Cardiology Flashcards
Down Syndrome associated with
AV canal defects
Turner Syndrome associated with
Bicuspid Ao Valve
CoArc
Turners: nonpitting edema of LE, Webbed neck, widely spaced nipples
Williams Syndrome associated with
Supravalvular Aortic Stenosis
Can sound like pulm stenosis on exam - systolic ejection murmur along L sternal border
Rheumatic Fever Criteria
Recent GAS infection +
“JONES CAFE PAL”
- Joints - polyarthritis
- Carditis (valvular disease +/- myo or pericarditis)
- subcutaneous Nodules
- Erythema marginatum
- sydenham’s chorea (later, 2wk-2yrs)
C – CRP Increased
A – Arthralgia
F – Fever
E – Elevated ESR
P – Prolonged PR Interval
A – Anamesis of Rheumatism (hx of rheumatic fever)
L – Leukocytosis
2 MAJOR OR 1 Major and 2 Minor
With GAS infection or Antistreptolysin O Ab
Secondary prevention, after a first episode of rheumatic fever, is essential to prevent RHD or to stabilize the disease process in patients already affected. This requires continuous daily oral penicillin or penicillin injections every 3 or 4 weeks.
Digitalis toxicity symptoms
Digoxin: increases the force of contraction of the muscle of the heart by inhibiting the activity of an enzyme (ATPase) that controls movement of calcium, sodium, and potassium into heart muscle
Abd pain, nausea, vomiting
PVCs, inverted T waves, AV block
HyperK
Alteration in color vision
Tx: Digoxin specific Fab Ab
Postpericardiotomy Syndrome
Pericarditis/Pericardial Effusion days to weeks after open cardiac surgery. Inflammatory or immune mediated.
chest pain, cough, SOB, tachycardia, hypotension, muffled heart sounds, enlarged heart on CXR, EKG shows low voltages or electrical altercans
Endocarditis Prophylaxis: Indications and Tx
Indications:
- prosthetic valve
- unrepaired cyanotic CHD
- repaired cyanotic CHD within 6 months OR with residual defects
- previous hx endocarditis
- cardiac transplant who develop valvulopathy
NOT for like VSD, AS, or non-cyanotic lesions.
Dental, Oral, or Resp procedures that put you at risk for transient bacteremia.
NOT for GI or GU procedures.
Amox 2g 1 hour prior to procedure
(Keflex, Azithro, Clinda alternatives)
Truncus Arteriosus Murmur
Ejection click (opening of the single valve)
Single S2
+ VSD (Systolic ejection murmur)
What 2 conditions cause EXTREME left axis deviation on EKG?
Tricuspid atresia
AV canal defect
LAD without LV hypertrophy in these two conditions due to their effects on the conduction system’s orientation
SVC Syndrome Signs
Signs: facial and upper extremity swelling, jugular venous distention, and inability to increase cardiac output on demand due to decreased venous return (air hunger, dizziness, syncope)
Associated with anterior mediastinal masses: lymphoma, teratoma, thyroid carcinoma, and enlargement of the thymus. Or just enlarged lymph nodes.
Extreme caution should be taken prior to sedating, anesthetizing, or initiating positive- pressure ventilation as they cannot ventilate well
How to treat a hypercyanotic TET spell
TOF: Overriding Ao, VSD, Pulm Stenosis, RVH
Hypercyanotic spell - fever, crying - something causing vasodilation that reduces SVR.
Decreased SVR means that the shunt shifts from R->L across VSD and less pulmonary flow so you’re delivering cyanotic blood to the body
Tx:
- knee chest to increase SVR
- 100% O2
- IV fluid bolus
- morphine to calm baby and decrease hyperventilation
Presentation and Tx of a VSD
Presents ~4 wks of age when pulm vascular resistance falls and you have L->R shunting, which leads to volume overload, pulm edema, and CHF
Tx: diuresis to treat pulm edema (Furosemide)
O2 is BAD. May increase shunting L->R worsening pulmonary edema
How does pulmonary stenosis cause cyanosis?
As stenosis worsens, RV pressure then RA pressure increases. If you have PFO, then shunts from RA -> LA, causing systemic desaturation. That responds to O2.
Infective Endocarditis Symptoms
Presentation:
- subacute (over several weeks) or acute (rapidly progressive)
- fever, malaise, anorexia
- new murmur (new or changing)
- splenomegaly, embolic phenomenon
- petechiae
children only rarely have
- Roth spots (small retinal hemorrhages)
- Janeway lesions (small painless hemorrhagic lesions on the palms and soles)
- Osler nodes (small tender intradermal nodules on the fingers and toes)
- splinter hemorrhages (linear streaks beneath the nail beds)
Occurs in:
- children with underlying congenital heart disease, but it can occur in children with normal hearts.
- Central venous catheters also pose an increased risk for infective endocarditis.
Patho:
transient bacteremia from the oropharynx, gastrointestinal tract, or genitourinary tract. The bacteremia interacts with damaged cardiac endothelium, platelets, and fibrin resulting in an infected thrombus on the surface of the endothelium
Endocarditis Organisms
Viridans streptococci (strep mitis) = abnormal cardiac valves (congenital heart disease, rheumatic heart disease, postoperative changes)
Staphylococcus aureus = an otherwise structurally normal heart.
The AACEK organisms (Aggregatibacter parainfluenzae, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella species) are gram-negative organisms that cause infective endocarditis, although less commonly than the Streptococcus and Staphylococcus species.
Chart of Murmurs
file:///Users/vicky/Downloads/C59.pdf
Acrocyanosis vs Central cyanosis
Acrocyanosis
- normal finding in newborns
- due to slow flow of blood across an area with a large arteriovenous difference (hands, feet)
Central cyanosis
- lips, mucous membranes
> 5 /dL of deoxygenated blood; easier to see in higher hemoglobin concentrations (newborns)
Other normal newborn findings
- liver 1 cm below costal margin
- 2/6 low-pitched, MUSICAL, midsystolic ejection murmur at the lower left sternal border
Cardiac manifestations of hyperthyroidism
- tachycardia
- HTN with a wide pulse pressure (dec peripheral vascular resistance)
- palpitations
- rarely arrhythmias
Tx: Propranolol. Started at diagnosis and continued until methimazole takes effect
First line therapy for Graves disease
- methimazole as the first-line treatment. some may go into remission with drugs alone, so it’s first line.
- radioactive iodine therapy, and thyroidectomy.
How does cyanotic congenital heart disease increase your risk of stroke?
Polycythemia in the setting of chronic cyanosis increases the risk of a thromboembolic event.
Many patients with cyanotic congenital heart disease are treated prophylactically with aspirin, warfarin, or other anticoagulants to help prevent thromboembolic events
Other manifestations of congenital heart disease: Heart failure, arrhythmias, pulmonary hypertension, and neurologic, hepatic, and renal dysfunction are complications of cyanotic congenital heart disease.
To pass CCHD screening you need
Oxygen saturations should be greater than 95%, with no more than a 3% difference between preductal and postductal oxygen saturations (R hand and R foot).
Cardiomegaly and “wall to wall” heart on CXR
Ebstein Anomaly
- displacement of tricuspid valve to RV leading to atrialization of the RV -> massive RA enlargement and “wall to wall” or “box shaped” heart
“egg on a string” CXR
d-TGA due to anterior-posterior relationship of the great arteries
“boot shaped heart’ and decreased vascular markings
TOF
normal sized heart with decreased vascular markings
conditions that obstruct pulm blood flow
pulm stenosis
tricuspid atresia
snowman sign
supracardiac total anomalous pulm venous return
tx for prolonged QT
propranolol
Pneumomediastinum on auscultation
Harsh systolic crunching sound due to subQ air
Sx: chest pain (radiating to neck, back, shoulders), dyspnea, subq emphysema
Anorexics can develop what valvulopathy
mitral valve prolapse
What drugs cause drug induced SLE?
Procainamide and Hydralazine
Sx: fever, myalgia, arthralgia, pericarditis, pleuritis, hepatomegaly, splenomegaly
+ ANA
Rib Notching is associated with
CoArc
Rib notching: due to erosion of inferior part of rib due to dilated intercostal collateral vessels. usually doesn’t appear until child is school aged.
3 sign on CXR: L paramedistinal area shows prestenotic and poststenotic dilation
Rhabdomyolysis can do what to the heart?
Causes Hyperkalemia, leading to prolonged PR, bradycardia and heart block!! Need to give Ca gluconate
Adolescent abusing IV drugs leads to what valvulopathy
Endocarditis and Tricuspid Regurg
(systolic murmur at LLSB that radiate to the R)
Likely due to staph aureus
Tricuspid Regurg associated with what physical findings
systolic murmur at LLSB that radiate to the R
jugular venous distension
hepatomegaly and LE edema (RHF)
Marfans is associated with what cardiac abnormality
Aortic root dilation (which may lead to aneurysm or dissection)
MVP
Marfans - tall, increased U:L body segment ratio, scoliosis, lens dislocation, myopia
Vascular Ring Etiologies and appearance on barium enema
Anterior Filling Defect of Esophagus: Pulmonary Sling (LPA coming off of RPA instead of PA trunk)
Posterior Filling Defect:
Double Aortic Arch
R Aortic Arch with Abberrant L subclavian artery
How does venous return relate to MVP?
Inversely.
Decreasing venous return (standing) -> decreased LV preload -> more laxity of the chordae tendinae -> will prolapse earlier so the murmur is longer and click is earlier.
Increasing venous return (squatting), will decrease the prolapse aka murmur is shorter and click is later
HyperCa on EKG
shortened QTc and abrupt upstroke of T wave
PDA closure in a preterm neonate depends on…
Usually conservative management! Do not pharmacologically close the PDA if the patient is stable and resp status not worsening because it will likely close on its own.
The “normal” course for a PDA in a term neonate is closure within 72 hours of birth. In preterm neonates, this course is delayed, and the PDA remains open in 10% of neonates born at 30 to 37 weeks’ gestation, 80% born at 25 to 28 weeks’ gestation, and 90% born at 24 weeks’ gestation.
By 7 days after birth, these rates decline to 2%, 65%, and 87%, respectively. Data from controlled studies indicate that spontaneous closure of PDAs frequently occurs.
While individual studies and meta-analyses have demonstrated the ability to close a PDA, both medically and surgically, no study has shown that closing a PDA improves long-term outcomes.
When does CHD with L->R shunting present
Congenital heart disease with left to right shunting, such as ventricular septal defects, atrioventricular canal defects, and anomalous pulmonary venous return often manifest with heart failure at approximately 1-2 months of age.
What cardiac effect of fetal alcohol syndrome
VSD
Dysmorphic features of fetal alcohol syndrome: microcephaly, short palpebral fissures, long smooth philtrum, thin vermillion border, midface hypoplasia, ptosis, epicanthal folds, micrognathia
What is Tietze syndrome?
Differs from costochondritis in that it is associated with visible swelling, erythema, and warmth - and is usually the 2nd costochondral cartilage
Most common cyanotic heart defect manifesting in first few days of life
Transposition of the Great Arteries
For what condition is an atrial septostomy helpful?
Transposition of the Great Arteries - to facilitate mixing of blood
When do ASDs become symptomatic?
2nd decade of life - usually with exercise intolerance
S3 vs S4
Both in diastole
S3: can be normal, increased filling of dilated LV (passive filling phase of diastole)
S4: never normal, blood entering poorly compliant stiff LV during atrial contraction
PDA is associated with what maternal risk factor?
Rubella
Unrepaired TET is associated with what?
Brain abscess, cerebral thrombosis, endocarditis.
There is R->L shunt across VSD.
Noonan is associated with
Pulmonary Stenosis
Male with phenotypic features of Turner’s (45X girl) but normal karyotype
T wave morphology in children
Newborns have upright T waves for up to 7 days after birth.
T waves in the right precordial leads (V4R and V1) then become inverted.
T waves then generally return to upright in early adolescence. But they may remain inverted after this time, and it does not necessarily indicate heart disease.
What does an ASD do to the heart?
RVH
There is a clear rsR’ in V1
Tall R waves and virtually no S waves in the special right precordial leads, V3R and V4R.
The S waves in V5 and V6 are more prominent than normal.
VSD, PDA, CoArc result in left or right hypertrophy?
LVH
And tricuspid atresia = left axis deviation and left ventricular hypertrophy (since it must pump blood to both the pulmonary and systemic systems)
Treatment of long QT
Beta-blockers
Rhabdomyosarcoma is associated with
Tuberous Sclerosis (Ash leaf spots, shagreen patches, seizures, intellectual disability, intracranial calfications, tumors in various organs including heart)
Kawasaki is associated with what in the abdomen
Gallbladder hydrops
Mucocele (hydrops) of the gallbladder is a term denoting an overdistended gallbladder filled with mucoid or clear and watery content
Brugada syndrome
right bundle-branch block pattern and ST-segment elevation in leads V1–V3.
Peripheral pulmonic stenosis vs stills murmur
PPS
- grade 2/6 systolic murmur heard best at the left upper sternal border, radiating to the right upper sternal border and into the posterior lung fields and axillae. The murmur is caused by turbulent flow at the acute angular origin of the relatively small-branch pulmonary arteries as they exit from the larger main pulmonary artery.
- usually resolves by 6 months
Stills
- musical-like” grade 2/6 midsystolic murmur heard best at the left lower sternal border and apex and is believed to be caused by blood flow in the left ventricle leading to vibrations in the left ventricular outflow tract and aorta.
It is most common among toddlers and young school-age children.
Neurocardiogenic (Vasovagal syncope) tx
Fludrocortisone - increases blood volume.
Can be diagnosed with tilt table test if history is unclear
ASD vs pulm stenosis
Both will have RVH but ASD = rSR pattern (volume overload) and PS = QR pattern.
ASD also has wide fixed split S2 and slightly prolonged QRS
Causes of sudden cardiac death/arrest:
HOCM
- most common cause of sudden death on athletic field
- AD inheritance, family hx of sudden death
- feels sx of decreased cardiac output prior to event like SOB/chest pain
Anomalous coronary artery
- 2nd most common cause
- also have preceding sx of SOB, chest pain, may also have syncope episodes
- no family hx
Prolonged QT
- not as common. does cause syncope with exercise
- AD inheritance
- seizure like events with ventr arrhythmias
- congenital deafness
Endocarditis: DUKE criteria
2 major
1 major and 3 minor
5 minor
Major:
- two positive BCx for orgs likely to cause IE (viridans, staph), or persistently positive BCx with less common orgs
- echo findings
- new murmur on exam
Minor:
- fever
- blood cultures not meeting major crtieria
- underlying heart disease
- IVDU
- vasculitis or immune effects like glomerulonephritis
HOCM vs AS
HOCM
- increases with valsalva (decreased preload)
AS:
- decreases with valsalva
