DRUGS USED FOR ANGINA PECTORIS

advertisement

DRUGS USED FOR

ANGINA PECTORIS

LAKSHMAN KARALLIEDDE

2011

ANGINA PECTORIS

SYMPTOM COMPLEX:

CONSTITUTES A CLINICAL SYNDROME

RATHER THAN A DISEASE

CAUSE:

TRANSIENT MYOCARDIAL ISCHAEMIA

OCCURS WHEN EVER THERE IS AN INBALANCE BETWEEN

MYOCARDIAL OXYGEN SUPPLY AND DEMAND

COMONEST CAUSE:

ATHEROMATOUS DISEASE OF CORONARY

ARTERIES

MAY ALSO BE A MANIFESTATION OF OTHER FORMS OF HEART

DISEASE e.g. Severe aortic valve disease, hypertrophic cardiomyopathy

DRUGS USED TO RELIEVE OR PREVENT THE

SYMPTOMS OF ANGINA

1. NITRATES

2. BETA BLOCKERS

3. CALCIUM ANTAGONISTS

4. POTASSIUM CHANEL ACTIVATORS

AS THE FUNDAMENTAL CAUSE OF ANGINA PECTORIS IS INSUFFICIENT

OXYGEN SUPPLY TO HEART MUSCLE, IT IS LOGICAL TO ATTEMPT TO

INCREASE THE OXYGEN SUPPLY BY ADMINISTERING OXYGEN- THAT IS

BY INCREASING THE INSPIRED OXYGEN CONCENTRATION SIMILARLY,

PATIENTS WITH ANGINA MAY SUFFER FROM SEVERE PAIN AND PAIN

RELIEF WITH A POTENT OPIATE e.g. Morphine NEEDS TO BE CONSIDERED TO MAKE THE PATIENT

MORE

COMFORTABLE, LESS ANXIOUS.

NITRATES

MODE OF ACTION :

ACTS DIRECTLY ON VASCULAR SMOOTH MUSCLE TO

PRODUCE ARTERIAL AND VENOUS DILATATION

EFFECT DURING ANGINA

1.REDUCES MYOCARDIAL OXYGEN DEMAND (LOWERS

PRE-LOAD AND AFTER LOAD)

2. INCREASES MYOCARDIAL OXYGEN SUPPLY

(CORONARY VASODILATATION)

NITRATE PREPARATIONS

1. SUBLINGUAL GLYCERYL TRINITRATE (GTN)

2. BUCCAL GLYCERYL TRINITRATE

3. TRANSDERMAL GLYCERYL TRINITRATE

4. ORAL ISOSORBIDE DINITRATE

5. ORAL ISOSORBIDE MONONITRATE

6. INTRAVENOUS GTN- FOR ACUTE MYOCARDIAL

INFARCTION/LEFT VENTRICULAR FAILURE -10 -200 µg /MIN

INTRAVENOUS INFUSION, TITRATING TO CLINICAL RESPONSE

AND BLOOD PRESSURE.

DURATION OF ACTION OF SOME NITRTATE PREPARATIONS

PEAK ACTION

DURATION OF

ACTION

10-30 minutes Sublingual GTN(Tablet 300-

500µg or metered dose aerosol 400µg/spray)

Buccal GTN (1-5 mg tablet 6 hourly)

Transdermal. GTN (5-10 daily)

Oral isosorbidedinitrate.(10-

20 mg 8 hourly)

Oral isosorbide mononitrate

( 20-60 mg once or twice a day)

4-8 minutes

4-10 minutes

1-3 hours

45-120 hours

45-120 hours

30-300 minutes

Up to 24 hours

2-6 hours

6-10 hours

SUBLINGUAL GTN- Administered

a. as a tablet – 300-500 µg to disolve under the tongue b. As metered-dose aerosol (400 µg per spray)

RELIEVES AN ATTACK OF ANGINA IN 2-3 MINUTES

UNWANTED EFFECTS

 HEADACHE

 SYMPTOMATIC HYPOTENSION –DIZZINESS, POSTURAL GIDDINESS,

BLURRING OF VISION

 RARELY SYNCOPE – FAINTING

ASK PATIENT TO SPIT TABLET IF ABOVE EFFECTS OCCUR

 NOT HABIT FORMING

 TEACH PATIENTS TO USE PROPHYLACTICALLY e.g.

Before exerting

 VIRTUALLY INEFFECTIVE IF SWALLOWED DUE TO EXTENSIVE FIRST PASS

METABOLISM IN THE LIVER

CONTINUOUS USE CAUSES PHARMACOLOGICAL TOLERANCE

THERFORE ATTEMPT TO INCLUDE A ‘NITRATE-FREE’ PERIOD OF 6-8 HOURS

A DAY

BETA BLOCKERS

MODE OF ACTION: LOWERS MYOCARDIAL OXYGEN DEMAND BY

A. REDUCING HEART RATE

B. REDUCING BLOOD PRESSURE

C. REDUCING MYOCARDIAL CONTRACTILITY

Can exaccerbate symptoms of peripheral vascular disease

May provoke bronchospasm in patients with obstructive airway disease e.g

asthma

Theoretically-Non- selective beta blockers may aggravate coronary vasospasm by blocking the coronary artery beta 2 recetors.

Advice: use a once daily cardio-selective preparation e.g atenolol 50-200mg daily slow release metoprolol 50-200mg daily bisoprolol 5-10 mg daily

BETA BLOCKERS SHOULD NOT BE WITHDRAWN ABRUPTLY (SUDDENLY)

BECAUSE OF THE POSSIBILITY OF A REBOUND EFFECT AND THE RISK OF

PRECIPITATING ARRHYTHMIAS, WORSENING ANGINA OR CAUSING

MYOCARDIAL INFARCTION (THE ‘BETA-BLOCKER WITHDRAWAL SYNDROME).

CALCIUM ANTAGONISTS

MODE OF ACTION

1. DECREASES MYOCARDIAL OXYGEN DEMAND BY REDUCING BLOOD

PRESSURE AND MYOCARDIAL CONTRACTILITY

TYPES

A. DIHYDROPYRIDINE CALCIUM ANTAGONISTS-NIFEDIPINE, NICARDIPINE

OFTEN CAUSE REFLEX TACHYCARDIA-BEST USED IN COMBINATION WITH

BETA BLOCKER-not used or caution when using

B. VERAPAMIL AND DILITIAZEM-SUITABLE FOR PATIENTS WHO ARE NOT

RECEIVING BETA BLOCKERS AS THEY DECREASE THE HEART RATE (

DANGEROUS ADDITIVE EFFECT)

CALCIUM CHANNEL ANTAGONISTS MAY REDUCE MYOCARDIAL

CONTRACTILITY TO A DEGREE THAT CAN AGGRAVATEOR PRECIPITATE

HEART FAILURE

UNWANTED EFFECTS

 PERIPHERAL OEDEMA

 FLUSHING

 HEADACHE

 DIZZINESS

POTASSIUM CHANNEL ACTIVATORS

MODE OF ACTION: DILATES ARTERIES AND VEINS

DOES NOT EXHIBIT TOLERANCE SEEN WITH NITRATES

NICORANDIL- 10-30 mg 12 hourly

Caution in: hypovolaemic patients

Patients with pulmonary oedema

Side effects: a. Headache b. Flushing c. Dizziness d. Weakness e. May cause a dose dependent increase in heart rate f. Myalgia g. Angioedema

ANTIPLATELET DRUGS

 ASPIRIN

 CLOPIDOGREL

THROMBOLYTIC AGENTS

 STREPTOKINASE

 ALTEPLASE

 RETEPLASE-

ASPIRIN

ANTIPLATELE T EFFECT BY INHIBITION OF THROMBOXANE A 2

NSAID, INHIBITS COX-1 AND COX -2 WHICH LEADS TO

DECREASED PROSTAGLANDIN SYNTHESIS

USES

THROMBO-EMBOLIC CVA, ISCHAEMIC HEART DISEASE-

PROPHYLAXIS (75MG/DAY) AND ACUTE TREAMENT (300 MG)

