Unit 3 Flashcards

1
Q

How does cardiac muscle differ from skeletal?

A

Cardiac muscle is a syncytium - muscle fibres separated by intercalated discs

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2
Q

What are 2 differences in action potentials in cardiac/skeletal muscle?

A

1 - cardiac muscle action potential caused by opening of fast sodium and slow calcium channels (vs fast sodium only)
2 - in cardiac muscle, after onset of action potential membrane potassium permeability decreases until calcium channels close
Both cause plateau in action potential

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3
Q

Describe the stages of cardiac muscle action potential

A

0 - fast sodium channels open
1 - fast sodium channels close
2 - slow calcium channels open. K+ channels close
3 - calcium channels close, k+ channels open

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4
Q

What is a difference in excitation-contraction coupling between cardiac and skeletal muscle?

A

In cardiac muscle calcium diffuse into the sarcoplasm from the T tubules, as well as the sarcoplasmic reticulum

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5
Q

Where is the sinus node located?

A

In the right atrium

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6
Q

How much of ventricular filling is active/passive?

A

80% passive
20% active

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7
Q

What are the pressure changes in the atria known as?

A

a wave - atrial contraction
c wave - ventricular contraction
w wave - flow of blood from veins

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8
Q

What is preload?

A

End diastolic pressure

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9
Q

What is afterload?

A

Pressure in aorta

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10
Q

Where does the energy for cardiac contraction come from?

A

70-90% fat metabolism
10-30% glucose/lactate

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11
Q

What is the Bainbridge reflex?

A

Stretch of the right atrial wall increases HR by 40-60%

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12
Q

What are the effects of vagal stimulation on the heart?

A

Mostly decrease in HR, slight reduction in contractility (vagus innervates atria not ventricles)

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13
Q

What are the effects of sympathetic stimulation on the heart?

A

Increase in HR and contractility

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14
Q

What are the effects of excess potassium ions on the heart?

A

Dilated, flaccid, reduced HR
High extracellular potassium decreases membrane potential - less negative, reduced intensity of action potential

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15
Q

What are the effects of excess calcium ions on the heart?

A

Spastic contraction - direct effect of ions to initiate contraction

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16
Q

What are the effects of deficiency of calcium ions on the heart?

A

Cardiac weakness

17
Q

What is the effect of increased body temperature on the heart?

A

Increased HR - increased permeability of cardiac membrane

18
Q

What are the effects of increased arterial blood pressure on cardiac output?

A

Minimal up to 160mmHg - cardiac output determined by venous return

19
Q

How is the tissue of the sinus node different to other heart muscle fibre?

A

Resting potential -55-60mV (vs -85-90mV)
Due to cell membrane being leaky to sodium and calcium
At less negative resting potential fast sodium channels blocked - only slow sodium channels open

20
Q

How does the sinus node self excite?

A

Sodium ions leak through membrane - funny currents
Resting potential slowly rises until L-type calcium channels activate
L-type channels inactivate and potassium channels open - repolarisation

21
Q

Which parts of the heart can exhibit intrinsic rhythmical activity?

A

Sinus node, AV node, Purkinje fibres

22
Q

What is the mechanism of vagal effects on the heart?

A

ACh increases permeability to potassium => hyperpolarisation

23
Q

Where is the majority of energy needed for heart contraction derived from?

A

Oxidative metabolism of fatty acids

24
Q

How does high atrial stretch increase heart rate?

A

Directly increased by 10-20%
Bainbridge reflex (vagus) - increases an additional 40-60%

25
What causes respiratory sinus arrhythmia?
Spillover of signals from the medullary respiratory centre into the adjacent vasomotor centre
26
What are the possible causes of a SA block?
Myocardial ischaemia, myocarditis, medication, fitness
27
What are the possible causes of a SA block?
Ischaemia of the AV node/bundle Compression of the AV bundle with scar tissue Inflammation of the AV node/bundle Extreme vagus stimulation Degeneration of the AV conduction system Medication (digitalis, beta blockers)
28
What are the types of second degree AV block? What causes them
Mobitz type I (Wenckeback periodicity) - progressive prolongation of PR until ventricular beat dropped. Usually abnormal AV node, normally benign Mobitz type II - fixed number of non-conducted P-waves. Usually associated with issue with His-Purkinje system, may require pacing
29
What is electrical alternans and what causes it?
Partial intraventricular block every other heartbeat Tachycardia, ischaemia, myocarditis, digitalis toxicity
30
What are the causes of premature contractions?
Ischaemia Calcified plaques Toxic irritation of AV node, purkinje system or myocardium
31
What are the classical features of VPCs?
Prolonged QRS High voltage QRS T wave has opposite electrical potential polarity opposite to QRS
32
What is long QT syndrome and why are they of potential concern?
Delayed depolarisation of ventricles Increased susceptibility to torsades de pointes
33
What are the possible causes of long QT?
Congenital - mutations of Na or K channels Acquired - hypomagnesaemia, hypokalaemia, hypocalcaemia, drugs (quinidine, fluoroquinolone, erythromycin)
34
What causes ventricular tachycardia?
Usually considerable damage to ventricles Digitalis
35
How can ventricular tachycardia be treated?
Lidocaine Amiodarone
36
What is the MOA of lidocaine?
Reduced sodium permeability of cardiac muscle membrane
37
What is the MOA of amiodarone?
Prolongs action potential and refractory period in cardiac muscle Slows AV conduction
38
What factors can predispose to circus movements?
Cardiac dilation Delayed velocity of contraction - blockage of Purkinje, ischaemia, hyperkalaemia Short refractory period - epinephrine, repeated stimulation