《病理生理学病理生理学 (3).pdf》由会员分享，可在线阅读，更多相关《病理生理学病理生理学 (3).pdf（15页珍藏版）》请在taowenge.com淘文阁网|工程机械CAD图纸|机械工程制图|CAD装配图下载|SolidWorks_CaTia_CAD_UG_PROE_设计图分享下载上搜索。
1、Cardiopulmonary Monitoring of ShockJames Simmons,MD1 and Corey E.Ventetuolo,MD,MS1,21Division of Pulmonary,Critical Care,and Sleep,Department of Medicine,Brown University,Providence,RI,USA2Division of Pulmonary,Critical Care,and Sleep,Department of Health Services,Policy,and Practice,Brown Universit
2、y,Providence,RI,USAAbstractPurpose of reviewWe will briefly review the classification of shock and the hallmark features of each sub-type.Available modalities for monitoring shock patients will be discussed,along with evidence supporting the use,common pitfalls and practical considerations of each m
3、ethod.Recent findingsAs older,invasive monitoring methods such as the pulmonary artery catheter have fallen out of favor,newer technologies for cardiac output estimation,echocardiography,and non-invasive tests such as passive leg raising have gained popularity.Newer forms of minimally invasive or no
4、ninvasive monitoring(such as pulse-contour analysis or chest bioreactance)show promise but will need further investigation before they are considered validated for practical use.There remains no“ideal”test or standard of care for cardiopulmonary monitoring of shock patients.SummaryShock and its unde
5、rlying etiologies are potentially reversible causes of morbidity and mortality if appropriately diagnosed and managed.Older methods of invasive monitoring have significant limitations but can still be critical for managing shock in certain patients and settings.Newer methods are easier to employ,but
6、 further validation is needed.Multiple modalities along with careful clinical assessment are often useful in distinguishing shock sub-types.Best practice standards for monitoring should be based on institutional expertise.Keywordshemodynamic monitoring;shock;pulmonary artery catheter;non-invasive ca
7、rdiac monitoringI.IntroductionShock is an important cause of intensive care unit admissions and mortality even with significant advances in medical care.The goal of this review is to provide an updated framework for monitoring these patients.We will briefly summarize the current classification of sh
8、ock,including distributive,cardiogenic,hypovolemic and obstructive Correspondence and request for reprints:Corey E.Ventetuolo,MD,MS,Assistant Professor of Medicine,Rhode Island Hospital,593 Eddy Street,APC 7,Providence,RI 02903,corey_ventetuolobrown.edu,Ph:401.444.0008,Fax:401.444.0094.Conflicts of
9、interestC.E.V.has served as a consultant for Bayer Pharmaceuticals and United Therapeutics.Her institution has received grant funding from Actelion.HHS Public AccessAuthor manuscriptCurr Opin Crit Care.Author manuscript;available in PMC 2018 June 01.Published in final edited form as:Curr Opin Crit C
10、are.2017 June;23(3):223231.doi:10.1097/MCC.0000000000000407.Author ManuscriptAuthor ManuscriptAuthor ManuscriptAuthor Manuscriptshock,and review various modalities to diagnosis and monitor shock states.Practical considerations and common pitfalls of cardiopulmonary monitoring in the intensive care u
11、nit will be discussed.II.Shock definition and epidemiologyShock is a state of cellular hypoxia due to an imbalance of oxygen delivery and oxygen consumption.This is most often due a reduction in relative tissue perfusion with circulatory failure.Cardiac output(CO)and systemic vascular resistance(SVR
12、)proportionally determine blood pressure.In turn,CO is a product of heart rate(HR)and stroke volume(SV).Systemic vascular resistance(SVR)is proportional to vessel length and blood viscosity,while it is inversely proportional to vessel diameter.Shock can arise if any of these variables are changed su
13、ch that CO or SVR is decreased.Shock can also occur if tissue is unable to utilize oxygen appropriately or if oxygen carrying capacity is not adequate,as can occur with mitochondrial dysfunction or poisoning with carbon monoxide,respectively.Clinically,shock can manifest as a decompensated patient w
14、ith evidence of end organ failure(e.g.,altered mental status,hypotension,or anuria)or more occultly without frank organ dysfunction(e.g.,lactic acidosis,mild decreases in blood pressure),referred to as cryptic or compensated shock.Shock is most commonly classified into four different underlying subt
15、ypes with different pathophysiologies:distributive,cardiogenic,hypovolemic and obstructive.Distinguishing features of these four shock states are described in Table 1.Mixed shock,with characteristics of more than one of these subtypes,can also occur.The relative frequency of each type of shock at a
16、given institution depends on the population served(e.g.,Level I trauma centers will see a higher level of hemorrhagic shock(1).A large(n=1679),multicenter randomized clinical trial(RCT)(the SOAP II trial)found distributive shock was most common(64%),followed by hypovolemic(16%),cardiogenic(15%),and
