SGD 2: RHD

SGD 2: RHD

Saldana Emmanuel, Sales Stephanie, Salonga Cryscel, San Diego Phoebe, San Pedro Rina, Sanez Eric, Sanidad Erica, Santos Emmalene, Santos

Jeniffer, Santos Joel, Santos Karen,Santos Mary Elaine

Elvie, 28 y/o housewife, dyspnea

3 days PTA Dental Procedure

2 days PTA •Cough productive of yellowish sputum accompanied by colds

•Pricking chest pain radiating to the back lasting more than 30 minutes occurring even at rest

•Fever at 38 degrees Celsius with joint pain and myalgia1 day PTA Dyspnea

Easy Fatigability

Admission

• Past Medical History– (+) frequent

streptococcal throat infection in childhood

– At age 16, diagnosed to have valvular heart disease with monthly injections of Benzathine Penicillin

• Family History(+) hypertension –

grandfather(+) heart disease - father

Physical Examination

• Drowsy, in respiratory distress, prefers the semi-sitting position

• BP: 130/60 mmHg PR: 124 beats/min • CR: 135 beats/min, irregularly irregular• RR: 40 cycles/min Temp: 38.5°C


• Cold, clammy extremities, no active dermatoses• No nasoaural discharge, with alar flaring• Moist buccal mucosa, hyperemic posterior

pharyngeal wall, tonsils not enlarged• Supple neck, distended neck veins at 4-5cm at

30°angle• Symmetrical chest expansion, (+) supraclavicular

retractions, coarse crackles over both lung fields

Physical Examination• Dynamic precordium, AB at 6th LICS AAL• (+) heave at the left lower parasternal area• (++) impulse at the 2nd LICS, • On auscultation at the apex, S1 was noted to vary

in intensity, followed by a grade 3/6 holosystolic murmur that radiates to the axilla, S2 is normal followed by an opening snap and a grade 3/6 diastolic rumbling murmur

• At the base, the pulmonic component of S2 is loud with a grade 3/6 diastolic blowing murmur


• Globular abdomen, liver is palpable• Extremity: grade 2 bipedal edema

Laboratory and Ancillary TestsCBC Patient Normal Values

Hgb 120 120-158 g/L

Hct 0.40 0.354-0.444

Platelet 305 165-415 x 109/L

WBC 19.9 3.54-9.06 x 109/L

Segmenters 0.91 0.40-0.70

Lympho 0.08 0.20-0.50

ASO >200 IU/L

ESR 100 0-20mm/hr

Chest X-ray:•Cardiomegaly with features of mitral valve pathology•Pulmonary edema•Haziness at right paracardiac border

ECG:•Atrial Fibrillation with rapid ventricular response•Non-specific ST-T wave changes

2D-Echo:•Mitral Stenosis, moderate to severe•Mitral regurgitation, moderate•Aortic regurgitation, moderate•LV and RV dilatation•Dilated LA and RA with no evidence of thrombus•Dilated main pulmonary artery

Diagnosis

• Rheumatic Heart Disease, active• Mitral stenosis, moderate to severe; Mitral

regurgitation, moderate; Aortic regurgitation, moderate; LV and RV dilatation; Dilated LA and RA with no evidence of thrombus; Dilated Main Pulmonary Artery; Pulmonary Hypertension; Congestive heart failure in atrial fibrillation with rapid ventricular response

• Class IV-D

Pathophysiology of Rheumatic fever/Rheumatic Heart Disease

Organism Factors

• Acute Rheumatic Fever is caused by infection of the upper respiratory tract with any strain of group A streptococci.

• A series of preceding streptococcal infections is needed to "prime" the immune system prior to the final infection that directly causes disease.

Host Factors• Findings of familial clustering of cases &

concordance in monozygotic twins—particularly for chorea—confirm that susceptibility to ARF is an inherited characteristic.

