Slide 1
Congestive Heart FailureDr Rita SinghBSc, BVMS, DipVetClinStud,
FANZCVSc, Dip ACVIM (Cardiology)
1
What is Heart Failure?Most are flawed:A state in which the heart
fails to maintain adequate circulation for the needs of the body
despite satisfactory venous pressureA clinical syndrome
characterized by exertional symptoms and caused by heart disease
Impaired cardiac function leading to elevated venous and capillary
pressures causing organs to become congested
First lets start with what is heart failureMost definitions of
HF as applied to veterinary medicine are flawed.
Definitions in human medicine include:a state in which the heart
fails to maintain adequate circulation for the needs of the body
despite satisfactory venous pressure
Or:
A clinical syndrome characterized by exertional symptoms and
caused by heart disease. These are human definitions relating often
to systolic dysfunction. Such signs as exertional symptoms are
difficult to recognize in domestic pets, particularly cats whom
spend 90% of their day sleeping.
The critical event in progression from heart disease to heart
failure is activation of neurohormonal abnormalities (SNS and
RAAS)
In veterinary medicine it is usually congestive heart failure
that is first recognized.Hence a better definition would be:
Impaired cardiac function leading to elevated venous and capillary
pressures causing organs to become congested2
Disease SyndromesMyxomatous mitral valve degenerationMiddle
aged-older small breed dogLarge breed dogDilated
cardiomyopathyLarge breed dog GSD, Boxer, Irish Wolfhound,
DobermanHypertrophic cardiomyopathyCats Maine Coon, Ragdoll,
Bengal, British Shorthair, American Shorthair, DSH
3
Pathophysiology
Myxomatous degenerationVery commonSmall breed dogsSoft murmur =
mild diseaseLoud murmur = mild/mod or severe ds
Myxomatous mitral valve degeneration is the cause of >95% of
heart failure in older small breed dogsDegeneration of the valves
results in regurgitation.In this disease the severity of the heart
murmur correlates with the severity of disease at the lower end of
the spectrumWhat this means is that a soft murmur ie grades
I-III/VI are likely to be due to mild disease that would not yet
result in heart failureA loud murmur ie grades IV-VI can have mild,
moderate or severe disease and usually further clinical signs or
diagnostics would be required to tell if respiratory signs are due
to heart failure. 4
Here is an video image of a dog with severe mitral regurgitation
due to myxomatous mitral valve degeneration. Degeneration of the
mitral valve results in valvular regurgitation. With each
contraction, more of the SV is recycled so there is a greater
volume of blood/beat. Preload, which is the amount of the blood
filling the heart in diastole, increases. To deal with this there
is eccentric (longitudinal) hypertrophy which increases chamber
size without wall thickness. Slippage of myocardial cells also
occurs.The result is enhanced early diastolic filling and decreased
LV stiffness.Diastolic function improves. However, the increase LV
chamber size increases wall stress
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PathophysiologyDilated cardiomyopathyLarge breed dogsSoft murmur
can = severe disease
It is important to consider dilated cardiomyopathy in any large
breed dog with a left apical systolic heart murmur.With this
disease, as opposed to MMVD, the murmur can be soft and still be
due to severe disease causing heart failure
6
Here is a video loop of dilated cardiomyopathy. With this
disease, the primary event is failure of the left ventricular
myocardium. Poor systolic pressure generation causes the EF to
decrease resulting in self induced volume overload and increased
wall stress. The cardiac chambers enlarge, first in systole then
also in diastole.The decreased force of contraction results in
impaired SV and CO. Eventually congestion and muscle fatigue occur
due to poor CO.
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PathophysiologyHypertrophic cardiomyopathyMost common feline
cardiac diseaseAny breedGenetic mutationHeart murmur heart
disease!
