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Physiology > Exam Final: Ch 14 Cardiac Output > Flashcards

Exam Final: Ch 14 Cardiac Output Flashcards

1
Q

Cardiac Output (CO)

A

= volume of blood pumped/min by each ventricle

- (SV)(HR)

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2
Q

Stroke volume (SV)

A
  • blood pumped/beat by each ventricle
    • Ex: 70 – 80 ml/beat and average HR = 70 BPM
    • CO = SV x HR thus at rest, CO ~ = 5500 ml/min = 5.5L….
      • TL blood vol. in body is also ~5.5 L
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3
Q

therefore, during exercise CO

A

↑ so does rate of blood flow through circulation

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4
Q

Without neuronal influences, SA node will

A

will drive heart at rate of its spontaneous activity

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5
Q

chronotropic effect)

A

Normally Symp & Parasymp activity influence HR

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6
Q

Autonomic innervation of SA node is

A
  • main controller of HR because nerve fibers modify rate of spontaneous depolarization
    • Symp (↑ HR)
    • Parasymp (↓HR)
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7
Q

NE & Epi stimulate

A

stimulate opening of pacemaker HCN channels

this depolarizes SA faster, increasing HR

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8
Q

ACH promotes opening of

A
  • K+ channels

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

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9
Q

Cardiac control center of medulla

A

coordinates activity of autonomic innervation

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10
Q

Sympathetic endings in atria & ventricles can stimulate

A

increased strength of contraction

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11
Q

Stroke Volume

Is determined by 3 variables

A
  • End diastolic volume (EDV)
  • Total peripheral resistance (TPR)
  • Contractility
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12
Q

End diastolic volume (EDV)

A

= volume of blood in ventricles at end of diastole

- ↑ EDV = ↑ SV; ↓ EDV = ↓ SV

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13
Q

Total peripheral resistance (TPR)

A
  • impedance to blood flow in arteries

- ↑ TPR = ↓ SV; ↓ TPR = ↑ SV

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14
Q

Contractility

A

strength of ventricular contraction ↓ contractility = ↓ SV

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15
Q

EDV

A

is amount of blood in ventricles just before they contract = workload (preload) on heart prior to contraction

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16
Q

SV is directly proportional to

A

preload and contractility

strength of contraction varies directly with EDV

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17
Q

Total peripheral resistance

A

afterload which impedes ejection from ventricle

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18
Q

Frank-Starling Law of the Heart

A

States that strength of ventricular contraction varies directly with EDV

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19
Q

intrinsic property of myocardium

A

When EDV ↑, strength of ventricular contraction ↑, thus SV (blood pumped/beat by each ventricle) ↑

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20
Q

Extrinsic Control of Contractility

- At any given EDV

A

strength of contraction depends upon level of sympathoadrenal activity = (positive inotropic effect);

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21
Q

positive inotropic effect);

A
  • NE (from symp. nerve endings) and Epi (from adrenal medulla) produce an increase in HR and contraction
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22
Q

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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23
Q

Venous return

A
  • return of blood to heart via veins

- controls EDV & thus SV & CO;

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24
Q

Venous return

dependent on

A

total blood volume & venous pressure

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25
Q

Veins hold most of blood in body (~70%) & are thus called

A

capacitance vessels;

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26
Q

capacitance vessels;

A
  • Have thin walls & stretch easily to accommodate more blood w/o ↑ pressure (=higher compliance)
  • have only 0-10 mm Hg pressure vs arteriole pressure of 90 – 100 mm Hg
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27
Q

Venous return is aided by

A
  1. Vasoconstriction caused by Symp (smooth muscle contraction)
  2. Skeletal muscle pumps (squeezes veins)
  3. Pressure drop during inhalation; promotes flow of venous blood to heart
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28
Q

Regulation of Blood Volume by Kidney

A

Blood volume ↓ as urinary excretion ↑

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29
Q

Urine formation begins with

A
  • with filtration of plasma in renal capillaries = glomeruli;
  • filtrate passes through and is modified by nephron
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30
Q

Volume of urine excreted

A
  • can be varied by changes in reabsorption of filtrate

- adjusted according to needs of body by action of hormones

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31
Q

ADH (vasopressin)

released by

A

Posterior pituitary when osmoreceptors in hypothalamus detect high osmolality

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32
Q

ADH high osmolality from

A

excess salt intake or dehydration

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33
Q

high osmolality causes

A
  • thirst and stimulates H20 reabsorption from urine;

