Critical Care Medicine
Shock; circulatory failure
Also known as
Low cardiac output
1. Description of the problem
What every clinician needs to know
Shock is a clinical syndrome where a primary circulatory problem causes impaired oxygen delivery to organs and peripheral tissues. Without rapid identification, restoration of oxygen delivery and treatment aimed at the underlying cause, a process of progressive multi-organ dysfunction and sequential organ failure will lead to death.
There are many causes of shock (the list below is not exhaustive) but they can be broadly divided into three different syndromes that have different clinical features:
Acute myocardial infarction/Cardiogenic shock
Valvular disease (i.e. severe aortic stenosis, acute mitral regurgitation)
Massive pulmonary embolus
Afterload problems (i.e. severe hypertension, flash pulmonary edema [may be associated with bilateral renal artery stenosis])
Hyperglycemic diabetic emergency (DKA/HONK)
Third-space losses (i.e., bowel obstruction, pancreatitis, ovarian hyperstimulation)
Clinical features of the condition
The broad range in the etiology of shock is reflected in the diversity of clinical features that may be seen at presentation. Impaired oxygen delivery will eventually affect all systems.
It is often possible to identify the cause for a patient becoming acutely unwell from his or her history and clinical findings. For example, a 50-year-old man with a history of hypertension and diabetes who develops severe central chest pain and is cold, clammy and hypotensive is most likely to have cardiogenic shock due to an acute MI.
However, there can be considerable overlap in clinical syndromes, especially if there are mixed etiologies or presentation later in the disease.
1. A patient with a cardiac arrest due to myocardial infarction may have cardiogenic shock, which is then complicated by a systemic inflammatory response or even overt sepsis. This alone has a broad differential, including an aspiration pneumonia, intravenous catheter infection or the pro-inflammatory response to global ischemia.
2. A patient with severe pancreatitis develops hypovolemia from intra-abdominal sequestration and sepsis from necrotic pancreatic tissue. There is also an association with acute MI.
3. Uncontrolled hemorrhage may progress from fluid-responsive hypovolemia with compensatory peripheral vasoconstriction to irreversible low-resistance vasoplegia if not corrected in time.
Tachypnea (Respiratory rate >20/min)
Tachycardia (HR >100 bpm)
Altered mental status (anxiety, confusion, obtundation)
Reduced urine output (<0.5 ml/kg/hr)
Gut hypoperfusion (nausea and vomiting, high aspirates, constipation)
Metabolic acidosis (base deficit >2 mEq/L)
Raised serum lactate (>2 mmol/L)
Cold, clammy skin
Delayed capillary refill time (> 2 secs centrally)
Hypotension (systolic BP <90 mmHg or 30 mmHg below baseline)
Pulmonary edema (crackles/effusions/wheeze on auscultation)
Raised jugular venous pressure
Warm, dilated peripheries
Hypotension (systolic BP <90 mmHg or 30 mmHg below baseline)
Specific features of infection
Specific features of anaphylaxis
Cold, clammy skin
Delayed capillary refill time (> 2 secs centrally)
Low jugular venous pressure
Postural hypotension (>20 mmHg systolic drop on lying to sitting or standing)
Hypotension (systolic BP <90 mmHg or 30 mmHg below baseline)
Reduced skin turgor
Dry mucous membranes
Key management points
If not treated urgently or aggressively enough, shock of any etiology will lead to death.
The key components of successful management of shock are:
1. Early recognition and prompt action
2. Ensure a suitable team, including an experienced clinician, are working together.
3. Manage your patient in an appropriate environment (e.g. resuscitation room, ICU).
3. Follow a logical ABC (airway, breathing, circulation) approach.
4. Address the treatable components of shock.
5. Establish suitable monitoring: cardiac monitor, pulse oximeter, arterial cannula, central venous catheter, urinary catheter, hemodynamic monitoring (cardiac output).
6. Perform focused history taking, clinical examination and diagnostic tests to establish the cause of shock.
7. Specific treatments dependent on the cause
8. Diagnostic tests, history taking, clinical examination, establishing monitoring devices and specific treatments dependent on etiology must be done in parallel with resuscitation.
9. Constantly re-evaluate the clinical condition and response to treatment and support.
2. Emergency Management
With any critically ill patient you should start with an A (airway), B (breathing) and C (circulation) approach. If at any point your patient does not have a patent airway, adequate respiratory effort or a pulse, you must follow a well-rehearsed Advanced Life Support algorithm, which may include airway maneuvers, bag and mask ventilation, tracheal intubation, CPR, vasoactive drugs and defibrillation.
Early consideration for elective intubation and mechanical ventilation should be given to any shocked patient in order to maximize oxygen delivery and reduce respiratory oxygen consumption as well as clear carbon dioxide and improve acidosis. This must be balanced against the potential for further cardiovascular collapse, which can occur as a result of the reduced sympathetic drive and reduced venous return occurring with sedation and positive intrathoracic pressure.
The following components should be addressed in order to optimize the hemodynamics of your patient:
1. Rhythm control
2. Rate control
3. Optimize preload
4. Optimize afterload
5. Optimize contractility
Acute rhythm disturbances can be a precipitant or contributing factor for hemodynamic compromise and shock. For example, atrial contraction becomes increasingly important at preserving ventricular end-diastolic volumes at increasing heart rates. This is even more important in elderly individuals. The development of atrial fibrillation may cause a fall in cardiac output of 20-40% . It can be particularly catastrophic with mitral valve disease.
Urgent cardioversion is indicated for VT, fast atrial fibrillation and supraventricular tachycardia in the presence of hypotension, myocardial ischemia or pulmonary edema, which are likely to be present in your shocked patient.
Cardiac output is the product of heart rate and stroke volume. It follows an almost linear increase up to a rate of 100 bpm. Higher than this and reduced ventricular filling time compromises stroke volume and reduced coronary blood flow (which occurs during diastole) impairs oxygen delivery to the heart.
As outlined above, urgent cardioversion should be considered for tachyarrhythmias.
Tachycardia is an appropriate response to physiological stress. It is not appropriate to manipulate a sinus tachycardia other than to treat the underlying cause.
