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Clinical Pharmacology > Cardio Drugs > Flashcards

Cardio Drugs Flashcards

1
Q

Heart Disease

A

Something is wrong with the heart

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2
Q

Acquired heart disease

A
  • Develop later in life
  • Most common in people
  • e.g. mitral valve endocardiosis
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3
Q

Congenital heart disease

A
  • from birth

- e.g. ventricular septal defect

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4
Q

Systolic dysfunction

A
  • want to improve contractility

- e.g. positive inotropic drug

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5
Q

Diastolic dysfunction

A
  • issue is with relaxation phase
  • Not able to get enough filling
  • e.g. Hypertrophic cardiomyopathy
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6
Q

Pressure overload heart disease

A
  • Stenotic pulmonic valve

- Heart has to work harder against that stenotic valve

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7
Q

Volume overload heart disease

A
  • More volume in the heart that it has to push out

- e.g. tricuspid valve endocardiosis

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8
Q

Congestive heart failure

A
  • Heart failure due to accumulation of fluid somewhere

- Location will vary depending on which side of heart failure

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9
Q

Right sided heart failure

A
  • Pleural effusion (cranial vena cava)
  • Abdominal effusion (back from the liver)
  • Abdominal effusion is more common than pleural effusion in dogs than cats
  • High pressure in sinudoids pressing on the liver parenchyma to go out into the abdominal cavity
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10
Q

Left sided heart failure

A
  • Pulmonary edema

- Cats can get pulmonary edema or pleural effusion (and pleural effusion is easier to manage)

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11
Q

What drug would you use for congestive heart failure?

A
  • Diuretics!
  • Removing excessive fluid
  • Furosemide is best at doing this quickly
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12
Q

Stage A Heart Disease

A
  • At RISK for heart disease, but don’t currently have it
  • Important for acquired diseases (e.g. endocardiosis)
  • Most common in small-breed dogs (<15 kg), middle-aged to aged dogs (these are stage A)
  • May recommend monitoring
  • Or for Dobermans that are at risk for DCM (may recommend these dogs go get an echocardiogram to look at systolic function)
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13
Q

Stage B1

A
  • MILD disease
  • Typically won’t do anything more than monitor the dog or cat
  • Don’t necessarily intervene with medications
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14
Q

Stage B2

A
  • Means the disease is MODERATE to severe
  • Severity: general rule of thumb is that severity is based on heart size
  • Atrial enlargement is considered more severe
  • High volume and high pressure, more likely caudal vena cava or main pulmonary vein
  • Monitor with echocardigoram, chest x-ray
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15
Q

Endocardiosis Stage B2 treatment

A
  • Pimobendan +/- ACE inhibitor +/- spironolactone
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16
Q

Stage C

A
  • You have had congestive heart failure
  • Prognosis varies depending on the response to treatment and how bad
  • Acute vs chronic
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17
Q

Treatment for acute congestive heart failure

A
  • Furosemide IV (high doses) + ACE inhibitor + Pimobendan +/- Spironolactone
  • Exception is with stenosis
  • Might not stop the Pimobendan here because furosemide and pimobendan were shown to have 3-6 months longer survival time than furosemide and ACE inhibitor
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18
Q

Chronic congestive heart failure

A
  • Prognosis is 1 year average

- Still treating with diuretics and likely an ACE inhibitor and Pimobendan +/- Spironolactone

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19
Q

Acute congestive heart failure

A
  • decompensated heart failure

- showing clinical signs; often emergent

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20
Q

Stage D Heart Disease

A
  • Congestive heart failure that is REFRACTORY to treatment
  • NOT GOOD
  • We don’t talk about this that much
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21
Q

Pimobendan Mechanism of action

A
  • Calcium sensitizer and phosphodiesterase inhibitor
  • Calcium sensitizer is positive inotropy/contractility
  • Phosphodiesterase inhibitor is vasodilation
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22
Q

Cost of Pimobendan

A

$80-100/month

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23
Q

Indication for Pimobendan

A
  • Endocardiosis B2
  • Likely endocardiosis C
  • Dilated Cardiomyopathy B2
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24
Q

EPIC study

A
  • Dogs with B2 endocardiosis

- Dogs with Pimobendan went 15 months longer

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25
Q

Pimobendan side effects

A
  • Don’t need to do kidney or liver monitoring
  • Can cause GI signs
  • May increase development of arrhythmias
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26
Q

PROTECT study

A
  • 9 month benefit for Dobermans with B2 dilated cardiomyopathy that were put on pimobendan
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27
Q

Pimobendan route

A
  • Oral
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28
Q

Contraindications for Pimobendan (Plumbs)

A
  • Hypertrophic cardiomyopathy, aortic stenosis, etc.

