Diastolic pressure is the blood pressure in the arteries at the peak of ventricular contraction

Frank–Starling law

Each ventricle must be able to change its force of contraction and therefore stroke volume in response to changes in venous return. The Frank–Starling law describes the mechanism by which changes in pressure alter stroke volume. It states that the force of ventricular contraction is increased when the ventricle is stretched prior to contraction. The myocardial fibers experience an increase in load due to the extra blood entering the heart. And the force of contraction of the cardiac muscle is proportional to its initial length. The capacity of the stretched heart to contract is a quality shared by all striated muscles.

The Frank–Starling law allows the heart to be synchronized with the venous return without depending on external regulation to make alterations. It is vital that stroke volume of both ventricles match so exactly that neither stagnation nor total emptying of the pulmonary circulation can occur, either of which would be fatal.

Ejection

When ventricular pressure rises further to exceed aortic pressure or pulmonary artery pressure, the aortic and pulmonary valves open and blood flows from the ventricles into the systemic circulation or the pulmonary circulation. The ejection phase of the cardiac cycle ends when the aortic valve snaps shut, producing the heart’s second sound. At the end of the ejection phase the volume of blood remaining in the left ventricle, its end-systolic volume (ESV), is about 50 mL. Thus, the stroke volume, the volume of blood ejected with each heart beat, is the difference between the end-diastolic volume and the end-systolic volume=120 mL−50 mL=about 70 mL. The ejection fraction is the fraction of the EDV that is ejected. The typical value for the ejection fraction is 70/120=0.58.

ejection takes about 0.30 s;

mitral and tricuspid valves closed;

aortic and pulmonary valves open;

peak pressure of about 25 mmHg (pulmonary circulation) or 120 mmHg (systemic circulation).

Right Ventricular Pressure

Normal ventricular pressures are easily distinguishable from atrial and arterial pressures. The right ventricular pressure wave consists of a rapid upstroke during isovolumic contraction, a systolic plateau, and a fall to near zero during isovolumic relaxation. There is, then, a gradual increase in pressure during diastole with a late diastolic increase associated with the a wave of atrial contraction (Fig. 14-3). The peak systolic and end-diastolic pressures, which vary with respiration, are measured routinely. End-diastole is identified as the point where the right atrial and ventricular tracings cross at the end of diastole or at the junction of the a wave and the rapid upstroke in the ventricular tracing. The former is the most accurate, but because simultaneous right atrial and right ventricular pressures are not routinely recorded, the latter is often utilized. The normal right ventricular systolic pressure is less than 30 mm Hg and the end-diastolic pressure is about 5 mm Hg.

Abnormal elevation of right ventricular systolic pressure occurs in outflow obstruction (e.g., pulmonary valve stenosis, pulmonary artery bands, or stenosis of the pulmonary artery branches), pulmonary artery hypertension, or lesions such as ventricular septal defects. In double-chambered right ventricle, anomalous muscle bundles obstruct the outflow portion of the right ventricle and create a proximal high-pressure chamber and a distal low-pressure chamber (Fig. 14-4).

Preload

In the intact heart, pressure is easily measured and used as a surrogate for volume. The end-diastolic volume can be assessed using pulmonary arterial wedge pressure, left atrial pressure, or central venous pressure. However, given the different diastolic compliances of individual ventricles, pressure provides a crude estimate of volume—the parameter that is actually sought. Echocardiography provides the best estimate of preload. This is readily measured either as end-diastolic dimension (M-mode), end-diastolic area (two-dimensional echocardiography), or end-diastolic volume (derived from two-dimensional echocardiography).

