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CVS & IBL - Physiology 🫁 > L1: Properties of the cardiac muscle > Flashcards

L1: Properties of the cardiac muscle Flashcards

1
Q

What are the properties of cardiac fibers?

A

rhythmicity, excitability, conductivity and contractility

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2
Q

What is the definition of rhythmicity?

A

The ability of cardiac fibers to give regular impulses (action potentials) causing the heart to beat regularly.

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3
Q

What is the origin of rhythmicity?

A

Myogenic (not neurogenic; nerves do not initiate it but control it).

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4
Q

What is the evidence that rhythmicity is myogenic?

A

The transplanted heart (no nerve supply) continues to beat.

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5
Q

What has the fastest rhythm?

A

SAN has the fastest rhythm (so, it is the pace maker of the heart).

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6
Q

What is the self-excitation of SAN due to?

A

Natural leakiness of the membrane to Na+

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7
Q

What is the rhythmicity of SAN, AVN, Bundle tissues, Purkinje fibers, and ventricles respectively?

A

Rhythmicity without vagus 120 / min

90 / min

45 / min

35 / min

25 / min

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8
Q

What is the mechanism of rhythmicity of SAN? (SAN action potential)

A
  1. Na influx through funny (If) slow Na channels, Ca influx through T (transient) Ca channel, decreased K efflux → membrane potential changes gradually from - 55 mV (resting) to - 40 mV. This is called Phase 4 (Pacemaker potential = pre-potential = diastolic depolarization (DD)).
  2. Ca influx through L (long-lasting) (Ica) Ca channels → membrane potential changes from – 40 mV (firing or threshold level) to + 10 mV. This is Phase 0 (Upstroke phase.
  3. K efflux (Ik) → membrane potential returns to - 55 mV (resting). This is Phase 3 (Repolarization).
  4. Then, the process is repeated throughout life.
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9
Q

What is the reason for the changing of the membrane potential from (-55mv) to (-40mv) in SAN action potential?

A

Na influx through funny (If) slow Na channels, Ca influx through T (transient) Ca channel, decreased K efflux

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10
Q

What is the reason for the changing of the membrane potential from (-40mv) to (+10mv) in SAN action potential?

A

Ca influx through L (long-lasting) (Ica) Ca channels

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11
Q

What is the reason for the changing of the membrane potential from (+10mv) to (-55mv) in SAN action potential?

A

K efflux (Ik)

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12
Q

What is the excitability of cardiac fibers?

A

The ability of cardiac fibers to respond to an adequate stimulus (to generate action potentials).

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13
Q

What is the ionic basis of action potential (AP) of cardiac muscle?

A
  1. Rapid Depolarization (Phase 0):
    - Opening of fast Na channels → rapid Na influx → membrane potential changes from - 85 (resting) to + 20 mV (overshoot) (total voltage of AP = 105 mV)
  2. Early Fast Partial Repolarization (phase 1):
    - Due to: K efflux & Inactivation of fast Na channels.
  3. Slow Prolonged Plateau (Phase 2):
    - The membrane remains depolarized (for 150 msec in atrial muscles & 300 msec in ventricular muscles) due to: slow Ca influx & decreased K efflux
  4. Rapid Repolarization (Phase 3) due to: increased K efflux & closure of Ca channels.
  5. Complete Repolarization to resting membrane potential (Phase 4):
    - The Na-K pump derives excess Na out and excess K in.
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14
Q

What causes rapid depolarization in cardiac muscle AP?

-85mv to +20mv

A

Opening of fast Na channels

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15
Q

What causes early fast partial repolarization in cardiac muscle AP?

A

K efflux & Inactivation of fast Na channels.

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16
Q

What causes the slow prolonged plateau in cardiac muscle AP?

A

slow Ca influx & Decreased K efflux

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17
Q

What causes rapid repolarization in cardiac muscle AP?

A

Increased K efflux & closure of Ca channels.

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18
Q

What is the function of the Na-K pump in cardiac muscle AP?

A

derives excess Na out and excess K in.

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19
Q

What is the conductivity of cardiac muscle fibers?

A

The ability of cardiac fibers to conduct excitation waves from one part of the heart to another.

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20
Q

What is the value of atrial conduction?

A

0.4 m/sec

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21
Q

From where to where does action potential travel in atrial conduction and what does it travel through?

A

The action potential travels from the SAN into the atria and to the AVN through:
- Atrial mass & Internodal bundles (Anterior, middle, and posterior).

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22
Q

What is the value of AV nodal conduction?

A

Velocity = 0.04 m/sec.

Total delay: 0.16 sec

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23
Q

What are the causes of slow conductivity in AVN?

A

the small size of fibers & few gap junctions.

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24
Q

What is the significance of AVN delay?

A
  • Gives time for atria to empty blood into ventricles.

- Protects ventricles from high pathological atrial rhythms.

25
Q

What is the value of Purkinje fibers conduction?

A

Velocity: 4 m/sec

26
Q

What are the causes of high velocity in conduction in Purkinje fibers?

A

large fibers & high permeability of gap junctions.

27
Q

What is the significance of high-velocity conduction in Purkinje fibers?

A

immediate transmission of cardiac impulse in the ventricles.

28
Q

What is the contractility of cardiac fibers?

A

The ability of the muscle to do mechanical work (contraction & relaxation).

29
Q

What are the steps of contraction of cardiac fibers? (Excitation-contraction coupling)

A

Action potentials pass over the muscle fiber membrane → spread to the interior along the transverse (T) tubules → open Ca++ channels → inc. entry of Ca++ into the sarcoplasm → act on the longitudinal sarcoplasmic reticulum (SR) → inc. release of Ca++ into the sarcoplasm → Ca++ bind to troponin → sliding between actin & myosin filaments → muscle shortening (contraction).

