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JMP Semester 1 > Week 8 The Heart, control, conduction, contraction > Flashcards

Week 8 The Heart, control, conduction, contraction Flashcards

1
Q

How does pacemaking signals in the Sino atrial node (SA node).

A

Sino atrial node cells have different ion channels involved in depolarization than other cardiac muscle cells.
leaky sodium channels (HCN)

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2
Q

What is the pathway for SA action potential.

A
  1. leaky Na channels (hits threshold at -40mV) (Na+ influx)
    (PHASE 4)
  2. Voltage gated Ca++ channels (fast depolarisation) (Ca influx)
    (PHASE 0)
  3. At peak Ca++ close and K+ open (K+ efflux) (repolarisation)
    (PHASE 3)
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3
Q

What is the order for action potential through cardiac tissue.

A
  1. SA node
  2. AV node
  3. bundle of His
  4. down left and right bundle branches
  5. Purkinje fibres
  6. Ventricular myocardium
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4
Q

What is the pathway for ventricular muscle action potential? (Phases)

A

PHASE 4:
Resting/input from other pacemakers
PHASE 0:
opening of fast Na+ channels. Huge depolarisation (voltage gated)
PHASE 1
Na channels close (the peak). Transient K+ channels open to let K+ out for a short time. (voltage gated)
PHASE 2
Ca-channels open and let Ca++ into the cell (this Ca++ inside negates the K+ efflux from the cell) therefore the potential remains stable. (plateau) (voltage gated)
PHASE 3
Ca++ channels close. DELAYED K+ channels open - fast efflux of K+ - potential returns to resting level.

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5
Q

List all ion channel types used in phase of AP

A

Phase 4- leaky Na+
Phase 0- fast voltage gated Ca++ in SA and Na+ in ventricle
Phase 1- voltage gated K+ (transient) (K+ efflux)
Phase 2- Voltage gated Ca++ (influx)
Phase 3- Delayed K+ in cardiac muscle and voltage K+ in SA.

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6
Q

What is the advantage of the plateau in cardiac action potential?

A

The advantage of the long plateau is to give the cell time to pool Ca+ to utilise for triggering a stronger muscle contraction. This contraction is not needed in the SA (sinoatrial) node thus the plateau is not present.

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7
Q

What is the advantage of a relatively long refractory period of cardiac AP

A

The long refractory period gives a better chance that ectopic beats will not be acted upon.

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8
Q

What is the absolute refractory period

A

Cell cant depolarise

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9
Q

What is the relative refractory period

A

the cell may be able to partially depolarise.

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10
Q

What is the P, QRS and T peaks on an ECG strip

A 
P = atrial depolarisation
QRS= Ventricle depolarisation
T= ventricle repolarisation
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11
Q

What is the P-Q interval

A

The delay at the AV node

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12
Q

What is the Q-T interval

A

The duration of action potential in the ventricles

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13
Q

How does surface body ECG work?

A

records from thebody surfaceand registers the differences in electrical potentialgeneratedby the heart. The signal recorded is determined by action potentialsgenerated

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14
Q

What are some features of skeletal muscle

A
  1. used in voluntary movement
  2. contraction initiated by ACh
  3. striated
  4. long cells
  5. multiple nuclei
  6. not electrically connected- needs to be nerve activated
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15
Q

What are some features of cardiac muscle

A
  1. contraction initiated from conducting system (electrically connected via gap junctions)
  2. are striated but not referred to as having them
  3. branched shape unlike skeletal muscles
  4. single nucleus
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16
Q

What are some features of smooth muscle

A
  1. contraction initiated in many ways, lots of hormone interaction
  2. elongated shape
  3. not striated
  4. single nucleus
  5. contraction initiated by external Ca concentration
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17
Q

What are the steps in excitation contraction coupling?

A
  1. ATTACHED STATE- actin is attached to myosin
  2. RELEASED STATE- ATP binds to myosin-causing detachment
  3. COCKED STATE- attached ATP changed to ADP (causes myosin to straighten)
  4. WEAK CROSS-BRIDGE STATE-myosin heads binds to new actin position.
  5. STRONG CROSS-BRIDGE STATE- Phosphate is released to make link stronger
  6. POST POWER STROKE STATE-loss of P causes myosin to bend and slide up the actin.
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18
Q

How does Ca concentration pathway differ in skeletal vs cardiac muscle

A

Skeletal- AP causes receptor activation (2 receptor chain) which then causes Ca++ release from SR.
Cardiac- During AP Ca++ enters the cell through channels. the increase in Ca++ activates SR receptors to release even more calcium.

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19
Q

What is the role of Potassium ATPase

A

Pump used to pump Na+ and K+ against their concentration gradients using ATP. this is to maintain a high external Na+ concentration.

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20
Q

what is the roll of a Na+/Ca++ exchanger (NCX)

A

Ca++ efflux
Na+ influx.
Uses high Na+ concentration gradient and no ATP.

21
Q

What does a cardiac glycoside do?

A

Inhibits the potassium ATPase.
Leading to reduced Na+ gradient and hence Ca++ cannot be exported by NCX.
This leads to higher internal calcium and an increase in contraction force

22
Q

what is the main roles of ATP in muscle contraction and relaxation?