17、obstructive(2%)shock among all comers with circulatory failure(2).The mortality for each type of shock varies widely.Septic shock is associated with an in-hospital mortality of 3054%(3,4),although death rates as low as 19%have been reported in recently completed RCTs(5).In-hospital mortality from ca
18、rdiogenic shock can range from 5080%(6,7).Outcomes for distributive shock also vary significantly with etiology,with mortality rates as high as 8090%from traumatic hemorrhage and as low as 19%from shock due to gastrointestinal bleeding(8,9).Hypovolemic shock patients tend to do well,with mortality r
19、ates under 10%(10).Obstructive shock includes disparate underlying conditions(i.e.,cardiac tamponade,pulmonary embolism),occurs less frequently and is less well studied,making outcome estimates difficult(11,12).IIa.Distributive ShockDistributive shock is defined by severe vasodilatation of the perip
20、heral vasculature and includes septic,anaphylactic,drug or toxin-induced,and neurogenic etiologies.Sepsis is the most common form and is attributable to dysregulation of the host response to infection and defined most recently as the use of vasopressors in the setting of a rising lactate despite flu
21、id resuscitation(3).A noninfectious but overtly robust systemic inflammatory response Simmons and VentetuoloPage 2Curr Opin Crit Care.Author manuscript;available in PMC 2018 June 01.Author ManuscriptAuthor ManuscriptAuthor ManuscriptAuthor Manuscriptsyndrome(SIRS)can mimic septic physiology,as typif
22、ied by burns or pancreatitis,among other causes.Anaphylaxis is mediated by a severe allergic reaction due to the release of immunoglobulin E and is usually accompanied by bronchospasm.Neurogenic shock is seen in severe brain or spinal cord injury.These causes lead to increased CO(via increased HR or
23、 SV)in response to tissue hypoperfusion from extreme vasodilation and increased permeability(low SVR)(Table 1).IIb.Cardiogenic ShockThis form of shock is defined by a primary intracardiac cause such as arrhythmia,ischemia,valvular dysfunction,or cardiomyopathy leading to decreased CO.Cool extremitie
24、s due to peripheral vasoconstriction and increased SVR in an attempt to maintain perfusion pressures characterize cardiogenic shock,as well as other findings such as elevated neck veins,rales from pulmonary edema,and leg edema from venous pooling.If the shock is more subacute or cryptic,then the ext
25、remities may be warm.IIc.Hypovolemic ShockReduced CO also occurs in hypovolemic shock,however this is due to reduced intravascular volume and low preload.Major causes include significant hemorrhage or volume depletion due to fluid losses from the kidneys(diuresis or salt wasting),the gastrointestina
26、l system(vomiting or diarrhea),or the skin(severe burns or heat stroke).Both hemorrhagic and non-hemorrhagic shock should lead to compensatory tachycardia and peripheral vasoconstriction in order to improve CO and perfusion pressure.IId.Obstructive ShockThis is a heterogeneous group of processes all
27、 with low CO due to an obstruction to forward flow.Pulmonary vascular causes that lead to right ventricle(RV)failure and in turn low CO include pulmonary embolism(thrombus,air,foreign body,tumor or amniotic fluid)or acute or subacute worsening of chronic pulmonary hypertension.Similarly,inadequate f
28、illing of the LV from acute tamponade,constrictive pericarditis,restrictive cardiomyopathy,or tension pneumothorax can lead to precipitous falls in CO.Obstructive shock can mirror cardiogenic shock on clinical exam due to peripheral vasoconstriction,increased jugular venous pressure,and tachycardia
29、but is notable for the absence of pulmonary rales.With such a diverse number of etiologies of shock,causes may present similarly or occur simultaneously.Diagnosing the underlying pathophysiology is of paramount importance to prevent significant end organ failure and death.Once treatment has begun,mo
30、nitoring for the improvement of shock as well as for the unmasking of other contributors is critical,as the treatments can vary greatly and run in opposition to each other.III.MonitoringIIIa.Blood pressure monitoringBlood pressure is perhaps the oldest form of perfusion monitoring outside of the phy
31、sical exam.It is monitored either statically by sphygmomanometers at the extremities or continuously via arterial catheters.Organ systems each autoregulate their own blood flow Simmons and VentetuoloPage 3Curr Opin Crit Care.Author manuscript;available in PMC 2018 June 01.Author ManuscriptAuthor Man
32、uscriptAuthor ManuscriptAuthor Manuscriptand as such there can be no absolute measurement of blood pressure that ensures or precludes adequate individual organ perfusion,hence the need for other modalities that are used in tandem.Generally,a mean arterial pressure(MAP)less than 65 mm Hg is considere
33、d pathological,and studies have shown that MAPs above this threshold were not associated with evidence of hypoperfusion or mortality(13).Lower targets and controlled hypotension(maintaining systolic blood pressure 70 mm Hg)may be preferable in trauma patients with hemorrhagic shock,although this app
