CARDIOVASKULAR MONITORING IN CRITICAL CARENAMA : MUHAMMAD FATHEE BIN BASREE(C11107348)SUPERVISOR : DR ALMUDAI, SpPDJOURNAL READINGNovember 2012

IntroductionHaemodynamic monitoring is a crucial part of bedside care of the critically ill patientOne of the main reasons for monitoring haemodynamicvariables is to detect an impending cardiovascular crisis before organ damage occurs. Another goal of haemodynamic monitoring is to allow clinicians to monitor the response to cardiovascular therapy. Many treatments have to be titrated to specific cardiovascular responses, thus making their use dependent on such monitoringFinally, the pattern of haemodynamic values often helps differentiate causes of haemodynamic instability and circulatory shock.

Most intensive care units monitor and display, as they have done for the last 20 years, only electrocardiography (ECG), heart rate (HR), blood pressure and pulse oximetry O2 saturation (SpO2).The effectiveness of haemodynamic monitoring therefore depends not only on the accuracy and validity of the available technology but also on the healthcare professionals ability to diagnose and effectively treat the underlying diseases for which the monitoring is used.With rapidly developing technology and improvement in our understanding of the pathophysiology of diseases, the utility of haemodynamic monitoring has changed significantly over time

Much of the monitoring is used to identify single haemodynamic values, such as blood pressure, HR or SpO2 (see above), and assess treatments specifically aimed to restore these values to normal ranges.This approach may seem reasonable but might be inappropriate under conditions commonly occurring in the intensive care unit

Static haemodynamic monitoring ofsingle variablesThe most common variables used in clinical settings are arterial blood pressure (BP), HR, SpO2, central venous pressure (CVP), pulmonary artery occlusion pressure (Ppao), cardiac output (CO) and mixed venous oxygen saturation (SvO2Threshold values for individual haemodynamic variables exist such that values above or below them may reflect cardiovascular compromise. Clearly, bradycardia (HR < 45/min) and tachycardia (HR > 130/min), hypotension (mean BP < 65 mm Hg) and hypertension (mean BP > 180 mm Hg) are usually not tolerated for prolonged intervals without resulting in end-organ dysfunction and/or death.

These values are often used as threshold single variable triggers to activate medical response teams. However, they represent the extreme of cardiovascular decompensation, whereas most patients can be in circulatory shock with sympathetic compensation with haemodynamic values within these broad limits

Systemic arterial blood pressureAfter pulse rate, arterial pressure is the most common haemodynamic variable monitored and recordedBlood pressure is not a single pressure value but a range of pressure values from systole to diastole. Therefore, for tissues other than the heart, if the back or venous pressure is not elevated, mean arterial pressure (MAP) is the best approximation of the organ perfusion pressure

Blood pressure is usually measured non-invasively using a sphygmomanometer and the auscultation techniqueBlood pressure can be measured automatically using computer-driven devicesSphygmomanometer-derived blood pressure measures display slightly higher systolic and lower diastolic pressures than simultaneously measured indwelling arterial catheters, but the MAP is usually similar and the actual systolic and diastolic pressure differences are often small except in the setting of increased peripheral vasomotor tone.

Accurate and continuous measurements of arterial pressure can be done through arterial catheterisation of easily accessible arterial sites in the arm (axillary, brachial or radial artery) or groin (femoral artery).Arterial catheterisation displaying continuous arterial pressure waveforms allows arterial waveform analysis, essential in the calculation of pulse pressure and pulse pressure variations and CO by pulse contour analysis

Blood pressure is physiologically regulated through baroreceptor reflex arcs that keep it constant despite changing CO, whereas CO varies with changing tissue metabolic demands. Thus, a normal blood pressure does not necessarily reflect haemodynamic stabilityHypotension (MAP < 65 mm Hg) should be considered as a pathological state of organ hypoperfusion and loss of autoregulation of blood flow.

Central venous pressure (CVP) or right atrial pressureCVP is also called right atrial pressure. CVP is the pressure in the large central veins proximal to the right atrium relative to atmosphere. CVP is usually measured using a fluid-filled catheter (central venous line or pulmonary artery catheter), with the distal tip located in the superior vena cava connected to a manometer or more often to a pressure transducer of a monitor, displaying the waveform in a continuous fashion.

