Download 60 Cardiovascular Formulary for the Hypertensive

Cardiovascular Formulary for the Hypertensive Cat
Drug
Trade Name*
Formulation(s)**
Dosage
Use
Amlodipine
Norvasc
1.25 mg tablets
.625 PO qd-bid
Antihypertensive
Diltiazem
Cardizem
30 mg tablets
7.5 mg PO tid
Lusitrope, Vasodilator,
Negative chronotrope
Diltiazem - LA
Dilacor XR
180, 240 mg caps.
30 mg PO bid
same
Cardizem CD
180, 240 mg caps.
45 mg PO qd
same
Enalapril
Enacard (Vasotec)
1, 2.5, & 5 mg tablets
.5 mg/kg PO qd
ACE-I (CHF, Hypertension)
Benazepril
Lotensin (Foretkor)
5 & 10 mg tablets
.25-.5 mg/kg PO qd-bid
same
Atenolol
Tenormin
25 mg tablets
6.25-12.5 mg PO qd
Negative chronotrope,
Antiarrhythmic, Lusitrope, Antihypertensive
Nitroglycerin
Nitrol, Nitro-Bid
2% ointment
1/8–¼ inch topically tid
for 24 hours
Venodilator (CHF)
LMW Heparin
Fragmin
Aspirin
2500 U/.2 ml
100 U/kg SQ qd
Anticoagulant
81 mg
40-80 mg q72h
Anticoagulant
FELINE HYPERTROPHIC
C A R D I O M YO PAT H Y
Clarke E. Atkins, DVM, Diplomate ACVIM (Internal Medicine & Cardiology)
Department of Clinical Sciences, College of Veterinary
Medicine
North Carolina State University, Raleigh NC, USA
[email protected]
Etiology and Pathophysiology
Hypertrophic cardiomyopathy (HC/HCM) is the most
prevalent feline cardiac disorder. It affects most commonly middle-aged cats (average 6.5 years), but
all ages are affected. There is a male predisposition
(>75%). In humans, there is an important hereditary
predisposition for HCM in 55% of cases. In people, this
disorder may be congenital or acquired, and probably
represents a group of diseases. Although the etiology
of feline HCM is unknown, the Persian and Maine coon
cat have appeared to be predisposed in some case series, suggesting a genetic influence. A case-controlled
study in our laboratory, which showed a trend toward
a predisposition for Maine coon cats, was validated
by work of Meurs, et al. which has shown that HCM in
Maine coon cats and Ragdolls is heritable as an autosomal dominant trait.
Cardiac lesions are typified by severe left ventricular
concentric hypertrophy and secondary left atrial dilatation. Asymmetric septal hypertrophy (ASH), present in
the majority of dogs and humans with HC, is present in
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only 30% of cats with HC. Histological cardiac myofiber
disarray is reported in 27% of affected cats and only in
those with asymmetric septal hypertrophy. Other histological features of feline HC include myocardial and
endocardial fibrosis and narrowed coronary arteries.
Dynamic aortic outflow obstruction, secondary mitral
insufficiency, myocardial ischemia, and systemic arterial embolism (SAE) may complicate this syndrome.
The left heart is predominately affected and clinical
signs manifested as sudden death or, more commonly,
acute left heart failure due to diastolic dysfunction. Pleural effusion is occasionally associated with HC. Systolic
function is usually adequate or enhanced but may decline with myocardial infarction. Tilley and Lord demonstrated an elevated resting left ventricular end diastolic
pressure (LVEDP) in feline HC. With the administration
of isoproterenol, mimicking endogenous, stress-related
sympathoadrenal activity, the LVEDP pressure doubled.
Left ventricular end diastolic pressure is indicative of
pressures in the left atrium and pulmonary veins, which
reflect the tendency for the development of pulmonary
edema. In addition, during stressful situations, acceleration of the heart rate reduces cardiac filling time and
myocardial perfusion. The former further diminishes
cardiac volume and the latter results in relative myocardial ischemia in a rapidly beating heart with high oxygen needs, thereby, aggravating diastolic dysfunction.
Stressful incidents, such as a car ride, restraint for an
ECG, confrontation with a dog, or an embolic event may
precipitate in left heart failure and pulmonary edema.