30
Q

What are the sources of calcium for myocardial contraction?

A

ECF: via Ca channels in the cell membrane & down the T tubules

S.R: via calcium-induced calcium-release.

31
Q

What does the force of contraction depend on?

A

the concentration of Ca++ in extracellular fluids

32
Q

What are the ionic reasons for the relaxation of cardiac muscle fibers?

A

Stoppage of Ca++ influx & pumping back of Ca++ from the sarcoplasm into SR & ECF via Ca++ pumps & Na+ Ca++ exchangers.

33
Q

What is a statement of starling law?

A

“Within limit, the greater the initial length of the cardiac muscle fiber, the greater the force of contraction”.

34
Q

What is the initial length of the cardiac fibers determined by?

A

diastolic filling (end-diastolic volume = EDV).

35
Q

How does EDV affect the force of contraction?

A

Inc. venous return (e.g., muscle exercise) → inc EDV (filling) → stretch of the muscle → inc the force of contraction

36
Q

What is the significance of increasing the force of contraction of cardiac muscle fibers in response to high venous return?

A

prevents stagnation of blood in the CVS.

37
Q

What happens in cases of overstretching concerning cardiac muscle fibers?

A

Dec. Contractility

38
Q

What is the nature of Starling law?

A

Myogenic

39
Q

What time does mechanical response take in relation to action potential?

A

1.5 times as long as AP.

40
Q

When does Contraction begin in relation to AP?

A

just after the start of depolarization

41
Q

When does contraction reach maximum in relation with action potential?

A

BY the end of plateau.

42
Q

When does relaxation begin in relation to action potential?

A

AT the end of plateau.

43
Q

When does Relaxation reach its med?

A

When RP is complete

44
Q

What are the excitability changes during action potential?

A

Absolute refractory period (ARP)

Relative refractory period (RRP)

Supernormal phase

45
Q

What is the excitability in ARP, RRP, and supernormal phase respectively?

A

Zero

Gradually increase

Above normal

46
Q

What is the stimulation in ARP, RRP, and supernormal phase respectively?

A

No response, whatever the strength of the 2nd stimulus

Strong stimulus → weak contraction

Weak stimulus → Strong contraction

47
Q

When do ARP, RRP, and supernormal phase occur respectively?

A

Rapid depolarization & plateau = Contraction

Rapid repolarization = 1st half of relaxation

At the end of AP = 2nd half of relaxation

48
Q

What is the effect of ARP, RRP, and supernormal phase respectively?

A

Prevents tetanus (continuous contraction)

Null

May cause extrasystole

49
Q

What are the Factors affecting rhythmicity (chronotropic), excitability (bathmotropic), conductivity (dromotropic), and contractility (inotropic)?

A

1- Nervous: Sympatyhaeic, Parasympathetic

2- Physical: Warming, Cooling, and Excessive warming/cooling

3- Chemical: Drugs and Hormones, Blood gases, Ions and typhoid/bacteria toxins

50
Q

How does the sympathetic nervous system affect cardiac properties?

A
  • Sympathetic → noradrenaline → inc Na influx → rapid depolarization → inc rhythmicity, excitability & conductivity.
  • Sympathetic → B1 adrenergic receptors → inc Ca influx → inc contractility of all cardiac muscles.
51
Q

How does the parasympathetic nervous system affect cardiac properties?

A
  • Basal parasympathetic discharge (vagal tone) to atrial structures only → acetylcholine → inc K efflux → hyperpolarization (inhibition)→ dec rhythmicity (of SAN from 120 → 70 /min), excitability & conductivity.
  • Strong vagal stimulation can stop rhythmicity, excitability & conductivity in atrial structures only. “Like in shocks”
  • Parasympathetic stimulation → muscarinic receptors → dec Ca influx → dec contractility of atrial muscle only.
52
Q

How does warming (fever) affect cardiac properties?

A
  • Moderate warming (fever) → inc ionic fluxes across the membrane → inc rhythmicity (10 beats/1°F), excitability, conductivity, and inc contractility (due to Increased metabolic reactions, Ca influx, and decreased viscosity).
53
Q

How does moderate cooling affect cardiac properties?

A
  • Moderate cooling: opposite effects to moderate warming.
54
Q

How does excessive cooling or warming affect cardiac properties?

A
  • Excessive warming or cooling → cardiac damage → stop the heart.
55
Q

How do drugs or hormones affect cardiac properties?

A
  • Catecholamines, Thyroxine, xanthene-derivatives (theophylline & caffeine) → inc all cardiac properties.
  • Cholinergic → dec all cardiac properties.
56
Q

How do blood gases affect cardiac properties?

A

Decreased O2: Mild hypoxia → inc rhythmicity, excitability, conductivity, and dec contractility “due to fatigue”

Increased CO2 (hypercapnia) → inc H+ (acidosis = dec pH) → dec rhythmicity, excitability, conductivity, and contractility (dec affinity of troponin to Ca)

57
Q

How do ions affect cardiac properties?

A
  • increased K+ (hyperkalemia) → dec K efflux → prolong repolarization → dec all cardiac properties. Marked K increase → stop the heart in diastole (irreversible
    relaxation)
  • increased Ca++ (hypercalcemia) → increases K efflux → hyperpolarization → dec rhythmicity, excitability, conductivity, and inc contractility. Marked Ca increase → stop the heart in systole (calcium rigor = irreversible contraction).
58
Q

How do typhoid or diphtheria toxins affect cardiac properties?

A

Dec rhythmicity, excitability, conductivity, and contractility (direct inhibition).

“However other organisms that cause fever increase cardiac properties due to warming”

CVS & IBL - Physiology 🫁 (12 decks)

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