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Pathophysiology III > Block I: CV III > Flashcards

Block I: CV III Flashcards

1
Q

what effect does the autonomic nervous system have on the heart?

A
  1. influences the rate of impulse generation (firing), depolarization, repolarization
  2. influences strength of ventricular contraction
  3. produces changes in heart and circulatory system faster than metabolic or humoral agents
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2
Q

what is the role of ACH

A
  1. decrease nerve firing rates

2. cholinergic vagal fibers stimulate membrane to become hyperpolarized (very negative)

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3
Q

what does ACH do on the molecular level in the myocardium

A
  1. increases K+ conductance of nodal tissue via M2 muscarinic receptors
  2. opens K+ channels to allow for repolarization (more negative environment inside cell)
  3. DECREASE HR
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4
Q

what effect does ACH have on M2 receptors?

A

decrease cAMP, inhibit Ca2+ from entering cell

-decrease HR

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5
Q

strong vagal stimulation may [] spontaneous discharge

A

abolish, halt

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6
Q

stimulation of sympathetic cardiac nerves [] depolarizing effect of Ih

A

speeds up, increase HR

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7
Q

spontaneous discharge [] upon sympathetic stimulation

A

increases

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8
Q

what hormone is released a sympathetic synapses

A

NE

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9
Q

what hormone is released at vagal/cholinergic synapses

A

ACH

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10
Q

what receptors does NE bind? what does this lead to?

A
  1. Beta-1
  2. increased intracellular cAMP
    - facilitates opening on L calcium channels
    - -increase ICa2+ and rapidity of depolarization phase
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11
Q

list catecholamines

A
  1. epi
  2. norepi
  3. dopamine
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12
Q

catecholamines bind receptors on target cells to [] muscle contraction

A

strengthen

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13
Q

what is the physiology behind catecholamines strengthening muscle contraction

A
  1. receptor couples with G protein
  2. G proteins activate adenyl cyclase
  3. concentrations of cAMP increase
  4. influx of calcium
  5. contraction strengthened because of increased intracellular calcium
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14
Q

sympathetic fibers [] the strength of myocardial contractoin

A

increase

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15
Q

[] arise in thoracic spinal cord and branch into superior, middle, and inferior cardiac nerves
-join at cardiac plexus, neural junction, at the root of the aorta in front of the trachea

A

sympathetic nerves

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16
Q

[] interact with beta-adrenergic receptors and pacemaker cells to

a. increase influx of Ca2 into cell
b. increase contractile stregnth

A

catechoalmines

increase HR and force contraction

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17
Q

what overall effects do catecholamines have on the heart

A
  1. increase strength myocardial contraction
  2. increase HR
  3. shorten conduction time through AV node
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18
Q

chronotropic changes describe []

A

heart rate
- decrease
+ increase

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19
Q

inotropic changes describe []

A

change in force myocardial contraction
-decrease
+ increase

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20
Q

this sympathetic hormone is released a post synpatic nerve endings

A

NE

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21
Q

this sympathetic hormones is released by adrenal medulla and reaches heart via the blood stream

A

epi

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22
Q

what does stimulation of beta receptors 1&2 cuase

A
  1. increase in heart rate (chronotropy)
    and force (inotropy)
    -pump more blood
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23
Q

what does stimulation beta 3 receptors cause

A

decrease myocardial contractiliy (- inotropic)

negative feedback
-safety mechanism to prevent overstimulation heart my sympathetic nervous system

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24
Q

what receptors provide negative feedback mechanisms to prevent overstimulation of heart

A

beta 3

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25
Q

parasympathetic [] the rate of contraction

A

decreases

i.e. rest and digest

26
Q

where are parasympathetic fibers found

A

medulla oblongata

27
Q

what nerve do parasympethic impulses travel by

A

vagus

28
Q

the parasympatheric impulses travel by way of [] nerve and synapse in the []

A
  1. vagus

2. cardiac plexus

29
Q

ACH [] conduction through the [] node

A
  1. slows

2. AV

30
Q

which one sympathetic/parasympathetic have a bigger impact on mycardial cells and why

