Patho Cardio Drugs

Anticoagulants can prevent the clotting process, but they do not break down clots that are already there. To do that you need a thrombolytic drug.

Anticoagulants = prophylactic.

Thrombolytics break down the thrombus (clot) itself, whereas fibrinolytics specifically break down the fibrin in the clots but leave the thrombus itself intact.

I could be wrong about that; the terms seem to be used interchangeably.

Tricky question. Anticoagulants do not actively break down existing clots themselves; however, they do help. By preventing any further clotting from happening, they allow your body's natural processes to break the clots up easier.

Heparin - Parenteral

Coumadin - Oral

Dabigatran

Pradaxa

Anticoagulant

It activates the enzyme Antithrombin III, a natural anticoagulant found in the body, greatly increasing its efficacy. This complex will go around inhibiting mainly thrombin and Factor Xa.

Fractionated Heparin is also called Low Molecular Weight Heparin (LMWH). It is heparin that has been processed to sort out only small molecules of heparin. Long story short, small molecules of heparin will affect thrombin less and affect Factor Xa more. This makes its effects more predictable.

thrombin

IIa

(II as in roman numeral for 2. "a" means activated)

subq for DVT prevention.

IV for treating DVT that has already occurred.

UFH (unfractionated heparin)

aPTT, as well as a platelet count

PT/INR

1.5 to 2.5

HAT - Heparin Associated Thrombocytopenia.

HIT - Heparin Induced Thrombocytopenia.

Xa, IIa

Less

Neither. If they've had HIT before, you don't give heparin.

"-parin"

Pretty easy. Ex: Enoxparin, Dalteparin.

Anticoagulant. Synthetic pentasaccharide that is used in place of heparin in patients with HIT. Has no risk of HIT. Binds only to antithrombin, leaves thrombin and platelets alone.

Heparin, LMWHs, and fondaparinux would all be fairly useless, since they all work mainly on antithrombin. This patient would need a Direct Thrombin Inhibitor, a class of drugs that work on thrombin and do not need antithrombin.

Work directly on Factor IIa (thrombin), without requiring the present of antithrombin. Given parenterally. Mainly used on patients with HIT.

Direct Factor Xa Inhibitors. Anticoagulants. Inhibit Factor Xa without needing antithrombin.

Inhibits clotting by interfering with Vitamin K and preventing synthesis of clotting factors II, VII, IX, and X, as well as Protein C and S.

Usually around 2.0-3.0.

For heart valves, up to 3.5.

plasminogen, plasmin

plasminogen

plasmin

An important enzyme in the blood that breaks down clots

Block either Beta or Alpha receptors (or both), blocking the SNS. This tends to lower BP. As such, they are often used to treat hypertension, or heart failure.

Inhibit Angiotensin-converting-enzyme. Used to treat hypertension and heart failure.

Reduce the activity of the RAAS. Cause relaxation of blood vessels, as well as a decreased blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart.

Angiotensin Receptor Blockers (ARBs)

ACE Inhibitor. Often used to treat hypertension or heart failure.

Often used to treat hypertension. Their main effects are:

- Vasodilation.

- Reduced force of heart contraction.

- Reduced heart rate.

- Reduced aldosterone production.

Works on the vascular smooth muscle, causing them to vasodilate.

(this only works on arteries; no effect on veins)

Reduces force of contraction, and reduces heart rate

<140 systolic

and

<90 diastolic

<150 systolic

and

<90 diastolic

Trade name Aldactone. Primarily used to treat heart failure.

BNP - B-Type Natriuretic Peptide. It is a hormone that the heart releases when it's too extended; a test for this can give an indication on how heart failure is improving or worsening.

white from the fluid, as opposed to clear (normal)

Alpha and Beta. Each with subtypes.

α1, α2

β1, β2, β3

The Sympathetic Nervous System (SNS)

Cathecholamines, specifically: epinephrine and norepinephrine

Arterial vasoconstriction

Decrease SNS outflow

Primarily cardiac effects.

+inotropic and +chronotropic.

