respiratory failure
DESCRIPTION
Respiratory Failure. 男性 , 50 岁 , 患喘息性支气管炎 30 年 , 三年来常下肢浮肿 . 三天前因受凉发烧 , 咳嗽加重 , 咳黄痰 . 当日上午患者神志恍惚 , 嗜睡 . 查 : T 38℃, 颈静脉充盈 , 肝大 , 双下肢凹陷性水肿 . 血气分析 : pH7.29, PaCO 2 10.7kPa(80mmHg), PaO 2 7.33kPa(55mmHg). BE -5mmol/L 血清钾 5.5mmol/L. RESPIRATION 4 distinct mechanisms: Ventilation - PowerPoint PPT PresentationTRANSCRIPT
1
Respiratory Failure
2
男性 , 50 岁 , 患喘息性支气管炎 30 年 ,
三年来常下肢浮肿 . 三天前因受凉发烧 , 咳嗽加重 , 咳黄痰 . 当日上午患者神志恍惚 , 嗜睡 . 查 : T 38 , ℃ 颈静脉充盈 , 肝大 , 双下肢凹陷性水肿 . 血气分析 : pH7.29, PaCO2
10.7kPa(80mmHg), PaO2 7.33kPa(55mmHg). BE
-5mmol/L 血清钾 5.5mmol/L.
3
4
RESPIRATION
4 distinct mechanisms:
Ventilation
Gas exchange External respiration
Transport of oxygen and carbon dioxide in the blood
Internal respiration
5
The Process of External Respiration
Pulmonary gas exchange
PiO2 159mmHg
PAO2 102mmHgPACO2 40mmHg
Pulmonaryventilation
PaO2 40mmHgPaCO2 46mmHg
PvO2 100mmHgPvCO2 40mmHg
6
Definition of RF Disorders of external respiratory function
PaO2 <60 mmHg (8.0kpa) while breathing air at rest, with or without PaCO2 >50 mmHg(6.67kpa).
judgment standard: PaO2 <60 mmHg , PaCO2 >50 mmHg
hypotonic hypoxia with (or without) respiratory acidosis
7
respiratory insufficiency: It is a condition in which respiratory function is inadequate to meet body’s needs during exertion. However, respiratory failure does so in rest.
a kind of respiratory insufficiency
a severe respiratory insufficiency
8
Classification1. According to blood gas:
1) type (hypoxemic RF) :Ⅰ
PaO2 <60 mmHg (8.0kpa)
2) type (hypercapnic RF) : Ⅱ PaO2 <60 mmHg (8.0kpa) ,
with PaCO2 >50 mmHg(6.67kpa)
9
2. According to primary site
central
peripheral
3. According to duration
acute
chronic
10
Section 1 Causes and pathogenesis of
respiratory failure
11
Chest WallChest Wall(muscle, ribs)(muscle, ribs)
ConductingConductingAirwaysAirways
DiaphragmDiaphragm(muscle)(muscle)
LungsLungsGas ExchangeGas Exchange
Pe
Pi
12
• Pathogenesis of RF:
Disorders of external respiratory function
pulmonary ventilation disturbance
pulmonary gas exchange disturbance
13
• Causes of RF
Disorders of:
Central Nervous System
Spinal Cord
Neuromuscular System
the chest wall and pleura
the airway
14
Ⅰ.pulmonary ventilation disturbance
i. Types and Causes
restrictive hypoventilation
obstructive hypoventilation
15
Mechanisms of Breathing:Mechanisms of Breathing:
• DiaphragmDiaphragm
Rib CageRib Cage
ContractContract
DiaphragmDiaphragmVolumeVolume
• External Intercostal Muscles External Intercostal Muscles IntercostalsIntercostals
ContractContractto Liftto Lift
RibRibSpineSpine
RibsRibs VolumeVolume
16
component elements causing ventilation disturbance
Lung elastic resistance increased
High spinal cord damaged
Anterior angle cell damaged
Inhibition of R. center
phrenic nerve damaged
weakness of R. M
thorax wall damaged
Airway straitness or block
17
Causes and mechanisms: impaired activity of respiratory muscle (dysfunction of
CNS, neural, muscle etc.) decreased compliance of thorax (chest malformation ,
pleura fibrosis) decreased compliance of lungs (pulmonary edema ,
inflammation , fibrosis, insufficient surfactant) thorax fluidify or pneumothorax
1. Restrictive hypoventilation:
18
2. Obstructive hypoventilation :
central airway obstruction
peripheral airway obstruction
19
above the forfication (between the glottis and the carina)
obstruction locates out of thorax ( paralysis, edema or inflammation of vocal cords ) inspiratory dyspnea
obstruction locates within thorax
expiratory dyspnea
why?
