Transcript Chapter 7 Body Systems - Kingwood Application Server

Chapter 20
Pulmonary Embolism
and Infarction
A
B
PE
C
D
Figure 20-1. A, Pulmonary embolism (PE). Bronchial smooth muscle constriction (B), atelectasis (C),
and alveolar consolidation (D) are common secondary anatomic alterations of the lungs.
Slide 1
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Anatomic Alterations of the Lungs
Slide 2

Blockage of the pulmonary vascular system

Pulmonary infarction

Alveolar atelectasis

Alveolar consolidation

Occasional bronchospasm
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Etiology
Slide 3

More than 600,000 cases reported yearly in
the U.S.

From this group, about 30,000 die annually

Diagnosis is missed in 70% or more of the
cases

Thus the possibility of a pulmonary embolism
should be considered for any unexplained
dyspnea, tachypnea, and chest pain
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Etiology

Blood clots—most common source of
pulmonary emboli


Slide 4
Most originate from deep veins in the lower part
of the body, i.e., leg veins
Other possible causes

Fat

Air

Amniotic fluid

Bone marrow

Tumor fragments
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Etiology
Risk factors

Slide 5
Venous stasis

Prolonged bed rest

Prolonged sitting

Congestive heart failure

Varicose veins

Thrombophlebitis
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Etiology
Risk factors

Slide 6
Trauma

Bone fractures

Extensive injury to soft tissue

Postoperative or postpartum states

Extensive hip or abdominal operation

Phlegmasia alba dolens puerperarum
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Etiology
Risk factors


Slide 7
Hypercoagulation disorders

Oral contraceptives

Polycythemia
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Multiple myeloma
Others

Obesity

Malignant neoplasm

Pregnancy

Burns
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Diagnosis and Screening
Slide 8

Chest x-ray

Electrocardiogram (ECG)

. .
Ventilation/perfusion scan (V/Q scan)

Fast computed tomography scan

Pulmonary angiogram
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Diagnosis and Screening
Additional tests used to detect blood clots
in veins
Slide 9

Fibrinogen test

Extremity venography

Duplex ultrasonography (DUS)

Magnetic resonance imaging (MRI)
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Overview of the Cardiopulmonary
Clinical Manifestations Associated
with PULMONARY EMBOLISM
The following clinical manifestations result from the
pathophysiologic mechanisms caused (or
activated) by Atelectasis (see Figure 9-7)—the
major anatomic alterations of the lungs associated
with pulmonary embolism (see Figure 20-1).
Bronchospasm (see Figure 9-10) also may explain
some of the following findings. It occurs rarely and
is of little clinical significance compared with the
atelectasis and increased physiologic dead space
caused by the embolism.
Slide 10
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Figure 9-7. Atelectasis clinical scenario.
Slide 11
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Figure 9-10. Bronchospasm clinical scenario (e.g., asthma).
Slide 12
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Clinical Data Obtained at the
Patient’s Bedside
Vital signs

Slide 13
Increased respiratory rate
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Stimulation of the peripheral chemoreceptors

Reflexes from the aortic and carotid sinus
baroreceptors

Increased heart rate

Systemic hypotension
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Figure 20-2. Dead-space ventilation in pulmonary embolism.
Slide 14
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Figure 20-3. Venous admixture develops in pulmonary embolism as a result of
bronchial smooth muscle constriction (shuntlike effect).
Slide 15
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Clinical Data Obtained at the
Patient’s Bedside
Slide 16
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Cyanosis
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Cough and hemoptysis
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Peripheral edema and venous distention
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Distended neck veins
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Swollen and tender liver

Chest pain/decreased chest expansion

Syncope, lightheadedness, and confusion
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Clinical Data Obtained at the
Patient’s Bedside


Abnormal heart sounds
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Increased second heart sound (S2)
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Increased splitting of the second heart sound (S2)

Third heart sound (S3) or ventricular gallop
Other cardiac manifestations

Slide 17
Right ventricular heave or lift
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Figure 20-4. A right ventricular lift can be detected in patients with a pulmonary
embolism if significant pulmonary hypertension is present.
Slide 18
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Clinical Data Obtained at the
Patient’s Bedside

Slide 19
Chest assessment findings
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Crackles

