respiratory failure sevda Özdoğan md, prof. chest diseases

RESPIRATORY FAILURE

Sevda Özdoğan MD, prof.Chest Diseases

Definition

If PaO2 <55 mmHg and/or PaCO2>45 mmHg in arterial blood gas values of a resting person who inhales room air on the sea level, the condition is called Respiratory Failure

Respiratory failure is a condition in which the respiratory system fails in its gas exchanging functions.

Normal ABG values

pH 7.35 – 7.45

PCO2 35 – 45 mmHg

PO2 80 – 100 mmHg

HCO3 22 – 26 mmol/L

BE -2 - +2

SaO2 >95%

Acidosis Alkalosis

pH < 7.35

PCO2 > 45

HCO3 < 22

pH > 7.45

PCO2 < 35

HCO3 > 26

Respiratory Acidosis

Think of CO2 as an acid

failure of the lungs to exhale adequate CO2

pH < 7.35

PCO2 > 45

CO2 + H2CO3 pH

Metabolic Acidosis

failure of kidney function

blood HCO3 which results in availability of renal tubular HCO3 for H+ excretion

pH < 7.35 HCO3 < 22

Respiratory Alkalosis

too much CO2 exhaled (hyperventilation)

PCO2, H2CO3 insufficiency = pH

pH > 7.45 PCO2 < 35

Metabolic Alkalosis

plasma bicarbonate

pH > 7.45 HCO3 > 26

Definition

If PaO2 <55 mmHg and/or PaCO2>45 mmHg in arterial blood gas values of a resting person who inhales room air on the sea level, the condition is called Respiratory Failure

Respiratory failure is a condition in which the respiratory system fails in its gas exchanging functions.

Classification

Acute Chronic

Hypoxemic Hypercapnic (Mixed)

Acute Respiratory Failure (ARF)

Characterized by acute life-treatening (reversible) derangements in ABG and acid-base status

Usually the patients do not have an underlying pulmonary disease

As the CO2 values increases rapidly respiratory acidosis occurs Kardiogenic pulmonary edema Respiratory depressing drug intoxications

Acute respiratory failure can occur in patients who already have chronic respiratory failure Eg: Acute exacerbations in advanced

COPD patients 5 mm Hg or more increase in the

stable PaCO2 value is diagnostic

Chronic Respiratory Failure (CRF)

Develops over several days or longer and may be clinically inapparent

Patients have an underlying disease Neuromusculer disease Advanced interstitial lung disease etc

Chronic hypoxemia and/or hypercapnia is irreversible with slow progression

Hypercapnia is compansated by metabolic alkalosis so pH remains in normal limits

Hypoxemic Respiratory Failure(Type I; Pulmonary Failure)

PaO2< 55 mmHg PaCO2 normal or decreased Acute and chronic forms of HRF can not

be differentiated only by ABG analysis Polystemia and corpulmonale is common

in chronic hypoxemia The initial signs of acute hypoxemia are

usually confusion and neurologic signs due to cerebral edema (impaired tissue oxygenation)

Tissue oxygenation is not only affected by PaO2 but also by cardiac output and hemoglobine concentration

Three pathophysiologic mechanisms account for the hypoxemia

Ventilation/Perfusion (V/Q) mismatch

Decreased perfusion in the areas of good ventilation (dead space ventilation)seen in

pulmonary embolism, pneumothorax asthma localised pneumonia,

Right to left shunt Perfusion of nonventilated areas of the

lung causes right to left shunt Massive pulmonary hemorragie, drowning, diffuse pneumonia, pulmonary edema (ARDS or Cardiac)

Diffusion limitation Thickening in the alveolocapillary

membrane causes diffusion abnormalities İnterstitial lung diseases

Hypercapnic Respiratory Failure(Type II; Pump failure)

PaCO2>45 mmHg and pH<7.30 in acute form (Respiratory acidosis) Eg: Drug overdose Trauma Cerebrovascular accident Infections

Chronic hypercapnia is compansated by metabolic alkalosis so pH remains within normal limits Neuromusculer diseases Thorax deformities Advanced COPD

Hypercapnic Respiratory Failure

Two pathophysiologic mechanisms account for the hypercapnia Alveolar hypoventilation

A decrease in minute ventilation without dead space ventilation cause hypercapnia (CNS, neuromusculer or chest wall diseases) PaO2 is also decreased but (PAO2-PaO2) is normal

V/Q mismatch Dead space ventilation is increased with

normal minute ventilation (airway diseases like COPD, asthma)

Hypoxemic Type I Pulmonary failure

V/Q mismatch Pneumonia, p.embolism, pneumothorax, asthma

Shunt Pneumonia, Kong.heart failure, Pulm.edema, DAH, ARDS, gastr.aspir, drowning

Diffusion limitation Fibrotic lung disease

Hypercapnic Type II Resp.pump failure

Alveolar hypoventilation CNS diseases (Drug, cerebral infarct, trauma, hypothyroidism), Neuromuscular diseases (Guillan-Barre, myastenia, MS, resp.muscle diseases),Chest wall diseases (pain, morbid obesity, Kyphoscoliosis)

V/Q mismatch COPD, Asthma, Cystic fibrosis

Types of respiratory failure and and the frequent causes

Perioperative Type III

Atelectasis Decreased FRC (supine position, obesity, upper abd incision, anesthesia)İncreased closing volume (overhydration, bronchospasm,increased secretions)