1) central airway obstruction:
20
Phase of expiration
(Ptr > Patm)
Phase of inspiration(Ptr <Patm)
Phase of inspiration(Ptr>Ppl)
Phase of expiration(Ptr<Ppl)
The effects on the phase of respiration on an extrathoracic variable obstruction
The effects on the phase of respiration on an intrathoracic variable obstruction
Ptr—intratrachel pressure Ppl—pleural pressurePatm—atmospheric pressure
PtrPatm
PtrPatm
PtrPtr
Ppl Ppl
21
peripheral airway character:
Wall: thin,without cartilage support;
Diameter changes with respiration ;
keep tight connection to
surrounding alveoli
2) peripheral airway obstruction (diameter <2mm ) :
22
causes and mechanism: chronic obstructive pulmonary disease
(chronic bronchitis , emphysema), severe pneumonia, atelectasis ,etc.
→ equal pressure point is moved up expiratory dyspnea
23
Equal pressure point
normal person makes forced expiration
Emphysema patients makes forced expiration
point thatIntra-airway pressure
= extra-airway pressure
24
Mechanism of chronic obstructive pulmonary disease (COPD)
1. inflammation stimulation, airway wall became thickening
2. Airway smooth muscle contraction
3. Retention of inflammatory secretion in airway
→inelastic resistance ↑
→ a great amount of gas keep in alveoli
4. Alveolar wall was damaged → elastic pull to peripheral airway ↓ , collapse occur in forced expiration.
→expiratory dyspnea
25
ii. Alteration of PaO2 , PaCO2 in
pulmonary ventilation disturbance
PaO2↓
PaCO2↑ ( type II RF )
26
Ⅱ . Pulmonary gas exchange disturbance
27
28
Respiratory Membrane Respiratory Membrane (Air-Blood Barrier)(Air-Blood Barrier)
29
Pulmonary gas exchange disturbance
diffusion impairment VA / Q mismatch
anatomic shunt
30
i. Diffusion impairment
Causes: area of R-M thickness of R-M diffusion time
31
1. Area of R-M
Normal adult R-M: 80 m2
At rest, used R-M:35~40 m2
area of R-M : atelectasis , pulmonary consolidation , lobar resection, emphysema
32
2. Thickness of R-M : pulmonary edema, fibrosis, formation of pulmonary hyaline membrane, hydremia
33
Alteration of PaO2 , PaCO2
PaO2↓
PaCO2 : N or ↓
according to compensatory ventilation
why?
34
Oxygenation of Blood
35
PO2
13.33
10.67
8.00
5.33
2.67
0 0.25 0.50 0.75 s
PCO2( kPa )
6.13PvCO2
PvO2
PaO2
PaCO2
Blood gas change when blood circulating through lungs
Real line stands for normal person;
broken line stands for patients with increased thickness of R-M
36
• CO2 O2 CO2/ O2
• Solubility 51.5 2.14 24• Molecular weight 44 32• square root of MW 6.63 5.66 1.17• Diffuse coefficient ratio 20/1
CO2 diffusivity is higher than O2
37
At restAt rest ::
(( VVAA)) : : ~ ~ 4L4L
(( Q) Q) : : ~ ~ 5L5L
VVAA/Q /Q : : 0.80.8
ii. ii. Ventilation-Perfusion Mismatch
ratio
38
• Ventilation-Perfusion Coupling
39
1.Types and Causes1) Hypoventilation of Partial alveoli ( VA/Q↓ )
functional shunt or
venous admixture
• Causes : Disorders of trachea or alveolus
40
functional shunt : alveolar Ventilation ( VA ) ,
alveolar Perfusion (Q) have not VA / Q
accordingly , even due to inflammation
venous blood flowing through these units have not been totally arterialized and mixes into arterial blood, this process is called as functional shunt, also as venous admixture.
41
O 2 CO 2
V 血 A 血
42
O 2↓ CO 2
V 血 V 血
43
2) Low perfusion of Partial alveoli ( VA/Q↑ ) dead space like ventilation:
alveoli at diseased region have low perfusion,while ventilation is not decreased,
alveolar ventilation can not be fully used.
• causes : Disorders of pulmonary vessel(vessel inflammation, occlusion , spasm )
44
O 2 CO 2
V 血 A 血
45
O 2 CO 2
V 血 A 血
46
2. Alteration of PaO2 ,PaCO2
N
PaCO2
PaO2 ?
47
1) blood gas change in functional shunt Asthma C.bronchitis VA / Q functional shunt
PaO2 ,PaCO2
compensatory
respiration ventilation
health region diseased region VA / Q VA / Q PaO2 ↑ , CaO2+ , PaO2 ↓ ,
CaO2 ↓ PaCO2 ↓ CaCO2 ↓ PaCO2 ↑ , CaCO2 ↑
PaO2 ↓ , PaCO2 ?
