Lecture 15 Flashcards

1
Q

Cardiac Failure

A

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

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2
Q

How Does the Heart Compensate for Acute Cardiac Failure

A

Increases sympathetic innervation and decreases parasympathetic innervation; increased sympathetic innervation strengthens muscle contractions in damaged and undamaged areas and increases the tone of vessels (especially veins) which increases mean systemic filling pressure

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3
Q

Compensatory Mechanisms by ANS for Acute Cardiac Failure

A

Baroreceptor Reflex
Chemoreceptor Reflex
CNS Ischemic Response

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4
Q

Acute Effects following Acute Heart Attack

A

Reduced cardiac output and damming of blood in the veins which increases venous pressure

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5
Q

Chronic Compensations following Acute Heart Attack (Compensated Heart Failure)

A

Partial heart recovery and renal retention of fluid; maximum pumping ability of the partly recovered heart is still depressed to less than 1/2 normal; any attempt to perform heavy exercise usually causes immediate return of symptoms of acute failure because heart can’t increase its pumping capacity to the levels required for exercise; an increase in right atrial pressure can maintain the cardiac output at a near normal level despite continued weakness of the heart

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6
Q

Pulmonary Edema

A

Left side of the heart fails without concomitant failure of the right side; blood continues to be pumped into the lungs but is NOT pumped adequately out of the lungs; this causes the mean pulmonary filling pressure to rise because of the shift of large volumes of blood from the systemic circulation into pulmonary circulation; pulmonary capillary pressure then increases; if this rises above colloid osmotic pressure, fluid begins to filter out of the capillaries into the lung interstitial spaces and alveoli

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7
Q

2 Major Problems of Left Heart Failure

A

Pulmonary Vascular Congestion and Pulmonary Edema

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8
Q

Arteriovenous Fistula

A

Overloads heart because of excessive venous return

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9
Q

Beriberi

A

Thiamin deficiency and weakening of the heart; decreased blood flow to the kidney results in fluid retention; this increases mean filling pressure

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10
Q

First Sound of a Heart

A

AV valves close at the onset of ventricular systole

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11
Q

Second Sound of a Heart

A

Semilunar valves close at the end of systole

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12
Q

Valvular Defects

A
Valvular lesions
Rheumatic valvular lesions
Heart murmurs
Aortic stenosis
Aortic regurgitation
Mitral regurgitation
Mitral stenosis
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13
Q

Left-to-Right Shunt

A

Blood flows backward and fails to flow through systemic circulation (Patent Ductus Arteriosus)

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14
Q

Right-to-Left Shunt

A

Blood flows from right to left side of the heart, bypassing the lungs (Tetralogy of Fallot)

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15
Q

Circulatory Shock

A

Generalized inadequate blood flow through the body, to the extent that the body tissues are damaged, especially because of too little oxygen and other nutrients delivered to the tissue cells

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16
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
Cardiogenic shock
17
Q

Cardiogenic Shock

A

Circulatory shock that results from diminished cardiac pumping ability

18
Q

Factors that Decrease Venous Return

A

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

19
Q

What causes powerful sympathetic reflexes?

A

Decrease in arterial pressure after a hemorrhage and decreases in pressures in the pulmonary arteries and veins in the thorax

20
Q

What do sympathetic reflexes result in?

A

Arterioles to constrict in most parts of the systemic circulation, veins and venous reservoirs constrict, and heart activity increases markedly

21
Q

After a shock, what compensatory mechanisms return blood volume back to normal?

A

Absorption of large quantities of fluid from 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, and increased thirst and increased appetite for salt

22
Q

Non-Progressive Shock

A

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

23
Q

Progressive Shock

A

Positive feedbacks; 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

Important factor in progressive shock is whether it is hemorrhagic in origin or not

24
Q

Factors in the Final Lethal Progression of Shock

A

Vasomotor failure, blockage of small vessels, increased vascular permeability, release of toxins by necrotic tissue, cardiac depression caused by endotoxin, and generalized cellular deterioration

25
Q

Neurogenic Shock

A

May occur with/without any loss of blood volume; vascular capacity increases so much that even the normal amount of blood becomes incapable of filling circulatory system adequately; loss of vasomotor tone resulting in massive dilation of the veins

26
Q

Causes of Neurogenic Shock

A

Deep general anesthesia (depresses vasomotor center enough to cause vasomotor paralysis), spinal anesthesia (blocks sympathetic nervous outflow), and brain damage (causes vasomotor paralysis)