34、roach remains controversial(14).A recent multicenter RCT comparing a MAP target of either 8085 mm Hg versus 6570 mm Hg showed no differences in survival at 90 days in patients with septic shock,though the higher target led to significantly less use of renal replacement therapy in patients with chron
35、ic systemic hypertension but also a higher incidence of atrial fibrillation(15).IIIb.Venous oxygen saturation monitoringMixed venous oxygen saturation(MvO2 or SvO2)is the percentage saturation of hemoglobin in the pulmonary artery measured from the distal tip of a pulmonary artery catheter(PAC).A de
36、creased SvO22 is a sensitive marker of decreased CO.The SvO2 drops in cardiogenic shock because the transit time of the blood in the peripheral vasculature is prolonged(CO is measured in liters per minute through a relatively fixed composite distance for that volume of blood to travel).Conversely,in
37、 distributive shock,the SvO2 is usually greater than 70%,due to a failure of the peripheral tissues to extract oxygen and microcirculatory shunt;very high values(90%)have been associated with worse outcomes(16).Ventriculoarterial uncoupling with concurrent cardiac dysfunction can also occur in septi
38、c shock and lead to low SvO2 in some cases(17).The major downside of SvO2 is that it can only be obtained by placement of a PAC,the limitations of which are discussed below.Central venous oxygen saturation(ScvO2)can be measured from a venous blood gas drawn from any central venous catheter(preferabl
39、y in the upper extremities),so it is often used as a practical substitute.Multiple studies have questioned the reliability of ScvO2 to predict SvO2(even allowing for+10%error)(1821).ScvO2 is generally regarded as not necessarily equivalent to SvO2 but potentially useful for trending changes with the
40、rapy.The degree and direction of changes in ScvO2 do correlate with SvO2 and a fiberoptic device for continuous ScvO2 monitoring was developed for this purpose(22).While monitoring central venous oxygen saturations may be useful for diagnosing causes of shock and for trending values in individual pa
41、tient(s),as a treatment target normalizing SvO2 does not improve morbidity or mortality in critically ill patients(5,23).Peripheral venous blood gases have no utility in differentiating shock subtypes.IIIc.Measures of central venous pressureCentral venous pressure(CVP)has a normal range of 57 mm Hg
42、in an adult spontaneously breathing patient while supine.The CVP is elevated in obstructive or cardiogenic shock,while it is decreased in septic or hypovolemic shock.CVP can be indirectly measured by the clinical assessment of jugular venous pressure or on ultrasound evaluation of the inferior vena
43、cava(IVC)(see Echocardiography).It can be measured directly via a simple manometer attached to a central venous catheter.The transducer should be aligned with the patients mid chest at the mid-axillary line,at the level of the left atrium.A common pitfall Simmons and VentetuoloPage 4Curr Opin Crit C
44、are.Author manuscript;available in PMC 2018 June 01.Author ManuscriptAuthor ManuscriptAuthor ManuscriptAuthor Manuscriptin CVP measurement is not accounting for the effect of positive end expiratory pressure(PEEP)with positive pressure ventilation(Figure 1)(24).PEEP may have direct effects on cardia
45、c preload,afterload,and ventricular compliance.PEEP can falsely elevate CVP measurements depending on pulmonary compliance and intrathoracic cavity pressure swings by creating resistance to flow.Direct measurement of CVP has the benefit of providing“hard”numbers to compare as the patients condition
46、changes,but requires a central line.CVP has traditionally been used to guide fluid management,but it is not clear that CVP is a precise or accurate measure in the critically ill or that measuring CVP improves outcomes.A systematic review confirmed that there is no relationship between CVP and circul
47、ating blood volume,nor does the CVP predict fluid responsiveness(25).Because of the lack of data supporting its use combined with the challenges related to assuring the accuracy of CVP in critically ill patients many physicians argue the CVP should no longer be used to guide management.IIId.Cardiac
48、echocardiography and ultrasonographyCardiac echocardiography is often useful in the evaluation of patients in shock,providing information about diagnosis(e.g.,assessing for valvular disease,changes in wall motion from acute coronary syndrome,acute cor pulmonale in pulmonary embolism,and pericardial
49、effusion with tamponade)and capturing serial changes in contractile function.Several studies have demonstrated the feasibility of this approach and a recent guideline on the appropriate use of point-of-care ultrasound and echocardiography in critically ill patients has been issued(2629).Echocardiogr
50、aphy may be limited by poor image acquisition due to body habitus as well as operator and interpreter experience.Standard 2-dimensional ultrasound can provide real time assessment of dynamic changes in the IVC which correlate with direct measurement of CVP and are used clinically to predict stroke v