Diagnosis and therapy of acute heart failure (HF) in dogs and cats require recognition of typical and atypical clinical signs, selective rapid diagnostic testing and decisive therapy, followed by close monitoring. Although these cases can be intimidating due to the 'crisis' atmosphere often present in the emergency room, most can be pulled back from a downward spiral with presence of mind and close observation to details.

Factors That Will Affect the Approach to Therapy

Do the Life-Threatening Clinical Signs Indicate Congestive or Low-Output (Hypotensive) Problems?

Congestive clinical signs include pulmonary oedema, ascites or pleural effusion. Low-output signs include cold extremities, hypotension, pale mucous membranes, weak pulses and slow capillary refill time (CRT). This differentiation is important because although both types of HF require immediate therapy, congestive signs need furosemide or mechanical relief and low-output signs (signalling concurrent dehydration or severe myocardial failure) may need fluid and inotropic support.

Are the Clinical Signs Typical of Right-Sided, Left-Sided or Biventricular HF?

Clinical signs of right-sided HF include jugular distension, hepatomegaly, ascites and/or pleural effusion. Left-sided HF signs usually include cough, coughing up foam, dyspnoea, pulmonary crackles and cyanosis. The differentiation matters because right-sided signs often require mechanical drainage acutely and left-sided failure requires immediate diuretic therapy.

Other Factors That Will Affect Therapy

Diagnosis of the HF as primarily systolic or diastolic in nature can help direct therapy. Systolic dysfunction is primarily characterised as poor contractility, and may need positive inotropic support. Diastolic dysfunction is clinically characterised as poor ventricular filling and may signal hypertrophic disease. Previous treatment status is important in the acute HF patient; animals may already be receiving furosemide ± angiotensin converting enzyme inhibitors, ± pimobendan, ± digoxin or other medications. Inappropriate previous therapy may lead to complications (e.g., dehydration, hypokalaemia). In addition, animals already receiving medications may now need higher doses, and the risk of drug interactions is increased.

The presence of an arrhythmia in an acute HF complicates therapy because the arrhythmia may require direct therapy in addition to the HF. Arrhythmias may actually cause the onset of HF (e.g., atrial fibrillation) or may lead to sudden death (e.g., hypoxia-or myocardial-related ventricular tachycardia).

Acute Congestive Heart Failure

Animals with acute congestive HF are at risk for death due to acute hypoxia or respiratory muscle failure after prolonged dyspnoea. They can be recognised by their history (abnormal heart on auscultation, dyspnoea, abdominal swelling, cyanosis, exercise intolerance due to dyspnoea or cough, pet may not have slept for several days) and physical examination findings. General findings consistent with congestive HF include weakness, depression, anxiety/panic and tachycardia (arrhythmias may be detected). Signs of left-sided HF include gallop rhythm, coughing up foam, dyspnoea, harsh lung sounds or pulmonary crackles and left-sided heart murmurs. Signs of right-sided HF include jugular distension, dull heart and breath sounds, hepatomegaly, dyspnoea/open-mouthed breathing if pleural effusion, positional discomfort if ascites and a right-sided heart murmur.

Additional testing to be done immediately: an electrocardiogram (ECG) strip should be recorded on every animal (10 second emergency lead II), whether or not an arrhythmia is detected. Immediate thoracic radiographs should not be attempted in dyspnoeic animals unless diagnosis is in doubt and waiting may kill the patient.

Emergency Therapy for Left-Sided Congestive Heart Failure

The aim of therapy for acute congestive HF is to increase oxygen delivery, increase cardiac performance and decrease stress. For any animal in acute congestive HF, the number one priority is to limit stress (e.g., no radiographs, limited and gentle restraint). Oxygen supplementation can be achieved via use of an oxygen cage, nasal oxygen, or flow-by oxygen. In cases of severe pulmonary oedema intubation may be necessary, and suction or postural drainage can remove copious amounts of pulmonary oedema.

