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Sys Path > Intro/Heart Failure > Flashcards

Intro/Heart Failure Flashcards

1
Q

What is the function of the heart?

A

So tissues receive adequate nutrients & oxygen, & waste products are removed

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2
Q

What is the first organ to form in the embryo?

A

heart

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3
Q

What chambers does the heart consist of in mammals and birds?

A

4 chambers (2 atria & 2 ventricles)

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4
Q

What are the 4 cardiac valves?

A
  1. Right atrio-ventricular (tricuspid)
  2. L atrio-ventricular (bicuspid or mitral)
  3. Aortic (semi-lunar)
  4. Pulmonic
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5
Q

Which ventricle is thicker in the adult animal?

A

L ventricle

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6
Q

Systemic circulation returns…

A

… non-oxygenated blood from the body to the R atrium via the vena cava

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7
Q
A
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8
Q

From R atrium blood passes through…

A

…right AV valve into right ventricle

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9
Q

From R ventricle blood is pumped ….

A

…into lungs via pulmonary (pulmonic) arteries

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10
Q

Blood passes from L atrium to….

A

…L ventricle through mitral valve

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11
Q

From lung…

A

… oxygenated blood returns to the L atrium via pulmonary veins

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12
Q

What are the 3 layers of the heart?

A
  1. pericardium (epicardium)
  2. myocardium (heart muscle)
  3. endocardium (atria, ventricles, & valves
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13
Q
A
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14
Q

What needs to be removed from heart to expose epicardium (is continuous with it)?

A

Pericardium

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15
Q

What is pericardium?

A

Double-layered serosal mb that covers heart & proximal part of great vessels

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16
Q

What is the parietal pericardium?

A

most external & thicker layer of pericardial sac

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17
Q

What is the visceral pericardium?

A

(aka epicardium); most internal & thinnest layer of pericardial sac that intimately covers myocardium

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18
Q

What are 2 serosal mbs of the pericardium composed of?

A

thin layer of mesothelium & CT which supports blood vessels, lymphatic vessels, nerves, & adipose tissue

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19
Q

What does the epicardial fat generally follow?

A

Coronary grooves

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20
Q

What is the pericardial space & what does it contain?

A

Present btwn epicardium & pericardium. Contains small amounts of clear lubricating fluid

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21
Q

What can sometimes be mistaken for lesions on the epicardial surface?

A

prominent lymph vessels

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22
Q
A
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23
Q

What is the myocardium?

A

Muscle of the heart

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24
Q

How does the heart pump blood to the lungs & systemic circulation?

A

through contraction (systole) & relaxation (diastole)

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25
Q

How does the myocardial muscle compare to skeletal muscle?

A

they are histologically similar but not identical

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26
Q

What kind of muscle is the myocardium?

A
  • involuntary, striated muscle w/ branched fibres (a nucleus in the center of the fiber) that connect to each other through intercalated disks (wht arrows), allowing them to work as a single functional unit.
  • these fibres contain abundant mitochondria (only seen by electron microscopy).
  • CT is present btwn cardiomyocytes
  • the sarcoplasm contains myofilaments arranged in discrete bands (A, I, Z, bands) & abundant myogloblin
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27
Q

What is the endocardium?

A

thin layer internal surface of heart

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28
Q

endocardium of heart is equivalent to what in blood vessels?

A

tunica intima

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29
Q

Endocardium is in close contact w/?

A

blood

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30
Q

Endocardium is microscopically composed of these 3 layers:

A
  1. endothelium (superficial)
  2. basal lamina
  3. sub-endothelial CT (elastin & collagen)
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31
Q

Part of the conductive system & Purkinje fibres are contained in which heart layer?

A

endocardium

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32
Q

What are Purkinje Fibers?

A

Specialized myocardial cells that are responsible for electrical impulse conduction (not to be confused w/ Purkinje cells in cerebellum)

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33
Q

What do heart valves allow for?

A

Unidirectional blood flow

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34
Q

What is normal morphology of the valvular leaflets (cusps)?

A

They are thin, smooth, partially translucent, lined by endothelium, glistening, & elastic

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35
Q

How do AV valves attach to papillary muscles of ventricular myocardium?

A

Chordae tendinae

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36
Q
A
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37
Q

How to do a postmortem exam of heart?

A
  • No universal method.
  • in neonates & young animals, it’s important to carefully check for congenital heart defects
  • method chosen largely depends on the species, disease suspected, & pathologist preference
  • once the heart has been opened, it is recommended to gently wash away excess blood from atria, ventricles, & major blood vessels
  • any abnormal change should be recorded & photographed for a second opinion if deemed necessary
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38
Q

What 12 things to look at on post mortem exam of heart?