PO2 and PCO2
Dissociation curve of O2 and CO2
C . O
2 an
d C
O2 (m
l/dl)
48
2) blood gas change in dead space like ventilation p. embolism P. arteritis, DIC VA / Q dead space like ventilation
other region Q
functional shunt health region diseased region VA / Q VA / Q
PaO2 ↓ , CaO2 ↓ PaO2 ↑ , CaO2 + PaCO2 ↑ , CaCO2 ↑ PaCO2 ↓ CaCO2 ↓
PaO2 ↓ , PaCO2 ?
PO2 and PCO2
Dissociation curve of O2 and CO2
C . O
2 an
d C
O2 (m
l/dl)
49
iii. anatomic shunt(true shunt)1 、 Under physiological conditionanatomic shunt: bronchia vein
venous blood pulmonary vein
A-V communicating branch
true shunt: there are totally no gas exchange in the blood flowing through anatomic shunt, so anatomic shunt also called as true shunt.
N : 2% - 3%
50
2 、 Under pathological conditionbronchiectasis flow of bronchial vein
shock flow of A-V shunt
true shunt
atelectasis
Consolidation like true shunt
of lung
PaO2 PaCO2
± or or
51
Ventilation disturbance ( PaO2↓
PaCO2↑ )
Gas exchange disturbancePaO2↓
PaCO2↑ ↓N )
restrictive
obstructive
diffusion impairment
V/Q mismatch
true shunt↑ ( V/Q=0 )
Hypoven-tilation
summary
RF
52
Section 2 The functional and metabolic
changes in RF
53
Total change direction
Dysf. of external R.
hypoxemia hypercapnia
Dist. of acid-base electrolyte
Effects on organ system
Com
p.
Discom
.
PaO2 < 60mmHgPaCO2 > 50mmHg
PaO2 < 30mmHg
PaCO2 > 80mmHg
54
Ⅰ. Acid-base Disorders and Electrolytes Disorders
i. Respiratory Acidosis——type Ⅱ RF : CO2 retention
Hyperkalemia: H+-K+ exchange Secretion from distal
renal tubules ↓hydrogen ion dissociate from H2CO3
carbonic acid
ii. Metabolic Acidosis ——Hypoxia →
production of lactic acid↑
excretion ↓
55
iii.Respiratory Alkalosis ----type I RFHypoxia compensation hyperventilation
→ PaCO2 ↓ Hypokalemia
56
Ⅱ . Respiratory system 1 、 Effects of PaO2↓and PaCO2↑
( 1 ) PaO2↓
PaO2 ↓ stimulate peripheral inhibit respiratory center
chemoreceptor excite respiration inhibit respiration
30mmHg<PaO2<60mmHg : excite respiration
PaO2<30mmHg : inhibit respiration
57
(2) PaCO2↑
• PaCO2 ↑ ( <80mmHg )→ stimulate center
chemoreceptor→respiratory center was excited→ventilation ↑
• PaCO2>80mmHg : respiratory center was
depressed
inhaling 30% O2
58
PaO2↓30~60mmHg
<30mmHg
peripheralchemoreceptor
Respiratory center
+
PaCO2↑>50mmHg
>80mmHg
-
The effects of PaO2↓and PaCO2 ↑ on R
centerchemoreceptor
+
-
59
2. Primary disorders of respiratory system1) pulmonary compliance↓
pulmonary juxtapulmonary-capillary extend reflex receptor
rapid light R. 2) obstructive hypoventilation→ins/exp dyspnea3) respiratory M. fatigue → contractibility of R.M. ↓ → rapid light R. 4) central RF: slow light R.,R. rhythm disturbance e.g.: tide-like R.
60
Tide-like R.(Cheyne-Stokes
Breathing)
Over low central excitability → R.pause→ PaCO2 ↑ → R.
center was stimulated →R occur→CO2was expelled out →
R. central excitability became very low
61
Ⅲ. cardiovascular system
cardiovascular center
Severe PaO2 ↓and PaCO2 ↑can inhibit
mild PaO2 ↓and PaCO2 ↑can excite
62
1 、 vasoconstriction and vasodilatation -blood redistribution :
• mild PaO2 ↓and PaCO2 ↑→ cardiovascular center → sympathetic nerve →norepinephrine → α-receptor
→ vasoconstriction• local metabolite(adenosine) → vasodilatation(heart)• direct effect → vasodilatation
→ blood redistribution skin, kidney, stomach-intestine: vasoconstriction brain, heart: vasodilatation
63
2 、 Heart : mild : heart rate ↑, myocardium contraction
force ↑,CO↑
severe: heart rate ↓, myocardium contraction,
force ↓, CO↓ ,blood pressure↓
right heart failure
64
3. Cor pulmonale• concept: Cor pulmonale is right heart
hypertrophy and even failure, which is caused by RF.
