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MD1S2: Physiology 202 > Cardiac muscle properties > Flashcards

Cardiac muscle properties Flashcards

1
Q

What are the cardiac muscle properties?

A

Property 1: Rhythmicity (Chronotropism)
Property 2: Conductivity (Dromotropism)
Property 3: Excitability (Bathmotropism)
Property 4: Contractility (Inotropism)

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2
Q

Property 1: What is rhythmicity?

A

Myogenic ability of the heart to beat regularly without nerve supply (automaticity)

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3
Q

+ve and -ve chronotropic effects

A

+ve chronotropic = increased heart rate
-ve chronotropic = decreased heart rate

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4
Q

How is rhythmicity initiated?

A

Pacemaker cells of the heart in the SA node

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5
Q

Why is the SAN the pacemaker of the heart?

A

Resting membrane potential (RMP) between -55 and -60 mv
RMP is unstable
SAN has higher rhythm and higher slope

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6
Q

Phases of pacemaker potential

A

Phase 0, 3 and 4

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7
Q

Events of phase 0 of pacemaker potential?

A

Rapid depolarization due to opening of L-type calcium channels

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8
Q

Events of Phase 3 of pacemaker potential?

A

Repolarization of pacemaker cells due to opening of K+ channels and closure of Ca++ channels

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9
Q

Events of Phase 4 of pacemaker potential?

A

Spontaneous depolarization/diastolic depolarization/prepotential/funny current (If) due to opening of slow Na+ channels

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10
Q

Rhythm of cardiac muscle fibers

A

SAN: Initiates heart beats from 90-110 beats/min
AVN: Initiates heart beats from 50-60 beats/min
Bundle branches: Initiates heart beats, 45 beats/min
Purkinje fiber: Initiates heart beats from 15-35 beats/min
Ventricles: Initiates heart beats from 25 beats/min

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11
Q

Property 2: What is conductivity?

A

The ability of the cardiac muscle to conduct cardiac impulse from one part to another

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12
Q

+ve and -ve dromotropic effect

A

+ve dromotropic = increased conduction
-ve dromotropic = decreased condution

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13
Q

What are the conducting fibers of the heart?

A

Atrioventricular bundle (Bundle of His)
Right and left bundle branches
Purkinje fibers

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14
Q

Describe the conduction of an impulse

A

(1) Pacemarker of the heart (SAN)
(2) Internodal and interatrial tract - (A) Connects SA node and AV node (B) Has a faster rate of conduction than the atrial muscles (C) Composed of three tracts, anterior, intermediate and posterior (D) Interatrial tract (Bachmann’s bundle which conducts impulses from the SAN to the left atrium)
(3) Atrioventricular node - (A) conducting path between atria and ventricles (B) Slow velocity of conduction (0.05 m/sec) (C) 0.1sec nodal delay (decremental conduction). Nodal delay due to fewer gap junctions and small fiber size
(4) Bundle of His - (A) Begins from AV node and passes through the interventricular septum (B) Divides into right and left bundle branches (C) Conduction speed 1-2m/sec
(5) Purkinje fibers - (A) Conduction velocity of 4-5m/sec (B) Largest conducting fiber + more gap junctions (C) Passes impulses to ventricular myocytes in the ventricular walls (D) Fast conduction enables both ventricles to contract simultaneously

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15
Q

Significance of AV nodal delay

A

(1) Allow atria to completely depolarize, contract and empty its blood before the ventricular depolarisation and contraction
(2) Limit the passage of the electrical signals that can activate the ventricles to allow sufficient time for ventricles to relax and to be filled with blood before they contract

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16
Q

Which fiber has the fastest and slowest conduction?

A

Fastest = Purkinje fibers
Slowest = AV node

SA node is not considered the slowest because it is not a conducting fiber

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17
Q

Property 3: What is Excitability?

A

Ability of the cardiac muscle to respond to stimulation

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18
Q

What is the resting membrane potential of the cardiac muscle cell?

A

-90 to -85mv (low excitability)

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19
Q

What are the phases of cardiac muscle action potential?

A

Phase 0 (Depolarization)
Phase 1 (Initial Repolarization)
Phase 2 (Plateau)
Phase 3 (Rapid Repolarization)
Phase 4 (Resting Membrane Potential)

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20
Q

Phase 0 of cardiac muscle action potential

A

Fast sodium channels open
Membrane potential reaches +20mv

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21
Q

Phase 1 of cardiac muscle action potential

A

Fast sodium channels close
Fast potassium channels open
Cells begin repolarizing

22
Q

Phase 2 of cardiac muscle action potential

A

Slow calium channels (L-type) open
Fast potassium channels close

A brief initial repolarization occurs, and the action potential then plateaus as a result of increased calcium ion permeability and decreased potassium ion permeability. The voltage-gated calcium ion channels open slowly during phases 0 and 1, and calcium enters the cell. Potassium channels then close, and the combination of decreased potassium ion efflux and increased calcium ion influx causes the action potential to plateau.

23
Q

Phase 3 of cardiac muscle action potential

A

Calcium channels close
Slow potassium channels open

24
Q

Phase 4 of cardiac muscle action potential

A

RMP (-90 to -80mv)

25
Q

SA Nodal potential vs Action potential of cardiac muscle BUT ON A GRAPH!!

