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Cardiology Flashcards

1
Q

degenerative valve disease predisposition

A

older dogs, mostly pure breeds, can also be large (GSD), small> large, males> female
- king Charles, dachshund, mini poodle, chihuahuas

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2
Q

cause degenerative valve disease

A

dogs mitral valve is most effected, cats not considered a common cause of valvular insufficiency

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3
Q

pathogenesis of degenerative valve disease

A
  • connective tissue disease
  • loss of valvular endothelial cells
  • activation of valvular interstitial cells
  • deposition of glycosaminoglycans (GAGs)
  • dissolution of ECM, oxidative damage
  • end result  thickening and elongation of the valve with loss of valvular function
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4
Q

symptoms of degenerative disease

A
  • respiratory distress: pulmonary edema, pleural effusion, pulmonary hypertension, expiratory airways collapse
  • cough: bronchial compression, pulmonary edema
  • syncope: arrhythmia, exertional/vasovagal
  • sudden cardiac death (rare)
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5
Q

diagnosis of degenerative valve disease

A
  • auscultation: detection of a typical heart murmur
    1. (pan/holo) systolic murmur
    1. point of maximal intensity : left apical area
    1. murmur intensity increases with severity
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6
Q

staging of degenerative valve disease

A

Asymptomatic:
- A (high risk of developing), B1 (mild), B2 (moderate)
- B1 – murmur present, no cardiac remodelling
- B2 – murmur present cardiac remodelling
Symptomatic:
- C (severe with CHF)
- D (worst with refractory CHF)

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7
Q

treatment of degenerative valve disease

A
  • Stage A + B1 nothing
  • B2 – pimobendane (ace inhibitor)
  • C – diet Na + restric, furosemide, spironolactone, pimobendane, ACE inhibitor, sedation, oxygen
  • D - same as C but higher dose of pimobendane and furosemide  torsemide
  • surgical treatment – mitral valve repair or hybrid procedures – transcatheter edge to edge repair
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8
Q

predisposition of canine DCM

A

sex, Dobermans, German boxers, huge breeds, cocker spaniels, dalmatians

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9
Q

cause of DCM canine

A

mostly idiopathic, but can be genetic basis too

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10
Q

canine pathogenesis of DCM

A

characterised by poor myocardial contractility with or without arrhythmia

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11
Q

canine signs of DCM

A

reduced exercise tolerance, weakness, syncope, lethargy, tachypnoea, cough, loss of muscle mass, anorexia, ascites

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12
Q

canine diagnosis of DCM

A

ECG and Holter, gallop sound, murmur
- radiography = generalised cardiomegaly

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13
Q

canine treatment of DCM

A

antiarrhythmic drug (lidocaine), with CHF: furosemide, long term therapy (pimobendane)

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14
Q

canine prognosis of DCM

A

generally guarded

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15
Q

predisposition of PDA

A

poodle, cocker spaniel, German spitz, German + Scottish shepherd, Shetland sheepdog, 3x more common in female than male

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16
Q

cause o PDA

A

genetic defect in structure of the ductus arteriosus

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17
Q

pathogenesis of PDA

A

with the birth the ductus remains open which leads to the shunting of the blood from the aorta to pulmonary artery during systole and diastole
- essence PDA leads to volume overload of the heart
- 1. decrease in stroke volume/CO
- 2. RAAS activation
- 3. Volume overload of the left ventricle

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18
Q

signs of PDA

A

asymptomatic when first diagnosed (usually)
- reduced exercise ability, tachypnoea, cough occurs sometimes

Continuous (systolic-diastolic heart murmur)
- best auscultated left cranially, over the axillary region
- systolic component of the murmur is louder than diastolic component
- precordial thrill

Hyperdynamic/kinetic (bounding) pulse – Corrigan pulse
- pulse pressure = SAP – DAP
- greater the difference between SAP and DAP pulse is stronger

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19
Q

diagnosis of PDA

A
  • Radiograph = cardiac elongation, LA and auricular enlargement and pulmonary over circulation
  • ECG = wide P waves, tall R waves and deep Q waves
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20
Q

treatment of PDA

A

Prevention of the CHF
Surgical - transthoracic approach – thoracotomy, ductal ligation

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21
Q

prognosis of PDA

A

patients with CHF, prognosis is worse

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22
Q

cause of reverse PDA + pathogenesis

A

present already at birth, or developing during the 1st several weeks of life

in which the flow Is directed from the pulmonary artery to the aorta. Occurs when the resistance in the pulmonary artery is higher than in the aorta

