Cardiovascular Flashcards

1
Q

The primary pathways by which the cardiovascular system can increase or decrease the
cardiac output include:

A
  • Changes in heart rate
  • Adjustments in myocardial contractility
  • Optimization of vascular size
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2
Q

The physiological control is via
1. __________ sensors
2. _______ and ______ nervous system
3. ____-______-_______ system

The drugs often provide their effect via _______ or ________ these systems

A

The physiological control is via
1. Pressure sensors
2. Sympathetic and parasympathetic nervous system (SNS and PSNS)
3. Renin-angiotensin-aldosterone system (RAAS)
The drugs often provide their effect via stimulating or blunting these systems

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3
Q

The ANS regulates the cardiovascular system by adjusting:
* Heart rate –> ______ receptor
* Vascular volume –> ______ in vasculature
* Myocardial __________

A

The ANS regulates the cardiovascular system by adjusting:
* Heart rate –> Beta 1
* Vascular volume –> alpha in vasculature
* Myocardial contractility

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4
Q

The intrinsic heart rate is determined via _________ of both arms of the ______

A

The intrinsic heart rate is determined via blockade of both arms of the ANS

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5
Q

When an animal is at rest, the ______ system is likely dominant
→ The resting heart rate is ______ than the intrinsic heart rate

A

When an animal is at rest, the PSNS is likely dominant
→ The resting heart rate is lower than the intrinsic heart rate

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6
Q

Patients with heart failure often have higher ________ heart rates → ____ is likely dominant over the _____

A

Patients with heart failure often have higher resting heart rates → SNS is likely dominant over the PSNS

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7
Q

The sympathetic stimulation of cardiac muscle ________ the force of contraction

A

The sympathetic stimulation of cardiac muscle ↑ the force of contraction

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8
Q

A change in contractile strength that is independent of muscle _________ is referred to as a change in _________ or _________

A

A change in contractile strength that is independent of muscle length is referred to as a change in contractility or inotropy

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9
Q

In the presence of inotropic stimulation by the SNS, cardiac output is _________ over
the basal state

A

In the presence of inotropic stimulation by the SNS, cardiac output is enhanced over
the basal state

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10
Q

Parasympathetic nerves exert the effects on cardiac output by ________ heart rate
and with that _____ ventricular filling time

A

Parasympathetic nerves exert the effects on cardiac output by slowing heart rate
and with that ↑ ventricular filling time

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11
Q

Cardiac output: ________ of blood pumped each ________ by ____ ventricle

A

Cardiac output: volume of blood pumped each minute by one ventricle

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12
Q

List the organizations involved in classifying cardiac disease in dogs.

A
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13
Q
A

Comparing classes between institutions is pretty similar.
Recognize organizations and their classification. Associated clinical symptom of patient with stages, you can be more sure of the treatment to use.

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14
Q

What plant is pictured below?

A

Digitalis purpurea

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15
Q

Digoxin is derived from?

A

Derived from the purple foxglove plant (Digitalis purpurea)

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16
Q

In patients with failing heart, digitalis glycosides cause:

  • It increases myocardial ________ (________)
  • Increased cardiac _______
  • Increased ______ with reduction of ______ secondary to a _______ in sympathetic tone
  • _________ in heart rate
  • No change in the myocardial _______ consumption
A

Digitalis glycosides: Digoxin
* It increases myocardial contractility (inotropism)
* Increased cardiac output
* Increased diuresis with reduction of edema secondary to a decrease in sympathetic tone
* Reduction in heart rate
* No change in the myocardial oxygen consumption

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17
Q

What is the MOA of digoxin?

A

Inhibition of Na+, K+-ATPase (sodium pump) in the cardiac myocytes
* The Na+, K+-ATPase is the cellular receptor for digitalis glycosides
* The ability of the pump to transport K+ inward and Na+ outward fails
* Increased Na+ intracellular augments transmembrane exchange of intracellular Na+ for extracellular Ca++ → increased intracellular Ca++

Increased Ca++ is stored in the sarcoplasmic reticulum
→ increases amount of Ca++ released by each action potential

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18
Q
A

Normally K+ comes in and Na+ out.

