treatment of congestive heart failure
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Treatment of congestive heart failure. Overview of congestive heart failure - PowerPoint PPT PresentationTRANSCRIPT
Overview of congestive heart failureOverview of congestive heart failureCongestive heart failure (CHF) is a condition in which the heart is unablCongestive heart failure (CHF) is a condition in which the heart is unable to pump sufficient blood to meet the needs of body. CHF can be incree to pump sufficient blood to meet the needs of body. CHF can be increased workload imposed on the heart. CHF is accompanied by abnormal ased workload imposed on the heart. CHF is accompanied by abnormal increases in blood volume and interstitial fluid; the heart, veins, and capincreases in blood volume and interstitial fluid; the heart, veins, and capillaries are therefore generally dilated with blood. Hence the term “congillaries are therefore generally dilated with blood. Hence the term “congestive(estive( 充血性充血性 )” heart failure, since the symptoms include pulmonary co)” heart failure, since the symptoms include pulmonary congestion with life heart failure, and peripheral edema with right heart failngestion with life heart failure, and peripheral edema with right heart failure. Underlying causes of CHF include arteriosclerotic heart disease, hyure. Underlying causes of CHF include arteriosclerotic heart disease, hypertensive heart disease, valvular heart disease(pertensive heart disease, valvular heart disease( 心瓣膜病心瓣膜病 ), dilated car), dilated cardiomyopathy(diomyopathy( 扩张性心肌病扩张性心肌病 ), and congenital heart disease(), and congenital heart disease( 先天性心脏先天性心脏病病 ). ). Left systolic dysfunction secondary to coronaryartery disease is thLeft systolic dysfunction secondary to coronaryartery disease is the most common cause of heart failure.e most common cause of heart failure.
Treatment of congestive heart failureTreatment of congestive heart failure
Heart FailureHeart Failure
Final common pathway for many cardiovaFinal common pathway for many cardiovascular diseases whose natural history resuscular diseases whose natural history results in symptomatic or asymptomatic left vlts in symptomatic or asymptomatic left ventricular dysfunctionentricular dysfunction
Cardinal manifestations of heart failure inCardinal manifestations of heart failure include dyspnea, fatigue and fluid retentionclude dyspnea, fatigue and fluid retention
Risk of death is 5-10% annually in patients Risk of death is 5-10% annually in patients with mild symptoms and increases to as hiwith mild symptoms and increases to as high as 30-40% annually in patients with advgh as 30-40% annually in patients with advanced diseaseanced disease
Main causesMain causes
Coronary artery diseaseCoronary artery disease HypertensionHypertension Valvular heart disease Valvular heart disease (( 心瓣膜病心瓣膜病 )) Cardiomyopathy Cardiomyopathy (( 心肌病心肌病 )) Cor pulmonaleCor pulmonale
Compensatory Compensatory changes in heart changes in heart failurefailure Activation of SNSActivation of SNS Activation of RASActivation of RAS Increased heart rateIncreased heart rate Release of ADHRelease of ADH Release of atrial natriuretic peptideRelease of atrial natriuretic peptide 心钠素心钠素 Chamber enlargement Chamber enlargement 心室腔扩大心室腔扩大 Myocardial hypertrophy Myocardial hypertrophy 心室肥厚心室肥厚
Classification of heart Classification of heart failurefailure Class I: No limitation of physical Class I: No limitation of physical
activityactivity Class II: Slight limitation of physical Class II: Slight limitation of physical
activityactivity Class III: Marked limitation of Class III: Marked limitation of
physical activityphysical activity Class IV: Unable to carry out Class IV: Unable to carry out
physical activity without discomfortphysical activity without discomfort
New classification of New classification of heart failureheart failure Stage A: Asymptomatic with no heart Stage A: Asymptomatic with no heart
damage but have risk factors for heart damage but have risk factors for heart failurefailure
Stage B: Asymptomatic but have signs Stage B: Asymptomatic but have signs of structural heart damageof structural heart damage
Stage C: Have symptoms and heart Stage C: Have symptoms and heart damagedamage
Stage D: End stage diseaseStage D: End stage disease
ACC/AHA guidelines, 2001ACC/AHA guidelines, 2001
心功能障碍
收缩功能 舒张功能
输出量
神经激素 心肌 1 受体RAA
CA 心缩力
顺应性
心肌肥大、重构 钠水潴留
血容量
静脉淤血
血管收缩
阻抗顺应性后负荷
血管肥厚、重构
前负荷
抗 RAA 系统药
改善舒张功能药正性肌力药
受体阻断药
利尿药
减前负荷药
减后负荷药
恢复心血管病理形态的药
CHF 的病理生理过程及可能治疗的环节 CHF 的病理生理过程及可能治疗的环节
长期病情心率
Strategy of treatment of Strategy of treatment of CHFCHF
The therapeutic goal for CHF is to increase cardiac The therapeutic goal for CHF is to increase cardiac output.output.
