Shock and heart failure

The core idea

Shock is inadequate tissue perfusion leading to cellular hypoxia, anaerobic metabolism and lactic acidosis. Because mean arterial pressure = cardiac output × systemic vascular resistance (SVR), every shock is a fall in cardiac output, a fall in SVR, or both. MAP is roughly diastolic pressure plus one-third of the pulse pressure; in resuscitation of septic shock, after fluids, a vasopressor (noradrenaline first) is titrated to a MAP of about 65 mmHg. Adequate resuscitation is judged by perfusion, best by a urine output of at least 0.5 mL/kg/h, falling lactate, mental state and capillary refill.

The four patterns

• Septic shock: bacterial products (endotoxin, the lipid A of Gram-negative lipopolysaccharide) activate macrophages via toll-like receptor 4, releasing TNF-alpha and IL-1. These induce inducible nitric oxide synthase; the large amount of nitric oxide is the final mediator of the vasodilatation and low SVR. Early sepsis gives warm peripheries, bounding pulses and a high cardiac output; late sepsis depresses the myocardium. In adults the urinary tract is the commonest source of Gram-negative septic shock, and elderly patients may have no urinary symptoms.
• Anaphylactic shock: IgE cross-linking triggers mast cell and basophil degranulation; histamine and leukotrienes cause vasodilatation, leaky capillaries, urticaria, angioedema and bronchospasm. First-line treatment in adults is adrenaline 0.5 mg IM (1 mg/mL).
• Neurogenic shock (cervical or high thoracic cord injury): loss of sympathetic outflow gives hypotension with bradycardia and warm, dry skin.
• Obstructive shock with tamponade: Beck's triad (hypotension, raised JVP, muffled heart sounds) and pulsus paradoxus, a fall in systolic pressure of more than 10 mmHg on inspiration. Normally inspiration slightly lowers systolic pressure. In tamponade the total heart volume is fixed by the fluid, so the inspiratory rise in right ventricular filling pushes the interventricular septum into the left ventricle, reducing LV filling and stroke volume; the normal dip is exaggerated, not reversed.

Compensation after haemorrhage, in time order

• The baroreflex is the first and fastest defence of blood pressure. When MAP falls acutely (say 100 to 60 mmHg), baroreceptor firing falls, so heart rate, contractility, total peripheral resistance and venous tone rise.
• Sympathetic constriction spares the brain and heart, which have little sympathetic constrictor control and strong autoregulation. Skin, gut, muscle and even kidney constrict hard; renal autoregulation is overridden, so oliguria appears early.
• Haemoglobin is normal immediately after a bleed because whole blood is lost; concentration falls only as interstitial fluid refills plasma or IV fluid is given, and keeps falling for a day or two as the kidney restores volume.
• Rising 2,3-BPG and acidosis shift the oxygen dissociation curve to the right, releasing more O₂ to tissues.
• A patient on a beta-blocker may not develop tachycardia; a normal pulse must not reassure in a bleeding patient on bisoprolol.

ATLS classes of haemorrhage (adult)

Systolic pressure usually holds until class III, so a young patient can look stable while losing a lot of blood. A closed femoral fracture can hide about 1–1.5 L and a pelvic fracture several litres.

Progressive and irreversible shock

If hypotension lasts long enough, compensation fails and positive feedback takes over. Low coronary perfusion causes myocardial depression, which lowers output further; vasomotor failure, capillary leak, acidosis, sludging of blood, release of toxins from ischaemic gut and disseminated intravascular coagulation follow. Eventually blood pressure no longer responds to transfusion even with a normal CVP, lactate is very high and ECG shows ischaemia. Rapid early restoration of volume prevents this transition.

Heart failure physiology

• Heart failure with reduced ejection fraction (systolic failure): weak contraction, dilated LV, EF below 40%.
• Heart failure with preserved ejection fraction (diastolic failure): a stiff, concentrically hypertrophied LV (hypertension, diabetes, ageing) relaxes poorly, so filling needs a high pressure; EF is normal, the left atrium enlarges and BNP rises. Filling depends on time and on atrial contraction, so atrial fibrillation with a fast rate can tip these patients into pulmonary oedema.
• Low output activates the sympathetic system, renin–angiotensin–aldosterone and ADH. Salt and water retention raise preload; vasoconstriction raises afterload. These help at first and harm long term (remodelling, fibrosis, congestion), which is why ACE inhibitors, beta-blockers and aldosterone antagonists improve survival. Spironolactone also corrects the hypokalaemia caused by loop diuretics.
• BNP is released from ventricular myocytes in response to stretch; it promotes natriuresis and helps diagnose heart failure.

Adult myocytes enlarge (hypertrophy) but do not divide (no hyperplasia).

Left and right heart failure

• Left failure: raised left atrial and pulmonary capillary pressure cause breathlessness, crackles and S3. Orthopnoea occurs because lying flat moves blood from the legs and abdomen into the thorax, raising pulmonary venous pressure; paroxysmal nocturnal dyspnoea adds reabsorbed oedema fluid. Chronic pulmonary congestion (for example mitral stenosis) lets red cells leak into alveoli, where macrophages ingest them and store haemosiderin: heart failure cells.
• Right failure: raised systemic venous pressure gives raised JVP, hepatomegaly and ankle oedema. The commonest cause of right failure is left failure.

Remember Find which term of MAP = CO × SVR has fallen, then check the skin and the JVP.

Exam trap Neurogenic shock combines hypotension with bradycardia; beta-blockade can also mask tachycardia in haemorrhage.

Exam trap Hb does not fall immediately after haemorrhage; red cell mass is the last thing to recover.

How FCPS asks about this

• First and fastest compensation for blood loss: arterial baroreceptor reflex; the CNS ischaemic response is the most powerful but appears only below about 60 mmHg.
• Restoration of plasma volume: transcapillary refill within hours; renal salt and water retention over 1–3 days; red cells over weeks.
• Pale, tachycardic man with normal Hb 20 minutes after a stab wound: no haemodilution yet.
• Warm shock with high cardiac output: septic or anaphylactic; final mediator of septic vasodilatation is nitric oxide; mast cell degranulation means anaphylaxis.
• Pulsus paradoxus in tamponade: inspiratory RV filling pushes the septum into the LV.
• Dilated LV with normal wall thickness in chronic MR: sarcomeres added in series (eccentric hypertrophy).
• Breathless HF patient with EF 62% and stiff thick LV: impaired relaxation (HFpEF); fast AF cuts filling time.