Transcript 77-year old male with a chief complaint of urinary intermittency

39 week/M by PA
with note of
occasional arrhythmia
NICU Rotation SGD . 07 January 2009
Interns Belandres, Bombase, D. Chan, Chu, Francisco
Circumstances of Delivery
Born
 Full Term 37 1/7 weeks by LMP
 39 weeks by PA
 2500g AGA
Cephalic via primary LSCS due to
NRFS
PRENATAL: Maternal Profile
 (+) 9 x PNCU’s c/o a midwife’s
clinic
 (-) cough/colds, HTN, BA, PTB,
DM/GDM, PROM, alcohol
intake, hep B, drugs, smoking
Course of Labor, Resuscitation
 14 hours PTC, (+) watery vaginal d/c with
irregular mild uterine contractions. On
admission, FHT noted to be 124/min,
regularly irregular.
 On delivery, thermoregulation, suctioning,
tactile stimulation done/given
 (-) meconium staining
Resuscitation
 Further thermoregulation, suctioning,
tactile stimulation done/given; 30 secs
  Good cry, tone and color noted. 
HR 130s, RR 40, Apgar 9.
 4 mins supportive care
  HR 130s, RR 40. Apgar 9.
Occasional arrhythmia noted.
  O2 sats taken: 98-99%
Post-natal course
 Roomed-in, monitored
  Persistent arrhythmia noted
 Admitted to NICU 2
Course in the NICU
Day 1
 Was received awake, active, comfortable, HR
122-134 irregular, RR 50-60, O2Sat 98%.
 AP, DHS, (-) murmurs, good pulses
 hooked to cardiac monitor
 (+) occ’l PVC’s noted
 thermoregulation done, feeding with EBM started,
3xBM noted, good UO
 A>> r/o CHD, PDA
Course in the NICU
Day 2
 Feeding increased
 (-) murmurs on auscultation
 Good cry, activity
Day 3-5
 (-) PVC’s on monitor
 (-) murmurs
 good cry/activity.
Course in the NICU
Day 6
 still (-) PVC’s
 15-L ECG done>> (N)
 good suck noted
 sent home
Discharge PE
 pink conjunctivate, anicteric sclerae, (-)
molding/caput, anterior fontanelle open and soft,
(-) overlap of sutures, (-) anterior neck mass, (-)
CLAD, head circumference 33cm
 equal chest expansion, (-) alar flaring, (-)
retractions, clear breath sounds, chest
circumference 31.4cm
 adynamic precordium, (-) heaves/thrills, normal
rate/regular rhythm, (-) murmurs appreciated
Discharge PE
 slightly globular soft abdomen, nonpalpable liver
edge, (-) masses, umbilical cord stump clean and
dry
 penile shaft straight, testes (B) descended
 peripheral pulses full and equal, pink color, skin
with good moisture and turgor,
patent
DUCTUS
arteriosus
the ductus arteriosus
 shunts right ventricular outflow to the distal
aorta
 facilitating bypass of the lungs by 90% of the
outflow; lung arterial circulation is still
vasoconstricted
 perfuses lower part of the fetal body
 (upper part, including coronaries and cerebral
perfused by LV output)
 Effectively a RL shunt
 * If RV output (flow to the lungs) is compromised by
other (congenital) heart disease, can be a critical,
essential shunt
the ductus arteriosus
 Effectively a RL shunt
 * If RV output (flow to the lungs) is compromised by
other (congenital) heart disease, can be a critical,
essential shunt
 Medial layer with circularly arranged smooth
muscle
 Patency = low oxygen tension +
endogenously produced prostaglandins
 (maternal NSAID use can close it during fetal life
and compromise fetal CV function)
 bifurcation of
the pulmonary
artery 
aorta just distal to
the left subclavian
artery
closure of the ductus
 At birth, changes in pressure gradient favors RV
output  lungs
 Pulmonary vascular pressure DEcreases with lung
expansion
 Systemic vascular resistance INcreases with loss of
placental circulation (which is low resistance)
 (systemic > pulmonary)
 Flow in the ductus becomes L  R
 High arterial PO2 constricts the ductus  closes
over days
closure of the ductus
 Functionally complete in
 ½ of neonates by the 24th hour of
life (10th to 18th hour)
 100% by the 4th day of life
PATENT ductus arteriosus
note again…
 Medial layer with circularly arranged smooth muscle
 Patency = low oxygen tension + endogenously
produced prostaglandins
 PERSISTENT PATENCY
 … in term infants: deficient muscular and
endothelial layers
 Persistence beyond 4 days usually will be unresponsive
to pharmacologic therapy
 … in PRE term infants: hypoxia and immaturity
Risk Factors
Infant
 Prematurity
 Chromosomal abnormalities (Down)
 Females : Males 2:1
 Hypoxia
 Asphyxia
 Coexistence with other congenital heart diseases (facilitates
survival)
 Right side outflow stenosis or atresia (TOF, Tricuspid or Pulmonary
atresia)
 Aortic coarctation
 TGA or TAPVR
 RDS/surfactant therapy
Maternal
 Rubella infection early in the pregnancy
Pathophysiology
 Consequences of a L to R shunt
 Hypoxia and Congestive Heart Failure
 Later in life, increase in pulmonary pressure
 pulmonary hypertension
 scarring and poor O2 exchange
 increasing pressure of R side/circulation
 R to L shunt
= Eisenmengerization
 Severity, significance related to size and ratio of
pulmonary : systemic vascular resistance
 Smaller and lower ratio = less
Signs and Symptoms
 Patient may be cyanotic, with bounding peripheral
pulses and wide pulse pressure
 in diastole, blood runs off  pulmonary artery
 Murmur
 “machinery,” “rolling thunder”
 after onset of 1st sound  wanes in late diastole
 2nd L ICS, sternal border, infraclavicular areas
 Increases and becomes more continuous with decreasing
pulmonary vascular resistance
 With increasing PVR, diastolic component wanes
 Heart Size / Dynamic Precordium / Heaves
 Increasing, with increasing PDA size
 2nd L interspace thrill radiating to the L clavicle
Diagnostics
 ECG
 NORMAL with small LR shunt
 LVH, Bi-VH if large
 CXR
 pulmonary artery prominence
 Increasing cardiac size with greater LR shunting
 2D Echo
 larger LA and LV dimensions
 Retrograde turbulent flow in the PA on doppler,
 as well as retrograde flow in the aortic during diastole
 Visualization on Cardiac Catheterization
Therapeutics
 MEDICAL
 Prostaglandin inhibition (10-14 days of life, more for
premature infants), intravenous agents
 Indomethacin 0.1 to 0.25 mg/kg q12 for 3 doses
 or Ibuprofen 10 mg/kg IV for first dose, then 5 mg/kg IV for
second and third doses after 24 and 48 h, respectively
 Fluid restriction
 theoretically, to decrease fluid conveyed by the shunt and
the load on the pulmonary circulation
 evidence not fully supportive
 Optimum oxygenation (support)
Therapeutics
 CARDIAC CATHETERIZATION
 Occlusion with coils (2.5-3mm)
 Even partial occlusion can lead to closure 
thrombus formation further reduces the shunt
 SURGICAL
 Ligation; approach: thoracotomy
 I: Congestive heart failure, failure of medical
therapy (note also risk of bacterial endocarditis)
 Low-risk, but complications involve nerve and
vessel ligations
thank you.