Adult Respriratory

What does ARDS stand for?

Acute Respiratory Distress Syndome

What is ARDS?

Sudden and progressive form of Acute Respiratory failure

Patho of ARDS?

Exact cause is unknown

ARDS causes diffuse alveolar damage and alveolar collapse = decreased lung compliance

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Once alveolar collapse - gas exchange ceases - body becomes starved of O2

What are the 3 phases of ARDS patho?

Phase 1: Injury/Exudative

Phase 2: Reparative/Proliferative

Phase 3: Fibrotic

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The course of each phase and overall disease is variable

Phase 1 of ARDS?

Injury/Exudative (Early phase)

* occurs 24-72 hours after initial injury
* With injury - the inflammatory response and immune system is stimulated
* The stimulation attracts neutrophils to pulmonary interstitium
* As condition worsens; fluid, protein & cellular debris flood alveolar space & interstitium
* disrupts surfactant
* collapse alveoli (atelectasis)
* Results = V/Q mismatch
* shunting, stiffening of lungs, decreased compliance, pulm HTN

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What is refractory hypoxemia?

* Sever V/Q mismatch and shunting of pulmonary capillary blood
* results in hypoxemia, that is still unresponsive to increase O2 concentration

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How is phase 1 characterized?

Interstitial & alveolar edema, atelectasis

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Pt breathes faster but suff. O2 can’t cross alveolar/cap membrane

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Pt may need vent after phase 1

What is phase 2 of ARDS?

Proliferative

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* begins 1-2 wks after initial injury
* Inflammatory response still active - influx of neutrophils, monocytes, lymphocytes & fibroblast continue
* they are attempting to repair lung
* Increased Pulmonary vascular resistance & Pulm HTN may occur due to fibroblasts & inflammatory cells destroying pulm. vasculature
* hypoxemia worsens due to thickened alveolar membrane

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When is phase 2 complete?

If phase 2 persist - widespread fibrosis results

* this phase is complete when diseased lung is replaced by dense, fibrous tissue

If it is stopped in time - lesions will often resolve

What is phase 3 of ARDS?

Fibrotic (Chronic/Late Stage)

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* Occurs approx. 2-3 wks after initial injury
* Patients who don’t recover - lung is remodeled by collagenous & fibrous tissue
* **NOT all pts who develop ARDS enter fibrotic stage**
* Decreased lung compliance - hypoxemia & pulm. HTN continue

Manifestations of ARDS

Develops as a result of an insult, condition, or noxious event that traumatizes the lungs

* injury can be direct or indirect

What are direct and indirect conditions of ARDS?

Direct

* Aspiration of gastric contents
* Bacterial/Viral pneumonia
* Sepsis
* Smoke inhalation, drowning

Indirect

* Sepsis
* Massive Trauma
* TBI
* Shock States (hypovolemic, cardiogenic, septic

**The most common cause is Sepsis**

What are signs/symptoms of ARDS?

Initially:

* lungs clear w/ inspiratory crackels
* **Hyperventilation: ABG= resp. alkalosis w/ mild hypoxemia**
* pH >7.45, PaCO2<35
* Chest X-Ray: minimal interstitial infiltrates

Progression:

* lungs w/ scattered to diffuse crackles & rhonchi
* Respiratory distress: dyspnea, tachypnea, retractions
* Syncope, light headed, dizzy
* Tachycardia
* N/V
* decreased LOC, lethargy, seizure

What is care for ARDS?

* frequently assess ABC’s
* treat underlying condition
* broad spectrum antibiotic then narrow
* Suction PRN
* Maintain tissue O2
* non-rebreather, ABG
* may require intubation
* Mobilize secretions & stimulate postural drainage
* Turn pt frequently & reposition to prone
* Improves oxygen by:
* redistributing lung infiltrates
* relieving/preventing atelectasis
* improve V/Q
* Maintain cardiac status
* fluids
* I/O, daily weight

What is Acute Respiratory Failure?

occurs when oxygenation, ventilation, or both are inadequate

Is ARF a disease?

Not a disease - a condition that develops as a result of one or more diseases involving the lungs or other body systems

Hypoxemia

conditions that interfere with adequate oxygen transfer

* causes decrease in arterial oxygen (PaO2) and saturation (SaO2)

Hypercapnia

Insufficient CO2 removal

* increase PaCO2

What are the two classifications of ARF?

* Hypoxemic
* Hypercapnic

What is Hypoxemic RF?

* Oxygenation failure
* PaO2 < 60mmHg on 60% oxygen
* Can be acute (min-hrs) or Chronic (several days)
* **Leads to Metabolic Acidosis**

**Most common form of RF - less optimal PaO2 despite supplemental O2**

* Main problem is inadequate exchange of O2 between alveoli & pulmonary capillaries

What is Hypercapnic RF?

