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| ==Natural History== | | ==HIV-TB Coinfection== |
| As the name implies, cardiogenic shock (CS) consists of a [[shock]] of [[cardiac]] origin, with adequate [[intravascular]] volume (therefore ruling out [[hypovolemic]] cause), with [[hypoperfusion]] of [[myocardium]] and peripheral tissues. There are different possible causes for this condition, of which the [[left ventricular]] [[myocardial infarction]] is the most common. There is also the possibility of mechanical [[complications]], arising from the [[myocardial infarction]], leading to the [[pump failure]] that is underneath CS, such as [[mitral regurgitation]] and [[ventricular septal defect]].<ref>{{Cite book | last1 = Hasdai | first1 = David. | title = Cardiogenic shock : diagnosis and treatmen | date = 2002 | publisher = Humana Press | location = Totowa, N.J. | isbn = 1-58829-025-5 | pages = }}</ref> The common basic mechanism underneath CS is the [[ischemia]]. Because of it, the [[myocardium]] fails to contract properly, thereby affecting [[cardiac output]]. This abnormality worsens the initial [[ischemia]], which then deteriorates even further the [[ventricular function]], creating the so called ''"downward spiral"''.<ref name="pmid10391815">{{cite journal| author=Hollenberg SM, Kavinsky CJ, Parrillo JE| title=Cardiogenic shock. | journal=Ann Intern Med | year= 1999 | volume= 131 | issue= 1 | pages= 47-59 | pmid=10391815 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10391815 }} </ref> When [[ischemia]] reaches a point that the [[left ventricular]] [[myocardium]] fails to pump properly, parameters like [[stroke volume]] and [[cardiac output]] will therefore decrease. The [[pressure]] gradient produced between the [[pressure]] within the [[coronary arteries]] and the [[left ventricle]], along with the duration of the [[diastole]], dictate [[myocardial]] [[perfusion]]. This will be compromised by the [[hypotension]] and the [[tachycardia]], worsening the [[myocardial]] [[ischemia]] and the [[perfusion]] of other vital organs. The fact that the [[heart]] is the only organ that benefits from a low [[blood pressure]], as [[afterload]] decreases, makes these [[hemodynamic|hemodynamical]] changes both beneficial and detrimental. The [[pump failure]] will then decrease the ability to push the [[blood]] out of the [[ventricle]], thereby increasing the [[ventricular]] [[diastolic pressure|diastolic pressures]]. This will not only reduce the [[coronary]] [[perfusion pressure]], as it will also increase the [[ventricle]] wall stress, so that the [[myocardial]] [[oxygen]] requirements will also raise, consequently propagating the [[ischemia]].<ref name="pmid10391815">{{cite journal| author=Hollenberg SM, Kavinsky CJ, Parrillo JE| title=Cardiogenic shock. | journal=Ann Intern Med | year= 1999 | volume= 131 | issue= 1 | pages= 47-59 | pmid=10391815 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10391815 }} </ref><ref name="ReynoldsHochman2008">{{cite journal|last1=Reynolds|first1=H. R.|last2=Hochman|first2=J. S.|title=Cardiogenic Shock: Current Concepts and Improving Outcomes|journal=Circulation|volume=117|issue=5|year=2008|pages=686–697|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.106.613596}}</ref><ref>{{Cite book | last1 = Hasdai | first1 = David. | title = Cardiogenic shock : diagnosis and treatmen | date = 2002 | publisher = Humana Press | location = Totowa, N.J. | isbn = 1-58829-025-5 | pages = }}</ref>
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| | Recommendations for the treatment of tuberculosis in [[HIV]]-infected adults: |
| | The recommended treatment of TB disease in HIV-infected adults (when the disease is caused by organisms that are known or presumed to be susceptible to first-line drugs) is a 6-month regimen consisting of: |
| | *For the first 2 months: An initial phase of [[isoniazid]] (INH), a [[rifamycin]], [[pyrazinamide]] (PZA), and [[ethambutol]] (EMB). |
| | *For the last 4 months: A continuation phase of INH and a rifamycin. |
| | *Patients with advanced HIV (CD4 counts < 100/µl) should be treated with daily or three-times-weekly therapy in both the initial and the continuation phases. |
| | *Twice weekly therapy may be considered in patients with less-advanced immunosuppression (CD4 counts ≥ 100/µl). |
| | *Once-weekly INH/rifapentine in the continuation phase should not be used in any HIV-infected patient. |
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| Other important reference to make in the setting of [[cardiac]] [[pump failure]] and [[hypoperfusion]] of the peripheral tissues is that this last one, leads to the release of [[catecholamines]]. [[Catecholamines]] such as [[norepinephrine]], will increase the [[heart]]'s [[contractility]] and peripheral [[blood flow]], by causing constriction of [[arterioles]], together with [[angiotensin II]], to maintain [[perfusion]], however, this will also increase the [[heart]]'s [[oxygen]] demand and have proarrhythmic and [[cardiotoxic|myocardiotoxic]] consequences. The increased [[SVR]] coupled with the low [[cardiac output]] will lead to an even more pronounced reduction of tissue perfusion.<ref name="ReynoldsHochman2008">{{cite journal|last1=Reynolds|first1=H. R.|last2=Hochman|first2=J. S.|title=Cardiogenic Shock: Current Concepts and Improving Outcomes|journal=Circulation|volume=117|issue=5|year=2008|pages=686–697|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.106.613596}}</ref>
