Cardio Drugs Flashcards
(192 cards)
1
Q
Heart Disease
A
Something is wrong with the heart
2
Q
Acquired heart disease
A
- Develop later in life
- Most common in people
- e.g. mitral valve endocardiosis
3
Q
Congenital heart disease
A
- from birth
- e.g. ventricular septal defect
4
Q
Systolic dysfunction
A
- want to improve contractility
- e.g. positive inotropic drug
5
Q
Diastolic dysfunction
A
- issue is with relaxation phase
- Not able to get enough filling
- e.g. Hypertrophic cardiomyopathy
6
Q
Pressure overload heart disease
A
- Stenotic pulmonic valve
- Heart has to work harder against that stenotic valve
7
Q
Volume overload heart disease
A
- More volume in the heart that it has to push out
- e.g. tricuspid valve endocardiosis
8
Q
Congestive heart failure
A
- Heart failure due to accumulation of fluid somewhere
- Location will vary depending on which side of heart failure
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
10
Q
Left sided heart failure
A
- Pulmonary edema
- Cats can get pulmonary edema or pleural effusion (and pleural effusion is easier to manage)
11
Q
What drug would you use for congestive heart failure?
A
- Diuretics!
- Removing excessive fluid
- Furosemide is best at doing this quickly
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)
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
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
15
Q
Endocardiosis Stage B2 treatment
A
- Pimobendan +/- ACE inhibitor +/- spironolactone
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
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
18
Q
Chronic congestive heart failure
A
- Prognosis is 1 year average
- Still treating with diuretics and likely an ACE inhibitor and Pimobendan +/- Spironolactone
19
Q
Acute congestive heart failure
A
- decompensated heart failure
- showing clinical signs; often emergent
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
21
Q
Pimobendan Mechanism of action
A
- Calcium sensitizer and phosphodiesterase inhibitor
- Calcium sensitizer is positive inotropy/contractility
- Phosphodiesterase inhibitor is vasodilation
22
Q
Cost of Pimobendan
A
$80-100/month
23
Q
Indication for Pimobendan
A
- Endocardiosis B2
- Likely endocardiosis C
- Dilated Cardiomyopathy B2
24
Q
EPIC study
A
- Dogs with B2 endocardiosis
- Dogs with Pimobendan went 15 months longer
25
Pimobendan side effects
- Don't need to do kidney or liver monitoring
- Can cause GI signs
- May increase development of arrhythmias
26
PROTECT study
- 9 month benefit for Dobermans with B2 dilated cardiomyopathy that were put on pimobendan
27
Pimobendan route
- Oral
28
Contraindications for Pimobendan (Plumbs)
- Hypertrophic cardiomyopathy, aortic stenosis, etc.
| - Caution in patients with cardiac arrhythmias
29
Monitoring for Pimobendan
- Cardiovascular parameters used to monitor heart function, including ECG, blood pressure, echo studies, and clinical signs
30
ACE Inhibitors examples
- Benazepril and Enalapril
31
ACE Inhibitors Mechanism
- Inhibit Angiotensin Converting Enzyme
- Blocks the RAAS system (which is involved in reabsorbing sodium and water as well as blocking aldosterone secondarily)
-
32
Cost of ACE Inhibitors
$20/month
33
Indication for ACE Inhibitors
- 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
34
ACE Inhibitors excretion
- For Enalapril: Kidney
| - Benazepril: kidney + other
35
ACE Inhibitors Adverse effects (Plumbs)
- GI distress primarily
| - Weakness, hypotension, renal dysfunction, and hyperkalemia could occur
36
Monitoring Enalapril (Plumbs)
- Serum electrolytes, serum creatinine, BUN, urine protein
- Blood pressure
- Periodic CBC with differential
37
Cardiac output equation
- Stroke volume x heart rate
38
Blood pressure equation
- Cardiac output x Systemic vascular resistance
| - Also, = stroke volume x heart rate x systemic vascular resistance
39
Three factors that impact stroke volume
- 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
40
RAAAS goal
- Goal is to maintain blood pressure
41
3 Main Stimuli of RAAAS
1. Decreased perfusion to the kidneys
2. Decreased sodium and chloride to the kidneys
3. Increased sympathetic tone in the autonomic nervous system
42
Effects of Angiotensin II (Should be able to list 7-8)
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
43
Aldosterone actions
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
44
Antidiuretic hormone action location
- Acts at the medullary collecting duct on the basolateral surface
45
Two main functions of antidiuretic hormone
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
46
What establishes medullary concentration gradient?
- Sodium and urea
| - Ascending loop of Henle has the Na/K/2Cl channel which is an ATPase
47
RAAAS pathophysiology in CHF
- 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
48
Ang II muscle hypertrophy and CHF
- Bad for the heart
49
Furosemide Mechanism
- Na/K/2Cl- inhibitor
| - Will immediately activate RAAS, even at normal doses
50
Location of action of Furosemide
- Proximal Loop of Henle
51
Indication of Furosemide
- Basically any congestive heart failure, acute or chronic
52
Contraindications of Furosemide
- Anuric patients
- Progressive azotemia and oliguria
- Patients with existing electrolyte or water balance abnormalities
- Impaired hepatic function
- Diabetes mellitus
53
Side effects
- 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
54
Monitoring for Furosemide
- serum electrolytes
- BUN
- serum creatinine
- glucose
- hydration status
- blood pressure
55
Benefits of ACE inhibitors
- Act pretty upstream in the RAAAS system
56
Drawbacks of ACE inhibitors
- Do not block everything
57
Telmisartin and Semintra MOA
- Angiotensin II receptor blockers
58
Drawbacks of Telmisartin and Semintra
- Mostly cost
59
Side effects of Telmisartan and Semintra
- Hypotensive patients or patients that are volume or electrolyte depleted
60
Route of administration of Telmisartan and Semintra
- Oral route
61
Antidiuretic hormone inhibitors
- Could in theory be used
- Expensive
- Ends in -vaptin
62
Spironolactone Mechanism of Action
- Aldosterone antagonist
63
Spironolactone location of action
- Distal convoluted tubule
64
Functions of Spironolactone
- Mild diuretic (potassium sparing diuretic)
Also blocks aldosterone's actions of causing hypertrophy and fibrosis of the heart
65
Sequential nephron blockade
- 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
66
Contraindications of Spironolactone
- Hyperkalemia, Addison's, anuria, acute kidney injury, or significant renal impairment
67
Monitoring for Spironolactone
- Serum electrolytes, BUN, creatinine
- Hydration status
- Blood pressure if indicated
68
Stenosis and use of Pimobendan
- Avoid Pimobendan in Stage B2 and C
| - Do NOT want to improve contractility in these cases
69
Effect of sympathetic arm of autonomic nervous system on contractility
- Sympathetic will increase contractility
70
Effect of parasympathetic arm of autonomic nervous system on contractility
- Parasympathetic will decrease contractility
71
Receptors on our heart that will increase contractility and respond to sympathetic tone
- Beta 1
72
Functions of Beta 1 receptors on the heart
- Increase sympathetic tone
- Increase contractility
- Increase electrical conduction
- Increase heart rate
- Increase relaxation as well (systole and diastole)
73
Beta blocker drug examples
- Atenolol, timolol, propanolol
74
Atenolol, timolol, propanolol MOA
- Block beta 1 receptors on the heart
75
Indications for Beta blockers
- 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)
76
Overdose signs of Beta Blockers
- Bradycardia, hypotension (lethargy, collapse, exercise intolerance)
77
Giving Beta blockers to a dog with DCM
- Don't do it
| - They have poor systolic function already, and you'd be decreasing systolic function even more
78
Contraindications of beta blockers
- 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
Adverse effects
- Bradycardia, inappetence, lethargy and depression, impaired AV conduction, CHF or worsening of heart failure, hypotension, hypoglycemia, and bronchoconstriction
80
Monitoring of beta blockers
- cardiac function, heart rate, ECG if necessary, BP if indicated
81
Parasympathomimetics
- Don't use that often
| - Other side effects not great (DUMBSLED)
82
Virchow's Triad
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
Hypertrophic cardiomyopathy
- 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
Where do clots tend to form in HCM?
- Left auricular appendage
- Tends to get very large, leading to blood stasis
- Then you get clots
85
Drugs used for HCM
- beta blockers
- Diltiazem (calcium channel blocker)
- At some point can add ACE inhibitor
- NO EVIDENCE that any of these work
86
Drugs for HCM stage B2
- Diltiazem
- Beta blockers
- +/- ACE Inhibitor
87
Amlodipine MOA
- Peripheral calcium channel blockers
| - Blood vessels --> vasodilation
88
Diltiazem MOA
- Central calcium channel blocker
89
Hypertrophic Obstructive Cardiomyopathy
- 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
Therapeutic goals of HOCM
- Decrease contractility
91
Treatment of choice for Stage B2 HOCM
- Beta blockers are treatment of choice
- Primary difference between HCM/HOCM?
- Would likely want to give an anti-platelet drug as well
92
Stage C HOCM Treatment
- Furosemide
- ACE inhibitor
- Beta blocker
- +/- Pimobendan (might counteract beta blocker)
- +/- Spironolactone
- ALSO an anti-platelet drug!
