n5315 pulmonary and shock core knowledge study objectives with advanced organizers university of texas
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N5315 Advanced Pathophysiology
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N5315 Advanced Pathophysiology
Pulmonary and Shock
Core Concepts and Objectives with Advanced Organizers
Age related Difference in pulmonary anatomy and physiology
1. Describe the age-related changes which occur in the alveoli, chest wall, and gas exchange.
o Pulmonary system loses elastic recoil, the chest wall stiffens, there are changes in gas
exchange and there is an increase in flow resistance
o Alveolar wall tissue is decreased with age which leads to a decrease in the alveolar
surface area available for gas diffusion.
o There is a decreased vital capacity, increased residual volume, and decreased
ventilation perfusion ratio.
2. Explain the structure and physiologic differences of the pulmonary system in the infant and
child.
o Infants and children have smaller airways and experience more obstructive episodes
from mucosal edema or secretion accumulation
o Infants have bigger tonsils
o Infants are nose breathers until 2-3 months and nasal congestion can be problematic
o Surfactant is produced by 20-24 weeks gestation and is secreted in the fetal airways by
30 weeks gestation.
A surfactant deficiency is seen in premature infants and causes respiratory distress
syndrome
o Chest wall compliance is high in infants
o Oxygen consumption is greater in infants because their high metabolic rate
o Children have less glycogen reserves and limits the effectiveness of the accessory
muscles, and fatigue and lactic acidosis may occur quickly
o Respiratory control is not mature in the neonate, so they do not respond as well to
hypoxia and hypercapnia as a child or adult would
o Infants are at an increased risk for apnea and hypoxia
3. Examine the process of ventilation, gas exchange and transport.
o Ventilation
Ventilation is the movement of air in and out of lungs
The brain stem houses the respiratory center which is responsible for controlling
ventilation by sending impulses to trigger the contraction and relaxation of the
respiratory muscles
Central chemoreceptors monitor arterial blood to help maintain the pH, PaCO2 and
the PaO2.
o Gas Exchange
The alveoli are the primary gas-exchange units of the lung, where oxygen enters
the blood and CO2 is removed
o Gas Transport
Deliver of Oxygen to the Cells
Ventilation of the lungs
Diffusion of oxygen from the alveoli into the capillary blood
, Perfusion of systemic capillaries with oxygenated blood
Diffusion of oxygen from systemic capillaries into the cells
Removal of CO2
Diffusion of CO2 from the cells into the systemic capillaries
Perfusion of the pulmonary capillary bed by venous blood
Diffusion of CO2 into the alveoli
Removal of CO2 from the lungs by ventilation and exhalation
Pulmonary Vascular Disorders
1. Analyze the etiology, clinical manifestations and pathophysiology of pulmonary
embolus, and pulmonary edema.
Disease Etiology Clinical Manifestations Pathophysiology
Pulmonary o Results commonly o Symptoms are o When the embolus lodges in the
Embolus from a proximal vague but may pulmonary circulation it triggers the
DVT in the lower include chest pain, release of serotonin, histamine,
extremities syncope, cough, catecholamines, angiotensin II,
o May arise from dyspnea, inflammatory mediators, and toxic
tissue fragments, a tachycardia, or oxygen free radicals
foreign body, an air unexplained anxiety o These cause vasoconstriction with
bubble, fat embolus o Hemoptysis may be further impedes blood flow and
from a fracture, or present causes an increase in the pulmonary
amniotic fluid o Important to artery pressure and can lead to right
understand risk ventricular dilation and increased
factors because of afterload
vague symptoms o The decrease or absent blood flow to
a portion of the lung leads to a V/Q
mismatch and a decrease in surfactant
production and causes atelectasis, and
hypoxemia
o May cause lung infarction, decreased
cardiac output, shock and death
Pulmonary o Most common o Dyspnea, o The accumulation of water in the
Edema cause is left-sided hypoxemia, pulmonary alveolar sacs.
heart failure. pulmonary rales, o Prevents the proper exchange of
o Other causes dullness to gases and leads to dyspnea, chest
ARDS, inhalation percussion, S3 heart pain and hypoxia
of toxic gases, sound and frothy o In left-sided heart failure the backup
increased sputum of blood into the lungs increases
pulmonary venous o May often have capillary hydrostatic pressure which
pressure and orthopnea, or pushes fluid out into the alveolar sacs
damaged alveolar paroxysmal o In post-obstructive pulmonary edema,
capillaries nocturnal dyspnea inspiration against an occluded
o Post-obstructive airway creates excessive intrathoracic
pulmonary edema negative pressure which leads to
or re-expansion increased venous return to the right
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