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Transcript of 2KULIAH KARDIOMIOPATI
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CARDIOMYOPATHY
Saharman Leman
Sub-bagian Kardiologi Penyakit Dalam Fk Unand /
Intensive Care Unit RSI Siti Rahmah Padang
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Definition
Disorders of the cardiac muscle of unknown
aetiology
A primary disorder of the heart musclethatcauses abnormal myocardial performance
and is not the result of disease or
dysfunction of other cardiac structures
myocardial infarction, systemic hypertension,
valvular stenosis or regurgitation
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Functional Classification
Dilatated (congestive, DCM, IDC)
ventricular enlargement and syst dysfunction
Hypertrophic (IHSS, HCM, HOCM) inappropriate myocardial hypertrophyin the absence of HTN or aortic stenosis
Restrictive (infiltrative)
abnormal filling and diastolic function
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IDIOPATHIC DILATED CARDIOMYPATHY
EPIDEMIOLOGY
ANNUAL INCIDENCE 5-8/100,000
PREVELANCE 36/ 100,000
INCREASED RISK ASSOCIATED WITH:
MALE GENDER BLACK RACE
HYPERTENSION
CHRONIC BETA-AGONIST USE
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ETIOLOGIES OF DILATED CARDIOMYOPATHY
0
5
10
15
20
2530
35
40
45
50
Disorder
IDCM
Myocarditis
Ischmic CM
InfiltrativediseasePeripartum CM
Hypertension
HIVCTD
Substance
abuse
Felker et al NEJM 2000
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1. IDIOPATHIC DILATED CARDIOMYOPATHY
PATHOLOGY
Four chamber dilatation
Mild to moderate ventricular
hypertrophy
Varying degrees of interstitial
fibrosis and myocyte
hypertrophy
Functional atrioventricular
regurgitation is common
Normal epicardial coronary
arteries
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IDIOPATHIC DILATED CARDIOMYOPATHY
PATHOGENESIS
Familial/genetic factors
Viral myocarditis and cytotoxic insults
Immunologic abnormalities Beta-receptor auto-antibodies
Abnormal T-cell function
Metabolic, energetic, and contractile
abnormalities Ca2+-ATPase
Myofibrillar ATPase
Creatine Kinase
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MOLECULAR DEFECTS IN DILATED
CARDIOMYOPATHY
Fatkin D, et al. NEJM 1999;341
GENESLamin A/C
-sarcoglycan
Dystrophin
Desmin
Vinculin
Titin
Troponin-T
-tropomyosin
-myosin heavy chain
Actin
Mitochondrial DNAmutations
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IDIOPATHIC DILATED CARDIOMYPATHY
CLINICAL PRESENTATIONS
Heart failure symptoms 75%-85%
Anginal chest pain 8%-20%
Emboli (systemic or pulmonary) 1%-4%
Syncope
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IDIOPATHIC DILATED CARDIOMYPATHY
CARDIAC IMAGING
CXR: enlargement of cardiac silhoutte
ECG: evidence of old MCI, conduction
abnormalities e.g LBBB, LV hypertrophy, AF or VT
24-hour ambulatory ECG (Holter) lightheadedness, palpitation, syncope
Two-dimensional echocardiogram or Radionuclide
ventriculographyto assess : LV ejection fraction,end-diastolic volume, diastolic function
Cardiac catheterization
age >40, ischemic history, high risk profile,
abnormal ECG
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IDCM:PROGNOSTIC FEATURES
VENTRICULOGRAPHIC FINDINGS
Degree of impairment in LVEF Extent of left ventricular enlargement
Coexistent right ventricular dysfunction
Ventricular mass/volume ratio
Global wall motion abnormalities
Left ventricular sphericity
CLINICAL FINDINGS
Favorable prognosis: NYHA < IV, younger age, femalesex
Poor prognosis: Syncope, persistent S3 gallop, right-sided heart failure, AV or bundle branch block,hyponatremia, troponin elevation, increased BNP,maximum oxygen uptake < 12 mg/kg/min
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IDIOPATHIC DILATED CARDIOMYPATHY
PREDICTING PROGNOSIS
Predictive Possible Not Predictive
Clinical factors symptoms alcoholism age
peripartum duration
family history viral illness
Hemodynamics LVEF LV sizeCardiac index atrial pressure
Dysarrhythmia LV cond delay AV block simple VPC
complex VPC atrial fibrillation
Histology myofibril volume other findings
Neuroendocrine hyponatremia
plasma norepinephrine
atrial natriuretic factor
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RIGHT
VENTRICULAR
BIOPSY
TECHNIQUE
ENDOMYOCARDIAL BIOPSY IN DILATED CARDIOMYOPATHY
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INDICATIONS FOR ENDOMYOCARDIAL
BIOPSY
Acute dilated cardiomyopathy with refractory heart failuresymptoms
Rapidly progressive ventricular dysfunction in anunexplained cardiomyopathy of recent onset
New onset cardiomyopathy with recurrent ventriculartachycardia or high grade heart block
Heart failure in the setting of fever, rash, and peripheraleosinophilia
Dilated cardiomyopathy in setting of systemic diseases
known to affect the myocardium (systemic lupus erythematosus,polymyositis, sarcoidosis)
Wu LA, et al. Mayo Clin Proc 2001;76:1030-8
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IDIOPATHIC DILATED CARDIOMYOPATHY
MANAGEMENT
Limit activity based on functional status
salt restriction of a 2-g Na+(5g NaCl)
diet fluid restriction for significant low Na+
initiate medical therapy
ACE inhibitors, diuretics
digoxin, carvedilol
hydralazine / nitrate combination
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IDIOPATHIC DILATED CARDIOMYOPATHY
MANAGEMENT
consider adding -blocking agents if
symptoms persists
anticoagulation for EF
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2. HYPERTROPHIC CARDIOMYOPATHY
First described by the French and Germans
around 1900
uncommon with occurrence of 0.02 to 0.2%
a hypertrophied and non-dilated left ventricle
in the absence of another disease
small LV cavity, asymmetrical septal
hypertrophy (ASH), systolic anterior
motion of the mitral valve leaflet (SAM)
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HYPERTROPHIC CARDIOMYOPATHYEPIDEMIOLOGY
Prevalence : 1 per 500inUS
Higher in Black individual
Inherited in an autosomal
dominant pattern Predominance in younger
Male
Commonest cause of
sudden death duringexertion in young people
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HYPERTROPHIC CARDIOMYOPATHYPATHOGENESIS
Misconception that outflow tract
obstruction
Impaired ventricular compliance as
consequence of inappropriate myocardial
hypertrophy
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HYPERTROPHIC CARDIOMYOPATHYPATOPHYSIOLOGY
Systole
dynamic outflow tract gradient
Diastole
impaired diastolic filling, filling pressure
Myocardial ischemia
muscle mass, filling pressure, O2 demand
vasodilator reserve, capillary density
abnormal intramural coronary arteries
systolic compression of arteries
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HYPERTROPHIC CARDIOMYOPATHYMYOCARDIAL DISARRAY
Normal Muscle Structure Myocardial Disarray
(Parallel alignment) (Disorganised alignment)
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HYPERTROPHIC CARDIOMYOPATHYTYPES
HCM or HOCM
Asymmetric septal (ASH) - withoutobstruction
Asymmetric septal (ASH) - with obstruction
Symmetric hypertrophy - concentric Apical hypertrophy
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65% 35%
10%
www.kanter.com/hcm
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HCM
Mitral
Valve in
normal
position
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HOCM
Mitral valve
presses
against
septum
MR
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SYMMETRIC
symmetric
or
concentric
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APICAL
Small
cavityremains
Apical Hypertrophy
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HYPERTROPHIC CARDIOMYOPATHYPHYSICAL EXAMINATIONS
Carotid impulse
Prominent a waves of JV pulse
Outflow murmur Mitral regurgitation
Atrial fibrilation
Embolic phenomena Heart Failure symptoms
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HYPERTROPHIC CARDIOMYOPATHY
DIAGNOSTIC APPROACH
ECG :
Abnormalities of ST segment and T waves
LVH
QRS complex tallest at mid precordial leads
Echo :
Concentric caused by pressure overload e.g. AS
Eccentric caused by volume overload e.g MR, AR
Septal thickening wall
Mitral valve anterior leafleat may be enlarged
MR
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HYPERTROPHIC CARDIOMYOPATHYDIFFERENTIAL DIANOSIS
Left Ventricular hypertrophy
Outflow obstruction secondary to valvularheart disease e.g AS, coarctation of aorta
and infiltrative disorder of myocardium
Pattern hypertrophy in hypertension is
concentric meanwhile in HCM is distinctive
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HCM vs Aortic Stenosis
HCM Fixed Obstruction
carotid pulse spike and dome parvus et tardus
murmur radiate tocarotids
valsalva, standing
squatting, handgrip
passive leg elevation
systolic thrill 4th left interspace 2nd right
