Respiratory: Respiratory Failure and ARDS

Marnie Quick, RN, MSN, CNRN

Normal Respirations: Tidal Vol; Inspiratory & Expiratory reserve Vol; Residual Vol; Vital Capacity; Anatomical dead space

Normal gas exchange in lung

Blood Supply to Lung

Respiratory Failure Not a disease process, sign of severe dysfunction Results when one or both gas exchanging systems

inadequate; atmosphere (to lung) or blood Alveolar ventilation inadeq to meet body’s need Commonly defined in terms of ABG’s:

PO2 of less than 50 mmHg PCO2 greater than 50 mmHg Arterial pH of less than 7.35

Predisposing factors for Resp Failure: Airways/alveoli; CNS; Chest Wall; Neuromuscular- Table in Lewis p 1801 Most common cause: COPD

Classification of Respiratory Failure

Hypoxemic Respiratory Failure Oxygenation failure- inadequate O2 transfer

between alveoli & pulmonary capillary bed PaO2: 60 mm Hg or less on 60 % O2 Inadequate O2 saturation of hemoglobin Causes tissue hypoxia> Metabolic acidosis; cell

death; decreased CO; impaired renal function Common causes: disorders that interfere with O2

transfer into the blood- respiratory or cardiac system (Lewis p. 1800 Table 68-1)

Hypoxemic Respiratory Failure Mechanisms that may lead to Hypoxemia: 1. Mismatch ventilation & perfusion (V/Q mismatch)

V/Q: Volume blood perfusing lungs each minute Each ml of air for each ml of blood 1:1= V/Q ratio of 1 Causes of V/Q mismatch:

Ventilation portion blocked (secretions in airway/alveoli, airway/alveolar collapse, decreased movement chest/ventilation)

Perfusion portion blocked (pulmonary embolus) Treat: O2(reverse hypoxemia); treat cause

Hypoxemic Respiratory Failure

Range of ventilation to perfusion (V/Q relationship) A. Absolute shunt, no

ventilation fluid in alveoli B. Ventilation partially

compromised- secretions C. Normal lung unit D. perfusion partially

compromised by emboli obstructing blood flow

E. Dead space: no perfusion- obstruction of pulmonary capillary

Hypoxemic Respiratory FailureMechanisms that may lead to Hypoxemia: 2. Shunt- Extreme V/Q mismatch

Occurs when blood leaves heart without gas exchange

Types: 1. anatomic shunt: O2

blood does not pass through lungs

2. intrapulmonary shunt- alveoli fill with fluid

Treatment: Mechanical ventilation to force O2 into lungs; treat cause

Hypoxemic Respiratory FailureMechanisms may lead to Hypoxemia: 3. Diffusion limitations

Alveoli membrane thickened or destroyed

Gas exchange across alveolar-capillary membrane can’t occur

Classic sign: hypoxemia present during exercise, not at rest

Treat the cause- pulmonary fibrosis; ARDS

Hypoxemic Respiratory FailureMechanisms may lead to Hypoxemia: Clinical Manifestations of Hypoxemia

Specific: Respiratory: Dyspnea; tachypnea; prolonged expiration;

intercostal muscle retraction; use of accessory muscles in resp;< 80% SpO2; paradoxic chest/abd wall movement with resp cycle (late); cyanosis (late)

Nonspecific: Cerebral: agitation, disorientation, delirium, restless,

combative, confusion, dec LOC, coma (late) Cardiac: tachycardia, hypertension, skin

cool/clammy, dysrhythmias (late), hypotension (late) Other: fatigue; need to pause to breath when

speaking

Hypercapnic Respiratory Failure Ventilatory failure with insufficient CO2 removal PaCO2 greater than 45 mm Hg Arterial pH less than 7.35 PCO2 rises rapidly and respiratory acidosis

develops: PO2 drops more slowly Common causes: disorders that compromise lung

ventilation and CO2 removal (Lewis Table 68-1)

