THE AIM OF THESE CASE STUDIES is to present and discuss the most common clinical presentations of feline heart disease and give a more detailed insight into the management of these patients, this first one examining a case in a dyspnoeic cat. A nineyear- old male, neutered DSH cat was presented to the cardiology service at Southern Counties Veterinary Specialists for the investigation of acute respiratory distress. The owners reported that the cat had been “off colour” for a few days; lethargic, inappetent, subsequently developing breathing difficulties. He was fully vaccinated and wormed, and had never travelled abroad.
On presentation, the patient was quiet, alert and responsive. Respiratory rate was 80 breaths/minute with severe respiratory effort. Prolonged expiratory phase and orthopnoea were noted. Mucous membranes were pink and capillary refill time was two seconds. Lung auscultation revealed increased respiratory sounds throughout the entire lung field. Cardiac auscultation revealed marked gallop sounds, a heart rate of 200 beats/minute and regular rhythm. A heart murmur was not detected. Femoral pulses were of fair quality and symmetric. The physical examination was otherwise unremarkable. Rectal temperature was
not measured initially to minimise stress.
Problem list and differential diagnoses
Tachypnoea and dyspnoea: a practical approach to forming a differential diagnosis list for the dyspnoeic patient is to consider the anatomic area associated with the breathing difficulty. Dyspnoea secondary to upper airway disease will typically present with increased upper respiratory sounds, stridor, marked inspiratory component. In this case, no signs of upper respiratory tract disease were noted. Dyspnoea secondary to lower airway disease is typically characterised by short inspiratory and long expiratory phase, with the exception of pleural space disease that is characterised by a restrictive breathing pattern (rapid rate, shallow depth of inspiration and paradoxical abdominal breathing). Causes include diseases affecting the thoracic trachea and bronchial tree, pulmonary parenchyma and pleural space; the most common of which include congestive heart failure (CHF) and secondary lung oedema and/or pleural effusion, feline asthma and bronchopneumonia (i.e. bacterial, viral, parasitic or fungal). Less common causes include diffuse parenchymal neoplastic disease (e.g. lymphoma), airway foreign body, trauma (causing pneumothorax, haemothorax or diaphragmatic hernia) and mediastinal mass. Pleural effusion occurs with: increased hydrostatic pressure (e.g. right or left CHF in cats), decreased plasma oncotic pressure (e.g. hypoproteinemia), lymphatic obstruction (e.g. neoplastic disease or idiopathic) and increased capillary permeability (eg vasculitis) (Côté, 2011). In addition to the breathing pattern described above, pleural diseases typically cause dull ventral lung and heart sounds, neither of which was
present in this case. Systemic causes of tachypnoea such as anaemia, sepsis and shock should be considered as well. Cardiac gallop sounds: associated with diastolic dysfunction and fairly specific for the presence of cardiomyopathy, whether primary (e.g. hypertrophic cardiomyopathy) or secondary (e.g. hyperthyroidism). Lethargy and anorexia: very unspecific signs in cats and can be a manifestation of many pathological processes.
Diagnostic plan and initial stabilisation
The presence of gallop sounds and acute dyspnoea in an older male cat raised the suspicion of heart disease and congestive failure. The diagnostic plan was therefore aimed at getting the most valuable information needed, as quickly as possible, in order to differentiate cardiogenic and noncardiogenic causes to the presentation.
The patient had presented in a fragile state and thus a “hands-off ” approach was adopted in order to minimise stress. Initial stabilisation was achieved by administering “flow by” oxygen supplementation in a calm, quiet environment with subdued lighting. Once the patient had relaxed, a rapid point-of-care thoracic ultrasound examination was performed with the patient in sternal position and minimally restrained. An assessment was made of left atrial size and also for presence/absence of pleural fluid. This revealed an enlarged left atrium (LA) with no pleural fluids (Figure 1). An enlarged LA was consistent with heart disease and therefore dyspnoea in this case was suspected secondary to pulmonary oedema and congestive heart failure. Thoracic radiographs were indicated to document the presence of pulmonary oedema; however, it was believed that the patient would benefit from further stabilisation prior to performing additional stressful investigation. An intramuscular injection of furosemide 2mg/kg was given and the patient was placed in an oxygen-enriched chamber for one hour. Respiratory rate decreased to 52 breaths/minute and the patient appeared more comfortable. Thoracic radiography was subsequently obtained (DV vie only in minimal restraint). It showed diffuse alveolar pattern and pulmonary venous congestion, consistent with lung oedema secondary heart failure (Figure 2). Systemic blood pressure was 95mmHg systolic (obtained with Park’s Doppler ultrasound).
