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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
What is the value of Purkinje fibers conduction?
Velocity: 4 m/sec
26
What are the causes of high velocity in conduction in Purkinje fibers?
large fibers & high permeability of gap junctions.
27
What is the significance of high-velocity conduction in Purkinje fibers?
immediate transmission of cardiac impulse in the ventricles.
28
What is the contractility of cardiac fibers?
The ability of the muscle to do mechanical work (contraction & relaxation).
29
What are the steps of contraction of cardiac fibers? (Excitation-contraction coupling)
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
What are the sources of calcium for myocardial contraction?
ECF: via Ca channels in the cell membrane & down the T tubules S.R: via calcium-induced calcium-release.
31
What does the force of contraction depend on?
the concentration of Ca++ in extracellular fluids
32
What are the ionic reasons for the relaxation of cardiac muscle fibers?
Stoppage of Ca++ influx & pumping back of Ca++ from the sarcoplasm into SR & ECF via Ca++ pumps & Na+ Ca++ exchangers.
33
What is a statement of starling law?
“Within limit, the greater the initial length of the cardiac muscle fiber, the greater the force of contraction”.
34
What is the initial length of the cardiac fibers determined by?
diastolic filling (end-diastolic volume = EDV).
35
How does EDV affect the force of contraction?
Inc. venous return (e.g., muscle exercise) → inc EDV (filling) → stretch of the muscle → inc the force of contraction
36
What is the significance of increasing the force of contraction of cardiac muscle fibers in response to high venous return?
prevents stagnation of blood in the CVS.
37
What happens in cases of overstretching concerning cardiac muscle fibers?
Dec. Contractility
38
What is the nature of Starling law?
Myogenic
39
What time does mechanical response take in relation to action potential?
1.5 times as long as AP.
40
When does Contraction begin in relation to AP?
just after the start of depolarization
41
When does contraction reach maximum in relation with action potential?
BY the end of plateau.
42
When does relaxation begin in relation to action potential?
AT the end of plateau.
43
When does Relaxation reach its med?
When RP is complete
44
What are the excitability changes during action potential?
Absolute refractory period (ARP) Relative refractory period (RRP) Supernormal phase
45
What is the excitability in ARP, RRP, and supernormal phase respectively?
Zero Gradually increase Above normal
46
What is the stimulation in ARP, RRP, and supernormal phase respectively?
No response, whatever the strength of the 2nd stimulus Strong stimulus → weak contraction Weak stimulus → Strong contraction
47
When do ARP, RRP, and supernormal phase occur respectively?
Rapid depolarization & plateau = Contraction Rapid repolarization = 1st half of relaxation At the end of AP = 2nd half of relaxation
48
What is the effect of ARP, RRP, and supernormal phase respectively?
Prevents tetanus (continuous contraction) Null May cause extrasystole
49
What are the Factors affecting rhythmicity (chronotropic), excitability (bathmotropic), conductivity (dromotropic), and contractility (inotropic)?
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
How does the sympathetic nervous system affect cardiac properties?
- 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
How does the parasympathetic nervous system affect cardiac properties?
- 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
How does warming (fever) affect cardiac properties?
- 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
How does moderate cooling affect cardiac properties?
- Moderate cooling: opposite effects to moderate warming.
54
How does excessive cooling or warming affect cardiac properties?
- Excessive warming or cooling → cardiac damage → stop the heart.
55
How do drugs or hormones affect cardiac properties?
- Catecholamines, Thyroxine, xanthene-derivatives (theophylline & caffeine) → inc all cardiac properties. - Cholinergic → dec all cardiac properties.
56
How do blood gases affect cardiac properties?
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
How do ions affect cardiac properties?
- 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
How do typhoid or diphtheria toxins affect cardiac properties?
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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