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Development of Barrel Chest in Emphysema

Dalam dokumen Color Atlas of Pathophysiology (Halaman 94-98)

Factor VII deficiency

B. Development of Barrel Chest in Emphysema

Plate4.7PulmonaryEmphysema

83 T

RL

T RL

·Vmax =

·Vmax =

RTL

RTL Chronic obstructive

lung disease Breakdown of connective

tissue in the lung

Elastase excess

Emphysema Panlobular Centrilobular

Aging etc.

Bronchioles Respiratory bronchioles Alveolar ducts

Alveoli Flaccid lung

Bronchial

obstruction Loss of

diffusion area Capillary

destruction Loss of

retractability (recoil)

Increased dead space

Deepened breathing Pulmonary hypertension

Pulmonary vasoconstriction Work:

Cardiac output (CO) Abnormal

distribution Abnormal diffusion

Hypoxemia Compensation

through inspiration

Right heart failure

‘cor pulmonale’

‘Blue

bloater’ ‘Pink puffer’ ‘Barrel chest’

‘Barrel chest’ in emphysema Normal inspiratory position

Tidal volume

Residual volume

Vital capacity

Functional residual capacity Total capacity

a1-proteinase inhibitor A. Emphysema

Pulmonary Edema

In pulmonary capillaries, as in systemic capil-laries (→p. 250), filtration is determined by the effective filtration pressure, i.e., the differ-ence between the hydrostatic and oncotic pres-sure gradients. An increase in effective filtra-tion pressure in the pulmonary vessels leads to pulmonary congestion, filtration of plasma water into the interstitial space results in inter-stitial pulmonary edema (→A1), and the pas-sage of plasma water into alveoli causes alveo-lar pulmonary edema (→A 2).

A rise in hydrostatic pressure in the pulmo-nary capillaries occurs when the left ventricleʼs forward pumping action is inadequate (→A 3, right). Causes are reduced myocardial power or excess demand on it (heart failure;

→p. 238), mitral valve stenosis or regurgita-tion (→p. 208 ff.). The resulting increase in left atrial pressure is transmitted backward into the pulmonary vessels.

The development of pulmonary edema is facilitated by abnormal lymphatic drainage (→A 4, left). Normally, an excess of filtered flu-id is removed via the lymphatics. However, the capacity of the pulmonary lymphatic system is low even under physiological conditions. If right heart failure occurs together with left heart failure, the systemic venous pressure rises and thus also the pressure at the point of drainage of the lymphatic vessels into the veins at the venous angle, so impairing lymphatic drainage.

The oncotic pressure in the capillaries is re-duced by hypoproteinemia (→A 5, left), favor-ing the development of pulmonary edema. Hy-poproteinemia is usually the result of hyperhy-dration, for example, an inappropriately high supply of fluids to patients with reduced renal excretion (e.g., due to renal failure; → p. 120 ff.). A reduction in plasma protein forma-tion in the liver (liver failure;→p. 188) or loss of plasma proteins, for example, via the kid-neys (nephrotic syndrome;→p. 114), also de-creases plasma protein concentration.

Finally, increased capillary permeability can result in pulmonary edema (→A 6, right). In-creased permeability of the capillary wall for proteins reduces the oncotic pressure gradient and thus increases the effective filtration pres-sure. Capillary permeability is increased by, for

example, inhalation of corrosive gases or pro-longed inspiration of pure O2(→p. 92).

Effects of pulmonary congestion are re-duced pulmonary perfusion, and thus impaired maximal O2uptake. The distension of the con-gested vessels prevents enlargement of the al-veoli and decreases lung compliance. In addi-tion, the bronchi are narrowed by the distend-ed vessels (→A 7) and resistance to breathing increases (→p. 80), discernable through dim-inution of the maximal breathing capacity and of FEV1(→Table 2 on p. 70).

In interstitial pulmonary edema the intersti-tial space between capillary and alveolus is in-creased. As a result, diffusion is disturbed (→A 8) with impairment mainly of O2uptake (→p. 74). If, due to physical activity, O2 con-sumption rises, O2concentration in blood falls (hypoxemia, cyanosis).

Any further pressure increase and damage to the alveolar wall causes the passage of fil-trate into the alveolar space. The fluid-filled al-veoli are no longer involved in breathing (gas-eous exchange) and a functional venoarterial (pulmonary arterial to pulmonary venous) shunt occurs along with a decrease in O2in the systemic arterial blood (central cyanosis).

Fluid enters the airways and thus also increases airway resistance. Increased filtration of fluid into the pleural space (pleural effusion) also impairs breathing.

Pulmonary edemas force the patient to breathe in the upright position (orthopnea;

→A 9). On sitting or standing up after being re-cumbent (orthostasis) venous return from the lower part of the body falls (even more in the fully upright position), and thus right atrial pressure and the right cardiac output decrease.

Less blood flows through the lungs, causing a fall in hydrostatic pressure in the pulmonary capillaries at the same time that pulmonary ve-nous flow from the upper parts of the lung is increased. Moreover, the decrease of central venous pressure facilitates lymphatic drainage from the lung. As a result, pulmonary conges-tion as well as interstitial and alveolar edemas regress.

