1 Banner University Medical Clinics, Scottsdale, AZ, USA
2 Robert Wood Johnson Barnabas Health, New Brunswick, NJ, USA
Background
Definition of disease
Shock syndrome is a condition that the European Society of Intensive Care Medicine (ESICM) defines as ‘generalized acute circulatory failure which is life threatening and is associated with inadequate oxygen utilization by cells.’
It is the final pathway of a state of cellular dysfunction where the circulation is unable to meet the demands of the tissues, resulting in cellular dysoxia, i.e. mismatch between oxygen delivery and oxygen consumption, resulting in increased blood lactate levels.
Disease classification
Shock syndromes are divided into four major groupings (hypovolemic, cardiogenic, distributive, and obstructive) along with the underlying diseases that cause each particular type of shock (see Differential diagnosis section).
It should be emphasized that despite this classification, circulatory collapse resulting in shock generally has overlapping pathophysiology. For example, hypovolemia can be found in cardiogenic shock or in septic (distributive) shock.
Incidence/prevalence
Circulatory shock accounts for one‐third of patients admitted to ICUs in the USA.
In the SOAP II trial (n = 1679), septic shock accounted for 62.2% (according to the ESICM, reported incidence of septic shock in patients admitted to the ICU varies between 6.3% and 14.7%). Cardiogenic shock accounted for 16.7%, hypovolemia accounted for 15.7%, and the rest were accounted for by other distributive and obstructive etiologies.
4.6% of ACS patients admitted to the hospital developed cardiogenic shock according to an observational study of 65 119 patients hospitalized.
Etiology
Circulatory failure or shock is a syndrome that is the final pathway for several etiological conditions that lead to circulatory collapse.
While circulatory shock is generally divided into four types (hypovolemic, cardiogenic, distributive, and obstructive), the conditions that contribute to development of any of these specific type are multitude as described in the Differential diagnosis section (Figure 18.1).
Pathology/pathogenesis
The underlying pathologic derangement in shock syndrome is a mismatch between global oxygen delivery (DO2) and oxygen consumption (VO2).
DO2 is responsive to changes in any of the three components of DO2 (cardiac output, Hb, and oxygenation) and VO2.
In the presence of adequate oxygenation and Hb, cardiac output drives DO2 to match VO2.
The normal DO2:VO2 ratio is 5:1 and is achieved by increasing cardiac output (CO) in response to increased demand from cellular respiration (consumption drives delivery) and at this ratio cellular respiration is not supply dependent.
When the ratio falls below 2:1, cellular respiration becomes supply dependent. This 2:1 ratio corresponds to maximal oxygen extraction by tissues and is the critical level at which tissue hypoxia (oxygen debt) results in anaerobic tissue metabolism leading to acidosis and lactic acid formation, hence elevated blood lactic acid levels.
Therefore, correction of DO2 by improving CO should improve survival from shock.
However, this is not the case as other regional and microcirculatory hemodynamic alterations become active in due course when restoration of DO2 is delayed.
Compensatory mechanisms that include extrinsic (autonomic nervous system and circulating norepinephrine from adrenals) and intrinsic (arteriolar and endothelium mediated) regional and microcirculatory autoregulation become overwhelmed with delay in treatment, resulting in systemic inflammatory response syndrome (SIRS). SIRS results in regional flow heterogeneity with shunting of blood supply to non‐critical areas of the body.
As shock state progresses, microcirculatory blood flow, microcirculatory oxygen diffusion, and microcirculatory oxygen utilization become ineffective resulting in microcirculatory failure. At this stage, even if the DO2 is re‐established with adequate CO, the downward spiral and the development of multiorgan dysfunction syndrome (MODS) is inevitable. At this point the patient may continue to decline even with adequate CO.
If measures to prevent this downward spiral are unsuccessful, death ensues.
Prevention
Screening
Critically ill patients are especially at risk for developing shock syndrome. Studies have shown that the shock syndrome is prevalent in approximately one‐third of patients admitted to ICU.
Critically ill patients should be routinely screened for the development of shock syndrome.
Screening involves monitoring and evaluating clinical, hemodynamic, and biochemical parameters.
