Respiratory insufficiency / failure

Respiratory
insufficiency / failure
Katalin Veres MD, PhD
3rd Department of Internal Medicine
Respiratory failure
the goal of breathing is to fill the blood
with the sufficient amount of oxygen
necessary for the tissues and clear the
blood of carbon dioxide
RF = the insufficiency of the breathing
to fulfill the above task - that is
insufficient respiratory performance of
the lungs
Definition
a functional acute or chronic disorder
severely affects the lungs’ ability to
maintain arterial oxygenisation or
carbon dioxide elimanation
frequently encountered medical
problem
major cause of death in the US
Respiratory failure
Physiologic definition
inability of the lungs to meet the
metabolic demands of the body
can’t take in enough O2 or
can’t eliminate CO2 fast enough to
keep up with production
Alveolar phase of breathing
Oxygen consumption
Resting oxygen consumption + work load (physical
+ metabolic) requirements
Hypoxia:
Hypoxemic
–
–
–
reduction of FIO2 (mountain sickness)
Ventilation/diffusion failure
Shunting - anatomic R→L shunts
circulation without ventilation = atelectasis!!!
Stagnation - mixed SatvO2↓
Ischemic
Anemic
Histotoxic
CO2 elimination
arterial CO2 level (PaCO2) depends on
the metabolic production rate (VCO2)
and the alveolar clearing
= alveolar ventilation (VA)
PaCO2 = k VCO2/VA
under normal circumstances these
values are relatively constant
Classification
failure of gas exchange – hypoxemia
Hypoxemic respiratory failure
(failure of oxygenation: PaO2<60 mmHg)
failure of ventilation – hypercapnia
Hypercapnic-hypoxemic respiratory
failure
(failure of ventilation: PaCO2>50 mmHg)
Classification
according to ventilatory pump–function:
partial or global
according to time length (duration):
chronic or acute
according to origin:
obstructive or restrictive
Classification
Acute/ chronic respiratory failure
+ acute exacerbation of a chronic
process
Partial or total (global) ARI
(hypoxia alone or + hypercapnia)
Ventilation/ Diffusion/ Perfusion
abnormalities
Obstructive or restrictive RI
Causes of ventilation problems
Central: CNS – spinal cord
Neurologic, neuromuscular, muscular failures
Thoracic cage – rib fractures, burns, scars, …
Compression of the lungs – hydrothorax,
hemothorax, pneumothorax
Airway obstruction
E.g. myasthenia gravis, GuillainBarré sy., muscle relaxants
Mechanical causes
Injuries
Drug action - e.g. opioids!
Upper airway obstruction – foreign body, stenosis, …
Lower airways – bronchospasm, asthma, ...
Problems in the lung-parenchyma itself
Clinical signs of
respiratory insufficiency
dyspnoea
use of ventilatory accessory muscles
cyanosis
progressive elevation of the resp. rate
tachycardia
agitation, confusion, somnolentia,
coma
Diagnosis
Inspection – dyspnoea, thoracic
movements, etc.
Respiratory rate, (VC, FEV?)
Pulsoximetry (capnography?)
Blood gases (arterial, venous) – repeated!
– Reaction to oxygen inhalation?
Asthma: peak flow
Further investigations:
Chest X ray?, CT, MRI
Sputum - bacteriology, serology
Laboratory testing
ECG, US (TEE?)
Hypoxic respiratory
failure
any condition that severely reduces arterial
oxygen tensio (<50 mmHg) and cannot be
corrected by increasing the inspired O2
concentration to > 50% (FiO2 > 50%)
low PaO2 is due to a large right-to-left
shunt in well-perfused but poorly
oxygenated lung tissue
anatomic features: edema, atelectasis or
consolidation, hyaline membranes
O2 reserve is minimal and patients become
symptomatic
Clinical manifestations
arterial hypoxemia increases ventilation by
stimulating carotid body chemoreceptors
activity of the sympathetic nervous system
tachycardia, tachypnea, anxiety,
diaphoresis, altered mental status,
confusion, cyanosis, hyper/hypotension,
bradycardia, seizures, lactic acidosis
Acute hypoxemic
respiratory failure
Shunt disease - intracardiac or
intrapulmonary
Severe V/Q mismatch - asthma, PE
Venous admixture due to low
cardiac output states, severe anemia
coupled with shunt and/or V/Q
mismatch
Features of hypoxemic
acute respiratory failure
medical history: hypertension, heart disease
present illness: acute shortness of breath
temporally related to some serious event
physical examination: evidence of acute
illness, tachypnea, tachycardia,
hypotension, diffuse crackles, signs of
consolidation
CXR, ECG, laboratory
Hypercapnic-hypoxemic
respiratory failure
life-threatening condition with inadequate
CO2 excretion (PaCO2 > 55 mmHg)
a rise in the PaCO2 level signifies reduced
alveolar ventilation or hypoventilation
mechanism for the failure in CO2 excretion
varies, usually associated with severe
airflow obstruction (e.g. COPD, asthma)
hypercapnia may also occur in normal
lungs: the control of breathing is altered
(e.g. sedative drug overdose) or the
neuromuscular apparetes is inadequte
Clinical manifestations
hypercapnia depresses central nervous
system activity
somnolence, lethargy, restlessness,
tremor, slurred speech, headache,
asterixis, papilledema, coma
Features of hypercapnichypoxemic acute respiratory
failure I.
