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Angina pectoris & mi new

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Nida Badvi
Nida Badvi

Angina and myocardial infarction are caused by reduced oxygen supply to heart muscles due to coronary artery spasm or obstruction. Angina presents as chest pain and comes in different types based on triggers and severity. It is treated with nitrates, beta blockers, calcium channel blockers, and ranolazine to prevent symptoms and disease progression. Myocardial infarction, also called a heart attack, occurs when blood flow decreases or stops to the heart, damaging the heart muscle. It is diagnosed through cardiac biomarkers and ECG and managed initially with analgesics, anticoagulants, and antiplatelet drugs, followed by lifestyle modifications and secondary prevention medications long-term.

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TREATMENT OF ANGINA & MYOCARDIAL INFARCTION By: DR: Nida Ayesha
Spasm/obstruction of coronary arteries Myocardial ischemia Reduced O2 supply to myocardium Chest pain---Angina pectoris Angina pectoris Chest pain due to ischemia of heart muscles
Weak relationship between severity of pain and degree of oxygen supply- there can be severe pain with minimal disruption of oxygen supply or no pain in severe cases Four types: Stable angina Unstable angina Microvascular angina Prinzmetals angina
Stable or Classical It occurs due to increase myocardial oxygen demand during exertion or emotion in a patient of narrow coronary arteries. It relieved by rest and nitroglycerine. . However, when myocardial demand increases, ischemia results. N.A.N
Variant or Prinzmetals Angina Transient impairment of coronary blood supply by vasospasm or platelet aggregation Majority of patients have an atherosclerotic plaque N.A.N
Prinzmetals Angina Spasm of a large coronary artery Transmural ischemia ST-Segment elevation at rest or with exercise More prolonged than in classical angina. It occurs more in women under age 50. N.A.N
Unstable angina: Also called Crescendo angina Acute coronary syndrome in which angina worsens Occurs at rest Severe and of acute onset Crescendo pain- pain increases every time
Microvascular angina: Also called Syndrome X Cause unknown Probably due to poor functioning of the small blood vessels of the heart, arms and legs No arterial blockage Difficult to diagnose because it does not have arterial blockage Good prognosis
Major risk factors Age Smoking Diabetes Mellitus DyslipidemiaHypertension Obesity Chronic psychological stress
Angina pectoris & mi new
Symptoms What is the cause of ischemia ? Inadequate blood supply and decreased oxygen supply are directly related to blockade or narrowed vessels either oxygen demand or oxygen supply
Aims of therapy Prevent disease progression (secondary prevention) Control symptoms
Drugs: 1. For treatment of acute attacks: Organic nitrates/nitrites 2. For prophylaxis: Organic nitrates Beta blockers Calcium channel blockers Ranolazine
Relaxation of vascular smooth muscles- vasodilatation NO-mediated guanylyl cyclase activation inhibits platelet aggregation Relaxation of smooth muscles of bronchi and GIT
Pharmacokinetics: Orally ineffective because of high first pass metabolism Administered sublingually to avoid first pass matabolism Tolerance: Repeated doses lead to tolerance Dose spacing is necessary Reasons for tolerance: 種 Capacity of vascular smooth muscle to convert nitrates to NO called true vascular tolerance
ADRs: Headache- may be severe May disappear after continued use or, Decrease dose Transient episodes of dizziness, weakness, pallor etc- symptoms of postural hypotension Rashes severe hypotension Uses: Angina pectoris, CHF, MI
