Antiarrhytmic drugs

By:Dr.Zharif

Vaughan Williams classification of Antiarrhythmic agents(International Classification):

I(Membrane Stabilizing agents)

Ia((Na+) channel block (intermediate association/dissociation)

Mech of action

block the fast sodium channel(depresses the phase 0 depolarization (reduces Vmax))By:

1.prolongs the action potential duration by slowing conduction.

2.decreased conductivity

3.increased effective refractory period

Indications:

supraventricular tachycardia, ventricular tachycardia, symptomatic ventricular premature beats, and prevention of ventricular fibrillation.

Procainamide treatment of atrial fibrillation in the setting of Wolff-Parkinson-White syndrome, and in the treatment of wide complex hemodynamically stable tachycardias. While procainamide and quinidine may be used in the conversion of atrial fibrillation to normal sinus rhythm, they should only be used in conjunction with an AV node blocking agent (ie: digoxin, verapamil, or a beta blocker), because procainamide and quinidine can increase the conduction through the AV node and may cause 1:1 conduction of atrial fibrillation, causing an increase in the ventricular rate.

Drugs 1a

Quinidine-

200-600mg every 4-6 hour peroral during attack

Procainamide-

250-750mg every 4-6 hour peroral or

10-15mg/kg I/V droplet with 25mg/min after that 1-6 mg/min

Disopyramide –

100-200 mg every 6-8 hours peroral

Ib((Na+) channel block (fast association/dissociation))

Mech.of action

fast onset and offset kinetics, meaning that they have little or no effect at slower heart rates, and more effects at faster heart rates

shorten the action potential duration and reduce refractoriness

tend to be much more specific for voltage gated Na channels than Ia

more activity with increasing heart rates

Indication

ventricular tachycardia and symptomatic premature ventricular beats, and prevention of ventricular fibrillation.

Drugs 1b

Lidocaine

1-3mg/kg i/v droplet 25-50mg/min till 1-4mg/min

Mexiletine-

200-400mg every 8 hours peroral

Ic((Na+) channel block (slow association/dissociation))

Mech.of action

decrease conductivity but have a minimal effect on the action potential duration. Of the sodium channel blocking antiarrhythmic agents

Indication :

life-threatening ventricular tachycardia or ventricular fibrillation, and for the treatment of refractory supraventricular tachycardia

Imaline(AJMALINE)-I/V 50mg till 75 mg 7-10 min

Gilurytmal(in russian)

Drugs 1c

Propafenone-

150-300mg every 8 hour i/v

Moricizine-

150-300 mg every 8-12 hour i/v

II(Beta blocker)

Mech of action

Beta blockers block the action of endogenous catecholamines (epinephrine (adrenaline) and norepinephrine (noradrenaline) in particular), on β-adrenergic receptors, part of the sympathetic nervous system which mediates the fight or flight response.

Drugs II

Propranolol

10-100 mg every 6 hour peroral

III(K+ channel blocker)

Mech of action

block the potassium channels, thereby prolonging repolarization. The prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias.

Side effect:

These agents include a risk of torsades de pointes

Drugs III

Amiodarone

600-1600mg/day 1-3 week

next 3rd week 200-400 mg/day

Sotalol (is also a beta blocker)

80-320 mg every 12 hours peroral

IV(Ca2+ channel block)

Mech of action

blocking voltage-gated calcium channels (VGCCs) in muscle cells of the heart and blood vessels

decrease in cardiac contractility

less contraction of the vascular smooth muscle of vessel-vasodilation

decreases total peripheral resistance,

decreases cardiac output.

low blood pressure

Drugs IV

verapamil

80-320 mg every 6-8 hours peroral

5-10 mg for 1-2 min i/v

V(Work by other or unknown mechanisms)

digoxin

1,25-1,5 mg fractional peroral in 24 hours

next 0.125-0,375 mg/day i/v

adenosine

6mg rapidly i/v

if no effect inbetween 1-2 minutes

12 mg rapidly i/v

Mnemonics

"some block potassium channels"

