Hemodynamics

[Clinical Art][Circulation] Hemodynamic Monitoring – Tissue Oxygenation and Cardiac Output

October 24, 2016 Cardiology, Clinical Skills, Critical Care, Hemodynamics No comments , , , , , , , , , , , , , , , ,

Key Points

  • No hemodynamic monitoring device will improve patient outcome unless coupled to a treatment, which itself improves outcome.
  • Low venous oxygen saturations need not mean circulatory shock but do imply circulatory stress, as they may occur in the setting of hypoxemia, anemia, exercise, as well as circulatory shock.
  • There is no "normal" cardiac output, only one that is adequate or inadequate to meet the metabolic demands of the body. Thus, targeting a specific cardiac output value without reference to metabolic need, or oxygen-carrying capacity of the blood, is dangerous.
  • Cardiac output is estimated, not measured, by all devices routinely used in bedside monitoring (though we shall call it measured in this text).
  • Cardiac output estimates using arterial pulse pressure contour analysis cannot be interchanged among devices and all suffer to a greater or lesser extent by changes of peripheral vasomotor tone commonly seen in the critically ill.
  • Since metabolic demands can vary rapidly, continuous or frequent measures of cardiac output are preferred to single or widely spaced individual measures.
  • Integrating several physiologic variables in the assessment of the adequacy of the circulation usually gives a clearer picture than just looking at one variable.
  • Integrating cardiac output with other measures, like venous oxygen saturation, can be very helpful in defining the adequacy of blood flow.

Clinical Judgement of Hypoperfusion

Tissue hypoperfusion is a clinical syndrome, thus the presentation depends on which organ(s)/organ system(s) are being hypoperfused.

Table 1 Common Clinical Presentations of Tissue Hypoperfusion
Brain/CNS altered mental status, confusion
Pulmonary system dyspnea on exertion
Gastrointestinal tract slowed bowel function, abdominal discomfort, nausea/vomiting, anorexia
Renal system decrease urine output, increased serum creatinine
Hepatic system increased transaminases
Extremities/constitutional cool extremities, poor capillary refill, general fatigue/malaise
SvO2 in the case of normal CaO2 and VO2, SvO2 would decrease
Serum lactate level elevated serum lactate level

Note that some factors other than tissue hypoperfusion are able to cause the "hypoperfusion"-like presentation(s) which are similar as the one discussed above. For example, in the sepsis, the elevated levels of lactic acid might be caused by reasons other than hypoperfusion. In another case, the low urine output of a patient might be caused by the patient's ESRD per se rather than the low perfusion of kidneys. Also, if the patient had hypoglycemia or severe hyponatremia (which cause the neurons to edema), he or she would definitely lose the consciousness (differential diagnosis? or differential clinical judgement).


Tissue Oxygenation

Although mean artieral pressure (MAP) is a primary determinant of organ perfusion, normotension can coexist with circulatory shock.

Since metabolic demand of tissues varies by external (exercise) and internal (basal metabolism, digestion, fever) stresses, there is no "normal" cardiac ouput that the bedside caregiver can target and be assured of perfusion adequacy. Cardiac output is either adequate or inadequate to meet the metabolic demands of the body. Thus, although measures of cardiac output are important, their absolute values are relevant only in the extremes and when targeting specific clinical conditions, such as preoptimization therapy.

How then does one know that circulatory sufficiency is present or that circulatory shock exists? Clearly, since arterial pressure is the primary determinant of organ blood flow, systemic hypotension (i.e., mean arterial pressure <60 mm Hg) must result in tissue hypotension. Organ perfusion pressure can be approximated as mean arterial pressure (MAP) relative to tissue or outflow pressure. But, if intracranial pressure or intra-abdominal pressure increases, then estimating cerebral or splanchnic perfusion pressure using MAP alone will grossly overestimate organ perfusion pressure. In addition, baroreceptors in the carotid body and aortic arch increase vasomotor tone to keep cerebral perfusion constant if flow decreases, and the associated increased systemic sympathetic tone alters local vasomotor tone to redistribute blood flow away from more efficient O2 extracting tissues to sustain MAP and global O2 consumption (VO2) in the setting of inappropriately decreasing DO2. Thus, although systemic hypotension is a medical emergency and reflects severe circulatory shock, the absence of systemic hypotension does not ensure that all tissues are being adequately perfused.


  • Arterial pulse oximetry: SaO2
  • Venous Oximetry: ScvO2, SvO2
  • Tissue Oximetry
  • StO2 vascular occlusion test

Arterial Pulse Oximetry

SaO2

Arterial blood O2 saturation (SaO2) can be estimated quite accurately at the bedside using pulse oximetry. Routinely, pulse oximeters are placed on a finger for convenience sake. However, if no pulse is sensed, then the readings are meaningless. Such finger pulselessness can be seen with peripheral vasoconstriction associated with hypothermia, circulatory shock, or vasospasm. Central pulse oximetry using transmission technology can be applied to the ear or bridge of the nose and reflectance oximetry can be applied to the forehead, all of which tend to retain pulsatility if central pulsatile flow is present. Similarly, during cardiopulmonary bypass when arterial flow is constant, pulse oximetry is inaccurate. The primary important functions of SaO2 are summarized below.

