-
which systolic murmur is heard at the RUSB
aortic stenosis
-
which systolic murmurs are heard at the LUSB
-
which systolic murmur is heard at ERBs point
HoCM
-
which systolic murmurs are heard at LLSB
-
which systolic murmurs are heard at the apex
- mitral regurg
- mitral valve prolapse
-
which diastolic murmurs are heard at LUSB
- Pulmonary insufficiency (PI)
- spilt S2
-
which diastolic murmur is heard of Erbs point
aortic insufficiency (AI)
-
which diastolic murmur is heard at LLSB
tricuspid stenosis
-
which diastolic murmur is heard at the apex
mitral stenosis
-
what is a delayed, non-suppurative sequelae of a pharyngeal infection with group A streptococcus
acute rheumatic fever
-
what is the most common age group for acute rheumatic fever
5-15 years old
-
what is the latent period before initial s/s appear for acute rheumatic fever
2-3 weeks
-
what are some specific symptoms that pts will complain about with rheumatic fever
- arthritis that affects numerous joints but emerges one joint at a time
- abnormal heart beat
- CP
- red patches on skin
- small painless lumps beneath skin
- rapid, involuntary movements in muscles of extremities or face
-
what are the major criteria of Jones criteria
- J= joints (migratory polyarthritis)
- O= carditis (heart involvement)
- N= nodules (subcutaneous)
- E= erythema marginatum
- S= Sydenham's chorea
-
this is a neurologic disorder, that has abrupt/rapid, involuntary, nonrhythmic movements, emotional disturbances and muscle weakness, and it ceases during sleep
sydenhams chorea
-
what are the minor Jones criteria in rheumatic fever
- other arthralgias (without arthritis)
- fever: 101-104 degrees f
- elevated acute phase reactants (ESR and CRP)
- prolonged PRI on ECG
-
what are the diagnostic tests for diagnosis group A strep pharyngitis infx
- positive throat culture
- positive rapid streptococcal antigen test
- elevated (especially rising) streptococcal antibody testing:
- - ASO (antistreplysin O)
- - Anti-DNase B
- - ASTZ (antistreptozyme)
-
what are the 3 circumstances that be used to make a presumptive dx for ARF
- chorea is the only manifestation
- indolent carditis may be the sole manifestation in pt who fail to seek early medical tx
- recurrent RF individuals with a hx of ARF should be presumed to have recurrence with any manifestations
-
how long should antibiotic therapy with PCN be started and maintained for in ARF
at least 10 days regardless of presence or absence of pharyngitis at time of dx
-
what meds can be used in a pt who is allergic to PCN but has ARF
- azithromycin
- clarithromycin
- clindamycin
-
when does rheumatic heart disease occur after the original illness
10-20 years after
-
what is the major cause of valvular heart dz world wide
ARF
-
what is the most commonly affected valve in ARF
mitral valve (mitral stenosis)
-
what is the most common cardiac valve lesion in the US
aortic stenosis
-
what are the etiologies behind aortic stenosis
- congenital (bicuspid, unicuspid)
- degenerative (calcific/"wear and tear")
- Rheumatic heart dz
-
what are the cardinal sxs of advanced AS and average survival after onset
- angina (5 years)
- exertional syncope (3 years)
- CHF (2 years)
- AFIB precipitates overt HF and can increase mortality rates
-
why is there angina with aortic stenosis
because there is an imbalance between myocardial supply and demand. the increased LVDP reduces coronary perfusion pressure gradient between the aorta and myocardium
-
why is there syncope with aortic stenosis
LV cannot increase cardiac output during exercise which leads to decreased cerebral perfusion pressure then syncope
-
why is there CHF with aortic stenosis
LV develops contractile dysfunction due to increased afterload which leads to increased LV diastolic volume/pressure.
The increased LA pressure backs up into the pulmonary vasculature, then there is increased alveolar congestions and that leads to CHF
-
what type of pulse will a pt with aortic stenosis have
pulses parvus et tardus
-
what are the clinical features of aortic stenosis
- pulsus parvus et tardus (weak and late)
- displace PMI
- narrow pulse pressure
- AFib
-
this type of murmur is harsh, has a crescendo-decrescendo "diamond shape", it is a systolic murmur. It is best heard at the RUSB with either the bell or diaphragm and radiates to the carotids
aortic stenosis
-
what will the EKG show is aortic stenosis
LVH
-
what will a CXR show with aortic stenosis
-
what will an echo show with aortic stenosis
- increased LV wall thickness
- determine the severity of dz
- increased valve pressure gradient (Doppler)
- reduced valve area
-
what is recommend for the initial diagnosis and assessment for aortic stenosis severity
Echo (class 1)
-
which diagnostic test is used in the assessment of LV wall thickness, size and function
echo (class 1)
-
if you have a pregnant pt with AS, which diagnostic testing do you want to use
echo (class 1)
-
what is recommended for re-evaluation of asymptomatic pts with aortic stenosis
transthoracic echo (TTE)
-
how often is severe AS re-evalutated with a TTE
every year
-
how often is moderate AS re-evaluated with a TTE
every 1-2 years
-
how often is mild AS re-evaluated with a TTE
every 3-5 years
-
what is the only effective therapy for adults with severe AS
aortic valve replacement
-
what type of treatment may be considered in young pts with congenital AS
balloon aortic valvuloplasty
-
what are the etiologies of aortic insufficiency (regurg)
- abnormalities of the valve leaflets (congenital; bicuspid valve, rheumatic; RA or rheumatic fever, infective endocarditis)
- dilation of the aortic root
- aortic aneurysm
- inflammation/CT dz (marfan syndrome, ehlers-danlos, IBD)
- trauma- aortic dissection
- syphilis
- annuloaortic ectasia
-
this is typically associated with rapid decompensation due to the inability to accommodate to increase end diastolic pressure (acute or chronic AR)
acute AR
-
this may be compensated for by ventricular dilation which leads to hypertrophy eventually leading to CHF (acute or chronic AR)
chronic AR
-
high LV stroke volume + reduced diastolic pressure = ??
