Return to site

Physiology and Pathophysiology

Describe the basic anatomy and functions of the pulmonary system including pulmonary circulation.

The respiratory system includes the lungs and a series of airways that connect the lungs to the external environment.

The structures of the respiratory system can be divided into two groups; The conducting zone, which brings air into and out of the lungs, and the respiratory zone, which is lines with alveoli, where gas exchange occurs.

Describe the basic anatomy and functions of the pulmonary system including pulmonary circulation

The Conduction Zone
Nose, nasopharynx, larynx, trachea, bronchi, bronchioles, and terminal bronchioles.
These structures function to bring air into and out of the respiratory zone for gas exchange and to warm, humidify and filter air before it reaches the critical gas exchange region Bonuses.
Trachea:
Main conduction airway
Divides into two bronchi, one leading to each lung.
The conducting airways are lined with mucous secreting and ciliated cells that function to remove inhaled particles. Large particles are filtered out in the nose, small particles are captured by mucous and swept upward by rhythmic cilia, causing sneezing.
The walls of the conducting airway contain smooth muscle:
Contains both sympathetic and parasympathetic innervations, which have opposite effects on airway diameter.

Pulmonary Vessels Physiologic Anatomy

Pulmonary Vessels
The pulmonary artery extends only 5 centimeters beyond the apex of the right ventricle and then divides into right and left main branches that supply blood to the two respective lungs.


The pulmonary artery is thin, with a wall thickness one third that of the aorta. The pulmonary arterial branches are very short, and all the pulmonary arteries, even the smaller arteries and arterioles, have larger diameters than their counterpart systemic arteries. This, combined with the fact that the vessels are thin and distensible, gives the pulmonary arterial tree a large compliance , averaging almost 7 ml/mm Hg, which is similar to that of the entire systemic arterial tree. This large compliance allows the pulmonary arteries to accommodate the stroke volume output of the right ventricle.


The pulmonary veins, like the pulmonary arteries, are also short. They immediately empty their effluent blood into the left atrium.

Bronchial Vessels Physiologic Anatomy

Bronchial Vessels
Blood also flows to the lungs through small bronchial arteries that originate from the systemic circulation, amounting to about 1 to 2 percent of the total cardiac output. This bronchial arterial blood is oxygenatedblood, in contrast to the partially deoxygenated blood in the pulmonary arteries. It supplies the supporting tissues of the lungs, including the connective tissue, septa, and large and small bronchi. After this bronchial and arterial blood has passed through the supporting tissues, it empties into the pulmonary veins and enters the left atrium , rather than passing back to the right atrium. Therefore, the flow into the left atrium and the left ventricular output are about 1 to 2 percent greater than that of the right ventricular output.

Lymphatics Physiologic Anatomy

Lymphatics
Lymph vessels are present in all the supportive tissues of the lung, beginning in the connective tissue spaces that surround the terminal bronchioles, coursing to the hilum of the lung, and then mainly into the right thoracic lymph duct . Particulate matter entering the alveoli is partly removed by way of these channels, and plasma protein leaking from the lung capillaries is also removed from the lung tissues, thereby helping to prevent pulmonary edema.

Gravitational Effects Physiology Anatomy

Gravitational Effects
Pulmonary blood flow is not distributed evenly in the lungs. When a person is standing, blood flow is lowest at the apex (top) of the lungs and highest and the base (bottom).
Regulation of pulmonary blood flow is accomplished by altering the resistance of the pulmonary arterioles. Changes in pulmonary arteriolar resistance are controlled by local factors, mainly 02.
Bronchial circulation is the blood supply to the conduction airways (not participating in gas exchange) and is a very small fraction of total pulmonary flow.

Define the lung volumes and capacities.

LUNG VOLUMES
Normal Tidal Volume
Approx. 500 ml
The volume of air that fills the alveoli plus the volume of air that fills the airways.
Inspiratory Reserve Volume
Approx. 3000 ml
The additional volume that can be inspired ABOVE tidal volume
Expiratory Reserve Volume
Approx. 1200ml
The additional volume that can be expired BELOW tidal volume.
Residual Voume
Approx. 1200ml
The volume of gas remaining in the lungs after a maximal forced expiration

Lung Capacites

LUNG CAPACITIES
Each lung capacity includes two or more lung volumes
Inspiratory Capacity (IC)
Approx. 3500ml
Compised of tidal volume plus the inspiration reserve volume.
Functional Residual Capacity (FRC)
Approx 2400ml
Composed of the expiratory reserve volume plus residual volume.
FRC is the volume remaining in the lungs after normal tidal volume is expired and can be thought of as equilibrium volume of the lungs.
Vital Capacity (VC)
Approx.4700ml
Composed of the inspiratory capacity plus the expiratory reserve volume.
It is the volume that can be expired after maximal inspiration.
Value increases with body size, male gender, and physical conditioning and deceases with age.
Total Lung Capacity (TLC)
Approx 5900ml
Composed of all the lung volumes; vital capacity plus residual volume.
Dead Space
The volume of the airways and lungs that does not participate in gas exchange.
Anatomic dead space is the volume of conducting airways, including the nose, trachea, bronchi and bronchioles.
Physiologic Dead space is the total volume of the lungs that does not participate in gas exchange.