HCM is the most common cause of heart disease in catsIt is
identified in any breed of cat however is known to occur with
increased predisposition in certain pedigree breeds including the
Maine Coon, Ragdoll, Burmese, Persian, Spynx, American Shorthair,
British Shorthair and BengalIt is considered to be an inherited
disease in these breeds and the genetic mutation has been
identified in the Maine Coon and Ragdoll breedsCats are much more
difficult than dogs in that the presence or absence of a murmur
including its grade tells us nothing about the severity of the
heart diseaseSo, cats can have heart murmurs with no underlying
structural heart disease or they can severe, end stage heart
disease with no murmur. This is just typical of anything to do with
cats in feline medicine they like to make things difficult!8
Here is a video image of severe HCM in a catConcentric
hypertrophy which is thickening of the LV wall, results in a
smaller sized LV cavity and a consequent inability to fill
normally. The main pathophysologic event is diastolic failure. This
is the inability to relax. Increased venous pressure and pulm
congestion occur due to imperfect LA emptying and incomplete
filling of LV.
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CompensationBaroreceptors detect reduced CO Stimulate SNS HR and
contractility Arteriolar constrictionNormalize haemodynamics
Regardless of whether the initiating factor is volume overload
from MMVD, systolic failure from DCM or diastolic failure from HCM,
If the disease is severe the eventual result is a decrease in
CO.
Baroreceptors in the aortic arch and carotid sinuss detect
reduced CO.
The SNS is stimulated.
Stimulation of cardiac B receptors via the SNS results in
increased HR, force of contraction and arteriolar constriction
The result is a normalization in haemodynamics 10
Compensation/1 receptors down-regulateCHF approx 50% cant
stimulateImproved rate and contractility diminishesWhat now??
However, it is well known that chronic SNS stimulation results
in down regulation of cardiac B1 receptors.With chronic SNS
stimulation, theses cardiac beta receptors internalize and eventual
degradeIn chronic CHF ~ 50% can no longer be stimulatedHence, the
improved HR and contractility diminishThe failing heart needs to
find another form of compensation11
Renal compensation
BP1 stimulation Renal perfusion Na+ resorption
Stimulates renal release of renin
12
Renin Angiotensin Aldosterone System
Sympatheticefferent activity
Diuretics
Na to distaltubule
Renal perfusion
K+, Ca++PGlANP
Reninrelease
Angiotensinogen(liver)
Angiotensin I(lung)Angiotensin IIACEThirstVasoconstrictionNa
retentionAldosteronesecretion(adrenal)
ADH secretion(pituitary)
This is the all important renin- angiotensin-aldosterone system
(RAAS)Discuss diagramRAAS acts to increase blood volumeWhile this
is helpful in situations such as acute blood loss, it is not
helpful chronically with heart disease as blood volume is normal to
start with.The result is increased blood volume and, eventually
congestion.13
Congestive Heart FailureCHF results from SEVERE heart
diseaseTreatment NOT required with mild or moderate changes
All these previously discussed changes stim of SNS, stim of RAAS
and fluid retention only occur with SEVERE heart disease.
The heart does not fail with mild or moderate changes.
Thus animals with MMVD or HCM must have a severely enlarged LA
to be in HF. The only exception to this is acute chordal rupture in
MMVD in which case there will be severe respiratory signs and a
suddenly loud murmur.
In DCM there should be severe systolic dysfunction (CHF not
likely if FS > 15%)
Anything less severe than this, and the dog or cats signs are
unlikely due to CHF and other causes of clinical signs should be
sort.
Thus, sometimes diagnosing CHF can be more difficult than one
would think.
1st image cat with respiratory signs, alveolar pattern, HCM with
severe LAE2nd Doberman with DCM, cough, increased respiratory rate.
