NSTEMI DrHafiz
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Transcript of NSTEMI DrHafiz
NON-ST ELEVATION MIBBH, Bangalore
Ahmad Hafiz
Nov 2011
ACUTE CORONARY SYNDROME SPECTRUM
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
WHAT IS NSTEMI?
Unstable angina = angina pectoris with at least one of three features:
1. it occurs at rest (or with minimal exertion) usually lasting more than 20 minutes (if not interrupted by nitroglycerin)
2. it is severe and described as frank pain and of new onset (i.e., within 1 month); and
3. it occurs with a crescendo pattern (i.e., more severe, prolonged, or frequent than previously). With or without ischemic ECG changes
NSTEMI = UA with evidence of myocardial necrosis on the basis of the release of cardiac markers
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
Davidson pg. 589
PATHOPHYSIOLOGY
UA/NSTEMI is caused by reduction in oxygen supply and/or increased myocardial oxygen demand superimposed on an atherosclerotic coronary plaque with varying degrees of obstruction
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
1. Plaque rupture or erosion with superimposed non-occlusive thrombus
2. Dynamic obstruction3. Progressive mechanical
obstruction4. Secondary unstable
angina related to increased myocardial oxygen demand and/or decreased supply
CLINICAL PRESENTATION
SYMPTOMS: chest discomfort epigastric discomfort shortness of breath nausea and vomiting excessive sweating palpitation, anxiety, sense of
impending doom, and feeling of being acutely ill
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
PHYSICAL EXAMINATION Resembling that of stable
angina Large NSTEMI may resemble
that of large STEMI e.g. diaphoresis, pale cool skin, sinus tachycardia, S3 or S4, basilar rales and sometimes hypotension
Signs of co-morbidities e.g. peripheral or cerebrovascular diseases
Autonomic disturbances e.g. pallor, sweating
Complications e.g. arrhythmia or heart failure
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
ECG CHANGES1. ST depression (70-80%)2. T wave inversion (10-20%)3. Both ST depression and T
wave inversion4. Post MI NSTEMI - ECG
changes variable (Ironically, even a residual ST elevation may be present)
5. Normal ECG
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
CARDIAC MARKERS
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
TROPONIN-T
Peak – 12 hours Troponin is released during MI from the
cytosolic pool of the myocytes Its subsequent release is prolonged with
degradation of actin and myosin filaments Differential diagnosis of troponin elevation
includes acute infarction, severe pulmonary embolism causing acute right heart overload, heart failure, myocarditis
Troponins can also calculate infarct size but the peak must be measured in the 3rd day. released in 2–4 hours and persists for up to 7 days.
BNP
B-type natriuretic peptide is a cardiac neurohormone released upon ventricular myocyte stretch as proBNP, which is enzymatically cleaved to the N-terminal proBNP (NT-proBNP) and, subsequently, to BNP. The usefulness of assessing this neurohormone was first shown for the diagnosis and evaluation of HF.
GLYCOGEN PHOSPHORYLASE ISOENZYME BB Peak – 7 hours Glycogen phosphorylase isoenzyme BB
(abbreviation: GPBB) is an isoenzyme of glycogen phosphorylase
Glycogen phosphorylase exists in 3 isoforms. One of these Isoforms is GP-BB. This isoform exists in heart and brain tissue
Because of the blood-brain barrier GP-BB can be seen as heart muscle specific. During the process of ischemia, GP-BB is converted into a soluble form and is released into the blood. This isoform of the enzyme exists in cardiac (heart) and brain tissue. GP-BB is one of the "new cardiac markers" which are discussed to improve early diagnosis in acute coronary syndrome. A rapid rise in blood levels can be seen in myocardial infarction and unstable angina. GP-BB elevated 1–3 hours after process of ischemia.
MYOGLOBIN (MB)
Myoglobin is used less than the other markers
Myoglobin is the primary oxygen-carrying pigment of muscle tissue
It is high when muscle tissue is damaged but it lacks specificity. It has the advantage of responding very rapidly, rising and falling earlier than CK-MB or troponin. It also has been used in assessing reperfusion after thrombolysis
CK-MB
Peak – 10-24 hours CK-MB resides in the cytosol and facilitates
high energy phosphates into and out of mitochondria
It is distributed in a large number of tissues even in the skeletal muscle
Since it has a short duration, it cannot be used for late diagnosis of acute MI but can be used to suggest infarct extension if levels rise again
This is usually back to normal within 2–3 days.
MANAGEMENT GUIDELINE
SuspicionEarly management-Emergency management-Hospital phase management-Pharmacotherapy
Late Management-Risk stratification-Life style modification-Secondary prevention drug therapy
ALGORITHM FOR EVALUATION AND MANAGEMENT OF PATIENTS SUSPECTED OF HAVING ACS
EMERGENCY MANAGEMENTABC, Pulse Oximeter, Attach ECG monitor and record 12-lead ECG,
High flow O2 by face mask
IV access [bloods for CBC, U&E, glucose, lipids, cardiac enzymes]
Brief assessment
History of CVS disease, risk factors for IHDExamination: pulse, BP, JVP, cardiac murmurs, scar from previous cardiac surgery
Aspirin 300 mg or Clopidogrel 75mg
Morphine 5-10 mg IV + metoclopramide 1 mg IV
GTN sublingually
Thrombolysis management
Beta blockers + ACEI
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
ACUTE REPERFUSION THERAPY
1. Thrombolysis2. PCI3. CABG
Aim :•Restore coronary patency•Preserves left ventricular function•Improves survival rate and reduced mortality rate.
