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Outline1.Compare fetal from neonatal circulation2. Identify the changes in the circulation of blood
after birth3.Discuss some conditions associated with
unsuccessful extrauterine transition4.Learn when to suspect congenital heart
FEATURESOF FETAL CIRCULATION
1. Gas exchange occur in the placenta(fundamental difference)a. right and left ventricles exist in parallel
circuitb. placenta provides for gas and metabolite
exchange2. *Four shunts in fetal circulation:
a. Placentab. Ductus Venosus (DV)c. Foramen Ovale (FO)- opening in between right and left atrium,
ensuring a good amount of oxygenated bloodentering both sides of the heart(since bloodfrom lungs entering left atrium is still
deoxygenated blood, the oxygenated bloodfrom the right atrium of the heart goes to theleft atrium(via foramen ovale), then to theleft ventricle and then to the entire body.
d. Ductus Arteriosus (DA)- since right ventricle receives mixed
blood(both oxy and deoxy), it pumps theblood towards the aorta through the ductusarteriosus.
*SHUNT=temporary DETOUR of blood in the body
NOTE: Foramen Ovale and Ductus Arteriosus are the major
shunts found in utero
Ductus Arteriosus attaches to the aorta AFTER theaorta arches, so the upper part of the body stillreceives the most amount of OXYGENATED BLOOD.
3. Pulmonary blood flow is lowa. Despite RV dominanceb. (*80- 90%) of blood is diverted to Patent
Ductus Arteriosusc. Purpose of pulmonary blood flow is
nutritional requirement for lung growthd. Allow lung to perform paraendocrine and
metabolic functione. *Pulmonary vascular resistance is high
due to constricted intrapulmonaryarteries
4. Fetal pulmonary arterial mean BP: increases withgestation (term: 50mmHg)
5. Total pulmonary vascular resistance: decreasesprogressively till term
*Blood flow to the lungs (PULMONARY CIRCULATION) isONLY FOR NOURISHMENT of the lungs, since the fetusdoesnot
breath on its own in utero, hence NO GAS EXCHANGEOCCURS in the lungs
FETAL CIRCULATION- oxygenated blood from placenta flows to the fetus
thru umbilical vein (PO2 30-35 mmHg)o ~ 50% enters hepatic circulation
o the rest bypasses liver and joins inferior venacava (IVC) via ductus venosus, and mixes withpoorly oxygenated IVC blood from the lower part
of fetal body (PO2 26-28 mmHg)- enters right atrium, favoring flow across foramen
ovale to the left atrium- blood then flows into left ventricle and ejected into
ascending aorta
fetal superior vena cava (SVC) blood w/cis less oxygenated (PO2 12-14 mmHg)enters the RA, preferentially traversesthe tricuspid valve flowing into the rightventricle
blood is ejected into pulmonary artery
(only 10% of RV outflow enters the lungs)
bypasses the lungs and flows thru theductus arteriosus into the descending
aorta to lower part of fetal body
FETAL BLOOD FLOW PATTERNS
Non uniform blood flow due to shunts (FO, DA)
Streaming pattern of flow from IVC--- RA---RV
RV Output: for Umbilical-Placental circulationo (For O2 and substrate uptake)
LV Output: for Fetal Bodyo ( For O2 and substrate delivery)
Combined Ventricular Output:- 2/3 main pulmonary trunkDAdescending aorta
(57% CVO; 87% RVO)o Pulmonary circulation
- 1/3 ascending aorta heart (3% CVO) / brain andupper fetal body (22% CVO); Descending aorta (10%CVO)
Branches of the PA are small (since the lungsreceive only 15% of combined ventricular output)
* It is small because it is constricted in utero* endothelin-1 or aspirin maintains the PA small
Combined ventricular output:RV: 55% LV: 45%
*parallel type of circulation due to the presence of
shunt Pressure in the RV is identical to that in the LV
(unlike in the adult)*This fact reflected in the ECG of the newborn, whichshows more RV force than that of adult
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Dimensions of the Cardiac Chambers
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Figure 2: Fetal Circulatory System
PLACENTA
Receives the largest amount of combinedventricular output (note: ventricular output=Right ventricle + Left ventricle) (55%)
Lowest vascular resistance in the fetus (*so,blood flow)
*Considered a separate organ where oxygenatedblood from placenta flows to fetus thru theumbilical vein(PO2= 30-35 mmHg)
MAIN AREA OF GAS EXCHANGE
SUPERIOR VENA CAVA (SVC)
Drains the upper part of the body, including thebrain
15% CVO
INFERIOR VENA CAVA (IVC)
Drains the lowest part of the body and theplacenta
70% CVO
***Since the blood is oxygenated in the placenta, theoxygen saturation in the IVC (70%) is higher than that
in the SVC (40%)***Highest PO2 is found in the umbilical vein (32 mm
Hg)
RIGHT VENTRICLE (RV)
Most of the SVC blood goes to the right ventricle
BRAIN and CORONARY CIRCULATION Receive blood with higher oxygen saturation
(PO2 of 28 mmHg) than the lower half of thebody (PO2 of 24 mmHg)
***1/3 of the IVC blood with higher oxygen saturation isdirected by the crista dividens to the Left Atrium (LA)
through the foramen ovale***2/3 enters the RV and main pulmonary and main
pulmonary artery (MPA)***Less oxygenated blood in the pulmonary artery (PA)flows through the widely open ductus arteriosus to the
descending aorta and then to the placenta foroxygenation
*Upper part of fetal body is perfused exclusively from
LV (w/ blood that has a slightly higher PO2).*Lower part of fetal body w/ blood derived mostly fromRV.