widened pulse pressure
-
what is the hallmark sign of AR
widened pulse pressure
-
what are the s/s of acute AR
acute pulmonary edema
-
what are the s/s of chronic AR
- prolonged asymptomatic period
- widened pulse pressure (bounding pulse, "water hammer" pulse)
- CHF sxs
- angina
- atypical CP ("uncomfortable awareness of a forceful heart beat)
-
if you are examining a pt with AR and you notice they have head bobbing with systole, what is that sign called
De Musset's sign
-
if you are examining a pt with AR and you notice they have a water hammer pulse, what is the name of that oulse
Corrigans pulse
-
what is the name of the pulse is the pt has capillary pulsations in the nail beds
Quincke's pulse
-
what is the name of the sign if a pt has pistol shot sounds over the radial or femoral artery
Traube's sign
-
what is the name of the sign is the pt has a to and fro femoral murmur
Duroziez's sign
-
this type of murmur has a high-pitched, blowing diastolic murmur, is heard best with the diaphragm in the 3rd left intercostal space (Erbs point) with the pt sitting up, leaning forward and exhaling
aortic regurg
-
this murmur is a low-pitched rumbling mid-diastolic sound attributed to normal diastolic blood flow from the left atrium hitting the anterior leaflet of the mitral valve
Austin-flint murmur
-
what can an ECG show if a pt has aortic regurg
- LVH
- strain pattern (chronic ischemia)
- LBBB
- LAE
- LAD
- Atrial fibrillation
-
what is used to confirm the presence and severity of acute or chronic AR
echo
-
this diagnostic testing is used for the dz and assessment of the cause of chronic AR
echo
-
this diagnostic testing is indicated in pts with an enlarged aortic root to assess regurg and the severity of aortic dilation
echo
-
this diagnostic testing is used for the re-evaluation of mild, moderate, or severe AR in pts with new or changing sxs
echo
-
this diagnostic testing is indicated for the initial and serial assessment of LV volume and function at rest in pts with AR and suboptimal echos
radionuclide angiography or MRI
-
this diagnostic testing is used when the noninvasive tests are inconclusive or to provide discrepant results from clinical findings with pts that have AR
cardiac cath
-
this diagnostic testing is used for chronic AR, it is reasonable for assessment of functional capacity and symptomatic response in pts with a hx of equivocal sxs
exercise stress
-
this diagnostic testing is used to assess sxs/functional capacity prior to athletic activity in a pt with AR
exercise stress
-
which medications benefit asymptomatic pts with severe AR with preserved LV function or pts with sxs or reduced LV function who are not surgical candidates
- ACE-I
- dihydropyridine CCB
- hydralazine)
-
what is the most common etiology of mitral stenosis
rheumatic fever/heart dz
-
what can worsen mitral stenosis
- A-fib
- tachycardia
- pregnancy (increased preload)
-
this type of pulmonary HTN is an increase in pressure due to backward transmission of elevated left atrial pressure
passive pulmonary HTN
-
this type of pulmonary HTN is due to pulm arterial/arteriolar vasoconstriction, hypertrophy of pulmonary artery
reactive pulmonary HTN
-
this murmur is low pitched, rumbling, decrescendo, diastolic murmur, it is associated with an opening snap, is best heard at the apex in the left lateral decubitus position with the bell
mitral stenosis
-
this type of murmur is seen on an EKG that has LAE (p-mitral) and/or RVH/RAD
mitral stenosis
-
which diagnostic testing is used for the diagnosis of MS
echocardiogram
-
this diagnostic test is used for the re-evaluation of pts with known MS and changing symptoms or signs
echocardiogram
-
this diagnostic study for MS should be performed to assess the presence or absence of left atrial thrombus and to further evaluate the severity of MS in pts considered for percutaneous mitral balloon valvotomy
TEE
-
how often is severe MS evaluated
every year with echo
-
how often is moderate MS evaluated
every 2 years with an echo
-
how often is mild MS evaluated
every 3-5 years with an echo
-
when is pharmacologic therapy appropriate for mitral stenosis
- stabilization prior to intervention
- to treat decompensation due to intercurrent illness
- for persistent symptoms after intervention
-
which medications may improve symptoms of mitral stenosis
diuretics and beta blocks
-
what are the etiologies of mitral regurg
- mitral valve prolapse (most common cause)
- congenital cleft leaflets
- left ventricular dilation (CHF, DCM, myocarditis)
- infective endocarditis
- Marfans
- acute MI
- myxoma
- MV annulus calcification
- chordae/papillary muscle/ischemia/rupture
- rheumatic fever
-
which leaflet is most often affected in mitral regurg
posterior leaflet
-
the severity of MR is based on what 5 things
- 1) size of the opening during regurg
- 2) the systolic pressure gradient between the LA and LV
- 3) systemic vascular resistance opposing the LV forward outflow
- 4) LA compliance
- 5) duration of regurg
-
what are the clinical features/signs and symptoms of mitral regurg
- dyspnea
- paroxysmal nocturnal dyspnea (PND)
- orthopnea
- palpitations
- peripheral edema
- arrhythmia (A fib)
-
acute mitral regurg will show what type of clinical signs in a pt
pulmonary edema
-
chronic mitral regurg will show what type of clinical signs in a pt
low cardiac output
-
what will your PE show in a pt with mitral regurg
- apical thrill (if severe MR)
- soft S1
- loud P2 and RV heave
-
this murmur is loud, high pitched, holosystolic at the apex that radiates to the axilla, will have a loud S2 and best heard at the apex/LLSB in the left lateral decubitus position with the diaphragm
