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225 Cards in this Set
- Front
- Back
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Why are arrhythmias clinical important?
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Arrhythmias may potentially compromise cardiac output and decrease oxygen delivery to the body tissues, predisposing the patient to sudden cardiac death.
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The level of compromise during an arrhythmia is dependent on what factors?
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Heart Rate
Site of Origin During of arrhythmia Other underlying cardiac and/or systemic disease(s) |
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The management of arrhythmias must consider what 3 main principles?
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Diagnosis of the arrhythmia with EKG
Consideration of possible underlying mechanisms/causes of the arrhythmia AND whether underlying heart disease is present Understand the personal patient goals of the arrhythmia treatment |
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When evaluating an arrhythmia, we need to take a deep breath, step back, and ask ourselves what questions?
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Is the EKG diagnostic?
What is the heart rate? Is there a P wave for every QRS? Is there a QRS for every P wave? What is the observed rhythm? Are there any enlargement patterns or conduction disturbances present? |
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How can we determine if an EKG reading is of diagnostic quality?
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Make sure it is free from artifacts: movement (patient & machine), tremors, breathing, electrical interference
Make sure the machine is calibrated for the paper speed and gain (amount of electricity being used) Make sure the complexes are completely shown on the paper Make sure all leads are shown on the paper |
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What "proportion" allows us to calculate an instantaneous heart rate from an EKG reading?
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At 25mm/sec paper speed, each large box = 0.2 sec
At 50mm/sec paper speed, each large box = 0.1 sec |
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When there are multiple rhythms present on an EKG reading, how is the rate expressed?
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Express the rate of ALL rhythms present
Example: Include both atrial and ventricular rates for AV block |
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When treating arrhythmias, what are the goals of treatment in a patient with clinical signs (including weakness, syncope, collapse, shock)?
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Reduce hemodynamic compromise!
Prevention of sudden cardiac death from hemodynamic compromise caused by the arrhythmia. |
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When treating arrhythmias, what are the goals of treatment in a patient without clinical signs?
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Prevent the arrhythmia from progressing to one which can cause clinical signs and/or sudden cardiac death (aka ventricular arrhythmias)
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Why is it so important for us as clinicians to have a good understanding of the medical therapies & drugs used in arrhythmia treatment?
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Every antiarrhythmic agent has the ptoential to induce further and perhaps more dangerous arrhythmias. So, it is our responsibility to be familiar with the actions and potential side effects of the antiarrhythmic therapies.
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What type of myocardial cells exhibit a fast response action potential?
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Atrial and ventricular muscle cells (working myocardiocytes) and Purkinje fibers (although purkinje cells can exhibit spontaneous depolarization, they fire at a slow rate)
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What type of myocardial cells exhibit slow response action potentials?
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SA node and AV node = modified muscle tissue that can spontaneously depolarize
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Of the "nodes" in the heart, which functions as the natural pace maker? Why?
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SA node functions as the natural pacemaker because its rate of depolarization is slightly faster than the AV node and other slow response action potential cells
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What factors may enhance the rate of spontaneous diastolic depolarization?
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Increasing body temperature (Hyperthermia)
Adrenergic/Sympathetic stimulation Hypoxia |
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What factors may depress the rate of spontaneous diastolic depolarization?
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Cholinergic/Parasympathetic stimulation
Increasing serum K+ concentrations Hypothermia |
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How are the antiarrhythmia agents classified?
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Type of ion channel or receptor the predominantly affect
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Class I and III antiarrhythmia agents work on what type of heart cells?
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Working myocytes (aka atrial & ventricular myocardiocytes)
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Class II and IV antiarrhythmia agents work on what type of heart cells?
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Specialized conduction cells (aka AV and SA node)
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What is the primary mechanism of action of Class I antiarrhythmia agents?
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Sodium channel blockade
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What are 2 of the most commonly used Class IA antiarrhythmia agents?
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QUINIDINE
Procainamide |
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What are 2 of the most commonly used Class IB antiarrhythmia agents?
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LIDOCAINE
Mexiletine |
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What are the indications associated with administration of Quinidine?
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Control and prevention of Ventricular Premature Complexes and Ventricular Tachycardia
Conversion of atrial fibrillation to sinus rhythm in the ABSENCE of myocardial disease |
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What routes of administration are used for Quinidine?
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IV and PO
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What are the toxicities associated with Quinidine?
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WEAK NEGATIVE IONOTROPE
IV ROUTE NOT RECOMMENDED IN DOG -> Development of severe hypotension from peripheral vasodilation Anorexia, vomiting, diarrhea Apparent deafness, ataxia, seizures Pharyngeal edema/dyspnea, laminitis, colic Prolongation of all EKG intervals Drug interaction with digoxin due to highly protein bound nature |
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What contraindications for quinidine therapy exist?
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Complete/3rd Degree AV block
Hypersensitivity 2nd Degree AV block Congestive Heart Failure Digoxin toxicity |
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What are the indications for use of Procainamide?
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Treatment of ventricular arrhythmias
Often used when Lidocaine is ineffective |
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What route(s) of administration are typically used with Procainamide?
