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{{Cardiogenic shock}}
[[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Cardiogenic_shock]]
{{CMG}}; {{AE}} {{JS}} {{sali}}
{{CMG}}; {{AE}} {{JS}} {{sali}} {{RG}}


==Overview==
==Overview==
[[Shock]] is a clinical [[syndrome]] resulting from the [[hypoperfusion]] of the [[tissues]]. Regardless of the underlying cause, this [[hypoperfusion]] leads to the failure to meet tissues' [[nutritional]] and [[oxygen]] needs, causing [[cellular]] dysfunction. The affected [[tissues]] lead to the production and release of [[inflammatory]] mediators that will further jeopardize [[perfusion]] through changes in the [[vasculature]]. The results of these changes are [[organ failure]] and death if treatment in not timely applied. According to the underlying cause, there will be different types of [[shock]], which will have similar presentations. It is mandatory to determine the underlying cause of the condition so that proper treatment may be started.<ref>{{Cite book  | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages =  }}</ref>
[[Shock]] is a clinical [[syndrome]] resulting from the [[hypoperfusion]] of the [[tissues]]. Regardless of the underlying cause, this [[hypoperfusion]] leads to the failure to meet tissues' [[nutritional]] and [[oxygen]] needs, causing [[cellular]] dysfunction. The affected [[tissues]] lead to the production and release of [[inflammatory]] mediators that will further jeopardize [[perfusion]] through changes in the [[vasculature]]. The results of these changes are [[organ failure]] and death if treatment in not timely applied. According to the underlying cause, there will be different types of [[shock]], which will have similar presentations. It is mandatory to determine the underlying cause of the condition so that proper treatment may be started. [[Cardiogenic shock]] is a clinical condition, defined as a state of systemic [[hypoperfusion]] originated in [[heart failure|cardiac failure]], in the presence of adequate [[intravascular]] volume, typically followed by [[hypotension]], which leads to insufficient ability to meet [[oxygen]] and [[nutrient]] demands of [[organs]] and other peripheral tissues. It may range from mild to severe [[hypoperfusion]] and may be defined in terms of [[hemodynamic]] parameters, which according to most studies, means a state in which [[systolic blood pressure]] is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right [[ventricular]] filling pressures that does not respond to isolated fluid administration, is secondary to [[heart failure|cardiac failure]] and occurs with signs of [[hypoperfusion]] ([[oliguria]], [[cool extremities]], [[cyanosis]] and [[altered mental status]]) or a [[cardiac index]] of < 2.2 L/min/m² (on [[inotropic]], [[vasopressor]] or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and [[pulmonary artery wedge pressure]] > 18 mm Hg.
 
'''Cardiogenic shock''' is a clinical condition, defined as a state of systemic [[hypoperfusion]] originated in [[heart failure|cardiac failure]], in the presence of adequate [[intravascular]] volume, typically followed by [[hypotension]], which leads to insufficient ability to meet [[oxygen]] and [[nutrient]] demands of [[organs]] and other peripheral tissues.<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> It may range from mild to severe [[hypoperfusion]] and may be defined in terms of [[hemodynamic]] parameters, which according to most studies, means a state in which [[systolic blood pressure]] is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right [[ventricular]] filling pressures that does not respond to isolated fluid administration, is secondary to [[heart failure|cardiac failure]] and occurs with signs of [[hypoperfusion]] ([[oliguria]], [[cool extremities]], [[cyanosis]] and [[altered mental status]]) or a [[cardiac index]] of < 2.2 L/min/m² (on [[inotropic]], [[vasopressor]] or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and pulmonary artery wedge pressure > 18 mm Hg.<ref>{{cite book | last = Hochman | first = Judith | title = Cardiogenic shock | publisher = Wiley-Blackwell | location = Chichester, West Sussex, UK Hoboken, NJ | year = 2009 | isbn = 1405179260  }}</ref><ref name="GoldbergGore1991">{{cite journal|last1=Goldberg|first1=Robert J.|last2=Gore|first2=Joel M.|last3=Alpert|first3=Joseph S.|last4=Osganian|first4=Voula|last5=de Groot|first5=Jacques|last6=Bade|first6=Jurgen|last7=Chen|first7=Zuoyao|last8=Frid|first8=David|last9=Dalen|first9=James E.|title=Cardiogenic Shock after Acute Myocardial Infarction|journal=New England Journal of Medicine|volume=325|issue=16|year=1991|pages=1117–1122|issn=0028-4793|doi=10.1056/NEJM199110173251601}}</ref><ref name="GoldbergSamad1999">{{cite journal|last1=Goldberg|first1=Robert J.|last2=Samad|first2=Navid A.|last3=Yarzebski|first3=Jorge|last4=Gurwitz|first4=Jerry|last5=Bigelow|first5=Carol|last6=Gore|first6=Joel M.|title=Temporal Trends in Cardiogenic Shock Complicating Acute Myocardial Infarction|journal=New England Journal of Medicine|volume=340|issue=15|year=1999|pages=1162–1168|issn=0028-4793|doi=10.1056/NEJM199904153401504}}</ref><ref>{{Cite journal  | last1 = Menon | first1 = V. | last2 = Slater | first2 = JN. | last3 = White | first3 = HD. | last4 = Sleeper | first4 = LA. | last5 = Cocke | first5 = T. | last6 = Hochman | first6 = JS. | title = Acute myocardial infarction complicated by systemic hypoperfusion without hypotension: report of the SHOCK trial registry. | journal = Am J Med | volume = 108 | issue = 5 | pages = 374-80 | month = Apr | year = 2000 | doi =  | PMID = 10759093 }}</ref><ref name="Hasdai-1999">{{Cite journal  | last1 = Hasdai | first1 = D. | last2 = Holmes | first2 = DR. | last3 = Califf | first3 = RM. | last4 = Thompson | first4 = TD. | last5 = Hochman | first5 = JS. | last6 = Pfisterer | first6 = M. | last7 = Topol | first7 = EJ. | title = Cardiogenic shock complicating acute myocardial infarction: predictors of death. GUSTO Investigators. Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occluded Coronary Arteries. | journal = Am Heart J | volume = 138 | issue = 1 Pt 1 | pages = 21-31 | month = Jul | year = 1999 | doi =  | PMID = 10385759 }}</ref><ref name="Fincke-2004">{{Cite journal  | last1 = Fincke | first1 = R. | last2 = Hochman | first2 = JS. | last3 = Lowe | first3 = AM. | last4 = Menon | first4 = V. | last5 = Slater | first5 = JN. | last6 = Webb | first6 = JG. | last7 = LeJemtel | first7 = TH. | last8 = Cotter | first8 = G. | title = Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. | journal = J Am Coll Cardiol | volume = 44 | issue = 2 | pages = 340-8 | month = Jul | year = 2004 | doi = 10.1016/j.jacc.2004.03.060 | PMID = 15261929 }}</ref><ref name="DzavikCotter2007">{{cite journal|last1=Dzavik|first1=V.|last2=Cotter|first2=G.|last3=Reynolds|first3=H. R.|last4=Alexander|first4=J. H.|last5=Ramanathan|first5=K.|last6=Stebbins|first6=A. L.|last7=Hathaway|first7=D.|last8=Farkouh|first8=M. E.|last9=Ohman|first9=E. M.|last10=Baran|first10=D. A.|last11=Prondzinsky|first11=R.|last12=Panza|first12=J. A.|last13=Cantor|first13=W. J.|last14=Vered|first14=Z.|last15=Buller|first15=C. E.|last16=Kleiman|first16=N. S.|last17=Webb|first17=J. G.|last18=Holmes|first18=D. R.|last19=Parrillo|first19=J. E.|last20=Hazen|first20=S. L.|last21=Gross|first21=S. S.|last22=Harrington|first22=R. A.|last23=Hochman|first23=J. S.|title=Effect of nitric oxide synthase inhibition on haemodynamics and outcome of patients with persistent cardiogenic shock complicating acute myocardial infarction: a phase II dose-ranging study|journal=European Heart Journal|volume=28|issue=9|year=2007|pages=1109–1116|issn=0195-668X|doi=10.1093/eurheartj/ehm075}}</ref>


==Differential Diagnosis==
==Differential Diagnosis==
Depending on the author and the source used there will be different ways of organizing the types of [[shock]]. Sometimes it might be difficult to differentiate, from the clinical standpoint, two types of [[shock]] since components of each type may combine in a single patient. The clinical presentation of [[shock]] is usually the result of a complexity of processes, such as the [[sympathetic]] and [[endocrine]] responses to [[hypoperfusion]], along with manifestations of [[organ failure]]. Patients who present with [[signs]] and [[symptoms]] of [[hypoperfusion]] following a diagnosed or suspected [[myocardial infarction]], are commonly suffering a cardiogenic shock as a [[complication]] of the [[MI]]. However, other clinical scenarios, not related to acute [[MI]], may present similarly:<ref>{{Cite book  | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages =  }}</ref><ref>{{cite book | last = Parrillo | first = Joseph | title = Critical care medicine principles of diagnosis and management in the adult | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2013 | isbn = 0323089291 }}</ref>
Depending on the author and the source used there will be different ways of organizing the types of [[shock]]. Sometimes it might be difficult to differentiate, from the clinical standpoint, two types of [[shock]] since components of each type may combine in a single patient. The clinical presentation of [[shock]] is usually the result of a complexity of processes, such as the [[sympathetic]] and [[endocrine]] responses to [[hypoperfusion]], along with manifestations of [[organ failure]]. Patients who present with [[signs]] and [[symptoms]] of [[hypoperfusion]] following a diagnosed or suspected [[myocardial infarction]], are commonly suffering a [[cardiogenic shock]] as a [[complication]] of the [[MI]]. However, other clinical scenarios, not related to acute [[MI]], may present similarly:<ref>{{Cite book  | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages =  }}</ref><ref>{{cite book | last = Parrillo | first = Joseph | title = Critical care medicine principles of diagnosis and management in the adult | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2013 | isbn = 0323089291 }}</ref>
:*'''[[Hypovolemic shock]]'''
:*'''[[Hypovolemic shock]]'''
::*More than a simple loss of [[intravascular]] volume, [[hypovolemic shock]] is a dynamic process in which the responses to the initial insult, and the period of time during which they are in practice, will dictate the response to treatment and therefore the [[outcome]]. Several causes may be in the origin of this type of [[shock]], including: [[hemorrhage]], [[dehydration]], [[GI]] or [[urinary]] losses and severe [[vasodilation|venodilation]] (in the setting of other conditions). There is a relationship between the clinical status of the patient and the amount of circulating [[blood]] volume, the [[signs]] may include  [[pallor]], [[cool extremities]], [[tachycardia]] and [[tachypnea]], [[oliguria]] and decreased [[consciousness]]. Compensatory mechanisms are responsible for tolerating initial [[blood loss]], however they begin to fail after about 20-25% of [[blood]] has been lost. This tolerance will be dictated mostly by the previous [[cardiac]] reserve of the patient, along with the velocity of loss of [[intravascular]] volume.
::*More than a simple loss of [[intravascular]] volume, [[hypovolemic shock]] is a dynamic process in which the responses to the initial insult, and the period of time during which they are in practice, will dictate the response to treatment and therefore the [[outcome]]. Several causes may be in the origin of this type of [[shock]], including: [[hemorrhage]], [[dehydration]], [[GI]] or [[urinary]] losses and severe [[vasodilation|venodilation]] (in the setting of other conditions). There is a relationship between the clinical status of the patient and the amount of circulating [[blood]] volume, the [[signs]] may include  [[pallor]], [[cool extremities]], [[tachycardia]] and [[tachypnea]], [[oliguria]] and decreased [[consciousness]]. Compensatory mechanisms are responsible for tolerating initial [[blood loss]], however they begin to fail after about 20-25% of [[blood]] has been lost. This tolerance will be dictated mostly by the previous [[cardiac]] reserve of the patient, along with the velocity of loss of [[intravascular]] volume<ref name="pmid29404656">{{cite journal |vauthors=Lier H, Bernhard M, Hossfeld B |title=[Hypovolemic and hemorrhagic shock] |language=German |journal=Anaesthesist |volume=67 |issue=3 |pages=225–244 |date=March 2018 |pmid=29404656 |doi=10.1007/s00101-018-0411-z |url=}}</ref><ref name="pmid23153876">{{cite journal |vauthors=Kobayashi L, Costantini TW, Coimbra R |title=Hypovolemic shock resuscitation |journal=Surg. Clin. North Am. |volume=92 |issue=6 |pages=1403–23 |date=December 2012 |pmid=23153876 |doi=10.1016/j.suc.2012.08.006 |url=}}</ref>.
::*When comparing [[hypovolemic shock|hypovolemic]] and [[cardiogenic shock]] (most commonly complicating acute-[[MI]]) some specific clinical [[signs]] of [[shock]] will be similar, however, others will be different, particularly [[signs]] of [[CHF]], such as the presence of distended [[jugular]] and peripheral [[veins]], presence of an [[S3]] sound and [[pulmonary edema]] on the cardiogenic type.
::*When comparing [[hypovolemic shock|hypovolemic]] and [[cardiogenic shock]] (most commonly complicating acute-[[MI]]) some specific clinical [[signs]] of [[shock]] will be similar, however, others will be different, particularly [[signs]] of [[CHF]], such as the presence of distended [[jugular]] and peripheral [[veins]], presence of an [[S3]] sound and [[pulmonary edema]] on the cardiogenic type.
::*When comparing [[hemodynamic]] data, similarities include: decreased [[cardiac index]], [[stroke volume]] index, [[cardiac output]], mixed [[venous]] [[oxygen saturation]] and increased difference in arteriovenous O<sub>2</sub> saturation and [[SVR]]. Differences to be noted include: decreased [[ventricular]] [[preload]], [[ventricular]] [[diastolic]] volumes and pressures, [[pulmonary wedge pressure]] and [[central venous pressure]].
::*When comparing [[hemodynamic]] data, similarities include: decreased [[cardiac index]], [[stroke volume]] index, [[cardiac output]], mixed [[venous]] [[oxygen saturation]] and increased difference in arteriovenous O<sub>2</sub> saturation and [[SVR]].  
::*When treating hypovolemic shock it's mandatory to rule out cardiogenic cause because part of the treatment for [[hypovolemic shock]], urgent intravascular volume replacement, may further jeopardize the [[cardiac]] condition in the cardiogenic form.
Differences to be noted include:  
:<math>\mbox{Shock index} = \frac{heart\ rate}{systolic\ blood\ pressure}</math>
 
