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VM741 BOD 2 > Exam 1: Cardio > Flashcards

Exam 1: Cardio Flashcards

1
Q

Which heart wall is thicker than the other?

A

L ventricular free wall & interventricular septum, 2-4x thicker than R

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2
Q

3 main lesions seen with valve leaflets

A

Insufficient (aka leaky, fail to close –> regurgitant blood flow)
Stenotic (aka narrowed, fail to open fully)
BOTH

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3
Q

3 layers of cardiac wall

A

epicardium (outer)
myocardium
endocardium

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4
Q

Frank Starling relationship

A

ventricular dilation increases sarcomere length –> increases contractility
If overload/excessive stretch –> contractility decreases
Acute volume overload of a chamber = dilation, chronic = dilation & hypertrophy

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5
Q

what vessels supply blood to the heart?

A

L & R coronary aa.
flow mostly during dyastole
heart takes ~75% oxygen

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6
Q

How does conduction impulse flow through the heart

A

Sinoatrial node (pacemaker) –> AV node –> R & L bundle branches

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7
Q

Arrhythmia

A

injured myocytes repeatedly depolarize and become pacemakers

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8
Q

Areas of the heart with differing disease features

A

mural/valvular endocardium
myocardium
pericardium

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9
Q

What happens when there is mural/valvular endocardium injury

A

altered unidirectional pattern of blood flow

blood flow in/out of chambers is impeded = changed preload or afterload

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10
Q

Semilunar stenosis causes what?

A

supra/subvalvular stenosis
increased afterload in affected chamber
concentric hypertrophy

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11
Q

Valvular insufficiency of either AV & SL causes what?

A

increased preload
eccentric hypertrophy
(can occur mildly with stenosis, but won’t be main issue)
Can be congenital or acquired

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12
Q

AV stenosis causes what?

A

decreased preload

increased atrial afterload in affected chamber

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13
Q

Valvular/Vegetative endocarditis

A
  • caused by proliferative inflammation and erosion of valvular endocardium (rough, yellow/grey/red/friable lesions)
  • may cause systemic embolism
  • undulant fever
  • secondary to this, can get distorting fibrosis
  • bacteremia involved
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14
Q

What happens when there is myocardium injury?

A

myocardium infarction
hypertrophy in response to increased workload
replacement fibrosis
dysrhythmia (acute, focal injuries to cardiomyocytes)

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15
Q

If see a dilated ventricular lumen and a normal/thin ventricular wall

A

increased preload, ineffective contractility
due to valvular insufficiency or vascular shunt
If no obvious inciting cause, consider dilated cardiomyopathy

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16
Q

If see hypertrophy or ventricular wall thickness

A

increased afterload
due to stenotic valve or shunt
If no obvious inciting cause, consider primary myocardial dz like hypertrophic cardiomyopathy

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17
Q

What happens when there is pericardium injury

A

Pericardium can’t stretch to accomodate fluid –> cardiac tamponade (fluid in sac compresses heart)

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18
Q

Clear fluid accumulated in pericardial sac

A

hypoproteinemia, heart failure

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19
Q

fibrinous fluid, pus accumulated in pericardial sac

A

infection

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20
Q

blood accumulated in pericardial sac

A

chamber rupture

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21
Q

Arrhythmia due to multiple disturbances to impulse formation/conduction

A

erratic filling and contraction –> decreased CO, tachyarrhythmia

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22
Q

Common forms of congenital blood flow shunts

A

patent ductus arteriosus
Patent foramen ovale/atrial septal defect
ventricular septal defect
(cause both increased pre and afterload)

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23
Q

Causes of restricted atrial and ventricular filling

A

fibrosis, cardiac tamponade, hypertrophic cardiomyopathy, reduced peri/myocardium compliance (–> increased venous P, congestive heart failure)

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24
Q

What happens in response to decreased CO?

