Cardiac output (Pt1): Electrical events and heart rate Flashcards

1
Q

CO =

A

HR x SV

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2
Q

Heart rate is driven by

A

waves of electrical activity that induce cardiac muscles to contract

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3
Q

2 types of pacemaker cells

A

ones in the AV node and SA node

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4
Q

AV node

A

connects atria and ventricles and delays the signal for 0.1ms- allows atria to contract before ventricles

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5
Q

Bundle of His

A

Fast conducting myocytes that connnect to the Purkinje fibres, only way activity can pass to the ventricles

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6
Q

Myocyte

A

cardiac muscle cell

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7
Q

Purkinje fibres- why are they wide

A

Wide allowing rapid conduction throughout the ventricle and simultaneous contraction of ventricles

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8
Q

Purkinje fibres are

A

nerves

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9
Q

Atrial excitation involves

A

SA node

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10
Q

ventricular excitation involves

A

AV node

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11
Q

what causes pacemaker cells of the SA node to trigger an AP

A

Low RMP

Na+ leakage, leading to depolarisation

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12
Q

Mechanism for APs in pacemaker cells of the SA node

A

sodium ions leaking in through the F type channels and calcium ions moving in through the T type (transient) channels cause a threshold graded depolarisation.
Rapid opening of calcium L-type channels responsible for rapid depolarisation
Reopening of K+ channels and closing o calcium channels responsible for repolarisation.

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13
Q

What is the overall driver of heart rate

A

SA node, overrides AV and purkinje fibres

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14
Q

Mechanism for contraction of ventricular myocytes

A

Rapid opening of VGNC responsible for rapid depolarisation phase
Prolonged ‘plateau’ of depolarisation (contraction) due to slow but prolonged opening of VGCCs and closure of K+ channels
Opening of K+ results in repolarisation

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15
Q

How does calcium produce contraction of cardiac muscle

A

excitation-contraction coupling

Entry of extracellular ca ions causes release of Ca from sarcoplasmic reticulum by binding to ryanodine receptors

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16
Q

Why does cardiac muscle have a long refractory period

A

Allows ventricles to fill prior to pumping

17
Q

vagus nerve (parasympathetic)

A

decr heartbeat

Innervates just SA and AV nodes

18
Q

Sympathetic ganglia

A
incr heartbeat (also regulate force/SV)
Innervates whole heart
19
Q

What do parasympathetic and sympathetic nervous system regulate

A

rate of depolarisation in the SA node

20
Q

At rest which one dominates

A

Parasympathetic

21
Q

Parasympathetic mechanism

A

Parasympthetic neurones release Ach
acts upon m2 muscarinic receptors of SA node
Incr K+ efflux, decr Ca influx
Hyperpolarises cell and decr rate of depolarisation
decr HR - bradycardia

22
Q

Sympathetic mechanism

A
Release noradrenaline
acts upon B1 adrenergic receptors of SA node
Incr NA+ and Ca2+ influx 
Incr rate of depolarisation
Incr heart rate
Tachycardia
23
Q

ECG

A

measures electrical activity of the heart

Summation of the spread of APs throughout the heart

24
Q

P

A

atrial depolarisation

25
Q

QRS

A

ventricular depolarisation

26
Q

T

A

ventricular repolarisation

27
Q

PQ

A

length of atrial contraction

28
Q

QT

A

length of ventricular contraction

29
Q

ECG provides info on

A
HR
rhythm
disturbances of rhythm and conduction (arrhythmia, pacemaker)
conduction velocity
orientation of heart
relative size of chambers
Condition of tissue within the heart
Damage to myocardium
Drugs
30
Q

Inspiration

A

faster
PQRST closer together
decr in vagal parasympathetic activity> incr in heart rate

31
Q

Expiration

A

Slower
PQRST further apart
Vagal paraympathetic activity increase> heart rate decrease

32
Q

sinus arrythmia

A

bnormal heart rhythms that start at the sinus node

33
Q

Third degree

A

complete failure of conduction atria to ventricles

beat independently

34
Q

Ventricular etopic beat

A

Aberrant firing of myocytes in ventricles-ill synchronised and fails to eject blood
Common after heart attacks

35
Q

ventricular fibrillation result

A

Random firing
Fibrillating ventricles can’t pump blood
Fatal

36
Q

Ventricular fibrillation caused by

A

Myocardial infarction
Electric shock
Drug intoxication
Impaired cardiac metabolism