Riyadh Ali

4/9/12
MDSC3311

Problem 1
Precordial Pain (part of body over heart and lower chest) and Breathlessness
VR is a 56-year-old East Indian male who works as an Assistant Manager at a tobacco
company. He presented to his primary care physician with a history of 2 episodes of chest
pain while climbing stairs last week. Each lasted for about 10 minutes and resolved with
rest. After initial inquiry and examination, his doctor ruled out non-cardiac causes of
chest pain and performed an ECG, which was normal. The doctor diagnosed him as
having Class II Angina Pectoris. The doctor identified the risk factors and advised the
patient to control risk factors and to undergo Stress test and prescribed Anti-anginal
agents and ACE inhibitor. VR was promoted to the rank of Manager and was transferred
to Guyana and could not be followed up.
Four years later, while on vacation in Trinidad, he was rushed to the emergency service
at Port of Spain General Hospital for sudden onset of substernal chest pain associated
with dyspnoea and diaphoresis, which began at around 4:00 am. The pain radiated to his
left arm and neck.
He smoked 20 cigarettes (one pack) per day for more than 15 years and has been
consuming alcohol in moderate amounts. His father had died suddenly at the age of 56,
of heart-related illness. There is no family history of diabetes mellitus.
Physical examination and investigations
Patient was anxious and in mild respiratory distress. His height was 5ft 7in and weight
186 lbs. His mucus membranes were pink and sclera, anicteric. There was no jugular
venous distension. Pulse=90/min. Heart sounds revealed soft S4 and lungs had basal
rales. BP =140/90 mm Hg. Other organ systems examination was unremarkable.

ECG showed evidence of an antero-septal acute STEMI. Lab investigations included a

complete blood count, electrolytes, BUN, BNP and cardiac enzymes. His lipid profile
revealed Total Cholesterol = 220 mg/dL, LDL= 130, HDL= 32. Coagulation panel and
creatinine were normal. Chest X-ray (portable) showed cardiomegaly.
The attending doctors quickly initiated treatment and his symptoms improved but
developed right bundle branch block (RBBB) and congestive cardiac failure. Antiarrhythmic
agents and drugs for cardiac failure were added to the treatment protocol.
He was discharged two weeks later advising him about management of his condition.

Definitions:
Angina Pectoris - Episodic constricting chest pain, often radiating to the left shoulder and down
the left arm, caused by an insufficient supply of blood to the heart. Coronary artery disease is a
common cause of angina pectoris. Class II refers to angina with moderate exertion.
ACE Inhibitor (Angiotensin Converting Enzyme Inhibitor) - Any of a class of drugs that cause
vasodilation and are used to treat hypertension and heart failure.
STEMI (ST elevation myocardial infarction) - Acute coronary syndrome (ACS) - Named
according to the appearance of the electrocardiogram (ECG/EKG) as ST segment elevation
myocardial infarction (STEMI)
S4 heart sounds a rare extra heart sound occurring immediately before the normal lub dub
Basal Rales crackling, rattling or clicking noises made in or near the base of the lungs, caused
by popping open of small airways collapsed by fluid
Cardiomegaly Enlarged heart
Right Bundle Branch Block - The right ventricle is not directly activated by impulses travelling
through the right bundle branch.
BNP

Issues:
1. Is there a relationship between the age, sex, race and occupation of the patient and his
complications?
2. What was the cause of his angina pectoris and what classes exist?
3. What are the risk factors for AP and how are they controlled?
4. Why was the ECG normal if the cause of the pain was cardiac?

5. How were non cardiac causes for the pain ruled out?
6. Why did the pain last for 10 mins and resolved with rest?
7. What does the stress test comprise and how do its findings help the diagnosis?
8. What is the significance of the patients social and family history?
9. Why was both an ACE inhibitor and anti anginal agent prescribed?
10. What was the significance of the time (4am) of the attack?
11. Is there a link between D. Mellitus and Heart disease?
12. What is the significance of the pain radiating to his left arm and neck?
13. What was the pateints BMI and was it abnormal?
14. Why was jugular venous distention considered important to look for?
15. What caused his increased pulse and BP and cholesterol?
16. What is the significance and causes of his cardiomegaly?
17. What prompted the acute chest pain during his visit?
18. What caused the development of the RBBB and CHF even as his symptoms improved?
19. Why were coagulation panel and creatinine levels investigated?
20. What were the treatment and management administered?

Problem Summary:
Aetiopathologenesis, diagnosis, treatment, complications of Ischaemic Heart Disease and Acute
Coronary Syndrome.