Class I "Some" = S = Sodium blocker

Class II "Block" = B =Beta blockers

Class III "Potassium"=P= Potassium channel blockers

Class IV "Channels" = C =Calcium channel blockers

Class I agents

Class IA “Double Quarter Pounder” (Disopyramide, Quinidine, Procainamide),

Class IB “Lettuce, Tomato, Mayo” (Lidocaine, Tocainide, Mexilitine)

Class IC “More Fries Please” (Moricizine, Flecainide, Propafenone)

Class III agents:

"A Big Dog Is Scary" (Amiodarone, Bretylium, Dofetilide, Ibutilide, Sotalol)

Class IV agents:

"Very Nice Drugs" (verapamil, nifedipine, diltiazem)

Russian classification for Antiarrhytmic drugs

Supraventricular arrhythmia

Drugs	During attack	Prophylactic	Start action	Prolong action
Izoptine	i/v 10mg(seldom 15-30 mg )with 1mg/min PerOS 40-120 mg till 160 mg	PerOS 40-120mg 4-6 times /day	i/v- 1st min. perOS-during 1 hours	4-8 hours
Quinidine	PerOS 0.2-0.6 g	PerOS 0.2-0.4g 4-6 times/day	30 min.	4-6 hours
Novocainamide	i/v 0.5-1 g or i/v every 2 min 0.1-0.2g or i/m o.5-1g or PerOS 1-1.5g	i/v 2-3mg/min or PerOS o.5g 4-6 times/day	i/v-1st minute perOS-30 min.	3-4 hours
Imaline	i/v 50 mg till 75 mg in duration 7-10 min or PerOS 0.05-0.1 g	perOs 0.05-1g 3-4 times/day	i/v-1st min.	6-8 hours
Ritmodan	i/v 2 mg/kg do 150 mg in duration 5 min. or perOS 0.2-0.3g	perOS 0.1-0.2g 3-4 times/day	i/v-1st min. perOS-30 min.	i/v-10 min perOS-4-6 hours
etmozine	i/v 2-2.5 mg/kg in duration 5-10 min	PerOS 0.2g 3-4 times/day	i/v-1st min perOS-24-48hours	i/v 20-25min perOS 6-8 hours
Obzidane	i/v 10mg in duration 7-10 min or PerOS 20-160mg	PerOS 20-80mg 4times/day	i/v- 1st min perOS-30 min.	i/v 2-4 hours perOS 3-6 hours
Kordaron	i/v 5mg/kg in duration 5 min	perOS: 1st week 200-400mg 3 times/day 2nd week 1-2 tab. 2 times/day 3rd week 1-2 tab./day 2 day rest in 1 week	i/v-1st min	i/v-20-30 min perOS- week

Ventricular arrhytmia

Drugs	During attack	Prophylactic	Start action	Prolong action
Lidocaine And trimecaine	i/v 80-100mg in duration 3-5 min seldom 150-200mg in duration 10-20 min.	i/v rapidly 80-100mg next droplet 2-3mg/min i/m 400-600mg in 3 hours	i/v-1st min. i/m- 10-15 min.	i/v-10-15min i/m 3hours
Mexitiline	i/v 75-250mg in duration 5-15 min or PerOS 0.3-0.4g	i/v rapidly 75-250mg next droplet or perOS 0.2-0.4g 3 times/day	i/v-1st min. perOS-30min.	i/v-3-8hours perOS- 6-8 hours
Diphenine		perOS:slow 0.1g 3-4 times fast 0.2g 5 times/day	3-5th day	Stop during 6-12 after stop taken

Ref:

1. Internal medicineRussian text book
2. Hospital therapyRussian text book
3. Cycle Russian therapy
4. American heart website
5. wikipedia

Cholecystocardial Syndrome (Botkin Syndrome)

Cholecystocardial Syndrome (Botkin Syndrome)

By:Dr.Zharif

–

this is the complex of clinical symptoms, which is manifested by pains in the region of heart (cardialgia), by metabolic disorders in the myocardium with disturbance of rhythm and conductivity, shortness of breath, sometimes by worsening in the coronary blood circulation as a result of the reflector and infectious-toxic actions on the myocardium, which are appeared as a result of the defeat by the pathologic process of gall bladder.

acalculous cholecystitis-35%,

the patients of elderly age - 70%.

