Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Small Animal Medicine II > Chronic Degenerative Valve Disease > Flashcards

Chronic Degenerative Valve Disease Flashcards

1
Q

What is chronic valvular disease? What valves are most commonly affected?

A

impaired valve closure leads to regurgitation or backflow of blood —> typically degenerative with time, most common in dogs

  • AV valves > semilunar valves
  • mitral valve > tricuspid valve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens with mitral insufficiency?

A

blood backflows into the LA from the LV during systole, resulting in increased volume of LA and LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens with tricuspid insufficiency?

A

blood backflows into the RA from the RV during systole, resulting in increased RA and RV volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When do aortic and pulmonic insufficiencies occur? How do each compare?

A

diastole

  • AORTIC - backflow from aorta to LV
  • PULMONIC - backflow from pulmonary artery to RV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Aortic insufficiency:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are 4 characteristics of normal valves?

A
  1. thin
  2. translucent
  3. flat edges
  4. chordae tendineae connect to papillary muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is myxomatous degeneration of the cardiac valves?

A

non-inflammatory progressive disarray of valve structure caused by a defect in the integrity of the leaflet from altered synthesis and/or remodeling by type VI collagen

  • AV nodes most common: mitral > tricuspid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the multifactorial mechanisms of valve degeneration?

A
  • aging
  • genetics
  • mechanical stress: valvular stress, endothelial dysfunction, myxomatous dysfunction
  • nodular thickening, deformity, weakening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is happening this these valves?

A

L = valve leaflets are diffusely thickened with ballooning and nodules at the edges

R = thickened and elongated chordae tendineae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the most common cardiac disease in dogs? What populations are most at risk?

A

CVD

  • middle-aged to older small breeds - Poodles, Chihuahuas, Dachshunds, Yorkies, Maltese + earlier onset in CKCS
  • males > females
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What unique manifestation of CVD has a genetic component?

A

mitral stenosis —> Bull Terriers affected at younger ages with similar disease progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does CVD typically begin? Progress?

A

long preclinical/asymptomatic stage —> B1-B2

NOT all patients progress - median time to CHF is 25-32 months and most dogs liver after >6 yrs of follow-ups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hemodynamic progression of DMVD:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 4 consequences of degenerative mitral valve disease?

A
  1. increased pressure and volume of LA
  2. increased pulmonary vein and capillary pressure over 25 mmHg
  3. pulmonary edema
  4. chronic elevations in systolic pulmonary arterial pressure causes pulmonary hypertension and right-sided disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are 5 sequelae resulting from the increased pressure and volume of the LA in cases of DMVD?

A
  1. CHF
  2. pulmonary hypertension
  3. left mainstem bronchus compression = coughing
  4. syncope
  5. left atrial tear - chronic endocardial damage from jet of high-pressure blood, resulting in blood in pericardium and shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are 5 common presentations of DMVD and their causes?

A
  1. murmur - can be incidental finding on physical exam, turbulent blood flow into LA
  2. cough - airway compression by LA, tracheal/bronchial collapse, pulmonary edema
  3. increased RR/respiratory distress - pulmonary edema
  4. syncope - reflex syncope, pulmonary hypertension, arrhythmia, left atrial tear
  5. weakness, exercise intolerance, weight loss - uncommon before end-stage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is DMVD diagnosed?

A
  • PE = mumur +/- cough
  • thoracic radiographs = cause of cough/dyspnea, evaluate LA chamber size (2 orthogonal views - lateral, dorsoventral)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is commonly seen on lateral and DV radiographs in cases of DMVD?

A

LATERAL = caudodorsal distribution of pulmonary edema

DV = caudal, R > L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are 6 purposes of performing echocardiographs in cases of DMVD?

A
  1. determine underlying issue (why is there a murmur?)
  2. determine LA size
  3. determine LV size and function
  4. assess mitral valve
  5. determine size of regurgitation
  6. determine if there is pulmonary hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why is BP typically monitored in cases DMVD?

A

systemic hypertension will increase rate of progression, causing concentric LV hypertrophy and target organ damage —> normal pressure in an unstressed dog should be 140/80; if >160 in consecutive readings, treat it

  • normotensive = <140 mmHg
  • prehypertensive = 140-159 mmHg
  • hypertensive = 160-179 mmHg
  • severely hypertensive = >180 mmHg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do the in-house SNAP and quantitative send-out NT-proBNP?

