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Cardiac Physiology
Gia Marzano, AC PNP Pediatric Cardiac Surgery
Rush Center for Congenital Heart Disease
Rush University Medical Center
Objectives Part 1
•
•
•
•
Fetal Circulation
Transition to Postnatal Circulation
Normal Cardiac Anatomy
Ductal Dependence and use of
PGE1
Objectives Part 2
• Basic principles of cardiac
physiology
• Basic categories of congenital heart
disease based on pathophysiology
• Application of physiology to your
bedside management
1
Fetal Circulation
Few Concepts
• Fetal heart starts developing
during the 3rd week of life
• By the 3rd month of development,
all major blood vessels are
present and functioning.
• Pulmonary Blood Flow is Low
• Gas Exchange (Oxygen) occurs
in placenta
More Concepts
• Pulmonary Resistance is High
– Lungs are still underdeveloped
– Small pulmonary arteries have a
thicker smooth muscle layer than
similar arteries in adults.
Fetal Circulation Overview
• Umbilical Circulation:
– Pair of umbilical arteries
carry deoxygenated blood &
wastes to placenta.
– Umbilical vein carries
oxygenated blood and
nutrients from the placenta.
• Placenta facilitates gas
and nutrient exchange
between maternal and
fetal blood.
2
Fetal Circulation Overview
• Oxygenated
blood from
placenta is
transported to the
fetus through the
Umbilical Vein
Fetal Circulation Overview
• Most of the
oxygenated blood
bypasses the liver
through the
Ductus Venosus
and mixes with
De-Ox Blood from
IVC
Fetal Circulation Overview
• Blood travels from
the IVC and enters
the RA
3
Fetal Circulation Overview
• 40 % of oxygenated
blood from the IVC
bypasses the RV and
is shunted to the LA
via the Foramen Ovale
• The rest mixes with
De-ox blood from the
SVC and enters the
RV
Fetal Circulation Overview
• Blood then travels to
the LV and is
distributed through the
aorta mainly to the
coronaries and upper
body (carotid and
subclavian arteries)
• Only 1/3 of this volume
goes to the lower body
Fetal Circulation Overview
• Most blood from the IVC
(60%) mixes with SVC
blood and enters the RV
from the RA
• Because the lungs are
non-functional, most (90%)
will be shunted away from
the pulmonary arteries
through the Ductus
Arteriosus to the
Descending Aorta and
Placenta for oxygenation
4
Fetal Circulation Overview
• Blood circulates to
the body and
returns to the
placenta via the
umbilical arteries
Fetal Circulation Overview
• Placenta reoxygenates blood
returning from the
umbilical arteries
• New fetal cardiac
cycle…
Fetal Circulation Overview
• Parallel circulation with shunts (PFO
and PDA) allows various lesions to
provide adequate transport of blood to
placenta for oxygenation and deliver it
to the tissues
• RV performs ~ 2/3 cardiac work  RV
larger and thicker at birth
5
Transitional and Post-Natal
Circulation
• What happens at birth ??
• The change from fetal to postnatal
circulation happens very quickly.
• 2 major events:
– Changes initiated by baby’s first breath.
– Elimination of the placenta
Transitional Circulation
• Clamping of the
umbilical cord:
– Eliminates the low
resistance placental
circulation
peripheral vascular
resistance increases
– decreases blood
volume returning to
the heart from IVC
Transitional Circulation
• With initiation of pulmonary
ventilation:
– Increased alveolar O2 pressure
vasodilates the pulmonary arteries
– Pulmonary vascular resistance
decreases significantly
6
Transitional Circulation
Increase
in
systemic
Vascular
resistance
+
Drop
in
pulmonary
Vascular
resistance
Pulm Blood flow
increases 8-10 X
Transitional Circulation
• Increased pulmonary
blood flow
increased
pulmonary venous
return into LA
 LAP >RAP
 the greater LAP
(and lower IVC flow)
closes the valve of the
foramen ovale,
preventing right-to-left
shunting.
Transitional Circulation
• PDA: changes from
R2L conduit of blood to
the descending aorta
to a L2R conduit of
blood to the lungs
• Ductus arteriosus
constricts and closes
functionally within
several hours after
birth, largely in
response to the
increase in oxygen
tension.
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Transitional Circulation
• PFO closure
• Ductus arteriosus
closure
• These events result
in the effective
separation of the
systemic and
pulmonary
circulations after
birth.
Ductal Dependence
The Ductus Arteriosus
• In fetus:
– large channel that allows
blood to bypass the lung
circulation to the Dao
and placenta for
oxygenation
– as big as the Dao !
(10mm)
– allows equalization of Ao
and pulm arterial P
The Ductus Arteriosus
Role of O2
• Thick muscular layer
• Towards late gestation, the muscle layer
thickens and the lumen becomes smaller
• After birth, increased arterial O2 causes
more constriction of the ductus
• Constriction decreases PO2 in the muscle
 severe hypoxia  cell destruction and
fibrosis
• Functional closure within 10-15 hrs after
birth
• Complete closure within 5-7 days, can be
up to 21 days
8
Ductus Arteriosus
Role of Prostaglandins
• Produced by the wall of the
ductus and placenta
• 2 types: PGI2 and PGE2
• Relax the ductus arteriosus
smooth muscle
• Metabolized in the lungs
• After birth, ↓↓ PG  ductal
closure
Ductus Arteriosus
in Congenital Heart Disease
• In many CHD cases (mainly
cyanotic), ductus does not close
normally after birth:
– TA/PA/TGA: arterial O2 remains low
after birth lower stimulus for
constriction
– Left-sided lesisons (Ao atreasia,
coarctation): arterial O2 increases
after birth but the high PAP/flow
keeps ductus patent
Ductus Arteriosus
in Congenital Heart Disease
Ductal Dependency
• Normally, ductus carries ~ 60 % of
combined C.O from the PA to the DAo
• If LV outflow tract is obstructed (e.g.
aortic valve atresia, coarctation,
interruption):
– larger portion of combined C.O crosses
the ductus (~90%) larger Ductus
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Ductus Arteriosus
in Lt sided lesions
Ductal Dependency
– After birth: need the ductus to provide most
of systemic blood flow (from PA to Ao)
Ductus Arteriosus
in Congenital Heart Disease
• If RV outflow is narrow (e.g.
pulmonary atresia, tricuspid
atresia)
– minimal blood from RV to ductus 
small ductus
Ductus Arteriosus
in Rt sided lesions
Ductal Dependency
• After Birth: Need the ductus to
maintain pulmonary blood flow
10
Prostaglandin Therapy
• Indomethacin: inhibits PG
production
• PGE1:
– relaxes the ductus arteriosus
smooth muscle cells.
– Effective within the first 7-10 days
after birth
– Dose: 0.05-0.1 mcg/kg/min
– IV/PO
Prostaglandin Therapy
Side Effects
•
•
•
•
•
•
•
Apnea
Fever
Flushing
Hypotension
Thrombocytopenia
Seizure
Pyloric gastric outlet obstruction
Questions?
11
Part 2
• Basic principles of cardiac physiology
including
Flow and pressure relationships
Oxygen delivery
Determinants of blood pressure and
cardiac output
Let’s start with a case…
• You are admitting a 4 day old female
who had no prenatal care and
presented to the ED with poor feeding,
respiratory distress, lethargy and poor
urine output. PGE infusion was started
in the ED.
• On exam, she is floppy with grunting
respirations and her skin appears gray.
Let’s start with a case…
• VS:T 97 P 190 R 70 BP 40/P SpO2 92%
• PE:
Chest: coarse BS with retractions
Heart: tachycardic, no murmur
Abd: soft, liver 4cm below RCM
Ext: gray, cool, cap refill 5 sec, poor
distal pulses
12
Let’s start with a case…
• Labs: WBC 8.2 Hg 11 Hct 33 Plt 189
Lytes:Na132/K5/Cl103/CO8/BUN13/Cr0.9
ABG: 6.99/32/54/8/-16/85%
CXR: cardiomegaly, increased PVM
ECHO: critical CoA
Questions…
• A nursing student asks “why is that baby
gray?” How will you answer?
• Then she asks why the baby is so
hypotensive. You explain…
• The MD decides to transfuse prbc and
asks you to get consent from the
parents. What will you tell them is the
reason for the transfusion?
Flow and Pressure
Relationship
(all you really need to know to
understand any concept in cardiac
critical care….seriously!)
13
Ohm’s Law
Pressure change (dP)
Flow (Q) = __________________
Resistance (R)
Increased P  Increased Q
Increased R  Decreased Q
Cardiac Physiology
• What is the purpose of the heart?
O2
Cardiac Physiology
Delivery of oxygen (DO2) is a direct
function of the cardiac output (CO) and
the arterial oxygen content (CaO2)
DO2 = CO x CaO2
14
Cardiac Physiology
Oxygen Delivery
DO2 = CO x CaO2
Cardiac Output (CO)
Arterial Oxygen Content (CaO2
art Rate (HR) x Stroke Volume (Hgb
(SV) x 1.39 x SaO2) + (0.003 x PaO
roke Volume is directly related to:
Preload
Afterload
Contractility
Cardiac Physiology
• What are we trying to achieve?
Maximize O2 delivery
Provide adequate end organ perfusion
Maintain BP
Determinants of
blood pressure
15
Ohm’s Law
BP = Flow(Q) x Resistance(R)
What is Blood Pressure?
BP
SVR (Afterload)
CO
Heart rate
Stroke Volume
Intravascular Volume
(Preload)
Contractility
Maintaining Blood Pressure
• Derrangement in:
– Volume status
– Cardiac function
– Vascular tone
– Heart rate
BP
CO
HR
Preload
SVR
SV
Contractility
16
Preload
• Derrangement in:
– Volume status
– Cardiac function
– Vascular tone
– Heart rate
BP
CO
HR
SVR
SV
Preload
Contractility
Determinants of Cardiac Output
• Preload
-“Resting fiber length before contraction”
-End diastolic ventricular volume
-If preload is increased, SV and capability for
pressure generation are increased.
• Frank-Starling Mechanism
-Compliance dependent
CVP
• CVP: Central venous pressure
– Transduced via RA lines or CVL
– Reflects the intravascular volume status of
the patient and the filling pressure of the
ventricle
– Relationship between CVP and BP is
important
17
Afterload (SVR)
• Derrangement in:
– Volume status
– Cardiac function
– Vascular tone
– Heart rate
BP
CO
HR
SVR
SV
Preload
Contractility
Afterload
• Any factor that resists the ejection of
blood from the heart (SVR or
obstruction)
• With increasing afterload, shortening is
decreased and slowed.
• Afterload reduction increases fiber
shortening.
• Decreasing afterload helps the heart
contract
Afterload
• Afterload (SVR) increased by
– Acidosis, hypoxemia, pain, hypothermia
– Aggressively treat/avoid these things
• Afterload reducers
– Milrinone, dobutamine, nitroprusside, NO
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Contractility
• Derrangement in:
– Volume status
– Cardiac function
– Vascular tone
– Heart rate
BP
CO
HR
Preload
SVR
SV
Contractility
Contractility
• Often impaired
• Requires treatment with inotropes
– Milrinone, epinephrine, dobutamine,
dopamine
– Calcium is an important component
Putting it all together…
• Decreased Cardiac Output can be
caused by:
– Decreased preload
– Increased (or decreased) afterload
– Impaired contractility
• All therapies aimed at maximizing these
parameters
19
Categories of CHD
Epidemiology of CHD
• Incidence estimated to be 8 to 10 cases
per 1000 live births (0.8% - 1%)
• Increased to 5% - 15% in parents with
CHD
• Prevalence increases as better
treatments are available
• Age at presentation varies greatly and
depends on type of lesion and severity
Age at Presentation
20
Epidemiology of CHD
Categories of CHD
• Patients with too much PBF  CHF
• Patients with too little PBF  Blue
• Patients with too little systemic blood flow
 Gray
Categories of CHD
• Acyanotic Congenital Heart Disease
– L  R Shunt (Volume load)
– Obstructive (Pressure load)
• Cyanotic Congenital Heart Disease
– Decreased PBF
– Mixing lesions
21
Acyanotic CHD
• LR Shunt lesions (Volume load)
– VSD, ASD, PDA, AV Canal
– Common denominator is communication
between systemic and pulmonary circulations
– Magnitude of shunt depends on size of defect
and relative SVR and PVR which will change
over time
Acyanotic CHD
• Obstructive lesions (Pressure load)
– CoA, AS, IAA
– Common denominator is obstruction of blood
flow/ventricular outflow
– Lead to left heart failure (pulmonary edema)
circulatory collapse
Cyanotic CHD
• Decreased PBF
– TOF, PS with PFO, tricuspid atresia,
pulmonary atresia
– Common denominator is obstruction to
pulmonary blood flow and a means of
shunting RL
22
Cyanotic CHD
• Mixing Lesions
– TGA, TAPVR, truncus arteriosus, HLHS
– Common denominator is that there is
complete mixing of systemic and
pulmonary venous return without
obstruction to PBF
Acyanotic CHD
• LR Shunt lesions (Volume load)
– Most common lesions are ventricular
septal defect (VSD) 20-25%, atrial septal
defect (ASD) 5-10%, patent ductus
arteriosus (PDA) 5-10, AV Canal 2%
– Common denominator is communication
between systemic and pulmonary
circulations
– Magnitude of shunt depends on size of
defect and relative SVR and PVR which
will change over time
23
Pathophysiology of VSD
• Qp:Qs is increased
• Increased PBF leads to decreased lung
compliance, increased WOB, pulmonary
edema
• Chronic increased PBF leads to
increased PVR (Eisenmenger’s
physiology)PHTN
Clinical Presentation - VSD
• History: poor feeding, diaphoresis with
feeds, delayed growth and
development, repeated pulmonary
infections
• Will present at 6 to 8 weeks of age
• Exam: tachypnea, holosystolic murmur
at LLSB, hepatomegaly
• CXR: cardiomegaly, increased PVM
24
CXR - VSD
Management - VSD
• Diuresis
• Inotropy with digoxin
• Surgical repair when optimal
Acyanotic CHD
• Obstructive lesions (Pressure load)
– Most common are coarctation of the aorta
(CoA) 8-10%, aortic stenosis (AS) 5%,
interrupted aortic arch (IAA) 1%
– Common denominator is obstruction of
blood flow/ventricular outflow
– Lead to left heart failure (pulmonary
edema) circulatory collapse
25
26
Ductal Dependence
• To provide pulmonary blood flow
(PBF) – Critical PS
• To provide systemic blood flow
(SBF) – Critical CoA
• To allow mixing - TGV
Pathophysiology of Critical CoA
• In fetal life, the descending aorta is
supplied by the PDA
• With closure of the duct, systemic
circulation is impaired which leads to
poor perfusion, acidosis and circulatory
collapse
Clinical Manifestations – Critical CoA
• History: CHF symptoms (poor feeding,
diaphoresis), poor urine output
• Will present in first few days to weeks of
life
• Exam: tachypnea, poor perfusion,
decreased femoral pulses, shock, often
NO MURMUR, usually gallop present
• CXR: cardiomegaly, pulmonary edema
27
Management – Critical CoA
• Diuresis
• Inotropy with dopamine or dobutamine
• Prostaglandin (PGE1) infusion to reopen ductus arteriosus and restore
systemic blood flow
• Balloon angioplasty vs. surgical repair
Cyanotic CHD
• Decreased PBF
– Most common lesions are Tetralogy of
Fallot (TOF) 10%, pulmonic stenosis with
PFO (PS) 5-8%, tricuspid atresia 1-2%,
pulmonary atresia (PA) <1%
– Common denominator is obstruction to
pulmonary blood flow and a means of
shunting RL
28
Tetralogy of Fallot
• Consists of four components
–
–
–
–
Large VSD
Right ventricular outflow tract obstruction
Right ventricular hypertrophy
Overriding Aorta
• Only two components are important
– VSD large enough to equalize pressure (R=L)
– RVOT obstruction – how severe determines if
patient shunts RL (“Blue Tet”) or LR (“Pink
Tet”)
Clinical Presentation of TOF
• History: cyanosis or hypoxic spells,
dyspnea on exertion, squatting
• Exam: cyanotic (“Blue Tet”), murmur
variable – usually loud (grade III-IV)
systolic ejection murmur with thrill
• CXR: boot shaped heart, decreased
PVM
29
CXR - TOF
Cyanotic CHD
• Mixing Lesions
– Most common lesions are transposition of
the great arteries (TGA) 5%, total
anomolous pulmonary venous return
(TAPVR) 1%, truncus arteriosus <1%,
hypoplastic left heart syndrome (HLHS)
<1%
– Common denominator is that there is
complete mixing of systemic and
pulmonary venous return without
obstruction to PBF
30
Pathophysiology of TGA
• Pulmonary and systemic circulations
are parallel
• Defects permitting mixing are essential
for survival – ASD, VSD, PDA
• Poor mixing results in hypoxia, acidosis
and death
Clinical Presentation of TGA
• History: cyanosis, poor feeding,
dyspnea
• Presents in the first few days of life
• Exam: systolic murmur of VSD may be
present, may have no murmur
• CXR: cardiomegaly, egg-shaped
cardiac silhouette
Management of TGA
• Treat acidosis
• Administer O2 to decrease PVR and
increase PBF (increase mixing)
• PGE1 to reopen ductus and increase
mixing
• Balloon atrial septostomy
31
Summary
• All congenital heart lesions can be
categorized based on flow and pressure
relationships
• Caring for these patients entails
maximizing oxygen delivery and
maintaining adequate blood pressure
Back to our case…
• You are admitting a 4 day old female
who had no prenatal care and
presented to the ED with poor feeding,
respiratory distress, lethargy and poor
urine output. PGE infusion was started
in the ED.
• On exam, she is floppy with grunting
respirations and her skin appears gray.
Questions…
• A nursing student asks “why is that baby
gray?” How will you answer?
32
Categories of CHD
• Patients with too much PBF  CHF
• Patients with too little PBF  Blue
• Patients with too little systemic blood flow
 Gray
Questions…
• Then she asks why the baby is so
hypotensive. You explain…
Contractility
• Derrangement in:
– Volume status
– Cardiac function
– Vascular tone
– Heart rate
BP
CO
HR
Preload
SVR
SV
Contractility
33
Questions…
• The MD decides to transfuse prbc and
asks you to get consent from the
parents. What will you tell them is the
reason for the transfusion?
Cardiac Physiology
Oxygen Delivery
DO2 = CO x CaO2
Cardiac Output (CO)
Arterial Oxygen Content (CaO2)
art Rate (HR) x Stroke Volume (Hgb
(SV) x 1.39 x SaO2) + (0.003 x PaO
34