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BVMS 3 > Module 15 Wk 1 > Flashcards

Module 15 Wk 1 Flashcards

1
Q

(Acquired cardiac diseases in dogs - Valvular problems and Cardiomyopathies)

What is concentric hypertrophy?

A

Pressure overload where wall grows thicker towards center of heart.

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2
Q

What is eccentric hypertrophy?

A

Volume overload where wall of heart grows towards the outside

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3
Q

What is MMVD?

A

Myxomatous mitral valve disease

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4
Q

What kinds of dogs is Myxomatous mitral valve disease most common in?

A
  • Highest prevalence in medium size breeds.
  • Older dogs
  • Mostly male
  • CKCS
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5
Q

Describe what Myxomatous mitral valve disease is?

A

Changes in the cellular constituents as well as the intercellular matrix of the valve apparatus

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6
Q

In Myxomatous mitral valve disease, what do the changes to the valve lead to?

A

Irregularity of the valves leads to an inability to close properly and prolapse of LA so Insufficiency/Regurgitation

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7
Q

What are consequences of Myxomatous mitral valve disease?

A
  • There is an increase in left atrial pressure, which leads to left-sided CHF.
    The left ventricle is experiencing a volume overload due to the LA accommodating more blood, so the LV has to get bigger to push more blood forward.
  • Due to pressure being high on the left, it may cause pulmonary hypertension on the right and lead to right-sided CHF as the arteries constrict.
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8
Q

What are the different stages of heart disease?

A

Stage A: dogs at risk for developing heart disease but no clinical signs or structural changes. Predisposed.

Stage B: structural changes are present
- B1: Clear valvular insufficiency, but no clear cardiac remodelling is present. Valve leaking but heart is not big yet as heart not noticed it yet.
- B2: Clear valvular and cardiac remodelling present. Heart bigger as has noticed it

Stage C: Current or past clinical signs of heart failure. Developed oedema.

Stage D: End-stage, refractory to treatment

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9
Q

T/F a dogs with Myxomatous mitral valve disease (MMVD) is commonly asymptomatic?

A

True

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10
Q

If there is clinical symptoms what would they be?

A
  • will have a cough is severe L CHF
  • dyspnoea
  • syncope
  • Exercise Intolerance
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11
Q

What should you hear when auscultating a dog with Mitral valve disease?

A
  • Left-sided apical systolic murmur!
  • Right side? If very loud or concomitant tricuspid regurgitation
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12
Q

What would you see on radiographs of a dog with mitral valve disease?

A

congested pulmonary vein, increased left atrial size, elevation of trachea and compression of the left principal bronchus

Cowboy legs tell you L atrium get bigge!!!!!!!

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13
Q

What diagnostic tool confirms mitral valve disease and why?

A

Echocardiography confirms disease! Mitral valve changes and dilatation of left atrium/ventricle

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14
Q

T/F with mitral valve disease NTproBNP and cradiac troponin I will both increase?

A

True

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15
Q

What are your treatment opyions for the different stages of mitral valve disease?

A

Stage A, B1: nothing
Stage B2: Pimobendan
Stage C: Pimobendan + Diuretics (clinical signs)

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16
Q

What does DCM stand for?

A

Dilated cardiomyopathy

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17
Q

What is dilated cardiomyopathy?

A

It is where the muscle cannot pump therefore the heart has to try compensate by stacking more muscles in series leading to volume overload.

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18
Q

What kind of dogs does DCM effect the most?

A

It mostly affects large/giant breeds of dogs that are often middle-aged/older. Mostly males over females.

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19
Q

What is the difference between primary and secondary DCM?

A

Primary is when you inherit DCM, whereas secondary is where it mimics DCM, but the heart muscle is not the problem.

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20
Q

What sort of things could cause secondary DCM?

A
  • Arrhythmia- induced
  • Metabolic; diabetes, systemic hypertension, hypothyroidism, acromegaly and pheochromocytoma
  • Drugs and toxins; chemotherapeutic agents, catecholamines
  • Nutrition
  • Myocarditis (inflammatory); infectious and non-infectious diseases
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21
Q

Describe DCM with big words babes

A

The Myocardium is sick leading to systolic Dysfunction. This causes low cardiac output (exercise intolerance) and Cardiac Remodelling stimulus (left eccentric hypertrophy). Resulting in Left (+ right) sided congestive heart failure.

ANDDDD a Sick heart = Arrhythmias = Syncope/Sudden Death.

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22
Q

What would a dogs history be if the had DCM?

A
  • Asymptomatic (occult)
  • Exercise intolerance
  • Cough (acute congestive heart failure)
  • Tachypnoea, Dyspnoea
  • Right sided problem: Pleural effusion, ascites
  • Syncope
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23
Q

On a clinical exam of a dog with DCM what would you find?

A
  • A low grade murmur or none
  • Arrhythmias
  • Weak pulse
  • Tachycardia
  • Prolonged capillary refill time
  • Left sided CHF: Dyspnoea
  • Right sided CHF: Ascites
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24
Q

How should you treat a dog with DCM?