Bradycardia is never physiologically appropriate in a shocked patient and may represent conduction disease, inferior myocardial ischemia, pharmacological effect of drugs such as beta-blockers or a state of impending cardiac arrest.
If the heart rate is less than 40 bpm consider giving positive chronotropes, such as atropine or glycopyrrolate. In cases of AV block, transvenous pacing should be instituted. Transcutaneous pacing may be used as a bridging measure. In patients who have transvenous pacing with shock, the rate should be set at 90-100 bpm for optimal cardiac output.
The circulation of a patient without an adequate effective arterial blood volume is like a bicycle with flat tires. Stroke volume increases as end-diastolic volume rises. In normal physiological states this continues until a plateau is reached. Only in poorly functioning and abnormally dilated hearts do you reach a state where over-distention can reduce cardiac output.
Preload responsiveness is where a rapid bolus of intravenous fluid results in a significant increase in stroke volume and cardiac output (>10-15%)
In pragmatic terms all shocked patients should receive repeated fluid challenges as long as they are preload responsive unless there is evidence that clinically significant pulmonary edema is developing. This includes patients with pump failure who may be fluid responsive and intravascularly deplete, secondary to diuretics, anorexia, vomiting etc., despite raised filling pressures.
NB: Preload responsiveness is physiologically normal in health, and aggressive preload optimization is not usually appropriate in the absence of concerns about cardiac output.
The type of fluid used is far less important than the rate of infusion; choose what you feel is appropriate for your patient. Preferably using a large-bore cannula, infuse 250-500 ml as fast as possible, using a pressure bag if necessary. This should be completed in 5 to 10 minutes, not 30 minutes to an hour as is often the case.
If you have a continuous cardiac output measurement device in place and you are concerned about the risks of giving too much fluid you have two options. First, you could give a very rapid push of 100 ml of colloid with a syringe and assess the response. The second is to perform a passive leg raise. Here the patient is tilted back and the legs are lifted to 45 degrees to achieve a rapid bolus from the venous capacitance in the legs into the central blood volume. This elegant method allows a “reversible” fluid challenge to be administered followed by an actual one if preload responsiveness is demonstrated.
The priority in shock is to resuscitate the intravascular space and restore capacity for oxygen delivery. In the short term there is no evidence of a difference between using isotonic sodium-based crystalloid solutions (0.9% NaCl or Hartmann's/Ringer's Lactate) or colloid solutions. This is despite the theoretical advantages of colloids being more efficient at intravascular volume expansion and maintaining oncotic pressure.
Choice of fluid should be individualized dependent on the fluid loss causing hypovolemia; for example:
Resuscitation with blood products is essential in hemorrhagic shock. Packed red cells (PRCs) are required to maintain the hematocrit and oxygen-carrying capacity. Without fresh frozen plasma (FFP), clotting factors will be depleted and a vicious cycle of impaired hemostasis, clotting factor consumption and ongoing hemorrhage will result in disseminated intravascular coagulation (DIC).
Estimation of transfusion requirements can be difficult, and acutely the hemoglobin or hematocrit is a poor guide as the fluid loss is from the intravascular space only and will not have compensated.
As a rough guide:
Up to 15% intravascular fluid loss can be compensated for with tachycardia only.
15-30% may result in a postural BP drop (>20 mmHg systolic/>10 mmHg diastolic), which you won't find unless you measure it.
It may not be until >30% intravascular fluid loss that hypotension occurs. Young patients compensate very well and may be close to cardiac arrest at this point.
Your institution should have a massive transfusion protocol for use in trauma or obstetric hemorrhage (for example). We would recommend the transfusion of 2 units of O Rh-ve blood in emergencies followed by units of PRC (via a blood warmer) and FFP in a ratio of 1:1. If >4 units of blood are required, then urgent re-measurement of platelet count, INR, APTR and fibrinogen levels is mandatory. If the platelet count is less than 100, supplementation is needed. Cryoprecipitate should be given if the fibrinogen is <1 g/L (some people would advocate <2).
Adjunctive treatment with intravenous calcium and tranexamic acid is recommended.
There are a wide range of methods to assess preload responsiveness. In general, clinical indicators such as peripheral temperature, capillary refill time, postural BP (lying and standing), JVP, urine output and thirst are not adequately reliable to optimize preload, although may be helpful in assessing hypovolemia due to fluid loss.
Central venous pressure (CVP) has been a traditional method of assessing intravascular volume status for many years. Unfortunately, it is a very poor surrogate for left atrial pressure or ventricular volume. In addition, measuring it accurately can be fraught with technical difficulty. There is no correlation between initial CVP reading and preload responsiveness. The arbitrary targeting of a certain CVP attainment is not an appropriate end-point and does not define adequate preload. The main utility of CVP measurement would be to stop fluid challenging a patient if he or she had a significant sustained rise in CVP, especially if the measurement is greater than 18 mmHg.
For a more detailed description of hemodynamic monitoring methods please see the linked chapter.
Since its invention in the 1970s the pulmonary artery catheter (PAC) has been the gold standard in cardiac output measurement of the shocked patient on the ICU. It has the advantage of allowing sampling of mixed venous blood from the pulmonary artery for blood gas analysis. The oxygen saturation of mixed venous blood (SvO2) allows calculation of the arterial-venous oxygen difference and the percentage of oxygen extracted from the metabolically active tissues. Several, albeit flawed, studies have failed to show a mortality benefit in using a PAC.
Several less invasive methods have come into widespread use, such as pulse contour analysis with thermodilution (LIDCO®/PiCCO®), esophageal Doppler (for mechanically ventilated patients) and even minimally invasive techniques such as bioimpedence. These all allow a validated, dynamic estimation of cardiac output and peripheral resistance. In addition, oxygen saturation measured from a central venous catheter (ScvO2) can be used to approximate SvO2.
Mean arterial Pressure (MAP) = Cardiac output (CO) x total peripheral resistance (TPR)
Patients with shock that does not rapidly correct with fluid resuscitation must have the use of continuous blood pressure (BP) monitoring via an intra-arterial catheter where available.
