Lecture 21 Cardiovascular system 2: Cardiac Function Flashcards

1
Q

Systole

A

contraction phase

ventricular systole 1/3 of cycle

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2
Q

Diastole

A

relaxation phase

ventricular diastole 2/3 of cycle

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3
Q

5 specific phases of cardiac cycle

A
ventricular filling 
atrial systole
isovolumic contraction 
ventricular ejection
isovolumic relaxation
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4
Q

Ventricular Filling

A
mid to late diastole
low Pressure in ventricle 
AV valves open, semilunar valves closed 
ventricular volume increased 
this is the P wave
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5
Q

Atrial systole

A

end of ventricular diastole
atrial contraction “tops off” ventricles after passive phase of ventricular filling
AV valves are still open

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6
Q

Isovolumic Contraction

A

beginning of ventricular systole
pressure rapidly increases as ventricles contract
AV valves close -> 1st hear sound “LUB”
semilunar valves still closed, so volume stays constant as Pressure increases
Volume is maximal
QRS phase

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7
Q

Ventricular Ejection

A
mid to late systole 
Pressure increase to maximal 
semilunar valves open 
blood ejected to arteries and ventricular volume decreases 
S-T segment (Plateau)
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8
Q

isovolumic relaxation

A
beginning of diastole 
P rapidly decrease 
AV valves stay closed until ventricular Pressure < atrial Pressure 
volume is the lowest 
T wave
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9
Q

Pressure in LV ranges

A

from about 0 during diastole to 120 mm Hg at peak of systole

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10
Q

Atrial BP in aorta and large arteries ranges

A
from 80 (diastolic) to 120 mm Hg (systolic) 
BP is sustained in diastole by closure of semilunar valves and elastic recoil of arteries
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11
Q

Volume in ventricles

A

is highest at end of diastole

lowest at end of systole

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12
Q

Wiggers cardiac output diagram correlates

A
electrical events (ECG)
pressure changes in atria, ventricles, and aorta, volume and heart 
volume changes in ventricles 
heart sounds
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13
Q

Cardiac Output

A

total blood flow per minute from one ventricle
RV and LV have the same output
CO is totaly blood flow to all tissues of the body (systemic circuit)
increased demand for O2 and nutrients is accommodated by increase in CO

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14
Q

Cardiac output (CO) =

A

hear rate (HR) X stroke volume (SV)

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15
Q

Stroke Volume

A

amount of blood ejected from each ventricle
end-diastolic volume (EDV) - end-systolic volume (ESV) = SV
resting values: 130 mL 60mL 70mL

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16
Q

Control of Cardiac output

A

Modulation of heart rate

Modulation of stroke volume

17
Q

Modulation of heart rate

Sympathetic (ANS)

A

sympathetic cardiac nerve (NE) -> B1 adrenergic receptors
->increased heart rate of peacemaker depolarization at SA node -> increases HR
E & NE secreted by the adrenal medulla also bind to B1 receptors to increase HR

18
Q

Modulation of heart rate

Parasympathetic (ANS)

A
vagus nerve (ACh) -> muscarinic receptors -> decreases HR at SA node 
parasympathetic control dominates at rest ("vagal tone")
19
Q

Modulation of Stroke Volume

Intrinsic control

A

Starling’s law of the heart (shows the relationship between SV and EDV)
increase in EDV -> Increase in force of contraction -> increase in SV
results from the length-tension relationship of cardiac muscle: increased filling stretches sarcomeres to a more optimal part of the L-T curve
EDV increases due to increased venous return to the heart
HOW YOU INCREASE STROKE VOLUME

20
Q

Modulation of Stroke Volume

Extrinsic control

A

sympathetic NS -> NE ->increase in contractility of the heart
adrenal medulla -> E & NE (neural & hormonal)
INCREASE STOKE VOLUME

21
Q

Contractility

A

beats stronger
builds up force more rapidly
greater SV

22
Q

Signal transduction pathway

A
  1. E and NE bind to B1 adrenergic receptors
  2. GPCR activates the cAMP second messenger system -> phosphorylation of proteins
  3. increase Ca2+ entry from the ECF and increase Ca2+ release from the SR
  4. increase actin-myosin crossbridge formation -> increase force and speed of contraction