Presentation on theme: "Chest Pain Epidemiology"— Presentation transcript:
1 Chest Pain Epidemiology 6 million ED visits/year5-7% ED patients3.3% AIS evacuations 2002, 3.5% in 2003, % in 2004, 3.2% in 20053 million patients admitted/year70% found not to have acute coronary event0.4% - 4.0% acute MI are sent home
2 Chest Pain Pathophysiology Chest pain syndromes difficult to diagnoseMultiple organ systems of the chestShare afferent (nerve) pathwaysPathology in any of these systems have similar pattern of complaintsMost patients have CP with acute coronary syndrome(ACS), others may present with only SOB, N/V, arm or jaw pain
3 Differential Diagnosis of Chest Pain Life-threatening causesAcute coronary syndrome(ACS)Aortic dissectionPulmonary embolismTension pneumothoraxEsophageal rupture (Boerhaave’s syndrome)Pericarditis; myocarditisAcute chest syndrome(in sickle cell disease)Myocarditis is the most common cause of sudden death in the young. Acute chest syndrome is the most common cause of death in sickle cell patients. Sickle cell patients presenting with chest pain should be presumed to have acute chest syndrome until proven otherwise. Progressive hypoxia, multilobar pneumonia, on chest x-ray, and falling hemoglobin levels are the most common clinical findings.
6 Chest Pain Evaluation Problems History Risk factors Physical exam Rhythm strip, 9 lead ECG, 12 lead ECGRisk stratification based on above factorsDo modified 9 lead by placing unit in the diagnostic mode.
7 The Initial Clinical Examination ECG can only help if it shows acute MIInitial ECG sensitivity 20% - 60% AMISensitivity of plasma CK-MB low first 4 hrsCan’t detect unstable anginaTherefore evaluation based on history, physical exam and ECG
8 History“The most important difference between a good and indifferent clinician lies in the amount of attention paid to the story of the patient”---Farquhar Buzzard
9 HistoryHelpful to group questions to target the three most common life threats;Consider ACS questionsPulmonary embolism(PE) questionsAortic dissection questions
10 History Cardiac Questions 2 most important historical informationage, genderAdvancing age, prevalence and severity of CAD increasesCan estimate pretest probability of CAD based on age and genderFurther refine pretest probability by classifying the chest pain as typical, atypical, or non-anginalCAD(coronary artery disease). A combination of autopsy data and large angiography studies allows us to estimate the pretest probability of CAD in patients based on age and gender alone.
11 Pretest likelihood of CAD based on age, sex, and symptoms Asymptomatic non-anginal CPAge Men Women Men Women% % % %% % % %% % % %% % % %
12 Pretest likelihood of CAD based on age, sex, and symptoms Atypical angina Typical anginaAge Men Women Men Women% % % %% % % %% % % %% % % %Atypical(variant) angina or Prinzmetal angina primarily occurs at rest and without provocation. The current thought is that variant angina is due to vasospasm of the coronary vessels. When studies are performed by angiogram, about 1/3 have no or insignificant atherosclerosis and about 2/3 have CAD in addition to spasm.
