5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

TABLE 21.4

Pulmonary Hypertension Severity Rating Based on Exercise Testing*

Class Description

Class 1 No remarkable limits. The patient performs regular physical activities (e.g., walking or climbing stairs) without causing pulmonary hypertension (PH) symptoms (e.g., tiredness, shortness of breath, or chest pain).

Class 2 Slight or mild limits. The patient is comfortable while resting, but regular physical activity (e.g., walking or climbing stairs) causes PH symptoms.

Class 3 Marked or noticeable limits. Comfortable while resting. However, regular physical activity (e.g., walking or climbing stairs) causes PH symptoms.

Class 4 Severe limits. Patient unable to do any physical activity without discomfort. PH symptoms may be present at rest.

*Exercise testing typically entails either (1) a 6-minute walk test, which measures the distance the patient can quickly walk in 6 minutes, or (2) a cardiopulmonary exercise test (CPET), which measures, in detail, how well the cardiopulmonary system functions while exercising on a treadmill or bicycle.

Left-Sided Heart Failure Versus Right-Sided Heart Failure

Although there are several clinical conditions that can cause right-sided heart failure and cor pulmonale (e.g., COPD, coronary artery disease, pulmonary embolic disease, pulmonic stenosis, tricuspid stenosis, and tricuspid regurgitation), left-sided heart failure (congestive heart failure) is more commonly the cause of PH. Because the respiratory therapist frequently encounters patients in left-sided or right-sided failure or a combination of both (biventricular failure) it is important to differentiate and identify the major signs and symptoms (although sometimes overlapping) associated with left-sided and right-sided heart failure. On the basis of the patient's history and physical examination, the common signs and symptoms caused by either left-sided or right-sided heart failure are presented in Box 21.5.

Box 21.5

Signs and Symptoms: Left-Sided Heart Failure Versus Right-Sided Heart

Failure

Right-Sided Heart Failure

•Shortness of breath

•Irregular fast heart rate

•Distended neck veins

•Peripheral edema and venous distention

•Distended neck veins

•Swollen and tender liver

•Ankle and feet swelling

•Pitting edema

•Heart palpitations

•Abdominal distention (bloating)—ascites

•Abdominal pain

•Urinating more frequently at night

•Anorexia

•Nausea

•Fatigue, weakness, faintness

•Weight gain

Left-Sided Heart Failure

•Shortness of breath

•Lightheadedness or fainting

•Frothy, blood-tinged sputum

•Crackles

•Cough and hemoptysis

•Orthopnea

•Paroxysmal nocturnal dyspnea

•Weak pulse

•Hypotension

•Decreased urine production

•Activity intolerance

•Fatigue, weakness, faintness

•Weight gain and fluid retention

•Heart palpitations

•Anxiety

•Excessive sweating

•Cyanosis

•Cool or clammy skin to touch

Management of Pulmonary Hypertension

Although, in general, pulmonary hypertension has no cure, treatment may help reduce the symptoms and slow the progress of the disease depending on the cause of the condition. The management of PH includes medicines, procedures, and other therapies. The precise treatment selection depends on what type of PH the patient has and its severity. Table

21.5 provides an overview of the treatment selections currently used to manage PH. In addition, several different treatments may be used to manage all types of PH. For example, therapies commonly used to treat all types of PH include the following:

TABLE 21.5

Treatment Selections Used to Manage Pulmonary Hypertension

As many as 25%–30% of patients with chronic thromboembolic pulmonary hypertension may never have had a diagnosed pulmonary embolism or even a history suggestive of pulmonary embolism, and 45%–55% may never have had a history of deep vein thrombus.

•Diuretics: To help decrease fluid buildup, including swelling in ankles and feet.

•Phosphodiesterase inhibitors: Especially in group I patients.

•Blood-thinning medications: To help prevent blood clots from forming or getting larger.

•Cardiac glycosides (digoxin, etc.): To help the heart to pump stronger or to control the heart rate.

•Oxygen therapy: To treat hypoxemia.

•Physical activity: To improve exercise tolerance.

•Inhaled nitric oxide (iNO) therapy: May be helpful in groups 1 and 4 (Box 21.3). An oral agent that mimics the effect of the inhaled gas is now available (riociguat).

The Emerging Role of the Respiratory Therapist in Pulmonary Vascular Disorders

In the future, the role of the respiratory therapist will, undoubtedly, expand in the diagnosis and management areas of patients with pulmonary vascular disease. For example, at the patient bedside, the perceptive respiratory therapist may likely be the first to recognize and report important signs and symptoms associated with left-sided heart failure or rightsided heart failure and, importantly, identify key signs and symptoms of deep venous thrombosis, pulmonary embolism, or pulmonary hypertension itself. Such information-gathering and timely communication may be lifesaving. In addition, the role of the respiratory therapist in the management of pulmonary vascular diseases will further broaden as inhaled gas (e.g., inhaled nitric oxide [iNO]) and various aerosolized medications (e.g., iloprost and treprostinil) continue to demonstrate long-term therapeutic benefits.2 Excellent patient education materials on this topic are available from the Pulmonary Hypertension Association website (https://phassociation.org).