interspace
systolic click absent present
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Hypertrophic Cardiomyopathy
Treatment algorithm
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HYPERTROPHIC CARDIOMYOPATHYMANAGEMENT
Medical management:
B-blockers
CCB, verapamil Disopyramide in decreasing outflow gradient
Endocarditis prophylaxis
Permanent Pacing
I C DAlcohol ablation of the septum
Injected 1-4 ml absolute alcohol into the septalperforator branch of LAD
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HYPERTROPHIC CARDIOMYOPATHYMANAGEMENT
Surgical therapy
Subaortic ventricular myotomy
Resection myocardium from proximal septum tobeyond mitral leafleat
Advantage :
Low mortality
Reduced symptoms Improved functional capacity
Heart transplantation
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3. Restr ic t ive Card iomyopathy
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RESTRICTIVE CARDIOMYOPATHY
Hallmark: abnormal diastolic function
rigid ventricular wall with impaired
ventricular filling
importance lies in its differentiation from
operable constrictive pericarditis
Characteristics by :Abnormalcompliance of the left ventricle and
short relaxation time
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RESTRICTIVE CARDIOMYOPATHYETIOLOGY
Non infiltrative cause
Associated with patchy endomyocardial fibrosis,
increased cardiac mass and enlarged atriaInfiltrative cause
Amyloidisis, primary caused by the deposition ofamyloid protein. Secondary caused by production
nonimunoglobulin protein and termed AASarcoidosis
Endomyocardial fibrosis
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RESTRICTIVE CARDIOMYOPATHYEXCLUSION GUIDELINES
LV end-diastolic dimensions 7 cm
Myocardial wall thickness 1.7 cm
LV end-diastolic volume 150 mL/m2
LV ejection fraction < 20%
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RESTRICTIVE CARDIOMYOPATHYCLASSIFICATION
Idiopathic
Myocardial
1. Noninfiltrative
Idiopathic
Scleroderma
2. Infiltrative
Amyloid
Sarcoid
Gaucher disease Hurler disease
3. Storage Disease
Hemochromatosis
Fabry disease
Glycogen storage
Endomyocardial
endomyocardial fibrosis
Hyperesinophilic synd
Carcinoid
metastatic malignancies radiation, anthracycline
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RESTRICTIVE CARDIOMYOPATHYCLINICAL PRESENTATIONS
Symptoms of right and left heart failure
Angina if CAD involve
Jugular Venous Pulse prominentxand ydescents
Echo-Doppler abnormal mitral inflow pattern
prominent E wave (rapid diastolic filling) reduced deceleration time (LA pressure)
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RESTRICTIVE CARDIOMYOPATHYDIAGNOSTIC APPROACH
ECG :
Low voltage
Poor R wave progression Pseudoinfarction pattern in the inferior leads
P pulmonal If pulmonary hipertension present
Atrial arrhythmia esp fibrillation
Sick sinus syndrome is common
Ventricular Tachiarrhytmia
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RESTRICTIVE CARDIOMYOPATHYDIAGNOSTIC APPROACH
Chest X-ray
Normal CTR and enlarged atria
Enlarged right ventricle may be seen if pulmonaryhypertension present
Echo
Severe biatrial enlargement
Thickened LV walls
Cardiac nuclear imagingCT scan and MRI
Cardiac catheterization and endomyocardial biopsy
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No satisfactory medical therapy
Drug therapy must be used with caution
diuretics for extremely high filling prssures vasodilators may decrease filling pressure
? Calcium channel blockers to improve
diastolic compliance
digitalis and other inotropic agents are not
indicated
RESTRICTIVE CARDIOMYOPATHYMANAGEMENT
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RESTRICTIVE CARDIOMYOPATHYDIFFERENTIAL DIAGNOSIS
Constrictive pericarditis
Chronic RV infarction RV dysfunction from RV pressure or RV
volume overload
Instrinsic RV myocardial disease Tricuspid valve disease
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Constrictive - Restrictive Pattern
Square-Root Sign or Dip-and-Plateau
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RESTRICTIVE CARDIOMYOPATHYRestriction vs Constriction
History provide can important clues
Constrictive pericarditis
history of TB, trauma, pericarditis, sollagenvascular disorders
Restrictive cardiomyopathy
amyloidosis, hemochromatosis Mixed
mediastinal radiation, cardiac surgery
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MYOCARDITIS
Inflammation of myocardium
Can be result of systemic disorder or
infectious agent
Viral-Coxsackie B, echovirus, influenza,
parainfluenza, Epstein-Bar, and HIV
Bacterial-C. Diptheria, N. meningitidis,
M. pneumonia, and beta-hemolytic strep
Frequently accompanied with
pericarditis
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MYOCARDITIS
Clinical Presentations
Fever, tachycardia out of proportion to
fever, myalgias, headache,rigors
Chest pain due to coexisting pericarditis
Pericardial friction rub
Severe cases may have CHF symptoms
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MYOCARDITIS
CLINICAL PRESENTATIONS
EKG-nonspecific changes, av block,
prolonged QRS suration, or ST
elevation(with pericarditis) CXR-Normal
Cardiac Enzymes- may be elevated
Differentail-ischemia or infarct, valvulardisease, and sepsis
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MYOCARDITIS
MANAGEMENT
Supportive care
Blood cultures Antibiotics for bacterial cause
Watch for signs of progressive heart
failure
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Pericardial disease
Fib di
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Fibrous sac surrounding
heart-dense network of
collagen fibres
Serous membranetwo continuous layers
separated by a small
amount of fluid lubricant
(10-20mls ) Layers are :
Visceral is inner layer
(epicardium)
Parietal is continuous with
diaphragm and outer walls of
great arteries
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ACUTE PERICARDITIS
Loose visceral pericardium and dense
parietal pericardium surround heart
Pericardial space may contain up to 50ml
normally
Etiologies of acute pericarditis-viral,
bacterial, fungal, malignancy, drugs,
radiation, connective tissue disorder,uremia, myxedema, post-MI, or idiopathic
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ACUTE PERICARDITISETIOLOGY
Idiopathic86%
Infective (viral or bacterial)7%
Following a myocardial infarction or cardiac surgery
(Dresslers syndrome)
Radiation therapy
Neoplastic disease (commonly lung or breast)6%
Connective tissue disease
Figures from Permanyer-Miralda et al 1985
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ACUTE PERICARDITISCLINICAL PRESENTATIONS
Retrosternal chestpainsharp orstabbing pain worseon insp and lyingflat
Friction rub (highpitched scratchingnoise)
Raised jugularvenous pressure
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ACUTE PERICARDITISDIAGNOSIS APPROACH
EKG-changes in four stages
1-ST elevation in I, V5 and V6,
PR depression in II, aVF and
V4-V6 2-ST segment normalizes, T
wave decreases
3-Inverted T waves in leads
with previous ST elevation 4-Return to normal ECG
In I, V5, or V6 ST:Twave ratio
>0.25 most likely acute
pericarditis
C C S
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ACUTE PERICARDITIS
DIAGNOSIS APPROACH
Chest Xray-normal and can help r/o other
disease
Other tests of value-CBC, bun and cr,streptococcal serology, viral serologies,
antinuclear/anti-DNA abs, thyroid function,
ESR, Cardiac Enzymes
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ACUTE PERICARDITISMANAGEMENT
Search for the underlying disease
No good evidence from randomised controlledtrials
Patients require bed rest
NSAID (aspirin, indomethacin) are generallyaccepted as effective for relieving symptoms ofchest pain
NSAID ketorolac tromethamine rapid results Colchicine may be a useful adjunct in those who
do not respond to NSAIDs alone
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ACUTE PERICARDITISPROGNOSIS
Pericarditis is usually a benign disorder
Diagnosis relates to underlying cause
But any cause can lead to an effusion andtamponade which can lead to death
Pericarditis can also progress to
pericardial constriction and heart failure
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CONSTRICTIVE PERICARDITIS
Occurs when fibrous thickening and loss
of elasticity interfere with diastolic filling
Cardiac trauma, pericardiotomy,intrapericardial hemmorhage, fungal or
bacterial pericarditis, uremic pericarditis
are most common causes
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CONSTRICTIVE PERICARDITISCLINICAL PRESENTATIONS
Sxs gradually develop-mimics restrictiveCM- CHF, DOE, and decreased exercise
tolerance Chest pain, orthopnea and pnd are
uncommon
Exam-Pedal edema, hepatomegaly,ascites, jvd, and Kussmauls sign.
