Pra

[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.

Pathophysiology of The Circulation

August 8, 2016 Cardiology, Critical Care, Hemodynamics, Physiology and Pathophysiology No comments , , , , , , , , , , , , ,

The Diastolic V-P Curve

Screen Shot 2016-07-25 at 5.40.29 PMFigure 31-4B plots LVEDV against LVEDP. As ventricular volume increases from zero, the transmural pressure of the ventricle does not exceed zero until about 50 mL (the unstressed volume) is added. Then LVEDP increases in a curvilinear manner with ventricular volume (the stressed volume) first as a large change in volume for a small change in pressure and then as a small change in volume for a large change in pressure. If the pericardium is removed, these V-P characteristics are more linear such that the large change in LVEDP at higher values of LVEDV is no longer evident. Thus the pericardium acts like a membrane with a large unstressed volume loosely surrounding the heart up to a given ventricular volume, but at greater LVEDV the pericardium becomes very stiff. At higher heart volumes, most of the pressure across the heart is across the pericardium, accounting for the very steep rise in the diastolic V-P relation.

Abnormality

  • Below factors shift the diastolic V-P curv up left
  • Diastolic dysfunction also suppress the cardiac function curve

In the presence of pericardial effusion, the volume at which the pericardium becomes a limiting membrane is reduced by the volume of the effusion. When the effusion is large enough, reduced end-diastolic volumes are associated with quite large end-DPs. In turn, pericardial pressure decreased VR by increasing Pra, thus keeping end-diastolic volume and QT abnormally low. Other common causes of diastolic dysfunction in critically ill patients signaled by high left atrial pressure and low ventricular end-diastolic volume are listed in Table 31-1.

Screen Shot 2016-07-25 at 6.31.10 PMThe End-Systolic V-P Curve

The contracting ventricle shortens against the aortic afterload pressure until its volume reaches the end-systolic volume; at that lower volume, the maximum pressure that can be generated is equal to the afterload pressure, so the aortic valve closes and ejection is over. If the afterload pressure were decreased, the ventricle could eject further to a lower end-systolic volume, where the maximum generated pressure equals the reduced afterload; hence, SV would increase.

The line connecting all end-systolic V-P points is an indicator of the pumping function or contractility of the heart because this line defines the volume to which the ventricle can shorten against each afterload for a given contractile state. Agents that enhance contractility shift the end-systolic V-P relation up and to the left; then the ventricle can shorten to a smaller end-systolic volume for each afterload, thereby increasing SV at a given LVEDV/LVEDP. Conversely, negative inotropic agents, myocardial ischemia, hypoxia, and acidemia depress the end-systolic V-P relation down and to the right. Then end-systolic volume is increased for a given pressure afterload, thereby reducing the SV at a given filling pressure.

Of note that diastolic dysfunction not only affect diastolic V-P curve (upper-left shift), but also we affect the end-systolic V-P curve/contractility (right shift), as decreased preload and resultant decreased contractility.


Control of Cardiac Output by The Systemic Vessels

The heart is a mechanical pump that generates flow in the circulation. Because QT is the product of HR and SV, it is often erroneously assumed that the heart controls QT. In fact VR to the right heart is controlled by the systemic vessels, so the heart is more accurately described as a mechanical pump having diastolic and systolic properties that determine how it accommodates the VR.

We use the classical Guyton view that mean systemic pressure (Pms), right atrial pressure (Pra), and resistance to venous return (RVR) govern VR. This conceptual model draws attention to how the resistance and capacitance of systemic vessels and their distribution exert control on the VR, especially through baroreceptor reflexes. This model also provides a graphical solution for the unique values of Pra and VR at the intersection of cardiac function and VR curves in health and in diverse critical illnesses.

We choose to downplay several potential shortfalls of this interpretation, which some regard as fatal flaws. Their analyses and interpretation of Guyton's experiments suggest that Pra is not the "back pressure" impeding VR, that Pms is an imaginative concept that ought not be interpreted as the pressure driving VR, and that Pms – Pra is the result of VR, not its cause. Our comparison of these two viewpoints reveals that the first provides more useful concepts for explaining the pathophysiology and treatment of the circulation in critical illness, so we build our discussion on Guyton's view.

Mean Systemic Pressure

When the heart stops beating, pressure equalizes throughout the vascular system, and its new value is the Pms (10-15 mm Hg). This pressure is much lower than the arterial pressure and is closer to the Pra. When flow stops, blood drains from the high-pressure, low-volume arterial system into the high-volume, low pressure venous system, which accommodates the displaced volume with little change in pressure. When the heart begins to beat again, the left heart pumps blood from the central circulation into the systemic circuit, thus increasing pressure there. At the same time, the right heart pumps blood into the lungs, thereby decreasing its pressure (Pra) with respect to Pms, so blood flows from the venous reservoir into the right atrium. Pressure on the venous side decreases slightly below Pms, whereas pressure on the arterial side increases considerably above Pms with succeeding heartbeats. This continues until a steady state is reached, when arterial pressure has increased enough to drive the whole SV of each succeeding heartbeat through the high arterial resistance into the venous reservoir. The Pms does not change between the state of no flow and the new state of steady flow because neither the vascular volume nor the compliance of the vessels has changed. What has changed is the distribution of the vascular volume from the compliant vein to the stiff arteries; this volume shift creates the pressure difference driving flow through the circuit.

Pms is the driving pressure for VR to the right atrium when circulation resumes. It can be increased to increase VR by increasing the vascular volume or by decreasing the unstressed volume and compliance of the vessels. The latter two mechanisms are mediated by baroreceptor reflexes responding to hypotension by increasing venous tone and usually occur together. The unstressed volume may also be reduced by raising the legs of a supine patient or applying military antishock trousers; both methods return a portion of the unstressed vascular volume from the large veins in the legs to the stressed volume, thereby increasing Pms and VR. When the heart has an improvement in inotropic state or a reduction in afterload, blood is shift from the central compartment to the stressed volume of the systemic circuit, thereby increasing Pms and VR; moreover, improved ventricular pumping function decreases Pra to increase VR further.

Venous Return and Cardiac Function Curves

Screen Shot 2016-07-26 at 7.07.47 PMBefore the heart was started in the discussion above, Pra was equal to the pressure throughout the vascular system, Pms. With each succeeding heartbeat, Pra decreases below Pms and VR increases. This sequence is repeated in a more controlled, steady state by replacing the heart with a pump set to keep Pra at a given value while VR is measured. Typical data are plotted in Figure 31-6. As Pra is decreased from 12 to 0 mm Hg (indicated by the thin continuous line), VR is progressively increased with the driving pressure (Pms – Pra). The slope of the relation between VR and Pms – Pra is the resistance to VR (RVR = delta[Pms – Pra]/deltaVR). When Pra falls below zero, VR does not increase further because flow becomes limited while entering the thorax. This occurs when the pressure in these collapsible great veins decreases below the atmospheric pressure outside the veins. Further decreases in Pra and CVP are associated with progressive collapse of the vein rather than with an increase in VR.

For a given stressed vascular volume and compliance, Pms is set and RVR is relative constant. In the absence of pulmonary hypertension or right heart dysfunction, LV function will determine Pra and, hence, VR to the right heart, along the VR curve. The corresponding cardiac function curve is drawn as the thick line. QT is described by the cardiac function curve, drawn as a thick continuous line relating Pra (abscisa) to QT (ordinate), in Figure 31-6. The heart is able to eject a larger SV and QT when the end-DP is greater because more distended ventricles eject to about the same end-systolic volume as less distended ventricles do. Accordingly, as Pra decrease, QT decreases along the cardiac function curve. However, VR increaseas Pra decreases until VR equals QT at a unique value of Pra, indicated by the intersection of the cardiac function and VR curves in Figure 31-6 (see point A in both panels).

When QT is insufficient, VR can be increased in several ways. A new steady state of increased VR is achieved by increasing Pms with no change in RVR, indicated by the interrupted VR curve in the left panel of Figure 31-6. This new VR curve intersects the same cardiac function curve at a higher value of QT at point B. This method of increasing VR is associated with an increase in Pra. Due to the steep slope of the cardiac function curve in normal hearts, large increase in VR occur with only small increases in Pra. Alternatively, VR can be increased by enhanced cardiac function by increasing contractility or decreasing afterload of th heart. This is depicted as an upward shift of the cardiac function curve, as in the right panel of Figure 31-6, such that greater QT occurs at each Pra. The increase on each VR curve by this mechanism is associated with a reduction in Pra. Further, in the normal heart, only a small change in VR is possible (from point A to point B in the right panel), and greater reductions in Pra do not increase QT further because VR becomes flow limited as Pra decreases to below zero. This explains why inotropic agents that ehance contractility are ineffective in hypovolemic shock.

Screen Shot 2016-07-30 at 2.20.14 PMWhen cardiac pumping function is depressed, as depicted by the interrupted line in Figure 31-7, VR is decreased from point A to point B for the same value of Pms as Pra increases. The patient must then retain fluid or initiate cardiac reflexes to increase Pms toward the new value required t omaintain adequate QT, as in chronic congestive heart failure. This is associated with a large increase in Pra from point B to point C, which in turn causes jugular venous distention, hepatomegaly, and peripheral edema. Diuretic reduction of vascular volumes will correct these abnormalities at the expense of decreasing Pms and VR. In contrast, inotropic and vasodilator drugs, which improve depressed cardiac function by shifting the interrupted cardiac function curve upward, increase QT and decrease Pra more effectively than in patients with normal cardiac function.

Resistance to Venous Return

At a given Pms and Pra, VR is increased by reduced RVR. The RVR is an average of all of the regional resistances. Each regional resistance (R) is weighted by its contribution to the entire systemic vascular compliance (C/CT) and to the fraction of the cardiac output draining from that region.

In most conditoins, RVR remains relatively constant, increasing only slightly with large adrenergic stimulation; even then the increase in regional resistances is offset by redistribution of blood flow to peripheral beds having low resistance and/or compliance. One illustraion of this effect is the opening of an abdominal arteriovenous fistula between the aorta and the inferior vena cava, which doubles VR at the same values of Pms and Pra (Figure 31-8). Consider aliquots of blood leaving the left heart simultaneously; the aliquot traversing the fistula returns to the right heart before the aliquot perfusing the lower body returns. When a greater fraction of the QT traverses the open fistula having a very low compliance and resistance, more blood returns to the heart because RVR decreases. This manifestation of reduced RVR may account for poorly explained hemodynamic changes in septic shock, when high QT is associated with increased blood flow to skeletal muscle, as if some metabolic stimulus increasese the fraction of QT perfusing the low resistance and low compliance skeletal muscle bed, thereby reducing RVR and increasing VR. For another example, systemic hypoxemia triples VR. It does so by increasing Pms through venoconstriction to cause 70% of this increase, while redistribution of QT toward vascular beds having reduced capacitance and resistance account for 30% of the change.

Screen Shot 2016-07-30 at 3.41.07 PMNote in Figure 31-8 that increased VR from A to B is associated with increased Pra when RVR is reduced without changing the cardiac function curve. In fact, Pra does not increase, and VR actually increases from A to C, as if arteriovenous shunting improved cardiac function from the continuous to the interrupted cardiac function curve shown in the figure. One explanation is that reduced SVR associated with arteriovenous shunting lowers the afterload on the left ventricle to improve cardiac function.