aVR case presentation

1. CASE
PRESENTATIO
N
Dr AsadullahSoomro
Adult cardiologist.

2. Complaints
69yr old male
presented to ER
Left arm numbness
with profuse sweating
and vomiting became cold
clammy
Symptom History
Medical History
Sudden onset one hour
Family History
No cardiac disorder before
Mildly hypertensive on diet control
No premature

3. Physical
Examination Conscious but restless
Cold & clamy
Pulse 110 / min
Blood pressure 80/50
JVP raised
Ejection systolic murmur
2/6 LSB
Normal 2nd
sound
S4 gallop
Chest clear

4. 12LEAD EKG
Total ST segment score
3+2+2+5+5+5=
22mm
5mm ST Segment depression i
V4 V5 V6
2mm ST Depression in lead
I, II
3mm ST Segment elevation
AVR
ELECTROCARDIOGRAPHIC
DIAGNOSIS?

5. LEFT MAIN
DISEASE
Electrocardiogram of patients with
resting pain from occlusion or sub
occlusion of “ Left Main
Coronary Artery “ frequently
show a combination of “
ST Elevation in AVR and ST
Depression in leads “1, 11
,V4 ,V5 ,V6 “sum of ST changes
>18 mm is 90 % sensitive for

6. LABORTARY
Wbc 7.7,Hb 13.8 ,Plt131,
Ptt 47.5 INR 1.0, glucose
7.8,Creatnine 123>167, K
3.8,Cholestrol 3.8,Tg 1.2
GOT 308, Ck46 > 1936
( MB 149) LDH 344 >1007
Trop –T 0.127.
ABG: PH 7.0, PCO2 56. PO2

7. DIAGNOSI
SACUTE MYOCARDIAL
INFARCTION
Complicated BY
CARDIOGENIC SHOCK
“ ? LEFT MAIN OCCLUSION”
RAPID ATRIAL FIBRILATION
ACUTE HEART FAILURE SYNDROME
( DE -NOVO)

8. CLINICAL COURSE
With in one hour of admission in ccu,
developed “rapid atrial
fibrilation” given DC shock but
not converted to sinus rhythm,
meanwhile suddenly became
severely dyspnoic , desaturated
hence intubated and ventilated ,
remain hypotensive despite
ionotropic support ,with low
urinary out put.
Developed asystole CPR done but
remain un successfull and expired.

9. CARDIOGENIC SHOCK AT
KFHH
•Total Acute MI 420
•Cardiogenic shock = 33
7.8%
•Saudi = 25
75 .7 %
•Non Saudi = 8
24.2 %

10. Type of MI
Anterior wall MI = 22 66.6%
bifasicular block =3
Atrial fibrillation = 4
Complete heart block =3
RBBB =2
Inferior MI , isolated = 0
Inferior post , Inferior with, Rv extension
=21.2%
Inferior-postero lateral 7
Old Anterior , acute Lat wall MI
Complete heart block =2
LBBB = 2 6%
Non ST = 2 6%

11. AGE
DISTRIBUTION
•< 30 – 45 YRS = 3
9.0%
•46-59 YRS =10
30.3%
•> 60 YRS =20 60.6
%
Age Range =

12. Streptokina
se 18
54.5%

13. CARDIOGENIC
SHOCK
•DM 11
33.3%
•Hypertensive 3
9.0%
•Both 9 27.2%
•Non 10
30.3%

14. CARDIOGENIC
SHOCK
Cardiogenic shock remains the most
frequent mode of death for patients
who are hospitalized for acute MI.
It is a state of tissue hypo perfusion
resulting from underlying cardiac
dysfunction ,characterized by
persistent systemic hypotension un
responsive to fluid, cool skin ,
alterd mental status ,markedly
diminished urinary output. systolic
BP< 90 mm. PAWP >15,reduced
cardiac output with cardiac index <

