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Physiology Winter 2012 > Physiology 12.5.12 Regulation of Cardiac Contraction > Flashcards

Physiology 12.5.12 Regulation of Cardiac Contraction Flashcards

1
Q

Characteristics of Cardiac Muscle (general- 7)

A

Functions as a synctium

Intercalated disks (gap junctions, connexons)

Very rich in mitochondria- continuous supply of ATP for contraction

Rich capillary supply- about one capillary per fiber-short diffusio distance for oxygen ,CO2, substrates, waste products

T-tubular system- importatnt in excitation-contraction coupling, ready acceess to interstitial flulid

network of SR- regulates intracelular Ca

Presence of SR-T tubule junction

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2
Q

When does Ca enter the cell>

A

during the PLATEAU PHASE of the cardiac AP

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3
Q

What deos Ca release trigger?

A

triggers release of additional Ca from the SR

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4
Q

What happens to Ca that is released from SR

A

Ca binds to Troponin C, leading to contraction of myofibrils

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5
Q

What happens to Ca during resting phase to lead to relaxaction

A

SR begins to pump Ca into SR via Ca-ATPase (causing relaxation)

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6
Q

What is Phospholambam

A

It nroamlly inhibits Ca-ATPase activity.

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7
Q

What do catecholamines lead to (what pathway)

A

increase and AC –> Increase in cAMP –> increases in cAMP-PK

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8
Q

What deos caMP phosphorylate

A

Phosphorylates Ca cahnnels (more Ca entry) adn phospholamban (relieving the inhibition of ATPase and producing more and faster Ca uptake by SR)

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9
Q

What does increase in cAMP lead to?

A

leads to

  1. increased speed of contraction
  2. Increased speed of relaxation
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10
Q

What do cardiac glycosides do?

A

They inhibit Na-ATPase (Na pump) and elevate intracellular Na

This reduces Na influx and Ca extrusion via Va/Ca exchange, resulting in elevated intracellular Ca

Inhibition of Na pump leads to increased CONTRACTILITY

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11
Q

What is an example of Cardiac Glycoside? What is is used to treat?

A

DIGOXIN

used to treat heart failure

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12
Q

What is Cardiac Output

A

Heart Rate x SV

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13
Q

What are intrinsic factors/regulation that affect heart (3)

A

Contraction of denervated heart

Starling’s Law

Rate-induced Regulation

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14
Q

What are extrinsic factors/regulations that affect herat (4)

A

Nerve control of heart beat

Sympathetic

parasympathetic

other hormones (O2, CO2, pH)

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15
Q

What happens when Phospholamban in phosphorylated (by increase in cAMP by catecholamines)

A

increase Ca ATpase activity –> Ca enters SR faster –> increase velocity of muscle relaxation

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16
Q

What can incerase cardiac contractility

A

Beta adrenergic agonist–> increase Ca in cell –> cardiac glycosides increase force of contraction)

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17
Q

What is the Frank-Starling’s law of the heart

A

Tension developed by heart is dependent on preload (or the end-diastolic volume or length of the tissue)

The greater the length (i.e. caused by stretch) ,the greater the tension

no neural input needed

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18
Q

Rate-induced increase in the force of contraction (intrinsic)

A

demonstrate changes in the F of contraction produced by changes in heart rate

In each case, underlying mechanism invovles chagnes in intracellular Ca concentration

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19
Q

What is the staircase or Treppe phenomenon?

A

i.e. exercise, HR and Contractility increase togethr.

It is important to note that increasing the HR increases the F of contraction independently of any simultaneous beta adrenergic-induced increase in contractiltiy.

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20
Q

How does increasing the HR increase the force of contraction (2 mechanisms- Ascending or positive Staircase)

A
  1. More rapid heart rate means more plateaus (phase 2 of cardiac cycle AP) per unit time, and Ca2+ enters cell every plateau
  2. If HR is suddenly increased, magnitude and duration of inward Ca current increase with each AP until new steady state is acheved. These mechanimss elevate intracellular Ca2+ that is available to the contractile proteins –hence a greater F of contraction (baseline Tension increase)
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21
Q

Why is it th 1st beat smaller?

A

when Incerase frequency, 1st beat smaller due to pre-mature contraction (not as much Ca to pump heart)

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22
Q

What is Premature Contraction and Post-extrasystolic potentiation

A

When a premature extra-systole occurs, F developed by the ventricle is smaller than normal and F developed during the subsequenct contraction is greater than normal (post-exxtra-systolic potentiation)

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23
Q

What causes the diminished force of premature contravtion

A

involves Frank-starling mechanism

Premature contraction occurs when resting fiber length was smalle (incomplete filling had occured)

Post

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24
Q

What causes the augmented contraction of post-extra-systolic contraction

A

Post-extra-systolic contraction occurs whent eh resting fiber was especially long (extra filling had occurred during the COMPENSATORY PAUSE)

25
Q

What can explain the weak premature contraction

A

When premature contraction cocurred- smaller than normal amt of Ca was released from SR since it takes about 500 msec for all of the Ca released during, and taken up after, the previous contraction to again become available for release

26
Q

Why is postextrasystolic contraction larger than normal

A

pool of releasable Ca is greater than normal, b/c Ca in SR had accumulated ruign last two heartbeats

