Download - Saturday Clinical Meeting
SATURDAY CLINICAL SATURDAY CLINICAL MEETINGMEETING
SATURDAY CLINICAL SATURDAY CLINICAL MEETINGMEETING
DEPARTMENT OF CARDIOLOGYDEPARTMENT OF CARDIOLOGY
1212THTH FEB 2005 FEB 2005
DETAILS OF THE CASE• 40 years old serving soldier• Resident of Rourkela• Non-smoker, non-diabetic, non-
hypertensive• Referred from CH(NC)• Date of admission – 24 Jan 2005• Informant – self• Reliability - good
PRESENTING COMPLAINTS
• Syncope
• Angina on exertion NYHA – III • Dyspnoea on exertion NYHA – III
6months
WHAT IS SYNCOPE ?WHAT IS SYNCOPE ?WHAT IS SYNCOPE ?WHAT IS SYNCOPE ?
SYNCOPE
• A transient loss of consciousness
• Spontaneous and full recovery
• Loss of postural tone
• No prolonged confusion
Discord in theEvaluation of Syncope
NeurologistNeurologist CardiologistCardiologist
SYNCOPE: CARDIAC ETIOLOGY
• OBSTRUCTION TO FLOW (3-11%)
– HOCM, AS, MS, myxoma
– PS, PE, Pulm HTN– Tamponade
• ARRHYTHMIAS (5-30%)
– Sick sinus, AV block
– VT, SVT
SYNCOPE: NONCARDIAC• Vasodepressor (1-29%)• Situational (1-8%)• Seizure• Psychogenic• Orthostatic (4-12%)• Drug-induced (2-9%)• Carotid sinus• Neuralgia• Neurologic (TIA, stroke, migraine)
HOW TO DISTINGUISH HOW TO DISTINGUISH
SEIZURES FROM SYNCOPE ?SEIZURES FROM SYNCOPE ?HOW TO DISTINGUISH HOW TO DISTINGUISH
SEIZURES FROM SYNCOPE ?SEIZURES FROM SYNCOPE ?
SEIZURE SYNCOPE
AURA + -
CYANOSIS + -
TONGUE-BITE + -
POST-ICTAL CONFUSION
+ -
POST-ICTAL AMNESIA
+ -
POST-ICTAL HEADACHE
+ -
WHAT ARE THE CAUSES WHAT ARE THE CAUSES OF CHEST PAIN WITH OF CHEST PAIN WITH
SYNCOPE ?SYNCOPE ?
WHAT ARE THE CAUSES WHAT ARE THE CAUSES OF CHEST PAIN WITH OF CHEST PAIN WITH
SYNCOPE ?SYNCOPE ?
CONDITION MECHANISMACUTE MYOCARDIAL INFARCTION LARGE AREA OF MYOCARDIUM
AT RISK, ARRHYTHMIAS
VASOSPASTIC ANGINA ARRHYTHMIAS(VT/VF)
ANGINA PECTORIS LARGE AREA OF MYOCARDIUM AT RISK, ARRHYTHMIAS
ACUTE PULMONARY EMBOLISM OBSTRUCTION TO CIRCULATION
PERICARDIAL TAMPONADE CARDIAC COMPRESSION
TENSION PNEUMOTHORAX CARDIORESPIRATORY EMBARRASSMENT
PLEURAL HEMORRHAGE CARDIORESPIRATORY EMBARRASSMENT
UPPER GE BLEED LOSS OF BLOOD
ACUTE PANCREATITIS HYPOVOLEMIA DUE TO CHEMICAL PERITOITIS, SEVERE PAIN
HISTORY • First episode of loss of consciousness while
running in August 2004• Duration : 2-3 seconds• Preceded by angina• Similar episodes since last 6 months• No associated h/o Palpitations Sphincter incontinence/tongue bite
• Patient presented with retrosternal
discomfort associated with breathlessness
initially during unaccustomed exercise
which progressed to discomfort while
doing routine activities
WHAT IS THE MECHANISM WHAT IS THE MECHANISM OF ANGINA IN HOCM ?OF ANGINA IN HOCM ?
WHAT IS THE MECHANISM WHAT IS THE MECHANISM OF ANGINA IN HOCM ?OF ANGINA IN HOCM ?
INCREASED MYOCARDIAL OXYGEN DEMAND
REDUCED MYOCARDIAL PERFUSION
MYOCARDIAL HYPERTROPHY SMALL VESSEL DISEASE
DIASTOLIC DYSFUNCTION ABNORMAL VASCULAR RESPONSES
MYOCYTE DISARRAY MYOCARDIAL BRIDGES
LEFT VENTRICULAR OUTFLOW OBSTRUCTION
INCREASED CORONARY VASCULAR RESISTANCE
ARRHYTHMIAS
• PAST HISTORY : Not significant
• FAMILY HISTORY : No h/o sudden cardiac death No h/o premature death
TREATMENT HISTORY
• Tab Atenolol 100mg 01 OD
• Tab Isoptin 40mg 01 TDS
• Symptomatic improvement with
medication
SUMMARY ON HISTORY• 40 years old serving soldier• No modifiable risk factors• No family h/o SCD• Presented with c/o syncope, AOE /
DOE III
CLINICAL EXAMINATION• Height 166cms• Weight 68.9 Kgs• Average built• Pulse 80/min, regular, bisferiens, no
radio-radial or radio-femoral delay• BP 130/90 mmHg
WHAT IS MEANT BY WHAT IS MEANT BY
BISFERIENS PULSE ?BISFERIENS PULSE ?
