Physiology Note - Heart Lung Interactions

 

                                                                        Heart Lung Interactions

DR NAMRATHA C

DrNB Final year resident

PD Hinduja National Hospital, Mahim, Mumbai

 

 

PHYSIOLOGY OF HEART LUNG INTERACTIONS

 

DEFINITION: The complex interactions between cardiovascular and respiratory physiology as a result of phasic changes in intrathoracic pressure during respiration.

 

PHYSICS: Let us understand the concept of pleural pressure which is normally negative. Consider thorax as the sealed container with lungs (elastic tissue) as the inner wall which has the tendency to collapse inward and rib cage and chest wall (elastic tissue) as the outer wall which has the tendency to spring outwards.

1)Elasticity of the lung tissue

HOOKE’S LAW: Within the elastic limit of a material, the deformation (strain) produced is directly proportional to the applied force (stress)

F=−kxF

where:

• F = restoring force (N)
• k = spring constant (stiffness)
• x= displacement (m)

The negative sign (–) indicates that the restoring force acts in the opposite direction to the displacement.

In terms of pressure and volume (as in lungs)

For elastic structures like lungs:

ΔP=E×ΔV

where:

• ΔP = change in pressure
• ΔV = change in volume
• E= elastance (stiffness of lung)

Basically, the more u stretches the more is the recoil force, (figure 1)

FIGURE 1: Pressure–Volume (P–V) curve of lungs

 

2)Surface tension: This tension tries to make each alveolus shrink, like soap bubbles collapsing.

Laplace’s Law for a sphere=2T/r ​

where T = surface tension, r = radius.

• Without surfactant, this force would be huge, making lungs collapse easily; surfactant reduces surface tension but doesn’t remove it completely, so some recoil remains.

Therefore, Lung recoil = Elastic recoil (fibres) + Surface tension recoil (fluid interface).
These two together are why, when you stop inhaling, your lungs don’t just stay inflated — they want to shrink back, pulling away from the chest wall and helping create that negative pleural pressure

 

So, now let us understand how pressure changes in lung and heart influence each other.

Shared thoracic space -Pascal’s Principle: Pressure applied to a confined fluid is transmitted undiminished in all directions throughout the fluid and to the walls of its container.

• Pascal’s Principle: Pressure applied to a fluid in a closed space is transmitted equally in all directions.
• The lungs, heart, and great vessels share the thoracic cavity.
• The pleural space is filled with fluid, and the pericardium (around the heart) is also a fluid-filled sac, so pressure changes in one part of the chest can be transmitted to others.

So, with this understanding of physics let us understand the interactions in various situations

 

 SPONTANEOUS BREATHING PATIENTS:

• Let us consider thoracic cavity as container containing two pumps, the smaller pump (circulatory pump) and the larger pump (respiratory pump). The respiratory pump acts as a suction pump, because on diaphragmatic contraction due to stimulus from neural drive by stimulating phrenic nerve, the thoracic cavity expands by causing drop in pressure causing more negative pleural pressure (Boyle’s law). The pressure gradient (Patm > Ppl) drives air into the lungs.

So, the inspiratory trigger is essentially the neural drive → muscle contraction → negative pleural pressure → air inflow.

This negative respiratory pump also draws blood from the systemic circulation into the heart, the heart acts as a positive circulatory pump and ejects blood towards the arterial tree.

The negative intrathoracic pressure is due to diaphragm contraction which lowers at inspiration

increases the intra-abdominal pressure: the thorax and abdomen have opposite pressure regimes at inspiration.

 

CARDIOVASCULAR CONSEQUENCES

Before understanding the effect respiratory variations on cardiovascular system let us understand the concept of circulation.

Preload-the passive stress at the end of the diastole of left ventricle. Contributed to by the end diastolic filling pressure and net end diastolic filling volume (EDV)

Afterload-the total myocardial stress during ejection of blood into the arterial tree. Contributed by the left ventricular systolic pressure, left ventricular systolic radius and wall thickness.