93
Anti-platelet drugs types of clots they work best on
- Primary hemostasis
| - Best for arterial blood clots
94
Anticoagulant drugs
- Secondary hemostasis
95
Intrinsic cascade clotting factors
12, 11, 9, 8
96
Extrinsic cascade clotting factors
7, 3 (both go to 10 or the common pathway)
97
Common pathway clotting factors
10, 5, 2, and 1
98
Vitamin K dependent factors
II, VII, IX, and X
99
Drug of choice for arterial blood clots
- Want something faster
| - Anti-platelet drugs (primary hemostasis)
100
Drug of choice for venous blood clots
- Slower; more time to block fibrin
| - Anticoagulants work better here potentially
101
For really bad clots
- Can use both anti-platelet and anti-coagulant drugs
102
Aspirin drug class
- Antiplatelet
103
Aspirin MOA
- Cyclooxygenase inhibitor (blocking thromboxane II)
104
Aspirin route
- PO
105
issues with Aspirin
- Doesn't work well
106
Clopidogrel drug class
- Antiplatelet medication
107
Aspirin and Clopidogrel length of efficacy
- Entire life of platelet
| - Platelets live 3-5 days
108
Clopidogrel MOA
- Blocks ADP
| - Inactive compound that goes to the liver --> cytochrome P450 --> converted to clopidogrel active metabolite (CAM)
109
Metabolism of Clopidogrel
- Liver
- Important because liver function varies
- Cats may over-respond or under-respond based on Cytochrome P450
110
Drug interactions with Clopidogrel
- Omeprazole we talked about
111
Aspirin contraindications (Plumbs)
- Patients with hemorrhagic disorders, asthma, or renal insufficiency
- Also in patients with bleeding ulcers
112
Adverse effects of aspirin
- Primarily gastric irritation
| - Severe blood loss could result
113
Monitoring aspirin
- Analgesic effect and/or antipyretic effect
- Bleeding times if indicated
- PCV or fecal occult blood tests if indicated
114
Clopidogrel contraindications
- In humans, if active pathologic bleeding is happening
115
Adverse effects of clopidogrel
- Hemorrhage
- Icterus (clopidogrel) - monitor liver values
- Don't need additional monitoring
- Measuring platelet function not fun and not easy or beneficial
116
Monitoring of clopidogrel
- vomiting, bleeding
| - Monitor litterbox for hematochezia, epistaxis, bruising (petechia and ecchymoses)
117
Considerations for surgery of a patient on anti-platelet drugs-
- Need to discontinue those medications 3-5 days prior to surgery
118
Warfarin MOA
- inhibits Vitamin K enzyme which will inhibit factors II, VII, IX, and X
119
Warfarin route
- oral medication
120
Contraindications of warfarin
- High risk of bleeding, but it's cheap
| - Would not be your first choice
121
Rivaroxaban MOA
- Factor Xa inhibitor
122
Rivaroxaban route
- oral medication
123
Rivaroxaban cost
- $200-300/month
- Not that much more effective than Clopidogrel
- Wouldn't necessarily pick this for a cat with an atrial thromboembolism
124
Indication for Rivaroxaban
- 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
Antithrombin III role
- Inhibits Factor Xa
126
Heparin route
- IV or SC
| - usually given as a CRI
127
Heparin MOA
- potentiates antithrombin III
128
Heparin cost
- $
| - Many different sizes
129
Lovenox or Enoxaparin route
- SC
130
Lovenox or Enoxaparin MOA
- potentiator of antithrombin III
131
Lovenox or Enoxaparin cost
- $$$$$$$
| - $200-300/month
132
Lovenox or Enoxaparin safety
- Quite safe
133
Lovenox or Enoxaparin safety precautions
- Use cautiously in patients with hepatic impairment or significant renal dysfunction as it can lead to drug accumulation
134
Side effects of Lovenox or Enoxaparin
- Hemorrhage possible
| - Anemia, thrombocytopenia, nausea, fever
135
Lovenox or Enoxaparin Monitoring
- Baseline CBC with periodic rechecks
- Urinalysis
- Routine coagulation tests usually insensitive
136
Primary clot prevention
- 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
Secondary clot prevention
- Had a clot and want to prevent future clots
138
Bradyarrhythmia value for a dog, cat, and horse
Dog: <70 bpm
Cat: <140 bpm
Horse: <20 bpm
139
Normal rhythm for a dog, a cat, and a horse
Dog: 70-160 bpm
Cat: 140-220 bpm
Horse: 20-40 bpm
140
Tachyarrhythmia for a dog, a cat, and a horse
Dog: >160 bpm
Cat: >220 bpm
Horse: >40 bpm
141
Bradyarrhythmia differentials
- Sick sinus syndrome
- Sinus bradycardia
- AV block (1°, 2°, 3°)
- Atrial standstill
142
Tachyarrhythmia differentials
- Sinus tachycardia
- Supraventricular arrhythmias (singlets, couplets, triplets, runs, atrial fibrillation)
- Ventricular arrhythmia
143
Sinoatrial node function
- Pacemaker of the heart
| - Propagates current across the atrium (P wave)
144
Atrioventricular node function
- 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
Purkinje cells
- 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
Ventricular myocytes
- Takes a longer time
| - Large positive lead (QRS complex)
147
Ventricular repolarization
- T wave
- There is a lot of variation in morphology
- If you have a QRS you have to have a T wave
148
Supraventricular complex
- 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
Ventricular complex
- 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
Ventricular premature complex
- singlet, doublet, triplet
| - 4+ = ventricular tachycardia
151
Ventricular escape
- if you come too late
152
Atrial fibrillation
- 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
Atrial fibrillation
- Have to have a pathologically large heart in small animals
154
Class Ia Vaughan Williams Anti-arrhythmics
- Type of sodium channel blocker
155
Class Ib
- Sodium channel blocker
| - **Used most often in vet med
156
Lidocaine, Mexiletine MOA
- Class Ib
157
Which type of Anti-arrhythmic medication is most often used?
