Cardiovascular Flashcards
Papers 2015-2019 JVIM, VCNA, JFMS,JVECC
What drugs are used for rate control of Afib?
Beta- blockers (class II)
- Atenolol
- Esmolol
K+ channel blocker (class III)
- Sotolol
- Amiodarone
Ca++ Channel blockers Class IV)
- Diltiazem
And digoxin
VCNA 2017. AFib Pariaut
What options are used for rhythm control of Afib?
Electric cardioversion
Lignocaine Na++ channel blocker ( class 1b) Amiodarone k+ channel blocker (class III)
VCNA 2017. AFib Pariaut
What are the causes of Afib?
Structural heart disease Lone AFib (giant and large breed dogs, structural normal heart with erratic rhythm with significant exercise +/- GA) High vagal tone (shortens the refractory period) Hypothyroidism Anaesthesia/opiates Rapid, large vol pericardial effusion GI disease Vol overload causing atrial stretch
VCNA 2017. AFib Pariaut + ettinger
Diltiazem mechanism of action?
Class IV antiarrhythmic; calcium-channel blocker (like verapamil or nifedipine).
- Inhibits the transmembrane influx of extracellular calcium ions in myocardial cells and vascular smooth muscle but does not alter serum calcium concentrations.
=> inhibit the cardiac and vascular smooth muscle contractility, thereby dilating main systemic and coronary arteries.
=> Decreased Total peripheral resistance, blood pressure, and cardiac afterload - Effects on cardiac conduction.
- slows AV node conduction
- prolongs refractory times.
Diltiazem rarely affects SA node conduction, but in patients with sick sinus syndrome (contraindicated) resting heart rates may be reduced.
Although diltiazem can cause negative inotropic effects, it is rarely of clinical importance (unlike verapamil or nifedipine). Diltiazem apparently does not affect plasma renin, aldosterone, glucose, or insulin concentrations.
Reduction in ventricular response rate is dose dependant.
Risk of hypotension
Plumbs
Sotolol : What is the mechanism of action?
- Non-selective beta-blocker
- Class III antiarrhythmic agent - potassium channel blocker:
selectively inhibiting potassium channels => prolongs repolarization and refractoriness without affecting conduction.
In supraventricular tachycardias, sotalol may be more effective in preventing recurrence of the arrhythmia rather than terminating it.
Plumbs
Where does an AV block originate from?
Conduction abnormalities along the AV nodes, bundle of His/Purkinje system or both.
Santilli JVIM 2016
What are the causes of AV nodal conduction abnormalities in dogs?
- Chronic fibrous or fibrous-fatty replacement of av bundles and branches
- Acute lymphoplasmacytic myocarditis (young dogs - Lev’s disease) with mild fatty-fibrous replacement
- infectious disease (Borrelia burgdorferi, bartonella vinsonii, bacterial endocardititis, parasitic - Trichinella spiraliz
- Immune med disease (MG, SLE)
- Neoplasia
- non-penetrating chest trauma
Santilli JVIM 2016
What proportion of dogs with AV nodal conduction disturbances had unchanged or progressed AV blocks after pacemaker implantation?
87%
Santilli JVIM 2016
In what dogs with AV conduction disturbances should pacemaker be considered the first line treatment?
High second degree AV block
Third degree AV block
2:1 second degree AV block
Santilli JVIM 2016
What proportion of dogs with AV noda conduction disturbances showed regression after pacemaker implantation?
What proportion of these returned to a normal sinus rhythm
13%
67%
consider acute lymphocytic myocarditis as a possible cause for these?
Santilli JVIM 2016
What drug is most effective at reducing progression to CHF or sudden death in Irish Wolfhounds with preclinical DCM, Afib or both?
Pimobendan > digoxin > benazepril
Vollmar JVIM 2016
What is the median time to CHF or sudden death in Irish Wolfhounds with preclinical DCM, Afib or both treated with:
- Pimobendan?
- Digoxin?
- Benazepril?
P: 1991 days (65m or ~5.5years)
D: 1263 days (41m or ~ 3.4 years)
B: 997 days (32m or ~ 2.6 years)
Vollmar JVIM 2016
Is there any evidence for starting pimobendan in preclinical DCM in Irish Wolfhounds?
