Respiratory Acidosis

S 40-cT

PaCO mm Hg

120 100 90 80 70 60 50

PaCO mm Hg

120 100 90 80 70 60 50

40

6.8 6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 Arterial blood pH

Steady-state relationships in respiratory acidosis: average increase per mm Hg rise in PaCO2

Chronic adaptation 0.3 0.3

FIGURE 6-1

Quantitative aspects of adaptation to respiratory acidosis. Respiratory acidosis, or primary hypercapnia, is the acid-base disturbance initiated by an increase in arterial carbon dioxide tension (PaCO2) and entails acidification of body fluids. Hypercapnia elicits adaptive increments in plasma bicarbonate concentration that should be viewed as an integral part of respiratory acidosis. An immediate increment in plasma bicarbonate occurs in response to hypercapnia. This acute adaptation is complete within 5 to 10 minutes from the onset of hypercapnia and originates exclusively from acidic titration of the nonbicarbonate buffers of the body (hemoglobin, intracellular proteins and phosphates, and to a lesser extent plasma proteins). When hypercapnia is sustained, renal adjustments markedly amplify the secondary increase in plasma bicarbonate, further ameliorating the resulting acidemia. This chronic adaptation requires 3 to 5 days for completion and reflects generation of new bicarbonate by the kidneys as a result of upregulation of renal acidification [2]. Average increases in plasma bicarbonate and hydrogen ion concentrations per mm Hg increase in PaCO2 after completion of the acute or chronic adaptation to respiratory acidosis are shown. Empiric observations on these adaptations have been used for construction of 95% confidence intervals for graded degrees of acute or chronic respiratory acidosis represented by the areas in color in the acid-base template. The black ellipse near the center of the figure indicates the normal range for the acid-base parameters [3]. Note that for the same level of PaCO2, the degree of acidemia is considerably lower in chronic respiratory acidosis than it is in acute respiratory acidosis. Assuming a steady state is present, values falling within the areas in color are consistent with but not diagnostic of the corresponding simple disorders. Acid-base values falling outside the areas in color denote the presence of a mixed acid-base disturbance [4].

Days

FIGURE 6-2

Days

FIGURE 6-2

Renal acidification response to chronic hypercapnia. Sustained hyper-capnia entails a persistent increase in the secretory rate of the renal tubule for hydrogen ions (H+) and a persistent decrease in the reabsorption rate of chloride ions (Cl-). Consequently, net acid excretion (largely in the form of ammonium) transiently exceeds endogenous acid production, leading to generation of new bicarbonate ions (HCO3) for the body fluids. Conservation of these new bicarbonate ions is ensured by the gradual augmentation in the rate of renal bicarbonate reabsorption, itself a reflection of the hypercapnia-induced increase in the hydrogen ion secretory rate. A new steady state emerges when two things occur: the augmented filtered load of bicarbonate is precisely balanced by the accelerated rate of bicarbonate reabsorption and net acid excretion returns to the level required to offset daily endogenous acid production. The transient increase in net acid excretion is accompanied by a transient increase in chloride excretion. Thus, the resultant ammonium chloride (NH4Q) loss generates the hypochloremic hyperbicarbonatemia characteristic of chronic respiratory acidosis. Hypochloremia is sustained by the persistently depressed chloride reabsorption rate. The specific cellular mechanisms mediating the renal acidification response to chronic hypercapnia are under active investigation. Available evidence supports a parallel increase in the rates of the luminal sodium ion-hydrogen ion (Na+-H+) exchanger and the basolateral Na+-3HCO^ cotransporter in the proximal tubule. However, the nature of these adaptations remains unknown [5]. The quantity of the H+-adenosine triphosphatase (ATPase) pumps does not change in either cortex or medulla. However, hypercapnia induces exocytotic insertion of H+-ATPase-containing subapical vesicles to the luminal membrane of proximal tubule cells as well as type A intercalated cells of the cortical and medullary collecting ducts. New H+-ATPase pumps thereby are recruited to the luminal membrane for augmented acidification [6,7]. Furthermore, chronic hypercapnia increases the steady-state abundance of mRNA coding for the basolateral Cl—HCO3 exchanger (band 3 protein) of type A intercalated cells in rat renal cortex and medulla, likely indicating increased band 3 protein levels and therefore augmented basolateral anion exchanger activity [8].

