Lecture 50 Flashcards

1
Q

What is LV remodelling?

A
  • Normal LV mass

- Increased relative wall thickness

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2
Q

What is concentric hypertrophy?

A
  • Increased LV mass
  • Increased relative wall thickness
  • Thick
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3
Q

What is eccentric hypertrophy?

A
  • Increased LV mass
  • Normal relative wall thickness
  • Dilated
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4
Q

Concentric hypertrophy

A
  • Increased wall thickness without LV enlargement
  • Increased LV mass
  • Often due to pressure overload
  • More sarcomeres in parallel to existing sarcomeres
  • This is a compensation for pressure overload (high afterload)
  • Thicker wall reduces wall stress (Laplace’s law)
  • -> The thicker the wall, the less wall stress. This is to maintain systolic function, CO and LVEDP
  • Can be a cause of LVH
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5
Q

What are some causes of concentric hypertrophy?

A
  • HTN

- Aortic stenosis

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6
Q

Eccentric hypertrophy

A
  • Increase in chamber size and normal relative wall thickness
  • increased LV mass
  • Often due to volume overload
  • Myocyte stretch–> new sarcomeres are added in SERIES to existing ones
  • This is a compensation for volume overload (high preload)
  • The head is bigger bc it has to pump a bigger SV with each beat
  • Bc you want to maintain SV, you have a bigger LVEDV and also increase ejection fraction
  • can be cause of LVH
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7
Q

What are some causes of eccentric hypertrophy?

A
  • Mitral and aortic regurgitation

- Ventricular septal defects

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8
Q

Diastolic dysfunction

A
  • Thick muscle due to hypertrophy–> shifts muscle
  • so you need higher LVEDP to achieve same LVEDV (PRELOAD)
  • If you have a stiff ventricle, you need a higher pressure pushing blood INTO ventricle in order for it to fill to a certain volume
  • So the PRELOAD PRESSURE is actually a BACK PRESSURE into the LA and pulmonary veins
  • This pressure causes fluid to leak out of the pulmonary capillaries, causing pulmonary congestion
  • Pts are also more sensitive to fluid loading (HF) or dehydration (decreased BP)
  • -> Ventricles being stiff cannot calibrate to new filling pressure
  • -> So you have decreased filling of ventricles
  • -> This means decreased CO and MAP
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9
Q

Other causes of LVH

A
  • Following MI or cardiac injury (endocarditis)
  • Systemic diseases (obesity, diabetes, renal failure)
  • Genetic causes–> hypertrophic cardiomyopathy
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10
Q

Clinical identification of LVH

A
  • Forceful apex beat (S3 and S4)

- ECG–> will show tall voltages, and inverted T wave

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11
Q

Treatment

A
  • NO DIRECT TREATMENT
    Treat underlying condition- valves etc
  • HTN–> decrease
  • Weight loss
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12
Q

LV remodelling

A
  • Following MI
  • Get increased LV volume and more spherical shape
  • Myocyte hypertrophy and apoptosis
  • Interstitial fibrosis
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13
Q

LV remodelling causes

A
  • RAAS defetcs
  • Adrenergic NS
  • Endothelin
  • Cytokines
  • Local factors

Leads to increase HF, mortality

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14
Q

How can LV remodelling be prevented/ reduced?

A
  • Angiotensin blocking

- B adrenergic blocking

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15
Q

RVH

A
  • Congenital–> e.g. transposition of great arteries
  • Pulmonary HTN
  • -> Lung disease, pulmonary embolus, chronic L HF
  • Right heart valves–> pulmonary stenosis/ regurgitation, tricuspid regurgitation
  • NB not as common as L heart valve disease
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16
Q

Hypertrophic cardiomyopathy

A
  • Autosomal dom condition
  • +ve fam history in most cases
  • Mutations in genes for sarcomere proteins
  • Most common is B cardiomyosin heavy chain
  • Others: cardiac myosin binding protein and cardiac troponin I and T
17
Q

Hypertrophic cardiomyopathy pathology

A

Characterised by very asymmetrical LVH. The septum becomes very thick and you get very thick wall muscles. This is hypertrophy, well beyond the scale of hypertension. Increase LV thickness

  • Cellular hypertrophy
  • Myocyte disarray
18
Q

Consequences of hypertrophic cardiomyopathy

A

The problem with hypertrophy is not normally that the cavity becomes smaller. But with hypertrophic cardiomypathy, the muscle can be so extensive that it actually blocks the flow of blood getting out of the heart- there is outflow tract obstruction (significant blockage)

  • LV outflow tract obstruction
  • Diastolic dysfunction
  • Ventricular arrhythmias–> sudden death
19
Q

Dilated cardiomyopathy

A
  • Heart is enlaged
  • many causes
  • most are idiopathic
  • Many may be genetic
  • -> Sarcomere proteins (diff ones to HCM), desmosomes, cytoskeleton or other cell-cell connections
20
Q

Exercise and the heart

A

Moderate exercise reduces risk of MI, stroke and DM

- Bradycardia is normal with increased exercise training–> greater range in HR possible

21
Q

Athlete’s heart

A
  • Only seen at elite level
  • We see in these athletes something that looks almost like hyertrophic cardiomyopathy
  • Eccentric hypertrophy
  • cardiac function normal
  • usually regresses with deconditioning
  • May become very enlarged esp RV
  • This type does not regress after deconditioning, possible cause of ventricular arrhythmias