Respiratory Failure Flashcards

1
Q

RESPIRATORY FAILURE

A

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

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2
Q

External Respiration

A
  • 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
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3
Q

Internal Respiration

A
  • the process by which gas exchange is performed and oxygen is used by the tissues
  • Its impairment does not led to respiratory failure
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4
Q

Normal values- didactic

A

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)
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5
Q

Respiratory failure: Pathophysiology

A

Isolated or combined dysregulation of

  1. Alveolar ventilation
  2. Capillary perfusion
  3. Alveolo-capillary diffusion
  4. Neuro-humoral control of respiration
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6
Q

Hypoxemia

A
• Alveolar ventilation ↓
• Diffusion abnormality
• V/Q mismatch
• intrapulmonary shunt RL
• Oxygen consumption, (VO2 )
↑: fever, chill, dyspnea, twitch
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7
Q

Hypercapnia

A
• CO2 production↑
fever, infection, epilepsy
• Alveolar ventilation ↓
• neuromuscular diseases or
fatigue of respiratory muscles
• obstructive ventilation disorder
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8
Q

Hypoxemia: mechanisms

A
  1. 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%)
  2. 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%)
  3. 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
  4. 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
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9
Q

Lung diseases that cause respiratory failure by primitive impairment of
VA / Q, diffusion and by right-left intrapulmonary shunts

A
  1. Lower respiratory airways ->COPD, Bronchitis, Bronchiectasis
  2. Parenchyma ->
    - Lung Abscess
    - Lung Cancer
    - Atelectasis
    - Interstitial Fibrosis
  3. Pulmonary Vessels -> Pulmonary Embolism , Heart failure
  4. Other pulmonary disorders ->
    - Cystic Fibrosis
    - Emphysema
    - Respiratory distress syndromes
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10
Q

Respiratory failure: Classification

By pH

A
  • Compensated with normal pH (7.4)

* Decompensated with pH < 7.35

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11
Q

Respiratory failure: Classification
According to Pathophysiology & arterial blood gas:
TYPE III &IV

A

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)

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12
Q

Type I Respiratory failure

A

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
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13
Q

Type II Respiratory failure

A

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

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14
Q

Syndrome component

Humoral component

A
Hypoxemia
 PaO2 < 60 mmHg
associated or not with:
Hypercapnia
 PaCO2 > 45 mmHg
±
acid-base disturbances
1. Respiratory acidosis
2. Respiratory alkalosis
3. Metabolic acidosis
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15
Q

Syndrome Component

Clinical component

A
= 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
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16
Q

Acute Hypoxemia – clinical aspect

A

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

17
Q

Acute Hypoxemia - clinical aspect - how it does affect the organs ?

A
  1. CNS
    - Similar to alcohol intoxication
    - Motor Instability, Mental alteration
  2. 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
  3. Respiratory:
    - Dyspnea, Tachypnea, increased respiratory effort
    - Acute PAH, Acute CorPulmonale
  4. 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)
18
Q

Chronic Hypoxemia

A

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)

19
Q

Chronic Hypoxemia –clinical aspect : organs

A

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

20
Q

Acute Hypercapnia– clinical aspect

A

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

21
Q

Chronic Hypercapnia– clinical aspect

A

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

22
Q

Respiratory failure complications

A

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)

23
Q

Respiratory failure

Diagnostic criteria: summary

A

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