Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

KIN 426 > Coronary circulation > Flashcards

Coronary circulation Flashcards

(89 cards)

Start Studying
1
Q

Where to the coronary arteries arise from?

A

the root of the aorta behind the right and left cusps of the aortic valve

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

What do the coronary arteries supply?

A

entire myocardium
right supplies right atrium and ventricle
left supplies left atrium and ventricle

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

What coronary artery is dominant?

A

right 50%
left 20%
both about 30%

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

what do the microcirculatory coronary vessels consist of?

A

terminal arterioles
precapillary sinuses
capillaries
venules

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

what are cardiomyocytes surrounded by?

A

capillaries that are aligned with them

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

what is the average length of a microcirculatory?

A

about 350um

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

During diastole, what do precapillary sinuses serve as?

A

blood reservoir

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

During systole, what do precapillary sinuses do?

A

disgorge the blood to sustain myocyte perfusion

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

How does most blood of the blood return after passing through the capillary beds?

A

to right atrium through coronary sinus
some through anterior coronary veins

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

What are the three vascular communications between vessels of the myocardium and cardiac chambers?

A

arteriosinusoidal
asterioluminal
thebesian vessels

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

What happens to the small arteries in ateriosinusoidal channels as they enter the chambers?

A

they lose their arterial structure and divide into irregular endothelium lines and sinuses that anastomose with other sinuses and capillaries to communicate with cardiac chambers

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

What are arterioluminal vessels?

A

small arteries or arterioles that open directly into the atria and ventricles

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

What are thebesian vessel?

A

small veins that connect capillary beds and communicate with cardiac and other thebesian veins
- communication through extensive plexus of subendothelial vessels
- do not give significant blood supply

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

What is the principal factor responsible for myocardial perfusion?

A

aortic pressure
generated by the heart itself
changes provoke parallel changes in coronary blood flow

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

What do abrupt changes in aortic pressure produce?

A

equally abrupt changes in coronary blood flow in the same direction

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

How is perfusion pressure maintained at a new level?

A

a return of blood flow toward the level observed before the induced change in perfusion pressure
*autoregulation of blood flow

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

What is autoregulation in the coronary arteries mediated by?

A

a myogenic mechanism, metabolic activity, endothelium

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

What will increased metabolic activity of the heart cause?

A

Decrease in coronary vascular resistance and a decrease in cardiac metabolism to increase coronary resistance

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

What is the position of the autoregulatory region affected by?

A

metabolic state of cardiac muscle

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

What are changes to coronary blood flow mainly caused by?

A

calibre changes of coronary resistance vessels in response to metabolic demands of the heart

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

What is coronary flow reserve?

A

the difference between maximal flow by vasodilator drugs and the flow in the physiological range

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

What is extravascular compression?

A

squeezing effect of the contracting myocardium on blood vessels
*LV hypertrophied = greater compression

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

When does maximal left coronary inflow occur?

A

Early diastole when ventricles have relaxed and extravascular compression is virtually absent

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

What is the flow pattern of the RCA?

