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MindMap Gallery Respiratory insufficiency mind map

Respiratory insufficiency mind map

Respiratory insufficiency refers to a pathological process in which the partial pressure of arterial oxygen (PaO₂) is lower than the normal range or accompanied by an increase in the partial pressure of carbon dioxide (PaCO₂) due to severe impairment of external respiratory function.

Edited at 2024-11-30 18:00:06

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Respiratory insufficiency mind map

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Respiratory insufficiency

Overview

Etiology and pathogenesis

Pulmonary ventilation dysfunction

obstructive hypoventilation

Central airway obstruction.

Extrathoracic obstruction (such as foreign body blocking the glottis): Inspiratory dyspnea is significant and there is a "three concave sign".

Intrathoracic obstruction (such as tracheal tumors): mainly expiratory dyspnea.

restrictive hypoventilation

Pulmonary causes

Severe pulmonary fibrosis and hardening of lung tissue caused by pulmonary edema.

Decreased alveolar surfactant

non-pulmonary causes

Organic diseases of central or peripheral nerves

Respiratory depression caused by overdose of anesthetics.

Decreased thoracic compliance

Large pleural effusion or tension pneumothorax compresses the lungs.

Alveolar hypoventilation

Oxygen inhalation and carbon dioxide discharge are blocked, the partial pressure of oxygen in the alveolar air decreases, the partial pressure of carbon dioxide in the alveolar air increases, and the blood flowing through the alveolar capillaries cannot be fully arterialized, resulting in a decrease in PaO2 and an increase in PaCO2.

Eventually leading to type II respiratory failure

Pulmonary ventilation dysfunction

diffusion disorder

Reduced alveolar membrane area

Due to the large reserve, ventilatory dysfunction will only occur when the alveolar membrane area is reduced by more than half.

Increased alveolar membrane thickness

When pulmonary edema, alveolar hyaline membrane formation, pulmonary fibrosis and alveolar capillary dilation or blood absorption lead to thickening of the plasma layer, the diffusion rate slows down due to the increase in diffusion distance.

Decreased diffusion time

When blood flow speed increases, the gas exchange time between bubbles and blood shortens. Patients with alveolar mesangial disease may develop hypoxemia during increased physical exertion.

Little alveolar-blood flow ratio disorders

Partial alveolar hypoventilation

Bronchial asthma, chronic bronchitis, airway obstruction caused by obstructive emphysema, etc. may lead to venous blood adulteration.

Partial alveolar blood flow is insufficient

Given pulmonary embolism, disseminated intravascular coagulation, pulmonary arteritis, pulmonary vasculature, etc.

Partial alveolar blood flow is reduced, VA/Q can be significantly greater than normal, and alveolar blood flow is small and ventilation is high, resulting in alveolar ventilation that cannot be fully utilized. This is called dead space ventilation, which can lead to a decrease in PaO2, and PaCO2 can be normal or decreased. It can also rise in extreme cases.

Increased anatomical shunting

Concept: A part of the venous blood flows directly into the pulmonary veins through the bronchial veins and very few intrapulmonary arterial-venous communicating branches.

To identify functional shunts and true shunts, inhaling pure oxygen for 30 minutes can effectively increase the PaO2 of functional shunts, while the PaO2 of true shunts has no significant improvement, and can be used to identify the two.

Changes in metabolic function

Acid-base balance and electrolyte disorders

Including metabolic acidosis, respiratory acidosis, respiratory alkalosis, and metabolic alkalosis.

respiratory system changes

Breathing exercises strengthen

It is compensatory in the early stage, increasing alveolar ventilation by deepening and accelerating breathing. Respiratory muscle fatigue: Long-term increased respiratory movement can lead to respiratory muscle fatigue, shallow and slow breathing, and reduced ventilation.

Pathological breathing patterns

Pathological breathing patterns: such as tidal breathing, paused breathing, etc., indicate damage to the respiratory center function.

Circulatory system changes

Early compensatory response: increased heart rate, increased cardiac output, and peripheral vasoconstriction to maintain blood pressure and tissue perfusion. Severe pulmonary heart disease: Long-term pulmonary hypertension leads to right ventricular hypertrophy and dilation, which can eventually develop into right heart failure.

Arrhythmia: Hypoxia, carbon dioxide retention and other factors can cause arrhythmia.

Severe pulmonary heart disease: Long-term pulmonary hypertension leads to right ventricular hypertrophy and dilation, which can eventually develop into right heart failure.

Drop in blood pressure: Severe respiratory insufficiency can cause serious damage to cardiac function, drop in blood pressure and even shock.

central nervous system changes

Pathogenesis of pulmonary encephalopathy

Hypoxia and carbon dioxide retention cause cerebral blood vessels to dilate and become congested

Hypoxia and acidosis damage the cerebral vascular endothelium and increase its permeability, leading to brain interstitial edema.

Acidosis can increase the activity of galuanic acid decarboxylase in brain cells, which increases the production of r-aminobutyric acid and leads to central depression.

Poisoning increases the activity of phospholipase and releases lysosomal hydrolase, causing damage to brain cells and tissues.

Hypoxia affects the function of potassium ions and sodium ion pumps on brain cell membranes, causing brain cell edema.

carbon dioxide anesthesia

When carbon dioxide retention causes PaCO2 to exceed 80mmHg, it can cause dizziness, headache, irritability, etc.

Changes in kidney function and gastrointestinal changes

Oliguria or anuria: Hypoxia and carbon dioxide retention can constrict renal blood vessels, reduce renal blood flow, and reduce glomerular filtration rate

Azotemia: Reduced renal function leads to the accumulation of metabolites in the body, and increases in blood urea nitrogen and creatinine.

Gastrointestinal mucosal damage: Hypoxia and carbon dioxide retention can cause gastrointestinal mucosal ischemia and hypoxia, leading to mucosal erosion and bleeding.

Digestive dysfunction: symptoms such as loss of appetite, nausea, vomiting, and abdominal distension.