Clinical “masks” are diverse in their manifestation, which can lead doctor into error.

Are separated cardial, allergic, thyrotoxic, neurotic, rheumatic, solar, gastrointestinal and other “masks”. One of the sufficiently frequently meeting “masks” is cardial.

History

Botkin, who first noted the possibility of reflector be ill in the heart with the gall bladder disease in clinical lectures (1883), since itself from the 25- summer age suffered the gall bladder disease, which flowed with the frequent assaults of colic, and it connected stenocarditic pains in the region of heart with the disease of gall bladder.

You will not hear complaints of the disorder of digestion, pain, inflation of stomach, patient will complain predominantly about the assaults be ill in the side of the hearts, which go with explicit changes in his function, by arrhythmia, by the difficulty of respiration, in a word, with the clear picture of stenocardia.

This attacks continues 8-10 hours, instead of 1/2 hours or several minutes, suddenly it turns yellow after such several assaults of patient.

But investigate it attentively from the very beginning, and you will ascertain that the liver is increased, the gall bladder diseases There is and so that the disorder of heart it is not accompanied by pains, but only by arrhythmia and by the strong difficulty of respiration or by the phenomena of so-called asthma, which reaches sometimes the strong degree.

Etiology

cholecystocardial syndrome can be developed with the following diseases of the bile-secreting ways:

• chronic acalculous cholecystitis;

• acute and chronic calculous cholecystitis

(maximally it is manifested during the bilious colic);

• choleduchlithiasis without the development of bilious hypertension, with bilious hypertension (with the development of mechanical jaundice);

• the pathologic processes, which lead to the contraction of the terminal division of common bilious duct (stenosing papillitis, the tumor of the large papilla of duodenum, infiltrative pancreatitis).

Pathogenesis

The pathogenesis of cholecystocardial syndrome has several mechanisms of the realization: reflector influences on the coronary vessels, the shifts of the metabolism of myocardium (especially at the moment of bilious colic) and the infectious-toxic action on the cardiovascular system with the sharp inflammatory process in the bile-secreting ways.

1. Reflector influence. The afferent pathologic pulsation, which emanate

s from extra and intramural nervous interlacements of the bile-secreting ducts with the spas

m of the sphincters Of

lyutkensa,Mirizzi,Oddi and the expansion of bilious ducts with biliar hypertension, can by means of the sympathetic and parasympathetic nerve fibers influence heart, causing the spasm of coronary vessels, the disturbance of rhythm and the like

2. Change in the metabolism of heart muscle. With the prolonged course of the gall stones disease with the frequent attacks of the biliar colic, complicated by chronic recurrent cholecystitis and associated disturbances of the functions of the liver and the pancreas, is developed the dystrophia of myocardium, connected with the complex disorders of electrolytic, enzyme and carbohydrate balance, which can lead to the disturbances of cardiovascular system.

3. Infectious-toxic action on the heart muscle with the sharp inflammatory process in the bile-secreting system (acute cholecystitis, purulent cholangitis to mechanical jaundice) with the disturbances in the system of homeostasis and the development of the acute dystrophia of myocardium, which is the reason for the increased excitability, disturbances of conductivity and contracting ability of myocardium. Besides the direct mechanisms of the forming of cholecystocardial syndrome, it is necessary to consider that with the age the frequency of morbidity increases by the ischemic disease of heart, by stenocardia and by the disturbances of rhythm, which makes especially unfavorable the flow of cholecystocardial syndrome.

Clinical pictures

pain in the region of heart (cardialgia or reflector stenocardia). .

The cardialgesic and stenocarditic forms of cholecystocardial syndrome are most common with the gall bladder disease (79% of patients).