Digoxin: K+ won’t come inside the cell. Na+ will be more inside –> allow exchange with Ca ++.

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19
Q

Digoxin increases contractility in both _______ and ______ myocardium, but ouput of the ______ heart increases minimally

A

Digoxin increases contractility in both normal and failing myocardium, but output of the normal heart increases minimally

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20
Q

Digoxin also _______ increases ______ vagal tone (________ _________ effect) and decreases ________ nervous activity

A

Digoxin also indirectly increases efferent vagal tone (cholinergic parasympathomimetic effect) and decreases sympathetic nervous activity

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21
Q

Digoxin possesses negative _________ characteristics resulting from ________ stimulation

A

Digoxin possesses negative chronotropic characteristics resulting from parasympathetic stimulation

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22
Q

Digoxin is well absorbed after ______ administration → ______ > _______

A

Digoxin is well absorbed after oral administration → Elixir > tablets

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23
Q

The drug Digoxin is distributed _______ throughout the body

A

The drug Digoxin is distributed widely throughout the body

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24
Q

What is the most important route of elimination for Digoxin?

A

Urinary excretion is the most important route of elimination

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25
Digitalis glycosides and their biotransformation products can follow the ____________ cycle
enterohepatic
26
* Digoxin is sufficiently absorbed by the oral route. The parenteral administration rarely used * Digoxin is indicated in congestive heart failure → 0.005 - 0.02 mg/Kg q 12, dogs * Supraventricular tachyarrhythmias → 0.0025 - 0.004 mg/Kg q 12, cats * Dilated cardiomyopathy (DCM) → 0.005 - 0.008 mg/Kg q 12, dogs; 0.003 - 0.004 mg/Kg q 12, cats
dont study numbers
27
List the clinical signs of Digitalis toxicity.
28
In dogs, Digoxin concentrations from 0.8 to 2.4 ng/ml have been considered ___________, whereas serum drug concentrations (SDCs) greater than 2.5-3 ng/ml are associated with increased probability of _______
In dogs, Digoxin concentrations from 0.8 to 2.4 ng/ml have been considered therapeutic, whereas serum drug concentrations (SDCs) greater than 2.5-3 ng/ml are associated with increased probability of toxicosis
29
Dobutamine and dopamine are ____________ agents.
Sympathomimetic
30
Dobutamine * It produces improvement in cardiac performance by binding ____ myocardial receptors. Through second messengers → increase ______cellular ________ * Dobutamine has a weak action on ____-receptors * It has a very _______ half-life (1-2 min) → usually administered by ? * The major indication → short term _____ in dogs and cats with _____ myocardial failure emergency * Doses: 2.5 to 20 mcg/Kg/min in dogs; 0.5-5 mcg/Kg/min in cats
Dobutamine * It produces improvement in cardiac performance by binding β1 myocardial receptors. Through second messengers → increase intracellular calcium * Dobutamine has a weak action on α-receptors * It has a very short half-life (1-2 min) → usually administered by constant-rate infusion (CRI) * The major indication → short term inotropic in dogs and cats with acute myocardial failure emergency * Doses: 2.5 to 20 mcg/Kg/min in dogs; 0.5-5 mcg/Kg/min in cats
31
Dopamine * It has wide spectrum of effects. At intermediates dosages dopamine has positive effects on cardiac ________, heart ____, and cardiac _____ → 2 to 10 mcg/Kg/min * Dopamine can only be administered ___ with a ____ * At low doses causes _______ * Activates ___ and ____ receptors * Effects are always in sync with _____ used
Dopamine * It has wide spectrum of effects. At intermediates dosages dopamine has positive effects on cardiac contractility, heart rate, and cardiac output → 2 to 10 mcg/Kg/min * Dopamine can only be administered IV with a CRI * At low doses causes vasodilation * Activates beta and alpha receptors * Effects are always in sync with amount used
