APPROACH TO CHEST PAIN - PowerPoint Presentation

1. APPROACH TO CHEST PAINDr.Aryakrishna A(JR1 MEDICINE)TDMC ALAPPUZHA

2. The most common reasons for which patients present for medical attention at ED or an OP clinicThe evaluation of non traumatic chest discomfort is inherently challenging owing to the broad variety of possible causes A minority of which are life-threatening conditions that should not be missed.

3. It is helpful to frame the initial diagnostic assessment and triage of patients with acute chest discomfort around three categories:Myocardial ischemiaOther Cardiopulmonary causesPericardial diseaseAortic emergenciesPulmonary conditions Non-Cardiopulmonary causes.

4. Chest discomfort is the third most common reason for visits to the ED More than 60 % of patients with this presentation are hospitalised for further testing15% of evaluated patients are eventually diagnosed with ACSThe most common diagnoses are Gastrointestinal causes.Fewer than 10% are other life-threatening Cardiopulmonary conditionsEPIDEMIOLOGY AND NATURAL HISTORY

5. CAUSES OF CHEST DISCOMFORTGastrointestinal 42%Ischemic heart disease 31%Chest wall syndrome 28%Pericarditis 4%Pleuritis 2%Pulmonary embolism 2%Lung cancer 1.5%Aortic aneurysm 1% Aortic stenosis 1%Herpes zoster 1%

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8. Angina pectoris Myocardial ischemia is precipitated by an imbalance between myocardial oxygen requirements and myocardial oxygen supply, resulting in insufficient delivery of oxygen to meet the heart’s metabolic demands. DEMAND SUPPLY MISMATCHMYOCARDIAL ISCHEMIA/INJURY

9. Myocardial oxygen consumption may be elevated by Increases in heart rateVentricular wall stressMyocardial contractilityWhereas myocardial oxygen supply is determined by coronary blood flow and coronary arterial oxygen content. When myocardial ischemia is sufficiently severe and prolonged in duration (as little as 20 min), irreversible cellular injury occurs, resulting in MI.

10. Ischemic heart disease is most commonly caused by atheromatous plaque that obstructs one or more of the epicardial coronary arteries. Stable ischemic heart disease usually results from the gradual atherosclerotic narrowing of the coronary arteries. Stable angina is characterized by ischemic episodes that are typically precipitated by a superimposed increase in oxygen demand during physical exertion and relieved upon resting.

11. Ischemic heart disease becomes unstable most commonly when rupture or erosion of one or more atherosclerotic lesions triggers coronary thrombosis. Unstable ischemic heart disease is classified clinically by the presence or absence of detectable myocardial injury and the presence or absence of ST-segment elevation on the patient’s electrocardiogram (ECG).

12. When acute coronary atherothrombosis occurs, the intracoronary thrombus may be partially obstructive, generally leading to myocardial ischemia in the absence of ST-segment elevation.Marked by ischemic symptoms at rest, with minimal activity, or in an accelerating pattern, unstable ischemic heart disease is classified as Unstable angina when there is no detectable myocardial injury Non–ST elevation MI (NSTEMI) when there is evidence of myocardial necrosis

13. When the coronary thrombus is acutely and completely occlusive, transmural myocardial ischemia usually ensues, with ST-segment elevation on the ECG and myocardial necrosis leading to a diagnosis of ST elevation MI (STEMI)

14. The term acute coronary syndrome which encompasses unstable angina, NSTEMI, and STEMI, is in general reserved for ischemia precipitated by acute coronary atherothrombosis.

