Lecture 30: Heart Control Flashcards

1
Q

Cardiac output (Q) averages

A
  • At rest: 4-6 L/min in average adult
  • Strenuous exercise: 15+ L/min
  • Increases occur with minimal changes in blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cardiac output is determined by 2 parameters

A
  • Stroke volume
  • Heart rate
  • Both intrinsic and extrinsic mechanisms can alter parameters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Normal adult heart rate

A
  • About 70 beats/min
  • Much higher in children
  • Sleep decreases heart rate by 10-20 beats/min
  • Anxiety, activity and exercise increase it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Heart rates of well-trained athletes

A
  • Lower resting heart rates
  • About 50 beats/min
  • Resting cardiac outputs are the same for sedentary and well-trained athletes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Intrinsic factors altering heart control

A
  • Relatively minor importance, evokes subtle effects
  • Atrial stretch (distension)
  • Temperature
  • Ionic Changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Atrial stretch or distension (intrinsic)

A
  • Stretch of SA node pacemaker cells
  • Increase excitability
  • Increases HR by 15%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Temperature (intrinsic)

A
  • Increase in temperature increases HR by increasing ionic permeabilities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ionic changes (intrinsic)

A
  • Alterations in electrolyte balance
  • Particularly K+ and Ca2+
  • Effects excitability of pacemaker cells
  • High Ca2+o or high K+o decreases HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Extrinsic control of the heart

A
  • Neurohormones
  • Sympathetics
  • PNS
  • Bainbridge reflex
  • Baroreceptor reflex
  • Higher center control
  • Respiratory
  • Chemoreceptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Sympathetics (extrinsic)

A
  • Accelerate

- Norepinephrine effects on SA node

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

PNS (extrinsic)

A
  • Decelerate

- Acetylcholine effects on SA node

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

Bainbridge reflex

A
  • Stretch of atrial receptors in veno-atrial junctions of left and right heart
  • Sensory impulses via vagus to cardiovascular center
  • Increase sympathetic and decrease parasympathetic output to heart
  • Therefore, an increase in HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bainbridge reflex stretching

A
  • Accounts for 50-60% of stretch effect (along with SA nodal stretch effect)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Baroreceptor reflex relationship

A
  • Inverse relationship between blood pressure and heart rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In hypotension, such as that induced by hemorrhage, in response to the loss of a moderate amount of blood,

A
  • Vagal tone diminishes
  • Sympathetic activity increases
  • Vagal activity ceases after BP declines to 20-30 mmHg below normal level
  • Further acceleration of heart in response to declines in BP is mediated exclusively by increases in sympathetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Higher center control (extrinsic)

A
  • Cerebral cortex, hypothalamus, thalamus
  • First two play roles in HR changes seen in excitement, anxiety
  • Hypothalamic responses seen with temperature changes
17
Q

Cortical and diencephalic centers

A
  • Initiate cardiovascular reactions that occur during excitement, anxiety, and other emotional states
  • Also during certain febrile disease states
18
Q

Respiratory (extrinsic)

A
  • Increase HR during inspiration
  • Decrease HR during expiration
  • Changes more pronounced in children
  • Mediated via stretch receptors in lungs, via changes in venous return (i.e. Bainbridge reflex and baroreceptor reflex)
19
Q

Chemoreceptors (extrinsic)

A
  • Stimulation of receptors produces slight effects on HR
  • Primary reflex effect of carotid chemoreceptor stimulation on SA node is inhibitory
  • Secondary effects via changes in pulmonary ventilation (small increase, small increased HR; large increase, marked increased HR)
20
Q

Hormones (extrinsic)

A
  • Epinephrine (like sympathetic norepinephrine) produces a positive chronotropy
  • Atrial natriuretic peptide (ANP), produced by atrial cells when stretched, affects blood volume, but probably has no effect on heart rate
21
Q

Stretch effect (intrinsic control of SV)

A
  • Starling’s Law of Heart (heterometric autoregulation)

- In simple terms cardiac output matches venous return

22
Q

Increased venous return in Starling effect leads to an increase in

A
  • EDV
  • Stretch of ventricular fibers (increased sarcomere length)
  • Force of contraction
  • SV
23
Q

Stretch effect is measured in

A
  • Heart lung preparation
  • Family of ventricular function curves are used as other parameters are changed
  • These other parameters are related to changes in contractility (inotropism)
24
Q

Changes in contractility

A
  • Inherent changes due to alteration of Cai, Ki, other ions
25
Q

Homeometric autoregulation

A
  • Pressure induced (Anrep effect)
  • Increase in afterload
  • Decrease in SV
  • Seen only at blood pressures above 160 mmHg
26
Q

Rate induced changes

A
  • Treppe/staircase
  • After period of rest
  • Ventricle responds to repetitive stimulation by increase in force of contraction
27
Q

Alteration of blood gases

A
  • Decreased Po2
  • Increased Pco2
  • Decreased pH
  • Last two probably via decrease in pHi (since acidosis of cardiac muscle depresses contractility)
28
Q

Inhibitory interactions between vago-sympathetic divisions

A
  • Direct and indirect vagal effects via sympathetic inhibition
29
Q

Increase in cyclic GMP causes

A
  • Decrease SV (direct)
30
Q

Decrease in cyclic AMP causes

A
  • Decrease SV (indirect)
31
Q

Increase in cyclic GMP due to

A
  • Increased breakdown of cyclic AMP
32
Q

Presynaptic inhibition of sympathetic terminals by vagal terminals effects

A
  • ACh from vagal terminals inhibits sympathetic NE release
33
Q

Presynaptic inhibition of parasympathetic terminals by sympathetic terminals effects

A
  • NPY from sympathetic terminals inhibits vagal ACh release