WHAT IS MEANT BY WHAT IS MEANT BY
BISFERIENS PULSE ?BISFERIENS PULSE ?
• BIS means twice
• FERIENS means beating
• It is a double-peaked arterial pulse, so there is a
mid-systolic dip
• Both tidal and percussion wave are appreciable
WHAT ARE THE CAUSES OF WHAT ARE THE CAUSES OF BISFERIENS PULSE?BISFERIENS PULSE?
WHAT ARE THE CAUSES OF WHAT ARE THE CAUSES OF BISFERIENS PULSE?BISFERIENS PULSE?
• Severe aortic regurgitation
• Aortic stenosis and regurgitation
• Hypertrophic obstructive
cardiomyopathy
• Hyperkinetic circulatory states
• Muscular exercise
GENERAL EXAMINATION
• Fever (-)• Pallor (-)• Cyanosis (-)• Clubbing (-)• Jugular venous pulse ‘a’ wave
prominent• Lymphadenopathy (-)
WHAT ARE THE CHANGES WHAT ARE THE CHANGES SEEN IN SEEN IN JVPJVP IN A CASE OF IN A CASE OF
HOCM ? WHY ?HOCM ? WHY ?
WHAT ARE THE CHANGES WHAT ARE THE CHANGES SEEN IN SEEN IN JVPJVP IN A CASE OF IN A CASE OF
HOCM ? WHY ?HOCM ? WHY ?
• Prominent ‘a’ waves are seen
• It indicates hypertrophy of
ventricular septum leading to lack of
compliance of right ventricle
CVS EXAMINATION• INSPECTION
Apex visible in 6th intercostal space 1cm outside MCL
Diffuse apical impulseNo precordial bulge
• PALPATIONDouble apical impulse felt S4+No thrillNo PSH
WHAT ARE THE CAUSES OF WHAT ARE THE CAUSES OF DOUBLE AND TRIPLE DOUBLE AND TRIPLE
APICAL IMPULSE ?APICAL IMPULSE ?
WHAT ARE THE CAUSES OF WHAT ARE THE CAUSES OF DOUBLE AND TRIPLE DOUBLE AND TRIPLE
APICAL IMPULSE ?APICAL IMPULSE ?
• Double apical impulse
Decreased LV compliance
Pre-systolic apical impulse due to forceful
atrial systole
• Triple apical impulse
Late systolic bulge of left ventricle that
occurs when heart is almost empty and is
in near iso-metric contraction
• AUSCULTATIONS1 normalS2 split – paradoxicalHarsh cresendo-decresendo mid-systolic murmur grade III/VI heard between apex and left sternal border not radiating to carotid or axillaMurmur increases with standing, exercise, Valsalva maneuver (strain)Decreases with squatting, isometric hand grip, Valsalva maneuver (overshoot)
WHAT ARE THE CAUSES OF WHAT ARE THE CAUSES OF PARADOXICAL SPLIT S2 ?PARADOXICAL SPLIT S2 ?
WHAT ARE THE CAUSES OF WHAT ARE THE CAUSES OF PARADOXICAL SPLIT S2 ?PARADOXICAL SPLIT S2 ?
MECHANISM CAUSESDELAYED ELECTRICAL ACTIVATION OF LV
LBBBRV PACINGRV ECTOPY
PROLONGED LV MECHANICAL SYSTOLE
SEVERE ASSEVERE SYSTEMIC HYPERTENSIONACUTE MYOCARDIAL INFARCTIONDURING AN EPISODE OF ANGINACARDIOMYOPATHYSEVERE ARLARGE PATENT DUCTUS ARTERIOSIS
INCREASE OF HANGOUT INTERVAL ON THE AORTIC SIDE
ANEURYSM OF ASCENDING AORTA POST-STENOTIC DILATION IN AS
EARLY PULMONIC CLOSURE
EARLY ELECTRICAL ACTIVATION OF RV AS IN TYPE B WPW SYNDROME. IN WPW SYNDROME, REVERSED SPLIT OCCURS ONLY WHEN THERE IS SIGNIFICANT PRE-EXCITATIONSEVERE TRICUSPID REGURGITATION
WHAT TYPE OF MURMURS WHAT TYPE OF MURMURS CAN BE HEARD IN HOCM ?CAN BE HEARD IN HOCM ?WHAT TYPE OF MURMURS WHAT TYPE OF MURMURS CAN BE HEARD IN HOCM ?CAN BE HEARD IN HOCM ?
• Harsh cresendo-decrescendo systolic
murmur
• Holosystolic murmur of mitral
regurgitation
• Diastolic rumbling murmur in patients
with severe MR
• Murmur of aortic regurgitation
• OTHER SYSTEM EXAMINATION : NAD
INVESTIGATION
HEMOGRAM WNL
RENAL PROFILE WNL
LIVER PROFILE WNL
INVESTIGATION
ECG NORMAL SINUS RHYTHMAXIS : (– 30°)LEFT ATRIAL ENLARGEMENTPOOR PROGRESSION OF R WAVELVH PRESENT LARGE NEGATIVE PRECORDIAL T WAVES
WHAT ARE THE ECG WHAT ARE THE ECG CHANGES FOUND IN HOCM ?CHANGES FOUND IN HOCM ?
WHAT ARE THE ECG WHAT ARE THE ECG CHANGES FOUND IN HOCM ?CHANGES FOUND IN HOCM ?
• ST-T wave abnormalities• QRS complexes, tallest in the
midprecordial leads• Prominent Q waves in precordial leads• Giant negative T waves• Evidence of LAE/RAE • Short PR interval• Prolongation of QTc• Features of WPW syndrome• Arrhythmias- VPCs, VT, SVT, AF
ECHO DIMENSIONS LA – 40mm IVS(D) – 27mm LVPW(D) – 10mm IVS(S) - 30mm LVPW(S) – 19mm LVEF – 77%ASH +GROUND GLASS APPEARANCE OF SEPTUMLVOT Δ RESTING 27 mmHgPOST-SORBITRATE 60 mmHg
HOLTER OCCASIONAL SVCS VPCS OF RBBB, LBBB MORPHOLOGYONE COUPLETONE RUN OF 3 BEATSNO SINUS PAUSEASYMPTOMATIC DURING RECORD
WHO ARE THE PATIENTS WHO ARE THE PATIENTS AT HIGH RISK FOR SCD ?AT HIGH RISK FOR SCD ?WHO ARE THE PATIENTS WHO ARE THE PATIENTS AT HIGH RISK FOR SCD ?AT HIGH RISK FOR SCD ?
COURSE OF EVENTS
FINAL DIAGNOSIS
A CASE OF HYPERTROPHIC OBSTRUCTIVE
CARDIOMYOPATHY, NYHA CLASS III, IN
NORMAL SINUS RHYTHM, WITH NO
EVIDENCE OF INFECTIVE ENDOCARDITIS
WITH HIGH RISK FOR SCD
MANAGEMENT PLAN
• PRIORITIES OF THERAPY
Alleviation of symptoms
Prevention of complications
Prevention of sudden cardiac death
Management of heart failure
TREATMENT• PHARMACOLOGICAL
Atenolol 100mg 1ODVerapamil 40mg 1TDS
• NON-PHARMACOLOGICALAlcohol septal ablation
IMPORTANT POINTS IMPORTANT POINTS TO REMEMBER TO REMEMBER ABOUT HOCMABOUT HOCM
IMPORTANT POINTS IMPORTANT POINTS TO REMEMBER TO REMEMBER ABOUT HOCMABOUT HOCM
• First described by Sir Russell Brock in 1958
• Eugene Braunwald described the unique hemodynamics
• Other terms used are idiopathic hypertrophic subaortic stenosis and muscular subaortic stenosis
• Defined as myocardial hypertrophy in absence of identifiable cause
• Prevalence is 1:500 to 1:1000• Autosomal dominant disease• Most common genetically
transmitted cardiovascular disease• Genetic basis first reported by
Seidman and Seidman (chromosome 14q11-12)
• Most common cause of SCD in young including trained athletes
• Common sites of ventricular involvement are septum, apex and mid-ventricle in decreasing order of frequency
• Obstruction present in 25% of cases
• Most characteristic is diastolic dysfunction rather than systolic
• Triad of dyspnea, angina, syncope• Most common symptom is dyspnea• Angina in 70-80% cases• MI in 15% cases• Syncope in 20%, over 50% have
pre-syncope
• B-blocker is the initial drug of choice• Advantages – decreased heart rate
response to exercise• Decreased outflow gradient with
exercise• Decreased oxygen demand• Improvement in diastolic filling
• Ca-channel blockers improves abnormal diastolic relaxation
• Disopyramide with negative inotropic effect decreases the gradient and improve symptoms
• Disopyramide added to B-blocker or Ca-blocker if symptoms persist
• Pacing of right ventricular apex reduces SAM
• Pacing or sensing atrium helps to maintain hemodynamic contribution of atrial contraction
• Used in patients with assd. sinus or AV node dysfunction
• Used in elderly patient with multiple co-morbidities who are at high risk for other therapeutic modalities
• Alcohol septal ablation is new therapeutic modality
• 100% alcohol is infused in first septal perforator artey
• Produces controlled MI of proximal septum
• Remodelling of basal septum region results in reduction of outflow obstruction