- Caution in patients with cardiac arrhythmias

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29
Q

Monitoring for Pimobendan

A
  • Cardiovascular parameters used to monitor heart function, including ECG, blood pressure, echo studies, and clinical signs
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30
Q

ACE Inhibitors examples

A
  • Benazepril and Enalapril
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31
Q

ACE Inhibitors Mechanism

A
  • Inhibit Angiotensin Converting Enzyme
  • Blocks the RAAS system (which is involved in reabsorbing sodium and water as well as blocking aldosterone secondarily)

-

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32
Q

Cost of ACE Inhibitors

A

$20/month

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33
Q

Indication for ACE Inhibitors

A
  • Endocardiosis B2
  • Some debate
  • SVEP studied show no big difference in Cavalier King Charles spaniels
  • VETPROOF study showed that ACE inhibitor got 3-4 months longer than a placebo
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34
Q

ACE Inhibitors excretion

A
  • For Enalapril: Kidney

- Benazepril: kidney + other

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35
Q

ACE Inhibitors Adverse effects (Plumbs)

A
  • GI distress primarily

- Weakness, hypotension, renal dysfunction, and hyperkalemia could occur

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36
Q

Monitoring Enalapril (Plumbs)

A
  • Serum electrolytes, serum creatinine, BUN, urine protein
  • Blood pressure
  • Periodic CBC with differential
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37
Q

Cardiac output equation

A
  • Stroke volume x heart rate
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38
Q

Blood pressure equation

A
  • Cardiac output x Systemic vascular resistance

- Also, = stroke volume x heart rate x systemic vascular resistance

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39
Q

Three factors that impact stroke volume

A
  • Contractility, afterload, and preload
  • Contractility is how long or hard your heart is contracting
  • Preload is how well the heart fills
  • Afterload is the pressure against which your heart has to pump
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40
Q

RAAAS goal

A
  • Goal is to maintain blood pressure
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41
Q

3 Main Stimuli of RAAAS

A
  1. Decreased perfusion to the kidneys
  2. Decreased sodium and chloride to the kidneys
  3. Increased sympathetic tone in the autonomic nervous system
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42
Q

Effects of Angiotensin II (Should be able to list 7-8)

A
  1. Peripheral vasoconstriction to increase Systemic Venous Resistance
  2. Direct effect on kidney to increase sodium absorption in the proximal tubules (increase water absorption –> increase preload –> increase stroke volume –> maintain blood pressure)
  3. Stimulate release of aldosterone from zona glomerulosa in the adrenal gland
  4. Stimulates sympathetic outflow in the brain to cause release of anti-diuretic hormone from posterior pituitary
  5. Goes to heart and stimulates hypertrophy and in chronic cases fibrosis (increased SVR which increases afterload on the heart which will cause hypertrophy of the heart)
  6. Aldosterone (at the distal convoluted tubule and collecting duct of the kidney - see separate flash card)
  7. Antidiuretic hormone (see separate flashcard
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43
Q

Aldosterone actions

A
  1. Aldosterone goes to the basolateral surface of the distal convoluted tubule and collecting duct to open channels to absorb sodium and pee potassium
  2. It can also open channels to absorb sodium in exchange for protons in the distal convoluted tubule and collecting ducts of the kidney
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44
Q

Antidiuretic hormone action location

A
  • Acts at the medullary collecting duct on the basolateral surface
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45
Q

Two main functions of antidiuretic hormone

A
  1. Induces insertion of aquaporin on the luminal surface at the medullary collecting duct, which will allow us to absorb free water due to medullary concentration gradient
  2. Acts on peripheral blood vessels to cause vasoconstriction
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46
Q

What establishes medullary concentration gradient?

