Lecture 14: HF, Sounds, Shock Flashcards

1
Q

Define Cardiac failure

A

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

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2
Q

Compensation for acute HF

A

Number of circulatory reflexes are activated in order to increase activation of the symapthetic innervation to the heart and decrease parasympathicteic innervation

  • strengthens muscle contraction
  • increases tone of most vessels, esp. veins- increases Psf
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3
Q

3 responses from ANS d/t acute HF :

A

Baroreceptor reflex

Chemoreceptor reflex

CNS ischemic response

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4
Q

Strong sympathietic stimulation d/t all ventricular function diffuesly damages but still functional:

A

Also if part of musculature is damaged—

Increases tone of most blood vessel of circulation and therefore increases venous return

Raises Psf!!! To 12-14 mm Hg

This increases tendency for flow from the veins back into the heart

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5
Q

Acute effects following AMI:

A

Reduced CO

Damming of blood in the veins- increased venous pressures

Causes compensation by sympathetic NS

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6
Q

Chronic compensation for MI- heart failure

A

Result from partial heart recovery and renal fluid retention.

Max. Pumping ability o the partylt recovered heart is stil depressed to less than 1/2 norm.

Heavy exercise generally causes return of symptoms back to acute HF stage….

Increase in r atrial pressure can maintain the CO at a near norm level despite continues weakness of the heart

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7
Q

Pressure changes in HF:

A

Increase in R atrial pressure

Decrease in mean Aortic pressure

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8
Q

Fall in capillary pressure reduces :

A

Chances of peripheral edema

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9
Q

Pulmonary edema and L HF:

A

L side of heart fails w/o concomitant failure of R side

Blood continues to be pumped to lungs but not adequately out of the lungs

Pulmonary filling pressure rises b/c of shift of large volumes from systemic into pulmonary circulation

Pulmonary capillary pressure increases

If rising to pressure = colloid osmotic pressure of plasma -28mm Hg fluids begins to filter out of capillary into lung lung interstitial spaces and alveoli resulting in pulmonary edema

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10
Q

2 major problems w/ L HF:

A

Pulmonary vasucular congestion

Pulmonary edema

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11
Q

Pulmonary edema onset:

A

Can occur so rapidly that if can cause death by suffocation in 20-30min.

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12
Q

What drug may function on a chronically failing heart by increasing the [ca++] in muscle fibers, thereby increasing the strength of contraction

A

Digitalis

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13
Q

What conditions can lead to high output heart failure?

A

Arteriovenous fistula: overloads heart-excessive venous return. Curve moves upwards.

Beriberi: heart muscle weakens d/t thiamine deficiency. Shift venous curve to the right. Results in decreased blood flow to kidneys.

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14
Q

What is first sound of heart?

A

AV valves closing- onset of ventricular systole

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15
Q

What is second sound of heart?

A

Semilunar valves closing- end of systole.

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16
Q

Distinguish btw left to right and right to left congenital defects

A

L to R: Patent ductus arteriosus- blood flows backwards and fails to flow through systemic circulation.

R to L: Tetralogy of fallot- blood flows from R to L side of heart- bypassing lungs.

17
Q

How is a patent ductus arteriosus L to R:

A

Blood flows backwards [L to R] from aortic arch to pulmonary arch

[essentially, L ventricle to R]

18
Q

How is tetralogy of FA loot a R to L defect:

A

W/ a defect in the interventricular wall blood will flow out of the R venticle into the L ventricle

[R to L]

19
Q

Define circulatory shock

A

Generalized Inadequate blood flow through the body, to the extent that the body tissues are damaged. Especially because of too little O2 and other nutrients delivered to the tissue cells

20
Q

List 2 factors that reduce CO and give ex:

A

Diminished blood volume~20%.
Decreased vascular tone.
Obstruction of blood flow.

Ex: MI, Heart arrhythmia, toxic heart state, severe heart valve dysfunction, circulatory shock that results from diminished cardiac ability-cardiogenic shock.

21
Q

Negative feedback mechanisms that attempts to return cardiac output and arterial pressure back to normal after cardiac shock?

A

Sympathetic reflex: initiated by arterial baroreceptors.

autoregulation for art. pressure as long as it doesnt drop elbow 70 mm Hg

22
Q

What results from sympathetic stimulation reflex after arterial baroreceptor has initiated the reflex?

A

Results in: arterioles and venous constriction and increase in HR up to 180 bpm

23
Q

Factors that cause a person to recover from shock:

A
  • baroreceptor reflexes
  • central nervous system ischemic response
  • reverse stress-relaxation of the circulatory system
  • Renin-angiotensin response
24
Q

What effects does renin cause?

A

Constricts peripheral arteries and causes DECREASED outputs of water and salt by the kidneys.

25
Q

What effect does ADH have?

A

Constricts peripheral arteries and veins and greatly increases water retention by the kidneys.

26
Q

What effect does epinephrine have in shock?

A

Constricts the peripheral arteries and veins and increases HR

27
Q

What are 4 compensatory mechanisms for returning blood volume back to normal?

A
  • Absorption of large quantities of fluid from GI tract
  • absorption of fluids into blood capillaries from GI tract
  • increased thirst and increased appetite for salt

-conservation of water and salt by the kidneys

28
Q

Progressive vs non-progressive shock

A

Non-progressive shock : sympathetic relaxes CAN compensate enough for shock. NEGATIVE feedback mechanisms

Progressive shock: POSITIVE feedbacks. Art. Pressure is low enough coronary blood flow is too low-decreasing heart muscle and CO even more. Important feature;hemorrhagic or not

29
Q

Lethal factors in progression of shock

A
  • Vasomotor tone
  • blockage of small vessels
  • increased vascular permeability
  • release of toxins by necrotic tissue.
  • cardiac depression d/t endotoxins
  • generalized cellular deterioration:decreased active transport, mito. Activity, lysosome breakdown, depression of cellular metabolism.
30
Q

Define neurogenic shock

A

Shock that occurs w/o blood loss.

Vascular capacity increases so much that even the normal amount of blood becomes incapable of filling the circulatory adequately

31
Q

Causes of neurogenic shock:

A

Major: loss of vasomotor tone, resulting in massive dilation of veins.

Others: general anesthesia, spinal anesthesia, brain damage

32
Q

Objective 4: Describe progressive changes that occur in cardiac output, Psf, and R atrial pressure after AMI:

A

Initially CO/ venous return drops d/t AMI. Then, Sympathetic innervation and partial recover will gradually increase CO again. It likely will never be as high as before.

This is with a compensated heart.

33
Q

What happens after AMI for a decompensated heart?

A

The heart is never able to come all the way back to the level req’d for critical CO level for fluid balance.

After decreasing initially it begins to improve…then it decreases again because it is unable to compensate.