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Introduction to management of shock for junior ICU trainees and medical students

Gavin Joynt

Types of shock

Cardiogenic Shock

  • blood flow decreased due to an intrinsic defect in cardiac function – either the heart muscle, or the valves are dysfunctional

  • classical example is acute anterior myocardial infarction, when the amount of damaged ischaemic muscle may be so great that the heart cannot pump anymore. The decreased contractility causes a decrease in stroke volume

  • typical haemodynamic picture: 

    • decreased cardiac output and blood pressure

    • high left ventricular filling pressures (backward failure)

    • increased systemic vascular resistance (from vasoconstriction, which is a sympathetic compensatory response to the low blood pressure)

    • increased heart rate (sympathetic compensatory response to the low blood pressure)

    • other features of cardiogenic shock such as the cool peripheries, decreased urine output and sweating can also be explained by the sympathetic compensatory response.

Hypovolemic shock

  • result of intravascular blood volume depletion

  • common causes:

    • haemorrhage

    • vomiting

    • diarrhoea

    • dehydration

    • third-space losses during major operations

  • primary abnormality is a decrease in preload. The decreased preload causes a decrease in stroke volume.

  • typical haemodynamic picture:

    • decreased cardiac output and blood pressure

    • low left ventricular filling pressures (because the ventricle is empty)

    • increased SVR (from vasoconstriction, which is a sympathetic compensatory response to the low blood pressure)

    • increased heart rate (sympathetic compensatory response to the low blood pressure)

  • Other features of hypovolaemic shock are similar to those seen in cardiogenic shock and include cool peripheries, decreased urine output and sweating that can also be explained by the sympathetic compensatory response.

Distributive Shock

  • occurs when the peripheral vascular dilatation causes a fall in SVR

  • most common causes:

    • septic shock

    • anaphylactic shock

    • acute adrenal insufficiency

    • neurogenic shock.

  • cardiac output is often increased but the perfusion of many vital organs is compromised because the blood pressure is too low and the body loses it’s ability to distribute blood properly

  • haemodynamic profile is usually characterised by:

    • normal or increased cardiac output with a low SVR

    • low to normal left ventricular filling pressures

    • low blood pressure

  • clinical features include:

    • warm peripheries

    • bounding pulses

    • tissue dysfunction despite this:

      • mental status changes

      • oliguria

      • lactic acidosis.

Obstructive Shock

Cardiac tamponade

  • extracardiac obstructive shock

  • mechanical obstruction to cardiac filling

  • pressures of the right cardiac chambers, the pulmonary artery, and the left cardiac chambers equilibrate in diastole

  • always consider cardiac tamponade when the CVP is high and BP low.

  • pulsus paradoxus

    • exaggeration of normal physiology in which there is a decrease of >10 mm Hg in systolic blood pressure during inspiration

    • important clinical finding in patients with suspected cardiac tamponade

Other forms

  • tension pneumothorax

  • massive pulmonary embolus

Principles of management

  • look for reversible causes such as acute valvular insufficiency, drug overdose, or tamponade

  • major goal of management is to return tissue oxygen delivery to normal. The treatment priority is therefore to increase cardiac output and blood pressure. Optimising the oxygen content of blood can also help to improve tissue oxygen delivery. The goal of improving cardiac output and blood pressure is usually accomplished with some combination of adjusting preload, increasing cardiac contractility and optimising SVR. Ensuring both good oxygenation and haemoglobin content optimises the oxygen content of the blood

  • occasionally, heart rate abnormalities, such as bradycardia, or tachyarrhythmias such as ventricular tachycardia, may cause or contribute to hypotension and must be treated.

Acute Cardiogenic Shock

  • primary goal is to improve myocardial muscle function

  • elevated SVR may also impair cardiac output because it increases afterload. Often in acute cardiogenic shock, the SVR is secondarily elevated (part of the baroreceptor response to shock) to maintain vascular perfusion pressure

  • inotropes, such as dobutamine, are indicated to increase myocardial contractility in the presence of normal or slightly decreased blood pressure and may have a secondary beneficial effect of decreasing SVR and improving afterload.

  • NB driving pressure for coronary artery perfusion is aortic diastolic pressure (this is because coronary artery perfusion occurs primarily during diastole). A low aortic diastolic pressure is common in severe shock seen in ICU and may be gently increased with vasopressors (agents that cause vasoconstriction and therefore increase SVR).  However, because of the increase in afterload, an agent that also increases cardiac muscle performance must also be used, and initial therapy with a single agent that has both inotropic and vasopressor effects (i.e. norepinephrine or high-dose dopamine) is indicated

  • if hypotension is not responsive to initial therapy, consultation should be obtained for consideration of a cardiac assist device such as intra-aortic balloon counterpulsation.

Hypovolemic Shock

  • return intravascular volume to normal

  • initial resuscitation:

    • colloid or crystalloid fluids are effective

      • choice of fluid should be based on the fluid type that has been lost.  For example, blood should replace blood and crystalloid should be used for vomiting and dehydration

      • because of the inherent complications of blood transfusion, mild to moderate blood loss (less than one liter in an adult), should be replaced by colloid (1-1.5 times volume of blood lost) or  crystalloid (crystalloid 2.5-3 times volume of blood lost)

      • crystalloid of choice is normal saline or lactated Ringer’s solution because it’s osmolality is similar to that of the intravascular volume. In large-volume resuscitation, however, excessive normal saline infusion may produce hyperchloremic metabolic acidosis. Colloid solutions (5% albumin and hetastarch) offer the most efficient intravascular volume expansion, but are expensive and no outcome benefit has been shown. Dextrose 5% in water does not offer significant expansion of intravascular volume because it is quickly distributed throughout body fluid compartments.

    • endpoints of therapy are to re-establish normal blood pressure, pulse, and organ perfusion. 

More on cardiogenic shock

Distributive Shock

  • vasodilation, resulting in a very low SVR, and diffuse capillary leak are the major features

  • because of capillary leakage, hypovolaemia contributes significantly to the shock before resuscitation and fluid requirements may be very large

  • end points of fluid resuscitation are the same as for hypovolaemic shock at this stage

  • if the patient remains hypotensive despite adequate fluid resuscitation (high CVP, pulmonary artery occlusion pressure, or pulmonary oedema) inotropes and/or vasopressors are necessary

  • anaphylactic shock is treated with subcutaneous epinephrine (0.3-1mg) and volume resuscitation. In circumstances of very low blood pressure and poor peripheral perfusion, titrated intravenous epinephrine (25-50µg per bolus) is indicated

  • acute adrenal insufficiency is treated with volume therapy, intravenous corticosteroids, and vasopressors.

  • septic shock

    • combination of inotropic and vasopressor effect is optimal. Dopamine (5 mg/kg/min and increased if necessary to 15-20 mg/kg/min) or adrenaline (0.05 mg/kg/min and increased if necessary to 2 mg/kg/min) provide both vasopressor and inotropic support

    • if mg/kg/min and increased if necessary to 2 mg/kg/min). The addition of dobutamine (5-10 mg/kg/min) may be beneficial if noradrenaline is used

    • i

Obstructive Shock

  • relief of the obstruction is life saving

    • if cardiac tamponade is present, urgent pericardiocentesis is essential

    • tension pneumothorax must be treated promptly with needle thoracostomy

    • massive pulmonary embolism requires urgent thrombolysis or surgical removal

  • keeping preload normal is important in patients with all forms of obstructive shock. Fluid resuscitation may improve the patient’s cardiac output and hypotension temporarily and buy time for definitive intervention. 

© Gavin Joynt April 2003

©Charles Gomersall, May, 2009 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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