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[Clinical Art][Circulation] Interpretation of Hemodynamic Waveforms

October 20, 2016 Cardiology, Critical Care, EKG/ECG, Hemodynamics, Mechanical Ventilation No comments , , , , , , , , , , , , , , , , , , , , , , , , ,

1st_ceb_insigniaBasic Knowledge

Mechanism of Hemodynamic Monitoring

The rapidly occurring events (represent mechanical forces) of cardiac chambers and vessels during cardaic cycle require conversion to an electrical signal to be transmitted and subsequently translated into an interpretable, graphic format. The pressure transducer is the essential component that translates the mechanical forces to electrical signals. The transducer may be located at the tip of the catheter (micromanometer) within the chamber or, more commonly, the pressure transducer is outside of the body, and a pressure waveform is transmitted from the catheter tip to the transducer through a column of fluid. These transducers consist of a diaphragm or membrane attached to a strain-gauge-Wheatstone bridge arrangement. When a fluid wave strikes the diaphragm, an electrical current is generated with a magnitude dependent on the strength of the force that deflects the membrane. The output current is amplified and displayed as pressure versus time.


Clinical Art

Pre-operations Before Recording

Old generations of transducers required calibration against a mercury manometer; fortunately, the factory-calibrated, disposable, fluid-filled transducers in clinical use today no longer need this. Table-mounted transducers do require balancing or "zeroing," which refers to the establishment of a reference point for subsequent pressure measurements. The reference or "zero" position should be determined before any measurements are made. By convention, it is defined at the patient's midchest in the anteroposterior dimension at the level of the sternal angle of Louis (fourth intercostal space). This site is an estimation of the location of the right atrium and is also known as the phlebostatic axis. A table-mounted transducer is placed at this level and the stopcock is opened to air (atmospheric pressure) and set to zero by the hemodynamic system. The system is now ready for presure measurements. It is important to emphasize that the pre-operation of the hemodynamic monitor is very important, because if the "zero" level is not properly set and the transducer not appropriately balanced, the hemodynamic data recorded would be misleading, even fatal.

Interpretation of pressure waveforms requires a consistent and systematic approach in Table 2-1. Careful scrutiny of the waveform ensures a high-fidelity recording without over- or under-damping. Each pressure event should be timed with EKG.

Table 2-1 A Systematic Approach to Hemodynamic Interpretation
1.Establish the zero level and balance transducer
2.Confirm the scale of the recording
3.Collect hemodynamics in a systematic method using established protocols
4.Critically assess the pressure waveforms for proper fidelity
5.Carefully time pressure events with the EKG
6.Review the tracings for common artifacts

At present, in the clinical setting, 3 pressure waveforms can be obtained at bedside with invasive hemodynaic monitoring devices (central venous cathether/CVC and pulmonary artery catheter/PAC), including right atrial pressure/Prapulmonary artery pressure/Ppa, and pulmonary artery wedge pressure/Ppw. The pressurewave form is recorded along with a synchronized EKG.

Normal Pressure Waveform

Atrial Pressure

The goal of measuring the atrial pressure is to measure the pressure in the ventricles  at the end of diastole, to idenfify a "filling pressure". The goal for any atrial pressure measurement is to obtain the measurement at the every end of diastole, when the atrial pressure is closest to the ventricular pressure. The normal Pra is 2-8 mm Hg and is characterized by a and v waves and x and y descents. The causes of a, v waves and x, y descents are listed below.

PS: The Rationale Reason for the Formation of Pra waveform

a wave represents the pressure rise within the right atrium due to atrial contraction follows the P wave on the EKG by about 80 msec
descet represents the pressure decay following the a wave and reflect both atrial relaxation and the sudden downward motion of the atrioventricular junction that occurs because of early ventricular systole  
c wave is sometimes observed after the a wave and is due to the sudden motion of the tricuspid annulus toward the right atrium at the onset of ventricular systole the c wave follows the a wave by the same time as the PR interval on the EKG
v wave when the tricuspid valve is closed, the pressure rise responsible for the v wave is due to passive venous filling of the atrium, represent atrial diastole. the peak of the right atrial v wave corresponds with the end of T wave on the surface EKG; the ORS alawys appears before the v wave is produced
y wave is due to rapid emptying of the right atrium when the tricuspid valve opens  

Atrial waveform interpretation in detail

v wave

The atrial pressures initially increase during systole as the contracting ventricles return blood to the atria, refilling the upper chambers. This rise in the atrial pressure is identified as the "v" wave. The upstroke of the v wave is the rise in atrial pressure as a result of atrial filling. Because it is produced as a result of ventricular contraction, its location is relative to the QRS on the EKG. Ejection eventually leads to the return of blood to the atria (left ventricular contraction refills the right atrium and produces the right atrial v wave; right ventricular contraction refills the left atrium and produces the left atrial v wave). Thus, the QRS causes the v wave, however, the QRS always appears before the v wave is produced.

PA

The normal pulmonary artery systolic pressure/Ppas is 15-30 mm Hg, the normal diastolic pressure/Ppad is 4-12 mm Hg, and the mean 9-18 mm Hg. The components pulmonary artery pressure include a rapid rise in pressure, systolic peak, a pressure decay associated with a well-defined dicrotic notch from pulmonic valve closure, and a diastolci trough.

PA and arterial pressure waveforms have similar morphology. Systole begins with the opening of the pulmonic valves. Prior to opening of the pulmonary valve, the pulmonary artery pressure is very low (the pulmonary vascular system does not need a high pressure system to perfuse). As the ventricles contact, they eject blood into the pulmonary artery. This causes an immediate rise in the arterial pressure. As blood enters the great vessels, the pressure rise quickly and steadily, producing a steep vertical rise. Late in systole, the rate of ejection slows as the pressure gradient between the right ventricle and pulmonary artery narrows. Although blood is still moving from the ventricle to the great vessels, the rate of movement is slowed to the point where the pressure begins to decline. This cause the early downslope in the arterial tracing that represents this period of reduced ejection. Like the right atrial v wave, the pulmonary artery systolic wave typically coincides with the T wave of the EKG.

Later, the ventricle begins to relax, causing the ventricular pressure to drop below the pressure in great vessels. This causes the pulmonic valves to close, producing a small rise in the PA pressure, known as the dicrotic notch. Following closure of the semi-lunar valves, the pulmonary artery continues to fall as blood leaves the great vessels to perfuse the tissues and lungs.

PAWP

The normal mean pulmonary artery wedge pressure/Ppw is obtained when the inflated catheter obstructs forward flow within a branch of the pulmonary artery, creating a static column of blood between the tip of the catheter and the j point in the pulmonary venous bed where it intersects with flowing blood. The Ppw tracing contains the same sequence of waves and descents as the Pra tracing. However, when referenced to the ECG, the waves and descents of the Ppw will be seen later than those of the Pra, because the pressure waves from the left atrium must travel back through the pulmonary vasculature and a longer length of catheter. Therefore, in the Ppw tracing, the a wave usually appears after the QRS complex, and the v wave is seen after the T wave.
screen-shot-2016-10-19-at-2-19-49-pmInterpretation of CVP and PAWP measurements

Correlation to the EKG

The easiest wave to evaluate an atrial tracing is to first locate the v wave. Generally, it will appear immeidately after the peak of T wave on a CVP waveform, however, it will be 80-120 ms after the T wave on a PAWP tracing. You can generally identify the v wave by ruling out other waves. It must be after the peak of the T wave. Once the v wave is identified, the a and c can be determined.

Observe the EKG rhythm. If the patient has a sinus rhythm, an a wave should be present. The a should be in the PR interval for a CVP. It is later in the PAWP, appearing within or even afte QRS. If the patient does not have a P wave, the a wave will be absent. If the P wave is not synchronized to the QRS, very large a wave may be present. These large a waves may appear as one very large wave during a cardiac cycle. The large a waves are called cannon a waves. They are actually exaggerated atrial pressures that occur when the atria contract against a closed AV valve, adding to the pressure that is already being generated due to the c or v wave.

If present, the c wave is generally within the QRS for a CVP. It will be after the QRS for a PAWP.

Where to Measure CVP and PAWP

At the very end of ventricular diastole, the atrial pressure equilibrates with the ventricular pressure, at the very end of ventricular filling. Measurement of the atrial pressure at the end of diastole provides the best opportunity to capture ventricular filling pressure. The location on the atrial pressure wave that best reflects end-diastolic pressure is the point just prior to the c wave. However, c wave is often absent or difficult to find, espeically true in the PAWP waveform, which is subject to considerable movement artifact from right ventricular systole and breathing. If we cannot use the mehtod based on c wave to measure the filling pressure, instead we can use other two ways to capture the filling pressure, where the second method for identification of the end-diastolic pressure is to take the mean of the highest and lowest a wave pressure; and the thrid method is used if the a wave is hard to interpret or absent, that is, the end-diastolic pressure can be estimated by identifying the Z point. Draw a line from the end of the QRS to the atrial tracing. The point where the line intersects with the waveform is the Z line. Note that for a PAWP waveform the Z line should be estimated as 0.08-0.12 seconds to the left of the end of the QRS (Z point is delayed 0.08-0.12 seconds from the QRS on the PAWP).


Respiratory Influences on Hemodynamic Data: Transmural Pressure

The Pra and Ppw are used as surrogates for RV and LV filling pressure (so the preload), but remember that when evaluating the patient's preload the end-diastolic volume of the ventricles should also be included in the interpretation. Here in this section we focus our discussion on the respiratory influecnes on the recorded hemodynamic data. OK, it is the transmural (intravascular minus pleural) pressure that represents the distending pressure for cardiac filling. During normal breathing, Ppl is slightly negative at end-expiration and intrathoracic vascular pressures measured at this point in respiratory cycle provide the best estimate of transmural pressure. Either a strip recording or the cursor method should be used to define the end-expiratory pressure.

One error is the assumption that during mechanical ventilation the lowest point in the pressure tracing reflects end expiration. While this is true during controlled ventilation, inspiratory efforts that trigger mechanical breaths produce a nadir in the pressure tracing. Identification of end expiration in the Ppw tracing is aided by the knowledge that expiration is usually longer than inspiration, two exceptions being marked tachypnea and inverse-ratio ventilation. Identification of end expiration from the pressure tracing should not be difficult when interpreted in relationship to the patient's ventilatory pattern. When confusion occurs, a simultaneous airway pressure tracing may be used.

The Pra and Ppw will overestimate transmural pressure if intrathoracic pressure is positive at end expiration. This can occur from an increase in end-expiratory lung volume due to applied positive end-expiratory pressure (PEEP) or auto-PEEP, or from increased intra-abdominal pressure due to active expiration or intra-abdominal hypertension.


Common Errors and Artifacts

screen-shot-2016-10-20-at-7-58-42-pmMost errors in the collection and interpretation of hemodynamic data are listed in Table 2-2.

Probably the most commonly observed artifacts relate to an improper degree of damping. The over-damped tracing indicates the presence of excessive friction absorbing the force of the pressure wave somewhere in the line from the catheter tip to the transducer. The tracing lacks proper fidelity and appears smooth and rounded because of loss of frequency response. This will result in loss of data and will falsely lower peak pressures. Typically, the dicrotic notch on the aortic or pulmonary artery waveforms is absent, and the right atrial or PAPW waveforms will lack distinct a and v waves.

Under-damping causes overshoot or ring artifact. This artifact typically appears as one or more narrow "spikes" overshooting the true pressure during the systolic pressure rise with similar, negatively directed waves overshooting the true pressure contour during the downstroke. This artifact may lead to overestimation of the peak pressure and underestimation of the pressure nadir. Tiny air bubbles that oscillate rapidly back and forth, transmitting energy back to the transducer, cause this artifact. Flushing the catheter or transducer often corrects this artifact; alternatively, introduction of a filter to the hemodynamic system may be necessary to eliminate this artifact.

Related to overshoot or ring artifact is catheter whip or fling artifact. This artifact is created by acceleration of the fluid within the catheter from rapid catheter motion and is commonly seen with balloon-tipped catheters in hyperdynamic hearts or balloon-tipped catheters placed in the pulmonary artery with extraneous loops. Similar to ring artifact, catheter whip causes overestimation of the systolic pressure and underestimation of the diastolic pressure. This artifact is difficult to remedy; eliminating the extra loops or deflation of the balloon can improve the appearance and limit this artifact.

Catheter malposition creates several interesting artifacts.

[Respiration][Circulation] Blood Flow to the Lung – General and Pulmonary Vascular Resistance

September 11, 2016 Cardiology, Critical Care, Hemodynamics, Mechanical Ventilation, Physiology and Pathophysiology, Pulmonary Medicine, Respirology No comments , , , , , , , , , , , ,

The lung receives blood flow via both the bronchial circulation and the pulmonary circulation. Bronchial blood flow constitutes a very small portion of the output of the left ventricle and supplies part of the tracheobronchial tree with systemic arterial blood. Pulmonary blood flow (PBF) constitutes the entire output of the right venticle and supplies the lung with the mixed venous blood draining all the tissues of the body.

There is about 250 to 300 mL of blood per square meter of body surface area in the pulmonary circulation. About 60 to 70 mL/m2 of this blood is located in the pulmonary capillaries.

Gas exchange starts to take place in smaller pulmonary arterial vessels, which are not truly capillaries by histologic standards. These arterial segments and successive capillaries may be thought of as functional pulmonary capillaries.

About 280 billion pulmonary capillaries supply approximately 300 million alveoli, resulting in a potential surface area for gas exchange estimated to be 50 to 100 m2.

Bronchial Circulation

The bronchial arteries arise variably, either directly from the aorta or from the intercostal arteries. They supply arterial blood to the tracheobronchial tree and to other structures of the lung down to the level of the terminal bronchioles. They also provide blood flow to the hilar lymph nodes, visceral pleura, pulmoonary arteries and veins, vagus, and esophagus. The bronchial circulation may be important in the "air-conditioning" of inspired air. The blood flow in the bronchial circulation constitutes about 2% of left ventricle output of the left ventricle. Blood pressure in the bronchial arteries is the same as that in other systemic arteries.

The venous drainage of the bronchial circulation is unusual. Although some of the bronchial venous blood enters the azygos and hemiazygos veins, a substantial portion of bronchial venous blood enters the pulmonary veins. Therefore, the bronchial venous blood entering the pulmonary venous blood is part of the normal anatomic right-to-left shunt. Histologists have also identified anastomoses, or connections, between some bronchial capillaries and pulmonary capillaries and between bronchial arteries and branches of the pulmonary artery. Thse connections probably play little role in a healthy person but may open in pathologic states, such as when either bronchial or PBF to a protion of lung is occluded. For example, if PBF to an area of the lung is blocked by a pulmonary embolus, bronchial blood flow to that area increases.

Pulmonary Circuation

The pulmonary vessels offer much less resistance to blood flow than do the systemic arterial tree. They are also much more distensible than systemic arterial vessels. These factors lead to much lower intravascular pressures than those found in the systemic arteries, which makes them more compressible. The pulmonary vessels are located in the thorax and are subject to alveolar and intrapleural pressures that can change greatly. Therefore, factors other than the tone of the pulmonary vascular smooth muscle may have profound effects on pulmonary vascular resistance (PVR). The transmural pressure difference across vessel walls is therefore a major determinant of PVR.

Because the right and left circulations are in series, the outputs of the right and left venticles must be approximately equal to each other over the long run. If the 2 outputs are the same and the measured pressure drops across the systemic circulation and the pulmonary circulation are bout 98 and 10 mm Hg, respectively, then the PVR must be about one tenth that of the systemic vascular resistance (SVR). Again, the low resistance to blood flow offered by the pulmonary circulation is due to the structural aspects of the pulmonary circulation.

The resistance is fairly evenly distributed among the pulmonary arteries, the pulmonary capillaries, and the pulmonary veins (from 15 mm Hg to 12 mm Hg, from 12 mm Hg to 8 mm Hg, from 8 mm Hg to 5 mm Hg, respectively). At rest, about one third of the resistance (PVR) is located in the pulmonary arteries, about one third is located in the pulmonary capillaries, and about one third is located in the pulmonary veins.

PVR

screen-shot-2016-09-11-at-3-44-33-pmThe relative small amounts of vascular smooth muscle, low intravascular pressures, and high distensibility of the pulmonary circulation lead to a much greater importance of extravascular effects ("passive factors") on PVR. Gravity, body position, lung volume, alveolar and intrapleural pressures, intravascular pressures, and right ventricular output all can have profound effects on PVR without any alteration in the tone of the pulmonary vascular smooth muscle.

Transmural Pressure On PVR

For distensible-compressible vessels, the transmural pressure difference is an important determinant of the vessel diameter. As the transmural pressure difference (which is equal to pressure inside minus pressure outside) increases, the vessel diameter increases and resistance falls; as the transmural pressure difference decreases, the vessel diameter decreases and the resistance increases. Negative transmural pressure differences lead to compression or even collapse of the vessel.

Lung Volume on PVR

Screen Shot 2016-09-06 at 12.48.46 PMTwo different groups of pulmonary vessels must be considered when the effects of changes in lung volume on PVR are analyzed: those vessels that are exposed to the mechanical influences of the alveoli and the larger vessels that are not – the alveolar and extraalevolar vessels.

As lung volume increases during a normal negative-pressure inspiration, the alveoli increase in volume. While he alveoli expand, the vessels found between them, mainly pulmonary capillaries, are elongated. As these vessels are stretched, their diameters decrease, just as stretching a rubber tube causes its diameter to narrow. Resistance to blood flow through the alveolar vessels increases as the alveoli expand because the alveolar vessels are longer (resistance is directly proportional to length) and because their radii are smaller (resistance is inversely proportional to radius to the fourth power). At high lung volumes, then, the resistance to blood flow offered by the alveolar vessels increases greatly; at low lung volumes, the resistance to blood flow offered by the alveolar vessels decreases.

One group of the extraalveolar vessels, the larger arteries and veins, is exposed to the intrapleural pressure. As lung volume is increased by making the intrapleural pressure more negative, the transmural pressure difference of the larger arteries and veins increase and they distend. Another factor tending to decrease the resistance to blood flow offered by the extraalveolar vessels at higher lung volumes is radial traction by the connective tissue and alveolar septa holding the larger vessels in place in the lung. Thus, at high lung volumes, the resistance to blood flow offered by the extraalveolar vessels decreases. During a forced expiration to low lung volumes, however, intrapleural pressure becomes very positive. Extraalveolar vessels are compressed, and as the alveoli decrease in size, they exert less radial traction on the extraalveolar vessels. The resistance to blood flow offered by the extraalveolar vessels increase greatly.

Because the alveolar and extraalveolar vessels may be thought of a 2 groups of resistances in series with each other, the resistances of the alveolar and extraalveolar vessels are additive at any lung volume. Thus, the effect of changes in lung volume on the total PVR gives the U-shape cruve. PVR is lowest near the functional residual capacity and increases at both high and low lung volumes.

There is another type of extraalveolar vessel called corner vessel, or extraalveolar capillary. Although these vessels are found between alveoli, their locations at junctions of alveolar septa give them different mechanical properties. Expansion of the alveoli during inspiration increases the wall tension of the alveolar septa, and the corner vessels are distended by increased radial traction, whereas the alveolar capillaries are compressed.

Also note that during mechanical positive-pressure ventilation, alveolar pressure (PA) and intrapleural pressure are positive during inspiration. In this case, and the resistance to blood flow offered by both alveolar and extraalveolar vessels increases during lung inflation. This is especially a problem during mechanical positive-pressure ventilation with positve end-expiratory pressure (PEEP). During PEEP, airway pressure (and thus alveolar pressure) is kept positive at end expiratory to help prevent atelectasis. In this situation, alveolar pressure and intrapleural pressure are positive during both inspiration and expriation. PVR is elevated in both alveolar and extraalveolar vessels throughout the respiratory cycle. In addition, because intrapleural pressure is always positive, the other intrathoracic blood vessels are subjected to decreased transmural pressure differences; the venae cavae, which have low intravascular pressure, are also compressed. If cardiovascular reflexes are unable to adjust to this situation, cardiac output may fall precipitously because of decreased venous return (for the reason see thread "Effects of Pressure Outside the Heart on Cardiac Output" at http://www.tomhsiung.com/wordpress/2016/09/effects-of-pressure-outside-the-heart-on-cardiac-output/) and high PVR.

Recruitment and Distention

During exercise, cardiac output can increase several-fold without a correspondingly great increase in MPAP. Although the MPAP does increase, the increase is only a few millimeters of mercury, even if cardiac output has doubled or tripled. Since the pressure drop across the pulmonary circulation is proportional to the cardiac output times the PVR, this must indicate a decrease in PVR.

Like the effects of lung volume on PVR, this decrease appears to be passive – that is, it is not a result of changes in the tone of pulmonary vascular smooth muscle caused by neural mechanisms or humoral agents. In fact, a fall in PVR in response to increased blood flow or even an increase perfusion pressure can be demonstrated in a vascularly isolated perfused lung. There are two different mechanisms that can explain this decrease in PVR in response to elevated blood flow and perfusion pressure: recruitment and distention.

Recruitment

At resting cardiac outputs, not all the pulmonary capillaries are perfused. A substantial proportion of capillaries, perhaps as large as one half to two thirds, is probably not perfused because of hydrostatic effects. Others may be unperfused because they have a relatively high critical opening pressure. That is, these vessels, because of their high vascular smooth muscle tone or other factors such as positive alveolar pressure, require a higher perfusion pressure than that solely necessary to overcome hydrostatic forces. Under normal circumstances, it is not likely that the critical opening pressures for pulmonary blood vessels are very great because they have so little smooth muscle. Increased blood flow increases the MPAP, which opposes hydrostatic forces and exceeds the critical opening pressure in previously unopened vesels. This series of events opens new parallel pathways for blood flow, which lowers the PVR. This opening of new pathways is called recruitment. Note that decreasing the cardiac output or pulmonary artery pressure can result in a derecruitment of pulmonary capillaries.

Distention

As perfusion pressure increases, the transmural pressure gradient of the pulmonary blood vessels increases, causing distention of the vessels. This increases their radii and decreases their resistance to blood flow.

Control of Pulmonary Vascular Smooth Muscle

Pulmonary vascular smooth muscle is responsive to both neural and humoral influences. These produce "active" alterations in PVR, as opposed to those "passive" factors discussed in the previous section.

The pulmonary vasculature is innervated by both sympathetic and parasympathetic fibers of the autonomic nervous system. The innervation of pulmonary vessels is relatively sparse in comparsion with that of systemic vessels. There is relatively more innervation of the larger vessels and less of the smaller, more muscular vessels. There appears to be no innervation of vessels smaller than 30 um in diameter. There does not appear to be much innervation of intrapulmonary veins and venules.

The effects of stimulation of the sympathetic innervation of the pulmonary vasulature are somewhat controversial. Some investigators have demonstrated an increase in PVR with sympathetic stimulation of the innervation of the pulmonary vasculature, whereas others have shown only a decreased distensibility with no change in calculated PVR. Stimulation of the parasympathetic innervation of the pulmonary vessels generally causes vasodilation, although its physiologic function is not known.

The catecholamines epinephrine and norepinephrine both increase PVR when injected into the pulmonary circulation. Histamine, found in the lung in mast cells, is a pulmonary vasoconstrictor. Certain prostaglandins and related substances, such as PGF2alpha, PGE2, and thromboxane, are also pulmonary vasoconstrictors, as is endothelin, a 21-amino acid peptide synthesized by the vascular endothelium. Alveolar hypoxia and hypercapnia also cause pulmonary vasoconstriction. Acetylcholine, the beta-adrenergic agonist isoproterenol, nitric oxide (NO), and certain prostaglandins, such as PGE1, and PGI2 (prostacyclin), are pulmonary vasodilators.

Gravity's Impact on PVR

Determinations of the regional distribution of PBF (see discussion below) have shown that gravity is another important "passive" factor affecting local PVR and the relative perfusion of different regions of the lung (see discussion below). The interaction of the effects of gravity and extravascular pressures may have a profound influence on the relative perfusion of different areas of the lung.

The Regional Distribution of Pulmonary Blood Flow

Interaction of Gravity and Extravascular Pressure

Experiments done on excised, perfused, upright animal lungs have demonstrated the same gradient of increased perfusion per unit volume from the top of the lung to the bottom. When the experiments were done at low pump outputs so that the pulmonary artery pressure was low, the uppermost regions of the lung received no blood flow. Perfusion of the lung ceased at the point at which alveolar pressure (PA) was just equal to pulmonary arterial pressure (Pa). Above this point, there was no perfusion because alveolar pressure exceeded pulmonary artery pressure, and so the transmural pressure across capillary walls was negative. Below this point, perfusion per unit volume increased steadily with increased distance down the lung.

screen-shot-2016-09-12-at-1-51-11-pmThus, under circumstances in which alveolar pressure is greater than pulmonary artery pressure in the upper parts of the lung, no blood flow occurs in that region, and the region is referred to as being in zone 1, as shown in Fingure 4-9. Any zone 1, then, is ventilated but not perfused. It is alveolar dead space. Fortunately, during normal, quiet breathing in a person with a normal cardiac output, pulmonary artery pressure, even in the uppermost regions of the lung, is greater than alveolar pressure, and so there is no zone 1. Some experiments have also demonstrated perfusion of the corner vessels under zone 1 conditions.

The lower portion of the lung in Figure 4-9 is said to be in zone 3. In this region, the pulmonary artery pressure and the pulmonary vein pressure (Pv) are both greater than alveolar pressure. The driving pressure for blood flow through the lung in this region is simply pulmonary artery pressure minus pulmonary vein pressure. Note that this driving pressure stays constant as one moves further down the lung in zone 3 because the hydrostatic pressure effects are the same for both the arteries and the veins.

The middle portion of the lung in Figure 4-9 is in zone 2. In zone 2, pulmonary artery pressure is greater than alveolar pressure, and so blood flow does occur. However, because alveolar pressure is greater than pulmonary vein pressure, the effective driving pressure for blood flow is pulmonary artery pressure minus alveolar pressure in zone 2. Notice that in zone 2 the increase in blood flow per distance down the lung is greater than it is in zone 3. This because the upstream driving pressure, the pulmonary artery pressure, increases according to the hydrostatic pressure increase, but the effective downstream pressure, alveolar pressure, is constant throughout the lung at any instant.

It is important to realize that the boundaries between the zones are dependent on physiologic conditions – they are not fixed anatomic landmarks. Alveolar pressure changes during the course of each breath. During eupneic breathing these changes are only a few centimeters of water, but they may be much greater during speech, exercise, and other conditions. A patient on a positive-pressure ventilator with PEEP may have substantial amounts of zone 1 because alveolar pressure is always high. Similarly, after a hemorrhage or during general anesthesia, PBF and pulmonary artery pressure are low and zone 1 conditions are also likely. During exercise, cardiac output and pulmonary artery pressure increase and any existing zone 1 should be recruited to zone 2. The boundary between zones 2 and 3 will move upward as well. Pulmonary artery pressure is highly pulsatile, and so the borders between the zones probably even move up a bit with each contraction of the right ventricle.

Changes in lung volume also affect the regional distribution of PBF and will therefore affect the boundaries between zones. Finally, changes in body position alter the orientation of the zones with respect to the anatomic locations in the lung, but the same relationships exist with respect to gravity and alveolar pressure.

Hypoxic Pulmonary Vasoconstriction

Alveolar hypoxia or atelectasis causes an active vasoconstriction in the pulmonary circulation. The site of vascular smooth muscle constriction appears to be in the arterial (precapillary) vessels very close to the alveoli.

The mechanism of hypoxic pulmonary vasoconstriction is not completely understood. The response occurs locally, that is, only in the area of the alveolar hypoxia. Connections to the central nervous system are not necessary: An isolated, excised lung, perfused with blood by a mechanical pump with a constant output, exhibits an increased perfusion pressure when ventilated with hypoxic gas mixtures. This indicates that the increase in PVR can occur without the influence of extrinsic nerves. Thus, it is not surprising that hypoxic pulmonary vasoconstriction persists in human patients who had received heart-lung transplants. Hypoxia may cause the release of a vasoactive substance from the pulmonary parenchyma or mast cells in the area. Histamine, serotonin, catecholamines, and prostaglandins have all been suggested as the mediator substance, but none appears to completely mimic the response. Decreased release of a vasodilator such as nitric oxide may also be involved in hypoxic pulmonary vasoconstriction. Possibly several mediators act together. More recent studies have strongly indicated that hypoxia acts directly on pulmonary vascular smooth muscle to produce hypoxic pulmonary vasoconstriction.

Physiologic Function of Hypoxic Pulmonary Vasoconstriction

The function of hypoxic pulmonary vasoconstriction in localized hypoxia is fairly obvious. If an area of the lung becomes hypoxic because of airway obstruction or if localized atelectasis occurs, any mixed venous blood flowing to that area will undergo little or no gas exchange and will mix with blood draining well-ventilated areas of the lung as it enters the left atrium. This mixing will lower the overall arterial PO2 (PaO2) and may even increase the arterial PCO2 (PaCO2). The hypoxic pulmomary vasoconstriction diverts mixed venous blood flow away from poorly ventilated areas of the lung by locally increasing vascular resistance. Therefore, mixed venous blood is sent to better-ventilated areas of the lung. The problem with hypoxic pulmonary vasoconstriction is that it is not a very strong response because there is so little smooth muscle in the pulmonary vasculature. Very high pulmonary artery pressures can interfere with hypoxic pulmonary vasoconstriction, as can other physiologic disturbances, such as alkalosis.

In hypoxia of the whole lung, such as might be encountered at high altitude or in hypoventilation, hypoxic pulmonary vasoconstriction occurs throughout the lung. Even this may be useful in increasing gas exchange because greatly increasing the pulmonary artery pressure recruits many previously unperfused pulmonary capillaries. This increases the surface area available for gas difusion and improves the matching of ventilation and perfusion. On the other hand, such a whole-lung hypoxic pulmonary vasoconstriction greatly increases the workload on the right venticle, and the high pulmonary artery pressure may overwhelm hypoxic pulmonary vasoconstriction in some parts of the lung, increase the capillary hydrostatic pressure in those vessels, and lead to pulmonary edema.

Effects of Pressure Outside the Heart on Cardiac Output

September 9, 2016 Cardiology, Critical Care, Mechanical Ventilation, Physiology and Pathophysiology, Pulmonary Medicine, Respirology No comments , , , ,

screen-shot-2016-09-09-at-9-37-40-pmIn the figure cited and the preceding dicussions in thread "Pathophysiology of the Circulation" at http://www.tomhsiung.com/wordpress/2016/08/pathophysiology-of-the-circulation/, values of Pms and Pra were expressed relative to atmospheric pressure. However, the transmural pressure of the right atrium exceeds the Pra by the subatmospheric value (about -4 mm Hg) of the Ppl surrounding the heart. Consider the effect of opening the thorax, which raises Ppl from -4 to 0 mm Hg: VR decreases from point A to point B in Figure 31-9 because Pra increases. This is indicated by the interrupted cardiac function curve shifted to the right by the increase in pressure outside the heart but parallel to the normal cardiac function curve (continuous line through point A). Normal VR can be restored (point B to point C) by increasing Pms by an amount equal to the increase in Ppl and Pra induced by thoracotomy. Then transmural Pra will be the same as at point A, and Pra will have increased from point A to point C at the same QT.

This mechanism for the decrease in QT with thoracotomy also partly explains the decrease in QT with PEEP. The Ppl within an intact thorax increases with passive positive-pressure ventilation, thereby increasing Pra and decreasing VR. When 8 mm Hg of PEEP (10 cm H2O) is added to the ventilator, the end-expiratory value of Ppl increases by about half that amount, for example, from -4 to 0 mm Hg. Accordingly, VR decreases with PEEP from point A to pint B in Figure 31-9, with no change in cardiac function or Pms. QT is returned to normal volume infusion or vascular reflexes that increase Pms by an amount equal to the increases in Ppl and Pra. Greater PEEP (20 cm H2O, as in the dotted line shown in Figure 31-8) decreases VR further (from point A to point D) and requires greater increases in Pms to return it to normal (from point D to point E). In one canine study, Pms increases as much as Pra when PEEP is added, so the observed decrease in VR must be due to an increase in RVR with PEEP. In either event, VR can be restored on PEEP by increasing Pms.

QT is much less suceptible to the deleterious effects of PEEP and increased mean intrathoracic pressure when Pms is high. In patients with reduced circulatory volume, vascular reflexes are already operating to maintain VR and Pms by reducing unstressed volume or vascular compliance. Such patients have little vascular reflex reserve and poorly tolerate intubation and positive-pressure ventilation without considerable intravenous infusion to increase vascular stressed volume. In contrast, well-hydrated or overhydrated patients may tolerate even large amounts of PEEP or increased mean intrathoracic pressure from elevated mechanical tidal volumes (VT) with no reduction in QT because their previously inactive vascular reflexes can increase Pms in well-filled systemic vessels by the amount that Ppl increases with PEEP. These considerations allow the physician to anticipate and treat the hypotension induced by ventilator therapy; the concept should not be interpreted as an indication for maintaining high circulatory volume in critical ill patients on ventilators because this often increases lung edema and provides even more QT than was already deemed sufficient. Further, pressure outside the heart can be increased by a variety of other concomitant conditions and complications of critical illness; all these actions increase pressure measured in the heart chambers and decrease heart volume and, as a consequence, are often interpreted as diastolic dysfunction.