Lecture 4 Flashcards

1
Q

Are the sizes of the LV and RV ever the same?

A

Yes, but due to diff functions - change in size.

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2
Q

Heart Growth in relation to Body Growth?

A

Parallel to the body.

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3
Q

Development and size changes of the heart? Factors involved?

A

Embryo -> First few months of life; Hyperplasia (increase in the number of cells)
Childhood -> hypertrophy (increase in cell size); within 6 months double the heart size, within 1 year - tripling of heart size
Factors like GF/Thyroxine influence growth

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4
Q

What does normal heart size depend on?

A
  1. Mass and Surface Area - adequate transport needed
  2. Genetics
  3. Blood Pressure - increase pressure thus increase heart size to deal with the increased pressure.
  4. Angiotensin/catecholamines
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5
Q

Definitions: LVH (SG), Relative Thickness of Heart

A
  1. LVH - increase in MASS relative to the size of the body; bigger heart per gram than we need
    Normal SG - 1.05 g/cm3
  2. Relative Wall Thickness - thickness of wall/diameter of lumen
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6
Q

What is Cardiac Remodelling…and why can it occur?

A
  1. Change the shape/size/function of the heart.
  2. Can occur after MI
  3. Pressure overloads - stenosis, afterload
    Volume Overloads - regurgitation, preload
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7
Q

What are 2 main types of hypertrophy patterns?

A
  1. Concentric - increase in mass, increase in wall thickness, addition of sacromeres in parallel, pressure overload
  2. Eccentric - increase in mass, no increase in wall thickness, enlargement/dilation, sarcomeres added in series, volume overload
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8
Q

What are consequences of Concentric Hypertrophy?

A

Increasing thickness, reduces the tension of the wall if dealing with high pressure - don’t have to contract as much thus reducing the worry of the heart. Due to the thickness, there is less volume in the LV. Leads to diastolic dysfunction. Ventricles can’t fill as well due to the stiffness of the ventricle. Ejection fraction stays the same.

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9
Q

What are the consequences of Eccentric Hypertrophy?

A

Increasing volume - promotes further dilation. To maintain normal SV need more blood coming in EDV because contraction isn’t as effective.

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10
Q

What is Decompensation?

A

When the heart can’t compensate anymore. Eccentric, eventually with increased filling to maintain SV - leads to further dilation - leads to increased LVEDV - leads to increased LVESV - but can’t contract as efficiently - Decease EF - decreased CO - increased LVEDP (more blood in the ventricle) - back pressures

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11
Q

What are some causes of LVH - 2 main categories?

A
  1. Environmental a) high BP - concentric b) Regurgitation - eccentric c) Renal Failure d) Infiltration - sarcoidosis - pn laid down in the heart
  2. Genetic a) Hypertrophic cardiomoypathy b) Fabry’s disease - missing an enzyme thus renal failure.
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12
Q

Identification of LVH

A
  1. Forceful Apex Beat
  2. Chest Xray - larger for eccentric
  3. ECG - large QRS, and inverted T
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13
Q

Is LVH a marker, symptom, disease, or cause?

A

Marker. It is a marker of underlying problem. Risk Factor.

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14
Q

Diastolic Dysfunction

A

In concentric hypertrophy - thick muscle - stiff - thus harder to fill and contract. Need an increased pressure to squeeze the same amount of blood out because the ventricle is stiffer. Back Pressures.
Increased Pul.VP - Edema.
More reliant on Atrial Kick. More sensitive to fluids.

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15
Q

Left Ventricular Remodelling - MI

A

Following MI - scar laid down, in some patients the muscles become thinner and stretch out.
Increase BV and Increase Spherical Shape of LV (protrusion like)
Increase stretch/elongation - Hypertrophy of cells or death
ANGIOTENSIN/SYMP/ENDOTHELIN promote remodelling.

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16
Q

RVH causes

A
  1. Congenital; Transposition of the Great Arteries, RV pushes against the systemic system
  2. Pulmonary Hypertension - lung disease/embolism/L Heart Failure - all cause increased pulmonary pressure - RV has to work harder.
  3. Right Heart Valves - pulmonary stenonis, regurgitation.
17
Q

Hypertrophic Cardiomyopathy

A
  1. autosomal mutation or spontaneous mutation - in sacromere -
  2. LVH accompanies with thicker septum/myocyte disarray
  3. Thick septum - causes obstructions in BF, blocks SL
  4. Treat with defibrillator.
18
Q

Dilated Cardiomyopathy

A
  1. idiopathic
  2. mutations in sacromeres (not the same as HCM)
  3. Cytoskeleton issue
19
Q

An athlete’s heart.

A
  1. Phenotypically like HCM, normal heart function
  2. Eccentric hypertrophy that regresses with de-conditioning
  3. May increase RV, may not regress.