describes about ischemia and its medications ,

1. ANTIISCHEMIC AGENTS
ADVANCED PHARMACOLOGY -1
PRESENTED BY
JITHIN MATHEW
FIRST MPHARM
DEPT OF PHARMACOLOGY

2. ISCHEMIA
 Imbalance Between the supply( perfusion) and Demand of
Heart for the oxygenated blood
 It comprises not only insufficiency of oxygen but also reduced
availability of Nutrient substrate
Reduction in coronary blood flow due to atherosclerotic
coronary arterial obstruction

5. ANGINA PECTORIS
Pain syndrome due to induction of n adverse oxygen demand/supply system in a portion of
myocardium . Insufficient supply of blood to heart muscle from narrowing of coronary artery
may cause angina
TYPES OF ANGINA
STABLE ANGINA
Occurs when increased physical activity ( hurrying across a street or climbing a
long stairs) which creates a greater demand for oxygen rich blood to reach heart muscle
UNSTABLE ANGINA
Occurs with lesser degree of exertion or while at rest unstable angina that occurs at
rest is the most serious form this type usually is caused by the formation of a ruptured plaque in
coronary artery

6. SYMPTOMS
 Some people have silent ischemia
 MI with sign& symptoms
 Chest pain
 Neck or joint pain
 Shoulder or arm pain
 Clammy skin
 Nausea and vomiting
CAUSES
 Coronary artery disease
 Blood clot
 Coronary spasm

7. PATHOPHYSIOLOGY OF ISCHEMIA

9. MYOCARDIAL INFRACTION
MI defined as a condition which is caused by reduced blood flow
in a coronary artery due to atherosclerosis & occlusion of an artery by thrombus
formation
CLINICAL MANIFESTATIONS
 Chest pain
 Dyspnoea
 Fatigue
 increased sweating
 Weakness
 nausea
 Light headness

11. ISCHEMIC STROKE
Ischemia occurs when part of the brain results in death of brain cells
movement ,sensation ,or emotion controlled by affected area are lost or
impaired
RISK FACTORS
• Age
• Gender
• Heredity
• Hypertension
• obesity

12. PATHOPHYSIOLOGY
Brain requires continuous supply of oxygen and glucose for neurons to function
If blood flow is interrupted neuronal metabolism is altered in 30 sec it may
cause cell death
Arthrosclerosis can leads to thrombus formation and contribute emboli
TYPES OF STROKE
 Ischemic
Thrombotic
Embolic
 Haemorrhagic

13. TYPES OF ISCHEMIA
 Cardiac ischemia
 Mesenteric ischemia
 Brain ischemia
 Acute limb ischemia
 Cutaneous ischemia

14. ANTI ISCHEMIC AGENTS
Coronary vasodilators
• Nitrites& Nitrates
Short acting (3-60 min)
Amyl nitrite, Nitro-glycerine,
ISD
Intermediate
acting
ISD, Nitro-
glycerine
Long acting( 6-60
hrs)
Erythryl
tetranitrate, Nitro-
glycerine
Based on duration of
action

15.  Beta adrenergic blocking agents- Atenolol, propranolol, Nadolol
 Calcium channel blockers - Amlodipine, Diltiazem, Felodipine,
Verpamine
 Potassium channel activators- Pinacidil
 Anti platelet drugs – Aspirin, clopidogrel
 ACE inhibitors - Captopril, Enalapril
 Cholesterol lowering mediators – Atorvastatin, Fenofivarate

16. Further treatments
 Surgical procedures of MI
 Angioplasty and stenting
 Coronary artery bypass surgery

17. ORGANIC NITRATES
Release of NO Radicle
Activation of Guanylate
cyclase
Activation of cyclic GMP
Dependent Kinase
DE phosphorylation of
myosin light chain
Vasodilation venules and
arterioles

18. MECHANISM OF ACTION

19. CVS
Dilates veins more than arteries – Peripheral pooling of blood-
decreased venous return- preload of heart decreases- end diastolic
pressure reduces- decreased cardiac work
RENAL & SPLANCHINIC SYSTEM
Blood flow decreases to compensate for vasodilation
PHARMACOLOGICAL
ACTIONS

20. LUNGS
Decongest lungs by shifting blood to systemic circulation
SMOOTH MUSCLE
Bronchi, Biliary tract and oesophagus are relaxed