Character pain

sharp pain 85% of patients

compressing pain 56-65% of patients

splitting pain13-58% of patients

Irradiation of pain from the right subcostal area into the leftist and into the region of the heart (more frequent during the combination of cholecystitis and pancreatitis);

Is possible the analgesic form of the cholecystocardial syndrome, when its only manifestation - disturbance of the rhythm of heart.

Arrhythmias of heart are also different:

ectopic rhythms (0,47%)

extrasystole (9,6-13,9%)

fibrillation arrhythmia (3,5-13,5%),

atrioventricular blockade and/or blockade of the right branch of His's bundle

Differential diagnostics

Between Cholecystocardial syndrome and IHD

Cholecystocardial syndrome is manifested by pains in the region of the hearts (cardialgias), whose appearance is connected with the viscero- visceral reflex on the vagus. First pains appear in by right subcostal area, then in the region of heart. Frequently the pain is localized in the region of the top of heart, and patient indicates its localization sufficiently accurately (by one finger).The pains prolonged, sharp pain, can be paroxysmal pain and be accompanied by dyspeptic phenomena.

harp paincardial Cholecystocardial syndrome important to consider connection be pain with the consumption of food, but one should remember that the pain can arise after physical load. Sometimes accompanied by jaundice.

Cholecystocardial syndrome is characteristic the syndrome of vegetative disfunction with the predominance of parasympathetic tone, neurotic syndrome is the practically integral part of the clinic of the pathology of the bile-secreting ways.

The combination of cardial complaints with the asthenoneurotic phenomena, the lability of pulse and arterial pressure can lead to the formulation of the erroneous diagnosis of vegetovascular dystonia.

During the attack in the blood are noted leukocytosis, neutrophilia, accelerated ESR, bilirubinemia, hyperglycemia, increase in the level of amylase.

On the ultrasound usually are well visible the large and small concrements of gall bladder, the diffuse or local thickening of the wall of the gall bladder (more than 4 mm) and an increase in its echodensity

The shadows of concrements are visible with the presence of the mixed or lime stones in the survey X-ray photograph. With cholecystography and cholegraphy cholesterol and pigment stones give enlightenments or defects of filling, frequently the shadow of gall bladder is absent.

On ECG during the attack of pain are noted negative waves R in the right breast and in lead 3 standard removal. They frequently take place of the disturbance of rhythm (extrasystole, atrioventricular blockade I st.), diffuse changes in the myocardium are noted.

Treatment

Cholecystoectomy

Ref:translated and edited from Russian Cardiology Website

#1 case study

By:Dr.Zharif



39 yo female was admitted to the hospital with a diabetic foot ulcer. She needed IV access for Unasyn IV and labs, and failed several peripheral line attempts.

A right IJ central line was placed. Immediately after the catheter was placed, she complained of SOB(dyspnea) and palpitations. Her SpO2 was 100%, breath sounds were equal and clear bilaterally.

What do you think is going on?
Is it a pneumothorax?

HR was 140 and irregular.


EKG showed AFib with RVR.(rapid ventricular respons) CXR showed that the triple lumen catheter (TLC) was at the level of the right AV junction.


TLC at the right AV junction on CXR


AFib due to a TLC at AV junction

What would you do?
Withdraw the central line. Repeat the CXR and EKG.

What happened?
The TLC was withdrawn 5 cm with conversion to sinus rhythm and no further complaints.


Central line in superior vena cava (SVC). This is the correct position for a TLC on CXR.


Conversion to NSR(normal sinus rhythm) after the TLC was repositioned

What your final Diagnosis????

correct diagnosis will answer on 26.11.2008
write your full diagnosis on discussion below k..
tq..

β-blocker drug (Antiadrenegic drug)treatment for IHD

By:Dr.Zharif

β-blocker drug (Antiadrenegic drug)treatment for IHD

Purpose of treatment :

1.Improve quality of life

2.Improve outcome of life

β-blocker drug (Antiadrenegic drug)

General Mechanism of action

block the action of endogenous catecholamines (epinephrine (adrenaline) and norepinephrine (noradrenaline) in particular),

on β-adrenergic receptors, part of the sympathetic nervous system which mediates the fight or flight response.

