results when exchange of oxygen and/or carbon dioxide between bloodand atmosphere is anadequate

not a disease but rather a condition resulting from disease involving lungs or other body systems

results from inadequate oxygen tranfer to blood

manifested by decreased O2 tension (PaO2) and saturation (SaO2)

caused by inadequte CO2 removal

manifested by an increased CO2 tension (PaCO2)

oxygenation failure

results from inadequate 2 transfer between alveoil and pulmonary capillary bed

• PaO2<60mmHg when cliet is recieving O2 concentration of >60%
• can be cased by:
  • pneumonia
  • pulmonary edema
  • pulmonary emboli
  • alveolar injury r/t inhalation of gas/smoke
  • alveoli injury/stress r/t ventilator induced lung injury
  • low cardiac output states
    • Heart failure
    • Shock 

ventilatory failure, problem is insfficient CO2 removal

• PaCO2>45mmHg in combination with acidemia (arterial pH<7.35 is evidence that body is unable to compensate for acidemia)
• caused by:
  • drug overdose of CNS depressants
  •  neuromuscular dissorders (myathnia gravis)
  • trauma or disease effecting the spinal cords role in lung ventillation
  • acute asthma

1) V/Q mismatch

2)shunt

3)diffussion limitation

4)hypoventilation

most common causes of

physiologic mehanisms that cause hypoxemia and subesquent hypoxemic respiratory failure

V/Q mismatch

Shunt

volume of blood perfusing the lung per minute (4-5 L) is approximatly the same as the amount of fresh gas reachign the alveoli (4-5L)

or 1mL of air for each 1mL of blood

1:1 ratio

V/Q=1

not equal throughout entire lung

apex >1 (more ventilation than perfussion)

base<1 (more perfussion that ventillation)

cause limited ventillation but have no effect on perfussion

• increased secretions in airway (COPD, aleoili pnemonia)
• bronchipspasms (athma)
• ataectasis (alveoli collapse)
• Pain (unrelieved or inadeuately managed)
  • interfears with chest wall movement
  • muscle rigidity causing systemic vasoconstriction
  •  activation of stress response
  •  increased O2 consumption/CO2 production

Causes limited perfussion with no effect on ventillation

• pulmonary embolism

administer O2 to increase PaO2 b/c not all gas exchange units are affected, the oxygenated blood will mix with the poorly oxygenated blood causing an overall PaO2 increase

subsequent interventions will focus on correcting cause of mismatch

occurs when blood exits the heart without paricipating in gas exchange

1. anatomic- blood passes through an anatomical channel in heart (ventricular septum defect)
2. intrapulmonary- blood flows through pulmonary capillaries without participating in gas exchange (alveoli filled with fluid)

patients are more hypoxemic than V/Q mismatch

may require machanical ventillation or high FIO2 to improve exchange

occurrs when gas exchange at the aveoil-capillary membrane is compromised (thichened or destroyed)

hypoxemia present during exersize but not at rest

• more likely to cause hypoxemia during exersize than at rest b/c of shortened time blood is in lungs for shorter time decreasing opportunity for diffusion across alveoli capillary membrane

worsened by 

• severe emphasima
• recurrent pulonary embolism
• thickening of the capillary (fibrotic)
• diseases that slow gas transportation

caused by

• pulmonary fibrosis
• interstitial lung disease
• ARDS

• generalized disease in ventillation that results in increase of PaCO2 and decrease in PaO2
• primarily a mechanism of hypercapnic respiration failure but may cause hypoxemia
• may be result of:
  • restrictive lung disase
  • CNS disease
  • chestwall dysfunction
  • acute asthma
  • neuromusclular disease

• severe morning headache
• Tachycardia (early sign)
• mild hypertension (early sign)
• cyanosis (late sign)
• rapid shallow breathing pattern
• tripod position
• dyspnea
• pursed lip breathing
• retractions
• change in I:E ratio (normal 1I:2E)
• paradoxical breathing
• orthopnea (more pillows)
• restlessness
• change in sleep patters