21. ADVERSE EFFECTS
1. Hypotension
2. Methemoglobinemia
3. Throbbing headache
4. Flushing
5. Tolerance
6. Constipation

22. CLINICAL USES OF NITRATES
Treatment& prophylaxis of classical Angina
Treatment of variant Angina
 Myocardial infraction
 Treatment of arrhythmia

23. CALCIUM CHANNEL BLOCKER
These are the drugs protect tissue by inhibiting
the entry of calcium ions into cardiac and
smooth muscle cells of coronary and systemic
arterial beds

24. CALCIUM CHANNEL BLOCKERS

25. MECHANISMOF ACTION

26. PHARMACOLOGICAL ACTIONS
 CVS
Produce vasodilation in heart muscle
SMOOTH MUSCLE
Relaxation by inhibit cyclic nucleotide phosphodiasterace –
increased C AMP


27. ADVERSE EFFECTS
 Swelling of legs
 Excess lowering of heart rate & Blood pressure
Depressing heart muscle

28. CLINICAL UESES OF CALCIUMCHANNEL BLOCKERS
 Supraventricular tachyarrhythmias
 Hypertension
 Reducing the frequency of attacks of angina

29. BETA BLOCKERS
These decreases the O2
demand lowering heart
rate& contractility
Blocking beta1
receptor by selective
beta1 antagonist

30. Mechanism of action

31. ADVERSE EFECTS OF BETA BLOCKERS
 Worsening of asthma
Depression & fatigue
 Impotence
Increased cholesterol level
Shortness of breath

32. CLINICAL USES OF BETA BLOCKERS
 treatment of myocardial ischemia
 Ventricular arrhythmia
 Pheochromocytoma
 hypertension

33. K CHANNEL OPENERS MECHNISMOF ACTION
Potassium channel openers
Activate potassium
channel
Increased potassium
permeability in cell
Hyperpolarisation
occurs

34. Closer of L-type calcium channels
Reduced intracellular free calcium
Leads to vasodilation

35. ADVERSE EFFECTS
 Vasodilation
Head ache
 Decreased BP
 Stomach pain
 Vomiting

36. ANTIPLATELITE DRUGS
These are the drugs which interfere with platelet function and may useful in the
prophylaxis of thromboembolic disorders
MECHANISM OF ACTION
Platelet sticks to the damaged blood vessels and they stick to each other and
release ADP thromboxane A2 Which promotes further aggregation thus a
platelet plug is formed which traps the RBC s
Prostacyclin's synthesised in the intima of blood vessels is a strong inhibitor of
platelet aggregation

37. CLINICAL USES OF ANTI PLATELET DRUGS
 Coronary artery disorders
 primary & secondary prevention of angina
 Cerebrovascular disorders
 Coronary bypass implants
 Venous thromboembolism

38. CHOLESTROL LOWERING DRUGS

39. Competitively inhibiting HMG-CoA Reductase first enzymes of
HMG CoA Reductase pathway
which is able to produce mevalonate used in the production of
cholesterol
Reduce LDL Levels by 30% to 40%
Reduce HDL level by 2% to 15%
Reduce triglycerides by 10% to 30%

40. MECHANISMOF ACTION

41. ADVERSE EFFECTS
o Mild transient GI disturbances
o Rash headache
o Myopathy
o Elevation of liver diseases
CLINICAL USES
Hyperlipidaemia
Coronary artery disorders

42. ACE INHIBITORS
ACE Inhibitors are produced its action by inhibiting Reni release
Renin Release
Angiotensinogen
Angiotensin 1
ACE inhibitors
Angiotensin11
Vasoconstriction

43. CLINICAL USES OF ACE INHIBITORS
 Hypertension
 Cardiac failure
 Following myocardial infraction , Ventricular dysfunction
 Diabetic nephropathy
 Progressive renal insufficiency

44. ADVERSE EFFECTS
 Neutropenia
Heavy proteinuria
 Hypotension
 Dry cough
 Hyperkalaemia

45. REFERENCE
 Text book of pharmacology , fourth edition by H.P Rang &
M.M Dale Page no 291- 295
 Essentials of medical pharmacology , third edition by K.D
Tripathi page no 476-481
 Text Book of Robbins pathologic basis of disease –
Robbins, Cotran, Kumar , prisin

46. THANK YOU