Shock

Shock is a state in which there is inadequate blood flow to the tissues to meet demand. Although shock and hypotension often coexist, hypotension need not be present and a normal blood pressure does not exclude the diagnosis of shock.

Evidence of hypoperfusion may be obtained by examining the patient’s conscious state, the temperature of the limbs and the urine output. Further information may be obtained by measuring arterial blood gases and serum lactate.

Assessment of the hypotensive patient

The simplest way to approach this is from a physiological standpoint

MAP = CO × TPR

CO = HR × SV

Therefore MAP = HR × SV × TPR

where MAP=mean arterial pressure, CO=cardiac output, TPR= total peripheral resistance, HR=heart rate and SV=stroke volume.

Stroke volume is dependent on preload, afterload and contractility but afterload is difficult to assess at the bedside.

Therefore the important parameters to assess are:

Both preload and contractility can be assessed with echocardiography but this may not be available in the emergency setting. Likewise peripheral resistance can be estimated by measuring cardiac output, central venous pressure and mean arterial pressure and calculating systemic vascular resistance, but these measurements are also unlikely to be immediately available.

In the emergency setting the assessment is based, therefore, on the heart rate, the jugular venous or central venous pressure (as a measure of preload) and the temperature of the peripheries (as a measure of total peripheral resistance (table 1). Echocardiography ± measurement of cardiac output should be considered after initial resuscitation.

The two commonest causes of shock in the ICU are distributive shock (due to sepsis) and hypovolaemic shock.

It is important to determine the type of shock. Although most previously unresuscitated, patients will require some fluid, the volume of fluid is dependent on the type of shock. Patients who already have pulmonary oedema should not be given further fluid.

Thus the two important initial questions are:

  1. What type of shock?
  2. Pulmonary oedema?

Table 1. Diagnostic clues to cause of shock in the emergency setting. *obstructive shock due to massive pulmonary embolus, cardiac tamponade or tension pneumothorax.

Cardiogenic shock

Cardiogenic shock is shock due to cardiac pump failure resulting from myocardial or valvular failure. The strict diagnosis requires the persistence of shock after correction of non-myocardial factors such as hypovolaemia, hypoxia, profound acidosis and arrhythmias.

The commonest cause of cardiogenic shock is myocardial ischaemia or infarction. Other causes are given in table 2.

In patients with cardiogenic shock due to myocardial ischaemia or infarction, the two main aims of treatment are to improve coronary perfusion and to increase cardiac output. Obviously improving coronary perfusion will, in itself, increase cardiac output.

Table 2. Causes of cardiogenic shock

Coronary perfusion can be improved by both definitive and supportive therapy. The definitive therapy of choice is percutaneous coronary intervention (angioplasty stenting). Alternatives include coronary artery bypass grafting and thrombolysis. The latter tends to be less effective in patients with cardiogenic shock.

Supportive therapy to improve coronary perfusion in severe cardiogenic shock is based on increasing diastolic blood pressure to increase coronary perfusion pressure and flow. The vasoactive agent of choice in a severely hypotensive patient is, therefore, norepinephrine because of its vasoconstrictive effect (which increases diastolic pressure) and its relative lack of chronotropy. If available, early consideration should be given to the use of intra-aortic balloon counterpulsation. This not only increases diastolic pressure but also decreases left ventricular afterload and increases cardiac output without an increase in myocardial oxygen demand.

As mentioned above, measures to improve coronary perfusion usually increase cardiac output. Other methods that may be attempted include careful administration of fluid in small boluses (~100 ml of crystalloid), careful administration of vasodilators (normotensive patients only) and administration of dobutamine at doses of up to 20μg/kg/min (normotensive or mildly hypotensive patients). When determining whether or not to give fluid, remember that a raised atrial pressure may be due to a fall in myocardial compliance and may not reflect a high preload.

Hypovolaemic shock

Hypovolaemic shock is the result of intravascular volume depletion. The common causes are:

The primary abnormality is a decrease in preload, which causes a decrease in stroke volume. The typical haemodynamic picture is of decreased cardiac output and blood pressure, low venous pressure, peripheral vasoconstriction and tachycardia.

