Page 292 - Clinical Small Animal Internal Medicine

260 Section 3 Cardiovascular Disease

Table 26.2 Doses of commonly used cardiac medications in dogs exert benefit by antimyocardial remodeling effects. A ret-
VetBooks.ir Drug Dose rospective study in Dobermans found that time to CHF
(see text for indications)
or SD was significantly prolonged with benazepril treat-
ment, with a 55–64% reduction of risk of those outcomes
compared to no treatment. While the strength of evi-
ACEI
dence is not as strong as that for pimobendan, the author
Benazepril 0.25–0.5 mg/kg q12–24h PO advocates the use of ACEI in preclinical DCM based on
Enalapril 0.25–0.5 mg/kg q12h PO the collective evidence in the human and veterinary lit-
erature, unless there is a specific contraindication to this
Positive inotrope class of drug. Evaluation of renal function one week after
Pimobendan 0.25–0.3 mg/kg q12h PO initiation and periodically thereafter is recommended.
Dobutamine 5–15 μg/kg/min IV CRI While there is good evidence in the human literature
Dopamine 1–5 μg/kg/min IV CRI that beta‐blocker therapy reverses LV remodeling,
improves LV systolic function and patient symptoms,
Diuretic and prolongs life in chronic heart failure, clinical data are
lacking on the use and efficacy of beta‐blockers in canine
Furosemide 2–5 mg/kg q8–12h PO or IV DCM. Concerns with beta‐blocker use typically include
0.5–1 mg/kg/h IV CRI hypotension or CHF due to bradycardia and negative
Spironolactone 2 mg/kg q24h PO inotropy when first administering; therefore, they must
Hydrochlorothiazide 0.5–2 mg/kg q12h PO be used with caution and uptitrated slowly.
Taurine supplementation should be initiated in any
Antiarrhythmic
case suspected or documented to be due to taurine defi-
Sotalol 1–3 mg/kg q12h PO ciency. L‐carnitine can be simultaneously added or initi-
Mexiletine 5–8 mg/kg q8h PO ated after three months if there is inadequate response
Diltiazem 0.5–3 mg/kg q8h PO (for immediate with taurine alone.
release formulation) The patient with clinically significant VA is worthy of
0.05–0.1 mg/kg IV slow bolus separate consideration. In humans, the risk of SD increases
followed by 1–5 μg/kg/min IV CRI with declining systolic function or a history of syncope,
Digoxin 0.003–0.005 mg/kg q12h PO (to max yet there is no clear evidence that any antiarrhythmic
(AA) drug is effective in preventing SD. In Dobermans,
0.25 mg/dog q12hr)
Lidocaine 2 mg/kg IV bolus (max. 4 boluses) increasing LVEDV, presence of VT, and VPCs yielding
instantaneous HR ≥260 bpm are associated with increased
followed by 30–70 μg/kg/min IV CRI risk of SD. There are no studies addressing the efficacy of
AA therapy in canine DCM. AA therapy may be consid-
Beta‐blocker
ered in any DCM patient with frequent VPCs (>1 per
Atenolol 0.25–1.0 mg/kg q12h PO minute) or VA with higher complexity or rate (couplets,
Carvedilol 0.1–0.5 mg/kg q12h PO triplets, or VT with instantaneous HR >180 bpm). Typical
choices for AA therapy include sotalol, a AA with both
Vasodilator
beta‐blockade and K+ channel blockade properties (initi-
Sodium nitroprusside 1–5 μg/kg/min IV CRI ating low doses and titrating upwards is often advised due
+
to the beta‐blockade), mexiletine, a Na channel blocker,
Supplements or a combination of the two.
Taurine 500–1000 mg q12h PO (<25 kg) Monitoring the preclinical patient should include
1000–2000 mg q12h PO (>25 kg) physical examination, echocardiography, and ECG or
L‐Carnitine 50–100 mg/kg q8h PO ideally Holter recording every 4–6 months. If AA ther-
Omega‐3 fatty acids 78 mg eicosapentaenoic acid and 497 mg apy is initiated, it is best to monitor therapeutic efficacy
docosahexaenoic acid per dog per day with Holter monitoring within 1–2 weeks of initiating
therapy. Due to a high degree of daily variability, an in‐
ACEI, angiotensin converting enzyme inhibitor; CRI, constant rate house ECG is an inadequate alternative.
infusion; IV, intravenous; PO, by mouth (per os).

The role of the renin‐angiotensin‐aldosterone system Overt DCM (ACVIM Stage C, CHF): Outpatient
(RAAS) in maladaptive cardiac remodeling and progres- Therapy
sion of systolic dysfunction is well known. In addition to Therapeutic goals in the CHF patient include resolu-
their mixed vasodilatory and natriuretic properties, ACEI tion of clinical signs and improvement in quality of life