A

compensatory mech to maintain tissue perfusion, systemic BP - activation of renin angiotensin aldosterone system, sympathetic activation

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25
Q

RAAsystem

A

kidneys release renin
Renin stimulates angiotensin formation in blood/tissues
Angiotensin II causes peripheral vasoconstriction, ADH release from pituitary (Na, water retention), & stimulates aldosterone release from adrenals (more na, water retention), which feedback loops to kidney

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26
Q

Heart disease causes decreased CO, what adaptations are used to increase CO

A 
Increase HR (sympathetic)
Increased SV by increasing contractility (hypertrophy), preload (dilation), decrease afterload (vasodilate), RAAs
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27
Q

With excessive stimulation of RAAs, you get

A

increased work, cardiac edema (adaptive response becomes part of the problem)

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28
Q

Why dose cardiac hypertrophy occur

A

-increased contractile myofilaments in mycardiocytes in response to increased work

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29
Q

What causes myocardial hypertrophy

A

chronic increased pressure/afterload (need to push out blood)
–>concentric hypertrophy, decreased compliance

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30
Q

What causes ventricular dilation and hypertrophy

A 
chronic preload (vol overload)
--> eccentric hypertrophy
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31
Q

What are the 2 mechanisms that cause cardiac edema

A

Backward failure –> increased systemic venous P –> edema

Forward failure (decreased CO) –> decreased BP causes activation of RAAs –> increased water retention –> edema

32
Q

Peripheral-dependent edema

ascites, hydrothorax, hydropericardium

A

Right sided cardiac lesion

e.g, R AV (tricuspid) insufficiency, pulmonic stenosis, pulmonary hypertension

33
Q

Pulmonary edema

A

Left sided cardiac lesion

e.g. Left AV (mitral) or aortic valvular insufficiency

34
Q

What characterizes heart failure?

A

decreased CO (forward failure)
pooling of blood back in venous system (backward failure)
OR both

35
Q

Acute heart failure

A

substantial change in HR or rhythm –> extreme drop in CO –> unexpected death, minimal lesions

36
Q

Pale mucous membranes, oliguria

A

Acute L or R ventricular forward failure

decreased co = decreased BP = increased sympathetic tone/RAAS

37
Q

Causes of acute left ventricular failure

A 
large ventricular septal defects
infarction of L ventricle
bacterial endocarditis
acute myocarditis
conduction failure
38
Q

Dyspnea, cough

Find L atrial dilation, pulmonary congestion, edema, hemosiderin-laden macrophages (heart failure cells)

A

backwards acute left ventricular failure

39
Q

Causes of R ventricular failure

A

pulmonary thromboemboli!!
acute myocarditis
infarction of right ventricle

40
Q

Jugular distention, hepatic & splenic enlargement, ascites, peripheral edema

Find congested liver, congested right atrium

A

backward acute right ventricular failure

41
Q

causes of acute biventricular failure

A

acute severe myocarditis
cardiac tamponade
primarily leads to signs of R heart failure, with time see signs of L heart failure

42
Q

Cor Pulmonale

A

right heart failure secondary to pulmonary disease

43
Q

Causes of cor pulmonale

A

chronic obstructive pulmonary disease (hypoxia or pulmonary hypertension)
dirofilariasis
acute pulmonary thromboembolism

44
Q

Congestive/chronic heart failure (CHF) is characterized by?

A

vascular congestion

edema within interstitium of tissues, body cavities

45
Q

Signs specifically of left heart CHF

A

rales (alveolar edema)
frothy pink expectorant, cough
tachypnea

46
Q

signs specifically of right heart CHF

A

generalized venous engorgement (jugular common)
hepatomegaly, ascites
pleural effusion, pericardial effusion, peripheral edema,
weight gain (retained fluid)

47
Q

Left sided CHF

A

Impaired contractility due to chronic preload OR afterload = left ventricular systolic dysfunction –> backup (congestion) in the lungs

Ventricular thickening/restriction OR other causes left ventricular diastolic dysfunction –> left sided CHF, backup in lungs

48
Q

Right sided CHF

A

same causes as left sided (just on R side ) –> backup in systemic circulation

49
Q

Ultimately, failure of 1 side of heart will result in failure of the other side due to what?

A

backward failure (increased afterload in the opposite ventricle)

50
Q

How to cut a heart

A
  1. vena cava across R atrium
  2. Cut to separate RV from other walls
  3. cut across L atrium
  4. bisect L ventricular free wall
51
Q

Normal R/L AV valve circumference ratio for dogs?

A

2:1

52
Q

On necropsy, where is it normal to find blood in the heart?

A

L ventricle should be empty - clotted blood = incomplete rigor
R ventricle should have some clotted blood

53
Q

For routine exam, what sample should be collected for histo?