A
  • radiographs arent to slay at helping
  • biomarkers again are not super slay but can hint to cardiac probs
  • ECG good to see arrhythmias as the arrive before cardiac remodelling
  • Treat with pimobenden
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25
Q

What is the survival time once clinical signs of DCM are present in dobermanns?

A

3-4months

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26
Q

What does ARVC mean?

A

Arrhythmogenic (right ventricular) cardiomyopathy

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27
Q

What is the pathophysiology of Arrhythmogenic (right ventricular) cardiomyopathy?

A

Fatty or fibrofatty replacement of the myocardial tissue, mainly affecting the right ventricle leading to eccentric volume overload = DCM Phenotype

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28
Q

What is HCM?

A

Hypertophic cardiomyopathy is a pressure overload phenotype causing concentric hypertrophy - rare in doggos and usually asymptomatic

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29
Q

(Clinical presentation and diagnostic considerations of the small animal cardiac patient)

Describe normal heart

A
  1. The ventricles begin to contract after they have been electrically activated which raises the pressure inside the ventricular chambers above that in the atria. The mitral and tricuspid atrioventricular valves close and tense
    S1 provides an audible signal of the beginning of mechanical ventricular systole
  2. At the end of systole the ventricular pressures fall and when pressures fall below the pressures in the aorta and pulmonary artery, the aortic and pulmonic valves close. S2 is subdivided into an aortic component (A2) and a pulmonic component (P2) and provides an audible marker for the end of systole and the beginning of diastole
  3. The normal cadence of S1 and S2 (lub-dup, where “lub” is S1 and “dup” is S2) is identified first—at the cardiac apex, S1 should normally be louder, longer, and lower pitched than S2.
    S3 and S4 is normally made by the sound of the blood moving between chambers, however this is normally not heard in SA
    bro idek come back to this
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30
Q

what are the 5 qualities of a heart murmour?

A
  1. Timing
  2. Intensity
  3. Location
  4. Quality: Pleateau, Crescendo-Decrescedo, Decrescendo, Continous or Machinery
  5. Pitch: Frequency (high/low, musical)
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31
Q

What is the timing of a murmur determined by?

A

By the phase of the cardiac cycle:
- Systolic (S1 to S2)
- Diastolic (S2 to S1)
- Continuous (machinery)

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32
Q

What is intensity of the murmour?

A

How loud it it

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33
Q

What are the 3 different shapes murmours can be?

A
  • Regurgitant (also called plateau-shaped or rectangular)
  • Ejection (crescendo-decrescendo or diamond-shaped)
  • Blowing (decrescendo)
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34
Q

Describe a sinus rhythm

A
  • Regular rhythm, characterized by a monotonous S1-S2 cadence.
  • Approximately 60 – 160 bpm in dogs, 140 – 220 in cats.
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35
Q

Describe a sinus arrhythmia

A

A reg irreg pattern associated with breathing. normal or slow HR

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36
Q

What is atrial fibrillation?

A

Generally rapid irregularly irregular rhythm. atrium going cra cra

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37
Q

What are normal lung sounds created by?

A

The turbulent movement of air in the tracheobronchial tree in large airways transmits to the chest wall.

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38
Q

When do you lung sounds are abnormal?

A

Louder

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39
Q

What are the 3 categories of abnormal adventitial lung sounds?

A
  1. Crackles = Fine or Coarse
  2. Wheezes
  3. Ronchi
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40
Q

Describe fine crackles

A

They have a short duration with a high pitch. They are quickly muffled and usually are at the beginning/end of breathing.

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41
Q

When are the fine crackles found?

A

In cases of

  • Bronchitis
  • Lung oedema
  • Pneumonia
  • Lung fibrosis
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42
Q

Describe course crackles

A

They are usually lower-pitched with a longer duration than fine. You can hear them over the trachea/mouth with or without your steth

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43
Q

What do course crackles indicate?

A

fluid in the large airways

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44
Q

Describe Wheeze sounds of the lungs?

A

They have a longer duration with a relatively high frequency compared to crackles

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45
Q

What causes wheezes?

A

Sinusoidal (musical), narrowing of airway, caused by vibration of small bronchial walls.

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46
Q

Describe roncho lung sounds?

A

Longer duration but have deeper frequency than wheezes. Snoring sound.

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47
Q

What is the difference between stridor and stertor?

A

Stridor is a harsh, high-pitched sound produced by obstruction of upper airways, whereas stertor is a low-pitched nasopharyngeal obstruction.

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48
Q

What is a anacrotic pulse?

A

weak and delayed

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49
Q

What is a pulsus alternans?

A

Strong/Weak alternation

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50
Q

What is a pulsus paradoxus?

A

Weak arterial pulse during inspiration, strong during expiration

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51
Q

What is a pulsus bigeminus

A

Regular alteration of the pulse pressure caused by premature ventricular contraction

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52
Q

Describe how hepatojugular reflex occurs?

A

Right heart failure is an increase in RA pressure leading to an increase of hydrostatic pressure in the caval veins, resulting in backward failure. And pressure on the liver leads to a rise in venous pressure.

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53
Q

What does CRT evaluate?

A

Peripheral perfusion

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54
Q

What is a cough?

A

A sudden expiratory effort in which a loud expulsion of air occurs.