SIGNS AND SYMPTOMS OF RESPIRATORY ACIDOSIS

Central Nervous System

Respiratory System

Cardiovascular System

Mild to moderate hypercapnia

Breathlessness

Mild to moderate hypercapnia

Cerebral vasodilation

Central and peripheral cyanosis

Warm and flushed skin

Increased intracranial pressure

(especially when breathing

Bounding pulse

Headache

room air)

Well maintained cardiac

Confusion

Pulmonary hypertension

output and blood pressure

Combativeness

Diaphoresis

Hallucinations

Severe hypercapnia

Transient psychosis

Cor pulmonale

Myoclonic jerks

Decreased cardiac output

Flapping tremor

Systemic hypotension

Severe hypercapnia

Cardiac arrhythmias

Manifestations of pseudotumor cerebri

Prerenal azotemia

Stupor

Peripheral edema

Coma

Constricted pupils

Depressed tendon reflexes

Extensor plantar response

Seizures

Papilledema

Signs and symptoms of respiratory acidosis. The effects of respiratory acidosis on the central nervous system are collectively known as hypercapnic encephalopathy. Factors responsible for its development include the magnitude and time course of the hypercapnia, severity of the acidemia, and degree of attendant hypoxemia. Progressive narcosis and coma may occur in patients receiving uncontrolled oxygen therapy in whom levels of arterial carbon dioxide tension (PaCO2) may reach or exceed 100 mm Hg. The hemodynamic consequences of carbon dioxide retention reflect several mechanisms, including direct impairment of myocardial contractility, systemic vasodila-tion caused by direct relaxation of vascular smooth muscle, sympathetic stimulation, and acidosis-induced blunting of receptor responsiveness to catecholamines. The net effect is dilation of systemic vessels, including the cerebral circulation; whereas vasoconstriction might develop in the pulmonary and renal circulations. Salt and water retention commonly occur in chronic hypercapnia, especially in the presence of cor pulmonale. Mechanisms at play include hypercapnia-induced stimulation of the renin-angiotensin-aldosterone axis and the sympathetic nervous system, elevated levels of cortisol and antidiuretic hormone, and increased renal vascular resistance. Of course, coexisting heart failure amplifies most of these mechanisms [1,2].

Pump

Cerebrum _

Voluntary control

Controllers

Brain stem

Automatic control

Spinal cord

Effectors

' Phrenic and intercostal nerves

Muscles of respiration

Ventilatory requirement

(CO2 production, O2 consumption)

Airway resistance

Lung elastic recoil

Chest wall elastic recoil Diaphragm

Load

Ventilatory requirement

(CO2 production, O2 consumption)

Airway resistance

Lung elastic recoil

Chest wall elastic recoil Diaphragm

FIGURE 6-4

Main components of the ventilatory system. The ventilatory system is responsible for maintaining the arterial carbon dioxide tension (PaCO2) within normal limits by adjusting minute ventilation (V) to match the rate of carbon dioxide production. The main elements of ventilation are the respiratory pump, which generates a pressure gradient responsible for air flow, and the loads that oppose such action. The machinery of the respiratory pump includes the cerebrum, brain stem, spinal cord, phrenic and intercostal nerves, and the muscles of respiration. Inspiratory muscle contraction lowers pleural pressure (Ppl) thereby inflating the lungs (aV). The diaphragm, the most important inspiratory muscle, moves downward as a piston at the floor of the thorax, raising abdominal pressure (Pabd). The inspiratory decrease in Ppl by the respiratory pump must be sufficient to counterbalance the opposing effect of the combined loads, including the airway flow resistance, and the elastic recoil of the lungs and chest wall. The ventilatory requirement influences the load by altering the frequency and depth of the ventilatory cycle. The strength of the respiratory pump is evaluated by the pressure generated (aP = Ppl - Pabd).

DETERMINANTS AND CAUSES OF CARBON DIOXIDE RETENTION

Respiratory Pump

Load

Depressed Central Drive Acute General anesthesia Sedative overdose Head trauma Cerebrovascular accident Central sleep apnea Cerebral edema Brain tumor Encephalitis Brainstem lesion Chronic Sedative overdose Methadone or heroin addiction Sleep disordered breathing Brain tumor Bulbar poliomyelitis Hypothyroidism

Abnormal Neuromuscular Transmission Acute High spinal cord injury Guillain-BarrS syndrome Status epilepticus Botulism Tetanus

Crisis in myasthenia gravis Hypokalemic myopathy Familial periodic paralysis Drugs or toxic agents eg, curare, succinylcholine, aminoglycosides, organophosphorus Chronic Poliomyelitis Multiple sclerosis Muscular dystrophy Amyotrophic lateral sclerosis Diaphragmatic paralysis Myopathic disease eg, polymyositis

Muscle Dysfunction Acute Fatigue Hyperkalemia Hypokalemia Hypoperfusion state Hypoxemia Malnutrition Chronic