- ADH release inhibited by low osmolality

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34
Q

Aldosterone

A

steroid hormone secreted by adrenal cortex

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35
Q

Aldosterone helps maintain

A

blood volume & pressure through reabsorption & retention of salt & water

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36
Q

Aldosterone Release stimulated by

A

salt deprivation, low blood volume, & low blood pressure

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37
Q

Renin-Angiotension-Aldosterone System

A

When there is a salt deficiency, low blood volume, or pressure, angiotensin II is produced

38
Q

angiotensin II is produced

A
  • starting w/ renin release from kidneys
  • –> renin cleaves angiotensin into angiotensin I
  • –> in lungs angiotensin converting enzyme (ACE) cleaves it to form angiotensin II
39
Q

Angio II causes

A
  • causes a number of effects all aimed at increasing blood pressure
    • triggers vasoconstriction, aldosterone secretion, thirst
40
Q

Atrial Natriuretic Peptide (ANP)

A
  • ↑ blood volume is detected by stretch receptors in left atrium
    • causes release of ANP (hormone)
41
Q

ANP (hormone)

A

inhibits aldosterone, promoting Na+ (natriureses) excretion and water excretion to lower blood volume, also promotes vasodilation

42
Q

Vascular Resistance to Blood Flow

A
  • Determines how much blood flows through a tissue or organ
    • Vasodilation = ↓ resistance = ↑ blood flow
    • Vasoconstriction = ↑ resistance = ↓ blood flow
43
Q

Blood Pressure (BP) is regulated by

A
  • mainly by controlling HR, SV, & total peripheral resistance (TPR)
    • Note: CO = HR X SV, thus BP = HR X SV X TPR
    • An increase in any of these can result in increased BP
44
Q

Sympathoadrenal activity raises

A

BP via arteriole vasoconstriction and by increased CO

45
Q

kidney plays role in BP by

A

regulating blood volume & thus stroke volume

46
Q

Baroreceptor Reflex Is activated by

A

changes in BP; which is detected by baroreceptors (stretch receptors) located in aortic arch and carotid sinuses

47
Q

Increase in BP causes walls of aortic arch and carotid sinuses

A

to stretch, increasing frequency of APs

48
Q

Baroreceptors are

A

tonically active and will send ↑ or ↓ frq APs to vasomotor & cardiac control centers in medulla

49
Q

Baroreceptors is most sensitive to

A

to decrease & sudden changes in BP

50
Q

Recall that when the parasymp (acts to ↓ BP) is on

A

the symp (acts to ↑ BP) is simultaneously turned off and vise versa

51
Q

Baroreceptor reflex helps

A

maintain BP on beat-to-beat basis:

52
Q

when going from laying to standing

A

BP ↓ b/c ~ 500 – 700 ml of blood moves from thoracic cavity to lower extremities –> ↓ venous return – > ↓ EDV –> ↓ SV and thus CO thus ↓ BP –> baroreceptors immediately ↓ frq of AP, which ↓ parasymp activity and ↑ symp activity

53
Q

Measurement of Blood Pressure Is indirect via

A

auscultation (to examine by listening)

54
Q

Measurement of Blood Pressure

- no sound is heard during

A

laminar flow (normal, quiet, smooth blood flow)

55
Q

Korotkoff sounds can be heard when

A

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

56
Q

cuff constricts

A

brachial artery creating turbulent flow & noise as blood passes

57
Q

1st Korotkoff sound is heard at

A

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

58
Q

Blood pressure cuff is inflated above

A

systolic pressure, occluding artery

59
Q

as cuff pressure is lowered

A

blood flows only when systolic pressure is above cuff pressure, producing Korotkoff sounds

60
Q

sounds are heard until

A

cuff pressure equals diastolic pressure, causing sounds to disappear

61
Q

Pulse pressure

A

= (systolic pressure) – (diastolic pressure)

62
Q

rise in pressure from diastolic to systolic levels =

A

= reflects stroke volume

63
Q

Mean arterial pressure (MAP)

A

represents average arterial pressure during cardiac cycle

64
Q

Mean arterial pressure (MAP)

has to be approximated because

A

period of diastole is longer than period of systole

65
Q

MAP =

A

= diastolic pressure + 1/3 pulse pressure

66
Q

Hypertension

A
  • Is blood pressure in excess of normal range for age and gender
    • (> 140/90 mmHg); afflicts about 20 % of U.S. adults
67
Q

Primary or essential hypertension is caused by

A

complex & poorly understood mechanisms

68
Q

Secondary hypertension is caused by

A

known disease processes

69
Q

Primary (Essential) Hypertension

A
  • Constitutes most of hypertensives
    • ~ 95% of high BP cases; increase in peripheral resistance is universal; CO & HR are elevated in many
  • Secretion of renin, Angio II, & aldosterone is variable
70
Q

development of hypertension

A
  • Sustained high stress (which increases Symp activity thus ↑ TPR and HR) and high salt intake act synergistically in
71
Q

Prolonged high BP causes

A

thickening of arterial walls, resulting in atherosclerosis

72
Q

Primary (Essential) Hypertension

- Kidneys appear to be

A

unable to properly excrete Na+ and H20

73
Q

Dangers of Hypertension

A
  • Patients are often asymptomatic until substantial vascular damage occurs
    • Contributes to atherosclerosis, increases workload of the heart leading to ventricular hypertrophy and congestive heart failure, often damages cerebral blood vessels leading to stroke, these are why it is called the “silent killer”
74
Q

Treatment of Hypertension

A
  • includes lifestyle changes such as cessation of smoking, moderation in alcohol intake, weight reduction, exercise, reduced Na+ intake
75
Q

Treatment of Hypertension

- Drug treatments

A
  • include diuretics to reduce fluid volume, beta-blockers to decrease HR, calcium blockers, ACE inhibitors to inhibit formation of Angio II, & Angio II-receptor blockers
76
Q

Circulatory Shock

Occurs when

A
  • there is inadequate blood flow to, and/or O2 usage by tissues
    • Cardiovascular system undergoes compensatory changes
    • Sometimes shock becomes irreversible & death ensues
77
Q

Severe allergic reaction can cause

A

a rapid fall in BP called anaphylactic shock

78
Q

anaphylactic shock

A

Due to generalized release of histamine causing vasodilation

79
Q

Rapid fall in BP called neurogenic shock can result from

A

decrease in Symp tone following spinal cord damage or anesthesia

80
Q

Cardiogenic shock is

A
  • common following cardiac failure resulting from infarction (myocardial necrosis caused by ischemia) that causes significant myocardial loss
    • Severe arrythmias or valve damage
81
Q

Septic Shock

- Refers to

A

dangerously low blood pressure resulting from sepsis (infection); Mortality rate is high (50-70%)

82
Q

Septic Shock Often occurs as a result of

A

endotoxin release from bacteria

83
Q

endotoxin

A
  • Endotoxin induces NO production causing vasodilation and resultant low BP
  • Effective treatment includes drugs that inhibit production of NO
84
Q

Hypovolemic Shock

A
  • Is circulatory shock caused by low blood volume
    • E.g. from hemorrhage, dehydration, or burns
    • characterized by decreased CO and BP
85
Q

decreased CO & BP

Compensatory responses include

A

sympathoadrenal activation via baroreceptor reflex

86
Q

Hypovolemic Shock

- low blood volume

A
  • Results in low BP, rapid pulse, cold clammy skin (b/c of vasoconstriction), low urine output
  • Blood is diverted to brain and heart at expense of other organs
87
Q

Congestive Heart Failure

A

Occurs when CO is insufficient to maintain blood flow required by body

88
Q

Congestive Heart Failure

- insufficient CO to maintain blood flow Caused by

A

myocardial infarction (most common), congenital defects, hypertension (↑afterload which impedes ejection from ventricle), aortic valve stenosis (thickened and hardened valve), disturbances in electrolyte levels

89
Q

Congestive Heart Failure

- insufficient CO to maintain blood flow Compensatory responses are

A

similar to those of hypovolemic shock (sympathoadrenal activation)
- Causes ventricular hypertrophy and ↑ blood volume

90
Q

Congestive Heart Failure

- Treatment

A
  • Digitalis: (blockage of Na+/K+ pumps in myocardial cells –> ↓ Na+ driving force thus diffusion is ↓ and there is ↓ Na+ available for Na+/Ca2+ exchanger thus ↑ Ca2+ –> ↑ strength of contraction)
  • Vasodilators like nitroglycerine, & diuretics

Physiology (27 decks)

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