27
Q

What is PVC

A

premature ventricular contraction

most common ventricular arrythmias
sensation of skipped beat, pauses, or palpitation

28
Q

What happens to HR after a carotid massage

A

carotid massage stimulates barorecepotr and produces increased Vagal Activity, leading to temp cessation of heart beat

29
Q

What does the heart beat look like after temporary cessation after carotid massage

A

the following heart beat after cessation shows greater force of contraction

this is due to changes in the availability of Ca2+ to teh contractile proteins

30
Q

Where does Sympathetic Nervous control come from (part of spine)- EXTRINSIC CONTROL

A

Stellate ganglia

Middle cervical ganglia

postganglionic neuron -NE

31
Q

What does PS

A

dorsal motor nucleus

nucleus amiguus (in the medulla)

postganglionic neurons- ACh

32
Q

What does the sympathetic NS innervate

A

all segments of the heart, pacemaker, conduction, and contractile cells

33
Q

What is the effect of sympathetic stimulation on heart

A

Increase frequency of contract ion (in HR)

increase velocity and speed of depol through heart (I funny)

Increase contractility of heart (Ca channels phosphorylated, inc Ca)

34
Q

How does sympathetic innervation affect AP graph

A

increase rate of rise of Phase 0

increase rate of repolarization of Phase 3 of pacemaker AP

Duration of systole is shorter

Shortening of Phase 4 (ventricular AP), shortens duartion of diastole

35
Q

What is the result of a simulataneous blockade of both PS and Sympathetic input to heart

A

resutls in rapid heart rate (~100 beats/min)

36
Q

What is Atopine? Function?

A

a muscarinic cholinergic antagonist (ACh blocker)

causes heart rate to increase consdierably

37
Q

What s Propanolol

A

Beta-1 adrenergic antagonist

decreases HR only slightly

38
Q

Does PS or Symp influence normal Heart Rate more?

A

In normal humans the intrinsic heart rate (~100 beats/min) is noramlly being restrained by PS (vagal) suppression

39
Q

What does increases arterial lead to (in terms of HR)

A

leads to decreased HR

40
Q

What is the Baroreceptor Reflex

A

Decrease in HR due to High ARTERIAL PRESSSURE

41
Q

Where are BaroR located

A

located at the bifurcation of internal and external carotid arteries where nerve endings can sense the pressure of teh artery

BaroR also locaetd in Aortic Arch. Here sigal is carried by vagus nerve to brainstem area

42
Q

What do ChemoR detect

A

sense arterial O2 pressure , and also located in same region as BaroR

43
Q

What does increase in arterial P do to sinus nerve?

A

causes sinus nerve to fire more requently

Singal is then carreid to glossopharyngeal nerve (CN #9) to meduall where CV control center is located

44
Q

What are consequences of Incrase in sinus pressure ()

A
  1. Increase vagal activity (decrease HR)

2. Decrease Sympathetic activity

45
Q

What is the Brainbridge reflex?

A
  1. Acceleration of HR by increase Right ATRIAL Pressure

2. Due to stimulation of atrial R

46
Q

What is a respiratory (sinus) arrythmia

A

in healthy indidivuals, lthe HR is Faster during inspiration than experiation

R-R is closer during inspiration

47
Q

Why is heart rate faster during inspriation (2 reasons)

A
  1. Increases venous return - increases HR (Brainbridge refelx)
  2. Decreases return of blood to left herat, decreases SV and reduces Arterial blood pressure0 increases HR (BaroR relex)

symp activity increases and vagal activity decreases

48
Q

What happens during expiration

A

vagal activity inc

sympathetic act decreases

49
Q

What is the clinical sign of absence of sinus arrythmia

A

Clinical sign of deterioration of ANS

i.e. sinus arrhythmia disappears in neuropathy that develops in some long-term diabetes

50
Q

What is the Valsalva maneuver?

A

Maneuver in which a person tires to exhale forcibly with a closed glottis (windpipe) so taht no air exits through mouth or nose

This impedes return of venous blood to heart

51
Q

What are examples of Valsalva maneuver

A

Stenuous coughing
Straining during a bowel movement
lifting a heavy weight

52
Q

How many phaes does normal response to Valsalva maneuver

A

4

53
Q

What is phase 1 of Valsalva maneuver

A

Squeezing lung forces blood out of lung into left atrium causing a mild rise in SV–reflex mechanism would decrease HR intially

54
Q

What is phase 2 of Valsalva maneuver

A

Venous return to right heart is reduced due to squeezing of the lung (pressure inside chest is increased)

This causes a fall in SV and CO–reflex mechanism would then incereas Symp NS activity increasing HR

55
Q

Phase 3 Valsalva

A

Upon termination of maneuver, P on chest is released. This allows lung to hold more blood and temporarily reduces left ventricular return and SV–reflex mechanism would increase HR slightly

56
Q

Phase 4

A

Venous return to right heart inc adn CO begins to inc.–HR returns to normal

57
Q

What does deviation from Valsalva maneuver signify

A

indicate abnormal heart funciton or abnromal ANS input to heart

58
Q

What are efects of Hypoxia, Inc CO2, and low pH?

A

Directly Decrease HR

through chemoreceptors and ventialtion increase HR

Physiology Winter 2012 (10 decks)

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