chest pain by dr.hassen alzubaidy

1. Chest pain presentation
Of
Two differential diagnosis
Myocardial infarction & acute pericardaitis
People & Disease Course
Dissertation

3.  Chest pain is discomfort or pain that feel anywhere along the front of the body
between the neck and upper abdomen.: in my study there are two patient
 First patient a 62-year-old man arrives to the emergency department
complaining of acute, severe precordial chest pain radiating to his arm and
neck. An ECG was done ,and the patient was diagnosed with myocardial
infarction .
 Second patient A 23- year-old woman is evaluate in the emergency department
for a 4- day history of substernal, sharp, intermittent chest pain that is
aggravated by deep breaths.. Ecg and chest x-ray was done and the patient was
diagnosed with acute pericardaitis

4. Non-central
 Pleural
 -Infection: pneumonia, bronchiectasis, tuberculosis
 -Malignancy: lung cancer, mesothelioma, metastatic
 -Pneumothorax
 -Pulmonary infarction
 -Connective tissue disease: rheumatoid arthritis, systemic lupus-erythematosus (SLE)
 Chest wall
 -Malignancy: lung cancer, mesothelioma, bony metastases
 -Persistent cough/breathlessness
 -Rib fracture
 -Intercostal nerve compression
 -Thoracic shingles (herpes zoster)

5.  Tracheal
 -Infection
 Cardiac
 -Massive pulmonary thromboembolism
 -Acute myocardial infarction/ischaemia
 Oesophageal
 -Oesophagitis
 Great vessels
 -Aortic dissection

6.  simple heart anatomy:
 The heart acts as two serial pumps that share several electrical and mechanical
components. The right heart circulates blood to the lungs where it is
oxygenated, and the left heart receives this and circulates it to the rest of the
body
 The heart receive its blood supply by special circulation called The coronary
circulation

8.  Simple heart physiology : the heart have an electrical wave
 The Sinoatorial (SA) node is situated at the junction of the superior vena cava
and RA. It comprises specialized aerial cells that depolarize at a rate influenced
by the autonomic nervous system and by circulating catecholamine this
depolarization wave propagates through both atria via sheets of atrial myocytes.
 The wave propagate from the right atrium to ventricles through the
atrioventricular node.
 The His–Purkinje system is comprised of the bundle of His extending from the
AV node into the interventricular septum, the right and left bundle branches
passing along the ventricular septum and into the respective ventricles

10.  History
 Examination
 Investigation

11.  First patient:
a 62-year-old man arrives to the emergency department complaining of acute,
severe precordial chest pain radiating to his arm and neck. He reports feeling like “
stone is standing on my chest” and states that his symptoms are accompnied by
nause . His chest pain began approximately 30 minutes ago. His medical history
includes hypertension, hyperlipidemia , and 50-pack/ year history of cigarette
smoking.

12.  vital signs: blood pressure 156/ 97 mmHg, pulse 113 bpm, respiratory rate 24
breaths/min
 He is tachycardic with normal S1 and S2 and without murmurs, rubs
 His jugular venous pressure is not elevated
 His abdomen is without masses. His lower extremities are without edema
 . He has 2+ pulses in his upper and lower extremities.

13.  An ST segment elevation myocardial infarction (STEMI) is most commonly the result of
atherosclerotic plaque rupture with subsequent acute thrombus formation and
completion occlusion of the arterial lumen. Rupture of the fibrous cap reveals the
highly thrombogenic extracellular lipid core, initiating platelet activation and
aggregation as well as thrombin activation .Less frequently, an erosion of a coronary
plaque can occur without plaque rupture but still resulting in thrombus generation.
Other rare causes of STEMI include coronary artery spasm, coronary artery dissection,
arteritis, cocaine abuse, and embolism to a coronary artery. All of these pathologic
mechanisms have a common final pathway to inducing myocardial ischemia and
ultimately infarction if artery patency is not established within approximately 30
minutes of occlusion. In other words, the lack of blood flow results in myocyte ATP
depletion and subsequent coagulation necrosis of the myocardium.