Describe the process of gas exchange and transport, as well as factors impacting gas exchange and transport.

Gas exchange depends on an approximately even distribution of gas (ventilation) and blood (perfusion) in all proportions of the lungs. When an individuals is in an upright position, gravity pulls the lungs down toward the diaphragm and compresses the lower portions or bases.

The alveoli in the upper portions or apexes of the lungs contain a greater residual volume of gas and are larger and less numerous than those in the lower portions. Surface tension increases as the alveoli become larger, and the alveoli in the upper portions of the lung are more difficult to inflate than the smaller alveoli in the lower portions of the lung. Therefore, during ventilation, most of the tidal volume is distributed to the bases of the lungs where compliance is greatest.


Factors Impacting Gas Exchange:
Body Position: The greatest volume of pulmonary blood flow will normally occur in the gravity dependent areas of the lungs. Body position has a significant effect on the distribution of pulmonary blood flow. Therefore, if a standing individual assumes a supine or side lying position, the areas of the lungs that are then most dependent become the best ventilated and perfused.


Alveolar Pressure: The pulmonary capillary bed differs from the systemic capillary bed in that it is surrounded by gas containing alveoli. If the gas pressure in the alveoli exceeds the blood pressure in the capillary, the capillary collapses and flow ceases. This is most likely to occur in portion of the lung where blood pressure is lowest and alveolar gas pressure is greatest, that is, the apex of the lung.

Describe ventilation/perfusion ratios and the lung zones.

Ventilation/Perfusion: The relationship between ventilation and perfusion is expressed as V/Q. The normal V/Q ratio is 0.8. This is the amount by which perfusion exceeds ventilation under normal circumstances (p1240 M&H)

VENTILATION/PERFUSION RATIO

Ideally, each alveolus in the lungs would receive the same amount of ventilation and pulmonary capillary blood flow (perfusion). In reality, ventilation and perfusion differ depending on the region of the lung.

· On average, the alveolar ventilation is about 4 L/min.
· Normal pulmonary capillary blood flow is about 5 L/min.

· In the upright lung, the ventilation/perfusion ratio progressively decreases from the apex to the base.

o The alveoli in the upper lung portions receive moderate ventilation and little blood flow.
The resulting ventilation/perfusion ratio is higher than 0.8 (ventilation > perfusion).

o In lower regions of the lung, the alveolar ventilation is moderately increased and the blood flow is greatly increased (since blood flow is gravity dependent).


Thus, the ventilation/perfusion ratio is lower than 0.8 (perfusion > ventilation).

· Two key relationships to remember are:
o When the ventilation/perfusion ratio increases, ventilation >perfusion.
o When the ventilation/perfusion ratio decreases, perfusion >ventilation.

*Most common cause of V/Q mismatch is hypoxemia R/T (from Video)
*Pneumonia
*PE
*COPD

Lungs are divided into Three Zones:
Zone 1- "No blood flow during all portions of the cardiac cycle", Is where alveolar pressure exceeds pulmonary arterial and venous pressures. The capillary bed collapses and normal blood flow ceases. Normally zone 1 is a very small part of the lung at the apex.


Zone 2- " Intermittent blood flow", is the portion where alveolar pressure is greater than venous pressure, but not greater than arterial pressure. Zone 2 is normally above the level of the left atrium
Zone 3- " Continuous blood flow," is the base of the lung. Blood flow through the pulmonary capillary bed increases in regular increments from the apex to the base.

Clinical manifestations - individuals are asymptomatic between attacks and pulmonary function tests are normal. At the beginning of an attack, the person experiences chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, and tachypnea. Severe attacks often use accessory muscles of respiration and both inspiratory and expiratory wheezing. Pulsus paradoxus (decrease in SBP during inspiration of >10 mmHg) may be noted. Usual findings are hypoxemia with associated respiratory alkalosis. If bronchospasm not reversed, individual experiences status asthmaticus → hypoxemia worsens → expiratory flows decrease further → effective ventilation decreases.