A

similar pattern to left
Because of lower pressure developed during systole by thin right ventricles, reversal of blood flow does not occur in early systole and constitutes a greater proportion of total coronary inflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What does pacing stress cause?
a rapid switch from lactate uptake to production (seen as a drop in the ST segment) *rapid reversal upon stopping
26
What drugs are typically used to treat chest pain?
organs nitrate, and nitrites that do not dilate the coronary vessels selectively
27
Do organic nitrates/nitrites have an effect on autoregulation?
little arterioles in the ischemic heart are likely already maximally dilated by the response to symptoms
28
In a patient with marked narrowing of a coronary artery, what is the result of administration of vasodilators?
fully dilate normal vessel branches parallel to the narrowed segment and reduce the head of pressure to partially occluded vessel *increase flow to other vessels = decrease in pressure gradient
29
What is coronary steel?
vasodilator further compromises blood flow to the ischemic myocardium and elicits pain and ECG changes indicative of tissue injury * observes with dipyridamole
30
What is the action of dipyridamole?
acts by blocking cellular uptake and metabolism of endogenous adenosine also decreased or eliminated coronary autoregulation because it dilates small resistance vessels
31
How do nitrites/nitrates alleviate chest pain?
decreasing cardiac work and MVO2 by relaxing great veins (decreasing preload) and decreasing BP (decreasing afterload)
32
What must the decrease in pressure work and MVO2 from nitrates/nitrites be greater than?
then the decrease in coronary blood flow and O2 supply consequent to the decrease in coronary perfusion pressure
33
What do nitrites and endogenous NO do?
dilate large coronary arteries and collateral vessels to increase blood flow to ischemic myocardium and alleviate chest pain
34
How does the ratio to endocardial and epicardial blood flow change if diastolic pressure in coronary arteries is low?
the ratio falls below one blood flow to endocardial regions is more severely impaired than epicardial regions - more damage in the inner wall than outer of the ventricle
35
What is the decrease in ratio to endocardial and epicardial blood flow reflected as?
an increased gradient of myocardial lactic acid and adenosine concentrations from the epicardium to the endocardium
36
How does sympathetic nerve stimulation affect coronary blood flow?
increases
37
In perfused hearts, what is eliminated by cardiac arrest or ventricular fibrillation?
mechanical effects of extravascular compression
38
The increase in coronary blood flow with sympathetic stimulation is a sum of what factors?
increase in metabolic activity by rate and contraction tends to dilate coronary resistance vessels
39
What is initially often observed with sympathetic stimulation?
vasoconstriction before vasodilation attributed to metabolic effects
40
What causes the initial vasoconstriction with sympathetic stimulation?
after B-adrenergic receptors are blocked to eliminate positive chronotropic and inotropic effects, direct reflex activation increases coronary resistance *The main function of sympathetic nerve fibres is to vasoconstriction
41
What is the function of A and B adrenergic receptors?
A - constrictors B - dilators
42
What control is coronary resistance predominately under?
local nonneuronal control
43
What does vagus nerve or Ach stimulation cause?
slight dilation of coronary resistance vessels and at a constant perfusion pressure increased coronary blood flow
44
What is vasodilation initiated by?
muscarinic receptors on endothelial cells that release NO
45
What occurs when NO synthase is inhibited by L-NAME?
vagal stimulation and Ach are less able to increase coronary blood flow
46
What is the relationship between myocardial metabolic activity and the magnitude of coronary blood flow?
close parallelism direct positive
47
What does a decrease in the ratio of O2 supply to demand cause?
releases vasodilator substances from the myocardium into interstitial fluid, where they can relax coronary resistance vessels
48
What causes a decrease in the ration of O2 supply to demand?
decrease in arterial blood O2 or coronary blood flow increase in cardiac metabolic rate
49
What would a decrease in O2 demand cause?
decrease the release of vasodilator and permit greater expression of basal tone
50
What are the three key factors that mediate vasodilation?
adenosine NO opening of KATP channels
51
What opens the KATP channels?
a decrease in oxidative metabolism in vascular smooth muscle, decreasing ATP opening will cause hyperpolarization
52
What does the hyperpolarization of the KATP membrane cause?
reduces the Ca2+ entry and relaxes the coronary smooth muscle to increase the flow *prevent Ca2+ overload and a decrease in ATP that will generate an outward current that decreases AP duration and limits entry of Ca2+ during phase 2 of AP
53
What signals an increase in NO?
in endothelial cells, hypoxia activates KATP channels that signal an increase in NO to relax vascular smooth muscle
54
What is through to be an AP role during O2 supply and demand imbalances?
protective role
55
What does adenosine do at low concentrations?
activate KATP channels and enhance NO release
56
What would occur if all three key vasodilator substances were inhibited?