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55
Q

What is the name of a couch with blood in it?

A

Haemoptysis

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56
Q

What are the 4 causes of a cough?

A
  1. Respiratory: upper or lower airway and pulmonary disease
  2. Cardiac: severe LSHF or LA dilation with compression of left mainstem bronchus
  3. Pleural space disease
  4. Toxic
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57
Q

what is Eupnoea?

A

normal, unlaboured breathing.

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58
Q

What is dyspneoea?

A

respiratory difficult

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59
Q

What is Orthopnoea?

A

Severe respiratory difficult with inability to lay down.

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60
Q

What is Paradoxical breathing?

A

Breathing pattern in which the chest moves in on inhalation and out on exhalation.

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61
Q

What is syncope?

A

Defined as transient loss of consciousness (TLOC) due to cerebral hypoperfusion, characterized by a rapid onset, short duration, and spontaneous complete recovery.

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62
Q

(Congenital heart diseases in dogs and cats)

What are the 3 types of murmurs?

A
  • Pathological
  • Non-pathological – functional
  • Non-pathological – Innocent
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63
Q

What are the most common CHD in dogs?

A
  • Pulmonic Stenosis (30%)
  • Patent Ductus Arteriosus (PDA, 17-25%)
  • Subaortic Stenosis (15%)
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64
Q

What are the most common CHD in cats?

A
  • Ventricular septal defect (VSD, 40-20%)
  • PDA (3-10%)
  • Tricuspid valve dysplasia (TVD, 5-10%)
  • Atrioventricular septal defect (AVSD, ASD, 5-10%)
  • Mitral valve dysplasia (MVD, 9-13%)
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65
Q

What breed of dogs has predispositions to Pulmonic and subaortic stenosis?

A

boxers

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66
Q

What breed of dogs has predispositions to PDA, persistent right aortic arch?

A

German shepards

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67
Q

What breed of dogs has predispositions to Pulmonic stenosis?

A

Bulldogs

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68
Q

What breed of dogs has predispositions to TVD?

A

labs

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69
Q

What breed of dogs has predispositions to MVD?

A

bull terrior

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70
Q

What is Pulmonic stenosis?

A

It is a structural malformation that obstructs the blood flow from the right ventricular outflow tract to the pulmonary artery.

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71
Q

What is the consequence of this obstruction of blood flow in pulmonic stenosis?

A

The heart tries to apply more pressure to push blood through, which results in concentric hypertrophy.
The narrowing of the right ventricular outflow tract can cause right ventricular concentric hypertrophy or decrease cardiac output.

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72
Q

In pulmonic stenosis what with RV concentric hypertophy or decreased cardiac output cause?

A
  • RV concentric hypertrophy will lead to an increase in o2 concentration, causing more cardiac damage and resulting in arrhythmias, sudden death or RSHF.
  • Decrease in cardiac output can cause LS volume depletion, forward failure or exercise intolerance.
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73
Q

What do you see on a radiograph of a dog with pulmonic stenosis?

A
  • increased cardiac silhouette.
  • Big RS heart, more than 2/3rds of the heart in front of the apex
  • pulmonary artery is prominent and bulging
  • increased sternal contact
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74
Q

On an ECG of dog with pulmonic stenosis what will you see?

A
  • Right axis deviation
  • Deep S waves in lead II, III with prolonged QRS duration: right bundle branch block (RBBB).
  • Arrhythmias possible.
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75
Q

What will you see on an echocardiograph of a dog with pulmonic stenosis?

A

On the short axis, you will see the increased thickness of the RV and will see at the level of the pulmonic valve that it is operating sufficiently along with turbulence

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76
Q

How would you treat pulmonic stenosis?

A

Balloon dilation under GA, inflate balloon catheter causing more opening of the tract

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77
Q

What is PDA?

A

Patent Ductus Arteriosus is a part of fetal curculation and at birth it should close itself and regress to form the ligamentum arteriosus due to an increase in pressure. If it does not close it stays patent and allows blood shunting from L to R

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78
Q

T/F with a PDA it can go R to L too?

A

True

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79
Q

What are the consequences of a PDA?

A

PDA means that saturated blood that is meant to go back into systemic circulation goes back to the lungs.

This can increase flow to the lungs, resulting in more blood on the left side of the heart, which causes eccentric hypertrophy of the left side and ultimately CHF.

It can also cause an increase in the pulmonary artery, which causes pressure overload in the right side. The blood shunts from R to L, which is an issue as unoxygenated blood is going into systemic circulation.

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80
Q

What can unoxygenated blood going into systemic circulation cause?

A

cyanosis

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81
Q

When a dogs has PDA what are the clinical signs (L to R)

A
  • Asymptomatic, loud continuous murmur on the left base (machinery murmur)
  • Exercise intolerance, left sided congestive heart failure (CHF)
    Bounding pulse (water hammer pulse)
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82
Q

What are the clinical signs of PDA when it is Right to Left?

A
  • No continuous murmur (evtl. systolic on the right secondary to tricuspid regurgitation)
  • Hindlimb weakness (differential cyanosis)
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83
Q

What dogs are predisposed to PDA

A

German Shepherd, Belgian Shepherd, Border Collie, and Australian Shepherd, as well as other large breeds such as the Newfoundland

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84
Q

On a radiograph of a dog with PDA what will you see?

A
  • Enlarged heart
  • RS is large
  • Inverted D
  • Knuckle with 3 bulges made up of the aortic arch, MPA and L Au
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85
Q

What is subaortic stenosis?

A

It is a malformation affecting the LV outflow tract, most commely via obstruction arising in the subvalvular level but valvular aortic stenosis is also possible

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86
Q

What are the consequences of subarortic stenosis?

A

obstruction causes narrowing of the LV outflow tract causing it to be underpressure which either results in LV concentric hypertrophy or lead to decrease in cardiac output.

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87
Q

What are the consequences of LV concentric hypertrophy or decreased cardiac output with subaortic stenosis?

A
  • If LV concentric hypertrophy occurs it will lead to an increase in O2 concentration whihc will cause more cardiac damage, kead to arrythmias, sudden death or LSHF.
  • If decreased cardiac output was to occur it will cause LS volume depeletion, forward failure, excerise intolerence or syncope.
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88
Q

What would the clinical findings be for a dog that has subaortic stenosis?

A
  • Asymptomatic, ”just a murmur”
  • Left cranial systolic crescendo-decrescendo murmur
  • Weak pulse
    Exercise intolerance, syncope, sudden death, left sided heart failure
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89
Q

What would an ECG look like of a dog with subaortic stenosis?

A
  • Tall T waves due to secondary to LV hypertrophy
  • S-T segment depression
90
Q

What would you see on an echocardiograph of a dog with Subaortic stenosis?

A
  • Opening should be straight but you will see a small area narrowing
  • on colour doppler - blood going back from aortic valve, velocity too high
91
Q

What do atrialventricular defects lead to?

A

Right ventricular eccentric hypertrophy

92
Q

T/F ventricular septal defects are most common in dogs?

A

False - cats

93
Q

What is Ventricular septal defect?

A

It is communiaction between the R and L ventricles

94
Q

What are the consequences of a Ventricular septal defect?

A

It leads to a R to L shunt causing an increase in flow through the lungs.

This causes volume overload on the left side leadinf to LS CHF.

It can also cause increased pressure in the pulmonary artery causing pressure overload on the right dide leading to shunt reversal causing central cyanosis.

95
Q

What are the clinical symptons of VSD?

A
  • Asymptomatic, ”just a murmur”
  • Right systolic murmur (L  R)
  • Strong pulse
  • Exercise intolerance
  • Left sided congestive heart failure.
96
Q

What are the predisposed breeds to VSD?

A

Boxer, Golden retriever, German shepherd, rottweiler, newfoundlan

97
Q

What is tetralogy of fallot?

A

It is a congenital heart defect characterized by a combination of four anatomical abnormalities in the heart.

  1. Ventricular Septal Defect (VSD):
    (A hole in the wall (septum) between the heart’s two lower chambers (ventricles). This allows oxygen-poor blood from the right ventricle to mix with oxygen-rich blood in the left ventricle.)
  2. Pulmonary Stenosis:
    (Narrowing of the pulmonary valve or the area below it, reducing blood flow from the right ventricle to the lungs for oxygenation.)
  3. Right Ventricular Hypertrophy:
    (Thickening of the muscle of the right ventricle due to the increased effort required to pump blood through the narrowed pulmonary valve.)
  4. Overriding Aorta:
    (The aorta, which normally arises from the left ventricle, is positioned above the VSD, allowing oxygen-poor blood from the right ventricle to enter the aorta and be distributed to the body.)
98
Q

What is the pathophysiology of Tricuspid Valve Dysplasia?

A
  • The tricuspid valve may be thickened, shortened, fused, or abnormally positioned. This prevents it from closing properly.
  • As blood leaks back into the right atrium with each heartbeat, the heart compensates by increasing the workload of the right ventricle.
  • Over time, the right atrium and ventricle become dilated due to the increased volume and pressure, potentially leading to heart failure.
99
Q

What breeds are predisposed to Tricuspid valve disease?

A

Labrador Retrievers, German Shepherds, Boxers, Golden Retrievers, and Old English Sheepdogs

100
Q

(Acquired cardiac diseases in dogs - Pericardial, Neoplastic and other conditions)

What is the function of the pericardium?

A
  • It attaches the heart to the mediastinum to prevent excessive motion.
  • It provides a nearly frictionless anatomical barrier.
  • It prevents the spread of an infection or neoplasm into the heart. Contributing to diastolic coupling of the right and left ventricles.
  • It prevents acute cardiac dilation.
  • Immunological, vasomotor, paracrine, and fibrinolytic activities.
  • The mesothelium of the pecardium is metabolically active and produces prostacyclin and other substances that modulate epicardial coronary arterial tone, fibrinolysis, and sympathetic neurotransmission.
101
Q

What is meant by pericardial effusion?

A

An increase in the physiological amount of fluid in the pericardial sac, which may result in the clinical signs of cardiac tamponade.

102
Q

What is cardiac tampade?

A

It is a critical condition where there is a sudden and/or excessive accumulation of Pericardial effusion which restricts appropriate filling of the cardiac chambers.

