5 Flashcards

(61 cards)

1
Q

what side of the heart goes to pulmonary circulation

A

right side

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2
Q

what side of the heart goes to systemic circulation

A

left side

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3
Q

is the CO in both sides of the heart the same

A

yes sinon accumulation

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4
Q

what are the two main differences entre pulmonary and systemic circulation

A

Pressure and VASCULAR RESISTANCE
SC requires high pressure to deliver o2 and blood to all organs.
PC not as much bc delivers to both lungs same amount.

SC has high total vascular resistance (flow controlled by arterioles that constrict and dilate)
PC has low total vascular resistance (flow controlled by oxygen)

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5
Q

what is the pressure in the SC and the mean ARTERIOLE pressure

A

120/80

MAP: 100

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6
Q

what is the pressure in the PC and the mean ARTERIOLE pressure

A

25/8

15

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7
Q

what are arterioles

A

small branches of arteries that lead to capillary beds

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8
Q

pressure drops before and after capillary bed. in SC the drop goes from what in artery to what in veins to what in RA to what in RV to what in PC

what does the drop in pressure correspond to

A

30 in artery –> 10mmHg in vein –> 2 in RA –> 25/0 –> 25/8

drop in pressure corresponds to water effusion to neighbouring tissues

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9
Q

pressure drops before and after capillary bed. in PC the drop goes from what in artery to what in veins to what in LA to what in LV to what in SC

what does the drop in pressure correspond to

A

12 in artery –> 8mmHg in vein –> 5 in LA –> 120/0 –> 120/80

low drop in pressure bc you don’t want water effusion to leave and enter air chambers.

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10
Q

what’s starlings law of the heart

A

Force of contraction of ventricle increases w increased end diastolic volume

–> blood will pump out as much blood as is delivered to it by vena cava and atria.

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11
Q

what’s end diastolic volume (EDV)

A

amount of blood in ventricles before ejection (before systole)

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12
Q

how do ventricles cope with increased EDV according to starlings law

A

increase diameter and increase force of contraction

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13
Q

what’s preload

A

degree of stretching of ventricles in diastole

its proportional to end diastolic volume

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14
Q

what’s stroke volume

A

the volume of blood pumped out by one contraction

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15
Q

what’s cardiac output

A

the volume of blood pumped out per unit of time

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16
Q

high preload has what implication on EDV

A

high EDV

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17
Q

high preload has what implication on SV and CO

A

high SV and high CO

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18
Q

when would EDV be increased

A

during exercise

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19
Q

what pathology results from too high preload?

A

heart failure.

limit to starlings law.

if preload keeps increasing above limit, ventricles WEAKEN and heart contractions will eventually start to weaken and CO will fall

same goes for too high atrial pressure, too high EDV too high ED fibre length, too high EDP

so eventually, high EDV –> low SV and low CO and MORE RESIDUAL VOLUME AT THE END OF SYSTOLE

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20
Q

theory underlying starlings law

A

actin and myosin are the contractile mechanisms of cardiac muscle. At rest they actually overlap.
so upon contraction, the overlap increases
in heart failure there’s no overlap

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21
Q

why is an enlarged heart problematic

A

if enlarged heart is not corresponding to increased ventricular wall thin¡canes than force of contraction will be reduced bc muscle fibres are stretched to a point where starlings law is no longer applicable.

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22
Q

what kinds of people have bigger hearts

A

athletes (Nadal)