CVP can also be measured non-invasively as jugular venous pressure by the height of the column of blood distending the internal and external jugular veins, when the subject is sitting in a semi-reclined position, such that the small elevations in CVP will be reflected in a persistent jugular venous distention.However, the accuracy of jugular venous distention to assess absolute CVP values has not been substantiated.

Still, if CVP is 10 mm Hg or less it has some physiologicalsignificance. For example, Jellenik et al. showed that if CVP is 10 mm Hg or less, then CO will uniformly decrease in ventilated patients in whom 10 cm H2O positive end-expiratory pressure (PEEP) is applied [17].However, if CVP is > 10 mm Hg, CO may increase, remain the same or decrease. There is no threshold value of CVP that identifies patients whose CO will increase in response to fluid challenge

Haemodynamic values measured by pulmonary artery catheterThe pulmonary artery catheter (PAC) is designed to estimate LV filling pressures by measuring PpaoIt can also measure pulmonary artery pressure (Ppa), CVP, SvO2, CO and right ventricular ejection fraction. Just as CVP is the back-pressure for system venous return to the right ventricle,Ppao is the back-pressure to pulmonary blood flow to theleft ventricle. Ppao can be used to identify the presence of a hydrostatic component to pulmonary oedema and to assess pulmonary vascularresistance.

Cardiac output can be calculated by measuring blood flow using dilution techniques with a thermal [26] or lithium indicator via PAC or CVP. As mentioned before, because there is no normal CO and because an accurate measurement of CO is less important than accurate documentation of trends in blood flow

Pulmonary artery pressureThe pulmonary vascular bed is a low resistance circuit with a large reserve that normally allows increases of CO with minor changes in the pulmonary artery pressure (Ppa). However, increases in the downstream venous pressure (e.g. left ventricular failure) or in the flow resistance (e.g. lung diseases and hypoxic pulmonary vasoconstriction) cause Ppa to increase if flow or CO remains constant. Although increases in CO alone do not normally cause pulmonary hypertension, with an increased pulmonaryvascular resistance the Ppa can be increased due to changes in CO. The normal range of values for Ppa is: systolic 1530 mm Hg, diastolic 412 mm Hg and mean 918 mm Hg [30]

Pulmonary artery occlusion pressurePulmonary artery occlusion pressure (Ppao) is measured as the stop flow (balloon occlusion) end-expiratory Ppa pressure.Unfortunately, the ability of healthcare professionals to accurately measure Ppao from either a strip chart recording or a freeze frame snapshot of the monitor screen is poor.Thus, it is difficult to assess the utility of Ppao as a therapeutic guide with any degree of confidence.

Balloon inflation of the pulmonary artery catheter forces the tip to migrate distally into smaller vessels until the tip occludes a medium-sized (1.2 cm diameter) pulmonary artery. This occlusion stops all blood flow in that vascular tree distal to the occlusion site until such time as other venous branches reconnect downstream to this venous draining bed about 1.5 cm from the left atrium.

Pulmonary oedema can be caused by either Pcap elevations, referred to as hydrostatic or secondary pulmonary oedema, or increased alveolar capillary or epithelial permeability, referred to as primary pulmonary oedema. Usually hydrostatic pulmonary oedema requires Pcap values in excess of approximately 18 mm Hg. However, if alveolar endothelial or epithelial cell injury is present, alveolar flooding can occur at much lower pulmonary capillary pressures

Haemodynamic profile analysis: grouping of static variablesOf the four categories of shock listed above, only distributive shock states following intravascular volume resuscitation are associated with an increased CO but decreased vasomotor tone Thus, CO, stroke work, DO2I and SvO2 are decreased in cardiogenic, hypovolaemic and obstructives hock but may be normal or even increased in distributive shock.Cardiogenic shock can be caused by impaired contractility, pump function or impaired diastolic compliance. The cardinal signs of cardiogenic shock are increased back pressure to cardiac filling (CVP and Ppao) and upstream oedema (peripheral and pulmonary).

Hypovolaemic shock represents a decrease in effective circulating blood volume and venous return. It can be caused by primary or secondary intravascular volume loss and increased unstressed vascular volume. The specific findings of hypovolaemic shock are decreased filling pressures. The specific findings of obstructive shock are often less specific but include decreased LV diastolic compliance and signs of cor pulmonale. Distributive shock represents loss of normal sympathetic responsiveness resulting in decreased vasomotor tone.