1)1) Inotropic agents that increase the strength of conInotropic agents that increase the strength of contraction of cardiac muscletraction of cardiac muscle
2)2) PDEI (phosphodiesterase inhibitors) agents that iPDEI (phosphodiesterase inhibitors) agents that increase cAMP to induce systoles and vasodilatatincrease cAMP to induce systoles and vasodilatationon
3)3) Calcium sensitizers extracellular fluid volumeCalcium sensitizers extracellular fluid volume4)4) adrenergic agonistadrenergic agonist5)5) adrenergic antagonistadrenergic antagonist6)6) Vasodilators: Calcium channel blocker Vasodilators: Calcium channel blocker 7)7) Decreasing RAS activity: ACEI and AT1 antagonist Decreasing RAS activity: ACEI and AT1 antagonist 8)8) Diuretic agentsDiuretic agents
Treatment of congestive heart Treatment of congestive heart failurefailure
ClassificationClassification1 Positive inotropic drugs1 Positive inotropic drugs Cardiac glycosidesCardiac glycosides β-adrenergic agonists (New dopamine receptor agonβ-adrenergic agonists (New dopamine receptor agon
ist)ist) phosphodiesterase inhibitors phosphodiesterase inhibitors Calcium sensitizersCalcium sensitizers2 Diuretics2 Diuretics3 Vasodilators3 Vasodilators Calcium channel blocker Calcium channel blocker Nitryl-vasodilatorsNitryl-vasodilators HydralazineHydralazine4 RAAS inhibitors: antiotensin converting enzyme inhibi4 RAAS inhibitors: antiotensin converting enzyme inhibi
tor and AT1 antagonisttor and AT1 antagonist5 β-receptor blocker5 β-receptor blocker
Classification1 Positive inotropic druClassification1 Positive inotropic drugsgsCardiac glycosides/Cardiac glycosides/ 强心苷类强心苷类
structure-activity relationship structure-activity relationship A cardiac glycoside molecule consists A cardiac glycoside molecule consists
of an aglyconeof an aglycone 苷元 苷元 or geninor genin 配基配基 , w, which possesses the same pharmacolhich possesses the same pharmacologic activity as the whole molecule cogic activity as the whole molecule combined chemically with one or morombined chemically with one or more sugars.e sugars.
