Page 284 - Feline Cardiology

Chapter 19: Congestive Heart Failure 291

right atrial dilation places heart failure high on the dif- an oxygen cage is not available and the cat is placed in
ferential list, and diuretic therapy can be started. an enclosure with supplemental oxygen, it is important
Medical treatment of acute heart failure includes to use a high oxygen flow rate to flush out the carbon
aggressive diuretic therapy with furosemide, oxygen sup- dioxide, as well as ice packs to cool the environment.
plementation, and possibly transdermal nitroglycerin Inhaled oxygen concentration should be decreased to
(see Table 19.1). Ideally, an intravenous catheter is placed 50% or less within 12 hours to avoid barotrauma induced
for repeated intravenous injections of furosemide, and by high fractional inspired oxygen.
can be done with as minimal restraint and stress as pos- Once the respiratory rate decreases to less than 50
sible, with a prepared oxygen cage ready to immediately breaths/minute and respiratory effort improves, the
place the cat into for rest and recovery after the injection. dose and frequency of furosemide may be decreased
However, if the cat is too unstable, 3–4 mg/kg furosemide (∼2 mg/kg IV q 6–8 hrs). Thoracic radiographs may be
can be given intramuscularly, and the cat placed in obtained 24 to 36 hours after acute diuresis to assess the
oxygen (at 50–60% fractional inspired oxygen) tempo- presence and severity of pulmonary edema, and help
rarily, until it is able to withstand gentle restraint for tailor continued heart failure treatment and transition
placement of an intravenous catheter. Initial furosemide to chronic oral dosing of furosemide. Some cardiologists
doses range from 2 to 4 mg/kg IV every 1 to 4 hours, feel that the patient’s clinical progression (improvement
depending on the cat’s response. Typically, an improve- of clinical signs) is sufficient information for making
ment in respiratory effort is expected within 4 hours such treatment decisions and do not obtain repeat
after the first injection of furosemide. If improvement radiographs at this time. Renal panels may be monitored
occurs within the first hour, as is common when conges- every 12 to 24 hours during the acute phase of treat-
tive heart failure was iatrogenic and/or mild, then the ment, to monitor for progressive electrolyte depletion Congestive Heart Failure
next dose of furosemide may be given only at 2 or 4 hours and severity of azotemia. Blood samples for measuring
after the first. However, if the cat continues to be severely electrolyte levels should be collected in a green top tube
dyspneic 1 hour after the first injection of furosemide, (lithium heparin). This is because a red top (plain) tube
then the second dose of furosemide may be given just 1 allows platelet activation/clumping, which releases
hour after the first. Hourly doses are sometimes neces- potassium and can mask clinically important hypokale-
sary in the worst cases, but if dyspnea worsens or remains mia. Potassium infusion (0.05–0.5 mEq/kg/hr IV) can be
severe after 2–3 hourly doses of furosemide, then the given for treatment of severe hypokalemia (K < 3 mEq/l),
diagnosis of heart failure may be questioned (is it actu- and frequent reevaluations of serum potassium concen-
ally primary respiratory disease causing dyspnea?), or tration are necessary. Oral potassium gluconate (2–4 mEq
the cat has acute, fulminant heart failure requiring addi- PO q 12 hr) may be used in cats with moderate hypoka-
tional therapy potentially with a constant rate infusion lemia that can tolerate oral medications. Hypokalemia
of furosemide, for more sustained diuretic effect, and often dramatically improves once the cat is discharged
possibly nitroprusside if it is not hypotensive and in a on lower dose oral furosemide for chronic heart failure
critical care setting with an experienced clinician. Acute therapy. Once the cat is stable and has normal to mildly
diuresis occurs 5 minutes after intravenous injection, increased respiratory rate or effort, the furosemide can
with a peak effect after 30 minutes, which lasts 2 to 3 be transitioned to oral administration (6.25–12.5 mg PO
hours. Venodilation is an acute ancillary effect of furose- q 12 hr). Concurrent use of intravenous fluids and
mide occurring 5 to 15 minutes after intravenous injec- administration of a diuretic to “protect the kidneys” by
tion, and is independent from the diuretic effect. Free minimizing the degree of dehydration and azotemia is
choice of water and encouragement of drinking is neces- counterproductive and ineffective, because each treat-
sary, since dehydration is very common and expected. ment negates the other.
Pulmonary edema causes hypoxemia because oxygen Nitrates such as nitroglycerin or sodium nitroprusside
cannot diffuse from the alveoli to the pulmonary capil- are vasodilators that function by increasing nitric oxide
laries. Increasing the inspired oxygen concentration production. Nitric oxide binds to guanylate cyclase,
increases the pressure gradient of oxygen to diffuse into which forms cyclic GMP from GTP. Cyclic GMP activates
the pulmonary capillary bed, which increases the arterial protein kinases that phosphorylate myosin light chains
oxygen tension. The percent inspired oxygen concentra- and cause smooth muscle relaxation and vasodilation.
tion is increased from room air (21%) to 40–60%. An Transdermal nitroglycerin causes systemic venodilation,
oxygen cage is the safest and most effective means to whereas intravenous nitroglycerin is a potent venodilator
supplement oxygen. The oxygen cage not only controls and arteriolar dilator. Although nitroglycerin has not
the percent of inspired oxygen, but it also regulates tem- been studied in cats, it is commonly given to cats with
perature and humidity, and removes carbon dioxide. If heart failure based on extrapolations from human