103
Q

What are the clinial signs of acute pericardial effusion?

A
  • acute hypotension
  • cardiogenic shock
  • weakness
  • dyspnea
  • collapse or sudden death.
104
Q

What are the clinical signs of chronic pericardial effusion?

A
  • Lethargy, exercise intolerance
  • Respiratory difficulty
  • Abdominal distension
  • Cough
  • Increased thirst
  • Vomiting
105
Q

What are common aetiologies of Pericarial effusion in dogs?

A
  • Neoplastic
  • Idiopathic
106
Q

T/F it is common for pericardial effusion to be congenitial in dogs

A

False - rare

107
Q

What is the most common and worst cardiac neoplasia that causes pericardial effusion?

A

Hemangiosarcoma

108
Q

What are the 3 neuroendocrine tumours that cause pericardial effusion in dogs, and which is the most common?

A
  • Chemodectoma – most common
  • Paraganglioma
  • Ectopic thyroid carcinoma
109
Q

What is the name of the neoplasm that comes from the pericardium itself that causes pericardial effusion?

A

Pericardial Mesothelioma

110
Q

What is the Cardiac neoplasia that causes pericardial effusion more commonly in cats than dogs?

A

Lymphosarcoma

111
Q

T/F The absence of cardiac mass doesn’t mean it is not neoplastic; it might be microscopic

A

True

112
Q

What is constrictive pericardial disease?

A

Where pericardium becomes stiff after inflamation and multiple epidodes of pericardial effusion.

113
Q

What may constrictive pericardial disease cause?

A

It may cause RSHF

114
Q

What are the two types of constrictive pericardial disease in dogs?

A
  • without fluid - constrictive pericarditis
  • with small amount - effusice constrictive pericardititis
115
Q

Where do cardiac hemangiosarcomas usually arise?

A

mass arising from right atrium and/or right auricle

116
Q

What dogs are predisposed to cardiac hemangiosarcomas?

A

German Shepherd Dog, Golden and Labrador retriever

117
Q

What is the trigger of chemodectomas? and there fore what breeds are predisposed?

A

Hypoxia as trigger so brachy predisposed

118
Q

What is pulmonary hypertension?

A

A pathological hemodynamic condition defined by an increased systolic/mean pulmonary arterial pressure (PAP).

119
Q

What does chronic PAP lead too?

A

Right sided concentric hypertrophy which potentially can cause right sided heart failure.

120
Q

What are causes of Pulmonary hypertension in dogs?

A
  1. Pulmonary arterial hypertension (includes cardiac shunts).
  2. Left heart disease
  3. Secondary to respiratory disease
  4. Thromboembolic
  5. Parasitic (Heartworms, Lungworms)
  6. Miscellaneous
121
Q

Where do adult heart woe=rns live what what do they do?

A

They live in the pulmonary arteries and damage the lungs causing pulmonary hypertenion.

122
Q

Where do the microfilarie live and what are the transmitted by?

A

They are present in the blood and transmitted by mosquitos

123
Q

What is the diagnosis for heart worm?

A

Positive antigen, microfilarie positiev, echocardiograph

124
Q

How do you treat heart worm?

A

Use of macrocyclic lactone for microfilariae or Use of Melarsomine as adulticide drug.

125
Q

What is endocarditis?

A

Infection of the heart valves

126
Q

What drug can predispose dogs to having endocarditis?

A

Corticosteroids

127
Q

What are the clinical signs in dogs of endocarditis?

A

Fever, new murmur, lameness.

128
Q

What is myocarditis?

A

Pathological infiltration of the myocardium by inflammatory cells.

129
Q

(Acquired cardiac Diseases in Cats)

What is a cardimyopathy?

A

A myocardial disorder in whihc the heart muscle is structurally and functionally abnormal.

130
Q

What does HCM phenotype mean?

A

This means you have increased ventricular wall thickness, not necessarily HCM.

131
Q

What is HCM?

A

Hypertrophic cardiomyopathy is a genetic disease which effect the sarcomeres which either increases diffuse or regional ventricular wall thickness or causes a mass.

132
Q

What breeds are predisposed to HCM in cats?

A
  • Maine Coon (A31P gene) – can also be affected without it being the gene defect.
  • Ragdoll (R820W gene)
  • Sphynx, Norwegian Forest, British Shorthair
133
Q

what other factors increase cats risk of being effected by HCM?

A
  • older
  • male
134
Q

What does HCM look like histologically?

A

The myocardial filaments are no longer in an organized parallel fashion which is called myofiber disorientation. Part of the muscle will also be replaced with fibrotic tissue that is not functional (interstitial fibrosis).

135
Q

Decribe the pathophysiology of HCM

A
  • The abnormal sarcomere function will lead to chnages in the myocardium.
  • This change is called concentric hypertrophy (pressure overload)
  • As time increases the heart will loose its elasticity and become stiffer causing the heart to not be able to relax.
  • This lack of relaxation causes diastolic dysfunction.
  • Aterial thromboembolism and CHF follow.
136
Q

What is a diastolic dysfunction?

