5. Patient no 1Patient no 1
55 Yrs Male Diabetic
AMI – Thrombolysed 2 days back– on
routine drugs
Chest pain today
ECG repeated show persistent ST
elevation in anterior leads and some
ST elevation in inferior leads
7. Dr. BadDr. Bad
Diagnosis: Re infarction/ Fresh Inferior
MI
Re occlusion of LAD and fresh RCA
lesion
Plan: Immediate CAG
PCI/Stenting
8. Dr.GoodDr.Good
Nature of chest pain
- Patient says it is different from the first day
- Pricking
- Related to deep inspiration/moving
Auscultation
- Triphasic pericardial rub
Persistent / new ST elevation is due to
pericarditis
Plan: Stop Heparin / Increase Aspirin/
Reassurance
9.
10. LESSON 1LESSON 1
CHESTPAIN ON 2ND
OR 3RD
DAY OF STEMI
– ALWAYS RULE OUT ACUTE
PERICARDITIS
MANAGEMENT IS COMPLETELY
DIFFERENT (in ischemia heparin to be
continued; in pericarditis it has to be stopped)
11. Patient no 2Patient no 2
Known CAD patient/ DM
Had ACS 2 months ago
On nitrates / oral antiplatelets/ statins/
beta blockers/ ACEI
Develops 2 episodes of syncope when he
got up in the morning and in the toilet
O/E : Pulse:66/mt R; BP 100/70 /
CVS&RS: No SAD
ECG – RBBB/AWMI
12. Dr. BadDr. Bad
Diagnosis: Probable Transient CHB/SA
Attacks
Plan:Immediate Temporary and then
permanent pacemaker therapy
13. Dr.GoodDr.Good
Compare with old ECG- previous ECG also
had RBBB/AWMI-PR is normal
Check postural BPSignificant postural
hypotension
Ask h/o malena Patient says yes
Rectal examination stool for occult blood
positive
HB/PCV / Urea / creatinine Normal
Plan: Stop dual antiplatelets / packed cell
transfusion/ Upper GI Scopy
14. LESSON IILESSON II
SYNCOPY IN CAD PATIENTS ON
DUAL ANTIPLATELET DRUGS
ALWAYS RULE OUT OCCULT UPPER
G.I BLEED
CHECK FOR POSTURAL
HYPOTENSION,OCCULT GASTRIC
BLEED (history, rectal exmn,)
H/O MALENA MAY NOT BE
FORTHCOMING IN SOME PATIENTS
SYNCOPY IN CARDIAC PATIENTS IS
NOT ALWAYS DUE TO CARDIAC
LESION
15. Patient no 3Patient no 3
Known case of severe LVD
Admitted for Cl.IV HF
Persistent dyspnea in spite of Diuretic
therapy and other standard HF therapy
Pulse 102/mt; BP 100/70; LV3
Basal creps / more on left side
RR 30/mt /SAO2 90%
ECG:Sinus Tachycardia/LBBB/LAE
17. Dr.GoodDr.Good
Good clinical examination
Reduced BS whole of Right chest
Dullness
X ray chest – large Right pleural effusion
Plan : Aspiration and analysis – treat the
cause
Patient became better
18. CAUSES OF NON CARDIACCAUSES OF NON CARDIAC
DYSPNEA IN HF PATIENTSDYSPNEA IN HF PATIENTS
Pleural effusion -Rt heart failure and
other causes
Associated wheezing- asthma
Renal failure – acidosis
Pulmonary embolism
Anemia – various causes
Pneumonia
Anxiety
19. LESSON IIILESSON III
DYSPNEA IN KNOWN LVD,HF
PATIENTS IS NOT ALWAYS DUE TO
CARDIAC CAUSES
ALWAYS KEEP LOOKING FOR
OTHER NON CARDIAC CAUSES
MANAGEMENT IS DIFFERENT FOR
EACH OF NON CARDIAC CAUSES
20. Patient no 4Patient no 4
Patient is admitted with Bilateral pitting
edema of legs and ascites with elevated
JVP
PR 110/mt ; BP 90/60
Heart sounds intensity ? III HS
Lungs clear
22. Dr.GoodDr.Good
Careful clinical examination – history – Ascites came
first
Pulsus paradoxus
JVP elevation on inspiration
Negative waves are prominent
Faint pericardial rub
Diastolic sound is probably pericardial knock
No murmurs
Does immediate Echo
Massive pericardial effusion-Tamponade
Aspiration and subsequent workup for the etiology
23. RHFRHF PERICARDIAL DISEASEPERICARDIAL DISEASE
JVP ELEVATEDJVP ELEVATED
POSITIVE WAVEPOSITIVE WAVE
JVP ELEVATEDJVP ELEVATED
NEGATIVE WAVENEGATIVE WAVE
NO SIGNIFICANT CHANGE INNO SIGNIFICANT CHANGE IN
RESPIRATIONRESPIRATION
INCREASE OF INSPIRATIONINCREASE OF INSPIRATION
LUNGS MAY SHOW CREPTSLUNGS MAY SHOW CREPTS LUNGS CLEARLUNGS CLEAR
PULSE VOLUME NORMAL ORPULSE VOLUME NORMAL OR
LOW /NO CHANGE INLOW /NO CHANGE IN
RESPIRATIONRESPIRATION
VOLUME LOW/ PARADOXICAL PULSEVOLUME LOW/ PARADOXICAL PULSE
MOST OFTEN MURMURMOST OFTEN MURMUR
PRESENTPRESENT
NO MURMURS /RUB MAY BE PRESENTNO MURMURS /RUB MAY BE PRESENT
OEDEMA COMES FIRSTOEDEMA COMES FIRST ASCITIES COMES FIRSTASCITIES COMES FIRST
24. WHERE OEDEMA STARTEDWHERE OEDEMA STARTED
Edema ascends – starts in legs and goes
up - CARDIAC
Edema descends – Starts in face and
descends down – NEPHRO
Edema in the middle – PERICARDIAL
OR HEPATIC
25. LESSON IVLESSON IV
IN PATIENTS PRESENTING WITH
SYSTEMIC VENOUS CONGESTION, IT
IS A GOOD PRACTICE TO RULE OUT
PERICARDIAL DISEASE
TREATMENT FOR HF LIKE
DIURETICS, DIGOXIN / ACEI MAY
WORSEN PERICARDIAL DISEASE BY
REDUCING PRELOAD AND
AFTERLOAD
26. Patient no 5Patient no 5
60 y male admitted with acute severe
chest and back pain / rolling with pain/
known HBP on irregular treatment ;
PR 120/min; BP 160/100;
ECG ST elevation Anterior chest leads /
no previous MI
No contraindication to thrombolysis
29. Dr.GoodDr.Good
History – pain is maximal at onset
Careful clinical examination
Inequality of pulses
AR is present
Pain radiating to back and below the umbilicus
into legs
Does an immediate Echo/TEE/CT scan
Confirms Acute Dissection of Aorta and plans
appropriate management
30. LESSON VLESSON V
IN ALL ACUTE SEVERE CHESTPAIN PATIENTS
ALWAYS NOTE THE FOLLOWING
PREDOMINANT BACKPAIN
MAXIMUM AT ONSET
INEQUALITY OF PULSES
PRESENCE OF AR
RADIATING INTO THE LEGS, BELOW
UMBILICUS
ALWAYS R/O DISSECTION BEFORE
THROMBOLYSIS
THROMBOLYSIS IS CONTRAINDICATED IN
DISSECTION
31. Patient no 6Patient no 6
Pt. was admitted with intermittent left
arm pain 3 hrs.
Known diabetic and hypertensive
Pt. is hemodynamically stable
ECG taken immediately showed ST
elevation in anterior leads
32.
33. Dr BadDr Bad
Diagnosis – Acute AWMI, ST elevation
V1 proximal LAD
Immediate CAG and Primary PCI in view
of proximal LAD
34. Dr GoodDr Good
Good history: The left arm pain radiates
from back of neck; related to movements
of neck; local tenderness +
Compares with old ecgs
All the previous ECGs look the same
Pt. has persistent ST elevation probably
due to LV aneurysm
Echo confirms the diagnosis
Gives simple symptomatic treatment- Pt.
becomes better
36. LV ANEURYSMLV ANEURYSM
Persistent ST elevation
>1mm in 3 Anterolateral leads
Inferior aneurysms are missed
Gold burgers’ sign – Tall R in avR
Pathological Q ‘must’
37. Causes of Persistent ST elevationCauses of Persistent ST elevation
IN ACUTE PHASE
Failure of thrombolysis
Recurrent ischemia
LV Dyskinesia
Pericarditis
ST elevation in aVL à IMPENDING RUPTURE
IN CHRONIC PHASE
LV Aneurysm
Severe dyskinesia
Associated LBBB
Metastatic tumors à no Q waves will be seen
38. LESSON VILESSON VI
IN KNOWN CAD PATIENTS, ALWAYS
COMPARE THE FRESH AND OLD
ECGS BEFORE PLANNING THE
MANAGEMENT
KNOWN CAD PATIENTS CAN ALSO
HAVE NON CARDIAC CHEST PAIN
CAREFUL HISTORY REGARDING THE
NATURE OF CHEST PAIN IS CRUCIAL
39. Patient no 7Patient no 7
35 y male comes with intermittent chest
discomfort, smoker
The ecg is taken and shown
40.
41. Dr. BadDr. Bad
ECG shows extensive non Q MI; in view
of his age , immediate CAG and plan
urgent revascularization
42. Dr . GoodDr . Good
Elicits good history: the chest pain is
clearly non cardiac
There is family h/o heart disease
Clinically examines the patient- Patient
has severe LVH shown by heaving apical
impulse and palpable 4th
heart sound with
normal BP
The ecg shows deep T inversion with Tall
R waves in lateral leads
Suspects Hypertrophic Cardiomyopathy
of Apical variety and proves by Echo.
45. PAIN- NOT CORONARY IF….PAIN- NOT CORONARY IF….
Pleuritic pain (i.e., sharp or knife-like pain brought on
by respiratory movements or cough)
Primary or sole location of discomfort in the middle or
lower abdominal region
Pain that may be localized at the tip of one finger,
particularly over the left ventricular (LV) apex
Pain reproduced with movement or palpation of the
chest wall or arms
Constant pain that persists for many hours
Very brief episodes of pain that last a few seconds or
less
Pain that radiates into the lower extremities
46. LESSON VIILESSON VII
WHEN DEEP T INVERISIONS ARE
ASSOCIATED WITH LVH IN THE
PRESENCE OF NORMAL BP SUSPECT
HYPERTROPHIC CARDIOMYOPATHY
• CLINICAL EXAMINATION FOR LVH,4TH
HEART SOUND AND FAMILY
HISTORY WILL HELP
• UNNECESSORY CAGs CAN BE
AVOIDED.
47. Patient no 8Patient no 8
3 year old child is brought for evaluation
of systolic murmur
No symptoms reported by parents
Child has no features of cyanosis or heart
failure
Normal milestones so far
48. Dr. BadDr. Bad
Immediately sends the child for echo
Echo report comes as normal study
Says it is innocent murmur and sends the
child
49. Dr. GoodDr. Good
Carefully examines the patient
There is pan systolic murmur at left sternal
edge
Then sends the patient for echo
When echo report comes as normal , doesn’t
accept it
Asks the echocardiographer to re do echo and
suggests to look for a apical VSD
Repeat echo report comes as small apical
trabecular VSD
Reassures, advises serial follow up and IE
prophylaxis
51. APPARENTLY NORMAL ECHOAPPARENTLY NORMAL ECHO
WITH LESIONSWITH LESIONS
Apical VSDs
SVC type of ASD
Coarctation of aorta
Pulmonary AV fistula
Bicuspid aortic valve
Dissection of aorta
52. LESSON VIIILESSON VIII
Most often apical trabecular VSDs
are missed by echo cardiographers
who usually do not auscultate
When investigation does not match
your clinical diagnosis suspect the
investigation rather than your
clinical diagnosis
53. Patient no 9Patient no 9
45y known CAD patient walks into op
with h/o palpitations
Stable hemodynamics
56. Dr. GoodDr. Good
Elicits history- previous h/o MI present
Notes intermittent cannon waves in neck
and varying intensity of S1-clinical signs of
AV dissociation
So diagnoses as VT and orders IV
lignocaine
NSR restored
57. Wide Complex Tachycardia –Wide Complex Tachycardia –
Clinical cluesClinical clues
VT SVT
Age >35 (85%) Age <35 years (70%)
Old MI (90%)
Structural Heart Disease
Most often normal hearts
Family h/o sudden death
Drugs (IC, III, LQTc ) Pre existing
BBB/ WPW
Electrolytes (K,Mg)
Intermittent and irregular cannon
waves
Regularly occurring cannon waves
(AVNRT)
Varying intensity of S1
Beat to beat variation of BP
Hemodynamic stability or instability does not differentiate VT from
SVT with aberrancy
58. LESSON IXLESSON IX
WHEN THERE IS WIDE QRS TACHY AND
IT IS DIFFICULT TO DIAGNOSE FROM
ECG WHETHER IT IS VT OR SVT WITH
ABERRANCY, CONCENTRATE ON
CLINICAL SIGNS
CERTAIN CLINICAL SITUATIONS,
INETERMITTENT CANNON WAVES IN
JVP, VARYING INTENSITY OF S1 FAVOUR
VT
DRUGS LIKE VERAPAMIL AND
ADENOSINE ARE DANGEROUS IN VT
59. Patient no 10Patient no 10
84 female was admitted with intermittent
occasional palpitation
On seeing ECG , patient was admitted in
ICU and monitored
Patient is hemodynamically stable
62. Dr.GoodDr.Good
Carefully sees the ECG
In computerized ECG , the leads are
simultaneously recorded
One can’t have VT in L1, L III and Sinus rhythm
in LII
Sees the patient clinically
Pulse is well felt during the ‘episodes of VT’
Identifies the tremor in left hand
The ECG changes are due to somatic tremor
artifacts due to ‘Parkinson Tremor’
63.
64. LESSON XLESSON X
WHEN MONITOR SHOWS
ARRHYTHMIA ALWAYS FEEL THE
PULSE
WHEN PULSE IS WELL FELT AND
REGULAR AT NORMAL RATE, AND
THE MONITOR IS SHOWING AN
ARRYTHMIA, SUSPECT SOMATIC
TREMOR ARTEFACTS
TREAT THE PATIENT NOT THE
MONITOR
66. Dr BadDr Bad
Pt. with Ami
Refractory cardiogenic shock
Pump in dopamine nor adrenaline
Plan IABP,CAG
67. Dr GoodDr Good
Does careful clinical examination
Loud systolic murmrur in LSE
JVP flat
Tachycardic
Does immediate echo
Picks up small hypercontractile LV and
acquired LVOT obstruction as well as IVC
collapse
Stops inotropes,gives fluids and small dose
of b blockers and the pt.improves
68. Lesson 11Lesson 11
Not all shocks in even in cardiac patients
are due to cardiac causes