Diagnosis
Differential diagnosis
Differential diagnosiss
Hypovolemic
Hemorrhagic:
Trauma
Gastrointestinal
Retroperitoneal
Non‐hemorrhagic:
External fluid loss
Dehydration
Vomiting
Diarrhea
Polyuria
Interstitial fluid redistribution:
Thermal injury
Trauma
Anaphylaxis
Increased vascular capacitance:
Sepsis
Anaphylaxis
Toxins/drugs
Cardiogenic
Myopathy:
Myocardial infarction:
Left or right ventricle
Myocardial contusion
Myocarditis
Cardiomyopathy
Post ischemic stunning
Septic myocardial depression
Pharmacologic:
Anthracycline cardiotoxicity
Calcium channel blockers
Mechanical:
Valvular failure (stenotic or regurgitant)
Hypertrophic cardiomyopathy
Ventricular septal defect
Arrhythmic:
Bradycardia
AV blocks
Tachycardia:
Supraventricular
Ventricular
Obstructive
Impaired diastolic filling (decreased preload):
Vena cava obstruction
Intrathoracic obstructive tumors
↑ intrathoracic pressure
Tension pneumothorax
Mechanical ventilation
Decreased cardiac compliance
Constrictive pericarditis
Cardiac tamponade:
Acute:
Post‐MI free wall rupture
Traumatic
Hemorrhagic
Chronic:
Malignant
Uremic
Idiopathic
Impaired systolic contraction:
Right ventricle:
Pulmonary embolus
Acute pulmonary hypertension
Left ventricle:
Saddle embolus
Aortic dissection
Distributive
Septic
Toxic shock syndrome
Anaphylactic
Neurogenic (spinal shock)
Endocrine:
Adrenal crisis
Thyroid storm
Toxins
Typical presentation
Typically, in adults, the systolic blood pressure is less than 90 mmHg and the mean arterial pressure is less than 70 mmHg. This is associated with tachycardia.
This tissue hypoperfusion can be identified early by paying attention to what is referred to as the ‘three windows’ of the body:
Cutaneous: skin becomes cold and clammy due to vasoconstriction or due to severely inadequate cardiac output with vasodilation.
Hyperlactatemia (>1.5 mmol/L) is typically present.
Clinical diagnosis
History
The state of circulatory shock is always a life‐threatening condition and is an emergency. It is imperative that the diagnosis is made as early as possible, preferably at the compensated stage.
In the compensated state hypotension may not be apparent, therefore reliance on the presence of hypotension is not recommended. Additionally, mortality is already increased if hypotension and hypoperfusion are present.
Because survival is dependent on early initiation of therapy for shock, diagnosis of shock is always a clinical diagnosis. Laboratory tests and imaging can be performed to support the diagnosis or to identify the underlying etiology; however, therapy should not be delayed to accommodate laboratory studies.
Just as circulatory shock is a common end pathway for a variety of etiologies, treatment of all forms of shock mainly follows a common pathway.
Physical examination
Physical exam is extremely important in recognizing shock and can be grouped into two main areas. The first is recognizing the physical signs of compensatory mechanisms that come into play during the initial phase (pre‐shock) of shock.
Examination is accomplished by paying attention to the physical manifestations in the ‘three windows’ of the body (cutaneous, neurological, renal). Early signs that reflect the body’s effort to compensate include tachycardia, dyspnea, and oliguria (urine output <0.5 mL/kg/h). Additionally, the extremities are cool and may get mottled.
Blood pressure may be elevated or even normal initially when the patient is in a compensated state with maximal sympathetic drive. Clinicians should consider the baseline blood pressure of the patient. Normotension in a patient who is otherwise hypertensive may indicate hypoperfusion. Frank hypotension (MAP <60–65 mmHg) will develop if untreated as the shock state progresses.
Other clinical signs may be sought to identify the type and etiology of the shock:
Hypovolemic shock – look for decreased JVP.
Cardiogenic shock – look for elevated JVP and presence of S3 and S4 with or without murmurs.
Obstructive shock:
Pulmonary embolus – look for signs of RV failure, dyspnea, and hypoxia.
Cardiac tamponade – look for Kussmaul’s sign, distant heart sounds, and pulsus paradoxus.
Septic shock – look for fever, abnormal WBC, warm extremities, and focus of infection.
Disease severity classification
Circulatory failure resulting in shock and its progression to death, irrespective of etiology, does not show abrupt changes and is rather a pathophysiologic continuum. However, three stages can be identified.
Stage
Explanation of stage
Pre‐shock
A stage in the shock continuum where compensatory mechanisms become active and an attempt to restore tissue perfusion is maintained. During this phase, mild tachycardia, mild to moderate reduction in blood pressure, and mild elevation of lactate levels may be the only manifestation in a patient with appropriate setting for development of shock
Shock
A stage where the compensatory mechanisms become overwhelmed by the underlying disease progression with or without therapy. Clinical parameters for the diagnosis of shock such as severe tachycardia, hypotension, progressive severe lactic acidosis, oliguria, altered mental status, and other evidence of tissue underperfusion become apparent
End‐organ dysfunction
Irreversible damage to multiple organs results in multiorgan failure. Resistant to therapy with worsening hypotension, severe reduction in cardiac output, acute renal failure, obtundation or coma, and finally death may ensue in this phase
Laboratory diagnosis
List of diagnostic tests
Hemoglobin level: check to assess hemorrhage and oxygen‐carrying capacity. Erythrocytosis may be evident in non‐hemorrhagic hypovolemic shock and in septic shock when extravasation of intravascular fluid into the interstitium.
WBC: leucocyte count is usually elevated despite the etiology of shock due to demargination of neutrophils but leucopenia can manifest in the case of late shock or sepsis.
Platelets: platelet count increases acutely due to stress of shock but thrombocytopenia can result with progression of sepsis or with massive resuscitation efforts to correct hemorrhage.
Arterial blood gases and electrolytes:
An anion gap acidosis usually associated with lactic acidosis indicates prolonged periods of tissue underperfusion.
Non‐anion gap acidosis in hypovolemia may indicate excessive diarrhea.
In hypovolemic shock, metabolic alkalosis may indicate vomiting.
BUN/creatinine: these may be initially normal even if there is underlying renal injury. Isolated increase in BUN without increase in creatinine may suggest GI bleed.
Coagulation studies: performed if coagulopathy as a result of shock is suspected.
ECG: helps detect myocardial ischemia and if pathologic tachycardia is suspected.
List of imaging techniques
Chest radiograph: to identify pneumonia, pulmonary edema, pneumothorax, and significant pericardial effusion.
The following are optional:
Abdominal radiograph is rarely needed unless intra‐abdominal obstructive processes are suspected.
CT scan of the chest and abdomen are useful in specific situations such as aortic dissection, intra‐abdominal hemorrhage, and pulmonary embolus.
Echocardiogram is useful for the diagnosis of multiple etiologies of shock such as pulmonary embolus, LV or RV failure, pericardial tamponade, and other repairable cardiac lesions such as acute mitral regurgitation or aortic regurgitation.
MRI (if the patient is able to tolerate it) is useful for the diagnosis of acute myocarditis and the presence of infiltrative cardiomyopathies resulting in restrictive filling and low cardiac output. It is also useful for accurate RV function assessment.
(Source: Reproduced with permission from Vincent et al. 2013.)
Potential pitfalls/common errors made regarding diagnosis of disease
Awaiting development of hypotension to identify development of hypotension is a common error and results in delay in useful interventions or searching for underlying etiologies in a timely manner.
Beware of the patient’s baseline systolic pressure. In a hypertensive patient, drop in pressure by 40 mmHg from baseline can signal development of shock state even if the MAP (<60–65 mmHg) does not meet the criteria for hypotension.
Once shock state is clinically identified, awaiting laboratory confirmation to start appropriate therapy is another common error encountered in the critical care setting.
Treatment
Treatment rationale
Treatment rationale of shock consists of efforts to maintain adequate perfusion to match oxygen delivery and oxygen consumption in addition to correcting the underlying etiology of the shock.
Initial approach is fluid resuscitation along with adequate oxygenation.
Vasoactive substances are then administered to maintain adequate perfusion.
Failure of vasoactive medications should lead to consideration for early institution of cardiac assist device support. Restoration of adequate cardiac output will not result in improvement once microcirculatory failure ensues.
If all aggressive measures fail and continuation becomes futile, palliation and comfort care are considered.
There are four phases of treatment: salvage, optimization, stabilization, and de‐escalation.
Managing the hospitalized patient
Stage
Four phases of treatment
Pre‐shock
Salvage Focuses on achieving adequate blood pressure and cardiac output and immediately correcting the underlying cause of shock:
Attempt at maintaining acceptable blood pressure (MAP >60–65 mmHg) is initiated
Life‐saving interventions are promptly initiated. For example: acute coronary revascularization or assist devices for cardiogenic shock from acute MI; prompt antibiotic coverage for septic shock; acute thrombolysis or thrombectomy in the case of massive PE; pericardiocentesis for tamponade, etc.
Shock
Optimization Focuses on factors that improve cellular oxygen delivery and availability:
Maintain adequate tissue oxygen availability by optimizing CO, SvO2 and lactate levels
Stabilization Focuses on preventing organ dysfunction even if hemodynamic stabilization has been established. Establishing hemodynamic stabilization in shock syndrome does not guarantee end‐organ function improvement:
Provide organ support and attempt to minimize complications
De‐escalation Focuses on weaning from vasoactive agents as the condition of the patient improves:
Wean from vasoactive agents and achieve negative fluid balance
End‐organ dysfunction
If SIRS and subsequent multiorgan failure/MODS develops, the risk of death increases substantially (>75%). Aggressive treatment may become futile and can perpetuate patient and family suffering. At this stage it is appropriate to involve the service of palliative care medicine and initiate goals of care conversation with patient/family
Table of treatment
Treatment
Comments
Conservative Fluid resuscitation Oxygen delivery (nasal cannula, high flow nasal cannula, or ventilator)
Fluid administration is a conservative initial measure to improve cardiac output and microvascular flow. Oxygen is administered to improve the oxygen content
Medical Norepinephrine (0.1–2.0 μg/kg/min) Dopamine (2–20 μg/kg/min) Epinephrine (0.05–2 μg/kg/min and titrated up) Vasopressin (0.03 U/min and titrated up) Dobutamine (2–20 μg/kg/min) Milrinone (0.125–0.75 μg/kg/min)
Once shock state is recognized, vasopressor support is recommended to maintain arterial perfusion pressure while inotropic support may be needed to enhance cardiac output of failing ventricles. All patients should be considered for resuscitation with vasoactive medications unless specific contraindication exist (e.g. arrhythmia prohibiting the use of pro‐arrhythmic drugs such as dobutamine or dopamine)
Surgical Various right and left ventricular devices, usually emergent/short‐term devices Pericardiocentesis Pulmonary thrombectomy
Patients who decline despite maximal medical therapy should be considered for early percutaneous short‐term or long‐term cardiac device support to ensure adequate oxygen delivery. The choice of device depends on the resources and the experience of the institution. Surgical pulmonary thrombectomy can be considered for acute PE resulting in obstructive shock
Radiologic Pulmonary thrombectomy
Considered in acute massive PE
Psychologic Spiritual care Palliative care
All patients and family should receive these interventions when appropriate
Prevention/management of complications
Critically ill shock patients frequently have multiple invasive catheters placed for monitoring and treatment purposes.
One of the most feared complications is the development of line‐related sepsis in addition to an existing shock from other etiology such as cardiogenic or hypovolemic shock. This can be prevented by vigiliant monitoring and removing indwelling catheters when not necessary and by limiting the use of indwelling catheters in general.
Development of ventilator‐associated pneumonia is another potential complication in patients with prolonged ventilator dependence. Application of prophylactic measures and daily assessment for the liberation from ventilator support should be instituted to prevent this complication.
Persistent hypotension despite aggressive efforts should raise concern for adrenal suppression/insufficiency. This can be managed by administering corticosteroids.
With the use of multiple vasoactive medications, development of arrhythmia is a common complication that may result in clinical decompensation. Clinicians should consider cardioversion or rhythm control versus rate control strategies carefully. It is important to carefully select vasoactive medications keeping the patient’s underlying risk factors in mind.
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