• HLA class II alleles• ↑levels of circulating MBL & polymorphisms

of TGF-β1 gene and immunoglobulin genes

Immune Response

Immune Response

• Epitopes present in the cell wall, cell membrane, and the A, B, and C repeat regions of the streptococcal M protein are immunologically similar to molecules in human myosin, tropomyosin, keratin, actin, laminin, vimentin, and N-acetylglucosamine.

• Human molecules—particularly epitopes in cardiac myosin—result in T cell sensitization.

Immune Response

• Laminin, another -helical coiled-coil protein like myosin and M protein, which is found in cardiac endothelium and is recognized by anti-myosin, anti-M protein T cells.

• Antibodies to cardiac valve tissue cross-react with the N-acetylglucosamine of group A streptococcal carbohydrate, and there is some evidence that these antibodies may be responsible for valvular damage.

Physical examination findings in MS, MR, AR?

Mitral Stenosis Inspection

o malar flush with pinched and blue fascies Palpation

Arterial pulse amplitude decreasedo RV tap along left sternal border signifies enlarged RV, diastolic thrill at

cardiac apex Auscultation:

o S1 accentuated and delayed and palpable at left sternal bordero S2 closely split with accented P2o OS readily audible in expiration

o Follows P2 closely, followed by a low pitched, rumbling diastolic murmur heard best at apex and does not radiate

o Soft grade 1 or 2/6 murmur heard at apex or left sternal border Hepatomegaly, ankle edema, ascites and pleural effusion if with

RV failure

Mitral Regurgitation• Usually asymptomatic for chronic mild-moderate MR• Palpation

– Arterial pressure usually normal but may show a sharp upstroke– Systolic thrill at cardiac apex– Palpable rapid filling wave (S3)– Apex beat displaced laterally– In acute severe MR

• Reduced arterial pressure• Normal or increased jugular venous pressure• Apical impulse not displaced

• Auscultation– Grade 3/6 holosystolic high-pitched decrescendo, my obliterate S2– Radiates from apex to base or to left axilla– Absent or soft S1– Premature A2 resulting in wide but physiologic splitting of S2– S3 often present– S3-S4 on those with severe MR

Aortic Regurgitation

• Inspection– Jarring of the entire body and bobbing motion of the head

with each systole– Abrupt distention (water hammer pulse) and collapse of

large arteries during late sytole and diastole (Corrigan’s pulse)

– Alternate flushing and paling of the skin at the root of the nail (Quincke’s pulse)

– Booming sound on femoral artery ( Traube’s sign)

Aortic Regurgitation• Palpation

– Elevation of systolic pressure (300 mmHg)– Depression of diastolic pressure– LV impulse is heaving and displaced laterally and inferiorly– Palpable diastolic thrill along the left sternal border, systolic

thrill in suprasternal notch transmitted in the carotid arteries• Auscultation

– Murmur is high pitched, blowing, decrescendo diastolic murmur heard best in 3rd ICS along the left sternal border

– Low pitched rumbling murmur at the apex (Austin Flint)– Soft S1, M1 and A2 often intensified– S3 and systolic ejection sound are audible– Occasionally S4 can also be heard– Auscultatory features are intensified by strenous handgrip, which

increases sytemic resistance

AUSCULTOGRAM

MR, MS, AR, AS

AUSCULTOGRAM

Differential Diagnosis for the Cause of Fever

Differential Diagnosis for the Cause of Fever

• Myocarditis• Pericarditis• Systemic Lupus Erythematosus (SLE)• Pneumonia• Pulmonary Tuberculosis (PTB)

Myocarditis Patient

Dyspnea (+) (+)

Chest Pain (+) (+)

Fever (+) (+)

history of recent flulike syndrome of fevers, arthralgias or pharyngitis, or upper respiratory tract infection.