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IV
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What toxicities are associated with procainamide?
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Anorexia, vomiting diarrhea
Weakness, hypotension Hypersensitivity |
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What contraindications exist for procainamide therapy?
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Hypersensitivity
Torsades de pointes 3rd or 2nd Degree AV Block Renal disease |
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What are the indications for use of Lidocaine?
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ACUTE termination of ventricular arrhythmia. Greatest effect in damaged myocardial tissue
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What route(s) of administration are used for Lidocaine?
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IV ONLY!!! In ALL species
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What toxicities are associated with Lidocaine?
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Cats more sensitive -> use at 1/10 dose
Nausea, vomiting Ataxia, drowsiness, depression, seizures, muscle tremors |
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What contraindications exist for Lidocaine?
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3rd and 2nd Degree AV block
HEPATIC DISEASE. 90% of lidocaine is metabolized by the liver |
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What indications call for the use of Mexiletine?
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ORAL maintenance of ventricular arrhythmias that initially responded to IV lidocaine...often used in combination with atenolol (II) to suppress life-threatening ventricular arrhythmias
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What toxicities are associated with Mexiletine?
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Nausea, vomiting
Ataxia, drowsiness, depression seizures, muscle tremors |
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What contraindications exist for Mexiletine?
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3rd Degree AV Block
RENAL DISEASE. 80% excreted in urine |
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What is the primary mode of action of Class II antiarrhythmia agents?
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Beta Blockers (Beta adrenergic antagonist)
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What are the general cardiac effects observed with use of Beta Blockers?
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Decrease contractility from potent negative ionotrope activity
Decrease relaxation rate = negative lusitrope Decrease heart rate = negative chronotrope Decrease conduction velocity |
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What are the general vascular effects observed with use of Beta Blockers?
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Smooth muscle contraction, most often observed as mild vasoconstriction and bronchoconstriction
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What are some examples of Non-selective Beta Blockers?
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Carvedilol
Propranolol Sotalol |
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What are some examples of selective beta blockers?
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Atenolol
Metoprolol |
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What are the indicators of use for Propranolol?
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Treatment of supraventricular tachycardia, including ventricular rate control of Atrial Fibrillation
Treatment of specific ventricular arrhythmias, such as Thyrotoxic |
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What toxicities are associated with Propranolol?
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POTENT negative ionotrope
Bronchoconstriction Bradycardia Hypotension Diarrhea |
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What contraindications exist for Propranolol?
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BRONCHIAL ASTHMA!
3rd and 2nd Degree AV block Acute Congestive Heart Failure Pulmonary disorders Hepatic Disease |
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What type of receptor do the specific beta blockers antagonize?
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Adrenoreceptor
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What benefit is there is using a specific versus non specific beta blocker?
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Specific beta blockers have less of an effect in bronchoconstriction and can be used with less concern in patients with pulmonary disease/problems.
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What is the primary mechanism of action for Class III antiarrhythmia agents?
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Lengthening of the action potential duration AND refractory period through blockage of the potassium channels
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Sotalol is listed as a Class III antiarrhythmic, but it contains properties of what other class(es) of antiarrhythmic agents?
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Class II
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What are the indications for use of Sotalol?
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Life threatening ventricular arrhythmias
BOXER DOG TREATMENT WITH ARVC Management of atrial tachyarrythmias |
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What route(s) of administration are used for sotalol?
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NO IV FORMULATION
So, mostly PO |
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What toxicities are associated with Sotalol?
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BRADYCARDIA
HYPOTENSION Proarrhythmogenic in some patients |
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What contraindications exist for Sotalol?
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Caution in animals with Congestive Heart Failure (Negative Ionotrope)
Caution in animals with airways disease (Beta Blocker activity) Chronic Renal Disease Hypotension |
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Amiodarone is listed as a Class III antiarrhythmic agent, but what other class(es) of agents does it share characteristics with?
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I, II AND IV - so, basically everything...
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What is the mode of action of Amiodarone?
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PROLONGS ACTION POTENTIAL (III)
Delays repolarization (III) Increase refractory period of SA/AV node & His-Purkinje system (III) |
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What indications call for the use of Amiodarone?
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LIFE-THREATENING Ventricular Arrhythmias
Management of unresponsive Supraventricular Tachyarrhythmias Chemical cardioversion of atrial fibrillation to sinus rhythm (I) |
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What toxicities are associated with Amiodarone?
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*Think of ALL toxicities for ALL classes*
GI signs Neutropenia Bradycardia Hepatotoxicity Injection site pain, urticaria Hypotension with IV administration |
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What contraindications exist for Amiodarone?
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Sinus bradycardia
Sick sinus syndrome 3rd Degree AV block Hepatic disease |
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What is the primary mode of action of class IV antiarrhythmics?
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Calcium channel blocker to slow conduction through the AV node
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What are the indications for Diltiazem?
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Ventricular rate response control of Atrial Fibrillation
Management of Supraventricular Tachyarrhythmias NOT derived from atrial fib |
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What route(s) of administration are used for Diltiazem?
