Cardiac Failure, Heart sounds, and Circulatory shock Flashcards

1
Q

What is cardiac Failure

A

Failure of the heart to pump enough blood to satisfy the needs of the body

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2
Q

What are the ways the sympathetic innervation compensates for acute cardiac failure

A

strengthens muscle contraction (both undamaged and damaged)

Increases tone of most vessels, especially the veins (note that this increases mean systemic filling pressure)

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3
Q

What are the 3 compensatory mechanisms by the ANS for acute cardiac failure

A

Baroreceptor reflex
Chemoreceptor relfex
CNS ischemic response

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4
Q

Sympathetic innervation raises the mean systemic filling pressure from from 7 mmHg to

A

12-14 mmHg thus increasing the tendency for blood to flow from the veins back to the heart

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5
Q

What are the acute dynamic changes after an MI

A

Reduced Cardiac output

Damming of blood in the veins—> increased venous pressure

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6
Q

Acute dynamic changes due to MI are compensated by

A

sympathetic innervation

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7
Q

Chronic dynamic changes due to MI are compensated by (compensated heart failure)

A

Compensated heart failure is the result of partial heart recovery and renal retention of fluid
Maximum pumping ability of the partly recovered heart is still depressed to less than one-half normal
Increase in right atrial pressure can maintain the cardiac ouput at a near normal level despite continued weakness of the heart

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8
Q

Why do patients with heart failure get pulmonary edema and not acute peripheral edema

A

As cardiac ouput decreases the right atrial pressure increases, the aortic pressure greatly decreases, and the capillary pressure reduces (this leads to reduced chance of peripheral edema)

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9
Q

Why does left heart failure lead to pulmonary edema

A

blood is pumped into lungs, but it is not pumped adequately out of the lungs
Therefore, the mean pulmonary filling pressure rises because of the shift of large volumes of blood form the systemic circulation to the pulmonary circulation
This leads to pulmonary capillary pressure increase
once pulmonary capillary pressure rises above or equal to the colloid osmotic pressure of the plasma (about 28mmHg) then fluid begins to filter out of the capillaries into the lung interstitial spaces and alveoli, resulting in pulmonary edema

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10
Q

What are the two major problems of left heart failure

A

pulmonary vascular congestion

pulmonary edema

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11
Q

What are two forms of high output cardiac failure

A

Arteriovenous fistula

Beriberi

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12
Q

Beriberi is what kind of deficiency

A

Thiamin

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13
Q

What is the first heart sound

A

AV valves close at the onset of ventricular systole

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14
Q

What is the second heart sound

A

Semilunar valves close at the end of systole

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15
Q

List 7 valvular heart defects

A

valvular lesions, rheumatic valvular lesions, heart murmurs, aortic stenosis, aortic regurgitation, Mitral regurgitation, Mitral stenosis

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16
Q

In a healthy person the arterial pressure can usually be reduced below about 45 mmHg before cardiac deterioration sets in. However, in a heart that already has a blocked major coronary vessel, deterioration begins when the coronary aterial pressure falls below

A

80 to 90 mmHg

17
Q

What is a rapid acting diuretic used in patients with flash pulmonary edema

A

furosemide

18
Q

The maximum percentage that the cardiac ouput can increase above normal is called

A

cardiac reserve

19
Q

Decompensation of the heart is caused by

A

the heart never being able to reach the cardiac ouput of 5 L/min, even as venous return increases due to fluid retention.

20
Q

Mitral regurgiation occurs during

A

systole

21
Q

Aortic regurgitation occurs during

A

Diastole

22
Q

When is it possible to hear mitral valves stenosis heart sounds

A

it is extremely quite due to the low pressure in the left atria. Best chance is in the last 2/3 of diastole

23
Q

What is Patent ductus arteriosus

A

(left-to-right shunt)-

Blood flows from aorta to pulmonary trunk

24
Q

Tetralogy of Fallot

A

(right-to-left shunt)

Blood flows from right atria to left atria

25
Q

Cardiac abnormalities that decrease the ability of the heart to pump blood

A
Myocardial infarction
Toxic state of the heart
severe heart valve dysfunction
heart arrhythmias
Circulatory shock that results from diminished cardiac pumping ability is called cardiogenic shock
26
Q

Factors that decrease venous return

A

diminished blood volume
Decreased vascular tone (especially of venous reservoirs)
Obstruction of blood flow

27
Q

Powerful sympathetic reflexes initiated by arterial baroreceptors and other vascular stretch receptors in attempt to return cardiac output to normal following cardiac shock

A

Arterioles constrict in most parts of the systemic circulation
The veins and venous reservoirs constrict
Heart activity increases markedly (up to 160-180 bpm)

28
Q

Autoregulation in cerebral and cardiac vessels maintains more-or-less normal pressure as long as the arterial pressue does not fall below

A

70 mmHg

29
Q

Factors that cause a person to recover from a moderate degree of cardiac shock

A
  • Baroreceptor reflex
  • Central nervous system ischemic response (activated at pressures below 50mmHg)
  • Reverse stress-relaxation of the circulatory system
  • Increased secretion of renin by the kidneys and formation of angiotensin II
  • increased secretion by the posterior pituitary gland of vasopressin (ADH)
  • Increased secretion by the adrenal medullae of epinephrine and norepinephrine
30
Q

Compensatory mechanisms that return blood volume back to normal

A

absorption of large quantities of fluid form the intestinal tract
absorption of fluids into the blood capillaries from the interstitial spaces of the body
conservation of water and salt by the kidneys
Increased thirst and increased appetite for salt

31
Q

What is progressive shock

A

when shock itself causes still more shock
- results from positive feeback
When arterial pressure falls low enough, coronary blood flow decreases below that required for adequate nutrition of the myocardium. This weakens the heart muscle and decreases cardiac output even more
- one of the most important features of progressive shock whether or not it is hemorrhagic in origin

32
Q

What is non-progressive shock

A

Sympathetic reflexes and other factors compensate enough to prevent further deterioration of the circulation (all of these are negative feedback mechanisms that attempt to return cardiac output and arterial pressure back to normal)

33
Q

Factors in the final lethal progression of shock

A
Vasomotor failure
blockage of small vessels (sludge blood) 
increased vascular permeability
release of toxins by necrotic tissue
cardiac depression caused by endotoxin
generalized cellular deterioration
34
Q

What is meant by generalized cellular deterioration

A

Diminished active transport of sodium and potassium though cell membrane
depressed mitochondrial activity
breakdown of lysosomes
depression of cellular metabolism of nutrients

35
Q

What is neurogenic shock

A

shock may occur without any loss of blood volume
the vascular capacity increases so much that even the normal amount of blood becomes incapable of filling the circulatory system adequately
one of the major causes of the above is sudden loss of vasomotor tone, resulting in massive dilation of the veins

36
Q

What are some causes of neurogenic shock

A

Deep general anesthesia- depresses vasomotor center enough to cause vasomotor paralysis
Spinal anesthesia- blocks sympathetic nervous outflow
brain damage- causes vasomotor paralysis