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Cardiovascular I > Regulation of Cardiac Output > Flashcards

Regulation of Cardiac Output Flashcards

1
Q

What are the three ways by wich heart rate can be altered?

A
  1. Rate of slow diastolic depolarization
  2. maximal diastolic potential
  3. threshold potential
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2
Q

What is the intrinsic rate of the sinoatrial node?

What modifies this rate in health individuals?

A

100 - 110

modified by normal “vagal” tone, decreasing heart rate to 60 - 100

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3
Q

What is the end neurotransmitter for the parasympathetic system?

What is the receptor type?

What impact does this system have on HR?

A

Acetylcholine

cholinergic (M2 - muscarinic receptors)

Decreases HR

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4
Q

What is the end neurotransmitter for the sympathetic system?

What is the receptor type?

What impact does this system have on HR?

A

Norepinephrine

adrenergic (B1- adrenoreceptors)

Positive chronotropy (Increase HR)

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5
Q

What are the effects of Norepinephrine (β1 agonists) effects on the current flow on the action potential phases?

What is the net effect?

A

•↑ 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

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6
Q

What are the effects of Acetylcholine (M2 agonists) on the current flow of the action potential phases?

What is the net effect?

A

•↓ 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

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7
Q

Give 4 examples of factors that have positive chronotropic effects.

A
  1. Sympathetic stimulation
  2. M2-Muscarinic receptor antagonist
  3. β1-adrenoceptor agonist
  4. Circulating catecholamines
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8
Q

Give four examples of factors that decrease heart rate

A

Parasympathetic stimulation

M2-Muscarinic receptor agonist

β1-blocker

Ca2+-channel blocker

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9
Q

What are the dromotropic effects of norepinephrine (β1 agonists)?

A

–↑ rate of depolarization (AP slope) —> ↑ conduction velocity

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10
Q

How do Parasympathetic acetylcholine effects (M2 agonists) impact conduction velocity?

A

–↓ rate of depolarization (AP slope ) –>↓ conduction velocity

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11
Q

Give 4 examples of factors that increase conduction velocity

A
  1. Sympathetic stimulation
  2. M2-Muscarinic receptor antagonist
  3. β1-adrenoceptor agonist
  4. Circulating catecholamines
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12
Q

List 5 examples of factors that decrease conduction velocity

A
  1. Parasympathetic stimulation
  2. M2-Muscarinic receptor agonist
  3. β1-blocker
  4. Na+ and Ca2+-channel blockers
  5. Ischemia/hypoxia
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13
Q

SV=?

A

SV=EDV-ESV

Volume of blood ejected in one heartbeat (ml/beat)

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14
Q

What are the six factors that increase EDV?

A
  1. Filling pressure: ↑ Central Venous Pressure (CVP)
  2. Decreased heart rate
  3. Increased Ventricular Compliance
  4. Increased atrial contractility
  5. Increased aortic pressure
  6. Pathological conditions
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15
Q

Explain how an increase in central venous pressure increases EDV

(2 main ways)

A

a. Decreased venous compliance, increased resistance

•Sympathetic venoconstriction

b. Increased thoracic blood volume

•Increased total blood volume
•Increased venous return by
–Increased respiratory activity
–Increased skeletal muscle pump activity
–Gravity (e.x.: head-down tilt)
–Increased CO

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16
Q

What is the result of increased filling pressure? (go through the steps that lead to increased EDV)

A

•↑ VR -> ↑ atrial filling pressure -> ↑ atrial pressure -> ↑ ventricular filling pressure ->↑ EDV

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17
Q

Describe how a decreased heart rate increases EDV

A

–↑ filling time -> ↑ EDV
–Relatively longer time in diastole vs. systole

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18
Q

How does Increased Ventricular Compliance increase EDV?

A

–↑ chamber filling volume (EDV) at a given filling pressure
↑ ventricular relaxation rate

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19
Q

What causes Increased atrial contractility? How does this increase EDV?

A

–Sympathetic stimulation
–Increased ventricular filling (EDV) from atria

20
Q

How does Increased aortic pressure increase EDV? Is this recommended as a stratagem?

A

–Increased afterload
–Increased ESV, decreased SV
–2° increase in preload for next cycle
–Not a “good” way to increase EDV

21
Q

Pathological conditions are capable of increasing EDV, what was discussed in class on this topic?

A

–Systolic failure
–Valve defects: aortic stenosis, aortic regurgitation
•Pulmonary valve stenosis & regurgitation (RV preload)

22
Q

Describe thefollowing 6 factors that result in decreased EDV…

  1. decreased filling pressure (CVP)
  2. Increased heart rate
  3. Decreased atrial contractility
  4. Decreased afterload
  5. Diastolic failure
  6. Mitral or tricuspid valve stenosis
A
  1. Decreased Filling Pressure (CVP)

–Decreased blood volume (Ex: hemorrhage)
–Gravity: venous pooling in the L.E. during standing

  1. Increased heart rate

–↓ filling time à ↓ EDV
–Shorter time in diastole

  1. Decreased atrial contractility

–Atrial arrhythmias (Ex: atrial fibrillation)
–May only impact EDV if combined with existing pathology

  1. Decreased afterload

–Increased ejection
–Decreased ESV, 2° decrease in EDV next cycle

  1. Diastolic failure

–Decreased ventricular compliance
•Pathologic ventricular hypertrophy or impaired relaxation (lusitropy)

  1. Mitral or tricuspid valve stenosis

–Decreased ventricular filling

23
Q

Define afterload

What is the direct measure?

What are the two indirect estimates?

A

The force opposing ventricular ejection (systolic pressure)

–Direct measure: maximum systolic ventricular pressure
–Indirect estimates:
•LV: aortic pressure (mean systemic arterial pressure)
•RV: pulmonary a. pressure (mean pulmonary arterial pressure)

24
Q

If you increase afterload, then a greater proportion of systole is spent in what phase?