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IV or PO
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What toxicities are associated with Diltiazem?
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Bradycardia, sinus arrest, 3rd-2nd AV block
Hypotension from peripheral vasodilation Aggravation of CHF from negative ionotropic effects Vomiting/inappetance (cats) |
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What contraindications exist for Diltiazem?
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3rd - 2nd Degree AV block
Sick sinus syndrome Concurrent use of Class II CHF |
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What effects does Digoxin have on myocardiocytes?
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Inhibits Na/K ATPase pump
Enhances vagal tone to AV node Acts as positive ionotrope through increase Ca/Na transport |
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When is Digoxin therapy indicated?
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Ventricular rate control of atrial fib.
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What toxicities are associated with Digoxin?
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Vomiting, diarrhea, anorexia
Development of 2nd - 3rd AV block Development of Ventricular Arrhythmias |
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What contraindications exist for Digoxin?
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3rd - 2nd Degree AV block
Renal disease Hypokalemia (increased risk of toxicity) |
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What are some examples of Anticholinergic agents? What is their 1 overall action on the heart?
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ATROPINE
Glycopyrolate Propantheline bromide Hyoscyamine Increase Heart Rate |
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Through what mechanisms do the anticholinergic agents increase heart rate?
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Increase automaticity of SA node
Improve conductivity through AV node Block vagal tone on AV/SA node |
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When is Atropine indicated for use?
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Treatment of Bradyarrhythmias
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Isoproterenol falls into what class of Drugs? What are its primary characteristics?
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Sympathomimetic!
Non-selective Beta Agonist Indicated for SERIOUS bradycardia |
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What 2 Sympathomimetic drugs are indicated for treatment of Symptomatic Sick Sinus Syndrome and are administered orally?
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Theophylline
Terbutaline |
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TRUE/FALSE: Some normal, old cats have premature atrial & ventricular complexes.
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TRUE! You should still evaluate for systemic hypertension and/or hyperthyroidism even though their "normal"
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AV dissociation and block are common in what age group of cats?
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Older
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Bradycardia in cats is most often associated with what?
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Hypothermia
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Are arrhythmias more hemodynamically significant in dogs or cats?
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DOGS!
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How is heart disease defined?
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Presence of structural or functional abnormality of the heart that, depending on its severity, can lead to heart failure
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How does heart failure manifest hemodynamically?
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Heart fails to pump enough blood to meet tissue needs at normal venous pressures
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What physiologic adaptations does the heart employ during a falling/decreasing cardiac output?
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Increase heart rate & contractility
Vasoconstriction Salt & Water retention Hypertrophy/remodeling of myocardium Cytokine activation --> inflammation |
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How is heart failure classified functionally?
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Class I = Heart disease present WITHOUT clinical signs
Class II = Clinical signs are apparent with strenuous exercise Class III = Clinical signs are apparent with everyday activities Class IV = Clinical signs are present at rest |
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What physical signs correlate with Right heart failure?
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Ascites
Pleural effusion Pericardial effusion - very little Jugular venous distention Hepatojugular reflex |
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What physical signs correlate with left heart failure?
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Pulmonary edema
Pleural effusion (CATS) |
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Heart failure signs can also be designated as "Backward" or "Forward". What clinical signs are consistent with Backward Heart failure/congestion?
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Ascites
Pleural effusion Pulmonary edema |
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Heart failure signs can also be designated as Backward or Forward. What clinical signs are consistent with Forward heart failure/congestion?
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Weakness
Lethargy Syncope Exercise intolerance Pale mucus membranes Poor peripheral pulse quality |
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What are the 2 main goals of Acute Therapy for heart failure? How are these goals achieved?
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Restore comfort at rest!!!! -> Mechanical removal of life-threatening fluid accumulations
Oxygen supplementation Reduce anxiety Reduce work of breathing Hemodynamic Stabilization!!!! --> Assess & optimize: Preload, Afterload, Heart Rate, Rhythm and Contractility |
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What are the goals of Chronic therapy for heart failure?
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Maintain acute hemodynamic gains
Improve quality of life Improve survival Minimize hospitalizations Optimize owner & patient compliance Moderately low salt intake |
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How might one relieve dyspnea from pulmonary edema in a patient with heart failure?
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FIRST: record respiratory rate & monitor every 10 min to ensure therapy
Take radiographs PRUDENTLY Drug therapy to reduce preload Sedate/analgesia with Opioids, Acepromazine Oxygen supplementation |
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What is the mechanism of action of the primary preload-reducing drug used in veterinary cardiology?
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Furosemide! (LASIX) is a POTENT diuretic
Inhibits active CL transport from Loop of Henle Effective even with low GFR/hypoalbuminemia Will activate RAAS is used ALONE |
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What are the relevant pharmacokinetics of Furosemide in Acute preload reduction therapy?
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Onset of action & peak within 30 minutes of IV administration versus 2 hours in PO administration
Acute treatment goal is to relieve symptoms Chronic treatment goal is to maintain patient at lowest effective dose Adverse effects include hypovolemia, hypokalemia and hyponatremia |
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Through what mechanisms might oxygen therapy be delivered to a veterinary patient?
