Difference between revisions of "Cardiogenic shock differential diagnosis"

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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]]. Differences to be noted include: decreased [[ventricular]] [[preload]], [[ventricular]] [[diastolic]] volumes and pressures, [[pulmonary wedge pressure]] and [[central venous pressure]].
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:*'''[[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>.
 
::*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>.
  
 
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Revision as of 16:55, 16 January 2020

Cardiogenic Shock Microchapters

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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]

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]

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.)[8][9]
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 — ↓

References

  1. Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
  2. Parrillo, Joseph (2013). Critical care medicine principles of diagnosis and management in the adult. Philadelphia, PA: Elsevier/Saunders. ISBN 0323089291.
  3. Lier H, Bernhard M, Hossfeld B (March 2018). "[Hypovolemic and hemorrhagic shock]". Anaesthesist (in German). 67 (3): 225–244. doi:10.1007/s00101-018-0411-z. PMID 29404656.
  4. Kobayashi L, Costantini TW, Coimbra R (December 2012). "Hypovolemic shock resuscitation". Surg. Clin. North Am. 92 (6): 1403–23. doi:10.1016/j.suc.2012.08.006. PMID 23153876.
  5. "Shock: Shock and Fluid Resuscitation: Merck Manual Professional".
  6. Pich H, Heller AR (May 2015). "[Obstructive shock]". Anaesthesist (in German). 64 (5): 403–19. doi:10.1007/s00101-015-0031-9. PMID 25994928.
  7. Smith N, Lopez RA, Silberman M. PMID 29261964. Missing or empty |title= (help)
  8. Parrillo, Joseph E.; Ayres, Stephen M. (1984). Major issues in critical care medicine. Baltimore: William Wilkins. ISBN 0-683-06754-0.
  9. Judith S. Hochman, E. Magnus Ohman (2009). Cardiogenic Shock. Wiley-Blackwell. ISBN 9781405179263.



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