Demystifying Congestive Heart Failure in Dogs -A Practical Approach to Diagnosis and Management starts in 1 day
What is heart failure?
MVD (Myxomatous Mitral Valve Disease)
is the most common cause of congestive heart failure in dogs. It is also called chronic valve disease or degenerative valve disease.
What happens:
The mitral valve inside the heart becomes thickened and weakened over time.
This can cause the valve to leak, allowing blood to flow backward inside the heart.
Over time, the heart may enlarge and fluid can build up in the lungs, leading to congestive heart failure.
Most commonly affects:
Older small breed dogs
Cavalier King Charles Spaniels are one of the classic breeds commonly affected
Large breed dogs can also develop MVD
Echocardiogram in dogs with MVD and congestive heart failure:
An echocardiogram is an ultrasound of the heart. It allows veterinarians to:
Evaluate the severity of the valve leak
Check heart enlargement
Assess heart function and blood flow
Monitor progression of the disease
Help guide treatment and medication decisions
Significant mitral valve regurgitation can lead to secondary enlargement (dilation) of the left atrium and left ventricle of the heart.
In simple terms:
The heart chambers become stretched and enlarged because blood is leaking backward through the mitral valve, forcing the heart to work harder over time.
In simple terms:
MVD is a condition where one of the heart valves wears out with age and starts leaking. The heart has to work harder to pump blood properly, and in advanced cases this can lead to fluid buildup in the lungs and congestive heart failure.
Congestive heart failure (CHF) secondary to dilated cardiomyopathy (DCM):
DCM is a disease where the heart muscle becomes weak and enlarged.
The heart loses its ability to contract effectively and pump blood normally.
This condition most commonly affects middle-aged to older large and giant breed dogs.
Breeds commonly associated with classic DCM include Doberman Pinschers and Great Danes.
Some cases have been associated with diet-related DCM, including:
Certain grain-free diets
Diets linked to taurine deficiency
On echocardiogram (heart ultrasound), dogs with DCM and congestive heart failure commonly show:
Poor heart muscle contractility (weakened pumping ability)
Enlargement (dilation) of the left ventricle
Enlargement (dilation) of the left atrium
Echocardiogram dogs with dilated cardiomyopathy and congestive heart failure have poor contractility as well as left ventricular and left atrial dilation.
In simple terms:
The heart becomes enlarged, weaker, and less efficient at pumping blood, which can eventually cause fluid buildup associated with congestive heart failure.
Conclusion:
Whether treating DCM or mitral valve disease whether left or right sided, medical management is the same for congestive heart failure.
Left-Sided Congestive Heart Failure
Can progress to pleural effusion and/or pulmonary edema (fluid buildup around or within the lungs).
Radiographs (X-rays) may show an interstitial-to-alveolar pulmonary pattern, most commonly in the perihilar to caudodorsal lung regions.
Other findings can include pulmonary venous congestion and cardiomegaly (enlargement of the heart).
Simple terms:
Fluid can begin to build up in or around the lungs, making breathing more difficult. Chest X-rays may show cloudy areas in the lungs, enlarged blood vessels leading to the lungs, and an enlarged heart.
Diagnostic tests for congestive heart failure
Thoracic radiographs (chest X-rays) are considered the gold standard for evaluating congestive heart failure (CHF).
However, there are important limitations:
Early or mild congestive heart failure can be difficult to detect on radiographs. Changes may resemble normal aging changes or harmless anatomical variations.
Radiographic findings do not always perfectly match the patient’s clinical signs. In some cases, symptoms may appear before obvious X-ray changes develop.
Interpretation of radiographs is somewhat subjective. A study published in the Journal of Small Animal Practice (JSAP) found that when radiologists reviewed radiographs of dogs with mitral valve disease without knowing the clinical history, there was significant variation in whether they diagnosed left-sided congestive heart failure.
Prior treatment can alter radiographic findings. For example, furosemide may reduce venous distension and fluid accumulation. If the patient received a dose before the radiographs were taken, the images may become more difficult to interpret.
In simple terms: congestive heart failure does not always “follow the rules.” Some pets with clear symptoms may have subtle or unclear X-ray findings, while others may show radiographic changes that are difficult to confidently interpret without considering the full clinical picture, including physical examination, history, respiratory rate, response to treatment, and additional diagnostics such as echocardiography.
- Radiographs from dogs with dilated cardiomyopathy (DCM) and congestive heart failure can sometimes look different from the “classic” heart failure pattern.
In this case, the main finding was a diffuse, marked interstitial lung pattern (a widespread hazy appearance in the lungs) that was most severe in the ventral lung fields (the lower/front parts of the lungs). This type of pattern can resemble pneumonia more than typical congestive heart failure.
Radiographs are not always straightforward, and some cases of heart disease can mimic respiratory
Echocardiography (heart ultrasound) is very helpful for determining the type of heart disease and how severe it is, but it is not always essential.
A definitive diagnosis of congestive heart failure can often be made based on the pet’s history, physical examination, and chest radiographs (X-rays) alone.