Yes - Vollmar JVIM 2016 found improved survival and significantly longer to sudden death or CHF in wolfhounds receiving pimobendan preclinical DCM and/or Afib
Vollmar JVIM 2016
For every 10 bpm increase in HR with dogs with Afib, what is the risk of all cause mortality increased by?
35%
Pedro JVIM 2018
What is the median survival time of dogs with AFib and a mean heart rate (measured by Holter)
- <125 bpm
- > 125bpm
<125 bpm = 1037 days
>125 bpm = 105 days
Pedro JVIM 2018
What is a benefit of Holter monitoring of Afib over ECG?
Holter monitoring allows ambulatory montiroing outsite the hospital setting, more accurately representing the dogs normal daily HR flucutations in its usual routine/environment.
ECG tents to over-estimate mean HR compared to Holter recordings in dogs with AFib
Pedro JVIM 2018
What Heart rate target should be aimed for with Holter readings in dogs with Afib?
<125 bpm
Pedro JVIM 2018
What are the options and aims for control of AFib?
Rhythm control: abolish the arrhythmia and restore sinus function:
- Electrical cardioversion
- Lignocaine
- Amiodarone
Rate control: - slow ventricular rate to reduce clinical signs and minimize deteriorationg of ventricular function
- Atenolol
- Esmolol
- Sotolol (mild)
- Diltazem
- Digoxin (mild)
VCNA 2017. AFib Pariaut
What does lignocaine do?
Lidocaine may also have benefit in dogs to terminate supraventricular tachycardia in the presence or absence of an accessory pathway and paroxysmal atrial fibrillation initiated by elevated vagal tone in large breed dogs with normal cardiac function
Class IB antiarrhythmic agent (membrane-stabilizing).
- combines with inactive fast sodium channels, => inhibits recovery after repolarization.
rapid rates of attachment and dissociation to sodium channels in ventricular conducting tissue more so than atrial tissue.
At therapeutic levels, lidocaine causes phase 4 diastolic depolarization attenuation, decreased automaticity, and either a decrease or no change in membrane responsiveness and excitability. These effects will occur at serum levels that will not inhibit the automaticity of the SA node, and will have little effect on AV node conduction or His-Purkinje conduction.
Plumbs
What is the mechanism of action of Atenolol?
What are the effects of Atenolol?
Relatively specific β1-blocker. At higher dosages,β2 blockade can occur.
Effects:
- no intrinsic sympathomimetic activity or membrane-stabilizing activity
- Negative inotropic and chronotropic actions =>
- decreased sinus heart rate,
- slowed AV conduction,
- decreased cardiac output at rest and during exercise,
- decreased myocardial oxygen demand,
- decreased blood pressure,
- inhibition of isoproterenol-induced tachycardia
Plumbs
What is the mechanism of action of Esmolol?
What effects does this drug have?
Class II antiarrhythmic drug.
Short acting beta1-adrenergic receptor blocker
- antiarrhythmic effect is thought to be due to its blockade of adrenergic stimulation of cardiac pacemaker potentials
- no intrinsic sympathomimetic activity or membrane-stabilizing activity
Cardiovascular effects include:
- negative inotropic and chronotropic activity
=> reduced myocardial oxygen demand.
- reduced systolic and diastolic blood pressures
- increases sinus cycle length,
- slows AV node conduction,
- prolongs sinus node recovery time.
Plumbs
What is the mechanism of action of Amiodarone?
Class III
- potassium channel blocker
- also blocks sodium and calcium channels and beta-adrenergic receptors.
Causes:
- prolongation of myocardial cell action-potential duration and refractory period.
Plumbs
What is the mechanism of action of Digoxin?
Suspected:
- increase the availability of Ca++ to myocardial fibers and to inhibit Na+-K+-ATPase with resultant increased intracellular Na+ and reduced K+
This leads to:
- decreased conduction velocity through the atrioventricular (AV) node
- prolonged effective refractory period (ERP).
+/- increase the PR interval, decrease the QT interval, and ST segment depression on ECG.
Plumbs
What are the effects of digoxin?
In patients with a failing heart includes:
- increased myocardial contractility (inotropism) with increased cardiac output;
- increased diuresis with reduction of edema secondary to a decrease in sympathetic tone;
- reduction in heart size, heart rate, blood volume, and pulmonary and venous pressures; and (usually) no net change in myocardial oxygen demand.