PHYSIOLOGY Pedia CVS by Dr.

Cacas 2015B
Outline 1. Compare fetal from neonatal circulation 2. Identify the changes in the circulation of blood after birth 3. Discuss some conditions associated with unsuccessful extrauterine transition 4. Learn when to suspect congenital heart diseases

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breath on its own in utero, hence NO GAS EXCHANGE OCCURS in the lungs

FEATURES OF FETAL CIRCULATION 1. Gas exchange occur in the placenta (fundamental difference) a. right and left ventricles exist in parallel circuit b. placenta provides for gas and metabolite exchange *Four shunts in fetal circulation: a. Placenta b. Ductus Venosus (DV) c. Foramen Ovale (FO) opening in between right and left atrium, ensuring a good amount of oxygenated blood entering both sides of the heart(since blood from lungs entering left atrium is still deoxygenated blood, the oxygenated blood from the right atrium of the heart goes to the left atrium(via foramen ovale), then to the left ventricle and then to the entire body. d. Ductus Arteriosus (DA) since right ventricle receives mixed blood(both oxy and deoxy), it pumps the blood towards the aorta through the ductus arteriosus.
*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 the aorta arches, so the upper part of the body still receives the most amount of OXYGENATED BLOOD.

2.

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 vena cava (IVC) via ductus venosus, and mixes with poorly 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/c is less oxygenated (PO2 12-14 mmHg) enters the RA, preferentially traverses the tricuspid valve flowing into the right ventricle blood is ejected into pulmonary artery (only 10% of RV outflow enters the lungs) bypasses the lungs and flows thru the ductus arteriosus into the descending aorta to lower part of fetal body

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Pulmonary blood flow is low a. Despite RV dominance b. (*80- 90%) of blood is diverted to Patent Ductus Arteriosus c. Purpose of pulmonary blood flow is nutritional requirement for lung growth d. Allow lung to perform paraendocrine and metabolic function e. *Pulmonary vascular resistance is high due to constricted intrapulmonary arteries Fetal pulmonary arterial mean BP: increases with gestation (term: 50mmHg) Total pulmonary vascular resistance: decreases progressively till term

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 circulation o (For O2 and substrate uptake) LV Output: for Fetal Body o ( 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 and upper fetal body (22% CVO); Descending aorta (10% CVO) Dimensions of the Cardiac Chambers Branches of the PA are small (since the lungs receive only 15% of combined ventricular output)
* It is small because it is constricted in utero * endothelin-1 or aspirin maintains the PA small

*Blood flow to the lungs (PULMONARY CIRCULATION) is ONLY FOR NOURISHMENT of the lungs, since the fetus does not

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, which
shows more RV force than that of adult

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High Ejects into the high resistance upper body circulation

Figure 2: Fetal Circulatory System

*afterload resistance the flow will encounter by the right ventricle *During fetal life, RV pumps blood against systemic BP and also performing greater volume of work than the LV.

PLACENTA Receives the largest amount of combined ventricular output (note: ventricular output= Right ventricle + Left ventricle) (55%) Lowest vascular resistance in the fetus (*so, blood flow) *Considered a separate organ where oxygenated blood from placenta flows to fetus thru the umbilical vein(PO2= 30-35 mmHg) MAIN AREA OF GAS EXCHANGE SUPERIOR VENA CAVA (SVC) Drains the upper part of the body, including the brain 15% CVO INFERIOR VENA CAVA (IVC) Drains the lowest part of the body and the placenta 70% CVO
***Since the blood is oxygenated in the placenta, the oxygen saturation in the IVC (70%) is higher than that in the SVC (40%) ***Highest PO2 is found in the umbilical vein (32 mm Hg)

FETAL CARDIAC OUTPUT Unlike the adult heart, which increases its stroke volume when the heart rate decreases, the fetal heart is unable to increase stroke volume when the heart rate falls Therefore the fetal cardiac output depends on the heart rate, when the heart rate drops as in fetal distress, a serious fall in cardiac output results combined ventricular output of both left and right ventricles ~450 ml/kg/min. ~ 65% of descending aortic blood flow returns to placenta; remaining 35% perfuses fetal organs and tissues

FETAL PULMONARY VASCULAR RESISTANCE (PVR) A. In the fetus: Pulmonary arteries (PA) : thicker medial smooth muscle 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 respiratory bronchiole 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 by hypoxia thereby develops it to smooth muscles allowing constriction hence decrease blood flow

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 the body (PO2 of 24 mmHg)
***1/3 of the IVC blood with higher oxygen saturation is directed 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 for oxygenation *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 from RV.