Hypercapic Respiratory Failure

Ventatory failure: Inability of the respiratory system to ventilate out sufficient CO2 to maintain normal PaCO2

Specific Causes: Airways/alveoli: asthma, COPD, cystic fibrosis CNS: drug overdose- depressant, brainstem

dysfuction, metabolic causing decreased LOC; high SCI injuries- decrease/absent diaphragm/chest movement

Chest wall: pain, flail chest, rib fractures, mechanical restriction, kyphoscoliosis, obesity

Neuromuscular: resp muscles weak/paralysis- MS, MG, MD, Guilain-Barre Syndrome

Hypercapic Respiratory Failure Clinical Manifestations Specific:

Respiratory: Dyspnea; dec resp rate or rapid with shallow resp; dec tidal vol; dec min ventilation

Nonspecific: Cerebral: AM headache; disorientation, progressive

sommolence; coma (late) Cardiac: dyshythmias; hypertension; tachycardia;

bounding pulse Neuromuscular: muscle weakness; dec deep tendon

reflexes; Tremor/seizures (late)

Collaborative Care for Respiratory Failure: Diagnostic tests History/physical assessment Pulse oximetry ABG analysis Chest X-ray CBC, sputum/blood cultures, electrolytes EKG Urinalysis V/Q scan- if pulmonary embolism suspected Hemodynamic monitor/pulmonary function tests

Collaborative care for Respiratory Failure Respiratory Therapy Main treatment- correct underlying cause & restore adequate gas

exchange in lung Elevate HOB Oxygen Therapy

Maintain PaO2 at least 60 mm Hg SaO2 at least 90%

Mobilization of secretions Hydration & humidification Chest physical therapy Airway suctioning Effective coughing & positioning

Positive pressure ventilation Noninvasive positive pressure ventilation Intubation with mechanical ventilation

Collaborative Care for Respiratory Failure cont Drug Therapy

Relief bronchospasm; reduce airway inflam and pulmonary congestion; treat pulmonary infections; reduce anxiety, pain

Medical supportive therapy Treat underlying cause

Nutritional therapy Enteral; parenteral Protein and energy stores

Collaborative Care: Artifical airways- tracheostomy and endotracheal tubes

Endotracheal tube

Taping an endotracheal tube

Suctioning with closed (inline) suctioning-used with tracheostomy or endotrach tubes

Complications of endotracheal intubation

1. Extubation Restraints

2. Aspiration Tube at right allows

for subglottal suctioning

Independent Lung Ventilation

Collaborative Care: Mechanical Ventilation Provide adeq gas

exchange Types- Positive, Neg Settings- Table 66-11 Modes- Table 66-12 Criteria to put on vent

RR > 35-45 pCO2 >45 pO2 <50

Types: Negative pressure ventilator

Types: Positive pressure mechanical ventilation with endotracheal tube (PPV)

Types: Positive pressure- Noninvasive (tight fitting mask) positive pressure ventilation (CPAP)

Settings and complications with mechanical ventilation

Ventilator settings (Table 66-11 p. 1761)

SETTING FUNCTION USUAL PARAMETERS

Respiratory Rate (RR) Number of breaths delivered by the

ventilator per minute

Usually 4-20 breaths per minute

Tidal Volume (VT) Volume of gas delivered during each

ventilator breath

Usually 5-15 cc/kg

Fractional Inspired Oxygen (FIO2) Amount of oxygen delivered by ventilator

to patient

21% to 100%; usually set to keep PaO2 > 60

mmHg or SaO2 > 90%

Inspiratory:Expiratory (I:E) Ratio Length of inspiration compared to length of

expiration

Usually 1:2 or 1:1.5 unless inverse ratio

ventilation is required

Pressure Limit Maximum amount of pressure the ventilator

can use to deliver breath 10-20 cm H2O above peak inspiratory

pressure; maximum is 35 cm H2O

Alarm settings Assess your patient – not

the alarm!!!!! Never turn alarms off Alarms sound when you

have low pressure or high pressure in the ventilator

Note “alarm silence” and “alarm reset” on picture to the right

Low Pressure

•Circuit leaks  •Airway leaks  •Chest tube leaks  •Patient disconnect from vent or tube

High Pressure

•Patient coughing  •Secretions or mucus in the airway  •Patient biting tube  •Airway problems  •Reduced lung compliance (as a pneumothorax)  •Patient fighting the ventilator  •Accumulation of water in the tube•Kinking of tube 

Modes of PPV Volume Ventilation

Predetermined tidal volume (TV) is delivered with each inspiration

Tidal volume (TV) is consistent, airway pressures will vary

Pressure Ventilation Predetermined peak inspiratory pressure Tidal volume (TV) will vary, airway pressures

will be consistent

Ventilator settings of Modes (Table 66-12 p.1761) Volume Modes

CMV; AC; SIMV Predetermined tidal volume (TV) is delivered with each

inspiration Tidal volume (TV) is consistent, airway pressures will vary

Pressure Modes PSV; PC-IRV

Predetermined peak inspiratory pressure Tidal volume (TV) will vary, airway pressures will be

consistent Other Modes

PEEP and CPAP

Ventilator settings- SIMV and IMV

Ventilator settings- Other modes Positive End-Expiratory Pressure

Positive pressure is maintained at the end of expiration

Pressure at end expiration keeps alveoli from collapsing, improving functional residual capacity (FRC)

Used with other modes on the ventilator Purpose is to improve oxygenation while limiting

risk of O2 toxicity Used to treat ARDS

PEEP

Ventilator settings- other modes Continuous Positive Airway

Similar to PEEP However, pressure in CPAP is delivered

continuously Prevents airway pressure from falling to zero Measured in cm H20 Can be administered noninvasively (by mask) or

through ETube or TTube Used in treatment of obstructive sleep apnea

Complications of Positive Pressure Mechanical ventilation Cardiovascular: decreased CO; inc intrathoracic pressure Pulmonary: Barotrauma; Volutrauma; alveolar

hypoventilation/hyperventilation; ventilator-associated pneumonia

Sodium and water imbalance Neurological: impaired cerebral bl flow>IICP Gastrointestional: stress ulcer/GI bleed; gas; constipation Musculoskeletal: dec muscle tone; contractures; footdrop;

pressure ulcers from BR Psychosocial: physical & emotional stress; fight vent

Nursing Care for complications Neurological – elevate head of bed, keep body

in proper alignment Respiratory – monitor cuff inflation, vent settings,

ABG’s, for hyperventilation, hypoxemia Cardiovascular – monitor NIBP and arterial

pressures, CO, capillary refill, HR & rhythm Gastrointestinal – set up schedule for BM, admin

laxatives, PPI, admin tube feedings Musculoskeletal – passive & active ROM, turn

q2h, keep body in proper alignment

Psychological needs- Need for information; regain control; to hope; to trust Involve in discision making, medication for

sedation (proplfol), analgesia (fentanyl), neuromuscular blocking agents (Nimbex)

Other problems when on mechanical ventilation Machine disconnection or malfunction Nutrition needs Weaning from ventilator/ extubation

Spontanenous breathing trial (SBT) Hospital protocol

Document progress Table 66-13 p.1767- readiness/assessment

Exhaled C02 (ETC02) normal 35-45Exhaled C02 (ETC02) normal 35-45

Used when trying to wean Used when trying to wean patient from a ventilatorpatient from a ventilator

Nursing assessment specific to Respiratory Failure Assess both airway and

lungs- note picture to right

Refer to hypoxic and hypercapnic respiratory failure symptoms

Table 68-4 p. 1806 Subjective data Objective data

Cyanosis

Relevant Nursing Problems related to Respiratory Failure Prevention of acute respiratory failure Nursing Care Plans (p.1807-09) Gerontology considerations Nursing Care Plans Mechanical ventilation

(NCP 66-1 p.1754) Suctioning procedure and oral care

(p.1757-8)

Acute Respiratory Distress Syndrome ARDS Sudden progressive form of acute respiratory

failure Alveolar capillary membrane becomes damaged

and more permeable to intravascular fluid Results in noncardiac pulmonary edema and

progressive refractory hypoxemia ARDS is NOT primary! Follows various pulmonary or systemic

conditions Sepsis is the most common cause

Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

Stages of Edema Formation in Stages of Edema Formation in ARDSARDS

AA, Normal alveolus and , Normal alveolus and pulmonary capillary pulmonary capillary

BB, Interstitial edema , Interstitial edema occurs with increased occurs with increased flow of fluid into the flow of fluid into the interstitial space interstitial space

CC, Alveolar edema , Alveolar edema occurs when the fluid occurs when the fluid crosses the bloodcrosses the blood--gas gas barrierbarrier

Fig. 68Fig. 68--88

Pathophysiology of ARDS

Phases of ARDS Injury or Exudate Phase Occurs 24-48 hrs post direct or indirect inj Systemic inflammatory response and damage to

the alveolar-capillary membrane. Increased capillary permeability Fluid enters the alveoli Dilutes and deactivates surfactant Alveoli stiffen and collapse Interstitial, alveolar edema & atelectasis>

noncardiogenic pulmonary edema Hypoxemia becomes refractory

Phases of ARDS Reparative or proliferative Phase 1-2 wks post initial insult Regeneration lung tissue may occur Hyaline membrane forms> CO2 cannot

diffuse across> respiratory acidosis Phase complete when diseased lung dense,

fibrous tissue

Phases of ARDS Fibrotic phase 2-3wks post insult Chronic or late phase Diffuse scarring and fibrosis>decease lung

compliance Dec surface area gas exchange> hypoxemia

continues> pulmonary hypertension Metabolic acidosis can occur> MOSD>

death

Surfactant keeping alveoli open Fibrotic lung

Clinical progression of ARDS Insidious onset- sym dev 24-48 hrs post

initial insult (direct or indirect lung injury) Course determined by nature of initial

injury, extent & severity of coexisting disease, and pulmonary complications

50% who develop ARDS die- even with aggressive treatment

Clinical manifestations of ARDS Progressive refractory hypoxemia> Hallmark sign Noncardiac pulmonary edema Early symptoms- labored R- dyspnea, tachypnea,

anxiety/restless, dry-nonproductive cough Later symptoms- cyanosis, adventitious breath

sounds, use of accessory muscles with retractions and decreased mental status

Diagnosis of ARDS ABG’s> refractory

hypoxemia Chest X-ray infiltrates>

white out/snow storm. Note progression picture to right

Pulmonary artery wedge 18 mm Hg & no evidence of heart failure

Identification of a predisposing condition for ARDS within 48 hrs of clinical manifestations

Complications of ARDS Hospital-acquired pneumonia Barotrauma Volu-pressure trauma Physiologic stress ulcer Renal failure

Collaborative Care for ARDS Respiratory therapy & medical support Oxygen Mechanical ventilation-

main treatment Positioning strategies

Proning CLRT-lateral rotation

bed Maintenance of CO &

tissue perfusion (fluids) Maintenance of nutrition

& fluid balance Treat underlying cause

Prone Device

•Prone positioning With position change to

prone, previously nondependent air-filled alveoli become dependent, perfusion becomes greater to air-filled alveoli opposed to previously fluid-filled dependent alveoli, thereby improving ventilation-perfusion matching.

No benefit in mortalityNo benefit in mortality

Rotoprone bed

Benefits to Proning >

Nursing assessment specific to ARDS & Relevant nursing problems R/T ARDS Assessment

Refer to respiratory failure assessment Assess for clinical progression and clinical

manifestations as stated above Nursing care plans- refer to resp failure Goals for recovery from ARDS

PaO2 within normal limits on room air SaO2 greater 90% Patent airway Lungs clear on auscultation