This document discusses respiratory failure, which occurs when the respiratory system fails in gas exchange. It defines two main types - hypoxemic respiratory failure, defined as low blood oxygen, and hypercapnic respiratory failure, defined as high blood carbon dioxide. The document then covers the anatomy and physiology of respiration, diagnostic evaluation of respiratory failure, treatment including mechanical ventilation, and specific causes of respiratory failure like infection, airway obstruction, and cardiac issues.

1. Moderator- Dr.John Israel
By-
Dr.Ranjith Kumar
Dr.Spandana

2.  a condition in which the respiratory system
fails in one or both of its gas-exchanging
functions
 a syndrome of inadequate gas exchange due
to dysfunction of one or more essential
components of the respiratory system

3. CNS (medulla)
Peripheral nervous system (phrenic nerve)
Respiratory muscles
Chest wall
Lung
Upper airway
Bronchial tree
Alveoli
Pulmonary vasculature

4.  Rhythmic respiration - initiated by a pacemaker cells in
the pre-Bötzinger complex on either side of the medulla
between the nucleus ambiguus and the lateral reticular
nucleus
 RESPIRATORY CENTER-Brain stem
 Incl.
(a)DRG
(b)VRG
(c)PRG/Pneumotaxic center-PONS
(d)Apneustic center
MEDULLA

5.  DRG-responsible for the basic rhythm of
respiration.
 VRG-When the respiratory drive for increased
pulmonary ventilation becomes greater than
normal,respiratory signals spill over into the
ventral respiratory neurons

6.  Pneumotaxic center - limits inspiration,
which has a secondary effect of increasing
the rate of breathing
 Apneustic center- slows down the inhibitory
signals from pneumotaxic center-regulates
intensity of respiration

8.  Chemosensitive area in the respiratory
center-beneath the ventral surface of
medulla
Sensitive to changes in blood PCO2/pH
Acute rise in PCo2 stimulates chemosensitive
area which inturn stimulates inspiratory area

9.  Decreased stimulatory effect of CO2 after the
first 1 to 2 days
 Part of this decline results from renal
readjustment of the H+ ion concentration
towards normal.
 Over a period of hours, the HCO3- ions also
slowly diffuse through the blood-brain and
blood–CSF barriers and combine directly with the
hydrogen ions adjacent to the respiratory
neurons

11.  Incl:
The Carotid and the Aortic bodies
 The Carotid bodies are located bilaterally in
the bifurcations of the common carotid
arteries.
 Their afferent nerve fibers pass through
Hering’s nerves to the glossopharyngeal
 nerves and then to the dorsal respiratory area
of the medulla.

12.  The aortic bodies are located along the arch
of the aorta
 Their afferent nerve fibers pass through the
vagi, also to the dorsal medullary respiratory
area.
 Decreased Arterial Oxygen Stimulates the
Chemoreceptors

14.  Reason for acclimatization is that, within 2 to 3
days, the respiratory center in the brain stem
loses abt. four fifths of its sensitivity to changes
in PCO2 and hydrogen ions.
 Therefore, the excess ventilatory blow-off of CO2
that normally would inhibit an increase in
respiration fails to occur, and low O2 can drive
the respiratory system to a much higher level of
alveolar ventilation than under acute conditions.

15.  Type-I : Hypoxemic respiratory failure
 Type-II : Hypercapnic respiratory failure
 Type-III : Perioperative respiratory failure
 Type-IV : Respiratory failure in shock

16.  defined as an arterial pO2(paO2) less than
55 mm Hg when the fraction of oxygen in
inspired air (FiO2) is 0.60 or greater
 Seen in
 Alveolar hypoventilation,
 Ventilation–perfusion mismatch,
 Shunt and
 Diffusion limitation
 Low FiO2 (high altitude)

17.  HYPOXEMIC RESP. FAILURE
INCREASED ALVEOLAR GRADIENT NORMAL ALVEOLAR GRADIENT
O2 responsive
V/Q mismatch
Non responsive
Shunt
PaCo2 Normal
Airway Ds.
1.COPD
2.Asthma
3.CF
ILD
Pulm Vasc. Ds.
PE
Intracard.Shunt
ASD,VSD,PFO
Intrapulm shunt
Pulm AVM
Alveolar filling
Pulm edema, ARDS,
TRALI,
pneumonia,
Aspiration
Alv. H’ge
Alv. proteinosis
Alveolar
hypoventilation
High altitude
Low inspired O2

18.  defined as an arterial pCO2 (paCO2) greater
than 45 mmHg
 Results from:
 (a) an increase in CO2 production,
 (b) a decrease in minute ventilation, and
 (c) an increase in dead-space ventilation

19.  RESP. PUMP FAILURE
CNS Anterior
Horn
Cells
Motor
Nerves
NMJ Muscles Airways
& Alveoli
Excessive
work of
breathing
Drugs
Medullary
CVA
OSA
Hypothyroi
dism
Ondine’s
curse(idiop
athic)
ALS
Polio
Cervical
spine
injury
GBS
Crtical
illness
polyneuro
pathy
Diphth.
Fish
toxins
Tick
paralysis
M.Gravis
LEMS
Botulism
OP
Poisoning
Myopathy
Drugs
Polymyosi
tis
Dermato
myositis
Muscular
dystrophi
es
COPD
CF
Asthma
PF
P.Edema
Chestwall
disorders
Scoliosis
Obesity
Sepsis,
M.acidosis
Tense
ascites,
AC syndr.
Upper
airway
obstruc.

20.  Results from lung atelectasis
 also called perioperative respiratory failure.
 After general anesthesia, decrease in FRC
leads to collapse of dependent lung units.

21.  Rx:
 frequent changes in position,chest
physiotherapy, upright positioning, incentive
spirometry.
 Noninvasive positive-pressure ventilation
may also be used to reverse regional
atelectasis.

22.  results from hypoperfusion of respiratory
muscles in patients in shock
 Normally, respiratory muscles consume <5%
of total cardiac output and oxygen delivery.
 Patients in shock often experience
respiratory distress due to pulmonary edema
(e.g., in cardiogenic shock), lactic acidosis,
and anemia.

23.  In this setting, up to 40% of cardiac output
may be distributed to the respiratory
muscles.
 Intubation and mechanical ventilation can
allow redistribution of the cardiac output
away from the respiratory muscles and back
to vital organs while the shock is treated

25.  Acute hypercarbic resp failure is
accompanied by change in pH i.e. acidemia
 Chronic condition result in renal
compensation & increased serum HCO3- conc.

26.  Acute and chronic hypoxemic respiratory
failure may not distinguished based on ABG
values
 Markers of chronic hypoxemia- polycythemia
or cor pulmonale provides clues to a long-
standing disorder
 Abrupt changes in mental status suggest an
acute event.

27.  The diagnosis of acute or chronic respiratory
failure begins with clinical suspicion of its
presence
 Confirmation of the diagnosis is based on
arterial blood gas analysis.
 Evaluation for an underlying cause must be
initiated early, frequently in the presence of
concurrent treatment for acute respiratory
failure

28.  Sepsis - fever, chills
 Pneumonia - cough, sputum production, chest
pain
 Pulmonary embolus - sudden onset of SOB or
chest pain
 COPD exacerbation – H/O heavy smoking, cough,
sputum production
 Cardiogenic pulmonary edema - chest pain, PND,
and orthopnea

29.  Noncardiogenic edema - the presence of risk
factors including sepsis, trauma, aspiration,
and blood transfusions
 Accompanying sensory abnormalities
/symptoms of weakness- neuromuscular
respiratory failure, H/O an ingestion or
administration of drugs or toxins.
 Additional exposure history may help
diagnose asthma, aspiration, inhalational
injury and some interstitial lung diseases

30.  Hypotension usually with signs of poor
perfusion- severe sepsis or massive
pulmonary embolism
 Wheezing suggests airway obstruction
• Fixed upper or lower airway pathology
• Secretions
• Pulmonary edema (“ cardiac asthma”)
• Bronchospasm