Shock Type IV

Hypoperfusion Cardiogenic (MI, Cardiac tamponade, PAH)Hypovolemic (Bleeding, dehydration)Septic (Endotoxemic, bacteriemic

Alveoloarterial oxygen gradient (PAO2-PaO2)

PAO2-PaO2=[PıO2-PaCO2/R]-PaO2

PıO2: inspired PO2R: Respiratory exchange ratio=0.8

PıO2 =(PB-PH2O)(FiO2)

(760-47)(21) = 149

PAO2-PaO2=[PıO2-PaCO2/R]-PaO2

=[149-PaCO2/0.8]-PaO2

Acute Hypoxemic Respiratory Failure:Acute Respiratory Distress Syndrome

(ARDS)

Acute severe alteration in lung structure and function due to several causes. It is characterized by acute dyspnea, severe hypoxemia, diffuse radiographic infiltrates.

It is a pulmonary edema due to increased vascular permeability

Risk Factors for ARDS

Direct insult Pulmonary contusion* Toxic gas inhalation* Neardrowning Pulmonary infection* Gastric aspiration* Pulmonary embolism Thoracic radiation Radiologic Contrast

Indirect insult Septisemia* Multisystem trauma* Hypertransfusion* Acute pancreatitis Drug overdose

(Neurogenic) DIC Cardiyopulmonary by-

pass High altitude Lung reexpansion

Insult direct/indirect

Inflamation

CellularNeutrophylMacrophage/monocytLymphocyt

HumoralComplemanCoagulation, Fibrinolysis

MediatorsCytokinesLipid mediatorsOxygen radicalesProteasesNitric oxidGrowth factorsNeuropeptides

Direct insult Pulmonary epithelium

and alveoli are subjected to the initial injury

Alveolar filling by edema, fibrin, collagen, neutrophlic aggregates and/or blood

Pulmonary consolidation

Indirect insult pulmonary

endothelial cell is subjected to the initial injury by mediators released from extrapulmonary foci

Microvessel congestion and interstitial edema

Intra-alveolar spaces are relatively spared

Pulmonary arterial pressure is increased in ARDS (>30 mmHg)

Clinical manifestation

Acute dyspnea, hypoxia, bilateral diffuse infiltration occuring most often 12-48 hours of the predisposing event (up to 5 days)

Diagnosis: Chest radiogram ABG analysis Risk factor evaluation

Hypoxia is refractory to oxygen treatment

There are no signs of left atrial hypertension (Pulmonary wedge pressure <18 mm Hg)

ALI/ARDS

Oxygenation Chest radiograph

Pulm Arterial Wedge Pressure

ALIPaO2/FIO2<=300 mmHg

Bilateral interstitial/alveolar infiltrates

<= 18 mm Hg/ no sign of left atrial hypertension

ARDSPaO2/FIO2<=200 mmHg

Bilateral interstitial/alveolar infiltrates

<= 18 mm Hg/ no sign of left atrial hypertension

Diagnostic criteria for ALI and ARDS

Differential diagnosis

Cardiac pulmonary edema

Infectious causes that cause diffuse pulmonary infiltrates and acute respiratory failure

Non infectious causes

Infectious causes of acute respiratory failure

Bacterial pneumonia

(S aureus, streptococus, legionella, salmonella, tb, mycoplasma, chlamydia)

Viral pneumonia(CMV, RSV, HSV,

VZV, adenovirus, influensa)

FungiH capsulatum,

coccidioides immitis, cryptococcus)

Parasites(PCP, Toxoplasma,

strongiloides stercoralis)

Noninfectious causes of acute respiratory failure

Cardiovascular Congestive heart failure

Drugs Aspirin Heroin Toxic gas inhalation Tricyclic antidepressants Acute radiation

Idiopathic Acute eosinophyl.pn Acute interstitial pn BOOP Idyopatic inters. Pn sarcoidosis

Immunologic Acute lupus pneumonitis Goodpasture’s sydr İdy. Hemosiderosis Hypersensitivity pn Pulmonary vasculitis with

hemorragia Metabolic

Alveolar proteinosis Neoplastic

Lymphangitic carsinomatosis

Leukemic infiltration Lymhoma

Miscellaneous Fat, amnion embolism High altitude edema

Treatment

Treatment of the predisposing factor

Cardiovascular supportive care Mechanic ventilation Fluid management

Pharmacological treatment

Cardiogenic Pulmonary Edema

Radiology of cardiac edema with central alveolar consolidation (bat wing pattern)

Increased cardiothoracic index Increased pulmonary wedge

pressure (>18 mm Hg)

Radiology of non cardiac pulmonary edema with the differences of cardiac edema

Cardiogenic pulmonary edema

Radiology of a casulty of 1999 Izmit earthquake (ARDS)

15.July

16.July

17.July

22.July

ARDS due to Gr(-) sepsis

21.May

23. May

26. May

21. May

29 .May

ARDS occured 24 hours after a traffic accident. Resolution due to MV on May 26 but progression on May 29

Pulmonary edema

Positional redistribution of the densities due to gravity

Ground grass appearance and pneumotocel formation on CT

Prognosis of respiratory failure

Morbidity and mortality depends on degree of respiratory failure and the underlying disease

Mortality is higher in old age with acute hypercapnic respiratory failure

In COPD patients with acute respiratory failure mortality is 10-20%

In ARDS patients mortality is around 50%