A
  1. ATP is required for myosin detachment. muscles cannot function/relax without ATP.
  2. Powering ion channels to ensure appropriate ion balance.
23
Q

What is a positive iontrope?

A

Pharmacological agents that increase myocardial contractibility. commonly through increases in Ca++ concentration

24
Q

What is a negative iontrope?

A

blocks Ca++ entry into cells - weaker contraction force - lower blood pressure

25
Q

What is the Atrial contributions to cardiac output during rest and exercise?

A

REST- Atria contribute 10% to ventricle filling (as there is lots of diastole time between contractions
EXERCISE- 30-40% ventricle filling (atrial kick) (as there is less time between contractions)

26
Q

What is the specific reason cardiac output can be affected by faulty atria?

A

Atria can have an affect on ventricle filling so determine stroke volume.
CO=SR X HR

27
Q

What is the relationship between HR and SV?

A
  1. both increase during exercise to increase CO.
  2. HR is linear and peaks.
  3. SV -peaks at moderate exercise but can be increased by training.
28
Q

Why does exercise lead to higher demand for cardiac output.

A

Muscles do more work.

need more O2 and need metabolites removed.

29
Q

What are examples of cardiovascular adjustments during exercise.

A
  1. increase in CO (approx 2.5x)
    through muscle movement increasing venous return.
  2. redistribution of Blood flow-away from GI to the skeletal muscles.
30
Q

What is post- exercise hypotension

A

blood pressure drops below normal (can last hours.)

31
Q

What is post exercise HR recovery

A

Accepted measure for fitness (faster the better)

32
Q

Why is rehydration important during exercise.

A

exercise generates lots of heat and causes large water losses through sweat. sweat is the main way heat is dissipated. If the water is not replaced can have large impacts on bodily function.
Low water = low blood volume.
Hence- increased viscosity, increased electrolytes, decreased venous return

33
Q

What is the phase order for SA node AP

A 
Phase 4 (rest)
Phase 0 (depolarisation)
Phase 3 (repolarisation)
Phase 4 (rest again)
34
Q

What is the phase order for cardiomyocyte

A 
Phase 4 (rest)
Phase 0 (depolarisation)
Phase 1 (peak/overshoot)
Phase 2 (plateau) 
Phase 3 (repolarisation)
Phase 4 (rest again)
35
Q

What effects can B1 receptor activation have?

A
  1. B1 receptor activation
  2. activates adenylate cyclase
  3. increases cAMP
  4. cAMP activates PKA (protein kinase A)
  5. PKA positively regulates:
    a) voltage gated Ca++ channels
    b) leaky Na+ channels
36
Q

What is the effect of B1 receptor ACTIVATION in the SA node?

A
  1. shortens AP duration as more Na+ influx. (this is the function of adrenaline (sympathetics in the heart)
    thus increases HR
37
Q

What is the effect of B1 receptor ACTIVATION in the cardiomyocytes?

A

Increases Ca+ influx hence increases force of contraction.

38
Q

What class of drug is Beta blockers?

A

Class 2 Adrenergic Antagonists

39
Q

What is the mechanism of action for beta blockers

A

They bind to B1 receptors and prevent sympathetic stimulation of heart muscle.
1.reducing AP in the SA node 2.reducing contractile forces in the cardiomyocytes

40
Q

When are beta blockers primarily used?

A

REDUCING HR

They are used for dysrhythmia control in the SA and AV nodes. (not used for ectopic signals)

41
Q

What class of drug is sodium channel blockers? and what happens with their use?

A

Class 1.

Reduction of HR

42
Q

What do sodium channel blockers do?

A
  1. They block voltage gated sodium channels.

2. hence main function at the cardiomyocytes (to reduce depolarisation speed)

43
Q

What are some odd effects of the differed class 1 subtypes?

A

a) decreases pacemaker ability due to K+ channel blocking
b) decreases pacemaker ability due to blocking of leaky Na+ channels
c) range of extra stuff.

44
Q

What is the class and primary mechanism of potassium channel blockers?

A

Class 3

  1. Blocks voltage gated K+ channels
  2. slows rate of depolarisation
  3. increases AP length in both SA and cardiomyocytes hence reducing excess cardiac activity.
45
Q

What is the class and mechanism of Calcium channel blockers

A

Class 4

blocks voltage gated Ca++ channels

46
Q

How do Calcium channel blockers achieve function in the heart.

A
  1. Blocks voltage gated Ca++ channels
  2. blocks conduction through the AV node as well as reducing automaticity in the SA node (slows depolarisation)
    Reduces HR.
  3. Not used for ectoptic disturbances.
47
Q

What is the two mechanisms of Digoxin?

A
  1. Activates K+ ATP channels in SA and AV. This effluxes K+ to hyperpolarise cell. causing longer AP to reduce HR
  2. Blocks Na+/K+ ATPase pump:
    * destroys NA+ gradient in cardiomyocytes
    * calcium can not be pumped out
    * more internal calcium = increased CO
    * used in heart failure.
48
Q

What is the main action of Digoxin?

A

Promotes muscarinic receptor action- boost parasympathetic effect in the heart.

JMP Semester 1 (12 decks)

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