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PFizz S2015 > CVS L4: Valvular heart disease > Flashcards

CVS L4: Valvular heart disease Flashcards

1
Q

First Heart Sound (S1)

A
  • Signals the beginning of ventricular systole
  • Generated by mitral and tricuspid valve closure – M1T1
  • Loudest over the apex
  • Heard best by using the diaphragm of the stethoscope
  • The intensity of S1 is determined primarily by:
    • -Valve mobility,
    • -Force of ventricular contraction &
    • -Velocity of valve closure
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2
Q

Variations of S1

A

Loud S1

  • Mitral stenosis
  • Short PR interval
  • Tachycardia
  • Hyperdynamic states

Soft S1

  • Mitral regurgitation
  • Long PR interval
  • Poor systolic function
  • Aortic/pulmonary regurgitation
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3
Q

Second Heart Sound (S2)

A
  • Generated by the closure of the aortic (A2) and pulmonic (P2) valves – A2P2
  • Best heard at the left upper sternal border (over the base of the heart)
  • A2 is the louder component and is audible at all locations on the chest wall
  • In normal, P2 is heard only at the upper left sternal border and is always less audible than A2 at this location
  • Abnormalities of S2- pay attention on:
  • Alterations in intensity
  • Alteration in timing of closure of valves
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4
Q

Variations of S2

A

Loud S2:

  • Systemic hypertension
  • Pulm hypertension
  • Atrial septal defect

Soft S2

  • Aortic stenosis
  • Pulmonic stenosis
  • Aortic regurgitation
  • Pulmonary regurgitation
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5
Q

Splitting of S2 (A2 P2):

A
  • Wide splitting of S2 (a widely split S2 having normal respiratory variation) occurs when P2 is delayed (e.g., RBB block)
  • Fixed splitting of S2 occurs when respiration- induced changes in filling are similar in both ventricles: e.g.,characteristic ASD
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6
Q

Paradoxical (Reversal) splitting of S2 (P2 A2):

A

Typically in:

  • LBB Block – because of delay in depolarization of LV
  • Severe Aortic stenosis – delay in closure of aortic valve
  • Normally the interval from A2 to P2 would lengthen during inspiration
  • In paradoxical splitting, the interval shortens during inspiration
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7
Q

Ventricular gallop (S3):

A
  • Occurs in early diastole; Corresponds to the end of the rapid filling phase of the ventricular diastole
  • Low-frequency sound, best heard with the bell of the stethoscope lightly applied to the apex (LV S3) or left lower sternal border (RV S3); best heard in the left lateral decubitus position
  • Caused by interplay between ventricular filling and existing ventricular (end-systolic) volume
  • Pathologic S3 is associated with abnormally high LV filling pressures, low cardiac output, and a dilated, poorly contractile LV (e.g., congestive heart failure)
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8
Q

Atrial gallop (S4)

A
  • A dull, low-frequency sound that precedes S1
  • Best heard over apex with the bell of the stethoscope in the left lateral position
  • The S4 is attributed to forceful atrial contraction to fill a noncompliant or stiff ventricle (e.g., coronary artery disease)
  • The S4 disappears in atrial fibrillation
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9
Q

Heart murmurs

A
    • Timing and duration
    • Intensity (grade I to VI)
    • Quality (blowing, harsh, rumbling)
    • Radiation (to the neck, axilla, or back)
  • All diastolic and continuous murmurs are abnormal and pathological
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10
Q

A midsystolic (or early systolic) ejection murmur:

A
  • begins with S1 and ends before S2
  • classically diamond-shaped (crescendo- decrescendo)
  • Ex. AS (2nd IS), HOCM (Apex, LLSB)
  • radiates to neck
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11
Q

Pansystolic (holosystolic) murmur:

A
  • begins with S1 and extend to S2
  • classically high frequency, blowing in quality, and relatively uniform in intensity
  • all pansystolic murmurs are pathologic
  • Ex. Mitral regurg (apex), VSD (LLSB), Tricuspid regurg (LLSB)
  • radiates to back/axilla or neck
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12
Q