coronary blood dlow would decrease at both rest and during exercise contractile dysfunction and signs of myocardial ischemia become evident
57
When is most of the O2 in coronary blood flow extracted?
during one passage through the myocardial capillaries * the O2 supply to myocardial cells is flow limited
58
What does complete elimination of coronary flow result in?
a quick depletion of high-energy phosphates and accumulation of lactate also, contractile akinesis occurs over time and evolves into MI and tissue necrosis
59
What is akinesis?
a particular area is lacking contraction
60
What does a modest reduction in coronary flow result in?
a decrease in myocardial O2 consumption (~10-50%), a transiently increased dependence on anaerobic glycolysis, oxidative free fatty acids at a decreased rate, and modest to severe contractile dysfunction
61
What is the classic symptom of MI?
angina pectoris - chest pain
62
What causes angina pectoris during ischemia?
high H+ concentration activates NHE and H+ is extruded from cells in exchange for Na+ ischemia inhibits Na+ K+ ATPase decreasing Na+ extrusion the increase in intracellular Na+ content enhances Na+Ca2+ exchange so that as Na+ leaves the vells Ca2+ enters = Ca2+ overload impairs myocardial contraction, possibly leading to cell death
63
What hastens recovery from ischemia during reperfusion?
inhibition of NHE or Na+Ca2+ exchange
64
What role does the NHE play against ischemic damage?
inhibition provides a protective role in an MI, intracellular acidosis develops, and Na+ accumulates in myocytes
65
What is one of the most common causes of serious cardiac disease?
diminished coronary blood flow as a consequence of coronary artery disease
66
What is the impairment of myocardial contraction during MI produced by?
decrease in O2 delivery metabolic substrates accumulation of lactic acid, K+. H+ in cardiac tissues
67
What does a decrease in ATP concentration do during a MI cause?
Due to the rate of oxidative phosphorylation decreased ATP concentration falls ADP is formed further hydrolyzed to AMP and converted to adenosine
68
What does an MI cause in adenosine?
about 100-fold increase in interstitial adenosine and stimulates adenosine receptors
69
Where are A1 receptors located?
on the plasma membrane of cardiomyocytes
70
What is the action of A1 receptors when stimulated (SA and in the ventricle)?
antiadrenergic effect in SA node = decrease in HR via same path as Ach in ventricle = decrease rate of O2 consumption
71
What are intravenous injections of adenosine used to treat?
supraventricular tachycardia stimulates A1 receptors on the AV node to rapidly decrease the ventricular rate
72
How do A1 receptors act on cardiac sensory nerve endings?
stimulation can result in chest pain
73
What does the rise of adenosine during ischemia link?
decrease of O2 delivery oxidative phosphorylation ATP content to chest pain
74
Where are the A2 receptors located?
on vascular smooth muscle of coronary arterioles
75
When stimulated what do A2 receptors cause?
vasodilation
76
What does intracoronary infusion of adenosine cause?
increase in coronary blood flow five-fold
77
What does the dramatic increase in adenosine formation cause during an MI?
increase in interstitial adenosine that stimulates A2 receptors, resulting in vasodilation
78
How does adenosine overall decrease the severity of ischemia?
by increasing coronary blood flow decreasing MVO2 by decreasing HR and contractility
79
What is myocardial stunning?
a relatively brief period of every ischemia followed my reperfusion maybe associated with mechanical dysfunction, can fully recover after a period of hours to days
80
How can myocardial stunning be prevented?
by preconditioning involves one or more brief occlusions of a coronary artery *prolonged occlusion in the absence of brief occlusions would impair the contractile force
81
How would long-term dipyridamole protect from ischemia-induced impairment of cardiac function?
preconditioning may involve adenosine release dipyridamole blocks cellular uptake of attention = rise in blood levels of adenosine A1 receptor antagonist would abolish the effect
82
When do collateral vessels develop?
if the narrowing of a coronary artery or branch occurs slowly and progressively
83
What is the function of collateral vessels?
supply sufficient blood to ischemic myocardium to prevent or decrease the extent of necrosis
84
How are collateral vessels developed?
originate from preexisting arterioles that undergo proliferative changes of endothelium and smooth muscle by arteriogenesis
85
What stimulates arteriogenesis?
shear stress is caused by enhanced blood flow velocity that occurs in arterioles proximal to occlusion
86
What is the process of arteriogenesis?
occlusion causes the pressure gradient along the proximal arterioles to increase because of greater perfusion pressure upstream stress-activated endothelium upregulates expression of MCP-1 that attracts monocytes to invade arterioles (and other adhesion molecules and growth factors) = remodelling and development of new enlarged collateral arteries
87
Are collateral arteries distinguishable from normal ones?
not after several months
88
What is capillary proliferation stimulated by?
VEGF expression is upregulated by hypoxia *mediated by adenosine release
89
Have any surgical attempts been able to enhance the development of collateral vessels?
no, they did not increase collateral circulation above that produced by coronary artery narrowing alone

KIN 426 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions