Brainscape's Knowledge GenomeTM

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


See full index

CV 2 > Regulation of Cardiac Output > Flashcards

Regulation of Cardiac Output Flashcards

1
Q

CO=

A

HRxSV

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

Factors affecting heart rate

A

atrial reflex
autonomic innervation
hormones

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

factors affecting stroke volume

A

Preload factors: venous return, filling time
Contractility factors: autonomic innervation, hormones
Afterload factors: vasodilation & vasoconstriction

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

chronotropy

A

changes in heart rate

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

impacts on sinoatrial node depolarization rate

A

Parasympathetic (vagal) input: acetylcholine -> cholinergic (M2 muscarinic receptors), negative chronotropy, decreases heart rate.

sympathetic input: norepinephrine–> adrenergic (beta adrenoceptors) - positive chronotropy, increases heartrate

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

Norepinephrine effects (beta 1 agonists)

A

Increases HR
↑ If
Increases slow depolarization rate (↑ steepness of phase 4)

↑ ICa (in all myocardial cells)
Increases slow depolarization rate (↑ steepness of phase 4)
Threshold more negative (reached sooner)

↓ IK
Increases steepness of phase 4 slow depolarization

Result: Shorter time for depolarization to threshold; ↑ HR

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

Parasympathetic N.S. effects

A 
Decreases HR
Acetylcholine effects (M2 agonists):

↓ If
Decreases slow depolarization rate (↓ steepness of phase 4)

↓ ICa:
Decreases slow depolarization rate (↓ steepness of phase 4)
Threshold more positive (takes longer to reach)

↑ IK
More negative maximum diastolic potential (KAch channel)

Result: Longer time for depolarization to threshold; ↓HR

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

Examples of Factors Which Can Influence the Firing Rate of the SA Node (Positive and Negative Chronotropic Factors)

A

Increasing heart rate: sympathetic stimulation (Muscarinic receptor antagonist, beta adrenoceptor agonist, circulating catecholamines)

Decreasing heart rate: parasympathetic stimulation (muscarinic receptor agonist, beta 1 blocker, Calcium channel blocker)

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

Dromotropy definition

A

changes in conduction velocity

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

Dromotropy affectors

A

Sympathetic norepinephrine effects (β1 agonists):
↑ rate of depolarization (AP slope)  ↑ conduction velocity

Parasympathetic acetylcholine effects (M2 agonists):
↓ rate of depolarization (AP slope )  ↓ conduction velocity

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

Examples of factors which can influence conduction velocity

A

Increasing conduction velocity: sympathetic stimulation (m2 muscarinic receptor antagonist, beta1-adrenoceptor agonist, circulating catecholamines)

Decreasing conduction velocity: parasympathetic stimulation (M2 muscarinic receptor agonist, beta-1 blocker, Na and Ca channel blockers, ischemia/ hypoxia

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

Stroke volume definition

A

SV = volume of blood ejected in 1 heartbeat (ml/beat)

SV = EDV - ESV

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

general affects on stroke volume

A

In general:
↑ SV when:
↑ Preload = ↑ End-diastolic volume (EDV)
↑ Contractility/Inotropy

↓ SV when:
↑ Afterload

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

6 Factors Which Can Promote ↑ EDV

A 
. ↑ Central Venous Pressure (CVP) 
decreased heart rate
increased ventricular compliance
increased atrial contractility
increased afterload
pathological conditions (systolic failure, valve defects)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Central venous pressure promotes increased EDV via

A

[Mean venous pressure/filling pressure/thoracic vena cava pressure]
a. ↓ venous compliance, ↑ resistance
Sympathetic venoconstriction

b. ↑ thoracic blood volume by:
↑ total blood volume 
↑ venous return through:
↑ respiratory activity
↑ skeletal muscle pump activity
↑ CO
Result:
↑ CVP --> ↑ VR --> ↑ atrial filling pressure                                ↑ ventricular filling pressure --> ↑ EDV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

promoting increased EDV via decreased heart rate

A

↑ filling time –> ↑ EDV

Relatively longer time in diastole vs. systole

17
Q

promoting increased EDV by increasing ventricular compliance

A

↑ chamber filling volume (EDV) at a given filling pressure

↑ ventricular relaxation rate (see section on lusitropy)

18
Q

promoting increased EDV via increased atrial contractility

A

Sympathetic stimulation

Increased ventricular filling (EDV) from atria

19
Q

promoting increased EDV via increased afterload

A 
Increased afterload
Ex: Increased aortic pressure
Increased ESV, decreased SV
2° increase in preload for next cycle                            
Not a “good” way to increase EDV
20
Q

pathological conditions that lead to increased EDV

A

Systolic failure
Valve defects: aortic stenosis, aortic regurgitation
Pulmonary valve stenosis & regurgitation (RV preload)
Not a “good” way to increase EDV

21
Q

effects of increased afterload

A

↑ Afterload –> ↑ ESV –> ↓ SV

22
Q

definition of afterload

A

force opposing ventricular ejection (Systolic pressure)

Pressure which contracting fibers must oppose for ejection
Direct measure: maximum systolic ventricular pressure
Indirect estimates:
LV: aortic pressure (mean systemic arterial pressure)
RV: pulmonary a. pressure (mean pulmonary arterial pressure)

↑ afterload –> greater proportion of systole spent in isovolumetric contraction phase

- -> ↓ SV and ejection fraction 

- -> ↑ ESV --> ↓ SV
23
Q

Examples of conditions which may increase afterload on the left ventricle/right ventricle:

A

Systemic hypertension/pulmonary hypertension

Stenotic aortic valve/stenotic pulmonary valve

24
Q

another word for contractility

A

inotropy

25
Q

Contractility/ inotropy in cardiac muscle

A

Not possible to increase force production via motor-unit recruitment or twitch summation

Contractility
Force generation that is independent of preload (EDV, sarcomere length)

↑ contractility = ↑ systolic function
↓ ESV
↑ SV and ejection fraction

Positive inotropic factors: ↑ contractility by ↑ [Ca2+]i
Negative inotropic factors: ↓ contractility by ↓ [Ca2+]i

26
Q

ESPVR (what does the acronym stand for)

A

end systolic pressure volume relationship

27
Q

how changes in contractility affect ESPVR

A

↑ contractility –> ↑ slope of ESPVR –> ↑ SV (independent of EDV)

↓ contractility –> ↓ slope of ESPVR –> ↓ SV
(independent of EDV)

28
Q

How the sympathetic NS impacts contractility

A

Activation of β1-adrenergic receptors on atrial and ventricular contractile myocytes:
↑ Ca2+ availability –> ↑ contractile force –> ↑ CO
How:
1.↑ Ca2+ influx via L-type DHDP channels:
↑ [Ca2+]i and ↑ Ca2+-dependent Ca2+ release from the SR
2. ↑ sensitivity of RYR to [Ca2+]i
3. ↑ SERCA activity (remove phospholamban inhibition), ↑ Ca2+ stores

CV 2 (3 decks)

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