32
___________ (Vetmedin®) Agents that have both _________ and ______ ionotropic properties * Pimobendan is an agent useful in the clinical management of canine heart failure caused by _____. Data on the use of pimobendan in _____ are limited
Pimobendan (Vetmedin®) Agents that have both vasodilatory and positive inotropic properties * Pimobendan is an agent useful in the clinical management of canine heart failure caused by DCM. Data on the use of pimobendan in cats are limited
33
What is the MOA of Pimobendan?
* Pimobendan increases the myocardial contractility by increasing affinity for Ca++ * It inhibits phosphodiesterase III (PDE III)→ responsible for vasodilating properties
34
Pimobendan Pharmacokinetics * The absorption is rapid after _____ administration * Pimobendan is metabolized to an active metabolite → potent inhibitor of ____ ____ * It is excreted into ___, and eliminated in the _____
Pimobendan Pharmacokinetics * The absorption is rapid after oral administration * Pimobendan is metabolized to an active metabolite → potent inhibitor of PDE III * It is excreted into bile, and eliminated in the feces
35
What are the adverse effects of Pimobendan?
* Pimobendan is well tolerated in dogs * At accidental overdosing, adverse signs are modest in severity * The primary adverse effect are GI effects →reduced appetite, diarrhea
36
As for all positive inotropic agents, pimobendan is contraindicated in patients with ?
outflow tract obstruction
37
Cytokines have been shown to depress ?
myocardial contractility
38
Elevated levels of circulating cytokines have been reported in patients with?
heart failure
39
List some examples of cytokines that are reported in patients with heart failure.
e.g. * Tumor necrosis factor (TNF-α) * Interleukin (IL-1β) * Interleukin (IL-6)
40
The production of TNF-α, IL-1β, and IL-6 in the heart tissue was reduced significantly by?
pimobendan
41
Pimobendan can only be given orally. This study showed how can we administerr it rectally. Consdering that if you are facing a patient that is in cirticaly stage and can be difficult to pill, did this studio and the most important thing they found is that for all the drugs, maybe you can find an IV presentation? But in the US there is no IV presentation for this drug. They found the amt of drug was similar and found metabolites in the serum. Importnat consideration: they have to give a little more amt of drug rectally than orally. normally 0.25 mg/kg ? First pass metabolism: it is bypassed here, but they found a part of the rectum does not bypass first pass metabolism. The metabolite is active, Demethyol Pimobendan
42
43
44
What is the MOA of ACEIs?
when renin i released, angio converted into angio 1. ACE enzyme converts to angio 2. This is a situation that happens in our body and under normal condition, inder hypertensions and not heart failure, if we acauvate he sysem by heart failure it is bad for the patient
45
How is angiotensin II blocked?
remodeling, after some time heart has to change myocytes it has and the amt of ?????
46
List the ACEIs currently in use for heart failure
Blue = not prodrug Red = ?? * Captopril is not a prodrug (Capoten®)→ it use has been surpassed (GI upset) Dosage: 0.5-2 mg/Kg 3 times daily PO. in dogs ¼ or ½ of a 12.5 mg tablet PO. 2 to 3 times daily in cats * Lisinopril is not a prodrug (Prinivil®, Zestril®) Dosage: 0.25 - 0.5 mg/Kg q 24 h PO. in cats 0.5 mg/Kg 1-2 times daily PO. in dogs * Enalapril (prodrug, Enacard®, Vasotec®and human generic drug is used, USA) → enalaprilat (metabolite) Dosage: 0.25-0.5 mg/Kg q 12-24 h PO. in dogs and cats * Benazepril (prodrug) Fortekor® has been approved for use in dogs in Canada, Europe, South America, and Asia. In USA (extra label) → benazeprilat Dosage: 0.25-0.5 mg/Kg q 12-24 h PO. in dogs and cats * Ramipril (prodrug, Altace®, Vasotop® Canada and UK) → ramiprilat Dosage: 0.125-0.25 mg/Kg q 24 h PO. in dogs * Imidapril (prodrug, Prilium® Canada and UK) → imidaprilat Dosage: 0.25 mg/Kg q 24h PO.