15. Other contributors Endothelial dysfunction, Microvascular disease, and vasospasm.Non-atherosclerotic processesCongenital abnormalities of the coronary vessels Myocardial bridgingCoronary arteritis Radiation-induced coronary disease

16. Conditions associated with extreme myocardial oxygen demand and impaired endocardial blood flow Aortic valve disease Hypertrophic cardiomyopathy Idiopathic dilated cardiomyopathy

17. Ischemic episodes are thought to excite local chemosensitive and mechanoreceptive receptors This in turn, stimulate release of adenosine, bradykinin, and other substances This inturn activate the sensory ends of sympathetic and vagal afferent fibers. The afferent fibers traverse the nerves that connect to the upper five thoracic sympathetic ganglia and upper five distal thoracic roots of the spinal cord.From there, impulses are transmitted to the thalamus. MECHANISMS OF CARDIAC PAIN

18. Within the spinal cord, cardiac sympathetic afferent impulses may converge with impulses from somatic thoracic structures, and this convergence may be the basis for referred cardiac pain. In addition, cardiac vagal afferent fibers synapse in the nucleus tractus solitarius of the medulla and then descend to the upper cervical spinothalamic tract, and this route may contribute to anginal pain experienced in the neck and jaw

19. PERICARDIAL DISEASESInflammation of the pericardium due to infectious or noninfectious causes can be responsible for acute or chronic chest discomfort.The visceral surface and most of the parietal surface of the pericardium are insensitive to pain.Therefore, the pain of pericarditis is thought to arise principally from associated pleural inflammation. Because of this pleural association, the discomfort of pericarditis is usually pleuritic pain that is exacerbated by breathing, coughing, or changes in position. OTHER CARDIOPULMONARY CAUSES

20. Moreover, owing to the overlapping sensory supply of the central diaphragm via the phrenic nerve with somatic sensory fibers originating in the third to fifth cervical segments, the pain of pleural pericarditis is often referred to the shoulder and neck. Involvement of the pleural surface of the lateral diaphragm can lead to pain in the upper abdomen

21. MYOCARDIAL DISEASESAcute inflammatory and other non-ischemic myocardial diseases can also produce chest discomfort.

22. Acute aortic dissection is a less common cause of chest discomfort but is important because of the catastrophic natural history .Acute aortic syndromes encompass a spectrum of acute aortic diseases related to disruption of the media of the aortic wall. DISEASES OF THE AORTA

23. 1. Aortic dissection involves a tear in the aortic intima, resulting in separation of the media and creation of a separate “false” lumen. 2.A penetrating ulcer has been described as ulceration of an aortic atheromatous plaque that extends through the intima and into the aortic media, with the potential to initiate an intramedial dissection or rupture into the adventitia. 3. Intramural hematoma is an aortic wall hematoma with no demonstrable intimal flap, no radiologically apparent intimal tear, and no false lumen. Intramural hematoma can occur due to either rupture of the vasa vasorum or, less commonly, a penetrating ulcer.

24. Each of these subtypes typically presents with chest discomfort that is often severe, sudden in onset, and sometimes described as “tearing” in quality. Acute aortic syndromes involving Ascending aorta tend to cause pain in the midline of the anterior chestDescending aortic syndromes most often present with pain in the backTherefore, dissections that begin in the ascending aorta and extend to the descending aorta tend to cause pain in the front of the chest that extends toward the back, between the shoulder blades.

25. Proximal aortic dissections that involve the ascending aorta (type A in the Stanford nomenclature) are at high risk for major complications that may influence the clinical presentationCompromise of the aortic ostia of the coronary arteries, resulting in MI; Disruption of the aortic valve, causing acute aortic insufficiencyRupture of the hematoma into the pericardial space, leading to pericardial tamponade.

26. Non-traumatic aortic dissections are associated with Hypertension or Conditions associated with deterioration of the elastic or muscular components of the aortic media, including Pregnancy, Bicuspid aortic disease or Inherited connective tissue diseases, such as Marfan and Ehlers-Danlos syndromes.

27. Although aortic aneurysms are most often asymptomatic, thoracic aortic aneurysms can cause chest pain and other symptoms by compressing adjacent structures. This pain tends to be steady, deep, and occasionally severe. Aortitis, whether of noninfectious or infectious etiology, in the absence of aortic dissection is a rare cause of chest or back discomfort.

