Lung function in chronic obstructive lung disease and coexistent left heart failure

APRIL

The American

Journal

1970

of Medicine VOLUME 48 NUMBER

4

EDITORIAL

Lung Function in Chronic Obstructive Lung Disease and Coexistent Left Heart Failure*

HARRY Boston,

BASS, M.D.,

MSc.

Massachusetts

* From the Department of Medicine, Peter Bent Brigham Hospital and Harvard Medical School, 721 Huntington Avenue, Boston. Massachusetts 02115. This study was supported by the John A. Hartford Foundation and U. S. Public Health Service Grant 5.Sol-FR05489. Manuscript received September 12, 1969.

Volume 48, April

1970

A common complaint of patients with either chronic obstructive lung disease or left heart failure is shortness of breath. When either of these conditions occurs alone, the characteristic symptoms and signs, chest roentgenograms and pulmonary function studies will help to establish the correct etiologic diagnosis and guide the clinician to administer appropriate therapy. However, when these conditions coexist the pathophysiologic processes interact to mutually conceal the characteristic findings of both chronic obstructive lung disease and left heart failure. Two of the chronic obstructive lung diseases are discussed, chronic bronchitis and emphysema; when both are referred to, the phrase chronic obstructive lung disease is used. Left heart failure refers to either an abnormally high left atrial pressure or left ventricular end-diastolic pressure. Emphysema and chronic bronchitis as defined by the Committee on Diagnostic Standards of the American Thoracic Society and as detected on random sample population surveys are common conditions [1,2]. Emphysema is defined as an anatomic alteration of the lung characterized by an abnormal enlargement of the air spaces distal to the terminal nonrespiratory bronchiole, accompanied by destructive changes of the alveolar walls. Chronic bronchitis is defined as a clinical disorder characterized by excessive mucous secretion in the bronchial tree and manifested by chronic or recurrent productive cough. Arbitrarily, these manifestations should be present on most days for a minimum of three months in the year and for not less than two successive years. Cough and sputum are usually not the symptoms that bring patients with chronic bronchitis to their physicians. Their presenting complaint, as with patients who have either emphysema or left heart failure, is shortness of breath. In patients with advanced chronic obstructive lung disease, chronic bronchitis and emphysema often coexist. Many of these patients experience shortness of breath on walking at their own pace on level ground or while washing or dressing. A sudden increase in the severity of their dyspnea is often related to either left heart failure or to acute infection which can in

413

EDITORIAL

itself precipitate left heart failure. Only by repeated physical examination, roentgenograms and pulmonary function studies can the proper diagnosis be established and the degree of chronic obstructive lung disease and left heart failure quantified [3]. Total lung capacity (TLC) is abnormally high in patients with either chronic bronchitis or emphysema. The maximal amount of air that can be expired after a complete inspiration (vital capacity, VC) is normal unless either left heart failure or bronchospasm coexist. However, the amount of air remaining within the lungs at the end of a normal breath (functional residual capacity, FRC) and after a forced breath (residual volume, RV) is abnormally high and accounts for the absolute increase in TLC. When left heart failure occurs in a patient who has normal lungs, there is either a proportionate decrease in all subdivisions of TLC or a relative sparing of RV (leading to a high RV:TLC ratio). In patients with chronic obstructive lung disease the occurrence of left heart failure produces a decrease in TLC that is accounted for by a decrease in the expiratory reserve volume (the volume of air expired between the end of a normal breath and the end of a forced breath) and RV. These patients have an abnormally low VC which shows little or no change after successful treatment of left heart failure [3]. Rales, wheezes or both may be heard at the bases of both lungs in patients with normal lungs and left heart failure. Patients with chronic obstructive lung disease and associated hyperinflation have hyperresonance on percussion and diminished breath sounds. However, when left heart failure is superimposed upon chronic obstructive lung disease, hyperresonance disappears, breath sounds improve, and rales, rhonchi and wheezes may be absent. Density of the media at an interface is the most important factor determining transmission or reflection of sound. If the density of the medium to which the sound is travelling is lower than that from which it came, reflection occurs at the interface. Respiratory sounds originate in muscle and blood (both of similar density) and travel to an interface at which a lower density medium, air, is present; at this interface reflection of sound occurs. In chronic obstructive lung disease there is a high RV and hyperinflation, leading to increased reflection and diminished breath sounds. With the occurrence of left heart failure air volume diminishes, transmission of sound improves, and breath sounds in patients with preexisting chronic obstructive lung disease revert towards normal. When left heart failure occurs, the inspiratory level of the diaphragm migrates cephalad, and diaphragmatic excursion between FRC and RV increases in both normal subjects and in the majority of patients with chronic obstructive lung disease. Left heart failure produces opposite changes in patients with selective destruction of parenchyma and vasculature of both lower lobes secondary to emphysema; the inspiratory level of the diaphragm is lower, and diaphragmatic excursion decreases. The change in the inspiratory level of the diaphragm and magnitude of diaphragmatic excursion in both situations is related to alterations in regional mechanics [5].

414

During normal breathing, with the patient erect, ventilation per unit volume in the lung will be greatest at the bases and least at the apices of the lungs [6,7]; conversely, physiologic dead space will be greatest in the upper lobes and least over the lower lobes [8,9]. In the normal lung, the occurrence of left heart failure will lead to selective transudation of fluid into the interstitial and alveolar spaces of the lower lobes [lo]. The resultant increase in interstitial pressure narrows small airways and secondarily causes a ventilation shift away from the lower lobes to the upper lobes in which there is a larger physiologic dead space. With the patient in the erect position there is also a zonal distribution of blood flow within the lungs, the apices receiving the least and the bases the largest amount of perfusion [ll]. Factors regulating the distribution of blood flow within the lungs are multiple and include pulmonary arterial and venous pressure, alveolar pressure, the ability to generate a negative interstitial pressure, the volume of flow per unit time, the lung volume at which distribution of blood flow is assessed, chemical factors and vascular tone [12-151. When left heart failure occurs due to an increase in either left atrial pressure (as seen in mitral stenosis) or left ventricular end-diastolic pressure, vascular redistribution occurs [16,17]. Hydrostatic forces produce a relatively higher venous pressure in the lower lobes compared to the upper lobes. Transudation occurs selectively at the lung bases producing a regional increase in interstitial pressure and secondarily a diminished retractile force on the walls of the extra-alveolar vessels, which close by virtue of their inherent tonus. The resultant increase in pulmonary vascular resistance leads to reduction of flow through the lower lobes with redistribution to the upper lobes. When emphysema causes selective parenchymal and vascular damage of both lower lobes the resultant changes mimic left heart failure in normal lungs. An expiratory roentgenogram will be helpful in differentiating emphysema in the lower lobes from left heart failure. In those with emphysema, there is no increase in density over the lower lobes secondary to fluid transudation; the vessels remaining show distinct and clear-cut margins. In those with heart failure, there is blurring of vessel margins at the bases, an increase in density over the lower lobes and lymphatic stasis [18,19]. Chronic bronchitis can replicate the changes produced in normal lungs by left heart failure. Associated with regional hypoventilation is regional hypoperfusion, both most common over the lower lobes [20]. This produces a shift in perfusion away from the lower lobes to the upper lobes. In patients with either emphysema or chronic bronchitis located selectively at the lower lobes of both lungs, the perfusion shift is accompanied by a ventilation shift; however, the two are not proportionate. The perfusion shift is usually greater than the ventilation shift, causing a ventilation to perfusion (V.& abnormality. This is reflected in the measurement of impaired mixing efficiency (ME) and low steady state diffusing capacity (Dr.,,) [21,

