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Sys Path > Cardiovascular-Heart defects > Flashcards

Cardiovascular-Heart defects Flashcards

1
Q

Function of heart

A

-perfusion of oxygen and nutrients and removal of waste products

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2
Q

Heart development

A

-first organ to form in embryo

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3
Q

Four cardiac valves

A
  1. Right AV (Tricuspid)
  2. Left AV (Bicuspid/Mitral)
  3. Aortic (semilunar)
  4. Pulmonic
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4
Q

three layers of the heart

A
  1. Pericardium (epicardium)
  2. Myocardium (muscle)
  3. Endocardium (atria, ventricles, valves)
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5
Q

Parts of the pericaridum

A
  1. Parietal- external, thicker layer
  2. Visceral- internal, thinner layer covering muscle (epicaridum)
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6
Q

pericardium serosa composition

A

-thin layer of mesothelium and connective tissue

**important for support of blood vessels, lymphatic vessels, nerves, adipose tissue

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7
Q

Pericardial space

A

-space between the epicardium and pericardium
-contains small amounts of clear lubricant fluid which is important for preventing friction between the layers

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8
Q

Myocardium

A

-muscle of heart
-contraction (systole), relaxation (diastole)

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9
Q

Myocardium histology

A

-involuntary striated muscle
-branched fibres connected through intercalated disks
-lots of mitochondria

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10
Q

Endocardium

A

-thin layer lining the internal surface of heart (equivalent to tunica intima of vessels)

-contains the purkinje fibres

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11
Q

Endocardium microscope layers

A

1.Endothelium
2.Basal lamina
3. Sub-endothelial connective tissue (elastin and collagen)

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12
Q

Purkinje fibres

A

-specialized myocardial cells
-responsible for electrical impulse conduction

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13
Q

Chordae tendinae

A

attach the papillary muscles of the ventricular myocardium to the AV valves

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14
Q

Postmortem exam of heart

A
  • silhouette
    -colour
  • wall thickness
    -shape
  • pericardial fluid
  • valves
  • size
  • fat deposits
  • endocardium
  • weight
    -post mortem changes
    -blood vessels
    -check for effusion or exudate
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15
Q

When do enlarged hearts occur?

A

-cardiac dilation or hypertrophy
- pericarditis
-tumour or pericardial effusion

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16
Q

Compensatory mechanisms when cardiac function is impaired

A
  1. Neurohumoral systems
  2. Cardiac dilation and hypertrophy
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17
Q

Neurohumoral system

A

**NE/ RAA

When activated, leads to vascular redistribution of blood, increase heart rate, increase in blood volume.
Leads to atrial natriuretic peptide secretion (counter mechanism)

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18
Q

Myocardial hypertrophy

A

-greater contractility and ejection force

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19
Q

Cardiac Dilation

A
  • increased stroke (blood) volume… AND contractile force and cardiac output

-occurs because the myofibrils become longer through addition of sarcomeres and myocyte lengthening (while diameter stays the same) which thins the wall and increased volume of chamber

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20
Q

Acute overload vs. chronic overload on the heart

A

Acute: leads to dilation

Chronic: causes hypertrophy

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21
Q

Cardiac hypertrophy cause

A

-can be primary (idiopathic) or secondary (occurs due to sustained increase in cardiac workload)

22
Q

What are ways that the heart workload can be increased?

A

1.pump more blood (volume overload)
2. pump at higher pressure (pressure overload)

23
Q

Is hypertrophy reversible?

A

yes, if workload demand is corrected

24
Q

Cons to cardiac hypertrophy

A
  • impaired intrinsic contractility
    -impaired ventricular relaxation
  • decreased compliance (not able to fill)
25
Q

Eccentric cardiac hypertrophy

A

-due to volume overload and leads to dilation

-thin ventricular wall and distended ventricle

26
Q

Concentric cardiac hypertrophy

A
  • due to reduced volume of the ventricular chamber

-thick ventricular wall and reduced ventricular space

27
Q

Cellular stages in cardiac hypertrophy

A
  1. Initiation- increase cell size (sarcomeres/mitochondria)
  2. Compensation- stable hyperfunction with no clinical signs
  3. Deterioration - degeneration of hypertrophied cardiomyocytes and loss of contractility followed by heart failure
28
Q

Heart shape- right sided cardiac hypertrophy/dilation?