A
26
Q

What are refractory periods?

A

Periods following action potentials during which the cardiac muscles don’t respond to a stimulus

27
Q

What are the two refractory periods?

A

Absolute refractory period (ARP): No impulse can excite the cardiac muscle. 0.25 to 0.3 second duration
Relative refractory period (RRP): Strong impulse can excite the cardiac muscle during rapid repolarization. 0.05 second duration

28
Q

What is the significance of the refractory period?

A

It prevents stimulation of the ventricle by another impulse → gives the ventricle sufficient time to empty their contents and refill before the next cardiac contraction

29
Q

At what point during the cardiac muscle potential does contraction and relaxation of the cardiac muscle occur?

A

Contraction occurs at the end of the plateau
Relaxation occurs at the rapid phase of repolarization

30
Q

What factors influence the rhythmicity of the cardiac muscle?

A

Nervous
Physical
Chemical

31
Q

How do nervous factors affect the rhythmicity of cardiac muscles?

A

Parasympathetic nervous system has -ve chronotropic = ↓ heart rate
Sympathetic nervous system has +ve chronotropic = ↑ heart rate

32
Q

What are the physical factors which affect the rhythmicity of the cardiac muscle?

A

Warming (fever) = +ve chronotropic effect (1°C increase = HR increase by 10-13 bpm)
Cooling = -ve chronotropic effect

33
Q

What are the chemical factors which affect the rhythmicity of the cardiac muscle?

A

Ions: Increase of Na+, K+, & Ca++ = ↓ heart rate
Drugs and hormones: Thyroxin and Catecholamines ↑. Digitalis ↓
Blood gases: Mild hypoxia ↑, alkalosis ↑, acidosis ↓
Toxins: Typhoid and diphtheria ↓

34
Q

How does hyperkalemia affect the heart?

A

Stops the heart during diastole

35
Q

How does hypercalcemia affect the heart?

A

Stops the heart during systole

36
Q

What can digitalis be used for?

A

Treatment of heart failure
Increases contractility, thereby improving cardiac output,
Reduces rhythmicity and conduction through the AV node and thus, used to treat atrial fibrillation and atrial flutter

37
Q

Property 4: What is contractility?

A

Ability of the healthy cardiac muscle to convert electrical and chemical changes into mechanical work (contraction) that pumps into circulation independent of preload and afterload

38
Q

+ve and -ve inotropic effects

A

-ve inotropic means decrease contractility while +ve inotropic means increase contractility

39
Q

What is the mechanism of contraction called?

A

Excitation contraction coupling

40
Q

Describe the mechanism of contraction of the heart

A
  1. Calcium enters via voltage gated L-type channels during plateau phase
  2. Calcium is sensed by ryanodine receptors (RyRs) on the sarcoplasmic reticulum causing the release of Ca++ (Calcium-Induced Calcium Release)
  3. Ca++ binds to troponin enabling cross bridge formation between myosin and actin.
41
Q

Describe the cross-bridge mechanism

A

Calcium binds to troponin C
Conformational change of troponin causes tropomyosin to move off the myosin-binding sites of actin
Myosin head loses the Pi group and binds the actin binding site
Powerstroke moves the thin filament to shorten thesarcomereand generate force
Disconnection of the cross-bridge from actin.
Re-energizing and repositioning of the cross-bridge
Removal of calcium ions

42
Q

Describe the mechanism fo muscle relaxation

A

Active reuptake of Ca++ into the SR by Ca++ pump (SERCA) and from the cell through Ca+2- Na+ exchanger.
Decrease in intracellular calcium concentration
Release of Ca++ ions from troponin C
Tropomyosin moves back to cover the active sites on actin
Cessation of the interaction between actin and myosin

43
Q

What are the factors affecting cardiac contractility?

A

Intrinsic factors:
1. Preload
2. Afterload
3. Healthy cardiac muscle
4. Frequency of stimulation

Extrinsic factors: (refer to flashcard 33)
1. Nervous
2. Physical
3. Chemical

44
Q

What is end diastolic volume (EDV)/preload?

A

Volume of blood in each ventricle at the end of diastole
End diastolic volume= 120ml

45
Q

What is end systolic volume (ESV)?

A

Volume of blood that remains in each ventricle at the end of systole
End systolic volume= 50ml

46
Q

What is stroke volume?

A

Volume of blood ejected from each ventricle per stroke
Stroke volume = 70ml

47
Q

Explain Frank-Starling’s Law

A

Within limit, the greater the initial length of cardiac muscle fiber (EDV), the greater the force of contraction

48
Q

What is afterload?

A

The resistance in front of the blood after starting ventricular contraction and ejection including aortic pressure, arterial wall rigidity and blood viscosity

49
Q

What does the force velocity curve show?

A

The initial velocity of shortening of cardiac muscle is inversely proportionate to the magnitude of afterload

50
Q

What factors increase afterload?

A

Increased arterial blood pressure
Stenosed (narrowed) valves

51
Q

How does frequency of stimulation affect the contractility of the heart?

A

Staircase (Treppe) phenomenon (Force frequency relationship)
Gradual increases in strength of cardiac muscle contraction due to repeated stimulation.
Produce thermal, chemical and ionic changes which increase force of contraction

MD1S2: Physiology 202 (20 decks)

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