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PPI > Arrhythmias and Heart Failure > Flashcards

Arrhythmias and Heart Failure Flashcards

1
Q

What are the two basic causes of arrythmias?

A

Two basic causes of arrythmias:
* Malfunction of the conduction system (more common):
* Abnormal impulse generation (abnormal automaticity):

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2
Q

Which is the more common cause of arrythmias,
a.Malfunction of the conduction system
OR
b.Abnormal impulse generation

A

Malfunction of the conduction system is the most common cause of arrhythmias

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3
Q

What are the two types of the malfunction of the conduction system?

A

Two types of malfunction of the conduction system:
1. Re-entry: re-excitation around a conducting loop, which produces tachycardia
2. Heart block

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4
Q

What is an arrythmia?

A

An arrhythmia is an abnormal heart rhythm.
Abnormal eletrical activity of the heart.

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5
Q

What is tachycardia?

A

Tachycardia is a heart rate over 100 beats per minute at rest.

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6
Q

What is the ST segment clinically important for?

A

The ST segment is clinically important for ischaemia and myocardial infarction.

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7
Q

What can the T wave indicate?

A

The T wave could indicate high potassium levels.

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8
Q

What is a normal heart beat?

A

A normal heart beat is 60-100 beats per minute.

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9
Q

What is bradycardia?

A

Bradycardia is a heart rate less than 60 beats per minute at rest.

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10
Q

What are the 3 stages of a heart beat?

A

The 3 stages of a heart beat are:
1. Atrial depolarisation
2. Ventricular depolarisation
3. Atrial and ventricular repolarisation

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11
Q

What does the P wave represent?

A

P wave represents atrial depolarisation

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12
Q

What does the QRS complex represent?

A

The QRS complex represnts ventricular depolarisation

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13
Q

What does the T wave represent?

A

The T wave represents ventricular repolarisation.

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14
Q

The heart is ?% electrical cells and ?% muscle cells?

A

The heart is 1% electrical cells and 99% muscle cells?

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15
Q

Normal heart rate/rhythm starts and ends where?

A

Normal heart rate/rhythm starts and ends in the SA node.

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16
Q

What does the PR interval allow for?

A

The PR interval allows for the ventricles to fill up.

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17
Q

How long shouldn’t the P-R interval be?

A

The P-R interval shouldn’t begreater than 0.2 seconds it could indicate issues

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18
Q

The term used for the release (discharge) of an electrical stimulus is “?”, and the term for recharging is “?

A

The term used for the release (discharge) of an electrical stimulus is “depolarisation”, and the term for recharging is “repolarisation

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19
Q

The SA node ? whilst the atria are refilling, and the AV node recharges when the ventricles are ?

A

The SA node recharges whilst the atria are refilling, and the AV node recharges when the ventricles are refilling

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20
Q

Any part of the heart can do what?

A

Any part of the heart can excite.

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21
Q

What can malfunction of the conduction system be caused by?

A

Malfunction of the conduction system can be caused by:
* unidirectional conduction block
* establishment of new loop of excitation
* conduction that outlasts the refractory period

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22
Q

What is the refractory period?

A

The refractory period is a period of time during which a cell is incapable of repeating an action potential

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23
Q

Describe normal conduction

A

Normal conduction:
SA node to atria to AV node to apex to bundle of HIS to purkinje fibres

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24
Q

What are autorhythmic cells?

A

Authorhythmic cells:
* Specialised muscle cells
* Spontaneously generate action potentials

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25
Q

What are the two types of autorhythmic cells?

A

Two types of auto rhythmic cells:
* Pacemaker cells
* Conducting fibres

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26
Q

What does the pulmonary artery do?

A

The pulmonary artery carries deoxygenated blood from the right ventricle to the lungs

27
Q

What does ventricular depolarisation allow for?

A

Ventricular depolarisation allows for contraction.

28
Q

What should the S-T segment b? What does it represent?

A

The S-T segment should be iso-electric
It represents the ventricles before repolarisation

29
Q

The PR interval is the time from onset of ? activation to onset of ? activation

A

The PR interval is the time from onset of atrial activation to onset of ventricular activation

30
Q

The QT interval is the duration of ? activation and recovery

A

The QT interval is the duration of ventricular activation and recovery

31
Q

What should the QT interval not be?

A

The QT interval shouldn’t be too wide or too narrow.

32
Q

What can more than one P wave for each QRS-T complex indicate?

A

More than one P wave for each QRS-T complex could indicate heart block

33
Q

What is heart block? What may it result in?

A

Heart block:
* Partial damage to AV node may lead to intermittent heart block
* Resulting in more than one P wave for each QRS-T complex

34
Q

What are extra-systoles?

A

Extra-systole= extra contraction

35
Q

What is abnormal impulse generation?

A

Abnormal impulse generation (abnormal automaticity):
* Beat originates from a part it shouldn’t (should be from SA node)
* Ectopic beats may originate in atria or ventricle in the absence of any nodal damage and initiate extra-systoles

36
Q

What might show on an ECG with atrial fibrillation?

A

Atrial fibrillation ECG:
* QRS complex may still be evident but superimposed on an irregular baseline
* No clear P wave

36
Q

What can the heart do if it has issues?

A

If the heart has issues, it can generate a beat from any area.

37
Q

Name the 4 types of arrhythmia

A

4 types of arrhythmia:
* Tachycardia: increased rate
* Bradycardia: decreased rate
* Fibrillation: disorganised contractile activity
* Flutter: very rapid but regular contractions

38
Q

What can ventriular fibrillation lead to?

A

Ventricular fibrillation can lead to cardiac arrest or death.

39
Q

Ectopic beat?

A

Ectopic beat: a part of the heart (not the SA node) generating a rhythm

40
Q

What is fibrillation?

A

Fibrillation:
* The heart generates multiple etopic beats
* multiple ectopic foci develop and discharge asynchronously
* there is no coordination

41
Q

Is atrial fibrillation or ventricular fibrillation more common?

A

Atrial fibrillation is more common than ventricular fibrillation.

42
Q

Which drugs are available for arrhythmias?

A

Arrhythmia drug treatment:
* Class I: Sodium channel blockers (e.g. lignocaine)
* Class II: Beta blockers (e.g. propranolol)
* Class IIi: Drugs that delay repolarization/slow heart rate (Amiodarone)
* Class IV: Calcium channel blockers (e.g. verapamil and nifedipine)
* Class V: “Atypical” (e.g. adenosine, digoxin and anticoagulants).

43
Q

Which symptoms are associated with arrythmia?

A

Symptoms associated with arrhythmia:
* Palpitations
* Dizziness
* Chest pain
* Dyspnea (breathing issues)
* Fainting
* Sudden cardiac death

44
Q

If heart rate is low what is the PR interval likely to be?

A

If heart rate is low, the PR interval is likely to be longer.

45
Q

If heart rate is high what is the RR interval likely to be?

A

If heart rate is high, the RR interval is likely to be closer.

46
Q

Which sites can be involved in arrhythmia?

A

Sites involved in arrhythmia:
* Ventricular
* AV node
* Atrial
* Sinus
* Supraventricular (atrial myocardium or AV node)

47
Q

What does a 3rd degree block have on an ECG?

A

On a ECG a 3rd degree block has many P waves

48
Q

What does an elevated ST segment indicate?

A

An elevated ST segment may indicate acute myocardium damage from myocardial ischaemia

49
Q

What does a depressed ST segment indicate?

A

A depresed ST segment may indicate myocardium damage and ischaemia.

50
Q

What does an ECG do?

A

ECG:
Show heart behaviour
Accurate & detailed detection of cardiac abnormalities which may be related to myocardium damage or issues with conduction

51
Q

What might a ventricular fibrillation ECG show?

A

Ventricular fibrillation ECG:
* Might not have any QRS-T waves (they won’t be completely flat)

52
Q

What does a delay at the AV node lasting for more than 0.2s result in?

A

A delay at the AV node lasting for more than 0.2s leads to a heart block.

53
Q

What is heart failure?

A

Heart failure:
- the heart’s inability to meet the metabolic requirements of the body
- heart could be pumping but not meeting metabolic demand/rate
- Disease of heart: associated with poor contracility of heart muscles, occurs when heart is unable to mainatin sufficient cardiac output to meet the demands of the body

54
Q

Chronic heart failure

A

Chronic heart failure
* Gradual inability of the heart to maintain blood supply

55
Q

Acute left ventricular failure

A

Acute left ventricular failure

Usually results from sudden inability of the heart to maintain blood
supply

56
Q

Left-sided heart failure

A

Left-sided heart failure
* an inability of the left ventricle to pump out enough blood and as a result,
* * blood backs up into the lungs,
* causes pulmonary oedema

57
Q

Right-sided heart failure

A

Right-sided heart failure
* Right ventricle fails to pump out enough blood,
* fluid backs up into the veins and capillaries
* causes systemic oedema particularly in the legs

58
Q

Heart failure causes

A

Causes of heart failure

Coronary artery disease
Diseases of the heart muscle
Abnormal heart rhythms
Leaky heart valves
High Blood Pressure
Infections: viral or bacterial
Some chemotherapy drugs
Toxins such as alcohol
Birth defects- congenital heart disease

59
Q

Heart failure treatments

A

Heart failure treatments
* Cardiac glycosides: e.g digoxin: inhibit na/K exchange, increase Na> decreased na/Ca exchange: increased Ca> increased contraction
* Angiotensin II blockers
* Beta-receptor agonists (Acute HD)
eg Dobutamine:Activate Beta 1-receptor in the heart and thus increase force of contraction
* Vasodilators: reduce afterload and peripheral vascular resistance
* Diuretics: fluid retention increases pre load.
* Diet
* Exercise
* Stop smoking
* Reduce alcohol intake
* Heart transplant

60
Q

Why are selective beta1 antagonists used in heart failure?

A

Selective beta1 antagonists are used in heart failure:
* To not increase the afterload which will happen if peripheral alpha receptors are stimulated> cause blood vessel constriction
* Increased afterload will increase heart workload and impair cardiac output more

61
Q

Angiotensin II mechanism of action

A

Angiotensin II mechanism of action
* Constrict Efferent arterioles
* Acts on CNS to increase ADH production Sympathetic tone
* Stimulate aldosterone secretion
* Na+ retention
* Increase fluid retention
* Vasoconstrict venous reservoir
* Increase blood volume

62
Q

What does blocking angiotensin II do?

A

Blocking angiotensin II: reduces workload on the heart by preventing: aldosterone secretion, fluid retention and blood volume increase

PPI (23 decks)

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