Cardiac glycosidesCardiac glycosides
O
OOHCH3
CH3
HOC18 H31O9
12
A
C
B
D17
3
DigitoxinDigoxin
= H at 12 C= OH at 12 C
Sugars- 3 mols. of digitoxose 3 分子洋地黄毒糖
Aglycones苷元
Unsaturated lactone不饱和内酯环
steroid nucleus甾核
Convey the pharmacological activity
Convey cardiotonic activity
Modulate potency and pharmacokinetic distribution
O
OOHCH3
CH3
HOC18 H31O9
12
A
C
B
D17
3
1. The relationship between structure and effects
The Indispensable parts of activity
C14
C
C
The number of -OH and glycose will decide water-solubility and lipid-solubility
活性基团活性基团 activity :: C17 C17 不饱和内酯环不饱和内酯环 Unsaturated lactone 、、 C14C14 羟基羟基 OHOH 、、 C3 C3 洋地黄毒糖洋地黄毒糖 digitoxose
脂溶性脂溶性 lipid-solubility : : C3 C3 洋地黄毒糖;水溶性洋地黄毒糖;水溶性 water-solubility :: C12C12 及其他位点的羟基数及其他位点的羟基数
Classification of cardiac glycosides
1. grade 1: in plant, cedilanide 2. grade 2: extract of digitalis Digitoxin (洋地黄毒苷) , Digoxin (地高辛) ,
Deslanoside (旋花毛地黄苷) , Strophanthin K(毒毛旋花子苷 K)
3.3. 地高辛和洋地黄毒苷地高辛和洋地黄毒苷 CC33 位均联结位均联结 33 个洋地黄毒糖,个洋地黄毒糖,地高辛地高辛 CC1212 位多一个羟基,毒毛花苷位多一个羟基,毒毛花苷 KK 的甾核上有的甾核上有多个羟基,所以多个羟基,所以脂溶性:洋地黄毒苷脂溶性:洋地黄毒苷 >> 地高辛地高辛 >>毒毛花苷毒毛花苷 KK 。。
Process of drug through bodyDrugDrug AbsorptioAbsorptio
n rate n rate (%)(%)
ProteiProtein-n-bindinbinding (%)g (%)
HeptoeHeptoenteral-nteral-circulatcirculation (%)ion (%)
BiotraBiotransformnsformation ation (%)(%)
Kidney Kidney excretioexcretion (%)n (%)
TT1/21/2
digitoxindigitoxin 90~10090~100 9797 2727 30~7030~70 1010 5~7 5~7 dayday
digoxindigoxin 60~8560~85 <30<30 6.86.8 5~105~10 60~9060~90 33~36 33~36 hh
CedilanideCedilanide 20~4020~40 55 Few Few Quite Quite fewfew
90~10090~100 33 h33 h
StrophanthiStrophanthin Kn K
2~52~5 55 Few Few 00 90~10090~100 12~19 12~19 hh
Pharmacologic actionPharmacologic action
I. Action of cardiac glycosides on the heartI. Action of cardiac glycosides on the heart
1.1.Positive inotropic actionPositive inotropic action :: Increasing coIncreasing contractility of cardiac muscle in heart failurntractility of cardiac muscle in heart failure. e.
(1) characteristic:(1) characteristic:A.A.myocardiac quick contractionmyocardiac quick contraction, Q-T period, Q-T period
↓ ①rate of force ↑↓ ①rate of force ↑ ② ②time to peak tension ↓time to peak tension ↓
B. no increase oxygen consumptionB. no increase oxygen consumption : : the increase in output is not accompanithe increase in output is not accompanied by an equivalent increase in oxygen ed by an equivalent increase in oxygen consumptionconsumption
Factors of oxygen consumptionFactors of oxygen consumption :: 11 )) Myocardia contractilityMyocardia contractility 22 )) Heart rate Heart rate 33 )) Myocadiac fiber length and toneMyocadiac fiber length and tone
Factors affect consumption of oxygen
I. The force of cardiac contraction
II. Heart rate
III. Volume of ventricular
C. Effect of positive inotropic act
① cardiac output is increased ② compensatory sympathetic tone is reduced ③ cardiac preload and afterload is decreased ④ heart rate is reduced ⑤ myocardiac fiber tone and oxygen consumption is decreased
⑥ increasing stroke volume causes a decrease in end-systolic volume
(2) Machanism of cardiac glycoside on positive inotropic action
A. Inhibiting Na+-K+-ATPase in therapeutic dose:
B. Increasing of calcium inward and induce the releasing of calcium from sarcoplasmic reticulum ( internal stores, by CICR)
α β↓ ↓
↓
↓
↓
glycoside→
Structure changes
Enzyme activity ↓
Na+↑, K+↓ in cell
Ca2+Na+exchange↓ in cell)↓
Na+-K+-ATPase is a recetor of glycoside