General goals - As well as an adequate cardiac output, organs require an adequate perfusion pressure. The brain and kidneys have a well-established autoregulatory system allowing maintenance of perfusion within a wide blood pressure range. Two primary goals of resuscitation in shock are to maintain cerebral perfusion to avoid the devastating effects of hypoxic brain injury or watershed infarction and to limit renal injury. There is a close association between mortality and severity of acute kidney injury (AKI), which is independently above its mark of overall hemodynamic compromise.
Drugs that increase blood pressure by increasing vascular tone are termed vasopressors. They are not benign and can have deleterious effects on peripheral perfusion, causing skin mottling, frank ischemia, lactic acidosis and infarction of digits all the way to limbs. This risk is escalated with dose and preexisting vascular disease. In addition, splanchnic circulation can be compromised, leading to mesenteric ischemia. As such, you must decide what your goals of therapy are, balance the risks, use the minimum dose required and be vigilant for the complications.
Some cardiac output monitoring devices estimate systemic vascular resistance (SVR). SVR is typically high in cardiogenic shock and hypovolemic shock and low in septic shock.
Systemic vascular resistance (SVR) = (MAP – CVP)/CO
As you can see, resistance can be high with a low blood pressure if cardiac output is low. There is no evidence that this derived variable is useful for titrating therapy.
As a starting point, an arbitrary target systolic BP of 90 mmHg and MAP of 65 mmHg is reasonable. This can be individualized with the considerations below:
The most common medical comorbidity is hypertension. In addition, the most common cause of death is related to ischemic heart disease. As a result, a high proportion of patients take anti-hypertensive drugs. These should be stopped if the patient is hypotensive. ACE inhibitors and angiotensin 2 receptor blockers should be held for the duration of cardiovascular instability as they impair the autoregulatory compensation for hypotension and reduce glomerular filtration. It is reasonable to consider continuing medications required for anti-anginal or anti-arrhythmic properties.
These hypertensive patients may require a higher MAP in order to maintain their glomerular filtration rate, and if they are oliguric with a MAP of 65 mmHg this can be titrated up to 75-80 mmHg as a trial.
Patients who are normally hypotensive or who are receiving renal replacement therapy for AKI or chronic renal failure could have a lower MAP target (down to 60 mmHg) if there are no signs of inadequate perfusion elsewhere.
In patients with significant head injury it is imperative to limit secondary brain injury by maintaining adequate cerebral perfusion pressure (CPP). This is ideally done with ICP monitoring in place, but in the acute setting targeting a MAP of at least 90 mmHg is recommended.
These patients usually have hypotension despite the compensatory rise in cardiac output. This often persists despite aggressive fluid resuscitation. At this point vasopressor support is required. For a detailed description of the drugs used please see the chapters on septic shock, anaphylaxis and spinal shock. In practice norepinephrine and dopamine are the predominant first-line drugs used. There is no clear evidence that one is superior to the other, but dopamine is associated with more tachyarrhythmias, especially atrial fibrillation, and we would recommend norepinephrine for first-line use. Please see
Cardiovascular drugs used in the treatment of shock
|DRUG||MECHANISM OF ACTION||ADVERSE EFFECTS||DOSE|
|Norepinephrine||Stimulates primarily alpha 1 adrenergic receptorsSome beta-1 adrenergic activityPotent vasoconstrictor: increases afterload||Increases myocardial workImpairs splanchnic and peripheral perfusion at mod/high doses||0-1 mcg/kg/min|
|Dobutamine||Inodilator Stimulates beta-1 and- 2 adrenergic receptors Increases intracellular calcium concentration Positively inotropic Positively chronotropic Vasodilator - afterload reduction||Hypotension Increased heart rate Increased myocardial oxygen demand Arrhythmogenic Patients receiving beta blockers may be relatively immune to its effect and require high doses.||5-20 mcg/kg/min No loading dose required. Hemodynamic actions are dose related.|
|Dopexamine||Inodilator Stimulates beta-1 and- 2 adrenergic receptors Increases intracellular calcium concentration Positively inotropic and chronotropic Vasodilator - afterload reductionPreferential increases in splanchnic blood flow||Hypotension Increased heart rate Arrhythmogenic Increased myocardial oxygen demand||0.25-2 mcg/kg/min|
|Dopamine||Dominant effect dependent on dose <2 mcg/kg/min - acts on dopamine receptors - vasodilatation 2-5 mcg/kg/min - beta-1 adrenergic receptors - inotropic 5-15 mcg/kg/min - beta-1 adrenergic receptors - inotropic and alpha-1 adrenergic receptors - vasoconstriction||Increased afterload at higher doses Tachycardia Arrhythmogenic (especially AF) Some evidence of worse outcomes compared to other 'inotropes'||0-20 mcg/kg/minNo loading dose required|
|Milrinone||Inodilator Type III phosphodiesterase inhibitor Increases intracellular cyclic adenosine monophosphate and as a result calcium Positively inotropic Arterial and venous dilatation - decreased SVR, PVR and PAOP No increase in myocardial oxygen demand||Hypotension Accumulates in renal failure||150-750 ng/kg/min Loading dose 50 mcg/kg - given slowly over 10 minutes - in practice omitted due to hypotension|
|Levosimendan||Inodilator Calcium sensitizer Binds to calcium saturated troponin C in cardiac myocytes - prolonging the conformational change and increasing contractile force. Stimulates ATP-sensitive potassium channels Positively inotropic Reduces SVR and PVR and PAOP Improves coronary perfusion No increase in myocardial oxygen demand Active metabolite with long half-life||Hypotension||0.05-0.2 mcg/kg/min Loading dose 3-12 mcg/kg/min over 10 minutes - in practice omitted due to hypotension|
|Epinephrine||Inoconstrictor Acts on alpha- and beta-adrenergic receptors Positively inotropic and chronotropic Potent vasoconstrictor||Tachycardia Arrhythmogenic Increased myocardial oxygen demand Vasoconstriction - increased afterload||0.01-1 mcg/kg/min|
|Vasopressin||Acts on type 1A vasopressin receptors to inducepotent vasoconstrictionUsed as an additional vasoconstrictor in norepinepherine-refractory hypotensive shock||Peripheral and mesenteric ischemiaIncreased myocardial oxygen demand||0.01-0.05 iu/min|
|GTN||Donates nitric oxide to dilate smooth muscleReduces blood pressure and afterloadUsed in decompensated heart failure with hypertensionUsed for myocardial ischemia if blood pressure permits||HypotensionHeadache||0-10 mg/hour|
For patients requiring significant vasopressor support (e.g. >0.2 mcg/kg/min of norepinephrine) it is worth considering relative glucocorticoid deficiency with consequent reduced vascular tone and catecholamine resistance. The clinical response to steroids does not correlate well with cortical levels or response to synthetic ACTH, and we would advocate a 100-mg bolus of hydrocortisone followed by an infusion of 8-10 mg/hr if a measurable clinical response in terms of vasopressor dose reduction occurs.
Do not forget to exclude hypovolemia in these patients.
High sympathetic drive, circulating catecholamines, renal hypoperfusion with angiotensin II (ATII) generation results in these patients usually having high TPR. If they are hypotensive, then further increases in resistance generated with vasopressors are likely to impair cardiac output further and should not be instituted without concurrently addressing Step 4 (optimizing contractility). If this is addressed, then norepinephrine or dopamine can be used with the same caveat as above.
It is not unusual for a patient with decompensating heart failure to present shocked, having gotten into a vicious cycle of organ hypoperfusion, catecholamine and ATII release, escalating afterload, impaired cardiac output, pulmonary edema and hypoxia, and worsening organ hypoperfusion. In these cases aggressive afterload lowering with GTN (1-20 mg/hr) is required to allow forward flow of cardiac output. This should be performed in preference to aggressive diuresis with furosemide, as these patients are often not intravascularly fluid overloaded and you risk decompensating them further and precipitating AKI.
Obstructive causes of pump failure such as PE, tension pneumothorax and pericardial restriction/tamponade require specific intervention.
Artificially increasing afterload with vasopressors without adequate volume resuscitation will worsen cardiac output and oxygen delivery.
Non-restoration of an adequate blood pressure and volume expansion may imply a number of etiologies.
1. Inadequate volume resuscitation. How sure are you that you have given enough fluid in to the right space? Is there ongoing fluid loss? This may not be apparent -- for example, unrevealed GI bleeding or third-space intra-abdominal sequestration.
2. Vasoplegia and capillary pooling due to profound/prolonged hypovolemia. This may progress to irreversible shock
3. Concurrent systemic inflammatory response and/or sepsis
4. Concurrent pump failure. This can be acute or acute on chronic.
5. Relative glucocorticoid deficiency precipitated by physiological stress
6. In trauma, clinical suspicion for occult bleeding, tension pneumothorax and tamponade must be high.
Control of bleeding through direct pressure, surgical intervention or radiological embolization is a priority. Until this has been achieved some people advocate “permissive hypotension.” In theory, allowing a lower blood pressure may allow reflex vasoconstriction and clot formation to maintain hemostasis. This is most likely to be of benefit in cases that involve penetrating trauma and where definitive control of bleeding will not be significantly delayed. Fluid is withheld unless the systolic BP is less than 70 mmHg or the radial pulse in not palpable.There is no evidence of benefit of this approach in blunt trauma or other forms of shock.
Even it your patient has an acceptable rhythm, at an acceptable rate, having been adequately fluid resuscitated and an appropriate perfusion pressure, inadequate oxygen delivery and shock may persist.
This situation predominantly arises when there is an element of pump failure, and further adjuncts are considered further down.
While it is reassuring to have a peripherally warm patient with normal mentation, clinical examination may not yield enough information. The best clinical indicator is urine output. Oxygen delivery should be adequate if the urine output is >0.5 ml/kg/hr. If it is lower it may still be adequate but acute tubular necrosis or significant antidiuretic hormone response has occurred.
Strong consideration should be given to the use of a hemodynamic monitoring device if not already in situ. These allow the patient's Cardiac Index (CI) to be derived. The CI is the cardiac output corrected for body surface area. The normal range is 2.2 - 4.0 L/min/m2.
The CI can be used to titrate inotropic drugs, which are usually indicated if the CI is below 2.0 L/min/m2. However, this should be done in conjunction with measures of global perfusion, and a higher CI may be required.
Anaerobic metabolism leads to pyruvate and lactic acid formation. This can be measured on blood gas analysis as a metabolic lactic acidosis. Low oxygen delivery can also be detected as low SvO2 or ScvO2, indicating increased oxygen extraction.
If lactic acidosis or Sv(c)O2 <70% persists after addressing Points 1 to 3, achieving optimal arterial oxygen saturation and a hemoglobin of 10 g/dl, then initiation or increase in ionotropic support may be indicated. Further detail is available in the chapter on low cardiac output.
Ionotropic agents increase cardiac contractility to shift the Starling curve up and to the left. This is usually achieved by increasing calcium concentration in the cytoplasm. This may be at the expense of increasing myocardial oxygen consumption.
Agents have different properties; see
Dobutamine, dopexamine and milrinone are inodilators and may lower the BP. Caution is advised with patients whose BP is borderline. It can precipitate the need for, or increase the level of, vasopressor support.
Dopamine (at doses >10 mcg/kg/min) and epinephrine are inoconstrictors.
All these drugs are pro-arrythmogenic, especially dopamine, and this can limit doses.
Patients with low output states post MI or coronary artery bypass may benefit from the calcium-sensitizing drug levosimendan. This drug can increase cardiac output without increasing myocardial oxygen demand and has active metabolites with a long half-life.
Acute myocardial infarction (AMI)
If AMI is suspected on the basis of chest pain, ECG changes and cardiac enzymes, urgent aspirin, clopidogrel, heparin anticoagulation and pain relief is required. Primary PCI is the gold standard but restoration of coronary vessel patency with thrombolysis may be performed if this is not available. Surgical revascularization may be required.
Another inotropic agent that may be useful is the calcium-sensitizing agent levosimendan. This drug can improve cardiac index without necessarily increasing myocardial oxygen demand. It has active metabolites with a long half-life and may have effects lasting for days after infusion ends. Whether it has a benefit on survival remains controversial.
Cardiogenic shock is usually a complication of AMI. In this instance reperfusion therapy as above is a priority. Other mechanical causes such as acute valvular dysfunction require urgent cardiothoracic intervention.
Intra-aortic balloon pump (IABP) counterpulsation can be life-saving in cardiogenic shock. A balloon is inserted in the descending aorta just distal to the left subclavian artery. It senses the cardiac cycle and is triggered to inflate during diastole. This improves diastolic BP and coronary perfusion, reduces afterload and improves the CI. It can be weaned by reducing the ratio of counterpulsations to cardiac contractions (e.g. 1:1 down to 1:3). Anticoagulation (usually with heparin) is required to prevent systemic embolization.
More advanced adjuncts such as left ventricular support devices and cardiopulmonary bypass are available but beyond the scope of this chapter.
A detailed description of the management of the underlying conditions contributing to shock should be sought under the individual chapters.
Suggestions not to be missed are outlined below:
Source control: removal of infected lines, drainage of collections and removal of infected tissue is an urgent priority.
Culture all potential sources.
Give broad-spectrum antibiotics as soon as possible.
Consider hydrocortisone 100 mg if norepinephrine >0.2 mcg/kg/hr is required with an 8-10 mg/hr infusion if significant improvement occurs.
Consider activated protein-C (APC) if there is multi-organ dysfunction and APACHE II score >25.
Use lung-protective ventilation strategies if mechanical ventilation is required to reduce the risk of ARDS.
Remove the trigger if known.
In addition to aggressive fluid resuscitation:
Intramuscular epinephrine 0.5 mg (repeat if necessary). Failure to give promptly is associated with death.
Steroid therapy: hydrocortisone 200 mg stat
Intubate early if airway compromise is likely.
Consider antihistamine as adjunct to epinephrine only.
Achieve hemostasis as soon as possible control by pressure, surgery or embolization.
Resuscitate with packed red cells when available.
Early use of FFP (consider 1:1 ratio with red cells)
Transfuse cryoprecipitate if the fibrinogen is <1-2 mg/dL.
Monitor platelets and transfuse if <100 cells/ml.
In cases of massive transfusion give tranexamic acid 2 g and consider IV calcium to aid thrombosis.
If bleeding continues despite correction of clotting parameters, consider performing a thromboelastogram (TEG) and administration of recombinant activated factor VII.
Actively seek evidence of:
Tension pneumothorax: needle decompression and intercostal drainage
Cardiac tamponade: pericardial drain
Massive hemothorax: drainage and cardiothoracic intervention
Bleeding related to long bone or pelvic fractures: reduction and stabilization
Intra-abdominal bleeding: surgical exploration or radiographic embolization
For acute myocardial infarction, aspirin, clopidogrel, opiate analgesia, nitrates and systemic anticoagulation should be instituted while emergent PCI is arranged.
Thrombolysis can be offered if this is not available.
Consider an IABP in cardiogenic shock.
Massive pulmonary embolus causing shock is an indication for thrombolysis.
Emergency Management: Checklist
All aspects of emergency treatment, diagnostics and monitoring must be done in parallel.
Call for senior help.
Ensure airway is unobstructed and GCS >8.
Apply supplemental oxygen if required.
Ensure adequate respiratory effort and oxygenation. Intubation and ventilation may be required.
Examine rate and character of pulse.
Insert two wide-bore IV cannulae.
Switch to advanced life support if cardiorespiratory arrest has occurred or is imminent.
Postural blood pressure
Measure oxygen saturations
GCS or AVPU score
Presenting problems and timing of events
Past medical history
Relevant family history
Focused systems inquiry
Collateral history from family and family practitioner
Arterial blood gas
Oxygen saturation probe
Blood pressure: intra-arterial catheter advised. Mandatory if vasopressors/inotropes are commenced.
Central venous catheter: advised. Mandatory if vasopressors/inotropes are commenced.
Continuous cardiac output monitor. Strongly advised if vasopressors/inotropes are considered/commenced.
Cardiovert VF, VT, SVT and acute AF.
Treat bradycardia <40.
Rate-control narrow complex tachyarrythmias if not cardioverting
Perform a rapid fluid challenge.
Repeat until no longer fluid response or risk of pulmonary edema.
Use vasopressor support if necessary to achieve an appropriate minimum MAP for your patient.
Use GTN for severe hypertension in decompensated heart failure.
Ideally use a continuous cardiac output monitoring device.
Titrate a positive inotrope to achieve:
A minimum cardiac index of 2.0 L/min/m2
+ clearance of serum lactate and metabolic acidosis
How do I establish a specific diagnosis?
The differential diagnosis of a shocked patient is very wide. Establishing a specific diagnosis can be as easy as spotting the knife sticking out of their chest. However, patients may present obtunded, hypotensive and acidotic with minimal clues as to the cause on physical examination.
In the acute setting, recognition of the shocked patient followed by resuscitation according to the approach above takes priority over making the specific diagnosis, which may require a panel of further investigations, collateral history and a thorough examination. Making a specific diagnosis is critically important, however, because every cause of shock has specific considerations that if not managed and treated will lead to additional morbidity and mortality.
To achieve a specific diagnosis I would advocate the approach below.
In principle the diagnostic approach to shock is the same as in any other presentation -- that is, combining history taking, physical examination, routine and specialist investigations and imaging. However, because of the severity of the situation this must be done rapidly and concurrently with resuscitative measures.
You should attempt to match the findings of the history, examination and investigations to the three categories of shock outlined above, remembering that features of all three can coexist and different underlying etiologies may have similar clinical features but different management. For example, tamponade, cardiogenic shock and massive pulmonary embolus may present with cold and shut-down peripheries, tachypnea, tachycardia, hypotension and raised JVP, but the treatment is different.
All aspects of the classic clinical history may yield vital information for diagnosis, tailoring treatment and prognostication. In addition to the symptoms and circumstances precipitating presentation, ensure an accurate history of comorbidities, vulnerability to disease (cardiac/immunosuppression/bleeding tendency), drugs and allergies and physical functional status. Information regarding smoking, alcohol and illicit drug use should be sought. Collateral history may be needed from relatives or family practitioner.
In trauma, an AMPLE history is a useful mnemonic.
Physical exam should be thorough and achieve:
The accurate measurement of vital signs (heart rate, postural BP, respiratory rate, oxygen saturations, temperature, capillary blood glucose).
An assessment of the airway, including compromise due to reduced conscious state (GCS < 8).
Thorough examination of the chest and adequacy of respiratory effort and oxygenation.
Cardiovascular exam, paying particular attention to (a) whether the patient is warm and vasodilated or cold, clammy and vasoconstricted; and (b) the degree of hypotension if present (postural maneuvers may elicit it).
-Signs of raised filling pressures (raised JVP, chronic edema, pulsatile liver)
-Presence of cardiac murmurs
5. Abdominal exam- tenderness, distention, organomegaly, altered bowel sounds should be carefully sought
6. Neurological exam- assessment of GCS, pupillary reflexes, meningism and localizing signs
Diagnostic tests should not delay essential treatment. Essential tests are listed below. Further tests such as ultrasonography, cross-sectional imaging and echocardiography can be of enormous value in selected patients.
Blood should be drawn at the same time as inserting two large-bore cannulae.
Urea/BUN, creatinine, Na, K+, Mg, Pi, Ca, HCO3, liver enzymes, CRP
Consider: cardiac enzymes, BNP, amylase
Full blood count, prothrombin time, activated partial thromboplastin time
Consider: fibrinogen, fibrin degradation products, blood grouping and cross-match
Dipstick the urine for glucose, blood, protein , leukoesterase and nitrites
An adequate septic screen is invaluable. In the septic shocked patient, acquisition of samples should not delay administration of appropriate antibiotics.
Blood cultures x3, urine analysis, sputum or bronchial alveolar lavage, pus from any site suppurating, stool culture
Consider: lumbar puncture, urinary pneumococcal and legionella antigens, atypical respiratory serology, stool for C. difficile toxin and ova/cysts/parasites
The ABG is crucial as it gives useful information about three critical things:
1. Respiration: Oxygen saturations can tell you if a patient is adequately oxygenated but the ABG allows you to assess the degree of compromise. For example, two patients may have saturations of 100% with an FiO2 of 0.8, but one has severe respiratory failure with a PaO2 of 105 mmHg (14 kPa) while another has much better gas exchange and a PaO2 of 480 mmHg (64 kPa). It is dangerous to remove supplemental oxygen from a shocked patient with respiratory failure in order to measure the ABG on air. The degree of impairment of oxygenation can be estimated by calculating the alveolar-arteriolar oxygen difference. PaCO2 will be low if your patient is attempting to compensate for a metabolic acidosis. A rising PaCO2 is often a sign of fatigue and imminent need for ventilatory support.
2. Acid-base balance: Metabolic acidosis is present if the base deficit is >2. Metabolic acidosis may be multifactorial (tissue hypoxia/AKI/Bicarbonate loss/hyperchloremia/exogenous acid), but worsening acidosis usually indicates worsening physiology. Severe acidosis can compromise many physiological systems, including the response to vasopressors and inotropes. Renal replacement therapy may be considered if a pH < 7.2 or base deficit > 10 has not responded to adequate CO2 removal and hemodynamic optimization. Raised serum lactate often indicates tissue ischemia, which may be global or regional. Raised serum lactate is a marker of critical illness and must prompt resuscitation aimed at optimizing oxygen delivery. Non-clearance may indicate critical ischemia such as infarcted bowel, or impaired liver function.
3. Additional values: Modern blood gas analyzers allow a range of additional parameters to be estimated that may all be useful in the acute setting, including hemoglobin, electrolytes (Na/K/HCO3/Cl), carboxyhemoglobin, methemoglobin.
In addition to a cardiac monitor a 12-lead ECG is essential for the accurate detection and interpretation of arrhythmias, myocardial ischemia (and old Q-wave infarction), structural abnormalities (such as ventricular hypertrophy) and conduction disease. A baseline ECG allows comparison and detection of dynamic changes.
The CXR is a mine of information, potentially yielding volume status, sources of infection, position of catheters and reasons for hypoxia.
Ultrasonography has a wide range of applications both diagnostically and to guide percutaneous intervention such as drain insertion. It is quick and portable and so is very useful for patients who are not stable enough to be safely moved. It may yield very limited information in obese patients and is operator-dependent.
CT scanning is the most widely used cross-sectional imaging method in critically ill patients. Modern scanners are capable of whole body imaging in a few seconds and can produce detailed 3-dimensional reconstructions. They have revolutionized modern trauma management. Transfer to the CT scanner involves risk. Cumulative radiation and the risks of contrast-induced nephropathy must be balanced against the potential benefits but should not prevent scanning when clinically indicated.
Echocardiography can provide a huge amount of diagnostic and prognostic information in the shocked patient. The right side of the heart is less able to compensate than the left, and right heart failure and pulmonary hypertension at not always clinically apparent. Right and left systolic and diastolic function can be measured. Regional wall motion abnormalities related to myocardial ischemia can be identified and valvular lesions can be characterized.
At a most basic level the cardiovascular system is a vehicle for delivering oxygen and glucose to all the tissues in the body and removing carbon dioxide.
Cardiac Output (CO) = Stroke volume x Heart rate
Stroke volume increases as end-diastolic volume rises. In normal physiological states this continues until a plateau is reached. Only in poorly functioning and abnormally dilated hearts do you reach a state where over-distention can reduce cardiac output.