Administration of nitrates: Sublingual Oral: For prophylaxis, require high doses due to first pass metabolism, isosorbide dinitrate (20 mg or more) every 4 h or mononitrate (20 mg or more) OD or BD Cutaneous: Ointment (2%) applied to 2.5-5 cm patch of skin
Transdermal nitrogycerine discs impregnated with nitroglycerine polymer- gradual absorption and 24 h plasma nitrate concentration Onset is slow Peak concentration in 1-2 h Interrupt therapy for at least 8 h a day to prevent tolerance
Ca2+ antagonists: Ca2+ influx Negative iono and chronotropic effects Peripheral vasodilatation Used in variant angina (spasm), exertional angina, unstable angina, MI, hypertension, antiarrhythmic
-Blockers: Effective in reducing severity and frequency of exertional angina May worsen vasospastic angina- contraindicated Reduce myocardial O2 demand by reducing cardiac work (-ve iono and chrono effects; decrease in BP during rest and exercise) All -blockers are equally effective
-Blockers Protective effect and symptom control All patients unless contraindicated Asthma (reversible airways obstruction) Severe peripheral vascular disease Heart block / bradycardia Hypotension
Dose depends on effect (no specific dose) Avoid sudden withdrawal if possible Monitoring Effectiveness Heart rate (50-60 bpm if tolerated) Blood pressure Toxicity Side effects (often overemphasised) Cold extremities Nightmares Fatigue (especially on initiation) Wheeze Impotence
Ranolazine: Reserve agent for treatment of chronic, resistant angina Inhibits cardiac late Na+ current Effects the Na+ dependent Ca2+ channels and prevents Ca2+ overload that causes cardiac ischemia Decreases cardiac contractility No change in HR, BP Prolongs QT interval so it is contraindicated with drugs that increase QT interval
Myocardial infarction MI also known as Heart attack When blood flow decreases or stop causing to a part of the heart, causing demage to the heart muscle.
CRITERIA FOR ACUTE MI It should be used when there is evidence of myocardial necrosis in a clinical settings along with acute ischemia Detection of rise and fall of cardiac biomarkers values Symptoms Significant st segments
CLINICAL FEATURES Chest pain Breathlessness Vomiting Collapse/ Syncope Anxiety
Diagnosis Biochemical marker of cardiac demage such as Trop I &T ECG is the gold standard method (Misleading when new bundle branch block or previous MI) X-Ray chest shows pulmonary edema/cardiomegaly
DIAGNOSIS CK more sensitive Start to rise at 4-6 hours,peak up to 12 hours Present in skeletal muscle Trop T & I are released within 4-6 hours & remain elevated for up to 2 weeks leucocytosis peak on 1st day C-reactive & ESR are raised
MANAGEMENT Immediate manage the patient 1st 12 hours Pt should be admited urgently to the hospital Analgesia- IV opiates, Morphine sulphate Anti emetic Metoclopramide Anti thrombolitic therapy
Antithrombolitic therapy Antiplatelet & anticoagulants oralAspirin 75 -325mg daily,1st 12 hours If any side effect seen combo of Aspirin with Clopidogrel for 1 week.
ANTICOAGULANTS Reduce risk of thromboembolic complications Prevent reinfections Aspirin LMW Heparin S/C BD Warfarin- persistant atrial fibrillation or Echo show mobile mural thrombus.
COMPLICATIONS Transmural MI Arythmias Ventricular fibrillations Atrial fibrillations Bradycardia Embolism Acute circulatory failure
Late Management Life style modifications Diet (weight control) Stop smoking Regular excersise
SECONDARY PREVENTION Antiplatelet Beta blockersa Statin ACE inhibitors Control Diabetes /Hypertension Rehabilitation Devices: implantable cardiac debrillator (high risk patient)
PROGNOSIS One quarter of all the case death occour within few minutes without medical care Half of the patient death occour within 24 hour Prognosis is better who survive to reach hospital is much better.

