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Ischaemic Heart Disease. Coronary Heart Disease.

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Ischaemic Heart Disease. Coronary Heart Disease. Late complications: 1-Pericarditis:can occure after MI as an early complication;occur days after infarction ... – PowerPoint PPT presentation

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Title: Ischaemic Heart Disease. Coronary Heart Disease.


1
Ischaemic Heart Disease.Coronary Heart Disease.
2
  • Atheroma of the coronary arteries
  • The commonest cause of changes in the luminal
    diameter of the coronary arteries is the presence
    of atheromatous plaques.
  • The lesions may encircle an artery or may be
    eccentric they may be discrete and localised or
    involve the greater length of the vessel.
  • Acute changes in the plaques may account for
    unstable angina,myocardial infarction and sudden
    death.,because expansion of the lesion occurs
    when the endothelial cells rupture,allowing
    haemorrhage into the plaque and platelet
    aggregation on the endothelial surface.

3
  • Clinical feasture
  • Symptoms
  • The cardinal symptom is angina pectoris. This is
    a chest discomfort precipited by exertion and
    relieved by rest. It is often descriped as a
    pressing or constricting feeling.
  • The patient may hold a clenched fist in front of
    the sternum to indicate the squeezing nature of
    the pain,and may describe radiating discomfort in
    the left arm and jaw,or even a choking sensation
    in the throat.

4
  • Dyspnoea frequently accompanies angina.
  • There is usually rapid relief of the symptom with
    sublingual nitrate tablets.
  • The pain of myocardial infarction may be similar,
    but generally begins at rest ,does not respond so
    well to nitrates, lasts longer than 20 minutes
    and is often associated with feeling of impending
    death,nausea,sweating and collapse.
  • Unfortunately, in many patients with I H D ,the
    first manifestation of disease may be sudden
    death. Prevention of atheroma is necessary to
    reduce this.

5
  • Signs
  • There are few physical findings in uncomplicated
    I H D.
  • There may be evidence of hypertension or
    hyperlipidaemia
  • .
  • Cardiac dilatation,hypertrophy ,and failure are
    all late features and are non-specific.
  • .Auscultation may reveals a fourth and third
    heart sounds over the apex in Pt complicated with
    Lt vent .faliure.
  • Orthopnoea,and fine basal crackles are present in
    Pt developing pulmonary oedema.
  • Some individuals have significant ischaemic
    episodes without symptoms.This may discovered by
    routine ECG.

6
Other anginal syndromes
  • The previous is a desciption of typical
    angina.Several other anginal syndromes occur
    which are less common.
  • 1-Crescendo angina and unstable angina
  • Both represent a state of preinfarction.In
    crescendo angina, a history of increasingly
    frequent attacks of angina with ever-diminishing
    levels of exertion is obtained.Unstable angina
    includes situations where episodes of pain are
    frequent,may occure without obvious cause and at
    rest.
  • Decubitus angina is angina occuring at rest in
    bed.

7
  • 2-Vasospastic angina
  • Some degree of arterial spasm is probably present
    in most episodes of angina, but spasm on normal
    coronary can occur(rarely),this spasm can be
    sever enough to cause infarction.
  • In Prinzmetals syndrome,rest pain is associated
    with acute ST segment elevation which resolves to
    normal with cessation of pain.
  • This condition is rare and almost involves
    coronary vasospasm.

8
Differential Diagnosis of Angina
  • With all causes of chest pain
  • 1-Angina pectoris.
  • 2-Angina due to Aortic valve stenosis.
  • 3-Acute Myocardial infarction.
  • 4-Aortic dissection.
  • 5-Acute pericarditis.
  • 6-Oesophageal spasm.

9
Chest Pain
  • 1-Cardiac ischemic pain
  • In a typical case the discomfort associated with
    myocardial ischemia is described as a compression
    or tightness in the chest which may also be felt
    in the throat, producing the choking feeling
    being called angina pectoris.
  • Siteretrosternal.
  • Radiationleft side ,jaw ,arm,and forearm.

