Unit 4: Musculoskeletal Disorders Gould: Chpt. 26: Porth: Chpt. 58
Unit 5: Respiratory Disorders
Gould: Chpt. 19: Porth: Chpt.28, 29
The main function of the respiratory system is gas exchange which provides body tissues with adequate O2 for cellular metabolism, and removes CO2, a by-product of metabolism
The respiratory system works in conjunction with the renal system to maintain blood pH and acid-base balance:
Facts for Review:
normal pH: 7.35 – 7.45
reflected in a HCO3- to H2CO3 ratio of 20:1
normal serum HCO3-: 24-31 mmol/L
normal serum CO2: 24-29 mmol/L, Pa CO2: 35-42 mm Hg
normal PaO2: XXXXXXXXXXmm Hg
arterial O2 saturation (SaO2) : 96%-98%
Base excess or deficit is essentially a measurement of HCO3- excess or deficit, and describes the amt of acid or base that must be added to
ing the blood pH to 7.4
O2 saturation (SaO2) reflects the degree to which O2 is bound to available sites on hemoglobin and therefore the oxygenation of the blood
CO2 + H2O H2CO XXXXXXXXXXH+ + HCO3-
lungs
kidneys
*
-H2CO3: ca
onic acid
-acidic conditions push the equation to the right: more CO2 from resp. acidosis leads to higher H+ levels and decreased pH
-the above equation represents the main buffer system in the body: the bica
onate-ca
onic acid buffer system: acts to buffer blood pH (Corwin)
-allows excess H+ in the system to be converted to ca
onic acid, resulting in fewer free H+ remaining in solution, preventing blood pH from falling
-Ca
onic acid can also be converted to CO2: hence, excess H+ can be removed from the system as CO2
-base excess represents (metabolic) alkalosis, and base deficit represents (metabolic) acidosis
-PaO2 represents the amount of O2 dissolved in the plasma
-O2 saturation: amount of oxygen bound to hemoglobin in comparison with the amount of oxygen Hb can ca
y
-adequate oxygenation of the blood is from 100 mm Hg to 60 mmHg (down from 100): in this range, saturation is still high, ~ 90%
Respiratory System Review: Anatomy
Upper Respiratory Tract: passageways that conduct air between the atmosphere and lungs: nose, nasal cavity, pharynx, larynx
Lower Respiratory Tract: trachea,
onchi,
onchioles and lungs (alveoli)
Lungs: right, three lobes; left, two lobes; lobes are divided into lobules
Each lung resides in a pleural cavity and is su
ounded by a double-layered pleura
parietal pleura attaches the lung to the thoracic wall and diaphragm; the visceral pleura covers the lung surface
layers are separated by a pleural cavity containing pleural fluid
fluid creates surface tension that helps to keep the naturally recoiling lungs inflated and reduces friction
Figure 23-12 Marie
Figure 9-2 Made
*
Respiratory System Review: Anatomy Cont’d
Each lobe has a
onchiole which
ings air to many alveoli
Alveoli: sac of simple squamous epithelium su
ounded by capillaries where gas exchange occurs
Figure 9-5 Made
Figure 23-9D Marie
The walls of the alveoli with their fused basement mem
anes form the respiratory mem
ane across which gas exchange occurs
endothelial cell
Respiratory
mem
ane
Nucleus of squamous epithelial cell
Red blood cell
Capillary
*
Ventilation-Perfusion Coupling
The ventilation:perfusion ratio (VE/Q) reflects the match of air flow through the alveoli to blood flow in the adjacent pulmonary capillaries
Gas exchange is most efficient when ventilation matches perfusion
The pulmonary arterioles will constrict or dilate in order to match ventilation with perfusion
Figure 27-21 Porth
Mismatch occurs when:
ventilated alveoli are not well perfused
perfused alveolic are not well ventilated
Figure23-19 Marie
*
-ventilation: the exchange of gases in the resp, system (Porth)
-two types: pulmonary ventilation ~ total exchange of gases between the atmosphere and the lungs; alveolar ventilation ~ exchange of gases within the alveoli
-mismatch: poor perfusion e.g. embolism; poor ventilation e.g. atelectasis
Respiratory Dysfunction
Respiratory Failure occurs when the lungs fail to adequately oxygenate the blood and prevent CO2 retention