Some biomarkers can also help support the diagnosis:
- NT-proBNP: a blood test that is usually elevated when there is increased stretch or stress on the heart muscle. It is not a perfect test and can produce false positives or false negatives, but it generally performs well in pets with respiratory symptoms. An elevated NT-proBNP level can strongly increase suspicion of congestive heart failure rather than primary respiratory disease.
Treatment
First, if the patient presents as a respiratory emergency, the priority is to provide oxygen supplementation if available and immediately reduce stress, as stress can significantly worsen breathing effort.
Stress reduction may include sedation when appropriate. Injectable options such as butorphanol can be used. If the patient is stable enough to take oral medications or will be hospitalized for monitoring, gabapentin or trazodone may be administered to help keep them calm and reduce anxiety.
Once the patient is stabilized, diagnostics should be performed in a controlled and stepwise manner. This may include:
- Thoracic radiographs (chest X-rays) to evaluate the lungs and heart
- Bloodwork to assess overall health and underlying contributors
- Focused cardiac ultrasound (point-of-care ultrasound) to quickly assess heart function and fluid status
The goal is to stabilize first, then proceed with diagnostics while minimizing stress and respiratory compromise.
The transporter in the luminal side of the thick ascending loop of Henle in the nephron is the Na⁺-K⁺-2Cl⁻ cotransporter (NKCC2).
Loop diuretics (like furosemide/Lasix) block this transporter. When it is blocked:
- Sodium cannot be reabsorbed back into the body
- Water follows sodium into the urine
- This results in increased urine production (diuresis)
Effects of loop diuretics (simple explanation):
- They make the kidneys remove more salt (sodium) and water
- This increases urine output
- This reduces fluid buildup in the body
As fluid is removed:
- Interstitial fluid decreases → less swelling/congestion in tissues
- Blood volume decreases → lower intravascular volume
- Preload decreases → the heart has less fluid to handle
In acute respiratory distress (fluid overload cases):
- Furosemide (Lasix) is commonly used to quickly remove excess fluid
- This can help improve breathing by reducing fluid in the lungs
Some veterinarians limit dosing to about 8 mg/kg over the first 4–6 hours because:
- Too much diuresis too quickly can reduce kidney blood flow
- This may increase the risk of kidney injury
Life-Threatening Pulmonary Edema (e.g., pink frothy fluid from the mouth with severe difficulty breathing)
This is an emergency. In severe cases, furosemide may be started as a continuous rate infusion (CRI) at approximately 0.6–1 mg/kg/hr after an initial IV bolus, depending on the patient’s condition and clinician judgment.
Hospital (Acute/Chronic Inpatient Management)
For hospitalized patients receiving higher doses of diuretics, it is important to closely monitor:
- Kidney values (renal function)
- Electrolytes (such as sodium, potassium, chloride)
These are typically checked every 12–24 hours, depending on stability and severity.
Oral (At-Home or Step-Down Therapy)
Once the patient is stable enough for oral medication, a common starting range is:
- 2–4 mg/kg/day total, divided into two doses per day
Treatment Goal
The goal is always to use the lowest effective dose that:
- Reduces pulmonary fluid (pulmonary edema)
- Keeps the lungs clear
- Helps the patient breathe comfortably
- Avoids stressing the kidneys as much as possible
If Pulmonary Edema Reoccurs
If symptoms return, the dose may be gradually increased by about 25% at a time, while carefully monitoring response.
In some cases, dosing may be increased up to 6–8 mg/kg/day total, but ideally not beyond this range due to limited added benefit.
Ceiling Effect (Important Concept)
At a certain point, increasing the dose no longer significantly increases urine production. Instead:
- You mainly increase the risk of kidney damage and dehydration
- This is called the “ceiling effect”
- This is why clinicians avoid routinely exceeding the upper dose range (around 6–8 mg/kg/day total)
Medication Form
Furosemide is available in:
- Tablets (multiple strengths)
- Liquid formulations (oral suspension or compounded liquid)
Torsemide (potent loop diuretic – furosemide alternative)
Torsemide is a loop diuretic that works through the same mechanism as furosemide (it helps the kidneys eliminate excess fluid by acting on the loop of Henle). However, it is more potent and longer-acting than furosemide.
In veterinary medicine, Torsemide is sometimes used in patients with heart disease or fluid overload that are not responding optimally to furosemide alone. Because of its increased potency, the starting dose is much lower compared to furosemide.
When transitioning a patient from furosemide to torsemide, veterinarians often estimate the dose using an approximate conversion where torsemide is about 10–20 times more potent than furosemide, depending on the case and clinical response. This is why the initial torsemide dose appears significantly smaller.
Torsemide is available in some countries and is used in veterinary cardiology. Access and familiarity may vary by region and clinician training, and some cardiologists with U.S. training may be more familiar with its use.
However here in Canada the preferred drug is Furosemide first then when patients get really refractory it gets replaced with Torsemide if possible.
- PU/PD (increased urination and thirst) is not just a side effect of furosemide, but an expected and necessary effect that helps save pets’ lives in many cases. It is important for owners to understand that increased drinking and urination are normal and required for the medication to work properly.