THROMBOLYSIS Indication:
Ischaemic chest pain > 30 minutes duration
Less than 12 hours from the onset of pain
ECG changes: new ST elevation of at least 2 mm in two
consecutive chest leads; or ST elevation of at least 1 mm in two
consecutive limb leads; or a new left bundle branch block.
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
FibrinolysisStreptokinase Dosage : 1.5 million units in 100 ml saline
Route of administration : IV infusion over 1 hour
Mode of action : Catalyze the conversion of plasminogen to active plasmin which further lyse the clots.
Side effects :-Allergic manifestations-Hypotension-Systemic bleeding
Note: production of circulating neutralizing antibodies following therapy may cause subsequent infusion with streptokinase ineffective
Alteplase Tissue plasminogen activators
MOA : specifically bound to fibrin-bound plasminogen
Route of administration:IV infusion over 90 minutes duration
Side effects :less compared to streptokinase- risk of intracranial bleeding
Other drugs: Tenecteplase –longer plasma half life
Reteplase - given as double bolus instead of infusion
First 30 mins Bolus dose 15mg
Followed by 0.75mg/kg
Next 60 mins 0.5mg/kg
(not > 35mg)
FULL THERAPEUTIC ANTICOAGULATION
Use either an infusion of unfractionated heparin or low molecular weight heparin(e.g., enoxaparin sodium).
In the context where pathology is not readily available, low molecular weight heparin is often easier to use
ADJUNCTIVE THERAPY
Consider intravenous beta-blocker (metoprolol 5 mg IV slow bolus at 0 min, 5 min and 10 min to give a total dose of 15 mg) then oral therapy (2). IV beta-blockers decreases mortality when given
early in acute myocardial infarction though the evidence is less clear in the reperfusion therapy setting;
it is more commonly used in the United States and parts of Europe and is routine therapy in Scandinavia.
ACE-inhibitors: when started within 24 hours reduce morbidity and mortality.
CONTRAINDICATIONS TO THROMBOLYTIC THERAPY
Active internal bleeding Previous history of subarachnoid or
intracerebral bleeding Uncontrolled hypertension Recent surgery (less than 1 month) Recent trauma High probability of active peptic
ulcer Pregnancy
PRIMARY PERCUTANEOUS CORONARY INTERVENTION
Primary percutaneous intervention is more effective than thrombolysis for treatment of AMI.
Death, non fatal reinfarction and stroke reduced from 14% with thrombolytic therapy to 8% with primary PCI
Keeley EC, et al. Lancet 2003;361:13-20
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
Treatment of choice to prevent reinfarction
Avoid hemostatic problems encounter with thrombolytic therapy
Preferred in case of presence of cardiogenic shock, bleeding risk, symptoms of more than 2-3h
Disadvantage
Expensive in terms of facilities and personnel, limited availability.
CORONARY ARTERY BYPASS GRAFTING (CABG)
surgical procedure performed to relieve angina and reduce the risk of death from coronary artery disease.
Arteries or veins from elsewhere in the patient's body are grafted to the coronary arteries to bypass atherosclerotic
narrowing and improve the blood supply to the coronary circulation supplying the myocardium.
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
HOSPITAL PHASE MANAGEMENT Coronary care units- provide intensive care. Duration of stay
depends on the condition of patient.
Activity – advise bed rest for first 12 hours, as increase workload to the heart may cause increase size of the infarct.
Diet – clear liquids for first 4-12 hours due to risk of emesis and aspiration. Diet should contain 50% complex carbohydrate and low fat contents.
Bowels – prevention of constipation by giving high fiber diet, laxative can be prescribed.
Sedation – Diazepam, oxazepam or lorazepam is given for sedation to enforced inactivity with tranquility.
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
LATE MANAGEMENT
Risk stratification and investigation
1. Left ventricular functions Assess by physical findings i.e tachycardia,3rd heart
sounds, crackles at lung bases Echocardiography and radionuclide imaging to assess LV
ejection fraction.
2. Arrhythmias Presence of ventricular arrhythmias during convalescence
phase may benefit from specific anti arrhythmic therapy such as implantable cardiac defibrillator.
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
3. Early post MI ischemia is managed like unstable angina
If no spontaneous ischemia, assess by exercise testing to look for residual ischemia-Good exercise tolerance – 1-4% chance of adverse event in 12 months
-Low exercise tolerance – consider revascularization by CABG
4. Other risk factors include age >75,diabetic
patient, prolonged sinus tachycardia, hypotension and silent ischemia
SECONDARY PREVENTION Long term drug therapy with low dose
aspirin, clopidogrel, beta blockers and ACEI
Cessation of smoking
Control of hypertension and hyperlipidemia
Regular exercise
Diet – diet high in fibers, fruit, oily fish, low in saturated fat, weight control
Returning to work after 4-6 weeks
ACS > NSTEMI > Pathophysiology > Clinical > Physical > ECG > Cardiac Markers > Emergency > Thrombolysis > PCI > CABG > Hospital > Late MGMT > Secondary Prevention
REFERENCE
2011 ACC/AHA Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction
http://content.onlinejacc.org/cgi/content/short/57/19/e215
Harrison's Principles ofInternal Medicine, 17e
Davidson’s Principles & Practice of Medicine, 20e
wikipedia Medscape
http://emedicine.medscape.com/article/811905-overview#aw2aab6b3
The End