Mechanism of pharmacological act
Na+-K+-ATPase is the receptor of cardiac glycosides , so cardiac glycosides act by inhibiting the membrane Na+-K+-ATPase pump → Na+ i
→ Na+ i
Bidirectional exchange
① Na+ enter ↓ → Ca2+ ↓ outer
② Na+ outer ↑→Ca2+ ↑ enter
→by Na + /Ca 2+exchanger
→ Ca2+ i↑
Ca2+ -induced Ca2+ release
Sarcoplasmic reticulum release Ca 2+
Enhance the increased cytosolic calcium concentration
Sarcoplasmic reticulum
→ Ca 2+ i↑
2.Negative chronotropic 2.Negative chronotropic actionaction
A. Continuous effect of positive A. Continuous effect of positive inotropic action inotropic action
decreasing sinus ratedecreasing sinus rate
heart rate is decreasedheart rate is decreased
Heart rate is decreased,Atropine can antagonize (block)
B. Increasing sensibility of myocardia to vagus nerve (increasing of potassiu(increasing of potassium outward and resting potential,m outward and resting potential, redreducing of automaticity).ucing of automaticity).
3. Affects of glycosides 3. Affects of glycosides to conductive tissuesto conductive tissues
A. Increasing conduction of the atrial A. Increasing conduction of the atrial muscle fibers, because increasing muscle fibers, because increasing excitation of vagus nerve (increasing excitation of vagus nerve (increasing of potassium outward).of potassium outward).
Increasing resting potential.Increasing resting potential.
Elevating rate of phase-0 Elevating rate of phase-0 depolarization. Acceleration rate of depolarization. Acceleration rate of depolarization phase-0 and atrial depolarization phase-0 and atrial fibers conductionfibers conduction..
B. Slowing (depress) conduction at the atrioventricular (A-V) node (inhibiting Na-K-ATPase, reducing resting potresting potentialential), and increase effctive refractory period
atrial fibrillation, atrial flutter, paroxymal (and) or supraventricular tachycardia
C. Increasing automaticity of Purkinjie fibres : toxicity
A.A. If If Na+-K+-ATPase was inhibited more tha was inhibited more than 30%, n 30%, cardiac glycosides cardiac glycosides would induce would induce toxicity by the overload of intercellular free calcium concentration in myocardiac. (decrmyocardiac. (decreasing easing inotropic action))
B.B. If intercellular potassium concentration waIf intercellular potassium concentration was lower level, s lower level, cardiac glycosides cardiac glycosides would eawould easily induce sily induce toxicity in myocardiac. (arrhythmyocardiac. (arrhythmia)mia)
Mechanism of toxicity act
4. Affects of cardiac glycasides to ECG (electrocardiography)
A. Therapeutic dose:T-wave can become low, flat, isoelectric
or invertedS-T segment falls below the isoelectric lineP-R interval is lengthened, which is
associated with slower or delayed A-V conduction
Q-T interval is shortened, ERP and APD is shortened in Purkenje fibers
B. Higher dose: arrhythmias
The affects on ECG
T wave
It is characterized by an descend ST segment on the ECG
P-R
Q-T
P-P
Directly inhibit or reflected decrease sympathetic activity
• Exciting increase the vagal activity
• Inhibit RAAS system, promote the excrete of ANP
• cause arrhythmias (toxic doses)
II. Action of cardiac glycosides onII. Action of cardiac glycosides on vascular and kidney • Vasoconstriction, increase in peripheral vascular resistance
• Diuretic , increase the blood flow through kidney and inhibit Na+-K+-ATPase → Na + decreased re-absorb
