cardiovascular lecture 2 Flashcards

1
Q

what purpose does the prolonged refractory period of cardiac muscle serve? (2)

A
  1. prevents tetanus

2. allows time for ventricles to fill with blood prior to pumping

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2
Q

what activity does “cardiac output (CO)” reference?

A

the amount of blood moved per unit of time (ex. volume of blood each ventricle pumps per minute or the volume of blood flowing through either the systemic or pulmonary circuit per minute); heart rate (HR) x stroke volume (SV)

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3
Q

route of blood through heart

A

right atrium –> tricuspid valve –> right ventricle –> pulmonary semilunar valve –> pulmonary trunk –> pulmonary arteries –> lungs –> pulmonary veins –> left atrium –> bicuspid valve –> left ventricle –> aortic semilunar valve –> aorta

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4
Q

what causes the first heart sound (“lub”)

A

closure of the AV valves

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5
Q

what causes the second heart sound (“dub”)

A

closure of the aortic and pulmonary valves

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6
Q

what are 3 conditions associated with a heart murmur

A
  1. stenosis (narrowing)
  2. regurgitation (insufficiency)
  3. septal defects
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7
Q

a stenotic valve/turbulent flow can be heard during systole or diastole?

A

systole

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8
Q

turbulent backflow can be heard during systole or diastole?

A

diastole

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9
Q

what does it mean when an electronic circuit is “in series”

A

components are connected end to end to form only one path for electrons to flow through the circuit

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10
Q

what does it mean when an electronic circuit is “parallel”

A

components are connected between the same two sets of electrically common points, creating multiple paths for electrons to flow

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11
Q

T/F: Systemic and pulmonary circulations are parallel

A

FALSE; they are in series; this allows for all of the blood to become oxygenated

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12
Q

T/F: organs in systemic circulation are in parallel

A

TRUE; this allows for each organ to receive 100% O2

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13
Q

Flow equals what

A

change in pressure/resistance (F=change in P/R)

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14
Q

during systole, are the ventricles relaxing or contracting?

A

contracting

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15
Q

during diastole, are the ventricles relaxing or contracting?

A

relaxing

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16
Q

wiggers diagram

A

PDF on carmen. Know it

17
Q

T/F: the right side of the heart and the left side of the heart have the same stroke volume and cardiac output

A

TRUE; the only difference is the pressure generated

18
Q

what kind of innervation/control does the atria have?

A
  1. Parasympathetic: muscarinic receptors (acetylcholine)

2. Sympathetic: beta-adrenergic receptors (NE)

19
Q

what kind of innervation/control does the ventricle have

A

Sympathetic ONLY (Ziolo yelled this at us like 800 times); beta-adrenergic receptors (EPINEPHRINE)

20
Q

under sympathetic control, what happens to the pacemaker potentials of the heart

A

they occur more quickly than under control circumstances (slide 27 for graph)

21
Q

under parasympathetic stimulation, what happens to the pacemaker potentials of the heart

A

they occur more slowly than under control circumstances (slide 27 for graph)

22
Q

what are 3 major ways to increase/speed up the heart rate

A
  1. deliver sympathetic hormone epinephrine
  2. release more sympathetic NT, NE
  3. reduce release of PS NT, acetylcholine
23
Q

what are 3 major factors influencing SV

A
  1. Preload: the end- diastolic volume aka the volume of blood in the ventricles just before contraction
  2. magnitude of sympathetic input to the ventricles
  3. Afterload: the pressure against which the ventricle pumps
24
Q

Frank-Starling mechanism aka ventricular function curve

A

plots the ventricular end-diastolic volume against the stroke volume; Frank Starling measures the PRELOAD, NOT contractility

25
Q

how do you increase the heart’s stroke volume? how do you further increase it?

A

fill it more fully with blood –> increased stretch of ventricle will align actin and myosin in a more optimal pattern of overlap; to further increase it, deliver sympathetic signals ie NE and epi –> will also cause heart to relax more rapidly and allow more time to refill

26
Q

increased contractility is due to what

A

sympathetic stimulation and an increase in Ca (slide 33, not sure what we need to know from the diagram)

27
Q

sympathetic signals ie NE and epi cause a stronger and more rapid contraction and what

A

a more rapid relaxation

28
Q

T/F: Parasympathetic nerves have a significant effect on the ventricular muscle

A

FALSE; the ventricle has NO parasympathetic innervation

29
Q

to increase SV, you can increase what

A
  1. end-diastolic volume
  2. NE delivery from sympathetic neurons
  3. epinephrine delivery from adrenal medulla
30
Q

to incrase HR, you can increase what

A
  1. NE delivery from symp neurons

2. epinephrine delivery from the adrenal medulla aka reduce PS

31
Q

T/F: Under normal circumstances, it is possible to increase SV without increasing HR and vice versa

A

FALSE; it’s not possible

32
Q

what is ejection fraction?

A

measurement of contractility; (EDV-ESV)/EDV **SV = EDV-ESV… **he said he “can see a question here”

33
Q

hypertrophic cardiomyopathy

A

increased heart wall thickness; myocardial disarray particularly in interventricular septum –> interferes with blood ejection (leads to angina, arrhythmias, and sudden cardiac death

34
Q

what is hypertrophic cardiomyopathy dependent on

A

preload