Hypotheses:
1. His history of smoking and moderate drinking lead to narrowing of coronary vessels and
angina.
2. He experienced Class II stable angina because his chest pain was resolved on rest, and
was initiated by moderate exercise.
3. Because the ECG was normal, a stress test was indicated.
4. Vessel narrowing lead to the inc. BP and inc. pulse.
5. S4 sounds indicate a hypertrophic ventricle.
6. A coagulation panel was done to make sure he didnt have a clot (thrombo embolism).
7. BNP and cardiac enzymes were used to determine the severity of damage to the
myocardium.
8. Treatment of acute STEMI lead to RBBB and CHF due to abnormal conduction of RBB
fibres.

Objectives:
1. Aetiopathogenesis of Angina Pectoris and its treatment.
2. What are the non-cardiac causes of chest pain?
3. Pharmacology of ACE inhibitors and anti anginal drugs (Drug, Mode of action,
Contraindications, Class and side effects).
4. Discuss the cardiac stress test.
5. Discuss the Aetiopathogenesis of Myocardial Infarction and the morphology of the heart
in Myocardial Infarction.
6. What are the clinical features of MI and the investigations conducted?
7. What are the treatments administered and management carried out following the MI and
the complications of MI?
8. Discuss the epidemiology of Ischaemic Heart Disease and the levels of prevention.
9. Discuss the lifestyle changes that should take place for the patient.

1) Angina Pectoris
This refers to intermittent chest pain brought on by transient ischemia of the myocardium.
The Canadian Cardiovascular Society classifies angina based on what level of physical
exertion brings it on:
Class 0: Asymptomatic
Class 1: Angina with strenuous Exercise
Class 2: Angina with moderate exertion
Class 3: Angina with mild exertion
(Walking 1-2 level blocks at normal pace
Climbing 1 flight of stairs at normal pace)
Class 4: Angina at any level of physical exertion

Further to this, there are three variants of Angina Pectoris:

1) Stable/Typical Angina Episodic Chest pain associated with physical exertion/some
form of increased myocardial oxygen demand. This includes tachycardia or hypertension
as brought on by fever, anxiety or fear. The pain is that of a crushing/squeezing
substernal sensation, which can radiate down the left arm or to the left jaw. In stable
angina, there is typically fixed atherosclerotic narrowing of one or more of the coronary
arteries. Hence, the myocardial oxygen supply may be sufficient under basal conditions
but may not be enough for increased exertion. Stable angina is typically relieved by rest
(reduce oxygen demand) or by using nitroglycerin (causes peripheral vasodilation thereby
causing the peripheral vessels to hold blood, lowering venous return to the heart and
therefore reducing cardiac work; Nitroglycerin can also directly dilate the coronary
vessels in high doses).
2) Unstable/Crescendo Angina There is an increasing frequency of pain, brought on by
progressively less exertion. The episodes of this tend to last longer and be more intense
than in stable angina. This is associated with disruption of plaques and superimposed
partial thrombosis (incomplete clot), embolization of the thrombus and/or vasospasm.
Unstable angina is known as pre-infarction angina since it is a sign of potentially
irreversible ischemia.
3) Variant/Prinzmetal Angina Angina due to coronary artery spasm. Typically respond
well to vasodilators (eg Nitroglycerin) and calcium channel blockers (reduce blood
pressure, eg. Amlodipine (Norvasc))
The prevalence of angina pectoris increases with age.
2) Non-Cardiac Causes of Chest Pain
Gastroesophageal (42% of all chest pain cases)
Reflux Esophagitis (heartburn/pyrosis) Aggravated by lying down, worse after
meals
Esophageal Spasm Also relieved by nitrates, as with ischemic cardiac pain, but not
brought on via exertion. Can be brought on by swallowing extremely hot/cold
substances, leading to chest pain
Esophageal Perforation By instruments passed down esophagus/forceful
vomiting/esophagitis/neoplasm cause sudden pain from neck to epigastrium that
worsens on swallowing
Gastritis Stomach lining becomes inflamed/swollen
Peptic Ulcer Disease Difficulty/pain on swallowing

Pulmonary
Pneumothorax sharp chest pain that may radiate to ipsilateral shoulder
Pulmonary Embolism dyspnea, chest pain on breathing/coughing
Pleuritis
Neoplasm
Bronchitis

Musculoskeletal
Costochondritis Tietzes Syndrome Inflammation of the costochondral junction
Rib Fracture
Myalgia (muscle pain)
Compression Radiculopathy

Dermatologic
Herpes Zoster can present as chest pain; usually described as a burning sensation

3) Pharmacology
ACE (Angiotensin Converting Enzyme) inhibitors -