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23
Q

sub aortic stenosis predisposition

A

German boxer, golden retriever, German shepherd, Rottweiler, Newfoundland

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24
Q

types of sub aortic stenosis predisposition

A

subvalvualr (most common), valvular, supravalvular, subaortic stenosis (during first 12 months of life)

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25
Q

pathogenesis of sub aortic stenosis predisposition

A

leads to pressure overload because of the stenosis making it difficult for blood to flow, concentric hypertrophy of LV

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26
Q

signs of sub aortic stenosis predisposition

A
  • weak pulses in severe cases
  • (holo)systolic ejection heart murmur best heard over left heart base
  • hypodynamic/kinetic (weak) pulse in cases of severe stenosis, precordial thrill
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27
Q

diagnosis of sub aortic stenosis

A

ECG: elevated R waves, elevation of ST segment, premature ventricular contractions
- Radiographs: show left atrial + ventricular enlargement, wide cranial cardiac waist (dilated ascending aorta)

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28
Q

treatment of sub aortic stenosis

A
  • Medical - beta blockers (reduce myocardial oxygen demand)
  • interventional – cutting and high pressure valvuloplasty
  • surgical – open heart surgery
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29
Q

prognosis of sub aortic stenosis

A
  • mild stenosis – normal life span
  • moderate – most dogs normal, some have occurrence of ventricular arrhythmia and SC
  • severe – most dogs die within 3 years
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30
Q

predisposition of pulmonic stenosis

A

small dogs (whereas subaortic is large) and brachycephalic

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31
Q

types of pulmonic stenosis

A

subvalvualr (rare), valvular (most common), supravalvular (rare)

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32
Q

pathogenesis of pulmonic stenosis

A

pulmonic stenosis leads to overload, same as subaortic stenosis but concentric hypertrophy

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33
Q

signs of pulmonic stenosis

A

normal pulse

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34
Q

diagnosis of pulmonic stenosis

A

ECG – right axis shift, deep S-wave in lead 1, narrow QRS complex (hypertrophy of RV), wide QRS complex (bundle branch block)
- radiographs: pulmonary trunk bulge, RAE and RVE

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35
Q

treatment of pulmonic stenosis

A

Balloon valvuloplasty
- success defined as reduction of pressure gradient for 50% from the starting pressure gradient
- possible complications:
o acute: arrhythmias and sudden cardiac death: perforation or rupture of PA
o chronic: restenosis (rare)

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36
Q

prognosis of pulmonic stenosis

A

depends on severity of stenosis. Mild may have normal life, but severe stenosis often die within 3 years of diagnosis

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37
Q

predisposition of ventricular septal defect

A

Very common in cats, in dogs seen most in WHWT, Lakeland terriers, English bulldogs

38
Q

types of ventricular septal defect

A

Restrictive
- small defects
- no equalisation of the pressures
- blood flows in the direction of the pressure gradient, from left to right
Non-restrictive
- large defects
- equal pressures L  R
- blood flow dependent on the pressure gradient:
o from left to right, from right to left, no flow-balance

39
Q

pathogenesis of ventricular septal defect

A
  • most often located high in the membranous part of septum, just below aortic valve and under the septal tricuspid leaflet
  • typically, volume overload of the left heart
    1. Underfilling of the systemic vasculature
    1. RAAS activation
    1. Volume overload of the left heart
40
Q

symptoms of ventricular septal defect

A
  • exercise intolerance and sides of L heart failure
  • holosystolic heart murmur can be heard
  • point of maximal intensity is dependent on the location of the defect:
    o over the right hemithorax – defect under the tricuspid valve
    o Parasternally – an RV inlet/outlet tract defect
    o over the left hemithorax, in the area of the heart – defect in the vicinity of pulmonary artery
41
Q

diagnosis of ventricular septal defect

A
  • Radiographs - L – R shunt cause left heart enlargement and pulmonary over circulation
  • ECG – normal or suggest LA or LV enlargement
42
Q

treatment of ventricular septal defect

A
  • cardiopulmonary bypass or transcatheter coil
    VSD with normal heart dimensions
  • yearly re-checks and monitoring of progression
    VSD with enlarged hearts and/or heart failure
  • medical therapy of heart failure
  • surgical treatment
43
Q

prognosis of ventricular septal defect

A

with moderate sized defect, often have normal life span

44
Q

predisposition of HCM

A

middle – older cats, more common in male, Maine coon, American shorthair, BSH, Persian, Bengal, most common in domestic

45
Q

cause of HCM

A

genetic mutation

46
Q

pathogenesis of HCM

A
  • Increased thickness of left ventricular myocardium, in absence of congenital aortic stenosis or systemic arterial hypertension
  • dynamic left ventricular outflow tract obstruction often accompanies hypertrophic cardiomyopathy as well as mitral valve apparatus and papillary muscle abnormalities
  • end stage hypertrophic cardiomyopathy
47
Q

signs of ventricular septal defect

A

heart murmur, cardiac gallop, respiratory distress, pulmonary edema, pleural effusion, arrhythmias

48
Q

diagnosis of ventricular septal defect HCM?