A

-broad base of heart

Examples: pulmonic stenosis, brisket disease

29
Q

What results from left sided cardiac hypertrophy/dilation?

A

increased length of the heart

Examples: aortic stenosis, feline hyperthyroidism

30
Q

What results from bi ventricular cardiac hypertrophy/dilation?

A

-a rounded, globose heart

Examples: hypertrophic cardiomyopathy

31
Q

Cardiac failure

A

-heart is unable to pump blood at rate sufficient to meet the metabolic demands of the tissues

32
Q

When does cardiac failure occur?

A

when the cardiac dysfunction is not properly compensated

33
Q

What does decreased cardiac output result in?

A

Decreased cardiac output via the aorta and/or pulmonic arteries (anterograde) leads to hypotension, depression, lethargy, and syncope

34
Q

What does an inability to adequately empty the venous reservoirs result in?

A

Inability to empty venous reservoirs (retrograde) leads to swollen abdomen, tachypnea, and dyspenia (from pleural effusion and pulmonary edema)

35
Q

Basic mechanisms in heart failure

A
  1. pump failure- weak contractility and emptying from fibrosis, inflammation, myocardial degeneration
  2. Outflow obstruction- stenosis or hypertension
  3. Blood flow regurgitation- valve insufficiency, endocardiosis, endocarditis, volume overload
  4. shunting of blood- congential heart defects or persistence of fetal circulation
  5. Restriction of filling- cardiac tamponade, pericarditis, tumour
  6. Conduction disorders- arrhythmias
36
Q

Retrograde vs anterograde components

A

Retrograde- systemic/pulmonary venous stasis

Anterograde- decreased cardiac output

37
Q

Diseases associated with right sided heart failure

A

-pulmonic stenosis
-pulmonary hypertension
- brisket disease
-hardware disease
- pulmonary fibrosis

38
Q

Diseases associated with left sided heart failure

A

-aortic stenosis
-systemic hypertension
-mitral endocardiosis
-mitral dysplasia
-feline hyperthyroidism

39
Q

Diseases associated with bilateral heart failure

A

-tetralogy of fallot
-hypertrophic cardiomyopathy

40
Q

Extracardiac lesions in right side heart failure

A

-systemic venous congestion, portal congestion and hypertension

-generalized edema, ascited, hydrothorax, passive liver congestion (nutmeg liver)

41
Q

Extracardiac lesions in left side heart failure

A

-pulmonary venous congestion
-pulmonary edema and intra-alveolar hemorrhage
-red cells phagocytized by alveolar macrophages leading to iron pigment within them= heart failure cells

42
Q

Brisket disease

A

-pulmonary hypertension, leads to hypertrophy RV, leads to right side heart failure and then ascites and SQ edema (brisket swelling) and nutmeg liver

43
Q

Mitral endocardiosis

A

-mitral insufficiency leads to passive congestion of the lung, pulmonary edema, intra-alveolar hemorrhages= heart failure cells

44
Q
A

Myocardial Hypertrophy
-greater contractility and ejection force

45
Q
A

Cardiac Dilation
-increased stroke volume

46
Q
A

Eccentric Hypertrophy
-thin vascular wall and distended ventricle

47
Q
A

Concentric Hypertrophy
-thick ventricular wall and reduced ventricular space

48
Q
A

Right sided heart
-broad base
-examples: pulmonic stenosis, brisket disease

49
Q
A

Left sided heart
-increased length
-Examples: aortic stenosis, feline hyperthyroidism

50
Q
A

Bi-ventricular heart
-globose (rounded)
-Examples: hypertrophic cardiomyopathy

51
Q
A

Brisket Disease= Right sided heart failure
-edema
-nutmeg liver/ congestion/necrosis

52
Q
A

Mitral insufficiency= left sided heart failure
-pulmonary edema
-congestion of lung
-intra-alveolar hemorrhage
-heart failure cells (iron laden macrophages)

Sys Path (10 decks)

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