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Cardiology Cardiology Document Transcript

  • CARDIOLOGY<br />
    • General aspects
    • Blood pressure
    • Chest pain
    • Know that chest pain in healthy children is generally not cardiopulmonary in origin
    • Recognize the CV causes of chest pain
    • Pericarditis: substernal chest pain with a squeezing or tightening character, worse with movement and lying down; feels better if they lean forward
    • Arrhythmias: especially SVT; pain improves when the arrhythmia resolves
    • Aortic dissection: possible if kid with Marfan of Ehler-Danlos
    • Syncope
    • Understand that the description of a syncopal episode usually directs the evaluation
    • Neurocardiogenic syncope: most common form. Almost always benign.
    • Occurs most commonly while person is standing, especially for long periods of time, but can occur with emotional stress or noxious stimuli (like blood). Usually have a prodrome of dizziness, nausea, change in hearing and vision.
    • MUST get a good famhx to rule out potential familial syndromes (like long QT)
    • Syncope with exercise is almost always abnormal and needs further eval (see below)
    • Good place to start for dx work up is an EKG even if suspect neurocardiogenic
    • Cardiac causes of syncope would include heart block, prolonged QT, sinus node dysfxn and pre-excitation syndromes (WPW)
    • Know the importance of CV eval in pts with syncopal or pre-syncopal episodes with exercise
    • Needs a complete and thorough CV eval and pt must not exercise until eval completed and dx made
    • Can include hypertrophic cardiomyopathy, arrhythmias and anomalies of the coronary arteries
    • Family hx is especially important, but even if it is negative they still need a w/u by a cardiologist
    • Murmur
    • Recognize the qualities of innocent heart murmurs and provide appropriate counseling
    • Most innocent murmurs:
    • Early systolic ejection
    • Short duration
    • Low intensity (grade 1 or 2)
    • Vibratory or musical quality
    • Still murmur
    • SEM, musical/vibratory like a plucked string
    • Heard best at lower precordium and decreases with inspiration and standing (decreased venous return)
    • PPPS (physiologic peripheral pulmonic stenosis)
    • Soft systolic ejection murmur heard best in the axillae and both hemithoraces
    • Due to the acute take off angle of branch pulmonary arteries and usually resolves by age 12 months
    • Other innocent murmurs include basal ejection systolic murmur, supraclavicular arterial bruit, venous hum
    • Recognize that a child with an innocent murmur requires no further evaluation
    • CHF
    • Diagnosis
    • Recognize irritability, dyspnea during feeding, and decreased volume with each feeding as sx of CHF in infants
    • CHD is the most common reason for CHF in children, and it usually develops during infancy
    • Due to increased workload on the cardiac muscle usually caused by structural defects
    • Excessive volume load: large AV septal defect, large VSD
    • Excessive pressure load: aortic stenosis, coarctation
    • Excessive volume and pressure: large VSD with coarctation
    • Less commonly due to actual problems with the myocardial performance, which can arise fro an inflammatory or infectious process that directly affects the myocardium and affects its contractility
    • Recognize si and sx of CHF
    • See above and next
    • Identify the importance of physical findings (e.g. edema, hepatomegaly, JVD, cardiomegaly, gallop rhythm) in CHF in older kids
    • The PREP questions like to point out this gallop rhythm; it is due to diminished systolic and diastolic function of the LV
    • As LV dysfunction increases, the right heart becomes affected as the increased pressure from the LV is transmitted through the pulmonary vascular system and then to the right heart (increased pressure against which the RV must pump); R sided heart failure leads to these classis findings of the hepatomegaly, SOB, crackles (less commonly seen in kids that adults), JVD
    • In older kids a dilated cardiomyopathy is a dx to consider with presentation of new CHF; for boards purposes think of this when they mention the kid having a recent URI
    • Know how an imaging study of the chest may help dx CHF
    • Enlarged cardiac shadow due to LVH my be seen
    • Pulmonary vascular congestion, pulmonary edema, effusions
    • Understand the association between systemic AV malformation and CHF in a newborn
    • A systemic AV malformation is essentially an extracardiac LR shunt
    • Blood flows via the AVM to the venous return and thereby overwhelms the right heart and results in right sided HF with its associated si/sx
    • These AVMs are often in the liver or brain
    • A murmur heard over a fontanelle = AVM
    • Recognize common causes of CHF in infants and children
    • Understand the role of the pulmonary vascular bed in the presentation of CHF in infants with large LR shunts
    • As the pulmonary vascular bed resistance decreases during the initial days/weeks of life, and the pulmonary pressures drop below the systemic pressures, the L R shunting will increase and therefore the condition will worsen. The left heart faces a higher afterload, and therefore there is increased back pressure to the pulmonary vasculature, and when it has a lowered resistance, the increased pressure from the LV is transmitted against the pulm vasculature and then to the R heart
    • Signs of R heart failure become evident as this occurs
    • Management
    • Plan the tx of CHF
    • Diuresis, diuresis, diuresis
    • Even when it does not yield a significant improvement in sx, it can be useful in improving lung fxn preoperatively
    • Congenital Heart Disease
    • General
    • Recognize the increased risk and plan appropriate eval of CHD in a newborn with congenital anomalies (e.g. trisomy 21, 18, FAS, 22q11, 45XO)
    • Need to et an echo early on in order to look for any associated CHD
    • Cri du Chat = VSD
    • Turner = Bicuspid aortic valves, coarctation
    • Tri 21 = Endocardial cushion defect
    • Tri 18 = VSD
    • Tri 13 = VSD
    • Cardiogenic shock
    • Know that and EKG and echo should be part of the eval of a patient with possible cardiogenic shock
    • Cardiogenic shock can mimic sepsis, especially in infants
    • Since cardiogenic shock is so immediately critical and life threatening, need to rule it out as quickly as possible, therefore doing the EKG and echo early and fast is warranted
    • Other studies, like a CBC and blood cx, can wait per PREP, and LPs can make the condition worse
    • Know that cardiogenic shock may be the initial finding in a newborn infant with CHD
    • Recognize findings of cardiogenic shock in the newborn
    • Gallop rhythm, hepatomegaly, tachypnea, lethargy, dehydration later signs, which are c/w the actual shock, are tachycardia, hypotension, decreased pulses/perfusion at which point the shock has gone from compensated to uncompensated
    • Know the tx of cardiogenic shock in the newborn infant
    • Giving fluids will worsen cardiogenic shock because it causes worsening congestion in the pulmonary circuit and adds more volume load to the already failing/dilated LV
    • If fluids are given to a pt in cardiogenic shock, will likely see and increase in HR as the heart attempts to increase CO (but is unable to increase SV due to poor pump)
    • The treatment = inotropics (dopamine) to increase contractility and thereby increase SV and CO
    • DO NOT GIVE MORE FLUIDS AND DO NOT OBTAIN FURTHER DIAGNOSTIC TESTS; you need to save the baby.