13 Cardiac QuestionsExample; 35y/o male with non-anginal CP has 5% pretest probability of CAD(1 in 20)same 35y/o with atypical angina 22% of CAD or (1in 5)same 35y/o with typical angina 70%(7in10)If patient has known previous CAD/MI raises risk of subsequent coronary event 5 timesIf patient has cardiac history ask about prior stress tests, cardiac caths, bypass surgery, stents
14 Cardiac Questions Character of Pain Many patients have atypical symptomsAsk questions in regard to nature (quality), severity(1-10), duration, modifying factors of the pain, and associated symptoms40% patients with AMI have atypical CP35% patients without AMI have typical CP
15 Cardiac QuestionsIn one study of 721 patients who were diagnosed with AMI, almost ½ presented without CPSOB, weakness, dizziness, syncope, abdominal painTypical angina is a deep, poorly localized chest or arm discomfort that is classically exertional and relieved with rest or nitrates
16 Analysis of Clinical Predictors of AMI Clinical features AMIchest pain radiation Odds ratioleft armright armboth armsnausea, vomitingdiaphoresisexertional CP
17 Analysis of Clinical Predictors of AMI Clinical features AMIOdds ratioburning/indigestion paincrushing/squeezing painrelief with nitroglycerinpleuritic paintender chest wallsharp/stabbing pain
18 Cardiac QuestionsAnother study of 251 patients with cardiac CP showed 88% respond to NTG, also 92% of noncardiac CP responded to NTGCan you give GI cocktail to R/O cardiac CP?a study of 97 patients who received GI cocktail showed 8 of 11 patients admitted with possible cardiac ischemia had complete or partial relief of CP
19 Cardiac Questions Risk Factors Diabetes, hypertension, smoking, high cholesterol, and family historyMost CAD patients have at least oneThe absence of risk factors does not exclude acute cardiac ischemia
20 Aortic Dissection History Male (75%)Seventh decadeHistory of hypertension (70%)Other risk factors;Marfan’s syndrome, atherosclerosis, prior dissection, or known aortic aneurysmMarfan”s syndrome is a generalized disorder of connective tissue with skeletal, ocular, and cardiac manifestations. The extremities are long and thin. The eyes show subluxation of the lens. Severe myopia and spontaneous retinal detachment are common. Cardiovascular defects include disruption and loss of elastic fibers in the media of the aorta. The lack of elasticity results in progressive diffuse dilatation of the proximal segment of the ascending aorta and severe aortic regurgitation. Heart failure and rupture of the aorta from dissecting aneurysm are the most common cause of death.
21 Aortic Dissection History Pain is sudden onset (83%)Severe or “worse ever” (90%)Sharp (64%) or tearing (50%)Location anterior chest (60%), back (53%)Migratory (16%), radiating (28%)Suspect dissection in patients with clinical changing picturePatients who complain of chest pain along with a neurologic deficit may have a dissection occluding a cerebral or spinal artery.
22 Aortic Dissection History Should address 3 basic concerns regarding a patient’s pain:quality (sudden and severe)radiation (especially to the back)intensity at onset (maximal)Aortic dissection and MI can coexist8% dissection involves coronary arteriesOne retrospective study showed that when all three questions were asked, physicians correctly diagnosed thoracic aortic dissection in 30 of 33 patients(91%); if one or more of these aspects were omitted, the correct diagnosis was suspected in fewer than half of all patients.EKG changes such as acute ST and T wave abnormalities are present in half of all patients with aortic dissection--- often confounding the initial diagnosis.
23 Pulmonary Embolism History Clinical diagnosis of PE is difficultSymptoms are variable and nonspecificCan range from dyspnea and fatigue to severe pleuritic CP and syncopeClassic description of pleuritic pain, dyspnea, and hemoptysis represents embolic pulmonary infarction and is seen most commonly in hospitalized patients
24 Pulmonary Embolism History Ambulatory patients often present with painless dyspneaCan have several weeks of intermittent symptomsPhysical exam is rarely diagnosticReproducible chest wall pain does not exclude diagnosis
25 Pulmonary Embolism History Wide spectrum of pain quality and locationPain that is peripheral, increases with deep breath, and not reproducible- suspect PEIsolated substernal, pleuritic CP less likely PESubsternal, anginal CP occurs 4% PERadiation to arm distinctly unusualPleuritic CP and leg pain more commonly PE than other diagnosis
28 Other ConditionsBoerhaave’s syndrome presents as spontaneous esophageal rupture after vomitingPain on swallowingSignificant number are recently, or acutely intoxicatedPericarditis refers pain to neck, shoulder and worsens with inspiration, swallowing, and lying supine
