Although many clinical features are common to all types of shock there are certain important respects in which they differ:
1 Inadequate tissue perfusion:
(a) Skin-cold, pale, blue, slow capillary refill
(b) Kidneys-oliguria, anuria
(c) Brain-confusion and restlessness
2 Increased sympathetic tone:
(a) Tachycardia, narrowed pulse pressure
(c) Blood pressure-may be maintained initially (despite up to a 25% reduction in circulating volume if the patient is young and fit), but later hypotension supervenes
3 Metabolic acidosis and tachypnoea
Additional clinical features may occur III the following types of shock.
1 Signs of myocardial failure, e.g. raised jugular venous pressure Ovp), pulsus alternans, ‘gallop’ rhythm, basal crackles, pulmonary oedema
1 Elevated JVP
2 Pulsus paradoxus and muffled heart sounds in cardiac tamponade
3 Kussmaul’s sign OVP rises on inspiration) in cardiac tamponade
4 Signs of pulmonary embolism (if present)
1 Signs of profound vasodilatation:
(a) Warm peripheries
(b) Low blood pressure
2 Erythema, urticaria, angio-oedema, pallor, cyanosis
3 Bronchospasm, rhinitis
4 Oedema of the face, pharynx and larynx
5 Pulmonary oedema
6 Hypovolaemia due to capillary leak
7 Nausea, vomiting, abdominal cramps, diarrhoea
1 Pyrexia and rigors, or hypothermia (unusual)
2 Nausea, vomiting
3 Vasodilatation, warm peripheries
4 Bounding pulse
5 Rapid capillary refill
7 Occasionally signs of cutaneous vasoconstriction
8 Other signs:
(b) Coma (rare)
The diagnosis of septicaemia is easily missed. In the elderly, the classical signs may not be present and, for example, mild confusion, tachycardia and tachypnoea may be the only clues, sometimes associated with unexplained hypotension, a reduction in urine output, a rising plasma creatinine and glucose intolerance.
Invasive monitoring is unnecessary in straightforward cases, such as a fit young man with moderate traumatic haemorrhage, but will be required in the more seriously ill patients and in those who fail to respond to initial treatment (see later). Clinical assessment must never be neglected.
Clinical indices of tissue perfusion
Pale, cold skin, delayed capillary refill and the absence of visible veins in the hands and feet indicate poor perfusion. Skin temperature measurements can help clinical evaluation as vasoconstriction is an early compensatory response.
Urinary flow is a sensitive indicator of renal perfusion and haemodynamic performance.
Alterations in blood pressure are often interpreted as reflecting changes in cardiac output. However, if there is vasoconstriction with a high peripheral resistance, the blood pressure may be normal, even when the cardiac output is reduced. Conversely the vasodilated patient may be hypotensive despite a very high cardiac output. The absolute level of blood pressure is also important, since hypotension may jeopardize perfusion of vital organs. The adequacy of blood pressure in an individual patient must always be assessed in relation to the premorbid value.
Blood pressure is traditionally measured with a sphygmomanometer, but automated instruments using a microphone to detect Korotkoffs sounds or continuous monitoring with an intra-arterial cannula, usually in the radial artery.
Central venous pressure (CVP)
This provides a fairly simple method of assessing the adequacy of a patient’s circulating volume and the contractile state of the myocardium. The absolute value of the cVP is not as important as its response to a fluid challenge (the infusion of 100-200 ml of fluid over 1-3 min). The hypovolaemic patient will initially respond to transfusion with little or no change in CVP, together with some improvement in cardiovascular function (falling heart rate, rising blood pressure and increased peripheral temperature). As the normovolaemic state is approached, the CVP usually rises slightly and stabilizes, while other cardiovascular values normalize. At this stage, volume replacement should be slowed, or even stopped, in order to avoid overtransfusion (indicated by an abrupt and sustained rise in CVP, often accompanied by some deterioration in the patient’s condition). In cardiac failure the venous pressure is usually high; the patient will not respond to volume replacement, which will cause a further, sometimes dramatic, rise in CVP. The CVP may be read intermittently using a manometer system or continuously using a transducer connected to an oscilloscope, similar to that used for intra-arterial monitoring.
Common pitfalls in interpreting CVP results are:
BLOCKED CATHETER. This results in a sustained high reading, with a damped waveform which often does not correlate with clinical assessment.
MANOMETER OR TRANSDUCER WRONGLY r-o s- ITIONED. Failure to level the CVP after changing the patient’s position is a common cause of erroneous readings.
INCORRECT CALIBRATION If an electronic transducer and oscilloscope are used, the system should be zeroed and calibrated prior to use.
ONE OR MORE INFUSIONS IN PROGRESS THROUGH THE CVP CATHETER. The CVP catheter maybe used for other infusions and the pressure measured intermittently. A falsely high reading will result if these fluids continue to be administered by an infusion pump while the pressure is recorded.
CATHETER TIP IN RIGHT VENTRICLE. If the catheter is advanced too far, an unexpectedly high pressure is recorded.
The catheter should be positioned in the superior vena cava. It is usually inserted via a percutaneous puncture of a subclavian or internal jugular vein.