Dr Zainuri_otot Pernapasan

Otot-otot Pernapasan dan Pengaturannya

dr. Zainuri Sabta Dep. Anatomi FK UII

Breathing

• Breathing (pulmonary ventilation) consists of two cyclic phases:

• inhalation, also called inspiration - draws gases into the lungs.

• exhalation, also called expiration - forces gases out of the lungs.

Costa

• 12 pasang• Posterior: melekat pada vertebra• Costa 1- 7 : di bagian anterior melekat ke

sternum melalui cartilago• Costa 8-10 : saling melekat satu dengan lainnya,

kemudian bersama-sama melekat pada costa ke 7 via cartilago costa

• Costa 11-12 : melayang, tidak memiliki perlekatan di bagian anterior

Cartilago Costa

• Cartilago hyaline• Menghubungkan 7 costa pertama ke sternum

dan costa 8-10 ke cartilago di atasnya

• memberikan dukungan elastisitas dan mobilitas dinding thorax.

3 muscles of respiration3 muscles of respiration External intercostalsExternal intercostals Internal intercostalsInternal intercostals Innermost intercostalsInnermost intercostals

These three muscle groups are innervated by collateral branches of the intercostals nerves, arteries and veins which run just superior to the ribs. The intercostal VAN run along the costal groove on the inferior inside of the ribs.

m. Intercostalis externus

• Lapisan superficial• Arah ke bawah depan (caudoventral)• Penempelan: dari tuberculum costa ke costochondral junction• Di anterior menjadi membrana intercostal• Fungsi mengangkat costa

Ext. int. muscle

m. Intercostalis internus

• Lapisan Intermediat• Arah ke bawah belakang (caudodorsal)• Dari sternum melekat ke angulus costa • Di posterior menjadi membrana intercostal• Fungsi menurunkan costa

int. int. muscle

m. Intercostal Innermost

• Lapisan otot paling dalam• Tidak menutup intercostal secara penuh• Meloncat melewati satu-atau lebih spatium

intercostal• Internal: fascia endotracheal dan pleura

parietal• External: n. intercostal dan vasa• Fungsi mengangkat costa

Otot-otot Pernapasan

Diaphragm—major inspiratory mm.

External intercostal muscles are inspiratory!

Intercostals & accessory mm also help under stress

Expiratory—normally passive, only use mm. to expel things (cough) & when in extreme states (aggressive exercise)

Abdominal mm—major expiratory mm

Internal intercostal muscles are expiratory

Diaphragma

Otot-otot PernapasanDuring inspiration, the scalene muscles and external intercostals contract. Both sets of muscles are therefore considered “primary,” and not “accessory,” muscles of respiration.

Scalene muscle

Muscles of Respiration1. The diaphragm muscle inserts vertically

into a horizontal membranous tendon. Because of its large zone of apposition with the chest wall, the diaphragm depresses like a piston, with little change in curvature until high lung volumes are achieved. This lowers pleural pressure, expands lower ribs, and sucks inward on upper ribs.

2. The crural diaphragm, which depresses the posterior section and doesn’t affect the ribs, is innervated by C4-5. The costal diaphragm is innervated by C3-4.

Otot-otot PernapasanInspiration – Active contraction of diaphragm (expanding rib cage), passive outwardmovement of abdominals (opposite for expiration)

Otot-otot yang mengangkat costae pada waktu menarik napas biasa ialah :

1.m. intercostalis externus2.m. levator costae3.m. serratus posterior superior 4.m. intercartilagineus

Pada keadaan dypsnoe berkontraksi juga : 1.mm. Scaleni, 2.m. sternomastoideus, 3.m. pectorales major4.m. pectoralis minor5.m. latissimus dorsi ,dan 6.m. serratus anterior

m. Levator costae

m. Pectoralis major

m. Pectoralis minor


Pada waktu mengeluarkan napas, costae turun oleh karena berat mereka, berat sternum, berat otot-otot yang menggantung pada mereka dan kekenyalan cartilago costalis

Pada keadaan dypsnoe, untuk meniup atau berbicara diperlukan juga kontraksi dari otot-otot :m. subcostalism. transversus thoracism. serratus posterior inferior m. obliquus abdominis externus et internus, m. rectus abdominis dan m. transversus abdominis

m. Transversus thoracis

m. subcostalis


m. Seratus post.inf. m. Rectus abd. m. Obliquus abd. Ext.m. Transversus abd.