Table 3 gives a rough guide to intravascular volume loss but it should be noted that there may be discordance between clinical signs and that changes in clinical signs are more important than absolute values. In particular, note that hypotension is a late sign of shock.

Table 3. Clinical features of hypovolaemic shock

It is important to realize that following resuscitation the main picture becomes one of distributive shock as a result of the inflammatory response to the primary insult, any surgical intervention and massive transfusion of blood and blood products.

The treatment of hypovolaemic shock is aimed at fluid therapy and definitive treatment of the underlying cause. Choice of fluid replacement is largely based on the type of fluid that has been lost. Because of the inherent complications of blood transfusion, mild to moderate blood loss (less than one litre in an adult), should be replaced by colloid (1-1.5 times volume of blood lost) or crystalloid (1.5-2 times volume of blood lost). In large-volume resuscitation, however, excessive normal saline infusion may produce hyperchloraemic metabolic acidosis and a balanced crystalloid (eg lactated Ringer’s solution or Plasma-Lyte may be preferable). Colloid solutions (5% albumin, gelatins) offer the most efficient intravascular volume expansion, but compared to crystalloids are expensive and do not reduce mortality. Dextrose 5% in water does not offer significant expansion of intravascular volume because it is quickly distributed throughout body fluid compartments.

In the initial stages of resuscitation it may be necessary to give a vasoconstrictor to maintain life while correcting hypovolaemia. A vasoconstrictor may also be necessary at a later stage if the patient goes on to develop distributive shock due to systemic inflammation.

Distributive Shock

Distributive shock occurs when peripheral vascular dilatation causes a fall in peripheral resistance. The most common cause of distributive shock is septic shock. Other, less common causes are anaphylactic shock, acute adrenal insufficiency and neurogenic shock. The 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 its ability to distribute blood properly. Clinical features include warm peripheries and bounding pulses, but with evidence of tissue hypoperfusion despite this. Evidence of hypoperfusion may include mental status changes, oliguria, or lactic acidosis.

Septic shock is covered in Severe sepsis and septic shock and anaphylactic shock in Anaphylaxis. Acute adrenal insufficiency is treated with volume therapy, intravenous corticosteroids, and vasopressors.

Obstructive Shock

Obstructive shock is characterised haemodynamically by decreased cardiac output, peripheral vasoconstriction and tachycardia. The JVP is usually, but not invariably, raised, depending on the cause.

Cardiac tamponade

Cardiac tamponade represents extracardiac obstructive shock, where there is a mechanical obstruction to cardiac filling. Always consider cardiac tamponade when the JVP is high and BP low. Pulsus paradoxus is an important clinical finding in patients with suspected cardiac tamponade. The treatment is urgent pericardiocentesis.

Tension pneumothorax

The treatment of tension pneumothorax is needle thoracostomy followed by insertion of an intercostal drain.

Massive pulmonary embolus

The mode of death from massive pulmonary embolus is cardiovascular failure as a result of right heart failure. Massive pulmonary embolus increases right ventricular afterload, enlarges the right ventricle and may cause deviation of the septum to the left, thus decreasing left ventricular volume and compliance (figure 1). Cardiac output and coronary blood flow (especially to the right heart) fall, resulting in decreased ventricular contractility and a cycle of cardiac decompensation.

Figure 1. RV distension and LV compression following massive pulmonary embolus

Pulmonary CT angiography is probably the investigation of choice for the unstable patient, although echocardiography may be helpful in experienced hands.

Supportive therapy includes fluid therapy and vasoconstriction. Fluid should be given cautiously as a marked rise in right ventricular end-diastolic pressure may result in a marked decrease in right sided coronary perfusion pressure and a shift of the interventricular septum to the left. Norepinephrine is the vasoactive agent of choice – by increasing mean arterial pressure it increases right ventricular coronary perfusion.

Definitive therapy is aimed at relieving the obstruction. The best treatment is not clear but intravenous thrombolysis with tissue plasminogen activator is probably the treatment of choice. All patients should receive anticoagulation with intravenous unfractionated heparin or subcutaneous low molecular weight heparin as soon as the diagnosis is suspected.

