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05 Sep 2024, 12:03
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Nitro-glycerine has long been famous for its relief of angina pectoris attacks but ruled out
for heart attacks on the theory that it harmfully lowers blood pressure and increases heart
rate. A heart attack, unlike an angina attack, always involves some localized, fairly rapid
heart muscle death, or myocardial infarction. This acute emergency happens when the
arteriosclerotic occlusive process in one of the coronary arterial branches culminates so
suddenly and completely that the local myocardium—the muscle area that was fed by the
occluded coronary—stops contracting and dies over a period of hours, to be replaced over a
period of weeks by a scar, or 'healed infarct.' In 1974, in experiments with dogs, it was
discovered that administration of nitro-glycerine during the acute stage of myocardial
infarction instantly reduced the extent of myocardial injury, provided that the dogs' heart
rate and blood pressure were maintained in the normal range.
Soon after, scientists made a preliminary observation of the clinical applicability of nitroglycerin in acute heart attack in human patients. Five of twelve human subjects developed
some degree of congestive heart failure. Curiously, the nitro-glycerine alone was enough to
reduce the magnitude of injury in these five patients, but the seven patients whose heart
attacks were not complicated by any congestive heart failure were not consistently helped
by the nitro-glycerin until another drug, phenylephrine, was added to abolish the nitroglycerin-induced drop in blood pressure. One explanation for this is that the reflex
responses in heart rate, mediated through the autonomic nervous system, are so blunted in
congestive heart failure that a fall in blood pressure prompts less of the cardiac acceleration
which otherwise worsens the damage of acute myocardial infarction.
It appears that the size of the infarct that would otherwise result from a coronary occlusion
might greatly be reduced, since the myocardial infarct is not determined at the moment of
coronary occlusion as previously thought. The fate of the stricken myocardial segment
remains largely undetermined, hanging on the balance of myocardial oxygen supply and
demand, which can be favorably influenced for many hours after the coronary occlusion. So
it is possible to reduce the myocardial ischemic injury during acute human heart attacks by
means of nitro-glycerin, either alone or in combination with phenylephrine. Other drugs are
also being tested to reduce myocardial infarct size, particularly drugs presumed to affect
myocardial oxygen supply and demand, including not only vessel dilators such as nitroglycerin but also antihypertensives, which block the sympathetic nerve reflexes that
increase heart rate and work in response to exertion and stress. Such measures are still
experimental, and there is no proof of benefit with regard to the great complications of
heart attack such as cardiogenic shock, angina, or mortality. But the drugs for reducing
infarct size now hold center stage in experimental frameworks.
1. According to the passage, the primary difference between a heart attack and an angina
attack is that a heart attack
(a) involves an acceleration of the heartbeat.
(b) cannot be treated with nitro-glycerin.
(c) takes place within a relatively short period of time and always results in a damage to the
muscle tissue of the heart.
(d) All of the above.
(e) Both b and c.
2. In the study referred to in the passage, the patients who developed congestive heart
failure did not experience cardiac acceleration because:
(a) the nitro-glycerin was not administered soon enough after the onset of the heart attack.
(b) the severity of the heart attack blocked the autonomic response to the nitro-glycerin
induced drop in blood pressure.
(c) administering phenylephrine mitigated the severity of the drop in blood pressure caused
by nitro-glycerin.
(d) phenylephrine abolished the drop in blood pressure caused by nitro-glycerin.
(e) doctors were able to maintain blood pressure, and thus indirectly, the pulse rate, in
those patients.
3. The passage provides information to answer all of the following questions EXCEPT:
(a) What are some of the physiological manifestations of a heart attack?
(b) What determines the size of a myocardial infarct following a heart attack?
(c) What effect does nitro-glycerin have when administered to a patient experiencing a
heart attack?
(d) What are the most important after effects of heart attacks?
(e) None of these.
4. It can be inferred from the passage that nitro-glycerine is of value in treating heart
attacks because it:
(a) lowers the blood pressure.
(b) stimulates the healing of an infarct.
(c) causes cardiac acceleration.
(d) dilates blood vessels.
(e) increases the myocardial infarct.
5. The author's attitude towards the use of nitro-glycerin and other drugs to treat heart
attack can best be described as one of:
(a) Concern
(b) Resignation
(c) Anxiety
(d) Optimism
(e) Pessimism.
6. It can be inferred that phenylephrine is administered in conjunction with nitro-glycerin
during heart attacks in order:
(a) to prevent cardiac acceleration caused by a drop in blood pressure.
(b) to block sympathetic nerve reflexes that increase the pulse rate.
(c) to blunt the autonomic nervous system which accelerates the pulse rate.
(d) to reduce the size of a myocardial infarct by increasing oxygen supply.