Thoracic cage motion1. Upper ribs move with a “pump-handle” motion about the vertebrae. This

elevates the manubrium and rotates it outward to open the chest.2. Middle ribs move with a “bucket-handle” motion that expands the rib

cage laterally.3. The 11th and 12th ribs move with a “caliper” motion.

Muscles of Respiration Type

1. Type I fibers are highly oxidative and slow to fatigue.2. Type IIa fibers are oxidative and relatively resistant to

fatigue.3. Type IIb fibers are glycolytic and fatigue rapidly.4. A normal diaphragm is 50% Type I and 25% Type IIa

fibers.

Control of Ventilation

Response to Changes in PO2, PCO2

Center of respiratory

a. Main Groups1. Pontine Respiratory Group (PRG)2. Medulla: Dorsal & ventral respiratory groups (DRG & VRG)

• rostral & caudal VRG—mainly expiratory nn.• medial VRG (nucleus ambiguous)—mainly inspiratory nn.

b. Vagus nerve—important modifier of output from each brainstem nucleus (↓ tone)c. Spinal-Muscle Anatomy

1. Major respiratory motor neurons found in cervical (C3-C5=phrenic), thoracic, lumbar cord2. Innervate intercostals, diaphragm, & abdominal mm3. Separate tracts for voluntary & involuntary mm

• Corticospinal tract (CST)—voluntary• Anteriolateral System—automatic (involuntary)

d. Pre-Botzinger Complex—contains anatomical site of pattern generator neurons

Boyle’s Law

• The pressure of a gas decreases if the volume of the container increases, and vice versa.

• When the volume of the thoracic cavity increases even slightly during inhalation, the intrapulmonary pressure decreases slightly, and air flows into the lungs through the conducting airways. Air flows into the lungs from a region of higher pressure (the atmosphere)into a region of lower pressure (the intrapulmonary region).

• When the volume of the thoracic cavity decreases during exhalation, the intrapulmonary pressure increases and forces air out of the lungs into the atmosphere.

Respiratory Cycle

Figure 10.9

Measurement of Lung Capacity

Figure 10.10A

Carotid and aortic bodies: sensitive to carbon dioxide, pH, and oxygen levels

Conscious control: resides in higher brain centers; ability to modify breath is limited

Regulation of Breathing: Nervous System Involvement

Regulation of Breathing

Figure 10.13

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Control of ventilation (chemoreceptors)

fig 13-33

peripheral chemoreceptors

in carotid & aortic bodies

Central chemoreceptors:

in medulla (brain interstitial fluid)

Stimulated by:

1. P.CO2 (via pH: most important)

Peripheral chemoreceptors:

see left (arterial blood)

Stimulated by:

1. P.CO2 (via pH)

2. P.O2

3. pH

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Control of ventilation ( arterial P.O2)

fig 13-34

Acts on peripheral chemoreceptors

( P.O2 depresses central chemoreceptors)

relatively insensitive (potentiated by P.CO2)

responds to P.O2, not O2 content (i.e. not to anemia or CO poisoning)


O2—mediated exclusively by peripheral chemoreceptors

Carotid bodies—site of peripheral chemoreceptors; also sens. to PCO2 & pH; found at bifurcation of common carotid arteries;

1. changes in output correlate w/ minute ventilation rates

2. glomus (type I) cells—principle output cells from carotid body

3. sustentacular (type II) cells—largely support structure


CO2—mediated by central & peripheral chemoreceptors

1. When hypoxia is coupled w/ hypercapnia (high CO2) response ↑

2. Central chemoreceptor system is main mediator of hypercapnic response

3. PCO2 response is much faster & stronger than pH response


pH—mediated by central & peripheral receptors but MAINLY CENTRAL

CSF surrounding brainstem is main chemoreceptorchanges of pH in CSF are very rapid, but imbalances take a long time to get to the brain (=> several days)

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Rhythmical nature of breathingRespiratory rhythm generator

located in medulla oblongata of brainstem

During quiet breathing

Inspiration: action potentials burst to diaphragm & inspiratory intercostals

Expiration: no action potentials; elastic recoil of lungs (passive process)

