Resp Disorders and Mechanical Ventillation

compare anatomy of right and left bronchi

right bronchus is shorter, wider, and more vertical than the left

VQ ratio

• what does high indicate?

• low?

amt of air that reaches the alveoli divided by amt of blood flow in the capillaries of the lungs

• high = ventilation typ normal, but alveolar perfusion is dec or absent (PE, dec CO)

• low = pulm circulation is adequate but not enough O2 available to the alveoli for perfusion (airway obstruction, pneumonia, pulm edema)

end tidal CO2 monitoring

• normal?

cont. capnography uses infrared light to measure exhaled CO2 at end expiration using a sensor attached to an ETT, tracheostomy tube, or nasal cannula

• compare w/ ABGs and use as trend

• normal: 30-45 mmHg

  • low = poor systemic perfusion (caused by hypovolemia, sepsis, dysrhythmias)

• values tend to be 2-5 mmHg less than PACO2

normal pH

7.35-7.45

• <7.35 = acidosis

• >7.45 = alkalosis

PaCO2

• regulated by ?

• normal?

regulated by the lungs

• normal: 35-45 mmHg

  • <35 = alkalosis

  • >45 = acidosis

remember: this is an ACID → more CO2 = ACIDosis

HCO3 (bicarbonate)

• regulated by ?

• normal?

regulated by the kidneys

• normal: 22-26 mEq/L

  • <22 = acidosis

  • >26 = alkalosis

remember: this is a BASE!!

compensation (2 types)

• partial = pH ABNORMAL

• complete = pH normal

normal PaO2

80-100 mmHg

common causes of respiratory acidosis

retention of CO2

• CNS depression (anesthesia, narcotics, sedatives, drug OD)

• neuromuscular disorders

• trauma: spine, brain, chest wall

• restrictive lung diseases

• COPD

• acute airway obstruction (late phase)

common causes of resp alkalosis

LOSS of CO2

• anxiety, pain, fever (think hyperventilation → expelling lots of CO2)

• stimulants

• CNS disorders

• hypoxia causing lung conditions

• pneumonia, atelectasis, asthma (early stage), ARDS, CHF

• pulm vascular disease

common causes of metabolic acidosis

GAIN OF ACID

• renal failure

• DKA

• lactic acidosis

• drug OD (salicylates, methanol, ethylene glycol)

LOSS OF BASE

• diarrhea (ASS-idosis)

• renal failure

common causes of metabolic alkalosis

GAIN OF BASE

• excess ingestion of antacids

• excess administration of Na Bicarb

LOSS OF ACID

• vomiting, NG suctioning

• low K+ and/or Cl-

• diuretics

• inc levels of aldosterone

Mallampati Scores

predict intubation difficulty or predict sleep apnea

• what structures in throat are visible when pt opens mouth

• think “more mouth = more easy”

• classes 3 and 4 = difficult intubation or probability of sleep apnea

does an OPA provide oxygen?

NO!! → must ventillate

nurse’s role in intubation

• gather supplies

• meds available

  • sedation, neuromuscular blocks, paralytics, fluids, vasopressors,

• watch monitor

clinical def of resp failure

• PaO2 =

• PaCO2 =

• pH =

• PaO2 = 60 or lower

• PaCO2 = 50 or higher

• pH = 7.25 or less

positive end expiratory pressure (PEEP)

reduce collapse of alveoli and small airways

• more pressure to force alveoli open

• inc PEEP dec CO

vent settings: 500/20/60/8

tidal volume / RR / FiO2 / PEEP

synchronized intermittent mandatory ventilation (SIMV) - vent setting

traditional mode

• can be assisted, controlled, or supported

• delivers mandatory breaths w/ FIXED volume

• UNCOMFORTABLE; pt CANNOT trigger

airway pressure release ventilation (APRV)

pt breathes spontaneously

• good for ARDS

pressure support (PS) — vent setting

all breaths pt initiated

• best for weaning

pressure controlled / assist (PC) — vent setting

• assisted or controlled

• preset pressure for a set time and rate

• pt needs adequate tidal volumes

volume controlled / assist (VC) — vent setting

• assisted or controlled

• preset tidal volume or rate

noninvasive positive pressure ventilation (NPPV)

• 2 types

• CPAP provides low levels of cont. positive airway pressure throughout the resp cycle

  • stents open larger airways and PREVENTS ALVEOLI FROM COLLAPSING

• BiPAP provides 2 levels of positive airway pressure — 1 cont. pressure during exhalation and 1 during inhalation to assist the ventilatory muscles

CI to non-invasive positive pressure ventilation (NPPV)

• actual complete apnea

• cardiovascular instability — hypotensive, uncontrolled dysrhythmia, active MI

• relative CI: claustrophobia, impaired sense of consciousness, very high aspiration risk, can’t clear secretions, recent gastroesophageal surgery, cranial / facial surgery, facial burns

nursing role for vented pt

• location of ETT → verify placement (auscultation and ETCO2 detector)

  • want bilateral breath sounds

• verify settings

• ensure emergency equipment available

• assess adequacy of CO and oxygenation

• monitor for alarms

• med management

• prevention of AE

• ABCEF bundle

• pt education

• involve pts and family in decision-making

what meds are commonly used for pts who require mechanical ventilation?

1. bronchodilators

2. sedation / anxiolytics

3. neuromuscular blockers / paralytics

4. analgesics

high pressure vent alarm

aka high peak airway pressure alarm

• vent exceeded preset pressure limit → will immediately cycle into expiration and gas flow ceases

• MOST COMMON

• causes: coughing, attempting to speak, pt / vent asynchrony, kinks, water in circuit, mucous plugs, bronchospasm, pulm edema, pneumothorax, ARDS

low pressure vent alarm

aka low tidal volume alarm

• causes: disconnection, air leak, tidal volume too low

high / low rate vent alarms

• high = pt agitated, pain , RASS too high

• low = oversedated, broken vent

think what causes high vs low RR

ABCDEF protocol

• Assess, prevent, and manage pain

• Both spontaneous awakening trials (SAT) and spontaneous breathing trials (SBT)

• Choice of analgesia and sedation

• Delirium — assess, prevent, and manage

• Early mobility and exercise

• Family engagement and empowerment

mechanical ventilation complications

• barotrauma

  • s&S: high peak airway pressures, dec breath sounds, tracheal shift, hypoxemia, subQ emphysema

• ventilator associated pneumonia (VAP)

  • bundle of practices

  • HOB at 30 degrees

  • SBT

  • PUD & DVT prophylaxis

  • daily oral care w/ CHG

  • ETT w/ subglottic suction

  • early mobility

• ETT out of position

• unplannned extubation

• tracheal damage

• damage to oral or nasal mucosa

• oxygen toxicity

• acid-base imbalance

• aspiration

acute respiratory failure

• causes?

• assessment findings?

most common MICU dx

• inability to oxygenate or remove CO2

  • oxygenation failure

  • ventilation failure

• acute vs chronic

• causes?

  • hypoventlation

  • intrapulmonary shunting

  • V/Q mismatch

  • diffusion defects

  • low CO

  • low Hgb

  • tissue hypoxia

• assessment findings?

  • lethargy, confusion, dysrhythmias, dec peripheral perfusion, tachypnea, bradypnea, tachycardia, HTN

oxygenation failure

• PaO2 <60

• normal or dec CO2

ventilation failure

hypercapnic resp failure

• CO2 >50

acute resp failure vs ARDS

• causes of ARDS?

ARDS = severe ARF

• ARDS = dyspnea, tachypnea, dec lung compliance, alveolar infiltrates on CXR

• Berlin Criteria

  • pt must have acute onset w/in 1 wk after some initial clinical insult

  • bilateral pulmonary opacities (CXR white, opaque) not explained by other conditions

  • altered PaO2:FiO2 ratio = giving high FiO2 and PaO2 not inc

• causes

  • aspiration, fat embolism, toxic inhalation, drowning, PNA, bypass, OD, sepsis, trauma

ARDS pathophysiology

1. acute phase = uncontrolled inflammation

2. proliferative phase = 1-3 wks after onset

3. fibrotic phase = 2-3 wks after onset

if untreated, leads to multi-organ dysfunction syndrome or multi-organ system failure and death

assessment findings in ARDS

initially:

• dyspnea, tachypnea, hypoxemia

• anxiety / agitation

• initial resp alkalosis

as it progresses:

• inc WOB, adventitious breath sounds

• worsening CXR

• difficulty ventilating due to dec compliance

• resp acidosis (body no longer able to compensate)

• refractory hypoxemia

pnemonia (PNA)

lower resp infection that inflames the alveoli in one or both lungs

• lots of causes (CAP, HAP, HCAP, VAP, ARF)

• can be bacterial, viral, fungal

ventilator acquired PNA

lung infect. that can develop in pts on a vent for more than 48hrs

• healthcare associated infect. (HAI)

• sx: cough, fever, chills, inc mucous, N, V, SOB

COPD

• hallmark signs

• chronic and acute exacerbation ABG

• tx?

chronic inflamm lung condition that causes obstructed airflow from lungs

• exacerbations can lead to ARF and/or ARDS

• hallmark signs: dyspnea, chronic cough, excessive sputum production

• chronic ABG: compensated resp acidosis, low PaO2

• acute exacerbation ABG: uncompensated resp acidosis, lower PaO2

• generally tolerate SpO2 >88%

• tx:

  • inhalers (albuterol)

  • short-term steroids — inhaled (mometasone, budenoside); oral (prednisone, cortisone, methylprednisolone, dexamethasone)

  • antibiotics

  • NPPV or intubation

  • palliative care in late stages

pulmonary embolism

• dx?

• tx?

blood clot, fat, septic, amniotic fluid in lungs

• usually originates from lower extremity DVT

• acute (new obstruction that requires immediate tx) vs chronic (older obstruction that has not been resolved; can worsen over time → pulm HTN → R HF )

• massive PE → shock, severe pulm HTN, cardiac / resp arrest

  • mortality rate 30-60%

• >50% of pts have NO sx

• dx: D dimer (positive = clot that’s beginning to break down), ultrasounds, VQ scan, CT angiogram, pulm angiogram, MRI

• tx: anticoagulation, thrombolytics, embolectomy, ventilation → SMALL TIDAL VOLUME AND LOWER PEEP b/c do not want to press emboli to brain