Transcript Evolution of MI and Assessment of Prognosis with ECG Evidences

Evolution of MI and Assessment
of Prognosis with ECG
Evidences
Dr.A.M.Thirugnanam,MD.MSICP,.(USA).Ph.d..
Interventional Cardiologist
International Institute of Preventive Cardiology.
First National Conference on ECG and
Electrophysiology-May-7th 2006, Hyderabad
Evolution of ECG changes in
Myocardial Infarction
What is myocardial
infarction?
sudden rupture of
unstable plaque
causing thrombus
formation, platelet
aggregation and
cytokines activation.
Diagnosis of Myocardial infarction
by different technique
Myocardial cell death – by Pathology
Markers of myocardial cell death- by
Biochemistry
ECG ST-T changes and Q wave - by ECG
Reduction of perfusion and myocardial tissue
and cardiac wall motion abnormalities by
Imaging technique
QRS criteria for the diagnosis of
myocardial infarction
Criteria are valid in the absence of LVH,
LAFB, RVH, LBBB,LBBB, COPD, or W-PW pattern
Definition of Myocardial Infarction
Typical rise and fall of troponin or rapid
rise and fall of cardiac biochemical
markers (CK,CK-MB, LDH), associated
with chest pain and ECG changes.
Pathological Q wave in established MI.
Hyper acute and Fully evolved
Phase
Hyper acute phase:
Begins immediately or
few hours after MI.
ECG characters: leads
facing injury shows ST
elevation and tall and
upright T wave.
Fully evolves phase:
starts hours to days.
ECG-deep T inversion
and Pathologic Q wave
Long term ST-T changes in MI
Characters of Reciprocal ECG
changes in MI
No Q wave
Increased height of R
wave
ST segment
depression
Upright T wave
Location of Myocardial Infarction
Characters of AMI:
Acute MI can be described as
Subendocardial, endocardial,
subepicardial, epicardial, intramural or
transmural depending on the location and
extension of damage.
Location of Myocardial segments
and related coronary arteries
Location of myocardial segments
and related coronary arteries
Transmural Infarction
Transmural MI involves full thickness of wall and
most of the MI are transmural.
Usually QS wave are present or absence of R
wave.
Indicative changes: QS, ST elevation and T
inversion in leads facing area of damage.
Reciprocal changes: absence Q wave, ST
depression and tall upright T wave.
Transmural MI
Pathologic Q wave
characters:
Any Q wave in V1-V3
Q wave >20mm in V4
Q wave >30mm in V5
Q wave >30mm in V6
Q wave >30mm in
I,II,AVF or AVL
Subendocardial Infarction (Nontransmural infarction)
This is limited to the inner half of the
myocardium, may extend transmurally.
Subendocardial flow greater during diastole and
subepicardial flow greater during systole.
Subendocardial MI occurs due to increased LV
filling pressure.
Subendocardial cells die in 15-30 min
ECG changes in Subendocardial
MI
Transient ST depression
and T wave changes.
Shallow- depressed ST
without alteration of QRS
complex.
Non-Q wave infarction.
Probably occurs as a
result of different
mechanism than
thrombosis.
Localization of Myocardial
Infarction
Variation of chest in
various individuals, exact
localization of an infarct
may be impossible.
V1, V2 lie over RV
V3 lies over Anterior
ventricular septum
V4-V6 lie over LV
V1,V
ST segment elevation and related
coronary artery-RCA
Inferior II,III,aVF,I,
aVL – RCA 85%, LCA
15%
ST elevation and related coronary
artery-Left anterior descending
Anterior V1,V2,V3,V4,
II, III, aVF- LAD artery
ST elevation and related coronary
artery
Extensive anterior
wall MI.
I, aVL, V1-V6, II, III,
aVF- LM or LAD and
LCx.
Extensive Anterior wall MI
Lateral MI- Left circumflex
ST elevation in I, aVL,
V5,V6- coronary
artery of OM or LCX
ST elevation and related coronary
artery-LCX / Right Postero-lateral
True posterior MI-V7,
V8, V9, V1, V2,
ST elevation in Postero-inferiorPDA / RCA
ST elevation and related Leads
Superior segmentInferior segment Anterior segment Antero septal
V3
Antero apical
Antero lateral
V5, V6, I, aVL.
Lateral
High lateral
V5, V6.
Postero lateral in V1-V3, V5, V6.
