Ami

AMIAMI

DefinitionDefinition

• AMI is almost always d/f formation of occlusive thrombus at the site of capture or erosion of an athermanous plaque.

H/OH/O

• Chest pain - retrostenal, tightness, construction, heaviness- radiate to

- asso: with pallor, vomiting , collapse, syncope

- Painless or silent MI occur in older patients and diabetic patients.

neck

U.L

epigastria

Physical signPhysical sign• Sign of sym: activation

- pallor, seating , tachycardia• Sign of vagal activation

- vomiting , Brady cardia• Sing of impaired myocardial function

- hypotension, oliguria, cold peripheries- narrow pulse pressure- JVP- 3rd heart sound , quiet 1st Ht sd- diffuse apical impulse-lung crepitations

• Sign of t/s damage

- fever

• Sing of complication

- MR, persicarditis

D/DxD/Dx

• Cardiac

• Aortic

• Oesphageal

• Lung & pleural

• M/s- skeletal

• neurological

InvestigationInvestigation

• Echo p-592

• ST → progressive loss of R-wave, de: Q wave, resolution of st , terminal T-wave inversion → deep Q wave and T ↓ → Q wave tends to persist but T-wave changes become less marked. (several wks or months)

[ Full thickness MI]

• Deep symmetrical t-wave inversion tog: with reduction in height of R-wave without Q wave or prominent ST

[ Partial thickness MI or non-ST elevation MI]

• II, III, avF → interoar

• I, II, avL → anterior

• V1 V4 → antero-septal

• I, avL, V4 V6 → anterio-lat:

• II, III, avf, V4 V6 → interio-lat:

• RV infarct → Rt precardium recording

Plasma biochemical markersPlasma biochemical markers

• CK-MB - 4-6 hr:, peak- 12 hr:, with in 48-72 hr:

• Troponin T & I - release with in 4-6 hr:, remain far 2 wk

• AST

• LDH

Other blood testsOther blood tests

• ESR - • Leucouftaris• CRP

CXR• Pul: oedema, Ht size - normal

- - d/t pre-existing myocar: damage

EchoEcho

• For assessing Lt & Rt ventricular function

• To detect - mural thrombus, cardiac rupture, VSD

- MR, pericardial effusion

• American college of cardiology & European society of cardiology defined MI as:

• Typical in cardiac troponin T or I, or CK-MB, above 99 th centile for normal

+

at least one of the following

• Ischaemic symptoms

• Dev: of patho: Q wave on ECG, ischaemic changes (ST or ↓)

• PCI

Early management of acute myocardial infarctionEarly management of acute myocardial infarction

Provide facilities for defibrillationProvide facilities for defibrillation

Immediate measures• High-flow oxygen

• I.V. access• ECG monitoring• 12- lead ECG

• I.V analgesia (opiates) and antiemetic

• Aspirin 300 mg

Reperfusion• Primary PCI or

thrombolysis

Detect and manage

acute complications• Arrhythmias• Ischaemia

• Heart failure

TrombolysisTrombolysis

• Restore coronary patency, pressure LV function and improve survival thrombolysis leads to reperfusion with relief of pain, resolution of acute ST and transient arrythmia. The sooner the patient is treated, the better the results will be.

• Streptokinase - 1.5 million unit in 100 ml of N/S over 1 hr:,

widely used regueme.

alteplase

• tpA

Reteplase

Relative C.I to thrombolytic therapy Relative C.I to thrombolytic therapy (potential candidates for I angioplasty)(potential candidates for I angioplasty)

• Active internal bleeding• Previous SAH or ICH• Uncontrolled hypertension• Recent surgery (within 1 mth)• Recent trauma (including traumatic

resuscitation)• High probability of active PU• Pregnancy

PCI (I percutaneous coronary intervention)PCI (I percutaneous coronary intervention)

• PCI is more effective than thrombolysis for the treatment of AMI

• Maintaining u/s patency

Asprin - 300 mg cheured, 75 mg daily →30% ↓ in morality

Aspirin+ clopidogrel → further 10%↓ in morality with no evidence of bleeding

AnticoagulantLM WH

Warfarin

Adjunctive therapyAdjunctive therapya/c - IV β-blocker →↓pain,

arrythmia and improve short term mart

β-blocker → C.I –heart failure

chr: - oral β-blocker – improve long- term survival

Nitrates and other agents – to relive pain

ComplicationComplication

• Arrythmia - VF, VT, VE, AF, AT, sinus bradycardia, Ht block

• Post-infarct angina

• a/c circulatory failure

• Pericarditis

• Mechanical complication - a/c pul: oedema d/f papillary m/s damage- USD – rupture of IV septum- MR- rupture of ventricle lead to cardiac temponade- Embolism- impaired vent: function, remodeling and vent: aneurysm

Late management of MILate management of MI• Risk stratification and further inv:

LV function - physical findings – tachy:, 3rd Ht sd, crackles

- ECG changes, CXR, Echo or radionucleclide imaging

Ischaemia - exercise tolerance test approximately 4 weeks after infarct, coronary angio-

graphy

- T with angioplasty or bypass graph

Arrhythmais - anti-arrythmic drugs

- implantable cardiac defibrillators

• Lifestyle modification

- stop smoking

- regular exercise

- diet (wt control, lipid lowering)

• 2 prevention drug therapy

- Anti platelet therapy (aspirin and/or clopidogrel)

- β blocker

- ACEI

- Statin

- control of D.M and Hypertension

RehabilitationRehabilitation

• Where there is no complication – pt can sit in a chair on 2nd day, walk to toilet on 3rd day, return home in 5 days, gradually activity and return to work in 4-6 wks.

• Majority → resume driving after 4-6 wks.

Stable AnginaStable Angina

• Symptom complex caused by transuent myocardial ischaemia

• d/t imblance b/t myocardial oxygen supply and demand

• Coronary atheroma is the most common cause of angina

• Other cause – AS , HOCOM

Unstable AnginaUnstable Angina

• Clinical $ charac: by new-onset or rapidly worsening angina (cresendo angina), angina on minimal exertion or angina at rest.

• Dx and risk stratification in stable angina.

Resting ECGResting ECG• ST & T wave changes

Exercise ECG- down-sloping ST ↓1mm or more is indicative of

ischaemia.- False (+)ve result - digoxin therapy

- LVH

- LBBB

- WPW$

Myocardial perfusion scanning stress Echo with

dopamineinfusion

Advice to patients with stable anginaAdvice to patients with stable angina

• Do not smoke

• Aim at ideal body wt

• Take regular exercise

• Avoid severe unaccustomed exertion and vigorous exercise after a heavy meal or in very cold weather

• Take sublingual nitrate before undertaking exertion that may induce angina

ManagementManagementThe management of angina pectoris involves:• A careful assessment of the likely extent and

severity of arterial disease• The identification and control of significant risk

factors (e.g. smoking, hypertension, hyperlipidaemia)

• The use of measures to control symptoms• The identification of high-risk patients and

application of treatments to improve life expectancy

Antiplatelet therapyAntiplatelet therapy

• Low-dose (75-150 mg) aspirin

Anti-anginal drug treatment

• Nitrates

• Beta-blockers

• Calcium antagonists

• Potassium channel activators

• Invasive treatment

• Percutaneous coronary intervention (PCI)

• Coronary artery bypass grafting (CABG)

ManagementManagementUnstable anginaUnstable angina

Unstable angina :risk stratification

High risk Low risk

Clinical Post-infarct angina

Recurrent pain at rest

Heart failure

No history of MI

Rapid resolution of symptoms

High risk Low risk

ECG Arrhythmia

ST depression

Transient ST elevation

Persistent deep T-wave inversion

Minor of no ECG

Changes

Biochemistry

Troponin T> 0.1μg/l Troponin T< 0.1 μg/l

N.B. There is a 5-to 10-fold difference in risk between the lowest and highest risk groups.

• The initial treatment should include bed rest, antiplatelet therapy (aspirin 300 mg followed by 75-325 mg daily long-term and clopidogrel 300 mg followed by 75 mg daily for 12 months, anticoagulant therapy (e.g. unfractionated or fractionated heparin) and a β-blocker, (e.g. atenolol 50-100 mg daily or metoprolol 50-100 mg 12 hourly)

• A dihydropyridine calcium antagonist (e.g. nifedipine or amlodipine)cane be added to β-blocker,but may cause an unwanted tachycardia if used alone; verapamil or dilteazem is therefore the calcium antagonist of choice if a β-blocker is contraindicated. An intravenous infusion of unfractionated heparin.

• Weight-adjusted subcutaneous low molecular weight heparin should be given if pain persists or recurs, infusions of intravenous nitrates

• Buccal nitrates may help, but such patients should also be considered for early revascularisation .

• Refractory cases or those with haemodynamic compromise should be considered for a glycoprotein IIb/IIIa receptor antagonist (e.g. abciximab, tirofiban or epitifibatide). Intra-aortic balloon pump or emergency coronary angiography.

• Most low-risk patients stabilise with aspirin, clopidogrel, heparin and anti-anginal therapy, and can be gradually mobilised. If there are no controaindications, exercise testing may be performed prior to or shortly following discharge.

• Coronary angiography should be considered with a view to revascularisation in all patient sat moderate or high risk, including those who fail to settle on medical therapy, those with extensive ECG changes, those with an elevated plasma troponin and those with severe pre-existing stable angina.

• This often reveals disease that is amenable to PCI. However, if the lesions are not suitable for PCI the patient should be considered for urgent CABG.