Evaluation and treatment Diagnosis supported by history of allergies and recurrent episodes of wheezing, dyspnea, and cough, or exercise intolerance. Further evaluation includes spirometry (showing decrease in FEV1). Evaluation requires rapid assessment of arterial blood gases and expiratory flow rates and search for underlying triggers.


Management begins with avoidance of allergens and irritants. Education is important (use of peak flowmeter and adherence to action plan).
Mild - short acting beta-agonist
Persistent - anti-inflammatory medications and inhaled corticosteroids. Leukotriene antagonists can be considered if symptoms not well controlled.
Severe - long-acting beta agonists

COPD

preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Airflow limitation that is not fully reversible (usually progressive and associated with abnormal inflammatory response of the lung to noxious particles or gases).


Chronic bronchitis - hypersecretion of mucus and chronic productive cough that continues for at least 3 months of the year for at least 2 consecutive years.


Patho - Inspired irritants result in airway inflammation with infiltration of neutrophils, macrophages, and lymphocytes into bronchial wall. Continued inflammation causes bronchial edema and increases size and number of mucous glands and goblet cells. Thick mucus unable to be cleared because of impaired ciliary function.


Clinical manifestation - decreased exercise tolerance, wheezing, and SOB. Productive cough and decreased FEV1, hypoxemia with exercise. FVC and FEV1 reduced and FRC and RV increase as obstruction and airway trapping occur. Obstruction → decreased alveolar ventilation and increased PaCO2. Hypoxemia → polycythemia. Hypoxemia → pulmonary HTN and eventually cor pulmonale.


Evaluation and treatment
Diagnosis - history of symptoms, physical exam, chest radiograph, PFTs, and blood gas analyses.
Treatment - bronchodilators (long-acting inhaled anticholinergics or long-acting inhaled beta agonists for symptomatic and FEV1 <60% predicted) and expectorants to reduce dyspnea and control cough.

Chest physical therapy may be helpful (deep breathing and postural drainage). Continuous oxygen may be needed (administer with care to individuals with severe hypoxemia and CO2 retention). Teaching includes nutritional counseling, respiratory hygiene, recognition of early signs of infection, and pursed-lip breathing
Acute exacerbations - antibiotics and corticosteroids
Late cough of disease - chronic oral corticosteroids

Emphysema

abnormal permanent enlargement of gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis. Major mechanism of airflow limitation is loss of elastic recoil.


Patho - Either infiltration of inflammatory cells and release of cytokines (neutrophils, macrophages, lymphocytes, leukotrienes, interleukins) or inherited alpha1-antitrypsin deficiency leads to inhibition of normal endogenous antiproteases. Increased protease activity breaks down elastin in connective tissue of lungs → destruction of alveolar septa and loss of elastic recoil of bronchial walls.


Clinical manifestations - DOE, tachypnea with prolonged expiration and use of accessory muscles for ventilation, barrel chest with hyperresonant sound on percussion. Individual often leans forward with arms extended and braced on knees and use pursed lips which helps prevent expiratory airway collapse.
Evaluation and treatment
Diagnosis - PFT measurements. Diaphragm appears flattened on radiograph and lung fields overdistended. High-resolution CT scanning may be indicated if PFT is not definitive.


Management - similar to chronic bronchitis; requires obtaining chest radiograph serum WBC count, arterial blood gas, and sputum sample. Individuals should receive oxygen. Inhaled bronchodilators should be administered. Oral corticosteroids and antibiotics should be prescribed immediately. Pharmacologic management is based on clinical severity, defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD). Inhaled anticholinergic agents and beta agonists should be prescribed. Long-term oral corticosteroids should be avoided, if possible.

Pneumonia (M & H, p. 1271-1273)

Pneumonia is an infection of the lower respiratory tract caused by bacteria, viruses, fungi, protozoa, or parasites. It is the 6th leading cause of death in the US, and is responsible for more disease and death than any other infection.

Risk factors for pneumonia include advanced age, immunocompromised status, lung disease, alcoholism, altered consciousness, impaired swallowing, smoking, malnutrition, immobilization, endotracheal intubation, cardiac or liver disease, or residence in a nursing home.


Pneumonia is classified as community-acquired (CAP), hospital-acquired (HAP), or ventilator-associated (VAP). See Box 35-1, M & H, p. 1271 for microorganisms responsible for each.

Pathophysiology: Aspiration of secretions is the most common cause of lower respiratory infections, so the nasopharynx and oropharynx offer the first line of defense. Inhalation of microorganisms in the air after an infected individual coughs, sneezes or talks is another route of transmission. Contaminated respiratory equipment, endotracheal tubes, or suctioning may introduce bacteria into the lungs.

Cough reflex and mucociliary are the second line of defense. Airway epithelial cells can recognize some pathogens directly, but the alveolar macrophages recognize pathogens and activate T and B cells with the induction of cellular and humoral immunity. Neutrophils are attracted, and these phagocytes kill microbes through the formation of phagolysosomes that are filled with degradative enzymes, antimicrobial proteins, and toxic oxygen free radicals.

Neutrophils also extrude a network of proteins called a neutrophil extracellular trap (NET) that capture bacteria that have not been phagocytosed. Release of inflammatory mediators and immune complexes bronchial mucous and alveolocapillary membranes causing the bronchioles to fill with mucous and debris. Further lung damage can be caused from microorgani sm toxin release damaging cell walls. The accumulation of exudate causes dyspnea and hypoxemia.


Figure 35-15, M & H, p. 1272 demonstrates the pathophysiologic course of pneumococcal pneumonia.
Viral pneumonia is seasonal, mild, and self-limiting. It can be a primary infection or a complication of another viral illness. Influenza is the most common cause of viral pneumonia. Viral pneumonia provides an environment for the growth of bacteria and the potential for serious systemic infection.

Clinical Manifestations: Pneumonia is usually preceded by an upper respiratory infection, typically viral. Subjective symptoms are cough (which may be productive or non-productive), dyspnea, fever, chills, malaise, and pleuritic chest pain. On physical examination we may find signs of pulmonary consolidation: inspiratory crackles, increased tactile fremitis, egophony, and whispered pectoriloquy.

Evaluation and Treatment: Diagnosis is made based on history, physical exam (tachypnea, tachycardia, crackles, bronchial breath sounds, pleural effusion), elevated WBC, positive sputum and blood cultures. Chest x-ray shows infiltrates of one or more lobes.


Prevention of pneumonia focuses on vaccination, prevention of aspiration, isolation of immunocompromised patients, good pulmonary hygiene, and procedures to prevent ventilator associated pneumonia.


Treatment for bacterial pneumonia is antibiotics, and antivirals may be used for viral pneumonia. (M & H, p. 1271-1273) pathogenesis of tuberculosis. (M & H, p. 1273-1274).

Tuberculosis (TB) is an infection caused by the acid-fast bacillus Mycobacterium tuberculosis. TB usually affect the lungs, but may invade other body systems. TB is the leading cause of death from a curable disease in the world.

Pathophysiology: TB is highly contagious and is spread via airborne droplets. Host susceptibility is influenced by host and parasite genetic polymorphisms, such as those that affect macrophages, tumor necrosis factor, and interleukins. TB is contained by the inflammatory and immune response systems in immunocompetent individuals, and latent TB infection (LTBI) develops with no clinical evidence of the disease. Microorganisms lodge in the lung periphery, usually in the upper lobe.

Bacilli multiply once they are inspired into the lung and cause pneumonitis. Some bacilli may move through the lymphatic system and lodge in the lymph nodes, where they trigger an immune response. Neutrophils and macrophages travel to the inflammation in the lung to begin phagocytosis and attempt to prevent the spread of the bacilli. TB is able to survive within macrophages, resist lysosomal killing, multiply within the cell, create a confined environment of well-formed granulomas, terminate its own central metabolism, stop replication, and enter a stage of dormancy that renders it resistant to host defense and drug therapy.

A granulomatomous lesion called a tubercle is formed as neutrophils, lymphocytes, and macrophages seal off the colonies of bacteria .A cheeselike material called caseous necrosis forms as the infected tissue within the tubercle dies. Scar tissue forms around the tubercle, preventing spread of the bacilli. The immune response is complete in about 10 days.

Manifestations: Latent TB is asymptomatic. Active TB develops gradually, and symptoms are usually not noticed until the disease is advanced. Typical symptoms are: weight loss, anorexia, fatigue, lethargy, low-grade fever, and night sweats. As the disease progresses, a productive cough, dyspnea, chest pain, and hemoptysis may be seen. Extrapulmonary TB may result in meningitis symptoms, neurological deficits, bone pain, and urinary symptoms.

Evaluation and Treatment: Diagnosis is made by a positive TB skin test, sputum culture, immunoassays, and chest x-ray. A positive TB skin test indicated the need for a chest x-ray to rule out active disease (I am going to disagree with the book here. A yearly CXR is not required if the patient is asymptomatic.) If someone has ever received the vaccine for TB (BCG), they will always have a positive skin test but this does not mean they have TB. Active TB is diagnosed when sputum cultures are positive for the bacilli, and chest x-ray shows nodules, calcifications, cavities, and hilar enlargement. Preventative measures include isolation of those with active TB.


TB is treated with a combination of up to four antibiotics (isoniazid, rifampin, pyrazinamide, and ethambutol) for 6-18 months, depending on the severity of the disease. (M & H, p. 1273-1274)
More information on TB is available on the CDC website. An excellent course is available here: http://www.cdc.gov/tb/webcourses/TB101/intro.html

(McCance and Huether 1275-1278)
1. Pulmonary embolism -

occlusion or partial occlusion of the pulmonary artery or its branches by an embolus. Most commonly results from DVT involving the lower leg.
Patho - as a result of thrombus lodging in pulmonary circulation, there is a release both or neurohumoral substances (serotonin, histamine, catecholamines, and angiotensin II), and of inflammatory mediators (endothelin, leukotrienes, thromboxanes, and toxic oxygen free radicals) → widespread vasoconstriction → further impedes blood flow → results in increased pulmonary artery pressures and can lead to right heart failure. Absent blood flow to lung segment causes VQ mismatch and decrease in surfactant production
embolus with infarction - an embolus that causes infarction of a portion of lung tissue.
embolus without infarction - an embolus that does not cause permanent lung injury
massive occlusion - an embolus that occludes a major portion of the pulmonary circulation
multiple pulmonary emboli - multiple emboli may be chronic or recurrent

Clinical manifestations - nonspecific. Evaluation of risk factors and predisposing factors is important in diagnosis. Sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia, and unexplained anxiety.

Evaluation and treatment - Chest x-ray, arterial blood gas, and ECG obtained immediately. CXR findings are nonspecific and often normal for 1st 24 hours until atelectasis occurs in the lung. Blood gas reveals hypoxemia with respiratory alkalosis. Treatment is oxygen and hemodynamic stabilization with fluids followed by rapid administration of anticoagulation. If massive life-threatening embolism - streptokinase, emergent percutaneous or surgical embolectomy.

Pulmonary Hypertension -

mean pulmonary artery pressure greater than 25 mmHg at rest. (normal is 15-18).
Patho - Idiopathic PAH characterized by endothelial dysfunction with overproduction of vasoconstrictors (thromboxane and endothelin) and decreased production of vasodilators (NO and prostacyclin).

Clinical manifestations - primary pulmonary or cardiovascular disease. 1st indication is often an abnormality seen on chest radiograph (enlarged pulmonary arteries and right heart border) or an ECG that show right ventricular hypertrophy. Fatigue, chest discomfort, tachypnea, and dyspnea on exertion, palpitations and cough are common. Exam may reveal peripheral edema, JVD, precordial heave, and accentuation of pulmonary compartment of 2nd heart sound.


Evaluation - definitive diagnosis only with right-sided heart catheterization. CXR, echocardiography and CT are used to determine the cause. Labs - arterial blood gas testing, LFTs, HIV serology, ECG, CXR, CT scan, PFTs, polysomnography, VQ scanning, and echocardiography.


Treatment - Oxygen, diuretics, and anticoagulants and avoidance of contributing factors (air travel, decongestants, NSAIDs, pregnancy, and tobacco). Meds include prostacyclin analogs (epoprostenol, eraprost, iloprost), endothelin receptor antagonists (bosentan, ambrisentan), and phophodiesterase-5 inhibitors.

Cor Pulmonale -

secondary to PAH and consists of right ventricular enlargement (hypertrophy, dilation, or both)
Patho - Pulmonary artery hypertension creating chronic pressure overload in RV → increases work of right ventricle → hypertrophy of normally thin-walled heart muscle and compromises RV myocardial perfusion. RV usually fails when pulmonary artery pressure equals systemic blood pressure.


Clinical manifestations - heart appears normal at rest, but with exercise, CO falls. ECG shows RV hypertrophy. Chest pain is common. Pulmonary component of second heart sound may be accentuated and pulmonic valve murmur may be present. Peripheral edema, hepatic congestion, and JVD often may be detected.


Evaluation - diagnosis made on basis of physical exam, radiologic exam, and ECG or echocardiogram or both.


Treatment - goal is to decrease workload of RV by lowering pulmonary artery pressure. Treatment is same as for pulmonary artery hypertension, and its success depends on reversal of underlying lung disease

Describe the four major histologic types of lung cancer. (See Table 35-4 in McCance & Huether pg. 128)

All Posts
×

Almost done…

We just sent you an email. Please click the link in the email to confirm your subscription!

OKSubscriptions powered by Strikingly