47
Use prodrug to help with bioavailability. If you use only _______ drug, the route of absorption is not ____
Use prodrug to help with bioavailability. If you use only parent drug, the route of absorption is not high
48
ACEIs are indicated in all cases of _____ heart failure
ACEIs are indicated in all cases of systolic heart failure
49
ACEIs can also be used in subclinical myxomatous mitral valvular disease (MMVVD)
ACEIs can also be used in subclinical myxomatous mitral valvular disease (MMVVD)
50
ACEIs have proven useful in the management of systemic _________, _____ and ______ cardiac disease and _______ renal disease b/c they ______ glomerular filtration.
ACEIs have proven useful in the management of systemic hypertension, clinical and subclinical cardiac disease and proteinuric renal disease b/c they reduce glomerular filtration
51
ACEIs work on what stages of heart failure?
52
In NYHA phase III and IV heart disease in dogs (_______ to _____ heart failure), due to MMVD or DCM ➢ Enalapril * improved survival by > _____% * ↓ _________ edema * Improving quality of life
In NYHA phase III and IV heart disease in dogs (moderate to severe heart failure), due to MMVD or DCM ➢ Enalapril * improved survival by > 100% * ↓ pulmonary edema * Improving quality of life
53
In chronic kidney disease (CKD) * ACEIs can be ___________ ➢ ___________ intraglomerular pressure ➢ __________ proteinuria ➢ _______ progression of lesions
In chronic kidney disease (CKD) * ACEIs can be beneficial ➢ Reduced intraglomerular pressure ➢ Decreased proteinuria ➢ Slow progression of lesions
54
* ACEIs are used with other ________ drugs (including _______) safely * ACEIs will potentiate the effects of _______ → the dose should be ________ * When ACEIs are administered with NSAIDs → NSAIDs may affect the beneficial effect of ACEIs by __________ formation of PGs ➢ __________ action is caused by generation of PGs
* ACEIs are used with other cardiovascular drugs (including diuretics) safely * ACEIs will potentiate the effects of diuretics → the dose should be reduced * When ACEIs are administered with NSAIDs → NSAIDs may affect the beneficial effect of ACEIs by blocking formation of PGs ➢ Antihypertensive action is caused by generation of PGs
55
* Enalapril is well absorbed _____. Bioavailability is ______ decreased by food
* Enalapril is well absorbed orally. Bioavailability is not decreased by food
56
Enalapril and its active form enalaprilat are excreted solely by the __________
Enalapril and its active form enalaprilat are excreted solely by the kidneys
57
Oral administration of __________ is absorbed at rate of ~40% → not affected by feeding
benazepril
58
Benazepril is eliminated equally in _____ and bile in _____. In cats, ~85% is excreted in the _____ and only 15% in the ______
Benazepril is eliminated equally in urine and bile in dogs. In cats, ~85% is excreted in the feces and only 15% in the urine
59
Captopril is well absorbed _____ (75%). - Feeding ____ bioavailability by 30-40%
Captopril is well absorbed orally (75%), but feeding ↓ bioavailability by 30-40%
60
* ACEIs can cause symptomatic _______ → mixed __________ effects ➢ When ACEIs are used in conjunction with other therapies → ? ➢ ____________ is reversed by altering the therapy * Azotemia, inappetence, weakness, lassitude * The major impact of ACEIs on the kidney, is through production of hypotension → reducing the kidney _______ pressure → reducing _______ ________ rate (both arrows --> Resulting in worsening of _______) Typically, diuretic cessation or reduction in dosages results in reversal of azotemia
* ACEIs can cause symptomatic hypotension → mixed vasodilation effects ➢ When ACEIs are used in conjunction with other therapies → vasodilator, diuretics, and sodium restriction ➢ Hypotension is reverse by altering the therapy * Azotemia, inappetence, weakness, lassitude * The major impact of ACEIs on the kidney, is through production of hypotension → reducing the kidney perfusion pressure → reducing glomerular filtration rate (both arrows --> Resulting in worsening of azotemia) Typically, diuretic cessation or reduction in dosages results in reversal of azotemia
