NeoRespCare 1.pptx PDF
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Tarlac State University
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Summary
This presentation provides an overview of neonatal respiratory care, covering topics such as placental exchange, pulmonary development, fetal circulation, and the transition period. It details different phases of lung development, including embryonic, pseudoglandular, canalicular, and alveolar stages. It also touches on the clinical aspects of respiratory distress syndrome and other complications important to neonatal care.
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Overview Part I Placental exchange Development of the Pulmonary System Development of the Cardiovascular System Fetal Circulation Part II Physiologic development Transition Period – Lung growth – Surface Forces Mechanics of ventilation – Ventilation Part III Neonatal...
Overview Part I Placental exchange Development of the Pulmonary System Development of the Cardiovascular System Fetal Circulation Part II Physiologic development Transition Period – Lung growth – Surface Forces Mechanics of ventilation – Ventilation Part III Neonatal Parenchymal Diseases RDS – BPD – Meconium Aspiration Syndrome TRANSITION PERIOD At birth, the neonate is required to make a transition from placental gas exchange to respiration that is dependent on the lung. The level of lung development greatly influences the success of this transition, and allows prediction of the possible need for supportive care. PLACENTAL EXCHANGE A low resistance circulatory system – blood can flow easily Provides for the exchange of nutrients and waste products, including oxygen delivery and CO2 elimination Umbilical cord: 2 arteries – deoxygenated blood from the fetus to the placenta 1 large vein – oxygenated blood to the fetus PLACENTAL EXCHANGE Maternal system uterine spiral arteries intervillous space chorionic villi where communication with the fetal circulation takes place Large maternal-fetal PO2 gradient Higher Hgb conc in the fetus Fetal hemoglobin e –ve.rend Respiratory system is composed of millions of air exchange units connected e –ve.Inter to outside by conducting airways mainly toInte PHASES OF LUNG DEVELOPMENT 0 26d 6wk 16wk 26wks 40 weeks Embryonic – covers primitive development PHASES OF LUNG DEVELOPMENT 0 26d 6wk 16wk 26wks 40 weeks Pseudoglandular – conducting airway system is developed; PHASES OF LUNG DEVELOPMENT 0 26d 6wk 16wk 26wks 40 weeks Canalicular respiratory portion (respiratory bronchioles) begins to PHASES OF LUNG DEVELOPMENT 0 26d 6wk 16wk 26wks 40 weeks Saccular – well defined gas exchange areas develop PHASES OF LUNG DEVELOPMENT 0 26d 6wk 16wk 26wks 40 weeks Alveolar – alveolar sacs; mature alveoli Embryonic Phase: Primitive development (first 5 weeks) 21-26 days after foregut Lung bud fertilization period Pulmonary 1st Sequestration branchin g 2nd Tracheoesophage al Fistula (TEF) branching Tracheal Agenesis/Stenosi s esophag us 3rd branching Pseudoglandular phase (weeks 6-16) Pseudoglandular phase Conducting airways are lower conduction airways, formed lymph vessels 1st 20 generations of conducting bronchial capillaries airways 1st 8 generations - cartilaginous walls - 9-20 generations – non respiratory bronchioles Congenital diaphragm atic hernia Congenit al lobar emphyse ma Bronchog enic cyst Canalicular phase (week 16-26) generati on 21- pulmona gas- 23 – ry exchang respirat capillari ing acini ory es bronchi oles Terminal sac phase (week rudimentar 27-36) y primary developme saccules refinement capillary nt of the divide to of the acini invasion surfactant subsaccule system s and alveolitransie nt tachyp nea of the newbor n pulmona ry interstiti al emphyse ma respiratory distress syndrome Alveolar phase (week 36- 8 years) alveolar Alveolar proliferati developm on ent subsacc polyhedr alveoli ules al shape The Heart he heart=a muscular double pump with 2 functions Overview The right side receives oxygen-poor blood from the body and tissues and then pumps it to the lungs to pick up oxygen and dispel carbon dioxide Its left side receives oxygenated blood returning from the lungs and pumps this blood throughout the body to supply oxygen and nutrients to the body tissues simplified… Cone shaped muscle Four chambers – Two atria, two ventricles Double pump – the ventricles Two circulations – Systemic circuit: blood vessels that transport blood to and from all the body tissues – Pulmonary circuit: blood vessels that carry blood to and from the lungs Valves three tricuspid one bicuspid (cusp means flap) “Tricuspid” valve – RA to RV Pulmonary or pulmonic valve – RV to pulmonary trunk (branches R and L) Mitral valve (the bicuspid one) – LA to LV Aortic valve – LV to aorta Pattern of flow Body Body to right heart to lungs to left heart to body RA RV Body, then via vena cavas and coronary sinus to RA, to RV, then Lungs to lungs via pulmonary arteries, then to LA via pulmonary veins, to LA LV, then to body via aorta LV From body via SVC, IVC & coronary sinus to RA; then to RV through Boby tricuspid valve; to lungs through pulmonic valve and via pulmonary arteries; to LA via pulmonary veins; to LV through mitral valve; to body via aortic valve then aorta Development of the Cardiovascular System Embryological development during week 4 (day 23) (day 28) (day 24) Day 22, (b) in diagram, heart starts Development of Cardiovascular System 3rd week - two tubes 4th week - heart surrounded by begins to beat myocardial tissue Heart begins to twist Tubes fuse form single and fold chamber Eventually will form four chambers Development of Cardiovascular System Sinus venosus - horns at bottom of embryonic heart - will become vena cava’s and portion of right atrium Truncus arteriosus - will form pulmonary artery and aorta Development of Cardiovascular System Bends in middle - S 5th week - heart takes shape on shape of adult Rapid growth heart Development of Developing veins and chambers arteries couple the Blood flow begins - heart to circulatory one way flow system Separate blood paths created Fetal Circulation Pressure in the fetal vasculature Systemic – Low resistance Placental – Low resistance Pulmonary – High resistance Characteristics of Fetal Circulation Normal shunts in the fetus Foramen ovale – bypasses lung Ductus arteriosus – bypasses lung Ductus venosus – bypasses liver Fetal Circulation Flow chart of the most oxygenated fetal blood Bypasses liver - ductus venosus Bypasses lungs - foramen ovale Fetal Circulation Flowchart of least oxygenated fetal blood Small amount feed lungs (high resistance) Most bypasses lungs - ductus arteriosus In the fetus, the RA received oxygenated blood from mom through umbilical cord, so blood R to L through the foramen ovale: fossa ovalis is left after it closes The pulmonary trunk had high resistance (because lungs not functioning yet) & ductus arteriosus shunted blood to aorta; becomes ligamentum arteriosum after 32 birth Overview Part I Development of the Pulmonary System Development of the Cardiovascular System Fetal Circulation Part II Physiologic development Transition Period – Lung growth – Surface Forces Mechanics of ventilation – Ventilation Part III Neonatal Parenchymal Diseases RDS – BPD – Meconium Aspiration Syndrome TRANSITION PERIOD Pulmonary Circulation In the fetus, blood flow to the lung is one-fifth to one-tenth the amount of found in the extrauterine life. There is high resistance to blood flow in the arterial bed of lung. Resistance – increased by hypoxia decreased by increasing O2 and by decreasing CO2 or hydrogen ion in pulmonary blood Fetal Lung Fluid Fetal lungs are fluid filled; approx 30ml/kg near term (~FRC) Contribute significantly to the amount of amniotic fluid aside from the kidney Necessary component of fetal lung growth; there must be some distention of the lung by the fluid for the lung to develop normally Can be decreased by carbonic anhydrase inhibitor , cyanide and epinephrine At birth, the secretion of lung fluid stops, and the liquid is absorbed into the lymphatic system and interstitium of the lung. Determination of Lung Development Too little amniotic fluid (oligohydramnios) chronic leaking of amniotic fluid diminished urine production hypoplastic (underdeveloped) lungs Potter’s syndrome / oligohydramnios sequence Decreased fetal breathing movements Diminished thorasic space congenital diaphragmatic hernia Determination of Lung Development Hormones Stimulates lung development/surfactant synthesis: Cortisol ACTH Thyroid hormones Estradiol Prolactin Epidermal growth factor Prostaglandins Inhibits surfactant synthesis Insulin Testosterone Lung Inflation at Birth Fetal respiratory movements ~ fetal well being - may be depressed by drugs / anesthesia Within minutes of birth, the lung is aerated and FRC is 95% of that found at 1 week of age Initial pressure to inflate the lungs: 20-40 cmH2O (can be as high as 70 cmH2O); succeeding inspiration pressures are lower Initial respiratory volume: 20 - 70 ml Initial residual volume: 20 - 30 ml These values occurs in term infants at birth; Preterm infants requires more effort to expand the lungs and have more tendency to deflate Lung Inflation at Birth During the first week of life, there is an increase in the compliance: 2 ml CMH2O to 4-6 ml cmH2O (appearance of surface active materials = surface tension) Stimulus for the newborn to breath decreasing O2 / increasing CO2 cutaneous stimuli Lung Growth Size increases as the child grows Grow fairly rapidly after birth; growth rate declines until a growth spurt during puberty Growth stops at about 17.9 years in girls, 19.8 yrs in boys Increase in lung volume is ~ 30-40 fold Weight increases approximately 15 fold from newborn to adult Larger in boys than in girls Lung Growth Frequency of Breathing – decreases form the neonatal period through adult life newborn: 40-60 breaths/min 5 years old: 20-30 breaths/min young adult: 15-20 breaths/min MECHANICS OF Inspiration VENTILATION Quiet breathing – contraction of the diaphragm When increased breathing needed – external intercostal muscles accessory muscles *nasal flaring Expiration generally passive Active phase of expiration: internal intercostal muscles abdominal muscles to push the diaphram up * In the newborn, expiration is interrupted before relaxation volume, effectively protecting FRC Lungs: organ for gas exchange Lungs expand by forces generated Lungs recoil secondary to by the diaphragm and intercostal muscles elastic and surface tension forces Pressure Volume Relationships Inspiration limb S shaped curve with flatter beginning and ending portion, and a moderately steep middle portion Expiration limb Hyster esis C shaped Hysteresis – caused in part by the surface forces within the lung Elastic Behavior Of The Lungs What makes the lungs to behave like balloon? Due to two things: 1. Compliance - stretchability of the lungs - change in lung volume per unit change in airway pressure 2. Elastic recoil - how quickly the lungs rebound after they have been stretched - depends on two factors: connective tissue in the lungs alveolar surface tension 45 Elastic Recoil The pressure required to counteract the tendency of the bronchioles and terminal air spaces to collapse is described Laplace Law P = 2 ST/ r P = pressure required to counteract tendency of air spaces to collapse ST = surface tension in the air spaces R = radius The main contributor to lung elastic recoil in the newborn is surface tension Laplace Law Surface Forces/Tension Depends on having air-liquid interface Surface Forces/Tension If an airless lung is inflated with liquid, the recoil pressure is half the amount found when the lung is inflated with air Significant part of the elastic recoil is caused by the surface tension present at the air- liquid interface In a system without any surface active material, the surface tension of water is fairly high. The forces at the surface of the air-liquid interface tend to pull the surface molecules away from the surface to a minimum Surface Forces/Tension The fluid that is initially present in the airways affects the ability of the lung to be inflated Amniotic fluid more resistance to movement > lung fluid > lung fluid with surfactant (least R) The pressure to collapse the lung is a combination of: elastic forces within the lung surface tension Surfactant: diminishes surface forces and reduces the tendency of the lungs to collapse Surfactant Production Secreted by Type II Alveolar Cells Surfactant Function Decreases inflation pressure Improves lung compliance Provides alveolar stability Decreases work of breathing Enhances alveolar fluid clearance Enhances foreign particle clearance Serves as a protective layer for cell surfaces Surfactant Composition Phospholipids (85%) Phosphoatidylcholine (Lecithin) – Major surfactant appears 18 weeks and peaks at 38 weeks Phosphatidylglycerol (PG) Phospgatidylethanolamine Phosphatidylinositol Sphingomyelin – Surfactant found in the amniotic fluid (decreases after 30 weeks) Neutral lipids (5%) Protein (10%) Determination of Lung Maturity Shake (Foam) Test LS ratio (Lecithin to sphingomyelin ratio) – Lungs mature when 2:1 (35 weeks) PG detection (Phosphatidylglycerol) – Lipid Absent until about 35 weeks gestation With advancing gestational age, increasing amounts of phospholipids are synthesized and stored in type II alveolar cells. Wk 20: start of surfactant production and storage. Does not reach lung surface until later Wk 28-32: maximal production of surfactant and appears in amniotic fluid Wk 34-35; mature levels of surfactant in lungs The amounts produced or released may be insufficient to meet postnatal demands because of immaturity. Conditions that Delays Surfactant Production Acidemia Mechanical Ventilation Hypoxia Hypercapnia Shock Maternal Diabetes Overinflation (A,B,C) Underinflation Smaller of Twins Pulmonary Edema Conditions that Accelerate Surfactant Production Maternal diabetes (D, Maternal infection F, and R) Placental Maternal heroin insufficiency addiction Betamethasone or Premature rupture of thyroid hormone membranes Abruptio placentae Maternal hypertension Prolonged labor without asphyxia Respiratory Distress Syndrome Decreased Surfactant = High Surface tension Preterm s High Small surface radius tension More pressure is needed to inflate the lungs ComplianceC = V/ P Ease at which the lung is deformed or distended It measures how much change in lung volume will take place for a given change in transmural pressure gradient, the force that stretches the lungs. (volume per unit pressure change) If compliance is decreased [decreased expansion of the lungs] large transmural pressure will be required to produce normal lung expansion. Lung is most compliant in the mid portion of the curve; less at both lower and upper parts of the curve Compliance Reduced when: – Pulmonary vessels are engorged with blood – Increased edema in the lung – Lung is stiff due to an inflammatory process – Parts of the lung have collapsed Specific Compliance – comparing compliance with a specific unit of lung volume such as the FRC Adult lung compliance is significantly greater than infant lung. Specific compliance has approximately the same value at all ages Pressure-volume loop : Normal vs RDS Low compliance : stiff lungs, extra work is required to br a normal volume of air Compliance Compliance FRC Newborn 4-6 ml/cmH2O 17 ml/kg Older children (8years old) 62.5 ml/cm H2O 1,000 ml 12 years old 110 ml/cmH2O 2,000 ml Specific compliance for each age: 0.055 to 0.062 ml/cmH2O/FRC Compliance of the respiratory system (lungs and chest wall) is less than lung compliance (2.67ml/cmH2O for newborn) RESISTANCE Resistance - inherent capacity of air conducting system and tissue to resist airflow Resistance to breathing results from - AIRWAY Resistance - Viscous Tissue Resistance Resistance Pressure difference between the beginning and end of a passageway Laminar flow < Turbulent flow Viscosity and density of inspired gas Diameter of the air passage Resistance decreases with increased lung and airway size If lung volume is exceedingly low, the small airways at the bottom of the lung will collapse resulting in atelectasis of the dependent areas of the lung. Contraction of the bronchial smooth muscle will also narrow airways and will increase resistance Nasal air passages represent about one-quarter of the total pulmonary resistance Newborns – obligate nose breathers AIRWAY RESISTANCE LESS Airways airway n ce Inspiration dilate and i sta lengthen res resistance E EAS NC R s I ti o n ecr e ed s u l a t INCREASE u m Airways are Acc Expiration compressed airway resistance borns: 50% of airway resistance is nasal resis Time Constants Resistance X Compliance = Time Constant A measure of how fast the lung or individual lung unit will empty or fill Newborn compliance ~ 0.005L/cmH2O flow resistance ~ 50 cm/H2O/L/sec time constant ~ 0.25 sec almost emptying the lung will take 0.75 sec Time Constants During rapid ventilation rate – may not have enough time to empty may result to increased lung volume and inadvertent PEEP The resistance of the system, if on mechanical ventilator, includes the endotracheal tube and the ventilator circuits May improve oxygenation but may result in reduced ventilation Either increased compliance or increased resistance will increase the time required to empty the lung or a particular unit of the lung May result to uneven ventilation to a partially obstructed part of the lung Alveolar Interdependence Alveoli are surrounded by other alveoli and interconnected by connective tissue. If alveolus starts to collapse, surrounding alveoli are stretched and they apply expanding forces on the collapsing alveolus, thereby help to keep it open. Work of Breathing During normal quite breathing, respiratory muscles work during inspiration to expand the lungs, whereas expiration is a passive process. Normally lungs are highly compliant and airway resistance is low, so only 3% of total energy is used by the body during quite breathing. Rate of breathing is regulated to produce maximum efficiency and minimize the work of breathing Newborn ~ 40 breaths/min RR or TV increases the amount of work done In patients with reduced compliance, there is tendency to take small, rapid breaths; in airway VENTILATION Definition Tidal volume (TV) – the volume of air moved in and out of the respiratory tract (breathed) during each ventilatory cycle. Inspiratory reserve volume (IRV) – the additional volume of air that can be forcibly inhaled following a normal inspiration. – can be accessed simply by inspiring maximally, to the maximal inspiratory level. Definition Expiratory reserve volume (ERV) – the additional volume of air that can be forcibly exhaled following a normal expiration. – can be accessed simply by expiring maximally to the maximal expiratory level. Vital capacity (VC) – the maximal volume of air that can be forcibly exhaled after a maximal inspiration. – VC = TV + IRV + ERV. Definition Residual volume (RV) – volume of air remaining in the lungs after a maximal expiration. – cannot be expired no matter how vigorous or long the effort. – RV = FRC - ERV Functional residual capacity (FRC) – volume of air remaining in the lungs at the end of a normal expiration. – FRC = RV + ERV Definition Total lung capacity (TLC) – volume of air in the lungs at the end of a maximal inspiration. – TLC = FRC + TV + IRV = VC + RV Minute volume – volume of air exhaled per minute Lung Volumes and Mechanics : Sick vs Well NBs Lung Normal RDS BPD volumes Functional 25-30 20-33 20-30 residual ml/kg capacity (FRC) Tidal volume 5-7 ml / 4-6 4-7 (TV) kg Compliance 1-2 ml/cm 0.3-0.6 0.2-0.8 H2O Resistance 25-50 cm 60-160 30-170 H2O/L/s VENTILATION Alveolar ventilation VA Anatomic dead space VD– non gas exchangeable part of the lung Total ventilation = VA + VD usually calculated per minute Minute Ventilation VE VE = frequency X tidal volume VD - estimated; 1ml/lbBW Newborn RR 40/min; TV 16.5ml; VD 4.1ml VE 660ml; VA 496ml Frequency decreases with increase in size. All volumes increase, generally in a linear relation to height VENTILATION Has a direct effect on PCO2 Alveolar ventilation VA = VCO2 x K PCO2 VCO2 – volume of CO2 expired in 1 min PACO2 – partial pressure of CO2 in the alveolus PaCO2 – partial pressure of CO2 in the arterial blood Because the production of CO2 (VCO2) in most instance is relatively constant, a change in VA will produce an expected change in PaCO2 but in the opposite if VA is halved, then the PaCO2 will Ventilation-Perfusion Relationships Neither ventilation nor perfusion (Q) is uniform throughout the lung. In an upright lung, both are better in the lower parts of the normal lung. Perfusion – because of increased hydrostatic pressure; upper part is limited because of the collapse of small vessels from surrounding pressures Ventilation – difference between upper and lower is lesser in degree Ventilation would quantitatively match the Q, giving maximum transport of O2 and CO2 in all areas of the lung Ventilation-Perfusion Relationships Ventilation would quantitatively match the Q, giving maximum transport of O2 and CO2 in all areas of the lung VA/Q PAO2 PACO2 Top 3 (adult) 130 25 mmHg mmHg Bottom