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PHYSIOLOGY Pedia CVS by Dr. Cacas UERMedicine2015B

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

091411 PHYSIOLOGY 7th Lecture (3rd LE) 1

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).

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

7 Phy3 - Pedia Cvs 2015b

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