A

L ventricular papillary muscle

54
Q

What is brisket/high altitude dz in cattle or heartworm dz an example of?

A

chronic hypoxia or acidosis –> chronic pulmonary arterial hypertension –> RIGHT ventricular dilation, hypertrophy –> backward failure –> cor polmonale

55
Q

Most important cause of congestive heart failure in dogs over 4 yrs old

A

Endocardiosis - chronic regenerative valvular dz (mostly AV valves)

56
Q

Endocardiosis

A 
Most common defect in general in dogs
thick, smooth, white opaque nodules at valve
mitral (left AV) most common site
no fever, murmurs common
myxomatous degeneration on histo
57
Q

Pathogenesis of endocardiosis

A

regurgitation –> L atrial dilation + left ventricular dilation (b/c decreased CO –> increased Renin –> increased preload) –> eccentric hypertrophy

58
Q

Causes of endocardial mineralizations/fibrosis

A

vit D toxicity
prolonged debiliation (e.g. Johne’s)
Renal dz
“jet lesions” - valvular insufficiency or stenosis

59
Q

4 mot important myocardial lesions in animals

A

hypertrophy
dilation
myocarditis
cardiomyopathy

60
Q

Primary cardiomyopathies

A

idiopathic (mebe genetic predisposition)
dilated cm
hypertrophic cm
restrictive cm

61
Q

Secondary cardiomyopathies

A

Identifiable cause
Nutritional (VitE/Se deficiency, Taurine deficiency cause DCM in cats)
toxic, trauma, metabolic - hyperthyroidism in cats

62
Q

Dilated cardiomyopathy

A

CHF often 1st sign
all 4 chambers flabby, enlarged - systolic dysfunction (sometimes from longterm mitral regurge)
Doberman pinschers, large breed dogs, boxers (genetic), Taurine def. in cats

63
Q

Hypertrophic cardiomyopathy

A

most common in cats (hypothyroid assoc’d) - genetic in Maine coon
ventricular hypertrophy without dilation - diastolic dysfunction
Seen as progressing to heart failure - seen in most cardiac dz

64
Q

Restrictive cardiomyopathy

A

seen in cats, but less common

decreased diastolic vol due to fibrosis, excessive moderator bands, endocardial fibroelastosis

65
Q

inotropic

A

modifying force or speed of contraction

66
Q

chronotropic

A

modify HR or rhythym

67
Q

Myocarditis

A

myocardial inflamm can cause cardiomyopathies

68
Q

causes of myocarditis

A

bact, fungal (coccidiomycosis), protozoan, parasite (NOT dirofilaria), viral (parvo, distemper), idiopathic

69
Q

Patent ductus arteriosus

A

allows continued partial shunting of blood, intitially not an issue (L to R shunt) but can progress to R - L shunt where deoxygenated blood goes into circulation b/c right heart was overloaded and compensatory mech’s were initiated

most common congenital cardiac defect

70
Q

R to L shunt

A

intitally get cyanosis

Large PDA, ventricular septal defect, tetralogy of fallot, persistent truncus arteriosis

71
Q

Tetrology of fallot

A

ventricular septal defect
subpulmonic stenosis
detraposed aorta
right ventricular hypertrophy

72
Q

What kind of stenosis is most common in critters? humans?

A
  1. subvalvular
  2. valvular
  3. supravalvular is rare
73
Q

valvular hematocyst

A

common in calves, puppies

incidental - usually resolves with growth

74
Q

persistent right aortic arch

A

ligamentum arteriosum band over esophagous –> megaesophagus
regurge in young dougs
german shepards

75
Q

Verminous arteritis

A

Strongylus vulgaris larvae migrate –> root of cranial mesenteric a. –> desctruction = arteritis, thrombosis, ischmeia downstream (colic) –> can have arterial rupture, or arterial occlusion (thromboembolism –> saddle thrombus)

76
Q

Cardiovascular tumors

A

Hemangiosarcoma (spleen, R atrium)
Common in skin of dogs: hemangioma, hemangiopericytoma
Metastasis/secondary - lymphosarcoma, mammary adenocarcinoma
Schwannomas (neurofibroma) - cattle

VM741 BOD 2 (5 decks)

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