29 Physical ExaminationStable patients with AMI rarely have physical findings on examVital SignsChest pain and hypotension-not good8% PE and 15% aortic dissection are hypotensive on presentationPatients with CP and hypotension are 3 times more likely to have AMI than normotensive pts
30 Physical Examination Vital Signs Fever, consider noncardiac cause, pneumonia, mediastinitisLow grade fever occurs 14% PE, only % PE pts had fever> 102FTachypnea is most common sign in PE, 15% PE pts had respiratory rate <20/min
31 Physical Examination Vital Signs Tachycardia is nonspecific sign May be only clue to early pericarditis, myocarditisBradycardia, esp. due to conduction defects, may be seen in right coronary occlusions
32 Physical Examination Vital Signs Fifth vital sign, pulse oximetry Hypoxia can occur in many conditionsPatient with low O2 saturations require supplemental oxygenO2 saturation is normal in ¼ of pts with PE
33 Physical Examination Head and Neck Check neck for Kussmaul’s sign (a paradoxical increase in jugular venous distension with inspiration)Seen in pericardial tamponade, right heart failure or infarction, PE, or tension pneumothorax)Subcutaneous air at the root of the neck suggests pneumothorax, or pneumomediastinitisCarotids bruits increase likelihood of CAD
34 Physical Examination Pulmonary Exam Look for respiratory distress:nasal flaring, intercostal retractions, and accessory muscle useListen for unilateral absence of breath sounds; consider pneumothorax, or massive pleural effusionPercuss the chest for infiltrates, effusions, and pneumothorax
35 Physical Examination Pulmonary Exam Wheezing and rales are important findings but are not specific for certain diseasesAsthma, foreign body, CHF, PE all may cause wheezingRales are rare in pts with AMI, but their presence with left heart failure, raises the likelihood of MI by twofold
36 Physical Examination Cardiac Exam A new murmur may signal papillary muscle ruptureMurmur of aortic insufficiency is an important finding associated with aortic dissectionS3 gallop secondary to CHF raises likelihood of MI 3 times
37 Physical Examination Cardiac Exam Hamman’s crunch- crunching sound of heart beating against mediastinal airPericardial rub(creaking of new leather) seen in pericarditisBeck’s triad(distant heart sounds, distended neck veins, and hypotension) seen in pericardial tamponade from proximal aortic dissection
38 Physical Examination Chest Wall Exam Even with chest wall tenderness, still have to consider life-threatening causesReproducible CP frequently seen in pts with PE and ACSCostochondritis is inflammation of the costal cartilages, may result in sharp, dull, or pleuritic CP, rarely has swelling of soft tissues
39 Physical Examination Chest Wall Exam Tietze’s syndrome- fusiform swelling and pain of only one upper costal cartilageCompression of cervical or thoracic nerve may produce dull chest pain mimickings angina (cervico-precordial angina)Pain worsens with neck movement, coughing, sneezing, or axial loading of the vertebraeCheck skin for herpes zoster (shingles); causes unilateral pain over 1-2 dermatones
40 Physical Examination Exam of the Extremities Look for edema, thrombosis, or pulse deficitsPeripheral edema frequently seen in right-sided and biventricular failureUsually absent in acute left heart failureUnilateral edema or palpable venous thrombus(cord) suggest DVT or PEBut most pts with PE have normal ext. exams
41 Physical Examination Examination of Pulses Exam for symmetry and qualityPulse deficit is defined as asymmetrical amplitude between the right and left sidesPulse deficits most common in type A dissections(ascending aorta)Measured BP difference occurs 15%Differences > 20mmHg between arms was an independent predictor of dissection
42 Physical Examination Neurologic Exam Altered mental status nonspecific findingAssociated with any cause of CP that leads to BP instability and cerebral hypoperfusion17% aortic dissection have focal neurologic deficits due to occlusion of carotid or spinal arteriesDistal aortic dissections can cause spinal cord ischemia
43 Diagnostic StudiesThe ECG is the most important test in the evaluation of CPThe initial ECG is insensitive in identifying acute coronary syndromeOnly 20%-60% pts presenting with acute MI have diagnostic changes on initial ECG
44 Diagnostic Studies ECG What diagnostic changes?at least 1 mm elevation in one or more inferior/lateral leadsor at least 2mm of elevation in one or more anterioseptal leads10% pts with AMI have LVH with repolarization changesTall peaked T waves may be earliest sign of AMI
47 Offshore Case Presentation # 1 Chief Complaintchest and arm painHistory of Present Illness38 y/o male c/o burning right sided chest and arm pain which began after he stood up from the supper table.
