The Diastolic V-P Curve
Figure 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.
- 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.
The 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
Before 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.
When 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.
Note 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.