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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
RAAsystem
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
26
Heart disease causes decreased CO, what adaptations are used to increase CO
``` Increase HR (sympathetic) Increased SV by increasing contractility (hypertrophy), preload (dilation), decrease afterload (vasodilate), RAAs ```
27
With excessive stimulation of RAAs, you get
increased work, cardiac edema (adaptive response becomes part of the problem)
28
Why dose cardiac hypertrophy occur
-increased contractile myofilaments in mycardiocytes in response to increased work
29
What causes myocardial hypertrophy
chronic increased pressure/afterload (need to push out blood) -->concentric hypertrophy, decreased compliance
30
What causes ventricular dilation and hypertrophy
``` chronic preload (vol overload) --> eccentric hypertrophy ```
31
What are the 2 mechanisms that cause cardiac edema
Backward failure --> increased systemic venous P --> edema Forward failure (decreased CO) --> decreased BP causes activation of RAAs --> increased water retention --> edema
32
Peripheral-dependent edema | ascites, hydrothorax, hydropericardium
Right sided cardiac lesion | e.g, R AV (tricuspid) insufficiency, pulmonic stenosis, pulmonary hypertension
33
Pulmonary edema
Left sided cardiac lesion | e.g. Left AV (mitral) or aortic valvular insufficiency
34
What characterizes heart failure?
decreased CO (forward failure) pooling of blood back in venous system (backward failure) OR both
35
Acute heart failure
substantial change in HR or rhythm --> extreme drop in CO --> unexpected death, minimal lesions
36
Pale mucous membranes, oliguria
Acute L or R ventricular forward failure | decreased co = decreased BP = increased sympathetic tone/RAAS
37
Causes of acute left ventricular failure
``` large ventricular septal defects infarction of L ventricle bacterial endocarditis acute myocarditis conduction failure ```
38
Dyspnea, cough | Find L atrial dilation, pulmonary congestion, edema, hemosiderin-laden macrophages (heart failure cells)
backwards acute left ventricular failure
39
Causes of R ventricular failure
pulmonary thromboemboli!! acute myocarditis infarction of right ventricle
40
Jugular distention, hepatic & splenic enlargement, ascites, peripheral edema Find congested liver, congested right atrium
backward acute right ventricular failure
41
causes of acute biventricular failure
acute severe myocarditis cardiac tamponade primarily leads to signs of R heart failure, with time see signs of L heart failure
42
Cor Pulmonale
right heart failure secondary to pulmonary disease
43
Causes of cor pulmonale
chronic obstructive pulmonary disease (hypoxia or pulmonary hypertension) dirofilariasis acute pulmonary thromboembolism
44
Congestive/chronic heart failure (CHF) is characterized by?
vascular congestion | edema within interstitium of tissues, body cavities
45
Signs specifically of left heart CHF
rales (alveolar edema) frothy pink expectorant, cough tachypnea
46
signs specifically of right heart CHF
generalized venous engorgement (jugular common) hepatomegaly, ascites pleural effusion, pericardial effusion, peripheral edema, weight gain (retained fluid)
47
Left sided CHF
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
Right sided CHF
same causes as left sided (just on R side ) --> backup in systemic circulation
49
Ultimately, failure of 1 side of heart will result in failure of the other side due to what?
backward failure (increased afterload in the opposite ventricle)
50
How to cut a heart
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
Normal R/L AV valve circumference ratio for dogs?
2:1
52
On necropsy, where is it normal to find blood in the heart?
L ventricle should be empty - clotted blood = incomplete rigor R ventricle should have some clotted blood
53
For routine exam, what sample should be collected for histo?
L ventricular papillary muscle
54
What is brisket/high altitude dz in cattle or heartworm dz an example of?
chronic hypoxia or acidosis --> chronic pulmonary arterial hypertension --> RIGHT ventricular dilation, hypertrophy --> backward failure --> cor polmonale
55
Most important cause of congestive heart failure in dogs over 4 yrs old
Endocardiosis - chronic regenerative valvular dz (mostly AV valves)
56
Endocardiosis
``` 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
Pathogenesis of endocardiosis
regurgitation --> L atrial dilation + left ventricular dilation (b/c decreased CO --> increased Renin --> increased preload) --> eccentric hypertrophy
58
Causes of endocardial mineralizations/fibrosis
vit D toxicity prolonged debiliation (e.g. Johne's) Renal dz "jet lesions" - valvular insufficiency or stenosis
59
4 mot important myocardial lesions in animals
hypertrophy dilation myocarditis cardiomyopathy
60
Primary cardiomyopathies
idiopathic (mebe genetic predisposition) dilated cm hypertrophic cm restrictive cm
61
Secondary cardiomyopathies
Identifiable cause Nutritional (VitE/Se deficiency, Taurine deficiency cause DCM in cats) toxic, trauma, metabolic - hyperthyroidism in cats
62
Dilated cardiomyopathy
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
Hypertrophic cardiomyopathy
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
Restrictive cardiomyopathy
seen in cats, but less common | decreased diastolic vol due to fibrosis, excessive moderator bands, endocardial fibroelastosis
65
inotropic
modifying force or speed of contraction
66
chronotropic
modify HR or rhythym
67
Myocarditis
myocardial inflamm can cause cardiomyopathies
68
causes of myocarditis
bact, fungal (coccidiomycosis), protozoan, parasite (NOT dirofilaria), viral (parvo, distemper), idiopathic
69
Patent ductus arteriosus
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
R to L shunt
intitally get cyanosis | Large PDA, ventricular septal defect, tetralogy of fallot, persistent truncus arteriosis
71
Tetrology of fallot
ventricular septal defect subpulmonic stenosis detraposed aorta right ventricular hypertrophy
72
What kind of stenosis is most common in critters? humans?
1. subvalvular 2. valvular 3. supravalvular is rare
73
valvular hematocyst
common in calves, puppies | incidental - usually resolves with growth
74
persistent right aortic arch
ligamentum arteriosum band over esophagous --> megaesophagus regurge in young dougs german shepards
75
Verminous arteritis
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
Cardiovascular tumors
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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