FETAL VASCULAR PRESSURE
R & L atrial pressure are equal ( due to foramenovale)
Afterload of fetal ventricles:
o RV:
Low
Ejects mostly into the low resistanceumbilical-placental circulation
o LV:
High
Ejects into the high resistanceupper body circulation
*afterload resistance the flow will encounter by theright ventricle
*During fetal life, RV pumps blood against systemic BPand also performing greater volume of work than the
LV.
FETAL CARDIAC OUTPUT Unlike the adult heart, which increases its stroke
volume when the heart rate decreases, the fetalheart is unable to increase stroke volume whenthe heart rate falls
Therefore the fetal cardiac output depends onthe heart rate, when the heart rate drops as infetal distress, a serious fall in cardiac outputresults
combined ventricular output of both left and rightventricles
~450 ml/kg/min.
~ 65% of descending aortic blood flow returns toplacenta; remaining 35% perfuses fetal organs
and tissues
FETAL PULMONARYVASCULAR RESISTANCE (PVR)A. In the fetus:
Pulmonary arteries (PA) : thicker medial smoothmuscle coat relative to their external diameter
*increase vascular resistance in the womb
Exaggerated in small arteries
B. Late Gestation
Only 50% of *PA associated with respiratorybronchiole are muscularized
*other PA remains open to allow pick-up of oxygen
fromcapillaries
PA within the alveolar wall are not muscularized
Contain *pericytes and intermediate cells(precursors of smooth muscle cells)
*pericytes and intermediate cells are triggered byhypoxia thereby develops it to smooth musclesallowing constriction hence decrease blood flow
CONDITIONSTHATCANCAUSEMEDIALTHICKENING: INCPVR
Fetal hypoxemia
Hypertension: *Pulmonary hypertension andpressure
Altered fetal blood flow
FACTORSTHATREGULATETHETONEOFFETALPULMONARYCIRCULATION:
Mechanical effects: *mechanical compression ofalveoli that comprises blood volume causingblood vessel resistance
Oxygenation state: *Oxygen is a potentvasodilator
Vasoactive substance: *i.e: PGI2, NO, O2
FACTORSINVOLVEDINTHECONTROLOF (PULMONARYVASCULAR RESISTANCE) PVR
VASOCONSTRICTION VASODILATATION
Physical NODecrease O2 Increase O2Leukotrienes PGI2Thromboxane A2Endothelin A activation PGD2Platelet derived growthFactor (PDGF)
ET B activation
Platelet activating factor (PAF)
AA metabolites
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PHYSIOLOGY Pedia CVS by Dr. Cacas UERMedicine2015BNEONATALCIRCULATION (CHANGESINTHE CIRCULATION
AFTER BIRTH)
Primary change in circulation after birth is a shiftof blood flow for gas exchange from the placentato the lungs
The placental circulation disappears:*Shorthypoxia due to cutting umbilical cord*beyond 42 weeks of gestation blood vessels necrose
(dissolve)
Pulmonary circulation is established (*Seriescirculation)
heart rate slows in response to an increase insystemic vascular resistance
with onset of ventilation, PVR is markedlyincreased
closure of DA and fall in PVR results in decreasein pulmonary arterial and right ventricularpressure
1st several wks of life PVR decreases furthersecondary to remodeling of pulmonaryvasculature
Circulatory Changes at Birth
- dec. w/ initiation of ventilation and oxygenation- due to partial pulmonary ****- pulmonary vasodilatation
At Birth:24 hrs closure of DA
- PA pressure half of SAP4 wks adult levels3-6 mos PA pressure cont. to dec
- PVR reaches adult levels
INTERRUPTIONOF THE UMBILICAL CORD RESULTSTOTHEFOLLOWING
An increase in systemic vascular resistance (SVR)as a result of the removal of the very-low-resistance placenta (shunt 1): *slows heart rate
Closure of the ductus venosus (shunt 2) as aresult of lack of blood return from the placenta
LUNG EXPANSION RESULTSINTHE FOLLOWING:
LA pressure increases as a results of theincreased pulmonary venous return to the LA
RA pressure falls as a result of closure of theductus venous
Functional closure of the foramen ovale (shunt 3)occurs as a results of increased pressure(because of the increased pressure from thepulmonary circulation) in the Left Atrium (LA) inexcess of Right Atrium (RA) pressure
A reduction of the PVR: *because intrapulmonaryarteries are no longer constricted by amnioticfluid
Increase in the Pulmonary Blood Flow (PBF): *due
to PVR
Fall in PA pressure
Closure of Patent Ductus Arteriosus (shunt 4):due to increased arterial oxygen saturation
CLOSUREOF CENTRAL SHUNTSAND SYSTEMICCIRCULATION
A. Closure of Foramen Ovale1. Ligation of umbilical cord/ removal of the
placenta/separation of the NB from umbilical/placental circulation
2. Decrease in IVC flow3. Decrease in RA pressure4. Increase pulmonary flow5. Increase LA pressure-> decrease RA will lead to
closure of foramen ovale
B. Closure of Ductus Ateriosus1. Exposure to increase oxygenation2. Decrease Prostaglandin E2 (PGE2) (removal of
placenta/ metabolism in the lungs): *PGE2keeps the ductus arteriosus open
3. Higher incidence of patency in preterm4. Causes L-R shunting
*If it does not close, congestions of lungs mayoccur. (L-R shunting -> increased PA flow ->increased blood flow in lungs)
C. Closure of Shunts Results in:1. Separation of the L and R sides of the heart2. Establishment of series circulation3. Cardiac output increases to meet demands4. Thyroid hormone, cortisol, catecholamines5. Associated with increased blood flow to
myocardium, renal and GI and a decrease inflow to adrenal, cerebral blood flow
*shunts should go after birth
PULMONARYVASCULAR RESISTANCE (PVR)
Decrease with the initiation of ventilation andoxygenation due to:1. Partial pulmonary vasodilatation caused by
physical expansion of the lung and prostacyclin2. Further pulmonary vasodilatation associated
with fetal oxygenation and Nitric Oxide (NO)production
*Nitric Oxide causes vasodilatation
Increase PBF and Decrease PVR
Mechanical and Humoral Factors: (all causesdilatation)1. Replace alveolar fluid with gas2. Decrease compression on pulmonary arterioles3. Gas-liquid interface in the alveoli produced4. Prostacyclin: dilatation
Figure 5: Fetal Lungs (before birth/ inhalation of O2)
In the Fetus Pulmonary Blood flow is diminished
Blood flow is diverted across ductus arteriosus
Arterioles are constricted
Figure 6: Fetal Alveoli transition to Neonatal Alveoli
After delivery Lungs expand with air and fetallung fluid leaves alveoli
*First few breaths must be effective to allowfluids to leave the alveoli
Figure 7: Pulmonary Blood Vessels at Birth
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*Pulmonary arterioles dilate causing increasein pulmonary blood flow (PBF)
Figure 8: Cessation of Shunt through Ductus Arteriosus
Ductus Arteriosus constricts
Blood flows through the lungs to pick up oxygen; bloodoxygen levels rise
FETALAND NATAL DEVELOPMENT
Fetal:PA and Systemic pressures are equal (DA that
connects the aorta and pulmonary artery)Neonatal:24 hours old: Closure of DA (ductus arteriosus)
PA pressure half of SAP(systemic arterialpressure)
4 weeks old: adult levelsPA PRESSURECONTINUESTODECREASE:
In 3-6 months
due to thinning of the muscular layer of the smallpulmonary arteries (vascular remodeling)
muscular involution***PVR- reaches adult levels by 3-6 months
CONGENITALCARDIACDISORDERS
IMPORTANT CONDITIONS ASSOCIATEDWITH ALTERED
DECREASEIN PVR AT BIRTH:1. Persistent Pulmonary Hypertension of theNewborn (PPHN)
o Failure to achieve/maintain the decreasein PVR that normally occurs at birth*decrease pulmonary blood flow,decrease systemic circulation