Severe systolic dysfunction and marked LAE and LVE
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Pathophysiology
Progression forward SV LA pressure Pulmonary capillary pressure
Pulmonary oedemaMedication is required
15
Natural HistoryOnce in heart failure:MMVD: Average survival 12
monthsDCM: 8 months (Dobermans 4 months)HCM: 18 months ?! (1
study)
Once in heart failure with intensive treatment, the average
survival for dogs with MMVD is ~ 12 months, for DCM is ~ 8 months
(and a very poor 4 months for Dobermans) and for cats with HF due
to HCM ~ 18 months (not my experience) .I find cats can either do
badly (and be euthanized in a period of weeks-months) or do well
and live for 12-18 months. It is hard to predict which category a
cat will be in and tend to be based on how they respond to initial
treatment for CHF (with regards to demeanor and appetite). I find
some cats just never regain their appetite despite appropriate
treatment of CHF while other can do very well If you have dogs that
have been previously diagnosed with CHF that are on frusemide +/-
pimobendan, benazepril that are still alive and doing well 3-4
years later, it is highly likely that these dogs were not in heart
failure to start with. 16
Diagnostic TestsMurmur, tachycardia, tachypneaO2 and frusemide
before echo!Body weight need to lose 7-10% BWRenal panel,
urinalysis prior if possible
If a dog or cat presents to you with a murmur (must be loud if
it is a small breed dog), tachycardia and tachypnea HF is high on
the list of differentials and I will usually commence treatment
immediately while organizing further diagnostic tests. Do not send
a dyspneac dog that you are highly suspicious could be in heart
failure for an echocardiogram prior to commencing frusemide. The
dog could be dead by the time the echo is done and I will rarely
echo such a dog immediately, I will usually do this 24-48hrs later
once the patient is stable. A baseline body weight and monitoring
during treatment is essential. Animals usually need to lose 7-10%
of their body weight to come out of heart failure and I will pay
close attention to this during therapy. If the animal has lost 10%
of its presenting body weight and is still dyspneac, one needs to
strongly consider that heart failure may not be the cause of the
respiratory signs.If possible, a renal panel and urinalysis are
useful prior to commencing therapy. If the patient becomes
azotaemic during therapy, once frusemide is in the system,
producing dilute urine, it is then impossible to tell if this it
just dehydration from the medication or renal failure. 17
RadiographsDiagnosisSeverity Stage disease via LA sizeCough due
to pulmonary oedema?
Thoracic radiographs are important for the diagnosis of CHF,
assessing the severity, staging the cardiac disease via assessment
of left atrial size and assessing potential causes of cough 18
Consensus Statement for Recognition of CHF in MMVD*Older than 7
yrsLoud murmur (IV/VI or >)Sinus arrhythmia absentTachycardic
(HR >120 bpm)Dyspneac (sleeping RR > 30)
**Cough on its own is not considered a sign of congestive heart
failure*** Beijerink, Campbell, Gavaghan, Singh and Wooley.
Published online via Vetforum, Boehringer Ingelheim, 2015
While severe CHF is easy diagnosis, mild CHF can be a little
more difficultThere are even some cases where a cardiologist is
unsure so it is not always as easy as one may think!In March 2014,
the 5 Australian cardiologists in collaboration with Boehringher
Ingelheim, put together a consensus statement on diagnosis of CHF
in MMVD. This has been released on the BI websiteThe consensus
statement says, that one should strongly consider CHF due to MMVD
if:1) The dog is older than 7 yrs and < 15kg2) The murmur is
loud (Grade IV/VI or more)3) The dog is tachycardic (HR >120
bpm) and sinus arrhythmia is absent4) The dog is dyspneac at rest
(sleeping RR > 30 breaths/minute)
If the dog statisfies these criteria, it is reasonable to
commence immediate treatment with frusemide and obtain confirmatory
radiographs once stable Also note that cough on its own in a dog
that is not tachycardic and has a normal sleeping RR is NOT
consistent with congestive heart failure and thoracic radiographs
are recommended in this instance rather than a treatment trial with
frusemide
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MMVD
Describe radiograph20
This is one of the most extreme examples of left atrial
enlargement without CHF that I have seen.This was a older small
breed dog whom presented with chronic coughDespite the extreme LA
enlargement, the lung fields are completely clear and the pulmonary
veins are small indicating that this dog is not in heart failure.