Late systolic murmur:

A
  • occurs in the latter part of systole, well after S1 and end in or after S2
  • all late systolic murmurs are pathologic
  • EX. MVP
  • radiates to apex, LLSB
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13
Q

Early diastolic: (decrescendo)

A
  • Ex. Aortic regurg
  • heard best Left sternal border, 3rd intercostal space
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14
Q

Middiastolic rumble:
(low pitched)

A
  • Ex. MS, TS
  • Apex w bell, lower left sternal border
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15
Q

Continous murmur

A
  • PDA
  • Left 1st and 2nd Intercostal space, Left sternal border
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16
Q

Patient 01: DDx

A 50 year old male presents with complaints of substernal chest pain, which increases with exertion, and shortness of breath which is starting to limit his lifestyle. He has no risk factors for coronary artery disease.

On Physical Exam you find the following:

  • Delayed carotid upstroke
  • Apical impulse is sustained but not displaced laterally
  • An ejection systolic murmur in the 2nd intercostal space
  • ECG: Left axis deviation with high voltage QRS in V4-V6
A

Most likely diagnosis: Aortic stenosis

Other possible differentials:

  • Mitral regurgitation
  • Mitral valve prolapse
  • Hypertrophic Obstructive Cardiomyopathy
  • Myocardial Infarction
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17
Q

Physical Exam of patient 02: DDx
BP 118/90 mmHg, Pulse 68 bpm, regular;
JVP 6 cm with normal “a” and “v” waves Carotids: Difficult to palpate, delayed upstroke Heart:

Palpation: Palpable “thrill” over the right 2nd interspace; Apical impulse is in 5th inter costal space, 2 cm lateral to the mid-clavicular line;

Palpable presystolic impulse followed by a sustained left ventricular lift.

Auscultation: A single S2 (P2) is heard at the upper left sternal border; Loud S4; Normal S1.
There is a loud systolic ejection murmur (crescendo- decrescendo) heard best at the right 2nd interspace that radiates widely to the neck. No diastolic murmurs.

A

Most likely diagnosis: Aortic stenosis

Other possible differentials:

  • Mitral regurgitation
  • Mitral valve prolapse
  • Hypertrophic Obstructive Cardiomyopathy
  • Myocardial Infarction
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18
Q

Causes of Aortic Stenosis:

A
  • Congenital: Patients below age 30
  • Rheumatic: Patients age 30-70; Accompanying AR and MS is frequent
  • Degenerative: Patients above 70; Prevalent in patients with diabetes or hypercholesterolemia
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19
Q

Pathophysiology of AS:

A

Stenosed aortic valve increases afterload on the LV

↓

Increased LV pressure during systole (systolic dysfn)

↓

Increased left ventricular wall thickness while the cavitary radius remains relatively unchanged due to parallel replication of sarcomeres producing “concentric hypertrophy”

↓

Decrease in ventricular compliance

↓

Significant increase in left ventricular end-diastolic pressure (diastolic dysfunction)

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20
Q
A
  • Pressure profile of AS
  • During ventricular ejection, LVP exceeds AP (gray area, pressure gradient generated by AS)
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21
Q

Clinical Manifestations of AS

A
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22
Q

Physical examination in AS:

A

Palpation of the carotid pulse reveals a pulsus parvus et tardus - both decreased (parvus) and late (tardus) relative to the apical impulse (low vol., slowly rising pulse)

Auscultation:

  • a midsystolic (early systolic) murmur is heard, loudest at the base of the heart, and often with radiation to the sternal notch and the neck
  • a high-pitched aortic ejection sound/click can be heard just after the first heart sound