During forced breathing (e.g. exercise, blowing up a balloon)

Active inspiration & expiration

Expiration with expiratory intercostals & abdominal muscles

Breathing is also modulated by centers in pons of brainstem & lungs

Ventilatory Pattern GeneratorFunction—rhythmically drives the mm. controlling inspiration & expirationNeural signals Stages

1. Inspiratory2. expiratory (phase I & phase II)

Reflexes & sensory Receptorsa. Sense presence of irritants via sensory receptors placed in different

locationsb. Reflexes

1. Reflexive coughing, sneezing, swallowing reflexes2. Dive reflex—causes breathing to stop when H2O is directed

towards facec. Sensor Types

1. Slowly adapting receptors (SARs)—major contributor to Hering Breuer Inflation reflex; continue to fire for a time after change in lung volume

2. Rapidly adapting stretch receptors (RARs)—mediate coughing, mucus production, & bronchoconstriction

3. Un-myelinated (slower conducting) receptors—mediate pulmonary chemoreflex (bradycardia, hypotension, & apnea) in response to chemicals

4. Hering Breuer Inflation reflex—shows influence of vagus; when inflate fully see temporary cessation of periodic breathing

Treatment of Respiratory Muscle Failure

• Muscle training, such as breathing through a resistor to improve strength, and voluntarily hyperventilating to improve endurance.

• For severe emphysema it is possible to surgically remove lots of the diseased tissue in order to reduce lung volume and hyperinflation.

• If hypercarbia is persistent, mechanical ventilation is required.

Diseases

a. Cheyne-Stokes breathing patterns—caused by head injuries or CNS dysfunction; => TV & breathing f ↑/↓ in periodic cycles

b. Apneustic Breathing patterns—may be caused by CNS injury; pattern of sustained inspiration w/ brief expiration

c. Sleep apnea—may occur briefly in normal indiv.d. Obstructive Airways or Drugs—may change ability to

respond to hypercapnic challenges

Respiratory Muscle FailureOne general rule is that lung failure is manifested as hypoxia, but respiratory muscle failure is manifested as hypoxia with hypercarbia.Respiratory failure is defined as PO2 <60 mmHg and PCO2 >45 mmHg. Hypercarbic respiratory failure results from decreased minute ventilation and increased dead space ventilation. This is caused by decreased respiratory muscle strength or increased mechanical load on the muscles (airway resistance, obesity, stiffened chest wall). Hypercarbia decreases PO2 by the alveolar air equation. Hypoxemic respiratory failure is usually caused by a right-to-left intrapulmonary shunt (V/Q = 0).Lungs will usually compensate with hyperventilation, and PCO2 will actually be a bit low. Hypoxemia is caused by fluid-filled alveoli (pulmonary edema or hemorrhage, pneumonia).

Respiratory Muscle FailureOne general rule is that lung failure is manifested as hypoxia, but respiratory muscle failure is manifested as hypoxia with hypercarbia.

Neuromuscular disorders that cause respiratory failure include kyphoscoliosis, obesity, cardiac surgery (severed phrenic nerve), trauma to spinal cord or thorax, stroke, Herpes Zoster, Guillain-Barre, ALS, MS, Polio, myasthenia gravis.1.Unilateral diaphragm paralysis occurs from stroke, trauma, Herpes Zoster involving the phrenic nerve, or transiently after open-heart surgery. Abdominal paradox is absent, but unilateral diaphragm paralysis can be diagnosed with the “sniff test.” The patient sniffs, and the normal half descends but the paralyzed half paradoxically rises.2.Bilateral diaphragm paralysis will have a VC that is only 50% of normal. That goes down to 25% when they lay down. Abdominal paradox is present, and patients cannot tolerate being supine.

Respiratory Muscle Failure

• The purely neuromuscular disorders (G-B, ALS, MS, etc) will have normal FRC and RV.

• CO2 retention occurs late in disease, when inspiratory muscle strength falls to 75% of normal. Chronic hypercarbia is associated with obesity.

• Lower spinal injuries paralyze the intercostals and expiratory muscles, but not the diaphragm. Therefore, MIP is relatively intact. However, they can’t cough or exhale strongly, so they are at high risk for pneumonia.

• Upper spinal injuries paralyze all the muscles, and these patients require a ventilator.

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