o Due to RDS, meconium aspiration, sepsis
o Effects: reduced pulmonary blood flow &reduced systemic deliveryManifestation: cyanosisTreatment:dilation of vessels
o Other findings: In utero events resulted
to endothelial dysfunction & impaired NO& ET-1 activity
*previously known as Persistent FetalCirculation
2. Congenital heart defects with largecommunications at the ventricular or greatvessel level (within PA or AORTA)
o Delayed fall in PVR in the presence ofincreased pulmonary blood flow orpressure
o Endothelial injury
o Remain unclear*In these instances, patient will remain desaturated
FETALAND NEONATAL CIRCULATION
Fetal Circulation Neonatal Circulation
Parallelcirculation
Intracardiacshunts
High PVR
Relatively lowCO
Gas exchangein the placenta
Seriescirculation
No IC shunts
Low PVR
Relatively high
CO
Lungs
Three cardiovascular structures unique to the fetus areimportant to maintain this parallel circulation: ductus
venosus, foramen ovale, ductus arteriosus
Transposition of Great Vessels (Ito yung sinasabi ni Dr.Cacas na yung right ventricle will go straight to the
systemic circulation via the aorta and left ventricle will goto the pulmonary circulation kaya walang oxygenation.
For the patient to thrive, PATENT DUCTUS ARTERIOSUS isneeded para magkaroon ng mixture ng oxygenated and
unoxygenated blood. Oxygen should not be given toprevent closure of the said shunt. To maintain the PDA,
prostaglandin should be administered.)
Differences between Neonatal and Older infantsCirculation:
1.) R-L or L-R shunting may persist across thepatent foramen ovale
2.) continued patency of DA may allow L-R, R-L orbidirectional shunting
3.) neonatal pulmonary vasculature constricts morein response to hypoxemia, hypercapnia andacidosis
4.) wall thickness and muscle mass of neonatal Land R ventricles are almost equal
5.) newborn infants at rest high O2 consumption;high CO
*normal DA has significant amount of circularlyarranged smooth ms in its medial layer*full term neonate, O2 is most important factor
controlling ductal closure
WHENTOSUSPECTA HEART PROBLEMINAN INFANT
A physician may suspect that one of these heartdefects is present if the child is not growing normally,has a heart murmur or has one or more signs (e.g., abluish tint to the skin called cyanosis)
Congenital Heart Disease-It is a heart-related problemthat is present since birth and often as the heart isforming even before birthIncidence: 1% (8-12 of 1000 live births)
CAUSES
1. Genetic2. Environmental factors: viruses, certain drugs,
radiation, living in high altitudes3. Rubella (German measles) during the first three
months of pregnancy have a high risk of having ababy with a heart defect (Congenital RubellaSyndrome)
4. Medications5. Drinking alcohol in pregnancy also can increase
the risk of heart defectsbabies with fetalalcohol syndrome (FAS)
6. Cocaine7. Smoking during pregnancy8. Chromosomal defects: Downs Syndrome
CLASSIFICATIONOF CONGENITAL HEART DISEASE
A. Cyanotic Heart Diseasea. Pulmonary Valve Atresiab. Total Anomalous Pulmonary Venous
Return (TAPVR)c. Ebstein Anomaly
B. Acyanotic Heart Diseasea. Left to Right Shunt
i. Ventricular Septal Defectii. Atrial Septal Defectiii. Patent DuctusArteriosusiv. Atrio-Ventricular Canal Defect
v. Partial Anomalous Venous Returnb. Obstructive Lesions
i. Pulmonary Stenosisii. Aortic Stenosisiii. Tricuspid Stenosisiv. Mitral Stenosisv. Coarctation of the Aorta
BASIC TOOLS & LABORATORYEXAMSINEVALUATINGACONGENITAL HEART DISEASEARE:
History/ Physical Exam
Chest X-ray
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15 leads ECG
Arterial Blood Gas
1.Heart Murmura. Evaluated in a timely mannerb. Ductal dependent cardiac lesions
2.Respiratory distress3.Shock4.Cyanosis with no respiratory distress
5.Circulatory collapse in the 1
st
few weeks of life
PHYSICAL EXAMINATION
INSPECTION:
Undressed/ radiant warmer
General appearance
Activity
Cyanosis ( generalized/ central/peripheral)
Peripheral perfusion
Respiratory pattern
Dysmorphic features (funny looking kid or FLK)
Thorax:
o Precordial area in particular
o Chest symmetry
o Location of PMI
ASSESSMENTOF PERIPHERALPERFUSION:
Low CO or CHF:
Pallor ( peripheral vasoconstriction caused by highcirculating endogenous catecholamines)
Mottled/ cyanosis of distal extremities/ delayed CRT
Cold extremities
Pulses weak and thready
Leads to metabolic acidosis & decrease coronaryperfusion
E.g. Hypoplastic L heart syndrome
Coarctation of the aorta
Critical aortic stenosis
PULSES:
Related to pulse pressure and stroke volume ( SBP-DBP)
Weak/ thready: Decrease CO
Bounding: due to wide pulse pressure
Systemic to pulmonary arterial connections
PDA/ aortopulmonary window/ AV malformations/extensive aorto-pulmonary collaterals
RESPIRATORYEFFORT:
Usually at the upper limits of normal
Respiratory pattern:Differ by the regularity of the tachypnea
Lack of normal variation in the RR
HEARTRATE:
Resting heart rate: 120-130/min
If < 90 or > 160: warrants investigation
Normal to have short transient decrease in HR:bowel movement, eating, hiccupping due toenhanced vagal tone
In intubated/ mechanically ventilated patients:bradycardia may be due to hypoxemia/ hypercarbia
Bradycardia in non-distressed patient: congenitalheart block
EDEMA:
Associated with CHD in Turners or Noonansyndrome
Seen in hands and feet
CHF:
o Eyelids
o Dependent areas ( sacrum)
HEART AUSCULTATION:
In the NB, requires patience/ calm the child
1st HS: single ( mitral & tricuspid valve closure)
2nd HS: ( aortic & pulmonic valve closure)
Single- 1st 6 hours OL
Split- 48 hours
Single S2: defect that equalize pulmonic & aorticpressure
o E.g. aortic/ pulmonic stenosis
HLHSTruncusarteriosusTransposition of the Great Arteries (TGA)
Quality of S2:o Loud pulmonic component
E.g. pulmonary hypertension
Systolic ejection click:o Normal: 1st few hours of life
o 24 hours old: abnormal ( dilatation of thegreat arteries/ malfunction of SL valves)
Innocent murmuro Soft murmur
o Non specific*not all murmurs are pathologic, usuallynot heard from diastolic
Loud harsh murmuro Usually pathologic
CYANOSIS:
Assessment affected by: lighting, reflected lightfrom wall paint, skin pigmentation, examinersexperience
Need 3-5 g of reduced hemoglobin/dl to detect it
Differential cyanosis (Coarctation/ Interrupted aorticarch)
Differentiate with a pulmonary condition*do ABG (Arterial Blood Gas) first then give Oxygen for
10minutes
CASE: At birth, a baby was noted to be cyanotic.What simple test can be done to determine
whether cause of cyanosis is cardiac or pulmonaryin cause?
HYPEROXIA CHALLENGE Hyperoxia test
Patients with O2 sats < 90 by pulse oximetry
Give 100% O2 x 10 minutes
PO2:
o > 200 torr ( CHD r/o)
o < 70 torr with normal pCO2 ( CHD, cyanotic)o 150-200 torr ( CHD unlikely but cant be r/o
completely; needs further tests)
HYPEROXIA HYPERVENTILATION TESTMay further differentiate if a cyanotic child has a CHD,
cyanotic type VS, PPHN***Rules:
Murmur associated with significant cyanosiswarrants 2D-echo
Absence of murmur does not rule out a CHD: e.g.TGA, TOF with PVA
*hyperventilation dilates blood vessels
ECG IN INFANTS AND CHILDREN
An electrocardiogram (EKG) is the visualrepresentation of the electrical conduction of theheart. As each signal travels from the atria to theventricles it can be recorded on paper.
The travel of this electrical signal is what is
represented as an EKG.
Figure 9: Cardiac Conduction System
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PEDIATRIC ECG
P wave: represents the electrical signal as ittravels through the atria, the atria contract andblood is forced into the ventricles.
QRS waves: represent the signal as it travelsthrough the ventricles, the ventricles contractand blood is forced into the arteries.
T wave: represents the heart at rest prior to thenext beat.
Figure 10: Pediatric ECG
DIFFERENCES BETWEEN INFANT ECG AND ADULTECG-reading of ECG for pediatric patients is essentially thesame except
1. Heart rate
Tachycardia accepted in newborn and decreaseswith age
2. Right Ventricular Hypertrophy
In utero, work of RV is greater
At birth- decrease in RVSP and increase insystemic resistance: LV becomes thicker than theRV
3. Right Axis deviation
May remain up to one yr of age
Figure 11:Adult ECG Interpretation
Routine Interpretation1) Heart Rate (Atrial and ventricular rates, if different)2) Rhythm (sinus or not sinus) by considering the P axis3) QRS axis, T axis, QRS-T angle4) Intervals: PR, QRS and QT5) P wave amplitude and duration6) QRS amplitude and R/S ratio; abnormal Q waves7) ST segment and T wave abnormalities
HEART RATEMethods to Calculate Heart Rate
1. Count the R-R cycle in six large divisions andmultiply it by 50
2. When the heart rate is slow, count the number oflarge divisions between two R waves and dividethat into 300 (1min=300 large division)
3. Approximate heart ratewhen R-R intervals are5,10,15,20 and 25 mm, the respective heartrates are: 300,150,100,75,60 beats/min
The easiest way to estimate heart rate is to use the...
Rule of 300 Provided that the rhythm is regular, heart ratecan be estimated by dividing 300 by the number of large boxes
in the R-R interval.
VENTRICULAR RATE
small squares (R-R interval) / 1500
big squares (R-R interval ) /300
Figure 12: Ventricular Rate
HEART RATES IN NORMAL CHILDRENAge Awake
RateMean Sleepin
g RateNewborn to 3
mo.85 to 205 140 80 to 160
3 mo. to 2 yrs 100 to 190 130 75 to 160
2 yrs 10 yrs 60 to 140 80 60 to 90
More than 10
yrs
60 to 100 75 50 to 90
RHYTHMSinoatrial (SA) Node:
Located in the right upper part of the atrial mass
The direction of atrial depolarization is from theright upper part toward the left lower partproducing the P axis in the left lower quadrant (0to +90 degrees)
What is Normal Sinus Rhythm?
During Normal Sinus Rhythm, the SA Node(Sinoatrial Node) fires electrical signals at aregular rhythm in accordance with the need formore or less oxygen by your body
Normal Sinus Rhythm is the ideal rhythm.
Sinus Rhythm1. P wave preceding each QRS complex (Every QRS
complex is preceded by a P wave but not every Pwave must be followed by a QRS as occurs ifthere is second or third degree AV block)
2. A usual rate of anywhere between 60-100 bpm.3. Regular but not necessarily normal PR interval
(PR interval will usually be 0.12 sec or greater)4. The P wave morphology and axis must be normal
Normal P axis (0 to +90 degrees)
***Remember (for Sinus Rhythm):
P axis to be between 0 to +90 degrees P waves must be upright in Leads I and AVF
Upright P wave in Lead II and inverted P wavein AVR
Figure 14: EKG Leads
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MEAN AND RANGE OF NORMAL QRS AXESAge Range
1 wk- 1 mo +110 (+30 to +180)
1-3 mo +70 (+10 to +125)
3 mo to 3 yr +60 (+10 to +110)
Older than 3 yr +60 (+20 to +120)
Adults +50 (-30 to +105)*Note: decreasing range with increasing age
Figure 13: Sample EKG
SIMPLIFIED SUMMARY of circulation
Blood from the placenta is carried to the fetus by the umbilicalvein. About half of this enters the fetal ductus venosus and iscarried to the inferior vena cava, while the other half enters theliver proper from the inferior border of the liver. The branch ofthe umbilical vein that supplies the right lobe of the liver firstjoins with the portal vein. The blood then moves to the rightatrium of the heart. In the fetus, there is an opening betweenthe right and left atrium (the foramen ovale), and most of the
blood flows through this hole directly into the left atrium fromthe right atrium, thus bypassing pulmonary circulation. Thecontinuation of this blood flow is into the left ventricle, and fromthere it is pumped through the aorta into the body. Some of theblood moves from the aorta through the internal iliac arteries tothe umbilical arteries, and re-enters the placenta, where carbondioxide and other waste products from the fetus are taken upand enter the maternal circulation.Some of the blood entering the right atrium does not passdirectly to the left atrium through the foramen ovale, but entersthe right ventricle and is pumped into the pulmonary artery. Inthe fetus, there is a special connection between the pulmonaryartery and the aorta, called the ductus arteriosus, which directsmost of this blood away from the lungs (which aren't being used
for respiration at this point as the fetus is suspended in amnioticfluid).
091411 PHYSIOLOGY 7th Lecture (3rd LE) 7
http://en.wikipedia.org/wiki/Placentahttp://en.wikipedia.org/wiki/Fetushttp://en.wikipedia.org/wiki/Umbilical_veinhttp://en.wikipedia.org/wiki/Umbilical_veinhttp://en.wikipedia.org/wiki/Ductus_venosushttp://en.wikipedia.org/wiki/Inferior_vena_cavahttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Umbilical_veinhttp://en.wikipedia.org/wiki/Liver#Lobeshttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Portal_veinhttp://en.wikipedia.org/wiki/Right_atriumhttp://en.wikipedia.org/wiki/Right_atriumhttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Right_atriumhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Foramen_ovale_(heart)http://en.wikipedia.org/wiki/Foramen_ovale_(heart)http://en.wikipedia.org/wiki/Foramen_ovale_(heart)http://en.wikipedia.org/wiki/Pulmonary_circulationhttp://en.wikipedia.org/wiki/Pumphttp://en.wikipedia.org/wiki/Aortahttp://en.wikipedia.org/wiki/Internal_iliac_arterieshttp://en.wikipedia.org/wiki/Umbilical_arterieshttp://en.wikipedia.org/wiki/Placentahttp://en.wikipedia.org/wiki/Carbon_dioxidehttp://en.wikipedia.org/wiki/Carbon_dioxidehttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Foramen_ovale_(heart)http://en.wikipedia.org/wiki/Right_ventriclehttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Aortahttp://en.wikipedia.org/wiki/Ductus_arteriosushttp://en.wikipedia.org/wiki/Respiration_(physiology)http://en.wikipedia.org/wiki/Fetushttp://en.wikipedia.org/wiki/Amniotic_fluidhttp://en.wikipedia.org/wiki/Amniotic_fluidhttp://en.wikipedia.org/wiki/Placentahttp://en.wikipedia.org/wiki/Fetushttp://en.wikipedia.org/wiki/Umbilical_veinhttp://en.wikipedia.org/wiki/Umbilical_veinhttp://en.wikipedia.org/wiki/Ductus_venosushttp://en.wikipedia.org/wiki/Inferior_vena_cavahttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Umbilical_veinhttp://en.wikipedia.org/wiki/Liver#Lobeshttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Portal_veinhttp://en.wikipedia.org/wiki/Right_atriumhttp://en.wikipedia.org/wiki/Right_atriumhttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Right_atriumhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Foramen_ovale_(heart)http://en.wikipedia.org/wiki/Pulmonary_circulationhttp://en.wikipedia.org/wiki/Pumphttp://en.wikipedia.org/wiki/Aortahttp://en.wikipedia.org/wiki/Internal_iliac_arterieshttp://en.wikipedia.org/wiki/Umbilical_arterieshttp://en.wikipedia.org/wiki/Placentahttp://en.wikipedia.org/wiki/Carbon_dioxidehttp://en.wikipedia.org/wiki/Carbon_dioxidehttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Foramen_ovale_(heart)http://en.wikipedia.org/wiki/Right_ventriclehttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Aortahttp://en.wikipedia.org/wiki/Ductus_arteriosushttp://en.wikipedia.org/wiki/Respiration_(physiology)http://en.wikipedia.org/wiki/Fetushttp://en.wikipedia.org/wiki/Amniotic_fluidhttp://en.wikipedia.org/wiki/Amniotic_fluid