| | Recommendations for the treatment of tuberculosis in [[HIV]]-infected adults are, with a few exceptions, the same as those for HIV-uninfected adults. The [[INH]]--[[rifapentine]] once weekly continuation phase is contraindicated in HIV-infected patients because of an unacceptably high rate of relapse, frequently with organisms that have acquired resistance to [[rifamycin]]s. The development of acquired [[rifampin]] [[drug resistance|resistance]] has also been noted among HIV-infected patients with advanced [[immunosuppression]] treated with twice weekly rifampin- or [[rifabutin]]-based regimens. Consequently, patients with [[CD4]]+ cell counts <100/µl should receive daily or three times weekly treatment. DOT and other adherence-promoting strategies are especially important for patients with HIV-related tuberculosis. |
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| The [[ischemia]] generated by all these processes increases the [[diastolic]] stiffness of the [[ventricle]] wall and this, along with the [[left ventricular dysfunction]], will increase the [[left atrial]] pressure. The increased [[left atrial]] pressure will propagate through the [[pulmonary veins]], generating [[pulmonary congestion]], which by decreasing [[oxygen]] exchanges, leads to [[hypoxia]]. The [[hypoxia]] will further worsen the [[ischemia]] of the [[myocardium]] and the [[pulmonary congestion]] will propagate its effect through the [[pulmonary arteries]] to the [[right ventricle]], hence jeopardizing its performance. Once [[myocardial]] function is affected, the body will put in motion compensatory mechanisms to try to increase the [[cardiac output]]. These include:<ref>{{Cite book | last1 = Hasdai | first1 = David. | title = Cardiogenic shock : diagnosis and treatmen | date = 2002 | publisher = Humana Press | location = Totowa, N.J. | isbn = 1-58829-025-5 | pages = }}</ref>
| | Management of HIV-related tuberculosis is complex and requires expertise in the management of both HIV disease and tuberculosis. Because HIV-infected patients are often taking numerous medications, some of which interact with antituberculosis medications, it is strongly encouraged that experts in the treatment of HIV-related tuberculosis be consulted. A particular concern is the interaction of [[rifamycin]]s with [[antiretroviral agent]]s and other antiinfective drugs. [[Rifampin]] can be used for the treatment of tuberculosis with certain combinations of antiretroviral agents. [[Rifabutin]], which has fewer problematic drug interactions, may also be used in place of rifampin and appears to be equally effective although the doses of rifabutin and antiretroviral agents may require adjustment. As new antiretroviral agents and more pharmacokinetic data become available, these recommendations are likely to be modified. |
| *[[Tachycardia]] and increased [[contractility]] through [[sympathetic]] stimulation
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| *Activation of the [[RAAS|renin/angiotensin/aldosterone system]], leading to fluid retention and consequently increased [[preload]]
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| However, these compensatory mechanisms eventually become maladaptive seeing that:<ref name="ReynoldsHochman2008">{{cite journal|last1=Reynolds|first1=H. R.|last2=Hochman|first2=J. S.|title=Cardiogenic Shock: Current Concepts and Improving Outcomes|journal=Circulation|volume=117|issue=5|year=2008|pages=686–697|issn=0009-7322|doi=10.1161/CIRCULATIONAHA.106.613596}}</ref><ref>{{Cite book | last1 = Hasdai | first1 = David. | title = Cardiogenic shock : diagnosis and treatmen | date = 2002 | publisher = Humana Press | location = Totowa, N.J. | isbn = 1-58829-025-5 | pages = }}</ref>
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| *[[Tachycardia]] and increased [[contractility]] will increase [[myocardium|cardiac muscle]] [[oxygen]] demand, thereby exacerbating the initial [[ischemia]];
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| *[[Vasoconstriction]], as a response to impaired [[cardiac output]], in order to try to maintain [[coronary artery]] [[perfusion]] and systemic [[blood pressure]] ([[SVR]]) increases [[myocardial]] [[afterload]], leading to an impairment in [[myocardial]] performance and an increase in its [[oxygen]] demand, worsening [[ischemia]];
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| *The activation of the neurohormonal cascade will promote retention of [[water retention|water]] and [[sodium]], in order to compensate for the [[hypotension]] and improve [[perfusion]], yet this will also exacerbate [[pulmonary edema]].