61
What are the adverse effects of ACEIs?
* Less common side effects → coughing and angioedema (humans) ➢ Coughing is thought to be related to ↑ levels of bradykinin
62
Carvedilol: adrenergic receptor antagonist (nonselective) → β1 ___ β2 ____ α1 ___ α2
Carvedilol: adrenergic receptor antagonist (nonselective) → β1 = β2 ≥ α1 > α2
63
Carvedilol * The ratio of β1/β2 to α1-receptor antagonist potency is ____:____ * Carvedilol reduces myocardial workload by lowering → Heart _____ → ________ vascular resistance
Carvedilol * The ratio of β1/β2 to α1-receptor antagonist potency is 10:1 * Carvedilol reduces myocardial workload by lowering → Heart rate → Peripheral vascular resistance
64
In human medicine __-blockers play a role in heart failure management by improving → ________ → ________ of life → _________ health → __________ capacity --> blunting of ______ activity
In human medicine β-blockers play a role in heart failure management by improving → survival → quality of life → cardiac health → exercise capacity --> blunting of SNS activity
65
The Harmful effects of Carvedilol on the SNS: * __________ and ____________ * ______________ with increased afterload * ______ activation * Myocardial ______ * ___________
The Harmful effects of Carvedilol on the SNS: * Tachycardia and arrhythmias * Vasoconstriction with increased afterload * RAAS activation * Myocardial remodeling * Fibrosis
66
In dogs with experimental mitral valve regurgitation Carvedilol (0.2 mg/Kg) 1. ____ heart rate 2. _____ function 3. _______ blood pressure 4. ____ ventricular contractile function 2-4 are unaffected
In dogs with experimental mitral valve regurgitation Carvedilol (0.2 mg/Kg) 1. ↓ heart rate 2. Renal function 3. Arterial blood pressure 4. Left ventricular contractile function 2-4 are unaffected
67
Carvedilol (0.4 mg/Kg) * ↓ heart rate * ↓ Renal function * ↓ Arterial blood pressure
68
Dogs in heart failure, carvedilol should be initiated at less than 0.2 mg/kg and titrate up to 0.4 mg/kg twice a day. Target dose in DCM The dosage is gradually increased until the target is reached: 0.5 – 1 mg/Kg BID
69
Diuretics * Use of potent _____-acting _______ is part of the management of CHF in human and in veterinary medicine: e.gs? * Their use is supplemented with: → ______ and ________ in most cases --> triple therapy → adding ________ (___) to the drug therapy --> quadruple therapy
Diuretics * Use of potent loop-acting diuretics is part of the management of CHF in human and in veterinary medicine * Furosemide * Torsemide * Bumetanide * Their use is supplemented with: → ACEIs and pimobendane in most cases --> triple therapy → adding spironolactone (MRB) to the drug therapy --> quadruple therapy
70
Patients receiving diuretics should be monitored!! Pronounced diuresis can _____ blood volume ➢ Dehydration lowers _______ (ventricular _____ pressure) ↓ preload reduces wall ______, myocardial ______ demand, and predisposition for ______ formation Reduction in venous return (without concurrent ______ inotropic effects) may lead to ___ cardiac output, __ renal perfusion, ______, ___ clearance of drugs Note: Inappetence and/or vomiting contribute further to dehydration and electrolyte loss
Patients receiving diuretics should be monitored!! Pronounced diuresis can reduce blood volume ➢ Dehydration lowers preload (ventricular filling pressure) ↓ preload reduces wall tension, myocardial oxygen demand, and predisposition for edema formation Reduction in venous return (without concurrent positive inotropic effects) may lead to ↓ cardiac output, ↓ renal perfusion, azotemia, ↓ clearance of drugs Note: Inappetence and/or vomiting contribute further to dehydration and electrolyte loss
71
Diuretics Monitored parameters * Serum electrolyte * Renal values → BUN (blood urea nitrogen) → serum creatinine * Body weight * State of hydration → skin turgor → packed cell volume → total protein → serum albumin and sodium
72
The _____ and ______ are both activated in heart failure. In virtually all cases, this activation is harmful to cardiac patients
The SNS and RAAS are both activated in heart failure. In virtually all cases, this activation is harmful to cardiac patients
73
In myxomatous mitral valve disease (MMVD), contractility is _______ maintained until patient reaches _______ stages.
* In myxomatous mitral valve disease (MMVD), contractility is partially maintained until patient reaches terminal stages
74
In heart failure, preload and afterload are both ________ and should be _________. Heart rate _____ but is usually high and can be reduced with _______.
In heart failure, preload and afterload are both elevated and should be reduced. Heart rate varies but is usually high and can be reduced with digoxin.
75
In dogs with DCM, the contractility is always _________ (and often very _________). This requires __________ support (in the ER) with _________ CRI, _______ (IV or PO), or ________ (IV or PO) and chronically with ________
In dogs with DCM, the contractility is always diminished (and often very profoundly). This requires inotropic support (in the ER) with dobutamine CRI, digoxin (IV or PO), or pimobendan (IV or PO) and chronically with pimobendan
76
What is an arrhythmia?
* An abnormality in the rate, regularity, or site of origin of the Electrical impulse (EI) * Disruption in impulse conduction: normal sequence of atrial and ventricular activation is changed
77
In many cases cardiac arrhythmias have no clinical importance, however arrythmias that lead to: very ____ or ______ heart rates or very _____ heart rates can have significant clinical implications if cardiac disease is present
In many cases cardiac arrhythmias have no clinical importance, however arrythmias that lead to: very slow or rapid heart rates or very irregular heart rates can have significant clinical implications if cardiac disease is present
78
Arrhythmias often are associated with * Imbalance of the _________ and _______ branches * Changes in serum electrolyte concentrations (2?) * Excessive _________ of cardiac tissue * _________ trauma
Arrhythmias often are associated with * Imbalance of the parasympathetic and sympathetic branches * Changes in serum electrolyte concentrations (K+ and Ca++) * Excessive stretch of cardiac tissue * Mechanical trauma
79
Classification of anti-arrhythmic drugs * Class I: ? * Class II: ? * Class III: ? * Class IV: ?
Classification of anti-arrhythmic drugs * Class I: Local anesthetics * Class II: β-adrenergic blockers * Class III: Potassium channel blockers * Class IV: Calcium channel blockers
80
Bradyarrhythmias * ___________ vagal tone: vagolytics * Increase __________ tone
Bradyarrhythmias * Decrease vagal tone: vagolytics * Increase sympathetic tone
81
List the different types of Tachyarrhythmias
82
Sinus tachycardia
* Pimobendan * ACEIs
83
Supraventricular tachyarrhythmias
* Digitalis: Digoxin * Calcium channel blockers: Diltiazem (IV) * β-adrenergic receptor blockers: Atenolol, Esmolol, Sotalol (II)
84
Ventricular tachyarrhythmias
* Lidocaine (IB) * Mexiletine (IB) * Sotalol
85
Bradyarrhythmia: Arrhythmia with heart rates that are _____ the normal range
Bradyarrhythmia: Arrhythmia with heart rates that are below the normal range
86
Bradyarrhythmias * These arrhythmias may be responsive to drugs that can increase heart rate → Decrease vagal tone (vagolytics) → Increase sympathetic tone
87
Bradyarrhythmia Vagolytics * _________: 0.4 mg/Kg SC * ___________ ________
Bradyarrhythmia Vagolytics * Atropine: 0.4 mg/Kg SC * Propantheline bromide
88
Propantheline bromide * It is an ____________ agent (like atropine) * Propantheline is not completely (variable) absorbed after ____ administration * As a __________, propantheline can lead to tachycardia, ↑ salivation, and vomiting
Propantheline bromide * It is an antimuscarinic agent (like atropine) * Propantheline is not completely (variable) absorbed after oral administration * As a vagolytic, propantheline can lead to tachycardia, ↑ salivation, and vomiting
89
Increase _________ tone Isoproterenol (ISO): β1 ___ β2 > > > > ___ * ISO __________ heart rate by stimulating the adrenergic receptors (β1 and β2) in the sinus and __________ node
