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U N I T 6
Respiratory Function
insertion of a filter to prevent emboli from traveling to
the lung may be indicated in life-threatening situations or
in cases where thrombolytic therapy or anticoagulation is
contraindicated.
Venous thromboembolism is often clinically silent
until it presents with significant morbidity and mortal-
ity. Thus, recognition of risk factors and appropriate pre-
ventative treatment are essential. Prophylactic measures
include early ambulation for postoperative and postpar-
tum patients and the use of graded compression elastic
stockings and intermittent pneumatic compression (IPC)
boots for bedridden patients. Intermittent pneumatic
compression boots provide intermittent inflation of air-
filled sleeves that prevent venous stasis. Some devices pro-
duce sequential gradient compression that moves blood
upward in the leg. Anticoagulant therapy may be used to
decrease the likelihood of deep vein thrombosis, throm-
boembolism, and fatal pulmonary embolism after major
surgical procedures (see Chapter 12). Low–molecular-
weight heparin, which can be administered subcutane-
ously, often is used. Warfarin, an oral anticoagulation
drug, may be used for persons with a long-term risk for
development of thromboemboli. Newer factor Xa inhibi-
tors are gaining popularity as an alternative to warfarin
due to their efficacy and fewer food and drug interactions.
Pulmonary Hypertension
The pulmonary circulation is normally a low-pressure
system designed to accommodate varying amounts
of blood delivered from the right heart. The main
pulmonary artery and major branches are relatively
thin-walled, compliant vessels. The distal pulmonary
arterioles also are thin walled and have the capacity to
dilate, collapse, or constrict depending on the presence
of vasoactive substances released from the endothelial
cells of the vessel, neurohumoral influences, flow veloc-
ity, oxygen tension, and alveolar ventilation.
Pulmonary hypertension
is a disorder characterized by
an abnormal elevation of pressure within the pulmonary
circulation—namely, the pulmonary arterial system.
62,63
Once present, pulmonary hypertension is self-perpetu-
ating. It introduces secondary structural abnormalities
of pulmonary vessels including smooth muscle hypertro-
phy and proliferation of the vessel intima. Although pul-
monary hypertension can develop as a primary disorder,
most cases develop secondary to other conditions.
Secondary Pulmonary Hypertension
Secondary pulmonary hypertension refers to an increase
in pulmonary pressures associated with other disease
conditions, usually cardiac or pulmonary.
10,15,16
Often
more than one disorder, such as COPD, heart failure,
and sleep apnea, contributes. Secondary pulmonary
hypertension may develop at any age. Mechanisms
include: (1) elevation of pulmonary venous pressure, (2)
increased pulmonary blood flow, (3) pulmonary vascu-
lar obstruction, and (4) hypoxemia.
Elevation of pulmonary venous pressure is com-
mon in conditions such as mitral valve disorders or left
ventricular diastolic dysfunction. In each of these altera-
tions, the elevated left atrial pressure is transmitted to
the pulmonary circulation. Continued increases in left
atrial pressure can lead to medial hypertrophy and
intimal thickening of the small pulmonary arteries,
causing sustained hypertension.
Increased pulmonary blood flow results from
increased flow through left-to-right shunts in congenital
heart diseases such as atrial or ventricular septal defects and
patent ductus arteriosus. If the high-flow state is allowed
to continue, morphologic changes occur in the pulmonary
vessels, leading to sustained pulmonary hypertension. The
pulmonary vascular changes that occur with congenital
heart disorders are discussed in Chapter 19.
Obstruction of pulmonary blood flow is commonly
due to pulmonary thromboemboli. Persons who are
promptly treated for acute pulmonary thromboembolism
with anticoagulants rarely develop pulmonary hyperten-
sion. However, in some persons chronic obstruction of
the pulmonary vascular bed develops because of impaired
resolution of the thromboemboli.
Continued exposure of the pulmonary vessels to
hypoxemia is a common cause of pulmonary hyperten-
sion. Unlike blood vessels in the systemic circulation,
most of which dilate in response to hypoxemia and
hypercapnia, the pulmonary vessels constrict. The stim-
uli for constriction are thought to originate in the air
spaces near the smaller branches of the pulmonary arter-
ies. In regions of the lung that are poorly ventilated, the
response is adaptive in that it diverts blood flow away
from the poorly ventilated areas to those areas that
are more adequately ventilated. This effect, however,
becomes less beneficial as more and more areas of the
lung become poorly ventilated. Pulmonary hypertension
is a common problem resulting from hypoxemia that
develops in persons with advanced COPD or interstitial
lung disease.
62
It also may develop at high altitudes in
persons with normal lung function. Persons who expe-
rience marked hypoxemia during sleep (such as those
with sleep apnea) often experience marked elevations in
pulmonary arterial pressure.
Secondary pulmonary hypertension is difficult to rec-
ognize in its early stages, when the signs and symptoms
are primarily those of the underlying disease. Pulmonary
hypertension may cause, or contribute to, dyspnea, present
initially with exertion and later at rest. Fatigue and syncope
on exertion also occur, presumably the result of reduced
cardiac output and elevated pulmonary artery pressures.
Diagnosis is based on radiographic findings and
echocardiography. Doppler ultrasonography is a reli-
able noninvasive method for estimating pulmonary
artery systolic pressure. Treatment measures are directed
toward the underlying disorder. Vasodilator therapy
may be indicated.
Primary Pulmonary Arterial Hypertension
Primary pulmonary arterial hypertension (PAH) is per-
sistent elevation in pulmonary artery pressure that occurs
in the absence of identified cardiopulmonary or other
secondary causes of pulmonary hypertension.
10,15,16,63–66
