Dog and Cat 11 Flashcards
Congestive heart failure clinical signs, what is the most important clinical sign
- Early ○ ↓ exercise tolerance ○ Tachypnoea with exertion - Then ○ Increased sleeping respiratory rate (should be less than 30 breaths per minute) - MOST IMPORTANT SIGN OF CHF § Used to decide whether treatment is working or not as well ○ Elevated resting RR - Finally ○ Dyspnoea ○ +/-Moist cough ○ Lethargy, anorexia Many dogs with significant pulmonary oedema do not cough
Congestive heart failure what are some less common clinical signs
○ Acute onset severe LSCHF with no prior signs
§ Chorda tendinea rupture - significant murmur
○ Syncope (fainting - lack of oxygen to the brain)
§ Severe coughing
§ Cardiac tamponade - rare cause
□ LA tear
§ Myocardial failure
§ Pulmonary hypertension -> decreased oxygen to the brain
§ Tachyarrhythmias
§ Atrial fibrillation- irregular QRS interval, no p waves, sometimes f waves
○ Ascites -> RSCHF (tricuspid)
○ Cardiac cachexia - heart working harder, required more energy however not eating as feeling unwell - breakdown muscle
Left sided congestive heart failure what are the general clinical presentations
○ CHF (wet): § Usually high-grade murmur (4-6/6), loud S1. § Tachycardia § Tachypnoea, dyspnoea § +/-crackles, wheezes - need large amount of fluid § Brisk pulses § Pale MM (hypoxia) - CO output poor, so vasoconstriction to preserve blood flow to essential areas § Cyanosis (severe hypoxia) ○ Low output signs (cold): § Low temperature § Cool extremities § Weak pulses § Slow CRT
Right sided congestive heart failure physical examination presentation
○ +/-tricuspid murmur ○ Ascites ○ +/-Jugular distention ○ Jugular pulses ○ Hepatojugularreflux ○ SQ oedema (rare) ○ Pleural effusion (rare)
What are 9 diagnostic techniques for Myxomatous (mitral) valve disease (MMVD)
- Signalment
- History
- Clinical signs
- PE
- Thoracic radiography
○ Assess LA size
○ Evaluate lungs for LSCHF
§ oedema, +/-venous congestion
○ RSCHF- CVC distention, hepatomegaly, pleural fissure lines - Blood pressure
- echocardiography - confirm diagnosis, assess contractility, severely - LA size, large dog echo
- lab testing - electrolytes and renal parameters, hydration
- +/- ECG only if arrhythmic
What are the 4 stages of Myxomatous (mitral) valve disease (MMVD), what defines these
Stage A
- At risk for developing disease
- Cavillers king Charles spaniel - NEED TO MONITOR FOR MURMUR
Stage B
- Structural heart disease (murmur) present but no clinical signs
- B1: no radiographic or echocardiographic evidence of cardiac remodelling
- B2: Hemodynamically significant, with evidence of remodelling (heart enlargement) on imaging
Stage C - in congestive heart failure
- Past or current signs of congestive heart failure
- May include some dogs requiring advanced stage D treatments from first onset of failure
Stage D
- Clinical signs of heart failure are refractory to ‘standard therapy’
Myxomatous (mitral) valve disease (MMVD) treatment in preclinical stage A
○ Client education ○ Disease prevalence ○ Clinical signs § Exercise intolerance § Cough § Tachypnoea ○ Annual checks NO survival benefit with any drugs
Myxomatous (mitral) valve disease (MMVD) treatment in stage B1 and B2
- Stage BI (valve disease, heart normal size)
1. Client education
§ Risk of failure
□ 30%most small breeds
□ Often takes years
§ Clinical signs
2. Baseline radiographs (or echo)
3. Weight loss if overweight
4. Mild salt restriction
5. Periodic monitoring
§ Sleeping RR at home(< 30/min)
§ Check-up q 6-12 months - Stage B2 (cardiomegaly)
1. Pimobendan - delays LSCHF or cardiac death (by 15 mo)
- reduces risk of LSCHF or cardiac death (by 1/3)
Myxomatous (mitral) valve disease (MMVD) treatment in stage C