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| The prolonged systemic [[hypoperfusion]] and [[hypoxia]] will cause a shift in [[cellular metabolism]], prioritizing [[glycolysis]], leading to a state of [[lactic acidosis]], which jeopardizes [[contractility]] and [[systolic]] performance, thereby affecting the previously described system.
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| All these factors affecting [[oxygen]] demand and [[cardiac]] performance create a vicious cycle that if not interrupted, may eventually lead to death. The [[therapeutic]] approach to cardiogenic shock focuses in disrupting this cycle.<ref>{{Cite book | last1 = Hasdai | first1 = David. | title = Cardiogenic shock : diagnosis and treatmen | date = 2002 | publisher = Humana Press | location = Totowa, N.J. | isbn = 1-58829-025-5 | pages = }}</ref>
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| Besides the area of original [[infarct]], remote territories may also exhibit some kind of [[myocardial]] damage, called [[myocardial stunning]], in response to an [[ischemic]] insult which further reduces [[myocardial]] performance. [[Myocardial stunning]] is the name given the [[myocardium]] which remains dysfunctional even though the restoration to normal [[perfusion]]. The pathophysiology of [[myocardial stunning]] is multifactorial and involves [[calcium]] overload in the [[sarcolemma]] and [[diastolic dysfunction]], as well as the release of [[myocardial]] depressant substances. This [[calcium]] overload is responsible for the activation of [[proteases]] called [[calpain|calpains]]. These and other [[proteases]] will be responsible for the degradation of [[Myofilament|myofilaments]], which will decrease the response to [[calcium]], thereby explaining the temporary [[myocardial]] dysfunction after [[reperfusion]]. Areas of [[stunned myocardium]] may remain stunned after [[revascularization]] due to the need to resynthetize new [[myofilament|myofilaments]].<ref name="pmid10221990">{{cite journal| author=Bolli R, Marbán E| title=Molecular and cellular mechanisms of myocardial stunning. | journal=Physiol Rev | year= 1999 | volume= 79 | issue= 2 | pages= 609-34 | pmid=10221990 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10221990 }} </ref> However, these regions retain contractile reserve and usually respond to [[inotropic]] stimulation. In contrast to [[stunned myocardium]], [[hibernating myocardium]] does respond earlier to [[revascularization]] since [[myocardial]] [[cells]] remain viable and when reperfused, [[calcium]] levels normalize.<ref>{{Cite book | last1 = Hasdai | first1 = David. | title = Cardiogenic shock : diagnosis and treatmen | date = 2002 | publisher = Humana Press | location = Totowa, N.J. | isbn = 1-58829-025-5 | pages = }}</ref><ref name="pmid9647607">{{cite journal| author=Bolli R| title=Basic and clinical aspects of myocardial stunning. | journal=Prog Cardiovasc Dis | year= 1998 | volume= 40 | issue= 6 | pages= 477-516 | pmid=9647607 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9647607 }} </ref><ref name="pmid1991384">{{cite journal| author=Marban E| title=Myocardial stunning and hibernation. The physiology behind the colloquialisms. | journal=Circulation | year= 1991 | volume= 83 | issue= 2 | pages= 681-8 | pmid=1991384 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1991384 }} </ref>
| | On occasion, patients with HIV-related tuberculosis may experience a temporary exacerbation of symptoms, signs, or radiographic manifestations of tuberculosis while receiving antituberculosis treatment. This clinical or radiographic worsening (paradoxical reaction) occurs in HIV-infected patients with active tuberculosis and is thought to be the result of immune reconstitution as a consequence of effective [[antiretroviral therapy]]. Symptoms and signs may include high [[fever]]s, [[lymphadenopathy]], expanding [[central nervous system]] lesions, and worsening of [[chest radiographic]] findings. The diagnosis of a paradoxical reaction should be made only after a thorough evaluation has excluded other [[etiologies]], particularly tuberculosis treatment failure. [[Nonsteroidal antiinflammatory agent]]s may be useful for symptomatic relief. For severe paradoxical reactions, [[prednisone]] (1--2 mg/kg per day for 1--2 weeks, then in gradually decreasing doses) may be used, although there are no data from controlled trials to support this approach. |
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| ===Right Ventricle Myocardial Infarction===