Hence, frusemide is not warranted in this patient. This dog was
part of a study I performed during my cardiology training looking
at dogs like this. Those that had a heart murmur due to MMVD and a
chronic cough but werent in CHF.If we look closely at this this
radiograph, we can see collapse of the mainstem bronchi on the
lateral view and severe collapse of the left lower airways on the
DV21
Bronchomalacia in Dogs With MMVD*Large LA compression of
bronchus vs airway diseaseDoes the syndrome of compression of the
left mainstem bronchus from a large LA actually exist?Small breed
dog with a murmur and cough but normal respiratory rate ?
* Singh et al, JVIM March/April 2012
In this study, 10 dogs with mod- severe LAE due to MMVD and
chronic cough without CHF were enrolled. These were the study dogs6
dogs without or with only mild LAE with chronic cough were the
control dogs. All dogs had echocardiography, thoracic radiographs,
fluoroscopy and bronchoscopy performed in an attempt to try and
characterize further the disease process occurring.Historically the
cough in this dogs was thought to be due to compression of the left
mainstem bronchus and I thought this was going to be the case in my
studyHowever, the results of this study led me to question if this
syndrome actually exists and to also question now best to treat
these dogs. 22
1. Left cranial and caudal segments of the left cranial lobar
bronchus2. Left caudal lobar bronchus3. Right middle lobar
bronchus
These are some images during broncoscopy of the airways of dogs
in this study,
Figure 1. Bronchoscopic evaluation of the left cranial and
caudal segments of the left cranial lobar bronchus from a dog in
group 1 (A) and a dog in group 2 (B) showing 90-100% static
collapse of both segments of this airway in both dogs with a large
LA and those without
Figure 2. Bronchoscopic evaluation of the left caudal lobar
bronchus from a dog in group 1 (A) and a dog in group 2 (B) showing
100% static collapse.
Figure 3. Bronchoscopic evaluation of right middle lobar
bronchus (arrows) from a dog in group 1 (A) and a dog in group (B)
showing 100% static collapse.
** Every dog in each group had airway inflammation**
Hence, our conclusions were that the large left atrium doesnt
actually cause compression of the left mainstem bronchus in these
patients as multiple other airways are also collapsed and dogs
without LAE also had collapse of similar airways.
It is now my opinion that these dogs should be approached as
though they have 2 separate diseases MMVD AS WELL AS chronic airway
disease and treated as such.
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This was on the of the control dogs in the studySmall breed dog,
chronic coughWhile the heart looks big on radiographs, he only had
mild LA enlargement on echo (LA:Ao 1.5)The reasons of the heart to
look big areShallow chestExpiratory film Both of these instances
will result in a smaller volume chest on radiographs and, in
relation, make the heart look bigger
This dog was not in heart failure. He had a chronic cough and
was treated with a combination of doxycyline/ theophylline and
later oral/inhaled corticosteroids24
Dilated Cardiomyopathy
Hypertrophic cardiomyopathy
HCM severe HFCats are more difficult than dogsThe left atrium
sits further forward n the lateral view making It harder to tell in
there is cardiomegaly on this viewIn this particular cat however,
there is a huge left auricle on the DV view.The lung pattern is
also more difficult in cats. In this particular cat it looks almost
miliary in appearance which may lead one to think that neoplasia
may be the cause of the cats signsHowever, due to the obviously
large left atrium, I would treat this cat with frusemide then
confirm this suspicious with echo (once stable).This cat had also
thrown a distal aortic thromboembolus hence, the presence of the
fentanyl patch for pain relief. 26
HCM, early CHF large LA27
HW catNot CHF28
Biomarkers?NT-proBNPCats CHF: 3 studies. 220 pmol/L - 90% sens,
88% spec for ddx CHF from respiratory causes of dyspneaScreening
for HCM: 100 pmol/L - 100% spec, 0-70% sens (44% severe ds)Dogs CHF
: 210 pmol/L - 80% sens, 82% spec
What are cardiac biomarkers. Biomarkers are tests performed on
products in the blood to aid in the detection of cardiac disease or
cardiac failure.NT-pro BNP is one such biomarker: It is a
degradation product of BNP BNP is rapidly produced by
cardiomyocytes in response to stimuli such as myocardial stretch or
hypoxia. BNP is produced where ever there are cardiomyocytes (most
from ventricle)It is a test vastly promoted by laboratories as an
aid in the detection of heart disease and heart failure in dogs and
cats
Cats. 3 studies: Dx CHF from non CHF causes of dyspneaCut off
220 pmol/L gave 90% sensitivity (ie 10% incorrectly dx has not
having CHF)88% spec (12% false +ve - incorrectly dx as having
CHF).BUT, no one looked at cats with HCM, no HF and respiratory
signs which is the only time I would personally find it
useful.There is now an in house snap test available which I think
is useful in the emergency situation in deciding if a cat
presenting with dyspnea could have CHF as the cause of its signs
when echocardiogram is not available.