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Angina pectoris & mi new

  • 1. TREATMENT OF ANGINA & MYOCARDIAL INFARCTION By: DR: Nida Ayesha
  • 2. Spasm/obstruction of coronary arteries Myocardial ischemia Reduced O2 supply to myocardium Chest pain---Angina pectoris Angina pectoris Chest pain due to ischemia of heart muscles
  • 3. Weak relationship between severity of pain and degree of oxygen supply- there can be severe pain with minimal disruption of oxygen supply or no pain in severe cases Four types: Stable angina Unstable angina Microvascular angina Prinzmetals angina
  • 4. Stable or Classical It occurs due to increase myocardial oxygen demand during exertion or emotion in a patient of narrow coronary arteries. It relieved by rest and nitroglycerine. . However, when myocardial demand increases, ischemia results. N.A.N
  • 5. Variant or Prinzmetals Angina Transient impairment of coronary blood supply by vasospasm or platelet aggregation Majority of patients have an atherosclerotic plaque N.A.N
  • 6. Prinzmetals Angina Spasm of a large coronary artery Transmural ischemia ST-Segment elevation at rest or with exercise More prolonged than in classical angina. It occurs more in women under age 50. N.A.N
  • 7. Unstable angina: Also called Crescendo angina Acute coronary syndrome in which angina worsens Occurs at rest Severe and of acute onset Crescendo pain- pain increases every time
  • 8. Microvascular angina: Also called Syndrome X Cause unknown Probably due to poor functioning of the small blood vessels of the heart, arms and legs No arterial blockage Difficult to diagnose because it does not have arterial blockage Good prognosis
  • 9. Major risk factors Age Smoking Diabetes Mellitus DyslipidemiaHypertension Obesity Chronic psychological stress
  • 11. Symptoms What is the cause of ischemia ? Inadequate blood supply and decreased oxygen supply are directly related to blockade or narrowed vessels either oxygen demand or oxygen supply
  • 12. Aims of therapy Prevent disease progression (secondary prevention) Control symptoms
  • 13. Drugs: 1. For treatment of acute attacks: Organic nitrates/nitrites 2. For prophylaxis: Organic nitrates Beta blockers Calcium channel blockers Ranolazine
  • 14. Relaxation of vascular smooth muscles- vasodilatation NO-mediated guanylyl cyclase activation inhibits platelet aggregation Relaxation of smooth muscles of bronchi and GIT
  • 15. Pharmacokinetics: Orally ineffective because of high first pass metabolism Administered sublingually to avoid first pass matabolism Tolerance: Repeated doses lead to tolerance Dose spacing is necessary Reasons for tolerance: 種 Capacity of vascular smooth muscle to convert nitrates to NO called true vascular tolerance
  • 16. ADRs: Headache- may be severe May disappear after continued use or, Decrease dose Transient episodes of dizziness, weakness, pallor etc- symptoms of postural hypotension Rashes severe hypotension Uses: Angina pectoris, CHF, MI
  • 17. Administration of nitrates: Sublingual Oral: For prophylaxis, require high doses due to first pass metabolism, isosorbide dinitrate (20 mg or more) every 4 h or mononitrate (20 mg or more) OD or BD Cutaneous: Ointment (2%) applied to 2.5-5 cm patch of skin
  • 18. Transdermal nitrogycerine discs impregnated with nitroglycerine polymer- gradual absorption and 24 h plasma nitrate concentration Onset is slow Peak concentration in 1-2 h Interrupt therapy for at least 8 h a day to prevent tolerance
  • 19. Ca2+ antagonists: Ca2+ influx Negative iono and chronotropic effects Peripheral vasodilatation Used in variant angina (spasm), exertional angina, unstable angina, MI, hypertension, antiarrhythmic
  • 20. -Blockers: Effective in reducing severity and frequency of exertional angina May worsen vasospastic angina- contraindicated Reduce myocardial O2 demand by reducing cardiac work (-ve iono and chrono effects; decrease in BP during rest and exercise) All -blockers are equally effective
  • 21. -Blockers Protective effect and symptom control All patients unless contraindicated Asthma (reversible airways obstruction) Severe peripheral vascular disease Heart block / bradycardia Hypotension
  • 22. Dose depends on effect (no specific dose) Avoid sudden withdrawal if possible Monitoring Effectiveness Heart rate (50-60 bpm if tolerated) Blood pressure Toxicity Side effects (often overemphasised) Cold extremities Nightmares Fatigue (especially on initiation) Wheeze Impotence
  • 23. Ranolazine: Reserve agent for treatment of chronic, resistant angina Inhibits cardiac late Na+ current Effects the Na+ dependent Ca2+ channels and prevents Ca2+ overload that causes cardiac ischemia Decreases cardiac contractility No change in HR, BP Prolongs QT interval so it is contraindicated with drugs that increase QT interval
  • 24. Myocardial infarction MI also known as Heart attack When blood flow decreases or stop causing to a part of the heart, causing demage to the heart muscle.
  • 25. CRITERIA FOR ACUTE MI It should be used when there is evidence of myocardial necrosis in a clinical settings along with acute ischemia Detection of rise and fall of cardiac biomarkers values Symptoms Significant st segments
  • 26. CLINICAL FEATURES Chest pain Breathlessness Vomiting Collapse/ Syncope Anxiety
  • 27. Diagnosis Biochemical marker of cardiac demage such as Trop I &T ECG is the gold standard method (Misleading when new bundle branch block or previous MI) X-Ray chest shows pulmonary edema/cardiomegaly
  • 28. DIAGNOSIS CK more sensitive Start to rise at 4-6 hours,peak up to 12 hours Present in skeletal muscle Trop T & I are released within 4-6 hours & remain elevated for up to 2 weeks leucocytosis peak on 1st day C-reactive & ESR are raised
  • 29. MANAGEMENT Immediate manage the patient 1st 12 hours Pt should be admited urgently to the hospital Analgesia- IV opiates, Morphine sulphate Anti emetic Metoclopramide Anti thrombolitic therapy
  • 30. Antithrombolitic therapy Antiplatelet & anticoagulants oralAspirin 75 -325mg daily,1st 12 hours If any side effect seen combo of Aspirin with Clopidogrel for 1 week.
  • 31. ANTICOAGULANTS Reduce risk of thromboembolic complications Prevent reinfections Aspirin LMW Heparin S/C BD Warfarin- persistant atrial fibrillation or Echo show mobile mural thrombus.
  • 32. COMPLICATIONS Transmural MI Arythmias Ventricular fibrillations Atrial fibrillations Bradycardia Embolism Acute circulatory failure
  • 33. Late Management Life style modifications Diet (weight control) Stop smoking Regular excersise
  • 34. SECONDARY PREVENTION Antiplatelet Beta blockersa Statin ACE inhibitors Control Diabetes /Hypertension Rehabilitation Devices: implantable cardiac debrillator (high risk patient)
  • 35. PROGNOSIS One quarter of all the case death occour within few minutes without medical care Half of the patient death occour within 24 hour Prognosis is better who survive to reach hospital is much better.