How can we measure venous function

Though the pulmonary artery catheter may be helpful in many circumstances, nevertheless its benefit has not yet been demonstrated in a prospective manner, and the results of a recent trial have put the basis for many controversial discussions about its benefit. On the other hand, these problems also hold for all new, even less validated alternative monitoring techniques like the transcardiopulmonary indicator dilution technique for measurement of cardiac putput as well as total and intrathoracic blood volume; the latter is postulated to represent a better indicator of preload than pulmonary capillary wedge pressure.

At present, however, pulmonary artery catheter monitoring is recommended in the hemodynamically unstable, critically ill patient. Echocardiography is making major inroads into the critical care units. In general, physical examination of critically ill cardiac patients is limited in its accuracy in predicting measured physiologic data. Diagnosis of many disease processes and pathophysiologic derangements are beyond the capabilities of routine invasive monitoring techniques and can only be made by bedside echocardiography.

Since its introduction in the early eighties, echocardiography has undergone a huge technological and clinical evolution. The indications of echocardiography as a diagnostic and monitoring tool in the peri-operative and critical care setting have increased exponentially because of its potential to accurately assess cardiovascular dynamics. TEE is able to assess global and regional left ventricular function and can reliable evaluate the different determinants of ventricular function such as preload, contractility and afterload.

The short axis view of the left ventricle is a basic and readily available part of this imaging technique. Moreover, its adequate visualization of the great vessels leads to an appreciation of cardiovascular interaction and helps to differentiate between cardiac and vascular causes of hemodynamic disturbances.

Selected cardiovascular agents and their hemodynamic effects. Turn recording back on. National Center for Biotechnology Information , U. Munich: Zuckschwerdt ; Search term. Hemodynamic monitoring Christian Kuhn and Karl Werdan. Goals of monitoring To assure the adequacy of perfusion. Early detection of an inadequacy of perfusion - decision making: is monitoring sufficient, or does the patient need active intervention?

Table I Cardiorespiratory parameters which are commonly monitored in the critically ill adapted from 2. Physiological basis of cardiac monitoring For cardiac monitoring, the right and left heart must be considered for their own with respect to function, structure and pressure generation.

Preload Preload refers to the amount of myocardial fiber stretch at the end of diastole, it also refers to the amount of volume in the ventricle at the end of this phase. Afterload Afterload refers to the tension developed by the myocardium during ventricular systolic ejection. Contractility Most forms of acute and chronic heart failure are characterized by an impairment of contractility, and many treatment options - like catecholamines and phosphodiesterase inhibitors - in the perioperative arena are targeted to improve contractility of the heart.

Monitoring techniques Hemodynamic monitoring using invasive techniques is the mainstay of today's practice of critical care and allows precise frequent determinations of cardiorespiratory variables. Central venous pressure The central venous pressure CVP reflects the pressure in the central veins - usually measured in the thoracic cavity - when they enter the right atrium.

Indications for CVP measurements include: Diagnostic measurements. Kidney function Diuresis depends strongly on heart function. Pulse oximetry Pulse oximetry monitors oxygenation. Arterial pressure monitoring Peripheral arterial lines A. Indications include Rapidly changing clinical circumstances in critically ill patients e. Pulmonary artery catheter The pulmonary artery catheter offers several advantages over central venous pressure monitoring. Table III Profiles of hemodynamic emergencies in the critically ill patient.

Major surgery: in the presence of myocardial dysfunction or for preoperative optimization of hemodynamics. Resuscitation: in case of hemodynamic instability during fluid replacement: to assess left ventricular function.

Related Testing The central venous pressure is measured by a central venous catheter placed through either the subclavian or internal jugular veins. Pathophysiology Low Central Venous Pressure Some factors that can decrease central venous pressure are hypovolemia or venodilation.

Elevated Central Venous Pressure Elevated Central Venous Pressure can occur in heart failure due to decreased contractility, valve abnormalities, and dysrhythmias. Clinical Significance Clinical utility of the central venous pressure can be seen in the assessment of cardiocirculatory status.

Review Questions Access free multiple choice questions on this topic. Comment on this article. Figure Central venous pressure. Image courtesy O. References 1. Front Physiol. Narrative review: clinical assessment of peripheral tissue perfusion in septic shock.

Ann Intensive Care. Martin GS, Bassett P. Crystalloids vs. J Crit Care. Senthelal S, Maingi M. Physiology, Jugular Venous Pulsation. Making care better in the pediatric intensive care unit. Transl Pediatr.

Berlin DA, Bakker J. Starling curves and central venous pressure. Crit Care. Utility of central venous pressure measurement in renal transplantation: Is it evidence based? World J Transplant. Is there an association between central venous pressure measurement and ultrasound assessment of the inferior vena cava?

Afr J Emerg Med. In a healthy person, CVP is close to zero, 6 and for an optimal performance, the heart will always try to keep the CVP as low as possible. Regardless of its cause, a high CVP will always have a negative impact on venous return and capillary blood flow. This could explain why high CVP values have been associated with increased mortality and higher renal failure incidence. However, it is important to remember that a high CVP may be the result of several pathological conditions and can be associated with different preload states.

Therefore, the therapeutic approach could be quite different according to the situation. An adequate echocardiographic evaluation may be helpful to find out the main mechanism involved. Causes for a high central venous pressure. Fluid administration aimed to achieve an arbitrary CVP value lacks of physiological rationale. Pursuing a fixed value of CVP, such as 12 cm H 2 O, can be deleterious in a patient with ventricular dysfunction, whereas for a patient with intra-abdominal hypertension, this CVP could be associated with a decreased preload.

However, since a healthy heart is associated with low CVP values, a significant CVP raise after fluid administration should be interpreted as an early sign of RV dysfunction.

Giving more fluids beyond this point could worsen cardiac function and impair venous return and capillary blood flow. Therefore, the role of CVP for guiding fluid therapy is not for defining how much, but rather when to stop giving fluids. It has been explained that an isolated CVP value is difficult to interpret. As CVP is defined by the interaction between RV function and the venous return, CVP and CO changes are determined by a unique peripheral venous return and central cardiac function relationship.

On the other hand, when changes in CO and CVP are in opposite directions, they usually result from a variation in cardiac function Fig. An adequate use of CVP measurements requires a solid knowledge of its physiological basis and limitations. In this regard, we strongly believe that, understanding these physiological boundaries, CVP measurement may still have a role in the hemodynamic assessment.

Both authors contributed to the original idea and writing of this manuscript. The authors declare no conflict of interest regarding this paper. ISSN: Descargar PDF. Autor para correspondencia. Table 1. Central venous pressure CVP : use and misuse.. Texto completo. Introduction Central venous pressure CVP is still the most frequent hemodynamic variable for deciding when to administer fluids. Figure 1. Table 2. Cecconi, C. Hofer, J. Alveolar hemorrhage Diffuse Alveolar Hemorrhage Diffuse alveolar hemorrhage is persistent or recurrent pulmonary hemorrhage.

There are numerous causes, but autoimmune disorders are most common. Most patients present with dyspnea, cough, hemoptysis Asthma Asthma Asthma is a disease of diffuse airway inflammation caused by a variety of triggering stimuli resulting in partially or completely reversible bronchoconstriction.

Symptoms and signs include dyspnea The DLCO increase in heart failure presumably because the increased pulmonary venous and arterial pressure recruits additional pulmonary microvessels. In erythrocythemia, DLCO is increased because hematocrit is increased and because of the vascular recruitment that occurs with increased pulmonary pressures due to increased viscosity. In alveolar hemorrhage, red blood cells in the alveolar space can also bind carbon monoxide, increasing DLCO.

In asthma, the increase in DLCO is attributed to presumed vascular recruitment; however, some data suggest it may also be due to growth factor—stimulated neovascularization. Transcutaneous pulse oximetry estimates oxygen saturation SpO2 of capillary blood based on the absorption of light from light-emitting diodes positioned in a finger clip or adhesive strip probe. Results may be less accurate in patients with. Pulse oximetry is able to detect only oxyhemoglobin or reduced hemoglobin but not other types of hemoglobin eg, carboxyhemoglobin, methemoglobin ; those types are assumed to be oxyhemoglobin and falsely elevate the SpO2 measurement.

ABG sampling can also accurately measure carboxyhemoglobin and methemoglobin. The radial artery is usually used. Because arterial puncture in rare cases leads to thrombosis and impaired perfusion of distal tissue, Allen test may be done to assess adequacy of collateral circulation. With this maneuver, the radial and ulnar pulses are simultaneously occluded until the patient's hand becomes pale. The ulnar pulse is then released while pressure on the radial pulse is maintained.

A blush across the entire hand within 7 sec of release of the ulnar pulse suggests adequate flow through the ulnar artery. Under sterile conditions, a to gauge needle attached to a heparin -treated syringe is inserted just proximal to the maximal impulse of the radial arterial pulse and advanced slightly distally into the artery until pulsatile blood is returned.

Systolic blood pressure is usually sufficient to push back the syringe plunger. After 3 to 5 mL of blood is collected, the needle is quickly withdrawn, and firm pressure is applied to the puncture site to facilitate hemostasis. Simultaneously, the ABG specimen is placed on ice to reduce oxygen consumption and carbon dioxide production by WBCs and is sent to the laboratory. Hypoxemia is a decrease in the partial pressure of oxygen PO2 in arterial blood; hypoxia is a decrease in the PO2 in the tissue.

Abnormalities in hemoglobin eg, methemoglobin , higher temperatures, lower pH, and higher levels of 2,3-diphosphoglycerate reduce hemoglobin SaO2 despite an adequate PaO2, as indicated by the oxyhemoglobin dissociation curve see Figure: Oxyhemoglobin dissociation curve Oxyhemoglobin dissociation curve Gas exchange is measured through several means, including Diffusing capacity for carbon monoxide Pulse oximetry Arterial blood gas sampling The diffusing capacity for carbon monoxide DLCO Arterial oxyhemoglobin saturation is related to P o 2.

Hb characterized by a rightward shifting of the curve has a decreased affinity for oxygen, and Hb characterized by a leftward shifting of the curve has an increased affinity for oxygen. Causes of hypoxemia can be classified based on whether the alveolar-arterial PO2 gradient [ A-a DO2], defined as the difference between alveolar oxygen tension PAO2 and PaO2, is elevated or normal.

PAO2 is calculated as follows:.