A

sympathetic, more synapses on base/myocardium

31
Q

muscarinic receptors are primarily on the [] while nicotinic is on the []

A
  1. heart

2. skeletal muscle

32
Q

what role does ACH have on nicotinic receptors

A

increase contractility of skeletal muscle via nicotinic receptors (opposite effect on heart)

33
Q

[] is the volume of blood flowing through either systemic or pulmonary circut in L/Min

A

CO

34
Q

[] is calculated by multiplying HR by stroke volume

A

CO

35
Q

[] is calculated by subtracting ESV from EDV

A

stroke volume

36
Q

what is a normal adult CO

A

5 L/min

37
Q

[] is the amount of blood ejected per beat and is useally measured by echocardiograph

A

ejection fraction

38
Q

what is a normal ejection fraction

A

55% or higher

39
Q

how is ejection fraction calculated

A

stroke volume/edv

40
Q

what is ejection fraction a good indicator of

A

ventricular function

41
Q

[] is the pressure generated at the end is diastole

A

pre-load (end of diastole is BEFORE contraction)

42
Q

pre-load is also called what

A

left ventricular end diastolic pressure

43
Q

[] is determined by EDV, the amount of venous return to ventricle and blood left in ventricle after systole or ESV

A

pre laod

44
Q

an increased preload normally increases

A

CO (think equation)

45
Q

[] is resistance during systole

A

afterlaod

46
Q

[] is dependent on arotic pressure and aortic valve function

A

afterload

47
Q

aortic systolic pressure is a good index of [] in left ventricle

A

after laod

48
Q

low aortic pressure leads to []

A

decreased afterload, heart contracts more rapidly

leads to increased CO (think equation)

remember this is supposed to be a high pressure system, so if pressure is low heart will work overtime to increase that pressure

49
Q

high aortic pressure leads to

A

increased afterload

-slows contraction and increases workload

50
Q

what are some determinants of the force of contraction

A
  1. changes in stretching of ventricular myocardium
    caused by changes in ventricular volume (preload)
  2. alteration of nervous system input to ventricles
  3. adequacy of myocardial oxygen supply
51
Q

what are positive inotropic agents

A
  1. Ne from sympathetic nerves

2. Epi from adrenal cortex

52
Q

what are some negative inotropic agents

A
  1. hypoxia
53
Q

average HR

A

70 BPM

54
Q

what is the carioexcitory and cardioinhibitory

A
  1. sympathetic speeds up HR

2. parasympathetic decreases HR, controls resting HR

55
Q

what are some neural reflexes of HR

A
  1. sinus arrythmia
  2. baroreceptor reflexes
  3. brainbridge reflex
  4. hormones and biochemicals
56
Q

sinus arrythmias change the heart rate during []

A

breathing

57
Q

describe the baroreceptor reflex

A

when BP falls, HR increases and arterioles constrict

58
Q

describe the bainbridge reflex

A

changes in heart rate form intravenous infusions, volume reveptors in atria innvervated by vagus nerve

59
Q

describe some hormones and niochemicals that have an effect on hert rate

A
  1. epi/ne

2. thyroid hormones

60
Q

describe the frank-starling law of the heart

A
  1. length-tension relationship of cardiac muscles
  2. volume of blood in heart at the end of diastole contributes to length of muscle fibers (Stretch(
  3. myocardial stretch determines force of contraction
    - more stretch, more contraction
  4. as contractility decreases, curve shifts down & to right to CO will also be decreased
    - contractility contributes to stroke volume and cardiac output
61
Q

describe Laplace’s law

A
  1. contractile force (wall distenction) within a chamber depends on the radius of chamber and thickness of wall
    - small chambers and thicker chamber walls equal decreases contraction force (tension)
  2. in ventriculat dilation, force needed to maintain ventricular pressure lessens available contractile force
    - more difficult for ventricle to eject blood

*anneruysm formation, dispensability in blood vessels, effects ventriculat dilation -> heart failure

Pathophysiology III (5 decks)

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