A
  • Sodium and urea

- Ascending loop of Henle has the Na/K/2Cl channel which is an ATPase

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47
Q

RAAAS pathophysiology in CHF

A
  • In a sick heart, your contractility fails, which will decrease stroke volume and blood pressure
  • This will activate RAAAS to increase preload, systemic vascular resistance, and afterload
  • This increases the work of the heart with increased afterload and preload
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48
Q

Ang II muscle hypertrophy and CHF

A
  • Bad for the heart
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49
Q

Furosemide Mechanism

A
  • Na/K/2Cl- inhibitor

- Will immediately activate RAAS, even at normal doses

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50
Q

Location of action of Furosemide

A
  • Proximal Loop of Henle
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51
Q

Indication of Furosemide

A
  • Basically any congestive heart failure, acute or chronic
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52
Q

Contraindications of Furosemide

A
  • Anuric patients
  • Progressive azotemia and oliguria
  • Patients with existing electrolyte or water balance abnormalities
  • Impaired hepatic function
  • Diabetes mellitus
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53
Q

Side effects

A
  • Fluid and electrolyte abnormalities
  • Hyponatremia is of greatest concern, but also hypocalcemia, hypokalemia, and hypomagnesemia may occur
  • Metabolic alkalosis is a side effect because you are losing positively charged ions
  • Otoxicity reported as well
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54
Q

Monitoring for Furosemide

A
  • serum electrolytes
  • BUN
  • serum creatinine
  • glucose
  • hydration status
  • blood pressure
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55
Q

Benefits of ACE inhibitors

A
  • Act pretty upstream in the RAAAS system
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56
Q

Drawbacks of ACE inhibitors

A
  • Do not block everything
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57
Q

Telmisartin and Semintra MOA

A
  • Angiotensin II receptor blockers
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58
Q

Drawbacks of Telmisartin and Semintra

A
  • Mostly cost
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59
Q

Side effects of Telmisartan and Semintra

A
  • Hypotensive patients or patients that are volume or electrolyte depleted
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60
Q

Route of administration of Telmisartan and Semintra

A
  • Oral route
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61
Q

Antidiuretic hormone inhibitors

A
  • Could in theory be used
  • Expensive
  • Ends in -vaptin
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62
Q

Spironolactone Mechanism of Action

A
  • Aldosterone antagonist
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63
Q

Spironolactone location of action

A
  • Distal convoluted tubule
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64
Q

Functions of Spironolactone

A
  • Mild diuretic (potassium sparing diuretic)

Also blocks aldosterone’s actions of causing hypertrophy and fibrosis of the heart

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65
Q

Sequential nephron blockade

A
  • Using furosemide in conjunction with spironolactone
  • Other portions of nephron hypertrophy chronically with furosemide, and if you block another part of the nephron (i.e. use another diuretic), you can prevent that
  • Monitor kidney values and electrolytes if used together
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66
Q

Contraindications of Spironolactone

A
  • Hyperkalemia, Addison’s, anuria, acute kidney injury, or significant renal impairment
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67
Q

Monitoring for Spironolactone

A
  • Serum electrolytes, BUN, creatinine
  • Hydration status
  • Blood pressure if indicated
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68
Q

Stenosis and use of Pimobendan

A
  • Avoid Pimobendan in Stage B2 and C

- Do NOT want to improve contractility in these cases

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69
Q

Effect of sympathetic arm of autonomic nervous system on contractility

A
  • Sympathetic will increase contractility
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70
Q

Effect of parasympathetic arm of autonomic nervous system on contractility

A
  • Parasympathetic will decrease contractility
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71
Q

Receptors on our heart that will increase contractility and respond to sympathetic tone

A
  • Beta 1
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72
Q

Functions of Beta 1 receptors on the heart

A
  • Increase sympathetic tone
  • Increase contractility
  • Increase electrical conduction
  • Increase heart rate
  • Increase relaxation as well (systole and diastole)
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73
Q

Beta blocker drug examples

A
  • Atenolol, timolol, propanolol
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74
Q

Atenolol, timolol, propanolol MOA

A
  • Block beta 1 receptors on the heart
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75
Q

Indications for Beta blockers

A
  • Pulmonic stenosis, aortic stenosis
  • Want to use a beta blocker to reduce contractility
  • Reduce contractility, heart rate, electrical conduction, and relaxation
  • Basically diastolic dysfunction
  • Arrhythmias (e.g. thyroid toxicosis in a cat with hyperthyroid would want to give methimazole and a beta blocker potentially)
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76
Q