A
  • Heart is too stiff and loses the ability to relax.
  • You need to put more force to push the blood inside of the ventricle.
  • Some blood will struggle to get in, therefore will rest in the left atrium = left atrial enlargement.
137
Q

How does HCM chnage the heart?

A

Common to develop left ventricular outflow tract obstruction from systolic anterior motion of the mitral valve which is a malposition of one of the parts of the valve.

138
Q

What are the different stages of HCM?

A

A -normal (predisposed)
B1- subclinical condition – HCM present but not as bad – In cats it is when the left ventricle starts to get bigger but the atrium is still small so there is not is not a compensatory mechanism, heart still coping
B2 – Left atrium starts getting big and not working as well and have the risk of clots.
C – Clinically see and treatment
D -not responsive to treatment

139
Q

How can you differentiate between stages of HCM?

A

echocardiography

140
Q

T/F In cat population over nine years, if there is a murmur, you have 43% of chance to have HCM as a cause for it

A

true

141
Q

What would you see clinicaly in a cat with HCM?

A
  • Asymptomatic, just a murmur/arrhythmia/gallop (higher chance of HCM?)
  • Dyspnoea
  • Paradoxical breathing if pleural effusion
  • Lameness/paresis
  • Collapse – seizures like face twitching
  • Lethargy
  • Ascites
142
Q

What would you see on an ECG of a cat with HCM?

A
  • There will be a presence of arrhythmia hinting to cardiac disease.
  • These could either be ventricular complexes or Atrial fibrillation
143
Q

Are cardiac biomarkers useful when diagnosisng a cat with HCM?

A

Yes useful if cat has dyspnoea (can differentiate if cardiac or respiratory origin).
Does not tell you what cardiac disease is present.
Cardiac troponin increases if cardiac damage is present.

144
Q

What would you see on echocardiography of a cat with HCM?

A
  • Increased thickness of ventricle
  • Identify left atrial enlargement
  • Identify signs of congestive heart failure
145
Q

What are the risks that for arterial thromboembolism?

A
  • Big left atrium.
  • Reduced systolic function of the left atrium.
  • Presence of spontaneous Echocontrast (Smoke).
  • Reduced velocity of blood flow in the left auricle.
  • Clot in the left auricle/atrium.
146
Q

What is Feline Arterial Thromboembolism (FATE)?

A

It is a sudden migration of a left atrial thrombus in the systemic arteries.

147
Q

What is the 5 P rule when it comes to fate clinical signs?

A
  1. Pallor - Discoloration
  2. Polar/Poikilothermy  Cold extremities
  3. Pulselessness
  4. Paralysis/Paresis
  5. Pain
148
Q

How should you monitor HCM

A

Resting respiratory rate will increase if cardiogenic pulmonary oedema is present.
Paradoxical breathing may develop if the cat has pleural effusion.

149
Q

How should you go about treating the different stages of HCM?

A

Stage A and B1: none

Stage B2: Clopidogrel (drug that makes it hard for platelets to interact and aggregate so reduces chance of clot)

  • Platelet aggregation inhibition will reduce risk of arterial thromboembolism.
  • Sometimes Rivaroxaban

Stage C: Diuretics + (Clopidogrel)
FATE: Heparin/Clopidogrel/Pain Management

150
Q

What is the prognosis for HCM in cats?

A

Prognosis is variable

  • If congestive heart failure developed, survival about one year.
  • FATE has a poor prognosis = estimate survival of 184 days if survive first episode.
151
Q

What are the three things that are HCM phenotype - so present lile HCM but the heart muscle isnt actually the problem.

A
  • Systemic Hypertension
  • Hyperthyroidism
  • Transient Myocardial Thickening (TMT) – myocardititis without knowing whats going on
152
Q

What is systemic hypertension?

A

Blood arterial pressure is increased

153
Q

What can systemic hypertension be caused by?

A
  • Kidney disease
  • HYperthyroidism which increases BP
  • hyperaldosteronism
  • Idiopathic
154
Q

How do you treat systemic hypertension?

A

Treatment with amlodipine to reduce BP if severe.

155
Q

T/F systemic hypertension can cause damage to organ?

A

True - If your blood pressure is high, think about a fast water jet with high pressure. Eject the water at things that will break just like high-pressure blood flow will damage organs.

156
Q

What is thyrotoxic cardiomyopathy?

A

Thyrotoxic cardiomyopathy is a condition in which the heart’s structure and function are adversely affected due to excessive thyroid hormone levels

157
Q

Whats does an increase of thyroid hormone do to the heart?

A
  • Faster heart rate leading to arrhythmias.
  • Increased output leading to cardiac remodelling.
  • Effect on blood pressure.
158
Q

How should you treat thyrotoxic cardiomyopathy?

A

Treat the Hyperthyroidism
Evtl. Atenolol (Betablocker) if very tachycardic
Treat CHF + clopidogrel if necessary

159
Q

What is transient myocardial thickening?

A

Left concentric hypertrophy caused by infiltrative process (inflammation? Oedema?) that over time regresses and normalizes.

160
Q

How shoulf you treat transient myocardial thickening?

A

It is the same treatment as HCM, only good prognosis if it completely resolves. NO tests, atrium may not appear as one with HCM.

161
Q

What is DCM?

