Chest Pain Dr Mohannad F Allehyani Emergency Medicine

  • Slides: 56
Download presentation
Chest Pain Dr. Mohannad F Allehyani Emergency Medicine Demonstrator KAUH – Faculty of Medicine

Chest Pain Dr. Mohannad F Allehyani Emergency Medicine Demonstrator KAUH – Faculty of Medicine

Goals Review the pathophysiology, diagnosis and treatment of life threatening causes of chest pain.

Goals Review the pathophysiology, diagnosis and treatment of life threatening causes of chest pain.

Epidemiology 5% of all ED visits Approximately 5 million visits per year

Epidemiology 5% of all ED visits Approximately 5 million visits per year

Visceral Pain Visceral fibers enter the spinal cord at several levels leading to poorly

Visceral Pain Visceral fibers enter the spinal cord at several levels leading to poorly localized, poorly characterized pain. (discomfort, heaviness, dull, aching) Heart, blood vessels, esophagus and visceral pleura are innervated by visceral fibers

Parietal Pain Parietal pain, in contrast to visceral pain, is described as sharp and

Parietal Pain Parietal pain, in contrast to visceral pain, is described as sharp and can be localized to the dermatome superficial to the site of the painful stimulus.

Initial Approach ABC’s first, always (look for conditions requiring immediate intervention) Aspirin for potential

Initial Approach ABC’s first, always (look for conditions requiring immediate intervention) Aspirin for potential ACS EKG Cardiac and vital sign monitoring Pain relief

History O- onset P-provocation /palliation Q- quality/quantity R- region/radiation S- severity/scale

History O- onset P-provocation /palliation Q- quality/quantity R- region/radiation S- severity/scale

History Change in pattern Associated symptoms: DOE, SOB, diaphoresis, vomiting, heart burn, food intolerance

History Change in pattern Associated symptoms: DOE, SOB, diaphoresis, vomiting, heart burn, food intolerance PHx Social history FHx

Physical Exam General Appearance and Vitals (sick vs not sick) Chest exam -Inspection (scars,

Physical Exam General Appearance and Vitals (sick vs not sick) Chest exam -Inspection (scars, heaves, tachypnea, work of breathing) -Auscultation (murmurs, rubs, gallops, breath sounds) -Percussion (dullness)

Physical Exam Neck: JVD, crepitence, bruits Abdomen Extremities: swelling, pulses, tenderness, Homan’s

Physical Exam Neck: JVD, crepitence, bruits Abdomen Extremities: swelling, pulses, tenderness, Homan’s

Differential Diagnoses Cardiovascular Acute myocardial infarction, Acute coronary ischemia, Aortic dissection, Cardiac tamponade, Unstable

Differential Diagnoses Cardiovascular Acute myocardial infarction, Acute coronary ischemia, Aortic dissection, Cardiac tamponade, Unstable angina, Coronary spasm, Prinzmetal's angina, Cocaine induced, Pericarditis, Myocarditis, Valvular heart disease, Aortic stenosis, Mitral valve prolapse, Hypertrophic cardiomyopathy Pulmonary embolus, Tension pneumothorax, Pneumothorax, Mediastinitis, Pneumonia, Pleuritis, Tumor, Pneumomediastinum Gastrointestinal Esophageal rupture (Boerhaave), Esophageal tear (Mallory. Weiss), Cholecystitis, Pancreatitis, Esophageal spasm, Esophageal reflux, Peptic ulcer, Biliary colic Musculoskeletal Muscle strain, Rib fracture, Arthritis, Tumor, Costochondritis, Nonspecific chest wall pain Neurologic Spinal root compression, Thoracic outlet, Herpes zoster, Postherpetic neuralgia Other Psychologic, Hyperventilation

Life Threatening Causes of Chest Pain Acute Coronary Syndromes Pulmonary Embolus Tension Pneumothorax Aortic

Life Threatening Causes of Chest Pain Acute Coronary Syndromes Pulmonary Embolus Tension Pneumothorax Aortic Dissection

Acute Coronary Syndromes - Epidemiology In a typical ED population of adults over the

Acute Coronary Syndromes - Epidemiology In a typical ED population of adults over the age of 30 presenting with visceral-type chest pain, about 15 percent will have AMI and 25 to 30 percent will have UA

