heart Flashcards
acyanotic congenital heart disease
-Left-to-Right Shunt Lesions:
-Atrial Septal Defect (ASD)
-Ventricular Septal Defect (VSD)
-Atrioventricular Septal Defect (AV Canal)
-Patent Ductus Arteriosus (PDA)
-Qp:Qs > 1
ASD- atrial septal defect
-opening in the atrial septum permitting free communication of blood between the atria
-Seen in 10% of all CHD
-assoc with fetal alcohol syndrome
-3 major types:
-Secundum ASD – at the Fossa Ovalis, most common.
-Primum ASD – lower in position & is a form of ASVD, MV cleft -> 25% of down syndrome
-Sinus Venosus ASD – high in the atrial septum, associated w/partial anomalous venous return & the least common
ASD- SS
-Rarely presents with signs of CHF
-Most asymptomatic -> may have easy fatigability or mild growth failure.
-Cyanosis does not occur unless pulmonary HTN present
-Hyperactive precordium, RV heave, fixed widely split S2
-2-3/6 systolic ejection murmur @ LSB
-Mid-diastolic murmur heard over LLSB
-Systolic murmur is caused by increased FLOW across the pulmonary valve, NOT THE ASD
-Diastolic murmur is caused by increased flow across the tricuspid valve & this suggest high flow Qp:Qs is 2:1
-paradoxical embolism- DVT clot goes to brain instead of lungs
ASD: tx
-Surgical or catherization lab closure for secundum ASD w/ a Qp:Qs ratio >2:1.
-Closure is performed electively between ages 2-5 yrs to avoid late complications (wait for it to close on its own)
-amplatzer is used
-Surgical correction is done earlier in children w/ CHF or significant Pulm HTN
-Once pulmonary HTN w/ shunt reversal occurs this is considered too late.
-Mortality is < 1%.
-endocarditis prophylaxis NOT required for ASD
VSD- ventricular septal defect
-abnormal opening in ventricular septum
-allows free communication between RV and LV
-25% of CHD
-fetal alcohol syndrome and down syndrome
-pulmonary artery is the determinant of flow
-left to right shunt occurs secondary to pulmonary vascular resistance being < systemic vascular resistance -> NOT the higher pressure in LV
-leads to elevated RV & pulmonary pressures/volume -> hypertrophy of LA & LV
-if the pulmonary HTN develops the blood switch to R->L shunt -> eisenmenger!
-holosystolic murmur at the LLSB
-4 types:
-Perimembranous (or membranous) – MC
-Infundibular (subpulmonary or supracristal VSD) – involves the RV outflow tract.
-Muscular VSD – can be single or multiple.
-AVSD – inlet VSD, almost always involves AV valvular abnormalities
-fatigue, failure to thrive,
VSD- SS
-Small - moderate VSD, 3-6mm, are usually asymptomatic and 50% will close spontaneously by 2yo
-Moderate – large VSD, almost always have symptoms and will require surgical repair
-2-3/6 harsh holosystolic murmur heard along LLSB, more prominent with small VSD, maybe absent with a very Large VSD.
-Prominent P2, Diastolic murmur.
-CHF, FTT, Respiratory infections, exercise intolerance hyperactive precordium
-Symptoms develop 1-6mo
VSD- tx
-Small VSD - no surgical intervention, no physical restrictions, just reassurance -> periodic follow-up and endocarditis prophylaxis.
-Symptomatic VSD - Medical treatment initially with afterload reducers & diuretics
-Indications for Surgical Closure:
-Large VSD w/ medically uncontrolled symptomatology & continued FTT.
-Ages 6-12 mo w/ large VSD & Pulm. HTN
-Age > 24 mo w/ Qp:Qs ratio > 2:1.
-Supracristal VSD of any size, secondary to risk of developing AV insufficiency
-larger the VSD -> aortic annulus -> incompetency of aortic valve -> aortic insufficiency
atrioventricular septal defect- AVSD
-results from incomplete fusion of endocardial cushions, which form lower portion of atrial septum, membranous portion of ventricular septum and septal leaflets of triscupid and mitral valves.
