Cardiogenic shock differential diagnosis
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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]
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- 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 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[3].
- When comparing 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 O2 saturation and SVR. Differences to be noted 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.
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- 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.[4] 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.
- 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 O2 saturation, right and left ventricular diastolic pressures, pulmonary artery diastolic pressure, serum lactate and CVP. Other causes may be observed on the table below.
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- 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 O2 saturation and increase of mixed venous oxygen saturation. It is important to note that, unlike cardiogenic and other types of shock, in the distributive kind there is an increase in venous oxygen saturation which, despite the increased O2 demand, might be due to the increased total body perfusion, that is responsible for diminishing the effectiveness of individual tissue perfusion.
| 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
- ↑ Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ Parrillo, Joseph (2013). Critical care medicine principles of diagnosis and management in the adult. Philadelphia, PA: Elsevier/Saunders. ISBN 0323089291.
- ↑ 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.
- ↑ "Shock: Shock and Fluid Resuscitation: Merck Manual Professional".
- ↑ Parrillo, Joseph E.; Ayres, Stephen M. (1984). Major issues in critical care medicine. Baltimore: William Wilkins. ISBN 0-683-06754-0.
- ↑ Judith S. Hochman, E. Magnus Ohman (2009). Cardiogenic Shock. Wiley-Blackwell. ISBN 9781405179263.