Pathophysiology

In abnormal ventricles, IVPGs are blunted22 or even reversed—the initial, faster phase is then lost; vortex formation predominates, slowing the progression of the wavefront toward the apex (see Fig. 11-2). Factors that can affect the formation of IVPGs include regional wall motion abnormalities, increased end systolic volume, and dyssynchrony of relaxation.15 The magnitude of pressure gradient formation also depends on ventricular size. In small ventricles, intraventricular gradient formation is enhanced. Vortex formation and propagation require that the ventricular diameter exceed the mitral diameter.4 In dilated, spherical ventricles, the difference in axial velocity between the blood already in the ventricle and blood coming through the mitral valve creates a larger vortex.4

DEVELOPMENTAL CHANGES IN DIASTOLIC FUNCTION

Atrial pressure exceeds ventricular pressure throughout filling, and from early gestation there is a clear distinction between passive and active filling, referred to as the E and A waves, respectively.5 The active velocities are higher than passive velocities in the fetus and in the newborn period, resulting in a ratio between the E and A waves which is below 1 in the normal fetus. This ratio, nonetheless, is highly dependent on preload. It cannot provide a load-independent assessment of ventricular function. It is, therefore, a particularly unsuitable measure in fetal life, when direct pressures cannot easily be measured. The patterns of ventricular filling change with age, with a relative increase in early diastolic filling, represented by the E wave, compared with the late diastolic component, or A wave, reflecting increasing ventricular compliance.78–80 Reference ranges between 8 and 20 weeks of gestation show a greater volume of flow passing through the tricuspid than mitral valve at all gestational ages. Maturational changes in ventricular properties in human fetuses accelerate after mid-gestation as diastolic filling increases mainly after 25 weeks. They are associated with a decrease in the ratio of the area of the myocardial wall to the end-diastolic diameter of the left ventricle. Thus, the decrease in left ventricular wall mass related to gestational age may be one important mechanism responsible for the alterations in diastolic properties noted in the fetal heart. These are co-incident with the reduction in placental impedance associated with normal adaptation of the spiral arteries.81,32

Pathophysiology

In abnormal ventricles, when intraventricular pressure gradients are blunted28 or even reversed, the initial, faster phase is then lost. Vortex formation predominates over columnar flow, decreasing the initial slowing of the progression of flow toward the apex. Factors that can affect the formation of intraventricular pressure gradients include regional wall motion abnormalities, increased end-systolic volume, and dyssynchrony of relaxation.15 The magnitude of pressure gradient formation also depends on ventricular size. In small ventricles intraventricular gradient formation is enhanced. Vortex formation and propagation require that the ventricular diameter exceed the mitral diameter.4

Right-Sided Heart Pressures

The right-sided heart pressures, as measured in the cardiac catheterization laboratory, consist of the central venous pressure (CVP) or right atrial (RA) pressure (RAP), right ventricular (RV) pressure (RVP), PAP, and PCWP. The CVP consists of three waves and two descents (Fig. 2-1, Box 2-3). The A wave occurs synchronously with the Q wave of the ECG and accompanies atrial contraction. Next, a smaller C wave appears, which results from tricuspid valve closure and bulging of the valve into the right atrium as the right ventricle begins to contract. After this, with the tricuspid valve in the closed position, the atrium relaxes, resulting in the X descent. This is followed by the V wave, which corresponds to RA filling that occurs during RV systole with a closed tricuspid valve. As the RV relaxes, the RVP then becomes less than the RAP, the tricuspid valve opens, and the atrial blood rapidly empties into the ventricle. This is signified by the Y descent.

Beginning in early diastole, the RV waveform reaches its minimum pressure shortly before or as the tricuspid valve opens. During the rapid filling phase of diastole, the ventricular pressure rises slowly and usually an A wave, which signifies atrial contraction, is seen just before the onset of ventricular systole. As ventricular contraction occurs, peak systolic pressure is rapidly reached. Just before the onset of contraction, and after the A wave, the RV end-diastolic pressure (RVEDP) can be determined.

The PAP is usually greater than the RVP during the time the pulmonic valve is closed, during ventricular relaxation and filling. During systole, RVP crosses over PAP by a small margin, causing the pulmonic valve to open, and the ventricle ejects blood into the PA. It is not uncommon for a 5-mm gradient to exist between the RV and PA during peak systolic contraction. The minimal PA diastolic pressure can also be measured just before the onset of contraction, as an estimate of the PCWP; however, the presence of increased pulmonary vascular resistance will invalidate this correlation. With an inflated balloon, the tip of the PA catheter is protected from pulsatile pressures and “looks forward” to the pressure in the pulmonary venous system and the left atrium. This “wedge” pressure shows many of the characteristics of the left atrial (LA) pressure (LAP). The differences between these two waves are considered in the discussion of LAP below.