  • SaO2 is routinely used to identify hypoxemia. Hypoxemia is usually defined as an SaO2 of <90% (PaO2 of <60 mm Hg).
  • SaO2 is also used to identify the causes of hypoxemia. The most common causes of hypoxemia are ventilation-perfusion (V/Q) mismatch (we will discuss this topic in the clinical art of respiratory medicine) and shunt. With V/Q mismatch alveolar hypoxia ocurs in lung regions with increased flow relative to ventilation, such that the high blood flow rapidly depletes alveolar O2 before the next breath can refresh it. Accordingly, this process readily lends itself to improve oxygenation by increasing FiO2 and minimizing regional alveolar hypoxia. Collapsed or flooded lung units will not alter their alveolar O2 levels by this maneuver and are said to be refractory to increase in FiO2. Accordingly, by measuring the SaO2 response to slight increases in FiO2 one can separate V/Q mismatch (shuntlike states) from shunt (absolute intrapulmonary shunt, anatomical intracardiac shunts, alveolar flooding, atelectasis [collapse]). One merely measures SaO2 while switching from room air FiO2 of 0.21 to 2 to 4 L/min nasal cannula (FiO2 ~0.3). Importantly, atelectatic lung units (collapse alveoli) should be recruitable by lung expansion whereas flooded lung units and anatomical shunts should not. Thus, by performing sustained deep inspirations and having the patient sit up and take deep breaths one should be able to separate easily recruitable atelectasis from shunt caused by anatomy and alveolar flooding. Sitting up and taking deep breaths is a form of exercise that may increaes O2 extraction by the tissues, thus decreasing SvO2. The patient with atelectasis will increase alveolar ventilation increasing SaO2 despite the decrease in SvO2, whereas the patient with unrecruitable shunt will realize a fall in SaO2 as the shunted blood will carry the lower SvO2 to the arterial side. Summary: SaO2 is used to identify V/Q mismatch and shunt, atelectasis and anatomical/flooding shunt, respectively.
  • Detection of volume responsiveness. Recent interest in the clinical applications of heart-lung interactions has centered on the effect of positive-pressure ventilation on venous return and subsequently cardiac output. In those subjects who are volume responsive, arterial pulse pressure, as a measure of left ventricular (LV) stroke volume, phasically decreases in phase with expiration, the magnitude of which is proportional to their volume responsiveness. Since the pulse oximeter's plethysmographic waveform is a manifestation of the arterial pulse pressure, if pulse pressure varies from beat-to-beat so will the plethysmographic deflection, which can be quantified. Several groups have documented that the maximal variations in pulse oximeter's plethysmographic waveform during positive-pressure ventilation covaries with arterial pulse pressure variation and can be used in a similar fashion to identify those subjects who are volume responsive.

PS: Intrapulmonary shunt fraction is increased in the following situations:

  • When the small airways are occluded; e.g., asthma
  • When the alveoli are filled with fluid; e.g., pulmonary edema, pneumonia
  • When the alveoli collapse; e.g., atelectasis
  • When capillary flow is excessive; e.g., in nonembolized regions of the lung in pulmonary embolism

Venous Oximetery

SvO2

SvO2 is the gold standard for assessing circulatory stress. A low SvO2 defines increased circulatory stress, which may or may not be pathological.

To the extent that SaO2 and hemoglobin concentration result in an adequate arterial O2 content (CaO2), then ScvO2 and SvO2 levels can be taken to reflect the adeuqacy of the circulation to meet the metabolic demands of the tissues. This is the truth. But attention must be paid that one needs to examine the determinants of DO2, global oxygen consumption (VO2), and effective O2 extraction by the tissues before using ScvO2, or SvO2 as markers of circulatory sufficiency.

Since VO2 must equal cardiac output times the difference in CaO2 and mixed venous O2 content (CvO2) (VO2 = CO x [CaO2 – CvO2]),if CaO2 remains relatively constant then CvOwill vary in proportion to cardiac output (CvO2 = CaO2 – VO2 / CO). Since the amount of O2 dissolved in the plasma is very small, the primary factor determining changes in CvO2 will be SvO2. Thus, SvO2 correlates well with the O2 supply-to-demand ratio.

Several relevant conditions may limit this simple application of SvO2 in assessing circulatory sufficiency and cardiac output (Table 32-1). If VO2 were to increase (as occurs with exercise), hemoglobin-carrying capacity to decrease (as occurs with anemia, hemoglobinopathies, and severe hemorrhage), or SaO2 to decrease (as occurs with hypoxic respiratory failure), then for the same cardiac output, SvO2 would also decrease. Similarly, if more blood flows through nonmetabolically extracting tissues as occurs with intravascular shunts, or mitochondrial dysfunction limits O2 uptake by tissues, then SvO2 will increase for a constant cardiac output and VO2 even though circulatory stress exists and may cause organ dysfunction.

Table 32-1 Limitations to the Use of SvO2 to Trend Circulatory Sufficiency
Independent events that decrease SvO2 independent of cardiac output
Event Process
Exercise Increased VO2
Anemia Decreased O2-carrying capacity
Hypoxemia Decreased arterial O2 content
Independent events that increase SvO2 independent of cardiac output
Event Process
Sepsis Microvascular shunting
End-stage hepatic failure Macrovascular shunting
Carbon monoxide poisoning Mitochondrial respiratory chain inhibition

ScvO2

SvO2 and ScvO2 covary in the extremes but may change in opposite directions as conditions change.

ScvO2 threshold values to define circulatory stress are only relevant if low (a high ScvO2 is nondiagnostic).

ScvO2 does not sample true mixed venous blood and most vena cacal blood flow is laminar, thus if the tip is in one of these laminar flow sites it will preferentially report a highly localized venous drainage site O2 saturation. Clearly, the potential exists for spurious estimates of SvO2. Most central venous catheters are inserted from internal jugular or subclavian venous sites with their distal tip residing in the superior vena cava, usually about 5 cm above the right atrium. Thus, even if measuring a mixed venous sample of blood at that site, ScvO2 reflects upper body venous blood while ignoring venous drainage from the lower body. Accordingly, ScvO2 is usually higher than SvO2 by 2% to 3% in a sedated resting patient because cerebral O2 consumption is minimal and always sustained above other organs.

Tissue Oximetry

Tissue O2 saturation (StO2) varies little until severe tissue hypoperfusion occurs.

StO2 coupled to a VOT allows one to diagnose circulatory stress before hypotension develops.

The most currently used technique to measure peripheral tissue O2 saturation (StO2) is near-infrared spectroscopy (NIRS). NIRS is a noninvasive technique based in the differential absorption properties of oxygenated and deoxygenated hemoglobin to assess the muscle oxygenation. Although there is a good correlation between the absolute StO2 value and some other cardiovascular indexes, the capacity of the baseline StO2 values to identify impending cardiovascular insufficiency is limited (sensitivity, 78%; specificity, 39%).

screen-shot-2016-10-24-at-12-52-46-pmHowever, the addition of a dynamic vascular occlusion test (VOT) that induces a controlled local ischemic challenge with subsequent release has been shown to markedly improve and expand the predictive ability of StO2 to identify tissue hypoperfusion. The VOT StO2 response derives from the functional hemodynamic monitoring concept, in which the response of a system to a predetermined stress is the monitored variable. The rate of DeO2 is a function of local metabolic rate and blood flow distribution. If metabolic rate is increased by muscle contraction, the DeO2 slope increases, whereas in the setting of altered blood flow distribution the rate of global O2 delivery is decreased. Sepsis decreases the DeO2. The ReO2 slope is dependent on how low StO2 is at the time of release, being less steep if StO2 is above 40% than if the recovery starts at 30%, suggesting that the magnitude of the ischemic signal determines maximal local vasodilation. This dynamic technique has been used to assess circulatory sufficiency in patients with trauma, sepsis and during weaning from mechanical ventilation.


Cardiac Output

There is no "normal" cardiac output (QT).

QT is either adequate or inadequate

Other measures besides QT define adequacy

Shock reflects an inadequate DO2 to meet the body's metabolic demand and cardiac output is a primary determinant of DO2. Indeed, except for extreme hypoxemia and anemia, most of the increase in DO2 that occurs with resuscitation and normal biological adaptation is due to increasing cardiac output. Since cardiac output should vary to match metabolic demands, there is no "normal" cardiac output. Cardiac output is merely adequate or inadequate to meet the metabolic demands of the body. Measures other than cardiac output need to be made to ascertain if the measured cardiac output values are adequate to meet metabolic demands. The two most common catheter-related methods of estimating cardiac output are indicator dilution and arterial pulse contour analysis.

Indicator Dilution

The principle of indicator dilution cardiac output measures is that if a small amount of a measurable substance (indicator) is ejected upstream of a sampling site and then thoroughly mixed with the passing blood then measured continuously downstream, the area under the time-concentration curve will be inversely proportional to flow based on the Stewart-Hamilton equation. The greater the indicator level, the slower the flow, and the lower the indicator level, the higher the flow. The most commonly used indicator is temperature (hot or cold) because it is readily available and indwelling thermistors can be made to be highly accurate.

Arterial Pulse Contour Analysis

screen-shot-2016-10-24-at-8-44-47-pmThe primary determinants of the arterial pulse pressure are LV stroke volume and central arterial compliance (pulse pressure ≈ SV / C). Compliance is a function of size, age, sex, and physiological inputs, like sympathetic tone, hypoglycemia, temperature, and autonomic responsiveness of the vasculature. Hamilton and Remington explored this interaction over 50 years ago developing the overall approach used by most of the companies who attempt to report cardiac output from the arterial pulse. The main advantage of these arterial pressure-based cardiac output monitoring systems over indicator dilution measurements is their less invasive nature.

However, since all these devices presume a fixed relation between pressure propagation alnog the vascular three and LV stroke volume, if vascular elastance (reciprocal of compliance) changes, then these assumptions may become invalid. Thus, a major weakness of any pulse contour device is the potential for artificial drift in reported values if major changes in arterial compliance occur.

[Clinical Art][Circulation] Interpretation of Hemodynamic Waveforms

October 20, 2016 Cardiology, Critical Care, EKG/ECG, Hemodynamics, Mechanical Ventilation No comments , , , , , , , , , , , , , , , , , , , , , , , , ,

1st_ceb_insigniaBasic Knowledge

Mechanism of Hemodynamic Monitoring

The rapidly occurring events (represent mechanical forces) of cardiac chambers and vessels during cardaic cycle require conversion to an electrical signal to be transmitted and subsequently translated into an interpretable, graphic format. The pressure transducer is the essential component that translates the mechanical forces to electrical signals. The transducer may be located at the tip of the catheter (micromanometer) within the chamber or, more commonly, the pressure transducer is outside of the body, and a pressure waveform is transmitted from the catheter tip to the transducer through a column of fluid. These transducers consist of a diaphragm or membrane attached to a strain-gauge-Wheatstone bridge arrangement. When a fluid wave strikes the diaphragm, an electrical current is generated with a magnitude dependent on the strength of the force that deflects the membrane. The output current is amplified and displayed as pressure versus time.


Clinical Art

Pre-operations Before Recording

Old generations of transducers required calibration against a mercury manometer; fortunately, the factory-calibrated, disposable, fluid-filled transducers in clinical use today no longer need this. Table-mounted transducers do require balancing or "zeroing," which refers to the establishment of a reference point for subsequent pressure measurements. The reference or "zero" position should be determined before any measurements are made. By convention, it is defined at the patient's midchest in the anteroposterior dimension at the level of the sternal angle of Louis (fourth intercostal space). This site is an estimation of the location of the right atrium and is also known as the phlebostatic axis. A table-mounted transducer is placed at this level and the stopcock is opened to air (atmospheric pressure) and set to zero by the hemodynamic system. The system is now ready for presure measurements. It is important to emphasize that the pre-operation of the hemodynamic monitor is very important, because if the "zero" level is not properly set and the transducer not appropriately balanced, the hemodynamic data recorded would be misleading, even fatal.

Interpretation of pressure waveforms requires a consistent and systematic approach in Table 2-1. Careful scrutiny of the waveform ensures a high-fidelity recording without over- or under-damping. Each pressure event should be timed with EKG.

Table 2-1 A Systematic Approach to Hemodynamic Interpretation
1.Establish the zero level and balance transducer
2.Confirm the scale of the recording
3.Collect hemodynamics in a systematic method using established protocols
4.Critically assess the pressure waveforms for proper fidelity
5.Carefully time pressure events with the EKG
6.Review the tracings for common artifacts

At present, in the clinical setting, 3 pressure waveforms can be obtained at bedside with invasive hemodynaic monitoring devices (central venous cathether/CVC and pulmonary artery catheter/PAC), including right atrial pressure/Prapulmonary artery pressure/Ppa, and pulmonary artery wedge pressure/Ppw. The pressurewave form is recorded along with a synchronized EKG.

Normal Pressure Waveform

Atrial Pressure

The goal of measuring the atrial pressure is to measure the pressure in the ventricles  at the end of diastole, to idenfify a "filling pressure". The goal for any atrial pressure measurement is to obtain the measurement at the every end of diastole, when the atrial pressure is closest to the ventricular pressure. The normal Pra is 2-8 mm Hg and is characterized by a and v waves and x and y descents. The causes of a, v waves and x, y descents are listed below.

PS: The Rationale Reason for the Formation of Pra waveform

a wave represents the pressure rise within the right atrium due to atrial contraction follows the P wave on the EKG by about 80 msec
descet represents the pressure decay following the a wave and reflect both atrial relaxation and the sudden downward motion of the atrioventricular junction that occurs because of early ventricular systole  
c wave is sometimes observed after the a wave and is due to the sudden motion of the tricuspid annulus toward the right atrium at the onset of ventricular systole the c wave follows the a wave by the same time as the PR interval on the EKG
v wave when the tricuspid valve is closed, the pressure rise responsible for the v wave is due to passive venous filling of the atrium, represent atrial diastole. the peak of the right atrial v wave corresponds with the end of T wave on the surface EKG; the ORS alawys appears before the v wave is produced
y wave is due to rapid emptying of the right atrium when the tricuspid valve opens  

Atrial waveform interpretation in detail

v wave

The atrial pressures initially increase during systole as the contracting ventricles return blood to the atria, refilling the upper chambers. This rise in the atrial pressure is identified as the "v" wave. The upstroke of the v wave is the rise in atrial pressure as a result of atrial filling. Because it is produced as a result of ventricular contraction, its location is relative to the QRS on the EKG. Ejection eventually leads to the return of blood to the atria (left ventricular contraction refills the right atrium and produces the right atrial v wave; right ventricular contraction refills the left atrium and produces the left atrial v wave). Thus, the QRS causes the v wave, however, the QRS always appears before the v wave is produced.

PA

The normal pulmonary artery systolic pressure/Ppas is 15-30 mm Hg, the normal diastolic pressure/Ppad is 4-12 mm Hg, and the mean 9-18 mm Hg. The components pulmonary artery pressure include a rapid rise in pressure, systolic peak, a pressure decay associated with a well-defined dicrotic notch from pulmonic valve closure, and a diastolci trough.

PA and arterial pressure waveforms have similar morphology. Systole begins with the opening of the pulmonic valves. Prior to opening of the pulmonary valve, the pulmonary artery pressure is very low (the pulmonary vascular system does not need a high pressure system to perfuse). As the ventricles contact, they eject blood into the pulmonary artery. This causes an immediate rise in the arterial pressure. As blood enters the great vessels, the pressure rise quickly and steadily, producing a steep vertical rise. Late in systole, the rate of ejection slows as the pressure gradient between the right ventricle and pulmonary artery narrows. Although blood is still moving from the ventricle to the great vessels, the rate of movement is slowed to the point where the pressure begins to decline. This cause the early downslope in the arterial tracing that represents this period of reduced ejection. Like the right atrial v wave, the pulmonary artery systolic wave typically coincides with the T wave of the EKG.

Later, the ventricle begins to relax, causing the ventricular pressure to drop below the pressure in great vessels. This causes the pulmonic valves to close, producing a small rise in the PA pressure, known as the dicrotic notch. Following closure of the semi-lunar valves, the pulmonary artery continues to fall as blood leaves the great vessels to perfuse the tissues and lungs.

PAWP

The normal mean pulmonary artery wedge pressure/Ppw is obtained when the inflated catheter obstructs forward flow within a branch of the pulmonary artery, creating a static column of blood between the tip of the catheter and the j point in the pulmonary venous bed where it intersects with flowing blood. The Ppw tracing contains the same sequence of waves and descents as the Pra tracing. However, when referenced to the ECG, the waves and descents of the Ppw will be seen later than those of the Pra, because the pressure waves from the left atrium must travel back through the pulmonary vasculature and a longer length of catheter. Therefore, in the Ppw tracing, the a wave usually appears after the QRS complex, and the v wave is seen after the T wave.
screen-shot-2016-10-19-at-2-19-49-pmInterpretation of CVP and PAWP measurements

Correlation to the EKG

The easiest wave to evaluate an atrial tracing is to first locate the v wave. Generally, it will appear immeidately after the peak of T wave on a CVP waveform, however, it will be 80-120 ms after the T wave on a PAWP tracing. You can generally identify the v wave by ruling out other waves. It must be after the peak of the T wave. Once the v wave is identified, the a and c can be determined.

Observe the EKG rhythm. If the patient has a sinus rhythm, an a wave should be present. The a should be in the PR interval for a CVP. It is later in the PAWP, appearing within or even afte QRS. If the patient does not have a P wave, the a wave will be absent. If the P wave is not synchronized to the QRS, very large a wave may be present. These large a waves may appear as one very large wave during a cardiac cycle. The large a waves are called cannon a waves. They are actually exaggerated atrial pressures that occur when the atria contract against a closed AV valve, adding to the pressure that is already being generated due to the c or v wave.

If present, the c wave is generally within the QRS for a CVP. It will be after the QRS for a PAWP.

Where to Measure CVP and PAWP

At the very end of ventricular diastole, the atrial pressure equilibrates with the ventricular pressure, at the very end of ventricular filling. Measurement of the atrial pressure at the end of diastole provides the best opportunity to capture ventricular filling pressure. The location on the atrial pressure wave that best reflects end-diastolic pressure is the point just prior to the c wave. However, c wave is often absent or difficult to find, espeically true in the PAWP waveform, which is subject to considerable movement artifact from right ventricular systole and breathing. If we cannot use the mehtod based on c wave to measure the filling pressure, instead we can use other two ways to capture the filling pressure, where the second method for identification of the end-diastolic pressure is to take the mean of the highest and lowest a wave pressure; and the thrid method is used if the a wave is hard to interpret or absent, that is, the end-diastolic pressure can be estimated by identifying the Z point. Draw a line from the end of the QRS to the atrial tracing. The point where the line intersects with the waveform is the Z line. Note that for a PAWP waveform the Z line should be estimated as 0.08-0.12 seconds to the left of the end of the QRS (Z point is delayed 0.08-0.12 seconds from the QRS on the PAWP).


Respiratory Influences on Hemodynamic Data: Transmural Pressure

The Pra and Ppw are used as surrogates for RV and LV filling pressure (so the preload), but remember that when evaluating the patient's preload the end-diastolic volume of the ventricles should also be included in the interpretation. Here in this section we focus our discussion on the respiratory influecnes on the recorded hemodynamic data. OK, it is the transmural (intravascular minus pleural) pressure that represents the distending pressure for cardiac filling. During normal breathing, Ppl is slightly negative at end-expiration and intrathoracic vascular pressures measured at this point in respiratory cycle provide the best estimate of transmural pressure. Either a strip recording or the cursor method should be used to define the end-expiratory pressure.

One error is the assumption that during mechanical ventilation the lowest point in the pressure tracing reflects end expiration. While this is true during controlled ventilation, inspiratory efforts that trigger mechanical breaths produce a nadir in the pressure tracing. Identification of end expiration in the Ppw tracing is aided by the knowledge that expiration is usually longer than inspiration, two exceptions being marked tachypnea and inverse-ratio ventilation. Identification of end expiration from the pressure tracing should not be difficult when interpreted in relationship to the patient's ventilatory pattern. When confusion occurs, a simultaneous airway pressure tracing may be used.

