Respiratory Failure Acute/Chronic Dr S Bianchi

Outline Structure & Function Control of Breathing Causes of Respiratory Failure Classification of Respiratory Failure Treatment Options in Respiratory Failure

Structure & Function

Respiratory Muscles and Work of Breathing: Health Rhythmic pumping of gas in and out of the lungs Inspiration mainly due to diaphragmatic function Expiration through passive relaxation Inspiration Overcoming elastic recoil of lungs (very small) Overcoming flow resistance (very small) Expiration Low energy expenditure

Respiratory Muscles and Work of Breathing: Disease Increased muscle activation and use of accessory muscles Inspiration Hyperinflation (COPD/Asthma) – increased elastic work (rubber band) Increase resistive work secondary to increased flow/respiratory rate Expiration Activation of expiratory muscles to overcome bronchoconstriction Consider effect of muscle weakness/paralysis versus increased airflow resistance Load versus capacity

Ventilation patterns (volunteer) Health Disease Airway Obstruction (Asthma/COPD)(straw) Expansion of ribcage, increased accessory muscle use, increased diaphragm work, inspiratory reduction in basal thoracic diameter (Hoover’s sign), increased expiratory abdominal muscle work. Airway Restriction (Obesity/Respiratory muscle weakness) Small amplitude chest excursion, reduced lung volumes, parameters often worse when supine.

Control of Breathing Beware the night! CORTEX ‘Wakefulness drive’ BRAINSTEM Central Chemoreceptors CAROTID SINUS Peripheral Chemoreceptors LUNGS Ventilatory output High pCO2 = + Low pO2 = + Awake = + Asleep = - CO2/O2 Negative Feedback loop Beware the night!

Stimuli & Control of Breathing Causes of Hypoxaemia (Pulse oximetry) Low FiO2 (altitude) Diffusion problems (fibrosis, COPD, heart failure, pulmonary hypertension etc.) V/Q mismatching (pneumonia, PE, COPD etc) Hypoventilation (muscle weakness, drugs, stroke, obesity, malnutrition etc.) Alterations in pCO2 Secondary to alveolar ventilation only pCO2 offers a better insight into ventilatory performance THM: VENTILATION (NOT OXYGENATION) IS IMPORTANT

Considerations in Respiratory Failure Central (brain/chemoreceptors) versus peripheral (lungs/muscles) Increased demand (load) versus inadequate response (capacity) Is the patient normal or is pre-existing disease present? Acute versus Chronic: all the same except the speed at which it develops

Disturbance of Central Control Cheyne-Stokes Respiration Alternating hyper/hypoventilation (60 second cycle) Severe cardiac disease Secondary to slow perfusion of peripheral chemoreceptors Agonal breathing Pre-terminal patients or opiate poisoning Groups of 4-8 breaths alternate with complete apnoea Hypoventilation OHS, hypothyroidism, respiratory muscle weakness, post sedation, REM sleep, loop diuretics causing metabolic alkalosis Hyperventilation Hyperthyroidism, post cortical CVA, liver cirrhosis, metabolic acidosis, anxiety and stress Overriding of normal drives by ‘emotional centres’, reticular activation centre and sympathetic nerves

Normal resting ventilation Cheyne-Stokes Respiration Idiopathic hyperventilation Diabetic acidosis (Kussmaul breathing)

Disturbance of End Organ Function Failure of the ventilation pump Increased load Metabolic CO2 production (exercise/infection) Flow resistance of airways (COPD/asthma) Elastic recoil (COPD/Fibrosis) Reduced capacity Reduced central drive (opiates/CVA) Strength & endurance of respiratory muscles (Neuromuscular disease/Diaphragm palsy) Sleep LOAD CAPACITY LOAD ++ CAPACITY Inc PCO2 Dec PO2 LOAD CAPACITY -- Inc PCO2 Dec PO2

Classification of Respiratory Failure

Signs & Symptoms of Type 1 Failure Cyanosis Increased respiratory rate (tachypnoea) Accessory muscle use Tachycardia Hypotension/peripheral shutdown Signs of underlying disease Confusion …

Symptoms & Signs of Type 2 Failure Non-specific Dyspnoea Anxiety Orthopnoea Altered mentation Morning headaches Myoclonus/seizures Drowsiness Decompensation during sleep Disturbed sleep Daytime hypersomnolence Nightmares Witnessed apnoeas Frequent chest infections Impaired cough reflex Signs Confusion Drowsiness Warm peripheries Flapping tremor Bounding pulses Myoclonic jerks Papilloedema

Treatment Options ABC Treatment for underlying condition Oxygen therapy CPAP NIV IPPV Others

Continuous Positive Airways Pressure (CPAP) POSITIVE PRESSURE APPLIED THROUGHOUT THE RESPIRATORY CYCLE TO A SPONTANEOUSLY BREATHING PATIENT STICK YOUR HEAD OUT OF A CAR WINDOW….. IMPROVES OXYGENATION by improving VENTILATION and improving V/Q RATIOS DECREASES THE WOB (think about pushing a car from stationary versus pushing an already moving car) – stops ‘complete airway collapse’ Time Flow CPAP Used predominantly in Type 1 (hypoxic) respiratory failure

Non-Invasive Ventilation (NIV) BI-PHASIC positive airway pressure – increases ventilation Overcoming inspiratory resistance to flow Unloading the inspiratory muscles Augmenting alveolar ventilation Improving V/Q ratio in low V/Q areas Lowering alveolar PCO2 Increasing alveolar PO2 FLOW TIME EPAP IPAP Predominantly used in Type 2 respiratory failure

Other therapies Respiratory stimulants Act via effects on brainstem respiratory centres Only effective if adequate ventilation capacity Doxapram – iv analeptic drug Theophyllines – po + inotropic effect on muscles Progesterone – acts on hypothalamus – impotence Acetazolamide – CA inhibitor causing metabolic acidosis (via kidneys) Protryptiline – antidepressant Caffeine – neonates with apnoea Rarely used in clinical practice

Summary Structure & Function Normal versus abnormal Acute versus acute on chronic versus chronic Control of Breathing Central versus peripheral damage Causes of Respiratory Failure Load versus capacity Classification of Respiratory Failure Type 1 or Type 2 Acute versus Chronic Treatment Options in Respiratory Failure Treatment of underlying cause Oxygen, Modes of ventilation, Drugs