- Stage C, Mild-moderate CHF
1. Drain ascites/pleural effusion directly
2. Decrease preload (atrial filling pressure)
§ Reduce blood volume
□ Diuretic (furosemide)
□ ACE Inhibitors
□ Moderate salt restriction, avoid salt loading
3. Control neurohormonalactivation
§ ACEI, +/-spironolactone, pimobendan
4. Reduce mitral regurgitation
Pimobendan - vasodilator as well - PROLONGS SURVIVAL
Myxomatous (mitral) valve disease (MMVD) treatment for stage D
Stage D - severe/refractory CHF Oxygen, sedate, cool, minimal stress. - As for milder disease plus: ○ Diuretics § Higher dose/frequency IV § combination therapy (add spironolactone) ○ Reduce preload § venodilator ○ Tachyarrhythmias § Control HR ○ Reduce afterload § Arterial vasodilator § Keep BP > 100mmHg ○ If low output signs § Additional positive inotropes § Care with vasodilator/diuretics § Consider PHT ○ Greater sodium restriction
What are some complications of treatment for Myxomatous (mitral) valve disease (MMVD) and monitoring
Complications of therapy - Prerenal azotaemia - Hypotension and renal injury - Hypokalaemia - Compliance ○ Too many pills! ○ PU/PD, incontinent - (never restrict water) Monitoring - 1-2 weeks after discharge - q 3-6 months if stable - More frequent for severe cases
Prognosis for congestive heart failure in most small breeds, CKCS and large breeds
- Most small breeds ○ Progression over years ○ Only 30% CHF ○ Median survival after CHF 6-10 mo - CKCS ○ Usually CHF within 1-2 yrsof murmur detection ○ 30% mortality within 3-4 y - Large breeds also usually progress more quickly
Primary cardiomyopathies what is it and list 5 main ones, what all called and how to diagnose
- Primary abnormality of the cardiac muscle: ○ Dilated cardiomyopathy (DCM) ○ Hypertrophic cardiomyopathy (HCM) ○ Arrhythmogenic right ventricular CM ○ Restrictive CM ○ Unclassified CM - ALL CAUSE POOR RELAXATION OF THE VENTRICLE - Diagnosis of exclusion
Secondary cardiomypathies what are they, causes and what need to treat
- Secondary dilated cardiomyopathy: ○ Doxorubicin (toxins) ○ Trauma ○ Tachycardia-induced ○ Taurine deficiency ○ Hypothyroidism (dogs) ○ Myocarditis ○ Infarction (embolisation) - Treat the primary disease!
Canine dilated cardiomyopathy (DCM) what is the primary problem, causes and pathogenesis (how leads to failure)
- Primary progressive decline in contractility
○ Myocardial failure = systolic dysfunction - Multiple genetic factors
Pathogenesis
-> decrease contracility, decrease output -> SNS, RAAS -> AV regurg, eccentric hypertrophy ->
Decrease contractility -> compensated via dilation - Dilation -> pulls apart of the mitral valve
Systolic cardiac failure -> CHF, output failure (more likely to present with exercise intolerance and lethargy
Canine dilated cardiomyopathy (DCM) signalment, presenting sign and cardiac finding
- Signalment ○ Large-giant pure breeds - Doberman pinschers § Highest prevalence of DCM § Usually present 5-7 years old § Autosomal dominant □ Males present earlier/more severely § Long preclinical phase (2-4 yrs) -> may not hear murmur for awhile ○ Some spaniels ○ Middle aged-older ○ Males - Presenting signs ○ Sudden death ○ Syncope ○ CHF (L > R) - Cardiac findings ○ Tachyarrhythmias common - due to large breed dogs ○ Mitral murmur
Doberman pinschers DCM prognosis, why and how to pre-screen
- Guarded to grave prognosis ○ 20%-40% sudden death ○ Ventricular arrhythmias and syncope § More sudden death ○ Severe LSCHF § Most dead within 3 mo □ Sudden death or □ Refractory heart failure ○ Bilateral failure -> MST 3 weeks Preclinical screening 1. Echocardiography - best § Reduced contractility □ Overt DCM 2-3 yrs 2. 24-hour ECG (Holter) - if don’t detect on ECG § 50 VPCs in 24 hrs+/-couplets, triplets § Diagnostic for DCM
