Respiration insuficiciency

Created by Jiří Kofránek

Struktura přednášky

Respiratory insufficiency (failure)

https://www.wikilectures.eu/w/Respiratory_insufficiency

symptoms

Cardiopulmonary monitoring

https://www.wikilectures.eu/w/Cardiopulmonary_monitoring

Stuffiness

But even with anemia

cardiac failure - mainly of the left heart (pulmonary edema)

Tachypnoea

auxiliary muscles

Cyanosis

>=50 g O2/l reduced Hb

150 g/l <75%

in anemia will not

50 g/l - anemia, pale

polycythemia vera >165 g/l men 160 women

JAK2 mutation clonal mutation (cyanosis)

g/l *0.06205784→ mmol/l

mmol/l*16.114→ g/l

central

differentiated from peripheral - tongue

but be careful . peripheral can be masked by hypoperfusion (fingers are pale)

peripheral

disturbances of consciousness - disorientation - up to delirium

https://www.wikilectures.eu/w/Glasgow_Coma_Scale

GCS, 15-13 OK, 12 -9 moderate, 8-3 impaired consciousness

GCS 15 ok

Respiratory rate

Respiratory rate above 22 - saturation OK,

Respiratory rate 30 - attention

I measure

O2 saturation

90% - PO2 60 mmHg

Respiratory rate above 22 - saturation OK,

Respiratory rate 30 - caution

O2 and CO2 saturation curves

https://egolem.online/bloodgases/#pribeh2a.md

Masks the decrease in saturation

Oxygen supplementation

Heart rate

Horowitz Index (1970)

PaO2/FiO2 norm 100 mmHg/0.21 = approximately 500 (300-500 is the norm)

P-F ratio PaO2 300-500 is the norm

300 - 200 mild damage

200-100 moderate damage

100 and less - severe damage (ARDS)

https://en.wikipedia.org/wiki/Horowitz_index

Astrup

PaO2 <60 mmHg

(60 mmHg corresponds to approximately 90% saturation)

PCO2 > 50 mmHg

pH <7.3 -> consider artificial ventilation

according to the laboratory

Type 1 partial (hypoxic)

Low PaO2

PaCO2 normal or low (respiratory alkalosis)

PaO2 <60 mmHg

PaCO2 normal or low → RALK

Early in lung disease (before respiratory muscles become fatigued)

Type 2 global (hypoxic-hypercapnic)

PaO2<60 mmHg

PaCO2 >50mmHg

according to time

Acute

Within a week

acute onset - aspiration, ARDS (3 days

Chronic

Months, years

can become acute

COPD, Asthma

Restrictive disease

Causes

hypoventilation

Obstruction

Diffusion

V/Q

Kyphoscoliosis

in seniors

Obesity

Muscular dystrophies (Duchene, ALS)

Myastenia gravis

antibodies against nicotinic receptors (to acetylcholine) ← Ig (worsens during the day)

Diaphragmatic fatigue (after tachypnoea)

CNS trauma, stroke

spinal cord injury C3-C5 (phrenicus)

opiates

pC02 will increase RAC

foreign body

Tumor, lymph nodes

Asthma, COPD

VA/Q

pneumonia

cardiogenic edema

noncardiogenic edema

ARDS

diffuse edema (ground glass X-ray)

wedge pressure <18 / cardiac cause ruled out

Acute respiratory distress syndrom v3.pptx

buffers

bicarbonate

protein

hemoglobin

phosphate (IC)

hyperventilation

Kussmaul breathing

sepsis, inspiration of gastric juice, hot air...

acute respiratory distress

Hyperventilation

Dogs with their tongues out hyperventilate dead space, not alveoli.

... while the alveoli do not hyperventilate - alveolar ventilation does not change

The goal is cooling - thermoregulation

Ventilation-without-perfusion - dead space

RL shunts

there is no ventilation and there is perfusion

12 / 5 000PO2 will decrease

breathing pattern low -CO2 - hypocapnia

O2 will not increase slightly increase

CO2 will decrease

compensation of respiratory acidosis

Oxygen delivery

Context