28. Pulmonary and pulmonary-vascular conditions that cause chest discomfort usually do so in conjunction with dyspnea and often produce symptoms that have a pleuritic nature. PULMONARY CONDITIONS

29. Pulmonary emboli (annual incidence, ~1 per 1000) Sudden onset dyspnoea and chest discomfort Typically pleuritic in patternThe chest discomfort associated with pulmonary embolism may result from Involvement of the pleural surface of the lung adjacent to a resultant pulmonary infarction Distention of the pulmonary artery Possibly,right ventricular wall stress and/or subendocardial ischemia related to acute pulmonary hypertension. PULMONARY EMBOLISM

30. The pain associated with small pulmonary emboli is often lateral and pleuritic and is believed to be related to the first of these three possible mechanisms. In contrast, massive pulmonary emboli may cause severe substernal pain that may mimic an MI and that is plausibly attributed to the second and third of these potential mechanisms. Massive or submassive pulmonary embolism may also be associated with syncope, hypotension, and signs of right heart failure.…

31. Primary spontaneous pneumothorax Secondary spontaneous pneumothoraxTension pneumothoraxPNEUMOTHORAX

32. Rare cause of chest discomfortEstimated annual incidence in 7 per 100,000 among men <2 per 100,000 among women. Risk factors include Male sexSmoking Family history Marfan syndrome. The symptoms are usually sudden in onset, and dyspnea may be mild; thus, presentation to medical attention is sometimes delayed. Primary spontaneous pneumothorax

33. Secondary spontaneous pneumothorax may occur in patients with Underlying lung disorders, such as chronic obstructive pulmonary disease, asthma, or cystic fibrosisUsually produces symptoms that are more severe. Secondary spontaneous pneumothorax

34. Tension pneumothorax is a medical emergency caused by trapped intrathoracic air that precipitates hemodynamic collapse.Tension pneumothorax

35. Most pulmonary diseases that produce chest pain, including pneumonia and malignancy, do so because of involvement of the pleura or surrounding structures. Pleurisy is typically described as a knifelike pain that is worsened by inspiration or coughing. In contrast, chronic pulmonary hypertension can manifest as chest pain that may be very similar to angina in its characteristics, suggesting right ventricular myocardial ischemia in some cases. Reactive airways diseases similarly can cause chest tightness associated with breathlessness rather than pleurisyPARENCHYMAL,PLEURAL OR VASCULAR

36. GI CONDITIONS Gastrointestinal disorders are the most common cause of nontraumatic chest discomfort Often produce symptoms that are difficult to discern from more serious causes of chest pain, including myocardial ischemia. Esophageal disorders, in particular, may simulate angina in the character and location of the pain. Gastroesophageal reflux and disorders of esophageal motility are common and should be considered in the differential diagnosis of chest pain NON CARDIO PULMONARY CAUSES

37. Acid reflux often causes a burning discomfort. The pain of esophageal spasm, in contrast, is commonly an intense, squeezing discomfort that is retrosternal in location and, like angina, may be relieved by nitroglycerin or dihydropyridine calcium channel antagonists. Chest pain can also result from injury to the esophagus, such as a Mallory-Weiss tear or even an esophageal rupture (Boerhaave syndrome) caused by severe vomiting. Peptic ulcer disease is most commonly epigastric in location but can radiate into the chest

38. Hepatobiliary disorders, including cholecystitis and biliary colic, may mimic acute cardiopulmonary diseases.Although the pain arising from these disorders usually localizes to the right upper quadrant of the abdomen, it is variable and may be felt in the epigastrium and radiate to the back and lower chest. This discomfort is sometimes referred to the scapula or may in rare cases be felt in the shoulder, suggesting diaphragmatic irritation. The pain is steady, usually lasts several hours, and subsides spontaneously, without symptoms between attacks. Pain resulting from pancreatitis is typically aching epigastric pain that radiates to the back.