48 Case Presentation # 1 History of Present Illness Pain is burning in qualityLocation is substernal and in the right arm5 on (1-10 scale) initially, now 2No radiation, duration > 2 hoursNo associated nausea, vomiting, SOB, or diaphoresisPain increased after climbing 3 flights stairs
49 Case Presentation # 1 Past History 2 weeks ago dx with acid reflux, had substernal chest pain. PMD stated ECG was normal, blood test normal, but cholesterol and BP were elevatedBegan Nexium, cholesterol, and BP meds, but quit taking themNo other past medical problems
50 Case Presentation # 1 Medications- none NKA Risk Factors + HTN, cholesterol, Family hx heart disease, smoker- diabetes
51 Case Presentation # 1 Physical Examination Vital signs: BP-140/88, P-76, RR-20, T-97.9, O2 sat.-98%; ECG- no acute changesAlert WM in NADskin warm, and dryHt -RR&R; Lungs- clear; Chest wall- nontender; Abd- soft, nontender; Ext- equal pulses
53 Case Presentation # 1 Treatment Plan, Physician Orders 4 baby ASA chew and swallowO2IV NS TKONTG SL q3-5min up to 3Nitrol paste 1” if BP stableMS if neededSend in emergently
54 Case Presentation #1 Final diagnosis: ACS Angiogram revealed two 95% blockages, 2 stents placed
55 Case Presentation # 2 Chief Complaint chest pain History of Present Illness32y/o male with squeezing, substernal chest pain that began while sitting in chair. Pain is worse with deep breathing and not relieved by drinking carbonated soda.
57 Case # 2Past HistoryHx of 2 previous episodes of chest pain while on rig. 1st workup was neg. 2nd revealed aortic valve problem and coronary blockage with stent placement 1998Hx of HTNMedicines- Toprol, Avapro, and ASA qdNKA
58 Case # 2Risk Factors+ HTN, smoker, Past Hx of CAD, Family Hx of MI- GF (both sides)- DM, elevated cholesterol
59 Case # 2Physical ExamVital signs- BP 160/80, P-94, RR-16, O2 sat 98%; ECG- no acute changesAlert WM in NADskin warm and dryheart- RR&R; Lungs- clear; Chest wall nontender; Abd- soft, nontender; Ext- equal pulses
61 Case # 2 Treatment Plan, Physician Orders IV NS TKONTG SL q3-5min up to 3Nitrol paste 1” if BP stableMS if neededSend in emergently
62 Case # 2 Final diagnosis: Work up revealed an ascending aortic aneurysmEmergent surgical repair, resection
63 Case # 3 Chief complaint Shortness of breath History of Present Illness53y/o awoke from sleep with SOB. Patient denies CP, nausea, vomiting, or diaphoresis. No hx of previous episodes in past. Denies cold, but did have coughing episode prior to SOB.
64 Case # 3 Past Medical History negative Medicine- none NKA Risk Factors + smoker- HTN, DM, cholesterol, Family Hx CAD
65 Case # 3Physical ExamVital signs- BP-130/90, P-104, RR-30, T-97.4, O2 sat- 95%; ECG- sinus tach, no acute changesAlert WM in mild distress, not SOB nowskin warm and dryHeart- RR&R; lungs- clear, no wheezes; Abd- nontender; Ext- no swelling, equal pulses