acuterespfailure.ppt

8/11/2019 acuterespfailure.ppt

1/31


2/31

Definition: Respiratory Failure

Failure of the respiratory system in one or

both of its gas exchange functions:

Oxygenation

Carbon dioxide elimination

Can be acute or chronic

Documented by PaCO2> 50 mm of Hg or

PaO2 < 60 mm of Hg.


3/31

Respiratory Failure Classification

Hypoxemic

PaO2 50 mmHg, can also see hypoxemia

Acute drop in blood pH (


4/31

Respiratory Failure: Causes

Upper airway dysfunction

Lower airway obstruction

Alveolar and pleural disease CNS causes


5/31

Respiratory Failure: Causes

1. Upper airways obstruction:

> Laryngomalacia

> Subglottic stenosis

> Laryngotracheobronchitis

> Tracheitis & Epiglottitis

> Retropharyngeal / Peritonsillar abscess

> Acute hypertrophic tonsillitis

> Diphtheria

> foreign body, trauma, vocal cord palsy


6/31

2. Lower airway obstruction:

> Bronchiolitis, Asthma, Foreign body

3. Alveolar and pleural disease:

> pneumonia, pulmonary edema, effusion

empyma, pneumothorax, ARDS

4. CNS causes:

> Infections, injury, trauma, seizures> tetanus, SMA, Polio

> AIDP, Phrenic nerve injury

> Myasthenia gravis, botulism,> Muscle dystrophies, Polymyositis

> Congenital myopathies, muscle fatigue


7/31

Respiratory Distress:

signs of impending respiratory failure

Tachypnea, diaphoresis

Exaggerated use of accessory muscles

Intercostal, supraclavicular and subcostalretractions

Paradoxical/abdominal breathing

In neuromuscular disease, the signs of respiratory

distress may not be obvious In CNS disease, an abnormally low respiratory

rate, and shallow breathing are clues to impending

respiratory failure


8/31

Arterial Blood Gases

Arterial Blood Gas analysis: single most

important lab test for evaluation of

respiratory failure.


9/31

Evaluation of Respiratory failure

The following parameters are important in

evaluation of respiratory failure:

1. PaO2

2. PaCO2

3. Alveolar-Arterial PO2 Gradient

4. Hyperoxia Test5. Blood pH


10/31

PaO2 / PaCO2

Normal value depends on :

a. Position of patient during sampling

b. Age of patient

PaO2(Upright) = 104.2 -- 0.27 x age (Yrs)

PaO2 (Supine) = 103.50.47 x age (Yrs)

PaCO2 : normal value= 35-45 mm of Hg

unaffected by age/ positioning


11/31

A - a Gradient

PAO2= FiO2 x (PB - PH20) - PACO2 / R A-a gradient = PAO2 - PaO2

PB = 760 mmHg (sea level)

PH20 = 47 mmHg (100% humidity)

(760 - 74) = 713

R = 0.8

A-a gradient =

[FiO2 x 713 - (PaCO2 / 0.8)] - PaO2


12/31

Sample ABG

7.34 / 58 / 92 / 21 / 94% on 100% Fi02

A - a gradient:

[1.0 x 713 - (58 / 0.8)] - 92

[713 - 72.5] - 92

[640.5] - 92 = 548.5

A - a gradient = 548.5

Severe defect in gas exchange/ hypoxemia


13/31

Alveolar-Arterial O2 gradient

Normal P(A-a)O2 gradient: 5-10 mm of Hg

A sensitive indicator of disturbance of gas

exchange.

Useful in differentiating extrapulmonary and

pulmonary causes of resp. failure.

For any age, an A-a gradient > 20 mm of Hgis always abnormal.


14/31

Causes of Hypoxemia

1. Low PiO2~ at high altitude

2. Hypoventilation~ Normal A-a gradient3. V/Q mismatch~ increased A-a gradient

4. R/L shunt~ increased A-a gradient


15/31

Hypoventilation-Diagnosis

PaO2

PaCO2 is always increased

A-a gradient is normal ( 10 mm of Hg)

Hyperoxia Test : dramatic rise in PO2


16/31

V/Q mismatch- Diagnosis

PaO2

A-a gradient is elevated

PaCO2may or may not be elevated

Hyperoxia test : Dramatic rise in PaO2


17/31

V/Q Mismatch

Most common cause of hypoxemia

Causes include

Decreased ventilation: COPD, ILD

Hypo/hyperperfusion: PE

Minute ventilation increases due to

chemoreceptor stimulation

Corrects with hyperoxia/100% oxygen


18/31

R-L shunt: diagnosis

PaO2is

PaCO2is usually normal unless shunt is severe(>60%)

A-a gradient is

Hyperoxia Test : Poor / No response


19/31

Shunt Physiology

Shunt occurs when deoxygenated bloodbypasses ventilated alveoli and mixes withoxygenated blood

Results in decreased arterial O2 content Intracardiac shunts:

ASD, VSD, PFO

Intrapulmonary shuntsPNA, Pulm edema, AVMs


20/31

Hypercapnia :

Causes

Acute Hypoventilation

CNS depression: drugs, stroke, seizure

Neuromuscular disease: ALS, MS, Guillain-Barre, MG,C-spine injury

Severe low V/Q mismatch

COPD, Asthma, ARDS Chronic hypoventilation

OSA, obesity


21/31

Status of ABG

It is not possible to predict PaO2and PaCO2

accurately using clinical criteria.

Thus, the diagnosis of Respiratory failure

depends on results of ABG studies.


22/31

Respiratory failure:

Interventions

Supportive therapy

Upon arrival to the bedside

Establish factors contributing to resp failure

Use ABG to identify type of resp failure

Choose therapies based on physiology and severity

Specific therapy


23/31

Assessment &Supportive Therapy

Secure the airway (ABCs)

Pulse oximetry, vital signs

Oxygen: by mask, nasal cannula, bag-valve mask

Proper positioning Nebulization if indicated

Blood sampling: Routine, electrolytes, ABG

Secure IV access

CXR: upright AP & lateral views


24/31

Hypoxemic / Non - Hypercapnic

respiratory failure

The major problem is PaO2.

If due to low V/Q mismatch; oxygen therapy. If due to pulmonary intra-parenchymal shunts

(ARDS), assisted ventilation with PEEP may

be needed.

If due to intracardiac R-L shunt: O2therapy is

of limited benefit. Surgical/advanced

intervention is often needed.


25/31

Hypercapnic Respiratory failure

Key decision is whether mechanical ventilation isrequired or not.

In Acute respiratory acidosis: Mechanicalventilation must be strongly considered.

Chronic Resp acidosis: patient should be

followed closely, mech ventilation is rarelyrequired.

In acute-on-chronic respiratory failure, the trendof acidosis over time is a crucial factor.


26/31

Mechanical Ventilation: Indications

1. PaO2< 55 mm Hg or PaCO2> 60 mm Hg

despite 100% oxygen therapy.

2. Deteriorating respiratory status despite

oxygen and nebulization therapy

3. Anxious, sweaty, or lethargic patient with

deteriorating mental status.

4. Respiratory fatigue: for relief of metabolic

stress due to work of breathing or underlying

condition (sepsis, MI, CHF, etc.)


27/31

Mechanical Ventilation: Strategies

Non-Invasive Ventilation:

CPAP / BIPAP

Invasive Ventilation:

AC, VC, PC, Bilevel ventilation


28/31

Non-Invasive Ventilation

BIPAP should be considered in patients withmild-moderate respiratory failure

Must have intact airway, airway-protective

reflexes, appropriate mentation NOT for: excessive secretions, obtunded

patient, vomiting, severe agitation

Bridge therapy to stave off intubation andreverse resp. failure acutely while othertherapies are administered


29/31

Non-Invasive Ventilation

Proven beneficial in clinical trials for:

Acute exacerbations of COPD, Asthma, CHF

Not clear for PNA, ALI

Unloads respiratory muscles and work-of-

breathing

Recruits alveoli with adjustable PEEP May increase cardiac output in CHF


30/31

Clinical Follow-up

Patients with respiratory insufficiency require

very close follow-up

Usually need close interval assessments

ICU or Intermediate/Step down units

Continuous pulse-ox monitoring, cardiac and

hemodynamic monitoring

Most need pulmonary and/or critical care input

and management


31/31

Thank you!

Date post:	02-Jun-2018
Category:	Documents
Upload:	chris-jara
View:	214 times
Download:	0 times

acuterespfailure.ppt

Documents