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Cardiovascular–Pulmonary Interactions 

Cardiovascular–Pulmonary Interactions
Chapter:
Cardiovascular–Pulmonary Interactions
Author(s):

John W. Kreit

DOI:
10.1093/med/9780190670085.003.0003
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date: 03 July 2020

The heart, great vessels, pulmonary circulation, and a portion of the systemic circulation are constantly exposed to non-atmospheric pressures. Figure 3.1 shows that the cardiovascular system can be divided into several “compartments” based on the prevailing external (extramural) pressure. Within the thorax, the visceral pleura completely surrounds both lungs, and the parietal pleura lines the chest wall, the diaphragm, and the mediastinum. It follows that the heart, aorta, superior vena cava, and pulmonary arteries and veins are constantly exposed to pleural pressure (PPL). On the other hand, alveolar pressure (PALV) is the external pressure on the pulmonary capillaries, which run through the walls of the alveoli. The blood vessels within the abdominal compartment are exposed to intra-abdominal pressure (PAB), while the extramural pressure on all other systemic vessels is atmospheric pressure (PATM).

Figure 3.1 The model divides the circulatory system into four “compartments” based on location and extramural pressure. Within the thorax, the right (R) and left (L) atria and ventricles, superior vena cava, aorta, and extra-alveolar (Ex-ALV) pulmonary vessels (arteries and veins) are exposed to pleural pressure (PPL), while the alveolar (ALV) vessels (pulmonary capillaries) are exposed to alveolar pressure (PALV). Systemic vessels within the abdominal compartment are exposed to intra-abdominal pressure (PAB). Upper body non-thoracic and lower body non-abdominal vessels are exposed to atmospheric pressure (PATM).

Figure 3.1 The model divides the circulatory system into four “compartments” based on location and extramural pressure. Within the thorax, the right (R) and left (L) atria and ventricles, superior vena cava, aorta, and extra-alveolar (Ex-ALV) pulmonary vessels (arteries and veins) are exposed to pleural pressure (PPL), while the alveolar (ALV) vessels (pulmonary capillaries) are exposed to alveolar pressure (PALV). Systemic vessels within the abdominal compartment are exposed to intra-abdominal pressure (PAB). Upper body non-thoracic and lower body non-abdominal vessels are exposed to atmospheric pressure (PATM).

These external pressures are generated solely or in part by the respiratory system and continuously change during spontaneous and mechanical ventilation. Since these pressures directly alter the internal (intramural) and transmural pressures of the heart chambers and systemic and pulmonary blood vessels, ventilation can have an enormous impact on cardiac and circulatory function. That’s why it’s so important for physicians who care for critically ill, mechanically ventilated patients to understand the interactions that occur between the pulmonary and cardiovascular systems. I will begin by reviewing certain aspects of normal cardiovascular physiology.

Essential Cardiovascular Physiology

Intramural, Extramural, and Transmural Pressure

As discussed in Chapter 1, the pressure inside a gas-filled (or liquid-filled) elastic structure is called the intramural pressure (PIM), and the external pressure is referred to as the extramural pressure (PEM). The pressure gradient across the wall of the structure is called the transmural pressure (PTM), which is calculated by subtracting the extramural from the intramural pressure.

PTM=PIMPEM
(3.1)

The main thing I want you to remember is that intramural pressures within a tube or circuit determine the rate and direction of flow, whereas the transmural pressure of an elastic structure determines its volume. In Chapter 1, we applied these principles when talking about the pressure needed to overcome viscous forces and elastic recoil during ventilation. In this chapter, we will use them to explain changes in blood flow between two portions of the circulatory system and changes in the volume and size of the heart chambers.

Before we move on, I want to remind you that any change in the extramural pressure of an elastic structure has a direct effect on its intramural pressure. For example, if you squeeze an inflated balloon, intramural and extramural pressure increase by the same amount. Similarly, changes in pleural, alveolar, and intra-abdominal pressure alter the pressure within the heart and the intrathoracic and intra-abdominal blood vessels.

Blood Flow and Waterfalls

Like gas flow, blood flow can occur only by overcoming viscous forces, and this causes a progressive fall in intramural (intravascular) pressure. Consider what happens when intravascular pressure initially exceeds but then falls below extramural pressure (Figure 3.2). Once this occurs, the vessel will collapse when a critical negative transmural (closing) pressure has been reached. Since veins and capillaries have little structural rigidity, they collapse shortly after transmural pressure becomes negative, and flow then stops. When this happens, though, the intramural pressure gradient disappears, the pressure within the collapsed segment equals the upstream driving pressure, the vessel opens, and flow resumes. But as soon as flow starts, intramural pressure falls and the vessel collapses. Of course, this vicious cycle doesn’t really happen. Instead, an equilibrium is reached in which the capillary or vein narrows but flow persists. Under these conditions, the pressure gradient driving flow is no longer the difference between the upstream and downstream ends of the vessel, but rather the difference between the upstream pressure and the pressure at the so-called choke point (which is just slightly less than extramural pressure).

Figure 3.2 The “waterfall effect” occurs when upstream intravascular pressure exceeds, and downstream pressure is less than, extramural pressure. As intravascular pressure falls during blood flow, the vessel will narrow once transmural pressure becomes negative. This produces a choke point, and flow is then determined by the gradient between upstream pressure and the pressure at the choke point.

Figure 3.2 The “waterfall effect” occurs when upstream intravascular pressure exceeds, and downstream pressure is less than, extramural pressure. As intravascular pressure falls during blood flow, the vessel will narrow once transmural pressure becomes negative. This produces a choke point, and flow is then determined by the gradient between upstream pressure and the pressure at the choke point.

It’s especially fitting to use the terms “upstream” and “downstream” because this situation is often compared to a waterfall. In Figure 3.3, the vertical distance between the upstream part of the river and the river below the waterfall represents the pressure gradient between the two ends of the blood vessel, while the top of the waterfall is analogous to the pressure at the choke point. If you think about it, you’ll see that the rate at which water rushes over the falls depends only on the vertical distance between the upstream portion of the river and the top of the waterfall (i.e., the slope of the riverbed). Just like the difference between the pressure at the choke point and downstream pressure in Figure 3.2 does not influence flow through the vessel, the height of the waterfall has no effect on how fast water flows over it. We will be talking a lot more about this waterfall effect throughout the rest of this chapter.

Figure 3.3 The rate at which water flows over a waterfall depends only on the slope of the river bed and is not affected by the height of the waterfall.

Figure 3.3 The rate at which water flows over a waterfall depends only on the slope of the river bed and is not affected by the height of the waterfall.

Cardiac Output and Stroke Volume

Cardiac output (CO) is equal to the product of heart rate (HR) and stroke volume (SV).

CO=HR×SV
(3.2)

Stroke volume is determined by the interaction of three factors:

  • Ventricular preload

  • Ventricular afterload

  • Ventricular contractility

Preload

Technically, preload is the length of the cardiac myocytes just before the ventricle contracts. Starling’s law tells us that, up to a point, the force of contraction increases with muscle cell length. Since we can’t measure the actual preload, ventricular volume at end-diastole is the most appropriate substitute. In clinical practice, however, we typically use end-diastolic pressure (EDP), which is related to end-diastolic volume (EDV) by ventricular compliance. Figure 3.4 is a ventricular function curve that shows the relationship between EDV and SV. Note that this curve has two parts—an ascending portion where SV varies significantly with preload, and a plateau where changes in preload have little effect on SV.

Figure 3.4 The relationship between left ventricular end-diastolic volume (LVEDV)  and the stroke volume (SV) generated during ventricular contraction. As muscle length  and ventricular volume increase, contractile force and SV rapidly increase,  then plateau.

Figure 3.4 The relationship between left ventricular end-diastolic volume (LVEDV) and the stroke volume (SV) generated during ventricular contraction. As muscle length and ventricular volume increase, contractile force and SV rapidly increase, then plateau.

There are three determinants of ventricular preload:

  • The rate at which blood enters the right atrium from the systemic veins (venous return)

  • Ventricular compliance

  • The duration of diastole, which is the time available for ventricular filling

Let’s take a closer look at the first two.

Venous Return

If we rearrange the equation used to calculate resistance in Chapter 1 (Equation 1.3), you can see that flow equals the intramural pressure gradient divided by resistance.

V˙=ΔPIM/R
(3.3)

We can use this equation to examine the factors that determine the rate at which blood returns to the right atrium (RA). Here, V˙ is the venous return, Δ‎PIM is the difference between mean systemic pressure (MSP) and right atrial intramural pressure (PraIM), and R is the resistance of the veins returning blood to the heart. The mean systemic pressure is determined only by the compliance of the systemic arteries and veins and the volume of blood they contain. In research studies, it is assumed to be the intravascular pressure during cardiac arrest.

Guyton and colleagues were the first to construct venous return curves (Figure 3.5). As expected, venous return increases as PraIM falls and the pressure gradient driving flow increases. Note that venous return stops when the curve intersects the x-axis; this is when PraIM equals MSP. Also notice that venous return does not increase indefinitely as PraIM falls; instead, it plateaus at a so-called critical pressure. As you may have guessed, this plateau, in spite of further decreases in downstream pressure, is due to a waterfall effect.

Figure 3.5 The relationship between venous return and intramural right atrial pressure (PraIM). As PraIM falls, venous return steadily increases, then plateaus once the critical pressure (PCRIT) has been reached. PCRIT is normally very close to atmospheric pressure. Mean systemic pressure and venous return at a given PraIM vary directly with intravascular volume. Increased venous resistance reduces the slope of the curve and decreases maximum venous return.

Figure 3.5 The relationship between venous return and intramural right atrial pressure (PraIM). As PraIM falls, venous return steadily increases, then plateaus once the critical pressure (PCRIT) has been reached. PCRIT is normally very close to atmospheric pressure. Mean systemic pressure and venous return at a given PraIM vary directly with intravascular volume. Increased venous resistance reduces the slope of the curve and decreases maximum venous return.

The extramural pressure of the jugular and axillary veins, which drain the head, neck, and arms, is PATM, whereas the inferior vena cava (IVC) is exposed to PAB. Since PraIM is the downstream pressure for both, a waterfall effect is created as soon as PraIM (and intramural venous pressure) falls below PATM or PAB. The back pressure for blood flow from the upper and lower body then becomes PATM and PAB, respectively, and further decreases in PraIM cannot increase venous return.

Figure 3.5 also illustrates that venous return depends on intravascular volume through its effect on MSP. Hypovolemia reduces MSP and the pressure gradient driving venous return. Volume loading increases MSP and venous return. Also note that increasing venous resistance reduces maximum venous return and decreases the slope of the venous return curve.

Ventricular Compliance

During diastole, blood flow from the atria to the ventricles is directly related to the pressure gradient between them (Equation 3.3). Also, if we rearrange the compliance equation from Chapter 1 (Equation 1.2), you can see that the volume of blood entering the ventricles is proportional to ventricular compliance and the change in ventricular transmural pressure:

ΔV=ΔPTM×C
(3.4)

If ventricular compliance is low (i.e., the ventricle is stiff), intramural and transmural pressure rise rapidly during diastole, the pressure gradient quickly disappears, flow stops, and there is relatively little ventricular filling (Figure 3.6). This means that a ventricle with low compliance will have relatively little end-diastolic volume (preload) for a given end-diastolic pressure. If ventricular compliance is high, much more blood can enter before pressure equalizes, and preload will be relatively high at the same end-diastolic pressure.

Figure 3.6 The relationship between left ventricular end-diastolic pressure (LVEDP) and volume (LVEDV). As ventricular compliance falls (arrow), progressively less blood enters the ventricle at the same intraventricular pressure (dashed lines).

Figure 3.6 The relationship between left ventricular end-diastolic pressure (LVEDP) and volume (LVEDV). As ventricular compliance falls (arrow), progressively less blood enters the ventricle at the same intraventricular pressure (dashed lines).

Ventricular compliance can be altered by a number of factors, including hypertrophy, ischemia, and infiltrative diseases, but for this discussion, I want to focus on the effect of the normal pericardium. Because it is relatively noncompliant, the pericardium limits the total volume of blood that the ventricles can hold. So, if the end-diastolic volume of one ventricle increases, the interventricular septum shifts toward the other ventricle, thereby reducing its compliance, diastolic filling, and preload. This is referred to as ventricular interdependence. As you’ll see later in this chapter, reciprocal changes in the volume within the right (RV) and left (LV) ventricles normally occur during the respiratory cycle. Abnormal ventricular interdependence occurs when this effect is exaggerated by pericardial or myocardial disease.

Afterload

Ventricular afterload is defined as the wall stress generated during systole. Wall stress (σ‎) is proportional to the intramural pressure needed to eject blood (PIM) and the internal ventricular radius (r), and inversely related to the thickness of the ventricle (T).

σ(PIM×r)/T
(3.5)

From a practical standpoint, it’s much easier to forget about ventricular radius and thickness (which you won’t know anyway) and simply remember that LV and RV afterload are directly proportional to mean systemic arterial (PSA¯IM) and mean pulmonary arterial (PPA¯IM) pressure, respectively. But, what determines these pressures? Well, if we rearrange Equation 3.3 and make a few substitutions, you can see that LV and RV afterload are also directly related to cardiac output and systemic (SVR) and pulmonary (PVR) vascular resistance, respectively.

LVafterloadPSA¯IM(CO×SVR)
(3.6)

RVafterloadPPA¯IM(CO×PVR)
(3.7)

Since the pulmonary circulation is a low-pressure, low-resistance circuit, RV afterload is normally low, and ventricular contraction must produce only a small amount of intramural pressure. The LV must generate much more pressure during systole because systemic blood pressure and vascular resistance are much higher, and afterload is proportionally increased.

Contractility

Ventricular contractility is the inherent ability of the ventricle to generate pressure during systole, and it’s reduced by any disease that damages the myocardium. As shown in Figure 3.7, differences in contractility are commonly represented by a series of ventricular function curves.

Figure 3.7 A series of ventricular function curves showing the effect of changes in contractility on the relationship between stroke volume (SV) and left ventricular end-diastolic volume (LVEDV).

Figure 3.7 A series of ventricular function curves showing the effect of changes in contractility on the relationship between stroke volume (SV) and left ventricular end-diastolic volume (LVEDV).

The Interaction of Preload, Afterload, and Contractility

Figure 3.8 shows how SV and LV end-diastolic volume are affected by changes in preload, afterload, and contractility. As you’ve already seen (Figure 3.4), changes in preload move stroke volume along a single curve. Increasing contractility or decreasing afterload shifts the curve upward and to the left, meaning that SV rises and end-diastolic volume falls. A decrease in contractility or an increase in afterload shifts the curve downward and to the right, thereby reducing SV and increasing end-diastolic volume.

Figure 3.8 A change in preload increases (A → B) or decreases (A → C) stroke volume (SV) along one ventricular function curve. A reduction in afterload or an increase in contractility (A → D) increases SV while reducing left ventricular end-diastolic volume (LVEDV). Decreased contractility or an increase in afterload (A → E) reduces SV and increases LVEDV.

Figure 3.8 A change in preload increases (A → B) or decreases (A → C) stroke volume (SV) along one ventricular function curve. A reduction in afterload or an increase in contractility (A → D) increases SV while reducing left ventricular end-diastolic volume (LVEDV). Decreased contractility or an increase in afterload (A → E) reduces SV and increases LVEDV.

Spontaneous Ventilation and Cardiovascular Function

The changes in PPL, PALV, PAB, and lung transmural pressure (PlTM) during a spontaneous breath are shown in Figure 3.9. As discussed in Chapter 1, PPL is normally negative (sub-atmospheric) at end-expiration. As the inspiratory muscles expand the chest wall, lung volume and elastic recoil increase. This causes a progressive drop in PPL, which reaches its lowest (most negative) value at the end of inspiration. Alveolar pressure is zero (atmospheric pressure) at end-expiration. During inspiration, PALV becomes negative as the lungs expand. This generates the pressure gradient between PALV and pressure at the mouth (PATM) that drives air into the lungs. As the lungs fill, PALV rises and returns to zero at end-inspiration. Lung transmural pressure is the pressure acting on the lungs. It equals PALV minus PPL, and the rise in PlTM during inspiration is what drives the increase in lung volume. Since PALV is zero (atmospheric pressure) at both the beginning and the end of inspiration (Figure 3.9), the rise in PlTM is due to the fall in PPL. As the lungs expand and the diaphragm descends, intra-abdominal volume decreases, which raises PAB.

Figure 3.9 Schematic representation of the changes in pleural pressure (PPL), alveolar pressure (PALV), intra-abdominal pressure (PAB), and lung transmural pressure (PLTM) during spontaneous breathing. Insp = inspiration; Exp = expiration

Figure 3.9 Schematic representation of the changes in pleural pressure (PPL), alveolar pressure (PALV), intra-abdominal pressure (PAB), and lung transmural pressure (PLTM) during spontaneous breathing. Insp = inspiration; Exp = expiration

During relaxed (passive) expiration, PlTM falls with lung volume, and PPL and PAB return to baseline levels. The elastic recoil generated during inspiration increases PALV, which drives gas from the lungs. Alveolar pressure and expiratory flow reach zero once the respiratory system has returned to its equilibrium volume. Based on our previous discussion, these pressure changes have predictable effects on RV and LV preload, afterload, and stroke volume (Figure 3.10).

Figure 3.10 Schematic representation of the hemodynamic changes that occur during spontaneous ventilation. Insp = inspiration; Exp = expiration; PraIM = intramural right atrial pressure; RVEDV = right ventricular end-diastolic volume; LVEDV = left ventricular end-diastolic volume

Figure 3.10 Schematic representation of the hemodynamic changes that occur during spontaneous ventilation. Insp = inspiration; Exp = expiration; PraIM = intramural right atrial pressure; RVEDV = right ventricular end-diastolic volume; LVEDV = left ventricular end-diastolic volume

The Effect on RV Preload

Since changes in pleural pressure cause a similar change in the pressures within the heart chambers, the drop in PPL reduces PraIM, which increases the pressure gradient driving venous return. Increased venous return augments RV filling and preload. Usually, this outweighs the increase in RV afterload (see The Effect on Pulmonary Vascular Resistance and RV Afterload), and RV stroke volume rises. Passive expiration reverses these hemodynamic changes, and venous return, RV end-diastolic volume, and RV stroke volume fall as PPL returns to its baseline level.

The Effect on LV Preload

Due to ventricular interdependence, the increase in RV volume reduces LV compliance and decreases diastolic filling. This reduces LV preload and stroke volume at the beginning of inspiration. Subsequently, increased RV stroke volume augments LV preload sufficiently to overcome the rise in LV afterload (see The Effect on LV Afterload), and LV stroke volume increases.

During expiration, LV preload and stroke volume transiently rise with the decrease in RV volume and improved LV diastolic filling but then fall due to the reduction in RV stroke volume.

The Effect on Pulmonary Vascular Resistance and RV Afterload

Recall that the pulmonary vasculature can be divided into two “compartments” based on the prevailing extramural pressure (Figure 3.1). The pulmonary capillaries are often referred to as alveolar vessels because they are exposed to alveolar pressure. The pulmonary arteries and veins are extra-alveolar and are exposed to pleural pressure.

Alveolar Vessels

The transmural pressure of the pulmonary capillaries (PcTM) is the difference between capillary intramural pressure (PcIM) and alveolar pressure (PALV).

PcTM=PcIMPALV
(3.8)

In turn, capillary intramural pressure depends on the location of each vessel relative to the left atrium.

At this point, it’s important to recall that a column of water (or blood) generates hydrostatic pressure. If you fill a 30-centimeter-long tube with water and hold it vertically, the pressure at the bottom will exceed the pressure at the top by 30 cmH2O. Similarly, when standing, the pressure inside the veins of the feet exceeds the pressure in the femoral veins by 1 cmH2O for every centimeter of vertical distance between them.

There is normally a continuous column of blood between the pulmonary capillaries and the left atrium. Since pulmonary venous resistance is very low, PcIM will be almost identical to intramural left atrial pressure (PlaIM) when they are at the same vertical height in the thorax. Hydrostatic pressure progressively increases and decreases PcIM by 1.0 cmH2O (0.74 mmHg) respectively, for every centimeter that the vessel is below or above the left atrial level.

We can consider PALV to be uniform throughout the lungs. Since PcIM varies with hydrostatic pressure, capillary transmural pressure and volume must decrease from the dependent to the non-dependent portions of the lungs. In 1964, West and colleagues famously divided the lungs into three “zones” based on the relationship between mean pulmonary artery pressure (PPA¯IM), PcIM, and PALV (Figure 3.11).

Figure 3.11 West’s zones of the lung are based on the relationship between mean pulmonary artery pressure PPA¯, intramural capillary pressure (Pc), and alveolar pressure (PALV). In Zone 1, the capillaries are collapsed, and no flow occurs. Vessel resistance decreases and blood flow increases from the top of Zone 2 to the bottom of Zone 3.

Figure 3.11 West’s zones of the lung are based on the relationship between mean pulmonary artery pressure PPA¯, intramural capillary pressure (Pc), and alveolar pressure (PALV). In Zone 1, the capillaries are collapsed, and no flow occurs. Vessel resistance decreases and blood flow increases from the top of Zone 2 to the bottom of Zone 3.

In the most dependent region (Zone 3), PPA¯IM is greater than PcIM, which exceeds PALV. Since capillary transmural pressure is positive throughout, the capillaries are filled with blood, their resistance is low, and flow is driven by the difference between PPA¯IM and PlaIM. As hydrostatic pressure increases from the top to the bottom of Zone 3, PPA¯IM (which is also affected by hydrostatic pressure) and PcIM increase, transmural capillary pressure rises, the capillaries dilate, resistance falls, and blood flow increases.

In Zone 1, the capillaries are far above the left atrial level, and both PPA¯IM and PcIM are less than PALV. This means that transmural pressure is negative along the entire length of the capillaries, which are collapsed and empty, and no flow occurs.

In Zone 2, PALV is greater than PcIM but less than PPA¯IM. This produces a waterfall effect, in which capillary flow is determined by the gradient between PPA¯IM and PALV and is independent of PcIM and PlaIM. Like in Zone 3, capillary resistance falls and flow increases from the top to the bottom of Zone 2 as both PPA¯IM and PcIM increase.

Based on this discussion, you can see that the overall resistance of the alveolar vessels increases with the number of capillaries in Zones 1 and 2.

Extra-alveolar Vessels

The transmural pressure of the pulmonary arteries and veins is the difference between intramural pressure and PPL. Unlike in other blood vessels, though, transmural pressure does not determine the radius and volume of the extra-alveolar vessels. That’s because the pulmonary arteries and veins are attached to the lung parenchyma, which provides outward radial traction. In this way, the extra-alveolar vessels are just like the bronchioles, which are pulled open by the “tethering effect” of the lung parenchyma.

Lung Volume and Pulmonary Vascular Resistance

Recall from our previous discussion that, during a spontaneous breath, the rise in PlTM is due solely to the drop in PPL. Since the left atrium is exposed to PPL, PlaIM also falls, which reduces both intramural and transmural capillary pressure. This narrows the alveolar vessels, increases their resistance, and increases the number of capillaries in Zones 1 and 2. At the same time, the increase in elastic recoil that accompanies lung inflation augments the outward traction on the extra-alveolar vessels, which increases their diameter and reduces their resistance. As shown in Figure 3.12, total pulmonary vascular resistance (the sum of alveolar and extra-alveolar resistance) and RV afterload are normally lowest in the tidal volume range and progressively increase between functional residual capacity and total lung capacity.

Figure 3.12 The change in pulmonary vascular resistance (PVR) between functional residual capacity (FRC) and total lung capacity (TLC). Total PVR is the sum of the resistance of the alveolar and extra-alveolar vessels.

Figure 3.12 The change in pulmonary vascular resistance (PVR) between functional residual capacity (FRC) and total lung capacity (TLC). Total PVR is the sum of the resistance of the alveolar and extra-alveolar vessels.

The Effect on LV Afterload

The fall in PPL during inspiration reduces LV end-diastolic pressure, but since most of the arterial circulation is outside the thorax, there’s no change in mean arterial pressure. It follows that the LV must generate more pressure to eject blood during systole, and its afterload increases. Left ventricular afterload falls during expiration as PPL returns to baseline.

Factors Affecting the Magnitude of Hemodynamic Changes

The hemodynamic effects produced by a spontaneous breath depend on three factors:

  • The magnitude of the fall in PPL

  • The magnitude of the rise in PlTM

  • Baseline ventricular function

Pleural Pressure

The magnitude of the fall in PPL during inspiration varies directly with lung volume, airway resistance, and inspiratory flow, and inversely with lung compliance. In other words, PPL becomes more negative with large, rapid breaths, when airway resistance is high, and when the lungs are stiff. Within the limits imposed by the critical pressure (Figure 3.5), the greater the fall in PPL, the greater the increase in venous return, RV and LV preload, and LV afterload.

Lung Transmural Pressure

Because it is due to the fall in PPL, the magnitude of the increase in PlTM during a spontaneous breath also varies directly with tidal volume, airway resistance, and inspiratory flow, and inversely with lung compliance. The greater the rise in PlTM, the greater the increase in capillary and total pulmonary vascular resistance and RV afterload.

Ventricular Function

The extent to which changes in ventricular preload alter LV stroke volume and blood pressure depends primarily on baseline LV preload (Figure 3.13). If preload is already high, an increase in LV end-diastolic volume will have little effect on stroke volume and blood pressure. If however, LV preload is low, the shape of the curve dictates that even a small increase in end-diastolic volume will significantly augment stroke volume. This leads to a characteristic, cyclical change in blood pressure in hypovolemic, “volume-responsive” patients.

Figure 3.13 When left ventricular end-diastolic volume (LVEDV) and stroke volume (SV) occupy a point on the ascending portion of the ventricular function curve, the increase in LV preload produced by a spontaneous breath (dashed line) will cause a relatively large rise in SV (A → B). When ventricular preload is high, the increase in LVEDV has little effect on SV (C → D).

Figure 3.13 When left ventricular end-diastolic volume (LVEDV) and stroke volume (SV) occupy a point on the ascending portion of the ventricular function curve, the increase in LV preload produced by a spontaneous breath (dashed line) will cause a relatively large rise in SV (A → B). When ventricular preload is high, the increase in LVEDV has little effect on SV (C → D).

As shown in Figure 3.14, the transient drop in LV preload and stroke volume early in inspiration causes blood pressure to fall. From mid-inspiration to early expiration, blood pressure rises with the increase in LV preload and stroke volume. Between mid-expiration and early inspiration, blood pressure decreases with the drop in LV stroke volume.

Figure 3.14 The variation in arterial blood pressure during spontaneous ventilation when LV preload is low.

Figure 3.14 The variation in arterial blood pressure during spontaneous ventilation when LV preload is low.

Spontaneous Ventilation and the Cardiovascular System: Take-Home Points

  • Spontaneous ventilation causes a cyclical decrease in PPL, which increases venous return, RV and LV preload, and LV afterload, and a cyclical rise in PlTM, which increases PVR and RV afterload.

  • The hemodynamic significance of these changes depends on the magnitude of the change in PPL and PlTM and on baseline ventricular function:

    • The change in PPL and PlTM varies directly with tidal volume, airway resistance, and inspiratory flow, and inversely with lung compliance.

    • The hemodynamic effect of a fall in PPL is greater in patients with low baseline LV preload.

Mechanical Ventilation and Cardiovascular Function

The pressure changes occurring during a passive (no patient effort) mechanical breath with constant inspiratory flow are shown in Figure 3.15A. Since atmospheric pressure is considered to be zero, the transmural pressure of the respiratory system (PALV – PATM) is simply PALV, which increases linearly with lung volume. The gradient between the pressure in the ventilator circuit (airway pressure; PAW) and PALV overcomes viscous forces and drives gas through the airways. Pleural pressure rises (becomes less negative) as the visceral pleura is forced outward against the parietal pleura, and reaches zero when the respiratory system expands to the equilibrium volume of the chest wall. Above this volume, the elastic recoil of the chest wall is directed inward, the parietal pleura is pushed against the visceral pleura of the expanding lungs, and PPL becomes positive (supra-atmospheric). The volume increase during inspiration is driven by the rise in PlTM. We saw that during a spontaneous breath, this is due solely to the fall in PPL. During mechanical inflation, PlTM increases because PALV rises out of proportion to PPL. As the thorax expands and the diaphragm is pushed into the abdominal compartment, PAB increases by about the same amount as PPL.

Figure 3.15 The change in airway (PAW), alveolar (PALV), pleural (PPL), lung transmural (PlTM), and abdominal (PAB) pressure during a mechanical breath shown as (A) pressure–time curves and (B) volume–pressure curves.

Figure 3.15 The change in airway (PAW), alveolar (PALV), pleural (PPL), lung transmural (PlTM), and abdominal (PAB) pressure during a mechanical breath shown as (A) pressure–time curves and (B) volume–pressure curves.

During passive expiration, PAW immediately returns to the level of extrinsic PEEP (PEEPE), and the gradient between PALV and PEEPE drives gas from the lungs. Alveolar pressure and PlTM fall with elastic recoil and lung volume, and expiratory flow stops when PALV equals PEEPE. Pleural pressure and PAB decrease with lung volume and return to their baseline levels at end-expiration.

Now look at Figure 3.15B. You were introduced to this alternative way of representing pressure changes in Chapter 1. It has the same information as Figure 3.15A, but I’m reintroducing the concept of volume–pressure curves because it will be easier to see how changes in tidal volume and compliance affect PPL and PlTM.

The hemodynamic effects of a mechanical breath are shown in Figure 3.16. Note that, for the most part, they are the opposite of those occurring during spontaneous breathing.

Figure 3.16 Schematic representation of the hemodynamic changes that occur during mechanical ventilation. Insp = inspiration; Exp = expiration

Figure 3.16 Schematic representation of the hemodynamic changes that occur during mechanical ventilation. Insp = inspiration; Exp = expiration

The Effect on RV and LV Preload

During mechanical inflation, the rise in PPL causes PraIM to increase, which reduces venous return and RV filling. The drop in RV preload and increase in RV afterload (see The Effect on RV Afterload) reduces RV stroke volume.

The decrease in RV end-diastolic volume transiently increases LV compliance, preload, and stroke volume, but, despite the drop in afterload (see The Effect on LV Afterload), LV stroke volume then falls with RV stroke volume.

Passive expiration reverses these hemodynamic changes. Venous return increases, which augments RV preload and stroke volume. LV preload and stroke volume initially fall with the increase in RV filling but then increase due to the rise in venous return and RV stroke volume.

The Effect on RV Afterload

Alveolar pressure normally increases more than PPL during mechanical inflation (Figure 3.15). Since PlaIM and PPL increase by the same amount, the increase in PALV must exceed the rise in PlaIM, and capillary transmural pressure falls. This increases the volume of Zones 1 and 2 and raises the resistance of the alveolar vessels. At the same time, the increase in elastic recoil that accompanies lung inflation augments the outward traction on the extra-alveolar vessels, which reduces their resistance. This means that the relationship between lung volume and total PVR (and RV afterload) is the same during spontaneous and mechanical ventilation (Figure 3.12).

The Effect on LV Afterload

The rise in PPL during inspiration increases LV end-diastolic pressure. This reduces the amount of pressure that the ventricle must generate to pump blood against the mean arterial pressure, and LV afterload falls. Afterload rises during expiration as PPL returns to baseline.

Factors Affecting the Magnitude of Hemodynamic Changes

The hemodynamic impact of a mechanical breath depends on:

  • The level and magnitude of the increase in PPL

  • The level and magnitude of the rise in PlTM

  • Baseline ventricular function

Pleural Pressure

During a mechanical breath, the increase in PPL varies directly with lung volume (Figure 3.17A) and inversely with chest wall compliance (Figure 3.17B). This means that, for a given tidal volume, there will be a larger rise in PPL when the chest wall is stiff (e.g., obesity, kyphoscoliosis). Also note that the actual level of PPL becomes much higher as tidal volume increases and chest wall compliance falls. Remember that venous return falls sharply as PPL (and PraIM) increase and stops completely once PraIM reaches mean systemic pressure (Figure 3.5).

Figure 3.17 (A) Volume–pressure curves illustrating the effect of tidal volume during a mechanical breath. A large tidal volume (VT-2) produces a larger increase and a higher level of pleural pressure (Δ‎PPL-2) and lung transmural pressure (Δ‎PlTM-2) than a small tidal volume (VT-1).(B) When chest wall compliance is low, the same tidal volume shown in (A) produces a much larger increase and a much higher level of pleural pressure (Δ‎PPL).(C) When lung compliance is low, the same tidal volume shown in (A) produces a much larger increase and a much higher level of lung transmural pressure (Δ‎PlTM).

Figure 3.17 (A) Volume–pressure curves illustrating the effect of tidal volume during a mechanical breath. A large tidal volume (VT-2) produces a larger increase and a higher level of pleural pressure (Δ‎PPL-2) and lung transmural pressure (Δ‎PlTM-2) than a small tidal volume (VT-1).

(B) When chest wall compliance is low, the same tidal volume shown in (A) produces a much larger increase and a much higher level of pleural pressure (Δ‎PPL).

(C) When lung compliance is low, the same tidal volume shown in (A) produces a much larger increase and a much higher level of lung transmural pressure (Δ‎PlTM).

Lung Transmural Pressure

Figures 3.17A and C show that the increase in PlTM during a mechanical breath is also directly related to tidal volume but inversely related to lung compliance. This makes sense if you remember that PlTM is the pressure needed to inflate the lungs. Remember that PVR and RV afterload increase with PlTM.

Ventricular Function

Like during spontaneous breathing, the degree to which changes in venous return alter LV stroke volume and systemic blood pressure depends primarily on baseline LV preload (Figure 3.18). If preload is high, a decrease in LV end-diastolic volume will have little effect on stroke volume. If, however, LV preload is low, any further decrease will cause a significant fall in stroke volume and blood pressure.

Figure 3.18 When left ventricular end-diastolic volume (LVEDV) and stroke volume (SV) occupy a point on the ascending portion of the ventricular function curve, the decrease in LV preload produced by a mechanical breath (dashed line) will cause a relatively large drop in SV (A → B). When ventricular preload is high, the fall in LVEDV has little effect on SV (C → D).

Figure 3.18 When left ventricular end-diastolic volume (LVEDV) and stroke volume (SV) occupy a point on the ascending portion of the ventricular function curve, the decrease in LV preload produced by a mechanical breath (dashed line) will cause a relatively large drop in SV (A → B). When ventricular preload is high, the fall in LVEDV has little effect on SV (C → D).

This leads to a characteristic, cyclical change in blood pressure. As shown in Figure 3.19, the transient rise in LV preload and stroke volume in early inspiration increases blood pressure. From mid-inspiration to early expiration, blood pressure falls with the drop in LV preload and stroke volume. Between mid-expiration and early inspiration, blood pressure rises with the increase in LV preload.

Figure 3.19 The variation in arterial blood pressure during mechanical ventilation in the presence of low LV preload.

Figure 3.19 The variation in arterial blood pressure during mechanical ventilation in the presence of low LV preload.

In patients with preexisting elevated RV afterload or reduced contractility, a marked increase in PlTM may precipitate acute or acute-on-chronic RV failure.

Patient Effort During Mechanical Ventilation

So far, we’ve only discussed the changes that occur during passive mechanical ventilation. What happens when patients actively inhale and exhale? By directly expanding the chest wall, inspiratory effort reduces the expected increase in PPL, PALV, and PAW. In fact, vigorous efforts may actually lower these pressures throughout most of inspiration. During active expiration, contraction of the abdominal musculature forces the chest wall down against the lungs, thereby increasing PPL and PALV. It should be evident, then, that patient effort can significantly change the usual hemodynamic effects of mechanical ventilation.

Positive End-Expiratory Pressure

Positive end-expiratory pressure may be set by the clinician (extrinsic PEEP; PEEPE) or result from dynamic hyperinflation (intrinsic PEEP; PEEPI). The sum of extrinsic and intrinsic PEEP is called total PEEP (PEEPT).

By itself, mechanical ventilation causes only intermittent increases in PPL and PlTM. As shown in Figure 3.20, PEEP not only augments these pressures during inspiration but continuously elevates them throughout the respiratory cycle. This magnifies the hemodynamic effects of mechanical ventilation in proportion to PEEPT. Based on the previous discussion and Figure 3.17, you can see that, for a given level of PEEPT, low chest wall compliance will accentuate the rise in PPL and the fall in RV preload, whereas low lung compliance will augment the increase in PlTM and RV afterload. Figures 3.17 and 3.20 are extremely important when considering the hemodynamic effects of mechanical ventilation and PEEP in different disease states. You will see them again in later chapters.

Figure 3.20 (A) Pressure–time curves showing that PEEP elevates airway (PAW), alveolar (PALV), pleural (PPL), and lung transmural (PlTM) pressure throughout the respiratory cycle.(B) Volume–pressure curves showing that PEEP sets a new, higher equilibrium volume (EV) for the respiratory system. The same tidal volume (VT) produces a similar increase in pleural pressure (Δ‎PPL-1 ≅ Δ‎PPL-2) and lung transmural pressure (Δ‎PlTM-1 ≅ Δ‎PlTM-2) with or without PEEP, but the actual values of these pressures are much higher after the addition of PEEP.

Figure 3.20 (A) Pressure–time curves showing that PEEP elevates airway (PAW), alveolar (PALV), pleural (PPL), and lung transmural (PlTM) pressure throughout the respiratory cycle.

(B) Volume–pressure curves showing that PEEP sets a new, higher equilibrium volume (EV) for the respiratory system. The same tidal volume (VT) produces a similar increase in pleural pressure (Δ‎PPL-1 ≅ Δ‎PPL-2) and lung transmural pressure (Δ‎PlTM-1 ≅ Δ‎PlTM-2) with or without PEEP, but the actual values of these pressures are much higher after the addition of PEEP.

The effect of compliance on the rise in PPL and PlTM produced by tidal inflation and PEEP can also be demonstrated mathematically. Recall that the compliance of the lungs (CL) and chest wall (CCW) equals the change in volume (Δ‎VL and Δ‎VCW) divided by the accompanying change in transmural pressure. If we do a little algebra:

CL= ΔVL/Δ(PALVPPL)andΔVL= CL×Δ(PALVPPL)CCW= ΔVCW/ΔPPLandΔVCW= CCW×ΔPPL

Since Δ‎VL must equal Δ‎VCW,

CCW×ΔPPL= CL×Δ(PALVPPL)CCW×ΔPPL= (CL×ΔPALV)(CL×ΔPPL)(CL×ΔPPL) + (CCW×ΔPPL) = (CL×ΔPALV)ΔPPL×(CL+CCW)= (CL×ΔPALV)ΔPPL= ΔPALV×CL/(CL+CCW)
(3.9)

Let’s say that we increase PEEP from 0 to 10 cmH2O. This increases end-expiratory alveolar pressure from 0 to 10 cmH2O, so Δ‎PALV = 10 cmH2O. If chest wall compliance is very low (let’s say CCW = 0.1 × CL), Equation 3.9 tells us that PPL increases by 9 cmH2O, but PlTM only increases by 10 – 9 = 1 cmH2O. If, on the other hand, lung compliance is very low and CL = 0.1 × CCW, PPL increases by only 0.9 cmH2O, but PlTM goes up by 9.1 cmH2O.

It’s usually assumed that venous return falls because of the PEEP-induced increase in PPL and PraIM; but it’s almost certainly not that simple. Several groups of investigators have shown that PEEP reduces venous return despite an equal increase in PraIM and mean systemic pressure. In the absence of a change in driving pressure, it was reasoned and subsequently proven in an animal preparation that PEEP reduces venous return by increasing venous resistance. As shown in Figure 3.5, this reduces the maximal venous return and decreases the slope of the descending portion of the curve.

Mechanical Ventilation and the Cardiovascular System: Take-Home Points

  • Mechanical ventilation causes a cyclical increase in PPL and PlTM. The increase in PPL (and PraIM) reduces venous return, RV and LV preload, and LV afterload. The rise in PlTM increases PVR and RV afterload.

  • Extrinsic and intrinsic PEEP produce a continuous elevation of PPL and PlTM, which further reduces venous return, RV and LV preload, and LV afterload, while increasing RV afterload.

  • The hemodynamic significance of these effects depends on the magnitude of the change in PPL and PlTM, the actual values of these pressures, and baseline ventricular function:

    • The level of PPL and the magnitude of its increase vary directly with tidal volume and the level of total PEEP and inversely with chest wall compliance.

    • The level of PlTM and the magnitude of its increase vary directly with tidal volume and the level of total PEEP and inversely with lung compliance.

    • The hemodynamic effect of a given rise in PPL will be greater in patients with low baseline LV preload.

    • The hemodynamic effect of a given rise in PlTM will be greater in patients with baseline RV dysfunction.

Additional Reading

Fessler HE. Heart–lung interactions: Applications in the critically ill. Eur Respir J. 1997; 10:226–237.Find this resource:

Feihl F, Broccard AF. Interactions between respiration and systemic hemodynamics. Part I: Basic concepts. Intensive Care Med. 2009;35:45–54.Find this resource:

Feihl F, Broccard AF. Interactions between respiration and systemic hemodynamics. Part II: Practical implications in critical care. Intensive Care Med. 2009;35:198–205.Find this resource: