Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PMCOL 343 > 4-cardio > Flashcards

4-cardio Flashcards

1
Q

what type of vessels is the main location of resistance in circulation

A

arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is afterload

A

the resistance that the heart has to pump against

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what determines afterload

A

arteriolar pressure and peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is preload

A

the stress on ventricular wall before systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what happens to afterload when you increase peripheral resistance

A

it increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what happens to afterload when you increase BP

A

it increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is another name of left ventricle end diastolic pressure

A

preload

weird question

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how do you find cardiac output

A

stroke volume x heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is venous return

A

rate of return of blood to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what does cardiac output equal in terms of veinous return

A

cardiac output=venous return

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

are veins or arteries more rigid

A

arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

are veins or arteries more elastic

A

veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is capacitance

A

ability to store blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

is venous capacitance bigger or smaller than arterial capacitance

A

venous>arterial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is another name for the intrinsic relationship in the heart

A

the Frank Starling relationship

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does the frank starling relationship tell us

A

that the force of contraction is proportional to initial fibre length (aka more blood in heart means more contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the measure of initial fibre length

A

left ventricular end diastolic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what happens during heart failure in the Frank Starling relationship

A

more blood in the heart doesnt cause more contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the extrinsic regulation of the heart contractility

A

baroreceptor reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what happens if BP increases in BR reflex

A

carotid sinus baroreceptors - CNS- enhances vagal flow- bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what happens if BP decreases in BR reflex

A

carotid sinus baroreceptors - CNS- decrease vagal flow- tachycardia +vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are 4 causes of congestive heart failure

A

myocardial infarction
ischemia
increase presure
increase volume load (increased afterload - hypertension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is ischemia

A

inadequate blood supply to an organ or part of the body, dead tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is infarction

A

obstruction of the blood supply to an organ or region of tissue, causing local death of the tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are 5 sings of congesttive heart failure

A

reflex tachycardia, enlarged heart, oedema, dyspnea (shortness of breath due to fluid build up), elevated venous pressure (swollen neck veins+ankles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is HF-ref

A

heart failure - reduced ejection fraction (decreased systolic volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is HF-pef

A

heart failure - preserved ejection fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is a main force that keeps circulation moving

A

the large pressure between arteries and veins (100-5mmHG)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

why are veins more elastic than arteries?

A

they have the capacity to store blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

why do arteries more muscular than veins?

A

they need to withstand higher pressures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what causes venous distention

A

heart is too weak to pump, resulting in the veins storing blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what happens to venous return in heart failure

A

decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what happens to cardiac output in heart failure

A

decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what happens to sympathetic outflow in heart failure

A

increases (caused by failure of heart to pump enough blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what happens to glomerular filtration in heart failure

A

decrease

36
Q

what does the “congestive” in congestive heart failure mean +what does it come from

A

enhanced sympathetic outflow leads to the circulatory congestion

37
Q

what does increased sympathetic outflow do to HR

A

increase

38
Q

what does increased sympathetic outflow in heart failure do to venous pressure

A

increase

39
Q

why is there edema in congestive heart failure

A

elevated venous pressure, fluid expelled from capillaries

40
Q

what happens to heart size in congestive heart failure

A

becomes large (maladaptive hypertrophy)

41
Q

why is renal blood flow decreased in congestive heart failure

A

because less cardiac output

42
Q

what does low renal blood flow cause

A

increase in renin release

43
Q

what happens to renin release in congestive heart failure and why

A

increase renin release because there is less renal blood flow

44
Q

what does renin cause the conversion of

A

angiotensinogen to angiotensin 1

45
Q

what happens to angiotensin 2 in congestive heart failure

A

increase

46
Q

what does angiotension 2 do to preload in congestive heart failure

A

increase

47
Q

what does angiotension 2 do to afterload in congestive heart failure

A

increase

48
Q

what are 3 ways to treat heart failure (broad)

A

enhance contractility
diuretics to reduce fluid intake
reduce cardiac work load

49
Q

what are 2 ways(drug types) to enhance contractility in congestive heart failure

A

cardiac glycosides and positive inotropic agents

50
Q

how can you reduce fluid intake and increase fluid loss in congestive heart failure