Boxer cardiomyopathy what is the most common one, what occurs, cause and clinical signs
Arrhythmogenic right ventricular cardiomyopathy - MOST COMMON
- Change in right ventricle -> fibro-fatty infiltration
Cause - Genetics
○ Familial
○ Autosomal dominant
○ Screen from 3 yo
- Clinical signs
○ ventricular arrhythmias - can be quite severe
○ Syncope episodes - if having these in this breed ECG
○ exercise intolerance
○ right heart failure
- sudden death - higher risk
Arrhythmogenic right ventricular cardiomyopathy what breed most common in, what are the 3 categories, clinical signs and prognosis
Boxer Category I: Concealed - Mild ventricular arrhythmias without clinical signs - Do well 2 years or more Category 2: Overt - Syncope, moderate ventricular arrhythmias. - Can do well for years with antiarrhythmics (beta blockers - sotalol) Category 3: Myocardial failure - As for 2, plus: - echo changes of poor systolic function - 50% present in CHF Likely to die of CHF or die suddenl
American cocker spaniels what mostly present as, what is the common cause and therefore treatment, follow up and prognosis
- Usually present in CHF
○ Treat heart failure
○ Treat with oral taurine and carnitine - hoping this is the cause - Follow up
○ Improved function by 3-6 mo on echocardiography
○ Once demonstrated -> Wean off cardiac drugs - Usually clinical recovery!
Irish wolfhounds what generally present as with heart and cause
- Autosomal recessive inheritance
- 2 presentation
1. Classic DCM
§ Biventricular failure
2. Atrial fibrillation with slow ventricular response
§ Asymptomatic at the start
§ May progress to CHF (3-4 years
§ DDx‘benign’ AF
□ (healthy!) heart on echo
DCM diagnosis what are the 3 techniques
1) Radiography ○ LSCHF(pulmonary oedema) - large left atrium ○ RSCHF(ascites, pleural effusion) ○ Usually generalised cardiomegaly 2) Echocardiography - Essential to confirm diagnosis ○ Usually LV + LA dilation ○ +/-RV/RA dilation ○ Systolic dysfunction § Fractional shortening < 15-20% 3) labwork - Biochemistry ○ Pre-renal azotaemia § low cardiac output ○ Hyponatraemia § Dilutional in severe CHF - NT-proBNP
What are some clinical signs for severe pulmonary oedema or low output (forward) failure due to primary cardiomyopathies
- Hypothermia
- Weak peripheral pulses
- Pale MM, slow CRT
- Cold extremities
+/- - Quiet heart sounds
- Mitral/tricuspid murmur
- Tachyarrhythmias
- Congestive signs
DCM treatment what are the 3 main aims and 2 treatments for preclinical DCM in dobermanns ALSO what need to control in all stages
AIMS 1. Control signs of CHF 2. Increase survival time 3. ↘ risk of sudden death Preclinical (occult) DCM Dobermanns - no CHF yet 1. ACEI - ace inhibitors ○ slow progression of ventricular remodelling ○ Delay CHF 2. Pimobendan ○ Delay onset clinical signs ○ Prolong survival Control arrhythmias/HR at all stages of disease
DCM treatment for mild/moderate and severe CHF
Mild-moderate CHF (furosemide, ACEI +) - know in this due to tachypnoea (same as previous lecture)
1. Pimobendan
○ Improved survival time over ACEI and furosemide alone
○ +/-spironolactoneto limit fibrosis and remodelling
- Pimobendan adds up to 9 months!
Severe CHF
1. Lots of furosemide
2. Nitroprusside
○ Don’t over-vasodilate as poor CO (don’t want too low BP)
3. Lots of inotropicsupport
○ Start pimobendan (IV/PO)
○ +/-Dobutamine CRI
4. ACEI when stable - long-term treatment
DCM prognosis after onset of CHF and cocker spaniels
- Poor after onset CHF
○ Sudden death can occur any time
○ Historically few weeks (Dobies) or months (others)
○ Good early response = longer survival - Better with Pimobendan!
