exam 3 - cardiac output, blood flow, and blood pressure: part #2 Flashcards

1
Q

three things that exercise training does

A
  1. increases the density of coronary arterioles and capillaries
  2. increases the production of nitric oxide for promoting vasodilation
  3. decreases the compression of the coronary vessels in systol, due to lower cardiac rate
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2
Q

what are cardiovascular changes during exercise affected by?

A
  • motor cortex
  • sensory feedback from contracting muscles
  • baroreceptor reflex
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3
Q

the blood flow through dynamically exercising muscles increases due to…

A
  • increased total blood flow (cardiac output)
  • metabolic vasodilation in the exercising muscles
  • diversion of blood away from the viscera and skin, due to vasoconstriction in these organs (by increased activity of adregnergic sympathetic fibers)
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4
Q

why does cerebral blood flow decrease during heavier exercise (>60% maximal oxygen uptake)?

A

becuse the person hyperventilates, which lowers blood CO2 and produces cerebral vasoconstriction

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5
Q

autoregulation

A
  • in a normal range of arterial pressures, cerebral blood flow is regulated almost exclusively by local intrinsic mechanisms
    • only when the mean arterial pressure rises to about 200mmHg do sympathetic nerves cause a significant degree of vasoconstriction in cerebral circulation
      • this helps to protect arterioles from bursting and to prevent stroke
  • achieved by myogenic and metabolic mechanisms
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6
Q

the role of carbon dioxide concentration in cerebral vessels (myogenic regulation)

A
  • when carbon dioxide concentration rises as a result of hypoventilation, the cerebral arterioles dilate
    • due to decreases in pH of cerebrospinal fluid
  • when arterial CO2 falls below normal during hyperventilation, the cerebral vessels constrict
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7
Q

hyperemic

A

blood flow to active brain regions exceeds the aerobic requirements of the active neurons

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8
Q

astrocytes role in cerebral blood flow

A
  • astrocytes secrete vasodilator chemicals (including prostglandin E2 and carbon monoxide) when stimulated by glutamate
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9
Q

neurovascular coupling

A
  • neurons, astrocytes, and arterioles function together so that increased neuronal activity in a local brain region is accompanied by an increased cerebral blood flow to that region (functional hyperemia)
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10
Q

bradykinin

A

a polypeptide secreted by sweat glands that stimulates vasodilation

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11
Q

what happens to cutaneous blood flow as the temperature warms?

A
  • decreased activity of the sympathetic vasoconstrictor (adrenergic) axons to the skin, allowing dilation
    • with further warming, there is increased activity of sympathetic cholinergic axons to the skin; these stimulate sweat glands
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12
Q

most important variables affecting blood pressure

A
  • cardiac rate
  • stroke volume (determined primarily by the blood volume)
  • total peripheral resistance
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13
Q

how does sympathetic stimulation affect blood volume indirectly?

A

by stimulating constriction of renal blood vessels and thus reducing urine output

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14
Q

changes in cutaneous blood flow occur as a result of changes in what?

A

sympathetic nerve activity

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15
Q

baroreceptors

A
  • located in aortic arch and carotid sinuses
  • stretch receptors
  • sensory nerve activity from baroreceptors ascends via the vagus (X) and glossopharyngeal (IX) nerves to the medulla oblongata, which directs the autonomic system to respond appropriately
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16
Q

what does the baroreceptor reflex consist of?

A
  1. aortic arch and carotid sinus baroreceptors as the sensors
  2. vasomotor and cardiac control centers of the medulla oblongata as the integrating centers
  3. parasympathetic and sympathetic axons to the heart and blood vessels as the effectors
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17
Q

the reflex of raising or lowering of blood pressure is due mainly to what? secondarily?

A
  • the reflex of raising or lowering blood pressure is due mainly to sympathetic nerve regulation of total peripheral resistance and secondarily to the reflex raising or lowering of cardiac output
18
Q

most important regulator of arterial blood pressure on a beat-to-beat basis? longer term regulation?