-account for 4% OF ALL CHD
-downs syndrome (trisomy 21), seen in 20-25%
-COMPLETE FORM
-Low primum ASD continuous with a posterior VSD.
-Cleft in both septal leaflets of TV/MV.
-Results in a large L to R shunt at both levels.
-TR/MR, Pulm HTN w/ increase in PVR.
-INCOMPLETE FORM
-Any one of the components may be present.
-MC is primum ASD, cleft in the MV & small VSD.
-Hemodynamics are dependent on the lesions.
atrioventricular septal defect- SS
-Incomplete AVSD maybe indistinguishable from ASD - usually asymptomatic.
-CHF in infancy.
-Recurrent pulmonary infections.
-Failure to thrive.
-Exercise intolerance, easy fatigability.
-Late cyanosis from pulmonary vascular disease w/ R to L shunt -> cyanosis is indicative of blood not going through pulmonary circulation!
-Hyperactive precordium
-Normal or accentuated 1st hrt sound
-Wide, fixed splitting of S2
-Pulmonary systolic ejection murmur w/thrill
-Holosystolic murmur @ apex w/radiation to axilla
-Mid-diastolic rumbling murmur @ LSB
-Marked cardiac enlargement on CX-Ray
atrioventricular septal defect tx
-Surgery is always required.
-Treat congestive symptoms.
-Pulmonary banding maybe required in premature infants or infants < 5 kg.
-Correction is done during infancy to avoid irreversible pulmonary vascular disease.
-Mortality low w/incomplete 1-2% & as high as 5% with complete AVSD.
patent ductus arteriosus (PDA)
-Persistence of the normal fetal vessel that joins the PA to the Aorta.
-Normally closes in the 1st wk of life.
-10% of all CHD, seen in 10% of other congenital hrt lesions and can often play a critical role in some lesions.
-Female : Male ratio of 2:1
-Often associated w/ coarctation & VSD
-dx- pulse and BP differentials in lower and upper extremities
-TORCH infection PDA assoc with -> rubella
eisenmenger syndrome =
pulmonary HTN due to congenital heart defect
-once you get here its too late
PDA- hemodynamics
-As a result of higher aortic pressure, blood shunts L to R through the ductus from Aorta to PA.
-Extent of the shunt depends on size of the ductus & PVR:SVR.
-Small PDA, pressures in PA, RV, RA are normal
-Large PDA, PA pressures are equal to systemic pressures. In extreme cases 70% of CO is shunted through the ductus to pulmonary circulation.
-Leads to increased pulmonary vascular disease.
PDA- SS
-Small PDA’s are usually asymptomatic
-Large PDA’s can result in symptoms of CHF, growth restriction, FTT.
-Bounding arterial pulses
-Widened pulse pressure
-Enlarged heart, prominent apical impulse
-Classic continuous machinary systolic murmur
-Mid-diastolic murmur at the apex
-doppler echo - confirms
PDA- tx
-Indomethacin, inhibitor of prostaglandin synthesis can be used in premature infants -> if it doesnt close -> surgery
-PDA requires surgical or catheter closure.
-Closure is required treatment heart failure & to prevent pulmonary vascular disease.
-Usually done by ligation & division or intra vascular coil.
-Mortality is < 1%
obstructive heart lesions
-Pulmonary Stenosis.
-Aortic Stenosis.
-Coarctation of the Aorta.
pulmonary stenosis
-pulmonary valve or subpulmonary ventricular outflow tract
-7-10% of all CHD.
-Most cases are isolated lesions
-Maybe biscuspid or fusion of 2 or more leaflets.
-Can present w/or w/o an intact ventricular septum
-obstruction of pulmonary flow -> decrease valve SA, decrease flow from left side, decrease opening
-compensate with RV hypertrophy
-associated with Noonan’s syndrome, secondary to valve dysplasia (high hairline, triangular face, transparent wrinkled skin, prominent nasolabial folds)
pulmonary stenosis hemodynamics
-RV pressure hypertrophy -> RV failure.
-RV pressures maybe > systemic pressure.
-Post-stenotic dilation of main PA.
-W/intact septum & severe stenosis -> R-L shunt through PFO -> cyanosis.
-Cyanosis is indicative of Critical PS.
pulmonary stenosis - SS
-Depends on the severity of obstruction.
-Asymptomatic w/ mild PS < 30mmHg.
-Mod-severe: 30-60mmHg, > 60mmHg.
-Prominent jugular a-wave, RV lift.
-Split 2nd heart sound w/ a delay.
-Ejection click, followed by systolic murmur.
-Heart failure & cyanosis seen in severe cases
-higher the pressure in the ventricle the higher the resistance through the valve
pulmonary stenosis tx
-Mild PS no intervention required, close follow-up.
-Mod-severe – require relieve of stenosis.
-Balloon valvuloplasty, treatment of choice.
-Surgical valvotomy is also a consideration
-if critical keep the PFO open with prostaglandin E -> surgery
aortic stenosis
-at or near aortic valve
-causes systolic pressure gradient of > 10mmHg
-7% of CHD
-supravalvular stenosis is found in williams syndrome
-3 Types
-Valvular – MC
-Subvalvular(subaortic) – involves the left outflow tract.
-Supravalvular – involves the ascending aorta -> least common.
aortic stenosis hemodynamics
-Pressure hypertrophy of LV and LA
-staged based on valvular SA and pressures:
-Mild AS- 0-25mmHG
-Moderate AS- 25-50mmHg
-Severe AS- 50-75mmHg
-Critical AS- > 75mmHg
aortic stenosis: SS
-Mild AS may present with exercise intolerance, easy fatigabiltity, but usually asymptomatic.
-Moderate AS – Chest pain, dypsnea on exertion, dizziness & syncope.
-Severe AS – Weak pulses, left HF, Sudden Death.
-LV thrust at the Apex.
-Systolic thrill @ rt base/suprasternal notch.
-Ejection click, 3-4/6 systolic murmur @ RSB/LSB w/ radiation to the carotids.
aortic stenosis tx
-surgery does not offer a cure
-reserved for pts with sx and resting gradient of 60-80mmHg
-subaortic stenosis- reserved for gradients of 40-50mmHg bc rapidly progressive
-Balloon valvuloplasty- standard of tx for children
-Aortic insufficiency & re-stenosis is likely after surgery and may require valve replacement.
-Activity should not be restricted in Mild AS.
-Mod-severe AS -> no competitive sports
-AVR is standard for adults
coarctation of the aorta
-narrowing of the aorta at varying points
-anywhere from transverse arch to the iliac bifurcation
-before the PDA and after subclavian
-98% of coarctations are juxtaductal (@ PDA)
-Male: Female ratio 3:1.
-7 % of all CHD
-assoc with bicuspid aortic valve, seen in >70%!!!!
-seen in turners syndrome
coarctation of aorta dx
-post ductal MC
-initial test- BP
-doppler echo- confirmatory
-imaging:
-scalloping of inferior border of ribs due to enlargement of intercostal arteries for collateral supply
-“3” sign
-red arrows point to rib notching caused by the dilated intercostal arteries
-yellow arrow points to the aortic knob
-blue arrow to the actual coarctation
-green arrow to the post-stenotic dilation of the descending aorta
coarctation of aorta hemodynamics
-Obstruction of left ventricular outflow -> increases systemic peripheral resistance -> pressure hypertrophy of the LV
coarctation of aorta- SS
-diminution or absence of femoral pulses.
-Higher BP - upper extremities > lower extremities.
-90% have systolic HTN of the upper extremities
-tinnitus, epistaxis, HA
-Pulse discrepancy between rt & lt arms.
-With severe coarc -> LE hypoperfusion, acidosis, HF, and shock!
-Differential cyanosis if ductus is still open
-2/6 systolic ejection murmur @ LSB
-murmur on the back
-Cardiomegaly, rib notching on X-ray
coarctation of the aorta tx
-With severe coarctation maintaining the ductus with prostaglandin E is essential!!!
-Surgical intervention, to prevent LV dysfunction.
-balloon Angioplasty is used by some centers -> adults
-Re-coarctation can occur, balloon angioplasty is the procedure of choice.
Examination of a 3-hr old infant reveals
dysmorphic features and cyanosis. Both the occiput and facial profile are flat, and the fontanelle is abnormally enlarged. The space between the great and second toe is wide, and there is a palmar crease extending across the left palm. Room air oximetry reveals a saturation 70%.
Of the following, the MOST likely lesion to be found on echocardiography would be
Atrioventricular septal defect
Coarctation of the aorta
Hypoplastic left heart
Total anomalous pulmonary venous return
Truncus arteriosus
-AVSD assoc with down syndrome
-AVSD- cyanosis
-down syndrome- Flat occiput and facial profile, Wide space between the first and second toes: “Sandal gap” deformity, Single palmar crease, Enlarged fontanelle: delayed suture closure
truncus arteriosus
cyanosis
-part of the spectrum of conotruncal defects
-aorta and pulmonary trunk are combined
-22q11.2 deletion syndrome (DiGeorge syndrome)
After a few days of poor feeding and
tachypnea, a 3-week-old presents with
hypotension, poor central and peripheral
pulses, and severe metabolic acidosis. A
gallop is audible, and the heart appears
enlarged on chest radiography.
Hepatomegaly is marked.
Of the following, the BEST intervention to produce a sustained improvement is
100% Oxygen administration
Dopamine infusion
Gamma globulin infusion
Phenylephrine infusion
Prostaglandin E infusion
hepatojugular reflex
-coarctation of the aorta
Prostaglandin E1 (PGE1): To reopen or maintain ductal patency, restoring systemic perfusion.
A term infant is born with a large ventricular septal defect. At what age is the infant most likely to first demonstrate clinical findings of CHF?
2 days
2 weeks
2 months
6 months
12 months
-2 months
adult congenital heart disease etiology
-US: 1,000,000 adults with congenital heart disease.
-20,000 more patients reach adolescents yearly.
-Cardiologists must:
-Have detailed knowledge of congenital disease, both repaired and unrepaired.
-Clearly define each patients surgical and corrective procedures.
surgical shunts in CHD
surgical procedures in heart disease
adult congenital heart disease: types
-Atrial Septal Defect.
-Coarctation of Aorta.
-Tetralogy of Fallot.
-Transposition of Great Arteries.
-Common Ventricle/Fontan Procedure.
-Ebstien’s Anomaly.
-Eisenmenger Syndrome.
-Pregnancy.
atrial septal defect: adult
-1/1500 live births.
-Secundum 75%
-Primum 15%
-Sinus Venosus 10%
-Cor Sinus (rare)
-Secundum:
-MC Atrial congenital heart defect (6-10%).
-Right axis deviation from RV and RA enlargement
-Primum
-Associated with other endocardial cushion defects (cleft AV valves, inlet type VSD).
-Left axis deviation is hallmark
-Sinus Venosus:
-Large, associated with anomalous pulmonary venous drainage (usually R superior PV).
-Coronary sinus (rare):
-Associated with unroofed coronary sinus
ASD- clinical: adult
-Majority repaired in childhood but may present in adolescence/adulthood.
-Asymptomatic: Murmur, abnormal ECG/CXR
-Symptomatic:
-Dyspnea/CHF.
-CVA/emboli.
-Atrial Fibrillation.
auscultation in ASD: adult
-Increased flow across PV -> systolic ejection murmur and fixed splitting of S2 (in part due to delayed right bundle conduction)
-Increased flow across TV produces a diastolic rumble at the mid to lower right sternal border
-Older pt loses pulm ejection murmur as shunt becomes bidirectional.
-signs of pulm HTN/ CHF may predominate.
dyspnea =
heart disease
ASD- therapy: adult
-Percutaneous Closure:
-Only for secundum (contraindicated in others).
-Adequate superior/inferior rim around ASD.
-No R-L shunting.
-Surgical Closure.
-Good prognosis:
-Closure age < 25, PA pressure <40.
-If >25 or PA>40, decreased survival due to CHF, stroke, and afib.
coarctation of aorta: adult
-Narrowing in proximal descending aorta.
-May be long/tubular but MC discrete ridge
-after PDA (closed)
-Natural hx: poor prognosis if unrepaired.
-Aortic Aneurysm/dissection
-saccular (berry) aneurysms
-CHF
-Premature CAD
-claudication
-HTN due to decrease blood to kidneys -> RAS
coarctation of aorta: clinical: adult
-Most repaired, but adult presentation may be:
-HTN.
-Murmur (continuous or systolic murmur heard in back or SEM/ejection click of bicuspid AV).
-Weak/delayed LE pulses.
-Rib notching (3-9) on CXR pathognomonic -> posterior intercostals
coarctation repair: adult
-Surgical correction
-1) Patch aortoplasty with removal of segment and end to end anastomosis or
subclavian flap repair.
-2) bypass tube grafting around segment.
-Despite surgery -> morbidity/mortality -> average age 38.
-70% of repaired patients still go on to develop HTN, pathology not well understood.
-Recurrence in 8-54% of repairs -> can undergo repeat surgery or balloon angioplasty.
-Aortic Aneurysm/rupture may occur despite successful repair and correction of HTN (freq around anastomosis site on patch repair)
-survival after the repair decreases over time -> CAD
tetralogy of fallot
-4 features:
-VSD
-Overriding Aorta.
-Pulmonic Stenosis.
-RV hypertrophy
-Variability correlates with degree of RVOT obstruction and size/anatomy of PA
-MC cyanotic heart disease
-40yo 95% mortality
-assoc- chromosome 22 deletion and digeorge
-mild- L -> R
-severe- R -> L (if RVOT is higher pressure than LV -> VSD)
-dx- echo
tetralogy: surgical tx
-within 1st year of life
-Complete Repair:
-Severe RVOTO: PGE1 infusion until surgery
-Takedown of prior shunt (if done)
-Patch VSD
-Resection of subpulmonic obstruction.
-Transannular patch around pulm valve annulus (usually leads to severe PI).
-Systemic – Pulmonary Shunt:
-this is done if ^ surgery wasnt possible at first
-Blalock-Taussig- palliative- connects subclavian artery to pulmonary artery with a graft -> f/u for pulm artery stenosis and Pulm HTN!!
-Waterston (RPA).
-Potts (LPA).
-Prior pulmonary valve atresia or anomalous LAD may have had prosthetic or homograft conduit ± valve placed between RV and PA.
-Conduits can undergo endothelial overgrowth and obstruction of “pseudo RVOT” – can Rx with balloon angioplasty or operative conduit replacement
-Acute hypoxia (tet spells):
-oxygen.
-Knee to chest position, squatting
-IM morphine
-AVOID ACEi
intracardiac pacemaker placement following atrial switch procedure
-pacer wire must go to LV via SVC baffle
L type transposition
-Atrial-ventricular AND ventricular-arterial discordance.
-Physiologically correct, anatomically incorrect.
-“Congenitally corrected” transposition.
-RV is systemic ventricle, TV is systemic AV valve.
-Asymptomatic for many years, often into adulthood.
the fontan patient
-Any congenital anomaly with an effective “single” or “common” ventricle may lead to a Fontan procedure.
-Tricuspid Atresia – also any other form of right sided hypoplasia or atresia.
-Double Inlet LV.
-Hypoplastic Left Heart.
-Some variations of Double Outlet RV
-Staged Procedure:
-Basic concept is to provide systemic venous return directly to pulmonary artery and bypass ventricle.
-Systemic-pulm shunt to stabilize pulm blood flow.
-Bi-directional Glenn or hemi-Fontan procedure -> SVC flow directed to PA and sys-pulm shunt ligated.
-Finally, Fontan procedure with IVC directed to PA.
-Older Fontan: includes RA in circuit; newer methods bypass RA
switch procedure
-thrombocytopenia after surgery (mechanical)
The aorta and pulmonary arteries are cut off close to the base where they connect to the heart. The coronary arteries are also detached from the base of the aorta. 2) The aorta and coronary arteries are attached to the base of the original pulmonary artery. The pulmonary artery is moved in front of the new aorta. 3) The pulmonary artery is then attached to the base of the original aorta and holes from the removed coronary arteries are patched.
hypoplastic left heart syndrome
-several anomalies:
-coarctation of the aorta
-hypoplasia of LV
-aortic and mitral valve stenosis or atresia
-cyanotic defect
-right heart pumps blood to body through PDA
-closure of PDA results in hypotension, shock, and death
-need PDA and ASD to survive
-maintain hypoxemia with normalized CO2 levels
-“40-40 club”
-PO2-PCO2
-dx- echo
-chronic hypoxia -> tissue damage
ebsteins anomaly
-Atrialization of RV, sail-like Tricuspid valve -> sig tricuspid regurgitation
-extends into the RV
-RA hypertrophy
-50% ASD/PFO!
-50% ECG evidence of WPW
-RF- gestational lithium exposure
-Age at presentation varies from childhood -> adulthood and depends on factors such as severity of TR, Pulm Vascular resistance in newborn, and associated abnormalities such as ASD
-CXR of pt with ebstein anomaly
-massive cardiomegaly - box shape appearance
-due to right atrial enlargement
-right atrial hypertrophy
-right side megaly = rotational changes in heart of RV or RA hypertrophy
-left side megaly = LV hypertrophy
-flat LA = LA hypertrophy
-nike swoop on top left = normal
coronary anatomy
CABG
-Aim to restore flow from the aorta to the coronaries distal to obstruction.
-N.B.- CABG does NOT rid pt of dz/ dz process (CAD).
-Done using vascular “conduits” (veins, arteries) with distal anastomosis to coronary artery then proximal anastomosis to the aorta.
-Can be done with/ without the assistance of cardiopulmonary bypass (“on-pump” or “off-pump”)
-indication
High-grade left main stem coronary artery stenosis (>50%)
Significant stenosis (> 70%) of the proximal left anterior descending artery, with 2-vessel or 3-vessel disease
Symptomatic 2-vessel or 3-vessel disease
Disabling angina despite maximal medical therapy
-failed PCI
-multivessel ds + DM2
-On Pump vs. off pump.
-Controversial topic. OPCAB may decrease cognitive/ neurologic dysfunction, post op AF, bleeding, operative time, ?mortality.
-But surgeon skill set required. ?Decreased patency on beating heart? Difficult positioning for distals
-anastomose distal to occlusion
cardiopulmonary bypass
-CPB machine diverts blood from the IVC/SVC, oxygenates blood, back to the body via aorta.
-Advantages: Quiet, bloodless field, better distal anastomoses. Still the standard.
-Disadvantages: Increase time in surgery, pt must be heparinized then reversed, platelet dysfunction, complications can include hypoperfusion, fluid retention, CVA.
-has to be fully heparinized -> bleed risk
aortic valve stenosis (AS)
-Aortic Stenosis from thickening, caclification, +/or fusion of aortic leaflets causing LV outflow obstruction.
-Pressure overload of LV -> LVH, increased myocardial oxygen demand.
-Seen in younger pt’s w/ congenital bicuspid valves.
-Older pt’s with hx of rheumatic fever.
-Symptoms may include angina, syncope, or CHF each with worsening prognosis if untreated
-Dx: Echo +/- cardiac cath on PE systolic murmur (crescendo-decrescendo) 2nd right intercostal space.
-Surgery indicated if symptomatic or based on cross sectional area of valve and gradient across the valve
-LDH, LAH, wet lungs, edema, right ventricular failure
Aortic valve insufficiency (AI)
-Incompetence of the aortic valve, backflow causes LV dilatation, LVH
-bobbing of the head, bobbing of the uvula
-pistol shots over femoral artery
-water hammer, corrigans pulse
-Causes: Bacterial endocarditis, hx of rheumatic fever, aortic root dilatation, bicuspid valve predisposes.
-Diagnosis: Echo, cath, on PE “blowing”, decrescendo diastolic murmur L sternal border.
-Surgery indicated if symptomatic with severe AI, acute w/ heart failure, impaired LV fxn, persistent bacteremia/sepsis or annular abscess formation
-mechanical valve lasts longer - pig needs another repair in the future
-mechanical requires anticoagulation
root repair guidelines
-Positive aortic valve replacement or repair, concurrent repair of the aortic root or replacement of the ascending aorta is indicated if the aortic root and ascending aorta diameter is greater than 45 mm.
-Independent of the need for aortic valve replacement or repair, repair of the aortic root or replacement of the ascending aorta is indicated if the aortic root and ascending aorta diameter is greater than 50 mm or the rate of increase is ≥5 mm per year
AVR: choice of prosthesis
-Patients’ age is probably the most important factor in recommending tissue or mechanical valve.
-Bioprosthetic valves are ideally suitable for older patients (>70 years) or those who are not likely to outlive the valve (co-morbidities).
-Mechanical valves should be recommended to younger patients (<60 years).
-If anticoagulation is a perceivable problem, tissue valves can be used in younger patients but the probability of reoperation is high
TAVR
-indications- society of thoracic surgeons operative risk score >8% or at a >15% risk of mortality at 30 days)
TAVR presentation
mitral valve regurgitation (MR)
-Incompetence of the mitral valve from mitral prolapse, rheumatic fever, papillary muscle dysfxn (post MI), ruptured chordae, dilatation of the annulus.
-Diagnosis: Echo/cath. On PE holosystolic murmur from apex to axilla.
-Symptoms may include dyspnea, palpitations, fatigue. Late onset.
-Indication for surgery based on cath/ echo findings
-Surgical treatment: for degenerative MR, dilated annulus, flail leaflet mitral repair or ring annuloplasty possible. Otherwise Mitral replacement.
-biphasic P waves
-afib, enlargement of atrial appendage
aortic dissection types
-2 classification types:
-DeBakey Type I involves ascending and descending, Type II ascending, Type III descending.
-Stanford Type A involves ascending +/- descending (= DeBakey Types I & II) -> surgery
-Type B descending only (= DeBakey Type III) -> medical management
-esmolol, cardiazem, clevaprex
-hydralazine - increases sheer forces -> increase risk for aneurysm rupture
-Surgery indicated for Type A (I & II).
-Type B (III) can be managed medically (control of HTN) unless complicated- uncontrollable HTN, persistent pain, rupture.
aortic aneurysm
-Dilatation of the thoracic aorta usually from atherosclerosis.
-Many pt’s are asymptomatic, may have chest pain.
-Diagnosis: CXR, CT, MRI
-2x the lumen of the natural aorta
-Indications for surgery: symptoms, >5.5 cm in diameter, rapid increase in diameter (>0.5 cm per year).
-Surgery: replace with a graft. Ascending repair, Bentall (if root involved), hemiarch, arch, elephant trunk (2 stage arch/descending), descending
frozen elephant trunk
-replace it with a graft
-must perfuse the patient
seldinger technique
swan ganz catheter