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23
Q

what’s the normal value for stroke volume

A

70mL

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24
Q

what’s the normal value for EDV

A

120 mL

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25
what's the normal value for ESV
50 mL
26
stroke volume in equation equals to
EDV - ESV
27
after load definition
resistance (impedence) of flow of aorta and large arteries.
28
opposite of overload
compliance (stretch)
29
so if you have high compliance what happens to afteload
decreases bc heart has to work less hard
30
in which kind of people is aorta elasticity (compliance) decreased and why
old people and smokers bc elastic fibres are replaced by collagen.
31
what happens if afterlaod increases
longer period of isovolumetric contraction of ventricle before valve opens, so shorter duration of ejection and shorter SV and higher EDV and so low CO
32
in a healthy heart is after load low or high
low
33
what's isovolumetric contraction
event in early systole where ventricles contract right before they eject.
34
what's inotropy
its the force of contraction of ventricular muscle. | its affected by neurones and hormones.
35
what's the impact of high inotropy on residual volume and stroke volume
high isotropy means low residual volume and high stroke volume
36
what increases inotropy?
``` high blood calcium levels b adrenergic agonists (adrenaline) drugs that stimulate calcium entry into myocardium (levosimendan) cardiac glycosides (digoxin) glucagon ```
37
what decreases inotropy?
insulin
38
what are the heart valves and how many cusps do they have
tricuspid (three cusps=leaflets) entre RA and RVwithstands lower pressure so 3 leaflets bas opens wider. mitral valve (2 cusps) entre LA and LV. 2 BC HAS to WHITSHAND GREATER PRESSURE semilunar aortic valce (3 cusps) semilunar pulmonary valve (3 cusps)
39
why is there no valve entre VC and RA
because pressure in VC is low so a valve would increase resistance too much
40
where do chordate tendinae attach
ventricular papillary muscles
41
what pathology results from inadequate closure of valves
mitral regurgitation (mitral bc its more dangerous if it occurs in left heart)
42
what keeps valves closed
chordate tendinae which bind papillary muscles
43
what are the two phases of ventricular systole
First phase: isovolumetric contraction phase Second phase: when pressure is high enough to open valves of aorta or pulmonary artery
44
to maintain normal CO is atrial systole necessary
no but its necessary for exercise. elastic recoil of ventricle is enough to suck in all the blood. during exercise diastole is too short to do that
45
what atrial fibrillation Sx and causes and WHAT YOU WOULD SEE IN A ECG
``` asynchronous contrition of atria diziness due to damage to atrial muscle common and not life threatening no P wave, normal QRS wave ```
46
what does the fist heart sound correspond to (S1)
Mitral and tricuspid valves closing- if sound is splitting then asynchronous closing of valves
47
what does the second heart sound correspond to (S2)
closing of aortic and pulmonary valves
48
what does the third heart sound correspond to (S3)
1/3 way through diastole due to turbulent flow during rapid filling of ventricles in early diastole
49
what does the fourth heart sound correspond to (S4)
Turbulent flow in ventricles during late filling | sign of decreased ventricular compliance
50
what is turbulent flow
some of the NRJ of the flow is diverted to sound --> you can hear sounds in air and blood when theres turbulent flow.
51
what are S3 and S4 also called
gallops (=sounds associated w diastolic filling, not a good sing, turbulent flow)
52
what tool can you use to investigate heart sounds
phonocardiogram
53
what's aortic stenosis
aortic valve doesn't open well so a blood goes through it makes a sound for as long as blood goes through damaged aortic valve. if AV valve isn't closing completely, you will also hear a noise in systole bas not as much
54
what's aortic regurgitation
valve opens okay but doesn't close well so blood comes back to venticle during isovolumetric relaxation. as blood goes back it makes a noise.
55
what's mitral stenosis
if mitral valve is narrow and blood cant get through easily, will be a small noise heard during the input of blood into ventricle during mitral diastole.
56
S2 is best auscultated where
erbs point- left sternal border 3rd ICS
57
S1 is best auscultated where
able the apex so
58
explain to me jugular venous pulse
bc no valve entre VC et RA, when RA contracts there's some back flow to IJV. that's jugular venous pulse
59
what are the 3 peaks of jugular venous pulse
a: atrial contraction before tricuspid valve closes c: increased pressure in atrium just after tricuspid closes bc valves bulges back into atrium v: valve bulges again as ventricles reaches peak of contraction.
60
which heart sound is the QRS complex in synch with
S1
61
what three mechanisms regulate venous return to the heart
1. one way valves in veins 2. muscular pumps effects 3. thoracoabdominal pumps (inspiratoim, thoracic pressure decreases so blood into VC. on exhalation pressure increases in thorax so blood to Riht atrium