Lecture 21 Cardiovascular system 2: Cardiac Function Flashcards Preview

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Flashcards in Lecture 21 Cardiovascular system 2: Cardiac Function Deck (22)
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1

Systole

contraction phase
ventricular systole 1/3 of cycle

2

Diastole

relaxation phase
ventricular diastole 2/3 of cycle

3

5 specific phases of cardiac cycle

ventricular filling
atrial systole
isovolumic contraction
ventricular ejection
isovolumic relaxation

4

Ventricular Filling

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

5

Atrial systole

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

6

Isovolumic Contraction

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

7

Ventricular Ejection

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

8

isovolumic relaxation

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

9

Pressure in LV ranges

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

10

Atrial BP in aorta and large arteries ranges

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

11

Volume in ventricles

is highest at end of diastole
lowest at end of systole

12

Wiggers cardiac output diagram correlates

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

13

Cardiac Output

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

14

Cardiac output (CO) =

hear rate (HR) X stroke volume (SV)

15

Stroke Volume

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

16

Control of Cardiac output

Modulation of heart rate
Modulation of stroke volume

17

Modulation of heart rate
Sympathetic (ANS)

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

Modulation of heart rate
Parasympathetic (ANS)

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

19

Modulation of Stroke Volume
Intrinsic control

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

Modulation of Stroke Volume
Extrinsic control

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

21

Contractility

beats stronger
builds up force more rapidly
greater SV

22

Signal transduction pathway

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