4-cardio Flashcards
1
Q
what type of vessels is the main location of resistance in circulation
A
arterioles
2
Q
where is renin released
A
kidneys
3
Q
what is afterload
A
the resistance that the heart has to pump against
4
Q
what determines afterload
A
arteriolar pressure and peripheral resistance
5
Q
what is preload
A
the stress on ventricular wall before systole
6
Q
in the shovel snow example, what is preload and afterload
A
preload=how much snow on shovel
afterload=how high lift snow
7
Q
what happens to afterload when you increase peripheral resistance
A
it increases
8
Q
what happens to afterload when you increase BP
A
it increases
9
Q
how do you find left ventricle end diastolic pressure / what is another name for it
A
pulmonary wedge pressure, it is the preload
weird question
10
Q
how do you find cardiac output
A
stroke volume x heart rate
11
Q
is left or right ventricular pressure bigger
A
left because it has to pump to the whole system
12
Q
what is venous return
A
rate of return of blood to the heart
13
Q
what does cardiac output equal in terms of vein
A
cardiac output=venous return
14
Q
are veins or arteries more rigid
A
arteries
15
Q
are veins or arteries more elastic
A
veins
16
Q
what is capacitance
A
ability to store blood
17
Q
is venous capacitance bigger or smaller than arterial capacitance
A
venous>arterial
18
Q
what is another name for the intrinsic relationship in the heart
A
the Frank Starling relationship
19
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)
20
Q
what does left ventricular end diastolic pressure =
A
=preload
21
Q
what is the measure of initial fibre length
A
left ventricular end diastolic pressure
22
Q
what happens during heart failure in the Frank Starling relationship
A
more blood in the heart doesnt make more contraction
23
Q
what is the extrinsic regulation of the heart contractility
A
baroreceptor reflex
24
Q
what happens if BP increases in BR reflex
A
carotid sinus baroreceptors - CNS- enhances vagal flow- bradycardia
25
what happens if BP decreases in BR reflex
carotid sinus baroreceptors - CNS- decrease vagal flow- tachycardia +vasoconstriction
26
what are 4 causes of congestive heart failure
infarction
ischemia
increase presure
increase volume load
27
what is ischemia
inadequate blood supply to an organ or part of the body, dead tissue
28
what is infarction
obstruction of the blood supply to an organ or region of tissue, causing local death of the tissue.
29
what are 5 sings of congesttive heart failure
reflex tachycardia, enlarged heart, oedema, dyspnea(shortness of breath), elevated venous pressure (swollen neck veins+ankles)
30
what is dyspnea
shortness of breath
31
what is a main force that keeps circulation moving
the large pressure between arteries and veins
32
what causes venous distention
heart is too weak to pump
33
what happens to venous return in heart failure
decreases
34
what happens to cardiac output in heart failure
decreases
35
what happens to sympathetic outflow in heart failure
increase (accumulate fluid)
36
what happens to glomerular filtration in heart failure
decrease
37
what does the "congestive" in congestive heart failure mean +what does it come from
enhanced sympathetic outflow leads to the circulatory congestion
38
what does increased sympathetic outflow do to HR
increase
39
what does congestive heart failure do to arterial pressure
maintain!
