Why ARF is so important?
•ARF is commonly encountered in emergency department and ICU.
•It has varied etiology, high morbidity and morality despite aggressive
monitoring and treatment.
•The aim of this discussion is to understand
-Classification
-Etiology
-Clinical features
-Diagnosis
-Management
What is Respiratory Failure
❖Inability of the respiratory system to
exchange gases and to oxygenate the
blood adequately
❖Respiratory failure is due to inadequate
gas exchange
➢Failure of oxygenation, Hypoxemia
➢Failure of removal of CO2, Hypercapnia
Mechanisms of Respiratory Failure
Pump failure
❖Failure in pulmonary ventilation
❖Includes Respiratory muscles and respiratory control mechanism
Lung failure
❖Failure in gas exchanges
❖Failure in Oxygenation
Lung Failure
Mismatch in blood gas exchanges due to the following different
pathologies:
oARDS
oAcute cardiogenic pulmonary oedema
oSevere status asthmaticus
oPneumonia
oAirspace collapse (atelectasis)
oPulmonary embolism
Classification of Respiratory failure
Respiratory Failure
Hypoxemic (Type-I)
Low PaO2 with normal or low PaCO2
Acute Chronic
Hypercapnic (Type-II)
Low PaO2 and high PaCO2
Acute Chronic
❖Hypoxemia and hypercarbic respiratory failure frequently coexist.
Classification of Acute Respiratory failure
❖Hypoxemic respiratory failure (Type-I)
PaO2 of <60mmHg with a normal or low PaCO2
❖ Hypercapnic respiratory (Type-II)
PaO2 of <60mHg and a PaCO2 of >45mHg
Mechanism of Hypoxemia
❖ Hypoventilation
❖ Alteration in gas diffusion
❖ Ventilation/perfusion ratio Mismatch
❖ Pulmonary shunt
FIO2
Ventilation without perfusion
(dead space ventilation)
Alteration in Diffusion
Perfusion without ventilation
(shunting)
Hypoventilation
Normal
Mechanism of hypoxemia
Hypoventilation
Brainstem
Spinal cord
Nerve rootAirway
Nerve
Neuromuscular
junction
Respiratory
muscle
Lung
Pleura
Chest wall
Sites at which disease may cause ventilatory disturbance
Hypoventilation
Causes of hypoventilation
❖Brainstem injury or disease
❖CNS depressant drugs
❖Spinal cord or nerve damage
❖Nerve injuries
❖Neuropathies
➢Guillain Barre
➢Critical illness neuropathy
❖Neuromuscular blockers
❖disease of the neuromuscular junction
➢myasthenia gravis
Causes of hypoventilation
❖Respiratory muscle
➢Fatigue
➢Disuse atrophy
➢Malnutrition
❖problem of increased resistance to airflow
➢Obstruction of the upper airway
➢Bronchospasm.
❖Decreased compliance of the lung itself, the pleura or the chest wall.
Diffusion Abnormality
Abnormality of the alveolar membrane or a reduction in the number
of capillaries resulting in a reduction in alveolar surface area
❖ Causes include:
➢Acute Respiratory Distress Syndrome
➢Fibrotic lung disease
Ventilation-perfusion Mismatch
❖ The efficacy of gas exchange is determined by the balance
between alveolar ventilation and pulmonary capillary blood flow
❖ This balance is commonly expressed as Ventilation-perfusion
ratio (V/Q)
Ventilation-perfusion Mismatch
V-Q RatioImplications Term Consequences
V/Q = 1 Perfect match of ventilation and perfusionV-Q Match Normal PaO2
V/Q > 1Ventilation > pulmonary capillary blood flowDead Space Ventilation↓PaO2
↑PaCO2
V/Q < 1 Pulmonary capillary blood flow > ventilationShunting /Venous admixture↓PaO2
Normal or ↑PaCO2
Dead Space Ventilation (Ventilation without perfusion)
❖If V/Q >1 there is excess Ventilation than pulmonary capillary blood flow.
