What drugs end in -pril?
ACE inhibitors
- block angiotensin converting enzyme
What do ARBs do?
Arbs block angiotensin II from binding to receptors that cause vasoconstriction
- end in -sartan
What is the vicious cycle of CHF?
- Decreased cardiac performance - impaired pumping ability due to MI, HTN, valve dysfunction, etc.
- Neurohoumoral compensation - incr. symp activity, incr. renin-angiotensin II, incr. aldosterone
- Increased cardiac workload - incr. vascular resistance, incr. fluid volume
- changes in myocardial cell function - structural damage, altered Ca+ transport
- -repeat–
What drugs increase myocardial contraction force?
- Digoxin
- Phosphodiesterase inhibitors
- Dopamine
- dobutamine
What drugs decrease cardiac workload?
- ACE-Inhibitors
- Beta blockers
- Diuretics
- Vasodilators
Improves cardiac pumping ability by elevating intracellular calcium levels and facilitating actin-myosin interaction in cardiac cells; Inhibits the sodium-potassium pump on the myocardial cell membrane. This transport system usually transports sodium out of the cell and transports potassium into it. Inhibition of this pump causes sodium to accumulate within the cell; Increased intracellular sodium leads to increased intracellular calcium; Because more calcium is stored in the cardiac cell, the sarcoplasmic reticulum releases more calcium during each action potential, thereby initiating greater actin-myosin interaction and a stronger cardiac contraction
Digitalis (Digoxin)
- improves symptoms of CHF
- makes pt feel better, but questionable evidence of actually increasing lifespan
What are the symptoms of digoxin toxicity?
- GI distress (nausea, vomiting, diarrhea)
- CNS disturbances (drowsiness, fatigue, confusion, visual disturbances)
- Arrhythmias
- digibind is used to treat toxicity, binds with the drugs and decreases toxic effects
Inhibit the phosphodiesterase enzyme that breaks down cyclic adenosine monophosphate (cAMP) in cardiac cells which enhances myocardial contractility; cAMP acts on membrane calcium channels to allow more calcium to enter the cell
Phosphodiesterase inhibitors
- IV for short term treatment
What are the types of phosphodiesterase inhibitors?
- Inamrinone
2. Milrinone
Decrease morbidity and mortality in patients with CHF; Reduces peripheral vascular resistance by preventing angiotensin II induced vasoconstriction and vascular hypertrophy/remodeling; Limits aldosterone secretion which prevents sodium and water retention; Promotes vasodilation by prolonging the effects of bradykinin
ACE inhibitors
- end in -pril
Stimulate cardiac beta-1 adrenergic receptors, which selectively increases myocardial contraction force; Reserved for patients who do not respond to other positive inotropic agents such as digoxin; May be associated with increased mortality
Dopamine and Dobutamine
Just as effective as ACE-Inhibitors in treating heart failure and preventing mortality; Reduce angiotensin II induced peripheral vascular resistance and cardiovascular hypertrophy/ remodeling by blocking angiotensin II receptors on the heart and vasculature
Angiotensin II Receptor Blocker (ARBs)
- end in -sartan
- as effective as ACE in decreasing mortality
block the effects of norepinephrine and epinephrine on the myocardium to normalize sympathetic stimulation and decrease heart rate
Beta blocker
- non selective are more helpful in CHF than selective
- Newer beta blockers such as carvedilol and nebivolol are especially useful because they also block alpha-1 receptors on the vasculature causing peripheral vasodilation
- end in -olol
What are the ADRs of beta blockers?
- Abnormally slow heart rate
2. Reduced contraction force
What can happened that will disturb the hemostasis balance?
- Insufficient levels of blood-clotting factors = inadequate clotting (hemophilia): Resolved by replacing the missing clotting factors or facilitating the synthesis of specific clotting factors
- Excessive clotting occurs during prolonged bed rest or when blood flow through vessels is partially obstructed: Rectified by drugs that prevent clot formation (anticoagulants, antiplatelets) or facilitate the removal of previously formed clots (fibrinolytics)
What are the 3 categories of drugs used to treat overactive clotting?
- Anticoagulant
- Antiplatelets
- Fibrinolytics
Control the function and synthesis of specific clotting factors; Used to prevent clot formation in the venous system (venous thrombosis)
Anticoagulants
Inhibit abnormal platelet activity; Used to prevent thrombus formation in the arteries that lead to myocardial infarction and ischemic stroke
Antiplatelets
Facilitate the destruction of blood clots; Used to reestablish blood flow through vessels that have been occluded by thrombi
Fibrinolytics
What are the primary anticoagulants?
- Heparin
- Warfarin (Coumadin)
- Direct thrombin inhibitors
- Factor Xa inhibitors
Often the initial treatment of venous thrombosis; Potentiates the activity of antithrombin. Antithrombin binds to several of the active clotting factors (thrombin, IXa, Xa) and renders them inactive; Poorly absorbed from the GI tract – given IV
Heparin
Preferentially inhibits factor Xa; Results in more predictable anticoagulant effect and less lab monitoring; Less risk of adverse effects such as hemorrhage and heparin-induced thrombocytopenia; Used for the treatment of acute venous thrombosis; Used for prevention of DVT’s following surgery or medical conditions
Low Molecular Weight Heparin (LMWH)
- ends in -parin
- as effective as heparin
- given subcutaneously
Interferes with vitamin K metabolism in the liver which impairs the hepatic synthesis of several clotting factors; In the liver, vitamin K acts as a catalyst in the final step of the synthesis of clotting factors II, VII, IX, and X. During this process vitamin K is oxidized to an altered form known as vitamin K epoxide. For the process to continue, vitamin K must be reduced to its original form; this drug blocks the conversion of vitamin K epoxide to vitamin K which impairs the synthesis of several clotting factors; A decrease in the level of circulating clotting factors results in a decrease in blood coagulation.
Warfarin (Coumadin)
- oral anticoagulant
- several days before full effect
- monitoring needed; lots of drug/drug and drug/food interactions
- cheap
- requires frequent INR monitoring
Bind directly to the active site on thrombin and inhibit thrombin’s ability to convert fibrinogen to fibrin; Approved for preventing stroke and systemic embolism in patients with Afib; May be helpful in preventing other coagulation disorders such as DVT
Direct throbbing inhibitor; Dabigatran (Pradaxa) - oral - Praxbind-antidote available - May have several advantages: More effective, Improved safety, Less drug-drug interactions, Reduced risk of hemorrhagic stroke,Fewer adverse effects