Increases HR and contractility.

Smooth muscle relaxation, bronchodilation, dilates some arteries.

Main thing to remember is the pulmonary effect: dilation of bronchial smooth muscle.

Beta 2

"-olol"s

ex: Metoprolol, propranolol

Beta 2

Beta receptors get activated by epinephrine and norepinephrine, and cause stress responses as a part of the SNS. Beta Blockers are BLOCKING this effect. So they're basically blocking the SNS; i.e., flight-or-flight type responses.

Bronchoconstriction

We want to target the Beta 1 receptor, which has more cardiac effects. Beta 2 receptors are more pulmonary, and blocking them can cause bronchoconstriction, which we probably dont want.

- Bradycardia

- Decreased AV node conduction (heart block)

- Reduced contractility

- Bronchoconstriction

Beta Blockers can mask S/S of hypoglycemia

When using, your body can up-regulate the blocked receptors and become more sensitive. If you've been taking them for a while and stop, the symptoms can come back even more severely. Can lead to angina, palpitations, MI, rebound hypertension.

Alpha 1 Blockers

Blocking vasoconstriction of vascular smooth muscle. So vasodilation.

Trade name Coreg. Combination of Nonselective Beta Blocker and Alpha 1 Blocker.

Carvedilol

Angiotensin II from Angiotensin I

Potassium. Inhibits potassium secretion, so the patient may end up with hyperkalemia.

ACE Inhibitors.

Ex: Lisinopril, Captopril, Enalapril

AT1 Receptor Blockers (ARBs)

Also called Angiotensin Receptor Blockers (ARBs). Mainly used to treat hypertension.

Hypertension, heart failure, and also kidney disease

Very little. They accomplish almost the same thing. The only notable difference is that ACE Inhibitors cause a characteristic cough, and ARBs dont.

Down-regulation leading to resistance. As you use Nitrates, your body down-regulates the receptors for them and everything becomes far less sensitive to them.

Both

Decrease it. Nitrates dilate the veins, which causes decreased preload.

Using them before activity to prevent activity-induced angina. Ex: you're about to go for a walk, and you know walking that distance will give you angina, so you pop a nitroglycerin tab to prevent it before it happens.

They can take 1 tab, and if it helps, they can take up to 3 more. If it the pain is not gone after 3, go to hospital. If the pain does not subside after the first tab, go to hospital.

Risk for them going bad. Nitroglycerin doesn't have a great shelf life. If they aren't using the tabs and just store them at home, they need to make sure to get new ones as needed.

Firstly, inhibits the Na/K Pump on the myocyte membrane. Secondarily, it inhibits Ca extrusion. The result is more calcium ions in the cell to be taken up by the SR, so more is available for release, giving stronger contractions.

contractility, heart rate

Atrial fibrillation

Whether the symptoms of HF are being managed. Activity tolerance, dyspnea, etc. Digoxin doesnt effect mortality; if it isnt helping their symptoms and improving their quality of life they shouldnt be on it.

osmotic diuretic

Loop Diuretics. Called that because there's a high ceiling for the amount that you give with increasing effects. In other words, the more you give the more effect it'll have.

This sounds obvious, but most of the other diuretics dont work this way; they have a max effect that you basically get with any dose above a certain point.

Oral and IV

Lasix

furosemide

Lasix (furosemide)

less

Also have an effect on water and sodium content of arteriole walls. Are potentially direct vasodilators.

Basically, they have some effects on blood vessels in addition to their mild diuretic poperties

Potassium

Potassium

Antiarrhythmic. Potassium channel blocker. Most commonly prescribed to treat dysrhythmias. Long onset, very long duration of effect.

Many drug interactions. Inhibits most cytochrome proteins in the liver.

Assume it will increase the levels of other drugs. It inhibits the liver's cytochrome proteins.

HMG-CoA Reductase Inhibitors.

Antilipemics.

statins

statins

Increases LDL catabolism and decreases LDL synthesis. Result is decreased LDL and overall cholesterol levels

Statin

Statin

liver

dilation