(+) (+)

Dilated cardiomyopathy (+) (+)

Arrhythmia (+) (+)

Heart Failure (+) (+)

Myocarditis Patient

Decompensation of heart failure (tachycardia, mitral regurgitation, edema)

(+) (+)

Leukocytosis (+) (+)

Elevated ESR (+) (+)

nonspecific ST or T-wave changes

(+) (+)

Frequent streptococcal throat infection in childhood

(+) rheumatic fever (+)

Pericarditis Patient

Males (+) (-)

Adults (+) (+)

Chest Pain (+) (+)

Pericardial friction rub (+) (-)

Dyspnea (+) (+)

Fever (+) (+)

Tachypnea (+) (+)

Tachycardia (+) (+)

Pericarditis Patient

Elevated ESR, segmenters (+) (+)

Frequent streptococcal throat infection in childhood

(+) rheumatic fever (+)

Pericardial effusion (+) (-)

SLE Patient

Females (+) (+)

Childbearing age (+) (+)

Fatigue (+) (+)

Fever (+) (+)

Arthralgia (+) (+)

Myalgia (+) (+)

edema (+) (+)

SLE Patient

Dyspnea (+) (+)

Chest pain (+) (+)

Multiple cytopenias (+) (-)

Tachypnea (+) (+)

crackles (+) (+)

Pneumonia Patient

Fever (+) (+)

Productive Cough (+) (+)

Dyspnea (+) (+)

Pleuritic Chest pain (+) (-)

Rales (+) (-)

Infiltrates on chest x-ray (+) (-)

PTB Patient

Males (+) (-)

Older than 65 (+) (-)

Productive cough (+) (+)

Fever (+) (+)

Weight loss (+) (-)

Hemoptysis (+) (-)

Chest pain (+) (+)

Anorexia (+) (-)

Fatigue (+) (+)

PTB Patient

Night sweats (+) (-)

Chest x-ray: patchy or nodular infiltrate

(+) (-)

REVISED JONES CRITERIA2002-2003 WHO Criteria for the Diagnosis of RF and RHD

Includes preceding streptococcal type A infection and a combination of major and minor

clinical manifestations

Harrison’s Principles of Internal Medicine, 17th ed.


SUPPORTING EVIDENCE OF A PRECEDING STREPTOCOCCAL INFECTION W/IN THE LAST 45 DAYS:

• Elevated or rising anti-streptolysin O or other streptococcal antibody, or•(+) Throat culture, or• Rapid antigen test for group A streptococcus


DIAGNOSTIC CATEGORIES

Primary Episode of Rheumatic Fever2 Major OR 1 Major + 2 Minor manifestationsPlus evidence of preceding group A streptococcal infection

Recurrent attack of RF in a patient without established RHD2 Major OR 1 Major + 2 Minor manifestationsPlus evidence of preceding group A streptococcal infection

Recurrent attack of RF in a patient with established RHD2 Minor manifestationsPlus evidence of preceding group A streptococcal infection



DIAGNOSTIC CATEGORIES

Rheumatic ChoreaInsidous onset rheumatic carditis

Other major manifestations or evidence of group A strep. infection not required

• Infective endocarditis should be excluded.

Chronic valve lesions of RHD Do not require any other criteria to be diagnosed as having

rheumatic heart disease• Congenital heart disease should be excluded.



“Probable Rheumatic Fever”

– with polyarthritis (or with only polyarthralgia or monoarthritis) and with several (3 or more) other minor manifestations, plus evidence of recent group A streptococcal infection.

– may later turn out to be rheumatic fever – advise regular secondary prophylaxis, follow up closely

and do regular heart examination (esp. in vulnerable age groups in high incidence settings)



The Duke Criteria

The Duke Criteria

• The diagnosis of infective endocarditis is certain only when vegetations obtained are examined histologically and microbiologically.

• Duke criteria is based on clinical, laboratory and echocardiographic findings.

• 2 major criteria, 1 major + 2 minor criteria, or 5 minor criteria allows a definitive diagnosis.

The Duke Criteria

• The diagnosis of infective endocarditis is rejected if:– Alternative diagnosis is established– Symptoms resolve and do not recur within 4 days

or less of antibiotic therapy– Surgery or autopsy after 4 days or less of

antimicrobial therapy yields no histologic evidence of endocarditis

The Duke Criteria

• Illnesses not classified as definite endocarditis or rejected are considered possible cases when either 1 major + 1 minor citeria or 3 minor criteria are identified.

• To fulfill a major criterion, the isolation of an organism that causes both endocarditis and bacteremia in the absence of endocarditis must take place repeatedly and in the absence of primary focus of infection.

The Duke Criteria

• Organisms that rarely cause endocarditis but commonly contaminate blood cultures must be isolated repeatedly if their isolation is to serve as a major criterion.

The Duke Criteria

• Major Criteria– Positive Blood Culture

• Typical microorganisms from two separate blood cultures*

• Persistently positive blood culture, defined as recovery of a microorganism consistent w/ infective endocarditis from:

– Blood cultures drawn >12 hrs apart– All of three, majority of four or more separate blood cultures,

with first and last drawn at least 1 hr apart– Single positive blood culture from Coxiella burnetti or phase I

IgG titer > 1:800

The Duke Criteria

– Evidence of Endocardial Involvement• Positive Echocardiogram

– Oscillating intracardiac mass on valve or supporting structures or in the path of regurgitant jets or in implanted material, in the absence of an alternative anatomic explanation

– Abscess– New partial dehiscence of prosthetic valve

• New valvular regurgitation*

The Duke Criteria

• Minor Criteria– Predisposition*– Fever >/= 38°C*– Vascular phenomena*– Immunologic phenomena*– Microbiologic Evidence*

Differential Diagnosis for the cause of dyspnea

Algorithm for Dyspnea Pathophysiology

DYSPNEA

RESPIRATORY

Gas Exchanger

Pulmonary embolismPneumoniaInterstitial lung disease

Pump

COPDAsthmaKyphoscoliosis

Controller

PregnancyMetabolic acidosis

Low output

Congestive heart failureMyocardial ischemiaConstrictive pericarditis

High output

AnemiaHyperthyroidismArteriovenous shunt

Normal output

DeconditioningObesityDiastolic dysfunction

CARDIOVASCULAR

PNEUMONIA

• infection of the pulmonary parenchyma

• results from the proliferation of microbial pathogens at the alveolar level and the host's response to those pathogens

• the most common way by which microorganisms gain access to the lower respiratory tract is by aspiration from the oropharynx

ETIOLOGY

Hospitalized patients

Outpatients Non-ICU ICU

Streptococcus pneumoniae S. pneumoniae S. pneumoniae

Mycoplasma pneumoniae M. pneumoniae Staphylococcus aureus

Haemophilus influenzae Chlamydophila pneumoniae Legionella spp.

C. pneumoniae H. influenzae Gram-negative bacilli

Respiratory viruses Legionella spp. H. influenzae

Respiratory virusesa

CLINICAL MANIFESTATIONS• Febrile• Tachycardia• Chills and/or sweats• Cough that is either nonproductive or productive of mucoid, purulent, or blood-

tinged sputum• Pleuritic chest pain• Nausea, vomiting, and/or diarrhea• Fatigue, headache, myalgias, and arthralgias

On physical examination:• increased respiratory rate and use of accessory muscles of respiration• increased or decreased tactile fremitus• on percussion note can vary from dull to flat, reflecting underlying consolidated

lung and pleural fluid, respectively• on auscultation, crackles, bronchial breath sounds, and possibly a pleural friction

rub may be heard on auscultation

CONGESTIVE HEART FAILURE

• Heart failure (HF) is a clinical syndrome that occurs in patients who, because of an inherited or acquired abnormality of cardiac structure and/or function, develop a constellation of clinical symptoms (dyspnea and fatigue) and signs (edema and rales) that lead to frequent hospitalizations, a poor quality of life, and a shortened life expectancy

• any condition that leads to an alteration in LV structure or function can predispose a patient to developing HF. – Coronary artery disease– Hypertension– Faulty heart valves– Cardiomyopathy– Myocarditis– Congenital heart defects– Arrhythmias– Chronic diseases : diabetes, severe anemia, hyperthyroidism, hypothyroidism,

emphysema, lupus, hemochromatosis and amyloidosis

ETIOLOGY

Type of Heart Failure Signs and symptoms

Chronic heart failure(A long-term condition with signs and symptoms that persist.)

• Fatigue and weakness • Rapid or irregular heartbeat • Shortness of breath (dyspnea) when you exert yourself or when you lie down • Reduced ability to exercise • Persistent cough or wheezing with white or pink blood-tinged phlegm • Swelling (edema) in your legs, ankles and feet • Swelling of your abdomen (ascites) • Sudden weight gain from fluid retention • Lack of appetite and nausea • Difficulty concentrating or decreased alertness

CLINICAL MANIFESTATIONS

Type of Heart Failure Signs and symptoms

Acute heart failure (An emergency situation that occurs when something suddenly affects your heart's ability to function.)

• Signs and symptoms similar to those of chronic heart failure but more severe, and start or worsen suddenly

• Sudden fluid buildup

• Rapid or irregular heartbeat with palpitations that may cause the heart to stop beating

• Sudden, severe shortness of breath and coughing up pink, foamy mucus

• Chest pain if caused by a heart attack

CLINICAL MANIFESTATIONS

Enumerate the precipitating factors of heart failure.

HEART FAILURE• Pathophysiologic state

wherein the heart loses its ability to pump sufficient amount of blood due to a structural or functional cardiac abnormality

HEART FAILURE• A majority of the patients’

symptoms of heart failure are due to impairment of left ventricular function.

• Hence, a condition that leads to an alteration in LV structure or function can predispose a patient to developing heart failure.

HEART FAILURE

HEART FAILUREPRECIPITATING CAUSES OF HEART FAILURE:

Differentiate low and high output failure, R/L sided heart failure, systolic

and diastolic dysfunction

Systolic Versus Diastolic Failure

Forms of Heart Failure

Sytolic Failure• Inability of the ventricle

to contract normally and expel sufficient blood

• Inadequate cardiac output with weakness, fatigue, reduced exercise tolerance (hypoperfusion)

Diastolic Failure• Inability to relax or fill

normally (elevation of filling pressures)

• Due to increased resistance to ventricular diastolic capacity, impaired ventricular relaxation, and myocardial fibrosis and infiltration

Management

Congestive Heart Failure

• Patients With Reduced Left Ventricular Ejection Fraction– If with fluid retention:

• Use diuretics (thiazides)

– Medications that should be AVOIDED:• Anti-arrhythmics• Calcium channel blockers• NSAIDs

Circulation; Journal of the AHA http://circ.ahajournals.org/cgi/content/full/119/14/1977


• Patients With Reduced Left Ventricular Ejection Fraction– Recommendations concerning aldosterone

antagonists:• carefully selected patients with moderately severe or

severe HF symptoms and recent decompensation or with LV dysfunction early after MI



• Patients With Refractory End-Stage Heart Failure (Stage D)– Intravenous Peripheral Vasodilators and Positive

Inotropic Agents:• hospitalized frequently for clinical deterioration, and

during such admissions, they commonly receive infusions of both positive inotropic agents (dobutamine, dopamine, or milrinone) and vasodilator drugs (nitroglycerin, nitroprusside, or nesiritide)



The Hospitalized PatientCommon Factors That Precipitate

Hospitalization for Heart Failure• Noncompliance with medical regimen, sodium

and/or fluid restriction• Acute myocardial ischemia• Uncorrected high blood pressure• Atrial fibrillation and other arrhythmias




Hospitalization for Heart Failure• Recent addition of negative inotropic drugs

(e.g., verapamil, nifedipine, diltiazem, beta blockers)

• Pulmonary embolus• Nonsteroidal anti-inflammatory drugs




Hospitalization for Heart Failure• Excessive alcohol or illicit drug use• Endocrine abnormalities (e.g., diabetes

mellitus, hyperthyroidism, hypothyroidism)• Concurrent infections (e.g., pneumonia, viral

illnesses)


SGD 2: RHD

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