- Owners must be prepared for their pets that will need more frequent bathroom breaks and must always have unlimited access to fresh water. Without this, there is a risk of dehydration, which can lead to kidney injury or worsening of existing kidney disease.
- When starting a pet on furosemide for the first time, owners should be informed that most urine production will happen within the first 1–2 hours after giving the oral dose. During this time, the pet may produce more urine than the bladder can comfortably hold.
For this reason, pets should be taken outside or offered litter box access several times after dosing. This helps improve comfort, reduces accidents in the house, and supports successful management at home.
Furosemide should be used with caution in terms of timing. It is not ideal to give before long periods without supervision, such as before leaving for work or overnight, as this can lead to urinary accidents and stress for the pet.
Side effects:
- Dehydration and prerenal azotemia (temporary kidney stress)
Furosemide works by making the kidneys remove more water and salts from the body, which reduces blood volume. If too much fluid is lost, this can lower kidney blood flow and temporarily increase kidney values (azotemia).
- Pets with existing kidney disease are more at risk.
- Electrolyte changes (salt imbalances)
- Low sodium
- Low potassium
- Low chloride- When chloride is lost, the body may retain bicarbonate, which can lead to a mild metabolic alkalosis (shift in body pH).
- Low blood pressure (hypotension)- This can occur if fluid loss is excessive, though it is uncommon when the medication is properly dosed and monitored.
- Ototoxicity (hearing effects)- This is very rare in veterinary patients but has been reported more commonly in humans at high doses.
Evaluation helps ensure the patient is tolerating the medication well. Typically, a chemistry panel or at minimum a renal (kidney) panel is completed before starting a diuretic or before adjusting the dose, and then repeated again in about 1–2 weeks.
What Can owners do:
Watch for signs of worsening kidney function or intolerance, including decreased appetite, vomiting, or diarrhea.
In practice, this often requires balancing two organ systems with opposite needs:
- The kidneys benefit from good blood flow and adequate fluid.
- The heart, when diseased, can become overloaded and cannot safely handle excess fluid.
Because of this, finding a “perfect” balance is not always possible. In many cases, treatment must prioritize what is most urgent. If a patient is struggling to breathe or showing signs of fluid buildup, controlling heart failure becomes the priority, even if it means accepting some degree of reduced kidney function.
How owners contribute: Role of diet at home
Home nutrition plays an important supporting role in helping maintain this balance:
- Helps reduce unnecessary strain on the heart and kidneys
- Supports stable hydration levels, making diuretic therapy more predictable
- Provides consistent sodium (salt) intake, which can influence fluid retention
- Helps maintain body condition and muscle mass, especially in chronic disease
When diet is consistent and appropriate for the condition, it can improve the effectiveness of treatment and make it easier to find a stable balance between heart and kidney needs.
Second Treatment Goal
Pos
Positive inotrope (sometimes with mild vasodilator effects). Preferred product: Vetmedin
What it does on the heart (simple explanation):
Vetmedin helps the heart pump stronger and more efficiently.
-
Increases contractility (positive inotrope):
Helps the heart muscle squeeze more forcefully, so each beat pumps more blood. -
Decreases preload (reduces volume load):
Lowers the amount of blood returning to the heart, so the heart doesn’t have to work as hard handling excess volume. -
Mild vasodilation:
Slightly relaxes blood vessels, making it easier for blood to flow forward and reducing resistance the heart pumps against.
summary:
It helps the heart pump stronger and work less hard at the same time by improving forward flow and reducing strain.
Administration:
- Available only as oral medication (tablet or chew).
Pimobendan (cardiac medication)
Pimobendan is a heart medication commonly used in dogs with heart disease. It is available in capsule sizes that allow flexible dosing based on body weight.
Typical dose:
- Usually 0.25–0.3 mg/kg by mouth, twice daily
- In more advanced (end-stage) heart disease, the total daily dose may be adjusted higher and sometimes divided into 3 doses per day, depending on the veterinarian’s assessment
How it helps:
- Improves the heart’s ability to pump blood more effectively
- Helps reduce strain on the heart
- Can improve energy level and breathing comfort in many patients
Side effects (generally uncommon):
-
Mild stomach upset
- decreased appetite
- diarrhea
- Most pets tolerate it well
Monitoring:
- Routine bloodwork is usually not required for pimobendan itself
- Your vet will still monitor the heart condition with check-ups and possibly imaging (like echocardiograms)
Pimobendan in Heart Disease (Dogs) When is it used?
Pimobendan is a heart medication that works best when started early, ideally in the preclinical stage of heart disease. This means the dog has heart changes (like valve disease or early heart muscle disease), but no signs of heart failure yet.
The goal is to diagnose conditions like mitral valve disease (MVD) or dilated cardiomyopathy (DCM) before they progress to congestive heart failure (CHF).