Abstracts European Veterinary Conference Voorjaarsdagen 2009
Diagnosis
Diagnosis of HC is not difficult, but does require special
testing to confirm clinical suspicions. Without the aid of
echocardiography, dilated and restrictive (RC) cardiomyopathies can be difficult to distinguish from HC
The ECG is abnormal in 35 to 70% of cases and can provide useful diagnostic information. Many ECG findings
are not specific, but left axis deviation and left anterior
fascicular block are strongly suggestive of HC, but also
may be recognized in RC, hyperkalemia, hyperthyroidism, hypertension and, rarely, DC. Other ECG abnormalities include P-mitrale and P-pulmonale (10% and 20%,
respectively), tall R waves (40%), wide QRS complexes
(35%), conduction disturbances (50%, including left
axis deviation in 25% and left anterior fascicular block
in 15%), and arrhythmias (55%, usually ventricular in
origin).
Thoracic radiographic findings suggestive of HC include cardiomegaly with a prominent left ventricle
and atrium, and pulmonary congestion and/or edema.
In the ventrodorsal projection, the heart may appear
“valentine-shaped,” reflecting the concentric ventricular hypertrophy and enlarged left auricle. Additionally,
the apex is often shifted to the right. On the lateral view,
the heart is enlarged with increased sternal contact,
left atrial prominence, left ventricular convexity, and a
prominent caudal cardiac waist. Pleural effusion may be
noted in 25 to 33% of cases in heart failure, but is usually of much less volume than that noted in DC. Nonselective angiography is of less risk in HC than in DC. This
procedure typically reveals normal or enhanced circulation, pulmonary venous tortuosity, left atrial enlargement, small left ventricular lumen, thickening of the left
Abstracts European Veterinary Conference Voorjaarsdagen 2009
ventricular wall, and papillary muscle enlargement. The
diagnosis of SAE (usually located at the aortic trifuracton: saddle thrombus) can be confirmed by the finding
of an abrupt termination of the dye column in the aorta
at its trifurcation.
Echocardiography is extremely useful for distinguishing HC from DC, but, because of overlap of echocardiographic reference values, differentiation of normal from
asymptomatic HC and HC from RC may be difficult.
Concentric left ventricular hypertrophy and left atrial
enlargement are features useful in confirming the diagnosis of HC. Cardiac function is normal to exaggerated,
due to diminished afterload and possibly hypercontractility. Systolic anterior mitral valve motion may be evident, suggesting dynamic aortic outflow obstruction. If
present, ASH, left atrial thrombi, pleural effusion, and/
or pericardial effusion may be evident.
Therapy
The treatment of HCM is different than that of DCM
(systolic myocardial failure) and entails the goals of reducing LVEDP, abolishing sinus tachycardia and other
arrhythmias, improving myocardial oxygenation, and
alleviating and preventing pulmonary edema. Positive
inotropic agents are not needed and generally contraindicated because they may increase LVEDP and aggravate outflow obstruction. The latter precaution should
be exercised in the use of arterial vasodilators and, to
a lesser degree, preload reducing agents (diuretics and
mixed or venodilators).
Diuretic therapy is indicated to eliminate pulmonary
edema. Furosemide is the diuretic of choice in emergencies because it reduces LVEDP and, hence, left atrial,
and pulmonary venous pressures through diuresis and
venodilation. In the emergency situation, treatment
with parenteral furosemide (2-4 mg/kg IV or IM) is accompanied by the use of topical nitroglycerin (1/8-1/4
inch tid-qid for first 24 hours, then “8 hours on, 8 off”
only if necessary) and oxygen supplementation (40%).
Although furosemide diuresis is usually successful, the
addition of enalapril (.25-.5 mg/kg sid) is indicated in
refractory cases or when biventricular failure (pleural
effusion) ensues. It should be kept in mind that drugs
which reduce preload (and afterload) may worsen outflow obstruction in hypertrophic obstructive cardiomyopathy (HOCM).
Drugs that enhance ventricular relaxation and slow the
heart include the beta adrenergic (atenolol), and calcium channel (diltiazem) blockers. Such therapy is indicated in treatment of the diastolic failure of HCM. Beta
blockers improve diastolic performance only indirectly,
enhancing ventricular filling by reducing heart rate and
improving myocardial perfusion. Traditionally, betablockers have been administered orally after stabilization (24 to 36 hours after institution of diuretic therapy)
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CARDIOLOGY
Clinical Signs
With the aid of ECG, thoracic radiographs, and echocardiography, a high percentage of cases of HC are diagnosed prior to the onset of symptomatology. Suspicion
is raised in such instances when the attending clinician
discovers a murmur, gallop, or arrhythmia. At the other
end of the spectrum, cats may die unexpectedly with
no prior signs. The most common clinical sign is the
sudden onset of dyspnea, with or without evidence
of SAE (the prevalence of which has ranged from 16
to 48%, in clinical and autopsy studies, respectively).
Physical examination typically reveals a well-fleshed,
dyspneic cat with audible pulmonary crackles, murmur
(50% of cases) typically loudest at the left apex, gallop (40%, usually S4), and/or arrhythmia (25 to 40% of
cases). Heart sounds may be muffled. The oral mucosa
is ashen, the pulses normal, weak, or absent (SAE), the
apex beat may be hyperdynamic, and the liver may
rarely be palpably enlarged. Cats with HC are generally
not hypothermic, providing information useful in differentiation from DC.
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to reduce and prevent elevations in LVEDP, to lower
systolic pressure gradients and myocardial oxygen requirements, to prevent stress-induced tachycardia and
reduce resting heart rate, and for its antiarrhythmic effects. When arrhythmias are present, this drug may be
initiated earlier in the disease course. This is the author’s
treatment of choice for asymptomatic HCM, for cats
with documented outflow obstruction (HOCM), and
when tachycardia persists.
Calcium channel blocking agents have been effective in
human HCM by reducing heart rate, myocardial oxygen
consumption, and diastolic dysfunction. In addition to
directly enhancing myocardial relaxation, these drugs
dilate peripheral and coronary arteries. Bright has demonstrated the utility of diltiazem (3-7.5 mg po tid) in the
treatment feline HCM, including those cases refractory
to the beta-blocker, propranolol. Unfortunately, current
packaging for human use, makes accurate feline dosing
of diltiazem difficult. Long-acting diltiazem may be substituted and includes Cardizem CD (45 PO sid; requires
disassembling capsules) or Dilacor (30 mg PO bid; requires disassembling capsules). Combining a calcium
channel blocker and a beta blocker has theoretical advantages and is often done, using a long-acting form of
each drug, one in the morning and one in the evening.
There is no role for amlodipine in the normotensive cat
with HCM as it has no theoretical or proven benefit and
it may precipitate hypotension.
A report by Rush, et al. demonstrated a reduction in wall
thickness with the administration of enalapril to cats
with HCM. This suggests a potential role for ACE-inhibitors in the treatment of HCM. These drugs are generally safe and do play a role in cases which are refractory
or in which pleural effusion is present. In asymptomatic patients, it is logical that the renin-angiotensinaldosterone system is not pathologically activated, and
hence ACE-inhibitors might not be useful. Recent data
from McDonald and colleagues, using an ACE-Inhibitor
in asymptomatic Maine Coon Cats and followed them
for one year, failed to show benefits in regression of hypertophy, improvement in diastolic function or onset of
CHF. While this does not prove “ineffectiveness” of this
drug class in HCM, it does not produce confidence of
their use. When used, at NCSU, we employ enalapril at
.5 mg/kg daily.
Other therapies, including oxygen, aspirin or low molecular weight heparin, home confinement, and moderate salt restriction should be instituted as needed. Taurine supplementation is not indicated in the treatment
of HCM. In asymptomatic cats with HCM, the author
advises home confinement, moderate salt restriction,
Beta- and/or calcium channel blockade, and aspirin indefinitely.
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Patient Monitoring
Cats with asymptomatic HCM should be evaluated at
12 month intervals, while those with symptoms should
ideally be seen more frequently until stabilized for a
period of time. The prognosis for asymptomatic HCM is
guarded to good, with a median survival of over 5 years.
