Page 89 - Small Animal Internal Medicine, 6th Edition

CHAPTER 3 Management of Heart Failure 61

have not yet developed signs of CHF (see Chapter 6). oxygen consumption; cage confinement is preferred. Envi-
However, evidence is lacking regarding the use of pimoben- ronmental stresses such as excess heat and humidity or
VetBooks.ir dan in dogs with early (stage B1) mitral valve disease, and it extreme cold should be avoided. When transported, the
animal should be placed on a cart or carried. Unnecessary
is not currently recommended at this stage. An ACEI gener-
ally is not advocated for dogs with preclinical mitral valve
avoided, when possible.
disease, unless it is used to reduce elevated blood pressure. patient handling and use of oral medications should be
However, some controversy remains, and although ACEIs do
not appear to delay onset of CHF in most dogs with mitral SUPPLEMENTAL OXYGEN
valve disease, some dogs with advanced stage B2 disease Oxygen administered by face mask or improvised hood,
might benefit from them. Doberman Pinschers, Irish Wolf- nasal catheter, endotracheal tube, or oxygen cage is beneficial
hounds, and probably other dogs with occult DCM also as long as the method chosen does not increase the patient’s
benefit from the introduction of pimobendan and an ACEI distress. An oxygen cage with temperature and humidity
before overt CHF develops (see Chapter 7). For cats with controls is preferred; a setting of 65° F is recommended for
preclinical (stage B) hypertrophic cardiomyopathy (HCM), normothermic animals. Oxygen flow of 6 to 10 L/min is
optimal strategy is not clear and consensus is lacking (see usually adequate. Concentrations of 50% to 100% oxygen
Chapter 8). may be necessary initially, but this should be reduced within
a few hours to 40% to avoid lung injury. When a nasal tube
MANAGEMENT OF MILD OR EARLY is used, humidified O 2 is delivered at a rate of 50 to 100 mL/
CHF SIGNS kg/min. Extremely severe pulmonary edema with respira-
Mild pulmonary edema can produce subtle and variable tory failure may respond to endotracheal or tracheotomy
clinical signs, including modest but persistent increases in tube placement, airway suctioning, and mechanical ventila-
resting respiratory rate (RRR; see later in this chapter), tion. Positive end-expiratory pressure helps clear small
reduced exercise tolerance, excessive panting (in dogs), or airways and expands alveoli. Positive airway pressures can
occasional cough. Detecting mild changes in RRR is easier adversely affect hemodynamics, however, and extended use
when owners know the animal’s baseline rate and periodi- of high oxygen concentrations (>70%) can injure lung tissue
cally have been monitoring the RRR. Thoracic radiographs (see Suggested Readings for more information). Continuous
are indicated when signs suggestive of decompensating CHF monitoring is essential for intubated animals.
appear, especially if this is the first episode. When radio-
graphic findings are consistent with mild cardiogenic pul- DRUG THERAPY
monary edema, initial therapy for CHF (furosemide, an Diuresis
ACEI, and pimobendan, if indicated), along with exercise Rapid diuresis can be achieved with intravenous (IV) furo-
restriction, often can be instituted on an outpatient basis. If semide; effects begin within 5 minutes, peak by 30 minutes,
the radiographs are nondiagnostic, but CHF is suspected, a and last about 2 hours. This route also provides a mild veno-
furosemide trial (such as 2 mg/kg/day) with or without an dilating effect. Some patients require aggressive initial doses
ACEI can be given for a week or so, with RRR monitoring. or cumulative doses administered at frequent intervals (see
If the clinical signs are caused by CHF, they usually resolve Box 3.1). Furosemide can be given by constant rate infusion
or substantially improve fairly quickly; in these cases addi- (CRI), which may provide greater diuresis than bolus injec-
tional CHF therapy, as indicated for the underlying disease, tion. The veterinary formulation (50 mg/mL) can be diluted
is added. An NT-proBNP test also can help in unclear cases, to 10 mg/mL for CRI using 5% dextrose in water (D 5 W),
in that if the result is not elevated, the patient is unlikely to lactated Ringer’s solution (LRS), or sterile water. Dilution to
have CHF. 5 mg/mL in D 5 W or sterile water also is described. The
patient’s respiratory rate, as well as other parameters (dis-
cussed in more detail later), guides the intensity of continued
TREATMENT FOR ACUTE CONGESTIVE furosemide therapy. Once diuresis has begun and respiration
HEART FAILURE improves, the dosage is reduced to prevent excessive volume
contraction or electrolyte depletion.
GENERAL CONSIDERATIONS
Fulminant CHF is characterized by severe cardiogenic pul- Vasodilation
monary edema, with or without pleural and/or abdominal Vasodilator drugs can reduce pulmonary edema by increas-
effusions or poor cardiac output. It can occur in stage C or ing systemic venous capacitance, lowering pulmonary
D patients. Therapy is aimed at rapidly clearing pulmonary venous pressure, and reducing systemic arterial resistance.
edema, improving oxygenation, and optimizing cardiac Although ACE inhibitors are a mainstay of chronic CHF
output (Box 3.1). Thoracocentesis should be performed management, more immediate afterload reduction usually is
expediently if marked pleural effusion exists. Likewise, large- desirable for animals with acute pulmonary edema. The
volume ascites should be drained, at least partially, to improve initial dose of an arteriolar vasodilator should be low, with
ventilation. Animals with severe CHF are greatly stressed. subsequent titration upward as needed on the basis of blood
Physical activity must be maximally restricted to reduce total pressure and clinical response. Arteriolar vasodilation is not