results from conditions that:
impair ventilation e.g. disease of the airways and lungs
impair fx’n of resp. center e.g. drug overdose hypoventilation
cause ventilation-perfusion mismatch e.g. obstructive or restrictive disease
involve chest wall injury/deformities
impair diffusion e.g. edema
disrupt blood flow in the lungs e.g. pulmonary embolus
involve resp. muscle failure e.g. muscular dystrophy
Defined by blood gases of:
PO2< 50 mm Hg (hypoxemia)
PCO2 > 50 mm Hg (hypercapnia) and resp. acidosis
Respiratory Insufficiency: state when blood gases are abnormal but cell fx’n can continue
Respiratory A
est: cessation of respiratory activity
*
-obstructive disease e.g. cystic fi
osis, cancer, aspiration, asthma
-restrictive disease: those in which lung expansion is impaired and total lung capacity is reduced e.g. kyphosis, pulmonary fi
osis, pleural effusion
Hypoxemia
Hypoxemia: condition of reduced arterial O2 concentration
Causes:
decreased O2 in air (hypoxia)
hypoventilation
impaired diffusion e.g. edema
shunt
hypoperfusion e.g. embolus
anemia
Manifestations:
~ tissue hypoxia and compensatory mechanisms
PO2 < 50 mm Hg, pH
tachycardia, slight BP, pale, cool, clammy skin ~ SNS compensation
hyperventilation ~ low O2 stimulation of peripheral chemoreceptors
impaired mental fx’n e.g. confusion, delirium
impaired sensory fx’n e.g. visual impairment
stupor and coma (late)
adycardia and BP (late)
cyanosis (late)
*
-decreased pH ~ anaerobic metabolism by cells
-shunt: blood moves from the venous side to the arterial side without first passing through the lungs
-recall; mild hypoxemia produces few manifestations because at 6o mm Hg, the O2 saturation is still ~90%
-peripheral chemoreceptors respond to O2 levels: create respiratory drive
-
adycardia and hypotension are considered preterminal conditions, indicating failure of compensatory mechanisms
Hypoxemia Cont’d
Compensations:
tachycardia, slight BP, pale, cool, clammy skin ~ SNS activity
hyperventilation ~ low O2 stimulation of peripheral chemoreceptors
polycythemia is only beneficial if hypoxemia is not acute or due to anemia
Cyanosis: bluish coloration of the skin and mucous mem
anes when large amts of blood hemoglobin are deoxygenated in the small BVs (5 g or more unsaturated Hb per 100 mls blood)
In anemia ~ impaired hemoglobin synthesis (e.g. iron-deficiency anemia), Hb is low, and the Hb present is oxygenated above 5 g /100 ml; no cyanosis
Cyanosis will also not develop in O2 saturation from ca
on monoxide poisoning because the CO binds to Hb (i.e. the Hb is saturated)
Those who are polycythemic may also be cyanotic without being hypoxic d/t H
Bluish coloration of skin is hard to detect in dark-skinned individuals: can be observed in nail beds or testing blood gas O2 levels
In providing O2 therapy for hypoxia, rate of administration must be closely monitored to prevent oxygen toxicity ~ body distu
ances (lung damage, visual and hearing abnormalities, fatigue while
eathing, anxiety, confusion twitching, convulsions)
*
-anemia: decrease in # of circulating functional RBC, abnormal Hb; both result in impaired oxygen ca
ying capacity
-ca
on monoxide poisoning: CO displaces O2 and binds to heme: manifests as
ight red coloring of the skin and mucous mem
anes
-note: normal saturation (~98%) is 14.7 g /100 ml
-O2 toxicity: alveolar injury caused by high oxygen concentrations (Lewis); is believed that high concentrations of O2 may inactivate surfactant and lead to acute respiratory distress syndrome
Systemic Hypoxia
Systemic hypoxia can result from:
Hypoxia results in reduced ATP synthesis impaired cellular fx’n, mem
ane integrity, waste removal cell swelling, toxification, pH, loss of enzymes and enzyme fx’n, release of destructive enzymes necrosis
Compensation mechanisms include: switch to anaerobic metabolism, SNS, erythropoietin secretion
Heart,
ain and kidney cells are most susceptible to hypoxia ~ high metabolic rate and O2 requirements
inadequate O2 in ai
respiratory disease or pulmonary edema causing impaired oxygenation in the lungs
ischemia
anemia: low concentration of functional hemoglobin or RBCs O2 ca
ying capacity
generalized edema
*
-hypoxia: decrease below normal levels of O2 in inspired gases, arterial blood or tissues; in this case, the tissue hypoxia is due to decreased perfusion (ischemic)
-inadequate O2 in air~ reduced atmospheric pressure, ca
on monoxide poisoning
-lung disease: hypoxic hypoxia: results from a defective mechanism of oxygenation in the lungs
-ischemia: ischemic hypoxia; tissue hypoxia d/t arterial obstruction or vasoconstriction
-anemia: anemic hypoxia hypoxia resulting from a decreased concentration of functional Hb or a reduced # of eryrthrocytes
-edema increases diffusion distance in tissues
- SNS manifests as tachycardia, BP~ TPR
-neurons cannot last longer than 5 minutes, cardiac muscle not longer than 20 minutes
-O2 requirements in
ain: NRG in
ain mainly provided by ATP:
ain receives 1/6 of CO and accounts for 20% of O2 consumption (Porth, pg 1160)
Hypercapnia
blood PCO2; occurs with hypoxia
Causes: same as hypoxia, esp. hypoventilation and ventilation-perfusion mismatch; also cellular metabolism or high ca
ohydrate diet
central chemoreceptors respond to CO2 by respiration rate; over time these receptors become less sensitive
peripheral receptors control respiration by responding to levels of O2 (hypoxic respiratory drive)
in persons with resp. disease causing chronic hypoxia and hypercapnia, administration of O2 may suppress respiratory drive ~ peripheral receptors respiration rate and further hypercapnia
Manifestations:
respiratory acidosis: CO2, pH, HCO3- (renal compensation)
vasodilation: headache, flushed skin
suppression of neural fx’n: lethargy, drowsiness, disorientation, coma
air hunger and rapid
eathing
*
-note: CO2 has vasodilator effects as a metabolite of cellular metabolism
-headache: ~ vasodilation of neural BVs
-high ca
diet: increases production of CO2 (Porth)
-respiratory drive: decreased sensitivity means that the central receptors no longer regulate respiration based on CO2 levels (there is a compensatory increase in bica
onate secretion into the CSF, which buffers the H+ ions); therefore rely on stimulation for ventilation by low O2 levels; hypoxia is the main stimulus for ventilation in those with chronic hypercapnia; administration of O2 at a level sufficient to increase PO2 above that needed to stimulate the peripheral receptors can lead to depression of ventilation
-vasodilation: recall that metabolites cause dilation of local arterioles
-suppression of neural fx’n: ~ acidosis as well as hypoxia
Aspiration
Aspiration: the passage of food, fluid or other foreign material into the trachea or lungs
Usually, the cough reflex removes material from the upper tract and passage into the lower tract is prevented by the vocal cords and epiglottis
Complete obstruction of upper tract inhibits the ability to speak or cough; blockage of the trachea is life-threatening ~ inadequate oxygenation
Sharp pointed objects and fatty or i
itating solids cause inflammation which causes swelling, edema and
onchoconstriction block air flow
Pointed objects may also form a “
idge” upon which other materials collect and cause obstruction
Peanuts and legumes may swell and become more firmly lodged
The right lower lung is usually the lodging site of aspirated objects
Wherever in the tract the object lodges, it obstructs air flow beyond that point
obstruction of a
onchus no air delivery and collapse distal to the obstruction (atelectasis)
Figure 19-20C Gould
*
-cough: inspire air, close the glottis, then forcefully expel the air against the glottis causing the unwanted material to move upward and out of the mouth or to swallow it
-milk ~ oil, vomitus ~ acid
-right lung: due to anatomy of
onchioles which go “straight” down compared to the left
Fluid Aspiration
If the alveoli are affected by inflammation, gas exchange is impaired; severe inflammation with the accompanying build up of fluids is called