II. Action of cardiac glycosides on II. Action of cardiac glycosides on neural and hormone
Clinical uses
1. Cardiac glycosides are given for CHF
Effects : Best go with atrial fibrillation
Better hypertension congenital heart disease
not good anaemia lack of vitamin B1 not useful pericarditis 心包炎
2. Some kinds of arrhythmias
Atrial fibrillation
Atrial flutter
Supraventricular Tachycardia
Toxic effects
1. Responses of stomach-intestines :
Anorexia 厌食 , nausea , vomiting ,
Abdominal pain and diarrhoea
2. CNS: visual disturbaces
3. Arrhythmia: 1) Tachycardia 2)AV block 3)Bradycardia <60 beat/min
Prophylaxis and treatment of the toxicity
• Clear the signal of toxic and the indication of withdraw
• Inspect the concentration of digoxin (3ng/ml), digitoxin(45ng/ml)
• If necessary ,potassium supplements and antiarrhythmic drugs ( phenytoin ,lidocaine,atropine )administered
• For severe intoxication ,antibodies specific to cardiac glycosides are available
Method of administration
• Classical : whole effect dose
quick or slow (have use digoxin within two weeks)
The suitable dose to the patients
• Maintain : 4 ~ 5 t ½
Digoxin 0.25mg/day , 6 ~ 7 day ( t ½ 33 ~ 36 hours)
Classification1 Positive inotropic drugsClassification1 Positive inotropic drugs -Adrenoceptor agonists
They are used intravenously in CHF emergenciesExample of -Adrenoceptor agonists :
Dobutamine ( 多巴酚丁胺 )• Exciting β1 Adrenoceptor → positive inotropic action →the volume of output↑• Exciting β2 Adrenoceptor→dilate the vascular → afterload↓
have benefits within short time
Classification1 Positive inotropic drugsClassification1 Positive inotropic drugs Phosphodiesterase- inhibitorsⅢ
Inodilator / inodilating drugs
Inhibiting the activity of PDE Ⅲ → cAMP↑→ causes an increase in myocardial contractility and vasodilatation →total peripheral resistance →cardiac output ↑
Examples:
Armirinone (氨力农) : Inhibits the excess product of NO, TNF and affects the neurohormone, anti-the forming of thrombus
milrinone (米力农) : stronger 20 time
vesnarinone (维司力农) : myocardial contract element’s the sensitivity to calcium
Classification1 Positive inotropic drugsClassification1 Positive inotropic drugs Calcium sensitizers
Pimobendan 匹莫苯 :
Inhibit PDE ; increase TnC’s sensitivity to calciumⅢ
Tn troponin— 肌钙蛋白; myosin -肌球蛋白; tropomyosin -原 ; Actin 肌动蛋白
Classification 2Classification 2 Diuretics
Diuretics inhibit sodium and water retention, →reduce the volume of blood, →venous pressure and the thus cardiac preload are reduced↓, increasing the efficiency of the heart as a pump→ cardiac output ↑, so reduce oedema due to heart failure
Heart failure
• Low-grade : Thiazides hydrochlorothiazide 氢氯噻嗪
• Higher-grade : Acute left heart failure
loop diuretics --- furosemide 呋塞米(速尿)
Spironolacton 螺内酯
( anti-aldosterone ,keep potassium and diuretics)
Antiotensin converting enzyme inAntiotensin converting enzyme inhibitor (ACEI) and AT1 antagonisthibitor (ACEI) and AT1 antagonist
Calcium channel blocker Calcium channel blocker Nitryl-vasodilatorsNitryl-vasodilators HydralazineHydralazine
Classification 3Classification 3 Vasodilators
bradykinin
aldosterone
ACEI and AT blocker
Classification 3Classification 3 VasodilatorsAngiotensin-converting-enzyme inhibitorinhibitor (ACEII )
Captopril Enalapril
Methanism of anti-CHF:
1) Humour: Inhibit ACE→angiotensin Ⅱ and aldosterone levels↓, reduce sodium retention, increase bradykinin levels , ANP 、 NO 、 PGI2↑, reduce the release of NA ET and renew the expression of βreceptor