• metabolic acidosis and cell death (body switches to anaerobic metabolism leading to cell death)
• decreased cardiac output
• impaired renal function

• physical asessment
• ABG analysis
• Chest x-ray
• CBC
• ECG
• serum electrolytes
• urinalysis
• V/Q lung scan
• Pulmonary angiogram
• pulmonary artery catheterization (extreme cases)

• History
  • tobacco use
  • trauma to chest/spinal chord
  • exposure to inhalants
• Medications
  • beta blockers
  • inhalants
  • O2
  • nebulizers
  • otc medications
  • CNS depressants
• Surgury
  • problems with intibation
  • thoracic surgery
• tachycardia
• fatigue
• sleep pattern changes
• headaches
• restlessness

• ineffective airway clearance
• ineffective breathing pattern
• risk for imballanced fluid volume
• anxiety
• ineffective gas exchange
• imballanced ntrition: less than body requirements

• ABG's and breath sounds within baseline (consult records/ history)
• no dyspnea (shortness of breath)
• effective cough

• oxygen therapy
• mobilization of secreations
  • effectve cough and positioning
  • chest physiotherapy (flutter valve, percussion)
  • hydration and humidification
  • airway suctioning
• positive pressure ventilation
  • Bipap (pressure varries for I&E)
  • CPAP (continuous pressure) 

• Reduce airway inflamation
  • corticosteroids
    • prednisone P.O.
    • solumedrol I.V.
• Reduce pulmonary congestion
  • I.V. diuretics
    • lasix
• treat pulmonary infections
  • I.V. antibiotics
    • vancomycin
    • rocephin
• reduce anxiety and severe pain
  • benzodiadapines
    • ativan
    • versed
  • narcotics
    • morphine
      • reduces respiration rate
      • increases action of diuretics

Structural-chest wall stiffens and costal cartilage calcifies

• barrel chested appearance
• kyphotic posture
• decreased chest wall movements
• mucous thickens
• decreased vital capacity
• increased residual volume
• increased functional residual capacity
• diminished lung sounds especially at base
• decreased PaO2/PaCO2 with normal pH

Decreased Defense Mechanisms- respiratory infections become more severe and last longer

• decreased cough effectiveness and secretion clearance
• increased risk of infection/pnemonia
  • less specific antibodies
  • less cel mediated immunity
  • less cillia funcion
  • less ciliary macrophage function
  • less sensation in pharynx
• decreased respiratory control
  • less response to hypercapnea/hypoxia
    • greater change in O2/CO2 needed to facilitate RR change
    • less ability to control acid-base balance
    • small incidents can significantly alter PaO2/CO2

• dyspnea
• tachypnea
• prolonges expiration (1:3, 1:4)
• intercostal muscle contractions
• use of acessory muscles for respiration
• SpO2<80%
• Pardoxic chestwall movement
• Cyanosis

Cerebral

• agitation
• disorientation
• delirium
• restless/combative behavior
• confusion
• decreased conciousness
• coma

Cardiac

• tachypnia
• hypertension
• skin cool, clammy, diaphretic
• dysrhythmias
• hypotension

Other

• fatigue
• unable to speak sentences without pausing for breath

• dyspnea
• decreased respiration rate or incresed with shallow respirations
• decreased tidal volume
• decreased minute ventilation

Morning headache

dissorientation

progressive somnolence

coma

dysrhythmias

hypertension

tachycardia

bounding pulse

muscular weakness

decreased tendom reflexes

tremors/siezures

pursed lip breathing

use of tripod position

a sudden and progresve form of respiratory failure in which alveolar capillary memberane becomes damamged and more permeable to intravascular fluid.

Fluid Filled alveoli sudilt in severe dyspnea, hypoxemia refractory to supplemental O2, reduced lung cmpliance and diffuse pulmonary infiltrates

50% mortality rate

gram-egative septic shock and ARDS has 70-90% mortality

Direct Lung Injury (aspiration or pnemonia most commonly)

indirect Lung Injury (Sepsis, massive trauma)