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Cardio Drugs Respons
Response of Cario Drugs
| Question | Answer |
|---|---|
| Bile Acid Binding Resins | Response: decrease LDL, increase TG and HDL |
| Statins | Response: Decrease LDL and TG, increase HDL |
| Cholesterol Absorption Blockers | Response: Decrease LDL and TGs, Increase HDL |
| Niacin (Nicotinic Acid) | Response: Decrease LDL, TGs and VDLD, Increase HDL |
| Fibrates | Response: Decrease LDL and TG, increase HDLIncrease HDL-C b/c of PPARalpha stim of apoA-I and apoA-II expression |
| Nitrates | DECREASE SYSTEMIC VENOUS CONTRACTION (dec work, dec O2 need Dec filling P (preload), Dec syst art contract (decr work, decrease O2 need, dec filling P, decr afterload), Dec pulm/syst edema (dec work), Dec large heart A contrac (inc O2 supp) |
| B-adrenergic Blockers | Response: decrease HR and contractility, arterial blood pressure (decrease O2 demand), increase coronary flow via increase time in diastole (increase O2 supply)HT: decrease CO, renin release and SNS to decrease BP (not sure how or why but it does) |
| Ca Channel Blockers | Response: DV: decrease HR and contractility (decrease O2 demand), All: decrease systemic arterial contraction (decrease O2 demand) and coronary artery contraction (increase O2 supply) |
| Ranolazine | Response: No affect on BP or HR, increase exercise tolerance, decrease anginal attacks |
| Aspirin | Response: PHENOMENAL decrease in risk of death or MI, can see benefits in 1st day of treat! |
| ADP Inhibitors | Response: decrease risk of death or MI, early is better |
| GP IIb/IIIa Receptor Inhibitor | Response: Decrease in risk of death or MI, early is better |
| Heparin | Heparin Response: LMWH > Heparin @ reducing death or MI in combo w/aspirin in unstable angina |
| Fondaparinux | Response: reduce death or MI in ACS (acute coronary syndromes like acute myocardial ischemia) similar to heparins |
| Direct Thrombin Inhib | Response: stable levels of x-coag (not yet proven beneficial in unstable angina) |
| Fibrinolytic (TPA) | Response: recanalize (re-allow flow) thrombotic occlusion, restore coronary flow, reduce infarct size, improve myocardial function and survival over short and long terms |
| Analgesics | Response: decrease pain, anxiety, restlessness, ANS, venous and arterial contraction (all decrease O2 demand) |
| Renin Angiotensin Inhib | dec V and A contrac, SNS, remodeling (for 2nd prevention), TPR (HT), increase renal Na/H2O excretionHF: Response: decrease venous and arterial contraction, VENTRICULAR REMODELING, SNS, preload and afterload, increase excretion of Na and H2O |
| Oral X-Coags | Response: decrease growth of existing thrombi, prevent new thrombi formation |
| Loop Diuretics | Response: increase renal excretion of Na, H2O, K, Ca, Mg, CI and H, relax systemic veins (increase venous capacitance): both cause decrease preload (decreased energy needs), diuretic effect causes decrease in edema (dec dyspnea, like in congestive HF) |
| Thiazide Diuretics | Response: increase renal excretion of Na, H2O, K+, Mg++, Cl- and H+ BUT decrease Ca excretion. Diuretic effect causes decrease in edema (decrease in dyspnea) and proload (dec E need), lower efficacy than loop diurs, activation of RAS (limits use in HT) |
| K+ Sparing Diuretics | Response: increase Na, H2O excretion, decrease Ca, K, Mg and H excretion. Low efficacy alone. |
| Aldosterone Antagonists | Increase excretion of Na, H20, Cl, decrease excretion of Ca, K, Mg and H. Low efficacy alone. Inhibit ventricular remodeling (slows progress of disease b/c aldosterone stim mineralocort in heart, promote fibrous lay down)HT: monother as eplerone |
| Direct Arterial Vasodilators | Response: decrease arteriolar contraction -> decrease afterload -> decrease O2 demand (work) |
| Digoxin | Response: decrease SNS, filling pressure, edema, AV conduction, increase CO, PNS, exercise tolerance and PR (b/c slower conduction @ AV node) |
| B agonists | Response: Increase CO, decrease filling P |
| Phosphodiesterase Inhibs | Response: increase contractility, rate of relax, CO, decrease venous and arterial contraction (DILATE ARTERIOLES), filling pressure and pulmonary arterial contraction |
| Nesiritide | Response: decrease venous (STRONG) and arterial contraction, and filling pressure, increase CO |
| Class IA | Response: decrease conduction and automaticity (b/c Na block), increase refractoriness (b/c K block), QRS (slower conduction, b/c Na channel block) and QT (increased refractoriness b/c K channel block) |
| Class IB | Response: decrease conduction, automaticity (only in abnormal, not in normal) and QT (NOT BIG CHANGE IN EKG) |
| Class IC | Response: decrease CONDUCTION, automaticity, increase QRS (VERY marked) |
| Class II | Response: decrease conduction, automaticity (normal and abnormal), increase PR (delay @ AV node) |
| Class III | Response: increase refractoriness, QT (*), decrease automaticity and PR (minor) |
| Class IV | Response: Decrease AV conduction, and automaticity, increase PR (delay @ AV node) |
| Adenosine | Response: Decrease AV conduction and sinus node rate, increase PR (longer conduction @ AV node) |
| Aliskiren | Response: decrease angiotensin II actions, venous and arterial contraction, SNS, TPRIncrease renal Na/H2O excretion |
Created by:
chavezc3
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