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define congestive heart failure
heart fails to meet oxygen demands of body

Forward failure
left heart failure- failure to pump to extremities: lethargy, weakness, exercise intolerance

Usually follows backward failure

Backward failure
RH- failure to collect systemic blood: lethargy, weakness, exercise intolerance hepatomegaly, ascites
LH- failure to collect pulmonary blood: dyspnea, pulm effusion

Usually occurs first

Pathophysiology of oedema formation in cardiac disease
venous congestion (backward failure)→ high capillary pressure → more fluid moves to tissues → lymphatic drainage overwhelmed.

Common cat presentation of cardiac disease
emergency dyspnoea. Usually don’t cough or have signs of forward failure

Haemodynamic model of heart failure
↓CO due to some initial trigger → ↓BP detected by baroreceptors → sympathetic Vc → ↑HR and contractility → ↑ strain on cardiomyocytes → heart failure progresses
Justification for ionotropes and vasodialators in cardiac disease

Neurohumoral model of heart failure
↓CO due to initial trigger → ↓kidney perfusion detected by juxtamedullary cells → RAAS activated → increase blood volume by reabsorbing more water/sodium → ↑preload → ↑CO back to normal for short term.

However, prolonged effect of RAAS causes volume overload and oedema (backward failure)

Justification for diuretics, ACE inhibitors, and aldosterone antagonists.

species differences in cardiac disease. Breed predispositions?
Dog: DCM Cat: HCM
Lg breed: DCM Sm breed: valvular dz

Why would a dog present with coughing?
Cat?
Dog- L atrial enlargement
Cat- dyspnea (pulm oedema, pleural effusion)
OR concurrent cardiac disease

Syncope versus seizure/collapse
– no warning
– occurs in exertion
– short duration, flaccid
– rapid recovery

Troponin-I
released in response to myocardial damage, usually once damage severe/end stage
Blood test available but not v. useful

BNP
hormone released in response to atrial stretch. The prohormone is stored in heart and cleaved when released. NT-proBNP is more stable than active hormone, and measured in blood test.
Used to document progression of heart disease, rule out cardiac component of respiratory disease, screen for cardiac disease in asymptomatic patients.

Why would you check kidney values in a cardiac workup?
Because you’re probably going to treat with diuretics, want to make sure kidney fn is normal. Also checks for underlying/concurrent disease.

Factors that affect cardiac radiographs
-phase of respiration (want inspiratory)
-obesity
-movement/rotation

Clockface: DV
Clockface: DV

What things do you look for on a chest film?
– cardiac size (# intercostal spaces)
– chamber size (clockface)
– great vessels: stenosis
– pulmonic vessels: pulmonary circulation
– lung pattern: oedema
– pleural effusion present?

Normal vertebral heart score
10 in dog
8 in cat

LA enlargement- what does it look like? Ddx?
LA enlargement- what does it look like? Ddx?
– terminal trachea and caudal border of heart get closer together, bulge at 2-3 on DV, no “cardiac waist”–
– indicates MMVD, DCM, HCM or PDA

LV enlargement Ddx?
LV enlargement Ddx?
– straightening of caudal heart on lateral, rounding 3-6 on DV. —
– MMVD, DCM, HCM, PDA, VSD

RA enlargement? Ddx?
RA enlargement? Ddx?
– bulge 9-11 on DV, cranial bulge in lateral–
– tricuspid insufficiency, pulmonic stenosis, DCM, HCM

RV and RA enlargement? Ddx?
RV and RA enlargement? Ddx?
– reverse ‘D’ on DV (bulge 6-9), increase sternal contact on lateral. — RV and RA enlargement.
– tricuspid insufficiency, pulmonic stenosis, DCM, HCM or Cor pumonale

aortic bulge? Ddx?
aortic bulge? Ddx?
– prominent aortic arch (lat) or bulge 12-1 DV —
– aortic stenosis, PDA

pulmonic bulge? Ddx?
pulmonic bulge? Ddx?
– bulge btwn 1-2 on DV, difficult to isolate (image is big RV + pulmonic bulge)
– pulmonic stenosis, PDA

What conditions might cause distended pulmonary arteries/veins?
left to right shunt and fluid overload.

What 3 criteria do you use to diagnose CHF from an x ray
What 3 criteria do you use to diagnose CHF from an x ray
1) big left atrium
2) big pulmonic veins
3) pulmonary oedema

Use of 2-D echocardiography
visualize moving heart and look for evidence of change in chamber demension or thickness of walls

Use of M-mode echocardiography
single US beam directed at portion of heart and plotted against time
– contractility, wall thickness and chamber dimensions can be measured objectively

Use of doppler echocardiography
Shows blood velocity, flow direction and character.
Used to investigate murmurs, stenosis

Catheterisation studies in Cardiac disease
Specialist centers, allows determination of chamber pressure, blood gas analysis and angiography.
Req’s GA + flouroscopy, thus mostly replaced by doppler US

Indications for ECG
– characterize arrythmias (rate/rhythm)
– detect chamber size (US better)
– detection of metabolic abnormalities (bioc better)
– evidence of conduction problems

Detecting heart rate from ECG
– at 25mm/s: number complexes in 15cm x 10
– at 50mm/s: number complexes in 15cm x 20

Detecting rhythm from ECG
R-R interval

def. sinus rhythm
a P for every QRS and a QRS for every P

What do changes in the P wave indicate?
Wide P wave: LA enlargement
Tall P wave: RA enlargement
(not good indicators)

What does do changes in QRS indicate?
Wide: LV enlargement
Tall: LV dialation/hypertrophy
small: effusion, obesity, hypothyroidism

What does alternating R waves indicate?
pericardial effusion

What does change in S wave indicate?
Deep S wave- RV enlargement
Wide S wave- right bundle branch block

What changes will show on ECG for electrolyte disturbances, hypoxia
prolonged QT or ST elevation (hypoxia)

Sinus arrythmia- normal finding
Sinus arrythmia- normal finding
R-R varied but a P for every QRS

Supraventricular premature complex
Supraventricular premature complex
Tachycardia
Abnormal or absent P wave
Normal QRS complex.

Supraventricular tachycardia
Supraventricular tachycardia
Extreme tachycardia (>300bpm)
Absent P wave
Normal QRS complex
Regular R-R

Atrial fibrilation
Atrial fibrilation
No P waves
irregular R-R
tachycardia
normal QRS

ddx for supraventricular premature complex/tachycardia
atrial stretch

ddx and PE findings for atrial fibrillation
-atrial stretch ass’d with DCM or endocardiosis
-marked pulse deficit, irregular rhythm

Ventricular premature complex
Ventricular premature complex
-wide weird QRS
– no P wave

Ventricular tachycardia
Ventricular tachycardia
more than 4 VPCs in a row

1st degree AV Block
1st degree AV Block
long PQ interval
Conduction across AV node slowed due to increased vagal tone

2nd degree AV Block- Mobitz type I (high vagal tone)
2nd degree AV Block- Mobitz type I (high vagal tone)
some P waves do not result in QRS.
P-R variable, increasing prior to a block

2nd degree AV Block- Mobitz type 2
2nd degree AV Block- Mobitz type 2
some P waves do not result in QRS
P-R interval is contstant

3rd degree AV block
3rd degree AV block
no relation between P and QRS. Ventricles beat at regular escape beat

Sinus arrest (high vagal tone)
Sinus arrest (high vagal tone)
no evidence of atrial activity for 2 R-R intervals

atrial standstill (hyperkalemia)
atrial standstill (hyperkalemia)
bradycardia
no P wave-
QRS wide and bizzare

What does high T wave indicate?
hyperkalemia

Sick Sinus Syndrome
Sick Sinus Syndrome
superventricular tachycardia + sinus arrest

electrical alterans (pericardial effusion)
electrical alterans (pericardial effusion)
beat to beat variation in R wave

left anterior fasicular block (cardiomyopathy)
left anterior fasicular block (cardiomyopathy)
sinus on lead 2/3 but not 1

insertable loop recorder
plant in subcut next to apex beat- constantly records ECG on 15m loop- can save if collapse

Indications to treat arrythmias
-haemodynamically significant
– life threatening
– bradycardia treat with pacemaker

Common congenital cardiac disease in dog
Subarotic stenosis > patent ductus arteriosis > mitral valve dysplasia > pulmonic stenosis > ventricular septal defect

Common congenital cardiac disease in cat
less common
VSD and AV valve dysplasia

Aortic stenosis
*pathophysiology* – narrowed left ventricular outflow tract, usually subvalvular → pressure rise in LV → LV concentric hypertrophy →
*signalment* – Boxers, GSD, Newfie, Rottie, Golden
*clinical signs* – exercise intolerence, syncope, L CHF, sudden death
*diagnosis*- systolic ejection harsh murmur PMI left heart base, poor pulse quality
ECG- ↑R wave amplitude and QRS duration, myocardial hypoxia
Rads- LV enlargement, post-stenotic dialation of aorta
US- LV wall thickening, abnormal anatomy
*treatment*- prophy abx for endocarditis, exercise restriction and A adrenergic blocking drugs
*prognosis*- good if moderately affected

PDA
*pathophysiology* – persistent foetal connection btwn aorta and pulmonary artery, blooc flows from L to R causes pulmonary hypertension, LV hypertrophy
*signalment* – CDC, poodles, GSD, Springer Spaniels, Collies, Shetland Sheep dog, Pom,
*clinical signs* – failure to thrive, L CHF (coughing, dyspnea), *continuous “machinery” type murmur*, bounding pulse, exercise intolerance, cyanosis vulva, head pink
*diagnosis*-
ECG- tall wide R wave, wide P wave (LA/V enlargement)
Rads- LA/V enlargement, bulges in great vessels (“3 knuckle”)
US- LA/V enlargement, ducts may be visible
*treatment*- Surgical occlusion of ductus
*prognosis*- good if surgical occlusion works, poor if not

Pulmonic Stenosis
*pathophysiology* -narrowed ventriular outflow, usually valvular. RV hypertrophy, RA dialation
*signalment* -boxers, beagles, Bull mastiffs, bull dogs, cocker spaniel, schnauzer, terrier, chihuahua
*clinical signs* – exercise intolerence, synchope, ascites, sudden death. Harsh L base systolic murmur.
*diagnosis*-
ECG- Deep S wave, tall P wave (R atrial enlargement)
Rads- Right AV enlargement, post stenotic pulmonic bulge
US- R vent hypertrophy, inc velocity on Doppler
*treatment*- B blockers, balloon valvuloplasty
*prognosis*- good in mild cases, otherwise poor

Mitral Valve Dysplasia
*pathophysiology* -malformation of mitral valve causing insufficiency or stenosis → eccentric LV hypertrophy→ LH failure & oedema
*signalment* -*English bull terrier*, Golden retriever, great dane
*clinical signs* – coughing, exercise intolerence, dyspnea, harsh pansystolic murmur over left apex
*diagnosis*-
ECG: LAV enlargement (tall R wave, wide QRS, wide P wave)
Rads: LAV enlargement
US: valve insufficiencies may be found, LAV enlargement
*treatment*- medical management as CHF
*prognosis*- poor, generally present in CHF

Tricuspid Valve Dysplasia
*pathophysiology* – malformation of tricuspid valve → regurg →RV hypertrophy → increased RAV pressures → increased systemic venous pressure → effusions
*signalment* – *labs*, golden retriever, GSD, Irish setters, Great Dane
*clinical signs* – right sided CHF (ascites, effusion), harsh systolic murmur over r apex, jugular venous distension
*diagnosis*-
ECG: tall R wave, wide QRS, wide P (RAV enlargement)
rads: generalized cardiomegaly (RAV enlargement)
US: RAV enlargement, tricuspid insufficiency
*treatment*- medical as CHF
*prognosis*- guarded if present in HF

Ventricular Septal Defect
*pathophysiology* – incomplete separation of the ventricles (L-R shunting), LV hypertrophy, pulmonary hypertension, lungs over perfused
*signalment* – *ESS*, Keeshonds, English Bulldog, Cat (rare)
*clinical signs* – left heart failure, may have shunt hypoxia/polycythemia. Pancystolic murmur over R ventral thorax
*diagnosis*-
ECG: Tall wide R wave, Wide P wave (LH enlargement)
Rads: LV enlargement, pulmonary oedema
US: may visualize defect
*treatment*- palliative (CHF)
*prognosis*- poor

Most common aquired cardiac disease in dog
– MMVD
-DCM
– Pericardial effusions

Most common acquired cardiac disease in cat
– HCM
– DCM

Pericardial effusions in Dogs
*pathophysiology* – idopathic or neoplasic (haemangiosarcoma, chemodectoma)
*signalment* – golden//giant breeds, GSD, Boxer tumours
*clinical signs* – lethargy, exercise intolerance, abdominal distension, pallor, prolonged CRT, weak pulses, tachycardia, ascites, hepatomegaly, pulsus paradoxus, jugular pulse
*diagnosis*-
rads: MASSIVE cardiomegaly
ECG: changing amplitude of R waves, small QRS
US: *gold standard*- effusion, masses, ascites
*treatment*- paracardiocentesis
*prognosis*- recurrence is common- treated with sub-total pericardiotomy

Angiostrongylosis
*pathophysiology* – infection with angiostronhylus vasorum, live in PA and RV of dogs. Eggs laid in pulm. paranchyma, snails/slugs intermediate hosts. PPP 50d
*signalment* – dogs
*clinical signs* – lower resp signs, R CHF, DIC may occur
*diagnosis*- eosinophilia, Thromocytopaenia (immune system), anaemia
rads: mixed parenchymal change, diffuse interstitial pattern, pulm. arterial enlargement
US: RV dialation and hypertrophy if severe, visualization of worms.
Larvae can be detected in faeces
*treatment*- fenbendazole and moxidectin
*prognosis*- good if subclinical, severe infections can be poor

Dirofilariasis
*pathophysiology* – dirofilaria immitis infection, long PP (6-7m). Female mosquito bites, passes microfilaria to blood, where it matures (3-4m). Causes pulmonary hypertension → RHF. May have inflam. response
*signalment* – dogs and cats in warm climates
*clinical signs* – cough, weight loss, tachypneoa, dypnea, abn. resp sounds, hepatomegaly, ascites, multi-organ involvement. Cats usually present per acute resp failure
*diagnosis*- can diagnose on MF detected in blood or adult worms
haem: anemia, ↑Neut, ↓Lymph ↑Eos, basos
rads: RH enlargemetn, pulm arteries enlarged/tortuous, interstitial/alveolar infiltrates in lungs
US: RV enlargement, worms may be seen
Ab test: have been exposed
Ag test: better but low sens. ELISA best
*treatment*- melarsomine but MONITOR for thrombi. Add doxycycline for bacteria living within worm. Surgical removal in high worm burdens.
*prevention*- avermectins, milbemycin. Easier than cure,w ill kill MF

Crensoma vulpis
“fox heartworm”, similar to Angiostronylus, affects older dogs, less severe effects, persistent coughing.

How should you treat a dog traveling to country with Dirofilaria
– if gone less than 1 mo: single avermectin treatment when back in UK
– if >1mo: treatment within 30 days of arrival, then monthly until 30 days after return

Dialated Cardiomyopathy aet and pathophysiology
idiopathic, doxyrubicin toxicity or taurine/carnitine deficiency (genetic) causes LV dialation. ↓CO causes neurohumoral activation (RAAS) and ↑volume → dialated LA → systolic LHF

DCM signalment and CS
*sig* – most common in dogs, usually middle aged males.
Great Dane, Irish wolfhound, Newfie, Irish setter, dobie, boxer, Old english sheepdog, springer and cocker spaniel.
Less common in cats now that commercial diets supplemented w taurine
*CS* – volume overload: poor CO, exercise intolerance, weakness (forward failure) ascites (2ary backward failure), tachycardia, arrythmias, low grade murmur/gallop rhythm.

DCM Diagnosic tests
Bloods: check T4/TSH, renal fn, electrolytes
Rads: cardomegaly (esp LA), dialated/distended vessels, oedema
ECG: Atrial fibrillation or other arrhythmia, LAV enlargement
US: dialated, rounded LAV, poor contractility (M-mode)

DCM treatment and prognosis
ACE inhibitors, furosemide, digoxin for arrhythmia, pimobendan. check up Q3mo for bloods. Prog is poor.

def. ARVC
arrythmogenic ventricular cardiomyopathy aka Boxer cardiomyopathy.
DCM with abnormal pectinate muscles, sudden death common. Treat/diag as DCM

Hypertrophic cardiomyopathy
*aet*- Genetic predispostion or hypertension, hyperthyroid, acromegaly → LV hypertrophy (diastolic failure) → LA enlargement → LHF → oedema
*sig*- CATS: main cool/ragdoll have genetic basis. Male MA/old
*CS*- poor chest compliance, systolic murmur, gallop rhythm, ↑HR, arrythmia, dyspnea, muffled heart sounds/crackles
*diag*- rads: R/LA enlargement = valentines heart, pulonary oedema, pleural effusion
ECG: normal or atrial enlargement (wide P wave), LV enlarge (tall R). LAFB common
US: check for fluid, visualize hypertrophy
*tx*- Treat underlying cause, diuretics/ACE inhib to ↓ preload, Clopridogrel/asprin to prevent embolism. amlodipine, pimobendan, ß blockers are controversial!
*prog*- poor, will die of heart disease

Restrictive cardiomyopathy, unclassified cardiomyopathy
similar to DCM in feline but different echocardiogram findings. May be early DCM.

Feline thromboembolism
*aetiology*- Secondary to cardiomyopathy, ↑ platelets, blood stasis leads to thrombus
*clinical signs*- acute onset pain/paresis, cyanotic nail beds, poor/absent peripheral pulses
*treatment*- opiods (analgesia/sedation), heparin/aspirin/clopidogrel. IVFT, treat heart disease and monitor ECG
*prognosis*- guarded to poor (20-30% recover, may reoccur)

Myocarditis
non specific cardiac disease, secondary to parasites?
ventricular arrhythmias common, diagnosis difficult. ACUTE DEATH COMMON.

Valvular Endocarditis (Myxomatous Mitral Valve Disease)
*aetiology*- ↑ GAG within connective tissue of valve → weakening → mitral insufficiency → neurohumoral activation → LAV dialation, systolic disfn
*signalment*- CAVIES, cocker, poodle, terrier, Dacshund, setter.
*clinical signs*- LOUD systolic murmur L apex. LHF → cough, dyspnea, exercise intolerance, lethargy, synchope, fem. pulse deficit
*diagnosis*- Rads defin.: CM (LAV) elevation of tracea/CVC, separated bronchioles, bronchograms
ECG- wide P waves, tall R wave, wide QRS (LAV↑). SVPC= atrial stretcch
US: thickened valve, enlarged chamber. Doppler confirms insuff.
*treatment*- Furosemide + ACE inhib + pimobendan +/- diruetics, +/-digoxin +/- spironolactone
*prognosis*- will die [eventually]

ISACHC stages of MMVD
Class Ia- asymptomatic- monitor + baseline rads
Class Ib- cardiomegaly no CS – monitor
Class II- milld CHF- ACEI + diuretics + pimobendan
Class IIIa- CHF- homecare possible – polypharmacy
Class IIIb- CHF- hospitalization- IV drugs, oxygen, dobutamine.

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