15. CARDIOGENIC
SHOCK
Incidence ranges from 5 -15% and
mortality is 70-80% despite advances
in medical management of acute MI. 1-5
% pts MI present to hospital in shock 5
-7% develop shock during
hospitalization. Shock may be due to
either sever left or right ventricular
dysfunction ( 85% due to primary
pump failure) 8% due to septal
rupture and acute MR 2% due to

16. CAUSES OF
CARDIOGENIC SHOCK
IN ACUTE MI
RV
Infarction
10%
RV
Infarction
10%
Mechanical Complications
Septal rupture, Pappilary muscle
dysfunction
Free wall rupture ( Tamponade)
Mechanical Complications
Septal rupture, Pappilary muscle
dysfunction
Free wall rupture ( Tamponade)
Large LV
MI
80%

17. CARDIOGENIC SHOCK
“EKG & Coronaries”
In the SHOCK registry the majority (86%) of
pts with primary pump failure had EKG
findings of acute transmural infarction with
ST elevation ,new Q waves or new LBBB. 51%
of all MI were Anterior 38% inferior 24%
lateral and 11% had posterior MI .10-15%
had atrial fibrilation.
14% pts with primary pump failure did not
have EKG findings of transmural MI but had
sub endocardial infarction with ST depression
or old LBBB. surprisingly with high mortality
77% vs 64%.Most often there is involvement of
all thee major coronary arteries with
predominant significant LAD stenosis (68 -80

18. LEFT MAIN SHOCK
SYNDROME
Left main stenosis is generally considered an
indication for CABG .How ever clinical outcome
in patients presenting to Duke university with
“ Left main shock syndrome” ,mortality
was disappointing 94 % in
patients who underwent salvage PTCA
or CABG and 100% in patients treated
medically.
Mortality can be reduced if diagnose early and
revascularization is achieved promptly, while
PTCA may be appropriate as a temporizing

19. CARDIOGENIC SHOCK
“ Diagnostic & therapeutic approach “
General measures
Support Ventilation
ntravascular volume
Aspirin/ Heparin
Diagnostic testing
PA Catheter
2D Echo
Transesophageal
Early cath
Phamacological
Support
Mechanical
support
Reperfusion
Revascularization
Inotrop
es
Vasopreso
rs
IABP
New
devices
Thrombolysis
PTC
A
CAB

20. THROMBOLYSIS
IN CARDIOGENIC SHOCK
Patients presenting with
cardiogenic shock with acute
MI should not be considered “
INELIGIBLE” for
thrombolysis .There are
dramatic case reports of
successful I/V thrombolysis for
acute MI with “left main

21. INTRA AORTIC BALOON
PUMP
It is a standard component of
therapy, superior to
vasopressors. It should be
considered early to augment
diastolic coronary blood
flow ,decrease LV after load
without increasing
myocardial oxygen
consumption.

22. ANGIOPLASTY IN
CARDIOGENIC SHOCK
Angioplasty demands a high
degree of technical experties
and support of highly skilled
operators because single stage
multi vessel PTCA for more
complete revascularization is
an approach alternative to
CABG. 30 day mortality
was 38% with successful
emergency PTCA with in six

23. CONCLUSION
Despite advancement in medical
technology which is not available
frequently ,prognosis remain
dismal”
Patient must be identified in early
phase of early LV failure ( Pre shock
or early phase shock) before frank
hypotension develops .
Current evidence suggest that early
reperfusion is critical if outcome is

24. Hospitals without special
experties or facilities for “
LVAD & IABP” , “high risk
PTCA” or “cardiac surgery”
should initiate supportive
measures & simultaneously
make a rapid decision
regarding appropriatness of
transfer to tertiary care
facility.
A decision with regard to
transfer should be based on
physicians estimate of

25. CONCLUSION
• Plethora of data currently
available on electro cardiographic
changes accompanying chest pain
should allow clinicians to make
faster and better decisions than
ever before .
• It is now clear that isolated ST
depression in leads V1 through V3
may indicate “ Left
Circumflex “ occlusion and