What studies show:
EPIC Study (dogs with mitral valve disease)
- Dogs had heart enlargement but no symptoms yet
- Pimobendan delayed the onset of congestive heart failure by about 15 months
- In simple terms: it helped dogs stay “stable and symptom-free” longer
PROTECT Study (Doberman Pinschers with preclinical DCM)
- Dogs had early heart muscle disease but were still asymptomatic
- Pimobendan delayed development of heart failure or sudden death by about 9 months
- In simple terms: it slowed disease progression and improved time before serious outcomes
QUEST Study (dogs already in congestive heart failure from MVD)
- Dogs already had heart failure symptoms
- Pimobendan improved survival time and quality of life
- In simple terms: dogs lived longer and felt better when already in heart failure
Who should receive Pimobendan?
Pimobendan is a medication with strong benefits and relatively few side effects, but it is not for every dog.
It is typically used for:
- Dogs with confirmed mitral valve disease and heart enlargement (even before symptoms)
- Dogs with preclinical dilated cardiomyopathy (especially Dobermans)
- Dogs with congestive heart failure due to valve disease or cardiomyopathy
Summery:
Pimobendan works best when started early in diagnosed heart disease, before heart failure develops. It can delay worsening of disease and improve both lifespan and quality of life in the right patients.
The following stages do NOT require Pimobendan:
-
Stage A – At Risk (Predisposed breeds)
- No heart disease is present yet
-
Higher-risk breeds only
- e.g., young Doberman
- e.g., Cavalier King Charles Spaniel
-
Stage B1 – Early structural heart disease
- Heart disease is present (example: mitral valve regurgitation / leaky mitral valve)
- Heart size is still normal
- No symptoms are seen
In simple terms: The heart is “leaking” slightly, but it is not enlarged and the pet feels normal and is as usual in routine.
Symptomatic / progressing stages (Pimobendan is typically needed):
-
Stage B2 – Enlarged heart stage
- Mitral valve disease (MMVD) is present
- The heart has become enlarged (working harder to compensate)
- Still may not show obvious symptoms yet, but disease is progressing
-
Stage C – Congestive heart failure (CHF)
- Heart is no longer able to keep up
- Fluid may build up in lungs or abdomen
- Symptoms present (coughing, fast breathing, fatigue, reduced exercise tolerance)
In simple Terms: The heart is struggling to pump effectively and the body is starting to show signs of fluid buildup and weakness.
If an echocardiogram is not available, chest radiographs (X-rays) can be used as an alternative at a primary care veterinary clinic to assess heart size.
One common measurement is the Vertebral Heart Score (VHS). This helps estimate whether the heart is enlarged.
When considering pimobendan based on radiographs:
A VHS greater than approximately 11.5 may suggest significant heart enlargement.
If two sets of chest radiographs taken about six months apart show progressive heart enlargement, it can also support starting pimobendan even without an echocardiogram.
How VHS is measured (simplified):
Take two measurements of the heart on the X-ray:
Long axis: from the carina (where the trachea splits) to the tip (apex) of the heart.
Short axis: the widest part of the heart, measured perpendicular to the long axis.
Place both measurements along the vertebral column starting at the front edge of the 4th thoracic vertebra (T4).
Add the two lengths together to get the VHS score.
Example:
Long axis = 7.3 vertebrae
Short axis = 7.1 vertebrae
Total VHS = 14.4
Interpretation:
Normal VHS is approximately 8.5–10.5
A VHS of 14.4 indicates severe cardiomegaly (enlarged heart)
Obstructive heart disease (e.g., subaortic stenosis, pulmonic stenosis, hypertrophic cardiomyopathy): Pimobendan may increase contractility, which can potentially worsen dynamic obstruction and contribute to further myocardial workload and hypertrophy.
Dogs with normal cardiac function: There is concern that unnecessary use of pimobendan could promote maladaptive cardiac changes over time, including hypertrophy.
Heart failure is a vicious cycle so the Goal: Suppress the RAAS system
The Renin-Angiotensin-Aldosterone System (RAAS)
Understanding basic anatomy and physiology helps make sense of this system.
When the kidneys detect decreased blood flow (reduced renal perfusion) such as in heart disease or low blood volume (hypovolemia) they release renin.
Renin starts a cascade by converting angiotensinogen (from the liver) into angiotensin I.
Next, angiotensin-converting enzyme (ACE) found mainly in the vascular endothelium, especially in the lungs converts angiotensin I into angiotensin II.
Effects of Angiotensin II
Angiotensin II has several important actions that initially help the body survive low blood pressure or low volume:
Vasoconstriction → narrows blood vessels, increasing blood pressure
Aldosterone release (from adrenal glands) → increases sodium and water retention in the kidneys while promoting potassium loss
ADH (antidiuretic hormone) release from the pituitary → increases water reabsorption
Overall result: increased blood volume and blood pressure
In Disease (Heart Failure)
While RAAS is protective in acute blood loss or dehydration, in chronic heart disease (e.g., heart failure) it becomes maladaptive:
Fluid retention increases circulating volume
This increases cardiac workload
Leads to worsening congestion, edema, and heart failure progression
Creates a vicious cycle of fluid overload and RAAS activation
Medications that Target RAAS
This is why RAAS-blocking drugs are important in managing heart disease:
ACE inhibitors (e.g., enalapril, benazepril) → reduce formation of angiotensin II
Aldosterone antagonists (e.g., spironolactone) → block aldosterone’s effects on sodium and water retention
Angiotensin receptor blockers (ARBs) → prevent angiotensin II from binding to its receptors
RAAS is a life-saving system in emergencies, but in chronic heart disease it becomes overactive and harmful. Blocking parts of this pathway helps reduce fluid overload and cardiac strain.
