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104 > Cvs > Flashcards

Cvs Flashcards

1
Q

Automaticity

A

initiate contraction independent of external stimuli

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2
Q

Rhythmicity

A

regular beats

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3
Q

Automaticity and Rhythmicity cause

A

Due to presence of Pacemaker cells → generate spontaneous & regular action potentials.

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4
Q

pacemakers their charge speed

A

SAN cells (90-105/min Normal pacemaker (fastest)→ o Vagal tone →↓ SAN rate
• AV node cells (60/min) in failure of SAN
• Purkinje cells (40/min) in failure of AVN. (idioventricular rhythm)

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5
Q

pacemakers their charge speed and define

A

SAN cells (90-105/min Normal pacemaker (fastest)→ o Vagal tone →↓ SAN rate
• AV node cells (60/min) in failure of SAN
• Purkinje cells (40/min) in failure of AVN. (idioventricular rhythm)

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6
Q

slow response action potential phase 4 name and define

A

Pre polarization
At – 60 mv:
A- Opening of funny Na+ channels→Causes inward Na+ (HCN?)
B- Activation of Na+-Ca++ exchanger due to spontaneous release of Ca++ from SR
• → move 1 Ca++ out for 3 Na+ in → Causes inward Na+
At -50 mv: Opening of T-type Ca++ channels →Cause inward Ca++

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7
Q

slow response action potential phase 4

A

Prepotential
At – 60 mv:
A- Opening of funny Na+ channels→Causes inward Na+ (HCN?)
B- Activation of Na+-Ca++ exchanger due to spontaneous release of Ca++ from SR
• → move 1 Ca++ out for 3 Na+ in → Causes inward Na+
At -50 mv: Opening of T-type Ca++ channels →Cause inward Ca++

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8
Q

slow response action potential phase 0 name and define

A

Depolarization
At -40 mV = firing level
1. Closure of funny channels & T-type Ca++ channels
2. Opening of L-type Ca++ channels Causes inward Ca++ current→ cause slow depolarization 3. Gradual opening of DRK+ channels

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9
Q

slow response action potential phase 3

A

Repolarization
1. Opening of DRK+ channels →cause outward K+
2. Closure of L-type Ca++ channels
3. Repolarization to -60 mV→ cause inactivation of K channel & Activation of funny channel

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10
Q

Factors affecting rate of SA nodal discharge= chronotropy= heart rate (rhythmicity) sympathetic

A

Mechanism:
✓ Sympathetic (norepinephrine)
✓ Bind β1 receptors →↑ c-AMP →
✓ ↑ funny current
1. Earlier depolarization starts earlier
2. ↑slope of phase 4.
Reach threshold in shorter time

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11
Q

Factors affecting rate of SA nodal discharge= chronotropy= heart rate (rhythmicity) para sympathetic

A

Mechanism:
✓ Vagus (acetylcholine)
✓ Bind muscarinic receptors →↓ c-AMP→ ✓ ↓ funny current.
1. Delayed depolarization
2. ↓slope of phase 4.
Reach threshold in longer time
Acetylcholine activates K+ channels (KAch)

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12
Q

Effect of catecholamines on SA nodal discharge

A

HR inc

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13
Q

Effect of body temp on SA nodal discharge

A

10 (fever) →↑ HR 10 beats/min.

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14
Q

Effect of Ca++ channel blocking drugs

A

↓ HR

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15
Q

Effect of hyperkalemia on SA nodal discharge

A

↑ conductance → ↓ slope of phase 4 → ↓ HR

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16
Q

Velocity of conduction depends on what

A

1- Number of gap junction (↓ conductance ability in hypoxia or ↑free Ca++ )
2- Amplitude & speed of upstroke of A.P.