Isovolumetric Indicators

The rate of rise in ventricular pressure during systole that begins in the isovolumetric contraction phase is a more load-independent indicator of LV systolic function. This parameter is better known as dP/dt, and Doppler-derived measurements correlate well with catheter-based invasive measurements. With echocardiography, the measurement of dP/dt is dependent on a mitral regurgitation (MR) jet. The contour of the MR jet reflects the rate of rise of LV systolic pressure until its eventual peak velocity. The time the jet velocity takes to rise from 1 m/s to 3 m/s is considered to indicate the dP/dt (Fig. 12-9). Since it is dependent on an MR jet and the stroke volume, this parameter is also preload sensitive. The corresponding pressure gradient at 1 and 3 m/s is 4 mmHg and 36 mmHg, calculated by the simplified Bernoulli equation [pressure gradient = 4 × (peak velocity)2]. Therefore, the time taken for the pressure gradient to rise by 32 mmHg reflects the dP/dt according to the formula:

dP/dt=32(mmHg)×1000/dT(milliseconds)

Normal values for this parameter are 1610 ± 290 mmHg/s.15

Ventricular Puncture.

Ventricular puncture provides valuable information concerning intraventricular pressure and the presence of ventriculitis, particularly when associated with serious localized infection (Table 35.17). Although only uncommonly necessary, ventricular puncture should be performed in any newborn with bacterial meningitis who is not responding favorably to apparently appropriate antibiotic therapy in terms either of clinical signs or of sterilization of lumbar CSF (see the section on management later). Severe ventriculitis may be present in an infant with improved or even a normal lumbar CSF WBC count. Indeed, the constellation of a deteriorating clinical state (e.g., apnea, bradycardia, or both and persistent fever) in the presence of decreasing CSF pleocytosis or even CSF sterilization should raise the suspicion of clinically important ventriculitis. Moreover, ventriculitis may evolve in a subacute fashion, with signs of increased intracranial pressure, either de novo or after apparent recovery from bacterial meningitis.260 The presence in ventricular fluid of bacteria (Gram stain or culture) or bacterial antigen (latex particle agglutination) and a WBC count in excess of approximately 100/mm3 indicates ventriculitis. Cranial ultrasonography often shows excrescences associated with the ependymal surface. Whether ventricular infection is localized and inaccessible to antibiotics depends on evaluation of a variety of factors. Favoring such a possibility is the presence of marked pleocytosis in ventricular CSF or evidence of intraventricular block of CSF flow (e.g., elevated intraventricular pressure and dilated ventricles) or both pleocytosis and CSF block. Management of such a situation is reviewed in subsequent discussions.

Ventricular puncture should be performed by a physician with expertise in the procedure and awareness of its hazards. In acute bacterial meningitis, the lateral ventricles are often small and may be tapped only with considerable difficulty. An ultrasound scan before the procedure is important. Indeed, ventricular puncture with ultrasound guidance is recommended if the ventricles are small. Ventricular puncture may be followed by the development of a cystic cavity.147,261 This development is particularly likely to occur if obstruction to CSF flow and increased intraventricular pressure, common complications of bacterial ventriculitis, are present. The subsequent cavitation along the needle track relates most probably to the combination of disruption of edematous, poorly myelinated, readily separable brain parenchyma and transmission of elevated intraventricular pressure. In the large, older series studied by Lorber and Emery,261 the approximately 50% of infants subjected to multiple ventricular punctures for the treatment of bacterial ventriculitis subsequently developed cystic cavities, demonstrable by ventriculography, at the sites of the taps. The incidence of significant cavity formation in infants with ventriculitis after a single tap is unknown but is probably relatively low. Although small diverticula from the lateral ventricles into the needle track are common after single taps, major cavity formation is very unusual.