    • Cyanotic Dz
    • Distinguish between central cyanosis and acrocyanosis
    • Acrocyanosis = transient bluish discoloration of the hands and feet in response to vasomotor instability or a cold environment. The perioral region can also be involved (spares the lips and mucous membranes), and the extremities may be cool on examination
    • Central cyanosis = due to deoxygenated blood or reduced hgb concentration (usually in the range of 4-6g/dL). Affected infants have bluish discoloration of the lips, tongue, mucous membranes, and occasionally nail beds. Cyanosis is usually clinically apparent when the O2 sat <70-80%
    • Causes = right to left shunt due to CHD or respiratory disease, hypoventilation, methemogobinemia
    • ID the clinical features of a tet spell
    • TOF =
    • RV outflow/pulmonary stenosis
    • VSD
    • Overriding aorta
    • RVH
    • Tet spell in an infant = distress, crying, inconsolability, hyperpnea, increased cyanosis, also during a tet spell, the murmur will be diminished or absent b/c the murmur is due to pulm stenosis (decreased volume or RH output therefore = decreased murmur)
    • Often occur in the morning or times of dehydration the spell is brought on by diminished pulmonary blood flow
    • Tx = increase pulm blood flow
    • Can be accomplished immediately by placing the patient in a knee to chest or a squatting position which will increase venous return and also increase systemic resistance
    • Increase in systemic resistance can also be accomplished pharmacologically
    • Know the cardiac causes of cyanosis in a newborn (cyanotic hours to days after birth)
    • TOF will present with cyanosis in the newborn period only when the pulmonary stenosis is severe and causes a significant RL shunt at the VSD
    • Transposition of Great Arteries (TAG) most common form of cyanotic heart disease to present in the first day after birth (overall is the second most common cyanotic heart disease, after TOF); the LV connects to the pulm artier and the RV connects to the aorta so that deoxygenated blood returning via the SVC into the RA enters the RV and then back out the aorta (not oxygenated). They can be profoundly cyanotic if there is no reliable method for mixing left and right sided blood (left sided/oxygenated blood into the right side via and ASD or VSD) These babies are often otherwise normal, healthy appearing babies
    • Tricuspid atresia (anatomy review: they do not have a tricuspid valve, therefore blood from the RA cannot get to the RV, and the only way it can get out of the RA would be through an ASD, taking blood from the RA to the LA to the LV; once in the LV the only way for blood to get oxygenated is via a left to right shunt across a VSD into the RV where it can then go to the lungs). The obligate right to left shunt of desaturated blood from the RA to the LA , then to the LV and then systemic causes the early cyanosis
    • Truncus Arteriosusoccurs when a single arterial outlet supports the coronary, systemic and pulmonary blood flow. Cyanosis occurs when the origins of the pulm arteries from the truncus are narrowed
    • Total Anomalous Pulm Venous Return usually lack a direct connection between the pulm veins and the LA; the pulm veins drain into the RA or into veins that eventually drain into the RA. There are three forms, depending on where the connection occurs. Supracardiac will drain into the left innominate vein and then into the SVC. Cardiac drain directly to the RA or coronary sinus. Infracardiac (subdiaphragmatic) go below the diaphragm, connect with the ductus venosus and then into the IVC. This third kind is most likely to have obstructed flow and therefore early cyanosis. Usually FTT and tachypnea are presenting signs, but if they have a severe obstruction, the cyanosis may be the presenting sign and pulm edema can develop rapidly
    • Recognize the absence of improvement in arterial oxygen content with 100% oxygen in comparison with room air is compatible with the dx of cyanotic CHD
    • Know the complications of polycythemia in a patient with CHD
    • Polycythemia leads to increased blood viscosity and can cause thrombotic events
    • If a pt has CHD that cannot be corrected, partial volume exchange transfusions may be necessary to maintain Hct <65% or lower depending on signs and symptoms of complications of polycythemia
    • Understand the prognosis for a patient with TOF
    • Surgical survival of >95%
    • Understand the prognosis for cognitive development in patients with cyanotic congenital heart dz
    • Most kids who’ve had cyanotic CHD, even after early repair, are likely to have some degree of cognitive impairment
    • Outcome is related to degree of pre-op hypoxia, intraoperative management (cardiac bypass time), and post op complications
    • If they have abnormal findings on neurologic exam they are more likely to have poorer school performance than kids with same lesions and no neurologic findings
    • If their lesions do not require surgical repair they are less likely to have poorer school performance
    • Kids with acyanotic heart disease are less likely to have poorer school performance than those with cyanotic heart disease
    • Know that relative anemia can be associated with a stroke in a patient with cyanotic CHD
    • Can be related to iron-deficient blood with decreased O2 carrying capacity as well as structural changes in the erythrocytes made under the iron-poor environment that can cause a higher viscosity despite the anemia
    • Know the immediate management of a child with a hypoxic episode
    • Best way to increase O2 delivery is through PRBC transfusion
    • Understand the role of ductus arteriosus in cyanotic CHD and the use of PGE-1 tx
    • Acyanotic heart disease
    • Recognize the major clinical findings in patients with cardiac anomalies such as VSD, ASD, PDA and aortic stenosis or pulmonic stenosis
    • ASD exercise intolerance due to left to right shunting, systolic murmur without a click (due to increased flow across the pulmonic valve, not due to flow through the ASD), fixed and split second heart sound due to increased time required for the dilated right ventricle to empty its contents
    • VSD usually a holosystolic murmur caused by the left to right shunt from LV to RV beginning with onset of systole. If small, the murmur may be high pitched and heard best along the sternal border. The second heart sound is normal.
