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Cardioresp > 5 > Flashcards

5 Flashcards

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
Q

what’s the normal value for ESV

A

50 mL

26
Q

stroke volume in equation equals to

A

EDV - ESV

27
Q

after load definition

A

resistance (impedence) of flow of aorta and large arteries.

28
Q

opposite of overload

A

compliance (stretch)

29
Q

so if you have high compliance what happens to afteload

A

decreases bc heart has to work less hard

30
Q

in which kind of people is aorta elasticity (compliance) decreased and why

A

old people and smokers bc elastic fibres are replaced by collagen.

31
Q

what happens if afterlaod increases

A

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
Q

in a healthy heart is after load low or high

A

low

33
Q

what’s isovolumetric contraction

A

event in early systole where ventricles contract right before they eject.

34
Q

what’s inotropy

A

its the force of contraction of ventricular muscle.

its affected by neurones and hormones.

35
Q

what’s the impact of high inotropy on residual volume and stroke volume

A

high isotropy means low residual volume and high stroke volume

36
Q

what increases inotropy?

A 
high blood calcium levels
b adrenergic agonists (adrenaline)
drugs that stimulate calcium entry into myocardium (levosimendan)
cardiac glycosides (digoxin)
glucagon
37
Q

what decreases inotropy?

A

insulin

38
Q

what are the heart valves and how many cusps do they have

A

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
Q

why is there no valve entre VC and RA

A

because pressure in VC is low so a valve would increase resistance too much

40
Q

where do chordate tendinae attach

A

ventricular papillary muscles

41
Q

what pathology results from inadequate closure of valves

A

mitral regurgitation (mitral bc its more dangerous if it occurs in left heart)

42
Q

what keeps valves closed

A

chordate tendinae which bind papillary muscles

43
Q

what are the two phases of ventricular systole

A

First phase:
isovolumetric contraction phase

Second phase:
when pressure is high enough to open valves of aorta or pulmonary artery

44
Q

to maintain normal CO is atrial systole necessary

A

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
Q

what atrial fibrillation Sx and causes and WHAT YOU WOULD SEE IN A ECG

A 
asynchronous contrition of atria
diziness
due to damage to atrial muscle
common and not life threatening
no P wave, normal QRS wave
46
Q

what does the fist heart sound correspond to (S1)

A

Mitral and tricuspid valves closing- if sound is splitting then asynchronous closing of valves

47
Q

what does the second heart sound correspond to (S2)

A

closing of aortic and pulmonary valves

48
Q

what does the third heart sound correspond to (S3)

A

1/3 way through diastole due to turbulent flow during rapid filling of ventricles in early diastole

49
Q

what does the fourth heart sound correspond to (S4)

A

Turbulent flow in ventricles during late filling

sign of decreased ventricular compliance

50
Q

what is turbulent flow

A

some of the NRJ of the flow is diverted to sound –> you can hear sounds in air and blood when theres turbulent flow.

51
Q

what are S3 and S4 also called

A

gallops (=sounds associated w diastolic filling, not a good sing, turbulent flow)

52
Q

what tool can you use to investigate heart sounds

A

phonocardiogram

53
Q

what’s aortic stenosis

A

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
Q

what’s aortic regurgitation

A

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
Q

what’s mitral stenosis

A

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
Q

S2 is best auscultated where

A

erbs point- left sternal border 3rd ICS

57
Q

S1 is best auscultated where

A

able the apex so

58
Q

explain to me jugular venous pulse

A

bc no valve entre VC et RA, when RA contracts there’s some back flow to IJV. that’s jugular venous pulse

59
Q

what are the 3 peaks of jugular venous pulse

A

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
Q

which heart sound is the QRS complex in synch with

A

S1

61
Q

what three mechanisms regulate venous return to the heart

A
  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

Cardioresp (23 decks)

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