The patient was hospitalised and an intravenous cannula was placed. Baseline biochemistry was performed to evaluate renal function and electrolyte status prior to starting an aggressive diuretic treatment. Furosemide 1mg/kg intravenous injection was repeated one hour after the initial injection. Additional doses were given according to the response to treatment, evaluated by the respiratory rate and effort (total dose 4mg/kg over the course of four hours). Once a satisfactory improvement was achieved, diuretic treatment was continued with furosemide 2mg/kg IV injections every eight hours. Respiratory rate and effort were monitored hourly overnight and blood pressure was measured every four hours.
A comprehensive echocardiographic examination was performed later that day after assuring the patient was stable enough to tolerate such a procedure. This showed marked concentric left ventricular hypertrophy (Figure 3), marked left atrial (LA) enlargement with poor LA function and spontaneous echo contrast (“smoke”). Diastolic dysfunction was noted with pseudo-normal pattern on spectral Doppler interrogation of mitral inflow (Figure 4). Systolic dysfunction was noted. There was no evidence of
left or right dynamic outflow tract obstruction. Pimobendan was started at 0.25mg/kg orally every 12 hours.
Hypertrophic cardiomyopathy (HCM) and left side congestive heart failure (CHF).
Discharge and chronic treatment plan
Overnight respiratory rate stabilised at 36 breaths/minute and respiratory effort normalised. Blood pressure had increased to 110mmHg. Repeated radiographs showed significant improvement of pulmonary oedema. Urea, creatinine and electrolytes were repeated to assess influence of diuresis. The patient remained in hospital for a further 48 hours and was switched to oral diuretic treatment (furosemide 2mg/kg orally every eight hours). Clopidogrel was started at 18.75mg total once daily. The patient was discharged once respiratory rate and effort were completely normal on oral medication and there was no evidence of pulmonary oedema on repeated thoracic radiographs.
Dyspnoeic cats often present in a fragile condition and often unable to tolerate additional stress caused by diagnostic procedures. Ill-timed diagnostic procedures, for example physical or chemical restraint for thoracic radiographs, may prove detrimental or even fatal for the patient. That said, determining the underlying cause for the dyspnoea is important to determine optimal treatment options (e.g. anti-inflammatory treatment for an asthmatic cat versus diuretics for a cat in CHF). This is a challenging situation for the practitioner who has to decide which test will provide the most information but without causing additional stress for a fragile patient.
Physical examination can provide clues for the underlying problem. Low rectal temperature, tachycardia and elevated respiratory rate can increase the index of suspicion for cardiomyopathy; however, more studies are needed in this area to generate specific and sensitive cut-off values. It should also be noted that it is not uncommon for cats in CHF to have lower heart rates (Smith, 2012). The clinician should also beware of over-interpreting the presence or absence of a heart murmur as those are not only commonly found in healthy cats (Wagner, 2010; Payne, 2015), they are also absent in a significant number of cats with cardiomyopathy (Payne, 2015; Smith, 2012). Left atrial enlargement (LAE) is a good predictor for presence of congestive heart failure in cats (Rush, 2002; Schober, 2006; Smith, 2012) as it correlates with the severity and chronicity of left ventricular (LV) dysfunction and filling pressures (Schober, 2007). Therefore, CHF should be assumed in a dyspnoeic cat with LAE until proven otherwise. Significant left atrial enlargement is fairly easily identified with basic echocardiographic examination; however, it is sometimes difficult to appreciate (Schober, 2014).