Other measures include:
decreased [[ventricular]] [[preload]], [[ventricular]] [[diastolic]] volumes and pressures, [[pulmonary wedge pressure]] and [[central venous pressure]].
::*When treating [[hypovolemic shock]] it's mandatory to rule out [[cardiogenic]] cause because part of the treatment for [[hypovolemic shock]], urgent [[intravascular]] volume replacement, may further jeopardize the [[cardiac]] condition in the cardiogenic form.


:*'''[[Obstructive shock]]'''
:*'''[[Obstructive shock]]'''
::*This form of [[shock]] results from an obstruction to the [[flow]] of [[blood]] through the [[cardiovascular system]], including the [[vessels]] and the [[heart]]. Therefore, different causes may give rise to this condition, such as: [[tension pneumothorax]], [[pulmonary emboli]], [[pericardial tamponade]] and [[constrictive pericarditis]].<ref name="urlShock: Shock and Fluid Resuscitation: Merck Manual Professional">{{cite web |url=http://www.merck.com/mmpe/sec06/ch067/ch067b.html#sec06-ch067-ch067b-490 |title=Shock: Shock and Fluid Resuscitation: Merck Manual Professional |format= |work= |accessdate=}}</ref> As in other types of [[shock]], the clinical response will be heavily dictated by the timespan during which the insult develops and urgent therapy must be applied.
::*This form of [[shock]] results from an obstruction to the [[flow]] of [[blood]] through the [[cardiovascular system]], including the [[vessels]] and the [[heart]]. Therefore, different causes may give rise to this condition, such as: [[tension pneumothorax]], [[pulmonary emboli]], [[pericardial tamponade]] and [[constrictive pericarditis]].<ref name="urlShock: Shock and Fluid Resuscitation: Merck Manual Professional">{{cite web |url=http://www.merck.com/mmpe/sec06/ch067/ch067b.html#sec06-ch067-ch067b-490 |title=Shock: Shock and Fluid Resuscitation: Merck Manual Professional |format= |work= |accessdate=}}</ref> As in other types of [[shock]], the clinical response will be heavily dictated by the timespan during which the insult develops and urgent therapy must be applied<ref name="pmid25994928">{{cite journal |vauthors=Pich H, Heller AR |title=[Obstructive shock] |language=German |journal=Anaesthesist |volume=64 |issue=5 |pages=403–19 |date=May 2015 |pmid=25994928 |doi=10.1007/s00101-015-0031-9 |url=}}</ref><ref name="pmid28613734">{{cite journal |vauthors=Dababneh E, Siddique MS |title= |journal= |volume= |issue= |pages= |date= |pmid=28613734 |doi= |url=}}</ref>.
::*To evaluate the [[hemodynamics]] of [[obstructive shock]] it is important to know the underlying etiology of the [[shock]], since different causes will present with different [[hemodynamic]] values. One example of cause of [[obstructive shock]] is [[cardiac tamponade]], which, similarly to the cardiogenic form, will likely present with: decreased [[cardiac index]], [[stroke volume]], stroke work, mixed [[venous]] [[oxygen saturation]] and increased difference in arteriovenous O<sub>2</sub> saturation, right and left [[ventricular]] diastolic pressures, pulmonary artery diastolic pressure, serum [[lactate]] and [[central venous pressure|CVP]]. Other causes may be observed on the table below.
::*To evaluate the [[hemodynamics]] of [[obstructive shock]] it is important to know the underlying etiology of the [[shock]], since different causes will present with different [[hemodynamic]] values. One example of cause of [[obstructive shock]] is [[cardiac tamponade]], which, similarly to the cardiogenic form, will likely present with: decreased [[cardiac index]], [[stroke volume]], stroke work, mixed [[venous]] [[oxygen saturation]] and increased difference in arteriovenous O<sub>2</sub> saturation, right and left [[ventricular]] [[diastolic]] pressures, [[pulmonary]] [[artery]] [[diastolic]] pressure, serum [[lactate]] and [[central venous pressure|CVP]]. Other causes may be observed on the table below.


:*'''[[Distributive shock]]'''
:*'''[[Distributive shock]]'''
::*The hallmark of this form of [[shock]] is the decrease of [[peripheral resistance]]. This may be present in a series of conditions that may lead to [[distributive shock]], such as: [[sepsis]], [[anaphylaxis]], [[toxic shock syndrome]] and [[adrenal crisis]].
::*The hallmark of this form of [[shock]] is the decrease of [[peripheral resistance]]. This may be present in a series of conditions that may lead to [[distributive shock]], such as: [[sepsis]], [[anaphylaxis]], [[toxic shock syndrome]] and [[adrenal crisis]].
::*When compared to [[cardiogenic shock]] it presents with similarities, such as: decreased [[cardiac index]], left and right [[ventricular]] stroke work and increased [[serum]] [[lactate]]. The differences reside in: overall decreased of [[SVR]], which after fluid resuscitation may become elevated, [[ventricular]] filling pressure, difference in arteriovenous O<sub>2</sub> saturation and increase of mixed [[venous]] [[oxygen saturation]]. It is important to note that, unlike [[cardiogenic shock|cardiogenic]] and other types of [[shock]], in the [[distributive shock|distributive]] kind there is an increase in [[venous]] [[oxygen saturation]] which, despite the increased O<sub>2</sub> demand, might be due to the increased total body [[perfusion]], that is responsible for diminishing the effectiveness of individual tissue [[perfusion]].
::*When compared to [[cardiogenic shock]] it presents with similarities, such as: decreased [[cardiac index]], left and right [[ventricular]] stroke work and increased [[serum]] [[lactate]]. The differences reside in: overall decreased of [[SVR]], which after fluid resuscitation may become elevated, [[ventricular]] filling pressure, difference in arteriovenous O<sub>2</sub> saturation and increase of mixed [[venous]] [[oxygen saturation]]. It is important to note that, unlike [[cardiogenic shock|cardiogenic]] and other types of [[shock]], in the [[distributive shock|distributive]] kind there is an increase in [[venous]] [[oxygen saturation]] which, despite the increased O<sub>2</sub> demand, might be due to the increased total body [[perfusion]], that is responsible for diminishing the effectiveness of individual tissue [[perfusion]]<ref name="pmid29261964">{{cite journal |vauthors=Smith N, Lopez RA, Silberman M |title= |journal= |volume= |issue= |pages= |date= |pmid=29261964 |doi= |url=}}</ref><ref name="pmid28238385">{{cite journal |vauthors=Alyeşil C, Doğan NÖ, Özturan İU, Güney S |title=Distributive Shock in the Emergency Department: Sepsis, Anaphylaxis, or Capillary Leak Syndrome? |journal=J Emerg Med |volume=52 |issue=6 |pages=e229–e231 |date=June 2017 |pmid=28238385 |doi=10.1016/j.jemermed.2017.01.012 |url=}}</ref><ref name="pmid17493496">{{cite journal |vauthors=Brown SG |title=The pathophysiology of shock in anaphylaxis |journal=Immunol Allergy Clin North Am |volume=27 |issue=2 |pages=165–75, v |date=May 2007 |pmid=17493496 |doi=10.1016/j.iac.2007.03.003 |url=}}</ref>.
 
