W3 Murmurs Valvular Heart Disease Flashcards
Rheumatic fever
Caused by
Affect which part of the heart
What do you see on histology
Major complication?
What are the JONES criteria? (major)
What are the minor criteria?
How do you diagnose?
How do you treat?
Which valve affected?
—GAS
—untreated pharyngitis
—affects all 3 layers (due to AI response)
—ASCHOFF BODIES on histology (cellular necrosis). Later becomes scar tissue
—devastating complication is valve destruction
Jones Criteria (MAJOR)
—Joints: migratory arthritis
—carditis (O = heart)
—Nodules, subcutaneous
—Erythema marginatum (rash with advanced edge and clearing center0
—Sydenham chorea involuntary movements
MINOR: CAFE PAL
—CRP increaased
—Arthralgia
—Fever
—Elevated ESR
—Prolonged PR interval
—Anamnesis of rheumatism
—Leukocytosis
Dx
—throat culture growing GAS
Or
—elevated anti-streptolysin O titers
PLUS
2 major criteria
OR
1 major and 2 minor
treatment
—penicillin
—anti-inflammatory like high dose aspirin/corticosteroids
mitral valve (40%)
Mitral stenosis
Patho: walk through the impact of a stenotic mitral valve
Presentation
—inflammation of valve leaflets > thickens and harder to open
rarer causes
—congenital stenosis
—carcinoid
—severe mitral annular calcification
—endocarditis
Impact
—high LA pressure > transmits to pulmonary vasculature > elevated hydrostatic pressure and causes Edema and SOB
—pulmonary HTN
—vasculature becomes hypertrophied
—RV pressure increases secondary to pulmonary HTN resulting in hypertrophy and dilation causing right sided heart failure
—chronic pressure leads to LA enlargement > stretching of the atrial conduction fibres causing afib
—afib results in loss of atrial kick and decline in CO
—stagnation of blood flow in LA + afib = thrombus formation and increase of stroke
PRESENTATION
—long asymptomatic course
—mild = dyspnea on exertion, reduced exercise capacity
—severe - Dyspnea at rest, pulmonary edema including PND & orthopnea, right sided HF (JVD, periph edema, abdominal distention), hoarseness as enlarged LA presses on laryngeal nerve
Mitral stenosis
Exam & diagnostics
What do you palpate ?
What do you hear? 3
What do you see on EKG? 2
What could you see on CXR? 3
—palpation may reveal right ventricular heave (palpate to feel this)
—loud S1 (closure of mitral valve) due to pressure gradient between LA & LV
—high pitched opening snap (diastole)
—descrescendo diastolic rumble
—EKG: possible afib as well as LA enlargement
V1 biphasic p wave
lead II has a wave with 2 peaks (camel hump) and long >110ms
—CXR: LA enlargement w/ pulmonary edema (3rd mogul, splaying of carina, double density sign, Kerley lines )
What can you see on ECHO if you’re looking for mitral stenosis? 7
—thickening of mitral leaflets
—abnormal fusion of their commissaries
—🔑LA enlargement
—possible intra atrial thrombus
—measure mitral valve area
—mean gradient across the valve
—pulm artery pressure
Mitral stenosis
Treatment
Medical? 4 main drugs. What’s the goal?
Avoid?
Percutaneous and surgical?
medical therapy
—GOAL: keep HR slow and in normal sinus rhythm (NSR)
—🔑 diuretics, salt restriction
—🔑 BBflecanide/digoxin to slow HR and increase filling time, also non-DHP CCB diltiazem/verapamil
—if afib, you lose atrial kick and higher HR. Consider cardio version and 🔑 anti-arrhythmic therapy for rhythm control: amiodarone
—🔑 consider anti-coags: dabigatran
—avoid vasodilators
percutaneous and surgical therapy
—moderate/greater pulmonary HTN
—balloon valvuloplasty, enter RA, poke hole in septum to LA , blow up balloon, breaks off calcification and the valve starts to move better. Risk is stroke embolising
—open valve surgery and replacement/repair (preferred)
Mitral regurgitation
Primary causes
Primary: disruption of MV apparatus
Secondary: LA enlargement pulling leaflets apart and making them floppy. HF
Primary causes:
—leaflets: myxomatosis degeneration, IE, R.fever
—mitral annulus: calcification
—chordae tendineae: rupture from damage
—papillary muscles: Ischemic
Mitral regurgitation
Pathology, explain the consequences of blood flowing back into the LA
—not all blood from LV is entering systemic circulation
—elevation of LV volume > inc LV pressure
—reduction of CO because not all blood is going forward, less organ perfusion
—regurgitated blood mixes with venous blood in LA and LV hits with more blood.
Mitral regurgitation
Severity depends on?
—size of valve orifice
—systolic pressure gradient between LA and LV
—systemic vas. Resistance opposing LV
—LA compliance
—duration of the regurgitation
diurese them to get volume off, and put them on HTN meds
Acute mitral regurgitation vs chronic?
acute
—normal LA size and compliance > high LA pressure > high pulm venous pressure > flash pulm congestion and edema
chronic
—increased LA size and compliance > normal LA and pulm venous pressure > however lower forward cardiac output
LA is dealing with more blood and pressure»_space;> hypertrophy over time.
Mitral regurgitation
Exam & diagnostics
Auscultation
CXR
EKG
—pansystolic apical murmur
—radiates to axilla
—S3 which indicates increase volume returning the LV in diastole, tenses chordae, hear a gallop sound
—displaced point of maximal impulse
—CXR: acute MR has more pulm edema (batwing)while chronic demonstrates left atrial and ventricular enlargement +/- edema
—EKG: LA enlargement and LV hypertrophy
Large R waves towards the hypertrophied side
Large R wave in V1 = abnormal (RVH)
Mitral regurgitation
Echo, what can you see?
—structural cause of MR
—grade the severity by Doppler
—determine LV and LA size and function
Catheterisation: useful for diagnosing an Ischemic cause and can grade the severity of MR
Mitral regurgitation
Treatment, medical therapy
For acute?
For chronic?
What the phrase to keep in mind?
—augment forward CO while reducing regurgitation into the LA.
—reduce pulm congestion
—keep them high and dry = faster HR to decrease diastolic filing time and diuretics
—acute can use vasodilators to reduce resistance to forward flow and diuretics to help w/ congestion
—chronic continue diuretics, vasodilators not as useful
Mitral regurgitation
Treatment - surgery?
—repair is preferred over replacement
—if not surgical candidate (high risk, too sick), consider placement of percutaneous mitral clip (clip the flaps so two holes are created in the valve so reduces the flapping around and less blood regurgitates back)
MV prolapse
Common in?
What do you see on echo ?
Which genetic disorders can be associated?
What type of tissue are the leaflets?
Dx?
Tx?
—common, in women
—asymptomatic
—billowing of MV leaflets into the LA
—may be genetic, marfan or ehlers-danlos
—leaflets enlarged, particularly posterior
—chordae lose tensile strength and replaced with loose myxomatous connective tissue (floppy, loose)
S/S
—dx made on echo, picked up incidentally
—maybe come in w/ palpitations or chest pain
Career HTN => LA dilation => afib
MV prolapse on PE?
Auscultation
Echo?
—pectus excavatum
—🔑midsystolic click heard at apex
—can alter murmurs by increasing preload (squatting) LV more full, delay prolapse, hear later click
ECHO
—confirmed diagnosis
—shows posterior displacement of one or both of the mitral valvue leaflets into the LA during systole
—benign, doesn’t require therapy
—if pt has palps, avoid stimulants
—can use BB for premature A of V beats
Aortic stenosis
Etiology
What is the disease course/patho?
—🔑calcification of aortic valve, degenerative, “wear and tear”, later in life
other etiologies
—atherosclerosis, endothelial dysfunction > lipid accumulation > inflammation > macrophages/foam
—congenital abnormality, ppl born with bicuspid valve
—rheumatic aortic stenosis
patho
—flow across valve impeded in systole
—develops over chronic course
—LV compensates by structurally changing
—Aortic valve narrows > inc afterload > 🔑 LV hypertrophies > decreases compliance of LV > LA hypertrophy in order to fill the stiff LV
Aortic stenosis
3 main manifestations ?
What would you not administer for this?
🔑 ASH: angina, syncope, heart failure
Angina
—secondary to imbalance between O2 demand and supply
—hypertrophy LV needs more O2
—reduces coronary perfusion secondary to elevated LV diastolic pressures and reduced pressure gradient
Syncope w/ exertion
—LV cannot increase CO during exercise
—reduced cerebral perfusion
Heart failure
—LV develops contractile dysfunction due to high afterload
🔑don’t administer nitroglycerine thinking they have angina but could have aortic stenosis, you’ll dilate and decrease preload and they’ll pass out! Rule out aortic stenosis, don’t assume it’s angina
Aortic stenosis
What do you hear on auscultation? describe the murmur, what else could you hear?
Type of pulse?
