Initial management is summarized in Figure 2.1.

1. If hypovolaemia or vasodilatation is likely, lay the patient flat and elevate the foot of the bed.

2. Give oxygen. Place an IV cannula. Attach an ECG monitor. Check oxygen saturation. Make a rapid clinical assessment (Table 2.2). Look carefully at the JVP, and assess skin temperature and perfusion. Investigations needed urgently are given in Table 2.3.

   Questions to ask yourself include:

   • Is there obvious haemorrhage from the gastrointestinal tract or other site (e.g. abdominal aortic aneurysm) (Chapters 73 and 74)?
   • Is there a major arrhythmia (Chapter 39)?
   • Is there ECG evidence of an acute coronary syndrome (ST segment elevation or depression, new left bundle branch block) (Chapters 45 and 46)?
   • Is there associated pulmonary oedema, indicating cardiogenic shock (Chapter 49)?
   • Is there fever, or other features pointing to sepsis (Chapter 35)?
   • Is pulmonary embolism possible (Chapter 57)? Hypotension and hypoxaemia without pulmonary oedema suggest pulmonary embolism or sepsis; in this setting, a raised JVP would favour pulmonary embolism and a low JVP sepsis.
   • Is tension pneumothorax a possibility (e.g. recent central vein cannulation) (Chapter 64)?
   • Could this be anaphylaxis (Chapter 38)? If the patient has recently been exposed to a potential allergen, and has urticaria, erythema, angio-oedema or wheeze, treat as anaphylaxis and give adrenaline 0.5–1 mg IM (0.5–1 mL of 1 in 1000 solution). Further management is detailed in Chapter 38.
3. If hypotension does not respond promptly, put in a bladder catheter so that urine output can be monitored. The urine output is a rough guide to renal blood flow and cardiac output; the target is >0.5 mL/kg/h.

The key points in the management of hypotension/shock are to:

• Make a diagnosis and give specific treatment (e.g. pericardiocentesis for tamponade, PCI for ACS, cardiac surgery for ruptured papillary muscle). Seek help from an intensivist and, in the case of cardiogenic shock, a cardiologist.
• Correct cardiac arrhythmias.
• Correct hypovolaemia while avoiding fluid overload.
• Correct hypoxia and biochemical abnormalities.
• Use inotropic/vasopressor therapy if there is refractory hypotension.

1. Make a diagnosis and give specific treatment:
   • Consider the causes in Table 2.1.
   • Echocardiography is indicated if the diagnosis remains unclear.
   • Give hydrocortisone 200 mg IV if the patient has been on previous long-term steroid treatment (prednisolone >7.5 mg daily) or you suspect acute adrenal insufficiency (Chapter 90).
2. Correct cardiac arrhythmias:
   • Ventricular tachycardia or supraventricular tachycardia with a ventricular rate >150 min should be treated with DC cardioversion (Chapter 121).
   • Acute atrial fibrillation: consider DC cardioversion if the ventricular rate is >140 min, after correction of hypoxia and electrolyte disorders. Otherwise, give amiodarone IV (via a central line; 300 mg in glucose 5% over 60 min, followed by 900 mg over 24 h). Most drugs used to control the ventricular rate in atrial fibrillation are contraindicated in hypotension. Digoxin is largely ineffective when sympathetic drive is high.
   • If there is severe bradycardia (heart rate <40 min), give atropine 0.6–1.2 mg IV, with further doses at 5-min intervals up to a total dose of 3 mg if the heart rate remains below 60 min. If there is little response to atropine, use an external transcutaneous pacing system or put in temporary pacing wire (Chapter 119).
3. Correct hypovolaemia:
   • If there is obvious hypovolaemia (appropriate clinical setting; low JVP with flat neck veins), give IV fluid (blood, colloid or crystalloid as appropriate to the cause). There is no role for a central line unless the patient needs inotropic medication.
   • If the evidence for hypovolaemia is less certain, but there are no clinical signs of fluid overload, give a fluid challenge, especially if the JVP is difficult to assess.
   • If systolic BP remains <90 mmHg despite correction or exclusion of hypovolaemia, search for and treat other causes of hypotension, of which sepsis is the most likely. In patients with acute bleeding, relative hypotension can be accepted until the bleeding is stopped surgically. In sepsis with prior systemic hypertension, a MAP >65 mmHg may be needed to prevent acute kidney injury.
   • There is no single value of LV filling pressure or CVP that should guide fluid replacement; instead, multiple methods should be used, including dynamic measures (e.g. pulse-pressure variability on the arterial line or the change in IVC diameter on leg raising).
   • Even in fluid-responsive patients, titrate fluid carefully to avoid hypervolaemia
   • If BP remains low, inotropic–vasopressor therapy will be needed.
4. Correct hypoxia and biochemical abnormalities:
   • Maintain PaO₂ >8kPa (60 mmHg), arterial saturation >90%.
   • Severe metabolic acidosis may contribute to hypotension. It is crucial to identify the cause of metabolic acidosis so that the correct treatment can be initiated. Causes of metabolic acidosis are given on p. 249. If arterial pH is <7.1 and falling, consider giving 50 mL of 8.4% sodium bicarbonate whilst waiting for a response to treatment of the underlying disease. Recheck arterial pH after 30 min.
5. Use inotropic/vasopressor therapy if there is refractory hypotension:
   • If systolic BP remains <90 mmHg (MAP <65 mmHg) with signs of hypoperfusion (associated with low central venous oxygen saturation) despite correction of hypovolaemia, start inotropic/vasopressor therapy whilst searching for the underlying cause.
   • Inotropes are not indicated for a low LV ejection fraction on echocardiography without signs of low cardiac output.
   • Invasive central venous and arterial pressure monitoring is recommended.
   • Choice of therapy and dosages are summarized in Tables 2.6 and 2.7.
   • Discuss with a cardiologist whether intra-aortic balloon counterpulsation (balloon pump) or left ventricular assist device is indicated as a bridge to definitive treatment (e.g. surgery for a ruptured papillary muscle).