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{| style="border: 2px solid #A8A8A8; font-size: 70%;" align="center"
{| style="border: 8px solid #A8A8A8; font-size: 180%;" align="center"
|+ <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>
|+ ''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>
| align="center" style="background: #A8A8A8; width: 100px;"| '''Type of Shock'''
| align="center" style="background: #A8A8A8; width: 100px;"| '''Type of Shock'''
| align="center" style="background: #A8A8A8; width: 50px;" | '''Etiology'''
| align="center" style="background: #A8A8A8; width: 50px;" | '''Etiology'''
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'''The following table outlines the major differential diagnoses of Shock on the basis of clinical manifestations.'''.<ref name="pmid8704488">{{cite journal |vauthors=Svavarsdóttir AE, Jónasson MR, Gudmundsson GH, Fjeldsted K |title=Chest pain in family practice. Diagnosis and long-term outcome in a community setting |journal=Can Fam Physician |volume=42 |issue= |pages=1122–8 |date=June 1996 |pmid=8704488 |pmc=2146490 |doi= |url=}}</ref><ref name="pmid8163958">{{cite journal |vauthors=Klinkman MS, Stevens D, Gorenflo DW |title=Episodes of care for chest pain: a preliminary report from MIRNET. Michigan Research Network |journal=J Fam Pract |volume=38 |issue=4 |pages=345–52 |date=April 1994 |pmid=8163958 |doi= |url=}}</ref><ref name="pmid19883149">{{cite journal |vauthors=Bösner S, Becker A, Haasenritter J, Abu Hani M, Keller H, Sönnichsen AC, Karatolios K, Schaefer JR, Seitz G, Baum E, Donner-Banzhoff N |title=Chest pain in primary care: epidemiology and pre-work-up probabilities |journal=Eur J Gen Pract |volume=15 |issue=3 |pages=141–6 |date= 2009 |pmid=19883149 |doi=10.3109/13814780903329528 |url=}}</ref><ref name="pmid21391528">{{cite journal |vauthors=Ebell MH |title=Evaluation of chest pain in primary care patients |journal=Am Fam Physician |volume=83 |issue=5 |pages=603–5 |date=March 2011 |pmid=21391528 |doi= |url=}}</ref><ref name="pmid11041906">{{cite journal |vauthors=von Kodolitsch Y, Schwartz AG, Nienaber CA |title=Clinical prediction of acute aortic dissection |journal=Arch. Intern. Med. |volume=160 |issue=19 |pages=2977–82 |date=October 2000 |pmid=11041906 |doi= |url=}}</ref><ref name="pmid2730190">{{cite journal |vauthors=Pate JW, Walker WA, Cole FH, Owen EW, Johnson WH |title=Spontaneous rupture of the esophagus: a 30-year experience |journal=Ann. Thorac. Surg. |volume=47 |issue=5 |pages=689–92 |date=May 1989 |pmid=2730190 |doi= |url=}}</ref><ref name="pmid7954018">{{cite journal |vauthors=Fleet RP, Dupuis G, Marchand A, Burelle D, Beitman BD |title=Panic disorder, chest pain and coronary artery disease: literature review |journal=Can J Cardiol |volume=10 |issue=8 |pages=827–34 |date=October 1994 |pmid=7954018 |doi= |url=}}</ref><ref name="pmid3270082">{{cite journal |vauthors=Bass C, Chambers JB, Kiff P, Cooper D, Gardner WN |title=Panic anxiety and hyperventilation in patients with chest pain: a controlled study |journal=Q. J. Med. |volume=69 |issue=260 |pages=949–59 |date=December 1988 |pmid=3270082 |doi= |url=}}</ref><ref name="pmid64694">{{cite journal |vauthors=Evans DW, Lum LC |title=Hyperventilation: An important cause of pseudoangina |journal=Lancet |volume=1 |issue=8004 |pages=155–7 |date=January 1977 |pmid=64694 |doi= |url=}}</ref><ref name="pmid9246027">{{cite journal |vauthors=Ros E, Armengol X, Grande L, Toledo-Pimentel V, Lacima G, Sanz G |title=Chest pain at rest in patients with coronary artery disease. Myocardial ischemia, esophageal dysfunction, or panic disorder? |journal=Dig. Dis. Sci. |volume=42 |issue=7 |pages=1344–53 |date=July 1997 |pmid=9246027 |doi= |url=}}</ref><ref name="pmid9594945">{{cite journal |vauthors=Ben Freedman S, Tennant CC |title=Panic disorder and coronary artery spasm |journal=Med. J. Aust. |volume=168 |issue=8 |pages=376–7 |date=April 1998 |pmid=9594945 |doi= |url=}}</ref><ref name="pmid17909127">{{cite journal |vauthors=Smoller JW, Pollack MH, Wassertheil-Smoller S, Jackson RD, Oberman A, Wong ND, Sheps D |title=Panic attacks and risk of incident cardiovascular events among postmenopausal women in the Women's Health Initiative Observational Study |journal=Arch. Gen. 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'''''Abbreviations:''''' '''ABG ('''[[arterial blood gas]]'''); ACE ('''[[Angiotensin-converting enzyme|angiotensin converting enzyme]]'''); BMI ('''[[body mass index]]'''); CBC ('''[[Complete blood counts|complete blood count]]'''); CSF ('''[[cerebrospinal fluid]]'''); CXR ('''[[chest X-ray]]'''); ECG ('''[[electrocardiogram]]'''); FEF ('''[[Spirometry|forced expiratory flow rate]]'''); FEV1 ('''[[forced expiratory volume]]'''); FVC ('''[[forced vital capacity]]'''); JVD ('''[[jugular vein distention]]''');''' '''MCV ('''[[mean corpuscular volume]]'''); Plt ('''[[platelet]]'''); RV ('''[[residual volume]]'''); SIADH ('''[[syndrome of inappropriate antidiuretic hormone]]'''); TSH ('''[[thyroid stimulating hormone]]'''); Vt ('''[[tidal volume]]''');''' '''WBC ('''[[White blood cells|white blood cell]]'''); Coronary CT angiography (CCTA); multidetector row scanners (MDCT); Cardiovascular magnetic resonance — CMRI; Myocardial perfusion imaging (MPI); single-photon emission CT (SPECT); Positron emission tomography (PET) scanning; Magnetic resonance (MR) angiography, Computed tomographic (CT) angiography, and Transesophageal echocardiography (TEE), late gadolinium enhancement (LGE); right ventricular hypertrophy (RVH), right atrial enlargement (RAE), functional tricuspid regurgitation (TR), Pulmonary artery systolic pressure (PASP; adenosine deaminase (ADA); Serum amyloid A (SAA), soluble interleukin-2 receptor (sIL2R); High-resolution CT (HRCT) scanning'''   
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="3" |Differentials on the basis of Etiology
! rowspan="3" |Disease
! colspan="10" |Clinical manifestations
! colspan="4" |Diagnosis
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! colspan="8" |Symptoms
! rowspan="2" |Risk factors
! rowspan="2" |Physical exam
! rowspan="2" |Lab Findings
! rowspan="2" |EKG
! rowspan="2" |Imaging
! rowspan="2" |Gold standard
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
!Onset
!Duration
!Quality of Pain
!Cough
!Fever
!Dyspnea
!Weight loss
!Associated Features
|- style="background: #DCDCDC; padding: 5px;" |
|
!'''[[Myocardial Infarction]]'''<ref name="pmid8704488">{{cite journal |vauthors=Svavarsdóttir AE, Jónasson MR, Gudmundsson GH, Fjeldsted K |title=Chest pain in family practice. Diagnosis and long-term outcome in a community setting |journal=Can Fam Physician |volume=42 |issue= |pages=1122–8 |date=June 1996 |pmid=8704488 |pmc=2146490 |doi= |url=}}</ref><ref name="pmid8163958">{{cite journal |vauthors=Klinkman MS, Stevens D, Gorenflo DW |title=Episodes of care for chest pain: a preliminary report from MIRNET. Michigan Research Network |journal=J Fam Pract |volume=38 |issue=4 |pages=345–52 |date=April 1994 |pmid=8163958 |doi= |url=}}</ref><ref name="pmid19883149">{{cite journal |vauthors=Bösner S, Becker A, Haasenritter J, Abu Hani M, Keller H, Sönnichsen AC, Karatolios K, Schaefer JR, Seitz G, Baum E, Donner-Banzhoff N |title=Chest pain in primary care: epidemiology and pre-work-up probabilities |journal=Eur J Gen Pract |volume=15 |issue=3 |pages=141–6 |date= 2009 |pmid=19883149 |doi=10.3109/13814780903329528 |url=}}</ref><ref name="pmid21391528">{{cite journal |vauthors=Ebell MH |title=Evaluation of chest pain in primary care patients |journal=Am Fam Physician |volume=83 |issue=5 |pages=603–5 |date=March 2011 |pmid=21391528 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]]
| style="background: #F5F5F5; padding: 5px;" |Commonly > 20 minutes
| style="background: #F5F5F5; padding: 5px;" |
*Same as [[stable angina]] but often more severe
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Nausea and vomiting]]
*[[Diaphoresis]]
*[[Presyncope]]
*[[Palpitation|Palpitations]]
*[[Lateral]] [[displacement]] of the [[apical impulse]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Dyslipidemia]], [[hypertension]], smoking,  family history of premature disease, and [[diabetes]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Hypotension]]
*[[Tachycardia]]
*[[S4]] [[Gallop rhythm|gallop]]
*[[Paradoxical splitting of S2]]
*[[Mitral regurgitation]] [[Heart murmur|murmur]]
| style="background: #F5F5F5; padding: 5px;" |
*Elevated [[cardiac enzymes]]
*↑[[Brain natriuretic peptide|B-Type Natriuretic Peptide]]
| style="background: #F5F5F5; padding: 5px;" |
*ST elevation MI (STEMI)
*Non-ST elevation MI (NSTEMI) or Non [[Q wave]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Echocardiography]]: ↓ EF
*CCTA: [[Coronory artery]] stenosis
*CMRI: Coronory vessels [[stenosis]]
*MPI on SPECT or PET scanning: Decreased [[myocardial]] perfusion.
| style="background: #F5F5F5; padding: 5px;" |
*CCTA combined with MPI
|- style="background: #DCDCDC; padding: 5px;" |
! rowspan="10" |Cardiac
|- style="background: #DCDCDC; padding: 5px;" |
!'''[[Aortic Dissection]]'''<ref name="pmid28847596">{{cite journal |vauthors=Takagi H, Ando T, Umemoto T |title=Meta-Analysis of Circadian Variation in the Onset of Acute Aortic Dissection |journal=Am. J. Cardiol. |volume=120 |issue=9 |pages=1662–1666 |date=November 2017 |pmid=28847596 |doi=10.1016/j.amjcard.2017.07.067 |url=}}</ref><ref name="pmid11922269">{{cite journal |vauthors=Kojima S, Sumiyoshi M, Nakata Y, Daida H |title=Triggers and circadian distribution of the onset of acute aortic dissection |journal=Circ. J. |volume=66 |issue=3 |pages=232–5 |date=March 2002 |pmid=11922269 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |Sudden severe progressive pain (common) or [[chronic]] (rare)
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |
* Tearing, ripping sensation, knife like
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Focal neurologic deficit]]
*[[Hypotension]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Hypertension]]
* Genetically mediated [[collagen disorders]]
* Preexisting [[aortic aneurysm]]
* [[Bicuspid aortic valve]]
* [[Aortic coarctation]]
* [[Turner syndrome]]
* [[Vasculitis]] ([[giant cell arteritis]], [[Takayasu arteritis]], [[rheumatoid arthritis]], [[syphilitic aortitis]])
| style="background: #F5F5F5; padding: 5px;" |
*[[Pulse]] deficit
*New [[Diastolic murmurs|diastolic murmur]]
*[[Diastolic]] decrescendo [[Heart murmur|murmur]]
*[[Focal neurologic deficit]]
*[[Hypotension]]
| style="background: #F5F5F5; padding: 5px;" |
* [[D-dimer]] <500 ng/mL rules out [[aortic dissection]]
* ↑Soluble ST2 (sST2)
* Measurements of soluble elastin fragments, smooth muscle [[myosin heavy chain]], high-sensitivity [[C-reactive protein (CRP)|C-reactive protein]], [[fibrinogen]], and [[Fibrillin|fibrillin fragments]]
| style="background: #F5F5F5; padding: 5px;" |
* Nonspecific ST and T wave changes
| style="background: #F5F5F5; padding: 5px;" |
*CXR: [[Mediastinal]] and/or [[aortic widening]]
*CTA: A compressed [[true lumen]]
*MRA: Detects differential flow between the true and false lumens, widening of the [[aorta]] with a thickened wall
*TEE: [[Intimal]] [[dissection]] flaps, true and false lumens, [[thrombosis]] in the false lumen
*[[Aortography]]: Distortion of the normal contrast column, Flow reversal or stasis into a false channel, Failure of major branches to fill, and [[Aortic]] [[valvular regurgitation]]
| style="background: #F5F5F5; padding: 5px;" |
*[[CT angiography]]
*[[Digital subtraction aortography]] (if high suspicion)
