13 respiratory failure

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Respiratory failure

Guo Yubiao, M.D & Ph.D Pulmonary & Critical Care Medicine

The first Affiliated Hospital of Sun-Yat Set University

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Male, 32Fever, cough with sputum for 3 daysNo finding on physical examination

Diagnosis: pneumonia X － ray: shadow in left lower lobe

August 16, 2003

August 20, 2003

Acute shortness of breathAnxiety

• RR 40/min, Cyanosis• ABG: PaO2 61mm Hg(FiO2 1.0) PaCO2 35 mmHg, pH 7.20• X-ray: clouded glass• Diagnosis ： ARDS Acidosis

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Intubation via mouthtracheotomy

Monitoring and ventilation

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Contents 0f outline

Definition

Etiology & Pathogenesis

Classification

Clinical manifestations

Diagnosis

Treatment

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Introduction

Be a frequently encountered medical problem A major cause of death in China Mortality from COPD, which ends in death from

respiratory failure, continues to increase More than 70% of patients with pneumonia are

attributed to respiratory failure About 1/3 patients in ICU in the United States,

about 500 000 persons, receive mechanical ventilation each year

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Introduction (cont.)

Short-term survival is more than 80% for acute respiratory failure not preceded by additional lung disease or systemic illness

Multi-system organ failure or pre-existing renal, liver, or chronic gastrointestinal disease with malnutrition substantially worsens outlook

About 17% of patients placed on mechanical ventilation require assistance for more than 14 days

Among those requiring this amount of mechanical ventilation, elderly patients have a 9% survival and younger patients a 36% survival

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Definition

Be a clinical syndrome of respiratory and metabolism dysfunction caused by any condition that severely affects the lung’s ability to maintain arterial oxygenation or carbon dioxide elimination.

Both acute or chronic respiratory failure may be divided into two main categories.• A failure of gas exchange – hypoxemia• A failure of ventilation – hypercapnia

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Classification

According to pathophysiology and arterial blood gas analysis: Type I: A failure of gas exchange

Hypoxemia, PaO2 < 60 mmHg Type II: A failure of ventilation

PaO2 < 60 mmHg, PaCO2 > 50 mmHg

PaO2 > 60 mmHg, PaCO2 >50 mmHg

Iatrogenic

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Classification

According to the involved site• Central respiratory failure

• Change of respiratory rhythm and frequency • Peripheral respiratory failure

• Dyspnea According to onset of respiratory failure

• Acute, develops in seconds or hours• Chronic, develops in days or longer, elevated HCO3-• Acute onset of Chronic respiratory failure• Have no definitive borderline

According to mechanisms• Pump failure• Lung failure

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Etiology

Airway obstruction• Airway inflammation, tumor, foreign bodies, fibrosis scar COPD and

asthma Alveolar or interstitial lung diseases

• pneumonia, emphysema, pulmonary tuberculosis, diffuse interstitial pulmonary fibrosis, pulmonary edema

Pulmonary vascular diseases• Pulmonary embolism, pulmonary vasculitis

Chest wall or pleural diseases• Flail chest caused by trauma, pneumothorax, severe spinal

deformity, massive pleural effusion Neuromuscular diseases

• Cerebrovascular diseases, craniocerebral trauma, cerebritis and sedative-hypnotic, poliomyelitis, polyneuritis, myasthenia gravis

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Respiratory Pump Failure（泵衰竭）

Pump failure is caused by dysfunction of respiratory pump

Low respiratory drive due to central or peripheral nervous system diseases, neuromuscular junction problem or fatigue of respiratory muscles→hypoventilation

manifested as type Ⅱ respiratory failure

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Lung Failure （肺衰竭）

Lung failure is caused by disorder of lung parenchyma, pulmonary vascular or airway obstruction

Airway obstruction → hypoventilation ， manifested as type Ⅱ respiratory failure

Disorder of lung parenchyma → dysfunction of oxygenation, manifested as hypoxemia

Disorder of pulmonary vascular system → ventilation/perfusion mismatch, manifested as hypoxemia

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Mechanisms & Pathophysiology

Hypoxemia• Alveolar ventilation ↓

• FiO2↓

• Diffusion abnormality• V/Q mismatch• A-V shunt

Hypercapnia(CO2 retention)• CO2 production↑

• Alveolar ventilation ↓

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Mechanisms of hypoxemia

FiO2↓• Altiplano or under a deep

well

• PAO2 & PaO2 ↓

Hypoventilation• VA = VE – VD

• The diffusion capacity of CO2 is 20 times of that of O2

25 20 15 10 5

肺泡分压(k

Pa)

0 2 4 6 8 10 肺泡通气量 (l/min)

PACO2

PAO2

PACO2 =0.863*VCO2/VA

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Mechanisms of hypoxemia –– Diffusion abnormality ( 弥散障碍 )

The factors that influence rate of gas diffusion across the respiratory membrane include: the partial pressure difference of the

gas between the two sides of the membrane,

the surface area of membrane the time of contact between blood

and alveoli the permeability of the membrane

Diffusion abnormality manifested as hypoxemia

100

80

60

40

动脉氧分

压

0.25 0.5 0.75 血液通过肺泡毛细血管时间

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Ventilation/perfusion mismatch （通气 / 灌流失衡）

Shunt （肺动 - 静脉分流）

V/Q=0.8V/Q>0.8 V/Q<0.8

Q > V(A-V shunt)

Normal V > Q(dead space effect)

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( 二 ) 通气 / 血流比例 V/Q

肺泡死腔通气 V/Q>0.8

静 - 动脉分流 V/Q<0.8 正常通气 / 血流 V/Q 0.8

VD PaCO2 － PeCO2

VT PaCO2

Qs CcO2 － CaO2

QT CcO2 － CvO2

VA 4.2L(R2.1, L2.1)

Q 5.0L(R2.5, L2.5)

见于肺不张， ARDS 见于 COPD正常


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Oxygen consumption, Oxygen consumption, (VO2 )(VO2 ) ↑↑::fever, chill, dyspnea, fever, chill, dyspnea, twitch (eg, 500ml/min)twitch (eg, 500ml/min)

Oxygen delivery (DOOxygen delivery (DO22 ）↓）↓ , Palev O2 , Palev O2 ↓↓ 800

100

20

10

肺泡氧分压

2 4 6 8 10 肺泡通气量 (l/min)

400

动脉氧分压(k

Pa)

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Mechanisms of hypercapnia

CO2 production↑:

• fever, infection, sepsis, epilepsy

Alveolar ventilation ↓• neuromuscular diseases or fatigue of respiratory muscles• obstructive ventilation disorder

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Influence of hypoxemia Central nervous system

Oxygen consumption of brain--3 ml/100g·min If jugular vein PaO2 <20mmHg:

unconsciousness, coma PaO2 <20mmHg: irreversible damage to nerve

cells in several minutes (4~5min) Mild hypoxemia: impaired concentration,

disorientation, hypomnesia Severe hypoxemia: dysphoria,

unconsciousness, coma

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Influence of hypoxemiaCardiovascular system

Myocardium oxygen consumption: 10 ml/100g/min

Early stage of acute hypoxia–stimulation of sympathetic nerve→HR 、 BP 、 CO

Chronic hypoxia → small pulmonary arteries contraction → pulmonary hypertension— Cor pulmonale

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PaO2↓ (<60mmHg) →stimulate the chemoreceptors → stimulate respiratory center → strengthen respiratory movement, MV , respiratory distress

PaO2↓(<30mmHg)→inhibition of respiratory center>stimulation of respiratory center → respiratory depression

Hyperventilation→CO2↓→inhibition of respiratory center

Severe hypoxemia → slow shallow irregular respiration or Cheyne-Stokes respiration

Influence of hypoxemiaRespiratory system

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Influence of hypoxemiahaematological system

Chronic hypoxemia →stimulate hematopoiesis of bone marrow → EPO production RBC haemoglobin saturation & O2 Delivery

capacity blood viscosity ， blood stream resistance

→ cardiac load & CO hypoxemia and blood viscosity → the risk of DIC

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Influence of hypoxemiaRenal & Digestive system

Renal blood vessels contraction, blood supply ↓when accompany with hypotension, DIC → Renal failure

Gastric mucosal erosion, necrosis, ulcer and bleedingHepatic cell impairment by hypoxia → ALT↑ ， jaundice

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Influence of hypercapnia Central nervous system

Cerebral blood flow: PaCO20.133kPa ， blood flow 4% → headache, intracranial pressure

Cerebrospinal fluid: H+ 、 HCO3 、 CO2enter blood-brain barrier →[H+] →stimulate subcortex & excitability

Consciousness: dizziness, asterixis, somnolence, coma, convulsion

Peripheral nerves: sympathetic nerve, adrenal gland, distal nerves ， catecholamine(CA)

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Influence of hypercapnia Cardiovascular system

HR, CO , BP With stimulation of sympathetic nerve, the skin and

abdominal vessels contract while coronary vessels dilate

Severe hypoxia and hypercapnia → directly inhibit cardiovascular center → depressed cardiac function, dilated vessels → BP↓, arrhythmia

Acute severe hypercapnia → ventricular fibrillation or cardiac arrest especially during intubation procedure

PaCO2 enhance cardiac inhibition by vagus

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Influence of hypercapnia Respiratory system

Stimulate respiratory center → strengthen respiratory movement, Ventilation

(PaCO2 0.133 kPa ， Ventilation volume 2 L/min)

Slight contraction of small pulmonary arteries Directly relax the bronchial smooth muscle PAO2 PaCO2 → rightward shift of the oxyhaemoglobin

dissociation curve (ODC)

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pH

pH

26.6mmHg

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Influence of hypercapniaurinary system

Mild CO2 retention →dilation of renal blood vessels → renal blood flow → urine

PaCO2 > 8 kPa, pH →renal blood vessels spasm → renal blood flow

HCO3 and Na+ reabsorption → urine

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Influence of hypoxemia & hypercapnia

Acid-base balance and electrolytes

Severe hypoxia → inhibition of cellular energy metabolism → insufficient energy production, production of lactic acid ↑ → sodium-potassium pump failure → metabolic acidosis, hyperkalemia → PCO2↑

Respiratory acidosis and metabolic acidosis pH is determined by HCO3/PaCO2 ratio

Slow CO2 retention → compensated by kidney, decreased elimination of HCO3

－

(It takes 1 ~ 3 days for kidney to compensate)

pH =HCO3

-

PaCO2

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Clinical manifestationAcute respiratory failure (1)

Dyspnea Dyspnea is a early symptom of respiratory failure. Increased breath rates Change in breath rhythm: Cheyne-Stokes respiration,

Biot’s respiration Accessory respiratory muscles involved in breathing → “three depressions sign”

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Cyanosis: Cyanosis is a typical sign of hypoxia, indicating arterial oxygen

saturation lower than 90%. The extent of cyanosis is associated with content of reduced

hemoglobin. So it is less readily detectable if anemia is present and more readily seen in polycythemia.

Peripheral cyanosis is associated with stasis, in which oxyhemoglobin is reduced more than it normally is because of the prolonged peripheral blood transit time, while the PaO2 could be normal.

Central cyanosis results from arterial hypoxemia.