❖This excess ventilation is called as Dead Space Ventilation (VD) which does not participate
in the gas exchange
❖Dead space ventilation includes Anatomical and physiological dead space
❖Anatomical dead space = gas in the large conducting airway that does not come in contact
with capillary blood
❖Physiological dead space = alveolar gas that does not take part in gas exchange with
capillary blood
❖In normal subjects VD is 20%-30% of total ventilation (VT)
❖VD / VT = 0.2 to 0.3
❖VD / VT > 0.3 results in both hypoxemia & hypercapnia
❖VD / VT > 0.5 results in hypercapnia
Dead Space Ventilation (Ventilation without perfusion)
DSV increase in
❖Alveolar-capillary interface destroyed e.g. emphysema
❖Blood flow is reduced e.g. CHF, PE
❖Overdistended alveoli e.g. positive- pressure ventilation
Shunting (Perfusion without ventilation)
❖If V/Q < 1,then Pulmonary capillary blood flow is relatively excessive than
ventilation
❖The excess blood not taking part in the gas exchange is called as intrapulmonary
shunting
❖ Shunting is of two types
➢True shunt = Total absence of gas exchange between capillary blood and alveoli
= V/Q = 0
= Found in Rt to left shunt of the heart
➢Venous admixture = Capillary blood that does not equilibrate completely with alveolar gas
= 0<V/Q<1
= As the admixture increases it becomes a true shunt
Shunting
❖Intra-cardiac
➢Any cause of right to left shunt e.g. Fallot’s, Eisenmenger
❖Intra-pulmonary
➢Small airways occluded ( e.g. asthma, chronic bronchitis)
➢Alveoli are filled with fluid ( e.g. pulm edema, pneumonia)
➢Alveolar collapse ( e.g. atelectasis, collapse)
FIO2
Ventilation without perfusion
(dead space ventilation)
Alteration in Diffusion
Perfusion without ventilation
(shunting)
Hypoventilation
Normal
Shunting
Consequences of Hypoxemic respiratory failure
❖Interrelationship of mechanisms
➢Hypoxemic respiratory failure is frequently caused by a combination of two
or more of these four mechanisms
❖Effects of hypoxemia
➢Build up of lactic acid → metabolic acidosis → cell death
➢CNS depression
➢Heart tries to compensate → ↑ HR and CO
➢If no compensation: ↓ O2, ↑ acid, heart fails, shock, multi-system organ
failure
Hypercapnic Respiratory Failure
Mechanism of Hypercapnia
❖Increase in CO2 production
➢parenteral feeding with high doses of carbohydrates
➢high body temperature
❖V/Q Mismatch : Deterioration in gas exchanges due to increased dead space ventilation
in COPD. Ventilation not adequate to eliminate CO2 Leads to respiratory acidosis
❖Deterioration in respiratory mechanics
Huge respiratory effort
Increase in respiratory work of breathing
Development of a rapid shallow breathing
↑ CO2
❖Alteration in the mechanism of control of the ventilation
Symptoms of Respiratory failure
❖Respiratory failure may of Sudden or gradual onset
❖A sudden ↓ in PaO2 or rapid ↑ in PaCO2 is a serious condition
❖When compensatory mechanisms fail, respiratory failure occurs
❖Signs may be specific or nonspecific
Management of ARF -Respiratory Therapy
❖ Mobilization of secretions
➢ Effective coughing and positioning
➢ Mobilization of secretions
➢ Hydration and humidification
➢ Chest physiotherapy
➢ Airway suctioning
❖ Oxygen therapy
❖Positive pressure ventilation
➢CPAP
➢BiPAP
➢Invasive ventilation
Management of ARF -Drug Therapy
❖ Relief of bronchospasm - Bronchodilators
❖ Reduction of airway inflammation - Corticosteroids
❖ Reduction of pulmonary congestion - IV diuretics
❖ Treatment of pulmonary infections - IV antibiotics
❖ Reduction of severe anxiety, pain, and agitation - Benzodiazepines & Narcotics
Management of ARF
❖ Medical Supportive Therapy
➢Treat the underlying cause
➢ Maintain adequate cardiac output
➢ Maintain Hb concentration
➢ Monitor BP, SPO2, urine output
❖Nutritional Therapy
➢Maintain protein and energy stores
➢Enteral or parenteral nutrition
➢Supplements
Case 1
❖ HISTORY:
➢68 year old man, retired truck driver, smoker (45 pack years), alcoholic, diabetic and
hypertensive
❖ CHIEF COMPLAINT:
➢ Productive Cough (Thick & rusty)
➢ High grade fever with chills for 4 days
➢ pain in his right chest that intensifies with inspiration
❖EXAMINATION:
➢SPO2 – 90 % in RA, BP- 152/90, HR-112/minute and regular, RR- 30/min, temperature
102.6 F.
➢CHEST - Bronchial breath sounds right ICA
❖ LABORATORY:
➢WBC 17,000/mm3; DC –N 88 L12
➢ABG : PH-7.42, PCO2- 30, PaO2- 56, HCO3- 20
Case 1
❖ What type of respiratory failure is this ?