|- style="background: #DCDCDC; padding: 5px;" |
!'''[[Aortic intramural hematoma]]'''
| style="background: #F5F5F5; padding: 5px;" |Sudden severe progressive pain (common) or [[chronic]] (rare)
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |
* Tearing, ripping sensation, knife like
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Focal neurologic deficit]]
*[[Hypotension]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Hypertension]]
* Genetically mediated [[collagen disorders]]
* Preexisting [[aortic aneurysm]]
* [[Bicuspid aortic valve]]
* [[Aortic coarctation]]
* [[Turner syndrome]]
* [[Vasculitis]] ([[giant cell arteritis]], [[Takayasu arteritis]], [[rheumatoid arthritis]], [[syphilitic aortitis]])
| style="background: #F5F5F5; padding: 5px;" |
*[[Pulse]] deficit
*New [[Diastolic murmurs|diastolic murmur]]
*[[Diastolic]] decrescendo [[Heart murmur|murmur]]
*[[Focal neurologic deficit]]
*[[Hypotension]]
| style="background: #F5F5F5; padding: 5px;" |
* [[D-dimer]] <500 ng/mL rules out [[aortic dissection]]
* ↑Soluble ST2 (sST2)
* Measurements of soluble elastin fragments, smooth muscle [[myosin heavy chain]], high-sensitivity [[C-reactive protein (CRP)|C-reactive protein]], [[fibrinogen]], and [[Fibrillin|fibrillin fragments]]
| style="background: #F5F5F5; padding: 5px;" |
* Nonspecific ST and T wave changes
| style="background: #F5F5F5; padding: 5px;" |
*CXR: [[Mediastinal]] and/or [[aortic widening]]
*CTA: A compressed [[true lumen]]
*MRA: Detects differential flow between the true and false lumens, widening of the [[aorta]] with a thickened wall
*TEE: [[Intimal]] [[dissection]] flaps, true and false lumens, [[thrombosis]] in the false lumen
*[[Aortography]]: Distortion of the normal contrast column, Flow reversal or stasis into a false channel, Failure of major branches to fill, and [[Aortic]] [[valvular regurgitation]]
| style="background: #F5F5F5; padding: 5px;" |
*[[CT angiography]]
*[[Digital subtraction aortography]] (if high suspicion)
|- style="background: #DCDCDC; padding: 5px;" |
!'''[[Penetrating atherosclerotic aortic ulcer]]'''<ref name="EggebrechtBaumgart2003">{{cite journal|last1=Eggebrecht|first1=Holger|last2=Baumgart|first2=Dietrich|last3=Schmermund|first3=Axel|last4=Herold|first4=Ulf|last5=Hunold|first5=Peter|last6=Jakob|first6=Heinz|last7=Erbel|first7=Raimund|title=Penetrating atherosclerotic ulcer of the aorta: treatment by endovascular stent-graft placement|journal=Current Opinion in Cardiology|volume=18|issue=6|year=2003|pages=431–435|issn=0268-4705|doi=10.1097/00001573-200311000-00002}}</ref><ref name="BossoneLaBounty2018">{{cite journal|last1=Bossone|first1=Eduardo|last2=LaBounty|first2=Troy M|last3=Eagle|first3=Kim A|title=Acute aortic syndromes: diagnosis and management, an update|journal=European Heart Journal|volume=39|issue=9|year=2018|pages=739–749d|issn=0195-668X|doi=10.1093/eurheartj/ehx319}}</ref><ref name="DeMartinoSen2018">{{cite journal|last1=DeMartino|first1=Randall R.|last2=Sen|first2=Indrani|last3=Huang|first3=Ying|last4=Bower|first4=Thomas C.|last5=Oderich|first5=Gustavo S.|last6=Pochettino|first6=Alberto|last7=Greason|first7=Kevin|last8=Kalra|first8=Manju|last9=Johnstone|first9=Jill|last10=Shuja|first10=Fahad|last11=Harmsen|first11=W. Scott|last12=Macedo|first12=Thanila|last13=Mandrekar|first13=Jay|last14=Chamberlain|first14=Alanna M.|last15=Weiss|first15=Salome|last16=Goodney|first16=Philip P.|last17=Roger|first17=Veronique|title=Population-Based Assessment of the Incidence of Aortic Dissection, Intramural Hematoma, and Penetrating Ulcer, and Its Associated Mortality From 1995 to 2015|journal=Circulation: Cardiovascular Quality and Outcomes|volume=11|issue=8|year=2018|issn=1941-7713|doi=10.1161/CIRCOUTCOMES.118.004689}}</ref>
| style="background: #F5F5F5; padding: 5px;" |Sudden severe pain
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |
* Tearing, ripping sensation, knife like
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Hypotension]]
*[[Back pain]]
*[[Hypovolemic shock]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Hypertension]]
*[[Smoking]]
*[[Hyperlipidemia]]
*[[Atherosclerosis]]
*Male gender
*Older age
*[[Bicuspid aortic valve]]
*Prior [[aortic]] surgery
*Prior aortic dilatation
| style="background: #F5F5F5; padding: 5px;" |
*[[Hypotension]]
| style="background: #F5F5F5; padding: 5px;" |
_
| style="background: #F5F5F5; padding: 5px;" |
_
| style="background: #F5F5F5; padding: 5px;" |
*CXR: [[Mediastinal]] and/or [[aortic widening]], diffuse or focal enlargement of [[thoracic]] [[descending aorta]], [[pleural effusion]], and deviated [[trachea]]
*CTA: Presence of false [[aneurysm]]
| style="background: #F5F5F5; padding: 5px;" |
*[[CT angiography]]
*Contrast-enhanced CT scan
|- style="background: #DCDCDC; padding: 5px;" |
|- style="background: #DCDCDC; padding: 5px;" |
|- style="background: #DCDCDC; padding: 5px;" |
![[Pericardial Tamponade]]<ref name="pmid20756103">{{cite journal |vauthors=Ewart W |title=Practical Aids in the Diagnosis of Pericardial Effusion, in Connection with the Question as to Surgical Treatment |journal=Br Med J |volume=1 |issue=1838 |pages=717–21 |date=March 1896 |pmid=20756103 |pmc=2406464 |doi= |url=}}</ref><ref name="pmid26320112">{{cite journal |vauthors=Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J, Brucato A, Gueret P, Klingel K, Lionis C, Maisch B, Mayosi B, Pavie A, Ristić AD, Sabaté Tenas M, Seferovic P, Swedberg K, Tomkowski W, Achenbach S, Agewall S, Al-Attar N, Angel Ferrer J, Arad M, Asteggiano R, Bueno H, Caforio AL, Carerj S, Ceconi C, Evangelista A, Flachskampf F, Giannakoulas G, Gielen S, Habib G, Kolh P, Lambrinou E, Lancellotti P, Lazaros G, Linhart A, Meurin P, Nieman K, Piepoli MF, Price S, Roos-Hesselink J, Roubille F, Ruschitzka F, Sagristà Sauleda J, Sousa-Uva M, Uwe Voigt J, Luis Zamorano J |title=2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS) |journal=Eur. Heart J. |volume=36 |issue=42 |pages=2921–64 |date=November 2015 |pmid=26320112 |doi=10.1093/eurheartj/ehv318 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]] or [[subacute]]
| style="background: #F5F5F5; padding: 5px;" |May last for hours to days
| style="background: #F5F5F5; padding: 5px;" |
*Sharp and stabbing [[retrosternal]] pain
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Pulsus paradoxus]]
*[[Pericardial friction rub|Pericardial rub]]
| style="background: #F5F5F5; padding: 5px;" |
*[[HIV]]
*[[TB]]
*[[Immunosuppression]]
*Acute trauma
| style="background: #F5F5F5; padding: 5px;" |
*[[Kussmaul's sign|Kussmaul sign]]
*[[Beck's triad (cardiology)|Beck triad]]
*[[Pulsus paradoxus]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Creatine kinase|Creatine kinase and isoenzymes]]
*Abnormal LFTs
*[[Antinuclear antibody|Antinuclear antibody assay]], [[erythrocyte sedimentation rate]] and [[rheumatoid factor]]
*[[HIV testing]]
| style="background: #F5F5F5; padding: 5px;" |EKG findings:
*[[Sinus tachycardia]]
*Low QRS voltage
*[[Electrical alternans]]
| style="background: #F5F5F5; padding: 5px;" |
*[[CXR]]: enlarged [[cardiac silhouette]] with clear lung fields
*[[Echocardiography]]: Chamber collapse, Respiratory variation in volumes and flows, [[IVC]] [[plethora]]
*[[Swan-Ganz Catheterization]]: Equilibration of average [[intracardiac]] [[diastolic pressures]] (usually between 10 and 30 mmHg) 
| style="background: #F5F5F5; padding: 5px;" |
*[[Echocardiography]]
|- style="background: #DCDCDC; padding: 5px;" |
![[Myocarditis]]<ref name="pmid3974674">{{cite journal |vauthors=Dec GW, Palacios IF, Fallon JT, Aretz HT, Mills J, Lee DC, Johnson RA |title=Active myocarditis in the spectrum of acute dilated cardiomyopathies. Clinical features, histologic correlates, and clinical outcome |journal=N. Engl. J. Med. |volume=312 |issue=14 |pages=885–90 |date=April 1985 |pmid=3974674 |doi=10.1056/NEJM198504043121404 |url=}}</ref><ref name="pmid17493945">{{cite journal |vauthors=Caforio AL, Calabrese F, Angelini A, Tona F, Vinci A, Bottaro S, Ramondo A, Carturan E, Iliceto S, Thiene G, Daliento L |title=A prospective study of biopsy-proven myocarditis: prognostic relevance of clinical and aetiopathogenetic features at diagnosis |journal=Eur. Heart J. |volume=28 |issue=11 |pages=1326–33 |date=June 2007 |pmid=17493945 |doi=10.1093/eurheartj/ehm076 |url=}}</ref><ref name="pmid21239404">{{cite journal |vauthors=Ukena C, Mahfoud F, Kindermann I, Kandolf R, Kindermann M, Böhm M |title=Prognostic electrocardiographic parameters in patients with suspected myocarditis |journal=Eur. J. Heart Fail. |volume=13 |issue=4 |pages=398–405 |date=April 2011 |pmid=21239404 |doi=10.1093/eurjhf/hfq229 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]] or [[subacute]]
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |
* Sharp & localized [[retrosternal]] pain reflects associated [[pericarditis]]
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Heart failure]]
*[[Sudden cardiac death]]
*[[Arrythmias]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Ischemic heart disease]]
*[[Valvular heart disease]]
| style="background: #F5F5F5; padding: 5px;" |
*[[S3]] and [[S4]] gallop
*[[Cardiac murmurs]]
*[[Pericardial friction rub]]
| style="background: #F5F5F5; padding: 5px;" |
* Serum [[cardiac troponin]] levels
* ↑ [[BNP]] or NT-proBNP level 
| style="background: #F5F5F5; padding: 5px;" |
*Nonspecific ST changes, single [[atrial]] or [[ventricular]] [[ectopic beats]], complex [[ventricular arrhythmias]]
| style="background: #F5F5F5; padding: 5px;" |
*[[CXR]]: Normal to enlarged with or without [[pulmonary]] [[vascular congestion]] and [[pleural effusions]]
*[[Echo]]: Left [[ventricular]] dilation, changes in left [[ventricular]] geometry (eg, development of a more spheroid shape), and wall motion abnormalities
* CMR: T1 and T2 signal intensity consistent with [[edema]], presence of LGE consistent with [[necrosis]] or [[scar]]
* Radionuclide ventriculography: ↓ EF
* [[Cardiac catheterization]]: Assessment of hemodynamic status
| style="background: #F5F5F5; padding: 5px;" |
*[[Endomyocardial biopsy]]
|- style="background: #DCDCDC; padding: 5px;" |
![[Hypertrophic cardiomyopathy]]<ref name="pmid8809524">{{cite journal |vauthors=Elliott PM, Kaski JC, Prasad K, Seo H, Slade AK, Goldman JH, McKenna WJ |title=Chest pain during daily life in patients with hypertrophic cardiomyopathy: an ambulatory electrocardiographic study |journal=Eur. Heart J. |volume=17 |issue=7 |pages=1056–64 |date=July 1996 |pmid=8809524 |doi= |url=}}</ref><ref name="pmid7199403">{{cite journal |vauthors=Pasternac A, Noble J, Streulens Y, Elie R, Henschke C, Bourassa MG |title=Pathophysiology of chest pain in patients with cardiomyopathies and normal coronary arteries |journal=Circulation |volume=65 |issue=4 |pages=778–89 |date=April 1982 |pmid=7199403 |doi= |url=}}</ref><ref name="pmid2295747">{{cite journal |vauthors=Webb JG, Sasson Z, Rakowski H, Liu P, Wigle ED |title=Apical hypertrophic cardiomyopathy: clinical follow-up and diagnostic correlates |journal=J. Am. Coll. Cardiol. |volume=15 |issue=1 |pages=83–90 |date=January 1990 |pmid=2295747 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]] or [[subacute]]
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |Typical or atypical chest pain
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[HF]]
*[[Arrhythmias]]
*[[Syncope]]
*Acute hemodynamic collapse 
| style="background: #F5F5F5; padding: 5px;" |
* Positive family history of sudden cardiac death
* [[Genetic mutation]]
| style="background: #F5F5F5; padding: 5px;" |