-a fourth heart sound (S4) is often present

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23
Q

ABNORMALITIES OF THE ARTERIAL PULSE: AS

A

pulsus parvus et tardus or Anacrotic pulse

24
Q

ABNORMALITIES OF THE ARTERIAL PULSE: AR

A

Water-hammer, Bisferiens pulse

25
Q

ABNORMALITIES OF THE ARTERIAL PULSE: HOCM

A

Bisferiens pulse

26
Q

ABNORMALITIES OF THE ARTERIAL PULSE: CHF

A

Pulsus Alternans

27
Q

ABNORMALITIES OF THE ARTERIAL PULSE: Cardiac tamponade

A

Pulsus Paradoxus

28
Q

Patient 03: DDx

A 24-year-old male presents with chest pain, dyspnea on exertion and episodes of syncope while playing. His family history is significant for similar illness in his brother who died suddenly while playing.

Physical Examination: Double peaked pulse (bisferiens pulse), Loud S4; A systolic murmur heard over lower left sternal border. The murmur increases by Valsalva but decreases by squatting and passive leg raising.

Laboratory:
EKG: Left axis deviation due to LV hypertrophy
Echo: Asymmetrical septal hypertrophy with marked thickening of the LV septal wall

A

Most likely diagnosis in patient: Hypertrophic Obstructive Cardiomyopathy (HOCM) or Idiopathic Hypertrophic Subaortic Stenosis (IHSS)

Other differentials:

  • Aortic stenosis
  • Restrictive cardiomyopathy
  • Glycogen storage diseases
  • Fabry disease
29
Q

Hypertrophic obstructive cardiomyopathy (HOCM):

A
  • AD, young
  • Subvalvular aortic stenosis due to severe hypertrophy of the septum of the left heart Manifested by a systolic murmur noted on physical examination
  • Obstruction of outflow tract in this case is dynamic
  • Greater obstruction occurs when preload is decreased - Standing and Valsalva’s maneuver (both decrease venous return) and the murmur becomes intense; deviation worsens and results in more obstruction to outflow
  • Both of these maneuvers cause a decrease in the intensity of murmur in case of organic AS, because less volume of blood flows across the stenotic aortic valve
30
Q

Patient 04: DDx

A 45-year-old salesman is referred for evaluation of a heart murmur. He had applied for a pilot’s license and was denied because of the murmur. He is asymptomatic and physically active. There is no history of chest pain, dyspnea, or spells of syncope. He has no family history of heart disease. He has never had high blood pressure or diabetes, doesn’t smoke, and takes no medications. He had suffered from infective endocarditis when he was 40 year old.

Physical Examination of patient 04:
BP - 148/44 mmHg; Pulse - 78 bpm, reg;
Carotids: Very brisk with sharp collapse (Waterhammer pulse)
Pulses are all very prominent and brisk; audible pulse over the femoral arteries.
JVP: 5 with normal a and v waves
Lungs: Clear
Heart:
Palpation: Apical impulse is in the 6th intercostal space, in the anterior axillary line. Auscultation: S1 and S2 are soft;

An early diastolic blowing murmur, heard best at the lower left sternal border;
An early systolic ejection murmur heard at the upper right sternal border.

A

most likely diagnosis in patient 04 is: Aortic Regurgitation

Other differentials:

  • Mitral stenosis
  • Pulmonary regurgitation
  • Tricuspid stenosis
  • Ventricular Septal defect
31
Q

Aortic regurg: Additional Testing

A
  • ECG: LVHwithmassivevoltageinthelateral precordial leads (V4-V6)
  • Chest X-Ray: Large heart, predominant left ventricular enlargement. No congestive heart failure
  • Echo: Marked left ventricular dilation, estimated EF 65%.
  • Doppler: Severe aortic regurgitation. The aorta is enlarged
32
Q

Causes for AR

A

Valvular site

  • Endocarditis
  • Rheumatic disease
  • Ankylosing spondylitis
  • Congenital

Aortic site

  • Aortic aneurysm
  • Heritable disorders of connective tissue - Marfan’s syndrome, Ehlers-Danlos syndrome, Osteogenesis imperfecta
  • Inflammatory - Aortitis (Takayasu), Syphilis, Ankylosing spondylitis, Rheumatoid arthritis and SLE
  • Aortic dissection
33
Q