A

diuretics

51
Q

what are 3 ways (drug types) to reduce cardiac work load

A

vasodilators, ACE inhibitors and ARBs, beta-blockers

52
Q

what is an example of a positive inotropic gent

A

cardiac digitalis glycosides / digoxin

53
Q

what does digoxin do to inotropy

A

positive effect

54
Q

what physiological benefits are there from digoxin’s positive inotropic effect

A

circulatory improvement
arterial BP preserved

55
Q

what are 3 things that cardiac glycosides cause in terms of chronotropy

A

Overall: negative chronotopy
- reflex tachycardia & vasoconstriction eliminated
- venous return increased
- circulatory improvement lowers ventricular filling pressure

56
Q

what are the 3 general effects of cardiac glycosides

A

positive inotropy
negative chronotropy
reduced oedema (due to improved glomerular circulation)

57
Q

what happens to the heart size when you use cardiac glycosides

A

smaller

58
Q

what are the 2 indirect effects of cardiac glycosides on supraventricular tissue

A

sensitization of baroreceptors, increased vagal tone (similar to ACh)

59
Q

where are the 2 direct effects of cardiac glycosides on the heart (which parts of the heart)

A

purkinje fibres and ventricular myocardium

60
Q

what do cardiac glycosides do to ventricular myocardium

A

increase force of contraction (positive inotropic effect)

ERP and APD reduced

61
Q

what do cardiac glycosides do to SA node + net effect

A

indirectly increase vagal outflow, decease sinus rate, leading to bradycardia

62
Q

which parts of the heart experience the indirect effects of cardiac glycosides

A

SA node and AV node

63
Q

what do cardiac glycosides do to AV node + net effect

A

indirectly increase vagal outflow - promotes AV block!

64
Q

what do cardiac glycosides do to purkinje fibres

A

directly increase automaticity and excitability

65
Q

what do cardiac glycosides do to the ventricles

A

directly increase inotropy (contractility)

66
Q

what is the therapeutic index of cardiac glycosides

A

low, 2-3x the therapeutic dose

67
Q

what are some cardiotoxic effects of cardiac glycosides (5)

A
  • arrhythmias
  • enhancement of effects seen with therapeutic dose
  • generation of after-depolarization
  • AV block
  • ectopic pacemakers in Purkinje fibres or ventricles
68
Q

what ion triggers the contractile machinery of the heart

A

ca++ entry through ca channels

69
Q

which ion exchange channel is occuring during phase 2 AP

A

Na+/Ca++ exchange (plateau)

70
Q

which gradient provides evergy for the extrusion of Ca++

A

Na+ gradient

71
Q

what is the mechanism of action of digoxin

A

inhibits the Na+/K+ ATPase pump, causing Na+ to accumulate in the cell after AP occurs, resulting in less Ca2+ to be removed by the NCX, and less Ca2+ to leave the cell during the plateau of an AP, thus increasing contractility

72
Q

what happens to Na+ gradient with digoxin

A

it is decreased

73
Q

what are 2 examples of catecholamines

A

dopamine and dobutamine

74
Q

what are dopamine and dobutamine used for

A

acute heart failure

75
Q

how do dopamine and dobutamine work

A

stimulate b1 adrenoceptors so they increase Ca++ influx through L-type Ca++ channel (increasing inotropy and chronotropy)

76
Q

what are two examples of phosphodiesterase inhibitors

A

amrinone and milrinone

77
Q

what are amrinone and milrinone used for

A

chronic heart failure

78
Q

how are amrinone and milrinone administered

A

orally or via IV

79
Q

what does phosphoodiesterase do

A

breaks down cAMP

80
Q

what is the mechanism of action for amrinone and milrinone

A

inhibit PDE, increasing cAMP, activate PKA, increase phosphorylation of L tyoe channels, increased Ca++ through L-type channels, increased contractility

81
Q

how do arteriolar vasodilators contribute to the therapeutic effects of amrinon and milrinone

A

vasodilation results in decreased afterload

82
Q

why is the RAAS a problem in heart failure?

A

during heart failure, the kidney thinks BP is low due to reduced CO, and will activate RAAS. This increases BP further and results in increased afterload

83
Q

name two ACE inhibitors

A

ramapril, captopril

84
Q

what is the mechanism of action for ramapril and captopril

A

inhibit synthesis of AT-II, resulting in decreased BP and decreased afterload

85
Q

name three angiotensin II receptor blockers (ARBs)

A

valsartan, losartan, candesartan

86
Q

what is the mechanism of action of ARBs?

A

inhibit AT-II receptors, resulting in decreased BP and decreased afterload

PMCOL 343 (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions