Cardio. DCM ARVC Flashcards
Pimobendan
MoA:
Other names:
-PDEIII inhibitor = inhibits degradation of cAMP = within myocytes:
increased cAMP = increased PKA = PKA (protein kinase A) phosphorylates:
- L-type Ca++ channels - > Ca++ influx
- increased Ca++ = increases SR release RyR
- deactivate phospholamban (allow SERCA to work) .:. enhances uptake in SR
- sensitized TN-C to Ca++
phospholamban in dephosphorylated state blocks SERCA
-PDEIII inhibitor = inhibits degradation of cAMP = within vascular smooth m = increased cAMP = decreased MLCK (myosin light chain kinase, which helps smooth m vasoconstrict/contract) = vasodilate
hence inodilator
Amrinone
milrinon
levosimendan
Cardiac glycoside:
Name:
MoA
MoA of hypoxia and how is this different from cardiac glycosides:
Digoxin
- inhibits Na/K ATPase pump
- increased Na intracellular = increase Na/Ca exhanger (3:1), increased intracellular Ca
hypoxia also decreases activity of Na/K ATPase exchanged but also ATPase dependant pumps within myocyte
positive inotrope - has very weak inotropic properties and has been largely supplanted by pimobendan
Dobutamine:
potent nonselective β agonist (with greater effect on β1 receptors) that is administered as a CRI
nonselective β stimulation, the positive inotropic effects come with some degree of peripheral vasodilation, so blood pressure must be monitored
DCM Age of onset in the Portuguese Water Dog
young are affected (2 to 32 weeks old)
Breeds DCM
Doberman Pinscher, Great Dane, Irish Wolfhound, and American Cocker Spaniel in North American
Europe: Airedale Terrier, Newfoundland, English
Cocker Spaniel, and Doberman Pinscher.
Peritoneal or pleural effusion:
modified transudate (nucleated cell count <2500/ml, total protein <4 g/dl)
Echo findings list 5:
- reduced left ventricular FS% and ejection fraction
- increased E-point septal separation with ventricular dilation
- Doppler studies evidence of mitral and tricuspid regurgitation
- low-velocity transaortic flow
- diastolic ventricular dysfunction, and possible pul-
monary hypertension (as a result of severe left-sided heart failure)
Is low FS pathognomonic?
No, many normal hearts contract apical-to-basilar direction, and this motion is not accounted for by
the FS%
most DCM cases with CHF should have moderate to severe atrial enlargement, and low FS% is not
pathognomonic for DCM
Treatments acute:
-Minimize stress, oxygen supplementation
-furosemide 2 to 6 mg/kg IV, then 1 to 2 mg/kg q2-3h as needed for resolution of pulmonary edema, then q8-12h for the first 3 days.
-Administer 2% topical nitroglycerin: 1 to 2 inches q8h.
-Treat life-threatening arrhythmias
-Sodium nitroprusside: 2.0 μg/kg/min. If mean BP remains higher than 70 mm Hg, increase incrementally to 4 μg/kg/min until patient is stabilized or mean pressure falls below 70 mm Hg - extremely effective with
furosemide in managing pulmonary edema
-Dobutamine (if severe heart failure or cardiogenic shock; ECG monitoring needed) increase by 2.5 μg/kg/min until heart rate increases excessively (>180 beats/min or >10% rise from baseline); maximum infusion rate 15 μg/kg/min
-ventricular ectopy develops, reduce rate.
-pimo
DCM chronic
Furosemide is given at 1 to 4 mg/kg PO q8-24h, spironolactone at 1 to 2 mg/kg PO q12h, with or without hydrochlorothiazide 2 to 4 mg/kg PO q12h
-spironolactone-hydrochlorothiazide (Aldactazide) at 1 mg/kg PO q24h in refractory cases
Angiotensin-Converting Enzyme Inhibitors initiated early in
Digoxin
Pimobendan
Diet/suppliments
Digoxin MoA in DCM
administered to improve systolic function and to slow
ventricular rate in animals with supraventricular tachyarrhythmias
(0.003 mg/kg PO q12h, adjusting dosage based on blood levels)
-blocks Na/K ATPase - incease Na/Ca++ exchanger 3:1
Pimo in DCM
- drug class:
- what study supports use in DCM in Dobies and when:
benzimidazole-pyridazinone
mainstay in the treatment of patients with DCH CHF
-PROTECT Study - administration of pimobendan to Doberman Pinschers with preclinical DCM prolongs the time to onset of clinical signs and extends survival
-pimobendan should be used earlier (preclinical phase) in Doberman Pinschers
DCM in some Cocker Spaniels is associated with ___
- low plasma taurine
- supplementation with taurine and l-carnitine appears to improve myocardial function
Dobermans and DCM
molecular deficiency in ____
______% Doberman Pinschers have ventricular arrhythmias without the classic ventricular dilation seen with DCM
present for:
most successful treatment consists of:
Why is holter imperative:
DCM more likely to develop if holter reveals:
calstabin-2 implicates this cytoskeletal protein abnormality as one of possible causes of DCM in this breed
25% to 30%
syncope or for arrhythmias noted on routine physical examinations
-sudden death is of great concern in this breed, and successful treatment of
sotalol alone or in combination with mexiletine
identify the causative arrhythmia (occasionally syncope caused by bradycardia in
this breed - recall Boxer paper)
> 50 ventricular premature complexes (VPCs) per 24 hours or with couplets or triplets
Atrial fibrillation common
Dalmation
Great Dane and Wolf Hound
fed a low-protein diet for prevention or treatment of urate stones that develop signs DCM
atrial fibrillation is the most common finding and in some cases develops before any other evidence of underlying myocardial disease - X-linked pattern of inheritance is suspected in some families of Great Danes