* Ventilation failure
* PaCO2 > 45, pH <7.35
* Can be acute or chronic
* **leads to Respiratory Acidosis**

Lungs are often normal

* Alveolar ventilation is inadequate for removing CO2 produced by the body
* Often reflects significant problems with resp. system

What are the 4 physiologic alterations that cause Hypoxemic Respiratory Failure?

1. V/Q mismatch - dead space
2. V/Q mismatch - intrapulmonary shunting
3. Diffusion abnormalities
4. Alveolar hypoventilation

Dead Space

the portion of the respiratory system where tidal volume doesn’t participate in gas exchange. It is ventilated but not well perfused.

\*\* the Q part of V/Q mismatch (perfusion)

What are the 3 types of dead space?

1. Anatomic - fixed by anatomy - doesn’t move
2. Physiologic - decreases pulmonary blood flow (varies situationally)
3. apparatus - any airway equipment being used to assist ventilation - increases dead space

What is anatomic dead space?

trachea, bronchi, & bronchioles - structures that don’t have alveoli

What is physiologic dead space?

Can change from min to min with alterations in CO & pulmonary blood flow

What are things that impair alveolar perfusion and increase pulmonary dead space?

* cardiovascular shock (blood flow to lungs decrease)
* Emphysema (enlarged alveoli with decreased SA and fewer alveolar capillary
* Pulmonary Embolism ( flow blocked by clot or air embolus)

What is V/Q mismatch - shunting?

A shunt occurs when blood exits the heart w/o having taken part in gas exchange

**extreme V/Q mismatch**

* the larger the shunt the lower oxygen content
* O2 therapy alone is not effective - leads to hypoxemia

What are the 2 types of shunts?

1. Anatomic
2. Intrapulmonary

What is an anatomic shunt?

a shunt that occurs when blood passes through an anatomical channel in the heart and bypasses the lungs

What is a intrapulmonary shunt?

a shunt that occurs when blood flows through the pulmonary capillaries w/o taking part in the gas exchange

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* seen in conditions where alveoli are filled with fluid
* pneumonia

What are common shunts?

* increased secretions in airway or alveoli (pneumonia, ARD’s, CF)
* Fluid in airway or interstitial space (Pulmonary edema)
* Bronchospasms
* Atelectasis - Most common shunt

What is diffusion abnormalities?

gas exchange across the avleolar - capillary membrane is compromised. Certain disease processes thicken or destroy membrane

Conditions that limit diffusion? (ARF)

* Emphysema (destroys alveolar walls)
* Pulmonary fibrosis, ARDS - alveolar membrane is damaged and becomes thicker (fibrosis)
* Inhalation of toxins - smoking

Common example = pulmonary edema

What is a classic sign of diffusion limitation?

Hypoxemia that presents during exercise but not at rest

What is alveolar hypoventilation?

decrease in ventilation that results in an increase in PaCO2

* lungs and airway are often normal however, person doesn’t take enough breaths/min to provide adequate O2

What causes alveolar hypoventilation?

**primary problem - hypercapnic RF but can also cause hypoxemia**

* CNS injury
* Neurotransmitter disease
* Restrictive lung disorder - obesity, scoliosis
* Restrictive lung disease - asbestos

what are manifestations of hypoxemic respiratory failure?

**frequently caused by more than on alteration**

* restlessness/agitation
* dysrhythmias
* Early = increase BP
* Late= Decrease BP
* Resp. distress
* Fatigue
* Cyanosis (late sign)

You will see:

* increase RR
* retractions
* use of accessory muscles
* decreased SpO2

What does prolonged hypoxemic respiratory failure lead to?

Cor Pulmonale

What are the 4 categories of Hypercapnic respiratory failure?

1. CNS problems
2. Neuromuscular conditions
3. Chest wall abnormalities
4. Problems affecting airways and/or alveoli

What can cause each category for Hypercapnic RF?

CNS - OD of opioids, head trauma

Neuromuscular - MS, Guillian-Barre, Muscular dystrophy

Restrictive disorders - obesity, scoliosis

Airflow obstructions - COPD

What are manifestations of Hypercapnic RF?

* morning HA
* drowsiness
* dyspnea
* dysrhythmias
* vasodilation/flushing

You will see:

* decreased RR
* bounding pulse
* HTN (early)
* HypoTN (late)
* extra heart sounds (S3, S4)

How to diagnose ARF (hypoxemic or hypercapnic)?

Pt’s can experience both

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* ABG’s
* PaO2< 50
* PaCO2 >50
* pH < 7.35
* CBC, sputum culture
* Chest X-Ray
* V/Q scan
* PAC - pulmonary artery catheter

What is care for ARF?

* maintain airway & breathing
* mobilize secretions
* teach effective coughing & deep breathing
* hydrate
* Elevate HOB 45 degrees
* Chest PT
* Suction
* Support breathing
* maintain adequate oxygenation & ventilation
* provide lowest O2 concentration possible to maintain PaO2 > 60 (SaO2 @ 90% or more)
* enhance V/Q matching by turning pt regular
* incentive spirometer

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What is treatment for all lung injuries?

Oxygen therapy

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* NIPPV
* BiPap
* CPap
* PEEP

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Can you recognize when to intubate?

* PaO2 < 80 and not improving with a nebulizer
* w/ COPD, PaO2< 60
* pH < 7.35 , PaCO2 > 55
* decrease LOC, unresponsive
* severe resp. distress
* resp. failure
* threatened airway obstruction
* Apnea
* Impaired alveolar ventilation (smoke inhaltion)

What is nutritional therapy for ARF?

* High protein - Low carb
* High protein - to prevent muscle loss
* low carb - carbs metabolize into CO2 = increase CO2

What is COPD?

Chronic Obstructive Pulmonary Disease

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* disease characterized by persistent airflow limitations
* enhanced chronic inflammatory response in airway, lungs, and pulmonary blood vessels
* It is preventable and treatable, but often progressive

What is the major risk factor for COPD?

Smoking

What is included in COPD?

Chronic Bronchitis

Emphysema

What is Chronic Bronchitis?

presence of coughing & sputum production for at least 3 months in each 2 consecutive years

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* increased mucus & inflammation which causes damage to lung tissue and destroys cilia

What is emphysema?

The destruction of alveoli without fibrosis

* air sacs supply O2 to blood, when they are damaged, less O2 enters blood

What is hallmark sign for Emphysema?

Shortness of breath

What is patho for Chronic Bronchitis?

* increased mucus & inflammation which causes damage to lung tissue and destroys cilia
* airway remodel takes place as lung attempts to repair itself
* fibrosis of small bronchi & bronchioles
* further constricting airway
* hypoxemia
* constriction of pulm. vasculature (Pulm. HTN)
* Overproduction of erythrocytes to compensate for low O2 (polycythemia)
* All results in an increase workload for Right side of heart
* causes dilation and hypertrophy
* LEADS to Cor Pulmonale

What are manifestations for Chronic Bronchitis?

* “Blue Bloaters”
* dusky to cyanotic color
* **Chronic cough w/ sputum**
* Resp. Acidosis
* Overweight
* clubbing of digits
* increase RR, wheezing, exertional dyspnea
* increased infections
* **manifestations of R-side HF**

What is patho for Emphysema?

recurrent pulmonary infections > increase macrophages & neutrophils > increase Proteolytic enzymes> increase enzymes decrease action of AAT = proteolytic enzymes breakdown infection & health lung tissue

What are the protease inhibitors that stop proteolytic enzymes?

AAT - alpha 1 antitypsin

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AAT is made in the liver and stored in lungs to protect lungs

Top 3 characteristics of Emphysema?

* Chronic cough
* sputum
* dyspnea

What are the two types of Emphysema?

1. Centrilobular - mostly from smoking
2. Panlobular - AAT deficiency

Manifestations of Emphysema?

* “Pink Puffer’s”

Early:

* Respiratory alkalosis
* moderate hypoxemia

Late:

* Respiratory acidosis (Inc. CO2, causes Pink color)
* severe hypoxemia

Others:

* weight loss/thin
* few infections
* minimal cough
* chronic dyspnea (worse w/ exertion)
* Pursed lip breathing
* Barrel chest
* Minimal cyanosis

What is collab care for Emphysema?

* **STOP SMOKING**
* Supplemental O2
* Avoid Large meals
* rest 30 min prior to eating, 5-6 small meals/day - High Protein & Calorie
* Hydrate (unless pt has HF)
* Immunizations
* flu, pneumonia
* Teach effective coughing
* Breathing retraining
* Chest PT & postural drainage
* Graded exercise - start slow

When to call the doctor for COPD?

* Unusual:
* increase/decrease in sputum
* increase/decrease in thickness or stickiness
* increase in difficulty breathing
* Sputum is new color or blood tinged
* Insomnia, need for more pillows
* Chest pain, fever, swelling in ankles, extreme fatigue, unusual drowsiness
* Unaccountable increase/decrease in weight
* Frequent morning HA or dizzy spells
* Confusion, disorientation, slurred speech

Drug therapy for COPD?

Bronchodilators

* Beta Agonists (SABA, LABA)
* Albuterol, Levabuterol, Formoterol
* Anticholinergices
* Ipratropium, Tiotropium
* Methylxanthines
* Aminophylline