    • This is the most common congenital heart defect
    • Majority close within one year
    • Symptoms would arise from increased strain on the RV due to increased volume/pressure as the systemic resistance increases and the LR shunt across the defect increases during the first few weeks of life, usually sx develop at about 4-8 weeks of age
    • PDAproduces a continuous machinery-like murmur that is usually loudest at the left infraclavicular area. If the opening is large there may be increased aortic pulse pressure and bounding pulses
    • Aortic stenosisis associated with a systolic ejection click and a murmur best heard at the RUSB with radiation to the neck. The findings do not change with position. An infant with severe congenital AS may present fairly early with the findings of the murmur, diminished perfusion and pulses, signs of pulmonary edema and also may appear to be in septic shock. If it does not present in newborn period it will present at some point in later infancy or childhood because the problem gets worse as the kid gets bigger and the stenosis becomes more critical and the LV wears out
    • Pulmonic stenosissystolic ejection murmur at the LUSB with an associated opening click, the murmur often radiates to the back and the axillae as the sound of turbulence flows through the branch pulmonary arteries. This is the second most common CHD after VSD. A critical stenosis can present shortly after birth because the RV cannot effectively pump against the stenotic valve. Cyanosis can be present due to right to left shunting at the level of the atria. They are ductal dependent in order for blood to get to the lungs, it has to traverse the PDA in order to enter the pulmonary artery; therefore they present as/when the duct is closing with severe cyanosis and cardiac collapse, but in general it is not a cyanotic lesion except in the critical newborn. The majority of affected children have no other associated sx but need to be monitored over time
    • Know the importance of PDA in the presentation of hypoplastic left heart syndrome and in coarctation of the aorta
    • In cases severe coarctation, keeping the PDA open can help relieve an acute aortic obstruction (since the coarctation is often due to a posterior shelf into the aorta that is created by the closure of the PDA due to a defect in the vessel media)
    • Note: clinically severe coarctation can mimic AS
    • Hypoplastic left heartan underdeveloped left heart is basically nonfunctional and so the RV must pump for both pulmonary and systemic blood delivery via the PDA. If the PDA is not kept open, then there is no way for blood to go systemic
    • Plan the initial management of a premature infant with PDA
    • Give IV indomethacin or ibuprofen-lysine in 3 successive doses.
    • If this does not close the PDA then may need surgical ligation.
    • Do not give the ibuprofen before you have echocardiographic confirmation of the PDA
    • Understand the immediate (e.g. referral) and long term (i.e. frequent BP measurements) management in a patient with coarctation
    • Because it can eventually cause left heart failure
    • Infectious and postinfectious diseases
    • Infective endocarditis
    • Know the indications for abx ppx in children with congenital heart lesions
    • Prosthetic cardiac valve or prosthetic material used for valve repair
    • Previous infective endocarditis
    • CHD:
    • Unrepaired cyanotic CHD, including palliative shunts and conduits
    • Completely repaired CHD with prosthetic material or device placed in the preceding 6 months
    • Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device
    • Cardiac transplant recipients who develop cardiac valvulopathy
    • Procedures that require ppx = any dental procedure that require extensive manipulation of the gingival or when perforation of the oral mucosa is likely; it is also reasonable to provide ppx for procedures involving the respiratory tract, infected skin, or musculoskeletal tissue; GI and GU tract procedures do not require ppx
    • Know the drugs of choice for the ppx of infective endocarditis
    • Oral amoxicillin (50mg/kg) can be given 30-60 mins prior to the procedure
    • If pcn allergic then clinda or cephalexin; if can’t do PO can do ampicillin, if can’t do PO and also pcn allergic then IV clinda
    • Know the clinical manifestations of infective endocarditis
    • Prolonged fever despite antibiotics, constitutional sx including anorexia, weight loss, malaise, night sweats, arthralgias, myalgias, splenomegaly, Janeway lesions, splinter hemorrhages, hematuria, glomerulonephritis, Roth spots in the eyes, Osler nodes
    • Cardiac manifestations include murmur, usually due to valvular insufficiency, possibly CHF
    • Know the management of infective endocarditis
    • Obtain blood cx from 3 to 5 sites prior to starting abx
    • 4-6 weeks of abx usually required
    • May need surgery if they develop CHF or severe regurg
    • Know the microbiology of infective endocarditis
    • Strep viridans (S. mitis and S. bovis) as well as staph aureus are the most common bacterial pathogens in kids
    • Enterococcus, coag neg staph, fungi and th HACEK organisms can also cause it
    • (HACEK = Haemophilus sp, Actinobacillus actinomycetemcomitants, cardiobacterium hominis, elkenella corrodens, kingella kingae) – these are gram negative oral and pharyngeal flora that are fastidious and slow growing and require special media to culture
    • Know the epidemiology of infective endocarditis, including risk factors
    • Know that a blood cx is the most important test for the dx of infective endocarditis
    • Get multiple cx before starting abx, do not need to wait until the pt is febrile as they are constantly bacteremic
    • Rheumatic fever
    • Identify the clinical manifestations of rheumatic fever
    • JONES CRITERIA
    • 5 major clinical manifestations
    • Carditis
    • Chorea
    • SubQ nodules
    • Polyarthritis
    • Erythema marginatum
    • Minor manifestations
    • Arthralgia
    • Increased ESR
    • Prolonged PR interval
    • Fever
    • Increased CRP
    • For dx must have 2 major or 1 major + 2 minor and evidence of recent or concurrent strep pyogenes infection (group A strep)
    • Know the lab findings of rheumatic fever
    • For dx there must be either a positive throat cx for GAS, or a positive rapid strep test, or elevated or rising ASO/strep antibody titer
    • Elevated ESR, CRP are minor diagnostic criteria
    • Identify the murmurs of mitral insufficiency and aortic insufficiency as the most common murmurs in rheumatic fever
    • Plan the initial management of acute rheumatic fever
    • Penicillin is always given in acute rheumatic fever (emycin if pcn allergic) then ppx begins immediately after acute tx
    • Salicylates and steroids for controlling acute sx (carditis and chorea)
    • The ppx management is continued for 5 years or until age 21; either a monthly pcn injection or BID pcn v-k
    • Myocarditis
    • Identify the major clinical manifestations of myocarditis
    • Suspected when there is a new murmur, sudden cardiac failure, arrhythmia or a combination of these
    • Signs may be subtle and may be just fever, fatigue and new murmur
    • Sx get worse as the myocardial function diminishes
    • PE findings of tachycardia, tachypnea, and a holosystolic murmur of mitral regurg, diminished pulse and perfusion, hepatomegaly
    • More common in infants and young children than older children, has a seasonal predilection (more in spring and summer)
    • Know the lab eval of myocarditis
    • Most common viral pathogen is coxsackie B, but many viral and bacterial pathogens have been implicated
    • Pericarditis
    • Know the etiologies and clinical manifestations of pericarditis
    • Etiologies = viral, bacterial, inflammatory, rheumatologic
    • Chest pain = substernal, positional (worse when laying down) and can be severe and worsen with deep inspiration, coughing, or movement of the upper torso. Pts usually prefer to sit up or lean forward
    • Pericardial effusion can develop and can lead to tamponade
    • Friction rub may be heard, but not always, and not hearing it does not rule out pericarditis or effusion
    • Know the lab eval of pericarditis
    • Viral titers, ASO titers may help determine the causative organism, also testing of the pericardial fluid if obtained
    • Echo is the most useful dx test
    • EKG might show tachycardia, elevated ST segments, decreased QRS voltages or electrical alternans
    • Know the microbiology of pericarditis
    • Bacterial causes include staph aureus (most common bacteria) as well as n. meningitides, h. flu, s. pneumo
    • Viral causes are often coxsackie A/B, echovirus, adenovirus
    • Rheum = collagen vascular disease, rheumatoid arthritis
    • Other = postpericardiotomy syndrome
    • Know the pathogenesis of pericarditis
    • Most often viral, less often bacterial (see above)
    • Know the tx of pericarditis, including the importance of surgical drainage
    • Pericardiocentesis is needed when there is evidence of large effusion or compromise of cardiac function (tamponade)
    • Anti-inflammatory agents are the key treatment, sometimes prednisone
    • If bacterial etiology may tx with abx
    • Kawasaki dz
    • Understand the proper use of echo in the eval and management of pts with KD
    • If pt meets dx criteria for KD then the echo is required in order to look for evidence of carditis
    • If it is an atypical case, then echo findings can help in confirming dx
    • Identify the cardiac complications of KD and the timing of onset; understand the prevention and treatment of the complications and the importance of follow up evaluation
    • About 50% of cases will show carditis by the end of the first week (acute phase)of sx, dilation (ectasia) may also appear at this phase
    • Coronary artery aneurysm usually appears at week 2-4 (subacute phase); its incidence is reduced greatly (from about 25% to 3% if pt is txed with IVIg during the acute phase)
    • Valvulitis and myocarditis can also occur
    • Rate and rhythm disorders, ischemia
    • Identify the clinical manifestations of common cardiac arrhythmias
    • Atrial arrhythmias = SVT, atrial ectopic tachycardia, atrial flutter, atrial fibrillation
    • Ventricular arrhythmias = ventricular tachycardia, ventricular fibrillation
    • Understand the clinical significance of a prolonged corrected QT
    • Can lead to ventricular dysrhythmias and sudden death
    • Using EKG patterns, identify PACs, PVCs, SVT and v tach
    • Understand the tx of SVT
    • SVT is the most common symptomatic dysrhythmia in kids.
    • Rapid, regular rate with narrow QRS (rate often nears 300BPM)
    • If relatively stable give IV adenosine
    • If unstable/crashing, they need immediate synchronized cardioversion
    • The boards don’t like you to try doing vagal maneuvers all that much
    • Systemic Disease affecting the heart
    • Know that hyperthyroidism should be considered in the eval of a pt with persistent sinus tachy
    • Likely will provide other clues about hyperthyroidism like weight loss, heat intolerance, etc, if this is a question they ask
    • Main thing, need to tell if it is sinus tachy or a dysrhythmia
    • Recognize that pts with Marfan syndrome may have associated cardiac dz that precludes participation in sports
    • Cardiac abnormalities can include dilation or aneurysm of arterial vessels, mitral valve dysplasia/prolapse/dysfxn, possible also to have same probs with tricuspid valve
    • Need to have their heart okayed before they can play or practice sports
    • Know the CV conditions associated with Turner syndrome
    • Bicuspid aortic valve and coarctation of the aorta
    • Recognize the si/sx of SVC syndrome
    • SVC obstruction can be due to
    • Extrinsic compression (i.e. tumor)
    • Intrinsic obstruction (i.e. clot, surgical anastomosis)
    • Abnormal hemodynamics due to elevated right atrial pressures
    • Have signs of superficial venous distention, venous congestion and facial and upper extremity swelling; as it progresses the jugular veins may become affected and there can be cerebral edema/seizures/death
    • Know the importance of CV evaluation when there is a fam hx of hypertrophic cardiomyopathy, MD, or Marfan
    • Hypertrophic cardiomyopathy is autosomal dominant inheritance, so if a parent has it all the kids need to be screened early and regularly as they have a 50% chance of inheriting it
    • MD – get cardiomyopathy
    • Marfan – see above
    • Identify the CV risk factors in kids and eval properly
    • Hyperlipidemia/chlesterolemia/triglyceridemia; these are familial and question often give clue about a parent with high cholesterol levels or an early ischemic event; need to screen the kids for same problem
    • If a parent has an early CV event then the kids should have an eval/screening