Case Study Pulmonary Embolism

Admitting History

A 32-year-old motorcycle enthusiast who smoked one pack of cigarettes per day fell from his bike while riding with a group of Harley “hogs” to the annual Sturgis Rally in North Dakota. Although his motorcycle sustained extensive damage, the man was conscious when the ambulance arrived. Before he was transported to the local hospital, he was treated in the field; splints and an immobilizer were applied. His injuries were thought to include a fractured pelvis, left tibia, and left knee.

En route to the hospital, a nonrebreathing oxygen mask was placed over the man's face. An intravenous infusion was started with 5% glucose solution. The patient was alert and able to answer questions. His vital signs were blood pressure 150/90 mm Hg, heart rate 105 beats/min, and respiratory rate 20 breaths/min. Various small lacerations and scrapes on his face and left shoulder were treated. Each time the man was moved slightly or when the ambulance suddenly bounced or turned sharply as it moved over the highway, he complained of abdominal and bilateral chest pain. The emergency medical technician (EMT) crew all thought his helmet and his youth had saved his life.

In the emergency department, a laboratory technician drew the patient's blood; several x-ray films were taken, and the man was given morphine for the pain. Within an hour the patient was taken to surgery to have the broken bones in his left leg repaired. He was transferred 4 hours later to the intensive care unit (ICU) with his left leg in a cast. Thrombosis and embolism prophylaxis had been started with low-dose heparin. Busy with another surgery, the physician ordered a respiratory care consultation for the patient.

Physical Examination

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ABGs on 100% oxygen were pH 7.25, PaCO2 69 mm Hg, 27 mEq/L, PaO2 37 mm Hg, and SaO2 59%. On the basis of these clinical data, the following SOAP was documented.

Respiratory Assessment and Plan

S N/A (patient not responsive)

O CTPA scan: No blood flow to right middle lobe; cyanosis; cough: small amount of bloodtinged sputum; vital signs BP 70/35, HR 160, RR 25 and shallow, T 37.5°C (99.2°F); palpation negative; dull percussion notes over right middle lobe; wheezing over both lungs; pleural friction rub over right middle lobe; ECG: Alternating among normal sinus rhythm, sinus

tachycardia, and atrial flutter; ABGs on 100% O2 pH 7.25, PaCO2 69, 27, PaO2 37, and SaO2 59%.

A

•Acute ventilatory failure with severe hypoxemia (ABGs)

•Pulmonary embolism and infarction (CTPA scan)

•Bronchospasm (wheezing)

P Contact physician stat. Discuss acute ventilatory failure and need for intubation and Mechanical Ventilation Protocol. Manually ventilate until physician arrives. Continue Oxygen Therapy Protocol via manual resuscitation at an FIO2 of 1.0—add continuous positive airway

pressure (CPAP) at 10 cm H2O. Increase Aerosolized Medication Protocol (continue med. neb. with 2 mL albuterol premix qid).

Discussion

Risk factors for development of a fatal pulmonary embolism include pelvis and long bone fractures, immobilization, malignant disease, and a history of thrombotic disease (including venous thrombosis), congestive heart failure, and chronic lung disease. Only about 10% of patients with pulmonary emboli do not have at least one of these risk factors. The symptoms of ultimately fatal pulmonary embolism include dyspnea (in about 60% of patients), syncope (in about 25% of patients), altered mental status, apprehension, nonpleuritic chest pain, sweating, cough, and hemoptysis (in a smaller percentage of patients).

The signs of acute pulmonary embolism and infarction include tachypnea, tachycardia, crackles, low-grade fever, lower extremity edema, hypotension, cyanosis, gallop rhythm, diaphoresis, and clinically evident phlebitis (in a small percentage of patients).

It is interesting to note that in surgical patients, at least half of the deaths caused by pulmonary embolism occur within the first week after the surgical procedure, most commonly on the third to seventh day after the operation. The remainder of the deaths, however, divide equally among the second, third, and fourth postoperative weeks. The current patient certainly had one of the obvious causes for pulmonary embolism—pelvis and long bone fractures and immobilization of the left leg, which was put in a cast after surgery.

At the time of the first assessment, the patient was not in any respiratory distress. His chest physical examination was basically unremarkable, as were the chest x-ray and ABGs. The patient might well have been placed on hyperexpansion therapy, such as incentive spirometry or even mask CPAP therapy, to be proactive in preventing atelectasis. This fact was particularly important for this patient, who was on morphine and might have been prone to hypoventilate because of his left shoulder and left anterior chest pain and tenderness.

By the time of the second assessment, however, things had changed dramatically; the patient demonstrated many of the signs and symptoms associated with a pulmonary embolism and infarction. The assessing therapist should have recognized the seriousness of the situation from the patient's complaints, history, physical findings, Wells score of 7, and ABGs. The patient's wheezing most likely was a result of pulmonary embolism and infarction, as was the atelectasis. However, a trial of aerosolized bronchodilation was not inappropriate given the patient's smoking history. The data were abnormal enough to prompt the therapist to suggest that the patient be transferred to the ICU and to prepare for ventilator support because acute ventilatory failure might not have been far off.