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Flow by
Face mask E-collar canopy Nasal catheter Oxygen cage Mechanical ventilation |
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What are the primary considerations of therapy for Transcutaneous Nitroglycerine ointment?
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Stagger doses to prevent tolerance
Useful for first 24 hours of treatment Indicated in canine AND feline CHF WEAR GLOVES! Applied primarily on abdominal veins/pinna |
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What drugs are useful for sedation of patients with Heart Failure?
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Butorphanol
Buprenorphine Acepromazine - Watch out for vasodilation in cats |
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What are the mechanisms of action of Enalapril? What drug class does it belong in?
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Inhibits synthesis of Angiotensin II
Inhibits degradation of bradykinin to produce vasodilation Prolongs survival time in dogs with DCM & CDVD May prolong survival in cats with FMD Adverse effects include hypotension and acute renal ischemic injury |
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What conditions causing heart failure would indicate afterload reduction therapy?
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CHF due to Mitral Regurgitation or DCM
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What drugs may be used in acute Afterload Reduction therapy? What is their primary mode of action?
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Hydralazine - Direct arteriolar vasodilator
Amlodipine - Vascular Calcium Channel Blocker Na-Nitroprusside |
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What is the Primary drug used to Improve Cardiac Contractility?
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Pimobendan
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What are the Direct Myocardial effects of Pimobendan?
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Sensitize myocardiocytes to calcium -->
Promotes efficient use of existing calcium Increases force of contraction Does NOT increase myocardial energy requirements |
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What are the balanced vasodilation effects of Pimobendan?
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Selective PDE III Inhibitor -->
Dilates arterial vessels & venous vessels Reduces preload AND afterload Improves cardiac function DOESN'T inhibit RAAS |
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Pimobendan is commonly used in combination with what other drugs?
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Enalapril
Furosemide |
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What effect does Dobutamine have on the heart?
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Positive Ionotrope
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How does Digoxin improve cardiac contractility?
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NEUROHORMONAL modulation
Decreases ventricular response to atrial fibrillation |
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The therapeutic goal of acute Atrial Fibrillation therapy is to slow the ventricular response rate. What drugs accomplish this task?
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Digoxin
Diltiazem Beta blocker |
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What drugs are indicated in the acute treatment of Ventricular Tachyarrhythmias?
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Lidocaine
Sotalol |
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What treatments are indicated for control of Bradyarrhythmias?
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Vagolytic drugs = Atropine, Propantheline
Beta 2 adrenergic receptor agonist = Methylxanthines Pacemaker |
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Why and when would ventilatory support be indicated for a patient with heart failure?
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Indicated in cases of refractory pulmonary edema --> If respiratory rate is not falling within 2 hours of start of therapy despite optimal care
Acts to relieve work of breathing & anxiety |
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What type of medical therapy in added in cases of Chronic CHF therapy?
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Additional diuretics, including Spironolactone +/- hydrochlorothiazide
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What are the benefits of Spironolactone in terms of Chronic CHF therapy?
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Acts as a competitive antagonist to Aldosterone
Potassium sparing diuretic |
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What are the pharmacodynamics of hydrochlorothiazide in relation to Chronic CHF therapy?
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Primarily acts in distal convoluted tubules
Impair sodium resorption Can result in profound electrolyte abnormalities when used WITH furosemide |
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What kind of harmful effects can chronic adrenergic stimulation have in patients with CHF?
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Norepinephrine induced cardiac toxicity/cardiac necrosis
Beta-1 receptor down regulation reduce myocardial response to increased sympathetic activity Loss of contractile force Stimulation of tachycardia & arrhythmias |
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When and how would you use beta blockers for treatment of Chronic CHF?
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Use after stabilization of Heart Failure in dogs with DCM or CDVD
Start very slow & titrate up dose over few months |
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What are the 5 clinical categories of Pulmonary Hypertension?
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1. Pulmonary Arterial Hypertension
2. PH with left heart disease 3. PH due to intrinsic lung disease 4. PH due to thrombotic or embolic disease 5. PH due to miscellaneous disorders |
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What is the most common condition lead to PH in veterinary patients?
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PH with Left heart disease = Pulmonary VENOUS hypertension
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Severe pulmonary hypertension can be a reflection of what vascular effects?
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Increase Pulmonary artery vasomotor tone and/or Pulmonary vascular remodeling
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What are the 2 most common diseases that lead to pulmonary hypertension from left heart disease?
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Mitral valve disease
DCM |
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What are the 3 primary mechanisms from which inadequate oxygenation of systemic arterial blood occurs in disorders of the lungs/hypoxemia?
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Intrinsic lung Disease (Collapsing trachea)
Impaired control of breathing (Diaphragm trauma) Residence at high altitude (Brisket Edema) |
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What hypercoagulable conditions might lead to thrombotic or embolic disease & pulmonary hypertension?
