Hayes Chapter 2 Flashcards

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1
Q

What are attempts to restore or mimic normal cardiac conduction physiology? (4)

A
  1. DDD pacing
  2. Algorithms to reduce RV pacing
  3. Ventricular rate regularisation
  4. CRT
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2
Q

What factors make up cardiac output? (2)

A

Heart rate x strike volume = cardiac output

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3
Q

What is strike volume? (2)

A

Amount of blood ejected with each ventricular contraction

Ie. end diastolic volume minus end systolic volume

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4
Q

Emotion & exercise increase cardiac output. The contribution of each is determined by what factors? (4)

A
  1. Age
  2. Type/intensity of activity
  3. Baseline cardiac fitness
  4. Presence of cardiac disease
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5
Q

In a normal heart, what affects end-diastolic volume? (4)

A
  1. Diastolic filling pressure
  2. Total blood volume
  3. Distribution of blood volume
  4. Atrial systole (preload)
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6
Q

In a healthy heart, what determined end-systolic volume? (2)

A
  1. Myocardial contractility

2. Afterload

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7
Q

What factors can influence myocardial contractility and afterload? (4)

A
  1. Metabolic changes
  2. Autonomic tone
  3. Drugs (work either on SA node or affect ANS)
  4. Cardiac rhythm
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8
Q

What are the two factors that heart conditions will affect? (2)

A
  1. Heart rate
  2. Stroke volume

Or both

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9
Q

What is chronotopic incompetence? (1)

A

Inability to increase heart rate during exercise or stress

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10
Q

Why will patients with poor LV function be less tolerant of chronotopic incompetence? (1)

A

Because their stroke volume is already lower (their heart is weak) and so they are more dependent on heart rate for cardiac output.

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11
Q

What cardiac diseases can impair myocardial contractility? (5)

A
  1. Coronary artery disease
  2. MI
  3. Non-ischaemic cardiomyopathy
  4. Valvular disease
  5. Pericardial disease
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12
Q

What is preload? (1)

A

End-diastolic volume that stretches the right or left ventricle of the heart TO ITS GREATEST DIMENSION

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13
Q

What is interventricular dyssynchrony? (1)

A

A mechanical delay in contraction of the right and left ventricles (usually >40ms)

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14
Q

What is intraventricular dyssynchrony? (1)

A

Difference in max strain time of different segments within ONE ventricle

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15
Q

What is pre-ejection time? (1)

A

Delay in time from QRS onset to onset of pulmonary or aortic flow

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16
Q

What are some metabolic problems that impact cardiac function? (3)

A
  1. Chronic acidosis
  2. Hypoxia
  3. Hypercarbia
17
Q

At low, moderate and extreme exercise, what are the biggest factors in increasing cardiac output? (2)

A
  1. Moderate/extreme exercise = increased heart rate

2. Low levels activity/rest = AV synchrony is most important

18
Q

Why are many paced patients more dependant on preload? (2)

A
  1. Because they have reduced ventricular compliance

2. This is why AV synchrony is SUPER important for them (just as important as RR)

19
Q

What is pacemaker syndrome? (1)

A

Ventriculoatrial conduction or atrial conduction against closed valves

20
Q

How does pacemaker syndrome affect haemodynamics? (4)

A
  1. Activates mechanical stretch receptors in walls of atria and pulmonary veins
  2. leads to vagal affects
  3. peripheral vasodilation
  4. hypotension
21
Q

What causes pacemaker syndrome?

A

Any loss of AV synchrony (including really long AV delays)

22
Q

Describe the MOST trial (mode selection trial)

A

Severe pacemaker syndrome occurred in 20% of subjects

23
Q

By how much can AV synchrony increase stroke volume?

A

By up to 50%

24
Q

Describe what happens of A.V. delays are too long?

A

Ventricular contraction doesn’t follow straight after atrial emptying, and AV valves float up towards atria (soft lub 1st heart sound = diastolic AV regurgitation)

25
Q

What is the downside of a really short AV delay?

A

Ventricular systole occurs before atrial emptying (loose atrial kick)

26
Q

Why can programming AV delays be tricky for heart failure patients?

A

Because they can have a big difference in RV and LV contraction time, so optimal AV timing may be different for each side of circulation

27
Q

How is right intra-atrial conduction delay measured?

A

From beginning of p wave (or signal recorded in RA) to onset of atrial depolarisation in the para-Hisian bundle region

Normal = 30-60ms

28
Q

How is interatrial conduction time measured?

A

Beginning of p-wave/signal recorded in RA to onset of left atrial depolarisation, measured at distal coronary sinus.

Normal = 60-85ms

29
Q

What are signs that AV optimisation might be helpful? (2)

A
  1. P wave duration >120ms

2. Absent or negative PR segment

30
Q

Describe the relationship between HR and AV delay

A

Linear relationship/inversely proportional. AV slickens up as HR increases

31
Q

Describe when AV delays may not shorten with increased heart rate (2)

A
  1. Conduction disease

2. Autonomic dysfunction

32
Q

Describe how lead position and inter/intra-atrial conduction delays affect AV timing

A

Lead site affects point of activation/when signal is sensed by lead.