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17
Q

Factors affecting rate of conduction(Autonomic)

A

Sympathetic→↑ conductance → ↑ velocity

Parasympathetic→dec conductance → dec velocity
, Digitalis→↓ velocity

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18
Q

Cardiac Myocyte Action potential phase 4

A

RMP)
K+ moves out via IRK

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19
Q

Cardiac myocyte phase 0

A

Depolarization from -90 to + 20mv
1. Inactivation of IRK
2. Opening of voltage gated Na+-channels: inward Na+ (Fast response )

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20
Q

Cardiac Myocyte phase 1

A

rapid small
repolarization
1. Closure of voltage gated Na+ channels
2. Opening of special K+ channels 3. Opening of Cl- channels

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21
Q

Cardiac myocyte phase 2

A

Plateau (around zero mV)
200 msec
Balance between
1. Outward positive via DRK+ channels 2. Inward positive via
A- Long lasting Ca++ channels
B- ↑Activity of Na+-Ca++ exchanger: Move 1 Ca++ out for 3 Na+ in

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22
Q

Cardiac myocyte phase3

A

Rapid late repolarization
1. Closure of long-lasting Ca++ & ↓ activity of Na+-Ca++ exchanger 2. Delayed rectifier K+ channels → causes outward K+
As membrane potential approaches RMP:
• Closure of DRK
• ↑Activity of inwardly rectifying K+ channels: →to reach -90 mV

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23
Q

Absolute refractory period (ARP)
Response and phase

A

No response to nay stimulus Cause: inactivation of Na+ ch

Phases 0, 1, 2, and part of phase 3 to -50 mv)

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24
Q

Relative refractory period (RRP) Response and phase

A

Respond to supra- threshold stimulus.

Follows ARP to -75 mv
25
Q

supernormal period response and phase

A

Respond to weaker stimulus → arrhythmias

Follows RRP
to fully repolarization

26
Q

Importance of refractory period

A

Prevents tetanic contractions (not suitable for pumping) As it occupies
whole systole and early diastole

27
Q

Effect of ischemia on electrical activity of the heart

A

Ischemia cause accumulation of K+ in ECF, due to:
A- Opening of KATP channels & Inhibition of Na+-K+ ATPase pump
2. Accumulation of K+ in ECF cause Membrane depolarization
3. Membrane depolarization →↓decreased number of active Na+ channels →↓Slope of phase 0.
4. ↓Slope of phase 0 & ↑intracellular Ca++→↓conduction velocity

28
Q

Relationship between Action potential &mechanical response
• Contraction

A

• Contraction after start of depolarization maximum at end of plateau

29
Q

Relationship between Action potential &mechanical response. Relaxation

A

Relaxation First half with Repolarization (phase 3)

30
Q

Explain Excitation contraction coupling

A

Membrane depolarization → open L-type Ca++ channels
2- Ca++ entry → open ryanodine sensitive- calcium channel on SR “Calcium- induced Calcium release”
3- Ca++ binds Troponin-C →contraction
4- Relaxation via removal of calcium from cytoplasm:
a. SERCA→ actively reuptake Ca++
b. Na+-Ca++ exchanger: move Ca++ out c. Calcium pump
5- Force of cardiac contraction (notropic state) depends mainly on Ca++

31
Q

Explain Excitation contraction coupling

A

Membrane depolarization → open L-type Ca++ channels
2- Ca++ entry → open ryanodine sensitive- calcium channel on SR “Calcium- induced Calcium release”
3- Ca++ binds Troponin-C →contraction
4- Relaxation via removal of calcium from cytoplasm:
a. SERCA→ actively reuptake Ca++
b. Na+-Ca++ exchanger: move Ca++ out c. Calcium pump
5- Force of cardiac contraction (notropic state) depends mainly on Ca++

32
Q

Positive inotropic mechanisms
Sympathetic

A

norepinephrine) or catecholamines → ✓ bind β1 receptors →↑c-AMP→
✓ Activates Protein Kinase → phosphorylates
a. L-type Ca++ channel
b. calcium release channel on SR

33
Q

Negative Inotropic Mechanisms:
Parasympathetic

A

(acetylcholine) →
✓ Bind muscarinic receptors (M2) → ↓c-AMP

34
Q

Positive inotropic mechanisms Drugs

A

Digitalis→ inhibits Na+-K+ ATPase →↑ Na+. Na+-Ca++ exchanger move 3Na+ out for 1Ca++ in. →↑Ca++ inside myocytes.
• Xanthine (caffeine)→ inhibit breakdown of c-AMP→↑c-AMP conc.

35
Q

Negative Inotropic Mechanisms: Drugs

A

• Calcium channel blockers (dihydropyridine) inhibit L-type Ca++ channels →↓ Ca++ entry
• Anesthetic drugs

36
Q

Regulation of Myocyte Relaxation (lusitropy)
1- Sympathetic / catecholamine

A

bind β1 receptors →↑ c-AMP →activate protein kinase
↑Activation of SERCA → rapid removal of Ca++ ↓binding of Troponin to Ca++.