Pathology of AR:

A
  • Valvular cusp abnormality
  • Aortic dilatation
  • Aortic inflammation
  • Aortic tears with loss of commissural support
34
Q

Pathophysiology of AR:

A

Regurgitant aortic valve produces a volume load on the left ventricle

↓
Increased end diastolic volume and pressure

↓
Elongation and replication of sarcomeres in series,

leading to increased ventricular volume

↓

Enlarged ventricular cavity producing “eccentric hypertrophy”

↓
Chronic AR leads to huge ventricular volumes

35
Q

A. regurgitation: Hemodynamic changes

A
  • An incompetent (leaky) aortic valve allows blood to regurgitate from aorta to LV during ventricular diastole
  • An elevated left ventricular end diastolic volume and pressure (↑ preload)
  • Increased left ventricular and aortic systolic pressures
  • Decreased aortic diastolic pressure
  • Widened aortic pulse pressure, i.e. waterhammer
  • Diastolic murmur appears
36
Q

Pressure profile in AR

A

Pressure profile in AR

37
Q

Clinical Manifestations of AR

A

Patient remains asymptomatic as the heart responds to the volume load
When the compensatory mechanisms fail, symptoms appear

Symptoms:
-Shortness of breath (due to pulm edema)

-Hypotension often with cardiovascular collapse

38
Q

Physical examination in AR:

A

i) Hyperdynamic (pounding) arterial pulses:
- A widened pulse pressure is responsible for several characteristic peripheral signs
- Palpation of the peripheral pulse reveals a sudden rise and then drop in pressure (water-hammer or Corrigan’s pulse)
- Head bobbing (DeMusset’s sign)
- Rhythmic pulsation of the uvula (Müller’s sign)
- Arterial pulsation seen in the nail bed (Quincke’s pulse)
ii) Apical impulse:

Hyperdynamic and displaced laterally – due to the increased volume and forceful contraction of the left ventricle

iii) Soft S1 & S2:

S2 is soft due to improper closure
S1 will be soft because of early mitral valve closure from aortic regurgitation and elevated ventricular pressures

iv) Auscultation for murmurs in AR:

Three murmurs may be heard:

  • A high-pitched, blowing, decrescendo early diastolic murmur heard best along the left sternal border - due to regurgitant flow into left ventricle (hall mark sign).
  • A crescendo-decrescendo, early systolic murmur due to an increased stroke volume flowing across the aortic valve, can be heard at the right upper sternal border with radiation into the neck.
  • Austin Flint murmur at the apex: a diastolic rumble from regurgitant flow from the aortic valve impinging on the anterior leaflet of the mitral valve producing functional mitral stenosis
39
Q

Causes of MS:

A

a) Rheumatic: Most common

Narrowing results from fusion and thickening of the commissures, cusps, and chordae tendineae

b) Calcific: Usually causes mitral regurgitation but can cause mitral stenosis
c) Congenital: Presents in infancy or childhood
d) Collagen-vascular: SLE and rheumatoid arthritis; Rare cause of MS

40
Q

Mitral Stenosis : Pathophysiology

A
  • Scarring & fusion of valve apparatus
  • Normal valve area: 4-6 cm2
  • Mild mitral stenosis:
    • – MVA <2-2.5 cm2
    • – Minimal symptoms
  • Mod mitral stenosis:
    • – MVA >1.5 cm2
    • – usually does not produce symptoms at rest
  • Severe mitral stenosis
    • – MVA < 1.0 cm2
    • – produces symptoms at rest (eg. dyspnea)

