This document discusses respiratory failure, including its definition, types, causes, clinical manifestations, diagnostic evaluations, management, and complications. Respiratory failure is when the respiratory system fails to adequately oxygenate the blood or eliminate carbon dioxide. It can be classified as hypoxemic or hypercapnic. Acute respiratory failure develops rapidly over hours while chronic develops over days. Management involves treating the underlying cause, providing oxygen supplementation, monitoring vital signs, and supporting respiratory function. Complications can affect the lungs, heart, gastrointestinal system, and risk of infection.
5. Control
• Resting respiration is the result of cyclical excitation
of the respiratory muscles by the phrenic nerve.
• Apneustic center
• Pneumotaxic center
• Central chemoreceptors
• Peripheral chemoreceptors
• Baroreceptors
6. Respiratory failure
Respiratory failure is a syndrome in which the
respiratory system fails in one or both of its gas
exchange functions
Oxygenation
Carbon dioxide elimination.
May be classified as either hypoxemic or hyper
capnic.
9. Acute & Chronic
• Acute respiratory failure develops over minutes to
hours; therefore, pH is less than 7.3
• Chronic respiratory failure develops over several
days or longer, allowing time for renal
compensation & an increase in bicarbonate
concentration. Therefore, the pH usually is only
slightly decreased.
14. Radiography
• Frequently reveals the cause
Echocardiography
• Not be performed routinely, useful test when a
cardiac cause of acute respiratory failure is
suspected.
15. Management
• Cardiac monitoring, blood pressure, pulse oximetry
& capnometry are recommended.
• Reverse/ prevent tissue hypoxia.
• Appropriate management of the underlying
disease
• Treated with O2 supplementation & ventilatory
assist devices
16. Diuretics
• First-line therapy generally includes a loop
diuretic such as furosemide, which inhibits
sodium chloride reabsorption in the ascending
loop of Henle.
Nitrates
• Nitrates reduce myocardial oxygen demand by
lowering preload & afterload.
Inotropic Agents
• The principal inotropic agents are dopamine,
dobutamine & digoxin.
17. Opioid Analgesics
• Morphine IV is an excellent adjunct.
• Reduces preload
• Causes arterial dilatation, which reduces
systemic vascular resistance and may increase
cardiac output.
Corticosteroids
• Effective in accelerating recovery from acute
COPD exacerbations & are an important anti-
inflammatory therapy in asthma.
18. Beta 2 Agonists
• These agents act to decrease muscle tone in
both small and large airways in the lungs.
• Includes beta-adrenergics, methylxanthines &
anticholinergics.
Anticholinergics
• Antagonize the action of acetylcholine with
muscarinic receptor on bronchial smooth
muscle.
19. Complications
• Pulmonary: Pulmonary embolism, barotrauma,
pulmonary fibrosis & complications secondary to
the use of mechanical devices.
• Nosocomial pneumonia
• Cardiovascular: Acute MI
• GI: Gastric distention, ileus, diarrhea, pneumo
peritoneum & stress ulceration
• Nosocomial infections
• ARF
• Nutritional: Malnutrition
20. Nursing diagnosis
• Impaired gas exchange
• Ineffective breathing pattern
• Impaired verbal communication
• Activity intolerance
• Self care deficit
• Impaired physical mobility
• Risk for impaired skin integrity
• Risk of imbalanced nutrition: less than body
requirement
left lung consists of an upper & lower lobe, whereas the right lung has an upper, middle, and
lower lobe. Each lobe is further subdivided into two to five segments separated by fissures, which are extensions of the pleura.
lobar bronchi (3R, 2L). segmental bronchi(10 R 8L) subsegmental bronchi, bronchioles, terminal bronchioles
whole process of gas exchange between the atmospheric air and the blood and between the blood and cells of the body is called respiration.
Diffusion- oxygen and carbon dioxide are exchanged at the air–blood interface.
Pulmonary perfusion is the actual blood flow through the pulmonary circulation.
Ventilation is the flow of gas in and out of the lungs, and perfusion is the filling of the pulmonary capillaries with blood.
lower pons stimulates the inspiratory medullary center to promote deep, prolonged inspirations
upper pons, control the pattern of respirations.
medulla & respond to chemical changes in the CSF fluid, an increase or decrease in the pH & change the depth & rate of ventilation to correct the imbalance.
aortic arch and the carotid arteries and respond first to changes in PaO2, then to PaCO2 and Ph
aortic and carotid bodies, respond to an increase or decrease in arterial blood pressure and cause reflex hypoventilation or hyperventilation
Hypoxemic respiratory failure is characterized by an arterial oxygen tension (PaO2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (PaCO2).
Hypercapnic respiratory failure is characterized by a PaCO2 higher than 50 mm Hg
Obstructive- hard to exhale. Asthma, emphysema, bronchitis
restrictive- difficulty fully expanding their lungs. Fracture, deformity
perfusion but no ventilation- shunt
ventilation but no perfusion- dead space
Alveolar hypoventilation- generator (CNS, Drug, lesions), pump(chest wall, NM system, Myasthenia, polio, Gbs), effector organs(lung, airways, copd,ards)
include restlessness, anxiety, confusion, seizures, or coma.
may result from hypoxemia and acidosis.
Enlargement of the right ventricle from hypertrophy or dilation or as a secondary response to disorders that affect the lungs
suspected on clinical grounds, This helps assess the severity of respiratory failure and helps guide management.
indicate anemia, contribute to tissue hypoxia, polycythemia may indicate chronic hypoxemic respiratory failure.
To exclude MI
Once the airway is secured, attention is turned toward correcting the underlying hypoxemia, the most life-threatening facet of acute respiratory failure. The goal is to assure adequate oxygen delivery
Correction of Hypoxemia
renal hypoperfusion & the use of nephrotoxic drugs