Sympathetic causes strong contraction ad rapid relaxation

37
Q

Regulation of Myocyte Relaxation (lusitropy) Ischemia

A

↓activity of Ca pump →↑ intracellular Ca++→ inhibits relaxation

Myocardial ischemia causes weak contraction and poor relaxation.

38
Q

Effect of changes in afterload:

A

On degree of shortening: (inverse relation). ↓by ↑afterload
B- On velocity: inverse relation

Zero velocity. Maximum velocity (Vmax)
When load ≥ maximum tension When load is zero
(Contraction remains isometric).

39
Q

Effect of changes in inotropic state: positive inotropic

A

On degree of shortening shifts active length-tension relationship upwards and left.
B- On velocity → Shifts load-velocity curve upwards and right→↑ velocity

40
Q

Effect of changes in preload:

A

A-On degree of shortening direct relation
B- On velocity
↑preload → shifts load-velocity curve upwards and right →↑ velocity

41
Q

Effect of ↑frequency: staircase phenomenon” or “treppe”

A

o ↑frequency → ↑ force of contractions till reach plateau o Cause: Ca++accumulation

42
Q

Stroke volume (SV): depend on

A

preload, afterload, inotropic state

43
Q

Changes in HR are more important than changes in SV.

A

Cause: In untrained person, HR ↑100% to 200% during exercise

44
Q

Doubling HR alone from 70 to 140 beat/min
(by artificial pacemaker or arrhythmias) →

A

↓ SV (due to shortening of diastolic time & filling)
→ no change in CO

45
Q

↑HR alone > 150/min→

A

Marked↓ in SV →↓ CO.
(↑HR cannot compensate for ↓in SV)

46
Q

↓HR alone < 60/min→

A

↓ CO
(↑SV cannot compensate for ↓ HR) (Limited capacity)

47
Q

During exercise (in physiology) Doubling HR

A

doubling CO due to ↑ SV

48
Q

Effect of changes in preload on SV and define preload

A

degree of stretching (sarcomere length) before contraction.
• Measured by EDV
• EDV depends on VR.
B- ↑VR→↑ EDV→↑ SV = direct relation = Starling’s law=
“heterometric autoregulation” → matches SV with VR.
C- In pressure-volume loop
• Ventricle start contraction at higher EDV (2a) and reach the same ESV = ↑ width → ↑SV. D-in performance of isolated cardiac muscle
↑preload →↑ amount and velocity of shortening

49
Q

Factors affecting preload:

A
  1. ↑VR (most important factor )
  2. Strong Atrial contraction →↑preload.
  3. ↑Heart rate → ↓diastolic time →↓preload
  4. ↓Ventricular compliance (myocardial infarction) →↑slope of EDVPR→ ↓ preload
    Effect of changes in preload on SV
50
Q

Effect of Afterload on Stroke Volume and define Afterload

A

Afterload= aortic pressure for left ventricle/ pulmonary pressure for right ventricle
➢ ↑afterload → shifts relationship between EDV and SV downward →↓ SV
➢ In Pressure-volume loop:
• Ventricle start contraction at the same EDV and
reach higher ESV = ↓SV
➢ in performance of isolated cardiac muscle:
↑afterload → ↓ amount and velocity of shortening →↓SV

51
Q

Effect of Inotropic State on Stroke Volume

A

➢ + ve inotropic → shifts relationship between EDV and SV upward → ↑SV
➢ In pressure-volume loop:
• + ve inotropic shifts ESPVR upwards & left
• Ventricle start contraction at the same EDV and reach lower ESV
➢ in performance of isolated cardiac muscle: + ve inotropic →↑ amount and velocity

52
Q

End Diastolic Volume =

A

volume of blood at end of diastole.

53
Q

ESV:

A

volume of blood at end of Systole.

54
Q

• Stroke volume:

A

volume of blood pumped by each ventricle/ beat

55
Q

• Cardiac Output :

A

volume of blood pumped by each ventricle /min.
•

56
Q

Cardiac index:

A

CO/ m2

57
Q

Cardiac Output increased in

A

Exercise (700%)
Excitement & anxiety (100%) Pregnancy

58
Q

Cardiac Output decreased in

A

Rapid arrhythmia
Heart failure
standing from supine position

104 (5 decks)

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