2) This therefore causes vasodilatation (include coronary artery) →reduction in peripheral resistance→ increase the cardiac output, Increase the blood flow of kidney so Improve the function of kidney
3) Prevent the remodel of the heart
AT1 antiagonists
Losartan (氯沙坦)The function just like ACEⅠ
It dosen’t influence bradykinin levels
Clinical utilize:
• CHF
• Protection of kidney
Calcium-channel blockers
Amlodipine 氨氯地平
Dilate artery
Dilate the coronary
Alleviate the LV Wall Tension
Vessel
Dilatation of the veins→ decreases preload
Dilatation of the artery→ decreases afterload
Decrease the oxygen demand of the heart
mechanism
Others --- Vasodilators
Nitrate esters: nitroglycerin , nitroprusside sodium 硝普纳
Hydralazine 肼屈嗪 direct dilate the vascular
Prazosin 哌唑嗪 ɑ- receptor blocker
Classification 4Classification 4 receptor blocker
Carvedilol 卡维地洛
labetalol 拉贝洛尔
Bisoprolol 比索洛尔
Carvedilol 卡维地洛
mechanism
• Anti RAAS system • Anti-arrthymias• Anti-myocardial ischemia
Cardiomyopathy 心肌病
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二 other action of cardiac gylcosides 1. Nerve system Toxic concentration:enhancing sym
pathetic activity increasing sympathetic impulse of p
reganglial and afterganglial fibers, can cause atrial fibrillation and ventricular tachycardia.
Therapeutic dose: increasing parasympathetic center in brain stem excitation------slowing rate of heart,inhibiting conduction
2. Effect of cardiac glycosides to kidney
①increasing renal blood flow and filtering rate of glomerulus
②competitive antagonism with aldosterone in proximal tubule
Clinical uses
1. Congestive heart failure *Depends in part on the cause of
the failure *Depends in part on the severity
of cardiac damage
A. The best therapeutic effect is the chronic, low-output form
Such as: heart failure with atrial fibrillation an rapid heart rate
B. The better therapy is
heart failure caused by hypertension, heart disease caused by coronary atherosclerosis Valvular stenosis( 瓣膜狭窄) Rheumatic valvulitis (风湿性瓣膜炎)
C. No better
Thyrotoxicosis (甲状腺中毒症) Thyroidism (甲状腺功能亢进)
Serious anemia Vitamin B deficiency Advanced valvular stenosis
D. No use pulmonocardiac disease activity carditis serious myocardia injured
(1) Activity rheumatic (2) other forms of infectious or toxic m
yocarditis , pulmonocardiac disease(3) advanced cardiomyopathy 心肌病(4) badly damaged hearts cardiopericarditis 心包炎
E. Acute heart failure
iv.Use strophanthin K cedilanide
}
2. Atrial fibrillantion
Ventricular rate ↑
↓
↓
↓
Atrial rate :400~650/min
Circulative blood flow ↓
Heart failure
Cardiac gylcosides
ventricular rate ↓ (atrial fibrillation)
Circulative blood flow volume ↑
(relive) sysptoms of heart failure
↓
↓
↓
•In atrial fibrillation, the same vagomimetic action helps control ventricular rate, thereby improving ventricular filling and increasing cardiac output.•Slowing conduction in A-V node,increasing concealed conduction (隐匿性传导) ,slowing ventricular rate.
Concealed conductionConcealed conduction
The impulses arriving at the AV The impulses arriving at the AV node are rapid and random in node are rapid and random in time. Most of these impulses time. Most of these impulses either fail to enter the AV node either fail to enter the AV node because it is refractory or because it is refractory or propagate only partway through it propagate only partway through it and give rise to the phenomenon and give rise to the phenomenon of concealed conduction.of concealed conduction.
