McCance Patho Chapter 35

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Alterations of Pulmonary Function

Inadequate alveolar ventilation in relationship to metabolic demand


Cheyne-stokes respirations

Alternating periods of deep and shallow breathing and apnea. caused by anything that slows the blood flow to the brain stem.

Kussmaul respirations

An increased ventilatory rate, large tidal volumes, and no expiratory pause (hyperpnea)

Most common cause of pulmonary edema

heart disease (left-sided)


an inflammatory obstruction of the small airways called the bronchioles. Most common in children and caused by a virus. Observed in adults with chronic bronchitis. Nonproductive cough, low-grade fever.


the presence of pus in the pleural space and is a complication of respiratory infection


circumscribed area of suppuration and destruction of lung parenchyma


inflamed lung tissue that causes the alveoli to fill with exudate


the presence of fluid with low protein content residing in the pleural space

most common cause of ARDS

either sepsis or multiple trauma, which damages the alveolar capillary membrane and results in severe pulmonary edema

Increased bronchial smooth muscle spasm and increased vascular permeability cause

Asthma. Asthma is an immunoglobulin E (IgE)-mediated response.

hypersecretion of mucus with a chronic productive cough that lasts for at least 3 months for a minimum of 2 consecutive years characterizes what disorder.
The mucus is thicker and will adhere to embedded bacteria. This condition is increased up to 20 times in smokers.

chronic bronchitis.

Pseudomonas aeruginosa, S. Aureus (MRSA), Klebsiella pneumoniae, Enterobacter species

Which pathogens are commonly associated with a pneumonia that is acquired while in the hospital?


collapse of alveoli


bluish discoloration of the skin caused by desaturation of hemoglobin


reduced oxygenation of arterial blood (PaO2)


coughing up bloody mucus


passage of fluid and/or solid particles into the lungs. Gastric fluid with pH less than 2.5 has serious consequences--leads to pneumonitis.


sensation of breathlessness, shortness of breath or respiratory distress


dyspnea when lying flat

paroxysmal nocturnal dyspnea (PND)

waking up with dyspnea during the night and needing to sit upright or stand to breathe


increased ventilatory rate


normal breathing. 16-18 breaths/minute, tidal volume of 400-800ml.


High pitched sounds made during inspiration


Whistling sound made during expiration


alveolar ventilation that exceeds metabolic demands. Lungs remove CO2 faster than it is produced leading to hypocapnia


selective bulbous enlargement of the end of a digit. associated with diseases that interfere with oxygenation. Rarely reversible


increased CO2 concentration of arterial blood (PaCO2 greater than 44mm Hg). Leads to increase in hydrogen ion in the blood--respiratory acidosis. Greatest concern is electrolyte abnormalities that may cause dysrhythmias.

restricted breathing (fibrosis)

small tidal volumes and rapid ventilatory rate


irregular, quick inspirations with an expiratory pause

obstructed breathing--small airway obstruction

increased ventilatory rate, small tidal volume, increased effort, prolonged expiration, wheezing

sigh breaths

help maintain normal lung function, 1.5-2 times the normal tidal volume, approximately 10-12 times/hour.

obstructed breathing--large airway obstruction

slow ventilatory rate, increased effort, prolonged inspiration or expiration and stridor or audible wheezing

central cyanosis

decreased arterial oxygenation (low PaO2) from pulmonary disease or cardiac right-to-left shunts. Seen in buccal mucous membranes and lips.


Decreased PaCO2 (less than 36mm Hg), results in respiratory alkalosis.

Amount of oxygen in the alveoli (PAO2) is dependent which two factors?

1) Fraction of air that is composed of oxygen (FiO2)
2) Amount of alveolar minute ventilation.