31.  Stridor suggests upper airway obstruction
 JVP suggests RV dysfunction due to
accompanying pulmonary hypertension
 Tachycardia and arrhythmias may be the
cause of cardiogenic pulmonary edema

32.  ABG
 Quantifies magnitude of gas exchange
abnormality
 Identifies type and chronicity of respiratory
failure

33.  Complete blood count
 Anemia may cause cardiogenic pulmonary edema
 Polycythemia suggests may chronic hypoxemia
 Leukocytosis, a left shift, or leukopenia
suggestive of infection
 Thrombocytopenia may suggest sepsis as a
cause

34.  Cardiac serologic markers
 Troponin, Creatine kinase- MB fraction (CK-
MB)
 B-type natriuretic peptide (BNP)
 Microbiology
 Respiratory cultures: sputum/tracheal
aspirate/broncheoalveolar lavage (BAL)
 Blood, urine and body fluid (e.g. pleural)
cultures

35.  Chest radiography
 Identify chest wall, pleural and lung parenchymal
pathology;
 Distinguish disorders that cause primarily V/Q
mismatch (clear lungs) vs. Shunt (intra-
pulmonary shunt; with opacities present)
 Electrocardiogram
 Identify arrhythmias, ischemia, ventricular
 Dysfunction
 Echocardiography
 Identify right and/or left ventricular dysfunction

36.  Pulmonary function tests/bedside spirometry
 Identify obstruction, restriction, gas diffusion
abnormalities
 May be difficult to perform if critically ill
 Bronchoscopy
 Obtain biopsies, brushings and BAL for
histology, cytology & microbiology
 Results may not be available quickly enough
to avert respiratory failure
 Bronchoscopy may not be safe in the if
critically ill

37.  ABC’ s
 Ensure airway is adequate
 Ensure adequate supplemental oxygen and
assisted ventilation, if indicated
 Support circulation as needed

38.  Treatment of a specific cause when possible
 Infection
 Antimicrobials, source control
 Airway obstruction
 Bronchodilators, glucocorticoids
 Improve cardiac function
 Positive airway pressure, diuretics,
vasodilators,
 morphine, inotropy, revascularization

39.  Mechanical ventilation is used to assist or
replace spontaneous breathing.
 Types:
 1.NIV
 2.Conventional MV
 3.Non-Conventional MV

40.  usually is provided with a tight-fitting face mask or nasal mask
 if patient can protect airway and is hemodynamically stable)
NIV has proved highly effective in patients with respiratory
failure arising from acute exacerbations of COPD
It is most frequently implemented as BiPAP ventilation or
Pressure Support Ventilation
 Both modes, which apply a preset positive pressure during
inspiration and a lower pressure during expiration at the mask,
are well tolerated by a conscious patient and optimize patient-
ventilator synchrony.

41.  Limitations of NIV
 Patient intolerance
 Tight fitting mask req for NIV can cause
both physical and pysh. discomfort
 Once NIV is initiated, patients should be
monitored;a reduction in respiratory frequency
and a decrease in the use of accessory muscles
(scalene, sternomastoid, and intercostals) are
good clinical indicators of adequate therapeutic
benefit

42. 1. COPD exacerbation
2. Cardiogenic pulmonary edema
3. Obesity /hypoventilation syndrome
4. NIV may be tried in selected pts with
asthma or non-cardiogenic hypoxemic
respiratory failure

43.  Cardiac or respiratory arrest
 Severe encephalopathy
 Upper airway obstruction
 Severe UGI bleeding
 Inability to protect airway

44.  Hemodynamic instability
 Inability to clear secretions
 High risk for aspiration
 Unstable cardiac rhythm
 Nonrespiratory organ failure
 Facial surgery, trauma, or deformity

45.  Conventional MV is implemented once a
cuffed tube is inserted into the trachea to
allow conditioned gas(warmed, oxygenated,
and humidified) to be delivered to the airways
and lungs at pressures above atmospheric
pressure.
 Care should be taken during intubation to
avoid brain-damaging hypoxia