A

IN-HOUSE = screening of patients suffering of respiratory distress, negative r/o cardiac disease

SEND-OUT = better for monitoring how patient is progressing

  • both used for monitoring improvement in patients —> heaper than using an echo each time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ACVIM classification of mitral valve disease:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is stage A mitral valve disease?

A

no disease or murmur, but the breed is considered high risk —> plan is to educate owners

  • CKCS
  • Poodles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is stage B1 mitral valve disease? What is necessary to distinguish this stage from others?

A

murmur or heart disease is present, but there is no significant changes structurally or clinically

  • thoracic rads - VHS < 10.5
  • echo - definitively shows no structural changes
  • BP - r/o hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What treatment is indicated for stage B1 mitral valve disease? What follow-ups are recommended?

A
  • no treatment indicated unless there is hypertension
  • continue life stage appropriate diet
  • normal exercise

recheck every 8-12 months or sooner if signs of HF develop + echo in 6-12 months depending on imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What should owners look for if it is determined their pet is in stage B1 mitral valve disease?

A
  • coughing, shortness of breath, rapid breathing while resting
  • exercise intolerance
  • collapse, fainting
  • weight loss, inappetance

good time to work on optimizing other aspects of the dog’s wellness plan - BCS, dental hygiene, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does stage B1 mitral valve disease tend to develop?

A
  • early stage that may or may not progress
  • lasts longer than stage B2
  • many dogs never develop heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What VHS is expected in stage A and B1 of mitral valve disease?

A

< 10.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is stage B2 mitral valve disease? What are the 2 major diagnostics used?

A

cardiac remodeling/enlargement from chronic valve disease is present with at least a grade III/VI murmur

  1. thoracic rads - VHS > 10.5 (must use echo for definitive diagnosis) or > 11.5 (no echo needed) + VLAS > 2.3
  2. echo - definitive diagnosis, LA:Ao > 1.6, LVDdn > 1.7
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How is stage B2 mitral valve disease defined by radiographs?

A

VHS - >10.5 is enlarged, 10.5-11.5 is a gray zone where echo is required for definitive diagnosis

VLAS - >2.3 is an enlarged LA

31
Q

How is stage B2 mitral valve disease defined by echocardiography?

A

LA:Ao - > 1.6; LA and aorta are usually close to the same size

LV diameter diastole - > 1.7

(definitive diagnosis shows moderate to severe heart remodeling/enlargement - high risk for developing LS-CHF)

32
Q

In what 3 situations is Pimobendan epecially started when the patient seems to be between stages B1 and B2 of mitral valve disease?

A
  1. echo findings show cardiac enlargement
  2. VHS >11.5
  3. incremental increase of 0.5 vertebral bodies in 6 months
33
Q

Mitral valve disease diagnosis/treatment strategies:

A
34
Q

How does stage B2 of mitral valve disease typically progress?

A
  • not all dogs progress to stage C
  • average time from B2 to CHF/stage C is 25-32 months (more likely if younger when diagnosed) with NO intervention
  • adding pimobendan (Vetmedin) can prolong progression!
35
Q

How does Pimobendan work?

A

induces calcium sensitization and inhibits phosphodiesterase (PDE3), exerting an inodilatory and vasodilatory effects —> afterload reducer

36
Q

What are the 3 major recommendations for treating stage B2 mitral valve disease? What follow-ups are recommended?

A
  1. MEDICATION - Pimobendan prolongs symptom-free survival in B2 dogs (no consensus on cats)
  2. DIET - life-stage appropriate with adequate proteins and modest Na restriction
  3. EXERCISE - normal, abbreviated strenuous exercise especially if the dog tires easily

recheck ever 4-6 months or sooner if there are signs of HF, take resting home RR at least once per week

37
Q

Management recommendations for mitral valve disease:

A
38
Q

What is the most easily monitored signs associated with development of stage C heart disease?

A

resting RR at HOME —> higher than 35/min resting or 30/min sleeping is associated with heart failure

39
Q

What are the main reasons that dogs cough with left heart disease?

A
  • pulmonary edema
  • LA presses on mainstem bronchus
  • BOTH
40
Q

What is indicative of stage C mitral valve disease? What is the most important diagnostic? What other tools can be used?

A

clinical signs and PE consistent with heart failure

thoracic radiographs —> determines presence of pulmonary edema (CHF)

  • echo - not as important, there are signs of heart failure
  • baseline CBC/Chem/UA - PCV/TS, BUN, CREAT, electrolytes, and USG to determine if patient can handle being on medications
  • BP - likely to be hypotensive
41
Q

How do patients present with stage C mitral valve disease?