* [[S4]]
* [[Systolic murmurs]]
* LV apical impulse
* Brisk [[carotid pulse]]
* ↑ [[JVP]]
* A [[parasternal lift]]
| style="background: #F5F5F5; padding: 5px;" |Non-specific
| style="background: #F5F5F5; padding: 5px;" |
* Prominent abnormal [[Q waves]]
* [[P wave]] abnormalities
* [[Left axis deviation]]
* Deeply inverted [[T waves]]
| style="background: #F5F5F5; padding: 5px;" |
[[Echocardiography]]:
* [[LV hypertrophy]]
* Systolic anterior motion of the [[mitral valve]],
* [[LVOT obstruction]] 
*[[Cardiac catheterization]]
**Pressure gradient
**Augmentation of the gradient
**[[Aortic pressure]]
**[[Left ventricular]] pressure
**Left [[atrial]] or [[pulmonary]] [[capillary wedge pressure]]
*[[Coronary angiography]]
**Obstructive [[epicardial]] [[coronary artery disease]]
**[[Genetic testing]] for [[HCM]]: [[Sarcomere]] [[mutation]] in an athlete with a maximal LV wall thickness in the "grey zone" 
| style="background: #F5F5F5; padding: 5px;" |[[Genetic testing]] for HCM
|- style="background: #DCDCDC; padding: 5px;" |
![[Stress cardiomyopathy|Stress (takotsubo)]]
[[Stress cardiomyopathy|Cardiomyopathy]]<ref name="pmid15687136">{{cite journal |vauthors=Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, Maron BJ |title=Acute and reversible cardiomyopathy provoked by stress in women from the United States |journal=Circulation |volume=111 |issue=4 |pages=472–9 |date=February 2005 |pmid=15687136 |doi=10.1161/01.CIR.0000153801.51470.EB |url=}}</ref><ref name="pmid26159108">{{cite journal |vauthors=Krishnamoorthy P, Garg J, Sharma A, Palaniswamy C, Shah N, Lanier G, Patel NC, Lavie CJ, Ahmad H |title=Gender Differences and Predictors of Mortality in Takotsubo Cardiomyopathy: Analysis from the National Inpatient Sample 2009-2010 Database |journal=Cardiology |volume=132 |issue=2 |pages=131–136 |date=July 2015 |pmid=26159108 |doi=10.1159/000430782 |url=}}</ref><ref name="pmid26332547">{{cite journal |vauthors=Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, Cammann VL, Sarcon A, Geyer V, Neumann CA, Seifert B, Hellermann J, Schwyzer M, Eisenhardt K, Jenewein J, Franke J, Katus HA, Burgdorf C, Schunkert H, Moeller C, Thiele H, Bauersachs J, Tschöpe C, Schultheiss HP, Laney CA, Rajan L, Michels G, Pfister R, Ukena C, Böhm M, Erbel R, Cuneo A, Kuck KH, Jacobshagen C, Hasenfuss G, Karakas M, Koenig W, Rottbauer W, Said SM, Braun-Dullaeus RC, Cuculi F, Banning A, Fischer TA, Vasankari T, Airaksinen KE, Fijalkowski M, Rynkiewicz A, Pawlak M, Opolski G, Dworakowski R, MacCarthy P, Kaiser C, Osswald S, Galiuto L, Crea F, Dichtl W, Franz WM, Empen K, Felix SB, Delmas C, Lairez O, Erne P, Bax JJ, Ford I, Ruschitzka F, Prasad A, Lüscher TF |title=Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy |journal=N. Engl. J. Med. |volume=373 |issue=10 |pages=929–38 |date=September 2015 |pmid=26332547 |doi=10.1056/NEJMoa1406761 |url=}}</ref><ref name="pmid15583228">{{cite journal |vauthors=Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, Rihal CS |title=Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction |journal=Ann. Intern. Med. |volume=141 |issue=11 |pages=858–65 |date=December 2004 |pmid=15583228 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]]
| style="background: #F5F5F5; padding: 5px;" |Commonly > 20 minutes
| style="background: #F5F5F5; padding: 5px;" |
*[[Substernal]] heaviness or tightness
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*Setting of physical or emotional stress or critical illness
| style="background: #F5F5F5; padding: 5px;" |Stress
| style="background: #F5F5F5; padding: 5px;" |
*[[Murmurs]] and [[rales]] may be present on [[auscultation]] in the setting of [[Pulmonary edema|acute pulmonary edema]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Catecholamines|Catecholamines transiently elevated]]
*↑TnT level
*↑[[Brain natriuretic peptide|BNP level]]
| style="background: #F5F5F5; padding: 5px;" |
*[[ST segment elevation]]
*[[ST depression]]
*[[QT interval prolongation]], [[T wave inversion]], abnormal [[Q waves]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Radionuclide]] [[myocardial perfusion]] imaging: Transient perfusion abnormalities in the left ventricular apex
| style="background: #F5F5F5; padding: 5px;" |
*[[Ventriculography]] and [[invasive coronary angiography]]
|- style="background: #DCDCDC; padding: 5px;" |
!'''[[Aortic Stenosis]]'''<ref name="pmid3984868">{{cite journal |vauthors=Green SJ, Pizzarello RA, Padmanabhan VT, Ong LY, Hall MH, Tortolani AJ |title=Relation of angina pectoris to coronary artery disease in aortic valve stenosis |journal=Am. J. Cardiol. |volume=55 |issue=8 |pages=1063–5 |date=April 1985 |pmid=3984868 |doi= |url=}}</ref><ref name="pmid16352020">{{cite journal |vauthors=Silaruks S, Clark D, Thinkhamrop B, Sia B, Buxton B, Tonkin A |title=Angina pectoris and coronary artery disease in severe isolated valvular aortic stenosis |journal=Heart Lung Circ |volume=10 |issue=1 |pages=14–23 |date=2001 |pmid=16352020 |doi=10.1046/j.1444-2892.2001.00060.x |url=}}</ref><ref name="pmid9924164">{{cite journal |vauthors=Munt B, Legget ME, Kraft CD, Miyake-Hull CY, Fujioka M, Otto CM |title=Physical examination in valvular aortic stenosis: correlation with stenosis severity and prediction of clinical outcome |journal=Am. Heart J. |volume=137 |issue=2 |pages=298–306 |date=February 1999 |pmid=9924164 |doi=10.1053/hj.1999.v137.95496 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]], recurrent episodes of [[angina]]
| style="background: #F5F5F5; padding: 5px;" |2-10 minutes
| style="background: #F5F5F5; padding: 5px;" |
*Heaviness/pressure/ tightness/squeezing/ burning ([[Levine's sign]])
*[[Retrosternal]]
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Dyspnea]] and decreased exercise tolerance
*[[Dizziness]] and [[syncope]]
*[[Angina pectoris]]
| style="background: #F5F5F5; padding: 5px;" |
*[[HTN]]
* Old age
| style="background: #F5F5F5; padding: 5px;" |
*[[S2]] is soft, single and [[Paradoxical splitting of S2|paradoxically split]]
*[[A2]] delayed and tends to occur simultaneously with [[P2]]
*[[Aortic]] [[Ejection murmur|ejection]] click
*[[Fourth heart sound|Fourth heart sound (S4)]] can also be heard
*Crescendo–decrescendo [[Heart murmur|murmur]] 
| style="background: #F5F5F5; padding: 5px;" |
*[[Schistiocytes]] on [[peripheral blood smear]]
| style="background: #F5F5F5; padding: 5px;" |
*Non specific (the voltage of the [[QRS complex]] is increased showing the presence of [[left ventricular hypertrophy]])
| style="background: #F5F5F5; padding: 5px;" |
*[[Echocardiography]]: [[aortic leaflets]] thickened and calcified, ↑ [[pulmonary artery pressure]])
*CMR: [[Myocardial fibrosis]], evaluation of [[aortic]] anatomy and size
*MDCT: Degree of [[aortic valve]] calcification
*PET: Measures active [[mineralization]] which correlates with [[stenosis]] severity
| style="background: #F5F5F5; padding: 5px;" |
**[[Echocardiography]]
|- style="background: #DCDCDC; padding: 5px;" |
![[Heart Failure]]<ref name="pmid12163209">{{cite journal |vauthors=Anker SD, Sharma R |title=The syndrome of cardiac cachexia |journal=Int. J. Cardiol. |volume=85 |issue=1 |pages=51–66 |date=September 2002 |pmid=12163209 |doi= |url=}}</ref><ref name="pmid18440336">{{cite journal |vauthors=Horwich TB, Kalantar-Zadeh K, MacLellan RW, Fonarow GC |title=Albumin levels predict survival in patients with systolic heart failure |journal=Am. Heart J. |volume=155 |issue=5 |pages=883–9 |date=May 2008 |pmid=18440336 |doi=10.1016/j.ahj.2007.11.043 |url=}}</ref><ref name="pmid27656000">{{cite journal |vauthors=Breathett K, Allen LA, Udelson J, Davis G, Bristow M |title=Changes in Left Ventricular Ejection Fraction Predict Survival and Hospitalization in Heart Failure With Reduced Ejection Fraction |journal=Circ Heart Fail |volume=9 |issue=10 |pages= |date=October 2016 |pmid=27656000 |pmc=5082710 |doi=10.1161/CIRCHEARTFAILURE.115.002962 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Subacute]] or [[chronic]]
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |
*Dull
*Left sided chest pain
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |
*[[Orthopnea]]
*[[Peripheral edema]]
*[[Hemoptysis]]
| style="background: #F5F5F5; padding: 5px;" |[[Dyslipidemia]], [[hypertension]], smoking,  family history of premature disease, and [[diabetes]]
| style="background: #F5F5F5; padding: 5px;" |
*[[S3]]
*[[Jugular venous pressure|Elevated JVP]]
*[[Peripheral edema]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Hyponatremia]]
* [[Hypoalbuminemia]]
* ↑ [[Brain natriuretic peptide|Serum brain natriuretic peptide (BNP) or NT-proBNP level]]
* A mild elevation in serum [[bilirubin]] (total bilirubin <3 mg/dL)
| style="background: #F5F5F5; padding: 5px;" |
*EKG findings are specific according to each cause of [[heart failure]]
*[[Q waves]], [[ST]] and [[T wave]] abnormalities in patients with prior MI
*New onset [[arrhythmias]] ([[atrial fibrillation]] and [[ventricular tachycardia]])
| style="background: #F5F5F5; padding: 5px;" |
*[[CXR]]: [[Cardiomegaly]]
*[[Echocardiography]]: ↓ EF
*[[Right heart catheterization]]: [[Pulmonary capillary wedge pressure]] >20 mmHg, [[right atrial pressure]] ≥12 mmHg) and/or decreased [[cardiac index]] (≤2.2 L/min/m2
| style="background: #F5F5F5; padding: 5px;" |
*[[Echocardiography]]
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="3" |Differentials on the basis of Etiology
! rowspan="3" |Disease
! colspan="10" |Clinical manifestations
! colspan="4" |Diagnosis
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
| colspan="8" |Symptoms
| rowspan="2" |Risk factors
! rowspan="2" |Physical exam
! rowspan="2" |Lab Findings
! rowspan="2" |EKG
! rowspan="2" |Imaging
! rowspan="2" |Gold standard
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
!Onset
!Duration
!Quality of Pain
!Cough
!Fever
!Dyspnea
!Weight loss
!Associated Features
|- style="background: #DCDCDC; padding: 5px;" |
! rowspan="5" |Pulmonary 
!'''[[Pulmonary Embolism]]'''<ref name="pmid17904458">{{cite journal |vauthors=Stein PD, Beemath A, Matta F, Weg JG, Yusen RD, Hales CA, Hull RD, Leeper KV, Sostman HD, Tapson VF, Buckley JD, Gottschalk A, Goodman LR, Wakefied TW, Woodard PK |title=Clinical characteristics of patients with acute pulmonary embolism: data from PIOPED II |journal=Am. J. Med. |volume=120 |issue=10 |pages=871–9 |date=October 2007 |pmid=17904458 |pmc=2071924 |doi=10.1016/j.amjmed.2007.03.024 |url=}}</ref><ref name="pmid2332918">{{cite journal |vauthors= |title=Value of the ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED) |journal=JAMA |volume=263 |issue=20 |pages=2753–9 |date=1990 |pmid=2332918 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]]
| style="background: #F5F5F5; padding: 5px;" |May last minutes to hours
| style="background: #F5F5F5; padding: 5px;" |
*Sharp or knifelike or [[pleuritic pain]]
*Localized to side of lesion
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Hemoptysis]]
*History of [[venous thromboembolism]] or [[coagulation]] abnormalities.
| style="background: #F5F5F5; padding: 5px;" | [[Hormone replacement therapy]]
[[Cancer]]
[[Oral contraceptive pills]]
[[Stroke]] 
[[Pregnancy]]
[[Postpartum]] 
Prior history of [[VTE]]
[[Thrombophilia]] 
| style="background: #F5F5F5; padding: 5px;" |
*[[S3]] or [[S4]] [[Gallop rhythm|gallop]]
*Low grade fever
*[[Tachycardia]]
*[[Tachypnea]]
*[[Hypoxia]] 
| style="background: #F5F5F5; padding: 5px;" |
*↑[[D-dimer]] ≥500 ng/mL
*[[Arterial blood gas|Arterial blood gases]] ([[Respiratory alkalosis]])
*↑[[Troponin|Troponin levels]]