15. There many risk factor for myocardial infarction,include:
Nonmodifiable risk factors for atherosclerosis include the
following:
 Age
 Sex
 Family history of premature coronary heart disease
 Male-pattern baldness

16.  Smoking or other tobacco use
 Diabetes mellitus
 Hypertension
 Hypercholesterolemia and hypertriglyceridemia, including inherited lipoprotein
disorders
 Dyslipidemia
 Obesity
 Sedentary lifestyle and/or lack of exercise
 Psychosocial stress

17.  1-ECG
 Show st elevation in V1-V4. Anterior ST segment elevation myocardial infarction

18.  creatine kinase (CK): are released during STEMI and are measureable within 4–
6 hours, peak within the first 24 hours, and normalize by 48–72 hours
 Troponin : They are released within 4–8 hours after symptom onset and
generally peak by 12–36 hours. Troponins can remain elevated for up to a week
after an acute event

19. Prevent progression of thrombosis
 Anti Thrombotic therapy
 Anti platelet agents: Aspirin
 Anticoagulants: Heparin
 ADP inhibitor :clopidogrel
Restore perfusion of partially occluded vessels
 High risk
 Early Percutaneous Coronary Intervention (Angioplasty) (PCI)
 Coronary Artery Bypass Graft (CABG)
 Low Risk
 Initially medical treatment
 General
 Pain control
 O2
 Organic Nitrates
 -blockers
 Statins
 ACE-Inhibitors

20. It's never too late to take steps to prevent a heart attack — even if you've
already had one. Here are ways to prevent a heart attack.
 Medications. Taking medications can reduce risk of a subsequent heart
attack and help damaged heart function better. Continue to take what
your doctor prescribes, and ask your doctor how often you need to be
monitored.
 Lifestyle factors. You know the drill: Maintain a healthy weight with a
heart-healthy diet, don't smoke, exercise regularly, manage stress and
control conditions that can lead to heart attack, such as high blood
pressure, high cholesterol and diabetes.
 .

21.  Epidemiology :
 Cardiovascular disease is the leading cause of death in the United
States; approximately 500,000-700,000 deaths related to the
coronary artery occur each year. Approximately 1.5 million cases of
myocardial infarction occur annually in the United States; the yearly
incidence rate is approximately 600 cases per 100,000 people.
 The incidence of cardiovascular disease increases with age, with
acute myocardial infarction being rare in childhood and
adolescence. Most patients who develop an acute myocardial
infarction are older than 60 years.

22. A 23- year-old woman is evaluate in the emergency department for a 4- day
history of substernal, sharp, intermittent chest pain that is aggravated by
deep breaths. The pain is worse when she lies down and improves when she
sits up and leans forward . She has had a 1-week history of nonproductive
cough, sore throat. Her medical history is unremarkable and she takes no
medications.

23.  temperature is 37.8°C (100.0°F), blood pressure is
118/54 mmHg, pulse is 90/min, and respiratary rate is 22 breaths/min.
oropharynx is erythematous. Cardiac examination discloses a three-
component scratchy rub that is loudest over the left sternal border, but no
murmurs. Pulmonary auscultation reveals normal breath sounds and no
crackles. There is no jugular venous distention an no chest wall tenderness

24.  Inflammation of the pericardial sac. the most common causes are :
 acute pericardaitis:

25.  1-ECG: A 12-lead electrocardiogram shows sinus tachycardia with diffuse,
concave upward, ST segment elevation (best seen in leads II, and V2–V6)
and PR segment depression (in most leads except aVR where PR segment
elevation is noted).

26.  2. Chest radiography (CXr ): Typically normal in acute pericarditis, and
usually reveals cardiomegaly with clear lung fields if a pericardial effusion,
with or without tamponade

27.  For most patients with idiopathic pericarditis, treatment consists of
combination therapy with NSAIDs (to decrease the inflammation) and
colchicine (which has been shown to decrease recurrences
 In acute pericarditis following myocardial infarction, aspirin is the
recommended NSAID to use
 Corticoid therapy should be reserved for autoimmune pericarditis

28.  You usually can't prevent acute pericarditis. You can take steps to reduce
your chance of having another acute episode, having complications, or
getting chronic pericarditis.
 These steps include getting prompt treatment, following your treatment
plan, and having ongoing medical care (as your doctor advises).

29.  Epidemiologic data on the incidence of acute pericarditis are lacking,
likely because this condition is frequently inapparent clinically, despite its
presence in numerous disorders. Lorell noted a diagnosis of acute
pericarditis in approximately 1 per 1000 hospital admissions.In addition,
acute pericarditis comprises 1% of emergency room visits in patients with
ST-segment elevation.In fact, the reported incidence of acute pericardial
tamponade is approximately 2% of penetrating trauma; however, this
condition is rarely seen in blunt