Flashcards in Cardiac Glycosides Deck (32):
Define what Congestive Heart Failure is:
Inability of the heart to provide the necessary output.
List the sequence of events for congestive heart failure:
1. Decreased cardiac output
2. Decreased peripheral bloodflow (anoxia)
3. Decreased renal bloodflow = increased renin production, increased angiotensin, increased aldosterone
4. Increased salt, increased ADH = water retention
5. Increased venous pressure = EDEMA
What occurs when there is insufficient blood flow that further complicates congestive heart failure?
- Reflex Sympathetic output
1. Increases heart rate
2. Increases peripheral resistance
3. Increases oxygen demand
Why are the reflex sympathetic output events undesired effects in CHF?
Increases burden on the heart
What is the target of drug therapy for CHF?
Block the sympathetic nervous system!
Causes of CHF?
1. Atherosclerotic coronary artery disease
2. Myocardial infarction
3. Myocarditis, various cardiomyopathies, valvular and congenital defects
4. Aortic stenosis
5. Systemic hypertension
6. Diet, humidity, exertion, anemia, infection
Name the acute symptoms of CHF
2. Shortness of breath
4. Decreased exercise tolerance
Chronic symptoms of CHF
1. Various arrhythmias
2. Hypertension (increased peripheral resistance)
Symptoms of Left Side Heart Failure:
1. Reduced cardiac output
2. Reduced blood pressure
3. Pulmonary congestion
**More acute in nature
Which side of the heart in heart failure has symptoms more acute in nature?
Left Side Heart Failure
Name the 6 goals of treatment for CHF
1. Slow heart rate to increase the filling time
2. Increase contractile force to improve the ejection fraction (make heart more efficient)
3. Increase cardiac output
4. Reduce retention of salt and water
5. Decrease angiotensin-induced increase in peripheral resistance (block angiotensin to decrease peripheral resistance)
6. Decrease sympathetic nervous system
What is the drug category of choice for CHF?
Name the preparations of Cardiac Glycosides
**digoxin (Digitek, Lanoxin)
Digoxin is metabolized by what organ of the body?
Indications for digoxin
2. Atrial fibrillation/flutter
What is the general mechanism of action and effects of cardiac glycosides?
1. Inhibits Na/K ATPase pump
2. Directly suppresses AV node conduction to increase ERP and decrease conduction velocity
3. Causes diuresis
Explain the effects of the inhibition of Na/K ATPase pump in the action of cardiac glycosides
- This results in increased Ca+ inside of cell
- Increases contraction of the heart
- Positive inotropic effect
What are the effects of suppressing the AV node conduction in cardiac glycosides?
- Slows down repolarization of myocytes following action potentials
- This results in prolonged action potential
***Slows heart rate = negative chronotropic effect
Name the diuretic effects that cardiac glycosides cause:
1. Decreases venous return
2. Allows heart to become more efficient
3. Decreases filling pressure
4. Decreases heart rate
5. Decreases heart size
What are the problems with cardiac glycosides?
1. Increased vagal ouput = can be blocked by atropine (anticholinergic drug)
2. Slowing of AV conduction = can slow too much which allows for ectopic foci = uncoordinated arrhythmias** can arise
3. Low therapeutic index = therapeutic dose is approximately 50-60% of the toxic dose
- Every patient must be titrated
List the general digoxin toxicities:
1. Block conduction between SA node and AV node
2. GI effects result from stimulation of chemoreceptor zones and vagal nucleus (parasympathetic effects)
3. Various CNS effects
Describe more in depth what happens when Digoxin blocks conduction between SA node and AV node
1. Bradycardia occurs because of the lack of conduction (AV block)
a. Because slows heart so much, heart betas before it is full (decreased CO)
2. Since conduction is blocked between upper and lower part of the heart, the lower part of the heart may start beating on its own (extra beats = extrasystoles)
3. **Causes Arrhythmias
List the GI effects that result from digoxin toxicity
2. Increase in salivation
5. Abdominal pain
List the CNS effects of digioxin toxicity
1. Headache = vasodilation, changes in edema in CNS
2. Fatigue = decreased muscle tone (Parasympathetic effect makes you feel fatigue)
4. Visual disturbances (blurry)
5. Green/yellowiah aura = patient knows that he is at toxic level of digitalis if he sees this aura
What are the treatment scenarios for digoxin toxicity
1. Discontinue drug
2. Give antidoe = digoxin immune fab (Digibind, DigiFab)
a. Antibodies bind with digoxin which are then excreted via urine
3. Administer Potassium chloride and anti-arrhythmic medications
Decreased intraceullular levels of what ion potentiates the effects of digitalis?
- K+ (potassium)
*Increasing K+ will decrease the effects of digitalis and is a reason why potassium chloride is used as a treatment of Digoxin Toxicity
The level of digoxin may be increased by concurrent use of what drugs?
- The red flag drugs in dentistry
○ *systemic azole antifungals
○ *macrolide antibiotics
○ This increased risk for toxicity
- Caution with vasoconstrictors - risk for arrhythmias
Know the red flag drugs in dentistry:
- Systemic azole antifungals
- Macrolide antibiotics
In summary, what does Digoxin do?
- Decreases heart rate which increases filling time
- Increases force of contraction so that it can increase ejection fraction
Other than Cardiac Glycosides, what drugs might be helpful for CHF?
1. ACE inhibitors
2. B1 agonists = increase force of contraction to increase cardiac output
3. Vasodilators = decrease preload/afterload; decrease filling pressure and work of the heart
5 dental considerations for a patient on cardiac glycosides
1. Decrease stress for the patient
2. Caution with use of local anesthetics with vasoconstrictors
3. Avoid using gingival retraction cords due to potency of vasoconstrictors
4. Do not recline patient fully: hard to breathe
5. General anesthesia decreases cardiac output and decreases perfusion = dangerous to a patient with CHF