Oxygen delivery (DO2) = CO x arterial oxygen content (Hb x SaO2 x 1.34)
Oxygen Consumption (VO2) = CO x (Arterial oxygen content - mixed venous oxygen saturation)
From the oxygen delivery equation it can be seen that DO2 will be reduced if cardiac output is impaired, hemoglobin is low (anemic hypoxia), or oxygen saturation is reduced (hypoxic hypoxia). When optimizing patients in the ICU, these parameters can be altered to try and improve oxygen delivery. However, hypoxia may still exist in spite of good cardiac output and arterial oxygen content if tissues are unable to extract and use oxygen from the hemoglobin. Tissues may become hypoxic if there is local hypoperfusion (stagnant hypoxia). Alternatively, cytotoxicity (cytotoxic hypoxia) can result in poor oxygen metabolism.
In health, oxygen delivery is far in excess of demand. Oxygen saturation measured from a central venous or PA catheter (SvO2 or ScvO2) can provide some clues as to the extent of oxygen extraction and balance between supply and demand.
Normal oxygen extraction is less than 25%, giving a central venous saturation >75%. If oxygen delivery is reduced or oxygen demand increased (by pain, fever, tachycardia, respiratory distress, etc.) then a compensatory increased extraction may occur down to 50%. Beyond this level of extraction tissues begin to undergo anaerobic metabolism, generating lactic acidosis.
In some instances tissue hypoxia occurs through impaired oxygen extraction or utilization. In severe sepsis, for example, SvO2 may be high at >80% despite the presence of lactic acidosis and multi-organ dysfunction. Organ dysfunction such as AKI may commonly occur in the absence of documented hypotension. Sepsis may induce complex dysfunction at the cellular level due to the pro-inflammatory state, which shuts down metabolic activity at the mitochondrial level.
A similar phenomenon can be observed post resuscitated cardiac arrest where global hypoxia impairs cellular function and a pro-inflammatory state also contributes.
The deleterious effects of impaired oxygen delivery begin before obvious organ dysfunction is clinically apparent; this could be classified as pre-shock. Using cardiac output monitoring has been shown to improve outcomes in pre-operative, peri-operative and immediate post-operative optimization protocols in high-risk surgery.
Once shock has been identified it is essential that the response is rapid. This was demonstrated in the well-known study of early goal-directed therapy for septic shock in the emergency department by Rivers et al.
For a detailed description of septic shock please see the relevant chapter.
Sepsis can be defined by the presence of two or more of the systemic inflammatory response (SIRS) criteria:
1. Temperature <36°C or >38°C
2. HR > 90 bpm
3. RR > 20
4. WCC <4 or >20
combined with proven or suspected infection.
Severe sepsis is defined as the presence of sepsis with organ dysfunction.
Septic shock is severe sepsis + hypotension or lactate >4 mmol/L despite fluid resuscitation.
Refractory septic shock is septic shock with addition of high vasopressor requirements to maintain a MAP > 60 mmHg.
Sepsis is primarily a disease of the vascular endothelium. Inflammation is essential for the host defense of infection. Pro-inflammatory mediators released from polymorphonuclear leukocytes (PMNs) such as interleukin-1 and tumor necrosis factor alpha promote further PMN aggregation at the site of infection and increase phagocytosis. This is normally tightly regulated, but an exaggerated, generalized and uncontrolled inflammatory response to infection can occur and leads to multi-organ dysfunction.
This often occurs in the presence of specific toxins associated with the infective organism such as lipopolysaccharide (LPS or endotoxin) found in the cell wall of gram-negative bacteria. Nitric oxide production by the endothelium is the main reason for the vasodilatation classically associated with sepsis. This redistribution of effective arteriolar blood volume and inability to compensate leads to hypotension. Interestingly, septic patients may have lower levels of antidiuretic hormone as well. For a given degree of hypotension septic patients tend to develop more AKI than cardiogenic shock patients.
The physiology of organ dysfunction is extremely complicated and important factors are micro-circulatory impairment, mitochondrial dysfunction and direct cytotoxic effects from activated members of the host’s immune system.
Cardiogenic shock usually occurs in the context of a large MI or complication of one such as acute mitral incompetence or tamponade. Ventricular impairment causes a fall in stroke volume and a resultant fall in cardiac output. Blood pressure is dependent on the cardiac output and peripheral resistance. Compensatory mechanisms to maintain the systemic blood pressure via a rise in resistance include high catecholamine levels, activation of the RAA system and vasopressin release. Unfortunately these have a tendency to cause further compromise in oxygen delivery through intense vasoconstriction and increased afterload. Coronary artery hypoperfusion due to hypotension compounds the problem, and a vicious cycle can spiral to death.
As always the clinical picture is often more complicated, and inflammatory vasodilatation may coexist due to post-MI SIRS or concurrent infection.
The fluid components of the human body are traditionally divided into three compartments. In a 70-kg man they would contain a total of 40 liters. 25 liters is intracellular. 15 liters is extracellular, comprising 12 liters interstitial fluid and 3 liters intravascular plasma volume. Blood volume is increased by the hematocrit.
Clinical hemodynamic responses to hypovolemia occur in response to a reduction in the effective arterial blood volume (EABV). Compensation for reductions in EABV occur through neural-hormonal responses via RAA and sympathetic nervous system activation, vasopressin release and suppression of atrial natriutetic hormone secretion. In acute hemorrhage this happens very quickly. If fluid loss is more chronic, such as diarrhea over several days, then there is time for fluid to shift from the intracellular space to the interstitial and then plasma through osmosis. In this context dehydration occurs that is not synonymous with hypovolemia. Clinical signs such as dry mucous membranes and reduced skin turgor indicate dehydration.
As a general rule the responses to reduced EABV are:
Up to 15% intravascular fluid loss can be compensated for with tachycardia only.
15-30% may result in a postural BP drop (>20 mmHg systolic/>10 mmHg diastolic), which you won't find unless you measure it.
It may not be until >30% intravascular fluid loss that hypotension occurs. Young patients compensate very well and may be close to cardiac arrest at this point.
Failure to correct hypovolemic shock fast or adequately enough can lead to irreversible shock, which is fatal. The potential mechanisms are complex but the net effect is the pooling of blood in capillaries and hypotension, which does not respond adequately to vasopressors.
In general, shock is under-recognized and under-treated even when overt organ dysfunction is present. Morbidity and mortality are increased even in the absence of obvious organ dysfunction when oxygen delivery is impaired. This makes measuring the incidence and impact of shock syndromes difficult in normal clinical environments.