39. Chest discomfort can be produced by any musculoskeletal disorder involving the chest wall or the nerves of the chest wall, neck, or upper limbs.Costochondritis causing tenderness of the costochondral junctions (Tietze’s syndrome) is relatively common. Cervical radiculitis may manifest as a prolonged or constant aching discomfort in the upper chest and limbs. The pain may be exacerbated by motion of the neck.MUSCULOSKELETAL AND OTHER CAUSES

40. Occasionally, chest pain can be caused by compression of the brachial plexus by the cervical ribs, and tendinitis or bursitis involving the left shoulder may mimic the radiation of angina. Pain in a dermatomal distribution can also be caused by cramping of intercostal muscles or by herpes zoster

41. As many as 10% of patients who present to EDs with acute chest discomfort have a panic disorder or related condition The symptoms may include chest tightness or aching that is associated with a sense of anxiety and difficulty in breathing. The symptoms may be prolonged or fleeting. EMOTIONAL AND PSYCHIATRIC CONDITIONS

42. APPROACH TO THE PATIENT

43. In patients who present with acute nontraumatic chest discomfort, the priorities of the initial clinical encounter include assessment of (1) the patient’s clinical stability (2) the probability that the patient has an underlying cause of the discomfort that may be life-threatening.

44. The high-risk conditions including ACS, acute aortic syndrome, pulmonary embolism, tension pneumothorax, pericarditis with tamponade and esophageal rupturePatients with these conditions may deteriorate rapidly despite initially appearing well. The remaining population with non-cardiopulmonary conditions has a more favorable prognosis during completion of the diagnostic work-up.

45. ASSESMENT OF A PATIENT WITH CHEST DISCOMFORT

46. QUALITY OF PAINPressure or tightness- MIPleuritic – d/s pleura, pericarditis, PE, pul.parenchymal processesTearing or ripping – acute aortic dissectionBurning – acid refluxSqueezing- esophageal spasmHISTORY

47. LOCATION OF DISCOMFORTSubsternal location + radiation to neck,jaw,shoulder,arms – MIRetrosternal –esophageal painSevere pain radiating to back, b/w shoulder blades- a/c aortic syndromeRadiation to trapezius ridge – pericardial painHighly localised pain-tip of finger-unusual for angina

48. PATTERNMI- builds over mins, exacerbrated by activity, mitigated by restAD,PE,spontaneous pneumotorax- pain reaches peak intensity immediately

49. PROVOKING AND ALLEVIATING FACTORSMI- prefer to rest, sit / stop walking‘warm up angina’Pericarditis –worse in supine, relieved sitting upright and leaning forwardGERD- incr. by alcohol,reclined postion, dec in sitting.

50. PUD- exacerbration by eating, 60-90 min after mealsSevere coronary atherosclerosis-can trigger postprandial angina Relief with Nitroglycerin- MI, esophageal spasm

51. ASSOCIATED SYMPTOMSMI- diaphoresis, dyspnea, nausea, fatigue, faintness,eructationPE- resp distress, hemoptysis, syncopeSyncope or presyncope –PE,AD,ischemic arrythmiasGi – nausea,vomiting

52. Risk factors- atherosclerosis, venous thromboembolismPredisposing conditions- history of connective tissue diseases such as Marfans syndromeDepression/prior panic attacksPAST MEDICAL HISTORY

53. GENERAL Appearance – severity of illness Acute MI – anxious ,uncomfortable,pale, cyanotic or diaphoretic Levine’s sign Body habitus – young ,tall man with spontaneous pneumothorax PHYSICAL EXAMINATION

54. VITALS Significant tachycardia and hypotension Acute MI with cardiogenic shock, massive pulmonary embolism, pericarditis with tamponade, or tension pneumothorax. Severe hypertension Acute aortic emergencies Can also present with profound hypotension when there is coronary arterial compromise or dissection into the pericardium

55. Sinus tachycardia Submassive pulmonary embolismTachypnoea and hypoxemia Pulmonary causePresence of low grade fever is non specific

56. SYSTEMIC EXAMINATION Respiratory system Localize a primary pulmonary cause LV dysfunction-pulmonary edema

57. JVP Normal Pericardial tamponade or acute right ventricular dysfunctionCardiac auscultation S3 or S4 reflecting myocardial systolic or diastolic dysfunction. Cardiovascular system