CONDITIONS THAT CAN CAUSE MEDIAL THICKENING: INC PVR Fetal hypoxemia Hypertension: *Pulmonary hypertension and pressure Altered fetal blood flow FACTORS THAT REGULATE THE TONE OF FETAL PULMONARY CIRCULATION: Mechanical effects: *mechanical compression of alveoli that comprises blood volume causing blood vessel resistance Oxygenation state: *Oxygen is a potent vasodilator Vasoactive substance: *i.e: PGI2, NO, O2 FACTORS INVOLVED IN THE CONTROL OF (PULMONARY VASCULAR RESISTANCE) PVR VASOCONSTRICTION Physical Decrease O2 Leukotrienes Thromboxane A2 Endothelin A activation Platelet derived growth Factor (PDGF) Platelet activating factor (PAF) AA metabolites VASODILATATIO
N

FETAL VASCULAR PRESSURE R & L atrial pressure are equal ( due to foramen ovale) Afterload of fetal ventricles: o RV: Low Ejects mostly into the low resistance umbilical-placental circulation o LV:

NO Increase O2 PGI2 PGD2 ET B activation

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NEONATAL CIRCULATION (CHANGES IN THE CIRCULATION AFTER BIRTH) Primary change in circulation after birth is a shift of blood flow for gas exchange from the placenta to the lungs The placental circulation disappears:*Short hypoxia due to cutting umbilical cord
*beyond 42 weeks of gestation blood vessels necrose (dissolve)

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*If it does not close, congestions of lungs may occur. (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 heart 2. Establishment of series circulation 3. Cardiac output increases to meet demands 4. Thyroid hormone, cortisol, catecholamines 5. Associated with increased blood flow to myocardium, renal and GI and a decrease in flow to adrenal, cerebral blood flow
*shunts should go after birth

Pulmonary circulation is established (*Series circulation) heart rate slows in response to an increase in systemic vascular resistance with onset of ventilation, PVR is markedly increased closure of DA and fall in PVR results in decrease in pulmonary arterial and right ventricular pressure 1st several wks of life PVR decreases further secondary to remodeling of pulmonary vasculature

PULMONARY VASCULAR RESISTANCE (PVR) Decrease with the initiation of ventilation and oxygenation due to: 1. Partial pulmonary vasodilatation caused by physical expansion of the lung and prostacyclin 2. Further pulmonary vasodilatation associated with fetal oxygenation and Nitric Oxide (NO) production
*Nitric Oxide causes vasodilatation

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 SAP 4 wks adult levels 3-6 mos PA pressure cont. to dec - PVR reaches adult levels INTERRUPTION OF THE UMBILICAL CORD RESULTS TO THE FOLLOWING An increase in systemic vascular resistance (SVR) as a result of the removal of the very-lowresistance placenta (shunt 1): *slows heart rate Closure of the ductus venosus (shunt 2) as a result of lack of blood return from the placenta LUNG EXPANSION RESULTS IN THE FOLLOWING: LA pressure increases as a results of the increased pulmonary venous return to the LA RA pressure falls as a result of closure of the ductus venous Functional closure of the foramen ovale (shunt 3) occurs as a results of increased pressure (because of the increased pressure from the pulmonary circulation) in the Left Atrium (LA) in excess of Right Atrium (RA) pressure A reduction of the PVR: *because intrapulmonary arteries are no longer constricted by amniotic fluid 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 CLOSURE OF CENTRAL SHUNTS AND SYSTEMIC CIRCULATION A. Closure of Foramen Ovale 1. Ligation of umbilical cord/ removal of the placenta/separation of the NB from umbilical/ placental circulation 2. Decrease in IVC flow 3. Decrease in RA pressure 4. Increase pulmonary flow 5. Increase LA pressure-> decrease RA will lead to closure of foramen ovale B. Closure of Ductus Ateriosus 1. Exposure to increase oxygenation 2. Decrease Prostaglandin E2 (PGE2) (removal of placenta/ metabolism in the lungs): *PGE2 keeps the ductus arteriosus open 3. Higher incidence of patency in preterm 4. Causes L-R shunting

Increase PBF and Decrease PVR Mechanical and Humoral Factors: (all causes dilatation) 1. Replace alveolar fluid with gas 2. Decrease compression on pulmonary arterioles 3. Gas-liquid interface in the alveoli produced 4. 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 fetal lung fluid leaves alveoli *First few breaths must be effective to allow fluids to leave the alveoli
Figure 7: Pulmonary Blood Vessels at Birth

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*Pulmonary arterioles dilate causing increase in pulmonary blood flow (PBF)
Figure 8: Cessation of Shunt through Ductus Arteriosus

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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 go to the pulmonary circulation kaya walang oxygenation. For the patient to thrive, PATENT DUCTUS ARTERIOSUS is needed para magkaroon ng mixture ng oxygenated and unoxygenated blood. Oxygen should not be given to prevent closure of the said shunt. To maintain the PDA, prostaglandin should be administered.)

Ductus Arteriosus constricts Blood flows through the lungs to pick up oxygen; blood oxygen levels rise FETAL AND 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 arterial pressure) 4 weeks old: adult levels PA PRESSURE CONTINUES TO DECREASE: In 3-6 months due to thinning of the muscular layer of the small pulmonary arteries (vascular remodeling) muscular involution
***PVR- reaches adult levels by 3-6 months

Differences between Neonatal and Older infants Circulation: 1.) R-L or L-R shunting may persist across the patent foramen ovale 2.) continued patency of DA may allow L-R, R-L or bidirectional shunting 3.) neonatal pulmonary vasculature constricts more in response to hypoxemia, hypercapnia and acidosis 4.) wall thickness and muscle mass of neonatal L and R ventricles are almost equal 5.) newborn infants at rest high O2 consumption; high CO
*normal DA has significant amount of circularly arranged smooth ms in its medial layer *full term neonate, O2 is most important factor controlling ductal closure

WHEN TO SUSPECT A HEART PROBLEM IN AN INFANT A physician may suspect that one of these heart defects is present if the child is not growing normally, has a heart murmur or has one or more signs (e.g., a bluish tint to the skin called cyanosis) Congenital Heart Disease-It is a heart-related problem that is present since birth and often as the heart is forming even before birth Incidence: 1% (8-12 of 1000 live births) 1. 2. 3. CAUSES Genetic Environmental factors: viruses, certain drugs, radiation, living in high altitudes Rubella (German measles) during the first three months of pregnancy have a high risk of having a baby with a heart defect (Congenital Rubella Syndrome) Medications Drinking alcohol in pregnancy also can increase the risk of heart defectsbabies with fetal alcohol syndrome (FAS) Cocaine Smoking during pregnancy Chromosomal defects : Downs Syndrome

CONGENITAL CARDIAC DISORDERS IMPORTANT CONDITIONS ASSOCIATED WITH ALTERED DECREASE IN PVR AT BIRTH: 1. Persistent Pulmonary Hypertension of the Newborn (PPHN) o Failure to achieve/maintain the decrease in 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 delivery Manifestation: cyanosis Treatment:dilation of vessels o Other findings: In utero events resulted to endothelial dysfunction & impaired NO & ET-1 activity *previously known as Persistent Fetal Circulation 2. Congenital heart defects with large communications at the ventricular or great vessel level (within PA or AORTA) o Delayed fall in PVR in the presence of increased pulmonary blood flow or pressure o Endothelial injury o Remain unclear
*In these instances, patient will remain desaturated

4. 5. 6. 7. 8.

FETAL AND NEONATAL CIRCULATION Fetal Circulation Neonatal Circulation Parallel Series circulation circulation Intracardiac No IC shunts shunts Low PVR High PVR Relatively high Relatively low CO CO Lungs Gas exchange in the placenta Three cardiovascular structures unique to the fetus are important to maintain this parallel circulation: ductus venosus, foramen ovale, ductus arteriosus

CLASSIFICATION OF CONGENITAL HEART DISEASE A. Cyanotic Heart Disease a. Pulmonary Valve Atresia b. Total Anomalous Pulmonary Venous Return (TAPVR) c. Ebstein Anomaly B. Acyanotic Heart Disease a. Left to Right Shunt i. Ventricular Septal Defect ii. Atrial Septal Defect iii. Patent DuctusArteriosus iv. Atrio-Ventricular Canal Defect v. Partial Anomalous Venous Return b. Obstructive Lesions i. Pulmonary Stenosis ii. Aortic Stenosis iii. Tricuspid Stenosis iv. Mitral Stenosis v. Coarctation of the Aorta BASIC TOOLS & LABORATORY EXAMS IN EVALUATING A CONGENITAL HEART DISEASE ARE: History/ Physical Exam Chest X-ray
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15 leads ECG Arterial Blood Gas

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2nd HS: ( aortic & pulmonic valve closure) Single- 1st 6 hours OL Split- 48 hours Single S2: defect that equalize pulmonic & aortic pressure o E.g. aortic/ pulmonic stenosis HLHS Truncusarteriosus Transposition 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 the great arteries/ malfunction of SL valves) Innocent murmur o Soft murmur o Non specific *not all murmurs are pathologic, usually not heard from diastolic Loud harsh murmur o Usually pathologic CYANOSIS: Assessment affected by: lighting, reflected light from wall paint, skin pigmentation, examiners experience Need 3-5 g of reduced hemoglobin/dl to detect it Differential cyanosis (Coarctation/ Interrupted aortic arch) Differentiate with a pulmonary condition
*do ABG (Arterial Blood Gas) first then give Oxygen for 10minutes

1.Heart Murmur a. Evaluated in a timely manner b. Ductal dependent cardiac lesions 2.Respiratory distress 3.Shock 4.Cyanosis with no respiratory distress 5.Circulatory collapse in the 1st 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 ASSESSMENT OF PERIPHERAL PERFUSION: Low CO or CHF: Pallor ( peripheral vasoconstriction caused by high circulating endogenous catecholamines) Mottled/ cyanosis of distal extremities/ delayed CRT Cold extremities Pulses weak and thready Leads to metabolic acidosis & decrease coronary perfusion E.g. Hypoplastic L heart syndrome Coarctation of the aorta Critical aortic stenosis PULSES: Related to pulse pressure and stroke volume ( SBPDBP) Weak/ thready: Decrease CO Bounding: due to wide pulse pressure Systemic to pulmonary arterial connections PDA/ aortopulmonary window/ AV malformations/ extensive aorto-pulmonary collaterals RESPIRATORY EFFORT: Usually at the upper limits of normal Respiratory pattern: Differ by the regularity of the tachypnea Lack of normal variation in the RR HEART RATE: 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 to enhanced vagal tone In intubated/ mechanically ventilated patients: bradycardia may be due to hypoxemia/ hypercarbia Bradycardia in non-distressed patient: congenital heart block EDEMA: Associated with CHD in Turners or Noonan syndrome 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)

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 pulmonary in 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 TEST May further differentiate if a cyanotic child has a CHD, cyanotic type VS, PPHN ***Rules: Murmur associated with significant cyanosis warrants 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 visual representation of the electrical conduction of the heart. As each signal travels from the atria to the ventricles 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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1. 2. 3.

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Count the R-R cycle in six large divisions and multiply it by 50 When the heart rate is slow, count the number of large divisions between two R waves and divide that into 300 (1min=300 large division) Approximate heart ratewhen R-R intervals are 5,10,15,20 and 25 mm, the respective heart rates 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 rate can be estimated by dividing 300 by the number of large boxes in the R-R interval.

PEDIATRIC ECG P wave: represents the electrical signal as it travels through the atria, the atria contract and blood is forced into the ventricles. QRS waves: represent the signal as it travels through the ventricles, the ventricles contract and blood is forced into the arteries. T wave: represents the heart at rest prior to the next beat.
Figure 10: Pediatric ECG

VENTRICULAR RATE small squares (R-R interval) / 1500 big squares (R-R interval ) /300
Figure 12: Ventricular Rate

HEART RATES IN NORMAL CHILDREN Age Awake Mean Rate Newborn to 3 85 to 205 140 mo. 3 mo. to 2 yrs 100 to 190 130 2 yrs 10 yrs DIFFERENCES BETWEEN INFANT ECG AND ADULT ECG -reading of ECG for pediatric patients is essentially the same except 1. Heart rate Tachycardia accepted in newborn and decreases with age 2. Right Ventricular Hypertrophy In utero, work of RV is greater At birth- decrease in RVSP and increase in systemic resistance: LV becomes thicker than the RV 3. Right Axis deviation May remain up to one yr of age
Figure 11:Adult ECG Interpretation

Sleepin g Rate 80 to 160 75 to 160 60 to 90 50 to 90

60 to 140 60 to 100

80 75

More than 10 yrs

RHYTHM Sinoatrial (SA) Node: Located in the right upper part of the atrial mass The direction of atrial depolarization is from the right upper part toward the left lower part producing the P axis in the left lower quadrant (0 to +90 degrees) What is Normal Sinus Rhythm? During Normal Sinus Rhythm, the SA Node (Sinoatrial Node) fires electrical signals at a regular rhythm in accordance with the need for more or less oxygen by your body Normal Sinus Rhythm is the ideal rhythm. Sinus Rhythm 1. P wave preceding each QRS complex (Every QRS complex is preceded by a P wave but not every P wave must be followed by a QRS as occurs if there 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 wave in AVR

Routine Interpretation 1) Heart Rate (Atrial and ventricular rates, if different) 2) Rhythm (sinus or not sinus) by considering the P axis 3) QRS axis, T axis, QRS-T angle 4) Intervals: PR, QRS and QT 5) P wave amplitude and duration 6) QRS amplitude and R/S ratio; abnormal Q waves 7) ST segment and T wave abnormalities HEART RATE Methods to Calculate Heart Rate

Figure 14: EKG Leads 091411 PHYSIOLOGY 7th Lecture (3rd LE)

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for respiration at this point as the fetus is suspended in amniotic fluid).

MEAN AND RANGE OF NORMAL QRS AXES Age 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 umbilical vein. About half of this enters the fetal ductus venosus and is carried to the inferior vena cava, while the other half enters the liver proper from the inferior border of the liver. The branch of the umbilical vein that supplies the right lobe of the liver first joins with the portal vein. The blood then moves to the right atrium of the heart. In the fetus, there is an opening between the right and left atrium (the foramen ovale), and most of the blood flows through this hole directly into the left atrium from the right atrium, thus bypassing pulmonary circulation. The continuation of this blood flow is into the left ventricle, and from there it is pumped through the aorta into the body. Some of the blood moves from the aorta through the internal iliac arteries to the umbilical arteries, and re-enters the placenta, where carbon dioxide and other waste products from the fetus are taken up and enter the maternal circulation. Some of the blood entering the right atrium does not pass directly to the left atrium through the foramen ovale, but enters the right ventricle and is pumped into the pulmonary artery. In the fetus, there is a special connection between the pulmonary artery and the aorta, called the ductus arteriosus, which directs most of this blood away from the lungs (which aren't being used 091411 PHYSIOLOGY 7th Lecture (3rd LE)