Right ventricular strain: definition, causes, echocardiography

Right ventricular strain

When assessing the right half of the heart, it is important to familiarize yourself with the principles of hemodynamics and conditions prevailing on the right side. Echocardiography is the first choice for assessing the right side of the heart, despite difficulties in visualizing it. Previously, the PA catheter ( Pulmonary Artery Catheter , also called Swan-Ganz catheter ) has been the first choice, but today the majority of patients can only be assessed using echocardiography.

A common question is the presence of right ventricular load. This condition implies that the right ventricle is pressure and/or volume loaded. The load itself leads to impaired right ventricular function, especially if the load becomes prolonged. However, most often the cause of the load is the primary problem. Among the causes are pulmonary embolism, pulmonary hypertension, septum defects, etc. Right ventricular load is thus an issue that is raised both in outpatient and emergency care. To evaluate the presence of right ventricular load, a variety of echocardiographic parameters are used.

Examination of the right ventricle with echocardiography

The right ventricle is relatively difficult to examine, which is due to the location of the ventricle in the thorax. It is localized immediately behind the sternum and thus is the most anteriorly located part of the heart. The right ventricle has a complicated anatomy. In cross-section (SAX, short-axis view), the the ventricle is rather a crescent-shaped appendage of the left ventricle. On longitudinal sections (A4C, apical four-chamber view), the right ventricle is a triangular structure (Figure 1).

Figure 1. SAX (short axis view), where the right ventricle appears as a crescent-shaped appendage of the left ventricle.

Systolic function of the right ventricle

The systolic function of the right ventricle is primarily a function of the following parameters:

• Contractility of the myocardium: all causes of reduced contractility, globally or regionally, lead to impaired right ventricular function.
• Preload: Preload is the volume of blood flowing from the right atrium to the right ventricle.
• Afterload: Afterload is the resistance that the the ventricle must overcome to pump blood out into the pulmonary artery. Resistance may increase in, for example, pulmonary hypertension or pulmonic stenosis.
• Heart rate.
• Synchronicity: Optimal contraction requires the majority of all ventricular myocardium to contract simultaneously. For this to be possible, the right leg must be intact. In the case of blockade of the right bundle of His (RBBB) , the ventricle can not depolarize normally, which affects the efficiency of contraction.

Left ventricular function affects right ventricular function via afterload. In the case of left ventricular failure, the pressure in the pulmonary vessels rises and the pressure rise propagates to the right ventricle.

Pulmonary vascular resistance (PVR)

Vascular resistance (R) is the resistance that must be overcome to force blood through a blood vessel. Vascular resistance is calculated by the ratio of the pressure difference (ΔP) and the flow over the vascular bed (Q):

R = ΔP/Q

Both ΔP and Q above the pulmonary vessels can be calculated by echocardiography, which makes it possible to calculate the resistance in the pulmonary vessels (pulmonary vascular resistance, PVR). This parameter is of utmost interest in investigating right ventricular load.

Pressure in the right atrium (right atrial pressure)

With the PA catheter (Swan-Ganz catheter), the right atrial pressure can be measured directly. Echocardiography (UCG) allows an indirect estimation of atrial pressure. This is done by assessing the diameter of the vena cava inferior and whether the diameter varies during the respiratory cycle. Thus, the pressure in the inferior vena cava is used as a proxy for pressure in the right atrium, which is possible because there is normally no valve between the vena cava and the right atrium. The following assessments are made for vena cava inferior:

• Diameter: Normally the diameter is less than 21 mm.
• How much does the diameter decrease during inspiration (tested by asking the patient to sniff). Normally, diameter decreases > 50% when inhaled or sniffing.

The measurement is made in the subcostal view (parallel to the longitudinal axis of the vena cava inferior ) after the departure of the hepatic veins, at the end of the exspiry. The patient should be lying on his back (the diameter varies with the body position). If the diameter is >21 mm or the decrease is < 50%, the pressure in the right atrium is higher than normal. The following thumb rules are used to estimate atrial pressure:

1. Normal diameter and respiratory variability: pressure is estimated at 3 mmHg (0-5 mmHg)
2. Normal diameter but reduced respiratory variation: pressure is estimated to be 8 mmHg (5-10 mmHg).
3. Increased diameter and reduced respiratory variability: pressure is estimated at 15 mmHg (10-20 mmHg).

This estimate becomes uncertain if there is a pronounced tricuspid regurgitation insufficiency (TI). Likewise, it may be affected by the patient's involvement and ability to ventilate. Athletes and younger people do not rarely exhibit a dilated vena cava inferior as a normal variant. Last but not least, some individuals have a valve between the inferior vena cava and right atrium; about this valve (eng. eustachian valve) is prominent, so the pressure in the right ventricle can differ significantly from the pressure in theinferior vena cava, and the pressure in the latter can not be used as a proxy for pressure in the atrium. (A prominent flap tends to prevent vena cava inferior from collapsing during inspiration, giving false elevated values).