mitral regurg
-
mitral regurg intensifies with what activity
should intensify with hand grip
-
what will an ECG show if a pt has mitral regurg
-
what is used for baseline evaluation of LV size and function, RV and left atrial size, pulmonary artery pressure, and severity of MR in any pt suspected of have MR
TTE
-
which diagnostic testing is used for annual or semiannual surveillance of LV function in asymptomatic pts with moderate to severe MR
TTE
-
which diagnostic testing is used to evaluate the MV apparatus and LV function after a change in signs or symptoms
TTE
-
this diagnostic test is reasonable in asymptomatic pts with severe MR to assess exercise tolerance and the effects of exercise on pulmonary artery pressure and MR severity
exercise Doppler echo
-
this is the most common cause of isolated MR requiring surgical repair
mitral valve prolapse
-
what are the etiologies of mitral valve prolapse
- congenital (associated with Ebsteins anomaly, ASD)
- Marfan, Ehlers-Danlos syndrome
- Rheumatic Heart Dz
- sequel of cardiomyopathy or MI
-
what is the hallmark macroscopic valvular lesion of MVP
excessive mitral leaflet tissue leading to folding and hooding
-
what are the signs and symptoms of mitral valve prolapse
asymptomatic
*key to clinical manifestations are ausculatory findings
-
what are the S/S of MVP syndrome
- stabbing chest pain
- dyspnea
- palpitations
- fatigue
- dizziness
- anxiety of panic disorder
-
what accentuates/alters mitral valve prolapse
bedside maneuvers that increase/decrease volume of LV
-
this diagnostic imaging is indicated for the diagnosis of MVP
echo
-
this diagnostic imaging can be effective for risk stratification in asymptomatic pts with physical signs of MVP or known MVP
echo
-
what are the etiologies of pulmonic stenosis
- rare
- congenital (most common)
- carcinoid syndrome (rare):
- - tumor with mets to the liver releases serotonin metabolites into the bloodstream forming endocardial plaques on the right side of the heart
-
what are the signs and symptoms of pulmonic stenosis
- asymptomatic
- exertional dyspnea
- symptoms of right HF
- exercise induced fatigue, syncope or CP
-
what will a PE show if a pt has pulmonic stenosis
- S2 split
- prominent right ventricular systolic impulse with a left para-sternal lift
-
this murmur is a crescendo-decrescendo, systolic murmur, it is heard best with either the bell or the diaphragm at the LUSB, is often accompanied by an early systolic ejection click
pulmonic stenosis
-
what is the management for pulmonic stenosis
- balloon valvuloplasty via catheterization
- treat the underlying RHF
-
what are the etiologies of pulmonic stenosis
- pulmonary HTN (most common)
- infective endocarditis
- rheumatic disease
- tetralogy of fallot
-
what are the signs and symptoms of pulmonary insufficiency
- asymptomatic
- exertional dyspnea
- exertional chest pain
- exertional syncope
- fatigue
- peripheral edema
- anorexia/adb pain
-
this murmur is an early diastolic ejection murmur with an ejection click heard at the pulmonic area
pulmonic regurg
-
this murmur is a high-pitched, decrescendo, diastolic murmur heard along the left sternal border
graham steel murmur
-
what are the etiologies of tricuspid stenosis
- rare
- rheumatic disease (most common)
- congenital
- carcinoid syndrome
- right atrial or metastatic tumors
-
what are the signs and symptoms of tricuspid stenosis
- peripheral edema
- abd distention/hepatomegaly
- fatigue
- palpitations
- JVP with giant "a" waves
- +/- kussmauls sign
-
this is a low-pitched, rumbling diastolic murmur that is best heard with the bell at the LLSB
tricuspid stenosis
-
what accentuates and diminishes tricuspid stenosis
inspiration, diminished with valsalva and expiration
-
what will an EKG show with tricuspid stenosis
RAE
* the absence of RVH in the presence of sxs of right-sided failure should suggest the diagnosis
-
what is the management of tricuspid stenosis
- preload reduction (diuretics)
- sx is usually reserved for pts undergoing other valve or CT sx
- valvulotomy/commissurotomy or valve replacement is indicated with diastolic pressure gradients >5mmHg or orifice <1.5-2 cm2
-
what are the etiologies are tricuspid regurg
- largely functional vs primary valve disease
- - dilated right atrium and right ventricle
- - pressure or volume overload
- rheumatic dz
- - rheumatic MS leads to TR due to pulmonary HTN with right ventricular enlargement
- infective endocarditis (IV drug use)
- congenital
- - ebstein anomaly is most common form
- carcinoid (rare)
- connective tissue d/o (marfan)
-
what are the signs and symptoms of tricuspid regurg
- peripheral edema
- fatigue
- palpitations
- Afib is usually present
-
what are the PE associated with TR
- RV heave
- ascites and peripheral edema
- ** severe TR pt may appear cachetic or chronically ill***
-
this murmur is a blowing holosystolic murmur, is best heard with the diaphragm along the LLSB
TR
-
what intensifies and diminishes TR
- intensifies with inspiration
- diminished by valsalva or standing
-
what is the most common congenital disorder in newborns
congenital heart disease
-
this syndrome is the development of pulmonary vascular disease due to chronic large left-to-right heart shunt
eisenmenger syndrome
-
what are the acyanotic lesions in congenital heart disease
- atrial septal defect (PFO- not a true ASD)
- VSD
- PDA
- Coarctation of the aorta
- aortic stenosis
- pulmonic stenosis
-
what are the classifications of ASD
- ostium secundum (75%)
- ostium primum (15%)
- sinus venosus (10%)
-
this is not a true ASD, it is significant in the context of increased right-to-left shunts which can lead to a paradoxical embolism
patent foramen ovale (PFO)
-
what are the 3 factors that shunt volume is dependent on
- size of defect (determined severity)
- pressure gradient between atria
- peripheral outflow resistance
-
if an infant has a large ASD, how may they present
- HF
- recurrent respiratory infections
- failure to thrive
-
what are the clinical features of ASD
- fatigue
- dyspnea on exertion or decreased stamina
- palpitations
- fixed spilt S2
- murmur
- increased frequency of atrial arrhythmias, especially atrial flutter and fibrillation (most frequent presenting symptom)
-
what are the causes of a RV heave in ASD
- hyperdynamic right ventricular impulse, most pronounced along the LSB
- precordial bulge due to atrial enlargement (large left-to-right shunt)
-
this is a soft, mid-systolic ejection murmur heard at the ULSB OR it can be a mid-diastolic murmur that may be also present at the LLSB due to increased flow across the tricuspid valve
ASD
-
a fixed S2 split is associated with what type of congenital heart disease
ASD
-
what will an ASD show on an EKG
- RAD (exception is it will be LAD with ostium primum type due to LAFB)
- RVH
- incomplete RBBB or complete RBBB
-
what is the treatment for an ASD
if volume of shunted blood is large or when the ration of pulmonary to systemic flow is 1.5 or greater, treatment is via surgical repair even is asymptomatic
-
how is surgical closure of an ASD completed
- cardiopulmonary bypass
- percutaneous transcatheter device closure
-
this is the most common congenital heart defect in infants and children
VSD
-
what are the classifications of VSD
- membranous (70%)
- muscular (20%)
- other (10%) near the aortic valve or mitral-tricuspid junction
-
how will a pt with a large VSD present
- secondary pulmonary HTN
- CHF by 2 years of age
-
how do adults present with VSD
- arrhythmias or sxs of right HF
- pulmonary HTN
- dyspnea on exertion
- peripheral edema
- fatigue
-
this is a harsh holosystolic/early systolic murmur best heard at the LLSB, mid-diastolic "rumble" heard at the apex (increased flow across the mitral valve) and is associated with a systolic thrill over the area of defect
VSD
-
how will infants with a VSD present within the first months of life
- FTT, delayed growth, poor feeding
- develop early symptoms of CHF
- tachycardia, tachypnea, hyperdynamic precordium, displaced PMI
-
which diagnostic study is used to see the location of the VSD and the shunts magnitude
echocardiogram with doppler
-
what will an ECG show in a pt with a VSD
- LAE
- LVH
- RVH (if pulmonary vascular dz)
-
how are large VSD's treated
- dietary interventions to facilitate weight gain
- diuretics are first line pharmacologic therapy (Furosemide is well tolerated)
- ACE inhibitors
- can add digoxin
-
what are the indications for surgical repair in the first few months of life
- CHF or pulmonary vascular dz
- pulmonary artery pressure >50mmHg
- LAE or LVH
- deteriorating left ventricular function
-
a PDA is common in which pt population
- premature births (most common)
- exposure to maternal rubella infx 1st trimester
-
what is the most common cause of CHF in premature newborns
PDA
-
a PDA that is associated with this syndrome will show as lower extremity cyanosis (feet), and upper extremities remain acyanotic
Eisenmenger's syndrome
-
how do large PDAs manifest
- fatigue
- dyspnea
- poor feeding
- recurrent lower respiratory tract infxs
- accessory muscle use
- apneic spells or symptomatic bradycardia
-
what is the most common finding with a PDA
the murmur
-
this murmur is a continuous machine-like murmur best head at the left infra-clavicular area
PDA
-
what does the exam show with PDA
- tachycardia
- bounding pulses
- wide pulse pressure
- hyperactive precordium (lifts, heaves)
- lower extremity cyanosis
- increased risk of endocarditis
-
what will the EKG show on a pt with a PDA
-
which diagnostic study is used to show the PDA location and flow and gives the estimation of right-sided systolic pressures
echocardiogram with doppler
-
what is the treatment of PDA in preterm infants
initial intervention is indomethacin or ibuprofen
-
how is a PDA treated in an older infant
- percutaneous device closure is recommended
- surgical ligation is an alternative
-
how long are antibiotics indicated for after percutaneous PDA closure (to prevent endocarditis)
6 months
-
what are the cyanotic lesions associated with congenital heart diseases
- tetralogy of fallot
- transposition of the great arteries
- ebsteins anomaly
-
what are the 4 primary abnormalities that develop in response to a single abnormal development of the outflow tract of the intra-ventricular septum
- VSD (caused by malalignment of the intraventricular septum)
- RV outflow obstruction (in effect pulmonic stenosis)
- RVH (due to high pressure load from PS)
- overriding aorta (receives blood from both ventricles)
-
this is the most common cyanotic heart defect diagnosed after infancy or age 1
tetralogy of fallot
-
what are the clinical features of tetralogy of fallot
- dyspnea on exertion
- - "tet spells" or "tet fits"
- - poor feeding, cyanosis during feeding
- - fussiness, tachypnea, cyanosis, agitation
- - hyperventilation, syncope
- - learn to squat after exercise or when symptomatic
- growth retardation
- development, puberty may be delayed
-
what are the consequences of chronic cyanosis assoc with tetralogy of fallot
- perioral and mucosal cyanosis
- - mild cyanosis noted around lips, mucus membranes and digits
- clubbing of digits- chronic hypoxemia
- erythrocytosis (aka polycythemia)
- hyperviscosity- stroke risk
-