The Pra and Ppw will overestimate transmural pressure if intrathoracic pressure is positive at end expiration. This can occur from an increase in end-expiratory lung volume due to applied positive end-expiratory pressure (PEEP) or auto-PEEP, or from increased intra-abdominal pressure due to active expiration or intra-abdominal hypertension.


Common Errors and Artifacts

screen-shot-2016-10-20-at-7-58-42-pmMost errors in the collection and interpretation of hemodynamic data are listed in Table 2-2.

Probably the most commonly observed artifacts relate to an improper degree of damping. The over-damped tracing indicates the presence of excessive friction absorbing the force of the pressure wave somewhere in the line from the catheter tip to the transducer. The tracing lacks proper fidelity and appears smooth and rounded because of loss of frequency response. This will result in loss of data and will falsely lower peak pressures. Typically, the dicrotic notch on the aortic or pulmonary artery waveforms is absent, and the right atrial or PAPW waveforms will lack distinct a and v waves.

Under-damping causes overshoot or ring artifact. This artifact typically appears as one or more narrow "spikes" overshooting the true pressure during the systolic pressure rise with similar, negatively directed waves overshooting the true pressure contour during the downstroke. This artifact may lead to overestimation of the peak pressure and underestimation of the pressure nadir. Tiny air bubbles that oscillate rapidly back and forth, transmitting energy back to the transducer, cause this artifact. Flushing the catheter or transducer often corrects this artifact; alternatively, introduction of a filter to the hemodynamic system may be necessary to eliminate this artifact.

Related to overshoot or ring artifact is catheter whip or fling artifact. This artifact is created by acceleration of the fluid within the catheter from rapid catheter motion and is commonly seen with balloon-tipped catheters in hyperdynamic hearts or balloon-tipped catheters placed in the pulmonary artery with extraneous loops. Similar to ring artifact, catheter whip causes overestimation of the systolic pressure and underestimation of the diastolic pressure. This artifact is difficult to remedy; eliminating the extra loops or deflation of the balloon can improve the appearance and limit this artifact.

Catheter malposition creates several interesting artifacts.

Mechanism of Pulmonary Edema

September 13, 2016 Cardiology, Critical Care, Hemodynamics, Physiology and Pathophysiology, Pulmonary Medicine, Respirology No comments , , , , , , , , ,

screen-shot-2016-09-12-at-8-32-24-pmPulmonary edema is the extravascular accumulation of fluid in the lung. This pathologic condition may be caused by one or more physiologic abnormalities, but the result is inevitably impaired gas transfer. As the edema fluid builds up, first in the interstitium and later in alveoli, diffusion of gases – particularly oxygen – decreases.

The capillary endothelium is much more permeable to water and solutes than is the alveolar epithelium. Edema fluid therefore accumulates in the interstitium before it accumulates in the alveoli.

The Starling equation describes the movement of liquid across the capillary endothelium, see the figure above. This equation describes the basic parameters that determine the net fluid movement between the vessel and the interstitium. On the other hand, the lymphatic drainage is another important factor which relieves the interstitial fluid accumulation by simply drainage – removing fluid from the interstitium. Any fluid that makes its way into the pulmonary interstitium must be removed by the lymphatic drainage of the lung. The pulmonary lymphatic vessels are mainly located in the extra-alveolar interstitium. The volume of lymph flow from the human lung is now believed to be as great as that from other organs under normal circumstances, and it is capable of increasing as much as 10-fold under pathologic conditions. It is only when this large safety factor is overwhelmed that pulmonary edema occurs.


screen-shot-2016-09-12-at-8-58-50-pmConditions That May Lead to Pulmonary Edema

The Starling equation provides a useful method of categorizing most of the potential causes of pulmonary edema.

Permeability (Kf)

Infections, circulating or inhaled toxins, oxygen toxicity, and other factors that destroy the integrity of the capillary endothelium can lead to localized or generalized pulmonary edema.

Capillary Hydrostatic Pressure (Pc)

The capillary hydrostatic pressure is estimated to be about 10 mm Hg under normal conditions. If the capillary hydrostatic pressure increases dramatically, the filtration of fluid across the capillary endothelium will increase greatly, and enough fluid may leave the capillaries to exceed the lymphatic drainage. The pulmonary capillary hydrostatic pressure often increases secondary to problems in the left side of the circulation, such as infarction of the left venticle, left ventricular failure, or mitral stenosis. As left atrial pressure and pulmonary venous pressure rise because of accumulating blood, the pulmonary capillary hydrostatic pressure also increases. Other causes of elevated pulmonary capillary hydrostatic pressure include overzealous administration of intravenous fluids by the physician and disease that occlude the pulmonary veins.

Interstitial Hydrostatic Pressure (Pis)

Some investigators believe the interstitial hydrostatic pressure of the lung to be slightly positive, whereas others have shown evidence that it may be in the range of -5 to -7 mm Hg. Conditions that would decrease the interstitial pressure would increase the tendency for pulmonary edema to develop. These include forced inspiration against an upper airway obstruction and potential actions of the physician, such as rapid evacuation of chest fluids or reduction of pneumothorax. Situations that increase alveolar surface tension, for example, when decreased amounts of pulmonary surfactant are present, could also make the interstitial hydrostatic pressure more negative and increase the tendency for the formation of pulmonary edema. Note that as fluid accumulates in the interstitium, the interstitial hydrostatic pressure increases, which helps limit further fluid extravasation.

The Reflection Coefficient (σ)

Any situation that permits more solute to leave the capillaries will lead to more fluid movement out of the vascular space.

Plasma Colloid Osmotic Pressurepl )

Decreased in the colloid osmotic pressure of the plasma, which helps retain fluid in the capillaries, may lead to pulmonary edema. Plasma colloid osmotic pressure, normally in the range of 25 to 28 mm Hg, falls in hypoproteinemia or over administration of intravenous solutions.

Interstitial Colloid Osmotic Pressureis)

Increased concentration of solute in the interstitium will pull fluid from the capillaries.

Lymphatic Insufficiency

Conditions that block the lymphatic drainage of the lung, such as tumors or scars, may predispose patients to pulmonary edema.

Other Conditions Associated with Pulmonary Edema

Pulmonary edema is often seen associated with head injury, heroin overdose, and high altitude. The causes of the edema formation in these conditions are not known, although high-altitude pulmonary edema may be partly caused by high pulmonary artery pressures secondary to the hypoxic pulmonary vasoconstriction.

[Respiration][Circulation] Blood Flow to the Lung – General and Pulmonary Vascular Resistance

September 11, 2016 Cardiology, Critical Care, Hemodynamics, Mechanical Ventilation, Physiology and Pathophysiology, Pulmonary Medicine, Respirology No comments , , , , , , , , , , , ,

The lung receives blood flow via both the bronchial circulation and the pulmonary circulation. Bronchial blood flow constitutes a very small portion of the output of the left ventricle and supplies part of the tracheobronchial tree with systemic arterial blood. Pulmonary blood flow (PBF) constitutes the entire output of the right venticle and supplies the lung with the mixed venous blood draining all the tissues of the body.

There is about 250 to 300 mL of blood per square meter of body surface area in the pulmonary circulation. About 60 to 70 mL/m2 of this blood is located in the pulmonary capillaries.

Gas exchange starts to take place in smaller pulmonary arterial vessels, which are not truly capillaries by histologic standards. These arterial segments and successive capillaries may be thought of as functional pulmonary capillaries.

About 280 billion pulmonary capillaries supply approximately 300 million alveoli, resulting in a potential surface area for gas exchange estimated to be 50 to 100 m2.

Bronchial Circulation

The bronchial arteries arise variably, either directly from the aorta or from the intercostal arteries. They supply arterial blood to the tracheobronchial tree and to other structures of the lung down to the level of the terminal bronchioles. They also provide blood flow to the hilar lymph nodes, visceral pleura, pulmoonary arteries and veins, vagus, and esophagus. The bronchial circulation may be important in the "air-conditioning" of inspired air. The blood flow in the bronchial circulation constitutes about 2% of left ventricle output of the left ventricle. Blood pressure in the bronchial arteries is the same as that in other systemic arteries.

The venous drainage of the bronchial circulation is unusual. Although some of the bronchial venous blood enters the azygos and hemiazygos veins, a substantial portion of bronchial venous blood enters the pulmonary veins. Therefore, the bronchial venous blood entering the pulmonary venous blood is part of the normal anatomic right-to-left shunt. Histologists have also identified anastomoses, or connections, between some bronchial capillaries and pulmonary capillaries and between bronchial arteries and branches of the pulmonary artery. Thse connections probably play little role in a healthy person but may open in pathologic states, such as when either bronchial or PBF to a protion of lung is occluded. For example, if PBF to an area of the lung is blocked by a pulmonary embolus, bronchial blood flow to that area increases.

Pulmonary Circuation

The pulmonary vessels offer much less resistance to blood flow than do the systemic arterial tree. They are also much more distensible than systemic arterial vessels. These factors lead to much lower intravascular pressures than those found in the systemic arteries, which makes them more compressible. The pulmonary vessels are located in the thorax and are subject to alveolar and intrapleural pressures that can change greatly. Therefore, factors other than the tone of the pulmonary vascular smooth muscle may have profound effects on pulmonary vascular resistance (PVR). The transmural pressure difference across vessel walls is therefore a major determinant of PVR.

Because the right and left circulations are in series, the outputs of the right and left venticles must be approximately equal to each other over the long run. If the 2 outputs are the same and the measured pressure drops across the systemic circulation and the pulmonary circulation are bout 98 and 10 mm Hg, respectively, then the PVR must be about one tenth that of the systemic vascular resistance (SVR). Again, the low resistance to blood flow offered by the pulmonary circulation is due to the structural aspects of the pulmonary circulation.

The resistance is fairly evenly distributed among the pulmonary arteries, the pulmonary capillaries, and the pulmonary veins (from 15 mm Hg to 12 mm Hg, from 12 mm Hg to 8 mm Hg, from 8 mm Hg to 5 mm Hg, respectively). At rest, about one third of the resistance (PVR) is located in the pulmonary arteries, about one third is located in the pulmonary capillaries, and about one third is located in the pulmonary veins.

PVR

screen-shot-2016-09-11-at-3-44-33-pmThe relative small amounts of vascular smooth muscle, low intravascular pressures, and high distensibility of the pulmonary circulation lead to a much greater importance of extravascular effects ("passive factors") on PVR. Gravity, body position, lung volume, alveolar and intrapleural pressures, intravascular pressures, and right ventricular output all can have profound effects on PVR without any alteration in the tone of the pulmonary vascular smooth muscle.

Transmural Pressure On PVR

For distensible-compressible vessels, the transmural pressure difference is an important determinant of the vessel diameter. As the transmural pressure difference (which is equal to pressure inside minus pressure outside) increases, the vessel diameter increases and resistance falls; as the transmural pressure difference decreases, the vessel diameter decreases and the resistance increases. Negative transmural pressure differences lead to compression or even collapse of the vessel.

Lung Volume on PVR

Screen Shot 2016-09-06 at 12.48.46 PMTwo different groups of pulmonary vessels must be considered when the effects of changes in lung volume on PVR are analyzed: those vessels that are exposed to the mechanical influences of the alveoli and the larger vessels that are not – the alveolar and extraalevolar vessels.

As lung volume increases during a normal negative-pressure inspiration, the alveoli increase in volume. While he alveoli expand, the vessels found between them, mainly pulmonary capillaries, are elongated. As these vessels are stretched, their diameters decrease, just as stretching a rubber tube causes its diameter to narrow. Resistance to blood flow through the alveolar vessels increases as the alveoli expand because the alveolar vessels are longer (resistance is directly proportional to length) and because their radii are smaller (resistance is inversely proportional to radius to the fourth power). At high lung volumes, then, the resistance to blood flow offered by the alveolar vessels increases greatly; at low lung volumes, the resistance to blood flow offered by the alveolar vessels decreases.

One group of the extraalveolar vessels, the larger arteries and veins, is exposed to the intrapleural pressure. As lung volume is increased by making the intrapleural pressure more negative, the transmural pressure difference of the larger arteries and veins increase and they distend. Another factor tending to decrease the resistance to blood flow offered by the extraalveolar vessels at higher lung volumes is radial traction by the connective tissue and alveolar septa holding the larger vessels in place in the lung. Thus, at high lung volumes, the resistance to blood flow offered by the extraalveolar vessels decreases. During a forced expiration to low lung volumes, however, intrapleural pressure becomes very positive. Extraalveolar vessels are compressed, and as the alveoli decrease in size, they exert less radial traction on the extraalveolar vessels. The resistance to blood flow offered by the extraalveolar vessels increase greatly.

Because the alveolar and extraalveolar vessels may be thought of a 2 groups of resistances in series with each other, the resistances of the alveolar and extraalveolar vessels are additive at any lung volume. Thus, the effect of changes in lung volume on the total PVR gives the U-shape cruve. PVR is lowest near the functional residual capacity and increases at both high and low lung volumes.

There is another type of extraalveolar vessel called corner vessel, or extraalveolar capillary. Although these vessels are found between alveoli, their locations at junctions of alveolar septa give them different mechanical properties. Expansion of the alveoli during inspiration increases the wall tension of the alveolar septa, and the corner vessels are distended by increased radial traction, whereas the alveolar capillaries are compressed.

Also note that during mechanical positive-pressure ventilation, alveolar pressure (PA) and intrapleural pressure are positive during inspiration. In this case, and the resistance to blood flow offered by both alveolar and extraalveolar vessels increases during lung inflation. This is especially a problem during mechanical positive-pressure ventilation with positve end-expiratory pressure (PEEP). During PEEP, airway pressure (and thus alveolar pressure) is kept positive at end expiratory to help prevent atelectasis. In this situation, alveolar pressure and intrapleural pressure are positive during both inspiration and expriation. PVR is elevated in both alveolar and extraalveolar vessels throughout the respiratory cycle. In addition, because intrapleural pressure is always positive, the other intrathoracic blood vessels are subjected to decreased transmural pressure differences; the venae cavae, which have low intravascular pressure, are also compressed. If cardiovascular reflexes are unable to adjust to this situation, cardiac output may fall precipitously because of decreased venous return (for the reason see thread "Effects of Pressure Outside the Heart on Cardiac Output" at http://www.tomhsiung.com/wordpress/2016/09/effects-of-pressure-outside-the-heart-on-cardiac-output/) and high PVR.

Recruitment and Distention

During exercise, cardiac output can increase several-fold without a correspondingly great increase in MPAP. Although the MPAP does increase, the increase is only a few millimeters of mercury, even if cardiac output has doubled or tripled. Since the pressure drop across the pulmonary circulation is proportional to the cardiac output times the PVR, this must indicate a decrease in PVR.

Like the effects of lung volume on PVR, this decrease appears to be passive – that is, it is not a result of changes in the tone of pulmonary vascular smooth muscle caused by neural mechanisms or humoral agents. In fact, a fall in PVR in response to increased blood flow or even an increase perfusion pressure can be demonstrated in a vascularly isolated perfused lung. There are two different mechanisms that can explain this decrease in PVR in response to elevated blood flow and perfusion pressure: recruitment and distention.

Recruitment

At resting cardiac outputs, not all the pulmonary capillaries are perfused. A substantial proportion of capillaries, perhaps as large as one half to two thirds, is probably not perfused because of hydrostatic effects. Others may be unperfused because they have a relatively high critical opening pressure. That is, these vessels, because of their high vascular smooth muscle tone or other factors such as positive alveolar pressure, require a higher perfusion pressure than that solely necessary to overcome hydrostatic forces. Under normal circumstances, it is not likely that the critical opening pressures for pulmonary blood vessels are very great because they have so little smooth muscle. Increased blood flow increases the MPAP, which opposes hydrostatic forces and exceeds the critical opening pressure in previously unopened vesels. This series of events opens new parallel pathways for blood flow, which lowers the PVR. This opening of new pathways is called recruitment. Note that decreasing the cardiac output or pulmonary artery pressure can result in a derecruitment of pulmonary capillaries.

Distention

As perfusion pressure increases, the transmural pressure gradient of the pulmonary blood vessels increases, causing distention of the vessels. This increases their radii and decreases their resistance to blood flow.

Control of Pulmonary Vascular Smooth Muscle

Pulmonary vascular smooth muscle is responsive to both neural and humoral influences. These produce "active" alterations in PVR, as opposed to those "passive" factors discussed in the previous section.

The pulmonary vasculature is innervated by both sympathetic and parasympathetic fibers of the autonomic nervous system. The innervation of pulmonary vessels is relatively sparse in comparsion with that of systemic vessels. There is relatively more innervation of the larger vessels and less of the smaller, more muscular vessels. There appears to be no innervation of vessels smaller than 30 um in diameter. There does not appear to be much innervation of intrapulmonary veins and venules.

The effects of stimulation of the sympathetic innervation of the pulmonary vasulature are somewhat controversial. Some investigators have demonstrated an increase in PVR with sympathetic stimulation of the innervation of the pulmonary vasculature, whereas others have shown only a decreased distensibility with no change in calculated PVR. Stimulation of the parasympathetic innervation of the pulmonary vessels generally causes vasodilation, although its physiologic function is not known.

The catecholamines epinephrine and norepinephrine both increase PVR when injected into the pulmonary circulation. Histamine, found in the lung in mast cells, is a pulmonary vasoconstrictor. Certain prostaglandins and related substances, such as PGF2alpha, PGE2, and thromboxane, are also pulmonary vasoconstrictors, as is endothelin, a 21-amino acid peptide synthesized by the vascular endothelium. Alveolar hypoxia and hypercapnia also cause pulmonary vasoconstriction. Acetylcholine, the beta-adrenergic agonist isoproterenol, nitric oxide (NO), and certain prostaglandins, such as PGE1, and PGI2 (prostacyclin), are pulmonary vasodilators.

Gravity's Impact on PVR

Determinations of the regional distribution of PBF (see discussion below) have shown that gravity is another important "passive" factor affecting local PVR and the relative perfusion of different regions of the lung (see discussion below). The interaction of the effects of gravity and extravascular pressures may have a profound influence on the relative perfusion of different areas of the lung.

