Respiratory Failure Flashcards
RESPIRATORY FAILURE
The inability of respiratory system to realize the gas
exchange between alveolar air and pulmonary
capillary at Rest and during Effort with the purpose
to maintain O2 and CO2 homeostasis in the arterial
blood determine RESPIRATORY FAILURE
External Respiration
- the process by which the gas exchange between the lungs and the atmosphere air at the level of the alveolo-capillary membrane is realized
- Any impairment led to respiratory failure
Internal Respiration
- the process by which gas exchange is performed and oxygen is used by the tissues
- Its impairment does not led to respiratory failure
Normal values- didactic
PaO2 = 96 mmHg (arterial blood)
– Varies with age, temperature, atmospheric pressure, O2 % in inspired air
– calculated by regression equation
– PaO2=100,1-0.323 x (age in years) ±5 mmHg
• SaO2 = 96% (hemoglobin saturation O2 in circulation)
• PaCO2 = 40-45 mmHg at an atmospheric pressure of 760 mmHg
– It does not depend on age, unaffected by environmental parameters
- HCO3 25 mEq/l
- pH blood 7.42
- mean PaP 15 mmHg (mean pulmonary artery pressure)
Respiratory failure: Pathophysiology
Isolated or combined dysregulation of
- Alveolar ventilation
- Capillary perfusion
- Alveolo-capillary diffusion
- Neuro-humoral control of respiration
Hypoxemia
• Alveolar ventilation ↓ • Diffusion abnormality • V/Q mismatch • intrapulmonary shunt RL • Oxygen consumption, (VO2 ) ↑: fever, chill, dyspnea, twitch
Hypercapnia
• CO2 production↑ fever, infection, epilepsy • Alveolar ventilation ↓ • neuromuscular diseases or fatigue of respiratory muscles • obstructive ventilation disorder
Hypoxemia: mechanisms
- Alteration of ventilation / perfusion ratio
(VA / Q) → VA / Q ratio = 0.8
Hypoxemia can be corrected by administering oxygen with a low concentration (24-40%) - Alveolar hypoventilation
Hypoxemia is associated with hypercapnia
If it acts as a single process → the number of mmHg with which PaO2 decreases = with no mmHg with which O2 increases. If not, other mechanisms are associated
Can be corrected by administering large amounts of oxygen (100%) - O2 diffusion capacity altered
If it is not severely altered → hypoxemia occurs only at exertion or altitude
Hypoxemia Correct easily with small amounts of O2 in the breathed air - Right to left intrapulmonary shunt
Pulmonary arterio-venous fistulas are present or Determined by perfusion of an
unventilated lung entities (atelectasis, pneumonia, pulmonary edema)
Hypoxemia cannot be corrected by O2
Lung diseases that cause respiratory failure by primitive impairment of
VA / Q, diffusion and by right-left intrapulmonary shunts
- Lower respiratory airways ->COPD, Bronchitis, Bronchiectasis
- Parenchyma ->
- Lung Abscess
- Lung Cancer
- Atelectasis
- Interstitial Fibrosis - Pulmonary Vessels -> Pulmonary Embolism , Heart failure
- Other pulmonary disorders ->
- Cystic Fibrosis
- Emphysema
- Respiratory distress syndromes
Respiratory failure: Classification
By pH
- Compensated with normal pH (7.4)
* Decompensated with pH < 7.35
Respiratory failure: Classification
According to Pathophysiology & arterial blood gas:
TYPE III &IV
Type III- results from lung atelectasis, also called perioperative respiratory failure, due to atelectasis that occurs so commonly in the Perioperative period
Type IV- This form results from hypoperfusion of
respiratory muscles in patients in shock (septic, hypovolemic,
cardiogenic)
Type I Respiratory failure
A failure of gas exchange
• Hypoxemia (PaO2 < 60 mmHg) • Main mechanism: ventilation / perfusion abnormalities • Other mechanisms: right to left intrapulmonary shunts (less often) Frequent Etiologies • Pneumonia • Pulmonary Edema • Fat tissue embolism • ARDS = a severe form of type-1 RF
Type II Respiratory failure
A failure of ventilation
Main mechanism: alveolar hypoventilation
Other mechanisms: VA / Q alteration may also be associated
Etiological categories
A. Normal lungs + hypoventilation
Respiratory center depression
Neuromuscular and medullary diseases (myasthenia, poliomyelitis)
Chest injuries
B. Lung disorders that cause disorders of ventilation and VA / Q
COPD, emphysema
Acute bronchitis, asthma, bronchiolitis
Syndrome component
Humoral component
Hypoxemia PaO2 < 60 mmHg associated or not with: Hypercapnia PaCO2 > 45 mmHg ± acid-base disturbances 1. Respiratory acidosis 2. Respiratory alkalosis 3. Metabolic acidosis
Syndrome Component
Clinical component
= tissue aspect - poorly correlated with laboratory data - not included in diagnosis definition - reflects tissue suffering = a set of clinical signs secondary to hypoxemia and / or Hypercapnia eg: • CNS • Cardiovascular
Acute Hypoxemia – clinical aspect
Has a recent onset (hours or days)
- The severity depends on the severity and rapidity of
installation
- Rapid installation can generate critical acid-base imbalance
- Acute RF → If associated with a sudden increase in PaCO2> 45 mmHg + Respiratory acidosis (pH <7.35) urgent treatment is needed
Acute Hypoxemia - clinical aspect - how it does affect the organs ?