(e) to increase the blood pressure.
for heart attacks on the theory that it harmfully lowers blood pressure and increases heart
rate. A heart attack, unlike an angina attack, always involves some localized, fairly rapid
heart muscle death, or myocardial infarction. This acute emergency happens when the
arteriosclerotic occlusive process in one of the coronary arterial branches culminates so
suddenly and completely that the local myocardium—the muscle area that was fed by the
occluded coronary—stops contracting and dies over a period of hours, to be replaced over a
period of weeks by a scar, or 'healed infarct.' In 1974, in experiments with dogs, it was
discovered that administration of nitro-glycerine during the acute stage of myocardial
infarction instantly reduced the extent of myocardial injury, provided that the dogs' heart
rate and blood pressure were maintained in the normal range.
Soon after, scientists made a preliminary observation of the clinical applicability of nitroglycerin in acute heart attack in human patients. Five of twelve human subjects developed
some degree of congestive heart failure. Curiously, the nitro-glycerine alone was enough to
reduce the magnitude of injury in these five patients, but the seven patients whose heart
attacks were not complicated by any congestive heart failure were not consistently helped
by the nitro-glycerin until another drug, phenylephrine, was added to abolish the nitroglycerin-induced drop in blood pressure. One explanation for this is that the reflex
responses in heart rate, mediated through the autonomic nervous system, are so blunted in
congestive heart failure that a fall in blood pressure prompts less of the cardiac acceleration
which otherwise worsens the damage of acute myocardial infarction.
It appears that the size of the infarct that would otherwise result from a coronary occlusion
might greatly be reduced, since the myocardial infarct is not determined at the moment of
coronary occlusion as previously thought. The fate of the stricken myocardial segment
remains largely undetermined, hanging on the balance of myocardial oxygen supply and
demand, which can be favorably influenced for many hours after the coronary occlusion. So
it is possible to reduce the myocardial ischemic injury during acute human heart attacks by
means of nitro-glycerin, either alone or in combination with phenylephrine. Other drugs are
also being tested to reduce myocardial infarct size, particularly drugs presumed to affect
myocardial oxygen supply and demand, including not only vessel dilators such as nitroglycerin but also antihypertensives, which block the sympathetic nerve reflexes that
increase heart rate and work in response to exertion and stress. Such measures are still
experimental, and there is no proof of benefit with regard to the great complications of
heart attack such as cardiogenic shock, angina, or mortality. But the drugs for reducing
infarct size now hold center stage in experimental frameworks.
1. According to the passage, the primary difference between a heart attack and an angina
attack is that a heart attack
(a) involves an acceleration of the heartbeat.
(b) cannot be treated with nitro-glycerin.
(c) takes place within a relatively short period of time and always results in a damage to the
muscle tissue of the heart.
(d) All of the above.
(e) Both b and c.
2. In the study referred to in the passage, the patients who developed congestive heart
failure did not experience cardiac acceleration because:
(a) the nitro-glycerin was not administered soon enough after the onset of the heart attack.
(b) the severity of the heart attack blocked the autonomic response to the nitro-glycerin
induced drop in blood pressure.
(c) administering phenylephrine mitigated the severity of the drop in blood pressure caused
by nitro-glycerin.
(d) phenylephrine abolished the drop in blood pressure caused by nitro-glycerin.
(e) doctors were able to maintain blood pressure, and thus indirectly, the pulse rate, in
those patients.
3. The passage provides information to answer all of the following questions EXCEPT:
(a) What are some of the physiological manifestations of a heart attack?
(b) What determines the size of a myocardial infarct following a heart attack?
(c) What effect does nitro-glycerin have when administered to a patient experiencing a
heart attack?
(d) What are the most important after effects of heart attacks?
(e) None of these.
4. It can be inferred from the passage that nitro-glycerine is of value in treating heart
attacks because it:
(a) lowers the blood pressure.
(b) stimulates the healing of an infarct.
(c) causes cardiac acceleration.
(d) dilates blood vessels.
(e) increases the myocardial infarct.
5. The author's attitude towards the use of nitro-glycerin and other drugs to treat heart
attack can best be described as one of:
(a) Concern
(b) Resignation
(c) Anxiety
(d) Optimism
(e) Pessimism.
6. It can be inferred that phenylephrine is administered in conjunction with nitro-glycerin
during heart attacks in order:
(a) to prevent cardiac acceleration caused by a drop in blood pressure.
(b) to block sympathetic nerve reflexes that increase the pulse rate.
(c) to blunt the autonomic nervous system which accelerates the pulse rate.
(d) to reduce the size of a myocardial infarct by increasing oxygen supply.
(e) to increase the blood pressure.
Archived Topic
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05 Sep 2024, 12:06
Kudos
Bookmarks
mobachat
Discussed here:
https://gmatclub.com/forum/nitroglyceri ... 64985.html
Hope this helps.
Archived Topic
Hi there,
This topic has been closed and archived due to inactivity or violation of community quality standards. No more replies are possible here.
Where to now? Join ongoing discussions on thousands of quality questions in our Reading Comprehension (RC) Forum
Still interested in this question? Check out the "Best Topics" block above for a better discussion on this exact question, as well as several more related questions.
Thank you for understanding, and happy exploring!
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