this murmur is a mild systolic murmur related to right ventricular outflow obstruction, is best hear LUSB, may hear a single loud S2, and/o a possible holosystolic VSD murmur
tetralogy of fallot
-
what will an ECH show on a pt with tetralogy of fallot
-
what will an CXR show on a pt with tetralogy of fallot
"boot-shaped heart" (right heart enlargement/prominent RV)
-
this diagnostic study defines the expected anatomy of tetralogy of fallot, it makes the dx, and it estimates the severity of the RVOTO
echocardiogram
-
what is the treatment for "tet spells"
- O2
- knee chest position
- fluid bolus
- morphine sulfate
- propranolol or esmolol
-
what type of repair do pts go under for tetralogy of fallot
intracardiac repair
-
what is the unoxygenated systemic circuit that is assoc with transposition of the great arteries
body ⇨ RA ⇨ RV ⇨ aorta ⇨ body
-
what is the oxygenated pulmonary circuit assoc with transposition of the great arteries
lungs ⇨ LA ⇨ LV ⇨ pulmonary artery ⇨ lungs
-
what is the most common cyanotic heart defect in the neonatal period
transposition of the great arteries
-
what are the clinical features associated with transposition of the great arteries
- "blue baby"
- generalized cyanosis first day of life which progresses (PDA closes)
- tachypnea
- palpable RV impulse
-
what may a CXR show on a pt with transposition of the great arteries
base of heart may narrow giving an "egg shaped" heart
-
what makes the dx of transposition of the great arteries
echocardiogram
-
what is the treatment for transposition of the great arteries
- rapid surgical correction is required, medical emergency
- - arterial switch)
PGE1 infusion alprostadil and/or balloon atrial septostomy
-
what are the histologic changes that occur with Eisenmenger syndrome
- pulmonary artiolar media hypertrophies
- intima proliferates
- vessels become thrombosed
-
what are the clinical features of Eisenmenger syndrome
- chronic cyanosis, digital clubbing
- prominent "a" wave when left to right shunt
-
which diagnostic test is used to identify the underlying defect and quantify the pulmonary artery pressure
echocardiogram with doppler
-
what is the treatment for Eisenmenger syndrome
- activity restriction and other interventions to reduce cardiovascular demands
- end stage sx in terminal pts
-
this is a congenital defect of the tricuspid valve in which the septal and posterior leaflets are malformed and displaced into the right ventricle leading to variable degrees of right ventricular dysfunction
ebsteins anomaly
-
this congenital heart disease may be associated with maternal lithium during the 1st trimester
ebsteins anomaly
-
what are the clinical features of ebsteins anomaly
- intrauterine demise
- incidental finding
-
when is endocarditis prophylaxis suggested for pts with ebstein anomaly
- it is suggested in cyanotic pts
- pts with prosthetic cardiac valves or with prosthetic material used for cardiac valve repair
-
what are the treatments for ebsteins anomaly
- endocarditis prophylaxis
- tricuspid repair or replacement with severe sxs
- arrhythmia treatment, if afib warfarin is recommended
-
in infective endocarditis, what causes the leaflet vegetation
platelet-fibrin thrombi, WBCs and bacteria (or other pathogens)
-
what are the 3 ways to classify infective endocarditis
- 1) by clinical course: acute (aggressive) and subacute (insidious in onset)
- 2) by host: native valve (MC), prosthetic valve, IV drug user
- 3) specific infectious organism ("bug")
-
which pathogen is more common found on native valve infective endocarditis
streptococcus
-
which pathogen is more commonly found with IVDU infectious endocarditis
S aureus
-
which pathogen is more commonly found with prosthetic valves with a recent sx < 1yr infective endocarditis
s. epidermidis
-
which pathogen is more commonly found with prosthetic valves with a remote surgery > 1 yr infective endocarditis
streptococcus
-
for community acquired infectious endocarditis, which valve is most commonly affected
MV
-
for IV drug uses what is the most common valve affected with infectious endocarditis
TV
-
what are the risk factors for infective endocarditis (7 risk factors)
- acquired valvular dz
- prosthetic valve
- CHD
- hypertrophic cardiomyopathy
- indwelling catheter
- IV drug use
- previous endocarditis
-
what changes are associated with/ within the heart that is affected by infective endocarditis
- endocardial surface injury (turbulent blood flow from valvular dz)
- thrombus formation at the site of injury
- bacterial entry into circulation (bacteremia)
- bacterial adherence to the injured endocardial surface
-
what are the acute sxs of infective endocarditis
- aggressive, high fever, shaking chills
- occurs and worsens over days
- typical IE causing organisms
-
what are the subacute sxs of infective endocarditis
- develops over weeks
- much less specific sxs
- may be easily overlooked or confused with less aggressive dz process (viral syndrome)
** more CHF type sxs
-
what are some common symptoms of infective endocarditis
-
what are some common signs of infective endocarditis
- fever
- murmur
- neurological abnormalities
- embolic event
-
which criteria is used to help dx infective endocarditis
duke criteria
-
what is the initial test of choice that detects large vegetations, quantifies valvular dysfxn, non-invasive and easy to obtain
TTE
-
which diagnostic study is more sensitive for the detection of small vegetaions and is useful for the evaluation of prosthetic valves
TEE
-
what are the major Duke criteria's
- positive blood cultures for IE
- evidence of endocardial involvement (+ echo for IE, new valvular regurgiation
-
what are the minor Duke criteria's
- predisposition- predisposing heart condition or IV drug use
