7: pulmonary disorders

Structures of the Respiratory System

Upper Respiratory Tract

• Nose

• Mouth

• Sinuses

• Pharynx

• Larynx

Lower Respiratory Tract

• Trachea

• Bronchi: R-3 + L-2 lobes

• Bronchioles

• Alveoli

Defenses of the Respiratory System

Mechanical	Surfactants	Macrophages
• Nose hair-filter air • Turbinate's-swirl air • Mucus Membrane-stick particulates • Trachea + Bronchi- Goblet cells (create sputum that triggers cough to expel debris) • Create sputum • Epithelial cells • Cilia • Sneeze + Cough	• Antimicrobial properties ()	• Immune defense

.

Controls Breathing

Primary Drive	Secondary
• Elevated levels of ____ • ___ and makes you take a breath	• Low ___

Alveoli

-Air → bronchioles → alveoli → capillaries

-Goal: O2 into blood

-O2 Penetrate Membrane + dissolve in water

-PO2: the amount of oxygen dissolved in the blood

-More O2= need more concentration or pressure

-Hemoglobin: uptakes O2 from blood

Controls Breathing

Primary Drive	Secondary
• Elevated levels of Carbon Dioxide (pCO2)  pH • pH becomes acidotic and makes you take a breath	• Low Oxygen (pO2)- hypoxemic

Hemoglobin Oxygen Dissociation Curve

• When there is lots of O2 around, ___

• When there is no O2 around, ____

Respiration

• Pull diaphragm down

• Expanding volume available to lungs

• Create a partial vacuum-air rushes in

• Create negative pressure space

Inhalation

• Relax

• Pressure in chest increases

• Pushes air out

Hemoglobin Oxygen Dissociation Curve

• When there is lots of O2 around,

• When there is no O2 around, hemoglobin will release O2 easily to compensate: more easily released bc drops it off sooner than if there were more O2

Respiration

• Pull diaphragm down

• Expanding volume available to lungs

• Create a partial vacuum-air rushes in

• Create negative pressure space

Inhalation

• Relax

• Pressure in chest increases

• Pushes air out

Ventilation + Perfusion (V/Q)

Ventilation

• Amount of air in alveoli: how much air we're able to breathe in through our abdominal muscles, respiratory structures, etc

Affected by:

• Resistance to airflow

• Lung compliance: conditions causing structure & function to change

• Lung volume and capacity

Perfusion

• Amount of air perfused to blood in pulmonary capillaries

Increase airway resistance:

-Bronchial constriction 

-Asthma

-Thickening of bronchial mucosa

-Chronic bronchitis

-Secretions: mucous

-Loss of lung elasticity

-Emphysema

.

How can we adjust respiratory rate (RR)?

Central chemoreceptors

• Measure ___

• Increase respiration when ___

Peripheral chemoreceptors

• Measure ___

• Increase respiration when PO2 less than 60 mm Hg

Hypoxemia

Cyanosis: ___

Impaired function of vital centers

• Agitated or combative behavior, euphoria, impaired judgment, convulsions, delirium, stupor, coma

• Hypotension and bradycardia

Activation of compensatory mechanisms

• Acute hypoxia → stimulation of the peripheral chemoreceptors → activates

• directly responsible, at least in part, for ___

Hypercapnia (happens after hypoxemia/ untreated hypoxemia)

• what is it? ____ 

Respiratory acidosis leads to:

• Increased ___

• Decreased ___

→Disorientation, somnolence, coma

• Decreased ___

• ___

→Headache; warm flushed skin

How can we adjust respiratory rate (RR)?

