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Cardio Drugs Respons

Response of Cario Drugs

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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