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Neuropsychic symptoms: Mental disorder, mania, coma, convulsionCirculatory system: Tachycardia, myocardial impairment, peripheral circulatory

failure, hypotension, arrhythmia, cardiac arrest.Digestive system : Hepatic function impairment: ALT↑ Gastrointestinal tract: mucosal erosion, stress ulcer,

gastrointestinal bleedingUrinary system: Renal function impairment: BUN↑ Proteinuria, hematuria, casts in urine


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Clinical manifestationChronic respiratory failure

Dyspnea: Excessive respiratory effort, prolonged expiration——rapid

shallow breathing——slow shallow breathing, Cheyne-Stokes breathing (CO2 narcosis, severe respiratory depression)

Neuropsychic symptoms: Irritation caused by increased PaCO2 in early stage: insomnia

at night, drowsiness during the day Depression caused by pulmonary encephalopathy in late stage:

apathy, convulsion, coma, tendon reflex weakened or disappearCirculatory system: Peripheral vesodilation, skin congestion, warm and sweaty

extremities, BP↑, CO↑, pulsus magnus, HR↑, pulsatile headache

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Diagnostic criteria

History of respiratory dysfunction that severely affects the lung’s ability to maintain arterial oxygenation or carbon dioxide elimination

Clinical manifestation of dyspnea and cyanosis Blood gas analysis

PaO2 < 60 mmHg, or plus PaCO2 > 50 mmHg

Breathing air on sea level and standard atmosphere pressure at rest

Exclude intracardiac shunt and decreased cardiac output, such as ventricular septal defect

In fact it is a pathophysiology & laboratory Diagnosis

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Diagnostic criteria The acute respiratory distress syndrome

(ARDS)

ARDS is a process of nonhydrostatic pulmonary edema and hypoxemia associated with a variety of etiologies:

Progressive dyspnea and hypoxia which can not be relieved by oxygen therapy

Bilateral infiltrates on chest radiograph PaO2/FiO2 <200 Excluding patients with signs of heart failure or a

pulmonary capillary wedge pressure (PCWP) >18 mmHg

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Treatment (outline of principle)

Etiology Management Keep airway open Oxygen therapy Ensure adequate alveolar ventilation, correct CO2 retention

Respiratory stimulant Mechanical Ventilation

General supportive care Transfer to ICU for critical care and treatment Infection control Management of electrolyte and acid-base disturbance Management of cor pulmonale, pulmonary encephalopathy, multi-

organ dysfunction syndrome(MODS). Nutrition support

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TreatmentEtiology Management

Management of any underlying diseases : upper airway obstruction, severe pneumothorax, massive pleural effusions

Eliminate any factors that cause respiratory failure secondary to infection or shock

Any inducement leading to acute deterioration of chronic respiratory failure ： infection, malnutrition, inappropriate medication usage

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Causes of Upper Airway Obstruction

CNS depression-anesthesia, drug overdose

Cardiac arrest Loss of consciousness Foreign body or tumor

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Treatment Keep airway open 保持气道通畅

Importance of airway open : Airway obstruction: resistance ↑ → WOB↑ respiratory muscle fatigue difficult to clear airway secretion → infection

deteriorate atelectasis → the surface area of gas exchange Complete airway obstruction → apnea, deathClear airway secretion : mucolytics manual suction

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Treatment Keep airway open保持气道通畅

Bronchodilators for patients with bronchospasm: β2-adrenoreceptor agonist, anticholinergic,

glucocorticoid, theophyllineMode of administration : parenteral first and then inhaleMechanical ventilation+ medications deliveryAirway humidify & nebulize

Establishing artificial airwayEndotracheal intubation Tracheostomy

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TreatmentOxygen therapy

Indications of oxygen therapy : Pump failure: improve ventilation Pneumonia, Pulmonary embolism, acute

attack of asthma Severe pulmonary edema, ARDS Acute deterioration or worsening of COPD

(pay attention to CO2 retention when giving oxygen therapy! )

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Inspired oxygen concentration: Inspired oxygen concentration should be the lowest value that

results in an oxygen saturation of over 90% (PaCO2 about 60mmHg).

High concentrations of inspired oxygen (>35%) are safe in patients with type respiratory failure, as there is no risk of CO2 Ⅰretention.

While in patients with type respiratory failure, who are Ⅱdependent on hypoxic drive for ventilation, oxygen therapy must be carefully controlled so that sufficient oxygen is supplied but without precipitating severe respiratory acidosis.

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Oxygen delivery device: ① Nasal cannula/prongs:

Advantage: allow patients to eat, drink, expectorate and speak Disadvantage: FiO2 delivered is not stable and affected by breathing; high

flow rates irritate nasopharyngeal mucosa Guide: Delivers 4% Oxygen per liter flow;

FiO2 (%)=21+4×oxygen flow rate (L/min) Flow rates should be limited to less than 7L/min.

② Mask: Simple oxygen mask, nonrebreathing mask with reservoir bag, Venturi mask. Advantage: FiO2 delivered is comparatively stable and is adjustable; less

irritative to nasopharyngeal mucosa Disadvantage: inconvenient for patients to expectorate, eat and drink


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Nasal cannula/prongs鼻导管吸氧

鼻导管给氧的上限量为 6L/min，大于这一流量时，由于管道和鼻咽内产生涡流，吸氧浓度不再增加。

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Simple oxygen mask常规面罩

常规面罩可提供较稳定的氧浓度，其输送的氧浓度大约为70% -80% 但是这两种方法都不能精确地监测 FiO2。因为随呼吸频率、每分钟通气量、室内空气的流动、输氧装置的放置等因素的不同而改变。故影响纠正低氧血症并防止高碳酸血症的发生的治疗观察。

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Venturi mask Venturi 面罩

Venturi面罩可较精确地调整 FiO2，但面罩必须佩戴正确才能使预期的氧量得到输送

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Side effects Inhibition of respiratory center in patients with type Ⅱ

respiratory failure, who are dependent on hypoxic drive for ventilation CO2 retention ↑

Absorption atelectasis/denitrogenisation 吸收性肺不张 ): nitrogen is replaced by more absorptive oxygen

Oxygen poisoning : High concentrations of inspired oxygen injury of pulmonary capillary epithelium

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TreatmentEnsure adequate ventilation, correct CO2 retention

Respiratory stimulant: mainly used in CNS depression Principles for respiratory stimulant ( 呼吸兴奋剂 ) :

Maintain potency of airway to avoid respiratory muscles fatigue and deteriorate CO2 retention

Be cautious when used in patients with frequent convulsion caused by cerebral anoxia, cerebral edema

Suitable for patients with normal respiratory muscle strength Not suitable for patients only with oxygenation failure Avoid sudden withdrawal Drug: coramine, lobeline, doxapram

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TreatmentNon-invasive positive pressure ventilation, NIPPV

Indications Conscious and cooperative Stable circulation Be able to protect airway No facial trauma, injury and deformity Be endurable to mask

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Different kind of masks 各款口鼻面罩

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TreatmentMechanical ventilation

Goals of Mechanical Ventilation: improve alveolar ventilation, decrease PaCO2; improve pulmonary gas exchange; Decrease work of breathing, reverse respiratory muscle fatigue.

Indications for mechanical ventilation : apnea; upper airway obstruction; impaired airway protection; inadequate handling of secretions; acute hypercapnia that is not quickly reversed by appropriate specific

therapy; severe hypoxemia; progressive patient fatigue despite appropriate treatment.

Adjust modes and settings for mechanical ventilation according to blood gas analysis and clinical judgment

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TreatmentManagement of electrolyte and acid-base disturbance

Respiratory acidosis improve alveolar ventilation

Respiratory acidosis + metabolic acidosis Etiology management of acidosis improve alveolar ventilation appropriate alkali supplement

Respiratory acidosis + metabolic alkalosis Avoid Iatrogenic factors

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Education

13 respiratory failure