❖What is the diagnosis ?
❖How will you manage this ?
Case 2
❖ HISTORY:
➢28 year student, tall and thin, smoker (5 pack years)
❖ CHIEF COMPLAINT:
➢ Sudden SOB
➢ Pain right chest
❖EXAMINATION:
➢BP- 90/40, HR-122/minute, RR- 30/min
➢CHEST – hyper resonant percussion and Absent breath sound right
hemithorax
➢ABG : PH-7.50, PCO2- 20, PaO2- 50, HCO3- 20
Case 2
❖ What type of respiratory failure is this ?
❖What is the diagnosis ?
❖How will you manage this ?
Case 3
❖ HISTORY:
➢23 years, footballer, got a chest injury while he was playing football.
❖CHIEF COMPLAINT:
➢ Pain right chest
➢ SOB
➢ Drowsiness
❖EXAMINATION:
➢BP- 150/90, HR-122/minute, RR- 14/min, shallow
➢CHEST – normal breath sound, crepitus and localized tenderness right hemithorax
➢ABG : PH-7.30, PCO2- 60, PaO2- 60, HCO3- 24
Case 3
❖ What type of respiratory failure is this ?
❖What is the diagnosis ?
❖How will you manage this ?
Case 4
❖ HISTORY:
➢78 year old man, retired teacher, ex-smoker (25 pack years), diabetic, IHD, Hypertensive
❖ CHIEF COMPLAINT:
➢ SOB
➢ High grade fever with chills for 4 days
➢ Desaturation at home
➢ Sneezing & rhinorrhea
❖EXAMINATION:
➢SPO2 – 78 % in RA, BP- 112/90, HR-122/minute and regular, RR- 38/min, temperature
102.6 F.
➢CHEST – coarse crepitations bilateral ISA
❖ LABORATORY:
➢WBC 11,000/mm3; DC –N 98 L2, CRP-112, D-DIMER-2590,Ferritin -726
➢Covid RTPCR –POSITIVE
➢ABG : PH-7.42, PCO2- 27, PaO2- 48, HCO3- 20
Case 4
❖ What type of respiratory failure is this ?
❖What is the diagnosis ?
❖How will you manage this ?
Case 5
❖ HISTORY:
➢72 year old man, Pujari, smoker (45 pack years), chronic exposure to fumes, diabetic
❖ CHIEF COMPLAINT:
➢ Productive Cough (Thick & yellowish)
➢ High grade fever for 4 days
➢ Increased SOB
➢Drowsy and disoriented
❖EXAMINATION:
➢SPO2 – 86 % in RA, BP- 152/90, HR-100/minute and regular, RR- 26/min, temperature 102.6 F.
➢CHEST – Labored breathing with use of accessory muscle, Bilateral poor air entry with prolonged
expiration and extensive polyphonic wheeze
❖ LABORATORY:
➢Hb- 17% WBC 16,800/mm3; DC –N 88 L12,CRP- 240,Na-125,K-2.8, RFT-WNL
➢ABG : PH-6.92, PCO2- 101, PaO2- 56, HCO3- 26
Case 5
❖ What type of respiratory failure is this ?
❖What is the diagnosis ?
❖How will you manage this ?
Case 6
❖ HISTORY:
➢88 year old female, K/C/O COPD extubated after 7 days of mechanical
ventilation and was doing well with NIV support.
➢Her ABG : PH-7.38, PCO2- 46, PaO2- 66, HCO3- 28 on that day.
➢On next day morning she was having severely hypoxemic with SPO2-
56% with high oxygen support.ABG Showed : PH-7.38, PCO2- 40,
PaO2- 46, HCO3- 28
❖EXAMINATION:
➢BP- 90/ 60 , HR-112/minute and regular, RR- 30/min,
➢CHEST - No breath sounds right hemithorax
❖ LABORATORY:
➢WBC 14,000/mm3; DC –N 88 L12
Case 6
❖ What type of respiratory failure is this ?
❖What is the diagnosis ?
❖How will you manage this ?