Transmural pressure-the distending pressure of the chamber, the difference between the internal expanding forces and collapsing external forces. For LV-difference between intracavitary pressure and pericardial pressure (equivalent to pleural pressure).

Mean systemic filling pressure: the mean pressure in the central circulation when there is no flow of blood. It is related to the effective blood volume, compliance of blood vessels and the pressure that blood vessels exert on vasculature. Normally it is equal to 7mmhg.

Factors affecting stroke volume

1.      RV Preload: Preload is the EDV (end diastolic volume), preload depends on venous return. Venous return in turn depends on the pressure difference between the mean systemic filling pressure and right atrial pressure. 60% of the blood volume is accommodated in the circulatory system without causing any vessel stretch. This is called the unstressed volume. Further addition of volume starts to stretch the vessel walls. This volume of blood that causes stretch of the vessel wall is known as the stressed volume. 40% of blood volume is the stressed volume. This part of the blood volume is hemodynamically active as it is responsible for the pressure generated on the vessel wall this pressure exerted is known as MSFP (mean systemic filling pressure)

ITP increases as during mechanical inspiration, the gradient between MSFP and RAP decreases and also the preload. Opposite happens in spontaneous inspiration when the gradient increases due to decreased ITP leading to increased preload.

Decreasing ITP can increase the VR up to a limit only, and beyond a certain point, the large vessels collapse at the entry to the thorax due to negative ITP limiting any further increase in VR. This is called critical closing pressure of the veins entering the thorax. Because ITP changes during each breath, VR gradient, and therefore the VR preload, varies during expiration and inspiration.

In volume-replete state, the drop in venous return (VR) from increased intrathoracic pressure (ITP) is partly balanced when ITP rises, such as during the use of positive end-expiratory pressure (PEEP), not only increases RA pressure but also causes increased MSVP by translocation of blood from pulmonary to systemic circulation and descent of diaphragm resulting in increased intra-abdominal pressure and compression of intra-abdominal capacitance vessels. This balance is lost in volume-deficient state, MSVP fails to rise adequately and VR may fall significantly. In a normal heart, PEEP reduces cardiac output (CO) to some extent in normovolemic and drastically in hypovolemia due to its effect on VR. In a failing heart, PEEP usually improves CO in part by reducing preload besides reducing transmural pressure.

 

2.      LV preload: Left ventricular (LV) preload averaged over time is equal to right ventricular (RV) output. Because RV preload and therefore RV stroke volume vary during inspiration and expiration, LV preload follows the pattern with a lag time equal to time taken by blood to transit pulmonary circulation. During mechanical inspiration, as the intrathoracic pressure rises while the venous return to RV decreases, the venous return  to LV increases due to squeezing of blood forward into the LV. Subsequently, reduced RV preload manifests as reduced RV stroke volume that reaches the LV after a few heartbeats, resulting in reduced LV preload.

3.      LV After load

Afterload is the pressure against which the heart must work to eject blood during systole. Afterload is often expressed as ventricular wall stress (σ).

 

where P is ventricular pressure; r is ventricular radius; and h is wall thickness.

Afterload increases by increase in transmural pressure and vascular resistance.

 

Transmural pressure: Intracavitary pressure − surrounding pressure. Thoracic cavity encloses heart and lung; heart is surrounded by pericardial cavity which is negative pressure. Since it is difficult to measure, pericardial pressure is equated with pleural pressure and it varies with. the respiratory cycle. In simple words, if surrounding pressure of the heart is negative, during the systole, ventricle has to overcome the extra load of outward distending forces on its wall due to surrounding negative pressure. Similarly, if the surrounding pressure is positive, it compresses the ventricles from outside, thereby aiding in systole.

 

 

 

 

 

 

 

Therefore, if the intrathoracic pressure  is positive (as during mechanical inspiration), it compresses the ventricle and aids in ejection. Transmural pressure becomes lower; however, in case of negative ITP (as during spontaneous inspiration) (transmural pressure = intraventricular − ITP).

 

DETERMINANTS OF RV AFTERLOAD: It is the variations in pulmonary vascular resistance (PVR) that play a more dominant role in deciding afterload. PVR varies significantly with lung volume

Pulmonary Vascular Resistance Variation with Lung Volume

Pulmonary vasculature can be divided into extra-alveolar vessels and intra-alveolar vessels. The former consists of vessels running in the lung interstitium, and the latter, capillaries exposed in alveolar space. When the lung volume increases the cross-sectional area of extra-alveolar vessels, it decreases in alveolar vessels and vice versa. As a result of this pulmonary vascular resistance, increase in both high and low lung volume and is minimum at functional residual volume. In addition to mechanical effects, at low lung volume during hypoventilation, alveolar hypoxia and resorption atelectasis may happen resulting in hypoxic vasoconstriction of pulmonary vessels. This adds to PVR (pulmonary vascular resistance) during low lung volume (figure 2,3).

PVR

                                       Lung volume

FIGURE 2: Pulmonary Vascular Resistance Variation with Lung Volume

 

 

 

FIGURE 3: Pulmonary vascular resistance across lung volumes and West’s zones of pulmonary blood flow The diagram illustrates the relationship between lung volume, pulmonary vascular resistance, and West’s zones of the lung. Pulmonary vascular resistance is lowest around functional residual capacity and increases at both high and low lung volumes due to alveolar and extra-alveolar vessel compression, respectively. On the right, West’s zones describe how regional blood flow is determined by the relative pressures of the alveoli (P_alv), pulmonary artery (P_PA), and pulmonary veins (P_PV): in Zone 1, alveolar pressure exceeds both arterial and venous pressures (P_alv > P_PA > P_PV), resulting in no flow; in Zone 2, arterial pressure exceeds alveolar pressure but venous pressure remains lower (P_PA > P_alv > P_PV), giving intermittent flow; and in Zone 3, arterial and venous pressures are both greater than alveolar pressure (P_PA > P_PV > P_alv), resulting in continuous flow.

VENTRICULAR INTERDEPENDENCE: LV and RV are enclosed in pericardium and they share a common interventricular septum. Therefore, diastolic filling pressure of one ventricle affects the diastolic filling pressure of the other. This is known as ventricular interdependence.

 

Effect of intraabdominal pressure; The negative intrathoracic pressure is due to the diaphragm which lowers at inspiration and increases the intra-abdominal pressure: the thorax and abdomen have opposite pressure regimes at inspiration. This increases intraabdominal pressure decreases venous return (figure 4)

FIGURE 4: Ventricular interdependence

So altogether, the magnitude of heart–lung interactions depend mainly

on four changes happening simultaneously.

1. Effect of phasic variations in ITP on the larger vessels and cardiac chambers

2. Effect of changes in lung volume on pulmonary circulation

3. Changes occurring due to ventricular interdependence (in series and parallel)

4. Effect of changes in intra-abdominal pressure due to diaphragm displacement on vessels in abdomen.

CLINICAL IMPLICATIONS-

A)AECOPD-

 

 

B)ACUTE LV DYSFUNCTION –( transmural pressure=intracavitary pressure -pericardial pressure(corresponding to pleural pressure)

 

 

 

 

WEANING INDUCED PULMONARY EDEMA AND FLUID RESPONSIVENESS

The risk factors for weaning-induced pulmonary oedema (WIPO) are COPD, cardiopathy (dilated and/or hypertrophic and/or hypokinetic cardiopathy and/or significant valvular disease) and obesity.

The WIPO is mainly induced by the shift from a positive to a negative pressure ventilation after disconnecting the ventilator. The inspiratory negativity of intrathoracic pressure may be accentuated by the resistance of the chest tube. This results in the heart–lungs interactions described above in spontaneously breathing patients, leading to unfavourable loading cardiac conditions (increase in right ventricular preload and afterload and increase in left ventricular afterload) and eventually to WIPO.

In patients with chronic right ventricular dysfunction, right ventricular enlargement during weaning may promote WIPO through the mechanism of biventricular interdependence. Conversely, in those with chronic left ventricular dysfunction, factors such as increased left ventricular afterload—driven by accentuated intrathoracic pressure negativity, elevated intra-abdominal pressure, and sympathetic-related arterial hypertension—are important contributors to WIPO. Regardless of ventricular dysfunction type, a positive fluid balance further adds to the risk of developing WIPO.

 

 

PREDICTION OF FLUID RESPONSIVENESS

Fluid administration is the first-line therapy in the early phases of shock states, except in patients with cardiogenic shock with pulmonary oedema.

 

 

A : Frank–Starling Relationship

• X-axis: Left ventricular end-diastolic volume (LVEDV) → i.e., preload.
• Y-axis: Stroke volume (SV).

1. Normal ventricular function:

Ø  The heart responds well to increased preload (steep part of the curve).

Ø  A fluid challenge increases LVEDV and produces a significant rise in stroke volume → preload responsive.

Ø  Once on the flat part of the curve, further fluids do not increase stroke volume → preload unresponsive.

2. Poor ventricular function:

Ø  Even with fluid loading, the stroke volume increases very little.

Ø  These patients are often fluid-unresponsive and may worsen with overload.

3. SVV (Stroke Volume Variation):

Ø  Large SVV = preload responsive.

Ø  Small SVV = preload unresponsive.

 

Figure B : Heart–Lung Interactions in Controlled (Positive Pressure) Ventilation

• Blue line (Airway pressure): Increases during inspiration (positive pressure ventilation).
• Red line (Arterial pressure waveform): Shows variations during respiration.

1. During inspiration (positive pressure):

Ø  Intrathoracic pressure rises.

Ø  Venous return to the right heart ↓ → right ventricular preload ↓.

Ø  At the same time, left ventricular afterload ↓ → left ventricular stroke volume ↑ (after a short delay).

2. Arterial pressure variations:

Ø  PP max = maximum pulse pressure during inspiration.

Ø  PP min = minimum pulse pressure during expiration.

Ø  SPV (Systolic Pressure Variation): Difference between max and min systolic pressure.

Ø  Delta up / Delta down: Reflect the effects of ventilation on preload/afterload.

Ø  Large variations (SPV, PPV) suggest preload responsiveness.

 

What happens in Spontaneous Breathing (opposite mechanics)

• In spontaneous inspiration:

Ø  Intrathoracic pressure becomes negative.

Ø  This increases venous return (RV preload) → RV stroke volume increases.

Ø  However, the negative pressure also increases LV afterload (more pressure needed to eject against the gradient).

Ø  As a result, LV stroke volume may decrease transiently.

• Clinically:

Ø  In positive pressure ventilation → arterial pressure rises during inspiration (due to reduced LV afterload).

Ø  In spontaneous breathing → arterial pressure falls during inspiration (pulsus paradoxus, seen in tamponade, severe asthma, etc.).

• Positive pressure ventilation: Inspiration reduces RV preload but reduces LV afterload → arterial pressure increases during inspiration.
• Spontaneous breathing: Inspiration increases RV preload but increases LV afterload → arterial pressure decreases during inspiration.

CONCLUSION-Heart–lung interactions arise from the interplay between the respiratory and circulatory systems within the confined thoracic cavity. They result from respiratory-induced changes in intrathoracic pressure, which are transmitted to the cardiac chambers, as well as from alterations in alveolar pressure that can influence the pulmonary microvasculature. Under normal physiological conditions, these interactions have little hemodynamic impact. However, in patients with acute respiratory failure, they may produce marked hemodynamic effects that can further aggravate the clinical state. In mechanically ventilated patients with ARDS, the application of PEEP may compromise hemodynamic, particularly when excessive PEEP leads to lung overdistension. More recently, heart–lung interactions have been increasingly applied to predict fluid responsiveness in ventilated patients. Several dynamic tests based on these interactions have been developed to guide decisions regarding fluid administration or removal, though their limitations must always be carefully considered.