A
  • beat-to-beat basis is the baroreceptor reflex
  • longer-term regulation achieved by the kidneys, through regulation of blood volume
19
Q

laminar flow

A

occurs when all parts of a fluid move in the same direction, parallel to the axis of the vessel

20
Q

turbulent flow

A

when some parts of a fluid move in different directions, churning and mixing the blood

turbulent flow causes vibrations of the vessel, which may produce sounds

21
Q

first Korotkoff sound

A

when the cuff pressure is equal to the systolic pressure

22
Q

last korotkoff sound

A

occurs when the cuff pressure is equal to the diastolic pressure

23
Q

pulse pressure

A

= systolic pressure - diastolic pressure

reflection of stroke volume

24
Q

causes of secondary hypertension

A
  • kidney disease
  • arteriosclerosis of the renal arteris
  • reduction of renal blood flow, which leads to elevated renin secretion
25
Q

explanation for association between dietary Na and hypertension

A
  • high salt diet increases plasma osmolality –> stimulates ADH secretion –> increased water reabsorption by the kidneys –> increasing blood volume –> increases cardiac output and blood pressure
26
Q

contributors to essential hypertension

A
  • inappropriately high levels of aldosterone secretion, because the person has normal or even elevated levels of renin
  • increased activity of the sympathoadrenal system, promoting vasoconstriction and raising peripheral resistance
  • peripheral resistance increased by secretion of paracrine regulators including:
    • increased endothelin (vasoconstrictor)
    • decreased nitric oxide (vasodilator)
27
Q

final common pathway in essential hypertension

A

kidney function

28
Q

dietary potassium influence on relationship between dietary salt and hypertension

A
  • a diet low in patassium enhances the ability of a high-sodium diet to raise BP, whereas a high potassium diet has the opposite effect
    • a potassium-rich diet increases renal flow and acts as a diuretic to lower blood volume and pressure
29
Q

“silent killer”

A

hypertension (because most patients are asymptomatic until substantial vascular damage has occurred)

30
Q

drugs that can be prescribed for hypertension

A
  • diuretics
  • drugs that block beta-1-adrenergic receptors (i.e. atenolol)
    • lower BP by decreasing cardiac rate
  • ACE (angiotensin-converting enzyme) inhibitors
  • calcium antagonists
  • various vasodilators
  • angiotensin II-receptor blockers (ARBs) - allows angiotensin II to be formed but blocks the binding of angiotensin II to its receptors
  • drugs that inhibit renin activity and reduce activity of renin-angiotensin-aldosterone system
31
Q

most commonly prescribed drugs for treatment of hypertension

A
  • ACE (angiotensin-converting enzyme) inhibitors
  • angiotensin II receptor blockers (ARBs)
32
Q

circulatory shock

A

occurs when there is inadequate blood flow and/or oxygen utilization by the tissues

33
Q

hypovolemic shock

A
  • circulatory shock that is due to low blood volume
  • caused by hemorrhage, dehydration, or burns
  • the sympathoadrenal system is activated by the baroreceptor reflex
    • this causes tachycardia and vasoconstriction (in skin, digestive tract, kidneys, and muscles)
  • a person in hypovolemic shock has low blood pressure, a rapid pulse, cold clammy skin, and reduced urine output
34
Q

septic shock

A
  • dangerously low BP that may result for sepsis, or infection
  • may occur through the action of a bacterial lipopolysaccharide called endotoxin
    • this endotoxin activates the enzyme nitric oxide synthase with macrophages
  • tx. with drugs that inhibit the production of nitric oxide
35
Q

anaphylactic shock

A
  • result of severe allergic reaction (bee stings, penicillin)
    • widespread release of histamine, causes vasodilation and decrease in total peripheral resistance
36
Q

neurogenic shock

A
  • rapid fall in BP
  • decreased sympathetic tone, usually because of upper spinal cord damage or spinal anesthesia
37
Q

cardiogenic shock

A
  • results from cardiac failure
    • inadequate cardiac output to maintain tissue perfusion
    • commonly results from infarction
    • may also result from severe cardiac arrhythmias or valve damage
38
Q

most common causes of left ventricular heart failure

A
  • myocardial infarction
  • aortic valve stenosis
  • incompetence of the aortic and bicuspid valves
39
Q

electrolyte concentration disturbances in heart failure

A
  • high blood K and low blood Ca can cause the heart to stop in diastole
  • low blood K and high blood Ca can arrest the heart in systole
40
Q

compensatory responses that occur during congestive heart failure

A
  • activations of sympathoadrenal system
    • stimulates cardiac rate, ventricle contractility, and arteriole constriction
    • increased renin secretion and reduced urine output
      • this occurs despite an increased secretion of atrial natriuretic peptide (which would have the compensatory effect of promoting salt and water excretion)
41
Q

treatment for CHF

A
  • first line of treatment:
    • angiotensin-converting enzyme inhibitors
    • angiotensin II receptor blockers
  • beta-adrenergic receptor blockers with digitalis to increase myocardial contractility
  • nitroglycerin (vasodilator)
  • diurectics
42
Q
A