The

American

Journal

of

Medicine

LUNG

223. When left heart failure occurs these patients have a further reduction in both the ME and D,,,.,, suggesting greater imbalance in VA:0 resulting from a larger shift in perfusion from the lower to the upper portions of the lungs. In patients with selective destruction of parenchyma and vasculature of both upper lobes due to emphysema, effective redistribution of perfusion and ventilation cannot occur with the onset of left heart failure. Instead, there is a closure of the basal units secondary to fluid transudation, which is detected by a reduction in TLC. An improvement (often a return to normal predicted values) in both ME and D,,, occurs, suggesting that the remaining units are both well ventilated and well perfused. The clinician can be confused by pulmonary function measurements in patients with emphysema in the upper lobes and coexistent left heart failure; hyperinflation is concealed and associated with changes towards normal oredicted values for FRC and RV. ME, D,,,,, and maximal expiratory flow rates at high lung volumes may appear normal or improved. The improved maximal expiratory flow rates at high lung volumes occur secondary to better elastic properties of the lung with left heart failure [23]. The abnormally high specific static compliance of chronic obstructive lung disease falls to or towards normal, and maximal negative transthoracic pressure improves with the occurrence of left heart failure. A simple test helpful in establishing the diagnosis of coexistent chronic obstructive lung disease and left heart failure and also in gauging the success of therapy for left heart failure is the serial measurement of forced

FUNCTION,

LUNG

DISEASE

AND

LEFT

HEART

FAILURE

-

BASS

vital capacity at one second (FEV,) and VC. In patients with chronic obstructive lung disease, left heart failure is associated with an increase to or towards normal in the FEV, and little or no change in VC. After successful therapy of left heart failure, the FEV, decreases. In both normal subjects and those with obstructive lung disease, the occurrence of left heart failure causes a decrease in expiratory flow rates at low lung volumes. This results from increased frictional resistance to alrfiow in small airways, which are narrowed secondarily to increased interstitial pressure. When left heart failure occurs in a patient who has emphysema localized in unusual regions, physical findings are bizarre, the interstitial pattern seen on chest roentgenograms unusual and abnormalities noted on lung function tests variable. In these patients interstitial fluid forms in areas of normal perfusion, leading to regional differences in compliance and an increase in interstitial pressure which causes narrowing of extra-alveolar vessels and ultimately redistribution of perfusion away from originally well perfused regions 1241. With repeated physical examination and serial analysis of chest roentgenograms and pulmonary function, it is possible to make the correct diagnoses and localize the regional abnormalities within the lungs. Also, serial studies of lung function help to quantify the degree of pulmonary and cardiac disease. One must remember that with improvement in cardiac function in a patient who has coexistent chronic obstructive lung disease, most indices of lung function deviate further away from the predicted normal value.

REFERENCES 1. American

Thoracic

cation Rev 2.

of

BG,

165,

Dis 85: in

Milne

6.

Bass

emphysema.

of

town.

Roentgenologic

failure.

Invest of

and 1967.

chronic

Amer

Rev

flow

Amer

13.

respiratory Resp

ENC.

Dis

H:

monary

compliance 1969.

Glazier

JB,

14.

disease

Radio1

4:

129,

tidal

of

analysis and

of

volumes.

Stand

J

J,

and

between

specffic

diaphragmatic

JMB,

from

Maloney

apex

excursion.

to

JE.

base

in

Pain the

pul-

MCF:

749,

18.

Lancet

JAM, of

Dolovitch inspired

LE:

MB. gas

10.

NR,

J Clin

Invest

West

JB,

11. West

JB,

isolated J Appl 12.

West

JB,

Dolovitch

regional 45:

Dollery

resistance caused

Milne

Trop

D,

Kaneko

K:

19.

the lungs. J Appl

in

Laws

in by

J Radio1

JE,

Physiol West

blood

interstitial M

20:

JB:

flow.

in

of

J.

left

175.

1965.