Shock is an important cause of emergency presentation and ICU unit admission and also commonly develops in hospital inpatients.
Vulnerability to poor outcome in shock has logical predisposing factors, with increasing age and burden of comorbid conditions being predictive for all forms.
The recognition of sepsis as a major cause of morbidity and mortality has had a renaissance in recent years, in no small part due to the international Surviving Sepsis campaign. Sepsis causes a similar number of deaths as acute myocardial infarction and more than breast cancer or colon cancer. There is evidence that the incidence of severe sepsis is increasing in Western societies, mostly due to the aging population. Despite developments such as early goal-directed therapy, the hospital mortality of severe sepsis remains around 30%.
Sepsis places a significant burden on healthcare resources, accounting for 40% of total ICU expenditure and costing up to $7.6 billion annually in Europe and $16.7 billion in the United States in 2000.
The most common cause of cardiogenic shock is acute myocardial infarction. As such, the incidence corresponds to trends in the prevalence of acute MI and management of classic risk factors. In addition, improvements in access and utilization of reperfusion techniques such as primary percutaneous coronary intervention (PCI) have reduced infarct size in many individuals. As such, the overall incidence of cardiogenic shock as a consequence of acute MI has decreased. The mortality from cardiogenic shock has halved to around 40% for the same reasons plus the availability of aortic balloon counter-pulsation.
In contrast, as more people survive acute MI, the burden of hypertension increases and as the population ages, the incidence of acute decompensated heart failure is increasing.
Trauma is a leading cause of death, accounting for 10% worldwide. The proportion of trauma deaths depends on a number of factors, including general life expectancy/socioeconomic conditions, road and work safety and the presence of conflict. Irrespective of this, trauma is the most common cause of death in the under-35 age group. Around 1/3 of deaths are attributable to hemorrhage, with another half caused by central nervous system injury.
What's the evidence?
2010. http://www.resus.org.uk/pages/als.pdf.(An update on current life support algorithms.)
Cecconi, M. "Haemodynamic monitoring in acute heart failure". Heart Failure Review. vol. 12. 2007. pp. 105-111.(An overview of hemodynamic monitoring used when assessing cardiac output.)
Pinsky, MR, Teboul, JL. "Assessment of indices of preload and volume responsiveness". Curr Opin Crit Care. vol. 11. 2005. pp. 235-239.(Overview of techniques used to assess preload responsiveness.)
Marik, PE, Baram, M, Vahid, B. "Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares". Chest. vol. 134. 2008 Jul. pp. 172-8.(A critique of the use of CVP measurement to optimize preload.)
Ho, AM, Karmakar, MK, Dion, PW. "Are we giving enough coagulation factors during major trauma resuscitation?". Am J Surg. vol. 190. 2005. pp. 479-84.
Erber, WN, Perry, DJ. "Plasma and plasma products in the treatment of massive haemorrhage". Best Pract Res Clin Haematol.. vol. 19. 2006. pp. 97-112.(Two good reviews of the use of blood products in massive transfusions.)
Rivers, E. "Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic Shock". N Engl J Med. vol. 345. 2001. pp. 1368-77.(A hugely influential but increasingly controversial RCT.)
"Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008". Crit Care Med. vol. 36. 2008. pp. 296-327.(An update on the recommended components (with evidence) for treating septic shock.)
De Backer, D. "SOAP II Investigators. Comparison of dopamine and norepinephrine in the treatment of shock". N Engl J Med. vol. 362. 2010. pp. 779-89.(An excellent RCT comparing these two commonly used vasopressors.)
Hochman, JS. "Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock". N Engl J Med. vol. 341. 1999. pp. 625-34.(A good study that demonstrated the advantage of early revascularization.)
http://www.trauma.org/archive/resus/permissivehypotension.html.(This site has an excellent bibliography of research in to pre-hospital/early fluid resuscitation in hemorrhagic shock, including this much-cited and criticized paper:)
Bickell, WH. "Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries". N Engl J Med. vol. 331. 1994 Oct 27. pp. 1105-9.
Andrew, D Bersten, Neil, Soni. Oh’s Intensive Care Manual.
Guyton and Hall Textbook of Medical Physiology.(Good base texts.)
Califf, RM, Bengtson, JR. "Cardiogenic shock". N Engl J Med.. vol. 330. 1994. pp. 1724-30.(Excellent review article.)
Singer, M.. "Cellular Dysfunction in Sepsis". Clinics in Chest Medicine. vol. 29. pp. 655-660.(More in-depth physiology of sepsis.)
Pearse, R. "Early goal-directed therapy after major surgery reduces complications and duration of hospital stay. A randomised, controlled trial". Crit Care. vol. 9. 2005. pp. R687-R693.
Goldberg, RJ. "Thirty-year trends (1975 to 2005) in the magnitude of, management of, and hospital death rates associated with cardiogenic shock in patients with acute myocardial infarction: a population-based perspective". Circulation. vol. 119. 2009. pp. 1211-9.
Jeger, RV. "Ten-year trends in the incidence and treatment of cardiogenic shock". Ann Intern Med. vol. 149. 2008. pp. 618-26.(Two useful studies looking at trends over many years.)
Martin, GS. "The epidemiology of sepsis in the United States from 1979 through 2000". N Engl J Med. vol. 348. 2003. pp. 1546-54.
Angus, DC. "Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care". Crit Care Med. vol. 29. 2001. pp. 1303-10.
Martin, GS, Mannino, DM, Moss, M. "The effect of age on the development and outcome of adult sepsis". Crit Care Med.. vol. 34. 2006. pp. 15-21.(Three interesting studies. Not surprisingly, older people have higher mortality. Those who survive often require prolonged rehabilitation and ongoing care after hospital.)
Kauvar, DS, Wade, CE. "The epidemiology and modern management of traumatic hemorrhage: US and international perspectives". Crit Care.. vol. 9 Suppl 5. 2005. pp. S1-9.(This study demonstrates how poor oxygen delivery may cause worse outcomes even at subclinical levels and early targeting can improve them. This excellent review article is available free on-line.)
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