10
  • The precipitating causes are typically those
    which will increase myocardial oxygen demand
    beyond the coronary .Excersion ,Emotional upsets
    ,Cold .
  • What increaseEmotions,stress,cold.
  • What decreaseRest,Nitroglycerin GTN.
  • Durationless than 10 minutes.
  • Special types of anginaUnstable angina
    it is more sever form of angina,if untreated
    can lead to myocardial infarction.

11
  • Myocardial infarction
  • It causes pain similar to angina in
    site,radiation and character but it is usually
    more sever and prolonged and persists despite
    taking glycerin trinitrate.
  • Autonomic symptoms usually in association
    ,sweating ,irritability,palpitation ,nausea,and
    ,vomiting are common ,particularly in inferior
    wall infarction. Pt. may also be
    breathless,restless with sensation of impending
    death.
  • With acute anterior infarction,tendency for
    sympathetic activity to dominate,--tachycardia,coo
    l pale periphery and normal or even slightly high
    Bl.pressure in early minutes.This contrasts with
    acute inferior infarction,which associated with
    massive vagal discharge ,producing a cold sweaty
    periphery,bradycardia,hypotension,nausea and
    vomiting.

12
  • Painless or silent myocardial infarction is not
    uncommon,particularly in diabetic patient and the
    elderly.

  • This patients may present later with
    complications from their infarct such as cardiac
    faliure or an arrhythmia , diagnosis may be made
    retrospectively from routine electrocardiogram
    (ECG).

13
  • Pericardial pain
  • Chest pain is usually more localized than
    ischemic pain.
  • Site retrosternal,may radiate to Lt shoulder.
  • Prodromamay be preceded by viral illness.
  • Naturestabbing and sharp.
  • Made worse by change in posture,respiration.
  • Helped by analgesics.,and NSAIDS.
  • Accompanied by pericardial rub.

14
  • Aortic dissection
  • The sudden development of a linear tear in the
    wall of the aorta is called acute dissection.
  • The length of aorta affected varies from a few
    centimetres to the whole vessel.
  • Siteretrosternal.
  • Onsetsudden.
  • Naturevery sever ,tearing pain.
  • Relived byNo ,tend to persist.
  • Accompanied by Hypertension,Syncope.sweating,.

15
  • Risk factors for coronary Ht disease
  • 1-Age increased in older age due to
    atherosclerosis.
  • 2-Male sex .
  • 3-Postive family history of IHD.
  • 4-Hypertension.
  • 5-Hyperlipidaemia.
  • 6-Diabetes mellitus.
  • 7-Obesity.
  • 8-Lack of exercise.

16
Investigations1-in angina
  • 1-Resting ECG
  • Recording the electrical activity of the
    heart ,usually normal in between attacks ,in
    attack it may show ST segment depression,T wave
    inversion.
  • 2-Excerise ECG
  • It is recorded whilst the patient walks or run
    on motorized treadmill or cycles.If there is ve
    history of chest pain and ve resting ECG you can
    do stress ECG,it will be very useful to confirm
    the diagnosis.

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  • 3-Cardiac scintigraphyOr Nuclear imaging
  • Myocardial perfusion scan at rest and with
    exercise,using contrast like thallium,
  • (Th -201) is rapidly taken immediately after IV
    injection,reflects the distribution of blood flow
    to the myocardium--areas of decreased myocardial
    perfusion means ischemia.(receive less thallium).
  • 4-EchocardiographyUse echoes of ultrasound waves
    to map the heart and study its functions.This can
    be used to assess ventricular wall
    involvement..and vent.function,

23
  • Regional wall motion abnormalities at rest
    reflect previous ventricular damage.
  • 5-Coronary angiography
  • This is occasionally usefull in Pt with chest
    pain and the diagnosis is un clear.This can be
    done through cardiac catheterisation.
  • Coronary angiography is performed using catheters
    designed to select Lt and Rt coronary
    artery,inject X- ray contrast medium.,then the
    coronaries can be visualized.
  • it is usefull because it shows the exact coronary
    affected ,with narrowing or obstruction .