Mitral valve is narrow

↓

Insufficient blood flows to LV during ventricular diastole

↓

Enlargement of LA with accumulated volume of blood

↓

Elevated left atrial pressure during ventricular diastole

↓

Elevated pulmonary venous pressure and elevated right-sided pressures (pulmonary artery, right ventricle, and right atrium)

↓
Dilation and systolic dysfunction of the right ventricle because of pulmonary hypertension

41
Q

Mitral stenosis: Hemodynamic changes

A
  • Narrowing of mitral valve reduces the amount of blood that flows forward through mitral valve
  • The left atrium enlarges and left atrial pressure builds up
  • There will be a pressure gradient between left atrium and left ventricle throughout the diastole
  • Mid Diastolic murmur appears
42
Q
A
  • Pressure profile in MS
  • During diastole, LAP exceeds LVP (gray area, pressure gradient generated by stenosis)
43
Q

Clinical Manifestations of MS:

A

Symptoms:

i) Dyspnea and orthopnea – due to elevated LAP, elevated pulm venous and capillary pressures
ii) Fatigue
iii) Hemoptysis

iv) Palpitations & Tachycardia - Increased left atrial size predisposes to atrial tachyarrhythmias
v) Hoarseness of voice – Enlarged LA can impinge on recurrent laryngeal nerve (Ortner’s syndrome)

44
Q

Physical examination of MS

A

i) Auscultation of heart:

  • The characteristic murmur of MS is a low pitched diastolic rumble (murmur) in the apex
  • Diastolic rumble occurs because of turbulent flow across the narrowed mitral valve orifice
  • In addition, an opening snap may be heard before the diastolic rumble (Opening snap is analogous to the ejection click described for aortic stenosis)
  • The opening snap is heard only when the patient has relatively mobile leaflets

ii) Auscultation of the lungs:

Reveals bilateral rales because of:

Elevated left atrial pressure

↓

Elevated pulmonary venous pressure

↓

Elevated pulmonary capillary pressure

↓

Accumulation of intra-alveolar fluid

45
Q

Mitral stenosis complications

A
  • Abnormal enlargement leads to loss of organized contraction of the left atrium and hence AF
  • Thrombus in the left atrium is observed due to stasis in LA (20% of patients with MS)
  • Embolic events lead to neurologic symptoms such as transient numbness/weakness of the extremities, sudden loss of vision or stroke.
46
Q

Mitral Regurgitation (MR) causes

A

Etiology:
Mitral valve prolapse is the most common cause, followed by coronary artery disease (ex. HOCM)

MR may be acute or chronic or congenital:
Acute causes:
-Ruptured chordae tendineae as in infective endocarditis; Trauma; Acute rheumatic fever

  • Ruptured or dysfunctional papillary muscles as in Ischemia; Myocardial infarction;Myocardial abscess
  • Perforated leaflet as in infective endocarditis
47
Q

Pathophysiology of acute MR:

A

In acute mitral regurgitation, the sudden volume overload on the LA and LV is not compensated for by chamber enlargement and hypertrophy

↓
Prominent atrial v waves with transmission of

this elevated LA pressure

↓

Elevated pressure in pulmonary capillaries

↓

Development of pulmonary edema

48
Q

MR chronic causes

A
  • -Inflammatory as in Rheumatic heart disease and Collagen vascular disease
  • -Infection as in Infective endocarditis
  • -Degenerative as in Myxomatous degeneration of the valve leaflets; Calcification of the mitral annulus
  • -Rupture or dysfunction of the chordae tendineae or papillary muscles as in Infective endocarditis; Trauma; Acute rheumatic fever; Myocardial infarction
49
Q

Pathophysiology of chronic MR:

A

Mitral valve fails to close properly during ventricular systole

↓
Regurgitation of blood into the LA from the LV

occurs during systole

↓

Enlargement of LA and LV to accommodate volume load

↓
Concomitant hypertrophy of the ventricular wall

↓
Increased diastolic filling of the left ventricle

50
Q

MR: Hemodynamic changes

A
  • An incompetent (leaky) mitral valve allows blood to regurgitate from LV to LA during ventricular systole
  • An elevated left atrial volume and pressure during ventricular systole
  • Left ventricular volume and also pressure increase during ventricular diastole
  • There is no pressure gradient between LA and LV throughout during ventricular filling
  • Systolic murmur appears
51
Q
A
  • Pressure profile in MR
  • An elevated LAP during systole w no gradient bw LVP and LAP during ventricular diastole
52
Q

Symptoms of MR:

A
  • The presentation of MR depends on how quickly valvular incompetence develops
  • Patients with chronic mitral regurgitation develop symptoms gradually over time Common complaints in chronic MR include: Dyspnea, easy fatigability, and palpitations Dyspnea - due to pulmonary edema
  • Fatigue - due to decreased forward blood flow to the peripheral tissues
  • Palpitations - due to atrial fibrillation
  • Common complaints in acute MR include: symptoms of left heart failure - shortness of breath, orthopnea, and shock
53
Q

Physical Examination in MR:

A

Laterally displaced and Hyperdynamic

Apical Impulse:

  • Reason for lateral displacement - The compensatory increase in left ventricular volume and wall thickness
  • Reason for hyperdynamic - The ventricle now has a low-pressure chamber (LA) into which to eject blood
  • When mitral regurgitation develops suddenly, the apical impulse is not displaced or hyperdynamic, because the LV has not had enough time for compensatory volume increases to occur.

ii) Holosystolic (pansystolic) Murmur:

  • Regurgitant flow into the LA produces a high- pitched murmur that is heard throughout systole
  • The murmur begins with S1, continues to the S2
  • Murmur is of constant intensity throughout systole
  • Unlike the murmur of AS, there is no variation in the intensity of the murmur as the heart rate changes
  • The murmur does not change in intensity with respiration
  • It is heard best at the apex and radiates to the axilla

iii) Muffled S1 and S2: The murmur often obscures the first and second heart sounds
iv) Loud S3: A third heart sound is heard in a patient with severe MR or if heart failure is present

54
Q

Mitral Valve Prolapse (MVP)

A

Other terms: Floppy valve, Barlow’s

Etiology

  • – Congenital
  • – Marfan’s syndrome
  • – Rheumatic heart disease
  • – Sequelae of MI

Pathophysiology

  • – Valve leaflet has redundant tissue
  • – Extra tissue balloons into LA, click sound
55
Q

MVP Physical Exam/Diagnosis

A

Thin, young females

Abnormalities: Associated skeletal abnormalities

Auscultation:

– Mid-systolic click & late systolic murmur

– Systolic murmur becomes louder and longer by Valsalva maneuver or on standing (decreasing venous return); by decr L. atrial vol.

56
Q

Physiologic maneuvers in the differential diagnosis of heart murmurs:

A
  1. Respiration:

Right-sided murmurs typically increase with inspiration, while left-sided murmurs generally are louder during expiration (“RILE”)

  1. Valsalva maneuver:
    Most murmurs decrease in length and intensity during the Valsalva maneuver
    Two exceptions are - the systolic murmurs of hypertrophic cardiomyopathy (HOCM) & mitral valve prolapse (MVP) – they become louder
  2. Handgrip (isometric exercise):

Murmurs of MR , AR and VSD increase with handgrip due to increase in afterload on LV

  1. Transient arterial occlusion:

Transient external compression of both arms by bilateral cuff inflation to 20 mmHg greater than peak systolic pressure augments the murmurs of MR, AR and VSD (due to increase in afterload on LV)

This maneuver does not affect the murmurs due to other causes

  1. Positional changes:
    i) Standing - Most murmurs diminish with standing due to reduced preload. Exceptions: the murmur of HOCM & MVP become louder
    ii) Squatting - Most murmurs become louder with prompt squatting (or usually passive leg raising), while the murmurs of HOCM and MVP typically soften and may disappear due to increased preload by incr VR

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