Central chemoreceptors

• Measure PCO2 + pH in cerebrospinal fluid

• Increase respiration when PCO2 increases or pH decreases

Peripheral chemoreceptors

• Measure PO2 in arterial blood

• Increase respiration when PO2 less than 60 mm Hg

Hypoxemia

Cyanosis: reduction of PO2 of the arterial blood (typically less than 60 mm Hg)

Impaired function of vital centers

• Agitated or combative behavior, euphoria, impaired judgment, convulsions, delirium, stupor, coma

• Hypotension and bradycardia

Activation of compensatory mechanisms

• Acute hypoxia  stimulation of the peripheral chemoreceptors  activates

• directly responsible, at least in part, for the acute blood pressure (BP) changes

Hypercapnia (happens after hypoxemia/ untreated hypoxemia)

• increase in the CO2 content of the arterial blood 

Respiratory acidosis leads to:

• Increased respiration

• Decreased nerve activity

→Disorientation, somnolence, coma

• Decreased muscle contraction

• Vasodilation

→Headache; warm flushed skin

True or false?

Both hypercapnia and hypoxemia will lead to respiratory failure if untreated.

True: Rationale: In both hypercapnia (PCO2 greater than 50 mm Hg), tissues accumulate carbon dioxide; in hypoxemia (PO2 less than 60 mm Hg), less oxygen is delivered to the tissues. In both cases, gas exchange is impaired, and respiratory failure will result unless the conditions are corrected (with oxygen, mechanical ventilation, etc

Antitussives 

MOA	Suppress ___
Drugs	___ ___
Contraindications	Head Injury, cough needed to ensure airway Caution: avoid CNS depressants  (enhance drowsiness)

Antitussives:

	Suppress cough reflex by direct action on medullary cough center of the brain
	Dextromethorphan (Robitussin) Codeine (narcotive: helps suppress cough)
Contraindications	Head Injury, cough needed to ensure airway Caution: avoid CNS depressants  (enhance drowsiness)

Expectorants: expect production of cough

MOA	____ • ___
Caution	Monitor for ___
Pearls	____

Expectorants

	Decrease viscosity/ pull water onto phlegm to produce more productive cough • Guaifenesin (Mucinex)
Caution	Monitor for GI effects, dizziness
Pearls	Full glass of water

Mucolytics: more powerful than expectorant

Moa	____ → ____
Caution	• ____, i.e. asthma patient • Separate ___

Mucolytics 

	Increase or liquefy respiratory secretions in high risk respiratory patients → Acetylcysteine (Mucomyst)
Caution	• Bronchospasm, i.e. asthma patient • Separate nebulizer – precipitates if mixed

Decongestants

• Usually ____

• Decrease ___

• ___ shrinks swollen membranes, opens passages

• Three varieties of decongestants:

• Oral

• Topical nasal sprays

• Topical nasal steroids

Decongestants

• Usually adrenergics/sympathomimetics (decoy as sympathetics)

• Decrease secretions by vasoconstriction

• Vasoconstriction shrinks swollen membranes, opens passages

• Three varieties of decongestants:

• Oral

• Topical nasal sprays

• Topical nasal steroids

Oral Decongestants

	-___ -Decrease ___ -___agonist: causes ___
SE	____
Cautions	• Caution with ____ • Assess for ___- HR, BP • Monitor for ___, limit use 3-5 days

Oral Decongestants

	-Pseudoephedrine (Sudafed) -Decrease nasal congestion-swollen nasal membranes, rhinitis -Alpha 1 agonist: vasoconstriction of respiratory tract mucosa
SE	insomnia, palpitations, nervousness (bc it’s sympathetic mimetic)
Cautions	• Caution with cardiac patients, HTN, hyperthyroid • Assess for adrenergic effects- HR, BP • Monitor for rebound congestion, limit use 3-5 days

Topical Nasal Decongestants sprays

	-rate of onset of action: ___ -where in the body does it affect? ___ ____ agonist: causes ____
Cautions	• Caution with cardiac patients, HTN, hyperthyroid • Assess for adrenergic effects- HR, BP • Monitor for rebound, limit use 3-5 days Avoid in pregnancy or glaucoma (affects pressure in eyes)

Topical Nasal Decongestants sprays

	-Immediate onset of action -Local effect , NOT generally systemic Aalpha 1 adrenergic receptor agonist: vasoconstriction
Cautions	• Caution with cardiac patients, HTN, hyperthyroid • Assess for adrenergic effects- HR, BP • Monitor for rebound, limit use 3-5 days

Nasal STEROID Decongestants

MOA	____ ___ effect to upper airway rate of onset: ____
SE	___
Cautions	• ___ • Stop smoking-irritant, i.e. asthma • Bronchospasm, i.e. asthma

Nasal STEROID Decongestants

	Fluticasone (Flonase) Anti-inflammatory effect to upper airway Takes time (weeks) to see full effect
SE	drying and burning/itching sensation
Cautions	• Immunocompromised patients • Stop smoking-irritant, i.e. asthma • Bronchospasm, i.e. asthma

Antihistamines

MOA	Competitively blocking ___ →block H2 from getting activated in cascade of inflammation
Medications	• 1st Generation: ____ • 2nd Generation: ___
Management of	• Seasonal allergic rhinitis (hay fever) • Itchy, watery eyes • Motion sickness • Sleep disorders • Urticaria (hives)
SE	• 1st: ___ • 2nd: ___
Cautions	• Respiratory disease due to ___ • Monitor for ____

Antihistamines

	Competitively blocking H1 receptors which reduces the effect of histamine →block H2 from getting activated in cascade of inflammation
Medications	• 1st Generation: diphenhydramine (Benedryl) • 2nd Generation: loratadine (Claritin)
Management of	• Seasonal allergic rhinitis (hay fever) • Itchy, watery eyes • Motion sickness • Sleep disorders • Urticaria (hives)
SE	• 1st: sedation, confusion, anticholinergic (dry mouth, dry eyes, etc) • 2nd: headache
Cautions	• Paradoxical effect: Respiratory disease due to thickening of bronchial secretions • Monitor for anticholinergic effects

Life Span Consideration Upper Respiratory Agents

-___ due to sedation

-Careful with combination of ___

-Caution with older adults– consider ___ function, use of other drugs,

-Monitor for safety concerns with CNS effects: Use topical nasal decongestants to avoid systemic effects when possible

-Teach when to seek further medical assessment of symptoms

-Teach use and expected side effects – rebound, GI effects, CNS effects, anticholinergic side effects

-Encourage fluids

Life Span Consideration Upper Respiratory Agents

-Care used in children due to sedation

-Careful with combination of OTC drugs

-Caution with older adults– consider renal/hepatic function, use of other drugs,

-Monitor for safety concerns with CNS effects: Use topical nasal decongestants to avoid systemic effects when possible

-Teach when to seek further medical assessment of symptoms

-Teach use and expected side effects – rebound, GI effects, CNS effects, anticholinergic side effects

-Encourage fluids

Respiratory Tract Diseases:

• Asthma- ____

• COPD – ___

• Emphysema – ___

• Chronic bronchitis – ___

• Characteristics:

• Bronchoconstriction

• Inflammation, mucosal edema

• Excessive mucus production

Respiratory Tract Diseases:

• Asthma- reversible airway obstruction

• COPD – chronic obstruction of airways

• Emphysema – damage to alveoli

• Chronic bronchitis – inflammation/mucus airway

• Characteristics:

• Bronchoconstriction

• Inflammation, mucosal edema

• Excessive mucus production

Asthma (Bronchial Asthma)

• chronic inflammatory disease of the airways that causes periodic "attacks" of coughing, wheezing, shortness of breath, and chest tightness.

Extrinsic (Atopic) Asthma

• Allergic Triad

→____

• Extrinsic Trigger: __

• Type I Hypersensitivity- Mediated by ___

Intrinsic (Nonatopic) Asthma

Not related to ___

• Cold

• Exercise

• Viral Upper Respiratory Infection

• Mediated by local IgE production

Pathologic Changes

• Wall ___

• Broncho ___

• Air flow ___

Asthma (Bronchial Asthma)

• chronic inflammatory disease of the airways that causes periodic "attacks" of coughing, wheezing, shortness of breath, and chest tightness.

Extrinsic (Atopic) Asthma

• Allergic Triad

→Asthma, Atopic Dermatitis, Allergic Rhinitis

• Extrinsic Trigger: environment

• Type I Hypersensitivity- Mediated by systemic IgE production

Intrinsic (Nonatopic) Asthma

Not related to an allergy trigger like pollen or dust

• Cold

• Exercise

• Viral Upper Respiratory Infection

• Mediated by local IgE production

Pathologic Changes

• Wall is inflamed and thickened

• Broncho hyperresponsiveness

• Air flow obstruction

Question: Which of the following occurs in asthma?

A. Airway inflammation

B. Bronchospasm

C. Decreased ability to clear mucous

D. All of the above

All of the above

Rationale: Inflammatory mediators lead to airway inflammation, edema of the mucous lining of the airways, bronchospasm, and impaired ability to clear secretions. All of these things cause the airways to narrow during an asthma attack.

Clinical Manifestations of Asthma

-Wheezing, crackle,  chest tightness 

-Anxiety, restlessness absent or diminished lung sounds use of accessory muscles tachypnea with hyperventilation tachycardia 

-Prolonged ___

-___

-Cyanosis, decreased O2 air trapping= respiratory acidosis

Diagnosis

• Peak Flow Meter

• How controlled the asthma is or if its getting worse

• Green=Good

• Yellow=Not Great

• Red= Bad

Asthma treatment

-Bronchodilators

→ ___

-Inhaled ___

-___ inhibitors

-__ Antagonists

-Reduce exposure to triggers

-Oxygen

Clinical Manifestations 

-Wheezing, crackles  chest tightness 

-Anxiety, restlessness absent or diminished lung sounds use of accessory muscles tachypnea with hyperventilation tachycardia 

-Prolonged exhalation

-Pulsus, paradoxus (abnormally large drop in systolic blood pressure during inspiration)

-Cyanosis, decreased O2 air trapping= respiratory acidosis

Diagnosis

• Peak Flow Meter

• How controlled the asthma is or if its getting worse

• Green=Good

• Yellow=Not Great

• Red= Bad

Asthma treatment

-Bronchodilators

→ Beta 2 agonists, xanthine's, anticholinergics

-Inhaled corticosteroids

-Mast cell inhibitors

-Leukotriene Receptor Antagonists

-Reduce exposure to triggers

-Oxygen

Medication Inhalation Devices

Metered Dose Inhaler (MDI)

• Uses a chemical propellant to push the medication out

• Spacer if Needed

Dry Powder Inhaler

• Delivers medication without using chemical propellants, but it requires strong and fast inhalation.

Nebulizer

• Delivers fine liquid mists of medication through a tube or a mask that fits over the nose and mouth, or with a mouthpiece, using air or oxygen under pressure.

Pearls

__ + __

• Two different medications, wait 5 min between

• Two doses, wait 1-2 min between

-take bronchodilator (opens bronchioles) first, then corticosteroid for max effect

BRONCHODILATORS: Beta 2 Agonists

MOA	• Dilates ___ • Long-term control (__)= ___ → Achieve and maintain control of ___ • Quick relief (___) = ___ →Used during ____
Uses	Short-acting beta 2 agonists (SABAs) Acute symptom relief →___ →___ Long-acting beta2 agonists (LABAs) Long term management →___ →___ →prevention of ___
SE	Tachycardia* Palpitations* Tremor* Cardiac arrhythmias Nervousness + anxiety Insomnia
Considerations	Nursing considerations : • Assess ___ • Vital Sign ___ • Teach use of ___

BRONCHODILATORS

Beta 2 Agonists

	• Dilates bronchi and increases rate and depth of respirations • Long-term control (prophylactic)= LABA → Achieve and maintain control of persistent constriction • Quick relief (rescue) = SABA →Used during periods of acute symptoms
Uses	Short-acting beta 2 agonists (SABAs) Acute symptom relief (albuterol preferred) →bronchospams →asthma Long-acting beta2 agonists (LABAs) Long term management →COPD →chronic bronchitis →prevention of bronchospams
SE	Tachycardia* Palpitations* Tremor* Cardiac arrhythmias Nervousness + anxiety Insomnia
Considerations	Nursing considerations : • Assess lungs sounds pre/post • Vital Sign pre/post • Teach use of inhalers

Bronchodilators- Anticholinergics

MOA	-Acetylcholine (ACh) causes bronchial constriction and narrowing of the airways -Anticholinergics block ___ -Result: ____  -Useful for patients unable to tolerate ___
Types	___: short acting ____: long acting
CI	Not used for ___
Cautions	Increase in ___

Bronchodilators- Anticholinergics

MOA	-Acetylcholine (ACh) causes bronchial constriction and narrowing of the airways -Anticholinergics block the parasympathetic nerve -Result: bronchoconstriction is prevented, airways dilate  -Useful for patients unable to tolerate B2 agonists—but not as effective
Types	Ipratropium (Atrovent)–short acting Tiotropium (Spiriva) –long acting
CI	Not used for acute asthma exacerbations
Cautions	Increase in anticholinergic effects when combined with other anticholinergics

Xanthine's: Theophylline

MOA	-Stimulate ___ -Cause ___ -Relief and prevention of ___
SE	-tachycardia -palpitations -ECG changes -nervousness & anxiety -irritable
Caution	Theophylline-___ • Toxicity: tachycardia, tonic-clonic seizures -Avoid caffeine (CNS stimulant)

Xanthine's: Theophylline

MOA	-Stimulate the CNS to promote bronchodilation -Cause smooth muscle relaxation in respiratory tract -Relief and prevention of bronchial asthma + bronchospasm for COPD
SE	-tachycardia -palpitations -ECG changes -nervousness & anxiety -irritable
Caution	Theophylline-narrow therapeutic index: 10-20 mcg/dL • Toxicity: tachycardia, tonic-clonic seizures -Avoid caffeine (CNS stimulant)

Corticosteroids 

End in -sone or -asone

MOA	-Reduces inflammation by ___  -May be combined with ___ Common:  -__ -___
Uses	COPD, Asthma Acute: IV PO, IM, PO, rectal, ocularly, Inhaled (inhalation doesn’t produce systemic effect)
SE	S’s of Steroids: causes -__ -__ -___ -___ -___ -___ -___ -___
Inhaled corticosteroid considerations	-after admin, rinse mouth to decrease risk of contacting possible fungal infection from candidiasis 1.bronchodilator first to help open airways 2.wait 5 min 3.administer corticosteroid

Corticosteroids 

End in -sone or -asone

MOA	-Reduces inflammation by decreasing number of mast cells in airway  -May be combined with bronchodilator Common:  -Prednisone -Beclomethasone
Uses	COPD, Asthma Acute: IV PO, IM, PO, rectal, ocularly, Inhaled (inhalation doesn’t produce systemic effect)
SE	S’s of Steroids: causes -Sugar: hyperglycemia -Soft bones: osteoporosis -Sick: decreased immunity/ sepsis -Sad: depression -Salt: water & Na+ retention (hypertension) -Sex: decreased libido -Swollen: water gain = weight gain -Sight: risk for cataracts
Inhaled corticosteroid considerations	-after admin, rinse mouth to decrease risk of contacting possible fungal infection from candidiasis 1.bronchodilator first to help open airways 2.wait 5 min 3.administer corticosteroid

Leukotriene Receptor Antagonists

Leukotrienes- substances released when ___

Leukotrienes cause ___

Result: coughing, wheezing, shortness of breath

Antileukotrienes (Leukotriene receptor antagonists): Montelukast (Singulair)

MOA	Prevent leukotrienes from ____
Uses	Prophylaxis and chronic treatment of ___
CI	NOT for ___ Teratogenic
Monitor/ assess	HA, n/v/d, elevated LFTs, myalgia

Leukotriene Receptor Antagonists

Leukotrienes- substances released when a trigger starts a series of chemical reactions in the body

Leukotrienes cause inflammation, bronchoconstriction, and mucus production

Result: coughing, wheezing, shortness of breath

Antileukotrienes (Leukotriene receptor antagonists): Montelukast (Singulair)

MOA	Prevent leukotrienes from attaching to receptors on cells in the lungs and in circulation
Uses	Prophylaxis and chronic treatment of asthma
CI	NOT for acute asthmatic attacks Teratogenic
Monitor/ assess	HA, n/v/d, elevated LFTs, myalgia

Chronic Obstructive Pulmonary disease (COPD)

Risk factors	#1 Risk Factor= Smoking Occupational risks= coal and dust Genetic defect- deficiency of alpha 1 anti-Trypsin • enzyme prevents enzymatic destruction of lung tissue • Deficiency= ___ -Air Pollution -Asthma
What is COPD	• Progressive airflow limitation leads to ___ • Not completely reversible • Leads to ____
Mechanisms of COPD	• Inflammation and fibrosis of the ___ • Hypertrophied mucous glands → excess mucus →Obstructed airflow • Loss of alveolar tissue →Decreased surface area for gas exchange • Loss of elastic lung fibers →Airway collapse, obstructed exhalation, air trapping
Tx	• Smoking cessation • Oxygen • Bronchodilators- Beta agonists, anticholinergics, xanthines • Steroids – IV or inhaled • Antibiotics those without COPD: healthy patients are stimulated to breathe out due to ___ COPD pt: stimulated due to ___. why is that important to know? ____
Nrsg implications	• Assess baseline for if they are getting worse, esp. CV disease with beta agonists • If inhalants used for exercise induced asthma use med 30 to 60 minutes prior to exercise • Monitor for anticholinergic effects • Steroid inhaler – not in acute infection, may take a few weeks to reach max effectiveness • Yearly flu vaccine a must (upper respiratory infection prevention) • If constricted breathing occurs use short acting inhaler (albuterol) for rescue • Monitor for appropriate dosing frequency • Refer to assess home environment for triggers/compliance • Review When to call PCP

Chronic Obstructive Pulmonary disease (COPD)

Risk factors	#1 Risk Factor= Smoking Occupational risks= coal and dust Genetic defect- deficiency of alpha 1 anti-Trypsin • enzyme prevents enzymatic destruction of lung tissue • Deficiency= alveolar wall destruction and less elasticity of lung -Air Pollution -Asthma
What is COPD	• Progressive airflow limitation leads to an abnormal inflammatory response of the lungs • Not completely reversible • Leads to pulmonary insufficiency, pulmonary hypertension, cor pulmonale (right heart damage)
Mechanisms of COPD	• Inflammation and fibrosis of the bronchial wall • Hypertrophied mucous glands → excess mucus →Obstructed airflow • Loss of alveolar tissue →Decreased surface area for gas exchange • Loss of elastic lung fibers →Airway collapse, obstructed exhalation, air trapping
Tx	• Smoking cessation • Oxygen • Bronchodilators- Beta agonists, anticholinergics, xanthines • Steroids – IV or inhaled • Antibiotics those without COPD: healthy patients are stimulated to breathe out dt high CO2 levels COPD pt: stimulated due to low O2. if you give them more O2, they'll lose their drive to breathe
Nrsg implications	• Assess baseline for if they are getting worse, esp. CV disease with beta agonists • If inhalants used for exercise induced asthma use med 30 to 60 minutes prior to exercise • Monitor for anticholinergic effects • Steroid inhaler – not in acute infection, may take a few weeks to reach max effectiveness • Yearly flu vaccine a must (upper respiratory infection prevention) • If constricted breathing occurs use short acting inhaler (albuterol) for rescue • Monitor for appropriate dosing frequency • Refer to assess home environment for triggers/compliance • Review When to call PCP