Myopathic disease eg, polymyositis

Increased Ventilatory Demand High carbohydrate diet Sorbent-regenerative hemodialysis Pulmonary thromboembolism Fat, air pulmonary embolism Sepsis

Hypovolemia

Augmented Airway Flow Resistance Acute

Upper airway obstruction Coma-induced hypopharyngeal obstruction Aspiration of foreign body or vomitus Laryngospasm Angioedema Obstructive sleep apnea Inadequate laryngeal intubation Laryngeal obstruction after intubation Lower airway obstruction Generalized bronchospasm Airway edema and secretions Severe episode of spasmodic asthma Bronchiolitis of infants and adults Chronic Upper airway obstruction Tonsillar and peritonsillar hypertrophy Paralysis of vocal cords Tumor of the cords or larynx Airway stenosis after prolonged intubation Thymoma, aortic aneurysm Lower airway obstruction Airway scarring

Chronic obstructive lung disease eg, bronchitis, bronchiolitis, bronchiectasis, emphysema

Lung Stiffness Acute

Severe bilateral pneumonia or bronchopneumonia Acute respiratory distress syndrome Severe pulmonary edema Atelectasis Chronic Severe chronic pneumonitis Diffuse infiltrative disease eg, alveolar proteinosis Interstitial fibrosis

Chest Wall Stiffness Acute

Rib fractures with flail chest Pneumothorax Hemothorax Abdominal distention Ascites

Peritoneal dialysis Chronic Kyphoscoliosis, spinal arthritis Obesity Fibrothorax Hydrothorax Chest wall tumor

FIGURE 6-5

Determinants and causes of carbon dioxide retention. When the respiratory pump is unable to balance the opposing load, respiratory acidosis develops. Decreases in respiratory pump strength, increases in load, or a combination of the two, can result in carbon dioxide retention. Respiratory pump failure can occur because of depressed central drive, abnormal neuromuscular transmission, or respiratory muscle dysfunction. A higher load can be caused by increased venti-latory demand, augmented airway flow resistance, and stiffness of the lungs or chest wall. In most cases, causes of the various determinants of carbon dioxide retention, and thus respiratory acidosis, are categorized into acute and chronic subgroups, taking into consideration their usual mode of onset and duration [2].

Posthypercapnic metabolic alkalosis. Development of posthypercap-nic metabolic alkalosis is shown after abrupt normalization of the arterial carbon dioxide tension (PaCO2) by way of mechanical ventilation in a 70-year-old man with respiratory decompensation who has chronic obstructive pulmonary disease and chronic hypercapnia. The acute decrease in plasma bicarbonate concentration ([HCO3]) over the first few minutes after the decrease in PaCO2 originates from alkaline titration of the nonbicarbonate buffers of the body. When a diet rich in chloride (Cl-) is provided, the excess bicarbonate is excreted by the kidneys over the next 2 to 3 days, and acid-base equilibrium is normalized. In contrast, a low-chloride diet sustains the hyperbicarbonatemia and perpetuates the posthypercapnic metabolic alkalosis. Abrupt correction of severe hypercapnia by way of mechanical ventilation generally is not recommended. Rather, gradual return toward the patient's baseline PaCO2 level should be pursued [1,2]. [H+]—hydrogen ion concentration.

Severe hypercapnic encephalopathy or hemodynamic instability

Severe hypercapnic encephalopathy or hemodynamic instability

• Consider intubation and use of standard ventilator support.

• Correct reversible causes of pulmonary dysfunction with antibiotics, bronchodilators, and corticosteroids as needed.

Observation, routine care.

Administer O2 via nasal cannula or Venti mask Correct reversible causes of pulmonary dysfuntion with antibiotics, bronchodilators, and corticosteroids as needed.

iz iZ

iz iz

• Consider use of noninvasive nasal mask ventilation (NMV) or intubation and standard ventilator support.

• Continue same measures.

FIGURE 6-8

Chronic respiratory acidosis management. Therapeutic measures are guided by the presence or absence of severe hypercapnic encephalopathy or hemodynamic instability. An aggressive approach that favors the early use of ventilator assistance is most appropriate for patients with acute respiratory acidosis. In contrast, a more conservative approach is advisable in patients with chronic hypercapnia because of the great difficulty often encountered in weaning these patients from ventilators. As a rule, the lowest possible inspired fraction of oxygen that achieves adequate oxygenation (PaO2 on the order of 60 mm Hg) is used. Contrary to acute respiratory acidosis, the underlying cause of chronic respiratory aci-dosis only rarely can be resolved [1,9].

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