• Mechanism of Cor pulmonale :
65
1) pulmonary hypertension :• pulmonary arteriole contraction : hypoxemia , hypercapnia →blood hydrogen ion [H+ ] ↑ →chemoreceptor → pulmonary artery contraction
• Pulmonary vessel becomes sclerosis, stegnosis : chronic RF → pulmonary arteriole contracts long-standing and
oxygen deficit long-term → pulmonary vessel’s smooth muscle cell and fibroblast become hypertrophy and proliferation.
• Some pulmonary disorders effects:
pneumonia , pulmonary fibrosis → pulmonary vessel became twist
66
2) cardiac diastole and contraction were confined : intrathoracic pressure ↑; hypoxemia, acidosis 3) resistance of blood flow is increased :Hypoxemia compensation RBC increased →blood became ropiness
67
Ⅳ. CNS1. PaO2 ↓ :• PaO2 decreased to 60mmHg →intelligence and
eyesight slight impairment
• PaO2 decreased to below 40~50 mmHg
→a series symptom of nerve and consciousness.
• PaO2 decreased to 20mmHg → nerve cell will become irreversible damaged
68
2. PaCO2 ↑ : PaCO2 is higher than 80mmHg→ carbon dioxide narcosis : headache, dizziness, dysphoria, flapping tremor, mental disorder , drowsiness, hyperspasmia, respiratory depression ,coma, even death
69
3.pulmonary encephalopathy:a kind of brain dysfunction caused by RF.
Mechanism:1) brain vessel :• hypoxia→ brain vessel dilation, blood flow↑ →brain
congestion• acidosis → blood vessel endothelium(BVE)
permeability↑ → brain interstitial tissue edema → intracranial pressure ↑, to oppress brain vessel
→ischemia, hypoxia, acidosis became severe
70
2) brain cell :• hypoxia → ATP↓,Na+-K+-ATPase↓→ brain cell edema• acidosis → glutamic acid decarboxylase (GAD ) activity ↑ → GABA↑ • acidosis → phospholipase ↑ → lysosome enzyme release → nerve cell and tissue damage
71
Ⅴ. kidney :
PaO2 sympathetic nervous system
renal blood vessel contract
renal blood flow
functional renal failure (oliguria, azotemia, metabolic acidosis)
72
Ⅵ . gastrointestinal tract : hypoxia and acidosis → excitation of sympathetic nerve → gastrointestinal tract wall vessel contraction (large amount of receptor) → ischemia CO2 retention→↑activity of carbonic anhydrase (CA) in acid cell in stomach →secrete more acid → pH of gastric juice ↓
→ gastrointestinal mucous membrane erosion,necrosis, bleeding ulcer
73
Section 3 Treatment Principle
74
1. Etiology treatmentCorrecting the cause and relieving the hypoxia
and hypercapniae.g. use of bronchodilators, antibiotics for respiratory infections,
establishment of airway (using endotracheal tube )
75
1) General Oxygen Therapy ( typeⅠ ): <50%O2
2) Controlled Oxygen Therapy ( typeⅡ ) :
Continuous low concentration (<30%O2 )
Low flux (1~2L/min)
2. Oxygen therapy
PaO2 =50 ~60mmHg
76
3. To decrease PaCO2
1) To unblock airway2) To strengthen respiratory driving force3) Artificial assisted respiration(mechanical ventilator) 4) To add nutrition
4. Treating the consequences of hypoxemia and hypercapnia
e.g. acidosis, heart failure.
77
Case analysisA man, fifty years old, has had bronchitis for thirty years. His lower limb often became swollen the latest three years. He caught a cold three days before and coughed aggravatly with yellow sputum. He became wandering and drowsiness in the morning of the day going to hospital.
P.E.: T 38 (centi-degree ), jugular vein engorged ℃ , liver swelling, double lower limb spitting edema.Blood gas: pH7.29, PaCO2 10.7kPa (80mmHg), PaO2 7.33kPa (55mmHg),BE -5mmol/L,serum K+ 6.5mmol/L.
Please answer the following questions:
1) What pathological processes are there existing in the patient? What are the pathogenesis?
2) What should we pay attention to when the patient inhaled oxygen?
78
DemandsTo grasp1. the concept and pathogenesis of RF2. the concept and pathogenesis of Cor pulmonale, and pulmonary
encephalopathy
To be familiar with1. The functional and metabolic changes in RF2. principle of inhaling Oxygen for type II RF
To learnTreatment Principle of RF