Cats: As a screening test for occult HCM, not useful. Using cut
off of 100 pmol/L 44% sensitivity for diagnosing cat with severe
HCM, 0% sens for mild and moderate disease. Specificity 100% (no
cat without HCM was misdiagnosed).Fox et al 2011 found > 99
pmol/L gave 100% spec and 70% sens (ie 30% not diagnosed).Thus not
a good screening test. If elevated, has good chance of having heart
disease, but will miss many with heart disease.
Dogs:Weekly variability in common in normal dogs. In 1 study
22/53 normal dogs had > result > 500 pmol/LMany extracardiac
effects on NT-proBNP documented in people including fluid intake,
HR, renal function, circadian patterns, physical activity,
genetics.Screening for MMVD (Chetboul 2009): Control dogs NT-pro
BNP 68-515 pmol/LMMVD, no heart enlargement 175-1101 pmol/LMMVD,
enlarged heart, no CHF 284-2007To much overlap. Not good for
detection of severity of the mitral regurg.Detection of resp
distress from CHF vs resp disease (Boswood 2008)CHF 171-8960Heart
disease but no CHF < 42-3910Resp disease only (no heart dis) 2
> Potent positive inotropePimobendan:Increases binding affinity
of calcium to cTNcInhibits cardiac PDE III reduces breakdown of
cAMP increase stimImproves myocardial contractility/ relaxation
Vasodilation
Positive inotropes increase heart rate and contractility, either
by direct or indirect stimulation of cardiac beta receptorsThe 2
positive inotropes used most commonly in congestive heart failure
are dobutamine and pimobendan
Dobutamine: Dobutamine is a synthetic analogue of dopamine It
causes stimulation of the cardiac sympathetic nervous system with
the cardiac B1 receptors being stimulated more than B2 receptors
which are stimulated more than alpha receptors. Stimulation of
cardiac B1 receptors results in an increased HR and contractility
while stimulation of B2 receptors causes vasodilation and of alpha
receptors vasoconstriction. Therefore dobutamine, through its
effect on B1 receptors causes an increased HR and contractility
with less effect on the vasculature.
Pimobendan Pimobendan increases the binding affinity of calcium
to cardiac troponin c. It also inhibits cardiac phosphodiesterase
III. This results in reduced breakdown of cAMP and increased B
stimulation. The overall effect is improved myocardial contraction
and relaxation as well as vasodilation.
36
Other DiureticsSpironolactone K+ sparingAldosterone
antagonistCombined with frusemide to limit hypokalaemia/ aid
diuresisHydrochlorthiazide/ chlorthiazide
Other diuretics that I will use in chronic CHF cases include
spironolactone which is potassium sparing diureticIt achieves this
action by inhibiting the action of aldosterone on the distal renal
tubular cellsSpironolactone has mild diuretic effects but is
commonly used in combination with frusemide to aid diuresis and
limit hypokalaemia that can be caused by frusemideIn addition to
this use, a strong link has been shown in humans between increased
aldosterone levels and worsening cardiac fibrosis. This is an
additional positive effect in that there may be some delay of the
progression of the disease although this has never been shown to be
the case clinically in veterinary patients.
