PCT - Respiratory System (A&P)

Anatomy of the upper airway

• soft palate

• palatine tonsil

• epiglottis

• vocal fold

• esophagus

• hard palate

• tongue

• pharynx (opa, npa, lpa)

• larynx

anatomy of the lower airway

• trachea

• alveoli

• main bronchi

• smaller bronchi

• bronchioles

bifurcation of the lungs

carina

trachea

conduit for air entry, 10-12cm, C-shaped cartilaginous rings, descends to level of fifth or sixth thoracic vertebra

hilum

point of entry for blood vessels and bronchi on each lung

lobes of the lung

3 in right lung

2 in left lung

pleura

visceral pleura lines the lungs

parietal pleura lines the thoracic cavity

small amount of synovial fluid between them to allow reduction of friction when breathing

bronchus

divides into smaller bronchi once it enters lungs

alveoli

balloon-like clusters of single-layer (cell) air sacs, functional site for gas exchange of oxygen and carbon dioxide with the pulmonary capillaries

surfactant

decreases surface tension to keep alveoli open

atelectasis

when alveoli collapse

total lung capacity

6 liters for an adult man

Tidal Volume (Vt)

volume of air that is inhaled/exhaled during a single respiratory cycle, normal is 5-7mL/kg (~500mL)

Inspiratory reserve volume

amount of air that can be inhaled in addition to normal Vt (around 3000mL)

Dead Space (Vd)

amount of space not participating in gas exchange

3 types:

• Anatomical

• Alveolar

• Physiological

Anatomical dead space

includes trachea and larger bronchi, air lingers but does not partake in gas exchange, typically 150mL or 30% of normal Vt

Alveolar dead space

not perfused alveoli

Physiological dead space

Anatomical dead space + alveolar dead space, created by intrapulmonary obstructions or atelectasis (alveolar collapse), mucus, inflammation, mechanical obstruction

Alveolar Volume

volume of air that reaches the alveoli and participates in gas exchange, approx. 350mL participating in gas exchange

Va = Vt - Vd

Minute Volume (Vm)

Amount of air that moves into and out of the respiratory tract per minute

Vm = Vt * RR

Minute Alveolar Volume (Va)

Amount of air that actually reaches the alveoli per minute and participates in gas exchange

Va = Vt- Vd * RR

Functional Residual Capacity (FRC)

Volume of gas remaining in lungs at the end of normal tidal volume exhalation, PEEP limits exhalation (increases FRC and keeps alveoli from collapsing)

Expiratory Reserve Volume

amount of air that can be exhaled following a normal exhalation, approx. 1200mL

residual volume

cannot completely empty your lungs, residual volume is the amount of air that remains in the lungs after maximal expiration, also approx. 1200mL

Vital Capacity

equal to the sum of tidal volume, inspiratory reserve volume, and expiratory reserve volume (Vc = Vt+Vir+Ver)

Fraction of Inspired Oxygen (FIO2)

Percentage of oxygen in inhaled air, increases when supplemental oxygen is given to a patient.

May decrease at altitude, in confined spaces, chemical vat

Expressed as decimal (i.e. breathing room air 21% O2, FIO2 0.21%)

Two phases of Ventilation

Inspiration (Inhalation)

Expiration

One cycle = one inhalation (one third) and one expiration (two thirds)

Regulation of Ventilation

regulated by pH of the CSF (cerebral spinal fluid) - directly related to the amount of CO2 dissolved in the blood (PaCO2)

Involves a series of receptors and feedback loops to sense CO2, pH, and O2 concentrations in the blood and plasma

These receptors send signals to the respiratory centre of the brain to alter ventilations accordingly, increase or decrease ventilation

neural control of ventilation

involuntary control of breathing originates in the brain stem in the pons and medulla, impulses descend through the spinal cord and can be overridden by voluntary control (breath holding)

Two motor nerves affect breathing

• phrenic nerve innervates the diaphragm

• intercostal nerve - innervates the external intercostal muscles between the ribs

Control center in the brain process to regulate breathing

CO2 increase/pH decrease travels along with nerve signal triggered by O2 sensor in artery indicating low O2 levels to breathing control centers in medulla and pons which send nerve signals to trigger contraction of intercoastal muscles and diaphragm

respiratory center

in the medulla, divided into 3 regions

3 regions of respiratory center

1. Respiratory rhythmicity center (inferior)

2. apneustic center

3. pneumotaxic center (superior)

respiratory rhythmicity center

sets RR, inhalation at 2 seconds, relaxes for 3 seconds allowing for passive exhalation

apneustic center

receives signals from the chest wall (mechanical stretch receptors) and bronchioles via the vagus nerve to inhibit inhalation and thus expiration occurs, PREVENTS OVEREXPANSION, INCREASES NUMBER OF INSPIRATIONS/min

pneumotaxic center

working opposite apneustic center, it inhibits inspiration and in times of increased demand it decreases influence of apneustic influence and increases respiratory rate