physiologic:
COPD: hypoventilation due to marked
wasted/dead space ventilation
neuromuscular or overdose:
hypoventilation due to decreased minute
ventilation
anatomic: mucus gland hyperplasia, alveolar
wall destruction, hypertrophied bronchial
muscle or mucous inpaction, upper airway
obstruction
Features of hypercapnichypoxemic acute respiratory
failure II.
medical history: chronic shortness of breath, history
of depression, waekness and wheezing
present illness: recent upper respiratory tract
infection, gradual worsening of shortness of breath,
increased cough, sputum and wheezing, drug
ovesdose, new or increased muscle weakness
physical examination: tachypnea, tachycardia,
prolonged exspiration, decreased breath sounds,
wheezing, pedal edema, reduced strength, altered
conscionsness
CXR, ECG, laboratory
Acute respiratory failure
Acute Lung Injury, Acute Respiratory
Distress Syndrome (ALI/ARDS)
Acute bronchospasm – severe asthma
Acute on chronic airflow limitation acute
exacerbation of COPD
Severe pneumonia
Pulmonary embolism
Pulmonary edema
Aspiration, inhalation
Acute lung injury,
Acute respiratory distress
syndrome (ALI/ARDS)
diffuse lung disease with severe
hypoxia - characterized by loss of
ventilated alveoli (loss of surfactant
activity, edema of the lung tissue)
→ reduced ventilated lung-capacity
→ reduced compliance
→ severe hypoxemia
(intrapulmonary shunts)
ALI/ARDS
ALI/ARDS
diffuse bilateral infiltration caused not
by LV insufficiency (Paop < 18 Hgmm)
PaO2/FiO2 < 300 (ALI) or 200 (ARDS)
lung compliance ↓
severe hypoxia – not reacting on
oxygen inhalation
ALI/ARDS
Pulmonary:
- infection/pneumonia
- aspiration/inhalation
- near drowning
- contusion
Extrapulmonary:
- sepsis
- trauma
- TRALI
- CPB
Acute bronchospasm,
severe asthmatic attack
Components of the insufficiency:
bronchospasmus
edema of the bronchiolar mucous
membranes
secretion – sticky secretions
obscruction of small bronchioli
air trapping – exhalation incomplete
the pressure never returns to zero! "dynamic
hyperinflation" (TLC↑, RV↑, FRC↑)
lung inflation - intrinsic or autoPEEP
respiratory work elevated - exhaustion!
Pneumonia
Epidemiology:
Infective agent:
Home aquired
Community aquired (CAP)
Hospital aquired (HAP)
Ventilator aquired (VAP)
Bacterial - pneumocc., haemophylus, staphylo., mycoplasma
Viral pneumonia (influenza, adenovirus, etc.)
Clinical appearance:
Typic pneumonia (sudden beginning, high fever, productive
cough, …)
Atypic pneumonia (less characteristic symptoms)
Pulmonary embolism
2/3 false diagnosis
non specific symptoms
risk factors draw attention to the
possible diagnosis
potencially lethal
mortality: 30%, if adequately treated:
2-8 (15)%
preventable
Pulmonary embolism
obstruction of blood flow to one or more
pulmonary arteries by thrombi
usually precipitated by DVT originating in
legs, pelvis, or upper extremities
primary or secundary hypercoagulable states
subclinical
submassive: normal BP, possible RV
hypokinesis or dilatation
massive: BP, RV afterload, PA systolic
pressure
Difficulty of diagnosis
– Multiple clinical presentations
– Nonspecific signs and symptoms
Risk factors: surgery, cancer,
immobilization, trauma, oral
contraceptives, pregnancy/postpartum,
advanced age, prior DVT, central
catheters, congestive heart failure,
hypercoagulable states (inherited or
acquired), polycythemia/dehydration,
obesity
Pulmonary edema
Dynamic balance state:
intravascular – interstitial – alveolar compartments
Starling equation
(fluid movement through
semipermeable membranes):
Qf = K /(Pc – Pi) – σ(Pc – Pi)/
K: filtration coefficient, σ: protein permeability, Pc, Pi: capillary
+ interstitial onkotic pressure
Factors:
alveolocapillary membrane permeability
hydrostatic pressure in the capillaries
onkotic pressure in the interstitium
capacity of the lymph-system
Common causes of
pulmonary edema
Cardial edema: main cause is the elevated
hydrostatic pressure in the pulmonary vessels
(AMI, CAD, CMP, MS, MI, hypertensive crisis…)
Non cardiac causes:
Chemical irritation (gases, fumes, aspiration of acidic
gastric content, etc.)
Fluid overload
Following upper airway obstruction, near drowing
Pneumothx (interstitial neg. pressure↓), re-expansion
High altitude
Infection, sepsis
Pharmacons, toxins
(sedato-hypnotica, salicylate overdose, paraquate, …)
…..
Chronic respiratory
failure
any process that affects the airways, lung
parenchyma, chest wall or neuromuscular
system can evolve into chronic respiratory
failure
obstruction / restriction
most severe cases of chronic hypoxic
respiratory failure, progressive lung
destruction also impairs ventilation, and
hypercapnia develops
supportive care
lung transplantation