Drugs that help modify or block excessive, maladaptive activation of the RAAS system, which can worsen heart failure.
Side effects are uncommon in clinical practice.
Routine monitoring of renal function, blood pressure, and potassium is recommended in patients receiving ACE inhibitors.
Enalapril is primarily renally excreted.
Blocking aldosterone causes increased sodium excretion and potassium retention, which makes it a potassium-sparing diuretic.
Compared to furosemide, it is a very weak diuretic, producing only about 5% diuresis versus roughly 25% with furosemide. Because of this, spironolactone is not used primarily for its diuretic effect. Instead, it is typically used alongside furosemide when treating conditions like pulmonary edema.
Its main role is blocking aldosterone, helping reduce the harmful effects of an activated RAAS (renin-angiotensin-aldosterone system). Its side effect profile is similar to ACE inhibitors.
Once-daily dosing can be more convenient for owners who have difficulty administering tablets.
Quadruple therapy (quad therapy)
Refers to the combined use of four medications: benazepril, spironolactone, furosemide, and pimobendan.
While this combination is physiologically logical for managing heart failure, more recent research has questioned how these drugs are used together and, in some cases, whether certain components remain necessary in all patients with heart failure.
This study questions the benefits of routine triple or quadruple therapy. However, there are important limitations to consider.
The data are retrospective, and treatment groups were not randomized, which introduces bias and limits how strongly we can interpret the results. More prospective, controlled studies are needed to confirm these findings.
It is also important to note that Stage C dogs are a challenging population to study. They are typically older and often have multiple comorbidities that may not be fully controlled. In addition, owner financial constraints can affect treatment decisions and follow-up care.
For example, if a dog experiences recurrent congestive heart failure and euthanasia is chosen due to cost or quality-of-life concerns, we cannot know how long that patient might have survived with continued treatment or medication adjustments.
In an ideal setting, most cardiac patients would receive furosemide and pimobendan, and in many cases, quadritherapy is considered optimal.
However, the use of RAAS blockers (such as ACE inhibitors and spironolactone) is still an area where the evidence is evolving, particularly regarding when and how to use them. This is where opportunity to develop individualized treatment plans based on each patient’s condition and the owner’s circumstances.
Treatment approach frameworks:
1. Full guideline approach (ideal candidates)
For patients with no financial or medication administration limitations, and for pets that take oral medications easily:
- Furosemide
- Pimobendan
- ACE inhibitor
-
Spironolactone
(All medications optimized to appropriate doses)
2. Adherence-first approach (most common)
For clients who are committed to doing the best for their pet but may have practical limitations:
- Prioritize a realistic, sustainable regimen
- Adjust based on ability to medicate consistently
- Focus on maintaining core therapy while minimizing missed doses
3. Minimalist approach (resource-limited or difficult compliance)
For clients who cannot afford or reliably administer multiple medications:
- Furosemide
- Pimobendan
- RAAS blockers may be omitted to maintain adherence and quality of life
These patients are considered refractory to standard therapy, often requiring high-dose diuretics such as furosemide (>8 mg/kg/day). Doses are typically increased gradually to control clinical signs while maintaining renal function as long as possible. At advanced (Stage D) disease, medications are often administered two to three times daily, reaching the maximum tolerated doses of multiple drug classes.
These cases are frequently complicated by comorbidities such as arrhythmias, pulmonary hypertension, and chronic kidney disease or renal failure, which further limit treatment options.
When continuing management of these patients, key considerations include:
- Owner capacity – whether the caregiver can manage intensive medication schedules (every 8–12 hours) and monitor a critically ill patient at home.
- Prognosis – generally guarded, with expected survival often ranging from 3 to 9 months in Stage D cases.
- Diuretic resistance – progression of disease is often associated with reduced response to diuretics over time, contributing to treatment failure.
Switching to injectable furosemide can improve bioavailability because it bypasses the gastrointestinal tract. Subcutaneous (SQ) administration is relatively straightforward and similar in teaching method to insulin injections used in diabetic patients.
Another option is switching from furosemide to torsemide, which may be more effective in some patients due to reduced diuretic resistance.
A sequential nephron blockade can also be used by adding a second diuretic such as hydrochlorothiazide. This works at the distal tubules, where the kidney may increase sodium reabsorption in response to loop diuretics, leading to compensatory changes. While this approach can improve diuresis, it also increases the risk of kidney injury and requires close monitoring.
If adequate fluid removal still cannot be achieved, treatment can shift toward reducing cardiac workload by targeting the vascular system:
- Arterial vasodilators (e.g., amlodipine, hydralazine) reduce afterload, making it easier for the heart to pump blood forward.