Vasopressors and inotropes

The effect of these agents in critically ill patients is dependent on both their pharmacological effects and the patient’s pathophysiology. In the hypotensive patient, norepinephrine may increase cardiac output, by increasing diastolic blood pressure and hence coronary perfusion, despite its minimal inotropic effect in healthy volunteers.

The majority of vasopressors and inotropes have very short half lives with the result that the dose can be easily titrated when delivered by continuous infusion. The appropriate dose is determined by the physiological effect in the individual patient, who should be monitored closely.

A continuous infusion is prepared by diluting a pre-determined drug dose in a specified volume (eg 3 mg norepinephrine added to normal saline to give a total volume of 50 ml). This solution is infused using an infusion pump at a set rate (eg 3 ml/h). Wards that use vasopressors and inotropes should have standard methods of dilution and infusion rate charts to convert the doses given below into infusion rates. It is safest to use the ward’s standard dilution method to avoid confusion and the infusion charts to avoid calculation error. Note that the doses given below are doses/min as the drug is given continuously.

Start with the starting doses given below and then increase or decrease the dose in response to the effect seen in the patient. For vasopressors titrate the infusion rate against the blood pressure (diastolic to maintain coronary perfusion, mean to maintain perfusion to other organs).

Most agents reach a new steady state within 15 minutes of a change in infusion rate with the majority of the response being seen in the first 10 minutes. When changing the infusion rate of vasopressors, the rate should be doubled or halved if the blood pressure is far below or above the target value. Smaller changes should be made if the blood pressure is close to the target value.

Vasopressors can cause severe soft tissue damage if the solution extravasates. Ideally these agents should be given via a central venous catheter, but in an emergency they can be given via a safely positioned and well functioning peripheral intravenous cannula for minutes to hours.

When choosing vasopressors or inotropes aim to restore blood pressure first. If organ perfusion remains poor despite an adequate blood pressure consider giving dobutamine e to increase cardiac output. While dopamine, norepinephrine and epinephrine have different effects, all of them are vasopressors and can be used to reverse hypotension. Your choice of vasopressor should take into account availability and the familiarity of ward staff with administration. You should, therefore, familiarize yourself with the drugs that are available in your ward.

Dopamine

Short acting agent with inotropic, chronotropic and vasoconstrictor effects. It increases urine output through a tubular effect without increasing creatinine clearance. Not recommended in septic shock if norepinephrine or epinephrine are immediately available. However, if these agents are not immediately available use of dopamine is preferable to leaving the patient hypotensive.

A reasonable starting dose is ~5 μg/kg/min. Dopamine should ideally be given through a central venous cannula, but in an emergency it can be given through a peripheral cannula, as described above.

Norepinephrine

Potent vasoconstrictor with minor direct inotropic and chronotropic effects. It may, however, increase cardiac output in hypotensive patients by increasing cardiac perfusion through its effect on diastolic blood pressure. Like dopamine, norepinephrine should only be administered through a central venous catheter. 0.05 μg/kg/min is a reasonable starting dose. Vasoactive agent of choice in septic shock but less likely to be available outside ICU.

Epinephrine

Similar to norepinephrine but has greater direct inotropic and chronotropic effects. Again, 0.05 μg/kg/min is a reasonable starting dose.

Dobutamine

Dobutamine has inotropic, vasodilator and chronotropic effects. Because of its vasodilator effects it should not be used alone in severely hypotensive patients but may be usefully combined with norepinephrine in this situation. It can be given peripherally, but because of its short half life patients who are dependent on its effects may deteriorate rapidly should it extravasate. The recommended dose is 0-20 μg/kg/min.

Immediately life-threatening shock

In emergency situations (eg immediately life-threatening shock or cardiac arrest) give epinephrine as a bolus. The dose should be given in mg as epinephrine is supplied as 1:1000 or 1:10,000 concentration.
In immediately life-threatening shock (eg systolic BP ≤ 50 mmHg or rapidly progressive shock) give epinephrine 0.1 mg IV, repeated as necessary.
The dose in cardiac arrest is 1 mg IV.