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Physiology > Let 15 Blood Volume , BP > Flashcards

Let 15 Blood Volume , BP Flashcards

1
Q

CO is what?

A 
Cardiac Output (CO), is the volume of blood pumped/min by each ventricle 
-(SV)(HR)
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2
Q

Define stroke volume

A

SV is blood pumped/beat by each ventricle

- CO=SVxHR thus at rest, CO= about 5500ml/min=5.5L

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3
Q

What is about the total blood volume in the body

A

about 5.5L

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4
Q

what is the main controller of HR

A

the Autonomic innervation of SA node b/c nerve fibers modify rate of spontaneous depolarization

  • symp (increases HR)
  • parasymp (decreases HR)
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5
Q

what stimulates the opening of pacemaker HCN channels

A

NE & Epi

-this depolarizes SA faster, increasing HR

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6
Q

What promotes opening of K+ channels

A

ACh, the resultant k+ outflow counters Na+ influx, slowing depolarization & decreasing HR

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7
Q

Cardiac control center of medulla does what

A

coordinates activity of autonomic innervation

-sympathetic endings in atria &ventricular can stimulate increased strength of contraction

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8
Q

What 3 variables determine SV

A
  • End diastolic volume(EDV)
  • Total peripheral resistance(TPR)
  • Contractility
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9
Q

Define EDV

A

volume of blood in ventricles at end of diastole; increase EDV= incr SV; dear EDV=decr SV

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10
Q

define TPR

A

impedance to blood flow in arteries; increase TPR= decreased SV; decreased TPR= increased SV

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11
Q

define contractility

A

strength of contraction decreases contractility=decreased SV

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12
Q

what is workload(preload)

A

EDV is amount of blood in ventricles just before they contract

  • SV is directly proportional to preload & contractility
  • strength of contraction varies directly with EDV
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13
Q

afterload which impedes ejection from ventricle comes from what

A

TPR

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14
Q

Frank-Starling Law of the Heart says what

A

states that strength of ventricular contraction varies directly with EDV
- when EDV increases, strength of ventricular contraction increases, thus SV increases

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15
Q

at any given EDV, strength of contraction depends upon level of what activity?

A

sympathoadrenal activity= positive inotropic effect; NE & Epi produce an increase in HR & contraction

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16
Q

Effect on SV is what effect

A

inotropic (positive)

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17
Q

what are the 2 ways CO is affected by sympathoadrenal activity

A
  1. positive inotropic effect on contractility

2. positive chronotropic effect on HR

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18
Q

effect on HR is what effect

A

positive chronotropic effect

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19
Q

what is venous return

A

return of blood to heart via veins

  • controls EDV & thus SV & CO
  • dependent upon total blood volume & venous pressure
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20
Q

what percentage of blood do veins hold

A

about 70% & are called capacitance vessels

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21
Q

describe capacitance vessels

A

they have thin walls & stretch easily to accommodate more blood w/o increased pressure (higher compliance)
-have only 0-10 mmHg pressure vs. arteriole pressure of 90-100mmHg

22
Q

venous return is aided by what ?

A
  1. vasoconstriction caused by symp(smooth muscle contraction)
  2. skeletal muscle pumps (squeezes veins)
  3. pressure to drop during inhalation; promotes flow of venous blood to heart
23
Q

urine formation begins with what

A

filtration of plasma in renal capillaries=glomeruli; filtrate passes thru & is modified by nephron
-volume of urine excreted can be varied by changes in reabsorption of filtrate

24
Q

ADH is released by what

A

posterior pituitary when osmoreceptors in hypothalamus detect high osmolality

25
Q

Aldoesterone

A

steroid hormone secreted by adrenal cortex

26
Q

what does aldosterone do

A

helps maintain blood volume & pressure thru reabsorption & retention of salt &water
release stimulated by salt deprivation, low blood volume, and low bp