Overdose signs of Beta Blockers

A
  • Bradycardia, hypotension (lethargy, collapse, exercise intolerance)
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77
Q

Giving Beta blockers to a dog with DCM

A
  • Don’t do it

- They have poor systolic function already, and you’d be decreasing systolic function even more

78
Q

Contraindications of beta blockers

A
  • Patients with overt heart failure
  • Greater than first degree heart block
  • Sinus bradycardia
  • May increase morbidity in cats with left-sided CHF caused by hypertrophic cardiomyopathy
79
Q

Adverse effects

A
  • Bradycardia, inappetence, lethargy and depression, impaired AV conduction, CHF or worsening of heart failure, hypotension, hypoglycemia, and bronchoconstriction
80
Q

Monitoring of beta blockers

A
  • cardiac function, heart rate, ECG if necessary, BP if indicated
81
Q

Parasympathomimetics

A
  • Don’t use that often

- Other side effects not great (DUMBSLED)

82
Q

Virchow’s Triad

A
  1. Stasis of Blood Flow
  2. Endothelial damage (exposure of tissue factor III)
  3. Hypercoagulability
  4. Some (Dr. Sellon) would argue that thrombolysis is the fourth corner of the triangle)
83
Q

Hypertrophic cardiomyopathy

A
  • Heart muscle gets very thick and lumen gets very thin
  • Big muscles contract well but lose ability to relax well
  • Diastolic dysfunction!
  • Left auricular appendage tends to get very large
84
Q

Where do clots tend to form in HCM?

A
  • Left auricular appendage
  • Tends to get very large, leading to blood stasis
  • Then you get clots
85
Q

Drugs used for HCM

A
  • beta blockers
  • Diltiazem (calcium channel blocker)
  • At some point can add ACE inhibitor
  • NO EVIDENCE that any of these work
86
Q

Drugs for HCM stage B2

A
  • Diltiazem
  • Beta blockers
  • +/- ACE Inhibitor
87
Q

Amlodipine MOA

A
  • Peripheral calcium channel blockers

- Blood vessels –> vasodilation

88
Q

Diltiazem MOA

A
  • Central calcium channel blocker
89
Q

Hypertrophic Obstructive Cardiomyopathy

A
  • Obstruction from the mitral valve (see an image)
  • Mitral valve flings open during systole and blocks the blood flow from leaving the heart
  • Dynamic stenotic lesion
90
Q

Therapeutic goals of HOCM

A
  • Decrease contractility
91
Q

Treatment of choice for Stage B2 HOCM

A
  • Beta blockers are treatment of choice
  • Primary difference between HCM/HOCM?
  • Would likely want to give an anti-platelet drug as well
92
Q

Stage C HOCM Treatment

A
  • Furosemide
  • ACE inhibitor
  • Beta blocker
  • +/- Pimobendan (might counteract beta blocker)
  • +/- Spironolactone
  • ALSO an anti-platelet drug!
93
Q

Anti-platelet drugs types of clots they work best on

A
  • Primary hemostasis

- Best for arterial blood clots

94
Q

Anticoagulant drugs

A
  • Secondary hemostasis
95
Q

Intrinsic cascade clotting factors

A

12, 11, 9, 8

96
Q

Extrinsic cascade clotting factors

A

7, 3 (both go to 10 or the common pathway)

97
Q

Common pathway clotting factors

A

10, 5, 2, and 1

98
Q

Vitamin K dependent factors

A

II, VII, IX, and X

99
Q

Drug of choice for arterial blood clots

A
  • Want something faster

- Anti-platelet drugs (primary hemostasis)

100
Q

Drug of choice for venous blood clots

A
  • Slower; more time to block fibrin

- Anticoagulants work better here potentially

101
Q

For really bad clots

A
  • Can use both anti-platelet and anti-coagulant drugs
102
Q

Aspirin drug class

A
  • Antiplatelet
103
Q

Aspirin MOA

A
  • Cyclooxygenase inhibitor (blocking thromboxane II)
104
Q

Aspirin route

A
  • PO
105
Q

issues with Aspirin

A
  • Doesn’t work well
106
Q

Clopidogrel drug class

A
  • Antiplatelet medication
107
Q

Aspirin and Clopidogrel length of efficacy

A
  • Entire life of platelet

- Platelets live 3-5 days

108
Q

Clopidogrel MOA

A
  • Blocks ADP

- Inactive compound that goes to the liver –> cytochrome P450 –> converted to clopidogrel active metabolite (CAM)