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Heartworm disease
Neoplasia DIC Hyperadrenocorticism IMHA PLN Surgery Sepsis Amyloidosis Pancreatitis (Cats) |
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What would be a typical signalment for a patient with Pulmonary Hypertension?
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Older, small-breed dog.
Essentially, it would be the same signalment for a dog with chronic degenerative mitral valve disease/airway disease |
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What are the chief complaints associated with pulmonary hypertension?
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Cough
Dyspnea Tachypnea Wheezin Exercise intolerance Syncope |
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What physical exam findings would you expect in a patient with Pulmonary Hypertension?
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Left apical systolic murmur (associated with CDVD)
Right apical systolic murmur (especially in chronic cases) Split S2 sounds (difference in closure times between aortic & pulmonic valves) Tachypnea Crackles Jugular venous distention |
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What radiographic findings might you expect in a patient with pulmonary hypertension?
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Noted enlargement of the pulmonary arteries
Potential for fluid opacity interstitial pattern in lung |
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What non-invasive test allows for the estimation of right heart & pulmonary arterial pressures in patients with PH?
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Echocardiography!
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What are the designations of degree of Pulmonary Hypertension based on?
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Mild - Systolic Pulmonary arterial pressure between 30-55mmHg
Moderate - systolic PA pressure between 56-79mmHg Severe - systolic PA pressure 80+mmHg |
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What is the primary mechanism of action for vasodilator therapy for pulmonary hypertension?
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Phosphodiesterase V inhibitor --> reduced cGMP degradation to increase vasodilation activity in lung tissue
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What is the basic, overarching goal in Pulmonary Hypertension therapy?
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Treat the underlying disease!!!
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What is the pathogenesis of the generation of vascular lesions in cases of heartworm disease?
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Inflammatory arteritis from antigenic stimulation of heartworms leads to a reduction in the arterial lumen and a corresponding increase in vascular resistance.
Thromboembolism is common in worm-ridden arteries, especially following adulticide therapy (in cats). |
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What pathophysiologic effectis might you expect from a "heart"worm infection?
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Villous myointimal proliferation leads to vasoconstriction & endothelial damage.
Vasoconstriction & endothelial damage incites inflammation, thrombosis, vasoconstriction, and pulmonary hypertension |
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What is caval syndrome in heartworm disease?
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Progression of heartworm disease where the worms have proliferated into the right heart and are spanning through the tricuspid valve.
Clinical signs include hemolytic anemia, hemoglobinuria, ascites and Pulmonary Hypertension |
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Why does Right heart failure develop as a consequence to heartworm disease?
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Right heart strain due to chronic pulmonary hypertension (from obstruction of worms) can lead to RHF
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Why might glomerulonephritis be a sequelae to heartworm disease?
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Deposition of antibody-antigen complexes in the kidney
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What clinical signs might you expect to see in a patient with heartworm disease?
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*Could be asymptomatic*
Weight loss Cough/hemoptysis/Tachypnea Exercise intolerance/syncope Ascites |
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What physical exam findings might you expect in a patient with heartworm disease?
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Increased adventitious lung sounds
Split S2 heart sounds (only 13%) Gallop sounds Murmur from tricuspid insufficiency (only 13%) Fever & hemoptysis |
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What diagnostic blood tests can you perform to confirm a heartworm infection?
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Antigen ELISA test
Microfilaria test (direct observation of microfilaria on blood smear) Knotts or Filter test |
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What conditions might lead to a false negative heartworm test?
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Prepatent infection
Low worm burden Immature female infection All male infection Kit not properly prepared (warmed) |
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Why should all animals with suspected heartworm disease be radiographically evaluated? What radiographic changes might you expect?
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Changes observed on thoracic radiographs are the best predictor of complications due to adulticide administration/treatment.
Pulmonary artery enlargement (especially cranial & caudal lobar arteries?) |
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What indications call for an echo in cases of heartworm disease?
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Suspicion of caval syndrome
Right heart failure (echo will tell us why) Murmur (echo will tell us why/where) Transesophageal echo Assists in adult worm extraction via direct visualization |
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What factors might influence the probability of post-adulticide complications?
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Extent of pulmonary vascular disease
Severity of infection Activity level of patient |
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What is the general adulticide therapy plan for a patient with Heartworm disease?
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Treat with Macrolide at preventative dosage (continue throughout treatment?)
Wait for 3 months Immiticide administration CAGE REST for 1 MONTH!!! Repeat Immiticide treatment (2 doses) CAGE REST for 1 MONTH!!! |
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What are the treatment goals for massive pulmonary thromboembolism due to post-adulticide heartworm treatment?
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HOSPITALIZE!
Supplement oxygen Give prednisone +/- Heparin therapy +/- Bronchodilator +/- Vasodilator |
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What heartworm condition requires surgery for treatment?
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Caval syndrome
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The Macrolide preventative for heartworm is prescribed to do what?
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Prevent further infection
Eliminate microfilariae Destroy developing L4 larvae |
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Why should you give the first dose of a macrolide heartworm preventative in a patient older than 6 months in a hospital setting?