27
Q

when there is a salt deficiency, low blood volume or pressure what is produced

A

angiotensin 2

28
Q

ANP is what

A

Atrial Natriuretic peptide

  • increase blood volume is detected by stretch receptors in left atrium
  • causes release of ANP hormone
  • inhibits aldosterone, promoting Na+ excretion & water excretion to lower blood volume, also promotes vasodilation
  • WORKS TO DECR. BP
29
Q

vascular resistance to blood flow determines what

A

how much blood flows through a tissue or organ

30
Q

vasodilation=

A

decrease resistance= increase blood flow

31
Q

vasoconstriction =

A

increase resistance = decrease blood flow

32
Q

how is bp regulated

A

by mainly controlling HR, SV, and TPR

-NOTE: CO=HRxSV thus BP=HRxSVxTPR

33
Q

What is the baroreceptor reflex

A

it is activated by changes in BP; which is detected by baroreceptors located in aortic arch & carotid sinuses

34
Q

no sound is heard during what flow

A

laminar flow= normal, quiet, smooth blood flow

35
Q

Korotkoff sounds are heard when?

A

when the sphygmomanometer cuff pressure is greater than diastolic (lowest BP) but lower than systolic (highest bp) pressure

36
Q

explain Korotkoff sounds

A

1st korotkoff sound is heard at pressure that blood is 1st able to pass thru cuff; represents systolic pressure
-last sound occurs when cuff pressure=diastolic pressure

37
Q

when do the korotkoff sounds disappear

A

sounds are heard until cuff pressure equals diastolic pressure

38
Q

define pulse pressure

A

systolic pressure- diastolic pressure

- rise in pressure from diastolic to systolic levels=reflects SV

39
Q

define mean arteriole pressure (MAP)

A

represents average arterial pressure during cardia cycle

  • has to be approx b/c period of diastolic is longer than period of systole
  • MAP = pulse pressure/3 + diastolic pressure
40
Q

what is hypertension

A

abnormally high bp

41
Q

what causes primary/essential hypertension

A

caused by complex & poorly understood mechanisms

42
Q

what causes secondary hypertension

A

caused by unknown disease processes

43
Q

primary/ essential hypertension is what

A

about 95% of high bp cases; CO & HR are elevated in many

- kidneys appear to be unable to properly excrete Na+ & H20

44
Q

Dangers of hypertension

A
  • patients usually asymptomatic until vascular damage occurs
    -contributes to atherosclerosis, increases workload of the heart leading to ventricular hypertrophy & congestive heart failure, often damages cerebral blood vessels leading to stroke.
    “silent killer”
45
Q

treatment of hypertension

A
  • lifestyle changes, ex; cessation of smoking, decrease in alcohol intake, weight reduction..etc
  • drug treatments: diuretics to reduce fluid volume, beta blockers to decrease HR, calcium blockers…etc
46
Q

what is circulatory shock

A

occurs when there is inadequate blood flow to & or 02 usage by tissues

  • cardiovascular system undergoes compensatory changes
  • sometimes shock becomes irreversible & death ensues
47
Q

other causes of circulatory shock

A
  • severe allergic rxn= rapid fall in bp called anaphylactic shock
  • rapid fall in bp called neurogenic shock can result from decrease in simp tone following spinal cord damage or anesthesia
  • cariogenic shock; is common following cardiac failure
48
Q

what is septic shock

A

refers to dangerously low bp resulting from sepsis(infection); mortality rate (50-70%)
- often occurs as a result of endotoxin release from bacteria

49
Q

what does endotoxin do

A

induces NO production causing vasodilation & resultant low bp
- treatment:drugs inhibiting production of NO

50
Q

what is hypovolemic shock

A

circulatory shock caused by low blood volume

  • ex; hemorrhage, dehydration, or burns
  • decreased BP and CO
  • results in low bp, rapid pulse, cold clammy skin, low urine output
51
Q

what is congestive heart failure

A

occurs when CO is insufficient to maintain blood flow
- caused by myocardial infraction, congenital defects, hypertension, aortic valves stenosis, disturbance in electrolyte levels

Physiology (6 decks)

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