46.  Admin. of mild sedatives-opioids, BZD
 Shorter-acting agents etomidate and propofol have
been used for both induction and maintenance of
anesthesia in ventilated patients because they have
fewer adverse hemodynamic effects
 Great care must be taken to avoid the use of
neuromuscular paralysis during intubation of patients
with renal failure, tumor lysis syndrome, crush
injuries, medical conditions associated with elevated
serum K+ levels, and muscular dystrophy syndromes

47.  To optimize oxygenation while avoiding
ventilator-induced lung injury due to overstretch
and collapse/re-recruitment.
 Normalization of pH through elimination of CO2
is desirable but the risk of lung damage
associated with the large volume and high
pressure.
 This has led to the acceptance of permissive
hypercapnia. This condition is well tolerated
when care is taken to avoid excess acidosis by pH
buffering.

48.  Ventilation strategy that allows PaCO2 to rise by
accepting a lower alveolar minute ventilation
 to avoid specific risks:
 Dynamic hyperinflation (“auto- peep”) and
barotrauma in patients with asthma
 Ventilator-associated lung injury, in patients
with, or at risk for, ALI and ARDS
 Contraindicated in patients with increased
intracranial pressure such as head trauma

50. 1. Assisted Control MV
 an inspiratory cycle is initiated either by the patient’s inspiratory
effort or, if none is detected within a specified time window, by a
timer signal within the ventilator.
 Every breath delivered, whether patient- or timer-triggered,
consists of the operator-specified tidal volume.
 Ventilatory rate is determined either by the patient or by the
operator-specified backup rate, whichever is of higher
frequency.
 commonly used for initiation of MV because it ensures a backup
minute ventilation in the absence of an intact respiratory drive
and allows for synchronization of the ventilator cycle with the
patient’s inspiratory effort.

51.  Patients with tachypnea due to nonrespiratory or
nonmetabolic factors, such as:
 Anxiety,
 Pain, and
 Airway irritation.
 Respiratory alkalemia may develop and trigger
myoclonus or seizures.

52.  Dynamic hyperinflation leading to increased
intrathoracic pressures (so-called auto-PEEP)
may occur-inadequate time is available for
complete exhalation between inspiratory
cycles.
 Auto-PEEP can limit venous return, decrease
cardiac output, and increase airway
pressures, predisposing to barotrauma

53.  The number of mandatory breaths of fixed
volume to be delivered by the ventilator are
set
 Between those breaths, the patient can
breathe spontaneously.
 In the most frequently used SIMV, mandatory
breaths are delivered in synchrony with the
patient’s inspiratory efforts.

54.  If the patient fails to initiate a breath, the
ventilator delivers a fixed-tidal-volume breath
and resets the internal timer for the next
inspiratory cycle.
 SIMV differs from ACMV in that only a preset
number of breaths are ventilator-assisted.
 SIMV allows patients with an intact respiratory
drive to exercise inspiratory muscles between
assisted breaths; thus it is useful for both
supporting and weaning intubated patients
 difficult in patients with tachypnea because they
may attempt to exhale during the ventilator-
programmed inspiratory cycle.

55.  This form of ventilation is pt triggered, flow-
cycled, and pressure-limited.
 It provides graded assistance and differs
from the other two modes in that the
operator sets the pressure level (rather than
the volume) to augment every spontaneous
respiratory effort.

56.  The level of pressure is adjusted by observing
the patient’s respiratory frequency
 With PSV, patients receive ventilator
assistance only when the ventilator detects an
inspiratory effort.
 PSV is often used in combination with SIMV to
ensure volume-cycled backup for patient
whose respiratory drive is depressed.

57.  Pressure Control Ventilation
 Inverse Ratio Ventilation
 CPAP-The ventilator provides fresh gas to the
breathing circuit with each inspiration and sets
the circuit to a constant, operator specified
pressure.
 CPAP is used to assess extubation potential in
pts who have been effectively weaned

58.  High frequency oscillatory Ventilation
 Airway Pressure Release Ventilation
 Extracorporeal Membrane Oxygenation
 Partial Liquid Ventilation
 Proportional Assist ventilation
 Neurally Adjusted Ventilatory Assist ventilation

59.  (1) Set a target tidal volume close to 6 mL/kg
of ideal body weight.
 (2) Prevent plateau pressure (static pressure
in the airway at the end of inspiration > 30
cm H2O.
 (3) Use the lowest possible Fio2 to keep the
Sao2 at ≥90%.
 (4) Adjust the PEEP to maintain alveolar
patency while preventing overdistention &
closure/reopening.