Pericardial knock-early diastolic soundmay be heard at apex
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CONSTRICTIVE PERICARDITISDIAGNOSIS APPROACH
EKG-not very helpful-may show low
voltage QRS and inverted T waves
CXR-pericardial calcifications seen in 50%
on lateral view(not diagnostic)
ECHO, CT, MRI are diagnostic
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CONSTRICTIVE PERICARDITISDIFFERENTIAL DIAGNOSIS
Consider acute pericarditis, myocarditis,
exacerbation of chronic ventriculardysfunction, or systemic process resulting
in decreased cardiac performance(sepsis)
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CONSTRICTIVE PERICARDITISMANAGEMENT
Supportive care
Symptomatic patients require admission
and pericardiectomy
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PERICARDIAL EFFUSION
Major causes are post cardiac surgery and
Neoplastic disease
Gradual accumulation of fluid (chronic) permits
progressive stretching of pericardium Patient may develop a substantial fluid without
significant increase in intrapericardial pressure
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PERICARDIAL EFFUSIONPATOPHYSIOLOGY
Significantly increased intrapericardialpressure impedes diastolic filling of theventricles
Therefore in order for the ventricles to fill theend-diastolic pressure must exceed thepericardial pressure
Global effusionpericardial pressure is equalaround heart
Therefore both ventricles have to increaseEDP to same amount for ventricles to fill
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PERICARDIAL EFFUSIONDIAGNOSTIC APPROACH
Clinical examinationSOB, orthopnoea,tachycardia (varying degrees)
Auscultationmay have muffled heart sounds
ECG may show low amplitude QRS complexesand alternating axis
CXRglobular appearance to heart andtherefore increased cardiothoracic ratio
Echosize of effusion and haemodynamiceffect of it
C X R ECHO
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C X R ECHO
PERICARDIAL EFFUSION
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PERICARDIAL EFFUSION
TREATMENT
Depends on the cause and nature
If acute the cause is treated and the
patient monitored
If persistent problem or life threatening
more dramatic action is called for
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Occurs when the fluid accumulation around theheart impairs filling to such an extent that there
is haemodynamic compromise.
It is a medical emergency and must be treatedpromptly.
Risk of death depends upon speed of diagnosis,
treatment and underlying cause of the
tamponade.
CARDIAC TAMPONADE
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CARDIAC TAMPONADECLINICAL PRESENTATIONS
Dyspnea and decreased exercise
tolerance-wt loss, pedal edema, ascites
Tachycardia, Narrow pulse pressure
Pulsus paradoxus
JVD, Muffled heart sounds, Hypotension
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CARDIAC TAMPONADEDIAGNOSTIC APPROACH
EKG-low voltage QRS with ST elevation and PRdepression possible
Electrical Alternans-classic findingP and R wave
beat to beat variability CXR-+/- enlarged cardiac silhoutte globular heart
ECHO :
- Size and location of effusion
- Any evidence of diastolic collapse- Swinging of the heart
- Decrease of insp. flow across MV
CARDIAC TAMPONADE
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CARDIAC TAMPONADE
DIAGNOSTIC APPROACH
IV Fluid Bolus-
improves RV filling and
improveshemodynamics
Pericardiocentesis-
therapeutic and
diagnostic
Admission to ICU or
monitored setting
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Terima Kas ih