A patient with heart failure can be a challenge to the veterinary nurse and clinician. Heart failure can be caused by venous congestion (congestive heart failure), arterial under-filling (low output heart failure), or a combination of both.

Congestive heart failure (CHF) that compromises breathing (pulmonary oedema, pleural effusion) is the most common presentation of heart failure in dogs and cats. The patient that arrives at the practice with respiratory distress and/or collapse needs to be handled in a calm but efficient manner. Stress should be avoided at all costs as this acutely increases the body’s metabolic demands and patients with heart failure do not have sufficient cardiac reserve to accommodate such an increase in demand.

Consequently, for patients with CHF, the saying ‘less is more’ is never more appropriate. As hypoxaemia is usually present, oxygen therapy and minimal handling is often the safest initial approach when dealing with these patients. Parenteral diuretics (for example, furosemide) are also indicated to remove excess fluid which gives rise to oedema.

Most patients will show clinical improvement with this approach, and more thorough investigations into the underlying cardiac disease can be performed when the patient is stable.

What is heart failure?

To answer that question, it is important to understand the role of the cardiovascular system. Its primary function is to provide a normal arterial blood pressure.

Normal arterial pressure is vital to maintain adequate perfusion to the organs of the body – especially vital organs, such as the heart, brain, and kidneys. This is achieved by a balance between cardiac output and vascular tone. Vascular tone refers to the degree of constriction experienced by a blood vessel. Vasoconstriction or vasodilation are influenced by different factors, such as neural activity, hormonal signals or autoregulation.

If cardiac output is compromised, arterial pressure falls, and compensatory mechanisms are activated in an attempt to return blood pressure to a more normal level. These compensatory mechanisms include increased fluid retention by the kidneys, vasoconstriction, and stimulation of the heart to increase heart rate and stroke volume (primarily via increased sympathetic tone). Although ultimately beneficial to restore adequate arterial pressures, the ‘trade-off’ is an increase in venous pressure, which if severe enough can cause fluid to leak (effuse) into the surrounding interstitial tissues (pulmonary oedema) or cavities (ascites, pleural effusion).

If mild compensation is sufficient to normalise arterial pressure without causing effusions, then affected patients will frequently not have clinical signs, or only develop signs if they undergo excessive exertion or stress. If more compensation is required to normalise arterial pressure, then this results in the development of effusions. The affected patient is considered to have developed congestive heart failure. 

If arterial pressure cannot be normalised, despite maximal activation of compensatory mechanisms, then low output heart failure is present. Affected patients usually have concurrent CHF, unless the fall in output is so acute that compensatory mechanisms have insufficient time to be activated – for example, with some arrhythmias or myocardial infarction. Although life saving in the short term, long-term stimulation of compensatory mechanisms causes progressive deterioration of cardiac function owing to fatigue of the heart muscle, termed ‘cardiac remodelling’.

Nursing a patient with acute, life-threatening CHF

The most common clinical signs and examination findings are listed in Table 1.

Patients with acute, life-threatening CHF are the most challenging case for the veterinary nurse, as these animals are almost invariably distressed and intolerant of handling, but also require intensive therapy and close monitoring. This makes nursing very difficult.

Nursing care will involve:

   minimal restraint of the patient while the veterinary surgeon performs a very quick physical examination

   preparation of oxygen supplementation

   placement of an IV catheter – but only if possible without stressing the patient further

   administration of diuretics, such as furosemide. Diuretics should be given parenterally (IV, IM, or SC).

The patient should be left to adjust to its new surroundings in an oxygen-rich environment. Ultimately the key to successful management is minimal handling and restraint. Remember, ‘less is more’.

Other nursing considerations include access to a plentiful water supply, a litter tray for cats, and remote monitoring of respiratory rate and effort. If continuous ECG is available, and the patient is not stressed further by electrodes attached to the limbs or thorax, then this method of monitoring of heart rate and rhythm is also useful.

The nurse should also prepare for thoracocentesis if required – usually cats (Figure 1).

Figure 1: An example of thoracocentesis being performed on a cat

What are the treatment goals in CHF?

The treatment aims for patients with CHF differ according to its nature.

Acute, life-threatening CHF cases should be stabilised by supplementing oxygen to reduce hypoxaemia; by administering drugs to reduce effusions (diuretics, vasodilators) and improve cardiac output (positive inotropes); and minimising stress by handling the patient as little as possible.

Quality of life in chronic CHF cases can be enhanced with drugs to improve haemodynamic function (pimobendan, furosemide); and length of life may be extended using drugs that decrease the deleterious effects of long-term stimulation of compensatory mechanisms (ACE inhibitors, spironolactone).

Case history 1

Louie is a 12-year-old male neutered Siamese cat. He presented to the clinic as an emergency because he had developed respiratory distress. He had muffled lung sounds on auscultation, a gallop rhythm, a pulse rate of approximately 200 beats/ minute, and a respiration rate of 58 breaths/minute. He was very distressed when handled.


Respiratory distress, gallop rhythm, and muffled lung sounds. Pleural effusion from CHF was suspected.