*[[Hypercoagulation]] workup
| style="background: #F5F5F5; padding: 5px;" |
*[[Tachycardia]] and nonspecific [[ST-segment]] and [[T-wave]] changes (70 percent)
*S1Q3T3 pattern
*New [[right bundle branch block]]
*Inferior Q-waves (leads II, III, and aVF)
| style="background: #F5F5F5; padding: 5px;" |
*[[Duplex Ultrasonography]]: [[DVT]]
*[[CXR]]: [[Westermark sign]], [[Hampton hump]], [[Palla's sign]]
*[[Echocardiography]]:
** [[RV]] dilation (ratio of apical 4-chamber [[RV]] diameter to [[LV|left ventricle (LV)]] diameter > 0.9)
** [[RV]] systolic dysfunction
*[[Ventilation-Perfusion Scanning]]: High probability
| style="background: #F5F5F5; padding: 5px;" |
*[[CT pulmonary angiography]]
|- style="background: #DCDCDC; padding: 5px;" |
!'''[[Pneumothorax|Spontaneous Pneumothorax]]'''<ref name="pmid3678419">{{cite journal |vauthors=Bense L, Wiman LG, Hedenstierna G |title=Onset of symptoms in spontaneous pneumothorax: correlations to physical activity |journal=Eur J Respir Dis |volume=71 |issue=3 |pages=181–6 |date=September 1987 |pmid=3678419 |doi= |url=}}</ref><ref name="pmid8553937">{{cite journal |vauthors=Seow A, Kazerooni EA, Pernicano PG, Neary M |title=Comparison of upright inspiratory and expiratory chest radiographs for detecting pneumothoraces |journal=AJR Am J Roentgenol |volume=166 |issue=2 |pages=313–6 |date=February 1996 |pmid=8553937 |doi=10.2214/ajr.166.2.8553937 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]]
| style="background: #F5F5F5; padding: 5px;" |May last minutes to hours
| style="background: #F5F5F5; padding: 5px;" |
*Sharp
*Localized [[pleuritic]]
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Respiratory distress]]
*[[Tachypnea]] 
*Asymmetric lung expansion
*Hyperresonance on [[percussion]]
*Decreased [[tactile fremitus]]
*[[Tachycardia]]
*Cardiac [[apical displacement]]
| style="background: #F5F5F5; padding: 5px;" |
* Smoking
* Positive family history
* [[Marfan syndrome]]
* [[Homocystinuria]]
* [[Thoracic]] [[endometriosis]].
| style="background: #F5F5F5; padding: 5px;" |
*[[Decreased breath sounds]] on involved side
*[[Respiratory sounds|Lung sounds]] transmitted from the unaffected [[hemithorax]] are minimal with [[auscultation]] at the [[midaxillary]] line
*Adventitious lung sounds ([[crackles]], [[wheeze]]; an ipsilateral finding)
*[[Pulsus paradoxus]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Respiratory alkalosis]] on [[Arterial blood gases|ABGs]]
| style="background: #F5F5F5; padding: 5px;" |
*Rightward shift in the mean electrical axis
*Loss of [[precordial]] R waves
*Diminution of the QRS voltage
*Precordial T wave inversions
| style="background: #F5F5F5; padding: 5px;" |
*[[CXR]]: White [[visceral]] pleural line on the chest radiograph
*[[CT]]: small amounts of [[intrapleural]] gas, atypical collections of [[pleural]] gas, and loculated pneumothoraces
| style="background: #F5F5F5; padding: 5px;" |
*CT scan
|-
!style="background: #DCDCDC; padding: 5px;" |[[Tension Pneumothorax]]<ref name="pmid8820023">{{cite journal |vauthors=Stark P, Leung A |title=Effects of lobar atelectasis on the distribution of pleural effusion and pneumothorax |journal=J Thorac Imaging |volume=11 |issue=2 |pages=145–9 |date=1996 |pmid=8820023 |doi= |url=}}</ref><ref name="pmid23179505">{{cite journal |vauthors=Jalli R, Sefidbakht S, Jafari SH |title=Value of ultrasound in diagnosis of pneumothorax: a prospective study |journal=Emerg Radiol |volume=20 |issue=2 |pages=131–4 |date=April 2013 |pmid=23179505 |doi=10.1007/s10140-012-1091-7 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]]
| style="background: #F5F5F5; padding: 5px;" |May last minutes to hours
| style="background: #F5F5F5; padding: 5px;" |
*Sharp
*[[Pleuritic]]
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Hypotension]]
*[[Jugular venous distention]]
*[[Respiratory distress]]
| style="background: #F5F5F5; padding: 5px;" |
*Trauma
| style="background: #F5F5F5; padding: 5px;" |
*[[Decreased breath sounds]] on involved side
*[[Respiratory sounds|Lung sounds]] transmitted from the unaffected [[hemithorax]] are minimal with [[auscultation]] at the [[midaxillary]] line
*Adventitious [[Respiratory sounds|lung sounds]] ([[crackles]], [[wheeze]]; an [[ipsilateral]] finding)
*[[Pulsus paradoxus]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Arterial blood gases|Respiratory alkalosis on ABGs]]
| style="background: #F5F5F5; padding: 5px;" |
*Significant elevation of the ST-T segment from leads V1 to V4
| style="background: #F5F5F5; padding: 5px;" |
*[[CXR]]: A distinct shift of the [[mediastinum]] to the [[contralateral]] side, collapse of the [[ipsilateral]] lung, and flattening or inversion of the [[ipsilateral]] [[hemidiaphragm]]
| style="background: #F5F5F5; padding: 5px;" |
*[[CT scan]]
|- style="background: #DCDCDC; padding: 5px;" |
![[Pleural Effusion]]<ref name="pmid3757561">{{cite journal |vauthors=Feinsilver SH, Barrows AA, Braman SS |title=Fiberoptic bronchoscopy and pleural effusion of unknown origin |journal=Chest |volume=90 |issue=4 |pages=516–9 |date=October 1986 |pmid=3757561 |doi= |url=}}</ref><ref name="pmid3581930">{{cite journal |vauthors=Collins TR, Sahn SA |title=Thoracocentesis. Clinical value, complications, technical problems, and patient experience |journal=Chest |volume=91 |issue=6 |pages=817–22 |date=June 1987 |pmid=3581930 |doi= |url=}}</ref><ref name="pmid15753638">{{cite journal |vauthors=Venekamp LN, Velkeniers B, Noppen M |title=Does 'idiopathic pleuritis' exist? Natural history of non-specific pleuritis diagnosed after thoracoscopy |journal=Respiration |volume=72 |issue=1 |pages=74–8 |date=2005 |pmid=15753638 |doi=10.1159/000083404 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]] or [[subacute]] or [[chronic]]
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |
*Dull
*[[Pleuritic]] pain
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" |
*Increasing lower extremity [[edema]]
*[[Orthopnea]]
*[[Paroxysmal nocturnal dyspnea]]
*[[Night sweats]]
*[[Hemoptysis]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pneumonia]]
| style="background: #F5F5F5; padding: 5px;" |
*Diminished or inaudible [[breath sounds]]
*[[Pleural friction rub]]
*[[Egophony]] (known as "E-to-A" changes)
| style="background: #F5F5F5; padding: 5px;" |
*[[Pleural fluid|Pleural fluid LDH levels above 1000 IU/L]]  [[Complete blood count|Nucleated cells]]
** [[Complete blood count|- Lymphocytosis]]
** [[Complete blood count|- Eosinophilia]]
** [[Complete blood count|- Mesothelial cells]]
*[[Pleural fluid]] culture and [[cytology]]
*[[Pleural fluid]] [[Anti-nuclear antibody|antinuclear antibody]] and [[rheumatoid factor]]
| style="background: #F5F5F5; padding: 5px;" |
*Typically not indicated
| style="background: #F5F5F5; padding: 5px;" |
*[[Chest X Ray]]: [[Pleural fluid]] on one or both sides
*[[Computerized tomography (CT)]] scan: Detects small [[pleural effusions]], ie, less than 10 mL and possibly as little as 2 mL of liquid in the [[pleural space]], Thickening of the [[visceral]] and [[parietal pleura]] 
*MRI: Characterize the content of [[pleural effusions]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Computed tomography]]
|- style="background: #DCDCDC; padding: 5px;" |
![[Acute chest syndrome]] ([[Sickle cell anemia|Sickle cell anemia)]]<ref name="pmid9057664">{{cite journal |vauthors=Vichinsky EP, Styles LA, Colangelo LH, Wright EC, Castro O, Nickerson B |title=Acute chest syndrome in sickle cell disease: clinical presentation and course. Cooperative Study of Sickle Cell Disease |journal=Blood |volume=89 |issue=5 |pages=1787–92 |date=March 1997 |pmid=9057664 |doi= |url=}}</ref><ref name="pmid7517723">{{cite journal |vauthors=Castro O, Brambilla DJ, Thorington B, Reindorf CA, Scott RB, Gillette P, Vera JC, Levy PS |title=The acute chest syndrome in sickle cell disease: incidence and risk factors. The Cooperative Study of Sickle Cell Disease |journal=Blood |volume=84 |issue=2 |pages=643–9 |date=July 1994 |pmid=7517723 |doi= |url=}}</ref><ref name="pmid10861320">{{cite journal |vauthors=Vichinsky EP, Neumayr LD, Earles AN, Williams R, Lennette ET, Dean D, Nickerson B, Orringer E, McKie V, Bellevue R, Daeschner C, Manci EA |title=Causes and outcomes of the acute chest syndrome in sickle cell disease. National Acute Chest Syndrome Study Group |journal=N. Engl. J. Med. |volume=342 |issue=25 |pages=1855–65 |date=June 2000 |pmid=10861320 |doi=10.1056/NEJM200006223422502 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute]]
| style="background: #F5F5F5; padding: 5px;" |May last minutes to hours
| style="background: #F5F5F5; padding: 5px;" |
*Chest tightness
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Sickle-cell disease|Sickle cell anemia]]
*Vaso-occlusive [[Crisis (charity)|crisis]]
*[[Pain]] crises 
| style="background: #F5F5F5; padding: 5px;" |
* ↑ [[WBC]]
* ↑ [[Hb]] levels
* ↓ [[fetal hemoglobin]] levels
* Smoking
* Vaso-occlusive pain events
| style="background: #F5F5F5; padding: 5px;" |
*[[Systolic murmurs|Systolic murmur]] may be heard over the entire [[precordium]]
| style="background: #F5F5F5; padding: 5px;" |
*↑[[Erythrocyte sedimentation rate]]
*[[Peripheral blood smear|Peripheral blood smears]]: [[Schistiocytes]]
*↑ [[Reticulocyte count|Reticulocyte count]]
| style="background: #F5F5F5; padding: 5px;" |
*[[EKG]] typically not indicated
| style="background: #F5F5F5; padding: 5px;" |
*Plain radiography of the extremities: [[Avascular necrosis]]
| style="background: #F5F5F5; padding: 5px;" | ---
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="3" |Differentials on the basis of Etiology
! rowspan="3" |Disease
! colspan="10" |Clinical manifestations
! colspan="4" |Diagnosis
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
| colspan="8" |Symptoms
| rowspan="2" |Risk factors
! rowspan="2" |Physical exam
! rowspan="2" |Lab Findings
! rowspan="2" |EKG
! rowspan="2" |Imaging
! rowspan="2" |Gold standard
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
!Onset
!Duration
!Quality of Pain
!Cough
!Fever
!Dyspnea
!Weight loss
!Associated Features
|- style="background: #DCDCDC; padding: 5px;" |
| rowspan="9" |Gastrointestinal
!'''Perforated [[Peptic Ulcer]]'''<ref name="pmid16928254">{{cite journal |vauthors=Vakil N, van Zanten SV, Kahrilas P, Dent J, Jones R |title=The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus |journal=Am. J. Gastroenterol. |volume=101 |issue=8 |pages=1900–20; quiz 1943 |date=August 2006 |pmid=16928254 |doi=10.1111/j.1572-0241.2006.00630.x |url=}}</ref><ref name="pmid15290658">{{cite journal |vauthors=Vakil NB, Traxler B, Levine D |title=Dysphagia in patients with erosive esophagitis: prevalence, severity, and response to proton pump inhibitor treatment |journal=Clin. Gastroenterol. Hepatol. |volume=2 |issue=8 |pages=665–8 |date=August 2004 |pmid=15290658 |doi= |url=}}</ref><ref name="pmid18289194">{{cite journal |vauthors=Giannini EG, Zentilin P, Dulbecco P, Vigneri S, Scarlata P, Savarino V |title=Management strategy for patients with gastroesophageal reflux disease: a comparison between empirical treatment with esomeprazole and endoscopy-oriented treatment |journal=Am. J. Gastroenterol. |volume=103 |issue=2 |pages=267–75 |date=February 2008 |pmid=18289194 |doi=10.1111/j.1572-0241.2007.01659.x |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute (medicine)|Acute]]
| style="background: #F5F5F5; padding: 5px;" |
*Minutes to hours ([[Gastroesophageal reflux disease|gastroesophageal reflux]])
*Prolonged ([[peptic ulcer]])
*5 to 60 minutes
