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Guyton > Unit 3 > Flashcards

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
Q

What causes respiratory sinus arrhythmia?

A

Spillover of signals from the medullary respiratory centre into the adjacent vasomotor centre

26
Q

What are the possible causes of a SA block?

A

Myocardial ischaemia, myocarditis, medication, fitness

27
Q

What are the possible causes of a SA block?

A

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
Q

What are the types of second degree AV block?
What causes them

A

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
Q

What is electrical alternans and what causes it?

A

Partial intraventricular block every other heartbeat
Tachycardia, ischaemia, myocarditis, digitalis toxicity

30
Q

What are the causes of premature contractions?

A

Ischaemia
Calcified plaques
Toxic irritation of AV node, purkinje system or myocardium

31
Q

What are the classical features of VPCs?

A

Prolonged QRS
High voltage QRS
T wave has opposite electrical potential polarity opposite to QRS

32
Q

What is long QT syndrome and why are they of potential concern?

A

Delayed depolarisation of ventricles
Increased susceptibility to torsades de pointes

33
Q

What are the possible causes of long QT?

A

Congenital - mutations of Na or K channels
Acquired - hypomagnesaemia, hypokalaemia, hypocalcaemia, drugs (quinidine, fluoroquinolone, erythromycin)

34
Q

What causes ventricular tachycardia?

A

Usually considerable damage to ventricles
Digitalis

35
Q

How can ventricular tachycardia be treated?

A

Lidocaine
Amiodarone

36
Q

What is the MOA of lidocaine?

A

Reduced sodium permeability of cardiac muscle membrane

37
Q

What is the MOA of amiodarone?

A

Prolongs action potential and refractory period in cardiac muscle
Slows AV conduction

38
Q

What factors can predispose to circus movements?

A

Cardiac dilation
Delayed velocity of contraction - blockage of Purkinje, ischaemia, hyperkalaemia
Short refractory period - epinephrine, repeated stimulation

Guyton (10 decks)

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