Loading presentation...

Present Remotely

Send the link below via email or IM


Present to your audience

Start remote presentation

  • Invited audience members will follow you as you navigate and present
  • People invited to a presentation do not need a Prezi account
  • This link expires 10 minutes after you close the presentation
  • A maximum of 30 users can follow your presentation
  • Learn more about this feature in our knowledge base article

Do you really want to delete this prezi?

Neither you, nor the coeditors you shared it with will be able to recover it again.


Clinical Case Presentation

No description

amr othman

on 4 December 2012

Comments (0)

Please log in to add your comment.

Report abuse

Transcript of Clinical Case Presentation

One hell of A maze ! Case Presentation So We Start Clinical Situation Diagnosis Aortic valve disease
Chest infection
Mild renal impairment Creatinine Clearance In case of dose adjustment Rocephin Lasix Active ingredient Renal impairment In chronic severe AR, vasodilator therapy may be used in select conditions to reduce afterload in patients with systolic hypertension to minimize wall stress and optimize LV function; in normotensive patients, vasodilator therapy is not likely to reduce regurgitant volume (preload) significantly and thus may not be of clinical benefit. Clinical Question Evidence Review Clinical Answer Background Foreground Aortic regurgitation (AR) is the abnormal retrograde flow of blood through the aortic valve during cardiac diastole.

AR may be caused by either valvular or aortic root pathology. Valvular abnormalities that may result in AR include bicuspid aortic valve (the most common congenital cause), rheumatic fever, infective endocarditis, collagen vascular diseases, and degenerative aortic valve disease.

Abnormalities of the ascending aorta, in the absence of valve pathology, may also cause AR, such as may occur with longstanding uncontrolled hypertension, Marfan syndrome, idiopathic aortic dilation, cystic medial necrosis, senile aortic ectasia and dilation, syphilitic aortitis, giant cell arteritis, Takayasu arteritis, ankylosing spondylitis, Whipple disease, and other spondyloarthropathies. Aortic stenosis is the obstruction of blood flow across the aortic valve. Aortic stenosis has several etiologies, including congenital (unicuspid or bicuspid valve), calcific (due to degenerative changes), and rheumatic.

Symptoms of aortic stenosis usually develop gradually after an asymptomatic latent period of 10-20 years. Exertional dyspnea or fatigue is the most common initial complaint. Ultimately, most patients experience the classic triad of chest pain, heart failure, and syncope.

Two-dimensional (2D) Doppler echocardiography is the imaging modality of choice to diagnose and estimate the severity of aortic stenosis and localize the level of obstruction. The only definitive treatment for aortic stenosis is aortic valve replacement Aortic Stenosis Aortic Regurgitation When the aortic valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta. This outflow obstruction leads to an increase in left ventricular (LV) systolic pressure. As a compensatory mechanism to normalize LV wall stress, LV wall thickness increases by parallel replication of sarcomeres, producing concentric hypertrophy. At this stage, the chamber is not dilated and ventricular function is preserved, although diastolic compliance is reduced. AR represents a condition of combined volume overload and pressure overload . As the disease progresses, recruitment of preload reserve and compensatory hypertrophy permit the ventricle to maintain normal ejection performance despite the elevated afterload. leaky valve:
Left ventricle load during diastole antegrade from the left atrium and from the retrograde from the aorta through the leaky valve The majority of patients remain asymptomatic throughout this compensated phase, which may last for decades. In many patients, however, the balance between afterload excess, preload reserve, and hypertrophy cannot be maintained indefinitely, and afterload mismatch or depressed contractility ultimately results in a reduction in ejection fraction. Guidelines of Management of Aortic Valve Disease clinical situation age 46
weight 60 kg
height 165 cm a. Natural History Presenting chief complaint Chest pain
Difficult breathing
Productive cough
Coloured sputum -Asymptomatic Patients With Normal Left Ventricular Function
-Asymptomatic Patients With Depressed Systolic Function
-Symptomatic Patients: History of the present illness Dyspnea grade III
No orthopnea
Paroxysmal nocturnal dyspnea
No lower limb edema
Productive cough
with colored sputum
The condition started
10 days before admission The onset of angina or significant dyspnea is usually an indication for valve replacement.Similar poor outcomes have been reported in the current era in symptomatic patients who do not undergo AVR. clinical situation
Rhematic heart disease
Mild aortic stenosis
Severe aortic regurgitation
No diabetes mellitus
No hypertension b. Diagnosis and Initial Evaluation stopped taking medication upon feeling better compliance ! Cardiac catheterization Investigational cardiac catheterization with coronary angiography a month ago, reporting normal coronaries but recommended for aortic valve replacement Class I

1)Echocardiography is indicated to confirm the presence and severity of acute or chronic AR. (Level of Evidence: B)

2)Echocardiography is indicated for diagnosis and assessment of the cause of chronic AR (including valve morphology and aortic root size and morphology) and for assessment of LV hypertrophy, dimension (or volume), and systolic function. (Level of Evidence: B) Sputum Culture GABHS
Sensitive to Resistant to
- Cefotaxime -Penicillin
- Ceftriaxone -Ampicillin
- Vancomycin Class III
1)Vasodilator therapy is not indicated for long-term therapy in asymptomatic patients with mild to moderate AR and normal LV systolic function. (Level of Evidence: B)

2)Vasodilator therapy is not indicated for long-term therapy in asymptomatic patients with LV systolic dysfunction who are otherwise candidates for AVR. (Level of Evidence: C)

3)Vasodilator therapy is not indicated for long-term therapy in symptomatic patients with either normal LV function or mild to moderate LV systolic dysfunction who are otherwise candidates for AVR. (Level of Evidence: C) Drugs upon
Admission Lasix 40mg Class I

Vasodilator therapy is indicated for chronic therapy in patients with severe AR who have symptoms or LV dysfunction when surgery is not recommended because of additional cardiac or noncardiac factors. (Level of Evidence: B) Tritace 2.5 mg Class IIa

Vasodilator therapy is reasonable for short-term therapy to improve the hemodynamic profile of patients with severe heart failure symptoms and severe LV dysfunction before proceeding with AVR. (Level of Evidence: C)

Class IIb

Vasodilator therapy may be considered for long-term therapy in asymptomatic patients with severe AR who have LV dilatation but normal systolic function. (Level of Evidence: B) Atrovent Rocephin Lab findings Serum Creatinine levels BUN levels elevated from 1 to 1.6 elevated from 17 to 29 over three weeks Orally Orally Nebulizer IV 1 ampoule 3 times daily 1 tablet once daily 1 tablet once daily 2 vials / 24 hours Class MOA Rocephin Active ingredient Class MOA Atrovent Active ingredient Class MOA Tritace Active ingredient Class MOA Therapy with vasodilating agents is designed to improve forward stroke volume and reduce regurgitant volume. These effects should translate into reductions in LV end-diastolic volume, wall stress, and afterload, resulting in preservation of LV systolic function and reduction in LV mass. Reduced end-diastolic volume and increased ejection fraction have been observed in small numbers of patients receiving long-term oral therapy with hydralazine and nifedipine for periods of 1 to 2 years; with nifedipine, these effects are associated with a reduction in LV mass. Less consistent results have been reported with ACE inhibitors, depending on the degree of reduction in arterial pressure and end-diastolic volume d. Physical Activity and Exercise e. Serial Testing In general, the stability and chronicity of the regurgitant lesion and the LV response to volume load need to be established when the patient first presents to the physician, especially if AR is moderate to severe. If the chronic nature of the lesion is uncertain and the patient does not present initially with one of the indications for surgery, repeat physical examination and echocardiography should be performed within 2 to 3 months after the initial evaluation to ensure that a subacute process with rapid progression is not under way. -LV functionality
-Ejection factor
-Vital signs (BP)
-In this case:
-Renal function Aortic Regurgitation Rheumatic fever is a late inflammatory, nonsuppurative complication of pharyngitis that is caused by group A-hemolytic streptococci.

Rheumatic fever results from humoral and cellular-mediated immune responses occurring 1-3 weeks after the onset of streptococcal pharyngitis.

Streptococcal proteins display molecular mimicry recognized by the immune system, especially bacterial M-proteins and human cardiac antigens such as myosin and valvular endothelium. Antimyosin antibody recognizes laminin, an extracellular matrix alpha-helix coiled protein, which is part of the valve basement membrane structure.

The valves most affected by rheumatic fever, in order, are the mitral, aortic, tricuspid, and pulmonary valves. Aortic Stenosis 1. Grading the Degree of Stenosis Mild (area 1.5 cm2, mean gradient less than 25 mm Hg, or jet velocity less than 3.0 m per second)
Moderate (area 1.0 to 1.5 cm2, mean gradient 25–40 mm Hg, or jet velocity 3.0–4.0 m per second)
Severe (area less than 1.0 cm2, mean gradient greater than 40 mm Hg or jet velocity greater than 4.0 m per second). Therapeutic decisions, particularly those related to corrective surgery, are based largely on the presence or absence of symptoms. Thus, the absolute valve area (or transvalvular pressure gradient) is not the primary determinant of the need for aortic valve replacement (AVR). 2. Natural History It appears that the progression of AS can be more rapid in patients with degenerative calcific disease than in those with congenital or rheumatic disease Previously
Diagnosed with Furosemide loop Diuretics Increase urine flow. These agents are ion transport inhibitors that decrease the reabsorption of sodium at different sites in the nephron. Ipratropium Symptomatic patients require early intervention, because no medical therapy for AS is able to improve outcome, compared with the natural history. However, patients who are unsuitable candidates for surgery or TAVI—or who are currently awaiting a surgical or TAVI procedure—may be treated with digoxin, diuretics, ACE inhibitors, or ARBs if they experience HF symptoms.Co-existing hypertension should be treated. Medical therapy: The Rationale of prescribing Lasix and Tritace Furosemide (Lasix) decreases preload
ACE inhibitor (Tritace) decreases afterload Recommendations: Adjusting doses of Tritace and Lasix while monitoring Renal Functions OR Using Ca channel blocker: Nifedipine -LV functionality & diameter
-Ejection factor
-Vital signs (BP)
-In this case:
-Renal function Parameters to be monitored: AVR as soon as possible In patients with severe aortic stenosis, atrial contraction plays a particularly important role in diastolic filling of the left ventricle. Thus, development of atrial fibrillation in aortic stenosis often leads to heart failure due to an inability to maintain cardiac output. Eventually, however, LV end-diastolic pressure (LVEDP) rises, which causes a corresponding increase in pulmonary capillary arterial pressures and a decrease in cardiac output due to diastolic dysfunction. The contractility of the myocardium may also diminish, which leads to a decrease in cardiac output due to systolic dysfunction. Ultimately, heart failure develops. In most patients with aortic stenosis, LV systolic function is preserved and cardiac output is maintained for many years despite an elevated LV systolic pressure. Although cardiac output is normal at rest, it often fails to increase appropriately during exercise, which may result in exercise-induced symptoms. Diastolic dysfunction may occur as a consequence of impaired LV relaxation and/or decreased LV compliance, as a result of increased afterload, LV hypertrophy, or myocardial ischemia. LV hypertrophy often regresses following relief of valvular (also called valvular) obstruction. However, some individuals develop extensive myocardial fibrosis, which may not resolve despite regression of hypertrophy. Increased LV mass, increased LV systolic pressure, and prolongation of the systolic ejection phase all elevate the myocardial oxygen requirement, especially in the subendocardial region. Although coronary blood flow may be normal when corrected for LV mass, coronary flow reserve is often reduced.

Myocardial perfusion is thus compromised by the relative decline in myocardial capillary density and by a reduced diastolic transmyocardial (coronary) perfusion gradient due to elevated LV diastolic pressure. Therefore, the subendocardium is susceptible to underperfusion, which results in myocardial ischemia.

Angina results from a concomitant increased oxygen requirement by the hypertrophic myocardium and diminished oxygen delivery secondary to diminished coronary flow reserve, decreased diastolic perfusion pressure, and relative subendocardial myocardial ischemia. 30-60 mg PO qDay
Adalat 30 mg Rocephin 1 gm two vials over 24hrs Rheumatic Fever clinical situation Medication History Digoxin : 0.25 QD
Anticoagulants :warfarin 2mg QD
Diuertics: 40 mg PO QD Questions Pathophysiology of Rheumatic Heart Disease, Aortic Stenosis & Regurgitation
Etiology of each Condition
Complications ACE-I produces a small increase in EF and significant decrease in LV volume and mass. Effective vasodilator therapy requires adjustment of dosage to achieve a decrease in arterial pressure. Competitive inhibitors of angiotensin-converting enzyme (ACE).( Reduce angiotensin II levels, decreasing aldosterone secretion.) Ramipril Anticholingeric Inhalation Ceftriaxone 3rd generation cephalosporin inhibit bacterial cell wall synthesis Inhibits vagally mediated refelexes by antagonizing
Ach action preventing increase in intracellular
Ca+ (M receptor) on bronchial smooth muscles
preventing brochoconstriction Atrovent nebulizer one ampoule 3 times daily Ramipril alone Ceftriaxone Ramipril & Furosemide interaction Medical Therapy Ceftriaxone & Furosemide Background question Foreground question What lead to deterioration of kidney functions?
Proper use of Rocephin
Treatment Guidelines for Aortic Stenosis and Regurgitation
Recommendations (change in plan)
Rationale lasix & tritace During the early phases of chronic AR, the LV ejection fraction (EF) is normal or even increased (due to the increased preload and the Frank-Starling mechanism). Patients may remain asymptomatic during this period. As AR progresses, LV enlargement surpasses preload reserve on the Frank-Starling curve with the EF falling to normal and then subnormal levels. The LV end-systolic volume rises and is a sensitive indicator of progressive myocardial dysfunction. Eventually, the LV reaches its maximal diameter and diastolic pressure begins to rise, resulting in symptoms (dyspnea) that may be worse during exercise. Increasing LV end-diastolic pressure may also lower coronary perfusion gradients, causing subendocardial and myocardial ischemia, necrosis, and apoptosis. Grossly, the LV gradually transforms from an elliptical to a spherical configuration. Acute aortic regurgitation:
left ventricle doesnt have enough time to dilate in response to volume load
Increased end diastolic pressure , increased pulmonary venous pressure, causing patient to develop dyspnea and pulmonary edema.
In severe cases, heart failure may develop and potentially deteriorate to cardiogenic shock. Early surgical intervention should be considered (particularly if AR is due to aortic dissection, in which case surgery should be performed immediately). Chronic aortic regurgitation
Chronic AR causes gradual left ventricular (LV) volume overload that leads to a series of compensatory changes, including LV enlargement and eccentric hypertrophy. LV dilation occurs through addition of sarcomeres in series (resulting in longer myocardial fibers) as well as rearrangement of myocardial fibers. As a result, the LV becomes larger and more compliant, with greater capacity to deliver a large stroke volume that can compensate for the regurgitant volume. The resulting hypertrophy is necessary to accommodate the increased wall tension and stress that results from LV dilation (Laplace law). In acute disease, small thrombi form along the lines of valve closure.
In chronic disease, there is thickening and fibrosis of the valve resulting in stenosis, or less commonly, regurgitation.

T-cells that are responsive to the streptococcal M-protein infiltrate the valve through the valvular endothelium, activated by the binding of antistreptococcal carbohydrates with release or tumor necrosis factor (TNF) and interleukins.

The acute involvement of the heart in rheumatic fever gives rise to pancarditis, with inflammation of the myocardium, pericardium, and endocardium.
Carditis occurs in approximately 40-50% of patients on the first attack; however, the severity of acute carditis has been questioned.
Pericarditis occurs in 5-10% of patients with rheumatic fever; isolated myocarditis is rare. Thank
You Amr Othman Khaled Elhady
Omar Essam Amr Asran
Omar Hegazi Made by: Supervised by: Dr. Nawal KhalafAllah
Dr. Aliaa Ramadan Furosemide alone RENAL
IMPAIRMENT !! PICO Patient problem Severe Aortic Regurgitation & Mild Stenosis Intervention Lasix & Tritace Comparison more like pacman Reduction of Preload (lasix) & Afterload (Tritace)
hypovolemia and hypotension likely to occur
Both contribute in Renal deterioration 1 Outcome Not together Rocephin...
how? 2 Outcome ? -Orthopnea is the sensation of breathlessness in the recumbent position, relieved by sitting or standing.

- Paroxysmal nocturnal dyspnea (PND) is a sensation of shortness of breath that awakens the patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position. - Dyspnea refers to the sensation of difficult or uncomfortable breathing. It is a subjective experience perceived and reported by an affected patient. DOE
Normally, but is indicative of disease when it occurs at a level of activity that is usually well tolerated. Streptococcal proteins (Esp. M protein) mimic

myosin muscle & laminin of valvular basement membrane Streptococcal proteins display molecular mimicry recognized by the immune system, especially bacterial M-proteins and human cardiac antigens such as myosin and valvular endothelium. Antimyosin antibody recognizes laminin, an extracellular matrix alpha-helix coiled protein, which is part of the valve basement membrane structure. Who touched
My kidney!! Side effects Interactions Drug Drug
Drug Disease Side effects Interactions 3 4 Questions Pathophysiology of Rheumatic Heart Disease, Aortic Stenosis & Regurgitation
Etiology of each Condition
Complications Background question Foreground question What lead to deterioration of kidney functions?
Proper use of Rocephin
Treatment Guidelines for Aortic Stenosis and Regurgitation
Recommendations (change in plan)
Rationale lasix & tritace kidney function deterioration Normal Liver Function Test
Blood picture
coagulation profile
Slightly low sodium
mild anemia explains hyponatremia
Full transcript