Increase sympathetic tone Isoproterenol (ISO): β1 = β2 > > > > α * ISO increases heart rate by stimulating the adrenergic receptors (β1 and β2) in the sinus and atrioventricular node
90
PE: Phenylephrine
91
Isoproterenol (ISO) * ISO is most used ____________ for ____-term treatment (CRI) * It can lead to _________ as well as cardiac ________ → blood __________ monitoring → electrocardiography should be performed
Isoproterenol (ISO) * ISO is most used intravenously for short-term treatment (CRI) * It can lead to hypotension as well as cardiac arrhythmias → blood pressure monitoring → electrocardiography should be performed
92
Sinus tachycardia is typically a response to: * _____ blood pressure * _______ * _______ * _______ * ______ cardiac output Sinus tachycardia → _______ If the sinus tachycardia is secondary to heart disease (_______ cardiac output), treating this condition with cardiac drugs is indicated ➢ __________ and _______
Sinus tachycardia is typically a response to: * Low blood pressure * Pain * Sepsis * Fever * Low cardiac output Sinus tachycardia → CHF If the sinus tachycardia is secondary to heart disease (low cardiac output), treating this condition with cardiac drugs is indicated ➢ Pimobendan and ACEIs
93
Supraventricular tachyarrhythmias (SVTA) * Usually caused by ________ cardiac disease and secondary _______ enlargement * They are not likely to completely resolve with antiarrhythmic drug treatment → Treatment is directed at _________ the rapid conduction through AV node
Supraventricular tachyarrhythmias (SVTA) * Usually caused by primary cardiac disease and secondary atrial enlargement * They are not likely to completely resolve with antiarrhythmic drug treatment → Treatment is directed at slowing the rapid conduction through AV node
94
Digitalis: digoxin * Slows conduction through the _________ node and slows the ________ response rate ↓ in heart rate is _____ significant and it may be necessary to add class ___ or ___ drugs * In cases of _______ or significant myocardial dysfunction ➢ It may be reasonable to give first digoxin. Once the heart disease is more stable add _______ or ________
Digitalis: digoxin * Slows conduction through the atrioventricular node and slows the ventricular response rate ↓ in heart rate is not significant and it may be necessary to add class II or IV drugs * In cases of CHF or significant myocardial dysfunction ➢ It may be reasonable to give first digoxin. Once the heart disease is more stable add atenolol or diltiazem
95
Calcium channel blockers (class IV): ______ and ________ * They _____ the ventricular response rate in STA → 24-hour Holter monitor Adverse effects of diltiazem are quite _____ In dogs → _______ and ________ block In cats → GI signs (_______ and ________)
Calcium channel blockers (class IV): diltiazem and verapamil * They slow the ventricular response rate in STA → 24-hour Holter monitor Adverse effects of diltiazem are quite rare In dogs → bradycardia and atrioventricular block In cats → GI signs (vomiting and anorexia)
96
Supraventricular tachyarrhythmias (SVTA) ____-adrenergic receptor blockers (class __) * ___________ (highlighted in red) * _________ * ________ (highlighted in red) * __________ * _________ * ___________
Supraventricular tachyarrhythmias (SVTA) β-adrenergic receptor blockers (class II) * Atenolol (highlighted in red) * Esmolol * Sotalol (highlighted in red) * Propranolol * Metoprolol * Carvedilol
97
Supraventricular tachyarrhythmias (SVTA) β-adrenergic receptor blockers (class II): Atenolol * Atenolol is a specific ____-blocking drug. Very high doses can produce _________ _________ inotrope → could _________ heart failure or myocardial dysfunction * It is most used in conjunction with __________ → to slow the heart rate in patients with atrial fibrillation or rapid SVTA Clinical monitoring → 24-hour Holter monitor