- fever- 100.4
- vascular phenomena- major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, janeway lesions
- immunologic phenomena- glomerulonephritis, osler's nodes, roth spots, RF
- microbiologic evidence- + blood culture but not meeting major criteria
- echocardiographic minor criteria eliminated
-
how many major and minor Duke criteria need to be present for definite IE
- 2 major
- 1 major and 3 minor
- 5 minor
-
how many major and minor Duke criteria need to be present for possible IE
- 1 major and 1 minor
- 3 minor
-
what are the different treatments for IE
- antibiotics 4-6 weeks of high dose IV abx therapy
- sx
- anti-coag
- prophylaxis
-
what is the appropriate initial therapy most pts will receive until cultures results are back for IE
vancomycin
-
if a pt has IE what is the treatment for strep
high dose PCN-G (12 million units daily)
-
if a pt has IE what is the tx for staph
nafcillin IV
-
what are some complications to be aware of in IE
- emboli
- CHF
- abscess formation
- intracranial hemorrhage
- immune complex glomerulonephritis
-
what are the indications for sx in IE
- mod-severe CHF caused by valvular dysfxn
- unavailable effective antimicrobial therapy:
- - fungi
- - brucella spp
- - pseudomonas aeruginosa
-
how much fluid is required for clinically evident cardiomegaly on CXR
200-250ml
-
this serves as a barrier to limit spread of infection from adjacent lungs to the heart
pericardium
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a pt presents to the ER with acute pleuritic CP. You do an EKG and notice distinctive EKG changes and upon auscultation you hear a pericardial friction rub, what is your presumptive dx
acute pericarditis
* may or may not also have a fever
-
what is the most common infectious cause of acute pericarditis
idiopathic/viral (coxsackie, CMV, HIV)
-
a pt reports to the ER stating that he is having pleuritic CP, upon getting his past hx he tells you he had a MI about 2 weeks ago. You listen to his heart and you hear a pericardial friction rub, what syndrome is associated with these sxs
dresslers
-
the highest mortality is associated with which type of pericarditis
purulent
-
which type of pericarditis is associated with PMNs, lymphocytes, histocytes (thin exudate)
serous acute pericarditis
-
which type of pericarditis has yellow exudate protein/fibrinogen which appears rough/shaggy. Is the most common type of pericarditis. The pericardium becomes thick, sometimes scar causing restriction of diastolic filling
serofibrinous ("bread and butter")
-
which type of pericarditis has purulence and an intense inflammatory response to bacteria
suppurative (bacterial)
-
which type of pericarditis has gross blood associated with it
hemorrhagic (TB/Ca)
-
what are the major clinical manifestations of acute pericarditis
- CP (sharp and pleuritis and exacerbated by position or coughing)
- friction rub (scratchy or squeaking sound best heard with diaphragm over the LSB
- ECG changes (new widespread ST elevation with/without PR depression)
- pericardial effusion
-
what will an ECG show on a pt with pericarditis
- diffuse ST elevation
- PR segment depression
- concave upsloping ST segment
-
what will a CXR show on a pt with pericarditis
water bottle heart with large effusion
-
when would you order a STAT echo
if tamponade is suspected
-
how much pericardial fluid must accumulate before the cardiac silhouette enlarges
200 mL
-
when do you need to get blood cultures on a pt with pericarditis
if fever great than 100.4 or signs of sepsis
-
what is the treatment for acute pericarditis
- viral or idiopathic pericarditis is self-limiting, lasts 1-3 weeks (rest and pain relief: combo colchicine + NSAIDS)
- NSAIDS are the maintstay of therapy, unless CI then use ASA
-
when would you not use NSAIDS on a pt with acute pericarditis
post MI--- use ASA instead
-
the likelihood of the this is determined primarily by the pressure-volume relationship
tamponade
-
what are some clinical features of pericardial effusion
- dyspnea
- dysphagia
- hoarseness
- hiccups
- increased JVP with dominant "x" descent
- arterial pulse normal to decreased
- decreased pulse pressure
- rub
- atypical CP
-
what are some clinical features of cardiac tamponade
- Becks triad (distant heart sounds, JVD, HoTN)
- atypical CP
- "small quiet heart"
- compression of surrounding structures
- tachycardia
- loss of "y" descent on JVP
- pulsus paradoxusshock
- death
-
what will an EKG show on a pt with an effusion
-
what will an EKG show on a pt with a tamponade and large effusion
- electrical alternan (pathognomonic)
- low voltage
-
this diagnostic test can identify fluid collections as small as 20ml, it assists in quantifying the volume and if ventricular filling is compromised, and can help direct placement of pericardiocentesis needle if needed
echo (effusion)
-
this diagnostic test can tell if a pericardial effusion led to the tamponade, can see if there is compression of the cardiac chambers, and assists with a differential dx
echo (tamponade)
-
if you suspect a pt has a tamponade, what can be used to get the direct measurement of intracardiac and intrapericardial pressures
cardiac cath
-
what is the tx for effusions
- mild: frequent observation with serial echos
- mod to severe: pericardiocentesis, definitive tx should it persist, is sx removal of part/all of the pericardium
-
what is the tx for a tamponade
- pericardiocentesis
- pericariotomy is recurrent
-
what are the etiologies of exudative effusion
- malignancy
- infectious/parainfections
- postpericardiotomy syndrome
- collagen vascular dz
-
what are the etiologies of transudative effusion
- radiation