- Class Ib
158
Class Ic Anti-arrhythmic
- Sodium channel blocker
159
Class II Anti-arrhythmic
- Beta blockers
| - e.g. -lols
160
Class III Anti-arrhythmic
- potassium channel blockers
161
Sotalol MOA
- Class III
| - Potassium channel blocker
162
Amiodarone MOA
- Class III
| - Potassium channel blocker
163
Class IV Anti-arrhythmic
- Calcium channel blockers
164
Diltiazem MOA
- Class IV
| - Central calcium channel blocker
165
Class Ib site of action
- Ventricular myocytes
| - Sodium channel blockers only affect ventricular myocytes
166
Lidocaine indication
- Ventricular arrhythmias
| - Ventricular tachycardia and ventricular premature complexes
167
Lidocaine contraindications
- 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
Side effects of lidocaine
- CNS signs: drowsiness, depression, ataxia, muscle tremors
169
Monitoring lidocaine
- ECG
| - Signs of toxicity
170
Beta blockers site of action
- Ventricles as well as nodes
- High sympathetic tone if agonized
- Will also influence ventricular myocyte
171
Beta blockers indication
- Ventricular and supraventricular arrhythmias
- Systemic hypertension
- Tends to be used in patients with arrhythmias or diastolic dysfunction
172
Beta blockers side effects
- Decreased contractility that is moderate to severe
- Can be pro-arrhythmic too
- Bradycardia
- Lethargy
- Inappetence
- Hypotension
173
Beta Blockers Contraindication
- 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
Action potential for ventricular myocytes
- 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
Nodal cell action potential
- 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
Class III blocker indications for use
- Ventricular or supraventricular arrhythmias
| - Often used in boxers with arrhythmogenic cardiomyopathy
177
Effect of Class III channel blockers on contraction
- No effect
| - They work by delaying repolarization to prevent depolarization
178
Side effect of class III channel blockers
- e.g. amiodarone, sotalol
- potential for negative inotropic, chronotropic, and proarrhythmic effects
- can worsen syncope or cause lethargy
179
Contraindications of sotalol
- Asthma, sinus bradycardia, 2nd or 3rd degree heart block, cardiogenic shock, or uncontrolled congestive heart failure
180
Calcium channel blockers/Class IV location of action
- nodal cells only
181
Calcium channel blockers/Class IV indication
- Supraventricular arrhythmias
182
Calcium channel blockers/Class IV Side effects
- Decreased contractility
- Won't impact ability to depolarize or repolarize
- pro-arrhythmic
- Bradycardia
- Lethargy, GI distress, hypotension, etc.
183
Calcium channel blockers/Class IV Contraindications
- 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
Digoxin Actions
- Increases parasympathetic tone by acting on muscarinic receptors on the SA and AV node
185
Digoxin Indication
- Supraventricular arrhythmias
186
Digoxin impact on contractility
- 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
Therapeutic index of digoxin
- LOW
| - Even lower in cachexic animals
188
Indications for digoxin
- Supraventricular arrhythmias, increase contractility
| - Supraventricular arrhythmias is when they use it primarily
189
Side effects of Digoxin
- Likes muscle (heart muscle > skeletal muscle > smooth muscle)
- GI signs first (vomiting, diarrhea, decreased appetite
190
Contraindications for digoxin
- 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
Pimobendan MOA
- direct calcium sensitizer and affects calcium at the level of the sarcomere
- Much better inotropic agent
- Usually use this instead of digoxin
192
Pimobendan function
- positive inotropic agent
