Eggena 5-1 Flashcards

1
Q

A chest x ray shows

A

dilated lymphatics from the excess fluid in the pulmonary interstitium

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2
Q

the ECG shows

A

Q waves and ST segment elevations.

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3
Q

A blood sample revaled

A

marked elevation of myocardial band isozyme of creatinine phosphokinase (MB-CPK) and troponin.

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4
Q

the woman sustained a massive transmural

A

myocardial infarction involving the inferior portions of the left ventricle, as indicated by the deep Q waves and ST segment elevations and the elevated MB-CPK.

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5
Q

isozyme most specific for myocardial infarction

A

MB-CPK

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6
Q

when muscle in the left ventricle has been injured, the ability of the left ventricle to develop pressure and eject blood into circulation during systole is

A

diminished (decreased cardiac output)

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7
Q

the diminished cardiac output had been sensed by the

A

baroreceptors in the carotid sinuses. it reflexively increased heart rate by increasing sympathetic tone. s

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8
Q

signs of sympathetic compensation

A

tachycardia

diaphoresis

pallor

peripheral cyanosis

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9
Q

Despite normal blood pressure, she remained in

A

circulatory shock.

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10
Q

pulse of patient in shock

A

wak and thready due to pulse pressure being reduced.

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11
Q

the pulse pressure depends on the amount of

A

blood ejected by the left ventricle during systole and upon the vigor with which the stroke volume is ejected.

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12
Q

soft first heart sound caused by

A

the inability to rapidly raise intraventricular pressure during early systole, which resulted in a slow closure of the mitral valve.

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13
Q

Cause of the third heart sound

A

A left ventricle cannot eject all the blood with which it fills during diastole and becomes distended. Early during diastole when blood flows rapidly into such a dilated left ventricular chamber, an abnormalheart sound is produced.

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14
Q

cause of the fourth heart sound

A

results when the left atrium ejects blood into a left ventricular chamber with walls that have been siffened by a recent myocardial infarction.

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15
Q

the left ventricular pressure during diastole is similar to

A

pulmonary artery wedge pressure

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16
Q

when the PAWP exceeds the plasma oncotic pressure

A

fluid accumulates in the pulmonary interstitium and becomes congested.

17
Q

the presence of edema fluid in her alveoli was detected as

A

moist rales

18
Q

congested lungs are stiffer than normal

A

and thus more work is needed to expand them on inspiration.

19
Q

the difficulty in breathing is made a little easier by taking shallow breaths, but

A

doing so more rapidly

20
Q

the ability of the left ventricle to eject a given stroke volume depends on four factors:

A

preload (proportional to PAWP)

afterload (proportional to mean aortic pressure)

ventricular muscle mass

ventricular contractility

21
Q

ventricular contractility

A

the ability of ventricular muscle fibers to generate tension, which is increased by beta-1-adrenergic receptor agonists or by stimulation of sympathetic nerves.

22
Q

three basic aims in the treatment of the patient

A

reduce preload (PAWP)

reduce afterload (peripheral vascular resistance)

increase left ventricular contractility

23
Q

to reduce preload

A

administer nitroglycerine (is a vasodilator that allows more blood to be stored in veins and less to the heart).

24
Q

to reduce afterload

A

phentolamine is prescribed. It lbocks the action of epinephrine and norepinephrine on alpha-1-adrenergic receptors.

25
Q

to increase cardiac output

A

administer dobutamine (makes the left ventricle pump more forcefully by stimulating beta-1-adrenergic receptors.