Pulmonary blood flow
Download
Report
Transcript Pulmonary blood flow
Catherine Bull M.S.N, P.N.P-C
Clinical Coordinator, Pediatric and Adult Congenital Cardiac Surgical Services
Department of Cardiothoracic Surgery
NYU Medical Center
Qs
Qp
Pulmonary blood flow
Systemic blood flow
~ 1 cup
~ 1 cup
Qp:Qs ratio is the amount of blood going to the lungs
compared to the amount of blood going to the body.
Qp : Qs
(LUNGS : BODY)
Qp : Qs
1:1
Blood flow to the body or the lungs is not 100%
ductal dependent
Transposition of the
Great Arteries
Total Anomalous Venous return
Truncus Arteriosus
NORMAL
TGA :
Aorta arises from
the anatomic RV
PA arises from the
anatomical LV
•
•
Parallel circulations
Mixing can occur at
PFO, PDA or VSD
• Most mixing occurs at
the PFO
•
Without a mixing:
– cyanosis, hypercarbia,
tachypnea, tachycardia
and acidosis may occur
n
NORMAL
To increase
SaO2 you
must increase
mixing:
PGE to open
duct
BAS
Volume
Oxygen
PDA
PFO
Arterial Switch
The aorta and the PA are
transected and the
coronary arteries are
removed.
The aorta and the
coronary arteries and
attached to the neoaortic
root
PA is attached to the
neopulmonary root
Decreased LV function
Coronary ischemia
Nitroglycerine/Heparin
▪ Usually a surgical problem
In older patients with IVS whose LV only exposed
to pulmonary pressures pre-operatively
Decreased cardiac output
Arrhythmias
Failure of pulmonary veins to
connect to the to the LA
Blood from both the systemic
and pulmonary venous
systems return to the RA
the RA, RV & pulmonary arteries
enlarge to compensate for the
increased volume
An ASD is essential for CO and
always present
NORMAL
NORMAL
Supracardiac: pulmonary veins attach to SVC.
NORMAL
Cardiac: pulmonary veins attach directly to the
heart via RA or coronary sinus
NORMAL
Infracardiac: pulmonary veins attach below the
diaphragm. Prone to obstruction.
Supracardiac
•
Unobstructed:
– May be asymptomatic at first
– CHF, FTT & frequent upper
respiratory infections will occur
•
Obstructed:
― Profound cyanosis within the
first few hours of life
― Typical “ground glass” CXR
― No PGE
― Surgical Emergency
Infracardiac
CXR:
Typical “ground
glass” appearance
of lung fields
Small heart
Attach pulmonary vein
confluence to
posterior LA and
close the ASD
Ligate the vertical vein
•Create a large ASD
and baffle veins from
the RA to LA
Unroof coronary
sinus and baffle
pulmonary venous
return to the LA
•Attach pulmonary vein
confluence to posterior
LA
•Ligate the vertical vein
•Close the ASD
Low cardiac output:
Noncompliant LV. Treated w/ inotropes.
Avoid aggressive volume overload-unresolved LA
hypertension & PHTN.
PHTN:
r/o pulmonary venous obstruction. Ventilation, O2, NO &
sedation to decrease PVR.
Respiratory failure:
Due to obstructed veins preop and resultant pulmonary
vascular congestion.
Treated with mechanical ventilation, paralysis, sedation,
PEEP & possibly ECMO.
Re obstruction
occurs in 10% of patients-usually obstructed infracardiac
type
NORMAL
CHF, mild cyanosis &
FFT within the first
month of life.
Can develop
pulmonary
hypertension by 3
months.
The pulmonary arteries
are excised from the
truncus
RV to PA conduit placed
VSD is closed in a manner
in which the truncal valve
recieves blood from the
left ventricle
PHTN:
preop overcirculation results in PA pressures=>Paralyze,
sedate, O2 and NO.
Low CO:
RV dysfunction=> volume (need a high CVP), inotropes &
vasodilators.
Cyanosis:
RL PFO =>will resolve with RV function.
Pulmonary blood flow is ductal dependant
Regular
Pulmonary Atresia
Real Pulmonary Atresia
Te t r a l o g y o f F a l l o t
Pulmonary
Atresia
w/ Intact
Ventricular
Septum
Pulmonary Atresia
w/ MAPCA’s
Tricuspid
Atresia
TOF is characterized by 4
cardiac anomalies:
Ventricular septal defect
Pulmonary stenosis or
pulmonary atresia/right
ventricular outflow tract
obstruction (RVOTO)
Overriding aorta
Right ventricular
hypertrophy
NORMAL
Hemodynamics depends on the amount of PS and
the size of the VSD
Severe PS:
Cyanotic
▪ RL shunt
▪ Qp<Qs
Mild PS:
▪ LR shunt
▪ Qp>Qs
▪ CHF
Pink Tet
Patch closure of VSD
Relieve RVOTO
Resect muscle below the
valve
Enlarge the pulmonary
artery above the valve
OR
transannular patch with
removal of valve
•
•
•
•
•
RV dysfunction
– Inotropes
– May have pleural effusions (esp. right) and ascites
Junctional Eptopic Tachycardia
– PREVENTION
– keep HR low with cooling, no chronotropic drugs, sedation
– Amiodarone
Cyanosis
– due to right to left shunt across PFO if present
Pulmonary insufficiency
– all patients with transannular patch
Residual VSD
– not well tolerated
•
Residual RVOTO
– well tolerated
Pulmonary valve &
main pulmonary artery
are atretic
Pulmonary blood flow
is supplied by
TOF/PA
PDA (most common)
multiple
aortopulmonary
collateral arteries
(MAPCAs)
TOF/PA w/ MAPAC’s
Blalock-Taussig
Shunt followed
by full repair
later in infancy
Pulmonary valve atresia with
no VSD
Hypoplastic RV (Variable)
Size of the RV is determined by
the size of the TV
High RV pressure
RV sinusoids (Variable)
May form due to high RV
pressure.
Steal coronary blood flow from
CA
NORMAL
RV Sinusoids
Need to do 2 things: establish pulmonary
blood flow and get the RV to grow
Pulmonary valve balloon angioplasty
▪ Works best when the leaflets of valve are only fused
BTS
Transannular patch
2 Ventricle Repair (Adequate RV without sinusoids)
Balloon angioplasty
+/- BTS
1 ½ Ventricle Repair (Borderline RV +/-sinusoids)
+/- Balloon angioplasty
BTS
+/- Transannular patch
Single Ventricle Repair (Inadequate RV +/- sinusoids)
BTS
Borderline RV +/-sinusoids:
BTS & transannular patch to
allow pulmonary
insufficiency and
subsequent RV growth.
▪ Adequate RV growth: complete
repair
▪ Inadequate RV growth:
Bidirectional Glenn procedure
(1 ½ ventricle repair)
NORMAL
The tricuspid valve is
absent w/ no
communication
between the RA and RV
Results in RV and PA
hypoplasia and a single
left ventricle
No VSD, PA, hypoplastic RV
Pulmonary blood flow is ductal dependant
Small VSD, hypoplastic PV, hypoplastic RV
(most common)
Pulmonary blood flow is ductal dependant
Large VSD, small to adequate PV & RV
Qp:Qs is variable
Cyanosis, hypoxemia and metabolic acidosis
usually occur within the first few days of life if
pulmonary blood flow is not adequate and the
PDA closes. Qp<Qs
Management strategies should be aimed at
balancing pulmonary and systemic blood flow
to maintain Qp=Qs.
Blalock Taussig
Shunt
Pallative shunt
between the right
innominate artery
and the RPA that
provides pulmonary
blood flow.
Variable Qp:Qs
Blood flow to the body is ductal dependant
Coarctation of the Aorta
Interrupted Aortic Arch
Hypoplastic Left
Heart Syndrome
NORMAL
Systemic blood flow is ductal
dependant
Blood to the upper body comes
from the LV & aorta: pre-ductal
sats are higher
Blood to the lower part of the
body comes from the PA and
PDA: post-ductal sats are lower
Decreased peripheral perfusion &
metabolic acidosis if duct closes
Type A= away
Type B
Type C= close
End-to-end anastomosis w/
PDA ligation
Pulmonary
hypertension
Issues related to
DiGeorge Syndrome
Recurrent laryngeal
nerve palsy
Pherenic nerve damage
Recurrent stenosis at
site of repair
Underdevelopment of
the left side of the heart
due to:
1.
2.
3.
4.
Mitral stenosis/atresia
Aortic stenosis/atresia
Hypoplastic left ventricle
Hypoplastic aortic arch
100% of systemic blood
flow is ductal dependent
NORMAL
NORMAL
The amount of blood flow
to the pulmonary and
systemic circulations
depends on the relationship
between SVR & PVR
As PVR falls blood will
naturally go to the lungs &
away from the body
•
1st few days of life: well appearing baby
(Qp=Qs) Sat 80%
Pink and warm
•
As the ductus closes blood flows into the lungs
resulting in CHF and decreased cardiac output.
(Qp>Qs 3:1) Sat >90%
– Ashen, tachypeanic, cool, difficulty feeding
•
There is progressive deterioration resulting in
pulmonary edema and cardiogenic shock.
(Qp>>Qs 5:1)
– Metabolic acidosis, cold & gray
Prevent the natural progression
Lower the systemic vascular resistance
Give extra circulating blood volume
The sick neonate requires aggressive
intervention
Goal is to re-establish systemic perfusion (Qp:Qs=1)
and provide blood flow to the systemic organs
▪ Lower the systemic vascular resistance
▪ Give extra circulating blood volume
1. Creation of
Neoaorta
2. Oversew
MPA
3. Atrial
septectomy
4. BTS/Sano
BT Shunt
Sano Shunt
Patient Management
Systemic blood flow is grossly indicated
by Lactate and BE/BD on ABG.
BD < -2 or Lactate > 2 indicates metabolic
acidosis and too little systemic blood flow.
BE > 0 or Lactate < 2 indicates adequate
systemic blood flow.
Pulmonary blood flow is indicated by
PaO2 on ABG.
PaO2 > 50 indicates too much PBF
PaO2 < 30 indicates too little PBF
O2 Sats = pulmonary blood flow
(gross measurement)
O2 Sat 80%= Qp:Qs of 1:1
Sats > 90%: too much pulmonary blood flow
Sats < 75%: too little pulmonary blood flow
O2 Sats in patients with single ventricle
physiology tell you how much blood is
going to the lungs-not necessarily how
well the lungs are working.
(ABG sat)
(VBG sat)
Ao Sat
SVO2
Qp/Qs= 80% 100% -
60% =20 =1
80% 20 1
PV sat
PA sat
(Assumed)
(ABG sat)
Not enough cardiac output
Sats>90%
Poor peripheral perfusion
Cool extremities
Tachypnea
Diaphoresis
Poor weight gain
“Norwood gray”
Too little pulmonary blood flow
Sats < 75%
Bounding pulses
Cyanotic with good perfusion
“Blue is better than gray!”
What affects Qp:Qs?
Systemic vascular resistance
(SVR)
Pulmonary vascular resistance
(PVR)
Always Remember BLOOD FLOWS THE
PATH OF LEAST RESISTANCE
•
Too little cardiac output
Lactate > 2.5, Sats>90%, PaO2 > 50
•
decrease the SVR or increase PVR
Too little pulmonary blood flow
Sats<75%, PaO2 < 30
decrease the PVR or fill the tank
*be very careful of increasing SVR in patients with
single ventricle physiology— DON’T DO IT!
The easiest way to increase CO is to
vasodilate the patient
Other ways to manipulate PVR & SVR
Temperature
FiO2
Ventilator changes
Sedation
Factors that PVR
Factors that PVR
Hypoxia PaO2 (NITROGEN)
Hypoventilation PaCO2
Hypothermia
Agitation
Hyperoxia PaO2 (OXYGEN)
Hyperventilation PaCO2
Normothermia
Analgesics
Factors that SVR
Hypothermia
Agitation
Catecholamines (high dose dopa,
epi)
NO
**Factor that SVR**
Normothermia
Analgesics/sedation
Vasodilators (Milrinone)
In all post-op patients w/ single
ventricle physiology you MUST do
two things ….
1. Ask yourself “is the patient warm, well
perfused and non-acidotic?”
If so then STOP and revaluate whatever you
where going to do next.
2. Relearn how to read an ABG
– 7.31/35/58/-4; lactate :5 like this?
– lactate :5; -4/58/35/7.31 or like this?
•
•
•
•
•
•
•
Sat 75-90%, PaO2 35-50, BE > 0,
Lactate < 2.5
Investigate, correct and
reinvestigate any metabolic
acidosis
Afterload reduction:
• Milrinone 0.25-0.75 mcg/kg/min
Volume:
• Based on perfusion and acid base status
• Anticipate volume requirement
Hgb= 13-15…..always above 11
Normal sinus rhythm
Normothermia to slightly cool but
not hot
Avoid unnecessary noxious stimuli
No baths or weights on night shift
Cluster cares
No excessive crying or IV sticks
Normothermia
Avoid dehydration
Weight gain- calories, calories, calories….
3KG baby needs 60 cc q 3h of 24 cal/oz formula to achieve 130
cal/kg/day- we do not always get here prior to DC
NG/PO feedings to achieve 10g/day wt gain
Acidosis
Arrhythmias
Anemia
Sats > 93%
Sats < 70%
Dehydration
A ventricle that is working double time
Variable cardiac output
Increased caloric requirement/difficulty
feeding
Tachypnea
A need for close supervision/follow-up
A risk for sudden death
•
Stressful hospitalization
– Fetal dx: long time to think and web surf
– Antenatal dx: no time to prepare
– Long hospitalization: 14-36 days
•
Transition home
– Most fragile between the 1st and 2nd stage
• Must have scale and pulse ox prior to DC
– 20% risk of death prior to the second stage
– Close follow-up by NP’s in clinic in addition to Nutritionist
•
Anticipation of future surgeries
High Risk Patient population:
Single Ventricle requiring staged repairs
Hybrid procedures and palliations
MBT shunts
PA, VSD, MAPCAs
Other complex lesions including heterotaxy
syndrome
Approximately 7 to 15% of these infants will
die unexpectedly at home before Stage 2.
Possible Causes
Coronary artery obstruction or spasm
Aortic arch obstruction
Low cardiac output
Arrhythmia
Shunt thrombosis
Sepsis or infection
Predictors
Intact atrial septum
Older age at the time of surgery
Post op arrhythmias
Airway complications
Decreased ventricular fx pre and post op
Anatomic subtypes
▪ Aortic atresia
▪ Small ascending aorta diameter
Infants with Complex Single Ventricle have
significant growth failure after Stage I
palliation.
Only 3.6% at or above 50th percentile in
weight at the time of Stage II palliation (Atz et
al, 2004)
Feeding difficulties and inadequate nutrition
can strongly influence outcomes!
All Single Ventricle
patients go home with
a scale and pulse ox
Family keeps daily log
of feeding, weight and
O2 saturations
Monitored by NPs
either by phone or in
high risk clinic
Family has “red flags”
to call for:
Weight loss: 30 grams of
weight in one day
Lack of weight gain: 20
grams of over 3 days
O2 sats drop below 70%
Weekly visits after discharge x 4 weeks
Every other week visits until Pre-Glenn Cath
(~3-4 months of age).
Special attention to Sats, weight, vomiting,
diarrhea, feeding difficulties, URI
Monitor
Pulse oximetry
Weight
BP
Echocardiogram as necessary
Monthly
Monitor EKG, Chest X-ray
Reduce interstage mortality to 0%
Improved nutritional status and weight gain
will positively influence timing of Stage II
palliation and outcome of surgical treatment.