Thoracic radiography can be specific but not sensitive for the presence of LAE (Schober, 2007; Schober, 2014) and often requires substantial physical or chemical restraint. In contrast, a point-of-care thoracic ultrasound examination is minimally stressful for most cats and thus was the test of choice in this case. In general practice, left atrial diameter of >16.5mm when measured from the right parasternal long axis view is 87 percent sensitive and specific for a diagnosis of heart failure (Smith, 2012). An additional benefit of a rapid echocardiographic examination is the ability to screen for the presence of pleural effusion.
Thoracocentesis is indicated when significant volumes of pleural fluid are present and usually results in a rapid improvement in respiratory effort and the patient’s comfort. Quantitative NT-proBNP assays are a useful tool in discriminating between cats with cardiac and noncardiac causes of dyspnoea (Connolly, 2009; Fox, 2009; Singletary, 2012). A shortcoming of these tests is the long period of time to get results,
making them unsuitable for the acute setting where decisions must be made rapidly. Recently, a pointof- care NT-proBNP assay has been shown to reliably differentiate cardiac and non-cardiac causes of pleural effusion (Hezzell, 2016), but results cannot be extrapolated for every dyspnoeic cat and more studies are needed.
- Diuretics. The loop diuretic furosemide is the corner stone of CHF treatment regardless of the underlying cause. Depending on severity, the initial bolus dose ranges from 1 to 4mg/kg (Ferasin, 2015); however, the author rarely uses a dose higher than 2mg/kg for the acutely decompensated feline patient (Fuentes, 2007). The peak effect of furosemide, when given subcutaneously (SC) or intravenously (IV), should be expected after about one hour (Harada, 2015). Furosemide injections of 1-2mg/kg can therefore be repeated hourly until clinical response is achieved. This is assessed by monitoring respiratory rates. It is important to note that furosemide must be given judiciously to minimise adverse effects such as hypotension, reduced renal perfusion and electrolyte depletion (Felker, 2009) and a maximal cumulative dose of over 12mg/kg/day should be avoided (Ferasin, 2015).
- Pimobendan. Pimobendan has been shown to improve survival time in pre-clinical and clinical heart disease in dogs (Boswood, 2016; Häggström, 2008; Summerfield, 2012). Unfortunately, studies are limited in cats and pimobendan is not licensed for their use. However, several retrospective studies have shown pimobendan can be safely used in cats (MacGregor, 2011; Gordon, 2012) and suggest significant clinical benefits (Reina-Doreste, 2014). As pimobendan is an inodilator (possessing both inotropic and vasodilatory effects) it is often used by cardiologists in cats with systolic dysfunction and low systemic blood pressure that show no echocardiographic evidence of obstructive disease (Ferasin, 2015).
- Anti-thrombotic medication. Feline arterial thromboembolism (FATE) is a catastrophic complication of feline cardiomyopathy with only 12 percent of cats presented to general practices surviving longer than seven days (Borgeat, 2014). Risk factors thought to be associated with FATE are LAE and poor left atrial function (Smith, 2003; Schober, 2006). There is little evidence for the use of anti-thrombotic drugs for the prevention of FATE; however, the FATCAT study demonstrated the superiority of clopidogrel in delaying recurrence when compared with aspirin (Hogan, 2015). For this reason the author uses clopidogrel in most cats with cardiomyopathy and LAE. The major limitation of clopidogrel is its bitter taste. Cats that will not tolerate clopidogrel should be given aspirin as an alternative.
Diagnosing and managing the acute heart failure cat is challenging and requires the delicate handling of an often vulnerable patient, the expertise to make the correct diagnosis, and careful attention to tailoring optimal treatment to the individual patient. The aim of this case report was to provide the reader with an insight into the reasoning behind the decisionmaking process in such cases. Further reading is recommended and readers are referred to the comprehensive review article “Management of acute heart failure in cats” published in the Journal of Veterinary Cardiology (Ferasin, 2015).
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