest probability is low Ahearn GS, Bounameaux H. Sem Respir Crit Care Med 2000;21:521-36. Tapson VF et al. Am J Respir Crit Care Med 1999;160:1043-66.

  31. Pulmonary Embolism:Laboratory Tests • Arterial blood gas • pO2usually abnormal (low) • pCO2usually abnormal (low) • Alveolar-arterial oxygen difference nearly always abnormal* • *May be normal, particularly in young patients • 150-1.25(pCO2)-pO2=A-a gradient on room air

  32. Pulmonary Embolus Workup Low Risk Intermediate Risk High Risk D Dimer Helical CT Helical CT - + - + - + D/C Dopplers Admit Admit Admit - + for D/C Admit Angio

  33. Pulmonary Embolus Rx • IV, O2, Monitor • Ventilatory and Oxygenation Support • IV Fluids • Heparin or Enoxaparin • Thrombolytics if low BP, Poor Oxygenation

  34. Case #3 • 75 year old female presents with SOB of two days duration • Tightness, DOE, Orthopnea, PND, leg swelling • Hx of HTN, MI, CAD • BP 210/110, P 60, R 24 • Rales in bases, JVD, ankle edema

  35. Heart Failure Pathophysiology Myocardial injury Fall in LV performance ANP BNP Activation of RAAS, ET, and others - Peripheral vasoconstriction Hemodynamic alterations Myocardial toxicity - Remodeling and progressive worsening of LV function Heart failure symptoms Morbidity and mortality

  36. Causes of CHF • CAD • HTN • Valvular Disease (aortic and mitral) • Cardiomyopathy (Etoh, amyloid, idiopathic, etc) • High Output: • Thyrotoxicosis • Anemia • AV Fistula • Beri Beri, Pagets

  37. Causes of Acute CHF Exacerbation • AMI/Ischemia • Arrhythmias (afib) • Accelerated HTN • Acute Valve Decompensation • Big PE (right sided failure, shock)

  38. Heart Failure Signs and Symptoms Symptoms Include: • Dyspnea Shortness of breath • Fatigue Feeling of tiredness • Peripheral Edema Swelling of legs and ankles • Orthopnea Pulmonary congestion • Weight gain Due to fluid retention • Rales Abnormal lung sounds

  39. Left Heart Failure SOB DOE Orthopnea Rales S3 Wheezes Tachycardia Fatigue Right Heart Failure Peripheral Edema Abdominal Swelling JVD Liver Enz Elevation HJR Most common cause is left heart failure, but COPD is common as well Right versus Left Heart Failure

  40. CHF Lab and Xray Findings • CXR: Vascular congestion, cardiomegaly, butterfly infiltrates, Kirley B lines, effusion • ABG or Pulse Ox: Hypoxia • ECG: LVH and strain patterns, nonspecific • Enzymes: Rule out AMI as a cause • Cardiac Output: Swan CO or CI, bioimpedance, etc. not practical in the ED. • BNP Levels: Elevated with atrial wall stretch >100 • Echocardiogram: Low EF, Valves

  41. Therapy of CHF in the ED • Airway Control • IV, O2, Monitor • Sitting Posture • Oxygenation Adjuncts: BiPAP, CPAP • Nitrates and Afterload Reducers • Diuretics • Continuous Monitoring of Urine Output, Hemodynamics • It’s Not That Simple

  42. Current Treatment of Acute Heart Failure Diuretics Vasodilators Inotropes Augment Contract- ility Decrease Preload And Afterload Reduce fluid volume

  43. Case #4 • 76 yo male presents with acute, severe chest pain of 15 minutes duration • Midsternal, radiates to back, pleuritic • Sweaty, vomiting, writhing, SOB • Hx HTN, PVOD • BP 220/140, P 110, R 24 • Normal Exam

  44. Thoracic Aortic Dissection

  45. Aortic Dissection: Clinical History • Risk Factors: HTN, collagen synthesis defects, pregnancy, aortic stenosis, advanced age • History: Severe, intermittent chest pain, tearing in nature, radiation to back, migratory • May be signs of peripheral embolus, inequality of pulses, stroke signs, or pulses lost • Usually hypertensive, but my be hypotensive if volume loss in chest or mediastinum

  46. Aortic Dissection: Lab and Xray • Chest Xray: Nonspecific. May have tortuous aorta, medistinal widening, pleural effusion, dilated aorta, separation of calcifcations from wall • ECG: nonspecific • Chest CT: Best screening test, unlikely if negative • Aortography or TEE: More specific, but less readily avalable

  47. Aortic Dissection: Treatment • ABC, IV (X2) O2, Monitor • Blood Pressure Control: • Nipride • Beta Blockers • Consulation with CT Surgery • Surgery if Proximal, Medical if Distal

  48. Case #4 • 44 yo alcoholic presents with acute onset of midsternal CP post vomiting • Pleuritic, diaphorsis, SOB, radiates to neck, back • Sweats and chills, no cough or sputum • BP 90/60, P 130, T 101 • No pain with palpation, clear lungs • Palpable sub q crepitance in left neck

  49. Esophageal Perforation • Acute onset pleuritic CP post vomiting • Fever, SOB, hemodynamic instability, sub q or mediastinal gas • EtOH, forced vomiting, instrumentation • Dx CXR, CT Chest,gGastrografin swallow, EGD • Rx: Abx, fluids, prepare for surgery

  50. Case #5 • 32 year old male with acute onset left sided CP, SOB • Four hours duration nonrelenting • Pleuritic, nonradiating, left sided • Hx HIV, AIDS • BP 110/60, P 110, R 28 • No breath sounds on left

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