Drug therapy almost always includes intra-venous or intramuscular use of furosemide. Furosemide is a potent loop diuretic that, when given intravenously, acts within 5 minutes, peaks within 30 minutes and dissipates after 2-3 hours. Furosemide should be administered frequently (initially every 1-2 hours) until the respiratory rate and dyspnoea start to decline. Monitor to be sure urination occurs within 1 hour of administration. After initial stabilisation, decrease dosing frequency to every 6-12 hours, based on the severity of respiratory distress and response to therapy.

Vasodilators provide acute decreases in arterial pressure, venous pressure, or both. Nitroprusside is a potent direct acting mixed vasodilator with a very short half-life (1-2 minutes), with dominant arterial dilating effects. Nitroprusside is indicated for use in severe, decompensated CHF caused by mitral regurgitation (MR) or dilated cardiomyopathy (DCM) to decrease afterload and increase forward flow. It is given only as continuous rate infusion (CRI) diluted in 5% dextrose, and patients must be monitored closely for hypotension (target mean arterial pressure is 70-80 mmHg). Hydralazine is a potent oral arterial vasodilator and is frequently used when nitroprusside is not available. Give crushed and mixed in water in acute situations. Glyceryl trinitrate (2% ointment) is a venodilator and preload reducing agent. It is applied to hairless skin for dermal absorption, but efficacy in dogs and cats is controversial.

Positive inotropes are drugs that increase systolic (contractile) function. The two medications used most frequently in acute congestive HF are dobutamine (intravenous) and pimobendan (oral). Dobutamine is a selective β₁ receptor agonist and increases contractility with little change in heart rate. It is administered as a CRI in 5% dextrose and titrated to effect (positive result is improved perfusion, negative effects are arrhythmias and tachycardia). Pimobendan is a rapid-acting oral positive inotrope with vasodilating properties that make it very useful for acute congestive HF.

Pimobendan may be given orally (crushed into water) with care to animals when dobutamine use is not feasible. Standard doses are used, but for most rapid absorption, pimobendan should be given on an empty stomach.

Sedation is a necessary part of early patient management in very stressed patients. Morphine sulphate reduces anxiety and decreases sympathetic tone if given intramuscularly or subcutaneously. Butorphanol or buprenorphine in low doses can be used to relieve anxiety in cats and should be given intramuscularly.

Emergency Therapy of Acute Right-Sided Congestive Heart Failure

Right-sided heart failure is only an emergency if the patient is collapsed or dyspnoeic. Collapsed patients with right-sided HF usually have pericardial effusion as the causative problem (and should undergo pericardiocentesis), and dyspnoeic animals usually have pleural effusion (very common in cats). Animals that are not in respiratory distress do not usually require sedation or pain management. Initial priorities in dyspnoeic animals remain the same: decrease stress and provide oxygen supplementation. If thoracic effusion is the suspected source of dyspnoea, thoracocentesis should be performed rapidly using low stress techniques. 'Exploratory' thoracocentesis can be life-saving in animals with severe dyspnoea. If the diagnostic centesis is positive for fluid but little is removed, consider sedation for more complete drainage. If centesis is positive for fluid and significant amounts can be removed, continue centesis until the patient is comfortable. If the centesis is negative for fluid or air with one try on each side, reconsider the diagnosis.

Once acute dyspnoea is relieved, patients with pleural effusion should be examined for jugular distension to confirm right-sided HF as the cause of the effusion. If the effusion is determined to represent HF (rather than chylothorax, etc.) furosemide can be administered after mechanical removal of pleural effusion. Furosemide cannot shift cavity fluid fast enough to be life-saving but is helpful as follow-up to drainage. Systemic vasodilators are not as helpful in pure right-sided HF as in left-sided HF, and use of systemic vasodilators may lead to low cardiac output signs if blood pressure (BP) drops and the right side of the heart cannot supply additional blood to the left side. Specific pulmonary vasodilators (sildenafil) can be useful if pulmonary hypertension is the cause of the right-sided HF. Pimobendan may provide needed inotropic support when used in conjunction with other therapies for heart failure. Lastly, ascites is generally not considered to be a life-threatening clinical problem, but large amounts of abdominal fluid reduce the available space in the thorax for lung expansion, limit diaphragmatic contraction and may lead to decreased appetite due to discomfort. Animals with severe ascites may be too uncomfortable to lie down and sleep. Abdominocentesis (usual goal is partial rather than total fluid removal) increases comfort for the animal while medical therapy is initiated.

