Download Free Medical Chest Pain PowerPoint Presentation

Chest Pain PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Angina, which is titled "Chest Pain", to know about the pathophysiology, diagnosis and treatment of life threatening causes of chest pain.

Tags : Angina, Chest Pain, pathophysiology, diagnosis, treatment

Published on : May 25, 2021 | Views : 2945 | Downloads : 11

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Chest Pain LSU Medical Student Clerkship, New Orleans, LA
Slide 2-

Goals Review the pathophysiology, diagnosis and treatment of life threatening causes of chest pain.
Slide 3-

Epidemiology 5% of all ED visits Approximately 5 million visits per year
Slide 4-

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 Because of dorsal fibers can overlap three levels above or below, disease of thoracic origin can produce pain anywhere from the jaw to the epigastrum
Slide 5-

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. The dermis and parietal pleura are innervated by parietal fibers.
Slide 6-

Initial Approach ABC’s first, always (look for conditions requiring immediate intervention) Aspirin for potential ACS EKG Cardiac and vital sign monitoring Pain relief Because of the wide differential, H+P will guide the diagnostic workup
Slide 7-

History O- onset P-provocation /palliation Q- quality/quantity R- region/radiation S- severity/scale T- timing/time of onset
Slide 8-

History Change in pain pattern Associated symptoms: DOE, SOB, diaphoresis, vomiting, heart burn, food intolerance PHx Social history FHx
Slide 9-

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) -Palpation (tenderness, PMI)
Slide 10-

Physical Exam Neck: JVD, crepitence, bruits Abdomen Extremities: swelling, pulses, tenderness, Homan’s
Slide 11-

Differential Diagnoses
Slide 12-

Life Threatening Causes of Chest Pain Acute Coronary Syndromes Pulmonary Embolus Tension Pneumothorax Aortic Dissection Esophageal Rupture Pericarditis with Tamponade
Slide 13-

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
Slide 14-

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 NOT present with these symptoms! Cardiac Risk Factors (Age, DM, HTN, FH, smoking, hypercholesterolemia, cocaine abuse)
Slide 15-

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 ischemia 5% of patients with AMI have completely normal EKGs
Slide 16-

ppt slide no 16 content not found
Slide 17-

ppt slide no 17 content not found
Slide 18-

Acute Coronary Syndromes – Cardiac Markers
Slide 19-

Acute Coronary Syndromes – Cardiac Markers
Slide 20-

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 complications: aneurysms, valve abnormalities, other structural destruction
Slide 21-

Echo
Slide 22-

Acute Coronary Syndromes - Treatment Aspirin Nitroglycerin Oxygen Analgesia
Slide 23-

Treatment Beta-Blockers Anticoagulation Anti-Platelet Agents Thrombolysis Percutaneous Coronary Interventions (PCI)
Slide 24-

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 Negative test has time limited value
Slide 25-

Acute Coronary Syndromes - Treatment STEMI (ASA, B-blocker, NTG, anti-platelet, anticoagulation, thrombolysis, PCI) NSTEMI (ASA, B-blocker, NTG, anti-platelet, anticoagulation, PCI) Unstable Angina (ASA, B-blocker, NTG, anticoagulation, risk stratification)
Slide 26-

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 AMI, this accounts for 25% of malpractice costs against EP’s
Slide 27-

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, Biomarkers No single globally accepted algorithm Mathematical models such as TIMI, GRACE, PURSUIT, and HEART can be helpful but are no substitute for clinical judgment
Slide 28-

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 creating a ventilation/perfusion mismatch
Slide 29-

Pulmonary Embolism – History Dyspnea is the most common symptom, present in 90% of patients diagnosed with PE Sharp pleuritic chest pain, syncope, Prolonged immobilization, neoplasm, known hypercoagulable disorder
Slide 30-

Pulmonary Embolism – Physical Exam Tachycardia, tachypnea, diaphoresis, hypotension, hypoxia, low grade fever, anxiety, cardiovascular collapse, right ventricular heave
Slide 31-

Pulmonary Embolism – Diagnostic Testing Sinus Tachycardia is the most frequent EKG finding Classic S1,Q3,T3 finding is seen in less than 20% ABG plays no role in ruling out PE D-Dimer in a low risk patient can be used to rule out PE
Slide 32-

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 palliative? Yes +1 <2 = Low risk, 2.5-6 = moderate risk, >6 = high risk
Slide 33-

Pulmonary Embolism – Diagnostic Imaging Algorithm
Slide 34-

Pulmonary Embolism – Treatment/Disposition Unfractionated heparin vs low molecular weight heparin (some studies suggest superiority of LMWH) Thrombolysis (for cardiovascular collapse) Floor vs ICU
Slide 35-

PE CXR
Slide 36-

ppt slide no 36 content not found
Slide 37-

ppt slide no 37 content not found
Slide 38-

ppt slide no 38 content not found
Slide 39-

ppt slide no 39 content not found
Slide 40-

ppt slide no 40 content not found
Slide 41-

Aortic Dissection - Pathophysiology Intimal tear of the aorta leads to dissection of the layers of the aorta creating a false lumen
Slide 42-

Aortic Dissection - Diagnosis Tearing chest pain radiating to the back Risk Factors: HTN, connective tissue disease Exam: HTN, pulse differentials, neuro deficits Radiology: Wide mediastinum on CXR, CT angio chest, echo
Slide 43-

ppt slide no 43 content not found
Slide 44-

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 that involve the ascending aorta as type A, regardless of the site of the primary intimal tear, and all other dissections as type B.
Slide 45-

ppt slide no 45 content not found
Slide 46-

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 De Bakey type I or type II) should be treated surgically whenever possible since these patients are a high risk for a life-threatening complication such as aortic regurgitation, cardiac tamponade, or myocardial infarction.
Slide 47-

Tension Pneumothorax - Pathophysiology Collection of air in the pleural space causes collapse of the ipsilateral lung and then cardiovascular collapse as intrathoracic pressures increase.
Slide 48-

Tension Pneumothorax - Diagnosis Risk factors: COPD; connective tissue disease, trauma, recent instrumentation, positive pressure ventilation Absent breath sounds unilaterally, hypotension, distended neck veins, tracheal deviation
Slide 49-

ppt slide no 49 content not found
Slide 50-

Tension Pneumothorax - Treatment Needle decompression Tube thoracostomy
Slide 51-

Esophageal Rupture - Pathophysiology Tear in the esophagus leads to leaking of gastrointestinal contents into the mediastinum Inflammation followed by infection cause rapid deterioration, sepsis and death
Slide 52-

Esophageal Rupture - Diagnosis Rare but devastating Risk Factors: Iatrogenic, heavy retching, trauma, foreign bodies, toxic ingestion Radiology: Mediastinal air on plain films or CT scan
Slide 53-

Subtle Not so subtle
Slide 54-

Imaging
Slide 55-

Esophageal Rupture - Treatment Antibiotics Supportive Care Small tears with minimal extraesophageal involvement can be managed conservatively Surgical consult for all regardless of size
Slide 56-

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