A
  • clinical signs of LS-CHF
  • tachypnea, respiratory distress
  • restlessness
  • cough

(because of the high prevalence of tracheobronchial disease in the population most at risk of MMVD, the presence of a left apical murmur in a coughing dog is not diagnostic of CHF)

42
Q

What are the 4 most common drugs used for treating stage C mitral valve disease?

A
  1. Furosemide
  2. Pimobendan (Vetmedin)
  3. Spironolactone
  4. ACEi

(blood work IS indicated to ensure patient can handle these medications)

43
Q

What is indicative of stage C mitral valve disease on thoracic radiographs? What is seen in cats?

A
  • LA/LV enlargement
  • pulmonary venous distention (ventral/central)
  • pulmonary edema - interstitial to alveolar (dorsocaudal)

pleural effusion

44
Q

Cat, left heart failure

A

pleural effusion compressing lungs

45
Q

Cat, left-sided CHF:

A

pleural effusion!

46
Q

What acute treatment for CHF is recommended?

A

emergency —> pet will likely be gasping for air, have harsh lung sounds, and an elongated neck

  • supplemental O2
  • Furosemide IV or IM
  • Pimobendan to optimize CO
  • tap chest if pleural effusion is suspected on PE
  • radiographs and echo after stabilized
47
Q

How are cardiac emergency patients maintained after stabilized?

A
  • restrict physical activity to reduce oxygen consumption (cage confinement preferred)
  • supplement O2 in the least stressful manner
  • eliminate environmental stresses, like excess heat, humidity, or cold
  • transport animal on a cart or carry
  • avoid unnecessary patient handling
  • avoid oral medications
48
Q

What diagnostics are performed once a patient with a cardiac emergency is stabilized?

A
  • baseline chest rads
  • baseline blood work - BUN, CREAT, Na, K, Cl, USG
49
Q

What are the top 6 treatments recommended for patients having a cardiac emergency?

A
  1. oxygen supplementation - edema fills lungs!
  2. Furosemide - IV or IM bolus, may need to give hourly until improved respiratory symptoms OR constant rate infusion
  3. Pimobendan - only oral available in US
  4. free access to water at all times
  5. control body temperature
  6. tap abdomen or chest as needed - alleviates symptoms (100-200 mLs!)
50
Q

How is anxiety associated with dyspnea treated? What needs to be monitored at the same time?

A

narcotics + anxiolytic —> Butorphanol/Buprenorphine + Trazodone

BP and respiratory response

51
Q

Why is it recommended to tap ascites resulting from heart failure ASAP?

A
  • painful!
  • renal congestion
  • intestinal edema = poor nutrient and drug absorption, bacterial translocation
  • hepatic congestion
  • pressure on diaphragm impairs breathing
52
Q

What 3 medications are recommended for dire emergencies with fulminant heart failure or poor response to initial therapy? What do they do?

A
  1. Dobutamine - improves LV function (continuous ECG monitoring recommended to avoid tachycardia or ectopic beats)
  2. Nitroprusside - redistributes venous blood flow by venodilation
  3. Hydralazine/Amlodopine - arterial dilation
53
Q

What medication is not commonly given to patients in dire emergencies with fulminant heart failure or poor response to initial therapy?

A

nitroglycerine —> poor absorption

54
Q

When can ACEi and Spironolactone be used in patients in stage C heart failure?

A

once renal values are proven to be normal and appetite/attitude are improved —> not necessarily part of standard acute therapy, but may help

(recommend Enalapril or Benazepril)

55
Q

Acute CHF treatment summary:

A
56
Q

When can patients suffering from acute heart failure go home? What is the 7 day treatment plan once home?

A

improved radiographs, clinical signs, and blood work, clients are educated to monitor respiratory rate

  • DAY 1-2 = continue Furosemide TID + Pimobendan
  • DAY 3-7 = try Furosemide BID, keep eye on RR + Pimobendan
  • DAY 7 = recheck renal panel +/- radiographs —> start ACEi and spironolactone if all normal while keeping on tapered Furosemide and Pimobendan
  • treatment is life-long!
57
Q

Why is Spironolactone required when ACEi are already used?

