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Understanding the pulmonary system

The pulmonary system delivers oxygen (O2) to the bloodstream and removes excess carbon dioxide (CO2) from the body. The delivery of O2 to the cells is essential for cell survival. The alveoli are the gas exchange units of the lungs. The lungs in a typical adult contain about 300 million alveoli.

A closer look at alveoli

Gas exchange occurs rapidly in the tiny, thin-membraned alveoli. Inside these air sacs, O2 from inhaled air diffuses into the blood as carbon dioxide diffuses from the blood into the air and is exhaled. Macrophages are present in the alveoli and protect from bacterial invasion through phagocytosis.

Alveoli consist of type I and type II epithelial cells:

  • Type I cells form the alveolar walls, through which gas exchange occurs.

  • Type II cells produce surfactant, a lipid-type substance that coats the alveoli. During inspiration, the alveolar surfactant allows the alveoli to expand uniformly. During expiration, the surfactant prevents alveolar collapse.

    This illustration shows a cross-sectional view of an alveolus.

    Structures of the pulmonary system

    The respiratory system is divided into the upper respiratory tract and the lower respiratory tract. The upper respiratory tract consists of the nose, mouth, nasopharynx, oropharynx, laryngopharynx, and larynx. The lower respiratory tract consists of the trachea, lungs, left and right mainstem bronchi, five secondary bronchi, and bronchioles. The left mainstem bronchus has two lobes, and the right mainstem bronchus has three lobes. Each lung is protected by a pleural membrane. The visceral pleura attaches to the outer surface of the lung, whereas the parietal pleura lines the inside of the thoracic cavity.

    Respiration

    Effective respiration requires gas exchange in the lungs (external respiration) and in the tissues (internal respiration). Three external respiration processes are needed to maintain adequate oxygenation and acid-base balance:

    1. Ventilation (gas distribution into and out of the pulmonary airways)

    2. Pulmonary perfusion (blood flow from the right side of the heart, through the pulmonary circulation, and into the left side of the heart)

    3. Diffusion (gas movement from an area of greater concentration to an area of lesser concentration through a semipermeable membrane): Deoxygenated blood enters the pulmonary capillaries, which have lower partial pressure of O2 in inhaled alveolar air.

    Ventilation

    Breathing, or ventilation, is the movement of air into and out of the respiratory system. During inspiration, the diaphragm extends downward to allow a greater area for lung expansion. The external intercostal muscles contract, causing the rib cage to expand and the volume of the thoracic cavity to increase. Air then rushes in to equalize the pressure. The air moves throughout the respiratory tract down to the alveoli, where gas exchange takes place. During expiration, the lungs passively recoil as the diaphragm and intercostal muscles relax, pushing air out of the lungs. CO2 is then expired.

    The mechanics of breathing

    Mechanical forces, such as movement of the diaphragm and intercostal muscles, drive the breathing process, which is a response to the changes in the atmospheric pressure within the alveoli and pleural cavity. In the figures that follow, a plus sign (+) indicates positive pressure, and a minus sign (–) indicates negative pressure.

    At rest
    • Inspiratory muscles relax.

    • Atmospheric pressure is maintained in the tracheobronchial tree.

    • Atmospheric pressure = pressure in the alveoli and lungs.

    • No air movement occurs.

    Inspiration
    • Inspiratory muscles contract.

    • The diaphragm descends.

    • Negative alveolar pressure is maintained.

    Expiration
    • Inspiratory muscles relax, causing the lungs to recoil to their resting size and position.

    • The diaphragm ascends.

    • Positive alveolar pressure is maintained.

    Pulmonary perfusion

    Blood flow through the lungs is powered by the right ventricle. The right and left pulmonary arteries carry deoxygenated blood from the right ventricle to the lungs. These arteries divide to form distal branches called arterioles, which terminate as a concentrated capillary network in the alveoli and alveolar sac, where gas exchange occurs. After the deoxygenated blood flows from the right side of the heart through the pulmonary circulation, oxygenated blood is delivered to the left side of the heart.

    Venules-the end branches of the pulmonary veins-collect oxygenated blood from the capillaries and transport it to larger vessels, which carry it to the pulmonary veins. The pulmonary veins enter the left side of the heart and distribute oxygenated blood throughout the body.

    Tracking pulmonary perfusion

    Pulmonary vascular resistance

    Pulmonary vascular resistance (PVR) refers to the resistance in the pulmonary vascular bed against which the right ventricle must eject blood. PVR is largely determined by the caliber and degree of tone of the pulmonary arteries, capillaries, and veins and is measured with the use of hemodynamic monitoring. Because these vessels are thin walled and highly elastic, PVR is normally very low. However, PVR may be easily influenced by vasoactive stimuli that dilate or constrict the pulmonary vessels or affect the tone of these vessels.

    Factors that increase PVR include:

    • vasoconstricting drugs

    • hypoxemia

    • acidemia

    • hypercapnia

    • atelectasis.

    Factors that decrease PVR include:

    • vasodilating drugs

    • alkalemia

    • hypocapnia

    • conditions that result in high cardiac output, such as during strenuous exercise.

    Diffusion

    Blood in the pulmonary capillaries gains O2 and loses CO2 through the process of diffusion (gas exchange). In this process, O2 and CO2 move from an area of greater concentration to an area of lesser concentration through the pulmonary capillary, a semipermeable membrane.

    Diffusion across the alveolar–capillary membrane

    This illustration shows how the differences in gas concentration between blood in the pulmonary artery (deoxygenated blood from the right side of the heart) and alveolus make this process possible. Gas concentrations depicted in the pulmonary vein are the end result of gas exchange and represent the blood that is delivered to the left side of the heart and systemic circulation.

      Ventilation and perfusion ratio

      Areas where perfusion and ventilation are similar have a ventilation-perfusion match (V̇/Q̇ match). Gas exchange is most efficient in such areas. For example, in normal lung function, the alveoli receive air at a rate of about 4 L/min, whereas the capillaries supply blood to the alveoli at a rate of about 5 L/min, creating a V̇/Q̇ ratio of 4:5, or 0.8 (the normal range for a V̇/Q̇ ratio is from 0.8 to 1.2).

      A V̇/Q̇ mismatch, resulting from ventilation-perfusion dysfunction or altered lung mechanics, indicates ineffective gas exchange between the alveoli and pulmonary capillaries and can affect all body systems by changing the amount of O2 delivered to living cells.

      Understanding ventilation and perfusion

      When V̇/Q̇ matches, unoxygenated blood from the venous system returns to the right side of the heart through the pulmonary artery to the lungs, carrying CO2. The arteries branch into the alveolar capillaries. Gas exchange takes place in the alveolar capillaries. This process is depicted in the below illustration, and possible causes of a V̇/Q̇ mismatch are described in the table that follows.

      Possible causes of a V̇/Q̇ mismatch

      CauseDescriptionIllustrationExplanation
      ShuntingReduced ventilation to a lung unit; perfusion is normal. Causes unoxygenated blood to move from the right side of the heart to the left side of the heart and into systemic circulation; it may result from physical defects or airway obstruction.

      When the V̇/Q̇ ratio is low, pulmonary circulation is adequate, but not enough O2 is available to the alveoli for normal diffusion. A portion of the blood flowing through the pulmonary vessels does not become oxygenated.
      Dead space ventilationReduced perfusion to a lung unit; ventilation is normal; occurs but the alveoli do not have adequate blood supply for gas exchange to occur, such as with pulmonary emboli and pulmonary infarction.

      When the V̇/Q̇ ratio is high, as shown here, ventilation is normal, but alveolar perfusion is reduced or absent. Note the narrowed capillary, indicating poor perfusion. This commonly results from a perfusion defect, such as pulmonary embolism or a disorder that decreases cardiac output.
      A silent unitA combination of shunting and dead space ventilation; occurs when little or no V̇/Q̇ is present, such as in cases of pneumothorax and acute respiratory distress syndrome.

      The silent unit indicates an absence of V̇/Q̇ to the lung area. The silent unit may help compensate for a V̇/Q̇ imbalance by delivering blood to better ventilated lung areas.

        Understanding the cardiac system

        The cardiac system:

        The heart is a cone-shaped muscle located within the mediastinum and is surrounded by a protective sac called the pericardium. The major blood vessels of the heart are the left and right coronary arteries, which branch from the base of the aorta. The heart is divided into four chambers: the right and left atria and the right and left ventricles. The right heart is responsible for delivering deoxygenated blood to the lungs and is a low-pressure system. The left heart is responsible for delivering oxygenated blood to the body and is a high-pressure system.

        The valves of the heart facilitate the flow of blood in a forward direction. The atrioventricular (AV) valves are the tricuspid and mitral valves. The semilunar valves are the pulmonic and aortic valves. The tricuspid valve is located between the right atrium and the right ventricle. The mitral valve is located between the left atrium and the left ventricle. The pulmonic valve is located between the right ventricle and the pulmonary artery. The aortic valve is located between the left ventricle and the aorta.

        A closer look at the heart

        Viewing coronary vessels

        Anterior view

        Posterior view

        On the level: Normal intracardiac pressures

        StructureNormal pressure
        Right atrium0–8 mm Hg
        Right ventricleSystolic: 15–25 mm Hg

        Diastolic: 0–8 mm Hg

        Pulmonary arterySystolic: 15–25 mm Hg

        Diastolic: 8–15 mm Hg

        Left atrium4–12 mm Hg
        Left ventricleSystolic: 110–130 mm Hg

        Diastolic: 4–12 mm Hg

        AortaSystolic: 110–130 mm Hg

        Diastolic: 70–80 mm Hg

          Cardiac conduction

          The conduction system of the heart begins with the heart's pacemaker, the sinoatrial (SA) node, which is located in the right atrium. When an impulse leaves the SA node, it travels through the atria along the Bachmann bundle and the internodal pathways on its way to the AV node and the ventricles. After the impulse passes through the AV node, it travels to the ventricles, first down the bundle of His, then along the bundle branches, and, lastly, down the Purkinje fibers.

          Cardiac conduction system

          Memory jogger

          To remember the path of cardiac conduction, use this mnemonic:

          Some Believe In Acting Badly Before Performing.

          The first letter of the words in the mnemonic stand for:

          Sinoatrial node

          Bachmann bundle

          Internodal pathways

          Atrioventricular node

          Bundle of His

          Bundle branches

          Purkinje fibers

          Events of the cardiac cycle

          The steps in the cardiac cycle, described here, are illustrated in the figure that follows:

          1. Isovolumetric ventricular contraction: In response to ventricular depolarization, tension in the ventricles increases. This rise in pressure within the ventricles leads to closure of the mitral and tricuspid valves. The pulmonic and aortic valves stay closed during the entire phase.

          2. Ventricular ejection: When ventricular pressure exceeds aortic and pulmonary arterial pressure, the aortic and pulmonic valves open and the ventricles eject blood.

          3. Isovolumetric relaxation: When ventricular pressure falls below the pressure in the aorta and pulmonary artery, the aortic and pulmonic valves close. All valves are closed during this phase. Atrial diastole occurs as blood fills the atria.

          4. Ventricular filling: Atrial pressure exceeds ventricular pressure, which causes the mitral and tricuspid valves to open. Blood then flows passively into the ventricles. About 70% of ventricular filling takes place during this phase.

          5. Atrial systole: Known as the atrial kick, atrial systole (coinciding with late ventricular diastole) supplies the ventricles with the remaining 30% of the blood for each heartbeat.

            Cardiovascular circuit

            The cardiovascular circuit is a continuous, closed, fluid-filled elastic system of arteries, capillaries, and veins. The heart acts as a pump for this system.

            Blood circulation

            Blood enters the right atrium from the vena cava and flows into the right ventricle during diastole. During systole, the heart muscles contract to send blood through the pulmonary trunk to the lungs for oxygenation. Blood returns to the left atrium through the pulmonary veins and flows into the left ventricle. Heart muscles contract again to drive blood through the aorta into the arterial system of the body. Because arteries become increasingly smaller, blood reaches capillary beds, where O2 is released to the cells of organs and tissues. Veins then carry the O2-poor blood back to the vena cava.

            Systemic vascular resistance

            Systemic vascular resistance (SVR) represents the resistance against which the left ventricle must pump to move blood throughout systemic circulation. SVR can be affected by:

            • tone and diameter of the blood vessels

            • viscosity of the blood

            • resistance from the inner lining of the blood vessels.

            SVR usually has an inverse relationship to cardiac output; that is, when SVR decreases, cardiac output increases, and when cardiac output decreases, SVR will increase.

            Although newer electronic monitors can automatically calculate SVR from hemodynamic measurements, the following formula can be used to calculate it by hand:

            On the level: Measurements of systemic vascular resistance

            Normal measurements of SVR range from 770 to 1,500 dynes/sec/cm–5.

              Cardiac output

              Cardiac output is the amount of blood the heart pumps in 1 minute. It is equal to the heart rate multiplied by the stroke volume (the amount of blood ejected with each heartbeat).

              Stroke volume depends on three major factors:

              Influences on stroke volume and cardiac output

              Understanding preload, contractility, and afterload

              If you think of the heart as a balloon, it will help you understand preload, contractility, and afterload. (See the images that follow.)

              Preload (blowing up the balloon)

              Preload is the stretching of muscle fibers in the ventricle. This stretching results from blood volume in the ventricles at end diastole. According to Starling law, the more the heart muscles stretch during diastole, the more forcefully they contract during systole. Think of preload as the balloon stretching as air is blown into it. The more the air, the greater the stretch.

              Contractility (the balloon's stretch)

              Contractility refers to the inherent ability of the myocardium to contract normally. Contractility is influenced by preload. The greater the stretch, the more forceful the contraction-or, the more air in the balloon, the greater the stretch, and the farther the balloon will fly when air is allowed to expel.

              Afterload (the knot that ties the balloon)

              Afterload refers to the pressure that the ventricular muscles must generate to overcome the higher pressure in the aorta to get the blood out of the heart. Resistance is the knot on the end of the balloon, which the balloon has to work against to get the air out.

                Effects of preload and afterload on the heart

                FactorPossible causeEffects on heart
                Increased preload
                • Increased fluid volume

                • Vasoconstriction

                • Increases stroke volume

                • Increases ventricular work

                • Increases myocardial O2 requirements

                Decreased preload
                • Hypovolemia

                • Vasodilation

                • Decreases stroke volume

                • Decreases ventricular work

                • Decreases myocardial O2 requirements

                Increased afterload
                • Hypovolemia

                • Vasoconstriction

                • Decreases stroke volume

                • Increases ventricular work

                • Increases myocardial O2 requirements

                Decreased afterload
                • Vasodilation

                • Increases stroke volume

                • Decreases ventricular work

                • Decreases myocardial O2 requirements

                  Quick quiz

                  Color my world

                  Trace the path of blood flow through the heart. Color sections blue where deoxygenated blood flows and red where oxygenated blood flows.

                  See Answer


                  Matchmaker
                  1. Cardiac output __________

                    A.the pressure that the ventricular muscles must generate to overcome the higher pressure in the aorta.

                    B.the stretching of muscle fibers in the ventricle.

                    C.the amount of blood the heart pumps in 1 minute.

                    D.the amount of blood ejected with each heartbeat.

                    E.the inherent ability of the myocardium to contract normally.


                  2. Stroke volume ___________

                    A.the pressure that the ventricular muscles must generate to overcome the higher pressure in the aorta.

                    B.the stretching of muscle fibers in the ventricle.

                    C.the amount of blood the heart pumps in 1 minute.

                    D.the amount of blood ejected with each heartbeat.

                    E.the inherent ability of the myocardium to contract normally.


                  3. Preload _________________

                    A.the pressure that the ventricular muscles must generate to overcome the higher pressure in the aorta.

                    B.the stretching of muscle fibers in the ventricle.

                    C.the amount of blood the heart pumps in 1 minute.

                    D.the amount of blood ejected with each heartbeat.

                    E.the inherent ability of the myocardium to contract normally.


                  4. Afterload _______________

                    A.the pressure that the ventricular muscles must generate to overcome the higher pressure in the aorta.

                    B.the stretching of muscle fibers in the ventricle.

                    C.the amount of blood the heart pumps in 1 minute.

                    D.the amount of blood ejected with each heartbeat.

                    E.the inherent ability of the myocardium to contract normally.


                  5. Contractility ____________

                    A.the pressure that the ventricular muscles must generate to overcome the higher pressure in the aorta.

                    B.the stretching of muscle fibers in the ventricle.

                    C.the amount of blood the heart pumps in 1 minute.

                    D.the amount of blood ejected with each heartbeat.

                    E.the inherent ability of the myocardium to contract normally.


                    Selected references