- uremia
- hypothyroidism
- trauma
-
this is a serious physiological state that develops as a consequence of chronic inflammatory changes to the pericardium (fibrosis, thickening, adherence, calcification)
constrictive pericarditis
-
what is the MC etiology of constrictive pericarditis
idiopathic/post viral
-
this type of pericarditis impairs diastolic filling without impairment of systolic filling
constrictive pericarditis
-
when do abnormalities occur with constrictive pericarditis
diastole
-
what are s/s of constrictive pericarditis
- dyspnea
- fatigue
- HoTN
- tachycardia
- abd pain
- right failure sxs (ascites, hepatosplenomegaly, peripheral edema, JVD)
-
what will an ECG show on a pt with constrictive pericarditis
- non specific ST and T wave changes
- tachycardia common
- low voltage
- AFib
-
what is the essential diagnostic test for constrictive pericarditis
TTE
-
which diagnostic study is superior for assessment of pericardial anatomy and thickness
CT scan
-
what is the normal consideration for pericardial thickness
<2mm
-
which diagnostic study confirms elevation and equalization of diastolic pressures, shows a dip and plateau from ventricular tracings with a prominent "y" descent, and is necessary to distinguish between constrictive pericarditis and restrictive cardiomyopathy
cardiac cath
-
what is the tx for constrictive pericarditis
the ONLY effective tx of severe constrictive pericarditis is sx removal of the pericardium
-
what type of pulse with cardiac tamponade have that constrictive pericarditis will not have
pulsus paradoxus
-
what sign can be visualized on a pt that can help you differentiate between constrictive pericarditis and cardiac tamponade
kussmaul's sign
-
what characteristics will be present with a pt that has constrictive pericarditis but wont be present with a pt that has tamponade
- kussmauls sign
- pericardial knock
- HoTN (variable)
-
what characteristics will be present with a pt that has tamponade but wont be present in a pt with constrictive pericarditis
- pulses paradoxus
- HoTN (severe)
-
which phase is when rapid Na+ channels open (-85mv), slow Ca++ channels open (-40mv)
phase 0
-
which phase is when the Na+ channels close which causes the Na+ flux to cease (outflow rectifier K+ channels open transiently)
phase 1
-
which phase is when the K+ channels open, Ca++ influx continues (plateau phase--responsible for prolonging the cardiac action potential, making it longer than a nerve action potential)
phase 2
-
which phase is the repolarization phase where the Ca++ channels close, K+ outflow continues (delayed rectifier K+ channel)
phase 3
-
which phase is when K+ channels are closed, active transport of Na+ and K+ to return to resting state concentrations. (inward rectifier K+ channels)
phase 4
-
what is the pulse rate of the SA node
60 to 100 bpm
-
what is the pulse rate of the AV junction
40-60 bpm
-
what is the pulse rate of the purkinje system
20 to 40 bpm
-
what are the 2 issues that cause arrhythmias
- altered impulse formation
- altered impulse conduction
-
what can cause altered impulse formation
- altered normal automaticityincreased sinus node automaticity (sympathetic; PAC,PJC, PVC)
- decreased sinus node automaticity (parasympathetic)
- escape rhythms
- enhanced automaticity of latent pacemakers
- ectopic beats and rhythms
- abnormal automaticity
- triggered activity
early after depolarizations (torsades de pointes) - delayed after depolatizations (digoxin-toxic rhythms)
-
what can cause altered impulse conduction
- conduction block
- transient versus permanent
- unidirectional versus bidirectional
- functional versus fixed
- reentry (WPW, Afib, Aflutter, VFib, Vflutter)
- primarily unidirectional (fixed path)
- include accessory pathways (WPW)
- multidirectional (unstable path)
-
how can you recognize a SVT arrhythmia
- appears as a narrow complex
- may be regular or irregular
- rate depends upon underlying arrhythmia mechanism
- are there any discernible P waves
- sinus tachycardia
-
what is the most frequent cause of a compensatory pause
PAC
-
this rhythm is a macro-re-entrant atrial rhythm, typically occurs in pts with pre-existing heart disease, will have atrial structural abnormalities, PE dz, TR, TS, hyperthyroidism, alcoholism, percarditis
atrial flutter
-
what will an EKG show for a pt with atrial flutter
 - saw toothed pattern
- atrial rate up to 350variation in conduction at AV node
- 2:1, 3:1, 4:1
-
this arrhythmia has symptoms that are rate related, can be paroxysmal or permanent, increased thromboembolic events, can lead to high output heart failure
atrial flutter
-
how is atrial flutter managed
- rate control- through atrial flutter rate is difficult to control:
- - CCB (verapamil/diltiazem)
- - BBB
- - Digoxing
- rhythm control/conversion:
- - synchronized cardioversion preferred for unstable or stable (internal or external DC)
- - rapid atrial pacing
- - chemical cardioversion (ibutilide DOC)
-
what is the definitive treatment for a stable pt with AFlutter
EP intervention, radiofrequency cath ablation
-
this arrhythmia is chaotic, uncontrolled atrial contractions with similar etiologies to aflutter
 - AFIB
-
what are the etiologies of Afib
- VHD (MS, MR)
- coronary heart dz
- HTN heart dz
- lone A-Fib
-
what is the most common arrhythmia requiring treatment
AFIB
-
what are the clinical features of AFIB
- sxs are rate related (rapid ventricular rate)
- range from asymptomatic pts to disabling sxs
- paroxysmal or permanent
- absent "a" waves on JVP or monitoring
- NO S4 heart sounds
-
what will an EKG show on a pt with AFIB
 - no discernible P-waves, irregular RR intervals
- Irregularly irregular
