Respiratory Muscles

2 types of respiratory failure

(1) lung failure Þ gas exchange failure manifested by hypoxemia

(2) pump failure Þ ventilatory failure manifested by hypercapnia Þ fatigue, central depression, mechanical defect

Anatomy and mechanical actions

costal diaphragm – anterior and lateral aspects of thoracic cage (origin: lower rib cage; insertion: central tendon)

crural diaphragm – located on posterior aspect (origin: lumbosacral spine; insertion: central tendon)

inspiratory muscles – diaphragm, parasternal intercostals, sternocleidomastoid, scalene, ext. intercostals, trapezius

expiratory muscles – internal intercostals, abdominal muscles (transverse abdominal muscle)

trangularis sterni – thin, inner aspect of sternum – very active during expiration

innervation – sternocleidomastoid CN XI; scalenes C1-C2; intercostals T1-T12; abdominal m T7-L1; diaphragm C3-C5

Structural and biochemical properties

muscle fiber classification – slow fibers (type I or red), 2 types of fast fibers (type IIa, IIb or white)

slow fibers have slow contraction kinetics but high endurance

fast fibers have fast contraction kinetics but less endurance

diaphragm is comprised of a mixture of fast and slow fibers – 50:50

other respiratory muscles have a slightly higher proportion of slow fibers – probably due to their function in posture

development of diaphragm – % of slow fibers slowly Ý from 0 to 50% between 0-1 years of age

length–tension relationship: optimal overlap of actin myosin = maximal force; excess overlap or too little overlap (hyperinflated lung) = less force

Clinical assessment of respiratory function

maximal inspiratory force (MIP) / negative inspiratory force (NIF) – tests inspiratory function at RV (most common)

maximum expiratory pressure (MEP) – tests expiratory function at TLC

gender and age determine MEP NOT body size

clinical utility of these tests:

(1) neuromuscular disease

more sensitive test for muscle weakness than spirometry or lung volume

assess clinical course of disease and treatment

identify patients at Ý risk for of ventilatory failure

(2) mechanically ventilated patients – predictor of ability to wean from ventilator (breathing pattern is better predictor)

breathing patterns: tachypnea Þ respiratory alternans (chest / abdomen alternate movement with each inspiration) OR abdominal paradox (abdominal wall moves in as chest wall moves out) Þ hypercapnia Þ bradypnea, ß ventilation

as respiratory muscle strength diminishes (40-50% of function) – patient becomes hypercapnic

Alterations in respiratory muscle function with disease

Diseases that Alter Respiratory Muscle Function

Primary Neuromuscular Diseases (muscular dystrophies, myasthenia gravis)

Neural Injury (spinal cord trauma, phrenic nerve paralysis)

Metabolic and Endocrine Disorders (malnutrition, hypo/hyperthyroidism)

Electrolyte Disturbances (hypo/hyperkalemia, hypo/hypercalcemia, hypomagnesemia, hypophosphatemia)

Arterial Blood Gas Disturbance (hypoxemia, hypercapnia, acidosis)

Primary Lung Disease (COPD, cystic fibrosis)

Hypoperfusion states (cardiogenic and septic shock)

Pharmacologic Agents (neuromuscular blockers)

structural disorders of thorax which lead to respiratory failure – kyphoscoliosis (cobb’s angle), obesity, etc

respiratory muscle function in myasthenia gravis – postural fall in vital capacity (suggests diaphragm weakness)

effects of spinal cord injury on respiratory muscle Þ high cervical injury (lose all respiratory muscles, requires ventilator), low cervical injury (lose all respiratory muscles except diaphragm - tend to be fine for resting respiratory demand, problems at high demand or cough), mid-thoracic injury (impaired cough due to problems with abdominal and lower intercostal); lumbar injury (below L1 – normal respiratory function)

phrenic nerve disease leading to diaphragm paralysis

causes – cardiac surgery (related to cardioplegia); idiopathic

consequences – tends to recover over a period of months

ß inspiratory capacity (loss of diaphragm contraction; intercostal force dissipated across flaccid diaphragm)

inward movement of abdominal wall during inspiration

if bilateral, vital capacity better upright than supine

effects of malnourishment: ß respir muscle strength/endurance; ß diaphragm mass/thickness/area; ß trace element

Management of respiratory muscle failure

diagnostic Þ physical exam (tachypnea, respiratory alternans, abdominal paradox, BP), respiratory muscle strength testing, electrolytes and trace elements, ABGs, nutritional assessment, assess cardiac output

therapeutic Þ correct electrolyte and trace element disorders; correct hypoxemia, hypercapnia, acidosis; improve cardiac output; pharmacological approaches (not very useful); rest therapy (mechanical ventilation); respiratory muscle training (patients who underwent muscle training – inspiratory muscle strength increased; dyspnea decreased)

Conclusions

respiratory muscle failure leads to hypercapnia but NOT hypoxemia

there are multiple causes of respiratory muscle dysfunction

management of respiratory muscle failure is directed towards the correction of the underlying factors