A

Dilated cardiomyopathy - Dilated left ventricle and potentially left atrium. Right side may be affected

162
Q

What are the two sub types of restrictive cardiomyopathy?

A
  • Endomyocardial form: endocardial scar (band) not enabling heart to relax very well
  • Myocardial form: normal ventricular walls and function, but increased size of left and right atrium.
163
Q

(Therapeutic Approaches -Understanding and management of Congestive Heart Failure in Small Animals)

Whats is stroke volume?

A

Amount of volume the pump moves during cycle.

164
Q

There are different way to define the type of heart failure:
* Anatomical side affected  Site differences
* Development of clinical signs  Type of failure
* Dependent on cardiac architecture  Pathomechanismus difference

A
165
Q

Cardiogenic shock is a type of forward failure, what are the clinical signs?

A
  • Weakness
  • Hypothermia
  • Hypotension
  • Perfusion Issue = «FORWARD»
166
Q

Explain tachycardia?

A

Very fast heart rate = less time to fill the heart and If not filled, cannot be pumped out.

167
Q

T/F Cardiac remodelling causes Tachycardia induced cardiomyopathy

A

True

168
Q

T/F LSHF leads to forwards failure?

A

False - LSHF is an increase in LA size which leads to an increase in hydrostatic pressure in pulmonary viens resulting in backwards failure

169
Q

What does LSHF with pleural effusion mean in terms of inflation of the lungs?

A

thye cannot inflate and cause paradoxical breathing

170
Q

Right heart Forwards failure does what?

A

Reduced ejection into pulmonary artery- low cardiac output

171
Q

What does Right heart Backwards failure cause?

A

Increased systemic venous pressure

172
Q

what does Left heart Forward failure cause?

A

Reduced ejection into aorta- low cardiac output

173
Q

What does LS Backward Failure cause?

A

Increased pulmonary venous pressure

174
Q

What is the difference of systolic and Diastolic failure?

A

Systolic heart failure is an ejection problem where as diastolic heart failure is a relaxation problem.

175
Q

What are common causes of LS systolic heart failure?

A

Dilated cardiomyopathy
Valvular/ congenital

176
Q

What are common causes of LS diastolic heart failure?

A

Hypertensive heart disease
Hypertrophic cardiomyopathy
Valvular/ congenital
Tachycardia-induced

177
Q

What are treatments of LS CHF

A
  • Oxygen supplementation: Ventilation?
  • Loop diuretics: Furosemide, Torasemide
  • Systolic Dysfunction?: Pimobendan or Dobutamine?
  • Arrhythmia treatment

Evtl. ACE inhibitor/spironolactone (mostly DCM)
Thoracocentesis if pleural effusion is present (cats).

178
Q

(The sporadic sick cow: Cardiac disease)

With RS backwards failure what happens and what are the clinical signs?

A

Blood backs up into circulation creating a high venous pressure which results in oeadema

179
Q

With RS forwards fairure what happens and what are the clinical findings?

A

There is a limiitation of blood being pumped to the lungs so see similare signs to L sided forward failure like low BP and fainting.

180
Q

T/F you dont see R and L sided forward failure much in bovines?

A

True

181
Q

What is LS backwards failure and what clinical signs do you see with it?

A

It is where the blood backs up into the lungs which tend to produce respiritory failure and cause pulmonary oeadema

182
Q

T/F normal to have mumromour and gallop/split sound when unwell in bovine?

A

True

183
Q

In bovine what are clinical signs of tramuatic pericarditits?

A
  • Muffled heart due to heart sitting in big bag of fluid
  • Splashing due to gas cap in the pericardium
  • pyrexia due to big abscess
  • CV signs
  • withers positive /thoracic pain
  • Non-specific signs – milk drop, slower to walk
184
Q

How would you go about diagnosing a cow with tramuatic pericardititis?

A
  • Clinical Signs +/- ultrasound (Easy)
  • Neutrophilia + increased globulins
185
Q

How would you treat a bovine with traumatic pericarditis?

A
  • Rarely successful
  • Broad spectrum abs- Rumenotomy (‘guddle’ for the wire)
  • Magnet
186
Q

Should you cull a cow with traumatic pericarditis?

A

Probs

187
Q

What is endocarditis?

A

Bacteria from a bacteraemia or septicaemia settle on valve leaflets causing granulomatous infection

188
Q

What is valve is more likely to be involved primarily with endocarditis?

A

Tricuspid

189
Q

What are the two diseases involved in traumatic pericarditis?

A

abscessation (chronic) and secondary cardiac tamponade (acute)

190
Q

What are the two diseases involved in endocarditis

A

abscessation (chronic) and secondary cardiac failure (slightly less chronic)

191
Q

What are the clinical signs of a bovine with endocarditis?

A
  • Murmur (variable)
  • Pyrexia (initially/intermittent)
  • Cardio-Vascular signs (Right side congestive/backward)
  • Abduction of the elbows (thoracic pain)
  • (+/-Withers positive)
192
Q

What would be increased in blood work of a bovine with endocarditis?

A

Globulins and neutrophils

193
Q

How would you go about atempting to treat bovine with endocarditiss?