24
Normal coronary angiography.
25
Coronary narrowing.
26
Treatement of angina
  • 1-Treatment of risk factors
  • Hypertension ,DM,Obesity,stop
    smoking.Hyperlipidemia.
  • 2-Medical treatement
  • 1- VasodilatorsNitrates
  • .Glyceryl trinitrate(GTN)-tablets,and,skin
    patches.
  • Isosorbide dinitrate(oral,short
    actingsustained release)
  • Isosorbide mononitrates-(oral some SR)
  • 2- Beta blockers.
  • Atenolol(B1-selective)
  • Propranolol(non-selective.both tacken orally..
  • 3- Calcium channel blockers.Nifedipin,Diltiazem,
    Verapamil.
  • 3-Surgical Coronary artery bypass grafting and
    angioplasty.

27
Treatment of unstable angin
  • 1-ICU admission.
  • 2-Bed rest and light sedation.
  • 3-Oxygen.
  • 4-Low dose aspirin.antiplatlet aggregator.
  • 5-Heparin IV ,to minimise thrombus formation.
  • 6-Nitrates (buccal or iv)
  • 7-Close monitoring of blood pressure during
    nitrate infusion.care about hypotension.
  • 8-B-blockers and Ca antagonists may be added when
    needed.

28
  • In vasospastic or prinzmetal angina,the aim of
    treatment is to prevent the powerful
    vasoconstriction
  • Combination therapy using long acting isosorbide
    mononitrate,calcium antagonists.
  • Beta-blockers may have to be added to counteract
    the reflex tachycardia and reduce the intensity
    of angina by reducing 02 demand during the attack.

29
  • Investigations in acute MI
  • 1-ECG Q-wave ,and riased ST segment in affected
    leads.
  • 2-Cardiac enzymes
  • Creatinin kinase CK --CK-MB(cardiac
    specific).increased withen few hours,and
    decreased in 24-48 hours.
  • Cardiac-specific troponins Troponin I .,are
    regulatory proteins,increased in cardiac injury.
  • Lactate dehydrogenase ( LDH)appers withen 12-24
    hours,and disappered late.
  • 3-A raised polymorphonuclear leucocyte count and
    elevated (ESR) are non specific companiments of
    acute MI.

30
Treatment of acute MI
  • Acute management
  • Analgesia and oxygen,bed rest.
  • .
  • If acute MI diagnosed ,Thrombolysis must be done
    with out delay .Six hours is the time limit
    withen which it is possible that measures to
    restore Bl.supply.
  • Thrombolytic treatement can achieve reperfusion
    in 50-70 of patients,and usually reduces the
    extent of ventricular damage and mortality rate.
  • Streptokinase (1.5 million units over one hour)
    is the agent most commonly used.
  • .

31
Asiprin ,as an antiplateletes,150 mg
chewed. Heparin. Nitrates,by infusion early
,later on we can use skin patches. B-blockers,-de
creased the rate of cardiac deathes. Follow up.
32
Complications of acute MI
  • Acute complications
  • 1-Very early after infarction,all kinds of
    cardiac arrhythmia can occur like
  • Ventricular extrasystoles
  • Ventricular tachycardia
  • Ventricular fibrillation.
  • Atrial fibrillation.
  • Sinus tachy or bradycardia.
  • Conduction disturbance.

33
  • 2-Cardiac failure.
  • 3-Cardiogenic shock.
  • 4-Thromboembolism ,due to Lt ventricular mural
    thrombus may form on the endocardial surface of
    the infarcted region.
  • 5-Acute ventricular septal rupture and ruptured
    papillary muscle.Treatment is early surgery for
    both.

34
  • Late complications
  • 1-Pericarditiscan occure after MI as an early
    complicationoccur days after infarction,clinicall
    y sharp chest pain aggrevated by movement.
  • 2-Post myocardial infarction syndrome(Dressler
    syndrome)
  • Late complicationIt is an autoimmune
    pericarditis ,(antibodies aginst cardiac myocytes
    were detected) occur weaks or months after
    infarction consists of pericarditis, fever,high
    ESR, and pericardial effusion.,treated by
    NSAIDs,and corticosteroids.Prognosis is good.
  • 3-Left ventricular aneurysm .
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