Hypovolemia is the often missed cause of
shock
The resultant lvot obstruction will
aggravate the shock
Positive inotropes will increase the
contraction and will worsen lvot
obstruction
Careful clinical examination and echo
will help to solve the issue
69. Patient 12Patient 12
55 y hypertensive and diabetic comes
with h/o breathlessness
Ecg shows LVH
Echo showed EF of 60 and gr 1 DD
70. Dr BadDr Bad
As EF is normal HF is unlikely and look
for non cardiac causes
71. Dr GoodDr Good
Careful history is suggestive of recent
onset breathlessness with orthopnea and
no cough or seasonal variation
Clinical examination showed LVH and
LA4
Carefully sees ecg to find la abnormality
in v1
Identifies gr 1 dd is with e/e’ of 16
Makes the the diagnosis of HFPEF and
treats accordongly
73. DIFFERENTIATION BETWEEN CARDIACDIFFERENTIATION BETWEEN CARDIAC
ASTHMA & CHRONIC PULMONARY DISEASEASTHMA & CHRONIC PULMONARY DISEASE
CARDIAC ETIOLOGY
1. DYSPNOEA PRECEDES
COUGH &
EXPECTORATION
2. PND & ORTHOPNOEA
3. ASSOCIATED WITH
ANGINA , SYNCOPE
4. NO SEASONAL
VARIATION
5. NO WEIGHT LOSS
6. ACUTE ONSET
7. RESPONSE TO
DIURETICS
8. PULSUS ALTERNANS
9. S3
10. CRACKLES OVER BOTH
LUNG BASES
PULMONARY ETIOLOGY
1. COUGH WITH
EXPECTORATION
PRECEDES DYSPNOEA
2. -----
3. -----
4. SEASIONAL VARIATION +
5. WEIGHT LOSS
6. GRADUAL ONSET
7. RESPONSE TO O2 &
BRONCHO DILATATION
8. PULSUS PARADOXUS
9. NO S3
10. RHONCHI OVER LUNG
FIELDS
Roadmaps In Cardiology – Dr. M. Chenniappan
74. Lesson 12Lesson 12
Any long standing hypertensives don’t
ignore dyspnea if EF is normal
HFPEF is increasing and it is going to be
the most common heart failure in future
Always look for LVH,LAA , e/e’ in
clincal,ecg and echo examination
In gr 1 dd e/e’ of >15 is definitely
suggestive of high LA pressures and flash
APO is common in this situation
76. CONCLUSIONCONCLUSION
Even in high tech era, the teaching of William
Osler (and Dr. G.A.S.) still stands tall.
Use high tech investigations to refine your clinical
knowledge rather than replace them
Spend time in listening to the patient and
examining your patient
90% of the time you will be rewarded with the
correct diagnosis without wasting time (of
yourself) and money(of the patient).
Be a Dr. Good !
77. More than a gold medal…More than a gold medal…
78. Golden day of the ecg club..Golden day of the ecg club..
When I have the opportunity to write
this type of letter to any one of you
Hope this day is not too far off !
96. Acute Aortic Dissection: Features
Sudden or dramatic onset of pain with gradually waning
The character of pain is often ripping, tearing or
stabbing
Can simulate the pain of acute MI or unstable angina
but is more commonly felt over back
Radiates to the neck, shoulders, abdomen, or lower
limbs if those arteries are involved in the process of
dissection
Features of acute M.I if the coronaries are involved in
the dissecting process
The murmur of AR if the aortic valve is involved
Asymmetry or absence of arterial pulses
Predisposing conditions like systemic hypertension,
marfan’s syndrome
97. HISTORY FAVOURING VTHISTORY FAVOURING VT
CAD PREVIOUS MI
HEART FAILURE
CARDIOMYOPATHY
DRUGS
ELECTROLYTE DISTURBANCES
HEMODYNAMIC STABILITY OR
INSTABILITY
Notas del editor
Figure 12-8. A and B, This study was from a patient with apical hypertrophic cardiomyopathy with marked apical hypertrophy and sparing of the basal half of the left ventricle. Panel A, taken in diastole, demonstrates the spade-like configuration of the left ventricle. Panel B, taken in systole, shows apical cavity obliteration.