84

4Respiration,Acid–BaseBalance

Plate4.8PulmonaryEdema

85 H2O

H2O H2O

1 4 5

8

2

7

9

3 6

Dyspnoa e.g. Hyperinfusion

Reduced vital capacity Hypoxemia

Orthopnea Alveolus

Interstitial space Plasma water Capillary Interstitial pulmonary edema Alveolar pulmonary edema

Abnormal diffusion Narrowing of alveoli and bronchi

Attempt to lower hydrostatic pressure Onphysical

work Decreased oncotic pressure

Increased

central venous pressure

Abnormal lym-phatic drainage

Increased vascular permeability Alveolus

Interstitial space

Lymphatics

Inhalation of corrosive gas

Increased hydrostatic pressure

Left heart failure Capillary

Abnormal ventilation A. Pulmonary Edema

Pathophysiology of Breathing Regulation

Numerous factors influence the respiratory neurons in the medulla oblongata (→A):

Ventilation is increased by acidosis, hyper-capnia, hypoxia, hormones (progesterone, tes-tosterone, ACTH), transmitters (blood [nor]epi-nephrine; cerebral histamine, acetylcholine, prostaglandins), and a decrease of Ca2+and Mg2+in cerebrospinal fluid (CSF). Pain, fear, an increase or moderate fall in body temperature, intense cold or heat stimuli to the skin, a drop in blood pressure, and muscular activity all in-crease ventilation.

Conversely, ventilation is reduced by alkalo-sis, hypocapnia, cerebral hypoxia, peripheral hyperoxia, ganglion blockers, high concentra-tions of atropine, catecholamines, endorphins, and glycin, increase of CSF, Ca2+ and Mg2+. Deep hypothermia, rise in blood pressure, and sleep also diminish ventilation.

Sleep apnea, an arrest of breathing lasting several seconds to minutes, results from re-duced sensitivity of the respiratory neurons to CO2(central apnea) or from a collapse of the airways due to relaxation of muscles during sleep (obstructive apnea). Sleep apnea is fa-vored by nonrespiratory alkalosis and obesity.

The apnea may stimulate the sympathic nerve tone with resulting tachycardia, arterial hyper-tension, and myocardial ischemia. The hypo-kapnia resulting from reduced respiratory drive during sleep may lead to cerebral vasodi-latation resulting in morning headaches.

Barbiturates (soporific drugs) and chronic respiratory failure decrease the sensitivity of the respiratory neurons to pH or CO2in CSF.

Lack of O2thus becomes the most important stimulus to breathing. In both cases the supply of O2-enriched air leads to hypoventilation and respiratory acidosis (→p. 96 ff.). This re-sponse is increased by, for example, uremia (→p. 120 ff.) or sleep. Because O2uptake varies within a wide range independently of alveolar ventilation (→p. 72), breathing is stimulated only when there is a marked diminution in al-veolar O2partial pressure and a fall in O2 satu-ration in the blood. The resulting increase in ventilation will again cease as soon as O2 satu-ration in the blood is normal; breathing is therefore irregular.

Normally the pH around the respiratory neu-rons or the pH in the CSF has a decisive influ-ence on ventilation. A shift in pH in the brain following rapid changes in PCO2is accentuated by the low buffering power of CSF (low protein concentration). Because CO2, but not HCO3or H+, quickly passes through the blood–CSF and blood–brain barriers, changes in CO2 concen-tration in the blood result in very rapid adapta-tion of ventilaadapta-tion, while adaptaadapta-tion after changes in blood pH or blood HCO3occurs only after a delay of several days. If sudden met-abolic acidosis occurs (→B, top; see also p. 96 ff.), respiratory compensation will thus oc-cur only slowly. Conversely, treatment of a part-ly compensated respiratory acidosis, for exam-ple, by infusion of HCO3, often leaves behind respiratory alkalosis (→B, bottom). Also, with a sudden fall of O2partial pressure in inspiratory air (at high altitude) ventilation is not immedi-ately and adequimmedi-ately raised. The onset of hyper-ventilation leads to hypocapnia, and the result-ing intracerebral alkalosis will then transiently inhibit any further rise in ventilation. Complete adaptation of breathing to a reduced O2supply requires an increase in renal HCO3excretion with subsequent decrease in HCO3 concentra-tion in plasma and (after a delay) in CSF.

Damage or massive stimulation of the respi-ratory neurons can cause pathological breath-ing (→C):

◆Kussmaul breathing (→C 1) is an adequate response of the respiratory neurons to metabol-ic acidosis. The depth of the individual breaths is greatly increased but breathing is regular.

◆Cheyne–Stokes breathing (→C 2) is irregu-lar. The depth of breathing periodically be-comes gradually deeper and then gradually more shallow. It is caused by hypoperfusion of the brain, or when breathing is regulated by a lack of oxygen. The delayed response of respi-ratory neurons to changes in blood gases re-sults in an overshooting reaction.

◆Biot breathing (→C 3) consists of a series of normal breaths interrupted by long pauses. It is an expression of damage to respiratory neu-rons. Gasping (→C 4) also signifies a marked disorder in the regulation of breathing.

86

4Respiration,Acid–BaseBalance

Plate4.9PathophysiologyofBreathingRegulation

87

HCO

3 –

2 3

5 6

1

4 pH 7.7

25 5 25

5

5

5

12

25

2.5

2.5

25

12

2.5

2.5

12

12 pH 7.4

pH 7.4

kPa Normal

mmol/L

pH 7.4

pH 7.4

Dalam dokumen Color Atlas of Pathophysiology (Halaman 94-98)