Effect

of

in-

Lancet

1:

192.

lung

on

pul-

the

regulation

214,

1961.

N,

Steinder

Shawdon

E:

failure

of RE:

and

Alterations

valve

simple Bass

the

118, 1965.

mitral

the

pul-

The

pul-

stenosis.

1962.

mitral

atrial

in

of

22:

Rev 41:

ventricular

293,

in

left

ENC.

gases

Braunwald

flow

pressure

Thoracalis

Physiol

35:

WF,

in

disease

H: The

regional

studies

non-traumatic pressure.

J

363,

Canad

radioisotope

for

34: diagnosis

disease.

pulmonary

by

technique

Circulation

roentgenologic

pulmonary

ventilation concept.

1349,

J

as Appl

a

determinant

Physiol

15:

20.

the CT,

lung:

DV:

Steady

perfusion

state

ratios

in

measure-

normal

21.

man.

Increased zone

edema. Naimark to

Physiol

19:

713,

Dollery

CT:

Distribution

of

pulmonary the

Circulation A:

vascular

isolated Res

Distribution and

vascular

17:

the

estima.

1966.

of early

Ass

chronic

Radio1

20:

3,

of

dog

blood

alveolar

lung

flow

in

blood

flow

and

the

pressure-

Bass

H.

in

Oriol

patients

Christie and

RE,

in

RV:

the

chest study.

A,

Place

with

REG.

film,

a

Brit

Bates

chronic

retro-

J

DV:

Radio1

Regional

bronchitis.

lntrapulmonary

emphysema.

Palmer

pulmonary

Pride

NB,

WH,

Clin Varvis

mixing

Sci CJ,

diffusing

capacity.

S,

RL,

Permutt

minants Physiol 24.

of

and

pathological

Clin

Sci

helium

in

1968.

DV.

Donevan

and

9:

17.

Bates J

of

1950.

DV: Appl

Influence

of

Physiol

14:

age 483.

1959. 23.

pressures.

1964.

NR,

495,

Bates

Emphysema

1962.

function

on

191. 1965.

BE:

radiological

750.

health 22.

BE:

dependent

relation

Volume 48, April 1970

Bates

Heard

Anthonisen lung

363,

1966.

Heard

perivascular

Dollery

MB,

ventilation CT,

JW.

spective

35: of

J Appl

pulmonary

Doppman

veins

Friedman

35:

Dead-space

ventilation-perfusion

ment

JP,

obstructive

1966.

Farhi

Anthonisen

lung. Maloney

Respiratory

scanning-a

Decreasing lung.

of

circulation.

blood

1960. 9.

Effect

AP:

Brit

Radiology

upright

on

circulation.

monary

Invest

dynamic

JB,

1969. Henderson

21:

BB.

S:

tion

distribution

Physiol

Permutt

monary

moveLab

whole

Glazier pressure

16. Lavender

1969. diaphragmatic

of the

JMB,

15. Fishman

conges-

1966.

Regional

the

functional

Relationship

Hughes size

Milic-Emill

relations

Hughes 1967.

86:

17.

Bass

615,

and pulmonary

investigation

corresponding

92:

in

prevalence

obstructive

method

A

ments Milne

H:

NH:

19: 45,

Ross

The

cardiac

Hauge

2: 203,

8.

and

classifi-

terstitial

Hampshire

chronic

alveolar 7.

asthma,

and

1962.

DO:

New

definition

monary

ENC.

tive

5.

762.

on

1962.

combined 4.

a

Statement

bronchitis,

Anderson

disease 3.

chronic

Resp

Ferris

Society.

Gianelli flow

of 23:

S Jr, upon

maximal 646, Ayers lung

Riley

expiratory

Bomberger-Barnes flow

from

the

B: lungs.

DeterJ

Appl

1967. SM.

Buehler

mechanics.

ME:

J Clin

Effect Invest

of 46:

pulmonary 1625,

blood

1967.

415