Functional haemodynamic monitoring: response to therapyA primary goal of resuscitation is to increase DO2I and to restore regional DO2I to those tissues that are hypoperfused. Thus, the primary functionalquestion usually asked of the haemodynamically unstable patient is will CO increase with fluid resuscitation and, if so, by how much? Physiologically speaking this equates to defining whether the patients CO increases with preload, provided by a volume challenge. Although specific patterns of haemodynamic values, as described above, reflect specific types of disease, they do not predict individual patient response to therapy.

The volume challengeOne of the methods used in assessing preload responsiveness is to infuse a small fluid bolus rapidly and evaluate the haemodynamic response by observing changes in arterial blood pressure, heart rate, CO, SvO2 and/or other relevant measuresA patient is considered to be a responder if there is an improvement in circulatory status, such as increasing MAP, stroke volume and CO or a decreasing heart rate

A fluid challenge must be conducted within the context of known or suspected tissue hypoperfusionImportantly, a volume challenge is only a diagnostic test to identify those who are preload responsive, and it should not be considered as a completion of fluid resuscitationIf clinical evidence of hypoperfusion persists, then volume responders should be given additional fluid resuscitation with minimal risk for worsening right ventricular failure or inducing pulmonary oedema.

Preload responsiveness in positive pressure ventilated patientsPositive pressure ventilation cyclically alters the pressure gradient for systemic venous return, proportionally altering right ventricular output on the next beat during inspiration. After about 24 beats, left ventricular filling and output are also proportionally altered. Thus, in patients whose ventricles are preload responsive, positive pressure ventilation will induce cyclical changes in stroke volume

The degree of changes in either arterial pulse pressure or systolic blood pressure in response to a series of increasing tidal breaths quantifies the degree of preload responsivenessArterial pressure pulse contour analysis has been used to estimate stroke volume variation and preload responsiveness [55]. Unfortunately, there are controversial results regarding the accuracy of the pulse contour algorithm used to calculate stroke volume using commercially available devices, and studies are limited

Preload responsiveness during spontaneous breathing

During spontaneous inspiration, venous return normally increases owing to a fall in intrathoracic pressure [65]. A normal right ventricle pumps this increased blood flow into the pulmonary circulation. Therefore CVP will decrease with decreasing intrathoracic pressure with each spontaneous inspiratory effort.

An inspiratory decrease in CVP of more than 1 mm Hg when intrathoracic pressure decreases more than 2 mm Hg accurately predicts preload responsiveness, whereas those patients whose CVP does not decrease in such a setting do not increase their CO in response to fluid challenge [66], but this approach requires central venous catheterisation.A change in inferior vena cava diameter during positive pressure ventilation can be also interpreted as CVP changes [67], but it requires complex echocardiographic technology and has minimal diagnostic utility at the Bedside.

Passive leg raisingPassive leg raising to 30 transiently increases venous return [68] in patients who are preload responsive. Since this only transiently increases CO and blood pressure [69] in responders, it is only a diagnostic test and cannot be considered as a treatment for hypovolaemia

It also can be repeated many times to reassess preload responsiveness without any risk of inducing pulmonary oedema in potential non-responders. One of the major limitations of this technique is that in severely ypovolaemic patients the blood volume mobilised by leg raising which is dependent on total blood volume could be small, which in turn can show minimal to no increase in CO and blood pressure, even in responders.

ConclusionA systematic approach to functional haemodynamic monitoring is the cornerstone of an effective resuscitation effort. If a patient responds to volume challenge or any equivalent preload responsiveness tests, then volume resuscitation should be initiated.

In preload responsive patients who, despite increase in CO in response to fluid resuscitation, cannot maintain an adequate perfusion, a decrease in vascular tone should be suspected and vasopressors should be given in addition to fluids. If a hypotensive patient is neither preload responsive nor exhibiting reduced vasomotor tone, then the problem is the heart or an obstruction in blood flow such as thromboembolic events.

In which case, both diagnostic and therapeutic actions must be taken simultaneously (e.g. echocardiography, dobutamine or thrombolytic therapy). This systematic approach can be incorporated in a protocolised cardiovascular management algorithm based on functional haemodynamic monitoring [71, 72], which in turn can improve patient-centred outcomes and cost of the healthcare system, by faster and more effectively response in order to diagnose and treat haemodynamically unstable patients both inside and outside of intensive care units.

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