109
Q

Metabolism of Clopidogrel

A
  • Liver
  • Important because liver function varies
  • Cats may over-respond or under-respond based on Cytochrome P450
110
Q

Drug interactions with Clopidogrel

A
  • Omeprazole we talked about
111
Q

Aspirin contraindications (Plumbs)

A
  • Patients with hemorrhagic disorders, asthma, or renal insufficiency
  • Also in patients with bleeding ulcers
112
Q

Adverse effects of aspirin

A
  • Primarily gastric irritation

- Severe blood loss could result

113
Q

Monitoring aspirin

A
  • Analgesic effect and/or antipyretic effect
  • Bleeding times if indicated
  • PCV or fecal occult blood tests if indicated
114
Q

Clopidogrel contraindications

A
  • In humans, if active pathologic bleeding is happening
115
Q

Adverse effects of clopidogrel

A
  • Hemorrhage
  • Icterus (clopidogrel) - monitor liver values
  • Don’t need additional monitoring
  • Measuring platelet function not fun and not easy or beneficial
116
Q

Monitoring of clopidogrel

A
  • vomiting, bleeding

- Monitor litterbox for hematochezia, epistaxis, bruising (petechia and ecchymoses)

117
Q

Considerations for surgery of a patient on anti-platelet drugs-

A
  • Need to discontinue those medications 3-5 days prior to surgery
118
Q

Warfarin MOA

A
  • inhibits Vitamin K enzyme which will inhibit factors II, VII, IX, and X
119
Q

Warfarin route

A
  • oral medication
120
Q

Contraindications of warfarin

A
  • High risk of bleeding, but it’s cheap

- Would not be your first choice

121
Q

Rivaroxaban MOA

A
  • Factor Xa inhibitor
122
Q

Rivaroxaban route

A
  • oral medication
123
Q

Rivaroxaban cost

A
  • $200-300/month
  • Not that much more effective than Clopidogrel
  • Wouldn’t necessarily pick this for a cat with an atrial thromboembolism
124
Q

Indication for Rivaroxaban

A
  • Primarily pulmonary thromboembolism
  • Most commonly used in hypercoagulable states (Cushing’s, IMHA, etc.)
  • Venous thromboembolism over an arterial thromboembolism (doesn’t work as fast)
125
Q

Antithrombin III role

A
  • Inhibits Factor Xa
126
Q

Heparin route

A
  • IV or SC

- usually given as a CRI

127
Q

Heparin MOA

A
  • potentiates antithrombin III
128
Q

Heparin cost

A
  • $

- Many different sizes

129
Q

Lovenox or Enoxaparin route

A
  • SC
130
Q

Lovenox or Enoxaparin MOA

A
  • potentiator of antithrombin III
131
Q

Lovenox or Enoxaparin cost

A
  • $$$$$$$

- $200-300/month

132
Q

Lovenox or Enoxaparin safety

A
  • Quite safe
133
Q

Lovenox or Enoxaparin safety precautions

A
  • Use cautiously in patients with hepatic impairment or significant renal dysfunction as it can lead to drug accumulation
134
Q

Side effects of Lovenox or Enoxaparin

A
  • Hemorrhage possible

- Anemia, thrombocytopenia, nausea, fever

135
Q

Lovenox or Enoxaparin Monitoring

A
  • Baseline CBC with periodic rechecks
  • Urinalysis
  • Routine coagulation tests usually insensitive
136
Q

Primary clot prevention

A
  • Don’t have a clot now and hope to prevent clots in the future
  • Most people want to prevent primary clots
  • No data, but most people give clopidogrel for primary clot prevention
137
Q

Secondary clot prevention

A
  • Had a clot and want to prevent future clots
138
Q

Bradyarrhythmia value for a dog, cat, and horse

A

Dog: <70 bpm
Cat: <140 bpm
Horse: <20 bpm

139
Q

Normal rhythm for a dog, a cat, and a horse

A

Dog: 70-160 bpm
Cat: 140-220 bpm
Horse: 20-40 bpm

140
Q

Tachyarrhythmia for a dog, a cat, and a horse

A

Dog: >160 bpm
Cat: >220 bpm
Horse: >40 bpm

141
Q

Bradyarrhythmia differentials

A
  • Sick sinus syndrome
  • Sinus bradycardia
  • AV block (1°, 2°, 3°)
  • Atrial standstill
142
Q