Systolic right ventricular pressure (RVSP, Right Ventric Systolic Pressure)

The systolic pressure in the right ventricle can be calculated if there is a tricuspid regurgitation insufficiency, which is present in the majority of all people. With Doppler, the maximum rate of tricuspid insufficiency is recorded, which is then used in the following formula to estimate the pressure difference between the right atrium and the right ventricle:

ΔP = 4v2

Then the estimated atrial pressure (measurement of the diameter of the vena cava inferior ) is added to ΔP, giving RVSP:

RVSP = ΔP + atrial pressure

Systolic PA pressure (PASP, Pulmonary Arterial Systolic Pressure)

PASP is equivalent to RVSP:

RVSP = PASP

This is provided that there is no obstruction between the right ventricle and the pulmonary artery. If obstruction exists, the pressure gradient is calculated over the RVOT and then the PASP is calculated according to the following:

PASP = RVSP - ΔPRVOT

Diastolic PA pressure (PADP, Pulmonary Arterial Diastolic Pressure)

In pulmonic regurgitation (PI), the maximum rate of leakage can be used to measure diastolic pressure in the pulmonary artery. First, the maximum rate of insufficiency is measured, with which the pressure difference is calculated:

ΔP = 4v2

ΔP and right atrial pressure are added to obtain PDAP:

PDAP = ΔP+ atrial pressure

MPAP (Mean Pulmonary Artery Pressure)

MPAP = (PSAP+ 2•PDAP) /3

MPAP can also be measured with pulsed wave doppler in RVOT. The acceleration time of the Doppler recording (AT, measured in milliseconds) is used in the following formula:

MPAP = 79 - 0.45•AT

If AT is <120 ms, the adjusted equation is used:

MPAP = 90 - 0.62•AT

This calculation is an uncertain left-to-right shunt (defect of the interatrial septum), bradycardia or tachycardia.

Pulmonary Vascular Resistance (PVR)

Pulmonary vascular resistance is calculated as the ratio between the pressure difference and the flow across the small circle of circulation:

PVR = ΔP/Q

ΔP and Q are estimated by the following parameters:

1. vmax****TI - If there is a tricuspid regurgitation insufficiency, its maximum rate can be measured and this gives an indication of the pressure drop over the lungs. The measurement is done with continuous wave doppler in apical four-chamber view .
2. VTI****RVOT - VTI in RVOT is used to estimate the flow over the lungs. The measurement is made in parasternal kortaxevyl with pulsed wave doppler.

After that, the following formula is used to damage PVR (mmHg):

vmaxTI /VTI

If the above quota is >0.175, PVR is likely to be increased (greater than 2 Wood Units).

If the ratio is 0.175 — 0.275, the following formula is used to estimate PVR (mmHg):

PVR = 10 • (vmaxTI/VTIRVOT)

Right ventricular load

In a series of conditions, pressure and/or volume load may rise in the right ventricle. This gives right ventricular load. Among the causes of right ventricular load are the following:

1. Pulmonic stenosis(PS) - this, generally, is a congenital heart malformation.
2. Pulmonary hypertension (primary, secondary) - high resistance of pulmonary vessels provides increased afterload for the right ventricle. Primary pulmonary hypertension is idiopathic. Among the causes of secondary pulmonary hypertension are pulmonary embolism, COPD (chronic obstructive pulmonary disease) and connective tissue diseases of the lungs.
3. Atrial septal defect - Since the pressure in the left atrium is higher than the pressure in the right atrium, the blood will be shunted from left to right, and the right side will be volumetric.
4. Tricuspid regurgitation - this is most often secondary to carcinoid heart disease or endocarditis.
5. Left ventricular dysfunction.

Under pressure and/or volume load, the right ventricle becomes dilated and this spreads to the right atrium, which is also dilated. The pressure in the right ventricle can become so high that the septum bulges into the left ventricle. High ventricular pressure also leads to tricuspid regurgitation insufficiency.

The most common of the above causes is left ventricular dysfunction. Dysfunction leading to increased pressure in the left ventricle can spread to the left atrium, to the pulmonary vessels and further to the right ventricle. The echocardiographic parameters that are of interest in this situation are the pressure in the pulmonary artery (PA pressure), as well as the resistance in the pulmonary vessels (PVR, Pulmonary Vascular Resistance).

In the case of signs of right ventricular load, it is fundamental to determine whether the load is due to increased resistance in the pulmonary vessels (increased PVR) or to increased pressure in the left ventricle. If left ventricular function is normal and the filling pressure in the left ventricle is normal, then increased PVR is the most likely explanation of right ventricular load. At high filling pressure on the left side, right ventricular load may be due to the propagation of pressure rise back to the right ventricle. At very high PA pressure without concomitant pulmonary edema, left ventricular function is likely to be normal.