The final class of diuretics used in the cardiac patient are the
thiazide diuretics. Drugs in this class include chlorthiazide and
hydrochlorthiazide. These drugs act by primarily reducing the
membrane permeability of the distal convoluted tubule to Na and
ClThey will also promote K+ loss at this siteI use this drug quite
frequently in my end stage congestive heart failure patients but
low doses must be used and frequent monitoring of renal parameters
and electrolytes is required when used in combination with high
dose frusemide and spironolactone.
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Mild- moderate HF - Dogs
Tachypnea (RR 40-60), dyspnea +/- coughTachycardicPulmonary
oedemaSevere regurgitation (MMVD) or systolic dysfunction
(DCM)Treatment is always indicatedFrusemide, ACEI, pimobendan
The following slides outline my approach to dogs in various
stages of heart failure. 38
Severe/ Fulminant HFMedical emergencyMarkedly dyspneac and
hypoxemicCoughing white/blood tinged frothRR 60- >100
breaths/minHANDLE GENTLY
39
Fulminant HF/O2Baseline RR, body weightIV frusemide 4-6 mg/kg
q30-60mins or CRI till RR < 60 OR lost 10% BWDelay radiographs/
echocardiographyConsider arteriolar dilators: oral hydralazine, IV
nitroprusside (BP)Positive inotropes: dobutamine, pimobendan (now
comes IV)
40
Ventilation
Intermittent positive pressure ventilation may be lifesaving in
this situation. It gives the patient a rest while giving a chance
of the drugs to workIn a patient that is not responding quickly to
treatment (or even prior) consider referral so that it can be
transported before it is to critical41
Refractory Chronic HFSleeping RR > 40 breaths/minMaximum
frusemide (4mg/kg q 8 hours)ACEI, pimobendan (tid) Spironolactone 2
mg/kg bidHydrochlorothiazide 1mg/kg 2x/week*+/- antiarrhythmics+/-
hydralazine or amlodipine
* Must monitor renal parameters
* Must monitor renal parameters carefully patients can be become
very azotaemic and hypokalaemic on this drug 42
Pulmonary arterial hypertensionPulmonary arteriolar constriction
secondary to pulmonary venous hypertensionExacerbates mild right
heart diseaseSevere clinical signs diuretic refractory ascites,
exercise intolerance, syncopeDx: PA cath (gold standard) or echo
(need TR or PI)
25255
43
PAH/No medically recognised Rx (except O2)
Prostacycline/selective endothelin receptor antagonists (Bosentan)
benefit some humansSildenifil (Viagra) phosphodiesterase V
inhibitor, only treat severe disease (PA pressure > 80 mm
Hg)$$$
Surgery Valvular Ds
Procedure of choice humansReplacement - potential for
thrombosisLifelong anticoagulant therapyRepair preferred
SurgeryDifficult in dogs:Very few trained veterinariansUS ~
$10,000 - $15,000Requires cardiopulmonary bypassHigh mortality
Other than a single surgeon in Japan whom is achieving 95%
succuss rates even on 2 kg dogsMost programs in the USA open with
great excitement then shut down due to poor success rates.46
Cats: HCMAsymptomatic: No treatment-blockers if systolic
anterior motion of the mitral valve WITH significant
obstruction
47
Cats: HCMCHF:Frusemide: 1-4 mg/kg
bid-tidACEiThoracocentesisDobutamine/ pimobendan?Heparin,
clopidogrel?Asprin, warfarin?
48
Questions?
I have tried to cover a lot of information in a very short
period of time so I am happy to entertain and questions.49
