Critical Care Exam 1

Module 1, 2 and 3

Define acute rsp failure

sudden decrease in arterial oxygenation with/without CO2 retention (hypoxemia w/ or w/out hypercapnia)

• PaO2 falls quickly

• PaCO2 may be norm, low, or high

What can be described as a special, severe form of acute rsp failure with major oxygenation problems?

ARDS

What is considered type 1 respiratory failure?

hypoxemia respiratory failure or “lung failure”

what is the primary problem in type 1 respiratory failure?

arterial oxygenation (low PaO2)

• problems with gas exchange in the lung

Oxygenation problems in lung (type 1 rsp failure) caused by poor matching of gas and blood examples:

• pulmonary shunt

• low V/Q ratios

• diffusion problems (early pulmonary fibrosis)

• hypoventilation (which increase PACO2 and reduces PAO2/PaO2)

Clinical causes of type 1 rsp failure

• atelectasis

• pneumonia

• pulmonary edema

Rsp failure signs/symptoms for mild hypoxia (rsp, cardiac, neuro)

rsp: increase rr, mild SOB, early rsp distress

cardiac: increase HR, mild hypertension, peripheral vasoconstriction

neuro: overconfidence, restlessness, anxiety, euphoria, lightheadedness, nausea, dizziness, fatigue

Rsp failure signs/symptoms for mod hypoxia (rsp, cardiac, neuro)

rsp: tachypnea, increased MV/hyperventilation, accessory muscle use, intercostal retractions

cardiac: tachycardia, arrhythmias, hypertension

neuro: agitation, impaired judgement, confusion, decreased night vision, disorientation, lightlessness, headache, tingling, loss of coordination

Rsp failure signs/symptoms for severe hypoxia (rsp, cardiac, neuro)

rsp: severe dyspnea, slowed/irregular breathing, cyanosis, rsp arrest

cardiac: hypertension → hypotension, tachycardia → bradycardia, cardiac arrest

neuro: confusion, somnolence, severe headache, unconsciousness, vision disturbances, slowed reaction time, coma

Rsp failure signs/symptoms for hypercapnia (rsp, cardiac, neuro)

rsp: dyspnea, increased WOB, diaphoresis, accessory muscle use, intercostal retractions, decreased Vt, rapid shallow breathing

cardiac: increase or decrease HR, BP changes, arrhythmias

neuro: restlessness, anxiety, headache, dizziness, altered mental status, confusion, somnolence, unresponsiveness, coma

normal PaO2

80-100

mild hypoxemia PaO2

60-79

mod hypoxemia PaO2

50-59

mod-severe hypoxemia

40-49

very severe hypoxemia

<40

How do you assess for rsp failure?

assessment of oxygenation (SpO2), ventilation (rr, pattern, Vt, WOB), acid-base (ABG), cardiac/circulatory status (BP, HR, cap refill, cyanosis, arrhythmias), neurologic status (lvl off consciousness, orientation, mental status), nutritional status (BMI, visual test)

what is considered type 2 rsp failure?

hypercapnic rsp failure, pump failure, or ventilatory failure

what is the primary problem of type 2 rsp failure?

ventilation (bulk movement of gas in and out of lungs)

• decreased ventilation → increased PaO2 (hypoventilation)

what’s the best index of alveolar ventilation?

PaCO2

what is an example of a chronic disease w/ acute problem

COPD exacerbation

• ventilatory failure may be acute, subacute, or chronic

Difference between acute ventilatory failure vs chronic ventilatory failure (ABG-wise)

Acute ventilatory failure = sudden increase in arterial PaCO2 with a corresponding decrease in pH

Chronic ventilatory failure = chronically elevated PaCO2, with a normal or near-normal pH owing to metabolic compensation

Acute ventilatory failure mechanism

sudden hypoventilation will result in an increased PaCO2 and decrease in pH (acute rsp acid)

Causes of acute ventilatory failure

• decreased ventilatory drive (anesthesia, sedative/narcotic overdose, head trauma, stroke)

• airway obstruction, neuromuscular disease (Guillain-Barré, myasthenia gravis, spinal cord injury)

• increased WOB/respiratory muscle fatigue (severe pneumonia, ARDS, CHF, pulmonary edema, shock, trauma, smoke/chemical inhalation, aspiration, near drowning)

if a pt’s PaCO2 is >45 and pH is <7.25 what is recommended

mechanical ventilation

mechanism of chronic ventilatory failure

long-standing hypoventilation leads to kidneys retaining HCO3 and pH normal or near normal

common causes of chronic ventilatory failure

• COPD (not all COPD pts)

• late-stage cystic fibrosis

• severe interstitial lung disease

• obesity hypoventilation syndrome

what is an example of an acute ventilatory failure superimposed on chronic ventilatory failure and what equipment could you use to help this pt?

COPD pt w/ an acute exacerbation

use NIV or HFNC

• can be hard to wean these pts off vent

signs/symptoms of rsp failure

• increased HR

• increased RR

• accessory muscle use

• intercostal retractions

• nasal flaring

• diaphoresis

• oxygen desaturation

• excitement

• restlessness

• anxiety

• headache

• altered mental status

• confusion

• somnolence

• coma

• rapid shallow breathing

severe rsp failure may be signaled by

• slowed/irregular breathing

• reduced chest expansion

• cardiac arrhythmias

• hypotension

rsp acidosis ABG

low pH, high PaCO2, normal or slightly high HCO3

causes of rsp acidosis

• hypoventilation from CNS depression (sedatives, opioids)

• neurologic disease

• decreased metabolic rate, pain, chronic CO2 retention

rsp alk ABG

high pH, low PaCO2, HCO3 normal or slightly low

causes of rsp alk

• hyperventilation from hypoxemia

• metabolic acidosis

• pain

• anxiety

• decreased BP

• inappropriate vent

metabolic acidosis ABG

low pH, low HCO3, norm or low PaCO2 (if compensated from hyperventilation)

causes of metabolic acid

• lactic acidosis (sepsis)

• keotacidosis

• renal failure

• GI losses of bicarb (diarrhea)

• ingestion of acids

metabolic alk ABG

high pH, high HCO3, norm or high PaCO2 (compensating with hypoventilation)

causes of metabolic alk

• vomiting

• NG suction

• renal H+ loss

• hypokalemia

• hypovolemia

• excess bicarb administration

changes made on NPPV based off ABG

Essentially, matching oxygenation and ventilation problems to FiO2, EPAP, IPAP, and flow:

• IPAP primarily affects ventilation (Vt, PaCO2), so ABG shows hypercapnia (high PaCO2); then increase IPAP to increase Vt and lower PaCO2

• EPAP functions like PEEP; it improves oxygenation by recruiting alveoli and improving V/Q, so if ABG shows hypoxemia (low PaO2), increase EPAP

  • avoid EPAP < 5 cmH2O

• Adjust FiO2 to maintain target SpO2/SaO2

• Flow (L/min) is auto-generated on this device

changes made on HFNC based off ABG

• Titrate FiO2 based on PaO2/SpO2; hypoxemia → increase FiO2

• Higher flows (30-60L/min) help wash out dead space, provide small positive pressure, and improve oxygenation

  • If pt is tachypneic w/ high WOB → increase flow to reduce WOB and improve oxygenation

indications for HFNC

• primary hypoxemic rsp failure (pneumonia, early ARDS, pulmonary edema) w/ minimal hypercapnia

• pts who need high FiO2 but cannot tolerate tight masks or NIV

• pts needing improved secretion clearance and humidification

setting changes for HFNC

• start w/ moderate flow (30-40 L/min) and FiO2 to achieve target SpO2 (>90%)

• if hypoxemia persists → increase FiO2 and/or flow

• If WOB is high → high flow to provide more support

• always reassess ABG and clinical status; failure to improve should consider NIV or intubation

benefits of HFNC

• precise FiO2 up to 100%

• High flows (30-60 L/min) with heated humidification → improved comfort, mucociliary clearance, less mucus plugging

• Provides low-level positive airway pressure, improving oxygenation and reducing atelectasis

• allows eating, drinking, talking, and better mobility compared to tight NIV masks

• can slightly aid CO2 removal via dead space washout

BiPAP vs CPAP

BiPAP

• 2 pressures:

  • IPAP (inspiratory) → ventilation (Vt, PaCO2)

  • EPAP (expiratory → oxygenation (PEEP effect)

• used for hypercapnic rsp failure, mixed hypoxemic/hypercapnic failure

• helps both oxygenation and ventilation

CPAP

• 1 constant pressure throughout respiratory cycle

• primarily improves oxygenation by splinting airways and recruiting alveoli

• commonly used for OSA and hypoxemic rsp failure when ventilation is adequate

when to use single limb circuits

NIV-specific devices

• used with dedicated NPPV machines

• 1 limb with a leak port (in-circuit or mask) to allow CO2 washout

• requires a mask with a leak port or exhalation valve to prevnt suffocation

• Best for noninvasive ventilation outside ICU, chronic NIV, sleep labs

when to use dual limb circuit

critical care ventilators

• inspiratory and expiratory limbs with exhalation valves

• less risk of CO2 rebreathing

• used in ICU, can deliver NIV via full-face mask without built-in leak port

• more sophisticated monitoring, but more expensive and often restricted to ICU

what type of mask would a pt in acute respiratory distress or failure need

full-face or total face mask (covers nose and mouth) for optimal gas exchange

what type of mask would a pt with chronic or nocturnal (OSA) need

nasal masks or nasal pillows may be appropriate

• can depend on pt comfort

what must all masks have

a proper seal and, for single-limb NIV devices, a leak port/safety valve

contraindications for NPPV

• inability to protect airway (low consciousness, high aspiration risk)

• active vomiting or nausea

• massive secretions or inability to clear secretions (aspiration risk)

• hemodynamic instability or cardiac arrest

• facial trauma or inability to fit mask

• uncooperative or agitated patients who cannot tolerate mask

recall when esophageal sphincter muscles matter

• when peak inspiratory pressures approach or exceed 20-25 cmH2O, the esophageal sphincter can open

• this can cause gastric insufflation, vomiting, and aspiration risk

goal Vt in initial BiPAP settings

target Vt: ~6mL/kg PBW

• adjust IPAP-EPAP difference to achieve this Vt while keeping peak pressures < 30 cmH2O

general risks of NIV

• gastric insufflation → vomiting → aspiration

• vent-induced lung injury (excessive Vt or pressures)

• skin breakdown from masks

• CO2 rebreathing if leak/flow inadequate

• delayed intubation if NIV is failing but not recognized

• pt discomfort, anxiety, claustrophobia

what you need to asses when placing pt on NIV

• gas exchange: ABGs

• WOB: rr, accessory muscle use, intercostal retractions, chest expansion

• hemodynamics: hr, bp, arrhythmias

• mental status: ability to cooperate, protect airway, remove mask if needed

• mask fit and skin integrity: check for leaks and pressure sores

• response to settings: adjust IPAP, EPAP, FiO2, based on ABG and clinical response

• readiness to discontinue NIV: once initial indication resolves, consider trials off NIV/CPAP

where does gas exchange occur

alevoli

elements that make up the conducting airways

• upper airways (nose, pharynx, larynx)

• larynx/trachea

• lower airways (bronchi, bronchioles

conducting airway problems that may affect oxygenation and/or ventilation

• airway obstruction

• increased secretions

• airway mucosal edema

• bronchospasm

problems that can occur in the upper airways

• upper respiratory tract infection

• upper airway edema

• tumor, abscess

• foreign body inhalation

• laryngeal abnormalities (vocal cord paralysis, laryngeal tumor, subglottic stenosis edema)

laryngeal edema may be caused by

• infection (croup, epiglottitis)

• artificial airways (cuff overinflated)

• trauma

• inhalation of noxious gases/flames

• angioedema (swelling under the skin caused by an allergic reaction)

OSA is caused by

decrease in upper airway muscle tone during sleep resulting in soft tissue obstruction and periods of apnea

lower airway problems

• airway inflammation

• mucosal edema

• excess secretions

• mucus plugging

• bronchospasm

• emphysema

• chronic bronchitis

• asthma

• cystic fibrosis

• bronchiectasis

bronchospasm, mucosal edema and asthma increase

airway resistance

physical principles of gas exchange

• diffusion follows concentration/partial pressure gradients (gas moves where there is less concentration/pressure)

• partial pressure is proportional to concentration of gas in a mixture

• each gas contributes to total pressure in proportion to its fraction

• CO2 is ~20 times more soluble than O2, so it diffuses more easily across barriers

• air is humidified in the airways, giving a water vapor pressure of 47 mmHg, which affects inspired PO2

diffusion of gas barriers

1. fluid and surfactant layer lining the alveolus

2. alveolar epithelium

3. epithelial basement membrane

4. interstitial space

5. capillary basement membrane

6. capillary endothelium into the blood and then into RBC’s

Fick’s law equation

Determinants of diffusion

• pressure gradient

• area

• distance

• solubility and MV are fixed

inspired oxygen formula

total pressure is the sum of partial pressures of what 4 gases

O2, N2, CO2, H2O

a decrease in inspired oxygen concentration (FiO2) or a decrease in barometric pressure (PB) will reduce… and may cause…

reduce inspired oxygen tension (PIO2) and may cause ambient hypoxia

a special case of ambient hypoxia d/t reduced barometric pressure at altitude

altitude hypoxia

norm PIO2 is 150 mmHg at sea level results in what PaO2

normal PaO2 in the range of 80-100 mmHg

Inspired oxygen tension (PIO2) must be

sufficient

PIO2 is deteremined by

barometric pressure and FiO2

the effectiveness of gas exchange and oxygen transfer across the lung can be assessed by

• measurement of arterial oxygen tension (PaO2)

• pulse oxi (SpO2)

• direct measurement of arterial oxygen sat (SaO2)

what can tell if there is adequate tissue for gas exchange

intrapulmonary shunt fraction (Qs/Qt)

• calculated using clinical shunt equation

blood oxygen content equation

the blood oxygen content equation helps you break down the question of

“where is the problem?”

normal CaO2

~20mL O2/100mL blood

factors that effect Hb or SaO2 may have significant effect on

CaO2 and O2 delivery to tissues

impairments to diffusion

• V/Q mismatch

• reduction in the available surface area for diffusion

• increase in diffusion distance

diffusion limitation causes

• interstitial lung disease (ILD): inflammation, edema fibrosis → increase distance, stiff lungs

• pulmonary vascular disease

• emphysema: destruction of alveolar walls → decrease surface area

• alveolar or interstitial edema: fluid in interstitium/alveoli → increase distance

hypoxemia from diffusion defects can appear during exercise which can be reversed with

administration of low-moderate O2

causes of V/Q mismatching

• hypoventilation

• ventilation-perfusion mismatch (low V/Q and right-to-left shunt)

• diffusion limitations

V/Q <1.0 but >0 means

under ventilation with respect to perfusion

• responds well to low-mod O2

V/Q = 0 means

absent ventilation with respect to perfusion

• shunt → atelectasis

V/Q > 1.0 means

over ventilation with respect to perfusion

• ventilation > perfusion

• often related to low blood flow

V/Q = n/o or undefined

ventilation without perfusion

• dead space units

no ventilation and no perfusion

silent unit

causes of low V/Q

• asthma

• bronchiectasis

• bronchospasm

• bronchiolar mucosal edema

• COPD

• cystic fibrosis

• decreased Vt

• focal pneumonia

• partial airway obstruction

• regional increases in fibrotic tissue

• retained secretions

causes of pulmonary capillary shunt (V/Q = 0)

• ARDS

• atelectasis

• complete airway obstruction

• consolidative pneumonia

• pneumothorax (large)

• pulmonary edema (with complete alveolar filling)

pts with significant pulmonary capillary shunt may experience

refractory hypoxemia

tx for refractory hypoxemia

requires PEEP/CPAP and mechanical ventilation to recruit alveoli

• high FiO2 will barely increase PaO2 in this case

causes of alveolar dead space

• pulmonary embolus (w/ complete occlusion of pulmonary vessel)

• obliteration of the pulmonary capillaries (emphysema)

what lung goes down to increase PaO2 in unilateral lung disease

“good” lung goes down

what is inhaled nitric oxide (iNO)

pulmonary vasodilator

• colorless, odorless, highly diffusible gas

• increases cGMP → vascular smooth muscle relation → pulmonary vasodilation

• improves blood flow to ventilated alveoli, enhancing V/Q matching

FDA approved use of iNO

improve oxygenation and reduce need for ECMO in term and near-term neonates w/ hypoxic rsp failure and pulmonary hypertension

adult/off-label uses of iNO

• ARDS (no mortality benefit)

• pulmonary artery hypertension, right ventricular failure

• persistent pulmonary hypertension of newborn

• primary pulmonary hypertension

• post-cardiac surgery

• cardiac transplant

• acute PE

• COPD

• congenital diaphragmatic hernia

• sickle cell disease

• testing pulmonary vascular responsiveness

what’s the most common type of bronchoscopy

flexible bronchoscopy

flexible vs rigid bronchoscopy

working channel for tools in flexible and separate channel for ventilation in rigid

what is the flexible bronchoscopy used for

• diagnostic (inspection, biopsies, washings)

• therapeutic (removing mucus plugs, secretions, small foreign bodies)

what is the rigid bronchoscopy used for

• large or difficult foreign body removal

• better control of airway and control of excessive bleeding