CCRN Test Guide

CCRN – 17%

PCCN – 14%

CCRN

 Acute pulmonary embolus

 Acute respiratory distress

syndrome (ARDS), acute

lung injury (ALI) &

respiratory distress

syndrome (RDS)

 Acute respiratory failure

 Acute respiratory infections

 Air-leak syndromes

 Aspiration

 Chronic conditions - COPD,

Asthma, Bronchitis,

emphysema

 Failure to wean from the

ventilator

 Pulmonary fibrosis

 Pulmonary hypertension

 Status Asthmaticus

 Thoracic surgery

 Thoracic Trauma (fractured

rib, lung contusion, tracheal

perforation)

PCCN

 Acute Respiratory Distress

Syndrome (ARDS/ALI)

 COPD Exacerbation

 Obstructive Sleep Apnea

 Pleural space abnormalities

& complications

(pneumothorax,

hemothorax, pleural

effusion, empyema)

 Pulmonary embolism

 Pulmonary Hypertension

 Respiratory depression

 Respiratory failure

 Respiratory infections (i.e.

pneumonia)

 Severe asthma

 Thoracic Surgery

(lobectomy,

pneumonectomy)

General Assessment

 Adventitious (added)

lung sounds:

 Crackles (rales) – heart

failure, effusions,

pneumonia

 Wheezes – narrowed

airways

 Rhonchi – Secretions in

large airways, pneumonia

Bronchial Vs Broncho-vesicular VS Vesicular Sounds

Arterial Blood Gases

*pH

*PaCO2 Lungs:

Fast compensation

*HCO3

Kidney:

Slow compensation

Normal Blood Gas values

Arterial

pH 7.35 – 7.45

PaO2 80 – 100

                                          PaCO2 35 - 45                                            

HCO3 22 – 26

Base

Excess/Deficit

- 2 to + 2

SaO2 95 – 100%

Venous

pH 7.32 – 7.42

Pa o2 28 – 48

Pa co2 38 – 52

HCO3 19 – 25

Sao2 50 – 70%

ABG Interpretation

pH: 7.35 ----- 7.40 ----- 7.45

Acid                            Alkaline

 PaCO2: 35 ----- 40 ----- 45

Alkaline                                 Acid

HCO3: 22 ----- 24 ----- 26

Acid                            Alkaline

ABG Analysis

1. Always assess the pH first!

2. Is it normal?

3. Is there acidosis or alkalosis?

4. Which other value (PaCO2 or HCO3) is trending

with the pH?

pH: 7.28 PaCO2: 54 PaO2: 196 HCO3: 26

If PaCO2 is the cause, it’s RESPIRATORY!

If HCO3 is the cause, it’s METABOLIC

 Look at the pH & CO2

If the pH & CO2 are both up or both down:

 saME = Metabolic

Example: pH: 7.32(↓) CO2: 32 (↓) HCO3: 18

 REverse = Respiratory

Example: pH: 7.28 (↓) CO2: 54 (↑)HCO3: 26

ROME – Respiratory Opposite, Metabolic Equal

 If pH is normal &

 PaCO2 and/or HCO3

- are abnormal, then the patient is

compensated.

 If pH is abnormal, &

 either PaCO2 or HCO3

- are abnormal, then the patient is

uncompensated.

 If pH is abnormal &

 PaCO2 and HCO3

- are both abnormal, then the patient is

partially compensated.

 If pH is abnormal &

 PaCO2 and HCO3

- are both trending toward acidosis or

alkalosis with the pH, then the patient has a mixed acidosis

or alkalosis

pH 7.36 PaCO2 48 HCO3 24

Compensated Respiratory Acidosis

pH 7.26 PaCO2 35 HCO3 16

Uncompensated Metabolic Acidosis

pH 7.30 PaCO2 58 HCO3 30

Partially Compensated Respiratory Acidosis

Respiratory Acidosis Causes

 Over-sedation

 Late respiratory failure

 Drug overdoses that cause

resp. depression

 COPD

 Brain stem dysfunction

 Extreme V/Q mismatch

 Pulmonary embolus, PNA

 Guillain Barre’

 K+ / PO-4 imbalances

 Excessive CO2 production

(Sepsis, TPN, Burns)

 Think hypoventilation!

(retaining CO2)

Respiratory Alkalosis Causes

 Early respiratory failure

 Anxiety or severe pain

 Excessive tidal volume or rate

on vent

 ARDs

 Heart failure

 Neurologic disorders

 Pulmonary embolus

 Salicylate overdose (adults)

 Decreased Cardiac

Output/Shock

 PaO2 < 60 (Cause & effect)

 Think hyperventilation!

(blowing off CO2)

Metabolic Acidosis Causes

 Acute kidney injury

 Drug overdoses

 Diabetic Ketoacidosis

 Sepsis

 Lactic Acidosis

 Toxins

 Aspirin overdose

 Liver failure

 Hyperkalemia

 Hyperchloremia

 Calculate an anion

gap!!!

 May lead to

hyperkalemia

 Suppresses myocardial

contractility

 (↓ CO, ↓ BP)

Anion gap: Normal < 11 - 12

Determination of the serum anion gap (AG) is primarily used in the differential diagnosis of metabolic acidosis

Na++ Cl-

K+ (don’t count) HCO3-

>12 – Metabolic acidosis

M: Methanol P: Propylene glycol

U: Uremia I: Isoniazid

D: DKA L: Lactic acidosis

E: Ethylene glycol

S: Salicylates

Serum AG  =  Measured cations - measured anions

Since Na is the primary measured cation and Cl and HCO3 are the primary measured anions (calculator 1):

 Serum AG  =  Na - (Cl  +  HCO3)

Metabolic Alkalosis Causes

 NG tube to suction

 Emesis

 Hypokalemia

 Hypochloremia

 Antacid abuse

 Excessive sodium bicarb infusion

 Inadequate renal perfusion

 Diuretics

 Excessive albuterol use

 Hyperaldosteronism (d/t RAAS activation)

Hypoxemia

3 Reasons:

 1. Hypoventilation

 ↓ total volume air

inhaled/exhaled

 ↓ Phosphate or

Magnesium levels

 OSA

 2. V/Q Mismatch

 PE, pneumonia, shunt

 3. DO2/VO2 imbalance

 ↓ Cardiac output

Is the ABG perfect?

 What does the PaO2 tell

you about O2 delivery to

the cells?

 What does oximetry tell

you?

 What does SVO2/ScvO2

tell you?

 Lactate?

Intrapulmonary Shunt

V/Q Mismatch

 Excessive blood flow in relation

to ventilation

 OR, ventilation without perfusion

 Examples:

 Asthma – small airways

restricted

 Pulmonary edema – alveoli

filled with fluid

 Atelectasis – Alveoli collapse

 Pulmonary embolus – nonembolized

regions of the lungs

PaO2 decreases as shunt increases

In general, PaCO2 stays about the same

Oxygen

Factoids

 Too much is NOT a good

thing!

 > 50% of hospitalized

patients receive O2 without

a written order

 O2 is a vasoconstrictor in

all vascular beds except

the lungs (vasodilator)

 Has negative inotropic

effects on the heart

 In the absence of

hypoxemia, O2 can ↓ C.O.

Administration

 Low flow

 Nasal cannula, face

mask, FM with reservoir

bag

 High flow

 Provides constant FiO2

 Delivers O2 at flow

rates > patient’s peak

inspiratory flow rate

 Venturi mask, ventilator

OXYGEN Delivery Methods

 Nasal Cannula 1 – 6 L

21% to 46% FiO2

 Face Mask 5 – 10 L

40% to 60% FiO2

 Partial RB 5 – 7 L

35% to 75% FiO2

 NRB 5 – 10 L

40% to 100% FiO2

 Exposure to FiO2 > 60% for

over 48 hours can be toxic

What’s the problem with too much O2?

 Too much is responsible for

cell injury

 Free radicals (unpaired O2):

 Denature proteins

 Damage cell membranes

 Break down DNA

 Cause inflammation

 ARDS: O2 metabolites assist

in destroying invading

organisms, but also destroy

the host

Symtoms

Eyes : Visual Field Loss, Near Sightedness, cataract formation, bleeding, fibriosis

Muscular : Twitching

Central : Seizures

Respiratory : Jerky breathing, Irritation, Coughing, Pain, SOB, Tracheobronchitis, ARDS

Asthma

Characteristics:

 Airway hyperactivity

 Inflammation

 Bronchial constriction

 Excessive mucus production

 Air trapping with

hyperinflation of the lungs

1ST Line Therapy:

 BRONCHODILATORS!!!!

 Beta2 agonist for acute

management

 Less accumulation

 Albuterol – onset < 5 min

 Effects last 2 – 5 hours

 Acute exacerbation

 Repetitive or continuous

Albuterol nebs:

 2.5 mg per treatment

 Continuous: 5 – 15 mg/hr

Asthma Treatment:

Albuterol and Anticholinergic Agents

Side effects of Albuterol:

 Tachycardia

 Tremors (stimulates Beta2

receptors)

 Hyperglycemia

 Hypokalemia

 Hypomagnesemia

 Hypophosphatemia

Anticholinergic Agents:

 Conflicting evidence

 Used in severe exacerbation

 Only in combination with Beta2

agonist

 Ipratropium Bromide

(Atrovent)

 Derivative of Atropine

 0.5 mg neb Q 20 min x 3,

then Q 2 – 4 hours or

 MDI 4 – 8 puffs

Asthma Treatment: Corticosteroids

 Reduces secondary airway inflammation & edema

 Prevents relapse

 Methylprednisolone or Prednisone

 7 – 10 days

 Neither is superior

 Benefit not seen until 12 hours after therapy started

 No need to taper

 Monitor for myopathies

Other thoughts on asthma treatment:

 No O2 unless ↓ O2 sats

 No CXR unless suspect PNA

 No ABG unless nonresponsive

to therapy

 No antibiotics unless there is

an infection!

 Hypercapnia is an ominous

sign

 Can consider Magnesium

Sulfate 1 - 2 gms over 2

hours

 Bronchodilation effects

 Try Heliox

 If need for mechanical

ventilation:

 Lower ventilation rate

 Prolonged expiratory

pause

 Decreased minute

ventilation

 Lower tidal volume

 Monitor for auto-PEEP

Chronic Obstructive Pulmonary Disease (COPD)

 Umbrella term for emphysema & chronic bronchitis

 Constant airflow obstruction

 Worsens over time

 Diagnosis: Pulmonary Function Test

 FEV1/FVC < 70%

 Forced expiratory volume in 1 sec

 *Must give bronchodilator first!

 Results vary by age, gender & height

 Expressed as % predicted

 Normal: 80%

 Shortness of breath

 Cough, +/- Sputum

COPD - Emphysema

 Air-trapping with chronic

hyperinflation of lungs

 Prolonged exhalation

 Barrel chest

 Enlarged right heart

 Elevated right sided venous

pressures (CVP)

Develop intrinsic PEEP from air trapping

 Bronchodilators – some thought to limited benefit

 Short course of corticosteroids – 7 to 10 days

 Methylprednisolone or Prednisone

 No advantage of IV over PO

 NNT = 10 (Steroids)

COPD Treatment:

Antibiotics

 Antibiotics are debated as

many infections are viral

 Strep pneumonia

 H. flu

 Problem: antibiotic

resistance

Oxygen Therapy

 Haldane effect disproven

General guideline:

 Keep low 90%, avoid high

concentration of O2

 If O2 needed, monitor for signs of

hypercapnia

 Non-invasive ventilation

Intubate if:

 -Respiratory distress with

hemodynamic compromise

 -Mental status change, somnolence

 -Worsening acidosis

 Monitor for intrinsic PEEP (auto-PEEP)

COPD vs. Asthma

COPD•

 Onset in mid-life

• Symptoms slowly

progressive

• Long smoking history

Asthma

• Onset early in life (often

childhood)

• Symptoms vary from day

to day

• Symptoms worse at

night/early morning

• Allergy, rhinitis, and/or

eczema also present

• Family history of asthma

Acute Respiratory Failure

 Oxygen or ventilation

disturbance

 Q > V (Perfusion

exceeds ventilation)

Signs:

 Increased work of

breathing

 Use of accessory muscles

 Increased minute

ventilation

 Because, they are

compensating for:

Increased dead space

 Hallmark sign of late

failure:

Increased PaCO2 /

Hypercapnia!!!

Who is at risk?

 COPD

 Pulmonary edema

 ARDS

 Drug OD

 Restrictive lung disease

Non-Invasive Ventilation (NPPV)

CPAP/BiPAP

 Continuous positive pressure

 Stabilizes airways during

exhalation

 Improves ventilation

 Keeps alveoli open

 Used to treat:

 COPD Exacerbation

 Pulmonary edema

 Obstructive sleep apnea

 Obesity Hypoventilation Syndrome

Non-Invasive Ventilation (NPPV) CPAP VS BIPAP

CPAP

 Simple mask & O2

 Set at 5 – 10 cm H20

 Increases functional

residual capacity

 Volume in the lungs at

end-expiration

 Does not augment tidal

volume

Bi-PAP

 Bi-level positive airway

pressure

 CPAP that alternates between

2 pressure levels

 Set IPAP & EPAP

 Higher mean airway

pressures, more alveolar

recruitment

 Larger tidal volumes

 Typical starting point:

IPAP 10 cm H20, EPAP 5 cm H20,

inspiratory time 3 seconds

 Inflammatory lung disease

It is not a primary disease, but a

result of:

 Sepsis

 Trauma

 Multiple blood transfusions

(TRALI, CRALI)

 Pancreatitis

 Cardiopulmonary bypass

 Pulmonary contusion

 Pneumonia/aspiration

What is happening?

IN ARDS

 INFLAMMATORY RESPONSE!

 Alveoli are infiltrated with

leukocytes

 Fibrin deposits in lungs

 Widespread endothelial &

alveolar damage

 Leaky capillaries

 Lungs get stiff

 decreased compliance

 Non-cardiogenic pulmonary

Edema

Signs:

 Tachypnea

 Progressive refractory

hypoxemia

 (refractory to increases in

FiO2)

Worsening P/F ratio

 (PaO2 divided by FiO2)

 CXR – Bilateral pulmonary

infiltrates

 Usually require mechanical

ventilation within 48°

What therapy will improve the PaO2 IN ARDS?

P/F Ratio:

PaO2

divided by

the FiO2

ANSWER : PEEP

Diagnosis OF ARDS:

 Pulmonary infiltrates on CXR

 **P/F Ratio:

 < 300 – Mild ARDS

 < 200 – Moderate ARDS

 < 100 – Severe ARDS

 Predisposing conditions

 Absence of left heart failure or left

atrial HTN

 PAOP abandoned to assist diagnosis

 Mimics pneumonia & cardiogenic

pulmonary edema

Berlin Criteria - 2012

ARDS Severity PaO2/FiO2* Mortality**

Mild 200 – 300 27%

Moderate 100 – 200 32%

Severe < 100 45%

*on PEEP 5+; **observed in cohort

Broncho-alveolar Lavage (BAL)

 Diagnostic that is highly

underutilized!

 Small bronchoscope

 Lavage with Normal Saline

 Sample examined for

neutrophils & protein

 Neutrophils:

 NL: 5%

 ARDS: Up to 80%!

 Protein:

 < 0.5 – pulmonary edema

 > 0.7 - inflammation

ARDS Treatment:

 Mechanical ventilation

 Lung Protective Ventilation (LPV):

 Low tidal volumes (6 ml/kg)

 Large tidal volumes over distend

& rupture distal air space

(volutrauma)

 Pressure related (barotrauma)

 ARDS Net trial – 9% reduction in

mortality

 Compared 6 ml/kg vs. 12 ml/kg

 Use predicted body weight

 End inspiratory plateau pressure

< 30

ARDS Management Con’t

 Low tidal volume (6 ml/kg)

 Permissive Hypercapnia

 PEEP:

 Like a stent to keep the

alveoli open

 When increasing PEEP,

monitor for signs of

decreased cardiac

output!!!

 Neuromuscular blockade if

dysynchrony with the

ventilator

Other therapies:

 Diuretics:

 FACTT Trial – Conservative

fluid management

 Some benefit

 Did not reduce inflammation

 Improving O2 delivery:

 -Cardiac Output:

Dobutamine

 -PaO2: PEEP

 -Hemoglobin: Transfuse only

if necessary!

 Steroids:

 No benefit from early steroids

 Some benefit days 7 – 14

 Methylprednisolone 2 – 3

mg/kg/day

 Inhibits fibrinolysis

 Prone Therapy:

 New evidence of benefit

 Must be done early, not rescue

strategy

 **Mortality increases with

advanced age & multi-organ

failure

ARDS summary

 Lower tidal volume (6 cc/kg)

 PEEP for hypoxia

 Plat

 Prone EARLY!!!!

 Plateau pressure < 30

 Monitor for ventilator

dysynchrony

 Neuromuscular blockage

 Peripheral nerve stimulation

 1 – 2 out of 4 twitches

Advantages of NM Blockade:

 Decreases barotrauma

 Decreases ventilator days

 Decreases pro-inflammatory

response

Capnography – PEtCO2

Ventilation

 Continuous with waveform

 Moderate or procedural

sedation

 Calculate the PaCO2 –

PEtCO2 gradient

 If: Low PEtCO2 & higher

PaCO2, could be:

 **Pulmonary embolus

 Pneumonia

 Over-distention of alveoli

from PEEP/TV

 Endotracheal tube in main

stem bronchus

Perfusion

 Resuscitation

 Low cardiac output states

 Correlation between PEtCO2

& Cardiac Output

 Other uses:

 Weaning the ventilator

 Head injuries

 Used with PCAs/sedating

agents

What do the waves mean?

What do the waves mean?

Pulmonary Embolus

General:

 70% have DVT

 Tachycardia

 Tachypnea

 Dyspnea

 Chest pain

 Hemoptysis

 Sudden right heart failure

 Increased PA pressures

 PEA Arrest

Diagnosis

 **Spiral (helical) CT Scan –

detector rotated around the

patient; 2-D view

 30 seconds to do scan

 Must be able to hold breath

for 30 seconds!

 Contrast infused to view

pulmonary vasculature

 93% sensitivity / 97%

specificity if clot is in one of

the main arteries

Other diagnostics:

 Ultrasound – DVT extremities

 V/Q Scan – only diagnose

25 – 30% of cases

 Underlying lung disease –

abnormal scan

 Pulmonary angiogram

 Most accurate

 Performed in < 20% of

patients with PE

Treatment:

 Unfractionated Heparin (UFH)

 Weight-based dosing

 Prevent progression

 Bolus, then continuous inf

 Goal: aPTT 50 – 80 sec

 Warfarin

 Used with UFH

 Start on 1st day of Heparin

therapy

 Goal: INR 2 – 3, then d/c

Heparin

 Continue for 6 weeks

 OR

 Low Molecular Weight

Heparin (LMWH)

 Enoxaparin 1 mg/kg Q 12

hours

 Cleared by the kidneys

(renal adjustment)

 Simplified dosing

 No need to monitor

coags

 Treat outpatient

PE with Hemodynamic Compromise

 Hypotension

 PEA Arrest

 Fibrinolytic therapy

 Alteplase – 0.6 mg/kg over

15 min

 OR

 Reteplase – 10 unit IV bolus,

repeat in 30 min

 12% chance of major

hemorrhage

 1% ICH

 Benefit > Risk

 IVC Filters

 Used if: DVT +

 1. Contraindication to

anticoagulation

 2. Pulmonary embolus while

on anticoag.

 3. Thrombus in right heart or

free floating

 4. No DVT, but ↑ risk of

hemorrhage

12 Lead ECG Findings

 Right axis deviation

 Transient Right BBB

 ST depression

 T wave depression in

V1 – V4

 Tall peaked T waves in II,

III, AVF

Other:

 ABG not overly helpful –

low PaO2

Pulmonary Arterial Hypertension (PAH)

 High pressure in the pulmonary

vasculature

 Leads to right sided heart

failure

 Causes: Idiopathic, medications,

systemic hypertension, OSA,

sclerotic diseases

Treatments for symptomatic

PAH (oral):

 Sildenafil (Viagra)

 Bosentan (Tracleer)

Rapid progression treatment:

 Epoprostenol (Flolan) –

Continuous IV

 Treprostinil (Remodulin

PAH Treatment Algorithm

PAH Treatment Algorithm

PAH Treatment Algorithm

Pulmonary Contusion

Mechanism of Injury

 Damage to the

parenchyma of the lung

 Localized edema

 Hemorrhage

 Rupture capillaries

Symptoms:

 Not always immediate –

24 to 72 hours

 Tachypnea

 Tachycardia

 Hypoxemia

 Hemoptysis – pink, frothy

 Crackles

 External signs of

ecchymosis, rib fractures

Pulmonary Contusion

Diagnosis & Treatment:

 CT Scan – most sensitive

 Differentiate between

atelectasis & aspiration

 ↓ P/F Ratio

 ↓ PaCO2 (d/t ↑ RR)

 Supportive treatment

 Severe – treat like ARDS

 Do not fluid overload!!!

Rib fractures

 4 – 8 most common

 9 – 12 concern with

rupture of spleen, liver

or diaphragmatic tear

 Chest x-ray

 Pain control – consider

epidural catheter

 **Prevent Pneumonia**

Hemothorax

 Blood in the pleural space

 Lung tissue is compressed, collapses

alveoli

 Often accompanied by a

pneumothorax

 Causes: trauma, thoracic surgery,

thoracic aneurysm

 > 400 mls - symptomatic

 Hypovolemia & shock

 Respiratory acidosis, dropping H/H

 Absent breath sounds affected side

 CT Scan

Chest tube 5-6th ICS,

midaxillary line

Thoracotomy if unable to

control bleeding

Pneumothorax

 Air in the pleural space

 Causes:

 Trauma

 Too much PEEP

 Rupture bleb

 3 types:

 Closed

 Tension

 Open

  Closed: Air enters

 through airways &

 cannot escape

  ↑ Intrathoracic chest pressure

  ↑ Pressure on lungs & heart 

 leads to tension pneumothorax

  Tension: Life

 threatening

  Air accumulates in pleural

 space & cannot escape

  Pressure collapses the lung

  Decreased capacity, decreased

 compliance

  Can lead to PEA Arrest

Pneumothorax

 Open: Penetrating

injury

 Air enters & exits

 Less dangerous

 Signs & Symptoms:

 Depends on size

 Dyspnea

 Restlessness

 Anxiety

 Chest pain

 SOB

 Cyanosis

 Decreased or absent breath

sounds on affected side

 Tracheal shift toward

unaffected side

Pneumothorax Treatment

 Chest x-ray

 ABG – low PaO2

 If it is small, treatment may not be necessary

 (air will be reabsorbed)

 Larger: Chest tube

 Needle decompression:

 14 – 16 gauge needle

 2nd ICS, midclavicular line

 Listen for air escaping

Chest Tubes

 Suction to re-expand the lung

 10 – 40 cm H20 suction (or

dry seal)

 Bubbling in water seal is

normal with pneumothorax

 When bubbling stops, air

evacuated pleural space

 Do NOT clamp chest tubes if

bubbling in H20 seal

chamber!!!

 Follow CXR

 Do NOT milk or strip chest

tubes…it creates up to -400

cm H20 pressure!!!

Advanced airways

Endotracheal Tubes

 Nasal or oral

 Smaller number – smaller

tube

 Placement confirmed via

waveform Capnography**

 Auscultate chest

 Chest x-ray

 ET tube – 2 – 3 cm above

carina

 Cuff pressure 20 – 30 cm H20

Tracheostomy Tubes

 Used if long term support

anticipated

 Emergency – obstruction

 Always have an extra trach at

the patient’s bedside

 Keep clean – avoid hydrogen

peroxide

 Deflate the cuff so the patient

can talk

 Use a 1 –way valve

Mechanical ventilation

Basic settings:

 Mode of ventilation

 Brand dependent, but usually pressure or volume

 Rate (breaths per minute)

 Tidal volume

 PEEP

 FiO2

Modes of ventilation - volume

CMV – Continuous Mandatory

Ventilation

 Little to no ventilatory

drive

 Preset tidal volume

without sensitivity to

spontaneous or

assisted breaths

 Rarely used!

AMV - Assisted Mandatory

Ventilation

 Also called assist control

 Preset tidal volume &

minimum rate of breaths

 Able to initiate breaths,

but will get set tidal

volume

 Can alter rate & pattern,

but not the tidal volume

 Reduces work of

breathing

Modes of ventilation - volume

SIMV – Synchronized Intermittent

Mandatory Ventilation

 Preset rate & tidal volume

 Allows patient to

spontaneously breath in

between

 Synchronized with patient

initiated breath

 Reduces competition between

patent & vent

 High set rate allows no time

for the patient to

spontaneously breath

 IMV + PS

Modes of ventilation - pressure

PS - Pressure Support

 Delivery of positive

pressure

 Patient decides when, how

fast & flow

 Assistance during

inspiration; must initiate

breath

 Set back up apnea mode

 Ideal pressure support to

achieve VT 6 – 8 ml/kg

 Used for weaning

Modes of ventilation - pressure

PCV – Pressure Control Ventilation

 Set inflation pressure

 Inspiratory time

adjusted to allow time

for inspiratory flow

rate to drop to zero at

end inspiration

Combo modes of ventilation

VC - Volume control

 Also called PRVC –

Pressure Regulated

Volume Control

 Pressure controlled

breaths

 Guaranteed minimum

volume

 Ventilator adjusts pressure

& flow to achieve minimum

VT

APRV – Airway Pressure Release

Ventilation

 Cycles between high & low

continuous positive airway

pressure

 P high – delivered for a

longer period of time

 P low – for shorter time

 Transition between high/low

deflates the lungs and allows

for CO2 removal

 Time spent in P high

determines the rate

Determine readiness

 Lighten sedation/analgesia

 Vital capacity

 RR during weaning

 NIF – Negative Inspiratory

Force

 PIP – Peak Inspiratory

Effort

 NIF & PIP of -20 cm H20

good sign for extubation

 Normal is – 70 to – 90

 Nutrition - Phosphate

Breathing Trials

 Should last < 2 hours

 CPAP

 Pressure support

 Decrease rate

 T-piece/SBT

 Monitor oximetry & PEtCO2

 Monitor minute ventilation

 Amount of air exchanged in

1 minute

 Normal is 5 – 10 L/min

Contraindications to extubation:

 Absence of gag reflex

 Unable to protect airway

 Absence of cuff leak (edema)

Post-extubation:

 Monitor for stridor (esp. inspiratory)

 Hypercapnia

Ventilator-Associated Events (VAE)

 CDC Definition - 3-Tiered

 Tier 1 – Ventilator Associated Condition (VAC)

 Hypoxemia more than 2 days

 Tier 2 – Infection-related VAC (IVAC)

 Hypoxemia in the setting of generalized infection or

inflammation

 Antibiotics instituted for a minimum of 4 days

 Tier 3 – Probable ventilator-associated pneumonia

(VAP)

 WBC present on sputum gram stain

 OR, pathogen

VAE (VAP) Prevention

 HOB elevation (30 – 45 degrees)

 Mouth/endotracheal tube care (oral w/chlorhexidine)

 Lung Protective Ventilator Strategies

 Early discontinuation of vent

 Appropriate analgesia & sedation (avoid benzos)

 Daily interruption of sedation

 Early mobilization with or without ambulation

 DVT Prophylaxis

 GI Prophylaxis

 Balanced IV fluid administration