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| Accounts for about 5% of the cases but represents as high [[mortality rate]] as [[left ventricular]] [[shock]]. The [[right ventricular]] regions more commonly affected by [[infarction]] are the inferior and inferior-posterior walls. The [[coronary arteries]] frequently occluded in this setting are the [[right coronary artery]], or the [[left circumflex coronary artery]], in a [[coronary artery dominance|left dominant system]].<ref name="pmid153103">{{cite journal| author=Isner JM, Roberts WC| title=Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease. Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction. | journal=Am J Cardiol | year= 1978 | volume= 42 | issue= 6 | pages= 885-94 | pmid=153103 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=153103 }} </ref><ref name="NgYeghiazarians2011">{{cite journal|last1=Ng|first1=R.|last2=Yeghiazarians|first2=Y.|title=Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies|journal=Journal of Intensive Care Medicine|volume=28|issue=3|year=2011|pages=151–165|issn=0885-0666|doi=10.1177/0885066611411407}}</ref> Patients with [[right coronary artery]] [[occlusion]], in a [[coronary artery dominance|right dominant system]], are at higher risk of developing [[papillary muscle rupture]] and therefore undergoing [[valvular heart disease]], such as [[mitral regurgitation]].<ref name="NgYeghiazarians2011">{{cite journal|last1=Ng|first1=R.|last2=Yeghiazarians|first2=Y.|title=Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies|journal=Journal of Intensive Care Medicine|volume=28|issue=3|year=2011|pages=151–165|issn=0885-0666|doi=10.1177/0885066611411407}}</ref><ref name="pmid7643642">{{cite journal| author=Reeder GS| title=Identification and treatment of complications of myocardial infarction. | journal=Mayo Clin Proc | year= 1995 | volume= 70 | issue= 9 | pages= 880-4 | pmid=7643642 | doi=10.1016/S0025-6196(11)63946-3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7643642 }} </ref><ref name="pmid2190052">{{cite journal| author=Lavie CJ, Gersh BJ| title=Mechanical and electrical complications of acute myocardial infarction. | journal=Mayo Clin Proc | year= 1990 | volume= 65 | issue= 5 | pages= 709-30 | pmid=2190052 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2190052 }} </ref>
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| [[Right ventricle]] failure may affect [[left ventricular]] performance by several means:<ref name="pmid12706920">{{cite journal| author=Jacobs AK, Leopold JA, Bates E, Mendes LA, Sleeper LA, White H et al.| title=Cardiogenic shock caused by right ventricular infarction: a report from the SHOCK registry. | journal=J Am Coll Cardiol | year= 2003 | volume= 41 | issue= 8 | pages= 1273-9 | pmid=12706920 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12706920 }} </ref><ref name="BrookesRavn1999">{{cite journal|last1=Brookes|first1=C.|last2=Ravn|first2=H.|last3=White|first3=P.|last4=Moeldrup|first4=U.|last5=Oldershaw|first5=P.|last6=Redington|first6=A.|title=Acute Right Ventricular Dilatation in Response to Ischemia Significantly Impairs Left Ventricular Systolic Performance|journal=Circulation|volume=100|issue=7|year=1999|pages=761–767|issn=0009-7322|doi=10.1161/01.CIR.100.7.761}}</ref>
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| *Decrease in [[right ventricular]] output leading to a decrease in [[left ventricular]] filling thereby affecting overall [[cardiac output]];
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| *Increased [[right ventricular]] telediastolic [[pressure]], leading to a shifting of the [[interventricular septum]] into the [[left ventricle]], therefore jeopardizing [[left ventricular]] filling and [[systolic]] function.
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| ===Cardiogenic shock and Inflammatory Mediators===
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| [[Image:Cardiogenic_shock.JPG|center|500px]]
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| ===The Pathophysiologic "Spiral" of Cardiogenic shock===
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| Among patients with acute MI, there is often a downward spiral of hypoperfusion leading to further ischemia which leads to a further reduction in cardiac output and further hypoperfusion. The [[lactic acidosis]] that develops as a result of poor systemic perfusion can further reduce cardiac contractility. Reduced cardiac output leads to activation of the sympathetic nervous system, and the ensuing [[tachycardia]] that develops further exacerbates the myocardial ischemia. The increased left ventricular end diastolic pressures is associated with a rise in wall stress which results in further myocardial ischemia. [[Hypotension]] reduces epicardial perfusion pressure which in turn further increases myocardial ischemia.
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| Patients with cardiogenic shock in the setting of [[STEMI]] more often have multivessel disease, and myocardial ischemia may be present in multiple territories. It is for this reason that multivessel angioplasty may be of benefit in the patient with cardiogenic shock.
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| The multifactorial nature of cardiogenic shock can also be operative in the patient with critical [[aortic stenosis]] who has "spiraled": There is impairment of left ventricular outflow, with a drop in [[cardiac output]] there is greater [[subendocardial]] ischemia and poorer flow in the coronary arteries, this leads to further [[left ventricular systolic dysfunction]], given the subendocardial ischemia, the left ventricle develops [[diastolic dysfunction]] and becomes harder to fill. Inadvertent administration of [[vasodilator]]s and [[venodilator]]s may further reduce cardiac output and accelerate or trigger such a spiral.
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| ===Pathophysiologic Mechanisms to Compensate for Cardiogenic shock===
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| [[Cardiac output]] is the product of [[stroke volume]] and heart rate. In order to compensate for a reduction in stroke volume, there is a rise in the heart rate in patients with cardiogenic shock. As a result of the reduction in [[cardiac output]], peripheral tissues extract more oxygen from the limited blood that does flow to them, and this leaves the blood deoxygenated when it returns to the right heart resulting in a fall in the mixed venous oxygen saturation.
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| ===Pathophysiology of Multiorgan Failure===
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| The poor perfusion of organs results in [[hypoxia]] and [[metabolic acidosis]]. Inadequate perfusion to meet the metabolic demands of the brain, kidneys and heart leads to multiorgan failure.
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| ++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++
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| Differential Diagnosis
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| {| style="border: 2px solid #A8A8A8; font-size: 70%;" align="center"
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| |+ <SMALL>''Classification of shock based on hemodynamic parameters.'' (CO, cardiac output; CVP; central venous pressure; PAD, pulmonary artery diastolic pressure; PAS, pulmonary artery systolic pressure; RVD, right ventricular diastolic pressure; RVS, right ventricular systolic pressure; SVO2, systemic venous oxygen saturation; SVR, systemic vascular resistance.)<ref name="isbn0-683-06754-0">{{Cite book | last1 = Parrillo | first1 = Joseph E. | last2 = Ayres | first2 = Stephen M. | title = Major issues in critical care medicine | date = 1984 | publisher = William Wilkins | location = Baltimore | isbn = 0-683-06754-0 | pages = }}</ref><ref name="isbn9781405179263">{{cite book | author = Judith S. Hochman, E. Magnus Ohman | authorlink = | editor = | others = | title = Cardiogenic Shock | edition = | language = | publisher = Wiley-Blackwell | location = | year = 2009 | origyear = | pages = | quote = | isbn = 9781405179263 | oclc = | doi = | url = | accessdate = }}</ref></SMALL>
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| | align="center" style="background: #A8A8A8; width: 100px;"| '''Type of Shock'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''Etiology'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''CO'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''SVR'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''PCWP'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''CVP'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''SVO2'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''RVS'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''RVD'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''PAS'''
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| | align="center" style="background: #A8A8A8; width: 50px;" | '''PAD'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC; width: 80px;" align=center rowspan=4 | '''Cardiogenic'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC; width: 20%;" | '''[[Ventricular septal defect|Acute Ventricular Septal Defect]]'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑ — ↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" | '''[[Mitral regurgitation|Acute Mitral Regurgitation]]'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑ — ↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" | '''[[Myocardium|Myocardial Dysfunction]]'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" | '''[[RV infarction|Right Ventricular Infarction]]'''
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓ — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓ — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓ — ↑
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" rowspan=2 align=center | '''Obstructive'''
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| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" | '''[[Pulmonary embolism|Pulmonary Embolism]]'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓ — ↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓ — ↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓ — ↑
| |
| |-
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" |'''[[Cardiac tamponade|Cardiac Tamponade]]'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓ — ↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↑
| |
| |-
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" rowspan=2 align=center | '''Distributive'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" | '''[[Septic shock|Septic Shock]]'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓ — ↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑ — ↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
| |
| |-
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" | '''[[Anaphylactic shock|Anaphylactic Shock]]'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓ — ↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↑ — ↑↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #DCDCDC;" align=center |↓
| |
| |-
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" rowspan=1 align=center | '''Hypovolemic'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" | '''[[Volume depletion|Volume Depletion]]'''
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↑
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |N — ↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓
| |
| | style="font-size: 90%; padding: 0 5px; background: #F5F5F5;" align=center |↓
| |
| |}
| |
| | |
| ==References==
| |
| {{Reflist|2}}
| |