Tachyarrhythmia differentials

A
  • Sinus tachycardia
  • Supraventricular arrhythmias (singlets, couplets, triplets, runs, atrial fibrillation)
  • Ventricular arrhythmia
143
Q

Sinoatrial node function

A
  • Pacemaker of the heart

- Propagates current across the atrium (P wave)

144
Q

Atrioventricular node function

A
  • funneling the electricity through the AV node
  • Also giving a pause for the ventricle to fill
  • The pause for this is the PR interval or PQ interval
145
Q

Purkinje cells

A
  • Bundle of His
  • Right and left bundle branch
  • Left bundle branch further divides into two additional pathways
  • Main goal to conduct electricity very quickly
146
Q

Ventricular myocytes

A
  • Takes a longer time

- Large positive lead (QRS complex)

147
Q

Ventricular repolarization

A
  • T wave
  • There is a lot of variation in morphology
  • If you have a QRS you have to have a T wave
148
Q

Supraventricular complex

A
  • Electricity will emanate from atrial myocyte
  • P’ wave (may or may not have a P wave)
  • Then it will go to AV node and have a normal QRS
149
Q

Ventricular complex

A
  • Rogue ventricular complex
  • Atrium will not depolarize
  • Does not go through Bundle of His (therefore SLOW)
  • Wider QRS complex on the ECG reading
  • Should still have a T wave
150
Q

Ventricular premature complex

A
  • singlet, doublet, triplet

- 4+ = ventricular tachycardia

151
Q

Ventricular escape

A
  • if you come too late
152
Q

Atrial fibrillation

A
  • Very chaotic
  • Hundreds of atrial myocytes firing
  • May run into each other
  • If you ever see ONE p wave that’s not atrial fibrillation
  • Should still get occasional QRS complexes
  • Sounds like shoes in a dryer
153
Q

Atrial fibrillation

A
  • Have to have a pathologically large heart in small animals
154
Q

Class Ia Vaughan Williams Anti-arrhythmics

A
  • Type of sodium channel blocker
155
Q

Class Ib

A
  • Sodium channel blocker

- **Used most often in vet med

156
Q

Lidocaine, Mexiletine MOA

A
  • Class Ib
157
Q

Which type of Anti-arrhythmic medication is most often used?

A
  • Class Ib
158
Q

Class Ic Anti-arrhythmic

A
  • Sodium channel blocker
159
Q

Class II Anti-arrhythmic

A
  • Beta blockers

- e.g. -lols

160
Q

Class III Anti-arrhythmic

A
  • potassium channel blockers
161
Q

Sotalol MOA

A
  • Class III

- Potassium channel blocker

162
Q

Amiodarone MOA

A
  • Class III

- Potassium channel blocker

163
Q

Class IV Anti-arrhythmic

A
  • Calcium channel blockers
164
Q

Diltiazem MOA

A
  • Class IV

- Central calcium channel blocker

165
Q

Class Ib site of action

A
  • Ventricular myocytes

- Sodium channel blockers only affect ventricular myocytes

166
Q

Lidocaine indication

A
  • Ventricular arrhythmias

- Ventricular tachycardia and ventricular premature complexes

167
Q

Lidocaine contraindications

A
  • Be careful in cats
  • Lidocaine should be used in caution in patients with liver disease, congestive heart failure, shock, hypovolemia, severe respiratory depression, or hypoxia
168
Q

Side effects of lidocaine

A
  • CNS signs: drowsiness, depression, ataxia, muscle tremors
169
Q

Monitoring lidocaine

A
  • ECG

- Signs of toxicity

170
Q

Beta blockers site of action

A
  • Ventricles as well as nodes
  • High sympathetic tone if agonized
  • Will also influence ventricular myocyte
171
Q

Beta blockers indication

A
  • Ventricular and supraventricular arrhythmias
  • Systemic hypertension
  • Tends to be used in patients with arrhythmias or diastolic dysfunction
172
Q