Cats presented in heart failure survive a median of approximately 18 months, while cats with emboli carry a
much poorer prognosis.
Abstracts European Veterinary Conference Voorjaarsdagen 2009
Cardiovascular Formulary for Cats
Drug
Trade Name*
Formulation(s)**
Dosage
Use
Amlodipine
Norvasc
1.25 mg tablets
.625 PO qd-bid
Antihypertensive
Diltiazem
Cardizem
30 mg tablets
7.5 mg PO tid
Lusitrope, Vasodilator,
Negative chronotrope
Diltiazem - LA
Dilacor XR
180, 240 mg caps.
30 mg PO bid
same
Cardizem CD
180, 240 mg caps.
45 mg PO qd
same
Enalapril
Enacard (Vasotec)
1, 2.5, & 5 mg tablets
.5 mg/kg PO qd
ACE-I (CHF, Hypertension)
Benazepril
Lotensin (Foretkor)
5 & 10 mg tablets
.25-.5 mg/kg PO qd-bid
same
Atenolol
Tenormin
25 mg tablets
6.25-12.5 mg PO qd
Negative chronotrope,
Antiarrhythmic, Lusitrope, Antihypertensive
Esmolol
Brevibloc
10 & 250 mg/ml injectable
50-500 (100 usually) ug/
kg IV
same
Sotalol
Betapace
80 mg tablet
2 mg/kg PO bid
Antiarrhythmic
Procainamide
Pronestyl, Procan SR
250 mg tablets
100 mg/ml inject.
2-5 mg/kg PO bid-tid
Antiarrhythmic
Furosemide
Lasix
12.5 mg tablets
50 mg/ml inject.
1-4 mg/kg PO bid-q48h;
Diuretic
.5-2 mg/kg SQ, IM, IV PRN
Nitroglycerin
Nitrol, Nitro-Bid
2% ointment
1/8–¼ inch topically tid
for 24 hours
Warfarin
Coumadin
Heparin
LMW Heparin
Fragmin
Aspirin
Digoxin
Taurine
Lanoxin
Venodilator (CHF)
1, 2, 2.5, 4 mg tabs.
.1-.2 mg QD
Anticoagulant
Multiple
250-300 U/kg SQ tid
Anticoagulant
2500 U/.2 ml
100 U/kg SQ qd
Anticoagulant
81 mg
40-8080 mg q72h
Anticoagulant
.05 mg/ml elixir
.125 mg tablets
.007 mg/kg PO q48h
(check serum [digoxin])
Positive inotrope, Negative chronotrope (CHF,
SVT)
250 mg tablets
250 mg PO qd
Taurine deficiency
*Selected name brands; some available as generic. **Most appropriate formulations for cats – other sizes available for many drug
S YS T E M I C A R T E R I A L E M B O L I S M I N C AT S
Clarke E. Atkins, DVM, Diplomate ACVIM (Internal Medicine & Cardiology)
Department of Clinical Sciences, College of Veterinary
Medicine
North Carolina State University, Raleigh NC, USA
[email protected]
cyanotic foot pads or nail beds, the latter not bleeding
upon quicking. If SAE is partial, a pulse (weak or even
normal unilaterally) may be detected, carrying a better
prognosis. If the attending clinician cannot ascertain
with certainty whether SAE is present, Doppler technology (Doppler diagnostic ultrasound or blood pressure
monitoring equipment) or non-selective angiography
may be used to confirm the diagnosis.
Physical Examination & Diagnosis
SAE is typically associated with an acute or peracute
presentation, usually with rear limb paralysis/paresis.
Classical findings include posterior limb pain, lack of
pulse, gradual (over days) hardening of the gastrocnemius and quadriceps muscles, lack of pulse and pale/
When SAE affects alternative sites, the signs may range
from sudden death (coronary or cerebral arteries or
proximal aorta) to an acute abdomen (aorta at level of
kidneys or mesenteric arteries) or to front leg lameness.
When affected, the kidneys can be isolated and are firm
and quite painful to palpation. Often (approximately
Abstracts European Veterinary Conference Voorjaarsdagen 2009
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CARDIOLOGY
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