26. • Entirely non diagnostic EKG may
become diagnostic when serial or
previous EKGS are obtained or
when posterior and right
precordial leads are recorded.
• A few hospitals around the world
are already using the “15 or 16”
lead EKG for routine admission
workups.
• Cardiologists and emergency
physicians should make an effort to
incorporate these leads in both
teaching and clinical practice and
request EKG machine vendors that

27. The electrocardiogram remains
a crucial tool in the
identification and management
of acute myocardial infarction.
EKG is single most effective
diagnostic test in Cardiology,
despite introduction of
computerized EKG
interpretation yet most
frequently misinterpreted in

28. •Some EKG leads are
underutilized in clinical
practice , but can be very
helpful in discriminating
infarct related artery
especially during inferior
injury with ST segment
elevation in V7—V9 and ST
depression in AVR are
probably related to left
“Circumflex “ occlusion.

29. • 12 lead ECG is of central
importance in the management of
acute MI because there is strong
evidence that patients with
“ST segment elevation”
benefit from reperfusion therapy
current data suggest that there is
no role of
“ thrombolytic therapy”
in non ST elevation MI however
role of glycoprotein clopidogrel
followed by primary angioplasty /

30. •The 12 lead EKG is only
moderately accurate to
determine the anatomic
location of AMI hence some
patient may not be offered
revascularization if 12 lead
ECG is used for decision making
how ever 15 lead EKG recording
i- e “V4R V8 –V9 “
Increases the probability of

31. •The early and accurate analysis
of “ST segment
deviation “ may influence
decision regarding use of
"reperfusion therapy “
and may identify infarct
related artery and proximal
occlusion result in most
extensive and sever myocardial
damage. It is crucial in decision
regarding urgency of

32. RIGHT
VENTRICULAR
INFARCTION• RV infarction is always associated with
occlusion of “proximal segment of
right coronary” artery. The most
sensitive EKG sign of RV infarction is ST
segment elevation of more than 1 mm in
lead V4R .This sign is rarely present
more than 12 hours after infarction.
•54% of inferior MI have ST
elevation in V4R. 18% of Pts
with acute inferior MI have ST
elevation in lead V1,which is
highly specific sign of RV
infarction. It is usually associated with

33. PAPILLARY MUSCLE
INFARCTION
• An autopsy study found that ST
segment depression of 1mm in
the initial EKG was a sensitive sign
for infarction of a papillary
muscle . Inferior ST depression
was seen exclusively in infarctions
of the “ Antero lateral
“papillary muscle ,where as ST
depression in leads 1,aVL
occurred only after infarction of

34. LATERAL & POSTERIOR
INFARCTION
• ST segment elevation in leads 1
,aVL,V5 & V6 and St segment
depression in V1 ,V2 & V3
suggest concomitant infarction of
the posterior wall ,however ,ST
elevation in V7 & V9 is always
detected and is more specific than
pre cordial leads in posterior MI
.When St elevation is more than
2mm it is probably a sign of “
Mega artery related “ ( either RCA

35. ANTERIOR PLUS
INFERIOR MI
• The combination of anterior plus
inferior ST elevation in the EKG
may give the impression of a
critical mass of myocardial
injury .How ever, it often results
from distal occlusion of long
LAD after D1 , which “Wraps
around“ the cardiac apex
( ST segment elevation
in V1,V2 & V3 along with ST

36. NON DIAGNOSTIC
EKG•15 to 18% of patients with MI do not have
changes in initial EKG & an additional 25%
show non specific changes ,( often associated
with branch arteries.) The probability of
detecting MI does increase by recording serial
EKGS . However because reperfusion therapies
are more effective when administered early.
• Approximately 8% of patients with cardiac
pain will display ST elevation only in posterior
leads (V7 through V9 ) or
right precordial leads ( V3R
through V6R ) leads .These patients may not
be offered reperfusion if 12 lead EKG is used
for decision making.
• It is reasonable to assume that a systematic
examination of lead aVR may increase