The Regional Distribution of Pulmonary Blood Flow

Interaction of Gravity and Extravascular Pressure

Experiments done on excised, perfused, upright animal lungs have demonstrated the same gradient of increased perfusion per unit volume from the top of the lung to the bottom. When the experiments were done at low pump outputs so that the pulmonary artery pressure was low, the uppermost regions of the lung received no blood flow. Perfusion of the lung ceased at the point at which alveolar pressure (PA) was just equal to pulmonary arterial pressure (Pa). Above this point, there was no perfusion because alveolar pressure exceeded pulmonary artery pressure, and so the transmural pressure across capillary walls was negative. Below this point, perfusion per unit volume increased steadily with increased distance down the lung.

screen-shot-2016-09-12-at-1-51-11-pmThus, under circumstances in which alveolar pressure is greater than pulmonary artery pressure in the upper parts of the lung, no blood flow occurs in that region, and the region is referred to as being in zone 1, as shown in Fingure 4-9. Any zone 1, then, is ventilated but not perfused. It is alveolar dead space. Fortunately, during normal, quiet breathing in a person with a normal cardiac output, pulmonary artery pressure, even in the uppermost regions of the lung, is greater than alveolar pressure, and so there is no zone 1. Some experiments have also demonstrated perfusion of the corner vessels under zone 1 conditions.

The lower portion of the lung in Figure 4-9 is said to be in zone 3. In this region, the pulmonary artery pressure and the pulmonary vein pressure (Pv) are both greater than alveolar pressure. The driving pressure for blood flow through the lung in this region is simply pulmonary artery pressure minus pulmonary vein pressure. Note that this driving pressure stays constant as one moves further down the lung in zone 3 because the hydrostatic pressure effects are the same for both the arteries and the veins.

The middle portion of the lung in Figure 4-9 is in zone 2. In zone 2, pulmonary artery pressure is greater than alveolar pressure, and so blood flow does occur. However, because alveolar pressure is greater than pulmonary vein pressure, the effective driving pressure for blood flow is pulmonary artery pressure minus alveolar pressure in zone 2. Notice that in zone 2 the increase in blood flow per distance down the lung is greater than it is in zone 3. This because the upstream driving pressure, the pulmonary artery pressure, increases according to the hydrostatic pressure increase, but the effective downstream pressure, alveolar pressure, is constant throughout the lung at any instant.

It is important to realize that the boundaries between the zones are dependent on physiologic conditions – they are not fixed anatomic landmarks. Alveolar pressure changes during the course of each breath. During eupneic breathing these changes are only a few centimeters of water, but they may be much greater during speech, exercise, and other conditions. A patient on a positive-pressure ventilator with PEEP may have substantial amounts of zone 1 because alveolar pressure is always high. Similarly, after a hemorrhage or during general anesthesia, PBF and pulmonary artery pressure are low and zone 1 conditions are also likely. During exercise, cardiac output and pulmonary artery pressure increase and any existing zone 1 should be recruited to zone 2. The boundary between zones 2 and 3 will move upward as well. Pulmonary artery pressure is highly pulsatile, and so the borders between the zones probably even move up a bit with each contraction of the right ventricle.

Changes in lung volume also affect the regional distribution of PBF and will therefore affect the boundaries between zones. Finally, changes in body position alter the orientation of the zones with respect to the anatomic locations in the lung, but the same relationships exist with respect to gravity and alveolar pressure.

Hypoxic Pulmonary Vasoconstriction

Alveolar hypoxia or atelectasis causes an active vasoconstriction in the pulmonary circulation. The site of vascular smooth muscle constriction appears to be in the arterial (precapillary) vessels very close to the alveoli.

The mechanism of hypoxic pulmonary vasoconstriction is not completely understood. The response occurs locally, that is, only in the area of the alveolar hypoxia. Connections to the central nervous system are not necessary: An isolated, excised lung, perfused with blood by a mechanical pump with a constant output, exhibits an increased perfusion pressure when ventilated with hypoxic gas mixtures. This indicates that the increase in PVR can occur without the influence of extrinsic nerves. Thus, it is not surprising that hypoxic pulmonary vasoconstriction persists in human patients who had received heart-lung transplants. Hypoxia may cause the release of a vasoactive substance from the pulmonary parenchyma or mast cells in the area. Histamine, serotonin, catecholamines, and prostaglandins have all been suggested as the mediator substance, but none appears to completely mimic the response. Decreased release of a vasodilator such as nitric oxide may also be involved in hypoxic pulmonary vasoconstriction. Possibly several mediators act together. More recent studies have strongly indicated that hypoxia acts directly on pulmonary vascular smooth muscle to produce hypoxic pulmonary vasoconstriction.

Physiologic Function of Hypoxic Pulmonary Vasoconstriction

The function of hypoxic pulmonary vasoconstriction in localized hypoxia is fairly obvious. If an area of the lung becomes hypoxic because of airway obstruction or if localized atelectasis occurs, any mixed venous blood flowing to that area will undergo little or no gas exchange and will mix with blood draining well-ventilated areas of the lung as it enters the left atrium. This mixing will lower the overall arterial PO2 (PaO2) and may even increase the arterial PCO2 (PaCO2). The hypoxic pulmomary vasoconstriction diverts mixed venous blood flow away from poorly ventilated areas of the lung by locally increasing vascular resistance. Therefore, mixed venous blood is sent to better-ventilated areas of the lung. The problem with hypoxic pulmonary vasoconstriction is that it is not a very strong response because there is so little smooth muscle in the pulmonary vasculature. Very high pulmonary artery pressures can interfere with hypoxic pulmonary vasoconstriction, as can other physiologic disturbances, such as alkalosis.

In hypoxia of the whole lung, such as might be encountered at high altitude or in hypoventilation, hypoxic pulmonary vasoconstriction occurs throughout the lung. Even this may be useful in increasing gas exchange because greatly increasing the pulmonary artery pressure recruits many previously unperfused pulmonary capillaries. This increases the surface area available for gas difusion and improves the matching of ventilation and perfusion. On the other hand, such a whole-lung hypoxic pulmonary vasoconstriction greatly increases the workload on the right venticle, and the high pulmonary artery pressure may overwhelm hypoxic pulmonary vasoconstriction in some parts of the lung, increase the capillary hydrostatic pressure in those vessels, and lead to pulmonary edema.

Pathophysiology of The Circulation

August 8, 2016 Cardiology, Critical Care, Hemodynamics, Physiology and Pathophysiology No comments , , , , , , , , , , , , ,

The Diastolic V-P Curve

Screen Shot 2016-07-25 at 5.40.29 PMFigure 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.

Abnormality

  • 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.

Screen Shot 2016-07-25 at 6.31.10 PMThe 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

Screen Shot 2016-07-26 at 7.07.47 PMBefore 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.

Screen Shot 2016-07-30 at 2.20.14 PMWhen 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.

Screen Shot 2016-07-30 at 3.41.07 PMNote 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.