The Cardiovascular Examination

Valvular Heart Disease and the Cardiac Exam
By:Charlotte Bai, M.D.
Internal Medicine Board Review
May 28, 2009

Overview
* Clinical syndromes
* Overview of cardiac murmurs and maneuvers
* Left sided valvular lesions
o Aortic stenosis and sclerosis
o Mitral stenosis
+ Rheumatic fever prophylaxis
o Acute and chronic aortic regurgitation
o Acute and chronic mitral regurgitation
* Right sided valvular lesions
o Tricuspid valve disease
* Prosthetic valves
* Endocarditis prophylaxis
* Questions

General Appearance
* Marfan Syndrome
o Tall, long extremities
o Associated with: aortic root dilitation, MV prolapse
* Acromegaly
o Large stature, coarse facial features, “spade” hands
o Associated with: Cardiac hypertrophy
* Turner Syndrome
o Web neck, hypertelorism, short stature
o Associated with: Aortic coarctation, pulmonary stenosis
* Pickwickian Syndrome
o Severe obesity, somnolence
o Associated with: Pulmonary hypertension
* Fredreich ataxia
o Lurching gait, hammertoe, pes cavus
o Associated with: hypertrophic cardiomyopathy
* Duchenne type muscular dystrophy
o Pseudohypertrophy of the calves
o Cardiomyopathy
* Ankylosing spondylitis
o Straight back syndrome, stiff (“poker”) spine
o Associated with: AI, CHB (rare)
* Lentigines (LEOPARD syndrome)
o Brown skin macules that do not increase with sunlight
o Associated with: HOCM, PS
“Spade” hands in acromegaly
* Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)
o Small capillary hemangiomas on the face or mouth
o Associated with: Pulmonary arteriovenous fistula
* Lupus
o Butterfly rash on face, Raynaud phenomenon- hands, Livedo reticularis
o Associated with: Verrucous endocarditis, Myocarditis, Pericarditis
* Pheochromocytoma
o Pale diaphoretic skin, neurofibromatosis- café-au-lait spots
o Associated with: Catecholamine-induced secondary dilated CM
* Sarcoidosis
o Cutaneous nodules, erythema nodosum
o Associated with: Secondary cardiomyopathy, heart block
* Tuberous Sclerosis
o Angiofibromas (face; adenoma sebaceum)
o Associated with: Rhabdomyoma
* Myxedema
o Coarse, dry skin, thinning of lateral eyebrows, hoarseness of voice
o Associated with: Pericardial effusion, LV dysfunction

Grading the Intensity of Cardiac Murmurs
* Grade 1
o Murmur heard with stethoscope, but not at first
* Grade 2
o Faint murmur heard with stethoscope on chest wall
* Grade 3
o Murmur hears with stethoscope on chest wall, louder than grade 2 but without a thrill
* Grade 4
o Murmur associated with a thrill
* Grade 5
o Murmur heard with just the rim held against the chest
* Grade 6
o Murmur heard with the stethoscope held away and in from the chest wall

Cardiac Murmurs


* Most mid systolic murmurs of grade 2/6 intensity or less are benign
o Associated with physiologic increases in blood velocity:
+ Pregnancy
+ Elderly
* In contrast, the following murmurs are usually pathologic:
o Systolic murmurs grade 3/6 or greater in intensity
o Continuous murmurs
o Any diastolic murmur

Diagnostic Testing
* ECHOCARDIOGRAM
Aortic Stenosis
Progression of Aortic Sclerosis
* Hemodynamic progression usually slow
o Average rate of increase in aortic jet velocity of 0.3 m/s per year
o Increase in mean transaortic gradient of 7 mmHg
o Decrease in AVA of 0.1 cm2 per year
* Severe AS
o Aortic jet velocity > 4 m/s
o Mean transvalvular pressure gradient > 50 mmHg
o AVA < 1.0 cm2

Pathophysiology of Aortic Stenosis
* Obstruction of LV outflow increases intracavitary systolic pressures and leads to LV pressure overload
* Initial compensatory mechanism is myocardial hypertrophy with preservation of systolic function
* Diastolic function impaired as a consequence of increased wall thickness and abnormal myocardial relaxation
* Increased wall stress and afterload causes eventual decrease in ejection fraction

Pseudostenosis
* Occurs in patients with impaired systolic function and aortic stenosis
o Unable to generate transvalvular gradient
* Careful diagnostic testing with dobutamine infusion protocols can aid in differentiating between true AS and pseudostenosis
* If the calculated AVA increases with augmentation of cardiac output, then pseudostenosis present
* If AVA does not increase with dobutamine, then obstruction fixed and true AS present

Clinical Presentation of Aortic Stenosis
* Cardinal symptoms:
o Angina
+ Occurs in >50% of patients, not sensitive due to prevalence of CAD
o Syncope
o CHF
* Sudden cardiac death rare, <1% per year
* In earlier stages, AS presentation more subtle
o Dyspnea
o Decreased exercise tolerance
* Rarely, AS diagnosed in the setting of GI bleeding
o Heyde’s syndrome
+ Bleeding caused by AVM
+ Concurrent AS occurs at prevalence rate of 15-25%
+ Associated with an acquired von Willebrand syndrome due to disruption of vW multimers through a diseased AV

Management of Aortic Stenosis
* Prognosis in asymptomatic disease excellent
* Conservative approach with monitoring for symptoms recommended
* When severe stenosis present-
o 38% of asymptomatic patients develop symptoms within 2 years
o 79% are symptomatic within 3 years
* Once symptoms occur, AVR needed
* LV dysfunction and severe AS have increased perioperative mortality with AVR
o But outcomes still favorable with surgery
* Nitroprusside may transiently improve cardiac function as a bridge to valve replacement
o Does not supplant AVR in symptomatic patients

Aortic Valve Replacement
* Prophylatic AVR in asymptomatic patients not routinely performed due to surgical risks
o Thromboembolism, bleeding associated with anticoagulation, prosthetic valve dysfunction, and endocarditis
o Occurs at a rate of 2-3% annually
o Only should be considered:
+ If other cardiac surgery (such as CABG) planned
+ Severe LVH or systolic dysfunction
+ Women contemplating pregnancy
+ Patients remote from health care
* Surgical valve replacement with operative morbidity and mortality of 10%
* Percutaneous balloon aortic valvotomy rarely used

Mitral Stenosis
* Usually associated with history of rheumatic fever
* >40% of cases of RHD result in mitral stenosis
o Women affected more than men (2:1)
* Presentation 20-40 years after the initial episode of rheumatic fever
o If infected at a young age, latent period is a few years

Clinical Presentation of Mitral Stenosis
* Significant MS leads to ↑LA pressure and pulm HTN
* Symptoms include dyspnea with ↑ cardiac demand
o Exercise
o Pregnancy
* Survival excellent with asymptomatic or minimally symptomatic patients
o >80% survival at 10 years
* Survival in symptomatic patients much worse
o 10 year survival drops to 15% or lower (if pulm HTN present)
* Findings consistent with severe MS:
o Transvalvular diastolic pressure gradient >10 mmHg
o MVA <1.0 cm2
o Severe pulmonary hypertension (>60 mmHg)

Management of Mitral Stenosis
* Atrial fibrillation
Mitral Valve Repair
* Percutaneous valvotomy
Rheumatic Fever Prophylaxis
* Primary prophylaxis
* Secondary prophylaxis
Acute Aortic Regurgitation
Acute Mitral Regurgitation
Chronic Valvular Regurgitation
Chronic Aortic Regurgitation
Chronic Mitral Regurgitation
Treatment of Chronic Mitral Regurgitation
Timing of Intervention for Left-Sided Valvular Conditions
OTHERWISE
Repeat TTE yearly, repeat clinical evaluation biannually
OTHERWISE
Repeat TTE at least yearly, repeat clinical evaluation at least biannually depending on the severity of the LV dilitiation
OTHERWISE
Clinical evaluation at least annually, depending on the severity of the mitral stenosis
OTHERWISE
Depending on the severity of AS, at least annual clinical evaluation with TTE to monitor for symptom onset
Intervention:
AVR
Chronic Severe MR
Chronic Severe AR
Mitral Stenosis
Aortic Stenosis
Tricuspid Valve Disease
* Tricuspid stenosis is rare
o Associated with rheumatic heart disease
* TR usually occurs secondary to:
o Pulmonary hypertension
o RV chamber enlargement with annular dilatation
o Endocarditis (associated with IV drug use)
o Injury following pacer lead placement
* Other secondary causes: carcinoid, radiation therapy, anorectic drug use, and trauma
* Primary causes: Marfan’s syndrome and congenital disorders such as Ebstein’s anomaly and AV canal malformation
* Echo is diagnostic in most cases
Tricuspid Regurgitation
* Severe tricuspid regurgitation is difficult to treat and carries a poor overall clinical outcome
* Symptoms are manifestations of systemic venous congestion
* Surgical intervention usually considered if other cardiac surgery planned
* Surgical options include valvular annuloplasty or replacement

Prosthetic Valves- Mechanical
* Three types:
o Ball-cage valve
o Single tilting disk valve
o Bileaflet valve
* Durable but require life long anticoagulation
* For operative procedures, warfarin typically is discontinued for 48-72 hours and restarted postop as soon as possible, except for:
o Mechanical mitral prosthesis
o Atrial fibrillation
o Prior thromboembolic events
Ball-cage valve
Single tilting disk valve
Bileaflet valve
Prosthetic Valves- Biological
* Biological Valves
o Composed of autologous or xenograft biological material mounted on stents and a sewing ring
o Warfarin therapy not required due to lower thromboembolic potential
o Valve durability less when compared to mechanical valves
o Newer stentless valves with increased longevity

Anticoagulation Guidelines for Mechanical Valves
Prosthetic Valve Complications
* Common complications include:
o Structural valve deterioration
o Valve thrombosis
o Embolism
o Bleeding
o Endocarditis
* Endocarditis prophylaxis required for patients with all types of prosthetic valves
* Suspect valve dehiscence or dysfunction in:
o Acute CHF in the immediate postop period
o New cardiac symptoms
o Embolic phenomena
o Hemolytic anemia
o New murmurs
* TEE is the diagnostic procedure of choice
* Postop TTE should be done 2-3 months after surgery

Valve Thrombosis
* Incidence with mechanical prosthesis of 2-4 % per year
* Suspect in patients with new murmur, change in cardiopulmonary symptoms, or an embolic event
* Diagnosis based on clinical presentation, TTE/TEE, and fluroscopy
* In small thrombus, treatment with heparin may be adequate
* Optimal treatment for left sided thrombosis is emergency surgery
* Consider thrombolytic therapy for right sided thrombosis or if surgery cannot be performed with left sided disease
Endocarditis Prophylaxis

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Heart Murmurs

Heart Murmurs
By: David Leder

Outline

I. Basic Pathophysiology
II. Describing murmurs
III. Systolic murmurs
IV. Diastolic murmurs
V. Continuous murmurs
VI. Summary

Basic Pathophysiology
Murmurs = Math
Describing a heart murmur

1. Timing
o murmurs are longer than heart sounds
o HS can distinguished by simultaneous palpation of the carotid arterial pulse
o systolic, diastolic, continuous
2. Shape
o crescendo (grows louder), decrescendo, crescendo-decrescendo, plateau

3. Location of maximum intensity
o is determined by the site where the murmur originates
o e.g. A, P, T, M listening areas
4. Radiation
o reflects the intensity of the murmur and the direction of blood flow

5. Intensity
o graded on a 6 point scale
+ Grade 1 = very faint
+ Grade 2 = quiet but heard immediately
+ Grade 3 = moderately loud
+ Grade 4 = loud
+ Grade 5 = heard with stethoscope partly off the chest
+ Grade 6 = no stethoscope needed

*Note: Thrills are assoc. with murmurs of grades 4 - 6

6. Pitch
o high, medium, low
7. Quality
o blowing, harsh, rumbling, and musical
8. Others:
i. Variation with respiration

+ Right sided murmurs change more than left sided

ii. Variation with position of the patient

iii. Variation with special maneuvers

+ Valsalva/Standing => Murmurs decrease in length and intensity

EXCEPT: Hypertrophic cardiomyopathy and Mitral valve prolapse

Systolic Murmurs
* Derived from increased turbulence associated with:

1. Increased flow across normal SL valve or into a dilated great vessel
2. Flow across an abnormal SL valve or narrowed ventricular outflow tract - e.g. aortic stenosis
3. Flow across an incompetent AV valve - e.g. mitral regurg.
4. Flow across the interventricular septum

Early Systolic murmurs
1. Acute severe mitral regurgitation
2. Congenital, small muscular septal defect
3. Tricuspid regurg. with normal PA pressures

Midsystolic (ejection) murmurs
* Are the most common kind of heart murmur
* Are usually crescendo-decrescendo
* They may be:
1. Innocent
2. Physiologic
3. Pathologic

Aortic stenosis
* Loudest in aortic area; radiates along the carotid arteries
* Intensity varies directly with CO
* A2 decreases as the stenosis worsens
* Other conditions which may mimic the murmur of aortic stenosis w/o obstructing flow:

1. Aortic sclerosis
2. Bicuspid aortic valve
3. Dilated aorta
4. Increased flow across the valve during systole

Hypertrophic cardiomyopathy
Pansystolic (Holosystolic) Murmurs
1. Mitral valve regurgitation
2. Tricuspid valve regurgitation
3. Ventricular septal defect
Diastolic Murmurs
* Almost always indicate heart disease
* Two basic types:

1. Early decrescendo diastolic murmurs
2. Rumbling diastolic murmurs in mid- or late diastole

Aortic Regurgitation
* Best heard in the 2nd ICS at the left sternal edge
* High pitched, decrescendo
* Blowing quality => may be mistaken for breath sounds
* Radiation:

Mitral Stenosis
* Two components:
1. Middiastolic - during rapid ventricular filling
2. Presystolic - during atrial contraction; therefore, it disappears if atrial fibrillation develops
Continuous Murmurs

1. Cervical venous hum
2. Mammary souffle
3. Patent Ductus Arteriosus
4. Pericardial friction rub
Back to the Basics
1. When does it occur - systole or diastole
2. Where is it loudest - A, P, T, M
I. Systolic Murmurs:
1. Aortic stenosis - ejection type
2. Mitral regurgitation - holosystolic
3. Mitral valve prolapse - late systole

II. Diastolic Murmurs:
1. Aortic regurgitation - early diastole
2. Mitral stenosis - mid to late diastole

Summary
A. Presystolic murmur
o Mitral/Tricuspid stenosis
B. Mitral/Tricuspid regurg.
C. Aortic ejection murmur
D. Pulmonic stenosis (spilling through S20
E. Aortic/Pulm. diastolic murmur
F. Mitral stenosis w/ Opening snap
G. Mid-diastolic inflow murmur
H. Continuous murmur of PDA

Heart Murmurs.ppt

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Valvular Heart Disease

Valvular Heart Disease

Medical Surgical I
Types
* Mitral Stenosis
* Mitral Regurgitation
* Mitral Valve Prolapse
* Aortic Stenosis
* Aortic regurgitation
* Tricuspid valve is affected infrequently
o Tricuspid stenosis – causes Rt HF
o Tricuspid regurgitation –causes venous overload

Tricuspid Valve
Rheumatic Heart Disease
* Inflammatory process that may affect the myocardium, pericardium and or endocardium
* Usually results in distortion and scarring of the valves
* Subjective symptoms
o Prior history of rheumatic fever
o General malaise
o Pain – may or may not be present
* Objective symptoms
o Temperature
o Murmurs
o Dyspnea
o polyarthritis
* Diagnosis
o H/P
o WBC and ESR
o C-reactive protein
o Cardiac enzymes
o EKG
o Chest x-ray
o Echo
o Cardiac cath
o Cardiac output
* Nursing Care
o Vital signs
o Rest and quiet environment
o Give antibiotics, digitalis, and diuretics
o Provide adequate nutrition
o Monitor I/O
o Explain treatment and home care

Mitral Stenosis
* Usually results from rheumatic carditis
* Is a thickening by fibrosis or calcification
* Can be caused by tumors, calcium and thrombus
* Valve leaflets fuse and become stiff and the cordae tendineae contract
* These narrows the opening and prevents normal blood flow from the LA to the LV
* LA pressure increases, left atrium dilates, PAP increases, and the RV hypertrophies
* Pulmonary congestion and right sided heart failure occurs
* Followed by decreased preload and CO decreases
* Mild – asymptomatic
* With progression – dyspnea, orthopneas, dry cough, hemoptysis, and pulmonary edema may appear as hypertension and congestion progresses
* Right sided heart failure symptoms occur later
* S/S
o Pulse may be normal to A-Fib
o Apical diastolic murmur is heard

Mitral Regurgitation
* Primarily caused by rheumatic heart disease, but may be caused by papillary muscle rupture form congenital, infective endocarditis or ischemic heart disease
* Abnormality prevents the valve from closing
* Blood flows back into the right atrium during systole
* During diastole the regurg output flows into the LV with the normal blood flow and increases the volume into the LV
* Progression is slowly – fatigue, chronic weakness, dyspnea, anxiety, palpitations
* May have A-fib and changes of LV failure
* May develop right sided failure as well

Mitral Valve Prolapse
* Cause is variable and may be associated with congenital defects
* More common in women
* Valvular leaflets enlarge and prolapse into the LA during systole
* Most are asymptomatic
* Some may report chest pain, palpitations or exercise intolerance
* May have dizziness, syncope and palpitations associated with dysrhythmias
* May have audible click and murmur

Aortic Stenosis
* Valve becomes stiff and fibrotic, impeding blood flow with LV contraction
* Results in LV hypertrophy, increased O2 demands, and pulmonary congestion
* Causes – rheumatic fever, congenital, arthrosclerosis
* Atherosclerosis and calcification is primary cause in the elderly
* Complications – right sided heart failure, pulmonary edema, and A-fib
* S/S – Early: dyspnea, angina, syncope

Aortic Regurgitation
* Aortic valve leaflets do not close properly during diastole
* The valve ring that attaches to the leaflets may be dilated, loose, or deformed
* The ventricle dilates to accommodate the ^ blood volume and hypertrophies
* Causes: infective endocarditis, congenital, hypertension, Marfan’s
* May remain asymptomatic for years
* Develop dyspnea, orthopnea, palpitations, ,and angina
* May have ^ systolic pressure with bounding pulse
* Have a high pitch, blowing, decrescendo diastolic murmur

Assessment for Valve Dysfunction
* Subjective symptoms
o Fatigue
o Weakness
o General malaise
o Dyspnea on exertion
o Dizziness
o Chest pain or discomfort
o Weight gain
o Prior history of rheumatic heart disease
* Objective symptoms
o Orthopnea
o Dyspnea, rales
o Pink-tinged sputum
o Murmurs
o Palpitations
o Cyanosis, capillary refill
o Edema
o Dysrhythmias
o Restlessness

Diagnosis
* History and physical findings
* EKG
* Chest x-ray
* Cardiac cath
* Echocardiogram

Medial Treatment
* Nonsurgical management focuses on drug therapy and rest
* Diuretic, beta blockers, digoxin, O2, vasodilators, prophylactic antibiotic therapy
* Manage A-fib, if develops, with conversion if possible, and use of anticoagulation

Interventions
* Assess vitals, heart sounds, adventitious breath sounds
* ^ HOB
* O2 as prescribed
* Emotional support
* Give medications
* I/O
* Weight
* Check for edema
* Explain disease process, provide for home care with O2, medications

Surgical Management of Valve Disease
* Mitral Valve
o Commissurotomy
o Mitral Valve Replacement
o Balloon Valvuloplasty
* Aortic Valve Replacement

Mechanical Valve
Porcine Valve
Tissue Valve

Valvular Heart Disease.ppt

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