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Potential for adverse reactions including:
Lethargy Inappetance Salivation Retching Hypotension/Tachycardia/Collapse |
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If a heartworm positive patient is contraindicated for arsenical treatment, what options are available for alternative treatments?
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Long-term ivermectin/macrolide treatment --> reduces worm lifespan & will eventually kill worms...over 2+ years.
Ivermectin/Doxycycline therapy to disrupt Wolbachia & kill worms |
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When would we want to perform a HW antigen test?
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If patient has never received prophylaxis
If there has been an extended break in preventative administration If a product switch occurs |
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What are the primary characteristics associated with HW infection in cats?
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More resistant to infection than dogs
Typically low number of adult worms Circulating microfilariae are SELDOM found (only persist ~30days) Aberrant migration is common |
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There are 2 main stages of heartworm disease in cats that commonly present with clinical signs. What stages are these and what are their clinical signs?
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(1) Arrival of immature heartworms in pulmonary vasculature.
Clinical signs include: Asthma --> wheezing, coughing, exercise intolerance, HARD (2) Death of adult worms. Clinical signs include: Pulmonary inflammation, Fatal & acute lung injury. |
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How is A definitive diagnosis of heartworm disease in cats performed?
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Echocardiogram & visualization of worms
Positive antigen test |
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TRUE/FALSE: Definitive diagnosis of a patent heartworm infection in cats is indicative of adulticide therapy.
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FALSE! Adulticide therapy is NOT recommended in cats.
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What is the main treatment modality for cats with HW disease?
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Administration of prednisolone
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TRUE/FALSE: Strictly indoor cats are still at risk for development of heartworm disease and should be placed on a monthly preventative.
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TRUE!
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What is the most common heart disease that affects canine veterinary patients?
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Chronic Degenerative Valvular Disease
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What are the 6 anatomical components of a normal mitral valve?
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Valve leaflets
Annulus fibrosus Chordae tendineae Papillary muscles Left atrium (Posterior wall) Left Ventricular muscle |
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What is the etiopathogenesis of CDVD/Mitral valve disease?
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UNKNOWN!
STERILE, degenerative disease that bears NO RELATIONSHIP to endocarditis nor is a sequelae to prior infection or a consequence of poor dental health |
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What breeds are predisposed to developing Mitral Valve Disease/CDVD?
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Cavalier King Charles Spaniel!!!
Dachshunds |
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What 2 factors determine the severity & volume of mitral valve regurgitation in CDVD?
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Regurgitant orifice area (ROA)
Left ventricular to left atrial pressure gradient |
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TRUE/FALSE: Mitral regurgitation imposes a pressure load on the left atrium and left ventricule and results in cardiac enlargement.
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FALSE! Mitral regurgitation results in a VOLUME overload of the left heart and results in cardiomegaly.
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How can cardiac enlargement cause coughing in a patient?
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Mainstem bronchial compression from increased heart size
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How does pulmonary edema develop as a result of MR/CDVD?
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An increase in Pressure in the left atrium (increased pressure to increase ejection of blood into left ventricle) leads to an increase in pulmonary venous pressures.
As venous pressure rise, fluid in the pulmonary capillaries is extruded into the tissues, producing pulmonary edema. |
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Acute pulmonary edema in MR is usually due to what?
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Rupture of the chordae tenindeae and corresponding acute increase in left atrial pressure
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Signs of Low cardiac output in MR is usually due to what? What are these clinical signs?
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Endocardial splitting (from jet lesions?) that occurs in the left atrium, progressing to perforation.
Syncope Weakness Collapse Pale mucus membranes Poor femoral arterial pulse quality |
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What are the stages for diagnosis & treatment of CDVD?
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Stage A = high risk with No known injury and No known clinical signs
Stage B = Structural injury with no clinical signs Stage C = Structural injury with Current or Past clinical signs Stage D = Structural Injury with Refractory signs |
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What is a typical signalment for a dog with CDVD?
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SMALL BREED DOGS!
Age is typically older (>10 years)...unless it's a Cavalier King Charles Spaniel |
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What physical exam findings might you expect in a patient with CDVD?
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Systolic murmur over LEFT APEX associated with mitral regurgitation
Gallop sounds (associated with severe cardiomegaly & CHF) Tachycardia |
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What diagnostics should you run in a patient with Stage A CDVD?
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yearly physical exam
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What diagnostics should you run in a patient with Stage B1 CDVD?
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Thoracic rads & blood pressure
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What diagnostics should you run in a patient with Stage B2 CDVD?
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Thoracic rads, blood pressure, +/- Echocardiogram
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What diagnostics should you run in a patient with Stage C or D CDVD?
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Thoracic rads, blood pressure, Echocardiogram is NOT RESPONSIVE to treatment OR thoracic rads are ambiguous.
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At what stage of CDVD do most cardiologists recommend ACE inhibitor treatment (ACE-I and beta blocker in large breeds)?
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Stage B2
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What therapy is indicated for a patient with Stage C or D CDVD?
