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CARDIOVASCULAR WORKSHOP
CASE 1.
A 68-year-old man was referred to hospital by his family doctor for investigation of
episodic chest pain. The patient described the pain as “crushing” and associated with
exertion. He had had this for 6 months and was eventually persuaded to seek medical
attention by his wife. On examination, he was in no distress and physical examination
was normal apart from a small pulsatile mass in the lower abdomen. Blood tests revealed
a hyperlipidemia but otherwise no abnormality. He was normotensive and ECG was
normal. ECG during exercise testing revealed reversible ST depression.
Questions:
1.
What is the clinical diagnosis?
(Answer)
2.
What is the cause of the chest pain?
(Answer)
3.
What is the most likely underlying cause?
(Answer)
4.
What is the significance of the hyperlipidemia?
(Answer)
5.
What is the abdominal mass due to?
(Answer)
6.
What are the possible complications of this lesion?
(Answer)
The patient was re-admitted 6 months later with a 12 hour history of severe, unremitting
chest pain radiating to the jaw and left arm. Over the past week, he had been having
increasingly frequent episodes of anginal pain, worse than usual and not always related to
exertion. On examination, he was distressed, pale, sweating, breathless and had a
tachycardia. ECG showed ST elevation with Q waves and emergency blood tests
revealed raised troponins and creatine kinase (CK-MB). There was a moderate
leukocytosis and ESR and C-reactive protein were elevated. The patient responded well
to therapy. On the second day, he complained of mild chest pain and an audible friction
rub was heard on auscultation of the heart. This resolved over the next 48 hours. Apart
from transient cardiac arrhythmias requiring no specific therapy, recovery appeared to be
progressing uneventfully. Unfortunately the patient died suddenly one week after
admission.
Questions:
7.
What condition did the patient have in the week preceding hospitalization?
(Answer)
8.
What condition has developed which necessitated hospital admission?
(Answer)
9.
What is the significance of the patient’s breathlessness?
(Answer)
10.
For how long do troponins and CK-MB remain elevated?
(Answer)
11.
Explain the leukocytosis and elevated ESR and CRP.
(Answer)
12.
What complication occurred on the second day?
(Answer)
13.
CASE 2.
What complication may have caused the patient’s demise on day 7?
(Answer)
A 75-year-old man with a long history of hypertension and congestive
cardiac failure was brought in dead to the A & E department. He was
known to have diabetes mellitus but no history of angina or myocardial
infarction. He was the subject of a Coroner’s autopsy. This showed severe
triple vessel coronary artery atherosclerosis. The heart was overweight and
dilated and showed a large area of scarring indicating an old, healed
myocardial infarct.
Normal heart
Patient’s heart
Questions:
1.
What name would you give to this heart condition?
(Answer)
2.
Why was there no history of chest pain in view of the post mortem
findings?
(Answer)
3.
What does the increased weight of the heart signify?
(Answer)
4.
What was the likely terminal event in this patient?
(Answer)
5.
What non-ischemic heart disease may resemble this condition?
(Answer)
6.
Hypertension typically causes concentric left ventricular hypertrophy.
Aortic stenosis would cause a similar appearance. Sudden death can occur
in patients with left ventricular hypertrophy from any cause.
What other myocardial diseases may result in sudden death?
(Answer)
1.
(Back)
Stable angina.
2.
(Back)
Myocardial ischaemia.
3. Coronary artery atherosclerosis. Stable angina can be caused by other cardiac
conditions such as aortic valve disease and in young patients hypertrophic
obstructive cardioangiopathy.
(Back)
4.
A known risk factor for atherosclerosis. Potentially controllable and important to
treat even in the presence of established coronary heart disease. Other risk factors include
hypertension, cigarette smoking and diabetes.
(Back)
5. An abdominal atherosclerotic aneurysm. Its presence is a confirmation of
established arterial disease in this patient.
(Back)
6. Rupture with massive haemorrhage. Risk increases with size, especially over 5cm
diameter. Thromboembolism from a mural thrombus to the lower limbs.
Obstruction to renal, lower mesenteric or vertebral arteries. Compression of
ureters; erosion of vertebrae.
(Back)
7.
(Back)
Unstable angina. This is due to plaque instability with mural thrombus and
vasospasm. It has a serious prognosis.
8.
(Back)
Myocardial infarction. This is usually due to thrombus superimposed on coronary
atheroma.
9.
(Back)
Pulmonary oedema due to left ventricular cardiac failure. This would suggest a
significant degree of myocardial damage.
10.
(Back)
Troponins up to 2 weeks.
CK-MB for 48-72 hours.
11. A polymorphonuclear leukocyte reaction occurs in the myocardium in response to
necrosis calling forth a leukocytosis which peaks on the first day. The ESR and
CPR are an indication of tissue necrosis.
Contraction band necrosis
Day 1-2
Day 1-2
Day 3-4
(Back)
12. Fibrinous pericarditis. This is a response to the underlying necrotic myocardium.
It indicates a transmural as opposed to a subendocardial infarct.
(Back)
13. Post mortem examination revealed a large haemopericardium due to rupture of
the wall of the left ventricle, resulting in cardiac tamponade. This occurs during
maximal softening of the myocardium usually between days 4 and 7. Rupture of
an aortic dissection into the pericardial cavity will have a similar effect.
(Back)
1.
(Back)
Chronic ischaemic heart disease or ischaemic cardiomyopathy.
2.
(Back)
Some cases of myocardial infarction are “silent”, especially in patients with
diabetes.
3.
(Back)
Left ventricular cardiac hypertrophy.
4.
(Back)
A cardiac arrhythmia. This is a common cause of death at the onset of infarction,
during convalescence and in the healed state.
5.
(Back)
Dilated cardiomyopathy. This occurs in a younger age group and gives rise to
congestive heart failure. An arrhythmia may cause sudden death.
6.
(Back)
Hypertrophic cardiomyopathy.
Myocarditis.