Wheezes

Pleural friction rub
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Clinical Data Obtained from
Laboratory Tests and
Special Procedures
Slide 20
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Arterial Blood Gases
Mild to Moderate Pulmonary Embolism

Acute alveolar hyperventilation with
hypoxemia
pH

Slide 21
PaCO2

HCO3 (Slightly)
PaO2

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Time and Progression of Disease
Disease Onset
Alveolar Hyperventilation
100
90
PaO2 or PaCO2
80
Point at which PaO2
declines enough to
stimulate peripheral
oxygen receptors
70
60
PaO2
50
40
30
20
10
0
Figure 4-2. PaO2 and PaCO2 trends during acute alveolar hyperventilation.
Slide 22
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Arterial Blood Gases
Extensive Pulmonary Embolism and
Infarction

Acute ventilatory failure with hypoxemia
pH

Slide 23
PaCO2

HCO3 (Slightly)
PaO2

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Time and Progression of Disease
Disease Onset
Alveolar Hyperventilation
Acute Ventilatory Failure
100
90
Pa02 or PaC02
80
70
Point at which PaO2
declines enough to
stimulate peripheral
oxygen receptors
Point at which disease
becomes severe and patient
begins to become fatigued
60
50
40
30
20
10
0
Figure 4-7. PaO2 and PaCO2 trends during acute ventilatory failure.
Slide 24
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Oxygenation Indices
QS/QT
DO2
VO2


Normal
O2ER

Slide 25
C(a-v)O2
Normal
SvO2

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Hemodynamic Indices
(Extensive Pulmonary Embolism)
Slide 26
CVP
RAP
PA
PCWP



 Normal
CO
SV
SVI
CI




RVSWI
LVSWI
PVR
SVR



Normal
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Three Major Mechanisms May
Contribute to the Pulmonary
Hypertension
Slide 27
1.
Decreased cross-sectional area of the
pulmonary vascular system because of the
embolus
2.
Vasoconstriction induced by humoral agents
3.
Vasoconstriction induced by alveolar hypoxia
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Abnormal Electrocardiographic
Patterns
Slide 28
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Sinus tachycardia
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Atrial arrhythmias
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Atrial tachycardia
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Atrial flutter
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Atrial fibrillation

Acute right ventricular strain pattern
and right bundle branch block

P-pulmonale
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Radiologic Findings
Chest radiograph
Slide 29
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Increased density
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Hyperradiolucency distal to the embolus
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Dilation of the pulmonary arteries
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Pulmonary edema

Right ventricular cardiomegaly

Pleural effusion
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Figure 20-5. Abnormal ventilation and perfusion lung scans in a patient with a right main
pulmonary artery embolism. A, A normal ventilation scan shows a uniform distribution of gas, with
the dark areas reflecting the presence of the radioactive gas and, therefore, good ventilation (right
lung is on viewer’s left). B, An abnormal perfusion scan. The dark area shown in the right lung
represents good blood flow. The white or light areas shown in the left lung represent decreased or
completely absent blood flow (right lung is on viewer’s left).
Slide 30
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Figure 20-6. Pulmonary emboli. Pulmonary angiogram shows numerous filling defects.
Trailing ends of the occluding thromboemboli are particularly well shown (arrows).
Slide 31
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General Management of
Pulmonary Embolism


Fast-acting anticoagulant heparin

Calciparine

Liquaemin
Slow-acting anticoagulant


Slide 32
Warfarin
• Coumadin
• Panwarfin
Unfractionated heparin
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General Management of
Pulmonary Embolism

Slide 33
Thrombolytic agents

Streptokinase
• Kabikinase
• Streptase

Urokinase
• Abbokinase

Activase
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General Management of
Pulmonary Embolism
Preventive measures
Slide 34

Vein filter

Heparin or warfarin therapy

Graduated compression stockings

Pneumatic compression
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General Management of
Pulmonary Embolism
Respiratory care treatment protocols
Slide 35

Oxygen therapy protocol

Aerosolized medication protocol

Mechanical ventilation protocol
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General Management of
Pulmonary Embolism
Pulmonary embolectomy

Slide 36
Last resort
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Classroom Discussion
Case Study:
Pulmonary Embolism
Slide 37
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