Cardiac Function Test
Cardiac Function Test
Case 1
He is mildly diaphoretic ("sweaty") but not in obvious distress. His vital signs are stable
except for a mild tachycardia (fast heart beat) of 123 beats per minute. There is no tenderness
to palpation of his arm and neck muscles and there is full range of motion at all of the joints.
His lungs are clear, his abdomen soft without tenderness and while there was tachycardia on
cardiac examination, no murmurs were heard.
2.What are the differential diagnosis in a patient presenting with chest pain?
Acute gastritis
Pulmonary embolism
Musculoskeletal chest pain
Aortic dissection
Anxiety
.
3. What is the pathophysiology related to laboratory diagnosis?
The disruption of sarcolemmal membranes of necrotic myocytes allows leakage of
intracellular macromolecules into the interstitial tissue and finally into
microvasculature and lymphatics which forms the basis of elevated cardiac enzymes.
4. What are acute coronary syndromes?
Unstable angina, acute myocardial infarction and sudden cardiac death are called as acute
coronary syndromes caused suddenly by acute plaque changes.
Case 2.
A 70-year-old man is working in his garden when he suddenly experiences crushing central
chest pain, starts sweating profusely and feels short of breath. An ambulance is called, but he
collapses in the interim and becomes unresponsive. Cardiopulmonary resuscitation is
commenced by the paramedics and continued until they reach hospital where no output can
be restored and the patient is declared dead.
The cause of ischaemic heart disease is reduced perfusion of coronary arteries relative
to myocardial requirement, and in over 90% of cases it is the result of atherosclerosis of
the coronary arteries with progressive narrowing of the affected coronary artery. Such
atherosclerotic plaques, which commonly show calcification, may rupture (‘acute
plaque change’) and result in overlying thrombosis, which may completely interrupt
perfusion, or progressive stenosis of the coronary artery may lead to critical narrowing
(defined as a pinpoint residual lumen, or narrowing of more than 75%)
3.If the patient had been successfully resuscitated, what complications might have occurred?
Complications include heart failure (which may be early or late), arrhythmias, rupture
of the heart muscle with collection of blood in the pericardial sac (cardiac tamponade),
pericarditis, extension of the infarct, mural thrombosis and embolism (e.g. a stroke) or
valvular dysfunction due to papillary muscle rupture.
4.Define sudden cardiac death. Mention four causes
Unexpected death from cardiac causes either without symptoms or within 1-24 hours of
symptom onset.
5.Name the types of infarct in myocardial infarction and mention the ECG changes.
ECG changes
Transmural -STEMI
6.what are the causes of silent MI and in what percentage of cases MI is silent
Case 3
49-year-old married white male school teacher was a 2 pack/day smoker with a history of
diabetes mellitus, hyperlipidemia and obesity, and a family history of coronary artery disease.
He was awakened from his sleep at 03:00 with crushing substernal chest pain which radiated
to his left arm and was accompanied by shortness of breath. When paramedics arrived, they
found the patient cool, clammy, bradycardic and hypotensive. Intravenous fluids and atropine
were given and he was transported to a suburban hospital.
On arrival in the emergency department at the hospital, the patient was in considerable
distress. He was still bradycardic. He had no jugular venous distention. He had decreased
breath sounds with occasional expiratory wheezes. At 04:01 his white blood cell count was
7,900/cu mm, hematocrit 45.8%, platelets 246,000/cu mm, creatine phosphokinase (CPK) 89
IU/L and troponin-I <0.4 ng/ml. Electrocardiogram showed ST-segment elevation in leads II,
III, AVF and V4-V6. Chest x-ray showed borderline cardiomegaly without signs of
pulmonary edema.
The patient was treated with morphine, atropine and aspirin, but he remained bradycardic and
hypotensive. He had decreasing pulse oximeter blood oxygen saturation despite supplemental
oxygen and he became cyanotic. He was intubated.
1. What are the risk factors associated with this condition?
4. Which type of infarct is complicated by free wall rupture and mural thrombi ?
Anterior wall MI
7. ECG shows ST segment elevation but troponin is not elevated in this condition why?
Troponin measurements are done within one hour in this case. Normally
troponins begin to rise after four hours.