Acute Coronary Syndromes - History “Typical” Chest Pain Story (Pressure-like, squeezing, crushing pain, worse

Acute Coronary Syndromes - History “Typical” Chest Pain Story (Pressure-like, squeezing, crushing pain, worse with exertion, SOB, diaphoresis, radiates to arm or jaw) The majority of patients with ACS DO

Acute Coronary Syndromes – EKG Findings STEMI - ST segment elevation (>1 mm) in

Acute Coronary Syndromes – EKG Findings STEMI - ST segment elevation (>1 mm) in contiguous leads; new LBBB T wave inversion or ST segment depression in contiguous leads suggests subendocardial

Acute Coronary Syndromes – Cardiac Markers Marker Initial Rise Peak Return to normal Benefits

Acute Coronary Syndromes – Cardiac Markers Marker Initial Rise Peak Return to normal Benefits Troponin 2 -4 hr 10 -24 hr 5 -10 days Sensitive and specific CK-MB 3 -4 hr 10 -24 hr 2 – 4 days Unaffected by renal failure LDH 10 hr 24 -72 hr 14 days Myoglobin 1 -2 hr 4 -8 hr 24 hours Very sensitive, powerful negative predictive value

Acute Coronary Syndromes – Cardiac Markers

Acute Coronary Syndromes – Cardiac Markers

Echocardiogram Wall abnormalities occur within minutes Will detect abnormalities in 80% of AMI Normal

Echocardiogram Wall abnormalities occur within minutes Will detect abnormalities in 80% of AMI Normal resting echo in setting of chest pain gives low probability Early screen for AMI

Echo

Echo

Acute Coronary Syndromes - Treatment Aspirin Nitroglycerin Oxygen Analgesia

Acute Coronary Syndromes - Treatment Aspirin Nitroglycerin Oxygen Analgesia

Treatment Beta-Blockers Anticoagulation Anti-Platelet Agents Thrombolysis Percutaneous Coronary Interventions (PCI)

Treatment Beta-Blockers Anticoagulation Anti-Platelet Agents Thrombolysis Percutaneous Coronary Interventions (PCI)

Stress echocardiograms Sensitivity 60 -90% Specificity 75% ? Should be employed with moderate to

Stress echocardiograms Sensitivity 60 -90% Specificity 75% ? Should be employed with moderate to high risk stratification Limitations of reader, image quality, and previous functional impairment

Acute Coronary Syndromes - Treatment STEMI (ASA, B-blocker, NTG, anti-platelet, anticoagulation, thrombolysis, PCI) NSTEMI

Acute Coronary Syndromes - Treatment STEMI (ASA, B-blocker, NTG, anti-platelet, anticoagulation, thrombolysis, PCI) NSTEMI (ASA, B-blocker, NTG,

Acute Coronary Syndromes - Disposition Mortality is twice as high for missed MI Missed

Acute Coronary Syndromes - Disposition Mortality is twice as high for missed MI Missed MI is the most successfully litigated claim against EP's. EP’s miss 3 -5% OF

Acute Coronary Syndromes - Disposition A single set of cardiac enzymes is rarely of

Acute Coronary Syndromes - Disposition A single set of cardiac enzymes is rarely of use Risk Stratification: goal is to predict the likelihood of an adverse cardiovascular event Combination of H+P, EKG,

Pulmonary Embolism - Pathophysiology Thrombosis of a pulmonary artery >90% arise from DVT Clot

Pulmonary Embolism - Pathophysiology Thrombosis of a pulmonary artery >90% arise from DVT Clot from a DVT travels through the venous system and lodges in the pulmonary vasculature

Pulmonary Embolism – History Dyspnea is the most common symptom, present in 90% of

Pulmonary Embolism – History Dyspnea is the most common symptom, present in 90% of patients diagnosed with PE Sharp pleuritic chest pain, syncope, Prolonged immobilization,

Pulmonary Embolism – Physical Exam Tachycardia, tachypnea, diaphoresis, hypotension, hypoxia, low grade fever, anxiety,

Pulmonary Embolism – Physical Exam Tachycardia, tachypnea, diaphoresis, hypotension, hypoxia, low grade fever, anxiety, cardiovascular collapse, right ventricular heave