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Diuretic to reduce preload --> Furosemide
ACE-Inhibitor to reduce preload AND afterload Positive ionotrope and afterload reducer --> Pimobendan Decrease in heart rate if atrial fib present --> Digoxin +/- Diltiazem |
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What clinical presentation of Body condition, Heart rate, Rhythm, and Cardiac murmur would you expect in a patient with cardiac disease? With Respiratory disease?
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Cardiac Disease:
Body condition = Thin Heart Rate = Rapid Rhythm = Regular (+/- arrhythmia) Murmur = Loud Respiratory Disease: Body Condition = Obese Heart Rate = Normal - slow Rhythm = Exaggerated sinus arrhythmia Murmur = Soft |
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Define endocarditis.
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Inflammation of the endocardial surface of the heart
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Define Infective Endocarditis?
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Microbial infection of the endocardial surface
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Define Vegetative endocarditis.
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Structures (vegetations) composed of platelets, fibrin, microbes, and inflammatory cells adhere to heart valves, septal defects, chordae tendineae, or the mural endocardium
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What is the epidemiology associated with endocarditis (and its various forms) in veterinary patients?
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Uncommon in dogs. RARE in cats
Large breed > Small Breed Males > Female Left-sided valves (Aortic & mitral) more commonly affected Geographic predisposition |
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What predisposing factors might lead to Endocarditis?
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Congenital aortic valve disease
Steroid use Any chronic bacteremia IV catheters Interventional cardiac catheterization Cardiovascular implants Immunosuppression/illness |
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What clinical signs might you expect in a patient with Endocarditis?
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FEVER!!!
Lethargy Anorexia Polyarthritis Back Pain Urinary signs Neurologic signs |
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What cardiovascular effects might you expect to find during physical examination of a patient with Endocarditis?
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Diastolic murmur (Aortic valve)
Increased arterial pulse pressure "New" murmur Change in old murmur Heart failure signs Syncope |
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What are the general principles of Endocarditis treatment?
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Killing infective organisms
Treat complications Provide long term A/B therapy |
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Why is endocarditis a difficult disease to cure?
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Poor penetration of A/B
Altered metabolic state of bacteria within lesion make susceptibility hard to predict Absence of adequate host-defense response makes clearance difficult |
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What is the prognosis for Infective Endocarditis?
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Extremely poor - median survival time of 2 months
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What are the main principles in prevention of infectious endocarditis?
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Prevent persistent bacteremia in an animal with a predisposition (anatomic)
Appropriate A/B selection for type of infection that may gain entry into systemic circulation |
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TRUE/FALSE: Pericardial disease is a common disease in dogs and cats.
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FALSE! It is relatively uncommon in dogs and of even lesser importance in cats.
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Why is diagnosis of pericardial disease causing right heart failure in the dog important?
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Because it's curable!!!
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What are the components of the parietal pericardium?
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Outer, fibrous pericardium
Inner, serosal layer |
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What is another name for the inner, serosal layer of the parietal pericardium?
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Visceral pericardium
Epicardium |
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What are the 2 classifications of Pericardial disease and what diseases can be found in each classification?
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Congenital Pericardial Disease:
Peritoneal Pericardial Diaphragmatic Hernia Absence Intrapericardial cysts Acquired Pericardial Disease: PERICARDIAL EFFUSION Pericardial Constriction |
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What are the 2 main etiologies for Pericardial effusion?
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Neoplasia = >50%
Idiopathic |
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What neoplasias are associated with Pericardial Effusion?
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HEMANGIOSARCOMA
Chemodectoma Mesothelioma Ectopic Thyroid carcinoma |
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What factors influence the effects of Pericardial effusion on cardiac function?
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Volume of effusate
Compliance characteristics of pericardium |
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What is cardiac tamponade?
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A syndrome of impaired ventricular filling due to the presence of intrapericardial fluid resulting in a continuum of hemodynamic abnormalities
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Clinical signs associated with cardiac tamponade are related to what cardiac conditions?
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Low cardiac output
Elevated venous pressure |
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Is a change in pressure due to pericardial effusion going to be evident in the left or right ventricle first?
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Right ventricle --> naturally lower filling pressures than left ventricle.
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TRUE/FALSE: Venous pressures that result in systemic congestion are lower than venous pressures that result in pulmonary congestion.
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TRUE!
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What is a typical signalment for a patient with pericardial effusion?
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Large breed dogs, especially German Shepherds and Retrievers
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What clinical signs would you expect to see in a patient with Pericardial effusion?
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Abdominal distention - Ascites
Weakness/syncope Lethargy Inappetance +/- Circulatory collapse |
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Upon physical examination, a dog with what cardiovascular signs would be highly indicative of cardiac tamponade?
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Tachycardia
Quiet/Muffled heart sounds Ascites/Jugular distention Hypokinetic arterial pulse Pulsus paradoxus (decrease in strength of arterial pulse ass'd with respiration) |
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What radiographic findings are typical for a patient with pericardial effusion?
