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

(36 cards)

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
QRS
ventricular depolarisation
26
T
ventricular repolarisation
27
PQ
length of atrial contraction
28
QT
length of ventricular contraction
29
ECG provides info on
``` 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
Inspiration
faster PQRST closer together decr in vagal parasympathetic activity> incr in heart rate
31
Expiration
Slower PQRST further apart Vagal paraympathetic activity increase> heart rate decrease
32
sinus arrythmia
bnormal heart rhythms that start at the sinus node
33
Third degree
complete failure of conduction atria to ventricles | beat independently
34
Ventricular etopic beat
Aberrant firing of myocytes in ventricles-ill synchronised and fails to eject blood Common after heart attacks
35
ventricular fibrillation result
Random firing Fibrillating ventricles can't pump blood Fatal
36
Ventricular fibrillation caused by
Myocardial infarction Electric shock Drug intoxication Impaired cardiac metabolism