REVIEWER Ventilation The process of moving gases into

The Concept of Ventilation

and out of the lungs
Def: Perfusion The ability of the cardiovascular system
Oxygenation: mechanisms that facilitate or impair body's to pump oxygenated blood to the tissues
ability to supply oxygen to cells and return deoxygenated blood to the lu
Respiration: act of inhaling, exhaling air to transport oxygen ngs
to alveoli
Ventilation: actual exchange of oxygen, carbon dioxide
Upper Respi. Tract: nose to pharynx Diffusion Exchange of respiratory gases in the
Lower Respi. Tract: epiglottis to alveoli alveoli and capillaries
Alveoli: functional portion of respiratory system
Breathing: contributes to vital oxygenation

RESPIRATORY PHYSIOLOGY
Respiratory Gas Exchange
 The thickness of the alveolar capillary membrane affects
the rate of diffusion.
 Hemoglobin carries O2 and CO2
 Oxygen transport = Lungs + cardiovascular (CV) system
 Carbon dioxide transport

Regulation of Respiration
 Neural Regulation
-CNS controls the respiratory rate, depth, and rhythm.
-Cerebral cortex regulates the voluntary control of
respiration.
 Chemical Regulation
-Maintains the rate and depth of respirations based
on changes in the blood concentrations of CO2 and
O2, and in hydrogen ion concentration (pH)
-Chemoreceptors sense changes in the chemical
content and stimulate neural regulators to adjust.

Alteration In Respiratory Functioning

Anatomy and Physiology
Hyperventilation: Ventilation in excess of that required to
 The work of breathing is defined as the amount of force
eliminate carbon dioxide produced by
needed to overcome the elastic and resistive properties
cellular metabolism
of the lungs
 Lung compliance refers to the degree of elasticity or
Hypoventilation: Alveolar ventilation inadequate to meet the
expandability of the lungs and thorax.
body’s oxygen demand or to eliminate
 Any condition that impedes lung contraction and
sufficient carbon dioxide
expansion causes a decrease in compliance.
 During normal, quiet ventilation only 2% to 3% of the
Hypoxia: Inadequate tissue oxygenation at the cellular level
total energy expended by the body is required by the
pulmonary system. When pathology occurs from
Cyanosis: Blue discoloration of the skin and mucous
disease, the work of breathing can increase significantly
membranes
above normal due to decreased lung compliance

Normal Ventilation
Pathophysiology of failure of ventilation
1. Flexibility of the rib cage
 PaCO2 is the index used to evaluate ventilation. When
2. Elasticity of the lungs
ventilation is reduced, PaCO2 is increased (hypercapnia).
3. Normal Airway proficiency
When ventilation is increased, PaCO2 is reduced
A. Ventilation = movement of gases into and out of the
(hypocapnia).
lungs
 Hypoventilation and V/Q (ventilation perfusion)
B. Perfusion = the flow of blood through body parts
mismatching are the two mechanisms responsible for
C. Diffusion = the flow of gases across the alveolar
hypercapnia. Hypercapnia greatly increases cerebral
capillary membranes from areas of higher to lower
blood flow. The patient may appear restless and anxious,
concentrations
and may demonstrate slurred speech and a decreased
level of consciousness.
Hypoventilation: >Measuring FVC (Forced Vital Capacity)
 In hypoventilation, CO2 accumulates in the alveoli and is  largest amount of air exhaled after breathing in deeply
not blown off in 1 sec
 Respiratory acidosis occurs
>Measures Forced Expiratory Volume
Ventilation Perfusion Mismatch  How much air a person can exhale w/in 1 sec
 Because the upper and lower airways do not play a part  Low reading show severity
in gas exchange, the volume of inspired gas that fills
these structures is referred to as physiologic dead PATHOPHYSIOLOGY of COPD
space. Environmental irritant --> bronchial inflammation and
 This dead space is normally 25% to 30% of the inspired damage --> mucus production --> inability to exhale fully
volume. (inhalation ↑ volume because there is residual air) -->
 major mechanism for the elevation of PaCO2 is an hyperinflation of lungs --> not enough O2 coming in and
increase in the volume of dead space retainment of CO2 --> respiratory acidosis --> cyanotic ↓ O2
--> ↑ RBC ( to compensate) --> ↑ pressure in the arteries from
the shift of blood due to ↓ O2 Pulmonary Hypertension -->
Diagnostic Assessment Right sided heart failure --> bloating of abdomen & legs
 Pulse oximetry (backflow of blood)
 ABG
 Pulmonary Capillary Wedge Pressure
 Pleural Fluid Analysis
 Pulmonary Angiography PATHOPHYSIOLOGY of Emphysema
 Ventilation-perfusion (V/Q scan) Hyperventilate for compensation ↓ O2
 Capnography Maintains “pink” normal complexion - no cyanosis, barrel
chest from accessory muscles usage

CHRONIC OBSTRUCTIVE PULMONARY DISEASE Environmental irritant --> inflammation --> alveoli sacs loss
-pulmonary disease that causes chronic obstruction of airflow elasticity --> air gets trapped in sacs --> HYPERINFLATION
from the lungs (diaphragm flattens) --> use of accessory muscles and
hyperventilate --> barrel chest --> anteroposterior diameter↑
Keypoints:
 Limited airflow; inflamed bronchioles - deformed and Diaphragm does 80% of the breathing
narrow w/ excessive mucus
 Inability to fully exhale (elasticity of alveoli sacs is loss + Hyperventilation causing ↑RR ---> less hypoxemia that chronic
air pockets develop) bronchitis, hence pink puffer
 Irreversible
 COPD is a term used as a “Catch all” for diseases that Clinical Manifestation
limit airflow and causes dyspnea  Dyspnea w/ activity
 Chronic cough - productive
Types of COPD  Smoker’s cough - in the morning
 Chronic Bronchitis “Blue Bloaters”  Recurrent lung infections - pneumonia
-cyanosis due to hypoxemia (O2 in the blood are lower
that normal) “LUNG DAMAGE”
-bloating: edema in belly and extremities; and
increased lung volume Nursing Responsibilities
 Monitor respi. System
 Emphysema “Pink puffers”  Lung sounds( may need suction)
-they have difficulty catching their breath and their  Keep O2 sat 88-93% (COPD pt are stimulated to breathe
faces redden while gasping for air. due to LOW O2 levels rather than high CO2 levels. Giving
too much O2 stops their breathing causes
Risk Factors/Etiology hypoventilation & CO2 will become toxic
>Enviromental (harmful irritants into lung)  Administer O2 as prescribed 1-2L/min
>Complications  Monitor effort of breathing
-heart disease: heart failure  Teach about pursed lip breathing, diaphragmatic
-pneumothorax: spontaneous from air sacs (emphysema) breathing
-lung infections: pneumonia
- ^ risk of lung cancer
MEDICATIONS: Regimen
Diagnostics Tests “Chronic Pulmonary Medications Saves Lungs”
>Spirometry
 How much volume the lungs can hold during Corticosteroids:
inhalation -↓ inflammation ↓ mucuos production in airway
 How much and how fast air is exhaled
Phosphodiesterase -4 Inhibitors (Roflumilast) >digitalis glycosides, IV diuretics, antiarrythmics
-used for people with chronic bronchitis and helps ↓COPD >if abnormal ABGs persist-->intubation + mech vent
exacerbation (not bronchodilator)
-“last” - could be their last day hence assess thoughts of Anticoagulation Therapy
suicide and report to physician -continue 3-6mos after embolic event
-hepatin therapeutic range: 2.0 - 2.5
Methylxanthines (Theophylline)
-given orally many times
-types of bronchodilator, used long-term in pts w/ severe Nursing Management:
COPD  Early ambulation, active & passive ROM
 DO NOT: sit/lie for too long, cross legs. Prolong IV
Short-Acting Bronchodilators catheters
-relaxes smooth muscles of bronchial tubes  Sequential compression devices
-emergency situation & quick relief  Deep breathing, incentive spirometry, nebulizer,
> Beta2 agonist - Albuterol percussion & postural drainage
>Anticholinergic - Atrovent

Long-Acting Bronchodilators
-same actions as short but effects last longer ACUTE RESPIRATORY DISTRESS SYNDROME
-used overperiod of time -milder form: acute lung injury
-scheduled: OD/BID -type of respiratory failure that occurs when the capillary
>Beta2 agonist - Salmeterol membrane around the alveoli sac start to leak fluid
>Anticholinergic - Spiriva -fluid will enter into the sac

Quick Facts:
>fast onset
PULMONARY EMBOLISM >usually already hospitalized with another condition
-obstruction of the pulmonary artery or one of its branches >develop due to systemic inflammation
by a thrombus that originates somewhere in the venous >high mortality rate
system or in the right side of the heart
Cause: MAJOR SYSTEMIC INFLAMMATION
Risk Factors/Etiology Indirect Cause:
 Trauma >sources outside the lungs
 Surgery >SEPSIS (body’s extreme response to an infection)
 Pregnancy >burns
 Heart failure >blood transfusion
 Age older than 50 >pancreatitis
 Hypercoagulable states >drug overdose
 Prolonged immobility
Direct Cause
>source is in the lungs
PATHOPHYSIOLOGY >pneumonia
Clot begins as a thrombus (usually DVT “deep vein >aspiration
thrombosis”) --> clot grows faster than fibrinolytic activities >inhalation injury
can break it down --> fragments break off (embolize) --> >drowning
travel to the heart --> lodges in the pulmonary artery or >embolism
smaller blood vessels
PATHOPHYSIOLOGY
Clinical Manifestation “ARDS”
 Dyspnea Atelectasis (alveolar sac fill with fluid and collapse,
 Substernal chest pain pulmonary edema) -- > Refractory Hypoxemia --> decrease in
 Mycardial infarction lung compliance (lung aren’t as elastic or stretchable +
 Tachypnea hyaline membrane develops) --> surfactant cell damaged
 Rapid and weak pulse (decrease in surfactant production) --> organ suffer
 Syncope
 Can sudden death Refractory Hypoxemia - there is inadequate arterial
oxygenation despite optimal levels of of inspired oxygen
Medical Management
Emergency Management:
>Nasal O2
>KVO (Keep Vein Open)
>dopamine - for hypotension
>ECG
 Nursing Intervention:
How it happens? >Maintain airway/function
>mech vent w/ PEEP (high 10-20cm H2O)
1. Exudative “The most frequently used baseline PEEPs were 5 and 10
>24 hrs after injury --> damage to capillary membrane --> cm H2O.”
leak protein-rich fluids (enters interstitium -> sac) = Why is it high?
pulmonary edema -↓ lung compliance
-edema in sacs
>damaged surfactant cells: ↓surface tension: collapse -↓ surfactant - collapsed sac
exhalation - PEEP open alveoli sacs that are collapsed, esp during
exhalation
>↓surfactant = unstable sac COLLAPSE - improved gas exchange, ↑ O2, keep clear of fluid
>PaO2 >60mmHg and O2 sat >90%
>ATELECTASIS --> Hypoxemia
Prone Positioning
>Hyaline Membrane (dead cells & protein): lung less elastic, >↑ O2 w/o ↑ O2 concentration
↓compliance, V/Q mismatch >improve V/Q, airflow (heart no longer compresses the
posterior parts of the lungs)
>Hallmark S/S : REFRACTORY HYPOXEMIA = O2 ↓ even >moves secretions to other area
though receiving high amounts of O2 >improves atelectasis

Pulmonary Artery Wedge Pressure

Early Stage: >measures left arterial pressure
 ↑RR to blow off CO2 >pulmonary catheter with balloon “wedged” in pulmonary
 O2↓ CO2 arterial branch
 pH ↑ - <18 mmHg --> ARDS
 Respiratory Alkalosis - >18 mmHG --> cardiac issue: heart failure
 Hyaline membrane formation prevents CO2 to pass >Administering drugs:
through = respiratory acidosis - Corticosteroids: help w/ systemic inflammation
- Antibiotics: preventing and treating infection
2. Proliferative - Fluis colloids or crystalloids solutions if cardiac output
>14 days after injury decreased along w/ drugs like that have an inotropic
>grow & reproduce cells quickly effect: helps with heart muscle contraction
>repair structure & reabsorption fluid
>lung tissue becomes very dense & fibrous
> ↓ lung compliance, worsen hypoxemia
RESPIRATORY FAILURE
3. Fibrotic
>3 weeks after injury Acute Respi. Failure:
>fibrosis of lung tissue, dead space in the lungs  PaO2 <50 mmHg (hypoxemia)
>major lung damage  PaCO2 >50 mmHg (hypercapnia)
>poor prognosis  Arterial pH <7.35
>but not all pts will enter this (worst case scenario)
Chronic Respi. Failure:
Clinical Manifestation  Deterioration in the gas exchange function of the lung
Early signs: subtle that has developed insidiously or has persisted for a
>normal lung sounds, or random crackles (fluid still in long period after an episode of acute respiratory failure
interstitium not in sac)
>difficulty in breathing “air hunger” Risk Factors/Etiology
>↑RR - low O2, respiratory alkalosis >Ventilatory failure:
>full respiratory failure -impaired function of CNS
>Refractory Hypoxemia! -neuromuscular dysfuntion
>Cyanosis -musculoskeletal dysfuntion
>Mental Status changes: tired, fatigue, confused -pulmonary dysfunction
>↑HR
>Retractions >Oxygenation failure:
>crackles throughout the lungs (pulmonary edema) -pneumonia, ARDS, heart failure, COPD, pulmonary
embolism, restrictive lung diseases
Diagnostic Tests
>Chest X-ray: white out appearance, bilateral infiltrates >postoperative period:
-anesthetic, analgesics, sedative that can enhance
opioids (hypoventilation)
PATHOPHYSIOLOGY Route of transmission:
Inhalation , aspiration, from blood and attack the alveoli sacs
Abnormality in any component of respiratory system (airways,
alveoli), CNS, PNS, respiratory muscles, chest wall Causes:
Bacteria: most common esp. in community acquired
pneumonia “streptococcus pneumoniae”
Ventilatory capacity < ventilatory demand
Atypical Bacteria:
Mycoplasma pneumoniae
Clinical Manifestation -that causes “walking pneumonia” which is milder form of
EARLY SIGNS pneumonia (no need complete rest hence “walking”)
>restlessness, fatigue, headache, dyspnea, air hunger,
tachycardia, and increased blood pressure
Virus: influenza, RSV (pedia)
LATE SIGNS
>confusion, lethargy, tachycardia, tachypnea, central Fungi: least common--->mostly affects immunosuppressed
cyanosis, diaphoresis (excessive sweating), and finally pts
respiratory arrest

PHYSICAL FINDINGS Diagnostic Tests:

>use of accessory muscles, decreased breath sounds  Notice: abnormal lungs sound when auscultating with a
stet may hear coarse crackles, rhonci (type of wheezing),
or bronchial breath sounds which should be noted only
Medical Management in the tracheal area and this lung consolidation
 Intubation mech vent  Chest X-ray, sputum culture

Nursing Intervention PATHOPHYSIOLOGY

 Assisting with intubation and maintaining mechanical Pathogen --> attacks alveoli --> alveolar inflammation, full of
vent fluid, WBCs, RBCs stuck & bacteria --> ↓ ability to
 Level of responsiveness, arterial blood gases, pulse inflate/deflate --> hypoxemia (O2 cant transfer across
oximetry, and vital signs capillary wall, CO2 retains) --> respiratory acidosis

Respiratory Acidosis: keep CO2 & can’t get O2

ABGs:
PNEUMONIA!!!! - PO2 <90 mmHg
-pH <7.35 mmHg
- a lower respiratory tract infection that causes inflammation -PCO2 >4.5 mmHg
of alveoli sacs
To compensate: the Kidneys start to conserve bicarbonate
Key Players: (HCO3) to hopefully ↑ the blood’s pH back to normal, so
>Germs: bacteria, Virus, Fungi HCO3 becomes >26mEq/L
>Lung Parenchyma: Alveoli, alveolar ducts, and bronchioles
(the trio in gas exchange) Clinical Manifestion
“PNEUMONIA”
Types:
>Productive cough, pleuritic pain (chest pain that is caused
1. Community Acquired Pneumonia by coughing, breathing etc.)
2. Hospital Acquired Pneumonia >Neuro changes
Pt must have developed 48-72 hrs after admission >Elevated labs: PCO2 >45 (co2 cant pass alveoli sacs),
Pag within 48-72 hrs upon admission, Community increased WBC (represents infection)
Acquired pa rin yun. Pero kapag lagpas 48-72 na, >Unusual breath sound
hospital acquired na. >Mild to high fever
>Oxygen saturation decreased (want >90%) will need
supplemental oxygen
Risk Factor: >Nausea and vomiting
 Prior infection; flu or cold >Increase heart rate and respirations
 Weak immune system >Aching all over with joint pain
 Immobile: strokes or any condition that causes decrease Activity intolerance with SOB
mental awareness or restrict ability to move
 Lung problems
 Post-op pt: not coughing deep breathing
Nursing Interventions
 Monitor lung system: improving? I THANK YOU. *BOW*
 Vital signs esp RR & O2 sat
 Color of skin
 Monitor ABG
 Collect sputum Cx (if ordered)
 Suction needed
 Breathing Tx: respiratory therapies, bronchodilators,
chest percussion

Education
 Incentive spirometer usage 10x q1-2hr while awake
 Stay hydrated 2-3L/day
-to keep secretions thin
-fever --> dehydration
-respiration causes 200-400mL water loss per day
-contraindicated: heart failure, renal failure

Antibiotics Groups for Bacterial Pneumonia

“Various Medications Frequently Treat Pneumonia Cases”

>Vancomycin: treat severe cases and is one of the few that

can treat bacteria that may be resistant to other antibiotics
-watch for hearing loss “ototoxicity”

>Macrolides: (Zithromax “Z-pak”)

-used in patients with penicillin allergy narrow-spectrum
targets mainly gram positive bacteria

>Tetracyclines: (Doxycycline)
-broad spectrum that targets gram positive and negative
bacteria

>Fluroquinolones: (Levaquin)
-treatment for severe infections that are found in the
hospital that are resistant

>Cephalosporins: (Keflex, Rocephin)

- watch with patients who are allergic to penicillin
-great for community acquired pneumonia

>Penicillin: (Penicillin G)
-narrow spectrum
-monitor if patient is allergic to cephalosporins
-decreases effectiveness of birth control

Education about antibiotics:

Take medications as prescribed and dont stop in the middle
of treatment, even if feeling better which helps decrease
resistance