A

Broad spectrum abs + NSAID’s

194
Q

In a PM room what would the heart of a Bovine who had endocarditis look like?

A

There would be classic vegetative lesion on right side of heart - these restrict blood flow and cause regurgitation, hearts doing 2x amount of work but blood not really going anywhere.

These lesions can be seen forming on the valves too.

195
Q

What predispositions are there to high altritude brisket disease?

A
  • age, pregnancy,
  • cold weather, rapid weight gain, intercurrent pulmonary diseases
  • Exposure to endotoxins, swainsonine, monocrotaline, and ionophores
196
Q

Discuss DCM in Holstein Friesians?

A

It is an autosomal resessive

197
Q

What could cause a secondary arrythmias in bovine?

A
  • Hypocalcaemia
  • Hypomagnesaemia
  • Endotoxin
  • Intestinal disease (acid/base imbalance)
  • Abdominal pain
198
Q

(Therapeutic Approaches -Interventions, Effusions and Other therapeutic Considerations )

T/F A valvular stenosis can be balloned better than a muscular stenosis?

A

True

199
Q

What are the different typrs of balloon catherters that can be used for PS?

A
  • standard
  • high
  • cutting
200
Q

What may be used to reduce stress on RS of heart when performing a PS ballooning?

A

Use of atenolol (betablocker) may be combined or used on own.

201
Q

When would you place a pacemaker implantation?

A

Bradyarrhythmias

  • High-grade second-degree atrioventricular block (II AVB)
  • Third degree AVB
  • Sick Sinus Syndrome
  • Atrial standstill
202
Q

What are the two types of pacemaker implantaions?

A
  • Transvenous
  • Epicardial (cats and very small animals)
203
Q

where are pacemaker implantations often placed?

A

Most often pace only the right ventricle

204
Q

How would you deal with pericardial effusion?

A

Pericardiocentesis

205
Q

How would you perform pericardiocentesis and thoracocentesis?

A
  • Sedation
  • Clip and prepare the area
  • Ultrasound guided
206
Q

What are the 3 effusion types in cardiac disease? and what are they made up of

A

Pure Transudate - low protein and no cells
Modified Transudate - high protein and no cells
Chylothorax in cats - mainly lymphocytes and truglceride

207
Q

(Diagnostic Approach to the Cardiorespiratory patient -From Dyspnoea to Cough)

How would you stabalise a patient with a cough?

A

Oxygen anf sedatuve with anxiolytic effects ie butorphanol

208
Q

A small dog with a cough - what is you go to cause?

A

Tracheobronchomalecia - a condition where the trachea (windpipe) and bronchi (airways leading to the lungs) are abnormally weak and prone to collapsing, leading to breathing difficulties.

209
Q

A Large dog with stridor- what is potentail cause?

A

Laryngeal paralysis

210
Q

Small dog with loud left sided heart murmour and cough - what you thinking?

A

Congestive heart failure

211
Q

What is orthopnoea?

A

Severe resp difficulty with the inability to sit down

212
Q

When cyanosis is central what does it mean?

A

There is systemic deoxygenation of arterial blood.

213
Q

When cyanosis is peripheral what does it mean?

A

There is localized reduction in oxygenated haemoglobin.

214
Q

When cyanosis is differential what does it mean?

A

There is deoxygenation of caudal part of body, with normal oxygenation of head and forelimbs.

215
Q

How does alveolar hypoventilation cause dyspnoea?

A

Due to air not reaching the lungs which could be caused by multiple things

  • Respiratory mechanics problem
  • Obstruction of the airways
  • Restriction of the lung’s expansion
  • Respiratory mechanics problem like Broken ribs, Diaphragm paralysis, Myopathies.
216
Q

What causes restriction on lung expansion?

A
  • Pleural effusion: Neoplastic, Infection, haemorrhage, hypoproteinemia, chylothorax, cardiac.
  • Pneumothorax: Traumatic, secondary to lung pathology, iatrogenic
  • Lung fibrosis
  • Diaphragm Impairment: Severe ascites, GDV
217
Q

What kind of dogs are predisposed to pulmonary fibrosis?

A

Middle to old age dogs esp. West Highland White & other terriers (“Westies’ disease”)

218
Q

What causes Impaired pulmonary diffusion?

A

Alveolar and interstitial disease processes that damage the alveoli or lengthen the path between alveoli and capillaries, in particular fluid and cell infiltration disrupt the gas exchange between alveoli and capillaries by reducing diffusion.

219
Q

What respiritory problems cause a cough?

A
  • Obstructive problems (BOAS, larynx paralysis)
  • Tracheobronchomalacia (Tracheal collapse)
  • Inflammatory (“-itis”, feline Asthma, pulmonary fibrosis)
  • Irritation (Aspiration pneumonia, foreign body)
  • Infectious
  • Neoplastic
  • Non-cardiogenic lung oedema
  • Pulmonary bleeding
220
Q

What cardiovascular problems cause a cough?

A
  • Left atrial enlargement + airway problem
  • Pulmonary oedema
221
Q

What intrathoracic problems cause a cough?

A
  • Pleural effusion
  • Mass (abscess, neoplasia)

BVMS 3 (10 decks)

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