—🔑 crescendo-descrendo systolic murmur at RUSB
— later crescendo, worse A.S because it’s taking longer to open the valve
—🔑pulses parvus (weak) and tardus (late) upstroke of the carotid artery owing to obstructed LVOT (outflow tract)
—🔑S4 (stiff, not compliant LV)
Aortic stenosis
Treatment
—monitor serial echocardiograms
—avoid harmful meds that result in hyPOtension (vasodilator, diuretics, nitroglycerine)
—NO therapy to slow progression
—only tx is surgery with AVR (aortic valve replacement) or now trans-aortic valve replacement (TAVR) when pt is symptomatic (angina, syncope, failure)
🔑SAVR is surgical
🔑TAVR is non-surgical, can be used in low risk pts now as of last year
Aortic regurgitation (insufficiency) AI
Results from? Chronic/acute — which are medical emergencies?
Those related to dilated aortic root?
Chronic
—congenital (bicuspid valve)
—rheumatic
—HTN
—syphilis
Acute
—🔑aortic dissection —medical emergency, LV cannot adapt quick enough
—🔑 endocarditis —medical emergency, LV cannot adapt quick enough
—aortic aneurysm
—annuloaortic ectasia
What is the patho of aortic regurgitation (insufficiency)
Severity depends on?
What is the difference between acute vs chronic
What can we see in acute?
What is the hallmark sign of chronic that you would find on PE?
—similar to MR, blood regurgitates back into the LV during diastole
—next contraction, LV has to pump regurg volume AND normal amount coming from LA
Severity
—depends on regurg orifice
—pressure gradient across the aortic valve during diastole
—duration of diastole
acute
—LV is normal size (no structural changes yet)
—new regurg volume causes inc in LV pressure
—pressure transmits back to the LA
—causing flash pulm edema and HF
—🚨surgical emergency requiring immediate valve replacement
chronic
—LV hypertrophy (structural changes taken place)
—causes inc SV
—systemic arterial pressure drops
—wide pulse pressure = high SV and low aortic diastolic pressure, like 160/40
—coronaries fill during diastole, therefore reduces coronary perfusion ➡️ produces angina
—negatively remodels the LV
Aortic regurgitation (insufficiency)
Presentation
🔑On PE, you’ll find 2
Murmur is best heard when?
What is the name of the other murmur associated with this valve dysfunction?
—dyspnea
—fatigue, angina, decreased exercise tolerance
—PE: bounding pulse, widening pulse pressure
(bounding pulse b/c regurgitated blood mixes with blood in LV, causing inc in volume ejected from LV = bounding pulse)
—diastolic murmur best heard when patient leans forward at the left sternal border
—austin flint murmur [know this] — mid diastolic, at the apex, heavy jet of AI impinging on the anterior leaflet of the mitral valve generating turbulence
Familiarise these “pimp” questions
not tested
Aortic regurgitation (insufficiency)
CXR (acute vs chronic) what do you see
Echo (diagnostic)
Cath
TX for acute and chronic?
CXR:
Acute: pulm edema, normal LV size
Chronic: enlarged cardiac silhouette, +/- pulm edema
Echo
—diagnositc can identify degree
cath
—LV function
TX acute
—hemodynamic stablisation before surgical correction
—IV vasodilators
—IV diuretics
TX chronic
—vasodilators for nonsurgical candidates w/ symptoms
—surgical therapy for SX pts
Tricuspid valve
Regurg/stenosis generally produce signs of what?
Stenosis: caused by? Murmur? Dx? Tx?
Regurg: caused by? PE? DX? TX?
—3 leaflets
—both regurg and stenosis produce signs of right HF elevated JVD, HSM, abdominal Ascites, peripheral edema
stenosis
—rare
—caused by rheumatic fever or carcinoid
—murmur is similar to MS with an OS but heard closer to the sternum intensifies on inspiration b/c increased right heart flow
—dx w/ ECHO
—no med therapy
regurgitation
—functional rather than structural
—rheumatic, carcinoid, ebsteins, connective tissue, IE, trauma, toxic (phen phen)
PE: JVD, prominent V wave, pansystolic at LLSB often w/ S3, pulsation liver from regurg flow from RV into systemic veins
—DX : EKG incomplete RBBB or RVH, ECHO is diagnostic, R.heart cath will show prominent V wave
—TX : mild moderate w/ HTN well tolerated. If RV develops, use diuretics
—surgical
Pulmonary valve
Stenosis: cause? When does it occur? Tx?
Regurgitation: cause? What type of murmur do you hear?
Diagnostic test for both?
stenosis
—rare, almost always congenital deformity.
—presents in 4-5th decade of life
—ECHO diagnostic
—mild/mod no intervention.
—severe: balloon valvuloplasty
regurgitation
—dilation of valve ring by enlarged pulm artery
—acquired from pulm HTN
PE: decrescendo diastolic murmur LSB
ECHO is diagnostic
Prognosis is good, rarely needs med
Summary of valve conditions
[SKILLS OSCE]
What is this
Left atrial enlargement
Lead V1 has biphasic p wave
[SKILLS OSCE]
What is this?