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Enlargement of cardiac silhouette
Lack of contour to cardiac silhouette Pulmonary vessels often small Edema is UNCOMMON |
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What results would you expect from an EKG in a patient with Pericardial Effusion?
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Sinus tachycardia
+/- QRS alternans (change in amplitude of R wave) Small QRS complexes |
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What is the most sensitive AND specific test for diagnosis of pericardial effusion?
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Echocardiography!
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What is the appropriate initial therapy for cardiac tamponade?
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Pericardiocentesis
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Why are diuretics NOT indicated for treatment of pericardial effusion?
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Diuretics reduce venous pressure and have no effect on reducing fluid volume in the pericardium (and other anatomic "spaces"). Diuretic treatment will likely only further limit ventricular filling by decreasing blood volume/end-diastolic volume
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How can you Cure Pericardial effusion?
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In cases of IDIOPATHIC PE, a subtotal pericardiectomy can be curative!
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Pericardial effusion of neoplastic derivation is treated how?
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Chemotherapy
Subtotal pericardiectomy for chemodectomas may be palliative |
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What is THE most common form of acquired heart disease in the cat?
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Myocardial disease
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What are the various types of myocardial diseases cats may acquire?
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HCM
RCM DCM ARVC Unclassified Thyrotoxic heart disease Hypertensive heart disease |
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What is the clinical definition of the most common primary heart disease in cats?
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Hypertrophic Cardiomyopathy = Hypertrophy of a non-dilated ventricle in the absence of outflow obstruction, hyperthyroidism, or any other disease process
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TRUE/FALSE: Genetics likely play a role in feline HCM.
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TRUE!
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Is HCM characterized by systolic or diastolic function? Why?
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Diastolic!
Diastolic function is the ability of the ventricles to fill without an inordinate increase in pressure. This function depends on Myocardial Relaxation Compliance. In HCM, this Relaxation Compliance is lost. |
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How are BOTH low Cardiac Output signs AND congestive signs manifested in cases of myocardial disease?
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Diastolic dysfunction leads to both an increase in the ventricular pressure and a decrease in the end-diastolic volume. The increase in pressure causes congestive signs. The decrease in diastolic volume causes low cardiac output.
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What is SAM?
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Systolic Anterior Motion of the Mitral Valve = The mitral valve leaflets fling back up into the atrium during systole.
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What is the pathophysiology associated with SAM?
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Cranial displacement of the mitral valve leaflets leads to obstruction of the left ventricular outflow tract and subsequent formation of a subvalvular pressure gradient.
Mitral valve regurgitation almost always accompanies SAM too! |
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What is the most likely signalment for a cat with HCM?
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Male cat > 6 years old.
BUT any cat can develop HCM. |
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What is a typical clinical presentation for Feline Myocardial Disease?
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Incidentally detected murmur/gallop rhythm
OR Signs associated with CHF, systemic thromboembolism, SCD |
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When diagnosing murmurs in cats, what is important to remember?
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Innocent and/or flow murmurs that are usually soft with varying intensity are NORMAL in healthy cats.
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TRUE/FALSE: A gallop rhythm is almost always indicative of clinically important heart disease.
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TRUE!
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What Radiographic findings are typical with Feline Myocardial Disease?
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Varying degrees of cardiomegaly
+/- Pulmonary edema Pleural effusion +/- ascites |
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TRUE/FALSE: Cats with cardiac disease typically present with a cough.
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FALSE!!!!
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When is preload reduction treatment indicated in cats? What therapies might be utilized?
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Indicated with pulmonary edema/pleural effusion is present.
Diuretic therapy with furosemide. Thoracocentesis when appropriate (respiratory distress from pleural effusion) |
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What are the 2 main modes of action in Diastolic Dysfunction therapy? What drugs can achieve these goals?
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Slow heart rate -> Beta Blocker
Speed myocardial relaxation -> Calcium Channel blocker |
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What drugs are typically used in therapy of Chronic CHF due to HCM in cats?
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Furosemide
+/- Enalapril |
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What is the clinical definition of Restrictive Cardiomyopathy?
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Atrial dilation with normal or nearly normal ventricular dimensions and wall thicknesses as well as normal to nearly normal systolic ventricular performance.
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What is ARVC
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Arrhythmogenic Right Ventricular Cardiomyopathy. Fatty or fibrofatty replacement of the right and sometimes left ventricular myocardium with corresponding arrhythmias.
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Administration of what endogenous and exogenous anti-inflammatory is associated with the development of heart failure in cats?
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Corticosteroids
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What diagnostic tests should you run in cases of feline subclinical heart disease?
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T4 - if patient is > 7 years old
Echocardiography +/- Thoracic radiographs |
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ALL patients with myocardial disease are predisposed to development of what condition?
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Intra-atrial/cardiac thrombi -->
FATE = Feline Arterial Thromboembolism. |
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What clinical signs might be observed in a case of FATE?
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Pain
Paresis/Paralysis of hind limbs Absent arterial pulses (femoral) |
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What is the only plausible therapy recommended for FATE?
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Analgesia.
Clot-busting drugs are $$$ and may or may not be efficacious/safe |