Indeed, in the last assessment, things had progressed to the point at which the patient was in severe respiratory acidosis with severe hypoxemia, and mechanical ventilation became necessary. Much more lung tissue than just the right middle lobe must have been embolized, and a repeat CTPA later in the patient's clinical course was almost certainly indicated and might have justified even more aggressive therapy. The treating therapist should recognize that the therapeutic options in such cases are limited by the amount of ventilation “wasted” in these patients because of their embolic disease. High minute volume ventilation may be necessary to improve (even slightly) the ABGs in such patients. Some centers would have considered an attempt at pulmonary embolectomy at this juncture.

One final note: The outlook for this patient was extremely poor. Indeed, he died during the fifth week of his hospitalization. He remained on ventilator support until the time of his death.

Self-Assessment Questions

1.Most pulmonary emboli originate from thrombi in the:

a.Lungs

b.Right side of the heart

c.Leg and pelvic veins

d.Pulmonary veins

2.The aortic and carotid sinus baroreceptors initiate which of the following in response to a decreased systemic blood pressure?

1.Increased heart rate

2.Increased ventilatory rate

3.Decreased heart rate

4.Decreased ventilatory rate

5.Ventilatory rate is not affected by the aortic and carotid sinus baroreceptors.

a.1 and 5 only

b.2 and 3 only

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PA R T V I

Chest and Pleural Trauma

OUTLINE

Chapter 22 Flail Chest

Chapter 23 Pneumothorax

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FIGURE 22.1 Flail chest. Double fractures of three or more adjacent ribs produce instability of the chest wall and paradoxical motion of the thorax. Inset, Atelectasis, a common secondary anatomic alteration of the lungs.

A flail chest causes a restrictive lung disorder, is often life-threatening in severe cases, and requires immediate medical intervention. The major pathologic or structural changes of the lungs that may result from a flail chest are as follows:

•Double fracture of numerous adjacent ribs

•Rib instability

•Lung volume restriction

•Atelectasis

•Lung collapse (pneumothorax)

•Pulmonary contusion (e.g., from trauma)

•Secondary pneumonia (e.g., from weak cough because of pain)

Etiology and Epidemiology

A blunt or crushing injury to the chest is usually the cause of flail chest. Such trauma may result from the following:

•Motor vehicle accidents

•Falls

•Blast injury

•Direct compression (trauma) by a heavy object

•Occupational and industrial accident

Overview of the Cardiopulmonary Clinical Manifestations Associated With Flail Chest

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by atelectasis (see Fig. 10.7) and consolidation (see Fig. 10.8)—the major anatomic alterations of the lungs associated with flail chest (see Fig. 22.1).

Clinical Data Obtained at the Patient's Bedside

The Physical Examination

Vital Signs

Increased Respiratory Rate (Tachypnea)

Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate. These include the following:

•Stimulation of peripheral chemoreceptors (hypoxemia)

•Paradoxical movement of the chest wall

Paradoxical Movement of the Chest Wall

When double fractures exist in at least three or more adjacent ribs, a paradoxical movement of the chest wall is seen. During inspiration the fractured ribs are pushed inward by the atmospheric pressure surrounding the chest and negative intrapleural pressure. During expiration (and particularly during forced exhalation), the flail area bulges outward when the intrapleural pressure becomes greater than the atmospheric pressure.

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As a result of the paradoxical movement of the chest wall, the lung area directly beneath the broken ribs is compressed during inspiration and is pushed outward with the flail segment during expiration. This abnormal chest and lung movement causes gas to be shunted from one lung to another during a ventilatory cycle.

When the lung on the affected side is compressed during inspiration, gas moves into the lung on the unaffected side. During expiration, however, gas from the unaffected lung moves into the affected lung. The shunting of gas from one lung to another is known as pendelluft (Fig. 22.2). As a consequence of the pendelluft, the patient rebreathes dead-space gas and hypoventilates. In addition to the hypoventilation produced by the pendelluft, alveolar ventilation also may be decreased by the lung compression and atelectasis associated with the unstable chest wall.

FIGURE 22.2 Lateral flail chest with accompanying pendelluft.

As a result of the pendelluft, lung compression, and atelectasis, the ventilation-perfusion ratio decreases. This leads to intrapulmonary shunting and venous admixture (Fig. 22.3). Because of the venous admixture, the patient's PaO2 and

CaO2 decrease. As this condition intensifies, the patient's oxygen level may decline to a point low enough to stimulate the peripheral chemoreceptors, which in turn initiate an increased ventilatory rate.

FIGURE 22.3 Venous admixture in flail chest.

Other Possible Mechanisms

•Relationship of decreased lung compliance to increased ventilatory rate

•Activation of the deflation receptors

•Activation of the irritant receptors

•Stimulation of the J receptors

•Pain, anxiety

Increased Heart Rate (Pulse) and Blood Pressure (e.g., caused by hypoxemia and paisn)

Cyanosis

Chest Assessment Findings

• Diminished breath sounds, on both the affected and the unaffected sides

Clinical Data Obtained From Laboratory Tests and Special Procedures

Pulmonary Function Test Findings

(Restrictive Lung Pathology)