- Venous vasodilators (e.g., isosorbide mononitrate) reduce preload, decreasing fluid returning to the heart.
Angiotensin receptor–neprilysin inhibitors (ARNIs) work by enhancing the body’s natural compensatory systems while also blocking harmful neurohormonal activation.
Neprilysin is an enzyme that breaks down natriuretic peptides, specifically atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP). These hormones are released when the heart is stretched due to volume overload, such as in congestive heart failure.
Natriuretic peptides are beneficial because they promote:
- Natriuresis (excretion of sodium)
- Diuresis (increased urine production)
- Vasodilation (widening of blood vessels)
They also counteract the renin–angiotensin–aldosterone system (RAAS) and reduce sympathetic nervous system activity, both of which are overactive in heart failure.
Sacubitril inhibits neprilysin, which prevents the breakdown of ANP and BNP. This allows these protective hormones to remain active longer, enhancing their beneficial effects.
When combined with an angiotensin receptor blocker (ARB), the medication also suppresses RAAS activity. Together, this dual action improves heart failure outcomes by reducing fluid overload and easing cardiac workload.
Drugs initially developed for treating diabetic patients work by targeting sodium–glucose co-transporters (SGLT) in the proximal convoluted tubules of the kidney. By blocking these transporters, they reduce glucose reabsorption, leading to glucose being excreted in the urine (glucosuria). Because water follows glucose, this also produces a mild diuretic effect.
These drugs have also been shown to have cardioprotective benefits in patients with heart failure, including those without diabetes. This has made them a promising emerging therapy beyond their original use. A recent review article highlights several proposed mechanisms behind their cardiorenal protective effects, which go beyond simple diuresis.
Although effective, they are still less commonly used in heart failure management compared to medications like Entresto.
Only a few centres in the world are able to surgically perform mitral valve repair, including annuloplasty and repair of damaged chordae tendineae. These procedures treat valve disease at its source, since the problem is mechanical in nature.
Because this type of surgery is highly invasive, patients must be placed on cardiopulmonary bypass (heart-lung machine). It is also a complex and expensive procedure.
A newer technique developed in the United States is TEER (Transcatheter Edge-to-Edge Repair). This is a minimally invasive, hybrid procedure involving both interventional cardiology and surgical principles. A device is inserted via a catheter to clip the two flailing mitral valve leaflets together, reducing mitral regurgitation and improving heart function. This procedure is still relatively new, costly, and not widely available in Canada.
Palliative treatment options include left atrial decompression. In heart failure, pressure builds up in the left atrium, which then backs up into the pulmonary veins, leading to pulmonary edema (fluid in the lungs).
Patients are typically referred after an initial diagnosis of congestive heart failure. Referral may also be made earlier, following evaluation of a heart murmur, to determine whether preclinical treatment is needed.
General practitioners may refer a case to a specialist at any stage when they feel the case exceeds their comfort level or when additional diagnostic information is required, such as echocardiography. However, referral is not mandatory, and many cases of congestive heart failure can be appropriately managed in general practice.
Referral is commonly considered when a patient is not responding as expected to heart failure medications or shows clinical deterioration despite treatment.
- Heart murmur diagnosed 3 years ago
- Exercise intolerance for one week a progressive cough for 5 days and increased respiratory rate and effort for 2 days
- Respiratory rate: 60 brpm (breaths per minute)
- Moderately increased respiratory effort
- HR: 180 bpm (Heart rate)
- Loud, grade 5/6 left apical systolic heart murmur as well as inspiratory crackles bilaterally.
- Chronic bronchitis (long-term airway inflammation)
- Pneumonia (lung infection)
- Tracheal or bronchial collapse (airway narrowing/collapse)
- Neoplasia (tumors/cancer)
Relationship Between Murmur Intensity and Mitral Valve Disease Severity
Heart murmur intensity does not always match how severe mitral valve disease is, but it can give helpful clues.
-
Grade 2 murmur
Usually suggests mild mitral valve disease, and the heart is often still normal in size. -
Grade 3–4 murmur
Can be linked to mild, moderate, or severe disease. The murmur is louder, but the exact severity must be confirmed with imaging (like an echocardiogram). -
Grade 5 murmur
Often associated with moderate to severe mitral valve disease. Dogs with advanced disease usually have at least a grade 3 or louder murmur.
Key Point (Simple Takeaway)
In small-breed older dogs, if they come in with breathing problems but:
- there is no murmur, or only a very soft murmur (grade 1–2)
then it is unlikely that congestive heart failure is the main cause of their respiratory signs. Other causes should be considered first.
Imaging is needed to look for radiographic signs of congestive heart failure and to assess pulmonary congestion.
Ideally, three-view chest X-rays, or at minimum a lateral and a DV (dorsoventral) view.
When evaluating heart disease in dogs, the DV view is preferred.
Why the DV (dorsoventral- Lay on back take picture of chest) view?
The caudodorsal (back lower) part of the lungs is better filled with air in this position, which makes it easier to see early fluid changes like pulmonary edema (fluid in the lungs) and signs of congestion in the blood vessels.