- evaluate for rapid ventricular response
-
for AFIB, when will you know if a pt is unstable and how is it treated
- HoTN
- ongoing ischemia
- severe heart failure
- cerebrovascular event
cardioversion
-
for AFIB, when will you know if a pt is stable and how is it treated
H&P and diagnostics
determine underlying etiology and treat
-
what are the three major therapeutic strategies in managing AFIB
- prevention of stroke
- rate control
- rhythm control
-
what is the preferred management as an initial approach for the majority of older pts with AFIB
rate control
-
what is the approach the is usually pursed in younger pts (<60) with AFIB
rhythm control
-
what are the 2 ways that rate control manages AFIB
- Pharmacological therapy:influenced by underlying cardiac condition
- pharmacologically we block the AV node with BB, CCBs (verapamil or diltiazem)
- Dig is used with those with systolic HF
- Electrically:anticoagulation required prior if pt is stable
- 3 weeks prior and 4 weeks after to decrease stroke risk
-
if you have a pt with AFib and there is no structural heart dz, what meds can be used for rhythm control
flecainide or propafenone
-
how soon should AFIB be cardioverted
within 48 hrs
-
a pt who has severe clinical instability due to Afib is less likely to have been in Afib for more than how many hours
48 hrs
-
what should be given to a pt with Afib prior to cardioversion
heparin
-
for pts with AFIB, what are the stroke risk determinants
- C- CHF
- H- HTN
- A- Age >75
- D- DM
- S- stroke or TIA
- * CHAD worth 1 pt for each letter
- * S worth 2 pts
-
what class of medications are usually tried first in pts with AFIB
beta blockers
-
what is the most common type of paroxysmal SVT
AVNRT
-
this represents a self sustaining electrical circuit that repeatedly depolarizes a region of cardiac tissue, unidirectional block, slowed conduction through a loop tissue, and MOST COMMON cause of narrow QRS complex tachycardia
re-entry
-
what is the most common cause of narrow QRS complex tachycardia
re-entry paroxysmal SVT
-
which type of PSVT will show a PAC on the EKG
AVNRT
-
which type of PSVT will show a delta wave, short PR, prolonged QRS (orthodromic or antidromic) or a concealed pathway
AVRT
-
which type of disease is more commonly seen if a pt has a MAT arrhythmia
lung dz
-
this type of WPW is usually associated with the bundle of kent left side of the heart, impulse travels down the bundle of kent and back up the AV node, can give a wide complex tachycardia difficult to distinguish between VT
type A: antidromic
* can be very dangerous because the AV node no longer can pause the impulse
-
which type of WPW has impulse that travels down the AV node and back up through the bundle of kent
type B: orthodromic
* less dangerous because the AV nod still influences the physiological block
-
explain the adult tachycardia ACLS algorithm
-
how is unstable AVNRT treated
cardioversion or adenosine
-
how is stable AVNRT treated
vagal maneuvers then adenosine
-
how is antidromic AVRT PSVT treated
IV procainamide-- remember this rhythm can be a wide QRS and look like Vtach
-
how is orthodromic AVRT PSVT treated
vagal maneuvers, IV adenosine
-
if a pt has an EKG done and they have a WPW and the are unstable how are they treated
cardiovert
-
what is recommended for pts with symptomatic arrhythmias (WPW)
catheter ablation
-
how is a pt with attach (ectopic and MAT) treated
- treat underlying cause
- rate control: verapamil used in MAT and slows AV nodal conduction used in pts with bronchospasm/advance COPD otherwise use BB
- ablation: those that can't tolerate pharmacologic therpay
-
this is a cariac beat arising from the ventricle usually with a wide complex QRS reflecting the ventricular origin
PVC
-
if a pt complains of palpitations or "skipped beats" and you do an EKG, what may be a finding on the EKG
PVC
-
how are PVCs treated
- asymptomatic= benign neglect
- symptomatic without underlying disease= BB
- treat underlying cardiac dz
-
what does an EKG look like if a pt has VTach
- wide QRS complexes
- rate >120
- regular rhythm with slight irregularity
- RAD, even extreme RAD
-
this type of Vtach is an abberant conduction associated with alternating R-R interval, and has an underlying A-fib
ashmans phenomenon
-
what are some causes of Vtach
- superimposed cardiac insult, previous MI more like to have Vtach
- ischemia
- electrolyte disturbance
- drug/medication toxicity
- prolonged QT
-
how is asymptomatic and non-sustained Vtach treated
- diagnostic eval:
- - potential unrecognized cardiac dz
- - treat underlying dz
-
how is acute sustained unstable vtach treated
- ACLS, immediate synchronized cardioversion
- if pulseless-- DFIB
-
how is acute sustained stable vtach treated
- consider urgent or elective cardioversion
- procainamide or amiodarone
-
how is acute sustained vtach torsade treated
defibrillation
-
how can vtach be prevented
ICD
-
how is primary vtach treated
-
how is secondary vtach treated
-
this arrhythmia is a disordered, uncoordinated, ventricular contractions leading to a pulseless state with no effective cardiac output that is invariably fatal without treatment
Vfib
-
this arrhythmia is the most common rhythm leading to SCD
Vfib
-
what is the ACLS protocol for adult cardiac arrest
-
what are the 5 H's that are reversible causes of Vtach/VFib/PEA
- hypovolemia
- hypoxia
- H+ (acidosis)
- hypo/hyperkalemia
- hypothermia
-
what are the 5 T's that are reversible causes of Vtach/Vfib/PEA
- tension pneumothorax
- tamponade
- toxins
- thrombosis, pulmonary
- thrombosis, coronary
-
what is the ACLS protocol for bradycardia
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