A
  1. Silouette in situ
  2. colour
  3. wall thickness
  4. shape
  5. pericardial fluid
  6. valves
  7. size
  8. fat deposits
  9. endocardium
  10. weight (total & ratios)
  11. post-mortem changes
  12. blood vessels
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39
Q

What do we look for when checking the heart in situ?

A

pay attention to relative size of heart

40
Q

Before cutting the pericardium, what should you check for?

A

presence of effusions or exudate

41
Q

enlarged hearts are called what and occur in?

A

Cardiomegaly; occur in cardiac dilation or hypertrophy, pericarditis, tumors, or pericardial effusions

42
Q

What is important to consider regarding cardiac damage?

A
  • cardiomyocytes lose their ability to regenerate soon after birth - therefore healing following damage is limited
  • functional reserve of the heart is reasonably good & compensatory mechanisms exist to mitigate damage
  • cardiac disease does not necessarily progress to heart failure
43
Q

What are the most important compensatory mechanisms of heart?

A
  1. activation of neurohumoral systems:
    - decreased CO & the resulting decreased circulating blood volume lead to the release of NE by cardiac nerves causing increased HR, augmentation of cardiac contractility & increased vascular resistance (via vasoconstriction).
    - similarly, there is activation of the renin-angiotensin-aldosterone system, which results in increased reabsorption of sodium & water by the kidneys & vasoconstriction
    - the resulting expansion of the blood volume induces secretion of atrial natiuretic peptide; this enhances sodium & water excretion & induces vasodilation as a counter mechanism
  2. cardiac dilation & hypertrophy
44
Q

What is overall enlargement of the heart called?

A

cardiomegaly

45
Q

What is cardiac output?

A

heart rate X stroke vol

46
Q

What does myocardial hypertrophy cause?

A

Greater contractility & ejection force

47
Q

MD?

A

myocardial hypertrophy

48
Q

MD?

A

cardiac dilation

49
Q

What is cardiac dilation in response to?

A

an increased workload in both physiologic & pathologic states

50
Q

What does cardiac dilatation (dilation) cause?

A

increased stroke (blood) volume

51
Q

MD?

A

cardiac dilation

52
Q

How does cardiac dilatation (dilation) work?

A
  • myocardial fibers stretch thereby increasing contractile force, stoke volume, & cardiac output (Frank-Starling relationship)
  • increased contractile force has limit, after which increased stretch will result in decrease in tension developed
  • chronic dilation of ventricle can occur through addition of sarcomeres & hence lengthening of myocytes
  • acute overload leads to dilation, chronic volume overload causes hypertrophy
53
Q

Two types of cardiac hypertrophy?

A

Primary (idiopathic) or secondary

54
Q

Where can cardiac hypertrophy occur?

A

biventricular, right ventricle, or left ventricle

55
Q

3 things about primary hypertrophy?

A

less common, irreversible, & mostly seen in Ca & Fe

56
Q

Hypertrophy occurs in the heart, …. does not

A

Hyperplasia (these cells cannot multiply

57
Q

How does hypertrophy develop secondarily?

A

due to sustained increase in cardiac workload over several days or weeks, or due to trophic signals (like hyperthyroidism)

58
Q

what counts as an increased workload?

A
  • pumping more blood (volume overload)
  • pumping @ higher pressure (pressure overload)
59
Q

Is hypertrophy reversible & how?

A

yes; if underlying workload demand is corrected

60
Q

Why does cardiac hypertrophy have limited benefits in pathological states?

A
  • Impaired intrinsic contractility, impaired ventricular relaxation, & decreased compliance
  • this can cause increased end diastolic pressure & ultimately lead to heart failure
61
Q

What are the two types of cardiac hypertrophy?

A
  1. Concentric: increase in myocardial mass w/ thick ventricular walls & reduced ventricular chamber volume (usually associated with pressure overload)
  2. Eccentric: increase in myocardial mass with enlarged ventricular chamber & relative thinning of the walls (accompanied by dilation & usually associated w/ volume overload)
62
Q

Cellular stages in cardiac hypertrophy:

A
  1. Initiation: increase in cell size (by increasing the number of sarcomeres/mitochondria)
  2. compensation: stable hyperfunction of the heart w/ no clinical signs
  3. deterioration: degeneration of hypertrophied cardiomyocytes & loss of contractility followed by heart failure
63
Q

How does right sided heart hypertrophy present and what are some examples?

A

broad base; pulmonic (arterial) stenosi, Brisket disease, pulmonary hypertension (cor pulmonale)

64
Q

How does left sided heart hypertrophy present and what are some examples?

A

increased length; aortic & sub-aortic stenosis, feline hyperthyroidism, systemic hypertension

65
Q

How does bilateral heart hypertrophy present and what are some examples?

A

globose (rounded); hypertrophic cardiomyopathy, various congenital heart defects (tetralogy of Fallot)

66
Q

How does myocardial hypertrophy present histopathologically?