Supraventricular tachyarrhythmias (SVTA) β-adrenergic receptor blockers (class II): Atenolol * Atenolol is a specific β1-blocking drug. Very high doses can produce bradycardia Negative inotrope → could exacerbate heart failure or myocardial dysfunction * It is most used in conjunction with digoxin → to slow the heart rate in patients with atrial fibrillation or rapid SVTA Clinical monitoring → 24-hour Holter monitor
98
Supraventricular tachyarrhythmias (SVTA) β-adrenergic receptor blockers (class II): Esmolol * Esmolol is an _________-acting blocker (half-life < 10 min) used for ____ administration (__) * Used for ____ termination of very ___ SVTA * Esmolol can cause ______ bradycardia and ________ myocardial function → It can stop the tachyarrhythmia quite abruptly leading to ?
Supraventricular tachyarrhythmias (SVTA) β-adrenergic receptor blockers (class II): Esmolol * Esmolol is an ultrashort-acting blocker (half-life < 10 min) used for IV administration (CRI) * Used for acute termination of very fast SVTA * Esmolol can cause sinus bradycardia and decrease myocardial function → It can stop the tachyarrhythmia quite abruptly leading to sinus arrest
99
Supraventricular tachyarrhythmias (SVTA) β-adrenergic receptor blockers (class II and III): Sotalol * Sotalol is a _____-_____ β-blocker and _______ channel blocker * Unlike other β-antagonists, it _______ the cardiac action potential and the ____ interval by delaying the slow outward ___ current → Supraventricular tachyarrhythmias → Ventricular tachyarrhythmias * Sotalol is a very effective and safe ventricular antiarrhythmic for veterinary medicine → frequently given in conjunction with _______ for refractory arrhythmias
Supraventricular tachyarrhythmias (SVTA) β-adrenergic receptor blockers (class II and III): Sotalol * Sotalol is a non-selective β-blocker and potassium channel blocker * Unlike other β-antagonists, it prolongs the cardiac action potential and the QT interval by delaying the slow outward K+ current → Supraventricular tachyarrhythmias → Ventricular tachyarrhythmias * Sotalol is a very effective and safe ventricular antiarrhythmic for veterinary medicine → frequently given in conjunction with mexiletine for refractory arrhythmias
100
The goal of treating a VTA are to _______ the number of abnormal ventricular complexes
The goal of treating a VTA are to decrease the number of abnormal ventricular complexes
101
VTA Local anesthetics (class IB): lidocaine and mexiletine Lidocaine * It inhibits the ______ sodium current and reduces the rate of rise of the ___ * Lidocaine is the common agent administered IV for acute treatment of ________ arrhythmias * It has a very high ____-pass metabolism in the liver → not effective if administered _____ * Side effects of lidocaine (neurological) → ? * ______ onset and offset of action → should be considered when given an ____ antiarrhythmic agent
VTA Local anesthetics (class IB): lidocaine and mexiletine Lidocaine * It inhibits the inward sodium current and reduces the rate of rise of the AP * Lidocaine is the common agent administered IV for acute treatment of ventricular arrhythmias * It has a very high first-pass metabolism in the liver → not effective if administered orally * Side effects of lidocaine (neurological) → depression, seizures, and vomiting * Rapid onset and offset of action → should be considered when given an oral antiarrhythmic agent
102
Ventricular tachyarrhythmias (VTA) Local anesthetics (class IB): lidocaine and mexiletine Mexiletine * Mexiletine is most useful for the ______ management of ventricular arrhythmias * It can cause similar neurological effects to _______. Mexiletine is safe. The most common adverse effects in animals is GI → _____ loss of appetite or vomiting * Mexiletine has a good _____ absorption (____ capsules) * It can be combined with _____
Ventricular tachyarrhythmias (VTA) Local anesthetics (class IB): lidocaine and mexiletine Mexiletine * Mexiletine is most useful for the chronic management of ventricular arrhythmias * It can cause similar neurological effects to lidocaine. Mexiletine is safe. The most common adverse effects in animals is GI → mild loss of appetite or vomiting * Mexiletine has a good oral absorption (oral capsules) * It can be combined with sotalol