| style="background: #F5F5F5; padding: 5px;" |
*Burning
*[[Substernal]]
*[[Epigastric]]
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" |
*[[Visceral]], [[substernal]], worse with recumbency, no radiation, relief with food, antacids
*[[Hematemesis]] or [[melena]] resulting from [[gastrointestinal bleeding]]
*[[Dyspepsia]]
| style="background: #F5F5F5; padding: 5px;" |
* Prolonged [[NSAIDs]] intake
* Smoking
* Alcohol abuse
* Spicy foods
* [[H-pylori infection]]
| style="background: #F5F5F5; padding: 5px;" |
*Not any auscultatory findings associated with this disease
*[[Enamel]] [[Erosion (dental)|erosion]] or other dental manifestations
| style="background: #F5F5F5; padding: 5px;" |
*↑Serum [[Gastrin]] Level
*[[Secretin Stimulation Test]]
*[[H-Pylori testing]]
| style="background: #F5F5F5; padding: 5px;" |
* [[EKG]] usually normal but may show [[T wave inversions]] in leads V2 through V4 consistent with [[myocardial ischemia]] in patients with [[peptic ulcer]] perforation
| style="background: #F5F5F5; padding: 5px;" |
*Upper [[Gastrointestinal]] [[Endoscopy]]: [[Biopsy]]
*[[Esophageal Manometry]]: To exclude an esophageal motility disorder
*Esophageal impedance pH testing: Monitors esophageal [[pH]]
| style="background: #F5F5F5; padding: 5px;" |
*Upper [[Gastrointestinal]] [[Endoscopy]]
|- style="background: #DCDCDC; padding: 5px;" |
![[Esophagitis]]<ref name="pmid3605035">{{cite journal |vauthors=Bott S, Prakash C, McCallum RW |title=Medication-induced esophageal injury: survey of the literature |journal=Am. J. Gastroenterol. |volume=82 |issue=8 |pages=758–63 |date=August 1987 |pmid=3605035 |doi= |url=}}</ref><ref name="pmid18763324">{{cite journal |vauthors=Parfitt JR, Jayakumar S, Driman DK |title=Mycophenolate mofetil-related gastrointestinal mucosal injury: variable injury patterns, including graft-versus-host disease-like changes |journal=Am. J. Surg. Pathol. |volume=32 |issue=9 |pages=1367–72 |date=September 2008 |pmid=18763324 |doi= |url=}}</ref><ref name="pmid10738847">{{cite journal |vauthors=Jaspersen D |title=Drug-induced oesophageal disorders: pathogenesis, incidence, prevention and management |journal=Drug Saf |volume=22 |issue=3 |pages=237–49 |date=March 2000 |pmid=10738847 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute (medicine)|Acute]]
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |
*Burning
*[[Epigastric]]
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" |
*[[Heartburn]]
*[[Abdominal pain]]
| style="background: #F5F5F5; padding: 5px;" |
* [[HIV]]
* [[Immunosuppression]]
| style="background: #F5F5F5; padding: 5px;" |
*No auscultatory finding
| style="background: #F5F5F5; padding: 5px;" |
*[[Cardiac troponin I (cTnI) and T (cTnT)|Troponin or other cardiac markers]]
*[[Leukopenia]]
*↓[[CD4|CD4 count]] 
*[[Human Immunodeficiency Virus (HIV)|Human immunodeficiency virus (HIV) test]]
| style="background: #F5F5F5; padding: 5px;" |
*ECG is done to rule out [[acute coronary syndrome]]
| style="background: #F5F5F5; padding: 5px;" |
*Double-contrast esophageal [[barium study]] ([[esophagography]])
*[[Endoscopy]]: [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
*[[Endoscopy]]
|- style="background: #DCDCDC; padding: 5px;" |
![[Esophageal perforation|Esophageal Perforation]]<ref name="pmid2730190">{{cite journal |vauthors=Pate JW, Walker WA, Cole FH, Owen EW, Johnson WH |title=Spontaneous rupture of the esophagus: a 30-year experience |journal=Ann. Thorac. Surg. |volume=47 |issue=5 |pages=689–92 |date=May 1989 |pmid=2730190 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute (medicine)|Acute]]
| style="background: #F5F5F5; padding: 5px;" |Minutes to hours
| style="background: #F5F5F5; padding: 5px;" |
*Burning
*Upper abdominal
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*[[Eating disorder|Eating disorders]] such as [[Bulimia nervosa|bulimia]]
*Repeated episodes of [[retching]] and [[vomiting]] with either recent excessive [[dietary]] or [[Alcohol|alcoho]]<nowiki/>l intake
*[[Subcutaneous emphysema]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Instrumentation]]/surgery
* Penetrating or blunt trauma
* Medications, other ingestions, foreign body
* Violent retching/[[vomiting]]
* Hernia/intestinal [[volvulus]]/obstruction
* [[Inflammatory bowel disease]]
* [[Appendicitis]]
* [[Peptic ulcer disease]]
| style="background: #F5F5F5; padding: 5px;" |
*Mild [[tachycardia]] or [[hypothermia]]
*[[Hamman's crunch|Hamman crunch (crackling sound upon chest auscultation occurs due to pneumomediastinum)]] 
| style="background: #F5F5F5; padding: 5px;" |
*↑Serum [[amylase]]
*↑[[C-reactive protein]] levels
| style="background: #F5F5F5; padding: 5px;" |
*[[EKG]] may be indicated to assess for [[myocardial ischemia]] due to [[Gastrointestinal bleeding|acute gastrointestinal bleeding]], especially if there is coexisting:Cardiovascular disease, significant [[anemia]] and advanced age
| style="background: #F5F5F5; padding: 5px;" |
*Plain chest films or chest [[CT]]: [[Pneumomediastinum]], Free air under the [[diaphragm]],  •[[Pleural effusion]]  •[[Pneumothorax]] (Macklin effect).    •[[Subcutaneous emphysema]]
*Plain abdominal films (or abdominal CT scout film):The appearance of [[pneumoperitoneum]]  -Free air under the diaphragm  -Cupola sign (inverted cup)  -Rigler sign (double-wall sign)  -Psoas sign  -Urachus sign 
| style="background: #F5F5F5; padding: 5px;" |
** Confirmed by water-soluble contrast esophagram
|- style="background: #DCDCDC; padding: 5px;" |
![[Mediastinitis]]<ref name="pmid3045478">{{cite journal |vauthors=Loyd JE, Tillman BF, Atkinson JB, Des Prez RM |title=Mediastinal fibrosis complicating histoplasmosis |journal=Medicine (Baltimore) |volume=67 |issue=5 |pages=295–310 |date=September 1988 |pmid=3045478 |doi= |url=}}</ref><ref name="pmid762913">{{cite journal |vauthors=Feigin DS, Eggleston JC, Siegelman SS |title=The multiple roentgen manifestations of sclerosing mediastinitis |journal=Johns Hopkins Med J |volume=144 |issue=1 |pages=1–8 |date=January 1979 |pmid=762913 |doi= |url=}}</ref><ref name="pmid3539049">{{cite journal |vauthors=Garrett HE, Roper CL |title=Surgical intervention in histoplasmosis |journal=Ann. Thorac. Surg. |volume=42 |issue=6 |pages=711–22 |date=December 1986 |pmid=3539049 |doi= |url=}}</ref><ref name="pmid7774324">{{cite journal |vauthors=Sherrick AD, Brown LR, Harms GF, Myers JL |title=The radiographic findings of fibrosing mediastinitis |journal=Chest |volume=106 |issue=2 |pages=484–9 |date=August 1994 |pmid=7774324 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute (medicine)|Acute]], [[Chronic (medical)|Chronic]]
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |
*Retrosternal irritation
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" |
*Nonspecific
| style="background: #F5F5F5; padding: 5px;" |
* Infection
* Esophageal perforation
* Post operative complication
| style="background: #F5F5F5; padding: 5px;" |
*Dysphagia
*Dysphonia
*Stridor
*[[Hamman's sign|Hamman sign]]
| style="background: #F5F5F5; padding: 5px;" |
*Positive organisms in sternal [[Culture collection|culture]]
*Leukocytosis
*Positive blood cultures
| style="background: #F5F5F5; padding: 5px;" |
*Diffuse ST elevation
| style="background: #F5F5F5; padding: 5px;" |
*CT: Localize the infection and extent of spread
*MRI: Assesses vascular  involvement and complications
| style="background: #F5F5F5; padding: 5px;" | CT scan
|- style="background: #DCDCDC; padding: 5px;" |
![[Pancreatitis]]<ref name="pmid6237447">{{cite journal |vauthors=Dickson AP, Imrie CW |title=The incidence and prognosis of body wall ecchymosis in acute pancreatitis |journal=Surg Gynecol Obstet |volume=159 |issue=4 |pages=343–7 |date=October 1984 |pmid=6237447 |doi= |url=}}</ref><ref name="pmid12094843">{{cite journal |vauthors=Yadav D, Agarwal N, Pitchumoni CS |title=A critical evaluation of laboratory tests in acute pancreatitis |journal=Am. J. Gastroenterol. |volume=97 |issue=6 |pages=1309–18 |date=June 2002 |pmid=12094843 |doi=10.1111/j.1572-0241.2002.05766.x |url=}}</ref><ref name="pmid8540502">{{cite journal |vauthors=Fortson MR, Freedman SN, Webster PD |title=Clinical assessment of hyperlipidemic pancreatitis |journal=Am. J. Gastroenterol. |volume=90 |issue=12 |pages=2134–9 |date=December 1995 |pmid=8540502 |doi= |url=}}</ref><ref name="pmid10352598">{{cite journal |vauthors=Lecesne R, Taourel P, Bret PM, Atri M, Reinhold C |title=Acute pancreatitis: interobserver agreement and correlation of CT and MR cholangiopancreatography with outcome |journal=Radiology |volume=211 |issue=3 |pages=727–35 |date=June 1999 |pmid=10352598 |doi=10.1148/radiology.211.3.r99jn08727 |url=}}</ref><ref name="pmid17378903">{{cite journal |vauthors=Stimac D, Miletić D, Radić M, Krznarić I, Mazur-Grbac M, Perković D, Milić S, Golubović V |title=The role of nonenhanced magnetic resonance imaging in the early assessment of acute pancreatitis |journal=Am. J. Gastroenterol. |volume=102 |issue=5 |pages=997–1004 |date=May 2007 |pmid=17378903 |doi=10.1111/j.1572-0241.2007.01164.x |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute (medicine)|Acute]], [[Chronic (medical)|Chronic]]
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |
*[[Epigastric]]
*Upper left side of the [[abdomen]]
*Pressure like
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" |
*Primary [[cirrhosis]]
*[[Primary sclerosing cholangitis]]
*Cystic fibrosis
*Autoimmune diseases
| style="background: #F5F5F5; padding: 5px;" |
* Alcohol abuse
* Smoking
* Genetic predisposition
| style="background: #F5F5F5; padding: 5px;" |
* Tachypnea
*Hypoxemia
*Hypotension
*Cullen's sign
*Grey Turner sign 
| style="background: #F5F5F5; padding: 5px;" |
*↑[[Amylase]] levels
*↑[[Lipase]] levels 
*↑ALT
*↑ALP
*Leukocytosis
| style="background: #F5F5F5; padding: 5px;" |
* T-wave inversion
* ST-segment depression
*  ST-segment elevation rarely
* Q-waves
| style="background: #F5F5F5; padding: 5px;" |
*[[Computed tomography|CT]]: focal or diffuse enlargement of the pancreas
*[[Magnetic resonance imaging|MRI]]: Pancreatic enlargement
| style="background: #F5F5F5; padding: 5px;" |
*CT Scan
|- style="background: #DCDCDC; padding: 5px;" |
![[IBD]]<ref name="ColbertSchmidt2017">{{cite journal|last1=Colbert|first1=James F.|last2=Schmidt|first2=Eric P.|last3=Faubel|first3=Sarah|last4=Ginde|first4=Adit A.|title=Severe Sepsis Outcomes Among Hospitalizations With Inflammatory Bowel Disease|journal=SHOCK|volume=47|issue=2|year=2017|pages=128–131|issn=1073-2322|doi=10.1097/SHK.0000000000000742}}</ref>
| style="background: #F5F5F5; padding: 5px;" |[[Acute (medicine)|Acute]], [[Chronic (medical)|Chronic]]
| style="background: #F5F5F5; padding: 5px;" |Variable
| style="background: #F5F5F5; padding: 5px;" |
*Painful bowl movments
*Bloody diarrhea
*pus or mucus in the stool
*Fistula
*sepsis
*pseudo  memberanous colitis
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |
*Gastric perforation
*Colon cancer
| style="background: #F5F5F5; padding: 5px;" |
* Genetic predisposition
* Alcohol abuse
* Smoking
* Microbiata and infections
| style="background: #F5F5F5; padding: 5px;" |
*Hypotension
*Abdominal tenderness 
| style="background: #F5F5F5; padding: 5px;" |
*Electrolyte disturbance
*Leukocytosis
| style="background: #F5F5F5; padding: 5px;" |
* T-wave inversion
* ST-segment depression
*  ST-segment elevation rarely
* Q-waves
| style="background: #F5F5F5; padding: 5px;" |
*[[Computed tomography|CT]]: Gastrointestinal inflamation
| style="background: #F5F5F5; padding: 5px;" |
*CT Scan
*Colonoscopy
*biopsy
|}
</small></small>