Right ventricular Postero basal
-
I, aVL
II, III, aVF
V1-V4
V1, V2,
V4
V1, V2,
V5, V6
I, aVL,
Large R
RV4
V6, aVF
Differentiation of RCA and LCXRV4 morphology-S/S
>1mm ST elevation –Proximal RCA93%/88%
ST down sloping -
LCX: 85/97%
Up sloping ST segment without ST
elevation – distal RCA: 74/92%
ECG changes in Anterior MI
V1-V3, especially V3 involves the anterior
wall of LV, which responsible for cardiac
output, involves greater muscle mass-LAD
V2- any Q wave or R<1mm
V3- any Q wave or R<2mm
Indicative changes in I, aVL, V1-V4.
Reciprocal changes in II, III, aVF.
Loss of R wave or Q in V1-V4 suggests
AWMI, in the absence of LVH.
Prognosis in AWMI
Persistent ST elevation in V5-V6 indicates apical aneurysm
formation.
AWMI predisposes to both stasis and clot formation.
Patient prone to BBB, AVB, SVT, ventricular aneurysm, CHF,
pulmonary edema, shock, LV clot and apical akinesis.
Ventricular dysrhythmias are seen immediately after MI, and tend to
be due to increased automaticity.
Anterior MI’s are associated with the greatest impairment of Left
ventricle and greatest mortality.
Bad prognosis in MI- VSR
Bad prognosis in AWMI- LV
aneurysm
Determination of extent of AWMI
Proximal occlusion of 1st diagonal- STE >1mm in
I or aVL. Without Rx patient will lose much of the
pumping force of the LV.
New LAFB- occlusion in the proximal of 1st
diagonal.
New LBBB- occlusion in proximal 1st septal
perforator, infarct penetrate deep into septum.
Limb leads are normal in AWMI.
Steps to prevent deterioration in
AWMI
Early thrombolysis. WP<60min.Door to needle time
should be less than 60min.
If possible shift patient to nearest PCI center. Door to
balloon time should be less than 3 hours.
Late thrombolysis in recurrent angina even after 24
hours age less than 65 years.
Ensure proper administration of Beta- blockers, ACEI’s,
Aspirin, clopidogrel, statin, anticoagulant, and IV
antiplatelets.
Diagnosis of cardiogenic shock in
AWMI
1) Persistent hypotension for more than 30
min,
2) Systolic Pressure less than 80mmhg,
3) Increased pulmonary capillary wedge
pressure.
4) Marked cardiac output reduction.
5) Urine output 20-30ml/hour.
Cardiogenic shock Incidence in
AMI
LV failure-74.5%
Acute MR-8.3%
VSR-4.6%
RV shock-3.4%
Tamponade-1.2%
Others-7.5%
Management of cardiogenic shock
in AWMI
If SBP>100mmHg, patient asymptomatic give
NTG 10-20mcg/min.
If SBP is 70-100mmHg, patient has signs and
symptoms, give dobutamine 2-20mig/min.
If SBP is 70-100mmHg, patient has signs and
symptoms, give dopamine 5-15mic/min
If SBP is <70mmHg, patient is symptomatic give
adrenalin 30mic/min
Inferior Wall MI- related artery RCA
Prognosis in inferior MI-RCA
Involved leads-II, III, AVF, - infarct on inferior surface of
the heart where it rests against the diaphragm.
Degree of STE in descending order-III, aVF, II.
Normally small portion of LV involved than in anterior MI.
Usually has a better outcome than anterior MI.
1st degree AVB, bradycardia are common.
Prognosis in IWMI-RCA
Acute inferior ischemia or infarction may cause
increased parasympathetic activity manifested as sinus
bradycardia and hypotension.
RV infarction is seen only in proximal RCA.
RVMI causes increased RV filling pressure and
decreased LV filling and systolic pressures.
Papillary muscle dysfunction and valvular insufficiency in
true posterior MI. ST depression in V1-V3 or STE in V7V9.
Prognosis in inferior Wall MI-RCA
RCA lesion causes SA node ischemia and there
by it leads to sinus bradycardia.
RCA related infarction manifested by sinus
bradycardia, AV block, hypotension and
dysrhythmias.
Vagal stimulation causes decreased oxygen
demand and decreased coronary flow.
Proximal RCA total occlusion can cause Sinus
bradycardia, AV nodal 2nd and 3rd degree block.
Treatment for RVMI complications
Hypotension- IV fluids
Bradycardia- IV atropine
AV node 2nd, 3rd degree block- IV
isoprenaline, temporary pacemaker,
permanent pacemaker
Hemodynamic instability- swan-ganz
catheter, to monitor PA pressure
Early PCI to maintain coronary flow, and to
prevent myocardial damage.
Posterior MI and related arteriesLCX or RCA
Posterior infarctions- related artery
may be LCX or RCA
Posterior MI’s are rare, and posterior surface lies
close to atria than to the inferior surface.
Involved leads: V1-V3, Tall R wave and ST
depression in V1-V2
PMI’s are associated with the lesions of LCX or
RCA.
No leads are looking directly to the posterior part
of the heart. We look mirror image of the
posterior portion.
If STE is not more than 1mm, patient may not
need thrombolytic treatment.
Apical MI- related artery is LAD
terminal territory
Apical involvement is reflected by STE in
V5-V6
Reciprocal changes are seen in RV5, RV6.
Loss of R wave progression in V5, V6.
Lead I-STE, T inversion
Lead III- STD, upright T wave,
Lateral Wall MI- related artery LCX
sometimes LAD
Occlusion of LCX
Indicative leads: aVL,
I indicates high lateral
and V4-V6 indicates
lower lateral.
LV Myocardial muscle loss and its
hemodynamic manifestations
Muscle loss > 8%= decreased compliance
Muscle loss > 10%= Decreased EF
Muscle loss > 15% = Increased LVEDP
Muscle loss > 20% =Increased LVDDV
Muscle loss > 25% = Clinical evidence of
heart failure
Muscle loss > 40% = Cardiogenic shock
and / or death
Assessment of LV Ejection fraction
only with ECG
If R wave is <3mm in V1-V3 and <5mm in V5V6, and the QRS duration is more than 120130msec, the EF will be less than 45%.
If R wave is < 1mm in V1-V3 and <3mm in V5V6, the QRS duration is more than 130msec, the
EF will be less than 30%
If there is no R wave in any lead, and the QRS
duration is more than 140msec, the EF will be
less than 20%.
Prognosis of Hemodynamic status
in MI
If no pulmonary congestion and hypo perfusion, mortality
less than 5%.( diuretics, inotropics and after load
reduction)
If PCWP >18mmHG and CI >2.2, mortality will be less
than 10%.( diuretics, after load reductions)
If PCWP <18mmHg, and CI<2.2, mortality will be less
than 25%.(inotropics, after load reductions)
If PCWP >18mmHg, and CI<2.2, mortality will be less
than 50%.(inotropics, after load reductions IABP)
Complications in Myocardial
Infarction
Aneurysm formation:
Interventricular tension
stretches the non-contracting
infarcted muscle, thus
producing infarct expansion.
Thin layer of necrotic muscle
and fibrous tissue that bulges
with each cardiac contraction.
Aneurysm is rarely seen with
multi vessel diseases.
ECG- Persistent ST elevation.
Prognosis in Aneurysm
It can occur weeks to
months after infarct.
May lead to CHF, mural
thrombi and
dysrhythmias.
Signs include precordial
bulge, double apical
impulse, S3,S4..
Cardiac Tamponade
Heart surrounded by fluid held in the
pericardial sac resulting in constriction of
the heart with a resulting decrease in
cardiac filling and a decrease in heart
sound.
It is seen with cardiac surgery, acute
pericarditis, ventricular rupture and aortic
dissection.
Diagnosis and treatment
Sudden decrease in BP, cardiac output, and an
increase in CVP, PAP, HR.
Signs and symptoms include a paradoxical
pulse, decreased ECG voltage, neck vein
distension, increased heart size, enlarged liver
and spleen, rales, wheeze, and decreased urine
output.
Treatment: Administration of steroids and
diuretics and pericardiocentesis.
Post Infarction syndromeDressler’s syndrome
It is a delayed form of acute pericarditis, can
occur 1 week to several months after AMI.
Antigen-antibody response to necrotic
myocardium.
Pericardial pain, fever, friction rub, pleural
effusion, pleuritis, tachycardia, and arthralgias
may accompany this syndrome.
Treatment: Aspirin, steroids.
Ventricular DysrhythmiasVentricular Fibrillation
Prognosis in Ventricular Fibrillation
Risk for ventricular
fibrillation is highest
for first 4 hour after
MI.