CONTRAINDICATIONS

1. THOSE UNDER AGE OF 16Y-CAN INCREASE INCIDENCE OF

REYE’S SYNDROME, LIVER/BRAIN DAMAGE

2. GASTRO-INTESTINAL ULCERS

3. BLEEDING DISORDERS

4. GOUT

5. HYPERSENSITIVITY TO ANY NSAID

6. GFR <10ML/MIN

ASPIRIN

CAUTION

1. ASTHMA

2. UNCONTROLLED HYPERTENSION

3. ANY ALLERGIC DISEASE

4. G6PD DEFICIENCY

5. DEHYDRATION

OTOTOXIC IN OVERDOSE

MAY INCREASE EFFECTS OF SULPHONYL UREAS AND OF METHOTREXATE

FOR ANALGESIA- 300-900 MG 4-6 HPOURLY –MAXIMUM DOSE4G/DAY

STOP 7 DAYS BEFORE SURGERY IF SIGNIFICANT BLEEDING IS EXPECTED

IF CARDIAC SURGERY OR PATIENT HAS ACUTE CORONARY SYNDROME-

CONSIDER CONTINUING

CLOPIDOGREL

ANTIPLATELET AGENTADP RECEPTOR ANTAGONIST

USE

PROPHYLAXIS OF ANTI-THROMBOTIC EVENTS IN NON—ST

ELEVATIONMYOCARDIAL INFARCTION AND IN ST ELEVATION

MYOCARDIAL INFARCTION-IN COMBINATION WITH ASPIRIN

MYOCARDIAL INFARCTION (WITHIN A ‘FEW’ TO35 DAYS)

ISCHAEMICCEREBROVASCULAR ACCIDENT- WITHIN 7 DAYS TO 6

MONTHS

PERIPHERAL ARTERIAL DISEASE

CONTRAINDICATION

ACTIVE BLEEDING

NOT RECOMMENDED WITH WARFARIN

CLOPIDOGREL

SIDE EFFECTS

 HAEMORRHAGE (ESPECIALLY GASTRO-INTESTINAL OR

INTRA-CRANIAL

 GASTRO-INTESTINAL UPSET

 PEPTIC ULCER

 PANCREATITIS

 HEADACHE

 FATIGUE

 DIZZINESS

 PARAESTHESIA

 RASH/PRURITUS

MONITOR FULL BLOOD AND FOR SIGNS OF OCCULT BLEEDING

STREPTOKINASE

THROMBOLYTIC AGENT

INCREASES PLASMINOGEN CONVERSION TO PLASMIN WHICH

INCREASES FIBRIN BREAKDOWN

USES

1. ACUTE MYOCARDIAL INFARCTION -1.5 MILLION UNITS

INTRAVENOUS INFUSION OVER 60 MIN

2. THROMBOEMBOLISM OF ARTERIES

3. PULMONARY EMBOLISM

4. CENTRAL RETINAL ARTERY THROMBOSIS

5. DEEP VEIN THROMBOSIS

OTHER DOSES-250,000 UNITS INTRAVENOUS INFUSION OVER

30 MIN, THEN 100,000 UNITS EVERYHOUR FOR UPTO12-72

HOURS

ALTEPLASE

(RECOMBINANT) TISSUE-TYPE PLASMINOGEN ACTIVATOR.

RECOMBINANT FIBRINOLYTIC

USE

ACUTE MYOCARDIAL INFARCTION (TOTAL DOSE 100MG-

REGIMEN DEPENDS ON TIME SINCE ONSET OF PAIN

0-6HOURS: 15 MG INTRAVENOUS BOLUS,FOLLOWED BY 50 MG

INTRAVENOUS INFUSION OVER 30 MINUTES AND 35 MG INTRAVENOUS

INFUSION OVER 60 MINUTES

6-12 HOURS-10 MG INTRAVENOUS BOLUS FOLLOWED BY 50 MG

INTRAVENOUS INFUSION OVER 60 MIN, AND FOUR FURTHER 10 MG

INTRAVENOUS INFUSIONS, EACH OVER 30 MIN)

DECREASE DOSE IF PATIENT WEIGHS LESS THAN 65 KG

RETEPLASE

RECOMBINANT PLASMINOGEN ACTIVATOR; THROMBOLYTIC

USED ONLY FOR MYOCARDIAL INFARCTION

DOSE-10 UNITS AS SLOW INTRAVENOUS INJECTION OVER 2 MINUTES,

REPEAT AFTER 30 MIN

Download