It gives a more consistent and natural appearance of the heart shape, which helps us better assess the size of the left side of the heart, especially the left ventricle and left atrium.
It is also more comfortable for dogs that are already having trouble breathing, since they can stay in a sternal (belly-down) position rather than being laid on their side.
In simple terms: the DV- Lay on back take picture of chest - view helps to see early fluid in the lungs more clearly, gives a more accurate look at heart size, and is easier for a struggling patient to tolerate.
Simple explanation of the phrase:
- Dorsal deviation of the trachea means the windpipe (trachea) is being pushed or pulled upward toward the spine instead of staying in its normal straight position.
On the dorsoventral (DV) view, cardiomegaly can be further assessed using the vertebral heart score (VHS), which helps estimate heart size relative to the spine.
Patients with left-sided congestive heart failure commonly show pulmonary venous distension.
In simpler terms: this means the veins carrying blood from the lungs back to the heart become enlarged because blood is backing up. When the left atrium becomes significantly enlarged, it can no longer efficiently receive blood from the lungs. As a result, pressure increases in the pulmonary veins, causing congestion or “backup” of blood within the lungs’ circulation.
That is what causes the distension. In Phoebe’s case, we can see that her cranial pulmonary vein is enlarged compared to the corresponding pulmonary artery.
In simpler terms: the vein bringing blood back to the heart from the lungs looks wider than the artery carrying blood to the lungs. This imbalance can contribute to fluid backing up and the appearance of distension.
Dogs with congestive heart failure (CHF) often develop fluid buildup in the lungs, known as pulmonary edema.
On radiographs (X-rays), this typically appears as an interstitial to alveolar lung pattern, meaning the lung tissue looks progressively more “fuzzy” as fluid moves from the supporting structures into the air spaces.
This change is most commonly seen in the perihilar region (around the center of the lungs where the airways and blood vessels enter) and the caudodorsal lung fields (the back and upper portions of the lungs).
In simpler terms:
CHF can cause fluid to leak into the lungs, and on X-rays this shows up as cloudy or hazy areas, especially near the middle and back upper parts of the lungs where blood flow is highest.
An alveolar pattern is also present in the right caudal lung field, with visible air bronchograms.
In simple terms: this means part of the lung appears more “solid” than normal because it is filled with fluid, cells, or debris, while the air-filled bronchi stand out within it. On the DV (dorsoventral) view, the caudal pulmonary veins are difficult to clearly identify because they are obscured by the surrounding lung changes. This makes the normal vascular structures less visible due to the overlapping pulmonary pattern.
When the blood vessels in the lungs are hard to see on an X-ray in a patient suspected of pulmonary edema, it usually means the lung tissue is becoming too “filled in” or too wet for the normal vascular pattern to stand out clearly.
In simple terms:
- Normally, you can see the lung blood vessels as thin branching lines on an X-ray.
- With pulmonary edema, fluid builds up in the lungs. That fluid can blur or “wash out” the normal vessel pattern.
- As a result, the vessels may look faint, hidden, or less distinct.
This doesn’t always mean the vessels are gone or reduced more often, they’re just harder to see because the surrounding lung tissue is no longer clear and airy.
In simple Terms: Fluid in the lungs can make the normal vascular markings look blurry or difficult to distinguish on X-ray.
Pheobe has Congestive Heart Failure. After making the diagnosis Pheobe's primary care vet started treatment:
2 weeks later followed up with specialist
At that time owner reported improvement in exercise tolerance with a normal respiratory rate and respiratory effort at rest. She still had a slight cough when she was waking up in the morning.
Resolved congestive heart failure. Heart was still enlarged and pulmonary veins where a little bit plump more importantly the pulmonary edema had completely resolved. Her lung pattern was normal (notice you can see the vessels lung vessels not on dorsal ventral view) Positive results.
On echocardiogram can further evaluate that advanced mitral valve disease with severe mitral regurgitation, resulting in marked enlargement (dilation) of the left atrium and left ventricle.
In simpler terms: the heart’s mitral valve is significantly weakened and not closing properly, causing blood to leak backward. This extra volume overload has led to significant enlargement of the heart chambers on the left side, specifically the left atrium and left ventricle.
Renal panel showed mild azotemia that was most likely prerenal since packed cell volume and total solids are elevated. Electrolytes : sodium, potassium, and chloride where on the lower end, and bicarbs on the high-end - all expected and typical in patients receiving a loop diuretic. Specialist didn't see a need to change her furosemide dose.
In Simple terms: Her kidney bloodwork showed a mild increase in values that can happen when the body is a bit dehydrated or has a lower circulating fluid volume. This is most consistent with what we call “prerenal changes,” meaning the kidneys themselves are not the primary issue.
Her red blood cell concentration and protein levels were a bit higher than normal, which can also support mild dehydration.
Her electrolytes (sodium, potassium, and chloride) were on the lower side of normal, and bicarbonate was on the higher side. These are expected changes in pets receiving a medication like furosemide (a diuretic that helps remove extra fluid from the body).