Diffusion of O2 from the alveoli into the blood is dependent on these two factors:

1) Ventilation--amount of air getting into the alveoli (V) and Perfusion--amount of blood perfusing the capillaries (Q) ratio V/Q
2) alveolocapillary barrier

Normal V/Q ratio



Inadequate ventilation of well perfused areas of the lung (low V/Q)

Alveolar Dead Space

Poor perfusion of well ventilated portions of the lung (high V/Q) resulting in wasted ventilation.

Most common cause of hypoxemia

compensatory hyperventilation and resultant respiratory alkalosis

Respiratory failure

Inadequate gas exchange in which PaO2 is = or <50 mmHg (hypoxemia) or PaCO2 is = or > 50 mmHg (hypercapnia) with a pH of = or <7.25

Flail chest

Results from fractures to the rib cage. Result in instability of chest wall, causing paradoxical movement of the chest with breathing.

Chest wall restriction

Such as with kyphoscoliosis, muscle weakness, trauma. Hypoventilation, decreased tidal volume, hypercapnea


Air in the pleural space

Primary pneumothorax

occurs unexpectedly in healthy individuals, usually men between 20-40 yrs old. Most often caused by rupture of blebs on the visceral pleura. (Birt-Hogg-Dube-syndrome)

Secondary (traumatic) pneumothorax

chest trauma or surgical procedure, rupture of bleb or bulla in COPD, mechanical ventilation

Iatrogenic pneumothorax

transthoracic needle aspiration

open pneumothorax (communicating)

Air is drawn in during inspiration and is forced out during expiration

Tension pneumothorax

Site of pleural rupture acts as a one way valve. Air enters during inspiration, but prevents its escape by closing during expiration. Air pressure increases above barometric pressure. Life threatening, immediate treatment required.

Pleural effusion

Presence of fluid in the pleural space

Transudative effusion

the fluid or transudate is watery and diffuses out of the capillaries as result of disorders that increase intravascular hydrostatic pressure or decrease capillary oncotic pressure. CHF, liver or kidney disorders that cause hypoproteinemia (decreases capillary oncotic pressure)

Exudative effusion

less watery, contains high concentrations of white blood cells and plasma proteins. Occurs in response to inflammation, infection or malignancy and involves inflammatory processes that increase capillary permeability.

pulmonary edema

Excess water in the lung. Dullness to percussion over the lung bases, inspiratory crackles, pink frothy sputum.


collapse of lung tissue

compression atelectasis

collapse of lung tissue caused by external pressure exerted on the lung

absorption atelectasis

results from gradual absorption of air from obstructed or hypoventilated alveoli

surfactant impairment

decreased production or inactivation of surfactant. Premature birth, ARDS, anesthesia, or mechanical ventilation.

Post-operative atelectasis can be prevented by...

Deep breathing, frequent position changes, early ambulation


persistent abnormal chronic dilation of the bronchi. Airway damage leads to bronchospasm and copious production of purulent mucous. Primary symptom is chronic productive cough.

Cylindrical bronchiectasis

airways are symmetrically dilated. commonly seen after pneumonia and is reversible

Bronchiolitis obliterans organizing pneumonia (BOOP)

alveoli and bronchioles become filled with plugs of connective tissue

Bronchiolitis obliterans

late stage fibrotic process that occludes the airways and causes permanent scarring of the lungs.

Causes of Pulmonary Fibrosis

Idiopathic Pulmonary Fibrosis, exposure to toxic gases, pneumoconiosis, silicosis, coal worker pneumoconiosis, asbestos exposure

Idiopathic Pulmonary Fibrosis (IPF)

Most common idiopathic interstitial lung disorder. Median survival is only 2 to 4 years. Thought to result from multiple injuries to different lung sites. Diffuse inspiratory crackles.


any change in the lung caused by inhalation of inorganic dust particles. Deposition of the materials in the lungs cause the release of proinflammatory cytokines, leads to chronic inflammation with scarring of the alveolocapillary membrane. Results in pulmonary fibrosis and progressive pulmonary deterioration.

In asthma, long-term airway damage that is irreversible is know as...

