Flashcards in Pharm 5 Cardio pt5 Deck (25)
How do ACE-I & ARBs lower bp?
reduction in systemic vascular resistance with either no effect or a minimal increase in cardiac output
BP reduction is not accomplished by changes in heart rate
How do ACE-I act on the kidneys?
ACE-I act on the renal vasculature to reduce arteriolar resistance, improved renal hemodynamics and improve diabetic nephropathy
CI of ACE-I
Pregnancy: Cat D
Precaution renal impairment
Why precaution ACE I if it protects your kidneys?
It's be helpful unless the kidney disease or CHF is too advanced.
ACE-I have interactions with _, can result in _
diuretics; hyperkalemia can occur with potassium-sparring diuretics or supplements; may increase lithium levels
Prototypical Angiotensin Receptor Blocker (ARB)
ARBs end in:
If Olmesartan 20 mg isn’t holding their bp, you can do what?
Example (only drug in its class)
Good & Bad thing about it
If on this drug for a few weeks and you miss doses, blood pressure does not go back up. It takes up to 2 weeks for bp to go back up.
Inhibits the Na-K-ATP-ase pump, causing an increase in intracellular sodium
This makes an Inotropic effect on cardiac cells through enhancement of excitation-contraction coupling triggered by membrane depolarization
Effects of Cardiac Glycosides (Digitalis) (6)
Inc force of myocardial contraction
Dec SA node by stimulating vagal activity
Prolong conduction to AV node due to this vagal activity
Inc refractory period of AV node
Inc peripheral vascular resistance
Dec heart rate through vegal mechanisms
IV Cardiac Glycoside
3 different types & each's effects
Low dose (below 8) - Inc myocardial contractility and CO, AV dilation
High dose (above 10) - tachycardia, arrhythmia, splanchnic, and renal vasoconstriction. Associated with symptomatic benefit.
continuous home pump infusion (for patients with CHF to improve their quality of life)
4 sites of action of drug that Treat CHF.
What's the mechanism for each?
What drug classes fall into each?
Venous system - Reduce preload. Venous dilators: Nitrates, ACE-inhibitors, Alpha-blockers
Arterial system - Reduce afterload. Arterial dilators: ACE-inhibitors, Hydralazine, Ca++ antagonists, Alpha-blockers
Kidney - Reduce blood volume. Diuretics
Left Ventricle - Inotropics: Digoxin; Myocardial protectants including B-blockers
Scenario to understand Cardiac Glycosides
Think of the AV Node as the neck of the funnel
Digitalis “narrows” the neck of the funnel
__ is the first drug found to slow conduction through the AV Node. Aka narrowing the neck of the funnel.
Digitalis slows down heart rate but __.
Due to this what is more effective?
Takes 18 hours to do so.
A shot of Verapamil takes a couple minutes to do it (more effective time-wise, doesn’t poison the heart, no drug-drug interactions)
Digitali comes in what forms? (3) (both are PO). Which is better absorbed?
tablets are 60-80% absorbed
elixir is 70-85% absorbed
Lanoxi-caps (solution filled capsules) are 90-100% absorbed
Digitalis Distribution (won't be writing this drug)
Highest concentrations are found in the myocardium, skeletal muscle, liver, brain and kidneys
It is not widely distributed in fatty tissues
Digoxin crosses the blood-brain barrier and the placenta
Digitalis Metabolism. How can it be especially dangerous?
How many days until steady state or elimination?
57-75% of digoxin is excreted by the kidneys unchanged
In patients with impaired renal function, significant accumulation may occur
This is especially dangerous because of the 36-hour half-life
6 days are required to reach steady-state or elimination
Digoxin vs Dialysis. Is it removed? Why?
Digoxin is not removed by dialysis because it is distributed in tissue and not blood
Adverse effects of Digitalis (that the boards will ask about)
yellow/green haloes/visual disturbances
How to assess a patient who sees haloes/visual disturbances
If it’s drug-related: Digitalis
If it’s the illness: Glaucoma
*BQ: Digitalis overdose presents itself with what EKG dysrhytmia? What causes it?
You can see any arrhythmia caused by digitalis. Tachy brady arrhythmia is most common. A patient who is tachycardic goes into bradycardia, then goes back and forth over a nonspecific period of time.
Due to the poisoning of the Na-K ATPase pump.