Overall, these results are consistent with her current treatment, and so the medical practitioners see there is no need to change her furosemide dose at this time.
At the time of diagnosis, a baseline kidney (renal) blood panel and chest X-rays are performed. Treatment is started with furosemide (a diuretic to remove excess fluid) and pimobendan (to support heart function). Usually wait until breathing improves before adding another medication.
A few days later, an ACE inhibitor and spironolactone are added if the patient is stable.
Follow-up monitoring plan:
- 1–2 weeks later: Repeat chest X-rays and kidney bloodwork to check response and kidney function
- If medications need adjustment, another kidney panel is repeated 1–2 weeks after each change
- If everything is stable and no changes are needed, monitoring is typically done every 3–4 months with chest X-rays and kidney bloodwork
At-home monitoring:
What owners can do- closely observe the pet at home. If there are any concerns such as changes in breathing, appetite, energy, or coughing the pet should be rechecked sooner.
(Owner Friendly) Other Management Strategies
ven that identification of increases in respiratory rates above the normal baseline has the best predictive value for impending clinical decompensation- Respiratory rate is really important thing which an owner can monitor at home.
Free apps available such as Cardalis app or Boehringer app which clients can use. You tap when the pet takes a breath and it can track their breathing rate and track trends over time it's functionality on the phone makes it handy.
** Importance of quality of life rather than the quantity
Free Grain Diet within the context of dilated cardiomyopathy ?
In Quebec there is still a lot of owners that go in with dogs that have giant hearts
on radiographs or that where diagnosed with heart murmurs and they are
on the famous grain free diets. The pulses in these formulated diets are the culprits.
It's not the lack of grain that causes the problem but rather what the grains have been replaced with. In nutrition usually there talk of either deficiency in something or a toxicity of something. So it would be more that these pulses elements have some level of toxicity of the heart muscle or are not well-used as a source of energy by the heart of some dogs. Two dogs on the same diet one is more prone then other is attributed to environmental and genetic factors which can increase the risk of early development of cardiomyopathy vs later in life.
Either way transitioning to a therapeutic diet is necessary as a first step. As without transition a lot of pets succumb to the condition due to arrhythmias or congestive heart failure.
It's the exact same therapy management however for better results a change in diet or addition of Taurine is needed.
The industry is lagging behind on the consequences of these formulations which lead pets to develop cardiomyopathy.
Nutraceuticals? There isn't a ton of research on them, certainly don't pose harm. If some provide a placebo effect which makes the owner think it's helping and maybe it is, but we will not fully know.
- Taurine - Is the basic go to
- Omega- 3 are beneficial the recommended dose 40 mg of EPA and 25 mg of DHA
- Coenzyme Q10
- Carnitine
Angiotensin II receptor blockers : Entresto when would you be looking to introduce those into your protocol?
- If a patient is hypertensive we use and angiotensin receptor blocker for
Treatment.
- Standard therapy is the go to for cardiomyopathy due to variety and complexity of cases.
Beta Blockers: Ophthalmic beta blockers
They can be Negative Inotropic= decrease contractility + Negative Chronotrope= Lower the heart rate.
In patients with early stages of valve disease in a B1 and B2 dog wouldn't really worry about it
If a dog is about to develop congestive heart failure there is a risk that by giving them a medication
Whether oral or ophthalmic drugs you get some level of absorption. If you lower the heart rate and
Decrease the heart rate and decrease their contractility then there is a risk that that's going to push them
Over the edge and they are going to develop pulmonary edema because of it. The approach is similar to the use of steroids, If a dog has reached a stage where there is no other option but to use Ophthalmic beta blockers for the purpose of quality of life to treat the condition. Be aware of the risks so monitor
The respiratory rate very closely at home take some baseline chest radiographs too. Factually in a patient that has a diseased heart which can get very large, where the left atrium is getting very big
And where the left ventricular function is not always as good those drugs can make them decompensate.
Diuretics and Renal insufficiency/ renal values that are trending upwards?
Importance on clinical signs. Developing azotemia is tolerated as long as the dog is doing all of their
Regular things. Being honest to owners when there is no choice but to start pet on diuretic even on the
Minimal dose if that helps to improve breathing but the kidney values are trending up however
Pet is not discomforted it's tolerated on a clinical level. Priority is placed on helping pet breathe
better and if azotemia is progressive
Creatinine number doesn't mean anything - you can have a dog with a creatinine of 150 that's
Completely fine because it's been gradually building up over the years and we can have dogs that went from
50 - 150 because they have an acute kidney injury and these dogs are going to be extremely sick.
If a diuretic is started and the patient gets really ill due to underlying kidney disease then try to
Back off on some of the drugs or to decrease the dose a little bit. Patient's comfort is always a priority.
Does Torsemide put more burden on the kidney vs Furosemide ? Yes
Always will be cautious to check renal panel. Being precise with dosing of furosemide if using it.
Vet comfort and choice of drug comes into play as well. Learning to use drugs and to practice and pay
Attention to the details of what has been done vs response to further improve therapy. Both medications
Can be dehydrating which is what worsens the kidneys.
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