A

isovolumetric contraction phase

25
Q

How can you increase the force production of cardiac muscle by motor-unit recruitment or twitch summation?

A

You can’t

26
Q

Slope of relationship between ESV and end-systolic LV pressure is an indicator of what?

The lower the ESV at a given pressure, the…

A

contractility

greater the contractility

27
Q

Activation of β1-adrenergic receptors on atrial and ventricular contractile myocytes has what effect on contractility?

For the bonus point, describe the pathway by which this is accomplished.

A

↑ Ca2+ availability -> ↑ contractile force -> ↑ CO

  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
  4. ↑ ECF Ca2+ influx, ↑ SR Ca2+ stores over time
28
Q

Describe how the effects of these inotropic agents…

  1. Adrenergic agonists (β1)
  2. Cardiac glycosides (digitalis derivatives)
  3. Decreased ECF [Na+]
  4. Increased ECF [Ca2+]
  5. Increased HR
A

All - ↑ Contractility

  1. Adrenergic agonists (β1) = ↑ Contractility

–Catecholamines (epinephrine, norepinephrine)

  1. Cardiac glycosides (digitalis derivatives)

–Inhibit Na+/K+ ATPase -> ↑ [Na+]i
–↓ Na+ gradient -> ↓ Na+/Ca2+ exchanger pump
–↓ Ca2+ extrusion -> ↑ [Ca2+]i

  1. Decreased ECF [Na+]

–↓ Na+ gradient -> ↓ Na+/Ca2+ exchanger pump
–↓ Ca2+ extrusion -> ↑ [Ca2+]i

  1. Increased ECF [Ca2+]
    a. ↑ [Ca2+]o -> ↑ Ca2+ influx (L-type Ca2+ channels) during AP à ↑ [Ca2+]i
    b. ↑ Ca2+ gradient -> ↓ Na+/Ca2+ exchanger pump
  • Decreased exchange of external Na+ for internal Ca2+
  • Decreased Ca2+ extrusion -> ↑ [Ca2+]i
  1. Increased HR

–Staircase phenomenon (Bowditch effect)
–Increased APs -> Ca2+ influx per unit time -> ↑ [Ca+]i–↑ [Ca+]i -> ↑ phospholamban phosphorylation -> ↑ SERCA2 activity -> ↑ Ca2+ storage for subsequent release

29
Q

What is the Anrep effect?

A

Increased inotropy due to increased afterload (observed experimentally)

–Partial compensation for ↑ ESV and ↓ SV due to ↑ afterload
–Otherwise, likely greater SV reductions would be observed

•Independent of innervation (intrinsic effect)

30
Q

How do muscarinic agonists (M2) affect contractility?

A

–Acetylcholine: ultimately ↓ adenylyl cyclase, PKA -> ↓ [Ca2+]i
–Opposite effect of β1 signaling

31
Q

How does Decreased ECF [Ca2+] impact contractility?

A

a. ↓ [Ca2+]o à ↓ Ca2+ influx via L-type Ca2+ channels during AP ↓ [Ca2+]i
b. ↓ relative Ca2+ gradient à ↑ Na+/Ca2+ exchanger

  • Increased exchange of external Na+ for internal Ca2+
  • ↑ Ca2+ extrusion à ↓ [Ca2+]i
32
Q

How do Ca2+ channel blockers impact contractility?

A

–Inhibition of L-type Ca2+ channels ->↓ Ca2+ influx during AP plateau -> ↓ [Ca2+]i

33
Q

What is the impact of increased ECF [Na+]?

A

–↑ Na+ gradient -> ↑ Na+/Ca2+ exchanger pump
–↑ Ca2+ extrusion -> ↓ [Ca2+]i

34
Q

Decreased affinity of troponin for Ca2+ has a negative inotropic action, what is an example of this?

A

↓ pH (acidosis)

35
Q

What is lusitropy?

A

Rate of relaxation

36
Q

What are two ways to increase lusitropy?

(Hint, both are β1-adrenergic agonists)

A
  1. Phosporylation of phospholamban (SERCA inhibitor)

–Removes phospholamban’s inhibition of SERCA -> promotes accelerated Ca2+ sequestering -> reduces Ca2+ available for binding with troponin

  1. Phosphorylation of Troponin I

•Enhances dissociation of Ca2+ from Troponin C

37
Q

If Dr. Montemayor asked us how one decreases the rate of relaxation you might respond with?

A
38
Q

But seriously, If Dr. Montemayor asked us how one decreases the rate of relaxation, what would you answer?

A

–Elevated Ca2+ levels
–Impaired SERCA
–Increase affinity of troponin C
–pH changes

39
Q

Positive inotropy and lusitropy increase diastolic function and SV for a given heart rate by?

A

Decreasing relaxation time and increasing force of contraction

40
Q

Summarize the effects of the sympathetic NS on HR, contractility and relaxation rate.

A

• ↑ HR

− ↑ conduction

  • ↑ contractility
  • ↑ relaxation rate
41
Q

List all formulas you can for CO!

A

CO = MAP/TPR = (DBP + (SBP-DBP)/3)/TPR = (O2 consumption)/([O2]arterial - [O2]venous) = HR * SV

42
Q

What is the formula for Pulse Pressure?

A

PP = SBP - DBP

43
Q

What is the formula for stroke volume?

A

SV = EDV - ESV

44
Q

What is the formula for the ejection fraction?

A

EF = SV/EDV

45
Q

What is the formula for net filtration pressure?

A

NFP = (Pc + πIF) – (πc + PIF)

46
Q
A

Cardiovascular I (18 decks)

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