A

Thoracic x-ray
- not suitable for diagnosis of HCM
- impossible to determine the type of cardiomyopathy
- suitable for diagnosis of pulmonary edema or pleural effusion
ECG
- neither sensitive, neither specific for diagnosis of HCM
- gold standard for diagnosis of arrhythmias
Biomarkers
- natriuretic peptides – arterial and B-type
- NT-pro BNP
o feline 1-step SNAP test, fast
o if positive in asymptomatic cat – follow with ECHO
o positive in respiratory distress – emergency and ECHO

49
Q

treatment of ventricular septal defect

A

enhance myocardial relaxation and ventricular filling, control pulmonary edema and suppress arrhythmias
- beta blockers (atenolol), diltiazem (ACEI), spironolactone

50
Q

prognosis of HCM

A

variable, asymptomatic cats is 5 years, median survival time with CHF 1-2 years

51
Q

predisposition of restrictive CM

A

older cats (2nd most common feline CM)

52
Q

cause of RCM

A

multifactorial

53
Q

pathogenesis of RCM

A

normal/decreased volume of the left ventricle, dilation of both atria, normal left ventricular myocardium thickness and severe diastolic

54
Q

signs of RCM

A

heart murmur, cardiac gallop, arrhythmias, body cavity effusion, pulmonary edema, arterial thromboembolism, poor appetite, vomiting and weight loss

55
Q

diagnosis of RCM

A
  • physical exam can show systolic murmur or mitral or tricuspid regurgitation
  • NT-proBNP may be helpful
  • radiographs: show LA or biatrial enlargement and LV or generalised heart enlargement
56
Q

treatment of RCM

A

pimobendane, atenolol or diltiazem

57
Q

prognosis of RCM

A

guarded to poor, some cats survive more than a year after diagnosis

58
Q

feline DCM predisposition

A

older cats, uncommon

59
Q

cause feline DCM

A

taurine deficienct

60
Q

pathogenesis of feline DCM

A

poor myocardial contractility

61
Q

signs of feline DCM

A

anorexia, lethargy, increased respiratory effort, hypothermia, jugular venous distension, bradycardia, increased lung sounds and pulmonary crackles

62
Q

diagnosis of feline DCM

A
  • Radiographs: generalised cardiomegaly with rounding of the cardiac apex
  • pleural effusion is common and may obscure the heart shadow
  • variable ECG: ventricular/supraventricular tachyarrhythmias, AV conduction disturbance and an LV enlargement pattern
  • plasma or whole blood taurine concentration measure to see if deficiency
63
Q

treatment of feline DCM

A

B2 – anticoagulation therapy
C – diuretics and anticoagulation therapy
D- diuretics, anticoagulation therapy and pimobendane
supplemental taurine

64
Q

prognosis of feline DCM

A

cats without deficiency of taurine prognosis is guarded to poor, with median survival time of 49 days even with pimobendane treatment

65
Q

complication of feline DCM

A

acute CHF, cardiogenic arterial thromboembolism, sudden cardiac death

66
Q

cariogenic arterial thromboembolism predisposition

A

not common in dogs

67
Q

cause of cariogenic arterial thromboembolism

A

HCM most common underlying disease in cats with arterial thromboembolism

68
Q

pathogenesis of cariogenic arterial thromboembolism

A

thrombi usually form in left heart, usually in an enlarged LA or auricle, neoplastic and systemic inflammatory disease is usually associated with it

69
Q

signs of cariogenic arterial thromboembolism

A

acute paresis/paralysis, extremely painful extremities, cyanosis of paw pads, cold extremities, pulselessness, poikilothermic, signs of poor systemic perfusion,

70
Q

diagnosis of cariogenic arterial thromboembolism

A

heart murmur (gallop)
- combination of acute onset paraparesis and absent femoral pulse
- blood glucose values lower, lactate high in blood from limbs affected by ATE
- abdominal US – presence of thrombus in distal aorta
- Xray, Echo
- azotaemia, metabolic acidosis, DIC, electrolyte abnormalities (low Na, Ca, K and high P), stress hyperglycaemia
- elevation in CK, ALT and AST
- myoglobinuria