58. Murmurs MR or VSD may indicate mechanical complications of STEMI. A murmur of aortic insufficiency may be a complication of proximal aortic dissection.Other murmurs may reveal underlying cardiac disorders contributory to ischemia (e.g., aortic stenosis or hypertrophic cardiomyopathy). Pericardial friction rubs reflect pericardial inflammation

59. Abdominal examination Localising tenderness - gastrointestinal cause of presenting complaintVascular pulse deficits- underlying c/c atherosclerosisEvidence of acute limb ischemia with loss of pulse and pallor in upper extremities – aortic dissection

60. Musculoskeletal Costochondritis- localized swelling/tenderness/redness Sensory deficits- cervical disc disease

61. Within 10min of presentationST elevation – diagnostic of MI Candidates for immediate interventions to restore flow in the occluded coronary artery. ST Segment depression, symmetric t wave inversions(>.2mV depth) –MI in the absence of STEMI. Indicative of higher risk of death or recurrent ischemia. Serial performance(30-60 min)-ED evaluation of suspected ACS. ELECTROCARDIOGRAPHY

62. Abnormalities in ST segment and T wave PE, ventricular hypertrophy, a/c & c/c pericarditis, myocarditis, electrolyte imbalance and metabolic disordersPanic disorder- hyperventilationPE- sinus tachycardia,rightward shift of ECG axis, S1Q3T3 patternPericarditis- the presence of diffuse lead involvement not corresponding to a specific coronary anatomic distribution and PR-segment depression

63. Helpful in identifying pulmonary processesPneumonia/ pneumothoraxPulmonary edemaWidening of mediastinum-aortic dissectionHamptons hump, westermarks sign- pulmonary embolismPericardial calcification in c/c pericarditisCHEST XRAY

64. Focused on the detection of myocardial injuryPresence of circulating proteins released from damaged myocardial cellsCardiac troponin is preferred over CK-MB for diagnosis of MI-superior cardiac tissue specificityShould be measured in all patients with suspected ACS at presentation and repeated in 3-6 hrsCARDIAC BIOMARKERS

65. Testing after 6 h is required only when there is uncertainty regarding the onset of pain or when stuttering symptoms have occurred. The development of cardiac troponin assays with progressively greater analytical sensitivity has facilitated detection of substantially lower blood concentrations of troponin than was previously possible. This evolution permits earlier detection of myocardial injury, enhances the overall accuracy of a diagnosis of MI, and improves risk stratification in suspected ACS. The greater negative predictive value of a negative troponin result with current-generation assays is an advantage in the evaluation of chest pain in the ED.

66. In addition, observation of a change in cardiac troponin concentration between serial samples is useful in discriminating acute causes of myocardial injury from chronic elevation due to underlying structural heart disease, end-stage renal disease, or interfering antibodies. The diagnosis of MI is reserved for acute myocardial injury that is marked by a rising and/or falling pattern—with at least one value exceeding the 99th percentile reference limit—and that is caused by ischemia.

67. D-dimer –exclusion of pulmonary embolismB-type natriuretic peptide –diagnosis of heart failure Also provide prognostic information among patients with ACS and those with pulmonary embolism.

68. Exercise electrocardiography Completion of risk stratifications of patients at low or moderate risk for ACS PROVOCATIVE TESTING FOR ISCHEMIA

69. Professional society guidelines identify ongoing chest pain as a contraindication to stress testing.

70. Detection of abnormal region wall motion –ischemic dysfunctionDiagnostic in patients with mechanical complications of MIPericardial tamponadeTTE-aortic dissection,intimal flap may be present in ascending aortaECHOCARDIOGARPHY

71. CT coronary angiography –detection of obstructive coronary diseaseCECT-detect focal areas of myocardial injuryExclude AD,pericardial effusion and pulmonary embolismCT ANGIOGRAPHY

72. Gadolinium enhanced CMR can provide early detection of MI, defining areas of myocardial necrosis accurately, and can delineate patterns of myocardial disease that are often useful in discriminating ischemic from non-ischemic myocardial injuryMRI

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