Muhammad Alyan .pharmaceutical management of mi

Mi management

1. Pharmacological management of MI
By
1.JavidRaza
2.Ibrahim
3.Tariq
4.Shakoor
5.Alyan
6.Fariha
7.joyce

2. •Contents
1.Overview to MI
2.Management
•Non pharmalogicalmanagement
•Pharmalogicalmanagement

4. Etiology
•Tobacco smoking
•> Hypertension
•> Drug abuse
•➤Obesity
•Stress
•Alcohol

6. •Clinical manifestations
•Chest pain / chest discomfort.
•Dyspnea.
•Fatigue
•Increased sweating
•Weakness
•Nauseaand Vomiting.
•Anxiety, sleeplessness, hypertension or
hypotension, arrhythmia.their common
symptoms are weakness, fatigue &
dyspnea

7. Management
Pharmacological management:
•Analgesics
Vasodilators-
-Nitrates
. -ẞ Blockers
. -Calcium channel blockers
• Anticoagulants–heparin
•Thrombolytic streptokinase,
•lipid lowering agents

8. Vasodilator
•Nitrates
•Amylnitrate
•Nitroglycerineor Glyceryl
trinitrate
•pentaerythritol
tetranitrate.
•Isosorbidedinitrate.

9. Anticoagulants include:
•Heparin
•Apixaban(Eliquis)
•dabigatran(Pradaxa)
•edoxaban(Lixiana)
•rivaroxaban(Xarelto)
•warfarin (Coumadin)

10. Thrombolyticsdrugs
•Streptokinase.
•Alteplase.
•Reteplase.
•Tenecteplase.
•Urokinase.
•Prourokinase.
•Anistreplase(APSAC)

11. Describing any drugs
•Pharmacokinetics of drugs
•MOA and pharmacological properties
•Indications
•Cautions/Contraindications
•Side effects

12. Vaspdilator
nitrates
pharmacokinetics of Nitroglyceren
•ABSORPTION
•Bioavailability:
• Oral: generally low (but isosorbidemononitrate>95%)
•Sublingual: 10-60%
. • Transdermal: 50-90%
•DISTRIBUTION
• In all body tissues including brain.
•BIOTRANSFORMATION
•> 99%, mainly in liver (by a high capacity nitrate-reductase).
Half-life: very variable
•sublingual nitroglycerin: 2-3 min
•oral isosorbidemononitrate: 4-5 hours11

13. Nitrates machanismof action
•Mechanism of action of nitratesInthe body, organic nitrates are
chemically reduced to release NO (nitrous oxide), a gas that can
dissolve in biological fluids and in cellular membranes.Nitrates-
formation of NO (nitric oxide)-activate guanylate cyclase->CGMP→
activate protein kinase→ dephosphorylationof light chain myosin→
relaxation of actin-myosin→→ smooth muscle relaxation -
vasodilatation

15. Indication
•Relief of acute
angina attack
•Prophylaxis of
stable angina
•(prior to exercise
GTN or long-acting)
•Left ventricular
failure

16. Beta blocker
•Competitive inhibitors of catecholamine at beta-adrenoceptor
sitesInhibitsympathetic stimulation of heart and smooth muscle

17. Indication
•Symptomatic angina
•Hypertension
•Acute coronary syndromes
•Post myocardial infarction
•Stable heart failure
•Arrhythmias
•Thyrotoxicosis/Benign essential tremor

18. Side effects
•Beta-1 effects Bradycardia, heart block, heart failure
•Beta-2 effects bronchospasm, worsening PVD, Raynauds
phenomenon
•Fatigue, depression, nightmares, impotence
•May mask hypoglycaemia and worsen glycaemic control in IDDM

19. Pharmacokinetics of CCB
• Absorption-typically oral form, but verapamil & diltiazem-also have
IV formulation.nifedipine, verapamil & diltiazem-all possess significant
first pass metabolism.
• Metabolism & excretion
-nifedipine& verapamil -excreted by kidney.
verapamil -excreted by liver.

20. Calcium channel blocker MOA
•CCBs has four effects:
•1) They act on vascular smooth muscle, reduce contraction of the arteries
and cause vasodilation.2
•2) They act on cardiac muscles (myocardium), they reduce the force of
contraction of the heart( Negative inotropic ).
•3) They slow down the conduction of electrical activity within the heart,
slow down the heartbeat (Negative chronotropic).4
•4) They block the calcium signal on adrenal cortex cells, they directly
reduce aldosterone production, which correlates to lower blood pressure.

21. Indications
•Symptomatic control of angina
•Coronary spasm
•Hypertension
•Arrhythmias
•Subarachnoid haemorrhage

22. Contraindication of CCB
•Known hypersensitivity to drug;
•sick sinus syndrome (unless pacemaker is in place and functioning).s
•second-or third-degree AV block.
•severehypotension (systolic <90 mm Hg or diastolic <60 mm Hg).
•patients undergoing intracranial surgery; bleeding aneurysms.

23. Anticoagulant drugs
Heaprin
Pharmacokinetics
•Heparin is not absorbed orally.
•If Injected i.v.-acts instantaneously.
•▸After s.c.injection anticoagulant effect develops after ~60 min.
•▸Bioavailability of s.c.heparin is inconsistent.
•▸Heparin does not cross blood-brain barrier or placenta (it is the
anticoagulant of choice during pregnancy).
•▸It is metabolized in liver by heparinase.
•▸Fragments are excreted in urine.

24. MOA of Heparin
•HEPARIN MOA1. Antithrombin (AT), is a native anticoagulant that
slowly binds to thrombin and other coagulants. Its full action requires
a cofactor, heparin.2. When heparin binds to AT, it induces a
conformational change that converts AT to a rapid and powerful
anticoagulant.3. With heparin attached, AT binds to a variety of
clotting enzymes, especially thrombin (factor II) and activated factor X
(Xa).4. This prevents the conversion of fibrinogen to fibrin.

25. Indication
•Deep vein thrombosis, pulmonary embolism.
•Ischemic stroke, transient ischemic attack.
•Coronary artery disease.
•Cardiac valve replacement or coronary angioplasty.
•Coagulation disorders like antiphospholipid syndrome and DIC.

26. Adverse effect
▸Bleeding due to overdose -most serious complication.
▸Thrombocytopenia -mild and transient.
▸Transient and reversible alopecia is infrequent. Serum transaminase
levels may rise.
▸Osteoporosis -long-term use of relatively high doses.
▸Hypersensitivity reactions -rare.

27. Contraindication
•►Bleeding disorders, history of heparin induced thrombocytopenia.
•▸Severe hypertension, threatened abortion, piles, g... ulcers.
•►Subacutebacterial endocarditis, large malignancies, tuberculosis.
•▸Ocular and neurosurgery, lumbar puncture.
•►Chronic alcoholics, cirrhosis, renal failure.

28. Thrombolyticsdrugs
streptokinase
Pharmacokinetics
•Metabolism:
No metabolites identified.
Elimination:
Streptokinase is cleared by the liver.
Time period approximately 23 min.

29. MOA
Recombinentstreptokinase and plasminogen together form a
stochiometric1:1 activator complex.oActivator complex converts
remaining plasminogen, present either in the blood or in a thrombus to
plasmin.oPlasmin lyses thrombi by converting insoluble fibrin into
soluble fibrin degradation products.

30. Indication
•Acute myocardial infarction (AMI)
•Deep vein thrombosis (DVT)
•Pulmonary embolism (PE)
•Acute ischemic stroke (AIS)
•Acute peripheral arterial occlusion.
•Occlusion of indwelling catheters.
•Intracardiacthrombus formation.

31. Lipid lowering drugs
Pharmacokinetics:
•30-90% oral absorption, 5-30% oral bioavailabilityEveningdosing (liver
cholesterol synthesis is greatest between midnight and 2 am)
•▸Maximal effects in one month followed by slow regression of
plaques as LDL is extracted
•Most have extensive hepatic metabolism (first pass effect) by CYP3A4
and CYP2C9
•Excreted in bile and feces, with some renal excretion (degree varies
among statins)

32. MOA of statin
•▸HMG-CoA reductase catalyzes the reduction of 3-hydroxy-3-
methylglutaryl-coenzyme A (HMG-CoA) to mevalonate, which is the rate-
limiting step in hepatic cholesterol biosynthesis
•▷Inhibition of the enzyme decreases de novo cholesterol synthesis,
increasing expression of low-density lipoprotein receptors (LDL receptors)
on hepatocytes.
•▷This increases LDL. uptake by the hepatocytes, decreasing the amount of
LDL-cholesterol in the blood.
• It also reduces blood levels of triglycerides and slightly increases levels of
HDL-cholesterol.

33. Indication
•Hyperlipidemiaand mixed
dyslipidemia.
•Primary dysbetalipoproteinemia.
•Hypertriglyceridemia.
•Atherosclerosis.
•Primary prevention of ASCVD
(atherosclerotic cardiovascular
disease)[6]

34. Side effects
•Cough
•Difficultywith swallowing
•Fastheartbeat
•fever and dizziness
•Itching
•muscle cramps, pain, stiffness, swelling, or weakness
•puffiness or swelling of the eyelids or around the eyes, face, lips, or tongue
•skin rash
•tightnessin the chest
•unusualtiredness or weakness

35. Nursing management of MI
•Obtain ECG daily.
•Always make sure the patient has 2 large-bore IVs.
•Monitor cardiac enzymes.
•Initiate treatment for acute MI.
•Administer morphine for pain.
•Start aspirin and nitroglycerin (0.4 mg sublingual)
•Provide oxygen if pulse oximetry is less than 94% at room air.