Beta blockers side effects

A
  • Decreased contractility that is moderate to severe
  • Can be pro-arrhythmic too
  • Bradycardia
  • Lethargy
  • Inappetence
  • Hypotension
173
Q

Beta Blockers Contraindication

A
  • Do not use in a patient with systolic dysfunction (e.g. dilated cardiomyopathy)
  • Contraindicated in patients with over heart failure
  • Use in caution in patients with renal insufficiency
174
Q

Action potential for ventricular myocytes

A
  • Sodium low in the cell and potassium high in the cell
  • When you hit threshold, sodium channels will open, and sodium will rush into the cell
  • Then the heart repolarizes as potassium moves out of the cell
  • In the plateau phase, cell doesn’t change charge as calcium moves in to cancel potassium moving out
  • VERY special to ventricular myocytes to allow calcium into the cells
175
Q

Nodal cell action potential

A
  • Degree of automaticity
  • Not a flat membrane potential
  • Calcium is constantly coming into the cell
  • Leaking channels determined by sympathetic tone or parasympathetic tone (sympathetic tone increases steepness; parasympathetic tone will decrease it)

-

176
Q

Class III blocker indications for use

A
  • Ventricular or supraventricular arrhythmias

- Often used in boxers with arrhythmogenic cardiomyopathy

177
Q

Effect of Class III channel blockers on contraction

A
  • No effect

- They work by delaying repolarization to prevent depolarization

178
Q

Side effect of class III channel blockers

A
  • e.g. amiodarone, sotalol
  • potential for negative inotropic, chronotropic, and proarrhythmic effects
  • can worsen syncope or cause lethargy
179
Q

Contraindications of sotalol

A
  • Asthma, sinus bradycardia, 2nd or 3rd degree heart block, cardiogenic shock, or uncontrolled congestive heart failure
180
Q

Calcium channel blockers/Class IV location of action

A
  • nodal cells only
181
Q

Calcium channel blockers/Class IV indication

A
  • Supraventricular arrhythmias
182
Q

Calcium channel blockers/Class IV Side effects

A
  • Decreased contractility
  • Won’t impact ability to depolarize or repolarize
  • pro-arrhythmic
  • Bradycardia
  • Lethargy, GI distress, hypotension, etc.
183
Q

Calcium channel blockers/Class IV Contraindications

A
  • Severe hypotension, sick sinus syndrome, or 2° or 3° degree AV block
  • Acute pulmonary congestion
  • Careful in older patients or those with heart failure, or hepatic or renal impairment
184
Q

Digoxin Actions

A
  • Increases parasympathetic tone by acting on muscarinic receptors on the SA and AV node
185
Q

Digoxin Indication

A
  • Supraventricular arrhythmias
186
Q

Digoxin impact on contractility

A
  • SOdium-potassium ATPase
  • Cardiac myocyte
  • Sodium moves out and potassium moves in
  • Digoxin inhibits thise so that intracellular sodium concentrations increase
  • When that happens, a bidirectional exchanger of sodium and calcium will activate to move calcium in and sodium out, or vice versa
  • This movement of calcium in will cause an increase in contractility
187
Q

Therapeutic index of digoxin

A
  • LOW

- Even lower in cachexic animals

188
Q

Indications for digoxin

A
  • Supraventricular arrhythmias, increase contractility

- Supraventricular arrhythmias is when they use it primarily

189
Q

Side effects of Digoxin

A
  • Likes muscle (heart muscle > skeletal muscle > smooth muscle)
  • GI signs first (vomiting, diarrhea, decreased appetite
190
Q

Contraindications for digoxin

A
  • Patients with ventricular fibrillation, frequent or complex ventricular tachycardia, or in digitalis intoxication
  • Caution in patients with renal dysfunction, heart failure, or Subaortic stenosis
  • Relatively contraindicated in cats with hypertrophic cardiomyopathy
  • Use with caution in patients with renal disease (eliminated by kidneys)
  • hypokalemia and hypomagnesemia should be corrected prior to digoxin as they compete for same ATPase binding site
191
Q

Pimobendan MOA

A
  • direct calcium sensitizer and affects calcium at the level of the sarcomere
  • Much better inotropic agent
  • Usually use this instead of digoxin
192
Q

Pimobendan function

A
  • positive inotropic agent

Clinical Pharmacology (7 decks)

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