==References==
==References==

Latest revision as of 13:14, 16 April 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3] Ramyar Ghandriz MD[4]

Overview

Shock is a clinical syndrome resulting from the hypoperfusion of the tissues. Regardless of the underlying cause, this hypoperfusion leads to the failure to meet tissues' nutritional and oxygen needs, causing cellular dysfunction. The affected tissues lead to the production and release of inflammatory mediators that will further jeopardize perfusion through changes in the vasculature. The results of these changes are organ failure and death if treatment in not timely applied. According to the underlying cause, there will be different types of shock, which will have similar presentations. It is mandatory to determine the underlying cause of the condition so that proper treatment may be started. Cardiogenic shock is a clinical condition, defined as a state of systemic hypoperfusion originated in cardiac failure, in the presence of adequate intravascular volume, typically followed by hypotension, which leads to insufficient ability to meet oxygen and nutrient demands of organs and other peripheral tissues. It may range from mild to severe hypoperfusion and may be defined in terms of hemodynamic parameters, which according to most studies, means a state in which systolic blood pressure is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right ventricular filling pressures that does not respond to isolated fluid administration, is secondary to cardiac failure and occurs with signs of hypoperfusion (oliguria, cool extremities, cyanosis and altered mental status) or a cardiac index of < 2.2 L/min/m² (on inotropic, vasopressor or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and pulmonary artery wedge pressure > 18 mm Hg.

Differential Diagnosis

Depending on the author and the source used there will be different ways of organizing the types of shock. Sometimes it might be difficult to differentiate, from the clinical standpoint, two types of shock since components of each type may combine in a single patient. The clinical presentation of shock is usually the result of a complexity of processes, such as the sympathetic and endocrine responses to hypoperfusion, along with manifestations of organ failure. Patients who present with signs and symptoms of hypoperfusion following a diagnosed or suspected myocardial infarction, are commonly suffering a cardiogenic shock as a complication of the MI. However, other clinical scenarios, not related to acute MI, may present similarly:[1][2]

Differences to be noted include:

<math>\mbox{Shock index} = \frac{heart\ rate}{systolic\ blood\ pressure}</math>

Other measures include: decreased ventricular preload, ventricular diastolic volumes and pressures, pulmonary wedge pressure and central venous pressure.

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.)[11][12]
Type of Shock Etiology CO SVR PCWP CVP SVO2 RVS RVD PAS PAD
Cardiogenic Acute Ventricular Septal Defect ↓↓ N — ↑ ↑↑ ↑ — ↑↑ N — ↑ N — ↑ N — ↑
Acute Mitral Regurgitation ↓↓ ↑↑ ↑ — ↑↑ N — ↑
Myocardial Dysfunction ↓↓ ↑↑ ↑↑ N — ↑ N — ↑ N — ↑
Right Ventricular Infarction ↓↓ N — ↓ ↑↑ ↓ — ↑ ↓ — ↑ ↓ — ↑
Obstructive Pulmonary Embolism ↓↓ N — ↓ ↑↑ ↓ — ↑ ↓ — ↑ ↓ — ↑
Cardiac Tamponade ↓ — ↓↓ ↑↑ ↑↑ N — ↑ N — ↑ N — ↑
Distributive Septic Shock N — ↑↑ ↓ — ↓↓ N — ↓ N — ↓ ↑ — ↑↑ N — ↓ N — ↓
Anaphylactic Shock N — ↑↑ ↓ — ↓↓ N — ↓ N — ↓ ↑ — ↑↑ N — ↓ N — ↓
Hypovolemic Volume Depletion ↓↓ ↓↓ ↓↓ N — ↓ N — ↓


The following table outlines the major differential diagnoses of Shock on the basis of clinical manifestations..[13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48]


Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell); Coronary CT angiography (CCTA); multidetector row scanners (MDCT); Cardiovascular magnetic resonance — CMRI; Myocardial perfusion imaging (MPI); single-photon emission CT (SPECT); Positron emission tomography (PET) scanning; Magnetic resonance (MR) angiography, Computed tomographic (CT) angiography, and Transesophageal echocardiography (TEE), late gadolinium enhancement (LGE); right ventricular hypertrophy (RVH), right atrial enlargement (RAE), functional tricuspid regurgitation (TR), Pulmonary artery systolic pressure (PASP; adenosine deaminase (ADA); Serum amyloid A (SAA), soluble interleukin-2 receptor (sIL2R); High-resolution CT (HRCT) scanning

Differentials on the basis of Etiology Disease Clinical manifestations Diagnosis
Symptoms Risk factors Physical exam Lab Findings EKG Imaging Gold standard
Onset Duration Quality of Pain Cough Fever Dyspnea Weight loss Associated Features
Myocardial Infarction[13][14][15][16] Acute Commonly > 20 minutes - - + -
  • ST elevation MI (STEMI)
  • Non-ST elevation MI (NSTEMI) or Non Q wave
  • CCTA combined with MPI
Cardiac
Aortic Dissection[49][50] Sudden severe progressive pain (common) or chronic (rare) Variable
  • Tearing, ripping sensation, knife like
- - + -
  • Nonspecific ST and T wave changes
Aortic intramural hematoma Sudden severe progressive pain (common) or chronic (rare) Variable
  • Tearing, ripping sensation, knife like
- - + -
  • Nonspecific ST and T wave changes
Penetrating atherosclerotic aortic ulcer[51][52][53] Sudden severe pain Variable
  • Tearing, ripping sensation, knife like
- - + -

_

_

Pericardial Tamponade[54][55] Acute or subacute May last for hours to days +/- + + - EKG findings:
Myocarditis[56][57][58] Acute or subacute Variable +/- + + -
Hypertrophic cardiomyopathy[59][60][61] Acute or subacute Variable Typical or atypical chest pain - - + - Non-specific

Echocardiography:

Genetic testing for HCM
Stress (takotsubo)

Cardiomyopathy[62][63][64][65]

Acute Commonly > 20 minutes - - + -
  • Setting of physical or emotional stress or critical illness
Stress
Aortic Stenosis[66][67][68] Acute, recurrent episodes of angina 2-10 minutes - - + -
Heart Failure[69][70][71] Subacute or chronic Variable
  • Dull
  • Left sided chest pain
+ +/- + + Dyslipidemia, hypertension, smoking, family history of premature disease, and diabetes
Differentials on the basis of Etiology Disease Clinical manifestations Diagnosis
Symptoms Risk factors Physical exam Lab Findings EKG Imaging Gold standard
Onset Duration Quality of Pain Cough Fever Dyspnea Weight loss Associated Features
Pulmonary Pulmonary Embolism[72][73] Acute May last minutes to hours + +/- + -  Hormone replacement therapy

Cancer Oral contraceptive pills Stroke  Pregnancy Postpartum  Prior history of VTE Thrombophilia 

Spontaneous Pneumothorax[74][75] Acute May last minutes to hours - - + -
  • Rightward shift in the mean electrical axis
  • Loss of precordial R waves
  • Diminution of the QRS voltage
  • Precordial T wave inversions
  • CXR: White visceral pleural line on the chest radiograph
  • CT: small amounts of intrapleural gas, atypical collections of pleural gas, and loculated pneumothoraces
  • CT scan
Tension Pneumothorax[76][77] Acute May last minutes to hours - - + -
  • Trauma
  • Significant elevation of the ST-T segment from leads V1 to V4
Pleural Effusion[78][79][80] Acute or subacute or chronic Variable + +/- + +/-
  • Typically not indicated
Acute chest syndrome (Sickle cell anemia)[81][82][83] Acute May last minutes to hours
  • Chest tightness
+ +/- + -
  • EKG typically not indicated
---
Differentials on the basis of Etiology Disease Clinical manifestations Diagnosis
Symptoms Risk factors Physical exam Lab Findings EKG Imaging Gold standard
Onset Duration Quality of Pain Cough Fever Dyspnea Weight loss Associated Features
Gastrointestinal Perforated Peptic Ulcer[84][85][86] Acute +/- - - +/-
  • Not any auscultatory findings associated with this disease
  • Enamel erosion or other dental manifestations
Esophagitis[87][88][89] Acute Variable + + - +/-
  • No auscultatory finding
Esophageal Perforation[18] Acute Minutes to hours
  • Burning
  • Upper abdominal
- +/- + -
    • Confirmed by water-soluble contrast esophagram
Mediastinitis[90][91][92][93] Acute, Chronic Variable
  • Retrosternal irritation
+/- + + -
  • Nonspecific
  • Infection
  • Esophageal perforation
  • Post operative complication
  • Positive organisms in sternal culture
  • Leukocytosis
  • Positive blood cultures
  • Diffuse ST elevation
  • CT: Localize the infection and extent of spread
  • MRI: Assesses vascular involvement and complications
CT scan
Pancreatitis[94][95][96][97][98] Acute, Chronic Variable - + + +/-
  • Alcohol abuse
  • Smoking
  • Genetic predisposition
  •  Tachypnea
  • Hypoxemia
  • Hypotension
  • Cullen's sign
  • Grey Turner sign 
  • T-wave inversion
  • ST-segment depression
  •  ST-segment elevation rarely
  • Q-waves
  • CT: focal or diffuse enlargement of the pancreas
  • MRI: Pancreatic enlargement
  • CT Scan
IBD[99] Acute, Chronic Variable
  • Painful bowl movments
  • Bloody diarrhea
  • pus or mucus in the stool
  • Fistula
  • sepsis
  • pseudo memberanous colitis
- + + +
  • Gastric perforation
  • Colon cancer
  • Genetic predisposition
  • Alcohol abuse
  • Smoking
  • Microbiata and infections
  • Hypotension
  • Abdominal tenderness 
  • Electrolyte disturbance
  • Leukocytosis
  • T-wave inversion
  • ST-segment depression
  •  ST-segment elevation rarely
  • Q-waves
  • CT: Gastrointestinal inflamation
  • CT Scan
  • Colonoscopy
  • biopsy

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