Action of β adregenic receptor (part of sympathethic nerves system)

-three known types of beta receptor, designated β₁, β₂ and β₃.

a) β₁-Adrenergic receptors are located mainly in the heart and in the kidneys.

b) β₂-Adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle.

c) β₃-receptors are located in fat cells

Respiratory system(β2 agonists receptor)

1.bronchodilation

2. Increase Respiratory Secretions

Cardiovascular system

Heart(β1 agonists receptor)

1.Increase heart rate

2.Increase AV conduction

3.Increase BP -rise in systolic and diastolic-NA

-rise in systolic and fall diastolic-Iso

Blood vessel(β2 agonists receptor)

1.Vasodilation

Eye(β2 agonists receptor)

1.Increase secretory activity of ciliary epithelia(caution to patient with glaucoma)

2.Increase Intraocular Pressure

GIT(not clinical significant)

1.Reduced peristalsis

2.Sphincter constricted

Bladder

1.Relaxed detrussor muscle

Uterus

1.Decrease contraction of uterus

Metabolic

1.Increase glycogenolysis- hyperglycaemia,hypelactidemia(β2)

2.Decrease insulin

3.Increase lipolysis

4.Increase lipid profile in plasma

5.Transient hyperkalemia followed by hypokalemia

CNS

Not produce any effect on CNS because poorly penetration in brain (hydrophilic)

Lipophilic drugs

Lipophilic drugs (metoprolol, propranolol, timolol) are

rapidly and completely absorbed from the gastr

ointestinal

tract but are extensively metabolised in the gut wall

and in the liver (first pass effect), so that the

ir oral

bioavailability is low (10–30%). These drugs may accumulate

in patients with reduced hepatic blood flow (i.

e.,

elderly, congestive heart failure, liver cirrhosis). Lipophilic

drugs present short elimination half-lives (1-5 h)

and they easily enter the central nervous sys

tem (CNS),

which may account for a greater incidence of

central

side-effects.

Hydrophilic drugs

Hydrophilic drugs (atenolol, esmolol) are absorbed incompletely

from the gastrointestinal tract and are excreted

unchanged or as active metabolites by the kidney.

They have longer half-lives (6–24 h), and do not interact

with other liver-metabolised drugs. They barely cross the

blood–brain barrier. Elimination half-life is increased

when glomerular filtration rate is reduced (i.e., elderly,

renal insufficiency).

Mechanism of action in IHD

The prevention of the cardiotoxic effects of catecholamines plays

The following mechanisms are also considered:

(a) Antihypertensive action.

Associated with a decrease in cardiac

output, inhibition of the release of renin and production

of angiotensin II, blockade of presynaptic a-adrenoceptors

that increase the release of norepinephrine from

sympathetic nerve terminals and decrease of central

vasomotor activity.1–9

(b) Anti-ischaemic action

b-blockers decrease myocardial oxygen demand by reducing

heart rate, cardiac contractility, and systolic

blood pressure.10 In addition, prolongation of diastole

caused by a reduction in heart rate may increase myocardial

perfusion.

(c) Reduction of renin release and

angiotensin II and aldosterone production by blocking of

b1-adrenoceptors on renal juxtaglomerular cells.

(d)Improvement of left ventricular structure and function,

decreasing ventricular size and increasing ejection fraction.

6–8 b-blockers may improve cardiac function because

they:

(i) reduce heart rate, prolong diastolic filling

and coronary diastolic perfusion time,

(ii) decrease myocardial

oxygen demands,

(iii) improve myocardial energetics

by inhibiting catecholamine-induced release

of free fatty acids from adipose tissue,

(iv) upregulate

b-adrenergic receptors

(v) reduce myocardial

oxidative stress.1;11;12

(e) The antiarrhythmic effect, the

result of direct cardiac electrophysiological effects

(reduced heart rate, decreased spontaneous firing of

ectopic pacemakers, slowed conduction and increased

refractory period of AV node),

reduces the sympathetic

drive and myocardial ischaemia, improves baroreflex

function and prevents catecholamine-induced hypokalemia.