Case management

   An oxygen kennel was prepared whilst the veterinary surgeon auscultated Louie. As soon as this was completed, Louie was given IM furosemide, placed in the oxygen kennel, and left alone to adjust to his new surroundings •   Equipment was prepared for ultrasound-guided thoracocentesis.

A large amount of pleural fluid was seen on thoracic ultrasound and 250ml of sero-sangrinous fluid was drained from his thorax

   Louie was placed back in the oxygen kennel
and his respiration rate improved to 30 breaths/minute.

   When Louie had calmed down sufficiently, an IV catheter was placed, blood sampling performed, and thoracic radiographs were taken. Radiographs showed an enlarged heart and a small amount of residual pleural fluid.

Case outcome

Louie was diagnosed with hypertrophic cardiomyopathy (HCM) and CHF. He went home the next day, and has come back for three further check-ups. Owing to his nature, he is dealt with quickly, calmly and efficiently, and goes straight home after minimal monitoring tests (radiographs, ultrasound, blood pressure and blood tests). His owner counts his respiration rate at home, which is important in order to gauge how well controlled his CHF signs are. His owner is in frequent communication with the veterinary surgeon to enable assessment of the cats, and has instructions to give an extra dose of furosemide if Louie has persistent tachypnoea. He is currently doing well.

Case discussion

Hypertrophic cardiomyopathy is the most common cardiac disease in cats, and Louie’s case is a typical presentation when CHF occurs. With HCM, the main heart chamber (left ventricle) becomes thicker. This causes stiffness and means that the ventricle cannot relax as it should. The left atrium may increase in size to cope with the increased pressure needed to fill the ventricle. In turn, if severe enough, this can lead to CHF with fluid accumulating as pulmonary oedema and/or pleural effusion. Furthermore, some cats will develop clots (thrombi) in the enlarged left atrium, which can embolise to the systemic arteries, particularly to the limbs.

Often affected cats will appear to be normal, and the first clinical sign can either be respiratory distress, aortic thromboembolism (ATE), or sudden death. The challenge with this particular case is the severity of the disease and Louie’s volatile nature. He is always handled in a locked room, away from barking dogs and other cats, and as calmly as possible to minimise stress. When cats develop signs of CHF, long-term prognosis can be poor, so management of these cases is directed at maximising quality of life.

Case history 2

Harry was a nine-year-old Cavalier King Charles spaniel, who presented as an emergency with respiratory distress, cough, and exercise intolerance. His respiration rate was 42 breaths/minute and pulse rate was 150 beats/minute.

A heart murmur had been recorded on routine examination two years earlier.


Respiratory distress, left apical heart murmur, and cough. Pulmonary oedema from CHF was suspected.

Case management

   An IV catheter was placed, and blood sampled for renal function and electrolyte analysis

   IV furosemide was administered

   Harry was attached to a continuous ECG

   He was placed in a ready-prepared oxygen kennel

   When he was stable enough, radiographs were taken. These showed cardiomegaly – particularly left atrial enlargement – which was compressing the mainstem bronchi. Pulmonary oedema was also present

   The next day, when Harry’s condition had stabilised, echocardiography showed a hugely distorted, thick and prolapsing mitral valve, and a large left atrium. This confirmed that degenerative mitral valve disease (DMVD) was the cause of Harry’s CHF

   Harry has come back to the clinic once since this episode, and currently, is doing very well. His owners monitor respiratory rate and effort at home and have instructions to give an extra dose of furosemide if necessary.

Case discussion

Degenerative mitral valve disease is the most common acquired heart disease in dogs (Figure 2). Both atrioventricular valves can be affected, but more commonly the mitral valve is affected. The valve leaflets start to degenerate and can become so distorted that they do not close properly, which leads to blood flowing back into the left atrium.

Figure 2: Cavalier King Charles spaniels are commonly affected by DMVD

In severe cases, such as Harry’s, the build-up of pressure in the left atrium and venous system results in pulmonary oedema. DMVD is a progressive disease and so usually the first clinical sign is a murmur picked up on routine examination. In some dogs, the disease process does not progress further to result in overt CHF, although exercise intolerance and cough can be present. In these cases, moderate exercise restriction and using a harness is recommended.

Prognosis varies from patient to patient, but if CHF if present, then the long-term prognosis is usually poor.


Management of patients with CHF can be quite challenging, when disease process, severity and temperament of the patient are taken into consideration. However, the saying ‘less is more’ can certainly be applied when dealing with heart failure cases. Good monitoring and record keeping is very important whilst oxygen supplementation and diuretics take effect. Nursing is very important in these patients as the primary treatment goal is maintaining quality of life.

Suggested reading

MARTIN, M., CORCORAN, B. (2006) Notes on Cardio-respiratory Diseases of the Dog and Cat Wiley Blackwell 2nd edition 

WARE, W. (2007) Cardiovascular disease in small animal medicine. Manson Publishing


Charlotte Pace

BA(Hons) RVN

Charlotte Pace qualified as a Veterinary Nurse in 2003, whilst working in practice in London. In the same year, she moved to the Royal Veterinary College to work as a medicine nurse. In 2006, she became the dedicated cardiology nurse for the Queen Mother Hospital for Animals.

Veterinary Nursing Journal • VOL 25 • No2 • February 2010 •