A
  • can be hard to evaluate microscopically w/o morphometric methods (measurement of cell size)
  • cardiomyocytes increase in width, nuclei increase in size, while sarcomeres, myofilaments, & mitochondria increase in number
  • hyperplasia (increase in the number of cells) does not occur in heart muscle cells
67
Q

What is cardiac failure?

A

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

68
Q

What happens when cardiac dysfunction is not properly compensated for?

A
  1. decreased CO via aorta &/or pulmonic arteries (anterograde component) -> hypotension, depression, lethargy, & syncope
  2. inability to adequately empty venous reservoirs (retrograde component) -> swollen abd (ascites), tachypnea, & dyspnea (resulting from pleural effusion & pulmonary edema)
69
Q

What are the basic pathophysiological mechanisms in heart failure?

A

Pump failure, outflow obstruction, blood flow regurgitation, shunting of blood, restriction of atrial/ventricular filling, conduction disorders

70
Q

Give an example of pump failure

A

weak contractility & emptying of chambers caused by myocardial degeneration, fibrosis, inflammation, &/or neoplasia

71
Q

Give an example of outflow obstruction

A

vascular or valvular stenosis, systemic of pulmonic hypertension

72
Q

Give an example of blood flow regurgitation

A

valvular insufficiency, endocardiosis, endocarditis, volume overload

73
Q

Give an example of shunting of blood

A

congenital heart defects or persistence of fetal circulation

74
Q

Give an example of restriction of atrial/ventricular filling

A

cardiac tamponade, pericarditis, tumour

75
Q

conduction disorders

A

arrythmias caused by fxnal or structural abnormalities in conduction system

76
Q

Where is congestive heart failure most commonly found & what are the most common signs?

A
  • most commonly found in dogs & cattle
  • signs: fluid retention, edema, venous congestion, & in some cases, cyanosis
77
Q

Types of congestive heart failure?

A

can be unilateral (L or R) or bilateral (biventricular), & acute or chronic

78
Q

Retrograde component of heart failure?

A

systemic/pulmonary venous stasis

79
Q

Anterograde component of heart failure?

A

decreased cardiac output

80
Q

Types of R-sided heart failure?

A
  1. pulmonic stenosis
  2. pulmonary hypertension
  3. brisket disease
  4. hardware disease
  5. pulmonary fibrosis
81
Q

Types of L-sided heart failure?

A
  1. Aortic stenosis
  2. systemic hypertension
  3. mitral endocardiosis
  4. mitral dysplasia
  5. feline hyperthyroidism
82
Q

Types of bilateral (or global) heart failure?

A
  1. tetralogy of Fallot
  2. hypertrophic
  3. cardiomyopathy
83
Q

What is cor pulmonale?

A

pulmonary hypertension & R-sided heart failure secondary to pulmonary disease

84
Q

Extracardiac lesions in R-sided heart failure?

A

Systemic venous & portal congestion & hypertension -> generalized edema, ascites, hydrothorax, & passive liver congestion (“nutmeg liver”)

85
Q

What might R sided heart failure occur secondarily to?

A

pulmonary hypertension (as in cor pulmonale, dirofilariasis, pulmonary thromboembolism, brisket disease in Cattle, & ascites syndrome in broilers)

86
Q

Extracardiac lesions in L-sided heart failure?

A

pulmonary venous congestion -> pulmonary edema & intra-alveolar hemorrhage -> red cells phagocytized by alveolar macrophages -> iron pigment in alveolar macrophages (“heart failure cells”)

87
Q

What is the fluid accumulation in the lungs caused by left sided heart failure called?

A

cardiogenic pulmonary edema

88
Q

pathogenesis of bilateral heart failure?

A

b/c the cardiovascular system is a closed circuit, failure of 1 ventricle will ultimately lead to failure of the other culminating in global or biventricular failure

89
Q

How does Brisket disease occur?

A

High altitude leading to pulmonary hypertension -> hypertrophy RV -> R sided heart failure -> ascites & sub Q edema

90
Q

Nutmeg liver

A

(Chronic passive congestion of liver).
Zonal pattern caused by congestion/necrosis/fibrosis of centrilobular regions.

91
Q

MD?

A

Congestion of liver

92
Q

MD?

A

Congestion of liver?

93
Q

Mitral endocardiosis in a dog leading to L-Sided heart failure?

A

mitral insufficiency (valve becomes v short, thick, nodular) -> passive congestion of lung -> pulmonary edema -> intra-alveolar hemorrhages -> “heart failure cells”

94
Q

MD?

A

mitral endocardiosis

95
Q

MD?

A

pulmonary congestion & edema

96
Q

MD?

A

pulmonary edema

97
Q

MD?

A

mitral endocardiosis

Sys Path (12 decks)

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