71
Q

treatment of cariogenic arterial thromboembolism

A

external warming, opioids, antiplatelet therapy, acepromazine not recommended
- antiplatelet therapy (sodium heparin, enoxaparin, dalteparin sodium)
- thrombolytic therapy (rt-PA)

72
Q

prognosis of cariogenic arterial thromboembolism

A

overall median long-term survival is approx. 6-9

73
Q

predisposition of pericardial effusion

A

Older golden retrievers, GSD, St. Bernard dogs, no predisposition, 6-9years

74
Q

types of pericardial effusion

A

Congenital (peritoneopericardial diaphragmatic hernia and pericardial cysts), acquired (pericardial effusion and constrictive pericarditis)

75
Q

cause of pericardial effusion

A

neoplastic, idiopathic, cardiovascular (R HF, rupture of left atrium), infections (intrapericardial FB or fungal infections), metabolic (toxic): (uraemia, coagulopathies)

76
Q

signs of pericardial effusion

A

weakness, lethargy, ascites, exercise intolerance, respiratory distress, collapse, cough, vomiting

muffled heart sound, depression, hepatomegaly, ascites/ distended jugular veins, hypodynamic pulse, pleural effusion, pale MM

77
Q

diagnosis of pericardial effusion

A

physical exam  ECG  X-rays  echo  Lab

78
Q

treatment of pericardial effusion

A
  • Pericardiocentesis – initial therapy result in short-term recovery
    o Left flank, ECG monitoring, right 4-6th IC space, +/- LA, 15-20cm long catheter, complete evacuation of the effusion
  • conversative therapy – periodic pericardiocentesis
  • surgical (total/subtotal pericardiectomy, pericardiotomy, tumour removal)
  • glucocorticoids, NSAIDs
79
Q

prognosis of pericardial effusion

A

idiopathic effusion = good to excellent, hemangiosarcoma = very bad, heart base tumours – cautious, mesothelioma = extremely bad, infectious = not great

80
Q

cause of heart murmur

A

many: structural abnormalities and considered pathologic, also some are nonpathological
- nonpathological murmurs are systolic in timing
o functional: anaemia or cardiac output is increased from fever/hyperthyroidism
o innocent: soft murmur, without evidence of structural cardiac disease/ physiological alteration (often in young puppies)

81
Q

pathogenesis of heart murmur

A

occur due to a turbulence in blood flow

82
Q

grades of heart murmur

A
  1. very soft, localised murmur; heard over listening intently in quiet surrounding
  2. soft murmur, yet heard easily
  3. moderate intensity murmur that radiates, equal in intensity to that of heart tones
  4. loud murmur, louder than normal heart tones
  5. loud murmur accompanied by a palpable precordial thrill
  6. very loud murmur accompanied by a palpable precordial thrill that can be heart with the stethoscope lifted away from the chest wall
83
Q

diagnosis of heart murmur

A
  • auscultation
  • echo
84
Q

echo: LA enlargement

A

mitral insufficiency, cardiomyopathies, PDA, subaortic stenosis, ventricular septal defect, mitral stenosis

85
Q

echo: RA enlargement

A

tricuspid insufficiency, chronic respiratory disease, interatrial septal defect, pulmonic stenosis

86
Q

echo: LV enlargement (hypertrophy)

A

HCM, subaortic stenosis

87
Q

echo: LV enlargement (dilation)

A

mitral insufficiency, DCM, aortic insufficiency, PDA, ventricular septal defect, subaortic stenosis

88
Q

echo: RV enlargement

A

pulmonic stenosis, tetralogy of fallot, tricuspid insufficiency, severe heartworm severe pulmonary hypertension

89
Q

jugular veins

A
  • persistent jugular vein distension – occurs with right sided CHF
  • distension alone: pericardial effusion, right atrial mass, DCM, cranial mediastinal mass, jugular vein thrombosis
  • pulsation +/- distension: tricuspid regurgitation, pulmonic stenosis, pulmonary hypertension, 3rd degree block, constrictive pericarditis, hypervolemia
90
Q

arterial pulse

A
  • weak pulse: DCM, subaortic stenosis, pulmonic stenosis, shock, dehydration
  • strong pulse: excitement, hyperthyroidism, fever, HCM
  • very strong: PDA, fever/sepsis, severe aortic regurgitation
91
Q

differential for cyanosis

A

reverse PDA

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