Identification/Therapy of Acute Low-Output Heart Failure

Animals with low-output HF will die of complications of limited oxygen and nutrient supply to vital organs (i.e., renal failure) and may show life-limiting signs of hypotension (mental deterioration, lack of appetite, weakness and collapse). The animals may have a history of known cardiac disease and the owners may report clinical signs including acute collapse (especially if arrhythmia is present) or a gradual decrease in function. Physical examination abnormalities typically include weakness, depression and tachycardia with weak femoral pulses with or without pulse deficits. Hypothermia is often present and the patient may have palpably cold ears, lips, tail and feet related to poor perfusion. Capillary refill time is typically prolonged and mucous membranes may be pale. Dehydration is a common cause of low cardiac output/hypotension in animals with poor cardiac function and physical findings of dehydration (dry mucous membranes, skin tent, sunken eyes) may be noted. In cats, a paradoxically low HR may be noted in the presence of hypothermia and hypotension.

Immediate diagnostic testing should include a brief ECG recording, regardless of auscultated findings. Immediate thoracic radiographs are indicated in dyspnoeic animals only, and only if there are not too dyspnoeic to survive the procedure. Biochemical testing (chemistry profile) may reveal evidence of dehydration, end-organ compromise (e.g., prerenal azotaemia) or electrolyte imbalances (these patients are often those already on cardiac therapy who are dehydrated and may be experiencing complications).

Treatment is aimed at alleviating the patient's most life-threatening problem. Poor cardiac output and hypotension may be due to acute arrhythmia, lack of preload (dehydration) or decrease cardiac function (usually systolic dysfunction). Therapy should acutely relieve cardiac output-compromising arrhythmias, increase cardiac output without leading to pulmonary oedema (increase preload with fluids, administer oral inotropes) and provide supportive care.

Therapy of Arrhythmias

Ventricular tachycardia (VT) at HR >160 bpm should be treated immediately with intravenous lidocaine in repeated boluses as needed until the VT is abolished. Supraventricular tachycardias (atrial tachycardia, other narrow complex tachycardias, atrial fibrillation) should be treated quickly in low cardiac output patients if the HR >240 bpm. The goal of therapy for supraventricular tachycardia is to slow the heart rate to <200 bpm in most patients. Intravenous or oral diltiazem is the treatment of choice for rapid resolution.

Increasing Preload

Rehydrate the dehydrated animal (assuming no congestive HF present) with intravenous fluids (half-strength saline or lactated Ringer's solution are good choices). Discontinue any previous furosemide therapy (this will be temporary). Monitor closely for increasing respiratory rate signalling development of pulmonary congestion. Subcutaneous fluid administration is strongly discouraged; the fluids cool off quickly, are erratically absorbed and cannot be removed if increased respiratory rate develops.

Positive Inotropic Support

Dobutamine or pimobendan can be used to increase cardiac output as outlined previously. Positive inotropes are most helpful in well hydrated myocardial disease patients.

Monitoring and Supportive Care

Monitoring potassium and magnesium concentrations in patients receiving fluids and diuretics is helpful to avoid life-threatening aberrations. Provide warmth for hypothermic patients, but allow the animal to self-regulate as needed (it is tempting but unhelpful to overheat animals that are hypothermic due to low cardiac output). Monitoring urination provides a way of assuring rehydration--be sure that dogs have 'urination opportunities' and that cats have a litter box. No exercise should be allowed in the first days of therapy. If animals have refractory inappetence, consider therapy with antacids.

References

1.  Stepien R, Boswood A. Cardiovascular emergencies. In: King, LG; Boag, A. eds. BSAVA Manual of canine and feline emergency and critical care (second edition). Quedgeley, Gloucester: British Small Animal Veterinary Association, 2007; 57-84.