Other mechanisms include:

Inhibition of cardiac apoptosis mediated via the activation of the b-adrenergic

pathway,

Inhibition of platelet aggregation,

Reduction of the mechanical stress imposed on t

he plaque,

Preventing plaque rupture

Resensitization of the b-adrenergic pathway and changes in myocardial gene expression,

i.e., an increase in sarcoplasmic reticulum calcium ATPase, mRNA and a-myosin heavy chain mRNA and a decrease in b-myosin heavy chain mRNA levels.15

exhibit antioxidant properties and inhibit vascular smooth

muscle cell proliferation.

Other Indication

· Hypertension

· Angina

· Mitral valve prolapse

· Cardiac arrhythmia

· Congestive heart failure

· Myocardial infarction

· Glaucoma

· Migraine prophylaxis

· Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism

· Essential tremor

· Phaeochromocytoma, in conjunction with α-blocker

also been used in the following conditions

· Hypertrophic obstructive cardiomyopathy

· Acute dissecting aortic aneurysm

· Marfan syndrome (chronic treatment with propranolol slows progression of aortic dilation and its complications)

· Prevention of variceal bleeding in portal hypertension

· Possible mitigation of hyperhidrosis

· Social anxiety disorder and other anxiety disorders

Adverse effect

Cardiovascular

1.Reduce heart rate,

2.Extreme bradycardia and AV block.

3.Impaired sinusnode function and AV-node conduction

4.Produce cold extremities and Raynaud’s phenomenon and worsen the symptoms in patients with severe peripheral vascular disease.

5.Coronospasm

Metabolic

Hypoglycaemia -In patients with insulin-dependent type I diabetes nonselective

b-blockers mask and selective b-blocker should therefore be preferred at

least in insulin dependent patients

In one study carvedilol decreased the new onset diabetes in

patients with heart failure.

Pulmonary

Increase in airway resistance and are contraindicated in patients with

asthma or bronchospastic chronic obstructive pulmonary

disease.

Central effects

Central effects (fatigue, headache, sleep disturbances,

insomnia and vivid dreams, depression) are less common

with hydrophilic drugs

In some patients the fatigue may

be related to a decrease in blood flow to skeletal muscles;

in other cases, it may be secondary to a central effect.

Sexual dysfunction

Impotence and loss of libido.

Abrupt discontinuation of b-blockers after chronic

treatment can lead to rebound symptoms (i.e., hypertension,

arrhythmias, exacerbated angina)

This increased risk is related with upregulation of badrenoceptors during chronic treatment

Contraindications

1. Asthma,
2. Symptomatic hypotension
3. Bradycardia
4. Severe decompensated heart failure
5. Chronic obstructive lung disease without bronchospastic activity
6. Peripheral vascular disease are not considered as absolute contraindications and high risk patients may obtain a significant benefit from this therapy.
7. Patients with heart failure and bradycardia due to sick sinus node or second or third degree AV-block may benefit from pre-treatment with pacemaker in order to tolerate b-blockers, although this approach has, however, not been formally tested.
8. Diabetes or intermittent lower limb claudication are not absolute contraindications for b-blockers use

I. Non-selective β₁, β₂ adrenergic antagonists

Carteolol + Low 2.5–20 mg once/twice daily

Nadolol 0 Low 40–320 mg once daily

Penbutolol + Moderate 20–80 mg once/twice daily

Pindolol ++ High 10–40 mg twice daily

Propranolol 0 High + 40–180 mg twice daily

Sotalol 0 Low +

Timolol 0 High 5–40 mg twice daily

II. Selective β₁adrenergic antagonists

Acebutolol + Moderate 200–800 mg once/twice daily

Atenolol 0 Low + 25–100 mg once daily

Betaxolol 0 Moderate 5–20 mg once daily

Bisoprolol 0 Moderate 2.5–10 mg once daily

Celiprolol + Moderate 200–600 mg once daily

Esmolol 0 Low Only i.v.

Metoprolol 0 High 50–100 mg once/twice daily

Nevibolol 0 2.5–5 mg once daily

III. α1- and β₁-adrenergic antagonists

Bucindolol + Moderate 25–100 mg twice daily

Carvedilol_ 0 Moderate 3.125–50 mg twice daily

Labetalol + Low 200–800 mg twice daily

ISA: Intrinsic Sympathomimetic Activity;

i.v.: Intravenous administration possible; AMI: Acute Myocardial Infarction; CHF: Chronic Heart Failure.

Acute Myocardial Infarction (AMI)

Intravenous dosing of b-blockers

Drug Loading dose Maintenance dose

Atenolol 5 ю 5 mg Oral, 50–100 mg/day

Esmolol 0.5 mg/kg over 1–5 min 0.05–0.3 mg/kg/min

Labetalol 20 mg in 2 min 2–10 mg/min

Metoprolol 2.5–5 mg i.v. bolus over 2 min; up to three doses Oral, 25–100 mg/12 h

Propranolol 0.15 mg/kg 0.10–0.20 mg/kg/min oral, 80–240 mg/day

Practical guidance on using b-adrenergic blockers in heart failure

Who should receive b-blocker therapy

_ All patients with chronic, stable heart failure

_ Without contraindications (symptomatic hypotension or bradicardia, asthma)

What to promise

Treatment is primarily prophylactic against death and new hospitalisations for cardiovascular reasons. Some patients will

experience improvement of symptoms.

When to start

_ No physical evidence of fluid retention (use diuretics accordingly)

_ Start ACE-I first if not contraindicated

_ In stable patients, in the hospital or in outpatient clinics

_ NYHA class IV/severe CHF patients should be referred for specialist advice

_ Review treatment. Avoid verapamil, diltiazem, antiarrhythmics, non-steroidal anti-inflamatory drugs

Beta-blocker

_ Bisoprolol, carvedilol or metoprolol

Dose

_ Start with a low dose

_ Increase dose slowly. Double dose at not less than 2 weekly intervals

_ Aim for target dose (see above) or, if not tolerated, the highest tolerated dose

Starting dose mg Target dose mg

Bisoprolol 1.25 once daily 10 once daily

Carvedilol 3.125 twice daily 25–50 twice daily

Metoprolol CR/XL 12.5–25 once daily 200 once daily

Monitoring

_ Monitor for evidence of heart failure symptoms, fluid retention, hypotension and bradycardia

_ Instruct patients to weigh themselves daily and to increase their diuretic dose if weight increases

Problem solving

_ Reduce/discontinue b-blocker only if other actions were ineffective to control symptoms/secondary effects

_ Always consider the reintroduction and/or uptitration of the b-blocker when the patient becomes stable

_ Seek specialist advice if in doubt.

Symptomatic hypotension (dizziness, light headedness and/or confusion)

_ Reconsider need for nitrates, calcium channel blockers and other vasodilators

_ If no signs/symptoms of congestion consider reducing diuretic dose

Worsening symptoms/signs (increasing dyspnoea, fatigue, oedema, weight gain)

_ Double dose of diuretic or/and ACE-I.

_ Temporarily reduce the dose of b-blockers if increasing diuretic dose does not work

_ Review patient in 1–2 weeks; if not improved seek specialist advice

_ If serious deterioration halve dose of b-blocker

_ Stop b-blocker (rarely necessary; seek specialist advice)

Bradycardia

_ ECG to exclude heart block

_ Consider pacemaker support if severe bradycardia or AV block or sick sinus node early after starting b-blockers

_ Review need, reduce or discontinue other heart rate slowing drugs, e.g., digoxin, amiodarone, diltiazem

_ Reduce dose of b-blocker. Discontinuation rarely necessary

Severe decompensated heart failure, pulmonary oedema, shock

_ Admit patient to hospital

_ Discontinue b-blocker if inotropic support is needed or symptomatic hypotension/bradycardia is observed

_ If inotropic support is needed, levosimendan may be preferred

Reference
1. Cycle clinical farmacology 6th year RSMU
2.Essential of Medical Pharmacology,KD Tripathi,JAYPEE
3.wikipedia
4.Escardio(Europian Society of Cardiology)