40
why is there edema in congestive heart failure
elevated venous pressure, fluid expelled from capillaries
41
what happens to heart size in congestive heart failure
becomes large
42
what happens to sympathetic outflow in congestive heart failure
increase
43
what happens to renal blood flow in congestive heart failure
decrease
44
what happens to cardiac output in congestive heart failure
decrease
45
why is renal blood flow decreased in congestive heart failure
because less cardiac output
46
what does low renal blood flow cause
increase in renin release
47
what happens to renin release in congestive heart failure and why
increase renin release because there is less renal blood flow
48
what does renin cause the conversion of
angiotensinogen to angiotensin 1
49
what happens to angiotensin 2 in congestive heart failure
increase
50
what does angiotension 2 do to preload in congestive heart failure
increase
51
what does angiotension 2 do to afterload in congestive heart failure
increase
52
what are 3 ways to treat heart failure (broad)
enhance contractility
diuretic+reduce fluid intake
reduce cardiac work load
53
what are 2 ways(drug types) to enhance contractility in congestive heart failure
cardiac glycosides and positive inotropic agents
54
how can you reduce fluid intake and increase fluid loss in congestive heart failure
diuretics
55
what are 2 ways(drug types) to reduce cardiac work load
vasodilators and beta-blockers
56
what is an example of a positive inotropic gent
cardiac/digitalis glycosides / digoxin
57
what do positive inotropic agents do
increase force of contraction
58
what do negative inotropic agents do
decrease force of contraction
59
what are 2 things that positive inotropic agents cause via the increased force of contraction
circulatory improvement and preserved arterial blood pressure
60
what are 3 things that negative chronotropics agents cause
- reflex tachycardia & vasoconstriction eliminated
- venous return increased
- circulatory improvement lowers ventricular filling pressure
61
what happens to the heart size when you use cardiac glycosides
smaller
62
what happens to edema with cardiac glycosides
it becomes reduced
63
what do cardiac glycosides do to baroreceptors
sensitize (indirect)
64
what do cardiac glycosides do to vagal tone
increase (indirect)
65
what are the indirect effects of cardiac glycosides like
ACh
66
what are the 2 indirect effects of cardiac glycosides on supraventricular tissue
sensitization of baroreceptors, increased vagal tone
67
where are the 2 direct effects of cardiac glycosides on the heart (which parts of the heart)
purkinje fibres and ventricular myocardium
68
what do cardiac glycosides do to ventricular myocardium
increase force of contraction (positive inotropic effect),
| ERP and APD reduced
69
what do cardiac glycosides do to SA node + net effect
increase vagal outflow, decease sinus rate (indirect) -bradycardia
70
where are the 2 indirect effects of cardiac glycosides on heart tissue
SA node and AV node
71
what do cardiac glycosides do to SA node + net effect
increase vagal outflow (indirect) - promotes AV block!
72
what is the net effect of cardiac glycosides on the SA node
bradycardia
73
what is the net effect of cardiac glycosides on the AV node
promotes AV block
74
what do cardiac glycosides do to purkinje fibres
increase automaticity and excitability
75
what do cardiac glycosides do to ERP
reduce
76
what do cardiac glycosides do to APD
reduce
77
what is the TI of cardiac glycosides
low, 2-3 of TI
78
what are some cardiotoxic effects of cardiac glycosides (5)
- arrhythmias
- enhancement of effects seen with therapeutic dose
- generation of after-depolarization
- AV block
- ectopic pacemakers in Purkinje fibres or ventricles
79
what causes the contractile machinery during AP
ca++ entry through ca channels
80
which ion exchange channel is occuring during phase 2 AP
Na+/Ca++ exchange (plateau)
81
which gradient provides evergy for the extrusion of Ca++
Na+ gradient
82
what is the mechanism of action of digitalis
inhibits the Na+/K+ ATPase pump
83
what happens to intracellular Na+ with digitalis
accumulation due to the AP
84
what happens to Na+ gradient with digitalis
it is decreased
85
what happens to Na+/Ca+ exchange with digitalis
it is reduced
86
what happens to the amount of Ca++ that leaves the cell during plateau phase of AP with digitalis
less leaves
87
what kind of dysrhythmia are cardiac glycosides good for
atrial and supraventricular
88
what is the role for cardiac glycosides in atrial dysrhythmias + How!?
control ventricular rate by impeding transmission through AV node
89
are cardiac glycosides good for ventricular dysrhythmias
bad
90
are cardiac glycosides good for do supraventricular dysrhythmias
good
91
are cardiac glycosides good for atrial dysrhythmias
good
92
how do cardiac glycosides help atrial dysrhythmias
impede transmission through AV node
93
what do cardiac glycosides do to AV node
impede transmission
94
are catecholamines positive or inotropic agents
positive
95
are phosphodiesterase inhibitors positive or inotropic agents
positive
96
what are 2 examples of catecholamines
dopamine and dobutamine
97
what are dopamine and dobutamine used for
acute heart failure
98
how do dopamine and dobutamine work
stimulate b1 adrenoceptors (increase force) so they increase Ca++ influx through L-type Ca++ channel (increase force more so than rate)
99
is the inotropic or chronotropic effect bigger in dopamine and dobutamine
inotropic (more force rather than rate)
100
what are two examples of phosphodiesterase inhibitors
amrinone and milrinone
101
what are amrinone and milrinone used for
chronic heart failure
102
what does phosphoodiesterase do
breaks down cAMP
103
what would a phosphodiesterase inhibitor do to cAMP level
increase
104
what does amrinone and milrinone do to contractility and how
increases because it increases Ca++ through L-type channels
105
what does amrinone and milrinone do to arteries
vasodilates
106
what does amrinone and milrinone do to force
increase
107
what does amrinone and milrinone do to afterload
lower