60.  As improvement in respiratory function is noted,
the first priority is to reduce the level of
mechanical ventilatory support.
 Patients on full ventilatory support should be
monitored frequently, with the goal of switching
to a mode that allows for weaning as soon as
possible
 Patients whose condition continues to deteriorate
after ventilatory support is initiated may require
increased O2, PEEP, or one of the alternative
modes of ventilation.

61.  Sedation and analgesia to maintain an acceptable level of
comfort-lorazepam, midazolam, diazepam, morphine,and
fentanyl
 Subcutaneous heparin and/or pneumatic compression
boots to avoid DVT
 To prevent decubitus ulcers- frequent changes in body
position , use of soft mattress overlays and air mattresses
 Prophylaxis against diffuse GI mucosal injury is indicated
for patients undergoing MV-H2 receptor antagonists,
antacids, and cytoprotective agents such as sucralfate

62.  Nutritional support - enteral feeding through
either a nasogastric or an orogastric tube
should be initiated and maintained whenever
possible.
 Delayed gastric emptying is common in
critically ill patients taking sedative
medications but often responds to
promotility agents such as metoclopramide.

63.  Pulmonary:
 Barotrauma
 Nosocomial pneumonia
 Oxygen toxicity
 Tracheal stenosis
 Intubated patients are at high risk for ventilator-
associated pneumonia as a result of aspiration from the
upper airways through small leaks around the
endotracheal tube cuff;
 The most common organisms - Pseudomonas aeruginosa,
enteric gram-negative rods, and Staphylococcus aureus.


64.  Hypotension resulting from elevated
intrathoracic pressures with decreased
venous return is almost always responsive to
intravascular volume repletion.
 Gastrointestinal effects of positive-pressure
ventilation include stress ulceration and mild
to moderate cholestasis

65.  The decision to wean:
 (1) Lung injury is stable or resolving.
 (2) Gas exchange is adequate, with low
PEEP/Fio2 (<8 cmH2O) and Fio2(<0.5).
 (3) Hemodynamic variables are stable, and
the patient is no longer receiving
vasopressors).
 (4) The patient is capable of initiating
spontaneous breaths.

66.  SPONTANEOUS BREATHING TRIAL
 The SBT is usually implemented with a T-
piece using 1–5 cmH2O, CPAP with 5–
7cmH2O
 Once it is determined that the patient can
breathe spontaneously, a decision must be
made about the removal of the artificial
airway, which should be undertaken only pt
has the ability to protect the airway, is able to
cough and clear secretions, and is alert
enough to follow commands

68.  Several studies suggest that NIV can be used
to obviate reintubation, particularly in
patients with ventilatory failure secondary to
COPD exacerbation
 In this setting, earlier extubation with the
use of prophylactic NIV has yielded good
results.

69.  Prolonged Ventilation- >21 days.
 A tracheostomy is thought to be more comfortable,
to require less sedation, and to provide a more
secure airway and may also reduce weaning time.
 In patients with long-term tracheostomy,
complications include tracheal stenosis, granulation,
and erosion of the innominate artery.
 MV for more than 10–14 days, a tracheostomy is
indicated

70.  Mortality in hypoxemic respiratory failure
depends on the underlying cause
 Mortality in ARDS appears to have improved
in recent years, but it remains high in the
elderly -mortality is 60%.
 Patients who develop sepsis after trauma
have a lower mortality than do patients with
sepsis that complicates medical disorders.

71.  Higher mortality in patients admitted with
hypercapnic respiratory failure
 For patients hospitalized with an acute
exacerbation of COPD, overall mortality is 8%
to 12%, but it may be as high as 28% for
those with significant comorbidities