Airway remodeling

An asthma episode that does not resolve with usual treatment

Status Asthmaticus

Alpha 1 antitrypsin deficiency

Genetic deficiency that causes early-onset emphysema in non-smokers. Alpha 1 antitrypsin normally inhibits the action of proteolytic enzymes that can destroy lung tissue.

The two disorders known as COPD

Chronic bronchitis and Emphysema

Clinical manifestations of emphysema

Barrel chest and wheezing

Acute Respiratory Distress Syndrome

ARDS (aka Acute Lung Injury {ALI}) aslo referred to as non cardiogenic pulmonary edema

Steps leading to ARDS

acute lung injury-->cytokines released-->neutrophils, macrophages, platelets accumulate-->neutrophils release inflammatory mediators and activate complement-->cell damage disrupts alveolocapillary membrane-->pulmonary edema occurs-->fibroblasts, lung cells proliferate-->acute respiratory failure

Clinical manifestation of ARDS

dyspnea and hypoxemia with poor response to O2 supplementation--hyperventilation and alkalosis--decreased tissue perfusion, metabolic acidosis and organ dysfunction--increased work of breathing, decreased Vt, and hypoventilation--hypercapnia, respiratory acidosis, and worsening hypoxemia--decreased cardiac output, hypotension, death

ARDS diagnosis criteria

1) acute onset of bilateral infiltrates on chest radiograph
2) low ratio of partial pressure of arterial oxygen to the fraction of
inhaled oxygen.
3) absence of clinical evidence of left atrial hypertension


chronic inflammatory disorder of the bronchial mucosa that causes bronchial hyperresponsiveness, constriction of the airways, and variable airflow obstruction that is reversible.


abnormal permanent enlargement of gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis. Expiration becomes difficult. Air trapping causes hyperexpansion of the chest. Disease is prolonged, increasing dyspnea, intermittent bouts of infection, culminate in cor pulmonale

centriacinar emphysema

destruction occurs in the respiratory bronchioles and alveolar ducts, usually in the upper lobes of the lung. Alveolar sac remains intact. Smokers

panacinar emphysema

Involves the entire acinus, damage randomly distributed and involving lower lobes. older adults and Alpha 1 antitrypsin deficient.


infection of the lower respiratory tract. Sixth leading cause of death in the U.S. Aspiration of oropharyngeal secretions is the most common route.

Hospital Acquired Pneumonia

The second most common nosocomial infection, but has the greatest mortality.


The most common cause of viral pneumonia

Tuberculosis (TB)

Infection caused by Mycobacterium tuberculosis. The leading cause of death from a curable disease throughout the world. Highly contagious and transmitted through airborne droplets.


TB--Neutrophils, lymphocytes, and macrophages seal off the colonies of bacilli, forming a granulomatous lesion.

Caseation necrosis

TB--Cheeselike material formed when infected tissues within the tubercle die.

TB manifestations

Latent TB is asymptomatic. Symptoms of active disease develop so gradually that they are not noticed until the disease is advanced. Common clinical manifestations include fatigue, weight loss, lethargy, anorexia, low-grade fever, night sweats.

Pulmonary Embolism (PE)

occlusion or partial occlusion of the pulmonary artery or its branches by an embolus. Most often results from DVT.

Virchow's triad

Increased risk for PE--hemodynamic stasis, hypercoagulability, and endothelial injury.

PE manifestations

sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia, and unexplained anxiety. ECG may show evidence of strain on the right side of the heart. Measure serum D-dimer, product of thrombus degradation by the fibrinolytic system.

Pulmonary Artery Hypertension (PAH)

Mean pulmonary artery pressure greater than 25 mmHg at rest. COPD is the most common lung disease associated with PAH, but any condition that causes chronic hypoxemia can result in PAH.

Cor pulmonale

right ventricular enlargement secondary to pulmonary artery hypertension. The right ventricle usually fails when pulmonary artery pressure equals systemic blood pressure.

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