5 WHAT IS PULMONARY INSUFFICIENCY?
Alden H. Harken M.D.

1. What is pulmonary insufficiency?

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The alveolar-capillary surface of the lung is the size of a singles tennis court. The purpose of the lung is to match alveolar ventilation (Va) to blood flow (Q). Mismatching leads to pulmonary insufficiency.

2. How is Va/Q mismatching characterized?

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Shunt: decreased ventilation relative to regional blood flow; pulmonary arterial (unoxygenated) blood “shunts” by hypoventilated alveoli
Dead space: decreased pulmonary regional blood flow relative to ventilation

3. How much energy is expended in the work of breathing?

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A healthy medical student expends about 3% of total oxygen consumption (energy use) on work of breathing. After injury, particularly a big burn, patients may increase fractional energy expenditure of breathing to 20% of their total energy use.

4. Which surgical incisions most significantly compromise a patient’s vital capacity?

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Intuitively an extremity incision or injury influences vital capacity least, followed sequentially by a lower abdominal incision, median sternotomy, thoracotomy, and upper abdominal incision. An upper abdominal incision is worse than a thoracotomy!

5. Is a chest radiograph helpful in assessing respiratory failure?

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Yes but the radiograph must be interpreted carefully. It can be difficult to standardize x-ray technique, especially in an intensive care unit.

6. What should you look for on the chest radiograph of a patient with impending respiratory failure?

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1. Are both lungs fully expanded?
2. Are there localized areas of infiltrate, atelectasis, or consolidation?
3. Are there generalized areas of infiltrate, atelectasis, or consolidation?
4. Are the endotracheal and other tubes in proper position?

7. Why is the local versus generalized distinction important in assessing respiratory failure?

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A local process may be produced by tumor or aspiration, and both are diagnosed and treated by bronchoscopy. Generalized multilobar infiltrates are more likely to represent a diffuse alveolar-capillary leak syndrome, such as adult respiratory distress syndrome (ARDS).

8. What is ARDS?

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A diffuse, multilobar capillary transudation of fluid into the pulmonary interstitium that dissociates the normal concordance of ventilation (Va) with lung perfusion (Q).

9. What governs fluid flux across pulmonary capillaries into the interstitium of the lung?

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Starling initially described the balance between intravascular hydrostatic pressure (Pc), which tends to push fluid out of the capillaries, and colloid oncotic pressure (COP), which sucks fluid back in across the capillary endothelial barrier (K):

Fluid flux = 5 K(Pc – COP)

10. What causes ARDS?

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Anything that increases lung dysfunction by promoting wet lung:

1. Heart failure backs up pulmonary intravascular Pc, forcing fluid into the pulmonary interstitium.
2. Malnutrition and liver failure decrease plasma protein and COP. Fluid is not sucked back out of the lung (if the total protein and albumin are low).
3. Sepsis may break down the capillary endothelial barrier (K), permitting water and protein to leak into the lung.

KEY POINTS: CLINICAL FEATURES OF ARDS

1. Severe hypoxemia refractory to increased inspired oxygen concentration
2. Diffuse pulmonary infiltrates
3. Low lung compliance
4. Large V/Q mismatch

11. Explain high-pressure versus low-pressure ARDS.

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Purists appropriately note that lung congestion resulting from high intravascular hydrostatic pressure secondary to heart failure is really not primary respiratory distress syndrome. If the pulmonary capillary wedge pressure (PCWP) is > 18 mmHg, the diagnosis is high-pressure pulmonary edema (not ARDS). A patient with pure mitral stenosis may have (high-pressure) lung congestion, whereas a malnourished patient may develop (low-pressure) lung congestion; neither of these is, strictly speaking, ARDS, although patients with ARDS frequently have components of both.

12. What is a normal COP?

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22 mmHg.

13. How is COP calculated?

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Of COP, 75% normally is created by serum albumin along with globulins and fibrinogen:

COP = 2.1 (total protein)

If an osmotically active molecule such as hetastarch is infused, this calculation is fouled up.

14. Define low-pressure ARDS.

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Low-pressure ARDS is a redundant term. To make the diagnosis of ARDS, the PCWP must be <18 mmHg. Pure ARDS exists only if the PCWP is > 4 mmHg less than the COP.

15. How can the pulmonary capillaries leak if the COP exceeds the PCWP?

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The current concept involves a septic expression of neutrophil CD11 and CD18 adhesion receptors, which stick to pulmonary vascular endothelial intercellular adhesion molecules. Septic stimuli provoke the adherent neutrophils to release intravascular proteases and oxygen radicals. Resultant endovascular damage breaks down the capillary endothelial barrier, permitting the lung leak-even at low hydrostatic pressure.

16. What is a Lasix sandwich?

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Many surgeons, when their backs are against the wall, give 25 g of albumin followed in 20 minutes by 20 mg of furosemide (Lasix) IV. They reason that the albumin pulls fluid out of the water-logged lung and the Lasix promotes diuresis to rid the patient of extra water. This therapeutic concept probably works only in patients who are not very sick. The sicker the patient, the faster the infused albumin leaks and equilibrates across the damaged endovascular endothelial barrier. Little water is sucked out of the sick lung in preparation for diuresis.