A

aldosterone breakthrough (continuous synthesis by adrenal gland) despite blocking RAAS occurs in 40% of dogs

  • adds another layer of protection from RAAS
58
Q

What is the overall long-term treatment recommended for stage C CHF?

A
  • DIET = low sodium, adequate protein, monitor weight
  • ACEi = Enalapril, Benazepril BID
  • FUROSEMIDE = BID, lowest dose possible to control RR
  • SPIRONOLACTONE = SID-BID
  • PIMOBENDAN = BID

(Dogs Are For Special People)

59
Q

What 5 additional long-term therapies are recommended for patients in Stage C CHF? What is avoided?

A
  1. fish oils/omega 3 FA supplementation
  2. treat arrhythmias
  3. cough suppressants
  4. bronchodilators
  5. surgical intervention

beta-blockers when in HF —> decreases myocardial contractility and worsens failure (can use once stabilized)

60
Q

What follow-up is recommended in patients in stage C CHF?

A

recheck every 2-4 months

  • must take resting home RR once per day
61
Q

What is stage D mitral valve disease?

A

refractory/end-stage heart failure —> may see right and left failure, pulmonary hypertension, severe arrhythmias (Afib), cardiac cachexia

  • now need Furosemide >8 mg/kg (resistance possible!)
62
Q

Why does treatment commonly fail at stage D heart failure? What is recommended at this point?

A

Furosemide has an unpredictable oral bioavailability, requires adequate renal blood flow, has a short half-life and duration, and can activate RAAS —> promotes diuretic resistance!

TORSEMIDE - 10-15x potency allows for SID dosage and has much more predictable oral absorption (monitor renal values!)

63
Q

What is considered in patients in stage D failure with persistent edema/congestion?

A
  • if the patient is azotemic with an increased dose of Furosemide, but feeling well, the dosage is likely tolerated
  • SQ Furosemide to assure proper dosage
  • oral Torsemide
  • NaCl restricted diet
  • add in Thiazide (distal tubule) at a lower dose
  • reduce afterload with Amlodipine to decrease BP
64
Q

What is considered in patients in stage D failure with renal insufficiency?

A
  • can increase diuretics in azotemic patients doing well
  • venous/arterial dilators to reduce preload and afterload (max out ACEi)
  • add a dose of Pimobendan for vasodilation and contractility
65
Q

What is considered in patients in stage D failure with comorbidities?

A
  • lower BP with Amlodipine (decreases afterload)
  • treat pulmonary hypertension with Sildenafil
  • treat arrhythmias
  • add another dose of Pimobendan for vasodilation and contractility
66
Q

What is considered in patients in stage D failure if there is difficulty giving meds?

A
  • must keep owner compliance!
  • change to SID drugs or different combinations
  • Spironolactone + Benazepril = Cardalis, less pills!
  • Torsemide SID > Furosemide BID
67
Q

What are the 5 important medications that reduce afterload in cases of stage D failure?

A
  1. ACEi - Enalapril, Benazepril
  2. calcium channel blockers - Amlodipine
  3. Hydralazine
  4. Nitroprusside
  5. Pimobendan

(ACEi = more mild)

68
Q

What are 4 options of positive inotropic agents used to preserve perfusion in cases of stage D failure?

A
  1. Pimobendan (calcium sensitization, PDE3 inhibitor)
  2. Dobutamine
  3. Dopamine
  4. Digoxin (Na/K ATPase competitor)
69
Q

What are the 7 aspects to treatment of stage D heart failure?

A
  1. DIURETICS - Torsemide, Hydrochlorothiazide
  2. DIET - severe sodium restriction
  3. ANTIARRHYTHMICS - Diltiazem, Digoxin
  4. REDUCE AFTERLOAD - low dose Amlodipine (decrease mitral regurgitation)
  5. surgical intervention
  6. max out or improve azotemia - stop/taper ACEi
  7. PULMONARY HYPERTENSION - Sildenafil
70
Q

What are 4 options to add to dietary therapy for stage D heart failure?

A
  1. omega 3 fatty acids - helps with cardiac cachexia
  2. appetite stimulants
  3. anti-nausea
  4. GI protectants

(patient MUST eat!)

71
Q

What 3 results of stage D heart failure that lead to euthanasia?

A
  1. recurrent/refractory CHF
  2. chordae tendinae rupture
  3. LA rupture
72
Q

Keys to success for treating Stage C and D heart failure:

A
73
Q

ACVIM diagnostics and treatment of heart failure:

A

Small Animal Medicine II (57 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions