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Cardiovascular pharmacology - Coggle Diagram
Cardiovascular pharmacology
hypertension treatment
hypertension with diabetes mellitus
ACE inhibitors, ARBs, Ca²⁺ channel blockers, thiazide uretics, β-blockers
hypertension in asthma
ARBs, Ca²⁺ channel blockers, thiazide diuretics, selective β-blocker (avoid nonselective β-blockers, ACE inhibitors)
hypertension with HF
diuretics, ACE inhibitors, ARBs, β-blockers(contraindicated in cardiogenic shock), aldosterone antagonist
hypertension in pregnancy
hydralazine, labetalol, methyldopa, nifedipine
primary hypertension
thiazide diuretics, ACE inhibitors, angiotensin Ⅱ receptor blockers, dihydropyridine Ca²⁺ channel blocker
calcium channel blockers
hypertension, angina, Raynaud phenomenon(dihydropyridines); subarachnoid hemorrhage(nimodipine); hypertensive urgency and emergency(nicardipine, clevidipine); hypertension, angina, AF(non-dihydropyridines)
block voltage-dependent L-type calcium channels of cardiac and smooth muscle→↓muscle contractility
hydralazine
severe hypertension, HF, can be used in pregnancy
↑cGMP→smooth muscle relaxation; arterioles>veins→afterload reduction
hypertensive emergency
nitroprusside: short acting, ↑cGMP→release of NO
fenoldopam: dopamine D₁ receptor agonist: ↓BP, ↑natriuresis (coronary, peripheral, renal, splanchnic vasodilation)
nitrates
vasodilate by ↑NO→↑ in cGMP and smooth muscle relaxation
vein>>arteries→↓preload
angina, acute coronary syndrome, pulmonary edema
contraindicated in right ventricular infarction
antianginal therapy
nitrate: ↓EDV, BP, contractility, ejection time, MVO₂, ↑HR
β-blocker: ↓BP, contractility, HR, MVO₂, ↑ejection time
goal is reduction of myocardial O₂ consumption; MVO₂ (↓EDV, BP, HR, contractility)
double: ↓BP, ↓↓MVO₂, no or little effect on EDV, contractility, HR, ejection time
ranolazine
angina refractory to other medication
inhibit the late phase of sodium current→reducing diastolic wall tension and oxygen consumption
milrinone
short term use in acute decompensated HF
selective PDE-3 inhibitor; ↑cGMP
lipid-lowering agents
ezetimib
↓↓LDH
prevent cholesterol absorption at small intestine brush border
fibrates
↓LDL, ↑HDL, ↓↓↓TG
myopathy, gallstone
upregulate LPL→↑TG clearance, activate PPAR-α to induce HDL synthesis
bile acid resins
↓↓LDH
↓absorption of other drugs and fat-soluble vitamin
prevent intestinal reabsorption of bile acids
niacin
↓↓LDL, ↑↑HDL, ↓TG
hyperglycemia, hyperuricemia
inhibit lipolysis in adipose tissue, reduce hepatic VLDL synthesis
HMG-CoA reductase inhibitors
↓↓↓LDH, ↑HDL, ↓TG
hepatotoxicity, myopathy
inhibit conversion of HMG-CoA to mevalonate
PCSK9 inhibitors
inactivation of LDL-receptor degradation, increasing amount of LDL removed from bloodstream
↓↓↓LDL, ↑HDL, ↓TG
myalgias, delirium, dementia, other neurocognitive defects
cardiac glycosides
HF, AF
cholinergic adverse effect, renal toxicity, hypokalemia
direct inhibition of Na/K ATPase→indirect inhibition of Na/Ca exchange→↑[Ca²⁺]i→↓HR
antidote: slowly normalize K⁺, cardiac pacer, anti-digoxin Fab fragments, Mg²⁺
digoxin
antiarrhythmics
sodium channel blockers (class1)
slow or block conduction, ↓ slope of phase0 depolarization
class 1A
both atrial and ventricular arrhythmias; SVT, VT
↑AP duration(活動電位持続時間), ↑effective refractory period, ↑QT interval
class 1B
↓AP duration, affect ischemic or depolarized Prukinje and ventricular tissue
acute ventricular arrhythmias, digitalis induced arrhythmias
class 1C
prolong ERP in AV node and accesory bypass tract
SVT, VT, AF
contraindicated in structural and ischemic heart disease
β-blocker (class2)
SVT, AF (ventricular rate control)
exacerbation of COPD and asthma, cardiovascular effects
decrease SA and AV node activity by ↓cGMP and Ca current
potassium channel blockers (class3)
AF, ventricular tachycardia
TdP
↑AP duration, ↑ERP, ↑QT interval
amiodarone is lipophilic and has class 1,2,3,4 effects
calcium channel blockers (class4)
nodal arrhythmias, AF(rate control)
↓conduction velocity, ↑ERP, ↑PR interval
other
adenosine: decreasing AV node conduction, very short acting
Mg²⁺: effective in TdP and digoxin toxicity
ivabradine
chronic stable angina in patients who cannot take β-bloccker
selective inhibition of funny sodium channel, prolonging slow depolarization phase, ↓SA node firing