Sustained ventricular
tachycardia, R on T
phenomenon,
torsedepointes,
multifocal VPC, and
ventricular bigeminy
can cause VF.
Supra ventricular Dysrhythmias in
MI
Bradycardia- Atropine
AV block- mortality greater in anterior infarcts
than in inferior infarcts.
Trifascicular block- usually associated with
anterior infarcts.
AV nodal ischemia- usually associated with
inferior infarcts.
Sinus tachycardia- Pericardial inflammation,
shock, hypotension, pulmonary congestion,
venous congestion and CHF.
Atrial Fibrillation- atrial infarction and CHF
Papillary muscle dysfunction- MI
It occurs in inferior or
posterior or inferoposterior MI.
Posterior papillary muscle
is most commonly
affected as it receives
blood supply from RCA or
dominant LCX.
Anterior papillary muscle
usually has blood supply
from the tributaries of
diagonals of LAD and
marginals of LCX.
Diagnosis and Prognosis of PMR
S1, S2 widely split.
Large V wave in PWP tracing.
Sudden onset of
breathlessness.
High pitched holosystolic
murmur.
Shock and Acute pulmonary
edema.
Complete rupture needs
immediate surgical correction.
Medical management: After
load reduction, IABP,
Nitroprusside, NTG.
Pericarditis in MI
It may be due to transmural infarction that produces
rough epicardial layer and irritation in pericardial surface
resulting in inflammation. It occurs usually 2-4 days after
MI.
Pericardial friction rub 1-3 days after MI.
Pain character: sharp, positional pain, and worsen in
recumbent. Relieved in leaning forward.
Treatment: Aspirin, NSAID’s
Post Infarction angina
It occurs within first 10 days of MI.
It suggests viable myocardium still subject to
ischemia.
Angina pectoris, S4, hypertension, hypotension
are common in high risk cases.
Treatment: Urgent PCI or CABG with IABP
Pulmonary Embolism
Common with CHF and
prolonged bed rest.
Symptoms: dyspnea,
pleuritic chest pain,
anxiety, hemoptysis,
diaphoresis and calf vein
thrombosis.
Signs: Tachypnea,
tachycardia, pleural pain,
hypotension, fever,
distended neck vein and
hypoxia.
Treatment: heparin,
STK,UK,TPA, GPIIbIIaRB
ECG changes with Electrolytes
abnormalities
Hypokalemia: serum
K+ <3
ECG changes in 303.5 K+
T wave may be flat,
inverted and ST may
be depressed.
Appearance of U
wave.
Hypokalemia – Serum K+ 2.7-3.0
U wave become taller
and T wave become
smaller.
Prolongs
repolarization as
indicated by U wave.
Fusion of T-U wave is
seen in K+ less than
2.7
Diagnosis and treatment
Long QT interval
Flat T wave and prominent U wave
Hypokalemia may produce PVC,
tachycardia, ventricular fibrillation.
Treatment: IV potassium
Hyperkalemia- serum K+ 5.5-7.5
ECG changes
Absence of P wave: sinovenrticular rhythm
or atrial paralysis. P wave flattens due to
intra-atrial block. It may develop into an AV
block with a prolonged PR interval. (5.57.5)
Sharp, pointed, tall T waves with narrow
base.(5.5-7.5)
Wide QRS and slurring of both initial and
terminal portions of the QRS.(7.0-8.0)
Hyperkalemia ECG changes
Prognosis and management of
Hyperkalemia
Hyperkalemia causes 1st and 2nd degree
AV block, atrial arrest, bradycardia and
ventricular fibrillation or a systole.
Always think of Hyperkalemia in the
absence of P wave.
Treatment: Insulin and glucose infusion.
Hypocalcaemia-less than 8
Decreased Ca2+ will cause increased Na+
entry into cells with repetitive firing of
nerves, skeletal muscle contraction is
unaffected.
Decreased calcium leads to depressed
cardiac contractility and arrhythmias.
Hypocalcaemia- ECG changes
Lengthened ST segment
and prolonged QT
interval. Slight short QRS
Short PR interval.
Flat T or inverted in
severe hypocalcaemia.
Sign and symptoms:
tetany, spasm, cramps,
numbness and tingling.
Hypercalcaemia- ECG changes
Slight increase in QRS.
Short ST segment of absent.
PR interval may be prolonged.
Short QT and abnormal Q.
Sign and symptoms: irritation,
somnolence, muscle
weakness, peripheral
neuropathies, anorexia, and
constipation.