Pulmonary Embolism – Diagnostic Testing Sinus Tachycardia is the most frequent EKG finding Classic

Pulmonary Embolism – Diagnostic Testing Sinus Tachycardia is the most frequent EKG finding Classic S 1, Q 3, T 3 finding is seen in less than 20% ABG plays no role in ruling out

Pulmonary Embolism – Wells Criteria Clinical Signs and Symptoms of DVT? Yes +3 PE

Pulmonary Embolism – Wells Criteria Clinical Signs and Symptoms of DVT? Yes +3 PE is #1 Diagnosis, or Equally Likely? Yes +3 Heart Rate > 100? Yes +1. 5 Immobilization at least 3 days, or Surgery in the Previous 4 weeks? Yes +1. 5 Previous, objectively diagnosed PE or DVT? Yes +1. 5 Hemoptysis? Yes +1 Malignancy w/ Treatment within 6 mo, or

Pulmonary Embolism – Diagnostic Imaging Algorithm

Pulmonary Embolism – Diagnostic Imaging Algorithm

Pulmonary Embolism – Treatment/Disposition Unfractionated heparin vs low molecular weight heparin (some studies suggest

Pulmonary Embolism – Treatment/Disposition Unfractionated heparin vs low molecular weight heparin (some studies suggest superiority of LMWH) Thrombolysis (for cardiovascular collapse)

PE CXR

PE CXR

Aortic Dissection - Pathophysiology Intimal tear of the aorta leads to dissection of the

Aortic Dissection - Pathophysiology Intimal tear of the aorta leads to dissection of the layers of the aorta creating a false lumen

Aortic Dissection - Diagnosis Tearing chest pain radiating to the back Risk Factors: HTN,

Aortic Dissection - Diagnosis Tearing chest pain radiating to the back Risk Factors: HTN, connective tissue disease Exam: HTN, pulse differentials, neuro deficits

Aortic Dissection - Classification De Bakey system: Type I dissection involves both the ascending

Aortic Dissection - Classification De Bakey system: Type I dissection involves both the ascending and descending thoracic aorta. Type II dissection is confined to the ascending aorta. Type III dissection is confined to the descending aorta. The Daily system classifies dissections

Aortic Dissection - Treatment Patients with uncomplicated aortic dissections confined to the descending thoracic

Aortic Dissection - Treatment Patients with uncomplicated aortic dissections confined to the descending thoracic aorta (Daily type B or De Bakey type III) are best treated with medical therapy. Medical Therapy: Goal to decrease the blood pressure and the velocity of left ventricular contraction, both of which will decrease aortic shear stress and minimize the tendency to further dissection. Acute ascending aortic dissections (Daily type A or

Tension Pneumothorax - Pathophysiology Collection of air in the pleural space causes collapse of

Tension Pneumothorax - Pathophysiology Collection of air in the pleural space causes collapse of the ipsilateral lung and then cardiovascular collapse as

Tension Pneumothorax - Diagnosis Risk factors: COPD; connective tissue disease, trauma, recent instrumentation, positive

Tension Pneumothorax - Diagnosis Risk factors: COPD; connective tissue disease, trauma, recent instrumentation, positive pressure ventilation

Tension Pneumothorax - Treatment Needle decompression Tube thoracostomy

Tension Pneumothorax - Treatment Needle decompression Tube thoracostomy

Esophageal Rupture - Pathophysiology Tear in the esophagus leads to leaking of gastrointestinal contents

Esophageal Rupture - Pathophysiology Tear in the esophagus leads to leaking of gastrointestinal contents into the mediastinum Inflammation followed by

Esophageal Rupture - Diagnosis Rare but devastating Risk Factors: Iatrogenic, heavy retching, trauma, foreign

Esophageal Rupture - Diagnosis Rare but devastating Risk Factors: Iatrogenic, heavy retching, trauma, foreign bodies, toxic ingestion

Not so subtle Subtle

Not so subtle Subtle

Imaging

Imaging

Esophageal Rupture - Treatment Antibiotics Supportive Care Small tears with minimal extraesophageal involvement can

Esophageal Rupture - Treatment Antibiotics Supportive Care Small tears with minimal extraesophageal involvement can

Take Home Points ABC’s first History is key Have a low threshold for missed

Take Home Points ABC’s first History is key Have a low threshold for missed MI