17. List the goals of therapy for ARDS.

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1. Reduce lung edema (typically with a diuretic).
2. Reduce oxygen toxicity (inspired oxygen concentration < 60% is safe).
3. Limit lung barotrauma (avoid peak inspiratory pressure in > 40 cm H2O).
4. Promote matching of Va and Q; frequently positive end-expiratory pressure (PEEP) is useful.
5. Maintain systemic oxygen delivery (arterial oxygen content x cardiac output).

18. What governs the distribution of lung perfusion (Q)?

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Mostly gravity. The dependent portions of the lung always are better perfused.

19. Discuss hypoxic pulmonary vasoconstriction (HPV).

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Most students believe that after dedicating the entire second year of medical school to pheochromocytoma and HPV, both entities may be safely forgotten. At least in the case of HPV, this is not true. A patient who has just undergone carotid endarterectomy illustrates the relevance of HPV. As the patient awakens from anesthesia, the blood pressure is 220/120 mmHg and arterial PO2 with 100% oxygen is 500 mmHg. So that the patient will not blow the carotid anastomosis, the surgeon urgently infuses nitroprusside. In 20 minutes, the blood pressure is 120/80 mmHg, but PO2 (still with 100% oxygen) has dropped to 125 mmHg!
Did the lab technician screw up the blood gas analysis? No-this is an example of the clinical significance of HPV, which directs pulmonary arteriolar delivery of deoxygenated blood toward ventilated alveoli and away from poorly ventilated lung regions. The patient was using HPV to attain a PO2 of 500 mmHg. All antihypertensive agents (e.g., nitroprusside) and most general anesthetics block HPV. The PO2 increment from 125 to 500 mmHg is due to HPV. HPV steered perfusion toward ventilated areas of the lung.
20. What governs the distribution of ventilation in lung? Show answer
KEY POINTS: THERAPEUTIC GOALS IN ARDS

1. Reduce lung edema
2. Reduce oxygen toxicity (FiO2 < 60%)
3. Minimize barotraumas (keep peak inspiratory pressure < 40 cm H2O)
4. PEEP to promote V/Q matching
5. Maintain systemic oxygen delivery (arterial oxygen content x cardiac output)

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A large pleural pressure gradient (more negative at the top of the lung by 20 cm H2O) squeezes gas primarily out of the dependent lung during each exhaled breath. The regional compliance of dependent lung is much better than that of lung apex, which still is distended with gas at the end of exhalation. The usual approach is to perfuse and ventilate dependent lung preferentially.

21. How does ARDS compromise lung function?

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The trachea is held open with cartilaginous rings, but terminal bronchioles are not. Wet lung collapses the terminal bronchioles, trapping distal alveolar gas. Persistent perfusion of these poorly ventilated regions is a shunt that results in hypoxia.

22. How long does it take for pulmonary arterial (deoxygenated) blood to equilibrate completely with trapped (poorly oxygenated) alveolar gas?

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About three fourths of a second. After that, no more oxygen is added, and no more CO2 is eliminated from the perfusing blood. Terminal bronchiolar closure producing trapped alveolar gas is bad.

23. What is the therapy for terminal airways closure and resultant shunt secondary to the wet lung of ARDS?

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PEEP should hold open terminal bronchioles, promoting ventilation of previously trapped alveoli and minimizing the shunt.

24. When may the patient come off mechanical ventilation and be extubated safely?

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The patient should be sufficiently alert to protect his or her airway, require an inspired oxygen concentration no greater than FiO2 = 0.4, and be comfortable breathing on a T-piece (without mechanical ventilation) for 60 minutes at a respiratory rate < 20 and a minute ventilation < 10 L/min. The patient should be able to generate a negative inspiratory force > -20 cm H2O. Finally, after 1 hour on the T-piece, oxygenation should provide a hemoglobin saturation > 85% without respiratory acidosis (see Chapter 6).

25. What is nitric oxide (NO)?

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NO is synthesized in vascular endothelial cells by constitutive nitric oxide synthase (cNOS) and inducible NOS (iNOS). Intuitively, inhaled NO should diffuse across ventilated alveoli to increase regional perfusion and improve matching of Va/Q.

26. Does inhaled NO work in ARDS?

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Almost 24 randomized controlled clinical trials have assessed the therapeutic efficacy of inhaled NO. Although systemic oxygenation and pulmonary hypertension improve transiently, ventilator time and ultimate survival are not influenced. Just say NO.

References
WEB SITES

1. http://www.ardsnet.org
2. http://www.nlm.nih.gov/medlineplus/ency/article/000103.htm

BIBLIOGRAPHY
1. Bartlett R: Pulmonary Insufficiency. New York, American College of Surgeons, Surgery WebMd Corporation, 2002.
2. Davidson TA, Caldwell ES, Curtis JR, et al: Reduced quality of life in survivors of acute respiratory distress syndrome compared with critically ill control patients. JAMA 281:354-360, 1999.
3. Gust R, McCarthy TJ, Kozlowski J, et al: Response to inhaled nitric oxide in acute lung injury depends on distribution of pulmonary blood flow prior to its administration. Am J Respir Crit Care Med 159:563-570, 1999.
4. Pesenti A, Fumagalli R: PEEP: Blood gas cosmetics or a therapy for ARDS? Crit Care Med 27:253-254, 1999.