- CNS
- Similar to alcohol intoxication
- Motor Instability, Mental alteration - CV → adrenergic stimulation of sympathetic nerve
- Palpitation due to Tachycardia & Arrhythmia, HTN, CO increases, cutaneous vasoconstriction and sweating
Severe Hypoxemia + acidosis→ hypotension -> Shock, Bradycardia, Depressed myocardium
with cardia arrest - Respiratory:
- Dyspnea, Tachypnea, increased respiratory effort
- Acute PAH, Acute CorPulmonale - Renal & Digestive system
- Renal blood vessels contraction→ Renal failure
- Gastric ulcer and bleeding,
- Hepatic cell hypoxia → ↑ALT, jaundice
SIGNS
- Cyanosis lips, mucosae, nail (↑ reduced Hbg, ↓ skin blood flow)
Chronic Hypoxemia
It develops in months or years
• Defines chronic respiratory failure
• Due to Chronic alveolar ventilation disorder
• Accentuated during sleep (nocturnal hypoventilation)
• Compensatory mechanisms may help to improve O2 transport and buffer respiratory acidosis
• PaO2 < 60 mmHg,
• Chronic RF:
– PaO2 <60 mmHg and / or PaCO2> 45 mmHg, pH = normal, increased BE and HCO3
– Common etiologies: COPD, neuromuscular diseases, restriction of chest mobility
(obesity, spondylitis), obstructive sleep apnea syndrome and hypoventilation (Pickwick)
Chronic Hypoxemia –clinical aspect : organs
Central nervous system - > Similar to neurosis or cerebral ATS
– Restless sleep, headaches and morning sleepiness
– Impaired memory and concentration, Loss of attention,
– Apathy, fatigue during daytime,↑ reaction time
– Personality changes, paranoia
• Cardiovascular
– Pulmonary Hypertension (PAH) –↑mPAP ← arteriolar spasm)
– Chronic Cor pulmonale
• Respiratory
– Chronic & Recurrent Dyspnea, sign & symptoms determined by right ventricle overload due to chronic PAH & chronic cor pulmonale (CCP)
– Signs
– Polyglobulia: RBC ↑ secondary to hypoxia ( ↑hematopoiesis )
– Digital hippocratism/ clubbing
– Edema by:
1) CCP; 2) By the association of hypercapnia which ↑ the renal reabsorption of bicarbonate and produces edema in the absence of right heart failure
Acute Hypercapnia– clinical aspect
Central nervos system
– hypercapnic encephalopathy if PaCO2 > 70
– cerebral vasodilation (VD) intracranial hypertension (ICH)
– coma (death)
– respiratory center depression when CO2 ↑↑↑
• Cardiovascular
– Mixture of vasoconstriction & vasodilation
• Perifery CO2 det. VasoDilation (skin)
• Central CO2 det. VasoConstriction (coronary vessels)
– Tachycardia with palpitation, BP↑, CO ↑ (CO-cardiac output; BP-blood pressure)
– Severe Hy → directly inhibit cv center → depress cardiac function, dilate vessels → BP↓, arrhyt.
– Acute severe hypercapnia → VF (ventricular fibrillation ) or cardiac arrest
• SIGNS
– tachypnea
– pulsus magnus
– warm and sweaty extremities
– skin congestion
Chronic Hypercapnia– clinical aspect
Headache, persistent (cerebral vasodilatation)
– Somnolence
– Muscular Fasciculation
– Flapping
– Papillary edema
Clinical picture similar to cerebral tumor determined by
chronic ICH
If PaCO2 increase slowly, the clinical signs are discrete
Respiratory failure complications
Death by hypoxemia and / or severe hypercapnia with respiratory acidosis
Visceral complications:
Pulmonary: pulmonary embolism, pulmonary fibrosis,
Renal: renal failure (increased risk of death)
Cardiovascular: arrhythmias (caused by the association of hypoxemia, acidosis, hyperkalemia, sympathomimetic use); hypotension (by decreasing cardiac output)
Infectious: nosocomial pneumonia
Gastrointestinal: pneumoperitoneum (complication of MV); gastroduodenal ulcer, esophagitis or gastric stress ulcers, potentiated by corticotherapy
Hematological: anemia, thrombocytopenia (in ARDS), DIC
Thrombocytopenia -> potentiate the risk of digestive hemorrhage)
Nutritional: protein-caloric malnutrition in chronic IR
A! PaCo2 can be increased with carbohydrates iv or oral
Chronic RF complications: polyglobulia, malnutrition,
pulmonary hypertension, chronic cor pulmonale
Dysfunction and contractile insufficiency of the
respiratory muscles (can be both cause and effect)
Respiratory failure
Diagnostic criteria: summary
Clinical manifestations of the disease that caused it
• History of lung disease or dysfunction
• Blood gas analysis
PaO2 < 60 mmHg, or / plus
PaCO2 > 45 mmHg
± respiratory acidosis
• Clinical pattern: Nonspecific, late or missing
Main Clinical manifestation of RF
– Dyspnea (subjective difficulties in respiration)
– Cyanosis
– Agitation, confusion, consciousness impairment
– Increased respiratory work, accessory muscles used, increased respiratory rate
• Exclude
– intracardiac shunt such as ventricular septal defect
– decreased cardiac output