- Best for cocker spaniels if taurine deficient - can go back to normal
What are the 3 main causes of dyspnoea in cats and therefore what need to be careful of
- FBD - feline asthma
- CHF - congestive heart failure - DON’T GIVE FLUIDS - important for stabilisation need to rule this out
- Pyothorax
Feline cardiomyopathies what is the most common types and how differ from dogs
- Primary cardiomyopathies ○ 62% of feline heart disease: § Hypertrophic (2/3) § Restrictive □ First two - DIASTOLIC FAILURE § Unclassified § Dilated - rare due to taurine in all cat foods § ARVC (< 1%) - Differences from dogs: ○ “Acute” presentations common - without clinical signs § CHF § Aortic thromboembolism § Sudden death ○ LSCHF -> Pleural effusion common § Usually modified transudate § Chylothorax
In terms of cat what supports cardiac origin in terms of clinical signs
- Normal to Low rectal temperature
- Murmur? - can get physiological cause in the exam room - stress
- Gallop rhythm
- Arrhythmia
- Bradycardia (or tachycardia)
- CAN HAVE NO MURMUR OR CLINICAL SIGNS AND BE IN HEART FAILURE
○ Echo important to diagnose in cats however need to be careful if in heart failure - NTproBNP - snap blood test
< 100 pmol/L: normal
< 270 pmol/L: unlikely
>270 pmol/L: likely
Feline dilated cardiomyopathy what are the 2 main causes and prognosis and treatment
Causes 1. Taurine deficiency - rare ○ Exceedingly rare now ○ Measure levels ○ Supplement § Improve clinically 3 wks § Echo improves 2-4 mo - Idiopathic? - more commonly ○ Poor prognosis ○ Pimobendan - OFF-LABEL
Feline hypertrophic cardiomyopathy (HCM) what results in, causes and what need to exclude
- PRIMARY LV concentric hypertrophy ○ Genetics + environment ○ Autosomal dominant § Maine coon, Ragdoll § Prognosis worse if homozygous ○ Males affected earlier/more severely Need to Exclude SECONDARY hypertrophy: ○ Hyperthyroidism ○ Hypertension ○ (Acromegaly)
Feline hypertrophic cardiomyopathy pathogenesis and clinical presentation with common and uncommon signs
Pathogenesis
-> protein defect -> ventriicle concentric hypertrophy -> stiff ventricle, diastolic relaxation imparied -> SNS, RAAS, LVOT obstruction -> progression to CHF
Clinical presentation
- murmur (2/3)
- gallop rhythm (1/3)
- arrhytmia
- CHF - usually acute
- other signs same as dog - tachypnoea, dyspnoea, lethargy, cough (sometimes
- ALSO - aortic thromboembolism (common) - cold extremities and PALE, not painful
- high risk of recurrence
- uncommon signs - weakness, sudden death
Feline hypertrophic cardiomyopathy what are the 3 main diagnostic techniques and the findings
Radiography - Mild ○ Normal - Advanced ○ Classic is ♥shape § Large LA and auricular bulge ○ Pleural effusion and/or pulmonary oedema 2. ECG ○ Arrhythmias ○ Left axis deviation ○ Not specific 3. Ultrasound -> essential for diagnosis - Increased diastolic wall thickness ≥ 6mm - +/-large LA - Diastolic dysfunction - SAM +/-LVOT obstruction
Feline hypertrophic cardiomyopathy treatment for pre-clinical and clinical acute
- Pre-clinical ○ No evidence any drugs prolong survival ○ Some use β-blockers for severe LVOT (left ventricular obstruction ○ Check annually - Clinical –acute ○ O2, furosemide ○ Thoracocentesis! ○ Pimobendan onlyfor refractory CHF ○ Thromboprophylaxis if large LA +/-thrombosis § Clopidogrel
Feline hypertrophic cardiomyopathy treatment when stable and when not to give beta-blockers
- When stable ○ ACEI ○ Beta-blockers for severe LVOT obstruction ○ Avoid corticosteroids - can worsen and bring on heart failure due to altered fluid dynamics ○ Limit stress - DO not give beta-blockers if ○ Hypotensive ○ Bradycardic ○ In CHF ○ Thromboembolism