Chemical control of ventilation

keeps concentrations of O2 and CO2 in blood, component of acid-base balance, within a narrow range

CO2 is the most powerful stimulant to affect the respiratory center (too much is acidosis), small increases as little as 1% can increase minute volume, whereas small change in PO2 has almost no effect (don’t use all the O2)

Hypercarbic Drive

amount of CO2 in bloodstream controlled by a negative feedback loop, primary stimulus to breathe

Chemoreceptors

monitor levels of CO2, O2, and the pH of the CSF and provide feedback to the respiratory center to modify rate and depth and respiration based on the body’s current needs

hydrogen ions to regulate ventilation

pH of blood has a powerful effect on respiratory center, CO2 and pH inversely rise and fall together causing a combined effect in the control of respirations

CO2 + H2O = H2CO3 = H +HCO3

central chemoreceptors

located adjacent to respiratory center in the medulla, monitor and sense minute changes in the pH of the CSF (H+)

H+ goes up, pH goes down, excitatory response to increase rate and depth of breathing

peripheral chemoreceptors

located in the carotid bodies and aortic arch, monitor and sense reduction in O2 and to a lesser degree CO2, pH in arterial blood

aortic arch detects levels of O2 and CO2 but not pH, carotid detects all three

control of ventilation by other factors

body temperature (febrile), medications, hypoxia, acidosis, metabolic rate

Accomplished mechanic of ventilation

pressure changes brought about by contraction and relaxation of the intercostal muscles and diaphragm

inhalation mechanics of ventilation

active process initiated by the contraction of the respiratory muscles with the net effect to increase the volume of the chest, the lungs undergo a comparable increase in volume and negative-pressure ventilation-air flows into the expanded lungs because pressure inside less than outside

Exhalation Mechanics of Ventilation

passive process at the end of inhalation, the respiratory muscles relax, natural elasticity of the lungs passively exhales the air

3 mechanics of ventilation

• relaxation - no movement

• inspiration - chest expands, diaphragm contracts

• expiration - chest contracts, diaphragm relaxes

**Respiration

Mechanism to ensure a constant oxygen supply and the removal of excess carbon dioxide

2 Kinds of Respiration

• external (pulmonary respiration) → environment and lungs

• internal (cellular respiration → glycolysis, citric acid, etc.) between blood and cells

4 parts of circulatory system

• pulmonary artery

• pulmonary vein

• arterial system

• venous system

hemoglobin carrying capacity

4 molecules of O2

Oxygen dissociation curve

Factors Affecting Affinity of Oxygen to Hemoglobin

3 main

• temperature (increase temp, decrease affinity)

• pH (increase in H+ ions, decrease affinity)

• Carbon dioxide (increase Co2, decrease affinity)

Bohr effect

changes in affinity of oxygen to bind to hemoglobin as a result of the shift in blood pH that occurs on a breath by breath basis, occurs at level of lungs and tissues

when blood is more alkaline, hemoglobin has a greater affinity for O2 and thus O2 is drawn toward hemoglobin at the alveolar/capillary level

when blood reaches tissue level, CO2 from cell. resp. diffuses from the tissue to the capillary blood

this shifts the blood pH toward the acidic side which weakens hemoglobin’’s hold on oxygen

blood that shifts toward acidic side of pH gives up O2 readily to the tissues

hemoglobin dissociation curve

1. oxygen from lungs

2. oxygen bonded to hemoglobin

3. oxygen released to tissue cells

hemoglobin in an alkaline state

strong affinity, draws O2 towards it

(if blood remained alkaline at tissue level, it would not release O2 to the tissues readily)

Hemoglobin in Acidotic state

weak affinity for O2, does not pick it up as readily, O2 bound to hemoglobin is released to tissue easily

(we attempt to compensate for this by providing supplemental oxygen which increases amount of O2 dissolved in blood plasma for transport)

False low Pulse oximetry cause

• cold extremities

• nail polish

• inflating the bp cuff

• ambient lighting (ambulance)

• states of decreased perfusion

Falsely high O2 Sat readings can be caused by

• anemia

• CO poisoning

CO affinity for hemoglobin

200 times greater than O2, blocks oxygen off from hemoglobin

cyanide poisoning and O2

prevents utilization of O2 at the cellular level

Oxygenation

to provide oxygen (hyperoxygenate: to provide supplemental oxygen in a high concentration)

PaO2

the partial pressure of oxygen in the arterial blood

SpO2

Saturation percentage of oxygen, should be >90%

ventilation

refers to the movement of air into and out of the lungs

normal Partial pressure of CO2 (PaCO2) is

35-45 mmHg

(hyperventilation blows off CO2 and therefore may result in PaCO2 or ETCO2 level of less than 35mmHg)

ETCO2

End tidal carbon dioxide

Hyperventilation

when minute volume (RR*Vt) exceeds body’s metabolic demands

impaired ventilation of upper airway

obstruction : fboa (foreign body obstruction of the airway), epiglottis, swelling

impaired ventilation of the lower airway

obstruction - asthma, bronchospasm

impaired ventilation in chest wall

pneumo/tension pneumothroax, flail chest

impaired ventilation at the neurological level

Neurogenic dysfunction - CNS depressant drugs, cervical spinal trauma, CVA (cerbrovascualr accident)

Cheyne-Stokes respirations

Gradually increasing rate and depth of respirations followed by gradual decrease of respirations with intermittent periods of apnea, associated with brain stem insult

Kussmaul respirations

deep gasping respirations, common in ketoacidosis (diabetic coma)

biot respirations

irregular pattern, rate, and depth with intermittent periods of apnea, results from increased intracranial pressure

agonal respirations

slow, shallow, irregular respirations or occasional gasps, results from cerebral anoxia, may be seen briefly after the heart has stopped as the brain continues to send signals to the respiratory muscles

hypoxia

not enough oxygen, occurs in acidosis

diffusion

• exchange of gases (O2 and CO2) between alveoli and pulmonary capillaries

• gas moves from an area of high to low concentration

• around 98% of body’s total O2 is bound to hemoglobin

conditions for diffusion

• alveolar and pulmonary capillary walls must not be thickened

• interstitial spaces between the alveoli and pulmonary capillaries must not be enlarged or filled with fluid

impaired diffusion causes

• inadequate oxygen in the air (smoke inhalation, CO poisoning)

• alveolar/bronchial pathologies, emphysema, bronchitis

• interstitial space pathologies (pulmonary edema, submersion aspiration, interstitial lung disease)

• capillary bed pathologies (severe atherosclerosis, pulmonary embolism)

atherosclerosis

hardening of arteries due to gradual plaque buildup

conditions for perfusion to occur

• adequate blood volume

• adequate hemoglobin within

• pulmonary capillaries must not be occluded

• there must be a functional left ventricle that allows for the smooth flow of blood through the pulmonary capillary bed

causes of impaired perfusion

inadequate blood volume - shock

inadequate hemoglobin - anemia

impaired circulation or flow - pulmonary embolus, myocardial infarction

general signs and symptoms of respiratory distress

stridor, wheezing, crackles, decreased LOC, accessory muscle use, tripod positioning, diminished breath sounds, tachycardia, tachypnea, pale, cool diaphoresis, bradycardia

stridor

partial obstruction of the upper airway

wheezing

bronchospasm/bronchoedma

decreased loc signs

disoriented, confused, combative, obtunded, (seizure), unconscious

perfusion

refers to circulation and oxygenation of blood as it circulates through the pulmonary capillary bed

Tachypnea, Tachycardia, pale, cool diaphoresis

Respiratory Distress due to SNS

purposes of O2

• increase the PO2 in alveoli and blood

• reduce ventilatory workload

• reduce myocardial workload

Non-Rebreather Mask (NRB Mask) Flow rates (non-COPD)

• 6 lpm - 60%

• 7 lpm - 70%

• 8 lpm - 80%

• 9 lpm - 90%

• 10-15 lpm - 95+%

Nasal Cannula Flow Rates (non-COPD)

1 lpm - 24%

2 lpm - 28%

3 lpm - 32%

4 lpm - 36%

5 lpm - 40%

6 lpm - 44%

Simple Face Mask Flow Rate (Non-COPD)

10 lpm - 40-60%

(mostly for peds)

nebulizer flow rate

typically ran at 8 lpm and used to deliver medications such as bronchodilators and epinephrine

BVM flow rate

at 15 lpm - 100% O2 supplied

indicated of apneic pts and those with inadequate respirations

PEEP

Positive End-Expiratory Pressure

BVM Technique

J (modified) jaw thrust

Airways (OPA/NPA)

Work together

Slow, small squeeze - 5-7 cc/kg, over 1-2 seconds at 10-12/min using low pressure

difficulties with BVM

Mask seal

Obese

Age

No teeth

Stiff lungs

Ventilation Correction Steps

Mask adjustment - reapply the mask consider 2-hand

Reposition airway - place head neutral or slightly extended

(Try PPV and reassess chest mvmt)

Suction mouth and nose - use a bulb syringe or suction catheter

Open mouth - lift jaw forward

(Try PPV and reassess chest mvmt)

Pressure increase - increase pressure in 5-10cm H2O increments max 40cm H2O

Alternative airway - place endotracheal tube or laryngeal mask

(Try PPV and assess chest mvmt and breath sounds)

edentulous patient

no teeth