3. Atrial flutteratrial rate : 320~360 beats/min, rapid and
regular In atrial flutter, the depressant effect of the
drug on atrioventricular conduction will help control an excessively high ventricular rate. The effects of the drug on the atrial musculature may convert flutter to fibrillation, with a further decrease in ventricular rate
Therapeutic action:
(1)Increasing block and ERP in atrioventricular (AV) node
heart rate decrease (ventricular rate)
(2) Shortening ERP of atrium
(convert) atrial flutter →atrial fibrillation
(3) After withdrawal cardiac glycosides, sinus rhythm may return, ERP increase (prolong ERP of shortened ERP in atrium)(4) Quinidine may convert atrial flutter to sinus rhythm , but may increase the risk of cardiac glycosides toxicity.
3. Paroxysmal supraventricular tachycardiaIncreasing function of vagal nerveEnhance vagal activityDecrease excitation of atriumNo use: supraventricular
tachycardia caused by glycosides------intoxication
Toxicity of cardiac glycosides1. Gastrointestinal and centre nerve systom occasions sickness , vomiting , purging 泄泻 ,
giddiness 眩晕 , confused vision , green vision or yellow vision , anorexia 厌食 , nausea , diarrhea , abdominal discomfort or pain , headache , fatigue
the drugs may stimulate the chemoreceptor of trigger zone (CTZ) in the area postrema of the medulla( 延髓极后区,化学感受区)
2. Toxic effects on the heart(1)Tachycardiac rhythm
abnormalities (arrhythmia)Atrioventricular (AV) node
Artial
Ventricular fibrillation
Bigeminy 二联律 , trigeminy 三联律
}Tachycardia
death
machanism
Severe inhibiting Na+-K+-ATPase
Depletion of K+ in cell
Resting potential or maximal diastolic potential
Change small(negative value)
(1)Automaticity easy to depolarization
(2) Delaying after depolarization↑迟后去极化
↓
↓
↓
}
(2) AV block
★ the development of AV block is due in part to the vagal effect of glycosides Na+-K+-ATPase is strongly depressed Resting potential↓
Phase 0 depolarization rate ↓
Conduction slows
★
↓
↓
(3)Sinus bradycardia
Sinus atrial node is depressed
↓
Automaticity ↓
Prevention of cardiac intoxication
1.Intoxication symptoms and signsGastrointestinal effectsNeurological effectsDrug concentration in blood can be
measured
2. Pathological situations
Ion pH of blood Oxygen deficiencyAgeDrug interaction
Treatment of cardiac glycosides introxication1. Administration K+ , orally or iv2. Administration of phenytoin treats s
evere tachycardiac rhythm abnormalities
ventricular tachycardia bigeminy 二联律 recovering activity of enzyme
ventricular tachycardiaVentricular fibrillation
Lidocaine :
}severe
Atropine:
Sinus bradycardiaAV conduction block
AdministrationAdministration
1 Digitalization 1 Digitalization Slow approach to “ digitalization”Slow approach to “ digitalization” Is the safest dosing technique.Is the safest dosing technique. Rapid approach to “digitalization”Rapid approach to “digitalization” can be achieved quickly with a can be achieved quickly with a
large loading dose (divided into large loading dose (divided into three or four portions and given three or four portions and given over 24~36 hours) followed by over 24~36 hours) followed by maintenance dosemaintenance dose
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2 Maintenance doses2 Maintenance doses3 Therapeutic method of Digoxin3 Therapeutic method of Digoxin tt1/2 1/2 36 hours 0.25 mg/day36 hours 0.25 mg/day 4~6 t4~6 t1/21/2 (6~7 (6~7 days) to approach steaddays) to approach stead
y-state level (Cy-state level (Cssss))